Paediatrics chapters
Bacillary dysentery
Shigellosis in children: the four Shigella groups, how they invade the colon, the picture of fever, cramps and bloody mucoid stools, stool microscopy and culture, antibiotics, complications such as HUS and seizures, and prevention.
- Bacillary dysentery is shigellosis: Shigella (non-motile Gram-negative rods; groups A dysenteriae, B flexneri, C boydii, D sonnei) spread faecal-orally with a very small infective dose, mainly in children 1-10 years.
- The organism invades the colonic mucosa, giving high fever, cramps, tenesmus and frequent small stools with blood, mucus and pus; febrile seizures and meningism can occur, and S. dysenteriae type 1 (Shiga toxin) can cause HUS.
- Stool shows many pus cells and red cells; culture confirms; treat with ORS, zinc, feeding and an antibiotic chosen by local sensitivity (WHO first choice ciprofloxacin; ceftriaxone if severe), and prevent with hand washing, safe water and breastfeeding.
On this page
Overview
Dysentery means acute diarrhoea with blood, mucus and pus (white cells) in the stool. When the cause is Shigella, it is called bacillary dysentery or shigellosis. It is the prototype of invasive, inflammatory diarrhoea in children, spreads easily in crowded homes, and can be complicated by seizures, dehydration and haemolytic uraemic syndrome (HUS). Exam questions test the organism, the stool findings, the choice of antibiotic and the difference from amoebic dysentery.
Causative organism
Shigella species are non-motile, Gram-negative rods. There are four groups:
| Group | Species | Point to remember |
|---|---|---|
| A | S. dysenteriae | Type 1 produces Shiga toxin: most severe disease, linked with HUS |
| B | S. flexneri | Common in developing countries |
| C | S. boydii | Less common |
| D | S. sonnei | Mildest; predominant in developed countries (Nelson); often resistant to amoxicillin and co-trimoxazole |
Pathogenesis
- Shigellae invade and destroy the surface epithelium of the colon.
- This produces inflammation, oedema, micro-abscesses and ulcers that bleed.
- The colon is selectively affected; the small bowel is spared.
- S. dysenteriae type 1 also releases Shiga toxin, which damages endothelial cells, including in the kidney.
Shigella needs only 10-100 organisms to cause disease (Nelson), so it spreads person to person easily, unlike Salmonella and cholera, which need large doses.
Epidemiology and transmission
- Humans are the main reservoir.
- Route: faecal-oral, via contaminated hands, food and water; flies and poor sanitation help spread.
- Commonest at 1-10 years; uncommon in the first 6 months, especially in breastfed babies.
- Incubation: 1-7 days (average 2-4 days).
- Untreated children can shed organisms for up to a month.
Clinical diagnosis
Symptoms and signs
- Abrupt onset of high fever (up to 40°C) lasting 1-3 days, malaise, anorexia.
- Crampy abdominal pain, urgency and tenesmus.
- Stools may start watery, then become frequent, small and mucoid with blood.
- Lower abdominal tenderness, not well localised.
- Dehydration from diarrhoea, vomiting and fever.
- Illness usually lasts 3-7 days.
Neurological picture
- Seizures are common, especially when the temperature is very high; Akbar puts them at up to about a third of children with Shigella diarrhoea.
- High fever with lethargy, seizures and neck stiffness can mimic meningitis.
A child with high fever and a seizure who passes bloody stools later may first be thought to have meningitis or a simple febrile seizure. Ask about diarrhoea and examine the stool.
"Shigella shakes the brain and scrapes the colon": high fever, seizures and bloody mucoid stools together point to shigellosis.
Clinical diagnosis in practice
In children, visible blood in loose stools is treated as dysentery. Most bloody diarrhoea in young children in Pakistan is bacterial, and Shigella is the prime suspect.
Investigations
Stool microscopy
- Many pus cells (white cells) and red blood cells.
- Mucus; no trophozoites of Entamoeba (if they are seen with ingested red cells, think amoebiasis).
Stool culture
- Isolation of Shigella from the stool confirms the diagnosis.
- Send a fresh stool sample before antibiotics; culture also gives the sensitivity pattern, which guides treatment.
Other tests
- Blood count: raised white count with a shift to the left (immature neutrophils).
- Blood culture: may be positive in toxic-looking children.
- Electrolytes, urea, creatinine: dehydration, acidosis, renal failure; check blood film, platelets and renal function if HUS is suspected (fragmented red cells, low platelets, rising creatinine).
Differential diagnosis
| Other causes of dysentery | Mimics |
|---|---|
| Enteroinvasive E. coli (same picture as Shigella); enterohaemorrhagic E. coli O157:H7 (bloody diarrhoea, HUS); Entamoeba histolytica; Campylobacter jejuni; Yersinia; non-typhoidal Salmonella | Intussusception (redcurrant-jelly stool, colicky pain, mass); inflammatory bowel disease |
Bacillary versus amoebic dysentery
| Feature | Bacillary (Shigella) | Amoebic (E. histolytica) |
|---|---|---|
| Onset | Acute, a few days | More gradual; often 1-2 weeks of symptoms |
| Fever | High | Mild or absent |
| Stools | Small, frequent, blood and mucus | Blood and mucus, often looser and larger |
| Stool pus cells | Many | Few (occult blood almost always present) |
| Organism seen | Shigella on culture | Trophozoites containing red cells |
| Seizures | Common | Rare |
| Extra-intestinal spread | Bacteraemia uncommon | Liver abscess |
Many pus cells = bacillary; few pus cells with red-cell-eating trophozoites = amoebic.
