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FM3-2: Parasites, STDs, etc > Intro to Parasites & Platyhelminthes > Flashcards

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
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2
Q

Th1 response against?

A

Protozoans

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3
Q

Th2 / eosinophilic response against?

A

Worms

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4
Q

Cyst

A

Dormant stage found encysted in a host (intermediate or definitive)

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5
Q

Hydatid

A

Specialized cysticercal form of cestode Echinococcus granulosus found in intermediate host, including humans, sheep, and ungulates.

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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
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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.
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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.
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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.
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10
Q

T saginata transmission

A

Ingestion of undercooked beef containing cysticerci (encysted larvae)

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11
Q

Difference in transmission b/w T solium / saginata

A

T solium eggs are infections for humans. T saginata eggs are not.

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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.
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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
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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.
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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
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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

FM3-2: Parasites, STDs, etc (11 decks)

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