11 - Parasitology: Nematodes Flashcards

1
Q

Describe some characteristics of the phylum Nematoda? Is their body segmented? What is the structure of their body cavity? What is it’s digestive system like?

A

Free-living parasites: ingestive and invasive.

Mostly dioecius round worms with unsegmented body.

Cavity filled with pressurized fluid; epidermis covered with tough elastic cuticle; development requires molting. Hydroskeleton for locomotion.

Complete digestive system.

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2
Q

What are the important round worm parasites in humans?

A
  1. Enterobius vermicularis
  2. Trichuris trichiura
  3. Ascaris lumbricoides
  4. Necator americanus
  5. Strongyloides stercoralis
  6. Trichinella spiralis
  7. Toxocara canis
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3
Q

What is the life cycle of enterobius vermicularis (pinworm)?

A

Eggs on perianal folds with larvae inside the eggs mature in 4-6 hrs.

Embryonated eggs ingested by humans and larva hatch in small intestines.

Adults in lumen of cecum and migrate to perianal region at night to lay eggs.

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4
Q

What is the appearance of enterobius vermicularis adult worms and eggs?

A

Adult worms can be 2-13 mm.

Up to 20000 eggs/females in perianal folds.

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5
Q

How is enterobius vermicularis transmitted? What is the epidemiology?

A

Ingestion of eggs, inhalation of egg-laden dust (eggs can survive indoors 2-3 weeks); autoinfection.

Occurs world-wide, common in temperate redions. Spread in crowded conditions such as daycares and schools.

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6
Q

What is the pathology associated with enterobius vermicularis?

A

Enterobiasis: intense perianal itching, secondary infections due to scratching.

Rare urogenital problems in females due to worm migration into vagina.

Psychological trauma.

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7
Q

How do you treat and prevent Enterobiasis from enterocius vermicularis?

A

Albendazole, mebendazole, pyrental pamoate.

Whole family repeated treatment to stop reinfection. Good personal hygiene, thorough house cleaning.

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8
Q

What is the life cycle of Trichuris trichiura (whipworm)?

A

Unembryonated eggs in feces.

Obligatory 2-cell stagef in soil.

Advanced cleavage. Embryonated eggs ingested and larva hatch in sm. intestine.

Adults in cecum.
(humans are only host).

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9
Q

What is the size and shape of the adult worms and eggs of trichuris trichiura?

A

Adult worm: 3-5 cm with skinny anterior portion.

3000,10000 eggs/day per female. Bile-stained eggs that are oval in shape with a blob on each end; ~50 microM.

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10
Q

What is the transmission and epidemiology of trichuris trichiura?

A

Ingestion of embryonated egggs; no direct person to person (soil stage!).

Worldwide: common in tropical regions (third most common worm infection). Use of human waste as fertilizer.

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11
Q

What is the pathology caused by Trichuris Trichiura?

A

Trichuriasis (depends on worm burden).

Low to moderate: usually none. Some bleeding and secondary bacterial infection. Anterior end of worm penetrates deep into intestinal mucosa.

High: disrupted mucosa; bloody stool, abd. pain, apandicitis. Anemia in kids. Impaired growth and cog development.

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12
Q

What is the immunity associated with Trichuriasis from Trichuris Trichiura? What is the treatment?

A

Some evidence for acquired immunity in natural infections.

3 days of albendazole, mebendazole, ivermecton; iron supplementation.

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13
Q

What is the life cycle of Ascaris lumbricoides (round worm)?

A

Fertilized egg from feces goes through obligatory soil stage.

Ingested by humans (only host) and migrates to the lungs to be coughed up and then swallowed and then grows in small intestine.

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14
Q

What is the structure and size of adult worms and eggs of Ascaris lumbricoides?

A

Fertilized egg is 45-75 microM and round. Unfertilized is oval.

Adult worm is long and round and boring.

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15
Q

What is the transmission and epidemiology of Ascaris Lumbricoides?

A

Ingestion of embryonated eggs; no person to person contact (soil stage)

Worldwide; tropical and subtropical regions. (most common worm infection)

Considered a US neglected disease of poverty.

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16
Q

What is the pathology of Ascaris lumbricoides (low and high)?

A

Called Ascariasis

Low: usually non; worms do NOT attach to intesine mucosa but adult may migrate into bile duct and liver.

High: abd. tenderness, obstruction, growth impairment in children. Stressed worms may migrate to nose or peritoneum through body wall.

17
Q

What is the immunity and diagnosis of ascaris lumbricoides? What about the treatment?

A

Immunity: inflammation from larva migration in lung, pneumonitis and eosinophilia.

Diagnosis: Bile-stained fertilized and unfertilized eggs in stool. (in pulm phase there’s eosinophilia in sputum).

Treatment: 1-3 days of albendazole, mebendazole, ivermectin.

18
Q

What is the life cycle of Necator Americanus and Ancyclostoma duodenale (hookworms)?

A

Eggs in feces and Rhabditiform larva hatches.

