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<taxonomicName id="4C3F01E7157A4843FF0EFF6189075EF7" ID-CoL="4KKVL" authority="Frenkel" authorityName="Frenkel" box="[136,258,223,249]" class="Pneumocystomycetes" family="Pneumocystaceae" genus="Pneumocystis" kingdom="Fungi" order="Pneumocystales" pageId="3" pageNumber="184" phylum="Ascomycota" rank="species" species="jirovecii">
<emphasis id="B94BA676157A4843FF0EFF6189075EF7" bold="true" box="[136,258,223,249]" italics="true" pageId="3" pageNumber="184">P. jirovecii</emphasis>
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prevalence and patients
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<emphasis id="B94BA676157A4843FDB1FF618ADA5EF4" bold="true" box="[567,735,223,250]" pageId="3" pageNumber="184">characteristics</emphasis>
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Among all renal transplant recipients tested (
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= 72, including
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,
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), the mean age was 52.5 ± 13.9 years, range 2176 years. The mean time after kidney transplantation was 78.7 months, ranging from 5 days to 19 years. Nine patients had undergone the second kidney transplantation, and two had undergone the third transplantation. One patient had undergone both kidney and heart transplantation. Immunosuppressive treatment included prednisone, calcineurin inhibitors (tacrolimus or cyclosporine), proliferation signal inhibitors (sirolimus or everolimus), mycophenolate mofetil, or azathioprine. Forty-four (61.1%) patients were receiving treatment combining three of the above drugs, 25 (34.7%) were receiving a dual combination, and 3 (4.2%) were treated with
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of immunosuppressant only (patients who required dialysis after kidney transplant failure). The routine anti-
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prophylaxis regimen contained co-trimoxazole at a dose of
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a day for 6 months after transplantation. Among all patients examined, 13 were receiving co-trimoxazole prophylaxis during sputum collection, and one patient was receiving only trimethoprim due to a previous allergic reaction to sulfamethoxazole.
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Nested
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amplifying the
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rRNA gene of
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<emphasis id="B94BA676157A4843FF0EFC4188FD5A18" box="[136,248,1023,1046]" italics="true" pageId="3" pageNumber="184">P. jirovecii</emphasis>
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was positive in eight of the 72 (11.11%) patients samples. Three of these eight patients showed symptoms compatible of pneumonia (including low-grade fever, dyspnea, and radiological presentation). In samples from only three patients (37.5%),
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presence was confirmed by IF staining, and only in one of these cases the number of cysts observed on the whole microscope slide was above five. That was the only case with both a positive result of IF staining and the presence of respiratory symptoms typical for PcP. Anti-
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therapy was introduced in this patient, in view of PcP suspicion. Due to the patient s allergy to sulfamethoxazole, it consisted of intravenous clindamycin (
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every 8 h on the first day and
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every 6 h afterwards) and primaquine for 29 days. The treatment was completed after the negative result of control
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analysis and pentamidine was introduced for prevention.
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The most important characteristics of
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<emphasis id="B94BA676157A4843FDBFF9AC8AAC5827" box="[569,681,1554,1577]" italics="true" pageId="3" pageNumber="184">P. jirovecii</emphasis>
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-positive and
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<emphasis id="B94BA676157A4843FF30F98D89205844" box="[182,293,1587,1610]" italics="true" pageId="3" pageNumber="184">P. jirovecii</emphasis>
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-negative patients are listed in
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statistically significant correlation with colonization was observed for the employment of a dual immunosuppressive regimen consisting of calcineurin inhibitors and prednisone (
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= 0.041, Fisher s exact test). Moreover, the mean eosinophil level was lower in
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positive patients, as compared to negative ones (
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= 0.040, Student s
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test). There were no significant differences in results of basic laboratory tests for other parameters,
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infection, or other co-morbidities.
</paragraph>
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<emphasis id="B94BA676157A4843FCB6FF228C045EB9" bold="true" box="[816,1025,156,183]" pageId="3" pageNumber="184">Multilocus typing</emphasis>
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Only
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rRNA was fully genotyped in all analyzed specimens. The ratios of efficient amplification of the other genetic fragments were 50% for
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, 62.5% for
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, and 87.5% for
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(
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). Since multilocus genotype is a combination of at least two loci, such complex analysis was not possible due to incomplete data required. Therefore, single genetic fragments were analyzed individually in order to verify the presence of any statistically significant correlations between
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distribution and patients data.
</paragraph>
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Three of the five previously described
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rRNA genotypes were identified: genotype 1 (wild
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) was found in four patients samples (50%), while genotypes 2 and 3 were detected in one (12.5%) and three (37.5%) other patients, respectively. The most common
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genotypes were
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1 and 2, both occurring in two (28.6%) cases. The remaining identified genotypes were
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5, 7, and 8, occurring in one case each (14.3%).
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polymorphisms were identified in four samples only, half of which referred to wild-type genotype (
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1), and the other half to
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2. Finally,
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typing revealed the presence of genotype 1 (wild-type only) in all five successfully amplified samples.
</paragraph>
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There were no significant differences in
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distribution and gender, immunosuppressive regimen, or PcP symptoms. However, it was observed that detection of
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2 genotype was significantly correlated with the ongoing prophylaxis regimen (
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0.047, Fisher s exact test). Moreover, both mean age (
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0.033, Student s
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test) and time after kidney transplantation (
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0.028, Student s
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test) were significantly lower in patients with detected wild-type
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rRNA genotype (44.5 years, 58.1 months, respectively) than in those with mutant genotypes (65.8 years, 78.3 months, respectively).
</paragraph>
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typing in patients with various pulmonary diseases was possible in 53% of available samples. Similarly, only genotype 1 was detected. Comparison of RTRs and patients with various pulmonary diseases (whose data on demographic, prevalence, and genotype distribution were described previously;
<bibRefCitation id="EFAE0795157A4843FB95FA338CE15BAA" author="Sokulska M &amp; Kicia M &amp; Wesolowska M &amp; Piesiak P &amp; Kowal A &amp; Lobo ML &amp; Kopacz Z &amp; Hendrich AB &amp; Matos O" box="[1043,1252,1421,1444]" pageId="3" pageNumber="184" pagination="809 - 815" refId="ref8777" refString="Sokulska M, Kicia M, Wesolowska M, Piesiak P, Kowal A, Lobo ML, Kopacz Z, Hendrich AB, Matos O (2017) Genotyping of pneumocystis jirovecii in colonized patients with various pulmonary diseases. Med Mycol 56: 809 - 815. https: // doi. org / 10.1093 / mmy / myx 121" type="journal article" year="2017">Sokulska et al. 2017</bibRefCitation>
) did not reveal any significant differences in
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distribution or
<taxonomicName id="4C3F01E7157A4843FAB2FA108DAE5BCB" box="[1332,1451,1454,1477]" class="Pneumocystomycetes" family="Pneumocystaceae" genus="Pneumocystis" kingdom="Fungi" order="Pneumocystales" pageId="3" pageNumber="184" phylum="Ascomycota" rank="species" species="jirovecii">
<emphasis id="B94BA676157A4843FAB2FA108DAE5BCB" box="[1332,1451,1454,1477]" italics="true" pageId="3" pageNumber="184">P. jirovecii</emphasis>
</taxonomicName>
prevalence.
</paragraph>
</subSubSection>
</treatment>
</document>