215 Centers for Disease Control, “Recommendations for Counseling Persons Infected with Human T-Lymphotropic Virus, Types I and II,†Morbidity and Mortality Weekly Report 42 (1993): 1–7.
216 C. Bartholomew, C. Saxinger, J. W. Clark, et al., “Transmission of HTLV-I and HIV Among Homosexual Men in Trinidad,†Journal of the American Medical Association 257 (1987): 2604–8.
217 H. Lee, P. Swanson, V. S. Shorty, et al., “High Rate of HTLV-II Infection in Seropositive IV Drug Abusers in New Orleans,†Science 244 (1989): 471–77.
218 P. S. Sarma and J. Gruber, “Human T-Cell Lymphotropic Viruses in Human Diseases,†Journal of the National Cancer Institute 81 (1990): 1100–6.
U.S. prostitute surveys showed HTLV-II incidence was highest among those women who were injecting drug users. See R. F. Khabbaz, W. W. Darrow, T. M. Hartley, et al., “Seroprevalence and Risk Factors for HTLV-I/II Infection Among Female Prostitutes in the United States,†Journal of the American Medical Association 263 (1990): 60–64. By 1991 the U.S. blood-bank industry conceded that both HTLV viruses had contaminated the American blood supply. See M. T. Sullivan, A. E. Williams, C. T. Fang, et al., “Transmission of Human T-Lymphotropic Virus Types I and II by Blood Transfusion,†Archives of Internal Medicine 151 (1991): 2043–48.
219 Serwadda’s group noted that in 1985 “the first recognized cases came from a small village on Lake Victoria, just north of the Tanzanian border. This village was one of many from which goods were traded across the border. The notion that the disease may have been transmitted sexually from Tanzania is interesting since it fits historically with the movements of the Tanzanian Army … and subsequent regular visits by the Tanzanian traders. Of the 15 traders tested for evidence of HTLV-III [HIV] antibodies, 10 were positive … . There have been no studies as yet to show whether the virus is endemic in Tanzania and, if so, whether it has been introduced from Uganda via traders and soldiers.†See Serwadda, Mugerwa, and Sewankambo, (1985), op. cit.
12. Feminine Hygiene
1 N. Friedman, “Everything They Didn’t Tell You About Tampons,†New West, October 20, 1980: 33–42; and R. E. Wheatley, M. F. Menkin, E. D. Bardes, and J. Rock, “Tampons in Menstrual Hygiene,†Journal of the American Medical Association 192 (1965): 113–16.
2 In 1977 a medical team from the University of Colorado Medical Center in Denver reported treating four young women (two of whom were teenagers) for vaginal ulcers, apparently caused by tampons. Two of the cases involved the so-called deodorant products (actually perfumed, rather than deodorized). All four women healed with cessation of tampon use. See K. F. Barrett, S. Bledsoe, B. E. Greer, and W. Droegemueller, “Tampon-Induced Vaginal or Cervical Ulceration,†American Journal of Obstetrics and Gynecology 127 (1977): 332–33.
3 The industry denied allegations that asbestos was ever used in their products, but also consistently refused to list the stabilizing fibers that were used to prevent the cotton tampons from falling apart.
4 D. E. Marlowe, R. M. Weigle, and R. W. Stauffenberg, “Measurement of Tampon Absorbency: Evaluation of Tampon Brands,†Bureau of Medical Devices, U.S. Food and Drug Administration, Rockville, MD, 1981.
5 In her outstanding piece of investigative journalism, Nancy Friedman notes: “The range of blood loss during menstruation is two to six ounces. A single superabsorbent tampon is capable of soaking up an ounce or more of fluid. Since menstruation is a gradual process lasting three to seven days, the question arises: If the tampon has absorbed all the blood leaving the uterus and still hasn’t reached saturation, what will it absorb? The answer: the normal secretions of the healthy vaginal walls.†Friedman (1980), op. cit.
6 M. Chrapil et al., “Reaction of the Vagina to Cellulose Sponges,†Journal of Biomedical Materials Research 13 (1979): 1.
7 A. Johnson, “Used Carboxymethyl Cellulose as Chromatographic Purifier for Staphylococcal Toxins,†Infection and Immunology 25 (1979): 1080–85.
8 K. F. Barrett, “Tampon-Induced Ulceration,†American Journal of Obstetrics and Gynecology 127 (1977): 332; R. K. Collins, “Tampon Induced Vaginal Laceration,†Journal of Family Practice 9 (1979): 127; and F. K. Beller, “Vaginal Tampon as Drug Carrier,†Medical World 30 (1979): 709.
