International surveillance and epidemiological significance
According to the rules in force since 1971, particularly dangerous infections are strictly regulated at the global level. They are divided into quarantine (conventions) diseases (plague, cholera, yellow fever, as well as eradicated smallpox) and infections requiring international monitoring, such as epidemic typhus and relapsing fever, poliomyelitis, and malaria.
In the modern world, the importation of such infections occurs rapidly. Historically known outbreaks include smallpox in Moscow (1960, imported from India) and cholera in the south of Russia (1971). Today, cholera remains the most likely threat to Russian healthcare: sporadic cases are annually recorded in regions with major water arteries, especially in the Volga region.
Cholera: pathogen and mechanisms of development
Cholera is a strict anthroponosis. The source of infection is always a human (a patient or a carrier). The disease is transmitted by the fecal-oral route, most commonly through water.
Features of the pathogen The seventh cholera pandemic is caused by the El Tor vibrio. Unlike the classical Asian vibrio, it survives longer in water, produces an exotoxin (choleragen), and more often leads to asymptomatic vibrio carrier state. 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 penetrate the blood (there is no vibrioremia), and all severe effects are associated with the action of the toxin.
- Choleragen activates adenylate cyclase in enterocytes, which leads to a sharp increase in cAMP and a massive release of isotonic fluid.
- In parallel, the synthesis of cGMP is suppressed, which blocks the operation of 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 periods of cholera
The classical course of the disease includes three successive stages characterized by the progression of exicosis (dehydration).
- Cholera enteritis. Begins suddenly, without prodrome. Watery diarrhea appears, and the stool quickly becomes colorless, resembling "rice water". Morphologically, serous enteritis, mucosal swelling, and hydropic dystrophy of cells are observed in the small intestine. Desquamated epithelium and accumulations of vibrios in the form of "fish schools" are found in the lumen.
- Cholera gastroenteritis. Sudden repeated vomiting, not preceded by nausea, joins the diarrhea. Fluid loss reaches critical values (up to 30 liters), hypovolemic shock, blood hemoconcentration, and metabolic acidosis develop. Blood pressure drops, diuresis decreases.
- Algid period. The most severe phase, accompanied by maximum mortality. Body temperature drops sharply, the skin becomes dry and wrinkled ("washerwoman's hands" sign), the voice disappears (vox cholerica). Cramps occur due to sodium loss.
Pathological anatomy of the algid period: the corpse is severely dehydrated and often assumes the "gladiator pose" due to ante-mortem spasms. The 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 via Troitzky shunts).
Plague: pathogenicity factors and development
Plague is caused by the bacterium Yersinia pestis and has historically claimed hundreds of millions of lives during three great pandemics. The infection is transmitted mainly vector-borne (through flea bites), with various rodents serving as the reservoir.
Mechanisms of immune evasion:
- Secretion of fibrinolysin and hyaluronidase for rapid spread and coagulation disorders.
- Antigenic mimicry (structural similarity to human tissues), which delays the immune response.
- Endocytobiosis: bacteria are not destroyed by phagocytes, but 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—the plague phlyctenule—is formed at the bite site, which evolves from a red spot to a pustule with purulent-hemorrhagic exudate, and then turns into a carbuncle. Next, the infection penetrates lymphogenically into regional nodes, causing their acute serous-hemorrhagic inflammation (formation of a primary bubo). When the lymphatic barrier is breached, the pathogen enters the blood, causing generalized sepsis and severe intoxication.
Briefly: answers to topical questions
What clinical and morphological forms of plague are distinguished in pathological anatomy?
Pathological anatomy distinguishes predominantly local, internally disseminated, and externally disseminated forms of plague.
- Predominantly local forms—cutaneous, bubonic, and cutaneobubonic.
- Internally disseminated forms (generalized)—primary septic and secondary septic.
- Externally disseminated forms—primary pulmonary, secondary pulmonary, and intestinal.
What biotypes of the cholera pathogen exist?
There are two main biotypes of the cholera agent belonging to the O1 serovar.
- Classical (Vibrio cholerae classica) is the causative agent of Asiatic cholera.
- El Tor (Vibrio cholerae biovar El Tor) is characterized by strong hemolytic activity, production of exotoxin (choleragen), high environmental stability, and a tendency to establish a carrier state.
To quickly memorize the classic cholera triad, use the "VDC" rule: Vomiting (sudden, without nausea) → Diarrhea (rice-water stool) → Cramps (resulting from sodium loss).
Class and exam questions
Does the cholera vibrio enter the bloodstream?
No, bacteremia is absent in cholera. The pathogen remains in the intestinal lumen, while the severity of the condition is due to massive exotoxin release and catastrophic fluid loss.
What is the morphological feature of the spleen in death from cholera?
Due to extreme dehydration (exicosis), the spleen becomes small and severely shrunken, which is a specific macroscopic sign in the algid period.
Why does acute renal failure develop in cholera?
A sharp drop in blood pressure and hypovolemic shock trigger a compensatory activation of the Trueta juxtamedullary shunt. This leads to severe ischemia of the renal cortex and the development of bilateral necrotic nephrosis.
What makes endocytobiosis dangerous in plague?
During endocytobiosis, the plague bacillus does not die inside macrophages. It uses the host cell as a shelter from circulating antibodies, preventing the immune system from stopping the generalization of the infection in time.
What else to study on this topic
- Pathogenesis and morphology of specific cholera complications: typhoid state and uremia
- Fulminant (dry) form of cholera and vibrio carriage
- Differences in the pathomorphosis of modern El Tor cholera versus the classical infection
- Primary pneumonic and secondary pneumonic forms of plague: pathogenesis features
- Features of the immune response and antigenic mimicry of Yersinia pestis
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