884
Correspondence
Use of Zidovudine Following Occupational Exposure to Human Immunodeficiency Virus SIR-The recent review of occupational exposures to bloodborne pathogens by Drs. Gerberding and Henderson [I] is a thorough discussion of complex issues. Fear of being injured by a needle contaminated with the human immunodeficiency virus (HIV) clearly weighs heavily on the minds of health care workers. Whether to use zidovudine after such exposure has been one of the most frequently asked questions at seminars on HIV. The authors suggest informing the exposed health care worker about the potential advantages and disadvantages of treatment, without making a recommendation. In my experience, this action is usually not adequate, and in some ways it is an abdication of responsibility. After all, if the infectious disease
Correspondence: Dr. Michael F. Para, The Ohio State AIDS Clinical Trials Unit, 4725 University Hospitals Clinic, 456 West Tenth Avenue, Columbus, Ohio 43210-1282.
Clinical Infectious Diseases 1992;15:884-5 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1505-0022$02.00
region, we decided to rule out this possibility. A CT scan is the diagnostic procedure for confirmation ofa psoas muscle abscess. Our patient's case was exceptional because S. milleri was isolated from blood cultures, which made us suspect the possibility of endocarditis, an intraabdominal abscess, or osteomyelitis of the lumbar column. For this reason, we performed a CT scan and thus were able to confirm the diagnosis.
M. A. Ibanez Perez de la Blanca, J. D. Mediavilla Garcia, R. Martinez, M. Omar Mohamed-Balghata, J. P. Arrebola Nacle, and J. Jimenez-Alonso Internal Medicine and Microbiology Services, Hospital "Virgen de las Nieves," Granada, Spain
References I. Gossling J. Occurrence and pathogenicity of the Streptococcus milleri group. Rev Infect Dis 1988;10:257-85. 2. Colman G, Williams RE. Taxonomy of some human viridans streptococci. In: Wannamaker LW, Matsen JM, eds. Streptococci and streptococcal diseases: recognition, understanding and management. New York: Academic Press, 1972:281-99. 3. Facklam RR. Physiological differentiation of viridans streptococci. J Clin Microbiol 1977;5: 184-201. 4. Tolosa C, Almirante B, Ordi J, Planes AM. Neumonia extrahospitalaria de evoluci6n fatal por Streptococo milleri. Med Clin (Bare) 1989;93:718. 5. Shlaes OM, Lerner PI, Wolinsky E, Gopalakrishna KV. Infections due to Lancefield group F and related streptococci (S. milleri, S. anginosus). Medicine (Baltimore) 1981;60: 197-207. 6. Pigrau C, Pahissa A. Abceso del psoas: una enfermedad enigmatica? [editorial]. Med Clin (Bare) 1990;95:456-8.
specialist or infection control practitioner cannot make a recommendation, who can? Unless a recommendation is made, the typical response to this information is, "Well, what would you do if it had happened to you?" For me, the major potential disadvantage in taking zidovudine is one that is just briefly mentioned in Gerberding and Henderson's review: delayed seroconversion. Most individuals are willing to accept the potential of drug toxicity and the lack of proofofefficacy, but the possibility that this therapy could delay or obscure detection of their own HIV infection is not acceptable to many. Review of studies with animal models for the use of zidovudine in this situation suggests that the drug suppresses viral replication and delays clinical manifestations, but it does not prevent infection. Therefore, it seems quite reasonable that early intervention with zidovudine after accidental exposure might delay seroconversion. Exposed health care workers not given zidovudine can be assured they are uninfected if they are seronegative 6 months after exposure. However, if treated with zidovudine, they would not have this reassurance. This potential delay in seroconversion is what most health care workers find objectionable about the use of zidovudine after exposure. Because I discuss this possibility during postexposure counseling, the majority of health workers whom I evaluate do not opt for therapy
Downloaded from http://cid.oxfordjournals.org/ at University of Birmingham on September 1, 2015
