Table 18.1 Nomenclature of bone tumors



Cholera is caused by the curved, flagellated Gram-negative bacillus, Vibrio cholerae. The organism is killed by temperatures of 100°C in a few seconds but can survive in ice for up to 6 weeks. One major pathogenic serogroup possesses a somatic antigen (O1) with two biotypes: classical and El Tor. The El Tor biotype replaced the classical biotype as the major cause of the seventh pandemic which began in the 1960s. Infection with the El Tor biotype generally causes milder symptoms, but can still cause severe and life-threatening disease.
     The fertile, humid Gangetic plains of West Bengal have traditionally been regarded as the home of cholera. However, a series of pandemics have spread the disease across the world, usually following trade routes. The seventh pandemic currently affects large areas of Asia and sub-Saharan Africa. A new serogroup (O139 Bengal) is responsible for many cases in Bangladesh, India and South East Asia.
     Transmission is by the faeco-oral route. Contaminated water plays a major role in the dissemination of cholera, although contaminated foodstuffs and contact carriers may contribute in epidemics. Achlorhydria or hypochlorhydria facilitates passage of the cholera bacilli into the small intestine. Here they proliferate, elaborating an exotoxin which produces massive secretion of isotonic fluid into the intestinal lumen. Cholera toxin also releases serotonin (5-HT) from enterochromaffin cells in the gut, which activates a neural secretory reflex in the enteric nervous system. This may account for at least 50% of cholera toxin’s secretory activity. V. cholerae also produces other toxins (zona occludens toxin, ZOT, and accessory cholera toxin, ACT) which contribute to its pathogenic effect.
• Incidence in U.S.
1. Previously, approximately 50 cases per year, mostly in travelers returning from endemic areas. From 1995 to 2009, 190 cases reported, 37 (61%) of which acquired outside the USA.
• Prevalence in USA: N/A
• Predominant sex: None
• Predominant age
1. In nonendemic areas, attack rates are equal in all age groups. In epidemic areas, children over the age of two are most commonly infected.
• Peak incidence
1. None in the USA.
2. Summer and fall in endemic areas
• Genetics: N/A
1. Familial disposition: N/A
2. Congenital infection: N/A
3. Neonatal infection: Illness is uncommon before the age of 2 years, likely because of passive immunity.
The incubation period varies from a few hours to 6 days. The majority of patients with cholera have a mild illness that cannot be distinguished clinically from diarrhoea due to other infective causes. In severe cases there is abrupt onset of profuse painless diarrhoea, followed by vomiting. As the illness progresses the typical ‘rice water’ stool, flecked with mucus, may be seen. There is massive fluid loss, and if this is not replaced the features of hypovolaemic shock (cold clammy skin, tachycardia, hypotension and peripheral cyanosis) and dehydration (sunken eyes, hollow cheeks and a diminished urine output) appear. The patient, though apathetic, is usually lucid. Muscle cramps may be severe. Children may present with convulsions owing to hypoglycaemia.
• Infection may result in asymptomatic illness or a mild diarrhea. The classic illness is described as the abrupt onset of voluminous watery diarrhea, which may lead to severe dehydration, acidosis, shock, and death. Vomiting may occur early in the illness, but fever and abdominal pain are usually absent. The typical “rice water” stools are pale with flecs of mucus and contain no blood. Muscle cramps may be prominent, and are due to loss of fluid and electrolytes. Untreated illness results in hypovolemic shock, and death may occur in hours to days. With adequate fluid and electrolyte repletion, cholera is a self-limited illness that resolves in a few days. The use of antimicrobials can shorten the course of illness.
• The organism responsible for this illness is one of several strains of V. cholerae. Most infections result from the 01 serotype, the El Tor biotype. In the USA, one outbreak occurred from the ingestion of illegally imported crab, and sporadic infection has been associated with the consumption of contaminated shellfish in Gulf Coast states. Most cases are seen in returning travelers. Transmission during epidemics is the result of the ingestion of contaminated water and, in some instances, contaminated food.
This is largely clinical. Examination of freshly passed stools may demonstrate rapidly motile organisms (although this is not diagnostic, as Campylobacter jejuni may give a similar appearance). A rapid dipstick test is now also available. Stool and rectal swabs should be taken for culture to confirm the diagnosis and to establish antibiotic sensitivity. Cholera should always be reported to the appropriate public health authority.

• Mild illness may mimic gastroenteritis resulting from a variety of etiologies.
• Sudden, voluminous diarrhea causing marked dehydration is uncommon in other illnesses.
Stool should be sent for culture and microscopy. Treatment should not be delayed while awaiting culture results.
• WBC may be elevated, and hemoglobin may be increased as a result of hemoconcentration.
• Elevated bun and creatinine suggests prerenal azotemia. Hypoglycemia may occur. Stool cultures on appropriate media may grow the organism. Wet mount of stool under dark field or phase contrast microscopy shows organisms with characteristic darting motility.

• The mainstay of therapy is adequate fluid and electrolyte replacement. This can usually be achieved using oral rehydration solutions containing salts and glucose. Some patients may require intravenous fluid and electrolyte replacement.
• Antimicrobial therapy can decrease shedding of fluid and organisms and can shorten the course of illness
1. Doxycycline 100 mg PO bid for 5 days, or
2. Septra, one DS tablet PO bid for 5 days
• Resistance to Septra is increasing in travel-associated infections
It is likely that asymptomatic chronic carriers exist, however, since they are difficult to identify, and their role in transmission of disease appears to be rather limited, there is no recommendation for treatment of these individuals.
The mortality of adequately hydrated patients is less than 1%.
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