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Year : 2014  |  Volume : 7  |  Issue : 5  |  Page : 655-660  

Role of advanced magnetic resonance imaging techniques in diagnosis of cerebral toxoplasmosis in immunocompromised patients: A case report

Department of Radio-Diagnosis, Dr. Dnyandeo Yashwantrao Patil Medical College, Pune, Maharashtra, India

Date of Web Publication10-Sep-2014

Correspondence Address:
Inderpreet Singh
S/O Dr. Harjeet Singh, Factory Road, Rampura Phul, Bathinda - 151 103, Punjab
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0975-2870.140487

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Cerebral toxoplasmosis commonly affects patients with advanced HIV infection. Toxoplasmosis can be severe and debilitating in patients with Central Nervous System (CNS) involvement and the condition may be fatal in patients if not suspected and treated early and adequately. Hence, imaging plays an important role in diagnosis and following during treatment in cases of suspected toxoplasmosis. We report a case of a 51-years-old man who was a known sero-positive since 2 years and presented with altered sensorium. Magnetic Resonance Imaging (MRI) scan of the brain showed multiple heterogeneously enhancing lesions in bilateral cerebral as well as cerebellar hemispheres and some of them showed "eccentric target sign." MR spectroscopy showed features of reduced NAA, mildly increased choline, and lipid lactate peak. MR perfusion study showed reduced perfusion favoring diagnosis of cerebellar toxoplasmosis. Patient was started on a combination of pyrimethamine plus sulfadiazine for toxoplasmosis. Follow up MRI after 20 days and 45 days from start of treatment showed significant resolution of the lesions supporting our radiological diagnosis.

Keywords: AIDS, MR perfusion, MR spectroscopy, toxoplasmosis

How to cite this article:
Singh I, Patil A, Kuber R, Patil P, Kulkarni VM. Role of advanced magnetic resonance imaging techniques in diagnosis of cerebral toxoplasmosis in immunocompromised patients: A case report. Med J DY Patil Univ 2014;7:655-60

How to cite this URL:
Singh I, Patil A, Kuber R, Patil P, Kulkarni VM. Role of advanced magnetic resonance imaging techniques in diagnosis of cerebral toxoplasmosis in immunocompromised patients: A case report. Med J DY Patil Univ [serial online] 2014 [cited 2021 Jan 27];7:655-60. Available from:

  Introduction Top

The human immunodeficiency virus (HIV) is a retrovirus that infects CD4 cells of the immune system and destroys or disrupts their function. In the more advanced stages of HIV infection, acquired immunodeficiency syndrome (AIDS) develops. Diseases of the central nervous system (CNS) in patients infected with the human immunodeficiency virus (HIV) result directly from HIV itself or from a variety of opportunistic agents like toxoplasmosis and cryptococcosis. [1] A resurgence of tuberculosis (TB) and neurosyphilis has also been documented. [1] Toxoplasmosis is commonly associated with acquired immunodeficiency syndrome (AIDS), is caused by ubiquitous parasite, Toxoplasma gondii. Transmission of the infection usually is by oral or trans-placental route. [2] Toxoplasmosis in association with AIDS is mostly due to reactivation of a chronic infection and (manifests) as toxoplasma encephalitis. Toxoplasma encephalitis usually occurs in AIDS patients with CD4 T-cell count <100/μL. [3] AIDS patients with sero-positive T. gondii, cerebral toxoplasmosis can be seen up to 30% of patients. [3]

Toxoplasmosis is one of the most common causes of focal brain lesions in AIDS patients and commonly localized to basal ganglia, although other sites in brain and spinal cord may be affected. [2] It is important to suspect possibility of toxoplasmosis as it responds rapidly to available antimicrobial drugs such as a combination of pyrimethamine plus sulfadiazine and is known to have good prognosis. It is also important to rule out differentials like primary CNS lymphoma, tuberculosis, pyogenic, and fungal infections. Imaging is important in case of symptomatic HIV patients, which have a more protracted course. Thus, we present this case to describe the radiological approach in a case of focal brain parenchymal lesion in HIV/AIDS.

  Case Report Top

A 51-year-old male, known HIV sero-positive, initially asymptomatic, came with complaints of generalized weakness since 2 months. He had associated intermittent headache localized to left fronto-parietal region with an evening low-grade fever. No history of seizure, trauma, tuberculosis, was present.

