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General features
- Gram negative cocci with kidney bean appearance
- Oxidase positive
- Ag variations: Pili, outer membrance proteins (OMPs)
- OMPs contain short LPS called LOS
- Lipid A and core oligosaccharide same
- Differences: Meningococcus has polysaccharide capsule (can cause toxic shock), Gonococcus grows more slowly than meningococcus
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Meningitidis: organism
- NP flora
- Multiple serogroups; A, B, C, W-135, and Y are most important
- Two classes of Pili, and multiple OMPs
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Meningitidis: Epi
- NP flora of 10%
- Inhalation of aerosolized droplets, close and prolonged contact
- Higher attack rates in families
- Disease in those that lack group specific Ab
- Most cases in kids < 6
- Group A - more severe
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Meningitidis: pathogenesis
- Attachment/invasion: pili for initial attachment to nonciliated NP epi; pass through to submucosa via vesicles
- Resisting Phagocytosis: Capsule prevents complement activated phagocytosis, LPS/LOS structure similar to sphongolipids -> ID as self, binds sialic acid to LOS side chains, which binds factor H
- Injury: disseminated endotoxic injury via endotoxin blebs, hyperproduction of toxins
- Immunity: group specific polysaccharide Ab, T-cell independent immune response in which IgG2 is predominant; Group B don't produce Ab
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Meningitidis: Clinical
- Disease: Acute purulent meningitis with scattered skin petechiae; Disseminated intravascular coagulation syndrome (part of endotoxin shock); many progress to fulminant DIC and hsock with bilateral hemorrhage destruction of renal glands; some patients with low grade fever, arthritis
- Tx: Penicillin still great
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Meningitidis: Prevention
- Refampin for prophylaxis (pencillin has poor tissue penetration in NP)
- quadrivalent vaccine
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Gonorrhoeae: Organism
- Chocolate agar, CO2 supplementation
- Outer membrane: LPS, LOS, phospholipids
- OMPs: Porin A + B, Opa (adherence protein)
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Gonorrhoeae: Ag Variation
- Pili: recombinational exchange between multiple pilin genes; results in silent pili or pili with changed antigenicity
- Opas: controlled via pentameric sequence, changed of which are due to replicative slippage; each opa gene has on/off switch which can be activated at random for for each cell
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Gonorrhoeae: Epi
- No effective means of control
- Hard to detect asymptomatic cases
- Major reservoir is asymptomatic patient
- 95% of men show symptoms
- 50% of women don't
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Gonorrhoeae: Pathogenesis
- Attachment/invasion: Adherance ligands (pili) attach to nonciliated epi cells; microcolinies move across cells; Opas help in between cell adhesion and in cervical/urethral adhesion; microvilli pull bacteria into cell via parasite directed endocytosis; exit into submucosa
- Survival: Scavenge iron; LOS sialyation binds factor H; pili/Opas prevent phagocytosis
- Spread/dissemination: Localized via sticky clusters held together by Opas; injury to fallopian tub via LPS/LOS and cell wall fragments; can reach the blood stream
- Immunity: Ag variations often degreats Abs
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Gonorrhoeae: clinical
- Genital: men - 2-7 days post infection, purulent discharge, dysuria, local extension to epididymitis or prostatitis; endocervis primary site in women, increase vaginal discharge, urinary frequency, dysuria, abd pain, menstrual abnormalities
- Other local infections: Rectal gonorrhea, pharyngeal gonorrhea
- PID: 10-20% of women with gonorrhea; fever, lower abd pain,a dnexel tenderness, leukocytosis; can cause infertility, ectopic pregnancy
- DGI: Fever, polyarthralgia, petechial, maculopapular rash
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Gonorrhoeae: diagnosis
- Smear: Genital site smear with bean shapped gram negative cocci in neutrophil; 95% specific/sensitive in men, 50-70% in women
- Culture: Men - urethral exudate; women - cervical/anal swabs
- Must specify gonorrhea
- Direct detection via nucleic amplification
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Gonorrhoeae: Treatment
- Third generation cephalosporins - ceftriaxone
- Prevention: safe sex
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