Neisseria Flashcards
Neisseria morphology:
Small, Gram-negative diplococci
Name the general virulence factors of Neisseria species:
Outer membrane is composed of LPS complexed with many other antigens/proteins
Type IV pili
Neisseria media:
Chocolate agar that is enhanced with CO2, oxidase, and (glucose and maltose)
Neisseria oxidase test:
Oxidase positive
Name the 2 species of Neisseria that cause human disease:
Neisseria meningitidis
Neisseria gonorrhoeae
Neisseria meningitidis causes ________ and _______.
Neisseria meningitidis causes meningitis and sepsis
Neisseria gonorrhoeae causes the _________ ________ disease gonorrhea.
Neisseria gonorrhoeae causes the sexually transmitted disease gonorrhea.
Describe the 5 steps of Neisseria meningitidis pathogenicity:
- N. meningitidis invades the nasopharyngeal cavity
- The type IV pilus is used to selectively attach to columnar cells of the nasopharynx
- Bacteria multiply and form large aggregates
- Within a few hours, pili undergo post-translational modification in the type IV pilus, which destabilizes some of the aggregates (bacteremia) while others are endocytosed (via capsule)
- LPS and other bacterial products cause systemic inflammation, activation of the complement system, cell damage, sepsis, shock, and death
Describe 3 virulence factors specific to Neisseria meningitidis and their function.
Major VF: Polysaccharide capsule allows it to avoid phagocytosis
Type IV pilus and other adhesins - allows adhesion to mucosal cells (nasopharynx)
LPS and outer membrane proteins - stimulates inflammation
Describe Neisseria gonorrhoeae pathogenicity:
Infection begins when the organism adheres to genitourinary epithelium mediated by pili and other surface proteins
exhibits genetic change by altering the protein structure of pili and by switching production of adhesins on and off, thereby evading the immune response
produces an intense local and acute inflammatory reaction
Describe the 6 virulence factors specific to Neisseria gonorrhoeae and their function.
Outer membrane proteins: PPORTL
Pilin – facilitates bacterial adherence to host cells and antigenic variation
PorB – prevents phagolysozyme fusion
Opa – facilitates phase variation to switch up membrane proteins
Rmp – protects other outer membrane proteins from degradation
Transferrin – obtain iron from host cell for metabolism
LPS / LOS (endotoxin) - causes local inflammatory response and tissue damage
The immune response to Neisseria species requires an intact _______ system.
The immune response to Neisseria species requires an intact complement system.
How does the polysaccharide capsule boost virulence of N. meningitidis?
Capsule is responsible for bloodstream invasion and CNS tropism
Transmission of N. meningitidis:
Respiratory droplet transmission via close contact
The majority of meningococcal disease occurs in ________ and ______ ________.
The majority of meningococcal disease occurs in infants and young children
There are key outbreaks of invasive meningococcal disease among ____.
MSM
There is a secondary peak in meningococcal disease among ________ and ______ ______.
There is a secondary peak in meningococcal disease among adolescents and young adults
Name the 2 possible outcomes of respiratory tract colonization by N. meningitidis:
clinical disease or a transient carrier state
What are the 3 primary most common outcomes of N. meningitidis?
Meningitis
Meningococcemia
Chronic meningococcemia
Meningitis can occur with or without ________.
Meningitis can occur with or without meningococcemia (most without).
Clinical manifestations of Meningitis:
Very rapid onset
Severe, fulminant, acute onset of headache, fever, neck stiffness/rigidity, altered mental status
May occur with seizures and cranial nerve deficits
Clinical manifestations of meningococcemia:
Sepsis that rapidly progresses to septic shock
Petechiae on extremities, especially legs that progresses rapidly to purpuric (violaceous) hemorrhagic bullae
Can see bilateral adrenal hemorrhage (Waterhouse-Freiderichson syndrome) and acute adrenal insufficiency
Hemorrhage and disseminated intravascular coagulation
Clinical manifestations of Chronic meningococcemia:
Relapsing fever, arthritis, and rash that mimics vasculitis
Name the 3 modes of diagnosis for Neisseria meningitidis:
Gram stain: Gram-negative diplococci from CSF sample
Culture on enriched media
Nucleic acid amplification testing (Multiplex PCR)
Name the 3 modes of treatment and prophylaxis for Neisseria meningitidis:
Preferred: ceftriaxone IV
Penicillin G: if bacteria is susceptible
Prophylaxis of close contacts: rifampin, ciprofloxacin, or single dose of ceftriaxone
Who is eligible for vaccination against Neisseria meningitidis (Serogroups A, C, Y W135)?
Adolescents: everyone age 11-12, booster at age 16
Adults with certain risk factors
Who is eligible for vaccination against Neisseria meningitidis (Serogroup B)?
Adolescents: consider age 16-18
Adults with certain risk factors
Describe transmission of N. gonorrhea.
Mucosal transmission via genital tract, mouth, anus, and eye via direct contact
commonly sexually transmitted
True or false: There must be direct contact for transmission of N. gonorrhea.
True
Women have a ______ risk of acquiring gonorrhea infection after exposure when compared to men.
higher
Describe the clinical manifestations of Primary Localized N. gonorrhea Disease.
Manifests as urethritis in men and cervicitis in women
Pharyngitis and proctitis (rare)
Neonatal conjunctivitis
Describe the clinical manifestations of Secondary Disseminated N. gonorrhea Disease.
Gonococcemia (bloodstream invasion) and septic arthritis with characteristic purulent skin lesions
Local dissemination with epididymitis/prostatitis in men
Pelvic inflammatory disease (PID) in women
Dermatitis
Endocarditis and meningitis are very rare
Name the 3 modes of diagnosis for N. gonorrhea :
Gram stain: Gram-negative diplococci from urethra, cervix, or joint fluid
Culture on enriched media
Choice Test: Nucleic acid amplification testing (Multiplex PCR)
Name treatment for N. gonorrhea:
Preferred treatment is Ceftriaxone IM injection
N. gonorrhea has wide-spread resistance to what drugs?
Widespread resistance to quinolones and azithromycin with increasing resistance reported to cephalosporins
