Preventing HPS begins with keeping homes and surrounding areas clean, airing closed buildings before entering them, and cleaning with a disinfectant solutions.
Sage Memorial Hospital, Ganado, Ariz, is a private, not-for-profit facility entirely owned and operated by the Navajo Nation Health Foundation. It is located in northeastern Arizona, in a very small community in the middle of the Navajo reservation. In 1999, it celebrated 100 years of promoting health in the community. This 42-bed hospital provides services to 900 inpatients and 55,000 to 60,000 outpatients per year, with 98% to 99% of its patients being Native Americans.
In early to mid 1993, cases of unknown etiology were being reported in New Mexico among members of the Navajo Nation; patients presented with common symptoms such as respiratory failure, fever, and shock, which were found to be due to hantavirus pulmonary syndrome (HPS), a recently discovered infectious disease having both respiratory and systemic symptoms. By the end of 1993, 53 cases had been reported (from several states). Of all reported cases, nearly 60% occurred in males, with their average age being 37.1 By the end of 1995, there had been 123 cases reported from 23 states, with a 51% fatality rate.2 HPS can strike anyone, regardless of ethnicity; today, Native Americans account for 23% of cases.1
The HPS patients seen in 1993 had a factor in common: they all lived in rural areas. According to Navajo elders and medicine people, many unexplained deaths were reported from 1918 to 1933, when above-average rainfall led to larger-than-usual crops of piñon nuts (which, in turn, led to an increase in the rodent populations that fed on the nuts). In Native American folklore, there is also a saying to the effect that if mice are allowed in a dwelling, they will take away the childrens breath.
Hantavirus is thought to have been present for thousands of years, but it was actually identified during the Korean Conflict near Koreas Hantaan River. It was named the Hantaan virus, and later was classified as the hantavirus. During the 1993 outbreak, the virus was named Muerto Canyon (later changed to Sin Nombre) and the resulting disease was called HPS.
There are several known types of hantavirus, but the most prevalent is the Sin Nombre/Four Corners virus. Rodents appear to be the only natural hosts and vectors for HPS.
In the United States, the hantavirus is carried by the deer mouse (Peromyscus maniculatus), which is the primary host, and also by the cotton rat (Sigmodon hispidus). It is believed that, in the southwestern United States, 10% to 30% of deer mice are infected. Hantavirus, however, has also been identified in other rodents, including the white-footed mouse (P. leucopus) and the rice rat (Oryzomys palustris). These rodents are found in all parts of the United States. Infected animals are only vectors; they do not become ill, but are infected through the inhalation of ex-
creta or airborne saliva of hantavirus carriers. So far, the disease has not shown any indication that it is transmissible from person to person. Common pets, such as dogs and cats, are not known to carry the virus, although a human could come into contact with the virus if a pet catches infected rodents and brings them home.
Studies3 performed using subjects from occupational groups frequently in contact with rodents (eg, farm workers, utility workers, park-service workers, heating and plumbing contractors) showed no evidence of viral infection. The risk of infection is greater when the number of rodents in the home increases.
Hantaviruses have a diameter of 60 to 120 nm, and members of the hantavirus genus have been classified as part of the family of Bunyaviridae. They belong to a group of RNA virus, and are surrounded by a lipid capsule containing glycoprotein spikes that enclose a trisegmented genome. The site of initial infection is unknown, but hantavirus shows a preference for the pulmonary vasculature, thus explaining its respiratory manifestations.
The diagnosis of HPS cannot be based on a single pathognomonic lesion. In fact, the early symptoms of the disease may lead to misdiagnoses implicating other pulmonary pathologies. Precious time may be lost before HPS is recognized.
The lung tissues of HPS patients show heavy edema with serous fluid effusions and a marked increase in vascular permeability, while the respiratory epithelium remains intact. Airway distortion is seen in patients who survive the disease for a few days, and this is followed by a thickening of the alveolar septa due to an increased number of type I pneumocytes. There is no pneumocyte type II hyperplasia, but there are focal hyaline membranes. The pleural cavity is filled with yellow, serous fluid.
