Bacillary Dysentery

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PatientPlus articles are written by UK doctors and are based on research evidence, UK and European Guidelines. They are designed for health professionals to use, so you may find the language more technical than the condition leaflets.

See also: Dysentery and Shigella written for patients

Synonym: shigellosis

This disease is notifiable in the UK, see NOIDs article for more detail.

Shigella is a genus of aerobic, non-motile, glucose-fermenting, Gram-negative bacilli that are highly contagious. They cause damage by two mechanisms.[1] Invasion of the colonic epithelium is dependent on a plasmid-mediated virulence factor whilst production of an enterotoxin is not essential for colitis but it enhances virulence.[2] In vivo experiments suggest that Shigella spp. modulate host-adaptive immune responses and affect the function of T lymphocytes.[3] 

Shigella spp. have considerable similarity with Escherichia spp. and its ubiquitous species E. coli but are classified separately for historical reasons. They are serotyped according to their somatic 'O' antigens.[4] Man and gorillas appear to be the only natural hosts.[5]

There are four species of shigellae. To give an indication of relative frequency in the UK the figures in parentheses are the number notified for England and Wales in 2010.[6]

  • Shigella sonnei (1,123)
  • Shigella flexneri (496)
  • Shigella boydii (85)
  • Shigella dysenteriae (42)

The numbers vary greatly from year to year with a peak of over 17,000 cases reported in 1992 to a trough of just over 1,000 in 2003. Since then there has been a gradual increase with a total of 1,747 in 2010. The order of frequency of the various species remains constant.

S. sonnei is the most common but also the mildest form. Many milder cases are probably never diagnosed and so never reported, so the true incidence may be substantially higher. In developing countries the predominant species is S. flexneri.

The organism is spread by faeco-oral contact via infected food or water, during travel, or in long-term care facilities, daycare centres, or nursing homes. Worldwide, shigellosis causes 80-165 million cases and 600,000 deaths annually, with the majority of cases occurring in the children of developing nations.[7] It tends to be most prevalent when flies are at their most prolific.[8] 

In July 2011, an increase in UK-acquired cases of S. flexneri was reported mainly in men who have sex with men (MSM) aged 30-50, some of whom were HIV-positive. A similar outbreak was also seen in Manchester in 2010/11 some of which was seen in MSM.[9] 

Occasional outbreaks are caused by infected foodstuffs. An outbreak of S. sonnei occurred in Norway, caused by infected imported fresh basil.[10] 

Shigella spp. are highly adaptive organisms. Reports from Beijing have shown a worrying trend in changing genotypes and antimicrobial resistance patterns.[11] 

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Risk factors

It is typically a disease of children although the elderly are vulnerable. Worldwide it is associated with overcrowding and poor sanitation.[12] There is evidence that it may be spread by swimming in infected waters. People who engage in anal sex and particularly oro-anal sex are also at risk.[9] 


  • A recent travel history may be pertinent.
  • The incubation period is one to three days but usually nearer to just one day.
  • There is acute watery diarrhoea which may be accompanied by mucus, pus or blood.
  • Abdominal pain and tenesmus.
  • Fever and malaise.
  • Mild cramps and diarrhoea which may persist for days to weeks after infection.
  • It is usually a self-limited disease of three days to one week and rarely lasts as long as a month.


  • Pyrexia
  • Lower abdominal tenderness
  • Normal or increased bowel sounds
  • Possibly dehydration
  • A fresh stool specimen should be sent for culture.
  • Methods using polymerase chain reaction (PCR) analysis may help to improve detection.[15] 
  • Red and white blood cells may be seen in the stool specimen.
  • FBC may show a leukocytosis and even a raised haematocrit if there is dehydration but often it is normal.
  • U&Es may be disturbed if there is dehydration.
  • Sigmoidoscopy is not usually necessary.
  • Sometimes a colonic biopsy is required to differentiate from acute ulcerative colitis.
  • Oral rehydration fluid should be given.
  • In children especially, antipyretic medicines can reduce temperature and help to prevent convulsions.
  • Antibiotics are often helpful both to reduce diarrhoea and fever (by about two days) and to limit spread to others. Resistance is, however, becoming a problem. A Cochrane review found that although antibiotics were generally helpful, no one particular group was more beneficial than another.[16] A third-generation cephalosporin is usually used first-line (eg, ceftriaxone). Ciprofloxacin is appropriate for HIV-positive patients. However, ciprofloxacin resistance has been reported in MSM and a change to a different antibiotic (as suggested by culture results) should be considered if necessary.[17] 
  • Antimotility agents are contra-indicated.[18]

