Describe Shigella and bacillary dysentery with its pathogenesis, diagnosis and treatment.

The Organism and Classification

• Gram-negative bacilli that are non-motile, non-capsulated and non-lactose fermenting (except S. Sonnei, a late fermenter); non-H2S-producing and anaerogenic (no gas)
• Non-motility is the useful contrast with Salmonella, which is motile
• Man is the only natural host, and there is no animal reservoir
• The infecting dose is remarkably small — as few as 10 to 100 organisms, because Shigella resists gastric acid. This is why it spreads readily by person-to-person contact and causes institutional outbreaks, unlike cholera or typhoid which need a large inoculum

Pathogenesis

A small inoculum survives gastric acid and reaches the colon → Organisms invade the M cells overlying lymphoid follicles → They are taken up by macrophages, induce apoptosis and escape into the cytoplasm → They spread laterally from cell to cell using actin polymerisation, without entering the lumen → Intense acute inflammation, mucosal ulceration and microabscesses in the colon → The infection remains superficial and localised to the mucosa — bacteraemia is rare → SHIGA toxin (chiefly S. Dysenteriae type 1) inhibits protein synthesis by cleaving 28S ribosomal RNA, damaging endothelium and causing haemolytic uraemic syndrome

Clinical Features and Diagnosis

• Incubation 1 to 4 days; begins with watery diarrhoea and fever, then evolves into dysentery — frequent small-volume stools containing blood, mucus and pus, with cramping abdominal pain and painful ineffectual straining (tenesmus)
• Complications — dehydration and electrolyte loss; haemolytic uraemic syndrome; febrile convulsions in children; toxic megacolon and perforation; rectal prolapse; protein-losing enteropathy and malnutrition; and reactive arthritis
• Specimen — fresh stool, ideally with blood or mucus, or a rectal swab, sent in buffered glycerol saline or Cary-Blair; the organism dies quickly, so prompt plating is essential
• Microscopy shows abundant pus cells, red cells and macrophages
• Culture on MacConkey and DCA or XLD agar, with colourless colonies; identified biochemically and by slide agglutination with group-specific antisera

Treatment, Prevention and Applied Aspects

• Rehydration — oral rehydration solution usually suffices, since fluid loss is less than in cholera
• Antibiotics are indicated in shigellosis, unlike most other bacterial diarrhoeas — they shorten the illness, reduce complications and limit transmission. ciprofloxacin, ceftriaxone or azithromycin, guided by local resistance, which is now extensive in India
• Avoid antimotility drugs such as loperamide; they prolong fever, delay clearance and may precipitate toxic megacolon
• Zinc and continued feeding in children, which reduce duration and prevent the nutritional deterioration that follows
• Prevention — handwashing is the key measure, because the infecting dose is so small that person-to-person spread dominates; also safe water, sanitation, food hygiene, exclusion of infected food handlers, and fly control
• Distinguish bacillary from amoebic dysentery — bacillary is acute with fever and numerous pus cells; amoebic is more insidious, with fewer pus cells, charcot-Leyden crystals and motile trophozoites containing red cells. The treatments differ entirely, and both are common in India