Toxic food-borne infections. Escherichiosis. Campylobacteriosis.

on methodical conference
department of infectious diseases and epidemiology
„____” ____________ 200 р.
Protocol № _____
Chief of Dept., professor __________ V.D. Moskaliuk
to a fifth year student of the Faculty of Medicine
on independent preparation for practical training
Educational degree and qualification degree:
Year of study:
Prepared by assistant professor
Infectious Diseases
Sydorchuk A.S.
Topic: Toxic food-borne infections. Escherichiosis. Campylobacteriosis.
1. Lesson duration: 2 hours
2. Aims of the lesson:
3.1. Students are to know:
• etiology of toxic food-borne diseases, escherichiosis, campylobacteriosis, types of pathogens,
their principal properties;
• epidemiology of toxic food-borne diseases, escherichiosis, campylobacteriosis;
• pathogenesis of toxic food-borne diseases, escherichiosis, campylobacteriosis and
morphology of organs afflicted by these pathogens;
• symptoms and development of typical and atypical toxic food-borne diseases, escherichiosis,
• clinical characteristic of toxic food-borne diseases, escherichiosis, campylobacteriosis;
• complications of toxic food-borne diseases, escherichiosis, campylobacteriosis;
• diagnosis of toxic food-borne diseases, escherichiosis, campylobacteriosis;
• laboratory methods of examination at toxic food-borne diseases, escherichiosis,
• differential diagnosis of toxic food-borne diseases, escherichiosis, campylobacteriosis
including distinguishing between similar diseases;
• treatment of toxic food-borne diseases, escherichiosis, campylobacteriosis with taking into
account of course severity;
• prophylactic and antiepidemic measures at toxic food-borne diseases, escherichiosis,
3.2. Students are to be able:
• to question a patient in order for obtaining of information on disease history and
epidemiologic anamnesis;
• to perform clinical examination of a patient;
• to formulate and to substantiate the diagnosis of toxic food-borne diseases, escherichiosis,
• to prepare a plan of additional patient examination;
• to evaluate results of laboratory examination;
• to determinate a course severity;
• to make differential diagnosis to distinguish between similar diseases (salmonellosis, cholera,
food borne diseases, typhoid fever etc);
• to prescribe adequate pathogen and etiotropic treatment;
• to prepare a plan and organize prophylactic and antiepidemic measures.
3.3. Students are to acquire the following skills:
• to conduct clinical examination of a salmonellosis patient and other acute intestinal diseases;
• to formulate and substantiate a clinical diagnosis;
• to prepare a plan of paraclinic patient examination;
• to take samples of material (stool, vomitory masses, suspicious food-stuffs, water after
irrigation of the stomach) for bacterioscopy and other quick analysis methods and
bacteriological examination for revealing of causative agents;
and to take samples of material (blood) for PCR (polimerase chain reaction) and other quick
analysis methods (ELISA) and serological examination for revealing of the agent or antibodies
against their;
• to evaluate results of paraclinic patient examination;
• to organize hospitalization and treatment of a toxic food-borne diseases, escherichiosis,
campylobacteriosis patient ;
• to provide emergency aid at severe toxic food-borne diseases, escherichiosis,
• to plan and organize prophylactic measures against toxic food-borne diseases, escherichiosis,
• to plan and organize antiepidemic measures to localize and liquidate a toxic food-borne
diseases, escherichiosis, campylobacteriosis source.
4. Advice to students.
Toxic food-borne infections is an acute transitory disease, caused by conditionally
pathogenic bacteria. These bacteria are capable to produce exotoxin (in food-stuffs). The
disease is accompanied with symptoms of the damage of the upper parts of the
gastrointestinal tract (gastritis, gastroenteritis) and by violation of the water-electrolyte
Many types of the conditionally pathogenic bacteria may be agents of the toxic
food-borne infections and produce exotoxin out of the human organism on the different
food-stuffs. Enterotoxins (thermoliable and thermostable) increase the secretion of the fluids
and salts into the stomach and intestine. Cytotoxins damage the membranes of the epithelial
cells and violate the protein synthetic processes. The agent, producing enterotoxins are
Clostridium perfringeus, Proteus. vulgaris, Proteus mirabilis, Bacillus cereus. These
enterotoxins are also formed by agents from the in families of Klebsiella, Enterobacter,
Citrobacter, Serrafia, Pseudomonas, Aeromonas, Edwarsiella. The majority of these
enterotoxins are thermoliable.
