Teaching Case

A 25-year-old male patient was admitted to the emergency service with disorder of consciousness associated with fever and right focal motor seizures for 5 days.
On admission, he was febrile, confused and found to have right-sided hemiplegia.
Routine haematological analyzes showed lymphopenia and cerebrospinal fluid analysis demonstrated a 5 white blood cell count and elevated protein with normal glucose level. Serum was reactive for HIV-1. Laboratory testing revealed also serum antitoxoplasma IgG and IgM antibody.

A Magnetic resonance imaging (MRI) of the brain with contrast demonstrated multiples lesions in the bilateral basal ganglia, frontal, temporal, parietal, occipital and cerebellar lobes with ring enhancement on post-contrast sequence adjacent oedema with the appearance of “eccentric target sign” (fig 1 d, stars). On T2 weighted sequence, those lesions had alternating hyper and hypointense zones with marked perilesional oedema corresponding to “concentric target sign” (fig 1 a, white arrows) and intra-lesional hemorrhagic foci on T2 * sequence (fig 1 b, red arrows). On diffusion-weighted sequence, there were high-signal-intensity rims and low-signal-intensity centres of these lesions. (fig 1 c, black arrows).
Repeat MRI of the brain with contrast 1 month after the diagnosis showed a resolution of the oedema and ring-enhancing lesion in the left occipital lobe and a decrease in the size of the ring-enhancing lesions and oedema in the right occipital and left temporal lobes (Fig 2 arrows).

Toxoplasmosis is caused by T gondii, an intracellular protozoan that is found worldwide. It is transmitted to humans primarily by ingestion of cysts in undercooked pork or lamb or contaminated vegetables or through direct contact with cat faeces [1].
Immunocompetent persons with an acute infection usually are asymptomatic. However, a latent phase ensues and is characterized by persistence of the organisms primarily in the brain, skeletal muscle, and heart. Chronically infected individuals who develop defects in cell-mediated immunity are at risk for reactivation of this latent infection.
The most common presenting symptom in patients with cerebral toxoplasmosis is headache. This is often accompanied by altered mental status and fever. Patients also may present with seizures, cranial nerve abnormalities, visual field defects, and sensory disturbances. Focal neurologic signs are common and include motor weakness and speech disturbances [2].
 
Cerebral toxoplasmosis presents clinical and cerebrospinal fluid non-specific signals. The clinical applicability of studies on the DNA of T. gondii, using the polymerase chain reaction, is still under investigation. This makes it very important to be able to recognize cerebral toxoplasmosis patterns on magnetic resonance imaging (MRI) performed at the initial stages of the clinical case [3].
 
MRI of brain and spine is key in the investigation of immunosuppressed patients who present with neurological symptoms such as altered mental status.
The leading diagnostic considerations for central neurological system (CNS) lesions with mass effect in a previously untreated Human immunodeficiency virus (HIV) patient, are cerebral toxoplasmosis and primary CNS lymphoma [4, 5, 6].
Definitive diagnosis of toxoplasmosis requires a compatible clinical syndrome, detection of the organism in a biopsy specimen, and solitary or multiple intracerebral lesions with mass effect on MRI of brain. Without treatment, toxoplasmosis can be fatal and in the majority of cases, therapy is initiated after making a presumptive, rather than definitive, diagnosis of toxoplasmosis.
One of the most commonly described findings of CNS toxoplasmosis is the postcontrast T1 “eccentric target sign” that has three alternating zones: an innermost eccentric enhancing core, an intermediate hypointense zone, and an outer peripheral hyperintense enhancing rim. A more specific imaging pattern is the more recently described “concentric target sign” on T2 weighted MRI. This focal lesion has alternating concentric layers of T2 weighted hypo- and hyperintensities [7].
This case demonstrates the importance of recognition of the key radiological features of CNS lesions in HIV patients to prevent delay of treatment.

Based on laboratory results and imaging studies, a diagnosis of cerebral toxoplasmosis was made and antitoxoplasma therapy was initiated.
After 5 days, the patient was completely conscious and no more febrile.