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Veterinary Microbiology, Concise Notes

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 2019
VETERINARY MICROBIOLOGY

Concise Notes

Notes of Veterinary Microbiology:

Writer: Farhan Qureshi
Ammar Tahir
Riaz Gul
Ammun Bashir
Salman Javeed
Hafiz Muhammad Anas
Supervision: Haroon Rashid Chaudhry
Mian Muhammad Khubaib Sattar
Muhammad Khalid Mansoor
Spiritual Mystique: Prof. Dr. Khushi Muhammad
DISCLAIMER: THIS IS AN HONEST EFFORT OF AN
UNDERGRADUATE STUDENT OF DVM, IT WAS NOT EDITED IN
ANY WAY FOR TRYING TO UNDERSTAND WHAT AN AVERAGE
STUDENT COMPREHENDS IN A LECTURE: ERRORS AND
OMISSIONS ACCEPTED, IT IS NOT TO BE USED AS REFERENCE.
OPENSOURCE, FEW COPYRIGHTS INFRINGED, APOLOGIES
Part I

THEORY LECTURES
GENERAL VETERINARY
MICROBIOLOGY
nd
DVM (2 SEMESTER)
Introductory Lecture:
General Microbiology:
General Microbiology includes physiology, biochemistry, control, growth, morphology and anatomy of
germs.

• Test/procedures take 3 minutes to 1 hour

• Pre-test takes more time (24 hours)
• Pre and post process of practical takes time
• Microbiology is not visible. It is micro.

General sizes of microorganisms:

• Bacteria — 10-6
• Virus — 10-9
• Prions — 10-10
• Fungus — 10-3-6
• Algae — 10-3-6
• These microorganisms are not visible with naked eye.
• Microbiology is a logic based or inference based study.
• Microbes are most enormous in the world.
• Level of microbes is 1012/ml or 1018/ml or 10 Trillion per ml in marshy water.
• Level of microbes in intestine is 1012/ml.
• Microbiology starts from microbiome.
• Microbiome decides the health of humans and animals or microbiome effectively controls the
health and disease status.
➢ If microbiome is normal, health is normal.
➢ If microbiome is not normal disease is caused.

SOP's in practicals:
• SOP's stands for "Standard operating procedure/protocol"
• Before each experiment, you should have SOP's.
• SOP's should be noted on practical notebook.

Introduction to microbiology:
Microbiology is the study of microbes.

Biosafety:
"Bio" means "life" and "safety" means "protection".

• Biosafety includes the safety of:

1. Product safety
2. Safety of life
Product safety:
Product safety includes:
• Safety of test
• Safety of germs

Safety of life:
 Safety of life includes:

• Safety of environment (lab, surroundings)

• Safety of personnel (Lab attendants, Lab assistants, supervisors, directors)
• Safety of surrounding populations (humans, animals, plants, faunna, flora)

Biosafety measurements in Microbiology Lab:

Following are the biosafety measurements in Microbiology lab:
i. Microbes causediseases so you should avoid direct contact with microbes.
ii. Chemicals are used to identify germs, these chemicals are toxic. You should avoid direct contact
with chemicals.
iii. Instruments of microbiology lab are costly. They should not be mishandled.
iv. Protection should be given to surrounding humans. You should not spread germs and chemicals.

Biosecurity:
Biosecurity means to provide security to personnel, building and infrastructure while working.
Infrastructure includes:

• Lock and key (guard,camera,thumb impression, retina scan)

• Equipment
• Chemicals
• Biological tests/Germs

Points:
➢ Biosafety is the protection of tests/germs in the lab.
➢ Biosecurity includes protection of tests/germs against notorious physical factors.
➢ Typhoid XDR:
• Disease spread in Karachi
• Disease spread through flies/ not properly cooked meat.
• Extreme drug resistance is produced by microbes causing the disease.

LECTURE NO.01:
Morphology of microorganisms:

• Bacteria
• Virus
• Fungus
• Algae

Bacteria:
Every bacterium has a unique shape.
Cocci (sing. Coccus):
Round shaped bacteria are called cocci.
Size:
Size ranges from 0.5 micrometer to 1 micrometer.
Example:
 • Mycoplasma ( micrococcus)
• Staphylococcus (cocci)

Division of cocci:
There are four main divisions of cocci:
i. staphylococci:
• Reproduce three dimensionally
• Grape like clusters
• For example, Staphylococcus
ii. streptococci:
• Reproduce in one dimension/single plane
• Form chains
• For example, Streptococcus
iii. tetrad:
• When cocci divide in two dimensions ( length and width ) they form tetrad.
• For example, Tetrad
iv. sarcina (p.sarcinae):
• When cocci divides in three dimensions at the same time they form a cube like structure
called sarcina.
Bacilli (sing. Bacillus ):

• Staff-like/Rod like bacteria

Size:

• Ranges from 3 micrometer to 10 micrometer in length.

• Ranges from 0.5 micrometer to 1 micrometer in width.
Division of bacillus:
There are three main divisions of bacillus:
i. streptobacillus:
• Long chains
• Divide by width
• For example, Bacillus
ii. Chinese letter formation:
• For example, Corynibacterium
iii. palisade:
• Stacks of coins
• Divide by length
• For example, Palisade
Sometimes bacteria have:

Filamentous / Branching shape:

• Like hairs
Size:

• More than 10 micrometer

• For example, Actinomycetes, Nocardia
Corkscrew:

• Spiral shaped
 • For example, Treponema, Spirilla

Comma shaped/vibrio:

• For example, Vibrio fetus( humans )

• Campylobacter (animals)

Square shaped bacteria:

• For example, hollacrula

Star shaped bacteria:

• For example, Stella

Viruses:
According to morphology viruses are of five types:
i. Enveloped:
➢ Icosahedral:
• Envelope is circular or disorganized.
• Size is 100nm
• For example Herpes viridae
• Some have size more than 100 nm (e.g. Orthomyxoviridae)
ii. Naked:
➢ Icosahedral (without envelope)
➢ Size is 30nm to 100nm
iii. Complex:
They are of two types:
i. Pox viruses:
• Large brick like
• Size is 300nm to 1500nm
ii. Bacteriophage:
• Size is 50nm
iv. Filamentous viruses:
• They have length in mm
• They have width in nm
• For example , Filonidae
v. Mega viruses:
• Live in insects and protozoans
• Not important for humans and animals
• Size is in micrometers
• For example, Megavirales

Fungus:
Fungus is of two types:
1. Unicellular
2. Multicellular
• Unicellular:
• Unicellular fungus is called yeast.
• They are round in shape
• Their size is 5 micrometer to 10 micrometer
• Overall range of size is 5 micrometer to 40 micrometer
• Maximum size is 40 micrometer
• For example, Saccharomyces
• Multicellular:
 • They have mycelium ,aerial spores and aerial hyphae
• Size is more than 10 micrometer
• For example, Aspergillus
➢ Some fungi are dimorphic/ bimorphic because they can exist as both unicellular and
multicellular at different temperatures.

Algae:
• Diverse in size
• Used as food source
• Photosynthetic
• They can cause poisoning but yeast cannot cause poisoning
• Size is 5 micrometer to 40 micrometer
• Blue Green algae have the size of 5 micrometer
• There isno algae of veterinary importance up till now.

LECTURE NO. 02:

Prokaryotes vs. Eukaryotes
Sr. No. Prokaryotes Eukaryotes

Term Before nucleus True nucleus

Primitive Modern

Groups Bacteria, Archeobacteria Algae, fungi, plants,

animals

Origin 3.5 billion years ago 2 billion years ago

Size 0.5 - 3 micrometer More than 5 micrometer

Cells Unicellular Unicellular/ Multicellular

Complexity Simple Complex

Nucleus location Free Center

• Free, attached to • Bounded in

cell membrane nucleus

• Circular • Linear

• One in bacteria, • Two or more than

two in some two in Eukaryotes
DNA
• Replication, • Replication and
transcription, translation takes
translation takes place in cytoplasm,
place in cytoplasm transcription takes
at the same time place in nucleus
but not at the same
• Cell membrane time
aids in genomic
process • No aid by cell
membrane in
genomic process
 Nuclear membrane None Yes

Nucleolus Absent Present

Chromosomes Usually one More than one

Chromosome shape Circular Linear

Operon Individually
Genes Multiple genes for a single Single gene for single
process process

DNA bases (G+C ratio) 28 - 73 40

DNA wrapping Non histonic proteins Histone proteins

Absent Present

• Inclusion bodies (Nucleus, E.R, Golgi

are present. apparatus, lysosome,
Membrane based mitochondria etc)
organelles • Respiration takes
place at the cell
membrane

Ribosomes 70S (50S+30S) 80S (60S+40S)

Ribosomal region Cell membrane or free Endoplasmic reticulum

Mitochondria Absent Present

Chloroplast If present, chlorophyll is Present, chlorophyll within

scattered chloroplast

Microtubules/
cytoskeleton/ cell
movement Simple or absent Present

Cell membrane No sterols Sterols

Cell wall Peptidoglycan or muramic Starch/ Chitin

acid

Reproduction Simple/ binary fission Complex (2 gametes)

Basal metabolic rate High Low

Fimbrae/ flagella/ cillia Simple Complex

LECTURE NO.03:
Introduction to Microbiology
The word “Microbiology" is derived from Greek words:

MIKROS → small

BIOS → life

LOGIA → study

• It is the study of microorganisms either unicellular, multicellular or acellular.

• Microbiology includes disciplines of Virology, Mycology, Bacteriology etc.

Prokaryotic Vs. Eukaryotic Organisms:

• Prokaryotic microorganisms are conventionally classified as lacking organelles and
includes:
→Eubacteria
→Archaebacteria
→Blue Green Algae
➢ Eukaryotic microorganisms exhibit cell organelles and include:

→Fungi

→Protists

→Algae
Additional Points:

• Only 1% of microorganisms are studied by culturing.

• The microorganisms which can be grown in culture media are studied by using
Molecular Biology. Their molecular study includes study of DNA, RNA & genes.

• Prions caused a disease called “Wasting Dear/Zombie Dear disease in America.

How Microbiologists Study Microbes:

Microbiologists traditionally relied on culture, staining and microscopy. However, 1% of
Microbes present in the environment are culturable. That's why Microbiologists often
rely on extraction or detection of nucleic acids either DNA or RNA.
Viruses & Prions:
• Viruses are not always classified as organisms as they have been identified either
as very simple microorganisms or very complex molecules.
• Prions are never considered as microorganisms and they have been investigated
by the virologists as the clinical effects traced to them were originally presumed
due to chronic viral infections and virologists identified them as “infectious agents.
Following are some infectious
→Mad cow disease in cattle.
→Scrapie disease in sheep.
→Wasting deer / Zombie deer disease in deers (America).

BRANCHES OF MICROBIOLOGY:
Two broad branches of Microbiology are as follows:
1. Pure Microbiology
2. Applied Microbiology
Pure Microbiology:
It includes the study of Microbes only for the sake of
study. No benefits or loses are studied. Pure
Microbiology has further seven divisions:

1. Bacteriology:
Study of bacteria is called Bacteriology.

2. Mycology:
Study of fungi is called Mycology.
3. Phycology:
Study of algae is called Phycology.

4. Immunology:
Study of immune system is called immunology.
5. Virology:
Study of viruses is called virology.

6. Microbial Physiology:
Study of microbial cell functions is called Microbial Physiology. It includes the study of
microbial growth, metabolism & cell functions.

7. MicrobialCytology:
Study of microscopic & sub-microscopic details of microorganisms is called Microbial
Cytology.
• APPLIED MICROBIOLOGY:
Study of microorganisms to determine benefits as well as
harmful effects of microorganisms.
Applied Microbiology is further divided into four branches:
1.Veterinary Microbiology:
Study of microbes of Veterinary importance such as probiotics & pathogens which
are related to Veterinary medicine.

2.Pharmaceutical Microbiology:
Study of microorganisms which are related to the production of antibiotics,
enzymes, vitamins, biologics and other pharmaceutical products & those microbes
which cause pharmaceutical contamination & spoilage.
3. Microbial Biotechnology:
Manipulation of microorganisms at genetics & molecular level to generate useful
products is called Microbial Biotechnology e.g. production of insulin from E.coli.

4. Food Microbiology:
Study of microorganisms causing food spoilage and food
borne illness. Use of microbes to produce food is called food Microbiology.
 • HISTORY OF MICROBIOLOGY:
Ancient History of Microbiology:
• Recent discovery of Mycobacterium DNA in the three thousand years old Egyptian
mummies reminds us that microorganisms have been around for a much longer
period of time.
• Infact, bacterium ancestors were the first living cells to appear on the earth.

Golden Age of Microbiology:

From 1857-1940 has been named Golden age of Microbiology. During this period, rapid
advancement spread hold mainly by Pasture & Robert Koch which led to the
establishment of
Microbiology as a science. During this era, salient achievements include;

➢ Discovery of immunity
➢ Discovery of disease causing agents
Koch's Postulates:
• Robert Koch a Germen physician discovered the cause of Anthrax (Bacillus
anthracis) in 1870s.
• He devised a theory relating micro-organisms to every specific disease. The
POSTULATES of that theory are as under.
• Same pathogen must be present in every case of the disease.
• Pathogen must be isolated from the diseased host & grown in a pure culture.
• Pathogen from the pure culture must cause the disease when it is inoculated into
susceptible lab. animal.
• The same pathogen must be isolated from the inoculated animal and it must be
same as original organism.

Vaccination:
Edward Jenner, a young British physician used scrapping of cowpox blisters to
vaccinate against smallpox.
• Edward Jenner is called the father of Vaccinology.
Fermentation:
• Microorganisms like yeast convert sugar into alcohol in the absence of air. This
process is called Fermentation.
• It is used to make wine & beer.
• In the presence of air bacteria converts alcohol into acetic acid or vinegar.

Pasteurization:
• It is the heat treatment of beverage & milk at 72°C for 30 minutes to kill
microorganisms (which cause spoilage of liquid in food) without compromising
on its quality.
• Now a day, it is only used for milk products.

Germ Theory of Disease:

• Microorganisms are the cause of diseases. In 1860's Joseph Lister used phenol,
carbolic acid as a disinfectant & antiseptic solution.
• This practice reduced the incidence of infection & death. Other surgeons readily
adopted it.
• Lister's technique was the earliest medical attempt to control infection caused by
microorganisms.
LECTURE NO.04:
SIZE OF BACTERIA:
Many sizes and most bacteria range from:

• 0.2 to 2.0 μm in diameter

• 2 to 8 μm in length
• Overall average size 1-10 μm .

SHAPE OF BACTERIA:
• Spherical / coccus (plural: cocci; means rounded)
• Rod Shaped / bacillus (plural: bacilli)
• Spiral
Cocci:
Cocci are usually round but can be oval or elongated. When they divide to reproduce,
they remain attached to each other.

CLASSIFICATION ACCORDING TO PLANE OFDIVISION:

Dipplococci:
Those cocci that remain in pairs after dividing are called diplococci.

Streptococci:
Those cocci that divide and remain attached in chainlike patterns are called streptococci.
Tetrad:
Those cocci that divide into two planes and remain in groups of four are known as
tetrads.

Sarcinae:
Those cocci that divide in three planes and remain attached in cube like groups of eight
is called sarcina.

Staphylococci:
Those cocci that divide in multiple planes and form grapelike clusters or broad sheets
are called staphylococci.

BACILLI:
Bacilli are the rod like bacteria e.g. Bacillus anthracis

Single bacillus:
Most bacilli appear as single rods, called single bacilli.
Diplobacilli:
Those bacilli which appear in pairs after division are called Diplobacilli.

Streptobacilli:
Those bacilli that are found in chains in single plane are called Streptobacilli.

MONOMORPHIC VS PLEOMORPHIC:
• Bacteria that maintain a single shape are called monomorphic or the bacteria
having same shape.
• Some bacteria can have many shapes known as pleomorphic. e.g.:
Corynebacterium pyogenese.
• Some bacteria occur in the shape of a star e.g. Stella.
• Some bacteria occur in the shape of rectangle e.g. Haloarcula.
• Some bacteria also appear triangular in shape.

FUNCTIONAL ANATOMY OF BACTERIA:

Cell Wall:
Acts as an antigen, provide protection and rigidity

Cell membrane:
Serve as a barrier through which materials enter and exit the cell

Capsule:
Acts as an antigen, has feeding importance, sticking features and cause disease

Mesosomes:
Has role in metabolism
FUNCTIONAL ANATOMY OF BACTERIA:
Fimbrae:
Helps in motility, jerky movement, has sticking feature and acts as an antigen

Pilus:
Helps in reproduction (conjugation)

Ribosomes:
Protein formation

Nucleoid:
Transcription and translation

FUNCTIONAL ANATOMY OF BACTERIA:

Chromosomes:
Hereditary material

Droplets:
Helpful in storage

Flagella:
Act as an antigen and helps in motility

Plasmid:
Have special features of resistance and infection.
LECTURE NO.05:
CULTURE MEDIA / GROWTH MEDIA
A nutrient material prepared for the growth of microorganisms in a laboratory is called a culture
medium.

• Solid / Semi-solid media known as Nutrient Agar

• Liquid media known as Nutrient Broth

INOCULUM:

Microbes that are introduced into a culture medium to initiate growth are called an inoculum24

PROPERTIES OF CULTURE MEDIA

1. It must contain the right nutrients for the specific microorganism we want to grow.i.e. MacConkey
Agar contains bile salt which is required for the growth of E. coli.

2. It should also contain sufficient moisture.

3. The pH of media must be properly, adjusted as per requirement of microorganism to be grown e.g.
pH 7.0-7.2 for bacteria and 5.5-5.6 for fungi.

4. Suitable level of oxygen or no oxygen at all.

5. The medium must initially be sterile that means it must initially contain no living microorganisms.
Most of these media, which are available from commercial sources, have premixed components and
require only the addition of water and then sterilization.25

AGAR & ITS PROPERTIES

When it is desirable to grow bacteria on a solid medium, a solidifying agent such as agar is added in a
medium. Agar is a complex polysaccharide derived from marine algae.

Properties of Agar
➢ Only a few microbes can degrade agar, so it remains solid.
• Agar liquefies at about 100°C (the boiling point of water) and at sea level remains liquid until
the temperature drops to about 40-45 degree celcius
• Agar media are usually contained in test tubes or petri dishes. The test tubes are called slants.

When they are allowed to grow microaerofiles with the tube held at an angle so that a large surface
area for growth is available. It has two portions

• Slant
• Butt

CHEMICALLY DEFINED MEDIA

Chemically defined media is that media whose exact chemical composition is known.

• Organisms that require many growth factors are described as fastidious.

• Organism of this type such as Lactobacillus are sometimes used in test that determines the
concentration of a particular vitamin in a substance.

Composition of Staphylococcus Medium 11025

COMPLEX MEDIA
These media are made up of nutrients including extracts from yeast, meat, plants or digests of protein
from these and other sources.

Composition of nutrient agar

REDUCING MEDIA
These media contains ingredients such as sodium thioglycolate that chemically combine with dissolved
oxygen and deplete the oxygen in the culture medium.

SELECTIVE MEDIA
Such type of media which suppress the growth of unwanted bacteria and encourages the growth of
desired microbes. e.g;

• Bismuth sulphite agar is one medium used to isolate the gram’negativeSalmonella typhi from
faeces.
 Salmonella typhi(GROWTH ON BISMUTH SULPHITE AGAR)

➢ Sabouraud’s dextrose agar which has a pH of 5.6 is used to isolate fungi that outgrows most
bacteria at this pH.

DIFFERENTIAL MEDIA

Such type of media which makes it easier to distinguish colonies of the desired organisms from other
colonies growing on the same plate.

• On blood agar, some bacteria show alpha haemolysis while other shows beta haemolysis.

• On manitol salt agar, Staphylococcus aureus produces yellow colonies while

Staphylococcusepidermis produces pink colonies
pH indicator phenol red

In Basic pH, color is RED

In Acidic pH, color is Yellow

On Eosin Methylene Blue (EMB) agar, E. coli produces black centered colonies with metallic sheen
while Enterobacter aerogenes gives dark centered colonies.

MACCONKEY AGAR IS A SELECTIVE AS WELL AS DIFFERENTIAL MEDIA. IT IS SELECTIVE AS IT ONLY

ALLOWS ENTERIC BACTERIA TO GROW AND DIFFERETIAL AS E. coli GIVES PINK COLOURED COLONIES
ON IT.

ENRICHMENT CULTURE MEDIA

• It is usually liquid and provides nutrients and environmental conditions that favor the growth of
a particular microbe but not others. It is also a selective medium but designated to increase
very small numbers of the desired type of organism to detachable levels e.g.;

Selenite F broth for the enrichment of Salmonella Species

LECTURE NO.06:
Transformation in bacteria
Transformation:

• Genes are transferred from one bacterium to another as naked”DNA in solution.

• First demonstrated over 70 years ago
• Not understood at that time
• Study of this phenomenon eventually led to the conclusion that DNA is the genetic material

Griffith’s Experiment:
The initial experiment on transformation was performed by Frederick Griffith in England in 1928 while
he was working with two strains of Streptococcus pneumoniae.

• One, a virulent strain, has a polysaccharide capsule that prevents phagocytosis. The bacteria
grow and cause pneumonia.
• The other, an avirulent strain, lacks the capsule and does not cause disease.
Purpose of Griffith’s Experiments:
• Griffith was interested in determining whether injections of heat-killed bacteria of the
encapsulated strain could be used to vaccinate mice against pneumonia.

➢ Prepare Killed Vaccine

First Experiment & Result:

• Injections of living encapsulated bacteria killed the mouse

Second Experiment & Result:

• Mice were injected with live non-encapsulated bacteria and

remained healthy

Third Experiment & Result:

• Dead encapsulated bacteria did not kill the mouse.

Fourth Experiment & Result:

➢ The dead encapsulated bacteria were mixed with live non-
encapsulated bacteria and injected into the mice, the mice died. In
the blood of the dead mice, Griffith found living, encapsulated
bacteria.
• Hereditary material (genes) from the dead bacteria had entered the
live cells and changed them genetically so that their progeny were
encapsulated and therefore virulent.
Bacterial Transformation in Broth:
Subsequent investigations based on Griffith’s research revealed that bacterial transformation could be
carried out without mice. A broth was inoculated with live non-encapsulated bacteria. Dead
encapsulated bacteria were then added to the broth. After incubation, the culture was found to
contain living bacteria that were encapsulated and virulent. The non-encapsulated bacteria had been
transformed; they had acquired a new hereditary trait by incorporating genes from the killed
encapsulated bacteria.

Components which caused Transformation:

Crucial experiments were performed in the United States by

• Oswald T. Avery and his associates

• Colin M. MacLeod
• Maclyn McCarty
• After years of research, they announced in 1944 that the component responsible for
transforming harmless S. pneumoniae
into virulent strains was DNA.
• Their results provided one of the
conclusive indications that DNA was
indeed the career of genetic
information.

Mechanism of Genetic Transformation in Bacteria:

• After death and cell lysis, bacteria, release their DNA into the environment.
• Other bacteria take up fragments of DNA and integrate them into their own chromosomes by
recombination.
• A protein called RecA binds to the cell’s DNA and then to donor DNA causing the exchange of
strands.
• A recipient cell with this new combination of genes is a kind of hybrid, or recombinant cell.
 • All the descendants of such a recombinant cell will be identical to it.
• Transformation occurs naturally among very few genera of bacteria, including Bacillus,
Haemophilus, Neisseria, Acinetobacter and certain strains of the genera Streptococcus and
Staphylococcus.

Competent and Competence:

• When a recipient cell is in a physiological state in which it can take up the donor DNA, it is said
to be competent. Competence results from alterations in the cell wall that makes it permeable
to large DNA molecules.
Lecture NO.07
Conjugation in Bacteria:
• Bacterial conjugation is the transfer of genetic material between bacterial cells by direct cell-to-
cell contact or by a bridge-like connection between two cells.
• Conjugation is mediated by one kind of plasmid that replicates independently from the
chromosomal DNA.
➢ The plasmids responsible for conjugation are transmissible between cells during conjugation.

Conjugation Vs. Transformation:

Conjugation differs from transformation in two major ways.

1. Conjugation requires direct cell-to-cell contact.

2. The conjugating cells must generally be of opposite mating type

• Donor cells must carry the plasmid

• Recipient cells usually do not carry that specific plasmid.
Conjugation in Gram Negative Bacteria:
In gram-negative bacteria, the plasmid carries genes that code for the synthesis of sex pilli that contact
the recipient and help bring the two cells into direct contact.

Conjugation in Gram Positive Bacteria:

Gram-positive bacterial cells produce sticky surface molecules that cause cells to come into direct
contact with each other (mating bridge).

Plasmid Replication in Conjugation:

In the process of conjugation, the plasmid is replicated during the transfer of a single-stranded copy of
the plasmid DNA to the recipient, where the complementary strand is synthesized.
1. Process of conjugation:
In E.coli, the F factor (fertility factor) was the first plasmid observed to be transferred between cells
during conjugation.

Donors carrying F factors (F+ cells) transfer the plasmid to recipients (F- cells), which become F+ cells
as a result.

2. Process of conjugation:
In some cells carrying F factors, the factor integrates into the chromosome, converting the F+ cell to an
Hfr cell (high frequency of recombination).

3. Process of conjugation:

• When conjugation occurs between an Hfr cell and an F- cell, the Hfrcell’s chromosome (with its
integrated F factor) replicates, and a parental strand of the chromosome is transferred to the
recipient cell.
• Replication of the Hfr chromosome begins in the middle of the integrated F factor, and a small
piece of the F factor leads the chromosomal genes into the F- cell. Usually, the chromosome
breaks before it is completely transferred.
• Once within the recipient cell, donor DNA can recombine with the recipient’s DNA. (Donor DNA
that is not integrated is degraded.)
• Therefore, by conjugation with an Hfr cell, an F- cell may acquire new versions of chromosomal
genes. However, it remains an F- cell because it did not receive a complete F factor during
conjugation.
Application of Conjugation for Mapping Gene Location:

• Conjugation is used to map the location of genes on a bacterial chromosome

➢ The genes for the synthesis of threonine (thr) and leucine (leu) are first, reading clockwise from
0.

Their locations were determined by conjugation experiments. Assume that conjugation is allowed for
only 1 minute between an Hfr strain that is his +, pro+, thr+, and leu+, and an F- strain that is his-, pro-,
thr-, and leu-.

If the F- acquired the ability to synthesize threonine, then the thr gene is located early in the
chromosome, between 0 and 1 minute. If after 2 minutes the F - cell now becomes thr+ and leu+, the
order of these two genes on the chromosome must be thr, leu37.
LECTURE NO.08:
TRANSDUCTION IN BACTERIA:
TRANSDUCTION:
Transfer of bacterial DNA from a donor cell to a recipient cell inside a virus that infects bacteria
(Bacteriophage) is called Transduction.

BACTERIOPHAGE:
These are group of viruses involved in transfer of genetic material from one bacterium to the other.
The carrier phage is called transducer or vector.

HISTORY OF TRANSDUCTION:

• Transduction was first described by Joshua Lederberg & Norton Zinder in 1952. Bacteriophage
are widely used as vectors in recombinant DNA Technology.
GENERALIZED TRANSDUCTION:

• Generalized transduction is mediated by phages where any DNA segment can be transferred by
the virus and may not integrate the segment to the bacterial chromosome.
• Here a portion of the donor bacterial DNA accidently get enclosed in a capsid.
• Upon lysis and further infection of the virus particle to another bacterium, the genetic material
of the donor is released and recombination occurs between the injected DNA segments and
homologous part of the recipient chromosome, forming a rDNA.
• All genes contained within a bacterium infected by a generalized transducing phage are equally
likely to be packaged in a phage coat and transferred.

SPECIALIZED TRANSDUCTION:

• Only certain bacterial genes are transferred by specialized transduction.

• In one type of specialized transduction, the phage codes for certain toxins produced by their
bacterial hosts, such as diphtheria toxin for Corynebacterium diphtheriae and erythrogenic toxin
for Streptococcus pyogenes, and Shiga toxin for E. coli O157:H7 are transferred by specialized
transduction.
COMPLETE TRANSDUCTION:

• In complete transduction, the transduced DNA fragment gets integrated within the recipient
bacterial chromosomes, forming a recombinant chromosome.
• This DNA fragment replicates along with recipient bacterial chromosome replication and passed
on to the daughter cells.

ABORTIVE TRANSDUCTION:

• In abortive transduction, the transduced DNA fragment may not get integrated within the
recipient bacterial chromosome, and remains in the cytoplasm as free particle.
• These DNA fragments cannot undergo replication.

LECTURE NO.09:
Fungal Spores:
Fungal Reproduction:

• Filamentous fungi can reproduce asexually by fragmentation of their hyphae.

• Both sexual and asexual reproduction in fungi occurs by the formation of spores.
• Fungi are usually identified by spore type.

Bacterial Endospore Vs. Fungal Spore:

• Fungi reproduce by producing cells called spores.

• While these fungal spores are somewhat resistant to destruction they are not usually
pathogenic to humans.
• Certain bacteria can produce a thick walled spore structure which allows them to survive
adverse environmental conditions for prolonged periods of time.
• The bacterial spore is more properly called an endospore because its function is to protect the
bacterial DNA from destruction by conditions or substances in the environment that destroy
non-endospore forming bacteria.
Fungal Spores Types:

• Spores are formed from aerial hyphae in a number of different ways, depending on the species.

There are two types of fungal Spores

• Asexual Spores
• Sexual Spores

1. Asexual spores:

These are formed by the hyphae of one organism.

When these spores germinate, they become organisms that are genetically identical to the
parent.
• Asexual spores are produced by an individual fungus through mitosis and subsequent cell
division; there is no fusion of the nuclei of cells.
• Two types of asexual spores are produced by fungi.
• Sporangiospore
• Conidiospore

1) Sporangiospore:
It is formed within a sporangium, or sac, at the end of an aerial hypha called a sporangiophore. The
sporangium can contain hundreds of sporangiospores. Such spores are produced by Rhizopus.
2) Conidiospore:
Conidiospore, or conidium (plural: conidia), a unicellular or multicellular spore that is not enclosed in a
sac. Conidia are produced in a chain at the end of a conidiophore. Such spores are produced by
Penicillium and Aspergillus

Arthroconidia:

Conidia formed by the fragmentation of a septate hypha into single, slightly thickened cells are called
arthroconidia
Blastoconidia:
Another type of conidium, blastoconidia, are formed from the buds of its parent cell. Such spores are
found in some yeasts, such as Candida albicans and Cryptococcus.

Chlamydoconidium:
A chlamydoconidium is a thick-walled spore formed by rounding and enlargement within a hyphal
segment. A fungus that produces chlamydoconidia is the yeast Candida albicans.
Sexual spores:

• It results from the fusion of nuclei from two opposite mating strains of the same species of
fungus.
• Sexual spores require two different mating strains and so are made less frequently than asexual
spores.
• Organisms that grow from sexual spores will have genetic characteristics of both parental
strains.
• A fungal sexual spore results from sexual reproduction, which consists of three phases:

1. Plasmogamy: A haploid nucleus of a donor cell (+) penetrates the cytoplasm of a recipient cell (-).

2. Karyogamy: The (+) and (-) nuclei fuse to form a diploid zygote nucleus.

3. Meiosis: The diploid nucleus gives rise to haploid nuclei (sexual spores), some of which may be
genetic recombinants
LECTURE NO.10:
"Viral Replication"
Introduction:

• Replication of virus is very complicated process.

• Viruses never reproduce by division.
• They are replicated by a process in which all components of virus are produced separately and
are assembled into intact virons.
• For replication of virus host is necessary
• Visuses are host specific.
• Host may be a bacteria, plant or an animal.
• Replication of viruses is studied for first time by experimenting on bacteriophage of the T series
[T2 , T4 and T6].

