A small animal model for early cerebral aneurysm pathology.

Prior studies, using systemic hypertension and elastase infusion, have induced cerebral aneurysm (CA) formation in mice. However, the CAs induced were rapidly formed, relatively large, and often ruptured. These features are not completely representative of human CAs. We set out to develop a mouse model representative of the early pathological features of human CA. Twenty male C57/BL6 mice were placed in a stereotactic frame. Low dose elastase solution (2µl/min) was manually injected into the right basal cistern. Human angiotensin II (0.11µl/h) was infused subcutaneously. Mice were observed for 2-3weeks prior to euthanasia. Early CA histopathological features including endothelial change (EC) and internal elastic lamina degeneration (IELD) were systematically sought at major cerebral arterial bifurcations. Brains were harvested from 11 of 15 mice, yielding 27 bifurcations. Sub-arachnoid haemorrhage (SAH) without CA formation was observed in one brain. Macroscopic CA without SAH was observed in another brain. Early CA features were observed in 8/11 (73%) brains. All bifurcations with IELD demonstrated EC: where EC was absent, IELD was also absent. EC severity appeared to correlate with IELD severity. EC and IELD were both severe within the CA. Using lower dose elastase solution than previously employed, we developed a model of early CA pathology. Our model demonstrated that the spectrum of known early CA pathology can be created at multiple bifurcations in mice, with EC severity appearing to correlate with IELD severity. This model permits the study of factors which potentially advance or retard the progression of CA formation.

Pulmonary Strongyloidiasis: The Varied Clinical Presentations.

Strongyloides stercoralis is a unique parasite. It can complete its life cycle entirely within the human host. As a result, an autoinfection cycle is set up. As long as there is an intact immune system, the host can control the parasitic burden, and the organism may persist for years after the initial inoculum. Most infected individuals experience mild gastrointestinal or pulmonary symptoms that may fluctuate for years. When cell-mediated immunity becomes impaired (ie, corticosteroid use, malignancy, acquired immunodeficiency syndrome), the parasite burden will grow, disseminate, and cause hyperinfection. Strongyloidiasis is endemic in the tropical and subtropical areas of the world; additionally, it is also endemic in the southeastern United States. Strongyloidiasis is associated with asthma, preexisting lung disease, and immunosuppression, including acquired immunodeficiency syndrome. Eosinophilia is not a prerequisite; therefore, the diagnosis of strongyloidiasis requires a high index of suspicion.