CLINICAL PARASITOLOGY

MEDICAL TECHNOLOGY ASSESSMENT PROGRAM 1 (MTAP 1)

KRISTINA MARIA R. PETALCORIN, RMT, DTA, MSMT(c)
FAR EASTERN UNIVERSITY - MANILA
CLASSIFICATIONS OF PARASITES:
▪ According to habitat:
1. Ectoparasites – resides OUTSIDE the host
2. Endoparasites – resides INSIDE the host
CLASSIFICATIONS OF PARASITES:
▪ According to Effect:
1. Pathogenic – causes diseases
2. Nonpathogenic – does not cause disease
TYPES OF HOSTS:

 DEFINITIVE HOST
• Sexual reproductive phase of the parasite
• Adult phase of the parasite
 INTERMEDIATE HOST
• Asexual reproductive phase of the parasite
• Juvenile stages of the parasite
TYPES OF HOSTS:
 RESERVOIR HOST
• Animal that harbors the same parasite as man
• Source of infection
 PARATENIC HOST
• Harbors the infective stage
• Transports the infective stage to the final host
• Parasite is in an arrested state of development.
TYPES OF HOSTS:

 CARRIER HOST
• Inside the host but no signs of infection
 VECTORS
• Usually, insects that actively transfers the infective stages
• Parasites is developing inside the vector
LIFE CYCLES:
 Three components:
1. Mode of transmission
2. Infective stage
3. Diagnostic stage
MODES OF TRANSMISSION:

 INGESTION – eggs, cysts or larvae

• Giardia lamblia, Ascaris lumbricoides,Trichinella spiralis
 BLOOD TRANSFUSION
• Trypanosoma spp., Plasmodium spp., Babesia spp.
 VECTOR
• Plasmodium spp., Microfilariae, Leishmania and Trypanosoma spp.
MODES OF TRANSMISSION:

 SEXUAL TRANSMISSION
• Trichomonas vaginalis
 PENETRATION
• Hookworms and S. stercoralis (exposure of skin to soil)
• Schistosoma spp. (exposure of skin to water)
• Plasmodium spp. and Microfilariae (mosquito bite)
MODES OF TRANSMISSION:

 INTRANASAL
• Acanthamoeba spp., Naegleria spp.
 INHALATION
• Enterobius vermicularis
 DIRECT CONTACT
• Enterobius vermicularis, Trichomonas vaginalis
MODES OF TRANSMISSION:

 TRANSPLACENTAL
• Toxoplasma gondii,Trypanosoma spp.,
 TRANSMAMMARY
• Strongyloides stercoralis
 INTIMATE ORAL CONTACT
• Trichomonas tenax, Entamoeba gingivalis
SOURCES OF INFECTION:
 SOIL
• Soil-transmitted Helminths (STH)
 WATER
• Schistosoma spp.
 FOOD
• Freshwater fish – Intestinal/ liver flukes
• Crabs – Paragonimus westermani
SOURCES OF INFECTION:

 ANIMALS (Cats, Rats)

 CONTACT TRANSMITTED
 AUTOINFECTION – host can be a direct source of infection
• Capillaria philippinensis, Hymenolepis nana, Enterobius vermicularis,
Taenia solium, Strongyloides stercoralis
SPECIMENS FOR DIAGNOSIS:

 Stool – eggs, cysts, scolex, adult worms

 Sputum – Paragoniumus westermani, Pneumocystis carinii
 Urine – T. vaginalis, Schistosoma haematobium
 Tissue biopsy – T. spiralis, Taenia solium
 Tissue Aspirate – Clonorchis sinensis, Giardia lamblia
 Swabs – E. vermicularis, T. vaginalis
AMOEBA
1. Entamoeba histolytica
 Pathogenic Note:
• E. dispar – morphologically the same with E. histolytica.
• Morphology – cannot be used for differentiation.
 Causes: • E. dispar vs. E. histolytica:
1. Antigenic testing
2. PCR
1. Amoebic dysentery 3. ELISA

2. Amoebic abscess
 World-wide cause of parasitic death
 Cysts and trophozoites in stool are diagnostic.
1. Entamoeba histolytica
 CYSTS:
• Round with one to four nuclei, with rounded
chromatoidal bar and young cysts may contain glycogen
vacuole.
 TROPHOZOITES:
• Rapid and directional motion, one nucleus with central
karyosome; ingested RBCs are diagnostic.
2. Entamoeba coli
 Commensal; Largest amoeba
 Cysts and trophozoites in stool are diagnostic.
 CYSTS:
• 1 to 8 nuclei with eccentric karyosome and splintered end
chromatoidal bar, uneven peripheral chromatin.
▪ TROPHOZOITES:
• Slow motility with one nucleus
3. Entamoeba hartmanii
 Commensal; “small-race E. histolytica”
 Cysts and trophozoites in stool are diagnostic.
 CYSTS:
• Resembles E. histolytica
▪ TROPHOZOITES:
• Resembles E. histolytica
4. Endolimax nana
 Commensal; Smallest amoeba
 Cysts and trophozoites in stool are diagnostic.
 CYSTS:
• 1 to 4 nuclei with blot-like karyosome.
▪ TROPHOZOITES:
• One nucleus with blot-like karyosome.
5. Iodamoeba butschlii
 Commensal
 Cysts and trophozoites in stool are diagnostic.
 CYSTS:
• One nucleus with large glycogen vacuole.
Stained with Iodine - brown
▪ TROPHOZOITES:
• One nucleus
6. Acanthamoeba spp.
 Pathogenic
 GAE – Granulomatous Amoebic Encephalitis
 Trophozoites and cysts – in CSF, brain and autopsy
 Cysts – Double cell wall with one nucleus “wrinkled cyst”
 Intranasal → bloodstream → CNS
 Keratitis – ocular pain and vision impairment
• Contact lens fluid contamination
7. Naegleria fowleri
 Pathogenic
 PAM – Primary Amoebic Encephalitis
 Trophozoites in CSF, brain tissue, autopsy, one nucleus with
slow motility 1. Amoeboid form
2. Flagellate form
 Has 3 morphologic forms 3. Cystic form

 Intranasal → bloodstream → CNS

FLAGELLATES
 INTESTINAL AND GENITAL FLAGELLATES:

PATHOGENIC NONPATHOGENIC
 Giardia lamblia  Chilomastix mesnili
 Trichomonas vaginalis  Trichomonas hominis
 Trichomonas tenax
FLAGELLATES:

 Presence of “flagella” for movement.

