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Microbiology Exam 5 > Etiologic agents of infant to adult > Flashcards

Etiologic agents of infant to adult Flashcards

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1
Q

what is the most common and serious manifestation due to Hib

A

meningitis

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2
Q

what is the gram staining of Hib

A

gram negative non motile cocobacilli/ pleomorphic rod

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3
Q

is Hib fastidious?

A

yes, fastidious growth requirements

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4
Q

what are the virulence factors of Hib and why are they important

A

Exopolysaccharide- antiphagocytic
lipooligosaccharide (LOS)- meningeal inflammation
Peptidoglycan- enhanced meningeal inflammation

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5
Q

what are the RF for Hib

A
  1. socioeconomic- crowding, smoking, short breast feeding

2. humoral immonodeficiences

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6
Q

what is the pathogenesis of Hib in unvaccinated children

A

window of infection >6mo to 6yo

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7
Q

what is the pathogenesis of Hib in vaccinated children

A

if child serconverts no window of infection

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8
Q

clinical manifestation of Hib meningitis

A

insidious onset

antecendent upper resp. tract infection and/or ottis media followed by meningitis symptoms

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9
Q

what are the possible sequelae for untreated Hib meningitis

A

permanent neuro damage
hearing loss
septic arthritis
purpura fulminans

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10
Q

Diagnosis of Hib

A

Culture and ID same as any bacteria

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11
Q

Treatment for Hib

A

ceftriaxone and dexamethasone

give steroid 15 min before AB

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12
Q

Prevention of Hib

A

prophylaxis with AB to decrease carriage and incidence

Hib polysaccharide conj. vaccine

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13
Q

what is the gram staining for s. pneumoniae

A

gram positive, lancet shape diplococci

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14
Q

what is s. pneumoniae hemolytic status and is it fastidious

A

alpha hemolytic

Not Fastidious- grows on blood agar

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15
Q

is s. pneumoniae catalase positive or negative and what does that mean

A

catalase negative

it is an aerotolerant anaerobe

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16
Q

Is s. pneumoniae encapsulated?

A

yes

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17
Q

what are s. pneumoniae’s virulence factors

A

antiphagocytic
lil or no crossreactivity
coagulase negative

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18
Q

what agent is responsible for pts with reoccuring meningitis

A

s. pneumoniae

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19
Q

which type of meningitis has the highest case of fatality rates

A

pneumococcal meningitis

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20
Q

what age is affected by s. pneumoniae the most

A

peaks in the young <5yo and the elderly

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21
Q

what season does s. pneumoniae peak

A

peaks late fall early winter but it is generally year round

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22
Q

what are the RF for s. pneumoniae

A
  1. antecedent RT infections or pneumococcal pneumonia
  2. if there is a CSF leak by deformity or trauma can lead to reoccurring infection
  3. IPD
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23
Q

what protein if detected in nose or ear drainage shows CSF leak

A

B2-transferrin

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24
Q

what is the primary site of damage in most bacterial meningitis

A

hippocampus die to neuronal loss

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25
Q

How would you be able to diagnose petechial-purpuric skin lesions (SPG) between s. pneumoniae and n. meningitides?`

A

s. pneumoniae will not be found in skin leision

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26
Q

Diagnoisis of s. pneumoniae

A

Culture and ID like any bacteria

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27
Q

what is the treatment for s. pneumoniae meningitis

A

IV cefotaxime and infussuion with vancomyosin and adjunctive dexamethasone (>17yo) until strain is proven to penicillin sensitive

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28
Q

what would you treat penicillin sensitive s. pneumoniae with

A

penicillin

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29
Q

why is vancomycin tolerance clinically importantant

A

related to relapse cases esp. pediatric pneumococcal meningitis

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30
Q

what is the best prevention for s. pneumoniae meningitis

A

conjugated s. pneumoniae vaccine (7 valent)

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31
Q

what is step is necessary if you discover pt. with n. meningitides?

A

n. meningitides is a reportable disease

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32
Q

what are the two pathogenic species of neisseria

A

n. meningitides

n. gonorrhoeae

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33
Q

where are non pathogenic species of neisseria located?

A

Normal flora of URT and mucosal surfaces

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34
Q

how do pathogenic and non-pathogenic neisseria differ

A

non pathogenic are non-encapsulated variants of pathogenic species

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35
Q

what is the gram staining of n. meningitides

A

Gram-negative diplococci kidney bean shape

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36
Q

is n. meningitides oxidase positive or negative

A

positive

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37
Q

is n. meningitides fastidious?

A

NO

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38
Q

what are the virulence factors for n. meningitides?

