Monday, 21 March 2016

Post 3: Streptococcus: the Flesh Eating Bacteria in the Far North & the Evolution of an Epidemic

Between the years 2007 to 2011, over 90 Queensland Grouper (Epinephelus lanceolatus) and a variety of wild fish and estuarine stingrays were found dead in the Cairns inlet in Far North Queensland (Bowater et al 2012). The symptoms were black patches of necrotic tissue and visible signs of both internal and external bleeding. The Department of Northern Fisheries diagnosed the problem as a disease called Streptococcus agalactiae, a flesh eating bacterium, which lead to septicaemia (Presence of bacterium in the blood) in the infected (Bowater et al 2012). This was the first recorded outbreak of S. agalactiae in Australia (Bowater et al 2012) and because it occurred in the wild, there was very little that responders could do besides removing the infected and deceased individuals from the environment. 

In the last 30 years, Streptococcus has been realised as an epidemic, with S. agalactiae being the leading cause of fast spreading infections in new born mammals (Brochet et al 2006). 
Other symptoms aside from skin necrosis and internal bleeding, infected fish can be seen swimming erratically and their eyes appear bulging (Abuseliana et al 2011). 

In an aquaculture or aquarium setting, antibiotics are the only realistic treatment for S. agalactiae when septicaemia is present. S. agalactiae has however evolved a number of resistances to antibiotics with 9 similtaneous antibiotic resistances being seen using PCR tests (Zeng et al 2006).
The first treatment should be a ten day course of the antibiotic Oxy-tetra Cycline (OTC) by either incorporating this into food or dosing the water body. If this treatment doesn't work, it becomes a trial and error process with other antibiotics to see what can irradicate the bacterium from the system.

A deceased Queensland Grouper that died during the Streptococcus outbreak in Cairns


References:

Abuseliana, A. Daud, H. Aziz, S. Bejo, S. Alsaid, M 2011, 'Pathogenicity of Streptococcus agalactiae Isolated from a Fish Farm in Selangor to Juvenile Red Tilapia (Oreochromis sp.)', 'Journal of Animal and Veterinary Advances', vol.10, pp. 914-919

Bowater, R. Forbes-Faulkner, J. Anderson, I. Condon, K. Robinson, B. Kong, F. Gilbert, G. Reynolds, A. Hyland, S. McPherson, G. O'Brien, J. Blyde, D 2012, 'Natural Outbreak of Streptococcus agalactiae (GBS) Infection in Wild Giant Queensland Grouper, Epinephelus lanceolatus (Bloch), and Other Wild Fish in Northern Queensland, Australia', 'Journal of Fish Dieseases', vol. 35, pp. 173-186

Brochet, M. Couve, E. Zouine, M. Vallaeys, T. Rusniok, C. Lamy, M. Buchrieser, C. Trieu-Cuot, P. Kunst, F. Poyart, C. Glaser, P 2006, 'Genomic Diversity and Evolution within the Species Streptococcus agalactiae', 'Microbes and Infection', vol. 8, pp. 1227-1243

Zeng, X. Kong, F. Wang, H. Darbar, A. Gilbert, G 2006, 'Simultaneous Detection of Nine Antibiotic Resistance-Related Genes in Streptococcus agalactiae Using Multiplex PCR and Reverse Line Blot Hybridization Assay', 'Antimicrobial Agents and Chemotherapy', vol. 50, pp. 204-209

















2 comments:

  1. That fish is absolutely ginormous! I assume that this bacterium infects fish indiscriminately (i.e. it is not specific to one group or another)? Is there any idea where this originated from or why it has becoming so prevalent in recent years?

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  2. Hi Tasmin,
    Yes so the disease has been documented to infect a variety of fish, mammals and even reptiles, however outbreaks in fish have been seen as very severe, which suggests fish have a unique susceptibility-this is thought to be because mammals and reptiles have very different virulence factors to fish.
    The streptococcus genus was first realized in the late 19th century, however work is still being done to determine the putative origin of S. agalactiae in Australia, generally involving gene sequencing. As to why it has become an epidemic, bacteria have the ability to exchange plasma with other bacterium and through this they can actually gain resistance to treatments and a variety of functions we're still learning about. This ability helps bacterial evolution to numerous antibiotic resistence

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