A Camping Trip Leads to Life-Threatening Respiratory Failure: Understanding Hantavirus Infection

Table of Contents

• Introduction: Why This Case Matters
• The Patient's Story: Initial Symptoms and Presentation
• Examination and Initial Test Results
• What the Scans Showed: X-ray and CT Findings
• Rapid Deterioration: ICU Admission and Critical Care
• Considering the Possibilities: What Could This Be?
• Reaching the Diagnosis: Hantavirus Confirmed
• Understanding Hantavirus: Transmission and Types
• What This Means for Patients
• Source Information

Introduction: Why This Case Matters

This detailed case report illustrates how a seemingly ordinary camping trip can lead to a life-threatening medical emergency. Hantavirus cardiopulmonary syndrome is a rare but serious condition that patients and doctors should be aware of, particularly those who spend time in rural areas or have exposure to rodents. The case demonstrates the rapid progression from mild flu-like symptoms to severe respiratory failure and shows how careful diagnostic detective work can identify the correct cause.

The Patient's Story: Initial Symptoms and Presentation

A previously healthy 52-year-old man presented to an emergency department in Buenos Aires, Argentina, in early autumn with a fever that had persisted for one week. He had been in his usual good health until seven days earlier when the fever developed. His initial visit to the emergency department showed a temperature of 38.0°C (100.4°F), and a test for SARS-CoV-2 (the virus that causes COVID-19) was negative. He was sent home with recommendations for supportive care.

Over the next seven days, his fever persisted and additional symptoms developed, including nausea, abdominal pain, and watery diarrhea. With poor oral intake and concerns about dehydration, he returned to the emergency department. This time, his vital signs were concerning: oxygen saturation was 89% while breathing room air (normal is 95-100%), which only improved to 93% with supplemental oxygen. He appeared confused but had no focal neurologic deficits.

Examination and Initial Test Results

The patient's medical history included gallstones treated with gallbladder removal two years earlier. He was fully vaccinated against COVID-19 but not against influenza. He took no regular medications and had no known drug allergies. He lived in Buenos Aires with his family, worked in an office, and had no pets or significant occupational exposures.

Notably, about one month before getting sick, he had undergone a dental root canal procedure. Most significantly, he had recently visited the rural Chascomús region of Argentina, where he had camped outdoors in a tent. He reported no known insect bites, contact with rodents, or other specific exposures.

On admission to the ICU, he had persistent low oxygen levels (88% saturation) requiring high-flow oxygen. Physical examination revealed dry mucous membranes suggesting dehydration, poor dental hygiene with decayed teeth, and crackles at the base of both lungs. His abdomen was soft with mild epigastric tenderness.

Laboratory tests revealed several concerning abnormalities:

• Elevated hematocrit (56.9%; normal 41-53%) indicating hemoconcentration
• High white blood cell count (16,500 cells/μL; normal 4,500-11,000) with predominance of neutrophils
• Low platelet count (54,000/μL; normal 150,000-400,000)
• Elevated blood urea nitrogen (49 mg/dL; normal 8-25 mg/dL) suggesting kidney impairment
• Normal creatinine level (1.23 mg/dL; normal 0.60-1.50 mg/dL)

Arterial blood gas measurements showed critically low oxygen levels (partial pressure of arterial oxygen 42 mm Hg; normal 80-100 mm Hg), high carbon dioxide levels (70 mm Hg; normal 35-45 mm Hg), and acidic blood pH (7.14; normal 7.35-7.45).

What the Scans Showed: X-ray and CT Findings

A portable chest X-ray performed in the emergency department revealed diffuse ground-glass opacities (hazy areas) in both lungs, predominantly in the lower lobes, with associated reticular opacities (net-like patterns). These findings were suggestive of fluid overload or possibly an underlying infection like atypical pneumonia.

CT scanning of the chest without contrast showed more detailed abnormalities:

• Interlobular septal thickening (thickening between lung segments) in both lungs
• Peribronchovascular thickening (around airways and blood vessels)
• Patchy ground-glass opacities and areas of consolidation (denser areas)
• Mosaic attenuation (patchy areas of different densities) and increased blood vessel diameters
• A nodular opacity with surrounding ground-glass changes in the right upper lobe (the "halo sign"), which can suggest fungal infection

Overall, these findings were consistent with pulmonary edema (fluid in the lungs), with the possibility of a superimposed infection.

