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Small Animal Final Year > Small Animal respiratory parasites > Flashcards

Small Animal respiratory parasites Flashcards

1
Q

O. osleri is a cause of?

A

(usually chronic) coughing in the dog

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2
Q

A. vasorum is an increasingly common cause of a variety of clinical signs, typically?

A

Respiratory difficulty and cough, but also signs (often neurological) secondary to the development of a coagulopathy

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3
Q

A. abstrusus is a rare cause of?

A

respiratory signs in (usually young) cats.

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4
Q

What is D. Immitis?

A

Dirofilaria immitis, the heartworm or dog heartworm, is a parasitic roundworm that is a type of filarial worm, a small thread-like worm, that causes dirofilariasis. It is spread from host to host through the bites of mosquitoes. The definitive host is the dog, but it can also infect cats, wolves, coyotes, jackals, foxes, and other animals, such as ferrets, bears, seals, sea lions and, under rare circumstances, humans.[1]

Dirofilaria immitis is commonly called the “heartworm”; however, adults often reside in the pulmonary arterial system (lung arteries), as well as the heart, and a major effect on the health for the animal is a manifestation of damage to the lung vessels and tissues.

Occasionally, adult heartworms migrate to the right heart and even the great veins in heavy infestations. Heartworm infection may result in serious disease for the host, with death typically as the result of congestive heart failure.

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5
Q

Name nematodes which have a lung phase but are not lungworms?

A
  • Toxocara cati
  • Toxocara canis
  • Ascaris suum
  • Parascaris equorum

•Usually migration does not cause clinical signs, unless large burdens

–often see in young puppies

–direct and indirect effects

•Seen often in young puppies as worms migrate through lungs

May be difficult to diagnose as signs occur before patent period and so faecal egg counts will be negative

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6
Q

Oultine common ascaris life cycle?

A
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7
Q

Name Primary cardiorespiratory parasites?

A

Most lungworms are from metastrongyloidea superfamily:

Oslerus osleri (Filaroides osleri) Dog

Filaroides spp. Dog

Crenosoma vulpis Dog

Aelustrongylus abstrusus Cat

Angiostrongylus vasorum Dog

Others from trichuroidae:

Capilaria aerophila Dog/Cat

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8
Q

What are the clinical signs of O. osleri?

A
  • Pre-patent period varies between 10-18 weeks
  • Nodules in which worms live appear around 2 months from infection
  • Immune response to adults in trachea and bronchus causes the worm to encapsulate
  • Clinical signs may include chronic cough
  • often dry rasping cough, particularly after exercise
  • more notable in young dogs: 6-12months

Spontaneous pneumothorax has been reported in a single dog

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9
Q

What is the best method of diagnosis for O. osleri?

A

Characteristic nodules (1-1.5cm) can be seen via bronchoscopy particularly at the tracheal bifurcation – most reliable method

–Small nodules contain immature worms

–Large nodules often contain tight coil of adults

–Sampling of tracheal mucus to identify eggs and larvae (characteristically coiled in appearance)

L1 in faeces or BAL fluid (+ eosinophils)

–Faecal L1 counts less reliable – variable shedding

–Requires experienced parasitologist

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10
Q

What is the prevelance of O. osleri?

A

UK distribution been reported on a number of occasions

–Prevalence of 6% in one study

–More prevalent in greyhounds and kennelled dogs

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11
Q

What is the appearance of O. osleri on bronchoscopy?

A
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12
Q

How do we treat Oslerus osleri?

A
  • Can be hard to treat, nodules remain, may even calcify and cough persists
  • Fenbendazole

–Licensed products: Panacur (MSD), Granofen – (Virbac)

–50mg/kg daily for 10 days

–Often need to repeat 4 weeks later

•Check in-contacts

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13
Q

Discuss Filaroid parasites?

