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. 1978;19(4):601-3.
doi: 10.1186/BF03547599.

Immunoglobulins in bovine ostertagiasis

Immunoglobulins in bovine ostertagiasis

P T Jensen et al. Acta Vet Scand. 1978.

Abstract

Lowered albumin levels with normal or slightly elevated γ-globulin levels are well known features of various gastro-intestinal disorders in cattle. Thus, this picture is a prominent finding in clinical ostertagiasis, where hypercatabolism of both albumin (Nielsen 1966) and IgG (Nansen 1970) has been demonstrated. The hypercatabolism is explained by gastric loss, and evidence suggests that this takes place as a non-selective loss of protein through the hyperplastic abomasal wall (Murray 1969). The albumin hypercatabolism is not compensated for by an increased synthesis, and thus leads to hypoalbuminaemia also during part of the non-diarrhoeal phase. The IgG hypercatabolism, on the other hand, is compensated for by increased synthesis, which may lead to elevated serum IgG levels, especially in phases without diarrhoea. There seems to be no comparative data available for IgG-1, IgG-2, IgM, and Ig A levels in ostertagiasis. The purpose of the present study was to analyse the influence of ostertagiasis on the serum levels of immunoglobulins, albumin and total protein in young cattle. The study comprised two groups of randomly selected Red Danish calves, approx. % year old. Half the calves (Group A) grazed the same paddock from May to late September and were exposed to heavy infection from August onwards as evidenced by high herbage larval counts, high faecal egg counts, and elevated serum pepsinogen levels (see Table 1). Most of the calves were clinically affected, and in the last part of August and September some had profuse diarrhoea. The other calves (Group B) were moved in mid July to a paddock not grazed earlier that season. Accordingly, these calves were exposed to only a relatively low pasture infection in the second half of the grazing season. None of them showed clinical signs, and pepsinogen levels were only slightly elevated (Table 1).

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References

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