BACKGROUND: The protozoan Haemoproteus belongs to the Phylum Apicomplexa, Class Sporozoa, and Order Haemosporina. Avian haemosporidian are protozoan parasites that use birds as hosts around the world. Many species of wild and domestic doves are natural hosts of different species of Haemoproteus. Blood-sucking arthropods are the main vectors of these blood parasites.OBJECTIVES: The aim of this study was the microscopic and molecular investigation of the protozoan Haemoproteus columbae in the blood of infected pigeons in Torkaman County, Iran.METHODS: Blood samples and tubes containing ethylenediaminetetraacetic acid (EDTA) anticoagulant were collected from 96 domestic pigeons randomly from 14 pigeon lofts and different parts of Torkaman County.Pigeons were also inspected for infection with the host-vector Pseudolynchia canariensis. In the next step, blood smears were stained with Giemsa and examined microscopically. Also, blood tubes containing EDTA were tested by PCR method on the cytochrome b gene.RESULTS: Microscopic and molecular examination of peripheral blood showed that 62 (64.58 %) and 73 (76.04 %) of the investigated pigeons were contaminated, respectively. Of the 62 infected pigeons infected with the Haemoproteus, 28 pigeons (66.66 %) were male, and 34 (62.96 %) were female. Also, the infestation with Pseudolynchia canariensis was observed in 4 (28.57 %) pigeon lofts.CONCLUSIONS: The preliminary investigation shows the high rate of Haemoproteus infection in pigeons in Torkaman County. Further studies to determine the prevalence and accurate identification of the species infecting pigeons in this region require PCR testing and sequencing of infected blood samples.

BACKGROUND: Congenital Toxoplasma gondii infection during pregnancy due to reduced maternal immune system could increase the risk of a child's autism disorder. OBJECTIVES: The aim of this study was to compare the Toxoplasma gondii infection in children with autism and normal children. METHODS: The research method was a case control study. The participants included 50 autistic children and 50 normal (N=100) children, aged between 3 and 12 years-old. They were matched according to age, socio-economic status, severity of the disorder, lack of physical and mental illness and other criteria considered in this research. From each group 5ml blood samples were collected to assess the prevalence of antibody against Toxoplasma gondii. To investigate the research hypotheses, the data were analyzed by Chi-square test. RESULTS: The results showed that children with autism had a higher level of frequency contamination with Toxoplasma gondii parasite infection than normal group (p < /em><0.001). CONCLUSIONS: Infection rate of Toxoplasma gondii in children with autism was significantly higher than in normal children.

BACKGROUND: Salmonellosis is a dangerous disease that can threaten the health of humans and animals. This disease can lead to economic losses annually; therefore, many studies have been conducted to prevent this disease.OBJECTIVES: The current study aims to design a recombinant chimera protein HBHA-Omp28 as a vaccine against Salmonella typhimurium.METHODS: The nucleotide and amino acid sequences of Omp28 and HBHA proteins were first extracted from the NCBI database. Then, the recombinant chimera of HBHA-Omp28 was bioinformatically assembled using a rigid linker. Epitope prediction of T and B cells, antigenicity, allergenicity, and physicochemical features assessments of HBHA-Omp28 were done using Immune Epitope Database (IEDB), ABCpred, VaxiJen, AllerTOP and ProtParam online servers, respectively. To assess the secondary and tertiary structures, the Self-Optimized Prediction Method with Alignment (SOPMA) and the Iterative Threading ASSEmbly Refinement (I-TASSER) server were used, respectively. Molecular docking between recombinant chimera and TLR4/MD2 receptor was assessed by ClusPro server. Finally, after codon optimization of nucleotide sequence of recombinant chimera to express in Escherichia Coli k-12 strain, the cloning of recombinant chimera in pET21-a (+) vector was examined.RESULTS: The designed recombinant chimera was classified as an antigenic and non-allergenic protein with molecular weight of 34.19 kDa. According to the results of molecular docking study, the HBHA-Omp28 protein was able to bind to TLR4/MD2 receptor using 9 hydrogen bonds. The results of cloning study demonstrated that HBHA-Omp28 successfully cloned into pET21-a (+).CONCLUSIONS: The designed recombinant chimera can be an appropriate vaccine against salmonella bacteria.

A 474-base pair segment covering the hypervaible region of VP2 gene from six Korean infectious bursal disease virus(K-IBDV) isolates(K1, K2, SH/92, 225, 269, 310) and one attenuated IBDV(DAE) were amplified using RT-PCR, sequenced, and compared with published sequences for IBDV. K-IBDV isolates(K1, K2, SH/92, 225, 269) and foreigh very virulent(vv) IBDV strains had 94.93-100% amino cid sequence similarity. K-IBDV isolate 310 and other K-IBDV isolates had 84.31%-86.07% amino acid sequence similarity. Attenuated strain(DAE), like other attenuated strain, has substitution at positions 279(D to N) and 284(A to T) as well as in the serine-rich heptapeptide region. Five K-IBDV isolates except 310 isolate share unique amino acid residues at positions 222(A), 256(I), 294(I) which are not present in other standard and attenuated strains. At the two hydrophilic region, K-IBDV isolates except 310 isolate had identical amino cids comparing with Belgium vv IVDV 894VB but had four amino acid substitutions comparing with Chinese vv IBDV F9502. The SWSASGS heptapeptide is conserved in all KIBDV isolates. The sequence of K-IBDV isolate 310 was markedly different from other IBDV strains, evolving from a separate lineage than the others. By phylogenetic analysis, Five K-IBDV isolates except 310 isolate were categorized in one group with foreign vv IBDV isolates but K-IBDV isolate 310 was categorized ina separate group which was differentiated form other compared IBDV strains.