A

group specific polysaccharides and LOS

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39
Q

why is the capsular polysacchride in n. meningitides impiortant

A

anti-phagocytic

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40
Q

what agent does the capsular poly saccharide of n. meningitides type most closely resemble and what do they have in common

A

E. Coli K1

they both have sialic acid which are human antigens and are poorly immunogenic

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41
Q

why is the LOS in n. meningitides so important

A

consists of an endotoxin (Lipid A)
can be antiphagocytic through molecular mimicry
Lipid A can cause DIC

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42
Q

what is the case rate endemic patterns of n. meningitides in the US

A

case rate is low (.5-1/100,000)

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43
Q

which serotype of n. meningitides causes the most infections in the US

A

serotype B

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44
Q

what is special about serotype Y n. meningitides

A

more likely cause pneumonia in older population

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45
Q

what countries is n. meningitides a hyperepidemic or epidemic

A

Africa and middle eastern countries

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46
Q

does US have n. meningitides epidemics?

A

potentially, specific serogroups are associated with epidemic which occur in cycles

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47
Q

how is n. meningitides transmitted

A

via aerosols and resp. droplets

48
Q

what is the POE and initial site of colonization of n. meningitides

A

nasopharynx

49
Q

what is the reservoir of neisseria spp.

A

humans

50
Q

which age is most commonly affected by n. meningitides

A

1 month to 22yo olds

51
Q

what are the age relationships with n. meningitides infections

A

infants and children
older children/adolescents
young adults esp. military and college students in dorms

52
Q

what is the seasonality to n. meningitides

A

late fall -> winter -> early spring

53
Q

what the RF for n. meningitides infection

A
  1. susceptibility (dorms, military)
  2. predisposing conditions/ actions (RT infect, smoke, binge drinking, bars, crowding, poor)
  3. Susceptible populations with disease predominates
54
Q

what is the pathogenesis

A

after colonization of nasopharynx n. meningitides invades blood the the meninges

55
Q

DIC is cause by thrombosis from loss of what to things

A

thrombomodulin and protein C receptor

56
Q

what is required to decrease DIC in your patients whith n. meningitides

A

give activated Protein C

57
Q

What type of immunity is helpful with n. meningitides

A

humoral anticapsular AB (protection) which most people have some groups
Functional compliment system

58
Q

what are the EARLY signs and symptoms for 16yo and younger pts with n. meningitides meningitis

A

early symptoms of sepsis (72% of pts) around 8 hours these symptoms include leg pain, cold extremities, abnormal skin color

59
Q

what are the LATE signs and symptoms for 16yo and younger pts with n. meningitides meningitis

A

late symptoms: meningism, impaired consciousness occurs 13-22 hours after early symptoms

60
Q

what are EARLY signs and symptoms of n. meningitides in adults

A

early symptoms: mild pharyngitis w.o exudate, slight fever, headache or flu-like with emesis

61
Q

what are LATE signs and symptoms of n. meningitides in adults

A

late: classic symptoms of meningitis can occur without early signs, also rash on ankles and wrist moving centrally if septicemia is present

62
Q

what are the possible sequelae with n. meningitides infections

A

nerve deafness
cns damage
necrosis of large area can result in amputation

63
Q

what is waterhouse-friderichsen symdrome

A

fulminant meningococcemia
-circulatory shock due to SIRS which results in septic shock
-bilateral hemorrhagic necrosis of adrenals which causes low cortisol and leads to hypotension and DIC
It is not limited to only n. meningitides

64
Q

what are signs of purpura fulminans

A

hypothermia, seizure, shock, thrombocytopenis, leukocytosis purpura
it is not limited to n. meningitides

65
Q

what serogroup of n. meningitides has the highest motality rate with purpura fulminans

A

serogroup C

66
Q

what other diseases besides meningitis, pupura fulmanins and waterhouse-frriderichsen syndrome can occur with n. meningitides

A

meningococcemia without CNS localization
Pneumonia
endocarditis

67
Q

diagnosis of n. meningitides if skin lesions are present

A

gram stain biopsy can reveal n. meningitides

68
Q

what step is important to do before establishing treatment of n. meningitides

A

MBC- many n. meningitides are resistant to AB

69
Q

what steps should be taken with potential n. meningitides carries

A

obtain nasopharyngeal culture to find carriers

70
Q

what is the treatment for n. meningitides carriers

A

rifampin

71
Q

what is the treatment for n. meningitides pt with disease

A

ceftriaxone or cefotaxime, or penicillin G or rBPI

72
Q

when does mortality rates of n. meningitides meningitis increase?

A 
meningococcal meningitis with meningococcal septicemia 
without shock (20%) HIGH
with shock (60%) VERY HIGH
73
Q

Prevention of n. meningitides

A

vaccine (2 different types)

do not give non-conj to children <55yo

74
Q

what serotype does n. meningitides vaccine not cover

A

B, which accounts for 1/3 of cases in US

75
Q

what type of species is c. neoformans?

A

fungus

76
Q

which form of cyptococcus is a major causative agent world wide

A

grubii (CnVG, serotype A)

77
Q

where does c. neoformans predominate

A

Central europe

78
Q

what is the infectious and pathogenic form of CnVN in humans

A

asexual yeast

79
Q

what is the distribution of CnVN or CnCG

A

worldwide, found in soil and pigeons and birds are carriers which disseminates fungi

80
Q

how does c. neoformans differ from other systemic mycosis

A

It is not thermally dimorphic!

