This section is from the book "A Manual Of Pathology", by Guthrie McConnell. Also available from Amazon: A Manual Of Pathology.
Typhoid Fever is an acute infectious fever caused by the Bacillus typhosus, and its characteristic lesion is ulceration of the lymphoid tissue of the small intestine, particularly the Peyer's patches. The upper part of the colon is also generally involved.
The lesions in the intestine correspond closely to the clinical course of the disease and indicate by their appearance the duration of the infection. The organisms gain entrance into the individual through the mouth in food, or more commonly in the water. They pass to the small intestine and there give rise to the various lesions. At first the mucous membrane becomes hypere-mic and swollen, the solitary follicles and the Peyer's patches become larger, through hyperplasia of the lymphoid tissue, their surfaces irregular and hyperemic. In the course of a few days they fade and become quite pale or grayish-white as necrosis begins. The Peyer's patch is elevated and sharply defined from the neighboring mucosa. Microscopically the intestinal wall presents a high-grade round-cell infiltration and an increase in epithelioid cells. During the second week there is a necrosis of the hyperplastic lymphoid nodes. The tissue is cast off in shreds. The greater part of the follicle may be sloughed off, leaving a long, irregular ulcer with a smooth floor lying parallel to the long axis of the intestine. The ulcers usually appear toward the end of the second week of the disease. They extend to varying depths, in some cases involving the lymphoid tissue alone, but at times the necrosis passes on to the submucosa and even to the serous covering. The ulcers rarely extend beyond the limit of the lymphoid tissue. Perforation is common. Ulceration is most marked in the small intestine near the ileocecal valve.
Fig. 153. - Ileum; Typhoid Fever (Early Stage) (Nicholls).
Peyer's patches and solitary follicles greatly swollen; superficial ulceration.
Fig. 154.-Typhoid Ulcer after Detachment of Slough. X 50 (Dürck).
The margins of the defect end abruptly; in the floor of the ulcer, which reaches into the submucosa, are seen a few necrotic portions of tissue with extensive infiltration of leukocytes. 1, Mucosa; 2, muscularis mucosae; 3, submucosa with overfilled blood-vessels; 4, muscularis.
By the end of the third week the necrosis and ulceration cease and reparative processes begin. The hyperplastic lymphoid tissue resumes its normal condition by disintegration and absorption of the newly formed cells. The ulcerated surfaces heal by granulation and cicatrization and by extensions from the surrounding mucous membrane.
The increase in the cellular elements in the lymph-nodes is the result of the proliferation of the endothelial cells of the lymphatic spaces, blood-capillaries, and reticulum of the lymphoid tissue, and a hyperplasia of the lymphoid cells. It is brought about by the action of a mild toxin. These cells give rise to necrosis in the lymph-nodes, liver, and spleen by thrombosis which interferes with the blood-supply. They may be found in the lung.
The complications of typhoid fever are several, but the most serious are hemorrhage and perforation. Small hemorrhages may be the result of oozing from the ulcerated surfaces. Its presence causes the stools to be dark brown in color. Severe hemorrhage follows the destruction of the walls of some larger vessel. The blood may remain in the intestine long enough to undergo changes and give rise to the "tarry stools." Occasionally the loss may be so sudden and large that the blood is discharged when still bright in color. Perforation follows extensive ulceration, and may occur by the end of the second week, but usually later during the third. It is more probably due to necrosis of the serosa than to an increase in internal pressure. The intestinal wall, however, may have become so thin that solid substances may lacerate it and escape into the peritoneal cavity. If the process has been comparatively slow, adhesions may have formed, so as to prevent a general infection. If this has not happened, general purulent peritonitis, nearly always fatal, will be set up.
The mesenteric lymph-nodes become enlarged, soft, and hyperemic, and show a cellular proliferation similar to that in the intestinal lymphoid tissue. As the processes within the intestine increase in severity these nodes show fatty metamorphosis, softening, and even necrosis. If the patient recovers connective tissue replaces the necrotic portions. The spleen becomes much larger, soft and flabby, and hyperemic. Sometimes it will be the seat of infarctions and abscesses. The muscles, particularly the recti, show Zenker's degeneration, a hyaline change. Minute hemorrhages may also be present in the muscles. The heart muscle undergoes a certain amount of cloudy swelling and at times is the seat of acute myocarditis. Acute endocarditis occasionally occurs, but is not as common as in other infectious diseases. There is no leukocytosis present unless pneumonic inflammations have arisen; acute bronchopneumonia and croupous pneumonia are quite common complications. The liver, in addition to parenchymatous changes, may show minute areas of focal necrosis. The kidneys are quite commonly the seat of acute parenchymatous nephritis and areas of necrosis are also frequently observed. Hemorrhagic areas may be found.