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Eur J Clin Microbiol Infect Dis, Volume 17, 1998 aspirate, and the patient was treated with

isoniazid, rifampin, pyrazinamide, ethambutol, theophylline, salbutamol, and oxygen. Despite treatment, he died of refractory hypoxemia. Mycobacterium tuberculosis sensitive to all drugs grew later in a L6wenstein's culture of a bronchial aspirate. Intrathoracic tuberculous adenopathies usually resolve after adequate treatment. In some cases the growing nodes can compress the neighboring structures, leading to mediastinitis, superior vein cava syndrome, pericarditis, or bronchoesophageal fistulae. Formation of large necrotic mediastinal lymph nodes has also been described in HIV-related TB caused by multidrugresistant Mycobacterium boris [6]. Both of our patients died after lymph node perforation into a major bronchus, resulting in acute respiratory failure. The irruption of a significant amount of caseum into a major bronchus, as we observed at bronchoscopy in case 2, could be responsible for the refractory hypoxemia and subsequent death. Drug-resistant strains and treatment non-adherence have been proposed as factors responsible for the lack of regression of intrathoracic tuberculous adenopathies [7]. The patient in case 1 was infected by a multidrugresistant strain of Mycobacterium boris. The incomplete response to treatment despite the patient's compliance supports primary resistance as the factor responsible for the treatment failure. Outbreaks of multidrug-resistant Mycobacterium bovis infection among HIV-infected patients have occurred in a French hospital in 1993 [8] and in two Spanish hospitals in Madrid and Mfilaga in 1996 [9, 10]. These cases illustrate the potential for human-to-human spread of multidrug-resistant Mycobacterium boris in HIVinfected patients. From June 1996 to February 1997, five cases of HIV-related Mycobacterium bovis infection had been diagnosed in our hospital, one of which was case 1 in the present report. The five strains shared identical IS6110 type and spoligotype, as did those isolated in Madrid and Mfilaga [9, 10]. The patient in case 2 had discontinued anti-tuberculous treatment 18 months earlier. A pre-existing mediastinal lymph node could have grown progressively as a result of nonadherence to the prescribed treatment. The Mycobacterium tuberculosis strain isolated was sensitive to all drugs administered. However, the treatment was probably started too late, because the lymph node drainage had already occurred. In summary, an adenobronchial fistulization should be considered in patients with tuberculous hilar and/or mediastinal adenopathies who develop acute respiratory failure. Fatal lymph node perforation into the airway is an u n c o m m o n complication in HIV-infected adults. Rapidly enlarging lymph nodes suggest treatment failure due to treatment non-adherence or to treatment ineffective against drug-resistant strains.

671

References
1. Barnes PF, Quoc Le H, Davidson PT: Tuberculosis in patients with HIV infection. In: Bass JB (ed): Tuberculosis. Medical Clinics of North America (1993) 77:1369-1390 2. Dupon M, Ragnaud JM: Tuberculosis in patients with human immunodeficiency virus 1. A restrospective multicentre study of 123 cases in France. Quarterly Journal of Medicine (1992) 85:719-730 3. Yates MD, Pozniak A, Grange JM: Isolation of mycobacteria from patients seropositive for the human immunodeficiency virus (HIV) in South East England: 1984-1992. Thorax (1993) 48: 990-995 4. Sharer RW, Kim DS, Weiss JP, Quale JM: Extrapulmonary tuberculosis in patients with human immunodeficiency virus infection. Medicine (1991) 70:384-397 5. Alam~ T, Dierckx P, Carlier S, Sergysels R: Lymph node perforation into the airway in AIDS-related tuberculosis. European Respiratory Journal (1995) 8:658-660 6. Schultsz C, Kuijper EJ, van Soolingen D, Prins JM: Disseminated infection due to multidrug-resistant Mycobacterium boris in a patient who was seropositive for human immunodeficiency virus. Clinical Infectious Diseases (1996) 23: 841-843 7. Pastores SM, Naidich DP, Aranda CP, McGuinnes G, Rom WN: Intrathoracic adenopathy associated with pulmonary tuberculosis in patients with human immunodeficiency virus infection. Chest (1993) 103:1433-1437 8. Bouvet E, Casalino E, Mendoza-Sassi G, Lariven S, Vall6e E, Pernet M, Gottot S, Vachon F: A nosocomial outbreak of multidrug-resistant Mycobacterium bovis among HIVinfected patients. A case-control study. AIDS (1993) 7:1453-1490 9. Blfizquez J, Espinosa de los Monteros LE, Samper S, Martfn C, Guerrero A, Cobo J, van Embden J, Baquero F, G6mezMampaso E: Genetic characterization of multidrug-resistant Mycobacterium bovis strains from a hospital outbreak involving human immunodeficiency virus-positive patients. Journal of Clinical Microbiology (1997) 35:1390-1393 10. Samper S, Martfn C, Pinedo A, Rivero A, Blfizquez, Baquero F, van Soolingen D: Transmission between HIV-infected patients of multidrug-resistant tuberculosis caused by Mycobacterium bovis. AIDS (1997) 11:1237-1242

