The Editors welcome submissions for possible publication in the Letters section. Authors of letters should: • Include no more than 400 words of text, three authors, and five references • Type with double-spacing • Send three copies of the letter and a transfer-of-copyright form (see Table of Contents for location) signed by all authors • Provide a self-addressed envelope if they want to be notified that the letter was received Letters commenting on an Annals article will be considered if they are received within 6 weeks of the time the article was published. Only some of the letters received can be published. Published letters are edited and may be shortened; tables and figures are included only selectively. Authors will be notified that the letter has been received. If the letter is selected for publication, the author will be notified about 3 weeks before the publication date. Unpublished letters cannot be returned. HIV Transmission in a Dental Practice To the Editors: We are astonished by the conclusion reached by Ciesielski and colleagues (1) that the small risk for being infected with human immunodeficiency virus (HIV) should not deter patients from seeking necessary dental care. This advice seems to contradict their own results. Although deviations from recommended procedures of infection control were noted, none could reasonably have been expected to cause the high rate of transmission of HIV from this dentist (5 of 1100 patients or 0.45%). Considering only those patients who had invasive procedures, the rate is even higher. No one with sound reason would choose to have an invasive procedure were this dentist still practicing. If there was nothing unique about this dentist in his practice, why is the risk not similar with other HIV-infected dentists? One possible explanation for not observing it elsewhere is that an unusual set of circumstances was needed to discover the cluster of cases. One patient needed to know that she had no other risk factors and that her dentist had the acquired immunodeficiency syndrome (AIDS); she also would have had to become symptomatic in an unusually short period of time. If the relationship had not been established for "Patient A , " it may never have been discovered for the other infected patients. This cluster of cases may turn out to be an aberration, but is it fair or wise to wait for another cluster before making safeguards and recommendations to protect the public? Daniel S. Berman, MD Barry D. Wenglin, MD White Plains Medical Association White Plains, NY 10605 Reference 1. Ciesielski C, Marianos D, Ou C, Dumbaugh R, Witte J, Berkelman R, et al. Transmission of HIV in a dental practice. Ann Intern Med. 1992;116:798-805.

To the Editors: Ciesielski and colleagues describe transmission of HIV to 5 of approximately 1100 exposed patients in a dentist's office (1, 2), the only known instance of occupational HIV transmission by health care personnel (2). The authors conclude that the preponderance of data indicate the probable viral source to be the dentist, who continued to practice den-

tistry despite having AIDS. This multipatient episode in one dental office stands in marked contrast to the more than 10 000 evaluated patients said to have been exposed to other HIVinfected health care workers without acquiring HIV infection (2). No evidence of sharps injury to the dentist's skin nor findings suggesting HIV transmission through contaminated instruments were noted. No postulated mechanisms of dentistto-patient transmission were presented. I note that a Kaposi sarcoma lesion in the dentist's palate was biopsied in 1987; considerable delay in complete healing of the palatal ulceration after biopsy is possible. In 1988, mucositis in the oropharynx was also evident, resulting from radiation treatment of the oral Kaposi sarcoma. I suggest that both merit serious consideration as factors promoting efficient HIV transmission. This conclusion is based on assumptions of specific conditions crucial for transmission: 1) a relatively high HIV level in the dentist's blood and at sites of the biopsied Kaposi sarcoma and oral mucositis, and 2) ulcerative or intermittently bleeding oral lesions as a consequence of biopsy and mucositis. That the dentist was actively practicing during times that he had " s o r e s " in his mouth has been bruited about Florida. Transmission might have occurred through body fluid-contaminated oral secretions that gained access to the lateral (open) edges of his face mask, and heavy droplets (> 5 microns in diameter) subsequently being nebulized by the dentist during his treatment of patients. The longer the mask was worn, the wetter with oral secretions it would have become (3). If the dentist's masked face was in close proximity to the open mouth of a patient, as is generally the case, dissemination of heavy droplet nebulae containing HIV to a fresh gingival incision may well have resulted in indirect contact transmission of HIV to some patients. Such an occurrence would be particularly likely if the dentist talked or sneezed during operative procedures (4). Transmission also could have occurred by direct contact if the dentist inadvertently touched the HlV-contaminated oral secretions on his mask or face and then touched a freshly incised patient site. Although it is known that saliva from HIV-infected men generally does not yield HIV (5), I am unfamiliar with studies of body fluid-contaminated oral secretions from persons with AIDS, who had the conditions described. N. Joel Ehrenkranz, MD Florida Consortium for Infection Control South Miami, F L 33143 References 1. Ciesielski C, Marianos D, Ou CY, Witte J, Dumbaugh R, Berkelman R, et al. Transmission of human immunodeficiency virus in a dental practice. Ann Intern Med. 1992;116:798-805. 2. Update: investigations of patients who have been treated by HIVinfected health-care workers. MMWR. 1992;41:344-6. 3. Davies WT. Filtration efficiency of surgical face masks: the need for more meaningful standards. Amer J Infect Control. 1991;19:16-8. 4. Riley RL, O'Grady F. Airborne Infection. New York: The MacMillan Co.; 1961:127. 5. Barr CE. Recovery of infectious HIV-1 from whole saliva: blood proves more likely virus transmitter. J Am Dent Assoc. 1992;123:3745.

