CNS infection Flashcards
Symptoms of Meningitis
headache
stiff neck
fever
photophobia
Symptoms of meningitis in peds
fever - cold hands & feet refusing food/vomiting pale blotchy skin blank staring stiff neck
Neisseria meningitidis
- Gram (), shape, where do you find it?
- what organism fo you find it on?
- Encapsulated?
- How many serotypes?
- Oxidase? Catalase?
- What does it ferment?
- What is growth inhibited by?
- Gram negative diplococci, facultative intracellular
- human-restricted
- encapsulated (nonencapsulated strains are nonpathogenic)
- 13 serotypes
- oxidase-positive, catalase positive
- ferments glucose and maltose, not sucrose or lactose
- growth inhibited by trace metals and fatty acids: chocolate agar, not blood agar
How is N. medingitidis transmitted?
Where does it colonize?
How do most infections present?
Airborn droplets
colonizes the nasopharynx (only reservoir) -> asymptomatic carrier, common in prisons, dorms, military, family of index case
Most infections resolve without symptoms: IgG-enhanced complement and neutrophils defend, leave lifelong immunity to infecting strain
Many individuals have some natural immunity by age 20; immune mothers passively immunize newborns
N. meningitidis pathogenesis
What happens if it enters the bloodstream?
Meningococcemia - colonizes favorite sites - joints (septic arthritis), meninges (meningitis, fatal if untreated, with treatment, may kill or leave damage)
May cause epidemics of meningitis
Most common cause in 2-18 yr age range
Together with Strep pneumoniae, causes >80% postinfant bacterial meningitis
N. meningitidis virulence factors
IgA protease: cleaves IgA, reduces defense of mucus membrane
Polysaccharide capsule (resists phagocytosis)
Endotoxin LOS (component of Gram (-) cell wall, causes fever, shock) - LOS is lower molecular weight
Is there a vaccine for N. meningitidis?
Ab to capsule is protective -> vaccine
deficiency inlate-acting complement components (c5-C9) is predisposing for complications
N. meningitidis diagnosis
1/3 cases adult, 2/3 pediatric
septic arthritis: joint pain-draw joint fluid
meningitis: Adults = classic fever, headache, stiff neck, progression to coma
young children: irritability, convulsions, lassitude, fever, abdominal discomfort, vomiting
BOTH DRAW CSF and ADMIT
Meningococcemia
Fever and hourly-spreding petechial skin rash (may be hard to see on dark skin) - draw blood and CSF, admit to ICU
Rarely may be present for weeks before symptoms become alarming (“chronic’)
5-15% develops 50% fatal Waterhouse-Friderichen syndrome: High fever, shock, widespread purpura, disseminated intravascular coagulation (DIC), thrombocytopenia, destruction of adrenal glands
N. meningitidis lab:
septic arthritis:
Meningitis:
Meningococcemia:
septic arthritis: joint fluid: gram stain and culture on chocolate agar
meningitis: CSF: increased PMNs, gram stain ( 50% sensitive) and culture on chocolate agar, Gram (-) cocci in CSF smear suffice for diagnosis, alternatively, latex agglutination test for capsule polysaccharide in CSF
Meningococcemia: Blood: gram stain and culture on chocolate agar. set of tests for DIC
N. meningitidis diagnosis: Lab
PCR testing gives simultaneous rapid results for many patients and sample types
PCR test targets meingitidis-specific DNA insertion sequence in blood buffy coat samples: no lumbar puncture.
differentiating N. meningitidis from N. gonnorrhoeae: only meningococci ferment maltose
How to treat N. meningitidis
Penicillin G unless allergic, or local history of drug resistance
Alternates: Ceftriaxone, cefotaxime, and cefuroxime; if severely allergic to penicillin, chloramphenicol
Fulminant meningococcemia: admit to ICU, support circulation and renal function
Prescribing glucocorticosteroids for the rash and arthritis bad, even though they are recommended for other types of meningitis
How to prevent N. meningitidis
Close contacts of index case get prophylactic rifampin, ceftriaxone, or ciprofloxacin (excreted efficiently into saliva)
Vaccines recommended for travels (Mecca outbreaks), college/boarding school students, 11-12 yrs (not suitable for < 2 yrs)
GBS: Bacteriology
gram (), shape, encapsulated?
Beta hemolytic?
Two virulence factors
S. agalactiae
encapsulated gram(+) cocci
beta hemolytic
polysaccharide toxin virulence factor
Pilus-like attachment virulence factor
serotype-specific antibody-mediated immunity
Normal vaginal flora transmits to neonate shortly before and during delivery
may also be normal flora in GI and upper respiratory tract
GBS risk group 1 pathogenesis
neonates of GBS+ mothers develop invasive disease
Most common cause of neonatal sepsis
Usually serotype 3 (of 10)
2 types: early disease pneumonia w/bacteremia presents with 1-7d postpartum prevented by intrapartum IV antibiotics
Late disease
bacteremia with meningitis
presents 1/12wk postpartum
GBS risk group 2 of 2
geriatric with predispositions
diabetes, malignancy, congestive heart failure
rare infections seem to be becoming more common; probably both improved reporting and older population, more diabetic and more immunosuppressed
GBS exam
Patient presents with pain, fever, other symptoms specific to site:
meningitis: spinal tap for gram(+) cocci in pairs or short chains
Cellulitis, abscess: gram stain and culture of appropriate sample (tissue biopsy, aspirate)
CT/MRI for deep abscesses
Echocardiogram for endocarditis
CAMP test: CAMP factor secreted by group B strep (and listeria) enhances activity of beta hemolysin form S. aureus
Hippurase/Hippurate test: Colorimetric test for hippurase, produced by GBS, Gardnerella vaginalis, Campylobacter jejuni, Listeria monocytogenes
GBS: Treatment
IV Penicillin or amoxicillin
If allergic, vancomycin
Surgical intervention may be needed: Heart valve replacement for endocarditis, abscess removal for cellulitis, amputation for diabetic foot
Pneumococcus Species Gram (), catalase?, where is it foun? Morphology? Capsule?
