Original Article
Toxoplasmosis of the Central Nervous System in the Acquired Immunodeficiency Syndrome
N Engl J Med 1992; 327:1643-1648December 3, 1992
- Abstract
- Abstract
Background and Methods.
Toxoplasmosis is the most common opportunistic infection of the central nervous system in patients with the acquired immunodeficiency syndrome (AIDS). To investigate its clinical course, we reviewed the records of 115 patients with AIDS and central nervous system toxoplasmosis treated at San Francisco General Hospital between 1981 and 1990.
Results.
The most common presenting symptoms were headache (in 55 percent), confusion (52 percent), and fever (47 percent). Focal neurologic deficits were present in 79 patients (69 percent). The median CD4 cell count at presentation was 50 per cubic millimeter (50× 106 per liter). Thirteen of 80 patients with clinical toxoplasmosis (16 percent) and 4 of 18 patients with pathologically proved disease (22 percent) had undetectable antitoxoplasma IgG antibodies by indirect immunofluorescence assay. Of 103 patients, 94 (91 percent) had enhancing lesions on CT. Single lesions were seen in 28 of 103 patients (27 percent) on CT, and such lesions were seen in 3 of 21 patients (14 percent) on magnetic resonance imaging. Over 90 percent of patients who eventually had clinical and radiographic improvement had evidence of improvement by day 14 of therapy. Adverse drug reactions occurred in 71 patients (62 percent) and led to a change in therapy in 50 patients (43 percent). Among the patients who survived a first episode of toxoplasmosis, the median survival was 265 days.
Conclusions.
Toxoplasmosis occurs in advanced stages of human immunodeficiency virus infection, and the absence of antitoxoplasma antibodies on immunofluorescence assay does not exclude the diagnosis. The clinical and radiographic response to therapy is usually rapid, but treatment is frequently limited by adverse drug effects. (N Engl J Med 1992;327:1643–8.)
Article Activity
- Article
TOXOPLASMOSIS of the central nervous system occurs in 3 to 40 percent of all patients with the acquired immunodeficiency syndrome (AIDS), and it is the most common opportunistic infection to cause encephalitis or focal intracerebral lesions.1 It is standard practice to provide empirical treatment for patients infected with the human immunodeficiency virus (HIV) who have intracerebral lesions that raise suspicion of toxoplasmosis, and to perform a biopsy only in patients who do not have a prompt clinical and radiographic response or who have no serologic evidence of previous infection.2 Information about the expected time of improvement would be useful and could allow more rational use of invasive diagnostic procedures.
In this retrospective review, we describe our experience with toxoplasmosis of the central nervous system in 115 patients with AIDS at San Francisco General Hospital. We specifically examined the role of serologic testing in the diagnosis of toxoplasmosis, the clinical and radiographic presentations, the time course of the initial response to therapy, and the usefulness of CT as compared with magnetic resonance imaging (MRI) in the clinical management of the disease.
Methods
From a review of diagnoses at discharge and of CT and MRI records for the period from January 1, 1981, through September 30, 1990, we identified 307 potential cases of toxoplasmosis at San Francisco General Hospital; the medical records for 281 of these patients were available for review. A patient was considered to have toxoplasmosis if there was histologic proof of central nervous system infection at either biopsy or autopsy, in addition to the appearance of brain lesions on CT or MRI consistent with a diagnosis of toxoplasmosis that improved after specific treatment. Histologic proof of toxoplasmosis was defined to include either the demonstration of tachyzoites in stained tissue sections (22 patients) or the demonstration of cysts containing Toxoplasma gondii surrounded by an inflammatory reaction (7 patients). Of the 281 medical records reviewed, 167 did not meet the definition of toxoplasmosis, because there was no follow-up available (52 patients), there was an alternative diagnosis (34 patients, with lymphoma diagnosed in 15), there was no response to antitoxoplasma therapy or there were one or more stable radiographic lesions when the patient was not being treated (17 patients), the illness was not associated with AIDS (8 patients), the diagnosis was made elsewhere (7 patients), or there were other reasons (49 patients), including no lesion apparent on CT or MRI, incorrect coding of diagnosis, and insufficient clinical data. One hundred fifteen patients met the definition of toxoplasmosis and constituted the study group. During this period, 2494 cases of AIDS were diagnosed at San Francisco General Hospital.
Clinical information was collected with a standardized data form. Each patient's serologic status at the time of presentation was recorded (if known). Dates of death were determined from medical records, from the AIDS Surveillance Branch of the Department of Public Health, or for patients who had left the area, by telephone conversations with health care providers or family members.
Before July 1990, serum was tested for antibodies to T. gondii at the California State Laboratory with an indirect immunofluorescence assay.3 A test was considered positive if there was a serum titer ≥1:16; a sample of cerebrospinal fluid was considered positive when an undiluted specimen was reactive. After August 1990, assays were performed in the clinical laboratory at San Francisco General Hospital with an enzyme-linked immunosorbent assay (ELISA) (Diamedix, Miami). Only two patients had antibody titers measured by ELISA.
One hundred fourteen study patients were treated for toxoplasmosis (one who had disease diagnosed by biopsy had brain herniation and was not treated). A clinical response was defined as an improvement in focal neurologic deficits, level of consciousness, or cognition. In patients who presented with persistent symptoms but had normal neurologic examinations, sustained improvement in symptoms was considered a clinical response. A radiographic response was defined as a decrease in the number or size of lesions on CT or MRI, in addition to the absence of new lesions; a decrease in edema or in the degree of enhancement after the use of intravenous contrast material did not constitute a response. A patient was considered to have relapsed if clinical and radiographic signs of toxoplasmosis reappeared or worsened after there had been an initial response to treatment and stabilization (both clinical and radiographic) of disease.
Only patients who completed at least 6 weeks (42 days) of treatment were included in the evaluation of relapse rates. Drug dosages varied from patient to patient and were dependent on the degree of toxicity and on the clinical judgment of the physician. Of 114 patients initially given pyrimethamine, 63 took 25 mg per day, 20 took 50 mg per day, 25 took 75 mg per day, 3 took 100 mg per day, and 3 took other or unknown dosages. Of 114 patients initially given sulfadiazine, 7 took 2 g per day, 84 took 4 g per day, 18 took 6 g per day, and 5 took other or unknown dosages. Of 43 patients treated with clindamycin (on a variety of dosing schedules), 15 initially took 1200 to 1800 mg per day, 21 took 1801 to 2400 mg per day, 1 took more than 2400 mg per day, and 6 took other or unknown dosages. A variety of dosages were subsequently used for long-term maintenance therapy; all the patients received medication daily. Drug toxicity was considered to be severe if it led to a change in the medical regimen or drug dosage and to be mild if no such alteration was necessary. Leukopenia was defined as a white-cell count of less than 2000 per cubic millimeter (2.0×109 per liter), thrombocytopenia as a platelet count of less than 75,000 per cubic millimeter (75×109 per liter), fever as a temperature above 38.4°C, and diarrhea as an increased frequency of stools, as reported by the patient.
