Essential to the web of life in every environment

Crucial role - made life comfortable to humans

A. BIOTECHNOLOGY
Food production - forms essential links to many food chains
 Plants Animals  Humans eat
2100 BC - Egyptians - used YEASTS  BREAD
1500 BC - High Complex Procedures
Fermenting cereal GRAINS  BEER
Fermentation process - cheese, yogurt, buttermilk
B. Probiotics - Bifidobacterium, Lactobacilli

C. Bioremediation - bacteria are used to destroy dangerous

chemical pollutants - DDTs, PCBs

D. Others: Cellulose - Headsets

HBA - diapers & plastics
Genetic Engineering -AA, hormones, Growth hormones
clotting factors enzymes

E. Synthesis of Antibiotics and vaccines

 CHARACTERISTIC
Cytoplasmic CELL
membrane PROKARYOTES
Contains enzymes of EUKARYOTES
Semipermeable layer not
COMPONENTS (BACTERIA)
respiration; active (FUNGI, functions
possessing PROTOZOANS)
of
secretions of enzymes, site prokaryotic membrane
Nucleus & Nuclear Single circular DNA,
of phospholipids no
& DNA Membrane bound, complex
Structure nuclear membrane or not
synthesis of DNA and basic CHONs
covered with CHONs
Cell Wall Rigid layer of murein or No peptidoglycan (In some
Localization of Nuclear Dense tangle of DNA in In nucleus surrounded by
peptidoglycan; exception: cases cellulose present)
structure cytoplasm; Nucleoid or nuclear membrane
Mycoplasma Cell wall present only in
nuclear equivalent fungi:
Glucans, mannans, chitin,
Extrachromosomal DNA Often present in the form of chitosan,
In organelles- mitochondria
cellulose
plasmids

Sterols
Organelles in cytoplasm Absent ; present only in
None Usually present
Mitochondria & chloroplasts
Mycoplasma in photosynthetic bacteria

Reproduction
Ribosomes Asexual,–by
Present 70sbinary
ribosomes In
80smost cases sexual,
ribosomes
transverse fission possibly asexual
MIND’S EYE
Coccus - round
variations: coffee bean,
lancet, diplococci
Bacillus - rod-shape
variations: club-shape, comma,
filamentous , coccobacilli

Spiral-coiled - Spirochetes - Treponema

Borrelia
Leptospira
Pleomorphic - Mycoplasma spp.
P C
L E
B L
A I L
N N U
E A L
S A
R R
Y
O A
F F R
I R
D A
S N
I S G
V I E
I O M
O N E
N N
T
s
Micrometers or Nanometers
Among the Smallest: Rickettsia, Mycoplasma
Among the Biggest: Bacillus megatorium
Bacillus anthracis
Cyanobacteria
Arrangement:
Singly, pairs,chains, clusters, pallisades, groups, etc.
CELL ENVELOPE
Composed of macromolecular layers surrounds bacterium
PARTS OF THE CELL ENVELOPE
Cell membrane and peptidoglycan layer
Outer membrane - Gram-negative
Capsule
Contains antigens

A. CELL WALL
Gram(+) - thick peptidoglycan ,teichoic acid, teichuronic acid
Portionpolysaccharides,
of cell envelope external to cytoplasmic
strong rigid cell wall
membrane & internal to the capsule
Confers
Gram osmotic
(-) - thin protection lipoprotein, phospholipid
peptidoglycan,
Confersmembrane
the Gram-staining
containscharacteristics
LPS, more complex
OUTER MEMBRANE
CELL WALL PEPTIDOGLYCAN
-Cross
Contain unique
linked LPS, various
peptidoglycan CHONs sacculus
- murein
NONTransmembrane
PEPTIDOGLYCAN CHONsCOMPONENTS
- porins,integral proteins bilayer
Envelope proteins-M proteins
gram-negative bacteria
CAPSULAR POLYSACCHARIDES
Dispensable,does not affect viability of the cell
FUNCTIONS
Barrier, filter, attachment site for phage and
conjugation, proteases and other enzymes
Form and rigidity,support to bacteria
Equalizes osmotic pressure
Absent in Mycoplasma - CELL WALL-LESS
Contains the - PEPTIDOGLYCAN
principal structural component -sugar backbone
COMPOSITION CELL WALL IN
1. Gram-Positive Bacteria - Multilayered
2. Gram - Negative Bacterai - Monolayered
ESSENTIAL FUNCTION OF CELL WALL COMPONENT
1. Cell wall growth
2. Sporulation
3. Cell septation
4. Competency for transformation
 Gram (+) Gram(-)

Peptidoglycan Multilayer Monolayer

Teichoic acid yes no

LPS no Yes

Lipoprotein & no yes

phospholipid
CELL WALL DEFECTIVE FORM (L- PHASE VARIANTS)
1. PROTOPLAST - Gram (+) bacteria w/o cell wall
2. SPHEROPLAST - Gram (-) bacteria w/o cell wall but with outer
membrane

TEICHOIC ACID - found only in Gm (+) bacteria

OUTER MEMBRANE - found only in Gram (-) organism
for attachment
 MADE UP OF POLYSACCHARIDE EXTERNAL TO CELL WALL
1. SLIME LAYER - loose attachment e.g. S. epidermidis
S. saprophyticus
Bacteroides fragilis
2. CAPSULE - tightly bound to cell wall
Encapsulated - Pneumococci, Meningococci
[Link], [Link]
K. Pneumoniae, C. burnetii
Size of capsule - 2-3x the bacteria
Hiss capsular direct stain - clear space or halo
Quellung reaction - capsular swelling with
specific antisera
Function : Antiphagocytic, antigenic,virulence
Not essential to life of bacteria
COMPOSITION OF CAPSULE OF DIFFERENT BACTERIA
1. COMPLEX POLYSACCHARIDE
Streptococcus, Enterobacteriaceae
2. HYALURONIC ACID
Group A - Streptococcus pneumoniae
3. SIALIC ACID
GROUP B - Streptococcus agalactiae
4. POLY-D-GLUTAMIC ACID
Bacillus anthracis
A. Streptococcus pneumoniae - showing a prominent capsule
B. Bacteroides spp. - has a slime layer surrounding the cell
 GLYCOCALYX
SLIME

CATHETER
SURFACE

CELL
CLUSTER
Aggregates of bacterial cells formed in soil and marine
environments and in surface of medical implants devices
(e.g. prostheses). They enhance nutrient uptake and often
exclude antimicrobials

ATTACHMENT

RESISTANCE

MATURATION

EXPANSION
BACTERIAL NUCLEIOD OR NUCLEAR BODY
Not a true nucleus & without nuclear membrane
and nucleolus
IN PROKARYOTIC
Cell appear as concentrated DNA in cytoplasm
bearer of hereditary characteristics
RIBOSOMES
Globular structures, composed of RNA molecules,
involve in protein synthesis
The bacterial nuclear region. A colored TEM of a thin section of
Escherichia coli with the DNA shown in red CNRI/CUSTOM
MEDICAL STOCKPHOTO, INC.)
PLASMA/CELL OR CYTOPLASMIC MEMBRANE
Physical & Metabolic barrier
Between interior and exterior of cell
Selectively permeable
Contain ELECTRON TRANSPORT SYSTEM
Made up of lipoprotein and lipopolysaccharide
Temporarily holds excess metabolites
1. Metachromatic Granules
C. diphtheriae which is made up of
volutin granules
Demonstrated by using LAMB stain

2. Much Granules
M. tuberculosis - gram+ granules
 Storage inclusions in bacterial cell. Substances such as polyhy-
droxybutyrate, stored in insoluble, concentrated form provides
an ample long-term supply of nutrients
 CLASSIFICATION BASED ON LOCATION
Flagella
1. Monotrichous - single polar flagellum
- Slender whip-like structure
- Organ of locomotion
2. Lophotrichous - bundle of flagella at one end
- Originate from cytoplasmic membrane
- Flagellin - functonal unit made up of protein
3. Amphitrichous - flagellum at both ends

4. Peritrichous - flagella present all around

the body
SWARMING PHENOMENON
- Exhibited by Proteus species

ANTIGENIC - FLAGELLAR H ANTIGEN

- Used for serologic classification
- Not vital to survival of bacteria
- Not required for virulence or viability
- Flagella can be dislodge but can regenerate
PILI (FIMBRIAE) - threadlike structures
1. Common pili - thousands of pili around
bacteria
2. Sex pili - one or two glycoprotein in a
bacterium

FUNCTIONS: Adhesion, sexual, virulence

pili found ONLY IN GRAM NEGATIVE
E.g. Neisseria gonorrhea
OUTER MEMBRANE
Found in Gram (-) bacterial membrane
Above Peptidoglycan layer composed of:
1. Lipid bilayer
2. Proteins - porins

LPS- LIPID A
- polysaccharide rich core and a polysaccharide
side chain
- Polysaccharide designated as  O antigen
- Lipid A portion - responsible for biologic effects of
endotoxin
GRAM NEGATIVE BACTERIA
more complex envelope than gm (+) bacteria

TEICHOIC ACID - only in Gram (+) bacteria

PILI - seen only in gram - negative bacteria

SPORES - seen only in certain gram + bacteria

 CHARACTERISTICS GRAM-POSITIVE GRAM -NEGATIVE
Outer membrane - +
Cell wall Thicker Thinner
Lipopolysaccharide (LPS) - +
Endotoxin - +
Teichoic Often present -
Sporulation Some strains -
Capsule Sometimes present Sometimes present
Lysozyme Sensitive Resistant
Antibacterial activity of More susceptible More resistant
Penicillin
Exotoxin production Some strains Some strains
Resistant structure which enable bacteria to withstand
adverse environmental conditions - VIABILITY
FOUND ONLY IN FEW BACTERIA:
1. Clostridium - gram (+) strictly anaerobic bacilli
2. Bacillus - gram (+) strictly aerobic bacilli
3. Coxiella burnetii
Location : Terminal, subterminal, central
Reverts to vegetative form when favorable.
DIPICOLINIC ACID - Makes spores resistant
 Cell division Elaboration of Free spore
and partitioning a spore coat

Terminal spore C. tetani

Central spore C. perfringens

Subterminal spore C. septicum, novyi, histolyticum

dificille, botulinum
1. CORE
Spore protoplast
Contains complete nucleus - chromosome
Glycolysis - protein-synthesis & energy-generating system
Cytochromes - lacking
Shortened electron transport pathway involve flavoproteins
UNIQUE ENZYMES
a. Alanine racemase
b. Dipicolinic acid synthetase
NO reduced pyridine nucleotides or ATP
Energy for germination stored as 3-phosphoglycerate
NOT ATP
HEAT RESISTANCE - ATTRIBUTABLE TO:
1. Dehydrated state
2. Presence of large amounts (5–15% of spore dry weight)
 CALCIUM DIPICOLINATE

2. Spore wall
Innermost layer surrounding inner spore membrane
Contains normal peptidoglycan
Becomes the cell wall of germinating vegetative cell

3. Cortex
Thickest layer of the spore envelope
Contains unusual type of peptidoglycan
Extremely sensitive to lysozyme
Its autolysis plays a role in spore germination
4. Coat
Composed of keratin-like protein with disulfide bonds
Impermeable Layer
- Confers relative resistance to antibacterial agents

5. Exosporium
Composed of proteins, lipids, and carbohydrates
Function ???? Unclear
Spores of Bacillus species (anthracis & cereus) possess
exosporium
1. Simple or Direct Stain

