BCG and protection against Mycobacterium tuberculosis infection.
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Biomedical subjects
Publications and source records attributed to M Bakir.
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Tick paralysis is a disease that occurs worldwide. It is a relatively rare but potentially fatal condition. The only way to establish the diagnosis is to carefully search for the tick paralysis. It is caused by a neurotoxin secreted by engorged female ticks. Tick paralysis generally begins in the lower extremities and ascends symmetrically to involve the trunk, upper extremities and head within a few hours. Although early-onset prominent bulbar palsy and isolated facial weakness without generalised paralysis are rare, there is no report in the English literature concerning isolated, reversible involvement of the upper trunk of brachial plexus caused by tick bite. We report a case of isolated, reversible involvement of the upper trunk of brachial plexus as a variant of tick paralysis. Diagnosis was confirmed with needle electromyography and nerve conduction examination. Within 2 weeks, the patient was fully recovered. The purpose of presenting this case is to remind clinicians that tick paralysis should be considered even in cases with atypical neurological findings admitted to the emergency department.
A prospective study of throat cultures and maxillary sinus aspirates from children with chronic sinusitis (n = 21), acute sinusitis (n = 28) or a clinical diagnosis of chronic adenoiditis (n = 41) was performed. Seventy-two bacterial pathogens were isolated from sinus aspirates from 52% of the study population. Haemophilus influenzae was most common pathogen, followed by Moraxella catarrhalis, Streptococcus pneumoniae, Staphylococcus aureus, and group A streptococci. Quantitative throat cultures had positive predictive values of 41%, 53% and 75% for H. influenzae, Strep. pneumoniae and M. catarrhalis, respectively, while negative predictive values were 93-98%, indicating that these three pathogens do not cause sinusitis when absent from the throat.
Pichia anomala is an emerging yeast causing serious nosocomial infections in newborn and immunocompromised children. We describe nosocomial port catheter infection due to P. anomala in three children who were receiving cancer chemotherapy, bloodstream infection in a preterm infant and in an infant with severe combined immunodeficiency. All patients were treated with amphotericin B. All isolates were susceptible to amphotericin B and fluconazole. No recurrence was observed during follow-up in four of five patients. The common clinical feature in all of our patients was the presence of prior antimicrobial therapy.
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We report a consanguineous Arab family with four children affected with bifid nose associated with renal agenesis and variable degree of anorectal malformations. We suggest that the combination of abnormalities in these children represent a previously undescribed autosomal recessive syndrome.
Two sibs from an inbred Arab family are described with an autosomal syndrome of choanal atresia, hypothelia/athelia and thyroid gland anomalies overlapping Bamforth syndrome, ANOTHER syndrome and methimazole embryopathy. In one case the syndrome described was lethal. Cases with similar features are reviewed and genetic mutations discussed.
The first metal complex of di-2-pyridylmethanone p-nitrophenylhydrazone (dpknph), i.e. the title compound, fac-[ReCl(C17H13N5O2)(CO)3]*C2H6OS, crystallizes as well separated pseudo-tetrahedral DMSO (DMSO is dimethyl sulfoxide) and pseudo-octahedral fac-[ReCl(dpknph)(CO)3] moieties. Two N atoms from dpknph, three C atoms from the carbonyl groups and one chloride ion occupy the coordination sphere around rhenium. The coordinated dpknph ligand forms a six-membered ring in a boat conformation, with the pyridine rings in a butterfly formation. The p-nitrophenylhydrazone moiety is planar, with all C and N atoms in sp2-hybridized forms. The molecules pack as stacks of interlocked fac-[ReCl(dpknph)(CO)3]*DMSO units via a network of non-covalent bonds that include solute-solute, solvent-solute and pi-pi interactions.
