Diagnosis Of Cerebral Toxoplasmosis Research Articles

Clinical manifestations and neuron-specific enolase cerebrospinal fluid concentration in HIV/AIDS patients with cerebral toxoplasmosis

Background. Cerebral toxoplasmosis (CT) is one of the most common cause of focal neurological defi cit in HIV/ AIDS group of patients. Timely diagnosis of CT and antiparasitic therapy contribute to decrease of lethal outcomes and disability. Aim. To study neurological manifestations, cognitive functions and neuron-specifi c enolase (NSE) concentration in cerebrospinal fluid (CSF), in HIV/AIDS patients with CT. Material and methods. The 35 patients (10 females and 25 males) from 28 to 50 years old with confirmed diagnosis of HIV/AIDS-associated CT were included in the investigation group. Neurological status, cognitive function and laboratory CSF changings had been studied in prospective investigation before and during the treatment with control points in the 1st and 10th days of the observation. Results. The method of neurological manifestation of CT evaluation had been developed and implemented in practice. The association between neurological defi cit severity (movement and sensory disorders), cognitive decline and increasing CSF concentration of NSE in HIV/AIDS-associated CT was determined that demonstrates the activity of encephalitic process. Conclusion. Dynamic evaluation of NSE concentration in CSF with clinical assessment of neurological manifestation in patients with HIV/AIDS-associated CT may be used for confirmation of specific antiparasitic treatment effectiveness and for increasing clinical criteria significance.

Evidence of Hearing Loss and Unrelated Toxoplasmosis in a Free-Ranging Harbour Porpoise (Phocoena phocoena).

Simple SummaryEvidence of hearing impairment was identified in a female harbour porpoise (Phocoena phocoena) on the basis of inner ear analysis. The animal live stranded on the Dutch coast at Domburg in 2016 and died a few hours later. Ultrastructural examination of the inner ear revealed evidence of sensory cell loss, which is compatible with noise exposure. In addition, histopathology also revealed multifocal necrotising protozoal encephalitis. A diagnosis of toxoplasmosis was confirmed by positive staining of tissue with anti-Toxoplasma gondii antibodies; however, T. gondii tachyzoites were not observed histologically in any of the examined tissues. This is the first case of presumptive noise-induced hearing loss and demonstration of T. gondii cysts in the brain of a free-ranging harbour porpoise from the North Sea.Evidence of hearing impairment was identified in a harbour porpoise (Phocoena phocoena) on the basis of scanning electron microscopy. In addition, based on histopathology and immunohistochemistry, there were signs of unrelated cerebral toxoplasmosis. The six-year old individual live stranded on the Dutch coast at Domburg in 2016 and died a few hours later. The most significant gross lesion was multifocal necrosis and haemorrhage of the cerebrum. Histopathology of the brain revealed extensive necrosis and haemorrhage in the cerebrum with multifocal accumulations of degenerated neutrophils, lymphocytes and macrophages, and perivascular lymphocytic cuffing. The diagnosis of cerebral toxoplasmosis was confirmed by positive staining of protozoa with anti-Toxoplasma gondii antibodies. Tachyzoites were not observed histologically in any of the examined tissues. Ultrastructural evaluation of the inner ear revealed evidence of scattered loss of outer hair cells in a 290 µm long segment of the apical turn of the cochlea, and in a focal region of ~ 1.5 mm from the apex of the cochlea, which was compatible with noise-induced hearing loss. This is the first case of concurrent presumptive noise-induced hearing loss and toxoplasmosis in a free-ranging harbour porpoise from the North Sea.

Detection and treatment of cerebral toxoplasmosis in an aplastic pediatric post-allogeneic hematopoietic cell transplant patient: a case report

BackgroundCerebral toxoplasmosis infection presents with non-specific neurologic symptoms in immunocompromised patients. With lack of measurable adaptive immune responses and reluctance to sample affected brain tissue, expedient diagnosis to guide directed treatment is often delayed.Case presentationWe describe the use of cerebrospinal fluid polymerase chain reaction and plasma cell-free DNA technologies to supplement neuroimaging in the diagnosis of cerebral toxoplasmosis in an immunocompromised pediatric patient following allogeneic hematopoietic cell transplantation for idiopathic severe aplastic anemia. Successful cerebral toxoplasmosis treatment included antibiotic therapy for 1 year following restoration of cellular immunity with an allogeneic stem cell boost.ConclusionsPlasma cell-free DNA technology provides a non-invasive method of rapid diagnosis, improving the likelihood of survival from often lethal opportunistic infection in a high risk, immunocompromised patient population.

