Zoonotic Nematodes Flashcards

1
Q

What is the species causing Baylisascariasis? What animal is the major definitive host?

A

Baylisascaris procyonis
Racoons

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2
Q

What syndromes can be caused in Baylisascariasis?

A
  1. Visceral larva migrans
  2. Ocular larva migrans
  3. Neural larva migrans
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3
Q

What species cause toxocariasis? What is the definitive host?

A
  • Toxocara canis - dogs
  • Toxocara cati - cats
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4
Q

Describe the lifecycle of toxocariasis

A
  1. Toxocara spp. can follow a direct (one host) or indirect (multiple host) life cycle. Unembryonated eggs are shed in the feces of the definitive host (canids: T. canis; felids: T. cati).
  2. Eggs embryonate over a period of 1 to 4 weeks in the environment and become infective, containing third-stage (L3) larvae.
  3. Infective eggs containing L3 larvae are ingested by a definitive host
  4. The infective eggs hatch and larvae penetrate the gut wall. In younger dogs (T. canis) and in cats (T. cati), the larvae migrate through the lungs, bronchial tree, and esophagus, where they are coughed up swallowed into the gastrointestinal tract; adult worms develop and oviposit in the small intestine. In older dogs, patent (egg-producing) infections can also occur, but larvae more commonly become arrested in tissues.
  5. Arrested larvae are reactivated in female dogs during late gestation and may infect pups by the transplacental (major) and transmammary (minor) routes
  6. In the small intestine adult worms become established. In cats, T. cati larvae can be transmitted via the transmammary route to kittens if the dam is infected during gestation, but somatic larval arrest and reactivation does not appear to be important as in T. canis.
  7. Toxocara spp. can also be transmitted indirectly through ingestion of paratenic hosts. Eggs ingested by suitable paratenic hosts hatch and larvae penetrate the gut wall and migrate into various tissues where they encyst.
  8. The life cycle is completed when definitive hosts consume larvae within paratenic host tissue, and the larvae develop into adult worms in the small intestine.
  9. Humans are accidental hosts who become infected by ingesting infective eggs
  10. Or undercooked meat/viscera of infected paratenic hosts .
  11. After ingestion, the eggs hatch and larvae penetrate the intestinal wall and are carried by the circulation to a variety of tissues (liver, heart, lungs, brain, muscle, eyes) . While the larvae do not undergo any further development in these sites, they can cause local reactions and mechanical damage that causes clinical toxocariasis.
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5
Q

Can toxocariasis be diagnosed through eggs in stool?

A

No - humans are not the definitive host and eggs are not produced

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6
Q

What type of host are humans in the toxocara lifecyle?

A

Accidental hosts

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7
Q

Describe the egg of T. canis

A
  • Toxocara eggs are golden in color
  • Spherical to slightly pear shaped
  • Thick-shelled, and have a pitted surface.
  • The size range for different species varies slightly; T. canis is slightly larger (80—85 µm) than T. cati (65—75 µm).
  • Toxocara sp. eggs are extremely hardy and can persist in the environment for years.
  • Eggs are not clinically diagnostic for human cases as humans are incapable of harboring adult worms that pass eggs.
  • Humans are paratenic hosts for Toxocara spp. and eggs are found only in the feces of definitive hosts (cats and dogs).
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8
Q

What are the clinical presentations of human toxocariasis?

A
  • Covert toxocariasis - asymptomatic or mild, transient symptoms
  • Visceral toxocariasis - most commonly in liver, lungs, CNS
  • Ocular toxocariasis - in posterior segment of eye
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9
Q

How is toxocariasis treated?

A
  • Covert - no tx required
  • Visceral - Albendazole x5 days
  • Ocular - steroids to control inflammation. Anti-helminthic drugs no consistent benefit shown
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10
Q

Describe T. canis adult worms

A
  • Adult Toxocara spp. measure approximately 4—6 cm long (males) and 6—10 cm long (females).
  • Like all ascarids, Toxocara have three “lips” on the anterior end of the worm.
  • They also possess large, spear-shaped cervical alae, which are broader in T. cati than T. canis..
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11
Q

Describe T. canis larvae

A
  • Toxocara spp. develop to third stage (L3) larvae in ovo.
  • When hatched, L3 larvae are about 350—400 µm long and about 15—20 µm in maximum width,
  • They have a straight esophagus extending about a third of the body length.
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12
Q

What is the most common infectious cause of eosinophilic meningitis?

