Intro to Parasites & Platyhelminthes Flashcards
1
Q
CDC top 5 neglected parasitic infections in the US
A
- Chagas – caused by Trypanosoma cruzi
- Cysticercosis – caused by Taenia spp
- Toxocariasis – caused by Toxocara canis or cati. Causes blindness.
- Toxoplasmosis – caused by Toxoplasma gondii. 2nd leading cause of food-borne deaths in US.
- Trichomoniasis – caused by Trichomonas vaginalis
2
Q
Th1 response against?
A
Protozoans
3
Q
Th2 / eosinophilic response against?
A
Worms
4
Q
Cyst
A
Dormant stage found encysted in a host (intermediate or definitive)
5
Q
Hydatid
A
Specialized cysticercal form of cestode Echinococcus granulosus found in intermediate host, including humans, sheep, and ungulates.
6
Q
Cestoda Type of parasite Digestive system Attachment Morphology Transmission
A
- Flatworms / Tapeworms. Flattened segmented bodies.
- No internal digestive system. Nutrients absorbed across cuticle.
- Attaches to gut wall via scolex
- Proglottids = segments. Mature from anterior to posterior. Specialized for hermaphroditic reproduction.
- Transmitted by ingestion of larval cysticerci or eggs
7
Q
Trematoda Type of parasite Digestive system Required intermediate host Attachment Reproduction (tissue vs blood flukes)
A
- Flukes w/ broad flattened bodies.
- Mainly affect the lungs, liver, and blood
- Simple digestive system. Single opening serves as mouth and anus.
- Requires 1 or more intermediate host, which always involves a snail.
- Have 2 suckers for attachment and locomotion.
- Tissue flukes reproduce hermaphroditically
- Blood flukes reproduce sexually and have sexually dimorphic forms.
8
Q
Pork / Beef Tapeworm Names Location (adults vs cysticerci) Definitive host Intermediate host Life cycle Prevention
A
- Pork = Taenia solium
- Beef = Taenia saginata
- Location: adults in intestine. Cysticerci found in any tissue.
- Definitive host: humans. Shed eggs and proglottids in feces.
- Intermediate host: pigs or humans for T solium. Only cattle for T saginata.
- Life cycle: Proglottids are full of eggs. Break off → stool. Cows / pigs eat stool, spread in blood and encysts in animal tissues. Human eats undercooked beef / pork → cysticercus evaginates and lives in human intestine. Individual worm may live 25 years.
- Prevention: cook / freeze pork / beef. Hygiene.
9
Q
T solium transmission
A
- Human ingestion of cyticerci in undercooked muscles of pigs → worms in gut (taeniasis).
- Human ingestion of eggs (may occur via autoinfection) → cysticercosis in muscle, brain, eyes, etc.
- Both forms can occur in same person due to autoinfection.
10
Q
T saginata transmission
A
Ingestion of undercooked beef containing cysticerci (encysted larvae)
11
Q
Difference in transmission b/w T solium / saginata
A
T solium eggs are infections for humans. T saginata eggs are not.
12
Q
Taenia Pathology
A
- Often asymptomatic. Abdominal discomfort, nausea, vomiting, diarrhea, weight loss. Superinfection can cause obstruction.
- Cysticercosis (T solium) = 1 cm cysticerci located in any tissue.
- Muscle cysts may cause lumps but no sxs
- Neurocysticercosis – sxs depend on where / how many cysticerci. Confusion, poor balance, hydrocephalus, seizures, headaches, death.
13
Q
Taenia Diagnosis (4)
A
- Observation of proglottids / eggs in stool. Discriminate T solium from T saginata from proglottids. Eggs are indistinguishable.
- Contrast studies show ribbon-like structures in intestine
- Cysticercosis: X ray shows calcified dead larvae. CT/MRI shows viable cysticerci
- CDC does immunoblot (Ab) w/ T solium Ag
14
Q
Taenia Treatment (4)
A
- Praziquantel, niclosamide, or albendazole for adult worms. Prolonged therapy for cysticerci.
- T solium: Dexamethasone reduces CNS inflammation that often occurs due to large inflammatory response from dying cysticerci.
