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Cattle I > Diarrhoea in adult cattle > Flashcards

Diarrhoea in adult cattle Flashcards

1
Q

Infectious causes of diarrhoea in adult cattle

A

Salmonellosis

BVD/Mucosal Disease

Liver Fluke

Johne’s Disease

Winter dysentery

Malignant Catarrhal Fever

Babesia (Red Water Fever)

Parasitic Gastroenteritis

Coccidiosis

(Rotavirus)

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2
Q

Nutritional causes of diarrhoea in adult cattle

A

Ruminal acidosis

Lush Pasture

Poor quality roughage

Excess dietary protein

Copper deficiency

Potato Poisoning

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3
Q

Toxic causes of diarrhoea in adult cattle (chemicals)

A

Salt poisoning

Copper Poisoning

Lead Poisoning

Nitrate Poisoning

Arsenic Poisoning

Mercury Poisoning

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4
Q

Toxic causes of diarrhoea in adult cattle (plants)

A

Mycotoxicosis

Alimentary tract carcinoma

Oak/Acorn Poisoning

Ragwort

Hemlock water dropwort

Dog’s Mercury

Rhododendron Poisoning

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5
Q

Miscellaneous causes of diarrhoea in adult cattle

A

Endotoxaemia

Displaced Abomasum

Peritonitis

Renal Amyloidosis

Haemorrhagic Bowel Syndrome[3]

Fat Necrosis

Cold Cow Syndrome

(Clostridium tertium)

(Yersinia pseudotuberculosis)

(Escherichia fergusonii)

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6
Q

Main serotypes of salmonella causing diarrhoea in adult cattle

A

S. typhimurium and S. Dublin

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7
Q

S. Typhimurium

A

ubiquitous and the origin in an outbreak is usually difficult to establish, but outbreaks can sometimes be associated with the purchase of animals.

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8
Q

S. Dublin

A

host adapted to cattle and outbreaks are associated with chronically infected animals, cattle can be latent carriers for years.

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9
Q

Pathogenesis of salmonellosis in adult cattle

A

Primarily occurs via the faecal oral route and cows are more susceptible when stressed e.g. around calving time.

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10
Q

Clinical signs of salmonellosis in adult cattle

A

Pyrexia

Profuse diarrhoea progressing to dysentery

Depressed, dehydrated, milk drop, toxaemia

Sometimes death

Mortality rates low in adults compared to calves

Some additional possible signs of S. Dublin whereas S. Typhimurium most causes GI signs

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11
Q

Additional clinical signs of S. Dublin

A

Abortion (6-9m)

pneumonia
polyarthritis
meningitis
osteomyelitis
tail and ear tip necrosis

Combination

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12
Q

Diagnosis of salmonellosis in adult cattle

A

All cases of diarrhoea in adult cattle are Salmonella until proved otherwise

Sample for culture

Slide agglutination

Serology of little value diagnostically

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13
Q

Treatment of salmonellosis in adult cattle

A

Antibiotics based on C&S
TMPS or pot. amoxicillin

Fluid therapy
Warm isotonic fluids orally
IV essential in severe cases - hypertonic saline

NSAID to counter toxaemia

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14
Q

Control of salmonellosis in adult cattle

A

Isolation and disinfection

Find source of S. Dublin carrier (not very practical)

Vaccinations (Bovivac S) to provide antibody protection to calves through colostrum

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15
Q

What is the main source of BVD infection?

A

PI calves

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16
Q

What happens if pregnant cow infected with BVD in first month of pregnancy?

A

Embryonic death, return to oestrus

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17
Q

What happens if pregnant cow infected with BVD in months 2-4 of pregnancy?

A

PI calf (antibody negative)

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18
Q

What happens if pregnant cow infected with BVD in months 5-9 of pregnancy?

A

Normal calf

Possibly malformations or abortions

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19
Q

Clinical signs of acute BVD infection in non-pregnant animals

A

Usually asymptomatic

Mild, often unnoticed diarrhoea

Transient milk drop and loss of appetite

Oculo-nasal discharge and occasional mouth ulceration

Occasionally more severe disease with profuse diarrhoea

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20
Q

What is mucosal disease?

A

Occurs in PIs when there is a mutation in the BVD virus to a cytopathic variant, or a PI is super-infected with a cytopathic variant

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21
Q

When do PIs most commonly develop mucosal disease?

