Poultry coccidiosis: recent advancements in control measures and vaccine development

Coccidiosis is recognized as the major parasitic disease of poultry and is caused by the apicomplexan protozoan Eimeria. Coccidiosis seriously impairs the growth and feed utilization of infected animals resulting in loss of productivity. Conventional disease control strategies rely heavily on chemoprophylaxis and, to a certain extent, live vaccines. Combined, these factors inflict tremendous economic losses to the world poultry industry in excess of USD 3 billion annually. Increasing regulations and bans on the use of anticoccidial drugs coupled with the associated costs in developing new drugs and live vaccines increases the need for the development of novel approaches and alternative control strategies for coccidiosis. This paper aims to review the current progress in understanding the host immune response to Eimeria and discuss current and potential strategies being developed for coccidiosis control in poultry.     

PREVALENCE OF ENDEMIC GOITRE IN SCHOOL CHILDREN: SHIRUR (DIST. PUNE,MAHARASHTRA)

A survey for estimation of goitre in school children in the Rural Health Training Centre, Shirur area was undertaken. A total of 4664 students from 17 schools were surveyed. The goitre prevalence was found to be 59.8% with visible goitre rate of 6.2% in pre- and peri-adolescent (10–19 years) age group. Thus a highly endemic goitre focus was located in Shirur, area in Pune District (Maharashtra). This area is located on the eastern tail-end slopes of Sahyadri Hills in Balaghat ranges, situated at an altitude of 533 metres. The area is generally drought prone and receives scanty rain, with poor agricultural practices. Environmental deficiency of iodine was found to be the main cause for this high prevalence of goitre.KEY WORDS: Goitre endemic, Iodine     

Coccidia: a review of recent advances on immunity and vaccine development

The genus Eimeria contains a number of obligate intracellular protozoan parasites with a complicated life-cycle involving both asexual and sexual stages of development. Coccidiosis is caused by Eimeria infecting primarily the intestine of the susceptible host, thereby seriously impairing the growth and feed utilization of poultry and other livestock. The desire to develop a vaccine against Eimeria has promoted active research to elucidate the mechanisms of protective immunity and identification of candidate vaccine antigens. Protozoa are unique in their modes of transmission and nature of disease manifestations, the significance of which should be considered in the development of a control strategy. An intricate and complex interplay of different cell populations and cytokines is involved not only in the pathogenesis of coccidiosis, but also in the development of protective immunity. Thus, comprehensive understanding of the events leading to protection following Eimeria infection will be crucial for the development of an effective vaccine.     

Differential reactive oxygen and nitrogen production and clearance of Salmonella serovars by chicken and mouse macrophages

The objective of the present study was to compare the uptake and killing of Salmonella serovars by murine and avian macrophage cell lines. We used Salmonella enterica serovars Enteritidis (SE338) and Typhimurium (SR11) for this study. Uptake of green fluorescent protein-labeled bacteria was measured using flow cytometry. Cell sorting and plating of viable infected macrophages demonstrated that bacterial clearance was significantly better with J774A.1 compared with HD11 cells. HD11 cells produced significantly higher amounts of nitric oxide (NO) than J774A.1 cells upon infection with SE338 and SR11, whereas J774A.1 cells exhibited greater superoxide production with SR11. Treatment of HD11 cells with recombinant chicken interferon gamma in the absence of bacteria enhanced NO production but did not induce increased levels synergistically with bacteria. Interferon treatment did not influence phagocytosis or increase killing by HD11 cells.     

HLA class I and II antigen phenotypes of North American Indians from Minnesota: implications for marrow transplants using unrelated donors

As a result of an appeal for a bone marrow donor for a North American Indian (Native American) patient, 261 Native Americans from our community were typed for HLA-A,B,DR antigens, and 51 were typed for HLA-A,B antigens only. The HLA antigen frequencies of the Native Americans were compared with those of 12,881 white bone marrow donors and were found to differ markedly. To investigate the implications these differences in HLA antigen frequencies would have for the location of unrelated bone marrow donors, the HLA types of 12 Native American bone marrow transplant patients from our institution were used to search among 5389 HLA-A,B,DR-typed white donors in the National Marrow Donor Program file and the file of 261 HLA-A,B,DR-typed Native American donors. In the white donor file, at least two donors were found that matched at all HLA-A,B,DR antigen loci of one Native American patient (8%). Using the Native American donor file, which was less than one-twentieth the size of the white donor file, and HLA-A,B,DR-matched donor was also found for one (8%) of the patients. These results suggest that although donors for nonwhites can be identified in a file of HLA-typed white volunteers, the probability of finding a suitably matched donor for such individuals is enhanced if donors representing racial or ethnic minorities are included in unrelated donor registries.     