There are 2 types of life cycle commonly seen in viruses They are:

i] Lytic Cycle

ii] Lysogenic Cycle

Key steps in the Viral Replication Cycle:

• Attachment
• Penetration (Entry)
• Uncoating
• Genome replication
• Assembly
• Maturation
• Release
1. Attachment:

• Virus are host specific and enters into the host or target cell
• This event is electrostatic, does not require any cellular or metabolic energy
• Virus exhibits cellular tropism
HIV T lymphocytes, macrophages

Rabies Muscle, neurons

Hepatitis A, B, C Liver(hepatocytes)

➢ Virus has host range and it may be narrow or broad

• Rabies virus is an example for broad range virus
• HIV is an example for broad range virus
• Viruses use receptors and anti-receptors for attachment and entry into host cell.
• Cellular receptors and anti-receptors are mostly protein but sometimes they may be
glycoprotein, carbohydrates or lipids.
• The presence of virus specific receptors is necessary.
• For example HIV- CD4 receptor, Rabies-Acetylcholine, phospholipids.
2) Penetration [entry]:
Penetration is energy dependent process. Virus may penetrate into host by:

• Endocytosis
• Translocation
• Fusion

3) Uncoating:

• Refers to the removal or degradation of capsid (uncoating), there by releasing the genome into
host cell.
• The virus genome is transported to the site where transcription/replication can begin.
• In some there is no degradation of capsid as capsid proteins play a role in viral transcription and
replication

4) Genome replication:

• Viral genetic material or genome is multiplied within the host

• Simultaneously viral structural proteins like capsids are synthesised
• Type of genetic material varies from virus to virus
• With respect to this all viruses are divided into seven groups by Dr. David Baltimor in 1971
• Dr. David Baltimor shared “ NOBEL PRIZE “with Renato Dulbecco, Howard Martin Temin in 1975
for their work on "interaction between tumor viruses and the genetic material of the cell".

Seven groups as follows:

• Double stranded DNA

• Single stranded DNA
• Double standard RNA
• Single stranded (+)ve sense RNA
• Single stranded (-)ve sense RNA
• Single stranded (+)ve sense RNA with DNA intermediate
• Double stranded DNA with RNA intermediate
1.Double stranded DNA:

Replication of genome of double stranded DNA virus

Example:Poxvirus, Herpes virus.

II. Single stranded DNA:

Replication of genome of single stranded DNA virus

Example: Pircovirus, Parvovirus

III. Double stranded RNA:

Replication of genome of double stranded RNA virus

Example: Reoviruses, Orbibiruses

IV. Single stranded (+)ve sense RNA:

Replication of genome of +sense single stranded RNA virus

Example: Toga virus& Hepatitis E virus.

V. Single stranded (-
)ve sense RNA:

Replication of genome of -sense single stranded RNA virus

Example: Rabies, Paramyxoviruses etc.

vi. Single stranded (+)ve

sense RNA with DNA
intermediate:

Replication of genome of single stranded (+)ve sense RNA virus with DNA intermediate

Example: Retrovirus
VII. Double stranded DNA
with RNA intermediate:

Replication of genome of double stranded DNA virus with RNA intermediate

Example: Hepadnaviruses

5)Assembly:

• Involves the collection of all components necessary for formation of viron.

• It takes place
at a

particular site in the cell.

• For example in pox viruses assembly occurs in the cytoplasm; in adenovirus it occurs in nucleus.

6) Maturation:
➢ Maturation is the stage of life cycle at which the virus becomes infectious.
• It involves structural change in virus particles.
 • For some
viruses

maturation occurs only after release of viurs particle from the cell.

7) Release:

• Newly formed viruses are released to outside of the cell either by lysis (as in bacteriophage) or
by budding(as in paramyxovirus, retrovirus)
• Generally non enveloped viruses release by cell lysis which results in the death of host cell
• Release of virus by budding may or may not kill cell

Conclusion:

In general terms, virus replication involves three broad stages carried out by all types of virus; the
initiation of infection, replication and expression of the genome, and, finally, release of mature virions
from the infected cell. At a detailed level, there are many differences in the replication processes of
different viruses which are imposed by the biology of the host cell and the nature of the virus genome.
It is possible to derive an overview of virus replication and the common stages which, in one form or
another, are followed by all viruses.

LECTURE NO.11:
General Characteristics of Viruses:
Virus:

• The word virus, is a Latin word means poison.

• In 1935, Wendell Stanley, an American chemist, isolated tobacco mosaic virus, making it
possible for the first time to carry out chemical and structural studies on a purified virus. At
about the same time, the invention of the electron microscope made it possible to see viruses.
Viral Size:
➢ Viruses range from 20 to 1000 nm in
length.
• Different viruses vary considerably in
size.
• Although most are quite a bit smaller
than bacteria, some of the larger viruses. For example: Adenovirus 90 nm, Poliovirus 30 nm.

General
Properties of Virus:

• Viruses are inert/crystalline outside the body of host as soon as they come into the host they
become living.
• They are obligatory intracellular parasites as, they absolutely require living host cells in order
to multiply.
 Distinctive
features of Viruses:

• Contain a protein coat (sometimes itself enclosed by an envelope of lipids, proteins, and
carbohydrates) that surrounds the nucleic acid.
➢ Multiply inside living cells by using the synthesizing machinery of the cell.
• Cause the synthesis of specialized structures that can transfer the nucleic acid to other cells.
➢ Virus contains a single type of nucleic acid, either DNA or RNA. (Both in a single virus not
present)
• Viruses have few or no enzymes of their own for metabolism.
• They lack enzymes for protein synthesis and ATP generation.
• To multiply, viruses must take over the metabolic machinery of the host cell.

Host Specificity

• Viruses are host specific.

• Most viruses are able to infect specific types of cells of only one host species
• In rare cases, viruses cross the host-range barrier, thus expanding their host range.
• The particular host range of a virus is determined by following factors;
• Virus ligand molecules which binds to certain receptors on host cell
• Availability within the potential host of cellular functions required for viral multiplication.
 • For the
virus to
infect
the host
cell, the
outer

surface of the virus must chemically react with specific receptor sites on the surface of the cell.

Viral Structure:

• Viruses may be Hexagonal, Octagonal or

have any other shape and have a 3D
structure.
• A virion is a complete, fully
developed, infectious viral particle
composed of nucleic acid and
surrounded by a protein coat outside of a
host cell, and is a vehicle of transmission
from one host cell to another.

1. Nucleic Acid:
 • A virus can have either DNA or RNA—but never both. The nucleic acid of a virus can be single-
stranded or double-stranded. There are viruses with the following possibilities as their genome.
• double-stranded DNA (dsDNA)
• Single-stranded DNA (ssDNA)
• Double-stranded RNA (dsRNA)
• Single-stranded RNA (ssRNA)
• +ve sense (Positive Sense)
• –ve sense (Negative Sense)
• Depending on the virus, nucleic acid can be linear or circular.
• In most of the RNA viruses (such as the influenza virus) the nucleic acid is in several separate
segments and called segmented genome.

2. Capsid and Envelope:

• The nucleic acid of a

virus is protected by a
protein coat called the
capsid.
• Each capsid is composed of protein subunits called capsomere.
➢ In some viruses, the proteins composing the capsomeres are of a single type.
• In other viruses, several types of protein may be present in a particular virus.
• In some viruses, the capsid is covered by an envelope which usually consists of some
combination of lipids, proteins, and carbohydrates which is derived from the host cell
membrane.
➢ Some viruses are not covered by an
envelope are known as Naked Virus /
non-enveloped viruses.
➢ The capsid of a non-enveloped
virus has following functions;
• protects the nucleic acid from
nuclease enzymes in biological
fluids
• promotes the viral attachment to susceptible host cells

• Depending on the virus, envelopes may or

may not be covered by spikes.
• Spikes are carbohydrate-protein
complexes that project from the surface of
the envelope.
• Some viruses attach to host cells by means of spikes.
• Spikes are such a reliable characteristic of some viruses that it can be used as a means of
identification.
• The ability of certain viruses, such as the influenza virus to clump red blood cells is associated
with spikes.
• Such viruses bind to red blood cells and form bridges between them. The resulting clumping is
called Hemagglutination.
LECTURE NO.12:
BACTERIAL GROWTH & MULTIPLICATION
Binary Fission:

• Normally bacteria reproduce by binary fission.

• It is asexual reproduction by a separation of the body into two new bodies. In the process of
binary fission an organism duplicates its genetic material and then divides into two parts, with
each new organism receiving one copy of DNA.
Budding:

• A few bacterial species reproduce by budding; they form a small initial outgrowth (a bud) that
enlarges until its size approaches to the parent cell and then it separates.
Generation Time:
➢ Time period required for a cell to divide is called the generation time. Some bacteria like E. coli
require 20 minutes for doubling under favorable condition while others like
Mycobacteriumtuberculosis requires 24 hours for doubling under favorable condition.

LOGARITHMIC PRESENTATION OF BACTERIAL POPULATION:

A few bacteria are inoculated into a liquid growth medium and the population is counted at intervals, it
is possible to plot bacterial growth curve that shows the growth of cells over time.

PHASES OF GROWTH:

• Lag Phase
• Log Phase
• Stationary Phase
• Death Phase
LAG PHASE:

• The period of little or no cell division is called the lag phase and it can last for 1 hour or several
days. The microbial population is undergoing a period of intense metabolic activity involving
synthesis of enzymes and various molecules.

LOG PHASE / EXPONENTIAL GROWTH PHASE:

• In this period, eventually cells begin to divide and enter a period of growth or logarithmic
increase called the log phase or exponential growth phase.
• Cellular reproduction is most active during this period and as the generation time is constant,
logarithmic plot of growth during the log phase is a straight line. The log phase is the time when
cells are most active metabolically and is referred for industrial purposes where a product is
needed to be produced efficiently.
STATIONARY PHASE:

• If the exponential growth continues unchecked, a large no. of cell could arise.
• For example, a single bacterium weighing 9.5x10 -11 gm / cell dividing every 20 minute for 24
hours can theoretically produce a huge mass of population but in reality, this does not happen.
• In this period, the growth rates slow down and the no. of microbial cell death balances the no.
of new cell and the population stabilizes. The metabolic activities of individual cell surviving also
slow at this stage.
DEATH PHASE / DECLINE PHASE:

• The no of deaths eventually exceeds the no. of new cells formed and the population enters the
death phase or logarithmic decline phase. This phase continues until the population is
diminished to a tiny fraction of the no. of cells in the previous phase or the population dies out
entirely. Many bacterial cells often undergo involution during this phase, meaning that their
morphology changes dramatically and makes them difficult to identify.

LECTURE NO.13:

Replication / Multiplication of Viruses

DNA Viruses, RNA Viruses & Retroviruses

Multiplication of Animal Viruses:

• For replication, a virus needs live host cells but it must stop synthesis of host proteins, so that
viral genes are translated.
• Research indicates that viruses use several mechanisms to inhibit expression of host cell genes.
Early proteins translated from the viral genome may block transcription, existing mRNA, or in
progress translation.
Attachment:

• Animal viruses have attachment sites that attach to complementary receptor sites on the host
cell’s surface.
• The receptor sites of animal cells are proteins and glycoproteins of the plasma membrane.
Moreover, animal viruses don’t possess appendages like the tail fibers of some bacteriophages.
• The attachment sites of animal viruses are distributed over the surface of the virus, and the
sites themselves vary from one group of viruses to another.
• In adenoviruses, which are icosahedral viruses, the attachment sites are small fibers at the
corners of the icosahedron.
• In many of the enveloped viruses, such as influenza virus, the attachment sites are spikes
located on the surface of the envelope. As soon as one spike attaches to a host receptor,
additional receptor sites on the same cell migrate to the virus. Attachment is completed when
many sites are bound
• Receptor sites are proteins of the host cell. The proteins have normal functions for the host and
are hijacked by the virus.
• Understanding the nature of attachment can lead to the development of drugs that prevent
viral infections. Monoclonal antibodies that combine with a virus’s attachment site or the cell's
receptor site may soon be used to treat some viral infections.

Entry:
Following attachment, entry occurs.

• Many viruses enter into eukaryotic cells by receptor-mediated endocytosis.

• A cell’s plasma membrane continuously folds inward to form vesicles.
These vesicles contain elements that originate outside the cell and are brought into the
interior of the cell to be digested.
• If a virion attaches to the plasma membrane of a potential host cell, the host cell will enfold the
virion and form a vesicle.
➢ Enveloped viruses can enter by an alternative method called fusion, in which the viral envelope
fuses with the plasma membrane and releases the capsid into the cell’s cytoplasm.
Uncoating:

• Viruses disappear during the eclipse period of an infection because they are taken apart inside
the cell.
• Uncoating is the separation of the viral nucleic acid from its protein coat.
• This process varies with the type of virus. Some animal viruses accomplish uncoating by the
action of lysosomal enzymes of the host cell. These enzymes degrade the proteins of the viral
capsid.
• The uncoating of poxviruses is completed by a specific enzyme encoded by the viral DNA and
synthesized soon after infection.
• Uncoating of influenza virus occurs at the lower pH in a vesicle.
• Uncoating of togaviruses occurs at ribosomes in the host cytoplasm.

Biosynthesis of DNA Viruses:

• Generally, DNA-containing viruses replicate their DNA in the nucleus of the host cell by using
viral enzymes, and they synthesize their capsid and other proteins in the cytoplasm by using
host cell enzymes.
• Then the proteins migrate into the nucleus and are joined with the newly synthesized DNA to
form virions.
• These virions are transported along the endoplasmic reticulum to the host cell’s membrane for
release.
• Herpesviruses, Papovaviruses, Adenoviruses, and Hepadnaviruses all follow this pattern of
biosynthesis.
• Poxviruses are an exception because all of their components are synthesized in the cytoplasm.

An example of multiplication of a DNA virus,the sequence of events in papovavirus is under:

Biosynthesis of RNA Viruses:

• The multiplication of RNA viruses is

essentially the same as that of DNA viruses,
except RNA viruses multiply in the host cell’s
cytoplasm.
• Several different mRNA formation
mechanisms occur among different groups of
RNA viruses.
• The major differences among the
multiplication processes lie in how mRNA and
viral RNA are produced.
• These viruses have RNA-dependent RNA
polymerase. This enzyme isn’t encoded in
any cell’s genome. Viral genes cause the
enzyme to be made by a host cell. This
enzyme catalyzes the synthesis of another
strand of RNA, which is complementary in
base sequence to the original infecting strand.
• Once viral RNA and viral proteins are
synthesized, maturation occurs by similar
means among all animal viruses.

Biosynthesis of Retroviruses:

• These viruses carry reverse transcriptase, which uses the viral RNA as a template to produce
complementary double-stranded DNA.
• This enzyme also degrades the original viral RNA.
• The name retrovirus is derived from the first letters of reverse transcriptase.
• The viral DNA is then integrated into a host cell chromosome as a provirus.
• Unlike a prophage, the provirus never comes out of the chromosome. As a provirus, HIV is
protected from the host’s immune system and antiviral drugs.
 • Sometimes the provirus simply remains in a latent state and replicates when the DNA of the
host cell replicates.
➢ In other cases, the provirus is expressed and produces new viruses, which may infect adjacent
cells. Mutagens such as gamma radiation can induce expression of a provirus. In oncogenic
retroviruses, the provirus can also convert the host cell into a tumor cell.

Maturation & Release:

• The first step in viral maturation is the

assembly of the protein capsid; this assembly
is usually a spontaneous process.
• The capsids of many animal viruses are
enclosed by an envelope consisting of
protein, lipid, and carbohydrate. Examples of
such viruses include orthomyxoviruses and
paramyxoviruses.
• The envelope protein is encoded by the viral
genes and is incorporated into the plasma
membrane of the host cell.
• The envelope lipid and carbohydrate are
encoded by host cell genes and are present in the plasma membrane. The envelope actually
develops around the capsid by a process called budding.
 • After the sequence of attachment, entry, uncoating, and biosynthesis of viral nucleic acid and
protein, the assembled capsid containing nucleic acid pushes through the plasma membrane. As
a result, a portion of the plasma membrane, now the envelope, adheres to the virus. This
extrusion of a virus from a host cell is one method of release. Budding doesn’t kill the host cell
immediately, and in some cases the host cell survives.
• Non-enveloped viruses are released through ruptures in the host cell plasma membrane. In
contrast to budding, this type of release usually results in the death of the host cell immediately.

LECTURE NO.14:
Requirements for microbial growth
Microorganisms need both physical and chemical requirements for their growth.

PHYSICAL REQUIREMENTS
1. SURFACE

• Microorganisms does not grow in air, they need certain medium for their growth. These
medium may be liquid or solid.

• In liquid medium bacteria can grow at very rapid rate up to 1012-14 , and if the liquid
media is mixed regularly or agitated the number can reach up to 1016-18. This is because in
liquid medium nutrients are easily dissolved and readily available.

• In solid medium bacterial growth rate is slow as compared to liquid medium however if
the nutrients are provided is solid medium bacteria can grow up to 106-8. Most commonly
used solidifying agent is agaragar.
 3. TEMPERATURE

On the basis of temperature, bacteria are divided into 3 classes:

PSYCHROPHILES(COLD LOVING):

These bacteria live in temperature range of -10 to 25 degree centigrade’s. Psychrophillic microbes grow
at -10 degree centigrade while other bacteria grow at 4 to 25 degree centigrade pschrotrophs. These
include staphylococcus, streptococcus, bacillus cereus and moulds etc. These microbes mostly cause the
spoilage of food. GLYCOLS.
MESOPHILES (MODERATE TEMPERATURE LOVING):

These microbes range from 25 to 40 degree centigrade. Most of these bacteria live at 37 degree
centigrade. About 99 percent of disease causing bacteria are included in this group. These bacteria do
not cause as much spoilage of food as psychrophiles

THERMOPHILES ( HEAT LOVING):

These bacteria live at 100 degree centigrade or above 100 degree centigrade. The bacteria living above
100 degree centigrade are called extreme thermophiles. These are not pathogenic bacteria. These
bacteria are found in volcanic, thermal springs, geezersetc.The application of these bacteria and their
products are in PCR TAQ Polymerase is isolated from thermus aquaticus.

STEROLS
3.HUMIDITY& LIGHT:

Bacteria grow at humid environment of humidity 40-60 percent. If bacteria are grown in dry
environment they will start to die.

UV light is bad for growth of bacteria. UV light will change the structure of DNA and cause mutation.
UV light will make loops in DNA THYMIDINE DIMERS

Simple light is necessary for some bacteria i.e. photosynthetic bacteria which need light to synthesize
their food. Some bacteria are not affected by light but they behave different in light and dark medium.

OSMOLARITY
ISOTONIC

➢ Microorganisms obtain almost all their nutrients in solution from the surrounding water. Thus,
they require water for growth, and their composition is 80-90 percent water. If the bacteria
are grown in hypertonic environment the water inside the cell will start to move outside the
cell and bacterial cell shrink and will die.

➢ If the bacteria are grown in hypotonic environment the water will start to move inside the cell
and bacterial cell will swell and burst.
 ➢ Different bacteria live in different osmotic pressure. Some organisms, called extreme
halophiles, have adapted so well to high salt concentrations that they actually require them
for growth.

➢ Obligate halophiles are organisms from such saline waters as the Dead Sea often require
nearly 30 percent salt.

➢ Facultative halophiles, which do not require high salt concentrations but are able to grow at
salt concentrations up to 2 percent, a concentrating that inhibits the growth of many
organisms. A few species of facultative halophiles can tolerate even 15 percent salt.

ACID AND BASE REQUIREMENTS

➢ Acid loving bacteria, Milk spoilage, Food spoilage, Sulphur loving bacteria, extreme
Acetinobacter, Lactobacillus, Fungus acid loving.

➢ 6.5-7.5 normal range of pH for most bacreia

➢ Base loving bacteria Disease causing bacteria

CHEMICAL REQUIREMENTS CHNOPS

CARBON

➢ Besides water, one of the most important requirements for microbial growth is carbon. It is
needed for all the organic compounds that make up a living cell.

➢ Half the dry weight of a typical bacterial cell is carbon.

➢ Chemoheterotrophs get most of their carbon from the source of their energy- organic materials
such as proteins, carbohydrates, and lipids.

➢ Photoautotrophs derive their carbon from carbon dioxide.

NITROGEN, SULPHUR AND PHOSPHOROUS

➢ In addition to carbon microorganisms need other elements to synthesize cellular material. For
example, protein synthesis requires considerable amounts of nitrogen as well as some sulphur.
Thesynthesis of DNA and RNA also require nitrogen and some phosphorous as does the
synthesis of ATP, these molecules are important for the storage and transfer of chemical energy
within the cell.

➢ Organisms use nitrogen primarily to form the amino group of the amino acids of proteins. Many
bacteria meet this requirement by decomposing protein containing material. Some bacteria use
nitrogen from ammonium ions NH4+ and some bacteria use direct nitrogen from environment.
This process is called nitrogen fixation.

➢ Sulphur is used to synthesize sulphur containing amino acids and vitamins such as thiamine and
biotin. Important natural sources of sulphur include sulphate ion SO4 -2 , hydrogen sulphide, and
the sulphur containing amino acids.

➢ Phosphorous is essential for the synthesis of nucleic acids and phospholipids of cell membranes.
A source of phosphorous is phosphate ion PO43-
TRACE ELEMENTS

➢ POTASSIUM, SODIUM, CHLORIDE, MAGNESIUM AND CALCIUM are also elements that
microorganisms require often as cofactor for enzymes.

➢ Microbes require very small amounts of other mineral elements such as iron, copper,
molybdenum and zinc. These are referred to as trace elements. Most are essential for the
functions of certain enzymes and usually act as cofactors.

OXYGEN

Oxygen is needed for the breakdown of food but some bacteria can live without oxygen. However the
energy extract is greater if the bacteria use oxygen. There are some bacteria that live in oxygen
environment and others without oxygen.

Toxic forms of oxygen are,

1. Singlet Oxygen 1O2- SOD

O2-+ O2- + 2H+ → H2O2 + O2

2. Super oxide free Radical O2- SOD

3. H2O2 Catalase

2 H2O2 →2H2O + O2
4. OH-

These forms of oxygen are present in the lysosomes of macrophage which engulf the pathogen
peroxidase like catalase but not O2

H2O2 + 2 H+→ 2H2O

CLASSIFICATION OF MICROBES ON THE BASIS OF OXYGEN DEMAND:

LECTURE NO.15:
Appendages external to bacteria:
1. Glycocalyx:

Unique substance used in bacteria. It is of two types:

• Capsule
• Slime
• Capsule:
• Thin layer
• General term
• Slime:
• Thick layer

Capsule Slime

All bacteria (99% of bacteria) Streptococcus

Composition is Lipopolysaccharide

Lipopolysaccharide gives 2 characters:

If it is present, bacteria forms mucoid/wet

colonies.

If capsule is not present, bacteria forms dull /

dry / rough colonies.

Rough strain:

Strains that do no have capsule.

Bacillus has protenacious capsule and always

form dull colonies.

Functions of Glycocalyx:

1. Protection against macrophages/immune organs.

2. Pathogenicity (disease causing ability)

3. Acts as an antigen (K antigen/capsular antigen which is unique for every bacteria). Typing is done on
the basis of K-antigen.

4. Used as identifier

5. Colonization (due to gummy nature)

6. Bacteria can use it for its own nutrition.

7. Food source for bacteria itself.

Point:

➢ Capsular antigen causes more diseases as compared to non-capsular antigens.

LECTURE NO.16:
Vaccination:

Vaccination/vaccine is an idea or thought to enhance the immunity of an organism.

Types of vaccines:

1. Wild Type Vaccines

2. Attenuated/Weakened Vaccines

3. Killed Vaccines

4. Toxin based Vaccines/Anti-toxins/Toxoids

5. Recombinant Vaccines

1. Wild Type Vaccines:

• Replicate in cells
• Do not cause disease

When they replicate:

• Mammary cells are formed.

• Immune cells are formed.
• Antibodies activate.
• Interferons are involved.
• Cytotoxic reactions take place.
• Inflammation occurs.
➢ All of them provide solid immunity.

Example: NDV vaccine, IBDV vaccine, Polio vaccine.

2. Attenuated/Weakened Vaccines:

• They require extraordinary media.

For example:

➢ Rabies virus, TB virus.

If we give a long time passage or short time passage to Rabies virus (passes from one media to another),
it loses its pathogenicity & gets weakened or attenuated.
3. Killed Vaccines:

• Antibodies are formed against receptors.

• Can be injected IV / IM / sub-cutaneous

For example:

• FMDV (Foot & month disease virus)

• Capsid remains outside. It acts on RNA & destroys it.
• HS ( Hemorrhagic septicemia)

Point: Measles & Mumps are preventable diseases.

4. Toxin based Vaccines/Anti-toxins/Toxoids:

• Virus & bacteria are not important. Their toxins are important.

Example: Tetanus.

5. Recombinant Vaccines:

It can involve:

• Subunits
• Whole organism
• DNA/RNA (Genomic Vaccines)

Point: Wild Type Vaccines & Attenuated / Weakened Vaccines are Live Vaccines.

LECTURE NO.17:
Quiz # 01: What is the mode of action of Viral Vaccines?

Viral Vaccines are of different shapes:

1. Live Vaccine:

• Virus with genome & peplomers

• Causes infection.
• When causes infection, it replicates in nucleus or cytoplasm.

After replication, there are 3 methods by which live Vaccines work:

1. Antibodies formation

• Vaccines bind to future viruses.

• Cannot attach the host so cannot cause disease.

2. Interferons:

• Antibodies ask neighbor cells to produce Interferons

• Block the replication of viruses.
3. T-Helper Activation:

• Activates T-cytotoxic.
• Tc destroys the cell containing the virus.

2. Fragments / Sub-units Vaccines:

• Fragments go to APC.
• APC present fragments to B-cells, B- cells secrete plasma cells , plasma cells release Antibodies.
• Recombinant subunits
• Most Vaccines are in this form.

3. Empty Capsid:

• Empty capsid works by one method i.e. production of Antibodies.

• Empty capsid is engulfed by APC (Macrophage), present it to B- cells , B-cells will form plasma
cells & plasma cells will form Antibodies.
• Replication is not necessary.

Working of Antibodies:

Antibodies work by covering the virus so that it does not enter the host. It is the best way of working.

LECTURE NO.18:
Quiz#02: What are the various routes used in vaccines?

Live Vaccines:

1. Intra oral (e.gND,IBD,Polio)

2. Intra Nasal (given because there can be some drug/chlorine in water or water is heated)

3. Eye drops

Killed Vaccines:

1. Injection (IM/Sub-cutaneous)

2. Alum precipitate/Gel based Vaccine (Sub-cutaneous/does not work in IM)

3. Bone Marrow

4. DNA / RNA are injected (In future)

5. Intra-food (In future)

Point: Killed Vaccines will be Sub-cutaneous either empty capsid or fragments.

Quiz#03: What are the causes of success / failure of vaccines?

LIVE VACCINES:

Following are the causes of success/failure of live Vaccines:

1. Adulteration (Addition of drug/disinfectant)

2. Fake / Fraud (Fake vaccine)

3. Dilution (Addition of water)

4. Tempered vaccine (Physically tempered e.g exposed to sunlight/heat, seal broken)

5. Expired Vaccine

6. High temperature

7. Untrained Vaccinator

8. Wrong injection site / area

9. Time of vaccination

10. Age of animal

11. Infection / Parasitic Load (If animal is sick / has parasites , vaccines will not work

Deworming should be done first)

12. Food (The one to be vaccinated should not be undernourished/should have ample food)

13. Immune depressed (The one to be vaccinated should not be immune depressant otherwise vaccine
will not work.

1-4 ... Production / Vaccination faults

7-9 ... Faults of staff

10-13... Faults of animal

Killed Vaccine:

1. Dilution

2. Toxins

3. Proteolytic Enzymes
LECTURE NO.19:
Quiz#04:Write a note on flagella?

• Flagella (Plural), Flagellum (Singular)

Life forms of bacteria having flagella:

1. Prokaryotic:

• Eubacteria (Flagellum)
• Archaebacteria (Archaellum)

2. Eukaryotic:

• Flagella of eukaryotic bacteria is belly dancer.

• Literal meaning of flagella is "whip"
• Always move counter-clockwise
• One protein ---- changes charge
• Clutch protein ----- works as clutch
• These rings are classically present in gram -ve bacteria.
• Flagella does not require ATP for movement. It requires protein motive force (Na +,H+)
• M-ring is embedded in cell membrane.
• RPM reaches 1000.

Functions of Flagella:

1. Main function is movement.

2. Acts as antigen (Antigen H)

3. Chemotactic Response

4. Help bacteria in causing disease.

• When it is to grow, a protein comes in hollow then attaches at tip.

• It grows form tip.
• In some bacteria, flagellin is 7.
• Most bacteria have 11 flagellin.
Mechanism of Movement:

• Run - Tumble run

• Flagella rotate (Bacteria move forward)
• In unfavorable conditions (Flagella stop , bacteria rotate backward)
• Thousand times more traversing than its body length.
• Efficient method but speed is slow.

LECTURE NO.20:
Growth of Viruses:

• Viruses cannot be grown on artificial media

(Agar/Broth)
• Viruses are thus grown in lab animals (Rats, pigs ,
ginny pigs , horses)
• 7-8 days embryonated eggs were used.
• For egg yolk (Thick & long syringe)
• After removing the syringe seal the egg with hot
wax.
• For egg, incubate at 99-100°F for 3 days till 10th
or 11th day.
• Before 11th day, (usually on 10th day, chilling is
done)
• Through chilling all vessels of embryo shrink, this is important to prevent embryo from bleeding.
If bleeding takes place, antibodies will act against them. Because of chilling, antigen-antibody
reaction will not take place.
• Then cut the sac with the help of scissor.

Growth in Cells:

• Embryo cells
• Neonatal cells
• Foetal cells
• Stem cells
• Bone Marrow cells
• Grown in minimum essential media (MEM)
• Baby Hamster kidney cell line.
• Tissue culture/cell culture (To form artificial/lab meat)
Part II

LABS/PRACTICALS
GENERAL VETERINARY
MICROBIOLOGY
DVM (2nd SEMESTER)
LAB NO.01:
DISINFECTION:
CHEMICAL METHODS:
Phenol & phenolics
(Lister was the first to use phenol to control surgical infections in the operating rooms)

• Bisphenol like hexachlorophene

• Biguanides like chlorhexidine
• Halogens like povidone-iodine
• Alcohol like 70% ethanol

Heavy metals & their compounds like

• Silver nitrate.
• Mercuric chloride
• Copper sulphate
• Zinc chloride

Surface active agents (surfactants)

• Soaps and detergents
• Acids anionic sanitizers
• Quaternary ammonium compounds(Quarts)
LAB NO.02:
STERILIZATION:
• It is the removal or destruction of all forms of microbial life including spores and viruses on an
object.

STERILANT & CONTAMINANT:

• A sterilizing agent is called sterilant, agent that kills microbes is called microbicidal or more
simply called germicides.
• Agent which specifically kills bacteria is called bactericidal.
• Agent which specifically kills fungi is called fungicidal.
• A sterile object that is still harboring microorganisms is called contaminant

SANITIZATION:
• It involves those procedures which reduce the number of pathogenic microbes or discourages
their growth.
MICROBIOSTATIC:
• They inhibit the growth of microbial agents but cannot kill them.
• Bacteriostatic inhibit the growth of bacteria.
• Fungistatic inhibit the growth of fungi.

DISINFECTION:
• In lab practice the term is most commonly applied to the use of chemicals to treat an inert (non-
living) surface.
ANTISEPSIS:
• This term is applied to the use of chemicals on living tissue and the chemical is called antiseptic.
• When someone is about to receive an injection, the skin is swabbed with alcohol, the process of
degerming which mostly results in the mechanical removal rather than killing microbes in a
limited area.
• In practice, the same chemical might be called a disinfectant for one use and an antiseptic for
another. Moreover, there are many chemicals suitable for swabbing a table top. It would be too
harsh to use on living tissue.
COMMERCIAL STERILIZATION:
• Sufficient heat treatment to kill endospores of clostridium botulinum in canned food is called
commercial sterillization.
• More resistant endospores of thermophilic bacteria may survive, but they will not germinate and
grow under normal storage conditions.

HOW ANTIMICROBIAL AGENTS WORK

ALTERATION OF MEMBRANE PERMEABILITY:

• Damage to lipids or proteins of plasma membrane by anti microbial agents causes cellular
contents to leak into the surrounding medium and interferes with growth of cell.

