CLASSIFICATION OF PARASITESCan you identify the

parasites in the pictures?

PARASITES

PROTOZOAMETAZOAN(Helminths)

SARCODINA

(Ameobas)

SPOROZOA

(Sporozoans)MASTIGOPHO

RA(Flagellates)

CILIATA(Ciliates)

PLATYHELMINTHES

(Flatworms)

NEMATHELMINTHES

(Round worms)

Balantidium coliC

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A They are single cell-like microorganisms. Shape: Spherical to oval (elongated). They belong in the Kingdom Protista. Most are unicellular. They are classified based on their mode of

locomotion (pseudopodia, flagella, cilia & w/o means of locomotion)

Not all are parasitic (some are facultative parasites [Acanthamoeba spp. & Naegleria fowleri]).

Habitation: Normally they reside in the soil or water & can invade or gain entrance in our body.

Reproduction: Simple (by Binary fission [Sarcodina & Mastigohora]); others involve union of 2 cells – Syngamy.

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A MOT: Intestinal & Luminal protozoa: Direct

contact (person-to-person) & ingestion of contaminated food & water. Blood & Tissue protozoa: direct contact or through vectors (carriers).

Stages: CYST (dormant)- the INFECTIVE STAGE – the stage of the parasite that enters the host ; TROPHOZOITE (motile) – the PATHOGENIC STAGE – the stage of the parasite that is responsible for disease production.

Diagnosis: Microscopic examination of body fluids, tissue specimens, or feces (small size); Special stains are also used to demonstrate the different protozoa.

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A KINGDOM Protista

SUBKINGDOM Protozoa PHYLUM Sarcodina

CLASS Lobosea• Entamoeba histolytica•Acanthamoeba spp.•Naegleria spp.

PHYLUM Sarcomastigophora SUBPHYLUM Mastigophora

•Intestinal flagellates•Giardia lamblia•Urogenital flagellates•Trichomonas vaginalis•Blood & Tissue flagellates•Leishmania spp.•Trypanosoma spp.

PHYLUM Apicomplexa CLASS Sporozoa

•Tozoplasma gondii•Plasmodium spp.

PHYLUM Ciliophora•Balantidium coli

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IMPORTANT PROPERTIES It is an intestinal

protozoa. Life cycle; Two stages:

(1) The non-motile cysts – found in non-diarrheal (hard) stools; (2) The motile trophozoites – found w/n the intestinal & extraintestinal lesions and in diarrheal (watery) stools.

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PATHOGENESIS & EPIDEMIOLOGY MOT: Ingestion

of the infective stage-cysts in contaminated food & water (by the fecal-oral route).

There is no animal reservoir.

Life cycle: refer to the illustration

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Contaminated food or drink

Excyst in

ileum

Metacystic trophozoites

(invade & colonize walls of l.intestine)

Trophozoites in walls & lumen of colons

Developing trophozoite –

precystic amoeba –

uninucleate cyst –

binucleate cyst –

mature cysts

(passed w/ feces)

binucleate cyst – mature cysts

(passed w/ feces)

1

2

34

5

6

7

Epidemiology: Found worldwide but is more common in tropical countries (areas with poor sanitation.

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Infections (millions)

Disease (millions)

Deaths (thousands)

Protozoa   malaria 800 150 1500

  amoeba 480 50 100

  toxoplasma 40 10

  trypanosoma 24 1.2 60

Nematodes  intestinal nematodes

2400 2.6 80

  filaria 250 3 <1

  onchocerca 30 5 50

Trematodes   schistosoma 200 20 1000

Cestodes   tapeworms 2.5

World annual rates of morbiditv and mortality

DISEASE: AMEBIASIS ACUTE INTESTINAL AMEBIASIS: Presents as dysentery (bloody, mucus-containing

diarrhea). Accompanied by lower abdominal discomfort,

flatulence & tenesmus. CHRONIC (may occur): Occasional diarrhea Weight loss Fatigue (In some patient) A granulomatous lesion called an

AMEBOMA may form in the cecum/in the rectosigmoid area of the colon (malignant tumor like in the colon).

