Eikenella corrodens Empyema

Eikenella corrodens Empyema

ii iii |111 Case Reports iiiii ill EikeneUa corrodens Empyema Christopher J. Papasian, Ph.D. Laboratory Service Peter S. Nelson, M.D. Medical Servi...

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ii iii |111

Case Reports iiiii ill

EikeneUa corrodens

Empyema Christopher J. Papasian, Ph.D. Laboratory Service Peter S. Nelson, M.D. Medical Service Veterans Administration Medical Center Kansas City, MO 64128 A 68-year-old man presented to the emergency room and was admitted to the hospital after complaining of a cough productive of copious amounts of green, foul-smelling sputum. Four months prior to admission (PTA) he underwent a total right pneumonectomy for squamous cell carcinoma; there was no evidence of metastatic disease at the time and he did not receive antineoplastic chemotherapy. Three months PTA, the patient developed a cough productive of a small amount of yellow-green sputum accompanied by a low-grade fever, night sweats, shortness of breath, and dyspnea on exertion. These symptoms steadily progressed to the point where he was producing 10 to 15 cups of putrid green sputum daily and was unable to sleep on his left side due to paroxysms of coughing. The patient also became anorexic and lost 20 pounds during this period; he attributed his appetite loss to the constant putrid odor and taste accompanying his sputum production. Physical examination revealed a well-developed, well-nourished man with stable vital signs and a temperature of 101. I°F. He was coughing continuously with production of copious amounts of putrid sputum. Breath sounds were absent in the right hemithorax, and there was dullness to percussion to the fifth thoracic vertebrae. A white blood cell (WBC) count on admission revealed 7.6 x 103 WBC/mm 3, with a marked left shift (15% polymorphonuclear neutrophils, 45% band cells, 30% lymphocytes, 7% monocytes, 1% eosinophils, 1% basophils, and 1% atypical lymphocytes). Chest x-ray revealed a fluid level in the

right hemithorax that was freely mobile. Thoracentesis permitted aspiration of 60 cc of purulent fluid that appeared identical to the patient's sputum. A chest tube was inserted and an additional 2000 cc of purulent fluid was removed. The patient subsequently underwent an open thoracotomy for drainage of the pleural space and repair of a bronchopleural fistula present at the right main bronchial suture line. Gram-stained smear of sputum obtained on the day of admission revealed numerous WBC and no epithelial cells. Sputum culture yielded predominant growth of Eikenella corrodens on blood and chocolate agars incubated at 35°C in an atmosphere of 95% air and 5% CO 2. Empyema fluid from the same day produced heavy growth of E. corrodens on blood and chocolate agars incubated as above. On CDC anaerobe blood agar incubated anaerobically (Bio-bag, Type A; Marion Scientific, Kansas City, MO) at 35°C, sparse quantities of Bacteroides melaninogenicus and an alpha-hemolytic Streptococcus spp. were also recovered. Eikenella corrodens was identified by means of its gram-negative coccobacillary appearance on Gram stain, its pitting of the blood agar plate, and characteristic profiles with Rapid NH (Innovative Diagnostic Systems, Inc., Atlanta, GA) and API 20E (Analytab Products, Plainview, NY). Antimicrobial susceptibilities determined by disk diffusion on Mueller Hinton agar with 5% sheep blood indicated that both E. corrodens isolates were susceptible to all antimicrobials tested, including amikacin, tobramycin, gentamicin, ampicillin, cefazolin, and cefoxitin. These results, however, must be interpreted with caution as agar dilution and microbroth dilution are the methods of choice for E. corrodens susceptibility testing and disk diffusion results are not well standardized (l). On admission, intravenous therapy with clindamycin (900 mg every 8 h) and gentamicin (160 mg loading dose followed by 100 mg every 8 h) was initiated. The patient's temperature and WBC differen-

tial count returned to normal by the fifth and twelfth days of hospitalization, respectively, with apparent resolution of his empyema. Eikenella corrodens is a capnophilic, glucose nonoxidizing, gram-negative rod that usually fails to grow on MacConkey agar and produces small colonies that tend to pit or corrode the surface of blood agar after several days (2). This organism is part of the indigenous microbiota of the human respiratory, genitourinary, and gastrointestinal tracts and has been implicated in a variety of serious infections, including endocarditis, meningitis, pneumonia, and other respiratory infections (3). Also, E. corrodens produces skin and soft tissue infections, osteomyelitis, and septic arthritis originating from bite wounds or hand injuries incurred during fist fights (2). Respiratory infections involving E. corrodens usually, though not invariably, are polymicrobic. Organisms frequently associated with E. corrodens include Streptococcus spp. and anaerobic respiratory flora (3). The polymicrobic nature of E. corrodens respiratory infections in conjunction with its presence as normal flora in the respiratory tract make sputum culture a fairly unreliable means of implicating E. corrodens in respiratory tract infections. The etiologic role of E. corrodens in pneumonia and pleuropulmonary processes resembling anaerobic infections has been clearly documented in a few reported cases in which E. corrodens was recovered from respiratory secretions obtained by transtracheal aspiration, or from empyema or pleural fluid obtained by percutaneous aspiration (3, 4). Usually E. corrodens is resistant to clindamycin; therefore, clinicians should be notified promptly when E. corrodens is implicated in a pneumonia or lung abscess, as clindamycin is frequently used empirically in these situations (4). Usually E. corrodens is susceptible to ampicillin and cefoxitin and shows variable resistance to aminoglycosides and most cephalosporins (3). i

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© 1989 Elsevier Science Publishing Co., Inc.

