Despite these concerns and contro- versies, many health-care institutions have initiated a chemoprophylaxis pro- gram that makes AZT available to health-care workers experiencing sig- nificant exposure to HIV. These pro- grams generally recommend at least the following procedures:

1) AZT should be administered imme- diately after the exposure, or as soon as possible.

2) Health-care workers must have im- mediate 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 informa- tion about safety and efficacy of AZT, and procedures for obtaining informed consent.

3) Criteria for high-risk exposures must be clearly defined and exposed em- ployees must be offered the opportu- nity to discuss the exposure with Employee Heal th 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 toxic- ity of AZT for occupational expo- sures to HIV is not entirely clear, it is important that the employee receive sufficient information to make an ed- ucated choice.

5) Since data are lacking on the terato- genicity of AZT, many programs elect to exclude pregnant workers or counsel them on the potential fetal risk. In addition, some protocols en- courage a pregnancy test before AZT

administration if pregnancy is a pos- sibility.

6) Baseline laboratory tests are gener- ally obtained before initiation of prophylaxis, and may include a com- plete blood count and blood chemis- tries.

7) The two regimens of AZT adminis- tration 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 fol- low-up blood work and counseling.

AZT has been the only approved chemotherapeutic agent for HIV-1 un- til 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 impossi- ble, 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 defini- tive information, they may never be forthcoming. Therefore, it remains critically important to prevent expo- sure, and we must continue to advo- cate 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 immunodeficien- cy virus infection among health care workers. Morbid. Mortal. Weekly Rep. 37:229-234.

2. Henderson, D. K. and J. C. Gerberd- ing. 1989. Prophylactic zidovudine after occupational exposure to the hu- man immunodeficiency virus: an in- terim analysis. J. Infect. Dis. 160:321- 327.

3. Ruprecht, R. M. et al. 1986. Suppres- sion 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 vi- res-infected cats: a model for therapy and prophylaxis of AIDS. Cancer Res. 47:3190-3194.

5. Schinazi, R. F. et al. 1990. Prophy- laxis with antiretroviral agents in Rhesus Macaques inoculated with sim- ian 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 acci- dental 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-inocula- tion 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 set- tings. 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

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

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-

3 8 0196-4399/92/$0.00 + 03.00 ©1992 Elsevier Science Publishing Co., Inc. Clinical Microbiology Newsletter 14:5,1992

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

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 fe- ver, 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 aden- opathies 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 parame- ters 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, choc- olate 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 incuba- tion, 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 cul- tures 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 re- tained 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,

.3-

%

Figure 1. Gram stain showing S. moni l i formis .

a cellular fatty acid profile was ob- tained by gas chromatography. The fatty acids were extracted and con- verted to methyl esters by using a methanolysis acid process (5). The extract was injected into a gas chro- matograph equipped with a capillary column (SPS-1, Supelco) and with a flame ionization detector.

The strain studied showed as princi- pal 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 acido- metric technique.

The patient was treated with penicil- lin G procaine 1,200,000 UI every 12 h for 10 d, with good response. By the end of 1 mo she showed no symp- toms and all laboratory tests were nor- mal.

Although rat-bite fever is an uncom- mon infection, a history of a bite from or contact with rodents suggest etio- logic 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-

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. monili- formis. Biochemical identification is laborious (6) due to the fastidious na- ture of the microorganism. However, identification of this microorganism to the species level using chromato- graphic analysis of fatty acids (7) is a safe, efficient, fast, and reliable proce- dure.

In our case it was possible to show that the positive VDRL test resulted from S. moniliformis infection as de- scribed 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 microor- ganism, it was performed by using an agar diffusion technique and by mi- crodilution, adopting the recommenda- tions for facultative bacteria. This technique, together with the absence of beta lactamase, made it possible to confirm the susceptibility of the micro- organism 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 thera- peutic failures.

References 1. M c H y g h , T. P. , R. L. Barlett , and

Clinical Microbiology Newsletter 14:5,1992 © 1992 Elsevier Science Publishing Co., Inc. 0196-4399/92/$0.00 + 03.00 39

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 chro- matographic. Acta Pathol. Microbiol. Immunol. Scand. Sect. B. 91:235- 239.

6. Morrison, R. 1985. Streptobacillus moniliformis and Spirillum minus, p. 400--405. In E. H. Lennette et al. (ed.), Manual of Clinical Microbiol- ogy, 4th ed. American Society for Mi-

crobiology, Washington, D.C.

7. Rowbotham, T. J. 1983. Rapid identi- fication of Streptobacillus monili- formis. Lancet ii:567.

8. Raffin, B. J. and M. Freemark. 1979. Streptobacillary rat-bite fever: a pediat- ric problem. Pediatrics 64:214-217.

9. Roughgarden, J. W. 1965. Antimicro- bial therapy of rat-bite fever, a review. Arch. Intern. Med. 116:39-54.

Letter to the Editor

This is in response to the letter sub-

mit ted by Patricia G. Rut land (Clinical Microbiology Newsletter, Vol. 13, No.

24, D e c e m b e r 15, 1991) that our letter

on the rapid f luorogenic tests for iden-

t if ication o f Gardnerella vaginalis con-

tained an error. She poin ted out

accurately that G. vaginalis should be

catalase negat ive and not catalase posi-

t ive as it stated in our letter (Clinical Microbiology Newsletter, Vol. 13, No.

19, October 1, 1991). At the t ime we

submit ted the manuscr ipt to Elsev ier

Science Publishing C o . , Inc. , we were

aware of the error immedia te ly , and

subsequent ly submit ted the corrected

page to the publ isher the next day.

Unfor tunate ly , due to a change of per-

sonnel at Elsevier and very unusual

c i rcumstances , the corrected vers ion

was not forwarded to the editors,

Thus our letter appeared in the news-

letter without the correct ion.

We thank Patricia Rut land for bring-

ing the error to our attention. We

hope that her letter and our reply will

reenforce for all the readers the correct

catalase react ion for G. vaginalis.

Pauline K. W. Yu, M. S. Clinical Microbiology Department of Laborator3' Medicine &

Pathology Mayo Clinic Rochester, MN 55905

Edi tor ' s note: We apologize to Ms.

Wu for any inconvenience caused by

the overs ight o f her correc ted manu-

script,

Editors

Mary Jane Ferraro

Paul A. Granato

Josephine A. More l lo

R. J. Zabransky

© 1992 Elsevier Science Publishing Co., Inc.

ISSN 0196-4399 CMNEEJ 14(5)33-40,1992

Elsevier

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