PubMed Health⌕ Search

Biomedical subjects

R Soeiro

Publications and source records attributed to R Soeiro.

At least 37 records · Page 2Linked to original sources
PubMed1987

Colonization of skin and development of peritonitis due to coagulase-negative staphylococci in patients undergoing peritoneal dialysis.

Coagulase-negative staphylococci, part of the normal skin flora, frequently colonize bioprosthetic devices and are the most common cause of peritonitis in patients undergoing peritoneal dialysis. Using the API STAPH-IDENT system (Analytab Products, Plainview, New York) and plasmid pattern analysis, we investigated the importance of chronic carriage of coagulase-negative staphylococci in the development of peritonitis due to these organisms. During a nine-month period, 182 surveillance cultures of pericatheter skin and anterior nares from 30 patients yielded 102 strains of coagulase-negative staphylococci. Twelve of these patients had 20 episodes of peritonitis due to these organisms. Staphylococcus epidermidis accounted for 75% of surveillance and 79% of peritonitis-associated strains. By plasmid pattern analysis of 47 surveillance and 16 peritonitis-associated strains, only three patients carried identical coagulase-negative staphylococci on two or more occasions, and only three patients developed peritonitis due to organisms cultured previously from body surface sites.

Coagulase↗
PubMed1986

Right-sided valvular endocarditis: etiology, diagnosis, and an approach to therapy.

Right- and left-sided endocarditis are two distinct entities, both clinically and experimentally. As such, they require different clinical approaches. The accurate diagnosis of right-sided endocarditis rests largely on a high index of suspicion which is often raised in the case of an intravenous drug abuser with fever, especially when pulmonary infiltrates are detected. Two-dimensional echocardiography can be expected to confirm the diagnosis in approximately 80% of the cases. Measurement of the echocardiographically visualized vegetation provides both prognostic and therapeutic information. When the vegetation is less than 1.0 cm in diameter, antibiotic therapy can be reasonably expected to cure the infection. Despite a prolonged fever, we recommend continued medical management in these cases, as lack of response to medical management is almost exclusively seen in cases in which echocardiographically determined vegetation size is greater than or equal to 1.0 cm, perhaps because of the slower metabolic rate of bacterial colonies within these large vegetations. If, however, after 3 weeks of antibiotic therapy, fevers persist in a patient in whom two-dimensional echocardiography reveals a vegetation of greater than or equal to 1.0 cm, surgical intervention should be contemplated. Prior to such intervention, the physician must be careful to exclude other sources of fever, such as abscesses, phlebitis, and drug reactions, as indicated in Table III. Also, adequate antibiotic levels should be documented prior to surgical intervention. Because of the adverse effect on vegetation size upon the response to antibiotics, there may be a role for anticoagulation in order to potentiate the effects of the antibiotic therapy; however, this is purely speculative at present.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Bacterial Agents↗
PubMed1986

Influence of vegetation size on clinical outcome of right-sided infective endocarditis.

Endocarditis involving right-sided valvular structures is largely a disease of intravenous drug abusers. The majority of these patients respond to antibiotic therapy with clearing of their bacteremia and preservation of their hemodynamic status. This study evaluated the prognostic value of echocardiographically determined vegetation size in 23 episodes of right-sided valvular endocarditis in 21 patients. Right-sided vegetations were visualized in 19 of 23 episodes (83 percent). Of these, a vegetation of 1.0 cm or greater was found in 11. No patient with an echocardiographically determined vegetation size of less than 1.0 cm required surgery, whereas four of 11 (36 percent) of those episodes in which the vegetation size was 1.0 cm or greater required surgery for persistent pyrexia (p less than 0.05). In all patients requiring surgery, a bioprosthetic tricuspid valve was placed at the time of initial surgery and in no patient did early reinfection occur. This study reconfirms the benign prognosis of right-sided valvular endocarditis. Further, although vegetations of less than 1.0 cm identify those patients who will respond to medical therapy, echocardiographically documented vegetations of 1.0 cm or greater are associated with a significantly lower response rate to appropriate medical therapy. The association of fever that persists for more than three weeks in the absence of another source of infection with an echocardiographically demonstrable right-sided vegetation of 1 cm or more identifies those patients who will require surgical intervention. Finally, tricuspid valve replacement can be performed at the time of initial surgery without undue concern for early reinfection or valve dysfunction.

Adult↗
PubMed1986

Immediate tricuspid valve replacement for endocarditis. Indications and results.

Tricuspid valve excision for tricuspid endocarditis in addicts is recommended to avoid early reinfection, continued sepsis, and late reinfection because of the resumption of intravenous drug abuse. Valvectomy is allegedly well tolerated hemodynamically by some, but it leads to heart failure in at least a third of patients. In our experience in 10 addicts with staphylococcal endocarditis who had failed to respond to antibiotic therapy, tricuspid valve replacement allowed all 10 to leave the hospital free of infection and free of heart failure. Resumption of drug addiction in three led to septic death, but not necessarily to tricuspid reinfection. Two returned to jobs requiring a high level of physical labor and tolerated this without difficulty. We find no need to follow the practice of tricuspid valve excision for tricuspid endocarditis in addicts. Those who refrain from drug abuse are well served by valve replacement. Those who do not are doomed with or without a tricuspid valve.

