What is Escherichiosis?
Escherichiosis (coli infection) – acute infectious diseases with fecal-oral transmission mechanism; the predominant lesion of the gastrointestinal tract with the development of enteritis or enterocolitis is characteristic, in rare cases, generalized forms with extraintestinal manifestations.
Brief historical information
Bacteria got their name in honor of the German pediatrician T. Escherich, who first discovered Escherichia coli (1886). Escherichia coli is a permanent inhabitant of the human intestines. The ability of E. coli to cause gastrointestinal lesions was experimentally proved by G.N. Gabrichevsky (1894) and clinically confirmed A. Adam (1922). Serological analysis conducted in the 40s by F. Kauffmann proved the difference in the antigenic structure of pathogenic and non-pathogenic E. coli, which formed the basis of their modern microbiological classification.
Causes of Escherichiosis
The causative agents are diarrheagenic (as defined by WHO) E. coli serovars, represented by mobile gram-negative bacilli of the genus Escherichia of the Enterobacteriaceae family. Morphologically, serovars are indistinguishable from each other. They grow well on ordinary nutrient media. Stable in the environment, stored for months in soil, water, feces. They tolerate drying well, are able to reproduce in foods, especially in milk. They die quickly when boiled and disinfected. In E. coli, somatic (O-antigen), capsular (K-antigen) and flagellar (H-antigen) antigens are isolated. Currently, about 170 antigenic variants of E. coli are known; more than 80 of them cause coli infection. Diarrheagenic serovars of E. coli are divided into 5 groups:
- enteropathogenic (EPKP);
- enterotoxigenic (ETKP);
- enteroinvasive (EICP);
- enterohemorrhagic (EHEC);
- enteroadhesive (EAKP).
In the materials of the WHO (1989), serogroups 071, 092, 0166, 0169 are also indicated in the number of ETCHs.
- Enteropathogenic E. coli includes about 15 serogroups and 29 serovars.
- Enteroinvasive E. coli includes about 9 serogroups and 13 serovars. Of greatest importance are strains 0124 and 0151.
- Enterotoxigenic E. coli includes 17 serogroups and 16 serovars.
- Enterohemorrhagic E. coli include serogroups 0157, 026, 0111, 0145.
- Enteroadhesive E. coli is not completely differentiated. They differ in their ability to quickly attach to intestinal epithelium.
The reservoir and source of infection is a person, patient, or carrier. Patients present a great epidemic danger; among them, the most dangerous are patients with Escherichiosis caused by EPEC and EICP, and the least dangerous are patients with Escherichiosis due to EECP, EHEC and EECP. The period of contagiousness of the source depends on the properties of the pathogen. With escherichiosis caused by ETEC and EHEC, the patient is infected only in the first days of the disease, with diseases caused by EECP and EPTK, 1-2 weeks (sometimes up to 3 weeks). Carriers excrete the pathogen for a short time, and children – for a longer time.
The transmission mechanism is fecal-oral, transmission routes are food, water and household. According to WHO, infection with ETEC and EICP is more likely to occur through the food route, and EPEC through the household. Among food products, dairy products (often cottage cheese), prepared meat dishes, drinks (compote, kvass, etc.), salads from boiled vegetables predominate. In children’s groups, as well as in hospital conditions, the pathogen can spread through care items, toys, hands of mothers and staff. With enterohemorrhagic escherichiosis, people become infected when they eat insufficiently thermally processed meat, as well as raw milk. Outbreaks of diseases associated with the use of hamburgers are described. Waterway transmission of Escherichiosis is less common; dangerously intense pollution of open reservoirs as a result of the discharge of uncontaminated domestic and wastewater, especially from infectious diseases hospitals. The natural susceptibility to Escherichiosis is quite high, but it varies in different age groups of the population. The transferred disease leaves unstable group-specific immunity.
The main epidemiological signs
The disease is ubiquitous; The epidemiological features of Escherichiosis caused by different serovars can vary significantly. EPKP – pathogens of enterocolitis in children of the first year of life. The incidence is usually recorded in the form of outbreaks in DDU and hospitals. Pathogens are transmitted, as a rule, in a contact-everyday way – through the hands of adults (puerperas and staff) and various objects (spatulas, thermometers, etc.). Foodborne outbreaks of infection are also known, mainly when artificially feeding young children. EIKP – causative agents of dysentery-like diseases in children older than 1 year and adults. Patients usually excrete bacteria within 1 week; the pathogen is transmitted through water and food. The epidemic process of dysentery-like escherichiosis occurs, as a rule, in the form of group diseases and outbreaks with the use of contaminated water and food. Diseases are distinguished by summer-autumn seasonality; they are more often registered in developing countries. ETKP – causative agents of cholera-like diseases in children under the age of 2 years and adults. These pathogens are widespread in countries with a hot climate and poor sanitary conditions. More often sporadic, less often group diseases are recorded. In the Russian Federation, ETCHs are rarely isolated, more often when deciphering “imported” cases of diseases that make up the main group of the so-called “travelers diarrhea”. Bacteria are isolated from patients for 7-10 days. Infection occurs through water and food. Contact-household transmission is unlikely, since the dose of the pathogen is important for infection. The epidemiology of Escherichiosis caused by EHEC is not well understood. It is known that diseases prevail among children over a year of age and adults, and outbreaks in nursing homes are also reported.It has been established that the natural biotope EGKP 0157: H7 is the intestines of cattle. An important influence on the incidence of escherichiosis is exerted by the sanitary and hygienic conditions of people’s lives (home improvement, provision of benign drinking water and food products, etc.). A common symptom of all forms of Escherichiosis is the lack of a relationship between morbidity and population groups by profession or occupation.
Pathogenesis during Escherichiosis
The mechanisms of the development of diseases depend on the affiliation of diarrheagenic Escherichia to specific groups. EPPs primarily cause disease in young children with damage to the predominantly small intestine. The pathogenesis of lesions is due to the adhesion of bacteria to the intestinal epithelium and damage to microvilli, but not invasion of the cells. The pathogenicity factors of ETEC are drank, or fimbrial, factors that facilitate adhesion to the epithelium and promote colonization of the lower parts of the small intestine, as well as determining the ability to toxin formation. Heat-labile, thermostable enterotoxin or both of these toxins are isolated. The effect of a high molecular weight labile toxin is similar to that of a cholera vibrio toxin [activation of the adenylate cyclase system with the formation of cyclic adenosine 3 ‘, 5’-monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP)]. These pathogens often become the etiological factor of secretory diarrhea in adults and children. EICPs, like shigella, penetrate and multiply in intestinal epithelial cells. Like shigella, they are motionless and often unable to ferment lactose (DNA homology analysis shows that EICPs are shigella, but because of the medical significance of the latter they were left in the genus Escherichia). Damage to the epithelium increases the absorption of bacterial endotoxin into the blood. The leading role in the pathogenesis of Escherichiosis due to EHECs is played by shigapodobny toxins of two types. Under their action, local necrotic lesions and hemorrhages develop. Penetrating into the blood, they enhance the toxic effect of the LPS complex, which can lead to the development of hemolytic-uremic syndrome and multiple organ failure (DIC, ITS, vascular endothelial damage in the glomeruli of the kidneys and acute renal failure).