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Penicillium janthinellum in sputum and bronchoalveolar lavage in an AIDS patient with pneumonia
LETTERS TO THE EDITORS
Penicillium janthinellum in sputum and bronchoalveolar lavage in an AIDS patient with pneumonia
Laboratory data showed a white blood cell count of 7 9 0 0 / m 3 , with 75% polyniorphonuclear cells, 8% bands, 10% lymphocytes, and 7% monocytes. A blood gas on room air test gave the follsowing results: p H 7.45, pCO2 33, pOz 56, H C 0 3 23 mnEQ/L, 0 2 saturation 91%. The chest X-ray revealed a dense right upper lung infiltrate with bilateral interstitial and alveolar infiltrates (Figure 1). The patient was started on trimethoprim-sulfamethoxazole (TS), 320 mg (IVD) every 6 h, erythromycin, 1 g (IV) every 6 h, and fluconazole, 100 mg (PO) every day, with a diagnosis of comrnunityacquired pneumonia. There was a need to rule out pulmonary tuberculosis and Pneumocystis cuvinii pneumonia (PCP), and sputum for Gram stain, culture and acid-fast smear was obtained. The day after admission, a bronchoscopy with bronchoalveolar lavage (BAL) was performed. Purulent secretions were noted and a sample was taken from the right upper lung. Culture of the sputum yidded abundant normal oropharyngeal flora and a moderate amount of a rapidly growing mold which was also isolated in large amounts from the BAL fluid in addition to Huemophilus inJuenzue (Figure 2). Both Gram stains and KOH preparations of the BAL fluid 5,tained with Calcofluor white revealed the presence of somewhat dichotomously branching septate fungal hyphae 3-6 pm in width. The fungus grew rapidly at 3OoC on Sabouraud dextrose agar (SDA) (Emmon',: modification) and on SDA with chloramphenicol. N o growth was noted on Mycosel agar (BBL). The organism was buff-colored and produced a slight yellow pigment on the reverse that was most pronounced on potato dextrose agar. Attempts to identifji the fungus were unsuccessful. The isolate was sent to the Fungus Testing Laboratory, Department of Patholom, University of Texas Health Science Center at San Antonio for identification. Blood cultures were negative. The isolate of H . in@enzae was sensitive to trimethoprim-sulfaniethoxazole and cefiizoxime. The patient remained febrile with a temperature up to 38.9"C. Erythromycin and fluconazole were discontinued and a new regimen of amphotericin B and ceftizoxime was begun. The patient began to defervesce but died 4 days later. An autopsy was not performed. The mold was later identified as Penicillium junthinellum (Maren A. Klich, USDA, Southern Regional Research Center, New Orleans, LA). Penicillium junthinellum Biourge (derived from the Latin junthinellus, meaning to be somewhat violet) is a
Clin Microbiol Infect 1997; 3: 261-264 Patients immunocompromised with acquired immune deficiency syndrome (AIDS) are at particular risk for infection with opportunistic fungi. Penicillium species are blue-green molds, and are ubiquitous in nature. They are frequently contaminants of clinical specimens, and isolation from the lung usually represents colonization after inhalation of conidia. We report pneumonia in an AIDS patient from whom Penicilliumjunthinellum was isolated in large quantities from expectorated sputum and bronchoalveolar washings. The patient died, and because an autopsy was not performed, the nature of the infection was not confirmed histopathologically or by culture from tissue. However, we assume that P junthinellum was the cause of severe bilateral pneumonia with consolidation in this patient. The patient was a 47-year-old male, HIV positive, with a CD4 count of zero. H e was a former intravenous drug user, and worked at a chemical plant. H e had been vacationing in Acapulco, Mexico 10 days prior to admission, and while there developed symptoms of cough producing a thick yellow-brown sputum with blood streaks, dull aching upper back pain, shortness of breath, fever, lethargy, weakness, and anorexia. H e also complained of a 10-lb weight loss over a 3-week period. He denied any diarrhea, abdonlinal pain, night sweats, or pleuritic chest pain. His past medical history included outpatient treatment of pneumonia twice before this admission. His niehcations included clotrimazole troches, clotrimazole cream, enalapril maleate 5 mg (PO) every day, trimethoprim-sulfamethoxazole DS 1 tablet (PO) every other day, N P H insulin 30 units (SC) every day, methadone 80 mg (PO) every day, rifabutin 300 mg (PO) every day, and azathioprine 100 ing (PO) five times a day. Physical examination revealed a cachectic, lethargic male in mild respiratory distress, alert and oriented to person, place and time. His temperature was 37.9"C on admission (maximum temperature 39.2"C), heart rate 104 beatdmin, respiratory rate 22/min, and blood pressure 106/60 mmHg. The physical examination was remarkable for bilateral crackles with increased vocal fremitus in the right mid-lung field on auscultation of the lungs. 261
