Large animal respiratory parasites Flashcards

1
Q

What makes lungworm a special parasite?

A

The lung is a very sensitive, important organ.

Unpredictable disease - no connection with season, region, history etc. Cannot have expectation as to when infections will occur. Serum antibodies and clinical signs, as well as excretion of stage: serum antibodies are suggestive of infection but may not be any clinical signs and visa versa: severe clinical signs and no antibodies – it doesn’t follow normal correlations.

Most of the time, antibiotics are given as they develop complications that require antibiotic administration.

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2
Q

Explain why lungworm is an unpredictable disease

A
  • The disease is dose dependent. Sometimes animals don’t show clinical signs when they ingest low numbers of the larvae. Cannot give oral treatment because it won’t reach the parasite. Antimicrobials don’t work for most parasites but can for lungworm. Use NSAIDs because this is a painful disease and to reduce inflammation: come due to inflammation caused by migration of larvae.
  • Unpredictability: there is no season preference of the disease, regional variation is null, can not have infection for years and then it develops again.
  • Serum antibodies suggest infection but they might not have clinical signs and visa vera: can have severe clinical signs without antibodies or infective stage in faeces.
  • There is a broad range of clinical stages
    • Mild to severe- there are not common clinical signs
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3
Q

Explain why lungworm is a speedy parasite

A
  • Direct lifecycle- needs no intermediate
  • Larvae in faeces can affect other animals and once animals have ingested them the larvae reach lungs in one week and PPP is 3 weeks so one animal can affect another in 3 weeks
  • Protective antibodies wane rapidly
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4
Q

Diagnosis of lung worm?

A
  • Diagnose with baermanns test NOT FEC.
    • Parasites are coughed up swallowed and L3 are excreted in faeces.
    • Don’t expect to find eggs in faeces.
    • Baermann technique is the only way of finding the larvae and diagnosing larvae in faeces.
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5
Q

What can lungworm have serious impacts on?

A
  • Sustainable livestock industry
    • Doesn’t just impact the lung but affects the body systemically.
  • Agricultural economy via:
    • wool production
    • Affects dam’s ability to conceive
    • milk production
    • carcass quality
    • weight gain (inappetence or anorexia)
    • Costs of drugs, labour and veterinary treatment
    • death or culling
  • In addition: reproductive performance
    • fertility drops
    • calving periods extend
  • The commonest respiratory disease in cattle in UK
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6
Q

Clinical signs of lungworm

A

Clinical signs range from a mild cough with a slightly increased breathing rate, to severe persistent coughing, with marked difficulty in breathing and even death.

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7
Q

Morphology of lungworms

A
  • Female up to 8cm
  • Male up to 5 cm
  • Very small buccal capsule so don’t eat a lot
  • Lung worms are in the family trichostrongyloidae and metastrongyloides
  • In general they have a direct lifecycle except for M. capilaris and metastrongulys apri.
  • Trichostronguloides have direct lifecycles
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8
Q

Life cycle of cattle lungworm: Dictyocaulus viviparous

A
  • P.P.P.= 3-4 weeks
  • First stage larvae (L1)
  • Third stage larvae (L3)
  • First stage larvae (L1)et out in the faeces.
  • Takes 3-5 days to develop into L3 on pasture
  • Good ability to disseminate.
  • Third stage larvae (L3)
  • PPP is three weeks so it take 3 weeks for one cow to infect another
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9
Q

Epidemiology of lungworm

A
  • Distribution
    • seen mainly in temperate areas.
  • Climate
    • larvae require moist, cool environment.
    • adverse weather conditions decrease larval survival and dispersal.
    • larvae can overwinter on pasture like GI nematodes.
  • Age
    • young animals are more susceptible.
  • Pilobolus fungi
    • facilitate the spread of lungworms larvae in a pasture.
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10
Q

