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I Pow

Publications and source records attributed to I Pow.

At least 37 records · Page 2Linked to original sources

A disease resembling louping-ill in sheep in the Basque region of Spain.

A clinical syndrome resembling louping-ill which primarily affects lambs and yearlings in the Basque region of Spain is described. The disease has been observed for several years during May and June after the sheep flocks have been taken to the mountain grazings where the sheep tick (Ixodes ricinus) is known to occur. Examination of the brain from one of the affected animals revealed histological changes indistinguishable from those caused by louping-ill virus. In addition antibody that reacted with louping-ill virus antigen was detected in the serum of 57 per cent of the sheep tested from the affected flocks but in only 0.8 per cent of sera from flocks free of the disease. These preliminary results suggest that louping-ill or a related tick-borne virus is responsible for ovine encephalomyelitis in Spain.

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Response of sheep to experimental concurrent infection with tick-borne fever (Cytoecetes phagocytophila) and louping-ill virus.

The pathogenesis of concurrent Cytoecetes phagocytophila and louping-ill virus infection was studied in two experiments. In the first experiment 18 four- to seven-year-old rams were used. Ten were infected with C phagocytophila and five days later eight of these animals and the remaining eight sheep were infected with louping-ill virus. The two rams infected with C phagocytophila alone developed no clinical signs apart from a transient pyrexia, while only three of the eight rams infected with louping-ill virus alone showed mild clinical signs. In marked contrast, all eight dually infected sheep developed severe clinical signs with pronounced depression and dysentery and three died and five were killed in extremis. They developed higher titres of viraemia and the antibody response was depressed while necrotising lesions affecting a variety of organs were detected at post mortem examination. Rhizomucor pucillus was recovered from these lesions in seven of the eight sheep. A second experiment using 10 sheep, five aged seven months and five aged two to three years, confirmed the findings of the first experiment indicating that the age of the animal had not significantly influenced the initial result. It was concluded that C phagocytophila infection could enhance the pathogenicity of louping-ill virus and that, operating together, the two pathogens facilitated fungal invasion. It is postulated that sudden deaths in sheep recently transferred to tick-infested pastures may be due to this newly described syndrome.

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Malignant catarrhal fever: experimental transmission of the 'sheep-associated' form of the disease from cattle and deer to cattle, deer, rabbits and hamsters.

Attempts to transmit malignant catarrhal fever (MCF) from 16 bovine cases of the 'sheep-associated' form of the disease are described. On two occasions disease was transmitted to bovine calves but transmission to red deer (Cervus elaphus) was not achieved. In addition, MCF was transmitted from one experimentally affected calf to a rabbit and on another occasion directly to rabbits with material from a field case which failed to transmit to a bovine calf or red deer. Subsequently each of these isolates was readily passaged through rabbits and one was also passaged to Syrian hamsters. Tissue from MCF-affected red deer consistently produced disease on inoculation into rabbits and deer but failed to cause disease in bovine calves. Contact infection between red deer occurred once and roe deer (Capreolus capreolus) were also shown to be susceptible to infection by inoculation. Passage of MCF in rabbits with an isolate from red deer failed to produce evidence of further adaptation even after 125 serial passages. Despite the failure to transmit disease from cattle to deer or from deer to cattle it is considered probable that there is only one sheep-associated agent which causes MCF in both species. The reasons for the anomalies in transmission of this form of the disease are discussed.

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Transmission of a malignant catarrhal fever-like syndrome to sheep: preliminary experiments.

The transmission of a malignant catarrhal fever-like syndrome to sheep is reported. Fetal sheep between 40 and 66 days gestation were inoculated intravenously with viable cells either from a red deer with clinical malignant catarrhal fever or from rabbits with the disease. Of the 21 fetuses in the experiment only five were born live and of these four developed clinical signs similar to malignant catarrhal fever in other species and died or were killed 10, 16, 47 and 175 days after birth. The fifth lamb remained unaffected. Histology of the four affected lambs revealed a generalised lymphoproliferation, with T-dependent areas of lymphoid tissues being affected, and an overall paucity of immunoglobulin containing cells. In addition arteritis and interstitial infiltration of many organs by lymphoid cells was present. The infectious agent was not reisolated in rabbits from lambs or passed to red deer housed in the same pen and it is thus considered possible that gene expression of the putative virus was incomplete.

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Malignant catarrhal fever.

