PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Rhodococcus”

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 1,153 records · Page 64Linked to original sources

Rhodococcus equi pneumonia in foals.

Rhodococcus (Corynebacterium) equi pneumonia is diagnosed by thoracic auscultation, radiographic and hematologic examination, and transtracheal aspiration. Treatment may be unsuccessful because of the organism's tendency to cause pulmonary abscesses. A 2-month-old, depressed, anorectic, febrile Quarter Horse colt, previously unresponsive to penicillin therapy, had loud, moist breath sounds in the ventral lung fields. Chest radiographs revealed pneumonia. Based on culture and sensitivity tests on organisms isolated from transtracheal washes, chloramphenicol and erythromycin, and then oral trimethoprim-sulfadiazine, were given, in addition to supportive therapy. The animal was fully recovered within 2 months.

Animals↗

Equine cell-mediated immune response to Rhodococcus (Corynebacterium) equi.

A lymphocyte blastogenic assay was developed to serve as an in vitro correlate of cell-mediated immunity to Rhodococcus (Corynebacterium) equi (R equi) in the equine species. Lymphocytes obtained from a group of experimental ponies showed no response in cell culture to R equi heat extract or lysozyme extract antigens. Ponies were assigned to groups for experimental inoculation. Three ponies were inoculated subcutaneously with live R equi, 3 were given live R equi by intranasal and intratracheal routes, and 4 ponies were left untreated. Lymphocytes from all inoculated ponies had a mitogenic response to R equi antigens in lymphocyte blastogenic assays performed between the 7th and 40th days after inoculation. Lymphocytes from noninoculated control ponies remained unresponsive to R equi antigens. Delayed-type hypersensitivity reactions developed in all experimentally exposed ponies after intradermal administration of the R equi antigen preparations. In a 2nd phase of experimentation, blastogenesis assays were performed on lymphocytes from horses in herds with endemic R equi infections. Results indicated that many of the animals had significant (stimulation index greater than 2) cell-mediated responses to the bacterium, but there was no distinct correlation between the immune response and clinical history. These data indicated that cell-mediated immunity is involved in the interaction of the equine immune system with R equi.

Animals↗

Equine humoral immune response to Rhodococcus (Corynebacterium) equi.

An enzyme-linked immunosorbent assay was developed to test equine serum for the presence of antibodies to Rhodococcus (Corynebacterium) equi. Experimental ponies had no detectable antibody to R equi before exposure to the bacterium. After experimental inoculation, animals in groups that received live R equi subcutaneously or intranasally/intratracheally developed high titers to R equi. Noninoculated controls remained seronegative. Serum was also collected from horses of various ages that were naturally exposed to R equi. There was a wide range of anti-R equi titers in these horses. Because experimentally infected horses seroconverted when some naturally infected foals did not seroconvert, the function of antibody in resistance to R equi infection remains unknown.

Animals↗

Immunity to and immunotherapy for Rhodococcus equi.

Immune responses to Rhodococcus equi were assayed in mares and foals on 7 studs in south-eastern Australia using skin test reactivity to the intradermal injection of culture filtrate and an indirect fluorescent antibody test. The prevalence of positive skin-test reactions did not differ between studs with a history of R. equi disease and those without but there were more mares with high antibody titres on studs with a disease history. A leucocyte extract prepared from mares that were skin-test positive was evaluated for its ability to protect foals exposed to experimental or natural challenge: 2 foals receiving leucocyte extract became skin-test positive and had resolving lesions present at post-mortem examination. All foals challenged experimentally developed serum antibody but only in those that became skin-test positive were the lesions resolving. In a field trial of leucocyte extract, using 450 foals over 2 foaling seasons, no significant difference was detected in morbidity or mortality rates between treatment and control groups. It is suggested that, since R. equi is so ubiquitous and most horses show immunological evidence of exposure, the development of clinical disease may be related to individual inability to cope with this organism. This may be due to inherited immunological unresponsiveness or to environmental factors which increase the challenge or decrease resistance.

Actinomycetales↗

[Key Rhodococcus enzymes in the catabolism of aromatic compounds].

