ne elevated at 12.04 (normal: <12), consistent with an ngoing inflammatory process. Bacterial cultures of CSF mained negative, and additional CSF evaluation showed egative viral PCR tests for cytomegalovirus, Epstein-Barr rus, enterovirus, and herpes simplex virus. Analysis of CSF so was negative for neuromyelitis optica antibody, associed with Devic's disease. Repeat neuroimaging on Octoer 7 revealed further caudal to rostral progression of the rainstem and spinal cord abnormalities observed on October 5. Because of progressive neurologic decline, the atient was transferred to a tertiary-care center.

On arrival at the tertiary-care center, the patient was omatose with a Glasgow coma score of 3 without demonrable cranial nerve function. A neurologic examination vealed flaccid quadriparesis and hyporeflexia. EMG vealed severe, acute polyradiculoneuropathy. Auditory oked potential testing indicated absent responses. With e presumptive diagnosis of idiopathic transverse myeli5, the patient was treated with methylprednisolone and asmapheresis. On October 15, CSF analysis revealed a eocytosis of 22 cells/mm3 (94% lymphocytes), red blood ll count of 2,519 cells/mm3 (normal: 0 cells/mm3), evated protein of 235 mg/dL, normal glucose, and rther elevated immunoglobulin G synthesis rate of 3 mg/24 hours (normal: -9.9 to 3.3 mg/24 hours). MRI the brain revealed new symmetric T2-signal abnormalies within the basal ganglia and medial temporal lobes, ith subtle leptomeningeal gadolinium enhancement. he ascending paralysis and coma appeared atypical of iopathic transverse myelitis, and the patient's clinical proession and brain imaging abnormalities were noted to semble those observed in rabies encephalitis (1). Once rabies was suspected, the patient's family was terviewed on October 16 for a history of potential expore. According to his family, the patient had handled a it with his bare hands in a semi-open cabin porch in northntral Minnesota on August 19, 2007. He had reported eling a needle prick sensation before releasing the bat. ecause no blood or wound was visible, the patient conuded he had not been bitten and did not seek medical tention. Neither the patient nor his family was aware that exposure constituted a rabies risk.

is

On October 17, specimens of the patient's serum, CSF, iva, and a nuchal biopsy were sent to CDC. Rabies virus tibodies were detected in stored CSF and serum samples llected before plasma exchange, confirming the suspected agnosis. However, no rabies virus antigens were detected the skin biopsy using fluorescent microscopy, and no bies virus amplicons were detected in saliva or skin

biopsy samples by reverse transcription-PCR; therefore, antigenic characterization and genetic sequencing of the rabies virus variant were not possible. Because of the poor prognosis, medical care was withdrawn after extended family discussions, and the patient died on October 20, the twenty-second day of hospitalization.

Public Health Investigation

After diagnosis of rabies, the Minnesota Department of Health assessed the need for rabies postexposure prophylaxis (PEP) among close contacts of the patient and healthcare workers and searched the likely site of rabies exposure. Family members, other close contacts, and health-care workers were interviewed using a standard questionnaire to identify possible exposures to the patient's saliva. Three of 14 family contacts and 51 of 524 health-care workers who participated in the man's care received rabies PEP, administered chiefly at the respective hospital emergency departments. The Minnesota Department of Health received no information from health-care providers suggesting incomplete PEP administration or adverse events resulting from rabies vaccination. Although a search of the cabin site on October 26 revealed no evidence of bat infestation, given the reported bat exposure on August 19, initial symptoms on September 19, and an incubation period of approximately 1 month, investigators concluded that a bite from a bat was the most likely source of rabies virus infection. Reported by: AH Yee, DO, RT Merrell, MD, AY Zubkov, MD, PhD, AJ Aksamit, MD, WT Hu, MD, PhD, EM Manno, MD, Mayo Clinic, Rochester; J Scheftel, DVM, A DeVries, MD, D Neitzel, MS, R Danila, PhD, KE Smith, DVM, PhD, Minnesota Dept of Health. CE Rupprecht, VMD, PhD, Div of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases; S Holzbauer, DVM, EIS Officer, CDC.

Editorial Note: This report describes the only reported case of human rabies in the United States in 2007 and the first case in Minnesota since 2000. Investigators determined that the likely source of rabies in this case was a bat. In Minnesota, bats and skunks are the only known reservoirs of rabies. In 2006, 42 rabid animals were reported in the state, including 17 bats and 20 skunks (2).

