= Solution
\b[The classical contrast is between ulceration centred on intestinal lymphoid tissue in enteric fever and granulomatous, often circumferential ulceration in intestinal <tuberculosis>.] The historical expression <continued fever> covered more than one illness. The characteristic bowel lesions meant here point especially to <typhoid fever>; they should not be attributed indiscriminately to <typhus> or every prolonged <fever>.
In <typhoid fever>, <Peyer's patches> and solitary lymphoid follicles, particularly in the terminal <ileum>, enlarge and become infiltrated. Their breakdown and <necrosis> lead to sloughing and ulceration. The larger ulcers characteristically follow the long axis of the <intestine>, reflecting the shape of the affected aggregated lymphoid patch on the side opposite the <mesentery>. Depending on their stage, one may see swollen patches, necrotic sloughs, open ulcers or healing surfaces. Depth varies; erosion into a <blood vessel> can cause <haemorrhage>, while full-thickness destruction can cause <intestinal perforation> and <peritonitis>.
Microscopically, the important cellular component includes swollen <macrophages> with ingested organisms and cellular debris; this is not simply a dense collection of <neutrophils> forming an ordinary <abscess>. The surrounding mucosal architecture may become severely disturbed. These current cellular descriptions refine the gross lesion recognized before the causative organism was identified.<Typhoid Fever in StatPearls>[Histopathology, mononuclear phagocytes, typhoid cells and lymphoid ulceration]{ref}<Infective disorders of the gastrointestinal tract>[Salmonella, macrophage-rich lymphoid infiltration and deep ulcers]{ref}
In historical <phthisis>, bowel disease frequently meant <intestinal tuberculosis> associated with <pulmonary tuberculosis>. Lesions commonly involve the terminal <ileum> and ileocaecal region, although other sites occur. Nodules in mucosal or submucosal lymphoid <tissue> undergo <caseous necrosis>, coalesce and break through the mucosa. The ulcerated surface tends to spread transversely and may encircle the bowel. The edges can be irregular and undermined, with additional <tuberculous granulomas> in the wall, serosal surface or draining <lymph nodes>. Progressive <fibrosis> may narrow the lumen and produce a <stricture>; thickened masses as well as ulcers can occur.<Abdominal tuberculosis of the gastrointestinal tract: Revisited>[Intestinal tuberculosis, morphology, ileocaecal involvement, caseating granulomas and obstructive complications]{ref}
A section from a tuberculous ulcer may show central <caseous necrosis> bordered by <epithelioid macrophages>, <giant cells> and <lymphocytes>. A section from an enteric-fever ulcer instead emphasizes destruction of lymphoid patches with macrophage-rich infiltration. A practical anatomical examination records site, orientation, depth, edges, intervening mucosa, serosal nodules and draining <lymph nodes>, rather than judging one detached fragment in isolation.
\b[Longitudinal lymphoid-patch ulcers favour the classical enteric-fever pattern; transverse, caseating and often stenosing lesions favour intestinal <tuberculosis>.] These are useful patterns rather than absolute rules. Modern <microbiological culture>, organism-specific molecular tests and appropriately sampled <histology> can establish the cause when gross appearances overlap.
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