To the Editors: In their report, Ciesielski and colleagues (1) state that " H I V does not remain viable for extended periods outside the body." This statement conflicts with the findings of Resnick and associates (2), who mixed highly concentrated, cell-free virus with human plasma and then dried it at room

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temperature. The titer of virus fell at a rate of 1 log per 9 hours, but infectious virus was still detectable at 3 days. Others have shown survival of HIV in water and lyophilized blood derivatives and on Petri dishes and cover slips (3). Ciesielski and associates (1) also state that HIV "is susceptible to commonly used germicides, including those used in the practice." The dental practice that was the focus of this report, however, used at least one germicide (alcohol) ineffective against HIV. When HIV was dried in the presence of serum (in an attempt to replicate clinical conditions [3]), 70% ethanol did not kill HIV even with contact times as long as 10 minutes (4), whereas the other germicide (2% glutaraldehyde) used rapidly killed HIV (4). Dental handpieces and other items that contact mucous membranes should be sterilized or should receive high-level disinfection (5). This process requires thorough cleaning of all surfaces and the use of a high-level disinfectant (for example, 2% glutaraldehyde). If the germicide manufacturer's instructions regarding concentration, shelf life, and contact time are meticulously followed, HIV and other pathogens are effectively killed. Ciesielski and coworkers (1) noted that the "handpieces were wiped with alcohol after each patient encounter; water lines were not flushed between patients." This procedure was clearly inadequate. Cleansing was not done, the germicide used was not a high-level disinfectant, and contact time was too brief. Possible persistence of HIV on dental equipment does not imply transmission. Indeed, we agree with Ciesielski and coworkers (1) that no evidence suggests that dental equipment transmits HIV. We also agree that dental handpieces were unlikely to have caused the reported outbreak, because epidemiologic evidence strongly suggested dentist-to-patient rather than patient-to-patient spread (1). However, the widespread but mistaken belief that HIV dies quickly outside the human body may lead to a false sense of security. Sattar and Springthorpe (3) have stated it well: "Although no cases of environmental spread of HIV have been documented, it would be foolhardy to assume that such transmission will never take place." Richard Frothingham, MD Daniel J. Sexton, MD Duke University Medical Center Durham, NC 27710 References 1. Ciesielski C, Marianos D, Ou CY, Witte J, Dumbaugh R, Berkelman R, et al. Transmission of human immunodeficiency virus in a dental practice. Ann Intern Med. 1992;116:798-805. 2. Resnick I, Veren K, Salahuddin SZ, Tondreau S, Markham PD. Stability and inactivation of HTLV-III/LAV under clinical and laboratory environments. JAMA. 1986;255:1887-91. 3. Sattar SA, Springthorpe VS. Survival and disinfectant inactivation of the human immunodeficiency virus: A critical review. Rev Infect Dis. 1991;13:430-47. 4. Hanson PJV, Gor D, Jeffries DJ, Collins JV. Chemical inactivation of HIV on surfaces. Br Med J. 1989;298:862-4. 5. Centers for Disease Control. Recommendations for prevention of HIV transmission in health-care settings. MMWR. 1987;36:1-18.