 Typical life cycle of flagellate is same as amoebas.
 Trophozoites are seen in loose, liquid or soft stool samples.
 Cysts are commonly seen in formed stool samples.
• Watery, liquid stool samples – processed within 30 mins.
• Formed stool samples – processed within 1 hour.
1. Giardia intestinalis
 Also known as: G. lamblia, G. doudenalis, L. intestinalis, L. duodenalis
 TROPHOZOITE:
• “Old man w/ eyeglasses”
• Falling leaf motility
• Has 4 pairs of flagella
 CYST:
• Ovoid-shaped
1. Giardia intestinalis
 LABORATORY DIAGNOSIS:
• Specimen: Stool, duodenal aspirates and biopsies
• Identification through PCR (Polymerase Chain Reaction)
 TRANSMISSION:
• Ingestion of contaminated drinking water
• Direct fecal-oral route
• Person to person contact (oral-anal sexual practices)
1. Giardia intestinalis
 PATHOGENESIS AND CLINICAL SYMPTOMS:
• Causative agent of Traveler’s diarrhea
• Only pathogenic intestinal flagellate.
• Patients are often completely asymptomatic.
• Affects the mucosal structure and function of the small
intestine causing diarrhea and malabsorption.
• Stools are watery and becomes steatorrheic or fatty stool.
1. Giardia intestinalis
 TREATMENT:
• Metronidazole, Tinidazole and Nitazoxanide
 PREVENTION AND CONTROL:
• Proper water treatment, personal hygiene, proper cleaning,
proper handling of food and avoidance of unprotected oral-
anal sex.
2. Chilomastix mesnili
 Nonpathogenic; commensal organism
 Largest flagellate
 TROPHOZOITE:
• Pear-shaped
• “Cork-screw motility”
 CYST:
• Lemon/ nipple-shaped
2. Chilomastix mesnili
 LABORATORY DIAGNOSIS:
• Liquid stools (reveals trophozoites)
• Formed stools (reveals cysts)
 EPIDEMIOLOGY AND TRANSMISSION:
• Poor personal hygiene and sanitation conditions
• Ingestion of infected cysts
• Hand to mouth, food and drink contamination
3. Dientamoeba fragilis
 “Amoeba-flagellate”
 TROPHOZOITE:
• Irregular and roundish in shape
• Progressive motility
 CYST:
• NO CYSTIC STAGE.
3. Dientamoeba fragilis
 LABORATORY DIAGNOSIS:
• Specimen of choice: Stool
• RT-PCR – most sensitive
 EPIDEMIOLOGY AND TRANSMISSION:
• Transmitted via the eggs of E. vermicularis and A. lumbricoides
• Fecal-oral, oral-anal and person-to-person route
3. Dientamoeba fragilis
 CLINICAL SYMPTOMS:
• Asymptomatic (most patients)
• Diarrhea and abdominal pain, bloody or mucoid stools,
nausea, vomiting, weight loss, eosinophilia and pruritus.
• Constipation, flatulence, weakness and fatigue
 TREATMENT:
• Tetracycline, Iodoquinol and Paramomycin
4. Enteromonas hominis
 Nonpathogenic
 TROPHOZOITE:
• Oval
• Jerky motility
 CYST:
• Oval to elongated
• Suspected as “yeast cells”
5. Retortamonas intestinalis
 Nonpathogenic
 TROPHOZOITE:
• Oval
• Jerky motility
• 2 anterior flagella
 CYST:
• Lemon/ pear-shaped
5. Retortamonas intestinalis
 LABORATORY DIAGNOSIS:
• Specimen of choice: Stool
 EPIDEMIOLOGY AND TRANSMISSION:
• Ingestion of infected cyst
• Poor sanitation and hygiene
 TREATMENT:
• Nonpathogenic (not indicated)
6.Trichomonas hominis
 Nonpathogenic; Medium sized intestinal flagellate
 TROPHOZOITE:
• Pear-shaped
• Jerky motility
• 3 to 5 flagella
 CYST:
• NO CYSTIC STAGE.
7.Trichomonas tenax
 Nonpathogenic; Smallest Trichomonas spp.
 Habitat: Mouth (oral scrapings)
 TROPHOZOITE:
• Oval to pear-shaped
• Has 5 flagella
 CYST:
• NO CYSTIC STAGE
8.Trichomonas vaginalis
 Persistent Urethritis, Persistent Vaginitis
 Largest flagellate
 TROPHOZOITE:
• Ovoid, round, pear-shaped
• Rapid jerky, tumbling motility
• 4 to 6 flagella
 CYST:
• NO CYSTIC STAGE.
8. Trichomonas vaginalis
 LABORATORY DIAGNOSIS:
• Specimen of choice: Urine, vaginal and urethral discharge
• Pap smears, fluorescent stains, monoclonal antibody assays,
cultures and Enzyme Immunoassays
• DNA-based assay
8.Trichomonas vaginalis
 EPIDEMIOLOGY AND TRANSMISSION:
• Sexual intercourse, transplacental, contaminated toilet and
underclothing, sharing of douche supplies, communal supplies.
• Resistant to change in environment.
• Survives in urine, wet sponges and damp towels for several
hours and in water for 40 minutes.
8.Trichomonas vaginalis
 PATHOGENESIS AND CLINICAL SYMPTOMS:
• PERSISTENT URETHRITIS
➢ Involvement of the seminal vesicle and prostate
➢ Enlarged tender prostate, dysuria, nocturia and epididymitis
➢ Releases thin, white urethral discharge
8.Trichomonas vaginalis
 PATHOGENESIS AND CLINICAL SYMPTOMS:
• PERSISTENT VAGINITIS
➢ Foul-smelling, greenish-yellow liquid vaginal discharge
➢ Burning sensation, edema and itching.
➢ Red lesions may be present (Strawberry cervix).
8. Trichomonas vaginalis
 PATHOGENESIS AND CLINICAL SYMPTOMS:
• INFANT INFECTIONS:
➢ Recovered from infants suffering from respiratory infection
and Conjunctivitis.
➢ Infected mother to infant through birth canal and during
vaginal delivery.
8.Trichomonas vaginalis
 TREATMENT:
• Metronidazole
 PREVENTION AND CONTROL:
• Avoidance of unprotected sex
• Avoidance of sharing douche equipment and communal
bathing, as well as close contact with potentially infective
underclothing, toilet articles, damp towels, and wet sponges, is
recommended.
HEMOFLAGELLATES
HEMOFLAGELLATES:
 Parasites located in blood and tissues with flagella.
 Leishmania and Trypanosoma spp.
 Four morphologic forms:
• Amastigote
• Promastigote
• Epimastigote
• Trypomastigote
TAKE NOTE!
LIFE CYCLE:

 Amastigotes and Trypomastigotes – found in human samples

 Amastigotes – found in tissue and muscle, CNS
 Trypomastigotes – visible in peripheral blood smears
 Promastigotes – seen if blood sample is collected immediately
 Epimastigotes – found primarily in the arthropod vector
LEISHMANIASIS:
 General term used to describe diseases caused by genus
Leishmania spp.
 Vector-borne disease transmitted by Sandflies.
 Diseases caused by Leishmania spp:
• Baghdad boils, Bay sore, Chiclero ulcer, Dum-dum fever,
Espundia, Forest yaws, Kala-azar, Oriental sore, Pian bois and
Uta.
1. Leishmania braziliensis complex
 Mucocutaneous
Leishmaniasis, Chiclero
ulcer, Espundia, Forest
yaws, Pian bois and Uta.
 L. braziliensis, L.
panamensis, L. peruviana, L.
guyanesis
1. Leishmania braziliensis complex
 LIFE CYCLE:
• Vector: Sandflies (Lutzomiya and Psychodopygus spp.)
• Infective stage: Promastigotes, Amastigote (in sandflies)
• Diagnostic stage: Amastigotes
 TRANSMISSION:
• Vector bite
1. Leishmania braziliensis complex

 CLINICAL SYMPTOMS:
• MUCOCUTANEOUS LEISHMANIASIS
➢ Large ulcers in oral or nasal mucosa areas
➢ Edema and secondary bacterial infections, numerous
mucosal lesions may cause disfigurement of the face.
➢ Death due to secondary bacterial infection.
1. Leishmania braziliensis complex

 TREATMENT:
• Antimony compounds, Liposomal Amphotericin B,
Fluconazole, Ketoconazole and Itraconazole.
 PREVENTION AND CONTROL:
• Control of sandfly population and reservoir hosts
• Vaccination
2. Leishmania donovani complex
 Visceral Leishmaniasis/ Kala-azar/ Dumdum fever
 L. infantum, L. chagasi
 LABORATORY DIAGNOSIS:
• Montenegro skin test
• Giemsa-stained slides of blood, bone marrow and etc…
• Cultured samples (visualization of Promastigotes)
• ELISA, DAT, Schizodeme and Zymodeme Analysis
2. Leishmania donovani complex
 CLINICAL SYMPTOMS:
• VISCERAL LEISHMANIASIS
➢ Kala-azar/ Dumdum fever
➢ Abdominal illness with hepatosplenomegaly, resembles
Malaria or Typhoid fever (early stages), diarrhea, anemia,
weight loss and emaciation.
➢ Kidney damage (Glomerulonephritis), darkening of skin
(Kala-azar - black fever) and death.
2. Leishmania donovani complex
 TREATMENT:
• Liposomal Amphotericin B, Sodium Stibogluconate,
Allopurinol (AIDS), combination of Paramomycin and
Miltefosine.
 PREVENTION AND CONTROL:
• Control of sandfly population and reservoir hosts
• Protection against sandflies.
3. Leishmania mexicana complex
 New World Cutaneous Leishmaniasis, Chiclero ulcer, Bay sore
 L. mexicana, L. pifanoi, L. amazonensis, L. venezuelensis, L. garnhami
 LABORATORY DIAGNOSIS:
• Giemsa-stained lesion biopsy material NNN – Novy McNeal Nicolle

• Culture on NNN medium (demonstrates Promastigotes)

• Serologic testing (monoclonal antibodies)
• Schizodeme, Zymodeme analysis, nuclear DNA hybridization
3. Leishmania mexicana complex
 CLINICAL SYMPTOMS:
• NEW WORLD CUTANEOUS LEISHMANIASIS
➢ Bay sore, Chiclero ulcer
➢ Single pus containing ulcer (self-healing), small red papule
(pruritus),
➢ Anergic and hypersensitivity immunologic responses,
healing does not occur.
3. Leishmania mexicana complex

 TREATMENT:
• Pentavalent antimonials (Sodium Stibogluconate),
Amphotericin B and Liposomal Amphotericin B.
 PREVENTION AND CONTROL:
• Control of sandfly population and reservoir hosts
• Protection against sandflies (repellants)
4. Leishmania tropicana complex
 Old World Cutaneous Leishmaniasis, Oriental sore, Baghdad
boils, Dry/ urban Cutaneous Leishmaniasis and Delhi boils.
 L. tropicana, L. aethiopica, L. major
 LABORATORY DIAGNOSIS:
• Giemsa-stained slides of aspiration and fluid
• Culture (reveals Promastigotes)
• Schizodeme, Zymodeme analysis, nuclear DNA hybridization
4. Leishmania tropicana complex

 CLINICAL SYMPTOMS:
• OLD WORLD CUTANEOUS LEISHMANIASIS
➢ Oriental sore, Baghdad boils and Delhi boils
➢ One or more containing pus that self heal
➢ Small red papule at the bite site causing intense itching.
4. Leishmania tropicana complex
 TREATMENT:
• Sodium Stibogluconate, Steroids, application of heat,
Paramomycin, Pentamidine and oral Ketoconazole
 PREVENTION AND CONTROL:
• Control of sandfly population and reservoir hosts
• Protection against sandflies.
• Vaccination and eradication of infected ulcers
TRYPANOSOMIASIS

