Culicoides from Western Turkey in relation to bluetongue disease of sheep and cattle.
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In order to investigate the contribution of lymphocytes to interstitial lung disease in animals with visna-maedi infection, we studied in parallel bronchoalveolar cells and lung tissue from slaughter-house animals (n = 29) and from colostrum-deprived lambs transtracheally inoculated with field isolates of visna-maedi virus (n = 9) or saline (n = 6). Lymphocyte subpopulations were identified in bronchoalveolar lavage by immunofluorescence and flow cytometry analysis and in lung tissue using indirect immunohistochemistry. In infected animals a lymphocytic alveolitis containing CD4 and CD8 lymphocytes was observed. Peribronchovascular lymphoid nodules comprise mostly CD4 lymphocytes. Alveolar lymphocytes of both subsets displayed increased expression of MHC class II antigens in animals with naturally occurring maedi but not in experimentally infected ones. A sequential process of lymphocyte attraction and activation is likely to occur in vivo as part of the alveolitis.
Eight ewes, divided into two groups based on age, with group 1 7-8 and group 2 1-3 years old, respectively, were administered 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) intravenously (IV) at cumulative doses of 2.0 to 34.6 mg/kg body weight. Two group 1 sheep, given cumulative doses of 2 and 8.5 mg/kg, developed persistent severe neurologic signs of body stiffness and rigidity, paucity of movement, intention body tremors, and abnormal body posture and stance similar to those signs in MPTP-induced disease in people and primates. After their acute onset, these persistent signs were nonprogressive up to the observation period of 32 days post infusion. None of the younger ewes had persistent neurologic symptoms at equivalent cumulative doses (9.0 mg/kg). The only pathologic changes were microscopic lesions in the central nervous system, consisting of bilaterally symmetrical neuronal chromatolysis and necrosis limited to the substantia nigra and locus ceruleus. These lesions were found in two persistently affected and two younger sheep, suggesting age-based differences in dose response and the threshold of clinical expression of disease. Serum MPTP half-life was 11 days. Thus sheep exposed to MPTP could be an alternative model to the primate for the comparative study of clinical, pathologic, and biochemical mechanisms in MPTP neurotoxicity and Parkinson's disease in people.
A nationwide survey of the occurrence of scrapie in France during the 12-year period 1968-1979 has shown the disease to be more widespread than previously thought. The data suggest that certain sheep raising practices, such as transhumance (nomadic grazing), pen and pasture alternations, and use of animals for milk production, may play a possible role in disease prevalence.
Starting from the clinical symptoms and the pathological-anatomical changes hints are given on the diagnosis of the rinderpest and how to distinguish it from other diseases. The paper discusses the differential diagnosis of the rinderpest with respect to mucosal disease, malignent catarrhal fever, Nairobi sheep disease, salmonellosis, pasteurellosis, and coccidiosis.
The sheep and goat pox viruses isolated in Kenya are not host specific as in the Middle East and India. The virus strains from one species are of a similar pathogenicity for the other, and the same virus appears to occur in the field outbreaks in mixed flocks. A silent infection with no skin lesions occurs in the field outbreaks. The virus grows well in lamb testis cell cultures, it does not haemadsorb nor haemagglutinate and is ether sensitive. Most strains could not readily be adapted to grow on the chorioallantoic membrane of embryonated eggs; one isolation only was made in this way. Staining of the virus inclusions showed that they were of DNA; the virus resembled that of lumpy skin disease in many characteristics. It was possible to cross-protect both species with virus of sheep or goat origin. A vaccine was made from tissue culture virus adsorped onto aluminium hydroxide gel and treated with formalin.
Ovine neuronal ceroid-lipofuscinosis represents another well studied model for human neuronal ceroid-lipofuscinosis (NCL). Accumulation of abnormal lipopigments in various retinal neurons, and loss of photoreceptors are similar to the lesions in human juvenile NCL and indicate that the sheep is a suitable model in which to study the pathogenesis of both NCL lipopigment formation and retinopathia pigmentosa. However, this latter process is not as advanced in NCL-diseased sheep as in human patients but far more obvious than in canine NCL in which retinopathy cannot be unequivocally documented. Ovine NCL shares with canine NCL peculiar lamellar inclusions in retinal pigment epithelial cells which may indicate an impaired catabolism of phagocytosed photoreceptor outer segments. As the peculiar lamellar inclusions seen in RPE cells of both NCL-diseased sheep and dogs do not very much resemble the phagocytosed photoreceptor outer segments, it may be assumed that in NCL the final steps in complete removal of these phagocytosed photoreceptor outer segments are also defective.
