Calf Problems: Infectious Diarrhoea and Other Conditions Flashcards

1
Q

Why do calves sometimes lose hair when they scour?

A

Faeces can be highly alkaline (bicarbonate) which causes chemical burns and hair loss at the rear end.

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2
Q

Why is the diagnosis of D+ in calves so problematic?

A

Subclinical infections are common.
Mixed infections are common.
Many complexities.

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3
Q

Clinical signs of D+ in calves.

A

Fever.
Change in abdominal contour.
D+:
- colour.
- consistency.
- blood.
Weight loss.
Inflammation in another body system.
- e.g. umbilicus.
Clinical biochemistry.

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4
Q
  1. Endemic pathogens causing calf D+.
  2. Exotic pathogens causing calf D+.
A
  1. Rotavirus (vac available).
    Coronavirus (vac available).
    Cryptosporidia (new vac available).
    Enterotoxigenic E. coli.
  2. E coli K99/F41 (vac available).
    Salmonella.
    *vacs will do nothing if passive transfer via colostrum is not achieved.
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5
Q

Calf age and likely agents causing D+.

A

0-6d old = enterotoxigenic E. coli.
6-21d old = rotavirus, coronavirus, cryptosporidium.
>21d old = coccidiosis (no vacs available).

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6
Q

Rotavirus.

A

Infection in almost 100% of calves.
Cows shed virus, colostrum contain specific antibodies.
Destruction of microvilli in enterocytes.
Immunity requires local antibody.
Immunity overcome by heavy challenge.
Several strains, some avirulent.
Thin, yellow white D+ - 2nd week of life.
Vac available and administered to dam. Calf immunity via colostrum.

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7
Q

Rotavirus disease pathogenesis.

A

Microvilli damage causes co-transport of glucose with sodium to stop due to non-structural protein NSP4 specifically inhibiting the symporter.
- If no sodium transport, no water pulled from the gut into circulation.
Damage causes disruption of intracellular junctions and fluids from extracellular space leach out into the gut lumen.
The release of amines and peptides can mimic enteric mural system, affecting gut movement with an elevated motility.

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8
Q

Coronavirus.

A

Widespread infection, virus in faeces of 65% cows (winter dysentery).
Commonly subclinical or part of mixed infection in calves.
D+ can be acute and severe leading to rapid death in calves.
Virus more commonly causes chronic debilitating D+ in older calves.

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9
Q

Coronavirus disease pathogenesis.

A

Massive loss of intestinal epithelium and villus stunting.
Greatly reduced absorption of intestinal fluid.
Basal crypt cells less affected so recovery can be rapid.

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10
Q

Cryptosporidia.

A

Extracellular protozoan, not host specific.
Zoonotic.
Infection widespread, favoured by dirty conditions.
Mixed infections common.
Earliest cases 5-7d old, age immunity at 3w old.
Profuse watery D+ for ~7d.
Poor response to anti-protozoals.
Oocysts resistant to disinfectant.
Better to prevent than to treat.

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11
Q

Pathogenic E. coli serotypes.

A

Enterotoxigenic E. coli (EETEC).
Verotoxigenic E. coli (VTEC).
Attaching and effacing E. coli (AEEC).
Enteroinvasive E. coli (EIEC).
Unclassified.
If calves getting D+ or dying of sudden death v eary in life, may be some justification to use ABX.

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12
Q

Enterotoxigenic E. coli.

A

Not a high incidence but can be v severe.
Seen in situations where calves do not get sufficient colostrum fast enough.
Invade through gut, through payer’s patches, through tonsil, into calf before has functional immune system w/ appropriate antibodies.
Clinical disease rare over 5d old due to loss of receptors on the gut epithelium for E. coli adhesins/toxins.
Specific antibody blocks the adhesion.
Sudden onset, profuse watery D+, severe dehydration leading to collapse of calf.
Sometimes sudden death.
Recovery takes a whle.
E. coli O157:H7 is an important zoonosis!

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13
Q

Nutritional D+ in calves.

A

Hopefully, mil bypasses rumen via oesophageal groove.
Acid (and rennin) causes paracasein to clot quickly.
Abomasum acts as reservoir, releasing small amounts of clot into SI by action of gastric enzymes.
Whey contains lactose and globulins and moves quickly into SI.
Poor clotting of casein can cause nutritional scours.
*milk needs to be fed at the right temperature and conc. and fed in such a way to make the oesophageal groove close.

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14
Q

What causes poor clotting of casein?

A

Failure of sufficient acid and enzyme secretion.
Poor quality milk product.
Farmer uses incorrect concentration of milk powder.
Farmer feeds at incorrect temperature.
Feeding times irregular.
Infection of the abomasum.
Overfeeding.

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15
Q

Nutritional scour in calves:
Check whether farmer is…

A

Mixing properly, add powder to water, whisk.
Correct concentration? Check instructions.
Correct temperature? = 42-45 degrees C when mixed.
Overfeeding?

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16
Q

Calf Diphtheria.

A

Usually superficial infection of mouth and elsewhere of calf with fusobacterium necrophorum (opportunistic).
In pre-weaned calves and those up to 6-9m old.
Physical abrasion allows bacteria in.
Usually single animal - poor hygiene.
Extensive salivation, some swelling, may be dull.
Dx on exam of mouth, halitosis, enlarged draining LNs and pain.
Tx w/ Penicillin or similar, nursing.
Good recovery.
Avoid coarse food and improve hygiene.

17
Q

Ruminal bloat in pre-weaned calves.

A

2 forms:
- milk fermentation in immature rumen.
- “immature rumen syndrome”.
Milk fermentation due to defective oesophageal groove closure or abomasal overfill/rapid drinking.
Clinical signs include pasty scours, bloat, colic - check for “10 to 4” appearance (swelling high on left and low on right of calf when stand behind).
Tx by stomach tube and occasional use of surfactants.
Withdraw milk and feed ORS for 24hrs, may need fistula.
Correct feeding errors, provide hard feed and wean early.

18
Q

Immature rumen syndrome.

A

Soon after weaning, often if weaned too early.
Calves eat large volumes of fibre and immature rumen cannot digest adequately.
Rumen dilated, calf still hungry, vicious circle.
Clinically - pot-bellied appearance with thin pasty faeces.
Tx by drastic reduction in roughage, use shavings as bedding, palatable concentrates, inoculate rumen with adult rumenal fluid.

19
Q
A