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The Enemy
Cholera is an infectious disease caused by Vibrio cholera. The comma-shaped bacillus bacterium thrives in aquatic environments and brackish water where it is found attached to crustaceans (Desselberger 2000). Vibrio cholera colonies thrive under conditions of low salinity and warm temperatures in estuaries, where they occur in the silt in a non-active form. Halpern et al. (2007), using the FISH technique, found that egg masses of midges harbor Vibrio cholerabacteria. In all these cases, this bacterium causes no infection to the organisms in the environment; it becomes dangerous only when it enters the human system that becomes infectious.
The Defense
Cholera is a non-inflammatory condition; it does not damage the mucosa of the small intestines. However, acute cholera can cause over-secretion of cytokines, such as interleukins, which cause inflammation of the intestinal mucosa (Satcher 2005). This leads to accumulation of neutrophils in the mucosa as an innate immune response to inflammation. Polymorphism in the LPLUNC1 gene, which is associated with increased susceptibility to cholera, increases the risk of infection (Satcher 2005). By contrast, adaptive immune responses to the bacterium are unknown. However, as V. cholera is a non-inflammatory microbe, high levels of secretory immunoglobulin A (sIgA) in serum offer protection against re-exposure to the pathogen (Satcher 2005). The intestinal slgA remains detectable in the blood for up to one year after infection by Vibrio cholera.
The War
Vibrio cholera, the microbe that causes cholera, normally completes its natural life cycle in estuarine ecology. Organisms, such as crustaceans, aquatic plankton and snails as well as silt in the estuary, mediate its life cycle (Nelson et al 2009). Vibrio cholera enters the digestive system of humans through the ingestion of contaminated water or food. Contaminated food, particularly seafood like crabs and oysters, when eaten raw, is another source of cholera infection. Also, Vibrio cholera can be ingested through contaminated drinking water, vegetables or fruits.
The bacterium is often transmitted from one person to another through ingestion of food or water contaminated with feces containing the bacteria (Nelson et al 2009). Once ingested, the bacteria multiply rapidly and produce toxins that stimulate secretion of electrolytes in the intestines leading to severe diarrhea and vomiting. Vibrio cholera in the intestines is excreted with each diarrhea to the environment, hence rapidly spreading to other people and resulting in an outbreak.
The Casualty
Cholera infections are often asymptomatic; however, within 1 to 5 days following an infection, patients show symptoms of severe diarrhea and vomiting. Dehydration and leg cramps also occur in some people due to loss of water through diarrhea (Slifko, Smith & Rose 2000). Dehydrated patients show signs of low blood pressure, weight loss and dry skin.
The Victory
Cholera diagnosis is recommended for patients with severe diarrhea and dehydration. Laboratory diagnosis techniques include stool PCR, gram staining and microscopy (Slifko, Smith & Rose 2000). Treatment involves the use of oral rehydration therapy and antibiotics. Prevention involves consumption of well-cooked food and peeled fruits for salads.
References
Desselberger, U 2000, ‘Emerging and re-emerging infectious diseases’, Journal of Infection, vol.40, no. 4, pp. 3-9.
Halpern, M, Landsberg, O, Raats, D, & Rosenberg, E 2007, ‘Culturable and VBNC Vibrio cholera: interactions with Chironomid egg masses and their bacterial population’,Microbial Ecology, vol. 53, no. 2, pp. 285-293.
Nelson, J, Harris, B, Morris, G, Calderwood, S & Camilli, A 2009, ‘Cholera Transmission: the host, pathogen and bacteriophage dynamic’, Nature Reviews Microbiology, vol. 7, no. 2, pp. 693-702.
Satcher, D 2005, ‘Emerging infections: Getting ahead of the curve’, Emerging Infectious Diseases, vol. 13, no. 1, pp. 1-6.
Slifko, T, Smith, H & Rose, J 2000, ‘Emerging parasite zoonoses associated with Water and food’, International Journal for Parasitology, vol. 30, no. 4, pp. 379-393.
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