During 2000-2007, a total of 25 cases of human rabies were reported in the United States (2). Eighteen (28%) cases were associated with suspected exposure to rabid bats or infection with bat rabies virus variants. Most of these human cases occurred in late summer or early autumn, coincident with a seasonal increase in the prevalence of rabid bats detected in the United States (2). Despite repeated documentation of human rabies attributable to bat exposures and identification of 1,212-1,692 rabid bats

in the United States during 2000-2006, the significance of bat exposures often is ignored (3,4).

The animal contact, incubation period, clinical presentation, and laboratory findings for the patient described in this report were typical of human rabies cases reported in the United States. However, a diagnosis of rabies was not considered until the clinical course appeared atypical of the presumptive diagnosis of idiopathic transverse myelitis and brain imaging abnormalities resembled those observed in rabies. One unusual facet of this case was the inability to detect viral antigens or nucleic acids in patient samples, although rabies virus antibodies were identified in the serum and CSF. The only other human rabies case in the United States in which viral antigens or nucleic acids could not be detected, since such laboratory methods became more widely available in the early 1990s, was a 2004 Wisconsin patient, who survived rabies after a bat bite (1,5). However, the Wisconsin patient was an adolescent girl treated successfully with a drug-induced coma and antiviral drugs, and the significance of any similarities between that case and the Minnesota case is unclear.

This report underscores the need for increased public awareness of the risks of direct contact with bats and other wild animals. After exposure, human rabies is preventable with timely and appropriate PEP, consisting of proper wound care and prompt administration of rabies biologicals (4). Rabies PEP is recommended for all persons with direct transdermal or mucous membrane exposure to a bat, unless the animal is found not to have rabies. However, bite lesions from certain animals, including bats, can be difficult to detect. Consequently, proper tailoring of health communications to medical practitioners and the public remains a challenge to ensure that appropriate PEP is administered when indicated but not unnecessarily.

Rabies should be considered in the differential diagnosis of human cases involving acute, rapidly progressive encephalitis, especially when the clinical course and neuroimaging findings are compatible, regardless of history of animal exposure (1,4). If a patient is unresponsive, interview of family members and close contacts might reveal potential exposures. Prompt diagnosis of rabies can enable rapid case investigation, implementation of appropriate infection-control measures, and consideration of experimental therapy (5).

Acknowledgments

The findings in this report are based, in part, on contributions by M Junna, MD, A Frye, MD, Mayo Clinic, Rochester, Minnesota; and R Franka, DVM, PhD, M Niezgoda, MS, L. Orciari, MS, and P Yager, Div of Viral and Rickettsial Diseases, National Center for Zoonotic, Vector-Borne, and Enteric Diseases, CDC.

References

1. Hu WT, Willoughby RE Jr, Dhonau H, Mack KJ. Long-term fol up after treatment of rabies by induction of coma. N Engl J M 2007;357:945-6.

2. Blanton JD, Hanlon CA, Rupprecht CE. Rabies surveillance in United States during 2006. J Am Vet Med Assoc 2007;231:540–56. 3. Liesener AL, Smith KE, Davis RD, et al. Circumstances of bat enco ters and knowledge of rabies among Minnesota residents submittin bats for rabies testing. Vector Borne Zoonotic Dis 2006;6:213-20 4. CDC. Human rabies prevention-United States, 1999: recommenci tions of the Advisory Committee on Immunization Practices. MMW 1999;48(No. RR-1).

5. Willoughby RE Jr, Tieves KS, Hoffman GM, et al. Survival afte treatment of rabies with induction of coma. N Engl J Med. 200 352:2508-14.

Report from the Advisory Committee on Immunization Practices (ACIP): Decision Not to Recommend Routine Vaccination of All Children Aged 2-10 Years with Quadrivalent Meningococcal

Conjugate Vaccine (MCV4)

At its February 2008 meeting, the Advisory Committ on Immunization Practices (ACIP) decided not to recor mend routine vaccination of children aged 2-10 year against meningococcal disease unless the child is at increase risk for the disease. This report summarizes the delibera tions of ACIP and the rationale for its decision and restats existing recommendations for meningococcal vaccinatio among children aged 2-10 years at increased risk for mer ingococcal disease. ACIP continues to recommend routi vaccination against meningococcal disease for all person aged 11-18 years and those persons aged 2-55 years wh are at increased risk for meningococcal disease (1–3).

