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266
81.4 Pathology
From the case reported:
It can invade any organ in the body. The disease may be dormant, invading
phagocytic and non-phagocytic cells. It spreads from cell-to-cell through actin
based motility and when very active is associated with high instability. The infection spreads throughout the body. It involves the skin, the subcutaneous tissues, the
musculoskeletal system, the urogenital system, the lung, the brain, and the spleen.
Neurological involvement is rare; 3 % in an Australian series. When it occurs, it
causes brain abscess, brain stem encephalitis, meningoencephalitis, and rarely
transverse myelitis. A 20 year prospective study in northern Australia, where the
disease is endemic, and only 14 cases presented with neurological complications,
two of which were myelitis. The case reported by the authors is the fi rst case of
transverse myelitis in Sri Lanka.
81.5 Clinical Picture
The case presented by the authors:
A 21-year-old man, from northern Sri Lanka, who health and worked in the farm,
where he was exposed to contaminated water and soil. The day before, he had low
grade fever, which resolved spontaneously. The day of presentation he had pain and
numbness in the lower limbs ending by fl accid paraplegia with urinary retention.
Exam showed normal vital signs. Neurological exam showed fl accid paraplegia
with sensory loss at T10 level. Elevated WBC, ESR, CRP. Radiography and CT of
the spine was normal, except left psoas abscess. MRI showed a left psoas abscess
which was multiloculated and measures 29.7 × 5.7 cm in size, with a fi nger-like
extension towards the spine. There was transverse myelitis at T4 with foci at T2 at
T2 weighted images. The central canal of the cord was dilated in all its length.
81.6 Diagonsis
Diagnosis is based on laboratory tests. The pus cultured on blood agar and
Macconkey agar on which non-lactose fermenting colonies. Further studies showed
identifi cation of Burkholderia pseudomallei . Other lab tests were negative. CSF
studies were not performed, due to the risk of introducing organisms into the CNS.
81.7 Management
Emergency ultrasound aspiration of the psoas abscess produced 350 ccs of purulent
fl uid. IV ceftazidime followed by cotrimoxazole and oral doxycycline for a year.
Residual neurological defi cits, including paraplegia, complete sensory loss, and
sphincter disturbance persisted.
81 Melioidosis
267
Reference
Nandasiri S, Wimalaratna H, Manjula M, Corea E. Transverse myelitis secondary to melioidosis:
a case report. BMC Infect Dis. 2012;12:232.
Reference
269
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_82
8 2
Mumps Viraemia
82.1 Definition
This is a condition of acute transverse myelitis (ATM) and Guillain-Barré syndrome
(GBS) occurring in association with mumps viremia.
82.2 Incidence
Myelitis due to mumps virus as the fi rst manifestation is very rare (Bansal et al.
1998 and Okada et al. 2002 ); whereas, neurological complication of mumps are
common especially in endemic areas. Meningitis is the commonest and encephalitis
occurs in less than 1 % of the cases. Rare manifestations are neural deafness, optic
neuritis, cortical blindness, neuropathy, facial palsy, Guillian-Barré syndrome, cerebellar ataxia, and hydrocephalus are the neurological manifestations of mumps.
Bajaj et al., reported a case of Guillian-Barré concomitant with acute transverse
myelitis due to mumps viremia and was the second cases in the literature.
82.3 Etiology
The virus causes ATM and at the same time leading to sensorimotor axonal polyradiculopathy (GBS). These changes may be direct effects of the virus or immune
mediated reaction.
Bajaj et al. ( 2001 )
270
82.4 Pathology
Neurological complications of mumps are: meningitis, encephalitis, myelitis, cranial nerve palsies, and rarely GBS. The area of myelitis shows increased vascularity, perivascular demyelination, proliferation of glial cells, degeneration of the
anterior horn cells, and perineural edema. These changes are not different from
other viral myelitis. Acute transverse myelitis may occur, especially in the thoracic
and lumbar regions, higher lesions are more accompanied by edema of the cord and
more demyelination. Associated viral pathology apart from neuropathy changes
are: parotitis, submaxillary sebadenitis.
References
Bajaj NP, Rose P, Clifford-jones R, Hughes PJ. Acute transverse myelitis and Guillain-Barré over-
lap syndrome with serological evidence for mumps viraemia. Acta Neurol Scand.
2001;104(4):239–42.
Bansal R, Kalita J, Misra UK, Kishore J. Myelitis: a rare presentation of mumps. Pediatr Neurosurg.
1998;28(4):204–6.
Okada Y, Fukasawa N, Tomomasa T, Inoue Y, Morikawa A. Atlanto-axial subluxation (Grisel’s
syndrome) associated with mumps. Pediatr Int. 2002;44(2):192–4.