A
  • Filaroides hirthi
  • Life cycle same as Oslerus osleri

–O. osleri reclassified as considered pathogenic

–F. hirthi not

•Infection generally asymptomatic

–Originally detected in breeding colonies of beagles

–Was considered ubiquitous and few dogs showed clinical signs

  • Worms live in alveoli
  • Diagnosis usually found at PM

–Radiographs often show diffuse broncho-interstitial patterns

–Rarely alveolar pattern

•Treatment rarely indicated

–When indicated, treat as O. Osleri

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14
Q

Discuss Crenosoma vulpis?

A
  • Usually a parasite of wolves and foxes
  • Occasionally affects dogs
  • Leads to chronic bronchopulmonary disease and productive cough
  • Indirect life cycle involves slugs / snails as intermediate hosts

–Paratenic hosts eating primary hosts also infective

  • Pre-patent period around 3 weeks
  • Highest incidence autumn due to acquisition of infections in summer

–Due to fluctuations in intermediate snail host

  • Adults live in bronchi and bronchioles where they cause bronchitis – NO nodules
  • Investigate and treat as Oslerus osleri

–Often more rapid response to treatment than with O. osleri

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15
Q

Discuss Capillaria aerophila?

A
  • Class: nematoda
  • Superfamily: trichuroidea
  • Infects the trachea and occasionally nasal passages and frontal sinuses – dogs and cats
  • Life cycle is both direct (major) and indirect (minor)

–Females deposit eggs in lungs

–Coughed up pass out into faeces

–5-6 weeks to reach infectivity

  • Long survival in environment
  • Ingestion of embryonated eggs completes the direct life cycle

–Ingestion by earthworms and hatching to infective larval stage occurs in indirect life cycle

•Ingestion by host completes indirect life cycle

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16
Q

What are the clinical signs of Capillaria aerophila?

A

•Clinical signs

–Light infections usually asymptomatic

–Moderate to severe infections

  • Rhinotracheitis and or bronchitis
  • Wheezing cough and sneezing

Dyspnoea in severe infections

17
Q

How is Capillaria aerophila diagnosed?

A

•Diagnosis

–Faecal egg count

–Rarely peripheral eosinophilia

–Radiographs may reveal mixed bronchial and alveolar patterns

–BAL cytology

•Treatment as for Oslerus and Crenosoma

18
Q

Do cats suffer respiratory parasitism?

A

Aelurostrongylus abstrusus - Feline lungworm

  • Class: nematoda
  • Superfamily: metastronglyoidea
  • Life cycle indirect

–definitive host (cats);

–intermediate host (snails/slugs)

–paratenic host (multiple – including rodents, birds, amphibians and reptiles)

•Has been reported in the UK

–Commoner in European mainland and USA (5% prevalence globally)

–Various reports of prevalence – Scotland ~10%

19
Q

What is the life cycle of Aelurostrongylus abstrusus?

A
  • L1 passed into faeces
  • L3 develops within intermediate host
  • Cat usually infected by ingesting the paratenic host (after they have eaten the intermediate host)

–May survive in intermediate host for up to 2 years

–Can remain viable as cyst form in paratenic host for up to 4 months

•L3 then released into the alimentary tract

–Travel to lungs via blood or lymphatics

•Adults reside in the alveolar duct and terminal bronchioles

–Loose living no nodule

–Eggs laid develop into L1 within the lung, coughed up and swallowed passing out in faeces

  • Pre-patent period between 4-6 weeks
  • Duration of patency around 4 months

–Some worms can survive in the lungs for several years

20
Q

What are the clinical signs of Aelurostrongylus abstrusus?

A

•Usually no clinical signs, self-limiting infestation in young cats

–Self-limiting infection usually resolved within 6-9 months

–Signs generally related to infective dose

•Experimental infections with 50 larvae usually subclinical, >800 clinical disease

–Signs in clinical cases usually limited to chronic mild cough

–Heavy experimental infections have also been associated with diarrhoea and weight loss

–In experimental infections signs most notable between 6-12 weeks post infection when egg laying is maximal

•Infections lead to multiple small raised subpleural greyish foci

–Various histological changes including muscular hypertrophy and hyperplasia of alveoli

–These changes are almost completely reversible following successful treatment

•Occasionally causes cough in young cats, rarely secondary infection and bronchopneumonia.