Immunodiagnostics of cerebral toxoplasmosis depending on permeability of blood-brain barrier

The aim of the work was to detect a diagnostic value of CNSToxoIndex - index of correlation between albumin concentration and anti-toxoplasma antibodies, which reflects local production of anti-toxoplasma IgG in CNS compared with their level in blood. Materials and methods: 30 HIV-infected persons with the IV clinical stage (16 man and 14 women) aged from 25 to 49 years with clinical and instrumental signs of cerebral toxoplasmosis were selected from the general array of the patients treated in the Regional Clinical Infectious Hospital. A retrospective parallel detection of IgG T. gondii was performed in serum and CSF in patients, whose results of ELISA or PCR on T. gondii were positive. Blood serum and CSF were obtained from patients at the same time. All samples for analysis were stored at -20 °C and then tested on the RT-2100C Rayto Life and Analytical Sciences Co., Ltd (China) immunoassay analyser for quantitative detection of the level of specific anti-Toxicoplasma IgG. Detection of albumin concentration in serum and CSF was performed on the Chemray-120 Automated Biochemical Analyzer Rayto Life and Analytical Sciences Co., Ltd (China) using the Liquick Cor-ALBUMIN Diagnostic Kit. Results: Specific IgG to T. gondii in blood plasma was found in 27 patients (90%) while in CSF only in 7 (23 %). The results of the research in this group of patients were represented by the following parameters: patient 1 (blood antiToxo IgG - 200 IU/ml, blood albumin - 36 g/l, CSF antiToxo IgG - 10 IU/ml, CSF albumin - 0.8 g/l, CNSToxolndex - 2.3); patient 2 (150 / 40 / 90 / 0.7 / 34.3, respectively); patient 3 (90 / 35 / 64 / 0.25 / 99.6); patient 4 (140 / 39/ 10/ 0.19/ 14.7); patient 5 (88 / 52 / 48 / 0.21 / 135.1); patient 6 (160 / 48 / 50 /0.15 / 100.0); patient 7 (122 / 42 / 15 / 0.17 / 30.4). Consequently, taking into consideration the diagnostic marker CNSToxolndex more than 10.0, cerebral toxoplasmosis was diagnosed only in six patients from seven, in whom anti-toxoplasma antibodies in CSF were detected. Patient 1, despite clinical symptoms similar to cerebral toxoplasmosis, and substitute signs of cerebral toxoplasmosis detected with the help of neuroimaging methods (volumetric formation of the right frontal lobe with a ring-shaped enhancement), availability of specific anti-toxoplasma antibodies in blood serum and CSF, diagnosis of cerebral toxoplasmosis has not been confirmed. M. tuberculosis DNA was found in CSF by PCR. Conclusions: CNSToxoIndex allows evaluating the local production of anti-toxoplasmic IgG in CNS and their diffusion from blood as a result of the blood-brain barrier damageand it is a powerful method of cerebral toxoplasmosis diagnostics in HIV-positive people as well.

