Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0348321 (Haemophilus)
 15,372 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The influence of cefodizime (CDZ) on CD4 and CD8 lymphocytes was investigated in patients with lower respiratory tract infection and underlying respiratory diseases. Ten men and one woman were treated with CDZ 1 g i.m. b.i.d. for ten days. The infecting organisms were Haemophilus influenzae (5), Streptococcus pneumoniae (2) and Escherichia coli (1). No adverse events were reported. Nine patients were clinically cured; two required further antibiotic therapy. Leucocyte counts decreased significantly during treatment. Lymphocyte counts and CD4 cells both increased significantly in absolute and relative numbers, while there was a much smaller increase in CD8 cells. This resulted in a significant increase in the CD4/CD8 ratio. These effects of CDZ might be of benefit for immunocompromised patients with bacterial infections.
Infection 1992
PMID:Changes in lymphocyte subpopulations in patients treated with cefodizime for acute lower respiratory tract infections. 152 80

One of every two Americans will be bitten by an animal or by another person at some point. Bites account for approximately 1% of all visits to emergency rooms; injuries inflicted by dogs are most common. The bacteria involved in infection of bite wounds include Pasteurella multocida, Staphylococcus aureus, Staphylococcus intermedius, alpha-hemolytic streptococci, Capnocytophaga canimorsus, and other members of the oral flora. Anaerobic bacteria are present in approximately one-third of bite wounds and are associated with the formation of abscesses and with relatively serious infections. P. multocida is found in infections of cat bites more than 50% of the time. The bacteriology of bite wounds inflicted by exotic animals reflects the animals' oral flora. Bites inflicted by humans are often more serious than those inflicted by animals. Infections of human bites are associated with alpha-hemolytic streptococci, S. aureus, Eikenella corrodens, Haemophilus species, and (in more than 50% of cases) anaerobic bacteria. The principles of management of bite wounds are discussed.
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PMID:Bite wounds and infection. 162 89

Infections of the respiratory airways are frequently responsible for exacerbations of chronic obstructive pulmonary disease (COPD) and attacks of asthma. However, the causal infectious agents in practice are rarely precisely identified. We have undertaken a prospective study with the aim of researching into the bacteria and viruses associated with these exacerbations. Forty-seven patients who were in hospital between 1987 and 1989 for attacks of asthma (13 episodes) or exacerbations of COPD (35 episodes) were included in this study. The microbiological analysis consisted of: 1) the bacteriology of expectorated material or the products aspirated by fibroscopy with direct examination, quantitative cytology and culture; 2) samples taken from the nasal airways to identify and isolate pneumotropic viruses and mycoplasma; 3) serial serology looking for antibodies against pneumotropic bacteria and viruses. One of more infectious agents were shown in 47% of the episode studies of which 57% were exacerbations of COPD and treated 23% attacks of asthma. In the cases COPD bacteria were identified in 13 cases including Haemophilus influenzae [3], Streptococcus pneumoniae [3], Pseudomonas aeruginosa [3]. Amongst the 14 viruses recovered, the influenza virus [8] and the respiratory syncytial virus (VRS) [4] predominated. In 14 cases of acute asthma only 4 infectious agents were shown; Mycoplasma pneumoniae, influenza A, VRS and parainfluenza virus. The influenza virus was the agent most frequently discovered (26%) during the course of exacerbation of COPD and of asthma.
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PMID:[Infectious agents associated with exacerbations of chronic obstructive bronchopneumopathies and asthma attacks]. 156 31

