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Bacterial dysentery is an infectious intestinal disease, contagious, caused by the bacteria of the bacillus (Shigella). Characteristic lesions occur in the intestines: large and straight. Dysentery, bloody diarrhea (dysentery), was described by Hippocrates as a clinical unit in antiquity. It is still endemic and epidemic in developing countries.
A few words about bacterial dysentery … – symptoms
Bacterial dysentery in the past caused significant mortality (among others Alexander Macedoński died of it). In accordance with the currently adopted etiological classification of infectious diseases, the diagnosis of “bacterial dysentery” applies to any disease with symptoms of intestinal catarrh, regardless of the severity of clinical symptoms, if bacteria belonging to the genus Shigella spp are detected in the excreta. In Poland, diseases are obligatorily registered by the sanitary services. and annual numerical reports sent to ECDC as required by the EU.
Bacterial dysentery and Shigella
The genus Shigella belongs to the order Enterobacteriales of the Enterobacteriaceae family of the intestinal bacilli. This family is found in the normal intestinal flora of animals and humans. Most are relatively pathogenic species, but Shigella are considered absolutely pathogenic, whether isolated from sick or healthy individuals.
Morphologically, Shigella are gram-negative short rods, immobile, growing on common bacteriological media under aerobic and anaerobic conditions. Genetically, Shigella is similar to Escherichia coli. They are a separate type (or only a clone) which, due to adaptation to intracellular parasitism, has lost a fragment of the genome and with it some of the metabolic properties that Escherichia coli has (e.g. for the breakdown of lactose, many sugars, gas fermentation and the formation of cilia), lost mobility and has become more demanding in terms of culturing conditions in the laboratory (new isolations require the presence of meat extract to grow on an agar medium and produce full antigenic structure).
The genus Shigella is divided into 4 species / groups marked with letters, differing in biochemical and antigenic properties, and 47 types and serological subtypes:
- S. dysenteriae (group A, 13 types),
- S. flex neri (group B, 6 types, 15 subtypes),
- S. boydii (group C, 20 types),
- S. sonnei (group D, 1 type, two varieties).
Factors determining bacterial dysentery
The listed varieties of Shigella differ in virulence and its determinant factors. They all produce factors responsible for Shigella’s invasive properties. These are antigens that mediate the adherence of bacteria and their passive penetration into the epithelial cells (enterocytes) of the mucosa of the large and rectal intestines. After penetration, bacteria have the ability to escape from phagocytic vesicles into the cytoplasm of the cell and synthesize proteins related to their ability to move inside the cytoskeleton, to multiply in epithelial cells and in the submucosal tissue of the large and rectal intestines, and move through intercellular junctions (bridges) to the next enterocytes.
In addition, two enterotoxins are produced:
- ShET 1 – by all 4 Shigella species,
- ShET 2 – by S. flexneri 2a.
They are responsible for the excretion of fluid into the intestinal lumen and blocking its reabsorption early in life, which causes watery diarrhea. A third enterotoxin related to the presence of a bacteriophage has also been described.
S. dysenteriae exotoxin 1, known as shiga toxin (stxA) (formerly neurotoxin), is heat labile and similar to the cytoxin (verotoxin) of enterohemorrhagic E. coli (EHEC, VTEC, STEC, e.g. O 157: H7, O104: H4) . It inactivates the 60s subunit of ribosomes in mammalian cells and inhibits protein synthesis in them. In patients, this toxin is responsible for the excretion of fluid, but also for the occurrence of systemic hemolytic uremic syndrome (HUS). It consists of 6 subunits, one biologically active – A and five – B, binding to the intestinal epithelial cell.
There is also an endotoxin in all types of Shigella LPS-O, heat-stable, consisting of the toxic lipid A and the immunogenic polysaccharide core (PS), which is the somatic antigen O. It is responsible for increased body temperature and stimulation of the immune system in the patient and for the occurrence of late immune reactions, e.g. Reiter’s syndrome.
In connection with the work on the oral vaccine against dysentery, it was found that the mentioned pathogenic properties of Shigella result from the action of many factors encoded in the genetic system of the bacterial cell.
The structure of surface antigens and the LPS complex as well as the ShET 2 toxin produced by S. flexneri 2a depend on the genes located on the chromosome. The ability of bacteria to invade (IpaBCDA genes) depends on the genes located on a large plasmid complex with a complex structure – 180-220 kDA (kilodaltons). For example, ipaC determines the entry of bacteria into the intestinal epithelial cell, and ipaB determines the lysis of the vacuoles and their release into the cytoplasm of the cell for intracellular multiplication. The VirG gene (IcsA) encodes the ability to form an actin tail and move bacteria around the epithelial cell and to be released from it. A similarly large plasmid is found in enteroinvasive E. coli EIEC. The loss of a plasmid by the strain screened in the laboratory causes it to lose its invasive properties.
Antimicrobial resistance is encoded by various smaller plasmids or complexes thereof. They can be transmitted between bacterial cells, such as the factor of infectious drug resistance to 4 different drugs (factor R), first described in 1949 in S. flexneri in Japan.