The results were analyzed by standard chi-square contingency tables for categorical variables and by Student's t-test for continuous variables. Survival times were calculated from the date of initial treatment and were analyzed according to the method of Kaplan and Meier; statistical significance was determined with the generalized Savage method of Mantel and Cox. Multivariate analysis was performed with the Cox regression. P values of less than 0.05 were considered to indicate statistical significance.
Results
Of the 115 patients studied, 111 had a first episode of toxoplasmosis. In 55 patients (48 percent), toxoplasmosis was the index AIDS diagnosis; the remaining 60 patients presented a mean of 7.4 months after a diagnosis of AIDS. The number of cases of toxoplasmosis diagnosed per year paralleled the overall number of new AIDS cases seen at our institution; the number of cases of both AIDS and toxoplasmosis increased proportionately from 1981 to 1987 and then stabilized. Moreover, the percentage of cases of toxoplasmosis that represented index diagnoses of AIDS remained constant. The 115 patients studied represented 4.6 percent of all patients with AIDS seen at San Francisco General Hospital over this period.
The majority of the 115 patients were male (110) and either homosexual or bisexual (98); all 5 female patients were heterosexual. Twenty-nine patients were intravenous drug users; 18 of these were also homosexual or bisexual (3 of the 5 female patients were intravenous drug users). The patients' mean age was 38±9.8 years (range, 22 to 62). Sixty-seven percent were white, and 24 percent were Latino; in contrast, Latinos made up only 12 percent of all patients with AIDS seen at our institution in the same period (P<0.001).
Extraneural toxoplasmosis was present in only three patients, two with concomitant pulmonary infection and one with chorioretinitis.
Clinical Features at Presentation
Most patients presented with headache and confusion, and almost half had fever (Table 1Table 1
Signs and Symptoms at Presentation In 115 Patients with Toxoplasmosis of the Central Nervous System.). Seizures were a presenting symptom in almost one third of patients, but they were the sole symptom in only five (4 percent). Only five patients did not present with headache, confusion, fever, or seizures. The duration of specific symptoms before presentation ranged from 5 to 28 days.On physical examination, focal neurologic deficits were identified in 79 patients (69 percent); hemiparesis, ataxia, and cranial-nerve palsies were the most common (Table 1). Fever, abnormal mental status, and psychomotor retardation were the most frequent nonfocal physical signs noted; only one patient in seven had a severely depressed level of consciousness at presentation.
Laboratory Features at Presentation
Standard laboratory tests of serum and cerebrospinal fluid revealed no consistent pattern in the patients tested (Table 2Table 2
Results of Laboratory Tests at Presentation in Patients with Toxoplasmosis of the Central Nervous System.); the cerebrospinal fluid was frequently normal, with only a mild elevation of protein. In contrast, almost 90 percent of patients had CD4 cell counts below 200 per cubic millimeter (200×106 per liter), and in two thirds the CD4 cell count was less than 100 per cubic millimeter (100×106 per liter).Serum antitoxoplasma IgG antibodies were assayed in 80 patients; surprisingly, 13 (16 percent) were negative (Table 3Table 3
Measurement of Serum Antitoxoplasma IgG Titers in Patients with Toxoplasmosis of the Central Nervous System.). The median titer measured by immunofluorescence assay was 1:256. Only two patients had titers measured by ELISA; one was positive, the other negative. IgM antibodies were undetectable in all eight patients tested. In patients with a pathologically proved diagnosis in whom IgG levels were measured, 4 of 18 were negative (22 percent). Cerebrospinal fluid IgG titers, tested in 16 patients who had positive serum titers, were positive in 14 (88 percent), with a median titer of 1:4. Both patients with negative serum titers who were tested had undetectable cerebrospinal fluid IgG titers against toxoplasma.Radiographic Features at Presentation
Of the 115 patients studied, 114 underwent CT (106 patients), MRI (21 patients), or both (13 patients). The results of CT scans with contrast material were available for 103 patients (Table 4Table 4
Radiographic Findings in 103 Patients Presenting with Toxoplasmosis of the Central Nervous System.). Enhancing lesions were seen in 94 patients (91 percent), and the lesions were ring-enhancing in 85 (82 percent). Cerebral edema was present in over three fourths of patients, and it caused a mass effect in 57 (55 percent). The median number of lesions seen was two; a single lesion was present in 28 patients (27 percent). The most common locations were the frontal, basal ganglia, and parietal regions (Table 4). The location of lesions seen on MRI study in 21 patients was similar, but the median number was four. As compared with CT, MRI revealed a solitary lesion in only 3 of the 21 patients (14 percent) (P not significant). Thirteen patients had both MRI and CT scans; in 3 the results were equivalent, whereas in the remaining 10 MRI showed an average of 3.8 more lesions per patient. In three patients, the CT scan was normal and the diagnosis was made only by MRI.Response to Therapy
All but one patient were initially treated with pyrimethamine, sulfadiazine, and leucovorin. Of the 114 patients treated, 6 died during the initial episode of toxoplasmosis, 3 were asymptomatic (with a normal neurologic examination at the start of treatment), 3 presented with seizures only (all of whom had no further seizures after treatment was started), and 6 had no clear clinical improvement with therapy (despite radiographic improvement in all 6 after a median follow-up of 93 days; range, 66 to 407). The remaining 96 patients showed clinical improvement after the start of therapy, allowing the time course of the clinical response to be determined (Fig. 1Figure 1
Time Course of Clinical (Circles) and Radiographic (Squares) Responses to Therapy of Toxoplasmosis of the Central Nervous System.). Between 90 and 95 percent of those who eventually improved clinically with treatment had done so by day 14; all such patients had improved by day 42. The six patients who did not have clinical improvement had primarily cognitive deficits at presentation that persisted.In patients with radiographic improvement, the time course of the response was similar to that observed in patients who improved clinically (Fig. 1). Of the 87 patients who had follow-up CT or MRI studies within the first 42 days, 6 did not improve and subsequently died, whereas the remaining 81 all improved. Over 95 percent of patients (78 of 81 ) responded radiographically by day 14; only 3 patients did not have radiographic improvement until after day 42.
