INTRODUCTION TO PARASITOLOGY

Parasitology basically is the study of parasites. Parasitology is the area of biology that deals
with the phenomenon of dependence of one organism on another living organism. The study deals
with the relationship between parasites and their host. As a biological discipline, the scope of
Parasitology is not determined by the organism or environment in question but by their way of life.

Areas of Parasitology
1. Medical Parasitology – deals with the human parasites and the diseases they cause
2. Veterinary Parasitology – deals with the animal parasites
3. Structural Parasitology – studies the structures of proteins from parasites
4. Quantitative Parasitology – involves the quantitative study of parasitism in a host population
5. Parasite Ecology – studies the ecological impact of parasites

Definition of Terms
Parasitology is a branch of science that is concerned with parasites and parasitism. Parasitism
is a form of symbiosis in which one organism (called parasite) benefits at the expense of another
organism usually of different species (called host). The association may also lead to the injury of the
host. In almost all cases of parasitic relationships, the parasite deprives the host of essential nutrients
and would produce disease.

1. Symbiosis – a relationship where unlike organisms exist together.

a. Commensalism – a form of symbiotic relationship in which two species live together and one
species benefits from the other without harming or benefiting the other.

b. Mutualism – a symbiotic relationship in which two organisms mutually benefit from each other.

c. Parasitism – a form of symbiotic relationship where one party or symbiont (e.i., parasites) benefits
to the detriment of the other party (host)
* Important Elements in Parasitism
1. Hosts – are organisms that harbor the parasite and provide nourishment to them.
2. Parasites – are organisms that usually depend on the host for survival and growth.

* Types of Hosts
1. Definitive Hosts – hosts that harbor the adult stage of the parasite or where the
sexual stage of the life cycle of the parasite occurs.
2. Intermediate Hosts – those that harbor the larval stage of the parasite or where
the sexual phase of the life cycle of the parasite occurs. (vectors)
3. Reservoir Hosts – are vertebrate host that harbor the parasite and may act as
additional source of infection in man.
4. Paratenic Hosts – hosts that serve as a means of transport for the parasite so that
the infective stage of a certain parasite may reach its final host.

Classification of Parasites
A. Based on Habitat
1. Ectoparasites – parasites that live outside the body of the host. Invasion of the body by
ectoparasites is called infestation.
2. Endoparasites – parasites that live inside the host’s body. Invasion of the body by endoparasites is
called infection and is the result of the entry where parasites multiply within the host.
B. Based on the ability to live independently of the host
1. Facultative parasites – parasites that can live independently of the host
2. Obligate parasites – parasites that must live inside the host. Most of the parasites that infect
humans belong to this classification.

C. Based on mode of living

1. Permanent parasites – remains in the host from early life to maturity (e.i. Plasmodium)
2. Intermittent parasites – simply visits the host during feeding time (e.i. non-pathogenic parasites)
3. Incidental parasites – parasites that occur in an unusual host (e.i. dog tapeworm in humans)
4. Transitory parasites – parasites whose larvae develops in a host while the adult is free-living (e.i.
dog tapeworm – Echinococcus granulosus)
5. Erratic parasites – parasites that are seen in an unusual organ, different from what it ordinarily
affects.

Sources of Exposure to Infection or Infestation

1. Contaminated soil or water (most common)
Ex. Ascaris Lumbricoides, Trichiuris Trichiura, Strongyloides Stercoralis, human hookworms)

2. Food containing the parasite’s infective stage

Ex. Taenia Solium – pork tapeworm
Diphyllobotrium Latum – fish tapeworm
Trichinella Spiralis & Taenia Solium – raw pork
Teania Saginata – improperly cooked or raw beef

3. A blood-sucking insect
Ex. Plasmodium spp – mosquitos (Anopheles mosquito)
Leishmaniasis – sand fly
Trypanosomes – tse-tse fly & reduviid bugs
Filariasis – Culex & Mansonia mosquitos

4. A domestic or wild animals harboring the parasite

Ex. Dog Tapeworm – E. Granulosus
Pigs, Cows, Birds
5. Contaminated clothing, beddings, or immediate environment the person has infected
6. Auto-infection

Modes of Transmission
1. Oral-fecal route
2. Skin penetration
3. Insect bites
4. Eggs inhalation
5. Transplacental or congenital infections
6. Transmammary infection
7. Sexual intercourse

Portal of Exit of Parasites

1. Anus (feces)
2. Ureter (urine)
3. Lungs (phlegm)
4. Vaginal discharges
Pathogenesis of Parasites
1. Trauma or physical damage
- manifestations may be due to the direct physical damage caused by the parasite in the
organ or at the point of entry of the parasite.

2. Lytic necrosis
- enzymes and other substances produced by parasites that are necessary for them to digest
food available in the immediate environment may cause harm to the tissue of the host.

3. Stimulation of host tissue reaction

- animal parasites provoke host tissue reactions in the form of cellular proliferation and
infiltration at the entry site of the parasite or may involve systemic increase in cell types especially
those in the blood circulation, may stimulates cancer cells in specific organ
Ex. Liver Flukes (Schistosoma japonicum & Clonorchis sinensis)

4. Toxic & allergic phenomena (immunopathology)

- proteins and other metabolites produced by the parasites may lead to hypersensitivity or
allergic reactions due to stimulation of antibody production.

