Intestinal Ulcers — Typhoid vs Tubercular: Orientation, Histology and Complications

Both typhoid (enteric) fever and intestinal tuberculosis target the ileocaecal region, because that is where lymphoid tissue is most abundant. Both produce ulcers over lymphoid follicles. The classic examination question is therefore about ulcer orientation: typhoid ulcers lie along the long axis of the ileum, tubercular ulcers lie across it (perpendicular to the lumen), and that orientation explains their different complications.

Typhoid follows an incubation of 6 to 30 days and presents insidiously with gradually rising fever, fatigue, anorexia, headache, malaise and abdominal symptoms. Rose spots (blanching, 2 to 4 mm erythematous macules) occur in fewer than 25% of patients. Delayed or inadequate treatment leads to meningitis, sepsis or intestinal perforation. The gut ulcer is therefore one stage of a systemic infection of the reticuloendothelial system.

Intestinal TB is nonspecific: abdominal pain, fever, weight loss and change in bowel habit, often with a delayed diagnosis. It occurs without a history of TB in many patients and with active pulmonary TB in only some (6–38%). Abdominal tenderness, ascites, organomegaly and an abdominal mass may be found; obstructive symptoms point to strictures. Patients are often anaemic with low albumin and raised CRP.

Salmonella Typhi and Paratyphi cross the gut epithelium, including by entry through the M cells overlying Peyer patches, and are taken up by mononuclear cells in the underlying lymphoid tissue. In contrast to non-typhoidal Salmonella, they spread through lymphatics and blood. The Peyer patches of the terminal ileum enlarge into plateau-like elevations up to 8 cm in diameter. Mucosal shedding over them creates oval ulcers oriented along the long axis of the ileum. The ileum and caecum are the sites usually involved, and the bowel wall becomes thickened.

• Microscopy: a predominantly monocytic infiltrate with swollen macrophages (typhoid cells) that often contain bacteria, red cells and debris. Neutrophils are rare, even at the ulcerated surface. Lymphoid nodules and diffuse areas of macrophages are present, and the inflammation can breach the muscularis propria and reach the serosa.
• Typhoid nodules (focal macrophage aggregates with small areas of necrosis) occur in the liver, bone marrow and lymph nodes; mesenteric nodes show necrotising lymphadenitis; the spleen is enlarged and soft.
• Closest mimic: Yersinia enterocolitis. The distinguishing feature is that deep, penetrating ulcers and abundant epithelioid granulomas characterise Yersinia and not typhoid.
• Time course: Peyer patches continue to enlarge, then necrose over several weeks. Haemorrhage (10–20%) and perforation (1–3%) classically occur in the third and fourth weeks; StatPearls says complications usually appear 2 to 3 weeks after onset.

Diagnosis and treatment, briefly. Blood culture is the gold standard (positive in about 50–66% of single cultures in endemic areas); bone marrow culture is the most sensitive (80–96%); Widal is widely used but has low sensitivity and specificity; stool culture is not suitable for acute diagnosis. For mild adult enteric fever where fluoroquinolone resistance is high, azithromycin (1 g loading dose, then 500 mg daily for 7 days) is the drug of choice; severe disease is treated with ceftriaxone 2 g IV daily for 10 days. See also diarrhoeagenic bacteria.

In GI tuberculosis the ileocaecal region is affected in about 90% of patients, following the distribution of lymphoid tissue. StatPearls adds that the terminal ileum and caecum are favoured because of a narrow lumen, relative stasis, minimal digestive activity and abundant lymphatic tissue. Infection arises from swallowed sputum, haematogenous or lymphatic spread, or ingestion of infected milk (M. bovis).

• Ulcer shape: ragged ulcers of varying number and size that are circumferential, with the long axis perpendicular to the lumen; fissures may extend into the muscularis propria. The mucosa is oedematous and haemorrhagic.
• Histology: epithelioid granulomas with caseation, throughout the full thickness of the wall (more frequent in ulcerative than hypertrophic lesions), with enlarged, caseating mesenteric lymph nodes. Acid-fast bacilli may be present even without granulomas, but the disease is paucibacillary so AFB stains are insensitive.
• Healing: fibrosis, strictures and stenosis, sometimes several centimetres long.
• Complications: bowel obstruction is common; perforation may occur.

Intestinal TB and Crohn disease share clinical, radiological, endoscopic and histological features, and no single lesion is strictly diagnostic. A 2026 review of colonoscopic features gives the useful contrasts below; diagnosis rests on biopsy with stains, PCR or culture, and response to treatment.

See the national regimens in TB treatment under NTEP and the drug pharmacology in anti-tubercular drugs. For the obstructive complication, see intestinal obstruction.