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227
Table 8.8
(continued)
Etiology Diagnosis and notes Treatment
Human
immunodeciency virus
(HIV)
• Primary HIV ulceration is
typically seen only in
uncontrolled HIV
• Endoscopy to rule out alternate
causes such as CMV
Antiretroviral therapy and
corticosteroids
Bacterial causes
• Oral and upper
respiratory ora
• Mycobacteria
including M.
tuberculosis and NTM
• Nocardia (rare)
• Actinomyces (rare)
• Endoscopy with tissue biopsy
• Culture may be challenging to
interpret given likelihood of
growing non-pathologic bacteria
Antibiotics, depending on
organism isolated
Candida spp.
• May see oral thrush
• Endoscopy reveals characteristic
white plaques; biopsy with yeast,
pseudohyphae with mucosal
invasion
• Treat with systemic antifungal
agents based on the patient
history; if no improvement in
3–5days, pursue EGD and
biopsy
Fluconazole
b
(discuss with
transplant team due to drug
interactions)
Other fungal
• Aspergillus
• Cryptococcus
• Histoplasmosis
• Blastomycosis
• Pneumocystis
• Endoscopy with tissue biopsy for
histopathology and culture
• Rare for Aspergillus to present as
localized esophagitis–more
commonly part of disseminated
disease
Antifungal selected for
specic fungus isolated
(discuss with transplant team
due to drug interactions)
Parasitic
• Trypanosoma cruzi
• Leishmania spp.
• Cryptosporidium
• Ascaris
• Serology
• Endoscopy with biopsy
Anti-parasitic medication
depending on etiology
a
Above dosing for normal renal function
b
Certain Candida species such as C. glabatra may have uconazole resistance
by clustered vesicles on an erythematous base, which rapidly rupture leaving an
ulcerated area. Diagnosis is made by scraping of ulcer base and staining with a
direct uorescent antibody. EBV infection causes oral hairy leukoplakia and post-
transplant lymphoproliferative disorder. CMV can present with oral manifestations,
with a study in renal transplant recipients reporting 1.32% incidence of ulcerations
involving buccal mucosa, palate, tongue, and oor of the mouth [163]. Candida
infection can present with erythematous candidiasis, angular cheilitis, and pseudo-
membranous candidiasis [164]. Rarely, one can see endemic mycoses present with
oral ulcers [165].
8 Infections intheAdult Solid Organ Transplant Recipient
228
Non-infectious causes include neoplasms, graft versus host disease, autoimmune
disorders such as Bechet’s, or side effects from immunosuppressive medications,
for instance, mycophenolate mofetil has been reported to cause painful oral ulcer-
ations [166], and cyclosporine is associated with gingival hypertrophy [167].
8.5 Urinary Tract Infections
Key Considerations for GI Infections
• The variety of organisms included on the enteric pathogen panel differs by
manufacturer. Cystisospora, Isospora, Microsporidia, and some travel-
related pathogens are not commonly included on most panels. O&P, aura-
mine, and trichrome stains may be necessary in some cases.
• Medications are a frequent cause of diarrhea in SOT recipients, and diar-
rhea itself is associated with uctuations in tacrolimus level with the
potential for tacrolimus nephrotoxicity or malabsorption.
• Updated guidelines now recommend PO daxomicin as rst line treatment
for C. diff infection, with PO vancomycin as an alternative.
• Diagnosis of CMV GI disease requires tissue biopsy; negative plasma PCR
does not rule out end organ involvement.
• Consider EGD in suspected candida esophagitis should rapid improvement
not occur after 3–5days of uconazole.
• Remember sexually transmitted infections as a cause of proctitis in sexu-
ally active SOT recipients.
Case
A 44-year-old woman who received a deceased-donor kidney transplant
11months ago presents with fatigue and dysuria. She was taken off trime-
thoprim/sulfamethoxazole for PJP prophylaxis at 6-months post-transplant. A
catheter-related UTI complicated her post-transplant course, but none since.
Her post-operative ureteral stent was removed. She has not had any episodes
of rejection. On exam, she is afebrile, with normal vital signs. She has no
tenderness over her transplanted kidney in the right lower quadrant and no
costovertebral angle tenderness. A urine dipstick is positive for leukocyte
esterase, nitrites, and protein.
After sending the urine sample for a formal urinalysis and reexive bacte-
rial culture, checking a complete blood count and chemistry panel, what
empiric treatment should be started?
