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Block 8 Week 2 > CNS infections- Kozel > Flashcards

CNS infections- Kozel Flashcards

1
Q

What are the 2 focal CNS syndromes?

A
  • brain abscess
  • subdural empyema
  • epidural abscess
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2
Q

What are the routine tests of CSF?

A
  • WBC count w/ diff (norm=0-5)
  • glucose conce (norm=50-80)
  • protein conc (norm=15-50)
  • gram stain
  • bacterial culture
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3
Q

If you have viral meningitis, what will your CSF labs look like?

A

WBC- 50-1000
cell type- mononuclear
glucose >45 mg/dl
protein <200

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4
Q

If you have bacterial meningitis, what will your CSF labs look like?

A

WBC 1000-5000
cell type- neutrophilic
glucose <40
protein 100-500

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5
Q

If you have tuberculous meningitis, what will your CSF labs look like?

A

WBC 50-300
Cell type- mononuclear
glucose <45
protein 50-300

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6
Q

If you have cryptococcal meningitis, what will your CSF labs look like?

A

WBC 20-500
Cell type - mononuclear
glucose 45

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7
Q

What are normal CSF labs like?

A

WBC -> 0-5/mm^2
glucose 50-80
protein 15-50

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8
Q

Why do you get increased WBC count in CSF when you have meningitis?

A

due to inflammation and immune response

-must be adjusted if evidence for blood in CSF

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9
Q

Why do you get decreased glucose in your CSF when you have meningitis?

A
  • increased glycolysis by leukocytes and bacteria
  • increased metabolic rate of brain and spinal cord
  • altered glucose transport b/w blood and CSF
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10
Q

Why do you get increased protein in your CSF when you have meningitis?

A
  • disruption of blood-brain barrier

- must be adjusted if evidence for blood in CSF

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11
Q

What are the contraindications for Lumbar Puncture (LP)?

A
  • Papilledema-increased cranial pressure

- neurological suggestion of intracranial mass

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12
Q

So your patient has a headache, nuchal rigidity, and fever but no altered mental status,,, is it more likely encephalitis or meningitis?

A

meningitis

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13
Q

What is meningitis?

A

inflammation of protective membranes covering brain and spinal cord-meninges

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14
Q

What is acute meningitis?

A

onset of symptoms over hours to several days

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15
Q

What is aseptic meningitis?

A

any meningitis for which a cause is not apparent after routine stains and culture of CSF

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16
Q

What are the symptoms of acute meningitis?

A
  • headache and neck stiffness associated with fever
  • confusion or altered consciousness
  • vomiting
  • inability to tolerate light (photophobia) or loud noises (phonophobia)
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17
Q

What is the initial management of acute meningitis?

A
  • lumbar puncture and CSF analysis
  • empiric antimicrobial therapy based on patients age
  • dexamethasone (corticosteroid) if appropriate
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18
Q

What are the three major causes of VIRAL meningitis and which causes the most cases?

A
  • Enteroviruses (85-95% of all cases)
  • Mumps virus
  • Herpesvirus
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19
Q

What are 5 major causes of bacterial meningitis and what bacter causes the most cases?

A
  • Streptococcus pneumoniae (61% of all cases)
  • H. influenza
  • N. meningitidis
  • S. agalactiae
  • Listeria monocytogenes
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20
Q

What are the 2 causes of spirochetal meningitis?

A
  • Treponema pallidum

- Borrelia burgdorferri

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21
Q

What is another way you can get meningitis (other than viruses, bacteria and spirochetal)?

A

protozoal and helminthic meningitis

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22
Q

What is the pathophysiology of bacterial meningitis?

A
  • mucosal/nasopharyngeal colonization
  • local invasion
  • intravascular survival
  • meningeal invasion
  • induction of subarachnoid space inflammation
  • alterations in BBB
  • cerebral edema and ICP
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23
Q

What is vasogenic cerebral edema?

A

increased BBB permeability

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24
Q

What is cytotoxic cerebral edema?

A

swelling of cellular elements of brain

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25
Q

What is interstitial cerebral edema?

A

obstruction of normal flow of CSF

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26
Q

What are the most common bacterial pathogens that babies less than 1 month old get?

A
  • strep agalactiae
  • E. coli
  • Listeria monocytogenes
  • Klebsiella spp.
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27
Q

What are the most common bacterial pathogens that babies get b/w 1-23 months?

A
  • Strep agalactiae
  • E. coli
  • H influenzae
  • Strep pneumoniae
  • N. meningitidis
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28
Q

What are the most common bacterial pathogens that people age 2-50 years old get?

A
  • Strep pneumoniae

- N. meningitidis

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29
Q

What are the most commmon bacterial pathogens that people over the age of 50 get?

