Letters to the Editor
114 doi:10.1053/jinf.2000.0686, available online at http://www.idealibrary.com on
An Unusual Case of Pulmonary Abscess Sir, We were interested to read the report of Veziris et al. describing a case of Gemella haemolysans empyema.1 We would like to report a case of a pulmonary abscess caused by this organism. A 37-year-old male smoker presented to the respiratory outpatients department with a history of back pain and persistent cough. He had been empirically treated in the community for community-acquired pneumonia with initially cefaclor 250 mg thrice daily for 1 week, amoxycillin 500 mg thrice daily for 1 week and then erythromycin 500 mg thrice daily for 1 week on a sequential basis. There was radiological evidence of consolidation in the lingula and right upper lobe prior to his referral. There had been no history of dental problems or excessive alcohol. At presentation his only positive respiratory finding was mucopurulent sputum and he was repeatedly apyrexial throughout his clinical course. Initial investigations revealed an ESR of 90 mm/h with a normal white cell count 11109/dl (neutrophils 85%), sputum cytology revealed no malignant cells and there was no growth on routine culture and no AAFB seen. His chest radiograph taken at the respiratory clinic revealed a clearing of his previous consolidation with bilateral hilar enlargement, with a cavitating lesion noted on lateral chest film. We proceeded to computerized tomography (CT) scanning of the thorax, which revealed bilateral cavitating lesions in the para-vertebral region with destruction of his thoracic vertebral body at T8. At this point the main clinical differential diagnoses were bronchogenic carcinoma or pulmonary abscess. The patient was admitted and a CT-guided biopsy of the lesion was scheduled, but unfortunately the patient developed focal fits. A CT scan of the head revealed a ring-enhancing lesion surrounded by oedema. The fits were controlled by sodium valproate and we proceeded to CT-guided Tru-cut biopsy of the lesion with cores sent for both histology and culture. The biopsy was consistent with a pulmonary abscess with no evidence of malignancy on histological examination, and cultures grew a Streptococcus spp. of the “milleri group” and Gemella haemolysans. The patient was commenced on high dose amoxycillin and metronidazole despite the absence of an associated anaerobe on culture. Neurosurgical transfer was arranged and the patient underwent burr-hole biopsy and drainage of his cerebral lesion. The brain biopsy was consistent with a metastatic abscess. The high dose antibiotics were continued for 3 months in view of the vertebral body destruction. In view of the microbial isolates from the pulmonary lesion, a dental radiograph was arranged which revealed a dental abscess in the right mandible and appropriate dental treatment was arranged. Despite these findings, even in retrospect, there were no dental symptoms. The patient made steady progress but has continued symptoms related to his established vertebral body destruction. This case adds to the evolving knowledge of this organism’s pathogenicity. Gemella haemolysans is a recognized cause of endocarditis,2 meningitis3 and has been implicated in postinfectious glomerulonephritis.2 Moreover, based on our experience and others1 this organism has now been implicated in causing both intrapulmonary sepsis, either empyema or abscess, in addition to metastatic brain abscesses. Co-isolation of a “milleri group” streptococcus reflects international data, with © 2000 The British Infection Society
up to 65% of abscesses growing more than one organism.4 In a recently published series a large proportion of patients with abscesses had an underlying predisposition.4 The only identifiable risk factor in this patient, dental abscess, was only identified on retrospect and had no associated clinical features. This highlights the need for careful appraisal of patients who may have a pulmonary abscess. Although Gemella morbillorum has been reported as a cause of lung abscess with associated empyema,5 we believe this is the first reported case of Gemella haemolysans as a cause of either pulmonary or brain abscess. A. De Soyza1, B. Higgins1 and K. Gould2 Departments of 1Respiratory Medicine and 2 Microbiology, Freeman Hospital, Newcastle, U.K.
References 1 Veziris N, Fuhrman C, Chouiad C, Marque E, Housset B, Lange J, Monnet I. Empyema of the thorax due to Gemella haemolysans. J Infection 1999; 39: 245. 2 Zingaro L, Bartoli E, Sechi L. Post infectious glomerulonephritis in a patient with Gemella haemolysans endocarditis. Am J Med 1999; 106: 125–126. 3 May T, Amiel C, Lion C, Weber M, Gerard A, Canton P. Meningitis due to Gemella haemolysans. Eur J Clin Microbiol and Inf Dis 1993; 12: 644–645. 4 Hirshberg B, Sklair-Levi M, Nir-Paz R, Ben-Siri L, Krivoruk V, Kramer MR. Factors predicting mortality of patients with lung abscesses. Chest 1999; 115: 746–750. 5 Da Costa CT, Porter C, Morris A, Quoraishi AH. Empyema thoracis and lung abscess due to Gemella morbillorum. Eur J Clin Microbiol and Inf Dis 1996; 15: 75–77. Accepted for publication 28 April 2000
doi:10.1053/jinf.2000.0691, available online at http://www.idealibrary.com on
Filamented Pseudomonas aeruginosa and a Markedly High Level of Endotoxin in Cerebrospinal Fluid Sir, In immunocompromised patients with Gram-negative bacterial infection, the administration of appropriate antibiotics is well recognized as an important chemotherapeutic strategy to reduce morbidity and mortality. However, the use of antibiotics sometimes causes the release of biologically active endotoxin from the bacteria. We wish to report a patient with Pseudomonas aeruginosa meningitis treated with cefozopran hydrochloride (CZOP) who had a markedly high level of endotoxin in cerebrospinal fluid, associated with filamentous forms of the bacteria. A 19-year-old Japanese man was admitted to the Jichi Medical School Hospital in February 1997 because of sustained fever. He had no history of frequent infections. He was diagnosed as having acute myelocytic leukaemia (AML-M4E). Following treatment with idarubicin and cytarabine (IDA/Ara-C), he achieved complete remission. Despite consolidation and maintenance therapy, he was admitted again in September 1998 because of bone marrow and meningeal relapse. He achieved complete