Analysis of the course and treatment of toxocariasis in children—a long-term observation

Toxocariasis is a helminthozoonotic disease caused by ascarid larvae of Toxocara genus: Toxocara canis and Toxocara cati. In the reported study, the clinical course of toxocariasis and administered therapy were evaluated in 103 children. The majority of the children (68.9%) were from the rural environment, with a prevalence of boys (62.1%). At diagnosis of infection, 36 (35%) children reported recurrent abdominal pain, 19 (18.4%) headache, 6 (5.8%) loss of appetite, 2 subfebrile conditions, and 2 arthralgia, Moreover, 23 (22.3%) children demonstrated symptoms of atopic diseases; in 30 (29.1%) children, moderate enlargement of lymphatic nodes was noted. In five children (4.9%), ophthalmic examination revealed unilateral changes in the eye: in two cases retinitis; in one case fibrotic lesions in the vitreous body, complicated 1 year from diagnosis by retinal detachment; and in other children parafoveal lesions and cataract. Only two children with ocular changes at diagnosis reported visual disorders. In 64.3% of children, eosinophilia was observed. A covert form of the disease was diagnosed in 95.1% of the children and an ocular form in 4.9%. In all the children, antiparasitic treatment was implemented, repeated several times in some of them. After therapy, the mean titer of specific antibodies, the number of children with abdominal pains and enlarged lymphatic nodes were decreased, while headaches maintained at unchanged levels. In approximately one fourth of the children with negative results of antibodies after the therapy, the symptoms of the disease were still reported. Evaluation of the efficacy of treatment is not easy due to non-characteristic symptoms and low kinetics of specific anti Toxocara IgG decrease; however, high IgG titers suggest non-effective treatment of concomitant infection requiring subsequent therapy. Due to risk of ocular form, which may develop in any stage of the disease, irrespectively of specific antibodies concentrations, it seems justified to implement antiparasitic treatment in all children infected with T. canis

HBV DNA suppression during entecavir treatment in previously treated children with chronic hepatitis B

The aim of this study was to assess HBV DNA suppression after 24 weeks of treatment with entecavir in previously treated children with CHB. Thirty children aged 5–17 years (25 males and 5 females) with CHB were treated with entecavir 0.5 or 1 mg daily. Twenty-two children were HBeAg-positive, eight were HBeAg-negative, and in eight HBV polymerase mutations were detected. After 24 weeks of treatment, mean and median HBV DNA levels and ALT activity were lower versus baseline, overall and in both subgroups. The overall median HBV DNA level decreased from 1.2 x 107 IU/mL to 3.3 x 102 IU/mL (p < 0.000004), in HBeAg-positive from 7.8x107 IU/mL to 6.3x103 IU/mL (p < 0.00004), and in HBeAg-negative from 2.5x104 IU/mL to 5.01x101 IU/mL (p < 0.03). The serum HBV DNA disappearance was observed in 7/8 (88%) HBeAg-negative and in 5/22 (23%) HBeAg-positive patients. The overall mean ALT activity decreased from 164+ 290 U/L to 34.1+ 18.9 U/L (p < 0.000007), in HBeAg-positive from 214+326 U/L to 38.59+19.2 U/L (p < 0.000074), and in HBeAg-negative from 27+14 U/L to 20+8 U/L (p < 0.03). Twenty-four weeks of treatment with entecavir results in suppression of HBV DNA in a substantial proportion of children previously treated ineffectively with CHB

Grzybicze powikłania zakażeń układu zastawkowego u dzieci z wodogłowiem wrodzonym

Mycotic complications of shunt infection in children with primary hydrocephalus. Recently, the incidence of fungal infections in children, including cbildren with shunt-dependent hydrocephalus, has increased. The analysis comprised 8 cbildren treated in the III Clinic of Pediatrics of ICZMP during the period of 12 months (12% of all infectious complications of the shunt system). The clinical picture of fungal infection included Symptoms of shunt dysfunction: febrile conditions, vomiting, distress and loss of appetite. The most common pathogens isolated from the cerebro-spinal fluid were fungi from the Candida species. Mean value of pleocytosis in the cerebro-spinal fluid was 812 cell/μ, and mean protein concentration was 311 mg/dl. Treatment consisted of monotherapy with Dillucan, monotherapy with Ancotil or combined treatment with Ancotil and Amphotericine B. The drugs were administered intravenously and intraventricolarly after removal of the shunt and application of external drainage. Sterility of cerebro-spinal fluid was obtained in the shortest time with the use of Ancotil. Propbylactic application of antifungal drugs decreases the frequency of infections in children with shunt-dependent hydrocepbalus

Association of TLR3 L412F Polymorphism with Cytomegalovirus Infection in Children.

