Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0004623 (bacterial infection)
 15,226 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Anorexia is a common symptom accompanying infections, but the teleology of the phenomenon remains unexplained. We hypothesize that anorexia may represent a prehistoric behavioral adaptation to fight infection by maintaining T helper (Th)2 bias, which is particularly vital in fighting bacterial pathogens. Specifically, we propose that anorexia may avert the reduction of Th2/Th1 ratio by preventing feeding-induced neurohormonal and vagal output from the gut. Emerging evidence suggests that the vagal and neurohormonal output of the gut during feeding promotes Th1 function, which is desirable in fighting viral infections. Since fever may be an adaptation to fight bacteria and "colds" are generally viral in origin, the adage "starve a fever and feed a cold" may reflect a sensible behavioral strategy to tilt autonomic and Th balance in directions that are optimal for fighting the particular type of infection. The ability to modulate T helper balance through the neurohormonal and autonomic axis by adjusting food intake may be the mechanism behind other unexplained clinical observations such as the improved outcomes of ICU patients after enteric versus parenteric feedings. Compared to the prehistoric period when bacterial infection was commonplace, the anorexic response may be less adaptive today when viruses and cancers have become common triggers of anorexia. By promoting host anorexia, cachexia, and insomnia, cancers and viruses can deter behaviors such as digestion and sleep that would raise vagal and Th1 activity against tumors and viruses. Hydration and sleep, unexplained but widely accepted recommendations for flu patients, may also work by promoting vagal and Th1 functions. Modulating feeding, hydration, and sleep may prove beneficial in treating other conditions associated with abnormal autonomic and Th balance.
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PMID:"Starve a fever and feed a cold": feeding and anorexia may be adaptive behavioral modulators of autonomic and T helper balance. 1582 88

This study describes an epizootic of respiratory tract disease caused by influenza virus infection in a large population of equines in Luxor and Aswan, Upper Egypt, during the winter of 2000. The epizootic started in January and the infection rate reached its peak in February before gradually decreasing until the end of April, 2000. Horses, donkeys and mules of all ages and both sexes were affected. Free movement of the infected equines and direct contact between the animals at markets facilitated the rapid spread of the disease. The cause of the epizootic was established by use of serological testing and the identification of the influenza virus in nasal secretions. Egg inoculation and the haemagglutination test were used to detect the influenza virus. Both haemagglutination inhibition (HI) and agar gel precipitation tests were performed to identify the isolated influenza virus using reference antisera against A/Equi-1 (H7N7) and A/Equi-2 (H3N8). Antibodies against the equine influenza virus were demonstrated in 416 (95.6%) out of 435 collected sera using the HI test. High rectal temperature, inappetence, conjunctivitis, redness of nasal mucosa, a serous to mucopurulent nasal discharge and a harsh dry cough were the most common clinical manifestations. Stress factors, such as using equines for heavy transportation and drawing, precipitated the onset of the disease, intensified the clinical syndrome, delayed recovery and facilitated secondary bacterial infection. The present study suggested that the absence of a vaccination programme against equine influenza was one of the principal causes of the spread of infection during this outbreak. In conclusion, the implementation of a national equine influenza vaccination programme, using an effective updated vaccine, is essential in Egypt.
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PMID:An epizootic of equine influenza in Upper Egypt in 2000. 1586 87