ТОКСОПЛАЗМОЗ ГОЛОВНОГО МОЗГА У БОЛЬНЫХ КО-ИНФЕКЦИЕЙ ТУБЕРКУЛЕЗ/ВИЧ

На сегодняшний день проблема церебрального токсоплазмоза у больных ко-инфекцией туберкулез/ВИЧ остается малоизученной. Цель исследования. Выявить особенности диагностики и лечения токсоплазмоза головного мозга у больных ко-инфекцией туберкулез/ВИЧ. Материал и методы. Обследованы 20 больных ко-инфекцией туберкулез/ВИЧ с церебральным токсоплазмозом. У всех пациентов диагностирован активный туберкулез, они получали противотуберкулезную химиотерапию. Лечение токсоплазмоза проводили бисептолом в сочетании с макролидами (кларитромицин, азитромицин) или клиндамицином. Результаты и обсуждение. Из 17 иммунологически обследованных больных у 16 содержание СD4 не превышало 78 кл/мкл (медиана 34,0 кл/мкл), у 16 из 20 пациентов диагностировали диссеминированный туберкулез легких и лимфатических узлов. Пациенты жаловались на слабость в конечностях, (9 человек), головную боль (7 человек), судороги и нарушения походки (по 5 человек). При неврологическом осмотре у 16 выявляли симптомы раздражения черепно-мозговых нервов, у половины – ригидность затылочных мышц и положительный симптом Кернига. Из 11 исследований ликвора нормальные показатели уровня белка выявляли в 8 случаях, глюкозы – 7 случаях, количества клеточных элементов – 8 случаях. У 10 пациентов была отрицательной проба Нонне-Апельта. Нормальный состав наблюдали у двух пациентов. Двусторонние токсоплазменные абсцессы находили у 17 больных, у остальных изменения были одиночными, крупных размеров (45-65 мм). Диагноз церебрального токсоплазмоза прижизненно верифицирован у 17 больных, у остальных стал патологоанатомической находкой. В стационаре умерло 12 из 20 больных, на аутопсии обнаруживали генерализованный туберкулез, признаков туберкулезного менингоэнцефалита не было. Антиретровирусную терапию присоединяли 9 больным, медиана продолжительности лечения перед этим составляла 43 дня. Зафиксировано два случая развития синдрома восстановления иммунной системы, повлекших смерть пациентов, остальные больные продолжили лечение, что привело к частичной регрессии клинической симптоматики и изменений в головном мозге. Приведен случай успешного лечения диссеминированного туберкулеза и токсоплазмоза головного мозга. Выводы. Церебральный токсоплазмоз у большинства больных ко-инфекцией туберкулез/ВИЧ развивался при содержании CD4 ниже 100 кл/мкл и протекал на фоне диссеминированного туберкулеза легких с поражением лимфоузлов. Больные предъявляли жалобы на слабость в конечностях и головную боль (9 и 7 человек), каждого четвертого беспокоили судороги и шаткость походки. У 16 определяли симптомы раздражения черепно-мозговых нервов, у половины – менингеальные знаки. В ликворе большинства пациентов выявляли нормальное содержание белка, глюкозы, клеточных элементов. Лечение токсоплазмоза и ко-инфекции туберкулез/ВИЧ является сложной задачей, залогом успеха является своевременная диагностика и присоединение антиретровирусной терапии.

Imaging features of central nervous system lesions in AIDS

Aims and objectives 1)To review and illustrate imaging patterns of the main pathological conditions that affects the central nervous system in HIV/AIDS, 2)To study the usefulness of imaging (CT and MRI of the central nervous system) in the diagnosis of neurological complications of AIDS, 3)To understand the impact of the immune status on the epidemiology and imaging of neurological complications of AIDS. Methods and materials We carried out a retrospective analysis of clinical biological and radiological data of HIV infected patients explored in our institution. Results Among the study period, 15 HIV infected patients were admitted for neurological symptoms. The main age was 37.6. Patients were predominantly male. Clinically, all patients had fever. CT was performed for all patients and MRI for 6 of them. The diagnosis of cerebral Toxoplasmosis was considered in 7 (46.66%) cases. Cerebral Cryptococcosis was found in 3 cases (20%), and cerebral Tuberculosis in 1 (6.66%). Progressive multifocal leukoencephalopathy (PML) was diagnosed in 4 (26.66%) cases. For one patient (6.66%), the diagnosis remained unestablished. The main age of patients was 37.6 year-old with masculine predominance. The principal symptom was a neurological deficit in 7 cases. Conclusion The introduction of Highly Active Anti Retroviral Therapy (HAART) has lead to a decline in the incidence of HIV related infections and neoplasms. Nevertheless, these are conditions are still seen. Imaging diagnosis relies to the radiological findings coupled with serological and CSF analysis. The radiologist should be aware of the changing epidemiology of HIV complications in correlation with immune status of the patient which helps establish the correct diagnosis and improve management and prognosis.

Cerebral Toxoplasmosis Masquerading Cns Lymphoma on FDG PET-CT in Post Renal Transplant Patient.

