Infections in Transplant recipients
Infections following transplantation are complicated by the use of
drugs that are necessary to enhance likelihood of survival of the
transplanted organ but also cause the host to be
immunocompromised.
Variety of organisms have been transmitted by organ transplantation
(see table 117-1)
From 2% to >20% of donor kidneys are contaminated with bacteria –
in most cases, with the organisms that colonize the skin or grow in
the tissue culture medium used to bathe the donor kidney while it
awaits implantation.
Use of enrichment columns and monoclonal-antibody depletion
procedures results in higher incidence of contamination.
Approx 2% of cryopreserved and peripheral blood stem cells
transfused as part of treatment for cancer are contaminated.
Results of cultures performed at the time of cryopreservation and at
the time of thawing were helpful in guiding therapy for the recipient.
In many transplantation centers, transmission of infections that may
be latent or clinically inapparent in the donor organ has resulted in
the development of specific-donor screening protocols.
Serologic testing focusing on such viruses such as HSV 1 and HSV
2; VZV, CMV, HHV 6, EBV, HHV-8, hepaB and C, HIV, HTLV -1 and
on parasites such as Toxoplasma gondii, skin testing for M.
tuberculosis. Investigation of patients dietary habits (consumption of
raw meat or fish or unpasteurized products) , occupations or
avocations (gardening or spelunking), and travel history (travel to
areas with endemic fungi) is mandatory. It is expected that the
recipient will have been likewise assessed.
INFECTIONS IN BONE MARROW AND HEMATOPIETIC STEM
CELL TRANSPLANT RECIPIENTS
BM or hematopoeitic stem cell transplantation for either
immunodeficiency or cancer patients results in a transient state of
complete immune incompetence.
Immediately after transplantation, both phagocytes and immune cells
(T&B cells) are absent, and the host is extremely susceptible to
infection.
BACTERIAL INFECTIONS.
1st month  bm or hematopoietic stem cell transplantation,
infectious complications are similar to those in granulocytopenic
patients receiving chemotherapy for acute leukemia.
1-4 week – due to anticipated neutropenia and high rate of bacterial
infection in this population, many centers give prohyplactic antibitiocs
to patients upon initiation of chemotherapy.
LEVOFLOXACIN – decrease the incidence of gram- negative
bacteremia among these patients
Bacterial infections are common in first few days after BM transplant.
Predominantly aerobic bacteria found in the bowel (
Pseudomonas, E.coli, Klebsiella) and those found in the
skin or in intravenous catheters (S. aureus and coagulasenegative staph)
Filamentous bacteria (Nocardia and organisms that cause
actinomycosis)  beyond 1st few days of neutropenia
Episodes of bacteremia due to encapsulated organisms  marked
the late post transplantation period (>6 months after BM
reconstitution).
FUNGAL INFECTIONS  beyond 1st week after transplantation,
become increasingly common.
Candida albicans  most common in granulocytopenic patients
Candida glabrata & aspergillus  increased used of prophylactic
fluconazole; resistant fungi
Candida % aspergillus  in patients with GVHD who required
prolonged or indefinite coursed of glucocoticoids and
immunospressive agents, high risk even after engraftment and
resolution of neutropenia. High risk of reactivation of fungal infection
(Histoplasmosis, Blastomycosis, Coccidiodomycosis) – endemic
areas.
PARASITIC INFECTIONS
Pneumocystis pneumonia (especially among patients being treated
for hematologic malignancies)  most patients receive maintenance
prophylaxis TMP-SMX (trimethroprim-sulfamethoxazole starting 1
month after engraftment and continuing for at least 1 year.
TMP-SMX- may also protect patients seropositive fo T. gondii which
may cause pneumonia & CNS lesion
advantage on maintenance daily for 1 yr after
transplanatation include protection against Listeria
monocytogenes and Nocardial disease as well as late
infections with S. pneumoniae & H. influenzae which
are consequence of the inability of immature BM to
respond to polysaccharide antigens
VIRAL INFECTIONS
BMT/HSCT reciepents are susceptible to infection with
variety of viruses, including reactivation syndrome caused by mist
HHVS (Table 117-3) and infections caused by viruses that circulate
in the community.