On October 17, 2007, the Food and Drug Administra tion added approval for use of quadrivalent meningococc conjugate vaccine (MCV4) (Menactra®, Sanofi Pasteu Swiftwater, Pennsylvania) in children aged 2-10 years: existing approval for use in persons aged 11-55 years ( Before licensure of MCV4, quadrivalent meningococc polysaccharide vaccine (MPSV4) (Menomune®, Sane Pasteur) was the only meningococcal vaccine available the United States. MPSV4 was recommended for routin use only among persons at increased risk for meningoco cal disease (1). Because clinical efficacy trials were not fe sible in the United States, MCV4 licensure was based o clinical trials in which the safety and immunogenicity o MCV4 was compared with MPSV4. Immunogenicity wa measured by serum bactericidal activity (SBA), a correlat

637 750

(372-487)

f protection. Rates of most solicited local and systemic dverse events after MCV4 vaccination were comparable to tes observed after administration of MPSV4 (5). The proortion of children aged 2-10 years who did not have etectable SBA (titer <1:8) at day 0 and seroconverted iter >1:32) by day 28 after MCV4 vaccination was 98.6% or serogroup A, 87.9% for serogroup C, 86.2% for erogroup Y, and 96.0% for serogroup W-135, similar to 'IPSV4 for all serogroups (Table) (5). Hence, MCV4 was ound to be safe and noninferior to MPSV4 for all erogroups.

During June 2007-February 2008, the ACIP Meningooccal Vaccine Workgroup considered use of MCV4 among ildren aged 2-10 years by reviewing data on MCV4 nmunogenicity and safety in this age group, the epideiology and burden of meningococcal disease, costfectiveness of various vaccination strategies, and rogrammatic implications. These data, expert opinion of orkgroup members, and feedback from partner organizaons were presented by the workgroup to the full ACIP at ie October 2007 and February 2008 ACIP meetings for s deliberation regarding a potential recommendation to accinate only those children at increased risk for meninococcal disease, among children aged 2-10 years.

ummary of ACIP Deliberations nd Rationale

ACIP evaluated data to determine the anticipated duraon of protection from a single dose of MCV4 in children ;ed 2–10 years. The duration of protection of MPSV4 is onsidered to be short (3-5 years), especially in young ildren, based on substantial declines in measurable levs of antibodies against group A and C polysaccharides by years after vaccination (6,7). Although SBA titers at 28 ys and 6 months after vaccination were significantly higher

in children aged 2-10 years who received MCV4 compared with children who received MPSV4 for all four serogroups (p<0.001) (5), the difference in magnitude of SBA titers between children in the two groups was not substantial (Table). Further, SBA activity among children aged 2–3 years who received MCV4 was lower than in children aged 4-10 years. Based on these data, ACIP concluded that evidence was insufficient to determine that 1 dose of MCV4 administered at age 2 years would provide protection against meningococcal disease through late adolescence and college entry.

ACIP also reviewed the burden of meningococcal disease among children aged 2-10 years. In the United States, during 1998-2007, overall rates of meningococcal disease were lower in children aged 2-10 years (0.68 per 100,000 population) than in infants aged <2 years and adolescents aged 11-19 years (3.9 and 0.81 per 100,000, respectively). Furthermore, 41% of cases in children aged 2-10 years occurred among children aged 2-3 years. In addition, among cases that occurred in children aged 2-10 years, 59% were caused by serogroups contained in MCV4 (A, C, Y, and W-135), compared with 77% of cases among youths aged 11-19 years. Annually, an estimated 160 cases of A/C/Y/W-135 disease and 13 deaths occur in children aged 2-10 years, compared with 250 cases and 15 deaths among youths aged 11-19 years (Active Bacterial Core Surveillance [ABCs], unpublished data, 1997-2006).

A cost-effectiveness analysis of vaccinating a cohort of U.S. children aged 2 years also was presented at the February 2008 ACIP meeting. A Monte Carlo simulation analysis was used in which multiple parameters were varied simultaneously over specified probability distributions. Data on age- and serogroup-specific meningococcal incidence rates during 1991-2005 and case-fatality ratios from ABCs were used, in addition to published estimates of meningococcal

disease complications (e.g., hearing loss and limb amputations) and vaccine efficacy (8). Duration of protection of 10 years from vaccination was assumed. Using standard cost-effectiveness methods, the analysis estimated that 205 meningococcal cases and 14 premature deaths could be prevented by vaccinating a cohort of 4 million children aged 2 years at a cost of $160,000 per quality-adjusted life year (QALY) saved. For a program conducting routine vaccination of children aged 11 years, the analysis estimated a cost of $90,000 per QALY saved. Hence, vaccinating children aged 2 years was determined to be less cost-effective than vaccinating children aged 11 years (8).

