Leprosy: general characteristics and forms
The disease is characterized by a long incubation period (on average 4–6 years, but sometimes more than 15 years) and an asymptomatic prodromal stage. The clinical presentation strictly depends on the patient's immune status.
There are three main forms:
- Tuberculoid leprosy. Develops in individuals with preserved resistance (often with HLA-DR2/DR3 haplotypes). It is distinguished by a benign course. Distinct macules with loss of sensitivity appear on the skin. Early involvement of peripheral nerves is characteristic, which can lead to lagophthalmos, hand muscle atrophy, and trophic ulcers of the feet. Granulomas consist of epithelioid and giant cells; caseous necrosis is absent in the skin, but it can develop in nerve trunks, forming a nerve abscess.
- Lepromatous leprosy. A severe generalized variant against the background of reduced immunity. The skin, ENT organs, eyes, nerves, and internal organs (testes, adrenal glands) are affected. A specific marker is Virchow lepra cells (large foamy macrophages filled with mycobacteria in the form of "cigarette packs"). Massive brown infiltrates form on the face, eyebrows and eyelashes fall out, forming facies leonina ("lion face"). The disease progresses rapidly, leading to mutilation (auto-amputation) of the phalanges.
- Undifferentiated leprosy. An intermediate variant that, depending on immune dynamics, can transform into the tuberculoid (with a predominance of epithelioid cells) or lepromatous (with a predominance of macrophages) type.
Pathomorphology of trachoma
Trachoma is a chronic purulent follicular keratoconjunctivitis caused by Chlamydia trachomatis. The infection is transmitted by contact, including via household items, or mechanically carried by flies.
Stages of morphogenesis:
- The pathogen gets onto the conjunctiva of the eyelids, causing purulent inflammation.
- Clusters of lymphocytes—follicles—form in the deep tissues, and the limbal epithelium undergoes hyperplasia.
- The inflammatory infiltrate penetrates the cornea, accompanied by the ingrowth of capillaries, which leads to the formation of a pannus.
- The outcome is tissue scarring. This not only leads to blindness but also impairs eyelid closure, which contributes to the addition of secondary bacterial flora.
Schistosomiasis: systemic granulomatous inflammation
Schistosomiasis is a severe helminthiasis in which larvae (cercariae) penetrate through the skin during swimming in water bodies. Having passed through the bloodstream, they settle in the portal and pelvic venous systems. Females lay eggs, the dissemination of which causes generalized granulomatous inflammation.
Features of organ involvement:
- Liver: The eggs secrete hepatotoxic substances. Granulomas with eosinophils are formed, and the production of fibrogenic cytokines is stimulated. Portal fibrosis develops, transitioning into cirrhosis with severe portal hypertension (ascites, esophageal varices).
- Urinary bladder: Confluent ulcerating plaques are formed. Productive inflammation with hematuria develops. This condition is considered a precancerous state of the urinary bladder.
- Lungs: The migration of eggs through anastomoses causes granulomatous arteritis, which leads to pulmonary hypertension and cor pulmonale.
Filariasis and particularly dangerous infections
Lymphatic filariasis is transmitted via mosquito bites. Adult helminths localize in the lymphatic vessels, causing reactive inflammation and sclerosis. The blockage of lymph outflow leads to severe lymphedema and elephantiasis of the limbs or genitalia. Microgranulomas may form in the lungs against the background of a high IgE concentration.
The group of particularly dangerous infections includes highly contagious diseases with a severe clinical course:
- Anthroponoses: epidemic and relapsing typhus.
- Anthroponoses (zoonoses): anthrax (an occupational disease of slaughterhouse and agricultural workers), tularemia, brucellosis.
- Quarantine infections: plague, cholera, smallpox, yellow fever.
Briefly: answers to topical questions
What stages of intestinal morphogenesis are distinguished in typhoid fever?
The morphogenesis of intestinal changes in typhoid fever includes five sequential stages distributed over the weeks of the disease.
- Stage of medullary swelling — develops in the first week, affecting Peyer's patches and solitary follicles.
- Stage of necrosis — occurs in the second week of the disease.
- Stage of ulceration — in the third week, necrotic masses are rejected with the formation of "dirty" ulcers.
- Stage of clean ulcers — in the fourth week, the ulcers clean up, and their base can become the serous membrane.
- Stage of ulcer healing — in the fifth and sixth weeks, scars form and lymphoid tissue is restored.
What cells make up the specific typhoid granuloma?
The specific typhoid granuloma consists of proliferating monocytes and reticular cells. Such cell clusters form against the background of persistent bacteremia in various internal organs. In particular, granulomas are found in the enlarged spleen (against the background of red pulp hyperplasia), lymph nodes, bone marrow, lungs, gallbladder, and kidneys of the patient.
Which intestinal complications are most characteristic of typhoid fever?
The most characteristic specific intestinal complications of typhoid fever are intestinal perforation and intestinal hemorrhage.
- Intestinal perforation — perforation of a typhoid ulcer (more often in the stage of clean ulcers), leading to the development of peritonitis.
- Intestinal hemorrhage — massive blood loss resulting from arrosion of blood vessels in the base of forming ulcers.
These complications are among the main causes of mortality in this disease.
What is Zenker's necrosis and in which muscles does it develop in typhoid fever?
Zenker's (waxy) necrosis is a variant of coagulative (dry) necrosis of skeletal muscles that occurs in severe infectious intoxications. In typhoid fever, this pathological process predominantly develops in the following muscles:
- Abdominal wall muscles
- Adductor muscles of the thigh
This type of necrosis is a characteristic morphological sign of a severe course of the infectious process and is accompanied by systemic inflammatory response syndrome and an increase in serum cytolysis markers.
What types of schistosomiasis are distinguished depending on the specific causative agent?
Depending on the specific species of the causative agent (blood fluke), three main types of schistosomiasis are distinguished:
- Urogenital schistosomiasis — caused by the urogenital schistosome (Schistosoma haematobium).
- Intestinal schistosomiasis — caused by Manson's schistosome (Schistosoma mansoni).
- Japanese schistosomiasis — caused by the Japanese schistosome (Schistosoma japonicum).
These diseases belong to the group of zoonoses and are natural focal infections.
What zoonotic particularly dangerous infections exist and who is in the risk group for contracting them?
Zoonotic particularly dangerous infections include anthrax, tularemia, and brucellosis; foot-and-mouth disease and glanders are sometimes included. The cited sources indicate the following risk groups:
- Anthrax — agricultural workers, slaughterhouse workers, wool-beaters, and brush-makers.
- Tularemia — specialists engaged in rodent trapping; workers processing their skins and meat; medical personnel of infectious disease departments and laboratories.
- Glanders — individuals in contact with sick animals, including grooms and veterinarians.
To remember the forms of leprosy: "TLN" — Tuberculoid (Tough immunity), Lepromatous (Losing immunity easily, "Leonine facies"), Undifferentiated (Unclear immunity).
What else to study on this topic
- Mechanisms of granuloma formation in helminthiasis
- Specific complications of urinary schistosomiasis
- Ophthalmological manifestations of lepromatous leprosy
- Differential diagnosis of types of granulomatous inflammation
- Classification and pathogenesis of quarantine infections
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