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)

We have to consider the exacerbation of chronic obstructive pulmonary disease(COPD) may be caused not only by infection, but also by acute exacerbation of chronic heart failure, pulmonary embolism, pneumothorax, or other cardiopulmonary complications. Because it is characteristic that the exacerbation of COPD is often recurensive, the most important thing is the administration during stable status. Approximately 40% of pathogens of the acute infectious exacerbation of COPD are Haemophilus influenzae, Streptococcus pneumoniae, Moraxella catarrhalis, Pseudomonas aeruginosa, Staphylococcus aureus, and Echelisia coli. Also, approximately 15% is exacerbated by atypical pathogens such as Chlamydia pneumoniae and approximately 30% is by viral infection. We should contemplate the possibility of pathogens according to the statistics, when we choose antibiotics empirically.
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PMID:[Administration of acute exacerbation of chronic obstructive pulmonary disease]. 1467 28

The incidence of lower respiratory tract infection (LRTI) in women of child-bearing age is approximately 64 per 1000 population. The spectrum of illness ranges from acute bronchitis, which is very common, through influenza virus infection and exacerbations of underlying lung disease, to pneumonia, which, fortunately is uncommon (<1.5% LRTI), but can be severe. Acute bronchitis is generally mild, self-limiting and usually does not require antibacterial therapy. Influenza virus infection in pregnant women has been recently related to increased hospitalization for acute cardiorespiratory conditions. At present, the safety of the newer neuraminidase inhibitors for the treatment of influenza virus infection has not been established in pregnancy and they are not routinely recommended. In influenza virus infection complicated by pneumonia, antibacterial agents active against Staphylococcus aureus and Streptococcus pneumoniae superinfection should be used. There are few data on infective complications of asthma or COPD in pregnancy. The latter is rare, as patients with COPD are usually male and aged over 45 years. Management is the same as for nonpregnant patients. The incidence and mortality of pneumonia in pregnancy is similar to that in nonpregnant patients. Infants born to pregnant patients with pneumonia have been found to be born earlier and weigh less than controls. Risk factors for the development of pneumonia include anemia, asthma and use of antepartum corticosteroids and tocolytic agents. Based on the few available studies, the main pathogens causing pneumonia are S. pneumoniae, Haemophilus influenzae, Mycoplasma pneumoniae and viruses. Beta-Lactam and macrolide antibiotics therefore remain the antibiotics of choice in terms of both pathogen coverage and safety in pregnancy. In HIV-infected pregnant patients, recurrent bacterial pneumonia, but not Pneumocystis carinii pneumonia (PCP), is more common than in nonpregnant patients. Trimethoprim/sulfamethoxazole (cotrimoxazole) has not definitely been associated with adverse clinical outcomes despite theoretical risks. Currently it is still the treatment of choice in PCP, where mortality remains high. In conclusion, there are few data specifically related to pregnant women with different types of LRTI. Where data are available, no significant differences compared with nonpregnant patients have been identified. In considering the use of any therapeutic agent or investigation in pregnant patients with LRTI, safety aspects must be carefully weighed against potential benefit. Otherwise, management strategies should not differ from those for nonpregnant patients. Further research in this area is warranted.
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PMID:Treatment of community-acquired lower respiratory tract infections during pregnancy. 1472 4

The spread of antibacterial resistance in bacteria that commonly cause childhood community-acquired respiratory tract infections (RTIs), such as acute otitis media, community-acquired pneumonia, and acute pharyngitis, is a major healthcare problem. One of the foremost concerns is the rapid increase in penicillin, macrolide, and multidrug resistance in Streptococcus pneumoniae. There is also a rising prevalence of macrolide resistance in Streptococcus pyogenes in pockets of the United States, and beta-lactamase production in Haemophilus influenzae is widespread. Although data are limited, some evidence suggests that resistance to antibacterials can impair bacteriologic and clinical outcomes in childhood RTIs. Optimizing antibacterial use is important both in the care of individual patients and within strategies to address the wider problem of antibacterial resistance. This involves encouraging judicious antibacterial use (i.e., reducing overuse for viral infection and prophylaxis), and preventing misuse through the wrong choice, dosage, and duration of therapy. Given that initial therapy is usually empiric, antibacterials used to treat community-acquired RTIs in children should ideally have the following properties: an optimal targeted spectrum of activity; high clinical and bacteriologic efficacy against respiratory pathogens, including resistant strains; simple, short-course therapy; and good tolerability and palatability. New antibacterials will continue to have a role in the treatment of RTIs in children, especially where resistance compromises existing therapies.
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PMID:Optimizing antibacterial therapy for community-acquired respiratory tract infections in children in an era of bacterial resistance. 1502 37