In response: Drs. Berman, Wenglin, and Ehrenkranz highlight the most puzzling aspect of our investigation—how HIV was transmitted to five patients in a Florida dental practice (1). Because we could not identify the specific incident, many hypotheses have been proposed. Most, although theoretically possible, seem unlikely. Dr. Ehrenkranz's hypothesis that the patients were infected by nebulized HIV-containing oral secretions seems rather improbable. Records from the dentist's oral examination conducted 2 weeks after biopsy of his palatal Kaposi sarcoma lesions in September 1987 do not indicate any delay in healing. None of the five patients were seen in the office during this time, and only two were seen during or near the time that the dentist was receiving radiation therapy (1). Although the dentist did develop oral mucositis immediately after receiving radiation therapy in June 1988, records from an oral examination in early July document that the reaction had subsided. The dentist's medical records also indicate that his oral Kaposi 794

sarcoma lesions were not exophytic or ulcerated, nor is there any indication that they bled intermittently. The lesions regressed after the radiation therapy and were not noted again until the spring of 1989, shortly before the dentist discontinued his practice. Neither the staff nor his patients indicated that the dentist sneezed frequently or in the faces of patients or that his face masks were ever tinged with blood. Further, it would seem very unusual for a face mask to be soaked with a dentist's oral secretions; in the absence of drooling, the moisture that accumulates on these masks originates from wet spray or splatter from the dental equipment and from moisture in the breath, which is exhaled through the mask. Drs. Berman and Wenglin question the risk of transmission by HIV-infected health care workers. To date, our investigation remains the only known instance of HIV transmission from an infected health care worker to patients. Eighty-four patients of HIV-infected health care workers from approximately 16 000 patients known to have been tested for HIV antibodies were found to be infected (2). Follow-up, thus far, has not shown transmission from a health care worker as the source of HIV infection for any of these persons. Although the risk for HIV transmission from infected health care workers to patients has not been well quantified, data from these investigations and modeled risk estimates indicate that this risk is very small (3) and may depend on various factors including the procedures done, the infection control precautions used, and the individual technique and skill of the health care worker. Carol Ciesielski, MD Donald Marianos, DDS Harold Jaffe, MD Centers for Disease Control Atlanta, GA 30333 References 1. Ciesielski C, Marianos D, Ou CY, Dumbaugh R, Witte J, Berkelman R, et al. Transmission of human immunodeficiency virus in a dental practice. Ann Intern Med. 1992;116:798-805. 2. Centers for Disease Control. Update: Investigations of patients who have been treated by HIV-infected health care workers. MMWR. 1992;41:344-6. 3. Chamberland ME, Bell DM. HIV transmission from health care worker to patient: what is the risk? [Editorial]. Ann Intern Med. 1992;116:871-3.

To the Editors: The continuing spread of HIV-infection is a daily concern of modern medical practice. Yet, considerable naivete exists about the increasing importance of heterosexual transmission of HIV. Two separate incidents in our practice illustrate this problem. In the first, a well-educated mother asked that her now college-age daughter be put on an oral contraceptive. "Wouldn't it be awful," she asked, "if she became pregnant while at school?" When asked if the issue of HIV infection had ever been discussed, she replied in a startled way: "How in the world could she ever get that?" One of us heard the same thing numerous times while working in a student health center of a major suburban college. The second case was more tragic. A 21-year-old woman had tested negative for HIV before beginning sexual relations with a young man to whom she eventually became engaged. Oral contraceptives were the only method of birth control used. The patient's partner tested positive for HIV when presenting for blood donation, and our patient's repeat test was also positive. Given the emphasis on education to combat the epidemic, we propose that the following label be attached to every package of oral contraceptives: WARNING: USE OF THIS PRODUCT WITHOUT OTHER PROTECTION MAY INCREASE YOUR RISK FOR EXPOSURE TO SEXUALLY TRANSMITTED DISEASES, INCLUDING THE HUMAN IMMUNODEFICIENCY VIRUS (THE CAUSE OF AIDS). Although shocking, such a warning may open people's eyes about exposure as a result of the increased risk resulting from sexual encounters with new or multiple partners.