9 J. P. Davis, J. Chesney, P. J. Wand, et al., “Toxic-Shock Syndrome,†New England Journal of Medicine 303 (1980): 1429–35.
10 J. Todd, M. Fishaut, F. Kapral, and T. Welch, “Toxic-Shock Syndrome Associated with Phage-Group-I Staphylococci,†Lancet II (1978): 1116–18.
11 F. Stevens, “The Occurrence of Staphylococcus aureus Infection with a Scarlatiniform Rash,†Journal of the American Medical Association 88 (1927): 1957.
12 H. Aranow and W. B. Wood, “Staphylococcal Infection Stimulating Scarlet Fever,†Journal of the American Medical Association 119 (1942): 1491.
13 T. Kawasaki, “Acute Febrile Mucocutaneous Syndrome with Lymphoid Involvement with Specific Desquamation of the Fingers and Toes in Children,†Japanese Journal of Allergology 16 (1967): 178–222.
14 Between 1975 and 1980 over 10,000 cases of Kawasaki syndrome were diagnosed in Japan.
15 Centers for Disease Control, “Toxic-Shock Syndrome—United States,†Morbidity and Mortality Weekly Report 29 (1980): 229–30.
16 See Table 1 in K. N. Shands, G. P. Schmid, B. B. Dan, et al., “Toxic-Shock Syndrome in Menstruating Women,†New England Journal of Medicine 303 (1980): 1436–42.
17 Centers for Disease Control, “Follow-up on Toxic-Shock Syndrome,†Morbidity and Mortality Weekly Report 29 (1980): 441–45.
18 The CDC’s results were:
Cases Controls
Tampon Brand (N = 42) (N = 114)
Rely 71% 26%
Playtex 19% 25%
Tampax 5% 25%
Kotex 2% 12%
OB 2% 11%
19 Food and Drug Administration, News Release PBD-42, September 25, 1980.
20 Centers for Disease Control, “Toxic-Shock Syndrome—Utah,†Morbidity and Mortality Weekly Report 29 (1980): 495–96.
21 D. B. Petitti, A. Reingold, and J. Chin, “The Incidence of Toxic Shock in Northern California,†Journal of the American Medical Association 255 (1986): 368–72.
22 According to the manufacturers, prior to 1977 all tampons were made primarily of rayon and cotton. After 1977, however, 65 percent of all tampons sold in the United States contained polyacrylate fibers, carboxymethyl cellulose, higher-absorbency rayon-cellulose, polyester, or other synthetics.
23 R. W. Tofte, K. B. Crossley, and D. N. Williams, “Clinical Experience with Toxic-Shock Syndrome,†New England Journal of Medicine 303 (1980): 1417.
24 “Report Rise in Toxic Shock Cases Unrelated to Tampon Use,†Hospital Practice, July 1982: 197–200; “S. aureus Bacteriophage May Be Implicated in Toxic Shock,†Hospital Practice, May 1983: 36–38; and B. Hanna and P. Tierno, “Staphylococcal Growth on Carboxymethyl Cellulose,†presentation to the Annual Meeting of the American Society of Microbiology, 1981.
25 It is likely that true Staphylococcus rates were 100 percent. As physicians became more familiar with TSS and recognized the speed with which the ailment could dangerously escalate, it became routine to give symptomatic menstruating females high doses of non-penicillinase antibiotics before taking vaginal samples and awaiting staph culture results.
26 Davis et al. (1980), op. cit.
27 These and many other comments in this chapter were made to the author during interviews conducted over the course of the TSS investigation.
28 J. Langone, “Riddle of the Tampon,†Discover, December 1989: 26–28.
29 P. M. Schlievert, K. M. Bettin, and D. W. Watson, �
�Purification and Characterization of Group A Streptococcal Pyrogenic Exotoxin Type C,†Infection and Immunology 16 (1977): 673–79.
30 P. Schlievert, “Activation of Murine T-Suppressor Lymphocytes by Group A Streptococcal and Staphylococcal Pyrogenic Exotoxins,†Infection and Immunology 28 (1980): 876–80.
31 Institute of Medicine, “Toxic Shock Syndrome: Assessment of Current Information and Future Research Needs†(Washington, D.C.: National Academy Press, 1982).
32 By that time Schlievert and his collaborators in Minnesota, Wisconsin, Colorado, and California were seeing clear autoimmune disorders in the women who had survived TSS bouts months earlier. Eleven of 123 women surveyed had developed lupus, and 40 percent had early symptoms of arthritis—a striking finding given that most TSS sufferers were under thirty-five years of age.
