Introduction
Cholera is an infectious disease that is caused by a bacterium known as Vibrio cholerae (Raufman, 1997). It is transmitted through consumption of water or food that contains traces of fecal matter. Even though an individual might not show signs or symptoms of the disease, his fecal material may transmit the disease if it contaminates drinking water or food. Cholera is caused by a fast toxin delivery mechanism that activates the adenyl cyclase system of the small intestine’s cells that are involved in secretion of enzymes (Raufman, 1997). Symptoms include vomiting, headache, and watery diarrhea. In severe cases, it may lead to quick dehydration, electrolyte imbalance in the body, and death (Sack et al, 2004). The most common treatment that is widely used for treatment of cholera is oral rehydration therapy. It is the most preferred form of treatment because it hydrates individuals who have lost a lot of water due to the effects of the disease. In severe cases, antibacterial drugs are used together with hydration to improve the recovery process. Globally, cholera affects between 3 million and 5 million people annually and causes between 100,000 and 130,000 deaths annually (Jackson, 2012).
The Epidemiological Triad Model
The Epidemiological triad refers to a model that explains how a disease is spread from a reservoir to a host. The model has three main components that include a causative agent, a host, and an environment (Raufman, 1997). The agent refers to the organism that infects such as a bacterium or virus. The host refers to the organism that is infected by the agent and that succumbs to the disease. The environment refers to the place and conditions under which an agent lives in, which facilitate its infectivity. According to the model, transmission involves the release of an agent from a reservoir trough an exit portal (Raufman, 1997). The agent is deposited into a host through a portal of entry. This is achieved through the action of a certain mode of transmission. After entry, the agent infects the host.
The causative agent for cholera is a bacterium known as Vibrio cholerae. It is a comma shaped gram-negative bacterium that possesses a flagellum at one end (Sack et al, 2004). Its pathogenicity includes secretion of a protein known as cholera toxin that causes watery diarrhea. The bacterium is transported to a host through contaminated water or food (Sack et al, 2004). The host for the agent is a human being. Food materials such as contaminated fish or leftover food materials are effective modes of transmission for the agent. The environment of the agent is the small intestines. The agents attaches to the walls of the small intestines from where it infects the host. The environment includes thick mucus and high PH that alter the proper functioning of the bacterium (Raufman, 1997).
Chain of infection
Vibrio cholerae possesses 155 different serogroups. However, only two of these groups, O1 and O139 are responsible for all reported cases of cholera (Faruque et al, 1998). Virulence factors of the bacterium include cholera toxin that causes watery diarrhea, and toxin co-regulated pilus. Cholera toxin is transported by a lysogenic bacteriophage, which ensures that the toxin gene retains its infectivity (Sack et al, 2004). The toxin co-regulated pilus binds colonies of bacteria for continuous infection. V. cholerae bacterium has two main reservoirs. These include humans and the aquatic environment. Humans are the primary reservoirs of the bacterium, and are in many cases asymptomatic carriers (Faruque et al, 1998). These bacteria can infect a host immediately after they are released from a reservoir. A very small infectious dose is required to cause an infection due to the high infectivity of the bacterium. Research studies have revealed that V. cholerae alters its model of gene transcription in order to enhance its survival in conditions such as high PH (Faruque et al, 1998).
V. cholerae exits the human reservoir through the anal opening. Humans discard infectious segments of the bacterium into the environment. Patients who show symptoms of infection release the largest portion of fragments into the environment that are responsible for most cases of cholera. Individuals who do not show symptoms even though they are infected shed the bacterium for only a day (Faruque et al, 1998). The bacterium exits aquatic reservoirs through drinking water or contaminated food such as fish.
The mode of transmission of V. cholerae is consumption of contaminated water, or food that has been prepared with contaminated water (Nelson et al, 2009). In rare cases, the bacterium is transmitted orally from an infected individual to a healthy individual. Person-to-person transmission is rare. After release form a reservoir and transmission through contaminated water or food, the bacterium then enters a susceptible host through the mouth, which acts as a portal of entry (Raufman, 1997). It enters through ingestion of contaminated water or food. The chain can be broken by washing hands carefully with clean water before handling food or after visiting a restroom (Nelson et al, 2009). In addition, drinking sterilized water and food that has been prepared using clean water can help break the chain. Susceptible hosts include young children, pregnant women, elderly people, infants, and individuals with health conditions that cause dehydration thus necessitating constant monitoring (Raufman, 1997).
Prevalence of cholera in the United States
There have been very few reported cases of cholera in the United States. Of all cholera cases reported from 1973, 90% of these cases happed between 2007 and 2012. A large percentage of reported cases have involved infected individuals travelling to America from other countries. In San Diego, cases of cholera are very rare. The most recent case of cholera was reported in 1992, which was after a couple of decades without a cholera case in the county (Glass et al, 1992). The situation is different in Haiti where more than 470,000 cases have been reported (Newton et al, 2011). However, the number of deaths is unclear because many people cannot afford medical treatment due to poverty. In the US, cases of cholera can be reported to any government hospital or Center for Disease Control and Prevention (CDC).
