ABSTRACT
Human parvovirus B19 [B19] exhibits a marked tropism to bone marrow, replicating exclusively in erythroid progenitor cells. Persistent B19 infection tends to occur in immunocompromised hosts and may manifest as pure red cell aplasia and chronic anemia. The aim of the present study was to assess the prevalence of B19 infection in patients with hematological malignancies receiving chemotherapy, and to highlight the relation between B19 infection and unexplained cytopenia[s]. The study included 30 adults and 18 children suffering from a variety of hematological malignancies and receiving chemotherapy. In addition, 10 healthy adults and 10 healthy children [age and sex matched as the studied patients] were included as controls. All patients had unexplained anemia, leukopenia, neutropenia and/or thrombocytopenia and had received a minimum of 4 courses of systemic chemotherapy. B19 infection was investigated both by serologic determination of specific IgG and detection of viral DNA in serum by nested PCR. IgG was detected in 24 [80%] adults and 11 [61.1%] children, while viral DNA was found in 16 [53.3%] adults and 5 [27.8%] children. Only one adult patient [3.3%] was positive for viral DNA and negative for IgG denoting an acute infection. Significant association was detected between unexplained anemia and IgG seropositivity in children. Meanwhile, unexplained thrombocytopenia was significantly associated with the presence of viral DNA in adults. In conclusion, patients with hematological malignancies receiving chemotherapy are at particular risk of persistent B19 infection. Moreover, it is important to consider B19 infection as a possible cause of unexplained cytopenia[s] in these patients. In such cases, administration of intravenous human immunoglobulin can reduce the viremia and correct the cytopenia[s]. Prospective studies are needed to define the serologic and clinical consequences of B19 infection in this group of patients
ABSTRACT
Staphylococcus aureus is recognized as one of the major causes of infections in humans occurring in both, the community and the hospitals. Community-acquired methicillin-resistant Staphylococcus aureus [CA-MRSA] appears to be a new emerging pathogen, which can cause fatal necrotizing pneumonia, skin, and soft tissue infections. Common features of these CA-MRSA strains are the presence of the Panton-Valentine leucocidin [PVL] genes. The aim of this study was to assess the prevalence of Panton-Valentine leucocidin [PVL] encoding genes lukF and lukS among Methicillin-resistant Staphylococcus aureus [MRSA] clinical isolates, and to investigate its association with various types of staphylococcal diseases. Forty seven MRSA isolates were recovered from unique patient clinical specimens: skin and soft tissue infections [SSTI], n=18; bronchoalveolar lavage [BAL] from clinically diagnosed cases of pneumonia, n=20 ; surgical site infections [SSI], n=7; and central venous line [CVL] catheter tip, n=2. Specimens were collected during the period between June 2005 through May 2006. All isolates were tested for the presence of mecA and PVL genes [lukS/F] by single target polymerase chain reaction [PCR]. All isolates were mecA gene positive. The PVL genes were detected in 8[17.02%] of the 47 MRSA isolates included in the study. The prevalence of PVL genes varies with the type of specimen from which MRSA isolates were recovered; 27.8% [5/18] among isolates associated with SSTI, 15% [3/20] among isolates from cases of pneumonia all of them were found to be community-acquired pneumonia; one of them was recovered from a case of acute necrotizing pneumonia. No PVL genes were detected from MRSA isolates recovered from cases of hospital acquired infections including SSI or CVL catheter tips. PVL genes are prevalent among community- acquired MRSA strains with no prevalence among hospital acquired strains. The presence of PVL genes is related to disease severity especially acute necrotizing pneumonia. Close surveillance of these strains is essential to monitor their spread, antimicrobial resistance profiles, and association with disease severity
ABSTRACT
Glycopeptides such as vancomycin are frequently the antibiotics of choice for the treatment of infections caused by methicillin resistant Staphylococcus aureus [MRSA]. Since vancomycin-intermediate Staphylococcus aureus [VISA] was first reported in Japan in 1997, there has been great concern that heterogeneous vancomycin-intermediate Staphylococcus aureus [hVISA] is the putative precursor of VISA. The aim of this study was to explore the prevalence of VISA and hVISA among MRSA strains isolated from hospitalized patients in Alexandria University Hospital over a 2 years period, and to investigate their clinical significance and mechanism of vancomycin resistance. Sixty two MRSA isolates were screened by using brain heart infusion agar supplemented with 4 micro g/ml vancomycin [BHI-V4] and macro E test. Minimum inhibitory concentrations [MICs] of vancomycin were determined by broth microdilution and standard E test. Population analysis profile [PAP] was performed for detecting the frequency of heterogeneous resistance for isolates grown on BHI-V4. Vancomycin intermediate resistant subpopulations of hVISA were viewed with scanning electron microscopy, and tested for the presence of van A gene by PCR. Twenty one [33.87 %] MRSA isolates grew on BHI-V4, 7 [11.29 %] isolates were suspected of having reduced susceptibility to vancomycin by macro E test. The PAP confirmed 6 [9.68 %] isolates as hVISA since they produced subpopulations with MIC of vancomycin of > 4 micro g/ml at frequency of 1 in 10[6] CFU/ml or higher. Vancomycin MIC values for all isolates were
ABSTRACT
