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Toxaemia

However, in case of acute clinical mastitis, it is widely accepted that animal welfare considerations should take prevalence. If both farmer and veterinarian are not familiar with non-antibiotic treatments, they should be advised to use broad-spectrum antibiotics immediately, because any delay (e.g. the 2-3 days it often takes between diagnosis and the return of microbiological test results) may seriously harm the animal. This approach should, however, only be taken after a sound clinical diagnosis, since antibiotic treatments themselves may lead to dramatic aggravation of the condition. For example, E. coli inflammations are able to develop into severe toxaemia, because increased levels of toxins are released into the animal tissues when E. coli cells are killed or stressed by antibiotic treatments. Also, if yeasts are the main cause or form part of the pathogen complex that causes mastitis, their growth and proliferation may be supported by the administration of anti-bacterial antibiotics (Crawshaw et al., 2005). [Pg.206]

Yarim GF, Karahan S, Nisbet C (2007) Elevated plasma levels of interleukin 1 beta, tumour necrosis factor alpha and monocyte chemotac-tic protein 1 are associated with pregnancy toxaemia in ewes. Vet Res Commun 31 565-573... [Pg.373]

Theileriosis is a tick-borne disease of cattle and sheep. The parasites are intracorpuscular but, unlike in babesiosis, the blood cells are not destroyed. The major symptoms are those of toxaemia and once the parasite has invaded the blood, there is high, rapid mortality. [Pg.216]

Pre- and perinatal events, e.g. maternal viral infection during second trimester toxaemia and/or hypoxia at birth... [Pg.259]

Jaundice may result from a diminished bilirubin uptake in the liver cell. This is possibly caused by bile acids, medication or chemicals (e.g. vermicides such as flavaspidic acid). Extensive periods of fasting (N.A. Gu.bert et at, 1907 E. Meyer et af, 1922) (<300 calories/day, >48 hours) and toxaemia with sepsis (14, 18, 23) can also give rise to unconjugated hyperbilirubinaemia. [Pg.218]

Baars JW, de Boer JP, Wagstaff J, Roem D, Eerenberg-Belmer AJ, Nauta J, Pinedo HM, Hack CE. Interleukin-2 induces activation of coagulation and fibrinolysis resemblance to the changes seen during experimental endo-toxaemia. Br J Haematol 1992 82(2) 295-301. [Pg.68]

Ahmed SM, Khan RM, Bano S, Ajmani P, Kumar A. Is spinal anaesthesia safe in pre-eclamptic toxaemia patients J Indian Med Assoc 1999 97(5) 165-8. [Pg.2152]

B26a. Brewer, T. H, Administration of human serum albumin in severe acute toxaemia of pregnancy. J. Obslet. Gynaecol. Brit. Commonwealth 70, 1001-1004 (1963). [Pg.284]

Amon, S.S. 1995. Botulism as an intestinal toxaemia. In Infections ofthe Gastrointestinal Tract, eds. M.J. Blaser, P.D. Smith, J.L Ravdin, H.B. Greenberg, and R.L. Guerrant, 257-271 New York, NY Raven Press. [Pg.414]

Chandra SV, Seth PK, Mankeshwar JK Manganese poisoning clinical and biochemical observations. Environ Res 7 374-380,1974 Charles JR Manganese toxaemia with special reference to the effects of liver feeding. Brain Journal of Neurology 50 30—43, 1927... [Pg.154]

Tularaemia results from systemic infection with the gram-negative bacteria Francisella tularensis. Wild rodents (in particular, hares) and other small-animal populations are the main reservoir of infection. In humans, most cases are sporadic, related to tick bites (Dermacentor) or direct contact with infected animals. Hunters are at greatest risk, but the disease also affects butchers, farmers, foresters, laboratory workers and veterinarians (Evans et al. 1985). The incubation period varies from 1 day to 10 days. The clinical manifestation is usually an ulcerated nodule at the point of inoculation, associated with enlargement and, later, breakdown of lymph nodes. Systemic symptoms and toxaemia may be severe. Minocycline is considered to be efficacious in most cases (100 mg twice per day for 4 weeks). [Pg.184]

Nutrient deficiencies in pregnancy may affect either or both the mother and the foetus. Many vitamin and mineral deficiencies (referred to in Chapters 5 and 6) are manifested in the foetus first. In the ewe, pregnancy toxaemia - which is basically a deficiency of glucose - is caused by the large demand for glucose by the foetus (often twin foetuses) and by a reduction in food intake in late gestation. [Pg.403]

Discuss the main factors contributing to pregnancy toxaemia (twin lamb disease) in sheep, and outline dietary strategies to prevent this. [Pg.403]

Sandler, M. and Goveney, J., Placental monoamine-oxidase activity in toxaemia of pregnancy. Lancet, 1962, p. 1096. [Pg.195]

Theobald, G. W. 1955. The Pregnancy Toxaemias or the Encymonic Atelositeses. Kimpson, London. [Pg.304]

Administration of chlorpromazine to a hypoglycaemic child successfully maintained on diazoxide and bedroflumethiazide was followed by marked hyperglycaemia (118 ). The combined use of diazoxide and chlor-methiazole in toxaemia of pregnancy shortly before delivery may have caused the severe depression, hypoventilation and hypotonia seen in 12 out of 13 infants in another similar case the mother had also received massive doses of anticonvulsants for grand mal 119C)... [Pg.170]


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See also in sourсe #XX -- [ Pg.130 ]




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Pregnancy toxaemia

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