Acute Disease↗
PubMed1984

Fv-1 host cell restriction of friend leukemia virus: microinjection of unintegrated viral DNA.

The murine gene Fv-1 has been shown to exert a major influence over the replication of ecotropic murine leukemia viruses. Studies of the replication of Friend murine leukemia virus have shown that the restriction of viral replication occurs intracellularly after the initiation of viral DNA synthesis. The precise mechanism of the block imposed by the Fv-1 gene product is not completely understood. Our studies of Fv-1 restrictive infection have shown a variable decrease in the accumulation of intracellular unintegrated form I viral DNA. Analysis by microinjection of the viral DNA formed in nonpermissively infected BALB/c cells indicates that this DNA is infectious. These studies indicate that the form I DNA accumulated in nonpermissively infected BALB/c cells contains the complete viral sequences necessary for the production of viral progeny, and therefore, they suggest that the Fv-1 host restrictive mechanism recognizes viral factors other than form I DNA alone. These results support the possibility that Fv-1 host restriction occurs after formation of infectious viral DNA, perhaps at the integration step itself.

Animals↗
PubMed1983

Rhodotorula rubra peritonitis in patients undergoing continuous ambulatory peritoneal dialysis.

Although still uncommon, fungal peritonitis is being reported with increasing frequency in patients with renal failure who are undergoing long-term peritoneal dialysis. Although most cases have involved Candida albicans, other opportunistic pathogens have been reported as well. Recently, three patients were seen with serious peritoneal infections due to Rhodotorula rubra, a "nonpathogenic" fungus. In two patients, peritoneal fibrosis made further peritoneal dialysis impossible. The third patient died from complications of peritonitis. Environmental cultures revealed a possible common-source outbreak. Literature review reveals that infection due to this organism is most unusual and occurs only in the hospital setting in patients with serious compromise of host defenses.

Adolescent↗
PubMed1983

Studies of the etiology of Crohn's disease using athymic nude mice.

Following injection of Crohn's disease tissue filtrates, lymphomas and hyperplastic lymph nodes developed in 16% of athymic nude (nu/nu) mice; whereas only 4% of control nude mice developed lymphadenopathy (p less than 0.025). One hundred forty coded sera from 111 patients (Crohn's disease = 36, ulcerative colitis = 28, diarrheal and other controls = 47) were assayed by indirect immunofluorescence for immunoreactivity with the lymphomas and hyperplastic lymph nodes. Coded sections were examined by two observers and scored on a 0 to 3 + scale. Fifty-four percent of the sera from patients with Crohn's disease were reactive with the Crohn's disease induced lymphoma by this assay. Eighty percent of sera from patients with symptomatic Crohn's disease were positive, whereas 22% of sera from patients in remission were positive. Sixty-six percent of sera from patients with symptomatic Crohn's disease reacted against hyperplastic lymph nodes induced by Crohn's disease filtrates. In contrast, only one control serum (from a patient with ulcerative colitis) reacted with the lymphomas or hyperplastic lymph nodes. Lymphomas induced by other means or arising spontaneously did not show immunofluorescence with Crohn's disease or control sera. Electron microscopy revealed C-type viral particles in five lymphomas induced by Crohn's disease filtrates and in one control lymphoma, but not in five hyperplastic lymph nodes and five control lymph nodes. Absorption of Crohn's disease sera with control lymphoma or with murine leukemia virus infected fibroblasts did not diminish immunoreactivity, whereas similar absorption with lymphomas induced by Crohn's disease filtrates abolished the immunofluorescence. These studies indicate that Crohn's disease tissue, when injected into athymic nude mice, induces lymphoid hyperplasia and lymphomas that contain an antigen(s) recognized by Crohn's disease sera.

Animals↗
PubMed1982

Studies with aphidicolin on the Fv-1 host restriction of Friend murine leukemia virus.

The murine gene Fv-1 exerts a major control over the replication of Friend murine leukemia virus (F-MuLV). An effect of the gene product has been determined to be at the level of accumulation and integration of viral DNA. Aphidicolin, an inhibitor of eucaryotic DNA polymerase alpha, was studied in murine cells infected either permissively or nonpermissively with regard to the Fv-1 genotype. Results indicated that inhibition of DNA polymerase alpha did not affect the accumulation of form III viral DNA in either permissive or nonpermissive cells. However, the normal accumulation of circular form I DNA in permissive cells was inhibited. The block in the accumulation of form I DNA resembled that occurring in some F-MuLV Fv-1-nonpermissive infections. Additionally, aphidicolin treatment resulted in the accumulation of novel low-molecular-weight viral DNA species, normally detectable in a nonpermissive infection of NIH cells with B-tropic F-MuLV. These data suggest that the Fv-1 gene product may interact with host DNA polymerase alpha to prevent viral replication.

