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erythema disappeared upon discontinuation of the antibiotic, there being no further dermatological problems. The normal EEG result and the CSF findings in our patient (pleocytosis with predominantly polymorphonuclear leukocytes, elevated protein level, reduced glucose level) suggest there was meningeal but not encephalic involvement [1, 9]. In the absence of antiMycoplasma pneumoniae antibodies in the CSF the most probable pathogenic mechanism of meningeal involvement would be an autoimmune one; however, the possibility of hematogenous dissemination from a respiratory source cannot be discarded [5, 6]. Aseptic meningitis caused by Mycoplasma pneumoniae has a benign prognosis [1, 3]; the recommended treatment is exclusively symptomatic since antibiotic therapy does not influence positively the natural course of the disease and could produce adverse drug reactions.

References 1. Couch RB: Mycoplasma pneumoniae. In: Mandel GL, Douglas RD, Bennet JE (eds): Principles and practice of infectious diseases. Churchill Livingstone, New York (1990) pp. 1446–1458 2. MacFarlane PI, Miller V: Transverse myelitis associated with Mycoplasma pneumoniae infection. Archives of Disease in Childhood (1984) 59 : 80–82 3. Hely MA, Williamson PM, Terenty TR: Neurological complications of Mycoplasma pneumoniae infection. Clinical Experimental Neurology (1984) 20 : 153–160 4. Pönkä A: Central nervous system manifestations associated with serologically verified Mycoplasma pneumoniae infection. Scandinavian Journal of Infectious Disease (1980) 12 : 175–184 5. Koskiniemi M: CNS manifestations associated with Mycoplasma pneumoniae infections: summary of cases at the University of Helsinki and review. Clinical Infectious Disease (1993) 17, Supplement 1 : 52–57 6. Tjhie JHT, Van de Putte EM, Haasnoot K, Van den Brule AJC, Vandenbroucke-Grauls CMJE: Fatal encephalitis caused by Mycoplasma pneumoniae in a 9-year-old girl. Scandinavian Journal of Infectious Disease (1997) 29 : 424–425 7. Kenny GE, Kaiser GG, Cooney MK, Foy HM: Diagnosis of Mycoplasma pneumoniae pneumonia: sensitivities and specificities of serology with lipid antigen and isolation of the organism on soy peptone medium for identification of infections. Journal of Clinical Microbiology (1990) 28 : 2087–2093 8. Foy HM, Kenny GE, Kaler J: Mycoplasma pneumoniae in Stevens-Johnson syndrome. Lancet (1967) 2 : 550 9. Maida E, Kristoferitsch W: Cerebrospinal fluid finding in Mycoplasma pneumoniae infections with neurological complications. Acta Neurologica Scandinavica (1982) 65 : 524

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Chronic Pulmonary Histoplasmosis in a Patient with a Recent History of Tuberculosis and Persistent Round Lung Lesions R. Pometta, C. Trovato, M.A. Viviani, T. Masini, D. Conte Histoplasmosis is a fungal infection which is caused by Histoplasma capsulatum and occurs worldwide. Endemic areas have been identified in the USA (Ohio, Nebraska and Louisiana), where histoplasmin skin testing gave positive results in up to 95% of the general population, and in Latin America, West Africa and Southeast Asia where up to 30% of the general population is positive [1, 2]. In Europe the infection is far less common, only sporadic cases having been reported [3]. Histoplasma capsulatum grows well in soil enriched with bird or bat guano, infection being acquired through the inhalation of airborne spores. Two different clinical forms of infection can be distinguished: an acute pulmonary form occurring in an otherwise healthy host, which is characterized by fever, hypoxia and pulmonary infiltrates, and a chronic form which is similar to tuberculosis. In the presence of a cellular immune deficiency disorder (e.g. AIDS), histoplasmosis may be disseminated with granuloma formation [1, 2, 4]. We report on a case of histoplasmosis in an Italian patient with a recent history of tuberculosis. The patient was a 41-year-old male Caucasian, a fitter by occupation, who was referred to our unit in May 1998 with left-sided chest pain which increased on inspiration, dyspnoea on exertion, progressive asthenia and a weight loss of 8 kg in the previous month from 104 to 96 kg (height 170 cm; decrease in body mass index from 36 to 33). The patient’s history revealed he had been hospitalized in October 1995, after a 2-month holiday in San Salvador, due to a sharp chest pain without fever or a productive cough. The results of blood tests were within normal range and no antibodies against HIV

R. Pometta (Y), C. Trovato, D. Conte Cattedra di Gastroenterologia-Istituto di Scienze Mediche, IRCCS Ospedale Maggiore, Via Francesco Sforza 35, I-20122, Milan, Italy e-mail: GASTRBIA6imiucca.csi.unimi.it M.A. Viviani Istituto di Igiene e Medicina Preventiva, IRCCS Ospedale Maggiore, Milan, Italy T. Masini Istituto di Anatomia e Istologia Patologica, IRCCS Ospedale Maggiore, Milan, Italy