Drug toxicity was noted in 71 of 114 patients (62 percent) at some time during initial or maintenance therapy (Table 5Table 5
Drug Toxicity in Patients Treated for Toxoplasmosis of the Central Nervous System.*). Severe toxicity requiring a change in medication or dosage occurred in 50 patients (44 percent), whereas 40 patients (35 percent) had mild side effects (more than one side effect in 24 patients). Rash, nausea or vomiting, and leukopenia were the most common toxic effects of drugs. Two thirds of the patients with rash and nausea or vomiting had these side effects within the first 21 days of treatment, whereas leukopenia occurred at any time during therapy (median, 26 days; range, 6 to 240). When they occurred, rash and leukopenia were usually severe enough to cause an alteration in therapy. Of the 114 patients initially treated with pyrimethamine and sulfadiazine, 43 had severe toxicity necessitating a change to pyrimethamine and clindamycin. The side effects resolved in all, but 11 had different toxic effects with the new regimen. Thus, side effects were more common in the patients treated with pyrimethamine and sulfadiazine (68 of 114 patients) as compared with those treated with pyrimethamine and clindamycin (11 of 43 patients, P<0.001), and they were more frequently severe (49 of 114 patients vs. 1 of 43 patients; P<0.001).Outcome
Of the 115 patients studied, 7 (6 percent) were lost to follow-up, 11 (10 percent) were alive at the end of the study period, and 97 (84 percent) had died (median follow-up, 245 days; range, 2 to 998). The mean survival of patients who died after surviving their first episode of toxoplasmosis was 265±212 days.
Univariate analysis of the various clinical, laboratory, and radiographic variables found the following variables to be associated with decreased survival: severely depressed level of consciousness (P<0.05), history of Kaposi's sarcoma (P<0.05) or Pneumocystis carinii pneumonia (P<0.005) as an AIDS-defining diagnosis, temperature greater than 38.4°C (P<0.05), and blood lymphocyte count ≤24 percent (0.24) (P<0.01). Multivariate analysis revealed, however, that only a history of P. carinii pneumonia (P<0.01) and a blood lymphocyte count ≤24 percent (P<0.01) were independent predictors of decreased survival.
Relapse
Ninety-six patients who responded to therapy and completed at least 6 weeks of treatment were followed for an average of 186 days (range, 43 to 996). Of 10 patients who stopped treatment, 6 relapsed an average of 83 days later (range, 15 to 248). Of the patients who continued treatment, 61 received pyrimethamine and sulfadiazine, 23 received pyrimethamine and clindamycin, and the remainder received pyrimethamine alone. Relapses occurred in six patients (10 percent) taking pyrimethamine and sulfadiazine (median follow-up, 182 days; range, 43 to 886) and five patients (22 percent) receiving pyrimethamine and clindamycin (median follow-up, 266 days; range, 60 to 996). No significant difference in mean relapse-free survival was found between the two treatment regimens.
Discussion
In the current study, toxoplasmosis occurred primarily in advanced HIV infection and was predicted by signs and symptoms of a mass lesion of the central nervous system. Unlike most published reports, in which the rate of detectable antitoxoplasma IgG antibodies approaches 100 percent in central nervous system disease,2 , 4 5 6 7 8 9 10 our study found that one in every six patients did not have detectable antitoxoplasma IgG antibodies. Five patients had repeat tests weeks to months later, and in each case these were also negative. In those patients with pathologically proved disease, the rate of seronegativity was similar.
There are several possible explanations for the high number of seronegative patients in our study. It is possible that some of these patients had newly acquired infections and were tested before they had mounted an IgG response. Given the low number of patients with recently acquired disease in the United States, however, as well as the lack of patients with detectable IgM in our series, it seems unlikely that newly acquired infection accounted for the high rate of seronegativity. An alternative explanation is that antibodies may have been present in some patients, but in concentrations too low to be detected by the immunofluorescence assay used at the California State Laboratory. Because the serum samples were no longer available, we were unable to confirm the results by batch testing. A recent study at San Francisco General Hospital, however, examined the reliability of the immunofluorescence assay.11 Two hundred forty-two serum samples were tested for antibodies to toxoplasma by both the immunofluorescence assay and ELISA; 159 were negative and 62 were positive by both methods, giving a concordance rate of 91 percent. Of 77 samples positive by ELISA, 15 had a negative immunofluorescence assay. In comparison, of 69 samples with a positive immunofluorescence assay, 6 were negative by ELISA. In virtually all cases in which discordant results were obtained, the samples had the lowest positive titers. It appears, therefore, that the immunofluorescence assay may be less sensitive in the detection of IgG directed against toxoplasma. Given this result and the findings in our study, we conclude that negative toxoplasma serologic status as determined by immunofluorescence assay should not be used to exclude the diagnosis of toxoplasmosis in patients with AIDS.
Our data are consistent with those of others who have reported finding solitary lesions on up to 39 percent of CT scans12 , 13 but on less than 20 percent of MRI scans.12 , 14 Despite the lower sensitivity of CT, only 3 of 106 patients (3 percent) had normal CT scans at presentation. CT would thus seem appropriate for use as an initial screening test in patients with advanced HIV infection who present with signs of toxoplasmosis. Patients with no lesions or solitary lesions on CT should undergo MRI to clarify the extent of involvement. Patients with solitary lesions on MRI, especially those with negative serologic tests, should be considered for early biopsy.
In our study, 95 percent of patients for whom there was radiographic evidence of a response to therapy had such evidence by day 14 of treatment. Clinical responses paralleled radiographic improvement. Since the large majority of our patients had follow-up CT scans, the results suggest that CT is adequate to detect early improvement after antitoxoplasma therapy.
Toxicity commonly complicates the treatment of toxoplasmosis. Reported rates of toxicity range from 38 to 71 percent, with medication changes required in 25 to 53 percent of patients.2 , 7 8 9 10 , 15 In the current study, side effects were noted in 62 percent of patients, with changes in the medication regimen required in 43 percent. Toxicity in general, and severe side effects in particular, were more frequently associated with sulfadiazine than with clindamycin. Similar results have been reported in other studies,10 , 16 , 17 although one recent report found no difference in rates of toxicity between these two drugs.18 In that study, however, a very high dose of clindamycin (4.8 g per day) was used. Our rates of toxicity may underestimate the problem; individual patients received drugs for varying lengths of time, often in different dosages at different points in their treatment. Moreover, some patients did not have continuous follow-up during the entire study period, and thus some side effects may have been unreported. Nevertheless, the rates of toxicity were high, underscoring the need for less toxic medications to treat toxoplasmosis in AIDS.
