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Coccidiosis in a Commercial Layer Flock

Eliz Braddon, SDV Lachlan LHPA

Posted Flock & Herd September 2011

History / Clinical Signs

A commercial layer operation in the Young district (southwest slopes of NSW) experienced a sudden increase in mortalities in one layer shed in Jan 2011. The deaths were occurring in birds in the bottom two rows of cages in the shed only and losses were approximately 10-15 birds per day when the LHPA was contacted.

A post-mortem was carried out on a number of birds at this point. The birds from this shed exhibited classic signs of Eimeria tenella. The carcases were pale with enlarged and hemorrhagic caeca.

Image of chicken caecum on <em>post-mortem</em>
Haemorrhage in ceca visible from serosa

Approximately 1 week later, severe losses (37 birds over 2 days) and a severe drop in egg production occurred in the second layer shed. These sheds are side by side but are operated under strict hygiene levels by staff. Post-mortem signs in these birds showed caecal cores of impacted dried feed material and circular white lesions visible from the serosal surface and signs of peritonitis. These carcases however were not anaemic. Laboratory examination of tissues showed histopathology of the ileum consistent with necrotic enteritis caused by coccidia (e.g. Eimeria burnetti). The liver histopathology was consistent with an endotoxaemic or septicaemic disease (e.g Gram negative bacteria, E.coli).

Image of chicken intestine
Image of chicken intestine, mucosal surface
Swelling in small intestine and lymphoid tissue visible. Impacted material removed


Clinical coccidiosis in adult layers is very unusual. Birds of this age would normally be considered to have developed natural immunity. In this instance, these birds were 30 weeks of age and in full lay when the outbreaks occurred. Predisposing factors included a change in grain quality in the feed mix, high humidity and environmental temperatures favouring sporulation of coccidia. Also despite these birds being cage birds, the cage construction included a belt floor which allowed access to faecal material.

The birds were treated with chlortetracycline and losses stopped within 5 days of treatment. In total, approximately 250 out of 35,000 birds died and egg production was down considerably for at least 2 weeks. Recommendations have also been made to improve the immune status of layers to coccidia prior to them being introduced to the layer sheds.

I would like to acknowledge and thank Ben Wells from Wells Avian Consulting for his much valued advice on this case.


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