Infection due to Streptobacillus moniliformis

Despite these concerns and controversies, many health-care institutions have initiated a chemoprophylaxis program that makes AZT available to health-care workers experiencing significant exposure to HIV. These programs generally recommend at least the following procedures: 1) AZT should be administered immediately after the exposure, or as soon as possible. 2) Health-care workers must have immediate access to program staff versed in the protocol, entry criteria, the risks for HIV infection associated with various types of occupational exposure, state-of-the-art information about safety and efficacy of AZT, and procedures for obtaining informed consent. 3) Criteria for high-risk exposures must be clearly defined and exposed employees must be offered the opportunity to discuss the exposure with E m p l o y e e Health Service staff, Emergency Room staff, or others identified as expert counselors. 4) The decision to enter into the AZT chemoprophylaxis regimen must rest entirely with the exposed employee. Since the efficacy, safety, and toxicity of AZT for occupational exposures to HIV is not entirely clear, it is important that the employee receive sufficient information to make an educated choice. 5) Since data are lacking on the teratogenicity of AZT, many programs elect to exclude pregnant workers or counsel them on the potential fetal risk. In addition, some protocols encourage a pregnancy test before AZT

administration if pregnancy is a possibility. 6) Baseline laboratory tests are generally obtained before initiation of prophylaxis, and may include a complete blood count and blood chemistries. 7) The two regimens of AZT administration generally followed are: (i) NIH regimen AZT 200 mg every 4 hr for 6 wk, or (ii) San Francisco General Hospital r e g i m e n - - A Z T 200 mg every 4 hr for 4 wk. No data are available to suggest that either regimen is more effective. 8) After the initial 2 wk of prophylaxis, the employee often will receive follow-up blood work and counseling. AZT has been the only approved chemotherapeutic agent for HIV-1 until recently. Unfortunately, evidence that it will prevent infection after an occupational exposure to HIV-1 is not available and controlled clinical trials would be impractical, if not impossible, due to the low rate of accidental infection. However, despite the lack of evidence, the general attitude among clinicians and experts in the field of HIV research and treatment is to provide a program that will offer AZT prophylaxis for employees with a documented high-risk exposure to HIV-infected blood or body fluids. While we eagerly await further studies that will provide us with more definitive information, they may never be forthcoming. Therefore, it remains critically important to prevent exposure, and we must continue to advocate and follow routine infection control precautions in the laboratory

setting to prevent direct contact with blood and body fluids. References 1. Centers for Disease Control Update. 1988. Acquired immunodeficiency syndrome and human immunodeficiency virus infection among health care workers. Morbid. Mortal. Weekly Rep. 37:229-234. 2. Henderson, D. K. and J. C. Gerberding. 1989. Prophylactic zidovudine after occupational exposure to the human immunodeficiency virus: an interim analysis. J. Infect. Dis. 160:321327. 3. Ruprecht, R. M. et al. 1986. Suppression of mouse viraemia and retroviral disease by 3'-azido-Y-deoxythymidine [letter]. Nature 323:467--469. 4. Tavares, L. et al. 1987. 3'-azido-3'deoxythymidine in feline leukemia vires-infected cats: a model for therapy and prophylaxis of AIDS. Cancer Res. 47:3190-3194. 5. Schinazi, R. F. et al. 1990. Prophylaxis with antiretroviral agents in Rhesus Macaques inoculated with simian immunodeficiency virus (abstract no. 962, p. 246). 30th Interscience Conference on Antimicrobial Agents and Chemotherapy, Atlanta, Georgia, 1990. 6. Looke, D. F. M. and D. I. Grove. 1990. Failed prophylactic zidovudine after needlestick injury. Lancet 335:1280, 1990. 7. Lange, J. M. A. et al. 1990. Failure of zidovudine prophylaxis after accidental exposure to HIV-I. N. Engl. J. Med. 322:1375-1377. 8. Durand, E., C. LeJeunne, and F. C. Hughes. 1991. Failure of prophylactic zidovudine after suicidal self-inoculation of HIV-infected blood. N. Engl. J. Med. 324:1062-1063. 9. Centers for Disease Control. 1987. Recommendations for prevention of HIV transmission in health-care settings. Morbid. Mortal. Weekly Rep. 36(Suppl 25):1S-19S, 1987.