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DISEASE: AMEBIASIS AMEBIC LIVER ABSCESS

(ALA): RUQ pain Weight loss Fever Tender enlarged liver The abscess has a

characteristic “anchovy-sauce” appearance

LUNG DISEASE (once the trophozoite penetrate the diaphragm from the right lobe of the liver).

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LABORATORY DIAGNOSIS & TREATMENT Stool Examination – positive

detection of trophozoites in diarrheal stools or cysts in formed stools.

Serological Testing – for invasive amebiasis

DOC: Metronidazole & Tinidazole for symptomatic intestinal amebiasis or hepatic abscess; Iodoquinol or Paromomycin for asymptomatic cyst carriers.

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PREVENTION Avoiding fecal contamination

of food and water. Observing good personal

hygiene such as proper hand washing.

Purification of water source. The use of “night soil” as

fertilizer should be avoided. Adequate cooking of

vegetables should also be observed.

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Acanthamoeba castellani & Naegleria fowleri They are minor protozoan pathogens. They are free-living amebas that cause

meningoencephalitis. Habitation: They are widely found in soil &

freshwater lakes; Acanthamoeba can survive in cold water, Naegleria can survive in thermal spring water.

Infective stage (for both): cyst & the pathogenic stage is trophozoite.

MOE/T: Naegleria: intranasal (swimming in contaminated water) – nasal mucosa – cribriform plate-brain; Acanthamoeba: skin or eyes (trauma).

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Targets: Acanthamoeba- immunocompromised individuals; Naegleria – healthy individuals, usually children.

Other than meningoencephalitis: Acanthamoeba – cause keratitis (cornea inflammation) – parasites have been recovered from contact lenses, lens cases & contact lens solutions.

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Acanthamoeba castellani & Naegleria fowleri

DIAGNOSIS, TREATMENT & PREVENTION DIAGNOSIS: Finding the parasite in the CSF. DOC: Amphotericin B – Naegleria infection;

Pentamidine, Ketoconazole, or Flucytosine – Acanthamoeba infections (Prognosis is poor even w/ treatment).

PREVENTION: Infection w/ Acanthamoeba can be prevented by

adequate boiling of water. (since dust carries the cysts) masks should be worn

while cleaning. Regular disinfection of contact lenses is also advised. There is no known means of prevention & control of

Naegleria infection.

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IMPORTANT PROPERTIES LIFE CYCLE: (1)

Trophozoite – pear-shaped w/ 4 pairs of flagella; (2) Cyst – oval & thick-walled w/ 4 nuclei. [1 cyst = 2 trophozoites during excystation in the intestinal tract].

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PATHOGENESIS & EPIDEMIOLOGY MOT (major): Ingestion of the

cyst in fecally-contaminated water & food.

Distribution: Approximately 50% are asymptomatic carriers.

Reservoirs: humans & (many) sp. of mammals.

Infection is common among male homosexuals (oral-anal contact).

High incidence is seen in day-care centers & among patients in mental hospitals.P

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DISEASE: DIARDIASIS Non-bloody, foul-

smelling diarrhea accompanied by nausea, anorexia, flatulence & abdominal cramps (for weeks or months) .

Malabsorption of fat may lead to the presence of fat in the stool (steatorrhea) of a patient.

The patient is afebrile (no fever). P

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LAB DIAGNOSIS, TREATMENT & PREVENTION DIAGNOSIS: Stool examination (+

cyst&/trophozoites); microscopic exam is negative the string test may be done.

TREATMENT: DOC is metronidazole or quinacrine hydrochloride.

PREVENTION: Drinking boiled, filtered, or iodine-treated

water (in endemic areas).Proper hygiene & waste disposal must also be

observed. (No prophylactic drug or vaccine is available).P

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IMPORTANT PROPERTIES Shape: Pear

w/ a central nucleus & 4 anterior flagella.

