MICROBIOLOGY AND PARASITOLOGY

MCC-4
bY: STEPHANIE E. MASIADO, SN

BACTERIA AND DISEASE 2.​ The validity of Koch's postulates lies in the ability of the
pathogen to grow in the laboratory using artificial culture
DEFINITION OF TERMS: media
●​ Infection-invasion of the body by pathogenic
microorganisms. The term is not synonymous with There are certain organisms that cannot be grown in artificial culture
disease media.
●​ Disease - result of an undesirable relationship between
the host and the pathogen, marked by Interruption in the 3.​ Viruses are obligate intracellular parasites that need to be
normal functioning of a body part or parts. grown in living cells.
●​ Symbiosis - prolonged and close interaction between 4.​ Mycobacteriumleprae, the causative agent of leprosy
organisms of different species. needs to be grown on foot pads of mice and armadillo
●​ Mutualism - a form of symbiosis in which both organisms 5.​ Not all people who acquire an infection develop overt
benefit from the relationship. disease.
●​ Commensalism- a form of symbiosis in which one 6.​ The reaction of humans to specific pathogens may differ
organism benefits from another organism without causing given a specific microorganism.
harm to it. 7.​ One individual might develop minor illness from a particular
●​ Parasitism-a form of symbiosis where one organism pathogen but the same pathogen may produce fatal infection
benefits from another organism and at the same time in another host.
causes harm to the other. 8.​ An issue involving Koch's postulates is the requirement that
●​ Pathogenicity-ability of an organism to produce disease. the cultured organism must be inoculated into a susceptible
An organism that can produce disease in humans is said animal
to be pathogenic 9.​ However, there are certain organisms that are species
●​ Virulence - describes the degree of pathogenicity of an specific There are organisms that produce disease only in
organism or the degree to which an organism can animals in the same manner that there are infectious agents
produce disease. that produce disease only in humans.
●​ Contamination-presence of unwanted materials 10.​ organisms that produce disease only in humans cannot be
(chemical, biological, or radiological) where they should tested using laboratory animals and vice versa. (plus ethical
not be or at concentrations above the normal. The issues)
presence of these substances may not necessarily lead to 11.​ There are certain pathogens that become altered when
harm. grown in artificial media. Some become less pathogenic
●​ Pollution-presence of contaminants that can cause while others may lose their pathogenicity, in which case
adverse biological effects to humans and communities. All Koch's Postulates cannot be applied
pollutants are contaminants but not all contaminants are
pollutants. Remember:
●​ Bacteremia - presence of bacteria in the blood. 1.​ Not all microorganisms can be grow inside the laboratory
●​ Septicemia - presence of actively multiplying bacteria in 2.​ Viruses needs living cells
the blood, usually from a source of infection. The 3.​ Not all people can develop disease
condition is called sepsis.
●​ Pyemia - presence of pus producing bacteria in the FACTORS THAT INFLUENCE THE OCCURRENCE OF INFECTION:
bloodstream. THE CHAIN OF INFECTION
●​ Viremia - presence of viruses in the blood.
●​ Toxemia - presence of toxins in the blood
THE CHAIN OF INFECTION

KOCH'S POSTULATES Infection

●​ is the invasion and multiplication of pathogenic
●​ Robert Koch was a German physician who made significant microorganisms in the body, which can lead to disease.
contributions to the field of microbiology. ●​ Pathogens include bacteria, viruses, fungi, and parasites.
●​ One of his greatest and most well known contributions was
proving that certain microorganisms caused specific Importance of Understanding the Chain of Infection:
diseases. ●​ Identifying the steps in the chain of infection helps in
●​ Koch's postulates pinpointing where interventions can be applied to prevent the
○​ The suspected causative agent must be absent spread of infections.
from all healthy organisms but present in all ●​ Effective infection control measures can break the chain at
diseased organisms various points, reducing the incidence of infectious diseases.
○​ The causative agent must be isolated from the
diseased organism and grown in pure culture COMPONENTS OF THE CHAIN OF INFECTION
○​ The cultured agent must cauve the same disease
when inoculated into a healthy susceptible 1.​ Etiologic agent- microorganism that causes the disease.
organism 2.​ Host- organisms that harbor the pathogen.
○​ The same causative agent must then be reisolated 3.​ Environment- external factors that affect the agent and
from the inoculated diseased organism the opportunity for exposure
4.​ Portal of Exit- path by which a pathogen leaves its host.
5.​ Mode of Transmission- way wherein the microorganism
LIMITATIONS OF KOCH'S POSTULATES
used to travel from one animal/person to the other.
6.​ Portal of Entry- path by which a pathogen enters new
1.​ Once all the above conditions are fulfilled, it can now be host.
concluded that the organism isolated is indeed the cause of
the disease understudy
ETIOLOGIC AGENT
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bY: STEPHANIE E. MASIADO, SN
The microorganism that causes the disease. ○​ Spread of pathogens through the air over long
Examples: distances.
●​ Bacteria: Staphylococcus aureus (causes skin infections). ○​ Examples: Tuberculosis, measles.
●​ Viruses: Influenza virus (causes flu)
●​ Fungi: Candida albicans (causes thrush). ●​ Vector-Borne Transmission:
●​ Parasites: Plasmodium species (cause malaria). ○​ Spread of pathogens through vectors like insects.
○​ Mechanical and Biological Transmission
ENVIRONMENT ○​ Examples: Malaria (mosquitoes), Lyme disease
(tick)
External factors that affect the agent and the opportunity for
exposure. PORTAL OF ENTRY

Examples: The path by which a pathogen enters a new host

●​ Climate: Warm, humid climates can promote the growth of
certain pathogens. Examples:
●​ Living Conditions: Overcrowded and unsanitary conditions ●​ Respiratory Tract: Inhalation of airborne pathogens.
can facilitate the spread of infections. ●​ Gastrointestinal Tract: Ingestion of contaminated food or
●​ Sanitation: Poor sanitation can lead to the contamination of water.
water and food sources. ●​ Broken Skin: Entry through cuts or abrasions.

HOST RESERVOIRS

The organism that harbors the pathogen. Continual sources of infectious agents where pathogens can live,
grow, and multiply.
Factors Influencing Susceptibility:
●​ Age: Infants and elderly are more susceptible. Types of Reservoirs:
●​ Immune Status: Immunocompromised individuals (e.g., HIV ●​ Animal Reservoirs- Animals that harbor infectious agents.
patients) are at higher risk. Examples:
●​ Underlying Diseases: Chronic conditions like diabetes can ○​ Anthrax: Cattle.
increase susceptibility. ○​ Plague: Rodents.
○​ Rabies: Dogs.
PORTAL OF EXIT
●​ Environmental Reservoirs- Water, soil, and plants
The path by which a pathogen leaves its host. Example: fungus Histoplasma capsulatum is associated with
soil. Water serves as a reservoir for Entamoeba histolytica, a
Examples: protozoan parasite that causes amoebiasis. Aquatic
●​ Respiratory Tract: Pathogens expelled through coughing or vegetation such as watercress and "kangkong" harbor
sneezing (e.g., influenza virus). Fasciola hepatica larvae which causes damage to the liver.
●​ Gastrointestinal Tract: Pathogens excreted in feces (e.g.,
Salmonella). ●​ Human Reservoirs- humans that harbour infectious agents.
●​ Blood: Pathogens transmitted through blood (e.g., HIV via Examples:
needles or insect bites). ○​ Respiratory Pathogens: Carriers of influenza.
○​ Sexually Transmitted Infections: Carriers of HIV
MODE OF TRANSMISSION
Types of Carriers:
1.​ Asymptomatic Carriers: Infected individuals who do not
Direct Contact show symptoms but can still spread the disease.
●​ Direct Transmission via Direct Contact: 2.​ Incubatory Carriers: Individuals who transmit the pathogen
○​ Immediate transfer of the pathogen from one host during the incubation period before symptoms appear.
to another. 3.​ Chronic Carriers: Individuals who harbor the pathogen for
○​ Examples: Touching, kissing, sexual contact. long periods, sometimes for life.
4.​ Convalescent Carriers: Individuals who have recovered
●​ Droplet Transmission: from the disease but still carry the pathogen.
○​ Spread of pathogens through respiratory droplets.
○​ Examples: Coughing, sneezing. Zoonotic Infections
●​ Diseases transmitted from animals to humans.
Indirect Contact Examples:
●​ Indirect Transmission: ○​ Anthrax: Transmitted from cattle to humans
○​ Transfer of the pathogen via an intermediate through contact with infected animals or animal
object or organism. products.
○​ Examples: Contaminated surfaces, food, water. ○​ Plague: Transmitted from rodents to humans
through flea bites.
●​ Vehicle Transmission: ○​ Rabies: Transmitted from dogs to humans through
○​ transmission of organisms through media such as bites.
food, water, milk, or biologic substances such as
blood and body secretions Human Carriers
○​ Fomites or inanimate objects such as beddings ●​ Typhoid Mary: An asymptomatic carrier of typhoid fever
and clothing mày also serve as vehicles. who infected numerous people in the early 20th century.
●​ HIV Carriers: Individuals who carry and can transmit HIV
●​ Airborne Transmission: without showing symptoms for many years.
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bY: STEPHANIE E. MASIADO, SN

PREVENTION AND CONTROL Production of Extracellular Substances

●​ Mechanisms Promoting Invasion:
Breaking the Chain of Infection: ○​ Intracellular Multiplication:
●​ Hand Hygiene: Regular handwashing with soap and water or ■​ Neisseria gonorrhoeae can enter and
using hand sanitizers. multiply within host cells. After
●​ Vaccination: Immunization to prevent infections like measles, multiplication, it is extruded from the
influenza, and hepatitis. host cell, causing direct destruction of
●​ Use of Personal Protective Equipment (PPE): Gloves, the host cells and allowing further
masks, and gowns to protect against exposure. infection.
●​ Environmental Sanitation: Proper disposal of waste, clean
water supply, and food safety measures. ○​ Enzymes:
■​ Collagenase: Produced by Clostridium
Public Health Measures: perfringens, this enzyme breaks down
●​ Surveillance: Monitoring and tracking the spread of infections collagen, a major component of
to implement timely interventions. connective tissue, contributing to
●​ Quarantine: Isolating infected individuals to prevent the diseases like gas gangrene.
spread of disease.
●​ Education: Informing the public about infection prevention CHEMICAL TOXIN PRODUCTION
and control measures.
Toxins are poisonous substances and are often the primary factors
HOW ORGANISMS PRODUCE DISEASE that contribute to disease production.
MECHANICAL INVASIVENESS
Two Major Types:
Invasiveness refers to the ability of pathogens to enter, survive, 1.​ Exotoxins
and multiply within the host. ●​ Produced inside mostly gram-positive bacteria as part of
their growth and metabolism.
Key Steps: ●​ Secreted into the surrounding medium.
●​ Colonization: The initial establishment of the pathogen at
the portal of entry. 2.​ Endotoxins
●​ Evasion of Host Immune Defenses: Strategies used by ●​ Integral components of the outer membrane of
pathogens to avoid detection and destruction by the gram-negative bacteria.
host's immune system. ●​ Released when the bacteria die and their cell walls break
●​ Production of Extracellular Substances: Substances down.
produced by pathogens that facilitate invasion and
damage to host tissues ENDOTOXIN

Endotoxins are part of the outer membrane of gram-negative

Colonization is the process by which pathogens establish themselves bacteria.
at the portal of entry.
●​ Mechanisms: Examples:
○​ Adhesins: Molecules that help pathogens adhere ●​ Salmonella, Shigella, Escherichia coli.
to specific target cells
○​ Examples: Gram-negative bacteria possess pili or Structure:
fimbriae that promote adherence to susceptible ●​ Lipopolysaccharide (LPS):
cells. ●​ Lipid A: Responsible for the toxic effects.
○​ Importance: Adhesion is crucial for pathogens to ●​ Polysaccharide: Antigenic component that triggers
invade surfaces and enter the host body. immune responses.

Evasion of Host Immune Defenses Mechanism.

●​ Immune Response: ●​ Released upon bacterial cell death and lysis.
○​ The host's immune system immediately responds ●​ Bind to receptors on immune cells, triggering
to destroy invading pathogens. inflammatory responses.

●​ Evasion Mechanisms: Effects:

○​ Capsules: Some bacteria have a capsule that ●​ Causes fever, inflammation, septic shock, and other
prevents phagocytosis, allowing them to evade systemic effects.
immune cells. ●​ Produce similar signs and symptoms across different
bacteria, though severity can vary.
○​ Enzymes:
■​ Coagulase: Secreted by
Staphylococcus aureus, this enzyme EXOTOXIN
promotes the formation of a protective
coagulum, hiding the bacteria from Exotoxins are proteins produced inside pathogenic bacteria, most
immune cells. commonly gram- positive bacteria, and secreted into the
■​ Survival in Macrophages: surrounding environment.
Mycobacterium tuberculosis can survive
and multiply inside macrophages by Characteristics:
inhibiting the fusion of phagosomes and ●​ Mainly proteins, often enzymes.
lysosomes.
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○​ Antibodies: Proteins produced by the immune
●​ Soluble in body fluids, allowing them to diffuse easily and system to neutralize pathogens.
be transported throughout the body. ○​ Cytotoxic T Cells: Immune cells that destroy
infected liver cells (hepatocytes).
Types of Exotoxins:
1.​ Cytotoxins: Kill host cells or disrupt their normal Mechanism.
functions. ●​ The immune system targets and destroys hepatocytes
2.​ Neurotoxins: Interfere with normal nerve impulse infected with hepatitis viruses.
transmission. ●​ This immune-mediated destruction leads to liver damage.
3.​ Enterotoxins: Affect the cells lining the gastrointestinal
tract, causing symptoms like diarrhea and vomiting. Measles and German Measles (Rubella)
●​ Measles:
Example: Botulism ○​ A highly contagious viral infection characterized by
a distinctive rash.
Mechanism: ○​ German Measles (Rubella): A viral infection
●​ Neurotoxin produced by Clostridium botulinum. similar to measles but generally milder. Immune
●​ Blocks the release of acetylcholine at neuromuscular
junctions, preventing muscle contraction. ●​ Response in Measles and Rubella:
○​ Rashes: The rashes seen in measles and rubella
Symptoms: are due to the immune response to the viruses.
●​ Muscle weakness, difficulty swallowing, respiratory
failure, paralysis. Mechanism
●​ The immune system's response to the virus includes the
Treatment: activation of immune cells and the release of inflammatory
●​ Administration of antitoxins. mediators.
●​ Supportive care, including mechanical ventilation if ●​ This immune activity causes the characteristic rashes.
necessary.
Mechanisms of Immune Response
●​ Antibody Production:
COMPARISON BETWEEN EXOTOXIN AND ENDOTOXIN
○​ B Cells: Produce antibodies that specifically target
viral antigens.
○​ Function: Neutralize viruses and mark infected
cells for destruction.

●​ Cytotoxic T Cells:
○​ Activation: Triggered by the presence of viral
antigens on infected cells.
○​ Function: Destroy infected cells to prevent the
spread of the virus.

●​ Inflammatory Response:
○​ Cytokines: Signaling proteins released by
immune cells to coordinate the immune response.
○​ Effects: Can cause tissue damage and
inflammation as a side effect of fighting the
infection.

CLASSIFICATION OF INFECTIOUS DISEASES

CLASSIFICATION BASED ON BEHAVIOR WITHIN A HOST AND
POPULATION

Communicable Diseases
●​ Diseases that spread from one host to another, either directly
(e.g., through physical contact) or indirectly (e.g., through
contaminated surfaces or vectors).
●​ Examples: Measles, tuberculosis, typhoid fever.
IMMUNOLOGIC MECHANISMS

Some diseases are caused not by the direct action of pathogens but Mechanisms of Spread:
by the host's immune response to the pathogen or its products. 1.​ Direct Contact: Physical interaction such as touching,
kissing, or sexual contact.
Examples: 2.​ Indirect Contact: "Through fomites (contaminated objects),
●​ Hepatitis vectors (insects), or airborne transmission.
●​ Measles
●​ German measles (Rubella) Contagious Diseases:
●​ A subset of communicable diseases that are easily and
rapidly spread from one person to another.
Hepatitis and Immune Response ●​ Examples: Measles, chickenpox.
●​ Hepatitis is an inflammation of the liver, often caused by viral
infections. Characteristics:
●​ Immune Response in Hepatitis: ●​ High transmission rate.
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●​ Often spread through respiratory droplets or close personal ●​ Persistent presence in a specific geographic area.
contact. ●​ Stable incidence over time.

Fulminant Infections: Epidemic Diseases

●​ Infections that result in the rapid death of the patient over a ●​ Diseases that affect a great number of people in a given
short period. locality in a short period.
●​ Example: Meningococcemia, where a patient may die within ●​ Example: Influenza outbreaks.
hours of hospital admission.
Characteristics:
Characteristics: ●​ Sudden increase in cases.
●​ Rapid onset and progression. ●​ Often linked to specific events or conditions.
●​ High mortality rate without prompt treatment.
CLASSIFICATION BASED ON THE SEVERITY OR DURATION OF A
Non-Communicable Diseases DISEASE
●​ Diseases that are not spread from person to person.
●​ Causes: Usually caused by organisms that normally inhabit Acute Diseases
the body and produce disease only occasionally or by ●​ Diseases that develop rapidly but last for a short period.
organisms introduced into the body through breaks in the ●​ Example: Common cold.
skin.
●​ Example: Tetanus, caused by "Clostridium tetani". Characteristics:
●​ Rapid onset of symptoms.
Characteristics: ●​ Short duration, typically resolving within days to weeks.
●​ Often related to environmental factors or internal flora.
●​ Not transmissible between individuals. Chronic Diseases:
●​ Diseases that develop slowly and last for long periods.
CLASSIFICATION BASED ON THE SOURCE OF THE ●​ Example: Tuberculosis.
MICROORGANISM
Characteristics:
Exogenous Infections ●​ Slow progression
●​ Infections where the source of the infectious agent is from ●​ Long-lasting, often persisting for months or years.
outside the body.
●​ Examples: DETAILED MECHANISMS AND EXAMPLES
○​ Cholera: Caused by ingestion of contaminated
water. Communicable vs. Non-Communicable
○​ Nosocomial Infections: Hospital-acquired ●​ Communicable: Spread through direct or indirect contact.
infections from the hospital environment. Examples include respiratory infections like influenza and
sexually transmitted infections like HIV.
Characteristics: ●​ Non-Communicable: Not spread between people, often due
●​ Acquired from external sources. to environmental factors or internal flora. Examples include
●​ Often associated with environmental exposure or healthcare tetanus and certain types of food poisoning.
settings.
Exogenous vs. Endogenous
Endogenous Infections ●​ Exogenous: Originates from external sources, such as
●​ Infections where the source of the causative organism is contaminated water or surfaces. Examples include cholera
from inside the body. and hospital-acquired infections.
●​ Example: ●​ Endogenous: Originates from within the body, such as
○​ Urinary Tract Infections (UTIs): Caused by normal flora become pathogenic. Examples include UTIs
Escherichia coli, part of the normal flora of the caused by E. coli
colon, entering the urinary tract.
Occurrence Patterns:
Characteristics: ●​ Sporadic: Random and infrequent occurrences, such as
●​ Originates from the host's own flora. isolated cases of tetanus.
●​ Often occurs when normal flora becomes pathogenic due to ●​ Endemic: Constant presence in a specific area, such as
changes in the host's environment or immune status. malaria in certain tropical regions.
●​ Epidemic: Sudden increase in cases in a specific area, such
CLASSIFICATION BASED ON THE OCCURENCE OF A DISEASE as seasonal flu outbreaks.
●​ Pandemic: Global spread, such as the COVID-19 pandemic.
Sporadic Diseases
●​ Diseases that occur occasionally and irregularly.
●​ Example: Sporadic cases of certain infections like tetanus. EXAMPLE: INFLUENZA (Flu)
Characteristics: Types:
●​ Random and infrequent occurrences. ●​ Seasonal Flu: Regular outbreaks can cause epidemics.
●​ No predictable pattern. ●​ Pandemic Flu: Global outbreaks, such as H1N1 in 2009.