A

6-24mo

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22
Q

Signs of mucosal disease

A

Profuse watery intractable diarrhoea with blood and tenesmus

Occasional pyrexia and depression

Weight loss

Erosions and uleration of the hard palate, under the surface of the tongue, oesophagus and buccal mucosa

Lesions around coronary band and interdigital space occasionally

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23
Q

Course of mucosal disease

A

Disease begins suddenly and animals may be affected for 2-3 weeks before they die. So, confirm diagnosis and euthanise.

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24
Q

Diagnosis of mucosal disease in PIs

A

Difficult to detect BVDv in acutely affected animals unless at the height of viraemia (ELISA, IPX, PCR).

However in PIs (including mucosal disease) the virus titre is much higher so all tests have high sensitivity.

Can use ELISA for paired serology

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25
Q

Treatment of mucosal disease

A

Acute BVD infection, usually self resolving. Mucosal disease no effective treatment, euthanasia on welfare grounds.

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26
Q

Control of mucosal disease

A

Screening to detect PI and remove.
Vaccination available - can disrupt testing.

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27
Q

Aetiology of liver fluke

A

Fasciola hepatica

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28
Q

Like cycle of liver fluke

A

Ova passed in faeces of infected animals

Hatch into miracidia within 9 days if temp is over 10 degrees

Invade snails to form cercaria after 6-8 weeks

Encyst on blades of grass to form metacercaria

Ingested

Migrate through gut wall and penetrate the liver where they tunnel for 6-8wks before entering bile ducts

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29
Q

Pre-patent period of liver fluke

A

10-12 weeks

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30
Q

How long is the whole life cycle of liver fluke?

A

Minimum of 17-18 weeks

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31
Q

What are the 2 cycles of liver fluke infection?

A

Summer infection of snails from over-wintered miracidia/carrier anials eggs

Autumn infection of snails

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32
Q

Summer infection of snails by liver fluke

A

Infection of snails from over-wintered miracidia or carrier animal’s eggs deposited in spring.

Infect cattle early autumn/winter causing signs from December to March.

Uningested metacercaria are capable of over-wintering.

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33
Q

Autumn infection of snails by liver fluke

A

Infection in the snails completes the following spring giving rise to disease from May to July.

Most snails die over winter so important in milder winters.

Will see more of this with climate change, snails survive milder winters.

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34
Q

What are the signs of liver fluke in cattle?

A

Diarrhoeais the most common presenting sign (often in association with ostertagia).

Chronic ill-thrift and anaemia reported

Weight loss, reduced milk yields and milk solids, also a variably reduced appetite.

Anaemia and submandibular oedema may occur in chronic cases.

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35
Q

Is liver fluke fatal in cattle?

A

rarely fatal on a reasonable plain of nutrition, but is more serious in animals out-wintered receiving little supplementary feed

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36
Q

What disease can follow liver fluke in cattle?

A

Black Disease (Infectious necrotic hepatitis), caused by Clostridium novyi, may occur in some animals as the necrotic tracts in the liver caused by parasite migration favour bacterial growth and toxin production.

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37
Q

Diagnosis of liver fluke in cattle

A

Faecal examination (floatation and sedimentation), faecal coproantigen test

Serology (ELISA) - shows infection within last 9mo

Biochem and haem - hepatocyte damage (GLDH), biliary inflammation (GGT), resultant protein loss, eosinophlia, non-regenerative anaemia

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38
Q

Treatment and control of liver fluke (not actual drugs)

A

Clinically affected animals are treated.

Cattle may be dosed prophylactically just once per year in December.
In wet springs a 2nd dose may be needed in out-wintered stock in May.

For dairy cows a treatment at drying may be a compromise.

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39
Q

Triclabendazole activity against liver fluke

A

Works against all stages from 2 days

Oral/pour on

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40
Q

When can triclabendazole be used in cattle?

A

NOT in lactation

In the dry period (50d mild w/d)

Not within 50d of calving (maiden dairy heifers)

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41
Q

Clostantel activity against liver fluke

A

Effective against adults and immature flukes 3-4wks

Injectable, oral

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42
Q

When can closantel be used in cattle?

A

NOT in lactation

NOT in dry period

NOT in last trimester (pregnant dairy heifers)

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43
Q

Nitroxynil activity against liver fluke

A

Effective against adults and immature fluke

Injectable

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44
Q

When can be nitroxynil be used in cattle?

A

NOT in lactation

NOT in dry period

NOT in last trimester (pregnant dairy heifers)

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45
Q

Albendazole activity against liver fluke

A

Effective against adults

Oral

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46
Q

When can albendazole be used in cattle?

A

In lactation (60hr milk w/d)

In dry period (60hr milk w/d)

In pregnant dairy heifers

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47
Q

Oxyclozanide activity against liver fluke

A

Effective against adult fluke

Oral

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48
Q

When can oxyclozanide be used in cattle?

