Parasites/helminths Flashcards
Giardias Etiology
G.lamblia
Giardias reservoir
beavers, dogs, cats, primates.
Giardias epidemiology
Common in children. Highly contagious. June-october. Common in the rocky mountains. Communicable as an STI.
Giardias Life cycle
Ingestion of cyst. Excystation in stomach. trophozoites pass to small bowel. Trophozoites encyst in the large bowel and then the cysts are excreted.
Giardias Symptoms
Intermittent episodes of watery diarrhea (no blood), cramps, abdominal distension, anorexia (malabsorption), vitamin B12 deficiency.
Giardias Diagnosis
O/P examination of multiple stool samples. ELISA for GSA65.
Giardias treatment
metronidazole.
Amebiasis etiology
Entamoeba Histolytica
Giardias trophozoites
exist freely in the intestine. bilobed adhesive disc with flagella and 2 nuclei. Feeds on the mucous and flattens the villi.
Giardias Cysts
Passed into the environment. Hyaline wall with 4 nuclei.
Amebiasis trophozoite
1 nucleus, non-flagellated, pseudopod, invasive and pathogenic.
Amebiasis Cysts
round with 4 nuclei. infectious.
Amebiasis Life cycle
ingestion of cysts. excystation in the colon. Highly motile. colonizes colon mucosa. encyst and are passed into the environment or invade the mucose to enter the blood stream and disseminate.
Amebiasis Epidemiology
Common in tropical/subtropical areas.
Amebiasis symptoms
Can range from asymptomatic to dysentery to extraintestinal manifestions. Acute amoebic colitis: cramps, tenderness, bloody stools, fever, vomiting, weight loss. Ulcers and right upper quadrant pain.
Amebiasis Mortality causes
peritonitis, cardiac failure and exhaustion
Amebiasis Lectin
adhesion
Amebiasis Phospholipases
Disrupt the cell membrane.
Amebiasis amebapore
peptide released that inserts ion channels into the host lipid structure causing lysis.
Amebiasis cyestein proteases
degrade mucus, antibodies, complement and cellular matrix.
Amebiasis Diagnosis
ELISA; differentiates between E. hystolitica and E. dispar (Commensal). Radiology will detect ascesses extraintestinal.
Amebiasis Treatment
Metronidazole and surgery for large abcesses.
Cryptosproridiosis etiology
Cryptosporidium hominis (humans) and C. parvum (bovine and human).
Cryptosproridiosis Oocyst
Infectious. Contains 4 sporozoites.
Cryptosproridiosis Sporozoites
motile. bind receptors on the surface of intestinal epithelium. Ingested into parasitophorous vacuole (near surface but still separated from the cytoplasm).
Cryptosproridiosis life cycle
Asexual and sexual reproduction inside the host
Cryptosproridiosis thin oocyst
Asexual. reinfect the host.
Cryptosproridiosis thick oocyst
Sexual. Shed into the environment. Highly infectious immediately after being released. Shedding can continue for weeks after the patient improves.
Cryptosproridiosis epidemiology
Person-to-person. Resistant to chlorine. Commonly associated with AIDS.
Cryptosproridiosis symptoms
watery (not bloody) diarrhea, dehydration, weight loss, fever, abdominal pain. Lasts for 2 weeks.
Cryptosproridiosis Diagnosis
Isolate oocysts from the stool (zinc sulfate centrifugal flotation) then use immunoflourescence or ELISA.
Cryptosproridiosis treatment
nitazoxanide or paroromycin.
Cyclosporiasis etiology
cyclospora cayetanensis
Cyclosporiasis epidemiology
common in latin america. contaminated water and imported food. Resistant to chlorine.
Cyclosporiasis description
Large oocyst that is autofluorescent. Acid-fast.
Cyclosporiasis life cycle
oocysts are shed in the feces and must sporulate in the environment which can take days to become infectious.
Cyclosporiasis symptoms
Low grade fever, chills, cramps, nausea, vomiting, explosive (not bloody) diarrhea, rapid weight loss, profound fatigue.
Cyclosporiasis treatment
bactrim.
Blastocystis hominis description
polymorphic. large central vacuole with multiple nuclei around the rin.
Blastocystis hominis epidemiology
comes from animal feces.
Blastocystis hominis treatment
metronidazole
balantidium coli description
Large microbe with a macronucleus and cilia.
balantidium coli epidemiology
zoonotic. Pigs.
balantidium coli complications
Gut perforation.
balantidium coli treatment
metronidazole or tetracycline.
Nematodes (roundworms) Morphology
elongated cylindrical body that tapers at the ends. covered with multi-layered cuticle. Presence of seperate sexes.
Enterobius vermicularis classification
“pinworm.” Nematode (roundworm). Causes enterobiasis. Most common helminth infection.
Enterobius vermicularis description
small (8-12mm) white worms.
Enterobius vermicularis epidemiology
person-to-person transmission or through the environment. Common in cosmopolitan and temperate regions. common in children.
Enterobius vermicularis life cycle
eggs are deposited in the perianal region. ingested (self-infection or transmission). larvae hatch in the small intestine. adults mature in the colon (2 months). gravid females migrate to the perianal region at night and deposit the eggs. eggs become infectious in 4-6 hours.
Enterobius vermicularis symptoms
perianal itching. secondary infections, sleep distrubance, abdominal pain.
Enterobius vermicularis Diagnosis
cellophane tape method. Take sample first thing in the morning or at night for three consecutive days. Also sample under the fingernails. Microscopic analysis.
