Pneumonia caused byCandida kruseiandCandida glabratain a patient with chronic myeloid leukemia receiving imatinib mesylate treatment

Abstract

In this report we describe a patient suffering from chronic myeloid leukemia (CML), who was treated for 4.5 years with imatinib and developed pneumonia caused by two Candida species, i.e., C. krusei and C. glabrata. The patient was in complete hematologic remission and molecular analyses did not display the presence of TLR2-R752Q, TLR4-D299G and TLR4-T399I polymorphisms that may predispose individuals to fungal infections. This case report indicates that in some patients, as previously observed, the long-term administration of targeted therapy might affect immunity and predispose patients to opportunistic and life-threatening fungal infections.

Chronic myeloid leukemia patient manifesting fatal hepatitis B virus reactivation during treatment with imatinib rescued by liver transplantation: case report and literature review

“…More specifically, imatinib can impair the immune response by preventing the differentiation of progenitor stem cells and inhibit delayed-type hypersensitivity, as shown in mice, indicating that the drug can potentially inhibit the T-cell response [15,16]. In fact, various opportunistic infections associated with imatinib treatment, including herpes zoster, candida species, and pulmonary tuberculosis, have been reported [3,17,18].…”

TLR2 and TLR4 polymorphisms in familial Mediterranean fever

“…The detection of TLR4-D299G and TLR4-T399I polymorphisms was performed by allele-specific polymerase chain reaction followed by restriction fragment length polymorphism (PCR-RFLP) analysis, as described previously [21,22]. In brief, the forward primers, in both reactions, were modified at the 5= end, creating restriction enzyme recognition sites (NcoI for the TLR4-D299G polymorphism and HinfI for the TLR4-T399I), so that if a polymorphism is present, PCR-RFLP analysis will create digestion fragments, visible on agarose gels [21,22]. The detection of TLR2-R753Q polymorphism was also performed by PCR-RFLP.…”

Toll-Like Receptor 4 Gene ( TLR4 ), but Not TLR2 , Polymorphisms Modify the Risk of Tonsillar Disease Due to Streptococcus pyogenes and Haemophilus influenzae

“…Detection of the TLR4-D299G and TLR4-T399I SNPs was performed by allele-specific PCR, followed by restriction fragment length polymorphism (PCR-RFLP) analysis, as described previously (16,29). In brief, in both reactions the forward primers were modified at the 5Ј end, creating restriction enzyme recognition sites (NcoI for the TLR4-D299G polymorphism and HinfI for the TLR4-T399I polymorphism), so that if a polymorphism was present, PCR-RFLP analysis would create digestion fragments visible on agarose gels (16,29). The primers for the detection of the TLR4-D299G SNP were forward primer 5Ј-GATTAGCATACTTAGACTACT ACCTC(G)CATG-3Ј and reverse primer 5Ј-GATCAACTTCTGAAAAAGCA TTCCCAC-3Ј.…”