Endemic Diseases Transmission:

●​ Diseases constantly present in a population at low levels. ●​ Spread through respiratory droplets from coughing or
●​ Examples: sneezing. Can also spread through contact with
○​ Malaria: Endemic in Palawan contaminated surfaces.
○​ Schistosomiasis: Endemic in Leyte.
Characteristics:
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●​ Rapid onset of symptoms. Directly caused by the initial
Impact: pathogen.
●​ Can cause widespread illness and significant mortality,
especially in vulnerable populations like the elderly and Secondary Infection:
those with pre- existing conditions. ●​ Infections caused by opportunistic pathogens after the
primary infection has weakened the body's defenses.
Prevention: ●​ Examples:
●​ Vaccination is the most effective way to prevent influenza. ○​ Pneumonia: Can occur after a primary viral
Good hygiene practices, such as handwashing and infection like influenza.
covering coughs, can reduce transmission. ○​ Fungal Infections: Common in patients with
compromised immune systems, such as those
with AIDS.
CLASSIFICATION BASED ON THE EXTENT OF HOST
INVOLVEMENT
Characteristics:
●​ Often more severe than the primary infection.
Localized Infections ●​ Can complicate the clinical course and treatment of the
●​ Infections where the invading organisms are limited to a primary infection.
relatively small area of the body.
●​ Examples: Subclinical (Inapparent) Infections
○​ Boils: Localized skin infections caused by ●​ Infections that do not cause noticeable illness.
bacteria, often Staphylococcus aureus ●​ Examples:
○​ Abscesses: Collections of pus that have built up ○​ Hepatitis A: Some individuals may carry the virus
within the tissue of the body. without showing typical symptoms.
○​ Polio: Some infected individuals may not show
Characteristics: symptoms but can still spread the virus.
●​ Confined to a specific area.
●​ Symptoms are localized, such as redness, swelling, and pain Characteristics:
at the infection site. ●​ No noticeable symptoms, making diagnosis challenging.
●​ Easier to treat and contain compared to systemic infections. ●​ Can still be contagious and spread to others.
●​ Important in public health for understanding disease
Systemic (Generalized) Infections transmission and control
●​ Infections where the causative organisms or their products
are spread throughout the body via blood or lymph.
DETAILED MECHANISMS AND EXAMPLES
●​ Examples:
○​ Sepsis: A life-threatening condition caused by the
body's response to an infection spreading Localized vs. Systemic:
throughout the body. ●​ Localized: Limited to a specific area, easier to treat and
○​ Bacteremia: Presence of bacteria in the blood, contain.
which can lead to systemic infections. ○​ Examples include skin infections like boils and
abscesses.
Characteristics: ●​ Systemic: Spread throughout the body, more severe and
●​ Symptoms are widespread and can affect multiple organ harder to treat.
systems. ○​ Examples include sepsis and bacteremia.
●​ Often more severe and harder to treat than localized
infections. Primary vs. Secondary:
●​ Requires systemic treatment, such as intravenous ●​ Primary: Initial infection, often acute. Examples include
antibiotics. influenza and the common cold.
●​ Secondary: Follows primary infection, often more severe
Focal Infections due to weakened defenses. Examples include bacterial
●​ Infections that start as localized but spread to specific parts pneumonia following influenza.
of the body and become confined to those areas.
●​ Examples: Subclinical Infections:
○​ Dental Infections: Infections in the teeth that can ●​ Characteristics: No noticeable symptoms, can still be
spread to other parts of the body, such as the contagious.
heart (endocarditis). ○​ Examples include asymptomatic carriers of
○​ Tonsillitis: Infections in the tonsils that can spread hepatitis A and polio.
to other areas, such as the ears or sinuses.
STAGES OF AN INFECTIOUS DISEASE
Characteristics:
●​ Initially localized but can cause secondary infections in other Once a microorganism invades a susceptible host, disease follows.
parts of the body. The development of the disease follows a sequence of events that
●​ Often requires targeted treatment to both the primary and tends to follow a similar pattern whether the disease is chronic or
secondary infection sites. acute. These periods are the following:
1.​ Incubation Period
Primary and Secondary Infections ●​ The time interval between the entry of the pathogen and the
Primary Infection appearance of initial signs and symptoms.
●​ An acute infection that causes the initial illness. Characteristics:
●​ Example: Influenza, which can weaken the immune system. ●​ Variable Duration: Can range from hours to months,
depending on the pathogen.
Characteristics:
Factors Influencing Duration:
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●​ Virulence of the Organism: More virulent organisms can STAGES OF AN INFECTIOUS DISEASE
cause disease faster.
●​ Number of Infecting Microorganisms: Higher numbers
can shorten the incubation period.
●​ Host Resistance: Stronger immune systems can prolong
the incubation period.
Examples:
●​ Influenza: Incubation period of 1-4 days.
●​ Hepatitis B: Incubation period of 1.5-6 months.
●​ Salmonella: Incubation period of 6 hours to 6
days.

2.​ Prodromal Period

●​ A relatively short period characterized by early, mild
symptoms of disease.
Characteristics: EXAMPLE: INFLUENZA (Flu)
●​ Non-Specific Symptoms: Symptoms such as fever, cough, Stages:
colds, general aches, and malaise. ●​ Incubation: 1-4 days
●​ Contagious Stage: Pathogens are actively replicating, and ●​ Prodromal: Early symptoms like fatigue and low-grade fever
the host is often contagious. ●​ Illness: High fever, severe cough, body aches
Examples: ●​ Decline: Symptoms begin to lessen
●​ Measles: Prodromal symptoms include fever, ●​ Convalescence: Full recovery in several days to weeks
cough, and malaise
●​ Influenza: Early symptoms can include fatigue Note:
and low-grade fever ●​ High transmission rate, especially during the prodromal and
illness periods.
3.​ Illness Period ●​ Importance of vaccination and early treatment
●​ The period during which the disease is most severe and
symptoms are most apparent. HOST RESPONSE TO INFECTION
Characteristics:
●​ Specific Symptoms: Symptoms specific to the disease Immunology
become evident. ●​ the study of the immune system and the immune
●​ Immune Response: The body's immune system is actively response.
fighting the infection. Immunogen
Examples: ●​ any substance capable of inducing an immune response,
●​ Influenza: Symptoms include high fever, severe whether humoral or cell mediated or both.
cough, and body aches Antigen
●​ Gastroenteritis: Symptoms include diarrhea, ●​ a substance recognized by the immune system, whether
vomiting, and stomach cramps by the B cell or the T cell, that serves as the target of the
immune response but may not necessarily lead to an
4.​ Decline Period immune response.
●​ The period during which the symptoms of the disease begin
to subside.
Characteristics: PROPERTIES OF ANTIGEN
●​ Decreasing Symptoms: Reduction in the severity of
symptoms. Antigens are substances that trigger an immune response, recognized
●​ Immune System Recovery: The immune system starts to by the body as foreign or non- self.
gain the upper hand over the pathogen. Example: Pig heart transplantation into a human being →
Examples: high chance of immune rejection due to genetic differences.
●​ Influenza: Fever and aches begin to lessen
●​ Gastroenteritis: Diarrhea and vomiting decrease Individual genetic variations influence immune responses to
environmental components (e.g., dust)
5.​ Convalescence Period
●​ The period during which the patient recovers and returns to Glycoproteins- carbohydrates and proteins can’t be an antigen due to
normal health. their molecular weight.
Characteristics:
●​ Recovery: Symptoms disappear, and the body repairs itself. CHEMICAL COMPOSITION AND COMPLEXITY
●​ Possible Complications: Some diseases may leave lasting
effects or complications.
Most organic substances can be antigenic, except pure lipids and
Examples:
nucleic acids.
●​ Influenza: Full recovery may take several days to
●​ Proteins are the most immunogenic due to their complex
weeks
structures and larger molecular size.
●​ Hepatitis B: Recovery can be prolonged, with
●​ Glycoproteins are more antigenic than pure proteins due to
potential for chronic infection.
their complex structure.

Molecular Size and Stability

●​ Molecules <10,000 daltons: weakly immunogenic or
non-immunogenic.
●​ Molecules >10,000 daltons: potent immunogens, but
stability is crucial.
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1 dalton= Function of Peripheral Lymphoid Organs
●​ Antigens brought to peripheral lymphoid organs
Examples: Insulin, a lipid (molecular weight: 5,800 daltons) vs. ●​ T cells and B cells recognize and respond to antigens
Immunoglobulin G (molecular weight: 150,000 daltons). ●​ Immune cells coordinate response to eliminate antigens

MODE OF ENTRY AND ADMINISTRATION CELLS OF THE IMMUNE SYSTEM

Protein antigens: smaller doses required for immune response. White Blood Cells
Polysaccharide antigens: larger doses required. ●​ White blood cells (WBCs) are a vital part of the immune
system.
Administration routes:
●​ intramuscular- 90 degrees There are three main types of WBCs:
●​ Intravenous- 25 degrees 1.​ Granulocytes (50-80%): neutrophils (engulf foreign cells),
●​ oral eosinophils (parasites and inflammation), basophils
(inflammation)
COMPONENTS AND FUNCTIONS OF IMMUNE SYSTEM 2.​ Lymphocytes (20-45%): B cells (plasma cells-producing
antibodies that targets pathogens and memory B cells), T
Central Lymphoid Organs: cells, NK cells
●​ Primary Sites for Immune Cell Differentiation and Maturation 3.​ Monocytes and macrophages (3- 8%): engulfing dead
●​ Bone marrow: origin of blood cells, differentiation of B cells cells,
and T cells
●​ Thymus: maturation of T cells Granulocytes
Neutrophils:
Bone Marrow ●​ Primary role: phagocytosis of bacteria and foreign particles
●​ Site of Hematopoiesis and Lymphopoiesis- location of ●​ Involved in acute inflammation
blood production or formed elements
●​ Precursor cells for lymphocytes Eosinophils
●​ Differentiation of B cells and T cells ●​ Primary role: anti-parasitic response and type I
●​ B cells mature in bone marrow hypersensitivity
●​ Release major basic protein, toxic to parasites
Antigen presenting cells (APCs)
●​ process and present antigens to T cells. Basophils:
●​ Primary role: allergies and histamine release
Types of APCs: ●​ Involved in type I hypersensitivity reactions
●​ Macrophages
●​ B cells
●​ Dendritic cells
●​ Langerhans cells
●​ Kupffer cells

APCs play a crucial role in initiating immune responses.

T Cell Maturation
●​ Immature T cells migrate to thymus
●​ Maturation and selection of competent T cells
●​ Mature T cells proceed to peripheral lymphoid organs

Peripheral Lymphoid Organs

●​ Lymph nodes
●​ Spleen
●​ Mucosa-associated lymphoid tissues (MALT)
○​ Tonsils
○​ Adenoids
○​ Peyer's patches
○​ Appendix

These organs trap antigens and facilitate encounters with T and B Lymphocytes
cells. B cells:
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●​ Primary role: humoral immunity and antibody production
●​ Differentiate into plasma cells and memory B cells
●​ Produce antibodies to neutralize or remove pathogens
●​ Differentiate into plasma cells and memory B cells
●​ Function as APCs
B cells play a crucial role in humoral immunity.

T cells:
●​ Primary role: cell-mediated immunity and cytotoxicity
●​ Differentiate into CD4+ and CD8+ T cells

CD4+ T cells:
●​ Helper T cells: activate cytotoxic T cells and stimulate B cell
differentiation
●​ Regulatory T cells: maintain self-tolerance and prevent
autoimmunity

CD8+ T cells:
●​ Cytotoxic T cells: kill infected cells or tumor cells

T cells play a central role in cell- mediated immunity.

Escape and Adaptive Immunity
NK cells: ●​ Microbes escaping innate Immunity are acted upon by
●​ Primary role: innate immunity and cytotoxicity adaptive immunity
●​ Recognize and kill infected cells or tumor cells ●​ Involves B cells and T cells
●​ Specific response to pathogens
INNATE VS ADAPTIVE IMMUNITY, LINES OF DEFENSE ●​ Activates Adaptive Immunity (final line of defense: immune
response)
Innate Immunity
●​ Innate immunity provides immediate protection against Adaptive Immunity
pathogens. Characteristics of Adaptive Immunity
●​ It's a nonspecific response, meaning it doesn't target specific ●​ Specific response
pathogens. provides the first line of defense, activates ●​ Acquired response -Delayed response (7-10 days)
adaptive immunity. ●​ Long-term protection Possesses memory

Characteristics of Innate Immunity Mechanisms of Adaptive Immunity

●​ Non-specific response ●​ Antibody production by B cells
●​ Active from birth, prior to antigen exposure ●​ Activation of cytotoxic T cells
●​ No memory or improvement after exposure ●​ Antigen processing and presentation
●​ Provides short-term protection ●​ Recognition of specific epitopes
●​ Activated within minutes of exposure
B Cells and Antibody Production
Functions of Innate Immunity ●​ Recognize specific antigens
●​ Kills invading microorganisms ●​ Undergo clonal expansion and differentiation
●​ Activates adaptive immune responses ●​ Produce antibodies to neutralize or remove pathogens
●​ Consists of first and second lines of defense
T Cells and Cell-Mediated Immunity
First Line of Defense ●​ Cytotoxic T cells recognize and kill infected cells
●​ Physical barriers: skin, mucous membranes ●​ Helper T cells assist B cells and cytotoxic T cells
●​ Chemical barriers: fatty acids, sweat (low pH) ●​ Memory T cells provide long-term protection
●​ Biological barriers: normal flora competition, immune
system priming Memory and Amplification
●​ Memory B cells and T cells recognize specific antigens
Second Line of Defense ●​ Rapid response upon re-exposure
●​ Inflammation and Natural Killer Cells ●​ Amplifiable response
○​ Inflammation
○​ Natural killer cells
○​ Recognition of pathogen- associated molecular
patterns (PAMPS)
○​ Activation of inflammatory cells and complement
system

PHAGOCYTOSIS AND COMPLEMENT SYSTEM

Elimination of Pathogens
●​ Phagocytosis: ingestion of microorganisms by inflammatory
cells
●​ Complement system: production of membrane attack
complex; Degradation of microorganisms
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Primary Immune Response Antibody structure:
●​ First exposure to antigen activates Th1 cells ●​ Heavy chains (H)
●​ Activation of inflammatory response and delayed type ●​ Light chains (L) -Variable regions (V)
hypersensitivity ●​ Constant regions (C)
●​ Stimulation of B cells to produce IgM and IgG ●​ Hinge region
●​ Antibodies detectable in serum after 7- 10 days ●​ Fab and Fc regions

Antibody Production Heavy Chains Structurally distinct for each immunoglobulin class
●​ Serum level of antibodies rises for several weeks 1.​ Gamma (γ) for Ig
●​ Declines and may drop to low levels 2.​ Mu (μ) for IgM
●​ Primary response duration varies depending on 3.​ Alpha (a) for IgA
antigen and dose 4.​ Delta (δ) for IgD
5.​ Epsilon (ε) for IgE
Secondary Immune Response
●​ Re-exposure to same antigen activates Th2 cells Light Chains
●​ Further production of antibodies (except IgM) ●​ Карра (к) or lambda (λ) chains
●​ Rapid antibody response of higher intensity ●​ Approximately 220 amino acid residues long

Memory Cells CLASSES OF IMMUNOGLOBULINS

●​ Persistence of antigen-specific memory cells
●​ Rapid response upon re-exposure IgG
●​ IgG predominant antibody ●​ Monomer, predominant in secondary immune response
●​ Major defense against bacteria and viruses
Class Switching ●​ 80% of serum immunoglobulins
●​ IgG modification to other antibodies (IgA or IgE) ●​ Four subclasses: IgG1, IgG2, IgG3, IgG4
●​ Occurs in response to specific needs
●​ Enables targeted immune response IgM
●​ Pentamer, largest immunoglobulin
Humoral Immunity ●​ J chain holds pentamer together
Types: ●​ Main immunoglobulin in primary response
●​ Innate humoral immunity ●​ Activates complement system
○​ Involves cytokines and complement system
○​ Provides immediate protection Adaptive humoral IgA
immunity ●​ Secretory immunoglobulin
●​ Adaptive humoral immunity ●​ Main immunoglobulin in secretions (colostrum, saliva, tears)
○​ involves the action of antibodies ●​ Monomer in serum, dimer in secretions
●​ Important in mucosal immunity
Targets of Antibody- Mediated Immunity
●​ Extracellular pathogens IgE
●​ Toxin-induced diseases ●​ Reaginic antibody
●​ Certain viral infections ●​ Mediates immediate hypersensitivity reactions
●​ Encapsulated pathogens (e.g., pneumococci, Haemophilus ●​ Defense against parasites (helminths) - Binds to mast cells
influenzae) and basophils
Mechanisms of Antibody-Mediated Immunity IgD
●​ Neutralization of toxins and pathogens ●​ Monomer, no known antibody function
●​ Opsonization and phagocytosis ●​ Surface marker for B cells
●​ Complement activation ●​ Antigen receptor
●​ Antibody-dependent cellular cytotoxicity ●​ Present in small amounts in serum (1%)
Importance: COMPARISON OF THE MAJOR CLASSES OF Ig
●​ Protects against infections and diseases
●​ Essential for vaccine-induced immunity
●​ Crucial for immune system function

ANTIBODIES

Antibodies are globulin proteins (immunoglobulins) that react

specifically with the antigens that stimulate their production

Functions of Antibodies
●​ Neutralize toxins and viruses
●​ Opsonize microbes for phagocytosis
●​ Activate complement system
●​ Prevent microbial attachment to mucosal surfaces

Antibodies (immunoglobulins):
●​ Y-shaped proteins
●​ Recognize specific antigens
●​ Neutralize or remove pathogens
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CELL MEDIATED IMMUNITY CELL ●​ Inhibit growth of pathogenic organisms

●​ Prime immune system of newborns
Functions of Cell-Mediated Immunity ●​ Protect organs and systems from invasive organisms
●​ Resistance and recovery from intracellular infections ●​ Synthesize essential vitamins
●​ Defense against fungi, parasites, and bacteria
●​ Transplant and graft rejection Vitamin K²- activation of clotting factors
●​ Main defense against tumor cells
Vitamin K Production
Components of Cell-Mediated Immunity ●​ Normal intestinal flora, specifically bacteria like Escherichia
1.​ Macrophages coli and Bacillus subtilis, produce vitamin K2 (menaquinone).
2.​ Natural killer cells This vitamin is necessary for the activation of clotting factors
3.​ Helper T cells (CD4+) II, VII, IX, and X.
4.​ Cytotoxic T cells (CD8+) ●​ Importance of vitamin K in blood coagulation

