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Nematodes > Cats and dogs > Flashcards

Cats and dogs Flashcards

1
Q

What is the superfamily of toxocara canis?

A

Acaridoidea

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2
Q

What is the life cycle of toxocara canis? How does this differ in young and old dogs?

A

Unembryonated eggs are excreted in the dogs faeces.
L1-L3 in the eggs, in the environment. They can remain like this for several years.
Host ingests embryonated eggs -> hatch in SI -> L3 perforates the walls.
Young dogs: L3 undergoes hepatic-tracheal migration. L4 returns to the intestine to develop into adults.
Older dogs: Larval encystment in tissues (somatic migration and hypobiosis)

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3
Q

When are encysted stages of larvae reactivated in female dogs?

A

Late pregnancy.

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4
Q

How can toxocara canis be transmitted?

A

Ingestion of eggs - followed by hepatic-tracheal migration, or somatic migration to the liver, lung, brain, heart, muscle and gut. Here it hypobioses.

Ingestion of L3 in paratenic host. No migration is ingested by this route.

Transplacental - larvae is mobilised 3 weeks prior to parturition and migrates to the lungs of the foetus as the life cycle is completed.

Transmammary - L3 is ingested in the first 3 weeks of lactation. There is no migration via this route.

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5
Q

What is the pre-patent period of toxocara canis if L3 has been ingested?

A

4-5 weeks

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6
Q

What is the pre-patent period of toxocara canis if infection is transplacental?

A

3 weeks

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7
Q

How can a male toxocara canis worm be differentiated from a female?

A

Male: 10cm
Female: 18cm

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8
Q

What are the features of the adult toxocara canis?

A

3 large lips.
No buccal capsule.
Cervical and caudal alae

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9
Q

What is the pathology of toxocara canis?

A

Heavy infection -> migrating larvae can cause pneumonia and pulmonary oedema in puppies.

Adult worms in intestine -> mucoid enteritis. If severe, it can occlude the gut.

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10
Q

What are the clinical signs of toxocara canis?

A

Coughing
Dyspnoea
Nasal discharge - heavy infections. Most common cause of mortality.
Pot bellied appearance.
Vomiting worms or passing worms in faeces.
Diarrhoea/constipation.

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11
Q

What is the epidemiology of toxocara canis?

A

5-80% infection rates.
Highest in <6 months.
Females highly fecund.
Eggs survive for years in the environment.
Constant reservoir in somatic tissues of the bitch.

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12
Q

What is the zoonotic importance of toxocara canis?

A

Geophagia - 10% of soil samples are positive. Here it can be picked up by children.
Can be found in the meat and liver if consumed and contaminated.

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13
Q

How is toxocara canis diagnosed?

A

Clinical signs.
Simultaneous pneumonia in the litter.
Eggs in faeces.
Worms in faeces.

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14
Q

How is toxocara canis controlled?

A

No drugs are fully effective at removing encysted larvae.

Anthelmintics during pregnancy: every day for 3 weeks pre-partum to 2 days post-partum.

Anthelmintics to pups: 2 weeks, 4 weeks, 1 month.

Anthelmintics to adults: 3-6 months.

Environmental: safe disposal of dog poo.

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15
Q

What is the superfamily of toxocara cati?

A

Ascaroidea

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16
Q

What is the life cycle of toxocara cati?

A

Unembryonated eggs are excreted in the dogs faeces.
L1-L3 in the eggs, in the environment. They can remain like this for several years.
Host ingests embryonated eggs -> hatch in SI -> L3 perforates the walls.
No migration with this species
Older cats: Larval encystment in tissues (somatic migration and hypobiosis)

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17
Q

How does transmission of toxocara cati differ from toxocara canis?

A

No transplacental transmission. Main infection is transmammary or from paratenic hosts.

No migration so clinical signs are usually in the GI

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18
Q

What is the superfamily of toxocaris leonina?

A

Ascaroidea

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19
Q

How is toxocaris leonina transmitted?