Malignant catarrhal fever is briefly reviewed and recent findings are described. Initially the disease was observed as a disease of cattle in Europe where, although no cause could be identified, circumstantial evidence implicated sheep as a source of infection and it was thus designated 'sheep-associated' malignant catarrhal fever. Subsequently the disease was observed in Africa where it became evident that a herpesvirus which normally infects wildebeest was the cause. It is now apparent that deer are highly susceptible to both forms of the disease, the sheep-associated form being a serious problem in farmed deer. The wide spectrum of clinical and pathological changes that occur in affected deer are described. A major constraint to studies of sheep-associated malignant catarrhal fever has been the absence of an experimental laboratory system. However, from affected deer it has been possible to transmit the disease to rabbits and thus has allowed detailed pathogenesis studies to be made which are summarised in this paper. It is suggested that the agent of sheep-associated malignant catarrhal fever is a virus and that when a particular subpopulation of T-lymphocytes is infected a profound immunological perturbation results; the lesions of malignant catarrhal fever being explained by a benign T-lymphocyte hyperplasia accompanied by a deregulation of cytotoxic natural killer lymphocytes that gives rise to tissue necrosis.

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Transmission of louping-ill virus in goat milk.

The course of louping-ill virus infection was examined in lactating goats. Seven goats were inoculated subcutaneously and titres of virus in blood and milk were monitored. All goats became viraemic with maximum titres of between 10(1.6) and 10(4.0) plaque forming units (pfu)/0.2 ml. Virus was also detected in the milk of all goats at maximum titres of between 10(0.6) and 10(5.7) pfu/0.2 ml. Only one of these goats exhibited clinical signs which were transient. In contrast, five of the 13 kids sucking these goats became infected and all showed marked clinical signs and one died and two were killed in extremis. It is considered that goats do not represent an efficient maintenance host for louping-ill virus but the excretion of virus in milk could represent a public health hazard.

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Pathogenesis of 'sheep-associated' malignant catarrhal fever in rabbits.

Pathogenesis studies of experimentally produced sheep-associated malignant catarrhal fever (MCF) in laboratory rabbits are described. Animals were examined at intervals after inoculation. The principal change was a proliferation of lymphoid cells which began as soon as three days and became quite pronounced by 13 days after inoculation. The appendix, mesenteric lymph node and spleen were most obviously affected. The reason for this was a progressive increase in T-lymphocytes, which appeared to be a hyperplasia rather than neoplasia in T-dependent areas of these organs. Lymphoid cells also accumulated in interstitial spaces of non-lymphoid organs. The use of cyclosporin-A suppressed the lymphoid proliferation but rabbits still developed clinical MCF after a similar incubation period. It is suggested that the agent of MCF might produce its effect by infecting and causing a dysfunction of lymphoregulatory cells, resulting in benign polyclonal T-lymphocyte proliferation. Terminal necrosis could be due to natural killer cell activity.

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Experimental louping-ill virus infection of black grouse (Tetrao tetrix).

Louping-ill virus was injected into the tarsal pads of four black grouse and the course of infection monitored. All developed viraemia of low intensity that lasted for four days and thereafter produced high titres of haemagglutination inhibiting antibody. No clinical signs were detected and mild neuropathological changes were present in only 1/4 brains collected on day 17 after inoculation. The mild response of black grouse to infection with louping-ill virus is thus similar to that found in other woodland and forest birds and contrasts with the generally fatal response of moorland and tundra grouse species. These findings give further support to the concept that louping-ill has been introduced to the moorland habitat only in the relatively recent past.

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A cytotoxic T-lymphocyte line propagated from a rabbit infected with sheep associated malignant catarrhal fever.

The propagation of a cell line from a rabbit affected with the sheep associated form of malignant catarrhal fever is described. Immunological and morphological characteristics of the cell indicated that it was a T-lymphocyte and the presence of electron dense cytoplasmic granules suggested that the cell could be further classified as a large granular lymphocyte. The cell line required a feeder layer and was cytotoxic to both primary cell cultures and cell lines, a characteristic of large granular lymphocytes. No evidence of the nature of the agent could be detected but as few as 10(2) cells transmitted the disease. These findings are discussed and the possibility that infection and subsequent dysfunction of large granular lymphocytes may have a central role in the pathogenesis of malignant catarrhal fever is considered. That cells with similar characteristics have been derived from Herpesvirus saimiri and H ateles infected marmoset lymphocytes suggests that the lymphoproliferation associated with infection by these two simian herpes-viruses and malignant catarrhal fever may have a similar pathogenesis.

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Immunosuppression in toxoplasmosis: studies in sheep with vaccines for chlamydial abortion and louping-ill virus.

Toxoplasma gondii infection was established in sheep seven days (acute infection) or 28 days (chronic infection) before they were given enzootic abortion (EAE) vaccine alone or simultaneously with louping-ill (LI) vaccine. Uninfected controls received the same vaccination schedule. The serological response of acute toxoplasma-infected sheep to initial LI vaccination was significantly depressed but after revaccination four weeks later these sheep demonstrated a response equal to that of the revaccinated controls. Infected sheep also gave a significantly poorer response to EAE vaccine than control animals, the effect being more marked in those with chronic infection. Revaccination evoked no clear response in any group but on three of five sampling days antibody titres of controls were significantly higher than those of infected sheep.

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