Ultrastructure and types of fimbriae in uropathogenic E-coli among bilharzial patients

The aim of this work was to study the association of different types of fimbriae of urinary E coli isolates with different disease entities. We collected a total of 57 urinary E. coli isolates from 3 groups of bilharrzial patients: group 1: with cystitis [21 isolates]; group 2: with pyelonephritis [18 isolates] and group 3: with urinary bladder carcinoma [18 isolates]. Each isolate was studied for: I. Fimbrial expression and type determination by haemagglutination [HA] of human and guinea pig erythrocytes. II. Electron microscopic [E/M] structure using negative staining, standard transmission and scanning electron microscopy. It was found that infection with mannose sensitive type 1 fimbriated E. coli dominated in group 1 and 3 [80.95% and 77.78% respectively]. In group2 [55.56%] were caused by mannose resistant P fimbriated E. coli. Although there was a perfect correlation between HA and the presence of fimbiriae by E/M [P< 0.01], yet E/M detected other types of fimibriae which could-have been missed by HA alone. Negative staining was the best technique in electron microscopy. We concluded that detection of P flimbriae in urinay E. coli strains may justify a vigorous antibiotic treatment to prevent development of pyelonephritis. Although type 1 fimbriae was associated with simple cystitis, yet follow up and complete investigations are recommended to detect an associated carcinoma

study of microbiological pattern of neonatal sepsis

The main of this [prospective] analytic study was to determine the microbiological pattern of bacterial infection in the neonatal intensive care unit of Kasr El Eini hospital, to investigate microbial colonization of neonates at birth before any interference and to examine whether surface cultures yielded information helpful in management. The study population comprised 70 high risk neonates whether full terms or preterm infants admitted to Kasr El Eini neonatal intensive care unit for a 6 months period from 1/3/2002 to 30/9/2002 babies with congenital anomalies were excluded from the study. The included neonates were subjected to laboratory studies as CBC, CRP, IT ratio, superficial cultures in the form of ear and throat swabs and deep culture in the from of blood culture. We defined neonatal sepsis by positive blood culture. The results showed that 70 out of 101 neonates included in the study developed sepsis [69.3%]. The incidence of early onset sepsis [49.5%] was higher than late onset sepsis [19.8%]. The highest incidence of sepsis was in the gestational age group 30 - <32 weeks and the weight group 1500 - <2500 grams. Clinical signs and laboratory investigation revealed no significance in relation to sepsis. The most prevalent organism recovered from blood culture was klebsiella [40%], followed by coagulase negative staph aureus, CONS [20%], staph aureus [15.7%] and enterobacter [15.7%]. Colonization detected by ear swabs was 68.5% in septic neonates and 64.5% in non septic neonates. The predominant organisms recovered from ear swabs in the septic group were CONS [38.6%] followed by staph aureus [18.6%] then klebsiella [5.7%]. Colonization detected by throat swabs was 55.7% in septic neonates and 42% in the non septic neonates. The most common organism recovered from throat swab in the septic group were klebsiella [15.7%] and E. coli [14.3%] followed by CONS and staph aureus [10%] each. Superficial swabs were of limited value in diagnosis of neonatal sepsis. Results of throat swabs were more significant than ear swabs with higher matching with blood culture [21.4% in contrast to 8.5% for ear swabs]. Mortality among septic neonates was 44.2% and among non septic neonates was 25.8%. Incidence of sepsis was still high in our unit [69.3%]. Early onset sepsis was much-higher than late onset sepsis. Klebsiella was the predominant organism causing sepsis followed by CONS and staph aureus. Superficial swabs were of limited value in diagnosis of neonatal sepsis. Throat swabs showed more matching with blood culture than ear swabs. Blood culture is still the gold standard for the diagnosis of neonatal sepsis

Role of thrombopoietin in thrombocytopenic patients with chronic viral hepatitis with and without liver cirrhosis

