Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Pathogenic Escherichia coli are responsible for a variety of diseases, including diarrhoea, haemolytic uraemic syndrome, kidney infection, septicaemia, pneumonia and meningitis. Toxins called cytotoxic necrotizing factors (CNFs) are among the virulence factors produced by uropathogenic (CNF1) or enteropathogenic (CNF2) E. coli strains that cause diseases in humans and animals, respectively. CNFs induce an increase in the content of actin stress fibres and focal contacts in cultured cells. Effects of CNFs on the actin cytoskeleton correlated with a decrease in the electrophoretic mobility of the GTP-binding protein Rho and indirect evidence indicates that CNF1 might constitutively activate Rho. Here we show that CNF1 catalyses the deamidation of a glutamine residue at position 63 of Rho, turning it into glutamic acid, which inhibits both intrinsic GTP hydrolysis and that stimulated by its GTPase-activating protein (GAP). Thus, this deamidation of glutamine 63 by CNF1 leads to the constitutive activation of Rho, and induces the reorganization of actin stress fibres. To our knowledge, CNF1 is the first example of a bacterial toxin acting by deamidation of a specific target protein.
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PMID:Toxin-induced activation of the G protein p21 Rho by deamidation of glutamine. 919 1

Disease associations of human T lymphotropic virus types I and II (HTLV-I and -II) infection were studied in 154 HTLV-I-infected, 387 HTLV-II-infected, and 799 uninfected blood donors. Adjusted odds ratios (ORs) and 99% confidence intervals (CIs) were derived from logistic regression models controlling for demographics and relevant confounders. All subjects were human immunodeficiency virus type 1-seronegative. HTLV-II was significantly associated with a history of pneumonia (OR, 2.6; 99% CI, 1.2-5.3), minor fungal infection (OR, 2.9; 99% CI, 1.2-7.1), and bladder or kidney infection (OR, 1.6; 99% CI, 1.0-2.5) within the past 5 years and with a lifetime history of tuberculosis (OR, 3.9; 99% CI, 1.3-11.6) and arthritis (OR, 1.8; 99% CI, 1.2-2.9). Lymphadenopathy (> or =1 cm) was associated with both HTLV-I (OR, 6.6; 99% CI, 2.2-19.2) and HTLV-II (OR, 2.8; 99% CI, 1.1-7.1) infection, although no case of adult T cell leukemia/lymphoma was diagnosed. Urinary urgency and gait disturbance were associated with both viruses. This new finding of increased prevalence of a variety of infections in HTLV-II-positive donors suggests immunologic impairment.
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PMID:Increased prevalence of infectious diseases and other adverse outcomes in human T lymphotropic virus types I- and II-infected blood donors. Retrovirus Epidemiology Donor Study (REDS) Study Group. 939 56

Five out of nine consecutive patients with HIV-related visceral aspergillosis observed by us since 1984 were diagnosed only at necropsy examination. The histopathological features of these five patients [two with isolated pneumonia, one with central nervous system (CNS) involvement, one with brain abscess and respiratory disease and one with pulmonary, pleural and kidney infection] have been evaluated according to epidemiological, clinical and radiological features. On the basis of our experience, life-threatening aspergillosis, which is often misdiagnosed or missed in the setting of HIV infection and AIDS, should be suspected in patients with far-advanced underlying disease and unexplained signs and symptoms, even in the absence of some presumed risk factors (i.e. neutropenia and prior steroid treatment). Plain chest radiography and bronchoscopy with broncholaveolar lavage may fail to reveal respiratory disease, CNS aspergillosis is not necessarily associated with suggestive neuroradiological features and disseminated disease may present with multiorgan failure. The unfavorable outcome of this emerging AIDS complication can be improved only by earlier diagnosis based on invasive techniques and appropriate and timely treatment.
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PMID:AIDS-related visceral aspergillosis: an underdiagnosed disease during life? 991 86

