Association of Epstein-Barr virus with systemic lupus erythematosus: relation to disease activity and flare-ups

To determine the prevalence of IgM, IgG and IgA antibodies against Epstein Barr, virus capsid antigens [EBV-VCA] in systemic lupus erythematosus [SLE] patients and to clarify their relation to disease activity and flare. The study comprised forty adults SLE patients; they were 35 females and 5 males, 'their ages ranged from 21-35 years [mean +/- SD 29.3 +/- 4.2] and forty normal subjects; 36 females and 4 males with a mean age value of 29.2 +/- 3.9 as a control group. Patients were subjected to thorough medical history taking, clinical examination, laboratory investigations, disease activity assessment and disease flare assessment within one year and detection of EBV IgG, IgM and IgA antibodies in the serum against EBV -VCA for patients and control groups. There was non significant difference as regards the prevalence of anti EBV IgG and IgM in both SLE patients and control groups. A significant difference of serum IgA antibody against EBV-VCA between SLE patients and control groups was found; 15/40 [37.5%] vs. 2/40 [5%]; p<0.001. The systemic lupus erythematosus disease activity index [SLEDAI] score was significantly higher in the SLE patients with IgA antibody against EBV-VCA than in the SLE patients without IgA antibody [29 +/- 7.7 VS 23.4 +/- 3.2; p<0.001]. As regard the disease flare we found that the SLE patients with IgA antibody against EBV-VCA had higher prevalence of disease flare compared to those without IgA antibody 10 [66.7%] vs. 2 [8%], p<0.001. The close clinical data association between EBV infection and SLE suggests a possible role of the EBV as a trigger in the Pathogenesis, disease activity and flare of SLE patients. Further, studies should be done to elucidate the complex relationship between EBV infection and SLE patients

association of HLA class II with hepatitis C virus induced autoimmunity

Patients with chronic hepatitis C virus [HCV] infection may suffer from some autoimmune disorders. The pathogenesis of autoimmunity in those patients remains unclear but may reflect the host's genetic predispositions. Human leukocyte antigen [HLA] may play a predominant role in this aspect. The aims of this study were to assess the production of autoantibodies in chronic HCV patients and to investigate for the presence of a possible link between the HLA-DRB1 alleles and production of autoantibodies in chronic HCV patients

Methods: This study included 60 HCV infected patients who were previously diagnosed as having chronic HCV infection. These patients were investigated for the presence of autoantibodies [ANA by ELISA, ASMA by indirect immunofluorescent technique, anti-ds-DNA by latex agglutination method, and LKM-1 by ELISA]. Also, they were investigated for HLA-DRB1 by PCR technique and reverse dot-blot hybridization. The studied individuals were divided according to the presence or absence of autoantibodies into two main groups: group I [HCV infected patients with autoimmunity], group II [Pathological control group, HCV infected patients without autoimmunity]. The results of this study showed that the most prevalent HLA-DRB1 broad types in group I were HLA-DRB1 *03, *04 and *16. Moreover, these three types were significantly higher in group I compared to group II [P < 0.05]. The most prevalent HLA-DRB1 broad types in group II were HLA-DRB1 *7 and *8 and the prevalence of each was higher in group II compared to group I and the difference was highly significant [P < 0.01]. The frequencies of the alleles 030101, 030501, 040702, 160101 and 160102 were significantly higher in group I than group II, while the alleles 0812 and 110103 were significantly lower in group I than in group II. In conclusion, the results of this study suggested that some HLA-DRB1 broad types and alleles may predispose to or protect from HCV-induced autoimmunity in Egyptian patients who suffer from chronic HCV infection. These findings may allow better selection of management strategies for these patients after detection of HLA-DRB1 types which may be helpful to predict those who are susceptible to HCV-induced autoimmunity

Impact of serum interleukin-10 in pathogenesis of chronicity in hepatitis C virus patients

Hepatitis C virus [HCV] has emerged as a major cause of liver disease worldwide. Most people who contact HCV infection become persistently infected, and the mechanism by which infection is established seems to be related to the lack of development of effective immune response. The aim of this study was evaluation of the role of IL-10 which is a marker of T helper-2 [Th-2] cell activities in the pathogenesis of chronicity of HCV

Methods: Forty five subjects were included in the study. They were divided into three groups as follows: group I [Control group] included 15 healthy individuals, group II included 15 individuals with positive ELISA test for hepatitis C antibodies but with negative PCR test for HCV RNA and Group III included 15 patients with positive ELISA test for hepatitis C antibodies and positive PCR test for HCV RNA. Complete history taking, full clinical examination and ultrasonography were done for all individuals included in this study. All individuals were subjected to the laboratory investigations including Liver function tests, measurements of liver enzymes, ELISA test for HCV antibodies, PCR for HCV RNA and determination of IL-10 by ELISA technique

