Cholera

Severe forms of plague

The pathoanatomical picture of the severe (likely pneumonic) form of plague is characterized by a lightning-fast course (2–3 days) and 100% mortality. The main changes revealed at autopsy are:

• Lungs: condensed, on cross-section show a mottled gray-red appearance, containing foci of necrosis and suppuration.
• Respiratory tract: serous-hemorrhagic inflammation in the trachea and bronchi, fibrinous deposits on the pleura.
• Internal organs: parenchymal fatty degeneration and reactive stromal inflammation.

The primary septic form progresses even more rapidly — death occurs in 24–36 hours. Due to this speed, specific morphological changes do not have time to form, and the diagnosis is confirmed solely by bacteriology.

Smallpox (Variola vera)

Although the disease has been officially eradicated, the cessation of universal vaccination leaves the population vulnerable to a potential pandemic. The causative agent is a large DNA virus transmitted via airborne and contact routes.

Pathogenesis and rash morphology: The infection goes through stages of minor and major viremia. The main impact is on the skin, sensitized at early stages. The rash evolves sequentially:

1. Papule: epidermis thickens due to proliferation of the Malpighian layer.
2. Pustule (multilocular vesicle): ballooning and reticular degeneration of the epidermis occur. The cavity fills with serous-purulent exudate, with central necrosis forming (umbilication).
3. Crust: by days 12–14, the exudate is absorbed, and the pustule dries out.

The most dangerous form is "black smallpox" (pustular-hemorrhagic). It involves massive diapedetic hemorrhages in the dermis. The exudate becomes bloody, and hemoglobin transforms into iron sulfide, turning the pustules blackish-gray. Mortality in this form is 100%.

Yellow fever (Febris flava)

A zoonotic vector-borne quarantine infection endemic to Latin America and Africa. Transmitted vector-bornely (via mosquito bites). The virus primarily multiplies in lymph nodes, then causes massive viremia.

Target organs and changes:

• Liver: multiple focal parenchymal necroses leading to hepatic jaundice (staining of the sclera, skin, and internal organs).
• Kidneys: development of icteric nephrosis and fatty degeneration, leading to oliguria and anuria in severe cases.
• Vessels: generalized vasculitis provokes multiple hemorrhages in the stomach, intestines, brain, and lungs.
• Heart: interstitial myocarditis and fatty degeneration.

Death most often occurs on days 7–8 from uremic coma against the background of toxic encephalopathy.

Autopsy specifics in quarantine infections

Autopsy of those who died from particularly dangerous infections requires the strictest safety measures to prevent the spread of the pathogen and staff infection.

• Prosector protection: a anti-plague suit (or two closed gowns with sleeve protectors, cap, mask, goggles, and two pairs of gloves) is mandatory. After work, the gear is incinerated in a closed room.
• Room: sewage in the dissection room must be completely shut off. Fluids are collected in special containers.
• Autopsy technique: organs are examined in situ (without being removed from body cavities).
• Body handling: organs are covered with quicklime and doused with lysol. The body is wrapped in sheets soaked in disinfectant. Burial is carried out at a depth of at least 3 meters, sprinkling layers of earth with quicklime.

Sepsis and SIRS syndrome

Sepsis is fundamentally different from other infections: it has no specific causative agent, is not contagious, and leaves no post-infection immunity. It is a macrobiological problem rooted in hyperergy — a distorted, hyper-intense response of the body to infection.

According to the ACCP/SCCM classification (1991), pathogenesis is based on SIRS syndrome (systemic inflammatory response syndrome). Its diagnosis requires temperature deviations (>38°C or <36°C), heart rate (>90/min), respiratory rate (>20/min), or leukocyte count (<4,000 or >12,000).

Morphologically, sepsis manifests as microcirculation disorders (stasis, sludge syndrome), diapedetic hemorrhages, dystrophy, and multiple small necroses in internal organs. The main cause of death in sepsis is multiple organ dysfunction syndrome (MODS).

Briefly: answers to topical questions

Class and exam questions

What else to study on this topic

• Pathogenesis and stages of septic shock development
• Specific complications of smallpox (meningoencephalitis, phlegmon, osteomyelitis)
• Morphological differences between gram-negative and gram-positive sepsis
• Mechanisms of multiple organ dysfunction syndrome (MODS) development

Other topics in "Chapter 16. Infectious and Parasitic Diseases"

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