A

In lactation (72hr milk w/d)

In dry period

In pregnant dairy heifers

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49
Q

Clorsulon activity against liver fluke

A
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50
Q

When can clorsulon be used in cattle?

A

NOT in lactation

In the dry period (60d milkd w/d)

Not within 60d of calving (dairy heifers)

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51
Q

Aetiology of Johnes disease

A

Mycobacterium avium subsp. paratuberculosis (MAP)

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52
Q

Signalment of typical cattle affected by Johnes

A

Over 3yo (peak 4-7yrs)

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53
Q

Transmission of Johnes disease

A

Faecal oral route
Transplacental can occur
Can be via milk and colostrum

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54
Q

Which animals are most likely to be infected with Johnes?

A

Young calves (but then long incubation period)

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55
Q

What can trigger clinical signs of Johnes?

A

stress such as calving, transport and malnutrition

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56
Q

Signs of Johnes

A

Early in the disease course signs are subclinical with poor performance and reduced milk yield in lactating cows.

Usually this progresses to chronic diarrhoea, classically bubbly scour which is intermittent at first, becoming persistent and profuse.

This is followed by weight loss, ill-thrift progressing to severe malabsorption with hypoproteinaemia.

Animals rarely show ventral oedema.

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57
Q

Diagnosis of Johnes

A

Should be possible on clinical grounds alone if previously in herd

Faecal exam (Ziehl-Neilsen stained) - low sensitivity as low nos passed and intermittent shedding

PCR from faeces

Serology - AB not usually detected until infection well established

PM- widespread gross lesions in intestine (thickened of wall and ridged appearance)

Johnin PPD - intradermal skin infection

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58
Q

Control of Johnes

A

Separate calves from their dams at birth (Welfare issues), feeding only clean colostrum from negative dams.

Avoid run off slurry from adult accommodation in calf house.

Store slurry for as long as possible before spreading and put on arable land only.

Allow drinking from only pipe line water.

Cull known positives and isolate suspects.
Cull on poor milk yield and weight loss.

59
Q

Johnes risk level classification

A

J0 - J5

J0 = low risk (green), repeat ELISA -ve (min 2 tests)

J1 = Low risk (green), ELISA -ve but only one test

J2 = low risk (green), ELISA -ve but +ve within previous 3 tests

J3 = High risk (yellow), ELISA -ve/+ve interchangeably

J4 = High risk (yellow), last ELISA +ve, all previous tests -ve

J5 = High risk (red), Repeat ELISA +ve (min 2 tests)

60
Q

Vaccination for Johnes

A

Only allowed in UK under special DEFRA licence if disease established on farm

Live vaccine given ASAP after birth (no older than 1 month)

Reduces no. of organisms excreted in faeces, does not eliminate infection

61
Q

Winter dysentery aetiology

A

Most outbreaks are believed to be due to coronavirus infection, but other viruses may be involved.

Explosive herd outbreaks are not uncommon and some herds may be repeatedly affected.

Typically seen in housed cattle during cold weather and usually affects adult cattle.

Typical outbreaks last about 2 weeks with up to 40% of the herd being affected, causing considerable economic loss.

62
Q

Signs of winter dysentery

A

Sudden onset diarrhoea with slight blood through to visible clots or dysentery.

Strong differential is salmonella.

Infected animals rarely have pyrexia, although they may be depressed, anorexic and lose condition.

Disease may spread rapidly to susceptible animals and clinical signs usually resolve within 2-3 days.

Marked reduction in milk yield, and may be accompanying respiratory signs in up to 50% of cows, with coughing and nasal discharge.

Mortality is not reported.

63
Q

Diagnosis of winter dysentery

A

History and no fever.

Faecal ELISA for coronavirus, often negative due to dilution factor and virus shedding largely preceding any clinical signs.

Antibodies to coronavirus are not uncommon in cattle so single serology is unhelpful. Paired serology 2-4 weeks apart looking for a rising titre.

(BVDv the most likely differential diagnosis).

64
Q

Treatment of winter dysentery

A

Often none is required, self-resolving. If signs are severe consider fluid therapy.

65
Q

Aetiology of malignant catarrhal fever

A

Caused by Ovine Herpes Virus 2 (OHV-2, previously BHV-3) a gamma-herpesvirus carried by healthy sheep.

MCF is an acute fatal condition affecting individuals but may sometimes occurs in outbreaks.

In most cases there is a history of contact with sheep in the previous 3 months.

In some cases it is difficult to differentiate from mucosal disease.

