A study of the pathology of experimental infection with Cooperia pectinata in calves

Winks, R. (1974). A study of the pathology of experimental infection with Cooperia pectinata in calves PhD Thesis, School of Molecular and Microbial Sciences, The University of Queensland. doi:10.14264/uql.2015.491

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Author Winks, R.
Thesis Title A study of the pathology of experimental infection with Cooperia pectinata in calves
School, Centre or Institute School of Molecular and Microbial Sciences
Institution The University of Queensland
DOI 10.14264/uql.2015.491
Publication date 1974-01-01
Thesis type PhD Thesis
Supervisor A. H. Waddell
Total pages 358
Language eng
Subjects 03 Chemical Sciences
Formatted abstract
The biochemical and pathological changes in calves infected experimentally with a single oral dose of 250000 infective larvae of the nematode, Cooperia peatinata were studied. Infections were patent from day 12, and faecal worm egg counts reached a maximum during the third week after infection. A second maximum egg count occurred terminally and was mainly due to a concentrating effect as the faecal output was reduced coincidental with a loss of appetite.

The effects of the worms on their host were remarkably consistent and 12 calves died of 13 in which the infection ran its full course. Clinical signs of infection were observed at the end of the third week, and the health of the calves then deteriorated rapidly until they died a week later with the characteristic signs of a shock syndrome.

Most larvae had a sojourn in the abomasum during the first two days after infection and some entered the abomasal crypts. From day four the larval and resultant adult populations had a log-normal distribution along the same region of the small intestine and at least 85% occupied the proximal 40% of this organ. Many worms migrated distally during the terminal stages of the infection. Between 10 and 75% of the larval dose was recovered at necropsy. Both the infectivity and pathogenicity of the larvae were affected by their age when administered.

Calves became ill and anorectic when lesions developed in the mucosa of the small intestine during the third week after infection. The villous structure altered in those regions most heavily parasitised, the mucosa became flattened and cuboidal cells replaced the normal columnar epithelial cells. Focal lesions developed in the mucosal epithelium and a profuse heterprophilic fibrinonecrotic exudate formed on the surface of the mucosa. Inflammatory cells infiltrated the lamina propria of the small intestine after infection. Eosinophil leucocytes increased in number from the first "week, mononuclear cells from the second and plasma cells from the third -week. In the moribund calves, however, few inflammatory cells were observed in those areas inhabited by worms. Numerous eosinophils accumulated in the mesenteric lymph nodes of moribund calves and many inflammatory cells were seen in the exudate in the small intestine. The number of globule leucocytes in the mucosal epithelium decreased during the second and third weeks and few were seen in dying calves. Mast cell numbers did not vary significantly during the course of the infection.

Reactivity in the lymphatic tissues increased from the end of the first week, and continued during the second and third weeks. In moribund calves these tissues became depleted. Degenerative changes also occurred in the thymus and only a thin flabby hypoplastic remnant remained in moribund animals.

Infected calves developed a severe hypoproteinaemia with decreased concentrations of both albumin and globulin. Major imbalances occurred in the body fluid compartments but diarrhoeic moribund calves were not dehydrated. Rather they showed an increased total body water with excess fluid in the interstitial space and peritoneal cavity which gave them a body weight advantage over pair-fed and watered uninfected partners. The plasma volume of the moribund calves was only 73% of the preinfection level and the packed cell volume in most infected animals increased terminally in proportion to the reduction in plasma volume. The half-life of body water showed a four-fold increase as the water intake of the calves decreased.

Injection of globulins extracted from antiserum produced in horses against calf thymocytes failed to modify the course of infection with C. pectinata.

The progression of these various changes observed during the course of the infection was discussed. The cellular changes in the tissues indicated that the calves attempted to mount an immunological response to the parasites but that protein-calorie deficiency induced generalised immunological exhaustion. The resultant hypoproteinaemia and ensuing circulatory collapse produced a state of shock which culminated in the death of the infected calves.
Keyword Calves -- Diseases
Cooperia pectinata
Additional Notes Other Title: Pathology of experimental infection with Cooperia pectinata in calves.

Document type: Thesis
Collection: UQ Theses (RHD) - UQ staff and students only
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Created: Wed, 13 May 2015, 21:37:10 EST by Ms Dulcie Stewart on behalf of Scholarly Communication and Digitisation Service