Return to work

When diarrhoea has settled, the vast majority are not a risk to others and may return to work with no further testing. The following need advice from Environmental Health officers or a Consultant in Communicable Disease Control (CCDC):

  • Food handlers who touch unwrapped food to be consumed raw or without further cooking.
  • Healthcare, nursery or other staff who have direct contact with people who are susceptible to infection or for whom infection with Shigella spp. would have very serious consequences. This includes simply serving food to them.
  • Children aged under 5 years attending nurseries, play groups, nursery schools, etc.
  • Older children or adults with poor standards of personal hygiene, like the mentally ill, handicapped or the elderly infirm.

Bacteraemia occurs primarily in malnourished children and carries a mortality rate of 20% as a result of acute kidney injury, haemolysis, thrombocytopenia, gastrointestinal haemorrhage and shock.[19][20] Haemolytic uraemic syndrome may complicate infections with Shigella spp. and E. coli and it carries a high mortality rate. Haemolytic uraemic syndrome is characterised by acute haemolysis, renal failure, uraemia and disseminated intravascular coagulation.[21] Seizures are the most common neurological complication and invariably occur with fevers.[22] 

Reiter's syndrome can occur. It is most common in men aged 20-40 and with the HLA-B27 antigen. It starts two to four weeks after infection and may be chronic and relapsing.[23] 

The disease tends to last from one day to one month with an average of one week. The person can be a carrier for the infection for up to four weeks but usually less. Mortality is rare but can occur in malnourished children and the elderly.

There are currently no vaccines against shigellae although substantial progress is being made.[25] Sanitation and clean water are important in developing countries. In developed nations the concern is hand washing and personal hygiene. Adhering to scrupulous hygiene measures in the preparation of fresh produce is also important.[26] 

It is estimated that the Shigella genus originated between 35,000 and 270,000 years ago.[13] By evolutionary standards that is very recent. The disease has been described by Hippocrates and Herodicus.

In 1897 the Japanese bacteriologist Kiyoshi Shiga (1871-1957) described Bacillus dysenteriae as the cause of bacillary dysentery. He had isolated the organism now known as Shigella dysenteriae from faeces and intestinal walls in patients suffering from dysentery. In 1900 he developed a dysentery antiserum. It was given a different name from Bacillus (now Escherichia coli) because it was not thought at the time that a commensal species could also have pathogenic strains. Koshi Shiga graduated MD from the Imperial University of Tokyo in 1896. He worked with Kitasato Shibasaburo who discovered the tetanus bacillus. Between 1901 and 1903 he worked with Paul Ehrlich in Berlin. His research also included work on leprosy, beriberi and tuberculosis.

Shigella spp. were investigated by the Japanese between 1932 and 1945 as an agent of biological warfare (considered to be a category B agent). Contamination of food supplies would be the most likely method. Biological warfare was used in the First World War but outlawed by the Geneva Convention in 1925. Japan started the development of biological weapons in 1932, using them on China and Manchuria in 1940 and, in 1942, the USA started to research biological weapons too.

