Journal of microbiology, immunology, and infection = Wei mian yu gan ran za zhi · 2007
Clinical characteristics of non-O1/non-O139 Vibrio cholerae isolates and polymerase chain reaction analysis of their virulence factors.
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Lee Ya-Ling, Hung Po-Pin, Tsai Che-An, Lin Yu-Hui, Liu Chun-Eng, Shi Zi-Yuan
Аннотация
BACKGROUND AND PURPOSE: Non-O1/non-O139 Vibrio cholerae can cause invasive extraintestinal disease as well as enteritis. The pathogenesis of invasive non-O1/non-O139 V. cholerae infections remains to be determined. This study compared the clinical manifestations and predisposing factors between bacteremic and non-bacteremic non-O1/non-O139 V. cholerae infections and examined virulence-associated genes in the pathogenic strains causing invasive disease.
METHODS: We retrospectively investigated clinical characteristics of 18 bacteremic patients and 18 non-bacteremic patients, including demographic, laboratory and clinical data. Fourteen clinical isolates (ten isolated from blood and four from stool specimens) were obtained for polymerase chain reaction tests of the presence of virulence-associated genes ctxA, ctxB and tcpA.
RESULTS: There was no difference in age, gender and gastrointestinal symptoms including abdominal pain and diarrhea, laboratory findings including leukocytosis and anemia, or underlying immunocompromised condition, except cirrhosis, between the bacteremic and non-bacteremic groups. Compared to patients with non-bacteremic infections, patients with non-O1/non-O139 V. cholerae bacteremia were significantly more likely to have cirrhosis and thrombocytopenia (0.0% vs 77.8% and 5.9% vs 72.2%, respectively; p<0.001). The cholera toxin genes (ctxA and ctxB) were found in only one strain (isolated from the stool specimen of a patient with enteritis) among fourteen clinical strains (7%). The tcpA gene, encoding the toxin-coregulated pilus, was present in thirteen of fourteen isolates (93%) [including ten isolates from blood, and three isolates from stool specimens].
CONCLUSIONS: Cirrhotic patients with thrombocytopenia were vulnerable to non-O1/non-O139 V. cholerae bloodstream invasion. The low prevalence of ctxA and ctxB genes in stool specimens indicates other toxins could have contributed to diarrhea. The fact that the tcpA gene was highly prevalent in clinical isolates in this study could imply an important role of tcpA in the pathogenesis of invasive disease caused by non-O1/non-O139 V. cholerae.
METHODS: We retrospectively investigated clinical characteristics of 18 bacteremic patients and 18 non-bacteremic patients, including demographic, laboratory and clinical data. Fourteen clinical isolates (ten isolated from blood and four from stool specimens) were obtained for polymerase chain reaction tests of the presence of virulence-associated genes ctxA, ctxB and tcpA.
RESULTS: There was no difference in age, gender and gastrointestinal symptoms including abdominal pain and diarrhea, laboratory findings including leukocytosis and anemia, or underlying immunocompromised condition, except cirrhosis, between the bacteremic and non-bacteremic groups. Compared to patients with non-bacteremic infections, patients with non-O1/non-O139 V. cholerae bacteremia were significantly more likely to have cirrhosis and thrombocytopenia (0.0% vs 77.8% and 5.9% vs 72.2%, respectively; p<0.001). The cholera toxin genes (ctxA and ctxB) were found in only one strain (isolated from the stool specimen of a patient with enteritis) among fourteen clinical strains (7%). The tcpA gene, encoding the toxin-coregulated pilus, was present in thirteen of fourteen isolates (93%) [including ten isolates from blood, and three isolates from stool specimens].
CONCLUSIONS: Cirrhotic patients with thrombocytopenia were vulnerable to non-O1/non-O139 V. cholerae bloodstream invasion. The low prevalence of ctxA and ctxB genes in stool specimens indicates other toxins could have contributed to diarrhea. The fact that the tcpA gene was highly prevalent in clinical isolates in this study could imply an important role of tcpA in the pathogenesis of invasive disease caused by non-O1/non-O139 V. cholerae.