A

Ingestion of eggs or paratenic host.
No migratory phase.
Less pathogenic.
No transplacental or transmammary transmission.

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20
Q

What is the pre-patent period of toxocaris leonina?

A

10 weeks.

Usually seen in pups from 2 months.

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21
Q

What is the superfamily of ancyclostoma caninum?

A

Ancyclostomatoidea

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22
Q

What is the life cycle of ancyclostoma caninum?

A

Eggs in faeces hatch and moult to L3.
L3 penetrates the skin and is carried by the blood to the heart and the lungs.
Moults to L4 in the bronchi.
A proportion also migrates to muscles where they lay dormant until pregnancy, when reactivated, they are passed in the milk for the first 3 weeks post-partum.
L4 is swallowed to the SI, moults to L5 and lays eggs.
Adults are blood feeders.

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23
Q

What is the pre-patent period of ancyclostoma caninum?

A

14-21 days

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24
Q

What are the clinical signs of ancyclostoma caninum?

A

Anaemia
Respiratory signs
Skin lesions
Protein losing diarrhoea

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25
Q

How is ancyclostoma caninum diagnosed?

A

Clinical signs.
Strongylate-like eggs in faeces.
Larval culture to differentiate from other species.

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26
Q

What is the ley term for ancyclostoma caninum?

A

Hook worm

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27
Q

How can ancyclostoma caninum be controlled?

A

Anthelmintic for encysted larvae.
Pedal dermatitis - responds poorly to treatment, but gradually subsides.

Anthelmintics during pregnancy - every day from 3 weeks pre-partum to 2 days post-partum.
Anthelmintics to pups 2 weeks, then 4 weeks then, 1 month.
Anthelmintics to adults every 3-6 months

28
Q

What is the ley term for uncinaria stenocephala?

A

Northern Hookworm

29
Q

What is the super family of uncinaria stenocephala?

A

Ancyclostomatoidea

30
Q

What is the life cycle of uncinaria stenocephala?

A

Infection by L3 orally or paratenic hosts.
Although L3 can penetrate through the skin, it rarely matures.
No evidence of transmammary transmission

31
Q

What diseases can be caused by uncinaria stenocephala?

A

Pedal dermatitis -> hypersensitivity reaction due to a previous exposure.
Rarely causes anaemia or diarrhoea.

32
Q

What is the superfamily of trichuris vulpis?

A

Trichuroidea

33
Q

What is the infective stage of trichuris vulpis?

A

L1 in the egg

34
Q

What is the life cycle of trichuris vulpis?

A

Hatches in GI tract.
L1 penetrates mucosal gland of large intestine.
All 4 moults to adult occur in these glands. Adults emerge with their anterior ends embedded in the intestine.

35
Q

What disease can be caused by a heavy infection of trichuris vulpis?

A

Colitis

36
Q

What is the shape of a trichuris vulpis egg?

A

Lemon

37
Q

What is the superfamily of angiostrongylus vasorum?

A

Metastrongyloidea

38
Q

What is the life cycle of angiostrongylus vasorum?

A

Direct host ingested an infected intermediate host.
L3 penetrates intestinal wall and migrates to the abdominal lymph nodes where they moult to L5.
L5 migrates through lymphatics to portal and hepatic veins and reach the RV and pulmonary arteries. Here they develop into adult worms.
Female worms produce eggs that are carried to the lung capillaries for embryonation.
L1 larvae penetrate the bronchial walls and alveoli, which are coughed up and swallowed.
L1 larvae are excreted into the faeces and can survive a few days before being ingested by the intermediate host for L1-L3 development.

39
Q

What is the intermediate host of angiostrongylus vasorum?

A

Slugs and snails

40
Q

What is the pre-patent period of angiostrongylus vasorum?

A

7 days

41
Q

How long can adult angiostrongylus vasorum live in the dog for?

A

<2 years

42
Q

What are the physical features that distinguish angiostrongylus vasorum?

A

Small red worms in pulmonary arteries.
<2.5cm
Female white ovaries coil around red intestine.
L1 passed in faeces are 330-360um, with cephalic button and wavy tail, with subterminal notch.