Pharmacokinetic/pharmacodynamic parameters were used to interpret susceptibility data for the oral agents tested in a clinically meaningful way. Among S pneumoniae isolates, >99% were susceptible to respiratory fluoroquinolones, 91.6% to amoxicillin, 92.1% to amoxicillin/clavulanic acid (95.2% at the extended-release formulation breakpoint), 90.6% to clindamycin, 80.4% to doxycycline, 71.0% to azithromycin, 72.3% to clarithromycin, 71.8% to cefprozil and cefdinir, 72.6% to cefuroxime axetil, 66.3% to cexime, 63.7% to trimethoprim/sulfamethoxazole, and 19.7% to cefaclor. Among H influenzae isolates, 28.6% were b-lactamase positive, but virtually all were susceptible to amoxicillin/clavulanic acid (98.3%, with 99.8% at the extended-release formulation breakpoint), cexime (100%), and uoroquinolones (99.8%), whereas 93.5% were susceptible to cefdinir, 82.8% to cefuroxime axetil, 78.1% to trimethoprim/sulfamethoxazole, 70.2% to amoxicillin, 25.1% to doxycycline, 23.2% to cefprozil, and 5% to cefaclor, azithromycin and clarithromycin. Most isolates of M catarrhalis were resistant to amoxicillin, cefaclor, cefprozil, and trimethoprim/sulfamethoxazole. Thus significant b-lactam and macrolide/azalide resistance in Streptococcus pneumoniae and b-lactamase production and trimethoprim/sulfamethoxazole resistance in untypeable Haemophilus influenzae are still present. The results of this study should therefore be applied to clinical practice based on the clinical presentation of the patient, the probability of the patient's having a bacterial rather than a viral infection, the natural history of the disease, the potential of pathogens to be susceptible to various oral antimicrobial agents, the potential for cross-resistance between agents with S pneumoniae, and the potential for pathogens to develop further resistance. Antibiotics should be used judiciously to maintain remaining activity and chosen carefully based on activity determined by pharmacokinetic/pharmacodynamic-based breakpoints to avoid these bacteria developing further resistance, particularly to fluoroquinolones.
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PMID:Susceptibility of Streptococcus pneumoniae, Haemophilus influenzae, and Moraxella catarrhalis to 17 oral antimicrobial agents based on pharmacodynamic parameters: 1998-2001 U S Surveillance Study. 1517 51