Because approximately 75% of cases of disease in children aged 2 years occur at age 24-29 months, the effectiveness of routine MCV4 vaccination of children aged 2 years in reducing the burden of disease is dependent on achieving high coverage at age 24 months (ABCs, unpublished data, 2008). However, achieving high coverage with MCV4 at age 24 months might be challenging. For example, during 1999-2006, before licensure of hepatitis. A vaccine for use in children aged 12-23 months, ACIP recommended administration of hepatitis A vaccine to children at age 2 years in states with historically high rates of hepatitis A. After that recommendation was in effect for 5 years in the 11 states where vaccination was recommended, 1-dose coverage was 54.4% (range by state: 8.6%74.4%) among children aged 24-35 months (9).

ACIP Decision and Continuing
Recommendations

Based on reviews of safety and immunogenicity data, the epidemiology of meningococcal disease, a cost-effectiveness analysis, and programmatic considerations, ACIP decided not to recommend routine vaccination against meningococcal disease for all children aged 2-10 years at its February 2008 meeting. ACIP continues to recommend vaccination for children aged 2-10 years at increased risk for meningococcal disease. These children include travelers to or residents of countries in which meningococcal disease is hyperendemic or epidemic, children who have terminal complement deficiencies, and children who have anatomic or functional asplenia. Health-care providers also may elect to vaccinate children aged 2-10 years who are infected with human immunodeficiency virus (HIV).* MCV4 is preferred to MPSV4 for children aged 2-10 years in these groups at increased risk and for control of meningococcal disease out

* Children with HIV infection likely are at increased risk for meningococcal disease, although not to the extent they are at risk for invasive Streptococcus pneumoniae infection. The efficacy of MCV4 among HIV-infected children is unknown.

breaks. In addition, if health-care providers or parents elec to provide meningococcal vaccination to other children. ir this age group, MCV4 is preferred to MPSV4. Recommen dations for use of MCV4 in persons aged 11-55 years including a recommendation for routine vaccination with MCV4 of persons aged 11-18 years, have been published previously and remain unchanged (1,3).

For children aged 2-10 years who have received MPSV and remain at increased risk for meningococcal disease, ACIP recommends vaccination with MCV4 at 3 years after receipt of MPSV4. Children who last received MPSV4 more than 3 years before and remain at increased risk for meningococcal disease should be vaccinated with MCV4 as soon as possible. For children at lifelong increased risk for meningococcal disease, subsequent doses of MCV4 likely will be needed. ACIP will monitor available data on duration of protection to determine whether recommendations for revaccination with MCV4 are indicated. Persons with a history of Guillain-Barré syndrome (GBS) might be at increased risk for GBS after MCV4 vaccination (3); there fore, a history of GBS is a precaution to administration c MCV4.

Effective meningococcal conjugate vaccines for infants might be available in the near future. Phase III clinical tri als for meningococcal conjugate vaccine in infants are ongoing, and published data suggest these vaccines are saf and immunogenic (10). Vaccines that provide protection against meningococcal disease early in life have the potential to greatly reduce the burden of meningococcal disease especially if they provide protection against serogroup f meningococcal disease.

References

1. CDC. Prevention and control of meningococcal disease: recomme dations of the Advisory Committee on Immunization Practices (ACI MMWR 2005;54(No. RR-7).

2. CDC. Recommendation from the Advisory Committee on Immuniza tion Practices (ACIP) for use of quadrivalent meningococcal con gate vaccine (MCV4) in children aged 2-10 years at increased risk for invasive meningococcal disease. MMWR 2007;56:1265–6.

3. CDC. Revised recommendations of the Advisory Committee of Immunization Practices to vaccinate all persons aged 11-18 years with meningococcal conjugate vaccine. MMWR 2007;56:794-5. 4. Food and Drug Administration. Product approval information-licering action, package insert: Meningococcal (groups A, C, Y, W-135 polysaccharide diphtheria toxoid conjugate vaccine Menactr Rockville, MD: US Department of Health and Human Services, Food and Drug Administration; 2005. Available at http://www.fda.gov/cbc label/menactralb.pdf.

