Gene expression of RD5 and Psp5 in extra intestinal Entamoeba histolytica isolated from liver abscesses.

Liver abscesses are known to be trophozoites of the amoeba parasite. They are devoured by the neutrophil cells in the liver and become large assemblies because these white cells do not eliminate the parasite and these white cells multiply. In this study, venous blood samples were taken from 61 patients have hepatic amoebosis and 61 healthy individuals as a control group. The patients attended Ghazi Al-Hariri Surgical Specialities Hospital, the Medical City, Baghdad, Iraq during the period from 15th January to 18th September 2021. The results showed that the mean age of patients was (41.84±15.88) years, while the mean age of the control group was (41.84±15.88) years with no significant difference (P>0.05). The prevalence rate of Entamoeba histolytica infection was 27 (44.2%) in males, and 34 (55.8%) in females with no significant difference. The mean anti-Entamoeba antibody IgA in urban areas was (1.95±1.25) and in the rural areas was (2.05±1.10), while the mean anti-Entamoeba antibody IgG in urban areas was (14.86±6.71), and in the rural areas was (13.55±7.43), with no significant differences (P>0.05). The mean anti-Entamoeba antibody IgA was (2.00±1.17) among the patient's group in comparison with the control group which was (0.09±0.17), while the mean anti-Entamoeba antibody IgG was (14.20±7.06) among the patients when compared with the control group which was (0.06±0.11) with highly significant differences (P<0.01). Expression of RD5 gene was investigated in E. histolytica in liver abscess patients and healthy controls by using qRT-PCR and the findings of amplification regarding atypical amplification plot. The amplification reaction had an early threshold cycle that was consistent with high levels of RD5 gene and the healthy controls. Psp5 gene was expression to investigated E. histolytica in liver abscess in 60 patients and (60) individuals as a control group by using qRT-PCR and the findings of amplification regarding atypical amplification plot. The amplification reaction had an early threshold cycle that was consistent with high levels of Psp5 gene and the healthy controls.

Identification of virulence factors in Vibrio cholerae isolated from Iraq during the 2007-2009 outbreak.

Thousands of people were infected with Vibrio cholerae during the outbreak in Iraq in 2007-2009. Vibrio cholerae was shown to be variable in its content of virulence determinants and in its antibiotic sensitivity. This study was designed to isolate and characterize clinical and environmental V. cholerae isolates and to determine antibiotic sensitivity, enzyme and toxin production, and the presence of virulence genes. Eighty clinical and five environmental bacterial isolates were collected and diagnosed by subjecting them to microscopic, biochemical, serological, and molecular analysis. The results revealed that 55% of clinical isolates belonged to the Inaba serotype, 32.5% to the Ogawa serotypes, and 12.5% to the Non-O1 serotype. All environmental V. cholerae isolates belonged to the Non-O1 serotype. All environmental isolates were sensitive to all examined antimicrobial agents, while all clinical isolates showed a high sensitivity (100%) to ampicillin, gentamicin, cephalothin, tetracycline, erythromycin, and ciprofloxacin, and a high resistance (97.5%) to co-trimoxazole, nalidixic acid, and chloramphenicol. It was found that all V. cholerae (O1) isolates were resistant to the Vibrio static O129 and all Non-O1 V. cholerae isolates were sensitive to the Vibrio static O129. All clinical and environmental isolates produced hemolysin (100%) and lecithinase (100%), while they showed various production rates of protease (90% of clinical and 60% of environmental) and lipase (50% of clinical and 20% of environmental). The ompW gene was amplified in all the clinical and environmental V. cholerae isolates, but not in other related and nonrelated bacteria. Multiplex PCR analysis showed that the toxR gene was amplified in all clinical and environmental isolates, while ctxA, ctxB, tcpA genes were amplified only in clinical (O1) isolates. This study indicates the differences in the production of some enzymes and toxins and in the content of virulence genes between clinical and environmental isolates in Iraq during the outbreak (2007-2009).