Centers for Disease Control and Prevention. Laboratory methods for the diagnosis of Vibrio cholera. Atlanta, Georgia: CDC, 1994 and Global Task Force on Cholera Control. Guidelines for cholera control. Geneva: WHO: 1992. Publication no. WHO/SDD/CER/80.4 Rev 4. Chapter 5; Etiology and Epidemiology of Cholera
This article gives the historical background of cholera, clinical manifestations, treatment, epidemiology and information regarding the cholera vaccine. Vibrio cholerae is the causative agent for cholera. It is a form of secretory diarrheal disease that causes large fluid and electrolyte outpouring into the bowel. Biotypes of serogroup O1 of Vibrio cholerae include classical and El Tor based on phenotypic features. El Tor is responsible for worldwide cholera cases while Classical is limited to Bangladesh. The O1 strain is further classified into two serotypes; Ogawa and Inaba on the bases of agglutination tests. An extremely rare third serotype, Hikojima has been identified presently. Knowledge of biotypes and serotypes is crucial during outbreaks. Ability to produce toxins makes the bacteria virulent.
Productions of toxins by O139 and O1 makes the strains extremely virulent thus cause epidemics. Outbreaks are also associated with these strains. Some isolates of the O1 strain do not produce enterotoxins thus cause no epidemics although they can cause periodic diarrhea. Cholera originated in Ganges Delta, India and spread worldwide in the 19th century. El Tor caused massive epidemic in Southeast Asia in 1961 which was considered the beginning of the seventh pandemic. Spread to Europe, Asia and Middle East was quick and in 1970 Africa was affected. Spread to 21 countries in Latin America left 12,000 deaths and one million victims. The increase in cholera cases was marked in the 1990s.It was during this time that West Africa and South Africa was affected too. Serogroup O139 affected India in 1992, spreading to Bangladesh and other Asian countries. By 1998 it had spread to 11 countries including the USA .Currently it is confined in Asia.O139 has similar epidemiology as the strain O1.Biotyping test for O1 is different from the O139 strain.
Pathogenesis results from O1 and O139. Following infection by the disease, rapid profuse diarrhea, poor circulation due to decreased blood volume, metabolic acidosis, and depletion of electrolytes, vascular collapse and death occur. Severe diarrhea causes significant loss of body weight causing hypovolemic shock and death.3/4 of initial infection with either strain can be asymptomatic depending on bacterial concentration.1/4 are symptomatic but with mild illness. Only 2 % progress to severe fatal cholera. Individuals with blood group O develop severe illness in comparison to other blood groups. Mortality rate is less than 1% with replacement of electrolyte and fluid intravenously (for patients in shock) or orally/Antimicrobial treatment can be given though it is not used primarily for treatment. However, illness duration, bacteria concentration in stool and stool volume is reduced. Constant monitoring of antimicrobial drugs should be done periodically and during epidemics due to increasing resistance.
Among unexposed people the epidemic affects all ages. However in endemic areas adults are unaffected as they display some form of immunity due to repeated exposure to the disease. However children in these areas are affected predominantly due to new exposure. The aged to who have decreasing immunity and low production of gastric acid tend to be most affected. Poverty ,makes the disease high risk due to lack of access to clean water, poor living conditions predisposing people to poor hygiene and consumption of food and drinks sold in the street. Cholera is linked to consumption of water fetch from shallow streams, rivers and open wells. Food has also been linked with the transmission of the disease especially undercooked and raw sea food. The strains O139 and O1 only die on exposure to acidity, sunlight and drying but thrive in moist alkaline foods where other microorganisms were eradicated by prior cooking. Neutral pH foods such as cooked grains, millet and cooked rice are good harbors for the bacteria. Vegetables and fruits grown in sewage and consumed raw transmit cholera. Freezing foods or drinks does not aid in prevention of cholera. Direct contact, through nursing patients, touching or handshakes does not cause cholera.
Outbreaks in hospitals are as a result of intake of contaminated food and water. Outbreaks of cholera in funerals are as a result of contaminated food served in the funeral ceremony due to involvement of an infected person. New oral vaccines have been developed over the past 15 years. However, the presently available vaccines have proven to be ineffective.
Tadars Online Text Book of Bacteriology by Kenneth Tadar, PhD.
Vibrio cholerae is a gram negative straight or curved rod. It is motile moving by use o flagella. Its forms of metabolism are respiratory and fermentation. It is oxidase positive. Vibrio is a member of the entreobacteriaceae family. Vibrio is differentiated from enteric bacteria because it is motile and oxidase positive. It is differentiated from pseudomonas because it is fermentative and oxidative. The bacterium grows in synthetic media with glucose as glucose is its sole supply of energy and carbon. Vibrio is majorly aquatic requiring seawater or relatively high concentrations of sodium chloride for growth. It has metabolic versality similar to pseudomonas. In liquid media vibrio is highly mobile via sheathed flagella while in solid media it forms many lateral unsheathed flagella.
