The possible causative agent is Corynebacterium diptheriae Sore throat, fever, shaking and chills, difficulty in breathing are all symptoms typically assocaited with C. diptheriae. The bacterium is Gram positive bacillus, non capsulated, non motile, toxin producing. They produce exotoxin called diptheria toxin, which is encoded by a prophage. The bacteria adheres to mucosal epithelium and infect them. The toxtosin released by endosomes stimulate localized inflammation followed by tissue destruction. Necrosis results from tissue destruction. The toxin belongs to AB toxin class. The B fragment binds to host cell and the A fragment toxin is innserted into the membrane and transported. It is proteolytically activated inside the cell. The toxin binds to a histidine residue of elongation factor 2 or eEF2. The active A fragment inhibits translocation of growing peptide chain on the ribosome. Thus, it inhibits protein synthesis. The toxin transfers NAD to dipthamide (elongation factor 2) to inactivate the elongation factor. Local tissue destruction makes the bacteria gain access into the circulation, anters the lymphatic and blood stream, to spread to other parts of the body. Systemic spreading causes diptheria toxin act on vital organs like kidney, myocardium, and nervous system. Innate immune responses against the bacterium includes Macrophages as the first line of defense. They use pattern specific receptors to attach and engulf bacteria. Neutrophils also mediate the same response. Macrophages further release cytokines to mediate inflammation. Solution The possible causative agent is Corynebacterium diptheriae Sore throat, fever, shaking and chills, difficulty in breathing are all symptoms typically assocaited with C. diptheriae. The bacterium is Gram positive bacillus, non capsulated, non motile, toxin producing. They produce exotoxin called diptheria toxin, which is encoded by a prophage. The bacteria adheres to mucosal epithelium and infect them. The toxtosin released by endosomes stimulate localized inflammation followed by tissue destruction. Necrosis results from tissue destruction. The toxin belongs to AB toxin class. The B fragment binds to host cell and the A fragment toxin is innserted into the membrane and transported. It is proteolytically activated inside the cell. The toxin binds to a histidine residue of elongation factor 2 or eEF2. The active A fragment inhibits translocation of growing peptide chain on the ribosome. Thus, it inhibits protein synthesis. The toxin transfers NAD to dipthamide (elongation factor 2) to inactivate the elongation factor. Local tissue destruction makes the bacteria gain access into the circulation, anters the lymphatic and blood stream, to spread to other parts of the body. Systemic spreading causes diptheria toxin act on vital organs like kidney, myocardium, and nervous system. Innate immune responses against the bacterium includes Macrophages as the first line of defense. They use pattern specific recep.

1. The possible causative agent is Corynebacterium diptheriae
Sore throat, fever, shaking and chills, difficulty in breathing are all symptoms typically
assocaited with C. diptheriae. The bacterium is Gram positive bacillus, non capsulated, non
motile, toxin producing. They produce exotoxin called diptheria toxin, which is encoded by a
prophage. The bacteria adheres to mucosal epithelium and infect them. The toxtosin released by
endosomes stimulate localized inflammation followed by tissue destruction. Necrosis results
from tissue destruction. The toxin belongs to AB toxin class. The B fragment binds to host cell
and the A fragment toxin is innserted into the membrane and transported. It is proteolytically
activated inside the cell. The toxin binds to a histidine residue of elongation factor 2 or eEF2.
The active A fragment inhibits translocation of growing peptide chain on the ribosome. Thus, it
inhibits protein synthesis. The toxin transfers NAD to dipthamide (elongation factor 2) to
inactivate the elongation factor. Local tissue destruction makes the bacteria gain access into the
circulation, anters the lymphatic and blood stream, to spread to other parts of the body. Systemic
spreading causes diptheria toxin act on vital organs like kidney, myocardium, and nervous
system.
Innate immune responses against the bacterium includes Macrophages as the first line of defense.
They use pattern specific receptors to attach and engulf bacteria. Neutrophils also mediate the
same response. Macrophages further release cytokines to mediate inflammation.
Solution
The possible causative agent is Corynebacterium diptheriae
Sore throat, fever, shaking and chills, difficulty in breathing are all symptoms typically
assocaited with C. diptheriae. The bacterium is Gram positive bacillus, non capsulated, non
motile, toxin producing. They produce exotoxin called diptheria toxin, which is encoded by a
prophage. The bacteria adheres to mucosal epithelium and infect them. The toxtosin released by
endosomes stimulate localized inflammation followed by tissue destruction. Necrosis results
from tissue destruction. The toxin belongs to AB toxin class. The B fragment binds to host cell
and the A fragment toxin is innserted into the membrane and transported. It is proteolytically
activated inside the cell. The toxin binds to a histidine residue of elongation factor 2 or eEF2.
The active A fragment inhibits translocation of growing peptide chain on the ribosome. Thus, it
inhibits protein synthesis. The toxin transfers NAD to dipthamide (elongation factor 2) to
inactivate the elongation factor. Local tissue destruction makes the bacteria gain access into the
circulation, anters the lymphatic and blood stream, to spread to other parts of the body. Systemic

2. spreading causes diptheria toxin act on vital organs like kidney, myocardium, and nervous
system.
Innate immune responses against the bacterium includes Macrophages as the first line of defense.
They use pattern specific receptors to attach and engulf bacteria. Neutrophils also mediate the
same response. Macrophages further release cytokines to mediate inflammation.