DAMAGE TO PROTEINS & NUCLEIC ACIDS:

• Hydrogen is responsible for three dimensional structure & shape which are susceptible to
breakage by heat or certain chemicals, breakage results in denaturation of proteins. DNA & RNA
are the carriers of genetic information of cell. Damage of these nucleic acids by heat, radiations
 of chemicals, is frequently lethal to the cell, the cell no longer replicate nor can it carries out
normal metabolic functions such as synthesis of enzymes

METHODS OF STERILIZATION:
PHYSICAL METHODS:

HEAT:

• Laboratory media, glasswares & hospital instruments are usually sterilized by heat.

THERMAL DEATH POINT (TDP):

• It is the lowest temperature at which all the microorganisms in a particular liquid suspension will
be killed in 10 minutes.

THERMAL DEATH TIME (TDT):

• The minimal length of time for all bacteria in a particular liquid culture to be killed at a given
temperature.

DECIMAL REDUCTION TIME (D value):

• DRT is the time, in minutes in which 90% of the population of bacteria at a given temperature
will be killed.

MOIST HEAT:
BOILING:

• Boiling kills the vegetative forms of bacterial pathogens, almost all viruses, fungi & their spores
within about 10 minutes usually much faster.
AUTOCLAVING:
• Some bacterial endospores can survive boiling even for more than 20 hours. So autoclaving is
preferred method of sterilization, unless the material to be sterilized can be damaged by heat or
moisture.

121 degree centigrade @ 15 psi for 15 minutes.

• Under these conditions steam will kill all organisms & endospores in about 15 minutes.
• The time for autoclaving (complete process) also depends upon the container size.

PASTEURIZATION:
• Classical pasteurization time is 30 minutes & temperature is 63 degree centigrade.
• High temperature short time (HTST) is 15 seconds for 72 degree centigrade.
• Ultra High Temperature (UHT) is 3 seconds for 140 degree centigrade.
DRY HEAT STERILIZATION:

DIRECT FLAMING:

• CULTURE LOOP/INOCULATING LOOP/PLATINUM LOOP is sterilized by putting it directly

on the flame.

HOT AIR STERILIZATION:

• 170 degree centigrade for about one and a half to two hours in hot air oven.

FILTRATION:
• It is used to sterilize heat sensitive materials such as some culture media, enzymes, vaccines &
antibiotic solutions.

HEPA FILTERS:
• High efficiency particulate air filters remove almost all microorganisms larger than about 0.3
micrometer in diameter.

MEMBRANE FILTERS:
• Composed of cellulose, esters or plastic polymers. These filters are only 0.1 mm thick. The pore
size includes 0.22 micrometer & 0.45 micrometer size. Filters are available with pore size as
small as 0.01 micrometer, a size which will retain viruses & even some larger protein molecules.

LOW TEMPERATURE:
• Low temperature reduces the metabolic rates of most of the microorganisms so that they cannot
reproduce or produce toxins.
HIGH PRESSURE:
• In presence of high pressure, the molecular structure of proteins & carbohydrates is altered
resulting in rapid inactivation of vegetative bacterial cells. Endospores are resistant to high
pressure.

DESSICATION:
• It is the condition in the absence of water, microorganisms cannot grow or reproduce but can
remain viable for years. This ability is used in laboratory when microbes are preserved by
lyophilization or freeze drying.

OSMOTIC PRESSURE:
• Higher concentration of salts & sugars create a hypertonic environment that causes water to leave
the cell. The principle of osmotic pressure is used in preserving food.

RADIATION:
IONIZING RADIATION:

• Gamma rays, X-Rays or high energy electron beam has less wavelength than about 1 millimeter.

NON-IONIZING RADIATION:

• Wavelength is more than 1 nm & best example is UV Light

RADIATION SPECTRUM:
LAB NO.03:
• QUANTITATIVE PLATING PROCEDUREMETHODS OF BACTERIOLOGICAL
CULTIVATION

1.PROCEDURE FOR REMOVING ORGANISMS FROM A BROTH CULTURE WITH

INOCULATING LOOP

2.PROCEDURE FOR INOCULATING A NUTRIENT BROTH

3.PROCEDURE FOR INOCULATING A NUTRIENT AGAR SLANT FROM AN AGAR PLATE

4.PROCEDURE FOR INOCULATING A NUTRIENT AGAR SLANT FROM A SLANT

CULTURE
5.STREAK PLATE METHOD

METHODS OF STREAKING
POUR PLATE METHOD
TUBE HANDLING PROCEDURE IN MAKING INOCULATIONS FOR POUR PLATES

BACTERIAL POPULATION COUNT

QUANTIFICATION OF BACTERIA

BACTERIAL TOTAL COUNT

Dry mass calculation

OD value measurement
BACTERIAL VIABLE COUNT

Quantitative plating procedure

OD Value measurement
LAB NO.04:
ANTIBIOTIC SENSITIVITY TESTING:
Kirby Bauer Method
(Disc diffusion method)
• It is a standardized system that takes all variables into consideration.
• Recommended medium in this test is Mueller Hinton II agar.
• ph 7.2 - 7.4
• Poured into petri plates to a uniform thickness of 4mm
• Inoculation of the surface of medium is made with a cotton swab from a broth or liquid media
• High potency disc are used that may be placed on the agar with mechanical dispenser or sterile
forceps.
• To secure the disc on to the medium it is necessary to press them down onto the
agar
After 16 to 18 hours incubation, plates are examined and the diameters of the zones are measured to the
nearest millimeter
Method:
• Label the petri plate with the name of sample/microorganism.
• Inoculate the surface of the medium with the swab. Cover the surface of agar evenly by swabbing
in three directions
• Allow 3 to 5 minutes for the agar surface to dry before applying discs.
• Dispense discs as follows
I. If an automatic dispenser is used, remove the lid from the plate place the dispenser over
the plate and push down firmly on the plunger. With the sterile tip of forceps tap each
disc lightly to secure it to medium
II. If forceps are used sterilize them first by flaming before picking up the disc. Keep each
disc at least 15mm apart from the edges of the plate and from other discs. Apply light
pressure to each disc on the agar with the tip of a sterile forceps or inoculating loop to
secure it to medium.
Place no more than 13 on a 150 mm plate, no more than 5 on a 100 mm plate.
Invert and incubate the plate for 16 to 18 hours at 37°C
Interpretation;
• After incubation, measure the zone diameters with a metric ruler to the nearest whole millimeter.
• The zone of complete inhibition is determined without magnification.
• Ignore faint growth or tiny colonies that can be detected by very close scrutiny.
• Large colonies growing within the clear zone might represent resistant variant or a mixed
inoculum and may require reidentification and retesting.
• Ignore the swarming characteristics of proteus measuring only to the margins of heavy growth.
Part III
Medical/Veterinary
One Health

STAPHYLOCOCCUS AUREUS INFECTIONS

STAPHYLOCOCCUS
Characteristics gram + (stains blue with gram
stain)
coccus (small, round
cell)
grow in grape-like cell
clusters
non-motile (has no
flagella)
non-spore forming (does not form a sturdy
vegetative
infectious
particle)
facultative anaerobic (may survive in both oxygen-rich
and oxygen-poor environments)
Grow on no enriched
media
Moderately sized white
or golden colonies
Commensals on skin and
mucous membranes
Comparatively stable in
environment
Cause pyrogenic
infections

COAGULASE + STAPHYLOCOCCI

Staphylococcus Aureus
Characteristics non-
encapsulated
beta-hemolytic (completely lyses RBCs on blood
agar,
forms a clear halo around it's colonies on blood
agar)
opportunistic
pathogen
Reservoirs humans (normal flora of the skin, nasopharynx,
oropharynx
and female
genitalia)
animals (primarily
cattle)
Transmission direct contact ("person-to-person")
perinatal ("mother-to-child")
zoonotic ("animal-to-human")
contaminated
food
Toxins staphylococcal enterotoxin (causes secretion of
histamine from mast cells " peristalsis " food
poisoning,
exfoliatin (disrupts desmosomes of skin
epithelium "
scalded skin syndrome, see
below)
toxic shock syndrome toxin-1 ("TSST-1", causes
massive
activation of helper T-cells " massive IL-2
secretion "
staphylococcal toxic shock syndrome
Diseases most common cause of skin infections (folliculitis,
cellulitis and impetigo), skin abscesses (pustules,
furuncles,
carbuncles), and wound infections (together
with
Streptococcus Pyogenes)
most common cause of acute infections
endocarditis
bronchopneumonia and pulmonary
abscesses
cystitis and renal abscesses (primarily if urinary
catheter)
meningitis and cerebral
abscesses
infective arthritis (primarily occurs in children and
elderly)
and osteomyelitis (primarily occurs in male
children)
septicemia (primarily if central venous
catheter)
 Food
Poisoning
most common cause of food poisoning
gastroenteritis (abdominal pain, vomiting and watery
Diarrhea)
spontaneously resolves in < 24 hours
caused by Staphylococcus Aureus contamination of food "
production and secretion of staphylococcal
enterotoxin (see
above) " ingestion of staphylococcal
enterotoxin-
containing
food may progress
to staphylococcal
toxic shock
syndrome

Scalded Skin Syndrome

epidermal skin shedding
primarily occurs around the umbilicus of neonates
caused by Staphylococcus Aureus infection of skin "
production and secretion of exfoliatin (see above)
may progress to staphylococcal toxic shock syndrome
Staphylococcal Toxic Shock Syndrome
- "STSS"
high fever, vomiting and watery diarrhea " diffuse
erythematous rash and focal epidermal skin shedding "
hypotension
may lead to septic shock " death
primarily occurs in menstruating females using tampons
caused by Staphylococcus Aureus septicemia " production
and secretion of TSST-1

Treatment beta-lactamase resistant penicillin’s

vancomycin (if resistant to beta-lactamase resistant
penicillin’s, "methicillin-resistant staphylococcus aureus",
"MRSA")
COAGULASE NEGATIVE STAPHYLOCOCCI

COAGULASE - STAPHYLOCOCCI

Staphylococcus Epidermidis
Characteristics - encapsulated
- gamma-hemolytic (does not lyse RBCs on blood agar)
- opportunistic pathogen

Reservoirs - humans (only reservoir, normal flora of the skin,

nasopharynx, oropharynx and GI tract)

Transmission - direct contact

Toxins - none in particular

Diseases Nosocomial Infections

- cystitis (primarily if urinary catheter)
- subacute infectious endocarditis (primarily if prosthetic
heart valves)
- infective arthritis (primarily if prosthetic joints)
- septicemia (primarily if central venous catheter)

Treatment - vancomycin
- trimethoprim-sulfamethoxazole

Staphylococcus Saprophyticus
Characteristics - non-encapsulated
- gamma-hemolytic
- obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

Transmission - direct contact

Toxins - none in particular

Diseases - second most common cause of cystitis (after Escherichia

Coli, see 18, primarily occurs in sexually active females)

Treatment - broad spectrum penicillins

- trimethoprim-sulfamethoxazole
STREPTOCOCCUS PYOGENES: PYOGENIC INFECTIONS
STREPTOCOCCUS PYOGENES: SCARLET FEVER AND
SECONDARY STREPTOCOCCAL DISEASES

STREPTOCOCCUS
Characteristics - gram +
- coccus
- grow in chains or in pairs
("diplococci"/”streptococci”)
- non-motile
- non-spore forming
- facultative anaerobic
- classified according to the structure of the C carbohydrate in their
respective cell walls ("lancefield antigen") as well as their
respective hemolytic abilities
Fastidious, require enriched
media
Catalase negative
Commensals on mucous
membranes
Cause pyrogenic infections
Streptococcus Pyogenes
Characteristics - encapsulated
- lancefield group A antigen ("group A Streptococcus")
- beta-hemolytic
- obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

Transmission - direct contact

- droplet nuclei ("respiratory spray")

Toxins - pyrogenic exotoxin ("erythrogenic exotoxin", causes scarlet fever

and streptococcal toxic shock-like syndrome, see below)

Diseases Invasive Diseases

- most common cause of skin infections (folliculitis, cellulitis and
impetigo), skin abscesses (pustules, furuncles, carbuncles), and
wound infections (together with Staphylococcus Aureus, see 1)
- most common BACTERIAL cause of acute pharyngitis ("acute
tonsillitis", "strep throat")
- otitis media and mastoiditis
- subacute infectious endocarditis
- septicemia

Cross Reactive Diseases

- rheumatic fever
- acute post-streptococcal glomerulonephritis ("diffuse proliferative
glomerulonephritis")

Scarlet Fever
- high fever and diffuse, brightly erythematous ("scarlet-red") rash
beginning on the trunk and neck and then progressing to the
extremities " shedding of the affected skin
- caused by Streptococcus Pyogenes septicemia " production and
secretion of pyrogenic exotoxin (see above)
- may progress to streptococcal toxic shock-like syndrome (see
below)

Streptococcal Toxic Shock-Like Syndrome

- "STLS"
- analogous to staphylococcal toxic shock syndrome (see 1)
- caused by Streptococcus Pyogenes septicemia " production and
secretion of pyrogenic exotoxin (see above)

Treatment - narrow spectrum penicillins

- beta-lactamase resistant penicillins (if skin infections, due to the
possibility that the skin infections might be of Staphylococcus
Aureus origin, see 1)
STREPTOCOCCUS PNEUMONIAE

Streptococcus Pneumoniae ("Pneumococcus")

Characteristics - encapsulated
- nolancefield antigen
- alpha-hemolytic (partially lyses RBCs on blood agar, forms a
greenish halo around it's colonies on blood agar)
- opportunistic pathogen

Reservoirs - humans (only reservoir, normal flora of the nasopharynx,

oropharynx and conjunctiva)

Transmission - direct contact

- droplet nuclei
- contaminated fomites (indigestible objects)

Toxins - none in particular

Diseases - most common cause of lobar pneumonia and pulmonary abscesses

- most common cause of meningitis and cerebral abscesses
- most common cause of otitis media (primarily occurs in children)
- sinusitis
- subacute infectious endocarditis and acute pericarditis
- septicemia

Treatment - narrow spectrum penicillins

- macrolides
THE "STREPTOCOCCUS VIRIDANS" GROUP, THEIR ROLE
IN CARIOGENESIS
ENDOCARDITIS LENTA AND ITS BACTERIAL DIAGNOSIS

Streptococcus Viridans
Species - S. Mutans
- S. Intermedius
- S. Salivarius

Characteristics - non-encapsulated
- nolancefield antigen
- alpha-hemolytic
- opportunistic pathogen

Reservoirs - humans (only reservoir, normal flora of the skin, nasopharynx,

oropharynx and oral cavity)

Transmission - perinatal

Toxins - none in particular

Diseases - most common cause of dental caries (primarily caused by S.

Mutans)
- most common cause of subacute infectious endocarditis
("endocarditis lenta", caused by all species of Streptococcus
Viridans)
- cerebral abscesses and hepatic abscesses (primarily caused by S.
Intermedius)
- septicemia (caused by all species of Streptococcus Viridans)

Treatment - narrow spectrum penicillins

- broad spectrum penicillins in conjunction with aminoglycosides (if
subacute infectious endocarditis, due to the possibility that the
subacute infectious endocarditis might be of enterococcus faecialis
origin, )
STREPTOCOCCUS AGALACTIAE, ENTEROCOCCUS
FAECIALIS

Streptococcus Agalactiae
Characteristics - encapsulated
- lancefield group B antigen ("group B Streptococcus")
- beta-hemolytic
- opportunistic pathogen

Reservoirs - humans (normal flora of the GI tract and female genitalia)

- animals

Transmission - perinatal

Toxins - none in particular

Diseases - most common cause of neonatal pneumonia

- most common cause of neonatal meningitis
- cystitis and endometritis
- endocarditis and peritonitis
- infective arthritis and osteomyelitis
- septicemia

Treatment - narrow spectrum penicillins

- aminoglycosides (if neonatal meningitis, due to the possibility that
the neonatal meningitis might be of Escherichia Coli origin,

-
Streptococcus Faecalis ("Enterococcus Faecalis")
Characteristics - non-encapsulated
- lancefield group D antigen ("group D Streptococcus")
- alpha-hemolytic
- facultative alkaliphilic (may survive in bothboth neutral- and
alkaline environments, thus may grow in bile)
- opportunistic pathogen

Reservoirs - humans (normal flora of the GI tract)

- animals

Transmission - trauma

Toxins - none in particular

Diseases - second most common cause of subacute infectious endocarditis

(after Streptococcus Viridans, see 7)
- wound infections
- cholecystitis (due to it's facultative alkaliphilic nature, see above)
- cystitis
- septicemia

Treatment - broad spectrum penicillins in conjunction with aminoglycosides

(due to high antibiotic resistance)
- vancomycin (if resistant to broad spectrum penicillins and/or
aminoglycosides)
PEPTOCOCCUS AND PEPTOSTREPTOCOCCUS

PEPTOCOCCUS
Species - P. Niger (all other species that previously were part of the Peptococcus
genus are now part of the Peptostreptococcus genus, see below)

Characteristics - gram +
- coccus
- grow in chains or in pairs
- non-encapsulated
- non-motile
- non-spore forming
- gamma-hemolytic
- opportunistic pathogen

Reservoirs - humans (normal flora of the nasopharynx, oropharynx, GI tract and female
genitalia)
- animals
- soil

Transmission - trauma

Toxins - none in particular

Diseases - wound infections (primarily if surgical)

- otitis media and mastoiditis
- sinusitis
- bronchopneumonia and pulmonary abscesses
- appendicitis, peritonitis and hepatic abscesses
- cystitis
- vulvovaginitis and pelvic inflammatory disease ("PID", endometritis,
salpingitis and oophitis)
- meningitis and cerebral abscesses
- infective arthritis and osteomyelitis
- septicemia

Treatment - narrow spectrum penicillins

- clindamycin
PEPTOSTREPTOCOCCUS
Species - P. Aerobius
- P. Magnus
- P. Micros

Characteristics - same characteristics, reservoirs, transmission, toxins, diseases and

treatment as Peptococcus (see above, Peptostreptococcus only differs from
Peptococcus in it's genome and the amino acid sequence of it's proteins)
NEISSERIA GONORRHOEAE

NEISSERIA
Characteristics - gram - (does not stain with gram stain, but stains red with gram
contrastain)
- curved coccus
- grow in pairs
- non-motile
- non-spore forming
- facultative anaerobic
- facultative intracellular (may survive both extracellularly and
intracellularly)

Neisseria Gonorrhoeae ("Gonococcus")

Characteristics - non-encapsulated
- obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

Transmission - sexual ( "sexually transmitted disease", "STD", "venereal disease")

- perinatal

Toxins - lipooligosaccaride ("LOS", analogous to LPS, )

Diseases In Males
- gonorrheal urethritis ("gonorrhea")
- prostatitis and epididymitis

In Females
- gonorrheal urethritis and cervicitis ("gonorrhea")
- pelvic inflammatory disease (see 9), tuboovarian abscesses, ectopic
pregnancies and infertility

In Both Males and Females

- pharyngitis (primarily if oral intercourse)
- proctitis (primarily if anal intercourse)
- meningitis and subacute infectious endocarditis
- dermatitis in conjunction with infective arthritis ("dermatitis-
arthritis syndrome")
- septicemia

In Neonates
- conjunctivitis and blindness

Treatment - third generation cephalosporins

-
 - third generation cephalosporins in conjunction with tetracyclines
(if gonorrheal urethritis and/or cervicitis, due to the possibility that
the urethritis and/or cervicitis may be of Chlamydia Trachomatis
orUreaplasmaUrealyticum origin)

NEISSERIA MENINGITIDIS
Neisseria Meningitidis ("Meningococcus")
Characteristics - encapsulated
- opportunistic pathogen

Reservoirs - humans (only reservoir, normal flora of the nasopharynx)

Transmission - direct contact

- droplet nuclei

Toxins - LOS

Diseases Meningococcemia
- spiking fever, diffuse petechial skin rashes and infective arthritis
- caused by Neisseria Meningitidis septicemia
- may progress to meningitis and/or waterhouse-friderichsen
syndrome (see below)

Meningitis
- intense headache, vomiting and stiff neck " delirium " coma
- permanent central neuropathies upon recovery
- caused by progression of meningococcemia (see above)

Waterhouse-Friderichsen Syndrome
- "fulminant meningococcemia"
- DIC " severe bilateral adrenal hemorrhage " adrenal crisis
- > 50% mortality if untreated (within 6-8 hours (!))
- caused by progression of meningococcemia (see above)

Treatment - narrow spectrum penicillins

- third generation cephalosporins
ENTEROPATHOGENIC (EPEC), ENTEROTOXIGENIC (ETEC)
AND ENTEROHEMORRHAGIC (EHEC) ESCHERICHIA COLI

ESCHERICHIA
Characteristics - gram -
- rod (thin, elongated cell)
- encapsulated
- motile (has flagellae)
- non-spore forming
- facultative anaerobic

Escherichia Coli
Characteristics - opportunistic pathogen

Reservoirs - humans (normal flora of the GI tract)

- animals

Transmission - direct contact

- fecal-oral
- contaminated water
- contaminated food
- contaminated fomites

Enteropathogenic Escherichia Coli ("EPEC")

Characteristics - gamma-hemolytic

Toxins - lipopolysaccaride ("LPS", "endotoxin")

Diseases - watery diarrhea (primarily occurs in infants)

Treatment - oral fluid and electrolyte replacement

Enterotoxigenic Escherichia Coli ("ETEC")

Characteristics - gamma-hemolytic

Toxins - heat-labile enterotoxin ("LT", inhibits the GTPase domain

of adenylate cyclase" ! cAMP " ! Cl- and HCO3-
secretion" ! intraluminal osmotic pressure " osmotic
diarrhea (see below), analogous to choleragen (see 23))
- heat-stabile enterotoxin ("ST", inhibits the GTPase domain
of guanylate cyclase" ! cGMP " same effect as LT, see
above)
- LPS

Diseases - most common BACTERIAL cause of gastroenteritis

("traveler's diarrhea", "montezuma's revenge", see 1,
primarily occurs in travelers)

Treatment - oral fluid and electrolyte replacement

Enterohemorrhagic Escherichia Coli ("EHEC")

Characteristics - gamma-hemolytic

Toxins - verotoxin ("shiga-like toxin", "SLT", inhibits the 60S

ribosomal subunit " # protein synthesis " necrosis and
inflammation " hemorrhagic colitis and hemolytic uremic
syndrome (see below), analogous to shiga toxin (see 13))
- LPS

Diseases Hemorrhagic Colitis

- low-grade fever, abdominal cramps, abdominal pain,
vomiting and purulent hemorrhagic diarrhea
- spontaneously resolves in < 1 week
- caused by EHEC infection of the GI tract " production and
secretion of verotoxin (see above) " necrosis of the
enterocytes
- may progress to hemolytic-uremic syndrome (see below)

Hemolytic-Uremic Syndrome
- "HUS"
- thrombosis and following thrombocytopenia "
sequestration of RBCs passing through the thrombi and
following hemolytic anemia " occlusion of the glomeruli
by the thrombi and following intrarenal azotemia and
uremia
- most common cause of hemolytic-uremic syndrome
- caused by verotoxin (see above) toxemia " necrosis of the
glomerular endothelial cells
Treatment - oral fluid and electrolyte replacement (if hemorrhagic
colitis)
- careful oral fluid and electrolyte replacement (if hemolytic-
-uremic syndrome, due to occlusion of the glomeruli, -

Uropathogenic Escherichia Coli ("UPEC")

Uropathogenic Escherichia Coli ("UPEC")

Characteristics - beta-hemolytic

Toxins - cytotoxic necrosis factor ("CNF", causes necrosis of the

transitional epithelial cells of the urinary tract " cystitis
and/or pyelonephritis, see below)
- LPS

Diseases - most common cause of cystitis (primarily occurs in sexually

active females) and pyelonephritis

Treatment - fluoroquinolones
- trimethoprim-sulfamethoxazole
Meningitis-Associated Escherichia Coli ("MNEC")

Characteristics - gamma-hemolytic

Toxins - cytotoxic necrosis factor ("CNF", causes necrosis of the

meningeal endothelial cells " neonatal meningitis, see
below)
- LPS

Diseases - second most common cause of neonatal meningitis (after

Streptococcus Agalactiae,
- most common cause of septicemia

Treatment - aminoglycosides (if neonatal meningitis, due to the

possibility that the neonatal meningitis might be of
Streptococcus Agalactiae origin,
- fluoroquinolones (if septicemia)
BACILLARY DYSENTERY

SHIGELLA
Species - S. Dysenteriae
- S. Flexneri
- S. Boydii

Characteristics - gram -
- rod
- non-encapsulated
- non-motile
- non-spore forming
- facultative anaerobic
- facultative intracellular
- obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

Transmission - direct contact

- fecal-oral
- vectorial (flies)
- contaminated water
- contaminated food

Toxins - shiga toxin (analogous to verotoxin (see 12), causes hemorrhagic

bacillary dysentery and hemolytic-uremic syndrome (see below))
- LPS

Diseases Bacillary Dysentery

- low-grade fever, abdominal cramps, abdominal pain, vomiting and
purulent hemorrhagic diarrhea
- spontaneously resolves in < 1 week
- primarily occurs in children and elderly
- analogous to hemorrhagic colitis
- caused by Shigella infection of the GI tract " production and
secretion of shiga toxin (see above) " necrosis of the enterocytes

Hemolytic-Uremic Syndrome
- see 12

Treatment - broad spectrum penicillins in conjunction with oral fluid and

electrolyte replacement (if bacillary dysentery)
- broad spectrum penicillins in conjunction with careful oral fluid
and electrolyte replacement (if hemolytic-uremic syndrome, due to
occlusion of the glomeruli,
SALMONELLAE CAUSING ENTERIC FEVER
SALMONELLA
Characteristics - gram -
- rod
- encapsulated
- motile
- non-spore forming
- facultative anaerobic
- facultative intracellular
- facultative alkaliphilic
Salmonella Typhi
Characteristics - obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

Transmission - direct contact

- fecal-oral
- contaminated water
- contaminated food

Toxins - LPS

Diseases Typhoid Fever

- "enteric fever"
- enterocolitis (high fever, headache, abdominal pain, vomiting and
watery diarrhea) and mesenteric lymphadenitis ("mock
appendicitis") " abdominal rash ("rose spots"),
hepatosplenomegaly and generalized lymphadenomegaly
- caused by phagocytosis of Salmonella Typhi by macrophages of
the gut-associated lymphoid tissue ("GALT") " survival of
Salmonella Typhi within the macrophages " dissemination of
Salmonella Typhi in virtually every lymphoid organ

Treatment - broad spectrum penicillins

- third generation cephalosporins
SALMONELLA GASTROENTERITIS
Salmonella Enteritidis
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily cattle and poultry)

Transmission - direct contact

- fecal-oral
- zoonotic
- contaminated food (primarily meat, milk and eggs)

Toxins - LPS

Diseases Salmonellosis
- gastroenteritis (see 1)
- spontaneously resolves in < 1 week
- caused by Salmonella Enteritidis infection of the GI tract

Treatment - oral fluid and electrolyte replacement

YERSINIA ENTEROCOLITICA AND YERSINIA
PSEUDOTUBERCULOSIS

YERSINIA
Characteristics - gram -
- bipolar (the extremities take up more stain than the center) rod
- non-spore forming
- facultative anaerobic
- facultative intracellular

Yersinia Enterocolitica
Characteristics - motile
- non-encapsulated
- obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily swine, cattle and birds)

Transmission - direct contact

- fecal-oral
- zoonotic
- contaminated water
- contaminated food (primarily meat and milk)

Toxins - yersinial enterotoxin (analogous to ST causes

enterocolitis (see below))
- LPS

Diseases - enterocolitis primarily occurs in children and in

immunocompromised) and mesenteric lymphadenitis ("mock
appendicitis")
- cellulitis, iritis and pharyngitis
- infective arthritis and osteomyelitis
- septicemia

Treatment - oral water and electrolyte replacement (if enterocolitis)

- third generation cephalosporins (if septicemia)

--
 Yersinia Pseudotuberculosis
Characteristics - same characteristics, reservoirs, transmission, diseases and
treatment as Yersinia Enterocolitica (see above, only differs in
toxins secreted, see below)
- (also causes a disseminated tuberculosis-like syndrome in animals,
thus "Pseudotuberculosis")

Toxins - cytotoxic necrosis factor ("CNF", causes necrosis of the

enterocytes of the small intestine " enterocolitis, see above)
- LPS

continued in 17

-
YERSINIA PESTIS
Yersinia Pestis
Characteristics - encapsulated
- non-motile
- obligate pathogen

Reservoirs - humans (only in epidemic periods, not normal flora)

- animals (primarily rats and other rodents)

Transmission - droplet nuclei (only in epidemic periods)

- zoonotic
- vectorial (fleas)

Toxins - LPS

Diseases The Bubonic Plague

- "the black death"
- fever and severe focal lymphadenomegaly ("buboae")
- caused by phagocytosis of Yersinia Pestis by macrophages "
dissemination of Yersinia Pestis in regional lymph nodes
- may progress to the septic plague (see below)

The Septicemic Plague

- large black gangrenous hemorrhages of the skin, meninges, GI
tract and genitourinary tract
- > 50% mortality if untreated (within 3-6 days (!))
- caused by Yersinia Pestis septicemia
- may progress to the pneumonic plague (see below)

The Pneumonic Plague

- pneumonia and severe black gangrenous hemorrhages of the lungs
- > 75% mortality if untreated (within 2-4 days (!))
- caused by secondary septicemic spread of Yersinia Pestis to the
respiratory tract or by primary inhalation of droplet nuclei (only in
epidemic periods)

Treatment - aminoglycosides
- tetracyclines
PROTEUS, PROVIDENCIA

PROTEUS
Species - P. Mirabilis
- P. Vulgaris
- P. Penneri

Characteristics - gram -
- rod
- motile
- non-spore forming
- non-encapsulated
- facultative anaerobic
- opportunistic pathogen

Reservoirs - humans (normal flora of the GI tract)

- water
- soil

Transmission - fecal-oral
- direct contact
- contaminated water

Toxins - LPS

Diseases - wound infections

- bronchopneumonia
- cystitis and urolithiasis
- septicemia

Treatment - cephalosporins
- aminoglycosides

-
PROVIDENCIA
Species - P. Stuartii
- P. Rettgeri
- P. Alcalifaciens

Characteristics - same characteristics, reservoirs, transmission and toxins as Proteus

(see above, only differs in diseases and treatment, see below)

Diseases - gastroenteritis (see 1, primarily occurs in travelers)

- wound infections (primarily if burned)
- bronchopneumonia (primarily if intubated)
- cystitis (primarily if urinary catheter) and urolithiasis
- septicemia

Treatment - fluoroquinolones
- tetracyclines
KLEBSIELLA, ENTEROBACTER, CITROBACTER

KLEBSIELLA
Species - K. Pneumoniae
- K. Rhinoscleromatis
- K. Ozeanae

Characteristics - gram -
- rod
- encapsulated
- non-motile
- non-spore forming
- facultative anaerobic
- opportunistic pathogen

Reservoirs - humans (normal flora of the skin, nasopharynx, oropharynx and GI

tract)
- animals
- water
- soil

Transmission - direct contact

- fecal-oral
- contaminated fomites

Toxins - LPS

Diseases - second most common cause of lobar pneumonia and pulmonary

abscesses (after Streptococcus Pneumoniae, see 5, primarily caused
by K. Pneumoniae)
- rhinoscleroma (granulomas of both the upper and lower respiratory
tract " airway obstruction, primarily caused by K.
Rhinoscleromatis)
- ozena (atrophic rhinitis in conjunction with chronic sinusitis,
primarily caused by K. Ozaenae)
- wound infections (primarily if burned, caused by all species of
Klebsiella)
- cystitis (primarily if urinary catheter, caused by all species of
Klebsiella)
- second most common cause of septicemia
caused by all species of Klebsiella)

Treatment - third generation cephalosporins

- fluoroquinolones
ENTEROBACTER
Species - E. Aerogenes
- E. Agglomerans
- E. Cloacae

Characteristics - gram -
- rod
- encapsulated
- motile
- non-spore forming
- facultative anaerobic
- opportunistic pathogen

Reservoirs - humans (normal flora of the GI tract)

- animals
- water
- soil

Transmission - direct contact

- fecal-oral
- contaminated fomites

Toxins - LPS

Diseases Nosocomial Infections

- skin infections (folliculitis, cellulitis and impetigo), skin abscesses
(pustules, furuncles, carbuncles), and wound infections
- bronchopneumonia and pulmonary abscesses
- cystitis and renal abscesses (primarily if urinary catheter)
- neonatal meningitis and cerebral abscesses
- subacute infectious endocarditis
- osteomyelitis and arthritis
- septicemia

Treatment - aminoglycosides
- tetracyclines
CITROBACTER
Species - C. Diversus
- C. Freundii
- C. Amalonaticus

Characteristics - gram -
- rod
- encapsulated
- motile
- non-spore forming
- facultative anaerobic
- opportunistic pathogen

Reservoirs - humans (normal flora of the GI tract)

- animals
- water

Transmission - fecal-oral
- direct contact
- perinatal
- contaminated food

Toxins - LPS

Diseases - neonatal meningitis and cerebral abscesses (caused primarily by C.

