Printer Friendly

Hantaviruses: An Overview And Radiographic Correlation.

In 1993 an outbreak of acute febrile illness was reported in the southwestern United States.[1] The affected patients came from rural areas of the Four Corners region that includes New Mexico, Arizona, Utah and Colorado.

In May of that year, the New Mexico Office of the Medical Investigator was notified of the unexplained deaths of a couple living in the same household -- a 21-year-old woman and a 19-year-old man who died within 5 days of each other.

The Indian Health Service also documented 5 deaths with similar symptoms occurring in a period of less than 3 weeks prior to May 17, 1993. The patients were described as having unexplained Adult Respiratory Distress Syndrome (ARDS). They also were listed as having acute bilateral pulmonary interstitial infiltrates in the initial and subsequent stages of the disease. Autopsy findings and laboratory tests did not indicate any known cause of this acute respiratory illness and septic shock. Reports of this outbreak led to collaborative efforts among clinicians, epidemiologists, biologists, public health educators and researchers in the search for a cause.[1-3]

This article outlines historical perspectives on these viral illnesses, clinical signs and symptoms, radiographic presentation, methods of treatment and ways to prevent infection. Radiologic technologists need to understand that rapid changes in the lung fields may be a sign of these types of viral infections and a patient's radiographs should be viewed by physicians as quickly as possible.

Historical Perspectives

Hantaviruses have been linked to Hemorrhagic Fever with Renal Syndrome (HFRS) and Hantavirus Pulmonary Syndrome (HPS). According to Hjelle[4,5] both diseases are transmitted by rodent vectors -- the HFRS virus is carried by Old World rodents and the HPS virus is carried by New World rodents. Although each virus appears to have a preferred rodent host, other small mammals can be infected as well. The rodent family associated with the spread of the disease in this country includes deer mice, white-footed mice, cotton rats and harvest mice. The Seoul virus, found in the commensal rat, occurs in many cities throughout the world.

Although the disease did not appear in Western medicine until the 1950s, historical evidence indicates that outbreaks of HRFS occurred for at least hundreds of years in Asia.[5] Outbreaks of the disease also have been reported in Canada, Brazil, Paraguay, Argentina, Norway and northern Europe.[6] Butler et al[1] and Marshall[6] reported the emergence of the hantaviral disease beginning in 1951, when American troops stationed in Korea were stricken by an unexplained and unfamiliar disease. Patients were afflicted with fever, chills and myalgia, followed by hemorrhagic manifestations such as gastrointestinal bleeding, subconjunctival hemorrhage and petechiae. Marshall[6] further noted that the disease progressed to acute renal failure, shock and pulmonary edema. In a 3-year period, approximately 3000 troops were diagnosed with Korean Hemorrhagic Fever with Renal Syndrome, with approximately 10% of the patients dying from complications. During this period, Western virologists began to realize that similar hemorrhagic fevers were prevalent outside southeast Asia. Illnesses discovered in Russia, China, Scandinavia, Brazil, Paraguay and Argentina all paralleled the cases treated in Korea.

It was not until 1976 that scientists were successful in isolating the agent in the tissue of the suspected rodent host captured near the Hantaan River in South Korea.[6] Since then, numerous related Hantaan viruses have been documented. According to Hjelle et al,[7] names of these viruses include Seoul, Puumala, Prospect Hill, Hantaan, Belgrade, Thottapalayam, Tchoupitoulas, Thailand and the Sin Nombre or Convict Creek. The latter virus also has been designated the Four Corners Virus (FCV) and the illness caused by FCV is now known as Hantavirus Pulmonary Syndrome (HPS). The host for this virus was found to be the deer mouse, peromyscus maniculatus.

In 1982 the Prospect Hill virus was isolated in Frederick, Md, and cases of infected rodents were reported from numerous cities throughout the United States. Studies conducted in Baltimore during this period revealed a widespread distribution of the Hantaan virus among rodents captured from 12 study sites, including both rural and residential locations.[8] In 1985 researchers located the Tchoupitoulas virus in New Orleans, the Puumala stereotypes in Sweden and similar viruses in infected rats throughout the United States.[6]

Transmission of the Virus

Hantaviruses are lipid-enveloped, trisegmented, single-stranded RNA viruses of the family Bunyavirdae. Each virus maintains its existence by infecting a single rodent species. The infections in the host are asymptomatic throughout life and spread through the saliva, urine and feces for many weeks following infection. Transmission of the viruses to humans is thought to occur after inhalation of dust particles laden with excreta from infected rodents, with some infections being related to rodent bites. The incubation period for human infections averages from 12 to 16 days, with a range of 4 to 42 days.[1] Hjelle[5] also notes that infection usually occurs after inhaling the excreta when sweeping floors or shaking rugs, especially in poorly ventilated closed spaces such as outdoor buildings, barns or storage sheds. The author further reports that no known cases of human-to-human transmission have been reported in the United States.

