scholarly journals Expanding Spectrum of Toxoplasma gondii: Thymoma and Toxoplasmic Encephalitis

2018 ◽  
Vol 5 (7) ◽  
Author(s):  
Daniel B Chastain ◽  
Joeanna I Sams ◽  
Gregory M Steele ◽  
Lindsey O Lowder ◽  
Carlos Franco-Paredes
Keyword(s):  
Toxoplasma Gondii ◽  
Parietal Lobe ◽  
Clinical Course ◽  
Toxoplasmic Encephalitis ◽  
Good’S Syndrome ◽  
Pathologic Findings

Abstract In this brief report, we describe a 76-year-old patient with thymoma who underwent craniotomy for a left parietal lobe mass with pathologic findings consistent with Toxoplasma gondii encephalitis in the absence of any features of thymoma with immunodeficiency/Good’s syndrome. His clinical course suggested likely Toxoplasma reactivation.

CAT SCRATCH SYNDROME

PEDIATRICS ◽  
1952 ◽  
Vol 10 (3) ◽  
pp. 311-318
Author(s):  
WILLIAM J. WATERS ◽  
SEYMOUR S. KALTER ◽  
JOHN T. PRIOR
Keyword(s):  
Skin Test ◽  
Laboratory Tests ◽  
Complement Fixation Test ◽  
Complement Fixation ◽  
Clinical Laboratory ◽  
Clinical Course ◽  
Diagnostic Value ◽  
Clinical Findings ◽  
Pathologic Findings ◽  
History Of

The clinical, laboratory and pathologic findings of a series of cases of cat scratch syndrome have been reviewed. In spite of a variable clinical course, certain features associated with a selected group of laboratory tests appear to be constant enough to be of diagnostic value. A history of contact with a cat and/or scratch which is usually associated with a peripheral skin lesion, lack of lymphangitis, presence of regional lymphadenopathy with tenderness to palpation are the most constant clinical findings. Fever, so frequently emphasized as a characteristic clinical sign, may be extremely variable in type and duration or entirely absent. A skin test with cat scratch antigen has been positive in all cases. Lacking this antigen, a negative Frei skin test in conjunction with a positive complement fixation test (Lygranum C. F.) is suggestive evidence for the diagnosis. With positive evidence from the above data, biopsy of an affected gland with its relatively nonspecific pathologic picture is not considered essential for the establishment of the diagnosis of cat scratch syndrome.

Cytomegalovirus-Associated Hemophagocytic Syndrome

PEDIATRICS ◽  
1985 ◽  
Vol 75 (2) ◽  
pp. 280-283
Author(s):  
ELIZABETH H. DANISH ◽  
BEVERLY B. DAHMS ◽  
MARY L. KUMAR
Keyword(s):  
Viral Infection ◽  
Epstein Barr Virus ◽  
Hemophagocytic Syndrome ◽  
Clinical Course ◽  
Underlying Disease ◽  
Barr Virus ◽  
Pathologic Findings ◽  
Immunosuppressed Patients ◽  
Epstein Barr ◽  
Herpes Group

Virus-associated hemophagocytic syndrome, first described by Risdall and co-workers in 1979,1 is a rare histiocytic proliferative syndrome characterzed by fever, hepatosplenomegaly, pancytopenia, and erythrophagocytosis by histiocytes that appear benign by histologic criteria. The clinical course and pathologic findings may be identical with another histiocytic disorder, familial erythrophagocytic lymphohistiocytosis, which occurs predominantly in infants. Diagnosis of virus-associated hemophagocytic syndrome depends entirely on evidence of concurrent viral infection, usually of the herpes group. Epstein-Barr virus has been associated with this syndrome in the few cases reported in children without underlying disease, whereas cytomegalovirus (CMV) has been implicated in immunosuppressed patients. We report a case of fatal CMV-associated hemophagocytic syndrome which occurred in a previously healthy infant.

Predictive value of Toxoplasma gondii antibody titres on the occurrence of toxoplasmic encephalitis in HIV-infected patients

AIDS ◽  
1996 ◽  
Vol 10 (13) ◽  
pp. 1521-1527 ◽  
Author(s):  
Francis Derouin ◽  
Catherine Leport ◽  
Sophie Pueyo ◽  
Philippe Morlat ◽  
Brigitte Letrillart ◽  
...  
Keyword(s):  
Toxoplasma Gondii ◽  
Predictive Value ◽  
Toxoplasmic Encephalitis ◽  
Antibody Titres

Clinical course and pathologic findings of successful second ABO-incompatible renal transplantation in a patient with donor-specific anti-HLA antibody

2007 ◽  
Vol 21 (s18) ◽  
pp. 54-59
Author(s):  
Mitsuru Saito ◽  
Shigeru Satoh ◽  
Takamitsu Inoue ◽  
Takeshi Yuasa ◽  
Atsushi Komatsuda ◽  
...  
Keyword(s):  
Renal Transplantation ◽  
Clinical Course ◽  
Pathologic Findings ◽  
Hla Antibody

scholarly journals Acute lead arsenate poisoning in beef cattle in Uruguay

2019 ◽  
Vol 31 (2) ◽  
pp. 307-310 ◽  
Author(s):  
Carlos O. Schild ◽  
Federico Giannitti ◽  
Rosane M. T. Medeiros ◽  
Caroline da Silva Silveira ◽  
Rubén D. Caffarena ◽  
...  
Keyword(s):  
Beef Cattle ◽  
Clinical Course ◽  
Lymphoid Organs ◽  
Lymphoid Tissues ◽  
Lead Arsenate ◽  
Pathologic Findings ◽  
Lead Levels ◽  
Baccharis Coridifolia ◽  
Orange Orchard ◽  
Toxic Plant