Streptococcus pneurnoniae Peritonitis


Secondary to a Tubo-Ovarian Abscess
M. Abalde, F. Molina, A. Guerrero, P. Llinares

Streptococcus pneumoniae can cause a wide range of infections. It has long been known to cause pneumonia, meningitis, sinusitis, and otitis media, and, less frequently, endocarditis, septic arthritis, and peritonitis.
M. Abalde, F. Molina, A. Guerrero Unidad de Microbiologfa Clfnica, Complejo Hospitalario Juan Canalejo, Las Jubias 84, E-15006 La Corufia, Spain P. Llinares (N~) Unidad de Enfermedades Infecciosas, Complejo Hospitalario Juan Canalejo, Las Jubias 84, E-15006 La Corufia, Spain

672 In cases of primary peritonitis where there is no obvious focus of infection, the origin is often assumed to be hematogenous, lymphatic, or intestinal, with spread occurring through an intact intestinal wall or vagina [1]. In the pre-antibiotic era. Streptococcus pneumoniae was frequently considered the cause of infection m children and adults with predisposing factors such as nephrotic syndrome or cirrhosis. In most cases of peritonitis secondary to a primary intra-abdominal process, the origin is endogenous due to organisms that colonize the mucous membranes of the genital and intestinal tract. The integrity of these membranes controls the invasive activity of the habitual flora, but if a lesion is present, the indigenous flora can escape and infect the peritoneum [1]. Streptococcus pneumoniae does not form part of the normal vaginal flora, but transitory colonization of the lower genital tract can occur due to predisposing factors such as the use of an intrauterine contraceptive device (IUD), recent childbirth, an abortion, a gynecological operation. orogenital contact, or upper respiratory tract infection. Colonization allows the organism to ascend to the endometrium, causing endometriosis, salpingitis. pelvic inflammatory disease, or abscesses and may lead to peritonitis. We report a case of Streptococcus pneumoniae peritonitis secondary to a tubo-ovarian abscess. Streptococcus pneurnoniae has been isolated only rarely in this type of infection. A 35-year-old female was admitted to hospital because of abdominal pain and fever, She had undergone a cesarean delivery 15 months earlier for dystocial dilatation: tubal ligature was performed at the same time. One month later she presented with dyspnea and fever and was admitted to the pneumology service. The chest radiograph was normal. Blood cultures were negative. and a scintigraph of the lower limbs ruled out pulmonary embolism. The patient was treated with ceftriaxone and was discharged 4 days later. There was no history of sinusitis, otitis, or lower respiratory tract infection. Four days prior to admission, she presented with pain in the left iliac fossa and was treated with norfloxacin. but without improvement, She was admitted to the gynecology department, but clinical examination, chest radiograph, abdominal ultrasound scan. and laboratory tests were unremarkable. Antibiotic treatment was not administered, and though fever persisted, there was less abdominal pain. Five days after admission, the patient developed intense abdominal pain and fever of 39~ accompanied by abdominal rebound tenderness. Surgery was performed, which revealed purulent generalized peritonitis originating in the left ovary and tube. Left adnexectomy and appendectomy were performed.

