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Cattle

Parasitic conditions

In the far north of Scotland, chronic liver fluke problems were diagnosed in seven herds of beef cows based on the demonstration of fluke eggs in faeces. In two cases, the disease had not been seen on the farms before. In another case, yearling cattle housed in December 2005 were ill thriven and scouring. They had not been treated with a flukicide at housing.

Reproductive tract conditions

The St Boswells Disease Surveillance Centre (DSC) investigated a stillbirth / ‘weak calf syndrome’ problem on one unit. A total of three of the 21 calved heifers and one of the 85 cows calving to a Charolais bull were affected. The bodily condition of the heifers and cows was said to be generally good, although a number of animals were recognised as being over-fat. Two calves were submitted for examination. The first of these was born to a heifer and had lived for a few hours after an assisted birth. This calf had been skinned prior to submission, but the carcase still weighed 46kg. It showed oedema of the muzzle and haemarthrosis of both shoulders. Examination of the brain revealed intense congestion of the meninges. The second calf examined was born to a cow and had died some 24 hours after an assisted calving. In this case the skinned calf carcase weighed 52.5 kg and was 100 cm long from crown to tail head. Internally three of the ribs on the left side of the chest were fractured at the junction with the sternum and there was associated bruising of soft tissues. Again blood was present within the synovial fluid of the left shoulder, right shoulder and right elbow joints. The lungs were expanded but oedematous and heavy, and the meninges were acutely congested. Further bacteriology, serology and histopathology failed to identify an infectious cause in either case and it was concluded that the gross findings were consistent with dystocia. The calf body weight in the first case was high for a heifer's calf and this, along with over condition in the heifers, was identified as the probable cause of the problem. Over-fat animals, apart from the physical barrier of fat in the pelvis, may also suffer from fat mobilisation, which reduces the available magnesium and in turn impacts on calcium mobilisation. Reduced calcium levels reduce the ability of the uterus to contract properly and proceed quickly through second stage parturition.

An Aberdeen Angus calf was submitted to the Dumfries centre from a suckler herd which had experienced 3 cases of stillbirth / ‘weak calf syndrome’. This calf had lived for 24 hours. Histopathological changes of a non-suppurative hepatitis and bronchopneumonia suggested a systemic infection and Bovine Virus Diarrhoea (BVD) virus was isolated from the thyroid gland by cell culture. Follow up sampling of the spring calf crop by a combination of antigen ELISA and PCR testing has identified one other calf persistently infected with BVD virus and the breeding herd was vaccinated prior to the breeding season.

The fourth abortion in a dairy herd in Dumfries and Galloway vaccinating for BVD and Bovine Herpes Virus type 1 (BHV1) was investigated. The calf was 3 weeks premature and the thyroid weighed 24g. Histopathology showed that there was no colloid present within cells of the thyroid gland but there was also evidence of a bacterial infection in the other tissues. The thyroid iodine content was low at 920mg/kg DM (normal range 1200 –2000mg/kg DM).

Generalised and systemic conditions

A one-year-old Aberdeen Angus cross heifer tested seropositive at the Edinburgh DSC for Malignant Catarrhal Fever (MCF). Its clinical signs comprised vague malaise, corneal oedema, enlargement of sub-cutaneous lymph nodes and skin lesions behind both elbows.

An eight-day-old Charolais cross calf was submitted for post mortem examination to the Perth DSC. This was the fourth recent death in this age group and the calf had been pyrexic and swaying on its feet. On examination, the carcass was jaundiced with bilateral cataracts. The liver was swollen and very firm and all joints examined had an excess of straw-coloured synovial fluid, some with fibrin tags. There was no gross evidence of enteritis. Salmonella Dublin was isolated from the liver and intestines. Salmonella Dublin had been isolated on the farm from scouring calves six months previously.

Four deaths had occurred over one month in a group of one-month-old Ayrshire calves. Pneumonia signs had been seen despite vaccination with a multivalent respiratory vaccine and antibiotic treatment with tilmicosin. A typical calf was submitted for post mortem examination to the Dumfries centre with anteroventral lung consolidation, a navel ill with abomasal adhesions, a thickened large intestine with a pasty scour, enlarged mesenteric lymph nodes and pale renal cortices. Salmonella Dublin was isolated in septicaemic distribution.

