Andes Virus and Hantavirus: Distinguishing Features and Risks

Log cabin in misty forest surrounded by camping gear and campfire
Dr. Abdolghader Pakniyat

Andes Virus and Hantavirus: Distinguishing Features and Risks

Peer-reviewed by Dr. Sabrina Berdouk.

Hantavirus is one of those diagnoses most emergency physicians may never personally see—but when it matters, it matters fast.

The early presentation can look like influenza, COVID-19, gastroenteritis, sepsis, pneumonia, myocarditis, or pulmonary edema. Then, in a subset of patients, the disease can abruptly transition into severe hypoxemia, shock, myocardial depression, dysrhythmia, renal failure, or hemorrhage. The ED challenge is not to diagnose every viral syndrome as hantavirus. The challenge is to recognize the rare patient whose viral prodrome plus exposure history plus early cardiopulmonary deterioration should trigger isolation, public health notification, and aggressive supportive care.

The two major clinical patterns

Hantaviruses are rodent-borne viruses that cause two major clinical syndromes.

The first is hemorrhagic fever with renal syndrome (HFRS), mainly associated with hantaviruses circulating in Europe and Asia. It can cause fever, thrombocytopenia, bleeding, acute kidney injury, oliguria, fluid overload and shock. Geography and travel history inform risk, but the syndromes can overlap. CDC HFRS overview.

The second is hantavirus pulmonary syndrome, also called hantavirus cardiopulmonary syndrome, classically associated with “New World” hantaviruses in the Americas. This is the syndrome most relevant to the recent Andes virus concern. CDC notes that HPS can begin with nonspecific flu-like symptoms and may progress to severe respiratory disease; nearly 4 in 10 patients with HPS die. This is a case-fatality estimate for HPS, not a fatality estimate for every hantavirus infection.

Andes virus: the important exception

Most hantaviruses are acquired from rodents through contact with urine, feces, saliva, nesting material, contaminated dust, or, less commonly, rodent bites or scratches. People are usually infected by inhaling aerosolized virus during activities like cleaning rodent-infested spaces, staying in cabins, camping, hiking, or working in rodent-exposed environments.

Andes virus is different. It is a South American hantavirus that can cause HPS and is the only hantavirus currently known to spread person-to-person. CDC describes this spread as rare and usually limited to close contact with a sick person, including direct physical contact, prolonged time in close or enclosed spaces, or exposure to body fluids.

Person-to-person transmission of Andes virus is documented but uncommon and is mainly associated with close or prolonged exposure. CDC’s May 2026 outbreak guidance reported no documented presymptomatic transmission. ECDC’s September 2026 advice still describes uncertainty about infectiousness; a precautionary extension of contact tracing before an ill-defined prodrome is not proof of presymptomatic spread.

Outbreak context: The M/V Hondius outbreak occurred in 2026 and was declared over at the end of June, according to ECDC’s 18 September 2026 advice. Earlier CDC statements about extremely low risk to the US public referred to that outbreak response, not a permanent risk estimate for every exposure or country.

The physiology: capillary leak plus cardiac dysfunction

The key pathophysiology is endothelial dysfunction.

Hantaviruses target small vessels and capillaries. In HPS, the pulmonary capillary bed becomes leaky. Plasma moves out of the intravascular space and into the lungs, creating rapidly progressive noncardiogenic pulmonary edema. At the same time, patients may develop myocardial depression and shock.

A useful mental model:

The tank is leaking, the lungs are flooding, and the pump may be failing.

That is why large-volume fluid resuscitation can be dangerous. These patients may be hypotensive, but their vascular permeability is abnormal. Too much crystalloid can worsen pulmonary edema. The ED approach is careful fluid, early vasopressors when needed, close cardiopulmonary monitoring, and early escalation to ICU or ECMO-capable care. CDC emphasizes careful fluid administration, oxygen, ventilation when needed, and monitoring/adjustment of cardiac function.

The timeline: the clue is often in the story

The incubation period is long enough that the exposure may not be obvious unless we ask.

For Andes virus, CDC’s May 2026 outbreak guidance lists an incubation period of 4–42 days, with a median of 18 days. Compatible illness can include fever, myalgia, chills, gastrointestinal symptoms or respiratory symptoms after exposure. These figures do not replace a public-health exposure assessment.

The classic clinical pattern has two phases:

Early phase: fever, chills, fatigue, headache, myalgias, back pain, nausea, vomiting, diarrhea, abdominal pain, and decreased appetite.