Rapid Deterioration: ICU Admission and Critical Care

The patient's condition deteriorated rapidly despite initial treatments. Doctors started empirical antimicrobial therapy with four medications: ceftriaxone, vancomycin, clarithromycin, and oseltamivir to cover various possible bacterial and viral infections.

Despite receiving high-flow oxygen at 50 liters per minute with 100% inspired oxygen, his oxygen levels remained critically low. He required endotracheal intubation (breathing tube placement) and mechanical ventilation (life support breathing machine) within his first hospital day.

He developed refractory shock (severe circulatory failure) requiring multiple vasopressor medications (drugs to support blood pressure) including norepinephrine and vasopressin. He also developed anuric acute kidney injury (complete cessation of urine output) requiring continuous renal-replacement therapy (dialysis).

His condition met the Berlin criteria for severe acute respiratory distress syndrome (ARDS), characterized by:

• Bilateral pulmonary opacities on imaging
• Acute onset within one week
• Severe hypoxemia with ratio of arterial oxygen to inspired oxygen <100 (his was 42)
• Absence of heart failure as the primary cause

Doctors used a pulmonary artery catheter to guide therapy, which showed:

• Right atrial pressure: 7 mm Hg
• Pulmonary artery pressures: 30/20 mm Hg (systolic/diastolic) with mean of 23 mm Hg
• Pulmonary artery wedge pressure: 11 mm Hg
• Cardiac output: 4.7 liters/minute
• Cardiac index: 2.6 L/min/m²
• Systemic vascular resistance: 1405 dyn·sec·cm⁻⁵ (indicating hypovolemic shock)

He received aggressive fluid resuscitation with lactated Ringer's solution, and his hemodynamic measurements improved. Although extracorporeal membrane oxygenation (ECMO, a advanced heart-lung support system) was considered for his severe respiratory failure, his oxygenation eventually improved with conventional mechanical ventilation.

Considering the Possibilities: What Could This Be?

The medical team considered several possible diagnoses before arriving at the correct one:

Community-Acquired Pneumonia: This was initially considered given his fever and respiratory symptoms. However, negative tests for SARS-CoV-2, influenza, pneumococcus, and the absence of productive cough or focal consolidation on imaging made typical bacterial or viral pneumonia less likely.

Myeloproliferative Disorder: His elevated hematocrit and white cell count initially suggested conditions like polycythemia vera, which could predispose him to fungal infections. However, his low platelet count and absence of organ enlargement on ultrasound made this unlikely.

Pulmonary-Renal Syndrome: Conditions like autoimmune disorders (Goodpasture's syndrome, vasculitis, or lupus) that affect both lungs and kidneys were considered but deemed unlikely due to absence of hematuria, red cell casts, or other autoimmune signs.

Hantavirus Cardiopulmonary Syndrome: This emerged as the leading possibility given his recent camping trip to an endemic area, rapid progression to respiratory failure, noncardiogenic pulmonary edema, hemoconcentration, thrombocytopenia, and leukocytosis. The capillary leak syndrome pattern matched hantavirus infection.

Reaching the Diagnosis: Hantavirus Confirmed

Diagnostic testing eventually confirmed hantavirus infection. Initial blood and sputum cultures showed no growth. Tests for HIV, dengue virus, and leptospira were negative. However, specialized testing revealed:

• Positive hantavirus-specific IgM antibodies (indicating recent infection)
• Positive nucleic acid amplification testing (NAAT) detecting viral RNA
• Later seroconversion with detectable IgG antibodies on follow-up testing 6 days after initial tests

These findings confirmed the diagnosis of hantavirus infection manifesting as hantavirus cardiopulmonary syndrome.