HSV – Within 1st 2 weeks after transplantation
HSV-1 from oropharynx
prophylactic ACYCLOVIR (or VALACYCLOVIR) to
seropositive BMT/HSCT recipients reduce mucositis
and HSV pneumonia ( a rare condition reported
exclusively in BMT recipients).
Esophagitis due HSV-1 & anogenital disease HSV2
may be prevented with acyclovir prophylaxis
VZV – Reactivation may occur in 1st month but more commonly after
several months after transplantation.
40% in allogeneic patients and 25% for autlogous
recipients.
Disseminated disease could be controlled by
ACYCLOVIR ( given prophylactic) to prevent sever
disease. Low dose (400mg orally, TID) appear to be
effective in preventing reactivation.
However, it may also inhibit the dev’t of VZV-specific
immunity. Thus administration for only 6 months after
transplantation does not prevent zoster from occurring
when treatment is stopped.
Low dose for 1 year may be effective
CMV – onset of CMV disease(interstitial pneumonia, BM
suppression, or graft failure) usually comes betweedn 30 days and
90 days after transplantation, when granulocyte count is adequate
but immunologic reconstitution has not occurred.
it develops earlier than 14 days after transplantation
may be evident as late as 4 months after the
procedure.
Great concern in the 2nd month after transplantation,
particularly in BMT/HSCT recipients.
In donor marrow is depleted of T cells – disease is
manifested earlier
aCD52 antibody (alentuzumab)  prevent GVHD in
nonmeloablative transplantation
patients who receive gancyclovir (for prophylaxis,
preemptive treatment, or treatment) may develop
infection even later than 4 months after transplantation
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-
-
-
-
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although CMV disease may present isolated fever,
granulocyotpenia, or gi disease, the foremost cause of
death from CMV infection in this setting is
PNEUMONIA
with the std use of CMV0negative filtered blood
products, primary CMV infxn should be a risk in
allogenic transplantation only when the donor is CMVseropositive and the recipient is CMV-seronegative.
Reactivation or superinfection is common in CMV
seropositive recipients and seropositice patients who
undergo BM transplantation excrete CMV, with or
without clinical findings
Serious CMV disease is common among allogenic
than autologous recipients and is often associated
with GVHD.
Finding of CMVin liver of a patient with GVHD does
not necessarily mean that CMV iis responsible for
hepatic enzyme abnormalities.
MANAGEMENT: Prophylaxis  Ganciclovir (or
valganciclovir) abort CMV disease during the period of
maximal vulnerability (from engraftment to day 120
after transplantation). Adverse effects: dose-related
BM suppression (thrombocytopenia, leucopenia,
anemia, and pancytopenia).
Suppressive treatment – PCR evidence of CMV or
urine cultures positive for CMV, entails unnecessary
treatment of many individuals (on the basis of a lab
test that is not highly predictive of disease) with drugs
that have adverse effects.
Treatment of CMV pneumonia in BMT/HSCT recipient
requires both IVIg and ganciclovir.
Foscarnet, for patients who cant tolerate ganciclovir,
although it may produce nephrotoxicity and
electroloyte imbalance.
Transfusion of CMV-specific T-cells from the donor
decreased viral load in small series of patients.
HHV-6&7 - HHV-6 , cause of roseola in children, is a ubiquitous
herpesvirus that reactivates (as determined by culture of the virus
from the blood) in 50% of transplant patients between 2 and 4 weeks
after surgery
EBV
appears to be asso with neutropenia, since, like CMV,
this can be found in marrow cells
although encephalitis developing after transplantation
has been asso with HHV-6 in CSF,the causality of the
association is not well defined.
May be found in lung samples after transplantation
susceptible to foscarnet ( and possibly to ganciclovir)
- Primary EBV infection can be fatal to transplant recipients
EBV reactivation can cause EBV-B cell
lymphoproliferative disease (LPD), which may be fatal
in patients taking immunospuppressive drugs.
Marrow ablation that occurs as part of BMT/HSCT
procedure may eliminate latent EBV from the host.
