Chronic Granulomatous Disease

The children with a disseminated infection with BCG following vaccination are likely to have a genetic deficiency of C3. This is where their macrophages have a reduced ability to produce oxygen intermediates which in turn leaves these children are susceptible to serious infections by pyogenic bacteria. Usually, gram-positive bacteria such as staphylococci, streptococci, pneumococci and Haemophilus types of infection. Therefore the children are at risk from infections of the lymph nodes, pneumonia and abscesses both inside and outside of the body. A diagnosis of Chronic Granulomatous Disease would be likely. These Children will have macrophages that can’t destroy the pathogen within the phagocyte due to having poor oxygen- dependent killing mechanisms, leaving mycobacterial to survive and proliferate inside host cells.

These children’s susceptibility to bacterial infections will cause Granulomas to appear inside their organs. Another less likely explanation of a disseminated BCG infection following a BCG vaccine could be because as it appears in someone with an impaired immune system along with the fact that Middle-East countries in recent years has seen a global rise in HIV and AID’s, therefore, the children should also be tested for the HIV virusQ3a.

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IgA and IgG are both transported around the body in the body fluids. IgA is the main antibody in the mucus secretions and IgG is the main antibody in the body’s blood and tissues and also has the ability to cross the placenta to the foetus. Therefore they must be of a high affinity to be transported in this way through the body’s fluids. IgA become bound to the poly-Ig receptor on the epithelial cells and transported across the epithelium in vesicles and released on the mucosal surface and then blocks pathogens and toxins from binding to their antigens. IgA and IgG are able to make strong bonds with antigens along with a complementary shape which depend on their molecule groups on the antigen and antibody At first a non-covalent bond is weak, once all the bonds combine, it will produce a very strong bond.

This shape is determined by the amino-acid residues in the hypervariable loops of the heavy and light chains. IgM has low affinity, however they do have high avidity, which means that they have ten binding sites as opposed to having only one which allows an antigen to bind via a number of epitopes of polymeric carbohydrate antigens. This is termed as multi-valanceQ3b.The surface of bacterium has many millions of identical polymeric carbohydrate epitopes and as IgM has ten combining sites then this will result in many strong bonds being produced. When the IgM is complexed it will expose a complement-binding site which results in the production of C3a and C5a which will trigger mast cell degranulation. C5a is a chemotactic for phagocytes and also a mast cell activator. Chemotactic molecules are bacterial peptides.

Bacteria has an amino-acid called formyl methionine (fMet) which have receptors on phagocytes for peptides which will initiate protein synthesis and any bacterial infection that is present will automatically be attracted to phagocytes. Phagocytes can also bind to bacterial carbohydrates because they have lectin and scavenger receptors that recognise generic bacterial carbohydrates. IgM is a serum antibody and if bacterium enters the body, these antibodies will opsonise bacteria for phagocytosis either directly or by activating complement.Q4Oral/Nasal aspirates are screened for respiratory viruses by extracting RNA, subjecting it to reverse-transcription polymerase chain reaction (RT-PCR) into DNA. DNA is then used to detect and amplify a short sequence of nucleotides specific to the virus. The sequence is separated, subjected to gel electrophoresis. If positive, are inoculated into cells for culture.

(A fluorescent-labelled antisera). If remains bound to cells, they fluoresce under illumination indicating viral antigen on the cell surface. Real-time RT-PCR assays are the best method of a primary diagnostic and provide rapid and accurate assessments. Positive samples will have an additional two probes that discriminate between seasonal and H1N1. Test amplifies the viral genetic material, enabling detection of new strains.ELISA testing H1N1 Influenza A. Easy to perform and highly specific.

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Both types of samples are added to wells. A series of incubation, washing and additives thus producing an antibody-antigen-sandwich and a developing blue dye. The colour changes from blue to yellow. The concentration of the IgG antibodies is directly proportional to the intensity of the colour.Haemagglutination-inhibition assay (HAI): Influenza virus particles have an envelope protein called hemagglutinin which binds to sialic acid receptor and to red blood cells. If the latter, are not bound to the virus, they will sink to the bottom and form a button. Those attached to the virus particles form a lattice that coats the well.

If a confirmed influenza A reacts weakly thus indicating an unknown variant of Influenza A. Further HAI and neuraminidase inhibition assay, or a PCR test will confirm strain variants.Nasopharyngeal swab can be tested initially for H1N1 in a culture. A culture of microbes from the patient is placed on non-selective medium. Cells that are not part of the normal flora are selectively cultured and identified. Results are rapid but with a high amount of false negative results and test can’t distinguish between different strains. (312 words)