262
C l i n i c a l M i c r o b i o l o g y a n d I n f e c t i o n , V o l u m e 3 N u m b e r 2 , A p r i l 1997
Figure 1 Chest X-ray on admission showing a dense right upper lung infiltrate with bilateral interstitial and alveolar
infiltrates
very common soil organism. Some authorities regard I? simplicissuin (Oudermans) Thorn to be a synonym of I? janthinellurn. Most taxonomists agree that this species is distinctly variable, with individual isolates showing considerable differences in colonial appearance. Generally, as with the clinical isolate recovered from this case, colonies are broadly floccose and spreading, radially furrowed and pale gray-green, with the colony reverse varying from colorless to pale dirty yellow or demonstrating reddish to purple colorations. Conidiophores are finely to coarsely rough (3-5 pin in diameter), and conidial heads irregular, often consisting of a simple whorl of cells supporting the conibogenous cells. Conidiogenous cells (phialides) are characteristic, very divergent (8-10 x 2-2.2 pm), and taper abruptly to long slender tips. Conidia are mainly elliptical to subglobose, delicately roughened (3-3.5 pm long axis), and arranged in delicate divergent twisted/tangled chains. Patients with severe dysfunction of cell-mediated immunity and HIV infection are at great risk for developing severe life-threatening illnesses caused by opportunistic fungal pathogens not previously recog-
nized to cause human infection. The genus Penicillium contains approximately 200 species, and is classified in a group of moniliaceous (lightly pigmented/clearcolored) molds which may cause opportunistic infections in humans. Other members of the group include Paecilomyces, Fusarium, Scopulariopsis, Acrernonium and Beauveria. These mycelial fungi can cause a variety of nosocomial infections in immunocompromised hosts and rarely can be isolated from bronchial secretions of patients with underlying pulmonary disease. However, demonstration of mycelial elements invading alveolar tissue is usually required to establish their role in pneumonia [1,2]. Related fungi of the genus Aspetgillus cause pneumonia in patients with AIDS who have had Pneumocystis carinii pneumonia [3] as well as a variety of frankly invasive manifestations [4-61. Penicillium species are ubiquitous in nature, and when recovered from clinical specimens are usually considered contaminants, but they are also known to cause human disease [7,8]. Systemic infections caused by Penicillium mamefei, a dimorphic fungus endemic to Southeast Asia, and Penicillium decumbens have been reported in patients with AIDS 19-12],
263
Letters t o t h e Editors
Figure 2 Yeast forms of Pmicillium jarithinellum in BAL washings stained with Grocott-Gomori methenamine-silver nitratc stain. Original magnification x200.
Penicillium janthinellum, a species of Penicillium well known to produce tremorgenic toxins, causes a neurologic disease in sheep and cattle known as rye grass staggers [13,14]. In a case report of soft drink food poisoning, P jantliinellum was identified as the causative mold [15]. This species of Penicillium, which was recovered from our patient's sputum and bronchoalveolar secretions, has not been previously reported to cause pneumonia. Bronchoalveolar lavage is the method of choice for sampling bronchial and alveolar secretions in patients with AIDS who have pneumonia, helping to make a diagnosis and direct therapy. In our patient, I! janthinellum was isolated in large quantities from expectorated sputum and bronchoalveolar washings, and thus we believe that this is likely to be the cause of the severe bilateral consolidation pneumonia. Although he was not neutropenic during his illness, he was severely immunocompromised, with a CD4 lymphocyte count of zero. This case points out once again the need for contemporary practitioners and laboratorians to be cognizant of the plethora of fungal agents capable of inciting disease in the host with abrogated immunity.