A
  • Strep pneumoniae
  • N. meningitidis
  • L. monocytogenes
  • Aerobic gram-negative bacilli
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30
Q

How come we have decreased levels of meningitis caused by h. influenzae?

A

due to shots!

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31
Q

Why is inflammation in the brain super bad? How do you rememdy this?

A

cuz it disrupts the BB and allows for penetration

-corticosteroids

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32
Q

YOu need an antibiotic with good BBB penetration if you dont have meningeal infammation, what properties does this antibiotic need?

A
  • low molecular weight
  • low degree of ionization at physiological pH
  • high lipid solubility
  • low degree of protein binding
  • absence of active efflux systems
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33
Q

FOr babies less than 1 month of age who have purulent meningitis, what therapy do you give them?

A

Ampicillin plus cefotaxime OR
ampicillin plus an aminoglycoside

(everyone is AMPed about KELS

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34
Q

For children 1-23 months who have purulent meningitis, what therapy do you give them?

A

Vancomycin plus third-generation cephalosporin (ceftriaxone or cefotaxime)

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35
Q

For people ages 2-50 years who have purulent meningitis, what therapy do you give them?

A

vancomycin plus 3rd generation cephalosporin (ceftriaxona or cefotaxime)

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36
Q

For people less than 50 years who have purulent meningitis, what therapy do you give them?

A

vancomycin plus ampicillin plus a third generation cephalosporin

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37
Q

If you are positive the microorganism causing meningitis is strep pneumo, what do you give them?

A

Vancomycin and 3rd generation cephalosporin

Alt: meropenem, fluorquinolone

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38
Q

If you are positive the microorganism causing meningitis is N. meningitidis, what do you give them?

A

Third generation cephalosporin

ALT:Penicillin G, ampicillin, fluoroquinolone

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39
Q

If you are positive the microorganism causing meningitis is Listeria monocytogenes, what do you give them?

A

Ampicillin or penicillin G

Alt: TMP-SMX, meropenem

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40
Q

If you are positive the microorganism causing meningitis is strep agalactiae, what do you give them?

A

ampicillin or penicillin G

Alt: third-generation cephalosporin

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41
Q

If you are positive the microorganism causing meningitis is H. influenzae, what do you give them?

A

third-generation cephalosporin

Alt: cefepime, meropenem, fluoroquinolone

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42
Q

If you are positive the microorganism causing meningitis is E. coli, what do you give them?

A

Third-generation cephalosporin

Alt: cefepime, meropenem, aztreonam, fluoroquinolone, TMP-SMX

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43
Q

What is the definition of chronic meningitis?

A
  • indolent onset greater than or equal to 4 weeks

- signs of chronic inflammation in CSF

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44
Q

What are the early symptoms of chronic meningitis?

A
  • headache
  • nausea
  • decreased memory and comprehension
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45
Q

Whats are the differences between acute meningitis and chronic meningitis?

A

in chronic meningitis:

  • onset is more gradual
  • fever is lower
  • associated with lethargy and disability
  • often immunocompromised
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46
Q

What are the etiologies of chronic meningitis?

A
  • mycoses
  • bacteria
  • parasites
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47
Q

What are the four mycoses that cause chronic meningitis?

A
  • cryptococcosis
  • coccidiodomycosis
  • histoplasmosis
  • candidiasis
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48
Q

What are the three bacteria that cause chronic meningitis?

A
  • Mycobacterium tuberculosis
  • Treponema pallidum
  • Borrelia burgdorferii
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49
Q

What are the three parasites that cause chronic meningitis?

A
  • Acanthamebiasis
  • Cysticerosis
  • Angiostrngylus cantonensis
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50
Q

What is the definition of encephalitis?

A

inflammatory process of the brain parenchyma

-> clinical or lab evidence of neurologic dysfunction

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51
Q

What are the symptoms of encephalitis?

A
  • fever and headache

- altered mental status -usually earlier than with meningitis

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52
Q

What is the CSF profile of encephalitis?

A
  • lymphocytic pleocytosis (elevated lymphocytes)- magnitude varies with etiologic agent
  • normal glucose
  • elevated protein
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53
Q

What is the most common way to encephalitis?

A

Viral encephalitis

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54
Q

What are the 2 ways you can get viral encephalitis?

A 
Herpesviruses
Arboviruses
HIV
Enteroviruses, primarily poliovirus
Rabies virus
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55
Q

What are the types of herpesvirus that cause viral encephalitis?

A

HSV-1 and HSV-2
Varicella Zoster virus
CMV
HHV-6

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56
Q

What are the non-viral causes of encephalitis (much less common)?