Pathogenic organisms of the toxic food infections are widely spread in the nature. They
may be everywhere: in the fecal matters of human and animals; in and the soil; in the water; in
an air and on the different subjects. The way of the spread of the infection is alimentary.
The factors of the transmission of the disease are solid products (sausages, eggs, meat and fish
canned food) and liquid products (soup, milk, juices, compotes, jellies, lemonade, beer,
cocktails). They are the nutritive mediums for bacteria.
The susceptibility to this group of diseases is very high, sometimes till 90-100 %. The
typical sign of the toxic food-borne infections is not only group but explosive character
of illness due to all participants of the outbreak become ill during a short period (over a
few hours). The diseases toxic food-borne infections are registered during the hole the year,
but especially in summer.
In toxic food infections exotoxin is contained in food, besides bacteria. Due to this
the incubation period is very short. Time of the of clinical manifestations development
after influence of toxins to the mucous membrane is from 30 minutes till 2-6 hours.
Pathogenesis and clinical manifestations of the disease depend of the type and
dose exotoxin, and also from other toxical substances microbial origin, containing in the
food-stuff. Enterotoxins (thermoliable and thermostable) are connected with the epithelial cells
of stomach and intestine and act to the fermental system of the epitheliocytes, but no cause
morphological changes in these organs. Enterotoxin activates ferments adenylcyclase and
guanylcyclase increasing formation of the biological active substance (cyclic
adenosinemonophosphates and cyclic guanidinmonophosphates) in the cells of the mucous
membranes. All these changes lead to the increase rate of secretion of water and salts into the
stomach and intestine and to the development of diarrhea and vomiting.
Pathological anatomy.
Cytotoxins damage the membranes of the epithelial cells and violates synthetic
processes. It may increase the permeability of the intestinal wall for different types of
the toxical substances, and for oneself microorganisms, development of intoxication and
violation of microcirculation and localized inflammatory alterations of the intestinal mucous
Clinical manifestations.
The clinical manifestations of the toxic food-borne infections caused by only
enterotoxins are less severe. In the majority of the cases of the disease there is no
fever and just considerable inflammatory changes of the mucous membrane of the
stomach and intestine.
The course of the disease become more severe due to accumulation of enterotoxin
and cytotoxin in the food-stuffs. The high fever and considerable change of the mucous
membrane of the gastrointestinal tract are observed.
In toxic food-borne infections there is combination of the signs of the damage of
the gastrointestinal tract (gastritis, gastroenteritis or gastroenterocolitis) and signs of the
general intoxication and dehydration. The incubation period is from 30 minutes to 24 hours
(generally 2-6 hours). The beginning of the disease is an acute. At first the nausea occurs.
Frequently the replated, agonizing and unrestrained vomiting occurs. Almost at the same
time with vomiting the diarrhea starts. Stool is watery from 1 to 10-15 times a day. In
considerable part of patients the disease is not accompanied by severe pain in the stomach
and increase of the body temperature of the body. However the disease may be with spasmatic
pains in the stomach, with the raise of the body temperature upto 38-39 C. The raise of the
body temperature takes place at the early hours of the disease and through 12-24 hours the
temperature is reduced to normal.
During objective examination of the patients the pale skin, sometimes cyanosis,
cold extremities are observed. The tongue is coated. Stomach is soft and painful in the
epigastrium during palpation. The cardiovascular system also suffers. There is bradycardia
(during hyperthermia - tachycardia). The arterial pressure decrease. In some cases collapse of
short duration develops. Due to repeated vomiting and plenty diarrhea the signs of
dehydration develop. It may be possible of the appearance of the muscle’s cramps of
extremities, decrease of the diuresis and reduced turgor of the skin. The liver and
pancreas are not expanded. In hemogram leukocytosis, neutrophylosis and temperate
accelerate ESR are noted.
