West Nile Virus A Growing Challenge for the Speech-Language Pathologist Features
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Features  |   May 01, 2004
West Nile Virus
Author Notes
  • Susan Brady, is the research coordinator of Marianjoy Rehabilitation Hospital’s Swallowing Center. For more information on this article, contact her at sbrady@marianjoy.org.
    Susan Brady, is the research coordinator of Marianjoy Rehabilitation Hospital’s Swallowing Center. For more information on this article, contact her at sbrady@marianjoy.org.×
  • Rhonda Miserendino, is a speech-language pathologist for the neuromuscular program at Marianjoy Rehabilitation Hospital in Wheaton, IL.
    Rhonda Miserendino, is a speech-language pathologist for the neuromuscular program at Marianjoy Rehabilitation Hospital in Wheaton, IL.×
  • Noel Rao, a physician, is the medical director of the Marianjoy’s neuromuscular rehabilitation program.
    Noel Rao, a physician, is the medical director of the Marianjoy’s neuromuscular rehabilitation program.×
Article Information
Swallowing, Dysphagia & Feeding Disorders / Healthcare Settings / Regulatory, Legislative & Advocacy / Features
Features   |   May 01, 2004
West Nile Virus
The ASHA Leader, May 2004, Vol. 9, 10-13. doi:10.1044/leader.FTR5.09092004.10
The ASHA Leader, May 2004, Vol. 9, 10-13. doi:10.1044/leader.FTR5.09092004.10
Until recently, West Nile Virus (WNV) was considered an exotic disease usually occurring in tropical and sub-tropical regions that resulted in a relatively benign fever-rash syndrome which only occasionally caused viral encephalitis (Solomon & Hughs, 2002). The first case of this virus appeared in the United States in 1999 with an outbreak of encephalitis in New York City. WNV has spread quickly across the United States with an annual increase in confirmed cases from 62 in 1999 to 8,734 in 2003, according to the Centers for Disease Control and Prevention. In 2002, Illinois and the Chicago metropolitan area were hit particularly hard by WNV, with the Illinois Department of Public Health confirming more than 800 human cases that resulted in 62 deaths. The following year, as reported by the Centers for Disease Control and Prevention, Colorado was the hardest hit with 2,477 confirmed human cases reported resulting in 45 deaths in 2003.
West Nile Virus was first isolated and identified in 1937 in an individual who was infected in the West Nile district of northern Uganda (Petersen & Martin, 2002). It is classified as an arbovirus and is a single-stranded RNA virus that is a member of the genus flavivirus (family Flaviviridae ) (Petersen & Martin, 2003). WNV is transmitted through a natural host of animals (enzootic process) that involves birds as the amplifying host and mosquitoes as the vectors (Solomon, 2003).
The virus is transmitted from bird to bird by mosquitoes, which then become the carriers after biting infected birds. The virus makes its way to the salivary glands of the mosquitoes and is transmitted to other birds when the mosquitoes feed again. WNV has been identified in over 110 species of birds, with crows and bluejays being the most common in the United States (Bender & Thompson, 2003).
WNV cannot be passed directly between individuals nor have horses or birds been found to transmit the virus directly (Campbell et al., 2002). According to CDC, humans and domestic animals are considered “dead-end” hosts because even though they can develop the clinical illness, they do not produce significant viremia to transmit the disease. The most common form of transmission to humans is through mosquito bite. The virus has been identified in approximately 29 different species of mosquitoes, but Culex pipens, Culex restuans, and Culex quinquefasciatus are believed to be the most common. There have also been reports of ticks carrying the virus in Asia and Africa (Bender & Thompson, 2003). Additionally, transmission of WNV to humans has been reported through blood products, organ transplants, intrauterine, and breast milk (Goldrick, 2003).
Diagnosis of WNV involves the detection of the IgM antibody to WNV in serum or cerebrospinal fluid. Some clinical trials evaluating the efficacy of alpha-interferon began in 2002; however, the main treatment for WNV infection is currently supportive, focusing on symptoms and the various problems associated with brain swelling, hydration through intravenous fluids, respiratory support, and prevention of secondary infections such as pneumonia. Prevention of WNV is based on reducing the number of mosquitoes and preventing mosquitoes from biting humans (Leggiadro, 2003). According to the CDC, the National Institutes of Health (NIH) has been working on developing a vaccine for WNV as well as investigating antiviral therapy for the disease. Antibiotics have not proven effective in the treatment of WNV, and no effective antiviral drugs have been discovered to date.
Clinical Presentation
