NEISSERIA GONORRHOEAE “The Violinist’s Last Clap”
General Features: Gram-, kidney bean-shaped diplococci, oxidase+, grows on chocolate
agar, does not have a capsule (“glass capsule case broken on the floor”)
Reservoir: human genital tract
Transmission: sexual contact (“detective flirting with woman at the bar”), birth (“mother
holding baby”), sensitive to drying and cold
Pathogenesis: pili allows for attachment to mucosal surfaces, inhibits phagocytic uptake,
has antigenic variation; has outer membrane proteins – OMP I, a structural antigen used
in serotyping; Opa proteins that has antigenic variation, allows for adherence; and IgA protease; organism invades mucosal
surfaces and causes inflammation
Disease: gonorrhea
• Male: urethritis, proctitis or orchitis
• Female: endocervitis and pelvic inflammatory disease, PID (“chandelier shaped as ovaries and uterus with candles
indicating inflammation”), this produces purulent discharge (“candles dripping hot wax onto table”), and can spread to the
peritoneum causing Fitz-Hugh-Curtis Syndrome, which can cause long, thin “violin-string” adhesions to the capsule of the
liver (“Fitz-Hugh-Curtis string orchestral band with violist’s violin in foreground”). This can also present with asymmetrical
arthritis (“statue crushing violist has a crack in one knee”) and proctitis
• Infants: ophthalmia and conjunctivitis that rapidly leads to blindness if untreated (“mother holding baby covering baby’s
eyes”)
Diagnosis: Intracellular gram- diplococci in PMNs (“white chairs in foreground shaped as neutrophils with high backs and
reflections to represent nucleus with two red pillows to represent diplococci”) from urethral smear from symptomatic male are
suggestive of infection
• Commonly: diagnosis by genetic probes with amplification; culture when done on Thayer-Martin medium
Treatment: ceftriaxone (“statue with 3 axes and 3 axe emblem on signs above orchestral band”), must also test for C.
trachomatis and assume coinfection (“clam shaped napkins on the table”) or treat with doxycycline; penicillin-binding protein
mutations led to gradual increases in penicillin resistance from the 1950s-70s; plasmid-mediated beta-lactamase produces high
level penicillin resistance