Christopher P. Hudson and Paul N. Levett ... Reprints or correspondence: Dr. C. P. Hudson, Department of Medicine,. University ... and Anthony L. Cunningham.
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susceptibility testing revealed that the organism was 0. anthropi and that it was susceptible only to trimethoprim-sulfamethoxazole (TMP-SMZ), ciprofloxacin, imipenem, and gentamicin (the typical susceptibility pattern for this organism) [2]. The patient was treated with vancomycin, rifampin, ciprofloxacin, and TMP-SMZ for 6 weeks, followed by ciprofloxacin and TMP-SMZ for 4 1/2 months. Her wound healed, and her symptoms have not recurred. 0. anthropi is an oxidase-positive, non-lactose-fermenting gram-negative bacillus. This organism (formerly CDC [Centers for Disease Control and Prevention] group Vd) was named 0. anthropi in 1988 and is the only species in the group. Other closely related oxidase-positive nonfermenters are the Achromobacter-like organisms: Achromobacter xylosoxidans, Agrobacterium radiobacter, and Achromobacter group B. Most of the early reports of infections due to these organisms, especially 0. anthropi, described catheter-related bacteremias [3]. Two of the three cases of pyogenic infection due to 0. anthropi recently reported by Cieslak et al. [1] involved a foreign body (a draining T tube in one case and a chest tube in the other); the third case did not involve a foreign body. Alnor et al. [4] studied bacterial adhesion to silicone tubing by Agrobacterium and Ochrobactrum and found that the binding abilities of both organisms were similar to those of Staphylococcus epidermidis and Staphylococcus aureus. Infections due to all three of the related Achromobacter-like organisms have been shown to be associated with prosthetic cardiac devices; these infections include a postoperative infection of an aortic prosthesis with A. xylosoxidans [5], prosthetic valve endocarditis due to A. radiobacter [6], and replacement valve endocarditis due to Achromobacter group B [7]. We believe this is the first report of a serious infection of a cardiac prosthetic device with 0. anthropi. Although it is an unusual pathogen, isolation of this species should not come as a surprise when infections involve catheters, silicone tubing, and foreign bodies. Kenneth C. Earhart, Ker Boyce, W. Dale Bone, and Mark R. Wallace Departments of Internal Medicine (Infectious Diseases and Cardiology Divisions) and Clinical Investigation, Naval Medical Center, San Diego, California
References 1. Cieslak TJ, Drabick CJ, Robb ML. Pyogenic infections due to Ochrobactrum anthropi. Clin Infect Dis 1996; 22:845-7. 2. von Graevenitz A. Oxidase-positive, indole-negative, saccharolytic nonfermenters. In: Murray PR, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of clinical microbiology. 6th ed. Washington, DC: American Society for Microbiology, 1995:526-7. 3. Cieslak TJ, Robb ML, Drabick CJ, Fischer GW. Catheter-associated sepsis caused by Ochrobactrum anthropi: report of a case and review of related nonfermentative bacteria. Clin Infect Dis 1992;14:902-7. 4. Alnor D, Frimodt-Moller N, Espersen F, Frederiksen W. Infections with the unusual human pathogens Agrobacterium species and Ochrobactrum anthropi. Clin Infect Dis 1994;18:914-20. 5. Olson DA, Hoeprich PD. Postoperative infection of an aortic prosthesis with Achromobacter xylosoxidans. West J Med 1982; 136:153-7. 6. Plotkin GR. Agrobacterium radiobacter prosthetic valve endocarditis. Ann Intern Med 1980;93:839-40.
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7. Mckinley KP, Laundy TJ, Masterton RG. Achromobacter group B replacement valve endocarditis. J Infect 1990; 20:262-3. The views expressed in this article are those of the authors and do not reflect the official policy or position of the U.S. Department of the Navy, the Department of Defense, or the U.S. Government. The Chief, Navy Bureau of Medicine and Surgery, Washington, D.C., Clinical Investigation Program sponsored this report #84-16-1968-606, as required by HSETCINST 6000.41A. Reprints or correspondence: LT K. C. Earhart, MC, USNR, c/o Clinical Investigation Department, Naval Medical Center, 34800 Bob Wilson Drive, San Diego, California 92134-5000. Clinical Infectious Diseases 1997; 24:281-2 This article is in the public domain.
