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References
Goffette S, Jeanjean AP, Duprez TP, Bigaignon G, Sindic CJ. Eosinophilic pleocytosis and myelitis
related to Toxocara canis infection. Eur J Neurol. 2000;7(6):703–6.
Moreira-Silva SF, Rodrigues MG, Pimenta JL, Gomes CP, Freire LH, Pereira FE. Toxocariasis of
the central nervous system: with report of two cases. 1. Rev Soc Bras Med Trop. 2004;37(2):169–
74. Epub 2004 Apr 13.
References
279
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_85
8 5
Toxoplasmosis of the Spinal Cord
85.1 Definition
Toxoplasmosis refers to both asymptomatic and symptomatic infection due to toxoplasma gondii parasite. Infection when symptomatic is usually short lived, rather
acute and self-limited. In the chronic form the parasite causes persistent or recurrent
clinical manifestations. The disease has many clinical manifestations, which are
beyond this paper. A few examples are:
• The congenital form is usually complicated by damage in the brain and eye
• The acquired form involves viscera, e.g. the heart, lungs, liver, brain.
We will focus this paper on spinal cord involvement.
85.2 Incidence
Toxoplasm of the central nervous system (CNS) is not uncommon in patients with
immunodefi ciency due to immunosuppression or AIDS. According to the Centers
for Disease Control (CDC) toxoplasma infection in the United States is approximately 60,000,000 may be infected with the parasite, mostly are asymptomatic.
According to National Health and Nutrition Examination Survey (NHANES) there
are about 4000 symptomatic cases and more common in females. Brain involvement in 50 % of patients with toxoplasma and autoimmune disease; whereas spinal
cord involvement is rare only sporadic cases.
Abstracted from Cosan et al. ( 2001 ) and Campbell et al. ( 2001 )
280
85.3 Etiology
Toxoplasmosis occurs by:
• accidentally swallowing cat or dog feces
• eating contaminated food (pork, lamb, venison)
• contaminated drinking water
• organ or blood transfusions
Toxoplasma tissue infection is caused by cysts in raw meat or by oocysts in cat
feces.
85.4 Pathology
The disease comprises the following:
• toxoplasmic lymphadenitis: reactive follicular hyperplasia with irregular clusters
of epitheliod histiocytes, monocytoid cells can also be seen.T. gondii can be
demonstrated.
• CNS: there is meningoencephalitis with necorsis and microglial cells. There are
similar changes in the heart, lung, liver, kidney, all of which are beyond this
paper.
Spinal cord involvement is in two pictures:
• Toxoplasmic myelitis: pathologically is due to tissue reaction
• Toxoplasmic arachnoiditis
– Granulomatous arachnoidits
– Adhesive arachnoiditis
– Arachnoiditis ossifi cans
– Arachnoiditis calcifi cans
These constrict and compress the cord causing ischemia and sometimes atrophy
of the spinal cord.
85.5 Clinical Picture
In immunocompetent individuals toxoplasmosis may produce acute symptoms with
fl u like and focal or diffuse meningoencephalitis, which may subside. In chronic
cases adult and infants with congenital toxoplasmosis there may be no symptoms.
When symptoms develop there may be fl u-like illness. In patients with immunodefi ciency the disease will persist with manifestations of meningoencephalitis. As
regards to the spinal cord myelitis it may develop in congenital toxoplasomosis
85 Toxoplasmosis of the Spinal Cord
281
leading to ascending fl accid paralysis (see report by Campbell et al.). In adults toxoplasma arachnoiditis of the spinal cord presenting with spinal paralysis (see Erhan
et al.) due to toxoplasma adhesive arachnoiditis.
85.6 Diagnosis
Diagnosis is base on:
1. Serological tests: IgG and IgM are positive in the acute infection and may not be
highly positive in the chronic infection. Indirect Florescent Antibody (IFA) and
Sabin-Feldman tests are rarely used clinically. IgM toxoplasma antibody may
not be detected in acute cases of immunocompromised patients. Compliment
fi xation test may be tried.
2. Pathological test: The demonstration of T. gondii tachyzoites and bradyzoites in
tissue specimens. In body fl uids by periodic acid-Schiff (PAS), IFA, immunohis-
tiochemical studies by staining (NeoMarkers)
3. Cerebral spinal fl uid (CSF): xathochroma and mononuclear pleocytosis
4. Fundus exam: may show chorioretinal scar
5. MRI of spinal cord: shows hyperintensive subarachnoid space thickened adhe-
sive arachnoiditis and spinal cord atrophy. Plaques of calcifi cation even ossifi ca-
tion may be detected.
The case described is isolated spinal cord toxoplasmosis with no visceral or cerebral changes.
85.7 Management
• Medical treatment of the organism using sulfadiazine and pyrimethamine.
• Surgical treatment: decompressive laminectomy and debridement of the arach-
noid scars and plaques.