Infection may be reacquired immediately after
transplantation by transfer if infected donor B cells.
Reactivation can occur in T-cell depleted autologous
recipients (patients being given antibioses to T cells
for treatment of a T-cell lymphoma with marrow
depletion).
EBV-LPD, becomes apparent as soon as 1 to 3
months after engraftment, causes high fever, and
cervical lymphadenopathy resembling the symptoms
of infectious mononucleosis but more commonly
presents as an extranodal mass..
In all cases, EBV-LPD is more likely to occur with
continued immnosuppression (especially that caused
by the use of antibodies to T-cell and cyclosporine or
other T-cell suppressive agents).
1st line treatment: Monoclonal anibody to CD20
(rituximab) for treatment of B cell lymphomas
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Ganciclovir has been postulated to have activity on
the basis of its ability to inhibit proliferation of B cells,
but is asso with high toxicity.
High-dose Ziduvidine – shows a promising effect for
treatment of EBV positive CNS lymphomas
Both interferon alpha and retinoic acid have been
used
As has IVIg
HHV – 8 – EBV related gamma herpesvirus which is usually asso
with Kaposi’s sarcoma, with primary effusion lymphoma, and
sometimes with multicentric Castleman;s disease, has rarely resulted
in disease in BMT/HSCT recipients.
Other (nonherpes) virus –
Both RSV and parainfluenza particularly type 3, can
cause severe or fatal pneumonia in BMT recipients.
Therapy with aerosolized ribavirin as well as RSV Ig
or monoclonal ab to RSV(palivizumab) has been
reported to lessen severity of RSV disease
Influenza also occurs in BMT recipients and generally
mirrors the presene of infection in the community.
(amantadine/rimantadine, ribavirin?), but have limited
effects, primarily reducing symptoms and shortening
the duration of illness. Neuraminidase inhibitors
(oseltamivir and zanamivir) are active against
Influenza Typa A and B and are a reasonable
treatment option.
Adenovirus occurs in 1st or 2nd month after
transplantation., is often asymptomatic.
Parvovirus B19 (presenting as anemia, or occasionally
as pancytopenia) can be treated with IVIg and
enterovirus can occur and being treated with
Pleconaril, a capsid binding agent.
Rotavirus are common cause of gastroenteritis in
BMT/HSCT recipients.
Polyomavirus BK is found at high titers in the urine of
patients who are highly immunosuppressed.
BK viruria may be asso with hemorrhagic cystitis.
PML by JC virus is rare among BMT/HSCT recipients
compared with the rate among patients with impaired
T cell function due to HIV infection.
INFECTIONS IN SOLID ORGAN TRANSPLANT RECIPIENTS
Organisms that cause infections in recipients of solid organt
transplant recipients are different from those that infect BMTHSCT
because solid organ recipients do not go through neutropenia.
As the transplantation procedure involves surgery, however, solid
organ recipients are subject to infections at anastomotic sites and to
wound infections.
Compared with BMT/HSCT, organ transplant patients are
immunosuppressed for longer periods (often permanently). Thus they
are susceptible to organisms as patients with chronic impaired T cell
immunity.
Early period (< 1month after transplantation),infections are most
commonly due to extracellular bacteria ( staph, strep, e. coli and
other gram-neg bacteria), which often originate in surgical wound or
anastomotic sites.
In subsequent weeks, consequences of the administration of agents
that suppress cell-mediated immunity and of the acquisition or
reactivation of virus and parasites become apparent.
CMV infection – first 6 months
HHV-6 reactivation – occurs within the 1st 2 to 4 weeks and may be
asso with fever and granulocytopneia
HHV6&7 – exacerbate CMV disease
CMV – asso not only with generalized immunosuppression but also
with organ specific, rejection-related syndromes, glomerulopathy in
kidney transplant patients, bronchitis obliterans in lung transplant ,
vasculopathy in heart transplant, and vanishing bile duct in liver
transplant.
Beyond 6 months, infections characteristic of patients with defects in
cell-mediated immunity – L. monocytogenes, Nocardia, various fungi
and intracellular parasites.
