Nisseria Meningitidis, Gonorrhea Flashcards
what are two pathogenic species of genus Nisseria?
N. meningitidis (meningococcus)
N. gonorrhoeae (gonococcus)
-
Nisseria
- bacteriology
- Biochemistry
- which was has a capsule
- what agar are they grown on?
THE ONLY gram negative cocci (diplococci)
Aerobic
Oxidase Positive
Meningococcus – glucose and maltose fermenting
Gonorrhea – glucose fermenting
Meningococcus - has capsule
Thayer Martin Agar (can also grow on chocolate agar, but this is not selective)
N. meningitidis (meningococcus)
epidemiology
how is it transmitted
Risk factors:
10% of the population are asymptomatic carriers (oropharynx)
Transmitted by close contact aerosols (eg partners)
Can be rapidly progressive and fatal
More frequently in children (most common cause of UK children)
Crowded living conditions
Immune defeciciency (complement def)
Respiratory viral infection
genetic factors (IL-1B genotype associated with more severity)
N. meningitidis (meningococcus)
- what serious diseases can manifest?
- what are the less serious manifestations
Meningitis – High mortality (HA, fever, vom, neck stiff, photophobia)
Meningococcemia - can occur with Meningitis; 25% mortatlity;
Endotoxic shock
Petichial rash (but not sensitive);
DIC can occur leading to grangrene lesions requiring amputation
Less Serious:
Chronic meningococemia – arthritis/dermatitis
Pneumonia
Urethritis
Pathogenesis of Meningococcus
Adherence to non ciliallted epithelial cells;Transcytosis of epithelial tissue
Bacteremia – (polysaccharide capsule allows for survival)
Acquire Iron from host
Induce shock in the host: cytokine storm; factor H sequestration
Can cross the BBB and multiple in the subarachnoid space
Virulence factors of Meningococcus
- what serotypes are most present in developed countries
- what is unique about Serotype B?
Serotypes B and C
Serotype B - capsule with polysialic acid
Type IV bundle forming Pilus (like EPEC) – binds to CD46
Lipo-oligo-saccharide – endotoxin
Complement factor H binding protein (has CHO that mimick Factor H binding site, uses Factor H to protect it from complement)
Diagnosis of Meningococcus
Need a Rapid Diagnosis
gram stain of CSF, see gram - diplococci with WBCs -> think meningococcal meningitis
Begin treatment immediately
Then do actual cultures
Treatment of Meningococcus
Ceftriaxone
prophylaxis of contacts with Rifampin
Vaccines for meningococcus
- why is there no vaccine for serotype B?
Menomune – capsule poly saccharide antigen (short term immunity; not good in children under 2)
Menactra – Conjugate vaccine – capsule + diphtheria toxoid
serotype B – no vaccine yet bc its capsule is coated with polysialic acid
sialic acid is a normal host cell component
Kingella -- bacteriology where does it colonize What growth culture is used? what can it cause? how is it treated ?
GN aerobic Coccobacilli in nisseria family
Colonizes child oropharnyx
Blood culture vials
Infectious arthritis & rare cause of endocarditis
Tx: Ampicillin or Ceftriaxone
Neisseria gonorrhoeae (gonococcal)
Bacteriology
Epi
Gram negative diplococci
Lots of asymptomatic carriers
second most commonly reported bacterial infection in the US
Neisseria gonorrhoeae (gonococcal)
- what diseases can it cause ?
males vs females vs newborns
Gonorrhea:
Males – urethriits (always symptomatic, purulent d/c; dysuria —- epididymitis, prostatitis)
Females: cervix is primary infection site; Vag d/c, abd pain; dysuria
—>alpingitis, ovarian abscess, PID and ectopic pregnancy
Newborns: conjunctivitis transmitted from mom
also - less bacteremia; arthritis
Pathogenic mechanisms of neisseria gonorrhoeae –
Colonization of the genital mucosa
ahdernece to non ciliated cells and transcytosis from there
can survive in neutrophils
Virulence factors of Neisseria gonorrhoeae
The Pili:
- PilE – the major subunit
- PilC — the adherent tip
- POR – outer membrane protein
- Opa – adherence factor; lymphocyte suppression
LOS: binds to specific receptor (asialogylcoprotein) of sperm and urethral epithelium
- IRON acquisition: transferrin binding proteins
Mechanisms of protection from immune response by N. gonorrhoeae
- repeat infections are common -
- infections persist for months in the untreated
- poor antibody response
- antigenic variation of the Pili proteins (PilE and PilS)
- Phase variation of the Opa (slipped strand – in vs out of frame)
- LOS Sialylation coating the pathogen – we won’t make antibodies to this
- Blocking antibodies: RMP (protein III) – stable antigen, but the antibodies produced to this antigen will inhibit complement and prevents action of the bactericidal Abs against Por