A 
Listeria monocytogenes
Rickettsia spp.
Ehrlichia spp.
Bartonella spp.
Mycoplasma pneumoniae
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57
Q

What is this:
focal, intracerebral infection that begins as a localized area of cerebritis and develops into collection of pus surrounded by a well-vascularized capsule

A

brain abscess

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58
Q

What are the sources of brain abscess?

A
  • contiguous spread- sinusitis, otitis media or matoiditis
  • hematogenous
  • trauma
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59
Q

What are the symptoms of brain abscess?

A

general-headache, nausea, vomiting, focal neurologic findings
-vary with the site of the abscess

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60
Q

What are the bacteria that can cause brain abscesses?

A
  • Streptococcus spp. (70%)
  • Enterobacteriaceae
  • S. aureus (10-20%) -
  • Pseudomonas spp.
  • Bacterioides spp.
  • Nocardia asteroides
  • Prevotella spp. -
  • Mycobacterium spp.
  • Fusobacterium spp.
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61
Q

What are the fungi that can cause brain abscesses?

A

Aspergillus spp. Mucorales
Candida spp.
Coccidioides spp.
Cryptococcus spp.

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62
Q

What are the protozoal and helmithinic causes of brain abscess?

A
  • toxoplasma gondii (most common)
  • Neurocysticercosis- larval form of Taenia solium; developing word
  • AND trypanosoma cruzi, Entamoeba histolytica, Shistosoma spp.
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63
Q

What are the predisposing conditions that can cause brain abscess?

A
  • sinus and dental infection
  • penetrating trauma
  • pulmonary infection
  • congenital heart disease
  • HIV infection
  • transplantation
  • neutropenia
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64
Q

What are the culprits of sinus and dental infections?

A
  • aerobic and anaerobic streptococci
  • bacteroides spp.
  • prevotella spp.
  • enterobacteriaceae
  • S. aureus
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65
Q

What are culprits of penetrating trauma?

A
  • S. aureus
  • aerobic streptococci
  • enterobacteriaceae
  • Clostridium spp.
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66
Q

What are the culprits of pulmonary infection?

A
  • fusobacterium
  • actinomyces
  • bacteroides
  • prevotella spp.
  • Nocardia spp.
  • S. aureus
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67
Q

What are the culprits of congenital heart disease?

A
  • streptococci

- S. aureus

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68
Q

What are the culprits of HIV infection?

A
  • toxoplasma gondii
  • Nocardia spp.
  • Mycobacterium spp.
  • Listeria monocytogenes
  • Cryptococus neoformans
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69
Q

What are the culprits of microbes associated with transplantation?

A
  • aerobic gram-neg bacilli
  • aspergillus spp.
  • candida spp.
  • mucorales
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70
Q

What is this:

  • gram negative cocci
  • pathogens are fastidious-> isolate on chocolate agar, and thayer-martin medium
A

Neisseria Meningitidis

Neisseriaceae

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71
Q

What does N. meningitidis produce?

A

indophenol oxidase

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72
Q

How do you kill N. meningitidis?

A

by drying, sunlight, heat and chemicals (super easy to kill)

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73
Q

What is the antigenic structure of N. meningitidis?

A
  • group specific capsular polysaccharide (12 groups)
  • type specific outer membrane proteins
  • type specific lipooligosaccharide (LOS)
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74
Q

What are the Group A, B, C, Y and W strains of N meningitidis?

A

Group A - classic epidemic strain
Group B - endemic strain
-Polymer of sialic acid
-Poorly immunogenic – seen as self
-Antigen expressed in neonatal tissue
Group C - endemic and occasional epidemic strain
Groups Y and W-135 - endemic strains

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75
Q

There is the meningitis belt in (blank) -> predominantly group A

A

sub-saharan Africa

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76
Q

What are the three meningococcal infections (caused by N. meningitis)?

A
  • meningococcemia (may occur with or without meningitis)
  • meningitis
  • petechia lesions
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77
Q

What do you see on the patients skin when they have fulimant (sudden onset) sepsis and meningitis?

A

purpura
petechia
ecchymoses

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78
Q

What is hemorrhage into skin?
What is petechiae?
What is ecchymoses?

A

purpura
small hemorrhagic spots
large irregularly formed hemorrhagic areas

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79
Q

petechiae correlate with the degree of thrombocytopenia due to (blank)

A

DIC

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80
Q

What are the viruence factors of N. meningitis?

A
  • antiphagocytic capsule
  • lipooligosaccharide
  • out membrane porins
  • pili
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81
Q

What makes up the lipooligosaccharide of N. meningitis and what does it do?
How is it released?

A
  • Lipid A, core oligosaccharide, LACKS O ANTIGEN
  • extremely toxic and produces inflammation
  • from bacterial surface as membrane blebs
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82
Q

What is the progression of infection of N. meningitis?

