The varicella zoster virus is the cause of this common childhood infection. It is a close relative of the herpes virus. After initial infection, the virus remains dormant in the dorsal root ganglia. During periods of stress or immunocompromised states, the virus may be reactivated and shingles (Herpes zoster) is the result. It is important to remember that a person with a shingles outbreak is infectious to anyone who has not been previously exposed to the virus.
The seroepidemiology of varicella in Italy.
Gabutti G, Penna C, Rossi M, Salmaso S, Rota MC, Bella A, Crovari P
Serological Study Group. Department of Health Sciences, Hygiene and Preventive Medicine Section, University of Genoa, Italy.
Epidemiol Infect 2001 Jun;126(3):433-40 Abstract quote
We conducted a seroepidemiological study to evaluate the potential impact of mass varicella vaccination on the transmission of varicella-zoster virus (VZV) in Italy, where vaccination is not mandatory.
We tested 3179 serum samples, collected from September 1996 to October 1997, for specific anti-VZV antibodies using a commercially available ELISA. The results confirmed that varicella typically involves children (82.1% seroprevalence among 10- to 14-year-olds) and that the mean age of acquiring the infection seems to be increasing. The results also revealed that southern Italy, compared to the rest of the country, has a greater circulation of VZV and an earlier age of acquisition.
The potential impact of mass vaccination among 12- to 18-month-old children on the epidemiological trend of the infection must be carefully considered, in that failure to reach high levels of coverage could lead to an increase in the mean age of acquisition, which is already occurring in Italy.
DISEASE ASSOCIATIONS CHARACTERIZATION
Severe invasive group A streptococcal infections: a subject review.
American Academy of Pediatrics. Committee on Infectious Diseases.
Pediatrics 1998 Jan;101(1 Pt 1):136-40 Abstract quote
The course of severe invasive group A beta-hemolytic streptococcal (GABHS) infections is often precipitous, requiring prompt diagnosis and rapid initiation of appropriate therapy. Therefore, physicians must have a high index of suspicion of this disease, particularly in patients at increased risk (e.g., those with varicella or diabetes mellitus). Although a relationship between the use of nonsteroidal antiinflammatory drugs and severe invasive GABHS infections has been suggested, at present data on which to base a clinical decision about the use or restriction of nonsteroidal antiinflammatory drugs in children with varicella are insufficient. When necrotizing fasciitis is suspected, prompt surgical drainage, debridement, fasciotomy, or amputation often is necessary. Many experts recommend intravenously administered penicillin G and clindamycin for the treatment of invasive GABHS infections on the basis of animal studies. Some evidence exists that intravenous immunoglobulin given in addition to appropriate antimicrobial and surgical therapy may be beneficial. Although chemoprophylaxis for household contacts of persons with invasive GABHS infections has been considered by some experts, the limited available data indicate that the risk of secondary cases is low (2.9 per 1000) and data about the effectiveness of any drug are insufficient to make recommendations. Because of the low risk of secondary cases of invasive GABHS infections in schools or child care facilities, chemoprophylaxis is not indicated in these settings.
Routine immunization of all healthy children against varicella is recommended and is an effective means to decrease the risk of invasive GABHS infections.
Varicella complicated by group A streptococcal facial cellulitis
J. Sánchez del Ríoa
J Am Acad Dermatol 2001;45:770-2 Abstract quote
An increase has been recently noted in the incidence of life-threatening group A -hemolytic streptococcal (GABHS) infections in children recovering from varicella.
We report our experience with a patient who required pediatric intensive care unit admission because of a serious GABHS infection 1 week after the onset of varicella.
Emergency physicians must look for this complication in patients with varicella remaining abnormally febrile and presenting unusual manifestations.
Zoster in patients infected with HIV: a review.
Vafai A, Berger M.
Centers for Disease Control and Prevention, Atlanta, Georgia 30333, USA.
Am J Med Sci 2001 Jun;321(6):372-80 Abstract quote
Varicella-zoster virus (VZV), a member of the human herpesvirus family, causes childhood chickenpox (varicella), becomes latent in sensory ganglia, and reactivates years later in immunocompromised and elderly persons to produce shingles (herpes zoster). Early in the AIDS epidemic, zoster was noted in adults and children infected with HIV. Severe and debilitating zoster-associated dermatological, ophthalmic, and neurological complications may occur in patients infected with HIV. Antiviral therapy can modify the duration of zoster and alleviate its attendant complications.
Varicella vaccine may boost the immunity and prevent virus reactivation. VZV immune globulin (VZIG) prevents or modifies clinical illness in persons who have been exposed to varicella or zoster.