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were detected. A chest radiograph showed multiple, bilateral, round lesions 2–3 cm in diameter, which were diagnosed as metastases of unknown origin. The findings on bronchoscopy were normal, and a bronchoalveolar lavage specimen was negative for both neoplastic cells and Mycobacterium tuberculosis. A test using a specific polymerase chain reaction (PCR) to detect Mycobacterium tuberculosis was also negative. A primary neoplastic lesion was excluded by means of upper and lower gastrointestinal tract endoscopy, abdominal CT, and thyroid and scrotal sonography. Thoracoscopy was performed and a brown, rubbery lesion 3 cm in diameter was removed. On transverse section of this specimen, caseous material was detected, but a Ziehl-Neelsen stain failed to show alcohol-acidfast bacilli and a test using a specific PCR was negative for Mycobacterium tuberculosis. As a skin induration of 25!28 mm was obtained in a tuberculin test using 10 tuberculin units, a presumptive diagnosis of tuberculosis was established. The patient was then started on a treatment regimen consisting of a daily dose of isoniazid (300 mg) and rifampicin (600 mg) for 6 months, and pyrazinamide (1.5 g) for the first 2 months. The patient experienced moderate improvement of his symptoms, but there was no change in the pulmonary lesions as seen on chest radiograph. On admission to our unit in May 1998 the patient was apyretic. The findings on physical examination were unremarkable. The results of an arterial blood gas analysis were normal. A chest radiograph showed multiple, round, well-defined opacities 2–3 cm in diameter in both lung fields with the exception of the apices (Figure 1). The findings on CT scan were similar to the findings in 1995 with the exception that a further lesion was detected in the left upper lobe. The results of all laboratory tests were again within normal range and no anti-HIV antibodies were detected. The findings on both bronchoscopy and culture of bronchoalveolar fluid were normal, with no evidence of atypical cells or

Figure 1 Chest radiograph showing multiple round lesions

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Mycobacterium tuberculosis. At this stage more detailed information was obtained on the patient’s previous occupational activities, revealing he had worked in 1987–1988 in a marble quarry and then in the Milan city underground construction project as tunnel excavator in Italy, and in 1990 as a driller near Moscow, Soviet Union. Subsequently he had done only unskilled labour outdoors. Taking into account these anamnestic details, chronic histoplasmosis was considered in the differential diagnosis, and both the periodic acid-Schiff and Grocott-Gomori stain were performed on stored formaldehyde-fixed material. The morphological findings were specific for Histoplasma capsulatum. Histoplasmosis is endemic in Italy but has seldom been reported [5–8]. Our patient could thus have acquired the infection in Italy, especially through work-related exposure. However, we think the infection was probably acquired during the patient’s stay in Central America, as symptoms appeared soon after his holiday there. Treatment of slowly progressive pulmonary histoplasmosis is recommended [1]. Itraconazole was chosen for treatment of our patient as recent clinical trials with this drug showed favorable results and it is less toxic than amphotericin B [1, 9, 10]. During the follow-up period the patient’s chest pain disappeared, and there were no drug-related side effects. The present report suggests that, in the presence of single or multiple round lung lesions, histoplasmosis must be considered in the differential diagnosis, even in countries where endemic Histoplasma capsulatum infection is rare.

References 1. Dismukes WE: Histoplasmosis. In: Bennett JC, Plum F, Gill GN, Kokko JP, Mandell GL, Ockner RK, Smith TW (eds): Cecil Textbook of Medicine. WB Saunders, Philadelphia (1996) pp. 1816–1819 2. Gurney JW, Conces DJ: Pulmonary histoplasmosis. Radiology (1996) 199 : 297–306 3. Sotgiu G, Mantovani A, Mazzoni A: Histoplasmosis in Europe. Mycopathologia et mycologia applicata (1970) 40 : 53–74 4. Bradsher RW: Histoplasmosis and blastomycosis. Clinical Infectious Diseases (1996) 22, Supplement 2 : 102–111 5. Confalonieri M, Gandola L, Aiolfi S, Parigi P, Mazzoni A: Histoplasmin sensitivity among a student population in Crema, Po Valley, Italy. New Microbiologica (1994) 17 : 151–153 6. Antinori S, Galimberti L, Bonaccorso C, Vago L, Nebuloni M, Esposito R: A case of fatal disseminated histoplasmosis of autochthonous origin in an Italian AIDS patient. European Journal of Clinical Microbiology & Infectious Diseases (1997) 16 : 545–546