43
Q

What is the pathogenesis of angiostrongylus vasorum?

A

Usually chronic.
Associated with adults in heart
Eggs and L1 in pulmonary arteries and alveoli.
Vessel blockage can result in congestive heart failure

44
Q

What are the acute and chronic clinical signs of angiostrongylus vasorum?

A

Acute: tachycardia, tachypnoea, heavy cough, blood in sputum.

Chronic: syncope, swellings due to reduced clotting, CNS haemorrhage due to clotting disorders, reduced appetite, anaemia, ascites, death due to heart failure.

45
Q

How can angiostrongylus vasorum be diagnosed?

A

Radiography, clinical signs, history is helpful but not diagnostic.
L1 in faeces or bronchoalveolar lavage.
Circulating antigen, DNA or specific antibodies.

46
Q

How can angiostrongylus vasorum be controlled?

A

Anthelmintic treatment.

Control is often impractical because the intermediate host is widespread.

47
Q

What is the super family of aelurostrongylus abstrusus?

A

Metastrongyloidea

48
Q

What is the intermediate host of aelurostrongylus abstrusus?

A

Slugs and snails.

49
Q

What is the paratenic hosts of aelurostrongylus abstrusus?

A

Birds, rodents, frogs

50
Q

What is the direct host of aelurostrongylus abstrusus?

A

Cat

51
Q

What is the lifecycle of aelurostrongylus abstrusus?

A

L1-L3 in the intermediate host.
Cat ingests paratenic host or L3 in the environment.
L3 penetrates the walls of the small intestine and migrates through the lymphatics/blood to the lungs.
Develops to adults in the alveolar ducts and terminal bronchioles.
L1 are coughed up, swallowed and excreted in faeces.

52
Q

What is the pre-patent period for aelurostrongylus abstrusus?

A

4-6 weeks

53
Q

What are the clinical signs of aelurostrongylus abstrusus?

A

Mild chronic cough

54
Q

How can aelurostrongylus abstrusus be treated?

A

Anthelmintics

55
Q

What is the super family of oslerus osleri?

A

Metastrongyloidea

56
Q

What is the life cycle of oslerus osleri?

A

L1 is ingested and moults to L2 in the intestine.
Migrates to the lungs to complete development,.
Adults in nodules in the tracheal bifurcation, females lay eggs which hatch to L1 and are coughed up and swallowed.
Passed into faeces or transferred to the pup by licking.

57
Q

What are the clinical signs of osleus osleri?

A

Dry cough

Weight loss - peaks at 6-12 months

58
Q

How can osleus osleri be diagnosed?

A

L1 in sputum or faeces.

59
Q

What is the ley term for dirofilaria immitus?

A

Heart worms

60
Q

What is the superfamily of dirofilaria immitus?

A

Filaroidea

61
Q

What is the life cycle of dirofilaria immitus?

A

Females release L1 (microfilarie) into the blood where they are ingested by feeding mosquitos.
Moults to L3 in mosquitos and transmitted to new host when feeding.
L3-L5 in skin/fat/muscle.
L5 migrates to the heart where they become adults.

62
Q

What is the pre-patent period of dirofilaria immitus?

A

6 months

63
Q

What disease is caused by dilofilaria immitus?

A

Right-sided heart failure.

Caval syndrome, if the vena cava is compromised.

64
Q

How can dilofilaria immitus be diagnosed?

A

Clinical signs.
Microfilarie in blood
ELISA, PCR

65
Q

What is the superfamily of thelazia callipaeda?

A

Spiruroidea

66
Q

What is the life cycle of thelazia callipaeda?

A

Adults reside in the conjunctival sac of the direct host and sheds L1 larvae.
L1 is ingested by the intermediate host when they feed on lacrimal secretions.
L1-L3 in IH.
L3 migrates to the flies mouthparts where they remain until the fly feeds on the tears of the DH.
L3 invades the conjunctival sac and becomes adults after about a month and 2 additional moults.

Nematodes (6 decks)

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