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)

Infections of the respiratory tract are among the most common causes for antibiotic prescribing. Their diagnosis within the community is generally limited to clinical criteria, and microbiological information is frequently lacking. Hospitalised patients with respiratory tract infections are more likely to undergo diagnostic sampling, but difficulties remain in reliably defining a microbial aetiology, thereby providing a confident basis for antibiotic selection. In considering the role of the cephalosporins in the treatment of respiratory tract infections, over 500 published articles have been reviewed. The pharmacokinetic considerations are discussed and the limitations of existing methodology are emphasised. Individual agents are reviewed by site of sepsis and conclusions are drawn from both comparative and non-comparative studies and in relation to currently recommended regimens. Although oral cephalosporins are widely used to treat upper respiratory tract infections, none is considered ideal, especially where Haemophilus influenzae is pathogenic. In the case of lower respiratory tract infections the beta-lactamase stable parenteral cephalosporins have become widely used to treat pneumonia in hospitalised patients, especially where Gram-negative enteric bacilli are of aetiological importance. However, the lack of activity of these drugs against Legionella spp., Mycoplasma pneumoniae and Coxiella burnetii must be emphasised. Another area of increasing use is in the treatment of infective exacerbations in patients suffering from cystic fibrosis of the lungs where Pseudomonas aeruginosa is pathogenic; ceftazidime in particular has proved a useful alternative to earlier antipseudomonal penicillin antibiotics.
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PMID:Treatment of respiratory tract infections with cephalosporin antibiotics. 331 1

Normally, the mucosa of the nasooropharynx, trachea, and, perhaps, the major bronchi is colonized with aerobic and anaerobic microbes. This epithelial surface coexists with the microbial flora and is not overgrown with it. Moreover, the physiologic functions of the mucosa--including a protective barrier, mucociliary clearance and humidification, and warming of respired air--are not impeded. How this flora is controlled and what is amiss when virulent or pathogenic bacteria can cause infection are fascinating questions. A balance is maintained during health in which epithelial cell integrity--a function of proper nutrition, available secretory immunoglobulins and glycoproteins, and ciliary motion--resists the microbe's attempt to attach via specialized receptors (pili) or by proteolytic destruction of local proteins. These interactions are reviewed in detail. When colonization is excessive and aspiration of more microbes into the lower airway occurs, infection is more probable. Certain bacteria such as Streptococcus pneumoniae and Hemophilus influenzae, which are associated with chronic bronchitis, illustrate a mechanism in which the host-microbial balance may be upset by selective impairment of a host protein, secretory IgA1. Alternatively, viral infection or cilotoxic microbes (mycoplasma) can favor colonization of bacteria when mucosal clearance mechanisms are impaired. Last, mucosal integrity can be breached by noxious gases or inflammation that may allow bacteria entry into the submucosal that provides a nidus for infection.
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PMID:Bacterial adherence to respiratory tract mucosa--a dynamic interaction leading to colonization. 332 Dec 69

Pneumonia is one of the most common causes of death from infectious disease in the United States. To examine the possible role of carbohydrates as adhesion receptors for infection, several pulmonary pathogenic bacteria were studied for binding to glycosphingolipids. Radiolabeled bacteria were layered on thin-layer chromatograms of separated glycosphingolipids, and bound bacteria were detected by autoradiography. The classic triad of infectious bacteria found in cystic fibrosis, Pseudomonas aeruginosa, Haemophilus influenzae, and Staphylococcus aureus, along with other bacteria commonly implicated in typical pneumonia, such as Streptococcus pneumoniae, Klebsiella pneumoniae, and certain Escherichia coli, bind specifically to fucosylasialo-GM1 (Fuc alpha 1-2Gal beta 1-3GalNAc beta 1-4Gal beta 1-4Cer), asialo-GM1 (Gal beta 1-3GalNAc beta 1-4Gal beta-1-4Galc beta 1-1Cer), and asialo-GM2 (GalNAc beta 1-4Gal beta 1-4Glc beta 1-1Cer). Bacteria maintained in nutrient medium bind better than the same cells suspended in buffer. They do not bind to galactosylceramide, glucosylceramide, lactosylceramide, trihexosylceramide, globoside, paragloboside, Forssman glycosphingolipid, or several other glycosphingolipids tested, including the gangliosides GM1, GM2, GM3, GD1a, GD1b, GT1b, and Cad. The finding that these pathogens do not bind to lactosylceramide suggests that beta 1-4-linked GalNAc, which is positioned internally in fucosylasialo-GM1 and asialo-GM1 and terminally in asialo-GM2, is required for binding. beta-N-Acetylgalactosamine itself, however, is not sufficient for binding, as the bacteria did not bind to globoside, which contains the terminal sequence GalNAc beta 1-3Gal. These data suggest that these bacteria require at least terminal or internal GalNAc beta 1-4Gal sequences unsubstituted with sialyl residues for binding. Other bacteria, including Mycoplasma pneumoniae, Streptococcus pyogenes, Salmonella species, and some E. coli, do not bind to the GalNAc beta 1-4Gal sequence. The biological relevance of these data is suggested by our finding that substantial amounts of asialo-GM1 occur in human lung tissue.
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PMID:Many pulmonary pathogenic bacteria bind specifically to the carbohydrate sequence GalNAc beta 1-4Gal found in some glycolipids. 341 84