Immunologic reactions of humans to various parasites

Reaction Mechanism Result Example

Type 1: Cell or Parasite Ag + IgE Anaphylactic Shock; Helminths: African
Anaphylactic attach to mast cells → bronchospasm; local Trypanosomiasis
histamine release inflammation
Type 2: Antibody- Ab + parasite Ag on Lysis of cell-bearing Trypanosome cruzi
mediated cell surface → parasite antigen
complement
activation
Type 3: Immune Antibody + Inflammation & tissue Malaria,
Complex extracellular antigen damage, complex Schistosomiasis,
complex deposition in organs & Trypanosomiasis
tissues
Type 4: Cell-mediated Sensitized T-Cell Inflammation, Leishmaniasis,
reaction with antigen mononuclear Schistosomiasis,
→ release of accumulation, Trypanosomiasis
lymphokines, macrophage
triggered cytotoxicity activation; tissue
damage

5. Opening of pathways for entry of other pathogens into the tissues

- the presence of parasites and the damage they produced to the tissues may favor the entry
and proliferation of other organisms, specifically bacteria. (Ex. Pinworms in the anus of the children)

General Life Cycle of Parasites

1. Source of infection
2. Mode of Transmission
3. Infective Stage (morphologic form that infects human)
4. Pathogenic Stage (morphologic form that is responsible for the pathology produced leading to
clinical manifestations)
5. Diagnostic Stage (morphologic form that can be detected through laboratory methods)
 Parasite enters &
Parasite comes in
establishes
contact with
residence in or on
human (mode of
human (infective
transmission)
stage)

Parasite comes in contact with soil or water &

other intermediate host (source of infection Parasite multiplies & competes w/ humans for
- parasite emerge from water, food, soil or nutritional needs (pathogenic stage)
intermediate hosts

Parasite emerges
from human
(diagnostic stage)
- parasite enters
outside
environment
General Life Cycle of the Parasite

CLASSIFICATION OF PARASITES (SUB-KINGDOM)

1. SINGLE-CELLED (PROTOZOA)
- Based on Motility and Mode of Reproduction
a. Amoeba (pseudopods)
b. Flagellates (flagella)
c. Sporozoa
d. Ciliates (cilia)
2. MULTICELLULAR METAZOA (HELMINTHS)
a. Nematodes
b. Cestodes
c. Trematodes

- Most parasitic protozoa reproduce by binary fission except sporozoa (reproduce sexually and
asexually)

Classification of Medically Important Parasites

Biologic, Morphologic and Physiologic Characteristics of Parasites (Comparison)

Protozoa
Amoeba Unicellular; cyst Binary fission Pseudopods Assimilation by
& trophozoite pinocytosis or
forms phagocytosis
Flagellates Unicellular; cyst Binary fission Flagella Simple diffusion
& trophozoite or ingestion via
forms cytostome,
pinocytosis or
Facultative phagocytosis
Ciliates Unicellular; cyst Binary fission Cilia anaerobe Ingestion via
& trophozoite or conjugation cytosome, food
forms vacuole
Sporozoa Unicellular, Schizogony & None Simple diffusion
frequently sporogony
intracellular,
multiple forms
including
trophozoites,
sporozoites,
cysts (oocysts),
gametes
Helminths
Cestodes Multicellular; Hermaphroditi No sigle Adults Absorption of
head w/ c organelle; usually nutrients from
segmented body usually anaerobic intestines
(proglottids); attachment to
lack of digestive mucosa;
tract; head possible
equipped w/ muscular
hooks &/or motility
suckers for (proglottids)
attachment
Trematode Multicellular; Hermaphroditi No single Adults Ingestion or
s leaf-shaped with c but organelle; usually absorption of
oral & ventral schistosoma muscle- anaerobic body fluids,
suckers, blind spp has directed tissue or
alimentary canal separate sexes motility digestive
contents
Nematodes Multicellular; Separate sexes No single Adults Ingestion or
round, smooth, organelle; usually absorption of
spindle-shaped, active anaerobic; body fluids,
tubular digestive muscular larvae tissue, or
tract; possibility motility possibly digestive
of teeth or aerobic contents
plates for
attachment
LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

I. SPECIMEN COLLECTION AND PROCESSING

1. Diagnosis of parasite infections often depend on observing parasite forms that include protozoa
ova, larva or adult forms.
2. Specimen includes stool, tissue, urine, sputum and blood

a. Stool sample should be free from antimicrobial agents that can inhibit parasitic growth. Barium
from enemas can obscure parasites during microscopic examination
- at least 3 grams of fecal sample on 3 consecutive days
- because urea and acidic pH inhibit some parasite and distort their morphology, stool
should be free of urine
- liquid stools best for trophozoites detection and formed stool for cyat and ova detection

b. Stool preservatives
- stool should not be preserve for longer hours
- 5 to 10% formalin for concentration procedures
- PVA for stained smear preparation
- Sodium Acetate Formalin = concentration procedures and stained smear preparation

c. Fecal Concentration Methods

a. Foramlin-Ethyl Acetate Sedimentation
b. Zinc Sulfate Flotation
c. Sheather Sugar Flotation

d. Blood Concentration Methods

3. Collection Methods
a. Cellophane / Scotch tape method (pinworm)
b. Entero Test – string test
c. Sigmoidocopy – to collect colon material