In Invernesshire, a three-day-old Charolais cross calf was found out-stretched with dysentery before it was euthanased. It was the third calf to die between two and five days of age. At postmortem examination there was marked hyperaemia of the small intestines. The abomasum contained some blood-tinged fluid and there was an area of oedema and haemorrhage in the abomasal mucosa. Neuropathology demonstrated large well-demarcated areas of haemorrhagic malacia in the internal capsule, thalamus and midbrain. The malacia in the midbrain was bilateral and approximately symmetrical. There was also extensive perivascular serum leakage in cerebral white matter cores, internal capsule, thalamus, midbrain, cerebellar peduncles and cerebellar white matter. The findings were consistent with Focal Symmetrical Encephalomalacia due to the epsilon toxin of Clostridium perfringens.

Toxic conditions

A one and a half-year-old bullock was submitted to the Perth centre, one of three found dead in the same morning after being put into a new field of fodder rape the previous day. The trachea was full of froth with multiple mucosal petechiae. The lungs were congested and emphysematous. The abomasum had a very congested mucosa and the intestines were grossly normal with well-formed faeces at the anus. Multiple resolving and suppurative abscesses were present throughout the liver parenchyma and the kidneys appeared autolysed. The blood was very dark in colour raising the possibility of nitrate poisoning. (Other signs suggestive of nitrate poisoning are petechial haemorrhages in the trachea, and congestion and haemorrhage of the gastrointestinal mucosa). Histopathology indicated acute nephropathy, acute pulmonary congestive changes and myocardial oedema supporting the diagnosis of nitrate toxicity. Liver lesions were suspected of being incidental in this case.

At the Edinburgh DSC, an investigation is ongoing into copper toxicity as a possible contributory cause of an unacceptable high mortality rate in Jersey dairy calves. For several years, the mortality rate in the pre-weaned calves has been higher than acceptable and at the the start of this investigation, three of the current 16 pre-weaned calves had died in the previous month. Affected calves have died after vague signs of ill-thrift and diarrhoea. Three calves, aged between one week and 10 weeks of age, were submitted for post mortem examination: high liver and kidney copper levels were detected, 18,200 – 21,000 and 393 – 792 m mol/kg respectively (normal respective reference ranges are 314-7850 and 141-314). Low-grade hepatopathy and enteropathy were confirmed in these calves although no enteropathogens were detected. Tests on the surviving calves have confirmed rotavirus and cryptosporidium infection and a degree of liver dysfunction; other factors in the investigation include calf feed analyses and assessing the calves’ immune, trace element and enteropathogen status. Jersey calves are known to be particularly susceptible to copper toxicity, and the hypothesis is that the problem is a combination of low-grade chronic copper toxicity combined with sporadic infections with enteropathogens.

Musculoskeletal Disease

An outbreak of chondrodystrophy was investigated in a Dumfries and Galloway suckler herd of 40 Aberdeen Angus and Saler cross cows in calf to two Charolais bulls. Two typical calves had been born two years earlier when only pit silage was being fed. In this instance 80% of calves born were affected with the predominant symptom being hyperextension of the fetlocks joints. The worst affected calves were unable to stand initially or walked on their accessory digits (Figure 1; click on PDF link on the right). Most straightened up within two to three days but others took two weeks. Only six of the total calf crop had obvious shortening of the long bones and none was noted with jaw deformities. One calf had two skin melanomas. There was no evidence of BVD involvement and no mycotoxins were detected in samples of silage being fed. The affected calves were low in manganese (26 – 49 nmol/l, normal range of 78 – 168nmol/l) but the silage contained adequate amounts – 118mg/kg DM (average 70mg/kg DM). Five of eight cows tested had low vitamin A levels (0.34 – 0.65umol/l, normal range 0.87-1.75umol/l). No significance was placed on this, as there were no other signs of vitamin A deficiency. This was an unusual outbreak due to the number of affected calves, the predominance of hyperextension, the fact that many were born in early spring (between the 27th February and 30th April) and that the diet fed was not typical of these cases. A 50:50 mix of arable silage: grass silage was used from housing until mid December. Approximately 10% straw was added to this along with minerals. After this point grass silage/straw/minerals were used.

Mammary diseases

Three milk samples were submitted from a Friesian herd experiencing problems with high cell counts. Staphylococcus aureus was isolated from two of the samples and Mycobacterium fortuitum was isolated as a profuse growth from the third case. The latter organism is an environmental organism, which can cause severe mastitis and usually does not respond to treatment.

Contact

Mr Colin Mason
SAC (Scottish Agricultural College) Work St Mary's Industrial Estate,
Dumfries
DG1 1DX

TelWork 01387 267260
Fax 01387 250028

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