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Viral Causes of Hearing Loss: A Review for Hearing Health Professionals
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Abstract
A number of viral infections can cause hearing loss. Hearing loss induced by these viruses can be congenital or acquired, unilateral or bilateral. Certain viral infections can directly damage inner ear structures, others can induce inflammatory responses which then cause this damage, and still others can increase susceptibility or bacterial or fungal infection, leading to hearing loss. Typically, virus-induced hearing loss is sensorineural, although conductive and mixed hearing losses can be seen following infection with certain viruses. Occasionally, recovery of hearing after these infections can occur spontaneously. Most importantly, some of these viral infections can be prevented or treated. For many of these viruses, guidelines for their treatment or prevention have recently been revised. In this review, we outline many of the viruses that cause hearing loss, their epidemiology, course, prevention, and treatment.
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Most cited references134
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Epidemiology and Transmission Dynamics of West Nile Virus Disease
Edward B. Hayes, Nicholas Komar, Roger Nasci … (2005)
West Nile virus (WNV) was first detected in the Western Hemisphere in 1999 during an outbreak of encephalitis in New York City. Over the next 5 years, the virus spread across the continental United States as well as north into Canada, and southward into the Caribbean Islands and Latin America (1). This article highlights new information about the epidemiology and transmission dynamics of human WNV disease obtained over the past 5 years of intensified research. Epidemiology WNV is transmitted primarily by the bite of infected mosquitoes that acquire the virus by feeding on infected birds. The intensity of transmission to humans is dependent on abundance and feeding patterns of infected mosquitoes and on local ecology and behavior that influence human exposure to mosquitoes. Although up to 55% of affected populations became infected during epidemics in Africa, more recent outbreaks in Europe and North America have yielded much lower attack rates (1,2). In the area of most intense WNV transmission in Queens, New York, in 1999, ≈2.6% of residents were infected (most of these were asymptomatic infections), and similarly low prevalence of infection has been seen in other areas of the United States (3,4). WNV outbreaks in Europe and the Middle East since 1995 appear to have caused infection in 1,000 potentially WNV-viremic blood donations were identified, and the corresponding blood components were sequestered. Nevertheless, 6 WNV cases due to transfusion were documented in 2003, and at least 1 was documented in 2004, indicating that infectious blood components with low concentrations of WNV may escape current screening tests (19). One instance of possible WNV transmission through dialysis has been reported (20). WNV transmission through organ transplantation was also first described during the 2002 epidemic (15). Chronically immunosuppressed organ transplant patients appear to have an increased risk for severe WNV disease, even after mosquito-acquired infection (16). During 2002, the estimated risk of neuroinvasive WNV disease in solid organ transplant patients in Toronto, Canada, was approximately 40 times greater than in the general population (16). Whether other immunosuppressed or immunocompromised patients are at increased risk for severe WNV disease is uncertain, but severe WNV disease has been described among immunocompromised patients. WNV infection has been occupationally acquired by laboratory workers through percutaneous inoculation and possibly through aerosol exposure (21,22). An outbreak of WNV disease among turkey handlers at a turkey farm raised the possibility of aerosol exposure (17). Dynamics of Transmission: Vectors WNV is transmitted primarily by Culex mosquitoes, but other genera may also be vectors (23). In Europe and Africa, the principal vectors are Cx. pipiens, Cx. univittatus, and Cx. antennatus, and in India, species of the Cx. vishnui complex (6,24). In Australia, Kunjin virus is transmitted primarily by Cx. annulirostris (11). In North America, WNV has been found in 59 different mosquito species with diverse ecology and behavior; however, 40%. Field studies during and after WNV outbreaks in several areas of the United States have confirmed that house sparrows were abundant and frequently infected with WNV, characteristics that would allow them to serve as important amplifying hosts (23,25,37). The importance of birds in dispersing WNV remains speculative. Local movements of resident, nonmigratory birds and long-range travel