A majority (60 percent) of the patients who stopped therapy relapsed. In addition, up to 22 percent of those who continued treatment also relapsed, regardless of the type of therapy. Although there was a trend toward higher relapse rates in the patients receiving pyrimethamine and clindamycin, relapse-free survival did not differ significantly between the two medical regimens. Previous studies have reported rates of relapse ranging from 0 to 46 percent in patients receiving maintenance therapy.7 , 10 In one retrospective series, none of the 25 patients who continued to receive daily therapy (pyrimethamine combined with either sulfadiazine or clindamycin) at the full dose and were followed for up to 503 days relapsed.2 In contrast, a study from Spain described a relapse rate of 40 percent in patients given twice-weekly pyrimethamine and clindamycin as maintenance therapy after successful primary therapy.19 It is unknown whether either relatively high dosages of pyrimethamine and clindamycin, their daily administration, or both are necessary for adequate suppression with these medications. The results of prospective studies currently in progress20 are needed to define the optimal drugs and dosages required to prevent reactivation of toxoplasmic encephalitis in patients with AIDS.
We are indebted to Gunnard Modin for assistance with the statistical analyses and to Drs. Julie Gerberding and Belle Lee for critical review of the manuscript.
Source Information
From the Medical Service, San Francisco General Hospital, and the Department of Medicine, University of California, San Francisco. Address reprint requests to Dr. Sande at the Medical Service, Rm. 5H22, San Francisco General Hospital, 1001 Potrero Ave., San Francisco, CA 94110.
- References
References
1
Luft
CrossRef | Web of Science | Medline2
Cohn
CrossRef | Web of Science | Medline3
Remington JS, Desmonts G. Toxoplasmosis. In: Remington JS, Klein JO, eds. Infectious diseases of the fetus and newborn infant. 3rd ed. Philadelphia: W.B. Saunders, 1990:89–195.
4
Luft
CrossRef | Web of Science | Medline5
Wong
Web of Science | Medline6
Navia
CrossRef | Web of Science | Medline7
Wanke
Web of Science | Medline8
Leport
CrossRef | Web of Science | Medline9
Carrazana
CrossRef | Web of Science | Medline10
Pedrol
CrossRef | Web of Science | Medline11
Miller CN, Sugai K, Yajko DM, et al. Evaluation of serologic kits for IgG toxoplasma antibodies. In: Program and abstracts of the 30th Interscience Conference on Antimicrobial Agents and Chemotherapy, Atlanta, October 21–24, 1990. Washington, D.C.: American Society for Microbiology, 1990. abstract.
12
Ciricillo
Web of Science | Medline13
Dina
Web of Science | Medline14
Levy
Web of Science | Medline15
Haverkos
CrossRef | Web of Science | Medline16
Leport
CrossRef | Web of Science | Medline17
Foppa
CrossRef | Web of Science | Medline18
Dannemann
Web of Science | Medline19
González-Clemente
Medline20
Katlama
CrossRef | Web of Science | Medline
- Citing Articles (105)
Citing Articles
1
Tali Siegal, Netta Levin. 2012. Infectious, metabolic, and endocrine complications. , 825-851.
CrossRef2
Katherine T Andrews, Ashraful Haque, Malcolm K Jones. (2011) HDAC inhibitors in parasitic diseases. Immunology and Cell Biology
CrossRef3
Nuzhat Husain, Praveen Kumar. (2011) Pathology of Tropical Diseases. Neuroimaging Clinics of North America 21:4, 757-775
CrossRef4
Kimberly E. Idoko, Isabel Gomez, Puneeta Sharma. (2011) Rhinocerebral Mucormycosis in an Inpatient With Acquired Immunodeficiency Syndrome. Infectious Diseases in Clinical Practice 19:6, 431-432
CrossRef5
Wai Kit Chew, Mak Joon Wah, Stephen Ambu, Ignacio Segarra. (2011) Toxoplasma gondii: Determination of the onset of chronic infection in mice and the in vitro reactivation of brain cysts. Experimental Parasitology
CrossRef6
M Nelson, H Manji, E Wilkins. (2011) 2 Central nervous system opportunistic infections. HIV Medicine 12, 8-24
CrossRef7
Ahmad Daryani, Mehdi Sharif, Masoumeh Meigouni. (2011) Seroprevalence of IgG and IgM anti—Toxoplasma antibodies in HIV/AIDS patients, northern Iran. Asian Pacific Journal of Tropical Medicine 4:4, 271-274
CrossRef8
Feng Tan, Xin Hu, Fang-Jun Luo, Chang-Wang Pan, Xiao-Guang Chen. (2011) Induction of protective Th1 immune responses in mice by vaccination with recombinant Toxoplasma gondii nucleoside triphosphate hydrolase-II. Vaccine 29:15, 2742-2748
CrossRef9
Melba Munoz, Oliver Liesenfeld, Markus M. Heimesaat. (2011) Immunology of Toxoplasma gondii. Immunological Reviews 240:1, 269-285
CrossRef10
Satoshi Utsuki, Hidehiro Oka, Katsutoshi Abe, Shigeyuki Osawa, Tomoya Yamazaki, Yoshie Yasui, Kiyotaka Fujii. (2011) Primary central nervous system lymphoma in acquired immune deficiency syndrome mimicking toxoplasmosis. Brain Tumor Pathology 28:1, 83-87
CrossRef11
Ashley H. Aiken. (2010) Central Nervous System Infection. Neuroimaging Clinics of North America 20:4, 557-580
CrossRef12
Feng Tan, Xin Hu, Chang-Wang Pan, Jie-Qiong Ding, Xiao-Guang Chen. (2010) Monoclonal antibodies against nucleoside triphosphate hydrolase-II can reduce the replication of Toxoplasma gondii. Parasitology International 59:2, 141-146
CrossRef13
Kei Suzuki, Masahiro Masuya, Takeshi Matsumoto, Naomi Ito, Kohshi Ohishi, Masayuki Maeda, Naoyuki Katayama. (2010) High-intensity signals in the basal ganglia from gadolinium-enhanced T1-weighted MRI as an early change in toxoplasma encephalitis in an AIDS patient. Journal of Infection and Chemotherapy 16:2, 135-138
CrossRef14
H. Kovari, C. Ebnöther, A. Schweiger, N. Berther, H. Kuster, H. F. Günthard. (2010) Pulmonary Toxoplasmosis, a Rare but Severe Manifestation of a Common Opportunistic Infection in Late HIV Presenters: Report of Two Cases. Infection 38:2, 141-144
