Etiology and pathogenesis
The causative agents of the disease are RNA-containing hantaviruses of the family Bunyaviridae. It is important to note that they do not have a direct damaging (cytopathic) effect on cells. The virus enters the body by binding to specific integrin receptors on the membranes of target cells, after which its replication occurs in the cytoplasm.
The main targets for hantaviruses are:
- Endothelial cells of blood vessels.
- Renal tubular epithelium.
- Macrophages and platelets.
The presence of specific receptors in tissues determines the specificity of the lesion: in HFRS, the kidneys are primarily affected, whereas in hantavirus pulmonary syndrome, the lungs are.
Epidemiology
HFRS is a classic natural focal zoonosis. In nature, the reservoir and source of infection are murid rodents (family Muridae). The animals themselves have a subclinical infection, but they actively shed the virus in urine, feces, and saliva.
Human infection occurs via several routes:
- Airborne (dust-borne) — the most frequent route. A person inhales dust containing dried rodent excreta (e.g., during agricultural or garden work).
- Alimentary — consumption of contaminated food or water.
- Contact — through damaged skin (including rodent bites) or unwashed hands.
The global incidence of HFRS reaches 150,000–200,000 cases per year. In Russia, the Privolzhsky Federal District is considered the most problematic region.
Clinical presentation
The diagnosis of HFRS is based on a combination of epidemiological history (countryside work, presence of rodents) and three leading clinical syndromes:
- Intoxication syndrome: sharp increase in temperature (up to 39°C), severe headache, weakness, thirst, nausea, and vomiting. Hyperemia of the face and neck and conjunctival injection are frequently observed.
- Nephropathic syndrome: lower back pain, bilateral positive Pasternatsky's sign, sharp decrease in urine volume (oliguria), and discoloration of urine (dark, turbid).
- Hemorrhagic syndrome: appearance of pinpoint hemorrhages (petechiae), e.g., on the mucous membrane of the soft palate.
The disease runs a cyclic course: the incubation period is followed by the initial stage, then the peak period (including oliguric and polyuric phases), and the convalescence stage.
Diagnostics and treatment
Laboratory and instrumental methods are used to confirm the diagnosis:
- Blood tests: complete blood count typically shows leukocytosis with a left shift. Biochemistry reveals elevated urea and creatinine levels.
- Urine tests: reveal protein (proteinuria), red blood cells (hematuria), casts, and decreased urine specific gravity (hyposthenuria).
- Specific diagnostics: detection of antibodies against hantaviruses using IIFA (IFA).
All patients with suspected HFRS are subject to mandatory hospitalization with gentle transportation. Treatment includes antiviral drugs (ribavirin) and massive infusion detoxification therapy. In case of complications, intensive therapy is indicated, up to hemodialysis.
Briefly: answers to topical questions
What is the pathogenesis of acute renal failure in HFRS?
The pathogenesis of acute renal failure in HFRS is associated with systemic microcirculatory vascular damage leading to organ and tissue ischemia, and a specific renal lesion resembling nephrosis-nephritis. The following mechanisms contribute to the development of renal failure:
- Ischemia — a consequence of microcirculatory disorders.
- Tubular compression — caused by serous-hemorrhagic edema of the interstitium.
- Tubular obstruction — associated with fibrin casts; during the polyuric period, their discharge and restoration of renal tubular patency are described.
- Tubular epithelial damage — dystrophic and necrotic changes.
What pathomorphological changes occur in the kidneys in HFRS?
Pathomorphological changes in the kidneys in HFRS are characterized by enlargement and marked capsular tension, which can lead to capsular rupture with hemorrhage into the perirenal tissue. The following changes are detected in renal tissues:
- Cortex — becomes pale.
- Pyramids and renal pelvis — contain multiple hemorrhages.
- Interstitium — serous-hemorrhagic edema develops.
- Tubular apparatus — dystrophic and necrotic changes of the tubular epithelium are observed.
Class and exam questions
What complications can occur in HFRS?
The most formidable complications include infectious toxic shock (ITS), acute renal failure (uremia), severe bleeding, rupture of the renal capsule, and hypopituitarism.
What diseases should HFRS be differentiated from?
Main differential diagnoses: leptospirosis, influenza, acute pyelonephritis, and acute glomerulonephritis.
Do hantaviruses have a direct destructive effect on cells?
No, hantaviruses do not have a direct cytopathic effect. Tissue damage is associated with the systemic response of the body and damage to the microvascular endothelium.
What else to study on this topic
- Mechanisms of hemorrhagic syndrome development
- Features of viremia and hantavirus penetration
- Cyclicity of the disease course (oliguric and polyuric periods)
- Hantavirus pulmonary syndrome: clinical presentation and outcomes
- Indications for hemodialysis in HFRS
- Pathomorphological changes in internal organs
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