Microbiology - bacterial meningitis Flashcards
Classic symptoms of meningitis
Fever Headache Stiff neck (nuchal rigidity) Photophobia
Symptoms of pediatric meningitis
Fever w/ cold hands and feet Refusing food or vomiting Fretful - dislike being handled Pale blotchy skin Blank staring affect Drowsy Stiff neck high pitched crying
Describe bacteriology Neisseria meningitidis: Gram stain (+/-) Morphology (rod / cocci) intracellular or extracellular Metabolism (aerobe, anaerobe, facultative) Encapsulated or unencapsulated Oxidase/Catylase reactions Fermentation (glucose/maltose/sucrose/lactose) Growth/agar type
Gram negative diplococci facultative intracellular Encapsulated strains are pathogenic (nonencapsulated strains are nonpathogenic) Oxidase-positive, catalyse positive Ferments glucose and maltose, not sucrose or lactose Growth inhibited by trace metals and fatty acids: grows on chocolate agar not blood agar Grows on Thayer-Martin medium
Transmission of Neisseria meningitidis:
airborne droplets
Reseviour/colonization for Neisseria meningitidis:
Colonizes nasopharynx (only resevior) - carriers are asymtomatic
What enhances Neisseria meningitidis spread and colonization?
concomitant upper respiratory viral infections
T/F Infection of Neisseria meningitidis often resolves w/o symptoms
true
What is immune mechanism against Neisseria meningitidis?
IgG-enhanced complement and neutrophils Defeat of infection leaves lifelong immunity to infecting strain
Can immunity be passed from mother to child?
Yes By 20 many have natural immunity; immune mothers passively immunize newborns
What is it called if Neisseria meningitidis enters bloodstream?
meningococcemia / meningococcal septicaemia
If Neisseria meningitidis enters bloodstream where does it go? What pathology is caused by colonization of those sites?
Joints: septic arthritis Meninges: meningitis, fatal if untreated, still may kill (
What is most common microorganism that causes meningitis in 2-18yr age range?
Neisseria meningitidis
Major virulence factors of Neisseria meningitidis:
IgA Protease: cleaves IgA, reduces defense of mucus membrane Polysaccharide capsule (resists phagocytosis) Endotoxin LOS (component of Gram(-) cell wall, causes fever, shock) *lipooligosaccharide (“LOS”) refers to low-molecular-weight bacterial lipopolysaccharides
What differentiates N. meningitidis vs N. gonorrhoeae What are 3 similarities?
Unlike N. gonorrhoeae, N. meningitidis has capsule as a virulence factor and can be part of normal flora as non-virulent strain. Only Meningococci ferment Maltose (meningitidis begins with M) Both: grow in Thayer-Martin medium have IgA protease as a virulence factor cause septic arthritis as a complication
What is an associated pathology of N. meningitidis infection?
5-15% develop 50%-fatal Waterhouse-Friderichsen syndrome: massive, usually bilateral, hemorrhage into the adrenal glands caused by fulminant meningococcemia Associated with high fever, shock, widespread purpura, results in adrenal insufficiency, and disseminated intravascular coagulation
Which virulance factor of N. meningitidis is responsible for septic shock and hemmorage?
LOS endotoxin - results in destruction of RBCs
Does a vaccine exist for N. meningitidis?
yes - Ab to capsule is protective
What predisposes infection with N. meningitidis?
Deficiency in late-acting complement C5-C9 Immuno-supressed state
Mechanism of bacterial destruction from late-acting complement cascade C5-C9
formation of membrane-attack complex pore
What are common clinical features of meningococcemia / meningococcal septicaemia
Fever joint pain petechial skin rash (spreads from trunk outward)
Clinical course of meningococcemia / meningococcal septicaemia
usually progresses rapidly (hourly spreading once invades bloodstream) occasionally progresses over several weeks as chronic infection
What is latex agglutination test ?
detects capsule polysaccharide in CSF
What are CSF features from meningitis caused by N. meningitidis
increased polymorphonuclear neutrophils
Treatment of choice for meningitis caused by meningiococcal meningitis?
Penicillin G Ceftriaxone, cefotaxime, and cefuroxime; if severely allergic to penicillin, chloramphenicol
T/F glucocorticoids are helpful for treatment of cerebral edema caused by meningiococcal meningitis
FALSE! glucocorticoids highly contraindicated!!
What is the vaccine for N. meningitidis?
Unconjugated = Menomune Conjugated = Menactra, may be more active in children, new
What populations are most susceptible to infection?
common in prisons, dorms, military, family of index case College students Convicts Travelers to the Middle East
Describe bacteriology of Group B strep (S. agalactiae):
Encapsulated Gram(+) cocci Beta-hemolytic
What are the virulance factors of
Polysaccharide toxin Pilus-like attachment
Where is reservoir for Group B strep?
Normal vaginal flora (15-45%) May also be normal flora in GI and upper respiratory tract
When do infants contract group B strep? What is transmission route?
transmits to neonate shortly before and during delivery Route: ascends from vagina/cervix to amniotic fluid, baby inhales bacteria > makes its way to blood stream
What is the most common cause of neonate sepsis?
group B strep infection
Which group B strep serotype is typically responsible for neonate sepsis?
Serotype 3
What is the clinical course of neonate sepsis?
