Case Report

DOI 10.3349/ymj.2010.51.1.131
pISSN: 0513-5796, eISSN: 1976-2437

Yonsei Med J 51(1): 131-137, 2010

Cerebellar Nocardiosis and Myopathy from Long-Term
Corticosteroids for Idiopathic Thrombocytopenia
Marlies Frank,1 Herbert Woschnagg,1 Günther Mölzer,2 and Josef Finsterer3
1

First Medical Department, 2Department of Radiology, 3Hospital Rudolfstiftung, Vienna, Austria.

Infection of the central nervous system with Nocardia sp. usually manifests as supratentorial abscesses. Supratentorial
and cerebellar abscesses from infection with Nocardia sp. following immunosuppression with long-term
corticosteroids for idiopathic thrombocytopenia (ITP) have not been reported. An 83 years-old, human immunodeficiency virus (HIV)-negative, polymorbid male with ITP for which he required corticosteroids since age 53 years
developed tiredness, dyspnoea, hemoptysis, abdominal pain, and progressive gait disturbance. Imaging studies of
the lung revealed an enhancing tumour in the right upper lobe with central and peripheral necrosis, multiple
irregularly contoured hyperdensities over both lungs, and right-sided pleural effusions. Sputum culture grew
Nocardia sp. Neurological diagnostic work-up revealed dysarthria, dysphagia, ptosis, hypoacusis, tremor,
dysdiadochokinesia, proximal weakness of the lower limbs, diffuse wasting, and stocking-type sensory
disturbances. The neurological deficits were attributed to an abscess in the upper cerebellar vermis, myopathy from
corticosteroids, and polyneuropathy. Meropenem for 37 days and trimethoprime-sulfamethoxazole for 3 months
resulted in a reduction of the pulmonary, but not the cerebral lesions. Therefore, sultamicillin was begun, but
without success. Long-term therapy with corticosteroids for ITP may induce not only steroid myopathy but also
immune-incompetence with the development of pulmonary and cerebral nocardiosis. Cerebral nocardiosis may not
sufficiently respond to long-term antibiotic therapy why switching to alternative antibiotics or surgery may be
necessary.
Key Words: Infection, brain abscess, opportunistic, antibiotics, steroid myopathy, immunosuppression

Received: January 22, 2008
Revised: May 9, 2008
Accepted: May 14, 2008
Corresponding author: Dr. Josef Finsterer,
Hospital Rudolfstiftung, Postfach 20, 1180
Vienna, Austria.
Tel: 43-1-71165, Fax: 43-1-4781711
E-mail: fifigs1@yahoo.de
∙The authors have no financial conflicts of
interest.

INTRODUCTION
Central nervous system (CNS) affection taking the form of supratentorial, cerebellar, or spinal cord abscesses from hematogenic dissemination of a pulmonary
infection with Nocardia sp. is a rare finding,1,2 and the induction of nocardiosis
due to long-term therapy with corticosteroids for idiopathic thrombocytopenia
(ITP) is more rarely found.3-5 Two of these cases developed supratentorial abscesses.
However, both cerebellar and supratentorial abscesses from Nocardia sp. in a
patient under corticosteroids for ITP, have not been reported.

CASE REPORT

© Copyright:
Yonsei University College of Medicine 2010

The patient is an 83 years-old, human immunodeficiency virus (HIV)-negative,
Caucasian male, with a history of recurrent nasal bleedings since childhood,
recurrent gingival bleedings, frequent cutaneous hematoma after minor traumata,
which were attributed to ITP diagnosed at age 52 years, splenectomy at age 52
years for the ITP, coronary heart disease resulting in two myocardial infarctions at

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131

Marlies Frank, et al.

age 52 years, corticosteroids for ITP since age 53 years,
steroid-induced diabetes mellitus since age 53 years, requiring insulin since age 78 years, arterial hypertension since
years, hyperlipidemia since age 53 years, percutaneous
transluminal coronary angioplasty at age 62 years, aortocoronary bypass grafting at ages 64 and 75 years, atrial
fibrillation since age 68 years, cataract surgery at ages 71
and 74 years, bilateral carotid artery stenosis requiring stent
implantation at age 72 years, a 6-fold stent placing for coronary stenoses at age 75 years, bilateral hypoacusis since
age 78 years requiring hearing devices bilaterally and
sensori-motor polyneuropathy since age 78 years. Since
age 82 years, he also noted a mild cognitive decline and
non-specific visual impairment and started to use a stick
for walking and a walker since two weeks prior to admission. His family history was positive for diabetes mellitus
and short stature in his mother. From age 68 years until
admission, he was taking phenprocoumon.
He was admitted at age 83 years because of chronic
tiredness, dyspnea, hemoptysis, and abdominal pain. Blood
chemical findings showed leucocytosis with a maximum
value of 38.8/nL (n, 4.0-9.0/nL) on hospital day (hd) 3,
thrombocytopenia with a minimum value of 4/nL (n, 150450/nL) on hd 15 and hd 18, renal insufficiency, and
elevated C-reactive protein with a maximum value of 34.7
mg/dL (n, ≤ 0.6 mg/dL) at hd 3 (Table 1). There were also
elevated glutamate-oxalate transaminase, glutamate pyruvate transaminase, and lactate dehydrogenase (Table 1).
Creatine-kinase was normal throughout hospitalization.
There was slight hypocalcemia (Table 1) and elevation of
ferritin to 3817 ng/mL (n, 30-400 ng/mL). Thyroid function
parameters were indicative of hyperthyroidism. The HbA1c
was 7.4% (n, ≤ 6%). X-ray of the lung revealed multiple
reticulonodular infiltrates up to one cm in diameter over

