Since 1992, Neisseria meningitidis serogroup B strains have caused several community- and school-based outbreaks in the United States (1). Response to such outbreaks is difficult because no serogroup B vaccine is licensed currently for use in the United States, and mass chemoprophylaxis has been evaluated only in restricted settings (2,3). This report describes the use of mass prophylaxis to control outbreaks of serogroup B meningococcal disease in Florida in two unusual settings: a hotel resort and a nursing home.

Miami-Dade County

During July-August 1995, the Miami-Dade County Health Department was notified of one probable and four laboratory-confirmed cases of serogroup B meningococcal disease among children vacationing at a local resort area. All of the cases occurred among county residents who either stayed at or visited Hotel A. One child died.

The first reported case was in a guest at Hotel A who developed a fever on July 8. On July 9, symptoms developed in a sister and brother staying at Hotel B who had visited Hotel A to play with other children. The sister died shortly after admission to a local hospital; N. meningitidis serogroup B was isolated from blood cultures. Her brother was admitted with fever, vomiting, leg pain, and a petechial rash, and gram negative diplococci were observed in the cerebrospinal fluid (CSF). However, cultures were negative for N. meningitidis.

For the investigation, a hotel-related confirmed case was defined as isolation of N. meningitidis serogroup B from the blood or CSF of a person with classic symptoms of meningitis who was staying at or visiting hotel A. A presumptive case was defined as detection of gram-negative diplococci in specimens from a normally sterile site (blood and CSF) in a person with classic symptoms who had close contact with a confirmed case-patient.

Investigators noted overcrowding at hotel A, where some rooms had as many as 12 residents. An estimated 730 persons stayed or worked at hotels A and B during the week before onset of symptoms in the first two cases (attack rate: 274 per 100,000 population). The Advisory Committee on Immunization Practices defines an outbreak of serogroup C meningococcal disease as three or more confirmed or probable cases occurring during a period of approximately 3 months in persons with a common affiliation but no close contact, resulting in a primary disease attack rate of at least 10 cases per 100,000 persons (4).

After consultation with epidemiologists at the Florida Department of Health and CDC, county health officials offered prophylaxis on site to all guests and employees at both hotels. Over a 2-day period, 480 persons (66% of the targeted group) received the recommended rifampin dosage. The hotel swimming pool, the site of organized activities for children, was closed.

Approximately 5 weeks after the first cluster of cases was identified, a case was diagnosed in a 17-year-old who provided child care at hotel A during the days before onset of symptoms. A secondary case (occurring at least 24 hours after onset in the primary case) was diagnosed in a child who had been in this 17-year-old's care and who had resided at the hotel since June. The child and her family had received prophylaxis at the time of the first meningitis cluster. The county again offered prophylaxis to all guests and employees at hotel A. No further cases were identified among visitors to the resort area.

Skilled Nursing Facility

On December 5, 1997, the Florida Department of Health was notified of a laboratory-confirmed case of N. meningitidis in a resident of a 104-bed skilled nursing facility. Within 5 days, two additional laboratory-confirmed cases were diagnosed from the facility; all three cases were serogroup B.

For the investigation, a suspected case of meningococcal disease was defined as clinical diagnosis of meningococcal disease in a nursing home resident or staff member; a case was confirmed by isolation of N. meningitidis from blood or CSF.

A nurse had been hospitalized on December 1 with confusion and fever following 2 weeks of influenza-like symptoms. His CSF contained elevated protein, decreased glucose, and a mononuclear cell count of 7500 per cc. Specimens for culture were not obtained until 3 hours after antibiotics were started and were negative for bacterial pathogens.

On December 2, a 90-year-old patient in the wing where the staff nurse was assigned was hospitalized with a fever of 104 F (40 C) and vomiting. She died the following day. Blood cultures were positive for N. meningitidis. On December 5, a 56-year-old nursing assistant who had cared for the first confirmed case-patient was hospitalized after abrupt onset of fever and stiff neck; her CSF was positive for N. meningitidis.

On December 5, the Florida Department of Health recommended chemoprophylaxis for all patients and staff. However, the facility had consulted a community physician who recommended administration of prophylaxis to all persons who had visited the facility during the previous 14 days, nasopharyngeal swabs for culturing of all patients and staff, and closure of the facility to all visitors.

Ciprofloxacin (750 mg) was administered to all 114 staff members, 103 of 104 patients, and to approximately 250 visitors. Nasopharyngeal swabs, obtained post prophylaxis from all available patients, were negative for N. meningitidis. The facility placed itself on quarantine from December 6 through December 10, permitting no visitors, discharges, or admissions.

On December 10, a 73-year-old man who resided on the same floor as the first confirmed case-patient was hospitalized with fever and lethargy. Blood cultures were positive for N. meningitidis. This patient had refused prophylaxis on December 6. No further cases were reported.

The state laboratory performed pulsed-field gel electrophoresis on the first two outbreak-related case-patients and on two serogroup B case-patients that were linked to each other in another county. The two isolates from the facility showed similar banding patterns, but were different from the controls from the other county. Multilocus enzyme electrophoresis (MEE) subtyping was not performed.