Clinical Microbiology Newsletter 11 : 14,1989

References •

1. Rubin, S. J., P. A. Granato, andB. L. Wasilauskas. 1985. Glucose-nonfermenting gram-negative bacteria, p p . 330-349. In E. H. Lenette, A. Balows, W. J. Hausler, Jr., and H. J. Shadomy (eds.), Manual of Clinical Microbiology, 4th ed. American So-

Bordetella bronchiseptica Endocarditis: A Tale of A Boy and His Dog John T. Sinnott IV, M.D. Christopher Blazejowski, M.D. Maria D. Bazzini, B.S. Division of lnfectious and Tropical Diseases Department of Internal Medicine University of South Florida College of Medicine Tampa, FL 33601 A 22-year-old man developed eczematoid dermatitis of the hands after undergoing surgery to stabilize a compound fracture of the humerus. During a routine postsurgical visit he complained of myalgias and was found to have a fever of 39°C. The wound had healed well and did not show drainage, but the patient's hands were red and excoriated. He attributed the erythema to his dog. This dog frequently bit the patient's hands and licked around the area of dermatitis. Because of the complaints of fever and myalgias, a complete blood count was ordered and blood cultures drawn. The complete blood count showed a mild normochromic, normocytic anemia with a white blood cell count of 13,000/mm 3. Seven days later the blood cultures grew Bordetella bronchiseptica and the patient was admitted to the hospital. A repeat physical examination disclosed a heart murmur of new onset and a splinter hemorrhage on the fourth f'mger of his left hand. An echocardiogram showed thickening of the mitral valve suggestive of endocarditis. He received six weeks of intravenous ampicillin with prompt clinical response and finally a cure. Blood cultures at the conclusion of therapy were negative.

Clinical Microbiology Newsletter i1:14,1989

ciety for Microbiology, Washington, D.C. 2. Stoloff, A. L., and M. L. Gillies. 1986. Infections with Eikenella corrodens in a general hospital: a report of 33 cases. Rev. Infect Dis. 8:50-53. 3. Goldstein, E. J. C., B. D. Kirby, and S. M. Finegold. 1979. Isolation of Ei-

Discussion Bordetella spp. are a closely related group of aerobic, gram-negative coccobacilli which cause disease both in animals and humans. Three species are recognized: B. pertussis and B. parapertussis, the common and uncommon causes respectively, of whooping cough in humans, and B. bronchiseptica which causes respiratory infection in animals (1). Initially, Bordetella bronchiseptica was named Brucella bronchiseptica but underwent six subsequent changes in taxonomy before DNA hybridization studies confmned its membership in the genus Bordetella (2). Isolates of B. bronchiseptica appear as smooth, translucent colonies which " p i t " as they age on Bordet-Gengou agar. Microscopically they are small, gram-negative coccobacilli, 0.3 by 1.0 Ixm in size. Unlike the other members of the Bordetella group, they demonstrate motility by peritrichous flagella. Isolates are characteristically inert biochemically. They do not ferment sugars, liquefy gelatin, or produce H2S. B. bronchiseptica produces urease and unlike the other Bordetella spp. is nitrate positive. Antibiograms show consistent susceptibility only to tetracycline, although our isolate was susceptible to ampicillin, trimethoprimsulfamethoxazole, and chloramphenicol (3). Clearly, susceptibility testing of individual isolates should guide therapy. B. bronchiseptica is best known as a respiratory pathogen which can cause atrophic rhinitis, tracheobronchitis, pneumonia, otitis media, and upper respiratory tract infections in cats and dogs (2). Wild animals such as racoons and skunks, as well as laboratory animals, have also exhibited similar clinical syndromes. An asymptomatic

© 1989 Elsevier Science Publishing Co., Inc.

kenella corrodens from pulmonary infections. Am. Rev. Respir. Dis. 119:55-58. 4. Javaheri, S., R. M. Smith, and D. Wiltse. 1987. Intrathoracic infections due to Eikenella corrodens. Thorax 42:700-701.

carrier state is also found in these animals (3). Cases of human disease are uncommon. Reported cases usually involve animal handlers with mild upper respiratory tract infection and/or sinusitis. Cultures from these patients have grown B. bronchiseptica (4-6). However, isolated instances of more severe forms of disease, such as a whooping cough-like illness with cavitary infiltrates resembling pulmonary tuberculosis and a fatal case of bronchopneumonia, have been documented (7, 8). B. bronchiseptica has been isolated from the CSF in a case of meningitis and from two patients with bacteremia and sepsis (9, 10). The sepsis occurred in an immunosuppressed patient with no zoonotic exposure documented (3, 10). Endocarditis attributed to this organism is a rare occurrence with only three reported cases. The fast recognized case was described in 1950, but it is not clear from this abbreviated review whether any animal-to-human transmission was involved (11). A second patient was described with aortic valve endocarditis, caused by both Staphylococcus epidermidis and B. bronchiseptica (12, 13). No animal contact was noted and the patient was successfully treated with penicillin, streptomycin, and tetracycline. A third patient was included in a review of 56 cases of endocarditis occurring over a 20-year period. Cure resulted from treatment with ampicillin and gentamicin (14). In conclusion, this is only the fourth documented case in which B. bronchiseptica produced clinical evidence of endocarditis. Our patient most probably acquired the organism from an animal reservoir, his dog, via repeated exposure to the dog's saliva.

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