',
M . Vanessa Gill Paul E. Sclzoch', Michael G. Rinaldi', Maren A.Klich', Burke A. Cunha' 'Infectious Disease Division and the Department of Pathology, Winthrop-University Hospital, Mineola, New York, USA, and School of Medicine, SUNY at Stony Brook, Stony Brook, New York, USA; 'Fungus Testing Laboratory, University of Texas Health Sciences Center at San Antonio, Sail Antonio, Texas, USA; 'United States Department of Agriculture, Southern Regional Research Center, New Orleans, LA, USA References 1. Rippon JW (ed). The pathogernc fungi and the pathogenic actinoniycetes. In: Medical Mycology, 3rd edn. Philadelphia: WB Saunders Company, 1988: 728-30. 2. Kogers AL, Kennedy MJ. Opportunistic hyaline hyphoniycetes. In: Balows A, Hausler WJ, Herrmann KL, Isenberg
264
C l i n i c a l M i c r o b i o l o g y a n d I n f e c t i o n , V o l u m e 3 N u m b e r 2, A p r i l 1 9 9 7
HD, Shadomy HJ, eds. Manual of clinical microbiology. Washington: American Society for Microbiology 1991: 659-73. 3. Denning DW, Follansbee SE, Scolaro M , Norris S, Edelstein H , Stevens DA. Pulmonary aspergillosis in the acquired immunodeficiency syndrome. N Engl J Med 1991; 324: 654-62. 4 Miller W T Jr, Sais GJ, Frank I, Gefter WB, Aronchick JM, Mder WT. Pulmonary aspergillosis in patients with AIDS: clinical and radiographic correlations. Chest 1994; 105: 37-44. 5 Wallace M R , Kanak RJ, Newton JA, Kennedy CA. Invasive aspergillosis in patients with AIDS. Clin Infect Dis 1994; 19: 222. 6 Staples CA, Kang E-Y, Wright JL, Phihps P, Muller NL. Invasive pulmonary aspergillosis in AIDS: radiographic, CT, and pathologic findings. Radiology 1995; 196: 409-14. 7 Kennedy MJ, Sigler L. Aspergillus, Fusarium, and other opportunistic moniliaceous hngi. In Murray PK, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of clinical microbiology, 6th edn. Washington, DC: American Society for Microbiology Press, 1995: 765-90. 8. Piehl M R , Kaplan RL, Haber MH. Disseminated penicdliosis in a patient with acquired immunodeficiency syndrome. Arch Pathol Lab Med 1988; 112: 1262-4. 9. Alvarez S. Systemic infection caused by Penicillium decuinbens in a patient with acquired immunodeficiency syndrome. J Infect Dis 1990; 162: 283. 10. Tsang DNC, Li PCK, Tsui MS, Lau YT, Ma KF, Yeoh EK. Penicillium marfie&: another pathogen to consider in patients infected with human immunodeficiency virus. Rev Infect Dis 1991; 13: 766-7. 11. Supparatpinyo K, Chiewchanvit S, Hirunsri P, Uthammachai C, Nelson KE, Sirisanthana T. Prnicillium marneffpi infection in patients infected with human immunodeficiency virus. Clin Infect Dis 1992;14: 871-4. 12. Jones PD, See J. Penicillium marrzefii infection in patients infected with human immunodeficiency virus: late presentation in an area of nonendemicity Clin Infect Dis 1992; 15: 744. 13. Gallagher RT, Latch GCM, Keogh RG. The Janthitrems: fluorescent tremorgenic toxins produced by Penicillium janthinellum isolates from ryegrass pastures. Appl Environ Microbiol 1980; 39: 272-3. 14. Lanigan GW, Payne AL, Cockrum PA. Production of tremorgenic toxins by Penicillium janthinellum biourgr: a possible aetiological factor in ryegrass. AJEBAK 1979; 57: 31-7. 15. Wang ZG. Identification of toxigenic mould in soft drink causing food poisoning. Chung-Hau Yu Fang i Hsueh Tsa Chih 1992; 26: 8-10.
Enterococcal joint prosthesis infection
Clin Microbiol Infect 1997; 3: 264-265
biologist. Extensive efforts are made to minimize the incidence of infection. It is common practice to identify risk factors and to avoid procedures such as urethral catheterization, in an attempt to guard against the most common infecting organisms. We report two cases of prosthesis infection which highlight the problems of identification and treatment of infection with enterococci.
