Biomedical subjects
Publications and source records attributed to H Lior.
Our improved toluidine blue-DNA agar was compared with methyl green DNase test agar for the detection of DNA hydrolysis by campylobacters. The toluidine blue-DNA agar gave clear-cut positive and negative reactions with campylobacter strains belonging to several species.
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Campylobacter jejuni is a common cause of inflammatory enteritis, which in normal hosts is usually self-limited and resolves without antibiotic therapy. C. jejuni bacteremia is very rare. We examined sera for bactericidal activity that might be important in limiting the extent of C. jejuni infection in man. We studied the ability of nonimmune sera and homologous and heterologous immune sera from infected patients to kill different fresh case isolates of C. jejuni in vitro. The reduction of the log10 concentration of viable C. jejuni (log10 killing) by fresh sera from nonimmune donors was only 0.2. Log10 killing by homologous acute sera varied from 0 to 3.8 (mean, 1.8). Convalescent sera showed remarkable log10 killing of only homologous C. jejuni, with values of 2.7 to 4.4 (mean, 3.7). The bactericidal effects of acute and convalescent sera were abrogated by heat and EDTA chelation, indicating mediation by complement. The role of classical complement pathway activation was supported by chelating sera with magnesium EGTA [ethylene glycol-bis(beta-aminoethyl ether)-N, N, N', N'-tetraacetic acid] and by reconstitution experiments with heat-inactivated sera, C2-deficient serum, and purified C2. The requirement of specific antibody for the serum bactericidal effect was indicated by the loss of bactericidal activity when immune sera were absorbed with homologous but not heterologous whole C. jejuni isolates. The presence of specific antibodies was further documented by agglutination of only homologous C. jejuni suspensions by heat-inactivated immune sera. Studies with polymorphonuclear leukocytes suggested that ingestion and killing of two C. jejuni strains were modest and variable in the presence of heat-inactivated homologous serum. In summary, the data document a potent serum bactericidal effect that develops rapidly and specifically during C. jejuni enteritis and may be an important factor in host defense against C. jejuni.
Complete toxigenicity studies were performed on 341 strains of Campylobacter spp., including 23 nonhuman isolates. Toxin profiles based on both cytotonic and cytotoxic factors were determined after analyzing responses in Vero, HeLa, CHO and Y-1 cells. Suckling mouse assays were consistently negative for all culture filtrates tested. Toxin-producing strains were frequently encountered among both the human and nonhuman strains of Campylobacter jejuni, C. coli, and C. laridis investigated. Strains isolated from outbreaks demonstrated parallels in serotype, biotype, and toxigenicity profile, although no clear association could be demonstrated. Biphasic culture conditions conducive to the production of both toxic factors were delineated for the propagation of test Campylobacter strains. Cytotonic effects of Campylobacter culture filtrates were determined in Vero and CHO cells, and cyclic AMP accumulation in cells exposed to these culture filtrates was compared with that in cells exposed to reference toxigenic strains of Vibrio cholerae and Escherichia coli. Partial neutralization of C. jejuni enterotoxin was demonstrated by using antitoxins to cholera toxin and E. coli heat-labile enterotoxin. No neutralization of C. jejuni cytotoxin could be achieved by using antitoxins to either Clostridium difficile cytotoxin or E. coli Verotoxin (0157:H7).
In a recent meat survey, 10 of 13 (77%) Campylobacter coli isolates were susceptible to cephalothin. These organisms were isolated from nine slaughter cattle from eight meat packing establishments. All 10 isolates grew at 43 degrees C but not at 25 degrees C, were catalase and oxidase positive, and were susceptible to nalidixic acid (30 micrograms) and cephalothin (30 micrograms). The cultures were subsequently identified as C. coli serogroup 20, biotype I (Lior scheme). Sodium dodecyl sulfate-polyacrylamide gel electrophoresis showed that protein and lipopolysaccharide profiles of whole cell preparations of the 10 cephalothin-susceptible strains and the reference strain for C. coli serogroup 20 were very similar. The plasmid profiles of these 11 strains were identical.
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Forty pediatric patients with idiopathic hemolytic uremic syndrome (HUS) were investigated for evidence of infection by Verotoxin-producing Escherichia coli (VTEC). Fecal VTEC (belonging to at least six different O serogroups including O26, O111, O113, O121, O145, and O157) or specifically neutralizable free-fecal Verotoxin (VT) or both were detected in 24 (60%) patients but were not detected in 40 matched controls. Ten of 15 of the former developed fourfold or greater rises in VT-neutralizing antibody titers, as did six other patients who were negative for both fecal VTEC and VT. A total of 30 (75%) patients had evidence of VTEC infection by one or more criteria. We concluded that a significant association exists between idiopathic HUS and infection by VTEC. The detection of free-fecal VT was the most important procedure for the early diagnosis of this infection because, in our study, VTEC were never isolated in the absence of fecal VT, whereas fecal VT was often present even when VTEC were undetectable.