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Eric C. Last, DO Lauri S. Last, DO, MPH 1046 Bellmore Road North Bellmore, NY 11710 Intracerebral Bacillary Angiomatosis in HIV To the Editors: I read with interest Spach and colleagues' first reported case of intracerebral bacillary angiomatosis in a patient infected with human immunodeficiency virus (1). We report a similar occurrence in a 37-year-old white male homosexual patient with the acquired immunodeficiency syndrome (AIDS) who presented in July 1990 with low-grade fever, dyspnea, and cough. Physical examination showed bilateral rales; chest radiographs and gallium scan results were compatible with a diagnosis of Pneumocystitis carinii pneumonia. The patient was treated with pentamidine, zidovudine, and steroids, resulting in resolution of clinical and radiologic findings. Several weeks later, the patient presented with abdominal pain and tenderness, lower back pain, and trigeminal neuralgia. Physical examination showed a 14-cm tender liver, tenderness to percussion over lumbar disks 1 to 3, and lancinating pain over the fifth faciocranial nerve. A computed tomographic (CT) scan of the abdomen before and during dynamic injection of contrast material showed a 1.5-cm defect in the midportion of the right hepatic lobe and a 4-cm defect in the interior margin of the right hepatic lobe; a 20-mc sulfur colloid nuclear flow study showed a vascular lesion in the right hepatic lobe. Two nuclear magnetic resonance imaging (MRI) scans of the spine showed increased signal densities consistent with vascular defects in L3 and L4. The patient refused biopsy; he was treated with erythromycin, 500 mg intravenously, every 6 hours for 3 weeks with complete resolution of symptoms. Repeat CT and MRI scans were normal. We believe that bacillary angiomatosis should be considered more frequently as a cause of neurologic dysfunction in patients with AIDS. "Empiric" therapy with erythromycin is a reasonable, less dangerous, and less costly alternative to other empiric therapies such as oral pyrimethamine, sulfadiazine, or intravenous acylovir. Pamela Jo Harris, MD 1810 Calvert Street, NW Suite Number Five Washington, DC 20009

potentials were consistent with bilateral injury to the distal brachial plexus. We believe that the patient suffered axillary vein thrombosis and bilateral brachial plexus injury secondary to neurovascular compression in the axillae due to rostrally secured vest restraint and concomitant distally secured wrist restraints. Hospital records supported the occurrence of the injury after admission, and the case was successfully litigated against the admitting institution. Scott and Gross (1) reported two cases of brachial plexus injury documented by electrophysiologic studies when vest and wrist restraints were secured in a similar manner. No mention was made of the duration of any deficits. Vogel and Bromberg (2) reported electrophysiologically documented brachial plexus injury in a patient restrained with vest restraint for a prolonged period; the patient showed improvement after modification of the restraint. The use of wrist restraints was not mentioned. Additional reports document the potential for injury due to the use of physical restraint (3, 4), and a recent study documents the lack of significant reduction in fall-related injury during the use of physical restraint (5). Ongoing research and attention to the appropriate use of physical restraint is needed. Mark B. Sheen, MD Marvin P. Rozear, MD Joel C. Morgenlander, MD Duke University Medical Center Durham, NC 27710 References 1. Scott TF, Gross JA. Brachial plexus injury due to vest restraints [Letter]. N Engl J Med. 1989;320:598. 2. Vogel CM, Bromberg MB. Proximal upper extremity compressive neuropathy associated with prolonged use of a jacket restraint [Abstract]. Muscle Nerve. 1990; 13:860. 3. Dube AH, Mitchell EK. Accidental strangulation from vest restraints. JAMA. 1986;256:2725-6. 4. Katz L. Accidental strangulation from vest restraints. JAMA. 1987; 257:2032-3. 5. Tinetti ME, Liu W, Ginter SF. Mechanical restraint and fall-related injuries among residents of skilled nursing facilities. Ann Intern Med. 1992;116:369-74.

Colchicine and Secondary Amyloidosis

Reference 1. Spach DH, Panther LA, Thorning DR, Dunn JE, Plorde JJ, Miller RA. Intracerebral bacillary angiomatosis in a patient infected with human immunodeficiency virus. Ann Intern Med. 1991;116:740-2.

Posey Palsy To the Editors: There has been growing public and legislative attention to potential hazards and appropriate use of physical restraint in patient care. We report a case of bilateral brachial plexus injury and unilateral axillary vein thrombosis due to the combined use of vest and wrist restraints. A 48-year-old male unrestrained driver suffered closed head injury in a head-on collision 17 months before his referral for bilateral hand weakness. On hospitalization after the accident, he was graded as Glasgow Coma Scale 14, with no evidence of acute cerebral injury by computed tomographic (CT) scan. His blood alcohol level was 200 mg/dL. A neurologic exam showed no focal abnormalities. Due to agitation, wrist and vest restraints were used, and he struggled with them repeatedly. During the use of restraints, marked arm swelling was noted, and axillary vein thrombosis was documented by venogram. His first recollection of this hospitalization was that both hands were "numb" and "heavy." He received extensive rehabilitation therapy and showed significant improvement, except for persistent bilateral hand weakness and numbness. On referral, a neurologic examination showed bilateral "claw hand" deformities with weakness and hypesthesia consistent with a distal brachial plexopathy. An electromyographic study, nerve conduction studies, and somatosensory-evoked

