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J Keystone

Publications and source records attributed to J Keystone.

16 recordsLinked to original sources

Reactivation of neurocysticercosis: case report.

A 37-year-old woman with a known history of longstanding neurocysticercosis presented with a three-day history of new onset headache. Several years prior to her current presentation, she had undergone cysticidal treatment and was assumed to be cured of active disease. Computed tomography and magnetic resonance imaging studies done three months prior to presentation showed multiple intracerebral calcified lesions consistent with resolved neurocysticercosis. Physical and laboratory findings were noncontributory. Imaging studies showed the same previously calcified lesions, but they were now surrounded by large amounts of edema. This case represents a unique report of reactivation of neurocysticercosis and raises interesting questions about the natural history of this infection.

Adult↗

Persistent MR contrast enhancement of calcified neurocysticercosis lesions.

PURPOSE: We sought to determine whether cysticercosis lesions in the brain continue to enhance after nodular involution and complete calcification, and to investigate the clinical significance of this finding with respect to seizure recurrence after cysticidal treatment. METHODS: Serial contrast-enhanced MR images were obtained in all patients with neurocysticercosis seen at our hospital over a 6-year period (1991-1997). From this group, all patients with nodular calcified lesions were selected for study. RESULTS: Sixteen of 29 patients with neurocysticercosis had nodular calcified lesions. Six of these 16 had rim enhancement of nodular calcified lesions for at least 1 year after imaging evidence of complete calcification. Three of these six patients with enhancing, calcified lesions continued to experience seizures. Three of the 10 patients without enhancement also continued to have seizures. CONCLUSION: Contrary to the literature, which states that enhancement and disease activity cease with calcification, six (38%) of 16 patients had lesions that continued to enhance after complete calcification. This abnormality may be a risk factor for posttreatment seizures or may suggest eventual resorption of the calcified lesion.

Adolescent↗

Development of severe secondary hypertension in a patient with systemic entomophthoromycosis.

The sudden onset of hypertension mandates investigation for secondary causes. We report the case of a young man with a very rare systemic fungal disease that included massive unilateral perirenal adenopathy. Treatment was associated with the abrupt onset of severe hypertension. Imaging studies suggested progressive constriction of one kidney with treatment, presumably as a result of healing adenopathy. We suggest that this case is a new example of hypertension secondary to constrictive perinephritis (Page kidney).

Adult↗

Imported malaria. Clinical presentation and examination of symptomatic travelers.

BACKGROUND: The diagnosis of malaria in nonendemic countries presents a continuing challenge. Increasing physician awareness of the variability in its clinical presentation will improve clinical management and health outcomes. METHODS: Charts of patients in whom malaria was diagnosed at two hospital-based tropical disease centers between September 1, 1980, and December 31, 1991, were reviewed. RESULTS: Of a total of 482 cases, 182 were caused by Plasmodium falciparum and 246 by Plasmodium vivax. Fifty-two patients with P falciparum malaria were hospitalized; 13 were classified as having severe falciparum malaria. Nineteen patients with P vivax malaria required hospitalization. The only death was caused by P vivax. Chemoprophylaxis was used by, or prescribed for, 46% of patients; however, of these, only half were compliant in taking their medication. Eighty-seven percent of patients with falciparum malaria presented within 6 weeks of return from travel to an endemic area. One third of patients with P vivax malaria presented more than 6 months after travel. The average time between onset of symptoms and physician contact was 6.7 days. Diagnosis was often delayed in those who sought care outside the referral center. Almost all patients had a history of fever, but only half were febrile at presentation. Presenting symptoms and signs were non-specific. Fifty percent of patients were thrombocytopenic. Other laboratory abnormalities were mild. CONCLUSIONS: Since the presentation of malaria is vague and nonspecific, the diagnosis should be considered in any appropriately symptomatic patient with a history of travel to a malaria-endemic area, and appropriate testing should be done. Up-to-date information on chemoprophylaxis should be provided to all travelers to malaria-endemic regions.