The enzyme apparatus involved in the catabolism of aromatic compounds in rhodococci is characterized by the presence of pyrocatechase and protocatechoate-3,4-dioxygenase as principal enzymes cleaving the aromatic cycle. Metapyrocatechase was found in about 30% of the rhodococci. All the enzymes are inducible. The inductor of pyrocatechase seems to be cyc-cys-muconate, and that of protocatechase appears to be 3-oxoadipate. The metapyrocatechase of rhodococci, in contrast to that of Pseudomonas, is not induced by benzoate, p-toluylate, p-xylene and phenol. The activity of metapyrocatechase rises 20-50 times comparing to the basal level only in the presence of p-cresol. The enzyme has a relatively low activity in rhodococci (50-200 nmole per 1 min per 1 mg of protein), though a very high affinity for methylcatechols. The activity of metapyrocatechase with methylcatechols is 2-5 times as high as that with catechol as a substrate, whereas the activity of pyrocatechase with methylcatechols is two times as low as that with catechol as a substrate. Such additional substrates as acetate, glycerol or fumarate have no effect on the qualitative composition of the key enzymes involved in the degradation of aromatic compounds in Rhodococcus carollinus 172. Glucose represses the synthesis of enzymes cleaving the aromatic ring by 100%. Fumarate taken in a 5-fold excess inhibits the activity of catechol oxygenases by 40%; if it is taken in a 1000-fold excess, it inhibits the enzyme activity by 100%.

Catechol 1,2-Dioxygenase↗

Reclassification of Mycobacterium phlei PN-bb as Rhodococcus bronchialis PN-bb.

Mycobacterium phlei PN-bb, induced in the parental strain PN by gamma-radiation and ethyl methanesulfonate, should be reclassified as Rhodococcus bronchialis PN-bb. The reclassification is based on the results of lipid analysis, DNA-DNA hybridization and several biochemical tests, performed in comparison with the parental strain PN, earlier reclassified as R. bronchialis, and R, bronchialis (N654).

Actinomycetales↗

Effect of cosubstrates on the dechlorination of selected chlorophenolic compounds by Rhodococcus erythropolis 1CP.

Effects of aromatic and nonaromatic cosubstrates on the rate of 2,4-dichlorophenol degradation by R. erythropolis 1CP were studied under growth and nongrowth conditions. Glucose and maltose were found to accelerate 2,4-dichlorophenol (initial conc. 50 mg/l) dechlorination from 11 days to 24 and 20 h, respectively. The stimulating effect was observed within the range of glucose concentration of 0.5-2.0 g/l in the medium. Ascorbic acid at a concentration of 10-70 mg/l as a nongrowth substrate also increased the decomposition of 2,4-dichlorophenol, though at a lower degree than glucose. Experiments with washed cells showed the limiting stage of chlorophenol degradation by R. erythropolis 1CP to be, possibly, aromatic ring dechlorination after its hydroxylation. As an additional source of electrons, glucose introduced into suspensions of washed cells grown on 3-hydroxybenzoate made it possible to eliminate the bottleneck in 2,4-dichlorophenol metabolism by significantly accelerating dechlorination of 3,5-dichlorocatechol. Based on the experimental and literature data, the enzyme systems involved in 2,4-dichlorophenol degradation by the culture R. erythropolis 1CP are assumed to be nonspecific.

Biodegradation, Environmental↗

Crystal structure of 2-hydroxyl-6-oxo-6-phenylhexa-2,4-dienoic acid (HPDA) hydrolase (BphD enzyme) from the Rhodococcus sp. strain RHA1 of the PCB degradation pathway.

2-Hydroxyl-6-oxo-6-phenylhexa-2,4-dienoic acid (HPDA) hydrolase (the BphD enzyme) hydrolyzes a ring-cleavage product of an aromatic compound generated in a biphenyl/polychlorinated biphenyl (PCB) degradation pathway of bacteria. The crystal structure of the BphD enzyme has been determined at 2.4 A resolution by the multiple isomorphous replacement method. The final refined model of the BphD enzyme yields an R-factor of 17.5 % at 2.4 A resolution with reasonable geometry. The BphD enzyme is an octameric enzyme with a 422 point-group symmetry. The subunit can be divided into core and lid domains. The active site of the enzyme is situated in the substrate-binding pocket, which is located between the two domains. The substrate-binding pocket can be divided into hydrophobic and hydrophilic regions. This feature of the pocket seems to be necessary for substrate binding, as the substrate is composed of hydrophilic and hydrophobic parts. The proposed orientation of the substrate seems to be consistent with the general catalytic mechanism of alpha/beta-hydrolases.

Amino Acid Sequence↗

[Rhodococcus equi pulmonary abscess in HIV infection].

RE is a well-known Gram positive bacillus which is usually pathogenic in animals. Disease in humans is rare, but incidence has clearly increased with the advent of AIDS. In humans, RE predominantly infect people with impaired cellular immunity so that it is considered an opportunistic agent. Its must common manifestation in immuno-compromised patients is a slowly progressive pneumonia which may cavitate. Even with early diagnostic and optimal and prolonged antibiotic therapy, the mortality of RE, infections remain high (20 to 55%). Problems in clinical and therapic management are illustrated in our two cases of cavitated pneumonia in two AIDS patients.

AIDS-Related Opportunistic Infections↗