81
Q

what parts of c. neoformans are not involved in infection

A

contains a sexual cycle but hyphae and spores are not cause of infections

82
Q

what the virulence factors for c. neoformans

A
  1. capsule (antiphagocytic, pevents Ag processing)

2. phenoloxidase production (antiphag, and resistant to Amphotericin B)

83
Q

how common is c. neoformans in HIV and AID pts

A

3rd most common CNS infection

84
Q

how opportunistic is c. neoformans in HIV and AIDS pts

A

4th most common opportunistic infection

85
Q

what is the transmission of c. neoformans

A

disease can occur in any population but is not believed to be person to person

86
Q

what is the poe of c. neoformans

A

respiratory tract with spread to CNS

87
Q

what is the age or gender relationship with c. neoformans

A

none

88
Q

what is the seasonality of c. neoformans

A

none

89
Q

what are the RF for Cg

A

tropical subtropical regions
rarely causes disease in HIV
incidence is rare

90
Q

what are the RF for CnVN and CnVG

A

worldwide
immunocomprimised individials
rarely caused in healthy people (immunocompetent)

91
Q

what is the primary site of infection in c. neoformans

A

lungs and cns

92
Q

what are symptoms of c. neoformans infection in people with functional immune system

A

asymptomatic pulmonary infection

93
Q

what are symptoms of c. neoformans infection in AIDS

A

fever, cough, dispnea, weight loss, headache, infiltrates on CXR
2-4 weeks to develo

94
Q

what is meningoencephalitis

A

progression of infection to basal ganglia and cortical gray matter
ICP >250 is common in mortality

95
Q

what are symptoms of meningoencephalitis

A

headache, fever lethargy. nausea, vomit. minimal nuchal rigidity, focal signs (mental status, memory/cognition)
ends with death

96
Q

besides lung and CNS a c. neoformans in aids pts can disseminate to where

A

anywhere

skin, eye, bone, urinary tract are common

97
Q

what is cryptococcal polysaccahridemia/antigenemia

A

positive serum Ag assay without any detection of fungi

since disease is fatal you sill treat any pt with positive serum Ag assay

98
Q

what type of pathogen is c. neoformans

A

facultative intracellular pathogen of macrophage

replicates inside and is released without response from immune system

99
Q

what would be seen with CSF examination with india ink in c. neoformans

A

5-7um spherical encapsulated yeast

cells of macrophage/monocyte lineage

100
Q

what would be seen with CSF examination with gram staining c. neoformans

A

gram positive eucaryotic cells

101
Q

what radiology test would you order in c.neoformans infection?

A

CXR or CT of lungs

and MRI or CT for meningitis

102
Q

what is the treatment for n c. neoformans

A

high does amphotericin B with 5-fluorocytosine for 2w
Fluconazole (400mg) or itaconazole for 8 weeks
maintain fluconazole (200mg) life long
TREAT ICP

103
Q

What are the two cellular forms of amoebaes

A

trophozoites are the feed form found in brain and environ

cyst are found in water never brain

104
Q

which cell form of amoebas are resistant to freezing water and chlorination

A

cyst

105
Q

where is N. fowleri found?

A

warm, freshwater lakes, puddles, ponds improperly chlorinated pools and brackish water in hot summer weather

106
Q

what CNS disease can N. fowleri cause

A

amoebic and acute primary meningoencephalitis

107
Q

what is the population at risk for N. fowleri

A

children and young adults

swimming in warm fresh water

108
Q

of the worlds cases of N. fowleri what percentage occur in US

A

1/2

109
Q

what is the POE of N. fowleri

A

nose

110
Q

what is the pathogenesis of N. fowleri

A

implants in nasal mucosa which goes through cribiform plate and can be found in perivascular and subarachnoid space

111
Q

What is the fulminate course of N. fowleri

A

2-7 days from onset to death

112
Q

what are the signs and symptoms of N. fowleri

A

2 day incubation with signs similar to bacterial meningitis

after 1-2 days manifest with diffused encephalitis then coma and death from cardiorespiratory failure, cerebral edema

113
Q

what is the most essential in diagnoising N. fowleri

A

Pt History!

114
Q

what difference will be observed in the csf of amoeba compared to bacterial infection

A

similar except may observe amoeba in CSF

115
Q

beside csf exam and pt history how else can you determine N. fowleri

A

lack of viral, bacterial and fungi findings
peripheral leukocytosis
Death occurs in a week
Brain biopsy would reveal Positive IFA, clusters of amoebic trophs, and intense PMNs in parychema

116
Q

what is the treatment for N. fowleri

A

Amphotericin B and Miltefosine

Prognosis is poor

Microbiology Exam 5 (7 decks)

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