66
Q

Epidemiology of malignant catarrhal fever

A

Incubation around 3-10 weeks, after a history of shared accommodation with sheep particularly at lambing time, therefore disease is often seen around May to June.

Also seen in cattle co-grazing with sheep.

67
Q

Clinical signs of malignant catarrhal fever

A

Pyrexia, enlarged lymph nodes, erosive stomatitis with classic ropes of saliva hanging from the mouth, crusting of the muzzle, constipation followed by diarrhoea, bilateral keratitis, blepharospasm, haematuria and encephalopathy.

Signs last for 3-7 days before the animal dies due to widespread vasculitis (the virus is epitheliotropic).

68
Q

Diagnosis of malignant catarrhal fever

A

Serology using IFAT, there is usually seroconversion by the time the animal is presented for examination.
Occasional peracute cases that have not seroconverted.

PCR for OHV-2 is available.

Gross pathology together with histopathology at post mortem examination is characteristic.

69
Q

Control of malignant catarrhal fever

A

Avoid housing cattle and sheep in the same building.

Avoid cattle access to lambs, placenta and discharge, good hygiene.

Sheep show no signs of the disease.

70
Q

Aetiology of Babesia (red water fever)

A

Due to tick borne infection with Babesia divergens (Ixodes ricinus)

Peak activity of ticks in spring and autumn

Incubation period 1-2 weeks

Cattle born in tick infested areas usually infected early in life.

71
Q

Immunity to Babesia

A

Young cattle born in tick areas are usually infected early in life and they do not develop signs, there is a possible role of colostral antibody.

Repeated challenge may be necessary to maintain immunity that develops or some persistently infected and preimmune.

Immunity may be overcome by massive challenge or stress.

Naive adults brought into a tick area are particularly susceptible.

Disease is usually seen in adults over 2 years of age.

72
Q

Signs of Babesia in cattle

A

Sudden onset acute haemolytic anaemia, pyrexia, raised pulse frequency and strength, rumen stasis, haemoglobulinuria (urine pink to black), pipe-stem diarrhoea due to spasm of anal sphincter and later constipation.

73
Q

Diagnosis of Babesia

A

PCV low, Leishman stain to detect paired divergent organisms lying near the edge of red blood cells.

74
Q

Treatment of Babesia

A

Imidocarb, need to inform Defra when using as it is under a special licence. Blood transfusion, 3-4 litres can be affective even in severe cases.

75
Q

Control of Babesia

A

Imidocarb can be used at a higher dose for prevention, only consider in a major problem area (questionable benefit). Control ticks using pour-ons (deltamethrin)

76
Q

Parasitic gastroenteritis in cattle

A

Occurs largely in the first grazing season and rarely seen in adult cattle.

Significant GI parasite numbers can occasionally be found in animals due to concurrent disease, receiving inadequate nutrition or in poor condition.

The disease has also been identified in show animals or bulls bred for sale that have been reared indoors and not exposed to parasites.

In the UK primarily due to Ostertagia ostertagi but may also involve Cooperia onchophora.

77
Q

Epidemiology of Ostertagia ostertagi

A

L3 over-winter and infect calves grazing the pasture in spring, these larvae are usually cleared by June.

Eggs deposited early in the season as a result of this infection are slow to develop through to L3, but this process accelerates as the season progresses and temperature rises resulting in peak pasture larval contamination in mid July.

Larvae ingested after October become inhibited hypobiotic L4 and over winter inside the calf.

78
Q

Signs of Ostertagia ostertagi

A

Profuse watery diarrhoea is the main clinical sign.
Reduced appetite and poor production can also result.

Type 1 Ostertagiasis: Scouring from mid-July onwards in first grazing season due to massive numbers of L3.

Type 2 Ostertagiasis: Scour towards the end of winter in animals not treated with a larvicidal anthelmintic at the end of the first grazing season prior to housing. Caused by synchronous activation of hypobiotic larvae in the gut. Can be severe with hypoalbuminaemia, anaemia and submandibular oedema. Worm egg counts can be variable.

79
Q

Diagnosis of Ostertagia ostertagi

A

Faecal worm eggs counts for diagnosis (>1,000 egg/g of faeces), counts expected to be high with heavy parasite burden, will depend on the species of parasite, chronicity of disease and the consistency of the faeces.

Total worm counts can be performed on fresh carcase samples of abomasal and intestinal contents.

Pepsin digestion is required to detect many of the immature parasites and should be carried out for suspected type 2 ostertagiasis.

Estimation of serum pepsinogen concentration is a useful biochemical indicator of abomasal glandular inflammation.