The full clinical spectrum of WNV is highly variable and is not completely known. The incubation period of WNV ranges from 3 to 14 days. Most WNV infections are clinically unapparent or present as a mild illness. Less than 1% of infected individuals develops acute neurological illness. Following a severe infection, a person may develop meningitis, encephalitis, or meningoencephalitis that may lead to permanent neurological damage of varying degrees and even death. The clinical symptoms of encephalitis include fever, headache, altered mental status (ranging from confusion to coma), paralysis, and sensory deficits (loss of deep tendon reflexes). The symptoms of meningitis include fever, headache, stiff neck, and increased number of lymphocytes in the cerebrospinal fluid. Mortality rates have been shown to increase with increased age (Leggiadro, 2003).
Severe generalized muscle weakness has been one of the most common clinical presentations of West Nile encephalitis, as exhibited by approximately 50% of patients in the U. S. (Leggiadro, 2003). Muscle weakness may affect limbs and the bulbar and respiratory musculature that may result in the need for mechanical ventilation and possible subsequent tracheotomy. Published reports have described WNV as a variant of Guillain-Barre syndrome (Gorson & Ropper, 2001). However, more recent published nerve conduction studies suggested that the most important pathological process was likely due to damage in the anterior horn cells of the spinal cord (myelitis) (Jeha et al., 2003). Other symptoms associated with severe WNV infection include high fever, headache, gastrointestinal symptoms, neck stiffness, tremor, convulsions, mental status changes (stupor, disorientation, coma), ataxia and extrapyramidal signs, cranial nerve abnormalities, optic neuritis, polyradiculitis and seizures.
Over the last few years, a growing number of speech-language pathologists have been faced with the challenges of treating patients following severe WNV infection. During the 2002 outbreak, Marianjoy Rehabilitation Hospital located in Wheaton, IL (a suburb located approximately 25 miles west of Chicago) admitted its first patients infected with WNV in late summer. Upon the first patient’s admission, SLPs at Marianjoy began to play an important role in patient rehabilitation. The specific areas of treatment for these patients included evaluation and treatment related to cognitive/communication skills and swallowing ability. The clinical experience at Marianjoy has demonstrated that the severity and length of the effects of severe WNV infection varied from patient to patient. The total length of hospitalization (acute and rehabilitation phase) following severe WNV infection ranged from 24 to 183 days (mean 88 days). Age range of the Marianjoy patient population was from 34 to 72 years old. Co-morbidities included diabetes, chronic obstructive pulmonary disease, coronary artery disease, chronic hepatitis B, myocardial infarction, hypertension, hypothyroidism, and end stage renal disease.
Upon admission to the rehabilitation hospital, the overall Functional Independence Measure (FIM) scores ranged from 31 to 68 with a mean score of 44 (possible maximum score of 126). At discharge, the overall FIM score range had improved from 52 to 90 with a mean score of 76. During inpatient rehabilitation, these patients were able to make significant functional gains in all targeted therapy areas. Patients who had multiple premorbid conditions appeared more vulnerable to severe WNV infections and had more severe complications with a slower recovery time, leading to longer hospitalization and higher medical costs. The majority of patients with WNV at Marianjoy required mechanical ventilation at some point during their hospitalization (all were successfully weaned from the ventilator). These patients also experienced cognitive/communication deficits and swallowing difficulty secondary to the infection.
The Role of the SLP
Initially, one of the primary roles of the SLP when treating a patient following severe WNV infection is to assist with the development of an augmentative and alternative communication system while the patient is ventilator-dependent. If the patient still has an oral-endotracheal tube while on mechanical ventilation, it is vital that the SLP instruct the patient, family, and medical staff on the use of a simple, low technology picture/word board as well as some hand gestures to facilitate communication for basic/immediate medical needs. If the patient has a tracheotomy, the SLP should be involved with the assessment for tolerance of an in-line one-way speaking valve in order to assist the patient with re-establishing verbal communication.
