I chose to investigate Vibrio cholerae from the genus Vibrio because I found that V. cholerae was a very interesting bacteria. According to our textbook, (Prescott’s Principles of Microbiology by Willey Joanne, Woolverton Chris, Sherwood Linda), V. cholerae has caused seven pandemics in various parts of the world, especially Asia, the Middle East and Africa. According to the 2009 Cholera annual report from the World Health Organization, (Weekly Epidemiological Record, 2010, 85(31):293-308), the US experienced less than 20 cases while around the world 45 countries experienced 221226 cases including 4946 deaths.
In 1883 Robert Koch, who is considered by our text and many others to be one of the founders of microbiology identified the Vibrio bacterium that caused cholera. Koch believed that the key to prevention was to improve hygiene and in sanitary drinking water. This is the reason that there are so few cases in the United States per year, because we have a high degree of sanitary drinking water throughout the United States. Our textbook describes its taxonomy as being one of many serogroups, the textbook identifies V. cholerae O1 and 0139 to be one of two serogroups that cause epidemics.
V. cholerae O1 also has two sterotypes and two biotypes. In 1992, the new strain, 0139 was discovered in Asia, but for the first time in recorded history, the 0139 strain actually displaced the 01 serogroup in India. Some of the genus Vibrio characteristics are that they are capable of fermentative and oxidative metabolism. According to Bergey’s Manual, they are related to enteric bacteria and Pseudomonadaceae and they are considered to be “Facultatively Anaerobic Gram-negative Rods” and on the level with the Family Enterobacteriaceae.
Read Chapter 8 Microbial Genetics
Vibrios are distinguished from enterics by being oxidase-positive and motile by means of polar flagella. V. cholerae as infectious bacteria, have the same goals as any other organism, to invade and infect the hose, to replicate and to transfer to another host. There are only a few ways that V. cholerae invade the human body. First, according to our text, it is transmitted through contaminated water that has been contaminated with fecal material containing V. cholerae from infected individuals. Such an outbreak is occurring right now in Haiti.
The source of the contamination can be from other cholera sufferer’s untreated diarrheal discharge into waterways or into groundwater or drinking water supplies. Because of the earthquake that occurred in Haiti the sanitary conditions of the water is probably the main source of transmission. A second way for transmission of V. cholerae to individuals is through contaminated food, either from fecal matter on the food from an infected individual or perhaps an infected individual that does not have good hygiene handling food and infecting others.
The third way that an individual can be exposed to V. cholerae, is through eating raw improperly cooked shellfish that were harvested in fecal-polluted coastal waters or even from shellfish that were harvested from non fecal-polluted waters and either undercooked or re-contaminated after cooking. In the United States this is usually how individuals are infected, this is because V. cholera is one of the most common bacteria found in surface waters. Strains have been found in marine coastal areas and in warmer estuaries in the United States.
According to the FDA, “The Bad Bug Book”, (www. fda. gov/Food/FoodSafety/FoodborneIllness/FoodborneIllnessFoodbornePathogensNaturalToxins/BadBugBook/default. htm). Once an individual has been infected and the bacteria is now inside the host, it has to survive the upper GI tract, which usually is very good at defending against invasion. Unfortunately for the host, cholera can grow very well in a high salt and low pH environment. The bacterial incubation period is usually from 12 to 72 hours.
When the bacteria get past the upper GI tract, they avoid the immune system by using their polysaccharide capsule which makes phagocytosis by the host immune system very difficult and will allow the bacteria to continue to replicate. It colonizes the small intestine The bacteria are not harmed by the strong stomach acid of the infected individual because of the polysaccharide capsule and attach themselves to the intestinal wall of the small intestine. They secrete a cholera toxin, called choleragen.
The bacteria are not invasive and the toxin that is secreted enters the intestinal epithelial cells, adding an ADP-ribosyl group, like pertussis toxin does which activated the enzyme adenylate cyclase which triggers the hypersectretion of water and choride ions and preventing sodium ions from being absorbed. The results are that the infected individual starts to lose large amounts of fluids, through vomiting, and a high amount of watery diarrhea. The individual will have painful stomach cramps and nausea and may lose up to 10 to 15 litres of fluid during the course of the infection.
The large amounts of fluid loss, is usually referred to as “rice-water,” and the diarrhea fluid contaminates water used by other individuals causing others to be infected as well. The amount of fluid loss that the individual loses can be large enough that the individual may have high levels of blood proteins and can lead to death from circulatory shock. In the intestinal tract V. cholerae can stimulate bacterial genes that can increase infectivity of subsequent hosts. The process is not well known, but the stimulated genes prepare the bacteria to be better, more infective colonizers in subsequent hosts. his process may be integral to fueling future epidemics. According to a paper published in Proc Natl Acad Sci USA in September 2006, that V. cholera cells will adjust to the host they invaded. They will “rearrange their transcriptional profile”, to adjust to the human host from the aquatic environment. It’s ability to infect and multiply within a host regardless of the range of environmental conditions. In studies on bacterial pathogenesis, virulence genes are usually the focus which is essential for pathogenesis.
The findings of this paper showed that the repression of MSHA pilus production suggested that not only is it critical for colonization but is also critical to the role in bacterial pathogenesis. It appears from the article that MSHA repression is critical in the early stages of the infection, to evade the host’s innate immune response. so when you think of V. cholera it is a very successful human pathogen because of transcriptional regulation and using a set of wide responses that are flexible so that the bacteria can respond to a wide ranging environment.
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