The therapeutic perspectives of flomoxef, SCE 2787, cefpirome, cefepime, latamoxef, cefotaxime and of piperacillin plus tazobactam were comparatively evaluated by their in vitro activity against 1119 clinical isolates of 83 bacterial species. Escherichia coli, Klebsiella spp. Enterobacter sakazakii, Proteus spp. and Shigella spp. were about equally susceptible to the cephalosporins (MIC90: 0.06 to 0.5 mg/l), while the MIC90 for piperacillin plus tazobactam was between 2 and 16 mg/l. Enterobacter cloacae, Enterobacter aerogenes and Serratia spp. were most susceptible to SCE 2787, cefpirome and cefepime (MIC90: 0.06 to 2 mg/l) followed by latamoxef, cefotaxime, flomoxef and piperacillin plus tazobactam. For Citrobacter spp., Providencia spp. and Yersinia enterocolitica MIC90 were between 0.06 and 0.5 mg/l. Flomoxef was between 2 to 4 log2 less active against these species but more active than piperacillin plus tazobactam (MIC90: 2 and 8 mg/l). Morganella morganii and Hafnia alvei were most susceptible to cefepime, cefpirome and latamoxef (MIC90: 0.13 to 0.5 mg/l) while cefotaxime (MIC90: 8 mg/l) and piperacillin plus tazobactam (MIC90: 8 and greater than 64 mg/l) were the least active compounds. SCE 2787, cefepime and cefpirome were the most potent beta-lactams against the majority of the 13 species of non-fermentative bacilli (NFB) investigated (MIC90: 0.5 to 16 mg/l). The oxacephems were the least active compounds against NFB. Cefepime was the most active of the compounds included against Pseudomonas aeruginosa (MIC90: 16 mg/l). Haemophilus spp., Neisseria gonorrhoeae and Bordetella pertussis were most susceptible to cefotaxime (MIC90: 0.03 to 0.06 mg/l). Latamoxef had the lowest activity of all compounds against gram-positive cocci. Flomoxef was the most active compound against penicillinase producing Staphylococcus aureus and about equally active as the other betalactams against methicillin susceptible staphylococci of other staphylococcal species.(ABSTRACT TRUNCATED AT 250 WORDS)
Infection 1991
PMID:In vitro activity and stability against novel beta-lactamases of investigational beta-lactams (cefepime, cefpirome, flomoxef, SCE2787 and piperacillin plus tazobactam) in comparison with established compounds (cefotaxime, latamoxef and piperacillin). 166 18

Sudden increases in prevalence of antimicrobial resistance among bacteria are seen in both hospital-acquired and community-acquired infections. Examples include precipitate change in amikacin susceptibility in a hospital after years of low resistance, the abrupt increase in prevalence of beta-lactamase-producing strains among gonococci isolated in one community, and rapid increase in resistance to ciprofloxacin among methicillin-resistant Staphylococcus aureus at a hospital shortly after the drug was introduced. Most dramatic are cases where organisms have abruptly become resistant to drugs that have worked clinically for decades (e.g. resistance to ampicillin in Haemophilus influenzae). Four types of mechanisms (other than laboratory artefact) for development of resistance can be postulated: introduction of resistant organisms into a previously susceptible population; acquisition of resistance by previously susceptible strains through genetic mutation or transfer of genetic material from another species or genus; emergence of a dormant resistance mechanism already present in the population; selection of resistant subpopulations of organisms. When any of these resistance mechanisms develop in a large proportion of the organisms, or in a few resistant organisms which are widely disseminated within the population, resistance can increase abruptly. It is likely that organisms will continue to use the mechanisms described here, and to develop additional ingenious ways to counter our antimicrobial weapons. Infection control personnel must rapidly uncover which mechanisms are involved so that appropriate measures (alternate drug regimens, isolation precautions, cohorting, etc.) can be instituted. Newer methods for typing of organisms can help identify which resistance mechanisms are involved in a given situation.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Abrupt changes in antibiotic resistance. 167 85

Infections caused by Haemophilus influenzae are a major worldwide health problem. In particular, nontypeable strains of H. influenzae are a common cause of otitis media in infants and children. A vaccine to prevent these infections would result in the prevention of substantial morbidity and cost savings. A problem in identifying an appropriate vaccine antigen has been the enormous antigenic heterogeneity among nontypeable strains of H. influenzae. The present study was undertaken to characterize the conservation of the P6 outer membrane protein (approximately 16,000 daltons) among strains of H. influenzae. A total of 20 type b strains and 20 nontypeable strains of diverse geographic and clinical origins was studied. Three approaches were taken. (i) Antigenic determinants recognized by monoclonal and polyclonal antibodies were present on P6 in all 40 strains tested. The molecular weight of P6 was identical in all strains. (ii) Comparison of the DNA sequences of the P6 genes from three epidemiologically and serologically unrelated strains demonstrated 100% homology at the amino acid level and 97 to 99% homology at the nucleotide level. (iii) Restriction fragment length polymorphism analysis demonstrated that the P6 gene and flanking sequences were highly conserved among all strains. These three independent series of experiments indicated that the P6 protein is highly conserved among strains of H. influenzae. P6 should receive serious consideration for inclusion in a vaccine to prevent infections caused by nontypeable H. influenzae.
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PMID:Molecular conservation of the P6 outer membrane protein among strains of Haemophilus influenzae: analysis of antigenic determinants, gene sequences, and restriction fragment length polymorphisms. 171 97