Results: there was a highly significant increase in the level of IL-10 in group II and group III when compared with control group [P<0.001], also, IL-10 showed a highly significant increase in group III when compared with group II [P<0.001]. There was also a highly significant positive correlation between IL-10 and each of the liver enzymes: ALT, AST, ALP and GGT. In conclusion, this study shows that patients with chronic HCV infection have an elevated level of serum IL-10 which reflects increased T-helper type 2 cell activities that may lead to suppression of Th1 cells which may contribute to the pathogenesis of chronic HCV infection. According to these findings, IL-10 assay may be used as a test to predict those who are liable to develop progressive chronic hepatitis C or the possible response to different lines of treatment. Moreover, the findings of this study drive the attention to the need to develop new therapeutic approaches to help in treatment of HCV patients applying immunological manipulations that suppress Th2 immune activity and stimulate Th1 immune response which is needed to control this type of infection. These possible new strategies for immunotherapy may help HCV patients for viral clearance or at least may allow better control of the infectious process

Lymphocytes subsets alterations in cases of co-infection with both hepatitis C virus and S. mansoni

The aim of this study was to investigate the presence of any possible alterations in different lymphocytes subsets in patients co-infected with HCV and S. mansoni which may be responsible for higher rate of viral persistence and aggressive course of hepatitis and liver fibrosis in these co-infected patients

Methods: 42 individuals were divided into four groups: Group I included normal control [n=10], Group II: patients with HCV mono-infection [n=9], group III: patients with S. mansoni mono-infection [n=11] and group IV of patients with HCV and S. mansoni co-infection [n=12]. For all subjects included in this study, count of lymphocytes subsets in the peripheral blood was done by flowcytometry applying a two color immuno-fluorescence technique using pairs of monoclonal antibodies conjugated with both fluorescein isothiocyanate [FITC] and phycoerythrin [PE]

Results: B lymphocytes [CD19+] showed no significant alterations in all groups while T lymphocytes [CD3+] showed a significant increase in both HCV mono-infection group and S. mansoni mono-infection group and a highly significant increase in the co-infection group. Natural killer [NK] cells [CD16+ and/or CD56+] showed a significant decrease in the group of HCV monoinfection patients, no significant alterations in the S. mansoni mono-infection group and a highly significant decrease in the co-infection group. T helper [CD4+] cells showed a significant increase in HCV mono-infection patients and in the co-infection group but with no significant alteration in S. mansoni mono-infection group while T cytotoxic [CD8+] cells showed a significant increase in both HCV mono-infection group and S. mansoni mono-infection group and a highly significant increase in the co-infection group. Activated T lymphocytes [CD3+ HLA-DR+] showed a highly significant increase in HCV mono-infection patients with no significant changes in S. mansoni mono-infection group and a significant increase in the co-infection group. The degree of increase of activated T lymphocytes was significantly higher in the HCV mono-infection patients compared to those co-infected with S. mansoni. In conclusion, results of this study suggest that co-infection of HCV patients with S. mansoni is associated with some immune system alterations that may explain the increased persistence and severity of HCV infection. Also, these findings suggest that there is an urgent need to introduce new therapeutic approaches that stimulate strong cellular immune responses which might limit the progression and severity of HCV infection in these co-infected patients

Hospital and community acquired methicillin resistant staphylococcus aureus infections and their association with panton-valentine leukocidin gene

Methicillin resistant S. aureus [MRSA], besides having established itself as a major hospital pathogen, is now beginning to prevail in the community. However, several notable differences were found to exist between hospital acquired strains [HA-MRSA] and community acquired strains [CA-MRSA]. Panton-Valentine leukocidin gene [PVL] is a cytotoxin which was found to represents an important virulence factor in some strains of S. aureus which cause some sorts of severe infections. The aims of this study were to assess the association of PVL gene with HA-MRSA and CA-MRSA and the role of this gene in pathogenesis of these infections

Methods: Two groups of patients with different types of infections were included in this study: the first group included 150 patients with hospital acquired infections and the second group included 85 patients with community acquired infections. All isolated S. aureus strains were tested for methicillin resistance by determination of MIC [minimum inhibitory concentration] using agar dilution method. All the detected MRSA isolates were tested for the presence of PVL gene by polymerase chain reaction [PCR]

Results: within the isolated CA S. aureus strains, MRSA isolates were found to be significantly higher compared to MRSA isolates from HA S. aureus infections [30/52: 57.7% and 25/74: 33.7% respectively]. PVL gene was detectable in 16/30 [53.3%] of CA-MRSA isolates while this gene was not found in any of HA-MRSA [0/25: 0%]. In CAMRSA isolates, PVL gene was found in 2/2 [100%] of cases with pneumonia, 8/10 [80%] of cutaneous abscesses, 4/4 [100%] of cases with furunclosis, 1/3 [33.3%] of finger pulp infections, 1/2 [50%] of breast abscesses while no isolates from cases with cellulites, impetigo or osteomyelitis harbored the PVL gene