May be susceptible to EBV-LPD from as early as 2 months to many
years after transplantation.
The prevalence of this complication is increased by potent and
prolonged used of T-cell suppressive drugs.
Among organ transplant patients, those with heart and lung
transplants- who receive most intensive immunosuppressive
regimens- are most likely to develop EBV-LPD.
KIDNEY TRANSPLANT
Early infections
often caused by bacteria asso with skin or wound
infections.
There is a role for perioperative antibiotic prophylaxis
Cephalosporins to decrease risk of postoperative
complications.
UTI developing soon after transplantation are usually
related to anatomical alterations resulting from
surgery.
UTI that occur >6 months after transplantation do not
seem associated with high rate of pyelonephritis or
relapse seen with infections that occur in 1st 3 months
and may be treated in shorter periods.
Prophylaxis with TMP-SMX for the 1st 4 months after
transplantation decreases incidence of early and
middle-period infections.
Middle-Period infections
predisposal to lung infection characteristic of those In
patients with T-cell deficiency with intracellular
bacteria, mycobacteria, nocardiae, fungi, viruses and
parasites.
50% of all renal transplant recipients with fever in 1 to
4 months after transplantation has evidence of CMV
disease.
CMV may also present with athralgias or myalgias
During this period, this infection may present as
primary disease, or may present as reactivation or
superinfection.
Px may have atypical lmphocytosis. Unlike
immunocompetent patients, however, they often do
not have lyphadenopathy or splenomegaly.
CMV may also cause glomerulopathy.
Ig enriched with ab to CMV decreases incidence in
group at higher risk (seronegative recipient of
seropositive kidneys)
Ganciclovir – useful prophylaxis and treatment of CMV
disease
Prophylacitv valacyclovir for the first 90 days after
renal transplantations shows 50 % reduction in CMV
disease and rejection at 6 months
Herpes group infection become evident within 6
months of infection.
HSV cause either oral or anogential lesions that are
responsive to acyclovir.
VZV may cause fatal disseminated infection in
nonimmunie kidney transplant recipiens, but in imunie
patients may cause reactivation zoster usually does
not disseminate outside dermatome.
HHV-6 may be reactivated and (usually
asymptomatic) may be associated with fever, rash,
suppression, encephalitis
EBV reactivation disease is more serious; it may
present as extranodal proliferation of B cells that
invade the CNS, naspharynx, liver, small bowel, heart
and transplanted kidneys.
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Disease may regress once immunocompetence is
restored.
HHV-8 asoo with development of Kaposi’s sarcoma
often appears within 1 year after transplantation,
although the range is wide (1 month – 20 years)
Papovavirus BK and JC have been cultured from the
urine of kidney transplant recipients. The excretion kf
BK virus is asso with urethral strictures
Patients may develop pulmonary infections with
Nocardia, Aspergillus, and Mucur as well as other
intracellular organisms.
In patients with IV catheter, L. monocytogenes is a
common cause of bacteremia > 1 month after renal
transplantation and should be seriously considered in
recipients presenting with fever and headache.
Salmonella bacteremia may lead to endovascular
infections and require a prolonged therapy.
Nocardia occur generally > 1 month after
transplantation and may follow immunosuppressive
treatment episode of rejection. May present as skin,
bones, and lungs or in CNS in single or multiple
abscesses.
TMP-SMX is often efficacious.
Late infections
 6 months after kidney transplantation include CMV retinitis and
a variety of CNS complication.
 Patients whose immunosuppression has been increased, are
at high risk of Subacute meningitis due to Cryptococcus
neoformans
 Listeria meningitis, acute and fatal
 “Transplant elbow” to patients who take glucocorticoids; a
recurrent bacterial infection in and around the elbow that is
thought to result from a combination of poor tensile strength of
the skin of steroid-treated patients.
 Bouts of cellulites due to S. aureus
 Susceptible to Aspergillus and Rhizopus which may present as
superficial lesions before dissemination
 M. marinum diagnosed by skin examination
 Protheteca wickerhamii by skin biopsy
 Warts caused BY HPV
HEART TRANSPLANTATION
Early infection
Sternal wound infection and mediastinitis as early complication
Common microbes in the skin are involved can also be due
Mycoplasma hominis can be cured with a combination of surgical
debridement (sometimes requiring muscle flap placement) plus
clindamycin and tetracycline.
