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Parasitology > Ascarids > Flashcards

Ascarids Flashcards

1
Q

Ascarid classification

A

Phylum: Nematoda
Order: Ascaridia
Family: Ascarididae

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2
Q

Which ascarids affect poultry?

A
  • Ascaridia galli

- Heterakis gallinarum

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3
Q

Which ascarid affects swine?

A

Ascaris suum

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4
Q

Which ascarid affects equids?

A

Parascaris equorum

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5
Q

Which ascarids affect cats and dogs?

A
  • Toxascaris leonina
  • Toxocara cati
  • Toxocara canis
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6
Q

Which ascarid affects raccoons and dogs?

A

Baylisascaris procyonis

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7
Q

Ascaridia galli - hosts

A

DH: birds in Galliforme order, ducks, waterfowl
PH: earthworm

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8
Q

Ascaridia galli - clinical signs

A
  • anorexia
  • unthriftiness
  • diarrhea
  • dull plumage
  • decreased egg production
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9
Q

Heterakis gallinarum - hosts

A

DH: birds in order Galliforme, ducks, geese, swan, waterfowl
PH: earthworm

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10
Q

Heterakis gallinarum - clinical signs

A

Usually asymptomatic

- thickening, inflammation, nodules in cecum

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11
Q

Signs due to Histomonas meleagridis

A

High pathology, most important in turkeys

  • cyanosis (blackhead)
  • histomoniasis
  • death 1 week post onset of signs
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12
Q

Ascaridia galli - life cycle

A

PH ingests L3 in egg –> DH ingests PH –> L3 released –> L3 enter SI –> L3 transient mucosal migration –> L4 emerges in SI –> adults in lumen of SI –> eggs in feces –> L1, L2, L3 in egg

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13
Q

Heterakis gallinarum - life cycle

A

DH ingests L2 in egg –> PH ingests L2 in egg –> DH ingests PH –> L2 released –> L2 hatch in gizzard, duodenum –> L2 enter liver, ceca, transient mucosal migration –> L3, L4, adult in ceca –> eggs in feces –> L1, L2 in egg

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14
Q

Heterakis gallinarum pathogenesis

A

Pale circular lesions in liver

  • typhlitis: mucosal thickening, cecal hemorrhage
  • vector of Histomonas meleagridis, multiply in nematode intestinal cells, ovaries, end up in egg –> nematode egg ingested by young bird, eggs hatch in SI and release protozoa in ceca
  • most pathogenic in turkeys*
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15
Q

Ascaridia galli and Heterakis gallinarum - diagnosis

A

Fecal float-eggs

Adults: largest nematodes in birds, may eliminate in feces, may see on necropsy

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16
Q

Ascaridia galli management

A
  • sanitation
  • break life cycle
  • ensure feed and water are not contaminated
  • treat range soil
  • avoid raising different species or different ages of birds together or in close proximity
  • older chickens possibly resistant
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17
Q

Heterakis gallinarum - treatment

A

Mebendazole: distributed to flock in food and water

- rear on hardware cloth, no access to earthworms

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18
Q

Ascaris suum - hosts

A

DH: swine
PH: dung beetle, earthworms

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19
Q

Ascaris suum - life cycle

A

Eggs in feces –> L1, L2, L3 in egg –> DH ingests PH (PH ingests L3 in egg) or DH ingests L3 in egg –> egg hatches, releases L3 in SI mucosa –> L3 hepatopulmonary migration (10-15 days) –> L4 in alveoli, bronchi, trachea –> L4 coughed up and swallowed –> L4, adult in SI

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20
Q

Ascaris suum - pathogenesis

A

Liver
- cell destruction, intestinal hepatitis, localized fibrotic areas, rxn to larvae (milk spots)
Lungs
- hemorrhage, bronchitis, edema, pneumonia in young pigs
SI
- catarrhal enteritis, adult worms interfere with nutrition, obstruction or perforation

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21
Q

Ascaris suum - clinical signs

A
  • coughing
  • rapid shallow breathing (thumps)
  • unthriftiness
  • colic
  • weight loss or reduced weight gain
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22
Q

Ascaris suum diagnosis

A
  • fecal float: eggs
  • necropsy: adult stages
  • clinical signs
23
Q

Ascaris suum - treatment and control

A
  • some approved drugs
  • eggs are extremely resistant
  • strict sanitation
  • facility specific
24
Q

Parascaris equorum clinical signs are due to different ______

A

Stages

  • larvae: coughing, bilateral mucopurulent nasal discharge
  • adults: unthriftiness, potbellied appearance, inappetence, decreased weight gain, colic, obstruction, diarrhea
25
Q

Parascaris equorum - life cycle

A

Eggs in feces –> L1, L2, L3 in egg –> DH ingests L3 in egg –> egg hatches, releases L3 –> L3 enters SI mucosa –> L3 hepatopulmonary migration –> L4 in alveoli, bronchi, trachea –> L4 coughed up and swallowed –> L4, adults in SI

26
Q

Parascaris equorum diagnosis

A
  • fecal float: eggs
  • necropsy: adults
  • history: peak prevalence at 4 months of age, decreases 6 months, age dependent resistance, immune response (attacks liver and lung stages)
27
Q

