Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
. 1978 Aug;25(3 Pt 2):351-5.
doi: 10.1111/j.1550-7408.1978.tb03901.x.

Ultrastruct of red-sore lesions on largemouth bass (Micropterus salmoides): associattion of the ciliate Epistylis sp. and the bacterium Aeromonas hydrophila

Ultrastruct of red-sore lesions on largemouth bass (Micropterus salmoides): associattion of the ciliate Epistylis sp. and the bacterium Aeromonas hydrophila

T C Hazen et al. J Protozool. 1978 Aug.

Abstract

Epizootic outbreaks of red-sore disease in several reservoirs in the southeastern United States have been reported to cause heavy mortality among several species of fish having sport and commercial value. The etiologic agent is said to be the peritrich ciliate Epistylis sp.; secondary infection by the gram-negative bacterium Aeromonas hydrophila produces hemorrhagic septicemia which results in death. However, in recent studies on the largemouth bass Micropterus salmoides, Epistylis sp. could be isolated from only 35% of 114 lesions from 114 fish, while A. hydrophila was found in 96% of the same lesions. Transmission and scanning electron microscopy of lesions associated with red-sore disease indicate that neither the stalk nor the attachment structure of Epistylis sp. have organelles capable of producing lytic enzymes. Since other investigators have shown that A. hydrophila produces strong lytic toxins, and in absence of evidence to the contrary, it is concluded that Epistylis sp. is a benign ectocommensal and that A. hydrophila is the primary etiologic agent of red-sore disease.

PubMed Disclaimer

Similar articles

Cited by

Publication types

MeSH terms

LinkOut - more resources