2. Differential Stain
a. GRAM STAIN
Gram (+) - Stains Blue / violet
Gram (-) - Stains pink / red
 All bacilli are gram negative EXCEPT
Mycobacterium, Corynebacterium,
Bacillus, Clostridium

All cocci are gram positive EXCEPT

Neisseria, Veilonella, Branhamella

NOTE: Spiral,if stainable, are usually gram

negative
Reagent Function Gram(+) Gram(-)

Crystal Primary purple Purple

violet stain
Grams mordant purple purple
iodine
alcohol 95% decolorizer purple Colorless

saffranin counterstain purple red

ACID FAST STAIN
1. Ziehl Neelsen – Hot Method
2. Kinyoun stain – Cold Method
Mycobacteria stains red vs. blue background,
resist decolorizer differentiate acid fast from
non acid fast

LIPID BILAYER (includes mycolic acid)

Responsible for acidfastness of Mycobacteria
Mycobacteria
Stain red - carbolfuchsin and resist decolorization of
acid alcohol

Mycolic acid
Cell wall - contain equal amounts of peptidoglycans,
arbinomannans, and lipids

LIPID BILAYER
> 50% of lipid components
Esterified mycolic acid
25% normal fatty acid
Glycolipid
- trehalose, mycolates, sulfolipids
- LOS mycosides & lipopolysaccharides
All bacteria are Non-acid fast EXCEPT
Mycobacterium

Partially acid fast Organisms

- Nocardia
- Cryptosporidium
- Gordonia
- Isospora
- Rhodococcus
- Tsukamurella
Ziehl- Kinyoun function Acid fast Non acid
neelsen method fast
method
Carbol Carbol Primary red red
Fuchsin Fuchsin stain

Acid Acid decolorizer red Colorless

alcohol alcohol

Methylene Malachite Counter- red Blue/

blue green stain green
SPECIAL OR SELECTIVE STAIN
Dyer Stain - cell wall
Fisher and Conn Stain - Flagella
Dorner Stain - Spore
[Link] - Metachromatic granules
Hiss Stain - Capsule
INDIRECT STAIN / NEGATIVE / RELIEF STAIN
Background will appear dark
E. G. India ink- capsule of Cryptococcus neoformans
CAPSULE STAIN. Capsules stains poorly, and so they stand out against the
India ink-stained background as a halo around the organism. This
photomicrograph shows Cryptococcus neoformans, an encapsulated yeast
 SHAEFFER-FULTON SPORE STAIN
Endospores of bacillus megatorium(2,335X) are visible as green, oval
structures inside and outside the rod-shaped cells. Vegetative cells, which
represent a non-spore-forming stage, and cellular regions without spore
stain red. (CDC/Courtesy of Larry Stauffer/Oregon State public Health lab)
FEATURE EXOTOXIN ENDOTOXIN
Source Gm+ & - Gram neg.
Location Secreted outer membrane
extracellularly Integral part
Toxicity great weak
Tissue affinity specific non specific
Chemical type polypeptide LPS
Stability heat labile heat stable
Antigenicity High Weak
Non pyrogenic pyrogenic
Convert to toxoid yes no
Incubation period- “first encounter” but no
symptoms yet
Prodrome - period of disease onset
Invasion period - period of maximal illness
Defervescence - manifestations decline
Convalescence - regains full strength
 Metabolism Results in  Reproduction
 Reproduction results in  Growth

 What is Microbial growth?

 an increase in a population of microbes (rather than an
increase in size of an individual)
 Result of Microbial growth?
 a discrete colony – an aggregation of cells arising from
single parent cell
METABOLISM
The process of building up chemical compounds
in the cell and their breaking down during activity
to receive the required energy and the building
elements. Sum up all the chemical processes that
occur within a cell

METABOLISM HAS TWO COMPONENTS

1. Anabolism (assimilation)
Synthesis of more complex compounds and
use of energy

[Link] (dissimilation)
Break down a substrate and capture energy
 Building and Breaking Down
Molecules

Anabolic Reaction
(Anabolism)
The phase of metabolism in which simple substances are
synthesized into the complex materials of living tissue.

Catabolic Reaction
(Catabolism)
The metabolic break down of complex molecules into
simpler ones, often resulting in release of energy.
GOAL OF METABOLISM
Conserve the energy released during
redox reactions by making high energy
compounds
ATP
There are different strategies for conserving this energy
All chemical reactions consist of transferring electrons
from a donor to an acceptor

OXIDATION-REDUCTION REACTIONS
Chemicals that donate electrons  OXIDIZED
Chemicals that accept electrons  REDUCED
Energy is released - during these electron transfers
To capture energy, bacteria need to intercept
the electrons during redox reactions
 CATABOLISM OR BREAK DOWN OF
CARBOHYDRATES
- Primary energy source for anabolic reactions
- GLUCOSE - a monosaccharide is used most commonly
- After Sugars are made or obtained  ENERGY SOURCE OF LIFE

CATABOLISM OF SUGAR BY DIFFERENT WAYS

1. AEROBIC CELLULAR RESPIRATION
2. ANAEROBIC CELLULAR RESPIRATION
3. FERMENTATION
AEROBIC RESPIRATION
Requires oxygen  results to COMPLETE breakdown
of glucose to CO2 & H2O and a lot of
Final electron receptor O2
Yield = 38 ATP
ANAEROBIC RESPIRATION
FERMENTATION
Yield=>22<38
Yield ATPATP
Does not require oxygen 
End products: Lactic acid/Alcohol
Only partially
Final breaks down
electron receptor glucose
is organic = makes less ATP
molecule
CATABOLISM - NUTRIENT BREAKDOWN & ENERGY
RELEASE
Primary catabolism of fuels (Glucose) results in energy
release proceeds through a series
Most efficient way to extract energy from glucose:
- GLYCOLYSIS
- KREBS CYCLE or TCA CYCLE
- ELECTRON TRANSPORT CHAIN
1. GLYCOLYSIS
Also called EMBDEN-MEYRHOF PATHWAY (EMP)

2. TRICARBOXYLIC ACID CYCLE (TCA)

Also known as CITRIC ACID CYCLE (TCA) or KREBS
CYCLE

3. RESPIRATORY CHAIN
Electron transport and Oxidative Phosphorylation
Glycolysis: Several glycolytic pathways
The most common one:
Glucose Pyruvic acid + 2 NADH + 2ATP
Final electron acceptor : never be O2
Sulfate reducer: final electron acceptor is Sodium
sulfate (Na2 SO4)
Methane reducer: final electron acceptor is CO2
Nitrate reducer: final electron acceptor is Sodium
nitrate (NaNO3)
NOTE: Anaerobic is less energy efficient
In the absence of an external electron acceptor, bacteria
need to regenerate NAD+ from NADH

It involves transfer of electrons to organic substrate

They do this by transferring the extra electrons back onto

the pyruvate
a. Homolactic Acid Fermentation
P.A Lactic Acid
E.g. Streptococci, Lactobacilli
b. Alcoholic Fermentation
P.A  Ethyl alcohol
E. g. yeast
d. Butylene-glycol Fermentation
c. P.A
Mixed acid fermentation
2,3, butylene glycol
[Link]
E.g.  lactic acid
acetic acid
H2 +Fermentation
e. Propionic acid CO2
succinic acid
P.A 2 propionic acid
Ethyl alcohol
E.g. Propionibacterium
E.g. E. coli and some Enterobacter
Consist of polymeric backbones of repeating N- acetyl
glucosamine and N acetyl muramic acid joined together
by a tetrapeptide bonds
Organisms use a variety of nutrients for:
1. Their energy needs
2. Build organic molecules & cellular structures

Most common nutrients contain necessary elements:

CARBON - OXYGEN - NITROGEN - HYDROGEN
Four elements make up 95% of dry weight of bacterium

Other 5%: Calcium, Copper, Iron, Magnesium,

Manganese, Phosphorus and Iron

TRACE ELEMENTS - Other elements needed

 CLASSIFICATION ACCORDING TO CARBON SOURCE
Carbon- skeleton or backbone of all organic molecules
I. AUTOTROPHIC or LITHOTROPHS
Use INORGANIC compounds = sole source of carbon like CO
a. Photolithotrophs - Derive energy from light
b. Chemolithotrophs - Oxidation of inorganic compounds
II. HETEROTROPHIC or ORGANOTROPHIC
Use ORGANIC compounds = carbon source = GLUCOSE
Cannot use CO2 as sole source of carbon
a. Phothorganotrophs - derive energy from ligth
b. Chemoorganotrophs - derived energy from organic cmpd.
Most medically imporant bacteria are
CHEMOORGANOTROPH
Nitrogen - major component of proteins and
nucleic acids
Assimilated by fixation, reduction,
and ammonia assimilation

Inorganic ions-Mg,K,Ca, iron, trace elements

Growth factors-B complex,amino acids,

purines,pyrimidines
Carbon dioxide-require CO2-capnophiles
Obligate Anaerobe
Acquire energy ONLY BY FERMENTATION
Most cannot survive in oxygen
E.g. [Link], perfringens Fusobacterium, Bacteroides
Oxygen is toxic for anaerobes which lack 2 enzymes:
1. Superoxide dismutase-destroys SOD
2. Catalase-destroys hydrogen peroxide

Facultative Anaerobes
Acquire energy by either RESPIRATION or FERMENTATION
Can survive with or without oxygen
Can grow both under aerobic and anaerobic condition
Most medically important bacteria belong here
E.g. E. coli, Staphylococcus aureus
Obligate Aerobe
Strictly require oxygen for growth
Acquire energy ONLY by RESPIRATION
Cannot survive without oxygen
E.g. Mycobacterium tuberculosis, Pseudomonas aeroginosa

Microaerophiles
Grow at low oxygen tension-damaged by
normal oxygen level oxygen
E.g. Campylobacter jejuni

Aerotolerant Anaerobes
Can resist exposure to oxygen, not killed

Capnophilic Bacteria
CATEGORY REQUIREMENT EXAMPLES
OBLIGATE AEROBE 15-21% 0₂ (As found in a Mycobacteria, fungi
C0₂ incubator or air)
MICROAEROPHILE 5% 0₂ Campylobacter,
Helicobacter spp
FACULTATIVE ANAEROBE Multiplies equally well in Enterobacteriaceae, most
the presence or absence of staphylococci, some
0₂ streptococci
AEROTOLERANT Reduced concentration of Most strains of
ANAEROBE 0₂ (Anaerobic system & Propionibacterium,
microaerophilic Lactobacillus, some
environment) Clostridium spp.
OBLIGATE ANAEROBES Strictly anaerobic Most Bacteroides species,;
environment (0% 0₂) many clostridium,
Eubacterium,
Fusobacterium spp.
Peptostreptococcus spp.;
Porphyromonas spp.
CAPNOPHILE 5% -10% CO₂ Some anaerobes, Neisseria,
Haemophilus sp.
 AEROBIC & ANAEROBIC IDENTIFIED BY GROWTH I LIQUID CULTURE
Obligate aerobic bacteria gather at top of test tube to absorb maximal amount
of oxygen
Obligate anaerobic bacteria gather at bottom to avoid oxygen
Facultative anaerobes gather mostly at the top, aerobic respiration is most
beneficial; but as lack of oxygen does not hurt them,
they can be found all along the test tube
Microaerophiles gather at upper part of test tube, not at top
Require O2, but at low concentration
Aerotolerant bacteria not affected by oxygen; evenly spread along test tube
TEMPERATURE
Affects proteins and lipid membranes
If too low, membranes become rigid and fragile
If too high, membranes become too fluid

