Mortality data in this table are voluntarily reported from 121 cities in the United States, most of which have populations of 100,000 or more. A death is reported by the place of its occurrence and by the week that the death certificate was filed. Fetal deaths are not included.

Pneumonia and influenza

↑ Because of changes in reporting methods in these 4 Pennsylvania cities, these numbers are partial counts for the current week Complete counts will be available in 4 to 6 weeks

tt Total includes unknown ages

TABLE V. Years of potential life lost, deaths, and death rates, by cause of death, and estimated number of physician contacts, by principal diagnosis, United States

*For details of calculation, see footnotes for Table V, MMWR 1984;33:2.

*Years of potential life lost for persons between 1 year and 65 years old at the time of death are derived from the number of deaths in each age category as reported by the National Center for Health Statistics, Monthly Vital Statistics Report (MVSR), Vol. 31, No. 13, October 5, 1983.

National Center for Health Statistics, Monthly Vital Statistics Report (MVSR), Vol. 33, No. 3, June 21, 1984, pp. 8-9. IMS America National Disease and Therapeutic Index (NDTI), Monthly Report, February 1984, Section III. **MVSR Vol. 33, No. 2, May 23, 1984, p. 1.

ACIP: Rabies - Continued

Bahmanyar M, Fayaz A, Nour-Salehi S, Mohammadi M, Koprowski H. Successful protection of humans exposed to rabies infection: postexposure treatment with the new human diploid cell rabies vaccine and antirabies serum. JAMA 1976;236:2751-4.

Bernard KW, Smith PW, Kader FJ, Moran MJ. Neuroparalytic illness and human diploid cell rabies vaccine. JAMA 1982;248:3136-8.

Boe E, Nyland H. Guillain-Barré syndrome after vaccination with human diploid cell rabies vaccine. Scand J Infect Dis 1980;12:231-2.

CDC. Systemic allergic reactions following immunization with human diploid cell rabies vaccine. MMWR 1984;33:185-7.

Corey L, Hattwick MAW. Treatment of persons exposed to rabies. JAMA 1975;232:272-6.

Greenberg M, Childress J. Vaccination against rabies with duck-embryo and Semple vaccines. JAMA 1960;173:333-7.

Helmick CG: The epidemiology of human rabies postexposure prophylaxis, 1980-1981. JAMA 1983;250:1990-6.

ACIP: Rabies - Continued

Hattwick MAW. Human rabies. Public Health Reviews 1974;3:229-74.

Hattwick MAW, Rubin RH, Music S, Sikes RK, Smith JS, Gregg MB. Postexposure rabies prophylaxis

with human rabies immune globulin. JAMA 1974;227:407-10.

Peck FM Jr, Powell HM, Culbertson CG. A new antirabies vaccine for human use. J Lab Clin Med 1955;45:679-83.

Rubin RH, Hattwick MAW, Jones S, Gregg MB, Schwartz VD. Adverse reactions to duck embryo rabies vaccine. Range and incidence. Ann Intern Med 1973;78:643-9.

Tierkel ES, Sikes RK. Preexposure prophylaxis against rabies. Comparison of regimens. JAMA 1967;201:911-4.

Tint H, Rosanoff El. Clinical responses to T(n)BP-disrupted HDCS (WI-38) rabies vaccine. Dev Biol Stand 1976;37:287-9.

Wiktor TJ, Plotkin SA, Koprowski H. Development and clinical trials of the new human rabies vaccine of tissue culture (human diploid cell) origin. Dev Biol Stand 1978;40:3-9.

World Health Organization. Sixth report of the Expert Committee on Rabies. Geneva, Switzerland: World Health Organization, 1973 (WHO technical report no. 523).

Sinnecker H, Atanasiu P, Bahmanyar M, Selimov M, Wandeler Al, Bogel K (Working Group 2, World Health Organization). Vaccine potency requirements for reduced immunization schedules and preexposure treatment. Dev Biol Stand 1978;40:268-70.

Epidemiologic Notes and Reports

Chromosomally Mediated Resistant Neisseria gonorrhoeae

United States

During 1983-1984, an increasing number of cases of ß-lactamase negative, penicillinresistant Neisseria gonorrhoeae were reported to CDC. Unlike penicillinase-producing N. gonorrhoeae (PPNG), which have plasmid-mediated resistance to penicillin, these ß-lactamase negative, resistant gonococci have chromosomally mediated resistance based on available data.

The first reported outbreak of chromosomally mediated (B-lactamase negative) resistant N. gonorrhoeae (CMRNG) in the United States occurred in Durham County, North Carolina (1). Since this outbreak, in which more than 200 cases were eventually detected, 16 other states have reported cases with resistant gonococci. Of these, Tennessee, New Mexico, and Oregon have reported more sustained outbreaks.