It exists only in the trophozoite form (infective & pathogenic form).

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ORA: Tr

ichom

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vagin

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PATHOGENESIS, EPIDEMIOLOGY & DISEASE MOT: Sexual contact HABITATION: Vagina & the prostate (male) Epidemiology: T. vaginalis infection is one of the most

common worldwide; the frequency is highest among sexually-active women (in their 30’s) & lowest in postmenopausal women.

Disease: TRICHOMONIASIS/VAGINITIS watery, foul-smelling, greenish vaginal discharge

accompanied by itching (pruritus) & burning sensation. Cervix is very red, w/ small, punctuate hemorrhages

giving rise to a “straberry cervix.” Infection in men is usually asymptomatic (some: manifest

symptoms of urethritis or prostatitis. PH

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Trichomoniasis (Protozoa: Trichomonas vaginalis)

LAB DIAGNOSIS, TREATMENT & PREVENTION DIAGNOSIS: Microscopic examination - + of

trophozoite (wet mount of vaginal & prostatic secretions).

TREATMENT: DOC is metronidazole PREVENTION: To prevent “ping pong” infections, there should be

simultaneous treatment of both sexual partners. Maintenance of the low pH of the vagina is also

helpful. The use of condoms can limit transmission of the

parasite. Health & sex education are also important.P

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ORA: Tr

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vagin

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IMPORTANT PROPERTIES Life cycle Vector: female

sandfly, Phlebotomus species.

Infective stage: promastigote

Pathogenic stage: amastigote

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PATHOGENESIS & EPIDEMIOLOGY Major MOT: Bite of the vector Target tissues: Organs of

reticuloendothelial system (liver, spleen, & bone marrow).

Epidemiology: Mediterranean basin, Middle East, China & some parts of Africa

Three distinct groups of species:1. L. donovani – visceral leishmaniasis2. L. tropica; L. mexicana; –

cutaneous leishmaniasis3. L. braziliensis – mucocutaneous

leishmaniasisPH

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donovani

visceral leishmaniasis/Dum Dum Fever Early nodule at

site of sandfly bite seen at times.

usually presents with chronic fever.

splenomegaly (very large)

Lymphadenopathy

dark skin

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KALA – AZAR means “black-

sickness”

High mortality from anemia and bacterial superinfections.

cutaneous leishmaniasis (L. tropica & L. mexica na) There are several

variants basically with skin nodules which ulcerate.

L. tropica complex - in Asia, Africa, and Mediterranean (called Oriental sore, Delhi or Bagdad boil).

L. mexicana complex and others - in Central and South America

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mucocutaneous leishmaniasis It begins as a

cutaneous ulcer and metastasizes to mucosa of nose and pharynx leading to destruction, obstruction and death.

L. braziliensis - in South  and Central America (called espundia).

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PATHOPHYSIOLOGY/LIFE CYCLE

Amastigotes ingested by

the mosquitoe

Amastigotes differentiate

into promastigot

es (inside gut of vector)

Transmitted to an

uninfected human during

next bite

Promastigotes are engulf by macrophages

(transform into..)

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LAB DIAGNOSIS, TREATMENT, PREVENTION DIAGNOSIS:o Biopsy preparation – amastigotes in a bone marrow, spleen,

or lymph node.o Serological Test – very high conc of IgG is indicative of

infection.o Skin Test – use a crude homogenate of promastigotes as the

antigen. TREATMENT: DOC- Sodium stibogluconate PREVENTION:1. Prevention of the bite from the sandfly:

a. Wearing of protective clothingb. Use of nettingc. Use of insect repellants.

