PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “MYCOBACTERIUM INFECTIONS”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources
PubMed1997

[Prevention of bacterial infections in immunocompromised hosts, excluding HIV infection and mycobacterium infections].

The immunocompromised host is an individual whose defense mechanisms against infectious agents are altered in such a significant way that he is abnormally susceptible to infections agents in general and bacterial "opportunists" in particular. The type of infection and etiologic agents vary with the nature and the severity of the immune defect. The goal of prophylactic treatments is to prevent the occurrence or recurrence of infections, and so, to reduce the infectious morbidity and mortality when the nature of severity of immunosuppression make these complications probable. Beside specific measures, which are detailed in this article, the strict application of the so-called universal precautions, particularly handwashing, remain at the basis of the prevention of bacterial infections in the immunocompromised host.

Bacterial Infections↗
PubMed2003

The fibrinolytic system in dissemination and matrix protein deposition during a mycobacterium infection.

The fibrinolytic system is known to play an important role in the inflammatory response to bacterial infections. In the present study, relationships between protein components of the fibrinolytic system and infectivity by Mycobacterium avium were analyzed. Infections were initiated through noninvasive intratracheal administration of M. avium 724 in mice individually deficient for plasminogen, tissue-type plasminogen activator, urokinase-type plasminogen activator, and urokinase-type plasminogen activator receptor, along with wild-type control mice. There were no differences in lung colony counts among all mouse genotypes throughout a 10-week infection. However, in tissue-type plasminogen activator and plasminogen-deficient mice an earlier dissemination of M. avium to other organs was observed. Nevertheless, the M. avium growth rates in the liver, spleen, and lung did not differ between the various mouse populations throughout a 10-week infection. Histochemical and immunohistochemical analyses at 5 and 10 weeks after infection demonstrated that plasminogen-deficient mice, compared to wild-type mice, had enhanced fibrin and fibronectin deposition, as well as increased neutrophil infiltration within liver granulomas. These results suggest that plasmin(ogen) plays a role in the turnover of extracellular matrix proteins within granulomas and has a limited effect in the early dissemination of M. avium from lungs. Thus, plasmin(ogen) functions in limiting progressive fibrosis in the granuloma during a chronic mycobacterial infection.

Animals↗
PubMed2005

Activation and mitogen-activated protein kinase regulation of transcription factors Ets and NF-kappaB in Mycobacterium-infected macrophages and role of these factors in tumor necrosis factor alpha and nitric oxide synthase 2 promoter function.

Previous studies have shown that primary murine macrophages infected with Mycobacterium avium produced lower levels of tumor necrosis factor alpha (TNF-alpha) and inducible nitric oxide synthase 2 (NOS2) compared to cells infected with nonpathogenic Mycobacterium smegmatis. TNF-alpha and NOS2 levels correlated with and were dependent on the activation of mitogen-activated protein kinases (MAPKs) p38 and extracellular signal-regulated kinase 1/2 (ERK1/2). To define the macrophage transcriptional responses dependent on ERK1/2 activation following a mycobacterial infection, we used RAW 264.7 cells transfected with a TNF-alpha or NOS2 promoter vector. We determined that macrophages infected with M. avium compared to M. smegmatis showed diminished TNF-alpha and NOS2 promoter activity. A more pronounced difference in promoter activity was observed when only the consensus ETS and NF-kappaB binding sites were used as promoters. Mutational analysis of the ETS and NF-kappaB binding sites present on the TNF-alpha and NOS2 promoters, respectively, showed that these sites were essential for a functional promoter. Moreover, the Ets/Elk but not the NF-kappaB transcriptional response was dependent on ERK1/2. This correlated with the requirement for ERK1/2 in TNF-alpha but not NOS2 promoter activity. Our data indicate that the increased Ets/Elk and NF-kappaB promoter activities associated with M. smegmatis-infected macrophages are responsible, at least in part, for the increased TNF-alpha and NOS2 production observed in these infected cells and that ERK1/2 is required for Ets/Elk activity and full TNF-alpha production.