The penetration of ofloxacin into bronchial secretions was evaluated in 16 patients after administration of a single oral dose of ofloxacin 400mg. Bronchial secretions were aspirated at bronchoscopy after 1 to 6 hours and serum was collected simultaneously. Ofloxacin concentrations were measured by a microbiological assay method. Considerable individual variations in serum and bronchial aspirate concentrations were recorded: bronchial aspirate concentrations varied between 1.1 mg/L and 4.5 mg/L but exceeded 1.5 mg/L in 14 of 16 patients between 1 and 6 hours. The ratio between simultaneous mean bronchial aspirate and serum concentrations ranged between 0.53 in the second hour and 0.92 in the fourth hour. It is likely that inhibitory activity will be sustained over at least 6 hours against most potential respiratory pathogens including Haemophilus influenzae, Branhamella catarrhalis, Gram-negative bacilli, Staphylococcus aureus, Legionella pneumophila and Mycoplasma pneumoniae. Streptococcus pneumoniae and Pseudomonas aeruginosa may have minimal inhibitory concentration (MIC) values lower than ofloxacin concentrations achieved in bronchial secretions, although some isolates are less sensitive. Clinical studies should establish the relevance of pharmacokinetic data to respiratory infections caused by organisms of borderline susceptibility.
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PMID:Penetration of ofloxacin into bronchial secretions. 348 25

Two immunochemical methods were used to identify Haemophilus influenzae and Streptococcus pneumoniae capsular antigens in the urine and serum of 162 children with acute lower respiratory tract infection. These methods were compared with standard bacterial blood culture. Viral and mycoplasma cultures of respiratory secretions were obtained simultaneously to determine the frequency of antigenuria at the time of nonbacterial acute lower respiratory tract infection. Urine from groups of well children and children with acute otitis media was tested for capsular antigens to determine the incidence of antigenuria. Antigenuria was found in 24% of children 2 months to 18 years of age with acute lower respiratory tract infection compared with a 2% incidence of bacteremia. Antigenuria was found in 4% of asymptomatic children and 16% of children with acute otitis media. One third of children with symptoms of acute lower respiratory tract infection and viral isolates from the oropharynx had bacterial antigenuria. The sixfold increase in frequency of bacterial antigenuria in children at the time of lower respiratory symptoms suggests that bacterial acute lower respiratory tract infection may be more common than identified by traditional culture techniques. Because bacterial antigen may come from other sites such as the middle ear, further studies are needed to determine the role of antigen detection in the diagnosis of pediatric acute lower respiratory tract infection.
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PMID:Use of bacterial antigen detection in the diagnosis of pediatric lower respiratory tract infections. 348 70

The activity of roxithromycin was determined by a microdilution method, in comparison with erythromycin, spiramycin and josamycin. Roxithromycin and erythromycin showed very similar MICs against staphylococci, Streptococcus pneumoniae, Str. pyogenes and Haemophilus influenzae. In most cases, spiramycin and josamycin appeared similarly or more active. The activity of roxithromycin against Mycoplasma pneumoniae, Legionella spp., Chlamydia psittaci and, to some extent, against Pasteurella spp. was also assessed, by suitable in-vitro methods. Roxithromycin has a promising potential for treating selected skin and respiratory infections.
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PMID:In-vitro activity of roxithromycin against respiratory and skin pathogens. 350 24

The folate inhibitor trimethoprim (TMP) is active against and potentially cidal to a few higher microorganisms and a wide spectrum of pathogenic bacteria except for Bacteroides, Branhamella, Brucella, Chlamydia, Clostridium, Mycobacterium, Mycoplasma, Nocardia, Neisseria, Pseudomonas and Treponema. These organisms tend to be more sensitive to sulfonamides (SUL) than to TMP, whereas TMP is 10- to 100-fold more active than SUL against most other bacteria. Synergy between TMP and SUL occurs at drug concentrations equal to or less than their respective MICs and is often seen in vitro with isolates that are sensitive or moderately resistant to one or both of the components. Synergy occurs over a wide range of ratios between TMP and SUL, the optimal being that between their respective MICs when acting singly. In vitro synergy is more impaired by bacterial resistance than by suboptimal TMP:SUL ratios. The vast majority of clinical isolates of Haemophilus, staphylococci, streptococci and enteric bacteria are inhibited in vitro by the minimum concentrations of drug attained in plasma during therapy. Exceptions are found among Enterobacter, Citrobacter, Serratia, Proteus and in particular Klebsiella where SUL resistance is common and isolates with TMP MICs of 5 mg/l or more may occur and lead to failure of TMP-SUL therapy in systemic infections. In the urinary tract drug concentrations that are synergistic and therefore inhibitory in vitro against isolates moderately resistant to SUL (MIC less than or equal to 1 g/l) and/or TMP (MIC less than or equal to 0.1 g/l) are present during TMP-SUL therapy. However, whether the synergy and the bactericidal effect of TMP-SUL observed in vitro play a role in vivo is controversial.
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PMID:The antimicrobial activities of trimethoprim and sulfonamides. 351 8