Case 1 A 75-year-old man underwent right total knee replacement with cefuroxime prophylaxis (three doses). Preoperatively he had no symptoms of prostatism, and a urine sample showed no significant bacterial growth. Postoperatively he developed urinary retention, requiring multiple urethral catheterizations, each with gentamicin cover followed by oral trimethoprim. He underwent transurethral resection of the prostate 3 weeks after his arthroplasty surgery. Eight months later he presented with swelling of the right knee and an abscess on the suture line. This discharged to reveal a sinus, from which Staphylococcus aureus was cultured. In contrast, culture of joint fluid obtained by arthrocentesis grew Enterococcus faecalis. At revision arthroplasty, there was established joint infection. The prosthesis and cement were removed and a cement spacer, incorporating gentamicin, ampicillin and flucloxacillin, was inserted. At operation, superficial and sinus tract swabs grew S. aureus, E. faecalis and Proteus sp., but cultures ofjoint fluid, bone, cement and joint tissue yielded pure growths of E. faecalis. The patient was treated with intravenous flucloxacillin, ampicillin and gentamicin for 2 weeks, followed by oral flucloxacillin and amoxycillin for 4 weeks, and the infection cleared. He is awaiting the second stage of revision surgery. Case 2 A 49-year-old woman with severe rheumatoid arthritis on long-term steroid therapy and azathioprine had multiple orthopedic procedures over 20 years. These included bilateral ankle arthrodeses, an osteotomy of her right tibia and subsequent knee arthroplasty, fusion of the left knee and bilateral total hip replacements. Replacement of the right hip was complicated by recurrent dislocations, requiring open reduction on two occasions and early revision of the acetabular component. Eighteen months later she presented with severe pain in the right hip and was unable to bear weight on that joint. Radiologic changes were consistent with infection. Joint fluid obtained by arthrocentesis grew E. faecalis and skin flora. A two-stage revision was planned. At surgery the joint was seen to be grossly infected. Multiple operative cultures grew I
Infection in a joint replacement is a disaster for the patient and a challenge for both surgeon and micro-
I
Penicillium janthinellum in sputum and bronchoalveolar lavage in an AIDS patient with pneumonia
Laboratory data showed a white blood cell count of 7 9 0 0 / m 3 , with 75% polyniorphonuclear cells, 8% bands, 10% lymphocytes, and 7% monocytes. A blood gas on room air test gave the follsowing results: p H 7.45, pCO2 33, pOz 56, H C 0 3 23 mnEQ/L, 0 2 saturation 91%. The chest X-ray revealed a dense right upper lung infiltrate with bilateral interstitial and alveolar infiltrates (Figure 1). The patient was started on trimethoprim-sulfamethoxazole (TS), 320 mg (IVD) every 6 h, erythromycin, 1 g (IV) every 6 h, and fluconazole, 100 mg (PO) every day, with a diagnosis of comrnunityacquired pneumonia. There was a need to rule out pulmonary tuberculosis and Pneumocystis cuvinii pneumonia (PCP), and sputum for Gram stain, culture and acid-fast smear was obtained. The day after admission, a bronchoscopy with bronchoalveolar lavage (BAL) was performed. Purulent secretions were noted and a sample was taken from the right upper lung. Culture of the sputum yidded abundant normal oropharyngeal flora and a moderate amount of a rapidly growing mold which was also isolated in large amounts from the BAL fluid in addition to Huemophilus inJuenzue (Figure 2). Both Gram stains and KOH preparations of the BAL fluid 5,tained with Calcofluor white revealed the presence of somewhat dichotomously branching septate fungal hyphae 3-6 pm in width. The fungus grew rapidly at 3OoC on Sabouraud dextrose agar (SDA) (Emmon',: modification) and on SDA with chloramphenicol. N o growth was noted on Mycosel agar (BBL). The organism was buff-colored and produced a slight yellow pigment on the reverse that was most pronounced on potato dextrose agar. Attempts to identifji the fungus were unsuccessful. The isolate was sent to the Fungus Testing Laboratory, Department of Patholom, University of Texas Health Science Center at San Antonio for identification. Blood cultures were negative. The isolate of H . in@enzae was sensitive to trimethoprim-sulfaniethoxazole and cefiizoxime. The patient remained febrile with a temperature up to 38.9"C. Erythromycin and fluconazole were discontinued and a new regimen of amphotericin B and ceftizoxime was begun. The patient began to defervesce but died 4 days later. An autopsy was not performed. The mold was later identified as Penicillium junthinellum (Maren A. Klich, USDA, Southern Regional Research Center, New Orleans, LA). Penicillium junthinellum Biourge (derived from the Latin junthinellus, meaning to be somewhat violet) is a
