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)

We conducted a case-control study to determine the incidence and clinical features of and risk factors for Pseudomonas aeruginosa infections in patients infected with human immunodeficiency virus (HIV). Twenty-five patients who had 37 episodes of P. aeruginosa infection from 1990 through 1992 were identified. Most of the patients (92%) were homosexual men with low CD4+ lymphocyte counts and a history of AIDS. The annual incidence rates of P. aeruginosa infection were 3.5% (1990), 6.3% (1991), and 8.7% (1992). Most infections were community-acquired (68%) and involved the respiratory tract (73%). Patients were more likely than HIV-infected controls to have AIDS and had more AIDS-defining opportunistic illnesses. The overall mortality was 36%. Recurrent episodes were common (39%). We conclude that P. aeruginosa infections may be an increasing problem in patients with extremely advanced HIV infection. Clinicians should consider including antibiotics with activity against P. aeruginosa in the empirical treatment for suspected bacterial infection in patients with advanced HIV infection.
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PMID:Serious Pseudomonas aeruginosa infections in patients infected with human immunodeficiency virus: a case-control study. 781 59

Otherwise infrequent, infections by non-tuberculous or atypical mycobacteria are now rising in AIDS. Infection with the Mycobacterium avium complex (MAC) is now the most frequent opportunistic bacterial infection, because of better detection of HIV positive patients. The incidence, which is probably underestimated, is now 14-33% in France. The Mycobacterium avium complex is responsible for 96% of infections by atypical mycobacteria in AIDS patients. Diagnosis of infection by MAC is bacteriological. The clinical picture is non-specific and associates high fever, profuse sweating, weight loss and asthenia, all of which make a severe alteration to the general condition. This infection persists in AIDS patients to a late phase of evolution where Immunodeficiency is profound, that is when the level of CD4 lymphocytes is low. Because of this, it is an increasing and preoccupying problem in patients, since it involves the prognosis of life. This shows the importance of prophylactic treatment for this pathology.
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PMID:[A new prophylactic agent in AIDS: Ansatipine. Disseminated Mycobacterium avium complex infection is now the most frequent of the opportunistic bacterial infections in AIDS]. 803 59

Changes in the level of CD4-bearing T-lymphocytes in injection drug users infected with the human immunodeficiency virus were evaluated in a sample of 318 subjects enrolled from a methadone program in the Bronx, New York, from 1985 through 1989. Follow-up continued through 1990. The percentage of CD4+ T-lymphocytes (CD4%) was used to maximize the stability of measurements. The rate of decline of the CD4% was determined using a random-effects assumption, and predictors of rate of decline were evaluated using an autoregressive model. The rate of CD4% decline was approximately 1.2 CD4% lost per 6 months, with a higher rate in recent seroconverters (2.2 CD4% lost). The most important predictors of decline of the CD4% in autoregressive models were current pyogenic bacterial infection (CD4% reduced by 2.75, 95% confidence interval (CI) 0.42-5.08), current report of a second constitutional symptom (CD4% reduced by 2.16, 95% CI 0.03-4.29), and history of bacterial infection (CD4% reduced by 1.49, 95% CI 0.09-2.89; proportion of prior CD4% lost increased by 0.14, 95% CI 0.01-0.27). Oral thrush was not related to an accelerated rate of CD4% decline.
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PMID:Correlates of the rate of decline of CD4+ lymphocytes among injection drug users infected with the human immunodeficiency virus. 810 Mar 95

