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[Specific prophylaxis of foot-and-mouth disease during summer pasturing husbandry].
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[Epidemiologic significance of permanent foot-and-mouth disease virus excretors].
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Serological evidence of arboviral infections among humans of coastal Kenya.
A serosurvey was conducted during September 1987 for evidence of human arboviral infections in the Coast Province of Kenya. Sera were collected from 1624 outpatients at three hospitals and tested for antibody to eight arboviruses by the indirect immunofluorescent antibody technique. Antibody prevalence rates were: Rift Valley fever, 2.8%; Sindbis, 2.6%; dugbe, 2.1%; dengue-2, 1.0%; West Nile, 0.9%; chikungunya, 0.7% and Nairobi sheep disease, 0.3%. Evidence of Crimean-Congo haemorrhagic fever viral antibody was not detected. The data suggested low arbovirus activity since 1982, when an epidemic of dengue occurred in this region, and revealed the first evidence of dugbe viral infection among humans in Kenya.
Ovine white-liver disease (OWLD). Changes in blood chemistry.
Changes in blood chemistry were examined in vitamin B12 deficient lambs which developed ovine white-liver disease (OWLD), and were compared with values of cobalt/B12 supplemented lambs on the same pastures, as well as clinically healthy, but sometimes B12 deficient, lambs on other pastures (H). In the OWLD group, signs of hepatic damage were seen concurrently with reduction in weight gain, or 1-3 weeks before, and comprised elevation of serum glutamate dehydrogenase (GLDH) and decrease of phospholipid and cholesterol. Drop of plasma glucose and elevation of gamma GT also came in the earlier phase of the disease. All other blood changes developed later, and were partly regarded as reflections of the inappetence or hepatic injury. The changes included a drop in packed cell volume (PCV) and mean corpuscular volume (MCV), elevation of serum iron, and reduction of total serum protein and urea. Generally Co/B12 supplementation prevented hepatic damage and normalized blood values. The clinically healthy H lambs also showed signs of hepatic damage, especially one year when they were B12 deficient, indicating that simple B12 deficiency causes a moderate liver damage as well. For diagnostic purposes, clinical pathology is recommended mainly on a flock basis.
Ovine white-liver disease (OWLD). Trace elements in liver.
Trace elements in liver were examined in vitamin B12 deficient lambs which developed ovine white-liver disease (OWLD), in cobalt/vitamin B12 supplemented lambs on the same pastures as well as clinically healthy, but sometimes subclinical B12 deficient lambs on other pastures (H). Liver Co was marginal to deficient in both OWLD lambs (S lambs) and H lambs. Supplementation with B12 or Co elevated liver Co. Liver copper was significantly lower in OWLD lambs than in the H lambs, and Co/B12 supplementation on pasture generally had no significant effect on the contents. Dosing lambs on OWLD pastures with copper oxide needles (SCuO), however, resulted in high/toxic liver Cu. Dosing with Co, Se and Cu glass boluses resulted in adequate liver Cu, except for 1 lamb with toxic amounts indicating dissolution and absorption of the bolus. OWLD lambs had significantly lower liver molybdenum than H lambs, and Co/B12 supplementation elevated values, while CuO treatment depressed them. Liver zinc, manganese and selenium are also reported.
Ovine white-liver disease (OWLD). Pathology.
Microscopic liver changes could earliest be found after 1 month on OWLD pasture, and include extensive fatty change with large spherical vacuoles in hepatocytes, varying size of hepatocytes and nuclei, and formation of Councilman bodies. Later came ceroid deposits, biliary hyperplasia and mesenchymal proliferation. Changes occurred in all lambs which died or were killed due to OWLD, and altogether 83% of the lambs grazing OWLD pastures showed typical or suspect changes. Widespread haemosiderosis of the spleen was common. In severely affected lambs, sclerosis of the Peyer's patches and of the germinative centres of the intestinal lymph nodes were seen, as were neuronal atrophy and patchy microcavitation of areas in the brain stem. Four had polyvasculitis. Cobalt/vitamin B12 supplemented lambs showed no specific changes. Lambs which grew well on other pastures (H lambs), but which were subclinically Co/B12 deficient some years, showed no fulminant hepatic OWLD, but 15% developed some features seen in OWLD. They showed no extensive fatty change. Results indicate that OWLD is a manifestation of B12 deficiency worsened by factors triggering early hepatic fatty change resulting in a more severe liver damage with loss of intracellular homeostasis rendering the hepatocytes vulnerable to other elements, like copper.
Ovine white-liver disease (OWLD). Treatment trials.
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Nephropathy in young lambs.
Renal disorders in lambs may be congenital, infectious, toxic, immunologically mediated or secondary to urethral obstruction. Congenital abnormalities are uncommon. Kidney infections often are only one aspect of more widespread diseases, for example, tick pyaemia or salmonellosis. Toxic diseases, which affect mainly the renal tubules, may be caused by bacterial, chemical or plant toxins, although in lamb nephrosis the cause is unknown. Immunecomplex glomerulonephritis is uncommon, and one form, mesangiocapillary glomerulonephritis of Finnish landrace lambs, is under genetic control. Urolithiasis may have secondary effects on the kidneys.
Ovine chlorellosis in the Sudan.
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[Comparative studies of the oral environment in domestic and wild animals].
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A veterinarian's glimpse at animal health in the People's Republic of China.
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[Toxoplasma gondii infection among wild and domestic animals].
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Prevalence of disease conditions and pregnancy in sheep and goats seen over a three year period in Enugu abattoir, Nigeria.
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Heartwater. An overview of the clinical signs, susceptibility and differential diagnoses of the disease in domestic ruminants.
Heartwater is a frequently fatal tick-borne disease of ruminants caused by Cowdria ruminantium. In domestic ruminants the incubation period varies considerably and depends on the route of infection, virulence of the isolate and amount of infective material administered. Adult cattle of all breeds appear to be equally susceptible to heartwater. It is generally accepted that calves up to the age of 3 weeks have a high degree of natural resistance which is not related to the immune status of the dam. Nervous symptoms are frequently seen in animals affected by the peracute and acute forms of heartwater and can easily be confused with similar signs caused by infectious conditions, toxic plants, acaricide and heavy metal poisonings.
The use of electro-encephalography and brain biopsy in the clinical diagnosis of heartwater.
Both electro-encephalography and brain biopsy were examined as possible aids in the confirmation of a clinical diagnosis of heartwater in field cases. Results showed that electro-encephalographic changes associated with heartwater were non-specific and probably caused by the associated brain oedema. Brain biopsy on the other hand appears to be a reliable technique for the confirmation of heartwater, and the technique if properly performed holds little risk for the animal.
[Pulpy kidney in the suckling lamb].
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