both lungs with predominance in the left lower lobe, a
pleural effusion in the horizontal interlobar fissure, and an
encapsulated effusion in the right-sided diagonal interlobar
fissure. X-ray of the lung five weeks earlier had been
normal. A CT-scan of the thorax showed an 11×7 cm,
enhancing mass lesion in the right upper lobe with central
and peripheral necrosis and multiple irregularly contoured
hyperdensities over both lungs (Fig. 1). Sputum cultures
grew Nocardia sp.
Clinical neurologic examination revealed slight dysarthria, dysphagia, bilateral ptosis, bilateral hypoacusis,
postural tremor, left-sided dysdiadochokinesia, weakness
for hip extension bilaterally (M5-), reduced tendon reflexes
on the upper limbs and absent tendon reflexes on the lower
limbs, diffuse wasting, stocking-type sensory disturbances
bilaterally, and ataxic stance. He was able to walk with a
walker. MRI of the cerebrum showed a hyperintense,
enhancing lesion of 4 mm in diameter in the cranial part of
the cerebellar vermis (Fig. 2). Additionally, there were small
hyperintense lesions in the occipital deep white matter and

Fig. 1. CT-scan of the thorax showing an enhancing mass lesion in the right
upper lobe with central and peripheral necrosis and multiple irregularly
contoured hyperdensities over both lungs.

Table 1. Hematological and Blood Chemical Values of the Described Patient during Hospitalisation for Nocardiosis
Parameter RL
hd 1
hd 2
hd 3
hd 7 hd 12 hd 18 hd 23 hd 30 hd 36 hd 44
Leuko
4.0 - 9.0/nL
30.5
32.5
38.8
22.6
32.1
13.2
14.8
20.5
21.8
22.3
Ery
4.2 - 5.5/pL
4.5
4.5
4.3
4.1
4.5
3.9
3.8
4.8
4.4
4.6
Thrombo 150 - 450/nL
32
27
28
12
9
4
6
17
12
15
BUN
9 - 20 mg/dL
42
42
42
31
53
39
nd
40
nd
nd
Krea
≤ 1.1 mg/dL
1.2
1.2
1.3
1.3
1.7
1.8
nd
1.7
nd
nd
CRP
≤ 0.6 mg/dL
14.4
13.9
34.7
5.3
1.5
3.2
nd
0.5
nd
nd
GOT
≤ 34 U/L
nd
30
nd
46
nd
60
nd
nd
nd
nd
GPT
≤ 44 U/L
nd
64
nd
103
nd
50
nd
nd
nd
nd
LDH
≤ 247 U/L
nd
317
nd
nd
nd
384
nd
nd
nd
nd
CPK
≤ 170 U/L
112
66
nd
nd
nd
39
nd
nd
nd
nd
Calcium 2.1 - 2.7 mmol/L 1.9
2.0
nd
1.8
1.6
nd
nd
1.9
nd
nd
RL, reference limit; hd, hospital day; Leuko, leukocyte count; Ery, erythrocyte count; Thrombo, thrombocyte count; BUN, blood urea nitrogen; Krea, creatinine;
CRP, C-reactive protein; GOT, glutamate-oxalate-transaminase; GPT, glutamate-pyruvate-transaminase; LDH, lactate-dehydrogenase; CPK, creatine-phosphokinase; nd, not done.

