TOXIC FOOD-BORNE INFECTIONS

Toxic food-borne infections are acute transitory diseases, 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 balance.

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Etiology

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 agents, producing enterotoxins are Clostridium perfringeus, Proteus vulgaris, Proteus mirabilis, Bacillus cereus. These enterotoxins are also formed by agents from the families of Klebsiella, Enterobacter, Citrobacter, Serrafia, Pseudomonas, Aeromonas, Edwarsiella. The majority of these enterotoxins are thermoliable.

Epidemiology

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 the soil; in the water; in 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 toxic food-borne infections are registered during the whole year, but especially in summer.

Pathogenesis

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 on the type and dose of exotoxin, and also from other toxical substances of 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 don't cause morphological changes in these organs. Enterotoxin activates ferments adenylcyclase and guanylcyclase, increasing formation of the biological active substances (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.

Anatomic pathology

Cytotoxins damage the membranes of the epithelial cells and violates synthetic processes. It may increase the permeability of the intestinal wall for different

Botulism. Toxic food-borne diseases. Campylobacteriosis. 93

types of the toxical substances, and for oneself microorganisms, development of intoxication and violation of microcirculation and localized inflammatory alterations of the intestinal mucous membrane.

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 up to 38-39 °Ñ. 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 observed.

Diagnosis

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.

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It is necessary to consider the simultaneous disease of the group of the persons, use one itself food-stuff, the features of this product, sanitary-hygienic state of commercive institutions, public nutrition when taking epidemiologic data. It is necessary to reveal the sick men or bacteriocarries among personnel of these institutions, because they may be a source of infection of the food.

Materials for bacterial examination are suspicious food products, vomitory masses, water after irrigation of the stomach, stool of the patient. Serological methods does not have independent meaning in the diagnostics.

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 failure of cranial blood circulation, subarachnoidal hemorrhage), with urological diseases (pyelonephritis, acute renal failure). During the diagnostics it is necessary to consider the food poisoning, poisoning by mushrooms, salts of hard metals.

Treatment

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, threeisault, acesault, quartasault, 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

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 foo'd at the temperature from 2 till 4 °Ñ.

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.

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CAMPYLOBACTERIOSIS

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. Campylobacter is derived from the Greek " campy lo", meaning curved, and "barter", meaning rod, so named to distinguish this genus from identically appearing vibrios.

Etiology

Campylobacters are motile, non-spore-forming, comma-shaped gram-negative rods. Originally isolated from aborted sheep fetuses in 1909, these and similar organisms were called Vibrio fetus. There are now 14 recognized species within the genus.

Three types of illnesses are associated with Campylobacter species-enteric, extraintestinal, and gastric. For each of these illnesses one Campylobacter species predominates while other species are less commonly present. The prototype for enteric infectionis C. jejuni, for extraintestinal infection it is C. fetus, and for gastric infection it is C. pylori.

The Campylobacters can be distinguished from other microorganisms oh the basis of several standard criteria and can be distinguished from one another on the basis of biochemical testing. Similar to other bacteria whose ecologic niche is the gastrointestinal tract of mammals, the serotypic diversity of C. jejuni is enormous. More than 90 different serotypes based on somatic O-antigens and 50 different serotypes based on heat-labile (capsular and flagellar) antigens have been identified.

Epidemiology

Campylobacteriosis is a worldwide zoonosis. Campylobacters are commonly found as commensals of the gastrointestinal tract of wild or domesticated cattle, sheep, swine, goats, dogs, cats, rodents. Primary Campylobacter infections of animals often occur early in life and may produce morbidity or mortality, but in most infected animals a lifelong carrier state with specific immunity develops. 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. Those in contact with the excreta of infected persons who; are not toilet trained (such as infants) are themselves at risk for infection. 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 Hays of life.

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Campylobacter jejuni infections occur year-round, but with a sharp peak òî summer and early fall. Campylobacter fetus infections show the same seasonal variation, but the peak is less marked.

Campylobacter jejuni and other Campylobacters are important causes of the acute diarrheal illnesses suffered by travelers visiting developing areas.

Pathogenesis

Not all Campylobacter infections produce illness. Although all factors responsible for this phenomenon are not known, two of the most important appear to be the dose of organisms reaching the small intestine and the specific immunity of the host to the pathogen ingested. 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.

Anatomic pathology

Campylobacter jejuni multiplies in human bile, a characteristic that aids

colonization of the bile-rich upper small intestine early in infection. The sites of

tissue injury include the jejunum, ileum, and colon, with similar pathologic features in

each. Inspection of affected tissues may reveal a diffuse, bloody, edematous, and

exudative enteritis, but pathologic examinations are generally performed on patients

with the most severe cases. Microscopic examination of rectal biopsy specimens

has shown a nonspecific colitis with an inflammatory infiltrate of neutrophils,

mononuclear cells, and eosinophils in the lamina propria; degeneration; atrophy;

loss of mucus; crypt abscesses in the epithelial glands; and ulceration of the mucosal

epithelium. Campylobacter outer membranes contain lipopolysaccharides with typical

endotoxic activity. Extracellular toxins with cytotoxic activities have been found, and

classic enterotoxins have been demonstrated, although generally at low concentrations.

Infected persons do not develop neutralizing antibodies to these toxins.

