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)
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.
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
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.
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
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
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
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.
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
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
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.
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
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
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.
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.
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