Trends of lungworm infections in the UK

A
  • Current trend: Rise in immunologically naïve populations who have either not been vaccinated or exposed to low levels of natural infection during their first grazing season.
  • Prevalence out of outbreaks reported in adults.
  • Don’t know where it came from
  • Some farmers are more cautious then others.
  • First season: decreasing because people use vacciantion
  • Second season- grazing season hasn’t reduced that much
  • Red- infection of cattle has increased – poor exposure means absence of immunity and increase naïve populations. Lungworm immunity doesn’t last that long.
  • Vaccinate animals to induce an immune response
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11
Q

Clinical presentation of lungworm

A
  • Cattle:cough, decreased milk production, and weight loss, enlarged lymph nodes (not usually).
  • Sheep and goats: cough, dyspnoea, catarrhal bronchitis, weight loss, lethargy. Greyish-green nodules. Goats are most susceptible and can die from pneumonia.
  • Horses:often seen in horse grazing with donkeys (natural host).
  • Pigs:dyspnoea, lethargy, weight loss, persistent cough
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12
Q

Diagnosis of lungworm?

A
  • Antemortem diagnosis:
    • Clinical signs, grazing history
    • Demonstration of larvae in faeces
    • Tracheal wash
    • Bronchoscopy and radiography
    • Serological tests
    • Failure of antibiotic therapy
    • Baermann technique is one of the best methods of diagnosis.
  • Postmortem diagnosis:
    • Demonstration and identification of lungworms & characteristics lung pathology
  • ‘Husk should be included in the differential diagnosis for persistent respiratory manifestations in animals especially in enzootic areas.’
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13
Q

Differential diagnosis for lung worm?

A
  • Lung abscess
  • Lung tumor
  • Bacterial bronchopneumonia
  • Necrobacillosis
  • Tuberculosis
  • Actinobacillosis
  • Hydatid disease
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14
Q

Treatment options for lungworms?

A
  • There is no resistance fortunately. The macrocyclic lactones are the most recent and most effective. Benzimidazoles are still effective.
  • Other clinical considerations:
    • Limited withdrawal period
    • Effective
    • Used in lactating cattle.
    • Use eprinomectin – no withdrawal period!!
    • Avoid using an anthelmintic where a lot od dead parasites occurs rapidly: too overwhelming for the body: inflammatory response to dead parasites.
    • Benzimidazoles take longer to kill the parasite.
      *
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15
Q

Control strategies of lungworm

A
  • Deworming
    • Strategic deworming using anthelmintics. Conjunction with treatment of GI nematodes
  • Vaccination (Bovilis® Huskvac, Intervet UK Ltd)
    • One vaccine, made up of irradiated L3 infective larvae (alive but cannot penetrate).
    • Two doses, 4wk apart at least 2 wk before animals can be turned out to allow the development of immunity.
    • Don’t use anthelmintics whilst using a vaccine.
  • Management Options
    • Supplementaryapproaches.
    • Sanitation and management.
    • Avoid mixing animals/ages on the same pasture.
    • Elimination of intermediate hosts (doesn’t apply for all lungworm species) – not in cattle species.
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16
Q

How to avoid a poor outcome in the management of parasitic pneumonia (lungworm)

A
  • DON’T wait for a husk to develop to suspect the diagnosis.
  • DON’T exclude the diagnosis because there is no history of lungworm infection.
  • DON’T exclude the diagnosis solely for geographic or seasonal reasons
  • DON’T withhold therapy if you are clinically suspicious
  • DON’T administer the vaccine to calves less than 8 weeks old due to MDA.
17
Q

Public health relevance of lungworm

A

Humans

  • Animal lungworms are strict animal parasites and don’t infect humans. However, there have been rare reports of human infections with the carnivore lung worm Eucoleusaerophilusin Morocco and Russia.

Animals

  • and a veterinary public health infrastructure that monitors the water/food supply and thwart infections via treatment and vaccination, and elimination of the intermediate/reservoir hosts.
18
Q

Future needs for lungworm?

A
  • Pathogenesis of disease
    • Identify host genetic determinants of resistance (hoping for natural resistance).
  • Better vaccines (long-lasting immunity)
    • New targets (e.g. more protective antigens, new virulence factors).
  • Controlling emergence of resistance
    • Monitor the development of new anthelmintic resistant strains