CATEGORIES BASED ON OPTIMUM TEMPERATURE

1. Hyperthermophiles = >70 -120⁰C
2. Thermophiles -high temp = 50-60⁰C
3. Mesophiles = 20-40⁰C- most pathogens belong in this group
4. Psychrophiles-low temp = 10-20⁰C
pH
Most bacteria grow at ph 6-8
Neutrophiles - pH 7.5-8- most medically
imptortant group belong here

Acidophilic - Peptosterptococci, lactobacilli

Halophilic - Vibrio species, Enterococci
Osmotic - high salt-halophile
high osmotic pressure-osmophile
Bacteria reproduce - Binary fission
1 parent cell forms 2 progeny cells
Exponential or logarithmic growth
One bacterium will produce 16 bacterium
after 4 generations
Doubling Time (Generation Time)
Different bacteria have ranges
Shortest/Fastest Generation Time
Slowest/ Longest Generation Time
 GENERATION OR DOUBLING TIME

Time required for a COMPLETE FISSION CYCLE

Time = 1 cell to undergo binary fission
or to divide into 2 cells
Each new fission cycle increases population
by a FACTOR OF 2
Favorable environment = Doubling effect continues
at a constant rate
LENGTH OF GENERATION TIME
A measure of the growth rate of an organism
AVERAGE GENERATION TIME
30 to 60 minutes under optimum conditions
Can be as short as 10 to 12 minutes
This growth pattern is termed EXPONENTIAL

EXPONENTIAL GROWTH
Occurs during a rapidly multiplying bacterial
population
Each cell gives rise to 2 cells, each of which divides
into 2 more, yielding a total of 4, and so on
LAG PHASE
Vigorous metabolic activityperiod of CELL ADAPTATION
and adjustment after metabolites are depleted
Increased in size , DNA & enzymes Synthesis
LOG OR EXPONENTIAL PHASE
Rapid cell division - Cells are in steady state
New cells are synthesized- Cell mass increase in number
Metabolically active
Generation time - can be observed
STATIONARY PHASE
Slowing growth,living cells equals dead cells
Nutrients used up
Waste products accumulate
SPORE PRODUCTION STARTS - dehydration
Dipicolinic acid helps stabilize nucleic acids
DEATH OR DECLINE PHASE
Final phase, decline in number of bacteria
More dead bacteria than viable
Spores continuously produced to survive
INCUBATION PERIOD
- “first encounter” but no symptoms yet

PRODROME - period of disease onset

INVASION PERIOD - period of maximal illness

DEFERVESCENCE - manifestations decline

CONVALESCENCE - regains full strength

I. COCCI
a. GRAM (+) COCCI
- Peptostreptococcus, Staphylococci
- Peptococcus
b. GRAM(-) COCCI
- Branhamella, Neisseria, Veillonella

II. BACILLI
a. Endospore Forming - Bacillus, Clostridia
b. Non-sporeforming
1. GRAM (+) - Eubacterium, Propionibacterium
Lactobacillus, Mobiluncus, Bifidobacterium
Actinomyces
2. GRAM(-) - Bacteroides, Prevotella, Porphyromonas
Fusobacterium, Leptotrichia

III. SPIROCHETES - Treponema, Leptospira, Borrelia

KINGDOM : Bacteria
PHYLUM : Firmicutes
CLASS : Cocci
ORDER : Bacillales
FAMILY: Micrococcaceae
Staphylococcaceae
GENUS : Staphylococci
SPECIES : aureus
epidermidis
saprophyticus
Gram (+) cocci , spherical
Singly, in pairs, grape-like clusters - bunch
Non-motile, non- sporeformer

Facultative anaerobic /aerobic

EXCEPT S. saccharolyticus - Obligate anaerobe

Mesophilic & Chemoheterotrophic

Capsulated  Slime layer or Biofilm - S. aureus
S. epidermidis
COLONIES ON BAP (18-24⁰ Culture)
Medium sized, cream-colored, white-light gold, buttery
Optimum Temperature: 18-40⁰C
1. Facultative Anaerobes
Grows most bacteriologic media
Aerobic & microaerophilic
2. Capnophilic
Increased CO2 tension for growth
3. Temperature ranges - Mesophilic
18 - 40⁰C; grows most rapidly at 37 ⁰C
4. Wide pH ranges
Grow on media containing 6.5%-10% NaCl
5. Complex Nutritional requirements
Enriched media containing nutrient broth or blood,
amino acids & various growth factors
SHEEP BLOOD AGAR - medium of choice for 1⁰ isolation
Solid media : Colonies - round, smooth, raised , glistening
CLASSIFICATION
Family Micrococcaceae
Three Clinically Significant Species : Human disease

A. Staphylococcus aureus
- Pathogen of man, 75% - cases of infections
- Binary fission
- Nasal carriage - 20-50% in humans
- Most virulent of all the Species
- Most purulent of all the cocci
B. Staphylococcus epidermidis
(STAPHYLOCOCCUS ALBUS)
Opportunistic disease in hospitalized patients,
with an impaired host resistance
Most frequently isolated species - Skin, RT, GIT
Opportunistic :
Hospitalized patients - impaired host resistance
Infection - those with PROSTHETIC DEVICES
Colonies - gray to white on primary isolation
Novobiocin test - SENSITIVE
C. Staphylococcus saprophyticus
Normal flora - female GUT, perineum & GIT
UTI : 10-20%
Sexually active females - displacement of normal flora
of vagina & perineum into urethra
2nd only to E. coli - cause of Community Acquired
Urinary Tract Infection
Honeymoon Cystitis
ADHESIN- adhere to human uroepithelium

Nosocomial Infection - use of indwelling catheter

Opportunistic pathogen & no exotoxins
NOVOBIOCIN TEST - RESISTANT
while S. epidermidis - Sensitive
NOTE:
BOTH: S. epidermidis & S. saprophyticus
Increasingly associated with 
OPPORTUNISTIC INFECTION
Not regarded as harmless commensals
Known as CONS - Coagulase-Negative Staphylococci

UPDATES
In recent years, species have been implicated in human
infections:
S. lugdunensis
S. schleiferi
S. caprae
 CULTUIRAL CHARACTERISTICS
Staphylococcus aureus
Fresh isolates - GOLDEN YELLOW PIGMENT
- CAROTENOID PIGMENTS - STAPHYLOXANTHIN

PIGMENT PRODUCTION
Variable trait, not related to pathogenicity
Produced only on prolonged incubation
Best demonstrated at 20-25⁰C - RT

Anaerobic condition or in broth = No pigment production

Sheep Blood Agar - Beta hemolytic
Colonies: Gray to deep Golden yellow color
METABOLISM
Respiratory and fermentative pathways

CATALASE TEST
ALL: CATALASE (+) = produced aerobically
Protective enzyme - a virulence factor
H2O2 = Toxic & biocidal  H2O & oxygen
Test to differentiate Staphylococci from Streptococci
POSITIVE: STAPHYLOCOCCI
Negative: STREPTOCOCCI
ENTEROCOCCI
2. Mannitol Salt Agar (MSA)
- Selective & Differential medium with 6.5% or 7-9% NaCl
- Colonies - Yellow-colored colonies
Result: Mannitol fermentation drop in medium’s pH(ACIDIC)
- Only Staphylococcus aureus ferments mannitol
- Growth on MSA - differentiate S. aureus from other species

STAPHYLOCOCCUS AUREUS STAPHYLOCOCCUS EPIDERMIDIS

A. CAPSULE OR SLIME LAYER
Called GLYCOCALYX
Network of loose fitting polysaccharide layer
Anti-phagocytic, chemotactic
SLIME - adherence -catheters & synthetic materials
[Link] 5 & 8 - Majority of infection & invasive
PEPTIDOGLYCAN
40-60% weight of diseases
cell wall
Poorly immunogenic
Called MUREIN OR MUCOPEPTIDE LAYER
Increase
PeptideH2O retention
link glycan - against
chains- desiccation
Cross-linked layers
Pathogenicity
BACKBONE OF factor - virulence
ALTERNATING:
1. N-Acetyl glucosamine (NAG )
2. N- Acetylmuramic Acid (NAM)

Osmotic stability, rigidity and shape

Endotoxin like properties activates complement
& release of cytokines
C. Protein AEFFECTS OF PROTEIN A
BIOLOGIC
1.
- Major
Chemotactic
CHON component of cell wall
2.
- Group
Anti - complementary
specific antigen - most strains only of S. aureus
3.
- Covalently
Antiphagocytic
linked to glycan layer
4.
- Binds
Adherence
FC receptors of IgG 1,2, 4 & ECM
5. Elicits
(-)hypersensitivity reaction
Binding of complement
6. Platelet injury
- PART OF MSCRAM
Microbial Surface
CLASSIFIED INTO: Components Recognizing Adhesive
Matrix
1. Mediates bacterialA attachment
BOUND PROTEIN
- Single polypeptide chain, cell wall component

2. FREE PROTEIN A
- Single polypeptide chain, extracellular,
released into the medium during cell growth
D. TEICHOIC ACID
- 40% of the dry cell mass
- ATTACHMENT OR ADHERENCE
- Composition: PO4-containing polysaccharides
SPECIES SPECIFIC
Poorly Immunogenic- (bound to peptidoglycan) 
Staphylococcus aureus
Stimulates antibody production
RIBITOL POLY A (Teichoic acid)
Ribitol teichoic acid with N-acetyl-D- glucosamine residue
Antibodies against teichoic acid used to detect =
SYSTEMIC STAPHYLOCOCCAL DISEASE
Not present in gram (-) bacteria
Staphylococcus epidermidis
GLYCEROL POLY B (Teichoic acid)
Glycerol Teichoic acid with glucosyl residues
E. CLUMPING FACTOR
- Cell wall component - adherence of organisms
to fibrinogen and fibrin
- Example of MSCRAM
A. COAGULASE
Marker for virulence - Invasive pathogenic potential
Best single test to identify pathogenic S. aureus
Formation of fibrin layer in abscess 
 LOCALIZING THE INFECTION - protection against
phagocytosis

TWO TYPES OF COAGULASE

1. FREE COAGULASE or CELL-FREE

- Produce during growth and multiplication

2. BOUND COAGULASE or CLUMPING FACTOR

- Fibrinogen  Fibrin = CLOT FORMATION
B CATALASE
All staphylococci = POSITIVE
Differentiates staphylococci from streptococci
Converts H2O2  H2O & O2 
Reduces killing by phagocytosis

C. LIPASES
Lipid hydrolyzing enzymes, invades cutaneous & SCT
HALLMARK OF STAPH. INFECTION: ABSCESS FORMATION

Liberates fatty acids causing:

1. Tissue irritation
2. Chemotaxis
3. Phagocytosis

D. HYALORUNIDASE
- Mucin-splitting enzymes, hydrolyses hyaluronic acid
in C.T. ground substance
- Facilitates SPREAD OF INFECTION
E. STAPHYLOKINASE or FIBRINOLYSIN
Dissolves fibrin clot resulting to  BLEEDING
A nuclease which cleaves either DNA or RNA

F. BETA-LACTAMASE or PENICILLINASE
Cleaves/destroy the beta-lactam ring conferring
 ANTIBIOTIC RESISTANCE
Resistant to penicillin and cephalosporin