Comment:
This patient has no indwelling hardware, no history of resistant UTI, and
no signs or symptoms concerning for a systemic infection. Her examination is
(continued)
J. Hu et al.
229
Urinary tract infections (UTIs) are common in SOT recipients, as they are in the
general population. Kidney transplant recipients have a higher risk for UTIs due to
surgical manipulation of the genitourinary tract and the associated risk related to
foreign bodies such as ureteral stents. A study of 4388 SOT recipients followed for
at least 1year found that UTI incidence varied based on the type of transplant. The
overall rate of UTIs was 4.4% over the study period; the incidence of UTIs
(expressed as the number of UTIs per 1000 transplant-days) was highest in kidney
transplant recipients (0.45), followed by kidney-pancreas (0.22), heart (0.07), liver
(0.06), and lung (0.02) [170]. The highest incidence of UTIs occurs in the rst
3–6months post-transplant. Bacteremia is due to a urinary source in over one-third
(37%) of cases in kidney transplant recipients [171]. The wide prevalence quoted in
studies of UTIs in kidney transplant recipients, 7–80%, is due to the lack of stan-
dardized diagnostic criteria, variable use of prophylactic antibiotics, over-
interpretation of asymptomatic bacteriuria (ASB), and uneven follow-up
duration [172].
8.5.1 Denitions
Clinical providers must be precise in their nomenclature when describing and diag-
nosing urinary infections. The terminology of simple and complicated should be
avoided and instead replaced with anatomical location of infection. Guidelines for
classication of urinary tract infections in kidney transplant recipients are given in
Table8.9. Other guidelines also exist for UTIs in SOT recipients in general and use
similar denitions [173]. Overuse of antibiotics for ASB should be avoided, and
reassuring, without tenderness over her graft or native kidneys, and she did
not experience nausea or vomiting. Her diagnosis is consistent with cystitis in
a kidney transplant recipient.
After consideration of prior microbiologic data and local resistance pat-
terns, empiric therapy choices include nitrofurantoin, fosfomycin, amoxicillin-
clavulanate, and third generation oral cephalosporins. Because she is past
6months post- transplant, her duration of treatment can be 5–7days. Longer
treatment courses have not shown benet in cases of cystitis [168, 169].
Empiric therapy with trimethoprim/sulfamethoxazole should be avoided,
given the risk of resistance to this antibiotic with recent use for prophylaxis.
Fluoroquinolones should also be avoided, given their side effect prole.
Antibiotics should be tailored based on culture results.
If the patient develops fever, tenderness, or pain over the allograft, ank
pain, or vomiting, she should present to the Emergency Department as she
may need volume resuscitation, IV antibiotics, and urgent assessment of her
allograft for concern for pyelonephritis versus graft rejection.
8 Infections intheAdult Solid Organ Transplant Recipient
230
Table 8.9
Classication of asymptomatic bacteriuria (ASB) and urinary tract infections (UTI) in
kidney transplant recipients
Classication Description
Laboratory
investigations of
urine
Asymptomatic
bacteriuria
No urinary or systemic symptoms of infection >10
5
CFU/mL
uropathogen
a, b
Cystitis Dysuria, urinary urgency/frequency, or suprapubic pain;
but no systemic symptoms and no ureteral stent/
nephrostomy tube/chronic urinary catheter
>10 WBC/mm
3 c
>10
3
CFU/mL
uropathogen
b
Pyelonephritis Fever, chills, malaise, hemodynamic instability, or
leukocytosis (without other apparent etiology); ank/
allograft pain; or bacteremia with same organism as in
urine
Dysuria, urgency, frequency, suprapubic pain may or
may not be present
>10 WBC/mm
3 c
>10
4
CFU/mL
uropathogen
b
Recurrent UTI ≥3 UTIs in prior 12-month period As mentioned
above
Other
considerations
Recent instrumentation, urethritis, prostatitis, infected
nephrolithiasis, obstruction, kidney abscess
As mentioned
above
WBC white blood cell, CFU/mL colony-forming units/milliliter
Adapted from Goldman, etal, with permission [172]
a
While routine treatment of ASB is not recommended (see Treatment section), if considering treat-
ment of ASB (e.g., in the immediate post-transplant period), a repeat urine culture is recommended
(with care to minimize contamination) to assess persistence of the same uropathogen. Spontaneous
resolution is common
b
Staphylococcus epidermidis (except if ureteral stent), lactobacillus, and Gardnerella spp. are
unlikely to be uropathogens. Regarding CFU/mL: while most patients with UTI will have
>10
5
CFU/mL of a uropathogen in a midstream urine sample, some patients with pyelonephritis
may have only 10
4
–10
5
CFU/mL of a uropathogen and some patients with cystitis may have even
fewer CFU/mL (most data on cystitis with low CFU/mL is only for E. coli). Not all labs report
<10
4
CFU/mL
c
While not an absolute criteria (depending on the performance characteristics of the urinalysis or
presence of neutropenia), <10 WBC/mm
3
should prompt consideration of a diagnosis other
than UTI
appropriate therapy in the setting of pyelonephritis and recurrent UTIs can be
selected.