Clin Microbiol Infect 1997; 3: 261-264 Patients immunocompromised with acquired immune deficiency syndrome (AIDS) are at particular risk for infection with opportunistic fungi. Penicillium species are blue-green molds, and are ubiquitous in nature. They are frequently contaminants of clinical specimens, and isolation from the lung usually represents colonization after inhalation of conidia. We report pneumonia in an AIDS patient from whom Penicilliumjunthinellum was isolated in large quantities from expectorated sputum and bronchoalveolar washings. The patient died, and because an autopsy was not performed, the nature of the infection was not confirmed histopathologically or by culture from tissue. However, we assume that P junthinellum was the cause of severe bilateral pneumonia with consolidation in this patient. The patient was a 47-year-old male, HIV positive, with a CD4 count of zero. H e was a former intravenous drug user, and worked at a chemical plant. H e had been vacationing in Acapulco, Mexico 10 days prior to admission, and while there developed symptoms of cough producing a thick yellow-brown sputum with blood streaks, dull aching upper back pain, shortness of breath, fever, lethargy, weakness, and anorexia. H e also complained of a 10-lb weight loss over a 3-week period. He denied any diarrhea, abdonlinal pain, night sweats, or pleuritic chest pain. His past medical history included outpatient treatment of pneumonia twice before this admission. His niehcations included clotrimazole troches, clotrimazole cream, enalapril maleate 5 mg (PO) every day, trimethoprim-sulfamethoxazole DS 1 tablet (PO) every other day, N P H insulin 30 units (SC) every day, methadone 80 mg (PO) every day, rifabutin 300 mg (PO) every day, and azathioprine 100 ing (PO) five times a day. Physical examination revealed a cachectic, lethargic male in mild respiratory distress, alert and oriented to person, place and time. His temperature was 37.9"C on admission (maximum temperature 39.2"C), heart rate 104 beatdmin, respiratory rate 22/min, and blood pressure 106/60 mmHg. The physical examination was remarkable for bilateral crackles with increased vocal fremitus in the right mid-lung field on auscultation of the lungs. 261
262
C l i n i c a l M i c r o b i o l o g y a n d I n f e c t i o n , V o l u m e 3 N u m b e r 2 , A p r i l 1997
Figure 1 Chest X-ray on admission showing a dense right upper lung infiltrate with bilateral interstitial and alveolar
infiltrates
very common soil organism. Some authorities regard I? simplicissuin (Oudermans) Thorn to be a synonym of I? janthinellurn. Most taxonomists agree that this species is distinctly variable, with individual isolates showing considerable differences in colonial appearance. Generally, as with the clinical isolate recovered from this case, colonies are broadly floccose and spreading, radially furrowed and pale gray-green, with the colony reverse varying from colorless to pale dirty yellow or demonstrating reddish to purple colorations. Conidiophores are finely to coarsely rough (3-5 pin in diameter), and conidial heads irregular, often consisting of a simple whorl of cells supporting the conibogenous cells. Conidiogenous cells (phialides) are characteristic, very divergent (8-10 x 2-2.2 pm), and taper abruptly to long slender tips. Conidia are mainly elliptical to subglobose, delicately roughened (3-3.5 pm long axis), and arranged in delicate divergent twisted/tangled chains. Patients with severe dysfunction of cell-mediated immunity and HIV infection are at great risk for developing severe life-threatening illnesses caused by opportunistic fungal pathogens not previously recog-
nized to cause human infection. The genus Penicillium contains approximately 200 species, and is classified in a group of moniliaceous (lightly pigmented/clearcolored) molds which may cause opportunistic infections in humans. Other members of the group include Paecilomyces, Fusarium, Scopulariopsis, Acrernonium and Beauveria. These mycelial fungi can cause a variety of nosocomial infections in immunocompromised hosts and rarely can be isolated from bronchial secretions of patients with underlying pulmonary disease. However, demonstration of mycelial elements invading alveolar tissue is usually required to establish their role in pneumonia [1,2]. Related fungi of the genus Aspetgillus cause pneumonia in patients with AIDS who have had Pneumocystis carinii pneumonia [3] as well as a variety of frankly invasive manifestations [4-61. Penicillium species are ubiquitous in nature, and when recovered from clinical specimens are usually considered contaminants, but they are also known to cause human disease [7,8]. Systemic infections caused by Penicillium mamefei, a dimorphic fungus endemic to Southeast Asia, and Penicillium decumbens have been reported in patients with AIDS 19-12],
263
Letters t o t h e Editors
Figure 2 Yeast forms of Pmicillium jarithinellum in BAL washings stained with Grocott-Gomori methenamine-silver nitratc stain. Original magnification x200.