2. Insecticide spraying (kill the sandfly)PH

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OTHER PARASITES:PARASITE PROPERTIE

SPATHO/

EPIDEMIOLOGY

DISEASE DIAGNOSIS TREATMENT

PREVENTION

Trypanosoma cruzi Vector: reduviid bug/kissing bug (Triatoma)

MOT: bite of the vectorOccurrence: rural Central & South AmericaAcute: USA; chronic: Latin Amerika

CHAGA’S disease (American trypanosomiasis)- ROMAÑA SIGN (facial edema), CHAGOMA (nodule near the bite site), fever, lympadenopathy, hepatosplenomegaly)

Acute – demostration of trypomastigotes in patient’s blood (serological test).Others – bone marrow aspiration, muscle biopsy, xenodiagnosis

DOC: acute phase – nifurtimox; alternative drug: benznidazole; chronic no effective drug

Protection from the bite of the reduviid bug; Improvement of housing conditions; insect control

T. brucei gambiense and T. brucei rhodesiense

Vector: tsetse fly (Glossina);Reservoir: humans (gambiense) & cattle & wild animals (rhodesiense) ;Infective & pathogenic stage – trypomastigote

Target tissues: skin, blood, lymph nodes, brain.Endemic in sub-Saharan Africa (natural habitat of tsetse fly); T. gambiense – west Africa & T. rhodesiense – east Africa

AFRICAN SLEEPING SICKNESS – trypanosomal chancer at the bite site, weekly fever, lymphadenopathy, WINTERBOTTOM’S SIGNS (lymph nodes enlargement), encephalitis, sleeping sickness (somnolence, muscle tremors), coma.

Microscopic examination (Serologic test-blood); Aspiration of the chancer (& CSF);

Effective drug- SURAMIN; Alternative drug – PENTAMIDINE (followed by MELASOPROL)

Protection against the bite of the fly; use of netting and protective clothing; clearing forest around the villages; using insect repellants; no vaccine available

Toxoplasma gondii (Apicomplexa)

Definitive host- domestic cat; Intermediate host – humans & mammals.Infective stage – cysts (oocysts); small intestine (host) – tachyzoites/bradyzoites)

MOT: ingestion of the cysts (in meat), transplacental transmission (infected mother to fetus-congenital infection),EPI: Occurs worldwide, infection is sporadic

TOXOPLASMOSIS – resemble infectious monocleosis w/ fever, jaundice; congenital infection – abortion, stillbirth, neonatal disease (encephalitis, chorioretinitis & hepatosplenomegaly); Cause of BLINDNESS in children.

Acute & congenital infection – IMMUNOFLUORESCENCE ASSAY for IgM antibodies.Microscopic examination – trophozoites; cysts in tissues

Congenital toxoplasmosis – SULFADIAZINE & PYRIMETHAMINE

Thorough cooking of meat to kill the cysts; Refrain from handling litter boxes; cats should not be fed raw meat.

PARASITE PROPERTIES PATHO/EPIDEMIOL

OGY

DISEASE DIAGNOSIS TREATMENT

PREVENTION

Plasmodium spp.: vivax malariae ovale falciparum (impt.)

Vector & definitive host: female Anopheles mosquito; humans (intermediate host)Life cycle: (1) SPOROGONY-sexual cycle (occurs in mosquito), (2) SCHIZOGONY – asexual cycle (occurs in humans).Infective stage: sporozoite.Erythrocytic phase – merozoites in the RBCs; Exoerythrocytic phase – sporozoites in the liver.

Main MOT: bite of the female mosquito; others: across the placenta, in blood transfusions, IV drug abuse.P. Falciparum – infects both young & old RBCs; P. vivax & ovale infects young RBCS; P. malariae infects old RBCs.Timing of fever cycle: Quartan malaria (4th day/72 hrs.) – P. malariae, Malignant tertian malaria (3rd day/ 24 – 48 hrs) – P. falciparum, Benign tertian malaria ( 3rd day/48 hrs) – P. vivax & P. ovale.EPI: Occurs worldwide (in tropical & subtropical areas – asia, africa & Central & South America. Philippines: Catanduanes, Cebu, Bohol, & Leyte are malaria-free; High endemicity – Palawan, Kalinga-Apayao, Ifugao, & Agusan del Sur; 70% of cases are due to falciparum

Malaria - paroxysms are divide into 3 stages: (1) cold stage – abrupt onset of chills accompanied by headache, myalgias, & arthralgias, (2) hot stage – spiking fever reaching up to 410C accompanied by shaking chills, nausea, vomiting & abdominal pain, (3) sweating stage – drenching sweats.Manifestations: splenomegaly & anemia, cerebral malaria & kidney damage, “blackwater fever” – dark color of urine due to kidney damage.

