Pathogenesis and outcomes of diseases

Pathogenesis and outcomes of purulent bone lesions

The pathogenesis of bone infections is vividly illustrated by the transition of acute hematogenous osteomyelitis into a chronic form. While an acute focal process may end in the patient's complete recovery, the generalized septic form (occurring predominantly in children) often ends fatally.

When the process becomes chronic, focal abscesses form within the bone marrow. The surrounding bone tissue undergoes necrosis, resorption, and sequestration—cavities containing fragments of dead bone (bone sequestra) form in the tissues. Against the background of purulent melting, the periosteum thickens and undergoes sclerosis, active periosteal bone formation occurs, leading to severe deformation of the affected bone segment.

Possible complications and outcomes:

• Pathological fractures and pseudoarthrosis formation.
• Formation of fistulous tracts through which small sequestra are discharged (the process may be accompanied by hemorrhages).
• Secondary amyloidosis resulting from prolonged purulent inflammation.
• Malignant transformation (tumor development) in the area of chronic inflammation.
• Development of sepsis.

The outcome of chronic osteomyelitis can be favorable only if adequate and radical surgical debridement of the lesion is performed.

Mechanisms of viral infections of the skin and nervous system

The varicella-zoster virus demonstrates a complex mechanism of development with the potential for prolonged persistence. The pathogen enters the respiratory epithelium, penetrates the bloodstream, and then concentrates in the skin, causing local vasculitis.

Morphologically, ballooning degeneration develops in the cells of the stratum spinosum of the epidermis. The cells die, forming itchy red vesicles that subsequently dry up into brownish crusts. After they fall off, small ulcers remain. Erosions with diapedetic hemorrhages and lymphohistiocytic infiltrates appear on the mucous membranes.

Following the primary infection, the virus enters a latent state, persisting for years in the satellite cells of the dorsal root ganglia of the spinal cord. Upon immunosuppression, it reactivates, leading to shingles (herpes zoster). The pathogen travels down the sensory nerves to the tissues. The disease manifests as radiculoneuritis, severe itching, burning, and acute pain (especially intense when the trigeminal nerve is affected). Complications in high-risk individuals include interstitial pneumonia, myelitis, and encephalitis, although the outcome of the disease is generally favorable.

Features of the pathogenesis and complications of measles

Measles is characterized by systemic involvement of the respiratory tract, skin, and lymphatic system. Microscopic examination of skin rash sites reveals hyperemia, perivascular infiltration, diapedetic hemorrhages, vacuolization of the epidermis, and the appearance of specific giant epithelial cells. In the lymph nodes, against the background of follicular hyperplasia, a pathognomonic sign of measles develops—giant multinucleated Warthin-Finkeldey cells.

Respiratory system involvement begins with serous-catarrhal pharyngitis and tracheitis. As it progresses, interstitial measles pneumonia develops. The alveoli and interalveolar septa are infiltrated by lymphocytes and macrophages, hyaline membranes are formed, and squamous metaplasia occurs in the bronchial epithelium.

Complications of measles:

• Secondary infection causes purulent-necrotic bronchitis and severe pneumonia.
• In severely weakened children, noma may develop—moist gangrene of the soft tissues of the face.
• Neurological disorders (meningitis, encephalitis).
• Gastrointestinal tract lesions (enteritis, colitis) and eye involvement (keratitis, conjunctivitis).

With proper treatment, the outcome of measles is favorable; however, in debilitated children, severe complications can lead to a fatal outcome.

Pathogenesis of pertussis and mumps

In pertussis (pertussis), the gram-negative bacterium Bordetella pertussis is transmitted via airborne droplets. The leading pathogenesis factor is the action of bacterial toxins and hemagglutinin. Hemagglutinin binds to carbohydrates on the epithelial surface and macrophage integrins, ensuring colonization of the respiratory tract and pathogen entry into cells. Bacterial toxins actively irritate nerve receptors, provoking characteristic paroxysms of spasmodic cough.

Mumps (epidemic parotitis) is caused by an RNA virus from the Paramyxoviridae family, possessing neuraminidase and hemagglutinating activity. Multiplying in the respiratory tract and T-lymphocytes, the virus exhibits a pronounced tropism for glandular tissues and the central nervous system. Macroscopically, the parotid glands enlarge bilaterally, acquiring a doughy consistency. Microscopically, the tissue is diffusely infiltrated by lymphocytes and plasma cells, interstitial edema develops, and detritus with neutrophils accumulates in the lumens of compressed ducts.

Class and exam questions

What else to study on this topic

• Pathogenesis and classification of rickets and osteomalacia.
• Morphological features and metastasis pathways of bone fibrosarcoma.
• Detailed pathomorphology of tuberculous arthritis.
• Pathogenesis of Duchenne muscular dystrophy and main causes of fatal outcomes.
• Morphological picture of testicular involvement (orchitis) in mumps.

Other topics in the section "Chapter 22. Diseases of the Musculoskeletal System"

Prepared by WhiteCoat Pro faculty in accordance with the medical school curriculum. For educational purposes only.