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Group B Streptococcus memorialhealth.com | Streptococcus suis News and Headlines by Microbes.info microbes.info | streptococcus roadback.org |
Streptococcus iniae is a species of Gram-positive, sphere-shaped bacteria belonging to the genus Streptococcus. It is an economically important pathogen in many species of fish, and may occasionally produce infection in humans. S. iniae has been called "one the most serious aquatic pathogens [...] causing high losses in farmed marine and freshwater finfish in warmer regions", with an estimated worldwide economic impact of US$100 million in 1997.[2]
[edit] HistoryS. iniae was first isolated in 1972 (and reported in 1976), from subcutaneous abscesses in a captive specimen of Amazon River Dolphin (Inia geoffrensis) suffering from an infection known as "golf ball disease".[1] The bacterium was found to be sensitive to beta-lactam antibiotics, and the dolphin was treated successfully with penicillin and tylosin.[1] In the 1980s, a purported new species of Streptococcus, named S. shiloi, was identified as one of the causes of an epidemic of meningoencephalitis (an inflammation of the brain and its surrounding membranes) affecting farmed rainbow trout and tilapia in Israel since 1986.[3] One year later, the use of DNA-DNA hybridization techniques revealed that S. shiloi was the same organism as S. iniae, and the original name was kept.[4][5] [edit] IdentificationStreptococcus iniae may be easily misidentified (or not identified at all) by conventional automated microbiology systems. Molecular genetics methods, such as DNA sequencing and DNA-DNA hybridization, can be useful for correct identification, although work by the U.S. Centers for Disease Control and Prevention has suggested they are unnecessary in most cases.[6] S. iniae is beta-hemolytic when incubated in anaerobic conditions, although it may be misidentified as alpha-hemolytic because, in some strains, zones of beta-hemolysis (complete destruction of red blood cells in the culture media) are surrounded by large zones of alpha-hemolysis (incomplete destruction of red blood cells with a greenish discoloration due to breakdown of hemoglobin).[7] It is catalase-negative and LAP-positive (like all streptococci), PYR-test and CAMP test-positive, does not hydrolyze sodium hippurate and does not grow in bile esculin agar.[5] It does not express any of the knownLancefield antigens.[5] [edit] Role in disease[edit] In fish Streptococcus iniae is highly pathogenic in freshwater, marine, and euryhaline fish, and is highly lethal: outbreaks may be associated with 30–50% mortality.[10] It is therefore one of the foremost economically important pathogens in intensive aquaculture.[2][11] In 1997, the global economic impact of S. iniae infection to the aquaculture industry was estimated at US$100 million (one-tenth of which in the United States).[2] As of 2007, infection had been reported in twenty-seven species of fish, including tilapia (genus Oreochromis and Tilapia), rainbow trout (Oncorhynchus mykiss), coho salmon (Oncorhynchus kisutch), Japanese amberjack (Seriola quinqueradiata), red drum (Sciaenops ocellatus), and barramundi (Lates calcarifer, which can be an asymptomatic carrier).[12][13][14] Common carp (Cyprinus carpio), channel catfish (Ictalurus punctatus), and goldfish (Carassius auratus) appear to be resistant.[2] The site of S. iniae infection and its clinical presentation vary from species to species. In tilapia, S. iniae causes meningoencephalitis, with symptoms including lethargy, dorsal rigidity, and erratic swimming behavior; death follows in a matter of days.[10][12][15] In rainbow trout, it is typically associated with septicemia and central nervous system damage. Symptoms are consistent with septicemia, and include lethargy and loss of orientation (as in tilapia), exophthalmia, corneal opacity, and external and internal bleeding.[8][15] [edit] In humansSee also: Cutaneous Streptococcus iniae infection Streptococcus iniae can cause opportunistic infections in humans. It is most commonly associated with bacteremic cellulitis, but has been known to cause endocarditis, meningitis, osteomyelitis, and septic arthritis.[13] Human infection with S. iniae was first identified in Toronto, Canada, between 15 and 20 December 1995, when three Asian patients were admitted to a hospital with cellulitis of the hand after injuring themselves while handling raw fish. All three were found to have bacteremia, initially attributed to Streptococcus uberis, but later correctly identified as S. iniae.[12][10] In February 1996, a Chinese man was admitted to the same hospital with sepsis one week after preparing a fresh whole tilapia, and was also diagnosed with S. iniae bacteremia.[12][10] A subsequent epidemiological investigation found other cases in the Toronto area, for a total of nine patients; all were of Asian descent and all had handled raw fish (mostly tilapia) before developing infection.[12] Other cases were later identified in the United States and elsewhere in Canada, and have since been reported in Asia (Hong Kong, Taiwan, and Singapore).[13][16][17] [edit] TreatmentSeveral antibiotics have been used successfully to treat S. iniae infection in fish. Enrofloxacin, a quinolone antibiotic, has been used to great effect in hybrid striped bass (Morone chrysops × M. saxatilis), although evidence suggested the development of a resistant strain.[18] Amoxicillin, erythromycin, furazolidone, and oxytetracycline have also been used (the latter with varying success, only in barramundi).[2] Vaccination against S. iniae has been attempted with limited success.[2] Penicillin has been suggested as the drug of choice for the treatment of S. iniae infection in mammals, including humans.[2][13][6] In the 1995–1996 cluster of human cases, all clinical isolates were susceptible to penicillin, several cephalosporins, clindamycin, erythromycin, and co-trimoxazole (MICs (0.25 mcg/mL); all nine patients were treated with parenteral beta-lactam antibiotics and recovered uneventfully.[12][10] A study of isolates submitted to the Centers for Disease Control and Prevention between 2000 and 2004 found all to be sensitive to beta-lactams, macrolides, quinolones, and vancomycin.[6] [edit] References
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