Animals↗
PubMed1994

Macrophage-T cell interaction in experimental mycobacterial infection. Selective regulation of co-stimulatory molecules on Mycobacterium-infected macrophages and its implication in the suppression of cell-mediated immune response.

The most important immunopathological consequence of experimental mycobacterial infection is the suppression of T cell-mediated immune response to both mitogens and mycobacterial antigens. We registered that there was decreased concanavalin A-induced spleen cell proliferation in infected susceptible BALB/c mice as compared to normal mice. In resistant (C3H/HeJ) mice, infection with the bacteria did not induce any suppression in the mitogen-induced lymphoproliferation. Likewise, delayed-type hypersensitivity (DTH) responses, to keyhole limpet hemocyanin and mycobacterial crude soluble antigen were suppressed in infected BALB/c mice but not in C3H/HeJ mice. This depressed T helper cell function may either be due to defective T cell-receptor occupancy by antigen-Ia complex or altered co-stimulatory signals provided by antigen-presenting cells. In the present study, we have investigated the status of certain co-stimulatory molecules on the infected macrophages from both susceptible and resistant mice. Our results demonstrate that upon mycobacterial infection, the macrophages are rendered incapable of delivering the co-stimulatory signals to T helper cells, possibly due to the involvement of prostaglandin, as inhibition of its biosynthesis by indomethacin reversed the defect. Furthermore, the selective regulation was bacteria-induced as killing of the bacteria by rifampicin abrogated the derangements in the expression of co-stimulatory molecules on the Mycobacterium-infected macrophages. Our observations revealed that upon infection with Mycobacterium tuberculosis, B7 was down-regulated while ICAM-1 was increased only in BALB/c but not in C3H/HeJ mice. Expression of VCAM-1 did not change during the infection in either strain of mice. We found that these changes in ICAM-1 and B7 expression on the surface of infected macrophages resulted in inhibition of DTH-mediating functions of T helper cells from BALB/c mice. The results obtained in this study describe not only a novel immune evasion strategy adopted by Mycobacterium, but also open up the possibility of immunotherapy of mycobacterial infection by selective manipulation of co-stimulatory molecules.

Animals↗
PubMed2005

Atypical Mycobacterium infections of the upper extremity.

BACKGROUND: We encountered five patients with atypical Mycobacterium infections in the upper extremity, and examined their outcomes. PATIENTS AND METHODS: Two patients were male and three were female. The average patient age was 67 (range, 63-75) years. A wide synovectomy was performed to diagnose all cases followed by a therapeutic regimen of Rifampicin, Isoniazid, and Ethambutol. RESULTS: The causative atypical organism was Mycobacterium marinum in three cases and Mycobacterium intracellulare in two cases. In one patient, inflammation recurred or did not disappear, and, therefore, three debridements were necessary. The average duration of antimicrobial therapy was 12 (range, 5-24) months. The average follow-up period was 26 (range, 5-66) months, and resolution had been achieved in all cases at the time of follow-up evaluation. CONCLUSION: Surgical debridement and appropriate mycobacterial culture or PCR method are critical to enable diagnosis and appropriate management.

Aged↗
PubMed2005

[A rare case of disseminated Mycobacterium kansasii infection].