15
Q
Fish Tapeworm Name Location Transmission Definitive host Intermediate host Endemic areas Pathology Diagnosis Treatment (3) Prevention
A
- Diphyllobothrium latum
- Location: lumen of intestine
- Transmission: ingestion of undercooked fish w/ plerocercoid (encysted larvae). No autoinfection as in Taenia.
- Definitive host: humans
- Intermediate host: copepod (crustacean) that infects fish
- Found in temperate zones where fish is major part of diet
- Pathology – Similar to beef tapeworm, but adult absorbs 80-100% of Vit B12 → anemia / neuro sxs
- Diagnosis – same as Taenia. Easily discriminated from Taenia by egg and proglottid. Clinical sxs of anemia.
- Treatment – Praziquntel or niclosamide. B12 supplements.
- Prevention – Hygiene, well cooked / frozen fish
16
Q
Diphyllobothrium latum life cycle
A
- 2 intermediate hosts
- Eggs shed into water supply and hatch into corcidium, which is ingested by a copepod (crustacean), where it encysts as a procercoid (1st larval stage).
- Copepod is ingested by fish, such as salmon
- Human eats undercooked fish → plerocercoid (2nd larval stage) matures into adult worm in intestine.
17
Q
Echinococcosis 2 kinds Endemic areas Location Transmission Definitive host Intermediate host Incidental host Immunity Prevention
A
- Echinococcus granulosus causes cystic echinococcosis / hydatid disease. Pastoral cycles w/ grazing animals (sheep / goats) and dogs.
- E multilocularis causes alveolar echinococcosis. Wild cycles w/ wolves and moose / caribou / elk. Humans exposed when hunters feed internal organs to dogs.
- Not endemic in US, but seen in immigrants
- Location: tissues, especially lungs and liver
- Transmission: ingestion of eggs from dogs. NOT from eating sheep meat.
- Definitive host: wild / domestic dogs that eat intestines of dead animals
- Intermediate host: ungulates (hoofed animals) and humans
- Humans are an incidental (dead end) host. Usually exposed when hunters feed internal organs to domestic dogs.
- Immunity – circulating Abs to hydatid cyst Ags. Causes more pathology than protection.
- Prevention: proper disposal of internal organs, deworm dogs, hygiene.
18
Q
Echinococcus life cycle
A
- Dogs poop out eggs, which are eaten by sheep. Larvae enter sheep circulation → hydatid cyst in liver / lungs.
- Dogs eat viscera of sheep. Protoscolices become adult worms in dogs.
- Humans acquire eggs through contact w/ infected dogs. Dead end host.
19
Q
Pathology of Hydatid Disease
Which parasite?
A
- Echinococcus granulosus
- May have latent period of 20 years
- Larvae makes large GRANULOMATOUS hydatid cysts, which cause problems when in tissues such as the liver (60%) and lungs (25%). Others include spleen, kidney, bone, CNS. Cysts may cause pain, nausea, and vomiting.
- Cyst rupture → release of protoscolices, which may induce ANAPHYLAXIS / death.
20
Q
Pathology of Alveolar Disease
Which parasite?
A
- Echinococcus multilocularis causes tumors in human liver that does not mature into cysts but invades / destroys surrounding tissues.
- May cause liver failure and spread to lungs / brain.
- Mainly in the liver, despite being called alveolar.
21
Q
Echinococcus Diagnosis (3)
A
- Live in endemic area, animal husbandry / hunting
- CT / US shows growing cysts
- Serology used for confirmation
22
Q
Echinococcus Treatment (3)
A
- Percutaneous drainage w/ instillation of hypertonic saline / alcohol. Plus albendazole.
- Surgical removal, avoiding rupture of cyst
- If inoperable, tx w/ albendazole alone, but cure rate is low b/c most of the cysts are dormant.
23
Q
3 species of Schistosomiasis Location of adult worms / eggs Endemic areas Transmission Definitive host Intermediate host Peak infection rate. Diagnosis (2) Treatment (2) Prevention
A
- Schistosoma mansoni. Adults in inferior mesenteric veins. Eggs in descending colon.