Middle Period infections
T. gondii  TMP-SMX
CMV – 1 to months after transplantation causes early signs and lab
abnormalities (usually with fever and atypical lymphocytosis
orleukopenia and thrombocytopenia) at 2 to 3 months, and produces
severe disease (pneumonia) in 3 to 4 months.
Ganciclovir is efficacious
Late infections
EBV infection usually present as a lymphoma-like proliferation of Bcells late after heart transplantation especially in patients on heavy
immunosuppression.
LUNG TRANSPLANTATION
Early infection
combination of ischemia and resulting mucosal
damage together with accompanying denervations
and lack of lymph drainage probably contributes to
high rate of pneumonia.
Prophylactic use od high doses broad spectrum
antibiotics for first 3-5 days after surgery decreases
incidence of pneumonia
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Gram negative organisms (pseudomonas and
enterobacteriaceae) are troublesome in first 2 weeks
after surgery.
It can also be caused by Candida, Aspergillus and
Cryptococcus.
Mediastinitis may occur at higher rate and most
commonly develops within 2 weeks of surgery,
Pneumonitis due to CMV usually present within 2
wekks and 3 months after surgery, with primary
disease occurring later than reactivating disease.
Middle-period infection
75 to 100% incidence of CMV infection.
More than half has CMV pneumonia
CMV can also cause bronchitis obliterans
Ganciclovir is more active against CMV and also HSV.
Prophlaxis is recommended.
Late infections
Incidence of Pneumocystisinfection is high among
heart-lung recipients.
TMP-SMX for 12 months after transplantation may be
sufficient for 12 months after transplantation.
EBV may cause either mononucleosis-like syndrome
or LPD.
The tendency of B cell blasts to present on lung
appears to be greater after lung transplantation than
after the transplantation of other organs.
LIVER TRANSPLANTATION
Early infections
Administratioin of systemic broad-spectrum antibiotics
for the first 5 days after surgery, even in the absence
of documented infection,
However, despite prophylaxis, infectious
complications are common and are correlated with the
duration of the surgical procedure and the type of
biliary drainage.
Operation lasting >12 hrs is asso with high likelihood
of infection.
Patients who have choledojejunostomy with drainage
of the biliary dure to a Roux-en- Y jejunal bowel loop
have more fungal infections thant those whose bile is
drained via a choledochocholedochostomy with
anastomosis of the donor common bile duct to the
recipient common bile duct.
Peritonitis and intraabdominal abscesses are common
complications of liver transplantation.
Bacterial peritonitis may result from biliary leaks and
primary and secondary infection after leakage of bile.
Abscesses within the 1st month after surgery may
occur not only over the liver but also in the spleen,
pericolic area and pelvis.
treatmentL antibiotic and drainage as necessary
Middle Period Infections
development of postsurgical biliary stricture
predisposes patients to cholangitis. These patients
may lack the characteristic signs and symptoms of
cholangitis: fever, abdominal pain and jaundice.
Alternatively, may be present but suggests graft
rejection.
Invasive studies of biliary tract (either T-tube
cholangiography or endoscopic retrograde
cholangiopancreatography) may lead to cholangitis.
For this reasons, prophylaxis with antibiotics covering
gram – negative and anaerobes is recommeneded
when these procedures are performed in liver
transplant patients
Reactivation of HepaB and C
High dose Hepa B Ig to prevent Hepa B. Long term
efficacy of lamivudive and aefovir in inhibiting hepa b
viral replication after transplantation is being studied
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Combination of interferon alpha and ribavirin is being
tested for treatment /prophylaxis of Hepa C.
CMV causes vanishing bile syndrome after liver
transplantation
PANCREAS TRANSPLANTATION
To prevent contamination of the allograft with enteric bacteria and
yeasts,some surgeons, instead of draining the pancreas through the
bowel, drain secretions into urinary tract or bladder.