Macrophages Protective Effects of Normal Flora

●​ Present antigens to T cells 1.​ Prevent pathogenic attachment and penetration
●​ Phagocytic cells, ingesting and destroying microbes 2.​ Aid digestion with enzymes (cellulase, galactosidase,
glucosidase)
Helper T Cells (CD4+) 3.​ Assist steroid metabolism
●​ Stimulate B cell differentiation
●​ Activate cytotoxic T cells Enzymes- lowering the activation in the substrate
●​ Subtypes: Th1, Th2, Th17 Steroid- a kind of hormones that is present in both males and females
(mainly in males)
Helper T Cell Subtypes
●​ Th1: triggers inflammation, IgM, and IgG synthesis ACQUISITION OF NORMAL FLORA
●​ Th2: promotes antibody synthesis and class
switching Newborns acquire normal flora from their mother's genital tract, skin,
●​ Th17: chemotactic for neutrophils, enhancing and environment.
inflammation ●​ Mother's genital tract during delivery
●​ Skin and respiratory tract of handlers
Cytotoxic T Cells (CD8+) ●​ Environmental exposure
●​ Destroy antigens via perforin-granzyme
mechanism Sterile Body Tissues and Fluids
●​ Main defense against intracellular pathogens ●​ Cerebrospinal fluid (CSF) in our brain
●​ Involved in transplant rejection and tumor ●​ Synovial fluid in joints causes friction free movement
destruction ●​ Blood- bacterization (presence of bacteria in blood)
●​ Urinary bladder- UTI causes by the E.coli
NORMAL HUMAN MICROBIAL FLORA AND MICROORGANISMS ●​ Uterus
PATHOGENIC TO MAN ●​ Fallopian tubes
●​ Middle ear
MICROBIAL ECOLOGY
●​ Paranasal sinuses
Microbial Ecology is the study of the relationships between Consequences of Bacterial Presence in Sterile Areas
microorganisms and their environment. ●​ Bacteria in CSF can lead to encephalitis.
●​ Relationships between microorganisms and their ●​ Central nervous system infections (meningitis)
environment ●​ Sepsis
●​ Interactions with humans and other organisms ●​ Organ dysfunction
●​ Study of microbial communities and ecosystems

NORMAL FLORA NORMAL FLORA ON DIFFERENT SITES OF THE BODY

SKIN AS A MICROBIAL HABITAT
Indigenous Microorganisms of the Human Body
Normal flora consists of the group of organisms that inhabit the body of
a normal healthy individual in the community. ●​ Constant contact with environment
●​ Non-pathogenic or pathogenic ●​ Exposed to microorganisms
●​ Opportunistic pathogens- can migrate to other site so ●​ Factors eliminating non-resident flora:
disease can produce ○​ Lysozyme
●​ Resident and transient flora ○​ Acidic pH
○​ Free fatty acids
○​ Skin sloughing
TYPES OF NORMAL FLORA
SKIN REGIONS AND THEIR MICROBIAL CHARACTERISTICS
Two types of flora: Resident and Transient
1.​ Resident flora: fixed types, regularly found in a given area:
permanent, capable of fighting transient flora 1.​ Axilla, perineum, and toe webs:
2.​ Transient flora: temporary, derived from the environment: ●​ Higher moisture and temperature
temporal visitors, mainly causes diseases ●​ Higher surface lipids
●​ Predominantly gram-negative bacilli
IMPORTANCE OF NORMAL FLORA
2.​ Hand, face, and trunk:
●​ Moderate moisture and temperature
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●​ Mixed flora PHARYNX AND TRACHEA

3.​ Upper arms and legs: ●​ The normal flora of the pharynx and trachea are similar to
●​ Lower moisture and temperature those found in the oral cavity.
●​ Predominantly gram-positive cocci ●​ However, there may be transient carriage in the pharynx of
potentially pathogenic organisms.
COMMON MICROORGANISMS ON SKIN REGION ●​ These include Haemophilus influenzae, Streptococcus
pneumoniae, Neisseria meningitidis and Mycoplasma
Axilla, perineum, and toe webs: Gram-negative bacilli (e.g., E. coli,
Klebsiella) CONJUNCTIVA

Dry sites (hands, forearms, feet, legs): ●​ The normal flora in the conjunctivae are very scanty because
●​ Staphylococcus epidermidis they are held in check by the flow of tears that contain
●​ Staphylococcus hominis lysozyme.
●​ Other regions: Mixed flora (e.g., Streptococcus, ●​ However, some bacteria may transiently colonize the
Corynebacterium) conjunctiva including Neisseria, Moraxella, and
Corynebacterium. Staphylococci and streptococci may also
FACTORS SHAPING SKIN FLORA be present.

●​ Hygiene and cleanliness DIGESTIVE TRACT FLORA

●​ Environmental exposure
ESOPHAGU AND STOMACH FLORA
●​ Skin conditions (e.g., acne, eczema)
●​ Antibiotic use
●​ Diet and nutrition ●​ Esophagus: transient mouth flora
●​ Stomach: minimal bacteria due to acidic environment
●​ Helicobacter pylori: survives acidic environment, causes
CLINICAL IMPLICATIONS OF SKIN FLORA
duodenal ulcers
●​ Infections (e.g., impetigo, folliculitis)
SCANTY FLORA IN THE SMALL INTESTINE
●​ Skin conditions (e.g., acne, eczema)
●​ Wound healing
●​ Immune system modulation ●​ Constant peristaltic movement limits bacterial growth
●​ Transient flora include streptococci, lactobacilli, and
Bacteroides
●​ The small intestine's constant movement and limited nutrient
availability result in scanty flora. The primary microorganisms
found in this region are:
1.​ Streptococci: facultative anaerobes
2.​ Lactobacilli: beneficial bacteria promoting
immune function
3.​ Bacteroides: anaerobic bacteria involved in
carbohydrate metabolism

DIVERSE FLORA IN THE LARGE INTESTINE

●​ Predominantly anaerobes (95%-99%)

●​ Bacteroides fragilis, Bifidobacterium/Lactobacillus bifidum,
Eubacterium, Peptostreptococcus, and Clostridium
●​ Facultative aerobes (1%-4%): Escherichia coli and other
Enterobacteriaceae
Reminder:
The large intestine's diverse flora plays crucial roles in:
Most microorganisms in the skin are found in its superficial
1.​ Fiber fermentation
layers(stratum corneum) and hair follicles. Anaerobes inhabit the
2.​ Short-chain fatty acid production
deeper structures and layers of the skin, such as hair follicles,
3.​ Vitamin synthesis (e.g., vitamin K, biotin)
sebaceous glands, and sweat glands
4.​ Immune system modulation
5.​ Diverse Flora in the Large Intestine
MOUTH AND RESPIRATORY TRACT
ORAL CAVITY The predominant microorganisms in this region include:
1.​ Bacteroides fragilis: anaerobic bacteria involved in
●​ The tongue and buccal mucosa are inhabited mostly by carbohydrate metabolism
Streptococcus viridans group, which includes S. mutans, S. 2.​ Bifidobacterium/Lactobacillus bifidum: beneficial bacteria
milleri, S. salivarius, and S. sanguis. promoting immune function
●​ Although they are part of the normal flora of the mouth, the
viridans streptococci have been implicated in the Intestinal Flora: Essential Functions
pathogenesis of dental caries. 1.​ Vitamin B complex and vitamin K synthesis
●​ The gingival crevices and the tonsillar crypts are primarily 2.​ Bile conversion to bile acids
inhabited by anaerobic flora. 3.​ Competition with transient flora for nutrients
4.​ Prevention of colonization by transient flora
5.​ Production of antimicrobial compounds
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gut) vitamin K es
GENITOURINARY TRACT FLORA
2.​ remora fish 1.​ 2.​ Mosquit
and sharks 2.​ Coral-algae oes
IMPORTANT NOTES: 3.​ Clownfish relationship transmit
●​ The genitourinary tract is a dynamic environment, influenced and sea s ting
by factors like age, hormonal levels, and PH. anemone 2.​ disease
●​ Genitourinary tract flora maintains homeostasis and prevents 3.​ Bees s
infections pollinating 3.​ Lice on
●​ Flora varies across different regions and life stages flowers human
●​ Imbalance of flora contributes to various clinical conditions hair

URINARY TRACT FLORA

FORMS OF PARASITES AND HOSTS
●​ Urinary tract is sterile above the distal 1 cm of the urethra PARASITE CLASSIFICATION
●​ Anterior urethra: S. epidermidis. enterococci, and
HABITAT BASED CLASSIFICATION
diphtheroids
●​ Mycobacterium smegmatis: normal commensal in secretions
Ectoparasites: live outside the host's body (e.g., fleas, lice, ticks)
Male Genitourinary Tract Flora infest the host's body, causing discomfort and disease.
●​ Penile urethra: Gardnerella vaginalis, bacteroides, and
alpha streptococci Endoparasites
●​ Urethral flora influenced by circumcision, hygiene, and ●​ live inside the host's body (e.g., helminths, worms, protozoa)
sexual activity ●​ Infect the host's body, often leading to severe health issues.

Female Genitourinary Tract Flora ABILITY TO LIVE INDEPENDENTLY

●​ Vaginal flora varies with age, hormonal levels, and pH
○​ Infants: Lactobacillus spp. Facultative parasites
○​ Pre-puberty: Staphylococcus epidermidis. ●​ can live independently (free-living) (e.g., Toxoplasma gondii)
Streptococci, diphtheroids, and Escherichia coli ●​ Facultative parasites. adapt to different environments.
○​ Puberty: Lactobacillus acidophilus,
corynebacteria, peptostreptococcus, streptococci, Obligate parasites
Bacteroides, and staphylococci ●​ require a host to survive (e.g., Plasmodium, Leishmania)
●​ Vaginal Flora is made up of: ●​ rely solely on hosts for survival
○​ Lactobacillus acidophilus
○​ Lactobacillus reuteri MODE OF LIVING
○​ Lactobacillus rhamnosus
○​ Lactobacillus crispatus Permanent Parasites: Remain in the host from early life to maturity
○​ Lactobacillus gasseri (e.g., Plasmodium).
○​ Lactobacillus iners
○​ Lactobacillus jensenii Intermittent Parasites: Visit the host during feeding time (e.g.,
non-pathogenic parasites).
Post-Menopause Flora
●​ Vaginal pH increases due to decreased glycogen production Incidental Parasites: Occur in unusual hosts (e.g., dog tapeworm in
●​ Normal flora: similar to pre- puberty humans).
●​ Fungi like Torulopsis and Candida (10%-30%)
Transitory Parasites: Larvae develop in hosts, adults are free-living
Role of Lactobacillus (e.g., Echinococcus granulosus).
●​ Produces lactic acid, maintaining vaginal acidity
●​ Prevents gonococcal infection Erratic Parasites: Found in unusual organs (e.g., Ascaris lumbricoides
●​ Essential for vaginal health in lungs or kidneys).MODE OF LIVING

INTRODUCTION TO PARASITOLOGY HOST OF PARASITES

SYMBIOTIC RELATIONSHIP TYPES OF HOSTS
THREE TYPES OF SYMBIOSIS
Definitive Hosts
●​ Harbor adult parasite stages or sexual reproduction (e.g.,
Commensalism Mutualism Parasitism humans for Ascaris, mosquitoes for Plasmodium)
●​ one ●​ both ●​ one ●​ Examples
species species species ○​ Humans (intestinal roundworm Ascaris)
benefits, benefits benefits ○​ Mosquitoes (malaria parasite Plasmodium)
the other , the ○​ Definitive hosts support parasite reproduction.
remains other is ○​ They are essential for parasite completion of life
unaffected harmed cycle.

1.​ Human 1.​ Normal 1.​ Tapewo Intermediate Hosts

body and intestinal rms in ●​ Harbor larval parasite stages or asexual reproduction (e.g.,
normal flora human cows for Taenia saginata, humans for Plasmodium)
flora (skin, producing intestin ●​ Examples:
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○​ Cows (cysticercus larva of beef tapeworm Taenia
saginata) Foodborne Parasites
○​ Humans (malaria parasite Plasmodium) ●​ Undercooked meat (Trichinella spiralis, Taenia solium)
○​ Intermediate hosts support parasite development. ●​ Raw fish (Diphyllobothrium latum)
○​ They facilitate parasite transmission. ●​ Contaminated produce (parasitic eggs, cysts)
●​ Examples:
Reservoir Hosts ○​ Pork tapeworm (Taenia solium)
●​ Vertebrate hosts harboring parasites, serving as additional ○​ Beef tapeworm (Taenia saginata)
infection sources (eg, migratory birds for Capillaria ○​ Fish tapeworm (Diphyllobothrium latum)
philippinensis)
●​ Examples: Vector-Borne Parasites
○​ Migratory birds (Capillaria philippinensis) ●​ Mosquitoes (malaria, filariasis)
○​ Rodents (hantavirus) ●​ Sand flies (leishmaniasis)
●​ Tsetse flies (trypanosomes)
Paratenic Hosts ●​ Examples:
●​ Hosts serving as parasite transport mechanisms (e.g., insect ○​ Plasmodium (malaria)
vectors) ○​ Leishmania (leishmaniasis)
●​ Paratenic hosts facilitate parasite transmission. ○​ Trypanosoma (Chagas disease)
●​ They play a crucial role in parasite dissemination.
●​ Examples: Animal Sources
○​ Insect vectors (mosquitoes, ticks) ●​ Animals as Parasite Sources
○​ Fish (parasite transmission to humans ●​ Dogs (Echinococcus granulosus)
●​ Pigs (Taenia solium)
●​ Cows (Taenia saginata)
●​ Birds (various parasites)
●​ Examples:
○​ Hydatid cyst (Echinococcus granulosus)
○​ Trichinella spiralis

Human-to-Human Transmission
●​ Direct contact (Entamoeba histolytica)
●​ Contaminated clothing/bedding (Enterobius vermicularis)
Personal hygiene practices prevent parasite transmission.
●​ Examples:
○​ Pinworm (Enterobius vermicularis)
○​ Dwarf tapeworm (Hymenolepis nana)

Autoinfection
●​ Autoinfection occurs when parasites reinfect the same host,
often through poor hygiene or contaminated environments.
●​ Examples:
○​ Strongyloides stercoralis (threadworm): Larvae
can penetrate skin, re-infecting the host.
○​ Enterobius vermicularis (pinworm): Eggs can
contaminate hands, clothing, and bedding, leading
to re-infection.
○​ Hymenolepis nana (dwarf tapeworm): Eggs can
hatch inside the intestines, re-infecting the host.

Transmission Modes
1.​ Direct contact: Touching contaminated skin,
clothing, or bedding.
SOURCES OF PARASITIC INFECTIONS 2.​ Fecal-oral transmission: Ingesting parasites or
eggs from contaminated hands, food, or water.
Contaminated Soil and Water 3.​ Autoinoculation: Scratching or touching
●​ Human feces-contaminated soil (helminths) contaminated areas, transferring parasites to other
●​ Waterborne parasites (amoebae, flagellates, blood flukes) body parts.
●​ Contaminated environments pose significant health risks.
●​ Proper sanitation and hygiene practices are crucial. Preventing Parasitic Infections
●​ Examples: ●​ Proper hygiene practices
○​ Ascaris lumbricoides ●​ Safe food handling and cooking
○​ Trichuris trichiura ●​ Vector control measures
○​ Strongyloides stercoralis ●​ Animal handling precautions

COMMON TYPES OF WORMS IN CATS AND DOGS MODES OF PARASITE TRANSMISSION

1.​ Roundworm Fecal-Oral Transmission

2.​ Hookworm ●​ Fecal-oral transmission is the most common mode.
3.​ Tapeworm
4.​ Whipworm
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●​ Fecal-oral transmission occurs when parasites or their ●​ Prevention: Safe sex practices, proper hygiene, and avoiding
eggs/cysts are ingested through contaminated food, water, contaminated water.
hands, or surfaces.
●​ Embryonated egg stage (Ascaris lumbricoides, Trichuris Respiratory Exit
trichiura) ●​ Sputum is an exit point for parasites infecting the respiratory
●​ Examples: tract.
○​ Intestinal roundworms ●​ Parasites: Paragonimus westermani, Ascaris lumbricoides
○​ Giardias (larval stage). Exit mechanism: Parasites or eggs are
coughed up in sputum.
Foodborne Transmission ●​ Clinical significance: Sputum analysis aids diagnosis of
●​ Food containing larval stages respiratory infections.
●​ Undercooked meat and contaminated food pose risks. ●​ Prevention: Avoiding contaminated water, proper hygiene,
●​ Proper cooking and handling prevent transmission. and vector control.
●​ Trichinella spiralis
●​ Taenia solium Genital Exit
●​ Taenia saginata ●​ Vaginal discharge is an exit point for sexually transmitted
●​ Diphyllobothrium latum parasites.
●​ Parasites: Trichomonas vaginalis.
Skin Penetration ●​ Exit mechanism: Parasites are shed in vaginal discharge.
●​ Parasites actively enter through skin from freshwater. ●​ Clinical significance: Vaginal discharge analysis aids
●​ Hookworms diagnosis of sexually transmitted infections.
●​ Strongyloides ●​ Prevention: Safe sex practices, proper hygiene, and regular
●​ Blood flukes screening.

Vector-Borne Transmission PREVENTION METHODS

●​ bite of blood-sucking arthropods such as mosquitos 1.​ Proper hygiene
●​ Malaria 2.​ Safe sex practices
●​ Leishmaniasis 3.​ Cough hygiene
●​ Trypanosomiasis 4.​ Proper waste disposal
●​ Filariasis
●​ Examples: MECHANISMS OF DISEASE PRODUCTION BY PARASITES
○​ Mosquitoes
○​ Sand flies Pathogenesis and Inapparent Infection
○​ Tsetse flies Inapparent Infection
●​ Other modes of transmission: ●​ Infection without symptoms or detectable harm
○​ Inhalation (pinworm) ●​ Inapparent infections can remain undetected for long
○​ Transplacental (Toxoplasma gondii) periods.
○​ Transmammary (Strongyloides) ●​ Relapses can occur, as seen in malaria.
○​ Sexual intercourse (Trichomonas vaginalis) ●​ Examples: Malaria, intestinal helminths

PORTALS OF EXIT OF PARASITES Trauma or Physical Damage

●​ Physical damage by parasites
Major Portal of Exits in Parasites ●​ Physical damage can lead to organ dysfunction.
●​ Anus (medically important roundworms) ●​ Hookworms cause intestinal damage, while Taenia solium
●​ Urine (Trichomonas vaginalis, Strongyloides stercoralis, causes neurocysticercosis.
Schistosoma haematobium) ●​ Examples: Hookworms (intestinal damage), Taenia solium
●​ Sputum (Paragonimus westermani, Ascaris lumbricoides (neurocysticercosis)
larval stage)
●​ Vaginal discharge (Trichomonas vaginalis) Mechanisms of Disease Production By Parasites
●​ Examples: Lytic Necrosis
○​ Roundworm eggs in feces ●​ Cell destruction by parasites
○​ Trichomonas vaginalis in urine ●​ Lytic necrosis leads to cell destruction.
●​ Plasmodium destroys erythrocytes, while Trypanosoma
destroys tissues.
Fecal Exit ●​ Examples: Plasmodium (erythrocyte destruction),
●​ The anus is the primary exit point for intestinal parasites. Trypanosoma (tissue destruction)
●​ Parasites: Medically important roundworms (e.g., Ascaris ○​ Plasmodium (malaria): Destroys erythrocytes (red
lumbricoides, Enterobius vermicularis, Trichuris trichiura). blood cells), causing anemia
Exit mechanism: Parasites or eggs are shed in feces. ○​ Trypanosoma (sleeping sickness): Destroys
●​ Clinical significance: Fecal examination for parasite eggs or tissues, including brain and nervous system cells
larvae aids diagnosis. ●​ Pathogenesis:
●​ Prevention: Proper hygiene, sanitation, and handwashing ○​ Parasite invasion and replication within host cells.
○​ Cell lysis (rupture) releasing parasitic progeny.
Urinary Exit ○​ Inflammation and tissue damage.
●​ Urine is an exit point for parasites infecting the urinary tract. ●​ Consequences:
●​ Parasites: Trichomonas vaginalis, Strongyloides stercoralis, ○​ Organ dysfunction (e.g., anemia, neurological
Schistosoma haematobium. disorders).
●​ Exit mechanism: Parasites or eggs are excreted in urine. ○​ Immune response activation.
●​ Clinical significance: Urine analysis helps diagnose urinary ○​ Potential for severe complications (eg., cerebral
tract infections and parasitic infections. malaria).
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Stimulation of Host Tissue Reaction ●​ Diagnostic stage (detectable form)

●​ Host tissue reactions occur when parasites stimulate an ○​ Detectable morphologic form
immune response, leading to inflammation, fibrosis, and ○​ Diagnostic stages facilitate laboratory detection
tissue damage. ○​ Examples: Plasmodium gametocytes, hookworm
●​ Schistosoma causes granuloma formation, while Trichinella eggs
triggers inflammatory responses.

