Lungworms of large animals Flashcards

1
Q

What are the superfamily’s of the lungworms for large animals?

A

Trichostrongyloidea

Metastrongyloidea

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2
Q

Trichostrongyloidea:

Direct or Indirect life cycle?

Species?

Disease caused?

Pathogenic?

A

Direct life cycle

Dictyocaulus

Parasitic Bronchits (mostly in dairy cattle)

Pathogenic

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3
Q

Metastrongyloidea:

Direct v. Indirect lifecycle?

Species in pigs and IMH?

Species in sheep/ goats (2)?

Pathogenic?

A

Indirect therefore IMH

PIgs:

  • *Metastrongylus**
  • *-IMH**: earthworm

Sheep/ Goats:

  • *Meullerius capillaris**
  • *-IMH:** snail/ slug
  • *Protostrongylus refescens
  • IMH:**snail

NOT PATHOGENIC

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4
Q

Dictyocaulus viviparus affects which species?

A

Cattle

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5
Q

Dictyocaulus arnfieldi affects which species?

A

Horse and Donkey

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6
Q

Dictyocaulus filaria affects which specie?

A

Sheep and goats.

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7
Q

Dictyocaulus eckerti affects which species?

A

Deer and other cervids (mammals of deer family)

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8
Q

Parasitic bronchitis is caused by which trichostrongyloidea species and in which animal?

A

Dictyocaulus viviparus in cattle.

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9
Q

Describe the life cycle of Dictyocaulus viviparus and the PPP.

A
  1. L1 in feces (NOT EGGS)
  2. Moults to infective L3. Ingested and penetrates mucosa.
  3. L4 develops in the mesenteric lymph nodes.
  4. Travels to the lungs via the lymphovascular route.
  5. Young adults in bronchioles and small bronchi.
  6. Adult worms in the mainstem bronchi/ trachea.
  7. Eggs hatch in the lungs. L1 migrate up trachea and swallowed.
  8. L1 excreted in feces.
  9. PPP= 26 days
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10
Q

Describe the Immune response to D. viviparus.

A
  • Strong immunity following infection but immune response can cause pathology.
  • Develops strong imune response after first infection.
  • Immunity is boosted by natural challenge. This will last approx 6 months however immunity will lose its efficacy if not challenged.
  • Therefore, after infection immunity will become strong and will continue to stay strong if challenged naturally, however if unchallenged for longer than 6 months immunity will lose its efficacy.
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11
Q

What are the clinical signs of Parasitic Bronchitis?

Mildly affected animals?

Moderately affected animals?

Severely affected animals?

A
  • Mildly affected:
    intermittent cough
  • Moderately affected:
    coughing at rest, tachypnoea( rapid breathing), hyperpnoea (increased depth of breathing)
  • Severely affected:
  • harsh cough
  • tachypnoea
  • dyspnoea (shortness of breath/ difficulty breathing)
  • mouth breathing -
  • pyrexia due to secondary bacterial infection
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12
Q

Parasitic Bronchitis: Pathogenesis

Penetration Phase

A

This occurs in days 1-7: Larvae are migrating to lungs (no pathology associated) (traveling thru GIT)

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13
Q

Parasitic Bronchitis: Pathogenesis

Prepatent phase:

A

Days 8-25.

  • L4 and young adults migrating up the respiratory tree.
  • Causes Acute Inflammatory response **(monocytes and eosinophils) **
  • Mucus/ cellular plugs- collapse of alveoli
  • Clinical signs are first seen in the pre patent phase.
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14
Q

Parasitic Bronchitis: Pathogenesis

Patent Phase

A

Days 26-60.

  • Clinical signs worsen.
  • Lesions form due to presence of worms in bronchi.
  • **Lesions form due to aspirated eggs/ larvae. –> Granulomatous response to aspirated eggs. **
  • Profuse inflammatory exudate.
  • hyperplasia of bronchial epithelium
  • over inflation of alevoli
  • interstistial emphysema (COPD) & edema
  • Increased eosinophils.
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15
Q

Parasitic Bronchitis: Pathogenesis

Postpatent phase

A

Days 61-90

  • Expulsion of adult worms due to immune response. The disease is beginning to resolve itself.
  • Most animals will gradually recover, and a strong immunity will be acquired.
  • Some animals clinical signs will increase and can potentially be fatal. This is due to either alveolar epithelialization or **Bacterial Infection. **
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16
Q

What is reinfection syndrome?

A
  • The immune response kills larve in the lungs therefore this is not a patent infection because adults don’t fully mature (NO L1’S) therefore they can’t produce eggs.
  • Since the adults don’t fully mature, and eggs are not produced, the only way to diagnose is based on clinical symptoms since a FEC cannot be performed.
  • The clinical symptoms involved in reinfection are coughing and slight tachypnea. (Mild syndrome)
17
Q

How do you diagnose parasitic bronchitis?

A
  1. clinical signs
  2. Grazing/ vx/ anthelmintic history
  3. L1 larvae present in the feces: Remember they are not present during the pre patent phase only during the patent phase
    - - Can use the Baermann technique which separates feces from larvae using the Baermann apparatus.
  4. Induce bronchoalveolar lavage and then test for eosinophils.
  5. ELISA- test for antibodies against adult and L3 antigens reflecting the exposure to infection.
18
Q

Epidemiology of Bovine Lungworm (Dictyocaulus viviparus)

A

Found in temperate regions iwth high rainfall.

In the UK the disease usually occurs in the summer months (July- October)

Infective L3’s can overwinter.

