Fig. 15.1 Hyperplastic lymphoid tissue of a Peyer's patch in the terminal ileum showing ulceration of the overlying mucosa (arrow) in a patient with typhoid fever. H&E x25. (from Isaacson and Hale 1995).

Fig. 15.2 Terminal ileum and cecum in typhoid fever. The Peyer's patches are enlarged, elevated, hemorrhagic and necrotic. The solitary lymphoid follicles of the cecum (on left) are enlarged and have a central hemorrhagic dimple. AFIP 62-4724-1. (Courtesy of Drs. Jerome Smith and Daniel Connor; from Connor DH, Chandler FW, et al (eds): Pathology of Infectious Diseases, Appleton & Lange, 1997).

Fig. 15.3 (A) Terminal ileum in early fastigium phase of typhoid fever. The formalin-fixed Peyer's patches are raised, convoluted, and have a shaggy necrotic base. AFIP 62-4724-3. (B) Formalin-fixed ileum during fastigium. The mucosa is bile-stained and the Peyer's patches are hemorrhagic. Massive intestinal hemorrhage is the most frequent and most feared complication of typhoid fever, developing in 5-10% of untreated patients, usually during the second or third week of illness (fastigium and early stage of lysis). (Courtesy of Drs. Jerome Smith and Daniel Connor; from Connor DH, Chandler FW, et al (eds): Pathology of Infectious Diseases, Appleton & Lange, 1997).


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After the initial bacteremia, the bacilli in the liver pass into the bile and reach the gallbladder, where they multiply rapidly. They then enter the intestinal tract for the second time, where further multiplication is restricted to the lymphoid tissue in the ileum and proximal colon. This second invasion coincides with the onset of clinical manifestations of the disease. There is an incubation period of 10 to 15 days before characteristic lesions of typhoid fever develop in the intestinal lymphoid tissues.

The Peyer's patches become swollen and hyperplastic by the end of the first week and the mesenteric lymph nodes are enlarged and soft. By the end of the second week the intestinal mucosa begins to ulcerate. The maximum inflammatory changes occur about the tenth day, after which they may resolve or, more commonly, progress to necrosis of the hyperplastic lymphoid tissue (Figs. 15.1 and 15.2), which then sloughs, leaving bile-tinged or hemorrhagic ragged ulcers of varying extent and depth (Fig. 15.3). The shape and position of the ulcers usually coincide with the Peyer's patches, being oval in the long axis of the intestinal lumen on the antimesenteric margin of the distal ileum.

Near the ileocecal valve, where perforation is most frequent, the ulcers are deeper than elsewhere in the ileum. Ulceration is in part caused by necrosis and bacterial damage and is partly due to microthrombosis of small blood vessels. The mesenteric lymph nodes continue to enlarge and become focally necrotic and hemorrhagic.


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