Toxic and Allergic Phenomena Others:

●​ Toxic phenomena: Parasites release toxins, damaging host ●​ Intermediate host: supports parasite development
tissues. ●​ Definitive host: harbors mature parasite
●​ Allergic phenomena: Parasite antigens trigger allergic ●​ Examples: Mosquitoes (intermediate), humans (definitive)
reactions.
●​ Examples:
○​ Anisakis (anisakiasis): Causes allergic reactions, Source of Infection
including anaphylaxis. ●​ Origin of parasite transmission
○​ Taenia saginata (beef tapeworm): Induces toxicity, ●​ Sources of infection determine transmission risk.
leading to gastrointestinal symptoms. ●​ Examples: Contaminated food, water, vectors
○​ Entamoeba histolytica (amoebiasis): Releases
toxins, causing intestinal damage. Mode of Transmission
○​ Trichinella spiralis (trichinosis): Induces allergic ●​ Fecal-oral transmission
responses, leading to muscle inflammation. ●​ Vector-borne transmission
●​ Pathogenesis: ●​ Direct contact transmission
○​ Parasite toxins or antigens stimulate host immune ●​ Examples: Malaria, hookworms, HIV
response.
○​ Release of histamine, cytokines, and chemokines. CLASSIFICATION OF PARASITES
○​ Inflammation, tissue damage, and allergic
reactions.
○​ Activation of immune cells (e.g., mast cells,
T-cells).
●​ Clinical Manifestations:
○​ Allergic reactions (e.g., hives, itching)
○​ Anaphylaxis
○​ Gastrointestinal symptoms (e.g., diarrhea,
abdominal pain)
○​ Muscle inflammation
○​ Respiratory symptoms (e.g., asthma)

Opening Pathways for Other Pathogens

●​ Parasites can facilitate opportunistic infections by
compromising the host's immune system, creating entry
points, or altering the microbiota
●​ Examples:
○​ HIV/AIDS: Immunocompromisation increases
susceptibility to opportunistic infections (e.g.,
Pneumocystis jirovecii, Toxoplasma gondii). 2.
○​ Malaria: Increases susceptibility to bacterial
co-infections (e.g., Salmonella, Streptococcus
pneumoniae).
○​ Schistosomiasis: Facilitates bacterial infections
(e.g., E. coli, Klebsiella).
○​ Hookworm: Increases susceptibility to viral
infections (e.g., HIV, HPV).

GENERAL LIFE CYCLE OF PARASITES

Components of Parasite Life Cycle

●​ Source of infection
●​ Mode of transmission
●​ Infective stage (morphologic form)
○​ Morphologic form infecting humans
○​ Infective stages initiate infection
○​ Examples: Plasmodium sporozoites, hookworm
larvae

●​ Pathogenic stage (disease- causing form)

○​ Disease-causing morphologic form
○​ Pathogenic stages cause clinical manifestations.
○​ Examples: Plasmodium trophozoites, Taenia
solium cysts
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TYPES OF PROTOZOA

Classification Based on Locomotion

●​ Flagellates (flagella)
●​ Ciliates (cilia)
●​ Amebae (pseudopodia)
●​ Sporozoans (no locomotion organs)

REPRODUCTIVE METHODS

Protozoan reproduction varies:

●​ Binary fission: simple cell division (flagellates, ciliates,
amebae)
●​ Merogony/schizogony: sporozoans undergo multiple cell
divisions: asexual reproduction where parasitic protozoan
replicates its nucleus inside a host cell and then causes cell
segmentation.
●​ Sexual recombination: sporozoans exchange genetic
material”
PROTOZOA
LIFECYCLE, DIAGNOSTIC METHODS AND EXAMPLES
Definition of Terms
●​ Infective stage refers to the stage of the parasite that
The protozoan life cycle consists of two main stages:
enters the host or the stage that is present in the
1.​ Trophozoite: active, feeding, and pathogenic
parasite's source of infection.
2.​ Cyst: dormant, non-motile, and infective
●​ Pathogenic stage refers to the stage of the parasite that
is responsible for producing the organ damage in the host
Diagnostic Methods:
leading to the clinical manifestations.
●​ Microscopic examination of body fluids, tissue specimens, or
●​ Encystation- process by which trophozoites differentiate
feces
into cyst forms.
●​ Special stains (e.g., Giemsa, Wright)
●​ Excystation- process by which cysts differentiate into
●​ Demonstration of trophozoite or cyst stages
trophozoite forms
Examples:
GENERAL PROPERTIES OF PROTOZOA ●​ Acanthamoeba (keratitis, encephalitis)
●​ Naegleria (meningitis)
●​ Trichomonas vaginalis (vaginitis)
Mode of transmission:
●​ Person-to-person
●​ Ingestion of contaminated food and water. FOUR MAJOR DIVISIONS/PHYLA
●​ Direct contact (blood) or through vector
●​ Single-celled organisms eukaryotic 1.​ Subphylum Sarcodina
●​ Spherical to oval or elongated shape a.​ Entamoeba histolytica (Intestinal and Urogenital
●​ Classification based on locomotion organ Protozoa)
●​ Not all protozoa are parasitic b.​ Acanthamoeba (free living amoeba, blood and
tissue protozoa)
2.​ Subphylum Mastigophora
a.​ Giardia lamblia (Giardianintestinalis)
b.​ Trichomonas vaginalis
c.​ Phylum Sarcomastigophora
i.​ Leishmania donovani complex
ii.​ Leishmania braziliensis complex
iii.​ Trypanosoma cruzi
iv.​ Trypanosoma Brucei gambiense and
Trypanosoma brucei rhodesiense
3.​ Phylum Ciliophora
a.​ Balantidium coli
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4.​ Subphylum Apicomplexa ●​ The drug of choice for symptomatic intestinal amoebiasis or
a.​ Plasmodium spp. hepatic abscess is metronidazole. The alternative drug
b.​ Toxoplasma gondii tinidazole is for both intestinal and extraintestinal
amoebiasis.
SUBPHYLUM SARCODINA ●​ Asymptomatic carriers should be treated with diloxanide
furoate, metronidazole, or paromomycin.
ENTAMOEBA HISTOLYTICA (INTESTINAL AND UROGENITAL
●​ Surgical drainage of amoebic liver abscess may be
PROTOZOA)
necessary if there is no improvement with medical therapy.
PROPERTIES AND LIFE CYCLE Prevention and Control
●​ Good personal hygiene. This includes proper handwashing,
●​ Intestinal and tissue ameba: the only known pathogenic especially for food handlers.
intestinal ameba. ●​ Proper waste disposal should be observed to avoid fecal
●​ Its life cycle consists of two stages-the non motile cyst contamination of water sources.
(infective stage) and the motile trophozoite (pathogenic ●​ The use of "night soil" (human feces) for fertilization of crops
stage). must be avoided.
●​ The trophozoite is found within the intestinal and extra ●​ Adequate washing and cooking of vegetables should be
intestinal lesions, and in diarrheal stools. Cysts are usually observed
found in non diarrheal, formed stools
ACANTHAMOEBA (FREE LIVING AMOEBA)
EPIDEMIOLOGY AND PATHOGENESIS INFECTION PROPERTIES AND LIFE CYCLE

●​ More common in tropical countries, especially in areas with ●​ Acanthamoeba castellani, together with Naegleria, is a minor
poor sanitation. The parasite is primarily transmitted by the protozoan pathogen but unlike Naegleria, Acanthamoeba
fecal oral route through ingestion of the cyst from usually causes infection in immunocompromised patients. It
contaminated food and water. is a free living amoeba that causes inflammation of the brain
●​ Water serves as the major source of infection of the parasite. substance and its meningeal coverings
Sexual transmission may also occur when a man has (meningoencephalitis).
unprotected sex with a woman who has vaginal amoebiasis ●​ The parasite is found widely in soil, contaminated freshwater
or through anal intercourse. lakes, and other water environments.
●​ The ingested cyst undergoes excystation in the ileum where ●​ It is able to survive in cold water. Like E. histolytica, the
it differentiates into a trophozoite (pathogenic stage). It then infective stage is the cyst while the pathogenic stage is the
proceeds to colonize the cecum and colon. trophozoite.
●​ The trophozoites may then undergo encystation and become
converted into cysts, which are then passed out with the
EPIDEMIOLOGY AND PATHOGENESIS
feces.
●​ Trophozoites are usually recovered in the feces of patients
with active infection (diarrheic stools) while cysts are found in ●​ There are two ways by which the parasite can be
formed, non diarrheic stools. acquired-through aspiration or nasal inhalation or through
●​ The trophozoites of E. histolytica secrete enzymes that direct invasion in the eye.
cause local necrosis producing the typical "flask shaped" ●​ People acquire the infection usually while swimming in
ulcer associated with the parasite. Invasion of the portal contaminated water. Inhalation of the cysts from dust has
circulation may occur leading to the development of abscess also been shown to occur. The trophozoites enter through
in the liver. the lower respiratory tract or through ulcers in the mucosa or
skin.
●​ The parasite then migrates through the blood stream and
DISEASE
invade the central nervous system. Eye infection with
Acanthamoeba occurs primarily in patients who wear contact
Amoebiasis lenses. The parasite has been recovered from contact
●​ Acute intestinal amoebiasis - presents as bloody, mucus lenses, lens cases, and contact lens solutions.
containing diarrhea (dysentery) accompanied by lower ●​ Tap water contaminated with the parasite is the source of
abdominal discomfort, flatulence (release of gas), and infection for contact lens users
tenesmus (feeling of incomplete defecation).
●​ Chronic infection: occasional diarrhea, weight loss, and
fatigue. In some patients, a lesion called an ameboma may
form in the cecum or in the rectosigmoid area of the colon,
DISEASES, TREATMENT, PREVENTION AND CONTROL
which may be mistaken for a malignant tumor in the colon.
●​ Extraintestinal amoebiasis- occurs when the parasite
enters the circulatory system. The most common Disease
extraintestinal form of amoebiasis is the amoebic liver Granulomatous amebic encephalitis
abscess. This is characterized by right upper quadrant pain, ●​ infection occurs primarily in immunocompromised
weight loss, fever, and a tender, enlarged liver. Abscess individuals. The parasite produces a granulomatous amebic
found on the right lobe of the liver may penetrate the encephalitis and brain abscesses in immune compromised
diaphragm and cause lung disease (amoebic pneumonitis). patients. Symptoms develop slowly and may include
Other organs that may become infected include the headache, seizures, stineck, nausea, and vomiting. The
pericardium, spleen, skin, and brain (meningoencephalitis) brain lesions may contain both the trophozoites and the
cysts. In rare instances, the parasite may spread and
Laboratory Diagnosis produce granulomatous lesions in the kidneys, pancreas,
●​ Diagnosis of intestinal amoebiasis is confirmed by the finding prostate, and uterus.
of trophozoites in diarrheic stools or cysts in formed stools.
Keratitis
Treatment
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●​ infection of the cornea of the eye. Symptoms include severe out the parasite with the feces which can then contaminate
eye pain and vision problems. Loss of vision may occur due water.
to perforation of the cornea.
Giardiasis (Traveler's diarrhea)
Laboratory Diagnosis ●​ infection is characterized by a non bloody, foul smelling
●​ Diagnosis is made by finding of both trophozoites and cysts diarrhea accompanied by nausea, loss of appetite,
in the cerebrospinal fluid as well as brain tissue and corneal flatulence, and abdominal cramps.
scrapings. ●​ The symptoms may persist for weeks or months.
●​ Histologic examination of corneal scrapings may also be Malabsorption of fat may lead to the presence of fat in the
done. Calcofluor white, a stain usually used to demonstrate stool (steatorrhea).
fungi, may be used to demonstrate the parasite in corneal ●​ Manifestations may vary depending on which nutrient
scraping specimens. becomes deficient due to the resulting malabsorption. These
Treatment may include deficiencies in fat soluble vitamins, folic acid,
●​ Pentamidine, Ketoconazole, or Flucytosine may be effective and proteins.
in the treatment of infection.
●​ For eye and skin involvement, topical miconazole, Laboratory Diagnosis
chlorhexidine, itraconazole, ketoconazole, rifampicin, or ●​ Diagnosis is made by the demonstration of the cyst or
propamidine may be used. trophozoite (or both) in diarrheic stools. Only cysts are
●​ Propamidine has been documented to have the best isolated from the stools of asymptomatic carriers.
success record. ●​ If microscopic examination of the stool is negative, string test
Prevention and Control may be performed which consists of making the patient
●​ Infection can be prevented through adequate boiling of swallow a weighted piece of string until it reaches the
water. duodenum.
●​ Regular disinfection of contact lenses is also advised. ●​ The trophozoites adhere to the string and can be visualized
Contact lens wearers are also advised to avoid using after withdrawal of the string.
homemade non sterile saline solutions.
Treatment
SUBPHYLUM MASTIGOPHORA ●​ As per recommendation of the Centers for Disease Control
and Prevention in the United States, the primary choice of
GIARDIA LAMBLIA (GIARDIANINTESTINALIS)
treatments for G. lamblia infection are metronidazole,
PROPERTIES AND LIFE CYCLE tinidazole, and nitazoxanide.

●​ Giardia lamblia is an intestinal protozoan that was initially Prevention and Control
known as Cercomonas intestinalis. ●​ avoidance of fecal contamination of water supplies through
●​ The parasite also exists in a cyst form and a trophozoite proper waste disposal.
form. The trophozoite is pear shaped or teardrop shaped ●​ Drinking water should be boiled, filtered, or iodine treated
with four pairs of flagella and has a motility likened to a especially in endemic areas.
falling leaf. ●​ Improvement of personal hygiene such as proper
●​ possesses a sucking disc which the parasite uses to attach handwashing is also recommended
itself to the intestinal villi of the infected human.
●​ The cyst is typically oval and thick walled with four nuclei. TRICHOMONAS VAGINALIS
●​ It divides through binary fission. Each cyst gives rise to two
PROPERTIES AND LIFE CYCLE
trophozoites during excystation in the intestinal tract.
●​ The parasite is a pear shaped organism with a central
EPIDEMIOLOGY AND PATHOGENESIS
nucleus, four anterior flagella, and an undulating membrane.
It exists only in the trophozoite form (infective and
●​ has a worldwide distribution through contaminated water pathogenic)
sources.
●​ About 50% of infected individuals do not present with
EPIDEMIOLOGY AND PATHOGENESIS
symptoms and serve as carriers. Other than humans, many
species of mammals may act as reservoirs. The infection is
also common among individuals engaging in oral anal ●​ Trichomonas vaginalis is not an intestinal pathogen.
contact. ●​ It causes urogenital infections and the main mode of
●​ The parasite is primarily transmitted through ingestion of the transmission is through sexual intercourse.
cyst from fecally contaminated water and food. The cyst ●​ It has been isolated from the urethra and vagina of infected
enters the stomach and is stimulated by the gastric acid to women as well as the urethra and prostate gland of infected
undergo excystation in the duodenum. The trophozoites then men.
attach themselves to the duodenal mucosa through the ●​ Infection is highest among sexually active women in their
sucking disks. Damage to the intestines is not due to thirties and lowest in post menopausal women.
invasion of the parasite but because of inflammation of the ●​ Occasionally the parasite may be transmitted through toilet
duodenal mucosa, leading to diarrhea with malabsorption of articles and clothing of infected individuals.
fat and proteins. The trophozoites may also infect the ●​ Infants may be infected as they pass through the infected
common bile duct and gallbladder. birth canal during delivery.
●​ The parasite invades the vaginal mucosa of infected women,
where they multiply through binary fission. The trophozoites
DISEASES, TREATMENT, PREVENTION AND CONTROL
feed on local bacteria and leukocytes. In men, the most
common infection site is the prostate gland and the urethral
Asymptomatic carrier state epithelium.
●​ infection with the parasite is usually completely
asymptomatic. The infected individual unknowingly passes
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DISEASES, TREATMENT, PREVENTION AND CONTROL ●​ Massive enlargement of the spleen (splenomegaly) is
characteristic, leading to hypersplenism and resulting
Disease anemia.
Trichomoniasis Infection in men ●​ Hepatomegaly or enlargement of the liver also occurs. In
●​ usually asymptomatic and men serve as the reservoir for light skinned patients, hyperpigmentation of the skin may be
infection in women. In men who develop symptoms, the seen (kala azar means "black sickness" or "black fever").
manifestations are those related to development of ●​ Involvement of the bone marrow leads to destruction of the
prostatitis(inflammation of the prostate), urethritis (manifest cellular components with the corresponding clinical effects-
as discharge), and other urinary tract involvement. Persistent anemia due to destruction of red blood cells, bleeding
or recurring urethritis is the most common symptomatic form tendencies due to reduction of platelets (thrombocytopenia),
of the infection. and increased risk for secondary infection because of
reduction of white blood cell (leukopenia).
Infection in women ●​ Glomerulonephritis or inflammation of the glomeruli of the
●​ also asymptomatic, some women may present with scant, kidney may also occur. The disease may be fatal if
watery vaginal discharge. In more severe cases, the untreated.
discharge may be foul smelling and greenish yellow in color.
This may be accompanied by itching (pruritus) and a burning Laboratory Diagnosis
sensation in the vagina. ●​ The diagnosis is made by finding of amastigotes in a bone
marrow, spleen, or lymph node biopsy preparation.
Infection in infants ●​ Serologic testing can be done (very high concentration of
●​ occurs as the infant passes through the infected birth canal IgG is indicative of infection)
of the mother during vaginal delivery. The infected infants ●​ Skin test is avalaible using a crude homogenate of
may manifest conjunctivitis or respiratory infection. promastigotes (leishmanin) as antigen

