Disease transmitted from mice to humans: name and symptoms

Introduction to Zoonotic Diseases

What are Zoonotic Diseases?

Zoonotic diseases are infections that originate in animals and can be transmitted to humans through direct contact, bites, aerosols, or contaminated materials. The pathogen maintains a natural reservoir in the animal host, allowing persistent circulation without causing severe disease in that species.

Rodents, particularly house mice, serve as reservoirs for several zoonoses. Their close association with human habitats increases exposure risk, especially in indoor environments where droppings, urine, and nesting material accumulate.

Key mouse‑associated zoonotic infections and their primary clinical manifestations:

Hantavirus pulmonary syndrome – fever, muscle aches, headache, followed by rapid onset of shortness of breath, cough, and fluid accumulation in the lungs.
Lymphocytic choriomeningitis virus (LCMV) – flu‑like symptoms, meningitis, encephalitis, and, in severe cases, neurological deficits.
Salmonella enterica serovar Typhimurium – abdominal cramps, diarrhea, fever, and occasional bacteremia.
Leptospira interrogans (leptospirosis) – high fever, chills, muscle pain, jaundice, and, if untreated, kidney or liver failure.

Recognition of these diseases relies on identifying exposure to mouse habitats and correlating characteristic symptom clusters with laboratory confirmation. Prompt diagnosis and supportive care reduce morbidity and prevent further transmission.

The Role of Rodents as Vectors

Rodents function as primary carriers of several zoonotic illnesses that affect humans. Their close proximity to human habitats, combined with high reproductive rates, creates frequent opportunities for pathogen exchange.

Hantavirus Pulmonary Syndrome – fever, muscle aches, headache, progressing to coughing and severe shortness of breath.
Lymphocytic choriomeningitis – fever, headache, stiff neck, confusion, occasionally meningitis.
Plague (Yersinia pestis) – sudden fever, chills, swollen lymph nodes (buboes), and, in septicemic forms, bleeding and shock.

Transmission occurs through distinct pathways. Inhalation of aerosolized urine, feces, or saliva releases viral particles directly into the respiratory tract. Bites and scratches introduce pathogens via skin breaches. Ectoparasites, especially fleas, acquire bacteria from rodent blood and transmit them to humans during feeding. Contamination of food or water supplies with rodent excreta provides another route for infection.

Effective mitigation relies on integrated pest management. Measures include sealing entry points, maintaining clean storage areas, using traps or rodenticides under professional supervision, and employing personal protective equipment when handling rodents or cleaning contaminated spaces. Monitoring rodent populations and testing for pathogen presence support early detection and rapid response.

Hantavirus Pulmonary Syndrome («HPS»)

Causative Agent and Transmission

Hantavirus Strains

Hantaviruses are RNA viruses carried primarily by rodents; human infection occurs through inhalation of aerosolized rodent excreta. The viruses are classified into distinct strains, each linked to a specific geographic region and clinical presentation.

Sin Nombre virus – western United States; causes hantavirus pulmonary syndrome (HPS) with rapid onset of fever, cough, dyspnea, and bilateral pulmonary infiltrates.
Andes virus – Southern Chile and Argentina; produces HPS similar to Sin Nombre but with a higher rate of person‑to‑person transmission.
Puumala virus – Scandinavia and the Baltic states; associated with a milder form of hemorrhagic fever with renal syndrome (HFRS) characterized by fever, headache, and transient proteinuria.
Hantaan virus – China, Korea, Russia; leads to classic HFRS presenting with high fever, flank pain, hemorrhagic manifestations, and acute renal failure.
Seoul virus – worldwide, especially urban environments; causes HFRS with moderate severity, including fever, myalgia, and renal impairment.
Dobrava virus – Balkans; results in severe HFRS with pronounced hemorrhage, hypotension, and renal dysfunction.

