Journal of Spine & NeurosurgeryISSN: 2325-9701

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Case Report, J Spine Neurosurg Vol: 4 Issue: 5

Left Cerebellary Toxoplasmosis with No Immunodefiency: Case Report

Bekar A1*, Eser P1, Yilmaz E2 and Sav A3
1Uludag University School of Medicine, Neurosurgery Department, Gorukle, Bursa, Turkey
2Uludag University School of Medicine, Infectious Diseases Department, Gorukle, Bursa, Turkey
3Ac─▒badem University School of Medicine, Atasehir, Istanbul, Turkey
Corresponding author : Prof. Ahmet Bekar
Uludag University School of Medicine, Department of Neurosurgery, Gorukle, 16059, Bursa, Turkey
Tel: +90 224-2952740; Fax: -90 224-4429263
E-mail: [email protected]
Received: July 22, 2015 Accepted: December 16, 2015 Published: December 23, 2015
Citation: Bekar A, Eser P, Yilmaz E, Sav A (2015) Left Cerebellary Toxoplasmosis with No Immunodefiency: Case Report. J Spine Neurosurg 4:5. doi:10.4172/2325-9701.1000202


Toxoplasmosis is caused by an infection with an obligate intracellular parasite, Toxoplasma gondii. The patients are usually immunocompromised. It causes a silent infection in healthy individuals. Trimethoprim sulfamethoxazole is the most common drug used for toxoplasmosis. A fifty year old male applied to our out-patient department with the complaint of right hemiparesis, walking difficulty, ear humming and facial asymmetry on May 2010. Magnetic resonance imaging revealed a left cerebellary mass lesion. He was operated and the pathological findings were consistent with ‘toxoplasmosis’; although we could not demonstrate an immunodeficiency in this patient.

Keywords: Cerebrallary mass; Toxoplasmosis; Immunocompromised patient


Cerebrallary mass; Toxoplasmosis; Immunocompromised patient


Toxoplasma gondii is an obligate, intracellular, opportunistic parasite causing a life-threatening disease ‘toxoplasmosis’; especially in acquired immunodeficiency syndrome (HIV) and immunocompromised patients. Cerebral white and grey matter, retina, lung alveolar layer, heart and skeletal muscle are the most common affected areas. Here, we report a case of cerebral toxoplasmosis who did not exhibit immunodeficiency.


A fifty year old male admitted to Uludag University, School of Medicine neurosurgery out-patient department on May 2010 with the complaint of right hemiparesis, walking difficulty, ear humming and facial asymmetry that persisted for two months. The neurological examination revealed ataxia, left cerebellary incapacity and left peripheral facial palsy (House Brackmann Grade III). The laboratory examinations were normal.
Magnetic resonance imaging (MRI) confirmed a peripheral enhancing mass lesion (18×22 mm) representing hyperintense hemorrhagic areas in T1-weighted images; hyperintense perilesional edema in fluid attenuated inversion recovery (FLAIR) images and hyperintense hemosiderin content in T2-weighted images in left middle cerebellar peduncle extending through pons and medulla oblongata (Figure 1A-1C).
Figure 1: Cranial magnetic resonance images.
The patient underwent elective operation 2 weeks after his application. He was operated under general anesthesia, in sitting position with the aid of an operation microscope. A midline suboccipital craniotomy was performed. The mass was removed subtotally, by leaving residual tumor adherent to the brain stem, not to compose additional neurological deficits. Immediate postoperative cranial tomography revealed postoperative changes. He was discharged 4 days after the operation without any problem.
Neuro-pathological examination revealed 1.5×1×2 cm, greyyellow- brown, soft tissue macroscopically with atypical lymphoid infiltration by T-cells richly and B-cells poorly. Preparations were consulted to another pathology center for T and B cell clonally.
Whence the consultation was reported and the diagnosis was confirmed as ‘toxo cerebellitis’ by demonstrating intracellular toxoplasma gondii, the patient was admitted to infectious diseases clinic (Figure 2A, 2B). Trimethoprim 10 mg/kg, sulfamethoxazole 50 mg/kg were ordered.
Figure 2: Pathologic specimens.
He was examined for immunodeficiency and additional tests for toxoplasmosis were not performed given the certain pathology report. In physical examination we did not determine a hepatosplenomegaly or lymphadenopathy. The laboratory examinations were normal. White blood cells were 5.74/ mm3 with the 16.8% lymphocyte ratio. HIV Ag/ab were negative. Although CD4/CD8 ratio was low, this finding was not considered as pathologic due to the normal CD4 and CD8 counts (Table 1). Abdominal ultrasonography, abdominopelvic and thorax CTs and chest x-ray for malignity research were reported as ‘normal’. Toxo IgG and toxo IgG avidity were reported as ‘positive’ and ‘high’, respectively. Toxo IgM was negative. Due to the herniation risk, we could not perform diagnostic lumber puncture. He was discharged with trimethoprim-sulfamethoxazole orally on the 23th hospitalization date. During the follow-ups, the patient rejected treatment and quitted follow-up.
Table 1: Immun panel.


Toxoplasma gondii is an obligate, intracellular opportunistic parasite causing a life-threatening disease ‘toxoplasmosis’; especially in acquired immunodeficiency syndrome (HIV) and immunocompromised patients. Individuals are infected by transplasental or oral route. Raw and uncooked meat including tissue cysts, oil or water including oocysts, unwashed vegetables and fruits are the most common sources of infection [1]. Besides, patients infected by unpasteurized goat’s milk are also reported in the literature.
Toxoplasma gondii infection can be diagnosed indirectly with serological methods and directly by PCR, hybridization, isolation, and histology [2]. Serology is frequently positive, but specificity is low because only one third of the cases show a high titrated IgG antibody [3], and only half of the cases show intrathecal antibody production for the agent [4]. Therewithal, the recent studies have denoted low sensitivity for polymerase chain reaction for toxoplasma gondii in plasma and cerebrospinal fluid [5,6] and occasional false-positive results [7]. In addition to all of these handicaps; the neuroradiological findings are also helpful for the diagnosis of toxoplasmic encephalitis. On the other hand, for a diagnosis, suspicion about the multiple lesions on MRI is required primarily.
Toxoplasmosis lesions are most commonly located in the cerebral hemispheric white and subcortical gray matter, such as thalamus and basal ganglia [8,9]. The characteristic finding is the asymmetric ‘target sign’ to which MRI is more sensitive then computed tomography.
Typically, toxoplasmic lesions are iso-hypointense on T1- weighted images with rim enhancement and have hyperintense foci on T2-wieghted images [10]. If there are multiple intracerebral lesions with mass effect or contrast uptake, some authors assert that the positive predictive value of MRI for toxoplasmosis can reach up to 100%; especially if at least one of these lesions is located in the basal ganglia or in the thalamus [11] but this is not pathognomonic to cerebral toxoplasmosis. Single toxoplasmic lesions are mentioned as ‘infrequently’ in literature [12,13].
Perilesional edema is associated with patient’s ability of inflammatory response formation [14]. The more edema formation means the more inflammatory response which is the sign of a good prognosis. Edema is also correlated with CD+4 quantity [15,16]. The definitive method of diagnosis is brain biopsy and this procedure is applied for the patients who did not response to 2-4 weeks’ empirical medication.


Our case is among the unique ones in literature of toxoplasma cerebellitis because of the single lesion with rim enhancement on T1, hyperintense hemorrhagic areas on T2 weighted MR images with cerebellar localization in a non-immunocompromised patient. To our knowledge, it is very rare in literature especially as a solitary lesion. They are curable lesions by antibiotherapy and surgery when needed.


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