To the Editors: We are writing to support the observations in the letter by Zemer and Langevitz that secondary amyloidosis could be treated with colchicine (1). We have followed a 52-year-old man with psoriatic arthritis for more than 10 years. He presented with skin rashes, deforming arthritis, mild uremia, and peripheral edema. His 24-hour urinary protein excretion was 2 g, and his creatinine clearance was 30 mL/minute. Renal biopsy showed amyloidosis, and he was started on topical agents for his skin rashes and on colchicine for amyloidosis. Thirty months later, peripheral edema and protenuria regressed. Serum creatinine and blood urea nitrogen levels decreased slightly (48 mg/dL and 3.2 mg/dL before treatment and 32 mg/dL and 2 mg/dL after treatment, respectively) and the creatinine clearance was 34 ml/ minute. During that time, he had had several exacerbations of the skin lesions. Follow-up biopsy was not done. Despite the absence of a widely accepted therapy for amyloidosis, colchicine appears to be effective in the treatment and prevention of amyloidosis and in delaying the onset of uremia and reversing the nephrotic syndrome (2, 3). One report (4) describes reversal of the nephrotic syndrome with colchicine in a patient with amyloidosis secondary to ankylosing spondylitis. These reports suggest the possibility that colchicine, in at least some cases, could be beneficial in not only preventing but also in reversing nephropathy in patients with secondary amyloidosis. A controlled study with biopsy confirmation is, however, required. Ali Serdar Fak, MD Cetin Ozener, MD Emel Akoglu, MD Marmara University School of Medicine Istanbul, Turkey

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References 1. Zemer D, Langevitz P. Reversal of the nephrotic syndrome by colchicine in amyloidosis of familial mediterranean fever. Ann Intern Med. 1992; 116:426. 2. Ravid M, Robson M, Kedar I. Prolonged colchicine treatment in four patients with amyloidosis. Ann Intern Med. 1977;87:568-570. 3. Gertz MA, Kyle R. Secondary systemic amyloidosis: response and survival in 64 patients. Medicine. 1991;70:246-56. 4. Escalante A, Ehresmann G, Quismorio F. Regression of reactive systemic amyloidosis due to ankylosing spondylitis following the administration of colchicine. Arthritis Rheum. 1991;34:920-2.

Genetics and Tuberculosis Resistance To the Editors: Dr. Stead neatly summarizes the case for an underlying genetic basis for resistance to infection by Mycobacterium tuberculosis. His challenge, in his concluding paragraph, to " . . . genetic engineers to identify the genes or genes responsible for enhanced resistance . . . " may be a long time in being answered (1). Although many homozygous genetic diseases probably arose as population responses to environmental pathogens, this course of investigation may not be fertile. Consider the sickle cell scenario, in which the heterozygous state conferred enough resistance to malaria to maintain the allele in the population, but at the expense of homozygous persons with severe disease. A current hypothesis on the genetic basis for resistance to tuberculosis is that lysosomal storage diseases (for example, Gauchers disease, Niemann-Picks disease, and TaySachs disease) arose in ghetto-bound Ashkenazi Jews living through Eastern European epidemics of tuberculosis (2, 3). In both cases, the response by natural selection appears to have been the creation of a homozygous disease state to achieve a " . . . pathogen-driven heterozygote advantage . . . " (3). A better understanding of tuberculosis and host resistance will still require detailed studies on the interaction between M. tuberculosis and lysosomal processing. Even if, as molecular cell biologists, we were able to localize enhanced resistance to a particular enzyme or cell process, there is no guarantee based on retrospective epidemiologic studies that pharmaceutical or gene therapy aimed at augmenting resistance in whites would work in blacks. Under what circumstances could we justify any " c u r e " that caused neurologic and other sequelae of lysosomal storage disease? Ibrahim A. Tangoren University of Pennsylvania School of Medicine Philadelphia, PA 19104-6067 References 1. Stead WW. Genetics and resistance to tuberculosis: could resistance be enhanced by genetic engineering? Ann Intern Med. 1992; 116:93741. 2. Rotter JI, Diamond JM. What maintains the frequencies of human genetic diseases? Nature. 1987;329:289-90. 3. O'Brien SJ. Ghetto legacy. Curr Biol. 1991;1:209-11.

