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446- ID and transplant > Opportunistic Infections in Solid Organ Transplantation > Flashcards

Opportunistic Infections in Solid Organ Transplantation Flashcards

1
Q

T or F: immunodeficiency is a spectrum

A

F- more a multidimensional problem

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2
Q

3 types of immunocompromised

A

increased sus
specific deficiency
truly immunocompromised

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3
Q

those with increased susceptibility immunocomp have increased chances of

A

normal infections
does not get atypical or strange infections

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4
Q

uncontrolled T2DM, chronic kidney or liver disease, solid organ tumors not on chemo, burn victims, etc are considered
1. increased susceptibility
2. specific deficiency
3. truly immunocompromised

A

1

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5
Q

patients on biologics, controlled HIV, structural lung disease are considered
1. increased susceptibility
2. specific deficiency
3. truly immunocompromised

A

2

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6
Q

pts that are post SOT, post stem cell transplant, severely uncontrolled HIV, severe bone marrow suppression are considered
1. increased susceptibility
2. specific deficiency
3. truly immunocompromised

A

3

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7
Q

opportunistic infections in solid organ transplant recipients are focused on by __________ (which subspecialty)

A

transplant infectious diseases

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8
Q

OI for SOTRs are typically more ____, _________, and _______

A

more severe
more rapidly progressing
more difficult to recognize

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9
Q

list 4 reasons why OI in SOTRs are more difficult to recognize

A

Immunosuppression may blunt inflam response
Use of steroids may mask fever/ inflam response
Surgical alterations in anatomy may hinder recognition
Noninfectious causes often mimic infection

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10
Q

4 categories of RFs for SOT

A

donor factors
recipient factors
intraoperative factors
postop factors

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11
Q

donor RFs for infections in SOTs include

A

latent infections
unrecognized active illness in donor

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12
Q

recipient RFs for infections in SOTs include

A

underlying illness
age
vax stat
allograft organ

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13
Q

intraoperative RFs for infections in SOTs include

A

surgical procedure
ischemic injury and OR duration = ↑ contamination risk

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14
Q

postop RFs for infections in SOTs include

A

Immunosuppression
Technical problems affecting allograft
Foreign devices
Hospital exposure

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15
Q

the most important reason for immune compromise in SOTRs is

A

T cell depletion

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16
Q

in SOTRs, pts receive ____________ to reduce risk of rejection but also wipes out T cells

A

T cell depleting agents (rATG or basiliximab)

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17
Q

in SCT, pts usually have _________ and hence are given ___________ which wipes out T cells

A

bone marrow cancer
myeloablative chemo

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18
Q

T or F: some pt’s T cells never recover after depletion

A

T- those who do have delayed recovery of 1-2yrs

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19
Q

__________________, more than any other feature, is responsible for the extent of immune system compromise

A

T cell depletion

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20
Q

what s considered “early period” after transplant

A

day 0 (transplant) - 30ds post SOT

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21
Q

what is the status of the immune system in the early period after SOT

A

immune function waning- possible donor derived or hospital acquired infections

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22
Q

what is the status of the immune system in the intermediate period after SOT

A

peak of immunosuppression, OI risk highest

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23
Q

when is the late period after SOT

A

> day 180

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24
Q

what is the status of the immune system in the late period after SOT

A

immunosuppression reduced- decreased risk of OI compared to intermediate period but higher baseline risk of OI compared to general population

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25
Q

what infections are most prominent in the early period post op

A

Nosocomial bacterial infections (ex- line related infxn, CA-UTI, sounds, VAP, C diff)

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26
Q

what infections are most prominent in the intermediate period post op

A

M tuberculosis or nontuberculous mycobacterial infections

Viral reactivation/ infxn: herpesviruses (HSV, VZV, CMV, EBV), BK virus

Fungal infxn: PJP, C. neoformans

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27
Q

what infections are most prominent in the late period post op

A

M. tuberculosis or nontuberculous mycobacterial infxn

Late viral OI, late CMV infection

Late fungal infection: invasive aspergillosis, other mold infxns

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28
Q

why are T cells important in preventing ID

A

Intracellular pathogens difficult to eradicate as they may hide in host cells (ex- viruses, mycobacteria)
Loss of T cell fxns predisposes to infxn with these organisms + those who require T cell assistance to activate innate response

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29
Q

early infections in SOT are predominantly

A

hospital acquired infections related to surgery, procedures, foreign devices installation, exposure to nosocomial pathogens by staff

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30
Q

when is the highest risk for infections post op

A

intermediate period

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31
Q

the cytomegalovirus is a group _____, ____ virus that is _______ (shape) and ________ (enveloped?_

A

group 2, dsDNA
icosahedral
enveloped

32
Q

seropositivity of cytomegalovirus is equal to

A

age

33
Q

how is CMV transmitted?