Management
Fluids and nutrition
- ORS for dehydration; IV fluids if severe or shocked.
- Continue breastfeeding and feeding; Akbar advises a high-protein, high-calorie diet during recovery.
- Zinc: 20 mg of elemental zinc daily for 14 days shortens the illness and improves weight gain and immunity.
- Vitamin A: Akbar notes a single large dose (200,000 IU) reduces severity.
- Antimotility (antidiarrhoeal) drugs are not given; they may prolong the illness and worsen toxicity.
Antibiotics
Antibiotics shorten the illness and reduce shedding and spread. Nelson: treatment gives a bacteriological cure in about 80% after 48 hours. Choose by recent local culture and sensitivity results; Akbar gives 5 days for all regimens.
| Drug | Notes (doses from Akbar) |
|---|---|
| Ciprofloxacin | 20-30 mg/kg/day in 2 doses; Akbar notes it is the WHO first choice for bloody diarrhoea |
| Ceftriaxone | 50 mg/kg/day IV or IM once daily; for severe or toxic children |
| Cefixime (oral third-generation cephalosporin) | 8 mg/kg/day in 1-2 doses; Nelson's oral choice for children |
| Azithromycin | 12 mg/kg on day 1, then 6 mg/kg/day for 4 more days |
| Nalidixic acid | Older option; resistance is common |
- Resistance is widespread: Nelson notes many S. sonnei strains resist amoxicillin and co-trimoxazole.
- Reassess after 48 hours: if there is no improvement in fever, blood in stool and appetite, change the antibiotic according to sensitivity.
An answer choosing co-trimoxazole or amoxicillin for shigellosis is usually wrong because of resistance; in Pakistan current practice starts with ciprofloxacin (or ceftriaxone/cefixime or azithromycin depending on local resistance). Check the current national guideline.
Complications
- Dehydration, acidosis, shock and acute renal failure.
- Febrile seizures, encephalopathy.
- Bacteraemia and metastatic infection (more in malnourished infants).
- Rectal prolapse (from straining).
- Haemolytic uraemic syndrome: haemolytic anaemia, low platelets and acute kidney injury, especially after S. dysenteriae type 1.
- Reactive arthritis after the infection (Akbar).
- Intestinal abscess and perforation (rare, Nelson).
- Malnutrition and persistent diarrhoea after repeated episodes.
Prognosis
- Excellent when dehydration is treated promptly.
- Mortality is highest in very young, malnourished infants who do not receive fluids.
Transmission and prevention
- Hand washing with soap, especially after defecation and before preparing or eating food.
- Safe drinking water and proper sewage disposal.
- Prolonged breastfeeding.
- Food hygiene; protect food from flies.
- Treat cases promptly to reduce shedding; exclude infected children from food handling and nurseries until well.
There is no routine vaccine against Shigella; prevention rests on hygiene, sanitation and breastfeeding.
Expect: Shigella as non-motile Gram-negative rods in four groups, with S. dysenteriae type 1 and Shiga toxin causing HUS; a tiny infective dose and person-to-person spread; abrupt high fever, cramps, tenesmus and small bloody mucoid stools; febrile seizures and meningism; stool with many pus and red cells and culture for confirmation; ORS, zinc, feeding and avoiding antimotility drugs; ciprofloxacin as WHO first choice, ceftriaxone for severe disease, cefixime or azithromycin by sensitivity; complications (HUS, rectal prolapse, seizures, reactive arthritis); and how to separate bacillary from amoebic dysentery.
Quick revision
- Dysentery = loose stools with blood, mucus and pus cells.
- Shigella: non-motile Gram-negative rods; A dysenteriae, B flexneri, C boydii, D sonnei.
- 10-100 organisms enough; faecal-oral; age 1-10 years.
- Invades colon: high fever, cramps, tenesmus, bloody mucoid stools; seizures.
- Stool: many pus and red cells; culture confirms; blood culture if toxic.
- ORS, feeding, zinc 20 mg for 14 days; no antimotility drugs.
- Ciprofloxacin (WHO first choice), ceftriaxone if severe; cefixime or azithromycin per sensitivity.
- Complications: dehydration, seizures, rectal prolapse, HUS, reactive arthritis.
Written by The House Job from standard references (Basis of Paediatrics by Pervez Akbar; Nelson Essentials of Paediatrics).
FAQ
Why do children with shigellosis get seizures?
Seizures are usually linked with the high fever of the illness, though toxins may contribute. They can make the child look as if they have meningitis before the bloody stools appear.
Is every child with bloody diarrhoea given an antibiotic?
In children, bloody diarrhoea is managed as presumed shigellosis and treated with an antibiotic chosen by local sensitivity, together with fluids, feeding and zinc.
Which Shigella causes haemolytic uraemic syndrome?
Shigella dysenteriae type 1, through Shiga toxin. Enterohaemorrhagic E. coli O157:H7 causes HUS by the same mechanism.
Why are antidiarrhoeal drugs avoided?
They slow the bowel, keep the organism and toxin inside longer and can worsen the illness; they do not help a child with dysentery.