A
  • gains access to nasopharynx
  • adheres via pili to epithelial cells of nasopharynx
  • remains local (carrier) or spreads via lymphatics to blood (bacteremia) and meninges (meningitis)
  • capsule prevents phagocytosis and complement-mediated lysis
  • tissue damage due to LOS (late onset sepsis)
  • DIC due to LOS
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83
Q

What will DIC caused by N. meningitis lead to?

A
  • hemorrhagic involvement of BVs

- shock

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84
Q

Why can you get multiple attacks of n. meningitis?

A

deficiencies of terminal complement proteins (C5, C6, C7 and C8)

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85
Q

How do you identify N. meningitis?

A
  • specimens (blood, CSF, NP secretiions found in carriers)
  • direct exam-> gram stain CSF
  • Isolation
  • Differential tests
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86
Q

How can you isolate N. meningitis?

A

(culture, incubate in CO2, blood agar, Thayer-Martin, chocolate agar)

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87
Q

What are the differential tests for N. meningitis?

A
  • gram neg diplococci
  • oxidase positive
  • oxidative production of acid from sugars (e.g glucose and maltose)
88
Q

Okay so you see growth on a chocolate agar plate, you see gram negative diplococci, you see an oxidase reaction, what are we looking at?

A

N. meningitis

89
Q

How do you transmit N. meningitis?
Whose most suscpetible?
Whats the carrier rate?
Does this cause epidemics?

A

-man to man transmission via airborne droplets
-1-40% (few carriers develop clinical disease)
yup, it can occur sporadically or in epidemics

90
Q

Why when your born will you not have any meningococcal meningitis but then become super suscpetible to it at 12 months and then you you gain immunity again?

A

transplacental antibodies that you lose almost all of it around 12 months and then you make your own immunity

91
Q

How can you get immunity to meningococcus? How does the immunity work?

A
  • due to anticapsular antibody

- immunity protects by complement-mediated lysis and opsonization

92
Q

In N. meningitis, the (blank) antibody is the major factor that determines resistance vs. susceptibility. Lack of antibody explains risk of children between (blank-blank) months.
Naturally occuring antibody probably due to carrier state and (blank) e.g. E. coli

A

anticapsular

cross-reacting bacteria

93
Q

There are 2 meningococcal vaccines, what are they, what do they do, who are they used on?

A

-Tetravalent meningococcal polysaccharide vaccine (MPSV4)
A purified polysaccharide that works on Groups A, C, Y and W-135
Only for people 56 and older

-Tetravalent meningococcal polysacchardie protein conjugate vaccine (MCV4)
Works on groups A, C, Y, W-135 polysaccharides.
Give routine immunization of adolescents (11-12 years) Booster at 16-18 years.

94
Q

What populations are at risk for meningococcal meningitis?

A
  • College freshmen living in dormitories
  • Microbiologists with potential exposure
  • Military recruits
  • Travelers to endemic regions
  • Terminal complement deficiencies
  • Anatomic or functional asplenia
95
Q

Why dont we have Group B vaccines for meningococcal meningitis?
Researchers are working on one though that targets (blank) binding protein.

A

cuz its poorly immunogenic

Factor H

96
Q

What kind of vaccine is the meningococcal vaccine?

A
  • Multivalent purified capsular polysaccharide

- Capsular polysaccharide-protein conjugate

97
Q

What is the treatment for meningococcal meningitis?

A
  • 3rd generation cephalosporin (ceftriaone or cefotaxime) OR Penicillin G or Ampicillin (readily penetrates inflamed meninges)
  • extensive supportive care
  • chemoprophylaxis for family contacts or epidemic situations-rifampin
98
Q

For N. meningitis-Chemoprophylaxis for family contacts or epidemic situations should use (blank)

A

rifampin

99
Q

How old do you have to be to have antibodies pass through the placenta? What does this mean?

A

Must be 35 weeks old in utero

It means if you are born before 35 weeks gestations you will be super susceptible to infections

100
Q

What are the species of importance for hemophilus?

A
  • H. influenzae
  • H. inluenzae biogroup aegyptius
  • H aegyptius
  • H. ducreyi
101
Q

What does H. influenzae biogroup aegyptius present as?

A

Brazilian purpuric fever

102
Q

What does H. aegyptius presents as?

A

acute, purulent conjunctivitis

103
Q

What does H. ducreyi present as?

A

veneral disease (soft chancre)

104
Q

What does Hemophilus look like on a gram stain?

A

gram negative rods

105
Q

What are the nutrional requirements for hemophilus?

A

X factor
V factor
Choclate agar
S. aureus

106
Q

What is X factor and where is it found?

What is V factor?

A

hematin-found in blood

NAD

107
Q

Why do you use chocolate agar to grow hemophilus?