 General term used to describe diseases caused by genus

Trypanosoma spp.
 “Nagana” – disease in cattle (T. brucei)
 “Chagas disease” – Carlos Chagas
1.Trypanosoma brucei gambiense
 West African Sleeping Sickness
 Gambian Trypanosomiasis
 Vector: Tsetse fly (Glossina spp.)
 LIFE CYCLE:
• Infective stage: Trypomastigote
• Diagnostic stage: Trypomastigote
1.Trypanosoma brucei gambiense
 CLINICAL SYMPTOMS:
• WEST AFRICAN SLEEPING SICKNESS
➢ Development of chancre surrounded by a white halo, fever,
malaise, headache, generalized weakness and anorexia.
➢ Lymphadenopathy, Winterbottom’s sign, erythematous rash,
pruritus, edema and Kerandel’s sign.
➢ Mental retardation, tremors, meningoencephalitis,
somnolence, character changes, coma and death.
1.Trypanosoma brucei gambiense
 TREATMENT:
• Melarsoprol, Suramin, Pentamidine and Eflornithine
 PREVENTION AND CONTROL:
• Control of Tsetse flies (destruction of breeding areas)
• Proper protective clothing and repellents
• Prompt treatment of infected persons
2.Trypanosoma brucei rhodesiense
 East African Sleeping Sickness
 Rhodesian Trypanosomiasis
 Vector: Tsetse fly (Glossina spp.)
 LABORATORY DIAGNOSIS:
• Blood slides stained with Giemsa
• CSF sediment
• Protein and IgM studies on CSF
2.Trypanosoma brucei rhodesiense
 EPIDEMIOLOGY:
• Cattle, sheep and wild game animals (Reservoir hosts)
 CLINICAL SYMPTOMS:
• EAST AFRICAN SLEEPING SICKNESS
➢ Fever, myalgia, rigors, mental disturbance, lethargy, rapid
weight loss and anorexia.
➢ Glomerulonephritis, Myocarditis and death.
2.Trypanosoma brucei rhodesiense
 TREATMENT:
• Melarsoprol, Suramin, Pentamidine and Eflornithine
 PREVENTION AND CONTROL:
• Early treatment to halt further transmission
• Treatment for infected animals
• Protective clothing and repellents
• Clearing of bush areas and control Tsetse fly population
3.Trypanosoma cruzi
 Chagas disease
 American Trypanosomiasis
 Vector: Reduviid, Triatomine bugs
 LABORATORY DIAGNOSIS:
• Giemsa-stained blood slides
• Lymph node biopsy and blood cultures
• PCR, ELISA (blood donor screening)
3.Trypanosoma cruzi
 CLINICAL SYMPTOMS:
• CHAGAS DISEASE
➢ Development of erythematous nodule (Chagoma), edema
and rash around eyes and face.
➢ Romaña’s sign, Myocarditis, Megacolon, Megaesophagus,
hepatosplenomegaly, cardiomegaly and death.
➢ Fever, chills, myalgia and malaise.
3.Trypanosoma cruzi
 TREATMENT:
• Nifurtimox, Benznidazole, Allopurinol and Ketoconazole
 PREVENTION AND CONTROL:
• Eradication of reduviid bug nest
• Educational programs (transmission, hosts)
• Vaccination
4.Trypanosoma rangeli
 Infection is generally asymptomatic, no signs of disease.
 Giemsa-stained blood smears.
 Vector: Reduviid bug
 Reservoir hosts: Monkeys, raccoons, dogs, cats and rodents.
 Treatment: Same with T. cruzi
 Prevention and control: Same with T. cruzi
SPOROZOA
 SPOROZOA
 Obligate intracellular parasite
 No apparent means of locomotion
 Life cycle:
1. Sporogony – sexual reproduction (arthropod)
2. Schizogony – asexual reproduction (man)
Plasmodium spp.
 Causative agent of Malaria
 Vector: Mosquito (Anopheles spp.)
 Charles Louis Alphonse – 1st to discover Malaria
 Morphologic forms:
1. Ring forms (early trophozoite)
2. Developing trophozoites
3. Immature and mature Schizonts
• Microgametocyte – male
4. Gametocytes (Micro- and Macro-) • Macrogametocyte - female
LIFE CYCLE:
 Vector: Anopheles spp.
 Infective stage: Sporozoites
 Transmission:
1. Mosquito bite
2. Blood transfusion
3. Sharing of needles and syringes
4. Congenital (mother to child)
 Relapse/ Recrudescence
 LABORATORY DIAGNOSIS:
 Giemsa-stained peripheral blood smears
 Thick and thin blood smears:
1. Thick smears – screening slides
2. Thin smears – differentiating Plasmodium spp.
 Best time to collect blood samples:
▪ Fever and chills - Paroxysms (resulting from release of
merozoites and toxic waste products from infected RBCs).
PATHOGENESIS & CLINICAL SYMPTOMS:

 Initial mosquito bite to exoerythrocytic cycle (Asymptomatic).

 Paroxysm (chills/ rigor and fever, profuse sweating and extreme
fatigue)
 Relapse (hypnozoites) – P. vivax and P. ovale
 Headache, lethargy, anorexia, Ischemia, nausea, vomiting and
diarrhea.
 Anemia, CNS involvement and Nephrotic Syndrome
MALARIAL RESISTANCE:

 G-6-PD deficiency
 Hemoglobinopathies (S, C, E)
 Thalassemia
 Duffy blood group (negative)
 1. Plasmodium vivax
 CLINICAL SYMPTOMS: Pigment: Schuffner’s dot (VS)
▪ BENIGN TERTIAN MALARIA
o Flu, nausea, vomiting, headache, muscle pains and photophobia.
o Paroxysms occur every 48 hours.
o Damage to the brain, liver and kidney and Ischemia.
o Relapse caused by hypnozoites.
 TREATMENT:
▪ Primaquine, Chloroquine, Tetracycline, Doxycycline, Azithromycin, Dapsone,
Quinine and etc…
1. Plasmodium vivax
 PREVENTION AND CONTROL:
1. Personal protection (netting, repellents)
2. Prophylactic treatment
3. Avoidance of sharing intravenous needles
4. Thorough screening of blood donors
5. Vaccination
2. Plasmodium ovale
Pigment: James dot (JO)
 CLINICAL SYMPTOMS:
▪ BENIGN TERTIAN MALARIA, OVALE MALARIA
o Paroxysm cycle (48 hours)
o Relapse (reactivation of hypnozoites)
 TREATMENT, PREVENTION AND CONTROL:
▪ Same with Plasmodium vivax
3. Plasmodium malariae
 LIFE CYCLE: Pigment: Ziemann’s dot (ZM)

▪ Infects mature RBCs

 CLINICAL SYMPTOMS:
▪ QUARTAN MALARIA/ MALARIAL MALARIA
o Paroxysms (72 hours)
o Recrudescence (Reactivation without hypnozoites)
 TREATMENT, PREVENTION AND CONTROL:
▪ Same with P. vivax
4. Plasmodium falciparum
 Black Water fever Pigments:
1. Maurer’s dot
 Malignant Tertian Malaria 2. Christopher’s dot
 RING FORM:
▪ 1 to 2 chromatin dots
▪ Multiple rings are seen (RBC)
 TROPHOZOITE:
▪ Fine pigments can be seen.
 4. Plasmodium falciparum
 LABORATORY DIAGNOSIS:
• Peripheral blood smears (thin/ thick smears)
• Mild to moderate – ring form and gametocytes
• Severe infection – trophozoites and schizonts
• Infect RBC at any age (mature/ young).
 LIFE CYCLE:
• Schizogony – capillaries and sinuses of internal organs
• Warmer months of late summer and early autumn
o AESTIVOAUTUMNAL MALARIA
4. Plasmodium falciparum

 CLINICAL SYMPTOMS:
▪ BLACK WATER FEVER & MALIGNANT TERTIAN MALARIA
❑ Chills, fever, severe diarrhea, nausea, vomiting, Paroxysms (36 to 48 hours).
❑ Black Water fever – marked Hemoglobinuria
❑ Acute renal failure, tubular necrosis, Nephrotic Syndrome, coma and death.
❑ Abdominal pain, vomiting of bile, rapid dehydration and severe diarrhea.
5. Plasmodium knowlesi
 Parasite of Old-World Monkeys
 Cross-reactivity with P. vivax interfere with PCR testing.
 CLINICAL FEATURES:
▪ Respiratory distress, acute renal or multiple-organ failure and shock.
 TREATMENT:
▪ Quinine, Chloroquine (no complications).
▪ IV Quinine and Chloroquine-Primaquine (severe disease).
PATHOGENESIS & CLINICAL SYMPTOMS:
Plasmodium DISEASE: PAROXYSM INCUBATION
spp. CYCLE: PERIOD:
P. falciparum Malignant Tertian 36 to 48 hours 8 to 15 days
Malaria
P. vivax Benign Tertian 48 hours 12 to 20 days
Malaria
P. malariae Quartan Malaria 72 hours 18 to 40 days

P. ovale Ovale Malaria 48 hours 11 to 16 days

Babesia spp.
 Texas Cattle fever/ Red Water fever
 B. microti, B. divergens
 “Maltese cross” appearance
 Vector: Tick (Ixodes spp.)
 Thick and thin blood smears
 LIFE CYCLE:
▪ Infective stage: Sporozoites
▪ Diagnostic stage: Trophozoite
MISCELLANEOUS
PROTOZOANS
1. Balantidium coli
 Balantidiasis
 Ciliate (Cilia – locomotion)
 TROPHOZOITE:
• Largest protozoan
• Rotary boring motility
• Micronucleus (small dot-like)
• Macronucleus (kidney bean-shaped)
1. Balantidium coli

 CYST:
• Subspherical to oval
• Double protective cyst wall
• Mature cyst - lose their cilia
2. Isospora belli
 Isosporiasis
 OOCYSTS:
• Oval and transparent
• Young oocysts divide into 2 sporoblasts
• SPOROBLAST:
▪ Roundish immature sac
▪ Small nucleus and granular cytoplasm
2. Isospora belli

 LABORATORY DIAGNOSIS:
• Fresh feces, duodenal specimens and intestinal biopsies
• Direct wet preparations
• Auramine-rhodamine permanent stain
• Acid-fast stain (confirmatory)
2. Isospora belli