Across all hantavirus infections, the incubation period ranges from 1 to 5 weeks. Early symptoms commonly include abrupt fever, chills, myalgia, and headache. Progression may involve:

Respiratory distress and pulmonary edema (predominant in HPS strains).
Oliguria, hematuria, and elevated serum creatinine (typical of HFRS strains).
Thrombocytopenia and gastrointestinal bleeding in severe cases.

Prompt recognition of these patterns enables early supportive care, which is critical for reducing mortality.

Modes of Transmission from Mice to Humans

Mice transmit infectious agents to humans through several well‑documented pathways. Direct contact with rodent fur, saliva, or bite wounds introduces pathogens into the skin or bloodstream. Inhalation of aerosolized particles containing mouse urine, feces, or nesting material releases viruses such as hantavirus and bacteria like Leptospira spp. Consumption of food or water contaminated with rodent excreta leads to gastrointestinal infection by agents such as Salmonella and Yersinia spp. Occupational exposure in laboratories, grain storage facilities, and pest‑control operations increases risk via prolonged proximity to infected rodents and their habitats. Indirect transmission occurs when ectoparasites—fleas, mites, or ticks—feed on infected mice and later bite humans, facilitating spread of plague‑related bacteria.

Primary transmission routes

Skin breach from bites or scratches
Inhalation of aerosolized urine, feces, or saliva
Ingestion of contaminated food or water
Contact with contaminated surfaces followed by hand‑to‑mouth transfer
Vector‑mediated transfer via fleas, mites, or ticks

Each route corresponds to specific clinical presentations, emphasizing the need for targeted preventive measures in environments where mouse populations intersect with human activity.

Clinical Manifestations of HPS

Early Symptoms

Rodent‑borne hantavirus infection begins with nonspecific signs that often resemble a mild flu. Within 2–3 weeks after exposure, patients typically experience:

Sudden fever ranging from 38 °C to 40 °C
Severe headache, frequently described as retro‑orbital
Profuse muscle aches, especially in the lower back, thighs, and shoulders
Unexplained fatigue and generalized weakness
Nausea, vomiting, or abdominal discomfort
Dizziness or light‑headedness, sometimes accompanied by a rapid heart rate

These early manifestations precede the development of respiratory distress that characterizes the later phase of the disease. Prompt recognition of the initial symptom cluster enables timely medical evaluation and isolation measures, reducing the risk of severe complications.

Late-Stage Symptoms and Complications

Late-stage disease progression after exposure to the rodent‑borne hantavirus is marked by rapid deterioration of pulmonary and cardiovascular function. Patients develop severe shortness of breath, hypoxemia, and diffuse pulmonary edema that often requires mechanical ventilation. Hemodynamic instability follows, with hypotension, tachycardia, and shock unresponsive to fluid resuscitation. Concurrent renal impairment manifests as oliguria or anuria, elevated serum creatinine, and electrolyte disturbances, indicating acute kidney injury. Hemorrhagic complications may appear as petechiae, ecchymoses, or pulmonary hemorrhage, contributing to further respiratory compromise. Neurological involvement includes confusion, seizures, or encephalopathy, reflecting hypoxic injury and systemic inflammation.

Complications that persist beyond the acute phase encompass:

Persistent pulmonary fibrosis leading to reduced lung capacity.
Chronic kidney disease with lasting reduction in glomerular filtration rate.
Cardiovascular sequelae such as arrhythmias and reduced myocardial contractility.
Neurocognitive deficits, including memory loss and reduced executive function.
Secondary infections due to prolonged intensive care stays.

Mortality rates increase sharply once these severe manifestations emerge, underscoring the necessity for early recognition and aggressive supportive care.

Diagnosis and Treatment

Diagnostic Methods

The rodent‑borne illness caused by hantavirus requires precise laboratory confirmation because clinical presentation overlaps with other febrile respiratory diseases.

Serological testing remains the primary tool. Enzyme‑linked immunosorbent assay (ELISA) detects hantavirus‑specific IgM during the acute phase and IgG during convalescence. Immunofluorescence assay (IFA) provides a confirmatory read‑out when ELISA results are equivocal.

