Epidemiology

There are 4 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 2005.^[3]

• Shigella sonnei (889)
• Shigella flexneri (334)
• Shigella boydii (114)
• Shigella dysenteriae (58)

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 but 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 1 million deaths and over 165 million cases each year, with the majority of cases occurring in the children of developing nations. It tends to be most prevalent when flies are at their most prolific.^[4]

Occasional outbreaks are caused by infected foodstuffs. An outbreak of Shigella dysenteriae type 2 occurred in Scandinavia, caused by infected sugar snap peas imported from Kenya.^[5]

Shigella spp. are highly adaptive organisms. Reports from South Vietnam have shown a worrying trend in changing genotypes and antimicrobial resistance patterns.^[6]

Risk factors

It is typically a disease of children although the elderly are vulnerable. Worldwide it is associated with overcrowding and poor sanitation.^[6] There is evidence that it may be spread by swimming in infected waters. It can also be transmitted by homosexual practices.^[7]

Presentation^[4][8]

History

• A recent travel history may be pertinent.
• The incubation period is 1 to 3 days but usually nearer to just 1 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 3 days to 1 week and rarely lasts as long as a month.

Examination

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

Differential diagnosis^[4]

• Amoebiasis
• Campylobacter infection
• Cholera
• Clostridium difficile colitis
• Colon cancer
• Crohn's disease
• E. coli
• Viral gastroenteritis
• Salmonellosis
• Ulcerative colitis
• Yersinia enterocolitica

Investigations^[4][8]

• A fresh stool specimen should be sent for culture.
• 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.

Management^[4][8]

• 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 2 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.^[9] A third-generation cephalosporin is usually used first-line (eg ceftriaxone). A quinolone is appropriate for HIV-positive patients.
• Antimotility agents are contra-indicated.^[10]

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 a shigella infection would have very serious consequences. This includes simply serving food to them.
• Children 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.

Complications^[4]

Bacteraemia occurs primarily in malnourished children and carries a mortality rate of 20% as a result of acute renal failure, haemolysis, thrombocytopenia, gastrointestinal haemorrhage and shock. Haemolytic uraemic syndrome may complicate infections with Shigella spp. and E. coli and it carries a mortality rate in excess of 50%. Haemolytic uraemic syndrome is characterised by acute haemolysis, renal failure, uraemia and disseminated intravascular coagulation. Seizures are the most common neurological complication and invariably occur with fevers.

Reiter's syndrome can occur. It is most common in men aged 20 to 40 and with the HLA-B27 antigen. It starts 2 to 4 weeks after infection and may be chronic and relapsing.

Prognosis^[4]

The disease tends to last from 1 day to 1 month with an average of 1 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.

Prevention

There are currently no vaccines against shigellae although substantial progress is being made in the development of nonliving vaccines.^[11] Sanitation and clean water are important in developing countries. In developed nations the concern is hand washing and personal hygiene. Preparation of fresh produce is also important.^[12]

History

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 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 was born in 1871 and died in 1957. He 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 was one species investigated by the Japanese between 1932 and 1945 as an agent of biological warfare and is considered a category B agent. Contamination of food supplies would be the 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.

In 1996 muffins and doughnuts were deliberately contaminated with S. dysenteriae in Dallas.^[14]