 LIFE CYCLE:
• I. belli has no intermediate host
• Humans– definitive host
• Infective stage: Mature oocysts
• Diagnostic stage: Oocysts
2. Isospora belli
 CLINICAL SYMPTOMS:
• Mild gastrointestinal discomfort to severe dysentery.
• Weight loss, chronic diarrhea, abdominal pain, anorexia,
weakness, malaise, eosinophilia and death.
• Presence of Charcoat-Leyden crystals.
• Malabsorption syndrome, foul-smelling stools (yellow and
loose consistency) and fecal fat.
3. Sarcocystis spp.
 S. hovihominis and S. suihominis
 Sarcocystic infection
 OOCYST:
• Oval and transparent
• 2 mature sporocysts
• 4 sausage-shaped sporozoites
• Double-layered clear wall
3. Sarcocystis spp.
 LIFE CYCLE:
• IS/ DS: Oocysts and sporocysts
• Infective stage to Definitive host: Bradyzoites
 LABORATORY DIAGNOSIS:
• Stool samples
• Human muscle samples (Sarcocysts)
4. Cryptosporidium parvum
 Cryptosporidiosis
 SCHIZONTS, GAMETOCYTES:
• 8 merozoites
• Not routinely seen in patients
 OOCYST:
• 4 small sporozoites
• Do not contain sporocysts
4. Cryptosporidium parvum
 LABORATORY DIAGNOSIS:
• Stool is the specimen of choice.
• Iodine/ Modified acid-fast stain
• Formalin–fixed with Giemsa stain
• Enterotest, ELISA and Indirect Immunofluorescence
• Intestinal biopsies (merozoites/ gametocytes)
• Zinc Sulfate and Sheather’s Sugar Flotation
4. Cryptosporidium parvum

 LIFE CYCLE:
• IS/ DS: Oocysts
• Sporozoites rupture (Autoinfection)
• Thin-shelled oocyst – Autoinfection
• Thick-shelled oocyst – Intact and passed out of the body
5. Blastocystis hominis
 Blastocystis hominis infection
 SAMPLE OF CHOICE: Stool
 VACUOLATED FORM:
• Most common form
• Large, central, fluid-filled vacuole
• 2 to 4 nuclei are present.
5. Blastocystis hominis
 LIFE CYCLE:
• Reproduces by binary fission/ sporulation
• Asexual and sexual reproduction and exhibits pseudopod
extension and retraction.
 TRANSMISSION:
• Travelling is a risk factor.
• Ingestion of contaminated food and water
6. Cyclospora cayetanensis
 Cyclospora cayetanensis infection
 OOCYST:
• Same with Cryptosporidum spp.
• An intestinal coccidian organism
• May form 2 sporocysts each containing 2 sporozoites.
6. Cyclospora cayetanensis
 LABORATORY DIAGNOSIS:
• Stool samples without formalin (fixative).
• Oocysts sporulate at room temperature.
• 5% Potassium Dichromate – visible sporocysts
• Modified acid-fast stain
• Autofluoresce under UV light microscopy
7. Toxoplasma gondii
 Toxoplasmosis, Congenital and Cerebral Toxoplasmosis
 OOCYST:
• Infective form for humans
• Round to slightly oval
• Contains 2 sporocysts
• Clear, colorless, 2-layered cell wall
7. Toxoplasma gondii
 TACHYZOITES:
• Actively multiplying
• Crescent-shaped
 BRADYZOITES:
• Slow-growing forms grow in clusters (inside a host cell)
• Form a cyst in host tissues and muscles
7. Toxoplasma gondii
 LABORATORY DIAGNOSIS:
• Blood samples (serologic methods)
• Determination of IgM in Congenital infections (Double-
sandwich ELISA), IgM and IgG (IFA).
• IgG (IHA and ELISA) and Sabin Feldman dye test
• Tachyzoites and bradyzoites (Microscopic examination)
➢ Seen in humans
7. Toxoplasma gondii
 LIFE CYCLE:
• Definitive host: Cats
• Intermediate host: Rodents
 TRANSMISSION:
• Hand to mouth transmission
• Ingestion of contaminated undercooked meat
• Transplacental and blood transfusion
8. Toxoplasma gondii
 CLINICAL SYMPTOMS:
• CONGENITAL TOXOPLASMOSIS
1. Degree of severity is dependent: (1) Ab protection from
the mother (2) Age of the fetus at the time of infection.
2. Hydrocephaly, microcephaly, intracerebral calcification,
chorioretinitis, convulsions and psychomotor disturbances
3. Develop mental retardation/ Retinochoroiditis
8. Toxoplasma gondii

 CLINICAL SYMPTOMS:
• TOXOPLASMOSIS IN IMMUNOCOMPROMISED:
1. Hodgkin’s lymphoma - opportunistic infection
2. Blood transfusion – screen potential donor
8. Toxoplasma gondii

 CLINICAL SYMPTOMS:
• CEREBRAL TOXOPLASMOSIS IN AIDS:
1. Headache, fever, altered mental status, lethargy, subsequent
focal neurologic deficit, brain lesions and convulsions.
2. Rise in IgG (spinal fluid) and presence of tachyzoites in the
CSF in microscopic examination.
8. Pneumocystis jiroveci

 Pneumocystosis, Atypical Pneumonia

 Old name: Pneumocystis carinii
 Classified as a fungus
 BAL – specimen of choice (AIDS)
9. Pneumocystis jiroveci

 LABORATORY DIAGNOSIS:
• Giemsa and Hematoxylin stain
• Gomori’s Methanamine Silver Nitrate stain
• Sputum, broncheoalveolar lavage (BAL), tracheal aspirate,
bronchial brushings and lung tissue
• Monoclonal Immunofluorescent stain
9. Pneumocystis jiroveci

 TRANSMISSION:
• Transfer of pulmonary droplets through direct person-to-
person contact.
• Common in patients with AIDS (immunosuppressed) and
malnourished infants and malignancy
• Pass through the placenta
9. Pneumocystis jiroveci
 CLINICAL SYMPTOMS:
• Cough, fever, rapid respirations and cyanosis.
• Interstitial Plasma Cell Pneumonia (death in AIDS patients)
• Kaposi’s sarcoma (malignant skin disease)
• Infected malnourished children – poor feeding, loss of energy,
rapid respiration rate and cyanosis
• Infiltrate on chest x-ray, breathing difficulties and lack of
proper Oxygen and CO2 exchange in lungs – Death
NEMATODES
NEMATODES:

 “Roundworms”
 Multicellular with internal organs
 3 morphologic forms: Eggs, larvae and adult worm
 Separate sexes (Dioecious)
LIFE CYCLE:
 Pinworms – ingestion/ inhalation of infected eggs
 Hookworm (larvae) – burrow through skin of the foot
 Adult female worm – lay eggs in the intestine
 Larvae – inside the eggs; require moist soil to continue development
 Trichinella spiralis, Dracunculus medinensis (reside in tissues)
 Facultative parasites (free-living)
LABORATORY DIAGNOSIS:
 Recovery of eggs, larvae and adult worms
 Cellophane tape preparation
 Stool samples, tissue biopsies and skin ulcers
 Concentration techniques:
1. FECT (Formalin Ether)
2. AECT (Acid Ether)
1. Enterobius vermicularis
 Enterobiasis: Pinworm infection
 Common name: Pinworm, Seatworm
 EGGS:
• Oval egg flattened on one side
• Unfertilized egg (unembryonated)
• Fertilized egg (embryonated)
1. Enterobius vermicularis
 ADULT:
1. FEMALE:
• Yellowish-white, organ systems
• Clear pointed tail “pinhead”
2. MALE:
• Yellowish-white
• Smaller than females
1. Enterobius vermicularis
 LABORATORY DIAGNOSIS:
• Cellophane tape preparation
❑ “Scotch tape swab”
❑ Perianal region
❑ Collect samples before defecation/ washing
• Recovered in stool samples (rare)
1. Enterobius vermicularis
 LIFE CYCLE:
• Humans are the only known host.
• Adult worms (reside in the colon)
• Copulation (mating), pregnant (gravid) female worm
• RETROINFECTION – migration of newly hatched larvae
from anal skin back into the rectum
• AUTOREINFECTION – reinfect themselves
1. Enterobius vermicularis
 EPIDEMIOLOGY AND TRANSMISSION:
• Hand to mouth contamination
• Responsible for transmission of Dientamoeba fragilis
 CLINICAL SYMPTOMS:
• Intense itching and inflammation of anal/ vaginal areas.
Intestinal irritation, mild nausea, vomiting, irritability and
difficulty in sleeping. Mild intestinal inflammation and
abdominal pain.
1. Enterobius vermicularis
 TREATMENT:
• Albendazole, Mebendazole and Pyrantel Pamoate
 PREVENTION AND CONTROL:
• Practicing proper personal hygiene, application of ointment in
the infected perianal area, cleaning of potentially infected
environmental surfaces (linens) and avoid scratching the
infected area.
2. Trichuris trichiura
 Trichuriasis: Whipworm infection
 Common name: Whipworm
 EGGS:
• “Barrel/ football-shaped”
• “Japanese lantern”
• Yellow-brown color
• Prominent hyaline polar plug
2. Trichuris trichiura
 ADULT:
• Anterior end
❑ Colorless with slender esophagus
• Posterior end
❑ Pinkish-gray color
• Male is smaller than female.
2. Trichuris trichiura

