Non‐O1, non‐O139 Vibrio cholerae bacteraemia in an Australian population

Abstract

This retrospective case series identifies the largest cohort of non-O1, non-O139 Vibrio cholerae bacteraemia in an Australian population from 2000 to 2013. We examine the risk factors, epidemiology, clinical presentations and mortality of non-O1, non-O139 V. cholerae bacteraemia in Victoria and compare them with published cases in the literature. This case series highlights the pathogenic potential of non-O1, non-O139 V. cholerae and identifies possible associations with host (underlying chronic liver disease and malignancy) and environmental factors (contaminated water supply and raw seafood). Clinicians should be aware of the morbidity and mortality associated with invasive non-O1, non-O139 V. cholerae infections, particularly in immunocompromised patients.

Non-O1, non-O139 Vibrio cholerae bacteraemia: case report and literature review

“…One hundred and twenty-eight articles described 350 cases of NOVC bacteraemia involving 347 patients, 3 of whom presented with a second episode (Additional file 1 : Table S1) (Petsaris et al 2010 ; Mannion and Mellor 1986 ; Lai et al 2012 ; Morris et al 1981 ; Anderson et al 2004 ; Pierce et al 2000 ; Hlady and Klontz 1996 ; Magnusson and Pegg 1996 ; Robins-Browne et al 1977 ; Eltahawy et al 2004 ; Marcenac et al 1991 ; Ferreira et al 2012 ; Zarate et al 2011 ; Goei and Karthigasu 1978 ; Trubiano et al 2014 ; Heath et al 2001 ; Guard et al 1980 ; Hsu et al 2013 ; Huhulescu et al 2007 ; Halabi et al 1997 ; Berghmans et al 2002 ; Kadkhoda et al 2012 ; Burns et al 1989 ; Ramsingh 1998 ; Briceno et al 2009 ; Young et al 1991 ; Lu et al 2014 ; Farmachidi et al 2003 ; Chong et al 1985 ; Choi et al 2003 ; Dalsgaard et al 2000 ; Marek et al 2013 ; Aguinaga et al 2009 ; Forné et al 1987 ; Prats et al 1975 ; Lopez-Brea et al 1985 ; Mirelis et al 1987 ; Royo et al 1993 ; Mauri et al 1987 ; Esparcia et al 2000 ; Fernández et al 2000 ; Lantero et al 1984 ; Folgueira et al 1991 ; Fernández-Monrás et al 1990 ; Catalá Barceló MT 1998 ; Fernández-Natal and Alcoba-Leza 1996 ; Calduch Broseta JV 2003 ; Rabadan and Vilalta 1989 ; Rubin et al 1981 ; Nedunchezian et al 1994 ; Pitrak and Gindorf 1989 ; Bonner et al 1983 ; Newman et al 1993 ; Namdari et al 2000 ; Patel et al…”

Two Cases of Bacteriemia Caused by Nontoxigenic, Non-O1, Non-O139 Vibrio cholerae Isolates in Ho Chi Minh City, Vietnam

“…However, other serogroups usually referred as non-O1 and non-O139 strains are occasionally reported to cause systematic infections. Patients with chronic syndromes, such as cirrhosis, hematologic abnormalities, renal dialysis, organ transplants, and immunosuppression, appear to be at increased risk of V. cholerae non-O1, non-O139 infections ( 7 – 11 ). Previous reports of retrospective studies originating from Taiwan ( 7 ) and Thailand ( 12 ) have described patients with cirrhosis and nontoxigenic Vibrio cholerae non-O1, non-O139 septicemia.…”

Non-O1/Non-O139 Vibrio cholerae Carrying Multiple Virulence Factors and V. cholerae O1 in the Chesapeake Bay, Maryland

“…However, infections other than cholera can be caused by nonepidemic V. cholerae serogroups that are collectively referred to as non-O1/non-O139 V. cholerae and are generally acquired through the consumption of raw or undercooked seafood. Non-O1/non-O139 V. cholerae infections are continuously reported worldwide (3,4), emphasizing their clinical significance. Although non-O1/non-O139 V. cholerae strains generally do not produce cholera toxin, other virulence factors contribute to their pathogenicity, including the hemolysin gene hlyA (5), the protease gene hapA (6), the cytotoxic actin cross-linking repeats in toxin gene rtxA (7), the sialidase gene nanH (8), the heat-stable toxin (NAG-ST) (9), a type 6 secretion system (T6SS) (10), and a type 3 secretion system (T3SS) (11).…”