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MS 2 - Unit 3 > Microbiology - bacterial meningitis > Flashcards

Microbiology - bacterial meningitis Flashcards

1
Q

Classic symptoms of meningitis

A

Fever Headache Stiff neck (nuchal rigidity) Photophobia

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2
Q

Symptoms of pediatric meningitis

A

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

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3
Q

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

A

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

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4
Q

Transmission of Neisseria meningitidis:

A

airborne droplets

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5
Q

Reseviour/colonization for Neisseria meningitidis:

A

Colonizes nasopharynx (only resevior) - carriers are asymtomatic

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6
Q

What enhances Neisseria meningitidis spread and colonization?

A

concomitant upper respiratory viral infections

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7
Q

T/F Infection of Neisseria meningitidis often resolves w/o symptoms

A

true

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8
Q

What is immune mechanism against Neisseria meningitidis?

A

IgG-enhanced complement and neutrophils Defeat of infection leaves lifelong immunity to infecting strain

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9
Q

Can immunity be passed from mother to child?

A

Yes By 20 many have natural immunity; immune mothers passively immunize newborns

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10
Q

What is it called if Neisseria meningitidis enters bloodstream?

A

meningococcemia / meningococcal septicaemia

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11
Q

If Neisseria meningitidis enters bloodstream where does it go? What pathology is caused by colonization of those sites?

A

Joints: septic arthritis Meninges: meningitis, fatal if untreated, still may kill (

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12
Q

What is most common microorganism that causes meningitis in 2-18yr age range?

A

Neisseria meningitidis

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13
Q

Major virulence factors of Neisseria meningitidis:

A

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

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14
Q

What differentiates N. meningitidis vs N. gonorrhoeae What are 3 similarities?

A

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

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15
Q

What is an associated pathology of N. meningitidis infection?

A

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

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16
Q

Which virulance factor of N. meningitidis is responsible for septic shock and hemmorage?

A

LOS endotoxin - results in destruction of RBCs

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17
Q

Does a vaccine exist for N. meningitidis?

A

yes - Ab to capsule is protective

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18
Q

What predisposes infection with N. meningitidis?

A

Deficiency in late-acting complement C5-C9 Immuno-supressed state

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19
Q

Mechanism of bacterial destruction from late-acting complement cascade C5-C9

A

formation of membrane-attack complex pore

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20
Q

What are common clinical features of meningococcemia / meningococcal septicaemia

A

Fever joint pain petechial skin rash (spreads from trunk outward)

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21
Q

Clinical course of meningococcemia / meningococcal septicaemia

A

usually progresses rapidly (hourly spreading once invades bloodstream) occasionally progresses over several weeks as chronic infection

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22
Q

What is latex agglutination test ?

A

detects capsule polysaccharide in CSF

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23
Q

What are CSF features from meningitis caused by N. meningitidis

A

increased polymorphonuclear neutrophils

24
Q

Treatment of choice for meningitis caused by meningiococcal meningitis?

A

Penicillin G Ceftriaxone, cefotaxime, and cefuroxime; if severely allergic to penicillin, chloramphenicol

25
Q

T/F glucocorticoids are helpful for treatment of cerebral edema caused by meningiococcal meningitis

A

FALSE! glucocorticoids highly contraindicated!!

26
Q

What is the vaccine for N. meningitidis?

A

Unconjugated = Menomune Conjugated = Menactra, may be more active in children, new

27
Q

What populations are most susceptible to infection?

A

common in prisons, dorms, military, family of index case College students Convicts Travelers to the Middle East

28
Q

Describe bacteriology of Group B strep (S. agalactiae):

A

Encapsulated Gram(+) cocci Beta-hemolytic

29
Q

What are the virulance factors of

A

Polysaccharide toxin Pilus-like attachment

30
Q

Where is reservoir for Group B strep?

A

Normal vaginal flora (15-45%) May also be normal flora in GI and upper respiratory tract

31
Q

When do infants contract group B strep? What is transmission route?

A

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

32
Q

What is the most common cause of neonate sepsis?

A

group B strep infection

33
Q

Which group B strep serotype is typically responsible for neonate sepsis?

A

Serotype 3

34
Q

What is the clinical course of neonate sepsis?

A

Early disease Pneumonia w/ bacteremia Presents 1-7d postpartum Prevented by intrapartum IV antibiotics Late disease Bacteremia w/ meningitis Presents 1-12wk postpartum

35
Q

Two highest risk groups for septicemia from group B strep? What are predisposing factors?

A

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

36
Q

Common sites of colonization for group B strep and associated pathology:

A

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

37
Q

What is alpha vs beta vs gamma hemolytic? Examples of each?

A

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)

38
Q

Lab tests for group B strep

A

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

39
Q

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?

A

Listeria monocytogenes Morphology on gram stain and motility on wet mount NOT from color on gram stain (both gram +)

40
Q

Preferred treatment for group B strep?

A

IV Penicillin or amoxicillin

41
Q

Secondary treatment for group B strep if allergic to IV Penicillin or amoxicillin?

A

vancomycin

42
Q

Describe the bacteriology of Strep pneumoniae (

A

Gram(+), catalase(-), alpha-hemolytic facultative anaerobe In culture, form diplococci in chains Pathogenic strains are encapsulated

43
Q

What differentiates strep pneumoniae and group B strep?

A

Morphology: diplococci in chains (strep pneumoniae) vs cocci in pairs or short chains (group B strep)

44
Q

what is the most common cause of community-acquired pneumonia, bacterial meningitis, bacteremia, and otitis media?

A

Strep pneumoniae

Also an important cause of sinusitis, septic arthritis, osteomyelitis, peritonitis, and endocarditis

45
Q

Who are the most susceptible populations to experiance spread of strep pneumonia ?

A

young children, or patients with pre-existing asthma, allergies, bronchitis, smoking, COPD, or HIV

46
Q

Where is reservior for Strep pneumoniae?

Is it normal flora?

A

colonizes upper respiratory tract

Yes - (20-50%) carried in healthy individuals and contained by innate immunity

47
Q

What are the virulance factors for Strep pneumoniae?

A

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

48
Q

What are the 2 types of Pneumococcal disease and which regions are affected?

A

1.Direct extension: sinuses, eustachian tubes, bronchi

2.Hematogenous spread: blood, joint fluid, peritoneum, CSF

49
Q

What is a common enzyme expressed by pathogenic strains of Strep pneumoniae?

A

pneumolysin

50
Q

Halmark clinical signs of direct extension type of pneumococcal disease:

A

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

51
Q

Most suseptible to Invasive pneumococcal disease:

A

patients younger than 5 or older than 65

Also anyone immunosuppressed

52
Q

Clinical course of pneumococcal meningitis:

A

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

53
Q

Pneumococcal meningitis CSF findings:

A

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

54
Q

Treatment for direct spreading pneumococcal disease

anything less than severe pneumonia:

severe pneumonia:

A

Direct spreading type:

Less than severe: amoxicillin or cephalosporin for everybody, fluoroquinolones or doxycycline for adults-only

Severe: vancomycin

55
Q

Treatment for invasive pneumococcal disease:

Antibiotics? Resistance? Steroids?

A

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

56
Q

Is there a vaccine for invasive pneumococcal disease?

A

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

MS 2 - Unit 3 (45 decks)

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