Total cross section for electron scattering from N2 in the energy range 600-5000 eV.
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Biomedical subjects
Publications and source records attributed to J Campos.
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We studied 10 trimethoprim-resistant (Tmpr) Haemophilus influenzae isolates for which agar dilution MICs were 10 to greater than 200 micrograms/ml. Trimethoprim resistance was transferred from two Tmpr H. influenzae isolates to a Tmps strain by conjugation or transformation. Wild-type Tmpr strains and Tmpr transcipients did not contain detectable plasmid DNA. The trimethoprim resistance gene was cloned into a cosmid vector, and recombinant plasmids were transduced into Escherichia coli. A 0.50-kilobase intragenic probe derived from a 12.9-kilobase fragment which encoded trimethoprim resistance hybridized with whole-cell DNA from Tmps and Tmpr strains. Southern blot analysis of restricted DNA from isogenic Tmps and Tmpr H. influenzae indicated that acquisition of trimethoprim resistance involved a rearrangement or change in nucleotide sequence. Hybridization was not seen with DNA derived from Tmpr E. coli containing dihydrofolate reductase I, II, and III genes or with Tmpr Neisseria meningitidis, Neisseria gonorrhoeae, and Pseudomonas cepacia. Southern hybridization with 12 multiply resistant encapsulated H. influenzae strains confirmed that the trimethoprim resistance gene was chromosomally mediated. Dihydrofolate reductase activity was significantly greater in cell sonicate supernatants of Tmpr strains in comparison with isogenic Tmps recipients. Differences were not found in the trimethoprim inhibition profile of dihydrofolate reductase activity in Tmps and Tmpr strains. We conclude that the mechanism of trimethoprim resistance in H. influenzae is overproduction of chromosomally located dihydrofolate reductase.
We examined clinical isolates of Neisseria meningitidis relatively resistant to penicillin G (mean MIC, 0.3 micrograms/ml; range, 0.1 to 0.7 micrograms/ml), which were isolated from blood and cerebrospinal fluid for resistance mechanisms, by using susceptible isolates (mean MIC, less than or equal to 0.06 micrograms/ml) for comparison. The resistant strains did not produce detectable beta-lactamase activity, otherwise modify penicillin G, or bind less total penicillin. Penicillin-binding protein (PBP) 3 of the six resistant isolates tested uniformly bound less penicillin G in comparison to the same PBP of four susceptible isolates. Reflecting the reduced binding affinity of PBP 3 of the two resistant strains tested, the amount of 3H-labeled penicillin G required for half-maximal binding was increased in comparison with that of PBP 3 of the two susceptible isolates. We conclude that the mechanism of resistance in these meningococci relatively resistant to penicillin G was decreased affinity of PBP 3.
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We studied the molecular epidemiology of multiply resistant Haemophilus influenzae type b in four day care centers after each had a case of invasive infection due to organisms resistant to four or more antibiotics. Colonization rates among 174 childhood contacts and 27 employees of the four separate day care centers were 28% in children (range, 13.5%-43.7%) and 22% (range, 18.7%-33.0%) in employees. All strains were type b, were biotype I, were type 12 by isoenzyme analysis, and harbored plasmids whose mass was 45 or 52 megadaltons. Restriction endonuclease analysis indicated that the plasmids were closely related to one another but that there were at least three distinct plasmids. The four index strains had two different outer membrane protein profiles and three distinct plasmid restriction patterns; an additional outer membrane protein profile and plasmid restriction pattern were found in carrier strains.
Eighty-three isolates of ampicillin and chloramphenicol resistant Haemophilus influenzae were tested for susceptibility to fifteen antibiotics by the agar dilution method. Fifty-four were from paediatric patients with H. influenzae disease and 29 from nasopharyngeal carriers (pre-school children). Twenty-five strains belonged to serotype b, one to serotype a, one to serotype c and the rest were non-typable. All strains produced beta-lactamase and inactivated chloramphenicol in a rapid bioassay, suggesting the production of chloramphenicol-acetyltransferase. The most active drugs were ceftriaxone, cefotaxime, latamoxef, aztreonam and desacetyl-cefotaxime (MIC90: 0.03, 0.06, 0.12, 0.25 and 0.25 mg/l, respectively). Cefuroxime, rifampicin and imipenem (MIC90 1 mg/l), and the combination of amoxycillin and clavulanic acid (MIC90 2:1 mg/l), also showed good activity. Cefaclor, erythromycin, tetracycline, trimethoprim, sulfamethoxazole and cotrimoxazole were the least active of the drugs studied. The excellent in-vitro activity of the new beta-lactam agents against H. influenzae resistant to ampicillin and chloramphenicol offers a therapeutic alternative in the treatment of serious infections caused by these micro-organisms.
We studied the efficacy of rifampin prophylaxis in reducing the prevalence of ampicillin- and chloramphenicol-resistant Haemophilus influenzae type b in four day care facilities after each center had individual cases of invasive infections (two meningitis, one pneumonia and one cellulitis) caused by multiply resistant organisms. Rifampin was given in a single daily dose of 20 mg/kg for 4 days. Cultures were taken pretreatment and 10 days after the last dose of rifampin. Included in the study were 174 children and 27 adults. We identified a total of 55 nasopharyngeal carriers; 45 received rifampin and 10 refused treatment. On the 10-day follow-up culture in the second sample, 95.5 and 20%, respectively, of treated and untreated children were no longer colonized with H. influenzae (P less than 0.001, Fisher's exact test). We conclude that rifampin can successfully reduce the prevalence of multiply resistant H. influenzae type b carriers attending day care centers.
