The distribution of gross lesions of tuberculosis caused by Mycobacterium bovis in feral ferrets (Mustela furo) from Otago, New Zealand

The distribution of gross lesions of Mycobacterium bovis was examined in 94 tuberculous feral ferrets (Mustela furo) collected from 1992 to 1995 from areas of Otago endemic for bovine tuberculosis. Overall, 56.4% of tuberculous ferrets had single-site lesions, 24.5% had multiple infections and 19.1% had generalised infections. The mesenteric lymph node was the most common site of infection (34.5% of all lesions), with the retropharyngeal (17%) and the prescapular lymph nodes (16.4%) also frequently infected. Only 2.9% of lesions involved the respiratory tract. Of single-site lesions, 60.4% were in the mesenteric lymph node. The high proportion of lesions in the alimentary tract suggests that the ingestion of infectious material, possibly carrion or prey, is an important source of infection. Peripheral lymph nodes contributed to 24.5% of all infections, suggesting that within species transmission by social contact such as fighting and mating also occurs. Open and respiratory lesions were found in 11.7% of tuberculous ferrets, which suggests that ferrets are potentially infectious and therefore may be involved in the transmission of bovine tuberculosis to domestic stock and other mammals. The distribution of gross M. bovis lesions in ferrets is compared to those observed in possums (Trichosurus vulpecula) and badgers (Meles meles).     

Intoxication in cattle caused by a batch of sugar beet pulp (author's transl)]

During the period from Dec. 7th 1972 to Jan. 8th 1973 76 cattle deaths were reported in 20 herds on the island of M?on and the adjacent south-eastern area of Sealand. The disease was characterized by a sudden onset and a rapid and invariably fatal course. Initially, there was a loss of appetite, depression, excessive salivation and incoordination. These symptoms progressed to paralysis and, in some animals, trmor and convulsions. Death usually ensued less than 2 hours after the first observation of symptoms. Losses in the herds varied from 1 to 12 animals. In herds with multiple incidents the majority of deaths occurred in the 24-hour-period following observation of the first case. Pathology: Gross lesions were few and inconclusive. Histology revealed marked dilatation of cerebral and maningeal blood vessels (arterioles, venoles and capillaries), with perivascular edema and haemorrhage. Adjacent neurons and glia cells showed various degrees of degeneration, apparently secondary to the vascular lesion. In all affected herds sugar beet pulp from one particular sugar mill had been used during the period preceding the outbreak. The syndrome was reproduced by feeding sugar beet pulp from this batch to two heifers. The heifers showed symptoms after 19 and 32 days' feeding, resp. and died after a few hours. Clinical and pathological features were identical with those observed in the spontaneous disease. Thus, it was proved that the particular batch of pulp was responsible for the disease. The investigation did not, however, reveal a toxic factor in this batch. Analyses for lead, arsenic, mercury, nitrite, alkyl phosphates, chlorinated insecticides and Cl. botulinum toxin were negative. Batches of the sugar beet pulp showed pronounced microbial deterioration, the flora being dominated by yeasts and filamentous fungi (moulds). Several species of fungi have been isolated but so fat their possible role in the etiology of the syndrome remains unsettled. The syndrome bears some resemblance to cerebrocortical necrosis (C.C.N.) but differs in several clinical and pathological details. It is tentatively suggested that the beet pulp may have contained one or more toxic substances that interfere with microbial activity in the rumen, resulting in a disturbance of synthesis or absorption of essential metabolites. The clinical, epidemiological and pathological findings are compatible with the hypothesis that the syndrome might be due to fungal toxins. Accordingly, the isolated fungi are now being studied in more detail.     

Prunus Stem Pitting

Prunus stem pitting disease was first described and recognized as a specific, infectious disease in 1967 and is now known to affect a number of Prunus species. Apricot trees affected by stem pitting show stunted terminal growth and chlorotic, drooping leaves that curl upward and lengthwise. The lower trunk may become enlarged at ground level or below with very thick, spongy bark. Removal of the bark from the affected lower trunk reveals pits and grooves on the woody cylinder. Wood pitting begins below ground, then gradually spreads into the roots and the trunk above ground. Stem pitting is caused by certain strains of the tomato ringspot virus. The causal agent is soil-borne and also graft transmissible but is not uniformly distributed through infected trees. Naturally infected apricot trees may show a slow decline, or rapid dieback of the terminal growth. The severity of symptoms is determined by the cultivar and the strain of tomato ringspot virus. Control measures for Prunus stem pitting should include: use of propagation material from healthy trees and rogueing of pitted trees in nurseries and orchards. Repeated use of infested nursery sites for stone fruit nurseries should be avoided     

The reproductive performance of New Zealand dairy cows after induction of calving

Induction of premature calving contributes to subsequent failure of some dairy cows to become pregnant and calve. Of a sample of 276 cows 16.7% failed to calve the following year despite the occurrence of oestrus relatively early after calving, and several matings. The cows which did conceive had a normal first-mating calving rate of 53.9%, requiring 1.7 matings per pregnancy. Two of the 18 survey herds under consideration suffered lengthy calving-to-first-mating oestrus intervals, presumably because the induced cows were in poor condition at the time of calving.     

Porcine parvovirus infection in a commercial piggery

Abstract

Extract

Madam:– We have recently been involved in a consultative role with a 60-sow commercial piggery. Over the year preceding the incident recorded here, this unit had approximately doubled in size by the purchase of improved large white gilts. An infertility problem involving irregular returns to service and small litter sizes was first noted around Christmas 1984. In early January 1985 all the adult stock were bled and serological tests undertaken. There was no evidence of infection with Aujeszky's disease virus or leptospires, but 42 sows had haemagglutination inhibition (HI) titres(2 Joo, H.O., Donaldson-Wood, C. and Johnson, R.H. 1976. A standardised haemagglutination inhibition test for porcine parvovirus antibody. Aust. vet. J., 52: 422–424.  [Google Scholar]) of >320 against porcine parvovirus (PP), and were considered to have been actively infected. (1 Johnston, R.H., Donaldson-Wood, C., Joo, H.O. and Allender, U. 1976. Observations on the epidemiology of porcine parvovirus. Aust. vet. J., 52: 80–84.  [Google Scholar]) Seventeen other gilts and sows in their second pregnancy had titres ?320 and were considered to be still susceptible to infection. These animals were bled again 75 days later and HI tests on the paired sera showed that 15 of the 17 had now scroconverted (minimum titre 1,280). Eleven of these animals were in early to mid-pregnancy during the period of seroconversion. Five of these animals subsequently failed to farrow, and the remaining six produced a mean of only 6.5 (S.D. 2.8) live piglets at birth. In contrast the two animals which did not seroconvert, and four other previously infected gilts with HI titre of >10,240 at the first bleeding, produced a mean of 9.8 (S.D. 1.7) live piglets. This was considered a satisfactory live birth rate for this age group, and was significantly higher (Student's t-test; P<0.05) than for the six sows which seroconverted and produced live pigs.