Bacterial dysentery – frequency of occurrence
Bacterial dysentery (shigellosis) is an anthroponosis, a disease that spreads only among humans, and the microorganism Shigella is a pathogen only for humans and only humans are its significant reservoirs in nature. Sometimes, dysentery (S. flexneri 4b) affects monkeys kept in captivity with an inadequate diet (e.g. lack of bananas).
The transmission of infection occurs:
- in the fecal-oral route, directly from the sick, convalescent or healthy carrier of the pathogen (asymptomatically infected),
- indirectly through water contaminated with human faeces (for drinking or recreation, epidemics in France and the USA),
- through food (dairy products, fruits, raw vegetables),
- through objects (doors, handles, bedding, walls in flush-flush toilets – splashes),
- by flies.
Shigella are sensitive to commonly used disinfectants. The survival time of bacteria outside the human body is short and depends on the Shigella variety, temperature and environmental conditions – S. sonnei survives the longest, up to 3 weeks in soil and moist toilets in winter. Infection can occur through dirty hands. An epidemic spread of infections in the communities of homosexual men (in Berlin and San Francisco) has been described. The infectious dose of the virulent strain is very small – it is enough to transfer 10-100 bacterial cells (much smaller than other intestinal bacteria).
Bacterial dysentery hatching period
The period of incubation of the disease is 24-72 hours, less frequently up to 7 days, its duration – on average from 48 to 120 hours. If left untreated, the disease may persist for several weeks, causing:
- dehydration,
- cachexia,
- death (especially in children and patients with AIDS).
In Poland, in the period when antibiotics were not yet available, the mortality of hospitalized patients was 10%.
The severity of the course of bacterial dysentery depends on the type of germ, the general condition of the patient, his age, nutritional and living conditions, and the climate. The last deaths due to dysentery were recorded in Poland in 1999 and they concerned elderly people in a nursing home. The incidence has significantly decreased, from 20-30 cases per 100. population in the last twenty years of the twentieth century to 0,20 per 100 thousand. at the beginning of the XNUMXst century.
Sporadic cases in former endemic areas of dysentery also occur less and less often, and also as epidemics of various ranges: limited to one environment (psychiatric hospital, children’s home, boarding house, prison, holiday camp for children or adolescents), often with secondary diseases spreading also by contact.
Bacterial dysentery in Poland
Currently, there are no large epidemics of dysentery in Poland, which spread through water, milk (Białystok), and cottage cheese in the years 1970-2000, and secondary illnesses appeared as a result of contact in the family of a sick or asymptomatic vector who excreted dysentery with faeces. Surviving dysentery causes permanent immunity only to the antigenic type that caused it, hence the possibility of repeated illness and the difficulty in creating an immunizing vaccine.
Where bacterial dysentery is most common
Dysentery is present all over the world, it is an endemic disease in countries with low hygiene standards and hot climates, sometimes also moderate (Africa, Asia, South America). It is estimated that about 165 million people suffer from dysentery annually, of which about 163 million in developing countries; 1,1 million people die annually, mainly children up to the age of 5. In some parts of Asia and Africa, dysentery is one of the leading causes of death for children under 5. In various countries, sporadic dysentery is mostly endemic, and its number varies seasonally. Epidemics occur during the period of natural disasters and population movements, in environments with significant overcrowding and very poor sanitary and hygienic conditions, e.g. in refugee camps, in combat areas. During World War I, more people died from dysentery in the Balkans than from hostilities. Mild and moderately severe illnesses also occur in summer youth camps, and may also occur in the home environment as a result of spreading contaminated food or water.
Dysentery cases after bacteriological confirmation that it is shigellosis are subject to mandatory registration in Poland, as well as in all European countries. An epidemiological investigation is required in the case of collective diseases ECDC data shows that in 2008 the incidence of dysentery was 1,8 per 100 inhabitants, people of all ages, women and men were affected, but the most cases were reported among children under 000 years of age. Most cases are reported in the fall months with peak cases in September. Most of the cases where the origin was established were imported. Most cases were reported from the United Kingdom (UK) 5, Bulgaria 1595 and Sweden 1094, from Poland 596 cases, including 33 confirmed by bacteriology, the incidence 31 per 0,06 population. The number of reported cases is decreasing every year, e.g. due to the lack of properly targeted bacteriological tests.
Dysentery is a threat to people traveling to and working in highly endemic countries. Sporadic infections among tourists, even those staying in reputable hotels, are brought to Poland every year.
There are different varieties of dysentery in the world in areas with different social and economic conditions. According to WHO data, it is estimated that S. sonnei is responsible for 15% of dysentery cases registered in developing countries and 77% in developed countries. Outbreaks caused by S. flexneri are most frequently registered in developing countries. S. dysenteriae 1 occurs mainly in the poorest countries in Africa and South America, causing about 6% of cases. These are cases of severe course and high mortality, spread epidemically – often caused by strains resistant to many antibacterial drugs. S. boydii is very rare. In Poland, in the years 1918-1970, a change in the etiological factor dominating in the recorded cases of dysentery was observed. S. dysenteriae 1 dominated during both world wars, S. flex neri – in the interwar and post-war period until 1970, and S. sonnei dominates until now.
Source: J. Cianciara, J. Juszczyk, Infectious and parasitic diseases; Czelej Publishing House