A
  • heating lyses erythrocytes to release X and V factors

- heating inactivates an inhibitor of V factor

108
Q

Why on earth would you need staph aureus to grow hemophilus?

A

satelliting-releases X and secretes V factor

109
Q

H. influenza needs what 2 things?

What does H. ducreyi?

A

X and V

X

110
Q

What is the antigenic structure of Hemophilus?

What do they nontypeable strains lack?

A

An antiphagocytic capsular polysaccharide
(types A-F)

Lack a Capsule (very common)

111
Q

What does the type b capsular polysaccharide of hemophilus do? What is it?

A

causes almost all systemic diseases

polyribitol phosphate

112
Q

H. influenzae infections can cause nasopharyngitis and spread where? What strain does this?

A

sinuses or middle ear-usually a nontypeable strain (one of the most common causes of nasopharyngitis)
blood or meninges or joints- predominantly type B

113
Q

What are some other causes of nasopharyngitis other than H influenzae?

A

strep pneumoniae, moraxella catarrhalis

114
Q

What besides nasopharyngitis, can H influenza cause and what strain causes this?

A

epiglottitis -encapsulated

pneumonia- primary or secondary to influenza virus infection

115
Q

What is this:
invasive disease in healthy person (doesnt kill in blood)
-has an antiphagocytic capsule
-blocks complement-mediated bacteriolysis
-has an endotoxin

A

Haemophilus influenzae type b meningitis

Hib meningitis

116
Q

What does the HiB endotoxin do? What does its capsule block?

A

induces meningal inflammation

complement-mediated bacteriolysis

117
Q

What are the lab specimens you want to grab for haemophilus?

A

nasopharyneal swab, blood, CSF

direct examine gram stain too!

118
Q

Whats sketchy about the haemophilus culture?

A

you have to inoculate it immediately cuz it doesnt survive well

119
Q

Isolation of haemophilus requires …?

Identification based on need for (blanK)

A

X and V -chocolate agar, S. aureus, satellite phenomenon, normal flora)
X and V factors

120
Q

How can you test for the capsular antigen of haemophilus?

A

latex agglutination

121
Q

How many kids are carriers for upper respiratory tract infections of haemophilus? What is the common carrier strain and what does it cause? Are there a lot of asymptomatic carriers of type b?

A

30-50% children
nontypeable
otitis media
no, very few

122
Q

Type (blank) of haemophilus produces almost all invasive disease

A

b

123
Q

What age group is most susceptible to H. influenzae meningitis?

A

6 months to 3 years

124
Q

How does antibodies mess with Hib?

A

anticapsular antibody (absence of Ab is primary risk factor)-> protects by opsonization and complement-mediated lysis

125
Q

How long does the maternal antibody protect an infant from Hib?

A

less than 6 months

126
Q

Exposure to Hib carriers and cross-reactive antigens protects children for (Blank) years

A

> 3 years

127
Q

WHy dont you give your 18 month and younger children a vaccine against Hib?

A

cuz in that young of children polysacchardies are poorly immunogenic

128
Q

What is the current Hib vaccine?

A

a protein conjugate

1) PRP coupled to diptheria toxoid
2) PRP coupled to nontoxic mutant diptheria toxin
3) PRP coupled to N. meningitidis OMP

129
Q

Who should get the Hib vaccine?

A

for all children at 2 months

130
Q

What is the vaccine type of the Hib vaccine?

A

capsular polysaccharide-protein conjugate

131
Q

How do you treat Hib infection?

A

Prompt tx DO NOT WAIT FOR CULTURE RESULTS

-broad spectrum cephalosporin with good CNS penetration i.e cefotaxime or cefrtriaxone

132
Q

What do you give to carriers of Hib? What do you give to susceptible contacts?

A

rifampin

rifampin

133
Q

What is the etiologic agent of Brazilian purpuric fever?

A

Hemophilus influenzae biogroup aegyptius

134
Q

What are the symptoms and affects of hemophilus influenzae biogroup aegyptius?

A
  • brazilian purpuric fever
  • invasive H. aegyptius following conjunctivitis
  • acute onset fever, vomiting and abdominal pain, followed by purpura, vascular collaspe and death
135
Q

What type of hemophilus infection causes acute, purulent conjunctivitis?

A

hemophilus aegyptius

136
Q

What type of hemophilus is this:

  • Chancroid (soft chancre); formerly rare in N. america
  • relativey common in Africa
  • Painful ulcers on genitalia
  • probable co-factor in transmission of AIDS in Africa
A

Hemophilus ducreyi

137
Q

What is this:

  • gram, ovoid or lancet shaped, in pairs; old cultures;
  • aerobic
  • encapsulated
  • older cultures undergo autolysis; the autolytic enzymes are activated by surfactants such as bile and detergents
  • rough-to-smooth conversion by transformation
  • relatively fastidious; grown on blood
A

Streptococcus pneumoniae

138
Q

What is the antigenic structure of strep pneumoniae?