mal. An echocardiogram showed no thickening, and the cavities and valves were normal. Abdominal echography showed a gallstone and a stone in the lower calix ofthe left kidney. An abdominal computed tomographic (CT) scan showed a large abscess in the left psoas muscle. The abscess was drained, and the patient's fever and pain disappeared. Cultures of pus yielded only S. milleri. S. milleri, traditionally included among the viridans streptococci on the basis of the classification system of Colman and Williams [2], corresponds to Streptococcus anginosus in Facklam's classification system [3]. At present, more cases of infection due to S. milleri are being reported because of better laboratory techniques. This organism's main pathological characteristic is its tendency to form abscesses in different organs. It has been isolated from dental, cerebral, and pleuropulmonary (pneumonia and empyema) abscesses and also in cases of endocarditis. Intraabdominal abscesses due to S. milleri (hepatic, pelvic, appendiceal, and peritoneal) are more common [4, 5] and are generally secondary to underlying abdominal pathology (Crohn's disease, diverticulitis, and cancer of the colon). Primary abscess of the psoas muscle is infrequent; Staphylococcus aureus (90% of cases) and Mycobacterium tuberculosis are the most common etiologic agents [6]. The clinical presentation of S. milleriinfections is often insidious, resulting in incorrect initial diagnoses such as infection of the urinary tract, masses in the kidney, intestinal diseases (neoplasms or appendicitis), or fever of unknown origin. In the present case the renal stone could have caused the renal infection by acting as a primary focus for the bacteremia. However, since the result of the urine culture was negative and the urologic studies showed no changes in the renal parenchyma or in the perirenal
CID 1992; 15 (November)
CID 1992; 15 (November)
with zidovudine. This is in contrast to the experience at San Francisco General Hospital and at the National Institutes of Health Clinical Center, where the majority of patients choose to receive zidovudine [2]. The review by Gerberding and Henderson mentions a standardized protocol for administering zidovudine. Do their institutions have standardized information that is provided to the exposed health care worker? Does this information discuss the potential for a delay in seroconversion? Do the authors offer a recommendation about therapy with zidovudine if asked?
SIR-We share Dr. Para's concern that zidovudine could suppress virus replication and result in seronegative infection or delayed seroconversion. In fact, the study protocol we administer and the information we provide to exposed health care providers explicitly point out this potential consequence of treatment. To date, delayed seroconversion after prophylaxis with zidovudine has not been observed. In all published anecdotal reports
Correspondence: Dr. Julie Louise Gerberding, The Medical Service 5H22, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, California 94110.
Clinical Infectious Diseases 1992;15:885 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1505-0023$02.00
A Leukemoid Reaction Caused by a Nasal Sympathomimetic SIR-Leukemoid reactions, with peripheral leukocyte counts exceeding 25,000-30,000/mm 3, generally result from acute toxic, inflammatory, malignant, or traumatic stresses [I]. Pharmacologically induced leukemoid reactions, however, are unusual. For this reason we report a previously unrecognized cause ofthis syndrome: the use of an over-the-counter phenylephrine hydrochloride solution (0.25% Neo-Synephrine [Sanofi Winthrop Pharmaceuticals, New York D. A 61-year-old engineer with long-standing multiple sclerosis was admitted to the hospital because of palpitations, dizziness, and mild dyspnea. The patient did not have fevers, chills, cough,
Correspondence: Dr. Mark M. Huycke, Infectious Diseases Section, Department of Veterans Affairs Medical Center, 921 Northeast l Jth Street, Oklahoma City, Oklahoma 73104-5028. © 1992 by The University of Chicago. All rights reserved.
1058-4838/92/1505-0024$02.00
Michael F. Para The Ohio State AIDS Clinical Trials Unit, Division of Infectious Diseases. The Ohio State University. Columbus. Ohio References 1. Gerberding JL. Henderson OK. Management of occupational exposures to bloodborne pathogens: hepatitis B virus, hepatitis C virus, and human immunodeficiency virus. Clin Infect Dis 1992; 14: 1179-85. 2. Henderson OK. Postexposure chemoprophylaxis for occupational exposure to human immunodeficiency virus type I: current status and prospects for the future. Am J Med 1991;91(suppl 3B):312S-19S.
of zidovudine treatment failure, antibodies (and usually seroconversion-related illness) appeared early (within weeks) after exposure to the human immunodeficiency virus (HIV). Similarly, in the animal models of zidovudine prophylaxis, infected animals demonstrate serological evidence of infection shortly after inoculation. Recent data demonstrate that lymphocytes from some health care providers occupationally exposed to (but not infected with) HIV proliferate in response to HIV antigens in tissue culture. This suggests that a cellular immune response to low-inoculum exposures could be an important defense against transcutaneous HIV infection. Theoretically, a virustatic agent that inhibits early replication and dissemination such as zidovudine could function as an adjuvant to this process.