 LABORATORY DIAGNOSIS:
• Stool sample
• Zinc Flotation method
• Adult worms (intestinal mucosa)
• Rectum (heavy infections)
2. Trichuris trichiura

 LIFE CYCLE:
• Infective stage: Embryonated ova
• Diagnostic stage: Unembryonated ova
• Larvae – small intestine
• Complete maturation (Cecum)
2. Trichuris trichiura
 EPIDEMIOLOGY:
• 3rd most common helminth
• Defecating into the soil/ using human feces as fertilizers
 CLINICAL SYMPTOMS:
• 500 to 5000 worms (heavy infection), chronic dysentery,
severe anemia and growth retardation. Rectal prolapse,
Tenesmus and peristalsis. Abdominal tenderness, pain,
weight loss, weakness, mucoid or bloody diarrhea.
3. Ascaris lumbricoides
 Ascariasis: Roundworm infection
 Common name: Large intestinal roundworm
 UNFERTILIZED EGGS: (Vitelline layer is absent.)
• Thin-shell (protection of amorphous mass of protoplasm)
• Corticated – Outer mammillated, albuminous coating
• Decorticated – Outer layer is absent.
UNFERTILIZED EGG (Ascaris lumbricoides)

CORTICATED DECORTICATED
3. Ascaris lumbricoides
 FERTILIZED EGG: (Vitelline later is present.)
• More rounded than unfertilized egg
• Chitin
❑ Thick Nitrogen-containing polysaccharide coating
❑ Between the embryo and mammillary albuminous material
❑ Less evident in corticated eggs
FERTILIZED EGG (Ascaris lumbricoides)

CORTICATED DECORTICATED
3. Ascaris lumbricoides
 ADULT:
• Creamy-white color
• Cuticle – surface covering
• Largest intestinal nematode
• Female: Larger and pointed tail
 Male: Slender and curved tail
3. Ascaris lumbricoides

 LABORATORY DIAGNOSIS:
• Stool sample
• Others: Small intestine, gallbladder, liver and appendix
• Adult worms - present in stool, vomited up or removed from
the external nares
• ELISA, DFS, Kato-katz/ Kato-thick and Conc. techniques
3. Ascaris lumbricoides
Animal Ascarids:
 LIFE CYCLE: • Toxocara cati
Visceral Larva Migrans
• Toxocara canis
 Liver-lung migration
 Infective stage: Embryonated eggs
 Diagnostic stage: Fertilized, unfertilized egg and adult worms
 Maturation of larvae – small intestine
 250, 000 eggs per day are passed in the feces
3. Ascaris lumbricoides
 CLINICAL SYMPTOMS:
• Vague abdominal pain, vomiting, fever and distention.
Obstruction of the intestine, appendix, liver or bile duct and
malnutrition.
• Discomfort from adult worms exits in the body through the
anus, mouth or nose.
• Lungs – low-grade fever, cough, eosinophilia and Pneumonia.
• Asthmatic reaction (presence of worms).
4. HOOKWORMS

Necator americanus
Most common STH (Soil
Transmitted Helminths).
Ancylostoma duodenale

Ancylostoma caninum ANIMAL HOOKWORMS:

• Causative agent of CLM

Ancylostoma braziliense (Cutaneous Larva Migrans)

• Treatment: Thiabendazole
4. HOOKWORMS
 Tropical anemia
 Necator americanus
• Common name: New World hookworm
• Necatoriasis
 Ancylostoma duodenale
• Common name: Old World hookworm
• Ancylostomiasis
4. HOOKWORMS
 EGGS:
• Unsegmented
• Embryonic cleavage
❑ 2, 4, 8 cell stage
• Thin, smooth, colorless shell
4. HOOKWORMS

 RHABDITIFROM LARVAE:
• Non-infective (feeding) stage
• Buccal cavity/ capsule (oral cavity)
• Genital primordium
 FILARIFORM LARVAE:
• Shorter esophagus than S. stercoralis
• Distinct pointed tail
4. HOOKWORMS

 ADULT:
• Buccal capsule:
1. Necator americanus
❑ Pair of cutting plates. “S-shaped”
2. Ancylostoma duodenale
❑ Consist of actual/ sharp teeth
❑ “C-shaped”
4. HOOKWORMS
 LABORATORY DIAGNOSIS:
• Stool samples
• Recovery and examination of buccal capsule
• “Harada-Mori technique”
 LIFE CYCLE:
• Infective stage: Filariform larvae
• Diagnostic stage: Egg/ ova
4. HOOKWORMS
 CLINICAL SYMPTOMS:
• Ground itch – Intense itching at the site of infection
• Sore throat, bloody sputum, wheezing, headache and mild
Pneumonia with cough (larvae migration to lungs).
• Mild gastrointestinal symptoms, mild anemia, wt. loss,
weakness Diarrhea, anorexia, edema, pain, enteritis
• Microcytic hypochromic Iron deficiency, weakness and
hypoproteinemia. Mortality – enormous loss of blood.
4. HOOKWORMS

 CLINICAL SYMPTOMS:
• Wakana disease (Pneumonitis)
• Miner’s anemia (Microcytic hypochromic)
• Animal hookworm: Creeping Eruption, CLM
5. Strongyloides stercoralis
 Strongyloidiasis – Threadworm infection
 Common name: Threadworm
 EGGS:
• Smaller than hookworms
• Well developed larvae is contained.
• “Chinese lantern”
• Thin hyaline shell
5. Strongyloides stercoralis

 RHABDITIFORM LARVAE:
• Short buccal cavity
• Prominent genital primordium
 FILARIFORM LARVAE:
• Long, slender
• Long esophagus
• Blue – genital primordium
• Notched tail • Red – esophageal bulb
• Green – buccal cavity
5. Strongyloides stercoralis
 ADULT FEMALE:
• Short buccal cavity
• Long and slender esophagus
• Colorless body (transparent)
• PARTHENOGENIC
❑ Male is not required for fertilization.
5. Strongyloides stercoralis
 LABORATORY DIAGNOSIS:
• Stool samples (severe diarrhea)
• Duodenal aspirates and stool (rhabditiform larvae)
• Enterotest
• Sputum (disseminated infection)
• Threadworm larvae (higher recovery in conc. samples)
• ELISA
5. Strongyloides stercoralis
 LIFE CYCLE:
• Direct – Similar to hookworms
• Indirect – Rhabditiform larvae are passed into the outside
environment (soil) and mature into free-living adults.
• Autoinfection – Rhabditiform develop into filariform larvae
inside the intestine and may enter the lymphatic system/
bloodstream.
5. Strongyloides stercoralis
 CLINICAL SYMPTOMS:
• Diarrhea and abdominal pain, Urticaria and eosinophilia.
• Vomiting, constipation, weight loss, anemia and Malabsorption
syndrome. Site of larvae penetration (itchy and red), recurring
allergic reactions, pulmonary symptoms (larvae to lung).
• Immunocompromised (suffer from severe autoinfections).
• “Cochin China Diarrhea/ Vietnam Diarrhea”
5. Strongyloides stercoralis

 TREATMENT: Ivermectin with Albendazole

 PREVENTION AND CONTROL:
• Proper handling and disposal of fecal material.
• Adequate protection of skin from contaminated soil.
• Thorough treatment of infected person (prevent
autoinfection)
6. Trichinella spiralis
 Trichinosis, Trichinellosis
 Common name: Trichina worm
 ENCYSTED LARVAE:
• Coiling up in the muscle fiber
• Striated muscle cell (nurse cell)
❑ Surrounds the coiled larva
6. Trichinella spiralis

 LABORATORY DIAGNOSIS:
• Examination of infected skeletal muscle.
• Laboratory findings: Eosinophilia and leukocytosis, elevated
Lactate Dehydrogenase (LDH), Aldolase and Creatinine
Phosphokinase (serum muscle enzymes)
• Bentonite Flocculation test, Beckman Intradermal test
 6. Trichinella spiralis
 LIFE CYCLE:
• Zoonosis – accidental infection, normal host is an animal.
• Consuming undercooked, contaminated meat (striated muscle)
• T. spiralis larvae in the intestine → matures into adult rapidly
• Gravid adult female → intestinal mucosa (lay eggs)
• Infant larvae → bloodstream → striated muscle (encyst)
• NO EGG STAGE.
6. Trichinella spiralis
 CLINICAL SYMPTOMS:
• Light infection: Diarrhea, headache and fever
• Heavy infection: Vomiting, nausea, abdominal pain, diarrhea,
headache and fever (intestinal phase)
• Eosinophilia, pain in pleural area, fever, blurred vision, edema,
cough and death (larval migration through the body)
• Muscular discomfort, edema, local inflammation, overall fatigue
and weakness (larvae settled into the striated muscle)
7. Dracunculus medinensis
 One of the largest adult nematode
 Dracunculosis, Dracunculiasis: Guinea worm infection
 Common name: Guinea worm
 LARVAE:
• 1st stage/ Rhabditiform larvae (Diagnostic stage)
• 3rd stage larvae
7. Dracunculus medinensis
 LIFE CYCLE:
• Ingestion of contaminated drinking water with infected
COPEPODS (freshwater fleas – Intermediate host).
• Copepods contain the 3rd stage larvae → intestine → larvae
mature into adult worm → penetrate the intestinal wall →
connective tissue/ body cavities.
• Copulation → subcutaneous tissue (lay 1st stage larvae) →
infected ulcer at the site of larvae deposit
8. Capillaria philippinensis
 Pudoc’s Mystery disease: Capillariasis
 Common name: Pudoc worm
 EGGS:
 Flattened bipolar mucus plugs
 “Guitar/ peanut-shaped”
 Striated
8. Capillaria philippinensis
 LIFE CYCLE:
• Intermediate host: Fresh water fish (Birot, Bagsang, Bagsit)
• Diagnostic stage: Ova
• Infective stage: Larvae
• Autoinfection
• MOT: Ingestion of raw/ undercooked infected fish
8. Capillaria philippinensis

