1.2.1 Clinical features
The incubation period ranges from a few hours to 5 days.
Depending on the strain involved, 60 to 75% of infections remain clinically unapparent.
Among symptomatic patients, at least 25 to 30% have severe disease but this proportion may be higher.
The initial manifestation is diarrhoea. Stools quickly lose their faecal content, taking on a characteristic “rice water” appearance and contain no blood.
Symptoms can range from simple watery diarrhoea to massive watery diarrhoea with losses of up to 500 to 1000 ml/hour in severe disease1 . The total stool output over 3 to 4 days of illness can reach 500 ml/kg.
Vomiting is often present, and is typically colourless without bile. Abdominal discomfort may be present but severe cramping is not a feature.
There is usually no fever; low-grade fever is possible, but as cholera does not induce a systemic inflammatory response, temperatures above 38 °C (axillary) should prompt a search for another cause of fever.
Continuing diarrhoea and vomiting cause volume depletion and further clinical signs and symptoms are those of increasing dehydration:
– Patients present with sunken eyes, dry mucous membranes and decreased skin turgor.
– The pulse becomes more rapid, then weak, and eventually non-palpable.
– Blood pressure drops progressively.
– Patients show deterioration in the level of consciousness (lethargy).
– Patients may arrive unconscious, in hypovolaemic shock.
In severe disease, cardiovascular collapse and death can occur within 12 to 72 hours without therapy12.
The large volume watery stools containing sodium, chloride, bicarbonates, and potassium contribute to acidosis and hypokalaemia.
Bicarbonate loss (40 mmol/litre of stool) and lactate production are responsible for a nearly universal metabolic acidosis in patients with severe dehydration. This acidosis is quickly corrected with appropriate rehydration fluid.
Potassium loss (20 mmol/litre of stool) also occurs and some degree of hypokalaemia is usually present. Clinical and biochemical evidence of hypokalaemia may be more apparent after 24 hours of rehydration therapy, particularly if ORS has not been used in rehydration.
1.2.2 Clinical diagnosis
At the beginning of the outbreak, laboratory investigations are performed in a group of patients presenting with compatible clinical signs of cholera, to confirm whether Vibrio cholerae is the causative pathogen and determine the sensitivity of the strain to antibiotics.
Once the cholera outbreak has been bacteriologically confirmed, diagnosis of subsequent cases relies on clinical case definition2 and clinical assessment only. A sudden onset of severe watery diarrhoea during a cholera epidemic is highly predictive of cholera.
1.2.3 Prognosis and case fatality rate
Without treatment, the prognosis of severe cholera is poor, with up to a 50% mortality rate.
In contrast, the case fatality rate in cholera cases treated in a well-functioning treatment structure is typically 1% or less.
After ingestion, vibrios pass through the gastric acid barrier and adhere to the mucosa of the upper small intestine without penetrating it. They secrete cholera toxin, which binds to mucosal receptors and is transported into the cell where it activates the enzyme adenylate cyclase, increasing cyclic adenosine monophosphate (cAMP). As a result, a shift in cell membrane ion transport occurs, with a net increase in ion concentration (mainly chloride and sodium) within the intestinal lumen. Water is drawn into the lumen in response to the increased ion concentration leading to the voluminous watery diarrhoea characteristic of cholera.
Cholera surveillance and early warning systems rely also on the standard clinical case definition for a presumptive diagnosis of cholera.