Eur J Clin Microbio! infect Dis, Volume iT; 1998 The pathological report indicated significant acute inflammation of the center of the left ovary with grampositive diplococci and polymorphonuclear collections forming microabscesses. The blood cultures were negative. Culture of the peritoneal fluid revealed mucoid Streptococcus pneumoniae serotype 3 that was sensitive to penicillin, cefotaxime, vancomycin, erythromycin. tetracycline, and chloramphenicol (MICs 0.03. 0.0i5. 0.5. 0.06, 0.5. and 2 l.tg/ml, respectively). The patient was asymptomatic after treatment with piperacillintazobactam. In later studies an H I V test was negative and the immunoglobin and complement levels were normal. Westh et al [2] reviewed 36 cases of pneumococcal infection of the internal genital tract in post-puberal women. There were ten puerperal infections, one postnatal infection, and 25 cases of salpingitic or cul-de-sac abscess. The principal predisposing factors of infection were recent childbirth, inflammatory pelvic disease associated with IUDs. and post-operative infection. Ovarian tube abscess was not mentioned A review of the literature revealed three cases of peritonitis secondary to an ovarian tube abscess caused by Streptococcus pneurnontae. The patients were young girls (2 were pre-menarche: the third had her second menstruation 3 days prior to admission) without previous risk factors. All of the pneumococci were serotype 1 [3]. Streptococcus pneumoniae colonization of the vagina may occur in girls when the organism is transferred from the upper respiratory tract as a result of poor hygiene or orogenital contact in sexual abuse. Moreover. the ascending route of the infection can be facilitated by the more alkaline secretions of prepubescent girls, which are less inhibitory to bacterial growth

[1].
The other two cases of Streptococcus pneumoniae ovarian tube abscess found in the literature did not present with peritonitis. The first case [4] was a 46-yearold female whose predisposing factors and serotype were not reported. The second case [5] was a postmenopausal female in whom Streptococcus pneumoniae serotype 7 was isolated. Rahav et ai. [5] pointed out that most ovarian tube abscesses present in pre-menopausal females, in whom the most common pathology is recurrent pelvic inflammatory disease. In post-menopausal females, however, genital tract instrumentation or prior abdominal surgery is involved most frequently In a review of internal female genital tract infe~ion caused by Streptococcus pneumoniae, Westh et al. [2] found 61% of pneumococci were serotype 1 or 3, A m o n g the five cases of Streptococcus pneumoniae ovarian tube abscess reported in the literature [3 5], three were due to Streptococcus pneumoniae serotype 1 and one to Streptococcus pneumoniae serotype 7. Some

Eur J Clin Microbiol Infect Dis, Volume 17, 1998 authors suggest the predilection of some serotypes for the genital tract and their ability to produce ovarian tube abscesses [3]. The interest in our case lies in the isolation of Streptococcus pneumoniae in peritonitis secondary to ovarian tube abscess in a pre-menopausal female without history of recurrent pelvic inflammatory disease, an infrequent occurrence. Of concern is the isolation of pneumococcus type 3, a serotype previously unreported in this type of infection, probably because all of the cases reported thus far, which were due to serotype 1, occurred in girls. Serotype 3 is more commonly encountered in adults. Serotype 3 is associated with high mortality; invasive infection with mucoid Streptococcus pneurnoniae type 3 can be rapidly fatal [6].

