AAAP: Spotty liver disease in layer hens
Campylobacter hepaticus causes spotty liver disease, resulting in mortality and production loss
[Excerpts of presentations at the 2025 annual meeting of the American Association of Avian Pathologists]
Campylobacter hepaticus is the causative agent of spotty liver disease, resulting in mortality and production loss in laying hens. The disease is primarily associated with free range laying birds and occurs most often at peak production.
Catherine Logue and colleagues at the University of Georgia, USA, used a C. hepaticus challenge model to assess if all layer breeds and bird types were susceptible to infection. The assessment was based on clinical signs, spotty liver lesions on necropsy and confirmation by histopathological analysis, microbiology and PCR confirmation.
For this study, five different bird types were assessed including Rhode Island White, Rhode Island Red, White Leghorn, broiler breeder and broiler. Thirty birds of each type were allocated into groups of 10 and challenged with one of three C. hepaticus challenge doses. All birds were housed in similar conditions and monitored. At intervals post-challenge, birds were removed and euthanized to assess for liver lesions and the presence of the challenge strain.
When compared by bird type, Rhode Island Red and Rhode Island White birds had the highest liver lesion scores while White Leghorn layers had significantly lower scores. Liver lesion scores for broiler breeders and broilers were comparable to the White Leghorn. Bacteriological analysis found that Rhode Island Red, Rhode Island White, and broiler breeders had similar prevalence rates (>80% positive) compared to White Leghorn and broilers, which had a lower prevalence (40-50%) but was not significantly different. Spotty liver disease can be replicated in all bird types using a C. hepaticus challenge resulting in lesions and positive birds on culture.
Spotty liver lesion persistence
Spotty liver disease and its etiologic agent Campylobacter hepaticus causes multifocal liver lesions in layers, resulting in reduced egg production, and increased mortality. A project by Roel Becerra and Catherine Logue, University of Georgia, USA, evaluated the potential persistence of liver lesions following challenge with C. hepaticus. The researchers hypothesized that liver lesions do not resolve without antibiotics. The researchers used 115 laying hens at 24 weeks of age. An oral challenge dose of C. hepaticus, (109 cfu/ml/hen) was given three times, one day apart, to 80 hens. At 16 days-post-challenge, the hens were divided into two groups: one group (n=40) was treated via feed with chlortetracycline for five days while the second group was untreated.
Also, 11 laying hens were added as sentinels/contact birds to both challenge groups at 16 days-post-challenge to evaluate horizontal transmission. At 16, 23, and 32 days-post-challenge, a subpopulation of hens per group were euthanized and necropsied to collect livers for histopathology, bile for bacteriology, and to score liver lesions.
Results found that liver lesions persisted in birds that did not receive chlortetracycline. However, in treated birds, liver lesion scores were significantly lower. Chlortetracycline was unable to clear the infection in treated birds or control transmission as more than 50% of treated and sentinel hens were positive on bacteriological analysis. This research confirms that C. hepaticus persists in flocks where antibiotics are not used.