G. OTHERS:
a. SLIME PRODUCTION
Produced by strains of CONS
Polysaccharide materials - Adherent to synthetic
material
Inhibits chemotaxis & phagocytosis
A. PYROGENIC EXOTOXINS
- Superantigen - Release of IL-1 & 6, alpha 2
mononucleosis factor
- Manifestations: Fever, capillary leak, circulatory
collapse, shock

B. ENTEROTOXINS A to E (A-E, G-J, K-R, U, V)

- Food poisoning (Phage Group 3)
- Heat-stable, Superantigen
- Gastrointestinal upset  Food poisoning

- Presentation: More of Vomiting than diarrhea

Stimulation of CNS Vomiting Center
1. Enterotoxin A
- Most common, acts on vascular smooth muscles
- Majority of food poisoning

2. Enterotoxin B
- Damage intestinal epithelium Pseudomembranous colitis

3. Enterotoxin A &D
- Responsible for staphylococcal food poisoning
- Inhibits water absorption
- Acts on EMETIC RECEPTOR SITE in the GIT  VOMITING
 THE SEQUENCE OF EVENTS IN A TYPICAL
OUTBREAK OF
STAPHYLOCOCCAL FOOD POISONING

Food containing protein is cooked (Bacteria, usually killed)

Then food is contaminated by worker with Staphylococci on

hands (Competing bacteria have been eliminated)

Food is left at room temperature. Organisms incubate in

food(temperature abuse) long enough to form and release toxins.
(Reheating will eliminate Staphylococci but not the toxin)

Food containing toxin is eaten

In 1 – 6 hours, Staphylococcal-intoxication occurs

FOOD POISONING
Self-limiting, food Intoxication  Enterotoxins
Toxins - heat-resistant not inactivated by brief cooking
Food contaminated by organisms/toxins
Meat products - HAM, PORK, BEEF, BURGERS
CLINICAL SIGNS & SYMPTOMS
SALADS - Potato & egg, baked foods
1. Severe crampy abdominal pain
2. Nausea and vomiting
INCUBATION PERIOD: 4 hours, course of 24 hours
3. Non-bloody diarrhea
CLINICAL ONSET: 2-6 hours after ingestion
4. NO FEVER differentiate it from infectious diarrhea
RECOVERY PERIOD: 6-8 hours
TREATMENT: Fluids & electrolytes

PREVENTION & CONTROL

1. Avoidance of food contamination
2. Control of personnel food preparation and distribution
C. EXOTOXINS
[Link] SHOCK SYNDROME TOXIN 1 - TSST 1
Formerly known as Exotoxin C & Enterotoxin F
Superantigen, Pyrogenic Exotoxin C
Most cases: Associated with female during menstruation
 Superabsorbent tampons
Also occur in: Non-menstruating women and men 
Surgical wound infection
CLINICAL PRESENTATION:
a. Hypotension
b. Fever and chills
c. Diarrhea
d. Extensive skin rash & desquamation
(Scarlatiniform rash)
e. Multi-organ Failure
2. EXFOLIATIN/EPIDERMOLYTIC TOXIN/ RITTER DISEASE
Superantigen
CausativeEXFOLIATIVE
BULLOUS agent: Phage DERMATITIS
Group 2 , immunogenic
Intraepidermal-splitting
Most severe form of tissues and necrosis
Disturbs
Starts adhesiveness
as erythema thenofwill
cellsspread
in Stratum granulosum
to the entire
SSSS of
body - Staphylococcal Scalded
the infant  Bullae Skin Syndrome
formation
Common - newborn and elderly
TYPES : a. Localized
EXFOLIATIVE TOXIN/SSSS
EPIDERMOLYTIC TOXIN
b. Generalized
1. EPIDERMOLYTIC TOXINSSSS
A
Chromosome -mediated , heat-stable

2. EPIDERMOLYTIC TOXIN B
Plasmid -mediated, heat-labile

Mechanism: Dissolves mucopolysaccharide matrix

D. CYTOLYSINS HEMOLYSINS
Exotoxins , tissue destruction & abscess formation
ALPHA CYTOLYSINS
Dermonecrotic activity , severe tissue damage , RBCs

BETA CYTOLYSINS/ SPHINGOMYELINASE C

LEUKOCIDINS
Heat labile, destroys rbcs, sphingomyelin around nerves
(-) phagocytosis, kills granulocytes, macrophage
Associated with:
DELTA CYTOLYSINS
a. Furunculosis disrupts
Thermostable, - Severe cellular
cutaneous infection
membranes
b.
byNecrotizing pneumonia
detergent-like actions
PANTON-VALENTINE LEUKOCIDIN
Has
NOTE:two All
Components
toxic to: PMNs, macrophages, platelets
a. S- leucocidin
b. F- leucocidin
Important virulence factor for CA-MRSA
 CUTANEOUS or SKIN INFECTIONS
1. FOLLICULITIS - a. Superficial b. Deep
Tender pustule that involves the hair follicle
Infection of one hair follicle e.g. Acne

2. FURUNCULOSIS (BOILS)
Coalition of folliculitis (single opening) with extension
to subcutaneous tissue
Formation of multiple sinus tracts
Signs& Symptoms
Systemic manifestation: Fever and chills
Treatment: Excision & Drainage
3. CARBUNCLE
Aggregate of connected furuncles, with several
pustular openings

4. IMPETIGO
Small area of erythema bullae rupture & heal 
honey-colored crust
Children - limbs and face
After Insect bites as Primary lesion  Satellite Lesions
Macule Pustule Crusting
Treatment: Antibiotics

5. WOUND INFECTIONS - e.g. Burns

6. ABSCESS - Typical lesion of Staphylococcus aureus

Hallmark of Staphylococcal infection
DEEP INFECTION
1. BONE & JOINT INFECTION (SEPTIC ARTHRITIS)
Bone - Primary infection - INSECT BITE
 Formation of sinus tract
 Affecting the bone  OSTEOMYELITIS

Joint Infection: Oxacillin, Clindamycin, Cephalosporin

SEPTIC ARTHRITIS
- Surgery
- Articular Cortisone injection

Both :Treatment: Minimum : 4-6 weeks / Surgical drainage

Pneumonia & Empyema
- Most common: Infants, children, elderly & debilitated
- Short Prodrome: Fever, rapid onset of respiratory distress
GIT symptoms
- CXR: Unilateral consolidation – Staphylococcal BPN

CXR-PA VIEW OF A 15Y/O WITH STAPHYLOCOCCAL ENDOCARDITIS MULTIPLE

SEPTIC EMBOLI REVEALING BORDERLINE CARDIOMEGALY MULTIPLE NODULAR
INFILTRATES, & BILATERAL PLEURAL EFFUSIONS.
ACUTE ENDOCARDITIS
- fever, malaise, peripheral emboli, may involve healthy
valves
- Treatment: Combination: Gentamicin & Nafcillin
at least 4 weeks

BACTEREMIA/ SEPTICEMIA
- Daptomycin with/without beta-lactams- usually for
refractory MRSA

DEEP ORGAN ABSCESSES

- Brain, kidney and lungs. Eyes, liver , spleen , CNS
1. MICROSCOPIC EXAMINATION
a. Gram Staining - gram-positive cocci in clusters

STAPHYLOCOCCI CHARACTERISTIC ARRANGEMENT SINGLY, IN

PAIRS, IN CHAINS, & IN CLUSTERS
GROWTH OF STAPHYLOCOCCUS
AUREUS ON SHEEP BLOOD AGAR
SHOWING BETA – HEMOLYTIC
PATTERN
S. EPIDERMIDIS S. SAPROPHYTICUS
BIOCHEMICAL TESTING DIFFERENCES
BETWEEN
STAPH. AUREUS AND STREP. PYOGENES
8. PROBLEMATIC CASES
MANAGEMENT AND TREATMENT
a. Beta Lactamase Production
1. FoodDOC - Cloxacillin,
Poisoning Methicillin
or Intoxication - NO ANTIBIOTICS
2. Treatment for Infection:
Nafcillin , Oxacillin
Mild to Moderate Infection : 7 days
Severe Cases : 14 days
b. PBP: Alteration
3. Abscess - Methicillin-
Do debridement / drainageResistant
+ Antibioticstrains
DOC -that
4. Infections VANCOMYCIN,
are Resistant toTEICOPLANIN
Penicillin: VANCOMYCIN
Two Resistant Strain To Vancomycin in the US:
a. VISA
b. VRSA
9. ALTERNATIVE DRUGS
5. First Generation Cephalosporin
Treatment
6. Third of MRSA
Generation Bacteremia & Endocarditis
Cephalosporin
a. Newer
7. Alternative Drugs
drugs: - Daptomycin,
Vancomycin Linezolid,
( Used in the Philippines)
Qiunupristin- dalfopristin
Erythromycin
Clindamycin
1. CA-MRSA - Community-Acquired MRSA
a. Increased risk of skin & soft tissue Infection
b. No known risk factors
c. Patients typically young & healthy
d. Necrotizing pneumonia in younger
e. Some strains- more virulent than HA-MRSA
f. (+) Panton-Valentine Leukocidin Gene
(+) Staphylococcus Cassette Chromosome MEC Type IV
g. Susceptible to broad arrays of antibiotics

TREATMENT
1. Mild-Moderate: TMX/ Doxycycline

2. Severe Cases: Daptomycin, Linezolid, Vancomycin,

Qiunupristin- dalfopristin
2.
4. VRSA
HA-MRSA
Vancomycin-Resistant Staphylococcus aureus
Hospital-Acquired Methicillin-Resistant S. aureus
Discovered & isolated in
Antibiotic resistance 2002 in the U.S.
Chromosome - mediated by a gene
TWO VRSA
distinct STRAINS:
penicillin-binding protein (PBP) PBP-2a
a. Vancomycin Resistance Gene van A from enterococci
PBP-2a
b. Nafcillin Resistance Gene mec A
Codes
Both for peptidoglycan
are susceptible transpeptidases
to antibiotic
3. VISA
Vancomycin - Intermediate Staphylococcus aureus
INFECTIONS : Worse
Also known - GISA outcomes, higher mortality
- Glycopeptide-Intermediate S. rates
aureus
(-) Panton
Isolated - U.K, Brazil, Asia Valentine
Japan, [Link] Gene
Complex infections on prolonged vancomycin therapy
TRANSMISSION: Health care settings
MECHANISM OF RESISTANCE:
MULTIDRUG RESISTANCE
Increase cell wall synthesis & alteration
- MIC :choice
Limited <_2 ug of/Mltherapeutic agents
- Intermediate Susceptibility: if MIC = 4-8ug/ml
- Resistant: MIC IS _> 16ug/ml
AFFECTED: Elderly, debilitated or chronically ill
- Associated : VANCOMYCIN TREATMENT FAILURE
ALTERNATIVE DRUGS FOR MRSA
a. Vancomycin - need to monitor MIC

b. Daptomycin - Cyclic lipopeptide

Binds to cell membrane  depolarization
inhibiting CHON, DNA, RNA synthesis 
Cell death

d.
c)Tedizolid
Linezolid- -Newer agent under
Alternative clinical
drug for trials
vancomycin

e. Telavancin
- Lipoglycopeptide derivative of vancomycin
- For complicated skin & skin structure
infection & pneumonia
- Inhibits cell wall synthesis
- interfere with polymerization & cross-linking
of peptidoglycan
- Depolarizes cell membrane & disrupts its functional
activity
f) Dalbavancin
g) Oritavancin Newer derivative of vancomycin

h) Ceftaroline - 3rd generation cephalosporin

- (+) Activity against MRSA

i) Fusidic acid - Old antibiotic

j) Mupirocin - For superficial localized infection

- Inhibits RNA & CHON synthesis

k) Retapamulin - Classified as Pleuromutilins

- Superficial localized infection
- Inhibits CHON synthesis binding to 50S
Beta Hemolysis + - -
 STREPTOCOCCUS
Domain : Bacteria
Kingdom : Bacteria
Phylum : Firmicutes
Class : Bacilli
Order : Lactobacillales
Family : Sreptococcaceae
Genus : Streptococcus
Species : pyogenes , pneumoniae
agalactiae, enterococci
viridans group
GENERAL CHARACTERISTICS
- Gram (+) cocci - chains , in pairs , singly
- Facultative anaerobes
- Normal flora of Oropharynx & GIT
- Complex nutritional requirements
- Growth & Hemolysis -
Aided by incubation at 37⁰ C & 10% C02

