- Email: [email protected]
Spread of multi-resistant Klebsiella pneumoniae in two Chicago hospitals
68
Infectious Diseases Newsletter September
treatment of fever is reasonable. Antipyretics, although seemingly harmless, may actually pose a number of problems. The sick elderly population is at greater risk of developing gastritis and gastric ulceration from nonsteroidal, anti-inflammatory drugs of all types, including salicylates. In addition, it should be noted that the elderly may have reduced renal and hepatic clearance, which can predispose to drug overdose. In the elderly population, serum creatinine elevations are not reliable in indicating mild impairment of renal function in the elderly because of age-related loss of muscle mass and a low glomerular filtration rate that may not be reflected in serum creatinine levels. The most commonly used antipyretic in the elderly is acetaminophen. No differences were found in the metabolic clearance of the glucuronide and glutathione-derived conjugates between young adults and the elderly, although the renal clearance of unchanged drug was 43% lower in the elderly. However, despite the decreased clearance, a re-
ll(9)
1992
duction in acetaminophen dosage has not been recommended for elderly patients. Except for patients with severe cardiopulmonary disease, young chiIdren, and individuals with CNS abnormalities, there are no data that suggest lowering temperatures in febrile patients is beneficial In fact, since all measurable host defense modalities are enhanced by fever, a strong argument can be made against using antipyretics that may deprive the patient of the benefits of fever. It is also important to emphasize that the absence of fever in a sick elderly patient does not exclude the presence of infection.
Bibliography Ashman RB, Mullbacher A: Infectious disease, fever, and the immune response. Immunol Today 5268271,1984. Collins KG, Exton-Smith AN: Thermal homeostasis in old age. J Am Geriatr Sot 31519-524, 1983. Curry G, Roger RJ, Muir JM, et al: Pharmacokinetics of salicylates in the elderly. Gerontology 25:49-56, 1979.
Gleckman R, Hibert D: Afebrile bacteremix A phenomenon in geriatric patients. JAMA284:1478-1481, 1982. Kluger MJ, Ringier DH, Anver MR: Fever and survival. Science 188:166-168, 1975. Miners JO, Penhall R, Robson RA, et al: Comparison of paracetamol metabolism in young adult and elderly males. Eur J Clin Pharmacol35:157-160, 1988. Roberts NJ, Jr: Temperature and host defense. Microbial Rev 43:241-259, 1979. Rudd AG, Banetjee DK: lnterleukin-1 production by human monocytes and ageing and disease. Age Ageing 18:43-46, 1989. Talbott JH: A Bibliographical History of Medicine. New York, Grune & Stratton, 1970. Wagner-Jauregg J: The treatment of dementia paralytica by malaria inoculation. In Nobel Lectures: Physiology of Medicine, 1922-1941. New York, Elsevier, 1965, pp. 159-160. Yoshikawa ‘IT, Norman DC: Aging and clinical practice. In Infectious Diseases, New York, Igaku-Shoin, 1987.
Address correspondence to Rican% Banaga. Infectious Disease Division, Winthrop University Hospital, Mineola, NY 11501.
Spread of Multi-Resistant KZebieUizpneumoniue in Two Chicago Hospitals Vincent Idemyor, PhaxmD,’ Charles E. Cherubin, MD,2 and Alex Kuritza, PhD3 ‘Dcpnmw~ofPhwmaceutica1 Services, Mercy Hospital andMedical Center, Chicago, Illinois; ‘Department Affa’rs, Me&al Centec Wilkes-Barre. Pennsylvania; ‘Clinical Microbiology Laboratory, Rwh-Presbyterian-St. Antimicrobial resistance has been a problem for clinicians since shortly after the introduction of penicillin nearly 50 years ago. Within the past 10 years, the process seems to have accelerated both within species and in the number of species involved. Concurrently, our knowledge of the mechanisms of resistance seems to be in a continuing process of change, with new agents being introduced, and gaining widespread use, and a growing frequency of resistance via unique
mechanisms being noted. The extended-spectrum cephalosporins (AKA third generation) are widely perceived by clinicians as broadly useful in the treatment of Gram-negative bacilhuy infections. Thus, use has grown substantially over the past 5 to 10 years. The development of resistance to these advanced cephalosporins has been particularly noteworthy in Klebsiellu pneumoniue. Although it is not the only resistant species reported, it has Q1992 Elsevier Science publishing 0278-2316/92/$0.00
+ 3.00
Co.,
Inc.
