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Septicopyemia and Syphilis

Sepsis, Septicopyemia, Endocarditis septica, Syphilis

For medical students2 min readUpdated 2026-10-10

Septicopyemia is a form of generalized infection characterized by the metastatic spread of pus and the formation of abscesses in various organs. Bacterial septic endocarditis stands out as a distinct pathology affecting the heart valve apparatus (including against the background of prior syphilis or rheumatic fever).

PathogensStaphylococci, streptococci, Pseudomonas aeruginosa, and Candida fungi.

Feature of LesionsCapsule formation around metastatic septic abscesses is delayed for a very long time.

Cardiac InvolvementAcute septic polypous-ulcerative endocarditis develops with purulent overlay.

DiagnosticsMicroorganisms are isolated from blood cultures in only one-third of cases.

Septicopyemia: Pathogenesis and Morphology

Septicopyemia proceeds as a unique allergic reaction, less turbulent than classic septicemia. The main sign is the presence of a purulent septic focus at the portal of entry, accompanied by purulent thrombophlebitis, lymphangitis, and lymphadenitis. Generalization of the infection occurs via the metastatic spread of pus.

Main Pathomorphological Manifestations:

Purulent metastases (embolic abscesses): Embolic purulent nephritis occurs in the kidneys, osteomyelitis in the bone marrow, and suppuration of infarcts with pleural empyema in the lungs. A characteristic feature is the prolonged absence of a capsule around these abscesses.
Heart: Acute septic polypous-ulcerative endocarditis develops. Unlike bacterial endocarditis, purulent overlays are present on the valves.
Immune and Hematopoietic Systems: Splenomegaly develops (spleen weight can reach 1500 g) — the so-called "septic spleen" with a tense capsule and abundant pulp scraping. Hyperplasia and myeloid metaplasia are observed in lymph nodes and bone marrow.
Vessels and Organs: Systemic vasculitis with hemorrhagic syndrome is observed, as well as pronounced fatty change in 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 heart valve cusps. The disease occurs against the background of a pronounced immune response disorder.

Classification of Forms:

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

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: Necrotic foci rapidly ulcerate and become covered with massive polypoid thrombotic overlays. An important detail: lymphocytes, histiocytes, and macrophages are present in the infiltrate, but neutrophils are absent. Thrombotic masses crumble easily, leading to thromboembolic syndrome.

General Changes and Syndromes in Endocarditis

The pathogenesis is based on the circulation of circulating immune complexes (CIC), 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 (skin petechiae) and Lukin–Liebman spots (necrosis in mucous membranes).
Kidneys: Immune complex-mediated diffuse glomerulonephritis occurs, often combined with infarcts.
Skin and Joints: Osler nodes on the palms (result of microembolism and sclerosis), clubbing of the fingers ("drumstick fingers"), and arthritis.

Purulent-Resorptive Fever and Pathomorphosis

Purulent-resorptive fever (I.V. Davydovsky's term) 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, and surgical 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. Upon healing of the valve foci, management shifts to addressing acquired heart defects and chronic glomerulonephritis.

Mnemonic

Tetrad in septic endocarditis: CVPE (Valvles — endocarditis, Vasculitis, Kidneys/spleen, Emboli).

Frequently asked questions

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

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

Primary period — characterized by the formation of a primary lesion (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 syphilitic rashes (syphilids) on the skin and mucous membranes.
Tertiary period (visceral, gummatous) — characterized by the development of granulomatous inflammation (gummas and diffuse gummatous infiltration) affecting internal organs, blood vessels, and the nervous system.

What does a primary syphilitic lesion (hard chancre) look like macroscopically?

Macroscopically, a primary syphilitic lesion (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 with scanty purulent exudate at the base. Characteristic macroscopic features of the formed ulcer are a smooth base and dense edges with a cartilaginous consistency.

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

Microscopic examination of the inflammatory infiltrate of a hard chancre reveals lymphocytes and plasma cells, along with a small number of neutrophils and epithelioid cells. The infiltrate is located at the base and edges of the ulcer, predominantly around small blood vessels. Many Treponema pallidum spirochetes are found between the cells.

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

In the secondary period of syphilis, syphilids appear on the skin and mucous membranes sequentially as roseolae, papules, and pustules. Pustules are filled with spirochetes; when they ulcerate, spirochetes are abundantly released into 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 adhesive coagulation (gummatous) necrosis with destroyed elastic fibers.
Cellular infiltrate — granulation tissue around the necrosis containing lymphocytes, macrophages, epithelioid cells, Langhans giant cells, and predominantly plasma cells. Small blood vessels showing signs of productive endovasculitis are also found here.
Periphery — a dense fibrous capsule with clear boundaries formed due to intensive connective tissue proliferation.

How does the aortic intima change macroscopically in syphilitic mesaortitis?

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

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

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

Interstitial keratitis — small infiltrates in the cornea and retina.
Hutchinson teeth — deformation of the upper central incisors due to hypoplasia of the chewing surface (crown is wider at the neck, with a semilunar notch on the cutting edge).
Deafness — caused by damage to the labyrinth and atrophy of the vestibulocochlear nerve (cranial nerve VIII) 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 junction zones between bone and cartilage (in the femur, sternum, and ribs). As a result of these processes, particularly when the tibias are affected, excessive bone formation occurs on the anterior surfaces of the lower leg, leading to the formation of a characteristic deformity — "saber shins".

Go deeper

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