Vibrio parahamolyticus and vibrio cholera are pathological to humans although their mode of pathogenesis is different. Vibrio parahaemolyticus is invasive colonizing the colon primarily. Vibrio cholera affects the small intestine by producing a toxin, enterotoxin. Vibrio vulnificus newly found bacteria causes primary septicemia, gastroenteritis and wound infections in human beings. Other bacteria discussed include Campylobacter jejuni and Helicobacter pylori. Vibrio cholerae causes severe diarrhea as it produces a toxin, enterotoxin that activates intestinal mucosa adenylate cyclase causing activation of pumps which pump water and electrolytes into the lumen of the intestine. Rapid diarrhea then results. One becomes hypotensive in an hour. Shock occurs in four to twelve hours. Death occurs between eighteen hours and several days if treatment is not given. Dehydration, anuria, acidosis and shock follow after infection. Diarrhea is freckled with debris of epithelial cells and mucus characteristic of rice water and also contains high concentration of bacteria. Cardiac complications and circulatory failure can occur due to loss of potassium ions. Mortality rates are 50%- 60% in untreated cases. Initial treatment is through administration of IV fluid to replace lost ions and fluid. Isotonic fluid is then given afterwards until diarrhea ceases. Glucose is added to the fluids being administered, oral administration is preferable to eliminate need for sterilization or intravenous administration. Antibiotics have no significance in curing cholera but significantly reduce fluid loss through diarrhea.
Oxford Journals, the Journal of Infected Diseases. Diagnosis of Vibrio cholera O1 infection in Africa.(Peer reviewed)
This journal provides information about identification of the strain O1 and diagnosis of cholera, rapid testing, stool collection, phenotype characterization, molecular characterization and quality management. Cholera is the cause of diarrhea in developing countries. Outbreaks result to high mortality rates. The disease is endemic in Africa. Late diagnosis results to high mortality rates due to few resources. For confirmation of a cholera outbreak it is crucial to isolate thee O1 strain off vibrio cholera. Rapid diagnostic methods are important for eliminating the disease. A rapid diagnostic test for stool specimen to detect the O139 or O1 strain is important for early detection and observation of an outbreak. There is lack of sensitivity in rapid diagnostic tests thus they should not substitute stool culture. However, stool culture is not available in endemic areas. For non-chlorinated stool specimens and rectal swab specimens not cultured immediately, the recommended transport medium is Cary Blair because it ensures preservation of the bacterial during its transportation.
When transportation of the specimen to the laboratory is delayed for a long time for instance, a week, the bile peptone medium is used to ensure viability. Stool samples should be collected in an environment free of detergent and chlorine to preserve Vibrio cholerae in transport medium and to favor growth in culture medium. Thorough analysis of filter papers against rectal swabs especially in epidemics is of outmost importance. For identification of the strain O139 or O1, fecal specimens are cultured in selective and non selective media including TCBS agar and 5% blood agar. Suspicious oxidase positive bacterial isolates are serotyped in monovalent antisera. Antimicrobial susceptibility tests detect bacterial resistance. Molecular characterization findings are crucial in identifying phenotypes and in detecting outbreaks. In addition, the lipopolysaccharide, the gene encoding for enterotoxin and the El Tor biotype characteristics are identified. Use of pulsated field gel in electrophoresis facilitates strain comparison. Quality management in laboratory tests ensures quality and reliable results.
American Journal of Tropical Medicine and Hygiene; Environmental Factors Influencing Epidemic cholera. (Peer reviewed)
This article focuses on the cholera outbreak that followed after the earthquake struck Haiti in 2010.This occurrence was a reassurance that the disease is still a major menace because millions of people were affected proving that the mechanisms of the disease and the relationship with the environment is not well understood. Vibrio cholerae is indigenous to the water environment. As a result complete obliteration of the bacteria is impossible. However, prediction of an outbreak through hydro climatology is possible. Prevention is also possible. Cholera epidemic areas are usually located nearby regional rivers. These areas experience periodic cholera outbreaks. This is because low river flows results to warm air temperature which favors bacterial growth. Epidemics occur as a result of breakdown of sanitation facilities during heavy rains thus accelerating interaction of contaminated water with human activities. Moreover, tidal encroachment of sea water containing Vibrio cholera from the inlet of the sea to inland areas contributes to spread. Cholera is a major health threat due to poor living conditions poor handling of food and drinking contaminated water and lack of sanitation facilities. Vibrio cholera inhabits in water bodies.
The emergence of new biotypes from its aquatic environment proves that it is impossible to completely eliminate the bacteria. Only prevention measures and control measures can be taken to minimize disease causing strains of the bacteria. In Latin America, South Asia and in Sub-Saharan countries, cholera is the most common water related disease. Recent research reveals that most outbreaks emerge from coastal areas proving a strong co-relation between the disease and the environment. In endemic regions simple treatment techniques such as oral rehydration and other medical techniques have reduced mortality rate from cholera by almost 30% especially in sub Saharan countries and Bangladesh. Endemic regions experience slightly higher mortality rates usually 3% or less or they can exceed 6% ,for example for Haiti 6.4% in 2010 and 6% for Madagascar in 2000.This major difference is due to lack of understanding how environme...
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