- ALL: CATALASE NEGATIVE

EXCEPT Strains of Enterococcus faecalis
Weakly catalase positive  PSEUDOCATALASE

- Grown on culture containing blood

1. CLINICAL OR PHYSIOLOGIC
- Pyogenic
- Oral
- Enteric

2. SEROLOGIC - Lancefield : A – H ; K – U

3. HEMOLYTIC PATTERN
Alpha - Incomplete
Beta - Complete
Gamma - Non hemolytic
Oldest/Classical way of Classification

4. BIOCHEMICAL IDENTIFICATION
Serologic (Lancefield): groups A-H, K-U; based on
AMINO SUGAR OF GROUP-SPECIFIC CHO
o Group A - rhamnose -N-acetylglucosamine
o Group B -rhamnose–glucosamine polysaccharide
o Group C - rhamnose-N- acetylgalactosamine
o Group D - glycerol teichoic acid containing
d- alanine and glucose
 SEROLOGIC BIOCHEMICAL HEMOLYTIC
CLASSIFICATION
(LANCEFIELD GROUPING) CLASSIFICATION PATTERN
(A-H/ K-U)

Group A Streptococcus pyogenes Beta hemolytic

Group B Streptococcus Beta Hemolytic
agalactiae
Group C Streptococcus Alpha or Gamma
equisimilis
Group D Enterococcus faecalis Alpha, Beta, Gamma
Enterococcus faecium
Streptococcus bovis
Group F Streptococcus milleri Alpha, beta, Gamma
Group
NA (NOT Streptococcus
APPLICABLE) pneumoniae Alpha Hemolytic
NA: S. viridans S. salivarius, S. sanguis, Alpha and Gamma
or Viridans Group S. mutans. S. mitis,
S. acidominismus
 Alpha prime
Small area of
intact RBC around
colony surrounded
by a wider zone of
complete hemolysis

Growth 6.5% NaCL broth

CAMP FACTOR
Diffusible substance of Group B, lyses sheep RBC in the presence of staphylococcal hemolysis
A. GROUP A STREPTOCOCCUS
Streptococcus pyogenes - Beta Hemolytic

STRUCTURE
CAPSULE - HYALURONIC ACID
- Group C Streptococcus - same component
- Anti-phagocytic
- Binds to H.A Binding CHON – CD44 
 Disruption of intracellular junction
 CELL WALL
1. CHON ANTIGENS - M, R , T
Responsible for TYPE SPECIFICITY
SEROLOGIC TYPING

M CHON ANTIGENS
Only in S. pyogenes (150 Serotypes )
Hair-like surface proteins projections
Anchored to cytoplasmic membrane

OUTER AMINO TERMINUS CHON

- HIGHLY VARIABLE ( > 100 Serotypes)

Features: 1. Acid Resistant

2. Heat resistant
3. Anti phagocytic

Inhibit activation of AP Pathway of Complement

 Two Types of M - Proteins
1. CLASS I M PROTEIN - associated with rheumatic fever

2. CLASS II M PROTEIN
Associated with Glomerulonephritis
Cross-react with human heart tissue
Can also occur in Class I
Rheumatic fever
Cross reactions - antibodies produced against
streptococcal antigens &human heart tissue
Binds Fibrinogen = (-) Alternate Complement Pathway

2.3.C-TCARBOHYDRATES
CHON ANTIGENS (POLYMERS )
Group Specific carbohydrate
Epidemiologic marker for routine surveillance
BASIS OF LANCEFIELD
Acid labile GROUPING OF STREPTOCOCCI
& heat Stable
N-acetyl-D-glucosamine
Not related to virulence = Antigenic Determinant
2. VIRULENCE FACTORS
a. Capsule - Non - immunogenic , anti-phagocytic

b. M-CHONS - Interferes with phagocytosis by

causing breakdown of C3b opsonin
Anti-complement binds with C3b,
Type Specific

c. LTA - Lipoteichoic Acid

Adherence to epithelial cells - skin , oral mucosa
Fibronectin Receptors  Streptococcal colonization

d. Protein F - Epithelial attachment (fibronectin binding)

to host cells
g.
e. C5a Peptidase
Protein - Inhibits attraction
G - (-) Phagocytosis ofFc
binds to phagocytes
segment ofbyIgG
destroying C5a
f. Hyaluronidase - Spreading factor
h. Capsule
Splits hyaluronic- Inhibits
acid ofphagocytosis; aids penetration
ground substance
Antigenic of epithelium
Erythrogenic Toxin
Current name : PYROGENIC EXOTOXINS A, B, C
SPE - STREPTOCOCCAL PYROGENIC TOXIN
Superantigens

TYPES OF TOXINS
1. Type A Toxins - Streptococcal Toxic Shock Syndrome (STSS)
- Fever - primary effect NOT THE RASHES
2. Type B toxins - Necrotizing fasciitis & Streptococcal
- Rashes dermal reactivity  Hypersensitivity Reaction
gangrene
- Heat labile, produced by lysogenic strains
(FLESH-EATING BACTERIA)
SPEs - STREPTOCOCCAL PYROGENIC EXOTOXINS
3. Type CSuperantigens
toxins - permeability of BBB & to bacteria
responsible for:
1. Scarlet fever
2. Toxic shock Syndrome
3. Flesh-eating Fasciitis
DICK TEST
- Intradermal injection of Erythrogenic toxin
(+) Erythematous skin reaction in person who lacks the
antitoxin or antibody

SCHULTZS CHARLTON REACTION

- Antitoxin injected intradermal to patient with scarlet
fever
(+) Blanching of Skin  Neutralization of Erythrogenic
toxin
E. Streptolysin O (SO)
- Oxygen-labile - hemolysis produce in absence of air
- Hemolysin , Cytolytic  PMNs. Platelets, RBCs
- Target: Cholesterol containing membrane 
 Leakage  Death
- BAP - shows Beta Hemolytic
- Immunogenic
- ASO TITER = 160-200 units ( High)
Recent infection or
Exaggerated immune response

F. Streptolysin S
- Oxygen-stable
- Non-immunogenic, Cytolytic
- Beta-Hemolytic
- Cardiotoxic
TISSUE DEGRADING ENZYMES
Enhance spread of bacteria by breaking down DNA ,
proteins, blood clots , tissue hyaluronic acid.
G. STREPTOKINASE
- Acts as Fibrinolysin Activates plasminogen 
Plasmin Digest fibrin  Spread of organisms

I WANT TO
BREAK
FREE!!!!!!!

FIBRIN CLOT WITH RBC , BACTERIA TRAPPED INSIDE

H. Streptodornase
A DNAse , digest NET (Neutrophil Extracellular Traps)
Contains serine proteases  (-) killing of bacteria
Types: A to D
Associated with PYODERMA & IMPETIGO
LOCAL SPREAD OF INFECTION

I. C5a Peptidase
Cleaves C5a - Potent Neutrophil attractant 
(-) influx of PMN early in infection
Early colonization of host tissue

J. Streptococcal Chemokine Protease (ScpC)

Prevents migration of neutrophils to the spreading
infection - NECROTIZING FASCIITIS
Degrades IL-8 - Attract Neutrophils
- No IL-8= Devoid of PMN
to site of infection
 CLINICAL SYNDROMES
Diffuse rapidly spreading  Tissues Minimal suppuration
 Lymphatics Blood

A. LOCALIZED INFECTION
c. Other Infections
[Link] OR SUPPURATIVE
- Pneumonia - Mastoiditis
a. Pharyngitis or Septic Sore throat
- Sepsis, Meningitis - Osteomyelitis
- Otitis media - Tonsillar abscesses 
b. Skin Infections
RETROPHARYNGEAL ABSCESS
- Pyoderma - Lymphangitis
- Non-bullous Impetigo - Lymphadenitis
d. Puerperal Sepsis
(Pyoderma)
- Introduced during or after delivery
Cellulitis - Erysipelas
- Serousanguinous - vaginal discharge
- Fever, facial flushing, abdominal distention,
pelvic tenderness
Streptococcal Sore Throat. This common form of pharyngitis is characterized by:
A) Enlarged and Reddened adenoids at the sides of the throat
B) White, pus-filled lesions on tonsils
2. Toxigenic Disease ( Non - Suppurative Sequelae )

a. SCARLET FEVER
Rash of the face & upper extremities
Shedding of the skin Erythrogenic or
Rash inducing toxin
- Strawberry Colored-tongue
- SpeC and SpeA
- Responsible for the rash of scarlet fever
B. Toxic Shock Syndrome Toxin 1 ( TSST 1 )
Formerly : Exotoxin C & Enterotoxin F
Superantigen, Streptococcal Pyrogenic Exotoxin C (SpeC)
- Most cases associated with Female
- Superabsorbent tampons ( menstruation )
- May occur in: Non-menstruating women
Surgical wound infection Men

- Clinical Presentation
a. Hypotension ( low blood pressure )
b. Fever and chills
c. Diarrhea
d. Extensive skin rash & desquamation
(Scarlatiniform rash)
e. Multisystem involvement
( Multiorgan failure & Shock )
3. Immunologic Disease
a. ACUTE RHEUMATIC FEVER
Associated with Class I M -Type CHON  URTI
M- PROTEIN = Cross react with human heart tissue
Serotypes - 1. 3, 5, 6, 14, 18, 19, 24, 27, 29.
Onset: 2-3 weeks after Streptococcus A infection

CLINICAL SIGNS AND SYMPTOMS

1. Fever
2. Migratory Polyarthritis
3. Chorea
4. Erythema marginatum late = 6 months after
5. Subcutaneous nodules
6. Carditis

THREE PATHOGENIC MECHANISMS

1. Antigenic Cross reactivity - Streptococcal antigens and
Heart tissues & joints
2. Direct toxicity by Streptococcal Exotoxins
3. Actual Invasion of the heart by Streptococci
 Supporting Evidence of Antecedent Group
A Streptococcal Infection
(+) Culture
(+) Streptococcal Antigen Test
Elevated or rising Streptococcal Antibody Titer
2 Major manifestations
1 Major and 2 Minor manifestations and

Evidence of previous Streptococcal infection

Indicative of High Probability of Rheumatic Fever

MINOR MANIFESTATIONS - arthralgia, fever

LABORATORY FINDINGS
1. Elevated Acute Phase Reactants :ESR, C-reactive CHON
2. ECG- prolonged P-R Interval
B. Acute Glomerulonephritis
Also known as Bright’s Disease
Clinical Manifestations
Type III Hypersensitivity Reaction
1.(Immune
Edema Complex
- facial,Mediated)
bipedal
Class
2. I or II M- Type 49
Fever
3. Hypertension producing skin infection
- headache, & URTI
dizziness,
Takes place 2-3 weeksnausea after infection
and vomiting
More
4. frequent after
Hematuria skin &
- gross infection than pharyngitis
microscopic
Ag-Ab
5. Complexes deposition into the glomeruli
Oliguria
6. Proteinuria ( Streptococcus M- proteins )
LABORATORY DIAGNOSIS
1. MICROSCOPY
Gram Stain of lesions