4. Sample Types and associated parasites

a. Feces: Gardia, Cryptosporadium, Entanoeba, Ascaris, Enterobius, etc
b. Blood: Plasmodium, Leishmania, Trypanosoma, Microfilariae
c. Skin: Onchocerca
d. Vaginal or urethral: Trichomonas
e. Eye scraping: Acanthamoeba
f. Tissue: Naegleria, Acanthamoeba, & Leishmania
g. Urine: Schistoc=soma & Trichomonas
h. Sputum: Ascaris & Strongyloides

II. MICROSCOPIC EXAMINATION

A. Direct wet preparation or direct wet mount

Purpose: To detect the presence of motile protozoan trophozoites; other stages detected include
cysts, oocysts, ova and larvae of worms.

Principle: A small portion of unfixed stool is mixed w/ saline or iodine then studied under the
microscope.
B. Concentration Methods
- can both used on both fresh and preserved specimens. It can be used to detect cysts,
oocysts and larvae of nematodes

Purposes:
1. To aggregate parasites present into a small volume of the sample that enables the detection of
small numbers of parasites that might not be detected in direct wet preparation.
2. To remove debris and other contaminants that might interfere with the microscopic examination.

Concentration Techniques:
1. Sedimentation (Formalin-Ethyl Acetate Sedimentation Procedure)
Principle: Based on the specific gravity- parsites are heavier than the solution than the fecal
debris.

2. Zinc Sulfate Floatation Technique

Principle: Based on the differences in specific gravity and the sample debris (heavier than the
parasites). The zinc sulfate has a specific gravity of 1.18 – 1.20 and is used as the concentrating
solution.

C. Permanent Stains
- serves as a final step in the microscopic examination for the detection of parasites. It is
designed to confirm the presence of cysts and/ or trophozoites of protozoans.

III. OTHER SPECIMENS & LABORATORY PROCEDURES

1. Duodenal Material
- this may be collected using nasogastric tube (NGT) or through the enteric capsule test
(Entero test).
- the collected fluid must be examined immediately to prevent rapid deterioration of
trophozoites, if there is any. Less than 2ml volume is recommended for this procedure. The sample
undergoes centrifugation prior to microscopic examination of the sediments.
- in the Entero- test, patient is advised to swallow gelatin capsule that cointains a coil of yarn
that is weighted, which will be released to the duodenum as the capsule dissolves in the stomach.
The free end of the yarn is attached to the neck or cheek of the patient and pulled out after 4 hours
of incubation. The bile stained material attached to the string is then examined under the
microscope by wet preparation followed by permanent stain application.

2. Sigmoidoscopy Material
- this is done by examination of the colon and collection of the material, which can be used
in biopsy examination. It is helpful in the diagnosis of Entamoeba histolytica infection.

3. Cellophane tape or Scotch Tape Preparation

- this is done to detect the presence of pinworm, Enterobius vermicularis. The female
parasite migrates to the anus and lays it eggs.
- done in the morning before defacation or washes.
- used to detect tapeworm eggs of Taenia spp.

4. Blood
- for blood-borne parasites (leishmania, trypanosoma, plasmodium and filarial worms)
- thin (spp identification) and thick (number) blood smear, blood from earlobe or fingertip.
- stain used: wright’s or giemsa
5. Cerebrospinal Fluid
- used to detect amebic infections.
- immediate examination ofr motility detection
- wet preparations to detect morphological characteistics (Naegleria, Acanthamoeba,
Trypanosoma, Toxoplasma gondii, Taenia solium (cystercosis) and Echinococcus.

6. Tissue and Biopsy Specimens

- utilized to detect the presence of Leishmania, Toxoplasma gondii, Trypanosoma, Taenia
solium, Trichinella spiralis.
- specimen of choice: liver abscess (if suspected amoebic liver abscess.

7. Genitourinary Secretions
- to detect blood fluke in urine (Schistosoma haematobium), Trichomonas vaginalis
- cotton swab collection, centrifuged urine sediments
- saline wet preparations for trophozoites demonstration.

PROTOZOA

Definition of Terms
Infective Stage – stage of parasite that enters the host or the stage that is present in the parasite’s
source of infection

Pathogenic Stage – stage of the parasite that is responsible for producing the organ damage in the
host leading to clinical manifestations

Encystation – process by which trophozoites differentiate into cyst forms

Excystation – process by which cysts differentiate into trophozoites forms.

