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2001 Central and peripheral nervous system infection, immunity, and inflammation in
the NHP model of Lyme borreliosis

Ann Neurol 2001 Sep;50(3):330-8   

Central and peripheral nervous system infection, immunity, and inflammation in
the NHP model of Lyme borreliosis.
Pachner AR, Cadavid D, Shu G, Dail D, Pachner S, Hodzic E, Barthold SW.
Department of Neurosciences, UMDNJ-New Jersey Medical School, Newark 07103,
USA. pachner@umdnj.edu


The relationship between chronic infection, antispirochetal immunity, and
inflammation is unknown in Lyme neuroborreliosis. In the nonhuman primate model
of Lyme neuroborreliosis, we measured spirochetal density in the nervous system
and other tissues by polymerase chain reaction and correlated these values to
anti-Borrelia burgdorferi antibody in the serum and cerebrospinal fluid, and to
inflammation in tissues. Despite substantial presence of Borrelia burgdorferi,
the causative agent of Lyme borreliosis, in the central nervous system, only
minor inflammation was present there, though skeletal and cardiac muscle, which
contained similar levels of spirochete, were highly inflamed. Anti-Borrelia
burgdoferi antibody was present in the cerebrospinal fluid but was not
selectively concentrated. All infected animals developed anti-Borrelia
burgdorferi antibody in the serum, but increased amplitude of antibody was not
predictive of higher levels of infection. These data demonstrate that Lyme
neuroborreliosis is a persistent infection, that spirochetal presence is a
necessary but not sufficient condition for inflammation, and that antibody
measured in serum may not predict the severity of infection.

PMID: 11558789 [PubMed - indexed for MEDLINE]

 

Original Message: Date: 11/30/2001 6:31:18 PM Eastern Standard Tim
In a message dated 11/6/2001 11:27:54 AM Eastern Standard Time, barb writes:
Barb (she was a dear Lyme friend) offered the following as proof of Borrelia persistence.  These emails were originally posted on Actionlyme and also sent privately.