Intracellular Toll-like receptor 3 (TLR3) recognizes viral double-stranded RNA (dsRNA) and activates antiviral immune responses through the production of type I interferons (IFNs) and inflammatory cytokines. This receptor binds to dsRNA molecules produced during human cytomegalovirus (HCMV) replication. TLR7 senses viral single-stranded RNA (ssRNA) in endosomes, and it can interact with endogenous RNAs. We determined the genotype distribution of single-nucleotide polymorphisms (SNPs) within the TLR3 and TLR7 genes in children with HCMV infection and the relationship between TLR polymorphisms and viral infection. We genotyped 59 children with symptomatic HCMV infection and 78 healthy individuals for SNPs in the TLR3 (rs3775290, c.1377C>T, F459F; rs3775291, c.1234C>T, L412F; rs3775296, c.-7C>A) and TLR7 (rs179008, c.32A>T, Q11L; rs5741880, c.3+1716G>T) genes. SNP genotyping was performed using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) and capillary electrophoresis. The HCMV DNA load was quantified by real-time PCR. We found an increased frequency of the heterozygous genotype TLR3 L412F in children with HCMV infection compared with uninfected cases. In individuals with a mutation present in at least one allele of the L412F SNP, an increased risk of HCMV disease was found, and this result remained highly significant after Bonferroni's correction for multiple testing (Pc < 0.001). The heterozygous genotype of this SNP was associated with the increased risk of HCMV disease in an adjusted model that included the HCMV DNA copy number in whole blood and urine (P < 0.001 and P = 0.008, respectively). Moreover, those with a heterozygous genotype of rs3775296 showed an increased relative risk of HCMV infection (P = 0.042), but this association did not reach statistical significance after correction for multiple testing. In contrast, the rs3775290 SNP of TLR3 and TLR7 SNPs were not related to viral infection. A moderate linkage disequilibrium (LD) was observed between the SNPs rs3775291 and rs3775296 (r2 = 0.514). We suggest that the L412F polymorphism in the TLR3 gene could be a genetic risk factor for the development of HCMV disease

TLR9 -1486T/C and 2848C/T SNPs Are Associated with Human Cytomegalovirus Infection in Infants.

Toll-like receptor 9 (TLR9) recognizes non-methylated viral CpG-containing DNA and serves as a pattern recognition receptor that signals the presence of human cytomegalovirus (HCMV). Here, we present the genotype distribution of single-nucleotide polymorphisms (SNPs) of the TLR9 gene in infants and the relationship between TLR9 polymorphisms and HCMV infection. Four polymorphisms (-1237T/C, rs5743836; -1486T/C, rs187084; 1174G/A, rs352139; and 2848C/T, rs352140) in the TLR9 gene were genotyped in 72 infants with symptomatic HCMV infection and 70 healthy individuals. SNP genotyping was performed by using polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP). Digested fragments were separated and identified by capillary electrophoresis. The HCMV DNA copy number was measured by a quantitative real-time PCR assay. We found an increased frequency of heterozygous genotypes TLR9 -1486T/C and 2848C/T in infants with HCMV infection compared with uninfected cases. Heterozygous variants of these two SNPs increased the risk of HCMV disease in children (P = 0.044 and P = 0.029, respectively). In infants with a mutation present in at least one allele of -1486T/C and 2848C/T SNPs, a trend towards increased risk of cytomegaly was confirmed after Bonferroni's correction for multiple testing (Pc = 0.063). The rs352139 GG genotype showed a significantly reduced relative risk for HCMV infection (Pc = 0.006). In contrast, the -1237T/C SNP was not related to viral infection. We found no evidence for linkage disequilibrium with the four examined TLR9 SNPs. The findings suggest that the TLR9 -1486T/C and 2848C/T polymorphisms could be a genetic risk factor for the development of HCMV disease

Frequency and distribution of <i>TLR</i> genotypes and their association with HCMV infection.

<p>Frequency and distribution of <i>TLR</i> genotypes and their association with HCMV infection.</p

Visualization of PCR-RFLP products for <i>TLR3</i> SNP (A) and <i>TLR7</i> SNP (B) genotyping.

<p>Gel image: A) rs3775290: 1. wild type CC, 2. heterozygous CT, 3. homozygous recessive TT; rs3775291: 4. wild type CC, 5. heterozygous CT, 6. homozygous recessive TT; rs3775296: 7. wild type CC, 8. heterozygous CA, 9. homozygous recessive AA. B) rs179008: 1. wild type AA, 2. heterozygous AT, 3. homozygous recessive TT; rs5741880: 4. wild type GG, 5. heterozygous GT, 6. homozygous recessive TT. Alignment markers (15 bp, 1 kbp).</p