Nalidixic acid-resistant mutants of Campylobacter jejuni and C. coli as well as "C. laridis" strains showed cross-resistance to another DNA gyrase subunit A inhibitor, enoxacin (MIC, 32 micrograms/ml), whereas C. fetus subsp. fetus, C. fetus subsp. venerealis, and "C. hyointestinalis" strains were all susceptible to enoxacin (MIC, less than or equal to 2 micrograms/ml). All Campylobacter species were resistant to novobiocin (MIC, 32 to 512 micrograms/ml), but most strains were susceptible to the other DNA gyrase subunit B inhibitors coumermycin A1 and clorobiocin.
A total of 525 specimens from 100 slaughter beef cattle were examined for the presence of Campylobacter jejuni and Campylobacter coli by direct plating and enrichment techniques. Isolates were identified by cultural, biochemical, antibiotic sensitivity, and immunofluorescence tests and further characterized with the aid of recently developed biotyping and serotyping methods. Fifty animals were positive for C. jejuni; only one was positive for C. coli. The distribution pattern of C. jejuni-positive animals, in decreasing order, was steers (55%), bulls (40%), heifers (40%), and cows (22%). Significantly higher isolation rates were obtained from the gall bladders (33%), large intestines (35%), and small intestines (31%) than from the livers (12%) or the lymph nodes (1.4%). C. jejuni isolation by the enrichment technique was 40.2% more frequent than by direct plating; 24-h enrichment resulted in 24% more isolations than 48-h enrichment. Eighty-four of 105 C. jejuni cultures were typable serologically and represented 13 serogroups. Biotype I accounted for 71% of biotyped cultures. Serogroup 7 biotype I was the most commonly encountered (24%) isolate. About one in three positive animals had C. jejuni strains representing more than one serogroup. C. jejuni serogroups encountered in slaughter cattle were similar to those commonly isolated from human sources.
More than 2,000 confirmed cases of food poisoning occurred in the four Atlantic provinces of Canada and in Ontario during the second and third quarters of 1984. Salmonella typhimurium phage type 10 was identified as the etiologic agent, and cheddar cheese was implicated as the source of infection. Strains isolated from infected humans and from cheese were indistinguishable by biotyping, antibiotic resistance typing, and phage typing. Plasmid analysis confirmed cheese as the source of infection and revealed the presence of two molecular subgroups of bacteriophage type 10. Group I strains carried 57-, 22.3-, and 3.4-kilobase (kb) plasmids; group II strains carried 57-, 4.6-, and 3.4-kb plasmids. Digestion with endonucleases HaeIII, HpaII, and AvaIII indicated that the 3.4-kb plasmids were identical. This outbreak was, therefore, caused by a mixed infection with two distinct but related bacteria. Group I strains are fairly common among Canadian S. typhimurium phage type 10 isolates, whereas group II strains appeared to be unique to this outbreak.
Outer membrane proteins of Campylobacter jejuni and other campylobacter species were analyzed for their antigenic potentials by immunoblotting. Polypeptides were resolved by sodium dodecyl sulfate-polyacrylamide gel electrophoresis, transferred electrophoretically, and reacted with rabbit antisera to C. jejuni. Each Campylobacter species analyzed demonstrated a unique outer membrane protein antigenic profile; interspecies antigen sharing was observed to be compatible with the degree of DNA relatedness between the species. The most highly conserved outer membrane protein antigen was the flagellum (molecular weight, 62,000). An aflagellate mutant was found to be untypable with the heat-labile system, in contrast to its parental isolate. The immunogenic potentials of C. jejuni proteins were examined by immunoblot analysis of sera from infected humans. Sera of convalescent patients, reacted with their homologous C. jejuni isolates, recognized a variety of campylobacter proteins. The most consistent immunogen in human infection was the flagellar protein. Patient sera assayed by the immunoblot technique were easily distinguished from control sera, which did not recognize specific campylobacter antigens. These findings suggest that the campylobacter flagellar protein is an essential determinant of the heat-labile antigen typing scheme and is the dominant immunogen recognized during C. jejuni infections in humans.
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During a five-day period, four neonates in a neonatal nursery developed Campylobacter entercolitis. Investigations suggested that cross-infection or common-source infection were unlikely and that the neonates acquired their infection during delivery from their respective mothers, three of whom were also found to harbour Campylobacter jejuni in their stools. This suggestion was confirmed with use of the Lior serotyping system in a blind fashion. Each neonate was infected with a different serotype, and each of the three culture-positive mothers had the same serotype as her neonate. Examination of multiple colonies from the stools of five individuals showed that each was likely to have been infected by only one serotype. The presenting clinical features in the four neonates provides further evidence that neonatal Campylobacter entercolitis typically manifests as a benign, self-limited, nonfebrile, diarrheal illness with bloody stools.
A biotyping scheme using improved media and methods for the detection of hippurate hydrolysis, rapid H2S production, and DNA hydrolysis was applied to 1,826 cultures of Campylobacter jejuni, Campylobacter coli and "Campylobacter laridis" isolates from human and nonhuman sources. Four biotypes were identified among C. jejuni: 57.3% of the isolates belonged to biotype I; 36.0%, to biotype II; 4.0%, to biotype III; and 2.7%, to biotype IV. C. coli organisms were differentiated into biotype I (67.0% of the isolates) and biotype II (33.0%). All "C. laridis" isolates belonged to biotype I. The combination of the biotyping scheme with the serotyping of campylobacters provided additional epidemiological markers by further differentiating the serogroups by species and biotypes.
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