ofMedicinell~ectiou Diseases,
Veterans Luke’s Medical Center, Chica.qo, Illinois
been particularly noteworthy for its plasmid-mediated resistance to these cepbalosporins and in particular to ceftazidime. The mechanism has been shown repeatedly to be an extended range beta-Iactamase of the TEM or SHV series. These new variants of the TBM-1 and SHV-1 were not noted prior to the introduction of the advanced cephalosporins. The fact that most of the extendedrange beta-lactamases have been reported from Europe probably repre-
69 Infectious Diseases Newsletter 1l(9) September 1992
sents investigators’ interests rather than a true geographic localization. In the late 198Os, Dr. John Quinn at Michael Reese Hospital in Chicago isolated and studied a Klebsiella pneumniae strainresistant to ceftazidime and axtreonam (but not to cefotaxime) from a patient receiving ceftaxidime. Over the next few years, such Klebsiellapneumoniae displaying this easily recognizable susceptibility signature were noted across the street at Mercy Hospital and Medical Center (MHMC) and at Rush-Ptesbyterian-St. Luke’s Medical Center (RPLMC) several miles to the north. These two centers are the focus of our report. The resistance patterns arc not confined to these three centers but have been seen in other hospitals in the Chicago area and in nursing home patients being seen at the two hospitals (personal communication from John Quinn). As the literature has indicated, there is a circumstantial connection between ceftazidime use and resistance in Klebsiellapneumoniae based on the extended TEM beta-lactamase. For example, at MHMC between 1988 and 1989, resistance of any advanced cephalosporin (cefotaxime, ceftriaxone, or ceftazidime) was only l-34 in Klebsiellapneumoniae. In 1990, the frequency of resistance to ceftaxidime (and axtreonam) jumped to 15% and has continued to maintain that level. No resistance to cefotaxime was noted based on the MicroScan semi-automated susceptibility system. At the same time, the number of grams of ceftaxidime used rose from l,OOOinl987to5,888inl99l,while the use of cefotaxime was stable at 12,000 per year. A similar pattern of resistance and of ceftaxidime consumption was evident at RPLMC. We selected 10 strains from each institution. All were Klebsiellapneumoniae and resistant by MicroScan to ceftaxidime and axtreonam but sensitive or moderately sensitive to cefotaxime. Susceptibilities were confirmed by manual microdilution testing. Other resistances
noted were to semisynthetic penicillins, ampicillin/sulbactam, ticarcillin/clavulanic acid, and the aminoglycosides, gentamicin and tobramycin. The latter resistance strongly suggested these were nosocomial strains. All isolates were universally susceptible to imipcnem. The MIC of these isolates to ceftazidime was >64 @ml but the cefotaxime MIC ranged from 1 to 32 udml. In contrast, an isolate from Dr. Quinn had a 32 ceftazidime MIC and an MIC for cefotaxime of 0.5 &ml. Thus, while by MicroScan, the pattern of ceftazidime resistance and cefotaxime sensitivity was reported. There was some variation evident among these isolates and they did not entirely resemble the strain described by Dr. Quinn. The plasmid fingerprinting of these strains revealed a single clonal pattern of the MHMC isolates but three or more patterns of RPLMC. These resistances were shown to be transferable, again suggesting a plasmid mediated resistance. Isoelectric focusing showed a consistent two bands among the MHMC isolates. These are now being confirmed by Dr. Karen Bush, and are tentatively identified as a TEM- 10 and an SHV- 1. The RPLMC isolates showed these bands and a variety of several others. This explains the difference in the MICs as compared to the TEM- 10 reference strain. It also illustrates the spread of a newly discovered extended beta-lactamasc carried probably via a plasmid from one hospital to another with the gradual addition of other beta-lactamascs making these strains resistant to one or several of the advanced cephalosporins frequently used in these hospitals’ patient population. Other points of interest are that this resistance primarily to ceftazidime arose in both hospitals despite a higher consumption of cefotaxime and the other aminothioxlyl, cephalosporins, ceftriaxone, and ceftizoxime. This also is the case at the Wilkes-Barre VAMC, where such ceftaxidime-resistant isolates of KlebQ1992 Elsevier Science Publishing Co., Inc. 0278-2316/92/%0.00 + 3.00
siellapneumoniae have been noted since January 1992. Although this resistance-pattern species does stand out, these findings am further circumstantial evidence suggesting the unique value of ceftaxidime in encouraging the development of extended TEM beta-lactamases. Perhaps the higher MICs for the Enterobacteriaceae, and the slower killing with this agent as shown by Eng and Cherubin, are factors in the close association between the use of this agent and the discovery of extended TEM and SHV beta-lactamases.