He underwent MRI brain with gadolinium, which showed multiple heterogeneously enhancing predominantly sub-cortical lesions of variable sizes in bilateral cerebral as well as cerebellar hemispheres. They were appearing heterogeneously hyperintense on T2WI and FLAIR, iso to hypointense on T1WI in left temporo-occipital region [Figure 1] and in left temporo-occipital regions. These lesions were also associated with perilesional edema. Similar intensity multiple lesions were noted in bilateral thalami, left external capsule on FLAIR [Figure 2]. The lesions also showed mild peripheral restriction on DWI [Figure 3] without blooming on GRE. The largest lesion was noted in left temporo-occipital region measured 4.6(AP) X 4.0(CC) X 3.6(TRANS) cm, which showed peripheral heterogeneous and irregular enhancement with an enhancing eccentric nodular solid component in the postero-lateral aspect towards the cortex, "Eccentric target sign" [Figure 4]. Perilesional edema with mass effect was also seen predominantly in the left temporo-parieto-occipital region with effacement of the overlying cortical sulci, occipital horn of the left lateral ventricle, and minimal mid line shift of 4 mm towards right. Other multiple smaller lesions were located in the right cerebellar hemispheres, left dentate nucleus, right temporal lobe, right para-hippocampal gyrus, bilateral thalami, left external capsule anteriorly, left precentral gyrus, sub cortical white matter of bilateral frontal gyri. These lesions showed nodular enhancement with minimal perilesional edema.
Figure 1: Axial FLAIR image (at the level of midbrain) showing heterogenous iso- to hyperintense signal abnormality lesion in left temporo-occipital region. Associated perilesional edema appearing is noted as ill-defi ned hyperintense signal

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Figure 2: Axial FLAIR image (at the level of thalami) showing heterogenous lesion in left temporo-occipital region associated with perilesional edema. Multiple similar intensity lesions are noted in bilateral thalami, left external capsule anteriorly

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Figure 3: Diffusion-weighted axial MR image showing multiple lesions showing peripheral restriction. The largest lesion noted in left temporooccipital region is showing mild peripheral restriction

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Figure 4: Post-contrast axial MR image showing peripheral heterogeneous and irregular enhancement with an enhancing eccentric nodular solid component in the peripheral postero-lateral aspect towards the cortex, "Eccentric target sign"

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Magnetic resonance spectroscopy was performed and it revealed lipid lactate peak with relatively low NAA, NAA/Creat ratio-0.22 (Opp. normal white matter NAA/Creat ratio-1.50), and mildly increased choline in peripheral enhancing component, Cho/Creat ratio 1.53 (Opp. normal white matter Cho/Creat ratio 1.16). Increased choline and reduced NAA were noted on high TE (TE-135) sequences in enhancing component [Figure 5], and Large lipid lactate peak was noted on low TE (TE = 30) [Figure 6].
Figure 5: MR spectroscopy (TE = 135) reveals increased choline and reduced NA

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Figure 6: MR spectroscopy (TE = 30) reveals a large lipid lactate peak

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MR perfusion was performed and revealed significant reduction in rCBV in left temporo-occipital lesion [Figure 7].
Figure 7: Reveals reduced rCBV in the region of left temporo-occipital lesion as compared to the opposite white matter

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On the basis of distribution of the lesion with characteristic enhancement pattern in the left temporo-occipital lesion, along with diffusion, MR spectro and perfusion imaging, the diagnosis of toxoplasmosis was considered with the left temporo-occipital lesion representing toxoplasma abscess, with differentials diagnosis of lymphoma.

Other biological and immunological studies showed increased neutrophils count, positive ToxoIgG and IgM antibodies and raised C-reactive protein and decreased CD4 cell count (35 μL). Ultrasound abdomen and chest radiograph were unremarkable.

Brain biopsy was deferred because of financial and technical constraints. Patient was started on a combination of pyrimethamine plus sulfadiazine.

Follow-up MRI scan was performed after 20 days, which showed persistence of the lesions in bilateral cerebral and cerebellar hemispheres. Axial FLAIR MR image at the level of midbrain [Figure 8] and at the level of thalami [Figure 9] revealed reduction in size of the left temporo-occipital lesion with reduced perilesional edema. The temporo-occipital lesion now measured approximately 3.7(AP) X 3.3(CC) X 2.7(TRANS) cms with surrounding perilesional edema. No midline shift was noted in present scan, thus indicating reduced mass effect.
Figure 8: Follow-up axial FLAIR MR image (at the level of midbrain) after 20 days of pyrimethamine and sulfadiazine combination reveals reduction in size of the left occipito-temporal lesion with reduced perilesional edema