Clinical manifestations

The clinical manifestations of infections due to all of the Campylobacter

species that cause enteric illnesses appear identical, C. jejuni may be regarded as

the prototype. Acute enteritis is the most common presentation of C. jejuni infection.

Symptoms may last from 1 day to 1 week or longer. Often there is a 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 may vary from loose stools to massive watery stools or grossly

bloody stools. Campylobacter enteritis is frequently self-limiting, with a gradual

improvement in symptoms over several days; however, illnesses lasting longer

than 1 week occur in about 10-20 % of patients seeking medical attention, and

relapses may be seen in another 5-10 % of untreated patients.

Infection may also be manifested as an acute colitis, with symptoms of fever, abdominal cramps, and bloody diarrhea persisting for 1 week or longer. Fever may be low grade or consist of daily peaks above 40 °Ñ. Initially, stools may be

Botulism. Toxic food-borne diseases. Campylobacteriosis. 97

watery, but as the illness progresses it may become frankly bloody; tenesmus is a common symptom. Because of the propensity of Campylobacter infection for young adults and this presenting clinical picture, it may be readily confused with ulcerative colitis or Crohn's disease.

Occasionally, acute abdominal pain may be the major or only symptom of infection. Although any quadrant of the abdomen may be affected, it has been

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right lower quadrant pain that has elicited the most attention. As with Yersinia enterocolitica and Salmonella enteritidis, C. jejuni may cause pseudoappendicitis. In most cases, the removed appendix has shown minimal or no inflammation. Enlarged mesenteric nodes (mesentericadenitis) and terminal ileitis also may be responsible for the symptoms.

Fever also may be the sole manifestation of C. jejuni infection. Temperature elevation may be so severe and persistent that typhoid fever is the initial diagnosis until C. jejuni is isolated from stools. Febrile convulsions in young children before the onset of the enteric phase of illness also may occur.

Campylobacter fetus infection. In contrast to C. jejuni, C. fetus less frequently causes diarrheal illness. Campylobacter fetus infection may cause intermittent diarrhea or nonspecific abdominal pain without localizing signs. The diarrheal illness may be manifested exactly like C. jejuni infection. Clinical manifestations are similar, and sequel are uncommon. Campylobacter fetus also may cause a prolonged relapsing illness characterized by fever, chills, and myalgias, without a source of the infection being demonstrated. Occasionally, secondary seeding to an organ will occur and lead to a more complicated infection and sometimes to a fulminant fatal course.

Campylobacter fetus infections appear to have a tropism for vascular sites; vascular necrosis occurs in patients with endocarditis and pericarditis. Thrombophlebitis may be associated with C. fetus bacteremia, but whether it is the primary event or a secondary manifestation of the infection is uncertain. Infections during pregnancy primarily have been manifested by upper respiratory symptoms, pneumonitis, fever, and bacteremia. Central nervous system (CNS) infections with C. fetus occur in neonates and adults. The prognosis is poor for premature infants. Infection is manifested as a meningoencephalitis with a cerebrospinal fluid polymorphonuclear pleocytosis; subdural effusion may complicate, infection.

Campylobacter 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.

Diagnosis

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.

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Differential diagnosis

Campylobacteriosis could take dysentery-like course, in this case it should be differentiated with shigellosis, salmonellosis, esherichiosis, intestinal yersiniosis, intestinal invagination. The main common signs of all these diseases are abdominal ache, hemocolitis, intoxication. For correct diagnostics the characteristic clinical signs of campylobacteriosis and corresponding laboratory findings should be considered.

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Treatment

Fluid and electrolyte replacement are the cornerstones for treating diarrheal illnesses. Patients with Campylobacter infections who are badly dehydrated should undergo rapid volume expansion using intravenous solutions of electrolytes in water. For those with less severe depletion, oral rehydration using glucose and electrolyte solutions.

C. jejuni is susceptible to a wide variety of antimicrobial agents, including erythromycin, the tetracyclines, aminoglycosides, chloramphenicol, nitrofurans.

C. fetus infections requires parenteral therapy, and erythromycin is not always effective. When isolates are susceptible, ampicillin treatment has been associated with good results. Patients with other serious infections also should be treated with parenteral gentamicin or other aminoglycosides, ampicillin, or chloramphenicol for at least 2 weeks.

Prophylaxis

Antimicrobial prophylaxis is effective, but because of increasing drug resistence and the possibilities of side effects, are recommending to avoid antimicrobial prophylaxis and, instead, use care in their consumption of contaminated food and water.

Control questions:

1. Etiology of botulism.

2. Epidemiology and pathogenesis of botulism.

3. Basic clinical manifestations of botulism.

4. Principles of botulism treatment.

5. Prophylaxis of botulism.

6. Etiology of toxic food-borne infections.

7. Sources and ways of transmission of infection.

8. Clinical features of toxic food-borne infections.

9. Differential diagnosis of toxic food-borne infections.

10. Laboratory methods of diagnosis and their estimation.

11. Prophylaxis of toxic food-borne infections.

12. Infectious agents of campylobacterioses.

13. Epidemiology of campylobacterioses.

14. Clinical manifestations of campylobacterioses.

15. Principles of campylobacterioses treatment.

16. Prophylaxis of campylobacterioses.

10.

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Date: 2014-12-21; view: 1502