History

Hallmark of cholera is the production of watery diarrhea 

Varying degrees of dehydration 

Difficult to differentiate from those infected by other enteric pathogens such as enterotoxigenic Escherichia coli or rotavirus. 

No other clinical illness produces such severe dehydration in a matter of a few hours as cholera. 

Onset of the disease is abrupt and characterized by the production of watery diarrhea without strain, tenesmus, or prominent abdominal pain, rapidly followed or sometimes preceded by vomiting. 

As the diarrhea continues, other symptoms of severe dehydration are present at this time, such as generalized cramps and oliguria. 

Physical

Alert patient most of the time despite the fact that the pulse is nonpalpable and blood pressure cannot be measured. 

Fever is observed in less than 5% of cases. 

Sunken eyes and washerwoman's hands are typical of patients with severe dehydration.

Patients look anxious and restless or sometimes obtunded, the eyes are very sunken, mucous membranes are dry, the skin has lost its elasticity and when pinched retracts very slowly, the voice is almost nonaudible, and the intestinal sounds are prominent. 

Although watery diarrhea is the hallmark of cholera, some patients do not have diarrhea but instead have abdominal distention and ileus, a relatively rare type of cholera called cholera "sicca." 

Management of these patients is particularly difficult because evaluation of the degree of dehydration is overshadowed
by the accumulation of fluid in the intestinal lumen.

Laboratory abnormalities reflect the isotonic dehydration characteristic of cholera.Increases in packed cell volume, serum specific gravity, and total protein are typically seen in patients with moderate to severe dehydration. 

 Biochemical and acid-base laboratory abnormalities typical of severe dehydration are prerenal azotemia, metabolic
acidosis with a high anion gap, normal or low serum potassium levels, and normal or slightly low sodium and chloride levels. The calcium and magnesium content in plasma is also high as a result of hemoconcentration. 

 The white blood cell count is high in patients with severe cholera. 

Hyperglycemia caused by high concentrations of epinephrine, glucagon, and cortisol stimulated by hypovolemia is more commonly seen than hypoglycemia,

Acute renal failure is the most severe complication of cholera.


Cholera has unique epidemiologic features. 

Two epidemiologic patterns, the epidemic and endemic patterns

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V. cholerae lives in aquatic environments, which are their natural reservoirs.  In its natural environment, V. cholerae lives attached to a particular kind of algae or attached to crustacean shells and copepods (zooplankton)When conditions in the environment such as temperature, salinity, and availability of nutrients are suitable, V. cholerae multiplies
and can survive for years in a free-living cycle without the intervention of humans. Otherwise, when conditions are not suitable for its growth, V. cholerae switches from a metabolically active state to a dormant state.  In this dormant state V. cholerae
cannot be cultured from the water on either standard or enrichment media but appears to survive under difficult environmental conditions. Immunofluorescent techniques using monoclonal antibodies have been used to detect dormant V. cholerae.
 V. cholerae may also persist in the environment and adopts a rugose form visible on a special agar, Luria agar. These forms are resistant to chlorination and may play a role in persistence of aquatic contamination during epidemics. Humans infected by V. cholerae may shed the bacteria for a long time, sometimes for months or years, but their importance as reservoirs is minimal in comparison to the aquatic environment.

From its aquatic environment, V. cholerae is introduced to humans through contamination of water sources and contamination of food. The cycle of transmission is closed when infected humans shed the bacteria into the environment and contaminate
water sources and food. Once humans are infected, incredibly high attack rates may occur, especially in previously nonexposed populations. Additional evidence of very high household transmission rates exists, as occurred during the last Latin American epidemic or more recently during the epidemic in Zaire in 1994. Transmission via contaminated water and food has been recognized for years. During the Latin American epidemic and more recent epidemics in Africa, acquisition of the disease by drinking contaminated water from rivers, ponds, lakes, and even tube well sources has been documented. Contamination of municipal water was the main route of transmission of cholera in Trujillo, Peru, during the epidemic in 1991. Drinking unboiled water, introducing hands into containers used to store drinking water,  drinking beverages from street vendors,  drinking beverages when
contaminated ice had been added,and drinking water outside the home were risk factors to acquire cholera.  On the other hand, drinking boiled water, acidic beverages, and carbonated water, as well as using narrow-necked vessels for storing
water, was protective. V. cholerae survives for up to 14 days in some foods, especially when contamination occurs after preparation of the food.  Cooking and heating the food eliminate the bacteria. Epidemics of cholera associated with the ingestion of leftover rice,  yellow rice in a restaurant,  raw fish,cooked crabs, eafood,  raw oysters,  and fresh vegetables and fruits  have been documented.

Transmission of cholera during funerals in Africa has been reported.Risk factors identified included eating at the funeral with a nondisinfected corpse and touching the body.  Eating rice at the funeral was the main risk factor for the acquisition of cholera in one study.  Person-to-person transmission is less likely to occur because a large inoculum is necessary to transmit disease. Anecdotal reports exist in the literature, however.Careful evaluation of these reports shows that other potential risk factors might have been implicated in the transmission. Other vehicles of transmission
such as insects and fomites are less likely to be important in epidemic situations.

Seasonality is another typical characteristic of cholera. Epidemics tend to occur during the hot seasons, and countries with more than one hot season per year may also have more than one epidemic, such as seen in Bangladesh. Data from the epidemic of cholera in Peru from 1991 to 1995 also confirm that outbreaks are associated with the warmest months of the year. Some host factors are important in the transmission of cholera. Among them, infection by H. pylori and the effect of the O blood group deserve special consideration. Recent data from Bangladesh show that people infected by H. pylori are at higher risk of acquiring cholera than are people not infected by H. pylori. Additionally, the risk of acquiring severe cholera among people infected by H. pylori was higher in patients without previous contact with V. cholerae, as measured by the absence of vibriocidal antibodies in the serum. H. pylori causes a chronic gastritis that induces hypochlorhydria, which in turn reduces the ability of the stomach to contain the Vibrio invasion. The impact of the association of these two infections is
particularly interesting because H. pylori infection is very common in persons of all ages in developing countries. An unexplained predisposition toward severe disease in persons with the O blood group has been observed in Asia and more recently in Latin America. 

Although mainly countries with poor sanitary conditions are affected by cholera, a few developed countries such as the United States, Canada, and Australia have reported indigenous cases. Two different V. cholerae O1 strains have been isolated from these regions, and these vibrios differ from the strain responsible for the seventh pandemic. Sporadic cases are reported periodically from these areas.