Acute respiratory infections in children aged less than 5 years in the Eastern Highlands of Papua New Guinea were investigated bacteriologically for 10 years from November 1978. Haemophilus influenzae and Streptococcus pneumoniae were responsible for 73% of all bacteria cultured from lung aspirate (83 samples), 85.5% from blood (1024 samples) and 92% from cerebrospinal fluid (155 samples). Nonencapsulated H. influenzae was carried by up to 90% of children and was the predominant haemophilus type cultured from lung tissue. Mixed infections of the lung with two types of H. influenzae (8 cases) and both H. influenzae and S. pneumoniae (18 cases), commonly together with other organisms of questionable pathogenicity, reflected the proximity of this organ to the upper respiratory tract. Serotype b accounted for 62% and 82% of H. influenzae isolated from bacteraemic pneumonia and meningitis cases, respectively. Polymicrobic bacteraemic pneumonia occurred in 16 children. Both H. influenzae and S. pneumoniae establish dense, unregulated long-term colonization in the nasopharynx during the neonatal period. Each inhibit autochthonous microflora by mechanisms that are currently unclear. Infections with two or more types occur in 30% (S. pneumoniae) and 60% (H. influenzae) of carriage-positive children. 70-75% of H. influenzae and S. pneumoniae isolates from blood concomitantly colonize the upper respiratory tract. Intense exposure of Papua New Guinean children to penicillin at all levels of health care since the 1940s has resulted in widespread relative resistance among pneumococci to this antibiotic. Resistant strains are now found in 32 serotypes, and in children penicillin resistance is present in 75% of all carriage strains and 52% and 22% of blood and cerebrospinal fluid isolates, respectively. Penicillin-susceptible and resistant pneumococcal serotypes commonly coexist in multiply populated carriage sites. Resistance to betalactam antibiotics is rare among H. influenzae strains and resistance has not been detected in either H. influenzae or S. pneumoniae to chloramphenicol, erythromycin, tetracycline or cotrimoxazole. It should not be assumed that the technology of respiratory bacteriology as it is practised in developed countries can be transferred to the third world for utilization in paediatric aetiology and carriage studies. Respiratory bacteriology strategies as they evolved in Goroka were subject to diverse influences. The type distribution of the major causative agents defied fashionable beliefs, generated the need for more precise epidemiological differentiation and, by virtue of their carriage density, cultural properties and response to commonly used antibiotics, required the introduction or development of compatible diagnostic procedures.
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PMID:The bacteriology of acute pneumonia and meningitis in children in Papua New Guinea: assumptions, facts and technical strategies. 175 Feb 63

The new oral cephalosporins cefpodoxime, cefixime, cefdinir, cefetamet and ceftibuten demonstrate enhanced activity against Enterobacteriaceae susceptible to the established compounds as well (e.g. cefuroxime, cefaclor, cefadroxil). In addition, cefpodoxime, cefixime, cefdinir, cefetamet and ceftibuten include in their spectrum species hitherto resistant to oral cephalosporins (Proteus vulgaris, Providencia spp., Yersinia enterocolitica). Besides, the majority of these compounds demonstrate relevant activity (MIC50 equal to or below 2 mg/l) against Enterobacter spp., Citrobacter freundii, Serratia spp. and Morganella morganii. Ceftibuten is the most potent oral cephalosporin against most of the Enterobacteriaceae. Non-fermentative bacilli (Acinetobacter spp., Pseudomonas spp.) remain completely resistant to oral cephalosporins (except some Acinetobacter species against cefdinir and Pseudomonas cepacia against ceftibuten). Antistaphylococcal activity for oral cephalosporins is highest for cefdinir followed by BAY 3522, cefprozil, cefuroxime and cefpodoxime. Loracarbef, cefaclor and cefadroxil are about equally active, while the other compounds are only weakly active (cefixime) or inactive (cefetamet, ceftibuten). Enterococci are insensitive to new generation oral cephalosporins as they have been to established compounds. The most active oral cephalosporins against hemolytic streptococci are cefdinir and cefprozil. Streptococcus pneumoniae, Streptococcus milleri and Streptococcus mitior are most susceptible to cefpodoxime, cefdinir, cefuroxime and BAY 3522. Penicillin resistant pneumococci have to be regarded as resistant to all oral cephalosporins. Fastidious pathogens like Haemophilus spp., Moraxella catarrhalis and Neisseria gonorrhoeae are more susceptible to cefpodoxime, cefixime, cefdinir, cefetamet and ceftibuten than to the other oral cephalosporins. The activity of oral cephalosporins is only weak against Listeria spp., Helicobacter pylori and anaerobic pathogens (except BAY 3522). Bordetella pertussis remains resistant to all absorbable cephalosporins. Progress in antibacterial activity of oral cephalosporins was mainly achieved by cefpodoxime, cefixime, cefdinir, cefetamet and ceftibuten against Enterobacteriaceae and the fastidious pathogens and against staphylococci and the nonenterococcal streptococci by cefdinir, BAY 3522, cefprozil and cefpodoxime.
Infection
PMID:Antibacterial activity of cefpodoxime in comparison with cefixime, cefdinir, cefetamet, ceftibuten, loracarbef, cefprozil, BAY 3522, cefuroxime, cefaclor and cefadroxil. 180 Mar 77