Bibliography Birnboii HC. Doly k A rapid extraction procedure for screening mcombmant plasmid DNA. Nucleic Acids Rea 7:1513-1523,1979. Chanal CM, Sirot DL, Labia R. et al: Comparative study of a novel plasmid-mediated beta-lactamase, CAZ-2, and the CTX-1 and CAZ-1 enzymes conferring resistance to broad spectrum cephalosporins. Antimicrob Agents Chemother 32:166&1655,1988. Eng RHK, Chuubm CE, Smith SM. Buccini F: Inocuhlln &ect of beta-lactam antibiotics on Enterokteriaceae. Antimicrob Agents Chemother 28:601606.1985. Jacoby GA, Medeiros AA: More extendedspectrum beta-lactamases. Antimicrob Agents Chemother 35:1697-1704.1991. Lachapelle J. Quinn JP,Miyashiro D, et al: Sequence of genes blT-10 and blT-11 which encode the extended-spectrum beta-lactamases TEM-10 and TEM-11. Program Absh 30th Jntersci Conf Antimicrob Agents Chemother 1990, abstr no 187. Petit A, Sirot DL, Chanal CM, et al: Novel plasmid-mediated beta-lactamase in clinicaJ isolates of Kkbsiellapnewnoniae more resistant to ceftaxidime than to other broad spectrum cephalosporins. Antimicrob Agents Chemother 32:626630,1988. Philippon A, Labia R, Jacoby G: Extended spectrum beta-lactamases. Antimicrob Agents Chemother 33:1131-1136,1989. Quinn JR,Miyashiro D, Sahm D, et al: Novel plasmid-mediated beta-lactamases (TEM-10) conferring selective resistance to ceftaxidiie and axtreonam in clinical isolates of nioe. Antimicrob Agents Chemother 33:1451-1456.1989.
70 Infectious Diseases Newsletter 1 l(9) September 1992 Rice LB, Wiley SH, Papanicolaou A, et al: Outbreak of ceftazidke resistance caused by extended-spectrum bcta-lactamases at a Massachusetts chronic care facility. Antimicrob Agents Chemother 34:2193-2199,199O.
II: High-level resistance to cefotaxime and ceftazidiie in Klebsiella pnewnoniue isolates from Cleveland, Ohio. Antimicrob Agents Chemother 35:1001-1003, 1991.
Sirot D, Chanal C, Labia R, et al: Comparative study of five plasmid-mediated ceftazidimases isolated in Kiebsiella pneumoniue. J Antimicrob Chemother 24:509-521.1989.
Vatopoulos AC, Philippon A, Tzouvelekis IS, et al: Prevalence of transferable SHV-5 type beta-lactamase in clinical isolates of Klebsiella pneumoniae and Escherichia coli in Greece. J Antimicrab Chemother 26:635-648,1990.
Thomson KS, Sanders CC, Washington JA
Vuye A, Verschraegen G, Claeys G: Plas-
mid-mediated beta-lactamases in clinical isolates of Klebsiella pneumoniae and Escherichia coli resistant to ceftazidime. Antimicrob Agents Chemother 33:757-761,1989.
