Suspected Viral Encephalitis Exposure

 

 

Purpose

The purpose of these policy guidelines is to recommend procedures for handling potential biological threats of Viral Encephalitis exposure.

 

Description of AgentlSyndrome

 

Alpha viruses

 

1.              Venezuelan equine encephalitis virus (VEE)

2.              Eastern equine encephalitis virus (EEE)

3.              Western equine encephalitis virus (WEE)

 

These viruses can be produced in large amounts in inexpensive and unsophisticated systems. They are relatively stable during storage and manipulation. Readily available strains may produce incapacitating or lethal infection.

 

Transmission

 

1.              Naturally occurring disease is mosquito-borne.

2.              Potential biological weapon threat from inhalation of aerosolized organism.

 

Incubation Period

       1.               VEE    1-6 days
       2.               EEE    7-14 days
       3.               WEE  7-14 days

 

Signs and Symptoms

 

Children and elderly are more susceptible to severe clinical illness and neurological sequelae.

 

1.   VEE:

a)    High fever (38 degrees C-40.5 degrees C), chills, headache, sore throat, malaise, myalgia, photophobia, vomiting are common.

b)    Only a small percent progress to more severe neurological involvement.

c)     Other common findings include:

                                                                   I.         leukopenia early followed by leukocytosis

                                                                II.         elevated serum AST levels

                                                             III.         elevated lymphocytes in CSF with neurological involvement

d)    Case-fatality rate: 10% for naturally occurring disease

 

2.   EEE:

a)    Febrile prodrome occurs up to 11 days before neurological disease occurs. Symptoms usually begin with malaise, headache and fever followed by nausea and vomiting.

b)    Progression to delirium, somulence and coma may occur within a few days.

c)         Other common findings include:

                                                                   I.         leukopenia early followed by leukocytosis

                                                                II.         elevated serum AST levels

                                                             III.         elevated lymphocytes in CSF with neurological involvement

d)    Up to 30% of survivors have severe neurologic sequelae (seizures, spastic paralysis, cranial neuropathies)

e)    Case fatality rate: 50-75% for naturally occurring disease.

 

3. WEE:

a)    Febrile prodrome occurs up to 11 days before neurological disease occurs. Symptoms usually begin with malaise, headache and fever followed by nausea and vomiting.

b)    Progression to delirium somulence and coma may occur within a few days.

c)     Other common findings include:

                                                                   I.         leukopenia early followed by leukocytosis

                                                                II.         elevated serum AST levels

                                                             III.         elevated lymphocytes in CSF with neurological involvement.

d)    Most adults recover completely without neurologic sequelae.

e)    Case fatality rate: 10% for naturally occurring disease

 

Diagnosis

 

1.     Clinical diagnosis with serologic confirmation. Early in disease, the virus may be cultured from serum or throat swabs but rarely after neurologic symptoms have developed.

2.     A single 1gM antibody elevation in serum 5-7 days after onset of illness is presumptive evidence of VEE (assuming no previous exposure)

3.     Other serum testing available includes 1gM ELISA, hemagglutination inhibition, complement fixation, and neutralization tests.

 

Treatment

 

1.               Supportive care is the mainstay of therapy.

2.               Symptom management may include anticonvulsant medication, airway protection, and antihyperthermia measures.

 

Prophylaxis

 

1.            Post exposure prophylaxis is not available.

2.            No licensed vaccine for EEE, WEE.

3.            Vaccines for VEE to homologous serotypes have been used in lab personnel with good result but are highly reactogenic and cross immunity to heterologous serotypes is weak.

 

Control Measures and Decontamination

 

1.            Person to person transmission has not been documented.

2.            Standard Precautions for patient care and patient care equipment.

3.            Private rooms are not necessary.

4.            Control of mosquito population in areas where patients are ill may reduce secondary transmission in both terrorist and naturally occurring events.

5.            Decontamination at the scene of a bioterrorist event would be more complex and requires direction from Health Department or CDC. High efficiency particulate respirators used at the scene of an aerosolizing event may offer some protection.

 

Notification

 

Internal:    At hospital notify______________________________

 

External:  All suspected cases of Viral Encephalitis are Class A2 Reportable and should be reported immediately to the Local Health Departments who will then contact the State Health Department and/or CDC.

 

Lab

 

Lab Data not yet available through CDC Website.

 

Biosafety level - 3 for lab with clinical isolates of VEE.

Biosafety level - 2 for labs with clinical isolates of EEEIWEE.

 

 

References

Association for Practitioners in Infection Control and Epidemiology, 2000. “APIC Text of Infection Control and Epidemiology”, 124-1 to 124-11

 

Center for Disease Control and Prevention. Disease Information via Internet http://www.cdc.gov/ncidod/dvbid/arbor/arboguid.pdf

 

US AMRIID’s Medical Management of Biological Casualties Handbook, Pgs. 49-53

 

Franz, D, Jahrling, B, Friedlander, A, etal. 1997, Clinical Recognition and Management of Patients Exposed to Biological Warfare Agents, JAMA, 278:5,pgs.399-41 1

 

 

Note:    These are guidelines that have been developed with data available as of 5/9/02.

 

 

Initially Prepared by

The Akron Regional Hospital Association

Emergency Preparedness Subcommittee

August 20, 2002