The antimicrobial activity of cefpodoxime, the active metabolite of the new cephalosporin ester cefpodoxime proxetil, in comparison to cefixime, cefotiam, cefuroxime, and cefotaxime was determined against a broad spectrum of freshly isolated gram-positive and gram-negative bacterial strains. Cefpodoxime was demonstrated to be inhibitory at concentrations of less than or equal to 1 mg/l against 90% of strains of Moraxella catarrhalis, Haemophilus influenzae, Escherichia coli (beta-lactamase- negative strains), Klebsiella spp., Serratia spp., Proteus mirabilis, Proteus vulgaris, Providencia spp., and Salmonella spp. This antimicrobial activity of cefpodoxime was generally superior to that of cefuroxime and similar to that of cefixime. Cefpodoxime was active at less than or equal to 1 mg/l against 50% of the members of beta-lactamase-producing Escherichia coli, Enterobacter cloacae, Enterobacter aerogenes, Citrobacter spp., and Morganella morganii. Cefpodoxime proved to be highly inhibitory against group A, B, and G streptococci and Streptococcus pneumoniae (MIC90 less than 0.015 mg/l). The MICs of cefpodoxime and those of the other cephalosporins were less than 2 mg/l for greater than or equal to 90% of the strains of Staphylococcus aureus and Staphylococcus epidermidis, with the exception of cefixime which had no activity with MICs below 8 mg/l against these bacteria. Pseudomonas spp., Acinetobacter spp., and Enterococcus spp. were resistant to cefpodoxime. The antibacterial activity of cefpodoxime was only to a minor degree influenced by different growth conditions with the exception of high inoculum sizes against some beta-lactamase producing strains of gram-negative bacilli.(ABSTRACT TRUNCATED AT 250 WORDS)
Infection
PMID:Cefpodoxime: comparative antibacterial activity, influence of growth conditions, and bactericidal activity. 180 Mar 79

Blood and cerebrospinal fluid (CSF) concentrations of cefmenoxime were determined either microbiologically or by means of HPLC in 20 children with proven or suspected bacterial meningitis. Sixteen children suffered from bacterial meningitis: causative organisms were Haemophilus influenzae type b (n = 10), Streptococcus pneumoniae (n = 4) and Neisseria meningitidis (n = 2). In these patients the cefmenoxime concentration in the CSF ranged from 0.9 to 12.2 mg/l, with a mean concentration of 4.63 mg/l 1.5-3 h after the last intravenous cefmenoxime application and 24-48 h after initiating therapy with 200 mg cefmenoxime/kg/d in four doses. In eight cases the bactericidal titers of the CSF were examined during therapy. Titers between 1:64 and 1:2,048, exceeding the minimal bactericidal concentration, were found. After five doses of cefmenoxime 50 mg/kg, two CSF cultures showed bacterial growth: one H. influenzae (bactericidal titer in CSF 1:256) and one S. pneumoniae.
Infection
PMID:Cerebrospinal fluid penetration of cefmenoxime in children with bacterial meningitis. 181 11


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