445
CORRESPONDENCE Reporting of Toxic Shock Syndrome
Use of trade names is for identification only and does not imply endorsement by the Public Health Service or by the US Department of Health and Human Services. Reprints or correspondence: Dr. Lisa A. Jackson, Meningitis and Special Pathogens Branch, Mailstop C09. Centers for Disease Control, Atlanta, GA 30333. The Journal of Infectious Diseases This article is in the public domain.
1992;166:445
Lisa A. Jackson and Anne Schuchat Meningitis and Special Pathogens Branch, National Center for Infectious Diseases. Centers for Disease Control. Atlanta. Georgia
References I. Schlievert PM, Kim MH. Reporting oftoxic shock syndrome Staphylococells aureus in 1982 to 1990 [letter]. J Infect Dis 1991;164:1245-6. 2. Centers for Disease Control. Reduced incidence of menstrual toxic shock syndrome-United States. MMWR 1990;39:421-3. 3. Gaventa S, Reingold AL, Hightower AW, et al. Active surveillance for toxic shock syndrome in the United States, 1986. Rev Infect Dis 1989; II(suppl):S28-34. 4. Latham RH, Kehrberg MW. Jacobson JA, et al. Toxic shock syndrome in Utah: a case-control and surveillance study. Ann Intern Med 1982;96:906-8. 5. Osterholm MT, Forfang JC Toxic-shock syndrome in Minnesota: results of an active-passive surveillance system. J Infect Dis 1982; 145:45864. 6. Davis JP, Chesney PJ, Wand PJ, et al. Toxic-shock syndrome: epidemiologic features, recurrence, risk factors, and prevention. N Engl J Med 1986;303: 1429-35. 7. Schuchat A, Broome CY. Toxic shock syndrome and tampons. Epidemiol Rev 1991;13:99-112. 8. Reingold AL, Hargrett NT, Shands KN, et al. Toxic shock syndrome surveillance in the United States, 1980 to 1981. Ann Intern Med 1982;96:875-80.
Downloaded from http://jid.oxfordjournals.org/ by guest on August 11, 2015
To the Editor-Schlievert and Kim [I] in a recent letter reported on the number of Staphylococcus aureus toxic shock syndrome (TSS)-related isolates submitted to their laboratory over a 9-year period. Because the number of isolates they considered "menstrual related" remained nearly constant from 1983 to 1990, they concluded that the decline in incidence of menstrual TSS reported by the Centers for Disease Control (CDC) national passive surveillance system [2] may not be accurate. We wish to clarify the basis for our conclusion that the incidence of menstrual TSS has decreased. The passive surveillance system relies on voluntary reporting of recognized cases and thus may be influenced by reporting bias. To ensure that the decline in menstrual TSS cases reported to the passive surveillance system during the early 1980s reflected a true decrease in the incidence of this syndrome rather than an artifact of decreased public attention to TSS and reduced voluntary reporting, CDC undertook a collaborative multistate active surveillance study during 1986 and 1987 [3]. The results of active case-finding efforts confirmed the trends detected by the passive system. In 1986, the rate of menstrual TSS was 1.0 per 100,000 women 15-44 years of age, a significant decrease from rates of 6-12 per 100,000 women in comparable age groups detected by similar active case finding efforts in 1980 [4-6]. Menstrual-associated cases accounted for about the same percentage (55%) of the total in both the active and passive systems during a comparable time period, further supporting the ability of the passive system to accurately reflect trends in disease [7]. The decline in incidence of menstrual TSS is also consistent with control measures implemented during that period. After Rely brand tampons were removed from the market in 1980, there was a dramatic drop in the number of menstrual TSS cases. Between 1980 and 1986, tampon absorbency was lowered by manufacturers. In 1985 polyacrylate-containing tampons were withdrawn from the market, which resulted in further decreases in tampon absorbency. These changes were accompanied by a decrease in reports of menstrual TSS to the passive surveillance system [2]. These measures would not be expected to affect the number of non menstrual cases, which is consistent with the relatively stable number reported in the 1980s. The largest decrease in the number of menstrual TSS cases reported was from 1980 to 1982; from 1983 to 1990 the incidence continued to decline, but at a slower rate [2]. The continued decrease in menstrual TSS after 1982 may not have been apparent to Schlievert and Kim from their laboratory data for several reasons.
First, their data are based on isolates that were voluntarily submitted for testing for toxin production. This is not a routine part of the diagnostic evaluation for TSS and physician interest in obtaining this information may well vary over time; thus the relevance of this information to the incidence ofTSS is unclear. Second, CDC classifies a case of TSS as menstrual-associated only if the onset ofsymptoms was during or within 24 h after the end of the menstrual period. In the 1986 active surveillance project, only 55%of the reported cases that met the case definition for TSS and occurred in females were classified as menstrual-associated [3]. TSS in females also occurred in association with use of barrier contraceptives, in the postpartum state, and in association with wound infections. Conversely, Schlievert and Kim classified as "menstrual-associated" any vaginal-cervical culture from 1982 to 1987 and from 1988 to 1990 any isolate from a female. This classification system will certainly inflate the number and proportion of cases considered to be menstrual TSS. Third, Schlievert and Kim assumed that all S. aureus isolates submitted to their laboratory were from patients with TSS, although the clinical characteristics of these patients are not known. In contrast, CDC reports only patients who meet a strict clinical case definition for TSS [8]. Finally, since the isolates were submitted primarily from a single state, the data may not reflect national trends. Recognition of toxin-producing S. aureus and the testing of isolates from patients with TSS for these toxins has provided important information on the pathogenesis of TSS; however, data obtained in this manner must be viewed with caution when used to draw conclusions about national trends in incidence of disease.