Penicillium janthinellum, a species of Penicillium well known to produce tremorgenic toxins, causes a neurologic disease in sheep and cattle known as rye grass staggers [13,14]. In a case report of soft drink food poisoning, P jantliinellum was identified as the causative mold [15]. This species of Penicillium, which was recovered from our patient's sputum and bronchoalveolar secretions, has not been previously reported to cause pneumonia. Bronchoalveolar lavage is the method of choice for sampling bronchial and alveolar secretions in patients with AIDS who have pneumonia, helping to make a diagnosis and direct therapy. In our patient, I! janthinellum was isolated in large quantities from expectorated sputum and bronchoalveolar washings, and thus we believe that this is likely to be the cause of the severe bilateral consolidation pneumonia. Although he was not neutropenic during his illness, he was severely immunocompromised, with a CD4 lymphocyte count of zero. This case points out once again the need for contemporary practitioners and laboratorians to be cognizant of the plethora of fungal agents capable of inciting disease in the host with abrogated immunity.
',
M . Vanessa Gill Paul E. Sclzoch', Michael G. Rinaldi', Maren A.Klich', Burke A. Cunha' 'Infectious Disease Division and the Department of Pathology, Winthrop-University Hospital, Mineola, New York, USA, and School of Medicine, SUNY at Stony Brook, Stony Brook, New York, USA; 'Fungus Testing Laboratory, University of Texas Health Sciences Center at San Antonio, Sail Antonio, Texas, USA; 'United States Department of Agriculture, Southern Regional Research Center, New Orleans, LA, USA References 1. Rippon JW (ed). The pathogernc fungi and the pathogenic actinoniycetes. In: Medical Mycology, 3rd edn. Philadelphia: WB Saunders Company, 1988: 728-30. 2. Kogers AL, Kennedy MJ. Opportunistic hyaline hyphoniycetes. In: Balows A, Hausler WJ, Herrmann KL, Isenberg
264
C l i n i c a l M i c r o b i o l o g y a n d I n f e c t i o n , V o l u m e 3 N u m b e r 2, A p r i l 1 9 9 7
HD, Shadomy HJ, eds. Manual of clinical microbiology. Washington: American Society for Microbiology 1991: 659-73. 3. Denning DW, Follansbee SE, Scolaro M , Norris S, Edelstein H , Stevens DA. Pulmonary aspergillosis in the acquired immunodeficiency syndrome. N Engl J Med 1991; 324: 654-62. 4 Miller W T Jr, Sais GJ, Frank I, Gefter WB, Aronchick JM, Mder WT. Pulmonary aspergillosis in patients with AIDS: clinical and radiographic correlations. Chest 1994; 105: 37-44. 5 Wallace M R , Kanak RJ, Newton JA, Kennedy CA. Invasive aspergillosis in patients with AIDS. Clin Infect Dis 1994; 19: 222. 6 Staples CA, Kang E-Y, Wright JL, Phihps P, Muller NL. Invasive pulmonary aspergillosis in AIDS: radiographic, CT, and pathologic findings. Radiology 1995; 196: 409-14. 7 Kennedy MJ, Sigler L. Aspergillus, Fusarium, and other opportunistic moniliaceous hngi. In Murray PK, Baron EJ, Pfaller MA, Tenover FC, Yolken RH, eds. Manual of clinical microbiology, 6th edn. Washington, DC: American Society for Microbiology Press, 1995: 765-90. 8. Piehl M R , Kaplan RL, Haber MH. Disseminated penicdliosis in a patient with acquired immunodeficiency syndrome. Arch Pathol Lab Med 1988; 112: 1262-4. 9. Alvarez S. Systemic infection caused by Penicillium decuinbens in a patient with acquired immunodeficiency syndrome. J Infect Dis 1990; 162: 283. 10. Tsang DNC, Li PCK, Tsui MS, Lau YT, Ma KF, Yeoh EK. Penicillium marfie&: another pathogen to consider in patients infected with human immunodeficiency virus. Rev Infect Dis 1991; 13: 766-7. 