ubiquitous virus known to cause febrile syndromes and exanthema subitum in children. Less
commonly, and particularly in organ transplant recipients, it may cause hepatitis, bone
marrow suppression, interstitial pneumonitis, and meningoencephalitis (201–207). In a recent
review, HHV-6 encephalitis occurs a median of 45 days (range 10 days to 15 months) after
transplantation. Mental status changes ranging from confusion to coma (92%), seizures (25%),
and headache (25%) were the predominant clinical presentations. Focal neurological findings
were present in only 17% of the patients. Twenty-five percent of the patients had fever,
occasionally reaching 40 8 C. Cerebrospinal fluid pleocytosis was generally lacking. Magnetic
resonance images of the brain may reveal multiple bilateral foci of signal abnormality
(nonenhancing involving both gray and white matter). HHV-6 can be detected in cerebrospinal
fluid by PCR or by viral isolation. HHV-6 viremia was documented in 78% of the patients.
Overall mortality in patients with HHV-6 encephalitis was 58% (7 of 12); 42% (5 of 12) of the
deaths were caused by HHV-6. Cure was documented in 7 of 8 patients who received
ganciclovir or foscarnet for7 days, compared with 0% (0 of 4) in those who did not receive
these drugs or received them for<7 days (p¼0.01) (203). A growing body of evidence
suggests that the more important effect of HHV-6 and HHV-7 reactivation on the outcomes of
liver transplantation may be mediated indirectly by their interactions with CMV (204). HHV-6
viremia is an independent predictor of invasive fungal infection (208).
CMV infection of the CNS is quite uncommon in SOT recipients. It may affect the brain
(diffuse encephalitis, ventriculoencephalitis, cerebral mass lesions) or the spinal cord
(transverse myelitis, polyradiculomyelitis). Diagnosis is very difficult and should be based
on clinical presentation, results of imaging, and virological markers. The most specific
diagnostic tool is the detection of CMV DNA by PCR in the CSF. Treatment should be initiated
promptly if CMV infection is suspected. Antiviral therapy consists of IV ganciclovir, IV
foscarnet, or a combination of both. Cidofovir is the treatment of second choice. Patients who
experience clinical improvement or stabilization during induction therapy should be given
maintenance therapy (209). Encephalitis caused by HSV has also been described (210,211).
Among causes of encephalitis, West Nile virus (WNV) has emerged as an important
cause of several outbreaks of febrile illness and encephalitis in North America over the past
few years. In a recent report, 11 transplant recipients with naturally acquired WNV
encephalitis were identified (4 kidney, 2 stem cell, 2 liver, 1 lung, and 2 kidney/pancreas).
Ten patients developed meningoencephalitis, which in three cases was associated with acute
flaccid paralysis. All patients had cerebrospinal fluid pleocytosis and WNV-specific IgM in the
cerebrospinal fluid and/or serum. Magnetic resonance images of the brain were abnormal in
seven of eight tested patients, and electroencephalograms were abnormal in seven of seven,
with two showing periodic lateralized epileptiform discharges. Nine of 11 patients survived
infection, but 3 had significant residual deficits. This viral infection should be considered in all
transplant recipients who present with a febrile illness associated with neurological symptoms
(212–214).
L. monocytogenesinfections can occur at almost any time, although the most common
occurrence is two to six months posttransplant (215). The incidence has significantly been
reduced since prophylaxis with cotrimoxazole is used (111).Listeriainfections may present as
isolated bacteremia or with associated meningitis (216,217). OLT recipients may present with
acute hepatitis (218). Brainstem encephalitis or rhomboencephalitis have been characteristi-
cally described in patients with listeriosis in which cranial nerve palsies or pontomedullary
signs may be observed. Cerebritis/abscess due toL. monocytogenes, without meningeal
involvement, is less common (219).
Incidence of cryptococcosis after organ transplantation is 2.6% to 5% and CNS is
involved in 25% to 72% of the patients (220–223).Cryptococcusis mostly a cause of meningitis,
pneumonia, and skin lesions (224–227). Cryptococcomas are rare (228). However, more
uncommon sites of infection have been also described in immunocompromised patients such
as hepatic cryptococcosis in an HT recipient (229). The patient developed fever, dyspnea, and
signs of liver damage. Diagnosis was made with liver biopsy and with cryptococcal antigen in
serum (229). Cryptococcosis is usually a late disease after transplantation, although rare
fulminant early cases have been reported (230). CSF analysis usually reveals moderate
Infections in Organ Transplants in Critical Care 401