H. injluenzae is the commonest cause of meningitis in the second year of life. The clinical features are described on generally the response to treatment is slow. About 25% of children have permanent residual neurological deficits such as deafness.
This is characterized by a dramatically rapid course and fatal outcome in children if appropriate treatment is not instituted. The onset is acute with high fever, pooling of oropharyngeal secretions, dysphagia and marked respiratory distress. Examination reveals a markedly swollen and inflamed epiglottis.
H. influenzae type b accounts for about 30% of all childhood bacterial pneumonias and 3-6% of pneumonias in adults.
This is made by isolation and culture of the organism. Counterimmunoelectrophoresis can be used to detect type b capsular antigen in 75% of patients.
Treatment is urgent, as delay may result in a high mortality, especially in patients with meningitis and epiglottitis. In these conditions the drug of choice is chloramphenicol50- 100 mg kg-l per day i.v. for children and 4 g per day i.v. for 7-10 days for adults. Cefuroxime can be given orally or, for meningitis 3 g 8 hourly. Ampicillin can be used for less severe cases, but resistance to this drug is increasing.
Children in close contact with an infected individual are at an increased risk of developing the disease. Rifampicin 20 mg kg-l for 4 days is helpful. Recently, conjugate vaccines have been developed in which a purified capsular polysaccharide is linked to a protein to improve immunogenicity. Primary vaccination is now recommended in the UK in the first year of life.
Cholera is caused by the curved, actively motile, 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. The El Tor biotype has replaced the classical biotype as the major cause of cholera. This is because the El Tor V. cholerae is hardier organism. Infection with the El Tor biotype is frequently unrecognized because it produces milder clinical symptoms; a chronic gall-bladder carrier state can result in about 3% of all infected adults. All three strains (Inaba, Ogawa and Hikojima) are pathogenic. The fertile, humid Gangetic plains of West Bengal have traditionally been regarded as ‘the home of cholera’. However, the seventh pandemic of cholera, which was caused by the El Tor biotype, affected large areas of Asia, North Africa and southern Europe. The pandemic has spread to South and Central America in recent years claiming thousands of lives. It has recently been suggested that the eighth cholera pandemic has begun and is due to a non-01 V. cholerae which may be an El Tor mutant. Humans are the only known natural hosts. Transmission is by the faecaloral route. Contaminated water plays a major role in the dissemination of cholera, although contaminated foods and contact carriers may contribute in epidemics. Achlorhydria or hypochlorhydria facilitates passage of the cholera bacilli into the small intestine, where they proliferate and elaborate an exotoxin with A and B subunits. The B subunit binds to specific GM1 ganglioside receptors and the A subunit activates the intracellular enzyme adenylate cyclase . This produces elevation of 3′,5′-cyclic-AMP, which in turn produces massive secretion of isotonic fluid into the intestinal lumen.
V. cholerae has recently been shown to produce a second toxin known as zonula occludens toxin (ZOT). This impairs the integrity of the ‘tight junctions’ between enterocytes allowing escape of water and electrolytes. A third toxin, accessory cholera toxin (ACE), which also produces intestinal secretion, has recently been identified.
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. Classically, however, three phases are recognized in the untreated disease. The evacuation phase is characterized by the abrupt onset of painless, profuse, watery diarrhoea, associated with vomiting in the severe forms. ‘Rice water’ stools, so called because of mucus flecks floating in the watery stools, are characteristic of this stage. If appropriate supportive treatment is not given, the patient passes on to the collapse phase. This is characterized by features of circulatory shock (cold clammy skin, tachycardia, hypotension and peripheral cyanosis) and dehydration (sunken eyes, hollow cheeks and a diminished urine output). The patient, though apathetic, is usually lucid. Muscle cramps may be severe. Children may, in addition, present with convulsions due to hypoglycaemia. At this stage renal failure and aspiration of vomitus present major problems. Should the patient survive this stage, then the recovery phase starts, with a gradual return to normal of clinical and biochemical parameters in 1-3 days. Cholera sicca is an uncommon but severe form of cholera. It presents with massive outpouring of fluid and electrolytes into dilated intestinal loops. Diarrhoea and vomiting do not occur and hence the disease is frequently not recognized. The mortality rate is high.
Diagnosis is largely clinical. Examination of freshly passed stools may demonstrate rapidly motile organisms. This is not diagnostic, as Campylobacter jejuni may also give a similar appearance. However, demonstration of the rapidly motile vibrios by dark-field illumination and subsequent inhibition of their movement with type-specific antisera is diagnostic. Stool and rectal swabs should be taken for culture.
With appropriate and effective rehydration therapy, mortality has decreased to less than 1%. Rehydration is mainly oral, but intravenous therapy is occasionally required.
ORAL REHYDRATION, for maintenance therapy or for correction of mild to moderate dehydration, is best carried out by giving a glucose-electrolyte solution. The World Health Organization (WHO) oral rehydration solution (ORS) is shown. Mildly dehydrated individuals are given ORS 50 ml kg-I in the first 4 hours followed by a maintenance solution of 100 ml kg-I daily until the diarrhoea stops. For moderate dehydration, ORS 100 ml kg-I is given within the first 4 hours followed by 10-15 ml kg-I per hour. Rice- and other cereal-based electrolyte solutions (Table 1.16) have been found to be as effective and actually reduce stool volume as well as rehydrating, so that they are replacing WHO ORS.
INTRAVENOUS REHYDRATION is required only for severely dehydrated individuals with features of collapse. Intravenous solutions recommended by WHO include Ringer’s lactate solution and the ‘Diarrhoea Treatment Solution’ (sodium chlo ride 4.0 g, sodium acetate 6.5 g, potassium chloride 1.0 g, and glucose 9.0 g, per litre). Several litres of intravenous fluid are usually required to overcome the features of shock. Maintenance of hydration is effectively carried out by oral rehydration solutions. Antibiotics such as tetracycline 250 mg four times daily for 3 days or doxycycline help to eradicate the infection, decrease stool output and shorten the duration of the illness dramatically. Drug resistance is becoming an increasing
PREVENTION AND CONTROL
Immunization with currently available parenteral vaccines results in poor immunity and is no longer recommended. Attenuated live oral cholera vaccines are under intensive evaluation. Chemoprophylaxis with tetracycline 500 mg two times daily for 3 days for adults and 125 mg daily for children is effective. The most effective preventive measures, however, are good hygiene and sanitary living conditions. compares the pattern of infection caused by V. cholerae with the patterns of infection caused by other gut organisms.