References
Campbell AL, Sullivan JE, Marshall GS. Myelitis and ascending fl accid paralysis due to congeni-
tal toxoplasmosis. Clin Infect Dis. 2001;15(10):1778–81.
Cosan TE, Kabukcuoglu S, Arslantas A, et al. Spinal toxoplasmosis Arachnoiditis associated with
osteoid formation: a rare presentation of toxoplasmosis. Spine. 2001;26(15):1726–8.
References
283
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_86
8 6
Trypanosomiasis
86.1 Definition
This is an infl ammatory condition of the spinal cord caused in Africa, by a trypanosome transmitted by a fl y tsetse in Africa; in South America, where it is commonly
called Chagas’ disease, it is transmitted by reduviid bug (called the kissing bug or
the assassin bug).
86.2 Incidence
There is no defi nite statistics about the trypanosomal myelopathy. In Africa the
disease is caused by a fl agellate protozoon, the trypanosome which has two species
of T. brucei , which involves the human disease. The others are T. brucei gambiense
(West Africa) T. brucei rhodesiense (East Africa). The trypanosome which causes
Chagas’ disease is T. cruzi . It is estimated that 16–18 million persons are infected
with T cruzi and death toll of 50,000 every year.
86.3 Etiology and Pathology
(From Meritt’s Neurology) In the African form of the disease, the organisms retain
their trypanososme form and multiply by longitudinal fi ssion. They are transmitted
from person to person by tsetse fl y, or occasionally by other fl eas, insects and by
mechanical contact. According to Kibiki and Murphy, T. brucei invades ova, has
marked tropism for the CNS giving rise to perivascular infl ammatory lesions,
immune complex formation and a generalized vasculitis. Demyelinating encephalitis is the terminal stage of the disease. A well described diffused meningoencephalitis is the usual dominant picture. The parasite itself may rarely be demonstrated in
Abstracted from Lury and Castillo ( 2005 ) and Kibiki and Murphy ( 2006 )
284
the nervous tissue as in the case reported by Lury and Castillo of Chagas’ disease.
Miliary granulomas may be detected consisting of microglia with lymphocyticplasmacytic perivascular and meningial infi ltrates. The organisms may be found in
glial and neurons. These lesions are scattered in the nervous system accompanied
by patch reactions in the meninges and parenchyma.
86.3.1 Stages of the Disease
The African type passes in two distinct stages:
• Fever (hemalymphatic)
• Lethargic (meningoencephalitis)
The incubation period varies, from 1 week from the infection or may not be
detected for months or years. The Rhodesian type usually has acute to subacute
course, the Gambian type is usually more chronic. The fever is accompanied by
exanthemia, lymphademitis, splenomegaly, arthrodyia, myalgia, and asthesia. This
may last for months or years and the organisms are found in the blood. The fi rst stage
may pass imperceptibly to the second stage, in which these symptoms are exaggerated with CNS involvement producing tremors, incoordination, convulsions, paralysis, confusion, headache, apathy, insomnia, or somnolence followed by coma. The
symptoms may last for a year and death ensues after intermittent infection.
86.3.2 The South American Type (Chagas’ Disease)
The acute stage starts by fever, conjunctivitis, palpebral swelling (where the bug
sticks) for blood sucking and they sometimes deposit their feces, which is rubbed by
the individual for itching. Swelling of the eye at the bit site is called Romaña sign.
The acute phase is uncommon and may last for a month. Fatigue, anorexia, nausea,
vomiting, enlarged lymph nodes, liver and spleen enlargements. In infants and
patients with AIDS, the phase may be fatal. This phase may subside without treatment. The second stage is the indeterminate stage, there may be no symptoms at all
and this stage may last for years. The chronic stage starts 10–40 years after the acute
stage; 20–30 % of the patients develop serious symptoms, for example: cardiac
arrhythmias, cardiac failure, cardiomegaly, even cardiac arrest; Esophagostasis and
colostasis leading to dysphasia and obstinate constipation. Acute exacerbations may
develop and occasionally with meningoencephalitis. The parasites are found in the
blood in the acute phase and may be transmitted to other people or to animals by the
reduviid bug or other insects, also through the placenta, through blood transfusion,
and organ transplants, or through breast fed infants and through eating uncooked
food contaminated with the feces of the vector bug.
86 Trypanosomiasis
285
86.3.3 Neurological Manifestations
According to Lury and Castillo from MRI studies the brain shows lesions in the corpus callosum, periventricular white matter, deep white matter, and subcortical regions
and the cerebellum. In the spinal cord, there are multiple intramedullary lesions. In
the African trypanosomiasis there is demyelinating encephalitis in the terminal stage.
In the spinal cord there is demyelinating myelopathy due to T. brucei which may be
reversible with specifi c therapy.
86.4 Clinical Picture
The different stages of the African and the American trypanosomiasis have been
referred to above. Specifi c picture for trypanososmal myelopathy:
• African trypanosomiasis: living under non-ideal conditions exposed to the tsetse
fl y, usually malnourished, and in poor hygienic conditions.
