What is the difference between mycoplasma pneumoniae and streptococcus pneumoniae
Pneumonia is an infection of the lungs that viruses, bacteria, and fungi can cause. A common cause of typical bacterial pneumonia is Streptococcus pneumoniae. Skip directly to site content Skip directly to page options Skip directly to A-Z link.
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Medically reviewed by Graham Rogers, M. What causes mycoplasma pneumonia? Who is at risk for developing mycoplasma pneumonia? What are the symptoms of mycoplasma pneumonia? How is mycoplasma pneumonia diagnosed? What are the treatment options for mycoplasma pneumonia?
How can I prevent mycoplasma pneumonia? How does mycoplasma pneumonia affect children? What are the complications of mycoplasma pneumonia? What is the long-term outlook? Read this next. Medically reviewed by Stacy Sampson, D. Medically reviewed by Karen Gill, M. Medically reviewed by Debra Rose Wilson, Ph. Can Pneumonia Be Contagious? The strains are indicated by their sequence ID listed in Table 1.
Only the variants with a frequency above 0. Hierarchical clustering was applied based on Euclidean distance and the average linkage method hclust. Using this procedure, we were unable to identify variants that were shared between all samples from the same group.
Although a number of variants were shared between some samples from the same group Table 2 , we did not find specific sequence differences between the strains from the group of symptomatic patients Groups 3 and 4 and those from the other groups Groups 1 and 2.
Variant frequencies for the different comparisons are shown in Tables 2 — 4. Two of the isolates that were sequenced were acquired at two different time-points from the same patient. The other isolate, HAPFUP, was taken 4 weeks later, after resolution of the infection following a course of antibiotics azithromycin.
One of these differences was localized to the P1 gene MPN , which encodes the major attachment protein of M. This triplet is part of a previously described tandem repeat of which the biological relevance is yet unknown Dorigo-Zetsma et al. Two of the strains C and C were isolated from the same patient at a single time point. These strains were analyzed separately because they displayed different colony morphologies on agar plates.
The sequences of these strains were found to be highly similar Figure 1 : only 5 SNPs were identified between these strains Table 4. Table 4. Variant frequencies of the isolates C and C with different colony morphologies. We determined the complete genome sequences of M. In addition, we analyzed the genomes of 3 M.
In a comparison of these sequences, we could not identify a specific genotype that is associated with M. Our previous findings on sequence variation among M. In the current analysis of whole-genome sequences of 20 different M. These findings are concordant with those of Xiao et al. In their analysis, the sequences of 15 M. Similarly, Lluch-Senar et al. However, they do report a high rate of variation among repetitive elements in the M. Although we were able to reliably determine the genomic sequences of M.
In routine microbiological diagnostics, asymptomatic patients are usually not tested for the presence of M. In addition, in our previous study on asymptomatic carriage of M.
Clearly, for genomic sequence analysis, culturing is a crucial step in obtaining pure, clonal bacterial isolates. Nevertheless, in future studies, we aim to obtain higher number of M. This should provide more insight in the physiology of asymptomatic colonization of the human respiratory tract by M. Another important issue to consider is whether or not M. Recent studies have indicated that multiple pathogens can be present in the respiratory tract of children and adults with RTI Spuesens et al.
As a consequence, we cannot rule out that pathogens other than M. Clearly, this may have obstructed the identification of potential genomic features that allow discrimination between pathogenic M. In conclusion, in this study we have shown that there is no specific genotype that can be associated with M. In addition, we found marked genetic differences between clinical isolates and the reference strains, which indicated that the latter strains may not be regarded as appropriate representatives of circulating M.
RJ provided the clinical information and some of the M. ES wrote the first draft of the manuscript and was responsible for the subsequent modifications. All authors were involved in the final modifications of the manuscript. The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. Supplementary File 1. Fast QC files. HTML files per strain.
Supplementary File 2. MUMmer alignments. The alignments of the generated genome assemblies to the M reference genome. Supplementary File 3. Generated contigs. Generated genome assemblies per strain. Supplementary Figure 1. The results of the optimization on the assembly statistics.
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