8.5.2 Risk Factors
Risk factors for UTI include demographic factors, history of genitourinary diseases,
and transplant-specic risks. In a study of nearly 29,000 kidney transplant recipi-
ents, 17% of patients in the rst month post-transplant developed UTIs. By 3years
after kidney transplantation, female transplant recipients experienced more UTIs
than male transplant recipients, 60% versus 47%. Factors that increased risk for UTI
in kidney transplant recipients were female sex, older age, indwelling catheters,
J. Hu et al.
231
diabetes, neurogenic bladder, and nephrolithiasis [174]. Specic transplant-related
risks include ureteral stents or urological structural abnormalities (e.g., malforma-
tions, bladder atony, kidney cysts or calculi, ureteric stenosis at ureterovesicular
anastomosis, and urinary stula), vesicoureteral reux, acute cellular rejection, and
deceased-donor graft. Risks for later-onset (>6 months post-transplant) UTIs
include prednisone dose >20mg/day and serum creatinine of >2mg/dL.However,
the type of long-term immunosuppressive is not clearly associated with UTI
risk [169].
8.5.3 Complications andOutcomes
UTIs in kidney transplant recipients result in serious health consequences. Blood
stream infections occur in kidney transplant recipients at 40 times the annual rate of
the general population. UTI caused 30–73% of blood stream infection in kidney
transplant recipients and 80% of those UTIs are from gram-negative rods (GNRs).
In a retrospective study of 116 hospitalizations for blood stream infections in kidney
transplant recipients, 83% occurred after the rst year of transplant and 71% were
community acquired. In this study, 57% of blood stream infections were from a UTI
source, followed by GI and surgical site infection sources. Sixty-ve percent of
bacteremic kidney transplant recipients developed acute kidney injury [175]. A
4-year retrospective study of kidney transplant recipients with severe UTIs requir-
ing hospitalization found that Klebsiella spp. and E. coli were the most common
pathogens, and between a quarter and a third of those bacteria produced extended-
spectrum beta-lactamase (ESBL). In these hospitalized kidney transplant recipients
with UTIs, 41% experienced acute kidney injury, 3.6% experienced graft loss, and
there was a 1.2% 1-year mortality [176].
8.5.4 Specic Organisms
GNRs, with E. coli being most common, account for >70% of UTIs in SOT recipi-
ents. Additional organisms to initially consider include Enterobacteriaceae,
Enterococci, Pseudomonas, Staphylococcus saprophyticus, and Streptococcus spe-
cies. SOT recipients are at higher risk for multi-drug resistant (MDR) organisms.
Less commonly, viral and fungal urinary infection can also occur.
Carbapenem-resistant Klebsiella pneumoniae (CRKP) and Extended-spectrum
beta-lactamase producing Klebsiella pneumoniae (ESBL-KP) are concerning patho-
gens for UTIs in SOT recipients. A 2015 study of kidney transplant recipients with
UTI found that CRKP UTIs were associated with ICU admissions, longer hospital
stays, and failure of antibiotic interventions compared to susceptible Klebsiella pneu-
moniae UTIs [177]. Although drug-resistant infections are more common, many rou-
tinely used oral antibiotics can still be used in outpatient management; it is a common
8 Infections intheAdult Solid Organ Transplant Recipient
232
misconception that MDR organisms automatically require intravenous antibiotics or
hospital admission unless otherwise clinically indicated. For example, some MDR
organisms may retain susceptibility to common oral antibiotics including uorquino-
lones, trimethoprim-sulfamethoxazole, nitrofurantoin, or fosfomycin, although the
latter two are not appropriate for treating upper tract UTI (use in cystitis only).