Beginning in 1985, relatively penicillin G-resistant (Penr) meningococci which did not produce beta-lactamase were isolated from the blood and cerebrospinal fluid of patients in Spain. We identified 16 Penr (mean MIC, 0.3 microgram/ml; range, 0.1 to 0.7 microgram/ml) and 12 penicillin-susceptible (Pens; mean MIC, less than or equal to 0.06 microgram/ml) strains of Neisseria meningitidis by the agar dilution technique using an inoculum of 10(4) CFU and questioned which disk susceptibility test would best differentiate these two populations. We compared the disk susceptibility of these strains using disks containing 2 (P2) and 10 (P10) U of penicillin G, 2 (Am2) and 10 (Am10) micrograms of ampicillin, and 1 microgram of oxacillin (OX1). We also investigated susceptibility with disks containing 30 micrograms of each of cephalothin (CF30), cefoxitin (FOX30), cefuroxime (CXM30), and cefotaxime (CTX30) and 75 micrograms of cefoperazone (CFP75) and determined by cluster analysis any correlation with the zone diameters obtained with P2 disks. Using the P2 and AM2 disks (in contrast to the P10 and AM10 disks), we correctly differentiated all the Penr from Pens isolates. In addition, the zone diameters with the P2 disk gave the best correlation with the penicillin G MIC determinations. All 16 Penr strains and 3 of 12 Pens strains showed zone diameters of 6 mm around OX1 disks, limiting the usefulness of OX1 disks. The zone diameters obtained with CF30, CXM30, and OX1 disks correlated with those obtained with the P2 disk, which suggests that these antibiotics have similar effects on these strains. In contrast, the data obtained with FOX30, CTX30, and CFP75 disks did not cluster with those obtained with the P2 disk, which suggests that there was a difference in the bacterial target or reflects their greater activity. We conclude that the P2 disk tests more readily identify Penr meningococci than do the standard P10 disk tests.
Thirty-five patients with meningitis caused by Haemophilus influenzae type b were admitted to our hospital from January 1981 to December 1984; 60% of the strains were resistant to ampicillin, 65.7% to chloramphenicol, and 57% to both antibiotics. No significant differences in age, sex, previous treatment, clinical symptoms, outcome, and mortality were found between the 20 patients whose strains were resistant to both ampicillin and chloramphenicol and the other 15 patients whose strains were susceptible to ampicillin, chloramphenicol, or both. Alternative therapeutic agents were a combination of carbenicillin and gentamicin and new cephalosporins. At present, cefotaxime is our treatment of choice for meningitis caused by H. influenzae type b.
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One hundred and twenty-eight lesions of the cavernous sinus were diagnosed and treated by endovascular embolization alone or combined with postembolization surgery. All patients presented with acute or subacute cavernous sinus syndrome. A complete angiographic evaluation included bilateral internal and external carotid and vertebral angiography. A total of 88 carotid-cavernous (c-c) fistulae (68 traumatic and 20 spontaneous) and 40 giant aneurysms were demonstrated. A complete anatomic cure or satisfactory clinical improvement was seen in 67 of 68 traumatic fistulae, in 14 of 20 spontaneous c-c fistulae and in 38 of 40 giant intracavernous aneurysms. An overall 15 per cent immediate and 2.7 per cent long-term morbidity with one death was observed. The technical and clinical complications involving endovascular therapy of each specific intracavernous vascular lesion are analyzed.
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A 42 year-old beekeeper who had an inhalant allergy to Compositeae pollen presented an adverse reaction while eating a honey which contained large numbers of Compositeae pollens. As she was not intolerant to honey of own production, which contained no Compositeae pollen, the adverse reaction seems to be attributed to these pollens.
From February 1981 to December 1983, 225 strains were isolated from pediatric patients infected with Haemophilus influenzae. Forty-one strains were found to be resistant to ampicillin, chloramphenicol, and other antibiotics. They were isolated from 20 patients with invasive diseases (meningitis, 16; bacteremia, 4) and 21 with noninvasive diseases (otitis media, 19; conjunctivitis, 2). During this period, 44 patients with invasive diseases were seen (meningitis, 28; bacteremia, 16). Strains resistant to both ampicillin and chloramphenicol occurred in 45.4% of cerebrospinal fluid and blood isolates and in 51% of cerebrospinal fluid isolates only. In this group, individual resistance to ampicillin was 50%; chloramphenicol, 52.2%; tetracycline, 54.5%; and sulfamethoxazole-trimethoprim, 63.6%. No epidemiological relationship could be found among the patients. The presence of asymptomatic carriers was investigated in two nurseries and in eight family groups. From a total of 125 individuals studied, 80 were found to be colonized by H. influenzae, and 36 carried multiply resistant strains. From patients and carriers, 77 strains were found to be resistant to ampicillin, chloramphenicol, and other drugs; 39 belonged to type b (cerebrospinal fluid, 16; blood, 4; ear, 7; and nasopharynx, 12), and 38 were non-type b. The most frequent pattern of resistance was ampicillin-chloramphenicol-tetracycline-sulfamethoxazole-trimethoprim (94.8%), followed by ampicillin-chloramphenicol-tetracycline (3.9%). The disk diffusion method correctly predicted multiple resistance. The mean inhibition zone diameters were: ampicillin, 12.8 mm; chloramphenicol, 15.2 mm; tetracycline, 9.9 mm; and sulfamethoxazole-trimethoprim, 10.8 mm. These resistant strains were susceptible to cefotaxime, moxalactam, cefoperazone, cefuroxime, rifampin, and gentamicin. Our data suggest that in Spain the resistance of H. influenzae to ampicillin and chloramphenicol is endemic and that other effective therapeutic modalities are needed.
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