Treat with anthelmintics and see if responds.

80
Q

Coccidiosis in cattle

A

Caused by the pathogenic species Eimeria zuernii, E. bovis and E. alabamensis.

Typically affects young calves usually 3-12 weeks old, but can cause problems in older animals with acute onset disease reported, which usually responds spontaneously in a few days.

81
Q

Signs of coccidiosis in cattle

A

Diarrhoea with blood and tenesmus but may be more subtle and chronic.

Variable depression and appetite reduction may also be seen.

Reduced production in dairy cows.

Rarely neurological signs are encountered, and the cause is unknown.

82
Q

Diagnosis of coccidiosis

A

Faecal coccidial oocyst count.

Pathogenic species should be identified as many animals may have high numbers of non-pathogenic species in their faeces.

Histopathology may be useful although mortality is unlikely in adult animals unless there are secondary complications.

83
Q

Treatment of coccidiosis in cattle

A

Potentiated sulphonamides: Act on asexual generation, not sufficient activity against gamonts and limited efficacy against mammalian coccidian but may suppress secondary bacterial infections.

Toltrazuril (Baycox) and Diclazuril (Vecoxan): Acts against various life cycle stages

Decoquinate (Deccox): Acts on sporozoites and trophozoites can be used in control.

84
Q

Rotavirus in cattle

A

Rapidly spreading watery diarrhoea which resolves spontaneously in affected cattle.

85
Q

Clinical signs of rotavirus in cattle

A

Rapid progressive outbreak of watery diarrhoea in adult cattle recover in 3-5 days, reduced milk yield.

86
Q

Diagnosis of rotavirus in cattle

A

Detection of rotavirus in faeces.

87
Q

Nutritional causes of diarrhoea in cattle

A

Ruminal acidosis

Lush pasture

Poor quality roughage

Excess dietary protein

Molybdenosis/copper deficiency

Potato poisoning

Toxins

88
Q

Ruminal acidosis

A

Sudden ingestion of a toxic dose of a carbohydrate rich feed such as wheat, barley or root crops.

Toxic dose depends on degree of processing of the grain and previous experience of the animal.

The typical history is one of either animals breaking into feed stores, piles of grain left when grazing stubble fields, insufficient trough space for cereal beef animals and failure to provide ad-lib intakes, increments in feed provision being too great, or too much feed given in one hit (as may happen on Christmas Eve or weekends)

89
Q

Pathogenesis of ruminal acidosis

A
  1. Ingestion of fermentable carbohydrate, proliferations of Strep. bovis, production of lactic acid, rumen pH falls from 6.5 to 5.5. Destruction of cellulolytitc bacteria and protozoa, and proliferation of Lactobacillus spp. which produces more lactic acid
  2. Increased osmolarity of rumen contents causing haemoconcentration and dehydration as fluid exits the extracellular fluid. Rumen stasis and chemical ruminitis due to high acidity of rumen contents (<pH 4.5). Endotoxin production. Absorption of acid and circulatory collapse. Metabolic acidosis.
  3. Either recovery, lamititis due to endotoxaemia or shock and death. Rumenitis (bacteria or fungal) and possible absorption of bacteria. In some case liver abscessation may follow.
90
Q

Signs of ruminal acidosis

A

In mild cases anorexia, rumen stasis and soft faeces.

In more severe cases profuse watery diarrhoea, possibly with visible grains, a falling body temperature, dehydration and sinking of the eyes, bloat, incoordination and apparent blindness, recumbency and death.

91
Q

Diagnosis of ruminal acidosis

A

History of access to excess carbohydrate feeds.

The heart rate can be used to assess the severity of the condition with 70-80/min mild, 100/min severe, 120+/min very severe.

Measurement of rumen liquor pH of less than 4.5, either by stomach tube, rumenocentesis or post mortem sampling, indicates acidosis.

Biochemistry can be helpful blood gas / Harleco measurement of base deficit or an increased anion gap. [Na++K+]-[Cl-+HCO3-]: Reference range 10-20 mmol/l. Value >30 mmol/l in case of acidosis.

92
Q

Treatment of ruminal acidosis

A

In mild cases:
- remove feed source
- Provide hay or straw only.
- After 6-8 hours if the affected animal is bright and alert it will probably recover.
- Monitor for 24 hours and begin very gradual re-introduction of the ration.

