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)

Fibrosing alveolitis is a rare, diffuse lung disease characterized by varying combinations of two histological features: thickening of alveolar walls and the presence of large mononuclear cells in the alveolar spaces. Clinical details of 10 children with fibrosing alveolitis are reported. The main symptoms in children are tachypnoea or dyspnoea, cough, poor weight gain, and cyanosis. The condition is similar to that in adults, but it is usually a more acute illness, and if untreated, more predictably fatal. Respiratory failure, pulmonary hypertension, and cardiac failure are the major complications. Less commonly, superimposed bacterial infection and pneumothorax occur. Chest x-rays often show a sequence of changes with a ground-glass appearance and fine mottling in the early stage of the disease, progressing to a picture of mainly hilar linear markings in those children who recover. The histological features at lung biopsy or necropsy are described; these correlated poorly with the radiological features, steroid responsiveness, and clinical course. Lung function tests in 3 older children showed evidence of markedly reduced lung volumes in 2. Static lung compliance in 4 children in the acute stage of the illness was normal in 3 and diminished in one. The response to steroid therapy was analysed in cases from the literature and the 10 reported cases. No spontaneous remissions occurred, all the survivors having been treated with corticosteroids. In children fibrosing alveolitis is almost always a corticosteroid-responsive disease. An appropriate course of prednisolone would be of at least 4 week's, but preferably of 8 weeks' duration, at a minimum daily dose of 2 mg/kg. After improvement the steroid withdrawal should be cautious and protracted, comprising at least a year's continuous treatment.
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PMID:Fibrosing alveolitis in infancy and childhood. 83 51

In a retrospective analysis of 2110 admissions to the pediatric intensive care unit, 564 cases of septic shock were identified (26.7% of the total admissions). Septic shock was defined in patients with: (1) clinical evidence of sepsis; (2) fever (greater than 38.3 degrees C) or hypothermia (less than 35.6 degrees C); (3) tachycardia; (4) tachypnea; and (5) inadequate organ perfusion. Inadequate perfusion was defined as hypotension or evidence of peripheral hypoperfusion (poor capillary refill or cyanosis with hypoxemia, oliguria, acidosis or altered mentation). Inotropic support was required to maintain an adequate blood pressure and perfusion in 268 of 564 patients (47.5%). Septic shock with confirmed bacterial infection occurred in 143 patients (143 of 564, 25.2%); these cases were caused by Haemophilus influenzae, type b (59 of 143, 41.3%), Neisseria meningitidis (26 of 143, 18.2%) and Streptococcus pneumoniae (16 of 143, 11.2%). Eight of 564 (1.4%) cases of septic shock were not clinically apparent on initial evaluation and were diagnosed within 24 hours after admission to the hospital. We conclude that septic shock occurs more frequently in children than previously appreciated and may develop after admission to the hospital.
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PMID:Septic shock in children: bacterial etiologies and temporal relationships. 233

Bacterial infections are frequent events in premature and newborn infants. The reason is a defective specific and nonspecific defence of bacterial organisms. Some immunoglobulins like IgM and IgA including secretory IgA are absent. Premature infants also show a decreased level of IgG. Cellular immunity is anatomically intact but functionally defective. A number of complement factors are lacking, the activation of the alternative pathway is impaired. Newborn infants with perinatal problems like asphyxia or difficult delivery, show defects of leucocyte function like decreased deformability, defective chemotaxis and defective killing of ingested bacteria. Certain diseases, like hypoxia and malformations of immature organ functions in this age group (decreased acid production in the stomach), facilitate bacterial colonization of surface epithelia and the invasion of tissues. Consequences of these pathogenetic mechanisms are an unimpaired propagation of bacterial organisms into the blood and meninges without localization of the infecting organisms at the entry site. Bacterial meningitis is not considered a separate disease entity but a complication of bacteremia and sepsis. Clinical symptoms are nonspecific at the onset of the infection. Fever is frequently absent; decreased appetite, vomiting, a bloated abdomen, diarrhea, tachycardia, tachypnea are early signs of a bacterial infection, a grey mottled appearance, cyanosis, jaundice, petechiae, apneic spells, seizure activity and a metabolic acidosis are symptoms of advanced infection. Successful treatment at this stage is often not possible. Every sign of a decreased well being of a newborn of premature infant warrants laboratory and bacteriologic work up for septicemia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Chemotherapy of severe bacterial infections in pediatrics]. 631 69

