Despite frequent use of immunosuppressive drugs in patients with inflammatory bowel disease (IBD) and reports of cytomegalovirus (CMV) infection following post-transplant immunosuppression, data on the frequency and clinical significance of CMV in patients with IBD are scant. Sixty-three patients with IBD (61 ulcerative colitis and two Crohn's disease) were evaluated for CMV using serology (IgM antibody, ì-capture ELISA), PCR for CMV DNA in colonic biopsy and histological assessment of haematoxylin and eosin-stained colonic biopsy. Positive result in any test was considered as CMV infection. Various parameters associated with CMV infection were analysed using univariate and multivariate analysis. Ten of 63 (15 . 8 %) patients (age 36 . 0 AE 11 . 2 years, 31 female) were infected with CMV (DNA alone in four, IgM antibody alone in two and both in four, inclusion body in one). Patients with CMV infection were more often female (8/10 vs 23/53, P , 0 . 05), had pancolitis (10/10 vs 33/53, P , 0 . 05), histological activity (9/10 vs 17/53, P , 0 . 005) and used azathioprine (5/10 vs 7/53, P ¼ 0 . 04; Fisher exact test for all). On multivariate analysis, female gender, pancolitis and histological activity were the independent factors associated with infection. Patients with CMV infection more often required surgical treatment for IBD (4/10 vs 4/ 53, P ¼ 0 . 01) and had fatal outcome (3/10 vs 0/53, P ¼ 0 . 003). CMV infection in patients with IBD may be common and is associated with poor outcome. PCR of rectal biopsy was the most sensitive method of detection followed by IgM antibody for diagnosis. INTRODUCTIONInfection with cytomegalovirus (CMV) is an important cause of morbidity and mortality after solid organ (kidney and liver) transplantation, as these patients receive multiple immunosuppressive drugs (Patel & Paya, 1997; Wiesner et al., 1993). Patients with inflammatory bowel disease (IBD), particularly those with severe, corticosteroid-refractory and -dependent states are frequently treated with immunosuppressive agents including corticosteroids, cyclosporine, azathioprine and methotrexate, either alone or in combination (Kho et al., 2001). Therefore, patients with IBD [ulcerative colitis (UC) and Crohn's disease (CD)] are expected to be at an increased risk of infection with CMV. However, data on CMV infection in patients with IBD is still scant and most studies used only histology and/or serology for diagnosis of CMV infection (Powell et al., 1961;Cooper et al., 1977;Berk et al., 1985;Eyre-Brook & Dundas, 1986;Vega et al., 1999;Cottone et al., 2001). Although histology is quite specific, it is of low sensitivity (Beaugerie et al., 1997). PCR has emerged as the most sensitive method for diagnosis of viral infection including that with CMV (Storch et al., 1994). However, only a few studies used PCR for diagnosis of CMV infection in IBD. With blood and buffy coat preparation of leukocytes as specimens, PCR failed to detect CMV in blood of patients with IBD in some of these studies (Adani et al., 2001). Demonstrati...

In vivo, ex vivo, and in vitro proton magnetic resonance spectroscopy was performed in 12 patients with intracranial tuberculomas with an aim of detecting the biochemical constituents of Mycobacterium tuberculosis in a granuloma. One dimensional (1D) single pulse and spin-echo sequences and 2D correlative spectroscopy were used for the ex vivo study to confirm the resonances seen on in vivo study. Spectroscopic studies of the perchloric acid and lipid extract of granuloma and M. tuberculosis were performed to look for similarity of resonance. In vivo study showed the presence of lipids at 0.9, 1.3, 2.0, 2.8 ppm, and phosphoserine at 3.7 ppm. All these resonances were confirmed on ex vivo study. In addition, distinct resonances of serine and phenolic lipids were seen on ex vivo and in vitro study of tuberculous granuloma, which have not been observed in other intracranial tumors. Lipid extract of granuloma and M. tuberculosis showed phenolic lipids at 7.1 and 7.4 ppm, a constituent of the cell wall of the bacteria in a tuberculoma. It appears that it may be possible to finger print the biochemicals of the cell wall of M. tuberculosis in a tuberculous granuloma and thus may help in detection and diagnosis of such lesions.

