Lymphoreticular and Hematopoetic Infections
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General Goal: To know the major cause(s) of  Hantavirus Pulmonary Syndrome, how it is transmitted, and the major manifestations of the disease.

Specific Educational Objectives: The student should be able to:

1. describe the common means of transmission of these diseases in general and for HPS.

3. describe the major manifestations of these diseases and for HPS.

4. describe the clinical case definition of HPS.

4. describe how you diagnose, treat and prevent HPS.

Reading: MEDICAL MICROBIOLOGY by P.R. Murray, K.S. Rosenthal, and M.A. Pfaller, 6th Edition. pp. 622-623.

Lecture: Dr. Neal R. Chamberlain


Hantavirus pulmonary syndrome is a relatively new disease reported in the U.S. The first cases of hantavirus pulmonary syndrome occurred in 1993 and were in the four- corner region of the United States in Arizona, Utah, Colorado, and New Mexico. This viral infection can cause significant pulmonary edema, and although relatively rare has a high mortality rate (35%).


The virus responsible for hantavirus pulmonary syndrome is a new-world hantavirus called Sin Nombre virus.


Sin Nombre virus causes cardiopulmonary signs and symptoms that have been called hantavirus pulmonary syndrome (Table Endo-2).



Portals of entry for the Sin Nombre virus include the respiratory and digestive tracts. Viral multiplication occurs in the endothelial cells. Viremia and fever occur 2–14 days after infection.

Viral antigens can be seen within the endothelium of capillaries throughout various tissues of the patient with hantavirus pulmonary syndrome. High concentrations of hantaviral antigens are seen in the pulmonary microvasculature and in follicular dendritic cells within the lymphoid follicles of the spleen and lymph nodes. Typical hantaviral inclusions are seen frequently in pulmonary endothelial cells. Antibodies produced to the hantaviral antigens damage the endothelial cells and increase capillary permeability. The increased capillary permeability in the lungs results in leakage of protein-rich plasma from the capillaries into the lungs and the pleura. This leakage causes the cardiopulmonary signs and symptoms detailed in Table Endo-2.


A clinical case definition has been developed for diagnosis of patients with hantavirus pulmonary syndrome and is described in Table Endo-3. The white blood cell count of patients with hantavirus pulmonary syndrome is usually elevated, with a marked left shift (bandemia). White blood cell precursors (band cells) may be as high as 50%, and atypical lymphocytes are frequently present. Atypical lymphocytes usually are observed at the onset of pulmonary edema. The platelet count in about 80% of individuals with hantavirus pulmonary syndrome is below 150,000. A dramatic decrease in the platelet count indicates a transition from the prodrome to the pulmonary edema phase (cardiopulmonary phase) of the illness. Early in the disease, chest radiographs show interstitial pulmonary edema, which progresses to alveolar edema with severe bilateral involvement. Pleural effusions are common and can be large enough to be observed in chest radiographs.

Therapy and Prevention

Treatment of hantavirus pulmonary syndrome involves supportive care. Improved sanitation standards and control of the rodent populations is important in preventing this disease.

Send comments and mail to Dr. Neal R. Chamberlain,
Revised 2/25/10
©2010 Neal R. Chamberlain, Ph.D., All rights reserved.

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