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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
Parascaris equorum - life cycle
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
Parascaris equorum diagnosis
- 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
Parascaris equorum - treatment and control
- some approved anthelmintics: fenbendazole, pyrantel tartate and pamoate - resistance control - eggs extremely resistant - strict sanitation - facility specific
28
Toxascaris leonina - hosts
DH: canids, felids, wild canids PH: rodents
29
Toxascaris leonina - life cycle
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
Toxascaris leonina - pathogenesis
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
Toxascaris leonina - clinical signs
Mixed infections - unthriftiness - potbellied appearance - diarrhea
32
Toxascaris leonina - diagnosis
- fecal float: eggs, smooth shell, more space | - adults: cervical alae on anterior end, feces, vomitus, necropsy
33
Toxocara cati life cycle
- 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
Toxocara cati - pathogenesis
- mechanical damage to SI - interference with nutrition - obstruction of SI
35
Toxocara cati - clinical signs
Often asymptomatic (even in kittens) - pot bellied appearance - failure to thrive
36
Toxocara cati - diagnosis
Adults - feces - vomitus - necropsy
37
Toxocara canis - life cycle
- 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
Toxocara canis - pathogenesis
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
Toxocara canis - diagnosis
- fecal float: eggs | - adults: cervical alae
40
Toxocara vs Toxascaris eggs
Toxascaris leonina: smooth surface, empty space within egg
41
Ascarids in dogs and cats - prevalence
- 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
_________ and ________ contribute to high prevalence even in well cared for pets
Transplacental transmission of Toxocara canis and hardy larvated eggs
43
Baylisascaris procyonis
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
Baylisascaris procyonis - life cycle
- raccoons ingest embryonated eggs or PH - humnas accidental hosts (ingest eggs) - VLM and OLM in humans - dogs: alternate DH
45
Why is B. procyonis a concern?
Raccoon latrines - children playing - dogs act as DH (shed eggs) - can spread near people
46
Toxocariasis
Parasitic disease caused by migrating larvae of 2 species of Toxocara roundworms - T. canis from dogs, and T. cati from cats
47
What are 2 major forms of toxocariasis?
- visceral toxocariasis | - ocular toxocariasis
48
Larva migrans
Migration of helminth larvae through tissue in suboptimal hosts
49
VLM
- preschool children | - organs invaded: hypersensitivity rxn, damage to organ
50
Neural larva migrans
Some enter CNS and rest migrate to body
51
OLM
Older children and young adults - opthalmologic lesions - larvae die --> granuloma - unilateral - partial/permanent blindness
52
Baylisascaris pathology
DH: no significant lesions | - other hosts: mechanical damage to tissues, granulomas, lung damage, CNS lesions, inflammation, hemorrhage, necrosis
53
Baylisascaris prevalence
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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