Pathophysiology of Gonorrhea

Neisseria gonorrhoeae is a gram-negative, intracellular, aerobic diplococci that affect cuboidal or columnar epithelium of the host. A wide variety of factors that affect the way mediate gonococcal virulence and pathogenicity.
Pathophysiology of Gonorrhea
Pathophysiology of Gonorrhea
Can assist the movement of gonococcal pili to the mucosal surface. Outer membrane proteins such as protein opacity-associated (Opa) increase attachment between gonococcal (form dense colonies on culture media) and also improves adhesion to phagocytes. Type plasmid-mediated production of TEM-1 beta-lactamase (penicillinase) also play a role in virulence.

Gonococci attached to the host mucosal cells (pili and Opa proteins play a major role) and within 24-48 hours, cells penetrate into the subepithelial space urethral tissue. Endotoxin in bacterial cells causing inflammation. Typical host response characterized by the invasion of neutrophils, followed by sloughing of the epithelium, submucosal microabscesses formation and discharge of pus (yellow) are emitted into the urethra and out of the urethra. Accumulation of pus in the urethra making urination painful. Endotoxin also causes inflammatory pain. Symptoms are usually milder in females. If left untreated, macrophage and lymphocyte infiltration of neutrophils replace. Untreated infection in women can spread to the fallopian tubes and abdominal tissues and cause PID (pelvic inflammatory disease). Infertile due to PID in women and disorders of the vas deferens in men.

The existence of births to mothers infected with gonorrhea caused the child has an infection in the eye that can cause blindness (ophthalmia nenoatorum). It can be prevented by 1% AgNO3 or penicillin in the eyes of newborns.

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