Search

Epitheliocystis is a skin and gill disease in fish caused by pathogenic intracellular bacteria. The disease has been reported in at least 90 species of marine and freshwater fish in both the southern and northern hemispheres. It affects a number of commercially important aquaculture species, including salmon, kingfish and bream. In infected fish, cysts typically develop in the gill epithelia, promoting the fusion of gill lamellae. Infections can lead to respiratory distress and death, particularly in cultured and juvenile fish with cases rarely reported in wild fish. Modern molecular techniques are challenging the conventional wisdoms regarding the epidemiology of epitheliocystis, showing now that a number of distinct bacterial pathogens from completely different phyla can cause this disease. Here, we review the state of knowledge, including updates on aetiology, host range, diagnosis and treatments. Traditionally, bacteria from the phylum Chlamydiae were the only known pathogenic agents of epitheliocystis, but aetiology is now recognized as being more complex, including a range of Proteobacteria. Notwithstanding recent advances in identifying the pathogens, the reservoirs and modes of transmission remain largely unknown. Recent genome sequencing of the growing number of epitheliocystis agents suggests that many bacteria causing this disease are unique to individual species of fish. Environmental conditions that approach or exceed animals' physiological tolerances (e.g. atypical temperature, salinity or pH levels) are thought to contribute to disease development and progression. Empirical data and evidence concerning epidemiology, aetiology and treatments are, however, in many cases limited, highlighting the need for more work to better characterize this disease across the different hosts and locales affected.

Dead animal bodies occur naturally in ecosystems, are regularly washed up along ocean beaches, and are a key component of many coastal food webs where scavenging animals consume carcasses. Microbes that decompose carcasses can, however, produce toxic chemicals during putrefaction. This is frequently assumed to have negative consequences for scavengers in the wild, but has been rarely quantified. In this study, we measured how changes in the microbial assemblages of decaying fish affect the toxicity of carcasses. We did this by allowing fish carcasses to decompose in the field for up to 31 days in the dunes of a sandy beach; an ecosystem where scavenging animals are common. Carcasses were sampled daily and the tissues tested for changes in culturable microbial communities using 100 μL samples of whole carcass homogenates on marine and sheep blood agar, and changes in cytotoxicity using Vero cell assays. Cytotoxicity peaked 11 days after deployment showing 95% rounded and detached cells. Cytotoxicity was lower in the early phases of decay as microbial communities developed and after approximately two weeks when carcasses dried. The peak in toxicity correlated with peaks in the abundance of Acinetobacter, and Vibrio and Alivibrio; microbes known to produce toxins. This trajectory of toxicity suggests an ecological model where microbes may predictably determine the palatability of carrion in food webs, making both fresh and aged carcasses the least risky proposition for scavenging animals. This ‘fresh and aged carcasses are best’ model is highly amenable to testing in the context of carrion-centred food webs in multiple systems, and it has practical applications in conservation where animal carcasses are provided to threatened, and often iconic, scavenger species.