Diarrhoea in adult cattle Flashcards

Question

Treatment of mucosal disease

Answer 1

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

Answer 2

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

Answer 3

Fasciola hepatica

Answer 4

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

Answer 5

10-12 weeks

Answer 6

Minimum of 17-18 weeks

Answer 7

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

Answer 8

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.

Answer 9

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.

Answer 10

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.

Answer 11

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

Answer 12

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.

Answer 13

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

Answer 14

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.

Answer 15

Works against all stages from 2 days Oral/pour on

Answer 16

NOT in lactation In the dry period (50d mild w/d) Not within 50d of calving (maiden dairy heifers)

Answer 17

Effective against adults and immature flukes 3-4wks Injectable, oral

Answer 18

NOT in lactation NOT in dry period NOT in last trimester (pregnant dairy heifers)

Answer 19

Effective against adults and immature fluke Injectable

Answer 20

NOT in lactation NOT in dry period NOT in last trimester (pregnant dairy heifers)

Answer 21

Effective against adults Oral

Answer 22

In lactation (60hr milk w/d) In dry period (60hr milk w/d) In pregnant dairy heifers

Answer 23

Effective against adult fluke Oral

Answer 24

In lactation (72hr milk w/d) In dry period In pregnant dairy heifers

Answer 25

NOT in lactation In the dry period (60d milkd w/d) Not within 60d of calving (dairy heifers)

Answer 26

Mycobacterium avium subsp. paratuberculosis (MAP)

Answer 27

Over 3yo (peak 4-7yrs)

Answer 28

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

Answer 29

Young calves (but then long incubation period)

Answer 30

stress such as calving, transport and malnutrition

Answer 31

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.

Answer 32

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

Answer 33

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.

Answer 34

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)

Answer 35

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

Answer 36

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.

Answer 37

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.

Answer 38

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).

Answer 39

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

Answer 40

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.

Answer 41

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.

Answer 42

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).

Answer 43

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.

Answer 44

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.

Answer 45

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.

Answer 46

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.

Answer 47

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.

Answer 48

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

Answer 49

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.

Answer 50

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)

Answer 51

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.

Answer 52

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.

Answer 53

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.

Answer 54

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.

Answer 55

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.

Answer 56

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.

Answer 57

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.

Answer 58

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.

Answer 59

Rapidly spreading watery diarrhoea which resolves spontaneously in affected cattle.

Answer 60

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

Answer 61

Detection of rotavirus in faeces.

Answer 62

Ruminal acidosis Lush pasture Poor quality roughage Excess dietary protein Molybdenosis/copper deficiency Potato poisoning Toxins

Answer 63

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)

Answer 64

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 (

Answer 65

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.

Answer 66

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.

Answer 67

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.

Answer 68

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.

Answer 69

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.

Answer 70

Poor quality feed availability, diarrhoea and loss of condition, poor production in dairy cows. No diagnostic tests other than to rule out other causes.

Answer 71

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.

Answer 72

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.

Answer 73

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.

Answer 74

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.

Answer 75

Salt poisoning Copper poisoning Lead poisoning Nitrate poisoning Arsenic poisoning Mercury poisoning

Answer 76

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

Answer 77

In acute disease there is diarrhoea, thirst, dehydration, prostration and death. In more chronic cases staggering, muscle tremors, reduced appetite and failure to thrive.

Answer 78

Electrolytes, Na+, Cl- and PCV estimations. Test water salinity using a conductivity meter.

Answer 79

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.

Answer 80

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.

Answer 81

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.

Answer 82

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.

Answer 83

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.

Answer 84

Mycotoxicosis Alimentary tract carcinoma/bracken poisoning Oak/acorn poisoning Ragwort Hemlock water sropwort Dogs mercury Rhododendron

Answer 85

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.

Answer 86

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.

Answer 87

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).

Answer 88

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.

Answer 89

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.

Answer 90

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

Answer 91

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

Answer 92

Endotoxaemia Left displaced abomasum Periotnitis Renal amyloidosis Haemorrhagic bowel sydrome/jejunal haemorrhagic syndrome Fat necrosis Cold cow syndrome Clostridium tertium Yersinia pseudotuberculosis Escherichia fergusonia

Answer 93

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.

Answer 94

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.

Answer 95

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

Answer 96

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.

Answer 97

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.

Answer 98

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).

Answer 99

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.

Answer 100

Clinical signs. Urinalysis reveals proteinuria, and blood biochemistry: hypoalbuminaemia (<10g/l), uraemia >30mmol/l. Histopathology required to confirm and differentiate from nephritis and nephrosis.

Answer 101

Caused by Clostridium perfringens type A. Acute collapse and death of dairy cows, usually in early lactation.

Answer 102

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.

Answer 103

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

Answer 104

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.

Answer 105

By rectal examination and presence of solid multinodular masses in the pelvic cavity. (May feel like a mummified foetus on rectal examination).

Answer 106

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

Answer 107

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

Answer 108

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

Answer 109

Move cows to another field, usually a rapid response. Fluid therapy in severe cases may be required.

Answer 110

Originally isolated from fattening cattle showing rapid onset ataxia and death within 12 hours. Experimental infection of calves has been shown to induce diarrhoea.

Answer 111

Haemorrhagic enteritis, diarrhoea usually bloody

Answer 112

Anaerobic bacterial culture of faeces or intestinal samples collected at PM

Answer 113

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

Answer 114

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

Answer 115

Bacterial culture and histopathology demonstrating necrotising entercolitis.

Answer 116

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

Answer 117

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

Diarrhoea in adult cattle Flashcards

(143 cards)