 CLINICAL SYMPTOMS:
• Abdominal pain
• Diarrhea
• Borborygmi (abdominal gurgling sound).
TAKE NOTE:
 UNHOLY THREE/ TRIAD OF INFECTION:
• Hookworm, Ascaris lumbricoides, T. trichiura
 HABITAT:
• Small intestine – T. trichiura, C. philippinensis, A. lumbricoides, S.
stercoralis and hookworms
• Large intestine – E. vermicularis, T. trichiura
• Muscle – T. spiralis
• Lymph nodes – W. bancrofti, B. malayi
TAKE NOTE:

 HEART AND LUNG MIGRATION:

 A. lumbricoides, S. stercoralis and Hookworms
FILARIAL WORMS
FILARIAE:

 Adult worm (tissue/ lymphatic system)

 Larvae (microfilariae - blood)
 Periodicity (nocturnal, diurnal and subperiodic)
 Viviparous/ larviparous
 Vector: Mosquitoes and flies
MORPHOLOGY:
 Two morphologic forms:
1. ADULT WORMS
• Creamy white
• Thread-like appearance
2. MICROFILARIAE (LARVAE)
• Distribution of nuclei within the tip of the nuclei.
• Presence of sheath (transparent covering)
LIFE CYCLE:

 Larvae → tissues (complete development)

 Adult worms → lymphatics, subcutaneous tissue, body cavities
 Adult female worms lay live microfilariae in blood or dermis.
 Microfilariae exit the body through blood meal (vector).
 Intermediate host: Vectors (Mosquitoes/ flies)
LABORATORY DIAGNOSIS:
 PERIODICITY
• Presence of parasites in bloodstream during a specific time
(nocturnal, diurnal or subperiodic).
• Helpful for specimen collection
 Giemsa-stained blood smear/ tissue of infected nodule
 Knott technique
PATHOGENESIS & CLINICAL SYMPTOMS:

 Lesions, eosinophilia, fever and chills

 ELEPHANTIASIS
• Enlargement of the skin and subcutaneous tissue
 CALABAR SWELLINGS
• Transient swelling of subcutaneous tissue
 Blindness
1. Wuchureria bancrofti
 Elephantiasis
 Common name: Bancroft’s filaria
 MICROFILARIAE:
• Thin and delicate sheath
• Numerous nuclei
• Anterior end – blunt and round
• Posterior end – pointed, free from nuclei
1. Wuchureria bancrofti
 LABORATORY DIAGNOSIS:
• Giemsa-stained blood smear
• Knott technique
• Sample collected during night (NOCTURNAL).
• Peak hours: 9:00pm to 4:00am
• Antigen and antibody detection
• PCR
1. Wuchureria bancrofti
 LIFE CYCLE:
• Vector: Aedes, Anopheles and Culex spp.
 CLINICAL SYMPTOMS:
1. Asymptomatic – Self-limiting
2. Symptomatic – fever, chills and eosinophilia, granulomatous
lesions, lymphangitis, lymphadenopathy, elephantiasis/ swelling
of lower extremities (breasts/ genitals), abscesses may occur.
1. Wuchureria bancrofti

 TREATMENT:
• Diethylcarbamazine (DEC) and Ivermectin with Albendazole
• Surgical removal of abscess
• Use of special boots “Unna’s phase boots”
• Elastic bandages (reducing size of enlarged limb)
2. Brugia malayi
 Malayan Filariasis/ Elephantiasis
 Common name: Malayan filaria
 MICROFILARIAE:
• Sheathed, round anterior end
• Numerous nuclei
• Presence of two nuclei (tip of the tail)
2. Brugia malayi
 LABORATORY DIAGNOSIS:
• Giemsa-stained blood smears
• Specimen collection during nighttime.
• Knott technique
 LIFE CYCLE:
• Vectors: Mosquito (Aedes, Anopheles or Mansonia spp.)
• Co-infection with W. bancrofti can be possible
2. Brugia malayi
 EPIDEMIOLOGY:
• Humans – Definitive host
• Infect felines and monkeys
 CLINICAL SYMPTOMS:
• Fever, lesions, chills, lymphadenopathy, lymphangitis and
eosinophilia, elephantiasis of the legs and genitals (rare).
2. Brugia malayi

 TREATMENT: DEC (Diethylcarbamazine)

 NEW TREND:
• Brugia timori – can also cause Malayan filariasis
• Tropical Eosinophilia (Occult Filariasis) – Pulmonary
and asthmatic symptoms. Microfilariae resides in the lungs.
Treatment is DEC.
3. Loa loa
 Loiasis
 Common name: African eye worm
 MICROFILARIAE:
• Sheathed
• Nuclei fill the organism
• Nuclei at the tip of the tail
3. Loa loa
 LABORATORY DIAGNOSIS:
• Giemsa-stained blood
• Corneal scrapings (adult worm)
• Knott technique
• Sample collection: 10:15am to 2:15pm (DIURNAL)
 LIFE CYCLE:
• Bite of Chrysops fly (vector)
3. Loa loa

 CLINICAL SYMPTOMS:
• Pruritus/ itchiness or localized pain, Calabar swelling
(anywhere in the body).
• Circulating adult worms in the tissue (no discomfort).
• Noticeable adult worms in the conjunctiva of the eye/
crossing under the skin of the bridge of the nose.
4. Onchocerca volvulus
 River Blindness, Onchocerciasis
 Common name: Blinding filaria
 MICROFILARIAE:
• Unsheathed
• Numerous nuclei
• Found in subcutaneous tissue
4. Onchocerca volvulus

 LABORATORY DIAGNOSIS:
• Giemsa-stained tissue biopsies
• Skin snips
• Ophthalmologic examination using a slit lamp.
• PCR (low infection)
4. Onchocerca volvulus
 LIFE CYCLE:
• Vector: Black fly (Simulium spp.)
• Adult worms encapsulate in the subcutaneous fibrous tumors.
• Adult worms coiled and microfilariae emerge.
• Microfilariae → infected nodules → subcutaneous tissues →
skin → eyes
4. Onchocerca volvulus

 CLINICAL SYMPTOMS:
• Severe allergic reactions, scratching (leading to secondary
bacterial infection).
• Lesions → blindness (eyes)
• Changes in skin appearance (loss of elasticity and location of
nodules)
5. Mansonella ozzardi
 Common name: New World Filaria
 MICROFILARIAE:
• Unsheathed
• Numerous nuclei that do not extend
at the tip of long, narrowed, tapered
tail.
• Do not exhibit periodicity.
6. Mansonella perstans
 Common name: Perstans filaria
 MICROFILARIAE:
• Unsheathed
• Nuclei extend at the tip of the tail.
 ADULT:
• Female is longer than male.
• Resides in pleural and peritoneal cavities
7. Dirofilaria immitis
 Common name: Dog heartworm
 Common filarial parasite in dogs
 Causes pulmonary diseases in humans
• Dead worms lodge in the pulmonary
vessels, these infarcts are referred as
“coin lesions” in chest radiography.
 SUMMARY:
FILARIAL HABITAT VECTOR SPECIMEN MICROFILARIA PERIODICITY
WORM
W. bancrofti Lymphatics Aedes and Blood Sheathed, nuclei absent Nocturnal
(Lower lymph Anopheles spp. in tail
nodes)

B. malayi Lymphatics Mansonia spp. Blood Sheathed, tail with 2 Nocturnal

(Upper lymph separate nuclei
nodes)

Loa loa Subcutaneous Chrysops fly, Blood Sheathed, nuclei Diurnal

tissue Deer fly, continuous up to the
Mango fly tip of the tail
 SUMMARY:
FILARIAL HABITAT VECTOR SPECIMEN MICROFILARIA PERIODICITY
WORM
O. volvulus Subcutaneous Black fly Skin snips/ Unsheathed, nuclei Non-periodic
tissue (Simulium skin shaving absent in the tail
spp.)