–Rarely in severe infections may develop pleural effusion

  • Recent reports of hypoventilation and respiratory acidosis in affected cats
  • Additional report of pulmonary hypertension and severe bronchopneumonia in young kittens – reversible with treatment
21
Q

How do we diagnose Aelurostrongylus abstrusus?

A

•Faecal examination – this has been shown to be the most sensitive method currently available

–may require repeated samples as intermittent shedding

–smear, flotation or Baermann

•Radiographs

–diffuse bronchial pattern

–may see associated nodules

•BAL may see larvae in wash fluid

–eosinophils (increased proportion and number)

•Sensitive PCR has been developed for pharyngeal swabs or faeces but not yet commercially available

22
Q

How do we treat Aelurostrongylus abstrusus?

A

Treatment

  • Fenbendazole –at 50mg/kg PO SID for 3 days – although may require longer course of 10-14 days
  • May require additional anti-inflammatory or bronchodilator therapy during treatment of respiratory signs worsen
23
Q

What can be seen here?

A

Bronchointerstitial lung pattern in 2 year old cat with A. abstrusus infection.

24
Q

Discuss Angiostrongylus vasorum?

A
  • Class: nematoda
  • Superfamily: metastrogyloidea
  • Sometimes called a heartworm – misnomer is a vascular worm in the main

–May be referred to as ‘French Heartworm’

•Adults live in the pulmonary arteries

–Slender worms up to 2.5cm long

•Life cycle-indirect: Dog is definitive host/slug or snail is intermediate host

–Indirect evidence that frogs may act as secondary intermediate hosts or paratenic hosts

25
Q

Is A. vasorum a problem I am likely to encounter clinically in the UK?

A
  • Historically regionally endemic in UK
  • Now accepted to be widespread in South of UK and wales, with reports arising of infections in northern UK and Scotland
  • Rural environments were the mainstay of distribution initially
  • Possibly becoming more widespread throughout the country due to increased fox urbanisation and more widespread travel with dogs
  • Also endemic in regions of Spain, France, Hungary, Germany, Italy, widespread in Ireland
26
Q

What is the Life cycle of A. vasorum?

A
  • Life cycle is indirect
  • Genus is ovo-viviparous
  • Eggs laid in pulmonary vessels
  • Carried into capillaries which then hatch
  • L1 larvae then penetrate into the alveoli

–Migrate into trachea and coughed up then swallowed

  • Passed out into faeces
  • Further development within intermediate host

–Snail/slug predominantly

–Infective stage reached in 17 days

–Infection can also occur via paratenic host

•After ingestion L3 larvae travel to abdominal lymph nodes

–Two further parasitic moults take place (L5)

–Liver heavily compromised between 10-25 dpi

–Proceeds from here to the vascular space (aberrant migration may occur at this point)

•Pre-patent period is 7 weeks

–Important with respect to onset of signs in young dogs

–Although in experimental studies this can vary from 5 ½ weeks to 10 weeks

27
Q

Clinical signs of A. vasorum infestation?

A

•Often complex presenting signs, not limited to respiratory tract

–Early stages of infection are often asymptomatic

–Recently established infections signs may also be minimal

  • Clinical signs when present typically involve three major body systems:
  • Cardiorespiratory– degree of signs associated with worm burden

–Various respiratory signs

  • Chronic cough,
  • ex intolerance, syncope
  • dyspnoea,
  • tachypnoea

–Signs often relate to degree of burden and duration of infection

–Productive cough with occasional haemoptysis

–Associated with larval migration through lung and airway

–Pulmonary hypertension – seen in heavy burdens, different reports as to whether this resolves with successful treatment (some studies suggest it doesn’t develop)

–Recent report of aortic rupture and the discovery of heavy adult and larval burden in haematoma in the thorax at PM

28
Q

What are the signs of A. vasorum infestation?

