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Branhamella catarrhalis as a cause of acute purulent pericarditis
Letters to the Editor
29I
Topical zoonosis
Accepted for publication 25 May I989 Sir, Drs Farrington and Rubenstein, in their editorial ' Topical Zoonoses ,1 aptly conclude 'there may soon be yet another bacterial zoonosis to add to the list of Acha and Szyfres '. A serious and often fatal zoonosis caused by an unusual and fastidious G r a m negative bacterium designated Dysgonic Fermenter type-2 (DF-2) has evoked m u c h recent interest. 2-6 Dysgonic Fermenter type-2 is part of the normal bacterial flora of the oral cavities of canines. 7 Infection of h u m a n beings with this organism usually presents as a severe community-acquired septicaemia often culminating in disseminated intravascular coagulation. 4 Although it was previously thought to be a zoonosis affecting predominantly the immunocompromised, an increasing n u m b e r of reports has described D F - 2 as the cause of serious illness even in the immunocompetent. ~ T h e paucity of case reports of D F - 2 infection from the United K i n g d o m ~,5 probably implies underdiagnosis. Dysgonic Fermenter type-2 has special growth requirements and there is a need for clinical and microbiological vigilance in actively seeking cases of D F - 2 sepsis. T h e lethal nature of this relatively ' n e w ' zoonosis should bring D F - 2 into prominence among a growing and formidable list. 6
Department of Medicine Hammersmith Hospital, London W I 2 oilS, U.K.
A. Zumla
References
I. Farrington M, Rubenstein D. Topical zoonoses. J Infect 1989; I8 : xo5-I IO. 2. Andrew JH, Waters MJ. Dysgonic fermenter z septicaemia. Rev Infect Dis I988 ; Io : Io63. 3. Fumarola D. Increasing evidence for pathogenic role of DF-2 organisms. Rev Infect Dis I988; IO: 668. 4. Zumla A, Lipscomb G, Corbett M and McCarthy M. Dysgonic fermenter type-2: an emerging zoonosis. Report of z cases and review. Q J Med I988; 68: 739-752. 5. Cook N, Brown EM, Pope N. DF-E septicaemia following a dog bite in the absence of local inflammation. J Infect I989; x : 77-78. 6. Cook GC. Canine associated zoonoses : an unacceptable hazard to human health. Q J Med I989; 261: 5-26. 7. Bailie WE, Stowe EC, Schmitt AM. Aerobic bacterial flora of oral and nasal fluids of canines with reference to bacteria associated with bites. J Clin Microbiol I978 ; 7:223-23 I.
Branhamella catarrhalis as a cause of acute purulent pericarditis
Accepted for publication 8 April I989 Sir, A 65-year-old man presented with shortness of breath and fever of 2 days' duration. He had a history of recurrent maxillary sinusitis as well as chronic obstructive pulmonary disease and had been digitalised because of atrial fibrillation. One m o n t h before onset, a form of lupus erythematosus had been diagnosed and treatment with prednisone begun. He had a malfitting, complete, removable denture and a partly retained carious third molar tooth, treatment of which he had refused. On admission to hospital, the patient was in poor general health, cachectic and dyspnoeic. He complained of chest pain. His temperature was 39"0 °C. A peripheral
29z
Letters to the Editor
white blood cell count was 38"9 x io9/1 and the serum C-reactive protein concentration was z6o rag/1. Rhonchi were heard in the right lung; the liver was palpable and tender. H e a r t sounds were quiet and blood pressure 8o/6o m m H g . An electrocardiogram revealed atrial fibrillation (I4O b e a t s / m i n ) and concave elevations of the S T - s e g m e n t . A chest X - r a y showed massive cardiac enlargement and p u l m o n a r y congestion. Echocardiography revealed pericardial effusion with a danger of cardiac tamponade. Pericardiocentesis yielded 70 ml turbid, yellowish fluid (white blood cell count 38-ox xoO/1 with 9 o % neutrophils, glucose concentration 3"I retool/l). Samples injected into blood culture bottles as well as cultured on agar yielded abundant growth of a G r a m - n e g a t i v e diplococcus. I t was positive in reactions for tributyrin hydrolysis, nitrate reduction, oxidase, catalase and D N A a s e but was O N P G - n e g a t i v e and did not ferment glucose, maltose or sucrose. T h e organism was identified as Branhamella catarrhalis. It produced fl-lactamase and was susceptible in vitro to cephalosporins, aminoglycosides, erythromycin, tetracycline, chloramphenicol and ciprofloxacin but resistant to vancomycin. Antibiotic treatment with intravenous cefotaxime and tobramycin was begun. T h e pericardial space was drained of turbid, blood-stained fluid. After I day of treatment this failed to yield any bacterial growth; the drain was