20 year old post renal transplant patient developed recurrent episodes of seizure. MRI revealed focal lesion in right parieto-occipital lobe with perilesional edema. FDG PET-CT revealed multiple hypermetabolic lesions in bilateral cerebral hemisphere. Subsequent biopsy from the lesion demonstrated bradyzoites of Toxoplasma gondii with inflammatory cells and thereby, a confirmatory diagnosis of cerebral toxoplasmosis was made. This case demonstrates the fact that increased FDG uptake in cerebral lesions in post transplant patient should be interpreted with caution and confirmed with histopathological correlation.

Cerebral Toxoplasmosis in an HIV-Negative Patient: A Case Report

Introduction: Toxoplasmosis is caused by infection with the obligate intracellular parasite Toxoplasma gondii. Toxoplasmosis is generally a late complication of HIV infection and usually occurs in patients with CD4+ T-cell counts below 200 cells/iL. Case Presentation: A case of cerebral toxoplasmosis is reported in a healthy 39-year-old woman who was admitted to hospital with the complaint of a headache. Gadolinium-enhanced brain magnetic resonance imaging (MRI) showed an irregular, ring enhancing, hyperintense lesion in the right temporoparietal lobe. Toxoplasma serology revealed raised IgG antibody levels. Based on the MRI features, biopsy, and serology, a diagnosis of cerebral toxoplasmosis was made. Conclusions: Cerebral toxoplasmosis can occur outside the setting of advanced HIV immunodeficiency or drug-induced immunosuppression. This highlights the fact that it should be considered in the differential diagnosis of opportunistic infections in HIV-negative patients.

Cerebral toxoplasmosis in children and adolescents from “Dr. Victor Babeş” Hospital pediatric HIV-cohort

Cerebral toxoplasmosis (Toxo) is rarely described in children. The Romanian pediatric cohort consists of children that have been infected parenterally in the late ’80s. We aimed to describe the prevalence, clinical findings and outcome of Toxo in children and adolescents from the Romanian Pediatric Cohort, that have been diagnosed in the “Dr. Victor Babes” Hospital, one of the main reference centers for HIV from Romania Cerebral toxoplasmosis was diagnosed based on CDC case definition (presumptive and definitive diagnosis). We reviewed retrospectively the charts of all 29 children diagnosed with Toxo starting 1996, recording the demographic, HIV markers, antiretroviral treatment, clinical and neuroimaging data, treatment and outcome of Toxo. The prevalence of Toxo was 4.8% from 604 patients followed in the Hospital. Out of 29 patients diagnosed with Toxo, 19 were girls and 28 had parenterally and 1 had vertically acquired HIV. The mean age at HIV diagnosis was 11.5±6.5 years, and 15.6±5.3 years at Toxo diagnosis. In 10 patients HIV was diagnosed concomitantly with Toxo. At onset 89.7% patients had focal neurological signs and 62.1% had headache. Median CD4 count was 60 (95% CI for median 27-95) lf/cmm. 28 patients had positive T. gondii IgG antibodies in plasma and/or cerebrospinal fluid. Only 6 patients had treatment with cotrimoxazole, most of them being treated with pyrimethamine/sulphadoxine combination and alternatively with atovaquone. 69% of patients had any adverse reactions to Toxo treatment. Most adverse reactions were cutaneous in 10 patients (5 severe) and anemia in 7 patients. Nine patients had antiretroviral therapy (ART) before Toxo diagnosis, out of them 1 had mono, 1 dual therapy, 6 were failing cART and one patient had immune reconstitution syndrome. Ten patients (34.5%) died. The median survival time was 117 months. In univariate analysis survival was correlated with shorter time from onset to admission (p=0.04) while on multivariate analysis diagnosis in the post-cART period was the only factor associated with longer survival (p=0.03). 14 of 19 patients recovered with sequels, most of them motor deficits. Cerebral toxoplasmosis in this particular pediatric cohort shared common features with that reported in adults pertaining to prevalence in pre-cART period and pathogenic mechanism. Survival was associated with a more rapid diagnosis of cerebral toxoplasmosis and with access to cART.

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

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.