2. CULTURE
Throat swab - posterior pharynx, tonsils
5% SBA - small colonies with wide Zone of beta
hemolysis
Streptococcal Selective Agar
TMX-SMX - inhibits growth of Non-Group A beta
hemolytic streptococci
PYR TEST (PYRROLIDONYL ARYLAMIDASE)
Presumptive identification of Group A Beta- hemolytic
streptococcus and Enterococci
Substrate= L- pyrrolidonyl -ɑ- naphthylamide
L- pyrrolidonylarylamidase or pyrrolidonyl aminopeptidase
degrades substrate in a 10 minute test
RESULT: (+) PYR = Streptococcus pyogenes
Enterococcus
Aerococcus
Gemella
(+) DEEP CHERRY RED COLOR
(-) YELLOW TO ORANGE COLOR
B. Bacitracin Test (TAXO-A)
- Presumptive identification of Group A Beta Hemolytic
Streptococci
- SBA - 0.04 Bacitracin disc is place on the plated
organism
- (+) Zone of Inhibition
SEROLOGY
A. ANTIGEN DETECTION
ELISA
LATEX AGGLUTINATION - SPECIFIC
- False (-) - if specimens contains low load of organisms
- Sensitivity - 60-95%
Two throat swab – from each patients
1st Swab – (+) - discard
2nd Swab if:
- 1st Swab (-)  Culture 2nd Swab BAP
or Strep. Agar Plate
B. ANTIBODY DETECTION
a. ASO - 3- 4 weeks after the recent infection
b. Anti-DNAse B - High sensitivity for both
pharyngeal and skin infection
 BILE ESCULIN TEST
PRESUMPTIVE TEST FOR ENTEROCOCCI
TEST GROUP GROUP Not A, Group D Group D Viridans S. pneu
METHOD A B B or D Enteroco Non- Group moniae
ccus Enteroco
ccus

HEMOLY BETA BETA BETA BETA, BETA, ALPHA ALPHA

SIS ALPHA ALPHA
or or
NONE NONE

PYR TEST + - - + - - -

Na++ - + - - - - -
Hippu-
rate

ONPG - - - - - - +

Esculin - - - + + - -
Beta hemolytic
Normal flora : Skin, Nasopharynx, GIT,
Female genital tract, male urethra
Occasional Colonizer: URT
Leading cause NEONATAL SEPSIS AND MENINGITIS
- High mortality rate

MODE OF TRANSMISSION
1. Endogenous Strain - Gaining access to sterile sites

2. Direct contact
a. Person to person - In utero
b. Birthing process - Delivery
c. Nosocomial transmission
Unclean hands of mother & health care personnel
 Clinical Infections in Infants
Sepsis, fever, meningitis, respiratory distress,
lethargy, and hypotension

1. Early Onset infection

(80% cases in NB ) - occur in utero, at birth or within
24 ⁰- first 5 days of life.
Vertical Transmission
- BACTEREMIA, PNEUMONIA

2. Late onset Infection

POST-PARTUM
- 7 days to 3SEPSIS
months after birth
- -Endometritis & wound
In older infants infection 
from exogenous sources
-pelvic abscess
Usually  SEPTIC
presents SHOCK
as  MENINGITIS

IMMUNOCOMPROMISED
- Bacteremia, Pneumonia, endocarditis, arthritis,
osteomyelitis, skin & soft tissue infections
GROUP B STREPTOCOCCI (STREPTOCOCCUS AGALACTIAE)
NORMAL INHABITANTSOF FEMALE GENITAL TRACT AND
MAY BE ACQUIRED BY NEONATES
OUTCOME
FACTORS Approx.
EARLY60%
ONSET
fatal:
(ATserious
OR Approximately
LATE ONSET (IN20%
THEfatal
sequelae
SOON AFTER
in many
BIRTH)
survivors NURSERY)
TREATMENT
AGE Take
< 7 DAYS
blood and CSF culture Gentamicin
1 WEEK – 3 MONTHS
and
RISK FACTORS Treat on suspicion
Heavily colonized mother ampicillin or
Lack of maternal
Gentamicin and ampicillin
lacking specific antibody Cefotaxime/Ceftriaxone
antibody
orPROM
Cefotaxime/Ceftriaxone Exposure to cross-
PREVENTION Antibiotic
Pre-termtreatment
delivery does Good hygiene
infection frompractices
heavily in
not abolish carriage
Prolonged labor , in nursery
colonized babies
mother, notcomplications
obstetric recommended Poor hygiene in nursery
TYPE OF DISEASE Blind treatment
Generalized of sick
infection Do not allow mothers to
Predominantly
baby who has
including risk factors
bacteremia, handle other babies
meningitis
Future??
pneumoniaImmunize
and
antibody-negative
meningitis females
of child-bearing age
TYPE OF GROUP B All serotypes but 90% Type III
STREPTOCOCCUSS meningitis mostly due to
Type III
VIRULENCE FACTORS
SIXEnzymes
B. CAPSULAR SEROTYPES
Protective
- DNAsebut ineffective once opsonized
1. Ia, Ib/c - Ia, Ib, II, III - causes most of the Human dses.
- Neuraminidase
- Hemolysin diseases
2. -Ia/c serotypes
Protease 3. III 4. III 5. IV 6. V
- Hippuricase
Double zone of Hemolysis
- Hyaluronidase
Contains
- CAMPGroup
FactorB-specific Antigens
Terminal Portion - repeating units of SIALIC ACID
NOTE: No evidence that these plays
Significant a role in
component ofvirulence
capsule
Critical virulence determinant
C. L- rhamnose - GroupLoss associated with loss of virulence
specific carbohydrates
- Major Antigenic determinants
 EPIDEMIOLOGY
Normal flora large intestines and genitalia
Reservoir , with propensity to infect:
1. Newborns
2. Decubitus ulcer of L.E. In Diabetic
- Peripheral Vascular Diseases
3. UTI in adults
4. Vaginal Colonization
15-20% (10-30%) - pregnant women vaginal carriers
Transient Vaginal Carriage

Neonatal Septicemia - acquired during delivery

or birthing process
High Risk: 1. Obstetric Complication
2. Prolonged Labor
3. PROM
4. Obstetric manipulation
 LABORATORY DIAGNOSIS
1. Culture - Blood, cervical swabs, sputum, spinal fluid =
BAP
- SBA - grayish white mucoid colonies- Small
Zone of Beta Hemolysis & surrounding
wide zone of beta hemolysis 
DOUBLE ZONE OF HEMOLYSIS
2. Antigen Detection
- CIE - Counter Immunofluorescence
- Latex Agglutination Test
- SCA for Serum, CSF, Urine
- Elisa Test

3. Detection of Carrier in Pregnant

Todd-Hewitt Broth - Gentamicin , Nalidixic or
Colistin and Nalidixic - suppresses normal vaginal
Allow growth of S. agalactiae
LIM - Sub-culturing
 POSITIVE CAMP REACTION
Indicated by enlarge zone of hemolysis shaped like a tip of the arrow
Streptococcus agalactiae intersecting with S aureus streak line
HIPPURICASE - hydrolyze hippuric acid forming =
Na+ benzoate & glycine
(+) NINHYDRIN - an indicator releases ammonia
Oxidative deamination of glycine
Ammonia reacts with ninhydrin forming:
RESULT: (+) DEEP PURPLE COLOR
(-) No change in color/slightly purple color
MODE OF MANAGEMENT & TREATMENT
1. Penicillin G & Ampicillin - DOC
Most strains sensitive

PREVENTION
2. Combination of Pen G or Ampicillin with
Aminoglycosides - Life threatening cases
1. Detection of Group B strep in expectant women
3.- Pregnant Carriers
Vaginal and rectal swab - 35-37 weeks of gestation

4. (+) Identified Newborns - Intrapartum prophylaxis &

2. Culture - Selective administration
Todd-Hewitt Broth  Subcultureantibiotic to infants
SBA - 35⁰C x 18-24
- 90%5%
hours with reduction
C02 of sepsis

[Link].
Ceftriaxone or Cefotaxime
B Carrot Broth (SCB)
 Production of orange or red pigment 
6. Vancomycin
Non-hemolytic isolates – no change in color
Pneumococcus , Diplococcus pneumoniae
Gram (+) cocci, non-motile, in pairs, short chains
Lancet shape - pointed end
Facultative anaerobe, alpha hemolytic, fastidious
> 90 different species - ENCAPSULATED STRAINS VIRULENT
NON-ENCAPSULATED STRAINS - AVIRULENT
Colonizer : Nasopharynx of healthy individuals - 5-75%
VIRULENCE FACTORS

1. Capsule - Antiphagocytic

2. Pneumolysin - Alpha -hemolysin, dermotoxin

3. Purpura-producing principle - Dermal hemorrahage

4. Neuraminidase – spreading factor

5. Amidase – Autolysin & for cell divisions

6. IgA proteases
 EPIDEMIOLOGY
Leading cause - Bacterial pneumonia & meningitis
- Above 5 y/o & in adult
Meningitis & pneumonia can be with or without bacteremia
One of the two most common causes of: Under 3 years of age
1. Acute sinusitis
2. Recurrent otitis media

NASOPHARYNX CARRIER
5 - 10% in Healthy adults
20 - 40% in Healthy children
STRUCTURES
1. Capsule - COMPLEX POLYSACCHARIDES
- > 90 different Serotypes
- Immunogenic
- Basis of NEUFELD QUELLUNG REACTION
- Type-Specific Antiserum - produces capsular
swelling
- Capsular Precipitation Test

2. Teichoic Acid – has two forms

a. C - Substance - Cell wall component, react with
human ɓ-globulin
CRP (C-Reactive Protein) - forms
precipitate
b. Bound to Plasma membrane

3. Peptidoglycans
MODE OF TRANSMISSION
1. Direct contact

2. Person to person with contaminated respiratory

secretions

COMPLICATIONS
a. Pneumonia with Pleural effusion - Empyema

b. Meningitis following otitis media or pneumonia

- acute, purulent

C. Life threatening Conditions

- Endocarditis
- Peritonitis
- Bacteremia
CLINICAL SYNDROMES
1. Pneumonia –
MOT: Aspiration of endogenous oral organisms
or through droplets
S/S: a. Productive cough, blood-tinged sputum or
Rusty colored sputum & sharp pleural pain

b. Lobar pneumonia
- localized in lower lobes or as
c. Bronchopneumonia
2. Sinusitis & Otitis media
- preceded by viral infection of URT

3. Meningitis
- follows bacteremia, infections of ear & sinuses
or head trauma

4. Bacteremia
associated with Pneumococcal pneumonia &
meningitis
DENSE CONSSOLIDATION OF THE LOWER LOBE CAUSED BY
STREPTOCOCCUS PNEUMONIIAE
 LABORATORY DIAGNOSIS
1. Microscopy - Gram staining - Sputum or secretions, CSF
- Gram (+) cocci in pairs
(Diplococci) with pointed end
or lancet shape.
3. Culture
- Complex nutritional requirements
- Media: a. Brain Heart Infusion
b. Trypticase Soy Broth with 5% Sheep RBC
c. Chocolate Agar
- Increased C02 - 5-10% preferred by S. pneumoniae
- SBA - large zone of ALPHA HEMOLYSIS, mucoid colonies