The first symptoms of HPS are similar to those of influenza or a severe cold with fever. Muscle aches in the shoulders, back, hips, and thighs are followed, a few hours later, by dizziness, headache, abdominal pain, vomiting, diarrhea, nausea, chills, tachypnea, and tachycardia. Upon auscultation, rales may be the only abnormality detected; they may indicate the onset of pulmonary edema (which is not cardiogenic in most HPS cases). After the first few days, as the disease progresses, the patient will develop cough, respiratory distress, respiratory difficulty that can be fatal in some cases (adult respiratory distress syndrome), and shock.
Laboratory findings indicate hypoxemia; platelet levels that are initially normal, but may decline later; mild proteinuria; initially normal white blood cell counts that can be followed by marked leukocytosis; prolonged prothrombin time; metabolic acidosis; and slightly elevated creatinine levels (usually >2.5 mg/dL). Detection of hantavirus immunoglobulin G (IgG) antibodies or hantavirus IgM in serum, increased aspartate aminotransferase, increased alanine transaminase, increased lactate dehydrogenase, increased hematocrit levels, and detection of a high viral load using the reverse transcriptase polymerase chain reaction test confirm the diagnosis.
In radiographic studies, hilar indistinctness is visible, with a marked interstitial edema, within a week of hospitalization. Kerley B lines are noted, and effusions are usually present.
For patients with HPS, arterial blood gas analyses show low Pao2 even when the fraction of inspired oxygen is high. Most patients require mechanical ventilation due to their severe hypoxemia. The most common cause of death in patients with HPS is cardiac dysrhythmia secondary to refractory hypotension and myocardial dysfunction.
Treatment of the patient with HPS includes supplemental oxygen administration via mechanical ventilation. Intravenous fluids should be given with caution (because of changes in vascular permeability), but the goal of reaching a pulmonary artery occlusion pressure of 12 to 15 mm Hg should be borne in mind. Extracorporeal membrane oxygenation has been tried for three patients who had very bad prognoses; it was successful. Broad-spectrum antibiotics should be given until HPS is confirmed. Another drug that is commonly used is ribavirin, which is delivered intravenously with good results.3 Inotropic agents are used to augment myocardial contractility, and it is important to maintain electrolyte balance and to monitor blood pressure carefully.
The pathogenesis of HPS is unclear, though hantavirus seems to exert a selective attraction of inflammatory cells to injured pulmonary epithelium (in this case, vascular).
It is important to remember that hantavirus is not transmitted from patient to patient, but via inhalation of particles carrying the virus. According to the Navajo Nation Hantavirus Project, HPS prevention starts with keeping homes and surrounding areas clean, airing closed buildings for at least an hour before entering them (in order to let out particles that may carry hantavirus), wearing dust masks and latex gloves when cleaning areas where rodents may live, trapping to get rid of rodents, and cleaning with a disinfectant solution. The best disinfectant for this purpose is one part chlorine bleach to 10 parts water. Hantavirus, once outside its host, cannot survive sunlight or use of detergents, or disinfectants such as chlorine and alcohol. After rodents are gone, the next step is to patch and seal holes in the building to prevent them from returning (although common house mice do not carry hantavirus).
In 1999, there were seven confirmed cases of hantavirus infection in New Mexico, with five resulting in death. Coconino County, Arizona, had one confirmed, nonlethal case in 1999. As of May 1999, 217 cases of HPS had been reported and confirmed in 30 states for the 6-year outbreak period.
The United States is not the only country with HPS cases. By the end of 1998, HPS had been confirmed in Argentina (approximately 200 cases), Brazil (14 cases), Chile (70 cases), Paraguay (more than 30 cases), and Uruguay (5 cases). It is presumed that hantavirus is also present in some countries in the Caribbean, but this has not yet been confirmed. N
Hector L. Bermudez, MD, CRT, is a member of the respiratory staff, Sage Memorial Hospital, Ganado, Ariz.
1. American Lung Association. Hantavirus Pulmonary Syndrome Fact Sheet. Available at: http://www.lungusa.org/diseases/hantavirus_factsheet.html. Accessed February 28, 2000.
2. Encarta Encyclopedia. Hantaviruses. Available at: http://www.encarta.msn.com/find/concise.asp?z=1&pt=2&ti=OAC94000. Accessed February 28, 2000.
3. Center for Disease Control and Prevention. All about Hantavirus. Available at: http://www.cdc.gob/ncidod/diseases/hanta/hps/noframes/phys/physindex.html. Accessed December 13, 1999.