Varicella-zoster virus vaccination is recommended for virtually all young children in the United States, Canada, and several other countries. Varicella vaccine is a live attenuated virus that retains some of its neurotropic properties. Herpes zoster caused by vaccine virus still occurs in immunized children, although the rate is much lower than in children who had wild-type varicella. It was commonly thought that 2 varicella vaccinations would protect children against the most serious complication of meningitis following herpes zoster; however, 2 meningitis cases have already been published. We now report a third case of varicella vaccine meningitis and define risk factors shared by all 3 immunized adolescents. The diagnosis in cerebrospinal fluid in this third case was verified by amplifying and sequencing portions of the viral genome, to document fixed alleles found only in the vaccine strain. Viral antibody was also detected in the cerebrospinal fluid by confocal microscopy. When compared with the other 2 cases, remarkably all 3 were 14 years old when meningitis occurred. All 3 were treated with intravenous acyclovir, with complete recovery. The adolescent in our case report also had recurrent asthma, which was treated with both prednisone tablets and beclomethasone inhaler before onset of meningitis. When the 3 cases were considered together, they suggested that immunity to varicella-zoster virus may be waning sufficiently in some twice-immunized adolescents to make them vulnerable to varicella vaccine virus reactivation and subsequent meningitis. This complication rarely happens in children after wild-type varicella.

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This research suggests that using a single test form with shift-based computerised assessments, spread over as many as two days, does not seriously compromise the integrity of the results. Since creating multiple unique-item forms is often not possible, shift-based testing with a single test form appears to be a fair method of accommodating a large number of students.

An inhibitory effect on Friend virus (FV) and Rauscher virus leukemia by the carcinogenic plycyclic aromatic hydrocarbons 7, 12-dimethylbenz [ a ] anthracene (DMlBA) and 3-methylcholanthrene was recently reported ( 1). The parameters used to show this were latent period, survival time, and spleen weight. Interference with "indirect neoplastic effects" (development of hemorrhagic necrosis and proliferation of erythroblasts in the spleen) was considered to play a greater role than interference with a "direct neoplastic effect" (proliferation of the neoplastic reticulum cells). To investigate the mechanism of this inhibitory effect, the weekly FV titers in spleen and liver of untreated and DMBAtreated mice were compared. Also compared were the weekly liver weight and blood picture (erythrocyte volume, nucleated blood cell count, and differential blood cell count) of splenectomized, untreated and DMBAtreated, FV-infected mice with those of nonsplenectomized mice.Materials and Methods. The FV was the same as that used in the previous study (1). The titer of the virus p o l was 10490 ID50/ml. For the induction of leukemia, adult BALB/c mice, weighing approximately 25 g, received a single intraperitoneal injection of 0.2 ml of a dilution of the virus in sucrose stabilizer. For the treatment with