All Posts Tagged With: "borrelia burgdorferi"

Canine and feline vector-borne diseases in Italy

Excerpt:

In Italy, dogs and cats are at risk of becoming infected by
different vector-borne pathogens, including protozoa, bacteria,
and helminths. Ticks, fleas, phlebotomine sand flies, and
mosquitoes are recognized vectors of pathogens affecting cats and
dogs, some of which (e.g., Anaplasma phagocytophilum, Borrelia
burgdorferi, Dipylidium caninum, Leishmania infantum, Dirofilaria
immitis, and Dirofilaria repens) are of zoonotic concern. Recent
studies have highlighted the potential of fleas as vectors of
pathogens of zoonotic relevance (e.g., Rickettsia felis) in this
country. While some arthropod vectors (e.g., ticks and fleas) are
present in certain Italian regions throughout the year, others
(e.g., phlebotomine sand flies) are most active during the summer
season.

Presence of Borrelia burgdorferi in endomyocardial biopsies

Excerpt:

Dilated cardiomyopathy (DCM) represents the third most common cause of heart
failure and the most frequent cause of heart transplantation. Infectious, mostly
viral, and autoimmune mechanisms, together with genetic abnormalities, have been
reported as three major causes of DCM. We hypothesized that Lyme disease (LD),
caused by spirochete Borrelia burgdorferi (Bb), might be an important cause of
new-onset unexplained DCM in patients living in a highly endemic area for LD
such as the Czech Republic.

Continued

Birds Play an Important Role in the Spread of Lyme Disease -Yale Study Finds

*********They had to spend thousands perhaps, even more to find that Birds are playing an important role in the spread of Lyme Disease??  What???   Are you telling me that birds stop at each border and request the right to fly over your state??  What a big waste of money….why doesn’t Yale and the Infectious Disease docs and other specialists at Yale, who say there is NO chronic Lyme, spend money finding a cure for Lyme disease instead of finding out what we patient’s already know.  Give me a break!!

*********It is time that patient’s start standing up and pushing back….sitting back and doing nothing is getting us no where.

*********We need to stop “fearing” city hall, when we can be city hall in these Lyme wars.

*********Just remember folks, Lyme isn’t just carried by ticks….look to birds, rodents, mice, we need to understand that it is up to us Lymie’s to take a stand.

Regards,

Linda

Article Excerpt:

New Haven, Conn. - The range of Lyme disease is spreading in North America and it appears that birds play a significant role by transporting the Lyme disease bacterium over long distances, a new study by the Yale School of Public Health has found. The study appears online in the journal Frontiers in Ecology and the Environment.

Researchers analyzed published records and concluded that at least 70 species of North American birds are susceptible to infection by black-legged ticks (Ixodes scapularis), the principal vector of the Lyme disease bacterium (Borrelia burgdorferi). The evidence also suggests that these bird species are dispersing infected ticks into areas that had previously been free of the disease, such as Canada.

Lyme disease bacterium is usually associated with small mammals such as mice and squirrels. Immature ticks (in the larval and nymphal stages) become infected with the bacterium when they feed on these mammals. During subsequent blood meals, an infected tick transmits the infection to other hosts, including humans. White-tailed deer-while playing an important role in maintaining and spreading tick populations-are a biological dead end for the bacterium because its blood is immune to infection.

Birds, however, are not immune and numerous species get infected and are capable of transmitting the pathogen onto ticks, the researchers found. What remains to be seen is whether the B. burgdorferi strains that can infect birds can also cause disease in humans. If so, the role of birds in the epidemiology of Lyme disease could be profound.
 

To read the whole article:

http://www.healthnewsdigest.com/cgi-bin/artman/search.cgi

Complement C3 in Bernese Mountain dogs

 Background: Previous research suggests that low serum concentrations of
the third component of complement (C3) are associated with both the
susceptibility to infectious agents such as Borrelia burgdorferi and the
development of glomerular disease. We hypothesized that low levels of C3
are associated with the coincident occurrence of B. burgdorferi
infection and glomerulonephritis in Bernese Mountain dogs. Continued

CD14 Signaling Restrains Chronic Inflammation

Current thinking emphasizes the primacy of CD14 in facilitating
recognition of microbes by certain TLRs to initiate pro-inflammatory
signaling events and the importance of p38-MAPK in augmenting such
responses. Herein, this paradigm is challenged by demonstrating that
recognition of live Borrelia burgdorferi not only triggers an
inflammatory response in the absence of CD14, but one that is, in part,
a consequence of altered PI3K/AKT/p38-MAPK signaling and impaired
negative regulation of TLR2. CD14 deficiency results in increased
localization of PI3K to lipid rafts, hyperphosphorylation of AKT, and
reduced activation of p38. Such aberrant signaling leads to decreased
negative regulation by SOCS1, SOCS3, and CIS, thereby compromising the
induction of tolerance in macrophages and engendering more severe and
persistent inflammatory responses to B. burgdorferi. Importantly, these
altered signaling events and the higher cytokine production observed can
be mimicked through shRNA and pharmacological inhibition of p38 activity
in CD14-expressing macrophages. Perturbation of this
CD14/p38-MAPK-dependent immune regulation may underlie development of
infectious chronic inflammatory syndromes.
 

