Shigellosis

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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: bacillary dysentery

This is a notifiable disease in the UK. See the Notifiable Diseases article for more detail.

Shigella is a genus of aerobic, non-motile, glucose-fermenting, Gram-negative bacilli that are highly contagious. Man and apes appear to be the only natural hosts. They cause damage by invasion of the colonic epithelium causing intense inflammation, and by the injection of type III effector proteins into host cells thereby altering their function.[1] This requires comparatively few bacteria to cause disease. In vivo experiments suggest that Shigella spp. modulate host-adaptive immune responses and affect the function of T lymphocytes.[2] 

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.[3]

'Dysentery' refers to diarrhoea with blood and/or mucus. Bacillary dysentery is a bacterial dysentery caused by Shigella infection. Shigella spp. can cause intestinal inflammation and symptoms of gastroenteritis without dysentery.

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 2013.[4]

  • Shigella sonnei (1003)
  • Shigella flexneri (686)
  • Shigella boydii (96)
  • Shigella dysenteriae (37)

The numbers vary greatly from year to year with a peak of over 17,000 cases reported in 1992 to a trough of around 1,000 in 2003. Since then there has been a gradual increase with a total of 1,822 in 2013. 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 around 160 million cases and more than a million deaths annually, with the majority of cases occurring in the children of developing nations.[5] 

In the UK, most cases are acquired during travel. Because it is primarily a disease of humans, it is most often acquired by drinking water contaminated with human faeces, or eating food washed with contaminated water.[6] It may also be readily transmitted between children at home or in childcare facilities. In recent years an increase in UK-acquired cases of S. flexneri and S. sonnei has been reported in men who have sex with men (MSM).[7] 

Occasional outbreaks are caused by infected foodstuffs. An outbreak of S. sonnei occurred in Norway, caused by infected imported fresh basil.[8] 

Shigella spp. are highly adaptive organisms, with reports from a number of countries showing changing genotypes and antimicrobial resistance patterns.

Risk factors

It is typically a disease of children although the elderly are vulnerable. Worldwide it is associated with overcrowding and poor sanitation. It may be spread by swimming in infected waters. People who engage in anal sex and particularly oro-anal sex are also at risk.[7] 

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History

  • 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.
  • It is usually a self-limited disease of three days to one week and rarely lasts as long as a month.

Examination

  • Pyrexia.
  • Lower abdominal tenderness.
  • Normal or increased bowel sounds.
  • Possibly dehydration.

A fresh stool specimen should be sent for culture where there is a history of travel, there is blood and/or mucus in the diarrhoea, or the diagnosis is otherwise suspected.

Other tests are not usually necessary.

  • 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.
  • Rarely, a colonic biopsy is required to differentiate from acute ulcerative colitis.

General measures

Oral rehydration fluid should be given. Where there is significant dehydration, admission may be required. (For further information on assessment and management of dehydration, see the separate Gastroenteritis in Adults and Older Children and Gastroenteritis in Children articles.)

Medication

  • In children especially, antipyretic medicines can reduce temperature and help to prevent convulsions.
  • Antibiotics are not recommended for healthy people with mild symptoms. They may be 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 to reduce duration of shigella dysentery, no one particular group was more beneficial than another.[9] Consider antibiotic use if there is severe disease, bloody diarrhoea or immunocompromise. Where indicated, seek advice from the local microbiologist and take into account sensitivity; however, usually ciprofloxacin or azithromycin are the treatment of choice.
  • Antimotility agents, such as loperamide, are contra-indicated.

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. General advice for those with an episode of gastroenteritis is that they may return to work or a school/childcare facility 48 hours after the last episode of diarrhoea or vomiting.

The Food Standards Agency advises for food handlers, this applies to those with confirmed infection with S. sonnei, but that for S. dysenteriae, S. flexneri and S. boydii further measures are required. Guidelines advise that: "In addition to the normal 48-hour exclusion, people handling and serving open ready-to-eat foods should seek medical clearance. This usually involves two consecutive negative stool samples taken at intervals of at least 48 hours. Anyone who has household contact with someone infected with these bacteria should inform their manager. They should be excluded from any work that involves direct handling or serving open ready-to-eat foods until medical clearance is obtained in the same way."[10] 

The following may also need extra precautions to prevent the spread of infection to others:

  • 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 - for example, those with mental illness, or with learning disability, or who are infirm elderly.

Complications are uncommon but may include the following:

  • Dehydration and electrolyte disturbance may occur. Occasionally where not rectified, this can have fatal consequences. Infants, the elderly and those with immunological compromise are more likely to have more severe disease and to require admission to hospital for rehydration. Pregnant women are also more at risk of dehydration.
  • Bacteraemia is more common in malnourished children and carries a high mortality.
  • Seizures may occur in young children and are common where there is fever.
  • Haemolytic uraemic syndrome may (rarely) complicate infections, usually those with S. dysenteriae and mostly affecting young children or the elderly. It is more commonly a complication of E. coli O157 and leads to haemolytic anaemia, thrombocytopenia and acute kidney injury.
  • Reactive arthritis (or Reiter's syndrome when arthritis is combined with uveitis and urethritis) can occur. It is most common in men aged 20-40 and with the HLA-B27 antigen. This is most often associated with S. flexneri infection.
  • Toxic megacolon is occasionally a complication of S. dysenteriae.

The disease tends to last from one day to one month with an average of one week. The more common form in the UK usually lasts for up to a week, whereas the tropical forms tend to be more severe and last for 2-4 weeks. Mortality is rare but can occur in malnourished children and the elderly. S. dysenteriae type 1 carries the highest mortality rate of 20-40% but is rare in the UK.

There are currently no vaccines against shigellae although substantial progress is being made.[12] 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. Public Health England has created some promotional material to warn men who have sex with men about the risk of shigella infection, advising of the need to change condoms between anal and oral sex, and about washing (hands as well as ideally buttocks and penis) after sex.[7] 

It is estimated that the Shigella genus originated between 35,000 and 270,000 years ago.[15] 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 with 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. Ashida H, Mimuro H, Sasakawa C; Shigella manipulates host immune responses by delivering effector proteins with specific roles. Front Immunol. 2015 May 7;6:219. doi: 10.3389/fimmu.2015.00219. eCollection 2015.
  2. 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.
  3. 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.
  4. Shigella Epidemiological Data; Public Health England
  5. 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.
  6. Gastroenteritis; NICE CKS, July 2015 (UK access only)
  7. Shigella: guidance, data and analysis; Public Health England
  8. 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.
  9. Christopher PR, David KV, John SM, et al; Antibiotic therapy for Shigella dysentery. Cochrane Database Syst Rev. 2010 Aug 4;(8):CD006784. doi: 10.1002/14651858.CD006784.pub4.
  10. Food handlers, Fitness to Work Guidelines; Food Standards Agency. 2009
  11. Shigellosis; Health Protection and Surveillance Centre, 2012
  12. 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.
  13. Trofa AF, Ueno-Olsen H, Oiwa R, et al; Dr. Kiyoshi Shiga: discoverer of the dysentery bacillus. Clin Infect Dis. 1999 Nov;29(5):1303-6.
  14. Riedel S; Biological warfare and bioterrorism: a historical review. Proc (Bayl Univ Med Cent). 2004 Oct;17(4):400-6.
  15. Shigella and Shigellosis; Todar's Online Textbook of Bacteriology

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 Laurence Knott
Document ID:
1840 (v23)
Last Checked:
25/05/2016
Next Review:
24/05/2021

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