Our objective was to evaluate the effect of intravenous immunoglobulin (IVIG) on absolute CD4+ lymphocyte count (CD4+ count) trends in human immunodeficiency virus- (HIV) infected children enrolled in a trial of IVIG for infection prophylaxis. To that end, we conducted a randomized, double-blind, outpatient trial comparing subjects treated with 400 mg per kilogram of IVIG every 28 days with those given 0.1% albumin placebo. CD4+ counts were measured at entry and every 12 weeks. Twenty-eight clinical centers in mainland United States and Puerto Rico participated. Previous reports showed IVIG efficacy for infection prophylaxis in 313 patients with entry CD4+ counts of > or = 0.20 x 10(9)/L (> or = 200/mm3). Two hundred and seventy-seven (89%) of these 313 children had three or more CD4+ counts measured during the trial and were included in evaluation of CD4+ count trends. Rates of CD4+ count decline, as measured by regression slopes, were compared between IVIG and placebo groups using generalized linear models, comparing unadjusted, age-adjusted, and standardized age-adjusted data. Potential covariate effects were assessed by modeling change in CD4+ count in terms of log change between successive measurements. Age-adjusted slope analysis showed slowing of CD4+ count decline by 13.5 cells/mm3 per month in IVIG compared with placebo recipients (95% confidence interval, 3.1-23.9, p = 0.012). Modeling log change between measurements documented a beneficial effect of IVIG that was cumulative over time and independent of other therapies. Occurrence of serious bacterial infection in the interval before CD4+ count measurement or death was independently associated with more rapid CD4+ count decline (p = 0.01 and p = 0.008, respectively). Zidovudine therapy was associated with a transient increase in CD4+ count. Benefits of IVIG include slowing of CD4+ count decline as well as previously reported reductions in serious and minor bacterial and viral infections in subjects with entry CD4+ counts of > or = 0.20 x 10(9)/L. This finding provides corroboration for the hypothesis that immunologic mechanisms contribute to the pathogenesis of CD4+ decline in HIV infection.
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PMID:Effect of intravenous immunoglobulin (IVIG) on CD4+ lymphocyte decline in HIV-infected children in a clinical trial of IVIG infection prophylaxis. The National Institute of Child Health and Human Development Intravenous Immunoglobulin Clinical Trial Study Group. 810 72

Mice with a retrovirus-induced immunodeficiency were challenged with Listeria monocytogenes and resistance to this facultative intracellular bacterium was analyzed. Early innate immunity was unaltered or enhanced. Although immunodeficient mice had reduced bacterial titers after these reached their peak on Day 3, infection with L. monocytogenes generally resulted in a low-grade persistent infection and occasionally there was a delayed resolution of bacterial infection. Endogenous cytokines are important in the containment of bacteria as mice often developed a high load of bacteria or succumbed to infection in the absence of cytokine action. There was a substantial heterogeneity in disease after bacterial challenge which probably reflects the variability found in retrovirus-infected mice during the later stages of this immunodeficiency syndrome.
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PMID:Mice with an acquired immunodeficiency (MAIDS) develop a persistent infection after injection with Listeria monocytogenes. 816 47

To determine the rates and characteristics of invasive bacterial infections in children infected with the human immunodeficiency virus type 1 (HIV-1), we conducted a prospective, longitudinal, observational cohort study of infants born to HIV-1-infected mothers between Dec. 1, 1985, and Sept. 30, 1989. Of 104 subjects whose HIV-1 infection status could be definitively determined, 21 were infected with HIV-1 and 83 were not. In all, 11 (48%) of 23 invasive infections occurred among 10 HIV-1-infected patients and 12 (52%) of 23 occurred among 11 uninfected subjects. Infections with Streptococcus pneumoniae (n = 8), all of which were community acquired, accounted for the greatest proportion (35%) of the organisms isolated from either the blood or the cerebrospinal fluid. Five episodes of pneumococcal bacteremia occurred in the HIV-infected patients; all resolved promptly after treatment was begun, and no serious focal infections developed. Of 13 instances of bacteremia with an organism other than S. pneumoniae, seven were nosocomial. The rate of community-acquired invasive bacterial infections among the HIV-infected children was nearly three times higher than the rate in the non-HIV-infected children (overall, 1.02 infections per 100 person-months vs 0.37 infection per 100 person-months; rate ratio, 2.8; p = 0.05). Most of the increased risk occurred in children > 1 year of age. In contrast, the difference in the rates of infection between those patients in the two groups who were less than 12 months of age was not significant (1.3 infections per 100 person-months vs 0.81 infection per 100 person-months; rate ratio, 1.6; p = 0.47). We conclude that the rate of invasive bacterial infection is higher in HIV-infected children than in their peers, especially after 1 year of age.
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PMID:Invasive bacterial infections in children born to women infected with human immunodeficiency virus type 1. 820 65

Despite significant knowledge of the molecular biology and genetics of adenovirus, no specific antiviral agent has been developed for use in adenovirus infections. This contrasts with the situation in herpes simplex virus (HSV) and human immunodeficiency virus (HIV) infections, in which antiviral agents target specific enzymes. Antiviral agents active against HSV and interferons have been used in the treatment of ocular adenovirus infections with limited effect. Some newer nucleoside analogues have inhibitory activity against adenovirus in vitro and their effect is being assessed in newly developed animal models. Live vaccines have been used in both the United States and Canada to protect military recruits against adenovirus-induced respiratory disease. However, the inoculating strains are not normally associated with epidemic keratoconjunctivitis (EKC). There is a low prevalence of antibody against strains of adenovirus inducing EKC. Until such time as specific antiviral agents against adenovirus are developed, the mainstays of therapy will remain topical antibiotics to eliminate any secondary bacterial infection and topical steroids to suppress the immune response against adenovirus or adenovirus-infected cells. Neither form of treatment is adenovirus specific.
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PMID:Antiviral agents for ocular adenovirus infections. 825 19