A major determinant of survival in patients with advanced viral or bacterial infection, or following severe trauma or burns complicated by multiple organ failure, is the combination of clinical signs termed the systemic inflammatory response syndrome (SIRS). SIRS is characterized by hypotension, tachypnea, hypo- or hyperthermia and leukocytosis as well as other clinical signs and symptoms, including a depression in myocardial contractile function. Heart failure complicating systemic sepsis or other causes of SIRS is usually not accompanied by coronary artery ischemia due to hypotension, myocardial necrosis, or marked cardiac interstitial inflammatory infiltrates, and thus the cause of cardiac contractile dysfunction in this syndrome has remained unclear. However, recent evidence has implicated an endogenous nitric oxide (NO) signalling pathway within cardiac myocytes and other cellular constituents of cardiac muscle, including the microvascular endothelium, as a possible contributor to the pathogenesis of heart failure in this syndrome. Cardiac myocytes are now known to express both constitutive NO synthase (cNOS) and inducible NO synthase (iNOS) activities. Activation of cNOS appears to modulate cardiac myocyte responsiveness to muscarinic cholinergic and beta-adrenergic receptor stimulation. Induction of iNOS by soluble inflammatory mediators, including cytokines, causes a marked depression in myocyte contractile responsiveness to beta-adrenergic agonists. Thus, inappropriate activation of cNOS or excessive or prolonged induction of iNOS in the myocardium may contribute to cardiac dysfunction complicating SIRS.
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PMID:Myocardial contractile dysfunction in the systemic inflammatory response syndrome: role of a cytokine-inducible nitric oxide synthase in cardiac myocytes. 753 82

The medical records of 53 horses with purpura haemorrhagica were reviewed. Seventeen of them had been exposed to or infected with Streptococcus equi, nine had been infected with Corynebacterium pseudotuberculosis, five had been vaccinated with S. equi M protein, five had had a respiratory infection of unknown aetiology, and two had open wounds; the other 15 cases had no history of recent viral or bacterial infection. The horses were between six months and 19 years of age (mean 8.4 years). The predominant clinical signs were well demarcated subcutaneous oedema of all four limbs and haemorrhages on the visible mucous membranes; other signs included depression, anorexia, fever, tachycardia, tachypnoea, reluctance to move, drainage from lymph nodes, exudation of serum from the skin, colic, epistaxis and weight loss. Haematological and biochemical abnormalities commonly detected were anaemia, neutrophilia, hyperproteinaemia, hyperfibrinogenaemia, hyperglobulinaemia and high activities of muscle enzymes. All of the horses were treated with corticosteroids; 42 also received non-steroidal anti-inflammatory drugs and 26 received antimicrobial drugs. Selected cases received special nursing care, including hydrotherapy and bandaging of the limbs. Most of the horses were treated for more than seven days and none of them relapsed. Forty-nine of the horses survived, one died and three were euthanased, either because their severe clinical disease failed to respond to treatment or because they developed secondary complications. Two of the four non-survivors had been vaccinated against S. equi with a product containing the M protein, one had a S. equi infection and the other had a respiratory infection of undetermined aetiology.
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PMID:Purpura haemorrhagica in 53 horses. 1291 29

Necrotising fascitiis is a rapidly progressive bacterial infection of the soft tissues and generally attacks the walls of the abdomen, the perineum, the limbs or, to a lesser degree, the cranio-cervical area. In the latter region, the infection involves the soft tissues of the neck, in a more or less extensive manner, and causes diffuse necrosis. Crepitation, areas with linear infiltration and others with fluctuation are detected on manual examination. Systemic symptoms such as fever, tachycardia, tachypnoea and signs of septic shock are always present, at least during the more advanced stages of the disease. Computed tomography may prove fundamental since it reveals an increase in the thickness and degree of impregnation of the cervical soft tissues, as well as the presence of liquid or gaseous infiltration in the thoracic areas, especially in cases of mediastinitis. Personal experience in a case is described which led to a review of the literature. The best approach in the management of this devastating condition is early diagnosis, adequate antibiotic treatment and radical surgical procedures, which may often need to be repeated several times.
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PMID:Cranio-cervical necrotizing fascitiis: case report and review of the literature. 1546 97