Obligatory soil stage occurs and forms a filariform larva which can penetrate the skin (ie the foot).

Migrates to small intestine.

19
Q

What are the life stages of the hookworm?

A

Filariform larva is the infective form.

Anterior end of adult has chewing abilities (teeth) that chew into the wall of the intestine and suck blood out of the patient.

20
Q

What is the epidemiology of hookworms? What is the pathology?

A

Worldwide; tropical conditions. Poor public sanitation; children and farmers without shoes.

Rash and itching near penetration. Microcytic anemia due to significant blood loss. Eosinophilic enteritis with abd. pain.

Severe: mental and physical retardation.

21
Q

What is the drug only used on flatworms? (not nematodes)

A

Praziquantal.

Inhibits their purine synthesis.

22
Q

How are hookworms diagnosed and treated? What are some ways to prevent them?

A

Eggs in (concentrated) stool, larva for species differentiation; anemia.

1-3 days albendazole, mebendazole, pyrantal pamoate; iron supplements/blood transfusion.

Public hygeine; wearing shoes, avoiding skin contact with contaminated soil.

23
Q

What are the three developmental options for Rhabditiform larvae or Strongyloides stercoralis?

A
  1. Direct: hookwork-like except larvae in feces; no amplification
  2. Indirect: sexual repro in soil, environmental amplification
  3. Autoinfection: matrucation in host, penetration of colonic mucosa or perianal skin. Host amplification.
24
Q

What is the transmission and epidemiology of Strongyloides stercoralis?

A

Penetration of the skin by filaform larvae; autoinfection possible.

Globally in tropical regions and warm temperate zones. Caused by poor public sanitation, often associated with agriculture. Domestic pets are reservoir hosts.

25
Q

What is the pathology of Strongyloides stercoralis? Where does a rash generally occur with autoinfection?
What can autoinfection lead to?

A

Strongyloidiasis

Pulm symptoms as in ascariasis and hookworm infections. Heavy worm load leads to dysentary, malabsorption, epigastric pain.

Rash on buttocks, legs, lower back due to autoinfection.

Autoinfection and immunosupression leads to hyperinfection and can eventually grow in all organs. (mortality ~85%).

26
Q

What is the immunity of Strongyloides stercoralis? How would you diagnose?

A

Inflammation from larval migration in lung causing pneumonitis.

Larvae in concentrated stool or sputum. Larval culture of fecal samples.

27
Q

What is the life cycle of Trichinella spiralis?

A

Ingestion of undercooked meats.

Adult worms and encysted larvae develop in a single vertebrate host.

Infected animals serve as definitive and potential int. host (can be pigs or bears).

Second host is needed to complete life cycle. Humans are dead end hosts.

28
Q

What is the structure of Trichinella spiralis? What do the females release?

A

Scale of mms.

Female releases about 1500 live larvae (no eggs) in about 4 weeks of life in the intestine.

Curly-looking larvae.

29
Q

What is the transmission and epidemiology of Trichinella spiralis? What is an example of a hosts?

A

Eating raw and undercooked meat (pork, wild game) containing cysts.

Strong association with pork consumption. Wide range of hosts: rodents.

30
Q

What is the pathology of Trichinella spiralis?

A

Trichinellosis, Trichinosis.

Mild infection is asymptomatic, flu-like.

More extensive: persistent fever, GI distress, muscle pain and weakness, periorbital edema, splinter hemorrhage beneath nails.

Heavy: muscle destruction (diaphragm), myocarditis, pneumonitis, death.

31
Q

What immunity is associated with Trichinella spiralis? How would it be diagnosed?

A

Humoral immune response, eosinophilia.

Myositis, fever, periorbital edema, eosinophilia. Muscle biopsy.

32
Q

What is the life cycle of toxocara canis (cati)?

A

Eggs passed in feces from dogs. Dogs take it up again to close the life cycle.

Other animals can take up embryonated eggs, which humans can get from meat with cysts.

Humans can also get cysts from bunnies.

Migrates all over the body - commonly in the eye and in the brain.

33
Q

How is toxocaris canis transmitted and what’s the epidemiology?

A

Ingestion of embryonate eggs; no person to person (soil stage).

Worldwide: 30%-100% of puppies infected. Common in warm climates because eggs develop in soil.

Commonly transmitted to puppies and children.

34
Q

What is the pathology of

toxocaris canis?

A

Toxocariasis.

Light infections often asymptomatic. Heavier ones lead to lead to severe damage in any location due to neural larva migrans.

Fever, enlarged liver, pulmonary symptoms, ocular disease, seizure, death.

35
Q

What is the immunity of toxocaris canis? How it is diagnosed?

A

Immune hypersensitivity common, eosinophilic granulomas.

Signs of ocular toxocariasis: eosiniphilia

Serology for larval antigens.

Habit of eating dirt, exposure to dogs Exposure to dogs.

36
Q

How is toxocaris canis treated?

A

albendazole, mebendazole; symptoms with steroids.