Primary Human Immunodeficiency Virus Type 1 Infection May Vary in Time, Place, and Person SIR-A recently reported case of severe primary human immunodeficiency virus (HIV) type 1 infection with rapid progression to AIDS and death [1] adds to the sizeable number of cases already published in the literature [2-5]. Are these isolated cases caused by a virulent strain that infects a patient with an impaired immune response, as was the case in the report by Holland et al. [1], or should we expect a growing number of cases of severe primary HIV-1 infection? The answer to this important question may lie in a greater understanding of the role of primary HIV-1 infection in AIDS epidemics. Symptomatic primary HIV-1 infection was first recognized in 1984 [6], but it has been postulated that, for AIDS epidemics to happen, high levels of viremia during primary HIV-1 infection are required [7]. An evolutionary balance may have ensured that HIV variants that cause relatively high levels of viremia but low rates of symptoms during primary HIV-1 infection were selected for in the early stages of the AIDS epidemic. After a period of rapid spread fueled by primary HIV-1 infection [7, 8], transmission from persons in the late stages of HIV infection increases in importance [8, 9]. These individuals have a high proportion of syncytium-inducing variants that result in more-severe primary HIV-1 infection in their partners [10]. All things being equal, severe cases of primary HIV-1 infections should appear when the first cases of AIDS occur or shortly thereafter, as we report elsewhere [5]. Some cases of symptomatic primary HIV-1 infection are associated with sexual contact with an AIDS patient [4]. Thus, symptomatic infection may reflect both the failure of an infected individual with HIV-related symptoms to adopt safer sexual practices and of the uninfected partner to recognize manifestations indicative of HIV infection. It follows that individuals in communities whose members are well educated and are highly motivated to avoid HIV infection should have a low rate of symptomatic primary HIV infection (as well as a low rate of incident infections). Conversely, individuals in communities whose members are not highly educated and have little motivation to avoid HIV infection should have a high rate of symptomatic seroconversions. In a population-based study [5], we found that heterosexual men with HIV-1 infection were more likely to have had a severe primary infection than were heterosexual women with HIV-1 infec-
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tion. The observed gender difference could be due to variations in sexual behavior. Heterosexual men with advanced HIV infection may be unable to have sex due to decreased libido or may choose to use a condom. In contrast, women with AIDS who do not have equal power in their sexual relationships may be unwilling to refuse unprotected sex, thereby exposing their partners at a time of viremia with syncytium-inducing variants. The significance of primary HIV-1 infection for public health would be best determined by instituting a program of surveillance in each locality. The rate of symptomatic primary HIV-1 infection may even predict future trends in AIDS cases. It is particularly important that countries with epidemics in communities whose members are not well educated should monitor cases of symptomatic primary HIV-1 infection as they may be an early indicator of failed health education. Christopher P. Hudson and Paul N. Levett Queen Elizabeth Hospital, Bridgetown, Barbados
References 1. Holland DJ, Dwyer DE, Saksena NK, et al. Dementia and pancytopenia in a patient who died of AIDS within one year of primary human immunodeficiency virus infection. Clin Infect Dis 1996;22:1121-2. 2. Tindall B, Hing M, Edwards P, et al. Severe clinical manifestations of primary HIV infection. AIDS 1989;3:747-50. 3. McLean KA, Holmes DA, Evans BA, et al. Rapid clinical and laboratory progression of HIV infection. AIDS 1990;4:367-8. 4. Keet I, Krijnen P, Koot M, et al. Predictors of rapid progression to AIDS in HIV-1 seroconverters. AIDS 1993; 7:51-7. 5. Hudson CP, Levett PN, Edwards CN, et al. Severe primary HIV-1 infection among black persons in Barbados. Int J STD AIDS 1997 (in press). 6. Anonymous. Needlestick transmission of HTLV-III from a patient infected in Africa [editorial]. Lancet 1984;2:1376-7. 