Molecular techniques supplement serology. Reverse‑transcription polymerase chain reaction (RT‑PCR) amplifies viral RNA from blood or respiratory specimens, delivering results within 24 hours and allowing genotype identification. Real‑time quantitative PCR quantifies viral load, supporting prognosis.

Viral culture is rarely performed because of biosafety constraints, yet when required, it utilizes Vero E6 cells under BSL‑3 conditions to isolate the pathogen for research purposes.

Imaging and routine laboratory panels assist in assessing disease severity but do not establish diagnosis. Chest radiography or computed tomography reveal pulmonary infiltrates; complete blood count often shows thrombocytopenia and leukocytosis.

Key diagnostic methods:

ELISA for hantavirus‑specific IgM and IgG
Immunofluorescence assay for confirmatory antibody detection
RT‑PCR for viral RNA from serum, plasma, or respiratory samples
Quantitative real‑time PCR for viral load measurement
Virus isolation in cell culture under high‑containment conditions (research use)

Combining serological and molecular results yields definitive identification, enabling timely clinical management and public‑health response.

Therapeutic Approaches

The rodent‑borne hantavirus infection presents with fever, myalgia, respiratory distress, and, in severe cases, pulmonary edema. Early recognition permits initiation of specific therapeutic measures that improve survival.

Evidence‑based interventions include:

Supportive care: aggressive fluid management, oxygen supplementation, and mechanical ventilation for respiratory failure.
Antiviral therapy: intravenous ribavirin administered within 48 hours of symptom onset reduces mortality in hemorrhagic fever with renal involvement; data for pulmonary syndrome remain limited.
Experimental agents: favipiravir and monoclonal antibodies targeting the viral glycoprotein have shown promise in animal models and early‑phase trials.
Critical‑care protocols: low‑tidal‑volume ventilation, prone positioning, and careful hemodynamic monitoring to avoid fluid overload.

Adjunctive strategies such as corticosteroids are not routinely recommended due to lack of definitive benefit. Ongoing clinical trials focus on combination antiviral regimens and immune‑modulating therapies, aiming to establish standardized treatment algorithms for this mouse‑derived viral disease.

Lymphocytic Choriomeningitis («LCM»)

Causative Agent and Transmission

LCMV Strains

Lymphocytic choriomeningitis virus (LCMV) is a rodent‑borne pathogen that can infect humans through direct contact with infected mice, contaminated bedding, or aerosolized excreta. The virus exists as several genetically distinct strains, each influencing disease severity and clinical presentation.

Prototype (Armstrong) strain – widely used in research; typically produces mild febrile illness in humans.
Weiss strain – associated with more pronounced neurological involvement, including meningitis and encephalitis.
Sofia strain – identified in European rodent populations; linked to atypical rash and arthralgia.
Mongolian strain – isolated from wild mice in Asia; reports suggest higher rates of hepatitis and elevated liver enzymes.
North American wild‑type strains – diverse genetic profiles; clinical outcomes range from asymptomatic seroconversion to severe hemorrhagic manifestations.

Human infection manifests after an incubation period of 7–13 days. Core symptoms include:

Fever, chills, and malaise.
Headache accompanied by neck stiffness.
Photophobia and mild to moderate confusion.
Myalgia and arthralgia.
In some strains, rash, gastrointestinal upset, or hepatic dysfunction.

Complications such as aseptic meningitis, encephalitis, or persistent neurocognitive deficits occur more frequently with neurotropic strains (e.g., Weiss). Immunocompromised patients may develop disseminated disease, characterized by prolonged fever, organ involvement, and elevated inflammatory markers. Early recognition of strain‑specific patterns assists clinicians in prognosis and management.

