Post by Admin/ Traveler on Nov 23, 2018 16:29:53 GMT
Residual Brain Infection in Relapsing-Fever Borreliosis
(Trav here - now it's noteworthy to notice that this article was actually "Published: 15 May 2006" - so this IS something that the IDSA has known about but chose to ignore.)
"Abstract
Background:
Neurological involvement is common in the spirochetal infection relapsing fever (RF) in both humans and experimental animals. RF is best known for antigenic variation caused by the sequential expression of variable outer membrane lipoproteins of 2 sizes, variable small (Vsp) and variable large (Vlp) proteins. Less understood is the persistence of RF borreliae in the brain after they are cleared from the blood, referred to as residual brain infection (RBI). Our goal was to investigate the phenomenon of RBI in RF
Methods:
We studied RBI in immunocompetent mice by culturing blood and perfused brain samples 1 month after intraperitoneal inoculation with Borrelia turicatae serotype 1 (Bt1). Mice deficient in Toll-like receptor 2 (TLR2−/−) or in B and T cells (scid) were included for comparison
Results:
All scid mice had persistent infection in blood and brain. RBI was found in 3 (19%) of 16 immunocompetent and TLR2−/− mice. RBI was caused by either persistence of the original serotype (Bt1) or newly emerged Vsp (n=1, renamed Bt3) or Vlp serotypes. The Vsp of Bt1 (Vsp1) and Bt3 (Vsp3) were 75% identical
Conclusions:
RBI in RF is relatively frequent and can occur by persistence of the original or newly emerged serotypes."
"Discussion
The major findings of the present study were as follows. (1) RBI occurs in close to 20% of immunocompetent mice inoculated with a neurotropic strain of B. turicatae. (2) TLR2 deficiency does not increase susceptibility to RBI. (3) The scid mutation confers 100% susceptibility to RF neuroborreliosis, independently of background genes. (4) Vestibular dysfunction is the main clinical manifestation of RF neuroborreliosis in mice. (5) RBI can be caused by persistence of the original infecting serotype or by newly emerged serotypes that spontaneously arise in the population...
...The present results reveal that persistent brain infection in RF borreliosis is not only a feature of antibody-deficient mice but that it also occurs in a significant percentage of immunocompetent mice. RBI can be caused by the persistence in the brain of the original or relapse serotypes after they had been eliminated from the blood. Future studies may elucidate how variations in VMPs modulate the ability of RF borreliae to enter the brain."
(Trav here - now it's noteworthy to notice that this article was actually "Published: 15 May 2006" - so this IS something that the IDSA has known about but chose to ignore.)
"Abstract
Background:
Neurological involvement is common in the spirochetal infection relapsing fever (RF) in both humans and experimental animals. RF is best known for antigenic variation caused by the sequential expression of variable outer membrane lipoproteins of 2 sizes, variable small (Vsp) and variable large (Vlp) proteins. Less understood is the persistence of RF borreliae in the brain after they are cleared from the blood, referred to as residual brain infection (RBI). Our goal was to investigate the phenomenon of RBI in RF
Methods:
We studied RBI in immunocompetent mice by culturing blood and perfused brain samples 1 month after intraperitoneal inoculation with Borrelia turicatae serotype 1 (Bt1). Mice deficient in Toll-like receptor 2 (TLR2−/−) or in B and T cells (scid) were included for comparison
Results:
All scid mice had persistent infection in blood and brain. RBI was found in 3 (19%) of 16 immunocompetent and TLR2−/− mice. RBI was caused by either persistence of the original serotype (Bt1) or newly emerged Vsp (n=1, renamed Bt3) or Vlp serotypes. The Vsp of Bt1 (Vsp1) and Bt3 (Vsp3) were 75% identical
Conclusions:
RBI in RF is relatively frequent and can occur by persistence of the original or newly emerged serotypes."
"Discussion
The major findings of the present study were as follows. (1) RBI occurs in close to 20% of immunocompetent mice inoculated with a neurotropic strain of B. turicatae. (2) TLR2 deficiency does not increase susceptibility to RBI. (3) The scid mutation confers 100% susceptibility to RF neuroborreliosis, independently of background genes. (4) Vestibular dysfunction is the main clinical manifestation of RF neuroborreliosis in mice. (5) RBI can be caused by persistence of the original infecting serotype or by newly emerged serotypes that spontaneously arise in the population...
...The present results reveal that persistent brain infection in RF borreliosis is not only a feature of antibody-deficient mice but that it also occurs in a significant percentage of immunocompetent mice. RBI can be caused by the persistence in the brain of the original or relapse serotypes after they had been eliminated from the blood. Future studies may elucidate how variations in VMPs modulate the ability of RF borreliae to enter the brain."