The duration of the disease in majority of the cases is 1-3 days. The toxical food
infection may be accompanied by severe complications. Hypovolemic shock and an acute
heart insufficiency, connecting with violations of electrolytic balance (hypokalemia) are
The diagnosis of the toxic food-borne infections is made according the results of the
clinical symptoms estimation, epidemiological and laboratory data. The typical signs are the
impetuous development of the disease after short incubation period, presence of
symptoms of gastritis, gastroenteritis or gastroenterocolitis in combination with
intoxication, dehydration, disposition to the vascular dystonia.
Differential diagnosis.
Differential diagnosis of toxical food infection is performed with acute intestinal
infections (cholera; acute shigellosis; gastrointestinal form of yersiniosis; rotoviral
gastroenteritis; campylobacteriosis; dyspeptic variants of preicteric period of viral hepatitis
and others), with surgical diseases (acute appendicitis; cholecystopancreatitis; thrombosis of
mysentrical vessels; perforation of ulcers in the stomach and duodenum), with gynecological
diseases (ectopic pregnancy; toxicosis of the pregnancy), with therapeutic diseases (myocardial
infarction; hypertension crisis), with neurological diseases (acute damages of cranial blood
circulation, subarachnoidal hemorrhage), with urological diseases (pyelonephritis; acute renal
insufficiency). During the diagnostics it is necessary to consider the food poisoning; poisoning
by mushrooms; salts of hard metals.
It is necessary to wash out a stomach and intestine to release them from microbes and
toxins as soon as possible. For a lavage it is better to use isotonic solution of Sodium
chloridum, boiled water or 1-2 % solution of sodium hydrocarbonate. Then give inside the
activated microspherical coal (SKN brand). Alternative preparations are Sillard P, Smecta,
Enterodes and other enterosorbents. Their early indication promotes the fastest improvement of
health state, preserves intoxication, development of the serious form of bacterial endotoxicosis.
In case of development of infection-toxic shock we should immediately infuse in blood colloid
and cristaloid solutions: Polyglucin, Reopoliglycin, donor Albumin, Trisol, Acesol, Quartasol,
and also glucocorticoides.
Etiotropic treatment is indicated only at serious forms with development of colitic
syndrome: Furazolidon or Enteroseptol. Antibiotics are indicated in case of development of
sepsis - Levomycetin, Gentamicin, Ampicillin, Ofloxacin (or Tarivid).
Prophylaxis of the toxical food infection is concluded in prevention of infection
of the food-stuff, of the reproduction of the microorganisms in the food. It is necessary
to keep the food-stuffs and prepared food at the temperature from 2 till 4 ºC.
The mechanization and automatization of the food objects, the elaboration of the
new methods of the preserving and storage of the food-stuff, the freezing at low
temperature are conductive to the successful prophylaxis of the toxical food infection.
Escherichiosis is an acute intestinal infection caused by E.coli, which mainly affect 1year-old babies. Classification includes enterohemorrhagic E.coli (EHEC), which produces
cytotoxins, enterotoxigenic E.coli (ETEC) elaborating enterotoxins. Then come enteroinvasive
E.coli (EIEC) invading intestinum epithelium, enteropathogenic E.coli (EPEC) that manifests
epithelial adherence and leads to attaching and effacing lesions. And finally, there is enteroaggregative E.coli (EAEC) demonstrating a stacked-brick adherence to epithelium cells. All
these classes are connected with different epidemic patterns and clinical syndromes. Infection
is caused by contact and alimentary route. Their mothers, who violate the anti-epidemic
regimen, also through contaminated food, toys, infect the babies. The disease frequently occurs
in summer and autumn. Bacilli carriers are frequently noted. Older children and adults get ill
principally. The incubative period is from 3 to 8 days. The disease has an abrupt onset. The
body temperature increases, weakness and anorexia appear. Stools occur frequently, they are
watery, yellow or orange, contain transparent mucus. If such stools occur five to seven times
daily, dehydration may occur. Toxemia is manifested by restlessness, recurrent regurgitation
and vomiting. The disease has a protracted course. Diagnosis is based on clinical
manifestations of the disease and bacteriologic tests of feces. The additional method of
laboratory diagnosis is serologic test (passive hemmagglutination test). Diagnostic titer is 1:801:160. The increase of antibody titer is discovered in 60-70% of the patients.