General Properties of Protozoa

1. Single-celled eukaryotic organisms that are spherical to oval or elongated in shape.
2. Classification is mainly based on the organ of locomotion.
3. Not all protozoa are parasitic
4. Some ar facultative parasites capable of free-living state that normally reside in the soil or water
but can cause severe illness when they gain entrance into the central nervous system or the eyes.
5. Majority reproduce by binary fission (flagellates, ciliates and amoeba), sporozoans reproduces by
both asexual and sexual means. Asexual reproduction is achieved through process of merogony or
schizogony; sexual recombination can occur leading to antigenic and genomic variation.
6. Parasitic protozoa infections are diagnosed to demonstrate trophozoite (motility, feeding and
dividing satge of the parasite), or cyst (dormant, non-motile form).

INTESTINAL PROTOZOA

ENTAMOEBA HISTOLYTICA
- An intestinal and tissue amoeba and is the only known pathogenic intestinal amoeba
- Life cycle consists of two stages:
o Trophozoite - motile, pathogenic stage; found within the intestinal and extra-
intestinal lesions, and in diarrheal stools.
o Cyst - non-motile, infective stage, usually found in non-diarrheal formed stools.
- Epidemiology: E. Histolytica is found worldwide but is more common in tropical countries
with poor sanitation.
 o Transmission: oral-fecal route through cyst ingestion from contaminated food and
water (as the major source of infection); sexual intercourse (when man has
unprotected sex with woman who has vaginal amoebiasis or through anal
intercourse.
- Pathogenesis: The ingested cyst undergoes excystation in the ileum where it differentiates
into a trophozoite, proceeds to colonize the cecum and colon, then undergo encystation and
become converted into cysts which are then passed out with the feces. Trophozoites are
usually recovered in the feces of patients with active infections, while cysts are found in
formed, non-diarrheic stools. The trophozoites of E. histolytica secrete enzymes that cause
local necrosis producing the typical “flask-shaped” ulcer associated with the parasite.
Invasion of the portal circulation may occur leading to the development of abscess in the
liver.

Life Cycle of Entamoeba Histolytica

- Disease: Amoebiasis
o Acute Intestinal Amoebiasis
o Extraintestinal Amoebiasis
o Asymptomatic Carrier State
- Laboratory Diagnosis: Stool specimen be examined within one hour of collection for
trophozoites motility appearance (finding trophozoites in diarrheic stools and cysts in
formed stools). Serologic testing is useful for invasive amoebiasis diagnosis.
- Treatment: Metronidazole; surgical drainage of amoebic liver abscess may be necessary if
untreated with medical therapy.
- Prevention and Control: Good personal hygiene – proper handwashing, proper waste
disposal, adequate washing and cooking of vegetables

GIARDIA LAMBLIA (GIARDIA INTESTINALIS/ GIARDIA DUODENALE)

- An intestinal protozoan that was initially known “Cercomonas intestinalis”.
- Also exists in trophozoite(pear-shaped or tear-drop shaped with 4 pairs of flagella and
characterized by a falling-leaf motility), described as resembling and old man with whiskers –
 old man facies, has sucking disc for attachment to intestinal villi of the infected human; and
cyst forms- typically oval and thick-walled with 4 nuclei (fully mature), divides through binary
fission, cyst gives rise to 2 trophozoites during excystation in the intestinal tract.
- Epidemiology: It has a worldwide distribution through contaminated water sources. The
infection is also common among individuals engaging in oral-anal contact. High incidence has
been in daycare centers and among patients in mental hospitals.
- Pathogenesis: The parasite is primarily transmitted through ingestion of the cyst from fecally-
contaminated water and food. The cyst enters the stomach and is stimulated by the gastric
acid to undergo excystation in the duodenum. The trophozoites then attach themselves to
the duodenal mucosa through the sucking disks. Damage to the intestines is not due to
invasion of the parasite but because of inflammation of the duodenal mucosa, leading to
diarrhea with malabsorption of fat and proteins. The trophozoites may also infect the
common bile duct and gallbladder.

Life cycle of Giardia Lamblia

- Disease: Giardiasis
o Asymptomatic Carrier State
o Giardiasis (Traveler’s Diarrhea)
- Laboratory Diagnosis
o Demonstration of the cyst or trophozoites in diarrheic stools.
o String Test may be performed if microscopic examination of the stool is negative
- Treatment: Metronidazole, Tinidazole, Nitazoxanide.
- Prevention & Control: Avoidance of fecal contamination of water supplies through proper
waste disposal. Drinking water should be boiled, filtered, or iodine-trreated especially in
endemic areas. Improvement of personal hygiene such as proper handwashing and the like.

TRICHOMONAS VAGINALIS
- A pear-shaped organism with a central nucleus, four anterior flagella and an undulating
membrane.
- Exists only in the trophozoite form (infective and pathogenic)
- Epidemiology: It is not an intestinal pathogen. It causes urogenital infections and the main
mode of transmission is through sexual intercourse. It has been isolated from the urethra
and vagina of infected women as well as the urethra and prostate gland of infected men.
 Infection is highest among sexually-active women and lowest in post-menopausal women. It
can be transmited occasionally through toilet articles and clothing of infected individuals.
Infants may be infected as they pass through the infected birth canal during delivery.
- Pathogenesis: The parasite invades the vaginal mucosaof infected women where divided by
binary fission. The trophozoites feed on local bacteria and leukocytes. Inmen, the most
common infection site is the prostate gland and the urethral epithelium.

