Page 941 - Hall et al (2015) Principles of Critical Care-McGraw-Hill

672 PART 5: Infectious Disorders

Findings can vary from normal to hyperintense lesions. Treatment is neurologic abnormalities, gastrointestinal symptoms, and seizures. The
60
supportive care; several vaccines are in the developmental stages. 61 diagnosis can be made by testing serum and CSF for IgM and neutral-
■ JAPANESE ENCEPHALITIS VIRUS izing antibodies. A fourfold increase in convalescent phase IgG antibody
titer is required to establish the diagnosis. Treatment is supportive. Case-
Japanese encephalitis virus (JEV) is an arbovirus of flaviviridae family, fatality rate is 10% to 15% with a high incidence of residual neurologic
spread to humans by mosquito bites (culex), and is a major public health abnormalities among survivors.
problem in Southeast Asia, causing around 50,000 cases and 10,000 deaths ■ MURRAY VALLEY ENCEPHALITIS VIRUS
per year especially in children below 10 years of age. JEV causes severe
62
fatal encephalitis with high mortality and survivors are left with Murray Valley encephalitis virus is found in Australia and New Guinea,
severe neurologic sequelae. JEV infection is most often asymptomatic. transmitted to humans by mosquitoes and mostly affects the aboriginal
When symptoms are present, they usually manifest as meningitis, children. Illness may progress rapidly in children with a case fatality rate
seizures, and motor paralyses. A progressive decline in alertness may of 15% to 30%. Diagnosis is made by the detection of IgM antibody in
take place, eventually progressing to coma. Recovery usually leaves the CSF or demonstrating a fourfold increase in IgG antibodies in paired
63
serious neurologic sequelae such as persistent altered sensorium, extra- acute and convalescent sera. MRI may show high signal intensities in
pyramidal syndrome, epileptic seizures, and severe mental retardation. basal ganglia. Treatment is supportive.
asymmetric hemorrhagic lesions of the thalamus are characteristically ■ TICK-BORNE ENCEPHALITIS VIRUS
The JE virus shows a fairly strong tropism for the thalamus, and bilateral
seen on MRI and CT. Hyponatremia from inappropriate antidiuretic Tick-borne encephalitis virus (TBE) is found in Eastern Russia, central
64
hormone secretion is reported. JEV specific anti-IgM antibody detec- Europe, and the Far East. The virus is transmitted to humans by ticks.
tion by ELISA may help establish a diagnosis. HSV, dengue virus, and Outbreaks of TBE viral encephalitis have been reported following
West Nile virus are the major viruses to be considered in differential ingestion of unpasteurized milk products from infected sheep and goat.
diagnosis. Treatment is usually supportive and there is no effective anti- Clinical spectrum of illness ranges from mild to severe encephalitis
viral treatment. Prevention is by vector control and vaccination. 62 along with myelitis- and poliomyelitis-like paralysis. 68,69 Diagnosis is
■ ST LOUIS ENCEPHALITIS made by the detection of IgM antibody in the serum and CSF or dem-
onstrating a fourfold increase in IgG antibodies in paired acute and
St Louis encephalitis (SLE) is endemic in western United States, with convalescent sera. In the early viremic phase, TBE virus may be cultured
from blood. Treatment is supportive.
large periodic outbreaks in the eastern United States, Central and South
America. It is the second leading cause of epidemic viral encephalitis in
the United States, after West Nile virus. The illness is mostly seen during PICORNAVIRIDAE
summer months when the vector, culex mosquito is active. Symptomatic Encephalitis causing viruses in the Picornaviridae family are distributed
illness is uncommon in children; among adults, 1 in 300 exposed to the worldwide and can be grouped into polio and nonpolio enteroviruses.
virus develop symptomatic illness. The incubation period is 4 to 21 days With a few exceptions, the predominant mode of transmission is by the
65
after the bite of an infected mosquito. Illness begins with a prodrome of ingestion of food or water contaminated with feces. Coxsackievirus A21
