Cattle Parasitology Flashcards
1
Q
What are the cattle nematodes? Abomasum, SI, LI?
A
- Abomasum = Haemonchus contortus, Ostertagia ostertagi, Trichostrongylus axei
- SI = Trichostrongylus colubriformis, Nematodirus helvetianus, Cooperia oncophora
- LI = Oesophagostomum radiatum, Bunostomum phlebotomum, Chabertia ovina, Trichuris spp
2
Q
How does ostertagia cause damage?
A
- Abomasal wall damage
- raised pH of gastric juice from 2 to 7
- Poorer digestion + bacterial overgrowth
3
Q
How does cooperia cause damage?
A
- Damage to intestinal mucosa
- Impaired absorption
4
Q
How is PGE diagnosed?
A
- Grazing history & signalment
- Clinical signs and seasonality
- Plasma pepsinogen- ostertagiosis
- Faecal egg counts = Standard McMaster’s salt flotation
- Post mortem
- Antibody ELISAs = Indicate exposure rather than infection
5
Q
When is PGE highest on pasture?
A
Summer time - July
6
Q
What are the differences in epidemiology between gastrointestinal worms and lungworms?
A
- PGE =
- Gut worms are ubiquitous
- Gut worm larvae survive for months at pasture
- Progressive pasture infectivity builds over time
- Consistent, predictable annual disease pattern
- Lungworms =
- Lungworm infection not present on all farms
- Lungworm Survival on pasture is short
- Most important source of infection year to year
are carrier animals - Pasture infectivity build-up can be very fast
- Disease risk varies and is difficult to predict
7
Q
What are at risk animals of lungworms?
A
- Youngstock - 1st / 2nd grazing seasons
- Bought in cattle - from naive herds
8
Q
What is the pathology and clinical presentation of lungworms?
A
- Prepatent phase = L4 larvae in alveoli, migrate towards
bronchi = Alveolitis, bronchiolitis, bronchitis - Patent phase (26 days+) = Adult worms in larger airways,
eggs and L1 larvae in the alveoli = - Obstructive bronchitis
- Aspiration pneumonia
- Secondary bacterial infections
- Pyrexia –associated with secondary bacterial infections
- Animals may never fully recover from clinical disease =
- Ongoing losses in milk production ~£100/cow
- Including treatment costs, fertility etc. ~£140/cow
9
Q
What are CS of mild lungworm?
A
Intermittent cough when exercised
10
Q
What are signs of moderate lungworm?
A
- Frequent cough at rest
- Laboured breathing
- Squeaks crackles on auscultation
11
Q
What are signs of severe lungworm?
A
- Severe tachypnoea
- Dyspnoea
- ‘Air Hunger Position’
- Mouth breathing
- Deep harsh cough
- Salivation, anorexia
- Death
12
Q
How is lungworm diagnosed?
A
- Signalment, history & clinical signs
- Post-mortem
- Oviviparous parasite- live L1 larvae passed in faeces =
- Patent infection >26 days = Baerman technique
- Antibody ELISAs = Serum or milk sample
13
Q
What is acute disease of fluke?
A
- 2-6 weeks post-infection
- Juvenile flukes migrating through liver parenchyma
- Tissue damage + haemorrhage
- Uncommon in cattle
14
Q
What is chronic disease of fluke?
A
- 10-12weeks post-infection
- Adult flukes within bile ducts
- Chronic anaemia, hypoalbuminaemia (bottle jaw)
- Weight loss + poor BCS
15
Q
How is fluke infection diagnosed?
A
- Signalment, history & clinical signs - Tricky in adult cattle/ subclinical infections
- Serum biochemistry = Serum albumen, GLDH & GGT
- Fluke egg sedimentation = Individual or composite samples
- Copro-antigen ELISA = Theoretically more sensitive (4 weeks+)
- Antibody ELISA = 2-4 weeks post-infection
- Post mortem/Abattoir feedback