A

capsular polysaccharide is major antigen and a C polysaccharide (teichoic acid)

139
Q

The major antigenic structure on strep pneumoniae is the capsular polysaccharide. How many distinct serotypes are there? What is this capsule essential for?
What kind of antigen does it have on it?

A

90
virulence
T independent antigen

140
Q

What kind of reaction does strep pneumoniae undergo and what is it?

A

Quellung reaction-> incubation of encapsulated bacteria with antibody makes capsule refractile

141
Q

What is the C polysaccharide (teichoic acid)?

A

cell wall carbohydrate that reacts with an acute phase protein (c-reactive protein)

142
Q

What does it mean to be a T-independent antigen?

A

little kids cant make antibodies to it. (less than 2 years of age)

143
Q

What are the types of pneumoccal infections?

A
  • pneumonia (usually lobar)
  • sinusitis
  • otitis media
  • meningitis
  • peritonitis, endocarditis, arthritis
144
Q

What are the causes of sinusitis?

A

strep pneumoniae

H. influenza

145
Q

Pneumococcal infection is the most common causes of otitis media in (blank)

A

young and elderly

146
Q

How does pneumococcal meningitis present?

What is the disease due to?

A

abrupt onset, toxicity, fulminant course and DIC
Inflammatory response to the bacterium and its products
(it produces the inflammatory response but doesnt get killed by it)

147
Q

What are the virulence factors associated with Strep. pneumoniae?

A
  • polysaccharide capsule (essential for virulence)
  • pneumolysin
  • peptidoglycan and lipoteichoic acid
148
Q

What does the polysaccharide capsule on s. pneumoniae do?

A

prevents phagocytosis
-anticapsular antibody protects by opsonization (cuz only gram neg can be killed via opsonization or complement mediated)

149
Q

What is pneumolysin and what does it do?

A

it is a porin that contributes to inflammation and has multiple effects

150
Q

What does the peptidoglycan and lipoteichoic acid do?

A
  • components of cell wall
  • activate alternative pathway
  • elicit production of IL-1 and TNF-alpha
  • largely responsible for inflammatory response
151
Q

The natural resistance of Strep pneumo is very (low/high)?

A

very high - 40-70% of normal individuals carry pneumococci in the nasopharynx

152
Q

What are the natural defensive barriers of strep pneumo?

A

Cough and epiglottal reflex
Mucus and cilia
Phagocytosis by alveolar macrophages
Splenic clearance from blood

153
Q

What are conditions that can alter strep pneumo resistance (5)?

A
  • Depressed action of cilia
  • Depressed epiglottal reflex
  • hyposplenia or asplenia
  • sickle cell disease
  • malnutrition
154
Q

What are the symptoms of pneumococcal pneumonia?

A
  • Sudden onset with shaking chill, fever and sharp pleural pain
  • Bloody, rusty sputum
  • Generally localized in lower lobes (lobar pneumonia)
155
Q

What was a pneumonic crisis?

A

dramatic recovery 5-10 days after initial chill caused by pneumococcal pneumonia prior to the creation of antibiotics

156
Q

For pneumococcal pneumonia:

  • what specimens do you look at?
  • What should you directly exam?
  • What do you isolate it on?
  • How do you identify it and differentiate it from strep viridians
  • How do you test for it?
A
  • sputum, body fluids; blood CSF, etc.
  • gram stain, DNA probe
  • blood agar
  • alpha hemolytic, optochin sensitive, bile soluble
  • serologic tests, test for free antigen in body fluids; pneumococcal C polysaccharide
157
Q

How do you get strep pneumonia?

Is incidence associated with predisposing factors?

A
  • enters and exits via upper respiratory tract (most endogenous)
  • no
158
Q

Unlike N. meningitidis and Hib, most healthy adults (blank) anticapsular antibody associated with strep pneumonia.

A

lack (i.e dont have a preexisting antibody)

159
Q

How do you prevent and control strep pneumonia?

A
  • prevent primary damage
  • isolation
  • immunize for pneumococcal and influenza
160
Q

What is the pneumovax and pnu-imune vaccine and how does it work?

A

Pneumovax and pnu-immune

Purified capsular polysaccharide that is polyvalent (23 serotypes) and works by induction of opsonic antibody

161
Q

The pneumovax and pnu-immune vaccines, covers (blank) percent of bacteremic cases. Is it effective?
How long does it last and at what age should you give it?

