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

Opportunistic Infections in Solid Organ Transplantation Flashcards

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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
what infections are most prominent in the early period post op
Nosocomial bacterial infections (ex- line related infxn, CA-UTI, sounds, VAP, C diff)
26
what infections are most prominent in the intermediate period post op
M tuberculosis or nontuberculous mycobacterial infections Viral reactivation/ infxn: herpesviruses (HSV, VZV, CMV, EBV), BK virus Fungal infxn: PJP, C. neoformans
27
what infections are most prominent in the late period post op
M. tuberculosis or nontuberculous mycobacterial infxn Late viral OI, late CMV infection Late fungal infection: invasive aspergillosis, other mold infxns
28
why are T cells important in preventing ID
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
29
early infections in SOT are predominantly
hospital acquired infections related to surgery, procedures, foreign devices installation, exposure to nosocomial pathogens by staff
30
when is the highest risk for infections post op
intermediate period
31
the cytomegalovirus is a group _____, ____ virus that is _______ (shape) and ________ (enveloped?_
group 2, dsDNA icosahedral enveloped
32
seropositivity of cytomegalovirus is equal to
age
33
how is CMV transmitted?
Usually shared by direct contact with blood or bodily fluids (Ex- sharing drinks/ sexual/ oral) Also shared vertically (possible, but not guaranteed transmission)
34
CMV is known as HHV ___
5
35
CMV attaches to ____ and it's latency site is ____
predominantly mucosal epithelium myeloid cells (ex- WBCs)
36
describe the process of going from primary to secondary infection
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
reactivation of CMV occurs in ___% infected pts and can be frequent of infrequent
90
38
list the 6 effects of CMV infection
↑ risk of opportunistic infections ↑ incidence of acute and chronic allograft injury/ rejection Chronic allograft nephropathy Bronchiolitis obliterans Coronary vasculopathy ↓ survival overall
39
list 3 RFs for CMV disease post SOT
CMV + donor/ recipient - serostatus Use of antithymocyte globulin induction Net state of immunosuppression Acute or chronic GVHD HLA mismatch Steroid use
40
what is latent CMV?
CMV IgG+, no active viral replication
41
what is CMV infection defined as
CMV IgG+, viral replication detected in any bodily fluid or by culture (asymp or symptomatic)
42
what is CMV syndrome defined as
not well defined, fever/ malaise, atypical lymphocytosis, leukopenia, elevated transaminases with viral replication
43
CMV disease is defined as
clinically evident disease and some form of tissue/ fluid diagnostics
44
what is gold standard for determining CMV disease
histopathyology
45
what is prophylaxis for CMV in a high risk SOT
valganciclovir
46
how to treat mod-severe CMV disease
ganciclovir IV
47
how to treat mild CMV syndrome
PO valganciclovir
48
valganciclovir and ganciclovir MOA
chain termination of viral DNA polymerase
49
VGCV is ___ PO absorbed than GCV
better
50
PO VGCV is converted to _____ by ______, then _____ eliminated
GCV by intestinal mucosa renally
51
renally eliminated VGCV is _____ unchanged, and _________ dose adjustment in renal failure
80-90% requires
52
what is the major toxicities of valganciclovir and ganciclovir
therapy limiting bone marrow suppression even with prophylactic doses- occurs up to ~20% pts
53
what is routine monitoring for VGCV and GCV
CBC at least monthly to monitor for marrow suppression
54
describe yeasts
unicellular, colourless, oval shaped fungi that reproduce by budding some are human commensals
55
describe molds
multicellular, colourful, branching shaped fungi with hyphae/ septa reproductive elements often environmental
56
describe dimorphic fungi
yeast in the heat (appears as yeast in human specimens), mold in the cold depends on environment
57
candida, cryptococcus are
yeasts
58
aspergillus spp, Mucorales/ Rhizopus, dermatophytes are
molds
59
histoplasma spp and blastomyces are
dimorphic fungi
60
describe the diseases caused by aspergillus in a pt that is severely immunodeficient, mildly immunodef, and a strong healthy patient
invasive pulmonary aspergillosis chronic cavitating pulmonary aspergillosis allergic bronchopulmonary aspergillosis (ABPA0
61
aspergillosis geography
ubiquitous worldwide saprophytes (breaks down decaying matter), inhaling constantly in most pts daily (not “black” mold in house)
62
how is aspergillosis acquired
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
what is the clinical presentation of invasive aspergillosis
immunocomp primary pulmonary infection (nodular diffuse lung disease) w/ fever which can disseminate since angioinvasive
64
what is the clinical presentation of chronic cavitating aspergillosis
captures aspergillus in cavities - less indolent lung infxn/ fungus balls
65
what is the clinical presentation of allergic bronchopulmonary aspergillosis
IgE mediated rxn to aspergillosis msot seen in pts with asthma
66
how is aspergillosis diagnosed
serum/ BAL galactomannan (antigen), culture, biopsy (septate hyphae)
67
how to treat aspergillosis
mold active azoles like voriconazole, posaconazole F2-6mths resolve RF like immunodeficiency, allergies, etc
68
3 major DDIs of azole antifungals
CYP450 P-gp OATP-1B1
69
many azole antifungals and caspofungin are CYP450 ___________
inhibitors
70
if you start a patient on antifungals, should always screen for DDI with
CYP3A4
71
P-gp is a ______ pump
efflux back into intsetines
72
OATP-1B1 is a ________ pump that goes into _______
influx liver
73
inhibition of OATP-1B1 results in
↑ systemic exposure of drug instead of hepatic CL = ↑ toxicity and effectiveness
74
rifampin is a 3A4 _____
inducer
75
voriconazole is a 3A4 _____
inhibitor
76
tacrolimus is a 3A4 _____
substrate

446- ID and transplant (18 decks)

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