Disease Phases

HFRS caused by the Hantaan virus has an abrupt onset and progresses through 5 distinct clinical phases, though in mild cases the individual phases may not be discernible.[1] In the febrile phase, the patient experiences headaches, abdominal and lumbar pain, facial flushing and widespread petechiae. The hypotensive phase begins after 3 to 5 days; during this phase shock and associated low cardiac output and increased systemic vascular resistance occur. In the third, oliguric phase, hypertension may develop due to diminished urine formation. During these first 3 phases, hemorrhagic complications may be evident. The fourth, diuretic phase, develops as renal failure in which hemorrhagic manifestations and electrolyte imbalances often are noted. Respiratory distress and pulmonary edema have been reported for a small portion of HFRS patients.

HPS begins with an initial or prodromal phase that usually lasts 3 to 6 days. Fever and myalgia are universal features but respiratory complications usually are absent in this phase. Nausea, vomiting and abdominal pain are common and often severe enough to result in admission to a hospital. Physical findings, laboratory results and chest radiographs may be normal at this stage. HPS may be mistaken for influenza or aseptic meningitis, except that sore throats, coryza (inflammation of the nasal membranes) and meningism (irritation of the brain and spinal cord) are not common in HPS patients.[1] In cases studied at the University of New Mexico's Medical Center, patients with HPS could be distinguished from those with septicemic shock by the high systemic vascular resistance and decreased cardiac index.[7]

The second phase is the cardiopulmonary phase, which involves a progressive cough and shortness of breath. Common physical findings include tachypnea, tachycardia, fever and hypotension. Tachypnea may be evident before a positive chest radiograph is demonstrated. During this phase, patients may require intubation and mechanical ventilation for management of progressive hypoxemia. The third, convalescent phase reveals improved respiratory and hemodynamic functions. In this stage, many patients can be weaned from ventilators in a matter of days and diuresis occurs. Patients who survive this respiratory phase of HPS recover completely.[1]

Radiographic Findings

Data collected from known cases of HFRS and HPS revealed the following findings, as reported by Butler and Peters[1] and shown in Figures 1, 2 and 3.

[Figures 1-3 ILLUSTRATION OMITTED]

* In the initials phases for HFRS and HPS, chest radiographs for most patients were normal.

* Patients' chest radiographs obtained within the first 48 hours after admission demonstrated evidence of interstitial edema, Kerleys B lines, hilar indistinctness or peribronchial cuffing.

* In some cases, extensive bibasilar or perihilar airspace disease was present.

* Pleural effusions were evident in a small percentage of patients upon admission, with this becoming radiographically evident for others after 48 hours.

* Cardiomegaly was not evident in these patients.

In the Four Comers region outbreak of this disease in 1993, 14 of the 18 confirmed cases resulted in death. Radiographic findings included the following:

* Initial radiographs in 11 cases showed interstitial and alveolar infiltrates, fluffy alveolar infiltrates in 2 cases and no abnormalities in 4 cases.

* A rapid progression to bilateral, diffuse infiltrates occurred in 16 cases, and 1 patient had interstitial infiltrates confined to the lower lobes.

* Pulmonary effusions occurred in 4 of the patients.

* Progressive pulmonary edema and hypoxia requiring intubation and ventilation occurred in 15 of the cases within 24 hours of admission.[2]

Although many of these radiographic manifestations are similar to ARDS, there are some differences that may assist in a differential diagnosis. For example, in HPS and HFRS, pulmonary effusions often are evident, but in ARDS this rarely occurs.

Treatment

The basic treatment for HPS and HFRS is aggressive supportive care. Pressor agents and inotropic agents that support blood pressure and adequate cardiac output are important.[2,7] The antiviral drug Ribavirin has been used experimentally and has decreased the mortality rate when administered early in the disease process.[2] Intubation with mechanical ventilation is necessary in cases of severe pulmonary edema and hypoxia. Currently, there are no effective vaccines against the New World viruses, but a promising vaccine has been developed for use against the viruses common in China.[5]

Research and Public Education

Medical investigators involved in the southwestern outbreak were able to identify the Hantaan virus as the cause of the deaths by 3 primary methods:

* The development of modern molecular techniques, such as the polymerase chain reaction, which allowed the amplification of previously undescribed hantavirus in autopsied victims.[4]

* The existing library of viral genetic information at the Department of Defense.

* The swift action taken by the medical investigators at the start of the outbreak. Scientists are developing coherent and effective health education programs to decrease human contact with rodents.[10]

Prevention and Precautions

The Centers for Disease Control and Prevention recommend the following steps to prevent transmission of the disease:

* Controlling rodent population.

* Wearing masks, gloves and protective clothing during clean up of rodent-contaminated areas.

