Pathophysiology of bacterial gill disease in trout

The pathophysiology of bacterial gill disease (BGD) was examined in naturally infected brook trout Salvelinus fontinalis, and experimentally infected rainbow trout Oncorhynchus mykiss. Blood gas, cardiovascular, respiratory and blood chemistry variables were monitored in rainbow trout with experimental BGD. Some trout were fitted with an extracorporeal post-branchial arterial loop, as well as additional cannulae and probes in order to record real-time physiological data during a BGD challenge. Naturally infected brook trout showed a hypoosmolality, with reduced serum [Na+] and [Cl−] and a haemoconcentration (p < 0.05). Similar blood chemistry findings were seen in experimentally infected rainbow trout, but only if trout were fed. Experimentally infected trout, fed, or unfed, developed a severe hypoxaemia (reduced PaO₂) within minutes of challenge. In addition to the hypoxaemia, a BGD challenge resulted in an increase in gill vascular resistance, PaCO₂ and ventral aortic pressure, while arterial pH fell. Fish do not have to be fed in order for a BGD bath challenge to cause hypoxaemia. However, feeding is necessary for BGD bacteria to proliferate on gill tissue (MacPhee et al. 1995, Dis. Aquat. Org 21, 163–170). A nonsteroidal antiinflammatory drug (NSAID) indomethacin, greatly mitigated the development of BGD-induced hypoxaemia, when given before challenge, suggesting that a prostanoid mechanism was responsible for the hypoxaemia. Sodium nitroprusside (SNP), a nitric oxide donor molecule, largely or completely reversed BGD-induced hypoxaemia, when given intravenously or intrarterially, after BGD challenge. SNP had no effect on the BGD-associated bronchial hypertension. SNP made no additional improvement in PaO₂ in BGD-challenged trout that had been pre-treated with NSAIDs indomethacin, or indomethacin and ibuprofen. In summary, evidence suggests that the pathogenesis of peracute, experimentally produced bacterial gill disease is largely due to a prostanoid-dependent gill vascular disturbance, leading to respiratory distress, involving a reduced PaO₂ and an increased gill vascular resistance. It is suggested that serum biochemical and haematological changes may be initiated indirectly, by the BGD-initiated gill vascular disturbance, which then leads to a disruption in gas exchange and subsequent hypoxaemia and bronchial hypertension.