Signs and Symptoms
Monkeys infected with B virus usually have no or only mild symptoms. In humans, however, B virus infection can result in acute ascending encephalomyelitis, resulting in death or severe neurologic impairment.
Disease onset in B virus–infected humans typically occurs within 1 month of exposure, although the actual incubation period can be a little as 3 to 7 days. Symptoms associated with B virus infection include
- Vesicular (small blister) skin lesions at or near the site of exposure
- Localized neurologic symptoms (pain, numbness, itching) near the wound site
- Flu-like aches and pains
- Fever and chills
- Headaches lasting more than 24 hours
- Muscular incoordination
- Shortness of breath
Initial symptoms include fever, headache, and vesicular skin lesions at the site of exposure. Neurologic symptoms vary. Respiratory involvement and death can occur 1 day to 3 weeks after symptom onset.
Disease progression depends on the location of the exposure (usually a bite or scratch) and on the number of infectious virus particles that get delivered by the exposure. Although vesicular lesions have sometimes been observed at the exposure site, they are not invariably observed. The first signs of disease typically include the onset of flu-like symptoms (e.g., fever, muscle ache, fatigue, and headache). Lymphadenitis, lymphangities, nausea and vomiting, abdominal pain, and hiccups have also been observed in patients. Once the virus spreads to the central nervous system (CNS), a variety of neurologic signs develop, including hyperesthesias, ataxia, diplopia, agitation, and ascending flaccid paralysis. CNS involvement generally heralds grave consequences. Most patients with CNS complications will die despite antiviral therapy and supportive care, and those who survive usually suffer serious neurologic sequelae. Respiratory failure associated with ascending paralysis is the most common cause of death.
Given the number of potential exposures for animal care workers, asymptomatic or mild human B virus infection has been postulated to occur, but no evidence for asymptomatic B virus infection or for latent infection has been observed in humans at elevated risk of infection. Antibodies produced in response to the human herpesviruses HSV-1 and HSV-2 (present in >80% of adults) are capable of neutralizing B virus in vitro but are not protective against B virus infection. Moreover, such antibodies complicate diagnostic testing for B virus due to their high level of cross-reactivity (i.e., they increase the potential for both false-positive and false-negative results).
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