Address correspondence to Charles E. MD, Departmentof Medicine/Infectious Diseases, Veterans Affain Medical Center, 1111 East End Boulevard, Wilkes-Barre, Pennsylvania 18711. Che~bii,
CASE REPORT
nberculous
Pericarditis in an Elderly Male with Lymphoma
Charles W. Stratton, MD Associate Professor 4 Padmlogy. Vamkrbil~Um’versiQ School
This 7 1-year-old white male was initially admitted to Vanderbilt University Medical Center because of a 2-week history of high fever and soaking night sweats. The past medical history was significant in that this man had been diagnosed 4 years earlier as having a well-differentiated malignant lymphoma, which had been diagnosed at another medical center by the biopsy of a neck lymph node after he had presented with cervical lymphadenopathy. He subsequently received chemotherapy and radiation for this lymphoma and had been without symptoms since the completion of this therapy. Physical examination revealed no palpable lymph nodes or hepatosplenomegaly. There was a two-component rub noted on cardiac auscultation. Otherwise, the physical exam was normal. The vital signs were stable with no fever. Laboratory values revealed a PCV of 28%. The WBC was 7,6OO/cmm with a normal differential. Liver function studies were normal. A chest roentgenogram revealed
ofMedicine,Nashville,
Tennessee
cardiomegaly. Follow-up computerized tomography of the chest showed bilateral pleural effusions with loculation in the right lung base as well as a pericardial effusion. An ultrasound guided thoracentesis showed pleural fluid with a lymphocytosis (5OO/cmm) having a monomorphic population of small lymphocytes. Pleural fluid was sent for appropriate cultures, including those for AFB and fungi. The pleural lymphocytosis was felt to be consistent with either a reactive process or a well-differentiated lymphoma. A bone marrow biopsy revealed a well-differentiated lymphoma. The bone marrow biopsy was cultured for AFB and fungi. An echocardiogram showed a left ventricular ejection fraction of 55%. There was no evidence of cardia tamponade by the pericardial effusion. Tuberculin skin tests were applied and were negative, first and second strength. The clinical impression of this initial admission was that these pleural and pericardial effusions represented a recurrence of lymphoma. The patient thus received chemotherapy with CyQ1992 Elsevier Science Publishing Co., Inc. 0278-2316/92/$0.00
+ 3.00
toxan, Vmcristine, and Prednisone. He did well and was discharged to be followed in the clinic. Over the next 3 months, the night sweats and fever seemed to be resolved. The patient did, however, net a 20-pound weight loss. In addition, he began to develop lower extremity edema. A magnetic resonance imaging study indicated pericardial effusion with thickened pericardium. The patient was felt to have a restrictive pericarditis without tamponade. He was readmitted to Vanderbilt Medical Center for a pericardiectomy. At tboracotomy, the pericardium was found to be thickened to approximately 4-5 mm with a shaggy exudate on the pericardial and epicardial surfaces and epicardial fibrous constriction. Approximately 100 ml of serious fluid was within the cavity. A section of the anterior pericardium was resected. Microscopic evaluation of the pericardium revealed granulomas by H&E and acid-fast bacilli by Fite staining. Cultures subsequently grew M. tuberculosis from the pericardium although the pleural fluid and
Infectious Diseases Newsletter September
treatment of fever is reasonable. Antipyretics, although seemingly harmless, may actually pose a number of problems. The sick elderly population is at greater risk of developing gastritis and gastric ulceration from nonsteroidal, anti-inflammatory drugs of all types, including salicylates. In addition, it should be noted that the elderly may have reduced renal and hepatic clearance, which can predispose to drug overdose. In the elderly population, serum creatinine elevations are not reliable in indicating mild impairment of renal function in the elderly because of age-related loss of muscle mass and a low glomerular filtration rate that may not be reflected in serum creatinine levels. The most commonly used antipyretic in the elderly is acetaminophen. No differences were found in the metabolic clearance of the glucuronide and glutathione-derived conjugates between young adults and the elderly, although the renal clearance of unchanged drug was 43% lower in the elderly. However, despite the decreased clearance, a re-
ll(9)
1992
duction in acetaminophen dosage has not been recommended for elderly patients. Except for patients with severe cardiopulmonary disease, young chiIdren, and individuals with CNS abnormalities, there are no data that suggest lowering temperatures in febrile patients is beneficial In fact, since all measurable host defense modalities are enhanced by fever, a strong argument can be made against using antipyretics that may deprive the patient of the benefits of fever. It is also important to emphasize that the absence of fever in a sick elderly patient does not exclude the presence of infection.
Bibliography Ashman RB, Mullbacher A: Infectious disease, fever, and the immune response. Immunol Today 5268271,1984. Collins KG, Exton-Smith AN: Thermal homeostasis in old age. J Am Geriatr Sot 31519-524, 1983. Curry G, Roger RJ, Muir JM, et al: Pharmacokinetics of salicylates in the elderly. Gerontology 25:49-56, 1979.