M. perstans Body cavities Culicoides spp. Blood Unsheathed, nuclei Non-periodic

continuous up to the
tip of the tail

M. ozzardi Body cavities Culicoides spp. Blood Unsheathed, nuclei Non-periodic

absent in the tail
 SUMMARY:
1. LYMPHATIC FILARIASIS:
• Wuchureria bancrofti, Brugia malayi, Brugia timori
2. SUBCUTANEOUS FILARIASIS:
• Loa loa, Onchocerca volvulus
3. SEROUS/ BODY CAVITY FILARIASIS:
• Mansonella perstans, Mansonella ozzardi
CESTODES
CESTODES:
 White to yellow
 Multicellular worms
 Flat/ Ribbon-like appearance
 Flatworms or Tapeworms
 Habitat: Small intestine
 NO DIGESTIVE TRACT
MORPHOLOGY AND LIFE CYCLE:
 Three morphologic forms:
1. Egg (Hexacanth embryo/ Oncosphere)
2. Larval stages (1st larval stage – hooklets)
3. Adult worm (Scolex, neck, proglottids, strobila)
 Intermediate host – required for larval development
 Hermaphroditic (self-fertilizing)
 Autoinfection (Hymenolepis nana)
MORPHOLOGY AND LIFE CYCLE:
1. Scolex (head) – attachment organ
a. Rostellum – Armed (with hooks), Unarmed (without hooks)
b. Suckers
2. Neck – region of growth
3. Proglottid – chain of segments (strobila)
a. Immature – no well-developed reproductive structures
b. Mature (medial) and Gravid – distal with ova
LABORATORY DIAGNOSIS:

 Specimen:
• Stool – eggs, gravid proglottids and scolex
• Biopsy of tissue – Echinococcus granulosus
 Serologic tests
PATHOGENESIS AND CLINICAL SYMPTOMS:

 Gastrointestinal discomfort, diarrhea and abdominal pain

 Nausea, dizziness, headache and weight loss
 Intestinal obstruction and Vitamin B12 – Macrocytic Anemia
• Diphyllobothrium latum
 Liver and lung involvement, persistent cough, localized pain,
eosinophilia and anaphylactic shock:
• Echinococcus granulosus
1. Taenia spp.
 Taenia saginata
• Common name: Beef tapeworm
• Taeniasis – Beef tapeworm infection
 Taenia solium
• Common name: Pork tapeworm
• Taeniasis – Pork tapeworm infection
1. Taenia spp.
 EGGS:
• Roundish egg
• Hexacanth embryo w/ radial striations
• 3 pairs of hooklets
• Yellow-brown shell (Embryophore)
• Nonembryonated/ embryonated
1. Taenia spp.

 SCOLEX:
• Equipped with four suckers
• T. solium
❑ Has rostellum and hooks
• T. saginata
❑ Lacks rostellum and hooks
1. Taenia spp.
 PROGLOTTIDS:
• Segments:
1. T. saginata – 1048
2. T. solium - 898
• Uterine branches:
1. T. saginata – 15 to 30
2. T. solium – 7 to 15
1. Taenia spp.
 LIFE CYCLE:
• Infective stage: Cysticercus larva
• Diagnostic stage: Eggs and proglottids
• Ingestion of raw/ undercooked beef/ pork.
• Intermediate hosts:
➢ Cow/ cattle (T. saginata) and pig (T. solium, T. asiatica)
1. Taenia spp.
 CLINICAL SYMPTOMS:
• Diarrhea, abdominal pain, change in appetite, slight weight loss,
dizziness, nausea and vomiting
• Laboratory test: Eosinophilia
• Cysticercosis (T. solium)
• Neurocysticercosis – headache, seizures, confusion, ataxia
and death
1. Taenia spp.
 Taenia asiatica
• Common name: Asian tapeworm/ Asian Taenia
• Acquired by eating raw pig liver
• Clinical symptoms: abdominal pain, nausea, weakness, weight
loss and headaches.
• Treatment: Praziquantel
 DIFFERENCE: Taenia saginata Taenia solium
Common name: Beef tapeworm Pork tapeworm

Intermediate host: Cattle/ cow Pig

Scolex: No rostellum Armed rostellum

No hooks

Number of proglottids: 1000 to 2000 Less than 1000

Gravid proglottid: 15 to 20 7 to 13
(Lateral/ uterine “Tree-like” “Finger-like”
branches)
Larva: Cysticercus bovis Cysticercus cellulosae
2. Hymenolepis diminuta
 Common name: Rat tapeworm
 Hymenolepiasis
 EGGS:
• 3 pairs of hooks
• Shell has distinct polar thickening and
no polar filaments
• Colorless embryophore
2. Hymenolepis diminuta
 SCOLEX:
• 4 suckers, rostellum (no hooks)
 PROGLOTTIDS:
• Rectangular
• Mature segment contains both female
and male reproductive organs
• Gravid proglottid: Sac-like uterus
3. Hymenolepis nana
 Common name: Dwarf Tapeworm
 Hymenolepiasis
 EGGS:
• Roundish to oval
• 3 pairs of hooklets
• Polar thickening and polar filaments
• Colorless embryophore
3. Hymenolepis nana
 SCOLEX:
• 4 suckers
• Short rostellum
• One row of hooks
 PROGLOTTIDS:
• Resembles H. diminuta
3. Hymenolepis nana
 LIFE CYCLE:
• IS/ DS: Embryonated egg
• Cysticercoid larvae → intestine ← adult worm
• No intermediate host is required.
• Autoinfection
• Transport hosts: Fleas, beetles, rats and house mice
DIFFERENCE: Hymenolepis nana Hymenolepis diminuta

Common name: Dwarf Tapeworm Rat Tapeworm

Scolex: Armed rostellum Unarmed rostellum

Eggs: With polar thickening and With polar thickening but

filaments without filaments

Infective stage: Eggs Cysticercoid larvae

Cysticercoid larvae

Final host: Man Rat

4. Dipylidium caninum
 Common names: Dog/ Cat Tapeworm,
Pumpkin seed Tapeworm
 Dipylidiasis
 EGG PACKETS:
• 6-hooked oncospheres
• Membrane-closed packets
➢ 5 to 30 eggs
4. Dipylidium caninum
 SCOLEX:
• 4 suckers
• Club-shaped armed rostellum
 PROGLOTTIDS:
• “Pumpkin seeds/ melon-shaped”
• Has both female and male reproductive
organs
• Eggs enclosed in an embryonic membrane
5. Diphyllobothrium latum
 Common name: Broad fish Tapeworm
Operculum
 Diphyllobothriasis
 EGGS:
• Coracidium – ciliated larval stage
• Smooth, yellow to brown shell
• Operculum
• Abopercular knob (terminal knob)
5. Diphyllobothrium latum
 SCOLEX:
• 4 cup-like suckers
• Almond/ spatulate spoon-shaped
• 2 prominent sucking grooves
 PROGLOTTIDS:
• Centrally located uterine structure
➢ “Rosette formation”
5. Diphyllobothrium latum
 LIFE CYCLE:
• Diagnostic stage: Unembryonated eggs
• Infective stage:
1. Coracidium – Cyclops (1st IH)
2. Procercoid – Fresh water fish (2nd IH)
3. Pleurocercoid – Man (final host)
5. Diphyllobothrium latum
 CLINICAL SYMPTOMS:
• Overall weakness, weight loss and abdominal pain.
• Vitamin B12 Deficiency
 TREATMENT:
• Praziquantel and Niclosamide
 PREVENTION AND CONTROL:
• Proper human fecal disposal, avoidance of eating raw/
undercooked fish and thorough cooking of all fish.
5. Diphyllobothrium latum
 SPARGANOSIS
• Transmission:
1. Water contamination with copepods
2. Medicines contaminated with infected animal by-products
• Sparganum – Infected subcutaneous tissue; white, wrinkled,
ribbon-shaped
• Treatment: Removal of sparganum and Praziquantel
6. Echinococcus granulosus
 Common name: Dog Tapeworm/ Hydatid Tapeworm
 Echinococcosis, Hydatid cyst, Hydatid disease, Hydatidosis
 EGGS: (Resembles Taenia spp.)
 HYDATID CYSTS:
• Larval stage (human tissues)
• Daughter cysts
• Brood capsules, hydatid sand
6. Echinococcus granulosus

 ADULT:
• Scolex – 4 suckers with 36 hooks
• Small neck
• 3 proglottids:
➢ Immature, mature and gravid
6. Echinococcus granulosus
 LABORATORY DIAGNOSIS:
• Biopsy samples – hydatid cyst fluid
• Care in choosing method → Anaphylaxis
• ELISA, IHA and Western blot
• Bentonite Flocculation test, Casoni test
• Radiography, Computed Tomography (CT), Ultrasound scan
6. Echinococcus granulosus
 LIFE CYCLE:
• Infective stage: Embryonated eggs
• Diagnostic stage: Hydatid cyst
• Accidental hosts/ dead-end hosts – humans
• Intermediate hosts – sheep
• Definitive hosts – wild canines/ dogs
• Eggs → larvae → intestine → bloodstream → lung and liver
6. Echinococcus granulosus
 CLINICAL SYMPTOMS:
• Enlargement of cysts → necrosis of infected tissue
• Rupture of cyst → process of biopsy procedure
• Anaphylactic shock, eosinophilia, allergic reactions and death
• Lung involvement – chest pain, coughing, shortness of breath
• Liver involvement – Obstructive jaundice
6. Echinococcus granulosus
 TREATMENT:
• Surgical removal of the cyst
• Mebendazole, Albendazole and Praziquantel
 PREVENTION AND CONTROL:
• Personal hygiene practices, discontinue feeding canines with
infected viscera, prompt treatment of canines and educational
programs.
7. Echinococcus multiocularis

 Accidental cause of hydatid cyst (Subartic, Europe and India)

 Primary definitive host: Foxes
 Intermediate host: Rodents (mice and voles)
TREMATODES
TREMATODES:

 Commonly known as flukes, blood flukes (Schistosomes)

 Hermaphroditic (self-fertilizing)
 Dioecious (separate sexes)
 Intermediate host – Mollusks (snails)
MORPHOLOGY:

 Morphologic stages: Eggs, multiple larval stages and adult worms

 Lid-like structure – Operculum (Fasciolopsis and Fasciola)
 Spines (Schistosoma spp.)
 Habitat: Intestine, bile duct, lung and blood vessels
LIFE CYCLE:
 Mode of transmission: Ingestion of metacercaria (water plants –
water chestnuts, fish, crab or crayfish)
 Metacercaria → intestine, bile duct, lung (adult stage)
 Eggs → feces/ sputum → fresh water (miracidium hatches) →
penetrates to the snails (1st IH) → Sporocyst → Rediae →
Cercariae
 Cercariae: Encyst on water plants, fish, crab and crayfish (2nd IH)
LIFE CYCLE:

 Penetration of cercariae in the skin.