Urinary protein-to-creatinine ratios and serum albumin concentrations were measured in 8 adult male dogs experimentally inoculated with Ehrlichia canis. Urinary protein concentration increased significantly, but transiently, during the acute phase of infection. Urinary protein-to-creatinine ratios were highest (mean, 8.6) during the third and fourth weeks after infection, and decreased to < 0.5 by 6 weeks after infection. Correspondingly, albumin concentration decreased significantly during the acute phase. Serum albumin concentrations were lowest (mean, 2.1 g/dl) the fourth week after infection and increased to > 3.0 g/dl by 11 weeks after infection. There was an inverse linear correlation between urinary protein-to-creatinine ratio and serum albumin concentration. The magnitude of proteinuria and its inverse relationship with serum albumin concentration suggested that hypoalbuminemia associated with acute E canis infection may be attributable primarily to increased renal loss of protein, rather than decreased hepatic synthesis as previously suggested. Another dog was subsequently inoculated with E canis from 1 of the experimentally infected dogs and a renal biopsy was performed during peak proteinuria (urinary protein-to-creatinine ratio = 22 and serum albumin = 1.1 g/dl). Immunofluorescent staining revealed mild to moderate deposits of anti-canine IgM, and to a lesser extent, anti-canine IgG and complement factor C3 in the glomerular tufts and mesangium. Ultrastructural evaluation revealed distortion and fusion of podocyte foot processes and increased microvilli on podocytes. These morphologic changes were consistent with transient glomerular leakage of protein of a magnitude that would significantly contribute to hypoalbuminemia during acute E canis infection. An underlying immunologic mechanism was suggested by positive glomerular immunofluorescence and previously described histologic findings.

Immunoglobulin reactions to Salmonella dublin in serum and milk from 4 groups of lactating cows were measured by an indirect ELISA. The groups consisted of (1) cows that were natural carriers of S dublin in the mammary gland, (2) experimentally infected cows that did not become carriers, (3) cows inoculated with a commercial S dublin bacterin, and (4) cows used as S dublin-negative controls. Milk and serum samples were obtained at monthly intervals. Models for predicting carrier status were developed by use of stepwise logistic regression. Independent variables consisted of serum and milk IgG and IgM titers to S dublin lipopolysaccharide and a ratio of IgG to IgM. The utility of a single sample vs multiple samples obtained at 1-month or 2-month intervals was tested by comparison of goodness-of-fit X2 P values for 8 models predicting carrier status. Immunoglobulin reactions specific to S dublin were a significant predictor of carrier status (P < 0.001). Serum IgG titers specific for S dublin were the most important variable for predicting carrier status. Two serum IgG titers to S dublin obtained 2 months apart was a better predictor of carrier status than measurement of the IgG:IgM ratio from a single serum sample. Immunoglobulin recognizing S dublin epitopes also were detected in milk samples. In milk, performing 2 ELISA 60 days apart to determine IgG and IgM reactions to S dublin appeared to be useful for the prediction of carrier status, but was not as accurate as models for serum immunoglobulin reactions.

We studied the uptake and sequential transneuronal passage of pseudorabies virus (PRV) in rat CNS by use of a combination of immunohistochemistry and in situ hybridization. Protocols for rapid detection of PRV by immunohistochemistry and in situ hybridization in rats with PRV infection of the CNS after intranasal instillation of a wild-type strain of PRV were optimized in vitro, using porcine kidney-15 cells. Pseudorabies virus-specific hybridization signals appeared in the cytoplasm and nucleus of PRV-infected porcine kidney-15 cells by postinoculation (PI) hour 6. In tissue sections of PRV-infected rats, PRV nucleic acids were detected in areas of the rat brain in close proximity to the areas in which PRV antigens were evident. The PRV was initially found in the nucleus of trigeminal ganglion neurons at PI hour 24. At PI hour 72, PRV antigens were observed in the mid-brain, and 24 hours later, in the telencephalon. We also found evidence of specific progressive transsynaptic transmission of the virus, and, on the basis of that, we have constructed a map of the synaptic contacts and pathways in the brain. Therefore, combined use of immunohistochemistry and in situ hybridization was useful for characterizing the pathogenesis of PRV in the CNS of rats after intranasal inoculation, following a pattern that mimics PRV infection of the natural host.