A

94%
60-80% effective
5 yrs (little or no booster effective)

-all adults age 65 or older in series and anyone aged 6-18 years w/ specific risk factors

162
Q

THe prevnar 13 polysacchride conjugate vaccine (PCV) for pneumoccocal pnemonia is made of what? How many serotypes does it cover? Is it a T independent antigen?
What ages is it recommended in? What does it reduce?

A 
polysaccharide protein conjugate
13
yes
ages 2-59, people 65 and older
carriage and produce herd immunity
163
Q

What was super cool about the vaccine for pneumococcal disease?

A

vaccinating children caused herd immunity amongst the elderly

164
Q

What is the vaccine for pneumococcus?

A

multivalent (23) purified capsular polysaccharide and (13) valent polysaccharide-protein conjugate

165
Q

How do you treat strep pneumo?

A

penicillin or ceftriaxone of susceptible

Alternative: vancomycin, macrolides, doxycycline, or a quinolone

166
Q

How do you get resistance to penicillin?

A

acquisition of penicillin binding protein with reduced affinity for antibiotic

167
Q

How does erythromycin work?

A

messes with protein synthesis (50 s) -> inhibits translocation of the ribosome

168
Q

How does doxycycline work?

A

it is a tetracycline-> messes with the 30s tRNA -> messes with protein synthesis

169
Q

How do you treat pneumococcal meningitis? why?

A

Ceftriaxone or penicillin + vancomycin
Ceftriaxone is more effective and has better CNS penetration
Vancomycin gives coverage if resistant to β lactam

170
Q

Can penicillin pass through the normal BBB? then why can we use it for pneumococcal meningitis?

A

No

inflammation makes the BBB permeable

171
Q

(blank) kills bacteria, releasing peptidoglycan and teichoic acids

A

penicillin

172
Q

(blank and blank) cause intense inflammatory reaction, contributing to increased intracranial pressure and irreversible brain damage. Can reduce inflammatory response by use of (blank)

A

PG and TA

corticosteroids

173
Q

What is the group b strep that causes meningitis?

A

S. agalactiae

174
Q

Where do you find group B strep normally?

A

genital (10-30% of normal women) and GI tract

175
Q

What is group B strep the leading cause of?

A

leading cause of neonatal sepsis and meningitis; extremely high mortality rate :((((

176
Q

Its easy to get strep agalactiae in adults who have (blank, blank or blank)

A

HIV, cancer, diabetes

177
Q

What is the key virulence factor of S. agalactiae? How do we deal?

A

antiphagocytic capsular polysaccharide

-Antibody to capsular polysaccharide is protective; is also protective for newborn child

178
Q

What are the three ways to get Group B strep infections?

A
  • early onset neonatal infection
  • late onset neonatal infection
  • infections in adults
179
Q

Tell me about early onset neonatal infections of group B strep?

A
  • First week of life
  • Acquired in utero or during birth
  • Bacteremia (most common), pneumonia and/or meningitis
180
Q

Tell me about early late onset neonatal infections of group B strep?

A

1 week to 3 months of age
Acquired from mother or another infant
Bacteremia and meningitis

181
Q

Tell me about group B strep infections in adults?

How does it present?

A

Patients generally older and have debilitating underlying conditions, e.g., diabetes mellitus, liver disease, malignancy

Presentations: bacteremia, pneumonia, bone/joint infection and skin and soft tissue infection

182
Q

What are the risk factors for early onset disease of group B strep?

A
  • Exposure to bacterium

- Absence of anticapsular antibody

183
Q

What are ways that babies can be exposed to group B strep?]

What are ways that babies can get an absence of anticapsular antibody?

A

Exposure to bacterium

  • Genital/GI carriage of bacterium (10-40% of normal women)
  • Prolonged membrane rupture
  • Intrapartum fever

Mother lacks antibody
Delivery at < 37 weeks gestation

184
Q

How do you diagnose group B strep in the lab?

A
  • gram stain of CSF
  • beta hemolytic
  • agglutination test for Lancefield Group B antigen
185
Q

T or F

there is more hemolysis with group B strep than group A strep

A

F! group A strep has more hemolysis

186
Q

How do you prevent group B strep?

A

-Universal screening: all pregnant women at 35-37 weeks gestation for vaginal and rectal colonization
-Additional/alternative risk factors
-Intrapartum antibiotic prophylaxis
(there is no approved vaccine)

187
Q

What are the intrapartum antibiotic prophylaxis and when do you use them?

A

penicillin G; ampicillin is alternative
At time of labor or rupture of membranes
All pregnant women who test positive for GBS colonization or have other risk factors

188
Q

What is the treatment of group B strep?