removed. On the third day, the patient was afebrile but echocardiography still showed pericardial fluid posteriorly. On day I5 the effusion had further decreased and medication was changed to oral ciprofloxacin. T h e patient was discharged on day 3o when antibiotic treatment was stopped and medication with decreasing dosage of prednisone continued. Out-patient surveillance up to I year showed no signs of pericarditis. Diseases now recognised to be caused by the opportunistic pathogen B. catarrhalis include otitis media, sinusitis, laryngitis, conjunctivitis and p n e u m o n i a as well as rarer systemic infections, e.g. septicaemia and meningitis.I. 2 A few cases of endocarditis but not pericarditis have also been r e p o r t e d ? O u r patient was receiving corticosteroid medication and had atrial fibrillation, chronic bronchitis, p n e u m o n i a and a dental focus of infection. T h e route of infection for the pericarditis was p r e s u m a b l y haematogenous. T h a t B. catarrhalis as well as other non-gonococcal, n o n - m e n i n g o coccal Neisseriae can produce life-threatening disease is becoming increasingly clear. ~ Neisseria mucosa, for example, has caused purulent pericarditis. 4 Neisseria meningitidis, on the other hand, has caused pericarditis even in the absence of meningitis. 5
Lahti Central Hospital,* SF-x585o Lahti 85, and Department of Bacteriology and Immunology,t University of Helsinki, SF-ooz9o Helsinki z9, Finland
Anja A. I. Kostiala*t§ T. Honkanen*
§ Address correspondence to: Dr A. A. I. Kostiala, Department of Bacteriology and Immunology, University of Helsinki, Haartmaninkatu 3, SF-oo29o, Helsinki, Finland. References I. Doem GV, Miller MJ, Winn RE. Branhamella (Neisseria) catarrhalis systemic disease in humans. Case reports and review of the literature. Arch Intern Med I98I ; x4I : I 6 9 O - I 6 9 2 . z. Feder HM, Garibaldi RA. The significance of non-gonococcal, non-meningococcal Neisseria isolates from blood cultures. Rev Infect Dis I984; 6: I8I-I88. 3. Turner HR, Taylor MR, Lockwood WR. Branhamella catarrhalis endocarditis in a patient receiving hemodialysis. South Med J I985; 78: IO2I-iO22. 4. Fainstein V, Musher DM, Young EJ. Purulent pericarditis due to Neisseria mucosa. Chest r978; 74:476-477 • 5- van Dorp WT, van Rees C, van der Meer JWM, Thompson J. Meningococcal pericarditis in the absence of meningitis. Infection I987; I5: Io9-I IO.
29I
Topical zoonosis
Accepted for publication 25 May I989 Sir, Drs Farrington and Rubenstein, in their editorial ' Topical Zoonoses ,1 aptly conclude 'there may soon be yet another bacterial zoonosis to add to the list of Acha and Szyfres '. A serious and often fatal zoonosis caused by an unusual and fastidious G r a m negative bacterium designated Dysgonic Fermenter type-2 (DF-2) has evoked m u c h recent interest. 2-6 Dysgonic Fermenter type-2 is part of the normal bacterial flora of the oral cavities of canines. 7 Infection of h u m a n beings with this organism usually presents as a severe community-acquired septicaemia often culminating in disseminated intravascular coagulation. 4 Although it was previously thought to be a zoonosis affecting predominantly the immunocompromised, an increasing n u m b e r of reports has described D F - 2 as the cause of serious illness even in the immunocompetent. ~ T h e paucity of case reports of D F - 2 infection from the United K i n g d o m ~,5 probably implies underdiagnosis. Dysgonic Fermenter type-2 has special growth requirements and there is a need for clinical and microbiological vigilance in actively seeking cases of D F - 2 sepsis. T h e lethal nature of this relatively ' n e w ' zoonosis should bring D F - 2 into prominence among a growing and formidable list. 6
Department of Medicine Hammersmith Hospital, London W I 2 oilS, U.K.
A. Zumla
References
I. Farrington M, Rubenstein D. Topical zoonoses. J Infect 1989; I8 : xo5-I IO. 2. Andrew JH, Waters MJ. Dysgonic fermenter z septicaemia. Rev Infect Dis I988 ; Io : Io63. 3. Fumarola D. Increasing evidence for pathogenic role of DF-2 organisms. Rev Infect Dis I988; IO: 668. 4. Zumla A, Lipscomb G, Corbett M and McCarthy M. Dysgonic fermenter type-2: an emerging zoonosis. Report of z cases and review. Q J Med I988; 68: 739-752. 5. Cook N, Brown EM, Pope N. DF-E septicaemia following a dog bite in the absence of local inflammation. J Infect I989; x : 77-78. 6. Cook GC. Canine associated zoonoses : an unacceptable hazard to human health. Q J Med I989; 261: 5-26. 7. Bailie WE, Stowe EC, Schmitt AM. Aerobic bacterial flora of oral and nasal fluids of canines with reference to bacteria associated with bites. J Clin Microbiol I978 ; 7:223-23 I.