Bacterial respiratory tract infections (RTIs), whether primary or subsequent to viral infection, are a frequent cause of morbidity and mortality worldwide. Treatment of these infections is most often empirical. Therefore, an antimicrobial's antibacterial spectrum must include the most likely pathogens: Streptococcus pneumoniae, the most frequent cause of community-acquired pneumonia (CAP), Haemophilus influenzae, Moraxella catarrhalis, and Staphylococcus aureus, as well as atypicals such as Mycoplasma pneumoniae, Legionella pneumophila and Chlamydophila (Chlamydia) pneumoniae. In addition, knowledge of antimicrobial resistance among these key pathogens is imperative for physicians to choose the most appropriate therapeutic agent. The latest data from global surveillance studies indicates that high-level resistance to penicillin (MIC > or =2 mg/l) among isolates of S. pneumoniae varies widely by geographic location. Rates exceed 20% in the USA, Mexico, Japan, Saudi Arabia, Israel, Spain, France, Greece, Hungary, and the Slovak Republic. In South Africa, Hong Kong, Taiwan, and South Korea rates exceed 50%. Penicillin non-susceptibility--including isolates exhibiting high-level resistance and intermediate susceptibility (MIC 0.12-1 mg/l)--is frequently found in association with macrolide resistance, which is found at a prevalence of 70-80% in some Asian countries. Trimethoprim-sulfamethoxazole (TMP-SMX) and tetracycline resistance, either individually or combined with macrolide resistance as multiple resistance, is also associated with reduced susceptibility to penicillin. Another concern about antimicrobial resistance in respiratory tract pathogens is beta-lactamase production among isolates of H. influenzae and M. catarrhalis. However, respiratory fluoroquinolones, of which levofloxacin has been available for the longest time, currently remain active against the great majority of common bacterial respiratory pathogens, including atypicals.
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PMID:Comparative antimicrobial susceptibility of respiratory tract pathogens. 1531 48

H9N2 influenza viruses are frequently isolated from chicken meat and bone marrow imported from China to Japan since 2001. These isolates were experimentally inoculated into specific pathogen-free chickens intranasally. Viruses were recovered from the meat and bone marrow of birds showing no overt signs. On the other hand, chickens co-infected with H9N2 virus and either Staphylococcus aureus or Haemophilus paragallinarum showed clinical signs severer than those shown by birds infected only with the virus alone or each of the bacteria alone. In addition, H9N2 viruses were more efficiently recovered from the chickens co-infected with S. aureus or H. paragallinarum than those from the birds infected with only the virus. The present results indicate that co-infection of H9N2 influenza virus with S. aureus or H. paragallinarum enhances the replication of the virus in chickens, resulting in exacerbation of the H9N2 virus infection.
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PMID:Co-infection of Staphylococcus aureus or Haemophilus paragallinarum exacerbates H9N2 influenza A virus infection in chickens. 1550 99

Progress in producing improved vaccines against bacterial diseases of cattle is limited by an incomplete understanding of the pathogenesis of these agents. Our group has been involved in investigations of two members of the family Pasteurellaceae, Mannheimia haemolytica and Haemophilus somnus, which illustrate some of the complexities that must be confronted. Susceptibility to M. haemolytica is greatly increased during active viral respiratory infection, resulting in rapid onset of a severe and even lethal pleuropneumonia. Despite years of investigation, understanding of the mechanisms underlying this viral-bacterial synergism is incomplete. We have investigated the hypothesis that active viral infection increases the susceptibility of bovine leukocytes to the M. haemolytica leukotoxin by increasing the expression of or activating the beta2 integrin CD11a/CD18 (LFA-1) on the leukocyte surface. In vitro exposure to proinflammatory cytokines (i.e. interleukin-1beta, tumor necrosis factor-alpha and interferon-gamma) increases LFA-1 expression on bovine leukocytes, which in turn correlates with increased binding and responsiveness to the leukotoxin. Alveolar macrophages and peripheral blood leukocytes from cattle with active bovine herpesvirus-1 (BVH-1) infection are more susceptible to the lethal effects of the leukotoxin ex vivo than leukocytes from uninfected cattle. Likewise, in vitro incubation of bovine leukocytes with bovine herpesvirus 1 (BHV-1) potentiates LFA-1 expression and makes the cells more responsive to leukotoxin. A striking characteristic of H. somnus infection is its propensity to cause vasculitis. We have shown that H. somnus and its lipo-oligosaccharide (LOS) trigger caspase activation and apoptosis in bovine endothelial cells in vitro. This effect is associated with the production of reactive oxygen and nitrogen intermediates, and is amplified in the presence of platelets. The adverse effects of H. somnus LOS are mediated in part by activation of endothelial cell purinergic receptors such as P2X7. Further dissection of the pathways that lead to endothelial cell damage in response to H. somnus might help in the development of new preventive or therapeutic regimens. A more thorough understanding of M. haemolytica and H. somnus virulence factors and their interactions with the host might identify new targets for prevention of bovine respiratory disease.
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PMID:Complexities of the pathogenesis of Mannheimia haemolytica and Haemophilus somnus infections: challenges and potential opportunities for prevention? 1598 39