Diversus)
- cystitis and renal abscesses (especially if urinary catheter, caused
by all species of Citrobacter)
- septicemia (caused by all species of Citrobacter)

Treatment - aminoglycosides
- chloramphenicol
CAMPYLOBACTER, HELICOBACTER

CAMPYLOBACTER
Characteristics - gram -
- helical rod
- motile
- non-spore forming
- non-encapsulated
- aerobic and microaerophilic (may survive in relatively oxygen-
poor environments)
- facultative alkaliphilic
- facultative intracellular

Campylobacter Jejuni
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily cattle and poultry)

Transmission - fecal-oral
- direct contact
- zoonotic
- contaminated food (primarily meat and milk)

Toxins - campylobacteral enterotoxin (analogous to choleragen (see 23),

causes gastroenteritis (see below))
- cytolethal distending toxin ("CDT", DNase, causes double-
stranded DNA-breaks " necrosis and inflammation "
hemorrhagic colitis and hemolytic-uremic syndrome, see below)
- LPS

Diseases In Children
- second most common BACTERIAL cause of gastroenteritis (see 1,
after ETEC, see 12)
- hemorrhagic colitis and hemolytic-uremic syndrome
- septicemia

Treatment - oral water and electrolyte replacement (if gastroenteritis and/or

hemorrhagic colitis)
- aminoglycosides (if hemolytic-uremic syndrome and/or
septicemia)

-
 Campylobacter Fetus
Characteristics - opportunistic pathogen

Reservoirs - humans (not normal flora)

- animals (primarily cattle, sheep and goats)

Transmission - direct contact

- fecal-oral
- zoonotic
- contaminated food

Toxins - LPS

Diseases InImmunocompromized
- meningitis, pleuritis, pericarditis and synovitis
- septicemia

Treatment - aminoglycosides
- macrolides

HELICOBACTER
Characteristics - gram -
- helical rod
- motile
- non-spore forming
- non-encapsulated
- aerobic and microaerophilic
- facultative alkaliphilic
- facultative intracellular
Helicobacter Pylori
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily cats)

Transmission - fecal-oral
- zoonotic

Toxins - vacuolating cytotoxin A ("VacA", causes chronic atrophic gastritis,

gastric adenocarcinoma and MALToma, see below)
- LPS

Diseases - most common cause of duodenal ulcers

- second most common cause of gastric ulcers (after aspirin)
- acute erosive gastritis
- chronic atrophic gastritis
- gastric adenocarcinoma and MALToma

Treatment - hydrogen ion/potassium antiporter inhibitors (if duodenal ulcers,

gastric ulcers and/or acute erosive gastritis)
- metronidazole in conjunction with broad spectrum penicillins (if
chronic atrophic gastritis, gastric adenocarcinoma and/or
MALToma)
VIBRIO AND AEROMONAS

VIBRIO
Characteristics - gram -
- curved rod
- motile
- non-spore forming
- non-encapsulated
- facultative anaerobic
- facultative alkaliphilic

Vibrio Cholerae
Characteristics - obligate isotonic (may only survive in isotonic environments)
- obligate pathogen

Reservoirs - humans (not normal flora)

- water

Transmission - fecal-oral
- contaminated water
- contaminated food

Toxins - choleragen (analogous to LT causes cholera gravis (see

below))
- LPS

Diseases Cholera Gravis

- severe watery diarrhea (>25 liter per day)
- may lead to hypovolemia " hypovolemic shock
- > 50% mortality if untreated (within hours (!))
- caused by Cholera Gravis infection of the GI tract " production
and secretion of choleragen (see above)

Treatment - oral water and electrolyte replacement

- tetracyclines
 Vibrio Parahaemolyticus
Characteristics - facultative hypertonic ("halophilic", may survive in both isotonic
and hypertonic environments, thus may survive in salt water)
- obligate pathogen

Reservoirs - humans (not normal flora)

- water (both fresh and salt water)
- animals (primarily fish and crustaceans)

Transmission - fecal-oral
- contaminated water
- contaminated food (primarily seafood)

Toxins - RTX toxin (causes gastroenteritis, hemorrhagic colitis and

hemolytic-uremic syndrome, see below)
- LPS

Diseases - wound infections

- gastroenteritis (see 1)
- hemorrhagic colitis and hemolytic-uremic syndrome
- septicemia

Treatment - oral water and elecrolyte replacement (if gastroenteritis,

hemorrhagic colitis and/or hemolytic-uremic syndrome)
- tetracyclines (if wound infections and/or septicemia)

AEROMONAS
Characteristics - gram -
- rod
- motile
- non-spore forming
- non-encapsulated
- facultative anaerobic
- facultative hypertonic

- 35 -
Aeromonas Hydrophilia
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- water (both fresh and salt water)
- soil

Transmission - fecal-oral
- contaminated water
- contaminated soil
- contaminated food (primarily seafood)

Toxins - aeromonas heat-labile enterotoxin ("ALT", "cytotonic

enterotoxin", analogous to choleragen , causes
gastroenteritis (see below))
- LPS

Diseases - gastroenteritis (see 1)

- wound infections (primarily if leech bites)
- endophthalmitis, keratitis and corneal ulcers
- bronchopneumonia
- cystitis
- septicemia

Treatment - oral fluid and electrolyte replacement (if gastroenteritis)

- tetracyclines (if all other diseases)

- 36 -
ACINETOBACTER

ACINETOBACTER
Characteristics - gram -
- pleomorphic rod (rod in log phase, coccobacillary rod (short
truncated rod) in stationary phase)
- encapsulated
- non-motile
- non-spore forming
- obligate aerobic

Acinetobacter Baumanii
Characteristics - opportunistic pathogen

Reservoirs - humans (normal flora of the skin)

- water
- soil

Transmission - direct contact

- droplet nuclei
- contaminated water
- contaimanted soil
- contaminated fomites

Toxins - LPS

Diseases Nosocomial Infections

- wound infections (primarily if surgical)
- bronchopneumonia (primarily if intubated)
- peritonitis (primarily if continuous ambulatory peritoneal dialysis)
- cystitis (primarily if urinary catheter)
- meningitis (primarily if external ventricular drainage catheter)
- septicemia

Treatment - carbapenems
- polymixins
PSEUDOMONAS AERUGINOSA
PSEUDOMONAS
Characteristics - gram -
- rod
- encapsulated
- motile
- non-spore forming
- obligate aerobic
Pseudomonas Aeruginosa
Characteristics - opportunistic pathogen

Reservoirs - humans (normal flora of the GI tract)

- water
- soil

Transmission - direct contact

- droplet nuclei
- contaminated water
- contaminated soil
- contaminated fomites

Toxins - exotoxin A ("exoA", ribosylates elongation factor 2 " # protein

synthesis " necrosis and inflammation, analogous to diphtheria
toxin,
- LPS

Diseases In Healthy
- endophthalmitis, keratitis and corneal ulcers (primarily if contact
lenses)
- otitis externa ("swimmer's ear")

In Immunocompromized
- second most common cause of acute infectious endocarditis (after
Staphylococcus Aureus, see 1)
- wound infections (primarily if burned)
- tracheobronchitis and bronchopneumonia (primarily if intubated)
- chronic bronchopneumonia and severe progressive pulmonary
abscesses (primarily if cystic fibrosis)
- cystitis and pyelonephritis (primarily if catheterized)
- meningitis (primarily if external ventricular drainage catheter)
- septicemia

Treatment - extended spectrum penicillins in conjunction with aminoglycosides

(due to high antibiotic resistance)
HAEMOPHILUS INFLUENZAE, H. PARAINFLUENZAE

HAEMOPHILUS
Characteristics - gram -
- pleomorphic rod
- non-motile
- non-spore forming
- facultative anaerobic

Haemophilus Influenzae
Characteristics - encapsulated
- opportunistic pathogen

Reservoirs - humans (only reservoir, normal flora of the nasopharynx,

oropharynx, oral cavity and conjunctiva)

Transmission - droplet nuclei

Toxins - LPS

Diseases In Neonates and Children

- acute laryngoepiglottitis ("obstructive laryngoepiglottitis")
- meningitis
- infective arthritis and osteomyelitis
- septicemia

Treatment - third generation cephalosporins

- chloramphenicol

- 39 -
HaemophilusParainfluenzae
Characteristics - non-encapsulated
- opportunistic pathogen
- same reservoirs, transmission and toxins as Hemophilus
Influenzae, see above)

Diseases In Teenagers and Adults

- otitis media and mastoiditis
- sinusitis
- bronchopneumonia (primarily if viral interstitial pneumonitis
and/or chronic bronchitis is already present)
- subacute infectious endocarditis
- septicemia

Treatment - broad spectrum penicillins

- broad spectrum penicillins in conjunction with beta-lactamase
inhibitors (if resistant to broad spectrum penicillins)
BORDETELLA PERTUSSIS, B. PARAPERTUSSIS,
B. BRONCHISEPTICA
BORDETELLA
Characteristics - gram -
- coccobacillary rod
- encapsulated
- non-spore forming
- obligate aerobic
Bordetella Pertussis
Characteristics - non-motile
- obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

Transmission - direct contact

- droplet nuclei

Toxins - tracheal cytotoxin ("TCT", disrupts mitochondria of bronchial

ciliated epithelial cells" ! cytochrome c release " ! activation of
caspases " apoptosis " #mucociliary clearance " pertussis, see
below)
- LPS

Diseases Pertussis
- "whooping cough"
- catarrhal stage (low-grade fever, myalgias, rhinorrhea and mild
non-productive cough, lasts > 2 weeks) " paroxysmal stage
(attacks of severe violent non-productive cough followed by an
inspiratory gasp ("whoop"), lasts > 4 weeks) "covalescent stage
(gradual decrease in number and severity of the attacks, lasts < 4
weeks)
- primarily occurs in neonates
- caused by Bordetella Pertussis colonization of the respiratory tract
" secretion of tracheal cytotoxin (see above)

Treatment - macrolides (if in catarrhal stage)

- intubation and mucous removal (if in paroxysmal stage)

-
Bordetella Parapertussis
Characteristics - same characteristics, toxins, diseases and treatment as Bordetella
Pertussis (see above)

Reservoirs - humans (not normal flora)

- animals (primarily sheep)

Transmission - direct contact

- droplet nuclei
- zoonotic

Bordetella Bronchiseptica
Characteristics - motile
- obligate pathogen
- same transmission, toxins, diseases and treatment as Bordetella
Parapertussis (see above)

Reservoirs - humans (not normal flora)

- animals (primarily swine, dogs and cats)
BRUCELLA, FRANCISELLA
BRUCELLA
Species - B. Melitensis
- B. Bovis
- B. Suis
Characteristics - gram -
- pleomorphic rod
- encapsulated
- non-motile
- non-spore forming
- obligate aerobic
- facultative intracellular
- obligate pathogen
Reservoirs - humans (not normal flora)
- animals (primarily sheep (B. Melitensis), cattle (B. Bovis) and
swine (B. Suis)
Transmission - zoonotic
- aerosolized ("airborne")
- contaminated food (primarily meat and milk)
Toxins - LPS
Diseases
Brucellosis
- "undulant fever"
- alternating fever (low in the morning, high in the evening),
alternating sweats and chills, headache, arthralgias,
hepatosplenomegaly and generalized lymphadenopathy
- lasts for months
- primarily occurs in farmers, abattoir workers and veterinarians
- caused by Brucella septicemia
Treatment - aminoglycosides in conjunction with tetracyclines (due to high
antibiotic resistance)
- trimethoprim-sulfamethoxazole

-
FRANCISELLA
Characteristics - gram -
- pleomorphic bipolar rod
- encapsulated
- non-motile
- non-spore forming
- obligate aerobic
- facultative intracellular

FrancisellaTularensis
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily rodents and birds)

Transmission - zoonotic
- aerosolized
- vectorial (mosquitoes, ticks and fleas)
- contaminated food (primarily meat)

Toxins - LPS

Diseases Ulceroglandular Tularemia

- "rabbit fever"
- black-based ulcerating papule at the site of initial infection, fever
and severe local lymphadenomegaly
- most common (80%)
- analogous to the bubonic plague (see 17)
- caused by initial FrancisellaTularensis infection of the skin

Occuloglandular Tularemia
- unilateral conjunctivitis, corneal ulcers, fever and severe
preauricular and/or cervical lymphadenomegaly
- caused by initial FrancisellaTularensis infection of the eye

Oropharyngeal Tularemia
- pharyngitis, vomiting, watery diarrhea, fever and severe mesenteric
lymphadenomegaly
- caused by ingestion of FrancisellaTularensis " initial Francisella
Tularensis infection of the oropharynx and GI tract

Pneumonic (Pulmonary) Tularemia

- interstitial pneumonitis and/or bronchopneumonia, fever and
severe hilar lymphadenomegaly
- > 30% mortality if untreated (!)
- caused by inhalation of FrancisellaTularensis " initial Francisella
Tularensis infection of the lungs

--
Treatment - aminoglycosides
- tetracyclines
LEGIONELLA

LEGIONELLA
Characteristics - gram -
- rod
- motile
- non-spore forming
- non-encapsulated
- obligate aerobic
- facultative intracellular

Legionella Pneumophilia
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- water

Transmission - aerosolized (through shower heads, air conditioners and cooling

towers)

Toxins - LPS

Diseases Mild Legionellosis

- "pontiac fever"
- low-grade fever, rhinorrhea, mild non-productive cough and
myalgias
- spontaneously resolves in < 1 week
- caused by Legionella Pneumophilia infection of the lungs in
healthy

Severe Legionellosis
- "legionaire's disease"
- high fever, headache, delirium, severe cavitating
bronchopneumonia, hemoptysis, vomiting, watery diarrhea and
anorexia
- > 40% mortality if untreated (!)
- caused by Legionella Pneumophilia infection of the lungs in
elderly smokers

Treatment - macrolides
- fluoroquinolones
BACILLUS ANTHRACIS, B. CEREUS
BACILLUS
Characteristics - gram +
- rod
- spore forming (forms a sturdy vegetative infectious particle)
- obligate aerobic
- facultative intracellular
Bacillus Anthracis
Characteristics - encapsulated
- non-motile
- obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily horses, cattle, sheep and swine)
- soil (primarily spores)

Transmission - zoonotic
- aerosolized
- vectorial (flies)
- contaminated soil
- contaminated food
- contaminated fomites (primarily wool and hides)

Toxins - lethal factor ("LF", causes ! TNF-alpha secretion from

macrophages " necrosis of host cells and septic shock " anthrax,
see below)

Diseases Cutaneous Anthrax

- painless necrotic black-based ulcerating papule
- may complicate by septicemia " septic shock
- > 5% mortality if untreated (!)
- most common
- caused by Bacillus Anthracis infection of the skin

Gastrointestinal Anthrax
- gastrointestinal necrosis and hemorrhage, abdominal pain,
vomiting and bloody diarrhea
- may complicate by septicemia " septic shock
- > 50% mortality if untreated (!)
- caused by ingestion of Bacillus Anthracis " Bacillus Anthracis
infection of the GI-tract

Pulmonary Anthrax
- severe hilar lymph node necrosis and mediastinal hemorrhage
 - may complicate by septicemia " septic shock
- 100% mortality if untreated (!)
- caused by inhalation of Bacillus Anthracis " Bacillus Anthracis
infection of the lungs

Treatment - narrow spectrum penicillins

- macrolides
Bacillus Cereus
Characteristics - motile
- non-encapsulated
- obligate pathogen

Reservoirs - humans (not normal flora)

- soil (primarily spores)

Transmission - contaminated food (primarily rice)

Toxins - bacillus heat-labile enterotoxin (analogous to choleragen (see 23)

causes diarrheal food poisoning (see below))
- bacillus heat-stabile enterotoxin (analogous to staphylococcal
enterotoxin (see 1), causes emetic food poisoning (see below))

Diseases Diarrheal Food Poisoning

- diarrheal gastroenteritis (abdominal pain, vomiting and watery
diarrhea)
- spontaneously resolves in < 24 hours
- caused by Bacillus Cereus contamination of food " production
and secretion of bacillus heat-labile enterotoxin (see above) "
ingestion of bacillus heat-labile enterotoxin-contaminated food

Emetic Food Poisoning

- emetic gastroenteritis (severe vomiting)
- spontaneously resolves in < 24 hours
- caused by Bacillus Cereus contamination of food " production
and secretion of bacillus heat-stabile enterotoxin (see above) "
ingestion of bacillus heat-stabile enterotoxin-contaminated food

Treatment - oral fluid and electrolyte replacement

GAS-GANGRENE CLOSTRIDIA

CLOSTRIDIUM
Characteristics - gram +
- rod
- encapsulated
- spore forming
- non-motile
- obligate anaerobic

Clostridium Perfringens
Characteristics - opportunistic pathogen

Reservoirs - humans (normal flora of the skin, GI tract and female genitalia)
- animals (primarily cattle, swine, poultry and fish)
- soil (primarily spores)

Transmission - direct contact

- fecal-oral
- contaminated soil
- contaminated food

Toxins - clostridium perfringens enterotoxin ("CPE", destroys the tight

junctions of the enterocytes" ! membrane permeability " !
intraluminal osmotic pressure " food poisoning, see below)
- bet2a+-toxin (forms pores in the enterocytes " massive influx of
Ca" ! activation of caspases " apoptosis of the enterocytes "
enteritis necroticans, see below)
- alpha-toxin (causes necrosis of host cells " gas gangrene, see

below)

Food Poisoning
- gastroenteritis (see 1)
Diseases - spontaneously resolves in < 24 hours
- caused by Clostridium Perfringens contamination of food "
production and secretion of CPE (see above) " ingestion of CPE-
contaminated food

Enteritis Necroticans
- abdominal pain, vomiting and bloody diarrhea
- caused by Clostridium Perfringens infection of the GI tract "
production and secretion of beta-toxin (see above)

Gas Gangrene
- large painful spongy gangrene of skin and muscle containing
pockets of gas ("crepitus") and thin black exudate
 - caused by Clostridium Perfringens infection of wounds "
production and secretion of alpha-toxin (see above)

Treatment - oral water and electrolyte replacement (if gastroenteritis)

- narrow spectrum penicillins (if enteritis necroticans)
- narrow spectrum penicillins in conjunction with surgical excision
(if gas gangrene)

--
CLOSTRIDIUM TETANI

Clostridium Tetani
Characteristics - opportunistic pathogen

Reservoirs - humans (normal flora of the GI tract)

- animals
- soil (primarily spores)

Transmission - direct contact

- zoonotic
- contaminated soil

Toxins - tetanus neurotoxin ("TeNT", "tetanospasmin", inhibits

neurotransmitter release from inhibitory neurons of motor neurons
" constant activation of the motor neurons " tetanus, see below)

Diseases Tetanus
- severe painful muscle spasms ("tetany") of the face and neck
leading to lockjaw ("trismus") and a sinister grin ("risus
sardonicus") " painful muscle spasms of the trunk
- may complicate by painful muscle spasms of the respiratory
muscles " death
- > 90% mortality if untreated (!)
- caused by Clostridium Tetani infection of wounds " production
and secretion of TeNT (see above) " uptake of TeNT into motor
neurons " retrograde axonal transport of TeNT into the CNS

Treatment - narrow spectrum penicillins in conjunction with tetanus antitoxin

and surgical excision
- muscle relaxants and intubation (if spasms of the respiratory
muscles)

-
CLOSTRIDIUM BOTULINUM, C. DIFFICILE
Clostridium Botulinum
Characteristics - opportunistic pathogen
Reservoirs - humans (normal flora of the GI tract)
- animals (primarily swine and fish)
- water
- soil (primarily spores)
Transmission - contaminated food (primarily smoked meat and canned vegetables)
Toxins - botulinum neurotoxin ("BoNT", inhibits acetylcholine release from
motor neurons " flaccid paralysis " botulism, see below)

Diseases Adult Botulism

- "foodborne botulism"
- flaccid paralysis of the head and neck leading to double vision
("diplopia") and difficulties of swallowing " flaccid paralysis of
the trunk
- may complicate by causing flaccid paralysis of the respiratory
muscles " death
- > 90% mortality if untreated (!)
- caused by Clostridium Botulinum contamination of food "
production and secretion of BoNT (see above) " ingestion of
BoNT-contaminated food

Infantile Botulism
- "floppy baby syndrome"
- constipation " asthenia and difficulties of swallowing
- caused by Clostridium Botulinum infection of the GI tract "
production and secretion of BoNT (see above)
Treatment - botulinum toxin antitoxin (if adult botulism)
- narrow spectrum penicillins (if infantile botulism)
- intubation (if paralysis of the respiratory muscles)
Clostridium Difficile
Characteristics - opportunistic pathogen

Reservoirs - humans (normal flora of the GI tract)

- animals
- water
- soil (primarily spores)
- sand (primarily spores)

Transmission - direct contact

- fecal-oral
- contaminated fomites

Toxins - toxin A ("clostridium difficile enterotoxin", causes watery

diarrhea, see below)
- toxin B ("clostridium difficile cytotoxin" , causes necrosis of the
simple columnar epithelial cells of the colon "pseudomembrane
formation, see below)

Diseases Pseudomembranous Colitis

- "antibiotics-associated colitis"
- colitis, pseudomembrane formation (coagulated pus) on the
luminal surface of colon and watery purulent diarrhea
- caused by excessive antibiotics treatment with broad spectrum
penicillins, cephalosporins and/or lincosamides " elimination of
the competing normal bacterial flora in the GI tract " overgrowth
of Clostridium Difficile in the GI tract " production and secretion
of toxin A and toxin B (see above)

Treatment - metronidazole
- vancomycin
CORYNEBACTERIUM DIPHTHERIAE
CORYNEBACTERIUM
Characteristics - gram +
- clubbed rod
- non-encapsulated
- non-motile
- non-spore forming
- facultative anaerobic
Corynebacterium Diphtheriae
Characteristics - opportunistic pathogen
Reservoirs - humans (only reservoir, normal flora of the skin and nasopharynx)
Transmission - direct contact
- droplet nuclei
Toxins - diphtheria toxin ("DT", analogous to exotoxin A , causes
diphtheria (see below))
Nasopharyngeal Diphtheria
Diseases - low-grade fever, headache, pharyngitis and pseudomembrane
formation on the luminal surface of the pharynx "
laryngeotracheobroncitis and pseudomembrane formation in the
larynx, trachea and bronchi " airway obstruction
- may complicate by diphtheria toxin toxemia " infective
myocarditis and peripheral neuropathies
- 10% mortality if untreated (!)
- caused by Corynebacterium Diphtheriae infection of the
nasopharynx
Cutaneous Diphtheria
- persistent ulcer covered by a grey pseudomembrane
- caused by Corynebacterium Diphtheriae infection of the skin
Treatment - narrow spectrum penicillins in conjunction with diphtheria toxin
antitoxin
- intubation (if pseudomembrane formation in the larynx, trachea
and brochi)

-
LISTERIA, ERYSIPELOTHRIX

LISTERIA
Characteristics - gram +
- rod
- motile
- non-encapsulated
- non-spore forming
- facultative anaerobic
- facultative intracellular

Listeria Monocytogenes
Characteristics - opportunistic pathogen

Reservoirs - humans
- animals
- insects
- water
- soil (primarily mud)

Transmission - direct contact

- sexual
- perinatal
- zoonotic
- contaminated soil
- contaminated food

Toxins - none in particular

Diseases In Neonates
- abortion, premature birth and stillbirth
- neonatal meningitis
- granulomatosis infantiseptica (abscess formation and granuloma
formation in multiple organs)
- septicemia

In Elderly and Immunocompromized

- meningitis and cerebritis
- septicemia

Treatment - broad spectrum penicillins

- aminoglycosides
ERYSIPELOTHRIX
Characteristics - gram +
- rod
- non-encapsulated
- non-motile
- non-spore forming
- facultative anaerobic
- facultative intracellular

ErysipelothrixRhusiopathiae
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily swine, poultry, fish and birds)
- water
- soil

Transmission - zoonotic
- contaminated food
- contaminated soil

Toxins - none in particular

Diseases Cutaneous Erysipeloid

- burning erythematous papule at the site of initial infection and low-
grade fever
- caused by ErysipelothrixRhusiopathiae infection of wounds
- may progress to diffuse erysipeloid (see below)

Diffuse Erysipeloid
- multiple burning red erythematous papules with necrotic centers,
headache, myalgias and arthralgias
- caused by progression of cutaneous erysipeloid (see above)
- may progress to septicemic erysipeloid (see below)

Septicemic Erysipeloid
- subacute infectious endocarditis and arthritis
- caused by progression of diffuse erysipeloid (see above) or by
ErysipelothrixRhusiopathiae infection of the GI tract "
ErysipelothrixRhusiopathiae septicemia

Treatment - narrow spectrum penicillins

- broad spectrum penicillins
MYCOBACTERIUM TUBERCULOSIS, M. BOVIS
ANTI-TUBERCULOSIS TREATMENT

MYCOBACTERIUM
Characteristics - acid-fast (stains red with acid-fast stain) gram +
- rod
- non-encapsulated
- non-motile
- non-spore forming
- obligate aerobic
- facultative intracellular

Mycobacterium Tuberculosis
Characteristics - obligate pathogen

Reservoirs - humans

Transmission - droplet nuclei

Toxins - none in particular

Diseases Primary Tuberculosis

- several medium-sized caseating calcifying granulomas in the
middle and lower lobes of the lungs ("gohn focus") and several
medium-sized caseating calcifying granulomas in the hilar lymph
nodes ("gohn complex")
- caused by primary Mycobacterium Tuberculosis infection of the
lungs
- may progress to pulmonary miliary tuberculosis, extrapulmonary
miliary tuberculosis, pulmonary reactivation tuberculosis and/or
extrapulmonary reactivation tuberculosis (see below)

Pulmonary Miliary Tuberculosis

- hundrends of tiny caseating calcifiying granulomas throughout the
lung parenchyma
- primarily occurs in neonates and in immunocompromized
- caused by absent or incomplete healing of the gohncompexes "
spread of the Mycobacterium Tuberculosis by the pulmonary
lymphatics " reentrance of Mycobacterium Tuberculosis through
the pulmonary arteries

Extrapulmonary Miliary Tuberculosis

- hundreds of tiny caseating calcifying granulomas throughout the
base of the brain, liver, spleen and kidneys
- primarily occurs in neonates and in immunocompromized
- caused by absent or incomplete healing of the gohncompexes "

--
 spread of the Mycobacterium Tuberculosis by the pulmonary veins
" entrance of Mycobacterium Tuberculosis into the systemic
circulation

Pulmonary Reactivation Tuberculosis

- low-grade fever, multiple large caseating cavitating granulomas
and large hemorrhaging cavernae in the upper lobes of the lungs,
productive cough and hemoptysis
- caused by escape of dormant Mycobacterium Tuberculosis bacteria
from the healed gohn complexes (see above) " spread of the
Mycobacterium Tuberculosis by the pulmonary lymphatics (see
above)

Extrapulmonary Reactivation Tuberculosis

- meningitis and multiple medium-sized caseating granulomas in the
brain
- pleuritis, pericarditis and peritonitis
- multiple medium-sized caseating granulomas in the kidneys
- orchidoepididymitis, oophoritis and multiple medium-sized
caseating granulomas in the testes and ovaries
- spondylitis of the vertebral bodies and multiple medium-sized
caseating granulomas in the intervertebral discs ("pott's disease")
- caused by escape of dormant Mycobacterium Tuberculosis for the
healed gohn complexes " spread of the Mycobacterium
Tuberculosis by the pulmonary veins (see above)

Treatment Primary Phase

- isoniazid in conjunction with rifampin and pyrazinamide (as well
as ethambutol if high antibiotic resistance)
- lasts 2 months

Secondary Phase
- isoniazid in conjunction with rifampin
- lasts 4 months (6 months if high antibiotic resistance)

Mycobacterium Bovis
Characteristics - obligate pathogen
- same toxins, diseases and treatment as Mycobacterium
Tuberculosis (see above)

Reservoirs - humans (not normal flora)

- animals (primarily cattle, primates and rodents)

Transmission - droplet nuclei

- zoonosis
- contaminated food (primariy meat and milk)
MYCOBACTERIUM LEPRAE AND OTHER NON-
TUBERCULOUS MYCOBACTERIA

Mycobacterium Leprae
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (possibly armadillos)

Transmission - direct contact

- droplet nuclei
- zoonosis

Toxins - none in particular

Diseases Paucibacillary Leprosy

- "tuberculoid leprosy"
- < 5 medium-sized granular hairless hypopigmented non-healing
skin lesions " local peripheral nerve thickening leading to partial
loss of sensation and asthenia in the affected areas
- caused by Mycobacterium Leprae infection of the skin in healthy

Multibacillary Leprosy
- "lepromatous leprosy"
- > 5 large nodular hairless hypopigmented non-healing skin lesions
leading to destruction of the nasal cartilage and deformation of the
face ("leonine facies") " multiple medium-sized granulomas in the
liver, spleen and lymph nodes leading to hepatosplenomegaly and
generalized lymphadenomegaly " generalized peripheral nerve
thickening leading to complete loss of sensastion and paralysis of
the arms and legs " unconscious damage and secondary infections
of the arms and legs leading to loss of fingers and toes
- caused by Mycobacterium Leprae infection of the skin in
immunocompromized

Treatment Paucibacillary Leprosy

- dapsone in conjunction with rifampin
- lasts 6 months

Multibacillary Leprosy
- dapsone in conjunction with rifampin and clofazimine
- lasts 2 years
Mycobacterium Avium & M. Intracellulare
Characteristics - opportunistic pathogen

Reservoirs - humans (not normal flora)

- animals (primarily cattle, swine and birds)
- water
- soil

Transmission - zoonotic
- aerosolized
- contaminated water
- contaminated food

Toxins - none in particular

Diseases Pulmonary Mycobacterium Avium-Intracellulare Complex

- ""pulmonary MAC"
- low-grade fever and productive cough
- primarily occurs if viral interstitial pneumonitis and/or chronic
bronchitis is already present
- caused by MAC infection of the lungs

Gastrointestinal Mycobacterium Avium-Intracellulare Complex

- "gastrointestinal MAC"
- low-grade fever and watery diarrhea
- primarily occurs in immunocompromized
- caused by MAC infection of the GI tract
- may progress to disseminated MAC (see below)

Disseminated Mycobacterium Avium-Intracellulare Complex

- "disseminated MAC"
- high fever, severe anorexia, severe anemia, hepatosplenomegaly
and generalized lymphadenomegaly
- caused by progression of gastrointestinal MAC (see above) "
MAC septicemia

Treatment - aminoglycosides
- macrolides
-
TREPONEMA PALLIDUM

TREPONEMA
Characteristics - gram -
- spirochete (helically-coiled cell)
- motile
- non-spore forming
- non-encapsulated
- microaerophilic

Treponema Pallidum
Characteristics - obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

Transmission - direct contact

- sexual
- perinatal

Toxins - none in particular (not even LPS (!))