Gleckman R, Hibert D: Afebrile bacteremix A phenomenon in geriatric patients. JAMA284:1478-1481, 1982. Kluger MJ, Ringier DH, Anver MR: Fever and survival. Science 188:166-168, 1975. Miners JO, Penhall R, Robson RA, et al: Comparison of paracetamol metabolism in young adult and elderly males. Eur J Clin Pharmacol35:157-160, 1988. Roberts NJ, Jr: Temperature and host defense. Microbial Rev 43:241-259, 1979. Rudd AG, Banetjee DK: lnterleukin-1 production by human monocytes and ageing and disease. Age Ageing 18:43-46, 1989. Talbott JH: A Bibliographical History of Medicine. New York, Grune & Stratton, 1970. Wagner-Jauregg J: The treatment of dementia paralytica by malaria inoculation. In Nobel Lectures: Physiology of Medicine, 1922-1941. New York, Elsevier, 1965, pp. 159-160. Yoshikawa ‘IT, Norman DC: Aging and clinical practice. In Infectious Diseases, New York, Igaku-Shoin, 1987.
Address correspondence to Rican% Banaga. Infectious Disease Division, Winthrop University Hospital, Mineola, NY 11501.
Spread of Multi-Resistant KZebieUizpneumoniue in Two Chicago Hospitals Vincent Idemyor, PhaxmD,’ Charles E. Cherubin, MD,2 and Alex Kuritza, PhD3 ‘Dcpnmw~ofPhwmaceutica1 Services, Mercy Hospital andMedical Center, Chicago, Illinois; ‘Department Affa’rs, Me&al Centec Wilkes-Barre. Pennsylvania; ‘Clinical Microbiology Laboratory, Rwh-Presbyterian-St. Antimicrobial resistance has been a problem for clinicians since shortly after the introduction of penicillin nearly 50 years ago. Within the past 10 years, the process seems to have accelerated both within species and in the number of species involved. Concurrently, our knowledge of the mechanisms of resistance seems to be in a continuing process of change, with new agents being introduced, and gaining widespread use, and a growing frequency of resistance via unique
mechanisms being noted. The extended-spectrum cephalosporins (AKA third generation) are widely perceived by clinicians as broadly useful in the treatment of Gram-negative bacilhuy infections. Thus, use has grown substantially over the past 5 to 10 years. The development of resistance to these advanced cephalosporins has been particularly noteworthy in Klebsiellu pneumoniue. Although it is not the only resistant species reported, it has Q1992 Elsevier Science publishing 0278-2316/92/$0.00
+ 3.00
Co.,
Inc.
ofMedicinell~ectiou Diseases,
Veterans Luke’s Medical Center, Chica.qo, Illinois
been particularly noteworthy for its plasmid-mediated resistance to these cepbalosporins and in particular to ceftazidime. The mechanism has been shown repeatedly to be an extended range beta-Iactamase of the TEM or SHV series. These new variants of the TBM-1 and SHV-1 were not noted prior to the introduction of the advanced cephalosporins. The fact that most of the extendedrange beta-lactamases have been reported from Europe probably repre-
69 Infectious Diseases Newsletter 1l(9) September 1992
sents investigators’ interests rather than a true geographic localization. In the late 198Os, Dr. John Quinn at Michael Reese Hospital in Chicago isolated and studied a Klebsiella pneumniae strainresistant to ceftazidime and axtreonam (but not to cefotaxime) from a patient receiving ceftaxidime. Over the next few years, such Klebsiellapneumoniae displaying this easily recognizable susceptibility signature were noted across the street at Mercy Hospital and Medical Center (MHMC) and at Rush-Ptesbyterian-St. Luke’s Medical Center (RPLMC) several miles to the north. These two centers are the focus of our report. The resistance patterns arc not confined to these three centers but have been seen in other hospitals in the Chicago area and in nursing home patients being seen at the two hospitals (personal communication from John Quinn). As the literature has indicated, there is a circumstantial connection between ceftazidime use and resistance in Klebsiellapneumoniae based on the extended TEM beta-lactamase. For example, at MHMC between 1988 and 1989, resistance of any advanced cephalosporin (cefotaxime, ceftriaxone, or ceftazidime) was only l-34 in Klebsiellapneumoniae. In 1990, the frequency of resistance to ceftaxidime (and axtreonam) jumped to 15% and has continued to maintain that level. No resistance to cefotaxime was noted based on the MicroScan semi-automated susceptibility system. At the same time, the number of grams of ceftaxidime used rose from l,OOOinl987to5,888inl99l,while the use of cefotaxime was stable at 12,000 per year. A similar pattern of resistance and of ceftaxidime consumption was evident at RPLMC. We selected 10 strains from each institution. All were Klebsiellapneumoniae and resistant by MicroScan to ceftaxidime and axtreonam but sensitive or moderately sensitive to cefotaxime. Susceptibilities were confirmed by manual microdilution testing. Other resistances