of migratory birds may both contribute to the spread of WNV (38,39). Although WNV was isolated from rodents in Nigeria and a bat in India, most mammals do not appear to generate viremia levels of sufficient titer to contribute to transmission (24,40–42). Three reptilian and 1 amphibian species (red-ear slider, garter snake, green iguana, and North American bullfrog) were found to be incompetent as amplifying hosts of a North American WNV strain, and no signs of illness developed in these animals (43). Viremia levels of sufficient titer to infect mosquitoes were found after experimental infection of young alligators (Alligator mississippiensis) (44). In Russia, the lake frog (Rana ridibunda) appears to be a competent reservoir (45). Nonmosquitoborne WNV transmission has been observed or strongly suspected among farmed alligators, domestic turkeys in Wisconsin, and domestic geese in Canada (17,46,47). Transmission through close contact has been confirmed in both birds and alligators in laboratory conditions but has yet to be documented in wild vertebrate populations (23,36,44). Control of WNV Transmission Avoiding human exposure to WNV-infected mosquitoes remains the cornerstone for preventing WNV disease. Source reduction, application of larvicides, and targeted spraying of pesticides to kill adult mosquitoes can reduce the abundance of mosquitoes, but demonstrating their impact on the incidence of human WNV disease is challenging because of the difficulty in accounting for all determinants of mosquito abundance and human exposure. One study indicated that clustering of human WNV disease in Chicago varied between mosquito abatement districts, suggesting that mosquito control may have some impact on transmission to humans (14). Persons in WNV-endemic areas should wear insect repellent on skin and clothes when exposed to mosquitoes and avoid being outdoors during dusk to dawn when mosquito vectors of WNV are abundant. Of insect repellents recommended for use on skin, those containing N,N-diethyl-m-toluamide (DEET), picaridin (KBR-3023), or oil of lemon eucalyptus (p-menthane-3,8 diol) provide long-lasting protection (48). Both DEET and permethrin provide effective protection against mosquitoes when applied to clothing. Persons' willingness to use DEET as a repellent appears to be influenced primarily by their level of concern about being bitten by mosquitoes and by their concern that DEET may be harmful to health, despite its good safety record (49). To prevent transmission of WNV through blood transfusion, blood donations in WNV-endemic areas should be screened by using nucleic acid amplification tests. Screening of organ donors for WNV infection has not been universally implemented because of concern about rejecting essential organs after false-positive screening results (50). Pregnant women should avoid exposure to mosquito bites to reduce the risk for intrauterine WNV transmission. Future Directions WNV disease will likely continue to be a public health concern for the foreseeable future; the virus has become established in a broad range of ecologic settings and is transmitted by a relatively large number of mosquito species. WNV will also likely continue to spread into Central and South America, but the public health implications of this spread remain uncertain. Observations thus far in North America indicate that circulation of other flaviviruses, such as dengue, viral mutation, and differing ecologic conditions may yield different clinical manifestations and transmission dynamics. Over the next few years, research efforts might well be focused in several areas. Research into new methods to reduce human exposure to mosquitoes is crucial and can help prevent other mosquitoborne illnesses. This should include development of new methods to reduce mosquito abundance, development of new repellents, and behavioral research to enhance the use of existing effective repellents and other personal protective measures against mosquito bites. A better understanding of the dynamics of nonmosquitoborne transmission is essential to prevent disease among infants of infected mothers and recipients of blood transfusions and transplanted organs. Currently available prevention strategies such as the dissemination of knowledge and products for personal protection from mosquito exposure and the application of existing techniques for reducing mosquito abundance in communities at risk of WNV transmission need to be vigorously implemented. National and international surveillance for WNV transmission will be important to monitor spread of the virus and the effect of control strategies. Finally, further research into the ecologic determinants of WNV transmission, including climatic factors and dynamics of reservoir and vector populations, could help in determining geographic areas of higher risk for WNV disease.
