GIT infection 33.pdf

Gastrointestinal bacterial Diseases Gastrointestinal Food Poisoning Staphylococcal food poisoning Bacillus cereus food poisoning Clostridium Perfringens Food poisoning Gastrointestinal Infection Campylobacter jejuni infection Salmonella spp. infection Escherichia coli infection...

Gastrointestinal bacterial Diseases Gastrointestinal Food Poisoning Staphylococcal food poisoning Bacillus cereus food poisoning Clostridium Perfringens Food poisoning Gastrointestinal Infection Campylobacter jejuni infection Salmonella spp. infection Escherichia coli infection Clostridium difficile infection Yersinia enterocolitica infection Cholera Bacillary dysentery (shigellosis) Gastrointestinal Food Poisoning Staphylococcal food poisoning Staph. Aureus transmission takes place via the hands of food handlers to foodstuffs such as dairy products, including cheese, and cooked meats. Inappropriate storage of these foods allows growth of the organism and production of one or more heat-stable enterotoxins which cause the symptoms. Nausea and profuse vomiting develop within1–6 hours. Diarrhoea may not be marked. Most cases settle rapidly but severe dehydration can occasionally be life-threatening. Antiemetics and appropriate fluid replacement are the mainstays of treatment. Suspect food should be cultured for staphylococci and demonstration of toxin production. Bacillus cereus food poisoning Ingestion of the pre-formed heat-stable exotoxins of B. cereus causes rapid onset of vomiting and some diarrhoea within hours of food consumption, which resolves within 24 hours. Fried rice and freshly made sauces are frequent sources; the organism grows and produces enterotoxin during storage If viable bacteria are ingested and toxin formation takes place within the gut lumen, then the incubation period is longer (12–24 hours) fever , watery diarrhoea and cramps are the predominant symptoms. The disease is self-limiting but can be quite severe. Rapid and judicious fluid replacement and appropriate notification of the public health authorities are all that is required. Bacillus cereus food poisoning Gastrointestinal Infection Escherichia coli infection Many serotypes of E. coli are present in the human gut at any given time. Production of disease depends on either colonisation with a new strain, or the acquisition by current colonising bacteria of a pathogenicity factor for mucosal attachment or toxin production. Travel to unfamiliar areas of the world allows contact with different strains of endemic E. coli and the development of travellers’ diarrhoea. Enteropathogenic strains may be found in the gut of healthy individuals and, if these people move to a new environment, close contacts may develop symptoms. At least five different clinico-pathological patterns of diarrhoea are associated with specific strains of E. coli with characteristic virulence factors. 1- Entero-toxigenic E. coli 2- Entero-invasive E. coli 3- Entero-pathogenic E. coli 4- Entero-aggregative E. coli 5- Entero-haemorrhagic E. coli A wide range of antimicrobial agents effectively inhibit the growth of E. coli. 1-β-lactams 2-Fluoroquinolone 3-Aminoglycosides and 4-Trimethoprim- sulfamethoxazole are often used to treat community and hospital infections due to E. coli Most common causes of travellers’ diarrhoe Antimicrobials in travellers’ diarrhoea Clostridium difficile infection Homework Cholera (Vibriosis) Cholera, caused by Vibrio cholerae serotype O1, is the archetypal toxin-mediated bacterial cause of acute watery diarrhoea. The enterotoxin activates adenylate cyclase in the intestinal epithelium, inducing net secretion of chloride and water. V. cholerae O1 has two biotypes, classical and El Tor, Following its origin in the Ganges valley, devastating epidemics have occurred, The seventh pandemic, due to the El Tor biotype, began in 1961 and spread via the Middle East to become endemic in Africa ,Since 2005, the number of cases of cholera have been increasing. El Tor is more resistant to commonly used antimicrobials than classical Vibrio, and causes prolonged carriage in 5% of infections. A new classical toxigenic strain, serotype O139, firstly discovered in Bangladesh in 1992 and started a new pandemic. Infection spreads via the stools or vomit of symptomatic patients or of the much larger number of subclinical cases. Organisms survive for up to 2 weeks in fresh water and 8 weeks in saltwater. Transmission is normally through infected drinking water, shellfish and food contaminated by flies, or on the hands of carriers.  Clinical features Severe diarrhoea without pain or colic begins suddenly and is followed by vomiting. Following the evacuation of normal gut faecal contents, typical ‘rice water’ material is passed, consisting of clear fluid with flecks of mucus. Classical cholera produces enormous loss of fluid and electrolytes, leading to intense dehydration with muscular cramps. Shock and oliguria develop but mental clarity remains. Death from acute circulatory failure may occur unless fluid and electrolytes are replaced. Improvement is rapid with proper therapy The majority of infections, however, cause mild illness with slight diarrhoea. Occasionally, a very intense illness, ‘cholera sicca’, occurs, with loss of fluid into dilated bowel, killing the patient before typical gastrointestinal symptoms appear. The disease is more dangerous in children. Diagnosis and management Clinical diagnosis is easy during an epidemic. Otherwise, the diagnosis should be confirmed bacteriologically. Stool dark-field microscopy shows the typical ‘shooting star’ motility of V. cholerae. Rectal swab or stool cultures allow identification. Cholera is notifiable under international health regulations. Maintenance of circulation by replacement of water and electrolytes is very important. Ringer-Lactate is the best fluid for intravenous replacement. Vomiting usually stops once the patient is rehydrated, and fluid should then be given orally up to 500 mL hourly. Early intervention with oral rehydration solutions that include resistant starch, based on either rice or cereal, shortens therefore the duration of diarrhoea and improves prognosis. Total fluid requirements may exceed 50 L over a period of 2–5 days. Accurate records are greatly facilitated by the use of a ‘cholera cot’, which has a reinforced hole under the patient’s buttocks, beneath which a graded bucket is placed. Three days treatment with tetracycline 250 mg 4 times daily, a single dose of doxycycline 300 mg or ciprofloxacin 1g in adults reduces the duration of excretion of V. Cholerae and the total volume of fluid needed for replacement Prevention