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Figure 9: Follow-up axial FLAIR MR image (at the level of thalami) after 20 days of pyrimethamine and sulfadiazine combination reveals reduction in the size of the bilateral thalamic lesions is seen

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Continued combination of pyrimethamine plus sulfadiazine was administered, following which MRI brain was done after 45 days of start of treatment. MRI brain showed persistent multiple foci of heterogeneously hyperintense lesions. The large left temporo-occipital lesion was further reduced in size. The perilesional edema in left temporo-parietal region was significantly reduced [Figure 10]. No new lesion was noted.
Figure 10: Follow-up axial FLAIR MR images after 45 days of pyrimethamine and sulfadiazine combination reveals further regression of the left occipito-temporal lesion and bilateral thalamic lesions

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  Discussion Top

Clinically, patients suffering from toxoplasma encephalitis present with complaints of headache, altered mental status, and fever. Commonly noted focal neurological signs are motor weakness, speech disturbances. Seizures, cranial nerve abnormalities, visual field defects, sensory disturbances, cerebellar dysfunction, movement disorders, and neuropsychiatric manifestations can also be noted. [4] Most common presentations in patients with cerebral toxoplasmosis are ocular and pulmonary diseases. [5] No radiological obvious ocular and pulmonary abnormality was noted in our case.

Diagnosis of toxoplasmosis is made by demonstration of tachyzoites in tissue biopsies or cytologic preparations of body fluids, isolation of T. gondii from body fluids or blood, or amplification of the parasite DNA in body fluids or blood. Toxoplasmosis in HIV-infected patients primarily mainly manifests as toxoplasmic encephalitis and is a common cause of focal CNS lesions.

MRI and CT scan findings are not pathognomonic for toxoplasma encephalitis. However, imaging studies are indispensable for the suspicion of the diagnosis to know associated complications and for evaluating the response. CT scan in patients with toxoplasma encephalitis reveals multiple, bilateral, hypodense, contrast-enhancing focal brain lesions in 70-80% of patients. These lesions have a predilection for basal ganglia and hemispheric cortico-medullary junction as seen in our case. A ring-like enhancement pattern with an eccentric nodule at the margins of the lesion is commonly noted on contrast study. [6] The enhancing nodule is a collection of concentrically thickened vessels while the rim enhancement is caused by an inflamed vascular zone that borders the necrotic abscess cavity "eccentric target" sign.

Three types of cerebral involvement by Toxoplasma gondii have been known. [7] Initially, the lesions consist of a mixture of free-living tachyzoites and encysted organisms, vascular reaction inflammation, and petechial hemorrhage forming a necrotizing abscess is seen. Following about 2-4 weeks, a fibrous capsule forms around a necrotic center. The third stage consists of a chronic abscess, in which the lesion consists of necrosis and free organisms.

The main differential diagnosis of focal brain lesions in HIV-infected patients is between CNS lymphoma and toxoplasmic encephalitis. [7],[8] Presence of more than one lesion increases the likelihood of toxoplasmosis rather than lymphoma, [9],[10] periventricular location and subependymal spread favor lymphoma over toxoplasmosis. [7],[8] No subependymal spread was noted in our case. Magnetic resonance imaging (MRI) is more sensitive than CT scan and is preferred imaging technique. Solitary lesions are noted only in 14% of toxoplasmosis patients, which helps in differentiating toxoplasmosis from lymphoma, which are commonly solitary. A small eccentric nodule alongside an enhancing ring, the "eccentric target sign" noted in more than 30% of cases is highly suggestive of toxoplasmosis, [1] as seen in our case.

Perfusion MRI can be diagnostic tool in differentiating toxoplasmosis from lymphoma. Using T1W gradient echo sequence with dynamic contrast acquisition of images, perfusion imaging shows significant rCBV values in toxoplasmosis are significantly reduced as seen in our case as opposed to lymphoma, which show increased perfusion. [1] Toxoplasmosis also reveals reduced rCBV even on SPECT. [7],[8] Low rCBV value noted in patients with toxoplasmosis lesions is due to the lack of vasculature within the abscesses. [9] Lack of significant peripheral response around the lesion can also be due to low immune status of the AIDS patients.