J ulie Louise Gerberding and David K. Henderson San Francisco General Hospital and University of California. San Francisco: and Warren G. Magnusen Clinical Centers. National Institutes of Health. Bethesda. Maryland
or dysuria; there was no change in his chronic lower-extremity spastic paresis. His medications on admission included baclofen, phenytoin, ibuprofen, diphenhydramine, and a 0.25% solution of phenylephrine hydrochloride (for relief of nasal congestion). On physical examination, the patient's blood pressure was 114/69 mm Hg, pulse was I35/min, respirations were 20/min, and temperature was 37.0°C. Except for paresis of the lower extremities, findings of the examination were normal. The initial white blood cell (WBC) count was 38,200/mm 3, with 92% neutrophils, 6% band forms, I% lymphocytes, and 1% monocytes; when repeated 4 hours later, the WBC count was 32,500/ mrrr'. The hematocrit was 43.5%, and the platelet count was 417,000/mm 3 . A work-up, including blood cultures, a urinalysis, and a chest roentgenogram, revealed no infection. All medications were continued except for the phenylephrine hydrochloride nose drops, and no other interventions were instituted. After 24 hours the patient's symptoms abated, and by 48 hours his WBC count had returned to 7,500/mm 3, with a normal differential cell count. He remained afebrile during this period. Since an inflammatory or traumatic cause for his leukocytosis was not apparent, we queried him concerning his use of the phenylephrine hydrochloride nose drops. Although he claimed
Downloaded from http://cid.oxfordjournals.org/ at University of Birmingham on September 1, 2015
Reply
Clinical Infectious Diseases 1992;15:885-6
885
Correspondence
Correspondence
Use of Zidovudine Following Occupational Exposure to Human Immunodeficiency Virus SIR-The recent review of occupational exposures to bloodborne pathogens by Drs. Gerberding and Henderson [I] is a thorough discussion of complex issues. Fear of being injured by a needle contaminated with the human immunodeficiency virus (HIV) clearly weighs heavily on the minds of health care workers. Whether to use zidovudine after such exposure has been one of the most frequently asked questions at seminars on HIV. The authors suggest informing the exposed health care worker about the potential advantages and disadvantages of treatment, without making a recommendation. In my experience, this action is usually not adequate, and in some ways it is an abdication of responsibility. After all, if the infectious disease
Correspondence: Dr. Michael F. Para, The Ohio State AIDS Clinical Trials Unit, 4725 University Hospitals Clinic, 456 West Tenth Avenue, Columbus, Ohio 43210-1282.
Clinical Infectious Diseases 1992;15:884-5 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1505-0022$02.00
region, we decided to rule out this possibility. A CT scan is the diagnostic procedure for confirmation ofa psoas muscle abscess. Our patient's case was exceptional because S. milleri was isolated from blood cultures, which made us suspect the possibility of endocarditis, an intraabdominal abscess, or osteomyelitis of the lumbar column. For this reason, we performed a CT scan and thus were able to confirm the diagnosis.
M. A. Ibanez Perez de la Blanca, J. D. Mediavilla Garcia, R. Martinez, M. Omar Mohamed-Balghata, J. P. Arrebola Nacle, and J. Jimenez-Alonso Internal Medicine and Microbiology Services, Hospital "Virgen de las Nieves," Granada, Spain
References I. Gossling J. Occurrence and pathogenicity of the Streptococcus milleri group. Rev Infect Dis 1988;10:257-85. 2. Colman G, Williams RE. Taxonomy of some human viridans streptococci. In: Wannamaker LW, Matsen JM, eds. Streptococci and streptococcal diseases: recognition, understanding and management. New York: Academic Press, 1972:281-99. 3. Facklam RR. Physiological differentiation of viridans streptococci. J Clin Microbiol 1977;5: 184-201. 4. Tolosa C, Almirante B, Ordi J, Planes AM. Neumonia extrahospitalaria de evoluci6n fatal por Streptococo milleri. Med Clin (Bare) 1989;93:718. 5. Shlaes OM, Lerner PI, Wolinsky E, Gopalakrishna KV. Infections due to Lancefield group F and related streptococci (S. milleri, S. anginosus). Medicine (Baltimore) 1981;60: 197-207. 6. Pigrau C, Pahissa A. Abceso del psoas: una enfermedad enigmatica? [editorial]. Med Clin (Bare) 1990;95:456-8.
