Pharyngitis: 62-kd polypeptide exotoxin, which causes local tissue

Pharyngitis:
(Simon, 2017)

Pharyngitis is an infection or irritation of the pharynx or
tonsils. (Acerra, 2017)

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The Pathophysiology of pharyngitis
involves infectious bacteria or viruses that sometimes invade the pharyngeal
mucosa directly, thereby causing a local inflammatory response. Irritation of
the pharyngeal mucosa can also be caused by many other viruses such as GABHS
which is the principal cause in children,  rhinovirus and coronavirus, .When
Streptococcal or GABHS infection is responsible for pharyngitis, it can be
identified by its characteristics of   local invasion and release of extracellular
toxins and proteases. (Simon,
2017) Some  80 M-protein serotypes of GABHS have been
isolated and few of those serotypes referred to as rheumatogenic forms, were
identified and linked to rheumatic fever and subsequent heart valve damage. GABHS
pharyngitis has typical incubation period of 2-5 days and is transmitted is via
respiratory droplets through close contact. (Simon, 2017)

 

 

Pediatric
Diphtheria:

 

Diphtheria is Corynebacterium diphtheria caused   toxin-mediated infectious disease. Diphtheria
organisms typically induce local inflammatory reaction after colonizing the superficial
layers of the patient’s skin lesions or respiratory mucosa. (Demirci,2017)

Corynebacterium Diphtheria’s major virulence is said to be its
special   ability to produce the potent 62-kd
polypeptide exotoxin, which  causes local
tissue necrosis  by inhibiting  protein synthesis .(Demirci,2017)

The Diphtheriae
toxin, carry’s the tox structural gene found in lysogenic
corynebacteriophages beta-tox +, gamma-tox +, and omega-tox +.(Demirci,2017)

The highly toxic
strains of C-Diphtheriae which have 2 or 3 tox + genes inserted into
the genome is regulated by the bacterial host and is iron dependent. The gene
regulator is inhibited when the iron concentration is low, thereby
increasing toxin production. The increase in toxin concentrations also extends C-Diphtheriae
toxic effects beyond the local area. (Demirci,2017) Toxin excreted
from the bacterial cell undergoes cleavage to form 2 chains, which are then held
together by an interchain disulfide bond between cysteine residues at positions
186 and 201. (Demirci,2017)

Although the myocardium and peripheral nerves are
affected the most, C-Diphtheriae toxin does not however target any specific
organ 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 are
either the primary focus of infection or the common sites infected. Patients
infected with C-Diphtheriae typically develop signs and symptoms of the
inflammation after a 2-4 days incubation period.

Pediatric
Mononucleosis and Epstein-Barr Virus Infection: 

 

Infectious mononucleosis
(IM) is a multisystem disorder caused by primary infection with Epstein-Barr
virus (EBV) and defined by the triad of fever, pharyngitis, and adenopathy. It is
a lifelong infection Primary infection with Epstein-Barr
virus is followed by latent infection.

(Bennett,2017)

The EBV virus lives in B lymphocytes and is intermittently shed
asymptomatically in oropharyngeal secretions, which is the principal mode
of  transmission among humans.

The virus which is usually acquired during early childhood through
sharing of saliva-bearing fomites can remain clinically silent ,but is not
highly contagious. But when adolescents and adults are infected it could lead
to a  clinical syndrome of infectious
mononucleosis between 25 and 50% of the time .

EBV enters B lymphocytes
through the C3d receptor on the surface of B cells or nasopharyngeal epithelial
cells. Once inside the cell, the virus expresses several  Epstein-Barr nuclear antigens that activate
EBV-encoded latent membrane proteins and other gene products responsible for
regulation of B-cell growth. The host response to acute EBV infection consists
of a vigorous and coordinated cellular and humoral immune response that
includes IgM and IgG antibodies directed at the viral capsid.