Infectious diseases belong to the most frequent reasons to seek emergency care. Life-threatening infectious emergencies, which require rapid diagnosis and hospitalisation, are, however, rare. Leading signs and symptoms are high fever combined with rapidly deteriorating general conditions, hypotonia, tachycardia, tachypnea, dyspnea, confusion, headache, or petechia or information about asplenia, immunosuppression or recent travel to the tropics. Life threatening situations, such as suspicion of invasive meningococcal infection or bacterial infection in an asplenic patient, septic-toxic shock, and acute bacterial meningitis with delayed hospitalisation require rapid start of empiric antibiotic therapy in the outpatient practice. In addition, acute infectious emergencies comprise situation for which post exposure prophylaxis is indicated.
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PMID:[Acute infectious emergencies in adults in medical practice]. 1599 31

Heart disease is among the leading causes of death in all populations. Cardiac dysfunctions are major complications in patients with advanced viral or bacterial infection, severe trauma and burns accompanied with multiple organ failure - collectively known as systemic inflammatory response syndrome (SIRS). SIRS, which is often subsequent to sepsis, is clinically featured by hypotension, tachypnea, hypo- or hyperthermia, leukocytosis and myocardial dysfunction. The striking association between inflammation and cardiac dysfunction not only prognoses likelihood of survival in patients with SIRS but also prompts the necessity of understanding the pathophysiology of cardiac dysfunction in SIRS, so that effective therapeutic regimen may be identified. Compelling evidence has shown significant and independent link among inflammation, sepsis, insulin resistance and cardiac dysfunction. Several cytokine signaling molecules have been speculated to play important roles in the onset of cardiac dysfunction under SIRS including endothelin-1 and toll-like receptor. Involvement of these pathways in cardiac dysfunction has been convincingly validated with transgenic studies. Nevertheless, the precise mechanism of action underscoring inflammation-induced cardiac contractile dysfunction is far from being clear. Given the substantial impact of inflammation and SIRS on health care, ecosystems and national economy, it is imperative to understand the cellular mechanisms responsible for cardiac contractile dysfunction under inflammation and sepsis so that new and effective therapeutic strategy against such devastating heart problems may be developed.
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PMID:A burning issue: do sepsis and systemic inflammatory response syndrome (SIRS) directly contribute to cardiac dysfunction? 1614 10

The aim of this study was to retrospectively review cases of cervical infection with descending mediastinitis, and to analyse the clinical character, diagnosis and treatment of this infection. Six patients were identified from December 1998 to June 2005. Their aetiology, associated systemic diseases, bacteriology, radiology, treatments and outcomes were reviewed. Four cases resulted from odontogenic infection, one from upper airway infection, and one had an unknown cause. Diffuse swelling in face and neck, chest distress, tachypnea, and fever were the main symptoms. Chest radiography showed a widening of the upper mediastinal shadow in four patients. Four patients underwent computed tomographic scanning that confirmed the diagnosis of descending mediastinitis, which suggests that routine use of this scan be highly recommended for early detection. Six different pathogens were identified through pus and blood culture. All patients underwent surgical drainage. Three patients received a tracheotomy. Of the six patients, four achieved good results, and there were two deaths. Early surgical drainage remains the main treatment for cervical infection with descending mediastinitis. Delayed diagnosis, inadequate drainage and multidrug-resistant bacterial infection were responsible for the deaths.
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PMID:Cervical infection with descending mediastinitis: a review of six cases. 1702 43

Sepsis, characterized by a systemic inflammatory state that is usually related to Gram-negative bacterial infection, is a leading cause of death worldwide. Although the annual incidence of sepsis is still rising, the exact cause of Gram-negative bacteria-associated sepsis is not clear. Outer membrane vesicles (OMVs), constitutively secreted from Gram-negative bacteria, are nano-sized spherical bilayered proteolipids. Using a mouse model, we showed that intraperitoneal injection of OMVs derived from intestinal Escherichia coli induced lethality. Furthermore, OMVs induced host responses which resemble a clinically relevant condition like sepsis that was characterized by piloerection, eye exudates, hypothermia, tachypnea, leukopenia, disseminated intravascular coagulation, dysfunction of the lungs, hypotension, and systemic induction of tumor necrosis factor-alpha and interleukin-6. Our study revealed a previously unidentified causative microbial signal in the pathogenesis of sepsis, suggesting OMVs as a new therapeutic target to prevent and/or treat severe sepsis caused by Gram-negative bacterial infection.
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PMID:Outer membrane vesicles derived from Escherichia coli induce systemic inflammatory response syndrome. 2059 24


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