To the Editors: Dr. Stead recently pointed out that strong innate resistance to tuberculosis is found in about twice as many whites as in blacks. Blacks, on the other hand, have greater resistance to malaria and yellow fever. Dr. Stead related these differences to genetic natural selection because blacks have been exposed to malaria and yellow fever for thousands of years but only recently to tuberculosis (1). How can we explain resistance to Coccidioidies immitis? Although blacks and whites have had only limited and very recent exposure to this organism, blacks are approximately ten times more likely than whites to develop extrapulmonary coccidioidal dissemination (2). Perhaps when the tuberculosis resistance gene is eventually sequenced, it will be found to be linked to resistance to C. immitis by some general mechanism of macrophage or lymphocyte function that is not yet defined. Roger Larson, MD University of California San Francisco Valley Medical Education Program Fresno, CA 93727 796

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References 1. Stead WW. Genetics and resistance to tuberculosis. Ann Intern Med. 1992;116:937-41. 2. Pappagianis D. Epidemiology of coccidioidomycosis. In: Coccidioidomycosis—A Text. New York: Plenum Publishing Corporation; 1980:75-8.

To the Editors: Dr. Stead's (1) excellent article on genetics and resistance to tuberculosis did not mention the tuberculization of the native American and Caribbean Indian populations. It is not clear whether tuberculosis was present before the arrival of the Spanish and American colonists. In Puerto Rico, the harsh working conditions by the incoming Spaniards described by de las Casas in his Historia de las Indias is believed to have led to the tuberculization of the native Indian population: "These Indians are unable to do heavy work and when they are confined they soon become emaciated and die throwing out blood from the mouth" (2). The decline of manpower in the Caribbean islands led to the introduction of slaves from Africa. Tuberculosis may have been readily passed to the new arrivals. The tuberculization of the American Indian, in particular the Indians of the Great Plains, after confinement on reservations, is well documented (3). Future epidemiologic and genetic studies should take into consideration the native Indian populations of the Americas. Bernard Christenson, MD San Pablo Medical Center Bayamon, Puerto Rico 00959 References 1. Stead WW. Genetics and resistance to tuberculosis. Ann Intern Med. 1992;116:937-41. 2. Casas FB. Historia de las Indias. Mexico: Fondo de Cultura Economica; 1965. 3. Ferguson RG. Tuberculosis among the Indians of the great plains. Transactions of the Fourteenth Annual Conference of the National Association for the Prevention of Tuberculosis; 1928.

In response: Dr. Tangoren's concerns are appropriate. As Rotter and Diamond (1) point out, a fatal recessive autosomal gene that otherwise would gradually be eliminated can be perpetuated if associated with relative resistance to a killer pathogen of the prereproductive period. A resistance mutation need not be tied, however, to such a deleterious gene. The greater resistance to tuberculosis in whites in Arkansas nursing homes (2) is not associated, for example, with Tay-Sachs disease. The fact that a possible candidate gene may soon be cloned (3) makes me optimistic that genetic engineers may devise a strategy to enhance resistance to initial infection by Mycobacterium tuberculosis. Dr. Larson raises an interesting point. Our data (2) show a distinct difference in infectibility by M. tuberculosis but no difference in the frequency of progression to clinical tuberculosis. We could find no comparable data on infectibility by C. immitis; that is, conversion of a negative coccioidin skin test from negative to positive. The ten times greater fatality rate from coccidioidomycosis among blacks and Filipinos (4) is not readily explained by natural selection. Much remains to be learned about population genetics of resistance to infections as well as efficiency of coping with pathogens after they produce infection. Dr. Christenson cites an additional example of group susceptibility to tuberculosis that supports the concept of natural resistance to tuberculosis. Even if tuberculosis existed in preColumbian America, it could not have been common enough to serve as a factor in natural selection. The combination of crowding into reservations and greater contact with white settlers around 1860 triggered an epidemic spread of tuberculosis in a highly susceptible population and was attended by high death rates (5). William W. Stead, MD Arkansas Department of Health Little Rock, AR 72205

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References 1. Rotter JI, Diamond JM. What maintains the frequencies of human genetic diseases? Nature. 1987;329:289-90. 2. Stead WW, Lofgren JP, Senner JW, Reddick WT. Racial differences in susceptibility to infection with M. tuberculosis. N Engl J Med. 1990;322:422-7. 3. Schurr E, Malo D, Radzioch D, Bust hman E, Morgan K, Gros P, et al. Genetic control of innate resistance to mycobacterial infections. Immunology Today. 1991;12:A42-5. 4. Pappagianis D, Linday S, Beall S, Williams P. Ethnic background and the clinical course of coccidioidomycosis. Am Rev Respir Dis. 1979; 120:959-61. 5. Ferguson RG. Studies in Tuberculosis. Toronto: University of Toronto Press; 1955:6-9.