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Herpes simplex virus infections.
Richard J. Whitley, Bernard Roizman (2001)
Herpes simplex virus (HSV) is a member of the herpesviridae family. Recognised since ancient Greek times, the virus frequently infects human beings, causing a range of diseases from mild uncomplicated mucocutaneous infection to those that are life threatening. In the past 50 years, substantial advances in our knowledge of the molecular biology of HSV have led to insights into disease pathogenesis and management. This review provides a contemporary interpretation of the biological properties, function, epidemiology, and treatment of HSV diseases.
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Virology, Pathology, and Clinical Manifestations of West Nile Virus Disease
Edward B. Hayes, James J. Sejvar, Sherif R. Zaki … (2005)
The impressive spread of West Nile virus (WNV) in the Western Hemisphere after its detection in 1999 during an outbreak of encephalitis in New York City has caused >16,000 human disease cases and >660 deaths in North America. Research on the signs, symptoms, and pathogenesis of WNV disease has greatly intensified in the past 5 years. The number of recognized cases of flaccid paralysis due to WNV infection has increased substantially, and research into prognosis and possible therapy has expanded. Genetic variation of the virus has been further characterized and continues to be explored. The pathology and pathogenesis of WNV disease have been described more completely than ever before. Several strategies are being pursued to develop effective vaccines to prevent WNV disease. This article highlights new information about the virology, clinical manifestations, laboratory diagnosis, pathology, and prognosis of WNV illness in humans. The expanded knowledge about WNV disease provides a new platform for future development of diagnostic tests, therapy, and vaccine development. Characteristics of West Nile Virus WNV is an arbovirus in the family Flaviridae. Its spherical, enveloped capsid has a diameter of ≈50 nm and contains single-stranded RNA that encodes the capsid (C), envelope (E), and premembrane (prM) proteins, as well as 7 nonstructural proteins that likely contribute to viral replication. The virus has 2 genetic lineages: lineage 1 strains are found in North America, Europe, Africa, Asia, and Australia; lineage 2 strains have been isolated only in sub-Saharan Africa and Madagascar. Lineage 1 strains have been further divided into 4 clades: Kunjin, Indian, A, and B (which includes an Indian isolate) (1). The isolates in clade B, which includes strains from the United States, are all virulent in mice; lineage 2 and other clades in lineage 1 comprise both virulent and attenuated strains (1). Differences in pathogenicity may be related to nucleotides that code for specific regions in the prM, E, or nonstructural proteins of the virus (1,2). WNV strains from the United States are closely related to strains from Israel, with 99.7% homology in nucleotide sequences, indicating that the strains in the United States almost certainly originated from the Middle East (3). The strain isolated in New York in 1999 is more virulent in American crows (Corvus brachyrynchos) than strains from Kenya and Australia (Kunjin virus, a subtype of WNV), and both the New York strain and the Kenyan strain experimentally killed house sparrows whereas the Australian strain did not (4). Two genetic variants of the North American WNV strain were isolated in Texas in 2002; the major variant differed from the New York 1999 isolate by 0.18% of nucleotides, and the minor variant by 0.35% (1). The 2 variants differed from each other by 0.5% of nucleotides, and their neuroinvasiveness in mice was similar to that of the New York 1999 isolate. In 2003, attenuated WNV strains were found in birds in Texas and Mexico, providing the first evidence of phenotypic variation of WNV strains in the Western Hemisphere (2,5). The reduced neuroinvasiveness and smaller plaque size of the Texas strains may be due to mutations in nonstructural proteins that result in lower levels of viremia; the attenuated strain from Mexico had a mutation in the E protein (2,5). Pathogenesis WNV is thought to replicate at the site of inoculation and then spread to lymph nodes and the bloodstream (6). Viral penetration of the central nervous system appears to follow stimulation of toll-like receptors and increased levels of tumor necrosis factor-α, which increases permeability