A

Angiostrongylus cantonensis

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13
Q

Describe the lifecycle of A. cantonensis

A
  1. Adult worms of A. cantonensis live in the pulmonary arteries and right ventricle of the normal definitive host.
  2. The females lay eggs that hatch in the terminal branches of the pulmonary arteries, yielding first-stage larvae. The first-stage larvae migrate to the pharynx, are swallowed, and passed in the feces. They penetrate or are ingested by a gastropod intermediate host.
  3. After two molts, third-stage larvae are produced
  4. 3rd stage larvae are infective to mammalian hosts. When the infected gastropod is ingested by the definitive host, the third-stage larvae migrate to the brain where they develop into young adults . The young adults return to the venous system and then the pulmonary arteries where they become sexually mature. Of note, various animals act as paratenic (transport) hosts: after ingesting the infected snails, they carry the third-stage larvae which can resume their development when the paratenic host is ingested by a definitive host.
  5. Humans can acquire the infection by eating raw or undercooked snails or slugs infected with the parasite; they may also acquire the infection by eating raw produce that contains a small snail or slug, or part of one. There is some question whether or not larvae can exit the infected gastropods in slime (which may be infective to humans if ingested, for example, on produce). Infection may also be acquired by ingestion of invertebrate paratenic hosts containing L3 larvae (e.g. crabs, freshwater shrimp).
  6. In humans, larvae migrate to the brain, or rarely to the lungs, where the worms ultimately die. Larvae may develop to fourth or fifth stage in the human host, but seem to be incapable of maturing fully.
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14
Q

What is the treatment for A. cantonensis infection?

A

Supportive
Larvae die on their own

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15
Q

Describe the lifecycle of Trichinella spiralis

A
  1. Trichinellosis is caused by the ingestion of undercooked meat containing encysted larvae of Trichinella species
  2. After exposure to gastric acid and pepsin, the larvae are released from the cysts
  3. Larvae invade the small bowel mucosa where they develop into adult worms
  4. Females are 2.2 mm in length; males 1.2 mm. The life span in the small bowel is about four weeks. After 1 week, the females release larvae
  5. Larvae migrate to striated muscles where they encyst
  6. Diagnosis is usually made based on clinical symptoms, and is confirmed by serology or identification of encysted or non-encysted larvae in biopsy or autopsy specimens.
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16
Q

How is trichinellosis diagnosed?

A
  • Serology by EIA
  • On observation of the larvae in muscle tissue following biopsies or autopsies
17
Q

What is the treatment for trichinellosis

A

Albendazole 1-2 weeks or Mebendazole

18
Q

What species causes dracunculiasis?

A

Dracunculus medinensis

19
Q

Describe the lifecycle of D. medinensis

A
  1. Humans become infected by drinking unfiltered water containing copepods (small crustaceans) which are infected with larvae of D. medinensis.
  2. Following ingestion, the copepods die and release the larvae, which penetrate the host stomach and intestinal wall and enter the abdominal cavity and retroperitoneal space.
  3. After maturation into adults and copulation, the male worms die and the females (length: 70 to 120 cm) migrate in the subcutaneous tissues towards the skin surface
  4. Approximately one year after infection, the female worm induces a blister on the skin, generally on the distal lower extremity, which ruptures. When this lesion comes into contact with water, a contact that the patient seeks to relieve the local discomfort, the female worm emerges and releases larvae.
  5. The larvae are ingested by a copepod
  6. After two weeks (and two molts) larvae have developed into infective larvae. Ingestion of the copepods closes the cycle.
20
Q

What is the vector for guinea worm disease?

A

Cyclops copepod (water flea)

21
Q

Where is guinea worm infection still endemic?

A

Few countries across West, Central, and East Africa
* Angola
* Chad
* Ethiopia
* Mali
* South Sudan
* Central African Republic

22
Q

What are some of the common complications for D. medinensis infection?

A
  • Pain
  • Blistering at site of worm emerging
  • Secondary bacterial infection
  • Tetanus status should be up to date
  • Loss of schooling and economic productivity
23
Q

What is the treatment for D. medinensis infection?

A
  • Anti-helminthic drugs are of marginal benefit
  • If the uterus has emerged, discharge the larvae by immersion in water and dispose of water hygienically
  • Traditional method is to tie the end of the emerging worm to a small stick and wind the worm out slowly over many days, taking care not to rupture the worm as this can cause severe allergic responses
24
Q

How is D. medinensis diagnosed?

A

Clinically through blister at site in an endemic area and visualization of worm and larvae emerging after being immersed in water