Thrombocytopenia is a common hematological defect among patients with chronic liver diseases. Thrombocytopenia secondary to liver cirrhosis and portal hypertension is a well known complication of advanced stage liver disease, but theories about the underlying pathogenetic mechanisms, mostly concentrating on splenic sequestration i.e. hypersplenism and destruction of platelets, have failed to solve the problem so far. Thrombopoietin [TPO] was recently cloned and identified as the primary cytokine involved in the megakaryocyte maturation and formation of platelets. The predominant site of TPO-production is the liver, where parenchymal cells are the TPO-producing cells. Therefore, thrombocytopenia in chronic liver disease may be related to deficient production of thrombopoietin. Thus, altered TPO production in patients with chronic liver disease may in part explain the thrombocytopenia found in these patients. To evaluate the relationship between serum TPO concentrations, circulating platelet count, and the state of liver pathology in patients with chronic viral hepatitis with and without liver cirrhosis, this study included ninety subjects divided into two main groups. Group A included sixty chronic hepatitis patients and group B included thirty apparently normal age- and sex-matched subjects taken as a control group. Etiology of the chronic hepatitis patients was either HBV or HCV. Group A was further subdivided into subgroup AI including thirty chronic hepatitis patients with liver fibrosis, while subgroup AII included thirty chronic hepatitis patients with liver cirrhosis, who were all of Child A group according to Child score. Ultrasonography as well as liver biopsy were used to differentiate the two subgroups. Thorough history taking, full physical examination, as well as biochemical blood tests in the form of serum albumin and total bilirubin were done. Prothrombin time, platelet counts, as well as serum TPO concentrations were all determined in addition to abdominal ultrasonography to evaluate the splenic size. Our data showed that serum albumin level was decreased and serum bilirubin level was increased in both subgroups AI fibrosis and AII cirrhosis compared to group B controls. Prothrombin time was prolonged in subgroup AII cirrhosis patients compared to both subgroup Al fibrosis and to group B controls. Splenic size was highly significantly increased in subgroup AII cirrhosis patients compared to subgroup AI fibrosis patients who showed larger spleen compared to group B controls as well. Serum TPO levels were significantly increased in subgroup Al fibrosis patients and significantly decreased in subgroup All cirrhosis patients compared to group B controls, moreover, TPO levels were highly significantly decreased in subgroup All patients compared to subgroup Al patients. Thus, our study clarified that decreased serum TPO levels parallel the increased serum biliruhin levels, the deterioration of the protein producing liver ability, as well as the prolonged prothrombin time. Thus, TPO concentrations decreased with the progression of liver disease and the reduction in the functional hepatic mass indicating that thrombocytopenia in chronic liver disease might highly be correlated with the hepatocellular damage. Our study also detected a negative correlation between the spleen size and the platelet counts, meanwhile we also demonstrated that the spleen size does not correlate with the TPO levels. In addition we demonstrated a significant positive correlation between TPO concentrations and platelet counts and a negative correlation between TPO concentrations and prothrombin time. Thus, we denoted that TPO concentration is an independent factor affecting positively the platelet counts in chronic viral hepatitis patients regardless of the splenic size, which is also partially implicated, also it is negatively related to the prothrombin time, which is an indicator of the functioning liver mass. This study concluded that serum TPO concentrations are increased above control levels in chronic viral hepatitis patients with liver fibrosis, but as the condition progresses to cirrhosis, the functioning liver mass decreases and so the TPO concentrations fall. Thus, the impaired TPO synthesis by the diseased liver may contribute to the development of thrombocytopenia in liver cirrhosis. Therefore, TPO deficiency due to reduced production, seems to be a major factor for thrombocytopenia in chronic liver disease although increased splenic sequestration of platelets in the enlarged spleen may also have an additional role. Our findings may suggest that recombinant TPO could possibly be an effective drug to treat patients with liver cirrhosis and severe thrombocytopenia during bleeding episodes or when undergoing surgical procedures. Moreover, it may decrease the incidence of splenectomy, with all its intraand postoperative hazards, done in such conditions

Ultrastructure and types of fimbriae in uropathogenic E-coli among bilharzial patients

The aim of this work was to study the association of different types of fimbriae of urinary E coli isolates with different disease entities. We collected a total of 57 urinary E. coli isolates from 3 groups of bilharzial patients: group 1: with cystitis [21 isolates]: group 2: with pyelonephritis [18 isolates] and group 3: with urinary bladder carcinoma [18 isolates]. Each isolate was studied for: I-fimbrial expression and type determination by haemagglutination [HA] of human and guinea pig erythrocytes, II- Electron microscopic [E/M] structure using negative staining, standard transmission and scanning electron microscopy. It was found that infection with mannose-resistant type I fimbriated Ecoli dominated in group 1 and 3 [80.95% and 77.78% respectively]. In group 2. 55.56% were caused by man- nose resistant P fimbriated Ecoli. Although there was a perfect correlation between HA and the presence of fimbriae by E/M [p< 0.01], yet E/M detected other byres of fimbriae which could have, been missed by HA alone. Negative staining was the best technique in electron microscopy. We concluded that detection of P fimbriae in urinay Ecoli strains may justify a vigorous antibiotic treatment to prevent development of pyelonephritis. Although type I fimbriae was associated with simple cystitis, yet follow up and complete investigations are recommended to detect an .associated carcinoma