- Schistosoma japonicum. Adults in superior mesenteric veins. Eggs in small intestine.
- Schistosoma haematobium. Adults in venous plexus (bladder). Eggs in bladder.
- In mansoni and japonicum, the eggs can flow into / get trapped in portal venules → chronic inflammation.
- Mansoni and haematobium are in Africa / Middle East.
- Japonicum is in southeast Asia, often in rice patties (stagnant water).
- Transmission – invasive: aquatic cercaria penetrate skin. Spread by water contamination w/ human waste and uptake by snails. Found in travelers. Not acquired in US. No person to person.
- Definitive host: humans
- Intermediate host: snails
- Peak infection rate in second decade. Mainly kids playing in water.
- Diagnosis – eggs in feces / urine is most common. Species differentiated by spikes and location. Serology.
- Treatment – Artemisinin early after exposure. Praziquantel later. Does not completely subside until the egg-induced granulomas heal.
- Prevention – treat infected pxs, proper waste disposal, eliminate snails (intermediate hosts), avoid contact w/ infested water.
24
Q
Schistosome Life Cycle
A
- Eggs are shed into the water, miracidium hatches and invades snail. Asexual reproduction in snail → release motile cercaria, which invades skin of humans, enters circulation → portal system.
- Adults mate and the couple migrates to the final venous location. Female burrows inside male. Pair may live 20-30 years inside a human. Good at avoiding immune system.
- Eggs are passed to environment or become trapped in body tissues → immune rxn / pathology
25
Q
Morphology of 3 Schistomes
A
- Japonicum doesn’t have any spikes on eggs. More associated w/ stagnant water, so it doesn’t need to grip on.
- Haematobium has terminal spike
- Mansoni has lateral spike.
26
Q
Early pathology of Schistosomiasis
A
Early (0-2 weeks): usually asymptomatic. Intensely itchy rash from invading cercaria. Multiple exposures may cause hypersensitivity. Rash goes away after 1-2 weeks, then fever, headache, nausea as schistosomula migrates. Sxs are much worse in visitors to the endemic area.
27
Q
Middle pathology of Schistosomiasis
A
- Middle (1-2 months): sxs mainly caused by immune response to eggs.
- Katayama Syndrome – Intense nocturnal fever, cough, headache, myalgia, abdominal tenderness w/ oviposition. Occurs in travelers who have never seen the pathogen before.
- Associated sxs include arthralgia, lymphadenopathy, splenomegaly
- Intestinal schistosomiasis → abdominal pain, diarrhea, bloody stool
- Urogenital shistosomiasis → hematuria
- Worse w/ Sj (more eggs) w/ occasional encephalitis
28
Q
Chronic pathology of Schistosomiasis
A
- Chronic (5-30 years)
- Eggs lodge in tissues: intestine, liver (Sm Sj), or bladder (Sh). Pathology is caused by the eggs, not the worms.
- Severe liver disease → periportal fibrosis → portal HTN, hepatosplenomegally, megaesophagus → rupture of varices. Also possible to get liver and colon cancer.
- Extensive fibrosis of bladder → mucosal thickening / ulceration → loss of bladder function and bladder cancer. Uremia, dysuria, and secondary infection may occur. Pseudopolyps may progress into bladder cancer.
- Ulceration of intestinal mucosa, abdominal pain, diarrhea
- Egg secretions → eosinic inflammatory response → granulomas surrounding dead eggs
29
Q
Schistosomiasis Immunity
A
- Adult organisms escape immunity by absorption of host proteins
- Some immunity to reinvasion in endemic areas. Immunity is involved in pathology (granuloma).
30
Q
Schistosome Dermatitis / Swimmer's Itching / Duck Schistosome Life cycle Pathology Endemic area Treatment (2)
A
- Dead-end invasion of humans. Cercaria penetrate skin but schistosomula fail to thrive
- Intensive pruritic inflammatory response lasts multiple days. Not lethal. Caused by immediate (IgE) and sometime delayed-type hypersensitivity.
- Common in WI lakes (including Devil’s lake)
- Tx w/ anti-pruritic and antihistamine lotions