Branhamella catarrhalis as a cause of acute purulent pericarditis
Accepted for publication 8 April I989 Sir, A 65-year-old man presented with shortness of breath and fever of 2 days' duration. He had a history of recurrent maxillary sinusitis as well as chronic obstructive pulmonary disease and had been digitalised because of atrial fibrillation. One m o n t h before onset, a form of lupus erythematosus had been diagnosed and treatment with prednisone begun. He had a malfitting, complete, removable denture and a partly retained carious third molar tooth, treatment of which he had refused. On admission to hospital, the patient was in poor general health, cachectic and dyspnoeic. He complained of chest pain. His temperature was 39"0 °C. A peripheral
29z
Letters to the Editor
white blood cell count was 38"9 x io9/1 and the serum C-reactive protein concentration was z6o rag/1. Rhonchi were heard in the right lung; the liver was palpable and tender. H e a r t sounds were quiet and blood pressure 8o/6o m m H g . An electrocardiogram revealed atrial fibrillation (I4O b e a t s / m i n ) and concave elevations of the S T - s e g m e n t . A chest X - r a y showed massive cardiac enlargement and p u l m o n a r y congestion. Echocardiography revealed pericardial effusion with a danger of cardiac tamponade. Pericardiocentesis yielded 70 ml turbid, yellowish fluid (white blood cell count 38-ox xoO/1 with 9 o % neutrophils, glucose concentration 3"I retool/l). Samples injected into blood culture bottles as well as cultured on agar yielded abundant growth of a G r a m - n e g a t i v e diplococcus. I t was positive in reactions for tributyrin hydrolysis, nitrate reduction, oxidase, catalase and D N A a s e but was O N P G - n e g a t i v e and did not ferment glucose, maltose or sucrose. T h e organism was identified as Branhamella catarrhalis. It produced fl-lactamase and was susceptible in vitro to cephalosporins, aminoglycosides, erythromycin, tetracycline, chloramphenicol and ciprofloxacin but resistant to vancomycin. Antibiotic treatment with intravenous cefotaxime and tobramycin was begun. T h e pericardial space was drained of turbid, blood-stained fluid. After I day of treatment this failed to yield any bacterial growth; the drain was removed. On the third day, the patient was afebrile but echocardiography still showed pericardial fluid posteriorly. On day I5 the effusion had further decreased and medication was changed to oral ciprofloxacin. T h e patient was discharged on day 3o when antibiotic treatment was stopped and medication with decreasing dosage of prednisone continued. Out-patient surveillance up to I year showed no signs of pericarditis. Diseases now recognised to be caused by the opportunistic pathogen B. catarrhalis include otitis media, sinusitis, laryngitis, conjunctivitis and p n e u m o n i a as well as rarer systemic infections, e.g. septicaemia and meningitis.I. 2 A few cases of endocarditis but not pericarditis have also been r e p o r t e d ? O u r patient was receiving corticosteroid medication and had atrial fibrillation, chronic bronchitis, p n e u m o n i a and a dental focus of infection. T h e route of infection for the pericarditis was p r e s u m a b l y haematogenous. T h a t B. catarrhalis as well as other non-gonococcal, n o n - m e n i n g o coccal Neisseriae can produce life-threatening disease is becoming increasingly clear. ~ Neisseria mucosa, for example, has caused purulent pericarditis. 4 Neisseria meningitidis, on the other hand, has caused pericarditis even in the absence of meningitis. 5
Lahti Central Hospital,* SF-x585o Lahti 85, and Department of Bacteriology and Immunology,t University of Helsinki, SF-ooz9o Helsinki z9, Finland
Anja A. I. Kostiala*t§ T. Honkanen*
§ Address correspondence to: Dr A. A. I. Kostiala, Department of Bacteriology and Immunology, University of Helsinki, Haartmaninkatu 3, SF-oo29o, Helsinki, Finland. References I. Doem GV, Miller MJ, Winn RE. Branhamella (Neisseria) catarrhalis systemic disease in humans. Case reports and review of the literature. Arch Intern Med I98I ; x4I : I 6 9 O - I 6 9 2 . z. Feder HM, Garibaldi RA. The significance of non-gonococcal, non-meningococcal Neisseria isolates from blood cultures. Rev Infect Dis I984; 6: I8I-I88. 3. Turner HR, Taylor MR, Lockwood WR. Branhamella catarrhalis endocarditis in a patient receiving hemodialysis. South Med J I985; 78: IO2I-iO22. 4. Fainstein V, Musher DM, Young EJ. Purulent pericarditis due to Neisseria mucosa. Chest r978; 74:476-477 • 5- van Dorp WT, van Rees C, van der Meer JWM, Thompson J. Meningococcal pericarditis in the absence of meningitis. Infection I987; I5: Io9-I IO.