82 Mumps Viraemia
271
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_83
8 3
Myelitis due to Sparganosis
83.1 Definition
According to Stedman’s Medical Dictionary Sparganosis is an infection with the
plerocercoid or sparganum of a pseudophyllidean tapeworm, usually in a dermal
sore resulting from application of infected fl esh as a poultice; infection may also
occur from ingestion of uncooked frog, snake, mammal, or bird intermediate or
transport host bearing the spargana, but not from fi sh with Diphyllobothrium larvae,
inasmuch as sparganosis is an infection with nonhuman pseudophyllidean tapeworms, usually species of Spirometra. Sparganosis may also develop from ingestion
of water containing procercoid-infected Cyclops.
83.2 Incidence
According to Kwon and Kim ( 2004 ) who reviewed the literature they found seven
cases involving the spinal cord and added one case of their own. Another case was
added by Bao et al. Six were males and three were females and the ages ranged from
10 to 59.
83.3 Etiology
See defi nition above. Human infection occurs by:
• Drinking untreated water containing infected pepods (fi rst intermediate host)
• ingesting raw or inadequately cooked fl esh of frogs or snakes that are infected
with sparganum (second intermediate host)
• Applying the fl esh of an intermediate host as a poultice to a wound.
Abstracted from Kwon and Kim ( 2004 )
272
83.4 Pathology
The spinal cord is most probably infected via blood stream. The parasite excites
chronic infl ammation and a sort of parasitic granuloma with adhesions around it.
The parasite may be detected as in the case by Kwon and Kim. The lesions may be
extradural, intradural, intramedullary, or cauda equine.
83.5 Clinical Picture
The disease is most common in East Asia. Exposure to contaminated water or eating
undercooked frog or snake meat or using the raw meat as poultices. The common
symptoms are: back pain, paresthesia, anesthesia, paresis or paralysis (paraplegia) and
sphincter disturbances especially incontinence.
83.6 Diagnosis
Diagnosis is based on:
1. Patient exposure and from endemic areas
2. Neurological assessment
3. Pleocytes: Eosinophils, monocytes, lymphocytes, occasionally plasma cells
4. Evoked potentials
5. Cerebral spinal fl uid (CSF): increased protein level
6. enzyme-linked immunoabsorbent assay (ELISA): test for sparganosis antibod-
ies is positive indicating that intrathecal production; IgG oligoclonal bands show
high sensitivity
7. MRI of spinal cord: mass in the spinal cord, nodular, and with mild enhance-
ment. The brain should be included to rule out its involvement. Other organs may
be involved as well.
8. Biopsy: will show chronic infl ammation and scar tissue formation
83.7 Management
Debulking the mass through laminectomy and removal of the parasite. Specifi c
therapy Praziquantel has been used to treat cerebral sparganosis but its effi cacy has
not been documented (Merk Manual).
Updates
Abstracted from Oh et al. (2011)
83 Myelitis due to Sparganosis
273
Sparganosis is a rare parasitic infection caused by the migrating plerocercoid
larva of the tape worm, Spirometra mansoni , which commonly invades the sub-
cutaneous tissue, skeletal muscle, and viscera. The CNS involvement is rare.
Few cases have been reported involving the thoracic spinal cord including their
case.
Case Report
A 51-year-old man complaining of progressive paresthesia of all the limbs and left
motor weakness of 4 months prior to coming in, he had a history of ingesting inadequately cooked frogs and snakes several years earlier. He was treated with cervical
laminectomy at C2-C3. The dura and the arachnoid were thickened yellow-white
discoloration, with adhesions to the cord. Aspiration of the compression fl uid was
done. Pathology revealed granulomatous infl ammation, tunnel-like cavities with
necrotic larvae of sparganum and psammoma like bodies and calcifi cations. Post-op
praziquantel; left sided paresis improved.
Reference
Oh SI, Koh SH, Pyo JY, Lee KY, Lee YJ. Sparganosis mimicking an intramedullary
tumor of the cervical cord. J Clin Neurosci. 2011;18(8):1128–9.
Abstracted from Boonyasiri et al. (2013)
The authors present a case of sparganosis of the spine with subarachnoid
serpiginous- mass from the preponitine levels to the oblongata, C7, T2 to T8 and
T12 until the end of the thecal sac and fi lling in the right S1 neural foramen.
Incidence
The parasite can be found everywhere in the body, only three cases have been
reported in the cauda equina. Boonyasiri et al., added a case of their own, fi rst diagnosed by molecular identifi cation.
Case Report
A 52-year-old woman living in rural Thailand, presented with lumbodorsal pain for
1 month. Paraparesis and radiculopathy for 2 weeks; bladder and bowel disfucntion
for 3 days. No history of ingestion of inadequately cooked frogs, snakes, or birds.
