Table 1.

Common forms of diarrhoea classified according to causative agent, pathogenic mechanism and clinical features.

Aetiology	Main site of action	Primary mechanism	Clinical features	Reference(s)
ETEC	Small intestine	Heat stable and heat labile toxins produced by the organism induce secretory diarrhoea	Watery stools associated with fever, abdominal cramps and vomiting	[22,27]
EPEC	Proximal small intestine	Attachment/effacement of enterocytes, alteration of intracellular calcium and cytoskeleton	Self-limiting watery diarrhoea occasionally accompanied with fever and vomiting.	[22,27]
EIEC	Distal ileum and colon	Tissue invasion and mucosal destruction	Watery occasionally bloody diarrhoea	[27]
EHEC	Colon	Elaboration of potent shiga-like cytotoxins l and ll	Bloody diarrhoea in 90% of cases and haemolytic uremic syndrome in 10%.	[22,27]
Vibrio cholerae enterotoxin	Endocrine cells on the villus surface of the intestinal epithelium	Enterotoxins cause an increase in cAMP or cGMP inducing cAMP-mediated alterations of ion transport.	Voluminous watery diarrhoea without abdominal cramps or fever; nausea and vomiting.	[31]
Shigella	M-cells of the colonic and rectal epithelium	Bacteria invade the intestinal epithelium damaging it and causing inflammation. Diarrhoea is due to epithelial damage and inflammatory mediators.	Abdominal cramps and pain with initial high volume watery stool that eventually reduces in volume, becomes stained with mucus and blood and associated with urgency and painful defecation.	[32,33]
Salmonella	Peyers patches of the small intestine	Bacteria invade the intestinal epithelium damaging it and causing inflammation. Diarrhoea is due to epithelial damage and inflammatory mediators.	Loose stools to profuse watery diarrhoea, nausea, vomiting and sometimes persistent headache, especially in S. typhi infection.	[33]
Yersinia enterocolitica	Intestinal epithelium of the terminal portion of the ileum	Bacteria invade the intestinal epithelium damaging it but inhibit host inflammatory responses	Abdominal pain and diarrhoea occasionally accompanied by fever, nausea, vomiting and malaise.	[33,34]
Norovirus	Sub-mucosa of proximal small intestines	Continuous viral replication in the sub-mucosa of the proximal small intestines is believed to interfere with normal intestinal function	Stomach pain, fever, nausea, vomiting, mild self-limiting and non bloody diarrhoea	[37,38]
Astroviruses	Epithelial cells of the proximal small intestines	Viral infection increases intestinal barrier permeability and causes sodium mal-absorption creating an osmotic pressure which pulls water and ions into the intestinal lumen.	Moderate to severe diarrhoea characterised by abdominal pain and vomiting.	[29,30]
Enteric adenoviruses	Intestinal epithelium, peyers patches in the ileum	Viral infection of the intestinal epithelium damages endothelial cells and interferes with smooth functioning of the intestines	Watery diarrhoea accompanied by vomiting, low grade fever and mild dehydration.	[39,40]
Cytomegalovirus	Entire gastrointestinal tract but frequently involves the oesophagus and colon	Viral infection causes intestinal inflammation, erosion and ulceration with inclusions in the stromal and endothelial cells. Causes distal oesophageal ulceration.	Acute watery diarrhoea, stained with blood and may be persistent	[5,41]
Cryptosporidium parvum	Surface epithelial cells lining the distal jejunum and ileum.	Protozoan invades minimally the intestinal mucosa causing self-limiting diarrhoea in immune competent individuals.	Mild to severe watery diarrhoea	[42]
Giardia lamblia	Small intestine	Colonisation of the intestine is an important step for diarrhoea. Initially, there is excystation followed by attachment to the intestinal epithelium and multiplication, then encystment. This process disrupts and distorts the microvilli of the intestine.	Asymptomatic, Stools are loose or semi-formed, mild abdominal discomfort	[24,43]
Entamoeba histolytica	Small intestines	Ingested cysts rupture in the small intestine releasing trophozoites which invade the mucin layer of the intestinal mucosa. Protozoan has an ability to kill and phagocytise host cells.	Lumpy mucoid stools with blood stains, diarrhoea, cramping, abdominal pain, flatulence, tenesmus rectal, headache and vomiting	[44,45]
Balantidium coli	Caecum and colon	Trophozoites produce proteolytic enzymes that digest the mucus coating of the colon facilitating tissue invasion, abscess formation, ulceration and perforation of the intestine.	Acute explosive watery diarrhoea, stools may be stained with blood. Cramping, halitosis, abdominal pain. Tenesmus, weight loss and intestinal perforations are seen in severe cases.	[5,46]

ETEC, enterotoxigenic E. coli, EPEC, enteropathogenic E. coli, EIEC, enteroinvasive E. coli, EHEC, enterohaemorrhagic E. coli.