A follow-up study of 179 cases of human immunodeficiency virus (HIV) seropositive neonates born from HIV seropositive mothers is reported. At the time of the present study, HIV infection resulting from maternofetal transmission was found in 50 cases, while 108 infants were not infected; HIV infection remained uncertain in 16 cases; 5 infants were lost for follow-up. Out of the 50 infected cases, 20 were less than two-year old, 17 were 2-5 year old and 13 were older than 5 years. Very few remained asymptomatic after the age of 6 months, the most common symptoms being adenopathies and/or hepatomegaly and/or splenomegaly. Twenty-six had an acquired immunodeficiency syndrome (AIDS). Six died, from pneumocystosis (3), cytomegalovirus infection (1) and septicemia (2). Virus culture and polymerase chain reaction were the most efficient laboratory methods for early diagnosis of HIV infection, both being positive in more than 95% of the infected cases after the age of 3 months. A close clinical and biological supervision is recommended in these infants and children because of the permanent threat of infectious diseases in relation to their immunodeficiency. Treatment associates: 1) antiviral therapy with AZT as soon as the HIV infection is diagnosed; 2) primary prophylaxis against pneumocystosis with trimethoprim-sulfamethoxazol; 3) IV immunoglobulins in the case of repeated bacterial infection; 4) regular evaluation of the nutritional status and psychological assistance.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Management of HIV-seropositive newborn infants. Personal experience apropos of 179 cases]. 839 76

Highly specialized, state-of-the-art diagnostic tests are available for identifying congenital and acquired immune defects. These methods should only be resorted to when less complicated means have created suspicion of an immune defect. The case history, including the family history, represents the core of the diagnostic procedure. Initially, only simple clinical investigations are indicated. These should enable the physician to exclude or delimit a defect in the immune system which then can be defined more closely by specific tests. Screening includes clinical chemistry (erythrocyte sedimentation rate, total serum protein, serum electrophoresis, C-reactive protein, blood count including differential blood count, ferritin, urine analysis, and a quantitative assay of the immunoglobulins A, G and M), bacteriological, serological, and radiological investigations, and finally skin tests with recall antigens. Thereby, it is usually possible to reliably detect primary B cell defects with humoral antibody deficiency syndromes. Lymphocyte subset counts, immunoelectrophoresis, and bone marrow biopsy are necessary for the differential diagnosis, or for the confirmation, of malignant lymphatic proliferation, especially in adults. IgG subclass defects as well as granulocyte dysfunction and complement defects must be excluded in patients who are susceptible to bacterial infection despite normal immunoglobulin concentrations. In suspected cases of primary or secondary (HIV, cytomegalovirus, Epstein-Barr virus) T cell defects, lymphocyte subset counts and, where applicable, T cell function tests are indicated. The majority of secondary immunodeficiency syndromes, in which the primary disease is known, do not currently require specialized diagnosis. Nevertheless, monitoring of the lymphocyte subsets in HIV-positive patients has already become standard practice in health care (for evaluating the prognosis and deciding on the therapy).
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PMID:[Laboratory diagnosis of immune deficiency]. 849 52

Infectious diseases remain among the most morbid events and are an important cause of death in ESRD. These events are related to an acquired immunodeficiency that progresses during the development of uremic retention, as part of the broader spectrum, displayed by the "uremic syndrome". A central role in the hose defense against bacterial infection is played by the phagocytic polymorphonuclear white blood cells, which are characterized by the capacity to ingest bacteria (phagocytosis), which is followed by the destruction of those bacteria (killing capacity). This article reviews the mechanisms of development and the potential causes that have been held responsible for this aspect of the defective immune function. The observed changes are attributed to alterations in receptor expression, although more convincing evidence points in the direction of metabolic functional disturbances, especially in the NAD(P)H-oxidase-dependent production of oxygen free radicals. The most important causative factors are: uremic toxicity, iron overload, renal anemia, dialyzer bioincompatibility, and the type of renal replacement therapy. It is concluded that the phagocytic defect in ESRD is multifactorial and that each factor should be managed by specific therapeutic approaches.
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PMID:Infectious morbidity and defects of phagocytic function in end-stage renal disease: a review. 850 9


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