Molecular diagnosis was performed. DNA was extracted from μm unstained serial
sections, cut from the formalin-fi xed paraffi n-embedded specimen, attached to glass
slides using DEXPAT kit (TaKaRa Bio Inc., Tokyo, Japan). The test was positive for
S. erinaceieuropaei. Laminectomy at L1 and L2; a scar with cystic formation was
noted and biopsied. The section showed larvae of cestode with the folding segments
and eosinophils. Calcareous corpuscles were evident, which is a sign of cestode. The
patient received corticosteroid therapy and praziquantel; however, the symptoms
persisted.
Updates
274
Reference
Boonyasiri A, Cheunsuchon P, Srirabheebhat P, Yamasaki H, Maleewong W, Intapan
PM. Sparganosis presenting as cauda equina syndrome with molecular identifi cation
of the parasite in tissue sections. Korean J Parasitol. 2013;51(6):739–42.
Reference
Kwon JH, Kim JS. Sparganosis presenting as a conus medullaris lesion: case report and literature
review of the spinal sparganosis. Arch Neurol. 2004;61(7):1126–8.
83 Myelitis due to Sparganosis
275
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_84
8 4
Toxocara canis
84.1 Definition
Toxocara canis is a round worm of dogs, which can cause visceral larva migration
syndromes in humans by ingestion of contaminated soil. Toxocara canis causes the
visceral larva to migrans in the central nervous system (CNS), brain and spinal cord.
84.2 Incidence
In the United State toxocara canis (TC) is a health problem. In different communi-
ties the prevalence is directly proportional to the infection rates depending on the
free access to dogs to public places. The incidence is higher in the south, Puerto
Rico, and minority areas as shown by enzyme-linked immunoabsorbent assay
(ELISA) test from 16 to 30 %. Involvement of the spinal cord is very rare, no defi nitive incidence is available.
84.3 Etiology
TC larva migrans induce TC syndrome, which involves the liver, lungs, skin, eyes,
and rarely the CNS. In the spinal cord the larva migrans cause transverse myelitis or
eosinophilic memingo-myelitis, cervical arachoiditis, meningo-encephalitis,
menigo-encephalo-myelitis, radiculitis, and sometimes spinal abscess. As a parasitic infection, it causes eosinophilic reaction. The migrant larvae reach the cord
through focal blood-spinal barrier disruption due to reactive infl ammatory process.
Abstracted from Goffette et al. ( 2000 )
276
84.4 Clinical Picture
The syndrome starts by fever, eosinophilia, hepatomegaly, and pulmonary symptoms,
which usually have a limited course. The patient usually was exposed to TC eggs and
develops dysesthesia, paresthesia, weakness of lower limbs, and mild sphincter dysfunction. A sensory level may be noted, the tendon refl exes are exaggerated, and
Babinski sign is usually positive.
84.5 Diagnosis
Diagnosis is based on:
1. History especially initial stages of fever, hepatomegaly and respiratory symptoms.
2. Patient from a community where there is free access of the dogs to public places.
3. Neurological assessment
4. Pleocytosis: Esinophils, monocytes, lymphocytes, occasionally plasma cells
5. Evoked potentials confi rm myelopathy
6. Cerebral spinal fl uid (CSF): increased protein level
7. enzyme-linked immunoabsorbent assay (ELISA): test for t. canis antibodies is posi-
tive indicating that intrathecal production; IgG oligoclenal bands may be negative.
8. MRI of spinal cord: slightly hyper-intense foci within the cord on T-1 weighted
images with slight contrast enhancement on post contrast T-1 weighted images
at the level of the lesion. Transverse T2 weighted images show hyper-intense
foci. MRI of the lesion is added evidence. For more details on the cerebral t.
canis see Moreira-Silva et al. ( 2004 ) .
84.6 Management
Goffette et al., treated giving methylprednisolone 32 mg daily and tapered over 2
weeks. Mebendazole up to 3 g daily, both for 30 days. During the antihelminthic
treatment Hexheimer’s reaction may develop and for that reason it is better to combine the antihelminthic with steroids in addition to its anti-infl ammatory action.
A follow-up with the therapy is useful:
• The CSF will normalize its cytosis and protein level, disappearance of the IgG
oligoclonal bands, and drop of the antibody titre.
• ELISA titre to t. canis in the blood may remain positive for months or years after
recovery.
• MRI: the pre-contrast T1-weighted scan no longer shows abnormality, but a
residual hypersignal on T2-weighted images may persist for sometime.
• Esinophilia drops down to normal
• Neurological recovery continues
84 Toxocara canis