specialist or infection control practitioner cannot make a recommendation, who can? Unless a recommendation is made, the typical response to this information is, "Well, what would you do if it had happened to you?" For me, the major potential disadvantage in taking zidovudine is one that is just briefly mentioned in Gerberding and Henderson's review: delayed seroconversion. Most individuals are willing to accept the potential of drug toxicity and the lack of proofofefficacy, but the possibility that this therapy could delay or obscure detection of their own HIV infection is not acceptable to many. Review of studies with animal models for the use of zidovudine in this situation suggests that the drug suppresses viral replication and delays clinical manifestations, but it does not prevent infection. Therefore, it seems quite reasonable that early intervention with zidovudine after accidental exposure might delay seroconversion. Exposed health care workers not given zidovudine can be assured they are uninfected if they are seronegative 6 months after exposure. However, if treated with zidovudine, they would not have this reassurance. This potential delay in seroconversion is what most health care workers find objectionable about the use of zidovudine after exposure. Because I discuss this possibility during postexposure counseling, the majority of health workers whom I evaluate do not opt for therapy
Downloaded from http://cid.oxfordjournals.org/ at University of Birmingham on September 1, 2015
mal. An echocardiogram showed no thickening, and the cavities and valves were normal. Abdominal echography showed a gallstone and a stone in the lower calix ofthe left kidney. An abdominal computed tomographic (CT) scan showed a large abscess in the left psoas muscle. The abscess was drained, and the patient's fever and pain disappeared. Cultures of pus yielded only S. milleri. S. milleri, traditionally included among the viridans streptococci on the basis of the classification system of Colman and Williams [2], corresponds to Streptococcus anginosus in Facklam's classification system [3]. At present, more cases of infection due to S. milleri are being reported because of better laboratory techniques. This organism's main pathological characteristic is its tendency to form abscesses in different organs. It has been isolated from dental, cerebral, and pleuropulmonary (pneumonia and empyema) abscesses and also in cases of endocarditis. Intraabdominal abscesses due to S. milleri (hepatic, pelvic, appendiceal, and peritoneal) are more common [4, 5] and are generally secondary to underlying abdominal pathology (Crohn's disease, diverticulitis, and cancer of the colon). Primary abscess of the psoas muscle is infrequent; Staphylococcus aureus (90% of cases) and Mycobacterium tuberculosis are the most common etiologic agents [6]. The clinical presentation of S. milleriinfections is often insidious, resulting in incorrect initial diagnoses such as infection of the urinary tract, masses in the kidney, intestinal diseases (neoplasms or appendicitis), or fever of unknown origin. In the present case the renal stone could have caused the renal infection by acting as a primary focus for the bacteremia. However, since the result of the urine culture was negative and the urologic studies showed no changes in the renal parenchyma or in the perirenal
CID 1992; 15 (November)
CID 1992; 15 (November)
with zidovudine. This is in contrast to the experience at San Francisco General Hospital and at the National Institutes of Health Clinical Center, where the majority of patients choose to receive zidovudine [2]. The review by Gerberding and Henderson mentions a standardized protocol for administering zidovudine. Do their institutions have standardized information that is provided to the exposed health care worker? Does this information discuss the potential for a delay in seroconversion? Do the authors offer a recommendation about therapy with zidovudine if asked?
SIR-We share Dr. Para's concern that zidovudine could suppress virus replication and result in seronegative infection or delayed seroconversion. In fact, the study protocol we administer and the information we provide to exposed health care providers explicitly point out this potential consequence of treatment. To date, delayed seroconversion after prophylaxis with zidovudine has not been observed. In all published anecdotal reports
Correspondence: Dr. Julie Louise Gerberding, The Medical Service 5H22, San Francisco General Hospital, 1001 Potrero Avenue, San Francisco, California 94110.
