Lesions Associated with Coccidiosis in Nursing Piglets

Abstract

Abstract. Of 45 piglets with diarrhea, 28 had coccidiosis, with no evidence of concurrent viral infection. Villous atrophy and necrotic enteritis were the characteristic lesions, and were more severe in piglets with combined viral and coccidial infections than with coccidiosis alone. Necrotic enteritis presumably was caused by bacterial invasion of the villous lamina propria at foci denuded of epithelium by coccidia, viruses or both. Consistent lesions associated with coccidia in piglets not infected by other primary enteric pathogens suggest that coccidia are the cause of significant clinical disease in nursing piglets 6 to 15 days old.

Lectin Histochemistry for Glycoconjugates in the Small Intestines of Piglets Naturally Infected with Isospora suis.

“…Clinical signs in affected pigs include yellowish to greyish diarrhea, dehydration, and weight loss in 5-to 14-day old piglets with high morbidity and low mortality [3,12,13]. Escherichia coli was frequently isolated from the small intestines of the coccidially infected piglets [3,7,11]. Eimeria tenella and Echinostoma caproni infection altered glycoconjugates composition in intestinal mucosa and may facilitate bacterial adherence to intestinal brush border [1,9].…”

Fibrinonecrotic enteritis of piglets in a commercial farm: a postmortem study of the prevalence and the role of lesion associated agents Isospora suis and Clostridium perfringens

“…Faecal sampling or scraping of gut mucosa studies allowed to identify the agent. However total percentage of FNE lesions suspected to be associated with I. suis was lower in comparison with others PWM categories and even with those of a previous report (Eustis & Nelson 1981). In field outbreaks of coccidiosis, gross fibrinonecrotic lesions are usually seen in less than 20% of the cases (Lindsay & Blagburn 1994).…”

“…Experimental studies found a diphtheric membrane in jejunum and ileum in one day old piglets receiving 200,000 (22% with FNE) to 400,000 oocysts (53% with FNE) while no gross lesions was seen in older pigs even with higher dosis (Stuart et al 1982). In the later, histopathological studies have shown segmental villous atrophy characterized by a slight to severe reduction of the height of the villi with flattened tips epithelial cells infected with asexual stages type 1 merozoites and rarely type 2 merontes (Eustis & Nelson 1981, Stuart et al 1982, Lindsay & Blagburn 1994, Perfumo et al 1998, Lindsay et al 1999, however neither coagulative necrosis of the mucosa nor inflammatory changes in the submucosa and muscle layers were reported. In a previous study, severe cases with not remnant enterocytes, only colonies or single rod-shaped Gram positive bacteria within the fibrinonecrotic material were identified (Perfumo et al 1998).…”

“…However PCR technique applied on formalin fixed tissue provides a useful tool to generate information related to the role of C. perfringens in the pathogenesis of FNE. According to a previous study (Eustis & Nelson 1981) necrotic lesion in piglets might be produced by bacterial invasion of the villous lamina propria at foci of denuded epithelium caused by I. suis which should favour the action of α toxin produced by C. perfringens type-A. Further α toxin, a phospholipase acting on membranes of erythrocytes, platelets, leukocytes, endothelial and muscle cells, might produce villous oedema, epithelial, vascular and muscular damage (Songer & Glock 1998, Songer & Trigo 1998 as was seen in our study in severe FNE lesions.…”

“…Grossly, it is characterized by a rigidity of the jejunum and ileum due to a thickening of the mucosa by a fibrinonecrotic membrane. Microscopically, superficial (involving villous cells) or deep (affecting cryptal cells), coagulative necrosis is seen with focal areas of fibrinonecrotic exudates (Eustis & Nelson 1981, Perfumo et al 1998). Although there is no doubt about the definition of the gross lesions, from the etiological point of view, several microorganisms, alone or in association, have been reported to be involved in the pathogenesis of FNE.…”