International Surveillance and Epidemiological Significance
According to regulations in effect since 1971, highly dangerous infections are strictly regulated at the global level. They are divided into quarantine/convention diseases (plague, cholera, yellow fever, and the eradicated smallpox) and infections requiring international monitoring, such as epidemic typhus, relapsing fever, poliomyelitis, and malaria.
In the modern world, the importation of such infections occurs rapidly. Historically, smallpox outbreaks occurred in Moscow (1960, imported from India) and cholera in the south of the region (1971). Today, cholera remains a significant global health threat: sporadic cases are annually recorded in regions with major water arteries, especially in river basin areas.
Cholera: Pathogen and Mechanisms of Development
Cholera is a strict anthroponosis. The source of infection is always a human (patient or carrier). The disease is transmitted via the fecal-oral route, most frequently through water.
Pathogen Characteristics The seventh cholera pandemic is caused by the El Tor vibrio. Unlike the classic Asian vibrio, it survives longer in water, produces an exotoxin (choleragen), and more frequently leads to asymptomatic vibrio carriage. The bacterium is comma-shaped, motile, prefers an alkaline environment (pH 7.6–8.2) and human body temperature, but is extremely vulnerable to gastric hydrochloric acid.
Pathogenesis of Diarrheal Syndrome Having passed the acidic environment of the stomach, vibrios actively multiply in the small intestine. The pathogen does not enter the bloodstream (vibrionemia is absent), and all severe effects are associated with the action of the toxin.
- Choleragen activates adenylate cyclase in enterocytes, leading to a sharp increase in cAMP and a massive release of isotonic fluid.
- Concurrently, the synthesis of cGMP is suppressed, which blocks the sodium pump and makes the reabsorption of water and electrolytes impossible.
As a result, the patient rapidly loses water, sodium, potassium, and bicarbonates, which triggers a cascade of metabolic disorders.
Clinical and Morphological Stages of Cholera
The classic course of the disease includes three sequential stages characterized by the progression of exicosis (dehydration).
- Cholera enteritis. Begins suddenly, without a prodrome. Watery diarrhea appears; the stool quickly becomes colorless, resembling "rice water." Morphologically, the small intestine exhibits serous enteritis, mucosal swelling, and hydropic cell degeneration. Sloughed epithelium and accumulations of vibrios resembling "schools of fish" are found in the lumen.
- Cholera gastroenteritis. Sudden, recurrent vomiting joins the diarrhea without preceding nausea. Fluid loss reaches critical values (up to 30 liters), leading to hypovolemic shock, hemoconcentration, and metabolic acidosis. Blood pressure drops, and urinary output decreases.
- Algid stage. The most severe phase, accompanied by maximum lethality. Body temperature drops sharply, skin becomes dry and wrinkled ("washerwoman's hands"), the voice is lost (vox cholerica).
Pathologic Anatomy of the Algid Stage: The corpse is severely dehydrated; due to premortem cramps, it often assumes a "gladiator posture." Blood is thick, serous membranes are dry and sticky, and the spleen is shrunken. The villi of the small intestine are completely devoid of epithelium, and necrotic changes develop in the kidneys due to ischemia (blood shunting through the Trueta shunt).
Plague: Pathogenicity Factors and Development
Plague is caused by the bacterium Yersinia pestis and historically claimed hundreds of millions of lives during three great pandemics. The infection is transmitted primarily vector-borne (through flea bites), with various rodents serving as reservoirs.
Mechanisms of Immune Evasion:
- Secretion of fibrinolysin and hyaluronidase for rapid spread and disruption of clotting.
- Antigenic mimicry (structural similarity to human tissues), delaying the immune response.
- Endocytobiosis: bacteria are not destroyed by phagocytes, but instead use their membrane for protection against antibodies.
Clinical and Morphological Forms: The basis of pathogenesis is the rapid development of hemorrhagic septicemia. In the cutaneous form, a primary affect forms at the bite site—the plague phlycten, which evolves from a red spot to a pustule with purulent-hemorrhagic exudate, and then turns into a carbuncle. Next, the infection spreads lymphogenically to regional lymph nodes, causing acute serous-hemorrhagic inflammation (primary bubo formation). Upon breaching the lymphatic barrier, the pathogen enters the bloodstream, causing generalized sepsis and severe intoxication.