Pathology of bacterial gill disease: ultrastructure of branchial lesions

The range of branchial lesions associated with bacterial gill disease (BGD) in rainbow trout, Oncorhynchus mykiss, was investigated through the ultrastructural examination of 23 separate outbreaks of the disease condition within commercially reared stocks. Diseased branchial tissues had a large and diffusely distributed monomorphic population of filamentous bacteria which were strictly epicellular. Although bacterial colonization was restricted to the branchial cavity, it was neither site nor cell specific: epithelial and chloride cells of the lamellae, filaments and lining tissues of the branchial cavity were all uniformly affected. The bacteria possessed an extensive glycocalyx which appeared to facilitate adhesion to the apices of the microridged sub-unit modification of the cell surface. Sites of colonization were accompanied by a diffuse pattern of cellular degeneration and necrosis that was generally restricted to the outer layers of epithelium. The polarity and nature of these changes suggest that the mechanism of interaction between the bacteria and host cells includes progressive hydropic changes as a sequel to primary membrane damage and consequent increased cell permeability. These cellular changes were accompanied by the range of stereotypical responses of the gill to damage frequently reported for BGD including lamellar fusion, epithelial hyperplasia, and squamous and mucous cell metaplasia, in addition to lamellar spongiosis..RE: 42 ref.; SC: CA; VE; 0I; ZA; 0VSource type: Electronic(1) http://upei-resolver.asin-risa.ca?sid=SP:CABI&id=pmid:&id=&issn=0140-7775&isbn=&volume=14&issue=1&spage=1&pages=1-20&date=1991&title=Journal%20of%20Fish%20Diseases&atitle=Pathology%20of%20bacterial%20gill%20disease%3a%20ultrastructure%20of%20branchial%20lesions.&aulast=Speare&pid=%3Cauthor%3ESpeare%2c%20D%20J%3bFerguson%2c%20H%20W%3bBeamish%2c%20F%20W%20M%3bYager%2c%20J%20A%3bYamashiro%2c%20S%3C%2Fauthor%3E%3CAN%3E19912256144%3C%2FAN%3E%3CDT%3EJournal%20article%3C%2FDT%3