Introduction to Pathogens Pathogens are microorganism like bacteria and viruses which causes infectious diseases in humans, animals or plants. Pathogens cause disease in two ways:Damaging cells: invading cells and organisms of the host and replicating on them. It is done by viruses.Producing toxins: Living pathogen produced exotoxins, while damaged pathogens produce endotoxins. It is done by bacteria(Bbc.co.uk, 2018).Staphylococcus AureusS.
aureus is a bacteria which causes infectious diseases, in order to initiate infection the pathogen must access to the host and get attached to it. The S. Aureus express a protein which will unite to the host. In addition, the strains present a Fibrinogen/fibrin protein which gets attach to the blood clots and traumatized tissues , this demonstrates that the Staphylococcus Aureus is a pathogen which damage the host creating and infection just like any other pathogen. Summary of virulence factors of Staphylococcus aureus.The evidence that these staphylococcal proteins are virulent bacteria (Pathogen) is in the study of defective mutants, in experimental infections and in vitro adhesion assays. Defective mutants to bind to fibronectin and fibrinogen have reduced virulence in endocrine diseases, which shows that the binding of bacteria to sterile vegetations causes damage to the endothelial surface of the heart valve. In addition, the soluble ligand-binding domain of fibrinogen, fibronectin and collagen-binding proteins expressed by recombinant methods strongly blocks the interactions of bacterial cells with the corresponding host protein.
The responsible for the symptoms during infectious of S. Aureus are caused for different types of toxins, those toxins damage the membrane.?-toxin?-toxin is the most potent membrane damaging. It is express right away when it gets attached to the membrane of susceptible cells. Those cells have a specific receptors for ?-toxin, which allows the low concentration of toxin to attach, causing smalls pores where the ions can pass.
When the concentration is higher, the toxin reacts non-specifically with membrane lipids, this creates bigger pores where the divalent and small molecules can pass.In humans, monocytes and platelets are very sensitive to ?-toxin as they carry stronger intermolecular forces which permits the toxins that are physiologically relevant. Then series of secondary reaction are produce it allow the release of eicosanoids and cytokines, this starts the production of inflammatory mediators. causing the symptoms of septic shock.?-toxinThe ?-toxin damage the membrane which produce sphingomyelinase lipid. Most of the human population does not express this toxin as a lysogenic bacteriophage needs to be inserted in the gene that encodes toxin.’Moreover, the majority of isolates from bovine mastitis express ?-toxin, meaning that the toxin is important in the pathogenesis of mastitis.
This is supported by the fact that ?-toxin-deficient mutants have reduced virulence in a mouse model for mastitis.’?-toxin and leukocidin?-toxin and leukocidin are two component protein which damages membranes.This proteins are are expressed separate but in order to damage the membrane the have to act together.
the ?-toxin express 3 proteins , the A and B components are weak and hemolytic, in the other hand, B and C components from leukotoxin has poor hemolytic activity.The Panton and Valentine (PV) leukocidin is different from the leukotoxin expressed by ?-toxin locus. Only a small part of S. Aureus isolates (2% survive) express the PV, while 90% of those isolated from severe dermonecrotic lesions express toxin. This shows the high rate of PV in necrotizing skin infections (Foster, 2018)Influenza AThe influenza is characterised by its RNA which needs to replicate in order to survive. This process is common in viruses, the influenza viruses evade the long term adaptive immune responses in many hosts as it is common in pathogens.
N-acetylneuraminic acid (sialic acid) is recognized on the surface of the host cell by influenza viruses. Sialic acids are nine-carbon acidic monosaccharides found at the terminus of many glycoconjugates. Carbon-2 of terminal sialic acid can bind to carbon-3 or carbon-6 of galactose, forming ?-2,3 or ?2,6 bonds; the result is terminal sialic acid. The rest of sialic acid is recognized and bound by HA peaks on the surface of influenza viruses. Sialic acids with ?-2,3 terminal bonds are also present in the human respiratory epithelium; consequently, humans and other primates can become infected with avian influenza virus.The virus is endocytosis after the binding of sialic acid to the HA protein of the influenza virus. First, the low pH triggers a change to HA, exposing a peptide in the viral envelope against the endosomal membrane, thereby opening a pore through which viral RNPs are released into the cytoplasm of the host cell. Second, the hydrogen ions in the endosome are pumped into the virus particle through the M2 ion channel.
The M2 protein is found only in the influenza A virus. The M2 protein is the target of the amantadine class of anti-influenza drugs, which blocks the activity of the ion channel and prevents the elimination of the virus. From the M2 channels RNPs is released from the viral matrix to cellular cytoplasm. Once RNPs are released, they are transported to the nucleus of the host cell by means of viral protein signals (NLS), which direct the cellular proteins to import the RNP. The nucleus is where the RNA synthesis of the influenza virus is located, both the messenger RNA (mRNA) that translates the viral proteins of the host cell and the vRNA segments that make up the genomes of the progeny virus.
The flu is encoded in negative sense vRNA. The blocking of messenger RNA occurs in a similar manner, to initiate the synthesis of the mRNA, the proteins PB1 and PB2 “steal” the primers in 5 ‘of the pre-mRNA transcripts of the host.The envelope proteins HA, NA and M2 are synthesized, from mRNA in ribosomes attached to the membrane to the endoplasmic reticulum, where they are folded and transported to the Golgi apparatus for post-translational modification.