Cardiopulmonary phase: cough, chest pain, dyspnea, hypoxia, pulmonary edema, hypotension, myocardial depression, and dysrhythmia.

The danger is the transition. A patient may initially look like they have a routine viral illness, then rapidly develop hypoxemic respiratory failure and shock.

When should an ER doctor think of hantavirus?

Do not screen every patient with fever for hantavirus. Instead, look for the pattern:

Viral prodrome + exposure risk + respiratory symptoms, shock, thrombocytopenia, hemoconcentration, renal injury, or unexplained pulmonary edema.

Ask specifically about:

Recent camping, hiking, cabins, barns, sheds, farms, or rodent-infested buildings
Cleaning or sweeping enclosed spaces with rodent droppings
Occupational exposure to rodents or contaminated environments
Travel to endemic areas, especially rural South America for Andes virus
Close contact with a symptomatic suspected or confirmed Andes virus patient
Cruise, aircraft, household, or enclosed-space exposure during a known outbreak

Continue evaluating common and treatable alternatives while assessing hantavirus exposure: sepsis, influenza/COVID-19, pneumonia, pulmonary embolism, myocarditis, cardiogenic edema, leptospirosis and other epidemiologically plausible infections. The clinical pattern is not specific for hantavirus.

Isolation: act before the test comes back

Use prompt infection-control assessment when hantavirus is plausible, especially with Andes-virus exposure. Do not assume that every hantavirus requires the same transmission-based precautions; identify the likely virus/exposure and involve infection prevention and public health.

For suspected or confirmed Andes virus, the US CDC isolation guidance recommends an airborne-infection isolation room, gown, gloves, eye protection and an N95-or-higher respirator on room entry. If the room is unavailable, obtain immediate infection-control advice on safe placement and transfer. Public health should determine precaution duration case by case. Follow current national/local requirements.

A practical ED workflow:

Recognize: compatible symptoms and exposure risk.
Isolate: use the applicable Andes-virus room/PPE precautions and an infection-control contingency if the recommended room is unavailable.
Notify: contact the responsible public-health authority early; US clinicians use their state, tribal, local or territorial department.
Support: oxygenation, cautious hemodynamic support and early critical-care/ECMO-centre discussion when deterioration is likely.

This is not because the ED should panic. It is because early containment protects staff and patients, and early consultation helps with testing, monitoring, and disposition.

Diagnosis: public health needs to be involved

Hantavirus testing is not usually an ED “send it and forget it” test.

CDC advises clinicians with compatible symptoms and exposure risk to contact their state, tribal, local, or territorial health department. CDC’s Viral Special Pathogens Branch can provide consultation through the CDC Emergency Operations Center, and CDC notes that specimens are not accepted without prior consultation.

Match the assay to the exposure. An Andes-specific assay may miss other New World hantaviruses; discuss the travel, rodent and contact history with the laboratory and public health. CDC testing update.
Diagnostic confirmation may include:

IgM positivity
Rising IgG titers
PCR positivity
Immunohistochemistry in fatal cases

Early negative tests need context. CDC’s May 2026 Andes guidance specifies that, if serum collected within 72 hours of symptom onset is negative for IgM and IgG, a second specimen should be collected more than 72 hours after onset. In the EU/EEA, September 2026 guidance recommends prompt RT-PCR with complementary serology for symptomatic contacts, consideration of repeat testing while symptoms persist, and immediate retesting with deterioration. Coordinate specimen choice, timing and release from isolation with public health; one early negative test is not an independent discharge rule.

Treatment: supportive care is the treatment

There is no specific antiviral treatment or vaccine currently available for Andes virus. Inactivated vaccines against particular HFRS hantaviruses have been used in Asia; these should not be represented as protection against Andes virus. WHO states that care is supportive and focuses on close clinical monitoring and management of respiratory, cardiac, and kidney complications.

For the ED, this means:

Give oxygen early.
Escalate respiratory support promptly, including intubation and ventilation when needed.
Treat shock with cautious fluid and early vasopressors.
Avoid reflexive large-volume crystalloid if pulmonary edema is developing.
Use broad-spectrum antibiotics if the patient is undifferentiated and bacterial sepsis remains possible.
Avoid NSAIDs when thrombocytopenia, renal injury, or hemorrhage is a concern.
Transfer early to an ICU or ECMO-capable center if the patient is deteriorating.

