619

Clinically

characterised by abdominal pain and diarrhoea, usually severe, lasting 2-10 days (6 days on average). Of the 9 patients 6 had animals at home. 4 patients had a history of severe gastrointestinal upset. Clearance of stools tooka long time-28-5 days (range 18-39) in tests done in our own laboratory and 25-5 (18-33) in tests done outside-indicating the need for prolonged monitoring. This is particularly important, in view of the fact that the complete life cycle of Campylobacter in man has not been established as it has for Salmonella infection. the illness

was

Medical Department, General Foods Ltd,

ALAN

Banbury, Oxon

transferable enzymes found in N. gonorrhaeae and H. in-

fluenzce. Laboratory of Bacteriology, Institute of Tropical Medicine, B2000 Antwerp, Belgium, and Department of Microbiology, University of Washington, Seattle, Washington 98195, U.S.A. Hôpital de Joliniont, Haine-Saint-Paul, Belgium

JONES

PETER PIOT MARILYN ROBERTS

GASTON NINANE

SYNOVIAL INFLAMMATION IN

SHIGELLA

INFECTION

mechanism

&bgr;-LACTAMASE PRODUCTION IN COMMENSAL NEISSERIACEÆ

SIR,-Siiice the emergence of p-lactamase-producing strains of Neisseria gonorrhaeae in 1976,’ there has been much concern that other Neisseriaceae, particularly N. meningitidis, which is closely related to the gonococcus, might acquire in vivo the R-plasmid encoding the TEM type p-lactamase which has been isolated from penicilliri-resistant N. gonorrhaeae and ampicillinresistant Hcemophilus influenzae. &bgr;-Iactamase-producing Branhamella catarrhalis isolates have been reported.2-4 Their enzyme is not of the TEM-type found in gonococci; and seeins to be unique on isoelectric focusing pattern and substrate profile.5,6 Using an agarose gel electrophoresis method’ we could not find a plasmid in any of eight isolates tested. We have isolated two &bgr;-lactamase-producing strains of N. perflava from the throat of healthy people in Belgium. The strains were recovered iri the same (Jolimont) over a period of 10 months during a surveillance programme on ,3-lactamase-’producing bacteria. The strains were gram-negative diplococci with yellowish and smooth colonies; no growth at room temperature; oxidase and catalase positive, D.N.A.se, o-nitrophenyl-p-D-galactopyranoside, and H2S negative; acid produced from glucose, maltose, and sucrose, but not from ldctose ; prototrophic on Catlin’s defined medium. &bgr;-Iactamaseproduction was shown with the chromogenic cephalosporin test.8 The minimum inhibitory concentration (M.l.c.) of benzylpenicillin for both organisms was 16 mg/1 in an agar dilution system with an inoculum of 104 colony-forming units. (Sensitive strains of N. perflava have m.i.c.s of less than 0.06 nig/I.) There was a marked inoculum effect on M.t.c. determinaiions. The isolates were resistant to oxacillin and sensitive to cephalothin (disc method). Plasmids were not found by agarose-gel electrophoresis.’ The enzyme is under investigation. We think that surveillance of 3-lactamase production in "commensal" Neisseriaceae (besides N. gonorrhaeae and N. meningitidis) is important because these may constitute a potential source of j3-lactamase transferable to other more pathogenic bacteria, including meningococci, coexisting in the upper respiratory tract. A 4.4x 106 dalton plasmid coding for 11-lactamase production in N. gonorrhaeae has been transferred to N. flava in vitro.9 However, in the two strains reported here, the 3-lactamase is different from the plasmid mediated and

of synovial inflamSIR,-Little is known of the mation in patients with Shigella infection.1,2 (P.G.E) has been established as a mediator of inflam’ination.1;4 Addition of Shigella endotoxin to cultured human synovial fibroblasts (derived from synovial tissue of patients undergoing

Prostaglandin t

laboratory

1. World Health Organisation Wkly epidem. Rec. 1976, 51, 293. 2. Ninane, G., Joly, J., Piot, P., Kraytman, M. Lancet, 1977, ii, 149. 3 Malmvall, B. E., Brorsson, J. E., Johnson, J. J. antimicrob. Chemother.

1977, 3, 374. 4. Percival, A., Corkill, J. E., Rowlands, J., Sykes, R. B. Lancet, ii, 1175. 5. Sykes, R. B., Percival, A. in Immunobiology of Neisseria gonorrhœœ (edited by Brooks et al.), p. 68, A.S.M., Washington, D.C., 1978. 6. Buu Hoi-Dang Van, A., Brive-Le Bouguenec, C., Barthelemy, M., Labia, R. Ann.Microbiol. 1978, 129B, 397. 7.Elwell, L. P., Roberts, M., Mayer, L. W., Falkow, S. Antimicrob. Ag. Chemother. 1977, 11, 528. 8. O’Callaghan, C. H., Morris, A., Kirby, S. M., Shingler, A. H. ibid. 1972,

i,283. 9. Eisenstein, B. I.,

Sox, T., Biswas, G., Blackman, E., Sparling, P. 1977, 195, 998.

F. Science,

Dose-resporise curve of stimulation of P.G.E and hyaiW6xo,&

acid

production in cultured human synovial fibroblasts by Shigella endotoxin.

P.G.É concentration in medium determined by radioimmunoassay and hyaluronic acid by a carbazol colour reaction, Vertical bars represent S.E.M.

menisectoniy) induced a dose-related increase in ,prQtaglandin

hyaluronic acid production by synovial fibroblast cul(figure). We have found a relationship between p.G.E and hyaluronic acid prodtiction by synovial fibroblast:>.5 We suggest that Shigella endotoxin may trigger a p;G.Emediated synovial inflammation and pathological acciimulation of joint fluid in patients with Shigella infections. E and tures

Arthritis Research Unit, Department of Physical Medicine and Rheumatology, Ichilov Hospital Medical Center and Sackler School of Medicine, Tel Aviv, Israel, and Department of Hormone Research, Weizmann Institute of Science, Rehovot

1. 2.

Noer, H. R. J. Am. med. Ass. 1966, 198, 693. Calin, A., and others. Ann. intern. Med. 1976, 84, 564. 3. DiRosa, M., and others. J. Path. 1971, 104, 15. 4. Floman, Y., and others. Clin. Orthop. 1977, 125, 214. 5. Yaron, M., and others. Arths. Rheum. 1978, 21, 694.

MICHAEL YARON

ILANA YARON URIEL ZOR

Synovial inflammation in Shigella infection.

619 Clinically characterised by abdominal pain and diarrhoea, usually severe, lasting 2-10 days (6 days on average). Of the 9 patients 6 had animals...
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