Case Report Infection Due to

StreptobaciUus monUiformis P. L6pez Service of Microbiology Hospital Santa Cruz y San Pablo Barcelona, Spain J. Euras

Service of Microbiology Hospital de Vic Vic, Barcelona, Spain

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A. Anglada Service of Internal Medicine Hospital de Vic Vic, Barcelona, Spain M. Garcia G. Prats Service of Microbiology Hospital Santa Cruz y San Pablo Barcelona, Spain

©1992 Elsevier Science Publishing Co., Inc.

Streptobacillus moniliformis is a gram-negative bacillus whose habitat is the oropharynx of rats, mice and other rodents (1). In human pathology it is isolated occasionally as one of the two etiologic agents of rat-bite fever (2). The spectrum of illnesses caused by this microorganism ranges from local infection to sepsis with or without ar-

Clinical Microbiology Newsletter 14:5,1992

thritis, endocarditis or other metastatic locations. The infection can be contracted through a bite or by ingestion of food contaminated by rodents.

.3-

Case Report Nine days prior to her visit to the hospital, a 54-yr-old woman living in a rural environment was bitten on her lower fight limb by a rat. Two days later, she experienced nausea and fever, along with pain, swelling, and functional impotence in her left ankle, left wrist, and right elbow, as well as pain on moving her fight knee. The remaining clinical examination was normal, including the absence of adenopathies and neurological alterations. Serologic analysis revealed an alpha-2 gamma-globulin level of 12.8 mg/dl/ 100 and a positive VDRL test. Other hematologic and biochemical parameters were normal. An arthrocentesis was performed on her left ankle. Five ml of joint fluid was obtained with diminished viscosity, 28,000 white blood cells/ml (86% segmented), and no crystals. Direct Gram stain examination of the joint fluid was negative. The fluid was inoculated onto blood agar, chocolate agar, and into thioglycolate broth, and incubated at 35°C in an atmosphere supplemented with CO 2. Blood cultures were also done at the time of admission. After 48 h incubation, round colonies 2 mm in diameter were observed on the blood plate; these were slightly shiny and of a fatty consistency. In the thioglycolate broth, growth in the form of woolly balls was observed. The blood cultures were negative. The Gram stain of the colony showed gram-negative bacilli and long, curved filaments intertwined with bulbous swellings in the central position (Fig. 1). The bacillus retained Giemsa stain and it was not acid-fast. The catalase and oxidase reactions were negative. In semisolid medium, cystine trypticase agar, the organism produced acid from glucose, galactose, maltose, and saccharose but not from salicin, lactose, arabinose, xylose, mannose, or mannitol. From a 48-h culture on blood agar,

Clinical Microbiology Newsletter 14:5,1992

%

Figure 1. Gram stain showing S. m o n i l i f o r m i s .

a cellular fatty acid profile was obtained by gas chromatography. The fatty acids were extracted and converted to methyl esters by using a methanolysis acid process (5). The extract was injected into a gas chromatograph equipped with a capillary column (SPS-1, Supelco) and with a flame ionization detector. The strain studied showed as principal methyl esters those of palmitic acid (16:0), linoleic acid (18:2), oleic acid (18:1), and stearic acid (18:0). The organism was susceptible to penicillin, clindamycin, tetracycline, chloramphenicol, and vancomycin by disk diffusion using Mueller-Hinton agar enriched with 5% horse blood. Using a microdilution technique (Sensititre), a MIC to penicillin ~<0.03 mg/ml was obtained. Beta-lactamase activity was not detected by an acidometric technique. The patient was treated with penicillin G procaine 1,200,000 UI every 12 h for 10 d, with good response. By the end of 1 mo she showed no symptoms and all laboratory tests were normal. Although rat-bite fever is an uncommon infection, a history of a bite from or contact with rodents suggest etiologic diagnosis of S. moniliformis or Spirillum minus (4). The colonies previously described appeared in the joint fluid culture on blood agar and the Gram stain appear-