The reason there are increased numbers during the summer months is because the small # of L3’s that have overwintered infect animals with no immunity and this causes an increase in environmental infection due to the cycle.

Small numbers are sufficient to cause disease due to the cycle.

**TRADITIONALLY DISEASE OF 1ST SEASON GRAZING CALVES BECAUSE THEY HAVE NEVER SEEN INFECTION BEFORE SO THEY HAVE NOT BUILT UP A STRONG IMMUNITY. **

19
Q

Comment on the increasing infections of boving lungworms in older cattle.

A

Recently, the disease is becoming more common in adult cattle possibly due to:

  1. Never have been exposed to the lungworm before (no infection) or vaccination.
  2. Cattle were treated with anthelmintic use in their 1st and 2nd years of life therefore never built up immunity.
  3. Both of these allows the cattle to be susceptible to infection if the burden is heavy.

TREND: becoming more common in adults and less common in 1st year grazing calves due to immediate tx. with anthelmintics.

20
Q

How do we prevent bovine lungworm?

A
  1. Vaccination with irradiated (live) L3’s ( 2 doses of 1000 irradiated L3’s).. This helps boost the immune response and allows release of some larvae to adults but not very patent, only a little bit.
  2. Vaccinate 1st season calves before turnout.
  3. Immunity boosted by infection.
  4. Oral Vaccine- Bovilus huskvac- Developed @ Glasgow vet School

NOTE: if giving the oral vaccine do not mix with un-vaccinated calves because the vaccinated calves WILL SHED some L1’s which are infective and therefore will infect un-vaccinated calves if they are mixed together.

21
Q

How do we treat boving lungworms?

A

ANTHELMINTIC DRUGS!

Use them early to reduce pathology.

Mildly affected animals: Tx and move to clean pastue.

Severely affected animals: house, hydrate, NSAID’s, antibitoics if pyrexic.

Give NSAID’s because this reduces the immune response which is the cause for the pathology in the first place.

22
Q

Dictyocaulus arnfieldi:

What species does it affect?

What is different about its life cycle v. D. viviparus?

PPP?

What ages is patency reached?

A
  1. Donkeys and Horses
  2. Similar life cycle to D. viviparus however there are EGGS IN FECES not L1’s.
  3. 2-4 months v. 26 days.
  4. Patency is reached in donkeys and foals/ yearlings but not in adult horses.
  5. UBIQUITOUS IN DONKEYS: A TRUE DEFINITIVE HOST.
23
Q

How do we diagnose Dictyocaulus arnfieldi for:

Donkeys?

Horses:

A
  1. Donkeys:
    - Eggs or L1’s in feces
  2. Horses:
    - Usually no eggs or L1’s
    - Mostly based on clinical signs (chronic cough and tachypnea)
    - Grazing/ anthelmintic history
24
Q

Dictyocaulus filaria:

What species does it affect?

PPP?

How do the clinical signs compare to that of D. viviparus?

How do we diagnose?

How do we prevent?

A
  1. Sheep and goats
  2. 5 weeks.
  3. Clinical signs are more mild than D. viviparus:
    - chronic cough
    - nasal discharge
    - dyspnea in severe cases.
  4. Diagnose L1 in feces.
  5. Tx flock and move to clean pasture.
25
Q

Metastrongyloid Lungworms:

Life cycle of Metastrongylus in Pigs and PPP?

A
  1. Eggs in feces
  2. L1 ingested by earthworms (IMH)
  3. Moults to L2-L3(infective)
  4. Earthworms are ingested by pigs.
  5. L3’s penetrate intestinal mucosa
  6. L4 in lymph node
  7. L4 travel via the lymphovascular route to the lungs.
  8. Adults in small bronchi and bronchioles.
  9. Eggs in Feces
  10. **PPP= 4 weeks **
26
Q

Metastrongylus spp. in Pigs:

Clinical symptoms?

Age prevalence?

Diagnoses?

A

Clinical symptoms:

Mostly light and asymptomatic

Heavy: coughing, dyspnea, nasal discharge.

Most prevalent in pigs 6-8 months old)

Diagnosis:

Eggs in feces- set up a fecal float.

27
Q

Muellerius capillaris:

Appearance?

IMH?

Pathogenic?

Diagnose at PM?

Diagnosis?

A
  1. Brown hair like worms found in alveoli. 1-3 cm)
  2. IMH: snails and slugs
  3. NOT pathogenic
  4. Lead shot nodules in lungs
  5. Diagnose L1’s in feces
28
Q

Protostrongylus rufescens:

Species affected?

Where do the adults reside?

Pathogenic?

IMH?

A

Sheep and goats

adults found in bronchioles

not pathogenic

snails

lung lesions larger then M. capillaris

heaviest infection in adult sheep/ goats.

29
Q

Identify this species. Is it pathogenic? What size is it?

A

Dictyocaulus filiaria. (L1 larvae in sheep feces)

Pathogenic

550-600 micrometers

30
Q

What species is this? Identify a prominent morphological stucture unique to this species.

A

Dictyocauls filiarai.

Anterior cuticular knob

31
Q

Identify this species. Is it pathogenic? What size is it?

A

Muelleris capillaris. (L1 larvae in sheep feces)

not pathogenic

320-400 Micrometers

32
Q

What species is this? Identify a prominent morphological stucture unique to this species.

A

Muelleris Capillaris

Tail dorsal spine.

33
Q

Identify this species. Is it pathogenic? What size is it?

A

Protostrongylus rufescens (L1 larvae in sheep feces)

Not pathogenic

320-400 micrometers

34
Q

Identify this species by its tail.

A

Protostrongylus rufescens.