Role of Cholera Toxin in <i>Vibrio cholerae</i> Infection in Humans - A Review

Abstract

Vibrio cholerae, the causative agent of Asiatic cholera, is a gram-negative motile bacterial species acquired via oral ingestion of contaminated food or water sources. Cholera has spread from the Indian subcontinent where it is endemic to involve nearly the whole world seven times during the past 185 years. V. cholerae serogroup O1, biotype El Tor, has moved from Asia to cause pandemic disease in Africa and South America during the past 35 years. A new serogroup, O139, appeared in south Asia in 1992, has become endemic there, and threatens to start the next pandemic. The facultative human pathogen V. cholerae represents a paradigm that evolved from environmental nonpathogenic strains by acquisition of virulence genes. The major virulence factors of V. cholerae, cholera toxin (CTX) encoded by the ctxAB genes residing in the genome of filamentous lysogenic bacteriophage (CTXɸ) and toxin coregulated pilus (TCP) encoded by vibrio pathogenicity island (VPI). CTX, a potent stimulator of adenylate cyclase, causes the intestine to secrete watery fluid rich in sodium, bicarbonate, and potassium, in volumes far exceeding the intestinal absorptive capacity, by ADP-ribosylation of the alpha subunit of the GTP-binding protein. Thus intestinal infection with V. cholerae results in the loss of large volumes of watery stool, leading to severe and rapidly progressing dehydration and shock. Without adequate and appropriate rehydration therapy, severe cholera kills about half of affected individuals. Today, cholera still remains a burden mainly for underdeveloped countries, which cannot afford to establish or to maintain necessary hygienic and medical facilities. During the last three decades, intensive research has been undertaken to unravel the virulence properties and to study the epidemiology of this significant human pathogen. This review provides an overview of the role of CTX in the occurrence of this disease in humans.

Detection of genes encoding ompW and ctxA of Vibrio cholerae isolated from shrimp and shellfish at Kedonganan fish market, Bali-Indonesia

“…Some virulence factors present in V. cholera are ToxR regulator, cholerae toxin (consisting of ctxA and ctxB), toxin-coregulated pilus subunit (TcpA), outer membrane protein U (ompU), outer membrane protein W (ompW), accessory cholerae enterotoxin (Ace), and zonula occludens toxin (Zot) (Waturangi et al, 2013;Ramazanzadeh et al, 2015). Cholerae toxin is responsible for the occurrence of diarrhea in cholera outbreaks (Sikora, 2013, Pal, 2014. The ctx gene is usually owned by V. cholerae pathogens of serogroups O1 and O139 (Maheshwari et al, 2011a;Dalusi et al, 2015) but non-O1/O139 are known to carry ctx genes such as the outbreak that occurred in the United States in 2011 caused by V. cholerae serogroup O75 that was transmitted through raw oyster consumption (Onifade et al, 2011).…”

A Review on Bacterial Food-Borne Disease

“…The most symptoms of vibriosis include: vomiting, diarrhea, abdominal cramps, and nausea may result. To prevent food infection must be avoided of contaminated waters to ishermen, storage shell ish in refrigeration to prevent the growth of vibrio and good cooking for shellish (Pal, 2014).…”

Molecular Mechanism of Cholerae Toxin (ctx) in Causing Diarrhea

“…Prior to 1992, only V. cholerae O1 was known to produce cholerae toxin and was the cause of endemic and epidemic outbreaks. Later, V. cholerae O139 is also known to produce toxins in quantities as large as serogroup O1 (Faruque, 1998, Pal, 2014. Today, V. cholerae serogroup O1 and O139 are considered to be pathogenic Vibrio groups that produce cholerae toxin (Dziejman et al, 2002;Ryan and Ray, 2004;Olaniran et al, 2011).…”