CrossRef15
H. A. Dabritz, P. A. Conrad. (2010) Cats and Toxoplasma : Implications for Public Health. Zoonoses and Public Health 57:1, 34-52
CrossRef16
Mary Patricia J. Craver, Peggy J. Rooney, Laura J. Knoll. (2010) Isolation of Toxoplasma gondii development mutants identifies a potential proteophosphogylcan that enhances cyst wall formation. Molecular and Biochemical Parasitology 169:2, 120-123
CrossRef17
Kazuhiro Horiuchi, Ichiro Yabe, Yasutaka Tajima, Takeshi Kondo, Yoshihiko Takizawa, Hideto Yamada, Hidenao Sasaki. (2010) A case of toxoplasma encephalopathy with specific MRI findings, diagnosed by IgG avidity index and nested PCR. Rinsho Shinkeigaku 50:4, 252-256
CrossRef18
Georgios Pappas, Nikos Roussos, Matthew E. Falagas. (2009) Toxoplasmosis snapshots: Global status of Toxoplasma gondii seroprevalence and implications for pregnancy and congenital toxoplasmosis. International Journal for Parasitology 39:12, 1385-1394
CrossRef19
Omar Lupi, Brenda L. Bartlett, Reshma Nair Haugen, Lady C. Dy, Aisha Sethi, Sidney N. Klaus, Jackson Machado Pinto, Francisco Bravo, Stephen K. Tyring. (2009) Tropical dermatology: Tropical diseases caused by protozoa. Journal of the American Academy of Dermatology 60:6, 897-925
CrossRef20
Ravindra Kumar Garg, Parthiv Desai, Minakshi Kar, Alok Mohan Kar. (2008) Multiple ring enhancing brain lesions on computed tomography: An Indian perspective. Journal of the Neurological Sciences 266:1-2, 92-96
CrossRef21
Carlos S. Subauste, Jose G. Montoya, Jack S. Remington. 2008. AIDS-associated Toxoplasmosis. , 399-413.
CrossRef22
Isabel Dellacasa-Lindberg, Niclas Hitziger, Antonio Barragan. (2007) Localized recrudescence of Toxoplasma infections in the central nervous system of immunocompromised mice assessed by in vivo bioluminescence imaging. Microbes and Infection 9:11, 1291-1298
CrossRef23
Chen-Hsiang Lee, Chun-Chung Lui, Jien-Wei Liu. (2007) Immune Reconstitution Syndrome in a Patient with AIDS with Paradoxically Deteriorating Brain Tuberculoma. AIDS Patient Care and STDs 21:4, 234-239
CrossRef24
John C.M. Brust. 2007. Les opioïdes. , 53-127.
CrossRef25
Irene Lindström, Deogratias H Kaddu-Mulindwa, Fred Kironde, Johan Lindh. (2006) Prevalence of latent and reactivated Toxoplasma gondii parasites in HIV-patients from Uganda. Acta Tropica 100:3, 218-222
CrossRef26
DE Eza, SB Lucas. (2006) Fulminant toxoplasmosis causing fatal pneumonitis and myocarditis. HIV Medicine 7:6, 415-420
CrossRef27
Martin Dedicoat, Nigel Livesley, Martin Dedicoat. 2006. Management of toxoplasmic encephalitis in HIV-infected adults (with an emphasis on resource-poor settings). .
CrossRef28
F. Brun Romero, M. Montes de Oca Arjona, A. Martín Aspas, J.A. Girón González. (2006) Toxoplasmosis. Medicine - Programa de Formación Médica Continuada Acreditado 9:58, 3760-3765
CrossRef29
TOORU YAMAMOTO. (2006) Nihon Naika Gakkai Zasshi 95:7, 1260-1262
CrossRef30
Jose E. Vidal, Adrian V. Hernandez, Augusto C. Penalva De Oliveira, Rafi F. Dauar, Silas Pereira Barbosa, Roberto Focaccia. (2005) Cerebral Toxoplasmosis in HIV-Positive Patients in Brazil: Clinical Features and Predictors of Treatment Response in the HAART Era. AIDS Patient Care and STDs 19:10, 626-634
CrossRef31
Yvette L. Kasamon, Richard F. Ambinder. (2005) AIDS-Related Primary Central Nervous System Lymphoma. Hematology/Oncology Clinics of North America 19:4, 665-687
CrossRef32
M Dedicoat, N Livesley, Martin Dedicoat. 2005. Management of toxoplasmic encephalitis in HIV-infected adults (with an emphasis on resource-poor settings). .
CrossRef33
P. Rivas González, M.L. Fernández Guerrero. (2005) Las infecciones del sistema nervioso central en pacientes con virus de la inmunodeficiencia humana en la era del tratamiento antirretroviral de gran actividad. Revista Clínica Española 205:6, 278-282
CrossRef34
Melanie Walker, Joseph R. Zunt. (2005) Parasitic Central Nervous System Infections in Immunocompromised Hosts. Clinical Infectious Diseases 40:7, 1005-1015
CrossRef35
Francois Durand, Marie-Pierre Brenier-Pinchart, Francois Berger, Patrice N. Marche, Renee Grillot, Herve Pelloux. (2004) Phosphatidylcholine-specific phospholipase C but not gamma interferon regulate gene expression and secretion of CC Chemokine Ligand-2 (CCL-2) by human astrocytes during infection by Toxoplasma gondii. Parasite Immunology 26:10, 419-422
CrossRef36
JG Montoya, O Liesenfeld. (2004) Toxoplasmosis. The Lancet 363:9425, 1965-1976
CrossRef37
Carlos José Castro-Sansores, Renán A Góngora-Biachi, Pedro González-Martı́nez. (2004) HIV-Encephalopathy as initial manifestation of acquired immunodeficiency Syndrome in Yucatán State, Mexico. Archives of Medical Research 35:1, 49-53
CrossRef38
Pasquale F. Finelli, Francis J. DiMario. (2003) Diagnostic Approach in Patients with Symmetric Imaging Lesions of the Deep Gray Nuclei. The Neurologist 9:5, 250-261
CrossRef39
Alexandra Coppin, Florence Dzierszinski, Sandra Legrand, Marlène Mortuaire, David Ferguson, Stanislas Tomavo. (2003) Developmentally regulated biosynthesis of carbohydrate and storage polysaccharide during differentiation and tissue cyst formation in Toxoplasma gondii. Biochimie 85:3-4, 353-361
CrossRef40
Tanya V. Aspinall, Edward C. Guy, Katherine E. Roberts, David H.M. Joynson, John E. Hyde, Paul F.G. Sims. (2003) Molecular evidence for multiple Toxoplasma gondii infections in individual patients in England and Wales: public health implications. International Journal for Parasitology 33:1, 97-103
CrossRef41
Peter K. Newman. 2003. Parasites and Neurological Disease, Overview. , 792-797.