© 1992 Elsevier Science Publishing Co., Inc.

ance led us to suspect the causal agent. The presence of gram-negative, long, curved filaments intertwined with bulbous swellings in the central position strongly suggests S. moniliformis. Biochemical identification is laborious (6) due to the fastidious nature of the microorganism. However, identification of this microorganism to the species level using chromatographic analysis of fatty acids (7) is a safe, efficient, fast, and reliable procedure. In our case it was possible to show that the positive VDRL test resulted from S. moniliformis infection as described for both etiologic agents of rat bite fever (6, 8). Although there are no data in the literature on standardized methods for susceptibility testing of this microorganism, it was performed by using an agar diffusion technique and by microdilution, adopting the recommendations for facultative bacteria. This technique, together with the absence of beta lactamase, made it possible to confirm the susceptibility of the microorganism to penicillin, which is the preferred antibacterial drug for treating infections caused by S. moniliformis (9), although spontaneous variations in 2 L-phase can be the cause of therapeutic failures. References 1. M c H y g h , T. P., R. L. Barlett, and

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J. L. Raymon. 1985, Rat-bite fever: report a fatal case. Ann. Emerg. Med. 14:1116-1118. 2. Jenkins, S. G. 1988. Rat-bite fever. Clin, Microbiol. News. 10:57-60. 3. Place, E. H. and L. E. Sutton. 1934. Erythema arthriticum epidemicum (Havershill fever). Arch. Intern. Med. 54:659---684. 4. Wilkins, E. G. L. et al. 1988. Rat-bite fever in a gerbil breeder. J. Infect.

16:177-180. 5. Lennart, L. 1983. Acidic methanolysis U alkaline saponification in gas chromatographic. Acta Pathol. Microbiol. Immunol. Scand. Sect. B. 91:235239. 6. Morrison, R. 1985. Streptobacillus moniliformis and Spirillum minus, p. 400--405. In E. H. Lennette et al. (ed.), Manual of Clinical Microbiology, 4th ed. American Society for Mi-

crobiology, Washington, D.C. 7. Rowbotham, T. J. 1983. Rapid identification of Streptobacillus moniliformis. Lancet ii:567. 8. Raffin, B. J. and M. Freemark. 1979. Streptobacillary rat-bite fever: a pediatric problem. Pediatrics 64:214-217. 9. Roughgarden, J. W. 1965. Antimicrobial therapy of rat-bite fever, a review. Arch. Intern. Med. 116:39-54.

Letter to the Editor This is in response to the letter submitted by Patricia G. Rutland (Clinical Microbiology Newsletter, Vol. 13, No. 24, D e c e m b e r 15, 1991) that our letter on the rapid f l u o r o g e n i c tests for identification o f Gardnerella vaginalis contained an error. She pointed out accurately that G. vaginalis should be catalase n e g a t i v e and not catalase positive as it stated in our letter (Clinical Microbiology Newsletter, Vol. 13, No. 19, O c t o b e r 1, 1991). At the time we submitted the manuscript to E l s e v i e r

Science Publishing C o . , Inc., we were aware of the error i m m e d i a t e l y , and subsequently submitted the corrected page to the publisher the next day. Unfortunately, due to a change of personnel at E l s e v i e r and very unusual circumstances, the corrected version was not f o r w a r d e d to the editors, Thus our letter appeared in the newsletter without the correction. W e thank Patricia Rutland for bringing the error to our attention. W e hope that her letter and our reply will

reenforce for all the readers the correct catalase reaction for G. vaginalis. Pauline K. W. Yu, M. S.

Clinical Microbiology Department of Laborator3' Medicine & Pathology Mayo Clinic Rochester, MN 55905 E d i t o r ' s note: W e a p o l o g i z e to Ms. W u for any i n c o n v e n i e n c e caused by the oversight o f her corrected manuscript,

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Clinical Microbiology Newsletter 14:5.1992