In the course of investigating suspected cases of viral haemorrhagic fever in South Africa patients were encountered who had been bitten by ticks, but who lacked evidence of infection with Crimean-Congo haemorrhagic fever (CCHF) virus or non-viral tick-borne agents. Cattle sera were tested by enzyme-linked immunoassay to determine whether tick-borne viruses other than CCHF occur in the country. The prevalence of antibody in cattle sera was 905/2116 (42.8%) for CCHF virus, 70/1358 (5.2%) for Dugbe, 21/1358 (1.5%) for louping ill, 6/450 (1.3%) for West Nile, 7/1358 (0.5%) for Nairobi sheep disease, 3/625 (0.5%) for Kadam and 2/450 (0.4%) for Chenuda. No reactions were recorded with Hazara, Bahig, Bhanja, Thogoto and Dhori viruses. The CCHF findings confirmed previous observations that the virus is widely prevalent within the distribution range of ticks of the genus Hyalomma, while antibody activity to Dugbe antigen was detected only within the distribution range of the tick Amblyomma hebraeum. Cross-reactivity for the nairoviruses, Hazara, Nairobi sheep disease and Dugbe, was detected in serum samples from 3/72 human patients with confirmed CCHF infection, and serum from 1/162 other patients reacted monospecifically with Dugbe antigen. The latter patient suffered from febrile illness with prolonged thrombocytopenia.
Copper homeostasis in mammals is maintained by the balance of dietary intake and copper excretion via the bile. Sheep have a variant copper phenotype and do not efficiently excrete copper by this mechanism, often resulting in excessive copper accumulation in the liver. The Wilson disease protein (ATP7B) is a copper transporting P-type ATPase that is responsible for the efflux of hepatic copper into the bile. To investigate the role of ATP7B in the sheep copper accumulation phenotype, the cDNA encoding the ovine homologue of ATP7B was isolated and sequenced and the gene was localised by fluorescence in situ hybridisation to chromosome 10. The 6.3 kb cDNA encoded a predicted protein of 1444 amino acids which included all of the functional domains characteristic of copper transporting P-type ATPases. ATP7B mRNA was expressed primarily in the liver with lower levels present in the intestine, hypothalamus and ovary. A splice variant of ATP7B mRNA, which was expressed in the liver and comprised approximately 10% of the total ATP7B mRNA pool, also was isolated. The results suggest that ATP7B is produced in the sheep and that the tendency to accumulate copper in the liver is not due to a gross alteration in the structure or expression of ATP7B.
During a large neuropathological survey of clinically normal sheep for evidence of scrapie, three adult Romney ewes from the same farm were found to have populations of distended neurons containing granular eosinophilic storage material. The affected neurons were confined to the striatum. The granules had the tinctorial properties of glycolipid and the ultrastructural appearance of spherical bodies containing concentric membranous whorls. The bodies resembled those of GM1 gangliosidosis. The restricted neuroanatomical distribution of changes together with the age of the sheep suggests a similarity to human type 3 GM1 gangliosidosis, which has not previously been reported in animals.
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OBJECTIVE: To estimate the likely geographical distribution and flock-prevalence of ovine Johne's disease (OJD) in Australia. DESIGN: A cross-sectional study design was used. PROCEDURE: The results of abattoir surveillance for OJD carried out during 2000 were analysed to estimate the prevalence of infected flocks in three regions of New South Wales and in other States. A Bayesian approach was used to adjust apparent prevalence estimates for the assumed flock-sensitivity and flock-specificity of abattoir surveillance, and to allow for uncertainty about the true values of these measures. RESULTS: The 95% probability limits for flock-prevalence at 31 December 2000 were 0.04%-1.5%, 8%-15% and 29%-39% for low, moderate and high prevalence regions of New South Wales respectively. The other States generally had an upper 97.5% probability limit of about 1% or less. Based on these estimates about 6 to 10% of flocks in New South Wales and 2.4 to 4.4% of flocks Australia-wide are likely to be infected. CONCLUSION: This study suggests that OJD has a highly clustered distribution in Australia, and provides estimates of the prevalence of infected flocks by State or region. Based on this analysis there were probably between 2000 and 3700 infected flocks in Australia at 31 December 2000, with more than 80% of these in a relatively small geographic area of central and southern New South Wales. Some States, such as Queensland and Western Australia, may have a prevalence equal or close to 0%, however the technique used was unable to demonstrate the absence of infection in these States with the intensity of surveillance undertaken to date.
Bacterial isolates (n = 38) previously cultured from sheep with Bolo disease were compared bacteriologically with known Corynebacterium spp. and Actinomyces spp. The isolates did not conform to any previously described species but closely resembled C. pseudodiptheriticum and C. urealyticum. More comprehensive tests are needed to classify this Corynebacterium sp. Bacterial cultures of this unclassified Corynebacterium sp. were used artificially to induce Bolo disease in Dohne Merino sheep (n = 20). Ten sheep were kept at Middelburg in the Cape Midlands (Northern Cape) under arid conditions and another 10 at Queenstown in the Eastern Cape in a more humid climate. Two suspensions containing 2.8 x 10(5) Corynebacterium sp. (inoculum A) and 2.8 x 10(9) Corynebacterium sp. (inoculum B) respectively were used to infect each sheep on 9 different sites on the skin. One sheep died during the course of the experiment. Corynebacterium sp. established itself on 81 out of 171 inoculation sites of the remaining sheep and caused typical lesions of Bolo disease, clinically and pathologically. Bolo disease lesions developed slowly over 175 days at Middelburg and 287 days at Queenstown. Weather conditions were unfavourable to the development of fleece-rot and mycotic dermatitis. No difference was seen in lesion development between rams and ewes or between sheep with 5 months' wool growth and those which were shorn before inoculation. More lesions developed with the higher concentration of inoculum B (49 sites positive) as compared to inoculum A (32 sites positive).