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
LA
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ATIO
N O
F
PA
RA
SIT
ES
PR
OTO
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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.
PR
OTO
ZO
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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A
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.
PH
YLU
M S
AR
CO
DIN
A: Enta
moeba
his
toly
tica
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
PH
YLU
M S
AR
CO
DIN
A: Enta
moeba
his
toly
tica
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.
PH
YLU
M S
AR
CO
DIN
A: Enta
moeba
his
toly
tica
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).
PH
YLU
M S
AR
CO
DIN
A: Enta
moeba
his
toly
tica
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).
PH
YLU
M S
AR
CO
DIN
A: Enta
moeba
his
toly
tica
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.
PH
YLU
M S
AR
CO
DIN
A: Enta
moeba
his
toly
tica
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.
PH
YLU
M S
AR
CO
DIN
A: Enta
moeba
his
toly
tica
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).
PH
YLU
M S
AR
CO
DIN
A: Aca
nth
am
oeba
& N
aegle
ria
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.
PH
YLU
M S
AR
CO
DIN
A: Aca
nth
am
oeba
& N
aegle
ria
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.
PH
YLU
M S
AR
CO
DIN
A: Aca
nth
am
oeba
& N
aegle
ria
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].
PH
YLU
M M
ASTIG
OPH
OR
A:
Gia
rdia
lam
blia
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
HYLU
M M
ASTIG
OPH
OR
A:
Gia
rdia
lam
blia
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
HYLU
M M
ASTIG
OPH
OR
A:
Gia
rdia
lam
blia
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
HYLU
M M
ASTIG
OPH
OR
A:
Gia
rdia
lam
blia
IMPORTANT PROPERTIES Shape: Pear
w/ a central nucleus & 4 anterior flagella.
It exists only in the trophozoite form (infective & pathogenic form).
PH
YLU
M M
ASTIG
OPH
ORA: Tr
ichom
onas
vagin
alis
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
YLU
M M
ASTIG
OPH
ORA: Tr
ichom
onas
vagin
alis
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
ichom
onas
vagin
alis
IMPORTANT PROPERTIES Life cycle Vector: female
sandfly, Phlebotomus species.
Infective stage: promastigote
Pathogenic stage: amastigote
PH
YLU
M M
ASTIG
OPH
OR
A:
Leis
hm
ania
spp.
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
YLU
M M
ASTIG
OPH
OR
A:
Leis
hm
ania
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
PH
YLU
M M
ASTIG
OPH
OR
A:
Leis
hm
ania
donovani
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
PH
YLU
M M
ASTIG
OPH
OR
A:
Leis
hm
ania
tro
pic
a
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).
PH
YLU
M M
ASTIG
OPH
OR
A: Le
ishm
ania
bra
zilie
nsi
s
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..)
PH
YLU
M M
ASTIG
OPH
OR
A:
Leis
hm
ania
spp.
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
YLU
M M
ASTIG
OPH
OR
A:
Leis
hm
ania
spp.
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.