Bladder drainage casuses a high rate or UTI and sterile cystitis.
Prophylactic antimicrobials or transplantation of islet cells only as
alternative.
MISCELLANEOUS INFECTION
IV catheter poses a risk of local and bloodstream infection, significant
insertion-site-infection is most commonly caused by S. aureus.
Coaugulase-neagative Staph are the most common isolates from the
blood.
Tuberculosis
-Occurring within 12 months after solid organ
transplantation.
- It has been rarely transmitted from the donor organ.
Virus-associated Malignancies
transplant patients may develop nonmelanoma skin or
lip cancers, that, in contrast to de novo skin cancers,
have high ratio of squamous cells to basal cells.
Among renal transplants, rates of melanoma are
modestly increased and rates of ca of kidney and
bladder are increased.
VACCINATION OF TRANSPLANT RECIPIENTS
recipients of allogenic BMTs must be reimmunized if
they are to be protected against pathogens.
In the absence of compelling data as to optimal timing,
it is reasonable to administer pneumococcal and HiB
conjugate vaccines to both autologous and allogenic
BMT recipients 12 months after transplantation and
again 12 months later.
pneumococcal and HiB are important for patients whi
have undergone splenectomy.
N. meningitides polysaccharide vaccibe, diphtheria,
tetanus, and inactivatedpolio vaccines can all be given
at these same intervals (12 and 24 months after
transplantation)
Some authorities, recommend (12, 14 and 16 months
after transplantation)
Because of risk of spread, household contacts of BMT
recipients should receive only inactivated polio
vaccine.
Live attenuated vaccines(MMR) can be given to
autologous BMT recipients 24 months after
transplantation and to most allogenic BMT recipients
at the same point if they are receiving ,aintenance
therapy with immunosuppressive drugs and do not
have ongoing GVHD.
Avoid all live-virus vaccines in patients who have
GVHD and/or taking high maintenance dose of
glucocorticoids.
Solid organ transplant recipients
all the usual vaccines and of the indicated booster
doses should be completed before
immunosuppression, if possible, to maximize
responses.
For taking immunosuppressive agents, the
administration of pneumoccocal vaccine should be
repeated every 5 years.
H influenzae conjugate vaccine is safe and should be
efficacious in this population; therefore, its
administration is recommended.
Person exposed to measles should receive Ig
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Seronegative for Varicella and comes in contact with a
person who has chicken pox should be given VZIg
asap (and certainly within 96 hrs) or, if this is not
possible, should be started immediately on a 10-14
day couese of acyclovir therapy.
Susceptible household contacts should receive live
vaccines
- Immunocompromised patients who travel may benefit
from some but not all vaccines.
CHAPTER 117 INFECTIONS IN TRANSPLANT RECEPIENTS
A. BONE MARROW TRANSPLANT
INFECTIONS: 1st month of bone marrow transplant
LEVOFLOXACIN: decreases bacteremia maong bone marrow
transplant px
1st few days: common org: aerobic( E coli, klebsiella, Pseudomonas
and thru skin or catheter ( Staph coag -/+)
beyond 1st few days; Filamentous bacteria ( Nocardia/
Actininomyctes)
Late posttransplant: encapsualted org (>6 months after BM
reconstitution)
beyond 1st week: fungal (candida)
TMP-SMX- prophylactic for Pneumocystis; 1 month after engrafment
and continiung for at least 1 year
- prophylactic also for Toxoplasma, Listeria, Nocardia,
Strep and haemophilus
ACYCLOVIR: prophylactic for seropositve BMT/SCT; reduce
mucositis and prevent HSV pneumonia
: 2 wks after BMT excretion of virus of seropositve HSV 1
