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Pathological Anatomy · Chapter 16. Infectious and Parasitic Diseases

Syphilis

Sepsis, Septicopyemia, Endocarditis septica

Septicopyemia is a form of generalized infection whose key distinguishing feature is the metastasizing of pus and the formation of abscesses in organs. Bacterial septic endocarditis stands out as an independent pathology affecting the heart valve apparatus (including against the background of prior syphilis or rheumatism).

PathogensStaphylococci, streptococci, Pseudomonas aeruginosa, Candida fungi.
Feature of the lesionsA capsule does not form around metastatic septic abscesses for a very long time.
Heart involvementAcute septic polypous-ulcerative endocarditis develops with purulent deposits.
DiagnosticsMicroorganisms are cultured from the blood in only a third of cases.
6 min readFor medical studentsUpdated Sep 25, 2026
Material prepared by WhiteCoat Pro editorial team based on platform study guidesReviewed by medical editor: Aulov A. A., general practitioner · 09/24/2026

Septicopyemia: pathogenesis and morphology

Septicopyemia proceeds as a peculiar allergic reaction, less turbulent than classical septicemia. The main sign is the presence of a purulent septic focus at the port of entry, which is accompanied by purulent thrombophlebitis, lymphangitis, and lymphadenitis. Generalization of the infection occurs via the metastasis of pus.

Main pathomorphological manifestations:

  • Purulent metastases (embolic abscesses): Embolic purulent nephritis occurs in the kidneys, osteomyelitis in the bone marrow, and infarction suppuration and pleural empyema in the lungs. A characteristic feature is the prolonged absence of a capsule around such abscesses.
  • Heart: Acute septic polypous-ulcerative endocarditis develops. Unlike bacterial endocarditis, purulent deposits are present specifically on the valves here.
  • Immune system and hematopoiesis: Splenomegaly develops (spleen weight can reach 1,500 g) — the so-called "septic spleen" with a tense capsule and abundant pulp scraping. Hyperplasia and myeloid metaplasia are observed in the lymph nodes and bone marrow.
  • Vessels and organs: Systemic vasculitis with hemorrhagic syndrome is observed, as well as pronounced fatty degeneration of parenchymal organs due to intoxication and hypoxia.

Septic (bacterial) endocarditis

This is an independent form of sepsis where the primary focus is localized directly on the cusps of the heart valves. The disease occurs against the background of a pronounced impairment of the immune response.

Classification of forms:

  1. Primary endocarditis (Chernogubov's disease): Occurs in 25% of cases. It affects initially intact heart valves.
  2. Secondary endocarditis: Develops on previously altered valves (about 70% against the background of rheumatism, 5% due to syphilis, atherosclerosis, brucellosis, or congenital malformations).

The course of the disease is most often subacute (up to 3 months) or chronic/protracted (sepsis lenta, lasting months and years). The mitral (40%) and aortic (30%) valves are most frequently affected.

Local changes on the valves: Necrosis foci rapidly ulcerate and become covered with massive polypoid thrombotic deposits. An important detail: the infiltrate contains lymphocytes, histiocytes, and macrophages, but neutrophils are absent. Thrombotic masses easily crumble, which leads to thromboembolic syndrome.

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General changes and syndromes in endocarditis

The pathogenesis is based on the circulation of immune complexes (ICCs), causing hypersensitivity reactions. A characteristic tetrad is formed: valvular endocarditis, vasculitis, kidney and spleen involvement, and thromboembolic complications.

Systemic Manifestations:

  • Vessels: Fibrinoid necrosis of the walls leads to microaneurysms. Vasculitis develops, manifesting as Janeway lesions (petechiae in the skin) and Roth spots (necroses in the mucous membranes).
  • Kidneys: Immune-complex diffuse glomerulonephritis occurs, often combined with infarcts.
  • Skin and joints: Osler nodes on the palms (the result of microembolism and sclerosis), thickening of the nail phalanges ("clubbing"), arthritis.

Purulent-resorptive fever and pathomorphosis

Purulent-resorptive fever (a term by I.V. Davydovsky) is a condition that arises during prolonged suppuration (e.g., in comminuted fractures of large bones). Pus and toxins are constantly absorbed into the blood, causing exhaustion and secondary amyloidosis. Unlike sepsis, there is no specific hyperergy here, and removal of the purulent focus dramatically improves the prognosis.

Therapeutic pathomorphosis: With the advent of antibiotics, the clinical picture has changed. In septicopyemia, there are fewer purulent metastases, and vasculitis has acquired a chronic productive character. When healing focal lesions on the valves, treating acquired heart defects and chronic glomerulonephritis comes to the foreground.

