Clinical Signs and Symptoms

Patients initially present with a nonspecific febrile illness. In addition, fever, muscle aches, headache, chills, dizziness, non-productive cough, nausea, and vomiting are noted. In about half of the patients malaise, diarrhea, and light-headedness are reported. Patients may report shortness of breath. Less frequent reports of arthralgias, back pain, and abdominal pain are noted. Cough and tachypnea develop around day seven. Once the cardiopulmonary phase develops, the disease progresses rapidly (53,54).

Laboratory findings include an elevated white cell count with a marked left shift of the myeloid cells. Atypical lymphocytes are frequently present. In the majority of cases, the platelet count is low. A rapid fall in the platelet count may herald the development of a pulmonary edema phase. The hematocrit may be elevated in about 50% of the cases. In severe cases of HPS, disseminated intravenous coagulation may occur, but this is rare. Proteinuria, mild elevation of liver enzymes, amylase, CPK, and creatinine has been reported. Within 24 hours of initial evaluation, hypotension and progressive evidence of pulmonary edema and hypoxia occur (53,54).

HPS has a characteristic radiologic evolution that begins with minimal changes of interstitial pulmonary edema progressing to alveolar edema with severe bilateral involvement. Pleural effusions are common (53).

HPS has been reported during pregnancy. Symptoms and signs, physical findings, and laboratory values were similar to nonpregnant patients, although fever was lower. No evidence of transplacental transmission was found (54).

Histologic evaluation of infected tissue show that viral antigens are distributed primarily within the endothelium of capillaries throughout various tissues. Histopatholgic lesions are mainly seen in the lungs and spleen. Immune complexes have been detected in the sera and may be responsible for the increased capillary permeability, vascular injury, platelet lysis, and kidney damage. Individuals with HLA-B*3501 have an increased risk of developing severe HPS, suggesting that CD8(+) T cell responses contribute to pathogenesis (55,56).

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