_ also good for Varicella- Zoster virus (low dose for the
entire year)
CMV: 30- 90 days after transplant: great concern on the 2nd month
-assoc w/ used of alpha CD52 antibody among GVHD px
-Ganciclovir- delay the devt of normal immune rsponse to
CMV, not really protective
- IVIg and Ganciclovir: tx for CMV pneumonia
HHV-6 / Roseola- 2-4 wks after surgery: ? foscarnet
EBV- fatal to transplant recepients
-lymphopriliferative disease (LPD) - 1-3 months after
engrfment
- tx: ? EBV specific T cells; Rituximab , ganciclovir;
zidovudine
HHV -8 - Kaposi' s Sarcoma, primary effusion sarcoma, castle man
RSV and Parainfluena- fatal pneumonia on BMT
- tx: aerosolized Ribavirirn, RSV Ig ,Palivizumab
Influenza- Oseltamivir and Zanamivir
Rotavirus- gastoenteritis
Polyomavirus BK- hemorrhagic cystitis
B. SOLID ORGAN TRANSPLANT
Early period( <1 month)- extracellular ( Staph, strep, e coli,)
- origin : surgical wound or anostomotic sites
CMV- 1st 6 months; sever systemic disease
HHV 6 reactivation- w/in 1st 2 to 4 wks; fever and granulocytopenia
CMV rejection related syndromes:
- glomerulopathy- kidney
-bronchilitis obliterans- lung transplant
-vanishing bile duct syndrome- liver transplant
Beyond 6 months: defects on CMI ( listeria , nocardia, fungi other
intracellular org)
EBV_LPD- 2 months to many years after transplant; heart and lung
transplants
1) KIDNEY TRANSPLANTS
-Early: due ti skin and wound infections; Tx:
Cephalosporins
-UTI- due to anatomical alterations from surgery
(pyelonephritis)-longer duration of tx
appear after 6 mos: shorter duration of tx
-Prophylaxis: TMP-SMX
-Middle period- lung infections w/ T-celldef( ICbacteria,
nocardia, fungi, virus, parasite)
-Legionella pnuemophilia- high mortality
- CMV- 1 to 4 months -fever, glomerulopathy; tx: administer
Ig w/ antibodies w/ CMV
-EBV reactivation- extranodal prolif of B cells; invade CNS,
nasopharynx, liver, small bowel heart and transplanted kidney
-PAPOVAVIRUS:BK-nepropathy; JC virus- progressive
multifocal leukoencephalopathy
- L. monocytogenes- most common cause of bacteremia
>= 1 month after renal transplantation
-NOCARDIA- skin, bones, lungs and CNS, multiple
abscess
-Late infection (>6 months) - CMV retinitis, transplant
ebow?, invasive fungal
2) HEART TRANSPLANTS
-early: sternal wound infxn and mediastinitis
-dx: sternal instability and failure to heal
-middle: toxoplasmosis, CMV ,CNS infxn
- late: EBV-lymphoma like
3) LUNG TRANSPLANTS
-eearly: ischemia and mucosal damage, denervtion and
lack of lymph drainage
- prophylactic broad spectrum 1st 3 to 4 days antibiotics
4) LIVER TRANSPLANTS
- infection on early; systemic broad spectrum antibiotic for
the 1st 5 days
- operation >12 hrs - inc incidence of infection
-PERITONITIS and Intraabdominal Abscess- Common
complication
-Peritonitis- from biliary leak and primary or 2ndary
infx,polymicrobil
-Abscess- w/in 1st month, spleen, liver, pericolic and
pelvis,Tx: antibiotic and drainage
-middle: Cholangitis- devt postsurgical stricture on biliaryfever abdominla paina nd jaundice
-Viral hepatitis- lamiduvine and adefovir for hepa B
5) Pancreas
-infection prevented by draining pancreas to urinary tract or
bladder
INdwelling cathter- S. aureus- bloodstream infxn w/in a week
Tuberculosis- w/in 12 months
VACCINATION:
For autologous and allogenic BMT recepients-(1 year and 2 years
after)
1) pneumococcal
-repeated every 5 years for px on immunosuppresants
-every 3 years w/ significant exposure risk
2) H. Influenza type b conjugate vaccines
Add: (12-14and 16 months after)
3) N. meningitides polysaccharide disease
4) diphtheia vaccines
5) tetanus vaccine
6) inactivated polio vaccine
OTHERS:
7) Live virus MMR- BMT recepients 24 mos after transplant