Bunyavirus diseases
المؤلف:
Stefan Riedel, Jeffery A. Hobden, Steve Miller, Stephen A. Morse, Timothy A. Mietzner, Barbara Detrick, Thomas G. Mitchell, Judy A. Sakanari, Peter Hotez, Rojelio Mejia
المصدر:
Jawetz, Melnick, & Adelberg’s Medical Microbiology
الجزء والصفحة:
28e , p572-574
2025-12-20
16
Hantaviruses are classified in the Hantavirus genus of the Bunyaviridae family. The viruses are found worldwide and cause two serious and often fatal human diseases: hemorrhagic fever with renal syndrome and HPS. It is estimated there are 100,000–200,000 cases of hantavirus infection annually worldwide. There are several distinct hantaviruses, each associated with a specific rodent host. The virus infections in rodents are lifelong and without deleterious effects. Transmission among rodents seems to occur horizontally, and transmission to humans occurs by inhaling aerosols of rodent excreta (urine, feces, saliva). The presence of hantavirus associated diseases is determined by the geographic distribution of the rodent reservoirs.
Hemorrhagic Fever with Renal Syndrome
Hemorrhagic fever with renal syndrome (HFRS) is an acute viral infection that causes an interstitial nephritis that can lead to acute renal insufficiency and renal failure in severe forms of the disease. Hantaan and Dobrava viruses cause the severe disease that occurs in Asia (particularly China, Russia, and Korea) and in Europe (primarily in the Balkans). Gener alized hemorrhage and shock may occur, with a case-fatality rate of 5–15%. A moderate form of HFRS caused by Seoul virus occurs throughout Eurasia. In a mild clinical form, called nephropathia epidemica, which is caused by Puumala virus and is prevalent in Scandinavia, the nephritis generally resolves without hemorrhagic complications and fatalities are rare (<1%).
Urban rats are known to be persistently infected with hantaviruses, and it has been suggested that rats on trading ships may have dispersed hantaviruses worldwide. Serosurveys indicated that brown Norway rats in the United States are infected with Seoul virus. Infected laboratory rats were proved to be sources of Hantaan outbreaks in scientific institutes in Europe and in Asia, but such infections have not been detected in laboratory rats raised in the United States. Hantavirus infections have occurred in persons whose occupations place them in contact with rats (eg, longshoremen).
HFRS is treated using supportive therapy. Prevention depends on rodent control and protection from exposure to rodent droppings and contaminated material.
Hantavirus Pulmonary Syndrome
In 1993, an outbreak of severe respiratory illness occurred in the United States, now designated the hantavirus pulmonary syndrome (HPS). It was found to be caused by a novel hantavirus (Sin Nombre virus). This agent was the first hantavirus recognized to cause disease in North America and the first to cause primarily an adult respiratory distress syndrome. Since that time, numerous hantaviruses have been detected in rodents in North, Central, and South America (see Table 1; Figure1).
Table1. Summary of Major Human Arbovirus and Rodent-Borne Virus Infections That Occur in the United States
Fig1. Geographic distribution of the New World hantaviruses paired to their unique rodent reservoirs (in italics). Hantaviruses known to be pathogenic are shown in red. (Reproduced with permission from MacNeil A, Nichol ST, Spiropoulou CF: Hantavirus pulmonary syndrome. Virus Res 2011;162:138. Copyright Elsevier.)
The deer mouse (Peromyscus maniculatus) is the primary rodent reservoir for Sin Nombre virus. Deer mice are widespread, and about 10% of those tested show evidence of infection with Sin Nombre virus. Other hantaviruses known to cause HPS in the United States include New York virus, Black Creek Canal virus, and Bayou virus, each having a different rodent host. HPS is more common in South America than in the United States. Andes virus is one causative hantavirus and is found in Argentina and in Chile. Choclo virus has been identified in Panama.
Infections with hantaviruses are not common, with relatively fewer subclinical infections, particularly with Sin Nombre virus. HPS is generally severe, with reported mortality rates of 30% or greater. This case-fatality rate is substantially higher than that of other hantavirus infections. The disease begins with fever, headache, and myalgia followed by rapidly progressive pulmonary edema, often leading to severe respiratory compromise. There are no signs of hemorrhage. Hantaviral antigens are detected in endothelial cells and macrophages in lung, heart, spleen, and lymph nodes. Pathogenesis of HPS involves the functional impairment of vascular endothelium. Person-to-person transmission of hantaviruses seldom occurs, although it has been observed during outbreaks of HPS caused by Andes virus.
Laboratory diagnosis depends on detection of viral nucleic acid by RT-PCR, detection of viral antigens in fixed tissues by immunohistochemistry, or detection of specific antibodies using recombinant proteins. An ELISA test to detect IgM antibodies may be used to diagnose acute infections. A fourfold rise in IgG antibody titer between acute and convalescent sera is diagnostic. IgG antibodies are long lasting. Isolation of hantaviruses is difficult and requires the use of containment facilities.
Current therapy for HPS consists of maintenance of adequate oxygenation and support of hemodynamic functioning.
The antiviral drug ribavirin is of some benefit as therapy in HPS. Preventive measures are based on rodent control and avoidance of contact with rodents and rodent droppings. Care must be taken to avoid inhaling aerosolized dried excreta when cleaning rodent-infested structures.
الاكثر قراءة في الفايروسات
اخر الاخبار
اخبار العتبة العباسية المقدسة