References 1. Hutchinson CM, Wilson C, Reichart CA, Marsiglia VC, Zenilman JM, Hook EW. CD4 lymphocyte concentrations in patients with newly identified HIV infection attending STD clinics. JAMA. 1991 ;266: 253-6. 2. Allard R. Beliefs about AIDS as determinants of preventive practices and of support for coercive measures. Am J Public Health. 1989;79: 448-52. 3. Stewart AL, Hays RD, Ware JE. The MOS short-form general health survey: reliability and validity in a patient population. Med Care. 1988;26:724-32. 4. Folkman S, Lazarus RS. Ways of Coping [Questionnaire]. Palo Alto, California: Consulting Psychologists; 1988. 5. Henry K, Sonnen M. Medical care following HIV testing [Letter]. JAMA. 1992;267:805-6.

Coping with HIV Infection: Why People Delay Care

The Hassle Factor To the Editors: Many persons infected with the human immunodeficiency virus (HIV) delay initiating care until their disease is advanced (1). We investigated factors associated with delay in seeking HIV-related care among 56 ambulatory patients who initiated care at San Francisco General Hospital between June 1990 and February 1991 and who had not had previous measurement of CD4 lymphocyte count. Participants were questioned regarding demographics (age, race, HIV risk group, income, employment status, education), substance use, social support, and beliefs regarding barriers to and benefits of treatment for the acquired immunodeficiency syndrome (AIDS) (2). We also assessed mental health, health perception (3), and use of avoidance as a strategy for coping with HIV antibody results (4). Participants were asked about the extent to which they coped with their infection by "wishful" thinking (for example, "hoped a miracle would occur") or avoidance behaviors (for example, "avoided being with people"). This was correlated with the period between a patient's first positive HIV antibody test (self-reported) and their first visit ("time known positive"). The distribution was skewed toward longer times; therefore, we log transformed the variable for correlational analysis. All of the patients were men; 55% were white, 20% were black, 18% were Latino, and 8% were of other racial groups. Ninety-one percent were homosexual, and 36% had used intravenous drugs. Only 13% of men had public or private health insurance. The median CD4 count was 445 cells (range, 65 to 1616 cells). The median time persons were known to be positive before initiating care was 99 days (range, 2 days to 5.5 years), with 13 men (23%) waiting over 1 year. Unemployment (r = 0.25; P = 0.05) and use of avoidance as a coping strategy (r = 0.34; P = 0.01) were significantly associated with a longer time known positive. Those with little social support tended to have longer times known positive (r = - 0.25; P = 0.06). Demographic variables, substance use, beliefs, and health status were not significantly associated with time known positive. In a regression analysis adjusting for race, intravenous drug use, and income, use of avoidance as a coping strategy remained independently associated with time known positive (t = 2.21; P = 0.03); unemployment and social support did not show such an association. Although our study is small and probably not generalizable to other HIV risk groups, our results suggest that increased effort is needed to help HIV-infected persons cope with antibody results and avail themselves of treatment. Such efforts should include linking HIV testing sites with treatment facilities (5). Mitchell H. Katz, MD Research Branch AIDS Office San Francisco, CA 94102-6033 Andrew B. Bindman, MD Miriam S. Komaromy, MD San Francisco General Hospital San Francisco, CA 94110

To the Editors: With the recent emphasis on "the hassle factor" in Internal Medicine, I offer, with due respect to David Letterman, a list of factors that do not usually get published.