A

Coagulopathies

–Clinically - anaemia, subcutaneous haematomas, internal haemorrhages, prolonged bleeding from wounds or after surgery

–Thrombocytopenia, prolonged APTT and OSPT, elevated D-dimer (previously measurement of FDPs was used) –via consumptive coagulopathy – chronic DIC

•Studies have shown deposition of immunoglobulins, complement and fibrinogen in pulmonary vessels

–Also causes immune mediated thrombocytopaenia

–Similar pathophysiology can lead to thrombopathia

–Parasite releases – or stimulates host to release – factors that modulate blood clotting?

Neurological dysfunction

–Paresis, depression, seizures, spinal pain, behavioural changes, ataxia and loss of vision have been described

–Associated with aberrant nematode migration or subdural haemorrhage secondary to coagulopathies

29
Q

Why are the signs of A. vasorum so diverse?

A

Adult antigens

– Cause Type III hypersensitivity (immune complex deposition)

– Complement activation

– Immune infiltrate in lungs and other tissues

Egg deposition/L1

– Pulmonary inflammation/granuloma formation

– Pulmonary arteriolar vasoconstriction

– End arteritis and fibrosis of vessels

30
Q

What are the clinical signs of A. Vasorum?

A
31
Q

What does A. Vasorum look like on histology?

A
32
Q

How is A. vasorum diagnosed?

A

•A. vasorum may be a difficult disease to diagnose, although signs may be very suggestive

–Clinically may take a number of diagnostic samples before a positive result is obtained

•Direct evidence:

–Problems due to intermittent shedding of larvae in faeces

–L1 in faeces (flotation techniques) using pooled samples

–L1 in faeces also detectable by smear methods

–L1 in bronchoalveloar lavage fluid (BAL)

•Supportive evidence:

–Radiograph may show alveolar infiltrates

–Routine biochemistry – generally unremarkable

  • Occasionally see hypercalcaemia
  • Reports of reduced fructosamine in affected dogs

–CBC – eosinophilia, increased APTT/OSPT, thrombocytopaenia

–Eosinophilic inflammation on BAL fluid

33
Q

What can be seen here?

A

A. Vasorum

34
Q

How do we diagnose A. vasorum?

A

•SNAP test

35
Q

What is the radiographic appearance of canine A. vasorum?

A
36
Q

Discuss A. Vasorum management?

A
  • Over recent years products have become licensed
  • Currently 2 products are licensed

–Advocate spot on - (Imidacloprid and Moxidectin) – licensed

–Milbemax/Milbactor/Milpro/Milquantel - (Milbemycin oxime and Praziquantel ) – licensed

–Fenbendazole – effective but unlicensed used at 25-50mg/kg orally for 7-21 days, some people suggest treating at weekly intervals every 3 weeks for 3 treatments

–Levamisole and ivermectin also effective

•alternative products are equally effective and licensed with fewer potential side effects

37
Q

So how do we treat A. vasorum?

A
  • Need to counsel owners about the risks of beginning therapy for Angiostrongylus
  • Considerations for supportive treatment in addition to anthelminthics with infections that have been identified

–Bronchodilators

•Aid with airway hyperresponsiveness

–Corticosteroids

•May reduce tendency for acute deterioration after beginning anthelminthic therapy

–Phosphodiesterase inhibitors – for ongoing PH

–Cage rest and possible oxygen therapy

•If dyspnoea present

–Considerations for haematological dyscrasias

•May be ongoing despite therapy for angiostrongylus

38
Q

Prevention of A. vasorum infestation?

A

No licensed drugs for prevention

  • However treatment in pre-patent period with milbemycin oxime or moxidectin decreases or prevents establishment of adult parasites
  • Unclear to what extent dogs are protected from reinfection by persistence of macrocyclic lactones nor how severity of disease relates to level or stage of infection
  • Dogs in endemic areas treated every 3 months with milbemycin are half as likely to test positive for A. vasorum as those treated with fenbendazole or untreated
  • Important to have an idea of local epidemiology
  • Difficult to control slugs and snails but can reduce time dogs are in contact by more active exercise regimes
39
Q

Compare Angiostrongylus case –
comparative radiographs at presentation and 7 days post treatment?

A

Small Animal Final Year (317 decks)

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