IFN-alpha/beta plays an essential role in innate immunity against viral and bacterial infection. Among the proteins induced by IFN-alpha/beta are the ubiquitin-like ISG15 protein and its E1- (Ube1L) and E2- (UbcH8) conjugating enzymes, leading to the conjugation of ISG15 to cellular proteins. It is likely that ISG15 conjugation plays an important role in antiviral response because a human virus, influenza B virus, inhibits ISG15 conjugation. However, the biological function of ISG15 modification remains unknown, largely because only a few human ISG15 target proteins have been identified. Here we purify ISG15-modified proteins from IFN-beta-treated human (HeLa) cells by using double-affinity selection and use mass spectroscopy to identify a large number (158) of ISG15 target proteins. Eight of these proteins were subjected to further analysis and verified to be ISG15 modified in IFN-beta-treated cells, increasing the likelihood that most, if not all, targets identified by mass spectroscopy are bona fide ISG15 targets. Several of the targets are IFN-alpha/beta-induced antiviral proteins, including PKR, MxA, HuP56, and RIG-I, providing a rationale for the inhibition of ISG15 conjugation by influenza B virus. Most targets are constitutively expressed proteins that function in diverse cellular pathways, including RNA splicing, chromatin remodeling/polymerase II transcription, cytoskeleton organization and regulation, stress responses, and translation. These results indicate that ISG15 conjugation impacts nuclear as well as cytoplasmic functions. By targeting a wide array of constitutively expressed proteins, ISG15 conjugation greatly extends the repertoire of cellular functions that are affected by IFN-alpha/beta.
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PMID:Human ISG15 conjugation targets both IFN-induced and constitutively expressed proteins functioning in diverse cellular pathways. 1600 40

In April 2004, two patients were admitted to hospital in Berlin, Germany, with clinical signs of acute respiratory infection after returning from a military exercise in their home country of Turkey. They were admitted to a high security infectious disease unit as epidemiological data pointed to an outbreak of unknown etiology. Samples taken at the time of admission proved to be strongly positive for Adenovirus by PCR, but negative for Influenza A/H1N1 virus, Influenza A/H3N2 virus, Influenza B virus, Respiratory syncytial virus, and SARS coronavirus. No evidence for bacterial infection was obtained by serological tests and blood cultures. The adenovirus detected was characterized further by genotyping and was identified as a species B2 virus with the highest similarity to adenovirus type 11a.
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PMID:Respiratory disease caused by a species B2 adenovirus in a military camp in Turkey. 1612 80

The expression of the Fcgamma-receptor I (FcgammaRI), CD64 on normal neutrophils is up-regulated during bacterial infections. CD64 is a promising diagnostic tool in the diagnosis of acute infections. The aim was to study surface expressions of CD64 on neutrophils and monocytes in patients with influenza A with and without complications and evaluate these as diagnostic tools in comparison with serum levels of HNL (human neutrophil lipocalin). CD64 expression on neutrophils and monocytes was evaluated by flow cytometry. HNL was assayed by a specific radioimmunoassay. 22 patients with influenza A with or without complications were included and the results compared with those of 29 patients with acute bacterial infections and 29 healthy subjects. Neutrophil expression of CD64 was increased in influenza A with raised proportion expressing CD64 in complicated compared to uncomplicated influenza. The expression was significantly higher in bacterial infections compared to both influenza groups. Serum levels of HNL were raised in all infection groups, but significantly more so in the group with bacterial infection. ROC-curve analysis showed that neutrophil expression of CD64 and the serum levels of HNL had similar diagnostic power in the discrimination between acute bacterial infections and influenza A. Monocyte expression of CD64 was raised in all infections with no differences between subgroups. We conclude that neutrophil expression of CD64 and serum levels of HNL are both promising assays in the distinction between infections caused by bacteria or influenza A, whereas CD64 could identify patients with complications of their influenza A infection.
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PMID:Cell surface expression of FcgammaRI (CD64) on neutrophils and monocytes in patients with influenza A, with and without complications. 1630 25

Children born without a spleen or who have impaired splenic function, due to disease or splenectomy, are at significantly increased risk of life-threatening bacterial sepsis. The mainstays of prevention are education, immunization, and prophylactic antibiotics. The availability of conjugate 7-valent pneumococcal vaccines for use in children to age 9 years at least, as well as conjugate meningococcal C vaccine in some countries, for use beginning in infancy, appear to represent beneficial additions, but not substitutions, to previous recommendations for the use of polysaccharide 23-valent pneumococcal and quadrivalent A, C, Y, W-135 vaccines. Routine immunization against H. influenzae type b should continue with non-immunized children older than age 5 years receiving two doses 2 months apart, similar to children who have not previously received conjugate pneumococcal vaccine in infancy. Annual influenza immunization, which reduces the risk of secondary bacterial infection, is also recommended for asplenic children and their household contacts. Many experts continue prophylaxis indefinitely although prophylaxis of the penicillin allergic child remains suboptimal.
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PMID:The prevention and treatment of bacterial infections in children with asplenia or hyposplenia: practice considerations at the Hospital for Sick Children, Toronto. 1633 16

