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FM3-2: Parasites, STDs, etc > Nematodes > Flashcards

Nematodes Flashcards

1
Q

General characteristics of nematodes

A

Roundworms
Cylindrical bodies w/ well-developed digestive and nervous systems. Reproduce sexually. Transmission can be ingestive (no intermediate host) or vector-borne (one intermediate host)

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2
Q 
Pinworm
Name
Location
Transmission
Definitive host
Pxs
Immunity
Diagnosis
Treatment
Prevention
A
  • Enterobius vermacularis
  • Location: adults in colon
  • Transmission: ingestion of eggs. Person to person. Aerosol transmission is possible.
  • Definitive host – humans. No intermediate host needed.
  • Common in kids in daycare centers. More common in poor communities
  • Pinworm infection is contained immunologically, but immunity is transient.
  • Diagnosis – persistent butt itch, restlessness, insomnia. Confirmed by observation of eggs w/ scotch tape test.
  • Treatment – pyrantel pamoate, mebendazole, albendazole. Thorough housecleaning to stop reinfection / transmission. Mebendazole does NOT work against the egg stage, just the worm stage, so it must be taken for 3 weeks.
  • Prevention – treat the entire family if one person is infected, even if they are asymptomatic.
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3
Q

Enterobius vermacularis life cycle

A
  • Eggs swallowed, hatch in intestine, adults mate and migrate to colon.
  • Female emerges from anus to lay eggs.
  • Perianal scratching facilitates transmission to mouth for autoinfection
  • Eggs in bed / clothes are transmitted to others
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4
Q

Enterobius vermacularis pathology (3)

A
  • Hypersensitivity rxn to pinworm proteins released when female degenerates during egg release.
  • Secondary infections may occur due to scratching
  • Occasional invasion of UG tract in females. Sxs such as dysuria / hematuria occur due to Coliform bacteria that the worms brought along.
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5
Q 
Whipworm
Name
Location
Definitive host
Transmission
Endemic areas
Life cycle
Immunity
Diagnosis
Treatment (3)
Prevention
A
  • Trichuris trichiura
  • Location: adults attach to colonic mucosa
  • Definitive host: humans. No intermediate host required.
  • Transmission: ingestion of embryonated eggs in soil. No person to person. Poor public hygiene and use of human waste as fertilizer spreads.
  • Found in tropical countries and poor communities in southern US. Less common than pinworm.
  • Life cycle – Eggs swallowed from soil or unwashed food (salad), hatch in intestine, adults mate and migrate to colon. Passed in feces. Eggs mature in soil for 2-5 wks.
  • Some acquired immunity
  • Diagnosis – eggs in stool
  • Treatment – ivermectin, mebendazole, or albendazole
  • Prevention – hygiene: hand washing, cooking raw fruits / vegetables
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6
Q

Trichuris trichiura pathology

A

Pathology – based on worm burden
• Low / moderate: usually asymptomatic. Bleeding / bacteremia.
• High: disrupted colonic mucosa, bloody stool, rectal prolapse, anemia
• Heavy: impaired growth and cognitive ability in kids

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7
Q 
Ascariasis
Name
Location
Definitive host
Transmission
Endemic areas
Immunity
Diagnosis
Treatment (3)
Prevention
A

Ascaris lumbricoides
•Location: adults free in upper intestine
•Definitive host: humans. No intermediate host required.
•Transmission: ingestion of eggs from soil (fecal-oral). No person to person. Spread via poor public hygiene and use of human waste as fertilizer.
•Up to 25% of world population infected, especially in tropical / subtropical. Appalachia / southern US. US neglected disease of poverty (NDP).
•Immunity – allergic inflammation from larval migration through lungs. May cause asthma.
•Diagnosis – eggs in stool, but hard to see.
•Treatment – Mebendazole, albendazole, or ivermectin
•Prevention – hygiene

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8
Q

Ascariasis Life Cycle

A
  • Eggs passed in feces. Eggs mature in soil for 3 weeks and are swallowed by kids playing in dirt or unwashed food (salad). Larvae hatch / invade intestinal mucosa.
  • Enter venous circulation → lungs → coughed up → swallowed again.
  • Mature / mate in SI; do not attach to mucosa. Live 1 year.
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9
Q

Ascariasis Pathology

A
  • Usually asymptomatic w/ low / moderate worm burden
  • Heavy load → intestinal obstruction, may require surgery
  • Stressed worms migrate to nose, ear, and may penetrate peritoneum or body wall.
  • Chronic infection → malnutrition → poor mental / physical development
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10
Q 
Hookworm
2 types
Location
Definitive host
Transmission
Endemic areas
Immunity
Diagnosis (2)
Treatment (3)
Prevention
A
  • Necator americanus (global)
  • Ancylostoma duodenale (Asia)
  • Location: attach to small intestine
  • Definitive host: humans. No intermediate host required.
  • Transmission – invades skin w/ soil contact. No person to person.
  • Found in southern US. Poor public sanitation. Kids / farmers w/o shoes. US NDP.
  • Immunity – asthma due to migration to lung
  • Diagnosis – anemia, confirmed by eggs in stool
  • Treatment – pyrantel pamoate, albendazole, and mebendazole
  • Prevention – hygiene, wear shoes
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11
Q