A) Young Cultures - round, grayish, glistening, wet ,

mucoid, domed-shape appearance

B) Old Cultures - Autolytic changes ( Autolysin –

Amidase )  collapse of colony’s
center  a coin with a raised rim
appearance. (Tend to dip down in
the center- Doughnut Shape

- Most organisms will grow within 48 hours of

inoculation.
4. Biochemical Test

5. Serologic Test
- Counter-Immunofluorescence
- Latex Agglutination - detects capsular
Polysaccharide Ag
- Specimen- urine, serum, CSF

STREPTOCOCCUS PNEUMONIAE - SUSCEPTIBLE

OTHER ALPHA HEMOLYTIC STREPTOCOCCI SPECIES - RESISTANT

P
OX BILE OR DEOXYCHOLATE INDUCE AUTOLYSINS
AUTOLYSINS CAUSE BACTERIAL CELL LYSIS
1. Alcohol / Drug Intoxication / Cerebral Impairment

2. Abnormality in the respiratory tract

- Viral infection , smoking

3. Abnormal circulatory dynamics - pulmonary congestion

& heart failure

4. Splenectomy

5. Chronic diseases - sickle cell anemia & nephrosis

1. Penicillin
2. Cephalosporin - Cefotaxime, ceftriaxone
3. Erythromycin or Azithromycin
4. Vancomycin & Imepenems - for severe infections
PREVENTION
[Link] PNEUMOCOCCAL VACCINES
a. PCV7 (Heptavalent Pneumococcal Conjugate Vaccine)
- Purified polysaccharides 7 serotypes conjugated
with diphtheria protein
- Prevents Bacteremic infections - Meningitis
Otitis media

b. PS23 (23-valent vaccine)

Composed of 23 purified capsular polysaccharides
Used for Adults - Elderly
Immunocompromised (splenectomized)
HIV
Patients on chemotherapy
Debilitated persons
- Booster Doses: 5 years after receiving initial vaccine

2. CHEMOPROPHYLAXIS
a. Oral penicillin
Hypogammaglobulinemia or splenectomized persons
- Previously classified - Group D Streptococci
- Gram (+) cocci
- Microbiota: GIT of humans & animals
- Female GUT
> 29 Species & all species contain cell wall
- Group D antigens

- SBAP - Non-hemolytic or Alpha hemolytic

- PSEUDOCATALASE REACTION
- weak bubbling in catalase test

- E. FAECIUM & E. FAECALIS

- Commonly identified species
- Little is known - arise to become prominent in
causing nosocomial infection
One of the most feared nosocomial pathogens isolated
from:
1. Urinary Tract 4. Bacteremia
2. Peritoneum 5. Endocarditis
3. Heart Tissue 6. Intra-abdominal
infections

- More resistant to antimicrobial agents

- commonly used in hospitals – Cephalosporin

DRUG RESISTANCE
[Link]
- First clinically relevant group of Gram(+) Streptococci

2. Acquire & disseminate resistance to vancomycin (VRE)

- Troublesome- Public Health concern
VIRULENCE FACTORS
CLINICAL INFECTIONS
1.
1. Serine Protease
UTI - most - Extracellular
common- surface
catheterization CHON
or urologic
E. faecalis – role in colonization
manipulations

2. Gelatinase -&2nd
2. Bacteremia adherence to heart
- prolonged valves
hospital and
stay,
Renal epithelialimmunocompromised
hemodialysis, cells
4. Intra-abdominal or Pelvic wound Infections –
3.
3. Cytolysin
Endocarditis - elderly with prosthetic heart valves
- Two
5. Burn sub-unit
patients toxinsinfection
-(5-10%)
Wound similar to
& bacteriocins
sepsis
E. faecalis
6. Ocular infections - occasional
4. Multidrug resistance - contributes to proliferation
7. Rare - CNS infection - neurosurgery & head trauma
- Respiratory Infection – in prolonged antibiotic
therapy.

8. Intestinal Infection - E. gallinarum & E. casseliflavus

 LABORATORY DIAGNOSIS

1. Microscopy - Gram Staining

2. Culture
- Trypticase Soy Broth or BHI with 5% Sheep blood -

- 35⁰C with C02 (low C02 level only)

- Contaminated material  SELECTIVE MEDIA

a. Bile Esculin Azide
b. Colistin- Nalidixic acid
c. Phenylethyl alcohol Chromogenic substrate
d. Cephalexin - Aztreonam - Arabinose Agar

- COLONIES: Small, cream or white, smooth, entire,

Alpha, Beta or non-hemolytic
 ANTIBIOTIC RESISTANCE
Six Vancomycin Resistance Phenotypes

1. Van A & Van B - most commonly encountered

Van A - inducible carried on transposons (TN1546)
- High-level resistance to vancomycin
&Teicoplanin (MIC Dose)
Van B - Chromosomal mediated, variable levels of
resistance to vancomycin & susceptibility
to Teicoplanin

2. Van C - Low levels of resistance to vancomycin

3. Van D - Some strains of E. faecalis - low levels of

resistance to vancomycin with susceptibility
or intermediate resistance to Teicoplanin

4. Van E & Van G - similar to Van C - low levels

of resistance to vancomycin
 MODE OF TREATMENT
1. Vancomycin
2. Daptomycin
3. Linezolid

4. Penicillin, Aminoglycosides or Vancomycin plus an

Aminoglycosides (Gentamycin or Streptomycin

5. Chloramphenicol - multidrug-resistance

6. UTI - Ampicillin, Nitrofurantoin, Tetracycline, Quinolones

 VIRIDANS STREPTOCOCCI
- Viridans - Greening, ALPHA HEMOLYTIC
- Normal flora: Oral cavity, Nasopharynx
(Oropharyngeal Commensals) GIT, Female Genital Tract
- Most prevalent members of the normal flora URT
- More than 30 species

- Fastidious organisms some requiring C02 for growth

- Opportunistic pathogens of low virulence
(Immunocompromised)
- Alpha hemolytic or also be non-hemolytic
 VIRIDANS GROUP
1. Streptococcus mitis Group

2. Streptococcus salivarius Group

3. Streptococcus bovis Group

- possess Group D antigen together with Enterococci

4. Streptococcus anginosus Group

- possess Lancefield Group A,C, F, G or N antigen
- some not groupable

5. STREPTOCOCCUS MUTANS
- production/synthesis of extracellular complex
polysaccharides (GLUCANS, DEXTRAN & LEVANS)
which leads to DENTAL CARIES  1⁰ contributor
- most commonly isolated group
 CLINICAL INFECTIONS
1. SUB ACUTE BACTERIAL ENDOCARDITIS
Insidious onset & protracted clinical course
(weeks to months)
Involved valve usually deformed or abnormal - MVP
Viridans Streptococci most common cause
Production of extracellular complex polysaccharides
- GLUCANS, DEXTRANS, LEVANS
Enhance attachment to host cell surfaces such as
cardiac endothelial cells
2. TRANSIENT BACTEREMIA
- Associated with endocarditis
- More common in children w/ hematologic malignancies
(Viridans Strep. bacteremia)

3. Fulminant Cardiovascular collapse

4. Meningitis
5. Oral Infections - GINGIVITIS AND DENTAL CARIES
6. Abscesses
7. Osteomyelitis
8. Empyema
VIRULENCE FACTORS : In some species
1. Polysaccharide capsule
2. Cytolysin
3. Hyalorunidase
4. DNAse
5. Streptolysin O

LABORATORY DIAGNOSIS
1. Gram staining
TREATMENT
2. Culture - Colonies: Minute to small gray, doomed, smooth
1. Penicillin with or without Aminoglycosides
or matte, alpha or non - hemolytic
2. Ceftriaxone
- Optochin Test - growth is not inhibited
3. Vancomycin - for resistant strains and allergy
- Bile Solubility Test - Not bile soluble
to penicillin
- Growth 6.5% NaCl - No growth at high alkalinity
Gram
TWO(-) diplococci , kidney
PATHOGENIC bean / coffee bean shaped
SPECIES
Flattened
1. Neisseria meningitides- canadjacent Side URT
be commensals
Non-sporeforming, aerobicalways
2. Neisseria gonorrhea- , facultative anaerobic, capnophilic
pathogenic
Most strains - Utilizes
3. Remaining glucose
- Normal florabyofoxidation by acid production
oronasopharynx
Oxidase (+); Catalase
- Grow(+)on
EXCEPT
BAP &N. ELONGATA
Nutrient media
Susceptible -Environmental
- Mesophilicconditions - drying, chilling , sunlight.
Iron- bind transferrin
4. Occasional for growth
- Colonizer - Strict human
of anogenital pathogens
membranes
Virulent Strains - Capsulated
 Grow on Chocolate
COLONY TYPES BASEDAgar not
ONonPOSSESSION
BAP OF PILI
1.5% CO2
T1 & T2--enhance
(+) PILIgrowth , needs humid air
UTILIZES
VirulentONLY
StrainsGLUCOSE OXIDATIVELY  Acid production
- initial isolation
Natural Host-: Non-
Subculture Humans piliated
Site
Small
of Infection
brown colonies,
: Non-ciliated
piliated
columnar & transitional cells
Involvement:
Responsible Urethra,
- Most casesendocervix,
of Acute anal
Gonorrhea
canal, pharynx,
conjunctiva
2. Flow
T3- T5of Seed
- ( -) -PILI
Mistaken for semen
CLAP disease
Avirulent - French word - Brothel
Strains
Large, granular, non-pigmented colonies
b. CHON 2
1. CAPSULE
Opacity - Associated Protein (OAP)
2. PROTEINS
Acts as an Adhesins – sticks to surfaces (adherence)
[Link]
CHON 1 Colonies
= 60%  Localized Disease
Transparent
Major OuterColonies
Membrane  PID
Porin& Disseminated
Protein (OMPP) Infections
Phase Variations
Also called P.I (Por)
Porins - Channels for nutrients & wastes
c. CHON
Por 3B - Major CHON in N. gonorrhea - survival
Rmp CHONs (Reduction
(-) Degranulation Modifiable
of PMNs CHONS)
(-) fusion of phagolysosomes
Binding sites for
Serotyping IgG Abs, (-) Complement Activation
of Gonococci
Contribute to the dissemination
Invasin -mediates penetration ofto Disease
host cells & dissemination
Porins
Many antigenic variations
No Antigenic variations
6. LIPO-OLIGOSACCHARIDES (LOS)
Fallopian tubes - Damage mucosa
Loss of ciliary activity
Sloughing off - ciliated epithelial cells
Pathogenesis: Release of Phospholipases & Proteases
Attracts PMNs - Elicits inflammatory response
LIPID A - Endotoxin - to the cells or mucosa
Lack O antigen found in LPS
BLEBS - Outer membrane CHONs release during growth
- contains LOS
7. IGA PROTEASES
Release
Cleaves by Autolysis
heavy chain  & Activates
inactivatesAlternate Complement
IgA 1 Hinge region 
Pathways
Inactive Fc & TNF - Responsible for signs & symptoms of
Fab fragments
Facilitates adhesionGonococcal Infection