CLINICAL AND GROSS DISEASE VARIANTS CHARACTERIZATION
Ramsay Hunt syndrome.
Sweeney CJ, Gilden DH.
Department of Neurology, Mail Stop B182, University of Colorado Health Sciences Center
J Neurol Neurosurg Psychiatry 2001 Aug;71(2):149-54 Abstract quote
The strict definition of the Ramsay Hunt syndrome is peripheral facial nerve palsy accompanied by an erythematous vesicular rash on the ear (zoster oticus) or in the mouth.
J Ramsay Hunt, who described various clinical presentations of facial paralysis and rash, also recognised other frequent symptoms and signs such as tinnitus, hearing loss, nausea, vomiting, vertigo, and nystagmus. He explained these eighth nerve features by the close proximity of the geniculate ganglion to the vestibulocochlear nerve within the bony facial canal. Hunt's analysis of clinical variations of the syndrome now bearing his name led to his recognition of the general somatic sensory function of the facial nerve and his defining of the geniculate zone of the ear.
It is now known that varicella zoster virus (VZV) causes Ramsay Hunt syndrome. Compared with Bell's palsy (facial paralysis without rash), patients with Ramsay Hunt syndrome often have more severe paralysis at onset and are less likely to recover completely. Studies suggest that treatment with prednisone and acyclovir may improve outcome, although a prospective randomised treatment trial remains to be undertaken. In the only prospective study of patients with Ramsay Hunt syndrome, 14% developed vesicles after the onset of facial weakness. Thus, Ramsay Hunt syndrome may initially be indistinguishable from Bell's palsy. Further, Bell's palsy is significantly associated with herpes simplex virus (HSV) infection. In the light of the known safety and effectiveness of antiviral drugs against VZV or HSV, consideration should be given to early treatment of all patients with Ramsay Hunt syndrome or Bell's palsy with a 7-10 day course of famciclovir (500 mg, three times daily) or acyclovir (800 mg, five times daily), as well as oral prednisone (60 mg daily for 3-5 days).
Finally, some patients develop peripheral facial paralysis without ear or mouth rash, associated with either a fourfold rise in antibody to VZV or the presence of VZV DNA in auricular skin, blood mononuclear cells, middle ear fluid, or saliva. This indicates that a proportion of patients with "Bell's palsy" have Ramsay Hunt syndrome zoster sine herpete. Treatment of these patients with acyclovir and prednisone within 7 days of onset has been shown to improve the outcome of recovery from facial palsy.
LABORATORY/RADIOLOGY/OTHER TESTS CHARACTERIZATION
Detection of herpes simplex and varicella zoster viruses in clinical specimens using direct immunofluorescence and cell culture assays.
Meqdam MM, Todd D, Al-Abosi M.
Department of Applied Biology, Jordan University of Science and Technology, Irbid.
Microbios 2001;105(411):111-8 Abstract quote
Patients (33 in toto) with a clinical diagnosis of herpes infections (simplex, zoster or chickenpox) were investigated for the presence of herpes simplex virus (HSV) and varicella zoster virus (VZV) in skin samples, using direct immunofluorescence and cell culture assays.
Five patients with nonherpetic vesiculobullous disorders were included as negative controls. Of the 33 patients, nineteen (57.6%) were positive for HSV or VZV and fourteen (42.4%) were negative. Five controls were all negative for HSV or VZV. Of the nineteen positive patients, HSV was isolated from eight (42.1%) patients, by both direct immunofluorescence and cell culture assays. VZV was isolated from eleven (57.9%) patients, eleven (100%) by direct immunofluorescence assay, and six (54.5%) by cell culture assays. HSV was isolated from one patient clinically diagnosed as chickenpox (VZV), but otherwise the positive laboratory results were concordant with the clinical diagnosis.
For epidemiological studies, atypical cases and immunocompromised patients the clinical diagnosis should be confirmed in the laboratory.
PROGNOSIS AND TREATMENT CHARACTERIZATION
Childhood vaccination against varicella: persistence of antibody, duration of protection, and vaccine efficacy.
Vessey SJ, Chan CY, Kuter BJ, Kaplan KM, Waters M, Kutzler DP, Carfagno PA, Sadoff JC, Heyse JF, Matthews H, Li S, Chan IS.
Merck Research Laboratories, Merck & Co, Inc, West Point, Pennsylvania 19482, USA.
J Pediatr 2001 Aug;139(2):297-304 Abstract quote
OBJECTIVE: To document the duration of protection afforded by Oka/Merck varicella vaccine over a 7-year period.