Less common pathogens include Mycobacterium tuberculosis, Salmonella,
CMV, and adenovirus which mainly cause hemorrhagic cystitis. Corynebacterium
urealyticum may be a pathogen in the setting of obstructive uropathy. Rarely
Mycoplasma hominis and Ureaplasma urealyticum can cause intra-parenchymal or
perinephric abscess or graft pyelonephritis in kidney transplant recipients.
Staphylococcus epidermidis, lactobacillus, Gardnerella vaginalis are unlikely
pathogens. Candida species are usually asymptomatic colonizers but can cause
upper tract infections with complications of candidemia and ureterovesicular fungal
balls. A urine culture with mixed ora represents contamination.
Special consideration should be given to BK virus in SOT recipients. It is a poly-
omavirus that is ubiquitous in the environment and causes both animal and human
infections. The median age of primary infection is 4–5years old. Primary infection
is usually a self-limited respiratory infection and rarely presents as acute cystitis.
BK virus develops a lifelong latency in kidney cells and transitional epithelial cells
of the genitourinary tract. Immunosuppression triggers viruria that in some cases
results in invasive kidney infections. In kidney transplant recipients, reactivation
occurs in native kidneys and can cause a high level of kidney graft failure—as high
as 50–80% within 2years of transplant. BK virus nephropathy is much rarer in non-
kidney solid organ transplantation, although when it does occur it tends to lead to
end stage kidney disease (ESKD) and signicant mortality. The most common man-
ifestations of BK virus reactivation infections are BK nephropathy and hemorrhagic
cystitis. The gold standard for diagnosis of BK nephropathy is kidney biopsy,
although BK viral loads in the blood and urine as well as the presence of decoy cells
(virally infected epithelial cells seen on cytology) in the urine assist in diagnosis and
are used in screening. The key treatment of BK virus nephropathy/reactivation
infections is reduction in immunosuppression medications (see Chap. 4) [178].
8.5.5 Diagnostic Considerations
In SOT recipients, the presentation of UTI may lack usual lower urinary tract symp-
toms such as frequency, urgency, and dysuria. Instead, symptoms such as fever,
malaise, and non-specic sepsis symptoms as well as leukocytosis may be the main
presentation, but not necessarily represent pyelonephritis as with immunocompe-
tent patients. Because of denervation of the allograft, the transplanted kidney may
not be tender to palpation. Pyuria >10 WBC/mL is usually present, and lack of
pyuria in the setting of UTI symptoms should spur evaluation for alternative etiolo-
gies. Notably, E. coli UTI in SOT recipients may only have 10
3
CFUs and still be
considered a UTI by transplant infectious disease specialists.
J. Hu et al.
233
8.5.6 Therapeutic Considerations
The Infectious Disease Community of Practice of the American Society of
Transplantation guidelines (2019) recommend against the routine urine testing in
asymptomatic SOT recipients after the rst 2months post-transplant. In the setting
of asymptomatic bacteriuria, the recommendation is to observe symptoms without
treatment. However, if there is persistent asymptomatic bacteriuria with an associ-
ated creatinine rise there is a weak recommendation for treatment with antibiotics.
Cystitis should be treated for 5–10days, and never for 3 days in SOT recipients.
Treatment of pyelonephritis should be for approximately 14days with an effort to
narrow antibiotics based on urine culture data. However, the course should be
extended for a longer duration depending on source control (such as in the setting of
perinephric abscesses that require drainage) [172].
8.5.7 Specic Treatment Recommendations By Condition
While the rate of UTIs in the 3–6-month period post-transplant is high, there is a
growing consensus that asymptomatic bacteriuria should not be treated in the
outpatient setting. The historical practice of “screen-and-treat" developed to prevent
cystitis, pyelonephritis, and allograft dysfunction. However, recent data suggest
against this practice and that treatment does not prevent subsequent cystitis or
pyelonephritis. Treatment of ABS does increase the incidence of resistant organ-
isms making subsequent true UTIs more difcult to treat [179–181].
Cystitis should be treated empirically with nitrofurantoin, fosfomycin,
amoxicillin- clavulanate, or an oral third-generation cephalosporin. Providers should
be wary of the risk for trimethoprim-sulfamethoxazole resistance in patients who
have been on prophylaxis. Fluoroquinolones should not be rst line given their side
effect prole and stewardship for more severe/complex infections. Empiric antibiot-
ics should be narrowed as much as possible based on the culture results. While
7–10 days of antibiotic therapy should be utilized in the rst 6-months post-
transplant, 5–7days can be considered for cystitis after 6months [172].