Modes of Transmission from Mice to Humans

Mice transmit pathogens to humans through several well‑documented pathways. Direct contact with rodent saliva, blood, or urine during handling, cleaning, or bites introduces infectious agents into the skin or mucous membranes. Inhalation of aerosolized particles containing dried droppings, urine, or nesting material allows viruses such as hantavirus to reach the respiratory tract. Consumption of food or water contaminated with rodent excreta spreads agents like Lymphocytic choriomeningitis virus and Yersinia pestis. Arthropod vectors that feed on infected mice, including fleas and ticks, can transfer bacterial or viral agents to humans during subsequent bites.

Key transmission routes include:

Dermal exposure: scratches, bites, or needle‑stick injuries while trapping or euthanizing rodents.
Respiratory inhalation: aerosolized rodent waste disturbed by cleaning activities or building renovation.
Oral ingestion: ingestion of contaminated food, beverages, or unwashed produce.
Vector‑borne transfer: fleas, ticks, or mites that acquire pathogens from mice and later bite humans.

Each route bypasses the species barrier by delivering the pathogen directly into a susceptible host compartment, establishing infection without intermediate hosts.

Clinical Manifestations of LCM

Early Symptoms

Early manifestations of rodent‑borne zoonoses that pass from mice to humans typically appear within days of exposure. Fever of 38‑40 °C often initiates the clinical picture, accompanied by chills and profuse sweating. Headache, ranging from mild pressure to throbbing pain, is common and may be localized or diffuse. Fatigue and generalized weakness develop rapidly, reducing physical stamina. Respiratory symptoms include dry cough and mild shortness of breath, sometimes progressing to wheezing. Gastrointestinal complaints such as nausea, loss of appetite, and occasional vomiting occur early in the disease course. Skin findings may consist of a maculopapular rash, frequently beginning on the trunk and spreading outward. In some cases, patients report conjunctival irritation or mild eye redness.

Typical early signs:

Elevated body temperature (fever)
Headache
Fatigue and weakness
Dry cough or mild dyspnea
Nausea and loss of appetite
Maculopapular rash
Conjunctival irritation

Recognition of these initial symptoms facilitates prompt diagnostic evaluation and timely therapeutic intervention.

Neurological Complications

The rodent‑borne infection transmitted by the common house mouse can affect the central nervous system, producing a spectrum of neurological signs. Viral invasion of the meninges and brain tissue leads to inflammation that may develop days after initial febrile illness.

Typical neurological manifestations include:

Headache of sudden onset, often severe
Neck stiffness indicating meningeal irritation
Photophobia and visual disturbances
Altered mental status ranging from confusion to coma
Focal deficits such as weakness or sensory loss
Seizures, both generalized and focal
Ataxia and gait instability

Diagnostic work‑up requires lumbar puncture with pleocytosis, elevated protein, and PCR or serology confirming the pathogen. Magnetic resonance imaging may reveal diffuse hyperintensities in the basal ganglia or thalamus. Antiviral therapy is limited; supportive care, seizure control, and intracranial pressure management are essential. Early recognition of neurological involvement improves outcomes, while delayed treatment increases risk of permanent deficits or fatality.

Diagnosis and Treatment

Diagnostic Methods

The rodent‑borne hantavirus infection presents with acute fever, myalgia, and either respiratory distress (Hantavirus Pulmonary Syndrome) or renal impairment (Hemorrhagic Fever with Renal Syndrome). Laboratory confirmation is essential for definitive diagnosis.

Serologic assays – Enzyme‑linked immunosorbent assay (ELISA) detects IgM antibodies within 5–7 days of symptom onset and IgG antibodies during convalescence. Immunofluorescence assay (IFA) provides comparable sensitivity and can be used when ELISA kits are unavailable.
Molecular detection – Reverse‑transcriptase polymerase chain reaction (RT‑PCR) amplifies hantavirus RNA from blood or tissue, confirming infection within the first week. Real‑time PCR quantifies viral load, aiding prognostication.
Virus isolation – Cell culture in Vero E6 or BHK‑21 cells yields live virus for research; it is rarely employed clinically due to biosafety constraints.
Antigen detection – Rapid immunochromatographic tests identify viral nucleocapsid protein in serum, offering point‑of‑care screening with limited sensitivity.