of the blood-brain barrier (7). WNV directly infects neurons, particularly in deep nuclei and gray matter of the brain, brainstem, and spinal cord (8–10). Collateral destruction of bystander nerve cells may contribute to paralysis (11). Immune-mediated tissue damage may also contribute to pathologic changes in some cases (12). Genetic susceptibility for severe disease in mice has been postulated to involve a deficiency in production of 2´–5´-oligoadenylate synthetase, but this genetic susceptibility has not been elucidated in humans (10). Although most nonfatal WNV infections appear to be cleared by the host immune response, the virus may persist in some vertebrate hosts (10,13). Clinical Manifestations The clinical spectrum of symptomatic WNV infection in humans has been further defined during the North American epidemics. About 80% of human infections are apparently asymptomatic (14). Of those persons in whom symptoms develop, most have self-limited West Nile fever (WNF), characterized by the acute onset of fever, headache, fatigue, malaise, muscle pain, and weakness; gastrointestinal symptoms and a transient macular rash on the trunk and extremities are sometimes reported (15,16). A recent follow-up study of WNF patients who sought medical attention found that difficulty concentrating and neck pain or stiffness were also prominent symptoms, and that fatigue and muscle weakness frequently lasted for ≈1 month after onset (16). Of the 98 patients interviewed, 31% were hospitalized, 79% missed school or work because of their illness, and the median time before patients felt fully recovered was 60 days. These patients probably represent the most severe WNF, but even without neurologic manifestations, WNV infection clearly can cause a notable public health problem, Additional nonneurologic clinical manifestations that may rarely occur during WNV infection include hepatitis, pancreatitis, myocarditis, rhabdomyolysis, orchitis, and ocular manifestations (17–24). Chorioretinitis may be more common than previously thought; a study in Tunisia found that 69% of 29 patients hospitalized with WNV disease had chorioretinitis (24). Cardiac dysrhythmias have been observed in some North American patients (Centers for Disease Control and Prevention [CDC], unpub. data) (22). Neuroinvasive disease develops in 4-fold higher than titers to other epidemiologically relevant flaviviruses included in the assay. However, PRNT may not discriminate between WNV infection and other flaviviral infections in patients with previous flavivirus exposure, because the neutralizing antibody in such cases may broadly cross-react to several related flaviviruses. WNV infection can also be diagnosed by detecting virus in CSF, serum, or tissues by isolation or nucleic acid amplification tests (NATs). WNV is best isolated in cell culture or suckling mice and identified by indirect immunofluorescence assay with specific monoclonal antibodies or by reverse transcriptase–polymerase chain reaction (RT-PCR). However, WNV is rarely isolated from the blood of patients with neuroinvasive WNV disease because viremia levels are typically low or absent by the time neurologic symptoms develop. Real-time RT-PCR and nucleic acid sequence-based amplification are the most sensitive NATs, able to detect ≥50 viral RNA copies per mL (≈0.1 PFU/mL), which is ≈1,000-fold more sensitive than culture (39). WNV can be detected in serum by NAT if the specimen is obtained early in infection and is readily detected by NAT, isolation, or IHC staining in brain tissue from persons with fatal cases. The sensitivity of RT-PCR among 28 patients with serologically confirmed neuroinvasive WNV disease was 57% in CSF and 14% in serum (40). The diagnosis of WNV encephalitis can be supported histopathologically, and there is no pathognomonic lesion. Differential diagnoses include arboviral and other viral encephalitides, rickettsial infections, and various noninfectious diseases. When serum samples and frozen tissues are not available, IHC testing of formalin-fixed tissues with specific monoclonal and polyclonal antibodies is particularly useful. Prognosis The clinical course of WNF ranges from a mild febrile illness of several days' duration to debilitating fatigue, aching, and weakness that may last for weeks or months (16,29,41). Although cases of meningitis without alteration of the patient's mental status or other focal neurologic features have a favorable prognosis, persistent headaches and fatigue may be reported (29). Patients