NEISSERIA Flashcards
What’s neisseria?
- it’s the only genus of gm - cocci that frequently cause disease
- usually diplococci –> 2 round bacteria
- N. gonorrhoeae (gonorrhea)
- N. meningitidis (bacterial meningitis and septicemia)
- non-motile (twitching motility from pili)
- attach to things via pili
- aerobic (but can grow anaerobically)
- grow best in on media supplemented with blood in presence of CO2
- obligate human pathogens
- don’t survive long outside host
- humans are only reservoirs -> need human to human transmission
What are the 2 major neisseria species?
N. meningitidis (meningococcus)
N. gonorrhoeae (gonococcus)
What’s N. meningitidis (meningococcus)?
- it’s found in the throat - the human nasopharynx is the only reservoir for N. meningitidis
- it colonizes the nasopharynx with no local symptoms (asymptomatic)
-it’s spread by airborne droplets. virus respiratory infections (e.g.influenza) may enhance the spread
-It’s virulence factors are it’s: - large capsule - heavily encapsulated (polysaccharide)
*outer membrane blebs which are profuse on N. meningitidis cell surface
~LPS endotoxin - produces hemolysin
- pili
- it colonizes the nasopharynx with no local symptoms (asymptomatic)
- it causes septicemia, meningitis, purpura fulminans
-it causes infection in the upper respiratory and meninges and ranges from transient bacteremia that are relatively benign to overwhelming infections that are rapidly fatal
What’s N. gonorrhoeae (gonococcus)?
-it lives in mucosal epithelial of male urethra or female cervix (distal urethra in both sexes)
-asympotmatic carriers greater among women
- these multiply rapidly and is spread via contact with genital secretions (shed in here) and to child during vaginal labor (conjunctivitis)
-its’s virulence factors are:
* don’t have flagella and aren’t motile (can’t move themselves around d)
* no capsule
* pili and strong adhesins
* LPS endotoxin
*IgA1 protease
~ extra cellular protease cleaves IgA1 (a major Ab)
- this protease removes Fc receptor (heavy chain portion) from the end of the Ab and this helps this bacteria to space from phagocytosis
** this protease is also produced by Haemophilus and streptococci
* phase/antigenic variation
-it causes disseminated gonococcal infection (DGI), pelvic inflammatory disease (PID), urethritis/cervitis/epididymitis
-it’s infection sit is in the genitals and the bacteria is localized inflammation, bacteremia that is rarely lethal (even when spread to bloodstream) but can become serious if disseminated.
What are the 3 general diseases of meningococci?
1) uncomplicated bacteremic process
2) metastatic infection of the meninges
3) overwhelming systemic infection - circulatory collapse and disseminated intravascular coagulation (DIC)
- individuals may lack IgA antibodies (that helps defend against this) that have specificity for the capsule polysaccharide
- higher known bacterial titers in blood
What happens when gonococci is introduced to the body?
-upon introduction, they attach to columnar epithelia or cervix or urethra
* via pili and surface protein to adhere because these aren’t capsulated
* adhesins are controlled by:
~ phase variation - presence/absence
~ antigenic variation - composition
**gonorrhea most present in ppl in their twenties
How do gonococci spread and multiple?
-attachement ot non-ciliated cells
* human Fallopian tubes and columnar epithelial cells have ciliated and non-ciliated cells
~ non-ciliated cells have microvilli
-ciliary stasis
* ciliated cell motility slows and ceases
-death of ciliated cells
* slough from epithelial surface
* can be elicited by LPS and peptidoglycan
-exocytosis
* vacuoles discharge bacteria into subepithelial connective tissue
-doens’t secrete exotoxins
-LPS (LOS - lipooligosaccharide and other cell wall components cause cell damage
* induce tumor necrosis factor-alpha (TNF - alpha)
~ sloughing of ciliated cells
~ non - ciliated cell lysis - release of factors that cause inflammation
What’s pelvic inflammatory disease (PID)
-gonococcal infection of female upper reproductive tract
* inflammation of uterus and fallopian tubes
* scarring of upper tract and adjacent orgfans
~ infertility
~ ectopic pregnancy - development of embryo in Fallopian tube rather than uterus
~ chronic pelvic pain
-epididymitis
* ascent of organism into upper reproductive tract of men
What is disseminated gonococcal infections?
- disseminated gonococcal infections (DGI)
- can result from pelvic inflammatory disease (PID) due to endotoxin
- pustular lesions of skin
- inflammation of tendons and joints
- suppurative arthritis
- more common in women
How do you encounter meningococci and how does it enter you?
- found in human nasopharynx - primarily reservoir for N. meningitidis, has also been found in dental plaque
- attach to nasopharyngeal epithelial cells and invade mucous membranes
- asymptomatic carriage induces humoral antibody response
- most individuals acquire immunity at age 20
- invasion of the blood stream only occurs in individuals deficient in complement (C5-C8)
- once in blood stream, travel through body
- type IV pili - attach organism to meninges in CNS
- lipoologosaccharide (LOS) damage to host tissue
- elicits host inflammatory response, resulting in hemorrhaging of blood into skin and mucous membranes (purpuric rash)
How does meningococcus survive in blood?
-serum antibodies recognitions
* target: LPS (LOS), protein I of the outer membrane (OM) and other surface proteins
* N. meningitidis divided into serogroups A, B, C, W135, X, Y, and Z depending on group-specific capsular polysaccharide antigens
-evasion
* strains alter LPS with host-derived N -acetylneuramic acid (sialic acid)
~ surface component of red blood cells (Camouflage)
* LOS is similar to antigens on human erythrocytes and may allow ‘self’ recognition
What are purpura fulminans in meningococcus?
- disseminated intravascular coagulation (DIC) due to ability to survive in bloodstream
- skin manifestations
- meningitis
- shock
- death
- response to LOS mediated by TNF-alpha and IL-1
- the higher the response, the greater the damage and risk of death
What is the treatment for neisseria ?
- most neisseria sp. are penicillin resistnat
- plasmid encoded b-lactamase first identified in 1976
- resistance to tetracycline was first described in 1986
- now reported in most parts of the world
- streptococcal derived
- resistance to other antibiotics is increasing
- antimicrobial chemoprophylaxis of close contacts is the primary means of preventing secondary cases of sporadic meningococcal disease.
How do you prevent neisseria?
-vaccine to meningococci
*quadrivalent (MPSV4) - derived abasing capsular polysaccharide from 4 serotypes (A,C,Y, and W135)
* tetravalent (MCV4) - polysaccharide-protein conjugate
~children <2 yrs don’t respond to polysaccharide vaccines
-vaccines to gonococci difficult to produce
* antigenic and phase variation
* protective intracellular components
-behavioral (gonococcal)
*condom use
* partner notification
* early diagnosis and treatment
What’s the phase variation in N. gonorrhoeae?
-slipped strand mispairing
* colony opacity-associated (Opa) genes (10+)
* encode outer membrane proteins
* opa’s presence results in neutrophils uptake
~ some gonococci lack Opa and avoid phagocytosis
* also controls other surface proteins, as well as LPS in gonococci and meningococci
