Gastrointestinal
bacterial Diseases
Causes of infectious gastroenteritis
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
Fried rice and freshly made sauces are frequent sources; the
organism grows and produces enterotoxin during storage
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.
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
Differential diagnosis of acute diarrhea and vomiting
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
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