noted were to semisynthetic penicillins, ampicillin/sulbactam, ticarcillin/clavulanic acid, and the aminoglycosides, gentamicin and tobramycin. The latter resistance strongly suggested these were nosocomial strains. All isolates were universally susceptible to imipcnem. The MIC of these isolates to ceftazidime was >64 @ml but the cefotaxime MIC ranged from 1 to 32 udml. In contrast, an isolate from Dr. Quinn had a 32 ceftazidime MIC and an MIC for cefotaxime of 0.5 &ml. Thus, while by MicroScan, the pattern of ceftazidime resistance and cefotaxime sensitivity was reported. There was some variation evident among these isolates and they did not entirely resemble the strain described by Dr. Quinn. The plasmid fingerprinting of these strains revealed a single clonal pattern of the MHMC isolates but three or more patterns of RPLMC. These resistances were shown to be transferable, again suggesting a plasmid mediated resistance. Isoelectric focusing showed a consistent two bands among the MHMC isolates. These are now being confirmed by Dr. Karen Bush, and are tentatively identified as a TEM- 10 and an SHV- 1. The RPLMC isolates showed these bands and a variety of several others. This explains the difference in the MICs as compared to the TEM- 10 reference strain. It also illustrates the spread of a newly discovered extended beta-lactamasc carried probably via a plasmid from one hospital to another with the gradual addition of other beta-lactamascs making these strains resistant to one or several of the advanced cephalosporins frequently used in these hospitals’ patient population. Other points of interest are that this resistance primarily to ceftazidime arose in both hospitals despite a higher consumption of cefotaxime and the other aminothioxlyl, cephalosporins, ceftriaxone, and ceftizoxime. This also is the case at the Wilkes-Barre VAMC, where such ceftaxidime-resistant isolates of KlebQ1992 Elsevier Science Publishing Co., Inc. 0278-2316/92/%0.00 + 3.00
siellapneumoniae have been noted since January 1992. Although this resistance-pattern species does stand out, these findings am further circumstantial evidence suggesting the unique value of ceftaxidime in encouraging the development of extended TEM beta-lactamases. Perhaps the higher MICs for the Enterobacteriaceae, and the slower killing with this agent as shown by Eng and Cherubin, are factors in the close association between the use of this agent and the discovery of extended TEM and SHV beta-lactamases.
Bibliography Birnboii HC. Doly k A rapid extraction procedure for screening mcombmant plasmid DNA. Nucleic Acids Rea 7:1513-1523,1979. Chanal CM, Sirot DL, Labia R. et al: Comparative study of a novel plasmid-mediated beta-lactamase, CAZ-2, and the CTX-1 and CAZ-1 enzymes conferring resistance to broad spectrum cephalosporins. Antimicrob Agents Chemother 32:166&1655,1988. Eng RHK, Chuubm CE, Smith SM. Buccini F: Inocuhlln &ect of beta-lactam antibiotics on Enterokteriaceae. Antimicrob Agents Chemother 28:601606.1985. Jacoby GA, Medeiros AA: More extendedspectrum beta-lactamases. Antimicrob Agents Chemother 35:1697-1704.1991. Lachapelle J. Quinn JP,Miyashiro D, et al: Sequence of genes blT-10 and blT-11 which encode the extended-spectrum beta-lactamases TEM-10 and TEM-11. Program Absh 30th Jntersci Conf Antimicrob Agents Chemother 1990, abstr no 187. Petit A, Sirot DL, Chanal CM, et al: Novel plasmid-mediated beta-lactamase in clinicaJ isolates of Kkbsiellapnewnoniae more resistant to ceftaxidime than to other broad spectrum cephalosporins. Antimicrob Agents Chemother 32:626630,1988. Philippon A, Labia R, Jacoby G: Extended spectrum beta-lactamases. Antimicrob Agents Chemother 33:1131-1136,1989. Quinn JR,Miyashiro D, Sahm D, et al: Novel plasmid-mediated beta-lactamases (TEM-10) conferring selective resistance to ceftaxidiie and axtreonam in clinical isolates of nioe. Antimicrob Agents Chemother 33:1451-1456.1989.