5. Pichichero M, Casey J, Blatter M, et al. Comparative trial of the safer and immunogenicity of quadrivalent (A, C, Y, W-135) meningococc polysaccharide-diphtheria conjugate vaccine versus quadrivalent polysaccharide vaccine in two- to ten-year-old children. Pediatr Infect Dis J 2005;24:57-62.

15. Gold R, Lepow ML, Goldschneider I, Draper TF, Gotshlich EC. Kinetics of antibody production to group A and group C meningococcal polysaccharide vaccines administered during the first six years of life: prospects for routine immunization of infants and children. J Infect Dis 1979;140:690–7.

7. Borrow R, Goldblatt N, Andrews J, et al. Antibody persistence and immunological memory at age 4 years after meningococcal group C conjugate vaccination in children in the United Kingdom. J Infect Dis 2002;186:1353-7.

3. Shepard CW, Ortega-Sanchez IR, Scott RD II, Rosenstein NE, ABCs Team. Cost-effectiveness of conjugate meningococcal vaccination strategies in the United States. Pediatrics 2005;115:1220–32. .CDC. Prevention of hepatitis A through active or passive immunization. MMWR 2006:55(No. RR-7).

). Snape M, Perrett K, Ford K, et al. Immunogenicity of a tetravalent meningococcal glycoconjugate vaccine in infants: a randomized controlled trial. JAMA 2008;299:173–84.

May is Healthy Vision Month. The focus of this year's ɔservance is raising awareness of sport-related eye injuries children and the importance of using protective eyewear. pproximately 100,000 of the eye injuries that occur each ear in the United States are sports related (1). Children ged <15 years account for nearly one third of all hospital Imissions for eye trauma and 43% of all sports and recreional eye injuries (2). Proper use of protective eyewear ould prevent most of these injuries (3).

Healthy People 2010 objectives include increasing the use protective eyewear among children participating in recreional activities and hazardous home situations (e.g., cookg and yard work) (objective 28-9). Additional information assist children, parents, coaches, and communities in ducing sport-related eye injuries is available from the ational Eye Institute's Healthy Vision Month website at tp://www.healthyvision2010.nei.nih.gov/hvm. Informaon regarding the Vision Health Initiative at CDC is availole at http://www.cdc.gov/diabetes/projects/vision.htm.

Notice to Readers

National Drinking Water Week May 4-10, 2008

This year marks the 100th anniversary of one of the most significant public health advances in U.S. history, the disinfection of drinking water. To highlight the importance of safe tap water and the need to reinvest in water infrastructure, the American Water Works Association and an alliance of other organizations are sponsoring National Drinking Water Week (1).

Safe drinking water is one of the most valuable resources of the United States. During the past century, many improvements in the health of the U.S. population, such as preventing tooth decay through community fluoridation and controlling infectious diseases, can be attributed. to improvements in drinking water quality (2). Disinfection has played a critical role in the provision of safe drinking water in the United States since 1908 (3). During 1900-1920, the incidence of typhoid fever in the United States decreased substantially, from 100.0 to 33.8 cases per 100,000 population (4,5). By 2006, incidence of typhoid fever had decreased to 0.1 per 100,000 population (only 353 cases), and approximately 75% of these cases occurred among persons returning from international travel (6,7). This decrease in waterborne illness can be credited to advances in public health, including implementation of drinking water disinfection in community water systems.

The United States has one of the safest public water supplies in the world. Nonetheless, an estimated 4-33 million cases of gastrointestinal illness associated with public drinking water systems occur annually in the United States (8). These estimates do not include illnesses that occur in the estimated 45 million persons served by small or individual water systems (9) or illnesses other than gastrointestinal illness. The continued occurrence of drinking water-associated disease highlights the importance of maintaining and improving the nation's water infrastructure.

CDC activities related to National Drinking Water Week include promoting waterborne disease prevention, reducing the adverse health effects from contaminated drinking water, improving access to safe water internationally, addressing terrorism concerns related to waterborne pathogens, strengthening waterborne disease outbreak surveillance and investigations, and supporting water-related programs at local and state health departments. Additional information regarding CDC activities is available at http://www.cdc.gov/health/water.htm, http://www.cdc.gov/ ncidod/dpd/healthywater, http://www.cdc.gov/nceh/ehhe/ water, http://www.cdc.gov/fluoridation, http://www.cdc.gov/