A

Usually shared by direct contact with blood or bodily fluids (Ex- sharing drinks/ sexual/ oral)
Also shared vertically (possible, but not guaranteed transmission)

34
Q

CMV is known as HHV ___

A

5

35
Q

CMV attaches to ____ and it’s latency site is ____

A

predominantly mucosal epithelium
myeloid cells (ex- WBCs)

36
Q

describe the process of going from primary to secondary infection

A

primary infection = worse due to no immune memory
recovery and establishment of latency = usually asymptomatic but can still be contagious
secondary disease = reactivation of latent virus due to loss of immune system control

37
Q

reactivation of CMV occurs in ___% infected pts and can be frequent of infrequent

A

90

38
Q

list the 6 effects of CMV infection

A

↑ risk of opportunistic infections
↑ incidence of acute and chronic allograft injury/ rejection
Chronic allograft nephropathy
Bronchiolitis obliterans
Coronary vasculopathy
↓ survival overall

39
Q

list 3 RFs for CMV disease post SOT

A

CMV + donor/ recipient - serostatus
Use of antithymocyte globulin induction
Net state of immunosuppression
Acute or chronic GVHD
HLA mismatch
Steroid use

40
Q

what is latent CMV?

A

CMV IgG+, no active viral replication

41
Q

what is CMV infection defined as

A

CMV IgG+, viral replication detected in any bodily fluid or by culture (asymp or symptomatic)

42
Q

what is CMV syndrome defined as

A

not well defined, fever/ malaise, atypical lymphocytosis, leukopenia, elevated transaminases with viral replication

43
Q

CMV disease is defined as

A

clinically evident disease and some form of tissue/ fluid diagnostics

44
Q

what is gold standard for determining CMV disease

A

histopathyology

45
Q

what is prophylaxis for CMV in a high risk SOT

A

valganciclovir

46
Q

how to treat mod-severe CMV disease

A

ganciclovir IV

47
Q

how to treat mild CMV syndrome

A

PO valganciclovir

48
Q

valganciclovir and ganciclovir MOA

A

chain termination of viral DNA polymerase

49
Q

VGCV is ___ PO absorbed than GCV

A

better

50
Q

PO VGCV is converted to _____ by ______, then _____ eliminated

A

GCV by intestinal mucosa
renally

51
Q

renally eliminated VGCV is _____ unchanged, and _________ dose adjustment in renal failure

A

80-90%
requires

52
Q

what is the major toxicities of valganciclovir and ganciclovir

A

therapy limiting bone marrow suppression even with prophylactic doses- occurs up to ~20% pts

53
Q

what is routine monitoring for VGCV and GCV

A

CBC at least monthly to monitor for marrow suppression

54
Q

describe yeasts

A

unicellular, colourless, oval shaped fungi that reproduce by budding
some are human commensals

55
Q

describe molds

A

multicellular, colourful, branching shaped fungi with hyphae/ septa reproductive elements
often environmental

56
Q

describe dimorphic fungi

A

yeast in the heat (appears as yeast in human specimens), mold in the cold
depends on environment

57
Q

candida, cryptococcus are

A

yeasts

58
Q

aspergillus spp, Mucorales/ Rhizopus, dermatophytes are

A

molds

59
Q

histoplasma spp and blastomyces are

A

dimorphic fungi

60
Q

describe the diseases caused by aspergillus in a pt that is severely immunodeficient, mildly immunodef, and a strong healthy patient

A

invasive pulmonary aspergillosis
chronic cavitating pulmonary aspergillosis
allergic bronchopulmonary aspergillosis (ABPA0

61
Q

aspergillosis geography

A

ubiquitous worldwide saprophytes (breaks down decaying matter), inhaling constantly in most pts daily (not “black” mold in house)

62
Q

how is aspergillosis acquired

A

inhalation of airborne conidia: most frequent causes clinical disease in immunocomp/ CGD (prolonged neutropenia as seen with heme malignancy, post transplant) or allergic disease

63
Q

what is the clinical presentation of invasive aspergillosis

A

immunocomp
primary pulmonary infection (nodular diffuse lung disease) w/ fever which can disseminate since angioinvasive

64
Q

what is the clinical presentation of chronic cavitating aspergillosis

A

captures aspergillus in cavities - less indolent lung infxn/ fungus balls

65
Q

what is the clinical presentation of allergic bronchopulmonary aspergillosis

A

IgE mediated rxn to aspergillosis msot seen in pts with asthma

66
Q

how is aspergillosis diagnosed

A

serum/ BAL galactomannan (antigen), culture, biopsy (septate hyphae)

67
Q

how to treat aspergillosis

A

mold active azoles like voriconazole, posaconazole F2-6mths
resolve RF like immunodeficiency, allergies, etc

68
Q

3 major DDIs of azole antifungals

A

CYP450
P-gp
OATP-1B1

69
Q

many azole antifungals and caspofungin are CYP450 ___________

A

inhibitors

70
Q

if you start a patient on antifungals, should always screen for DDI with

A

CYP3A4

71
Q

P-gp is a ______ pump

A

efflux
back into intsetines

72
Q

OATP-1B1 is a ________ pump that goes into _______

A

influx
liver

73
Q

inhibition of OATP-1B1 results in

A

↑ systemic exposure of drug instead of hepatic CL = ↑ toxicity and effectiveness

74
Q

rifampin is a 3A4 _____

A

inducer

75
Q

voriconazole is a 3A4 _____

A

inhibitor

76
Q

tacrolimus is a 3A4 _____

A

substrate

446- ID and transplant (18 decks)

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