MR spectroscopy can be useful technique in differentiating toxoplasmosis from lymphoma. MRS in toxoplasmosis reveals lipid-lactate peak, which is due to their destructive nature and the super-added infiltration with lipid-laden macrophages. [9] In AIDS patients, cerebral lymphoma may have necrosis and can reveal a similar lipid peak if the voxel is placed over the necrotic, rather than cellular enhancing portion, of the lesion. [11],[12]

Tuberculosis which is rampant in our country also needs to be considered as a differential of any focal lesion in the brain in immune-compromised patients. Tubercular abscess can also be multiple. However they show restriction on diffusion with corresponding low ADC values, as opposed to toxoplasma abscess which shows high ADC values. [13],[14]

Tubercular lesions show lipid peaks, which is quiet characteristic without significant elevations of other peaks. [15]

Increased diffusion in toxoplasmosis lesions suggests lower viscosity of the abscess fluid compared to that found in pyogenic abscesses. It is found that ADC ratios of toxoplasmosis lesions (mean + SD: 1.63 = 0.41) differed significantly from those in necrotic lymphoma brain lesions (mean + SD: 1.14 + 0.25) in AIDS patients. It is found that ADC ratios of >1.6 solely associated with toxoplasmosis. [16]

Pyogenic abscess also show diffusion restriction with low ADV values. MRS in the pyogenic infections also show presence of amino acids in addition to lipid and lactate. Pyogenic brain abscesses contain significant quantity of neutrophils and proteins, which are released in the necrotic cavity. The destruction of these neutrophils results in the release of a large amount of proteolytic enzymes that hydrolyze the proteins into amino acids at 0.9 ppm, which are particularly absent in tuberculosis. [17]

Fungal lesions such as those in aspergillosis can mimic the abscesses in toxoplasmosis. However, polymorphonuclear impairment and subsequent impairment of fungicidal ability are not typically seen in AIDS. Thus, aspergillosis is relatively uncommon in these patients. [14] The possibility of aspergillosis should be considered if there is hemorrhage associated with the lesions. [18],[19] Subtle or well defined ring enhancement may be noted in fungal abscesses, which may be related to the patient's immune status. [15],[20] It is noted that diffusion-weighted images showed restricted diffusion predominantly in the wall of the fungal abscess, whereas the core of the abscess did not exhibit reduced diffusion, a pattern unlike that demonstrated by pyogenic and tuberculous abscesses. [15]

Conservative approach is specifically useful in surgically inaccessible lesions. Treatment of toxoplasmosis encephalitis in AIDS patients is divided into an acute and a maintenance phase. Acute therapy usually lasts for 3-6 weeks but is continued in cases who have not achieved a complete response. After that, maintenance therapy is continued to avoid relapse. Combination of Pyrimethazine/Sulfadiazine and folinic acid is considered the standard regime for treatment of the toxoplasmosis encephalitis. [20] Short course of corticosteroids is helpful in patients with significant cerebral edema and elevated intracranial pressure. If the therapy is discontinued, toxoplasmosis can re-occur. [1]

Primary prophylaxis is recommended in T gondii-seropositive patients with CD4 T-cell count <100/μL regardless of the clinical status and in patients with CD4 T-cell count <200/μL if an opportunistic infection or malignancy develops. [21]

Thus, we conclude that any intraparenchymal lesion/lesions should be evaluated with special sequences as diffusion weighted, MR perfusion and MR spectroscopy to differentiate the different types of opportunistic infections as toxoplasmosis, tuberculosis, pyogenic and fungal infection and neoplastic lesions as lymphoma. This is important specially as infections like toxoplasma, if diagnosed early, do have good response to antimicrobial drugs and have better prognosis than other infections/neoplasms.

  References Top

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2.Khan AN, Turnbull I, Okaili AR. Toxoplasmosis, CNS. Available from: [Last accessed on 2014 Sep. 1].  Back to cited text no. 2
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12.Laissy JP, Soyer P, Tebboune J, Gay-Depassier P, Casalino E, Lariven S, et al. Contrast-enhanced fast MRI in differentiating brain toxoplasmosis and lymphoma in AIDS patients. J Comput Assist Tomogr 1994;18:714-8.  Back to cited text no. 12
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21.Carr A, Tindall B, Brew BJ, Marriott DJ, Harkness JL, Penny R, et al. Low-dose trimethoprim-sulfamethoxazole prophylaxis for toxoplasmic encephalitis in patients with AIDS. Ann Intern Med 1992;117:106-11.  Back to cited text no. 21


  [Figure 1], [Figure 2], [Figure 3], [Figure 4], [Figure 5], [Figure 6], [Figure 7], [Figure 8], [Figure 9], [Figure 10]


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