ECMO can be lifesaving in selected severe cardiopulmonary failure. The often-cited 80% survival came from the later group of a single-centre observational HCPS series: 20 of 25 patients survived, versus 34 of 51 overall. This is not an Andes-specific outcome guarantee or randomized proof of one timing strategy. Early expert-centre consultation remains important. Original study.

Ribavirin has been studied in HPS but has not been shown to be effective for HPS treatment.

Primary references: CDC HPS clinician brief; WHO hantavirus overview; WHO HFRS vaccine-standardization page. HFRS vaccine use in parts of Asia is not evidence of protection against Andes virus.

Disposition: don’t be reassured too easily

Suspected HPS or Andes-virus illness needs urgent, monitored clinical assessment because deterioration can be abrupt, and admission is generally appropriate when the syndrome is clinically plausible. Respiratory failure, shock or evolving organ dysfunction require critical-care assessment. Do not extend that disposition rule to every asymptomatic exposure or every mild non-HPS hantavirus presentation.

Patients with suspected HPS should be treated as potentially unstable even before confirmation. CDC notes that most HPS patients develop some degree of hypotension within 24 hours of initial evaluation, with progressive pulmonary edema and hypoxia often requiring mechanical ventilation. Fatal cases may involve severe myocardial depression progressing to bradycardia, electromechanical dissociation, ventricular tachycardia, or ventricular fibrillation.

For asymptomatic contacts, follow current public-health advice for the exposure and jurisdiction. ECDC’s September 2026 advice for sporadic imported EU/EEA cases recommends 42-day self-monitoring after the last exposure, with active follow-up for higher exposures; it does not recommend routine testing or quarantine of asymptomatic contacts in that setting. New compatible symptoms require self-isolation and immediate notification. Do not automatically transfer May cruise-outbreak restrictions to every later event.

POCUS-guided resuscitation: leaking, failing, bleeding, or mimicking?


POCUS can play an important role when a suspected hantavirus patient begins to deteriorate.

It does not diagnose hantavirus.

POCUS can help a trained clinician assess shock physiology and important alternatives, but findings may be mixed, technically limited or nonspecific. Use it with serial clinical assessment and other investigations; it cannot guarantee recognition before deterioration.

The key question is:

Is the patient leaking, failing, bleeding, or mimicking another emergency?

Lung ultrasound may show B-lines or pleural fluid, supporting assessment of increased lung density/fluid. These findings are not specific for hantavirus or one type of edema, and superiority over chest radiography in this infection has not been established here. ACEP lung-ultrasound guidance.

This matters because repeated crystalloid boluses may worsen oxygenation if the pulmonary capillaries are already leaking.

Cardiac POCUS can support assessment of ventricular function, pericardial fluid and possible obstructive or cardiogenic causes. Quantifying stroke volume and interpreting RV strain require appropriate technique and clinical context; RV strain alone does not diagnose pulmonary embolism.

IVC size and respiratory variation must be interpreted with ventilation, right-heart function and the rest of the examination. They do not independently establish hypovolemia, fluid responsiveness or the safety of giving fluid.

In hantavirus cardiopulmonary syndrome, the patient can be vascularly dry but lung-wet.

A small, collapsible IVC should not automatically trigger large-volume fluid resuscitation.

Instead, use small fluid challenges only when appropriate.

Then reassess repeatedly:

the lungs,
the heart,
the blood pressure,
and the oxygenation.

If pulmonary edema, shock, or myocardial dysfunction is emerging, move early to vasopressors, ventilatory support, ICU care, and ECMO-capable transfer.

In this setting, POCUS is one component of serial bedside assessment, alongside perfusion, blood pressure, oxygenation, laboratory findings and the response to treatment.

The ED bottom line

Hantavirus is rare, but it is an emergency medicine diagnosis because the patient can crash quickly.

The pattern to remember is:

Exposure risk + viral prodrome + pulmonary edema/hypoxia/shock = think hantavirus.

The action plan is:

Isolate early. Call public health early. Support the physiology early. Transfer early if cardiopulmonary failure is developing.

For the worried well, assess exposure risk and coordinate with the health department. For the crashing patient, do not wait for the test. Treat the lungs, support the circulation, protect the team, and get help early.


Author

  • EM Physician & RDMS(AB). Uses POCUS daily in trauma/critical care. Empowers frontline clinicians via EM Mastery Academy and RecapEM.

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