Clinical Infectious Diseases 1992;15:885 © 1992 by The University of Chicago. All rights reserved. 1058-4838/92/1505-0023$02.00
A Leukemoid Reaction Caused by a Nasal Sympathomimetic SIR-Leukemoid reactions, with peripheral leukocyte counts exceeding 25,000-30,000/mm 3, generally result from acute toxic, inflammatory, malignant, or traumatic stresses [I]. Pharmacologically induced leukemoid reactions, however, are unusual. For this reason we report a previously unrecognized cause ofthis syndrome: the use of an over-the-counter phenylephrine hydrochloride solution (0.25% Neo-Synephrine [Sanofi Winthrop Pharmaceuticals, New York D. A 61-year-old engineer with long-standing multiple sclerosis was admitted to the hospital because of palpitations, dizziness, and mild dyspnea. The patient did not have fevers, chills, cough,
Correspondence: Dr. Mark M. Huycke, Infectious Diseases Section, Department of Veterans Affairs Medical Center, 921 Northeast l Jth Street, Oklahoma City, Oklahoma 73104-5028. © 1992 by The University of Chicago. All rights reserved.
1058-4838/92/1505-0024$02.00
Michael F. Para The Ohio State AIDS Clinical Trials Unit, Division of Infectious Diseases. The Ohio State University. Columbus. Ohio References 1. Gerberding JL. Henderson OK. Management of occupational exposures to bloodborne pathogens: hepatitis B virus, hepatitis C virus, and human immunodeficiency virus. Clin Infect Dis 1992; 14: 1179-85. 2. Henderson OK. Postexposure chemoprophylaxis for occupational exposure to human immunodeficiency virus type I: current status and prospects for the future. Am J Med 1991;91(suppl 3B):312S-19S.
of zidovudine treatment failure, antibodies (and usually seroconversion-related illness) appeared early (within weeks) after exposure to the human immunodeficiency virus (HIV). Similarly, in the animal models of zidovudine prophylaxis, infected animals demonstrate serological evidence of infection shortly after inoculation. Recent data demonstrate that lymphocytes from some health care providers occupationally exposed to (but not infected with) HIV proliferate in response to HIV antigens in tissue culture. This suggests that a cellular immune response to low-inoculum exposures could be an important defense against transcutaneous HIV infection. Theoretically, a virustatic agent that inhibits early replication and dissemination such as zidovudine could function as an adjuvant to this process.
J ulie Louise Gerberding and David K. Henderson San Francisco General Hospital and University of California. San Francisco: and Warren G. Magnusen Clinical Centers. National Institutes of Health. Bethesda. Maryland
or dysuria; there was no change in his chronic lower-extremity spastic paresis. His medications on admission included baclofen, phenytoin, ibuprofen, diphenhydramine, and a 0.25% solution of phenylephrine hydrochloride (for relief of nasal congestion). On physical examination, the patient's blood pressure was 114/69 mm Hg, pulse was I35/min, respirations were 20/min, and temperature was 37.0°C. Except for paresis of the lower extremities, findings of the examination were normal. The initial white blood cell (WBC) count was 38,200/mm 3, with 92% neutrophils, 6% band forms, I% lymphocytes, and 1% monocytes; when repeated 4 hours later, the WBC count was 32,500/ mrrr'. The hematocrit was 43.5%, and the platelet count was 417,000/mm 3 . A work-up, including blood cultures, a urinalysis, and a chest roentgenogram, revealed no infection. All medications were continued except for the phenylephrine hydrochloride nose drops, and no other interventions were instituted. After 24 hours the patient's symptoms abated, and by 48 hours his WBC count had returned to 7,500/mm 3, with a normal differential cell count. He remained afebrile during this period. Since an inflammatory or traumatic cause for his leukocytosis was not apparent, we queried him concerning his use of the phenylephrine hydrochloride nose drops. Although he claimed
Downloaded from http://cid.oxfordjournals.org/ at University of Birmingham on September 1, 2015
Reply
Clinical Infectious Diseases 1992;15:885-6
885
Correspondence
