Epidemiology and Reservoirs of Infection
Infections caused by hantaviruses consistently occupy a leading place among natural focal diseases. The pathogens belong to the group of rodent-borne viruses. Unlike many other viral hemorrhagic fevers, hantaviruses are non-transmissible—their spread is not related to bites from mosquitoes, ticks, or other blood-sucking arthropods.
The main reservoir and source of infection are wild rodents, in which the infection is asymptomatic but accompanied by massive and prolonged shedding of the stable virus into the environment via urine, feces, and saliva. Based on ecological niches, reservoirs are divided into two groups:
- Forest complex rodents: bank vole (Myodes glareolus), grey-red vole (Myodes rufocanus), striped field mouse (Apodemus agrarius), and East Asian field mouse.
- Steppe complex rodents: deer mice (Peromyscus maniculatus) and cotton rats (Sigmodon).
Human infection occurs via three main routes:
- Aerogenic (dust-inhalation): This is the primary mechanism. The virus enters the respiratory tract via inhalation of contaminated dust during the cleaning of old buildings, agricultural work, logging, or sleeping on hay.
- Fecal-oral: Alimentary transmission via food and water contaminated with rodent excreta, as well as contact transmission via unwashed hands.
- Direct contact: When infected excreta come into direct contact with broken skin, during the skinning of animal carcasses, or from a rodent bite.
Human susceptibility to the infection is extremely high.
Pathogenesis and Effects on the Body
The leading disease mechanism is the vasotropic action of the virus. Upon entering the body, the pathogen causes systemic destructive lesions in the walls of small blood vessels. Viremia typically lasts from 4 to 7 days.
Depending on the specific viral serotype, different target organs are affected:
- In HFRS (hemorrhagic fever with renal syndrome), primary pathological changes occur in the kidneys, adrenal glands, hypothalamus, myocardium, and intestines.
- In cardiopulmonary syndrome, the virus shows a marked tropism for the pulmonary capillary endothelium, causing massive lung injury.
Hemorrhagic Fever with Renal Syndrome (HFRS)
The incubation period for HFRS ranges from 7 to 45 days, but most commonly lasts 2–3 weeks. The disease begins acutely with high fever. The clinical course is characterized by strict cyclical phases:
- Febrile phase
- Oliguric phase: Sharp decrease in urine output (diuresis).
- Polyuric phase: Compensatory increase in urine volume.
- Convalescence: Gradual recovery.
HFRS is frequently complicated by severe manifestations, including acute kidney injury (uremia), rupture of the kidney or its capsule with massive hemorrhage into the surrounding retroperitoneal tissue, pulmonary edema, and eclampsia. Systemic vascular damage leads to gastrointestinal bleeding, as well as hemorrhages in the brain and myocardium.
Case fatality rate directly depends on the strain: European virus variants cause death in 1–2% of cases, whereas Far Eastern strains are more aggressive, with mortality reaching 5–10%.
Hantavirus Cardiopulmonary Syndrome (HCPS)
This clinical form gained widespread attention following a major outbreak in the USA in 1993, which demonstrated an extremely high case fatality rate (over 50%). The causative agent was the Sin Nombre virus (serotype 5), with deer mice as the natural reservoir. Geographically, this syndrome is distributed across North, Central, and South America.
The incubation period is about 6 weeks. The disease begins with a short prodrome featuring fever, which rapidly progresses to severe cardiopulmonary failure accompanied by massive interstitial pneumonia. The prognosis for HCPS is extremely guarded, with mortality rates reaching 50–60%.
Immunity and Diagnostic Principles
A prior infection confers robust, lifelong immunity. Re-infection with a homologous viral serotype has not been documented, and protective antibodies can be detected in human blood for up to 25 years.
Microbiological diagnostics employ the following methods:
- Virological: Isolation of the pathogen from patient blood and urine (effective only during the acute phase).
- Serological: Detection of specific antibodies in paired sera and urine.
- Viral antigen detection: Rapid identification of viral proteins in clinical samples.