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Cerebellar Nocardiosis and Myopathy from Long-Term Corticosteroids for Idiopathic Thrombocytopenia

subcortically bilaterally (Fig. 2). Lumbar puncture was
recommended, but contraindicated due to ITP. No manifestations of nocardiosis other than in the lung and cerebrum were detected.
For ITP, the patient received prednisolone 50 mg/d until
hd 9. For the general infection, he initially received amoxicillin between hd 2 and hd 4. From hd 4 to hd 7, he received
caspofungin and between hd 5 and hd 7 piperazillin. Meropenem was started on hd 8 and maintained until hd 45. He
had never developed fever during the entire hospitalization. After dismissal, the patient was switched to a longterm therapy with trimethoprim-sulfamethoxazol. Shortly
after admission, oral anticoagulation was stopped because
of severe thrombocytopenia of 4,000/nL (Table 1). Since hd
23, corticosteroids had to be restarted because of deteriorating ITP (Table 1). His therapy at dismissal included
danazol, furosemide, pantoprazole, atorvastatin, metoprolol, enalapril, amiodarone, prednisolone, folic acid, and
insulin in addition to the antibiotic. At the three month
follow-up, dimension of the pulmonary lesions had regressed. On the contrary, the cerebral lesions had progressed

A

B
Fig. 2. T1-weighted MRI images of the brain show a slightly enhancing mass
lesion in the cerebellar vermis (A) and a hyperintense lesion in the right occipital
lobe (B).

despite trimethoprim-sulfamethoxazol, promting a switch
to sultamicillin and then to meropenem. Unexpectedly, the
patient died from acute myocardial infarction shortly
thereafter. Autopsy excluded a pulmonary malignancy as
the underlying cause of nocardiosis and confirmed that
antibiotic therapy was not effective in eradicating the
cerebral infection, although cerebral tissue cultures were
negative for Nocardia sp.

DISCUSSION
Nocardiosis is an opportunistic local infection with consecutive hematogenic spread in half of the cases from the
Gram-positive, filamentous, eosinophilic organism Nocardia
sp. The most frequently found species is N. farcinica,6,7
followed by N. asteroides,8-10 N. paucivorans,11 N. otitidiscaviarum,12 N. brasiliensis,13 N. cyriacigeorgica,14,15 or N.
transvalensis.14,16,17 Nocardiosis is an uncommon disease,
but its frequency has increased due to the high number of
immunosuppressive treatments, improved diagnostic facilities, and increasing survival times of patients with malignancy.18 Patients become infected by inhalation, direct
traumatic cutaneous inoculation, or by eating contaminated
food.19 The most common primary site of nocardiosis is the
respiratory tract, being the origin of hematogenic dissemination with a high incidence to the skin, subcutaneous
tissue, or CNS.6,19,20 Extra-pulmonary manifestations of
nocardiosis include CNS abscesses or meningitis,6 chorioiditis,6 intraocular vasculitis,21 or renal abscesses.22 Most
patients have an underlying chronic diseases or suffer from
endogenous or drug-induced immunosuppression with for
instance TNF-alpha blockers, but Nocardia can also infect
healthy subjects.23 Culture or biopsy followed by identification of the infectious species by PCR is recommended
because of the specific therapeutic strategies associated
with each species and their different sensitivity to antibiotics.6 Because of the high relapse rates, treatment is recommended to be continued for 12 months.24
CNS nocardiosis usually manifests as cerebral abscesses
or rarely as meningitis or chorioiditis. The abscesses usually
develop supratentorially but cerebellar abscesses have
been also reported (Table 2).2,25-27 Though the preference of
Nocardia sp. for the CNS is well known, CNS abscesses
from Nocardia sp. are rare and account for only 1-2% of
brain abscesses.1,28 In almost half of the patients with pulmonary nocardiosis, dissemination is associated with brain
abscesses.10 Early detection and treatment is important
because the mortality is three times higher than that of
other bacterial cerebral abscesses.28 Since the literature
about CNS nocardiosis takes the form of anecdotal reports,
small case series, or retrospective studies (Table 2), an

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Marlies Frank, et al.

Table 2. Previous Reports during the Last 10 Years about Cerebral Nocardiosis
Reference
Abscess localisation
N
34
Hashimoto, et al.
Cerebrum
1
Kennedy, et al.35
Cerebrum
4
8
Borchers, et al.
Both hemispheres, cerebellum
1
Nakamura, et al.10
Cerebrum
1
Oztürk, et al.36
Cerebrum
1
19
Aboal, et al.
Cerebrum, recurrent
1
Dahan, et al.37
Cerebrum
1
38
Ghalib, et al.
Cerebrum, multiple
1
39
Kilincer, et al.
Cerebrum, cerebellum
2
Ozaras, et al.40
Cerebrum
1
41
Pieroth, et al.
Cerebrum, multiple
1
Sonesson, et al.23
Cerebrum, multiple
1
42
Oshiro, et al.
Right parietal, rupture, meningitis
1
17
Yorke, et al.
Cerebrum
1
Börm, et al.43
Left parietal
1
Valarezo, et al.28
Cerebrum
2
44
Montoya, et al.
Cerebrum
1
Shin, et al.28
Cerebrum, multiple
1
45
Mooraki, et al.
Cerebrum
1
Schriever, et al.6
Cerebrum, multiple
1
46
Murray, et al.
Cerebrum, multiple
1
47
Malincarne, et al.
Right fronto-parietal
1
Lee, et al.48
Cerebrum
7
26
Eisenblätter, et al.
Cerebellum
1
49
Weber et, al.
Cerebrum
2
Acar et, al.50
Cerebrum
1
51
Vialle, et al.
Cerebrum
2
Kayacan, et al.27
Frontal lobe, cerebellum
1
Durmaz, et al.25
Cererbum, cerebellum, spinal cord
1
1
Fleetwood, et al.
Cerebrum
3
Marlowe, et al.52
Cerebrum
1
53
Hartmann, et al.
Right frontal
1
54
Prieto de Paula, et al.
Cerebrum, meningitis
1
Palomares, et al.55
Left occipital
1
56
Cosnett, et al.
Cerebrum
1
Mogilner, et al.57
Chorid plexus
1
Oerlemans, et al.2
Cerebellum
1
58
Orsolon, et al.
Cerebrum
1
Fuzier, et al.59
Cerebrum
1
Machado, et al.60
Right frontal
1
61
Pyhtinen, et al.
Cererbum, multiple
1
Ogg et, al.62
Cerebrum
1
Peters, et al.20
Cerebrum
1