Parascaris equorum - treatment and control

A
  • some approved anthelmintics: fenbendazole, pyrantel tartate and pamoate
  • resistance control
  • eggs extremely resistant
  • strict sanitation
  • facility specific
28
Q

Toxascaris leonina - hosts

A

DH: canids, felids, wild canids
PH: rodents

29
Q

Toxascaris leonina - life cycle

A

Eggs in feces –> L1, L2, L3 in egg –> DH ingests PH or DH ingests L3 in egg –> no somatic migration!! –> L3 enter SI mucosa –> L3, L4 SI mucosa –> L4 adults in SI lumen –> adults in SI
PH: PH ingests L3 in egg –> somatic migration –> disseminate to tissues –> L3 arrest

30
Q

Toxascaris leonina - pathogenesis

A

Toxascariasis

  • no somatic migration so no mammary or transplacental transmission
  • rarely infections are reported in humnas
  • mixed infections are more pathogenic
  • Toxocara spp. more common than Toxascaris leonina
31
Q

Toxascaris leonina - clinical signs

A

Mixed infections

  • unthriftiness
  • potbellied appearance
  • diarrhea
32
Q

Toxascaris leonina - diagnosis

A
  • fecal float: eggs, smooth shell, more space

- adults: cervical alae on anterior end, feces, vomitus, necropsy

33
Q

Toxocara cati life cycle

A
  • DH ingests L3 in egg: migration of larvae
  • DH ingests PH: no migration
  • transmammary: infection only when queen is lactating
  • L3 arrests, reactivates –> mammary glands –> nursing kitten –> ingests L3, enters SI crypts
34
Q

Toxocara cati - pathogenesis

A
  • mechanical damage to SI
  • interference with nutrition
  • obstruction of SI
35
Q

Toxocara cati - clinical signs

A

Often asymptomatic (even in kittens)

  • pot bellied appearance
  • failure to thrive
36
Q

Toxocara cati - diagnosis

A

Adults

  • feces
  • vomitus
  • necropsy
37
Q

Toxocara canis - life cycle

A
  • DH (> 6 months old): ingests L3 in egg, L3 penetrate SI and hatch, L3 hepatopulmonary migration +/- ALD, L4 coughed up and swallowed, L4 and adults in SI
  • PH ingests L3: somatic migration, L3 arrest, reactivated, DH ingest PH
  • L3 ALD, reactivate: mammary glands, pup ingests L3, L4, adults in SI
  • L3 ALD, reactivate: transplacental, fetal liver, neonatal lungs, L3 to stomach, L4, adults in SI
38
Q

Toxocara canis - pathogenesis

A

Transplacental most important

  • age dependent resistance
  • puppies: verminous pneumonia, enteritis, ulcers in SI, occlusion of SI, death with transmammary/placental
  • clinical signs: potbelly, diarrhea, vomiting, unthriftiness
39
Q

Toxocara canis - diagnosis

A
  • fecal float: eggs

- adults: cervical alae

40
Q

Toxocara vs Toxascaris eggs

A

Toxascaris leonina: smooth surface, empty space within egg

41
Q

Ascarids in dogs and cats - prevalence

A
  • Toxocara common worldwide
  • virturally all pups born with T. canis
  • geographic distribution of Toxascaris leonina more focal than Toxocara
  • infection with Toxascaris leonina less frequent
42
Q

_________ and ________ contribute to high prevalence even in well cared for pets

A

Transplacental transmission of Toxocara canis and hardy larvated eggs

43
Q

Baylisascaris procyonis

A

Ascarid of raccoons, occassionally found in dogs

  • midwest, NE west coast, emerging in SE
  • direct transmission: young raccoon ingests egg with L2, hepatopulmonary migration
  • indirect transmission: PH (small mammals, birds), older raccoons ingest PH
44
Q

Baylisascaris procyonis - life cycle

A
  • raccoons ingest embryonated eggs or PH
  • humnas accidental hosts (ingest eggs)
  • VLM and OLM in humans
  • dogs: alternate DH
45
Q

Why is B. procyonis a concern?

A

Raccoon latrines

  • children playing
  • dogs act as DH (shed eggs)
  • can spread near people
46
Q

Toxocariasis

A

Parasitic disease caused by migrating larvae of 2 species of Toxocara roundworms
- T. canis from dogs, and T. cati from cats

47
Q

What are 2 major forms of toxocariasis?

A
  • visceral toxocariasis

- ocular toxocariasis

48
Q

Larva migrans

A

Migration of helminth larvae through tissue in suboptimal hosts

49
Q

VLM

A
  • preschool children

- organs invaded: hypersensitivity rxn, damage to organ

50
Q

Neural larva migrans

A

Some enter CNS and rest migrate to body

51
Q

OLM

A

Older children and young adults

  • opthalmologic lesions
  • larvae die –> granuloma
  • unilateral
  • partial/permanent blindness
52
Q

Baylisascaris pathology

A

DH: no significant lesions

- other hosts: mechanical damage to tissues, granulomas, lung damage, CNS lesions, inflammation, hemorrhage, necrosis

53
Q

Baylisascaris prevalence

A

Occurs in raccoons across US and Canada

  • midwestern, northeastern, western states
  • isolated in Texas, Florida, Appalachia
  • > 90% adult raccoons infected

Parasitology (28 decks)

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