Uccessful Treatment of Cerebral Toxoplasmosis with Clindamycin: A Case Report

Toxoplasmosis is caused by infection with the obligate intracellular parasite Toxoplasma gondii. Toxoplasmosis is generally a late complication of HIV infection and usually occurs in patients with CD4 + T-cell counts below 200/μl. Co-trimoxazole (trimethoprim plus sulfamethoxazole) is the most common drug used in India for the treatment of AIDS-associated cerebral toxoplasmosis. Other alternative drugs used for the treatment of cerebral toxoplasmosis are clindamycin plus pyrimethamine and clarithromycin with pyrimethamine.A 30-year-old male known case of retroviral disease presented to Kasturba Medical College, India, with complaints of fever, headache and vomiting. Computed tomography scan of his brain showed irregular ring enhancing lesion in the right basal ganglia. Toxoplasma serology revealed raised IgG antibody levels. Based on the CT features and serology, diagnosis of cerebral toxoplasmosis was made. He was treated with clindamycin alone as he had history of sulfonamide allergy. The patient was symptomatically better after 48 hours. After 21 days, repeat CT of brain was done which was normal. The patient showed good clinical improvement within 48 hours and the lesion resolved completely within 3 weeks. The authors recommend using clindamycin without pyrimethamine in resource poor settings and in patients who do not tolerate sulfa drugs.

An unsuspected case of cerebral toxoplasmosis: case report and literature review

Toxoplasmosis caused by Toxoplasma gondii is one the most frequent opportunistic infections among the immunocompromised patients and commonly affects the brain of those individuals with advanced human immunodeficiency virus (HIV) infection with acquired immune deficiency syndrome (AIDS). Cerebral toxoplas-mosis can be a challenging histopathological diagnosis when it presents as the early sequela of clinically unsuspected immuno-suppression. We report a case with problematic histopathological diagnosis of cerebral toxoplasmosis because of the patient’s unsuspected HIV status, the clinico-radiological impression of metastatic malignancy, and the compounded difficulty of identifying the typical T. gondii organisms in frozen section material. However, this case highlights the need to always contemplate a non-neoplastic infective cause as the basis for observed necrosis in brain biopsies, regardless of the clinical suspicion under which the histopatholo-gical examination has been requested.

Pyogenic brain abscess in toxoplasmosis lesion in a patient with AIDS

Introduction Brain abscesses remain common among HIV-infected immunocompromised patients. In addition to the pyogenic organisms found in the healthy host, toxoplasma gondii, mycobacteria, fungi, protozoa, and Listeria species have all been reported as causative pathogens. We report here an unusual case of a brain abscess caused by Streptococcus acidominimus in an HIV-infected patient that partially responded to initial antimicrobial treatment. Case A 29-year-old Hispanic female with AIDS (CD4 18cells/μl and viral load 34 350 copies/ml) not on highly active antiretroviral treatment (HAART) and an active history of IV heroin abuse was found disoriented and confused. A brain CT scan revealed an irregularly shaped ring-enhancing lesion in the left frontal lobe with extensive vasogenic edema producing left-to-right shift (Fig. 1a). The immunoglobulin G (IgG) antitoxoplasma antibody was negative. The patient was sent to the operating room for emergent craniotomy and brain biopsy during which, a pocket of pus was found and the fluid was drained and sent for culture. As the finding was believed to be consistent with a pyogenic brain abscess, the patient was placed on empiric antibiotics including vancomycin, cefepime, and metronidazole, pending further microbiologic data. Postoperatively the patient was aphasic and right-sided hemiparesis was notable in the neurologic examination. Final cultures of the aspirate yielded Streptococcus acidominimus and her antibiotic regimen was changed to ceftriaxone and metronidazole for a total of 8 weeks of treatment.Fig. 1: MRI series of the pyogenic brain abscess in toxoplasmosis lesion in a patient with AIDS.Seven days after neurosurgery the patient was awake, alert and cooperative with a marked improvement of her neurologic signs (normal speech, hemiparesis resolved). Brain MRI at weeks 1, 2 and 3 (Fig.1b–e) after the initiation of treatment did not show any decrease in the abscess size. However, the edema and midline were significantly diminished. At this point the immunoglobulin M (IgM) antitoxoplasma antibody was positive and therapy for Toxoplasma gondii encephalitis started. Two weeks after the initiation of pyrimethamine, sulfadiazine and leukovorin the brain MRI revealed significant decrease of abscess size (Fig. 1f). Discussion The incidence of focal neurological diseases in patients AIDS has decreased after the introduction of the highly active antiretroviral therapy [1]. The initial approach to management of expansive brain lesions in HIV-infected patients include considering the diagnosis of cerebral toxoplasmosis [2], the most common cause of intracranial mass lesion in HIV-infected patients. However, the differential diagnosis should also include viridans streptococci, methicillin-resistant Streptococcus aureus, Gram-negative bacilli, listeria monocytogenes, Mycobacterium tuberculosis, Nocardia and Rhodococcus species. Differently from cerebral toxoplasmosis, brain abscesses are usually characterized by a peripheral uniform ring enhancement after the injection of contrast, a central high signal on T2-weighted and markedly hyperintense signal on DWI, indicating restricted diffusion [3]. Conclusion Streptococcus acidominimus is a Gram-positive facultative anaerobic organism of the Strepotococcus viridans group, which includes oropharyngeal commensals that have been cultured on dental plaque [4]. As is the case for 20% of patients with brain abscesses, the primary source of infection in our patient's case remained cryptogenic despite a full investigation. On further questioning, however, the patient described the routine of holding the needle in her teeth just prior to injecting heroin. We hypothesize that transient bacteremia from the intravenous injection lead to the bacterial seeding of a preexisting brain lesion. However, initial antibiotics alone did not decrease the lesion. Serum toxoplasma IgG can be negative in 5% of patients with end stage AIDS. It was only after treating for toxoplasmosis that our patient's lesion finally resolved.

