Lee Ya-Ling, Hung Po-Pin, Tsai Che-An, Lin Yu-Hui, Liu Chun-Eng, Shi Zi-Yuan
Division of Infectious Disease, Department of Internal Medicine, Taichung Veterans General Hospital, Taichung, Taiwan.
J Microbiol Immunol Infect. 2007 Dec;40(6):474-80.
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.
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.
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].
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.
非O1/非O139群霍乱弧菌可引起侵袭性肠外疾病以及肠炎。侵袭性非O1/非O139群霍乱弧菌感染的发病机制尚待确定。本研究比较了菌血症性和非菌血症性非O1/非O139群霍乱弧菌感染之间的临床表现和易感因素，并检测了引起侵袭性疾病的致病菌株中的毒力相关基因。
我们回顾性调查了18例菌血症患者和18例非菌血症患者的临床特征，包括人口统计学、实验室和临床数据。获取了14株临床分离株（10株从血液中分离，4株从粪便标本中分离），用于对毒力相关基因ctxA、ctxB和tcpA的存在情况进行聚合酶链反应检测。
菌血症组和非菌血症组在年龄、性别以及包括腹痛和腹泻在内的胃肠道症状、包括白细胞增多和贫血在内的实验室检查结果，或除肝硬化外的潜在免疫功能低下状况方面均无差异。与非菌血症感染患者相比，非O1/非O139群霍乱弧菌菌血症患者患肝硬化和血小板减少症的可能性显著更高（分别为0.0%对77.8%和5.9%对72.2%；p<0.001）。在14株临床菌株中，仅在1株菌株（从一名肠炎患者的粪便标本中分离）中发现霍乱毒素基因（ctxA和ctxB）（7%）。编码毒素共调节菌毛的tcpA基因在14株分离株中的13株（93%）中存在[包括10株从血液中分离的菌株和3株从粪便标本中分离的菌株]。
伴有血小板减少症的肝硬化患者易发生非O1/非O139群霍乱弧菌血行感染。粪便标本中ctxA和ctxB基因的低流行率表明其他毒素可能导致腹泻。本研究中tcpA基因在临床分离株中高度流行这一事实可能意味着tcpA在非O1/非O139群霍乱弧菌引起的侵袭性疾病发病机制中起重要作用。
