Planctomycetes DNA in febrile aplastic patients with leukemia, rash, diarrhea, and micronodular pneumonia.

We found Planctomycetes DNA in 2 out of 100 blood samples from patients suffering from leukemia with neutropenia induced by chemotherapy, as well as fever, rash, pneumonia, and diarrhea. Antibiotic-resisting Planctomycetes may be pathogenic in these patients.

Broad-spectrum antibiotic resistance of Planctomycetes organisms determined by Etest.

OBJECTIVES: The in vitro susceptibility of Planctomycetes organisms to antibiotics has seldom been studied and when it has, a variety of methods have been used. The objective of the study was to expand the knowledge of Planctomycetes antibiotic susceptibility patterns. METHODS: Planctomyces maris, Planctomyces brasiliensis, Blastopirellula marina, Planctomyces limnophilus, Gemmata obscuriglobus and Rhodopirellula baltica reference strains were tested for in vitro susceptibility to 18 antibiotics, representing 11 antibiotic families, using the Etest method. RESULTS: All Planctomycetes organisms were found to be resistant to ß-lactams, with MICs of > 32 mg/L for penicillin G and imipenem, and MICs of > 256 mg/L for ampicillin, cefalotin and ceftriaxone. The organisms were resistant to nalidixic acid and vancomycin (MIC > 256 mg/L), but susceptible to tetracycline (MICs < 0.016-0.5 mg/L) and doxycycline (MICs < 0.016-1 mg/L). The MIC of gentamicin ranged from 1 mg/L (P. limnophilus) to > 256 mg/L (B. marina and P. brasiliensis); the MIC of erythromycin ranged from 0.032 mg/L (P. limnophilus) to 2 mg/L (P. brasiliensis); the MIC for ciprofloxacin ranged from 0.008 mg/L (R. baltica) to > 32 mg/L (P. brasiliensis); and the MIC for colistin ranged from 0.125 mg/L (P. limnophilus) to 96 mg/L (B. marina). CONCLUSIONS: In addition to shedding new light on the biology of Planctomycetes organisms, these data could be used for the further phenotypic characterization of Planctomycetes organisms, and for the optimization of culture media for the primary isolation and growth of Planctomycetes organisms from contaminated specimens.

Molecular evidence for mother-to-child transmission of multiple variants by analysis of RNA and DNA sequences of human immunodeficiency virus type 1.

We have examined the viral selection that may occur during transmission by studying the env gene sequences from four cases of mother-to-child transmission of human immunodeficiency virus type 1. The V3 region sequences were directly amplified from both plasma viral RNA and peripheral blood mononuclear cells containing proviral DNA from mothers at delivery and at the time of diagnosis for children. Transmission occurred perinatally in three cases. The similarity of the viral sequences in each infant sample contrasted with the heterogeneous viral populations in the mothers. Phylogenetic analysis indicated the transmission of one or a few closely related maternal minor virus variants. In contrast, the child virus population in the fourth case was as heterogeneous as that of his mother, and phylogenetic analysis strongly suggested the transmission of multiple maternal variants. This case of multiple transmission was confirmed by analyzing sequences obtained at three times after delivery. Strains with sequences corresponding to the syncytium-inducing phenotype were also transmitted in this fourth case, and this was associated with the rapid development of disease in the child. There was no evidence for transmission of particular viral variants from mother to infant. We have thus described a particular case of vertical human immunodeficiency virus type 1 transmission with the transmission of multiple maternal variants to the infant and a rapid, fatal outcome in the child.

Mutation in splicing consensus sequences causes lack of TCR membrane expression due to exon excision.

T-cell antigen receptor (TCR) membrane-negative T-cell mutants can be divided into two groups: 1) those which lack one of the six TCR polypeptides and 2) those which contain a mutated TCR chain. The present experiments reveal a new mechanism for the development of TCR membrane-negative T-cell variants: mutations in splicing consensus motifs causing excision or misreading of an entire exon (exon 3 of the TCRAC or TCRBC genes). C27.15 cells transcribe a TCR alpha chain consisting of TCRAVJCexon1Cexon2-encoded amino acids plus six new amino acids. The assembly defect seems to be that the truncated alpha chain does not interact with CD3 delta molecules; consequently, no TCR alphabeta/CD3 deltaepsilongammaepsilon complexes are formed. E6.E12 cells transcribe a TCR beta chain composed of TCRBVDJCexon1Cexon2-encoded amino acids plus twenty-seven new amino acids, which seem not to form a transmembrane region. The truncated beta chain does associate with CD3 gammaepsilon heterodimers, yet no TCR alphabeta/CD3 deltaepsilongammaepsilon complexes are made. This may be due either to low assembly of TCR beta/CD3 gammaepsilon trimers or to lack of access of the mutated TCR beta/CD3 gammaepsilon trimers to the TCR alpha/CD3 deltaepsilon compartment in the endoplasmic reticulum.