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A 44-Year-Old Man With Sore Throat and Fatigue After Using an Old Camper Van FREE TO VIEW

Vanessa Yap, MD; Jessica Abrantes, MD; Lucas Cruz, MD; Ulysses Wu, MD; Bimalin Lahiri, MD
Author and Funding Information

aDivision of Pulmonary and Critical Care Medicine, University of Connecticut School of Medicine, Farmington, CT

bPrimary Care Internal Medicine Residency Program, University of Connecticut School of Medicine, Farmington, CT

cInternal Medicine Residency Program, University of Connecticut School of Medicine, Farmington, CT

dInfectious Disease Program, Saint Francis Hospital and Medical Center, Hartford, CT

ePulmonary and Critical Care Section, Saint Francis Hospital and Medical Center, Hartford, CT

CORRESPONDENCE TO: Vanessa Yap, MD, 263 Farmington Ave, Farmington, CT 06030

Copyright 2016, American College of Chest Physicians. All Rights Reserved.

Chest. 2016;150(2):e49-e52. doi:10.1016/j.chest.2016.02.668
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Published online

A 44-year-old man from Connecticut with no significant past medical history presented to the ED with a 2-week history of sore throat and fatigue, subsequently developing cough, dyspnea, fevers, and chills. The patient reported buying an old camper van and noticed a large infestation of rodent droppings, which he had cleaned thoroughly from the cabin. He used the camper van on several camping trips in Vermont, and symptoms started on his return.

Figures in this Article

On admission, his temperature was 38.4°C; respiratory rate, 30 breaths/min; pulse, 122 beats/min; and oxygen saturation, 79% on room air. He was alert, oriented, but in mild respiratory distress. Examination revealed the following: oropharynx clear; regular rhythm, tachycardic with no murmurs; crackles at bilateral lung bases; no rashes, clubbing, edema, or cyanosis.

Laboratory work is summarized in Table 1.

Table Graphic Jump Location
Table 1 Laboratory Work: Results

BNP = B-type natriuretic peptide.

Chest imaging (Figs 1, 2) showed alveolar edema with moderate bilateral pleural effusions. The patient was admitted to the ICU because of impending respiratory failure, and he was continued on empiric broad-spectrum antibiotics. The patient was then intubated and went into shock, requiring vasopressors.

Figure 1
Figure Jump LinkFigure 1 Chest radiograph, showing moderate bibasilar patchy opacities.Grahic Jump Location
Figure 2
Figure Jump LinkFigure 2 Chest CT scan without contrast, showing ground-glass alveolar opacities in both lungs with moderate bilateral pleural effusion.Grahic Jump Location

What is the diagnosis?

Diagnosis: Hantavirus pulmonary syndrome

Hantavirus pulmonary syndrome (HPS) is a severe respiratory disease most commonly caused by the Sin Nombre virus, a member of the genus Hantavirus, hosted by the deer mouse. The hantaviruses are a genus of more than 21 enveloped single-stranded negative-sense RNA viruses belonging to the Bunyaviridae family. These viruses are borne by rodents and insectivores, with representative species in most parts of the planet. It causes two distinct febrile illnesses in humans involving an element of vascular leak: hantavirus pulmonary syndrome, also known as hantavirus cardiopulmonary syndrome, as seen in North and South America; and hemorrhagic fever with renal syndrome, as seen in Asia and Europe.

HPS was first recognized after an outbreak in 1993 that occurred in Arizona, Colorado, New Mexico, and Utah (Four Corners region, United States). The index cases were identified from New Mexico when two young, healthy, long-distance runners succumbed to a rapidly progressive pulmonary infection, both dying within days. The causative agent for the illness was determined to be an unidentified North American member of the Hantavirus genus. The clinical syndrome caused by this agent, ultimately named Sin Nombre virus (SNV), came to be called HPS.

HPS is characterized by a vague viral prodrome followed by rapidly worsening respiratory distress, noncardiogenic pulmonary edema, and hemodynamic compromise. There have been 639 reported cases of HPS through April 2014 in the United States. Case counts have varied from 11 to 48 per year, with a case fatality rate of 35%. Most of the cases reported in the United States have been from the Southwest; less than 3% of cases are associated with exposures in the eastern United States, but infections have been reported in 34 US states, this being the first from Connecticut.