Campylobacteriosis refers to the group of the infections caused by gram-negative
bacteria of the genus Campylobacter. Among the most common bacterial infections of humans
in all parts of the world, campylobacters cause, both diarrhoeal and systemic illnesses and are
highly associated with gastritis and peptic ulcer disease. Originally isolated from aborted sheep
fetuses in 1909, these and similar organisms were called Vibrio fetus. There are now 14
recognised species within the genus. Three types of illnesses are associated with
Campylobacter species-enteric (C. jejuni), extraintestinal (C. fetus), and gastric (C. pylori).
Campylobacteriosis is a worldwide zoonosis. The vast reservoir in animals is probably
the ultimate source for most enteric Campylobacter infections of humans. Direct contact with
infected animals may result in transmission. Household pets, especially young dogs and cats
with diarrhea, have been implicated as vectors for campylobacteriosis. Since healthy dogs, cats,
rodents, and birds may excrete campylobacters.
As with other enteric pathogens, fecal-oral person-to-person transmission of C. jejuni
has been reported. Perinatal transmission, from a mother who was not necessarily symptomatic
may be due to exposure in utero, during passage through the birth canal, or during the first days
of life. Among exposed persons who become ill, the incubation period varies from 1 to 7 days,
a characteristic that is probably inversely related to the dose ingested. Often there is prodrome
with fever, headache, myalgia, and malaise 12-24 hours before the onset of intestinal
symptoms. The most common symptoms are diarrhea, malaise, fever and abdominal pain.
Diarrhea myay vary from loose stools to massive watery stools or grossly bloody stools.
Relapses may be seen in 5-10 % of untreated patients.
C. fetus has been shown to cause a variety of other types of localized infections,
including septic arthritis, spontaneous bacterial peritonitis, salpingitis, lung abscess, empyema,
cellulitis, urinary tract infection, vertebral osteomyelitis and cholecystitis.
A clinical diagnosis of enteric campylobacteriosis may be made by demonstration of the
organisms in direct microscopy of feces or isolation of the organisms. The use of serologic
methods for diagnosis is at present a research only.
Treatment include a variety of antimicrobial agents, including erytromycin, the
tetracyclines, aminoglycisides, chloramphenicol, nitrofurans.
5. Test questions.
1. Etiology, epidemiology, and incidence of food poisoning.
2. Pathogenesis of food poisoning.
3. Anatomic pathology of food poisoning.
4. Main clinical symptoms and signs of food poisoning.
5. Classification of food poisoning.
6. Laboratory methods of food poisoning.
7. Differential diagnosis of food poisoning.
8. Treatment of food poisoning.
9. Prevention and control of food poisoning.
10. Pre-exposure food poisoning
11. Etiology, epidemiology, and incidence of escherichiosis.
12. Pathogenesis of escherichiosis.
13. Pathological anatomy of escherichiosis.
14. Main clinical symptoms and signs of escherichiosis.
15. Laboratory diagnosis of escherichiosis.
16. Differential diagnosis of escherichiosis.
18. Treatment of escherichiosis.
19. Escherichiosis prophylaxis.
20. Etiology, epidemiology, and incidence of campylobacteriosis.
21. Pathogenesis of campylobacteriosis.
22. Pathological anatomy of campylobacteriosis.
23. Main clinical symptoms and signs of campylobacteriosis.
24. Laboratory diagnosis of campylobacteriosis.
24. Differential diagnosis of campylobacteriosis.
26. Treatment of campylobacteriosis.
27. Campylobacteriosis prophylaxis.
6. References.
A. Basic:
1. Infectious diseases / E. Nikitin, M. Andreychyn – Ternopil, Ukrmedknyga, 2004. – P.
67-77; 91-94.
2. Understanding infectious disease / Paul D. Ellner, Harold C. Neu – Mosby Year
Book, 1992. – P. 166-169.
3. Reese R.E. A practical approach to infectious diseases. – Little, Brown & Company,
Boston-Toronto, 1986. – P. 284-286; 288-289; 299-300.
4. Berkow R. The Merck Manual of diagnosis and therapy. – Merck Sharp, 1987. – P.
88-89; 197-204; 780-782.