Chronic enterocolitis - types. Ulcerative colitis, Crohn disease, Whipple disease. Microscopic & gross pathomorphology
Enterocolitis (aka colenteritis) just means inflammation of the digestive tract, involving the small and large intestine. It can be viral, bacterial, fungal, parasitic or autoimmune. The common symptoms are malabsorption, diarrhea, nausea, vomiting, abdominal pain, fever, and possibly blood in the stool.
Common bacteria are Salmonella, Shigella, E. coli, Campylobacter, common viruses are enterovirus, rotavirus, norwalk virus, adenovirus.
As well as dividing types based on etiology, we can add the following types:
- Necrotizing enterocolitis
- Necrosis of the intestine occurs with inflammation, most common in premature babies. General GI symptoms as expected, exact cause is unclear, but is thought to combine poor blood flow and infection
- Antibiotic-associated enterocolitis (Pseudomembranous enterocolitis)
- Antibiotics clear out normal gut bacteria and Clostridium difficile spreads causing inflammation throughout the gut. Can cause watery diarrhea as well as other expected symptoms
- Hemorrhagic enterocolitis
- Caused by strains of E.coli that produce Shiga toxin causing bloody diarrhea and other complications
- Organisms often transferred via unpasteurized milk
Ulcerative Colitis & Crohn's
Together these form IBD, inflammatory bowel disease. It is chronic and arises from inappropriate mucosal immune activation.
Ulcerative colitis is limited to the colon and rectum, extending only into the mucosa and submucosa. It’s progression is stepwise, not missing out sections. However Crohn's disease can affect any part of the GI tract, is frequently transmural and does skip, it doesn’t have to be continuous.
Both disorders are more common in women, and more common in the west. The exact cause of IBD is uncertain, however most believe it comes from errors in interaction between intestinal microbiota, intestinal epithelial dysfunction and aberrant mucosal immune responses. Primary factors we shall consider:
- Genetics - risk is increased when family member has disease (NOD2 mutation increases susceptibility)
- Mucosal immune response - immunosuppressors help with symptoms, suggesting the mucosal immune response is of central importance to the pathogenesis
- Epithelial defects - defects in tight junctions present in Crohn's (NOD2 polymorphisms)
- Microbiota - data suggests it’s important but we don’t know how
Morphology
- Crohn's
- Most common sites are terminal ileum, ileocecal valve and cecum
- Disease limited to small intestine in 40% of cases
- Presence of multiple, separate, delineated areas, known as skip lesions
- Lesions do however coalesce into elongated serpentine ulcers along the axis of the bowel with fissures frequently developing and the formation of a cobblestone appearance
- The intestinal wall thickens due to transmural edema, inflammation, fibrosis and hypertrophy of muscularis propria