Acquired immunodeficiency syndrome and opportunistic infections

This article presents a clinical case of late diagnosis of cerebral toxoplasmosis and cytomegalovirus retinitis of right eye in a 32-year-old patient who was unaware of her HIV status. In addition, this article reviews the literature reflecting clinical, diagnostic, and treatment issues of some opportunistic infections in AIDS.

Use of the serum reactivity against Toxoplasma gondii excreted–secreted antigens in cerebral toxoplasmosis diagnosis in human immunodeficiency virus-infected patients

Despite the development of serological and molecular methods in recent years, the diagnosis of cerebral toxoplasmosis in human immunodeficiency virus (HIV)-infected patients still presents difficulties. In the present study, we investigated whether cerebral toxoplasmosis induced changes in the reactivity of serum toward Toxoplasma gondii excreted-secreted antigens (ESA) in order to develop an assay for evaluating HIV-infected patients with cerebral toxoplasmosis. The antigen selection was based on those produced by tachyzoites, since it is the form of the organism responsible for disseminating the infection, as well as stimulation of the humoral and cellular immune responses. By using an ELISA containing pooled ESA recovered from infected culture supernatants with tachyzoites-RH strain (ESA-ELISA), we found that ESA had a high specificity for sera from patients with cerebral toxoplasmosis. The reactions were compared with an ELISA using crude tachyzoites antigen, widely used in traditional serology. The assays were performed on 293 serum samples separated as follows: 100 sera from patients with cerebral toxoplasmosis and AIDS (symptomatic), 99 sera from individuals with chronic toxoplasmosis (asymptomatic) and 94 sera from healthy individuals without toxoplasmosis (control). The crude tachyzoite antigen in ELISA was able to distinguish both groups of sera with toxoplasmosis, as similar reactivity were observed in sera from patients with cerebral toxoplasmosis and those from chronic individuals. In contrast, ESA-ELISA distinguished sera from symptomatic and asymptomatic individuals (three times more reactive in the former group, 12.6 versus 4.2). The assays were reproducible based on immunoblotting and statistical analysis. These data suggest the utility of ESA-ELISA in the diagnosis of cerebral toxoplasmosis in HIV-infected patients, since it provided clear evidence that anti-ESA antibodies are present principally in patients with active infection. The absence of a significant amount of antibodies distinguished the patients without clinical symptoms of infection.

