Pharyngitis: corynebacteriophages beta-tox +, gamma-tox +, and omega-tox

Pharyngitis:(Simon, 2017)Pharyngitis is an infection or irritation of the pharynx ortonsils. (Acerra, 2017)The Pathophysiology of pharyngitisinvolves infectious bacteria or viruses that sometimes invade the pharyngealmucosa directly, thereby causing a local inflammatory response.

Irritation ofthe pharyngeal mucosa can also be caused by many other viruses such as GABHSwhich is the principal cause in children,  rhinovirus and coronavirus, .WhenStreptococcal or GABHS infection is responsible for pharyngitis, it can beidentified by its characteristics of   local invasion and release of extracellulartoxins and proteases. (Simon,2017) Some  80 M-protein serotypes of GABHS have beenisolated and few of those serotypes referred to as rheumatogenic forms, wereidentified and linked to rheumatic fever and subsequent heart valve damage. GABHSpharyngitis has typical incubation period of 2-5 days and is transmitted is viarespiratory droplets through close contact. (Simon, 2017)  PediatricDiphtheria: Diphtheria is Corynebacterium diphtheria caused   toxin-mediated infectious disease.

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Diphtheriaorganisms typically induce local inflammatory reaction after colonizing the superficiallayers of the patient’s skin lesions or respiratory mucosa. (Demirci,2017)Corynebacterium Diphtheria’s major virulence is said to be itsspecial   ability to produce the potent 62-kdpolypeptide exotoxin, which  causes localtissue necrosis  by inhibiting  protein synthesis .(Demirci,2017)The Diphtheriaetoxin, carry’s the tox structural gene found in lysogeniccorynebacteriophages beta-tox +, gamma-tox +, and omega-tox +.(Demirci,2017)The highly toxicstrains of C-Diphtheriae which have 2 or 3 tox + genes inserted intothe genome is regulated by the bacterial host and is iron dependent. The generegulator is inhibited when the iron concentration is low, therebyincreasing toxin production. The increase in toxin concentrations also extends C-Diphtheriaetoxic effects beyond the local area. (Demirci,2017) Toxin excretedfrom the bacterial cell undergoes cleavage to form 2 chains, which are then heldtogether by an interchain disulfide bond between cysteine residues at positions186 and 201. (Demirci,2017)Although the myocardium and peripheral nerves areaffected the most, C-Diphtheriae toxin does not however target any specificorgan of the body.

Toxin absorption can lead to necrosis of kidney tubules,thrombocytopenia, cardiomyopathy, and demyelination of nerves. (Demirci,2017)In 90% or more of the patients, the tonsils, pharynx, nose and the larynx areeither the primary focus of infection or the common sites infected. Patientsinfected with C-Diphtheriae typically develop signs and symptoms of theinflammation after a 2-4 days incubation period.PediatricMononucleosis and Epstein-Barr Virus Infection:  Infectious mononucleosis(IM) is a multisystem disorder caused by primary infection with Epstein-Barrvirus (EBV) and defined by the triad of fever, pharyngitis, and adenopathy. It isa lifelong infection Primary infection with Epstein-Barrvirus is followed by latent infection.(Bennett,2017)The EBV virus lives in B lymphocytes and is intermittently shedasymptomatically in oropharyngeal secretions, which is the principal modeof  transmission among humans.The virus which is usually acquired during early childhood throughsharing of saliva-bearing fomites can remain clinically silent ,but is nothighly contagious.

But when adolescents and adults are infected it could leadto a  clinical syndrome of infectiousmononucleosis between 25 and 50% of the time .EBV enters B lymphocytesthrough the C3d receptor on the surface of B cells or nasopharyngeal epithelialcells. Once inside the cell, the virus expresses several  Epstein-Barr nuclear antigens that activateEBV-encoded latent membrane proteins and other gene products responsible forregulation of B-cell growth. The host response to acute EBV infection consistsof a vigorous and coordinated cellular and humoral immune response thatincludes IgM and IgG antibodies directed at the viral capsid. 

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