Laboratory Diagnosis Treatment

●​ Diagnosis is made by the finding of the characteristic ●​ The present recommended drug of choice is liposomal
trophozoite in a wet mount of vaginal or prostatic secretions, amphotericin B (Ambisome). Sodium stibogluconate has also
urine, and urethral discharges. been found to be effective but the development of resistance
Treatment may occur.
●​ The drug of choice for treatment of trichomoniasis is
metronidazole. All sexual partners of an individual with the Prevention and Control
infection must be simultaneously treated to prevent "ping ●​ Control of the vector population is important in the prevention
pong" infections. of infection.
Prevention and Control ●​ The use of insect repellents, protective clothing, and
●​ The best way to prevent infection is to practice safe sex. The installation of screens may be helpful.
use of condoms can limit the transmission of the parasite. ●​ Prompt treatment of infected humans is essential to help halt
Health and sex education are important. Maintenance of the the spread of the disease.
acidic pH of the vagina may also be helpful.
LEISHMANIA BRAZILIENSIS COMPLEX
PHYLUM SARCOMASTIGOPHORA
IMPORTANT PROPERTIES
LEISHMANIA DONOVANI COMPLEX
●​ L. braziliensisis the causative agent of mucocutaneous
leishmaniasis which involves skin, cartilage, and mucous
IMPORTANT PROPERTIES membranes.
L. donovani is the causative agent of visceral leishmaniasis (also ●​ Infection with L. braziliensis occurs most commonly in Brazil
known as kalaazar or dum dum fever). and Central America, primarily in construction and forestry
●​ The complex consists of (1) L. donovani chagasi which is workers.
mainly seen in Central America (mainly Mexico, West Indies, ●​ The complex consists of L. panamensis (Panama and
and South America) and is transmitted by the Lutzomyia Colombia), L. peruviana (Peruvian Andes), and L.
sandfly; guyanensis (The Guianas, parts of Brazil and Venezuela).
●​ L. donovani donovani found in parts of Africa and Asia ●​ Infection is transmitted by sand flies (Lutzomyia and
(Thailand, India, China, Burma, and East Pakistan) and is Psychodopigus)through skin bite. The promastigotes invade
transmitted by the Phlebotomus sandfly; and the reticuloendothelial cells where they transform into
●​ L. donovani infantum, also transmitted by the Phlebotomus amastigotes (diagnostic stage).
sandfly and is found mainly in Mediterranean Europe, Near ●​ Reproduction of the amastigotes result in tissue destruction.
East, and Africa. The promastigote is injected into the human ●​ The amastigotes are taken up by the vector during a blood
host through bite of the sand fly. After entry into the host, it meal and are transformed into promastigotes.
loses its flagella, is engulfed by macrophages, and
transforms into amastigotes. The organs of the DISEASES, TREATMENT, PREVENTION AND CONTROL
reticuloendothelial system (liver, spleen, and bonemarrow)
are the most severely affected Disease
Mucocutaneous Leishmaniasis
DISEASES, TREATMENT, PREVENTION AND CONTROL ●​ also called espundia, begins with a papule at the site of
insect bite, then forms metastatic lesions, usually at the
Disease mucocutaneous junction of the nose and mouth. Disfiguring
Visceral Leishmaniasis granulomatous, ulcerating lesions destroy the nasal cartilage
●​ (Kala azar, DumdumFever) After an incubation period of 2 but not the adjacent bone. Death can occur from secondary
weeks to 18 months, the disease begins with intermittent infections.
fever, weakness, and weight loss.
Laboratory Diagnosis
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●​ Diagnosis is confirmed by demonstration of amastigotes in Laboratory Diagnosis
clinical specimens. Ulcer biopsy specimens are used for the ●​ Acute disease is diagnosed by the finding of trypomastigotes
diagnosis of mucocutaneous leishmaniasis. in thick or thin films of the patient's blood. Other diagnostic
●​ Microscopic examination of Giemsa stained ulcer biopsy methods that can be used include bone marrow aspiration,
specimens reveals the diagnostic amastigotes. muscle biopsy, culture on special medium, and
●​ Culture of infected material may show the promastigotes. xenodiagnosis.
●​ Serologic testing may also be done ●​ Xenodiagnosis entails allowing an uninfected laboratory
Treatment raised reduviid bug to feed on an infected patient. After
●​ At present, the most widely used drug for the treatment of several weeks, the intestinal contents of the bug are
mucocutaneous leishmaniasis is sodium stibogluconate. examined for the presence of the parasite.
●​ Alternative drugs include liposomal Amphotericin B and oral
antifungal drugs (fluconazole, ketoconazole, and Treatment
itraconazole). ●​ The drugs of choice for treatment are benznidazole and
Prevention and Control nifurtimox but these are less effective during the chronic
●​ The most important preventive measure is the control of the phase of the disease. Alternative agents are allopurinol and
insect vector. ketoconazole
●​ Protection from sand fly bites by using netting, window
screens, protective clothing, and insect repellents. Prevention and Control Prevention
●​ Prompt treatment can also help prevent spread of the ●​ involves protection from the bite of the reduviid bug,
disease. improvement of housing conditions, and insect control.
●​ Education regarding the disease and its transmission
TRYPANOSOMA CRUZI
TRYPANOSOMABRUCEI GAMBIENSE AND TRYPANOMA BRUCEI
PROPERTIES AND LIFE CYCLE RHODESIENSE
●​ The parasite is found primarily in South and Central America
and is transmitted by the bite of the reduviid or triatomid bud PROPERTIES AND LIFE CYCLE
(Triatomaor "cone nose" bug or "kissing bug"). ●​ The two species are similar in morphology and life cycle.
●​ It is usually transferred to a human host when the feces of Their life cycles involve the tsetse fly (Glossina) as the
the bug containing the infective trypomastigotesis deposited vector. Humans are the reservoir for T. brucei gambiense,
near the bite site. while domestic animals(especially cattle) and wild animals
●​ The feces are then introduced into the bite site when the serve as the reservoir for T. brucei rhodesiense.
host scratches the bite area. ●​ The infective and pathogenic stage is the trypomastigote.
●​ Other routes of transmission include blood transfusion, The trypomastigotes spread from the skin to the blood then
sexual intercourse, transplacental transmission, and through to the lymph nodes and the brain.
the mucous membranes when the bite site is near the eye or ●​ T. gambiense infection (West African or Gambian Sleeping
mouth. Humans and animals (domestic cats and dogs, and Sickness) is chronic while T. rhodesiense infection (East
wild species such as armadillo, raccoon, and rat)serve as African or Rhodesian Sleeping Sickness)is more rapidly
reservoir hosts fatal. The disease is endemic in sub Saharan Africa which is
●​ The trypomastigotes invade the surrounding cells and the natural habitat of the tsetse fly. T. gambiense causes
transform into amastigotes. The amastigotes then reproduce disease along the water courses in West Africa while T.
leading to destruction of host cells. These are then rhodesiense causes disease mostly in the arid regions of
transformed back into trypomastigotes, which invade the East Africa.
blood, penetrate other cells in the body, and transform back
into amastigotes Different cell types may be affected. DISEASES, TREATMENT, PREVENTION AND CONTROL
However glial cells, reticuloendothelial cells, and especially
myocardial cells are the most frequently affected. Disease
●​ The disease is primarily seen in rural areas because the African Sleeping Sickness
reduviid bug lives in the walls of rural huts and feeds at night. ●​ The initial lesion is an indurated ulcer called chancre at the
site of the insect bite. Intermittent weekly fever and
DISEASES, TREATMENT, PREVENTION AND CONTROL lymphadenopathy then develop. Enlargement of the
posterior cervical lymph nodes (Winterbottom'ssign) is
Disease commonly seen. Other manifestations seen during this stage
Chagas Disease (American Trypanosomiasis) include red rash accompanied by pruritus, localized edema,
●​ The acute phase of the disease begins with a nodule and a delayed pain sensation (Kerandel'ssign).
(chagoma) near the bite site and unilateral swelling of the
eyelid with conjunctivitis (Romana's sign). Encephalitis
●​ The eyelid swelling may be due to the bug feces being ●​ is characterized by headache, insomnia, and mood changes.
accidentally rubbed into the eye. This is accompanied by Muscle tremors, slurred speech, and apathy follow,
fever, chills, malaise, myalgia, and fatigue. progressing to somnolence (sleeping sickness) and coma.
●​ rapid and fulminating disease may follow with the parasite
Hepatosplenomegaly, enlargement of lymph nodes spreading in the blood. Death is seen usually within 9-12
(lymphadenopathy) months following infection in untreated patients
●​ and myocarditis with cardiac arrhythmia characterize the
chronic phase of Chagas disease. Laboratory Diagnosis
●​ Cardiac muscle is the most frequently and most severely ●​ Microscopic examination of Giemsa stained slides of the
affected tissue. blood, lymph node aspirations and CSF will reveal the
●​ CNS involvement may also be seen in the form of trypomastigotes during the early stages of the disease.
meningoencephalitis and cysts. ●​ Aspiration of the chancre or enlarged lymph nodes may also
●​ Death may occur due to cardiac failure and arrhythmias. reveal the parasites.
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●​ Serologic tests can also be helpful as well as detection of the ●​ Diagnosis is based on the finding of trophozoites and cysts
presence of IgM and proteins in the CSF of patients. The in the stool specimen.
presence in the serum and/or CSF of IgM is considered ●​ Due to its large size, the parasite can be readily detected in
diagnostic. fresh, wet microscopic preparations.
Treatment
Treatment ●​ The current recommended treatment of patients with
●​ Several drugs are available for the treatment of both East balantidiasis involves two and drugs-oxytetracycline
African and West African Sleeping Sickness, which include iodoquinol. Metronidazole may also be used as alternative to
melarsoprol, suramin, pentamidine, and eflornithine (Zeibig, treat infected patients.
2013) Prevention and Control
●​ Preventive measures are similar to those for amoebiasis.
Prevention and Control ●​ These include maintenance of sanitary hygiene, proper
●​ Preventive measures involve protection against the bite of disposal of pig feces, and boiling of drinking water.
the fly. Use of netting and protective clothing are
recommended. Use of fly traps and insecticides may be SUBPHYLUM APICOMPLEXA
helpful. Clearing the forest around the villages are also
PLASMODIUM SPP.
helpful measures.
PROPERTIES AND LIFE CYCLE
PHYLUM CILIOPHORA
●​ Malaria is caused by five plasmodia species:
BALANTIDIUM COLI
○​ Plasmodium vivax
PROPERTIES AND LIFE CYCLE ○​ Plasmodium malariae
○​ Plasmodium ovale
●​ Balantidium coli is morphologically more complex than E. ○​ Plasmodium knowlesi
histolytica. It has a primitive mouth called a cytostome, a ○​ Plasmodium falciparum
nucleus, food vacuoles, and a pair of contractile vacuoles. ●​ The vector and definitive host is the female Anopheles
●​ The infective stage is the cyst and the pathogenic stage is mosquito.
the trophozoite, which invade Protozoa the mucosal lining of ●​ The sexual cycle (sporogony) occurs primarily in
the terminal ileum, cecum, and colon. mosquitoes, and the
●​ It is the largest protozoan to infect humans. The trophozoites ●​ asexual cycle (schizogony) occurs in humans (intermediate
typically exhibit a rotary, boring motility (through cilia) and hosts).
contain two nuclei (a small dot like micro nucleus adjacent to ●​ The infective stage is the sporozoite from the saliva of the
a kidney bean shaped macronucleus). The cyst also biting
contains two nuclei although the micro nucleus may not be ●​ mosquito, which is taken up by the liver cells. This is called
readily observable. the exoerythrocytic phase.
●​ Multiplication and differentiation of sporozoites into
EPIDEMIOLOGY AND PATHOGENESIS merozoites occur during this stage. P. vivax and P. ovale
produce a latent form (called hypnozoite or sleeping form) in
●​ The parasite has a world wide distribution. The most the liver, which is the cause of the relapse or recrudescence
common and most important reservoir is the pig. Monkeys seen in vivax and ovale malaria.
may occasionally act as reservoirs of the parasite. ●​ Merozoites (pathogenic stage) are released from liver cells
●​ The main source of infection is water contaminated by pig and infect the red blood cells.
feces and the mode of transmission is through the fecal oral ●​ The parasite’s life cycle now enters the erythrocytic phase.
route. Person to person transmission via food handlers has These merozoites multiply and are eventually released to
been implicated in outbreaks. infect other red blood cells.
●​ The cysts are found in contaminated water, which when ●​ Some merozoites then develop into
ingested, undergoes excystation in the small intestines. microgametophytes(male gametocytes) and
From there, the trophozoites travel to the large intestines microgametocytes(female gametocytes). The gametocytes
where they produce ulcers similar to those seen in containing red blood cells are ingested by the mosquito
amoebiasis. during feeding. Sexual reproduction then ensues.

DISEASES, TREATMENT, PREVENTION AND CONTROL EPIDEMIOLOGY AND PATHOGENESIS

Disease ●​ Infection with plasmodia occurs worldwide. It occurs primarily

Balantidiasis in tropical and subtropical areas, especially in Asia, Africa,
●​ Most infected individuals are asymptomatic. A dysenteric and Central and South America.
type of diarrhea resembling amebic dysentery may occur in ●​ Sixty nine percent (69%) of cases in the Philippines are due
patients with high parasite load. to Plasmodium falciparum while the remaining 31% are due
to Plasmodium vivax (World Malaria Report 2013).
Acute infections ●​ The primary vector is Anopheles flavirostris, which breeds in
●​ may manifest with liquid stools containing pus, blood, and clear, slow flowing streams near foot hills and forests.
mucus while chronic infections may manifest with a tender ●​ In the 2014 Asia Pacific Malaria Elimination Network
colon, anemia, wasting, and alternating diarrhea and (APMEN) VI held in Makati City, Philippines, then Secretary
constipation. of Health Doctor Enrique Ona reported an 83% reduction in
malaria cases from 2005 to 2013, with a 92% decrease in
Extraintestinal infection malarial deaths.
●​ is rare and may involve the liver, lungs, mesenteric nodes, ●​ The main mode of transmission of malaria is the bite of the
and urogenital tract. female mosquito vector.
●​ However, the parasite can also be transmitted through blood
Laboratory Diagnosis transfusion (transfusion malaria), intravenous drug abuse
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with sharing of IV needles(“main line malaria”), and artesunate, artemether lumafantrine, atovaquone proguanil,
transplacental transmission(congenital malaria). quinine, quinidine, pyrimethamine sulfadoxine (Fansidar),
●​ Most of the pathologic findings result from the destruction of and doxycycline (Murray, 2014).
red blood cells. P. falciparum and P. knowlesi can infect both ●​ Artemisin based combination therapies(ACTs) are now
young and old red blood cells leading to high levels of recommended for uncomplicated malaria and for chloroquine
parasitemia. resistant vivax malaria.
●​ P. vivax and P. ovale mainly infects young red blood cells, ●​ Artesunate is the drug of choice for severe malaria, in
while P. malariae infects old red blood cells. Plasmodium combination with either amodiaquine, mefloquine,or
knowlesi is a natural parasite of macaque monkeys sulfadoxine pyrimethamine.
throughout the Southeast Asia region. Cases of infection
have been noted in Thailand, Singapore,Brunei, Indonesia, Prevention and Control
Myanmar, Vietnam, and the Philippines(Murray, 2014). ●​ Chemoprophylaxis of malaria for travellers to endemic areas
●​ The red blood cells infected by P. knowlesi have normal consists of mefloquine or doxycycline. Travelers to areas
morphology. All developmental stages of the parasite may be where the other plasmodia are found should take
seen in the peripheral blood chloroquine starting two weeks before arrival and continued
for 6 weeks after departure, followed by a 2 week course of
DISEASES, TREATMENT, PREVENTION AND CONTROL primaquine if exposure was high.
●​ Other preventive measures include avoidance of the bite of
Disease the vector through the use of mosquito netting, window
Malaria Paroxysms of malaria are divided into three stages: screens, protective clothing, and insect repellants.
1.​ cold stage ●​ The mosquitoes usually bite from dusk to dawn, so
2.​ hot stage protection is important during the night. Reduction of
3.​ sweating stage. mosquito population is also helpful, including the use of
These paroxysms are considered partially as allergic responses to the insecticide sprays, as well as drainage of stagnant water in
schizonts and to the antigens released following the release of the swamps and ditches.
merozoites.
●​ A malarial paroxysm presents with abrupt onset of chills TOXOPLASMA GONDII
(rigors) accompanied by headache, muscle pain (myalgia), PROPERTIES AND LIFE CYCLE
and joint pains (arthralgia).This stage lasts for approximately
10–15 minutes or longer. ●​ The definitive host of the parasite is the domestic cat or other
●​ Spiking fever lasting 2–6 hours follows, reaching up to 41 °C, felines while humans and other mammals serve as the
accompanied by shaking chills, nausea, vomiting, and intermediate hosts.
abdominal pain. This is then followed by drenching sweats. ●​ The parasite develops in the intestinal cells of the cat and
●​ The timing of the fever cycle is 72 hours for P. malariae, in passes to the tissues through the bloodstream. These are
which symptoms recur every 4th day (quartan malaria). then passed in the cat’s feces and mature into infective
Malaria caused by P. vivax, P. ovale, and P. falciparum recur oocysts in the external environment.
every 3rd day (tertian malaria). ●​ Infection in humans begins with the ingestion of oocysts
●​ P. falciparum causes malignant tertian malaria since it (infective form) in undercooked meat or from contact with cat
causes severe infection which is potentially life threatening feces.
due to extensive brain (cerebral malaria) and kidney ●​ In the small intestines, the oocysts rupture into trophozoites
damage. (tachyzoitesor bradyzoites). Tachyzoites are the rapidly
●​ The dark color of the patient’s urine is due to kidney damage multiplying forms responsible for the initial infection while
giving rise to the term “black water fever.” bradyzoites are shorter, slow growing forms seen in chronic
●​ P. vivax and P. ovale cause benign tertian malaria that is infections.
characterized by relapses that can occur up to several years
after the initial illness and is due to the latent hypnozoites in
EPIDEMIOLOGY AND PATHOGENESIS
the liver.