Enterobius vermicularis Treatment
mebendazole or albendazole for all members of the household.
Ascaris lumbricoides classification
Largest intestinal nematode.
Ascaris lumbricoides epidemiology
transmission via contaminated soil. common in children. world wide distribution especially in warm climates.
Ascaris lumbricoides life cycle
eggs are ingested. larvae are released in the duodenum. larvae penetrate the mucosa. travel to the lungs. oropharynx. swallowed. mature in the duodenum. Can live for 2 years. Release 200,000 eggs/day.
Ascaris lumbricoides presentation
asymptomatic. high worm load: blockages, loeffler’s syndrome (eosinophil accumulation in the lungs), abdominal pain.
Ascaris lumbricoides diagnosis
detection of eggs in a stool sample.
Ascaris lumbricoides treatment
mebendazole or albendazole.
Trichus trichiura classification
Nematode (roundworm). “whipworm”
Trichus trichiura description
small (40mm) with whiplike morphology. Have eggs with capsules tapered at the ends.
Trichus trichiura epidemiology
contaminated soil. common in children. world wide distribution.
Trichus trichiura life cycle
eggs are ingested. larvae are released in the duodenum. mature in the colon. release the eggs in feces.
Trichus trichiura presentation.
asymptomatic. high worm load: frequent, painful passoage of stool with mucus, blood and water. rectal prolapse. growth retardation and anemia.
Trichus trichiura diagnosis
presence of eggs in stool sample.
Trichus trichiura treatment
albendazole or mebendazole.
Hookworm classification
nematode (roundworm)
Hookworm etiology
Necator americanus and ancylostoma duoddenale.
Hookworm description
small (12mm) feed on blood from the intestinal mucosa.
Hookworm epidemiology
inadequate disposal of feces leads to contaminated soil. Larvae can penetrate the skin.
Hookworm life cycle
eggs hatch in soil. Larvae (filiform) penetrate the skin. travel to the lungs. oropharynx. swallowed. mature in the duodenum. eggs are excreted into the soil.
Hookworm presentation
blood-filled pruritic lesion at the site of penetration (ground itch). Anemia due to continual blood loss.
Hookworm diagnosis
presence of eggs in the stool
Hookworm treatment
mebendazole.
Strongyloides stercoralis classification
nematode (roundworm) “threadworms” small (12mm).
Strongyloides stercoralis epidemiology
tropical/subtropical areas. related to poor sanitation.
Strongyloides stercoralis life cycle
larvae penetrate the skin. travel to lungs. oropharynx. swallowed. mature in the mucosa of the duodenum. larvae are released in the feces. free living multiplication cycle in the soil.
Strongyloides stercoralis presentations
diarrhea, abdominal pain, constipation, malabsorption, signs of larval migration. Autoinfection can result in chronic infections. Life threatening in patients with defect in cell mediated immunity.
Strongyloides stercoralis diagnosis
presence of larvae in the stool, duodenal aspirate or sputum in hyperinfected person.
Strongyloides stercoralis treatment
thiabendazole.
Trematodes (flukes) morphology
flattened, leaf-like, suckers, hermaphroditic. 2 intermediate hosts and 1 definitive.
Clonorchis sinensis classification
Trematode (fluke). “chinese liver fluke” small (20mm).
Clonorchis sinensis epidemiology
far east. transmission occurs via ingestion of larvae in raw fish.
Clonorchis sinensis life cycle
fish containing encysted larvae is ingested. excytation occurs in the duodenum. larvae go into the biliary duct. mature. eggs are released. eaten by aquatic snails. larvae (cercariae) are released. cercariae encyst under the scales or flesh of a fish.
Clonorchis sinensis presentation
usually asymptomatic unless it becomes chronic.
Clonorchis sinensis diagnosis
presence of eggs in stool sample with a geographic history
Clonorchis sinensis treatment
praziquantel
Tapeworm classification
trematode (fluke). Taeniasis.
Tapeworm etiology
taenia solium (pork) and taenia saginata (beef)
Tapeworm description
large (3-9m). with scolex head structure. eggs are released in proglottids and are immediately contagious.
Tapeworm epidemiology
humans. world wide distribution.
Tapeworm life cycle
eggs are ingested by pigs or cows. hatch in the duodenum. larvae penetrate the cell wall. larvae (cysticerci) develop in the muscle. Human ingests poorly cooked meat. matures into a tapeworm in the jejunum. proglottids are released in the feces
cysticercosis
T. solium can develop cysticercosis in humans if infective eggs are ingested.
Tapeworm presentation
usually asymptomatic with one worm. may have mild GI symptoms. Cysticercosis can cause blindness or seizures depending on where the worm goes.
Tapeworm diagnosis
eggs/proglorrids in the stool sample. Cysticrosis shows lesions on CT scan with histological demonstration to confirm.
Tapeworm treatment
praziquantel
Diphyllobothrium latum classification
trematode (fluke). “fish tapeworm”. eggs are released singly not in proglottids.
Diphyllobothrium latum epidemiology
widespread from alaska to the great lakes.
Diphyllobothrium latum life cycle
larvae in the muscle of fish. ingested. larvae are released in the duodenum. mature in the jejunum. eggs are released in the feces. hatch in fresh water. work the way up the food chain.
Diphyllobothrium latum presentation
asymptomatic. Worm competes for B12 so anemia.
Diphyllobothrium latum diagnosis
presence of eggs in the stool ID of the adult worm.
Diphyllobothrium latum treatment
praziquantel