Early disease Pneumonia w/ bacteremia Presents 1-7d postpartum Prevented by intrapartum IV antibiotics Late disease Bacteremia w/ meningitis Presents 1-12wk postpartum
Two highest risk groups for septicemia from group B strep? What are predisposing factors?
neonates and geriatric populations especially w/ Predispositions: Diabetes Malignancy Congestive heart failure *rare infections in geriatric cases but becoming more common; probably both improved reporting and also population becoming older, more diabetic, more immunosuppressed
Common sites of colonization for group B strep and associated pathology:
Meninges: meningitis - spinal tap for Gram(+) cocci in pairs or short chains Under skin or in deep tissue: Cellulitis, abscess: Gram stain and culture of appropriate sample (tissue biopsy, aspirate) Edocardium: endocarditis CT/MRI for deep abscesses Echocardiogram for endocarditis
What is alpha vs beta vs gamma hemolytic? Examples of each?
Refers to hemolytic activity of bacteria when colonized on blood agar alpha - partial hemolysis - agar under the colony is dark and greenish (Strep pneumoniae, Strep viridans) beta - complete hemolysis - area around colony appears lightened (yellow) and transparent (Streptococcus pyogenes, Listeria monocytogenes, Clostridium perfringens) gamma - non-hemolytic (Enterococcus faecalis - aka group D strep)
Lab tests for group B strep
CAMP test Hippurase test Hemolysis test - CAMP factor secreted by B-group strep (and Listeria) enhances activity of β-hemolysin from S. aureus – shows enhanced hemolysis Colorimetric test for hippurase, produced by GBS, Gardnerella vaginalis, Campylobacter jejuni, Listeria monocytogenes
What other bacteria (besides group B strep) would show up as CAMP test positive and hippurase test positive? How could you differentiate from group B strep?
Listeria monocytogenes Morphology on gram stain and motility on wet mount NOT from color on gram stain (both gram +)
Preferred treatment for group B strep?
IV Penicillin or amoxicillin
Secondary treatment for group B strep if allergic to IV Penicillin or amoxicillin?
vancomycin
Describe the bacteriology of Strep pneumoniae (
Gram(+), catalase(-), alpha-hemolytic facultative anaerobe In culture, form diplococci in chains Pathogenic strains are encapsulated
What differentiates strep pneumoniae and group B strep?
Morphology: diplococci in chains (strep pneumoniae) vs cocci in pairs or short chains (group B strep)
what is the most common cause of community-acquired pneumonia, bacterial meningitis, bacteremia, and otitis media?
Strep pneumoniae
Also an important cause of sinusitis, septic arthritis, osteomyelitis, peritonitis, and endocarditis
Who are the most susceptible populations to experiance spread of strep pneumonia ?
young children, or patients with pre-existing asthma, allergies, bronchitis, smoking, COPD, or HIV
Where is reservior for Strep pneumoniae?
Is it normal flora?
colonizes upper respiratory tract
Yes - (20-50%) carried in healthy individuals and contained by innate immunity
What are the virulance factors for Strep pneumoniae?
Major virulence factor is capsule - protects bacterium against phagyctosis and classic complement unless anti-capsule IgG is already present (protective)
IgA protease, teichoic acid
strong inflammatory response underlies most of the clinical disease symptoms
What are the 2 types of Pneumococcal disease and which regions are affected?
1.Direct extension: sinuses, eustachian tubes, bronchi
2.Hematogenous spread: blood, joint fluid, peritoneum, CSF
What is a common enzyme expressed by pathogenic strains of Strep pneumoniae?
pneumolysin
Halmark clinical signs of direct extension type of pneumococcal disease:
sinusitis, otitis media, bronchitis, pneumonia
Patient looks ill, anxious
rales in most patients, dullness to percussion in half
on xray:
lobar consolidation in adolescents and adults
scattered consolidation, bronchopneumonia in infants and young children
Most suseptible to Invasive pneumococcal disease:
patients younger than 5 or older than 65
Also anyone immunosuppressed
Clinical course of pneumococcal meningitis:
Develops over hours or days, neurologic signs often prominent, admit for antibiotics and MRI
ØMental status changes
ØLethargy
ØDelirium
ØBrudzinski(+) (knees bend when lift head)
ØCranial nerve palsies
ØFocal neurologic defects
Pneumococcal meningitis CSF findings:
typical of bacterial meningitis
Elevated opening pressure
Elevated WBC count and neutrophil level
Elevated protein
Decreased glucose
Highly elevated lactic acid
Gram stain and culture are positive unless antibiotic treatment began >4hrs prior to tap
Treatment for direct spreading pneumococcal disease
anything less than severe pneumonia:
severe pneumonia:
Direct spreading type:
Less than severe: amoxicillin or cephalosporin for everybody, fluoroquinolones or doxycycline for adults-only
Severe: vancomycin
Treatment for invasive pneumococcal disease:
Antibiotics? Resistance? Steroids?
Invasive type:
Initial antibiotics are vancomycin plus ceftriaxome or cefotaxime
If resistant (based on antibiotic susceptibility testing), add rifampin, meropenem, or chloramphenicol
Steroids - can be used in addition to antibiotics, early in the antibiotic course
Mutations inhibit binding of antibiotics to cell wall but dont block it completely - increase in dosage can sometimes overcome resistance however they’re carried on a transposon that includes resistance genes for multiple antibiotics, so if there’s resistance to any, probably many
Is there a vaccine for invasive pneumococcal disease?
Yes - Prevnar7 - vaccine raises protective IgG against the capsules of the seven serotypes that most commonly caused invasive disease
very effective (knocked down levels of invasive disease caused by THOSE 7 STRAINS by 90%), especially for childhood cases
-other disease causing strains not vaccinated against are causing “replacement disease”
New vaccine Prevnar13 vaccine adds 6 more strains, can be given as a booster