We describe and illustrate lesions in an outbreak of lead arsenate poisoning in beef cattle that ingested pesticide residues stored in an abandoned building of a former orange orchard. Of 70 exposed cattle, 14 had diarrhea, paresis, ataxia, recumbency, and/or seizures. Ten of the affected animals died after a clinical course of 12–18 h. Pathologic findings in 3 steers included extensive necrohemorrhagic, ulcerative rumenitis, omasitis, and abomasitis; lymphocytolysis in lymphoid organs; and nephrosis. Hepatic arsenic and lead levels in cases 1–3 were 20, 24, and 31 ppm, and 8.3, 25, and 9.4 ppm, respectively. Lesions in the forestomachs and lymphoid tissues have been rarely reported in cases of lead arsenate poisoning. In southern South America, these lesions are indistinguishable from those produced by Baccharis coridifolia, a toxic plant that contains macrocyclic trichothecenes, thus these conditions should be considered in the differential diagnosis of necrotizing lesions in alimentary and lymphoid organs.

Intracranial parenchymal schwannoma

1993 ◽  
Vol 79 (2) ◽  
pp. 217-222 ◽  
Author(s):  
Gian Piero Casadei ◽  
Takashi Komori ◽  
Bernd W. Scheithauer ◽  
Gary M. Miller ◽  
Joseph E. Parisi ◽  
...  
Keyword(s):  
Parietal Lobe ◽  
Clinical Course ◽  
Cystic Degeneration ◽  
Resonance Imaging ◽  
Imaging Studies ◽  
Content Type ◽  
Imaging Characteristics ◽  
Benign Nature ◽  
Peripheral Enhancement

✓ The clinical, radiological, and pathological features of nine cases of intracranial parenchymal schwannoma are described. The clinical course in four patients 23 years of age or younger mirrored the indolent nature of this neoplasm. Imaging studies included computerized tomography in eight patients and magnetic resonance imaging in three. The lesions were well demarcated with only mild surrounding edema. Five tumors were deep within the temporoparieto-occipital region, three were in the cerebellum, and one lay peripherally in the parietal lobe. Over two-thirds of the nine tumors were either cystic (five) or contained areas of cystic degeneration (two). One lesion was frankly hemorrhagic. A variety of imaging characteristics and contrast enhancement patterns were observed, including those of a cyst with a mural nodule and peripheral enhancement. Of the four solid neoplasms, two enhanced homogeneously while the other two demonstrated heterogeneous enhancement. Six tumors were resected totally. The follow-up period ranging from 2 months to 2 years has shown no recurrences. Microscopically, immunohistochemically, and ultrastructurally, the tumors were indistinguishable from peripheral schwannomas. A possible mechanism underlying the histogenesis of these rare lesions is discussed. The importance of recognizing this tumor is stressed, particularly in younger patients, given its benign nature, radiological resemblance to other tumors such as pilocytic astrocytoma, and favorable response to resection.

scholarly journals Migratory Activation of Primary Cortical Microglia upon Infection with Toxoplasma gondii

2011 ◽  
Vol 79 (8) ◽  
pp. 3046-3052 ◽  
Author(s):  
Isabel Dellacasa-Lindberg ◽  
Jonas M. Fuks ◽  
Romanico B. G. Arrighi ◽  
Henrik Lambert ◽  
Robert P. A. Wallin ◽  
...  
Keyword(s):  
T Cells ◽  
Toxoplasma Gondii ◽  
Mhc Class Ii ◽  
Glial Cells ◽  
Costimulatory Molecule ◽  
Toxoplasmic Encephalitis ◽  
Immune Functions ◽  
Content Type

ABSTRACTDisseminated toxoplasmosis in the central nervous system (CNS) is often accompanied by a lethal outcome. Studies with murine models of infection have focused on the role of systemic immunity in control of toxoplasmic encephalitis, while knowledge remains limited on the contributions of resident cells with immune functions in the CNS. In this study, the role of glial cells was addressed in the setting of recrudescentToxoplasmainfection in mice. Activated astrocytes and microglia were observed in the close vicinity of foci with replicating parasitesin situin the brain parenchyma.Toxoplasma gondiitachyzoites were allowed to infect primary microglia and astrocytesin vitro. Microglia were permissive to parasite replication, and infected microglia readily transmigrated across transwell membranes and cell monolayers. Thus, infected microglia, but not astrocytes, exhibited a hypermotility phenotype reminiscent of that recently described for infected dendritic cells. In contrast to gamma interferon-activated microglia,Toxoplasma-infected microglia did not upregulate major histocompatibility complex (MHC) class II molecules and the costimulatory molecule CD86. YetToxoplasma-infected microglia and astrocytes exhibited increased sensitivity to T cell-mediated killing, leading to rapid parasite transfer to effector T cellsin vitro. We hypothesize that glial cells and T cells, besides their role in triggering antiparasite immunity, may also act as “Trojan horses,” paradoxically facilitating dissemination ofToxoplasmawithin the CNS. To our knowledge, this constitutes the first report of migratory activation of a resident CNS cell by an intracellular parasite.

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