The geographic distribution of hantaviruses is determined by the geographic distribution of their host reservoirs. In the United States, SNV chronically infects the deer mouse Peromyscus maniculatus. The deer mouse habitat occupies a huge area of the North American continent, making SNV the most likely cause of most HPS cases. Most cases occur during the late spring and early summer months, and HPS occurs almost exclusively in people who sleep or work in areas where they may be exposed to rodents. Transmission occurs through inhalation of air contaminated by aerosolized rodent urine, feces, or saliva and through rodent bites. HPS is nearly always acquired within closed spaces, such as peridomestic buildings on farms or ranches, or the cabs of abandoned pickup trucks. Indoor acquisition is likely due to higher murine population densities; less ultraviolet light for desiccation; and higher likelihood of performing activities that stir up virus-carrying dust particles without the diluting effect of outdoor air, leading to the possible inhalation of higher concentrations of the virus. The time between exposure and symptomatic illness is usually 1 to 5 weeks, with a median incubation time of 18 days.

The primary site of infection is the lung, where the virus elicits an inflammatory response enabling widespread dissemination to vascular endothelial cells. This leads to severe vascular permeability, capillary leak, noncardiogenic pulmonary edema, hypoxia, lactic acidosis, elevated systemic vascular resistance, and myocardial depression. The proximate cause of death in patients is usually cardiogenic shock. The disease comprises four clinical phases: prodrome, pulmonary edema and shock, diuresis, and convalescence. During the prodromal phase, patients present with nonspecific complaints almost indistinguishable from influenza. Headache and abdominal pain may be quite prominent and can progress over the next 7 to 10 days and include nonproductive cough and dyspnea. Patients will be febrile, tachycardic, tachypneic, and hypoxic, which heralds the development of worsening respiratory failure and hypotension. Patients who survive the shock phase enter the diuretic phase with rapid (24-48 h) resolution of respiratory and hemodynamic abnormalities. Patients then enter the convalescent phase of the illness, which typically lasts for a few months, but some patients have taken up to 2 years for full recovery.

Confirmatory testing includes detection of hantavirus-specific immunoglobulin M, rising titers of hantavirus-specific immunoglobulin G, detection of hantavirus RNA by PCR, or detection of hantavirus antigen by immunohistochemistry. However, because confirmatory testing is often not immediately available, a peripheral blood smear may facilitate a more timely diagnosis. In the right clinical setting, the presence of four of five of the following criteria was shown to be 96% sensitive and 99% specific for hantavirus: myelocytosis, greater than 10% immunoblasts, hemoconcentration, thrombocytopenia, and the absence of toxic granulations in neutrophils.

Treatment is predominantly supportive in nature. No specific therapy has been shown to be effective. Ribavirin was used at the initial outbreak in an open trial and more recently in a double-blind placebo-controlled trial, but has not been shown to improve clinical outcomes. Empiric broad-spectrum antibiotics are recommended because it overlaps with other infectious etiologies. Judicious intravenous fluids should be administered given the widespread capillary leak despite the risk of worsening pulmonary edema. Patients with HPS should be admitted to the ICU for close monitoring as they can decline precipitously. Extracorporeal membrane oxygenation has been used successfully in patients with refractory HPS.

At present no hantavirus vaccines are approved by the US Food and Drug Administration or European Medicines Agency, although inactivated virus vaccines are used in Asia. Patients with high-risk occupations are advised to wear face masks to decrease the chance of inhaling infected excreta.

Clinical Course

The patient was continued on antibiotics until serology tests returned positive results for hantavirus (Sin Nombre serotype) IgM and IgG antibodies (6.21 and 9.11, respectively; cutoff, < 2). The patient was eventually weaned off vasopressors and extubated 7 days later, after diuresis. The patient continued to improve clinically and was eventually discharged home.

  • 1.

    HPS should be suspected in patients with rodent exposure and who present with vague viral prodromes, even outside of the southwestern United States.

  • 2.

    Transmission occurs through inhalation of aerosolized urine, feces, or saliva of the rodent host, and the largest risk factor is the entering of enclosed spaces with rodent infestation.

  • 3.

    Presumptive diagnosis can be made when a patient with known exposure has a nonspecific viral prodrome, pulmonary interstitial edema on imaging, with four of five of the following: hemoconcentration, thrombocytopenia, myelocytosis, absence of toxic granulation in neutrophils, and more than 10% immunoblasts on peripheral blood smear.

  • 4.

    Patients undergo serological confirmation, and treatment is largely supportive.

  • 5.

    Patients require ICU admission for monitoring, mechanical ventilation, vasoactive agents, and possibly extracorporeal mechanical oxygenation.

Financial/nonfinancial disclosures: None declared.

Other contributions:CHEST worked with the authors to ensure that the Journal policies on patient consent to report information were met.


Figure Jump LinkFigure 1 Chest radiograph, showing moderate bibasilar patchy opacities.Grahic Jump Location
Figure Jump LinkFigure 2 Chest CT scan without contrast, showing ground-glass alveolar opacities in both lungs with moderate bilateral pleural effusion.Grahic Jump Location


Table Graphic Jump Location
Table 1 Laboratory Work: Results

BNP = B-type natriuretic peptide.


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