The diagnostic timeline for hantavirus follows a specific pattern:

• IgM antibodies become detectable 1-3 days after symptom onset, peak around day 10, and decline by approximately day 30
• IgG antibodies start rising 3-5 days after symptom onset and remain elevated long-term
• Viral RNA can be detected by NAAT before and up to approximately 10 days after symptom onset

In Argentina, the enzyme-linked immunosorbent assay (ELISA) test for hantavirus has a sensitivity of 96.6% and specificity of 90.6%, approaching 100% sensitivity during the cardiopulmonary phase of illness.

Understanding Hantavirus: Transmission and Types

Hantaviruses are RNA viruses belonging to the Bunyaviridae family that are found worldwide. In the Americas, more than 20 genotypes have been identified. These viruses are hosted by rodents of the Muridae family (including various mouse and rat species), which carry chronic asymptomatic infections and excrete the virus through urine, saliva, and feces, contaminating their environment.

Human infection typically occurs through:

• Inhalation of aerosolized virus particles from rodent excreta
• Direct contact with rodent urine, droppings, or nesting materials
• Rarely, bites from infected rodents

In Argentina, eight hantavirus genotypes have been linked to hantavirus cardiopulmonary syndrome, including:

• Andes virus (unique for potential human-to-human transmission)
• Lechiguanas virus
• Laguna Negra virus
• Orán virus

Andes virus outbreaks in the Patagonia region have been associated with mortality rates as high as 40%. Argentina has the highest incidence of hantavirus cardiopulmonary syndrome in the Americas.

The disease progresses through four phases:

1. Incubation: 2-4 weeks after exposure without symptoms
2. Prodromal phase: 3-5 days of fever, fatigue, muscle aches, and sometimes gastrointestinal symptoms
3. Cardiopulmonary phase: 2-4 days of rapid respiratory deterioration, pulmonary edema, and shock
4. Convalescence: Gradual recovery that may take weeks, with persistent fatigue and polyuria (excessive urination)

The severe illness results from both direct viral infection and a dysregulated immune response that causes profound capillary leak syndrome, leading to fluid accumulation in the lungs and circulatory failure.

What This Means for Patients

This case highlights several important points for patients:

Travel History Matters: Always inform your doctors about recent travel, especially to rural areas or regions where specific diseases are known to occur. This patient's camping trip to the hantavirus-endemic Chascomús region was crucial information for diagnosis.

Recognize Early Symptoms: Early hantavirus infection presents with non-specific flu-like symptoms—fever, fatigue, muscle aches—that may include gastrointestinal symptoms like nausea, vomiting, and abdominal pain. These symptoms typically develop 1-5 weeks after exposure to rodents or their droppings.

Seek Prompt Medical Attention: If you develop respiratory symptoms (cough, shortness of breath) along with fever after potential rodent exposure, seek medical care immediately. Early recognition and supportive care are essential for survival.

Prevention is Key: When spending time in rural areas or places with rodent activity:

• Avoid areas with signs of rodent infestation (droppings, nests, dead rodents)
• Air out closed buildings before entering
• Wear gloves when handling wood, hay, or other materials that might harbor rodents
• Disinfect areas with rodent evidence with bleach solution
• Seal holes and gaps in homes to prevent rodent entry
• Store food in rodent-proof containers

Treatment Approach: There is no specific antiviral treatment for hantavirus infection. Care is supportive, focusing on:

• Careful fluid management to address capillary leak without worsening pulmonary edema
• Oxygen therapy and mechanical ventilation for respiratory failure
• Blood pressure support with vasopressor medications when needed
• Renal replacement therapy (dialysis) for kidney failure
• Treatment of secondary infections if they occur

With advanced supportive care in intensive care units, survival rates have improved, though the disease remains serious with significant mortality risk, especially in the first 24-48 hours of hospitalization.

Source Information

Original Article Title: Case 15-2025: A 52-Year-Old Man with Fever, Nausea, and Respiratory Failure

Authors: Martín Hunter, M.D., Ignacio Lopez Saubidet, M.D., Tomás Amerio, M.D., and Maria V. Leone, M.D.

Publication: The New England Journal of Medicine (May 29, 2025; 392:2049-2057)

DOI: 10.1056/NEJMcpc2412526

This patient-friendly article is based on peer-reviewed research from The New England Journal of Medicine. It maintains all significant medical findings, data points, and clinical details from the original case report while making the information accessible to patients and caregivers.