The SLP should also be involved with the evaluation and treatment of cognitive/communication skills following severe WNV infection. It is important for the SLP to identify potential areas that require remediation and to provide direct treatment in order to maximize the patient’s cognitive/communication functioning. Infected patients at Marianjoy demonstrated a wide range of cognitive/communication deficits. Severity of these deficits was also highly variable, ranging from severe confusion and an inability to follow one-step directions or communicate their basic wants/needs to mild memory deficits and numerical reasoning difficulty at the complex level. One patient was completely unresponsive initially even to pain stimulus. During recovery, however, the patient recovered sufficiently to be discharged to home with outpatient therapy at home. Many of the WNV patients at Marianjoy demonstrated confabulation, disorientation, memory deficits, and a reduced awareness of their deficits. Fortunately, these patients were still able to read simple sentences and benefited from memory notebooks to assist with recall of daily information and long-term biographical information. Calendars also proved useful in assisting patients with their orientation. Overall, the majority of the patients made functional recovery with their cognitive/communication skills, however, some continued to demonstrate residual deficits and required ongoing therapy after discharge from the hospital.
Dysphagia following severe WNV infection was also common in the WNV patient population at Marianjoy, and was thought to be secondary to the neurological damage. This may have been further compromised by the presence of the tracheotomy tube. Completing an instrumental assessment of the swallow in this patient population is highly recommended, not only to define the physiology that might be causing the swallowing disorder, but also to determine diet level/swallow safety strategies as well as to provide direction for appropriate use of rehabilitative/ swallowing treatment exercises to assist with recovery. The majority of WNV patients at Marianjoy demonstrated tracheal aspiration (with and without a cough response) during the modified barium swallow examination in the early stages of recovery.
Swallowing therapy included diet modification, compensatory swallow safety strategies, and swallowing rehabilitation/strengthening exercises. The majority of WNV patients were nil per os (npo), with supplemental tube feedings at the beginning of their rehabilitation. All of them, however, eventually returned to oral feedings (without supplemental tube feedings) following swallowing therapy prior to their discharge from the hospital.
A Key Role in Recovery
In the treatment of patients with WNV, the SLP plays an important role on the rehabilitation team. The SLP works closely with these patients to assist them during their recovery in the area of cognitive/communication and swallowing ability. All of the patients admitted to Marianjoy Rehabilitation Hospital with severe WNV infection were able to demonstrate significant functional improvement during their inpatient rehabilitation stay, however, none had complete recovery to their premorbid functional status and required prolonged recuperation.
As with any disorder, providing education to the patient, family, and medical staff on the effects of the disorder and how it may impact the patient’s cognitive/communication skills and swallowing ability is a key role for the SLP. This can be extremely challenging due to the wide clinical spectrum of effects associated with severe WNV infection. When identifying possible prognostic variables for recovery, it is important to remember that patients with multiple premorbid conditions are at a higher risk for more severe complications leading to a longer recovery time following severe WNV infection. Additionally, patients initially presenting with profound muscle weakness and axonal neuropathy were associated with lower functional outcomes and increased cost of care.
It is important for all the members of the rehabilitation team, especially the SLP, to recognize the potential complications of WNV and to provide appropriate interventions to maximize recovery and minimize additional complications.
Prevention of West Nile Virus
  • Avoid mosquito bites

  • Apply insect repellent containing DEET

  • Wear long sleeves, long pants, and socks when outdoors

  • Consider avoiding outdoor activities during peak mosquito hours (dusk to dawn)

  • Drain standing water

  • Install or repair window screens

  • Report dead birds to local authorities

  • Check with local authorities regarding mosquito abatement program

Source: The West Nile Virus: What You Need To Know CDC Fact Sheet

Reported Human Cases of WNV in the United States
  • Year, Number of Cases, Number of Deaths, Number of States
  • 1999, 62, 7, 1
  • 2000, 21, 2, 3
  • 2001, 66, 9, 10
  • 2002, 4156, 284, 40
  • 2003, *8734, 208, 46

*Reported cases as of Dec. 10, 2003 Source: The Centers for Disease Control and Prevention Web site

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May 2004
Volume 9, Issue 9