Hookworm life cycle

A
  • Eggs in feces matures in soil to rhabditiform larva → infectious filariform
  • Filariform larvae invade skin → circulation → lodges in lungs
  • Larvae coughed up and swallowed. Matures in intestine. Poop out eggs.
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12
Q

Hookworm pathology (4)

A
  • Initial itching at penetration sites, usually b/w toes
  • Heavy infection → larval migration through lungs → bronchitis
  • Prolonged infection → asthma
  • Intestinal blood loss → anemia (main pathology) → reduced mental / physical development in kids
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13
Q 
Strongyloides stercoralis
Location
Definitive host
Transmission
Pxs
Immunity
Treatment
Prevention
A
  • Location: small intestine
  • Definitive host: humans
  • Transmission: filariform larvae penetrate skin or rhabditiform larvae may be ingested. Autoinfection can cause long-term infection.
  • US NDP. Poor public sanitation, kids / farmers w/o shoes
  • Immunity - asthma
  • Treatment – ivermectin (DOC), thiabenazole. Treat all cases. HYPERINFECTION requires prolonged treatment.
  • Prevention – hygiene, wear shoes, wash veggies / food
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14
Q

Strongyloides Life Cycle

A
  • Eggs are laid in intestinal mucosa. 3 possibilities from there:
  • Direct – similar to hookworms, except larvae are in the feces. Larvae live in soil and then infects skin (no amplification)
  • Indirect – sexual reproduction in soil (instead of intestines) if conditions are right (warm / moist soil). Environmental amplification. Then enter through skin.
  • Autoinfection – larvae mature in host and enter colonic mucosa or perianal skin → host amplification. Pxs are usually immunocompromised, such as using steroids. Worm may live 40 years in single person. Direct transmission b/w individuals may occur.
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15
Q

Strongyloides Pathology (4)

A
  • Pulmonary problems like Ascaris
  • Intestinal infection is usually asymptomatic unless burden is high → chronic intestinal malabsorption / dysentery
  • Rash on butt, legs, and lower back w/ autoinfection
  • Autoinfection + immunosuppression → HYPERINFECTION w/ disseminated larvae / adults → bowel perforation, which can be lethal.
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16
Q

Strongyloides Diagnosis (5)

A
  • Gram stain of sputum is easiest.
  • Wet mount of stool stained w/ iodine to detect larvae. Eggs not found in poop.
  • Fecal smear stained w/ auramine O, showing orange / yellow fluorescence w/ UV light
  • Agar plate culture. Takes 2-3 days.
  • Serology done at CDC
17
Q 
Trichinosis
Name
Location (larvae vs adults)
Transmission
Definitive host
Incidental host
How common?
Diagnosis
Treatment
Prevention
A
  • Trichinella spiralis
  • Location: adults in intestine, larvae in muscle
  • Transmission: raw / undercooked pork / bear meat containing encysted larvae
  • Definitive host: meat eating animals (pigs, bears, walrus)
  • Incidental host: humans (dead end)
  • Rare. Only 20 cases / year in US. Most often associated w/ home-made sausage
  • Diagnosis: Eosinophilia, periorbital edema, myositis, fever; serology after 3 weeks
  • Treatment – If infection 3 weeks) pork
18
Q

Trichinosis Life Cycle

A
  • Eat undercooked meat w/ encysted larvae
  • Adults mate in small intestine. Female embeds in mucosa. Larvae are live-birthed (no eggs) and enter lymphatics / blood. Encyst in muscle.
  • Larvae develop into an encapsulate spiral, which is viable for 10 years.
19
Q

Trichinosis Pathology

A
  • Pathology – severity is related to number of cysts
  • Mild pathology from adult worms: nausea / cramps
  • Localized inflammation occurs around cysts
  • Degeneration of muscle cell architecture.
  • Severe sxs – fever, muscle pain, weakness, conjunctivitis, cardiac / neural dysfunction
20
Q 
Toxocariasis
Name
Location (adults vs larvae)
Definitive host
Incidental host
Transmission
Immunity
Treatment
Prevention
A
  • Toxocara canis / cati
  • CDC top 5
  • Location – adult worms free in upper intestine of dogs. Larvae found in any tissue in humans.
  • Definitive host: dogs (most dogs are infected unless dewormed)
  • Incidental host: humans
  • Transmission: ingestion of embryonated eggs in soil. No person to person. Most commonly transmitted by puppies and acquired by kids. More common in warmer climates. NDP.
  • Immunity – asthma and immune hypersensitivity
  • Treatment – Only treat severe cases. Short course of albendazole or mebendazole. Corticosteroids for sxs.
  • Prevention – disposal of dog waste and deworm dogs.
21
Q

Toxocara Life Cycle

A
  • Dogs: Sexual cycle produces eggs in feces.
  • Humans infected by ingestion of eggs in soil from dogs. Larvae burrow through intestine and wander for months in any tissue in humans. Does not progress to adults.
22
Q

Toxocara Pathology

A
  • Light infection: self limited
  • Heavy worm loads → severe necrosis of any tissue, especially in kids
  • Visceral larva migrans: enlarged liver, pulmonary complications, ocular lesions (may cause blindness), neuro sxs
23
Q

Toxocara Diagnosis

A
  • History of geophagia (eating dirt) or exposure to dogs
  • ELISA for larval Ags, but can cross w/ Ascaris
  • No eggs in stool b/c infection does not progress to adults in humans

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

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