Briefly: answers to topical questions

What periods are distinguished in the pathomorphological course of acquired syphilis?

Three successive periods are distinguished in the pathomorphological course of acquired syphilis.

  • Primary period — characterized by the formation of the primary affect (hard chancre) and the development of the primary infectious complex.
  • Secondary period — caused by the hematogenous spread of the pathogen with the development of vasculitis and the appearance of a syphilitic rash (syphilids) on the skin and mucous membranes.
  • Tertiary period (visceral, gummatous) — characterized by the development of granulomatous inflammation (gummas and diffuse gummatous infiltration) with involvement of internal organs, blood vessels, and the nervous system.

What does the primary syphilitic affect (hard chancre) look like macroscopically?

Macroscopically, the primary syphilitic affect (hard chancre) initially appears as a reddish thickening of the mucous membrane measuring 3–5 mm. After 1–2 weeks, this thickening turns into a superficial ulcer, at the bottom of which is scanty pus-like exudate. Characteristic macroscopic signs of the formed ulcer are a smooth bottom and dense edges with a cartilaginous consistency.

Which cells predominate in the inflammatory infiltrate of the hard chancre upon microscopic examination?

Lymphocytes and plasma cells are detected in the inflammatory infiltrate of the hard chancre; a small number of neutrophils and epithelioid cells are also present. The infiltrate is localized at the bottom and edges of the ulcer, predominantly around small blood vessels. There are many pale treponemes between the cells.

What types of syphilids are most characteristic of skin and mucosal involvement in the secondary period of syphilis?

In the secondary period of syphilis, syphilids appear on the skin and mucous membranes, sequentially taking the form of roseolae, papules, and pustules. Pustules are filled with pale spirochetes; upon their ulceration, spirochetes abundantly enter the external environment.

What zones does a syphilitic gumma consist of upon microscopic examination?

Upon microscopic examination, a syphilitic gumma consists of three zones.

  • Center — a zone of coagulative (gummatous) necrosis of a sticky consistency with destroyed elastic fibers.
  • Cellular infiltrate — granulation tissue around the necrosis, containing lymphocytes, macrophages, epithelioid cells, Pirogov-Langhans giant cells, and predominantly plasma cells. Small blood vessels with phenomena of productive endovasculitis are also detected here.
  • Periphery — a dense fibrous capsule with clear boundaries, formed due to the intensive development of connective tissue.

How does the intima of the aorta change macroscopically in syphilitic mesaortitis?

Macroscopically in syphilitic mesaortitis, the inner lining of the aorta (intima) undergoes sclerosis and acquires the specific appearance of "shagreen skin". It becomes uneven, wrinkled, and nodular. These changes occur as a result of the formation of cicatricial retractions in the middle layer of the aorta, where destruction of the elastic framework and uneven sclerosis of the wall take place following the proliferation and maturation of granulation tissue.

What pathomorphological signs make up the classic Hutchinson triad in late congenital syphilis?

The classic Hutchinson triad in late congenital syphilis consists of three pathomorphological signs.

  • Parenchymatous keratitis — small infiltrates in the cornea and retina.
  • Hutchinson teeth — deformation of the upper central incisors due to hypoplasia of the masticatory surface (the crown is wider at the neck, with a crescent-shaped notch on the cutting edge).
  • Deafness — caused by damage to the labyrinth and atrophy of the VIII pair of cranial nerves against the background of syphilitic changes in the cerebral vessels.

What is "white pneumonia" and for which form of syphilis is it characteristic?

"White pneumonia" is interstitial pneumonia accompanied by the formation of whitish layers of fibrous tissue in the lungs. This pathomorphological sign (a term proposed by R. Virchow) is characteristic of early congenital syphilis, which manifests in newborns and infants during the first two months of life.

What specific changes develop in the zones of endochondral ossification in early congenital syphilis?

In early congenital syphilis, syphilitic osteochondritis and periostitis develop in the areas where bones meet cartilage (in the femurs, sternum, and ribs). As a result of these processes, particularly when the tibias are affected, excessive osteosynthesis occurs on the anterior surfaces of the lower leg, leading to the formation of a characteristic deformity known as "saber shins".

How to memorize

The tetrad in infective endocarditis: V-K-E-S (Valvular endocarditis, Vasculitis, Kidneys/spleen, Embolism).

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What else to study on this topic

  • Mechanisms of circulating immune complex (CIC) formation in bacterial endocarditis
  • Differential diagnosis of septicemia and pyosepticemia
  • Morphological differences between rheumatic and bacterial endocarditis
  • Thanatogenesis and complications of purulent-resorptive fever
  • Secondary amyloidosis in chronic purulent processes

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