Laboratory Diagnosis ●​ Infection by T. gondii occurs worldwide. Infection is usually

●​ The diagnosis of malaria is based on examination of Giemsa sporadic but outbreaks associated with ingestion of raw meat
stained or Wright stained thick and thin smears of the blood. or contaminated water can occur.
The thick blood smears are used for screening purposes ●​ Individuals who are severely immunocompromised are more
while the thin blood smears are used to differentiate the likely to develop severe disease.
various Plasmodium species. ●​ The parasite can be transmitted in two ways: (1) ingestion of
●​ Characteristic trophozoites will be seen within the infected improperly cooked meat of animals that serve as
red blood cells. P. falciparum will show characteristic intermediate hosts, and (2) ingestion of oocyst from
crescent shaped or banana shaped gametocytes. contaminated water. Transplacental transmission may occur,
●​ Infection with P. falciparum is highly considered if there are with severe consequences on the fetus. Sharing of needles
> 10 infected red blood cells consisting only of ring forms. by IV drug abusers as well as blood transfusion are less
●​ P. knowlesi should be suspected if there is a higher average common modes of transmission of the parasite
merozoite count of 16/red blood cell as compared to
10–12/red blood cell of P. malariae. DISEASES, TREATMENT, PREVENTION AND CONTROL

Treatment Disease
●​ The drugs of choice for acute malaria infection are 1.​ Infection in immunocompetent individuals – usually
chloroquine or parenteralquinine. However, chloroquine does asymptomatic. Acute infection may manifest non specific
not affect the hypnozoites of P. vivax and P. ovale. symptoms such as chills, fever, headache, and fatigue. This
●​ For vivax and ovale malaria, primaquine is given to destroy may be accompanied by inflammation of lymph nodes
the hypnozoites. For chloroquine resistant strains of P. (lymphadenitis).Chronic infection may manifest with
falciparum other agents may be used including mefloquine +
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lymphadenitis, hepatitis, myocarditis, and encephalomyelitis. ●​ Capillaria, the major source of infection for the intestinal
Chorioretinitis leading to blindness may also occur nematodes is soil contaminated with human feces.
2.​ Congenital infection – occursin infants born to mothers ●​ Ascaris, Enterobius, and Trichuris are transmitted through
who were infected during pregnancy.The manifestationsvary ingestion of the embryonated ova.
depending on when the infection was acquired. ●​ Necator, Ancylostoma, and Strongyloides are transmitted by
a.​ Infection during the first trimester of pregnancymay skin penetration.
result to miscarriage,stillbirth, or severe infection ●​ Capillaria philippinens is, transmitted by ingestion of
(encephalitis,microcephaly,hydrocephalus,mentalr undercooked or raw infected fish, is endemic in certain areas
etardation, pneumonia).If the infant acquiresthe in the Philippines, particularly Northern Luzon.
b.​ infection during the last trimester,symptomsmay ●​ blood tissue nematodes in the Philippines: filarial worms
not develop until monthsto years after delivery. Wuchereria and Brugia. The filarial worms, found in specific
The most common manifestation is chorioretinitis locales in the Philippines, are transmitted by the bite from
with or without blindness. arthropod vectors (usually mosquitoes).
3.​ Infection in immunocompromised hosts – usually ●​ The muscle worm, Trichinella is an intestinal tissue
manifest with neurologic symptoms similar to patients with nematode acquired by ingesting improperly cooked or raw
diffuse encephalopathy,meningoencephalitis,or brain tumors. pork meat containing the worm’s encysted larva.
Reactivation of latent toxoplasma infection is common. Other
Sites of infection include the lungs, eye, and testes.

Laboratory Diagnosis
●​ Demonstration of high antibody titers through
immunofluorescence assay is essential for the diagnosis of
toxoplasma infection.
●​ Microscopic examination of Giemsa stained preparations will
show the crescent shaped trophozoites during the acute
infection.
●​ Cysts may be seen in the tissues.
●​ Prenatal diagnosis can be done through ultrasonography
and amniocentesis with PCR analysis of the amniotic fluid
(method of choice).

Treatment
●​ Infection in immune competent hosts is usually self limiting
and does not require specific therapy. The regimen of choice
for immunocompromised patients, especially those with
AIDS, is initial high dose pyrimethamine plus sulfadiazine
given for an indefinite period.
●​ Alternative regimen for those who develop symptoms of drug
toxicity is clindamycin plus pyrimethamine.
●​ For pregnant women, clindamycin or spiramycin may be
given.

Prevention and Control

●​ The most effective preventive measure is through adequate
cooking of meat.
●​ Pregnant women should refrain from eating undercooked
meat and should avoid contact with cats and refrain from
handling litter boxes.
●​ Cats should not be fed raw meat

NEMATODES
GENERAL PROPERTIES OF NEMATODES
THREE GROUPS OF NEMATODES
Nematodes
●​ Nematodes or roundworms are unsegmented, bilaterally
symmetrical worms with elongated, cylindrical bodies. 1.​ Intestinal nematodes
●​ The life cycle of these parasites consists of three stages— a.​ Ascaris lumbricoides (large intestinal roundworm)
embryonated egg or ova, embryonated larva, and adult b.​ Enterobius vermicularis (pinworm, seat worm)
worms. c.​ Trichuris trichiura (whipworm)
●​ body covering is called the cuticle. d.​ Ancylostoma duodenale (old world hookworm) and
●​ have separate sexes, with the female worm being larger than Necator americanus (new world hookworm)
the male worm. e.​ Strongloides stercoralis (LThreadworm)
●​ Most patients with nematode infection are asymptomatic. f.​ Capillaria Philippinensis (Pudocworm)
●​ The nematodes may be divided into three groups based on
their primary location in the body—intestinal nematodes, the 2.​ Intestinal tissue nematodes
intestinal tissue nematodes, and the blood tissue a.​ Wuchereria bancrofti (Bancroft's filarial worm) and
nematodes. Brugia Malayi (Malayan Filarial worm)
●​ The intestinal nematodes important in the Philippines include
Enterobius, Ascaris, Trichuris, Necator, Ancylostoma, 3.​ Blood tissue nematodes
Strongyloides, and Capillaria. a.​ Trichinella spiralis (Muscleworm, Trichina)
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Laboratory Diagnosis
INTESTINAL NEMATODES ●​ Diagnosis is established by finding of the eggs in a stool
specimen.
ASCARIS LUMBRICOIDES LARGE INTESTINAL ROUNDWORM
●​ In cases of heavy worm burden, the adult worm may be
PROPERTIES AND LIFE CYCLE present in the stool or be regurgitated.
●​ Larvae may be recovered from the sputum during the
Ascaris lumbricoides is the largest intestinal roundworm infection pulmonary phase of the disease.
among humans.
●​ The adult worm is creamy white in color with an outer Treatment
covering of cuticle. ●​ Drugs that have been proven effective are mebendazole,
●​ Humans acquire infection through ingestion of food or water albendazole, and pyrantel pamoate
contaminated with human feces containing the infective
embryonated ova. Prevention and Control
●​ Upon entry into the small intestines, larvae are released from ●​ proper disposal of human feces,
the eggs, penetrate the intestinal wall, enter the blood to go ●​ health education of the population,
initially to the liver, and finally localize to the lung. ●​ Improved personal hygiene.
●​ In the lungs, the larvae gain entrance into the air sacs and ●​ avoid using human feces as fertilizer.
migrate into the bronchioles. ●​ A program of mass chemotherapy is recommended
●​ The larvae are then coughed up with the sputum which is especially for children and in areas with high incidence of
swallowed thereby returning the worm to the intestines. parasitism.
●​ The larvae mature into adult worms in the small intestines,
where they lay their eggs that are eliminated with the feces. ENTEROBIUS VERMICULARIS (PINWORM, SEATWORM)
●​ The eggs are capable of surviving in soil, sewage, or water
PROPERTIES AND LIFE CYCLE
for several years.
●​ The egg of E. vermicularis is typically oval and flat on one
EPIDEMIOLOGY AND PATHOGENESIS
side. The adult worms are small and yellowish white in color.
The common name pinworm is based on the appearance of
●​ Ascaris infection is considered as the most common a clear, pointed tail of the adult female that resembles a
helminth infection worldwide. pinhead.
●​ The parasites are more common in areas characterized by ●​ Humans acquire the infection through ingestion of the eggs
warm climates and poor sanitation. of the worm. As it reaches the small intestines, larvae
●​ Areas that use human feces as fertilizer or where children emerge from the eggs and mature into adult worms in the
defecate directly on the ground are highly susceptible to large intestines.
infection with the parasite. ●​ Once the female becomes impregnated, it migrates to the
●​ Young children are the most affected when they play in soil perianal region where egg laying occurs, usually at night.
contaminated with human feces. ●​ The infective eggs may dislodge from the body due in part to
●​ Adult worms produce little damage in the intestines. intense scratching of the anal area, and deposit in dust, soil,
However, since the adult worms obtain nourishment from linens, and clothing. Some infective pinworm eggs may
ingested food, they may contribute to development of migrate back into the host body rather than be dislodged
malnutrition. leading to a retro infection.
●​ The major damage occurs during larval migration to the ●​ Autoinfection occurs as a result of hand to mouth
lungs where inflammation occurs transmission. It is also possible to ingest the eggs through
breathing them in, as the eggs are so small.
DISEASES, TREATMENT, PREVENTION AND CONTROL
EPIDEMIOLOGY AND PATHOGENESIS
Disease: Ascariasis
●​ Asymptomatic infection is usually seen with low worm ●​ Pinworm infection occurs worldwide, especially in temperate
burden. regions.
●​ Symptomatic infection occurs due to migration of the ●​ People at risk for pinworm infection are children, their
parasite through the host. caretakers, institutionalized persons, and those in unsanitary
●​ During larval migration, the larvae may induce allergic and crowded living conditions.
reactions, manifesting as asthmatic attacks accompanied by ●​ Deposition of eggs in the anal area incite a hypersensitivity
eosinophilia (called Loeffler’s syndrome). Penetration of the reaction that leads to the prominent manifestation of the
lung capillaries by the larvae as they enter the air sacs can disease-anal itchiness.
lead to pneumonia. ●​ Vigorous scratching of the anus can lead to development of
●​ The presence of multiple adult worms in the intestines can mucosal breaks in the anus which can become secondarily
lead to abdominal pain (most common complaint), vomiting, infected.
fever, and abdominal distention. ●​ Like Ascaris, some pinworms may obstruct the appendix
●​ Mature worms may entangle with each other forming a mass leading to appendicitis
that can cause intestinal obstruction.
●​ In addition, due to the erratic nature of the mature worms,
DISEASES, TREATMENT, PREVENTION AND CONTROL
the adult parasite can travel to different organs of the body.
●​ An adult worm can obstruct the appendix leading to
appendicitis. Disease: Enterobiasis
●​ Other organs that can be obstructed include the liver and the ●​ Most cases of enterobiasis are asymptomatic.
bile ducts. Due to the tough, flexible body of the worm, it may ●​ intense itching with inflammation in the anal area (pruritus
cause perforation of the intestines, leading to peritonitis ani) or the vaginal area which occurs most frequently at
which can be fatal. Secondary bacterial infections may also night.
occur in the damaged tissues. ●​ Other symptoms may include intestinal irritation and mild
nausea.
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●​ infected persons may be deprived of sleep and become resemble those of inflammatory bowel disease and include
irritable abdominal pain and tenderness, weakness, and dysentery

Laboratory Diagnosis Laboratory Diagnosis: confirmed by demonstrating the presence of

●​ demonstration of the eggs or adult females using the Scotch characteristic eggs in stool specimens.
Tape method or cellophane tape method.
●​ The small size of the eggs may make recovery from stool Treatment: Drugs of choice for treatment are mebendazole or
difficult albendazole.

Treatment Prevention and Control: health education, proper sanitation, good

●​ Drugs of choice for treatment are albendazole, personal hygiene, and avoidance of use of human feces as fertilizer.
mebendazole, or pyrantel pamoate.
●​ It is recommended that household members also undergo ANCYLOSTOMA DUODENALE (OLD WORLD HOOKWORM) AND
treatment as pinworm infection is considered a group NECATOR AMERICANUS (NEW WORLD HOOKWORM)
infection.
PROPERTIES AND LIFE CYCLE
Prevention and Control
●​ Good personal hygiene, clipping of fingernails, thorough There are two common species of hookworms, Ancylostoma
washing of beddings, and prompt treatment of infected duodenale and the Necator americanus, both of which share the same
persons four stages in the life cycle: eggs, rhabditiform larvae, filariform larvae,
●​ To avoid ingestion and/or inhalation of the eggs, it is and adults.
recommended to thoroughly clean the house using a damp ●​ The eggs of the two hookworms vary only in size. The
mop in areas including the floor under the beds, the rhabditiform larva is the immature, newly hatched larva.
windowsills, and overdoors ●​ The filariform larva is the non feeding, infective larva that has
a distinct pointed tail.
●​ The adult worms of the two hookworms are differentiated by
TRICHURIS TRICHIURA (WHIPWORM)
the appearance of their buccal capsule. The N. americanus
PROPERTIES AND LIFE CYCLE buccal capsule is equipped with a pair of cutting plates while
that of A. duodenale consists of teeth.
●​ The eggs of the human whipworm have a characteristic ●​ Unlike the other intestinal roundworms, the infective stage
barrel or football shape with a prominent hyaline plug at each for hookworms is the larva and transmission through skin
end of the egg. penetration by the filariform larva. The feet or legs are the
●​ The anterior end of the adult worm appears colorless while usual sites of penetration.
the posterior end is pinkish in color. The male worm has a ●​ After penetration, the larvae are carried by the blood to the
recognizable curled tail. The posterior end is larger and lungs, migrate to the air sacs, pass up the bronchi and
resembles the handle of a whip while the anterior end trachea, are coughed up and then swallowed with sputum
resembles the whip itself. > ●​ Once in the small intestines, the larvae mature into adult
●​ Humans acquire the infection through ingestion of food or worms and attach themselves to the intestinal wall using
water contaminated by human feces containing the infective their cutting plates or teeth. The adult worms feed on blood
eggs. The larvae emerge from the eggs in the small from the capillaries of the intestinal villi. Mating occurs in the
intestines, become immature adults, and migrate to the colon small intestines, where thousands of eggs are laid each day.
where complete maturation and mating occurs. Thousands The eggs are then passed out with the feces.
of eggs are produced each day, which are then passed in the
feces. EPIDEMIOLOGY AND PATHOGENESIS

EPIDEMIOLOGY AND PATHOGENESIS ●​ Hookworms are found worldwide, especially in tropical

countries.
●​ The whipworm is the third most common roundworm ●​ Walking barefoot on soil puts one at risk of acquiring the
affecting humans. infection.
●​ tropical countries and areas with poor sanitation practices. ●​ Irritation of the skin at the site of penetration may be seen,
●​ The parasite, like Ascaris, is seen in locales where human as well as inflammatory reactions in the lungs during the
feces is used for fertilizer and where humans defecate larval phase. The major damage to the host is due to chronic
directly on the soil. blood loss at the site of attachment in the small intestines.
●​ Children are at highest risk for development of infection
when they play in contaminated soil. DISEASES, TREATMENT, PREVENTION AND CONTROL
●​ Infection is acquired primarily by ingesting food or water
contaminated by human feces containing the infective eggs. Disease: Hookworm Infection
●​ Penetration of the skin by the filariform larvae produces a
DISEASES, TREATMENT, PREVENTION AND CONTROL pruritic papule or vesicle. This is called "ground itch."
●​ Pneumonia with eosinophilia may occur during the lung
●​ Severity and occurrence of manifestations of trichuriasis are phase. The presence of adult worms in the intestines can
related to the intensity of the worm burden. Heavy infection manifest nausea, vomiting, and diarrhea.
in children resemble manifestations of ulcerative colitis, a ●​ As the worm feeds on blood, a microcytic, hypochromic
chronic inflammatory condition of the colon that has an anemia akin to iron deficiency anemia may occur.
autoimmune etiology. ●​ Intestinal sites may be secondarily infected by bacteria
●​ Manifestations may include chronic dysentery (bloody,
mucoid diarrhea), severe anemia, or growth retardation. Laboratory Diagnosis:
●​ Rectal prolapse and hyperperistalsis are also seen in ●​ Stool examination. Occult blood in the stool and blood
infected children. Rectal prolapse occurs due to irritation and eosinophilia are frequent findings.
straining during defecation. Manifestations in adults
 MICROBIOLOGY AND PARASITOLOGY
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●​ Peripheral blood smear will show microcytic, hypochromic ●​ the parasite can stimulate recurrent allergic reactions
anemia. Larvae may be recovered from sputum. resulting to urticaria and eosinophilia.
●​ In patients with very high worm burden, which is seen in
Treatment: mebendazole and pyrantel pamoate. Iron replacement autoinfection, malabsorption syndrome may occur due to
therapy is recommended for the anemia. In severe cases, blood involvement of the biliary ducts, pancreas, small intestines,
transfusion and colon. This can lead to steatorrhea (fat in the stool) and
resulting nutrient deficiencies, epigastric pain and
Prevention and Control: Wearing shoes or any protective footwear. tenderness, and increasing diarrhea.

STRONGLOIDES STERCORALIS (THREADWORM) Laboratory Diagnosis

●​ Eggs, although not commonly present, may be recovered
PROPERTIES AND LIFE CYCLE
from stool of patients with heavy worm burden who have
severe diarrhea.
●​ The eggs of Strongyloides stercoralis are similar to those of ●​ The usual diagnostic method is through the recovery of the
hookworms except for two features-Strongyloides ova are rhabditi form larva in fresh stool samples
smaller and contain well developed larvae. The rhabditiform ●​ Examination of duodenal aspirates may also yield the larvae.
larva of Strongyloides differ from that of hookworms in Larvae may also be recovered from sputum during the lung
having a longer buccal cavity and a smaller genital phase of the parasite's life cycle.
primordium.
●​ Like hookworms, the infective stage is the filariform larva Treatment: ivermectin with mebendazole and thiabendazole as
●​ Strongyloides stercoralis is unique among the intestinal alternative drugs.
roundworms for having two distinct life cycles-one within the
host and a free living cycle in soil. Prevention and Control: thorough health education of the population
●​ Humans acquire the infection through three possible means. at risk, proper sanitation and sewage disposal, wearing of protective
The first is through direct skin penetration by the infective footwear, and prompt treatment of infected individuals.
filariform larva, as that of hookworm acquisition. This direct
mode of transmission marks the beginning of the human
CAPILLARIA PHILIPPINENSIS (PUDOCWORM)
cycle. The direct or human cycle resembles that of the
hookworm life cycle where a lung phase also occurs. It PROPERTIES AND LIFE CYCLE
differs from the hookworm cycle in that it is usually the
rhabditid form larvae that are passed out with the feces ●​ The parasite was first described in the Philippines in 1963,
instead of the eggs. The rhabditiform larvae transform when the first human case died from the infection. From
directly to the infective filariform larvae in warm, moist soil. 1967-1968, outbreaks of the infection occurred leading to the
●​ In the second, the indirect mode, rhabditi form larvae are death of more than a hundred infected individuals.
passed out in the feces which transform into filariform larvae ●​ Unlike the other intestinal roundworms, migratory fish eating
in the soil. These mature into adult, free living, non parasitic birds are the natural hosts. Typically, the unembryonated
adult worms. This is the free living cycle which occurs in soil. eggs are passed out to the external environment with the
The adult female worm lays eggs that develop into rhabditi feces of the birds or infected humans, usually in fresh water.
form larvae, which transforms into the infective filari form The eggs become embryonated and are ingested by fresh
larvae that can then enter a host to start a direct life cycle. water fish (usually bagsit in the Ilocos region). The larvae
●​ Infection may also occur through autoinfection. This occurs encyst in the tissues of the fish.
when the rhabditi form larvae develop into filariform larvae in ●​ Humans acquire the infection by eating improperly cooked or
the intestines of the infected person. These then enter the raw freshwater fish. Once in the small intestines, the larvae
lymphatic system or the bloodstream of the infected host, mature into adult worms that burrow into the wall of the
thus starting a new cycle. intestines, where the worms lay eggs. Some of the eggs may
become embryonated in the intestines which leads to
EPIDEMIOLOGY AND PATHOGENESIS development of autoinfection.