STUDY DESIGN: The subjects were healthy children 1 to 12 years of age originally enrolled in clinical studies to evaluate the primary immune response to varicella vaccine 6 weeks after vaccination. Each was monitored for antibody persistence, breakthrough infection, and household exposure to varicella to produce estimates of vaccine efficacy.
RESULTS: The 6-year cumulative varicella antibody persistence rate was 99.5% (95% CI: 98.9%, 100.0%). The annual breakthrough rate through 7 years ranged from 0.2% to 2.3% per year; the estimated cumulative event rate was 6.5%. Comparison of the observed average annual breakthrough rate with the age-adjusted expected annual incidence rate of varicella in unvaccinated children corresponded to an estimated vaccine efficacy of 93.8% to 94.6%. Eighty vaccinated children were exposed to varicella in the household, resulting in 8 (10%) cases of infection. When compared with the historical attack rate of 86.8% in unvaccinated susceptible persons exposed to varicella in the household, this yields an estimated vaccine efficacy of 88.5% (95% CI: 80.9%, 96.1%). Varicella cases in vaccinated children generally were mild.
CONCLUSION: The live attenuated varicella vaccine is highly effective in inducing persistent immunity and long-term protection against breakthrough varicella infection.
Varicella vaccine exposure during pregnancy: data from the first 5 years of the pregnancy registry.
Shields KE, Galil K, Seward J, Sharrar RG, Cordero JF, Slater E.
Worldwide Product Safety & Epidemiology, Merck Research Laboratories, Merck & Co., Inc., USA.
Obstet Gynecol 2001 Jul;98(1):14-9 Abstract quote
OBJECTIVE: To assess the risks of congenital varicella syndrome and other birth defects in offspring of women who inadvertently received varicella vaccine during pregnancy or within 3 months of conception.
METHODS: Pregnant women inadvertently exposed to varicella vaccine, reported voluntarily, were enrolled in the Pregnancy Registry for VARIVAX (Merck & Co., Inc., West Point, PA). The pregnancies were monitored and the outcomes ascertained from questionnaires completed voluntarily by the health care providers. The rates of congenital varicella syndrome and congenital anomalies were calculated for seronegative women prospectively reported to the registry.
RESULTS: From March 17, 1995 through March 16, 2000, 362 pregnancy outcomes were identified from prospective reports. Ninety-two women were known to be seronegative to varicella, of whom 58 received their first dose of vaccine during the first or second trimester. No cases of congenital varicella syndrome were identified among 56 live births (rate 0%, 95% confidence interval [CI] 0, 15.6). Among all the prospective reports of live births, five congenital anomalies were reported. No specific pattern was identified in either the susceptible cohort or the sample population as a whole.
CONCLUSION: No abnormal features have been reported that suggested the occurrence of congenital varicella syndrome or other birth defects related to vaccine exposure during pregnancy. Because of the small numbers, this study has limited precision, so continued surveillance is warranted. However, these results should provide some assurance to health care providers and women with inadvertent exposure before or during pregnancy.
Immunization of HIV-infected children with varicella vaccine.
Levin MJ, Gershon AA, Weinberg A, Blanchard S, Nowak B, Palumbo P, Chan CY
AIDS Clinical Trials Group 265 Team. University of Colorado School of Medicine, Denver, USA.
J Pediatr 2001 Aug;139(2):305-10 Abstract quote
OBJECTIVE: To determine the safety and immunogenicity of varicella vaccine in children with human immunodeficiency virus (HIV) infection. Children (n = 41) who were mildly affected by HIV (Centers for Disease Control and Prevention stage N1 or A1) and had no history or serum antibody indicative of prior varicella infection were immunized with two doses of live attenuated varicella vaccine.
RESULTS: A minority of the vaccine recipients had mild local or systemic reactions. Vaccination had no effect on the clinical stage of HIV or the HIV RNA plasma load. CD4 cell percentage and CD4 cell count were marginally decreased at week 4 after the first vaccination; this effect was no longer present at week 8 after vaccination. Two months after the second dose of vaccine, 60% of vaccine recipients had anti-varicella antibody in their serum, and 83% had a positive lymphocyte proliferation assay response to varicella antigen.
CONCLUSION: On the basis of its safety and immunogenicity, varicella vaccine should be considered in the childhood vaccines given to mildly affected HIV-infected children.
Henry JB. Clinical Diagnosis and Management by Laboratory Methods. Twentieth Edition. WB Saunders. 2001.
Tzank-This cytologic preparation utilizes a swab of a blister base smearing it on a glass slide. The characteristic viral inclusion bodies of herpes will be present in an active lesion.
Send mail to
email@example.com with questions or comments about this web site.
Copyright © 2001 The Doctor's Doctor