Diagnosis of cerebral toxoplasmosis by detection of Toxoplasma gondii tachyzoites in cerebrospinal fluid

Sirs: In patients with human immune deficiency syndrome, cerebral toxoplasmosis is one of the typical opportunistic diseases. Compared to cardiac and pulmonary involvement, cerebral manifestation is more common and mediated by the neurotoxic potential of the HIV [1]. Usually, toxoplasmosis can be diagnosed by detecting organism-specific antibodies (IgG, IgM) in blood samples and cerebrospinal fluid (CSF). However, in immunodeficient patients, in particular those with HIV infection in a progressive stage (CD4+-cell count less than 200), the diagnosis of cerebral toxoplasmosis may cause difficulties if only relying on antibody detection. Other diagnostic options are either less specific, less available or more invasive [2, 3]. In the present report, we detected Toxoplasma gondii (Tg) tachyzoites in lumbar CSF in a patient with cerebral toxoplasmosis. To the best of our knowledge, cytologic detection of Tg tachyzoites in lumbar CSF is described for the first time. A 50-year-old female with a 9 year history of untreated HIV infection (CD4+-T-lymphocytes 210/μL corresponding to stage C2 of the CDC 1993 criteria, and HIV viral load more than 100,000 HIVRNA-Genome/ml) with rapid progressive symptoms of encephalitis was admitted to our hospital. The patient was somnolent and disoriented, and she showed signs of basal meningitis consisting of paresis of right-sided cranial nerves VI and VII. In the MRI scan multiple and disseminated T2-lesions were found in supraand infratentorial regions, in particular in the brainstem and cerebellum, where lesions showed ring-shaped contrast enhancement. Meningeal enhancement was described as well. Apart from the MRI results suggestive of opportunistic infection, CSF findings showed a pleocytosis (66 leukocytes/μl), elevation of total protein (1474 mg/dl) and accordingly a moderate dysfunction of the blood-CSF barrier (CSF/serum quotient of albumin 24.0 10–3, ref.-range < 8.0 10–3). The differential cell count of the CSF revealed 87 % lymphocytes, 3 % neutrophils, 1 % eosinophils, 5 % plasma cells and the remaining 4 % were apoptotic cells. There was no evidence for infection with Cryptococcus. Serum anti-Tg IgM-antibodies were within the normal range (normal range < 20 U/L) and IgG-antibodies were slightly increased (113 U/L, normal range < 90 U/L). In CSF antibodies against Tg were not elevated. However, interpretation of these results were difficult given the immune deficient condition of the patient. CSF cytology, however, revealed the presence of mostly intracellular organisms (small bow-shaped organisms with slightly eccentrically placed nuclei) morphologically suggestive as Tg tachyzoites and bradyzoites (Fig. 1) in accordance with the previous literature [4]. These findings were confirmed by post-mortem examination of brain tissue. The autopsy revealed the diagnosis of disseminated focal necrotizing Tg encephalitis involving the cerebrum, cerebellum and brainstem. In addition to inflammatory changes typical for HIV encephalitis, Tg organisms were described in multiple brain regions confirmed by immunohistochemical staining. Leptomeningeal infiltration was also found in several regions primarily in parasagittal and right-sided prefrontal regions. Overall the neuropathology findings were in accordance with the MRI findings. The patient refused antiviral as well as anti-toxoplasma treatment, only support measures were provided owing to the patient’s request. She died two weeks after admission to the hospital and 9 years after she was diagnosed with HIV. A possible way to detect Tg organisms is a direct cytologic examination of CSF. However, this procedure is associated with a low sensitivity as described in a large retrospective study where tachyzoites were seen in only 2 out of 6,090 examined CSF’s both of which were ventricular specimens [4]. So far, only five cases exist in the literature where a direct identification of Tg organisms was possible by cytologic examination of CSF [4–8]. However, in all reported cases Tg organisms were detected only in ventricular CSF but not in lumbar CSF. Therefore, it was discussed that lack of detection of tachyzoites in lumbar CSF was due to obstructive hydrocephalus inhibiting the passover of tachyzoites from the ventricles to the subarachnoid space [3]. In our patient a hydroLETTER TO THE EDITORS

Cerebral toxoplasmosis in an allogeneic peripheral stem cell transplant recipient: case report and review of literature

We present a patient who underwent allogeneic peripheral stem cell transplantation (PSCT) for chronic myelocytic leukemia. Twenty months after the PSCT he experienced status epilepticus. Magnetic resonance imaging (MRI) revealed a focus in the ventral thalamus-hypothalamus region. Using stereotactic biopsy with histology and specific polymerase chain reaction investigation from brain tissue, cerebral toxoplasmosis was diagnosed and treated with antiparasitic therapy. Early recognition of such serious and potentially lethal disease enabled prompt specific treatment. This case report emphasizes the role of stereotactic biopsy in diagnosis of cerebral toxoplasmosis. Other methods such as MRI are non-invasive but not sufficiently specific and sensitive.

