Hantavirus Cardiopulmonary Syndrome Clinical Presentation
- Author: Juliet D Caldwell, MD; Chief Editor: Rick Kulkarni, MD more...
History
The clinical course of Hantavirus cardiopulmonary syndrome (HCPS) advances through several sequential stages.
Following exposure, an incubation period of about 3 weeks ensues. The aerosolized virus enters the lung, is taken up by local phagocytes, and is transported to local lymph nodes where it prepares to disseminate. The prodrome/febrile phase lasts 3-10 days and is marked by the onset of fever, chills, and myalgias, often severe, and is the likely clinical correlate to viral dissemination. It is nearly impossible to distinguish HCPS from any other nonspecific viral syndrome during this period. Disease severity progresses quickly, and patients often develop nausea, vomiting, weakness, and sometimes diarrhea and headache. Andes virus HCPS of South America differs slightly, presenting with facial flushing, fine petechiae, and conjunctivitis. Though rhinorrhea, pharyngitis, otalgia, and coryza are notably absent in most Hantavirus infections, a dry cough is common and often heralds sudden deterioration and progression to the cardiopulmonary phase of disease.[25]
The cardiopulmonary phase lasts anywhere from 2-7 days and presents with sudden respiratory distress and, often, cardiovascular collapse within hours of arrival to the hospital. This phase of the illness correlates with massive capillary leakage into the pulmonary vascular bed. Immune response always precedes the abrupt deterioration into the cardiovascular phase of disease supporting the hypothesis of an immune-mediated pathogenesis.[8] Clinical deterioration is precipitous and results in pulmonary edema, bronchorrhea, shock, and sometimes coagulopathy (Andes virus) and preterminal arrhythmias. Mean time from onset of first symptom to cardiopulmonary failure is 5 days. See the image below.
Clinical progression of hantavirus cardiopulmonary syndrome. Among survivors, recovery is nearly as rapid as decline and is often accompanied by a period of diuresis. During the convalescent period, the patient typically recovers with little or no residual deficits. Several months of fatigue and decreased exercise tolerance are often the only sequelae.
Early diagnosis is difficult because the common presenting symptoms of HCPS overlap with those of other, less ominous, viral illnesses. Risk factors for rodent exposure must be sought and are often the key to potential early diagnosis.
Consider diagnosis of HCPS in patients with the following:
- Fever
- Severe myalgias (often in the back and legs)
- Exposure to mice or mouse droppings
Other symptoms may include the following:
- Malaise
- GI symptoms such as nausea and vomiting, diarrhea, and abdominal pain
- Headache
- Cough
Risk factors to seek in the history include the following:
- Peridomestic rodent infestation
- Entering or disturbing seasonally closed or infrequently opened buildings
- Occupational exposure to rodents
Risk also varies with rodent abundance and distribution, which, in turn, depends on several factors, including the following:
- Geographic region (highest incidence in the Southwest United States)
- Seasonality (increased incidence in spring and summer)
- Weather patterns (Outbreaks may follow El Nino conditions of a temperate wet winter.)
The most common prodromal symptoms are the following:
- Fever
- Chills
- Myalgias (often in the back and legs)
Other common prodromal symptoms include the following:
- Nausea/vomiting
- Diarrhea
- Headache
- Cough (usually nonproductive)
- Malaise
- Dizziness
- Dyspnea (usually not observed at presentation but often heralds the cardiopulmonary phase of HCPS)
Consider another diagnosis with the following symptoms:
- Sore throat
- Rhinorrhea
- Conjunctivitis (except Andes virus)
- Rash (except Andes virus where petechiae are common)
- Coryza
- Otalgia
Physical
Physical findings vary substantially with the stage of disease at presentation.
The most frequent initial physical findings in Hantavirus cardiopulmonary syndrome (HCPS) are as follows:
- Tachypnea
- Fever
- Tachycardia
Crackles or decreased breath sounds are noted in most patients on lung examination.
Abdominal tenderness is present in about 10% of patients and may be severe. One patient underwent an exploratory laparotomy before HCPS was recognized.
Petechiae is not observed despite thrombocytopenia (except Andes virus).
Hallmarks of the cardiopulmonary phase of HCPS include the following:
- Hypotension
- Respiratory distress with bilateral alveolar infiltrates on radiograph
Causes
In the United States, Hantavirus cardiopulmonary syndrome (HCPS) is primarily caused by the Sin Nombre virus (SNV) and is transmitted via inhalation of aerosolized virus from dried rodent excreta (see Background and Pathophysiology).
The vector of SNV is the deer mouse, P maniculatus. SNV causes no obvious harm to mice, and they therefore never develop immunity. Infected rodents thereby become chronic, persistent viral shedders.
The incidence of HCPS closely parallels the distribution and number of infected deer mice in a geographic area.[8] Deer mouse populations are influenced by specific environmental conditions.
The El Nino conditions present during the 1993 Navajo outbreak increased the number of deer mice seen that year. The wet and mild conditions encouraged an unusually high population of pinons, a favorite source of food for mice. This, in turn, allowed for a 10-fold increase in the number of deer mice found that year in the Four Corners region of the United States.
Because of horizontal viral transmission via intra-rodent aggressive behaviors such as biting, high rodent density also increases the percentage of mice infected.[8] Thirty percent of deer mice in the Four Corners region tested positive for SNV in the 1993 outbreak.
All agree that some type of rodent exposure, whether occupational or sporadic, is the greatest risk factor for contracting Hantavirus. Some controversy exists as to whether occupational exposure on farms or in laboratories is as great a risk factor as sporadically entering rarely opened or seasonally closed rodent-infested buildings.[10, 26, 11]
Occupations at greatest risk for exposure are as follows:
- Grain farmers
- Agricultural workers
- Feedlot employees
- Field biologists
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