Outcome
Favorable
Favorable
Recovery
Recovery
Recovery
Ni
Recovery
Satisfactory
Satisfactory
Ni
Favorable
Fatal
Fatal
Ni
Favorable
Favorable
Favorable
Favorable
Satisfactory
Favorable
Ni
Favorable
Favorable
Favorable
Satisfactory
Ni
Favorable
Favorable
Fatal
Satisfactory
Ni
Favorable
Ni
Favorable
Ni
Favorable
Favorable
Ni
Ni
Favorable
Ni
Fatal
Favorable

N, number of patients; Ni, not indicated.

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Cerebellar Nocardiosis and Myopathy from Long-Term Corticosteroids for Idiopathic Thrombocytopenia

optimal treatment approach has not yet been established.
Abscesses with Nocardia sp. represent a diagnostic and
therapeutic challenge, since they are associated with high
mortality rates, particularly in immunocompromised patients. Cerebral abscesses are managed either conservatively
with stereotactic aspiration, or by open craniotomy and
enucleation.29 Surgical treatment is indicated if the lesions
are large and readily accessible or in case of progression of
the lesions within two weeks after initiation of the antibiotic
treatment. There is growing evidence that the size of the
cerebral lesion and clinical and immune status of the patient are relevant to surgical decision making. In spite of the
existing controversy with regard to the surgical management of these lesions, an early diagnosis through stereotactic aspiration and the beginning of an antibiotic therapy
are essential for a favorable outcome.19 In most cases of
cerebral nocardiosis the overall prognosis is favorable
upon adequate antibiotic or surgical therapy.30 However,
there are several cases with poor outcome (Table 2).18,25,31
The patient presented herein is interesting because of
severe side-effects to long-term corticosteroid treatment
for ITP, including pulmonary and cerebral nocardiosis,
induction of diabetes shortly after initiating corticosteroids
at age 53 years, cataract, and possibly steroid myopathy.
Whether corticosteroids could be responsible also for arterial hypertension, dermal atrophy, or dermal bleedings
remains speculative. Since arterial hypertension had occurred already prior to the administration of steroids, a causal
relationship is rather unlikely. It also remains elusive if
myopathy was due to the side-effects of corticosteroids
alone or due to other causes. The combination of thrombocytopenia, diabetes, and hypoacusis has been reported
together with the thiamine-responsive megaloblastic anemia syndrome,32 but anemia was not a dominant feature in
the present patient. The combination of diabetes, hyperlipidemia, arterial hypertension, atrial fibrillation, thrombocytopenia, sensorineural hearing loss, the renal cyst, myopathy, and cataract could also be attributed to a systemic
metabolic defect as the underlying pathology. Unfortunately, however, further diagnostic work-up into this direction
was limited due to the ITP. The cause of the markedly
elevated ferritin levels remains elusive, but could be explained with the chronic infection. Pulmonary malignancy
was definitively excluded at autopsy. The slightly reduced
calcium levels were attributed to hypoalbuminemia. That
the antibiotic therapy definitively eradicated the infection
with Nocardia sp. remains speculative since negative
culture results cannot be reliably interpreted as evidence
that the infection was eradicated. Whether the patient was
resistent to the applied antibiotics and would have profited
from linezolid, as has recently been reported,33 is unknown.
The present case shows that long-term therapy with

corticosteroids for ITP may induce immune-incompetence,
resulting in the development of pulmonary and cerebral
nocardiosis. Cerebral nocardiosis may not sufficiently
respond to long-term antibiotic therapy and may necessitate switching to alternative antibiotics or surgery. Longterm corticosteroid therapy may induce secondary steroid
myopathy or enhance primary metabolic myopathy.

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