* Spraying areas of contamination with a disinfectant solution (eg, dilute hypochlorite solutions, ethyl alcohol [70%] or most general-purpose household disinfectants).

* Using universal precautions when treating patients in the acute stages of the disease; respiratory precautions should be included if respiratory droplets or other modes of aerosol transmission are likely.

Role of the Technologist

Radiologic technologists often are involved in the assessment and treatment of patients experiencing the initial stages of HPS or HFRS. Careful evaluation of a patient's condition should be completed prior to performing any radiographic procedure. Thorough documentation of a patient's history may provide the interpreting physician with added insight into the etiology of the patient's disease process. Knowledge of the patient's activities prior to the onset of illness also may provide clues that lead to diagnosis. While obtaining a clinical history, the technologist should note what activities the patient was involved in recently, such as camping or cleaning cupboards, garages, sheds or any outdoor structures, especially those with poor ventilation. Inhalation of infectious particles can occur whenever rodent droppings are disturbed.

Changes occurring on chest radiographs during the first 48 hours of treatment also are key indicators for the clinician to evaluate and compare to the clinical history. In many cases, the initial chest radiograph was normal, but within a few hours, follow-up radiographs demonstrated a rapid progression of bilateral infiltrates and Kerley B lines. Comparison between current and previous chest radiographs is critical in the treatment of patients infected with the Hantaan virus. Technologists often are first to view a patient's radiographs, while an attending physician may not look at the radiographs for some time. Therefore, if rapid changes are seen on the radiographs, the attending physician and nursing personnel should be notified as quickly as possible. Consistency in technical factors on successive chest radiographs also is important in facilitating an accurate interpretation as the disease progresses.

As with ARDS, the signs and symptoms of these disease processes may include dyspnea, hypoxemia and increased respiratory effort. The radiologic technologist should document all clinical signs and should look for any changes in a patient's condition each time a procedure is performed.

Summary

The radiographic manifestations of HPS and HFRS are similar to other disease processes, such at ARDS. Therefore, a comprehensive assessment of clinical symptoms, radiographic manifestations and laboratory values may be the only way to differentiate these 2 processes from those that occur more often. As more information becomes available about these and other emerging viruses, an accurate diagnosis may be possible in a shorter time. Recent outbreaks of the disease resulted in death for a significant number of patients, but through the research of health care professionals, data banks now are available that will facilitate assessment and treatment in the future.

References

[1.] Butler JC, Peters CJ. Hantaviruses and hantavirus pulmonary syndrome. Clin Infect Dis. 1994;19:387-395.

[2.] Duchin JS, Koster FT, Peters CJ. Hantavirus pulmonary syndrome: a clinical description of 17 patients with a newly recognized disease. N Engl J Med. 1994;330:949-955.

[3.] Nichols ST, Spiropoulou CF, Morzunov S. Genetic identification of a hantavirus associated with an outbreak of acute respiratory illness. Science. 1993;262:914-917.

[4.] Hjelle B. Hantaviruses, with emphasis on Four Corners hantavirus. Available at: http://www.blocklabs. wisc.edu/ed/hanta.html. Accessed July 7, 1997.

[5.] Hjelle B. Frequently asked questions about hantavirus pulmonary syndrome and hemorrhagic fever with renal syndrome. Available at: http://www.outbreak. org/cgiunreg/dynaserve.exe/hantavirus/faq.html. Accessed May 5, 1997.

[6.] Marshall E. Hantavirus outbreak yields to PCR. Science. 1993;262:832-836.

[7.] Hjelle B, Jenison S, Mertz G, Koster F, Foucar K. Emergence of hantaviral disease in the southwestern United States. West J Med. 1994;161:467-473.

[8.] Childs JE, Korch GW, Glass GE, LeDuc JW, Shah K. Epizootiology of hantavirus infections in Baltimore: isolation of a virus from Norway rats and characteristics of infected rat populations. Am J Epidemiol. 1987;126(1) :55-67.

[9.] Centers for Disease Control and Prevention. Hantavirus Illness in the United States. Available at: http:// main.street.net/hantavirus.html. Accessed July 21, 1997.

[10.] Kreeger KY. One year later, the hantavirus investigation continues. Available at: http://www.uct.acza/ microbiology/newhanta.html. Accessed May 5, 1997.

Virginia Vanderford, M. Ed., R. T. (R)(M), is assistant professor of radiologic sciences at Weber State University in Ogden, Utah.
COPYRIGHT 1999 American Society of Radiologic Technologists
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 1999 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Author:VANDERFORD, VIRGINIA
Publication:Radiologic Technology
Geographic Code:1USA
Date:Mar 1, 1999
Words:2390
Previous Article:Diagnosis and Treatment Of Esophageal Strictures.
Next Article:Trends in Numbers of R.T.s.
Topics:

Terms of use | Privacy policy | Copyright © 2018 Farlex, Inc. | Feedback | For webmasters