Strep pneumoniae
Gram (+), catalase (-), faculative anaerobe
In culture, form diplococci in chains
Pathogenic strains are encapsulated
Most common cause of community-acquired pneumonia, bacterial meningitis, bacteremia, and otitis media, as well as an important cause of sinusitis, septic arthritis, osteomyelitis, peritonitis, and endocarditis
A major childhood pathogen worldwide with deaths from pneumonia and meningitis
Pneumococcus pathogenesis
Ealisy colonizes upper respiratory tract using adhesion virulence factors (20-50% carrier rates in pop.)
infections peak in Fall and Winter when carriers congregate more closely
in healthy adults and older children, contained by innate immunity
in young children, or in patients with pre-existing asthma, allergies, bronchitis, smoking, COPD, bacteria can spread
Two types of pneumococcal disease
- Direct extension: sinuses, eustachian tubes, bronchi
- Hematogenous spread: blood, joint fluid, peritoneum, CSF
Capsule protects bacterium against phagocytosis and classic complement unless anti-capsule IgG is already present (protective)
Pathogenic strains all produce pneumolysin, some also produce hemolysin, neuraminidage, hyaluronidase, but exact contribution of these exotoxins to pathogenesis is unclear
infection raises a strong inflammatory response, which underlies most of the clinical disease symptoms
Pneumococcus exam
Diseases of direct extension (Non-invasive disease):
Sinusitis, otitis media, bronchitis, pneumonia
PNEUMONIA ->
pneumonia causes significant morbidity and mortality (10-20%)
patient looks ill, anxious
predispositions: asthma, COPD, chronic bronchitis, smoking or frequent exposure to cigarette smoke
stethoscope: can hear rales in most patients, dullness to percussion in half
radiology findings:
adolescents and adults: lobar consolidation
infants and young children: scattered parenchymal consolidation, bronchopneumonia
Pneumococcus: Exam
Diseases of hematogenous spread (invasive disease): Meningitis, septic arthritis, pericarditis, endocarditia, osteomyelitis
bimodal distribution: patients younger than 5 or older than 65
Anyone who is immunosuppressed
meningitis develops over hours or days, neurologic signs often prominent, admit for antibiotic and MRI
- mental status changes
- lethargy
- delitium
- brudzinski(+)
- cranial nerve palsies
- focal neurologic defects
Pneumococcus: Lab
Non-invasive disease
Invasive disease
Non-invasive: can usually be treated based on exam, optional gram stain
invasive disease: gram stain and culture of appropriate samples (blood, sputum, CSF, abscess aspirates or biopsies). Blood cultures usually positive.
- begin antibiotic-sensitivity testing
- urine-antigen testing is available, useful for pneumonia in young children who don’t produce enough sputum for testing
Meningitis spinal tap findings are typical of bacterial meningitis
- elevated opening pressure
- elevated WBC count and neutrophil level
- decreased glucose
- highly elevated lactic acid
- gram stain and culture are positive unless antibiotic treatment began >4hr b4 tap
Pneumococcus treatment
noninvasive disease
anything less than severe pneumonia: proceed with treatment using antibiotics that include S. pneumoniae among other probable causes: amoxicillin or cephalosporin for everyone, fluoroquinolones or doxycycline for adults-only, outpatient
severe pneumonia: admit, vancomycin becomes another antibiotic option
Pneumococcus treatment for invasive disease
admit patient, take samples, start antibiotics, start cultures, perform antibiotic susceptibility testing on cultures
initial antibiotics are vancomyvin plus ceftriazone and cefotaxime
if isolate testing comes back resistant, add rifampin, meropenem, or chloramphenicol
steroids may be used with caution in addition to antibiotics, early in the antibiotic course
cellulitis and septic arthritis may require surgical care in addition to antibiotics
Pneumococcal antibiotic resistance
conferred by mutations changing the bacterial cell wall sites to which the antibiotics bind such that binding affinity is lowered
consequently, an increase in dosage can sometimes overcome resistance for this pathogen. “MIC” (minimum inhibitory concentration) describes the dosage necessary to kill the patient’s isolate
The resistance is carried on a transposon that includes resistance genes for multiple antibiotics, so if there is resistance to any, there is resistance to many
Pneumococcus prevention
Prevnar7 vaccine raises protective IgG against the capsules of the seven serotypes that most commonly caused invasive disease prior to 2000.
Universal childhood vaccination with Prevnar7 starting in 2000 knocked down levels of invasive disease 90%
childhood cases of invasive disease caused by those serotypes essentially disappeared (more effective than anyone expected)
Rates of carriage of those serotypes dropped as herd immunity was achieved
rates of disease caused by other serotypes of pneumococcus increased (‘replacement disease”)
prevnar13 vaccine, providing coverage for the original seven plus 6 of the newly-problematic serotypes, is now available
may be used for childhood vaccination series
may be given as a booster to those who received the prevnar 7 series