Reported by: R Duany, MD, MA Cruz, MPH, S Atherley, MPH, JA Suarez, V Sneller, PhD, L Vaamonde, MD, K Mavunda, MD, E Sfakianaki, MD, Miami-Dade County Health Dept; E Jennings, Hernando County Health Dept, Spring Hill; R Sanderson, DJ Katz, PhD, R Hopkins, MD, Bur of Epidemiology, P Fiorella, PhD, Bur of Laboratory Svcs, WG Hlady, MD, Florida Dept of Health. Meningitis and Special Pathogens Br, Div of Bacterial and Mycotic Diseases, National Center for Infectious Diseases, CDC.

Editorial Note

Editorial Note: Organization-based outbreaks of meningococcal disease previously have been identified in military barracks, schools, universities, among jail inmates, and in a Job Corps center (3,5-8). The Florida serogroup B outbreaks occurred in institutions that have not been reported previously as settings for meningococcal outbreaks.

Crowding may have contributed to the outbreak at the resort hotel, where the hotel pool was the center of activities for a large number of children, and investigators noted room overcrowding. Crowding previously has been identified as a factor in the transmission of N. meningitidis at a university campus bar (7) and among jail in-mates (5), and outbreaks have been reported among children participating in school-based group activities (6). In the nursing home outbreak, the first illness occurred in a nurse who had had symptoms of a respiratory infection during the preceding 2 weeks. Coincident upper respiratory infections have been suggested as predisposing risk factors for the subsequent development of meningococcal disease and spread of infection (9). Guidelines for evaluation and management of suspected outbreaks are available only for serogroup C (4); these guidelines were adapted for use in the Florida clusters of serogroup B cases.

The primary tool in the control and prevention of meningococcal disease is identification and chemoprophylaxis of close contacts. Serogrouping of isolates also is necessary to determine whether an outbreak exists and whether vaccination should be considered. Pulsed-field gel electrophoresis and MEE may be useful for identifying the particular strain involved and for linking cases. In the nursing home outbreak, electrophoresis was able to establish that at least three of the four cases were related. Because MEE was not performed on isolates from either outbreak, it is not known whether the Florida outbreaks were caused by the ET-5 strains that have emerged recently as important causes of disease in Europe and the Americas (1).

When an outbreak is confirmed, a decision must be made on the appropriateness of more extensive control measures. Chemoprophylaxis of small, well-defined populations is the only available mass intervention for serogroup B outbreaks.

In many situations, the disadvantages of mass chemoprophylaxis (i.e., expense, side effects, and the emergence of resistant organisms) outweigh the benefits. However, in outbreaks involving small populations (e.g., an outbreak in a nursing home or a single school), administration of chemoprophylaxis to all persons within this population may be effective in preventing larger outbreaks (3).

To be effective, mass prophylaxis must be given simultaneously to all persons at risk. Otherwise, persons may reinfect each other. That may have been the explanation for the occurrence of the second cluster of cases in the hotel outbreak.

Although mass prophylaxis was justified for staff and patients in the nursing home outbreak, more than 250 casual contacts received prophylaxis unnecessarily, which has implications for the development of resistant strains (3). The extensive inappropriate treatment and testing suggests the need for education of medical students and public health professionals about appropriate public health responses to outbreaks of meningococcal disease.

References

1. Fischer M, Perkins BA. Neisseria meningitidis serogroup B: emergence of the ET-5 complex. Sem Pediatr Infec Dis 1997;8:50-6.

2. CDC. Serogroup B meningococcal disease -- Oregon, 1994. MMWR 1995;44: 121-4.

3. Jackson LA, Alexander ER, Debolt CA, et al. Evaluation of the use of mass chemoprophylaxis during a school outbreak of enzyme type 5 serogroup B meningococcal disease. Pediatr Infect Dis J 1996;15:992-8.

4. CDC. Control and prevention of meningococcal disease and control and prevention of serogroup C meningococcal disease: evaluation and management of suspected outbreaks. MMWR 1997;46(no. RR-5):13-21.

5. Tappero JW, Reporter R, Wenger JD, et al. Meningococcal disease in Los Angeles County, California, and among men in the county jails. N Engl J Med 1996;335:833-40.

6. Zangwill KM, Schuchat A, Riedo FX, et al. School-based clusters of meningococcal disease in the United States. JAMA 1997;277:389-95.

7. Imrey PB, Jackson LA, Ludwinski PH, et al. Meningococcal carriage, alcohol consumption, and campus bar patronage in a serogroup C meningococcal disease outbreak. J Clin Microbiol 1995;33:3133-7.

8. Jackson LA, Schuchat A, Reeves MW, Wenger JD. Serogroup C meningococcal outbreaks in the United States. JAMA 1995;273:383-9.

9. Moore PS, Hierholzer J, DeWitt W, et al. Respiratory viruses and mycoplasma as cofactors for epidemic group A meningococcal meningitis. JAMA 1990;264:1271-5.

   
   

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