Imaging supports clinical assessment. Chest radiography or computed tomography reveals bilateral infiltrates and pleural effusion in pulmonary cases, while ultrasonography may show renal enlargement and edema in renal syndrome. Routine blood work typically shows thrombocytopenia, elevated serum creatinine, and increased transaminases; these parameters, combined with specific laboratory tests, establish the diagnosis.

Early application of serology and PCR shortens the interval between symptom onset and treatment initiation, improving patient outcomes.

Therapeutic Approaches

The rodent‑borne infection most commonly associated with human cases is hantavirus disease, which manifests as fever, myalgia, headache, and, in severe forms, acute respiratory distress with pulmonary edema. Early recognition of these clinical signs is essential for initiating treatment.

Therapeutic management focuses on supportive care and, when available, antiviral interventions:

Hospitalization in an intensive‑care setting for patients with respiratory compromise.
Supplemental oxygen or mechanical ventilation to maintain adequate oxygenation.
Intravenous fluid administration calibrated to avoid fluid overload, which can worsen pulmonary edema.
Broad‑spectrum antibiotics are not indicated unless a bacterial co‑infection is confirmed.
Ribavirin, a nucleoside analogue, has demonstrated modest efficacy when started within the first 48 hours of symptom onset; dosing follows weight‑based protocols and requires monitoring for hemolytic anemia.
Corticosteroids are not routinely recommended, as clinical trials have not shown consistent benefit.
Experimental therapies, such as monoclonal antibodies targeting viral glycoproteins, are under investigation in clinical trials and may become available pending regulatory approval.

Adjunctive measures include strict infection‑control practices to prevent nosocomial spread and patient education on avoiding rodent exposure. Continuous monitoring of renal function, coagulation parameters, and cardiac status is advised throughout the acute phase.

Prevention and Control Measures

Rodent Control Strategies

Exclusion Techniques

The rodent‑borne illness most frequently associated with transmission from mice to people is hantavirus pulmonary syndrome. Early manifestations include fever, chills, muscle aches and headache. Within a few days, respiratory distress develops, characterized by rapid breathing, coughing and pulmonary edema; the condition can progress to respiratory failure if untreated.

Exclusion techniques interrupt the chain of transmission by preventing mouse access to human environments. Effective measures include:

Sealing cracks, gaps and utility openings larger than ¼ inch with steel wool, caulk or metal flashing.
Installing door sweeps and weather stripping on exterior doors and windows.
Maintaining a clearance of at least 18 inches between stored items and walls to eliminate nesting sites.
Storing food in airtight containers and removing spillage promptly to deny attractants.
Removing vegetation, debris and clutter within 30 feet of structures to reduce habitat proximity.
Using snap traps or live‑catch traps in identified activity zones, followed by proper disposal of captured rodents.

Regular inspection of building envelopes, prompt repair of structural breaches and diligent housekeeping together create a hostile environment for mice, thereby reducing the risk of hantavirus exposure and its severe pulmonary complications.

Sanitation Practices

The disease transmitted from rodents to humans, most commonly hantavirus infection, presents with fever, muscle aches, and respiratory distress that can progress to severe pulmonary syndrome. Lymphocytic choriomeningitis virus, another rodent‑borne pathogen, causes fever, headache, meningitis, and encephalitis.

Effective sanitation practices reduce exposure to these pathogens. Key actions include:

Sealing entry points such as gaps around doors, windows, and utility lines to prevent rodent ingress.
Removing food sources by storing waste in sealed containers and cleaning spills promptly.
Maintaining dry, clutter‑free environments; moisture attracts rodents and provides nesting material.
Conducting regular inspections of storage areas, basements, and attics for droppings, urine stains, or nesting debris.
Disinfecting contaminated surfaces with EPA‑registered rodent‑borne disease cleaners after any sign of infestation.
Employing integrated pest management, combining traps, baits, and professional extermination when populations exceed safe thresholds.

