Typhoid Fever and Associated Infections

Leprosy: General Characteristics and Forms

The disease is characterized by a prolonged incubation period (averaging 4–6 years, but sometimes over 15 years) and an asymptomatic prodromal stage. The clinical presentation strictly depends on the patient's immune status.

Three main forms are distinguished:

1. Tuberculoid leprosy. Develops in individuals with preserved cell-mediated immunity (often associated with HLA-DR2/DR3 haplotypes). It has a benign course. Distinct hypopigmented skin macules with loss of sensation appear. Early involvement of peripheral nerves is characteristic, which can lead to lagophthalmos, hand muscle atrophy, and trophic foot ulcers. Granulomas consist of epithelioid and giant cells; caseous necrosis is absent in skin lesions, but it may develop in nerve trunks, forming a nerve abscess.
2. Lepromatous leprosy. A severe generalized variant occurring against the background of depressed cell-mediated immunity. The skin, ENT organs, eyes, nerves, and internal organs (testes, adrenals) are affected. A specific marker is Virchow cells (large foamy macrophages packed with Mycobacterium leprae resembling bundles of cigars). Massive brownish infiltrates form on the face, eyebrows and eyelashes are lost, resulting in facies leonina (leonine facies). The disease progresses rapidly, leading to mutilation (autoamputation) of the phalanges.
3. Borderline (dimorphous) leprosy. An intermediate variant that, depending on immune dynamics, can shift toward the tuberculoid type (with a predominance of epithelioid cells) or the lepromatous type (with a predominance of macrophages).

Pathomorphology of Trachoma

Trachoma is a chronic purulent follicular keratoconjunctivitis caused by Chlamydia trachomatis. The infection is transmitted by direct contact, fomites, or mechanically by flies.

Morphogenetic stages:

• The pathogen infects the conjunctival mucosa, causing purulent inflammation.
• Lymphocyte accumulations (follicles) form in the deeper tissues, and the limbal epithelium undergoes hyperplasia.
• Inflammatory infiltrates invade the cornea, accompanied by capillary ingrowth leading to the formation of a pannus.
• The end stage is tissue scarring. This not only leads to blindness but also disrupts eyelid closure, predisposing the eye to secondary bacterial infections.

Schistosomiasis: Systemic Granulomatous Inflammation

Schistosomiasis is a severe helminthiasis in which larvae (cercariae) penetrate the skin during swimming in contaminated water. After entering the bloodstream, they settle in the portal and pelvic venous systems. Females lay eggs, and their dissemination triggers generalized granulomatous inflammation.

Organ involvement features:

• Liver: Eggs release hepatotoxic substances. Granulomas with eosinophils form, and fibrogenic cytokine production is stimulated. Portal fibrosis develops, progressing to cirrhosis with severe portal hypertension (ascites, esophageal varices).
• Urinary bladder: Confluent ulcerating plaques develop, accompanied by productive inflammation and hematuria. This condition is considered a precancerous state of the bladder.
• Lungs: Migration of eggs through vascular anastomoses causes granulomatous arteritis, leading to pulmonary hypertension and cor pulmonale.

Filariasis and Highly Hazardous Infections

Lymphatic filariasis is transmitted via mosquito bites. Adult helminths localize in lymphatic vessels, causing reactive inflammation and sclerosis. Blockage of lymph drainage leads to severe lymphedema and elephantiasis of the limbs or genitalia. Microgranulomas may form in the lungs against a background of high IgE concentration.

Highly hazardous infections comprise highly contagious diseases with a severe clinical course:

• Anthroponoses: epidemic typhus and relapsing fever.
• Anthropozoonoses: anthrax (an occupational disease of abattoir and agricultural workers), tularemia, brucellosis.
• Quarantinable diseases: plague, cholera, smallpox, yellow fever.