Bovine GIT 1 Flashcards
Alimentary problems in the adult cow as recognised by the farmer.
Diarrhoea.
Excess salivation.
Bloat.
Pain.
Poor production and/or weight gain.
Diarrhoea.
A sign rather than diagnosis.
Difficult to definitively diagnose cause.
Can look for presence/absence of oral lesions.
- can give info about rest of GIT.
Can be due to net increase in secretion or malabsorption.
In ruminants ~80% water reabsorbed in SI which is opposite to horse.
Acute diarrhoea leads to loss of electrolytes (dehydrate), chronic diarrhoea leads to loss of nutrients and some electrolytes (lose body condition, fat and muscle).
Diagnosis of diarrhoea.
History.
Group exam.
Individual exam.
Faecal exam.
Clinical pathology.
Difficult unless isolate pathogens.
Diagnosing diarrhoea Hx.
Here or single animal.
Previous occurrence?
Age group.
Duration of diarrhoea.
Nutrition?
Water source?
Production effects.
Diagnosing diarrhoea - group and individual exam.
Drooling.
Abdominal pain.
Tenesmus.
CE - esp. assessing level of dehydration.
Diagnosis of diarrhoea - faecal exam.
Consistency.
Colour.
Smell.
Mucoid.
Blood.
Samples.
- need to know what to do with them and know how to interpret the results.
Exam of animal.
Oral cavity for lesions.
Perineal region.
Abdominal pain?
TPR.
Body condition.
Level of hydration/dehydration.
Any lameness?
Nervous signs?
APHA diseases that cause diarrhoea.
Johne’s disease (less common now compared to a decade ago).
Salmonellosis due to S. Dublin.
Salmonellosis due to S. Typhimurium.
Malignant catarrhal fever.
Acute BVDV infection (control programmes).
Mucosal disease (control programmes).
Fasciolosis (better controlled).
Traumatic reticuloperitonitis.
Ruminal bloat.
Winter dysentery (large outbreaks).
Abomasal ulceration.
Ruminal acidosis.
Reasons cows may eat poisonous plants or chemicals.
Usually sensible and discriminate eaters but:
- may become confined to area with little food.
- may be exposed to dumping of potentially harmful material.
- may be exposed to excessive lush pasture.
Dietary induced diarrhoea.
Common cause of diarrhoea.
Hx of husbandry changes important.
Ruminal overload; frosted foods; grass scour; excess fodder beet.
Coccidiosis.
Increasing incidence - indoor intensification in housed confined calves, often insufficient bedding.
Locusts survive months in faeces but only a few hours in sunlight.
Parasites are ubiquitous but disease due to build up of predisposing factors.
Acute-chronic d+, smelly, often greenish, can get mucoid/blood.
Poor weight gain or actual weight loss.
Self-limiting.
Dx from GROUP exam.
Tx/preventative meds:
- Diclazuril orally or perhaps sulphonamides.
- Decoquinate in feed preventative med.
Helminth parasitism.
Obvious cause of chronic D+ in young stock.
Most important are:
- Ostertagiasis type I and type II.
- Fasciola hepatica (Liver Fluke)
Salmonellosis.
Disease in calves, growing and adult cattle.
Causes enteritis, abortion, septicaemia.
>70% of isolates are usually:
- Salmonella enterica subspecies enterica.
- serotype Typhimurium (S. Typhimurium) — numbers falling.
- serotype Dublin (S. Dublin).
Serotype prevalence varies from year to year.
Reportable under Zoonosis Order 1989 (but not a notifiable disease).
- if isolated in laboratory, needs to be typed.
Transmission of Salmonellosis?
Faecal-oral.
In feed, on vet, in slurry, rodents, birds.
Conjunctival.
Respiratory.
Dose dependent.
High infective dose in normal animals (10^10 in adults, 10^8 in calves).
General Salmonellosis epidemiology.
Initial infection.
Outcome depends on interaction among host immune status, infective dose, and serotype.
Incubation period 1-4d.
Clinical cases excrete 10^8/gram faeces.
S. Typhimurium epidemiology.
Peak incidence in October-December.
- weather changes — wet.
- calves are housed, stocking densities increase.
Established in calf trade environment historically.
Not host-specific.
Mainly causes enteritis/septicaemia.
- in calves not immuno-competent.
Infections resolved after 3-16w.
Tends to be epidemic.
S. Dublin epidemiology.
Endemic in wetter areas (west).
Host-adapted.
Active carriers shed for up to a year.
Passive carriers shed while exposed.
Latent carriers shed when stressed.
Congenital? - can get into repro tract.
Association with Fasciola Hepatica.
Not closely associated with calf sales.
Sites of carriage of salmonella within the animal.
Caecal contents.
Terminal ileum.
Ileal/caecocolic LNs.
Gall bladder.
She’d in faeces.
Carriage for ~4w (Typhimurium).
Carriage for yrs (Dublin).
Lab Dx in salmonellosis.
Faecal culture.
Environmental samples.
Pathology especially guy lesions.
Histopathology.
Culture of lesions.
Culture of abattoir.
Serology.
Reporting and confirmation of salmonellosis.
Report to DEFRA under Zoonosis Order 1989.
Send to reference lab.
Serotyping.
Phage typing - for tracking.
Plasmid analysis.
Pulse field gel electrophoresis.
Gene sequence? PCR?
European Centre for Disease Control recording.
Why is salmonella dublin relatively easy to treat?
It is very sensitive.
A high percentage of S. Dublin were sensitive to a high number (16) of antimicrobials.
Why is S. Typhimurium less easy to treat?
A much lower percentage of S. Typhimurium are sensitive to 16 different antimicrobials.
Likely to be resistant.
Antimicrobial sensitivity testing aids selection of therapy.
Why is S. Typhimurium less easy to treat?
A much lower percentage of S. Typhimurium are sensitive to 16 different antimicrobials.
Likely to be resistant.
Other bacteriological issues in treatment and control.
Vacs containing killed culture.
Organisms sensitive to disinfectants but resistant to drying (survive >1yr).
Wide range of reservoir hosts.