flu-like symptoms such as fever, headache, myalgia, nausea, and vomit- is transmitted via respiratory secretions.
ing. Clinical features of SLE include altered sensorium, seizures, cranial
nerve palsies, eyelid and lip tremors, nystagmus, ataxia, myoclonic move- ■ POLIOVIRUS
ments, and coma. A unique feature in SLE is the development of urinary Poliovirus is a neurotropic virus, the causative agent of paralytic polio-
symptoms such as dysuria, urgency, and incontinence prior to the myelitis. The virus is primarily transmitted by fecal oral route with
appearance of central nervous system signs. CSF analysis is consistent pharyngeal spread occurring during epidemics. Incubation period is 1
with viral meningitis with mild elevation in protein, normal to mildly to 2 weeks and over 90% of infections are asymptomatic. Presentation
decreased glucose, and WBC counts ranging from 50 to 500 cells/µL of symptomatic illness is similar to a viral illness. Initial symptoms are
with mononuclear cell predominance. Syndrome of inappropriate headache, fever, nausea, vomiting, and malaise. In infants this may
secretion of antidiuretic hormone (SIADH) has been documented in progress to meningoencephalitis with altered sensorium and seizures.
one-third of patients. A positive serum IgM ELISA provides a presump- Paralytic polio occurs in less than 1% of all polio infections and may
tive diagnosis of SLE, but a fourfold increase in convalescent phase IgG present as asymmetric flaccid paralysis, diaphragmatic and respira-
antibody titer is required to establish the diagnosis. False-positive serol- tory muscle paralysis leading to respiratory failure. Lower extremities
ogy due to cross-reaction with other flaviviruses, especially West Nile are more often involved than the upper extremities. Poliovirus causes
virus, can occur. The presence of SLE-specific IgM antibody in the CSF damage only to the motor neurons, therefore the sensation is preserved.
is indicative of infection of the central nervous system, and by day 7 of Oral polio vaccine (OPV) has been associated with a few cases of acute
illness, 100% of CSF samples will yield a positive result. Abnormalities flaccid paralysis. Outbreaks of poliomyelitis due to vaccine derived
specific to SLE have not been identified in brain imaging. MRI of the strains of virus have occurred, when OPV was administered in areas
brain may show hyperintense lesions in the basal ganglia, substantia with low immunization rates. This is unlikely to occur in the USA, as the
nigra, and thalamus. Treatment is supportive. There are no approved Advisory Committee on Immunization Practices has recommended the
antiviral agents available for the treatment of SLE, though interferon- use of inactivated polio vaccine for primary immunization since 2000.
α-2b may reduce the severity and duration of complications associated Early in the illness, CSF evaluation reveals predominance of polymor-
with SLE. 47,66 Case-fatality rate is 3% to 30% with higher rates seen in phonuclear cells with a shift to lymphocytic predominance after a few
persons over the age of 60 years. days. CSF protein concentration is often elevated to 100 to 300 mg/dL
■ POWASSAN VIRUS and the glucose concentration is normal. Virus can be cultured from
pharyngeal secretions and stool. CSF culture for the virus is unreliable.
Powassan virus is a rare cause of encephalitis in the New England states The diagnosis can be confirmed by PCR amplification of poliovirus
and eastern Canada. Rodents are the reservoir for the virus, which is RNA in the CSF. Serologic testing by demonstrating a fourfold increase
transmitted by ticks to humans. Infection occurs mostly during summer in convalescent phase antibody titer can also be used to establish the
months and asymptomatic infection is more common than symptomatic diagnosis. At the present time, treatment of poliomyelitis is supportive.
illness. The incubation period is about 8 to 34 days. When symp- None of the available antiviral agents have demonstrated any benefits in
67
tomatic, patients often present with fever, headache, confusion, focal the treating this enterovirus-associated acute paralysis.

section05_c61-73.indd 672 1/23/2015 12:48:46 PM