Neisseria & Bacteroides Flashcards
Neisseria sp. • Gram? shape? • LPS? • common where? • O2 use? • pathogenic species? Host?
• Gram− diplococci
• Lipooligosaccharide (vs. LPS): lack O antigen extensions
• common oral flora and other mucous membranes
• facultative anaerobe
• pathogens: N.gonorrhoeae and N.meningitidis
Host: only humans
Virulence Factors of N. gonorrhoeae
Ag variation (pilin) phase variation pili IgA protease lack of Opa sialic acid on LOS shedding of endotoxin
antigenic variation of pilin
Gonococci at different infection sites in an infected individual often express different pilin genes
because they adhere to different cell surface receptors on distinct mucosal epithelial cells.
ØPilE single chromosomal copy of pilin structural gene
ØStrains contain 10-15 copies of PilE variants lacking promoter and 5-end
of gene called PilS genes
ØPilS genes recombine with PilE creating unlimited antigenic variants of PilE
ØResult is that antigenic structure of pilus protein is constantly changing
phase variaiton
nassiera and E.coli
effects on Opa expression
on/off switch for surface protein expression
In Neisseriae: Slipped Strand Mispairing resulting from presence of multiple identical repeated sequences at 5-end of gene. Replication errors due to strand misalignment creates reading frame errors.
Often, premature stops, but also results in ON/OFF switch.
Multiple Opa (Colony Opacity) protein copies scattered across genome; Slipped strand mispairing results in frequent variation in Opa protein expression or complete absence of Opa
E. coli and other Gm- rods simple inversion of promoter
N. Gon surface attachment
Pili mediate bacterial attachment to non-ciliated epithelia
bacteria proliferate and shed into secretions;
Does N. Gon have a capsule
no
IgA protease of N. gon, how can cleaved IgA be useful
Usefulness of cleaving IgA: Coating of bacteria with IgAFab fragments (does not activate complement and also blocks binding by other IgG and IgM)
Serum-resistant virulent strains cause:?
disseminated gonococcal infections:
Serum-resistant virulent strains
lack what protein/ significance?
how do they avoid phago?
Strains lack Opa proteins (colony opacity proteins = outer-membrane proteins) Neutrophils unable to engulf bacteria lacking Opa proteins.
Sialic acid on LOS (Lipidoligosaccharide of outer membrane) binds complement regulatory proteins, prevents complement-based phagocytosis
endotoxin shedding of n. gon
Shedding of lots of endotoxin (LOS of these bacteria, LIPID A) Binds TLR-4 (especially on dendritic cells, macrophage & B cells) secretion of pro-inflammatory cytokines that can lead to shock
Gonorrheal Diseases diseases via Sexual transmission
urogenital infections
§ Frequently (almost) asymptomatic
o urethritis in men, urethral pus secretion (leukocytes with many gonococci)
o cervicitis in women, frequently some urination sensitivity but no other symptoms
(infection tracing is important to prevent re-infection)
Opthalmia Neonatorum
o destructive eye infection, acquired during birth
o Application of erythromycin ointment into both eyes of newborns is mandatory in many states
and is considered standard neonatal care
Pelvic Inflammatory Disease (PID) in women
future impacts?
Initial infection of cervix, fallopian tubes and vaginal wall glands can lead to PID (15-30%):
o gonococci enter abdominal cavity, cause liver disease
o tissue scarring causes fallopian tube abnormalities which lead to ectopic pregnancies
and sterility
Urethral and testicular tubule scarring caused by and can lead to?
resulting from epididymitis
leads to sterility and increased urethral infections by other microbes
Disseminated Gonococcal Infection (without apparent genital infection) causes:
skin lesions, suppurative arthritis of a major joint, and heart valve destruction.