Implementation requires documented cleaning schedules, routine monitoring for signs of rodent activity, and training staff to recognize contamination and apply appropriate decontamination procedures. Compliance with these measures directly lowers the risk of human infection from mouse‑originated diseases.

Personal Protective Measures

Handling Rodents and Contaminated Areas

Rodent‑borne diseases such as hantavirus present a clear occupational hazard; direct contact with mice or their excreta can initiate severe respiratory illness. Effective control relies on strict handling protocols and thorough decontamination of affected zones.

Safe rodent handling requires:

Disposable nitrile gloves, fluid‑resistant gown, and eye protection.
Use of sealed cages or traps; avoid manual capture.
Placement of traps inside a biosafety cabinet or well‑ventilated area.
Immediate disposal of dead or captured rodents in biohazard containers.
Hand washing with antimicrobial soap after glove removal.

Decontamination of contaminated sites includes:

Removal of bedding, food, and debris into sealed bags.
Application of a 1 % bleach solution or EPA‑registered disinfectant to surfaces, followed by a 10‑minute contact time.
Vacuuming with a HEPA‑filter equipped unit to capture residual particles.
Regular monitoring of humidity and ventilation to reduce aerosol formation.

Personnel should be trained to recognize early symptoms—fever, muscle aches, gastrointestinal upset, and rapid onset of pulmonary distress—and to report them to occupational health services without delay. Prompt medical evaluation and supportive care improve outcomes and limit further transmission.

Awareness and Education

Rodent‑borne infections pose a measurable risk to public health, especially when the pathogen spreads from mice to people. The most documented condition of this type is hantavirus pulmonary syndrome, caused by inhalation of aerosolized virus particles from rodent droppings. Early manifestations include fever, muscle aches, and headache; progression leads to coughing, shortness of breath, and rapid development of pulmonary edema, which can be fatal without prompt medical intervention.

Effective mitigation relies on structured awareness programs that translate scientific knowledge into practical actions. Key components include:

Distribution of concise fact sheets outlining transmission routes and early warning signs.
Community workshops that demonstrate safe cleaning practices and proper protective equipment usage.
Integration of rodent‑control modules into school health curricula, emphasizing identification of high‑risk environments.
Regular briefings for healthcare providers on diagnostic criteria, reporting protocols, and treatment options.

Education campaigns must target populations with frequent exposure to mouse habitats, such as agricultural workers, pest‑control staff, and residents of rural dwellings. Materials should be available in multiple languages, employ visual aids, and reference local health authority contacts for rapid response. Continuous evaluation of outreach effectiveness—through surveys, case‑report analysis, and incident tracking—ensures adjustments align with emerging epidemiological data and community feedback.

Public Health Implications

The rodent‑borne pathogen most frequently associated with human infection from mice is a hantavirus, notably the Sin Nombre virus, which causes febrile illness, respiratory distress, and, in severe cases, pulmonary edema. A second concern, lymphocytic choriomeningitis virus, produces fever, headache, meningitis, and encephalitis. Both agents illustrate the broader public‑health challenges posed by zoonotic transmission from commensal rodents.

Surveillance systems must integrate rodent population monitoring with clinical case reporting to detect clusters early.
Infection control protocols for laboratory and healthcare workers should include personal protective equipment and strict handling procedures for rodent specimens.
Community education campaigns need to emphasize rodent exclusion, safe cleaning practices, and avoidance of aerosolized rodent excreta.
Environmental management programs should prioritize sanitation, waste reduction, and habitat modification to lower rodent densities in residential and occupational settings.
Outbreak response plans must provision rapid diagnostic testing, antiviral support where available, and coordination with veterinary services to interrupt animal‑to‑human transmission chains.

Effective mitigation relies on coordinated action across epidemiology, environmental health, and clinical care sectors.