Genotypic Characterization of Streptococcus infantarius subsp coli Isolates from Sea Otters with Infective Endocarditis and/or Septicemia and from Environmental Mussel Samples

University of California, Davis, Veterinary Medicine: Pathology, Microbiology and Immunology, 5318 VM3A, One Shields Avenue, Davis, CA 95616 USA.
Journal of clinical microbiology (Impact Factor: 3.99). 10/2012; 50(12). DOI: 10.1128/JCM.02581-12
Source: PubMed


Pulsed-field gel electrophoresis (PFGE) was used to type 128 Streptococcus infantarius subsp. coli isolates from sea otters and mussels. Six SmaI PFGE groups were detected, with one predominant group representing 57% of
the isolates collected over a wide geographic region. Several sea otter and mussel isolates were highly related, suggesting
that an environmental infection source is possible.

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    • "Infection by Streptococcus infantarius subsp. coli and other pathogenic streptococci has been associated with fatal vegetative valvular endocarditis, septicemia, and thromboembolic disease in southern and northern (Enhydra lutris kenyoni) sea otters, especially for otters stranding in Alaska (Burek et al. 2005; Counihan-Edgar et al. 2012). More recently, the facultatively anaerobic, beta-hemolytic, pyogenic bacterium Streptococcus phocae (Skaar et al. 1994; Romalde et al. 2008) has been reported from numerous marine animals. "
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    ABSTRACT: Recent studies have implicated beta-hemolytic streptococci as opportunistic pathogens of marine mammals, including southern sea otters (Enhydra lutris nereis), but little is known about their prevalence or pathophysiology. Herein, we focus on risk factors for sea otter infection by a single beta-hemolytic streptococcal species, Streptococcus phocae. Streptococcus phocae was first identified as a marine mammal pathogen in 1994, and the first report in southern sea otters was in 2009. Its broad host range encompasses fish, pinnipeds, cetaceans, and mustelids, with S. phocae now recognized as an important pathogen of marine species worldwide. We assessed risk factors and lesion patterns for S. phocae infection in southern sea otters. Using archival necropsy data, S. phocae prevalence was 30% in fresh dead otters examined 2004-2010. Skin trauma of any type was identified as a significant risk factor for S. phocae infection. The risk of infection was similar regardless of the cause and relative severity of skin trauma, including mating or fight wounds, shark bite, and anthropogenic trauma. Streptococcus phocae-infected sea otters were also more likely to present with abscesses or bacterial septicemia. Our findings highlight the importance of S. phocae as an opportunistic pathogen of sea otters and suggest that the most likely portal of entry is damaged skin. Even tiny skin breaks appear to facilitate bacterial colonization, invasion, abscess formation, and systemic spread. Our data provide important insights for management and care of marine species.
    Full-text · Article · Nov 2015 · Journal of wildlife diseases
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    • "Because of a decline in the southwestern stock of northern sea otters in Alaska and slow population recovery of southern sea otters in California, these populations are currently listed as ''threatened'' under the United States Endangered Species Act (US Fish and Wildlife Department 2008; US Geological Survey 2010). Causes of the decline and slow recovery are multifactorial and mediated through complex interactions among sea otter populations and numerous biotic and environmental factors, including infectious diseases (Kreuder et al. 2003, Goldstein et al. 2009, Miller et al. 2010b, Counihan-Edgar et al. 2012). Epidemiological studies have demonstrated that southern sea otters are at high risk for exposure to gastrointestinal protozoal pathogens and opportunistic bacteria in the coastal waters of central California (Miller et al. 2008, Miller et al. 2010a). "
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    ABSTRACT: Abstract Since 2002, an increased number of northern sea otters (Enhydra lutris kenyoni) from southcentral Alaska have been reported to be dying due to endocarditis and/or septicemia with infection by Streptococcus infantarius subsp. coli. Bartonella spp. DNA was also detected in northern sea otters as part of mortality investigations during this unusual mortality event (UME) in Kachemak Bay, Alaska. To evaluate the extent of exposure to Bartonella spp. in sea otters, sera collected from necropsied and live-captured northern sea otters, as well as necropsied southern sea otters (Enhydra lutris nereis) unaffected by the UME, were analyzed using an immunofluorescent antibody assay. Antibodies against Bartonella spp. were detected in sera from 50% of necropsied and 34% of presumed healthy, live-captured northern sea otters and in 16% of necropsied southern sea otters. The majority of sea otters with reactive sera were seropositive for B. washoensis, with antibody titers ranging from 1:64 to 1:256. Bartonella spp. antibodies were especially common in adult northern sea otters, both free-living (49%) and necropsied (62%). Adult stranded northern sea otters that died from infectious causes, such as opportunistic bacterial infections, were 27 times more likely to be Bartonella seropositive than adult stranded northern sea otters that died from noninfectious causes (p<0.001; 95% confidence interval 2.62-269.4). Because Bartonella spp. antibodies were detected in necropsied northern sea otters from southcentral (44%) and southwestern (86%) stocks of Alaska, as well as in necropsied southern sea otters (16%) in southcentral California, we concluded that Bartonella spp. exposure is widely distributed among sea otter populations in the Eastern Pacific, providing context for investigating future disease outbreaks and monitoring of Bartonella infections for sea otter management and conservation.
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