Animals↗
PubMed1981

Host restriction of Friend leukemia virus: gag proteins of host range variants.

The host response to murine ecotropic leukemia viruses is mainly controlled by the mouse Fv-1 gene. This locus controls virus replication at an intracellular stage and prevents provirus integration. Biological studies suggest that the Fv-1 effector molecule recognizes at least one virion structural protein. We have produced host range variants of B-tropic Friend murine leukemia virus in order to study the primary structure of potential viral target proteins. Our results show that conversion of B-tropism to NB-tropism is associated with changes in the primary structure of three gag proteins--p15, p12, and p30. These results suggest that host range conversion is due to a recombinational event, presumably between the parental virus and an endogenous murine virus. They also open the possibility that p12 and p30 may be involved in host range restriction.

Amino Acid Sequence↗
PubMed1981

Fv-1 host restriction of Friend leukemia virus: oligonucleotide analysis of host range variants.

The Fv-1 murine gene controls predominantly the replication of leukemia viruses of murine cells. Forced passage by B-tropic Friend leukemia virus in the restrictive host cells (NIH, Fv-1n/n) results in viral progeny capable of replicating efficiently in murine cells of any Fv-1 type, which are denoted as NB-tropic virus. We have studied the RNase T1-resistant oligonucleotide pattern of a series of NB-tropic Friend virus isolates and have been able to show changes from the parental B-tropic virus which occur at the 5' end of the genome. Cloned NB-tropic virus falls into three classes, demonstrating either four, one, or no apparent changes in the genome. These results suggest the possibility that conversion to NB tropism occurs by a recombination mechanism but, since change to NB tropism can occur without any observable oligonucleotide alteration, they do not confirm that any single oligonucleotide is diagnostic of NB tropism.

Friend murine leukemia virus↗
PubMed1981

Fv-1 host restriction of Friend leukemia virus: analysis of unintegrated proviral DNA.

The murine gene Fv-1 predominantly controls the outcome of infection by murine ecotropic retroviruses. The inhibition of virus replication by the Fv-1 gene product has been determined to be at an early stage in virus replication. Mechanistically, its effect appears to be on the accumulation of unintegrated proviral DNA or its integration or both. We investigated the synthesis of unintegrated proviral DNA, using several clones of B-, N-, or NB-tropic Friend murine leukemia virus. Our results indicate that the accumulation of B-tropic proviral DNA in NIH cells may be inhibited at either the level of linear (form III) or covalently closed circular DNA (form I), depending upon the degree of restriction of the clone of virus used. We confirmed that there is an effect of the Fv-1 gene on the accumulation of form I DNA of either B- or N-tropic Friend murine leukemia virus. However, the decrease in infectious centers effected by the Fv-1 gene did not correlate quantitatively with the effect on form I proviral DNA produced by N-tropic Friend murine leukemia virus in nonpermissive cells. Lastly, we demonstrated in nonpermissively infected NIH cells that a rapidly migrating doublet of viral DNA is formed.

Animals↗
PubMed1980

Expression of viral RNA in Friend virus-induced erythroleukemia cells.

The regulation of expression of the Friend virus complex (FV) was studied in clones of H-2 congenic erythroleukemia cell lines. Molecular probes specific for each of the two FV components were generated and hybridized to RNA extracted from clones differing with respect to virus production or viral envelope antigen expression. Sequences representing the defective component of FV continued to be transcribed in cells regardless of virus production. The presence of helper virus-specific sequences, however, was shown to be directly related to virus expression. Molecular hybridization with cytoplasmic and nuclear RNA extracted from the H-2 congenic clones representing various stages of viral expression demonstrated a direct correlation between the level of transcription of FMuLV-specific sequences and the degree of virus expression. These data suggest that regulation of FV expression is primarily related to the cessation of helper virus transcription in the cell lines studied. In this paper we provide further evidence that the defective viral components is responsible for the rapid malignancy associated with Friend disease.

Animals↗
PubMed1976

Host restriction of Friend leukemia virus: synthesis and integration of the provirus.

Host restriction of exogenous infection by murine leukemia viruses is controlled in vitro predominantly by the murine Fv-1 locus. The mechanism of this host restriction was investigated by comparing the early events in the replication of N-tropic versus B-tropic Friend leukemia virus in NIH 3T3 cells. These cells, which are Fv-1nn in type, are permissive for the N-tropic strain, but nonpermissive for the B-tropic strain, which replicates permissively in Balb/c cells. We have studied the synthesis, intracellular location, and molecular form of virus-specific DNA early in replication by means of molecular hybridization with a virus-specific DNA probe. Our results suggest that in the permissive infection viral DNA rapidly becomes integrated with cellular DNA. However, in the nonpermissive infection, although almost equal amounts of both positive and negative strand viral DNA are synthesized, integration of the provirus does not occur.

Cell Line↗