For severe cases:
- separate from the rest of the group,
- penicillin orally,
- multivitamins may assist,
- Magnesium hydroxide (milk of magnesia) drench (Not bicarbonate as it fizzes producing more gas).
- Rumen probiotics may help.
- Intravenous NaHCO3 1.3% or 300ml 8.4% .
- Rumen lavage using wide bore stomach tube.
- Rumenotomy can be difficult when rumen is bloated and full of fluid.
- Empty contents and give isotonic fluids.

In severe outbreaks mortality can be high. Euthanasia if there is a welfare issue.

93
Q

Prevention of ruminal acidosis

A

Cereal beef animals need gradual introduction to their full ration, built up over at least 2-3 weeks, increase the number of feeds per day so that there is cereal left over from previous feed, then go on to ad-lib.

Make sure that there is adequate feed space and plenty of straw available as roughage, a minimum of 1kg per head per day is required.

94
Q

Diarrhoea due to lush pasture

A

More likely to occur in spring in herds that are not buffer fed, causes diarrhoea.

No diagnostic tests other than to rule out other causes.

95
Q

Diarrhoea due to poor quality roughage

A

Poor quality feed availability, diarrhoea and loss of condition, poor production in dairy cows.

No diagnostic tests other than to rule out other causes.

96
Q

Excess dietary protein causing diarrhoea

A

High protein, low energy diet causing diarrhoea and reduced production.

High blood urea may provide supportive evidence.

No definitive diagnostic tests other than to rule out other causes.

97
Q

Molybdenosis/copper deficiency causing diarrhoea

A

Persistent diarrhoea caused by grazing land rich in molybdenum, usually confined to ‘teart’ pastures of Somerset.

Low liver and blood copper and improved health status after copper supplementation support the diagnosis.

98
Q

Potato poising causing diarroea

A

Waste potatoes that are green or decayed and sprouting/seed potatoes can cause (solanine) poisoning in cattle.

Typically nervous signs found including restlessness and incoordination.

Appetite loss, excess salivation, vomiting and diarrhoea or constipation also occurs.

99
Q

Toxic causes of diarrhoea in adult cattle

A

A range of chemicals, plants and mycotoxins can cause enteritis and diarrhoea in adult cattle.

These conditions tend to be rare and diagnosis depends on knowledge of possible exposure with detection of toxin concentrations or causative agents on post mortem examination.

100
Q

Toxic chemicals that can cause diarroea in adult cattle

A

Salt poisoning

Copper poisoning

Lead poisoning

Nitrate poisoning

Arsenic poisoning

Mercury poisoning

101
Q

Salt poisoning

A

Seen on salt marshes and other coastal areas where grazing cattle drink from drainage ditches contaminated by sea water with no alternative water source.

102
Q

Signs of salt poisoning

A

In acute disease there is diarrhoea, thirst, dehydration, prostration and death.

In more chronic cases staggering, muscle tremors, reduced appetite and failure to thrive.

103
Q

Diagnosis of salt poisoning

A

Electrolytes, Na+, Cl- and PCV estimations.

Test water salinity using a conductivity meter.

104
Q

Copper poisoning

A

Diarrhoea is an occasional sign, another sign being a haemolytic crisis occurring causing haematuria and jaundice most consistently.

Diagnosis:
Whole blood copper concentrations >50µmol/l suggestive of toxicity. Liver and kidney copper analysis to confirm diagnosis.

105
Q

Lead poisoning

A

Diarrhoea is a feature of chronic lead toxicity. In addition there is depression, loss of condition and performance and infertility.

Diagnosis:
Lead analysis of blood samples or kidney samples in dead animals.

106
Q

Nitrate poisoning

A

Typically occurs after eating brassicas or after access to fertilisers. Acute toxicity manifests as diarrhoea, abdominal pain, muscle tremors, weakness, dyspnoea, rapid weak pulse, brownish coloured mucous membranes and convulsions.

Diagnosis:
Detection of methaemoglobin in fresh blood.

107
Q

Arsenic poisoning

A

Arsenicals are now rare, but sometimes used in horticulture, also old mine waste used in farm walls can be a source.

Poisoning results in profuse diarrhoea (often haemorrhagic), weakness, salivation, incoordination, vomiting and abdominal pain.

Diagnosis: On PM extremely reddened abomasal mucosa, arsenic detection in rumen content or liver of animals that die. Analysis of blood samples, urine, faeces and milk will detect recent exposure. Test hair sample to detect chronic intoxication.

108
Q

Mercury poisoning

A

Organomercury compounds have been used as seed dressings and intoxication is possible if animals access stores.

Clinical signs include diarrhoea, inappetence, incoordination and blindness.

Diagnosis:
Raised mercury concentration may be detected in blood samples, urine and faeces. Analysis of mercury concentration in samples of liver and kidney possible at PM examination.