A novel protein tyrosine phosphatase gene is mutated in progressive myoclonus epilepsy of the Lafora type (EPM2)

Progressive myoclonus epilepsy of the Lafora type or Lafora disease (EPM2; McKusick no. 254780) is an autosomal recessive disorder characterized by epilepsy, myoclonus, progressive neurological deterioration and glycogen-like intracellular inclusion bodies (Lafora bodies). A gene for EPM2 previously has been mapped to chromosome 6q23- q25 using linkage analysis and homozygosity mapping. Here we report the positional cloning of the 6q EPM2 gene. A microdeletion within the EPM2 critical region, present inhomozygosis in an affected individual, was found to disrupt a novel gene encoding a putative protein tyrosine phosphatase (PTPase). The gene, denoted EPM2, presents alternative splicing in the 5' and 3' end regions. Mutational analysis revealed that EPM2 patients are homozygous for loss-of-function mutations in EPM2. These findings suggest that Lafora disease results from the mutational inactivation of a PTPase activity that may be important in the control of glycogen metabolism.      

Invasive pneumococcal infection in children, 1981-92: A hospital-based study

Objective: To document the pattern and sequelae of invasive pneumococcal infection in hospitalized children.
Methodology Retrospective review of Streptococcus pneumoniae (Sp) isolates from normally sterile sites from 1981 to 1992 at three paediatric centres in Sydney for demographic data, spectrum of disease, predisposing conditions, mortality, and sequelae from meningitis.
Results: Four hundred and thirty-one episodes in 417 patients were identified. Foci of infection were: meningitis, 34%; pneumonia, 29%; bacteraemia without apparent focus, 30%; and other foci, 7%. Sixty-one per cent of all cases and 64% of cases with meningitis were less than 2 years old. Predisposing conditions were present in 37%, were significantly more common in patients over age 2 years and were more common with foci other than meningitis. Overall mortality was 6.6% whereas the mortality for those with meningitis was 8%. Neurological sequelae were identified in 34% of previously normal children, and severe hearing loss occurred in 11.5%.
Conclusions The high morbidity and mortality from invasive pneumococcal infection in children justifies further evaluation of preventive strategies.     

Isolation and functional characterization of chicken intestinal intra-epithelial lymphocytes showing natural killer cell activity against tumour target cells.

Intestinal intra-epithelial lymphocytes (IEL) of SC or FP chickens were isolated and examined for their natural killer (NK)-cell activity against chicken tumour cell lines, LSCC-RP9 (RP9), LSCC-RP12 (RP12), MDCC-MSB-1 (MSB-1) and MDCC-CU36 (CU36). In general, IEL of satisfactory yield and of good viability were obtained with EDTA treatment of the gut tissues, followed by rapid passages of the resultant cells through nylon-wool columns and centrifugation on two-step Percoll density gradients (45% and 80%). In 4-hr and 16-hr 51Cr-release assays, the NK-cell activity of chicken IEL depended not only upon the type of target cells but also upon the incubation time and the host genetic background. RP9, MSB-1 and CU36 were susceptible to NK lysis by IEL and by spleen cells, while RP12 was resistant to lysis even after a prolonged incubation. In kinetic studies the cytotoxicity was detactable from 2 hr after incubation and progressively increased up to 16 or 18 hr. The IEL of SC chickens revealed significantly higher levels of NK-cell activity against RP9 than FP-strain chickens, whereas their splenic NK-cell activity was not significantly different. Against MSB-1 targets, however, IEL of SC and FP chickens showed similar levels of NK-cell activity while their spleens did not (being higher in FP). When tested in FP chickens, IEL NK-cell activity was inhibited by the addition of unlabelled homologous target cells. In general, NK-cell activity was higher in the jejunum and ileum than in the duodenum and caecum. Efforts to enrich IEL NK-effector cells by discontinuous Percoll gradients were not successful. The results of the present study show that IEL of chicken intestine contain effector cells that can mediate NK-cell activity against chicken tumour cells.     

Examination of whether persistently indeterminate human immunodeficiency virus type 1 Western immunoblot reactions are due to serological reactivity with bovine immunodeficiency-like virus.

The bovine lentivirus, known as bovine immunodeficiency-like virus (BIV), is genetically, structurally, and antigenically related to human immunodeficiency virus type 1 (HIV-1). It is not known whether sera from persons exposed to BIV proteins would show either positive or indeterminate reactivity on HIV-1 antibody tests. We used a BIV Western blot (immunoblot) analysis to examine human sera characterized as HIV-1 antibody positive, HIV-1 antibody negative, HIV-1 persistently indeterminate, HIV-1 p17 antibody positive only, HIV-1 p24 antibody positive only, human T-cell leukemia virus type 1 (HTLV-1) p19 antibody positive only, or HTLV-1 p24 antibody positive only. None of these sera were positive by Western blot to BIV-specific proteins. Many of these sera, however, displayed strong reactivities to bovine cell culture antigens on blots prepared from both mock-infected and BIV-infected cell cultures. The HIV-1 p17 and p24 antibody-positive and the HTLV-1 p19 and p24 antibody-positive sera were further examined by Western blot to bovine leukemia virus (BLV) and were found to be negative. We examined sera from laboratory personnel at risk for BIV exposure, including two laboratory workers who were exposed to BIV by accidental injection with BIV-infected cell culture material, and found no evidence of seroconversion to BIV-specific proteins. We tested 371 samples of fetal bovine sera, each sample representing serum pooled from one to three fetuses. All samples were negative by BIV Western blot. To date, we have not detected any human sera with antibody to BIV-specific proteins. Our data indicate that persistently indeterminate results on HIV-1 Western blot are not caused by a human antibody response to BIV proteins.