Things Primary Care Physicians Do Well that Nobody Else Can Do 10) 9) 8) 7) 6) 5) 4)

Write jury duty and airline refund excuse letters Fill out drivers license forms Certify medical necessity Complete life insurance forms Compose special bus transportation privileges letters Support issuing handicapped license plates Perform rectal exams that subspecialists do not have time for 3) Sign nursing home verbal orders and death certificates 2) Call in prescriptions for patients whose friends have recommended a drug and given them some to try 1) Handle any illness, hospital referral, or consultation occurring after 3 P.M. on a Friday I am sure that your readers can add many more entries to this list of factors that make primary care internal medicine somewhat less exciting than it seemed in training. John G. Meharg, Jr., MD 11 East Lancaster Avenue Shillington, PA 19607

Annals " B a g s " the Bag To the Editors: I wholeheartedly applaud your decision to " b a g " the bag. I have become increasingly concerned with the number of journals mailed in plastic bags with apparent disregard for the environment and the abuse of the natural resources required to produce these bags. I hope the decision of the Annals will encourage other publishers to eliminate plastic mailing bags and to use acid-free, recycled paper. Janis Quinlisk, MLS, MAT Ohio Valley Medical Center, Inc. Wheeling, WV 26003 To the Editors: I was absolutely delighted to see your editorial, "Plastic bags and permanent paper: Annals and its environments." On behalf of my five-year-old, I thank you. The issue of Annals was spotless, and the policy of replacement without charge will have to satisfy even the worst nitpicker. The prospect of recycled glossy paper is also immensely appealing. Bravo to you, and to Annals, for taking several very good ideas and translating them by hard work into action. Henry Schneiderman, MD University of Connecticut Health Center Farmington, CT 06030

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• Volume 117 • Number 9


Comportment and Health Care Reform To the Editors: A national debate is going on about changing the American health delivery system. Our present medical compensation system pays much for the care of medical catastrophes and poorly for preventive care to head them off. All of us (including me) would like to be medically pampered without any personal out-of-pocket expense and (read my lips) no new taxes. Yet, we cannot afford the cost or the omissions of the medical care system as presently designed. We must consider the role of behavior and responsibility. For instance, a man who has severe emphysema but continues to smoke five dollars worth of cigarettes a day may be hospitalized every two months, requiring fifty thousand dollars worth of intensive and critical medical care each time, so that he can go out and smoke again. Expensive and life-saving care for millions of such cases runs up the rates for private insurance, Medicare, or Medicaid. Should society (that is, private or government insurance) permit such a patient only three strikes (that is 3 trips to the intensive care unit) before he strikes out? Should society then say that the patient (or his family or concerned friends) should pay out of pocket to permit him four, five, or more such strikes? Might not the willfully destructive behavior of many people be lessened if they saw that there would be no more free lunch at the hospital? Should this arrangement be considered for alcoholics and drug abusers and all types of intentionally noncompliant citizens who basically say, "I'll damage my body as much as I wish, and society should help me no matter the cost, because I'm helpless to change or I don't give a damn!"

While I was admitting a millionaire Texan for care of his alcoholic cirrhosis at the Mayo Clinic many years ago, his butler opened an extensive portable bar in his private hospital suite. I told the patient that he, of course, shouldn't drink. His answer was, "Doc, let me tell you how it is. I'll do the drinking and you do the doctoring." He died of his cirrhosis in a few weeks, but the bill for his wasted medical service was paid out of his oil fortune, not any other citizen's tax payment or insurance premium. Today, such wasted medical dollars are shared by us all. Such diverse persons as Billy Graham and Malcolm X have preached the value of individual comportment and the sanctity of our bodies. So, should the coming changed medical delivery system introduce a factor of citizen comportment or compliance in determining how the limited medical dollars will be spent? To those tearful people of tender mercies who think we should help everyone, no matter what the cause, I answer that the time has come to decide whether to spend big dollars on noncompliant people or save some to upgrade our care of pregnant women and infants and children, which happens to be almost as bad as in the poorest third world countries. Most third world countries have already made the decision to spend their meager medical funds on the young citizens of tomorrow, not the profligate older citizens of today. Phil Ball, MD 4915 North Nebo Road Muncie, IN 47304

Correction Fastidious Mycobacterium in Seven Patients with AIDS The appendix table in this report (1) contained several errors. Patient 4 received rifampin, ethambutol, ciprofloxacin, and clofazimine. Patient 5 received isoniazid, rifampin, and pyrazinamide. Ascites and anasarca were observed in Patient 6. A corrected version of this table is available from the authors (reprint requests). Reference 1. Wald A, Coyle MB, Carlson LC, Thompson RL, Hooton TM. Infection with a fastidious mycobacterium resembling Mycobacterium simiae in seven patients with AIDS. Ann Intern Med. 1992; 117; 586-9.


1 November 1992 • Annals of Internal Medicine • Volume 117 • Number 9

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Comportment and health care reform.

Letters The Editors welcome submissions for possible publication in the Letters section. Authors of letters should: • Include no more than 400 words...
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