A
  • Empiric treatment of neonatal infection: ampicillin + aminoglycoside
  • Specific treatment: penicillin G
189
Q

Should you give prophylaxis for GBS for the following:

Previous pregnancy with a positive GBS screening culture (unless a culture was also positive during current pregnancy)

A

no

190
Q

When is GBS intrapartum prophylaxis indicated?

A
  • previous infant with invasive GBS disease
  • GBS bacteriuria during current pregnancy
  • Positive GBS screening culture during current pregnancy
  • GBS status unknown + any of the following: delivery at less than 37 weeks, amniotic membrane rupture greater than 18 hrs, and intrapartum temp greater than 100.4 celcius
191
Q

When is GBS intrapartum prophylaxis NOT indicated?

A
  • GBS bacteriuria during previous pregnancy
  • negative vaginal and rectal GBS culture in late gestation during current pregnancy regardless of intrapartum risk factors
  • planned cesarean delivery performed in the absence of labor or membrane rupture (regardless of culture status)
192
Q

What is this:
encapsulated yeast, and causes an opportunistic infection. There are four serotypes of capsular polysaccharide and 2 species. Globally, this is the most serious and life-threatening of the pathogenic fungi.

A

Cryptococcus

193
Q

What are the four serotypes of the capsular polysaccharide of cryptococcus? WHat is it called and why is it important?

A

A, B, C, and D

-cryptococcal antigen and is the foundation for diagnosis

194
Q

What are the 2 species of cryptococcus and what serotypes are they?

A

C. neoformans (serotypes A and D)

C. gatti (serotype B and C)

195
Q

What is the most serious and life-threatening of the pathogenic fungi?

A

cyptococcus

196
Q

What is the most common cause of cryptococcus meningitis?

A

cryptococcus neoformans

197
Q

Where will you find cryptococcois?

A

worldwide

198
Q

(blank) is a ubiquitous saprophyte that is acquired from an environmental source such as pigeon dropping and trees (eucalyptus trees)

A

Cyptococcois

199
Q

Who does cyptococcois infect?

A

everyone but its usually a subclinical infection that exhibits latency until you immune system is low or something (i.e opportunisitic infection)

200
Q

Where do you typically see cryptococcosis in HIV/AIDS patients and how does it present and how do you control it?

A
  • sub-saharan Africa
  • latent infection activated with loss of T cell function
  • well controlled in developed countries due to HAART
201
Q

What happened with cryptococcois in the US?

A

we had an outbreak of C. gatti in pacific northwest

202
Q

What is this:
infection begins as a pulmonary infection
variable in presentation; relatively common with C. gattii

A

pulmonary cryptococcosis

203
Q

What is this:
most common clinical form of cryptococcois and is highly neutropic.
Is this fatal?

A

cryptococcal meningitis

Yes, if untreated

204
Q

What are some other manifestations of cryptococcois other than pulmonary cryptococcosis, nd cryptococcal meningitis?

A
  • skin lesions
  • ocular infection
  • prostatic involvement (possible asymptomatic reservoir)
205
Q

What are the opportunistic ways that cryptococcosis can infect patients?

A
  • HIV/AIDS
  • immune suppresion (i.e transplants)
  • C. gatti-> can infect people without immunosuppresion.
206
Q

To diagnose cryptococcus you need to look at what specimens? directly examine what?
identify what?
detect antigens where and which ones?

A
  • Blood, CSF
  • India ink negative stain of CSF for encapsulated yeast
  • culture
  • capsular antigens (CrAg) in the serum, plasma, or CSF
207
Q

How can you detect the cryptococcal antigenic capsule?

A
  • latex agglutination
  • enzyme immunoassay
  • lateral flow immunoassay
208
Q

What is the most sensitive test for cryptococcus?

A

Antigen (most specific) and culture

209
Q

How do you treat cryptococcosis?

A

Antifungal agents used alone or in combination

  • Amphotericin B
  • Flucytosine
  • Fluconazole
210
Q

What are the three phases of treatment?

Is treatment the same for all patient populations?

A

induction, consolidation, maintenance

NO (different for HIV-infected, organ transplant recipients, norm)

211
Q

What is IRIS?

A

Immune reconstitution inflammatory syndrome -> occurs at initiation of HAART-> an overwhelming inflammatory response to previoulsy acquired opportunistic infection

212
Q

Cryptococcus neoformans occurs entirely in (blank) patients

A

HIV/AIDS

213
Q

How do you diagnose c. neoformans

A

using CSF or serum CrAg

-> use lateral flow assay

214
Q

How do you treat symptomatic patients of c. neoformans?

A

Induction-> amphotercin B, flucytosine, fluconazole
Consolidation-> fluconazole
Maintenance-> fluconazole

215
Q

How do you prevent cryptococcal disease?

A

-screen and treat
screen all AIDS patients for CrAg prior to initiation of ART> Treat prior to ART use.
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