The structure of the first metal compound of pyridyl N,N'-coordinated di-2-pyridyl ketone oxime (dpk-o), fac-tricarbonylchloro(di-2-pyridyl-kappaN ketone oxime)rhenium(I) dimethyl sulfoxide solvate, [ReCl(C(11)H(9)N(2)O)(CO)(3)].C(2)H(6)OS, (I), is reported. The coordinated atoms (two N atoms from the pyridyl rings, three C atoms from the carbonyl groups and one Cl atom) are in a distorted octahedral arrangement, with the major distortion being due to the constraints associated with the binding of dpk-o. The packing of the molecules shows antiparallel tapes of (I), with a network of classical (O...H-O) and non-classical (O...H-C) hydrogen bonds between the dimethyl sulfoxide solvate molecule and the complexed metal moiety.
The association of neural tube defects (NTDs) with Down syndrome (trisomy 21) and altered folate metabolism in both mother and affected offspring provide a unique opportunity for insight into the etiologic role of folate deficiency in these congenital anomalies. We describe here the case of a male child with trisomy 21, cervical meningomyelocele, agenesis of corpus callosum, hydrocephaly, cerebellar herniation into the foramen magnum, and shallow posterior cranial fossa. Molecular analysis of the methylenetetrahydrofolate (MTHFR) gene revealed homozygosity for the mutant 677C-->T polymorphism in both the mother and child. The plasma homocysteine of the mother was highly elevated at 25.0 micromol/L and was associated with a low methionine level of 22.1 micromol/L. Her S-adenosylhomocysteine (SAH) level was three times that of reference normal women, resulting in a markedly reduced ratio of S-adenosylmethionine (SAM) to SAH and significant DNA hypomethylation in lymphocytes. The child had low plasma levels of both homocysteine and methionine and a reduced SAM/SAH ratio that was also associated with lymphocyte DNA hypomethylation. In addition, the child had a five-fold increase in cystathionine level relative to normal children, consistent with over-expression of the cystathionine beta synthase gene present on chromosome 21. We suggest that altered folate status plus homozygous mutation in the MTHFR gene in the mother could promote chromosomal instability and meiotic non-disjunction resulting in trisomy 21. Altered folate status and homozygous TT mutation in the MTHFR gene in both mother and child would be expected to increase the risk of neural tube defects. The presence of both trisomy 21 and postclosure NTD in the same child supports the need for an extended periconceptional period of maternal folate supplementation to achieve greater preventive effects for both NTD and trisomy 21.
BACKGROUND: Vancomycin-resistant enterococci (VRE) are increasingly important as pathogens in liver transplant patients. To guide control efforts, we conducted an epidemiological study of the frequency, source, and modes of transmission of VRE at our center. METHODS: During September 1998 through August 1999, we obtained weekly surveillance cultures from consenting liver transplant patients and surfaces in their rooms. Pooled handwash specimens from personnel also were obtained. Specimens were processed on selective media to detect VRE, and isolates were typed by pulsed field gel electrophoresis. Information was collected from patient records concerning in-hospital treatment and clinical course. RESULTS: Serial cultures were obtained during 33 admissions of 29 patients. VRE were detected in initial specimens from 6 admissions, and nosocomial acquisition of VRE occurred in 12 (44%) of the remaining 27 admissions. Seven different strain types of VRE were detected. The initial site of acquisition was stool in all cases; bile became culture-positive in only two patients. Overall, 16 (55%) of the 29 patients became colonized, usually after transplantation. VRE were detected in environmental cultures during 10 admissions and in 2 of 21 pooled handwashes. No statistically significant differences in clinical status or treatment were found when colonized patients were compared to noncolonized controls. The only VRE infection resulted from a choledochojejunostomy anastomotic leak. CONCLUSION: Alimentary tract colonization by VRE occurred commonly in liver transplant patients, probably by cross-transmission. The clinical consequences were modest in the patients studied, but colonized transplant patients provide a substantial reservoir for continued VRE transmission in hospitals.