109
Q

Toxic plants and fungi causing diarrhoea in adult cattle

A

Mycotoxicosis

Alimentary tract carcinoma/bracken poisoning

Oak/acorn poisoning

Ragwort

Hemlock water sropwort

Dogs mercury

Rhododendron

110
Q

Mycotoxicosis

A

Some fungi produce potentially pathogenic toxins e.g. Fusarium species produce T2 toxin.

Cases result from ingestion of contaminated feed.

Haemorrhagic syndrome seen with T2 toxin results in dullness, anorexia, milk drop, bloody diarrhoea, occasional hair loss and multiple petechial haemorrhages of the mucous membranes.

Death usually follows.

Mycotoxins have been incriminated in the Pyrexia-Pruritis-Haemorrhagic (PPH) syndrome.

111
Q

Alimentary tract carcinoma/bracken poisoning

A

Squamous cell carcinomas of the mouth, pharynx, oesophagus and fore stomachs believed to be caused by chronic exposure to bracken (ptaquiloside toxicity) and papilloma virus.

Only seen in adult cattle, usually over 8 years (suckler cows) 20% of cases also have bladder tumours.

Clinical Signs:
Related to the site of the tumour.

Treatment: None.

112
Q

Oak/acorn poisoning

A

Constipation is seen early in the disease process with diarrhoea often dark/tarry or bloody developing later.

Diagnosis:
Based on detecting acorns in the rumen contents collected at post mortem, can be difficult as disease occurs some time after ingestion. Elevated blood urea and creatinine concentrations are indicative of compromised renal function (used prognostically).

113
Q

Ragwort toxicity

A

Disease is caused by ingestion of pyrrolizidine alkaloid found in ragwort. Toxin causes cross-linkage of DNA, megacytosis and death of hepatocytes with fibrous and portal hypertension.

Signs:
Diarrhoea possibly melaena, tenesmus with or without rectal prolapsed, weight loss. Hepatic encephalopathy. Poor prognosis once clinical signs are present.

Diagnosis:
Raised GGT. Liver biopsy, histopathology.

114
Q

Hemlock water dropwort toxicity

A

Diarrhoea, abdominal pain, excess salivation or foaming of the mouth, hyperpnoea, dilated nostrils, bellowing, pupillary dilation, rapid pulse, staggering gait, circling, muscle tremors and convulsions.

115
Q

Dogs mercury toxicity

A

Watery diarrhoea, sometimes preceded by constipation, salivation and loss of appetite. Later weakness, jaundice and production of pinkish or blood-stained urine.

116
Q

Rhododendron toxicity

A

Principle signs are diarrhoea, depression, anorexia, salivation, abdominal pain, bloat, vomiting (sometimes projectile) and dyspnoea.

117
Q

Miscellaneous causes of diarrhoea in adult cattle

A

Endotoxaemia

Left displaced abomasum

Periotnitis

Renal amyloidosis

Haemorrhagic bowel sydrome/jejunal haemorrhagic syndrome

Fat necrosis

Cold cow syndrome

Clostridium tertium

Yersinia pseudotuberculosis

Escherichia fergusonia

118
Q

Endotoxaemia

A

Toxic conditions such as coliform mastitis, metritis or other co-incidental illnesses may cause signs of acute diarrhoea or dysentery.

Diagnosis based on clinical history and failure to identify other causes of diarrhoea.

119
Q

Peritonitis aetiology

A

Numerous causes of peritonitis including traumatic reticulitis/pericarditis, rupture of the uterus or vagina, leaking of liver or umbilical abscesses, abomasal ulceration, penetration of the abdomen, or following surgery.

In acute diffuse peritonitis fluid moves into the peritoneal cavity and the gut becomes atonic.

Haemoconcentration, toxaemia and shock develop.

120
Q

Clinical signs of peritonitis

A

Severity relates to the degree of sepsis (localised to diffuse), tachycardia (Heart rate 100-120/min), pyrexia followed by falling temperature as toxaemia develops, rumen and gut stasis, pain with spontaneous grunting, distension of the abdomen, foul diarrhoea and dull “pings” on abdominal auscultation

121
Q

Diagnosis of peritonitis

A

Haematology: Can be useful but cattle may have normal blood picture even when close to death. May see neutrophilia, raised total WBC count, raised globulin:albumen ratio, raised fibrinogen.

Abdomenocentesis: Very useful in acute diffuse peritonitis. Findings include turbid, pus, fibrin clumps, total protein >50g/l, >40% neutrophils.

