Shigella sonnei, Shigella flexneri, Shigella dysenteriae, Shigella boydii
Shigellae are gram-negative, immobile, facultatively anaerobic rod-shaped bacteria. They are the causative agents of shigellosis (shigella dysentery). The only relevant source of infection is humans (sick, convalescent and asymptomatic excretors).
The risk of infection depends primarily on the quantity of pathogens excreted and the stool consistency as well as the hygienic behaviour of the infected persons. Therefore, the greatest danger comes from acutely ill persons. Non-human infections occur mainly in captive monkeys, but are generally of no importance in the epidemiology of shigellosis.
The genus Shigella belongs to the family Enterobacterales and can be divided into 4 species or subgroups (UG) based on their biochemical characteristics and specific O-antigens:
- S. dysenteriae (subgroup A)
- S. flexneri (subgroup B)
- S. boydii (subgroup C)
- S. sonnei (subgroup D)
The strains within subgroups A-C can be subdivided into serovars. S. sonnei is serologically uniform and consists of one serovar. In Austria, about 80 % of shigelloses are caused by Shigella sonnei.
Shigellae are distributed worldwide. In Central Europe Shigella sonnei and Shigella flexneri are endemic. A large proportion of all cases of shigellosis in Austria are imported by travellers (about 60-70% of reported cases), with the pathogens most frequently being imported from Egypt, India and Morocco. Inadequate hygienic conditions and cramped living quarters (camps, retirement homes, kindergartens, schools) favour the spread of the disease.
Transmission usually occurs through direct or indirect smear infection via contaminated hands. The infection can spread indirectly via food, drinking water, bath water or contaminated objects. The pathogens causing shigellosis can also be easily transmitted during sexual anal contact. Education due to the increased risk of transmission among MSM (men who have sex with men) is especially important in the context of the clustered occurrence of multidrug-resistant Shigella strains. Where appropriate, mostly in developing countries, flies play a role as vectors. The infectious dose of Shigella is very low. Even a minimal amount (10-200 germs) is sufficient to cause clinical symptoms. The reason for this is a relatively high acid tolerance compared to Salmonella.
Incubation period: 0.5 to 4 days, rarely longer. All shigellae produce an endotoxin consisting of lipopolysaccharides, which is responsible for the inflammatory irritation of the intestinal mucosa. Invasion into the epithelial cells of the colon is facilitated by the ipaH (invasion plasmid antigen H) gene. Some Shigella species (primarily Shigella dysenteriae 1) also produce an exotoxin (Shiga toxin) that can lead to severe disease with CNS involvement. The disease varies between mild courses with minor watery diarrhea and severe disease. The occurrence of bloody-mucous stools corresponds to the clinical picture of dysentery (hence the name shigella dysentery, bacterial dysentery). Typical bacterial dysentery begins with fever, cramping abdominal pain, and watery diarrhea. The presence of mucus, pus and blood, which are absent in mild cases, are characteristic of dysentery stools. In typical cases, 20 to 30 bowel movements occur daily, which are associated with a painful urge to defecate (tenesmus). The amount of stool produced in each case is small. Shigellosis is often accompanied by abdominal cramps and vomiting. In severe cases, epithelial necrosis and ulcers may occur in the colon. In rare cases, Reiter's syndrome (caused primarily by S. flexneri) and hemolytic uremic syndrome (caused by Stx-positive Shigella spp.) may also occur.
The duration of the disease varies depending on the course and is on average 7 days. Contagiousness exists primarily during acute infection (i.e., as long as the person shows symptoms of illness) and as long as the pathogen is excreted in the stool; this may be 1-4 weeks after the acute phase of illness. Excretion over a longer period is rare. In asymptomatic carriers, excretion may continue for several months. About half of all shigelloses have an abortive course, which occurs as mild, short-lived diarrhea without blood in the stool. These forms are epidemiologically particularly dangerous because they are usually not recognized.
Treatment with antibiotics shortens the duration of the disease and reduces the excretion of the pathogen. In industrialized countries, Shigella infections are mostly caused by S. sonnei. They are often mild illnesses, and antibiotic therapy is not mandatory but may be indicated to prevent secondary infections. Due to the widespread and rapidly developing resistance in shigella, therapy must always be guided by the antibiogram. The attending physician decides on the necessity of antibiotic administration. Motility inhibitors should not be used in the treatment of shigellosis. Parenteral compensation of fluid and electrolyte loss is primarily used in patients with chronic underlying diseases and in very young and elderly patients.
Appropriate hand hygiene or personal hygiene to prevent fecal-oral transmission of shigellosis from person to person is the most important preventive measure. Shigella is often spread through toilet facilities in schools and kindergartens, so adequate cleaning is always necessary in these areas. Due to the lower "hygiene awareness" of young children, thorough hand washing with soap and water after visiting the toilet should be practiced and controlled, especially in kindergartens.
Teachers, students, school staff and employees, and visitors to other children's community facilities who have or are suspected of having shigellosis shall not use school facilities or similar facilities or attend their functions until medical judgment indicates that they are no longer likely to spread the disease. Persons suffering from or suspected of suffering from shigellosis or excreting shigella may not work or be employed in the commercial production, handling or marketing of foodstuffs if they come into contact with the latter in the process. This also applies mutatis mutandis to employees of restaurants, canteens and other areas in and for communal catering.
Differentially, a multitude of other pathogens of intestinal infections as well as non-infectious causes have to be distinguished. Mild forms of shigellosis may be confused with salmonellosis or with infections of viral origin such as noroviruses, adenoviruses or rotaviruses. In the presence of bloody stools, infections with Campylobacter, Yersinia enterocolitica, enteroinvasive and enterohaemorrhagic E. coli, Clostridium difficile, Aeromonas, in case of return from warm countries amoebiasis or lamblia, in elderly persons additionally carcinoma, in children intussusception should be considered.
Clinically and anamnestically only a tentative diagnosis can be deduced. The diagnosis of shigellosis can only be made by bacteriological stool examination. Fresh stool (possibly also freshly taken rectal swabs) is the most suitable material for examination. At least the rectal swabs must be transported in buffered medium.
In the primary laboratory, the pathogen is detected from the stool either conventionally by isolation using selective agar and subsequent biochemical and/or serological identification, or using PCR systems. However, this molecular biological detection cannot distinguish between Shigella and EIEC (Enteroinvasive Escherichia coli), therefore, if the PCR result is positive, this method requires additional isolation or identification of the pathogen.
Shigella isolates are sent by the primary laboratories to the National Reference Centre for Shigella in Austria. The strains received by the reference centre are typed by means of serotyping, biochemotyping, phage typing (only for Shigella sonnei), MLST (multilocus sequence typing) and cgMLST (core genome multilocus sequence typing). Antibiotic resistance testing is performed on all isolates.
Last updated: 10.10.2022