11. Supparatpinyo K, Chiewchanvit S, Hirunsri P, Uthammachai C, Nelson KE, Sirisanthana T. Prnicillium marneffpi infection in patients infected with human immunodeficiency virus. Clin Infect Dis 1992;14: 871-4. 12. Jones PD, See J. Penicillium marrzefii infection in patients infected with human immunodeficiency virus: late presentation in an area of nonendemicity Clin Infect Dis 1992; 15: 744. 13. Gallagher RT, Latch GCM, Keogh RG. The Janthitrems: fluorescent tremorgenic toxins produced by Penicillium janthinellum isolates from ryegrass pastures. Appl Environ Microbiol 1980; 39: 272-3. 14. Lanigan GW, Payne AL, Cockrum PA. Production of tremorgenic toxins by Penicillium janthinellum biourgr: a possible aetiological factor in ryegrass. AJEBAK 1979; 57: 31-7. 15. Wang ZG. Identification of toxigenic mould in soft drink causing food poisoning. Chung-Hau Yu Fang i Hsueh Tsa Chih 1992; 26: 8-10.
Enterococcal joint prosthesis infection
Clin Microbiol Infect 1997; 3: 264-265
biologist. Extensive efforts are made to minimize the incidence of infection. It is common practice to identify risk factors and to avoid procedures such as urethral catheterization, in an attempt to guard against the most common infecting organisms. We report two cases of prosthesis infection which highlight the problems of identification and treatment of infection with enterococci.
Case 1 A 75-year-old man underwent right total knee replacement with cefuroxime prophylaxis (three doses). Preoperatively he had no symptoms of prostatism, and a urine sample showed no significant bacterial growth. Postoperatively he developed urinary retention, requiring multiple urethral catheterizations, each with gentamicin cover followed by oral trimethoprim. He underwent transurethral resection of the prostate 3 weeks after his arthroplasty surgery. Eight months later he presented with swelling of the right knee and an abscess on the suture line. This discharged to reveal a sinus, from which Staphylococcus aureus was cultured. In contrast, culture of joint fluid obtained by arthrocentesis grew Enterococcus faecalis. At revision arthroplasty, there was established joint infection. The prosthesis and cement were removed and a cement spacer, incorporating gentamicin, ampicillin and flucloxacillin, was inserted. At operation, superficial and sinus tract swabs grew S. aureus, E. faecalis and Proteus sp., but cultures ofjoint fluid, bone, cement and joint tissue yielded pure growths of E. faecalis. The patient was treated with intravenous flucloxacillin, ampicillin and gentamicin for 2 weeks, followed by oral flucloxacillin and amoxycillin for 4 weeks, and the infection cleared. He is awaiting the second stage of revision surgery. Case 2 A 49-year-old woman with severe rheumatoid arthritis on long-term steroid therapy and azathioprine had multiple orthopedic procedures over 20 years. These included bilateral ankle arthrodeses, an osteotomy of her right tibia and subsequent knee arthroplasty, fusion of the left knee and bilateral total hip replacements. Replacement of the right hip was complicated by recurrent dislocations, requiring open reduction on two occasions and early revision of the acetabular component. Eighteen months later she presented with severe pain in the right hip and was unable to bear weight on that joint. Radiologic changes were consistent with infection. Joint fluid obtained by arthrocentesis grew E. faecalis and skin flora. A two-stage revision was planned. At surgery the joint was seen to be grossly infected. Multiple operative cultures grew I
Infection in a joint replacement is a disaster for the patient and a challenge for both surgeon and micro-
I