CORRESPONDENCE Reporting of Toxic Shock Syndrome
Use of trade names is for identification only and does not imply endorsement by the Public Health Service or by the US Department of Health and Human Services. Reprints or correspondence: Dr. Lisa A. Jackson, Meningitis and Special Pathogens Branch, Mailstop C09. Centers for Disease Control, Atlanta, GA 30333. The Journal of Infectious Diseases This article is in the public domain.
1992;166:445
Lisa A. Jackson and Anne Schuchat Meningitis and Special Pathogens Branch, National Center for Infectious Diseases. Centers for Disease Control. Atlanta. Georgia
References I. Schlievert PM, Kim MH. Reporting oftoxic shock syndrome Staphylococells aureus in 1982 to 1990 [letter]. J Infect Dis 1991;164:1245-6. 2. Centers for Disease Control. Reduced incidence of menstrual toxic shock syndrome-United States. MMWR 1990;39:421-3. 3. Gaventa S, Reingold AL, Hightower AW, et al. Active surveillance for toxic shock syndrome in the United States, 1986. Rev Infect Dis 1989; II(suppl):S28-34. 4. Latham RH, Kehrberg MW. Jacobson JA, et al. Toxic shock syndrome in Utah: a case-control and surveillance study. Ann Intern Med 1982;96:906-8. 5. Osterholm MT, Forfang JC Toxic-shock syndrome in Minnesota: results of an active-passive surveillance system. J Infect Dis 1982; 145:45864. 6. Davis JP, Chesney PJ, Wand PJ, et al. Toxic-shock syndrome: epidemiologic features, recurrence, risk factors, and prevention. N Engl J Med 1986;303: 1429-35. 7. Schuchat A, Broome CY. Toxic shock syndrome and tampons. Epidemiol Rev 1991;13:99-112. 8. Reingold AL, Hargrett NT, Shands KN, et al. Toxic shock syndrome surveillance in the United States, 1980 to 1981. Ann Intern Med 1982;96:875-80.
Downloaded from http://jid.oxfordjournals.org/ by guest on August 11, 2015
To the Editor-Schlievert and Kim [I] in a recent letter reported on the number of Staphylococcus aureus toxic shock syndrome (TSS)-related isolates submitted to their laboratory over a 9-year period. Because the number of isolates they considered "menstrual related" remained nearly constant from 1983 to 1990, they concluded that the decline in incidence of menstrual TSS reported by the Centers for Disease Control (CDC) national passive surveillance system [2] may not be accurate. We wish to clarify the basis for our conclusion that the incidence of menstrual TSS has decreased. The passive surveillance system relies on voluntary reporting of recognized cases and thus may be influenced by reporting bias. To ensure that the decline in menstrual TSS cases reported to the passive surveillance system during the early 1980s reflected a true decrease in the incidence of this syndrome rather than an artifact of decreased public attention to TSS and reduced voluntary reporting, CDC undertook a collaborative multistate active surveillance study during 1986 and 1987 [3]. The results of active case-finding efforts confirmed the trends detected by the passive system. In 1986, the rate of menstrual TSS was 1.0 per 100,000 women 15-44 years of age, a significant decrease from rates of 6-12 per 100,000 women in comparable age groups detected by similar active case finding efforts in 1980 [4-6]. Menstrual-associated cases accounted for about the same percentage (55%) of the total in both the active and passive systems during a comparable time period, further supporting the ability of the passive system to accurately reflect trends in disease [7]. The decline in incidence of menstrual TSS is also consistent with control measures implemented during that period. After Rely brand tampons were removed from the market in 1980, there was a dramatic drop in the number of menstrual TSS cases. Between 1980 and 1986, tampon absorbency was lowered by manufacturers. In 1985 polyacrylate-containing tampons were withdrawn from the market, which resulted in further decreases in tampon absorbency. These changes were accompanied by a decrease in reports of menstrual TSS to the passive surveillance system [2]. These measures would not be expected to affect the number of non menstrual cases, which is consistent with the relatively stable number reported in the 1980s. The largest decrease in the number of menstrual TSS cases reported was from 1980 to 1982; from 1983 to 1990 the incidence continued to decline, but at a slower rate [2]. The continued decrease in menstrual TSS after 1982 may not have been apparent to Schlievert and Kim from their laboratory data for several reasons.
First, their data are based on isolates that were voluntarily submitted for testing for toxin production. This is not a routine part of the diagnostic evaluation for TSS and physician interest in obtaining this information may well vary over time; thus the relevance of this information to the incidence ofTSS is unclear. Second, CDC classifies a case of TSS as menstrual-associated only if the onset ofsymptoms was during or within 24 h after the end of the menstrual period. In the 1986 active surveillance project, only 55%of the reported cases that met the case definition for TSS and occurred in females were classified as menstrual-associated [3]. TSS in females also occurred in association with use of barrier contraceptives, in the postpartum state, and in association with wound infections. Conversely, Schlievert and Kim classified as "menstrual-associated" any vaginal-cervical culture from 1982 to 1987 and from 1988 to 1990 any isolate from a female. This classification system will certainly inflate the number and proportion of cases considered to be menstrual TSS. Third, Schlievert and Kim assumed that all S. aureus isolates submitted to their laboratory were from patients with TSS, although the clinical characteristics of these patients are not known. In contrast, CDC reports only patients who meet a strict clinical case definition for TSS [8]. Finally, since the isolates were submitted primarily from a single state, the data may not reflect national trends. Recognition of toxin-producing S. aureus and the testing of isolates from patients with TSS for these toxins has provided important information on the pathogenesis of TSS; however, data obtained in this manner must be viewed with caution when used to draw conclusions about national trends in incidence of disease.