Blood exam of Giemsaistained smears ( + trophozoites in the infected RBCs).P. falciparum – w/ “banana-shaped” gametocytes.NOTE: If more than 5% of RBCs are parasitized, the diagnosis is usually P. falciparum malaria.

DOC: CHLOROQUINE , PRIMAQUINE – for vivax & ovale malaria, MEFLOQUINE/ QUININE+DOXYCYCLINE = for chloroquine-resistant strains of falciparum, in severe cases (cerebral malaria/blackwater fever) – PARENTERAL QUINIDINE or QUININE

CHEMOPROPHYLAXIS (mefloquine/doxycycline) of malaria for traveler to endemic areas.Other preventive measures: (1) avoidance of the bite of the vector thru the use of mosquito, window screens, protective clothing, & insect repellants (protection is important during the night). (2) reduction of mosquito population is also helpful (by using insecticide sprays). No vaccine is available.

OTHER PARASITES:

PARASITE PROPERTIES PATHO/EPIDEMIOL

OGY

DISEASE DIAGNOSIS TREATMENT

PREVENTION

Balantidium coli Largest protozoan to infect humans.Reservoir host: domestic animals especially pigs. Infective stage: cystsPathogenic stage: trophozoites

It is worldwide.MOT: ingestion of the cysts in food & water contaminated w/ animal or human feces.

Extraintestinal lesions do not occur.Most infected individuals are asymptomatic.

Stool examination Tetracycline Avoiding contamination of food and water by feces of domestic animals

CESTODES/TAPEWORMS Flat worms w/ 2 main parts:

(1)head/scolex w/ hooks, suckers or sucking grooves, (2) body divided into PROGLOTTIDS (multiple segments)

A series of proglottids is called STROBILA.

All are hermaphroditic. GRAVID PROGLOTTIDS contains both

male & female reproductive organs and are capable of laying eggs.

Intermediate hosts: cattle, pigs & fish.

Infection is acquired thru ingestion of the undercooked or raw flesh of the infected intermediate host.

PARASITE IMPORTANT PROPERTIES

PATHOGENESIS &

EPIDEMIOLOGY

DISEASE DIAGNOSIS TREATMENT PREVENTION

Taenia saginata (beef tapeworm)

Infective larva: cysticercusPathogenic stage: adult worms (10 m long)Intermediate hosts: cattlesDefinitive hosts: humans

Cosmopolitan (universal) distribution occuring worldwide.Endemic in Africa, South America & eastern Europe. Taenia saginata is more common in the Philippines than infection w/ T. solium (pig tapeworm)

Taeniasis – mild abdominal cramps & malaise; itchiness in the anus (PRURITUS ANI)

Stool examination – demostration of proglottids or eggs.

DOC is praziquantel Proper waste disposal & adequate cooking of beef; freezing of meat at -20oC for 10 days may kill the encysted larvae.

Taenia solium (pork tapeworm)

Infective larvae: cysticercus cellulosae.Pathogenic stage : small worms & adult worms (5 meters in length)Intermediate host: pig

MOT: similar w/ T. saginata.Worldwide in distribution but endemic in certain areas in Asia, South America & Eastern Europe

Taeniasis [asymptomatic, although anorexia & diarrhea may occur] caused by the adult worms & cysticercosis [muscle pain, in the eyes-uveitis & renitis] caused by the larvae (in the brain it is known as NEUROCYSTICERCOSIS – most feared & severe complication).