P. M. Schlievert, K. M. Shands, B. B. Dan, et al., “Identification and Characterization of an Exotoxin from Staphylococcus aureus Associated with Toxic-Shock Syndrome,†Journal of Infectious Diseases 143 (1981): 509–16; and P. M. Schlievert and J. A. Kelly, “Staphylococcal Pyrogenic Exotoxin Type C: Further Characterization,†Annals of Internal Medicine 96 (1982): 982–86.
33 Centers for Disease Control, “Toxic Shock Syndrome, United States, 1970–1982,†Morbidity and Mortality Weekly Report 31 (1982): 201–4.
34 Centers for Disease Control, “Update: Toxic-Shock Syndrome—United States,†Journal of the American Medical Association 250 (1983): 1017.
35 A. L. Reingold, “Epidemiology of Toxic-Shock Syndrome, United States, 1960–1984,†Morbidity and Mortality Weekly Report 33 (1982): 19ss—22ss.
36 When averaged over the population as a whole for the various states, acute TSS cases occurred, for example, in:
State Per capita (all ages, both genders)
Utah 1:10,288
Minnesota 1:14,201
Wisconsin 1:17,363
Colorado 1:22,228
Oregon 1:30,978
Ohio 1:73,956
Washington 1:93,917
Indiana 1:99,368
California 1:100,713
Michigan 1:110,262
Texas 1:122,633
New York 1:532,065
Based on cumulative reports, 1975–83, to the CDC.
See Petitti, Reingold, and Chin (1986), op. cit.
37 S. F. Berkley, A. W. Hightower, C. V. Broome, and A. L. Reingold, “The Relationship of Tampon Characteristics to Menstrual Toxic Shock Syndrome,†Journal of the American Medical Association 258 (1987): 917–20.
38 G. Faich, K. Pearson, D. Fleming, et al., “Toxic Shock Syndrome and the Vaginal Contraceptive Sponge,†Journal of the American Medical Association 255 (1986): 216–18; and A. L. Reingold, “Toxic Shock Syndrome and the Vaginal Sponge,†Journal of the American Medical Association 255 (1986): 242–43.
39 S. M. Wolfe, “Dangerous Delays in Tampon Absorbency Warnings,†Journal of the American Medical Association 258 (1987): 949–51.
40 The chart was as follows:
Absorbency Ranges of Absorbency in Grams
Tampons come in the following standardized industry-size absorbencies. Junior absorbency Less than 6
Regular absorbency 6 to 9
Super absorbency 9 to 12
Super Plus absorbency 12 to 15
41 L. E. Markowitz, A. W. Hightower, C. V. Broome, and A. L. Reingold, “Toxic Shock Syndrome: Evaluation of National Surveillance Data Using a Hospital Discharge Survey,†Journal of the American Medical Association 258 (1987): 75–78.
42 K. L. MacDonald, M. T. Osterholm, C. W. Hedberg, et al., “Toxic Shock Syndrome: A Newly Recognized Complication of Influenza and Influenzalike Illness,†Journal of the American Medical Association 257 (1987): 1053–58; and Centers for Disease Control, “Toxic Shock Syndrome Associated with Influenza,†Morbidity and Mortality Weekly Report 35 (1986): 143–44.
43 S. J. Sperber and J. B. Francis, “Toxic Shock Syndrome During an Influenza Outbreak,†Journal of the American Medical Association 257 (1987): 1086–87.
Langmuir and his colleagues hypothesized the existence of such a scourge, combining TSS and influenza, which they dubbed Thucydides syndrome after the great Greek chronicler, and said might have been the cause of the 430–427 B.C. plague of Athens. See A. D. Langmuir, T. D. Worthen, J. Solomon, et al., “The Thucydides Syndrome: A New Hypothesis for the Cause of the Plague in Athens,†New England Journal of Medicine 313 (1985): 1027–39; and B. B. Dan, “Toxic Shock Syndrome: Back to the Future,†Journal of the American Medical Association 257 (1987): 1094–95.
44 J. K. Todd, M. Ressman, S. A. Caston, et al., “Corticosteroid Therapy for Patients with Toxic Shock Syndrome,†Journal of the American Medical Association 252 (1984): 3399–3402.
45 L. K. Altman, “Bacteria Are Linked to Deadly Childhood Disease,†New York Times, December, 3, 1993: A28.
46 A. L. Bisno, “Staphylococcal Endocarditis and Bacteremia,†Hospital Practice, April 15, 1986: 139–58.
47 D. Y. M. Leung, H. C. Meissner, D. R. Fulton, et al., “Toxic Shock Syndrome Toxin-Secreting Staphylococcus aureus in Kawasaki Syndrome,†Lancet 342 (1993): 1385–88.