CrossRef42
James S Lewis Jr, Hanna Khoury, Gregory A Storchand John DiPersio. (2002) PCR for the diagnosis of toxoplasmosis after hematopoietic stem cell transplantation. Expert Review of Molecular Diagnostics 2:6, 616-624
CrossRef43
David J.P. Ferguson, Stephen F. Parmley, Stanislas Tomavo. (2002) Evidence for nuclear localisation of two stage-specific isoenzymes of enolase in Toxoplasma gondii correlates with active parasite replication. International Journal for Parasitology 32:11, 1399-1410
CrossRef44
Shuang Wei, Florentina Marches, Ben Daniel, Sabrina Sonda, Kim Heidenreich, Tyler Curiel. (2002) Pyridinylimidazole p38 mitogen-activated protein kinase inhibitors block intracellular Toxoplasma gondii replication. International Journal for Parasitology 32:8, 969-977
CrossRef45
Patrick Bastien. (2002) Molecular diagnosis of toxoplasmosis. Transactions of the Royal Society of Tropical Medicine and Hygiene 96, S205-S215
CrossRef46
Meriem K. Bensalem, Joseph R. Berger. (2002) HIV and the central nervous system. Comprehensive Therapy 28:1, 23-33
CrossRef47
ROBERT LICHO, SCOTTN LITOFSKY, MARTIN SENITKO, MARIE GEORGE. (2002) Inaccuracy of TI-201 Brain SPECT in Distinguishing Cerebral Infections from Lymphoma in Patients with AIDS. Clinical Nuclear Medicine 27:2, 81-86
CrossRef48
Joseph R Zunt. (2002) Central Nervous System Infection During Immunosuppression. Neurologic Clinics 20:1, 1-22
CrossRef49
D. J. Skiest. (2002) Focal Neurological Disease in Patients with Acquired Immunodeficiency Syndrome. Clinical Infectious Diseases 34:1, 103-115
CrossRef50
J Sparano. (2001) Clinical aspects and management of AIDS-related lymphoma. European Journal of Cancer 37:10, 1296-1305
CrossRef51
Jeffrey M. Jacobson, Richard Hafner, Jack Remington, Charles Farthing, Jeanne Holden-Wiltse, Elizabeth M. Bosler, Carol Harris, Dushyantha T. Jayaweera, Clemente Roque, Benjamin J. Luft. (2001) Dose-escalation, phase I/II study of azithromycin and pyrimethamine for the treatment of toxoplasmic encephalitis in AIDS. AIDS 15:5, 583-589
CrossRef52
K. Sugane, M. Takamoto, K. Nakayama, T. Tada, T. Yuasa, K. Kurokawa. (2001) Diagnosis of Toxoplasma Meningoencephalitis in aNon-AIDS Patient Using PCR. Journal of Infection 42:2, 159-160
CrossRef53
Emanuel N. Vergis, John W. Mellors. (2000) NATURAL HISTORY OF HIV-1 INFECTION. Infectious Disease Clinics of North America 14:4, 809-825
CrossRef54
Christine Lacascade, Anne-Marie Conge, Vincent Baillat, Isabelle Pages, Marie-France Huguet, Jacques Reynes, Jean-Pierre Vendrell. (2000) In Vitro Anti-Toxoplasma Gondii Antibody Production by Peripheral Blood Mononuclear Cells in the Diagnosis and the Monitoring of Toxoplasmic Encephalitis in AIDS-Related Brain Lesions. JAIDS Journal of Acquired Immune Deficiency Syndromes 25:3, 256-260
CrossRef55
Christine Lacascade, Anne-Marie Conge, Vincent Baillat, Isabelle Pages, Marie-France Huguet, Jacques Reynes, Jean-Pierre Vendrell. (2000) In Vitro Anti-Toxoplasma Gondii Antibody Production by Peripheral Blood Mononuclear Cells in the Diagnosis and the Monitoring of Toxoplasmic Encephalitis in AIDS-Related Brain Lesions. Journal of Acquired Immune Deficiency Syndromes256-260
CrossRef56
Bruno C. De Medeiros, Carlos R. De Medeiros, Betina Werner, Jose Zanis Neto, Giovanni Loddo, Ricardo Pasquini, Luiz F. Bleggi-Torres. (2000) Central Nervous System Infections Following Bone Marrow Transplantation: An Autopsy Report of 27 Cases. Journal of Hematotherapy <html_ent glyph="@amp;" ascii="&"/> Stem Cell Research 9:4, 535-540
CrossRef57
Benjamin J. Luft, Arlene Chua. (2000) Central nervous system toxoplasmosis in HIV pathogenesis, diagnosis, and therapy. Current Infectious Disease Reports 2:4, 358-362
CrossRef58
D.J Skiest, W Erdman, W.E Chang, O.K Oz, A Ware, J Fleckenstein. (2000) SPECT Thallium-201 Combined with Toxoplasma Serology for the Presumptive Diagnosis of Focal Central Nervous System Mass Lesions in Patients with AIDS. Journal of Infection 40:3, 274-281
CrossRef59
Ildiko Vastagh, Ilona Jelencsik, Peter Barsi, Katalin Balint, Janos Szlavik, Imre Szirmai. (1999) Single cerebral Toxoplasma abscess: first manifestation of HIV infection. European Journal of Neurology 6:6, 725-726
CrossRef60
François Raffi, Jacqueline Franck, Hervé Pelloux, Francis Derouin, Véronique Reliquet, Pierre Ambroise–Thomas, Jean Pierre Aboulker, Catherine Leport, Henri Dumon. (1999) Specific anti-Toxoplasmic IgG antibody immunoblot profiles in patients with AIDS-associated Toxoplasma encephalitis. Diagnostic Microbiology and Infectious Disease 34:1, 51-56
CrossRef61
ANDREW HELFGOTT. (1999) TORCH Testing in HIV-Infected Women. Clinical Obstetrics and Gynecology 42:1, 149-162
CrossRef62
Miguel A. Pagano, Mart