Same for Taenia saginata. Cysts in tissues – Surgical removal and CT scan

DOC: PRAZIQUANTEL (intestinal infection & for cysticercosis); ANTICONVULSION (for neurocysticercosis); ALBENDAZOLE (alternative drug for cysticercosis)

Proper waste disposal & adequate cooking of pork meat.Treating patients to prevent autoinfection.Proper hygiene to prevent contamination of food w/ the eggs of the parasite.

Diphyllobothrium latum (fish tapeworm)

The longest of the tapeworms (13 meters in length).Infective larvae: PLEROCERCOID/ SPARGANUM First intermediate host: copepodsSecond intermediate host: fish (e.g. trout)

MOT: ingestion of improperly cooked or raw fish contaning the infective larvae.Has worldwide distribution but is endemic in countries where eating raw fish is a custom.

DIPHYLLOBOTHRIASIS – abdominal discomfort & diarrhea, deficiency of Vit B12 leading to megaloblastic anemia.

Demonstration of characteristics eggs in stool of infected individuals.

DOC: PRAZIQUANTEL Proper waste disposal & adequate cooking of fish.Freezing for 24 – 48 hrs at -180C kills all larvae.

INTESTINAL CESTODES

PARASITE PROPERTIES

PATHO/EPIDEMIOLOGY

DISEASE DIAGNOSIS TREATMENT

PREVENTION

Hymenolepis nana (dwarf tapeworm)

There is no obligatory intermediate animal host (though can be ingested by rice/flour beetles – intermediate hosts).Direct life cycle.

MOT: ingestion of food or water that is contaminated by the eggs of the parasite.Autoinfection may also occur.Dwarf tapeworm is the most common in the US; it is endemic in the southeastern US, mostly in children;also seen in East Asia & the Philippines.

HYMENOLEPIASIS – severe case is hyperinfection syndrome (high worm burden); secondary bacterial infections

Finding the eggs in the feces

DOC: PRAZIQUANTEL

NO specific means of prevention.Proper disposal of human waste & environmental sanitation may help limit the spread of the parasite. Rodent control must be observed.Food must be properly stored & protected from infestation w/ flour & grain bettles.

EXTRA-INTESTINAL CESTODEPARASITE PROPERTIE

SPATHO/

EPIDEMIOLOGY

DISEASE DIAGNOSIS TREATMENT

PREVENTION

Echinococcus granulosus (dog tapeworm)

Primarily a zoonotic infection.Definitive host: dogsAccidental/dead-end host: humans.Intermediate host: sheep.

MOT: ingestion of food & water that is contaminated by dog feces (w/ the parasite).Common in the Mediterranean region, the Middle East & Australia.

HYDATID CYST DISEASE – liver dysfunction, obstructive jaundice (liver cysts); cough & bloody sputum (pulmonary cysts); increased intracranial pressure-headache, vomiting & seizures (cerebral cysts); rupture of the cyst may lead to fatal anaphylactic shock.

Microscopic examination of specimen (sputum) - + protoscoloces.CT scan – in the case of liver & brain involvement.Serologic tests – indirect hemagglutination test.

ALBENDAZOLE, accompanied or not by surgical removal of the cyst.Hypertonic saline or 1% formalin may be injected into the cyst.Surgical removal – prevent anaphylaxis.

Reduce the infected populations & minimizing transmission.CHEMOPROPHYLAXIS should be given to dogs in endemic areas.Health education is essential.

TREMATODES (FLUKES) Flat, fleshy, leaf – shaped worms Member of the phylum

Platyhelminthes. Flukes have a digestive tract (unlike

cestodes). Have 2 muscular suckers: ORAL

TYPE - beginning of an incomplete digestive system; VENTRAL SUCKER – serves for attachment.

(most) Hermaphroditic, except for Schistosoma spp. (blood flukes).

Never use humans as intermediate hosts.