value of routine screening of TT virus in blood transfusion practice

To clarify the prevalence of TT virus [TTV] infection in blood donors as well as recipients to predict the value of its routine screening and to minimize the incidence of transfusion associated hepatitis [TAH], the present study included 180 subjects divided into three groups. Group A included 50 consecutive healthy blood donors with elevated ALT at the time of donation and group B included 100 consecutive healthy volunteer blood donors with normal ALT; both groups were negative for the serological markers for hepatitis A, hepatitis B and hepatitis C viruses. Group C included 30 blood product recipients in whom post-transfusion follow up revealed elevated ALT and negative hepatitis A-C markers. All subjects were subjected to laboratory evaluation in the form of serum ALT as well as a panel of A-C hepatitis viruses studies which was carried out using ELISA II technique to detect HbsAG, anti HCV antibodies and anti HAV IgM. TTV DNA was amplified and detected using polymerase chain reaction, followed by gel electrophoresis

Circulating leptin and tumor necrosis factor: a in patients with sepsis: correlation with microbiologic findings

Forty-six critically ill patients with culture proven bacteremia participated in this study and classified into two groups [30 patients with severe sepsis and 16 patients with septic shock]. The control group composed of 20 subjects before elective surgery. Body mass index [BMI] was calculated for all subjects. Leptin and TNF-alpha concentrations were determined for all participants. Leptin and TNF- alpha were reassessed in eight patients who survived after severe sepsis. Blood cultures were obtained for all patients. Specimens from other sites were obtained as appropriate. All samples were cultured and the isolates were identified by standard microbiologic procedures. All patients received a full standard supportive care and an empiric antimicrobial treatment that was modified to reflect the in vitro susceptibility testing whenever appropriate. The study concluded that septic patients had an elevated leptin and TNF-alpha levels correlating with the severity of the disease. Patients with a pure Gram-negative infection had significantly higher leptin and TNF- alpha levels than those with a pure Gram-positive sepsis

Anticardiolipin antibodies in chronic hepatitis C virus infection: is there an aetiopathogenetic link to antiphospholipid syndrome?

Chronic hepatitis c virus [HCV] has always been linked to extrahepatic autoimmune phenomena and found to be associated with various diseases known as extrahepatic manifestations of HCV. In addition, a variety of autoantibodies are detected in HCV patients. Recently HCV has been implicated as a cause of antiphospholipid syndrome [APS] which is usually defined by the association of clinical manifestations that comprise venous and/or arterial thrombosis, recurrent fetal losses, and thrombocytopenia, along with the presence of anticardiolipin [ACL] antibodies and/or lupus anticoagulant. Anticardiolipin antibodies can be induced by various infections diseases, however, they are not associated with thrombotic events as in the case of autoimmune diseases in which they are b2-glycoprotein I dependent and produce thrombotic events. To clarify whether an aetiopathogenesis exists between HCV and APS and meanwhile to study the prevalence, nature, and clinical significant of ACL auto antibodies in serum samples of HCV patients, the present study included one hundred and thirty subjects divided into three groups: a included 50 patients with chronic HCV infection, group b included 30 patients with APS [15 patients with primary and 15 with secondary type], and group c included 50 apparently normal age and sex-matched subjects taken as a control group. Clinical events as well as proper history of APS manifestations were recorded. The prevalence of ACL antibodies was detected by Elisa as well as its IgG and IgM isotypes, its B2-glycoprotein dependence was also evaluated. The present of cryoglobulins and other autontibodies as lupus anticoagulant [LA] and antinuclear antibodies [ANA] were determined as well, using indirect immunofkuorescence. HcVRNA and its viraemia titre were determined by RT-PCR and its quantitative testing. Our data showed that the prevalence of ACL antibodies in chronic HCV patients was found to be 42% which proved to be more than that in the normal controls [0%] but, its presence had no clinical significance. Our study clarified also that there is no significant association between a ACL antibodies and the presence of other auto antibodies or cryoglobulins in those patients. Furthermore, all HCV patients with positive ACL antibodies in our study were B-2 glycoprotein I independent. We concluded that the presence of ACL antibodies in chronic HCV patients seem to be an epiphenomenon and their presence has neither a clinical nor a laboratory significance in this category of patients. Thus, testing for HCV infection in APS patients or follow-up for the possibility of APS development in HCV patients might not be recommended. Thus, our study failed to implicate HCV as an aetiopathogeinc factor for APS