48 J. M. Musser, P. Schlievert, A. W. Chow, et al., “A Single Clone of Staphylococcus aureus Causes the Majority of Cases of Toxic Shock Syndrome,†Proceedings of the National Academy of Sciences 87 (1990): 225–29.
49 TSST-1 can stimulate rapid proliferation of T cells in doses of less than 10-9M, which means a person could have virtually undetectable amounts of the toxin in his or her blood and develop acute Toxic Shock Syndrome.
50 For a succinct description of the immune system effects of TSST-1, see A. K. Abbas, A. H. Lichtman, and J. S. Pober, Cellular and Molecular Immunology (Philadelphia: W. B. Saunders, 1991), 304.
51 B. N. Kreiswirth, J. S. Kornblum, and R. P. Novick, “Genotypic Variability of the Toxic Shock Syndrome Exoprotein Determinant,†in J. Jeljaszewicz, ed., The Staphylococci (Stuttgart: Gustav Fischer Verlag, 1985).
52 M. C. Chu, B. N. Kreiswirth, P. A. Pattee, et al., “Association of Toxic Shock Toxin-1 Determinant with a Heterologous Insertion of Multiple Loci in the Staphylococcus aureus Chromosome,†Infection and Immunity 56 (1988): 2702–8.
53 Plasmids were self-contained units of DNA that could be exchanged from one microbe to another either as random events, or in response to specific survival pressure when a population of bacteria were exposed to antibiotics. For further details of both the TSST-1 and penicillin-resistance transposons, see: Murphy, E. “Transposable Elements in Gram-Positive Bacteria.†Chapter 9. Eds. D. E. Berg and M. M. Howe. Mobile DNA. Washington, D.C.: American Society for Microbiology, 1989.
13. The Revenge of the Germs
1 There are thousands of natural and synthetic antibiotics, relatively few of which have been tested and marketed. The most commonly used are as follows:
2 A. L. Bisno, “Staphylococcal Endocarditis and Bacteremia,†Hospital Practice, April 15, 1986: 139–58.
3 A. L. Panililo, D. H. Culver, R. P. Gaynes, et al., “Methicillin-Resistant Staphylococcus aureus in U.S. Hospitals, 1975–1991,†Infection Control and Hospital Epidemiology 13 (1992): 582–86.
4 M. Truneh, “Phage Types and Drug Susceptibility Patterns of Staphylococcus aureus from Two Hospitals in Northwest Ethiopia,†Ethiopian Medical Journal 29 (1991): 1–6.
5 E. E. Udo and W. B. Grubb, “Transfer of Resistance Determinants from a Multi-Resistant Staphylococcus aureus Isolate,†Journal of Medical Microbiology 35 (1990): 72–79.
6 For overviews of the antibiotic resistance crisis, see M. L. Cohen, “Epidemiology of Drug Resistance: Implications for a Post-Antimicrobial
Era,†Science 257 (1992): 1050–55; S. M. Finegold, “Antimicrobial Therapy of Anaerobic Infections: A Status Report,†Hospital Practice, October 1979: 71–81; L. O. Gentry, “Bacterial Resistance,†Orthopedic Clinics of North America 22 (1991): 379–88; A. Gibbons, “Exploring New Strategies to Fight Drug-Resistant Microbes,†Science 257 (1992): 1036–38; M. Lappe, Germs That Won’t Die (Garden City, NY: Anchor Press, 1982); S. B. Levy, The Antibiotic Paradox (New York: Plenum Press, 1992); H. C. Neu, “The Crisis in Antibiotic Resistance,†Science 257 (1992): 1064–73; Panlilio et al. (1992), op. cit.; and M. Toner, “When Bugs Fight Back,†Pulitzer Prize-winning series of reports in the Atlanta Constitution, August 23, 1992—October 16, 1992.
7 D. P. Levine, B. S. Fromm, and B. R. Reddy, “Slow Response to Vancomycin or Vancomycin Plus Rifampin in Methicillin-Resistant Staphylococcus aureus Endocarditis,†Annals of Internal Medicine 115 (1991): 674–80.
8 D. S. Kernodle and A. B. Kaiser, “Comparative Prophylactic Efficacy of Cefazolin and Vancomycin in a Guinea Pig Model of Staphylococcus aureus Wound Infection,†Journal of Infectious Diseases 168 (1993): 152–57; and R. P. Wenzel, “Preoperative Antibiotic Prophylaxis,†New England Journal of Medicine 326 (1992): 337–39.
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