●​ Thread worm infection occurs worldwide but is more EPIDEMIOLOGY AND PATHOGENESIS
common in tropical, sub tropical, and warm, temperate
areas. ●​ Capillaria philippinensis is endemic in the Philippines,
●​ The parasite is frequently seen in agricultural areas where especially in the Ilocos region. Cases have also been seen in
there is constant contact with soil. As in hookworm infection, Thailand.
irritation at the site of skin penetration also occurs (ground ●​ The parasite is also found in other parts of the Philippines
itch). including Zambales and Southern Leyte. The large number
●​ The larvae in the lungs can produce an inflammatory of worms that develop within the infected host is responsible
reaction similar to Ascaris. The adult worms in the small for the pathology seen.
intestines can initiate an inflammatory reaction on the ●​ Adult worms can cause micro ulcers in the intestinal mucosa
intestinal wall, resulting in diarrhea. This is especially seen in that if severe, can lead to malabsorption syndrome
autoinfection, where significant damage can occur in the
intestinal mucosa which may lead to secondary bacterial DISEASES, TREATMENT, PREVENTION AND CONTROL
infection and sepsis
Disease: Intestinal Capillariasis
DISEASES, TREATMENT, PREVENTION AND CONTROL ●​ Intestinal capillariasis is characterized by abdominal pain
with a gurgling stomach (borborygmus) and chronic diarrhea.
Disease: Strongyloidiasis (Cochin China Diarrhea) The chronic diarrhea leads to weight loss which is
●​ Migration of the larvae into the lungs lead to pneumonitis aggravated by the accompanying loss of appetite (anorexia),
●​ The presence of numerous adult worms in the intestines lead nausea, and vomiting.
to diarrhea and abdominal pain. ●​ Malabsorption of fat, carbohydrates, and proteins as well as
electrolyte abnormalities can be fatal.
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●​ Symptoms of filariasis may vary depending on the species.
Laboratory Diagnosis The clinical course may be divided into three
●​ demonstration of the characteristic eggs in stool specimens. stages-asymptomatic, acute, and chronic.
In high worm burden, larvae as well as adult worms may also
be demonstrated in stool. 1.​ Asymptomatic stage is characterized by the presence of
thousands of microfilariae in the peripheral blood. Adult
Treatment worms may be found in the lymphatic system without clinical
●​ The drug of choice for treatment is albendazole, with manifestations of filariasis.
mebendazole as alternative, especially for adult patients. 2.​ Acute stage of infection is marked by fever, with
●​ Chemotherapy is given for at least 20 days in order to totally inflammation of the lymph nodes (lymphadenitis), particularly
eradicate the parasite. those of the male genitalia (in bancroft'sfilariasis) and of the
●​ Relapses may occur if the treatment regimen is not followed. extremities(due to Brugia). In females, involvement of the
lymphatics of the breast may be seen. Recurrent attacks are
Prevention and Control characterized by epididymitis(inflammation of the
●​ Preventive measures include adequate and thorough epididymis), orchitis (inflammation of the testes), retrograde
cooking of seafood before consumption, especially in lymphangitis, and localized inflammation of the arms and
endemic areas. legs.
●​ proper human waste disposal, health education, and prompt 3.​ Chronic filariasis: develops slowly after several years of
treatment of infected persons infection. Manifestations include chronic edema and
repeated acute inflammatory episodes. The edema and
BLOOD AND TISSUE NEMATODES fibrosis gradually lead to lymphatic obstruction of the legs
and genitalia (especially the scrotum). The enlarged
WUCHERERIA BANCROFTI (BANCROFT’S FILARIAL WORM) AND
extremity hardens with loss of skin elasticity producing
BRUGIA MALAYI (MALAYAN FILARIAL WORM)
elephantiasis. Obstruction of the lymphatics of the tunica
PROPERTIES AND LIFE CYCLE vaginalis of the testes lead to accumulation of edema fluid in
the scrotum (called hydrocele). Hydrocele, chronic
●​ W. bancrofti and B. malayiare both mosquito borne epididymitis, and lymphedematous thickening of the scrotal
parasites. skin are commonly seen in bancroft's filariasis. Deformities
●​ Both have two important morphologic forms-the adult worm resulting from Malayan filariasis are not as severe and
and the larvae (called microfilariae). The adult male is include enlargement of the epitrochear, inguinal, and axillary
usually the size of the female worm. Both are threadlike in lymph nodes
appearance with creamy white color. The microfilariae have
a delicate transparent covering called a sheath. Laboratory Diagnosis
●​ Humans acquire the infection through the bite of a mosquito ●​ Examination of Giemsa stained peripheral blood smear is the
vector. The infective larvae migrate to the tissues, mature, diagnostic method of choice demonstrating the microfilariae.
and localize in the lymphatics, subcutaneous tissues, or ●​ In light infections, the blood specimen (approx. 1 ml) may be
internal body cavities. immersed in 10 ml of a 2% formalin solution to lyse the red
●​ Migration of the parasites exhibit periodicity, where the blood cells. Optimal sampling collection is at night, especially
parasite is present in the bloodstream during specific times for species that demonstrate nocturnal periodicity (usually
of the day, which corresponds to the feeding schedule of the Wuchereria).
mosquito vector. ●​ The ideal times for specimen collection are between 9:00 pm
●​ Migration may occur at night (nocturnal), during the day and 4:00 am, the peak periods for the appearance of the
(diurnal), or with no clear cut timing (sub periodic). mosquito vectors. Antigen detection methods and serologic
EPIDEMIOLOGY AND PATHOGENESIS tests have been developed as alternative diagnostic
methods.
●​ Majority of filarial worm infections worldwide are caused by
Wuchereria bancrofti. Infections in Asia are frequently due to Treatment
Brugia malayi.In the Philippines, bancroftian filariasis is more ●​ The recommended drugs for treatment are
common. Mosquito vectors for W. bancrofti include Culex diethylcarbamazine (DEC) and ivermectin in combination
spp., Anopheles spp., Aedes spp., and Mansonia spp. The with albendazole.
typical vectors for B. malayi are Mansonia and Aedes ●​ Microsurgery may be necessary to remove the obstructing
mosquitoes.In rural areas in the Philippines, the major vector parasite from the lymphatics.
is Anopheles minimus falvirostris.In urban areas, the parasite ●​ Other supportive measures include anti inflammatory drugs
is transmitted chiefly by Culex spp., which can breed in to reduce the inflammation.
latrines, sewage, and ditches.
●​ Fourty four (44) provinces in the Philippines have been Prevention and Control
identified by the Department of Health (DOH) as endemic. ●​ The WHO Division of Control of Tropical Diseases
These provinces are mainly in the Southern portion of the recommends mass treatment in endemic areas. In the
Philippines. To date, the following provinces have been Philippines, a Filariasis Control Program was implemented in
declared filaria free: Southern Leyte, Sorsogon, Biliran, 2001 which entailed mass treatment in endemic areas using
Bukidnon, Romblon, Agusan del Sur, and Dinagat Islands. a combination of DEC and albendazole. This resulted in the
The manifestations of filariasis are due to the obstruction of elimination of infection in some endemic areas.
the lymphatic vessels by the adult worms, causing edema of ●​ Other measures include the use of mosquito nets and
the limbs. The adult worms cause inflammatory and fibrotic repellents, the use of insecticides to control the mosquito
reactions. Microfilariae cause less severe pathology. vectors, wearing of protective clothing, and thorough health
education of the population.
DISEASES, TREATMENT, PREVENTION AND CONTROL

Disease: Filariasis
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INTESTINAL - TISSUE NEMATODES the giving of analgesics and antipyretics to relieve muscle
pain and fever.
TRICHINELLA SPIRALIS (MUSCLEWORM, TRICHINA)
●​ Corticosteroids may be given for severe infections.
PROPERTIES AND LIFE CYCLE Thiabendazole may be given during the early stages of the
disease, especially during the first week, to kill the adult
●​ There are two important morphologic forms of the worms. The drug has no effect on the migrating larvae.
parasite-larva and adult worm. The larvae have a coiled
appearance and encysts in muscle tissues, surrounded by Prevention and Control
striated muscle cells called nurse cells. ●​ Health education is important in preventing infection.
●​ The usual, natural host is the pig but any mammal can be ●​ It is also important to thoroughly and adequately cook meat
infected. Humans are accidental hosts and acquire the before consumption.
infection by ingestion of raw or improperly cooked pork meat ●​ Freezing meat may also kill the encysted larvae.
containing the encysted larva. ●​ Avoidance of feeding pork scraps to hogs may help break
●​ The larvae are released from the cysts with exposure to the life cycle of the parasite.
gastric acid and pepsin, after which they invade the mucosa ●​ Other measures include strict meat inspection and keeping
of the small intestines where they mature into adult worms. pigs and other farm animals in rat free pens
●​ After mating, the gravid female "gives birth" to the larvae in
the intestinal submucosa
●​ Among the nematodes, the life cycle of the muscle worm has
no egg stage. The larvae then migrate through the
bloodstream and localize to striated muscles where they
undergo encystation,
CESTODES
EPIDEMIOLOGY AND PATHOGENESIS GENERAL PROPERTIES OF CESTODES

●​ Infection with T. spiralisis seen worldwide, especially in parts Cestodes

of Europe and the United States where meat can be eaten ●​ subkingdom Metazoa, phylum Platyhelminthes.
raw. Aside from the pig, other animals that may be infected ●​ These parasites are considered as primitive worms.
include deer, bear, walrus, and rodents (rats). Patients ●​ They absorb nutrients and eliminate waste products through
harboring a hundred or more worms are usually their outer surface called the tegument.
symptomatic. Encystation of the larvae may lead to ●​ Commonly known as tapeworms, these parasites are flat
inflammation, then granuloma formation, which can later and consist of three distinct regions-the head, neck, and
become calcified body (proglottids). The head contains an organ of
attachment called the scolex, which may consist of either
DISEASES, TREATMENT, PREVENTION AND CONTROL hooks, suckers, or sucking grooves.
●​ The body is divided into multiple segments (hence, the name
Disease: Trichinosis, Trichinellosis tapeworm) called proglottids. A series of proglottids is called
●​ Trichinosis may be divided into three phases- entericphase, strobila (plural strobili).
invasion phase, and convalescent phase. ●​ All cestodes are hermaphroditic (self fertilizing) with each
●​ These correspond to the incubation and intestinal invasion proglottid containing both male and female reproductive
stage (enteric phase), the larval migration and muscle organs
invasion stage (invasion phase), and the encystation and ●​ Each proglottid is capable of laying eggs (now called a
encapsulation stage of the larva (convalescent phase). pregnant proglottid or gravid segment). The neck serves as
●​ The enteric or intestinal phase may manifest with diarrhea, the region of growth and connects the head to the body of
abdominal pain, and vomiting. In the invasion phase, the worm.
potentially any organ with striated muscles may be the target ●​ The worm grows by adding new proglottids from the neck.
of the parasite. Symptoms may Include periorbital and facial The oldest proglottids are found at the most distal part of the
edema, conjunctivitis, fever, muscle pain (myalgia), splinter body of the parasite. A typical cestode life cycle is divided
hemorrhages, rashes, and peripheral eosinophilia. into three stages-egg, larva, and adult worm.
Involvement of the heart can lead to life threatening ●​ oncosphere, first larval or motile stage. It is equipped with
myocarditis. small hooks (called hooklets) that eventually enable the
●​ During the convalescent phase, the manifestations start to parasite to pierce the wall of the intestines.
decline. ●​ The eggs are excreted in the feces of infected hosts and are
●​ The disease is self limiting, hence full recovery is expected. transmitted to the intermediate hosts (cattle, pig, or fish).
Rare causes of death are congestive heart failure and ●​ Infection in humans is usually acquired through ingestion of
respiratory paralysis. the undercooked or raw flesh of the intermediate host
containing the infective larvae.
Laboratory Diagnosis ●​ After ingestion, the ingested larvae are transformed into
●​ Definitive diagnosis is done by demonstrating the encysted adult worms in the intestines of the infected host.
larvae in muscle biopsy specimens. ●​ The adult worm then undergoes self impregnation with the
●​ Blood examination results include eosinophilia, leukocytosis, gravid segment rupturing to release the eggs in the
and elevated serum muscle enzyme levels (lactate intestines.
dehydrogenase, aldolase, creatine phosphokinase).
●​ Serologic tests are available. False negative results may be TWO GROUPS OF CESTODES
seen during early infection, hence it is often necessary to
perform multiple tests 1.​ Intestinal cestodes
2.​ Extra Intestinal Cestode
Treatment
INTESTINAL CESTODES
●​ The disease is self limiting and therefore does not require
medication. Supportive measures include bed rest as well as
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1.​ Taenia Saginata (Beef Tapeworm) ●​ Infection with the pork tapeworm is acquired through
2.​ Taenia Solium (Pork Tapeworm) ingestion of improperly cooked or raw pork meat which
3.​ Diphyllobothrium latum (Broad type fishworm) contains the infective larva called cysticercus cellulosae.,
4.​ Hymenolepis nana (Dwarf Tapeworm) ●​ can also occur following the ingestion of food or water
contaminated with human feces that contain the eggs of the
TAENIA SAGINATA (BEEF TAPEWORM) parasite. Therefore, unlike the beef tapeworm, Taenia solium
has two infective stages-eggs and larvae.
Properties and Life Cycle ●​ Pigs serve as the intermediate host while humans serve as
both intermediate and definitive hosts. (5 m)
●​ In cases where infection is acquired through ingestion of
undercooked or raw pork meat, the infective stage is the
larval form which transforms into adult worm in the intestines
of infected individuals (humans serve as the definitive hosts.)
●​ ingested worm eggs hatch in the small intestines, burrow
through the wall of the intestines into a blood vessel, and
disseminate to various organs (e.g. eyes, brain, skeletal
muscle-encycst to form larvae. (humans serve as
intermediate hosts.)

●​ The intermediate host is cattle where the eggs enter the Epidemiology and Pathogenesis
blood vessels within the cattle's intestines. ●​ T. solium infection is more prevalent in underdeveloped
●​ eggs are transported to the skeletal muscles of the cattle communities with poor sanitation and where people eat raw
where they develop into cysticerci (larvae). or undercooked pork. Higher rates of illness have been seen
●​ acquired by ingestion of improperly cooked or raw beef in people in Latin America, Eastern Europe, sub Saharan
containing the infective larva (called cysticercus). Africa, India, and Asia (Centers for Disease Control and
●​ larvae mature into adult worms(pathogenic stage)in the small Prevention).
intestines within a period of approximately three months. ●​ Adult worms produce little damage in the intestines.
●​ a length of as much as 10 meters. Encysted larvae may produce damage in the tissues where
●​ Humans serve as the definitive hosts. they disseminate. For instance, in the brain, they may
manifest as space occupying lesions.
Epidemiology and Pathogenesis ●​ larvae may encyst in various tissues of the body, they evoke
●​ Taenia saginata infection is common in areas of the world little inflammatory response.
where beef is routinely eaten, especially undercooked beef. ●​ when the encysted larvae die, they may release substances
●​ It has been found to be endemic in Eastern Europe, Russia, that may induce an allergic reaction in the host which may
Eastern Africa, and Latin America (Centers for Disease potentially be fatal due to the development of anaphylactic
Control and Prevention). shock.
●​ The adult worms do not produce significant damage in the
small intestines. Disease
1.​ Taeniasis- the disease produced by the adult worm. Most
Disease: Taeniasis cases are asymptomatic but in the presence of high worm
●​ Majority of patients are asymptomatic. burden, manifestations may be similar to beef tapeworm
●​ Those with high worm burden may complain of diarrhea, infection.
abdominal pain, loss of appetite with resultant weight loss, 2.​ Enterobiasis
and body malaise. The gravid proglottids may reach the 3.​ Cysticercosis- the result of larval encystation in various
anus where egg laying may occur resulting in itchiness in the tissues of the body. Skeletal muscles: muscle pain. Brain:
anal region (pruritus ani). (neurocysticercosis) is the most feared and most severe
involvement. It may present with symptoms associated with
Laboratory Diagnosis increased intracranial pressure such as seizures, headache,
●​ A fecal specimen from infected patients is the procedure of and vomiting. Ocular cysticercosis may lead to visual
choice. disturbances due to development of inflammation of the uvea
●​ Eggs or gravid proglottids may be recovered from the stool (uveitis) and retina (retinitis).
although eggs are less often found than the proglottids
Laboratory Diagnosis
Treatment ●​ Microscopic examination of stool specimens.
●​ The drug of choice against the adult worm is ●​ Demonstration of ova or proglottids may help establish the
praziquantel diagnosis (demonstration of the cyst in tissue, through
biopsy or CT scan.)
Prevention and Control
●​ Proper waste disposal and sanitation practices Treatment
adequate cooking of beef Freezing of beef meat ●​ The drug of choice for treatment of intestinal
for approximately 10 days may kill the encysted infection is praziquantel.
larvae. ●​ Alternative drugs include albendazole,
●​ Prompt treatment of infected persons help prevent paromomycin, and quinacrine hydrochloride.
spread of the disease. ●​ Surgical removal of the larvae may be necessary.
●​ Anticonvulsants may be given in cases of
TAENIA SOLIUM (PORK TAPEWORM) neurocysticercosis.