70 Infectious Diseases Newsletter 1 l(9) September 1992 Rice LB, Wiley SH, Papanicolaou A, et al: Outbreak of ceftazidke resistance caused by extended-spectrum bcta-lactamases at a Massachusetts chronic care facility. Antimicrob Agents Chemother 34:2193-2199,199O.
II: High-level resistance to cefotaxime and ceftazidiie in Klebsiella pnewnoniue isolates from Cleveland, Ohio. Antimicrob Agents Chemother 35:1001-1003, 1991.
Sirot D, Chanal C, Labia R, et al: Comparative study of five plasmid-mediated ceftazidimases isolated in Kiebsiella pneumoniue. J Antimicrob Chemother 24:509-521.1989.
Vatopoulos AC, Philippon A, Tzouvelekis IS, et al: Prevalence of transferable SHV-5 type beta-lactamase in clinical isolates of Klebsiella pneumoniae and Escherichia coli in Greece. J Antimicrab Chemother 26:635-648,1990.
Thomson KS, Sanders CC, Washington JA
Vuye A, Verschraegen G, Claeys G: Plas-
mid-mediated beta-lactamases in clinical isolates of Klebsiella pneumoniae and Escherichia coli resistant to ceftazidime. Antimicrob Agents Chemother 33:757-761,1989.
Address correspondence to Charles E. MD, Departmentof Medicine/Infectious Diseases, Veterans Affain Medical Center, 1111 East End Boulevard, Wilkes-Barre, Pennsylvania 18711. Che~bii,
CASE REPORT
nberculous
Pericarditis in an Elderly Male with Lymphoma
Charles W. Stratton, MD Associate Professor 4 Padmlogy. Vamkrbil~Um’versiQ School
This 7 1-year-old white male was initially admitted to Vanderbilt University Medical Center because of a 2-week history of high fever and soaking night sweats. The past medical history was significant in that this man had been diagnosed 4 years earlier as having a well-differentiated malignant lymphoma, which had been diagnosed at another medical center by the biopsy of a neck lymph node after he had presented with cervical lymphadenopathy. He subsequently received chemotherapy and radiation for this lymphoma and had been without symptoms since the completion of this therapy. Physical examination revealed no palpable lymph nodes or hepatosplenomegaly. There was a two-component rub noted on cardiac auscultation. Otherwise, the physical exam was normal. The vital signs were stable with no fever. Laboratory values revealed a PCV of 28%. The WBC was 7,6OO/cmm with a normal differential. Liver function studies were normal. A chest roentgenogram revealed
ofMedicine,Nashville,
Tennessee
cardiomegaly. Follow-up computerized tomography of the chest showed bilateral pleural effusions with loculation in the right lung base as well as a pericardial effusion. An ultrasound guided thoracentesis showed pleural fluid with a lymphocytosis (5OO/cmm) having a monomorphic population of small lymphocytes. Pleural fluid was sent for appropriate cultures, including those for AFB and fungi. The pleural lymphocytosis was felt to be consistent with either a reactive process or a well-differentiated lymphoma. A bone marrow biopsy revealed a well-differentiated lymphoma. The bone marrow biopsy was cultured for AFB and fungi. An echocardiogram showed a left ventricular ejection fraction of 55%. There was no evidence of cardia tamponade by the pericardial effusion. Tuberculin skin tests were applied and were negative, first and second strength. The clinical impression of this initial admission was that these pleural and pericardial effusions represented a recurrence of lymphoma. The patient thus received chemotherapy with CyQ1992 Elsevier Science Publishing Co., Inc. 0278-2316/92/$0.00
+ 3.00
toxan, Vmcristine, and Prednisone. He did well and was discharged to be followed in the clinic. Over the next 3 months, the night sweats and fever seemed to be resolved. The patient did, however, net a 20-pound weight loss. In addition, he began to develop lower extremity edema. A magnetic resonance imaging study indicated pericardial effusion with thickened pericardium. The patient was felt to have a restrictive pericarditis without tamponade. He was readmitted to Vanderbilt Medical Center for a pericardiectomy. At tboracotomy, the pericardium was found to be thickened to approximately 4-5 mm with a shaggy exudate on the pericardial and epicardial surfaces and epicardial fibrous constriction. Approximately 100 ml of serious fluid was within the cavity. A section of the anterior pericardium was resected. Microscopic evaluation of the pericardium revealed granulomas by H&E and acid-fast bacilli by Fite staining. Cultures subsequently grew M. tuberculosis from the pericardium although the pleural fluid and