with WNV encephalitis or focal neurologic manifestations often have persistent neurologic deficits for months or years (28,29). Of 35 patients hospitalized with WNV disease in New York, only 13 (37%) reported full recovery in physical, cognitive, and functional abilities 12 months after illness onset (41). Many patients with WNV-associated poliomyelitislike syndrome do not recover, but some improvement in limb strength may occur over time (42,43). The overall case-fatality rate for neuroinvasive WNV disease is ≈9% (26). Clinical Management Management of severe WNV illness remains supportive. Patients with severe meningeal symptoms often require pain control for headaches and antiemetic therapy and rehydration for associated nausea and vomiting. Patients with severe encephalitis should be observed for development of elevated intracranial pressure and seizures, and patients with encephalitis or paralysis must be monitored for inability to protect the airway. Acute neuromuscular respiratory failure may develop rapidly, particularly in patients with prominent bulbar signs; prolonged ventilatory support may be required (22,30,34). Ribavirin, interferon-α, WNV-specific immunoglobulin, and antisense gene–targeted compounds have all been considered as specific treatments for WNV disease, but no rigorously conducted clinical trials have been completed. Nonspecific immunoglobulin and plasmapheresis should be considered for patients with Guillain-Barré syndrome but are not indicated for patients with paralysis due to damage of anterior horn cells (30). Vaccine Development Two vaccines are available for vaccinating equines: an inactivated WNV vaccine and a recombinant vaccine that uses canarypox virus to express WNV antigens (44,45). An inactivated vaccine is also being studied for use in humans (46). A chimeric live virus vaccine incorporating the genetic sequences for E and prM antigens into a 17-D yellow fever virus backbone has been shown to be efficacious in hamsters and is undergoing initial clinical trials in humans (46). Another chimeric vaccine incorporating WNV genetic sequences into a backbone of attenuated serotype-4 dengue virus–induced protective immunity in monkeys (44). A DNA vaccine that elicits expression of WNV E and prM antigens has been used in mice, horses, and birds (44). Vaccination of crows with Kunjin virus, a subtype of WNV, protected against WNV, and a DNA vector, which elicited expression of attenuated Kunjin virus, provided protective immunity against WNV in mice (46). Future Directions Since the 1990s, WNV has gained notoriety as a cause of severe neuroinvasive disease in humans. As WNV isolates and genetic sequences accumulate over an increasing geographic and clinical range, the virus shows signs of genetic modifications that likely interact with host factors in causing different patterns of neuroinvasiveness and neurovirulence. Several areas warrant research focus over the next few years. More efficient diagnostic assays will help with both clinical diagnosis and disease surveillance. Improved knowledge about the pathogenesis and natural history of WNV disease is crucial to developing effective treatment, and promising therapies need to be carefully evaluated in controlled clinical trials. Given the focal distribution of WNV outbreaks, and the uncertain distribution of future cases of WNV disease, prospective clinical studies need to be designed with the flexibility to gather information from widely dispersed and changing locations. The development of a safe and effective vaccine for humans is a clear priority for prevention, and the public health strategies and recommendations for vaccination deserve careful thought. Given the relatively low incidence of WNV neuroinvasive disease and the focal occurrence of WNV epidemics thus far, vaccination will likely require targeting to higher risk groups to approach the cost-effectiveness of many recommended public health prevention strategies.
Author and article information
Journal
Title:
Trends in Hearing
Abbreviated Title:
Trends in Hearing
Publisher:
SAGE Publications
ISSN
(Print):
2331-2165
ISSN
(Electronic):
2331-2165
Publication date Created:
October
17 2014
Publication date
(Electronic):
July
29 2014
Publication date
(Print):
October
17 2014
Volume: 18
Page: 233121651454136
Affiliations
Article
DOI: 10.1177/2331216514541361
SO-VID: 5906805c-d722-467e-b154-aebfc0757f22
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2014
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