Pyelonephritis in kidney transplant recipients with complicating factors (e.g.,
hardware, abscess, bacteremia, and many more) should be admitted to the hospital for
management. Otherwise, outpatient management can be considered if there is appro-
priate coordination with transplant and infectious disease consultants. Stable inpa-
tients can be treated with ceftriaxone, ampicillin-sulbactam, or ciprooxacin if prior
cultures do not show antibiotic resistance. Patients with signs of clinical instability
should receive empiric therapy with piperacillin/tazobactam, cefepime, or a carbape-
nem. Detailed inpatient management is beyond the scope of this book, but in general,
consultation with a transplant infectious disease specialist is often indicated due to the
increasing rates of multi-drug-resistant organisms. The transplant team will also need
to be involved, especially in severe infections (e.g., septic shock) in which reduction
8 Infections intheAdult Solid Organ Transplant Recipient
234
of immunosuppressive medications is recommended. Advanced imaging may also be
required to assess for upper tract disease such as kidney abscess or structural abnor-
malities that could lead to obstruction and to ensure source control. Treatment dura-
tion should be approximately 14days (usually longer in the presence of abscess), and
antibiotics should be narrowed to reect coverage of culture results [172].
For recurrent UTI treatment and prevention, interventions have not been ade-
quately tested in SOT recipients. Recommendations for SOT recipients with recurrent
UTIs are identical to those for immunocompetent patients. Behavioral interventions
including hydration, timed voiding, front to back wiping in females, and avoidance of
serial anal and vaginal intercourse is recommended. Vaginal estrogen for post-meno-
pausal women decreased the frequency of recurrent UTIs by 12fold [182]. Post-coital
antibiotics in females, and assessment for BPH with obstruction and prostatitis in
males are also recommended. Non-antimicrobial interventions such as cranberry juice
and probiotics are not well supported [172]. Additionally, given the higher risk of
recurrent UTI in the SOT population, primary care providers should strongly consider
consultation with an infectious disease specialist.
Early postoperative infections are usually addressed by the transplant team. For
donor-derived infections, trimethoprim-sulfamethoxazole used for PJP prophy-
laxis in the rst 6–12 months will serve as dual prophylaxis against many UTI
organisms in kidney transplant recipients, but increases the risk of trimethoprim-
sulfamethoxazole resistant organisms in breakthrough or subsequent infections.
One study showed a two-third reduction in UTIs for those receiving trimethoprim-
sulfamethoxazole versus no antimicrobial prophylaxis. In patients who cannot tol-
erate trimethoprim/sulfamethoxazole some authors recommend uoroquinolones or
fosfomycin specically for UTI prophylaxis, and guidelines are to limit such pro-
phylaxis to the rst month post-transplantation [174].
Ureteral stents are used in kidney transplant recipients to reduce the risk of ste-
nosis of the ureterovesicular anastomosis. Ureteral stents may increase the risk for
UTI, and they are typically removed within 2–4weeks of transplantation to decrease
the risk for UTI [174].
A summary of key considerations for UTIs in SOT recipients is given in
Table8.10.
8.5.8 Sexually Transmitted Infections (STIs)
Sexually transmitted infections (STIs) in SOT recipients should be diagnosed and
treated similarly to the general population. STIs are often overlooked in immunocom-
promised populations. They manifest throughout the genitourinary tract as urethritis,
epididymitis, prostatitis, vaginitis, and cervicitis, as well as proctitis in the gastrointesti-
nal tract. Common pathogens include N. gonorrhea, C. trachomatis, and T. vaginalis.
Additional considerations include M. genitalium, U. urealyticum, T. pallidum, herpes
simplex virus 1 & 2, and HIV.Therapy is based on causative organism. It is important to
remember that people opt for transplantation to return to a fuller life, which includes sex.
J. Hu et al.
235
8.6 Infections oftheCentral Nervous System
Case
A 45-year-old man who underwent liver transplant 18months prior is brought
to the primary care clinic by his family who is concerned about confusion.
