Acute human immunodeficiency virus infection presenting as disseminated gonococcal infection. (Case Report).
Gonorrhea is a common sexually transmitted disease that F may cause a disseminated infection. We present a case of disseminated gonococcal infection (DGI) associated with acute human immunodeficiency virus (HIV) infection. To our knowledge, this is the first report in the literature of this codiagnosis, but it may represent an underdiagnosed problem. An increasing amount of data shows a significant immunologic benefit of early antiretroviral treatment in patients with acute HIV infection before seroconversion. The possibility of acute HIV infection should be considered in patients who present with another sexually transmitted disease (STD) such as gonorrhea, because these diseases can be transmitted together in a single sexual exposure.
Gonorrhea is a common bacterial sexually transmitted disease, usually manifesting in men as acute urethritis. (1) The incubation period is typically 2 to 5 days but can be 10 days or more. Disseminated gonococcal infection (DGI) is a result of bacteremic spread of the organism, occurs in approximately 0.5 to 3% of infections, and usually presents clinically as an arthritis-dermatitis syndrome. Our patient did report a characteristic discrete papular rash, but this was resolved by the time of his presentation to the hospital; however, he never had signs or symptoms of arthritis or any other manifestation of DGI. Gonorrhea is a common diagnosis in HIV infected persons given their similar modes of transmission, and has been used as a marker of high risk behavior in this population. (2)
Acute HIV infection (also called primary HIV infection or PHI) has a similar incubation period as DGI (3) The rate of transmission of HIV during a heterosexual encounter varies with the level of viral load in the infected partner, and in one large study, the rate of transmission from an infected female to a male partner was similar to that from an infected male to a female partner. (3a) Soon after the transmission event, there is a very rapid rise in HIV particles in the bloodstream, and widespread seeding of lymphoid tissues. For the first approximately 22 to 27 days, standard serologic tests such as ELISA for HIV- 1 and -2 are negative and will miss the diagnosis of acute HIV infection. The diagnosis must be made by serum or plasma p24 antigen tests or by measurement of plasma HIV viral RNA, which will be extremely high. Therefore, if the diagnosis is not suspected, it will be very commonly missed in the clinical setting because the routine HIV test, the ELISA, has not yet turned positive in this situation .
The most common symptoms of acute HIV infection are fever, fatigue, rash, headache, pharyngitis, sweats, myalgias or arthralgias, and lymphadenopathy. Thrombocytopenia is observed in about 45% and leukopenia is seen in 40% of cases. (3) Our patient's symptoms, including the transient rash, were likely to be entirely due to the acute HIV infection, rather than DGI, and it was the leukopenia and thrombocytopenia that led us to perform the diagnostic test of HIV RNA viral load. The diagnosis of DGI was made by routine blood cultures and likely would have been undiagnosed had the patient not had those cultures done. Because there are few reported cohorts of patients with acute HIV infection, the incidence of other STD infections at the time of diagnosis with acute HIV infection is unknown. In addition, it is unknown whether the immunologic alterations induced by the acute retroviral syndrome would predispose a patient to DGI.
Acute HIV infection before seroconversion is a diagnosis not commonly made despite the fact that most patients with acute HIV are symptomatic. It can be confused with many other viral syndromes such as Epstein-Barr mononucleosis. (4) However, its diagnosis has large prognostic and therapeutic implications for the patient and for public health. A significant amount of the spread of HIV to new partners occurs during the acute HIV infection period, as the HIV viral load is extremely high, making transmission more efficient, and the source patient is not yet aware of his or her HIV positive status. (5) Furthermore, for the individual patient, early treatment with antiretroviral medications may confer substantial benefit in preserving specific cytotoxic CD8+/- cell immune function against HIV-infected cells. (6) This very early treatment before seroconversion may then allow for novel strategies to control HIV infection that will potentially alter the natural history of HIV infection in that patient and allow for better immune control of the disease. (7) Such novel treatment strategies, for example antiretroviral drug treatment interruptions or structured intermittent therapy, are currently being evaluated in clinical trials for their efficacy in this unique patient population.
We present a case of coinfection during a single sexual exposure of disseminated Neisseria gonorrhoeae and HIV. Though the blood cultures were positive for gonorrhea, not all of the patient's clinical features were consistent with DGI, and this prompted a search for an alternative diagnosis. The ELISA test for HIV antibodies was negative but a diagnosis of acute HIV was made by very high HIV RNA viral load. In patients with high-risk exposures and the diagnosis of one sexually transmitted disease, consideration should be given to the diagnosis of other similarly transmitted diseases, as these diseases can be transmitted together. The diagnosis of acute HIV infection may have profound implications for the individual patient as well as the public health.
ACCEPTED July 18, 2002.