Uropathogenic strains of Escherichia coli [UPEC] cause the vast majority of urinary tract infections [UTI] in both community and hospital settings. They exhibit a variety of virulence properties that determine the severity of infection. The aim of this study was to determine the prevalence of two urovirulent genes [papC and cnf1] and production of haemolysin among UPEC strains causing community acquired [CA] and hospital acquired [HA] UTI, to test the susceptibility of these strains to different antimicrobial agents and to screen for extended spectrum beta-lactamase [ESBL] production. One hundred UPEC strains were collected during the period from June 2005 to May 2006 from cases of CA [50 strains] and HA [50 strains] UTI. Of them, 40 strains were isolated from upper UTI cases, and 60 strains were isolated from lower UTI cases. PapC and cnf1 genes were detected by real-time TaqMan PCR assay. Haemolysin production was detected phenotypically. The double disk synergy method was used to screen ESBL production. Fifty strains [50%] possessed one or more of the studied virulence factors. They were significantly more frequent among isolates causing upper UTI [75%] than those causing lower UTI [33.33%, X[2] =6.404, p= 0.011], but, no significant difference was found between CA and HA strains. HA-UPEC strains showed significant higher resistance to third and fourth generation cephalosporins, quinolones, and nitrofurantoin. No resistance to carbapenems was detected among our strains. Quinolone resistance was detected in 52% of the strains, with significant prevalence among lower UTI and HA strains. Forty two strains [42%] were multidrug resistant [MDR], with more significant prevalence among HA strains. Both quinolone resistant and MDR isolates exhibited significantly lower virulence score than did the susceptible isolates. Twenty eight strains [28%] were found to be ESBL producers, 79% of them [22/28] were quinolone resistant with no significant differences regarding their source. None of the ESBL producers possessed any of the studied virulence genes. Overall, the results showed that virulence factors were more prevalent among isolates causing upper UTI. Quinolone resistance itself may be a virulence factor in lower UTI with an observed association between it and ESBL production. Further studies are needed to clarify these relations
ABSTRACT
The increased use carbapenems for the treatment of infections caused by multiresistant Pseudomonas aeruginosa [P. aeruginosa] has resulted in the development of carbapenem resistant [CR] P. aeruginosa. In recent years, the metallo-B-lactamases [MBLs] have emerged as one of the most feared resistance mechanisms because of their ability to hydrolyse virtually all B-lactam agents including the carbapenems, and because their genes are carried on highly mobile elements. This study was carried out to investigate the prevalence of MBLs among clinical isolates of carbapenem-resistant P. aeruginosa, and to characterize their molecular types. A total of 134 non-repetitive clinical isolates of P. aeruginosa were collected and tested for carbapenem resistance by disk diffusion method with imipenem and meropenem. Minimum inhibitory concentrations [MICs] were determined by the microdilution technique according to CLSI guidelines. Carbapenem-resistant isolates were screened for the presence of MBLs by imipenem EDTA double disk synergy test. Isolates with screen positive results were confirmed by EDTA inhibition of imipenem hydrolysis with their crude cell extracts, and by PCR using primers for detection of bla[IMP-1], bla[IMP-2], bla[VIM-1], bla[VIM-2], and intI1 genes. Out of the 134 P. aeruginosa clinical isolates included, 75 [56%] isolates were CR, among them MBL phenotype was detected in 30 [40%] isolates by the double disk synergy test. EDTA sensitive hydrolysis of imipenem by crude cell extracts confirmed 14 [46.7%] isolates as MBL producers. PCR detected MBL genes among 15 [50%] isolates; 11 [73.3%] isolates were positive for bla[VIM-2], and 4 [26.7%] isolates were positive for bla[IMP-1]. The integrase gene [intI1] was detected in all of the 15 genotypically MBLpositive isolates. No isolate harboring bla[IMP-2], or bla[VIM-1] was detected. Continued screening for MBLs production among CR P. aeruginosa isolates will be essential to control dissemination of this important resistant mechanism, ensure optimal patient care, and the timely introduction of appropriate infection control procedures. PCR is an important step, since EDTA based screening tests can give false positive results
ABSTRACT
Helicobacter pylori [H. pylori] is the main cause of several gastro-duodenal diseases, and is also related to a variety of extragastric diseases, including liver diseases. It was classified as class I carcinogen. Several risk factors for the development of hepatocellular carcinoma [HCC] are identified. Continuing attempts are being made to identify other risk factors. The objective of this study was to evaluate the presence of H. pylori DNA in human HCC to determine if H. pylori may contribute to the development of this disease. Liver specimens from 33 patients with HCC as well as from 6 patients who did not have malignancy; 4 had cholelithiasis and 2 had hepatic hemangioma considered as control, were studied. Liver samples were examined by polymerase chain reaction [PCR] for the presence of genomic 16S rRNA of Helicobacter genus using specific primers. Besides, other genes; 26 kDa cell surface protein, cag A, and vac A, specific for H. pylori and mdh specific for E. coli were also screened by PCR. In addition, the specimens were examined for H. pylori by immunohistochemical procedure using anti-H. pylori antibody. Helicobacter genus-specific 16S rRNA was found in 12 out of the 33 [36.4%] samples of HCC tissues, whereas none of the 6 control liver specimens were found to harbor this rRNA. The H. pylori species-specific 26 kDa protein gene was detected in 11 of the 12 [91.7%] samples positive for the Helicobacter 16S rRNA gene thus confirming the presence of H. pylori DNA in 33.3% of the HCC samples. Within these 11 HCC samples, the cag A gene was detected in only 3, whereas the vac A and mdh genes were not detected. Helicobacter pylori immunostaining was recognized in 7 HCC specimens [21.2%], which were also positive for H. pylori species-specific DNA detection by PCR with statistically very high significant association [p = 0.0001]. The presence of microscopic evidence of hepatitis [10 cases] and cirrhosis [15 cases] presented a significant association with both H. pylori DNA detection [p = 0.0320 and 0.0260 respectively] and immunoreactivity [p = 0.0075 and 0.0158 respectively]. These data indicate that the detection of H. pylori by means of molecular methods and immunohistochemistry in human HCC tissue supports the concept of the possible association between H. pylori and HCC development. However, their eventual role in hepatocarcinogenesis, although it is plausible, remains to be proven