Life Cycle of Trichomonas Vaginalis

- Disease: Trichomoniasis
o In Men: Prostatitis, Urethritis (recurring, most symptomatic form)
o In Women: Vaginitis (itchiness, red cervix), dysuria
o In Infants: infected infants manifest conjunctivitis or respiratory infection (when
infants passes through infected birth canal during delivery)
- Laboratory Diagnosis: Trophozoite in wet mount of vaginal or prostatic secretions, urine and
urethral discharges.
- Treatment: Metronidazole to prevent “ping-pong infection”
- Prvention & Control: Safe sex, Health & sex education, pH maintenance of the vagina

BALANTIDIUM COLI
- A mophologically more complex than E. histolytica that has a primitive mouth called a
Cytostome, a nucleus, food vacuoles and a pair of contractile vacuole.
- Infective stage is the cyst; pathogenic stage is the trophozoite – exhibits a rotary, boring
motility through cilia and contain 2-nuclei (a smalldot-like micronucleues adjacent to a
kidney bean-shaped macronucleus)
- Largest protozoan to infect humans.
- Epidemiology: Has a worldwide distribution. Most common and important reservoir is the
pig. Main sourceof infection is water contaminated with pig feces; mode of transmission is
fecal-oral route; person-to-person transmisssion via foodhandlers
- Pathogenesis: Found in contaminated water
 - Disease: Balantidiasis – a dysentery type of diarrhea resembling amebic dysentery. Acute
infections may manifest with liquid stools containing pus, blood and mucus. Chronic
infections manifest a tender colon, anemia, wasting and alternating diarrhea and
constipation.
- Laboratory Diagnosis: Trophozoites and Cysts in stool specimen by wet microscopic
examinations
- Treatment: Oxytetracycline and Iodoquinol (recommended); metronidazoel (alternative)
- Prevention & Control: Good sanitation, proper disposa of pig feces, boiling of drinking water.

Balantidium Coli Lyfe Cycle

BLOOD & TISSUE PROTOZOA

ACANTHAMOEBA (FREE-LIVING AMOEBA)

- A free-living amoeba that causes inflammation of the brain subsatnace and its meningeal
coverings (meningoencephalitis).
- Found widely in soil, contaminated fresh water lakes and other water environment and may
cause immunocompromised patients. The parasite able to survive in cold water
- Cyst is the infective stage; trophozoite is the pathogenic stage.
- Epidemiology:
o Mode of transmission: Through aspiration or nasal inhalation or direct invasion in
the eye (through swimming in contaminated water)
o Trophozoites can enter lower respiratory tract or through ulcers in mucosa or skin
then migrates through the bloodstream and invade the CNS.
o Eye infection with acanthamoeba occurs primarily in patients who wears contact
lenses (wash with contaminated water)
- Disease:
o Granulomatous Amebic Encephalitis – may develop brain abscesses. S/S= headache,
seizures, stff neck, nausea and vomiting. It can also spread and produce lesions in
the kidneys, pancreas, prostate and uterus.
o Keratitis – infection of the cornea of the eye. S/S include severe eye pain and vision
problems, eye blindness.
- Laboratory Diagnosis: Finfing of both trophozoite and cysts in the CSF, brain tissue, corneal
scrapings; histologic examination of corneal scrapings
 - Treatment: Pentamidine, Ketoconazole or Flucytosine. For eye infection- topical miconazole,
chlorhexidine, itraconazole, ketoconazole, rifampicin or propamidine (best record)
- Prevention & Control: Adequate boiling water, regular disinfection of contact lenses is also
advised, avoid home-made non-sterile saline solutions.

Life Cycle of Acanthamoeba spp.

NAEGLERIA FOWLERI
- Free-living protozoan found worldwide in soil and contaminated water environment, can
survive in thermal spring water
- The only amoeba with three identified morphologic forms- trophozoite, flagellates and cyst
forms.
o Trophozoite – “slug-like” motility, only exist in human
o Flagellate – “pear-shaped” and equipped with 2 flagella responsible for “jerky or
spinning movement”
o Cyst – non-motile
- Epidemiology: Naegleria infection is acquired transnasally when swimming in contaminated
water. It will penetrate the nasal mucosa and cribriform plate, enters the central nervous
system and rapidly produces fatal menigitis and encephalitis (primary amoebic
meningoencephalitis. They usually produce infection in children. It could also be inhaled
through dust containing the parasite. Entire life cycle occurs in the external environment.
- Disease:
o Asymptomatic Infection – most common clinical presentation in patients with
colonization of the nasal passages.
o Primary Amoebic Meningoencephelitis (PAM) – result of colonization of the brain by
amoeboid tropozoites leading to rapid tissue destruction. Patients initially complains
of sore throat, nausea, vomting, fever and headache. Eventually, patient develop
signs of meningeal irritation (kernig’s sign), as well as alterations in their senses of
smell and taste. If untreated the patients may die within one week after symptoms
have appeared.
- Laboratory Diagnosis: Based on the finding of the ameboid trophozoites in the CSF.
- Treatment: It is ineffective due to its rapid fatal course. Ampotericin B is a drug of choice
combined with miconazole and rifampicin if detected earlier.
- Prevention and Control: Adequate chlorination of swimming pools and hot tubs is
recommended.
 Life Cycle of Naegleria Fowleri

