Pathogenesis of Cholera: Recent Prospectives in Rapid Detection and Prevention of Cholera

Abstract

Cholera, also known as "blue death" is a potentially epidemic and life-threatening secretory diarrhea characterized by numerous voluminous watery stools, often accompanied by vomiting and resulting in hypovolemic shock and acidosis. The causative agent of this water-borne disease belongs to certain members of the species Vibrio cholerae (V. cholerae) which can also cause mild or unapparent infections. V. cholerae is a facultative anaerobic, Gram-negative bacilli, which possess the characteristic feature of darting motility under wet-mound preparations. Other members of the species may occasionally cause isolated outbreaks of milder diarrhea, whereas others-the vast majority-are free-living and not associated with disease. The emergence of new, virulent, drug-resistant strains of Vibrio is the main cause of protracted outbreaks leading to high fatality rates. The subsequent loss of fluid volume causes a drop in blood pressure and circulatory shock. If the patient remains untreated, they become progressively weaker, sometimes to the point of death, within 12-24 h of the onset of symptoms. The severity and fatality of the disease depend on the strain of Vibrio. The cholera toxin-producing (CT-producing) V. cholerae manifests the most fatal disease known as cholera gravis. Throughout most of the twentieth century, cholera was caused by V. cholerae of the O1 serogroup, and the disease was largely confined to Asia and Africa. The emergence of a pandemic in 1992 was caused by an unknown serogroup of V. cholerae (O139) wherein the targets were India and Bangladesh. The pathogenesis and virulence of the bacteria are due to an enterotoxin it producescholera toxin (CT). The mechanism of action of CT is discussed in this chapter at a later stage. Attempts have been made to produce vaccines through a number of trial-and-error methods, and still the possibility of an effective vaccine which gives a good prophylactic measure is under consideration. The identification of the bacteria as well as toxin detection is one of the main elements in the clinical microbiology field. The identification and confirmation of this epidemic disease commend from the morphological identification of Vibrio and end with serotyping and biotyping in addition to toxin detection by various means of assays-both in vitro and in vivo. This chapter will cover all of the mentioned areas of clinical microbiology with respect to cholera infection in addition to the recent outbreaks and epidemics which occurred across the globe.

Cholera rages in Africa and the Middle East: A narrative review on challenges and solutions

“…PCR requires a sample to be grown in pure culture without requiring viable strains. PCR can also detect the pathogen in food, water, and rectal swabs, it does not require a stool sample as most of the tests 129 …”

Intestinal colonization against <i>Vibrio cholerae</i>: host and microbial resistance mechanisms

“…In a separate study recently, to determine the significance and involvement of T6SS in V. cholerae colonization, T6SS mutants were designed and orally administered to mice, the results obtained proved that T6SS is important to V. cholerae successful colonization as the mutant strains show significantly lower intestinal colonization compared to wild-type V. cholerae with functional T6SS system [45] . Furthermore, V. cholerae can produce mucolytic enzymes, such as sialidases, peptidases, and sulphatases, to digest the mucus and, with the aid of its single flagellum, can propel itself into the thick mucosal layer to the intestinal epithelial surface to adhere [46] , [47] . Also, a study by Wang et al proved that the pathogen could utilize mucins as an energy source through the gluconeogenesis pathway during and after colonizing the gut, mucin is the major component of mucus [48] .…”

What are the drivers of recurrent cholera transmission in Nigeria? Evidence from a scoping review

“…The mechanism by which biological factors drive cholera transmission appears to be largely genetic-based, as opined by Adewale et al [57], Marin et al [58], and Oyedeji et al [42]. Generally, genetic mutation has been demonstrated to be linked with the emergence of new, virulent and drugresistant strains of V. cholerae [3]. For example, Hu et al [59] argue that the seventh cholera pandemic became prominent in 1961 after V. cholerae underwent series of mutations, with suitable niches in the Middle East and gene sources from Makassar to aid the genetic events.…”

“…Cholera is often characterised by a rapid onset of watery diarrhoea, with or without vomiting, and an extensive dehydration [2]. When prompt rehydration therapy is not administered for severe cases, cholera can result in severe clinical sequel including lethargy, unconsciousness, confusion, and a drop in blood pressure and circulatory shock as well as death [3]. The case fatality rate (CFR) from untreated cholera cases can be as high as 30-50%, although the value could be as low as 1% with adequate and prompt care [2].…”