They noticed that he has become progressively more confused and fatigued
over the last 10days. They note word-nding difculties, trouble remember-
ing the names of his children, and being confused about the time of day. He
has been sleeping more and taking naps in the afternoon, which is unusual for
him. Yesterday morning, he began complaining of a headache, and this morn-
ing he was difcult to rouse from sleep. In the ofce, his temperature is
38.1°C, heart rate 92bpm, blood pressure 104/54mmHg, respiratory rate 16
breaths/min, and oxygen saturation 98% on ambient air. He is sleepy but
arousable and able to participate in conversation; however, he cannot recall
the events of the last week and thinks the year is 1958.
His strength, reexes, and a limited cranial nerve examination of the pupils,
extraocular movement, facial, and oropharynx motor function are normal.
Comment:
This patient is presenting with acute to subacute onset of altered mental
status accompanied by a fever. In a solid organ transplant recipient, these
symptoms should prompt immediate referral to the emergency department for
rapid evaluation and treatment. While the neurologic symptoms may be non-
specic, the possibility of meningoencephalitis must be considered in this
population. In this case, the duration of symptoms is longer than what would
be expected for bacterial meningitis, however, meningoencephalitis due to a
fungal pathogen, such as cryptococcus, is of high concern.
This patient should undergo immediate testing in an emergency setting,
including complete blood counts, basic chemistries, neuroimaging with con-
trast, and a lumbar puncture. Cerebrospinal uid should be sent for cell count
with differential, glucose, protein, bacterial cultures, fungal cultures, PCR for
herpes viruses (HSV, VZV, EBV, and CMV), PCR for enteroviruses, and cryp-
tococcal antigen. Although this patient’s presentation is less consistent with
bacterial meningitis, empiric antibiotic therapy should be started while
awaiting laboratory data. Infectious disease specialists should be consulted
early to guide additional evaluation and management.
Table 8.10 Key considerations for urinary tract infections
• Asymptomatic bacteriuria rarely requires treatment in SOT recipients
• Urinary anatomy is important; SOT recipients may not have specic urinary symptoms with
upper tract infection
• Many resistant bacteria still have non-beta lactam oral options, especially for cystitis
• In kidney transplant recipients, BK virus reactivation is a notable cause of graft dysfunction
8 Infections intheAdult Solid Organ Transplant Recipient
236
Infections of the central nervous system (CNS) are less common in solid organ
transplant (SOT) recipients now compared to previous eras due to more tailored
immunosuppressive regimens, improved immunization rates, and routine surveil-
lance. The current incidence of opportunistic CNS infections in this population is
estimated to be 1–2%, down from 7% in older studies [183]. However, CNS infec-
tions remain a signicant cause of morbidity for SOT recipients, with some studies
suggesting mortality rates as high as 73% [184]. Furthermore, mortality rates with
CNS fungal infections after solid organ transplantation may be as high as 90%. SOT
recipients may not present with typical meningeal symptoms of CNS infection and
therefore clinicians should have a high index of suspicion in a patient with fever,
headache, and/or altered mental status [185]. Like most infectious complications in
SOT recipient, the risk for different CNS infections varies according to time after
transplantation (See Table8.1) [186].
8.6.1 Diagnostic Considerations (Table8.11)
A SOT recipient with onset of fever and altered mental status should undergo a
rapid evaluation including CBC, peripheral blood cultures, and a lumbar puncture
(LP) to evaluate for CNS infection. A head CT should generally be performed prior
Table 8.11 Common CNS infections in solid organ transplant recipients by time since
transplantation
Time course Infections Special considerations
Initial 30days
post-transplant
• Reactivation of latent fungal,
mycobacterial and viral
infections
• Donor-derived infections
• Nosocomial infections (MRSA,
Candida species, Aspergillus
species)
• Viral prophylaxis in the immediate
post-transplant period makes
reactivation of viral infections less
likely
1–6months
post-transplant
• Opportunistic infections
(Nocardia, Listeria,
Toxoplasmosis, endemic
mycoses)
• Reactivation of viral infections
(EBV, VZV, HSV, CMV,
HHV-6)
• Viral prophylaxis often decreases
3–6months after transplant,
increasing risk for reactivation
syndromes
>6months
post-transplant
• Opportunistic infections
(Nocardia, Listeria,
Cryptococcus, Aspergillus)
• Community-acquired infections
• Reactivation of previous
infections (Herpes viruses, JC
virus)
• Incidence of opportunistic fungal
CNS infection is highest >12months
after transplant
Reprinted with permission from Pizzi etal. [183] with special consideration comments added
J. Hu et al.