Don't take the i out of Enterobacteriaceae

i

in combination with one o f the cephalosporins that behave like antibiotic B. A second use of PBPs in the disciplines o f infectious diseases and clinical microbiology is in the study o f antibiotic resistance. Several investigators have shown that some laboratory-derived mutants with resistance to beta-lactam antibiotics possessed one or more PBPs with altered affinity for the antibiotic in question. This was demonstrated in E. coli and two species o f Bacillus. Attention was then turned to clinical isolates. Strains of penicillin-resistant Streptococcus pneumoniae and Neisseria gonorrhoeae that do not produce beta-lactamase have one or two PBPs that show decreased binding o f penicillin compared to that shown by penicillin-susceptible strains o f the same species. Knowledge of the PBP affinity patterns o f

penicillin-resistant bacteria may allow rational selection of alternatives to penicillin among other beta-lactam type antibiotics. In addition, PBP affinity patterns may prove to be good markers for epidemiologic studies o f the appearance and spread of non-beta-lactamase antibiotic resistance in a hospital, community, or country.

References 1. Blumberg, P. M., and J. L. Strominger. 1974. Interaction of penicillin

with the bacterial cell: Penicillinbinding proteins and penicillin-sensitive enzymes. Bacteriol. Rev. 38:291335. 2. Curtis, N. A. C., D. Orr, G. W. Ross, and M. G. Boullon. 1979. Competition of [3-1actam antibiotics for the penicillin-binding proteins of Pseudomonas aeruginosa, Enterobacter cloacae, Klebsiella aerogenes, Proteus rettgeri, and Escherichia coli: Comparison with antibacterial activity and effects upon

bacterial morphology. Antimicrob. Agents Chemother. 16:325-328. 3. Georgopapadakou, N. H., and F. Y.

Liu. 1980. Penicillin-binding proteins in bacteria. Antimicrob. Agents Chemother. 18:148-157. 4. Hakenbeck, R., M. Tarpay, and A. Tomasz. 1980. Multiple changes of penicillin-binding proteins in penicillinresistant clinical isolates. Antimicrob. Agents Chemother. 17:364-371. 5. Spratt, B. G. 1977. Properties of the penicillin-binding proteins of Escherichia coli KI 2. Eur. J. Biochem. 72:341-352. 6. Spratt, B. G. 1978. The mechanism of action of penicillin. Sci. Prog. (Oxf.) 65:101-128. 7. Suzuki, H., Y. Nishimura, and Y. Hirota. 1978. On the process of

cellular division in Escherichia coli: A series of mutants of E. coli altered in the penicillin-binding proteins. Proc. Natl. Acad. Sci. U.S.A. 75:664-668. 8. Tomasz, A. 1979. From penicillinbinding proteins to the lysis and death of bacteria:A 1979 view. Rev. Infect. Dis. 1:434-467.

Editorial llU

Don't Take the i out of Enterobacteriaceae

Karla M. Tomfohrde, M.S. Associate Director, Technical Services Analytab Products Plainview, New York 11803 During the last several months much has been written concerning the "request for an opinion" by S. P. Lapage (2) on the change in the name Enterobacteriaceae to Enterobacteraceae and the concomitant change in type genus from Escherichia to Enterobacter, which appeared in the July 1979 issue of IJSB. From what I have seen and read, it appears that clinical microbiologists in the United States are opposed to this change. In recent years we have seen many changes in the nomenclature o f the Enterobacteriaceae. New organisms such as Enterobacter gergoviae, Enterobacter sakazakii, and Serratia odorifera have been described. Several other organisms have been split into more than one species (e.g., Klebsiella pneumoniae and K. oxytoca; Yersinia enterocolitica into

four groups with three new species to be described). In addition, several organisms, including Hafnia alvei, Morganella morganii, and Providencia rettgeri, have been moved into new genera. Clinical microbiologists have accepted these changes or additions, if at times reluctantly, because they are based on scientific facts (i.e., deoxyribonucleic acidrelatedness tests, biochemical profiles, antibiotic susceptibility patterns, and pathogenicity). This current proposal, however, is based not on scientific data, but rather on a desire to eliminate exceptions to the rules o f taxonomy. This may be fine for the taxonomist, but it is unacceptable to the clinical microbiologist. It is true that this appears to be only a slight change. And, as stated by Lapage (2): This course has the merit o f producing a minimal disturbance of existing nomenclature, because for practical purposes the only change is a small difference in spelling, i.e., the omission of the letter i

from the presently used family name. Such a change is unlikely to cause much difficulty for future bacterial systematists, because it should be no more disturbing than changes produced by emendation of the spelling of names that have been inadvertently spelled incorrectly (e.g., emendation o f Hemophilus to Haemophilus). The change does not affect the first part o f the word, and therefore it should seldom disturb the position of the family name in alphabetized lists. This situation has been well summarized by Farmer et al. (1): • . . rejection o f the name Enterobacteriaceae is totally undesirable and would cause much needless confusion to microbiologists, other scientists, students, editors, literature searchers, abstract preparers, and especially to computer programmers (two words are different regardless o f how similar their spelling).

