Reactivation of Varicella-Zoster Virus in Facial Palsy Associated With Infectious Mononucleosis

Facial palsy with infectious mononucleosis, although well-recognized, is rare in children, and its pathogenesis is uncertain. To our knowledge there has been no previous report describing varicella-zoster virus reactivation as a cause of facial palsy associated with infectious mononucleosis. We report such a patient in whom serology showed reactivation of varicella-zoster virus. Case report. A 17-month-old male child was admitted to the hospital because of fever, cervical lymphadenopathy and left sided facial palsy. He had had chickenpox 8 months before admission. Fever and left cervical lymphadenopathy appeared 3 days before admission, and the day before admission his mother noted asymmetry of the left side of his face. Otorrhea of the left ear appeared on the day of admission. On physical examination his consciousness level was normal. Lymphadenopathy was present, and lymph nodes in the left parotic area were strikingly enlarged. Bilateral membranous tonsillitis was present. Paralysis of the facial nerve on the left side was accompanied by difficulty in closing the left eye. The remainder of the neurologic examination was normal. No other abnormality was found on general medical examination, and there was no hepatosplenomegaly. Otoscopic examination of the ears by an otolaryngologist revealed bilateral exudative otitis media. The following laboratory data were obtained: hemoglobin 11.3 g/dl; hematocrit 34.7%; white blood cell count 31 800/mm3 with 81% lymphocytes (15% atypical lymphocytes); aspartate aminotransferase 133 units/l; alanine aminotransferase 152 units/l; lactate dehydrogenase 1281 units/l; amylase 242 units/l; and C-reactive protein 1.0 mg/dl. A culture of the purulent material from the left ear grew Moraxella catarrhalis, susceptible in vitro to multiple antibiotics, but no pathogenic bacteria were isolated from the throat culture. Computed tomography of the brain revealed no abnormalities. He was treated with antibiotics, prednisone (1.5 mg/kg/day) and acyclovir (80 mg/kg/day for 7 days). The fever subsided and otorrhea ceased the day after admission. Clinical findings including the lymphadenopathy and membranous tonsillitis resolved within several days. The facial nerve paralysis also improved and prednisone was stopped after gradually decreasing the dosage. Ten days after hospitalization the facial nerve paralysis had improved to the point where the facial asymmetry was noticeable only when the child cried. He was discharged home without medications. The paralysis of the left facial nerve resolved within 3 weeks. We collected the patient’s sera during the acute and convalescent phases and subjected them to microbiologic examination (Table 1). The development of specific antibody titers to different Epstein-Barr virus (EBV) antigens confirmed the diagnosis of infectious mononucleosis. The patient had no herpetic vesicles characteristic of varicella-zoster virus (VZV) infection during the entire observation period. However, serologically there was strong indication of reactivation of a previous VZV infection because the VZV-IgM antibody was positive and the IgG antibody titer was highly elevated.Table 1: Antibody titers to miscellaneous microorganisms in acute and convalescent phasesDiscussion. Although facial nerve paralysis is a well-known neurologic manifestation of infectious mononucleosis, it is rare in children. 1 The pathogenesis of facial palsy with infectious mononucleosis is uncertain. As possible mechanisms of facial palsy associated with EBV infection, direct viral invasion of the neurons and a central nervous system allergic response to the infective agent have been suggested. 2 In our patient further factors that can be considered as possible causes of the facial palsy are otitis media caused by M. catarrhalis and reactivation of VZV. Otitis media is a well-known cause of facial palsy. However, there are no previous reports implicating VZV reactivation as the cause of facial paralysis in infectious mononucleosis. 3–5 Ramsay Hunt syndrome is characterized by acute facial palsy associated with a herpetic eruption on the auricle. Sometimes facial palsy develops without the herpetic eruption, a syndrome known as zoster sine herpete. The syndrome is caused by reactivation of latent VZV concealed in the geniculate ganglion. The exact mechanism of reactivation remains unclear but is presumably triggered by preceding stress, such as fever, an upper respiratory infection or exposure to cold. Recently the usefulness of detecting VZV DNA in oropharyngeal swabs by PCR was described for the early diagnosis of zoster sine herpete in a patient with acute peripheral facial palsy. 6 Furuta et al. 7 suggested that VZV reactivation is a major cause of delayed facial palsy after dental treatment and orofacial surgery. In general herpesviruses, including EBV, induce a concomitant release of interleukin-6, and this could facilitate the reactivation of other latent infectious agents within the host, enhancing the possibility of coinfection in the central nervous system. 8 The VZV load in saliva samples reflected the kinetics of viral reactivation in patients with Ramsay Hunt syndrome. 9 To confirm participation of VZV reactivation in a patient with facial palsy, VZV detection from saliva or oropharyngeal swabs by PCR is needed. Because this test was not done in our patient, we were unable to determine whether reactivation of VZV was a major cause of his facial palsy. Possibly the positive VZV IgM antibody test is the result of his having had chickenpox 8 months before. However, usually IgM antibody cannot be detected a few months after chickenpox infection. We thought that the high titer of VZV IgG and the positivity of IgM in our case suggested reactivation of VZV. Although the prognosis for facial palsy associated with infectious mononucleosis is generally favorable, the facial palsy in Ramsay Hunt syndrome is usually more severe than that in Bell’s palsy. Because early administration of acyclovir and prednisone was beneficial in the patient with Ramsay Hunt syndrome, 10 combination therapy should be considered in patients with facial palsy associated with infectious mononucleosis when reactivation of VZV is suspected.