Comparisons were made in the mortality associated with an inhaled dose of viable Haemophilus pleuropneumoniae type 5, strain J45, between adult C3H/HeN and C3H/HeJ mice. Mice of both strains were also challenged with Escherichia coli strains O111:B4 and J5. The 50% lethal dose (LD50) of H. pleuropneumoniae in C3H/HeN mice was calculated to be 10(6.5) CFU. At a mean dose of 10(6.7) CFU a 46% mortality rate occurred in C3H/HeN mice, whereas only 10% of the C3H/HeJ mice died (P less than 0.01). Deaths occurred significantly earlier in C3H/HeN mice (P less than 0.01). No deaths occurred later than 12 h postinfection in either group. Pulmonary lesions in the mice that died were similar to those in pigs that die during the acute phase of H. pleuropneumoniae infection. In surviving mice of both strains, a mild resolving interstitial and bronchopneumonia was present which was not typical of subacute H. pleuropneumoniae infections in swine. Quantitative bacterial isolations from the lungs, liver, and spleen indicate that H. pleuropneumoniae did not multiply in the lungs, was rapidly cleared, and did not become systemic. No deaths occurred in the mice inoculated with E. coli J5 or O111:B4 at mean doses of 10(6.3), 10(7.2), and 10(8.5) CFU, and 10(6.4), 10(7.5), and 10(8.2) CFU, respectively. The difference in the mortality rate between the C3H/HeN and C3H/HeJ mice suggests that endotoxin may be involved in acute deaths in pigs infected with H. pleuropneumonia. As indicated by the E. coli challenge, however, other factors are also likely to be involved. Because of the differences in the pathology and microbiology following H. pleuropneumoniae pulmonary infections in mice and pigs, mice do not appear to be an accurate model of the overall disease in swine.
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PMID:Resistance of C3H/HeJ mice to the effects of Haemophilus pleuropneumoniae. 352 83

During a 14-month study period, 92 patients admitted to the University Clinic for Infectious Diseases with pneumonia were investigated to determine the prevalence and severity of Legionnaires' disease (LD). The diagnosis of LD was based on positive serology. Antibodies to 10 different legionella antigens--Legionella pneumophila serogroups 1-6, Fluoribacter (Legionella) bozemanae, F. dumoffii, F. gormanii, and Tatlockia (Legionella) micdadei--were measured by the microagglutination (MA) and indirect fluorescent antibody (IFA) techniques. LD was diagnosed in 22 patients showing a 4-fold or greater rise of MA titers. 10 patients showed a 4-fold or greater rise of IFA titer, 2 had standing high titer. One patient died. Legionella infection was the second most common cause of pneumonia. However, in half of the cases legionella infection occurred concomitantly with Streptococcus pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae, Chlamydia psittaci, or viral infections. All 22 LD cases were sporadic. LD had been contracted abroad by 6 patients. Two of the legionella pneumonias were hospital-acquired. Half of the LD patients were older than 60 years. The majority of cases occurred during the winter months. Neither clinical chemistry parameters nor clinical features could distinguish LD from other types of pneumonia.
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PMID:Prevalence of Legionnaires' disease in pneumonia patients admitted to a Danish department of infectious diseases. 353 3

A single bolus of either Escherichia coli endotoxin, sonicated suspension of Haemophilus pleuropneumoniae, or pyrogen-free normal saline was intratracheally instilled in six week old specific-pathogen-free pigs. Pigs exposed to E. coli endotoxin developed fever, leukopenia followed by leukocytosis, and endotoxemia. Leukocytosis was the only clinical abnormality noted in pigs receiving the sonicated suspension of H. pleuropneumoniae. At one day postexposure, focal areas of atelectasis and consolidation were observed in the caudal lung lobes of animals receiving either E. coli endotoxin or the sonicated suspension of H. pleuropneumoniae. Lesions were characterized by a neutrophilic bronchitis and bronchiolitis with alveolitis in the surrounding tissue. Increased numbers of alveolar macrophages and evidence of phagocytosis were observed by light and electron microscopy. No clinical abnormalities or lesions were observed in animals receiving normal saline. Lesions typical of acute porcine Haemophilus pleuropneumonia were not produced by either E. coli endotoxin or sonicated suspension of H. pleuropneumoniae, indicating that multiple virulence factors are probably involved in lesion development.
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PMID:Acute inflammatory effects of intratracheally instilled Escherichia coli endotoxin and sonicated suspension of Haemophilus pleuropneumoniae in swine. 353 96


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