Diseases Primary Syphilis

- a single small painless depressed ulcer with elevated margins
("chancre") at the site of initial infection, fever, headache, anorexia
and local lymphadenomegaly
- primarily occurs on the external genitalia, periorally (if oral
intercourse) or perianally (if anal intercourse)
- occurs 3-6 weeks after initial infection
- spontaneously resolves in 3-6 weeks
- caused by Treponema Pallidum infection of the skin
- may progress to secondary syphilis (see below)

Secondary Syphilis
- small flat erythematous rashes of the palms and soles, small
painless papules ("condyloma lata") of the groin and axilla, and
generalized lymphadenomegaly
- occurs 12-18 weeks after initial infection
- spontaneously resolves in 3-6 weeks
- caused by Treponema Pallidum septicemia
- may progress to tertiary syphilis (see below)

Tertiary Syphilis
- nodular well circumscribed caseating granulomas ("gummas") of
the skin, liver and bone, obliterative endarteritis of the vasa
vasorum leading to aortic aneurysm ("cardiovascular syphilis"),
meningitis, obliterative endarteritis of the cerebral arteries leading
 to cerebral infarct, and permanent central neuronal damage leading
to general paresis and tabes dorsalis ("neurosyphilis")
- occurs 3-15 years after initial infection
- occurs in 30% of untreated patients
- caused by Treponema Pallidum accumulation in tissues

Early Congenital Syphilis

- small flat erythematous rashes of the palms and soles, condyloma
lata (see above) of the groin and axilla, osteitis, rhinitis (snuffles"),
hepatosplenomegaly and generalized lymphadenomegaly
- occurs immediately after birth
- spontaneously resolves in 1-3 weeks
- caused by intrauterine Treponema Pallidum infection "
Treponema Pallidum septicemia
- may progress to late congenital syphilis (see below)

Late Congenital Syphilis

- gummas (see above) of the cartilage of the nose, the bone of the
hard palate and the teeth leading to deformation of the face
("bulldog facies"), gummas of the tibia and fibula leading to
deformation of the legs ("saber shins"), and neurosyphilis (see
above)
- occurs 1-3 years after birth
- caused by Treponema Pallidum accumulation in tissues

Treatment - narrow spectrum penicillins

- tetracyclines
BORRELIA

BORRELIA
Characteristics - gram -
- spirochete
- motile
- non-spore forming
- non-encapsulated
- microaerophilic

Borrelia Burgdorferi
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily deer and rodents)

Transmission - vectorial (ticks)

Toxins - none in particular

Diseases Early Localized Lyme Disease

- a single large round flat painless enlarging erythematous rash with
central necrosis ("erythema chronicum migrans") at the site of
initial infection, fever, headache, myalgias, and local
lymphadenomegaly
- occurs 1 week after initial infection
- spontaneously resolves in < 1 month
- caused by Borrelia Burgdorferi infection of the skin
- may progress to early disseminated lyme disease (see below)

Early Disseminated Lyme Disease

- disseminated small erythema chronicum migrans (see above),
relapsing arthritis, carditis leading to AV block, meningitis, cranial
nerve damage leading to cranial nerve neuropathies, peripheral
nerve damage leading to peripheral neuropathies, and generalized
lymphadenomegaly
- occurs 1-3 months after initial infection
- caused by Borrelia Burgdorferi septicemia
- may progress to late disseminated lyme disease (see below)

Late Disseminated Lyme Disease

- chronic arthritis and permanent central neuronal damage leading to
encephalopathies
- occurs 3-6 months after initial infection
- occurs in 10% of untreated patients
- caused by Borrelia Burgdorferi accumulation in tissues
Treatment - broad spectrum penicillins (if early localized lyme disease and/or
early disseminated lyme disease)
- third generation cephalosporins (if late disseminated lyme disease)

Borrelia Recurrentis
Characteristics - obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

Transmission - vectorial (body lice)

Toxins - none in particular

Diseases Relapsing Fever

- high fever, headache, myalgias and disseminated skin rashes for <
1 week " afebrile period for > 1 week " progressively shorter
and milder periods of fever and progressively longer afebrile
periods until it completely disappears
- caused by Borrelia Recurrentis septicemia

Treatment - narrow spectrum penicillins

- tetracyclines
LEPTOSPIRA

LEPTOSPIRA
Characteristics - gram -
- spirochette
- motile
- non-encapsulated
- non-spore forming
- obligate aerobic

Leptospira Interrogans
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals

Transmission - zoonotic
- aerosolized
- contaminated water
- contaminated soil
- contaminated food

Toxins - none in particular

Diseases Anicteric Leptospirosis

- "fort bragg fever"
- spiking fever, headache and myalgias (primarily of the calves, back
and abdomen) " meningitis (usually subclinical)
- most common
- caused by Leptospira Interrogans infection of the GI tract " mild
septicemia

Icteric Leptospirosis
- "weil's disease"
- enterocolitis (see 14) and mesenteric lymphadenitis ("mock
appendicitis") " meningitis, infectious interstitial nephritis leading
to intrarenal acute renal failure and uremia, and hepatitis leading
jaundice and coagulopathies
- caused by Leptospira Interrogans infection of the GI tract " severe
septicemia

Treatment - narrow spectrum penicillins

- broad spectrum penicillins
BACTEROIDES, FUSOBACTERIUM AND VEILLONELLA

BACTEROIDES
Species - B. Fragilis
- B. Ovatus
- B. Vulgatus

Characteristics - gram -
- pleomorphic rod
- encapsulated
- motile or non-motile depending on the species
- non-spore forming
- obligate anaerobic
- opportunistic pathogen

Reservoirs - humans (normal flora of the nasopharynx, oropharynx, oral cavity,

GI tract (99% of the normal flora of the GI tract (!)), and female
genitalia)
- animals

Transmission - trauma
- zoonosis

Toxins - none in particular (not even LPS (!))

Diseases - otitis media and mastoiditis

- sinusitis
- gingivitis and periodontitis
- pharyngitis and retropharyngeal abscesses
- bronchopneumonia and pulmonary abscesses
- peritonitis, subphrenic abscesses and hepatic abscesses
- vulvovaginitis and pelvic inflammatory disease
- meningitis and cerebral abscesses
- subacute infectious endocarditis
- osteomyelitis and infective arthritis
- septicemia

Treatment - metronidazole
- lincosamides
FUSOBACTERIUM
Species - F. Necrophorium
- F. Nucleatum
- F. Polymorphum

Characteristics - same characteristics, reservoirs, transmission, toxins, diseases and

treatment as Bacteroides (see above)

VEILLONELLA
Species - V. Atypica
- V. Dispar
- V. Parvula

Characteristics - gram -
- curved coccus
- encapsulated
- non-motile
- non-spore forming
- obligate anaerobic
- opportunistic pathogen
- same reservoirs, transmission and toxins as Bacterioides (see
above)

Diseases - gingivitis and periodontitis

- pharyngitis and retropharyngeal abscesses
- bronchopneumonia and pulmonary abscesses
- meningitis and cerebral abscesses
- subacute infectious endocarditis
- osteomyelitis and infective arthritis (primarily if prosthetic joints)
- septicemia (primarily if central venous catheter)

Treatment - narrow spectrum penicillins

- broad spectrum penicillins
RICKETTSIA

RICKETTSIA
Characteristics - gram -
- pleomorphic rod
- encapsulated
- non-motile
- non-spore forming
- obligate aerobic
- obligate intracellular

Rickettsia Rickettsii
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily dogs and rodents)

Transmission - zoonotic
- vectorial (ticks)

Toxins - LPS

Diseases Rocky Mountain Spotted Fever

- fever, headache, myalgias, and maculopapular rashes beginning on
the palms and soles and then progressing towards the trunk
- spontaneously resolves in < 3 weeks
- 20% mortality if untreated (!)
- caused by Rickettsia Rickettsii septicemia

Treatment - tetracyclines
- chloramphenicol

Rickettsia Prowazekii
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (possibly flying squirrels)

Transmission - zoonotic
- vectorial (body lice)

Toxins - LPS
Diseases Acute Epidemic Typhus
- fever, headache, myalgias and maculopapular rashes beginning on
the trunk and then progressing towards the extremities (except the
palms, soles and face)
- spontaneously resolves in < 3 weeks
- 10% mortality if untreated (!)
- caused by Rickettsia Prowazekii septicemia
- may progress to chronic epidemic typhus (see below)

Chronic Epidemic Typhus

- "brill-zinsser disease"
- fever, headache and myalgias
- occurs years after initial infection
- caused by reactivation of latent Rickettsia Prowazekii " Rickettsia
Prowazeki septicemia

Treatment - tetracyclines
- chloramphenicol

Rickettsia Typhi
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily rodents)

Transmission - zoonotic
- vectorial (fleas)

Toxins - LPS

Diseases Endemic Typhus

- similar to epidemic typhus (see above)
- caused by Rickettsia Prowazekii septicemia

Treatment - tetracyclines
- chloramphenicol

Rickettsia Akari
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily rodents)

Transmission - zoonotic
- vectorial (mites)
Toxins - LPS

Diseases Rickettsialpox
- small erythematous vescicular papule at the site of initial infection
" fever, headache and disseminated small erythematous vesicular
papules
- spontaneously resolves in < 1 week
- caused by Rickettsia Akari septicemia

Treatment - tetracyclines
- chloramphenicol
COXIELLA, BARTONELLA

COXIELLA
Characteristics - gram -
- pleomorphic rod
- spore forming
- non-motile
- non-encapsulated
- obligate aerobic
- obligate intracellular

Coxiella Burnetti
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily cattle and sheep)

Transmission - zoonotic
- aerosolized
- contaminated food (primarily milk)

Toxins - LPS

Diseases Acute Pulmonary Q Fever

- fever, headache and interstitial pneumonitis
- caused by Coxiella Burnetti infection of the lungs
- may progress to chronic q fever (see below)

Acute Gastrointestinal Q Fever

- fever, headache and hepatitis
- caused by Coxiella Burnetti infection of the GI tract
- may progress to chronic q fever (see below)

Chronic Q Fever
- fever, headache and subacute infectious endocarditis
- occurs years after initial infection
- caused by reactivation of latent Coxiella Burnetti " Coxiella
Burnetti septicemia

Treatment - tetracyclines
- chloramphenicol
BARTONELLA
Characteristics - gram -
- pleomorphic rod
- motile
- non-spore forming
- non-encapsulated
- obligate aerobic
- facultative intracellular

Bartonella Henselae
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily cats)

Transmission - zoonotic
- vectorial (fleas)

Toxins - none in particular

Diseases Cat Scratch Disease

- a single purulent papular lesion at the site of initial infection, low
grade fever and local lymphadenomegaly
- spontaneously resolves in < 3 months
- caused by Bartonella Henselae infection of the skin
- may progress to bacillary angiomatosis and/or bacillary peliosis
(see below)

Bacillary Angiomatosis
- cystic congested vascular proliferations in the skin and mucous
membranes
- primarily occurs in immunocompromized
- caused by Bartonella Henselae infection of vascular endothelium

Bacillary Peliosis
- cystic congested vascular proliferations in the liver and spleen
- primarily occurs in immunocompromized
- caused by Bartonella Henselae infection of vascular endothelium

Treatment - tetracyclines in conjunction with surgical drainage (if cat scratch

disease)
- tetracyclines (if bacillary angiomatosis and/or bacillary peilosis)
Bartonella Quintana
Characteristics - obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

-
Transmission - vectorial (body lice)

Toxins - none in particular

Diseases Acute Trench Fever

- high fever, headache, myalgias (primarily of the calves, back and
abdomen) and skin rashes for < 1 week " afebrile period for > 2
weeks " progressively shorter and milder periods of fever and
progressively longer afebrile periods until it completely disappears
- primarily occurs in homeless
- analogous to relapsing fever (see 40)
- caused by Bartonella Quintana septicemia
- may progress to chronic trench fever, bacillary angiomatosis and/or
bacillary peliosis (see below)

Chronic Trench Fever

- relapsing high fever, headache, myalgias and skin rashes in
conjunction with subacute infectous endocarditis, hepatic abscesses
and splenic abscesses
- primarily occurs in immunosuppressed
- caused by progression of acute trench fever (see above)

Bacillary Angiomatosis
- see above

Bacillary Peliosis
- see above

Treatment - tetracyclines
- macrolides
CHLAMYDIA

CHLAMYDIA
Characteristics - gram -
- coccus
- spore forming
- non-motile
- non-encapsulated
- obligate aerobic
- obligate intracellular

Chlamydia Trachomatis
Characteristics - obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

Transmission - direct contact

- sexual
- perinatal

Toxins - LPS

Diseases In Males
- most common cause of non-gonococcal urethritis ("chlamydia")
- prostatitis and epididymitis

In Females
- most common cause of non-gonococcal urethritis and cervicitis
("chlamydia")
- pelvic inflammatory disease, tuboovarian abscesses, ectopic
pregnancies and infertility

In Both Males and Females

- trachoma ("follicular keratoconjunctivitis") and blindness
- lymphogranuloma venerum (painless ulcer at the site of initial
infection and local lymphadenitis), rectal stricture and elephantiasis
- reiter's syndrome (septic oligoarthritis of the large joints)
- septicemia

In Neonates
- conjunctivitis and blindness
- neonatal interstitial penumonitis

Treatment - tetracyclines in conjunction with third generation cephalosporins

(if non-gonococcal urethritis and/or cervicitis, due to the possibility
that the urethritis and/or cervicitis may be of Neisseria
 Gonorrhoeae and/or UreaplasmaUrealyticum
origin)
- tetracyclines (if trachoma and/or conjunctivitis)
- macrolides (if neonatal interstitial pneumonitis)

Chlamydia Psittaci
Characteristics - obligate pathogen

Reservoirs - humans (not normal flora)

- animals (primarily birds)

Transmission - zoonotic
- aerosolized

Toxins - LPS

Diseases Parrot Fever

- "psittacosis"
- fever, headache, myalgias and interstitial pneumonitis
- caused by Chlamydia Psittaci infection of the lungs

Treatment - tetracyclines
- macrolides

-
MYCOPLASMA, UREAPLASMA

MYCOPLASMA
Characteristics - gram -
- pleomorphic (neither coccus nor rod, due to no cell wall (!))
- motile (but has no flagella, unknown mechanism (!))
- non-spore forming
- non-encapsulated
- facultative anaerobic

Mycoplasma Pneumoniae
Characteristics - obligate pathogen

Reservoirs - humans (only reservoir, not normal flora)

Transmission - direct contact

- droplet nuclei
- contaminated fomites

Toxins - none in particular

Diseases - most common BACTERIAL cause of interstitial pneumonitis

- pharyngitis and tracheobronchitis
- wound infections (primarily if surgical)
- meningitis and cerebritis
- subacute infectious endocarditis and acute pericarditis
- infective arthritis
- septicemia

Treatment - tetracyclines
- macrolides

UREAPLASMA
Characteristics - gram -
- pleomorphic (neither coccus nor rod, due to no cell wall (!))
- non-encapsulated
- non-motile
- non-spore forming
- facultative anaerobic
UreaplasmaUrealyticum
Characteristics - opportunistic pathogen

Reservoirs - humans (only reservoir, normal flora of the female genital tract)

Transmission - sexual

Toxins - none in particular

Diseases In Males
- second most common cause of non-gonococcal urethritis (after
Chlamydia Trachomatis, see 45)
- prostatitis and epididymitis

In Females
- second most common cause of non-gonococcal urethritis and
cervicitis (after Chlamydia Trachomatis, see 45)
- pelvic inflammatory disease, tuboovarian abscesses, ectopic
pregnancies and infertility

In Both Males and Females

- cystitis and pyelonephritis
- wound infections (primarily if surgical)
- infective arthritis
- septicemia

In Neonates
- neonatal interstitial pneumonitis
- neonatal meningitis
- septicemia
Treatment - tetracyclines in conjunction with third generation cephalosporins
(if non-gonococcal urethritis and/or cervicitis, due to the possibility
that the urethritis and/or cervicitis may be of Neisseria
Gonorrhoeae and/or Chlamydia Trachomatis
origin)
- tetracycline (if all other diseases)
Part IV
Veterinary Bacteriology
Short Notes

MICR-02403[3(2-1)]
DVM 4TH SEMESTER (2017-22)

DISCLAIMER: THIS IS AN HONEST EFFORT OF AN

UNDERGRADUATE STUDENT OF DVM, IT WAS NOT EDITED IN
ANY WAY FOR TRYING TO UNDERSTAND WHAT AN AVERAGE
STUDENT COMPREHENDS IN A LECTURE: ERRORS AND
OMISSIONS ACCEPTED, IT IS NOT TO BE USED A REFERENCE.

ASSIGNED BY:
Dr. Haroon Rashid Chaudhary
Dr. Muhammad Khalid Mansoor
Dr. Muhammad Khubaib Sattar

SUBMITTED BY:
Salman Javeed (29)
Hafiz Mohammad Anas (09)
 Lecture# 01
Escherichia
VETERINARY BACTERIOLOGY AND MYCOLOGY
In veterinary problem caused by fungi are of less importance as compared to bacteria. So our
main focus will be on bacteriology. It doesn’t mean that we are going to ignore mycology at all,
we will discuss mycology a bit less as compared to bacteriology. Mycology is not of importance
as there is least chance of Fungal diseases in animals as it requires cool &moist environment
which is not available to a fungi. The most of the problem in veterinary caused by fungus are due
to eating food contaminated with fungi. Sometimes abortion may also occur

Escherichia
History:
Discovered by Escherich in 1880 in babies’ feces.

Morphology:
❖ Size :3-5 micron by 0.6 micron..
❖ Bacilli with peritrichous flagella and sluggishly motile.
❖ Some are non-motile.

Gram Reaction:
❖ They give G -ve reactions.
❖ Non-acid fast.
❖ Non sporing.
Antigens:
❖ O: somatic antigen (LPS,LP).
❖ K:capsule(LPS)
❖ Flagellar: protein based..
❖ Common antigen: also common with Salmonella and other coliforms. Designated as
CA.
❖ Fimbria

Toxins:
❖ Enterotoxins (role in diarrhea )
❖ Colicin(antibacterial agent as well as has a role in diarrhea ). They do colonization and
kill other bacteria and due to disturbance in microflora population they cause diarrhea.

Biochemical Reactions:
Agar

❖ Can grow on common agar like nutrient agar.

❖ No special need of nutrients.
❖ Grows well in blood agar.
❖ Colony appears as opaque , convex and 3mm in size .

Temperature:

Temperature ranges from 28-44oC however 37oC is the optimum

temperature and colony grows within 18-24 hours

Differential Media

❖ MacConkey agar: colony appears pink.

❖ EMB: black centered colony with metallic sheen.
Sugar test:

❖ Allare sugar fermenters.

❖ Can be aerobic or facultative anaerobic.
Physiochemical Reactions(tolerance/resistance):

❖ Chemicals: can be killed by common disinfectants.

❖ Physically:
✓ Death occurs when heated at 60oC for 2 hours or
✓ 20 -30 minutes at 100oC.
 ✓ Autoclave gives immediate effect
❖ If fecal matter/organic matter is abundant then it is not destroyed by heat rather stays
there and increases its colony.

Groups of bacteria:
❖ Septicemic: causes septicemia, as infection is in blood so spreads in whole body and
signs like fever ,inflammation are evident
❖ Enterotoxin: causes diarrhea
❖ Enterohaemorrhagic: it produces toxic effect over the cells.
❖ Enteroaggregation: they begin to colonize in villi folds & intestinal lining and then enter
into the lumen. It is not dangerous but it causes malabsorption.

Diseases:
Horse:

❖ Septicemic form present.

❖ Causes Sleeping Foal Disease.
❖ Diarrhea and fever are typical signs.
Cattle/Buffalo:

❖ Diarrhea in young ones that’s why called acute undifferentiated neonatal diarrhea.
Sheep/Goat:

❖ Diarrhea in lambs.
Cats/Dogs:

❖ Diarrhea, fever called Fading Pup disease.

Poultry:

❖ Causes early chick mortality. If chick survives somehow ,the microbe turns to be
septicemic. If somehow recovered from diarrhea the microbe becomes septicemic and
moves in joints to cause Arthritis (joint ill). This is common in poultry and horse and
indicates chronic stage of infection.
❖ If passes to umbilical cord of fetus then causes Naval ill.
Humans:

❖ Same as above mentioned diseases

Distribution/Spread:
❖ Feco-oral route..
❖ Mechanically via flies
 ❖ Habitat:
❖ Found in sewerage,canals,guttersand intestine

Drug of choice:
❖ Chlortetracycline
❖ Tetracycline
❖ Oxytetracycline
❖ Doxycycline
NOTE:

✓ But not recommended usually as cause toxicity and deculturation of teeth in

children.
✓ So we prefer Neomycin, colistin which are Lumen active drugs and minimally
absorbed from gut hence less toxic effects
✓ We also use Yogurt and saccharomyces as probiotic.
✓ Can also use pre biotic.
✓ ORS is used to remove dehydration.
❖ When septicemic form passes into urinary tract it causes urinary tract infections
particularly in females that’s why called as Urinary tract invasive
❖ One serotype also causes mastitis. Ciprofloxacin is used against mastitis
❖ One serotype also affects reproductive tract

Human Diarrhea Treatment:

Following combination is used:

❖ Ciprofloxacin
❖ vibramycin
❖ Flagel
❖ along with ORS.
 Lecture# 02
STAPHYLOCOCCUS

Staphylococcus
The word staphylococcus is derived from two words:

staph→ meaning grape like or cluster.

coccus→ meaning round in shape.

History:
It was discovered in Scotland by a surgeon Sir Alexander Ogston in pus from surgical
abscesses. More than 50 species have been identified. It is most problematic in Human hospitals.
Doctors, nurses & other employee in the hospitals are full of this. It is most commonly found in
their nasal secretions.

Habitat/Ecological Niche:
❖ Lives in nectar (flower, sugar, sweat)
❖ Upper respiratory tract of all animals. (nose, pharynx, oral mucosa)
❖ Lives in tissue→ most commonly in mammary gland and enter through skin.
❖ Abundantly present on skin.
Morphology:
❖ They are cocci. (1µm in diameter)
❖ They reproduce at more than one axis.
❖ Teichoic acid + gram +ve cell wall is present.
❖ Gram +ve in gram reaction.
❖ They are nonsporing&non acid fast.
Antigens:
❖ Leucocidin→ kills the leukocytes.
❖ enterotoxins→ causes diarrhea. (increases the motility & increases the water transfer into the
lumen)
❖ vomitoxins→ triggers the vomiting center.
❖ coagulase→ increases the coagulation.
❖ hyaluronidase→ causes the tissue penetration.
 ❖ phosphatase→
❖ fibrinolysin→ reduces the clotting.
❖ Hemolysin α, β, γ→ causes hemolysis.
❖ Necro-toxins→ necrosis.
❖ Lethal toxins.

Modern problem:
The name of the modern problem is Super Bug& this is the transfer of resistant gene
from one bacteria to another bacteria and so on. Transmission is of two types

Horizontal:Horizontal transmission is the transmission of resistant genes between members of

the same species that are not in a parent-child relationship.

Vertical: In case of vertical transmission the resistant genes are transferred from parent to
daughter bacteria.

In hospitals Doctors, nurses have abundant staphylococcus in their oral & nasal mucosa.
They use antibiotics & also inject antibiotics to the patients. Due to this the niche of bacteria
developing is becoming more and more resistant and less sensitive. They are becoming resistant
to more than one drugs. This phenomena is called multi drug resistance. Staphylococcus is
aMDR bacteria

It is also MRSA, means methicillin resistant staphylococcus aureus. Methicillin is an

antibiotic.

The only choice of drug that is being used against it, is cephalosporin III & IV.
Salmonella:
It causes typhoid. It is most common now a days in Karachi. It is resistant even against
the III generation, so it is also called as XDR (extreme drug resistant). TB is also XDR.

Neisseria gonorrhoeae: Itis also MDR

Syphilis: most common problem of European countries, also MDR.

STD→ MDR
So cefepime is now on trial bases against such cases such as MDR, XDR.

Physiochemical properties:
❖ They are halophiles means salt loving.
❖ osmotolerant→ they tolerate the osmotic pressure.
❖ Optimal temperature for their growth is 37oC and their temperature range is 4-44oC.
❖ Psychrophile: Sensitive to temperatures over 20oC. Optimum growth at 15oC or below. Found in
very cold environments (North pole, ocean depths). Seldom cause disease or food spoilage.
❖ Psychrotroph:Optimum growth at 20 to 30oC. Responsible for most low temperature food
spoilage.
❖ Due to psychrophilic nature staphylococcus are also found in fridges. When there is temperature
variation from 4-10oC and then up-to 2oC, it begins to grow; in milk, meat, cream custard etc.
❖ In Pakistan main cause of food poisoning is load sheading. When there is temperature variation
staphylococcus begins to grow and when you take such food contaminated with staphylococcus,
will produce vomitoxins, enterotoxins which will lead to diarrhea and this diarrhea will recover
itself after one day. So this is self-limiting poisoning. It causes food poisoning in dogs, cats &
human.
❖ It also serve as Sag (super antigen).
Benefits:
❖ It is beneficial at the same time as it produces fibrinolysin that is used in the heart attack to
dissolve the clotting.
❖ For tissue penetration in chronic infection we use hyaluronidase to penetrate the fibrosis, Ca
crystals etc.
 ❖ Diseases:
❖ It causes tick pyemia in sheep. Major skin problem. Fever & nodule may be observed at the
place of tick.
❖ In cattle horses goat & sheep causes mastitis. Staphylococcus is the number one cause of
mastitis.
❖ All skin problems.
❖ Wound problems. Causes infection in the wounds so wounds failed to heal.
❖ It is the major cause of surgical wounds problems. That is the reason why ceftriaxone is
necessary for surgery. It was only recommended for surgery patients just for three days.
❖ Oxidil and Rocephin was also reserved for surgery but we used them in case of every infection as
a result staphylococcus is becoming resistant to them.
❖ Ofloxacin was reserved for typhoid but we used it so badly that it is now not useable.
❖ Pefloxacin was also reserved for typhoid.
Staphylococcus is very:
❖ Resistant
❖ Osmotolerant
❖ Chemo-resistant (disinfectant can’t affect them)
❖ It is becoming super Bug day by day.
 Lecture# 03
BRUCELLA

BRUCELLA
History
In 1886 David Bruce, a British army surgeon, isolated a coco-bacillus that he named
“Micrococcus melitensis” from the spleen of a man who had died of “Malta Fever”(1). This
disease was endemic, but confused with other diseases, especially malaria. The human disease
was associated with people who consumed goat milk and had other close contact with goats.
The organism soon was isolated from these animals. A similar microbe was isolated from the
udder of cows, and from swine. In about 1920 the genus was renamed Brucella and its species
became respectively Br. Melitensis, Br. Abortus, and Br. Suis. The disease caused by
BrucellaMelitensis is known as brucellosis.

Habitat:
There is no habitat of brucella but it is found in soil.

Spread:
It is obligatory parasite that always require host cell to grow. It does not travel without
diseased animal.

Vector:

Its vector may be flies, insects, mosquitoes and small animal. Its means it is found in
rodents and diseased animals.

Morphology:

• 0.6 – 2.0µm in length.

• 0.3 – 0.5µm in width.
• It is gram negative bacteria.
• It is non-acid fast. (it is not true acid fast bacteria but a modified acid fast bacteria)
• It is non sporing.
 • It is non motile.
• MZN +ve (as it is modified acid fast bacteria so modified ziehlneelsen stain. It don’t even
decolorize by HCl & maintain color).

Antigens:

There are following antigens:

• O: that is somatic antigen.

• K: that is capsular antigen made up of LPS.
• As there is no flagella present so H antigen is absent.

Proportion of Ag used for diagnostic purposes:

A- Antigen : M- antigen
20 : 01 → B. abortus.
01 : 20 → B. Melitensis.

Note: If abortion and MZN positive then the case is of Brucella.

Cultural characteristics:

• Optimum temperature for growth is 37oC.

• Capnophile (CO2 loving require 5-10% CO2).
• Require Brucella agar & hemin so we add blood agar otherwise can’t grow. If we give
more time then it grow vigorously. Colony of Brucella is round, translucent, convex,
glistening and capsulated.

Location:

❖ Specifically found in Mediterranean region & Arabian region but generally found
all over the world.
❖ Someone bought goats and sheep from Malta island and went to other place and
observed that abortion started there. Then reason came to known that is being
due to bacteria brucella. As it has origin from Malta island so brucellosis is also
known as Malta fever.
❖ Note: two bacteria most commonly cause abortion
Brucella

Vibrio(campylobacter)
 Brucellosis can be detected by brucella agar.

Risk factors:
In 2003, a list was published OIE, that give risk factor of different bacteria:

❖ Type I = beneficial such as lactobacillus.

❖ Type II = dangerous.
❖ Type III = highly dangerous having zoonotic importance such as brucella.
Brucella was categorized in type 2 & 3. In type 2 & 3 bacteria were zoonotic, also rodents, wild
life, insects was categorized in it and were dangerous. So brucella growth in labs was prohibited.
Only sophisticated labs can grow it.

Diseased animal handling should be restricted.(self biosecurity measures). It is so harmful that

it can cross barrier from intact skin, hands, patagial infection, conjunctiva, and eyes surrounding
area.

Resistance to physiochemical agents:

• It can survive for 10mints at 60. If we keep it in such conditions it will die.
• At 100 it immediately die.
• It can also die with common disinfectant. But if organic matter is present in fetal
membrane or cow then its killing is difficult.

Zoonosis/transmission cycle:

• It spread by milk, meat, milk products(unpasteurized milk, uncooked meat), hunted

wildlife. We drink boiled milk so can’t get brucella.
• It takes hematogenous route, obligatory pathogen.
• It can grow in every cell of body.
• It infects lymph node of gravid uterus localize in female & testis in male . although
spread in whole body but destroyed there. In uterus and testis they are abundant as
there is present erythritol(4C alcohol). Brucella is erythritol loving and can grow in
artificial media as well. From gravid uterus brucella invade joints and grow.
• It is also present in reproductive secretion, milk, saliva, urine, fecal matter and found in
all of the reproductive and secretion.

What it does to body: (it causes abortion, abortion and abortion)

When you brought cows and these were infected or it mated with infected bull then
there is following sequence of abortion cases:
 ❖ 1st time → chances of abortion 80-100%. Minimal level of abortion is 80%.
❖ 2nd time→ chances of abortion 60-90%. Minimal level of abortion is 40%.
❖ 3rd time→ chances of abortion 30-60%. Minimal level of abortion is 0%.
So it is immunized by infection.

Transmission:
❖ It is transmitted by
o Insects
o Animal
o Human
o Intercourse
❖ It is like STD.
❖ If the assistant intercourse technology (AI artificial insemination ) is not correct. This
may also lead to brucellosis.
❖ It is also spread from mother to calves.

Types

• Br. Abortus → cattle

• Br. Melitensis→ sheep, goat & cattle. This is of zoonotic importance and cause Malta
fever.
• Br. Canis → dog
• Br. Swiss → pig
• Br. Neotame

Note:
❖ cat is resistant to brucella.
❖ In chicken brucella cause early chick mortality. In backyard poultry this problem
is more.
❖ these bacteria are not specie specific but the viruses are specie specific.

Signs and symptoms:

❖ Late term abortion. (last or end trimester abortion but in goat last month abortion and
in dogs last 15-20 days abortion)
❖ Most of the time dead fetus.
❖ Placenta retained (cotyledons bind), post parturient pyometra
❖ Milk retention.
Pathology:
❖ Metritis and endometritis.
❖ Inflammation of cotyledons, fetal death after spreading, inflammation of fetal
membrane.
❖ Fetal lungs, stomach, fetal membrane are full of it.
❖ Fetal rejection.
❖ In male severe orchitis, arthritis, or arthralgia(in males joint movement painful).
❖ Both in male and female cause undulating fever.
❖ In male abscessation of testis and fibrosis and infertility and sterility.
Treatment

❖ No treatment recommended.
❖ According to WHO antibiotics treatment like ciprofloxacin &probiotics is
recommended.
❖ In Pakistan and India Ciprofloxacin+Oxytetracycline is used with double or triple dose
is used.
❖ Vaccination + probiotics for 21 days.
Prevention:

❖ Disinfect the farm properly with carbolic acid ,slaked lime, caustic soda.
❖ Placental membrane and foetus should be buried deep and cover it with slaked lime .
❖ Don’t allow dogs ,cats to eat it otherwise abortion may occur.
❖ Incinerate the waste.
❖ All far equipment like milk machines and AI rods should be disinfected.
❖ Make quarantine cells,keep infected animals there for 40 days.
Vaccination

❖ Vaccinate the whole farm.