 Schistosomule → blood vessels (liver, intestine and bladder)
 Dioecious → copulation → eggs → urine/ feces → miracidium →
sporocyst → cercariae (snail – IH)
LABORATORY DIAGNOSIS:

 Specimen:
• Feces, duodenal aspirate, rectal biopsy, sputum and urine
 Eggs and adult worms (can be recovered).
 ELISA – blood flukes (Schistosoma spp.)
PATHOGENESIS AND CLINICAL SYMPTOMS:

 Eosinophilia
 Allergic and toxic reactions
 Tissue damage
 Jaundice
 Diarrhea
1. Fasciolopsis and Fasciola spp.
 Fasciolopsis buski
• Common name: Large intestinal fluke
• Fasciolopsiasis
 Fasciola hepatica
• Common name: Sheep liver fluke
• Fascioliasis, sheep liver rot
1. Fasciolopsis and Fasciola spp.
 EGGS:
• Oblong undeveloped miracidium
• Operculum
 ADULT:
• F. buski – no shoulder
• F. hepatica – with shoulder
1. Fasciolopsis and Fasciola spp.
 LABORATORY DIAGNOSIS:
• Stool – recovery of eggs
• Fasciola:
➢ Enterotest, ELISA and Gel diffusion
 LIFE CYCLE:
• F. buski adult – resides in the small intestine
• F. hepatica adult – resides in the bile ducts
1. Fasciolopsis and Fasciola spp.
 EPIDEMIOLOGY:
• Mode of transmission: Ingestion of raw water plants
• Reservoir host: Rabbits, pigs and dogs
• Food sources: Water chestnuts, lotus and water caltrop
• Fasciola hepatica (sheep and cattle)
1. Natural host – sheep
2. Accidental host - humans
1. Fasciolopsis and Fasciola spp.

 CLINICAL SYMPTOMS:
• FASCIOLOPSIASIS
➢ Abdominal discomfort, inflammation and bleeding in the
infected area, jaundice, diarrhea, gastric discomfort and
edema.
➢ Malabsorption syndrome, intestinal obstruction and death.
1. Fasciolopsis and Fasciola spp.

 CLINICAL SYMPTOMS:
• FASCIOLIASIS
➢ Headache, fever, chills, pain in liver area, eosinophilia,
jaundice, liver tenderness, anemia, diarrhea and digestive
discomfort
➢ Biliary obstruction
1. Fasciolopsis and Fasciola spp.

 CLINICAL SYMPTOMS:
• HALZOUN
➢ Pharyngeal fascioliasis
➢ Laryngopharyngitis due to eating of raw infected liver of
sheep and goat → young adult attach to pharynx → Asphyxia
Fasciola gigantica

 Common name: Giant liver fluke, Tropical liver fluke

 1st and 2nd IH – same with Fasciola hepatica
2. Clonorchis sinensis
 Common name: Chinese liver fluke
 Clonorchiasis
 EGGS:
• Miracidium
• Operculum
• Thick rim (shoulders)
• Small knob
2. Clonorchis sinensis

 ADULT:
• Flattened
• Lancet-shaped
• Hermaphroditic
• Oral and ventral suckers are small
2. Clonorchis sinensis
 LABORATORY DIAGNOSIS:
• Eggs or duodenal aspirates
• Adult worms (removed during surgery or autopsy procedure)
 LIFE CYCLE:
• Ingestion of undercooked fish with encysted metacercariae
• Maturation – liver
• Adult worm – bile ducts
3. H. heterophyes/ M. yokogawai
 Heterophyes heterophyes
• Common name: Heterophid fluke
• Heterophyiasis
 Metagonimus yokogawai
• Common name: Heterophid fluke
• Metagonimiasis
3. H. heterophyes/ M. yokogawai

 EGGS:
• Presence of shoulders
• Lack small terminal knob
• Operculum
• H. heterophyes has thicker shell
3. H. heterophyes/ M. yokogawai

 LABORATORY DIAGNOSIS:
• Stool samples
 LIFE CYCLE:
1. Ingestion of contaminated undercooked fish
2. Adult worms – reside in the small intestine
4. Paragonimus westermani
 Common name: Oriental Lung fluke
 Paragonimiasis/ Pulmonary distomiasis
 EGGS:
• Miracidium (thin shell)
• Operculum
• Terminal shell thickening
• Opercular rim (shoulders)
4. Paragonimus westermani

 ADULT:
 Oval
 Red to brown colored
 Cuticle (spines)
4. Paragonimus westermani
 LABORATORY DIAGNOSIS:
• Sputum samples – recovery of egg
 LIFE CYCLE:
• Ingestion of undercooked crayfish/ crabs
• Immature flukes → intestinal wall → peritoneal cavity →
diaphragm → lung tissue (encystation)
• Reservoir hosts: Pigs and monkeys
4. Paragonimus westermani

 LIFE CYCLE:
• 1ST IH – Brotia aspirate (snail)
• 2nd IH – Sundathelpusa philippina, Parathelphusa mistio,
Sundathelphusa grapsoides (crabs)
4. Paragonimus westermani
 CLINICAL SYMPTOMS:
• Pulmonary discomfort – cough, fever, chest pain, increased
production of “blood-tinged” sputum and Hemoptysis.
• Chronic bronchitis, eosinophilia and fibrous tissue
• CEREBRAL PARAGONIMIASIS
➢ Seizures, visual difficulties and decreased precision of
motor skills
5. Schistosoma spp.

 Schistosoma mansoni
• Common name: Mansoni’s fluke
 Schistosoma japonicum
• Common name: Blood fluke
 Schistosoma haematobium
• Common name: Bladder fluke
A. Schistosoma mansoni

 EGGS:
• Oblong
• LARGE LATERAL spine
• Anterior end is tapered
and slightly curved.
B. Schistosoma japonicum

 EGGS:
• Small
• Roundish
• SMALL LATERAL spine
C. Schistosoma haematobium

 EGGS:
• Oblong
• Large, prominent
TERMINAL spine
5. Schistosoma spp.
 ADULT:
• Separate sexes
• Male surrounds the female
• Thin female resides in the
gynecophoral canal of the thicker
male.
5. Schistosoma spp.
 LABORATORY DIAGNOSIS:
• Stool and rectal biopsy (S. mansoni and S. japonicum)
• Urine (S. haematobium)
 LIFE CYCLE:
• Penetration of cercariae in the skin → schistosomule
(bloodstream – maturation)
• Veins (intestinal tract – S. mansoni and S. japonicum)
• Veins (bladder – S. haematobium)
5. Schistosoma spp.

 EPIDEMIOLOGY:
• RH – monkeys, cattle, other livestock, rodents, dogs and cats
• Schistosoma japonicum – Philippines
• Transport of organism – slave trade
5. Schistosoma spp.
 CLINICAL SYMPTOMS:
• Inflammation at the cercaria penetration site.
• Acute infection – abdominal pain, fever, chills, weight loss,
cough, bloody diarrhea and eosinophilia.
• Painful urination and hematuria (S. haematobium)
• Development of necrosis, lesions and granulomas.
• Obstruction of the bowel ureters, secondary bacterial
infections and CNS involvement.
5. Schistosoma spp.
 CLINICAL SYMPTOMS:
• KATAYAMA FEVER
➢ Systemic hypersensitivity reaction to the schistosomulae.
➢ Rapid onset of fever, nausea, myalgia, malaise, fatigue, cough,
diarrhea and eosinophilia
• NEPHROTIC SYNDROME (S. japonicum/ haematobium)
• BLADDER CANCER (S. haematobium)
• SALMONELLA INFX. (S. mansoni/ japonicum)
5. Schistosoma spp.
 CLINICAL SYMPTOMS:
• SWIMMER’S ITCH
➢ Accidental infection with cercariae
➢ Penetration of fork-tailed cercariae in the skin
➢ Severe allergic reactions and secondary bacterial infections
➢ Topical medications
5. Schistosoma spp.
 TREATMENT:
• Praziquantel
• Oxamniquine (S. mansoni only)
 PREVENTION AND CONTROL:
• Proper human waste disposal, control of snail populations,
avoidance of human contact in contaminated water and
educational programs.
• Mass treatment
6. Opistorchis felineus

 Common name: Cat liver fluke

 1st IH – Bulimus pentacolata (snail)
 2nd IH – Barbus barbus, Tinca tinca (fish)
7. Echinostoma ilocanum

 Common name: Garrison’s fluke

 1st and 2nd IH – (Pila luzonica – snail)
 Eggs: “straw-colored”
TAKE NOTE:
EGGS: EMBRYONATED EGGS: IMMATURE WHEN
WHEN LAID LAID
Schistosoma spp. Paragonimus westermani

Heterophyes Fasciola hepatica

Opistorchis felineus Echinostoma ilocanum

Clonochis sinensis Fasciolopsis buski

TAKE NOTE:
LIVER INTESTINES

Fasciola hepatica Fasciolopsis buski

Fasciola gigantica Echinostoma ilocanum

Clonorchis sinesis Heterophyes heterophyes

Opistorchis felineus
TAKE NOTE:
LUNGS BLOOD

Paragonimus westermani Schistosoma japonicum

Schistosoma haematobium

Schistosoma mansoni
REFERENCES:

 Clinical Parasitology: A Practical Approach by Elizabeth Zeibig (2nd edition)

 Medical Parasitology in the Philippines by Belizario and de Leon
 https://www.cdc.gov/dpdx/index.html