ABSTRACT
It is known that nucleic acids from formalin-fixed tissues are not nearly as good templates for DNA amplification as those extracted from fresh tissues. However, specimens stored in most pathologic archives are initially fixed in formalin. The possibility of an infectious etiology of several diseases including Alzheimer's underscores the usefulness of archived tissue in assessing the association of infectious agents with specific pathology. In this report, we describe in detail a method resulting in robust amplification of HSV1 and Human Herpes type (HHV) 5 viral DNA targets using formalin-fixed Alzheimer brain frontal and temporal tissue as source of amplification template. Herpes simplex type 2 viral DNA was not detected in the limited samples examined in this study. Amplicons were verified by sequence analysis. Brain tissue stored in formalin longer than 1 year prior to post-formalin-fixation analysis gave rise to significantly shorter amplicons consistent with the observation that template DNA integrity decreases significantly with increasing time of storage in formalin. Thus, this report should be useful in PCR-based investigations assessing the regional presence of viral DNAs in formalin-fixed brain tissue.
Subject(s)
Alzheimer Disease/virology , Brain/virology , DNA, Viral/analysis , DNA, Viral/genetics , Herpesvirus 1, Human/genetics , Herpesvirus 2, Human/genetics , Nucleic Acid Amplification Techniques/methods , Specimen Handling/methods , Brain/drug effects , Formaldehyde/administration & dosage , Humans , Organ Preservation Solutions/administration & dosageABSTRACT
BACKGROUND: Although vasculopathy is a recognized complication during acute meningitis, to our knowledge, no previous reports have been published of this phenomenon developing months after successful treatment. OBJECTIVE: To report a unique case of a late-developing vasculopathy after pyogenic meningitis in an adult. REPORT OF A CASE: A 51-year-old woman was seen with severe headache 2 months after treatment of Haemophilus influenzae type C meningitis. Initial arteriography showed no abnormality; a second arteriogram showed progressive multifocal intracranial stenosis affecting mainly the internal carotid arteries. Findings from pathologic examination disclosed diffuse collagenosis consistent with chronic vascular injury from meningitis. The arterial lesions stabilized, and the patient remained asymptomatic. CONCLUSION: Progressive intracranial arterial stenosis can evolve months after meningitis and should be added to the list of recognized vascular complications.