HIV infection with concomitant cerebral toxoplasmosis and disseminated histoplasmosis in a 45-year-old man

Although disseminated histoplasmosis is a common opportunistic infection in HIV patients in endemic areas, it is not widely known in Japan. We report a rare case of a man from Ghana infected with HIV who was hospitalized in Japan and who suffered from coinfection with cerebral toxoplasmosis and disseminated histoplasmosis. The diagnosis of cerebral toxoplasmosis was confirmed by a brain biopsy, and the therapy for the disease resulted in almost complete resolution of the brain lesion. However, fever of unknown origin continued for 2 weeks, and disseminated histoplasmosis was diagnosed by examination of a blood smear and by the detection of the histoplasma genome in the peripheral blood by means of polymerase chain reaction. The isolate was confirmed to be Histoplasma capsulatum var. duboisii. Therapy with amphotericin B was initiated, and no histoplasma genome in the peripheral blood was detected 3 days later. Unfortunately, the patient died after 10 days from acute respiratory syndrome. This case highlights that histoplasmosis should be included in the differential diagnosis of opportunistic infections in AIDS patients when patients have a history of travel to or arrival from endemic areas.

Clinical features, outcome and survival from cerebral toxoplasmosis in Edinburgh AIDS patients

Nineteen cases of cerebral toxoplasmosis (CTOX) are reported from a group of Edinburgh AIDS patients. All patients were severely immunodeficient at the time of presentation with CD4 count < 50 cells/mm3. Thirteen patients had suffered a previous AIDS-defining illness. In Edinburgh, CTOX has developed in 48% of patients who are seropositive for toxoplasma and have a CD4 count < 50 cells/mm3. It is estimated that at least half of the toxoplasma seropositive patients will develop CTOX if they survive for 21 months after reaching a time in their illness when the CD4 count = 50 cells/mm3. The incidence of CTOX in toxoplasma-seronegative patients with a CD4 count < 50 cells/mm3 is 1.3%. All patients showed improvement on treatment and there was no correlation between clinical or radiological features and patient survival. Those patients unable to tolerate first choice anti-toxoplasma therapy had a significantly shorter survival than the remainder but there was no single therapeutic regimen which conferred a survival advantage. Eighteen patients had died at the time of study and the median survival following diagnosis of cerebral toxoplasmosis was 10 months (range 3-38 months). Postmortem examination of the brain was available in 8, 4 of whom had concomitant cerebral lymphoma. The survival from AIDS or CD4 count = 50 cells/mm3 did not differ significantly between those with treated CTOX and a control group who had no toxoplasma infection, suggesting that treatment is reasonably effective. CTOX is a disease associated with severe HIV-related immunodeficiency and, in those with a CD4 count < 50 cells/mm3, occurs more than 35 times as frequently in toxoplasma-seropositive than toxoplasma-seronegative patients. Treatment is effective but the outcome of treated disease cannot be predicted from presenting clinical or radiological features. Concomitant space-occupying cerebral pathology is evident in 50% of post-mortem examinations.

Weber's syndrome due to a possible solitary brainstem toxoplasmosis as a presenting sign of AIDS

We report the case of a young man, with a previous history of parenteral drug abuse, who developed a Weber's syndrome. Brain computed tomographic scan and nuclear magnetic resonance imaging showed a single ring enhancing lesion in the right mesencephalic site. After the demonstration of seropositivity for human immunodeficiency vims, a presumptive diagnosis of cerebral toxoplasmosis in an AIDS patient was made and a specific treatment was started. A partial neuroradiological and clinical improvement were obtained. Opportunistic cerebral lesions, as first manifestation of AIDS, should be always considered in subjects at risk for AIDS who present a brainstem syndrome.