Secondary bacterial infections often complicate respiratory viral infections, but the mechanisms whereby viruses predispose to bacterial disease are not completely understood. We determined the effects of infection with respiratory syncytial virus (RSV), human parainfluenza virus 3 (HPIV-3), and influenza virus on the abilities of nontypeable Haemophilus influenzae and Streptococcus pneumoniae to adhere to respiratory epithelial cells and how these viruses alter the expression of known receptors for these bacteria. All viruses enhanced bacterial adhesion to primary and immortalized cell lines. RSV and HPIV-3 infection increased the expression of several known receptors for pathogenic bacteria by primary bronchial epithelial cells and A549 cells but not by primary small airway epithelial cells. Influenza virus infection did not alter receptor expression. Paramyxoviruses augmented bacterial adherence to primary bronchial epithelial cells and immortalized cell lines by up-regulating eukaryotic cell receptors for these pathogens, whereas this mechanism was less significant in primary small airway epithelial cells and in influenza virus infections. Respiratory viruses promote bacterial adhesion to respiratory epithelial cells, a process that may increase bacterial colonization and contribute to disease. These studies highlight the distinct responses of different cell types to viral infection and the need to consider this variation when interpreting studies of the interactions between respiratory cells and viral pathogens.
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PMID:Respiratory viruses augment the adhesion of bacterial pathogens to respiratory epithelium in a viral species- and cell type-dependent manner. 1643 19

We report the clinical and histopathological features of four cases of pulmonary bacterial infections associated with extensive necrosis, which were fatal within a few hours (two cases of group A Streptococcus, one case of Staphyloccocus aureus and one case of Haemophilus influenzae infection). These bacterial infections are extremely severe conditions due to the production of necrotizing toxins. Histological findings are distinctive, showing extensive hemorrhagic necrosis, widespread layers of bacteria, and very few or no inflammatory cell components. These dramatic infections are extremely rare, occuring with no apparent underlying disease, both in immunodeficient and immunocompetent patients. The main differential diagnosis is a viral infection, difficult to diagnose on histological examination alone. The diagnosis is based on histological and microbiological results.
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PMID:[Histological diagnosis of lung bacterial necrotizing infections: a study of four fulminant cases]. 1649 88

Prevention of exacerbations of chronic obstructive pulmonary disease (COPD) can involve removing the cause or reducing the patient's vulnerability to the cause. This article addresses the following issues: What is the problem during an exacerbation, what are the causes of an exacerbation, what can prevent exacerbations, and who are we? The difference between a patient with COPD during an exacerbation and after recovery is small. It is unlikely that patients with early COPD experience less exposure to exacerbation causes than those with severe disease; it is just that the consequences are more severe for those with severe disease. Interventions that produce small absolute benefits can therefore have a disproportionately large effect on exacerbation reduction. Recognized causes include season, cold weather, pollution events, bacterial infection, viral infection, and treatment withdrawal. Countries with warmer climates have much larger mortality in cold weather than those with colder climates. Reducing exacerbations in more temperate climates may be altered as much by changes in clothing and bedroom heating as by changes in treatment. Taking more exercise in cold weather may be the underlying reason for the reduction of exacerbations after pulmonary rehabilitation. Influenza vaccination reduces influenza severity and reduces transmission from health care workers to patients. There are a number of pharmacologic interventions shown to reduce (the effect of) exacerbations, including inhaled corticosteroids, long-acting beta-agonists, long-acting anticholinergics, mucolytics, and perhaps antibiotics that reduce Haemophilus carriage. The effect of the bronchodilators is additive to inhaled corticosteroids; how far the other interventions are complementary is unclear. So far, we have had a very medical response to COPD exacerbations. Altering social and behavioral aspects is likely to be complementary.
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PMID:Prevention of exacerbations: how are we doing and can we do better? 1663 95


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