8. BETA- LACTAMASES
PPNG = Penicillinase-Producing Strains of N. gonorrhea
ARCHITECTURE OF NEISSERIAL
CELL WALL
?
1. Urethritis predominant manifestation in men
2. Cervicitis - ENDOCERVIX - most common infected site
3. Conjunctivitis
4. Pharyngitis
5. PID - Pelvic Inflammatory Disease or Salphingitis = 10-20%
- Most frequent complication in women
- Ascending infection Uterine tubes  Sterility 
Scarring of the tubes
6. Acute proctitis
7. Vulvovaginitis
8. Prostatitis
9. Epididymitis - Resulting to obstruction - Permanent sterility
10. DISSEMINATED GONOCOCCAL INFECTION (D G I)
Gonococcemia
a. Septicemia - LOS
b. ARTHRITIS, TENOSYNOVITIS
d. GONOCCOCAL
- Most commonARTHRITIS
cause of septic arthritis inSYNDROME
- DERMATITIS
- (1- 3% -ofwomen)
Result sexually
gonococcal active adults
bacteremia
c. FITZ-HUGH- CURTIS
- Fever , chills, SYNDROME
malaise, arthritis , distal joints - involve
- Perihepatitis - complication of gonorrhea or
11. Others:
Anorectal Infections chlamydial
- 30-60% ininfection
women with genital
- Seen in women marked by:
infection
1. Fever Infections
Oropharyngeal
2. Upper quadrant pain
INCIDENCE:- Peritoneal spread
Asymptomatic - Affects  Hepatic
: Women = 90%Capsule & Subcapsular space
Men = 40%
Undiagnosed - Favors spread of disease
12. OPTHALMIA NEONATORUM
- 1% Silver Nitrate
- 1% Tetracycline
- 0.05% Erythromycin Eye Ointment
ORGANISMS COLONIAL MORPHOLOGY PRIMARY ISOLATION
SITES
N. gonorrheae Small, grayish white, translucent, Male: Urethra
raised with entire edge Female: Endocervix
Usually easily emulsified
Smaller than N. meningitidis
Up to 5 different colony
morphologies from primary
culture

N. meningitidis Bluish-gray or tan( Sero Nasopharynx and

group 6 may be yellowish) oropharynx(Carriers)
Sero Group A & C may be mucoid, Spinal fluid= Meningitis
translucent, and convex with Blood: meningococcemia
smooth glistening surface; may be LRTI: Meningococcal
greenish cast in agar around pneumonia
colonies
Weak pathogen
mistaken for N.
meningitidis
found in
nasopharynx of
children
 Organisms Growth on CARBOHYDRATE UTILIZATION DNAse
MTM,ML,
NYC Glucose Maltose Lactose Sucrose or
Medium Fructose
N. gonorrheae + + - - - -
N. meningitidis + + + - - -
N. lactamica + + + + - -
N. sicca - + + - + -
N. subflava - + + - +/- -
N. flavescens - - - - - -
N. elongata - -/w - - - -
M. catarrhalis - - - - - +
 OXIDASE TEST
Filter paper is moistened with a few drops of 1% tetramethyl-p-
phenyldiamine dihydrochloride. With a wooden applicator growth from
an agar medium is smeared on the paper.
(+) TEST: Development of purple color within 10 seconds
3. GENETIC PROBES
a. Nucleic Acid Assays
Detect Gonococcal Ag - Cervical, urine , urethral discharge

b. PCR

4. SEROLOGY TEST
a. Coagglutination Test - Uses monoclonal Abs
b. Fluorescent Antibody Test
Uses monoclonal Abs - recognition of epitopes on Por
- Specific & sensitive
EPIDEMIOLOGY
Disease - Humans
MOT: Unprotected Sexual contact
Incubation Period: 2 - 7 Days
MALE INCIDENCE:
Peak Incidence: 15-24 y/o
Infection Risk:
a. Asymptomatic Carrier
1. Women = 50% after single exposure
3-5% Uncommon
Cases
AHU Strain- seen: 15-19
Arginine, y/o
Hypoxanthine, Uracil = isolated
2. Men = 20% after exposure to infected women
CasesCarrier:
b. Symptomatic seen: 20-24y/o
95%

2nd only to Chlamydia as most commonly reported STD

FEMALE INCIDENCE:
Reservoir: Asymptomatic
Asymptomatic - 50% Infected Individuals
Common
Blood-borne in females= 1%  Purulent arthritis
Dissemination
Septicemia- rarely
 - Estimated 62 million - New cases each year
- Highest Rates - Sub-Saharan Africa
- South & Southeast Asia
- Caribbean & Latin America
- Second most commonly = Reported communicable disease
MEDICAL MANAGEMENT AND TREATMENT
1. Penicillin
2. Fluoroquinolones
3. Ceftriaxone & Cefixime
4. Doxycycline for >8 years old
5. Erythromycin for <8 years old
Gram (-) diplococci , coffee bean-shaped , encapsulated
Oxidase and catalase positive
UTILIZES GLUCOSE AND MALTOSE OXIDATIVELY
Colonizer - Naso-oropharynx = 3-30% (Asymptomatic)
Obligate parasites of human
Carriage - Non-encapsulated Strains

CULTURAL CHARACTERISTICS
Solid Medium - Smooth, round , most gray-white
Encapsulated strains - mucoid
BAP - Transparent , non-pigmented colonies
1. CAPSULE
Composed of Polysaccharide
Immunogenic
Resist phagocytosis & facilitates meningeal invasion
Serogroups A, B, C, Y, & W135 - Epidemic Meningitis
Serogroup
3. LOS LAYER A (Endotoxin)  PURPURA- Pandemic Meningitis
Serogroup B - shock,
Cause of fever, Community-Acquired
vascular necrosis,Meningitis
inflammatory
Serogroup
response Y - Meningococcal Pneumonia
Very potent ,10x more than other endotoxins
2. PILI
Adherence
4. IGA PROTEASES& colonization
Mucosa heavy
Cleaves of oropharynx
chain of IgA1
Mediates attachment
Attachment to meningeal tissues
& Invasiveness

5. CELLULAR MEMBRANE CHONS - Por , Opa, Rmp

EPIDEMIOLOGY
Worldwide distribution
Epidemics- common in Developing countries
Serogroups A,B, C - 90% of cases
Serogroup B - common in the U.S.
- Epidemics & Outbreaks
- Community Acquired Meningitis
Serogroup A - Common in Asia and Africa
- Pandemic Disease
Serogroup C - Localized outbreaks
Serogroup Y - Meningococcal pneumonia
Serogroups
MODE A, B, C, X, Y & W135
OF TRANSMISSION: Respiratory Droplets
- Commonly
- Humans associated
- only Natural with Meningococcal Disease
carrier
- High Risks: - Epidemic Meningitis
a. Children Younger than 5 years old
b. Complement Deficiency (MAC)
 VIRULENCE NEISSERIA HEMOPHILUS STREPTOCOCCUS
FACTOR MENINGITIDIS INFLUENZAE PNEUMONIAE
CAPSULE + + +
IgA PROTEASE + + +
PILI + + -
ENDOTOXIN + + -
OUTER
MEMBRANE + + -
PROTEIN (OMP)
 PATHOGEN CAPSULE IMPORTANT VACCINE
TYPE
N. meningitidis Polysaccharide A, B, C, Y W-135 Good for A and C;
poor for B
H. influenzae Polysaccharide B Hib vaccine for <1
year olds
S. pneumoniae Polysaccharide Many Pneumovax:
23-valent most
common type
Streptococcus Polysaccharide rich Ia, Ib, II) III in ???
agalactiae in sialic acid neonatal
(Group B) meningitis
Escherichia coli Ki in meningitis ???
 PATHOGEN HOST(PATIENT) IMPORTANT MORTALITY SEQUELAE
CLINICAL (a) (a, b)
FEATURES
N. meningitidis Children and Acute onset 7-10 <1
Adolescents (6-24hr); skin
rash
Hemophilus Children <5 Onset often 5 9
influenzae years of age less acute (1-2
days)
Streptococcus All ages, but Acute onset 20-30 15-20
pneumoniae especially may follow
children < 2 pneumonia
years of age and and/or
elderly septicemia in
elderly

(a = percentage of treated cases

(b = major CNS deficits; in addition up to 10% of patients develop deafness)
1. Meningitis - Most common complication
INCUBATION PERIOD - 3 days
- Purulent Meningitis
2. Meningococcemia or Septicemia
Vasculitic purpura - Hallmark of Meningococcemia
3. Other Accompanying Manifestations
a. Meningitis
b. Arthritis
c. Pericarditis
d. Urethritis
e. Organ system involvement - Pneumonia
f. DIC
g. Shock
3. WATERHOUSE- FRIEDERICHSEN SYNDROME
Hemorrhage in the adrenal glands with hypoadrenergic
state
Most severe form of Meningococcemia, fulminant
Characterized by:
a. High fever
b. Widespread purpura
c. DIC or Massive hemorrhage
d. Adrenal Insufficiency- necrosis of the adrenals
e. Vascular collapse
f. Shock
g. Death - in 6-8 hours
1. Culture - Blood and CSF
2. Gram-staining of CSF - paired kidney bean organisms
3. Latex Agglutination test
 CELLS/ mL PROTEIN(mg/dl GLUCOSE(mg/dl) CAUSES
NORMAL 0-5 15-45 45-85 -

SEPTIC 200- 20,000 HIGH >100 <45 Bacteria<

(PURULENT) Mainly Amoeba,
MENINGITIS neutrophils Brain
or abscess
polymorpho-
nuclear
ASEPTIC 100-1,000 Moderately high Normal Viruses< TB,
MENINGITIS or Mainly (50-100) Leptospira,
MENINGOENCEP mononuclear fungi, brain
HALITIS abscess,
partially
treated
bacterial
meningitis
ORGANISMS COLONIAL MORPHOLOGY PRIMARY ISOLATION
SITES
N. gonorrheae Small, grayish white, translucent, Male: Urethra
raised with entire edge Female: Endocervix
Usually easily emulsified
Smaller than N. meningitidis
Up to 5 different colony
morphologies from primary
culture

N. meningitidis Bluish-gray or tan( Sero Nasopharynx and

group 6 may be yellowish) oropharynx(Carriers)
Sero Group A & C may be mucoid, Spinal fluid= Meningitis
translucent, and convex with Blood: meningococcemia
smooth glistening surface; may be LRTI: Meningococcal
greenish cast in agar around pneumonia
colonies
Weak pathogen
mistaken for N.
meningitidis
found in
nasopharynx of
children
 Organisms Growth on CARBOHYDRATE UTILIZATION DNAse
MTM,ML,
NYC Glucose Maltose Lactose Sucrose or
Medium Fructose
N. gonorrheae + + - - - -
N. meningitidis + + + - - -
N. lactamica + + + + - -
N. sicca - + + - + -
N. subflava - + + - +/- -
N. flavescens - - - - - -
N. elongata - -/w - - - -
M. catarrhalis - - - - - +
MODE OF TREATMENT AND PREVENTION
1. Penicillin - DRUG OF CHOICE
2. Chloramphenicol
3. 3rd Generation Cephalosporin
4. Vaccines – Polyvalent vaccines - A,C, Y , and W135

PROPHYLAXIS
Rifampicin, Minocycline, Ciprofloxacin

VACCINES
1. Meningococcal Vaccine - Menactra
- Contains Polysaccharide Antigens A,C,Y & W-135
- Not Protective against Serogroup B
- Group B Polysaccharide poorly immunogenic

2. Quadrivalent Vaccine - Serotypes A,C,Y & W-135