The unexpected occurrence of a fever higher than 38 degrees Celsius at least twice in 48 hours after childbirth is a common problem. A well-executed clinical examination of a patient with a high fever is necessary to determine the origin of the infection. It is necessary to remain vigilant because it could be a sign of severe infection threatening a mother's life. The fever can sometimes remain moderate while the infection progresses at lightning speed. This is especially the case in weak patients (e.g., those with tuberculosis, AIDS, or malnutrition); thus it will be necessary to keep an attentive eye on them. Major causes to be familiar with and to recognize include malaria (always to be considered), uterine infection (the most common postpartum infection), kidney infection, tender breasts, pneumonia, meningitis, or appendicitis. Things health workers should consider if they suspect uterine infection are birth history, endometritis, and the fact that, in the absence of treatment, the infection can spread to the Fallopian tubes and eventually to the general circulation (septicemia). Special cases include uterine infections accompanied by retention of placental debris or membranes, fever after abortion, and fever after cesarean section. Health workers must consider all cases of retention, even those without a fever, as a potential infection. They must administer antibiotic treatment within 5 days after emptying the uterus. The treatment of choice for fever following an abortion is 3 g ampicillin for 7 days. In cases of infection after an abortion, health workers should consider uterine perforation and retention. Fever usually occurs 4-5 days after a cesarean section. Antibiotic treatment is usually necessary.
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PMID:[Postpartum infections]. 1234 37

Human T-lymphotropic virus types I and II (HTLV-I and -II) cause myelopathy; HTLV-I, but not HTLV-II, causes adult T-cell leukemia. Whether HTLV-II is associated with other diseases is unknown. Using survival analysis, we studied medical history data from a prospective cohort of HTLV-I- and HTLV-II-infected and -uninfected blood donors, all HIV seronegative. A total of 152 HTLV-I, 387 HTLV-II, and 799 uninfected donors were enrolled and followed for a median of 4.4, 4.3, and 4.4 years, respectively. HTLV-II participants had significantly increased incidences of acute bronchitis (incidence ratio [IR] = 1.68), bladder or kidney infection (IR = 1.55), arthritis (IR = 2.66), and asthma (IR = 3.28), and a borderline increase in pneumonia (IR = 1.82, 95% confidence interval [CI] 0.98 to 3.38). HTLV-I participants had significantly increased incidences of bladder or kidney infection (IR = 1.82), and arthritis (IR = 2.84). We conclude that HTLV-II infection may inhibit immunologic responses to respiratory infections and that both HTLV-I and -II may induce inflammatory or autoimmune reactions.
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PMID:Respiratory and urinary tract infections, arthritis, and asthma associated with HTLV-I and HTLV-II infection. 1507 5

Sepsis represents a clinical syndrome following an infection and it is characterized by classical signs of systemic inflammatory response syndrome (SIRS): fever or ipothermia, tachycardia, tachipnea, leucocytosis or leucopenia. There may also be symptoms related to a specific infection such as a cough in pneumonia or burning with urination in a kidney infection, and abdominal pain in an intraabdominal sepsis. Common locations for the primary infection include lungs, brain, urinary tract, skin and soft tissues, and mainly abdominal organs. Patients who develop sepsis have an increased risk of complications and death and face higher healthcare costs and longer treatment. The infection is caused most commonly by bacteria, but can also be by fungi, viruses, or parasites. Severe sepsis is sepsis causing poor organ function or insufficient blood flow; septic shock is the situation with ipotension and/or need for high dosage of inotropes or vasopressors and multiple organ failure syndrome is when multiple organ dysfunction or failure is present. Outcomes depend on the severity of disease with the risk of death from sepsis being as high as 30%, severe sepsis as high as 50%, and septic shock as high as 80%. Prevention, early diagnosis, and treatment, both medical (antibiotics) and surgical (source control), together with the prompt intensive care and organ support are crucial to increase survival rate.
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PMID:[Surgical sepsis]. 2575 9