n J. Segura, Guillermo A. Di Lorenzo, Mar
CrossRef63
S Alfandari, J M. Bourez, E Senneville, L Maulin, Y Mouton. (1998) Methotrexate for suspected cerebral lymphoma in AIDS. AIDS 12:10, 1246-1247
CrossRef64
Leena Ketonen, Rosinda C. De La Pe$nTa, Javier Villanueva-Meyer. (1998) MR and TL-201 Spect Imaging with Pathologic Correlation for the Assessment of CNS Lymphoma vs. Toxoplasmosis in AIDS Patients. Journal of Neuro-AIDS 2:1, 21-42
CrossRef65
Kee-Hyun Chang, Moon Hee Han. (1998) Invited. MRI of CNS parasitic diseases. Journal of Magnetic Resonance Imaging 8:2, 297-307
CrossRef66
V. Soriano, M. Gutiérrez, J. González-Lahoz. (1998) Detection of HTLV-II proviral sequences in HIV-immunosuppressed patients with HTLV indeterminate serological patterns. Journal of Infection 36:2, 243-244
CrossRef67
Chumpitazi, Simon, Polack, Peyron, Picot, Ricard, Ambroise-Thomas. (1998) Human platelet inhibition of Toxoplasma gondii growth. Clinical and Experimental Immunology 111:2, 325-333
CrossRef68
Philippe Lesprit, Anne-Marie Zagdanski, Arnaud de La Blanchardiere, Martine Rouveau, Jean-Marie Decazes, Jacques Frija, Philippe Lagrange, Jacques Modai, Jean-Michel Molina. (1997) Cerebral Tuberculosis in Patients with the Acquired Immunodeficiency Syndrome (AIDS). Medicine 76:6, 423-431
CrossRef69
F Dalençon, Y Amjaud, C Lafforgue, F Derouin, H Fessi. (1997) Atovaquone and rifabutine-loaded nanocapsules: formulation studies. International Journal of Pharmaceutics 153:1, 127-130
CrossRef70
François Raffi, Jean-Pierre Aboulker, Christian Michelet, Véronique Reliquet, Hervé Pelloux, Alain Huart, Isabelle Poizot-Martin, Philippe Morlat, Benoît Dupas, Jean-Marie Mussini, Catherine Leport. (1997) A prospective study of criteria for the diagnosis of toxoplasmic encephalitis in 186 AIDS patients. AIDS 11:2, 177-184
CrossRef71
May-Lill Garly, Eskild Petersen, Court Pedersen, Jens D. Lundgren, Jan Gerstoft. (1997) Toxoplasmosis in Danish AIDS Patients. Scandinavian Journal of Infectious Diseases 29:6, 597-600
CrossRef72
Hugo M. Weigel, Erwin De Vries, Rosa M. Regez, Jeanette H. Henrichs, Jos J. A. M. Ten Velden, P. H. Jos Frissen, Jan T. M. Van Der Meer. (1997) Cotrimoxazole is Effective as Primary Prophylaxis for Toxoplasmic Encephalitis in HIV-infected Patients: A Case Control Study. Scandinavian Journal of Infectious Diseases 29:5, 499-502
CrossRef73
Katherine L. Heilpern, Bennett Lorber. (1996) FOCAL INTRACRANIAL INFECTIONS. Infectious Disease Clinics of North America 10:4, 879-898
CrossRef74
Peter Berlit, Octavian Popescu, Yvonne Weng, Rolf Malessa. (1996) Disseminated cerebral hemorrhages as unusual manifestation of toxoplasmic encephalitis in AIDS. Journal of the Neurological Sciences 143:1-2, 187-189
CrossRef75
Horatio B. Fung, Harold L. Kirschenbaum. (1996) Treatment regimens for patients with toxoplasmic encephalitis. Clinical Therapeutics 18:6, 1037-1056
CrossRef76
C. Hellerbrand, F. D. Goebel, R. Disko. (1996) High predictive value ofToxoplasma gondii IgG antibody levels in HIV-infected patients for diagnosis of cerebral toxoplasmosis. European Journal of Clinical Microbiology & Infectious Diseases 15:11, 869-872
CrossRef77
Kenneth Tomkovich, Justin Gooding, Huey Jen Lee. (1996) Ring-enhancing brain lesion in a 42-year-old man. Academic Radiology 3:11, 968-970
CrossRef78
B.K Kleinschmidt-Demasters, Catherine Amlie-Lefond, Donald H Gilden. (1996) The patterns of varicella zoster virus encephalitis. Human Pathology 27:9, 927-938
CrossRef79
UWE GROSS, WOLFGANG BOHNE, CARSTEN G. K. LÜDER, RAIMOND LUGERT, FRANK SEEBER, CHRISTINE DITTRICH, FABIAN POHL, DAVID J. P. FERGUSON. (1996) Regulation of Developmental Differentiation in the Protozoan Parasite Toxoplasma gondii. The Journal of Eukaryotic Microbiology 43:5, 114S-116S
CrossRef80
H. Klinker, P. Langmann, E. Richter. (1996) Pyrimethamine alone as prophylaxis for cerebral toxoplasmosis in patients with advanced HIV infection. Infection 24:4, 324-327
CrossRef81
Klaus Becker, Helmut Jablonowski, Dieter Häussinger. (1996) Sulfadiazine-Associated Nephrotoxicity in Patients with the Acquired Immunodeficiency Syndrome. Medicine 75:4, 185-194
CrossRef82
T. C. Brightbill, M. Judith Donovan Post, George T. Hensley, Armando Ruiz. (1996) MR of Toxoplasma Encephalitis: Signal Characteristics on T2-Weighted Images and Pathologic Correlation. Journal of Computer Assisted Tomography 20:3, 417-422
CrossRef83
Oona Dunlop, Vibeke Rootwelt, Mette Sannes, Anne K. Goplen, Michael Abdelnoor, Kjell Skaug, Kåre Baklien, Anne Skar, Kjetil Melby, Bjørn Myrvang, Johan N. Bruun. (1996) Risk of Toxoplasmic Encephalitis in AIDS Patients: Indications for Prophylaxis. Scandinavian Journal of Infectious Diseases 28:1, 71-73
CrossRef84