Further reading & references

  1. Shigella; Microbiology in, 2013
  2. Carayol N, Tran Van Nhieu G; Tips and tricks about Shigella invasion of epithelial cells. Curr Opin Microbiol. 2013 Feb;16(1):32-7. doi: 10.1016/j.mib.2012.11.010. Epub 2013 Jan 11.
  3. Salgado-Pabon W, Celli S, Arena ET, et al; Shigella impairs T lymphocyte dynamics in vivo. Proc Natl Acad Sci U S A. 2013 Mar 19;110(12):4458-63. doi: 10.1073/pnas.1300981110. Epub 2013 Feb 15.
  4. Hoare A, Bravo D, Martinic M, et al; The normal chain length distribution of the O antigen is required for the interaction of Shigella flexneri 2a with polarized Caco-2 cells. Biol Res. 2012;45(1):21-6. doi: 10.1590/S0716-97602012000100003.
  5. Nizeyi JB, Innocent RB, Erume J, et al; Campylobacteriosis, salmonellosis, and shigellosis in free-ranging human-habituated mountain gorillas of Uganda. J Wildl Dis. 2001 Apr;37(2):239-44.
  6. Shigella Epidemiological Data; Public Health England
  7. Bowen A et al; Shigellosis, Centers for Disease Control and Prevention, 2011
  8. Njuguna HN, Cosmas L, Williamson J, et al; Use of population-based surveillance to define the high incidence of shigellosis in an urban slum in Nairobi, Kenya. PLoS One. 2013;8(3):e58437. doi: 10.1371/journal.pone.0058437. Epub 2013 Mar 7.
  9. Shigella; Public Health England
  10. Guzman-Herrador B, Vold L, Comelli H, et al; Outbreak of Shigella sonnei infection in Norway linked to consumption of fresh basil, October 2011. Euro Surveill. 2011 Nov 3;16(44). pii: 20007.
  11. Qu F, Bao C, Chen S, et al; Genotypes and antimicrobial profiles of Shigella sonnei isolates from diarrheal patients circulating in Beijing between 2002 and 2007. Diagn Microbiol Infect Dis. 2012 Oct;74(2):166-70. doi: 10.1016/j.diagmicrobio.2012.06.026. Epub 2012 Jul 31.
  12. Vinh H, Nhu NT, Nga TV, et al; A changing picture of shigellosis in southern Vietnam: shifting species BMC Infect Dis. 2009 Dec 15;9:204.
  13. Todar K; Shigella and Shigellosis, Microbial World, 2009
  14. Burke A et al; Shigellosis, Merck Manual, 2009
  15. Mokhtari W, Nsaibia S, Gharbi A, et al; Real-time PCR using SYBR Green for the detection of Shigella spp. in food and stool samples. Mol Cell Probes. 2013 Feb;27(1):53-9. doi: 10.1016/j.mcp.2012.09.002. Epub 2012 Oct 5.
  16. Prince Christopher R H, David KV, John SM, et al; Antibiotic therapy for Shigella dysentery. Cochrane Database Syst Rev. 2010 Jan 20;(1):CD006784.
  17. Gaudreau C, Ratnayake R, Pilon PA, et al; Ciprofloxacin-resistant Shigella sonnei among men who have sex with men, Canada, 2010. Emerg Infect Dis. 2011 Sep;17(9):1747-50. doi: 10.3201/eid1709.102034.
  18. Bhattacharya SK, Sur D; An evaluation of current shigellosis treatment. Expert Opin Pharmacother. 2003 Aug;4(8):1315-20.
  19. Shigella spp; Public Health Agency of Canada, 2011
  20. Boyce T; Overview of Gastroenteritis, Merck Manual, 2012
  21. Walker CL, Applegate JA, Black RE; Haemolytic-uraemic syndrome as a sequela of diarrhoeal disease. J Health Popul Nutr. 2012 Sep;30(3):257-61.
  22. Papaconstantinou HT, Thomas JS; Bacterial colitis. Clin Colon Rectal Surg. 2007 Feb;20(1):18-27. doi: 10.1055/s-2007-970196.
  23. Hamdulay SS, Glynne SJ, Keat A; When is arthritis reactive? Postgrad Med J. 2006 Jul;82(969):446-53.
  24. Shigellosis; Health Protection and Surveillance Centre, 2012.
  25. Barry EM, Pasetti MF, Sztein MB, et al; Progress and pitfalls in Shigella vaccine research. Nat Rev Gastroenterol Hepatol. 2013 Apr;10(4):245-55. doi: 10.1038/nrgastro.2013.12. Epub 2013 Feb 19.
  26. Cairncross S, Valdmanis V; Water Supply, Sanitation, and Hygiene Promotion

Disclaimer: This article is for information only and should not be used for the diagnosis or treatment of medical conditions. EMIS has used all reasonable care in compiling the information but make no warranty as to its accuracy. Consult a doctor or other health care professional for diagnosis and treatment of medical conditions. For details see our conditions.

Original Author:
Dr Laurence Knott
Current Version:
Peer Reviewer:
Dr Adrian Bonsall
Document ID:
1840 (v22)
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