Introduction: The frequency of fetopathogenic viruses and Toxoplasma gondii infections in the TORCH group (Toxoplasma gondii, rubella virus, cytomegalovirus (CMV), herpes simplex virus) together with Parvovirus B19 (B19) in pregnant women with bad obstetric history (BOH) and/or concurrent pregnancy complications was investigated. Methodology: Sixty women (20-35 years) with BOH and/or antecedent pregnancy complications were studied. Twenty-nine healthy pregnant women matched for age, parity and gestational age served as controls. Sera were analyzed for IgM antibodies for B19 and TORCH agents by ELISA. Cord blood and 33 placental tissues from six malformed newborns were tested for B19 DNA by PCR. Results: Out of 60 high-risk pregnant women, 47 (78%) had BOH while 23 (38.3%) had underlying complications including polyhydramnios (n=10), oligohydramnios (n=6) and intrauterine growth restriction (n=7). Adverse outcomes occurred in 36 (60%) high-risk cases.  All 16 cases with polyhydramnios/oligohydramnios resulted in preterm stillbirths while the remaining 20 cases resulted in seven abortions, six newborns with congenital malformations, four full-term stillbirths and three cases of non-immune hydrops fetalis (NIHF). IgM positivity to T. gondii, rubella, cytomegalovirus, herpes simplex virus and B19 virus was 8.3%, 15%, 30%, 3.3% and 13.6% respectively. B19 infection caused NIHF in three cases and cardiac anomaly in one. All placental tissues and cord blood were negative for B19 DNA. None of the controls had IgM antibodies to any pathogen. Conclusions: Women with BOH and/or pregnancy complications had a high frequency of TORCH and parvovirus B19 infections causing fetal wastage, IUGR, NIHF and congenital malformations.

Backgound and Objectives:Parvovirus B19 (B19) being a non-enveloped DNA virus is hence thermo-stable to the current methods of viral inactivation. Therefore transfusion of blood or its component from a viremic donor to non-immune recipients may result in transfusion-transmitted B19 infection with occasional sinister complications. The serologically naïve blood donor population in our country has not been studied. Hence a study was designed to find the sero-status of B19 virus in normal voluntary blood donor population (relatives of recipients) as an indirect measure of the susceptibility to B19 in north Indians together with seroepidemiology of B19.Methods:An in-house anti-B19 IgG ELISA was standardized using cloned, baculovirus expressed, and purified VP1/VP2 capsid proteins as antigen. Anti-B19 IgG antibodies in sera (diluted 1:400) of 1000 healthy voluntary blood donors (18-60 years; mean 30.5 years) were analyzed and their epidemiologic data were documented.Results:A total of 399 (39.9%) donors were seropositive for B19 virus. Seroprevalence was higher in males than females (44% vs 27%) and it increased with increasing age (P<0.01). Socioeconomically, B19 IgG antibody positivities were 61.8%, 61.1%, and 44.4% in low, medium, and high income groups respectively with unskilled laborers having higher seroprevalence in low (48.5%) and middle (58.7%) income group (P<0.05). Housing conditions revealed B19 seroprevalence as 42.6% in donors living in small houses compared to 20.4% in larger houses (P<0.01) but no difference with religion.Conclusions:Seroprevalence to B19 in normal voluntary blood donors was low leaving a large proportion of north Indians susceptible to B19 infection.

Acquired pure amegakaryocytic thrombocytopenic purpura is a relatively rare bone marrow failure disorder characterized by severe thrombocytopenia with total absence or marked reduction of bone marrow megakaryocytes in the absence of other haematological abnormalities (Hoffman, 1991). We report a case of acquired pure amegakaryocytic thrombocytopenia secondary to parvovirus infection, which was treated with intravenous immunoglobulin.A 9-month-old male child was noticed to have skin purpura in late November 2003, of 2 weeks duration, followed by epistaxis and haematochezia. He had developed a cough a week prior to the other symptoms. The child developed an intracerebral bleed and was found to have a platelet count of less than 10 ·