Vivian Y. Kim, Jay S. Duker. (1996) Ocular Manifestations of Human Immunodeficiency Virus. Seminars in Ophthalmology 11:1, 93-106
CrossRef85
L.M. Samkoff, M. Daras, B.S. Koppel, A. Hirschfeld, H. Donnenfeld. (1996) Toxoplasma gondii myelitis in AIDS. European Journal of Neurology 3:1, 50-54
CrossRef86
Cabot, Richard C.Scully, Robert E., Mark, Eugene J., McNeely, William F., McNeely, Betty U., Ronthal, M.Vonsattel, J.-P.. (1995) Case 33-1995. New England Journal of Medicine 333:17, 1135-1143
Full Text87
G. Orefice, G. Volpe, G. Liuzzi, M. D'Abbraccio, M. Coppola, P. Tullio Cataldo. (1995) Weber's syndrome due to a possible solitary brainstem toxoplasmosis as a presenting sign of AIDS. European Journal of Neurology 2:4, 375-377
CrossRef88
Bernadine R. Donahue, Jessie W. Sullivan, Jay S. Cooper. (1995) Additional experience with empiric radiotherapy for presumed human immunodeficiency virus–associated primary central nervous system lymphoma. Cancer 76:2, 328-332
CrossRef89
H. Manji, B. Sweeney, S. Connolly, A. Hughes, R.F. Miller, M.J.G. Harrison. (1995) Movement disorders in AIDS: Infective, neoplastic and iatrogenic causes. Parkinsonism & Related Disorders 1:1, 13-19
CrossRef90
GIULIANA CARREGA, ANDREA CANESSA, PAOLA ARGENTA, MARIO CRUCIANI, DANTE BASSETTI. (1995) T Cell Blastogenic Responses to Toxoplasma gondii Trophozoites among HIV-Infected Patients. AIDS Research and Human Retroviruses 11:6, 741-746
CrossRef91
Daniel K. Resnick, Christopher H. Comey, William C. Welch, A. Julio Martinez, William W. Hoover, George B. Jacobs. (1995) Isolated toxoplasmosis of the thoracic spinal cord in a patient with acquired immunodeficiency syndrome. Journal of Neurosurgery 82:3, 493-496
CrossRef92
V. Menéndez, J. Valls, M. Espuña, A. Pérez, M. A. Barranco, P. Carretero. (1995) Neurogenic bladder in patients with acquired immunodeficiency syndrome. Neurourology and Urodynamics 14:3, 253-257
CrossRef93
S. Romagnani. (1994) Immunologic and clinical aspects of human immunodeficiency virus infection. Allergy 49:9, 685-695
CrossRef94
Christopher A. Hunter, Carlos S. Subauste, Jack S. Remington. (1994) The role of cytokines in toxoplasmosis. Biotherapy 7:3-4, 237-247
CrossRef95
Fedor Heidenreich, Gabriele Arendt, Sebastian Jander, Helmut Jablonowski, Guido Stoll. (1994) Serum and cerebrospinal fluid levels of soluble intercellular adhesion molecule 1 (sICAM-1) in patients with HIV-1 associated neurological diseases. Journal of Neuroimmunology 52:2, 117-126
CrossRef96
Thomas R. Hedges. (1994) Ophthalmoplegia associated with AIDS. Survey of Ophthalmology 39:1, 43-51
CrossRef97
Cabot, Richard C.Scully, Robert E., Mark, Eugene J., McNeely, William F., McNeely, Betty U., Basgoz, NesliMattia, Anthony R.. (1994) Case 4-1994. New England Journal of Medicine 330:4, 273-280
Full Text98
T. Weber, R. Beck, E. Stark, J. Gerhards, K. Korn, J. Haas, W. L
CrossRef99
Paddock, Christopher D.Suchard, David P.Grumbach, Kevin L.Hadley, W. KeithKerschmann, Russell L.Abbey, Nancy W.Dawson, Jaqueline E.Anderson, Burt E.Sims, Kimetha G.Dumler, J. StephenHerndier, Brian G.. (1993) Fatal Seronegative Ehrlichiosis in a Patient with HIV Infection. New England Journal of Medicine 329:16, 1164-1167
Full Text100
Luft, Benjamin J.Hafner, RichardKorzun, Ann H.Leport, CatherineAntoniskis, DianaBosler, Elizabeth M.Bourland, D. DavidUttamchandani, RajFuhrer, JackJacobson, JeffreyMorlat, PhilippeVilde, Jean-LouisRemington, Jack S.the ACTG 077p/ANRS 009 Study Team. (1993) Toxoplasmic Encephalitis in Patients with the Acquired Immunodeficiency Syndrome. New England Journal of Medicine 329:14, 995-1000
Full Text101
J. Zufferey, A. Sugar, P. Rudaz, J. Bille, M. P. Glauser, J. P. Chave. (1993) Prevalence of latent toxoplasmosis and serological diagnosis of active infection in HIV-positive patients. European Journal of Clinical Microbiology & Infectious Diseases 12:8, 591-595
CrossRef102
J-P. Vendrell, M-F. Huguet, J. Ngou, C. Michard, A. Serre, J. Reynes, N. Atoui, M. Segondy, F. Pratlong. (1993) In-vitro synthesis of antibodies to Toxoplasma gondii by lymphocytes from HIV-1-infected patients. The Lancet 342:8862, 22-23
CrossRef103
REINHARDT W. FLØ, ARVID NILSEN, PÅL VOLTERSVIK, GUNNAR HAUKENES. (1993) Serum antibodies to viral pathogens and Toxoplasma gondii in HIV-infected individuals. APMIS 101:7-12, 946-952
CrossRef104
(1993) Central Nervous System Toxoplasmosis in AIDS. New England Journal of Medicine 328:18, 1352-1354
Full Text105
Pietro Caramello, Brunella Forno, Anna Lucchini, Anna Maria Pollono, Alessandro Sinicco, Paolo Gioannini. (1993) Meningoencephalitis Caused by Toxoplasma gondii Diagnosed by Isolation from Cerebrospinal Fluid in an HIV-positive Patient. Scandinavian Journal of Infectious Diseases 25:5, 663-666
CrossRef