Clinical course of infection
After ingestion, most bacteria die because of the unfavorable environment of the stomach. Bacteria that survive halt production of proteins in order to conserve energy to use during infection (Faruque et al, 1998). After reaching the small intestines, V. cholerae secretes flagellin that facilitates formation of flagellum that enables it to move through the thick mucus of the small intestines (Faruque et al, 1998). The bacterium halts production of flagellin after adhering to walls of the small intestines. It then starts producing a protein known as cholera toxin that causes watery diarrhea. The cholera toxin comprises six distinct protein subunits. They include one copy of A subunit and six copies of B subunits. A complex of B subunits and ADP-ribosylates G proteins is transported into the cell through the process of endocytosis (Faruque et al, 1998). The disulfide bonds that bind the five B subunits are reduced thus freeing a bound A1 subunit. The A1 subunit binds with a human protein known as ADP-ribosylation factor 6. This results in production of cAMP (cyclic adenosine 5¹-monophosphate) (Faruque et al, 1998). cAMP then facilitates secretion of water, sodium ions, chloride ions, potassium ions, and hydrogen carbonate ions into the lumen causing dehydration (Faruque et al, 1998).
Confirmation of cholera
Cholera is confirmed using a rapid dip-stick test and other laboratory tests. Additional tests are carried out on samples to determine the degree of resistance of the bacterium for proper medication. In addition, laboratory tests using stool and swab samples are also used. Cholera is confirmed by isolation of V. cholerae from patient samples.
Vaccine
A vaccine for cholera is available. However, most people are not vaccinated because preventive measures are enough to protect individuals from cholera infection (Williams et al, 2010). The vaccine is administered through the mouth and is dissolved in water for ease of administration. Vaccination includes two doses for adults and children, and three doses for infants. The vaccine is not strong enough to provide immunity for a long period. Therefore, a booster is needed after vaccination to improve sustain the effects of the vaccine for a longer time. The booster is administered after two years, a time when the effectiveness of the vaccine has reduced (Williams et al, 2010). The vaccine is not very effective in providing immunity against cholera because it only provides immunity against one serogroups of the bacterium. This implies that it is important to take preventive measures or increased immunity.
Treatment
Treatment options include use of fluids, electrolytes, and antibiotics. Oral rehydration therapy is the best treatment because it replaces lost water and electrolytes in the body (Milner et al, 2011). Treatment with antibiotics is usually coupled with hydration for improved efficiency. Antibiotics used include Doxycycline and azithromycin Faruque et al, 1998).
Conclusion
Cholera is an infectious disease that is caused by a bacterium known as Vibrio cholerae. The disease is transmitted through consumption of food or water that is contaminated with fecal material. Based on the Epidemiological Triad Model, cholera has three main components. They include an agent (V. cholerae), a host (a human), and an environment (the small intestines).Major symptoms include dehydration, headache, and watery diarrhea. Globally, cholera affects between 3 million and 5 million people annually and causes between 100,000 and 130,000 deaths annually. Cases of cholera are rare in the United States. However, the disease has infected more than 470,000 people in Haiti. The country experienced the worst cholera outbreak in 2010. The disease is prevalent in third world countries that cannot afford quality health care services due to poverty. Cholera is confirmed by the isolation of the bacterium from samples of patients. Treatment options include use of fluids, electrolytes, and antibiotics. A vaccine is available but it only provides immunity against one type of V. cholerae.
References
Faruque, S., Albert, J., & Mekalanos, J. (1998). Epidemiology, Genetics, and Ecology of Toxigenic Vibrio cholerae. Microbiology and Molecular Biology Reviews: MMBR, 62 (4), 1301-1314.
Glass, R., Libel, M., and Bennett, D. (1992). Epidemic Cholera in the Americas. Science, 256, 1524-1525.
Jackson, P. (2012). Fearing Future Epidemics: The Cholera Crisis of 1892. Cultural Geographies, 20(1), 43-65.
Milner, S., Greenough, W., Asuku, M., Feldman, M., Makam, R., and Loon, I. (2011). From Cholera to Burns: A Role for Oral Rehydration Therapy. Journal of Health and Population Nutrition, 29(6), 648-651.
Nelson, J., Harris, B., Morris, J., Calderwood, B., & Camilli, A. (2009). Cholera Transmission: The host, Pathogen, and Bacteriophage Dynamic. Nature reviews. Microbiology, 7 (10), 693-702.
Newton, A., Heiman, K., Schmitz, A., Bohm, S., Mahon, B., and Mintz, E. (2011). Cholera in Haiti. Emerging Infectious Diseases Journal, 17(11), 2166-2169.
Raufman, J. (1997). Cholera. The American journal of medicine, 104, 386-394.
Sack, A., Sack, R., Nair, B., & Siddique, K. (2004). Cholera. Lancet, 363,223–233.
Williams, L., Collins, A., Bauaze, A., and Edgeworth, R. (2010). The Role of Perception in Reducing Cholera Vulnerability. Risk Management, 12, 163-184.