❖ RB51 & S19 are non capsulated attenuated vaccines used.
❖ RB51 is most recommended as it is considered more safe.
❖ S19 causes abortion in pregnant.
 Lecture# 04
MYCOBACTERIUM

Mycobacterium
History

Recorded since Pharaoh times .Related with poor living conditions like poor people,
poor environment, poor sanitation. That’s why also called poor man’s disease.

Morphology

❖ Slender rod shaped Bacilli.

❖ 1-4 micrometer long X 0.2-4 micrometer wide.
❖ Acid fast and Ziehl-Neelsen positive.
❖ Not discolored even by acid due to mycolic acid present in their cell walls.
❖ It is gram +ve but not demonstrable (can’t be stained).
❖ Aerobic (requires high oxygen tension ).
❖ Obligate pathogen (can’t survive in an artificial media ).
Generation time

14 days

Agars

❖ Glycerol, cholesterol, albumin and other things like serum proteins, mycobactinrequired .
❖ Requires mycobactin for fastidious growth.
Mycobactin Preparation

❖ Kill the microbes and put it in the Agar .This allows growth of mycobacterium.
❖ Lowenstein Jenson medium and Egg dose medium are mostly used for this bacterium.
❖ If we add agar in above mentioned things then it will become agar for that bacterium
otherwise broth.
❖ In broth it is friable and not mixed .this property is present in some but not in all.we have
to shake it well or add something to make it mixed.
 ❖ Mycobacterium leprae does not grow artificially but grows in Armadillo.

Growth Time

❖ On Agar takes normally 24 days to 3 months to grow.

Resistance

❖ Highly resistant.
❖ At 60ᵒC 15 minutes required to kill.
❖ At 10ᵒC takes 3-4 sec only and dies.

Optimum Temperature

❖ 37-38ᵒC
❖ Favorable oxygen is required
❖ Mycobacterium avian requires 40ᵒC (it can’t grow on 37ᵒC )
Pathogenesis

❖ Mycobacterium piscium can’t affect mammals and birds.

❖ Mycobacterium Avian Complex disease.
❖ Mycobacterium tuberculosis causes chronic debilitating disease in bovine.
❖ Mycobacterium John’s causes John’s disease &paratuberculosis.
Signs

❖ Weight loss.
❖ Continuous diarrhea.
❖ Wasting with mild fever.
❖ Dehydration.
❖ Bacteria replicate in villi of ilium so no absorption.
❖ Lymphadenitis.
❖ High mortality.
Test

❖ Delayed hyper sensitivity test.

❖ Cross react Mycobacterium John’s and mycobacterium avian PPD of them as well cross.
Treatment
 ❖ No treatment.
❖ Slaughter and culling.

Tuberculosis
Introduction

• It is most prevalent communicable infectious disease.

• Usually involves lungs but effect the other organs or tissues in the body.

Etiology

• Pulmonary TB is caused by Mycobacterium tuberculosis.

• Poor hygiene.

• Reduced immune status.

Transmission

• It is airborne disease.

• Airborne droplets coughed or sneezed by the patient.

Signs and Symptoms

• Weight loss, fatigue, productive cough, fever.

• Hemoptysis.

• Pleuric Pain.
 Lecture# 05
ACTINOMYCES VS ACTINOBACILLUS

Actinomyces vs Actinobacillus
Feature Actinomyces Actinobacillus
Size ❖ 1.5 × 0.4 micro meter. ❖ 1.5 micro meter × o.4
micro meter.

Morphology ❖ Filamentous, ray fungus, ❖ Coccobacilli,

branching form. Diplobacilli,
❖ Gram +ve. Filamentous form.
❖ Non acid fast. ❖ Not so much Fastidious
as can grow on any
media like blood
/serum.
❖ G-vebacteria.
❖ Non acid fast& non
sporing.

Habitat ❖ Actinomyces species ❖ Can’t live in soil for

are ubiquitous, occurring longer time but in hay
in soil and in it can live for longer
the microbiota of animals, time.
including the human ❖ Obligate parasite
microbiota. They are ❖ Lives in upper GIT
known for the important &also moves to rumen,
role they play in soil
reticulum.
ecology.
❖ Present in intestine of
horse.

Colony Size ❖ 0.5 -1 micro meter. ❖ Forms translucent

❖ Fastidious growing. colony with a size of 1-
❖ Grows well on brain 1.5mm size at 37ᵒC.
infusion, Egg Dorset, ❖ By adding glucose
Loeffler’s media. /serum growth is
 ❖ Gives yellow color colony. increased and makes 4-
❖ Grows anaerobically. 5mm colony.
❖ Rarely caprophile.
❖ Forms granules.
Optimum ❖ 37ᵒC. ❖ 37ᵒC.
Temperature ❖ It is anaerobic. ❖ It is aerobic.

Resistant ❖ Takes 20 minutes to be ❖ It dies in 15 minutes at

killed at 60 ᵒC. 60 ᵒC.
❖ Forms pellicle in Broth.

Pathogenesis ❖ It is a pus forming ❖ Actinobacilli resides in Hay

microorganism. etc. ,when this hay, fodder or
❖ Same epidemiology and other roughage is given to
etiology as that of animal it causes micro cuts in
actinobaccillus. mouth of animal. Bacterium
enters in body through these
cuts.
❖ Inflammation.
❖ Liquefaction.
❖ Bone break.
❖ Forms Sulphur granules.

Clinical Signs ❖ Swelling outside the mouth ❖ Wooden tongue.

either unilateral or bilateral. ❖ Swelling occurs in soft tissue
❖ Bone is involved always i.e. and buccal cavity including
lower jaw bone. tongue, lips, Salivary glands,
❖ Yellow pus or greyish white lymph nodes.
pus.
❖ Liquified calcium material
of bone.
Treatment ❖ Hot fermenter Iodex. ❖ No vaccination.
❖ Remove pus. ❖ Pen strep in high dose IM.
❖ Glycerin. ❖ Oxytetracycline.
❖ KI or NaI orally or
parentally.
❖ Use pulsit.
 Lecture# 06

SALMONELLA
SALMONELLA
Salmonella is not a genus, it is actually specie but it is written as the genus.But it has the
serotype/varieties.

History:

In 1884, Salmon and Smith discover it first time. That’s why it is named by the name of
Salmon.

General Characteristics:

❖ It is gram +vet bacterium.

❖ Size is about 2-4 by five micrometer.
❖ Sometimes it is short and sometimes it is long rod shaped.
❖ All are motile except S.gallinarium and S.pullorum.
❖ Non sporing.
❖ Non acid fast.

Antigens and toxins:

❖ O antigens, somatic antigen, LPS based

❖ Hantigens , flagellar antigens having the flagellin protein
❖ Further classification is based on these antigens
❖ Vi antigens. These are the variable antigens and cause the disease in mice. These are also
called the virulent antigens.

Growth/agars:

❖ They can grow at the ordinary media/agar and not require any condition like the blood
agar, serum, protein etc.
❖ But this growth is at the low in the number. So, the special media is required.
❖ We can grow it on the ;
▪ Selenite broth
▪ Tetrathionate broth
❖ So first it is grow in the selenite broth and then it is grown on the Tetrathionate.
 ❖ After that it is bring to the normal MacConkey agar. It will produce the mucoid convex
colonies. Colonies will be non lactasefermenting(cream yellow color)
❖ Brilliant green agar is also used to grow
❖ Some of the varieties grow very fast while other grows very slow.

Habitat:

❖ It lives mostly in the intestine.

❖ Where it lives (Intestine) all the other microbes are present there. They are also
present in the sewerage water.

Colonies:

❖ Mucoid
❖ Convex
❖ Non-lactose fermenting
❖ Cream yellow
❖ Minute colonies/dew drops colonies

Resistance to physical and chemical agents:

Very resistant

❖ 55ᵒC for 1 hour

❖ 60ᵒC for 20 minutes

They are obligatory to semi obligatory pathogens and reside and affect the lymph nodes,
liver, spleen, bone marrow, WBCs,(especially macrophages), intestine and gall bladder. Here it
causes the acute inflammation. It resides also in the joints of the calves.

Require cells for growth:

❖ Intestine
❖ Lymph nodes
❖ Liver
❖ Spleen
❖ Gall bladder
❖ Bone marrow
❖ WBCs(macrophages)

Transmission:

❖ Face-oral route (in animals)

❖ House fly (as a vector in the human)
❖ Inhalation (only in the small chicks)
Diseases:

1. Salmonella abortus

Abortion is normally occurs in the typhoid but in such case there is the abortion in the
last two months. It is due to the species like S.abortus ovis(in caprine and ovis) and
S.abortus equi (in horses).

Neonatal death after the 2-4 days of birth.

Characteristics signs:

❖ High grade fever

❖ Ovary inflammation (oocytis)
❖ Inflammation of ovary and placenta.
❖ Cause abortion
❖ Diarrhea
❖ Enteritis

Note: This is non zoonotic disease.

2. Salmonella Dublin:

It is present in the cattle and buffalo. It is not in the large animals but it is present in the
calves.

Characteristic signs:

• Fever
• Diarrhea
• Constipation
• Death

In Poultry

➢ Salmonella pullorum causes the pullorum disease.

➢ Salmonella gallinarium causes the fowl typhoid.
➢ Salmonella paratyphi causes the avian paratyphoid.

If feces of birds are the yellow in color than there are the chances of the presence of the
salmonella species.

All the above mentioned species of Salmonella causes the ECM (early chick mortality)
Adult Birds:

❖ Signs appear on the ovaries, ulceration and infections of reproductive track. The
fluff of the on birds carries them and they are transferred to the other chicks by
means of inhalation.
❖ They are also non zoonotic and thus the eating of the meat of the infective birds
does not cause the diseases in human or other animals.

1. Salmonella typhimurium:

It is in case of the dog, cat, cattle, horses, sheep, goat human and poultry.

Signs and effects:

❖ Severe Diarrhea
❖ Dysentery
❖ Fever
❖ Acute colic pain

Vector is very important in this case.

Prevention:

❖ Vaccines to the human especially the hostalized persons.

❖ For animals the disinfectants are used and the environment is made clear.

Treatment:

The antibiotics do not work against them which do not enter the cells.

❖ Chloramphenicol
❖ Quinolone ( they work against them because they can enter the cell)
❖ Cefexime
❖ Ceftriaxome
❖ Cefipim

Testing:

❖ Widal test (human)

❖ ELISA based tests.
 Lecture# 07

ENTEROBACTERIACEAE

Enterobacteriaceae
• It is an opportunistic bacteria.
• It doesn’t cause disease itself.
• It causes secondary infection after the infection with E.coli& salmonella. So it act as
secondary invader. It can behave like E.coli& salmonella.
• Enterobacteriaceae family contains a large number of genera that are
biochemically and genetically related to one another. This group of
organisms includes several that cause primary infections of the human
gastrointestinal tract. Members of this family are major causes of
opportunistic infection (including septicemia, pneumonia, meningitis and
urinary tract infections). Examples of genera that cause opportunistic
infections are: Citrobacter, Enterobacter, Escherichia,Hafnia, Morganella,
Providencia and Serratia.

Arizona
Morphology

Similar to salmonella and E.coli.

❖ Size :3-5 micron by 0.6 micron..

❖ They are with peritrichous flagella and sluggishly motile.
❖ Some are non-motile
History

It was discovered in Arizona state, USA.

Habitat

It resides in

❖ Intestine
❖ Sewerage
Antigens

❖ antigen that is somatic.

❖ H antigen that is flagellar.
❖ No exotoxins but has endotoxins.
It can affect the turkey and chicks.

Growth/agars

Growth media requirement is same as E.coli and salmonella. So of salmonella is given below

❖ They can grow at the ordinary media/agar and not require any condition like the blood
agar, serum ,protein etc.
❖ But this growth is at the low in the number . So, the special media is required.
❖ We can grow it on the ;
▪ Selenite broth
▪ Tetrathionate broth
❖ So first it is grow in the selenite broth and then it is grown on the Tetrathionate.
❖ After that it is bring to the normal MacConkey agar. It will produce the mucoid convex
colonies.colonies will be non lactasefermenting(cream yellow color)
❖ Brilliant green agar is also used to grow
❖ Some of the varieties grow very fast while other grows very slow.

Incubation period

Its incubation period(duration between the occurrence of infection and appearance of signs of
disease) is 48hrs at 43ᵒC.

Proteus
Morphology

They are cocci shape and filamentous

size
1-3µm × 0.5 µm

Growth

❖ Swarming growth on agar that is contaminated.

❖ Highly motile and high reproduction.

Incubation period
 ❖ 20-40hrs at 37ᵒC

Antigens

❖ Othis is somatic.
❖ H this is flagellar.

Affects

❖ Overpopulation in intestine causes diarrhea.

Klebsiella
❖ It is aerogenes and cause pneumonia in human.
❖ It is non motile.

Antigens

❖ Othis is somatic
❖ K this is capsular.

Diseases

It causes

❖ pneumonia in fowls
❖ airsacculitis in chicks
❖ metritis and mastitis

shigella
❖ there are 10 serotypes of this bacterium.
❖ It causes disease only in human but rarely in dogs, cats and rabbits.
❖ It causes diarrhea or dysentery that is very painful and bloody.
❖ It has no flagella no spores and no capsule.

Antigens

Only O antigen is present that is somatic.

Treatment

❖ Quinolones
❖ Cefixime

Prevention
 ❖ Good sanitation.
❖ Use probiotics and prebiotics.

Yersinia entercolitica

The organisms are invasive (usually without systemic spread).

Typically the infection is characterized by diarrhea, fever and abdominal
pain. Y.
enterocolitica infections are seen most often in young children. Y.
enterocolitica can be
transmitted by fecal contamination of water or milk by domestic animals or from
eating meat
products.
 Lecture# 08

Pasteurella

Pasteurella
History:
Named after the name of Pasteur. Similar toSalmonella gallinarium. It is a part of upper
respiratory tract’s natural microflora. It only cause disease when there is stress to animal.

Morphology:
❖ These are rod like or ovoid Coccobacilli.
❖ 1.0µm × 0.5µm -0.8µm.
❖ On the lab media the size is about the 5 by 1.
❖ Gram –ve.
❖ Non motile.
❖ Non-sporing.
❖ Profound capsule is present (capsule cause the disease).

Note:
All the pathogenic bacteria are non-sporing except

❖ Clostridium.
❖ Bacillus.

Habitat:
❖ Found in dust.
❖ Aerosol with humidity.
❖ Upper respiratory track.
❖ Lives commensally and does not cause the disease.
❖ Important for the lab animals, dogs, sheep and cats.

Staining:
❖ It takes bipolar staining which include Leishman stain and giemsa stain.
Size:
❖ If we take it direct from the animals its replication is fast, so its size remain small.
❖ But when we take it and grow it on the lab media then its size is greater (5 × 1µm).

Cultural characteristics:
❖ No specific agar.
❖ It will grow in every agar but show no growth in Mcckonkey agar.
❖ We modify the agar by adding the sample from the infected animal and injecting the
serum in the ear vein of rabbit (or guinea pig). The rabbit will die 24-40 hour with
fever, septicemia etc. After that you will take the liver or heart of rabbit and then
grow the pasturellamultocida in it(in broth or agar).
❖ Growth is so rapid that 8-12 hours causes the turgidity in broth. CYS broth is ideal for
it.

Biochemical reactions:
❖ Gives positive test with indole + hydrogen sulphide.
❖ Converts nitrates into the nitrites.
❖ Negative reaction with urease.
❖ Sugar reactions are non specific. These are varied reactions(produce acid without gas)

Colony size:
❖ 2-3mm colony iridescent/non-iridescent(both)
❖ Always gives mucoid colony due to capsule. But bacillus is capsulated but gives the dull
colony because its capsule is of protein.

Susceptibility:
❖ Very susceptible
❖ Dies in heat, sunlight and dry condition.
❖ Common disinfectants are most effective against it.
❖ 15 minutes are required to kill it at 55⁰C.

Diseases:

1. HS:
Most important disease after mastitis and caused by E2 (imp) and B2 strain. It is disease of
cattle and buffalo but its origin is from sheep and goat. So we also have to vaccinate sheep
 and goat along with cattle and buffalo to avoid disease as sheep goat and rabbit harbor and
potentiate the P.multocida.

Signs:

❖ Open mouth
❖ Gurgling sound (First low pitch than high pitch)
❖ Moist rales (moist Gurgling)
❖ wheezing sound (dry Gurgling)
❖ Inappetence.(off feed)
❖ No rumination.
❖ Inflamed neck, brisket and throat.
❖ High grade fever.
❖ Death will be due to strangulation (anoxia, hypoxia) in 48 hours.

Postmortem lesions:

❖ Sever signs of septicemia (LPS in blood).

❖ Bacteremia (bacteria in blood).
❖ Ulceration.
❖ Liver: Hepatitis, hemorrhages and hepatomegaly.
❖ Spleen: acute inflammation, hemorrhages and splenomegaly.
❖ Disturbed bile duct.
❖ Most important sign: if you cut or remove cartilaginous mass of trachea then you will
observe froth that can move toward lungs
❖ Severe tracheitis (hemorrhagic )

All these signs are also in poultry in case of fowl cholera. If symptoms are 40 percent less then it
will be in sheep when it is being transported. That’s why it is also called shipping fever or
transportation sickness. High grade fever and tracheitis are present in it. It is non lethal form and
it is due to Mannheimiahemolytica.

Both P.mutocida and Mannheimiahemolytica are related with humidity, cold weather, extreme
cold weather and rain. It is mostly in Monsoon season of rain.

Prevention:
Vaccination that is lipopolysaccharide based. It is either twice a year or once a year.

Treatment:
❖ Cephtiophorsodium (animal dies as injection is delivered to the animal because
lipopolysaccharide act as the endotoxin and as a result animal dies.
Protocols that should be followed:
Head of animal is down, lacrimation, difficulty in breathing (dyspnea).

So,

❖ (1). First of all give NSAIDs. It will inhibit all the prostaglandins.
❖ (2). Also give anti inflammatory (corticosteroids and steroids)
❖ Also give anti histaminic.
❖ Also use bronchodilators.
❖ Warm the animal in winter.
❖ Provide good ventilation.
❖ There should be the gap of 30 minutes to 1 hour between 1st and 2nd injection. After that
fever will be down and animal will feel a little good.
❖ After 2 hours you have to give bactericidal but we don’t. we always use bacteriostatic
(OTC in higher dose)
❖ If animal is fallen down then cut the trachea(tracheostomy) that there are chances of
animals to survive.

Note:
❖ Clamaxole, penicillin and ampicillin is not recommended in respiratory infections
in 3rd world countries as there is greater bacterial range. Instead we mostly use
Tylosin in case of HS and other respiratory infections.
❖ Mycoplasma is common player in our area. It replicate along with HS (P.
mutocida). There is no treatment of mycoplasma. It cause pleuropneumonia.
Erythromycin and clarithromycin are effective against it.
 Lecture# 09

RHODOCOCCUS EQUI
Rhodococcusequi
Formerly called as Corynebacterium Equi

Morphology:
❖ Shape: Rods or cocci
❖ Size: 5 micro meter length

General Characteristics:

❖ Gram-positive
❖ Aerobic soil saprophyte
❖ Non-Motile
❖ Catalase positive
❖ Oxidase Negative
❖ Weakly acid fast

Cultural Characteristics:

❖ Rhodococcusequigrows on non-enriched media such as nutrient agar and produces

characteristic mucoid salmon-pink colonies with no hemolysis, features reflecting capsule
formation and pigment production. Blood and MacConkey agar plates inoculated with suspect
material are incubated aerobically at 37 C for 24 to 48 hours.

Habitat:
Rhodococcusequiis an inhabitant of both soil and the intestinal tracts of animals. It can replicate at
warm temperatures in soils enriched with faeces of herbivore.
Clinical infrctions:

Clinical signs:
❖ Clinical signs vary with the age at which the foal becomes infected.
❖ Acute disease often occurs in one month-old foals=>sudden onset of fever, anorexia and signs
of
bronchopneumonia.
❖ In 2 to 4 month-old foals and lesions can be well advanced before the animal exhibits coughing,
dyspnoea, weight loss, exercise intolerance and characteristic loud, moistrales on auscultation
of the lungs. Occasionally diarrhea can also occur.

Treatment:
Combination of oral rifampin and erythromycin for 4 to 10 weeks and supportive therapy.

Control:
➢ No commercial vaccines are available.

➢ On farms where the disease has occurred, foals shouldbe kept under observation and examined
clinicallytwice weekly until they are 4 months of age.
 Lecture# 10
PSEUDOMONAS

CAMP
Test:

PSEUDOMONAS
Pseudomonas is a psychotropic bacterium and can grow below 10C with the production of odor,
slime, pigment and fluorescence on poultry meat surfaces. It is also known as “blue green pus
bacteria” that opportunistically infects humans, especially those who are immuno-
compromised. Pathogen of plants, animals and humans.

Habitat
Ubiquitous. Pseudomonas bacteria can be found in soil, marshes, coastal marine habitats, and
plant and animal tissue; generally, these bacteria can tolerate a variety of physical conditions.
Spread
The bacteria can be spread in hospitals via the hands of healthcare workers, or by hospital
equipment that is not properly cleaned.

Antigens
Somatic: O antigen.cell wall lipopolysaccharides
Flagellar: K antigen.

Characteristics

➢ Rod shaped
➢ Gram negative
➢ Non sporing
➢ Catalase positive
➢ Non-Lactose fermenting
➢ Oxidase positive
➢ Growth of pseudomonas on spoiling foods can generate a "fruity" odor.
➢ Can cause disease both in plants and animals
➢ Sensitive to Galium

Morphology

➢ Slender
➢ 1.5-3.0 * 0.5 microns in size
➢ One or more flagella
➢ Non capsulated some exceptions are mucoid

Cultural Charateristics
➢ Obligate aerobe but grows anaerobically if nitrate is available
➢ Produce large opaque irregular colonies with distinctive mawkish or earthy smell

➢ 6-42 degree celsius(optimum is 37C)

Risk factors
Nosocomial
Immuno compromised patients
Resistant antibiotics
Transmission
Via water aerosols, aspiration and fecal contamination
Inhabits skin, colon and upper respiratory tract.

Pathology
It is the second-most common infection in hospitalized patients. This pathogenesis may in part
be due to the proteins secreted by P. aeruginosa. The bacterium possesses a wide range
of secretion systems, which export numerous proteins relevant to the pathogenesis of clinical
strains
Signs and Symptoms
➢ Fever and chills.
➢ Pneumonia
➢ Body aches.
➢ Light-headedness.
➢ Rapid pulse and breathing.
➢ Nausea and vomiting.
➢ Diarrhea.
➢ Decreased urination.

Usefulnes
➢ Act as bio-control agent for crops probably b acting as siderophore for other microbes
➢ Can metabolise chemical pollutants serving the prcocess of bio-remediation
Prevention
To prevent spreading Pseudomonas infections between patients, healthcare personnel must
follow specific infection control precautions. These precautions may include strict adherence to
hand hygiene and wearing gowns and gloves when they enter rooms where patients infected
with Pseudomonas are staying. Healthcare facilities must also follow proper cleaning
procedures to prevent the spread of Pseudomonas. Certain protocols should be followed to
prevent device-associated infections, wound infections etc. A breakdown in these protocols
may lead to infections with Pseudomonas or other healthcare pathogens.

Treatment
Treatment may involve one or more of the following types of antibiotics:

➢ ceftazidime.
➢ ciprofloxacin (Cipro) or levofloxacin.
➢ gentamicin.
➢ cefepime.
➢ aztreonam.
➢ carbapenems.
➢ ticarcillin.
➢ ureidopenicillins
 Lecture# 11
COXIELLA BURNETII

Disease Agent:
• Coxiella burnetii

Disease Name:
• Q fever

Background:
• Described in 1935 by E. H. Derrick in abattoir workers
in Australia as a disease of unknown origin and, therefore, termed “query fever.”
• Isolated in 1937 by Burnet and Freeman who identified the organism as a Rickettsia
species.
• Cox and Davis isolated the pathogen from ticks in
Montana in 1938 and described its transmission. The
agent was then officially named Coxiella burnetiithe
same year.
• No longer regarded as closely related to Rickettsia
species
• Classified (Category B) as bioterrorism agent by the
CDC.

Disease Agent Characteristics:

• Small, Gram-negative, pleomorphic coccobacillus; obligate intracellular bacterium that
lives inmacrophages.
• Order: Rickettsiales; Family: Rickettsiaceae
• Size: 0.5-0.8 mm ¥ 1.2-3 mm
• Nucleic acid: Rickettsial genomes are among the
smallest of bacteria. Coxiella is approximately 1600 kb.
• Physicochemical properties:
Resistant to heat, low orhigh pH, 0.5% sodium hypochlorite, UV irradiation,
and environmental conditions, such as desiccation, drying, and sunlight, because of the
presence of aspore stage. It can survive for 7-10 months on wool at15-20°C, for more than
1 month on fresh meat in coldstorage, and for 40 months in skim milk at room temperature.
It can be isolated from infected tissues storedin formaldehyde.
• The microorganism exists in two antigenic forms:
phase I and phase II. Phase I is highly infectious,
whereas phase II is sporelike, metabolically dormant,
and avirulent.
Transmission:
• Inhalation of aerosols or contaminated dusts containing air-borne bacteria derived from
infected
ruminants or their products. A single inhaled organism may produce clinical illness.
• Bacteria are shed in milk, urine, and feces of infected
animals. High numbers of organisms in the amniotic
fluids and placenta during birthing (e.g., 109
bacteria/g placenta)
• Contact with contaminated wool
• Ingestion of unpasteurized contaminated milk or
meat
• Ideal for aerosol dissemination. Secondary infection is rare but sometimes with
pneumonic patients.

At-Risk Populations:
• Farmers, veterinarians, or those who handle potentially infected livestock, especially
animals giving
birth
• A threat as a bioterrorist weapon for susceptible
populations
Vector and Reservoir Involved:
• Greater than 40 tick species are involved in transmission among domestic animals and
are considered to
be the organism’s primary vector; tick bites are rarely

Blood Phase:
• Bacteremia documented during both acute andchronic infections, with and without
symptoms.
• The organism replicates in macrophages. This couldresult in eventual cell lysis and the
dissemination offree bacteria in plasma.
Incubation Period:
• 20 days (range: 14-39 days)

Mortality:
• 1-2% in acute infection
• Approximately 65% in untreated chronic infection.

Primary Disease Symptoms:

• Humans are the only species that exhibit illness as aresult of infection.
• Acute disease is characterized by high fever (usually40°C) and headache (usually retro-
orbital). The feverlasts approximately 7-14 days. Other signs and symptoms include
hallucinations, diarrhea, weight loss,facial pain, and speech impairment. A rash is rarely
observed in Q fever, in contrast to other rickettsial infections.
• Pneumonia or hepatitis in 30-50% of infections,depending on route of exposureI,e
(inhalation oringestion)
• Infrequently causes endocarditis, pericarditis, myocarditis, or meningoencephalitis.

Severity of Clinical Disease:

• May progress to chronicity in approximately 1% ofthose infected if untreated, in which
case mortalityincreases. Chronic disease is defined as Q fever lasting6 months.
• Predominantly occurs in individuals with underlyingvalvular heart disease, vascular
aneurysms, or vascular grafts manifesting primarily as culture-negativeendocarditis.

Treatment Available/Efficacious:
• Doxycycline (acute) and doxycycline and hydroxychloroquine (chronic illness).

Other Prevention Measures:

• Vaccine is available in some parts of the world(formalin-inactivated phase I organisms),
and its useis recommended for exposed or high-risk individuals(livestock handlers,
abattoir workers, veterinarians,and laboratory workers) who do not have immunity.
 Lecture# 12

BACILLUS
Bacillus
It is an etiological agent of anthrax ---a common disease of livestock and occasionally in humans.
The classification of bacterium is as follows

Class :Bacilli

Scientific name: Bacillus anthracis

Family: Bacillaceae

Phylum:Firmicutes

Morphology

❖ Gram +ve bacteria.

❖ Large sized (3-8micron x 1-2 micron).
❖ Spore forming.
❖ Non motile.
❖ Facultative anaerobe.
❖ May exist as single, paired or long chained.
❖ Capsulated (polypeptide capsule consists of D-glutamic acid.
❖ Antiphagocytic, plasmid encoded and resistant to Antibiotics.

Staining
➢ With Spore stain: spore appear as pink & bacilli appear blue.
➢ With gram stain: Bacilli is violet blue or surrounded by hallo zone
➢ With polychrome methylene Blue(Mc Fadyean’s reaction):Bacilli is
surrounded by Purplish pink capsule .it is diagnostic for Anthraces.
Agars
Grows well on common agars .However when grown on following agars and media it
shows certain characters

1- Nutrient Broth: Produces floccular turbidity. It appears as cotton wool in the

tube.
2- Nutrient agar: gray white, irregular colonies with Medusa head appearance
3- Blood agar: Produces non-hemolytic, gray white colonies with irregular
margins.
4- Gelatin stab: Slow liquification and inverted fir tree appearance.

Biochemical Characteristics

It iscatalase, nitrate reduction, starch hydrolysis and gelatin liquefaction test

positive.

litmus milk: Soft card is formed and digested quickly

Resistance
➢ Vegetative forms are destroyed – 600C in 30min.
➢ Spore form – viable for years in soil.
➢ Autoclaving – kills anthrax spores.
➢ 4% KmNo4 in 15 mts - kills anthrax spores.
➢ Susceptible to many antibiotics like penicillin etc.

Antigens

B. anthracis contain 2 plasmid encoded virulence factors:

1) Capsule >>>linear γ-D-glutamic acid polymer.

2) Exotoxin (Trimer) consists of:

A- Protective Antigen (PA): It form Membrane channel that allow Edema Factor
(EF) and Lethal Factor (LF) to enter the mammalian cell via endocytosis.

B- Lethal Factor (LF): Both PA and LF are required for lethal activity.

C- Edema Factor (EF): Both PA and EF are required for edema to occur.
Pathogenesis
Anthrax

Synonyms: Splenic fever.

Characters: Zoonotic, highly infectious disease -- primarily affecting herbivores

animals such as cattle, sheep, horses, mules and goats & secondary affecting
man.

Etiology: B. anthracis which belong to family Bacillaceae.

Susceptibility: Herbivores animals such as cattle, sheep, horses, mules, goats, pigs, dogs.
Human is accidental host while birds are resistant.

Mode of transmission & source of Infection:

Herbivores animals infection by >>>> ingestion or inhalation of spores in the soil.
Carnivoresbecome infected through consumption of infected animals that have
died from anthrax.

Human infected through:

1) broken skin (injuries).

2) Inhalation anthrax spores from contaminated animal products as flesh, bones,

hides, hair & wool.

3) Ingestion of infected animal meat. N.B: Accidentally via biting flies (Minor
route) during sever outbreaks.

Clinical signs:
1- Per acute course of illness: Mainly in cattle & sheep. Lasts approximately for 1-2
hours.
Characterized by: Sudden death of the animal (1st indication for anthrax).

2- Acute course of illness: Mainly in equines. Lasts approximately 96 hours.

Characterized by: Fever, enteritis, septicemia >>>> death.

3- Course of illness Subacute / chronic: Mainly in swine, dogs and cats. *

Characterized by: Dysphagia, dyspnea, sever enteritis
 Diagnosis:
1) Sampling: Blood sample >>> only taken from ear, tail vein or natural openings
of the dead animals. Blood smear stained With Gram stain (or Methylene blue)
- With Polychrome Methylene Blue (Mc Fadyean’s reaction)

2) Isolation & Identification

Don’t Open the carcass of the dead animal

3) Laboratory animal inoculation:

4) Serological test: ELISA for PA, LF and EF. Ascoli test: 1- Procedure :2-
Result :+ve reaction >>>> formation of a ring of precipitate at the junction of the
2 fluids in the capillary tube.