Today, most clinical microbiolo-

gists will accept the inevitability of taxonomic and nomenclature changes. These will be accepted when they are supported by scientific data. H o w ever, " n i t p i c k y " changes such as this one are not acceptable. In this case,

as stated in the popular song, " E n o u g h is enough, is enough, is enough . . . . "

References I. Farmer, J. J., D. J. Brenner, and W. H. Ewing. 1980. Enterobac-

teriaceae. ASM News. 46:275-279. 2. Lapage, S. P. 1979. Proposal of Enterobacteraceae nom. nov. as a substitute for the illegitimate but conserved name Enterobacteriaceae Rahn 1937: Request for an opinion. Int. J. Systemat. Bacteriol. 29:265-266.

Case Report

Capnocytophaga Bacteremia Submitted by Nettle M. Warwood, B.S. Clhtical Microbiology Laboratory University of Mhmesota Hospitals Mhtneapolis, Mbtnesota 55455 A fourryear-old white female was admitted to the University o f Minnesota Hospitals on September 4, 1980. She had a one-month history of a chest cold, fever, hemoglobin o f 8.6 mg/dl, and a sore throat that was assumed to be a viral infection. Her chest cold had persisted, and she had been treated with ampicillin and trimethoprim-sulfamethoxazole; her hemoglobin had risen to 10.5, and she was later noted to have swelling and tenderness in her right leg. At the end o f August she had been taken to her local hospital because of pain. At that time her white blood count (WBC) was found to be about 120,000/mm 3, and she was referred to our hospital. On admission, she was noted to be a normal, well-nourished child except that her liver and spleen were each 3 cm below the right costal margin, and a chest x-ray showed increased heart size. She had purpura in the antecubital fossae, but no petechiae.

M a n y small, shotty, matted nodes were felt in the anterior and posterior cervical and inguinal regions. H e r hemoglobin was 5.2 m g / d l with a hematocrit of 15. H e r W B C was 170,000/mm 3, with 90% blasts. Her bone m a r r o w was packed with peroxidase-positive blasts with granules. She was diagnosed as having acute myelogenous leukemia with secondary anemia, decreased platelets, and lymphadenopathy. A double-exchange transfusion was performed on the first day, and she was begun on a course o f antileukemic therapy. She remained stable until the fourth day o f hospitalization, when her temperature increased. On the sixth day, she was still febrile to 102.4°F. A blood culture collected in the afternoon was negative, but a blood culture collected that evening and two more collected the next day yielded growth of Staphylococctts attreus. The organism was susceptible to cephalothin, chloramphenicol, clindamycin, erythromycin, gentamicin, methicillin, tetracycline, and trimethoprim-sulfamethoxazole and was resistant to penicillin. She was treated with cefazolin; later her therapy was changed to nafcillin and gentamicin.

Editors: D o n n a J. Blazevic, L. R. McCarthy, and Josephine A. Morello Subscription Rates in U.S. and Canada: one year $54.00; two years $103.00; three years $146.00. All other countries: one year $62.00; two years $118.50; three years $168.00. Single copies are $2.50 in U.S. and Canada; $2.90 in all other countries. Single issues are available in quantity (prices available upon request). Volume I (1979), 24 issues $42.50. Volume2 (1980), 24 issues $46.50. All subscriptions are payable in advance. Foreign subscriptions are sent guaranteed air mail. First class postage paid in U.S. and Canada. Address correspondence regarding subscription to: Clinical Microbiology Newsletter, G. K. Hall & Co., 70 Lincoln St., Boston, Massachusetts 02111. Please include zip code in subscription address. The Clinical Microbiology Newsletter is published twice monthly. All rights, including that of translation into other languages, reserved. Photomechanical reproduction (photocopy, microcopy) of this newslener or parts thereof without special permission of the publisher is prohibited. Editorials and letters printed in this Newsletter are published for the interest of the readers and do not necessarily reflect the opinions of the editors.

On the seventh day after admission, the patient developed hemorrhagic crusts with erosions and a vermillion border on her lips, but no blister formed. The next day both upper and lower lips had developed erosions that were thought to be related to her cytopenia or chemotherapy. She also developed mouth ulcers. Her hemoglobin on the eighth day was 7.8 m g / d l with less than 500 W B C s / m m ~, and she was transfused with four units o f platelets. She continued to appear septic with spiking temperatures for the next two weeks, although all blood cultures remained negative. On the fifteenth and sixteenth days she was noted to have a red throat with white plaques and desquamation o f the mucosal lining o f the palate. On the seventeenth day she developed a papular macular rash. At the beginning of her third week of hospitalization, she was noted to be severely immunocompromised. The next day a blood culture was drawn that five days later was reported to be growing a thin gram-negative rod that was subsequently identified as a Capnocytophaga species. The organism was susceptible to cephalothin, chloramphenicol, clindamycin, erythromycin, penicillin and tetracycline, and it was resistant to gentamicin. Before these results were reported, the patient's therapy had been changed to gentamicin and cephalothin. Three days later she was reported to be afebrile and in good spirits. Her mouth ulcers healed and she continued to do well nearly two weeks later. Capnocytophaga is a newly described genus of gliding bacteria that is identical to the CDC group DF-I and Bacteroides ochraceus (1). Sometimes found as normal flora in the mouth, it is commonly responsible for