Adult↗

Evaluation of the Merifluor immunofluorescent assay for the detection of Cryptosporidium and Giardia in sodium acetate formalin-fixed stools.

The Merifluor Cryptosporidium/Giardia direct immunofluorescent assay (MFDFA) was used for the blinded detection of Cryptosporidium and Giardia in 100 previously tested sodium acetate formalin (SAF)-preserved fecal specimens. Examination for ova and parasites by formalin-ether concentration followed by iron-hematoxylin and Kinyon staining had demonstrated Cryptosporidium (n = 32), Giardia (n = 20) and both Giardia and Cryptosporidium (n = 5). The MFDFA detected one additional specimen with Cryptosporidium and another with Giardia and was rapid, accurate, and simple to perform.

Acetates↗

Induction of circulating group II phospholipase A2 expression in adults with malaria.

High levels of interleukin 1 and tumor necrosis factor are found in both cases of malaria and cases of septic shock. Since both interleukin 1 and tumor necrosis factor induce expression of the proinflammatory enzyme phospholipase A2 (PLA2), we examined serum PLA2 levels in 14 adults with malaria. Mean serum PLA2 activity was elevated 40-fold above normal (P less than 0.001). Serum PLA2 activity correlated with PLA2 immunoreactivity (r = 0.987; P less than 0.001) by an enzyme-linked immunosorbent assay specific for human group II PLA2, showing that serum PLA2 in cases of malaria is host derived. This article describes the novel finding of elevated PLA2 levels in cases of malaria, further strengthening the notion that mediators of the host response in cases of malaria are similar to those in cases of septic shock.

Adult↗

Global distribution of a variant of the circumsporozoite gene of Plasmodium vivax.

The global distribution of a newly described variant of the Plasmodium vivax circumsporozoite (CS) gene was determined by genetic analysis of wild isolates. Whole blood specimens were collected on filter paper from patients infected with P. vivax in South America. West Africa, and the Indian subcontinent. P. vivax DNA was released from the filter paper samples, and the CS gene was amplified by polymerase chain reaction and analyzed for genetic variation. Amplified DNA was probed with oligonucleotide probes that hybridize with the predominant CS repeat region (PV210) and the variant CS repeat region (PV247) of P. vivax. The PV247 variant was found in all three geographically diverse areas. In addition, five of six consecutive patients studied had simultaneous infection with both the predominant and variant forms of P. vivax. These findings suggest that a single-epitope vaccine based on the predominant CS domain is unlikely to be protective on even a regional basis.

Africa, Western↗

Immune-mediated thrombocytopenia of malaria.

Thrombocytopenia frequently complicates malarial infections but the mechanism has not been elucidated. We studied 28 patients with malarial infections and noted that 16 of 17 thrombocytopenic patients had elevated levels of platelet-associated IgG (PAIgG). In all thrombocytopenic patients studied, the level of PAIgG returned to normal as the platelet count rose to normal levels. To study the mechanism of the elevated platelet-bound IgG, IgG and F(ab')2 from patients with recurrent Plasmodium falciparum infections was purified and radiolabeled. Labeled and unlabeled P. falciparum antigen was also prepared. IgG did not nonspecifically bind to malaria-damaged platelets. Binding studies with 3H-malarial antigen demonstrated platelets have saturable binding sites for malarial antigen. Increasing concentrations of malarial antigen displaced the 125I-IgG antimalarial antibody from the platelets. The binding of 125I-IgG and 125I-F(ab')2 was similar and this excluded significant immune complex binding. The thrombocytopenia that complicates at least some malarial infections is caused by immune mechanisms; specific IgG binds to platelet-bound malaria antigen through the Fab portion of the immunoglobulin molecule.

Binding Sites, Antibody↗

Travelers' health.

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Communicable Disease Control↗