LEISHMANIA SPP
- Are obligate intracellular parasites
- Has 3 morphologic forms:
o Amastigote – pathogenic and diagnostic stage found primariy in tissue and muscle,
CNS within macrophages and in cells of reticuloendothelial system (RES)
 Typically round to oval in shape and contains a nucleus (blepharoblast), and
a parabasal body adjacent to the blepharoblast
 Kinetoplast – (blepharobast and the parabasal body)
o Promastigote – infective stage, maybe seen only if a blood sample is collected and
examined immediately after transmission
 Long and slender in shape; kinetoplast located in its anterior end and a
single free-flagellum extending from the anterior portion
o Epimastigote – found primarily in the vector
- Epidemiology and Pathogenesis
o Vector: female sandfly (phlebotomus and lutzomyia genera)
o Worldwide distribution
o Natural reservoir includes rodents, ant eaters, dogs and cats
o In endemic areas, paradite maybe transmitted in a human-vector-human cycle.
o 3 major strains: differs in the tissues affected and the resulting clinical manifestations

1) L. donovani (Visceral leishmaniasis/ Kala-azar/ Dumdum fever)

 Leishmania donovani complex consist of the following:
o L. donovani chagasi – seen mainly in Central America-
Mexico, West Indies and South America, vector: lutzomyia
sandfly
o L. donovani donovani in Africa and Asia – Thailand, China,
India, Burma and East Pakistan, vector: phlebotomus sandfly
o L. donovani infantum – mainly in Mediterranean Europe,
near East and Africa; vector is phlebotomus sandfly.
 The promastigote is injected into human host through bite of the
sandfly where after entry into host loses its flagella and engulf by
 macrophages then transform into amastigotes. Severely affected are
the RES organs that includes liver, spleen and bone marrow.

Life Cycle of Leishmania Spp

- Disease: Visceral Leishmaniasis/ Kala-azar/ Dumdum Fever

o After incubation of 2 weeks to 18 months, disease begins with intermittent fever,
weakness and weight loss
o Massive splenomegaly leading to hypersplenism resulting to anemia.
o Hepatomegaly also occurs
o Hyperpigmentation in patients with light-skinned patients (kala-azar- “black fever or
black sickness”)
o Bone marrow involvement – anemia (cell lysis, thrombocytopenia, leukopenia)
o Occurrence of Glomerulonephritis (inflammation of the kidney’s glomeruli)
o Disease may be fatal if untreated
- Laboratory Diagnosis:
o Montenegro skin test – screening test
o Definitive diagnosis is done by amastigote demonstration in Giemsa stained blood
smear specimen; bone marrow and lymph node biopsies of infected areas; blood
culture which demonstrate promastigote forms
o Serologic tests: ELISA (Enzyme-Linked Immunosorbent Assay), IFA (Indirect
Fluorescent Antibody) or DAT (Direct Agglutination Test)
- Treatment:
o Drug of choice: Amphotericin B (Ambisome)
o Sodium stibogluconate- effective but may develop resistance
- Prevention and Control:
o Vector control – use of insect repellents, protective clothing and screen installations
o Immediate trreatment of infection to stop the spread of disease.
2) L. tropica (Old World Cutaneous leishmaniasis)
 Leishmania tropica complex consists of:
o L. tropica
o L. aethiopica
o L. major
 Vector: Phlebotomus sandfly; attacks the human lymphoid tissue of the skin
 Disease: Old World Cutaneous Leishmaniasis
o Also known as “Oriental Sore/ Baghdad or Delhi Boil
o Characterized by one or several pus-containing ulcers that may heal
spontaneously.
o Initail lesion – small, pruritic red papule at he bite site
o Thick skin plaques with multiple nodules may develop especially on
the limbs and face.
 Laboratory Diagnosis:
o Giemsa-stained slides of aspirated fluids from beneath the ulcer bed
– diagnostic procedure of choice
o Microscopic examination reveals amastigote form
o Culture procedure shows promastigote form
 Treatment:
o Drug of choice – sodium stibogluconate
o Steroids with heat application at the infected lesions
o Alternative drugs: Meglumine antimonite, Pentamidine, Oral
ketonazole, Paramomycin ointment for ulcers
 Prevention and Control
o Same with those of Leishmaniasis
o Vaccine against L. tropica (under clinical trials yet)

3) L. braziliensis (Mucocutaneous leishmaniasis)