5) Fluorescent labeled antibody staining:

6) PCR:

Treatment:
1- Large doses of antibiotics with immune serum.
2- Penicillin & tetracycline are the most active.

Prevention and control:

1- Notification of the authorities.
2- Quarantine the area.
3- Don’t open the carcass or examine postmortem & minimize the contact.
4- Passive immunization. Vaccination:
Animal Vaccine
Human Vaccine - Pasteur Vaccine -
Spore Vaccine - Sterne attenuated spore vaccine -
UK Vaccine - US Vaccine Simultaneous Method: The best method is to inject 10-20 c.c.
of hyper immune serum in one shoulder & at the same time a dose of used vaccine is
injected into the other shoulder.
 Lecture# 13

CLOSTRIDIUM

Clostridium
History:

First described in 1880 by Prazmowski, the genus Clostridium is composed of a

heterogeneous group of bacteria that are characterized by their rod-like
morphology.

Classification:

Currently, more than 200 species and about 5 subspecies belonging to genus
Clostridium have been identified. A majority of these are free living saprophytes
while a few are pathogenic to human beings (e.g, C. botulinum, C. difficile, and C.
tetani)

Scientific classification

Domain: Bacteria

Phylum: Firmicutes

Class: Clostridia

Order: Clostridiales

Family: Clostridiaceae

Genus: Clostridium

Morphology:

Rod shaped (straight rods or slightly curved)

Colonies can be convex, spherical and shaped

The ends also vary from rounded to pointed ends depending on the strain.

Gram Reaction:

• Gram positive
• Spore Forming

Toxins:

• Neurotoxins
• Botulinum Toxin (BoNT)
• Tetanus Toxin (TeNT)
• Enterotoxin
• Cholesterol-dependent Cytolysins
• Binary Bacterial Toxins

Biochemical Reactions:

• Can grow on common agar like nutrient agar.

• No special need of nutrients

Physiochemical Reactions(Tolerance/Resistance):

The vegetative cells of clostridia are heat-labile and are killed by short heating at
temperatures above 72–75 °C. The thermal destruction of Clostridium spores
requires higher temperatures (above 121.1 °C, for example in an autoclave) and
longer cooking times (20 min, with a few exceptional cases of > 50 min recorded
in the literature). Clostridia and Bacilli are quite radiation-resistant, requiring
doses of about 30 kGy, which is a serious obstacle to the development of shelf-
stable irradiated foods for general use in the retail market.The addition of
lysozyme, nitrate, nitrite and propionic acid salts inhibits clostridia in various
foods.

Species Of Clostridium:

• C. botulinum
• C. perfringen
 • C. sporogenes
• C. bifermentans
• C. leptum
• C. difficile

* Sporulation factor and temperature has also been shown to cause

morphological changes of such species as C. perfringens in cultures.

Diseases:

• Clostridium botulinum can produce botulinum toxin in food or wounds and

can cause botulism. This same toxin is known as Botox and is used in
cosmetic surgery to paralyze facial muscles to reduce the signs of aging; it
also has numerous other therapeutic uses.
• Clostridium perfringens causes a wide range of symptoms, from food
poisoning to cellulitis, fasciitis, and gas gangrene.
• Clostridium tetani causes tetanus.
• Clostridium sordellii can cause a fatal infection in exceptionally rare cases
after medical abortions.

Distribution/Spread:

• Feco-oral route
• Mechanically

Habitat:

Clostridium species are ubiquitous and thus found in various environments across
the world. Oxygen tolerance among these species also varies considerably with
some being strict anaerobes. For this reason, oxygen concentration in a given
environment will influence the type of species present.

Drug Of Choice:

In general, the treatment of clostridial infection is high-dose penicillin G, to which

the organism has remained susceptible. Clostridium welchii and Clostridium tetani
respond to sulfonamides. Clostridia are also susceptible to tetracyclines,
carbapenems (imipenem), metronidazole, vancomycin, and chloramphenicol.
 Lecture# 14

SPIROCHETES

Spirochetes
These are helically coiled bacteria.
These include:

1.TREPONEMA
General Characteristics
❖ gram -ve
❖ spirochete
❖ motile
❖ non-spore forming
❖ non-encapsulated
❖ microaerophilic
Treponema Pallidum
Characteristics - obligate pathogen
Reservoirs - humans (only reservoir, not normal flora)
Transmission
❖ direct contact
❖ sexual
❖ perinatal
Toxins - none in particular (not even LPS)
Diseases
Primary Syphilis
- a single small painless depressed ulcer with elevated margins
❖ ("chancre") at the site of initial infection, fever, headache, anorexia
❖ and local lymphadenomegaly
- primarily occurs on the external genitalia, periorally (if oral
❖ intercourse) or perianally (if anal intercourse)
- occurs 3-6 weeks after initial infection
- spontaneously resolves in 3-6 weeks
 - caused by Treponema Pallidum infection of the skin
- may progress to secondary syphilis (see below)
Secondary Syphilis
❖ small flat erythematous rashes of the palms and soles, small
❖ painless papules ("condyloma lata") of the groin and axilla, and
❖ generalized lymphadenomegaly
❖ occurs 12-18 weeks after initial infection
❖ spontaneously resolves in 3-6 weeks
❖ caused by Treponema Pallidum septicemia
❖ may progress to tertiary syphilis (see below)
Tertiary Syphilis
❖ nodular well circumscribed caseating granulomas ("gummas") of
❖ the skin, liver and bone, obliterative endarteritis of the vasa
❖ vasorum leading to aortic aneurysm ("cardiovascular syphilis"),
❖ meningitis, obliterative endarteritis of the cerebral arteries leading
❖ to cerebral infarct, and permanent central neuronal damage leading
❖ to general paresis and tabes dorsalis ("neurosyphilis")
❖ occurs 3-15 years after initial infection
❖ occurs in 30% of untreated patients
❖ caused by Treponema Pallidum accumulation in tissues
Early Congenital Syphilis
❖ small flat erythematous rashes of the palms and soles, condyloma
❖ lata (see above) of the groin and axilla, osteitis, rhinitis (snuffles"),
❖ hepatosplenomegaly and generalized lymphadenomegaly
❖ occurs immediately after birth
❖ spontaneously resolves in 1-3 weeks
❖ caused by intrauterine Treponema Pallidum infection "
❖ Treponema Pallidum septicemia
❖ may progress to late congenital syphilis (see below)
Late Congenital Syphilis
❖ gummas (see above) of the cartilage of the nose, the bone of thehard palate
and the teeth leading to deformation of the face("bulldog facies"), gummas
of the tibia and fibula leading to
❖ deformation of the legs ("saber shins"), and neurosyphilis (see
❖ above)
❖ occurs 1-3 years after birth
❖ caused by Treponema Pallidum accumulation in tissues
Treatment - narrow spectrum penicillins
- tetracyclines
 2.BORRELIA
General Characteristics
❖ gram -ve
❖ spirochete
❖ motile
❖ non-spore forming
❖ non-encapsulated
❖ microaerophilic
Borrelia Burgdorferi
Characteristics - obligate pathogen
Reservoirs - humans (not normal flora)
- animals (primarily deer and rodents)
Transmission - vectorial (ticks)
Toxins - none in particular
Diseases
Early Localized Lyme Disease
a single large round flat painless enlarging erythematous rash withcentral necrosis
("erythema chronicum migrans") at the site ofinitial infection, fever, headache,
myalgias, and local
lymphadenomegaly
- occurs 1 week after initial infection
- spontaneously resolves in < 1 month
- caused by Borrelia Burgdorferi infection of the skin
- may progress to early disseminated lyme disease (see below)
Early Disseminated Lyme Disease
- disseminated small erythema chronicum migrans (see above),
relapsing arthritis, carditis leading to AV block, meningitis, cranial
nerve damage leading to cranial nerve neuropathies, peripheral
nerve damage leading to peripheral neuropathies, and generalized
lymphadenomegaly
- occurs 1-3 months after initial infection
- caused by Borrelia Burgdorferi septicemia
- may progress to late disseminated lyme disease (see below)
Late Disseminated Lyme Disease
- chronic arthritis and permanent central neuronal damage leading to
encephalopathies
- occurs 3-6 months after initial infection
- occurs in 10% of untreated patients
- caused by Borrelia Burgdorferi accumulation in tissues
Treatment
- broad spectrum penicillins (if early localized lyme disease and/or
early disseminated lyme disease)
- third generation cephalosporins (if late disseminated lyme disease)
Borrelia Recurrentis
Characteristics - obligate pathogen
Reservoirs - humans (only reservoir, not normal flora)
Transmission - vectorial (body lice)
Toxins - none in particular
Diseases
Relapsing Fever
- high fever, headache, myalgias and disseminated skin rashes for <
1 week " afebrile period for > 1 week " progressively shorter
and milder periods of fever and progressively longer afebrile
periods until it completely disappears
- caused by Borrelia Recurrentis septicemia
Treatment
- narrow spectrum penicillins
- tetracyclines

3.LEPTOSPIRA
General Characteristics
- gram -ve
- spirochette
- motile
- non-encapsulated
- non-spore forming
- obligate aerobic
Leptospira Interrogans
Characteristics - obligate pathogen
Reservoirs - humans (not normal flora)
- animals
Transmission - zoonotic
- aerosolized
- contaminated water
- contaminated soil
- contaminated food
Toxins - none in particular
Diseases
Anicteric Leptospirosis
- "fort bragg fever"
- spiking fever, headache and myalgias (primarily of the calves, back
and abdomen) " meningitis (usually subclinical)
- most common
- caused by Leptospira Interrogans infection of the GI tract " mild
septicemia
Icteric Leptospirosis
- "weil's disease"
- enterocolitis (see 14) and mesenteric lymphadenitis ("mock
appendicitis") " meningitis, infectious interstitial nephritis leading
to intrarenal acute renal failure and uremia, and hepatitis leading
jaundice and coagulopathies
- caused by Leptospira Interrogans infection of the GI tract " severe
septicemia
Treatment
- narrow spectrum penicillins
- broad spectrum penicillins.
 MYCOLOGY

MYCOTOXINS
Mycotoxins are metabolites (toxic compounds) that are naturally
produced by certain types of moulds (fungi). Moulds that can produce
mycotoxins grow on numerous foodstuffs such as grains, forages, cereals,
dried fruits, nuts and spices.
A mycotoxicosis is a disease caused by mycotoxins, unlike a mycosis,
which is a disease caused by fungal growth (not due to its toxins).

Characteristics
• Low molecular weight, heat-stable substances
• Unlike many bacterial toxins, non-antigenic; exposure does not induce
a protective
immune response
• Many are active at low dietary levels
• Specific target organs or tissues affected
• Toxic effects include immunosuppression, mutagenesis, teratogenesis
and
carcinogenesis
• Accumulation in tissues of food-producing animals or excretion in milk
may result inhuman exposure
Epidemiological and clinical features of mycotoxicosis
• Outbreaks usually seasonal and sporadic
• No evidence of lateral spread to in-contact animals
• Certain types of pasture or stored feed may be involved
• Clinical presentation is usually ill-defined
• Increased susceptibility to infectious disease may be evident
• Severity of clinical signs is influenced by the amount of mycotoxin
ingested; recovery is related to duration of exposure
• Occurrence of vaccination failure may be increased
• Antimicrobial medication is ineffective
Confirmation requires demonstration of significant levels of mycotoxin
in feed or in from affected animal
Fig: Factors affecting mycotoxin production and manifestations of
clinical disease

Important Mycotoxins, their origin and effects on

 LIVESTOCK

Mycotoxins Fungal species Grain Effect onlivestock

Ergot alkaloids

Ergotamine Clavicepspurpurea Rye, Impaired lactation,

Ergocryptine barley, impaired heat
Ergocornine wheat, regulation, gangrene
Ergocristine oats, and of extremities in
Ergovaline triticale livestock

Agroclavine Claviceps fusiformis Millet Impaired lactation in

Setoclavine pigs
Chanoclavine
Elymoclavine

Dihydroergosine Clavicepsafricana Sorghum Impaired lactation in

Dihydroelymoclavine pigs and cattle,
impaired heat
regulation and
reduced growth in
cattle

Aflatoxins

Aflatoxin B1 Aspergillus flavus Maize, Liver damage,

Aflatoxin G1 Aspergillus rice, livestock carcinogen.
parasiticus peanuts, Impaired immunity,
 and stunting
oilseeds

Ochratoxins

Ochratoxin A Aspergillus Barley, Kidney damage in

Ochratoxin B ochraceus maize, and pigs,
Penicillium sorghum
verrucosum

Fumonisins

Fumonisin B1 Fusarium Maize Liquefaction of brain

Fumonisin B2 verticillioides in horses, fluid
Fumonisin B3 Fusarium accumulation in lungs
proliferatum of pigs

Trichothecenes

T-2 toxin Fusarium equiseti Wheat, Fever; gastroenteritis;

HT-2 toxin Fusarium poae oats, and bleeding from the
Scirpentriol Fusarium barley nose, throat, and
Neosolaniol sporotrichioides gums; exhaustion of
the bone marrow in
livestock

Deoxynivalenol Fusarium Maize, Vomiting, feed

Nivalenol graminearum wheat, refusal in pigs and
Fusarium culmorum barley, and other livestock
Fusarium triticale
crookwellense
Zearalenone Fusarium Maize, False estrus in pigs,
graminearum wheat, infertility in cattle
Fusarium barley, and and sheep
culmorumFusarium sorghum
equiseti

Phomopsin Diaporthetoxica Lupines Liver disease in

livestock
 Lecture# 15
DERMATOPHYTES

DERMATOPHYTES

General characteristics
Dermatophytes are the cutaneous fungi which infect only the keratinized tissue by liberating
keratinase enzyme which helps them to invade into keratinized tissue like stratum corneum layer of
skin, hair and nail.

It is a group of 40 related fungi that belong to three genera

1. Microsporum
2. Trichophyton
3. Epidermophyton
They are restricted to non-viable skin because most are unable to grow at 37®C or in the
presence of serum.

Many species have particular keratinase, elastase and other enzymes which make them host
specific.

Several are capable of sexual reproduction- produce ascospores thus belong to genus
Arthroderma.

In skin they produce:

1. Hyaline hyphae
2. Branching hyphae
3. Septate hyphae
4. Chains of Arthroconidia
E. floccosum is the only pathogen in this genus which produces macroconidia.

They are highly contagious and frequently transmitted by exposure to shed skin scale, nails,
hairs containing hyphae and conidia.

They remain viable for long periods on fomites.

Classification

❖ According to shape and site of infection:

1. Microsporum:
• Spindle shaped
• Infect skin and hair

Examples

➢ Microsporumcannis
➢ Microsporumgypseum
➢ Microsporumgallinae
➢ Microsporumnanum
2. Trichophyton:
• Pencil shaped
• Infect skin, nail and hair
Examples

➢ Trichophyton rubrum
➢ Trichophyton tonsurans
➢ Trichophyton mentagrophytes
3. Epidermophyton:
• Club shaped
• Infect skin and nail
Example

➢ Epidermophyton floccosum

❖ According to the habitat

1. Antropophilic
• Live in the human body.
Examples

➢ some Trichophyton species

➢ E. floccosum
2. Geophilic
 • Usually habitat in the human body
Examples

➢ M. gypseum
3. Zoophilic:
• Usually habitat in animals
Examples

➢ M. cannis (dogs and cats)

➢ M. gallinae (fowl)
➢ M. nanum (pigs)
➢ M. equinum (horses)
➢ M. verrucosum (cattle)

Immunity

Trichophytid reaction: Trichophytin is a crude antigen preparation that can be used to detect
immediate or delayed type hypersensitivity.

Chronic, non-inflammatory dermatophyte reaction

Poor cell mediated immune response to dermatophyte antigen

Immediate type hypersensitivity with elevated IgE

Allergic reaction – dermatophytid (usually vesicle and often in hand)

Clinical findings
COLONY MORPHOLOGY:
Part IV
Veterinary Virology
 Understanding
Lectures (Systemic
Veterinary
Virology Lectures)

This file has not been

changed and depicts what a Muhammad Ammun Bashir
good student picks up in a
lecture delivered in an Teacher: Dr. Haroon Rashid
effort to understand
teaching style and effort) Chaudhry
Muhammad Khalid Mansoor

11/23/2018
Lecture # 1

Dated: 1/10/18

Introduction
History

1. Named poisonous/poison

General characteristics

2. Filterable virus
A virus that is small enough to pass through a fine-pored filter
3. Size
Small sized viruses (30nm) such as picorna virus (0.03μm resolving
power)
Large sized viruses (300nm) such as pox virus (0.3μm resolving
power)
Large virus seen as a small dot under the microscope
4. Shape
2 main classical shapes
1. Icosahedral shape (Hexagone&Pentagone)

2. Helical shape
 5. Forms (2 Forms)
1. Crystal ( In air)
2. Living (Inside host)
6. Non enveloped virus/Naked Virus
a. Fixed and short range sized
7. Enveloped virus
a. Not fixed and large range sized
b. Envelope made up of host cell membrane (up to 70 %
proteins in envelope are virus origin)
c. Round Envelope (Round shape)
d. Irregular Shape of envelope (Large cell membrane of host)
8. Common shapes of viruses
1. Astrovirus (Star shaped)

2.Filoviruse (Filamentous Shaped)

3. Bacteriophage virus (Complex shaped)

4. Poxviruse (Complex Shaped)

5. Minute viruse( Minute shape/Dot shape)

6. Corona Viruse (Crown shaped)

 7. Rhabdoviruse (Bullet shaped)

Classification OF Viruses

➢ 2 major categories
1. RNA based
a. Single standard RNA (90%) are more stable
b. Double standard RNA (5-10%) are less stable such as
birnaviridae
2. DNA based
a. Single standard DNA (5-10%) such as parvoviruse
b. Double standard DNA (99%)

Identification Of viruses (steps)

1. DNA based or RNA Based

2. Single standard/Double Standard
3. Enveloped/Non enveloped
4. Shape
5. Genome (Latest)
Taxonomy of viruses

➢ Named to virus according to their disease in host

➢ Importance to family because viruses are host specific (Except
Bird flu virus and Rabies virus) , sex specific, species specific
(Feline panleukopenia of cats) and age specific (Polio virus)
a. Adenoviridae
b. Canine parvovirus (Parvo dog disease)
c. Picornaviridae
d. Poxviridae
e. Parvoviridae
f. Retroviridae
g. Coronaviridae
h. Birnaviridae
i. Rhabdoviridae
j. Herpesviridae

Biochemical Reactions

➢ Viruses do not give chemical test (Enzymes Present)

Genomic & Replicating Enzymes

➢ Polymerase enzymes
➢ Reverse transcriptase enzymes
➢ Matrix enzymes
➢ Invading enzymes
Lecture # 02

Dated: 5/10/18

Adenoviridae
Adeno (Greek word ) means pertaining to gland/gland

Viridae means virus family

Important virus in vet. Point of view

1. Mastadenovirus (Mammals)
2. Avianadenovirus (Birds)

General Characteristics

➢ Size (70-90nm)
➢ Icosahedral symmetry
➢ Non enveloped virus
➢ Double standard linear DNA
➢ Capsid made up of 10-11 proteins(II-X) such asII (Hexagone),III
(Pentagone), core protein and terminal protein
➢ Peplomers made up of protein (HA/HI in rat & monkey’s RBCs)
➢ Intranuclear replication
➢ Intanuclear basophilic inclusion bodies (Structural proteins of
virus, genome of virus and enzymes of virus)
➢ Mild resistance to environment pressure (56 degree Celsius for 10
mins)

Diseases

➢ Humans (Imuno-compromised)
1. Hepatitis (Mian)
 2. Cause Sever disease
➢ Mammals
1. All species
2. Mild disease
3. Gastroenteritis
4. Hepatitis

Important Diseases In Animals

➢ Dogs
1. Canine Adeno virus type 1/CAV-I
2. Canine Adeno virus type 2/CAV-II
➢ Birds (specially in poultry, turkey and quail)
1. Inclusion body hepatitis/IBH (Normally in broilers)
2. Hydropericardium syndrome/HPS (Normally in broilers)
3. Egg drop syndrome/EDS (Normally in layers)
Above 3 disease also present in breeder

Canine Adeno virus type 1/CAV-I

Gastroenteritis

Hepatitis

Incubation time (7-10days)

Transmission (urine, feces and saliva)

Mortality in pups (70-100%)

Mortality in adults (10-30%)

Morbidity (100%)

Route Of Infection (oral)

 ➢ Oral Oral tonsils Endothelial layer of organs Liver
Kidney (Secretion)
➢ Remains 2-3 weeks in kidney after finishing of disease

Gastroenteritis signs

➢ Vomiting
➢ Diarrhea
➢ Abdominal cramps
➢ Loose feces
➢ High grade fever

Treatment

➢ Supportive treatment
1. Oral rehydration solution/ORS
2. IV
3. Vitamin B-complex
➢ Antiemetics
➢ Prevention is better than cure (Vaccination)
I. CAV-I is mild vaccine (Protect against CAV-I and CAV-II)
II. Reservoir of vaccine is stray dogs and wild dogs (Africa)

Canine Adeno Virus Type 2/CAV-II/Kennel cough

Signs

➢ Tracheitis
➢ Laryngitis
➢ Cough
➢ Pneumonic signs
➢ Shortness of breath
 ➢ Vomit (Sever)
➢ High grade fever

Same route of transmission as canine adeno virus type 1

Mortality (less)

Morbidity (High)

Treatment

➢ Formaldehyde (Naked virus)

➢ Glutaraldehyde
➢ Quartz (Anti-protein)

Vaccination

➢ At 8-10 weeks because of maternal antibodies & 12-14 weeks

➢ Booster at 2 years

Inclusion Body Hepatitis/IBH

Death on back

IBH occurs when feed engorgement is toxic and least water intake in
birds

During 20-36 days of age

Mortality up to 30%

Characteristic Lesions

➢ Enlarged liver with scattered hemorrhage and necrosis,

➢ Intramuscular hemorrhage
➢ Anemia
Diagnosis

Hepatic lesion based

Egg drop syndrome

➢ It is characterized by drop in egg production

➢ Infected hens may lay abnormal eggs

Signs

Inflammatory lesions are found in the oviduct, particularly the pouch

shell gland.

Diagnosis

➢ HI

Control

➢ Use inactivated vaccine before laying begins

Lecture # 03

Dated: 08/10/18

Asfarviridae (African swine fever virus)

General Characteristics

Enveloped DNA virus

Icosahedral symmetry

Replicates in cytoplasm of host cell and in soft ticks of ornithodoros

species
African swine Fever

Disease of pig characterized by fever, hemorrhageages in many tissues

High mortality rate

Endemic in sub-saharan Africa and Sardinia

Pathogenesis and pathology

Infection in domestic pigs is usually acquired via the oro-nasal route

Virus replication in tonsils and in regional lymph nodes

Spreading Of Disease

Blood stream to lymph nodes, bone marrow, spleen, lung, liver and
kidney

Lesions

➢ Splenic enlargement
➢ swollen hemorrhage gastro-hepatic
➢ Renal lymph nodes
➢ Sub capsularpetitation in kidney
➢ Oedema of lungs
➢ Hydrothorax

Clinical signs

➢ Incubation period (19 days)

➢ Fever
➢ Depression
➢ Cutaneous hyperemia
➢ Dyspnea
 ➢ Diarrhea
➢ Bleeding from nose

Diagnosis

➢ ELISA
➢ Samples of blood & serum

Control

➢ Prohibiting import of pig and pig products

Lecture # 04

Dated: 12/10/18

Papovaviridae (old name)

Papillomaviridae (new)
General characteristics
➢ Non enveloped (naked virus)
➢ Icoshedral symmetry
➢ Double standard DNA virus
➢ Circular in nature
➢ Size is fixed 55nm
➢ Physio-chemically resistant (60 degree Celsius at 30 mins)
➢ Replication occur in skin mucous membrane and sometime
in organs

More than fifty types area reported in the human

80% population is infested by it

Spread
Due to weak immune system

Transformation
Sexually from male to female
Direct contact

RX:
• Surgical removal
• With hard inert substance tighten the base
• Vaccination

Types of papilloma and fibro papilloma:

1. Fibro
2. Fibro
3. Cutaneous
4. Alimentary track (dangerous)
5. Fibro
Frond cause mastitis
It is the tumor causing virus
Lecture # 05
Dated: 15/10/18
Parvoviridae
General Characteristics
Size (less than 30nm)
Icosahedral Symmetry
Non enveloped virus
LinearDna
Single standard DNA
Intranuclear replication
Intranuclear inclusion bodies
Disease
1.Panleukopenia of cats/Feline panleukopenia viruse disease
Spread through
➢ Contact
➢ Aerosol
➢ Fecal
➢ Urine
➢ Clinical signs:
➢ High grade fever
➢ Cerebral Degeneration
➢ Abortion and fertility in queens
➢ Diarrhea
➢ Vomting
Depression
Treatment
Supportive therapy
Iv infusion+ Antibiotic+antidiarrheal+antiemetic
Prevention Control
➢ Vaccination (8-10 week)
➢ Booster (Booster)
Parvovirus/Canine parvovirus disease
Signs
➢ Myocardial degeneration
➢ Diarrhea
➢ Vomiting
➢ Fever
➢ Panlekuopenia
Vaccination
3 shots
Epidemiology
Morbidity (90-100%)
Mortality (70-100%)
SMEDI (Porcinus)
Still birth
Mumification
Embryonic Death
Infertility
Lecture No 6
Dated:9/10/18
Circoviridae
General Characteristics
Smallest virus (17-22nm)
Circular DNA
Non-enveloped
Icosahedral virus
Single standard
Intranuclear replication
Stable at 60 degree Celsius for 30 mins
Daignosis
PCR
ELISA
Disease
PMWS (Post weaning wasting syndrome)
PCV-2 (Porcine circoviruse)
Beak And Feather Disease
➢ Feathers shed off
➢ Beak deformity
➢ Hair follicle deformity
➢ Not transmitted to humans
➢ Only in parrots
Chicken Anemia Virus/CAV
➢ Sever Anemia
➢ Lymphocytopenia
➢ Target T cells
➢ Mortality (10-50%)
➢ Morbidity (90-100%)
Route OfTransmission
➢ Vertical
➢ Horizontal
Lecture NO 7
Dated: 22/10/18
Poxviridae
Complex symmetry
Ovoid shape
Brick shape
Pox virus
➢ 220-450 nm X 140-260nm
Parapox virus
➢ Ovoid shape
➢ 250-350 nm X 160-190 nm
➢ Largest virus that effect both animal and bird
➢ Very resistant to environment
➢ Very sensitive to disinfectant and heat
➢ Viral factories are in the cytoplasm
➢ Over thousand enzymes of viral origin
POXVIRIDAE
Entemopox virus (Fish birds reptiles mammals)
Cordopox virus (Have virus to each of invertebrate )
Chicken
Cow
Bird
Camel
Fowl
Buffalo
Poxviridae mostly cross react
Immunity give cross protection
Best antigen(complex protein)
Best immunogen
Best and cheap vaccine
STEP FOR VACCINE PRODUCTION
1. Vesicles
2. Material Taken
3. Heat Treatment
4. Esterification
5. Injected to Animal
6. Immunity Gain
TRANSMISSION
• Aerosol
• Contact
• Abrasion
Small mammals (rodent mouse insect)
1. Macule
2. Papule
3. Vesicle
4. Pustule
5. Scab
It is self-limiting disease but severe to such extent that death
occur
Small pox occur in human
Chicken pox occur in chicken
Cow pox occur in cattle and us of veterinary importance
Vaccina virus infect both buffalo and human
In fowl pox lesion are produced at different sight and mostly on
mouth and foot
Big Macule ----- Pock Lesion
Sheep Pox -------Mouth and Udder
Rabbit Pox --------- Mouth and Udder
Canary Pox ------ Like Fowl Pox
Camel pox like a florid pox and whole body is filled with lesion
Cutaneous pox ----upper part of body like udder etc. Is infected
Transmission
Animal contact --------mice, wools and almost whole class of
rodent
Cow pox can be seen in cat
Direct contact, mechanical contact, flies by cutting
By biting insects
Aerosols
Orf
Sheep to human
Mouth thrash ----- commissure, buccal cavity, inguinal region, off
feed production loses
Recovery occur in 3-4 week
Human ----- mouth, hand, and neck rashes is produced
Orf Types
1. Respiratory ---- lacrimal, nasal secretion, rhinitis, weight loss,
mouth lesion produced
2. Cutaneous
3. Florid
Signs oforf
Drooling saliva and smacking of lips
Orf related to BPS
Sign of orf also match to FMD and RP
Lumpy skin disease
Whole body ----- lump of skin is produced
Boss torus ---- more sensitive
Boss indicus ---- resistant somewhat

FOWL POX
Commissure, combs, and wattles are infected
DIAGNOSIS
PCR
ELISA
HA
Lesion Development
Classical best antigen
Safe, gave cross protection, long term or lifelong immunity
It can be grow in labs and egg culture
Most define sign of virology is high-grade Fever
High Grade Fever is observed in viral disease and septicemic form
of bacterial disease
PATHOGENESIS
Pathogenesis’s according to route
1st it cause lymph adenitis1
Lecture No 8
Dated: 5/11/18
Herpesviridae
Oldest infection known to man
To creep or to spread ----- lesion extend from one place to other
Disease of respiratory system
Less generalized disease
10-20% mortality range
Some cause generalized infection unto death
Spread via
Sex (Sexual), contact, aerosols (respiratory), insect (mechanical)
Mostly this disease is occur to immunodepressed or
immunocompromised animal
Mostly occur during intercourse
Mortality is always less and healthy animal recover fastly and in 1-
3 week
Rapid disease have rapid rate of division so have short incubation
period 3-4 days
Other disease can take 7 day
Cause latent disease --- latency comes and cause hidden infection
Show latency in sacral ganglia
It is one of the tumor causing virus and have ability of tumor
causing and latency
DNA virus, 120-200 nm size, enveloped virus, bilipid layer having
8-10 protein that act as antigen
Icosahedral capsid and is much smaller 50-60 nm in size have a
linear DNA genome and become circular in latency phase powder
like substance is present between capsid and lipid bilayer
(Enveloped) and is called integument
Intranuclear replication occurs virus protein is produced inside the
nucleus, intranuclear inclusion bodies
Very week not survive in environment
And not replicate above 37 centigrade
Every Disinfectant can destroy it
Heat, sunlight, desert, hot weather not survive
Survive in moist, having more organic matter Area
It can even killed by soap or any lipid soluble disinfectant.
It have strains for each species
Produce very hard pain
SUB-FAMILIES
Alpha-herpsviridae ---- human, cattle, porcine, equine, ovine,
Caprine.
Cause generalized infection and genital or respiratory infections
B-herpsviridae ------- cytomegalo virus, ----- Large morphology and
are tumor causing virus
Gemma- herpvirinae
• Marek's disease virus
• In this disease T cell and B cell of the body recognized it a
body part
• Virus will combine with host cell membrane and fusion occur
and then goes to the nucleus and control the machinery.
• After entering the nucleus it will merge with chromosome
and remain as latent or inactive
• After entering the nucleus it will replicate and produce ds
DNA and hexagonal capsid
• After that packing will occur and release in ER.
• Endoplasmic reticulum produce or in vesicle hoes to Golgi
apparatus where it processed and 8 protein are produced and
then exocytosis is occurred
• No fusion ----no entry of virus into body ------- no infection
spread
• Exocytosis -------- can cause cell death (but not common)
ANTIGEN BENEFITS
Immunity
Diagnosis (ELISA)
Vaccine formation
Lecture No 9
Dated:12/11/18

Birnaviridae
Double stranded RNA
60 nm
Non enveloped
Icosahedral symmetry
Core protein are 5 in number
• VP -1
• VP-2
• VP-3
• VP-4
• VP-5
VP-2
Diagnostic test is based on it.
If it (Immunogenic) is not used in vaccine, than vaccine will not
work.
It also pathogenic and cause lysis of lymphocyte B
In Birnaviridae reversion is also occurs.
Three groups
1. AvaiBirna
2. EquiBirna
3. EntomoBirna

INFECTIOUS BURSAL DISEASE (IBD)

