All Posts Tagged With: "endothelial cells"

Link: http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=21079313&retmode=ref&cmd=prlinks

Excerpt:

Bacillary angiomatosis is a recently described infectious disease that
usually affects immunosupressed hosts with a previous history of contact
with cats. We report a rare case of bacillary angiomatosis in an
immunocompetent 59-year-old woman with no history of previous exposure to
cats, and atypical clinical features (fever and subcutaneous nodules with
ulceration on the left ankle).
Histopathology of the lesion showed extensive ulceration and reactive
tumor-like vascular proliferation of the blood vessels with swollen
endothelial cells and an inflammatory infiltrate including neutrophils and
lymphocytes in the dermis and subcutis. Staining with the Warthin-Starry
method demonstrated the presence of clustered bacilli located in the
extracellular matrix adjacent to the proliferating endothelial cells.
Diagnosis was confirmed with the detection of Bartonella spp. DNA in the
affected skin and in bone marrow using polymerase chain reaction.

Full article: http://www.biomedcentral.com/content/pdf/1471-2202-11-121.pdf

Excerpt:

Conclusions

Anti-C. pneumoniae antibodies, obtained commercially, identified both typical intracellular and atypical extracellular C. pneumoniae antigens in frontal and temporal cortices of the AD brain. C. pneumoniae, amyloid deposits, and neurofibrillary tangles were present in the same regions of the brain in apposition to one another. Although additional studies are required to conclusively characterize the nature of Chlamydial immunoreactivity in the AD brain, these results further implicate C. pneumoniae infection with the pathogenesis of Alzheimer’s disease

Full article: http://www.emedicine.com/derm/topic4.htm

Excerpt:

Acrodermatitis chronica atrophicans (ACA) is the third or late stage of European Lyme borreliosis (LB). This unusual, progressive, fibrosing skin process is due to the effect of continuing active infection with Borrelia afzelii. Buchwald first delineated it in 1883; Herxheimer and Hartmann described it in 1902 as a tissue paper–like cutaneous atrophy. It is evident on the extremities, particularly on the extensor surfaces, beginning with an inflammatory stage with bluish red discoloration and cutaneous swelling and concluding several months or years later with an atrophic phase. Sclerotic skin plaques may also develop. Physicians should use serologic and histologic examination to confirm this diagnosis.

Pathophysiology: B afzelii is the predominant, but may not be the exclusive, etiologic agent of ACA. Another genospecies of the Borrelia burgdorferi sensu lato complex, Borrelia garinii, has also been detected.

ACA is the only form of LB in which no spontaneous remission occurs. Its pathophysiology is not yet fully understood. ACA appears to be associated with long-term persistence of Borrelia organisms in the skin; several nonspecific reactions together with a specific immune response may contribute to its manifestations.

The persistence of the spirochetes despite a marked cutaneous T-cell infiltration and high serum antibody titers may be connected with resistance of the pathogen to the complement system; the ability to escape to immunologically protected sites (eg, endothelial cells, fibroblasts); and the ability to change antigens, which may lead to an inappropriate immune response. Lack of protective antibodies, with a narrow antibody spectrum and a weak cellular response with down-regulation of major histocompatibility system class II molecules on Langerhans cells, has been observed in patients with LB.

The use of new, highly sensitive diagnostic methods has revealed persistent
infections to be a common feature of different tick-borne diseases, such as
babesiosis, anaplasmosis and heartwater. Antigenic variation can contribute to
disease persistence through the continual elaboration of new surface structures,
and we know in several instances how this is achieved. Continued