- involves the skin, cartilage and mucuos membranes
- occurrence of infection most common in Brazil and Central America
primarily in construction and forestry workers.
 Leishmania braziliensis complex consist of:
o L. panamensis (Panama and Columbia)
o L. peruviana (Peruvian Andes)
o L. guyanensis (Guianas, parts of Brazil and Venezuela)
 Vector: Sandflies(Lutzomyia and Psychodopigus) through skin bite
o Promastigote invade the RES cells where they transform into
amastigotes (diagnostic stage). Amastigote reproduction results in
tissue destruction.
o Amastigotes are taken up by the vector during blood meal and are
transformed into promastigotes.
 Disease: Mucocutaneous Leishmaniasis/ Espundia
o Espundia begins with papule at the bite site then forms metasttic
lesions at the junction of the nose and mouth
o Disfiguring granulomatous, ulcerating lesions destroy the nasal
cartilage and death may occur in secondary infections.
 Laboratory Diagnosis:
o Amastigote demonstration by ulcer biopsy
o Microscopic examination of giemsa-stained ulcer biopsy specimens
o Culture shows promastigotes
  Treatment
o Sodium stibogluconate but resistance may develop
o Amphotericin B
o Oral anti-fungal drugs: Fluconazole, ketoconazole and itraconazole
 Prevention and Control:
o Use of nets, window screens, protective clothing, insect repellents to
avoid insect vector
o Immediate attention to treat disease

TRYPANOSOMA SPP
- Are hemoflagellates
- Diagnostic stage: trypomastigote, curved-shaped, assuming the letters C, S or U
- Kinetoplast of trypomastigotes is posteriorly located with single large nucleus located
anteriorly
- Trypomastigotes visibly seen in peripheral blood.

TRYPANOSOMA CRUZI
- Found in South and Central America transmitted by Reduvid bite or Triatomid bud (Triatoma
or “Cone-nose” bug or “kissing bug”)
- Transferred to human host when the feces of the bug containing the trypomastigote is
deposited near the bite site, where feces are introduced to the bite site and when the host
scratches the biten area; could be transmitted by blood transfusion, sexual intercourse,
transplacental transmission and through mucuos membrane
- Resevoir hosts: humans, animals- domestic cats and dogs, wild species such as armadillo,
racoon and rat.
- Disease: Chagas Disease (American Trypanosomiasis)
o Acute phase – begins with a nodule (chagoma) near the bite site and Romana’s sign
(unilateral swelling of the eyelid with conjunctivitis; fever, chills, malaise, myalgia and
fatigue
o Chronic phase – Hepatosplenomegaly, Lymphadenopathy, myocarditis with cardiac
arrhythmia, cardiac muscle frequently and most affected tissue, meningoencephalitis
and cysts
- Life cycle of Tryponasoma Cruzi
 - Laboratory Diagnosis:
o Trypomastigote demonstration in thick or thin blood film
o Bone marrow aspiration, muscle biopsy, culture on special medium and
xenodiagnosis
o Xenodiagnosis and serologic tests are useful in the chronic form of the disease
- Treatment:
o Drug of choice: Benznidazole, Nifurtimox (less effective during chronic stage)
o Alternative: Allopurinol and Ketokonazole
- Prevention and Control
o Protectio from infected reduviid bug
o Improve housing conditions
o Insect control (pesticides)
o Health education

TRYPANOSOMA BRUCEI GAMBIENSE and TRYPANOSOMA BRUCEI RHODESIENSE

- Trypomastigote – infective and diagnostic stage
- Vector: TseTse fly
T. Brucei Gambiense T. Brucei Rhodesiense
Reservoir hosts Humans Domestic & Wild animals
Disease West African or Gambian East African or Rhodesian
Sleeping Sickness Sleeping Sickness
Occurrence Sub-Saharan Africa East Africa Arid regions

- Disease: African Sleeping Sickness

T. Brucei Gambiense T. Brucei Rhodesiense
Virulence Less virulent More virulent
Manifestations Chancre- red rash, pruritus
Cervical lymphadenopathy (Winterbottom’s sign), localized
edema, delayed pain sensation (Kerandel’s sign), encephalitis
characterized by headache, insomnia and mood changes, muscle
tremors, slurred speech
Incubation period of infection Infection has a shorter incubation period. Death is usually seen
within 9-12 months of infection if untreated with could be due to
 glomerulonephritis and myocarditis

- Life Cycle of T. brucei

- Laboratory Diagnosis:
o Giemsa-stained blood smear, lymph node aspirations
o Trypomastigote demonstration on CSF
o Aspiration of chancre will reveal trypomastigote
o IgM and protein detection on serologic test – considered diagnostic
- Treatment:
o Melarsoprol, Suramin, Pentamidine, Eflornithine
o Drug of choice depending on whether the patient is pregnant or not, patient’s age
and stage of the disease.
- Prevention and Control
o Protection against fly insect bite
o Netting, fly traps, protective clothing, insecticides
o Cleaning of the environemnt especially forest