673 mammals, soil, beach sand, and natural waters. It has been very rarely isolated from humans [2]. Staphylococcus sciuri, however, may be an important reservoir of genetic determinants of methicillin resistance [3]. In a recent study the methicillin resistance gene, mecA, was shown to be present in each strain of Staphylococcus sciuri investigated [4]. Strains of Staphylococcus sciuri expressing resistance to methicillin have been reported to spread among healthy chickens in a chicken farm in Japan [5]. We describe a case of endocarditis due to Staphylococcus sciuri; to our knowledge, this is the first such case to be reported in the English literature. A 37-year-old male was admitted to our department in 1997 with persistent unexplained fever (maximum 38.5 C). He complained of fatigue and dyspnea that had been increasing for more than 1 month. The patient had a known asymptomatic combined aortic failure since childhood. H e was a former intravenous drug abuser whose last admitted relapse occurred in 1995. H e was treated in 1992 for acute endocarditis of the left side, caused by Enterococcus faecalis. Lichen planus (arms and legs) was established in 1995. One week before admittance in 1997, he had had dental surgery (root filling treatment) and had taken prescribed endocarditis prophylaxis, 300 mg of clindamycin, 1 h preoperatively. Physical examination showed no altered consciousness or focal neurologic abnormalities. T e m p e r a t u r e was 37.7~ pulse 90 beats/min, and blood pressure 140/ 8 0 m m H g . Results of oral mucosa examination and fundoscopy were normal. Cardiac examination revealed a grade V/VI holosystolic murmur and a grade III high-pitched diastolic m u r m u r with puncture maximum at the lower left sternal border. Laboratory studies disclosed a total leukocyte count of 8.2x109/1, with 60% polymorphonuclear leukocytes and 3% band forms; hemoglobin of 15.2 g/dl; a platelet count of 226 109/1; an erythrocyte sedimentation rate of 18 mm at l h ; and C-reactive protein of 25 mg/1. Urea, creatinine, albumin, sodium, potassium, bilirubin, aspartate aminotransferase, alanine aminotransferase, and urinalysis were all normal. A test for H I V antibodies was negative. A chest radiograph revealed slight cardiac enlargement. A n echocardiogram disclosed marked aortic regurgitation with a systolic gradient of 49 m m H g and an average gradient of 28 mmHg, i.e., marked deterioration compared to the previous examination in 1992. There were no signs of left ventricle dysfunction. Transesophageal echocardiogram showed several flapping vegetations, up to 11 mm long, in the aortic valves. Three sets of blood cultures were obtained on admission, and an additional three sets the next day. All six

References
1. Levinson ME, Bush LM: Peritonitis and other intra-abdominal infections. In: Mandell GL, Bennett JE, Dolin R (eds): Mandell, Douglas and Bennett's principles and practice of infectious diseases. Churchill Livingstone, New York (1995) pp. 705-740 2. Westh H, Skibsted L, Kornre B: Streptococcus pneumoniae infections of the female genital tract and in the newborn child. Reviews of Infectious Diseases (1990) 12:416-422 3. Sirotnak AP, Eppes SC, Klein JD: Tuboovarian abscess and peritonitis caused by Streptococcus pneumoniae serotype 1 in young girls. Clinical Infectious Diseases (1996) 22:993-996 4. Hadfield TL, Neafie R, Lanoie L: Tubo-ovarian abscess caused by Streptococcus pneumoniae. Human Pathology (1990) 21 : 1288-1289 5. Rahav G, Ben-David L, Persitz E: Postmenopausal pneumococcal tubo-ovarian abscess. Reviews of Infectious Diseases (1991) 13 : 896-897 6. Hsueh PR, Wu JJ, Hsiue TR: Invasive Streptococcus pneumoniae infection associated with rapidly fatal outcome in Taiwan. Journal of the Formosan Medical Association (1996) 95, Supplement 5:364-371

Endocarditis due to sciuri


G. Hedin, M. Widerstr~3m

Staphylococcus

Staphylococcus sciuri, first described in 1976 by Kloos


et al. [1], is a coagulase-negative staphylococcus that has been isolated from the coats of rodents, ungulates, carnivora, and marsupials and, occasionally, from other G. Hedin (~) Department of Clinical Microbiology, Ostersund Hospital, S-83183 Ostersund, Sweden M. Widerstr/3m Department of Infectious Diseases, Ostersund Hospital, S-83183 Ostersund, Sweden

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