non-motile

fastidious

oxidase+ (produces acid from maltose & glucose)

colonizes: nasopharynx/pharynx

endemic disease worldwide esp cold/dry mo

transmission: respiratory droplets in prolonged close contact 

prevalence: highest in school-aged children

*outer membrane components:

1. capsule-antiphag; incr survival in blood/CSF

2. outer mem proteins: two major OMPs, PorA & PorB (=> hydrophilic pores, stim endocytosis & inflammation)

3. Lipooligosaccharide: antigenic variability

4. Pili (fimbriae): antigenic variability; adherence

5. more proteases

[LOS = N. meningitidis endotoxin]

No repeating O-antigen subunits of sugars

lipid A (type of LOS) interaction w/ TLR4 & MD2 (mem prot; these both present on monocytes, macroph, dendritic cells, & other phagocytes)

*LOS circulating =morbidity/mortality

life-threatening: 1. acute bacterial meningitis 

2. meningococcemia

not: 1. pneumonia (usually preceded w/ URT infection; symptoms: cough, chest px, fever/chills, pharyngitis perhaps)

2. arthritis

3. urethritis

meningococcemia 

pt may also have meningitis

*prominent hemorrhagic skin lesions

LOS loosely attached to outer mem (released into circulation; stim monocytes/dendritic cells/endothel cells => release cytokines)

[N. meningitidis invade vasc endothel & prod procoagulants]

once N. meningitidis produces procoagulants (this is the cause of skin lesions)

activate factor XII

characteristics: small petechial sking lesions (trunk & LE) may coalesce => lg hemorr lesions

may => Waterhouse-Friderichsen Syndrome

hemorrhagic adrenalitis (=> massive hemorrhage in 1 or both adrenals)

most common bacterial agent: N. meningitidis

characterized by: overwhelming bact infec, low BP, shock, DIC, widespread purpura, rapidly develop adrenocortical insufficiency

N. meningitidis meningitis

#1 cause of bacterial meningitis in children <5 yoa in US (before 1995, was H. influenzae)

untx: 100% fatality 

w/ antibiotic tx: 10%

onset: abrupt, typical meningeal signs

frequently seen in: children; complement deficiencies

severe headache

stiff neck

bright-light phobia

fever/vomiting

drowsy/less responsive

rash (anywhere)

gram stain: gram- w/ coffee-bean shape

culture: growth on chocolate agar

oxidase test+ (dark blue/purple color change)

carbohydrate utilization test: maltose AND glucose positive

1. transferrin binding protein (Fe acquisition)

2. lactoferrin binding protein (")

3. Hb Binding protein (")

also, pilin: antigenic variation (prior exposure cannot protect against different bacterium)

men: urethra

women: uterine cervix (higher risk of infection after single exposure; carriage may be asymptomatic)

local spread: 

male-gonococcal urethritis

female-cervicitis

disseminated forms:

skin lesions

endocarditis

arthritis

opthalmia neonatorum

2-6d after exposure

dysuria

itching

purulent discharge

testicular px

(95% acute)

frequently asymptomatic

cervical discharge (seen on swab test; normal/negative=white & positive=yellow)

lower abdominal px

cervical-vaginal tenderness

dysuria

pelvic inflammatory disease

early symptoms: dyspareunia & abdominal px

transmission: sexual contact

1. salpingitis

2. endometritis

caused by the close proximity of these structures to each other (propelled by menstruation)

neisseria gonorrhoeae

mother-->child (delivery)

symptoms: lid edema, redness, purulent discharge, swelling, px

gram stain: lots of bacteria & inflamm cells

may lead to blindness (rapid progression; severe ulcerative keratitis & perforation)

types of disseminated gonococcal infection (DGI)

occur when N. gonorrhoeae infections are left untreated

1. gonococcal skin papules

2. septic arthritis (joint is NOT infected, just an immune response) vs poly arthritis (joint not infected, host response) vs mono arthritis (organism in blood eventually gets into 1 joint-this joint is infected)

*N. gonorrhoeae is the #1 cause in 16-45 yoa (staphylococcus aureus is #2 in this case, #1 in all other age groups for septic arthritis)

1. gram stain (+ for PMN & gram- intracellular diplococci)

2. culture on thayer martin agar (+ w/ growth)

=> N. gonorrhoeae

urethritis: more PMNs w/ diplococci in 1st sample

cystitis: same # PMNs in both samples

gram-

aerobic 

oxidase+

diplococcus

normal flora of URT (esp in children)

virulence not known (possibly LPS); some w/ pili/fimbriae (attachment to epithelium)

URT infections (otitis media/sinusitis): children

[3rd most common cause behind S. pneumoniae & non-typable Haemophilus influenzae]

LRT: adults

gram-

diplococcus

chocolate/blood agar culture: opaque & non-hemolytic

fermentation tests: does NOT use sucrose, glucose, maltose, or lactose

non-motile

not pigmented

no fermentation

gram-

non-fastidious

only gram- organism part of normal skin flora (skin & distal urethra of healthy people)

emerging nosocomial pathogen

*commonly isolated from wounded US troops in Iraq

1. capsule (antiphagocytic)

2. LPS

3. bacteriocins

4. no known cytotoxins

5. resistance to antibiotics

(produces biofilms)

pneumonia (assoc w/ ventilator use)

bacteremia/septic shock

meningitis (usually after neurosurgery)

log phase: bacilli

stationary phase: coccobacilli

colonies (non-pigmented) may be mucoid (from capsule)

*oxidase- (as opposed to both Neisseria & Moraxella, which are oxidase+)

superoxal test

similar to catalase test except 30%, not 3% H202 is used

N. gonorrhoeae: rapid/strong bubbles=positive

(other Neisseria: no/weak bubbling)