PLASMODIUM SPP
- Malariae is caused by plasmodium spp, P. Malariae, P. Ovale, P. Vivax, and P. falciparum
- Vector and definitive host: Female Anopheles Mosquito
- Sporogony – sexual cycle (occurs primarily in mosquito)
- Schizogony – asexual cycle (occurs in humans as intermediate host)
- Sporozoite – infective stage (saliva of the biting mosquito
- Merozoites – pathogenic stage, release from liver cells and infects the red blood cells
- Exoerythrocytic phase – multiplication and diffrentiation of sporozoites into merozoites
- Life Cycle of Plasmodium spp:
- Merozoites once released from liver cells will infect red blood cells. The parasite’s life cycle
now enters the erythrocytic phase. These merozoites now multiply and are eventually
released to infect other red blood cells. This periodic release of merozoites causes typically
recurrent symptoms seen in malaria patients. Some merozoites develop into
microgametocytes (male gametocytes) and macrogametocytes (female gametocytes). These
red cells containing gametocytes are ingested by the mosquito during feeding thus sexual
reproduction ensues.
- Epidemiology and Pathogenesis:
o Occurs worldwide, primarily in tropical and sub-tropical areas, Asia, Africa, Central
and South America
o Secretary Ona in Philippines, reported once that out of 53 provinces, 27 are malaria-
free including Cavite, Batangas, Marinduque, Catanduanes, Albay, Masbate,
Sorsogon, Camarines Sur, Iloilo, Aklan, Capiz, Guimaras, Bohol, Cebu, Siquijor,
Western Samar, Eastern Samar, Northern Samar, Northern Leyte, Southern Leyte,
Biliran, Camiguin, Surigao del Norte, Benguet, Romblon, Batanes, and Dinagat
Islands.
o Main mode of transmission of malaria is the bite of the female mosquito vector,
blood transfusion (transfusion malaria), intravenous sharing of needles of drug
abusers (“main-line malaria), and transplacental transmission (congenital malaria)
- Disease: Malaria
o Paroxysms of Malaria
 Cold Stage: Abrupt onset of chills (rigors), headache, muscle pain (myalgia)
and joint pains (arthralgia), approximately last for 10-15 minutes or longer
 Hot Stage: Fever spiking up to 41⁰C lasting 2-6 hours with shaking chills,
nausea, vomiting and abdominal pain.
  Sweating Stage: Drenching sweats
 Splenomegaly often present and anemia is prominent.
- Laboratory Diagnosis
o Gram-stained; Wright’s stained, thick and thin blood smear
o Thick smear – for screening purposes; thin smear – for differentiation of plasmodium
spp.
o Best time to collect blood – midway between paroxysms of chills and fever or before
onset of fever (presence of great number of intracellular organisms)
o Trophozoites – seen in infected red blood cells.
 P. falciparum- crescent-shaped or banana-shaped gametocytes (>10 infected
red blood cells with ring forms)
 P. malaria – rosette schizont-diagnostic (10-12 red blood cells)
- Treatment:
o Drug of choice: Chloroquine or parenteral quinine
o Artemisin-based combination therapies (ACTs) are now recommended for
uncomplicated malaria
o Artesunate in combination with either amodiaquine, mefloquine or sulfadoxine-
pyrimethamine- drug of choice for severe malaria
- Prevention and Control
o Chemoprophylaxis of malaria for travelers to endemic areas (mefloquinine or
doxycycline)
o Chloroquine – 2 weeks before arrival and continued for 6 weeks after departure
followed by a 2-week course of primaquine if exposure was high.
o Avoidance of vector bite, netting, window screens, protective clothing, insect
repellents, from dusk to dawn
o Environment protection
TOXOPLASMA GONDII
- Definitive host – domestic cats or other felines
- Intermediate host – humans and other mammals
- Infective form – oocysts (found in undercooked meat). Oocysts when in small intestine will
rupture into trophozoites known as tachyzoites (rapidly multiplying forms responsible for the
initial infection) or bradyzoites (shorter, slow-growing forms seen in chronic infections).
- Epidemiology and pathogenesis:
o Infection occurs worldwide. Infection usually sporadic but outbreaks associated with
ingestion of raw meat or contaminated water can occur. Individuals who are severely
immunocompromised are more likely to develop severe disease.
o Transmission:
 Ingestion of improperly cooked meat that serves as intermediate hosts
 Ingestion of oocyst from contaminated water

Less common MOT are the following:

 Transplacental transmission
 Sharing of needles by IV drug abusers
 Blood transfusion
- Life cycle of Toxoplasma Gondii
- Disease: Toxoplasmosis
o Infection in immunocompetent individuals – usually asymptomatic
 Acute infection may manifest non-specific symptoms such as chills, fever,
headache, and fatigue, lymphadenitis, hepatitis, myocarditis and
encephalomyelitis, chorioretinitis leading to blindness
 Congenital infection – occurs in infants through infected mothers during
pregnancy
 Infection in immunocompromised hosts – usually manifest neurologic
symptoms (diffuse encephalopathy, meningoencephalitis, brain tumors).
Infection I lungs, eyes and testes.
- Laboratory Diagnosis:
o High antibody titers demonstration through immunofluorescence assay
o Giemsa-stained preparations showing crescent-shaped trophozoites during acute
infection. Cyst in tissues
o Prenatal diagnosis – ultrasonography and amniocentesis with PCR of the amniotic
fluid (method of choice)
- Treatment:
o Pyrimethamine plus sulfadiazine
o Alternative: Clindamycin plus pyrimethamine
o For pregnant women- clindamycin or spiramycin
- Prevention and Control
o Adequate cooking of meat
o Refrain from eating undercooked meat, avoid contact with cats and litter
boxes, especially pregnant individuals