122
Q

Treatment of peritonitis

A

Often disappointing response when signs are severe need to be aggressive or euthanase the affected animal.

Fluid therapy: Hypertonic 3l, or isotonic fluids 40l.

NSAIDs

Antibiotics: High levels for at least 14 days. Intraperitoneal antibiotics probably of no benefit over intravenous dosage.

Peritoneal lavage: May be attempted.

123
Q

Renal amyloidosis aetiology

A

A disease of older cattle that is characterised by renal enlargement, profuse diarrhoea and subcutaneous oedema.

Sporadic cases are seen in cattle usually over 5 years old often evident shortly after calving and commonly with a history of a long standing suppurative illness (lameness, mastitis or endometritis).

124
Q

Signs of amyloidosis

A

Profuse diarrhoea due to amyloid deposition and oedema, subcutaneous oedema in submandibular, pre-sternal and ventral abdomen regions.

Thin but bright and afebrile.

Enlarged kidney is palpable per rectum.

Affected animals do not usually survive for more than a month once clinical signs develop.

125
Q

Diagnosis of renal amyloidosis

A

Clinical signs.

Urinalysis reveals proteinuria, and blood biochemistry: hypoalbuminaemia (<10g/l), uraemia >30mmol/l.

Histopathology required to confirm and differentiate from nephritis and nephrosis.

126
Q

Treatment of renal amyloidosis

A

None

127
Q

Aetiology of haemorrhagic bowel syndrome/jejunal haemorrhagic syndrome

A

Caused by Clostridium perfringens type A.

Acute collapse and death of dairy cows, usually in early lactation.

128
Q

Clinical signs of haemorrhagic bowel syndrome/jejunal haemorrhagic syndrome

A

Acute onset depression, reduced milk production, tachycardia, ruminal stasis, abdominal distension and tar-like bloody faeces rather than overt diarrhoea.

Usually death occurs within 6-36 hours of animals showing clinical signs.

129
Q

Diagnosis of haemorrhagic bowel syndrome/jejunal haemorrhagic syndrome

A

PM examination confirms jejunal haemorrhage, isolation of Clostridium perfringens on anaerobic culture and exclusion of alternative diagnosis.

130
Q

Fat necrosis aetiology

A

Seen in adults usually 2-3 months following calving in animals that were overfat in late pregnancy.

Calcified deposits develop in mesorectum, mesocolon, intrapelvic fat and mesenteric fat.

Diarrhoea is due to impaired venous return and compression of the rectum.

131
Q

Diagnosis of fat necrosis

A

By rectal examination and presence of solid multinodular masses in the pelvic cavity.

(May feel like a mummified foetus on rectal examination).

132
Q

Treatment of fat necrosis

A

Some cases respond to corticosteroids, some may spontaneously regress, others do not.

133
Q

Cold cow syndrome

A

Uncommon sporadic reports of outbreaks of diarrhoea in dairy herds in spring after turn-out, sometimes associated with particular pastures on some farms.

134
Q

Clinical signs of cold cow syndrome

A

Ataxia or drunkenness, anorexia, depression, hyperpnoea, in some cases animals are cold to touch, there is milk drop, profuse diarrhoea, perineal oedema and collapse.

135
Q

Treatment of cold sow syndrome

A

Move cows to another field, usually a rapid response.

Fluid therapy in severe cases may be required.

136
Q

Clostridium tertium causing diarrhoea in cattle

A

Originally isolated from fattening cattle showing rapid onset ataxia and death within 12 hours.

Experimental infection of calves has been shown to induce diarrhoea.

137
Q

Clinical signs of Clostridium tertium

A

Haemorrhagic enteritis, diarrhoea usually bloody

138
Q

Diagnosis of Clostridium tertium

A

Anaerobic bacterial culture of faeces or intestinal samples collected at PM

139
Q

Yersinia pseudotuberculosis

A

Outbreaks have been reported in cattle on water-logged pastures in Australia in winter and early spring. Not typically described as a UK problem

140
Q

Clinical sign sof yersinia pseudotuberculosis

A

Profuse foul smelling watery brown-green coloured diarrhoea, which may be sometimes blood tinged.

141
Q

Diagnosis of yersinia pseudotuberculosis

A

Bacterial culture and histopathology demonstrating necrotising entercolitis.

142
Q

Escherichia fergusonii

A

E. fergusonii has been found to be the cause of sporadic cases of diarrhoea, mastitis and abortion.

143
Q

Diagnosis of Escherichia fergusoni

A

Based on the isolation of E. fergusonii in diagnostic samples in the absence of other recognised infectious or parasitic causes.

Cattle I (38 decks)

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