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.

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

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.

Known or suspected mechanisms of persistence in babesial parasites include cytoadhesion and rapid
variation of the adhesive ligand in Babesia bovis and genetic diversity in
several merozoite stage proteins of different Babesia spp. In Anaplasma,
extensive variation in the pfam01617 gene family accompanies cycling of organism
levels in chronic infection. One result from the pioneering research at
Onderstepoort is the definition of a related polymorphic gene family that is
likely involved in immunity against heartwater disease. We are beginning to
understand the sizes of the antigenic repertoires and full definition is close,
with the possibility of applying simultaneous high-throughput sequencing to the
order of 1000 small genomes. We also, for the first time, can consider modifying
these genomes and looking at effects on persistence and virulence. However,
important biological questions remain unanswered; for example, why we are seeing
a new emerging Anaplasma infection of humans and is infection of endothelial
cells by Anaplasma significant to persistence in vivo.

http://eutils.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&id=19967928&retmode=ref&cmd=prlinks
PMID: 19967928  [PubMed – in process]

Onderstepoort J Vet Res. 2009 Mar;76(1):53-8.

Persistence mechanisms in tick-borne diseases.

Barbet AF.

Department of Infectious Diseases & Pathology, College of Veterinary Medicine,
University of Florida, Gainesville, Florida, USA.