(1.) Sparling PF, Hardsfield HH. Neisseria gonorrhoeae, in Mandell GL, Bennett JE, Dolin R (eds): Principles and Practice of Infectious Diseases. Philadelphia, Churchill Livingstone, 2000, ed 5, pp 2242-2258.
(2.) Do AN, Hanson DL, Dworkin MS, Jones JL; Adult and Adolescent Spectrum of HIV Disease Project. Risk factors for and trends in gonorrhea incidence among persons infected with HIV in the United States. AIDS 2001:15:1149-1155.
(3.) Kahn JO, Walker BD. Acute human immunodeficiency virus type 1 infection. N Engl J Med 1998;339:33-39.
(3a.) Quinn TC, Wawer MJ, Sewankambo N, Serwadda D, Li C, WabwireMangen F, et al. Viral load and heterosexual transmission of human immunodeficiency virus type I: Rakai Project Study Group. N Engl J Med 2000;342:921-929.
(4.) Rosenberg ES, Caliendo AM, Walker BD. Acute HIV infection among patients tested for mononucleosis. N Engl J Med 1999;340:969 (letter).
(5.) Yerly S, Vera S, Rizzardi P, Chave JP, Vemazza PL, Flepp M, et al; Swiss HIV Cohort Study. Acute HIV infection: impact on the spread of HIV and transmission of drug resistance. AIDS 2001;15:2287-2292.
(6.) Rosenberg ES, Altfeld M, Peon SH, Phillips MN, Wilkes BM, Eldridge RL, et al. Immune control of HIV-l after early treatment of acute infection. Nature 2000;407:523-526.
(7.) Altfeld M, Walker BD. Less is more? STI in acute and chronic HIV-1 infection. Nat Med 2001;7:881-884.
RELATED ARTICLE: Case Report
A 43-year-old black man was admitted to a Houston hospital with a 1-week history of fever, chills, and rash. The rash was described by the patient as erythematous with discrete papules, and appeared initially on the bilateral inner thighs, then briefly generalized, and disappeared after 2 days of the onset of fever. He also reported a mild sore throat, cough productive of clear sputum, and some nonbloody diarrhea. He did not report dysuria, urethral discharge, joint symptoms, or headache. The patient did not have a history of homosexual contact or any recent sexual exposures, except for a single episode of insertive vaginal sex with a prostitute approximately 2 weeks before the present illness. He had a history of IV drug use, but none in the last 6 years. He had never before been tested for HIV infection.
The physical examination revealed that the patient had a body temperature of 101.3 [degrees]F, blood pressure of 140/75 mm Hg, and pulse of 60 beats/mm. His oropharynx was clear and there were no meningeal signs. There was diffuse, less-than-1-cm lymphadenopathy present in the axillary, cervical and inguinal areas, which were non-tender and mobile. There was a soft, II/VI systolic injection murmur at the left sternal border. There was no rash on presentation, and he had no signs of joint inflammation or tendonitis. There were no genital lesions.
Initial laboratory findings revealed a white blood count of 1,900 cells/[mu]l with a predominance of lymphocytes, hemoglobin of 11.5 g/dl, and a platelet count of 52,000/[mu]l. Serum electrolytes and liver function tests were normal, as were the chest x-ray and urinalysis. A DNA probe of the urethra was negative for chlamydia and gonorrhea. Cultures of other mucosal surfaces, such as the rectum and pharynx, were not obtained. However, two sets of blood cultures at the time of admission grew Neisseria gonorrhoeae. ELISA for HIV-1 and HIV-2 was negative.
Because of the recent high-risk sexual exposure to a prostitute and the clinical findings of leukopenia and thrombocytopenia, which are not characteristic of DGI, the diagnosis of acute HIV infection before seroconversion was considered. HIV RNA viral load by polymerase chain reaction was performed (Roche Amplicor, version 1) and was positive with a value of more than 750,000 copies/ml, consistent with the diagnosis of acute HIV infection. Bone marrow biopsy and transesophageal echocardiograms were normal.
The patient was treated with IV ceftriaxone for DGI. Despite extensive counseling on the importance of treatment for his acute HIV infection, he left the hospital against medical advice and was lost to follow-up.
* Diagnosis of acute retroviral syndrome is important to individual patients as well as to public health.
* Acute human immunodeficiency virus infection should be considered in a patient with recent high-risk behavior and a compatible clinical syndrome that resembles mononucleosis.
* Sexually transmitted diseases can be transmitted together, and the diagnosis of one should lead to a consideration of others, including acute human immunodeficiency virus infection.
From the Division of Infectious Diseases, Department of Internal Medicine, University of Texas at Houston Medical School, Houston, TX.
Reprint requests to Ben J. Barnett, MD, Division of Infectious Diseases, Department of Internal Medicine, University of Texas at Houston Medical School, 6431 Fannin Street, JFB 1.728, Houston, TX 77030. Email: Ben.J.Barnett@uth.tmc.edu
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