Properties and Life Cycle Prevention and Control

●​ Important preventive measures for pork tapeworm
infection are the same as that for beef tapeworm
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and include proper waste disposal and sanitary ●​ Accidental ingestion of rice or flour beetles containing the
measures, thorough cooking of pork meat, and the infective larvae and that may have gotten into food is another
prompt treatment of infected persons to prevent way by which the infection may be acquired. Rodents serve
the spread of the parasite. as additional source of infection
●​ Once the eggs (infective stage) gain entrance into the
DIPHYLLOBOTHRIUM LATUM (BROAD FISH TAPEWORM) human host after ingestion of contaminated food and water,
the eggs transform into cysticercoid larvae.
Properties and Life Cycle ●​ The larvae mature into adult worms capable of self
●​ The longest of the tapeworms (13 meters.) reproduction.
●​ Its eggs consist of ciliated larvae called coracidia (s. ●​ two pathways for the eggs-the eggs may be passed to the
coracidium). One end of the egg is occupied by a lid outside environment through the feces or some of the eggs
structure called an operculum may remain inside the human host. Those that remain inside
●​ Its scolex contains a pair of long sucking grooves. The gravid the human host hatch into larvae and mature into adult
segments contain a uterine structure that is centrally located worms, thereby starting a new cycle within the human host.
and assumes a rosette formation. This type of re-infection is called autoinfection.
●​ ingestion of improperly cooked or raw fish containing the
plerocercoic (infective stage), the precursor larval stage. Epidemiology and Pathogenesis
After ingestion, the plerocercoid attaches to the intestinal ●​ The dwarf tapeworm is the most common tapeworm
mucosa and matures into the adult worm. recovered in the United States.
●​ The adult worm self fertilizes and the eggs are passed out ●​ It has a worldwide distribution and is also found in East Asia
with the stool. If the eggs come to contact with fresh water, and the Philippines. It is common in areas with inadequate
the coracidium hatches and is ingested by the first sanitation and hygiene. Children and persons living in
intermediate host, a tiny crustacean called a copepod crowded areas are at risk of developing infection. The
(Cyclops sp.). parasite produces little damage in the small intestines.
●​ After ingestion, the coracidium develops into the larval stage
called the procercoid. The copepod is then eaten by a Disease: Hymenolepiasis
freshwater fish (second intermediate host) where the ●​ Most patients are asymptomatic. In cases of high worm
procercoid develops into the plerocercoid. burden, patients may complain of nausea, weakness, loss of
●​ Definitive hosts for the parasites are humans and other fish appetite, diarrhea, and abdominal pain. In young children
eating mammals such as dogs, cats, bears, and seals. with heavy infection, anal itchiness (pruritus ani) may occur
leading to headaches due to difficulty sleeping
Epidemiology and Pathogenesis ●​ Autoinfection may lead to hyper infection syndrome which
●​ D. latum infection occurs in countries where raw freshwater can result in secondary bacterial infection and spread of the
fish is consumed. worms to other tissues of the body.
●​ Little damage is produced in the small intestines of the
human hosts. In some individuals, the parasite may compete Laboratory Diagnosis: Stool examination.
with the host for vitamin B12, leading to a deficiency of this Treatment: Praziquantel. Niclosamide can be an alternative
vitamin drug.
Prevention and Control: proper hygiene and waste
Disease disposal, control of transport host population, and rodent
1.​ Asymptomatic disease the most common presentation control. Proper storage of grains and flour must be observed
among most individuals infected with the parasite. to prevent infestation with flour and grain beetles. Prompt
2.​ Diphyllobothriasis-may manifest with symptoms of treatment of infected individuals must be instituted to prevent
gastrointestinal involvement, which may include diarrhea and the spread of the parasite.
abdominal discomfort. When the adult worm attaches itself to
the jejunum and ileum, the patient may develop deficiency of EXTRA INTESTINAL CESTODES
vitamin B12, leading to anemia similar to pernicious anemia
and is characterized as megaloblastic anemia resulting from 1.​ Echinococcus Granulosus (Dog Tapeworm or hydatid
lack of maturation of red blood cells. Tapeworm)

Laboratory Diagnosis: finding of the characteristic eggs and/or the ECHINOCOCCUS GRANULOSUS (DOG TAPEWORM OR HYDATID
proglottids (less frequent)in a stool specimen. TAPEWORM)
Treatment: praziquantel. An alternative drug is niclosamide.
Prevention and Control: Proper sanitary procedures, Properties and Life Cycle
thorough cooking of fish prior to consumption, and the ●​ zoonotic type of infection.
prompt treatment of infected individuals to prevent spread of ●​ Dogs are the most important definitive hosts while sheep are
the parasite. Freezing of the fish for 24-48 hours at-18 °C usually the intermediate hosts.
can kill all larvae. ●​ Humans are considered as accidental and dead end hosts.
The eggs of E. granulosus are identical to those of Taenia
HYMENOLEPIS NANA (DWARF TAPEWORM) spp. and are thus not diagnostic. The diagnostic stage of the
parasite is its larval form, which is encased in a cyst wall and
Properties and Life Cycle is called the hydatid cyst.
●​ does not require an obligatory intermediate animal host. The ●​ Infection is acquired after ingestion of eggs (infective stage)
eggs are directly infectious and humans get the infection from food and water contaminated by dog feces or through
after the accidental ingestion of the eggs of the parasite. contact with contaminated dog feces.
●​ ingestion of fecally contaminated food or water. One may ●​ Eggs transform into larvae in the intestines, penetrate the
also acquire the eggs by touching one's mouth with intestines, and migrate through the bloodstream to different
contaminated fingers or through ingestion of contaminated tissues in the body, particularly the liver and the lungs.
soil.
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●​ The hydatid cyst (pathogenic stage) then develops in the ●​ The eggs of the trematodes vary in appearance and are the
infected tissues. Dogs acquire the parasite by eating the primary morphologic stage that are usually recovered from
visceral organs of the intermediate host. humans.
●​ humans never serve as intermediate hosts for the flukes.
●​ Epidemiology and Pathogenesis ●​ In general, flukes have two intermediate hosts except for the
●​ E. granulosus infection is common in Africa, Europe, Asia, blood flukes (only one intermediate host).
the Middle East, Central and South America, and in rare ●​ Common to all trematodes, the first intermediate hosts are
cases, North America (Center for Disease Control and mollusks (snails and clams) where asexual reproduction
Prevention). takes place.
●​ The embryos develop into large, fluid filled hydatid cysts, ●​ The second intermediate host varies depending on the
which act as space occupying lesions. parasite.
●​ the cyst fluid contains antigens that can sensitize the host. ●​ Sexual reproduction of flukes occurs in humans. In most
Rupture of the cyst, either spontaneously or during trauma or cases, humans acquire the infection through ingestion of
surgical removal, may lead to the release of these antigens undercooked or raw second intermediate host. Skin
leading to anaphylaxis and widespread dissemination of the penetration by the infective larvae is the major mode of
parasite. transmission for blood flukes.

Disease: Echinococcosis Hydatid Cyst Disease TWO GROUPS OF TREMATODES

●​ patients are asymptomatic during the early stages of the
disease. 1.​ Blood dwelling Flukes
●​ cysts enlarge, necrosis of the infected tissues occur. 2.​ Tissue dwelling Flukes
Involvement of the liver may result in obstructive jaundice.
Patients with lung involvement may manifest with cough,
BLOOD DWELLING FLUKES
chest pain, and shortness of breath. Other organs that may
be infected include the spleen, kidneys, heart, bone, and SCHISTOSOMA SPP.
central nervous system, including the brain and eyes (Center
for Disease Control and Prevention).Cyst rupture may lead Properties and Life Cycle
to anaphylactic shock leading to death of the patient. ●​ Three schistosomes are frequently associated with human
disease, namely: Schistosoma mansoni, Schistosoma
Laboratory Diagnosis japonicum, and Schistosoma haematobium.
●​ examination of biopsy specimen; (2) serologic tests (e.g., ●​ Blood flukes are dioecious.
ELISA or indirect hemagglutination test); and (3) radiography ●​ Known as the "romantic parasites," the male and female
to demonstrate the hydatid cysts (e.g.,CT scan or worm are usually in a state of copulation(en copula).
ultrasound). Care should be exercised when doing biopsy to ●​ Female worms are usually larger than the male worms.
prevent rupture of the cyst. ●​ The schistosomes are also obligate intravascular parasites.
Treatment ●​ The eggs are found in fresh water contaminated with the
●​ In cases when surgery is possible, removal of the feces or urine of infected humans.
cyst has been considered as the treatment of ●​ Once in the water, eggs develop into a miracidium, that will
choice. then locate a snail as its host, where it transforms into
●​ medical management alone may prove effective, cercariae. Infection is acquired through skin penetration by
especially if the cyst is located in inaccessible the fork tailed cercaria (larval form). The parasite migrates
areas. into the bloodstream where they undergo maturation.
●​ Drugs that have been proven effective include ●​ The location of the adults varies by species: after skin
mebendazole, albendazole, and praziquantel. penetration, the worms enter the veins surrounding the
Prevention and Control intestinal tract; localize in the veins surrounding the urinary
Improvement of personal hygiene practices, prevention of bladder.
contamination of food and water with dog feces, avoidance ●​ The adult worms lay thousands of eggs per day. The eggs
of feeding pet dogs with contaminated viscera, and the produce enzymes that enable them to travel through the
prompt treatment of infected canines and humans. tissue.
Chemoprophylaxis should be given to dogs in endemic ●​ The eggs then find their way into the colon (for S. japonicum
areas. Health education is essential and S. mansoni) or into urine (for S. haematobium) from
which they are excreted
TREMATODES
Epidemiology and Pathogenesis
GENERAL PROPERTIES OF TREMATODES
●​ Schistosoma mansoni and Schistosoma haematobium are
both distributed throughout Africa. S. mansoni is also found
●​ commonly known as in South America while S. haematobium is also prevalent in
flukes, belong to the class the Middle East. Schistosoma japonicum is endemic in
Trematoda Indonesia, some parts of China, and Southeast Asia,
●​ Hermaphroditic or including the Philippines.
dioecious (reproduce via separate ●​ It is the only schistosome for which domestic animals (e.g.,
sexes). water buffalo and pigs) act as important reservoirs. Most of
●​ Morphologically, flukes the findings are caused by the presence of eggs in the liver,
are fleshy, leaf-shaped worms. spleen, or walls of the gut or the urinary bladder,
●​ flukes have a digestive ●​ Eggs of S. japonicum in the liver may induce granuloma
tract. formation leading to fibrosis and portal hypertension, as well
●​ flukes have two muscular as damage the walls of the small and large intestines.
suckers-an oral type, which is the ●​ Eggs of S. mansoni may damage the walls of the distal
beginning of an incomplete colon.
digestive system and a ventral sucker which serves for
attachment.
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●​ Eggs of S. haematobium may induce granuloma and fibrosis enter a freshwater fish where they encyst to become the
in the walls of the urinary bladder metacercariae. The larvae excyst in the duodenum, enter the
biliary ducts, and differentiate into adults. The adult worms
Disease: Schistosomiasis (Bilharziasis) produce eggs that are excreted in the feces. Humans
1.​ Asymptomatic infection - the most common form of the acquire the infection by ingesting raw or undercooked
disease. Chronic infection may become symptomatic. freshwaterfish containing the infective metacercariae.
2.​ Early acute infection - characterized by pruritic papules
seen at the site of entry of the parasite. This is called Epidemiology and Pathogenesis
"swimmer's itch" or "clam digger's itch." This is followed after ●​ Clonorchissinensis is found in Asia including Korea, China,
2-3 weeks by fever and chills, abdominal pain, cough, bloody Taiwan, Vietnam, Japan, and Asian Russia (CDC).
diarrhea, and weight loss. Painful urination (dysuria) and ●​ parasites that inhabit the bile ducts can damage the biliary
blood in the urine (hematuria) may also occur in patients tract (may lead to cancer of the bile ducts). The egg has also
infected with S. haematobium. been associated with the development of gallstones(stones
3.​ Katayama fever - a systemic hypersensitivity reaction to the in the gall bladder or cholelithiasis).
migrating schistosomes, usually associated with S.
japonicum. It is characterized by a rapid onset of fever, Disease
myalgia, body malaise, cough, diarrhea, and eosinophilia ●​ Most patients are asymptomatic. In heavy worm burden,
occurring 1-2 months after exposure to the parasite. patients may manifest a fever, upper abdominal pain,
●​ Swollen lymph nodes (lymphadenopathy) and anorexia, hepatomegaly, diarrhea, and eosinophilia. Liver
enlargement of the liver and spleen dysfunction may also occur in chronic infection associated
(hepatosplenomegaly)may also occur. It can lead with heavy worm burden.
to hepatic dysfunction, leading to portal
hypertension. The most common cause of death in Laboratory Diagnosis: Fecalysis or duodenal aspirates
this case is internal bleeding from ruptured Treatment: praziquantel. An alternative drug is albendazole.
esophageal varices Prevention and Control: Infection can be prevented by
4.​ Associated conditions - include development of nephrotic thorough cooking of fish prior to consumption; health
syndrome in S. japonicum and S. haematobium infection. education, proper waste disposal to avoid contamination of
●​ Infection with S. mansoni or S. japonicum may bodies of freshwater, and prompt treatment of infected
predispose to repeated Salmonella infections. persons.
●​ S. japonicum is associated with the development
of hepatocellular carcinoma or liver cancer while FASCIOLA HEPATICA (SHEEP LIVER FLUKE)
S. haematobium has been implicated in the
development of cancer of the urinary bladder. Properties and Life Cycle
●​ The first intermediate host for the parasite is the snail while
Laboratory Diagnosis the second intermediate hosts are edible aquatic plants
●​ Diagnosis relies on demonstration of characteristic eggs in (kangkong and watercress).
the feces or rectal biopsy specimen ●​ Humans acquire the infection by ingesting raw edible aquatic
Treatment plants or by drinking water contaminated by metacercariae
●​ The recommended drug for all three species is (infective stage).
praziquantel. An alternative drug for S. mansoni is ●​ Upon ingestion, the metacercariae excyst in the duodenum
oxamniquine. Anti malaria drugs such as or jejunum, releasing the young flukes.
artemether and artemisinins have also been ●​ The parasite burrows through the liver parenchyma until it
proven effective. finally enters the bile ducts where they mature.
Prevention and Control ●​ The adult worms (pathogenic stage) live in the biliary
●​ There are two objectives of schistosomal control: passages of the liver. Immature eggs are carried by the bile
(a) control of transmission through snail control, into the intestines and subsequently excreted with feces.
health education, and provision of sanitary ●​ The eggs mature in the water and infect the first intermediate
facilities and water supply; and (b) control of host. The cercariae escape the snail host, usually at night,
disease. then encyst on the surface of aquatic plants, forming
●​ Chemotherapy using praziquantel is the main metacercariae.
thrust of the Philippine program for ●​ The natural host for the completion of the life cycle is the
schistosomiasis control (Department of Health). sheep, however the parasite may also be found in cattle. In
●​ In order to prevent infection, swimming in endemic sheep raising countries, ingestion of raw sheep liver
areas should be avoided. containing the adult worm also serves as an additional mode
of transmission.
TISSUE DWELLING FLUKES ●​ Humans serve as accidental hosts.
CLONORCHIS SINENSIS (ASIAN LIVER FLUKE, CHINESE LIVER
FLUKE) Epidemiology and Pathogenesis
●​ The Fasciola hepatica is found worldwide, especially in
Properties and Life Cycle sheep and cattle raising countries, and where humans
●​ There are three morphologic stages of the parasite-egg, consume raw watercress such as Asia, Europe, and the
larva, and adult. Middle East.
●​ The first intermediate host is the freshwater snail while the ●​ The acute or invasive phase corresponds to the migration of
second intermediate host is a freshwater fish. Within the egg the parasite through the liver parenchyma, which leads to
is the developed miracidium, that is released once the egg traumatic and necrotic lesions in the liver.
comes into contact with fresh water ●​ The severity of the destruction is proportional to the number
●​ The miracidium penetrates the first intermediate host and of metacercariae ingested.
develops into a sporocyst that contains numerous larval ●​ The chronic phase corresponds to the localization of the
stages called the rediae. The larvae are then released into adult worms to the bile ducts. The worm can obstruct the bile
the water where they transform into cercariae. The cercariae duct and stimulate inflammation. During migration from the
 MICROBIOLOGY AND PARASITOLOGY
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bY: STEPHANIE E. MASIADO, SN
intestines to the liver, the parasite may wander to other sites sputum has a foul, fishy odor and is most pronounced in the
(e.g., lungs, subcutaneous tissues, brain, or orbit) where morning.
abscesses may develop ●​ The disease may mimic pulmonary tuberculosis.
●​ In rare cases, the immature flukes may migrate to the brain
Disease: Fascioliasis or Sheep Liver Rot leading to cerebral paragonimiasis, which may manifest as
●​ Migration of the larval worm through the liver irritates the seizures, visual disturbances, and reduced motorskill
organ, manifesting as tenderness and hepatomegaly. precision
Characteristic clinical features include right upper quadrant
pain, fever and chills, and marked eosinophilia. Laboratory Diagnosis
●​ Hepatitis may develop with biliary obstruction. Some worms ●​ Demonstration of the characteristic eggs in sputum or feces
may cause necrotic foci in the liver. Ingestion of raw sheep (when sputum is swallowed).
liver may lead to temporary lodgment of the adult worm in ●​ A chest x-ray may be done which may show a ring
the pharynx leading to suffocation. shadowed opacity with several contiguous cavities giving the
appearance of a cluster of grapes.
Diagnosis: rests on finding of eggs in stool specimen, although the Treatment
appearance of the eggs of F. hepatica may be indistinguishable from ●​ The drug of choice for treatment is praziquantel.
the eggs of another fluke, Fasciolopsis buski. Examination of a sample An alternative drug is bithionol.
of the patient's bile may aid in the differentiation. If the eggs are Prevention and Control
present in bile then this is indicative of F. hepatica. ●​ adequate and thorough cooking of freshwater
Treatment: crabs or crayfish
●​ dichlorophenol (bithionol). An alternative drug is ●​ health education
triclabendazole. ●​ control of snail population and elimination of
reservoir hosts.
Prevention and Control Preventive ●​ Prompt treatment of infected persons
●​ proper human waste disposal, improvement of FASCIOLOPSIS BUSKI (LARGE INTESTINAL FLUKE)
hygiene, control of snail population, and avoidance
of consumption of raw aquatic plants and Properties and Life Cycle
contaminated water. In endemic areas it is highly ●​ the first intermediate host is a snail while the second
recommended to boil water before consumption or intermediate hosts are edible aquatic plants(e.g., watercress
use. and lotus). Humans acquire the parasite by ingestion of raw
●​ Avoidance of ingesting of raw sheep liver is also or inadequately cooked aquatic vegetation that carries the
important, as well as prompt treatment of infected encysted metacercariae.
individuals. ●​ The metacercariae excysts in the duodenum and attaches to
the intestinal wall where they attain maturity. The adult
EXTRA-INTESTINAL CESTODES worms lay eggs, that are released together with the feces
PARAGONIMUS WESTESNI (ORIENTAL LUNG FLUKE) into water, where they hatch and infect the first intermediate
host. The eggs develop into cercariae which encyst as
Properties and Life Cycle metacercariae on the surface of the aquatic plants. Other
●​ the first intermediate host for Paragonimus is a snail while animals such as pigs and dogs may also serve as the
the second intermediate hosts are crabs or crayfish. Humans reservoir hosts.
acquire the infection by ingesting raw or undercooked crabs
or crayfish that contain the infective encysted metacercaria. Epidemiology and Pathogenesis
The larva excysts in the small intestines, migrate through the ●​ F. buski is the largest intestinal fluke that can infect humans.
intestinal wall, through the peritoneal cavity, into the Infection with the parasite is common in Asia and the Indian
diaphragm then into the lung parenchyma where they subcontinent, particularly in areas where pigs are raised and
mature. where freshwater aquatic vegetation is ingested raw.
●​ The adult worms enter the bronchioles and are then coughed ●​ No locally acquired cases in humans or pigs have been
up or swallowed. Eggs in the sputum or feces reach fresh reported in the Philippines. Pathologic changes are due to
water, hatch, and penetrate the first intermediate host, where damage to the intestinal mucosa by the adult fluke.
they differentiate into free swimming cercariae. The
cercariae leave the snail host and encyst in freshwater crabs Disease: Fasciolopsiasis
that are eaten by humans. ●​ with heavy worm burden, patients may experience
abdominal discomfort with inflammation and bleeding in the
Epidemiology and Pathogenesis affected area. Patients may also suffer from malabsorption.
●​ P. westermani infection occurs most commonly in Asia, in ●​ Intoxication may result from absorption of worm metabolites
countries like China, the Philippines, Japan, Vietnam, South by the host, leading to allergic symptoms such as edema of
Korea, Taiwan, and Thailand (CDC). Pigs, monkeys, and the face, abdominalwall, and lowerlimbs.
other animals that eat crayfish and crabs serve as reservoir ●​ Profound intoxication can result in death.
hosts.
●​ The worms exist in a fibrous capsule within the lung which Laboratory Diagnosis
communicates with a bronchiole. Within this cyst is blood ●​ Demonstration of the eggs in stool specimen. Examination of
tinged purulent material containing eggs. Secondary bile samples and duodenal aspirates may help differentiate
bacterial infection frequently occurs. F. buski eggs from those of F. hepatica.
Treatment
Disease: Paragonimiasis ●​ The drug of choice for treatment is praziquantel.
●​ The early stages of the disease are usually asymptomatic. Prevention and Control
Patients may later experience symptoms related to ●​ Adequate washing and cooking of aquatic plants
pulmonary involvement including cough productive of blood before
tinged sputum (hemoptysis), fever, and chest pain. The ●​ consumption can help prevent infection.
●​ proper disposal of human waste,
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bY: STEPHANIE E. MASIADO, SN
●​ control of snail population, and
●​ prompt treatment of infected persons.