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7. Confalonieri M, Aiolfi S, Gandola L, Scartabellati A, Colavecchio A, Cannatelli G, Mazzoni A: Disseminated histoplasmosis and idiopathic CD4c T-lymphocytopenia. An autochthonous Italian case. Presse Medicale (1995) 24 : 459 8. Confalonieri M, Nanetti A, Gandola L, Colavecchio A, Aiolfi S, Cannatelli G, Parigi P, Scartabellati A, Della Porta R, Mazzoni A: Histoplasmosis capsulati in Italy: Autochthonous or imported? European Journal of Epidemiology (1994) 10 : 435–439 9. Wheat J, Hafner R, Korzun AH, Limjoco MT, Spencer P, Larsen RA, Hecht FM, Powderly W: Itraconazole treatment of disseminated histoplasmosis in patients with the acquired immunodeficiency syndrome. AIDS Clinical Trial Group. American Journal of Medicine (1995) 98 : 336–342 10. McKinsey DS, Kauffman CA, Pappas PG, Cloud GA, Girard WM, Sharkey PK, Hamill RJ, Thomas CJ, Dismukes WE: Fluconazole therapy for histoplasmosis. Clinical Infectious Diseases (1997) 23 : 996–1001

Otitis Media due to Corynebacterium jeikeium I. de Miguel-Martínez, A. Ramos- Macías, A.M. Martín-Sánchez After decades of confusion about their clinical significance, coryneforms have been recognized as opportunistic pathogens in humans. Several species, such as Corynebacterium jeikeium (CDC group JK), are now known to cause diseases such as nosocomial septicemia, endocarditis, pneumonia, meningitis, osteomyelitis, infectious arthritis, and cutaneous infections, especially in immunocompromised hosts [1, 2]. To the best of our knowledge, Corynebacterium jeikeium has not been mentioned in the literature as a microorganism involved in chronic otitis media. A 67-year-old man presented with a 5-month history of otorrhea, progressive hearing loss, and postauricular pain in the left ear. He had been using a retroauricular hearing aid in the same ear for the past 3 years. Otologic examination revealed a purulent discharge with the presence of odor, and central perforation of

I. de Miguel-Martínez, A.M. Martín-Sánchez Department of Microbiology, Hospital Universitario Insular de Gran Canaria, Universidad de Las Palmas de Gran Canaria, Apartado 550, Las Palmas de Gran Canaria, Spain A. Ramos-Macías (Y) Department of Otolaryngology, Hospital Universitario Insular de Gran Canaria, Universidad de Las Palmas de Gran Canaria, Avenida Rafael Cabrera n79 47c, E-35002 Las Palmas de Gran Canaria, Spain

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the tympanic membrane with tympanosclerotic areas in the middle ear mucosa. An ossicular necrosis in the long process of the incus was observed under microscope exploration of the left ear. A sample of the middle ear discharge was obtained. The middle ear fluid was aspirated into a Teflon catheter fitted with a tuberculin syringe, and specimens were inoculated into an agar transport medium (Portagem; bioMérieux, France). The sample was plated onto 5% sheep blood agar, chocolate agar, and Brucella agar (bioMérieux). Microscopic examination of the sample revealed the presence of numerous polynuclear cells and numerous pleomorphic gram-positive rods, arranged in V forms or palisades. After 24 h of growth on sheep blood agar at 37 7C, colonies were catalase positive, nonhemolytic, small (0.5 to 1 mm), glistening, low convex, and greyish white. The organism was an aerobe. After recognition as coryneform bacteria, this isolate was identified to the genus level by the API Coryne identification system V1.0 database (API, bioMérieux) supplemented with 1% Tween 80 to promote growth [1]. Its analytical profile was 2100104, the value of the percentage of identification was 87.7%, and the T index was 0.83. Besides the API Coryne system, several complementary tests were used to further characterize the organism. A fructose test (BBL-Cristal gram-positive ID system; Becton Dickinson, USA) was negative, as was DNasa examined on DNA medium (bioMérieux). The CAMP reaction with a b-hemolysin-producing strain of Staphylococcus aureus ATCC 25923, also was negative. After a 4 h incubation period, the API ZYM system (API, bioMérieux) was used according to the manufacturer’s instructions to detect enzymatic activities, Lipase (C14), esterase lipase (C8), leucine arylamidase, and alkaline phosphatase were positive. Corynebacteria can be distinguished by their cell wall and fatty acids constituents. The cell wall characteristics were determined by thin-layer chromatographic analysis and cellular fatty acids by gas chromatography. The cell wall contained arabinose, galactose, and mycolic acids. Cellular fatty acids were 14 : 0, 15 : 0, 16 : 1, 16 : 0, 18 : 1, and 18 : 0. On the basis of these findings, the strain was identified as Corynebacterium jeikeium [2–4]. In the present study antibiotic susceptibility was determined by the disk diffusion method, using MuellerHinton antibiotic medium supplemented with 5% sheep blood. The disk contained 10 mg of penicillin, 10 mg of gentamicin, 30 mg of tetracycline, 15 mg of erythromycin, 25 mg of trimethroprim-sulfamethoxazole, 5 mg of rifampin, 30 mg of vancomycin, 30 mg of teicoplanin, and 5 mg of ciprofloxacin [5]. The strain was susceptible only to vancomycin and teicoplanin. After treatment with teicoplanin adminis-