More in Pakistan
8-10 day vaccination is done and at 24 day booster is given
Not come in young chick
Occur at 18 day of chick age
At day 12 is also reported
Mild strain only used for ND.
 For IBD we called it cold strain, produce immunity but not
produce sign and symptoms.
Intermediate strains produce immunity and also produce
sign and symptoms.
Hot strain produce high immunity and clear sign and
symptom.
Pakistan only reached intermediate strains.
Control not do vaccination but if they do than use clod strain
in drinking water and nasal spray.
Intermediate vaccine done than cold will not work.
In control shed either vaccine is not done if do they repeat it
every year.
CLINICAL FINDINGS
Ruffed feather pulsating cloaca, dullness red and white faces
mortality 10-20% morbidity 100%
POST-MORTEM SIGN
• Streaked thigh of blood.
• Hemorrhagic streak on liver.
• Hemorrhagic streak at junction of Proventiculus and gizzard.
• Gland of cloaca is large 3 times.
• Bloody strict hemorrhagic.
• Bursa inflamed.
DIAGONOSIS
RT-PCR
AGPT (specific test used in field)

Control
Vaccinations
Effect
B lymphocytes
HIV of Avian
Cause immunodepression in birds
In immunodepression vaccine not work
As IBD end ND will occur so the solution is that;
When IBD is cured than
• Do vaccination of all bird specially of ND
• Use of diuretics
• Aspirin
• Light antibiotics
• Liver degenerating
• Give hepamer, getepar etc.
Management
Restricted feeding - to decrease activity of liver and kidney
Feed Dilution by corn meal, oat meal etc.
Lecture # 10
Dated: 16/11/18
Orthomyxoviridae
Old called Myxovirus - mean pertaining to mucous membrane
Paramyxoviridae – (pertaining to)
Othomyxoviridae – (true to, true to mucous membrane)
Paramyxoviridae
1. Type A - no veterinary importance
2. Type B - veterinary importance
3. Type C - veterinary importance
General Characteristics
• 80-120 nm
• Enveloped
• HA / NA peplomers
• Linear segmented ss RNA , genetic assortment occur
• Helical Capsid
• Very sensitive to reagent
PORCINE INFLUENZA VIRUS
• AI + PIV = Genetic assortment and new one produced
• Mutation very high
• Genetic drift occur
• Genetic shift occur
Equine influenza virus is one of the very common disease of
horse specially racing horse
Avian influenza virus effect layer broiler and breeder
Migratory birds - transcontinental transmission occur
Route of transmission
Naso oral route - tonsillitis - lungs - viremia
Clinical sign
Breathes shortness
Cause pneumonia and it’s all sign also appear
In AIV ------ Proventiculus big red dot
In ND ------Proventiculus small red dot
Sign of Avian influenza virus;
Inflamed comb
Wattles
Nares
Sinusitis
Seems like whole head is red / blue and swelling
Trachea passage is Inflamed
 Sinus highly inflamed
Mucous in whole respiratory tract
Redent eye ( Big red eye )
Bumble foot ( feet below part large and swell)
Shank - inflamed and swollen

Vaccinations
Sometime work and Sometime not work
Serotherapy is also failed
LIVE VACCINE
Work but dangerous (mutation)
Not recommended
Only solution of disease
Supportive therapy is only solution
Respiratory stimulants
Antibiotic
Bronchodilator
In AIV Very high mutation is occurred
Low pathogenic avian influenza
Mild pathogenic avian influenza
High pathogenic avian influenza
Spreadness
March is ideal time for it
Transmitted by Inhalation aerosols, orally and water
Brooder work------ environment temperature Increased------ than
cold water supply and bird sneezing on it and disease is spread.
LPAI and HPAI Seen in Paramyxovirdiae also.
Morbidity 100%
Mortality depend upon strain
Losses
Egg
Weight
Chick less production
Lecture # 11
Dated: 19/11/18
Bornaviridea
Borna –Virus
Size(50to60mm)
Enveloped virus
Single standarad RNA negitive sense virus RNA genome
JoestDogest –inclusion bodies produces in nucleus
Route
Naso oral route
Target olfactory system of nose for entry
Spread-intra axonal
Cause peri vascular caughing
Non soppurative encephalitis
Infalamatin of membrane of brain
Sings
In horse donkeey ,mule,cat,dog,human,sheep, is reported
Antibodies is reported in scheizopherinia patient
Incordination ,settingposition,ataxia,headpressing,blindness,singl
e or double side,sheviring,fever and other Nervous sings
Loss of sense of hearing ,tremors
Hipocapus
Its more active
Usually it is a chronic disease
Milid attack---can be survive
Severe attack—death occure
Mortality reached 100%
Course of disease 3-4day
 Understanding Lectures (RNA
Viruses)
Course Title:
Systemic Veterinary Virology
Course Code:
Micro-502
Assigned By:
Dr. Haroon Rashid Ch
Assigned To:
M. Ammun Bashir
Roll No:
07
Semester:
5th
Session:
2016-21
Lecture # 12

Dated: 7/12/18

Paramyxoviridae (Veterinarians Favorite)

Previously classified as myxoviridae

General Characteristics

6. 5 main genera
7. Size is 150 nm or more
8. Single standard RNA virus
9. Negative Sense
10. Complete genome ( Differ from orthomyxoviridae)

11. Enveloped Virus

12. The capsid is helical shaped (15-18 nm in size)
13. Virus Coded Protein
➢ HA Protein (Helps in the entry)
➢ NA protein
➢ F protein (Important in disease-causing)
➢ M protein
➢ G protein (Helps in an entry)
k. Labile to physiochemical agents
110
Diseases

New-Castle Disease

Signs
l. Bloody litter in VELOGENIC VISCEROTROPIC NEWCASTLE
DISEASE (VVND)/Doyle form/
m. Peracute form
n. Beaches form/Mesogenic (Acute form) give signs
o. 90-99 % death & 100 morbidities in VVND
p. 60-80 % mortality in beach form
q. 20 % mortality in mild form/lentogenic
Forms According To System

Nervine Form

Beach Form
➢ Torticollis

➢ Stargazing
➢ Paralysis
➢ Incoordination
111
GIT Form

3. Bloody diarrhea
4. Copious diarrhea
5. Dysentery (Not in copious amount)
6. Dehydration
7. Death

Postmortem

➢ White comb
➢ White wattle
➢ Hemorrhagic crop
➢ Profused and small hemorrhages in proventriculus (DD from bird flu)
➢ Hemorrhagic enteritis
➢ Cecal tonsil become hemorrhagic

Respiratory Forum

➢ Pneumonia
➢ Labored Breathing
➢ All respiratory signs

Vaccine Form

3. Cold strain (Lasota)

4. Intermediate strain
5. Hot strain

Vaccination

5. 1st day
6. 7th day
7. 14th day

Lecture # 13

Dated: 14/12/18

Astroviridae (Star shaped)

General Characteristics

112
 3. 28-30 nm (Larger than Circovirus)
4. SSRNA
5. Intracytoplasmic replication
6. Very resistant
7. 60 degree Celsius for 5 min.
8. Opportunistic bacteria

Disease

4. Self-limiting diarrhea
5. Encountered when immunity is weak (Especially in young ones)

Host

➢ Cattle
➢ Buffalo
➢ Sheep
➢ Goat
➢ Pig

Treatment (Humans)

4. Wash hand after washroom

Lecture # 14

Dated: 21/12/18

Picornaviridae

Smallest RNA virus

113
4 viruses

5. Aphthous virus (FMD)

6. Enterovirus (Pigs)
7. Hepatovirus (Chickens)
8. Cardiovirus (Pigs)

General Characteristics

III. 30 nm
IV. Icosahedral symmetry
V. 60 total protein
VI. 4 major proteins (VP1,VP2,VP3& VP4)
VII. VP1,VP2 & VP3 important for diagnostic
VIII. VP4 (Inner Protein )
IX. VP4 helps in replication
X. The only RNA is infectious
XI. Intracytoplasmic Replication
XII. Very stable to physiochemical characteristics
XIII. The only choice is formalin (Toxic) & Glutaraldehyde (Expensive)
XIV. Quaternary ammonium compounds (Quat) is the best choice

Disease

Foot and mouth (FMD) Disease

➢ Encountered twice in a year ( Extreme Summer & Winter)

Serotypes

➢ 80-200 are serotypes

➢ Important serotypes are O, A, C, Asia 1, Sat 1, Sat 2 & Sat 3
114
 ➢ O, A & Asia 1 (Pakistan)

Signs & Symptoms

➢ Oral ulcers (Necrosis)

➢ High fever
➢ Anorexia
➢ Foot ulcers (laminitis, Sedentary, Lameness, Necrosis)
➢ Abortion
➢ Off rumination
➢ Salivation
➢ Smacking of lips
➢ Froth
➢ Diarrhea

Treatment

➢ No treatment
➢ Vaccination
➢ Supportive treatment can be done (Vitamin B complex, antipyretic,
glycerin & KMnO4
➢ Chemical cautery (Glycerin + very small amount of KMn04/Formalin +
very small amount of KMnO4)
➢ The best combination is glycerin & boric acid
➢ Pinky solution used orally

Lecture # 15

Dated: 4/1/19

Caliciviridae

General Characteristics

➢ 27-40 nm
➢ Non-enveloped
➢ Cup-shaped
➢ + sense RNA (Rapidly Replicate)
➢ Single standard
➢ Icosahedral symmetry
➢ Intracytoplasmic replication in Upper respiratory tract, blood cells &
Humans (GIT & Liver)
➢ Very stable in the environment
➢ No disinfectant works

115
 Cup Shaped Virus

➢ Hepatitis virus in humans

➢ Sapo like a virus (Self-limiting gastroenteritis)
➢ Norwalk like a virus (Self-limiting gastroenteritis)
➢ Laguvirus
➢ Vesivirus

Transmission

➢ Flies &feco-oral routes in humans

Treatment

➢ Wash hands after washroom (Humans)

Disease

➢ Hepatitis E in humans

Feline calicivirus disease

➢ Vesivirus
➢ Infect 2-6 month cats
➢ Upper respiratory tract infection
➢ Africa & Asia (Prevalence)

Sines

➢ Pharyngitis
➢ Laryngitis
➢ Nasal discharge
➢ Fever
➢ Vomiting

116
 ➢ Oral Lesions
➢ Depression

Solution

➢ Vaccination
➢ No seroprotection

Swine Vesicular exanthema Virus

➢ Also known as picorna of swine

➢ Infect pigs
➢ Eradicate from Europe since 1956
➢ San Miguel sea lion virus (Vesivirus)

Rabbit hemorrhagic disease

➢ Also known as European brown hare disease

➢ Use to control the rabbit population in America
➢ Humans (Patches on the skin)
➢ The incubation period is 3 to 5 days
➢ Death within one week

Signs

➢ Hematuria
➢ Blood from oral mucosa
➢ Convulsions
➢ DIC (Disseminated intravascular coagulation)
➢ Mortality is high
DIC Factors
➢ Old age
➢ Apoptosis
➢ Bacterial DIC (Hospital Required)
➢ Viral DIC

Transmission

➢ Feco-oral route
➢ Inhalational route
➢ Vetor-born

Treatment

➢ Fortam used in humans

➢ Seprin used in humans
117
 ➢ Ephor sodium is used in Case of DIC (HS)
➢ Rocephin used in sheep and goat

Vaccine

➢ Killed vaccine
➢ Live attenuated vaccine
➢ No vaccination in humans

Lecture # 16

Dated: 7/1/19

Coronaviridae (Crown shaped)

General Characteristics

➢ 120-160 nm
➢ SSRNA
➢ Intracytoplasmic replication
➢ Very labile in environment
➢ Disinfectant effectively control it
➢ Helical/Tubular/Oval/Round/Kidney Nucleocapsid

Host

➢ Human
➢ Pig
➢ Cat
➢ Dog
➢ Cattle

Route

• Feco-oral route
• Inhalational route

Repliaction

• Rbcs
• Wbcs

Disease

Feline Coronavirus (FCoV)

• Transmissible diarrhea in babies

118
Transmissible Gastroenteritis virus (TGEv)

• Causes acute, rapidly spreading disease in swine characterized by diarrhea

and vomiting

Porcine epidemic diarrhea

Turkey Cov

Bovine Cov

Canine Cov

Signs

• Diarrhea
• Dehydration
• Vomiting

Treatment

• Sodium salt drip

• Normal salts drip
• Mother mouth cud
• Probiotics

Feline infectious peritonitis

• Same signs and symptoms

Avian infectious bronchitis (IB)

• Respiratory disease in winter

Signs

• Nasal discharge
• Cloudy air discharge
• Asphyxia
• Cheasy plug in trachea

Treatment

• Expectoration
• Ammonium chloride
• Ultimately death

Vaccine
119
 • H120 vaccine at 0 day, 7 day & 14 day

Lecture # 17

Dated:11/1/19

Rhabdoviridae (Rod-Shaped)

General Characteristics

9. linear, non-segmented RNA genome of negative polarity encased in a

ribonucleoprotein complex
10. Bullet- or cone-shaped
11. six genera; Vesiculovirus, Lyssavirus, Ephemerovirus,
Cytorhabdovirus, Novirhabdovirus, and Nucleorhabdovirus
12. Rhabdoviruses usually contain five major proteins: a large RNA-
dependent RNA polymerase (L), a surface glycoprotein (G), a
nucleoprotein (N), a protein component of the viral polymerase (P) and
a matrix protein (M)
13. The G protein forms the surface peplomers which interact with host
cell receptors, facilitating endocytosis of the virion. In addition, the G
protein induces virus-neutralizing antibodies and cell-mediated
immunity. Replication occurs in the cytoplasm (with the exception
ofnucleo-rhabdoviruses)
14. Virions (100 to 430 nm x 45 to 100 nm) are stable in the pH range of 5
to 10
15. Rapidly inactivated by heating at 56"C, by treatment with lipid solvents
and by exposure to UV light

120
Clinical infections

16. Transmitted by bites of mammals, arthropod vectors or direct contact.

Infection may also be acquired through environmental contamination
17. The best known and most important member of the Rhabdoviridae is
rabies virus, a Lyssavirus (Greek lyssa, rage or fury)
18. A number of distinct Lyssavirus genotypes produce clinical signs
indistinguishable from rabies
19. Domestic animals are the vesicular stomatitis Indiana virus and the
vesicular stomatitis New Jersey virus. Bovine ephemeral fever virus, of
significance in some countries, is the type species of the genus
Ephemerovirus. Some fish diseases, such as infectious haematopoietic
necrosis, viral haemorrhagicsepticaemia and spring viremia of carp are
also caused by rhabdoviruses

Rabies

3. This viral infection, which affects the central nervous system of

most mammals including man, is invariably fatal
4. Most clinical cases are due to infection with rabies virus
(genotype 1)
5. Genetic sequencing and antigenic studies have been used to
categorize lyssaviruses into seven genotypes and four
serotypes

121
 6. Classical rabies caused by genotype 1 lyssavirus is endemic on
continental land masses with the exception of Australia and
Antarctica

Epidemiology

8. Two epidemiologically important infectious cycles are

recognized, urban rabies in dogs and sylvatic rabies in wildlife
9. Raccoons, skunks, foxes, and bats are important reservoirs of
rabies virus in North America
10. In continental Europe, the principal reservoir is the red fox. The
vampire bat is an important reservoir of the virus in Central and
South America and in the Caribbean islands
11. In developed countries, the control of stray dogs and vaccination
programmes have reduced the importance of urban rabies and
have focused attention on wildlife reservoirs

Pathogenesis

b. Following introduction into the tissues, the virus enters

peripheral nerve endings
c. There may be limited replication locally in myocytes or other
tissue cells
d. The virus is transported to the central nervous system by
retrograde axoplasmic flow and becomes widely disseminated in
nervous tissue by the intra-axonal spread

Clinical signs

e. Prodromal, furious (excitative) and dumb (paralytic) phases

f. In dumb rabies, muscle weakness, difficulty in swallowing,
profuse salivation and dropping of the jaw are the usual features
g. The furious phase is characterized by an increase in
aggressiveness and hyperexcitability, and there is a tendency to
bite it inanimate objects and at other animals
h. Hydrophobia
Control
i. Commercial vaccines available for the immunization of domestic
carnivores by parenteral inoculation contain inactivated virus
(genotype 1) and are potent and safe

Vesicular stomatitis

j. Vesicular stomatitis is clinically similar to foot-and-mouth

disease
122
Epidemiology

k. South America and the USA

l. Tropical and subtropical regions

Pathogenesis
m. The virus probably enters the body through abrasions on the
skin or mucous membranes or following an insect bite.
n. Vesicles which develop at the site of infection may coalesce.
Spread may occur locally by extension from primary lesions
o. Although secondary lesions at distant sites may develop, it is
unclear how the transfer of the virus occurs and if these lesions
result from viremia or following
environmental contamination
Treatment and control
p. Specific treatment is not available. Measures aimed at
minimizing secondary infections may be beneficial.

Bovine ephemeral fever

q. This arthropod-borne viral disease of cattle and water buffalo

occurs in tropical and subtropical regions of Africa, Asia, and
Australia.
r. The virus causes subclinical infection in many other ruminant
species including Cape buffalo, wildebeest, waterbuck and deer

Epidemiology

2. Culicoides species are involved in the transmission of the virus

3. In tropical areas where bovine ephemeral fever is endemic,
subclinical infections are common

Pathogenesis

➢ Blood-sucking insects acquire the virus when feeding on animals

during the brief viraemic stage of the disease
➢ The virus, which multiplies in the insect vector, is shed in its saliva and
is transmitted to a new host through wounds during feeding
➢ Many of the changes observed in infected animals are attributed to
host response rather than to direct viral damage

Clinical signs

3. The incubation period is up to eight days

123
 4. A biphasic high fever is commonly observed
5. Affected animals become depressed, anorexic, lame and
constipated.
6. Milk production drops dramatically
7. Muscle stiffness and ruminal stasis may develop
8. Pregnant animals may abort
9. Recumbency may be accompanied by salivation and ocular and
nasal discharge
10. Muscular fibrillation and paresis frequently occur,
reflecting the accompanying hypocalcemia

Treatment

c. Affected animals should be rested.

d. Anti-inflammatory drugs such as phenylbutazone, flunixin
meglumine and ketoprofen have proved useful for the
treatment
e. Intravenous or subcutaneous administration of calcium
borogluconate is recommended
f. Oral drenching should be avoided during the acute phase
of the illness because swallowing may be impaired.

Control

c. Vector control is usually impractical in endemic areas

Lecture # 18

Dated: 14/11/18

Bunyaviridae

124
5 Genera

General Characteristics

d. 80-120 nm
e. Enveloped RNA virus
f. SSRNA virus
g. Segmented genome (3 segments)
h. Very labile & lethal virus
i. Zoonotic virus

Life cycle

125
Genus (5)

Bunyavirus

• Fetus abnormal during pregnancy

• Transfer by midges, ticks, mosquitoes, and sandfly

• Monster babies

Phlebovirus

• Transfer by mosquito &aedes

126
 • Rift valley fever

Hantavirus

127
• Transfer by class Rodentia

Isopouvirus

• Arbovirus
• Infect plants

Nairovirus

• Nairobi sheep disease

• Crimean-Congo haemorrhagic fever (CCHF) is a widespread disease

caused by a tick-borne virus (Nairovirus) of the Bunyaviridae family

128
 Signs & Symptoms

• Hemorrhagic fever
• Hepatic necrosis
• Immunodeficency

Replication

• Replicate in WBC

Zika virus

• Out break in Brazil

Life cycle & Pathogenesis

129
 • Microcephalus

Lecture # 19

Dated: 20/1/19

Filoviridae

Introduction

130
 • These are long threadlike viruses, hence the name (filum
means thread)
• Marburg and Ebolaviruses causing hemorrhagic fever belong to the
genus Filovirus
• These agents cause severe or fatal hemorrhagic fevers
and are endemic in Africa

Characteristics

• Pleomorphic viruses (mostly filamentous)

• They range in size from 80 to 800–1000 nm.
• Enveloped
• Single-stranded (-) RNA genome
• The nucleocapsid is helical

Epidemiology

Pathogenesis

131
 • The floviruses replicate efficiently, producing large amounts of virus in
monocytes, macrophage, dendritic cells, and other cells
• Viral cytopathogenesis causes extensive tissue necrosis in
parenchymal cells of the liver, spleen, lymph nodes, and lungs
• The breakdown of endothelial cells leading to vascular injury and
hemorrhage

Marburg Virus
• Marburg disease is a hemorrhagic fever that occurred simultaneously
in laboratory workers in Marburg, Frankfurt (Germany) and Belgrade
(Yugoslavia) in 1967
• In each case the infection arose from tissues of African green monkeys
to which the laboratory workers had been exposed imported to
laboratories from Uganda

Chronology of Marburg Hemorrhagic Fever Outbreaks

132
 Ebola Virus

• In 1976, two severe epidemics of hemorrhagic fever occurred in Sudan

and Zaire with high fatality
• The causative virus was morphologically identical to the Marburg virus
but antigenically distinct
• The virus responsible was named Ebola virus after the Ebola river
• In 1979 Ebola re-emerged in Sudan, with serial person to-person
spread
• Another epidemic occurred in Kikwit, Zaire, in 1995
• Three distinct strains of Ebola virus have been recognized
1. Zaire strain (EBO- Z)
2. Sudan strain (EBO-S)
3. Reston strain (EBO-R)

133
 Laboratory Diagnosis

Electron microscopy

• In the blood and in the cytoplasm of the affected cells filamentous

viruses can be seen by electron microscopy

Isolation of virus

• Virus can be cultured in vero cells from the blood during the febrile
phase
• Virus isolate is identified by electron microscopy and direct
immunofluorescence
• Virus culture must only be attempted in laboratories with required
biosafety level

Serology

• Indirect immunofluorescence can be used for detection of

antibodies in the serum

Treatment, Prevention, and Control

• Antibody-containing serum and interferon therapies have been tried

in patients with filovirus infections
• Infected patients should be quarantined, and contaminated animals
should be sacrificed
• Handling of the viruses or contaminated materials requires very
stringent isolation procedures

Reoviridae

Introduction

• Reoviridae constitutes a diverse family of viruses that infect humans,

many mammals, other vertebrates (including birds), plants and insects
• The family Reoviridae derives its name from the prototype virus which
was known as the Respiratory enteric orphan virus
• The term "orphan virus" refers to the fact that some of
these viruses have been observed not associated with any known
disease
• The family Reoviridae is divided into nine genera
• Four of the genera are able to infect humans and animals
• Orthoreovirus, Rotavirus, Coltivirus, and Orbivirus

134
 Rotaviruses
• Double-stranded, segmented (11 segments) RNA genome
• Three- layered capsid, icosahedral
• Diameter: 70 nm, Naked
• Rotavirus causes gastroenteritis, especially in babies under two years
of age
• Symptoms may include vomiting, diarrhea, fever and dehydration
• 215 000 child deaths occurred during 2013 due to rotavirus infection
compared to 528 000 in 2000
• Acquired by fecal-oral route, especially during winter and summer
seasons in communities where personal hygiene is inadequate

Diagnosis, Treatment & Control

Diagnosis

• ELISA
• Immune electron microscope

135
Treatment

• Management consists of replacement of fluids and restoration of

electrolyte balance either intravenously or orally, as feasible

Control

• In view of the fecal–oral route of transmission, wastewater treatment

and sanitation are significant control measures
Vector-Borne Infections

Introduction

• Many human and animal virus infections are restricted to very defined
geographical areas of the world
• This geographical restriction and the observation that direct contact
between an infected individual and a subsequent victim was not always
necessary for transmission of infection led early investigators to the
conclusion that an intermediate was responsible for transmission of the
virus between people
• Following intense study, it was shown that haematophagous (blood
sucking) insects can transmit viruses from their natural animal reservoir
to a susceptible host of a different species
• some species of mosquitos, sand flies, biting midges and ticks

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 Arboviruses and their Hosts
• Arboviruses are acquired by an insect either directly from its mother
whilst still an egg (vertical transmission) or as an adult female when it
takes a blood meal from an infected animal or person
• The viruses can only be acquired and spread if they establish a
viraemic infection in which virus is found in the blood of the infected
vertebrate host
• For efficient transmission the virus must be present in sufficient
quantity to ensure that the insect takes up an infectious dose during the
blood meal
• Once the virus has been ingested, it typically replicates within the
insect without causing any significant disease
• When the virus infects members of its animal reservoir it is also unlikely
to cause significant disease as the virus and host will have usually
established a mutually acceptable co-existence over a long period of
interaction
• Some examples of arboviruses that cause severe diseases in
vertebrates are shown in Table

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 Yellow Fever Virus
• Dengue virus is a member of the Flavivirus family
• As indicated in Fig. Yellow fever virus infections are restricted to
regions of tropical South America and sub-Saharan Africa
• This reflects the geographical habitat of the primary mosquito vectors
that transmit the virus, and in particular of Aedes aegypti
• In recent times in excess of 200,000 cases of yellow fever with
approximately 30,000 deaths have been recorded each year
• Approximately 90% of this disease burden falls in Africa where large
outbreaks occur, whilst the remainder are in South America

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Disease syndromes of the alphaviruses and flaviviruses

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Yellow Fever Virus Vaccine

• Yellow fever vaccine is recommended for people aged ≥9 months who

are traveling to or living in areas at risk for yellow fever virus
transmission
• Yellow fever vaccine may be required for entry into certain countries
• Yellow fever vaccine is available only at designated vaccination centers
• For most travelers, a single dose of yellow fever vaccine provides long-
lasting protection and a booster dose of the vaccine is not needed.
However, some travelers may require a booster dose
• Yellow fever vaccine is a live-attenuated virus vaccine that has been
available since the 1930s
Dengue virus
• Dengue virus infection causes disease ranging from asymptomatic or
mild to the severe dengue haemorrhagic fever and dengue shock
syndrome
• Dengue virus infects monkeys which act as an animal reservoir from
which the virus can be transmitted to humans
• The virus is maintained in a jungle cycle similar to that described for
yellow fever virus.

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 • Dengue virus is transmitted between humans primarily by Aedes
aegypti mosquitos and, to a lesser extent, by Aedes albopictus, which
occur in all tropical and sub-tropical region of the world
• Dengue virus is endemic in South-East Asia, the Pacific, East and
West Africa, the Caribbean and the Americas and is now considered to
be a major international disease threat with up to 40% of the world’s
population potentially at risk
• Current estimates suggest that there may be as many as 400 million
Dengue virus infections every year up to 500,000 people,
predominantly children, are hospitalized with severe Dengue virus
disease of whom approximately 2.5% die

Prevention and Treatment of Dengue Virus Infection

• There is currently no vaccine to prevent dengue virus infection

• The presence of an animal reservoir makes elimination of
dengue virus unachievable
• Consequently, the only preventative measures are aimed at reducing
exposure to infected mosquitos
• Treatment of infected patients is generally supportive to reduce the
impact of blood and fluid loss in the circulatory system and to reduce
the impact of tissue damage
• Early treatment of patients with dengue haemorrhagic fever can reduce
mortality from levels of 10% seen with untreated individuals to 1% if
treated
Chikungunya virus
• Chikungunya virus was first identified in 1952 in Tanzania and was
subsequently found to be responsible for several large outbreaks
• In 2005–2007, an outbreak on Reunion Island in the Indian Ocean
resulted in almost a third of the entire population becoming infected,
and this marked a rapid increase in the incidence and geographical
range of Chikungunya virus
• The virus has now been found in many parts of South-East Asia, with
small numbers of cases also reported in Australia and in Italy and
France in Europe
• The animal reservoir of Chikungunya virus is not clear, but there is
evidence suggesting the involvement of rodents, birds and small
mammals in Africa

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 • The virus is transmitted between the various hosts by several different
Aedes mosquito species within which it can replicate
• During the Reunion Island outbreak it became clear that the primary
vector was Aedes albopictus
• Unfortunately, Aedes albopictus has a greater geographical distribution
than Aedes aegypti and this alteration in insect host preference of the
virus has consequently been associated with its increased spread
across tropical and subtropical regions of the world

Prevention and treatment of Chikungunya virus infection

• No vaccine is available for Chikungunya virus and no alternative form

of protective treatment has been discovered
• For this reason the major effort for protection is focused on control of
the mosquito vector, as for dengue virus
• Similarly, no drugs that attack the virus have been approved for use
and treatment is thus restricted to addressing the symptoms of disease
• Treatment primarily takes the form of anti-inflammatory drugs to reduce
the joint pains that are characteristic of the disease
West Nile virus in the USA
• West Nile virus is a member of the Flavivirus family
• West Nile virus can cause a fatal neurological disease in humans

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 • However, the majority of infections are asymptomatic and only
approximately 20% result in overt disease of which a small proportion
then develop serious acute neurological complications
• West Nile virus is transmitted from one vertebrate host to another by
mosquitoes within which the virus also multiplies
• The virus is able to infect a very wide range of invertebrate and
vertebrate hosts, including humans and birds
• In 1999, West Nile virus was detected during an outbreak of
encephalitis in New York, the first time that it had been seen in the
Americas
• Following the first signs of its presence the virus spread relentlessly
across the USA and southern Canada, and after five years was present
from the east to the west coast of the continent

Prevention and treatment of West Nile virus infection

• While effective vaccines for prevention of West Nile virus in horses are
available there is no human vaccine
• No antiviral drugs to treat West Nile virus infections are routinely
available and treatment for West Nile disease is limited to supportive
therapy to address the symptoms

Laboratory Diagnosis

• The alphaviruses and flaviviruses can be grown in both vertebrate and

mosquito cell lines, but most are difficult to isolate
• Infection can be detected through the use of cytopathologic studies and
immunofluorescence
• Detection and characterization can be performed by RT-PCR testing of
genomic RNA or viral mRNA in blood or other samples
• After isolation, the viral RNA can also be distinguished by the finding of
RNA “fngerprints” of the genomic RNA
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 • A variety of serologic methods can be used to diagnose infections,
including hemagglutination inhibition, enzyme-linked immunosorbent
assays, and latex agglutination
• The presence of specific IgM or a fourfold increase in titer between
acute and convalescent sera is used to indicate a recent infection

Disclaimer

This is part of a series, priced minimally to try to keep alive

open source effort, we dont have copyrights for this and dont
believe in copyright, we believe knowledge in whatever form
must be free to all humanity. Some things may be copied, we
apologize to original source as it is a student effort to keep alive
knowledge sharing. We also apologize for any mistakes and
own it, as it is a part of series to understand teaching practice
and student perception of the lecture delivered. Nothing has
been edited and original student perception is depicted.

Haroon Rashid Chaudhry

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Literature Cited.

1. Veterinary Microbiology and Microbial Disease, P. J. Quin, B. K. Markey, M.

E. carter, W. J. Donelly, F. C. Leonard, Blackwell
2. All the Microbiology Notes which come in all shapes and sizes from the
Internet

Disclaimer:

We bring this opensource Concise Notes book to you and be sure not any of the
money earned will be spent on us but will be given to the Outdoor hospital of CVA,
IUB, BWP and UVAS, Lahore-Pakistan for the treatment of the sick animals.

A further note that the price of the book has been limitized to the least possible price
only cut off the printing charges and transit charges. We believe in the freedom of
scientific knowledge as I recall my early days in Cathedral High School, Hall Road,
Lahore Pakistan despite me being a muslim I was given a free copy of the catholic
Bible to read but I guess it is not the case anymore even in the muslim country like
Pakistan we have to buy our holy book at twice the charges and that may be the case
for Bible as well. Freedom of literature be it scientific or religious is the true essence
which will lead us to prosperity in the third world countries.

We as a team don’t hold any copyright of this book and authorship is only to suffice
the need of the opensource project any similarity observed is purely unintentional and
if we need to hang someone please blame it on the compiler Haroon Rashid Chaudhry.
These are common scientific knowledge we dispense to our veterinary and medical
students and similarity is bound to occur but it is mentioned here that it is a
compilation rather than an authored book. The literature from where this is taken has
been mentioned above.

We apologize the living legends of microbiology for using their work but it is for the
impoverished nations which can’t afford their original masterpieces at very high cost
and their books limitize to the reference book section of the libraries, we want to
promulgate their work but through careful manipulation and keep it cost free- I hope
they realize our predicament.

It is supposed to be open source and free

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 ****THE END****

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