Mycobacterium kansasii infection has been reported to be about 20 percent of non-tuberculous mycobacteriosis, and its disseminated type is uncommon and the prognosis is reported to be generally poor. We experienced one case of disseminated Mycobacterium kansasii infection. A 81 year-old man who had been short-bowel syndrome due to the operation for superior mesenteric artery occlusion since 1998 was admitted on April 24th, 2001 to our hospital because of slowly progressive consciousness disturbance and anorexia. He had shown progressive productive cough and respiratory failure and laboratory findings were C-reactive protein elevation and pancytopenia. Human immunodeficiency virus (HIV) antibody was negative. Chest X-ray and computed tomography showed diffuse miliary nodules and infiltrative shadow. Sputum examination was positive for mycobacteria. The cultured isolate was identified as Mycobacterium kansasii. Bone marrow aspirations revealed inflammatory granuloma with necrosis. He was diagnosed as disseminated Mycobacterium kansasii infection and heart failure, and was treated by anti-tuberculosis drugs and diuretics. Treatment was very effective and Chest X-ray findings and respiratory failure had been completely improved. In this case we speculated that the malnutrition due to short-bowel syndrome could be one of the most suspected reasons of Mycobacterium kansasii dissemination. Disseminated Mycobacterium kansasii infection has been rarely reported comparing with the other mycobacterial infections in Japan. However, due to the increasing numbers of immunocompromised hosts with aging, HIV infection, cancer, and steroid therapy, this type of infection will become more common and its earlier diagnosis and adequate treatment will be important to improve the prognosis.

Aged↗
PubMed1994

Atypical Mycobacterium infections of the upper extremity.

Thirty-three patients with culture-positive atypical Mycobacterium infections of the upper extremity underwent surgical debridement and antimicrobial therapy. The causative atypical organism was M. marinum in 12 cases, M. avium-intracellulare in 7, M. terrae in 4, M. chelonei in 4, M. kansasii in 3, M. fortuitum in 2, and M. ulcerans in 1. The tenosynovium was the most common location of infection (14 patients). The average follow-up period was 36 months. Duration of antimicrobial therapy averaged 10 months. The average delay between onset of symptoms to correct diagnosis was 1 year. There were seven superficial infections; six were caused by M. marinum and one was caused by M. ulcerans. All of these cutaneous infections resolved following incisional or excisional biopsy and pharmacologic therapy. The remaining 26 infections involved the deeper tissues, and M. avium-intracellulare was the most common organism. The immune status of the host was an overwhelming predictor of eventual outcome. In the 15 patients with competent immune systems, resolution occurred in 13. However, in the immunocompromised patient population, only 4 of the 10 had resolution of deep infection at time of the follow-up evaluation.

Adolescent↗
PubMed2001

[Beta-defensins in plasma and bronchoalveolar lavage fluid in patients with non-tuberculous mycobacterium infection].

We measured the levels of beta-defensin 1 and 2 (HBD-1, 2), novel antimicrobial peptides in plasma and in bronchoalveolar lavage fluid (BALF) from patients with with non-tuberculous mycobacterium infection (NTM). Plasma HBD-2 levels in NTM patients before treatment were higher than those in the controls, while the HBD-1 levels were similar to the control levels. High levels of HBD-2, but not of HBD-1, in BALF were also observed in NTM patients. In NTM, a positive correlation was found between HBD-2 levels in BALF and plasma, and also between HBD-2 and IL-1 beta levels in BALF. NTM patients with cavities or ectasia on chest radiography had higher HBD-2 levels in BALF than those without. Plasma HBD-2 levels in NTM patients were markedly decreased after successful treatment, while those of patients with an intractable mycobacterium infection maintained the same high plasma HBD-2 levels as those before treatment. These findings suggest that HBD-2 may participate in the host defense and plasma HBD-2 levels may reflect disease activity in pulmonary NTM.

Biomarkers↗
PubMed1978

Problems in diagnosis and therapy of Mycobacterium fortuitum infections.

Mycobacterium fortuitum was isolated 11 times from 8 patients during a 6-year period. Six of the isolates were from sputum; one was from aspiration of a lymph node, and 4 were from wound cultures. The isolation from sputum was believed not to be associated with pulmonary infection in all 6 instances. The difficulty in diagnosis and therapy of infections with Mycobacterium fortuitum is illustrated by these cases and by others from the literature. Amikacin and doxycycline may offer some therapeutic benefit for patients with Mycobacterium fortuitum infections.

Adolescent↗