Cases in these outbreaks were detected either by routine screening of all gonococcal isolates (New Mexico) or screening of primary treatment failure isolates (Tennessee, Oregon) for susceptibility to penicillin at the local or state levels. Screening was performed by disk agar diffusion or by growth on penicillin-containing media. Gonococcal isolates that grew on media containing 1.6 μg/ml of penicillin or produced a zone of inhibition less than 26 mm, with a 10 μg penicillin disk, were submitted to CDC for confirmation of resistance. Minimum inhibitory concentrations by the agar dilution susceptibility test were determined for antimicrobials that included penicillin, ampicillin, tetracycline, cefotaxime, cefuroxime, cefoxitin, spectinomycin, and trimethoprim/sulfamethoxazole. Isolates resistant to penicillin and ampicillin were equally resistant to tetracycline by agar dilution susceptibility testing.

Of all CMRNG isolates submitted to CDC for agar dilution susceptibility testing during 1983-1984, 11.0% were susceptible to less than 2 μg/ml of penicillin; none were susceptible to less than 2 μg/ml of tetracycline; and only 47.0% were susceptible to less than 0.5 μg/ml trimethoprim and 9.5 μg/ml sulfamethoxazole (trimethoprim/sulfamethoxazole). All isolates were susceptible to spectinomycin, cefoxitin, cefuroxime, and cefotaxime. Immunologic characterization demonstrated that all CMRNG isolates were serogroup llb (the majority of the same serovariant) based on serotyping by experimental monoclonal antibodies to major outer membrane protein (2). Of the 18 New Mexico cases, two distinctly different serovariants were detected within serogroup llb.

Neisseria gonorrhoeae - Continued

Clinical and epidemiologic information were obtained for patients whose isolates were tested. Excluding North Carolina, of the 16 other reporting states, over half of the CMRNG cases were from Tennessee, New Mexico, and Oregon.

Tennessee: All the 14 Tennessee patients were heterosexuals, and two patients could be linked to interstate travel to Virginia or North Carolina. Strains from the Tennessee cases were immunologically similar and had similar antimicrobial susceptibility patterns consistent with continued endemic transmission within the state.

New Mexico: Of the 18 CMRNG patients from New Mexico, seven were heterosexual (three males, four females), and 11 were homosexual males. All heterosexual patients and seven homosexual patients were infected with gonococcal strains immunologically identical, with similar antimicrobial susceptibility patterns. Strains from these cases were more resistant to penicillin than strains from the other four homosexual patients. Heterosexual CMRNG patients could not be linked to homosexual CMRNG patients by sexual history or naming of sexual contacts. All homosexual patients were clustered within Albuquerque; heterosexual patients were more widely distributed throughout the state. Based on immunologic studies of the gonoccoci recovered from these individuals and examination of temporal and geographic variables for heterosexuals versus homosexuals, at least two separate outbreaks with no demonstrable common source occurred in New Mexico. No evidence for interstate or foreign transmission into New Mexico could be identified for any of the cases.

Oregon: Of the eight cases reported from Oregon, all occurred among homosexual males. Gonococcal strains from these individuals shared identical immunologic and antimicrobial susceptibility patterns. No epidemiologic evidence for interstate or foreign transmission could be documented for any of these cases, suggesting only endemic transmission within the homosexual community in Oregon. No additional cases have been reported from Oregon since March 1984.

Reported by M Kimberly, DrPh, State Laboratory Director, W De Vault, CE Chapman, MD, G Conrad, Venereal Disease Control, RH Hutcheson, Jr, MD, State Epidemiologist, Tennessee State Dept of Health; JM Mann, MD, L Nims, Scientific Laboratory, A Chowning, E Montes, Venereal Disease Control, HF Hull, MD, State Epidemiologist, Health Svcs Div, New Mexico Dept of Health and Environment, L Foster, MD, D Harger, H Horton, Venereal Disease Control, C Schade, MD, JA Googins, MD, State Epidemiologist, State Health Div, Oregon Dept of Human Resources; Sexually Transmitted Diseases Laboratory Program, Center for Infectious Diseases, Div of Sexually Transmitted Diseases, Center for Prevention Svcs, Div of Field Svcs, Epidemiology Program Office, CDC.

Editorial Note: Seventeen states, including North Carolina, have reported cases of CMRNG to CDC since 1983. The majority of these cases were detected as primary therapeutic failures to the penicillins or tetracyclines. Gonococcal strains from the majority of U.S. outbreaks and cases have generally been immunologically similar (serogroup IIb) with similar antimicrobial susceptibilities.