• American trypanosomiasis (Chagas’ disease): Living in Southern America or the
southern most part of the United States, living in non-hygienic homes, thatch style
homes, which harbor the vector bugs. Many patients are poorly nourished and
some have a lowered immune system, such as AIDS, etc. The skin signs may be
present (Romaña sign) or skin nodules (“chagoma”). Splenomegaly, cardiomeg-
aly, etc., maybe detected as well.
Neurological symptoms of the myelopathy include motor and sensory loss,
sphincteric dysfunction, cerebral or cerebellar manifestations may be detected in
both diseases.
86.5 Diagnosis
Diagnosis is based on:
1. Environmental conditions
2. Cutaneous manifestations: insect bites Romaña’s sign, chagoma, etc.
3. Serum fl uorescent antibody for trypanosome in a tissue biopsy
4. Blood test for the parasite
5. Parasite antibody in blood
6. CSF: positive for trypanosome antibody and trypanosomes may be found
7. MRI (abstracted from Lury and Castillo): multiple areas of enhancement in the
spinal cord and contrast enhancement in T1-weighted images. Brain images
show infra and supra tentorial lesions and tumor like masses.
86.5 Diagnosis
286
86.6 Management
In the African case of trypanosomiasis, Kibiki and Murphy treated the patient with
metronidazole, ciprofl oxacin, ceftriaxone for infections. Supportive treatments
include nutritional multivitamins. In the case of Lury and Castillo the patient with
American trypanosomiasis was started on a treatment of nifurtimox however he
continued to decline and subsequently died. Antiprotozoal agents, nifurtimox or
benznidazole (not available in the United States) are used to treat infections caused
by the protozoan T cruzi . According to the CDC the goals of pharmacotherapy are
to eradicate the infection, to reduce morbidity, and to prevent complications.
Medication administered in the acute phase of American trypanosomiasis is usually
effective; however in the later, chronic stages it becomes less effective. There is no
preventative therapy or vaccine for the disease.
References
Kibiki GS, Murphy DK. Transverse myelitis due to trypanosomiasis in a middle aged Tanzanian
man. J Neurol Neurosurg Psychiatry. 2006;77(5):684–5.
Lury KM, Castillo M. Chagas’ disease involving the brain and spinal cord: MRI fi ndings. AJR Am
J Roentgenol. 2005;185(2):550–2.
86 Trypanosomiasis
287
© Springer International Publishing Switzerland 2016
I.M. Eltorai, Rare Diseases and Syndromes of the Spinal Cord,
DOI 10.1007/978-3-319-45147-3_87
8 7
Compression Myelopathy due to Typhoid Spondylodiscitis
87.1 Definition
This is a condition of spinal infection by Salmonella typhi, resulting in spondylodiscitis and epidural abscess resulting in compression myelopathy.
87.2 Incidence
The authors reviewed the literature and found only nine reported cases and added
one case of their own, which was the fi rst in southeast Asia.
87.3 Etiology
Salmonella typhi is from an infected source (food) it passes the blood stream
through the GI tract causing typhoid fever. Extraintenstinal infection is rare 5–10 %.
Involvement in the spine is very rare and usually occurs in patients with poor sanitary hygiene and living in endemic areas. Debilitating causes were diabetes and
sickle cell anemia.
87.4 Pathology
The organisms will cause spondylitis, discitis with or without epidural abscess. The
level most commonly involved is the lumbar and lower dorsal region. One case was
in the upper dorsal. One case had psoas abscess. In the presence of an abscess, the
cord is compressed.
Abstracted from Suwanpimolkul et al. ( 2010 )
288
87.5 Clinical Picture
A 57-year-old male diabetic not well controlled, ingested raw vegetables, which
was contaminated. His symptoms included low back pain, paraparesis, bladder and
bowel dysfunction. Physical exam showed tenderness at T12, tight paraspinal muscles, paraparesis, and sensory level at T12. Blood cultures were negative.
Radiography showed mild thoracolumbar kyphosis, narrowing T11-T12 disc. MRI
showed spondylitis of T11 and T12 and discitis, erosion of the adjacent vertebral
endplates, extension of the infection to the epidural space causing cord
compression.
87.6 Management
Surgery consists of:
1. Laminectomy T11-T12, discotomy and debridement of epidural abscess, culture
showed S. typhi
Medical consists of:
1. IV Ciprofl oxacin and thimethoprim-sulfamethoxazole, followed by oral treat-
ment for 5 months.
Patient was doing well 2 months post-antimicrobial treatment.
Reference
Suwanpimolkul G, Nilgate S, Suankratay C. Typhoid spondylodiscitis: the fi rst reported case in
Southeast Asia and review of the literature. J Med Assoc Thai. 2010;93(1):137–41.
87 Compression Myelopathy due to Typhoid Spondylodiscitis