Meningococcal disease is one of the most important causes of morbidity and mortality among children in many parts of the world. Main reservoir of carriage and site of meningococcal dissemination appears to be the upper respiratory tract. Colonization of Neisseria meningitidis and lactamica and factors affecting this carriage were determined in a group of healthy children aged 0-10 years. Meningococcus and N. lactamica carriage were detected in 17 (1.23%) and 245 (17.7%) of 1382 subjects, respectively. Number (%) of serogroups for meningococci was 1 (6), 5 (29), 0 (0), 1 (6), 1 (6), and 9 (53) for A, B, C, D, W135, and Y, respectively. Having more than three household members, elementary school attendance, pharyngeal carriage of Streptococcus pneumoniae and Haemophilus influenzae were associated with carriage of meningococci, whereas age less than 24-month was associated with carriage of N. lactamica. There was a reverse carriage rate between N. meningitidis and N. lactamica by age which may suggest a possible protective role of N. lactamica against meningococcal colonization among pre-school children.
We report a baby with severe micromelic dwarfism characterized by severe shortening of the humeri, femora and tibiae with hypoplastic radii, ulnae and fibulae which are of normal shape. We suggest that this case is similar to the case reported by Baxova et al [(1993), Paediatr Radiol 23:446-449] confirming the identity of this new bone dysplasia.
Three cases with the rare condition of tuberculous pericarditis are reported.
Contamination of clinical specimens by Mycobacterium gordonae is a significant endemic problem in many laboratories. To investigate this problem, 84 cases at 1 hospital were retrospectively identified during 20 months. The overall rate of specimen contamination was 2. 4%, and 72 of the contaminated specimens were respiratory. A case-control comparison showed that the risk of respiratory specimen contamination was significantly increased if the specimen was expectorated (odds ratio [OR], 3.62; 95% confidence interval [CI], 1. 36-9.50) or if the patient consumed fluids within 2 days before specimen collection (OR, 8.92; 95% CI, 1.40-71.20). Cultures of tap water, ice, and iced drinking water all yielded M. gordonae at 10(-2)-10(0) cfu/mL. A culture survey of consenting patients showed contamination of 8 (24%) of 34 sputum specimens collected immediately after a tap water mouth rinse. These findings demonstrate that endemic specimen contamination arises from mycobacteria in hospital tap water and provide a foundation for control efforts.
We report a baby with congenital bowing of the long bones, camptodactyly, talipes equinovarus and radiological features resembling both Stüve-Wiedemann syndrome and Schwartz-Jampel syndrome type 2. The baby had, in addition, agenesis of the corpus callosum. This feature has not been reported in either of these syndromes. It is possible that this baby has a previously undescribed syndrome.
Renal-coloboma syndrome is a developmental disorder involving optic nerve colobomas and renal hypoplasia/insufficiency, which exhibits autosomal dominant inheritance and a highly variable phenotype (OMIM:120330). Mutation in the PAX2 gene was found to result in the renal-coloboma phenotype. We report on an Arab family with autosomal dominant inheritance of a syndrome characterized by a variable combination of optic nerve colobomas, renal abnormalities, vesicoureteral reflux, lax joints and arthrogryposis multiplex. Apart from the arthrogryposis multiplex which has not been described in the renal-coloboma syndrome, the features of the syndrome in this family are very similar to the renal-coloboma syndrome. However sequencing of all 12 axons of PAX2 gene revealed no mutation in this family. The disorder in this family is likely to represent a new syndrome with features overlapping with the renal-coloboma syndrome.
To determine the impact of bacillus Calmette Guerin (BCG) vaccination on IgE production in ovalbumin (OVA)-sensitized newborn mice, four groups (I, II, III, IV) of BALB/c mice were immunized on the first day of life with live BCG, killed BCG, BCG diluent, and saline, respectively. No injection was applied to mice in group V (control). All mice except group V were sensitized and challenged with OVA in the fourth and sixth weeks, respectively, and serum total IgE levels were determined at 8 weeks, 2 weeks after the second OVA challenge. IgE levels of all groups were significantly higher than the control group except for group II (p = 0.95). Mice in group II showed significantly lower IgE values than group IV and I (p = 0.007 and p = 0.003, respectively). We concluded that heat-killed BCG may downregulate IgE response to OVA in newborn mice.