7. Hudson CP. Concurrent partnerships could cause AIDS epidemics. Int J STD AIDS 1993;4:249-53. 8. Hudson CP. AIDS in rural Africa: a paradigm for HIV-1 prevention. Int J STD AIDS 1996; 7:236-43. 9. Hudson CP. Stable prevalence of HIV-1 in African populations. AIDS 1994; 8:1739-40. 10. Nielsen C, Pedersen C, Lundgren J, Gerstoft J. Biological properties of HIV isolates in primary HIV infection. AIDS 1993; 7:1035-40. Reprints or correspondence: Dr. C. P. Hudson, Department of Medicine, University of Cape Town, 916 Groote Schur Hospital, Observatory 7925, Cape Town, South Africa. Clinical Infectious Diseases 1997; 24:282-3 © 1997 by The University of Chicago. All rights reserved. 1058-4838/97/2402-0040$02.00
Reply SIR-We agree with Hudson and Levett that the high viral load in patients who undergo HIV-1 seroconversion is likely to facilitate transmission of HIV-1 to their sexual contacts. Syncytiuminducing strains may be present in individuals who have undergone seroconversion (and in AIDS patients) and are associated with high viral loads, symptomatic primary infection, and more-rapid immune decline [1]. However, it must be remembered that nonsyncytium-inducing viruses are also detected in individuals who have
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undergone HIV-1 seroconversion (and in AIDS patients) as well as in conjunction with high viral load and transmission [2]. Our report demonstrates severe progressive symptomatic primary infection with a macrophage tropic nonsyncytium-inducing virus [3]. The investigators' hypothesis that individuals in communities whose members are well educated and are highly motivated to avoid. HIV infection should have a lower rate of symptomatic primary HIV1 infection than individuals in communities whose members are not well educated and highly motivated to avoid HIV infection is speculative given the many factors that may influence recognition of clinical HIV-1 seroconversion. These factors include medical and community awareness (especially in cases where patients are from communities whose members are not considered at risk of HIV infection), patient reporting of symptoms and presentation to medical services, and the availability of specialized HIV diagnostic tests. It is reasonable that surveillance for HIV seroconversion illness (as currently performed in Australia [4]) be performed to provide data on new HIV infections and to answer issues such as those raised by Hudson and Levett. Early recognition of primary HIV infection may also allow patients to receive antiretroviral therapy during this period of high viral load [5]. Dominic E. Dwyer, David J. Holland, Nitin K. Saksena, Hassan Naif, Donald R. Packham, Jean Downie, and Anthony L. Cunningham Departments of Virology and Infectious Diseases, Centre for Infectious Diseases and Microbiology, Westmead Hospital, Westmead, and the University of Sydney, Westmead, New South Wales, Australia References
1. Nielsen C, Pedersen C, Lungren JD, Gerstolf J. Biological properties of HIV isolates in primary HIV infection: consequences for the subsequent course of infection. AIDS 1993; 7:1035-40. 2. Daar ES, Moudgil T, Meyer RD, Ho DD. Transient high levels of viremia in patients with primary human immunodeficiency virus type 1 infection. N Engl J Med 1991; 324:961-4. 3. Holland DJ, Dwyer DE, Saksena NK, et al. Dementia and pancytopenia in a patient who died of AIDS within one year of primary human immunodeficiency virus infection. Clin Infect Dis 1996;22:1121-2. 4. The National Centre in HIV Epidemiology and Clinical Research. Australian HIV Surveillance Report. 1996; 2(4):1-32. 5. Kinloch-deLoes S, Hirschel BJ, Hoen B, et al. A controlled trial of zidovudine in primary human immunodeficiency virus infection. N Engl J Med 1995;333:408-13.
Reprints or correspondence: Dr. Dominic E. Dwyer, Departments of Virology and Infectious Diseases, Centre for Infectious Diseases and Microbiology, Westmead Hospital and the University of Sydney, Westmead, New South Wales 2145, Australia. Clinical Infectious Diseases 1997; 24:283 © 1997 by The University of Chicago. All rights reserved. 1058-4838/97/2402 -0041$02.00
Risk Factors for Acute Otitis Media SIR-In their meta-analysis of risk factors (or indicators) for acute otitis media (AOM) in children, Uhari and co-workers chose to pool individually the crude risk ratios (calculated from the figures