Conclusion: our results revealed that PVL gene is strongly associated with CA-MRSA while it is not associated with HA-MRSA. PVL gene is mostly associated with primary necrotic infections [abscesses, furunclosis and Pneumonia], but not with invasive and secondary infections commonly encountered in HA S. aureus infections. The results of this study drive the attention to the current increase of CA-MRSA in Egypt which makes implementation of infection control guidelines of great concern to prevent more dissemination of MRSA in the community or to hospitals. A wide scale study of CA and HA-MRSA is recommended on the national level in Egypt to investigate the general prevalence rate, pathogenesis and the changes in antibiotic resistance and their relations to PVL gene and other genetic and virulence factors which may allow better management and control of these infections

Assessment of T helper 1 and T helper 2 cytokines and their correlations with viral load in HCV patients co-infected with S. mansoni

The aim of this study was to investigate the effect of infection with S. mansoni on the balance between Th-1 and Th-2 cytokines in patients with chronic hepatitis C virus [HCV] infection and to show the relations between these two groups of cytokines to the degrees of viral load in these patients. 44 individuals were classified into 4 groups: group I of control subjects [n=10], group II of patients with S. mansoni mono-infection [n=9], group III of patients with chronic HCV mono-infection [n=13] and group IV of patients with both S. mansoni and HCV co-infection [n=12]. For individuals of all studied groups, interferon-gamma and IL-2 [cytokines of Th-1 cells] and IL-4 and IL-10 [cytokines of Th-2 cells] were measured. Viral load was measured for patients of group III [HCV mono-infection] and group IV [co-infected patients]. The results showed that Th-1 cytokines [IFN-gamma and IL-2] were significantly higher in HCV mono-infection patients and significantly lower in patients co-infected with HCV and S. mansoni compared to normal subjects group. In S. mansoni mono-infection group, IFN-gamma was decreased while IL-2 was normal compared to normal control group. Th-2 cytokines [IL-4 and IL-10] were significantly higher in the three patients groups compared to the control group but the degree of increase of IL-4 showed no significant difference between S. mansoni mono-infection patients and HCV mono-infection patients while the degree of increase of IL-10 was higher in S. mansoni mono-infection patients compared to HCV monoinfection patients. The degree of increase of both IL-4 and IL-10 was significantly higher in the coinfection patients compared to the HCV mono-infection patients. Viral load was significantly higher in the co-infected group compared to HCV mono-infection group and in both groups, the viral load was positively correlated with Th-2 cytokines and negatively correlated with Th-1 cytokines [except IL-2 in the group of HCV mono-infection patients]. In conclusion, these results suggest that HCV patients co-infected with S. mansoni suffer from strong activation of Th-2 cells and so increase of Th-2 cytokines that suppress Th-1 cells and related cytokines which is the type of immune response needed in face of HCV. This Th-1/Th-2 imbalance allows more viral replication and higher viral load in these patients compared to HCV patients who are not co-infected with S. mansoni and this may give an explanation to the rapid hepatic deterioration of these co-infected patients

Rapid diagnosis and characterization of diarrheagenic Escherichia coli in Egyptian children using multiplex PCR

Escherichia coli [E.coli] is the most important etiologic agent of childhood diarrhea and represents a major public health problem in developing countries. Aim of this work was to investigate the role of diarrheagenic E.coli in Egyptian children below 5 years age using multiplex PCR and to evaluate multiplex PCR in rapid diagnosis of enteric infections caused by diarrheagenic E.coli strains. Rectal swabs were taken from 83 children under 5 years age with diarrhea and 33 age-matched controls. All E.coli isolates were O serotyped using E.coli O polyvalent and monovalent antisera and subjected to multiplex PCR assay with specific primers, eae primer of eaeA [gene of intimin of EHEC and EPEC], primer bfpA of bfpA [structural gene for the bundle-forming pilus of EPEC], primers VT1 and VT2 of vt1 and vt2 genes [genes of shiga toxins 1 and 2 of EHEC respectively], primer LT of eltB [gene of labile toxin of ETEC], primer ST for estA [gene of stable toxin of ETEC], primer SHIG of ial [invasion-associated locus of the invasion plasmid found in EIEC] and primer EA of pCVD [the nucleotide sequence of the EcoRIPstI DNA fragment of pCVD432 of EAEC]. The study revealed that diarrheagenic E.coli strains were significantly isolated from patients more than control using multiplex PCR. Out of 70 E.coli strains isolated from patients, 17[24.3%] isolates were proved to be diarrheagenic by multiplex PCR where 53 [75.7%] isolates were non diarrheagenic. Out of 30 E.coli isolates recovered from control group, 1 [3.3%] isolate was proved to be diarrheagenic by multiplex PCR where 29 [96.7%] isolates were non diarrheagenic[Chi-square=18.5 and p