Based on epidemiologic data, foreign importation has been infrequently documented for these CMRNG strains in the United States (3). In contrast, foreign importation contributes to the largest proportion of PPNG in the United States, although domestic transmission became more important after 1976 (4).

Cases of CMRNG may be detected by screening for penicillin resistance at the local or state levels to guide appropriate therapy and permit rapid follow-up of cases. Screening by disk agar diffusion or with penicillin-containing media will identify chromosomally mediated resistance to penicillin. Disk susceptibility testing to tetracycline and trimethoprim/sulfamethoxazole should be performed only by standardized procedures using appropriate controls (5,6). Inconsistent results to these two antimicrobials may be seen with disk susceptibility testing (5,6).

Based on agar dilution susceptibility testing, infections caused by CMRNG should clinically respond to therapy with recommended dosages of spectinomycin, cefoxitin, cefotaxime, or ce

Neisseria gonorrhoeae - Continued

furoxime. CDC treatment guidelines for PPNG infections provide the recommended schedules for these antimicrobials and emphasize the importance of the immediate use of spectinomycin as primary therapy for gonorrhea cases when treatment failures are suspected (7).

Since 1975, gonorrhea has generally declined in the United States (8). PPNG increased dramatically between 1976 and 1982 but decreased in 1983 (8). Unfortunately, cases of CMRNG have been reported with increasing frequency since the North Carolina outbreak. Because the extent and prevalence of CMRNG infections are not yet fully understood, screening of all ß-lactamase negative (nonpenicillinase-producing) primary treatment failure gonococcal isolates for penicillin susceptibility (1) is encouraged at the local and state levels to improve surveillance and guide appropriate therapy. Screening at the community level should be most cost-effective, since the majority of these CMRNG strains are equally resistant to tetracycline, thereby preventing unnecessary and usually ineffective retreatment with a tetracycline. Because of high secondary treatment failure rates with tetracycline, tetracycline should not be used as the drug of choice for either PPNG or CMRNG infections that have failed primary therapy with penicillin or ampicillin. Spectinomycin, cefoxitin, or cefotaxime should be used to treat CMRNG infections at dosages recommended for PPNG (7).

More active surveillance for these CMRNG infections will be required to determine their accurate prevalence, and support control activities.

References

1. CDC. Penicillin-resistant gonorrhea-North Carolina. MMWR 1983;32:273-5.

2. Tam MR, Buchanan TM, Sandstrom EG, Holmes KK, et al. Serological classification of Neisseria gonorrhoeae with monoclonal antibodies. Infect and Immun 1982;36:1042-53.

3. CDC. Gonorrhea surveillance reports, 1975-1984.

4. Jaffe HW, Biddle JW, Johnson SR, Wiesner PJ. Infections due to penicillinase producing Neisseria gonorrhoeae in the United States: 1976-1980. J Infect Dis 1981;144:191-7.

5. Biddle JW, Swenson JM, Thornsberry C. Disc agar diffusion antimicrobial susceptibility tests with beta-lactamase producing Neisseria gonorrhoeae. J Antibiot 1978;31:352-8.

6. Barry AL. "Diffusion test procedures." The antimicrobic susceptibility test: principles and practices. Philadelphia, Pennsylvania: Lea & Sebiger 1976:180-207.

7. CDC. Sexually transmitted diseases treatment guidelines, 1982. MMWR Supplement, 1982;31: 35S-62S.

8. CDC. Gonorrhea-United States, 1983. MMWR 1984;33:361-3.

Fatalities from Occupational Heat Exposure

Presented below are two of several fatalities from occupational heat stroke reported to the National Institute for Occupational Safety and Health (NIOSH) since 1977.

Indiana: In July 1980, a 24-year-old white male, who was employed at a surface coal mine, collapsed and later died after performing heavy labor in a hot environment. The worker, 5 feet 9 inches tall and weighing about 200 pounds, had been employed at the mine for 11⁄2 weeks. On the day of the reported incident, he was assigned to load 40-pound bags of explosives into vertically drilled holes in preparation for blasting the material overlying the coal seam. He began work at 6:00 a.m., and at 3:40 p.m., informed a co-worker that he did not feel well. He walked about 50 yards to a shady area and collapsed. The outdoor dry bulb temperature was 39.4 C (103 F).

The worker was moved to a nearby hospital where his rectal temperature registered 42.2 C (108 F). By the time he was transferred to the intensive care unit (ICU), his temperature exceeded 43.3 C (110 F). He was treated with an ice pack and intravenous fluids but died at 6:30p.m. The autopsy report listed systemic hyperthermia with extreme generalized dilation of capillaries (cardiovascular shock) and cerebral edema as the immediate causes of death.