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

Current data concerning epidemiology, clinical picture, pathogenesis, prevention and treatment of Avian influenza H5N1, data of pharmacodynamics and pharmacokinetics of antiviral drugs--neuraminidase inhibitors and M2 channels inhibitors, also the recommendation of WHO for prevention prevalence of infection were discussed in the review. Strategic measures of WHO aims to protect humans from contact with infected poultry, in case of contact, to prevent transmission of this infection from human to human and occurrence of pandemic. Infected birds were the major source of the H5N1 influenza virus among humans in Asia. Mainly humans became infected by eating infected birds, by poor hygiene procedures when cooking infected birds, or by close contact with infected poultry. At present transmission of the H5N1 influenza from human to human by aerosol way hasn't been registered, but ongoing monitoring for identification mutation and adaptation of H5N1 influenza virus to human is needed. Season influenza and avian H5N1 influenza differ by the ways of transmission, clinical picture, severity, pathogenesis, response to treatment. Diagnostic of infection is difficult due to non-specific initial symptoms, in most cases disease begins with disturbance of under respiratory ways and in rare cases--from upper respiratory ways. High viral titre is identified in pharynx but not in nose. Initial symptoms of the H5N1 influenza are: fever greater then 38 degrees Celsius, mild cold, cough and shortness of breath, practically all patient have viral pneumonia, later secondary bacterial infection occurs, mild to severe respiratory distress, diarrhea, vomiting and abdominal pain. Conjunctivitis is rarely diagnosed contrary to season influenza. Sometimes gastrointestinal disorder begins a week early then respiratory symptoms. Complication also includes renal and multi organ failure. The cytokine storm is commonly developed during H5N1 influenza. For treatment and for prevention (under certain conditions) of the H5N1 influenza neuraminidase inhibitors such as oseltamivir (Tamiflu) and zanamivir (Relenza) are recommended. Currently circulatory of the H5N1 strains are fully resistant to an older class of antiviral drugs--the M2 channels inhibitors (amantadine and rimantadine). The knowledge of epidemiology, pathogenesis, clinical picture, treatment of the H5N1 influenza in humans, in spite of progress isn't complete. Future coordination of scientific investigation of the H5N1 influenza in humans should be provided not only in the countries where infection was revealed, but all around the world.
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PMID:[Epidemiology, clinical picture, prevention and treatment of Avian influenza]. 1657 38

Acute respiratory bacterial infection is the most common complication of influenza and a leading cause for excess rate of outpatient visits, hospitalization, and death (pneumonia). Influenza promotes bacterial infection as stated by epidemiologic evidence of temporal association between outbreaks or peaks of both influenza and bacterial pneumonia. The bacteria involved are Streptococcus pneumoniae, Haemophilus influenzae, Staphylococcus aureus. However, Gram-negative rods, Klebsiella pneumoniae, Pseudomonas aeruginosa, anaerobes and methicillin resistant S. aureus may be involved in institutionalized elderly patients. Various studies confirm that antibiotics are over-prescribed in patients with influenza or influenza like illness, even in the absence of bacterial infection signs, and in patients without comorbidity. No data has proven the benefice of antibiotic prescription in influenza-infected patients without bacterial infection. Neuraminidase inhibitors may be of interest for the management of influenza infected patients, because they can decrease the risk of bacterial complications and the use of antibiotics.
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PMID:[Using antibiotics in case of influenza]. 1660 May 51

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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