Soluble L-selectin, vascular endothelial growth factor and endothelin-1 in patients with ulcerative colitis

Recent evidence increasingly suggests that ulcerative colitis [UC] is the result of dysfunctional immunoregulation manifested by an inappropriate production of mucosal cytokines. An abnormal microcirculatory system has also been implicated in its pathogenesis. The objective of this study was to assessed serum concentrations of soluble L-selectin [sL-selectin] and vascular endothelial growth factor [VEGF] and the plasma level of endothelin-1[ET-1] in the patients with UC, compared with healthy controls, and to analyze the results depending on the stage of the disease. This study was conducted on two groups of subjects, the patient group including 30 patients with active ulcerative colitis [UC], and the control group which included 15 healthy volunteers. We assessed serum sL-selectin, VEGF and Plasma ET-1 Level at the beginning of the study in patients and controls then measured again in patients after remission. The levels of sL-selectin, VEGF, and ET-1 were significantly higher in active UC than those in the controls [p < 0.001]. But in remission there was no significant difference between UC patients and controls in VEGF and ET-1 levels. We also found that serum Level of sL-selectin, VEGF, and Plasma Level of ET-1 were significantly higher in patients with active UC compared with patients in remission [p < 0.001]. In addition, it is shown that UC patients in remission have significantly lower levels of sL-selectin than controls. There was a significant positive correlation among the serum levels of VEGF and the plasma level of ET-1; that is, elevated VEGF, and ET-1 levels correlated well with each other in active UC patients [r= 0.631, p < 0.001]. The most common form of the disease observed in our patient population was of mild to moderate severity. Pro-inflammatory cytokines, including sL-selectin, VEGF, and ET-1 appear to play a significant role in the pathogenesis of ulcerative colitis [UC]. Their levels were higher during exacerbation while it is low in periods of remission in UC patients

Prediction of small-for-gestational age infents by quantitative assessment of diastolic notch in uterine artery flow velocity waveforms

To assess the performance and clinical usefulness of the notch depth index [NDI] in predicting small-for-gestational age infants [SGA] in comparison to the previously defined abnormalities in uterine blood flow velocity waveforms; peak systolic over protodiastolic velocities [A/C] ratio. Presence of protodiastolic notch and resistance index [RI]. This prospective clinical study included evaluation of pulsed Doppler abnormalities uterine artery velocity waveforms in 673 nulliparae with normal singleton pregnancies at 16-18 weeks and at 26 weeks gestation. Main outcome measures: Delivery of small for gestational age [SGA] infants. SGA developed in 11% of nulliparae. Although early Doppler screening was associated with high false positive results, yet two-stage screening avoided false negative cases. NDI was found to be a better predictor than other Doppler indices [A/C ratio, protodiastolic notch and RI]. NDI improved, both sensitivity and PPV as determined by other Doppler indices. NDI measurements were clinically useful in predicting for gestational age infant than other conventional Doppler indices

Role of estimation of serum CA125 in the diagnosis and prognosis of spontaneous bacterial peritonitis

Cancer antigen [CA] 125 is the only known glycoprotein marker increased by active synthesis by peritoneal epithelium in the presence of ascites alone. The aim of this work is the evaluation of diagnostic and prognostic significance of serum CA125 in cases with spontaneous bacterial peritonitis [SBP]. Two groups of patients were examined for serum level of CA125. Group I: 20 patients with cirrhotic ascites and SBP, diagnosed by ascitic PMN count >/= 250/mm[3] and positive ascitic fluid culture. Group ll: 24 patients with sterile cirrhotic ascites. Other causes of CA 125 elevation [mainly malignancies and gynecological diseases] were excluded. All cases with SBP were treated and the serum CA 125 level was re-tested in the 10 patients who completed therapy. Significantly elevated levels of serum CA125 were found in patients with SBP [group I] which were more than that found in group II [338.8 +/- 89.9 vs. 149.3 +/- 58.6, p<0.001]. This increase of CA125 in SBP cases was not related to amount of ascites, type of causative bacteria, cause of cirrhosis, liver and kidney function tests, or ascitic PMN count. Therapy of SBP led to significant decrease of CA 125 in survivors [1 55 +/- 37.85vs. 309.5 +/- 42.4, p< 0.001]. The sensitivity, specificity and diagnostic accuracy of serum CA 125 in diagnosis of SBP [when the cut- off level was 240/Uml] were 100%, 83.3% and 90.9% respectively, although it had no prognostic value. In conclusion serum CA 125 can be used as easy and rapid screening test to diagnose of SBP