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Coccidiosis in replacement gilts.

2005 
COCCIDIOSIS in pigs is normally associated with fiveto 15day-old sucking pigs. Diarrhoea with up to 20 per cent mortality results, and subsequent growth may be compromised. Isospora suis infection is invariably diagnosed in such cases (Cook 1996, Taylor 1999). Disease due to coccidiosis in weaned pigs is rarely reported, although in 1994 it was estimated that 5·3 per cent of breeder-finisher units and 12·5 per cent of weaner-producer units were infected with Eimeria species of coccidia (Taylor 1999). This short communication describes an outbreak of severe diarrhoea and death due to coccidiosis in a group of replacement gilts. The gilt replacement breeder unit concerned comprised 500 gilts. Animals arrived every fortnight in groups of 55, at 170 to 175 days of age. The pigs took two or three days to adapt to their non-medicated ration. Well water supplied both the farmhouse and the straw yards in which the pigs were housed. There was no obvious sign of significant rodent populations; however, birds and semiferal cats had free access to the straw yards. On March 3, 2004, a group of 55 replacement gilts arrived on the unit. Within one week, the faeces of approximately 25 per cent of the group were loose, but the animals remained bright and ate well. No investigation into the cause of the diarrhoea was undertaken at this time. A tylosin (Tylan G250 Premix; Elanco) and flubendazole (Flubenol Premix; Janssen)medicated ration was fed to the entire unit for seven days. No further problems occurred until a batch of 55 gilts arrived on April 30, 2004. Moderate inappetence was noted in this group, and seven days after arrival, two gilts were discovered dead in the yard. Over half the group was quiet, depressed and inappetent, with severe yellow, watery diarrhoea. One live, affected gilt and faecal samples (A to E) from five further gilts were submitted to Veterinary Laboratories Agency (VLA) – Thirsk the following day. The gilt was quiet, with a ‘tucked-up’ appearance, and had watery, yellow faecal staining of the perineum. Slight thickening of the mucosa of the distal jejunum and proximal ileum was seen on postmortem examination. A serofibrinous coating to the mucosal surface was most pronounced in the area of the mesenteric attachment. The caecal and large intestinal mucosae were relatively normal. The small intestinal contents were yellow in colour and had a creamy consistency, whereas the caecal contents were watery. The large intestinal contents were sparse, mucoid and bright mustard coloured. There was slight serosal congestion of the small intestine. The mesenteric lymph nodes were greatly enlarged, as were the coeliac lymph nodes. Coccidial oocysts counts using the modified McMaster technique gave results of 5,280,000 and 6,660,000 oocysts gram of faeces (opg) for the small intestinal and caecal contents, respectively. The limit of detection was 50 opg. Culture of the intestinal contents using standard operating procedures for the VLA identified no pathogens. Ileal mucosal scrapes revealed no evidence of Lawsonia intracellularis. Representative samples of gut were fixed, dehydrated and embedded in paraffin. The sections were cut at 4 μm and stained with haematoxylin and eosin, and a 4 μm section of ileum was stained with Giemsa. Histological examination of the jejunum and ileum revealed moderate villous atrophy, with extensive invasion of surface enterocytes by coccidial organisms. Crypt hyperplasia with numerous mitotic figures was seen, as was a moderate mixed inflammatory response in the lamina propria. Serofibrinous exudates were present on damaged mucosal surfaces, intermingled with coccidial forms and necrotic cellular debris (Fig 1). Higher magnification of the jejunal epithelium revealed almost total invasion of the enterocytes by coccidial forms (Fig 2). Mild lamina proprial infiltrates of inflammatory cells were seen in the large intestine. Coccidial oocysts were numerous within the lumen; however, no coccidial forms were seen within enterocytes. The faecal samples submitted at the same time as the gilt were examined for coccidial oocysts using the modified McMaster technique and the improved modified McMaster technique; the results are shown in Table 1. The coccidial forms were identified as 30 per cent Eimeria debliecki, 24 per cent Eimeria polita, 20 per cent Eimeria perminuta and 13 per cent Eimeria suis. The remaining oocysts were speciated as Eimeria neodebliecki and Eimeria porci. Three faecal samples were collected from a subsequent delivery of gilts as they arrived on the unit. No coccidial oocysts were found in these samples. Salmonella Derby was isolated from sample C by enrichment culture, and from two more gilts on the unit. A screen of six gilts on the source unit resulted in three isolations of salmonella. Six species of Eimeria were identified in this case, with clinical disease apparent in the gilts seven days after arrival. The distal jejunum and proximal ileum were most severely affected on postmortem examination. Mondal and others
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