This report was received from a the authors in a published literature article and refers to a 36 year old female patient with multiple sclerosis. The patient's medical history included chickenpox. Past drug therapy included: BETASERON, COPAXONE and TYSABRI. On 13-OCT-2011, the patient's lymphocyte count was 3370. On 03-NOV-2011, GILENYA was initiated, but discontinued after 5 days when it was realized that her VZV antibody was negative despite a childhood history of chickenpox. Although advised to wait at 4-6 weeks before VZV vaccination, the patient was vaccinated with a dose of ZOSTAVAX vaccine live (manufacturer unknown) (dose, route and lot number were not reported) on 09-NOV-2011. On 23-NOV-2011, the patient lymphocyte count was 1550 and her 3 year old daughter developed chickenpox (MARRS case # 1304USA006039). On 08-DEC-2011, fingolimod was GILENYA reinitiated. On 23-JAN-2012, she developed influenza and had an multiple sclerosis (MS) relapse requiring 5 days of intravenous methylprednisolone. She had not been previously vaccinated for influenza. At that time, her lymphocyte count was 190. On 25-MAR-2012, she developed a urinary tract infection and was found to have leukopenia (300) and thrombocytopenia (98,000). These were ascribed to sepsis and returned to baseline values on 30-MAR-2012 (WBCs 7400 and platelets 224,000) with cephalosporin treatment. On 10-MAY-2012, the patient CD4/8 ratio was 0.2 and CD4 10%; unfortunately, an absolute CD4 lymphocyte count was not available nor could it be calculated; her absolute white blood cell count at the time was 5000. On 09-JUL-2012, she developed shingles in a left T8-11 distribution that resolved in association with course of acyclovir 800 mg five times for 2 weeks. On 28-SEP-2012, she had recurrent shingles that involved the lower thoracic dermatomes bilaterally. She was retreated with acyclovir and recovered within 10 days. On 27-FEB-2013, repeat varicella antibody testing, performed 16 months after zoster vaccine live (manufacturer unknown) administration and following 2 bouts of zoster, was again negative. An immunoglobulin assay was normal with the exception of a slightly diminished IgG of 629. Recent case reports continue to raise concerns about a possible association between fingolimod and serious herpes infection. One patient developed zoster cranial polyneuritis with a high VZV copy number in the CSF 42 months after the initiation of fingolimod 0.5 mg daily. Another patient developed encephalopathy and brainstem infarction attributed to VZV encephalitis and vasculopathy three months after the initiation of fingolimod when his absolute lymphocyte count was 190. The patient described appears to have transmitted VZV to her daughter after inoculation following a very short course of fingolimod. Furthermore, during the first year of fingolimod treatment, she has had 2 discrete episodes of recurrent herpes zoster. These observations suggests the possibility that zoster vaccine efficacy was attenuated in patients who had recieved fingolimod immediately prior to vaccination, even a short course, and that VZV control may be diminished during treatment with fingolimod leading to recurrent zoster in some patients. A blunted immune response to vaccination to varicella would not be surprising in the setting of the administration of immunosupressive drugs as it has been observed with influenza and pneumococcal vaccinations. It is unlikely that either her influenza infection or the corticosteroid administration for the MS relapse occurring on its heels contributed to her bouts of shingles as there was a 6 month hiatus between them and the first onset of zoster. The zoster vaccine was a live-attenuated virus (Merck) that is extremely safe and highly immunogenic. It reduces the risk of developing zoster by 51.3% (95% (1=44.2-57.6). It had been proposed that vaccinated individuals may shed the attenuated virus increasing the herd immunity following vaccination efforts; however, early studies by the manufacturer failed to confirm transmission of the vaccine virus in contacts. While transmission of the live attenuated varicella virus to contacts was infrequent, it has been described. The incubation period from time of exposure of VZV to the clinical expression of varicella is typically 14-15 days, precisely the time from our patient's vaccination to the development of her daughter's varicella. And transmission may occur in the absence of the rash. As our patient's 3 year old daughter had not been otherwise exposed to VZV, it is likely that the source of her viral infection was her mother's inoculation two weeks earlier. Although our patient had been advise to wait 4-6 weeks from time of discontinuing the fingolimod, zoster vaccination was administered the day after she had received 5 days of fingolimod. Zoster vaccine should not be administered to persons with primary or acquired immunodeficiency. It is quite possible that the immunological compromise attending fingolimod administration favored VZV shedding, although the patient suffered no ill effects at the time of inoculation. Although disseminated and persistent varicella infection has been reported in immunosuppressed individuals who have been vaccinated with varicella, our patient seemed to tolerate the vaccination without complication. Furthermore, her MS did not worsen following the vaccination. While on fingolimod, the patient experiended separate episodes of thoracic herpes zoster 8 and 10.5 months following zoster inoculation. Both recurrences resolved within 10 days of acyclovir administration. Although the zoster vaccine is not totally effective in preventing episodes of herpes zoster and recurrent herpes zoster has been described in immunocompetent individuals, recurrent herpes zoster is rare in vaccinated immunocompetent individuals. Among immunocompetent adults vaccinated after a recent episode of herpes zoster, the rate of recurrent herpes zoster was only 0.99 per 1000 patient years. This case report must be interpreted cautiously. Viral cultures were not obtained from her dauther or from the patient's lesions during the recurrent episodes of zoster. Transmission of the varicella Oka vaccine to non-vaccinated individuals has been documented on rarely. Furthermore, the multidermatomal nature of her second episode of shingles is unsual as well, though the symptoms and lesion appearance strongly suggested recurrent zoster. Despite a history of childhood varicella, she was VZV antibody negative and remained VZV antibody negative after ZOSTAVAX and two bouts of shingles. There was no evidence of a primary immunodeficiency either clinically or by laboratory examination suggesting that fingolimod may have blunted the humoral response to immunization and recrudescent infection. Cell mediated immunity is fundamental to viral reactivation and clinical expression of the disease; the incidence of herpes zoster was substantillay increased with hematological and solid tumors, HIV infection, hematopoietic stem cell, and organ transplantation, as well as with other conditions affecting cell mediated immunity. Whether fingolimod which inhibits the egress of naive and central memory T cells, but not effector memory cells truly predisposes to increases the risk of and aggressiveness of VZV remains uncertain. Current data suggests that there was be no relationship between the degree of lymphopenia associated with fingolimod and the occurrence of all herpes infections Vigilance for unsual complications of VZV during treatment with fingolimod is warranted. Sepsis was considered to be an other important medical event per internal review. This is one of the several reports from the same source. Additional information has been requested.