The chemokine CXCL13 in acute neuroborreliosis

OBJECTIVE: Recent studies have suggested an important role of the B-cell chemoattractant CXCL13 in acute neuroborreliosis (NB). Our aim was to confirm the diagnostic role of CXCL13 and to evaluate its relevance as a therapy response and disease activity marker in NB. Continued

Do infections trigger juvenile idiopathic arthritis?

Microbiology and Clinical Microbiology Department, Cerrahpasa Medical
Faculty, Istanbul University, Kocamustafapasa, 34303, Istanbul, Turkey.

Juvenile idiopathic arthritis (JIA) is a disease that was prominent with
increased inflammation response in immune system, appeared mostly with
peripheral arthritis and endogenous and exogenous antigens play a role
in the pathogenesis of disease. Two major reasons were thinking to be
considerably important. First of them is immunological predisposition
and the second one is environmental factors. Continued

Ineffectiveness of Tigecycline Against Persistent Borrelia burgdorferi

Center for Comparative Medicine, Schools of Medicine and Veterinary Medicine,
University of California at Davis, One Shields Avenue, Davis, California 95616;
Division of Infectious Diseases, Department of Medicine, State University of New
York at Stony Brook, Stony Brook, New York 11794. Continued

Neurological Spectrum of Baggio-Yoshinari Syndrome

INTRODUCTION: Lyme disease (LD) is a tick-borne disease, caused by Borrelia burgdorferi sensu lato spirochetes, transmitted by Ixodes ricinus complex ticks, which leads to multiple systemic clinical manifestations. In Brazil, a different syndrome is described that mimics LD symptoms, but that also manifests high frequencies of recurrent episodes and immune-allergic manifestations. It is transmitted by the Amblyomma cajennense tick and the etiological agent is an uncultivable spirochete with atypical morphology. Due to its particularities, this emerging zoonosis has been called Brazilian LD-like syndrome or Baggio-Yoshinari Syndrome (BYS).
OBJECTIVE: To describe the neurological spectrum of BYS.
PATIENTS: Thirty patients with neurological symptoms of BYS were analysed.
RESULTS: Mean age of patients was 34.2 ± 13.3 years old (6 to 63 years); 20 were females and 10 males. A high number of recurrent episodes (73.6%) and severe psychiatric or psycho-social disturbances (20%) were distinguishing features. Erythema migrans similar to those seen in the Northern hemisphere was identified in 43.3% of patients at disease onset. The recurrence of skin lesions diminished as the disease progressed. Articular symptoms (arthritis) happened in nearly half of patients at BYS onset and during relapsing episodes.
CONCLUSIONS: The BYS is considered a new tick borne disease in Brazil that differs from classical LD observed in the Northern hemisphere. BYS replicates most of the neurological symptoms observed in LD, except for the additional presence of relapsing episodes and the tendency to cause chronic neurological and articular manifestations. 

http://www.scielo.br/pdf/rbr/v49n5/en_v49n5a03.pdf

Infectivity of Borrelia burgdorferi

Central Role of the Holliday Junction Helicase RuvAB in vlsE Recombination and Infectivity of Borrelia burgdorferi

Lyme disease is the most prevalent tick-borne infection in North America and Eurasia. It is caused by the bacterium Borrelia burgdorferi and is transmitted to humans via the bite of infected ticks. These spirochetes can cause both acute and chronic infection and inflammation of the skin, joints, heart, and central nervous system. The persistence of infection despite the presence of an active immune response is dependent upon antigenic variation of VlsE, a 35 kDa surface-exposed lipoprotein. A large number of different VlsE variants are present in the host simultaneously and are generated by recombination of the vlsE gene with adjacent vls silent cassettes. To try to identify factors important in vlsE recombination and immune evasion, we selected mutants in genes involved in DNA recombination and repair and screened them for infectivity and vlsE recombination. Mutants in genes encoding RuvA and RuvB (which act together to promote the exchange of strands between two different DNA molecules) had reduced infectivity and greatly diminished vlsE recombination. In immunodeficient mice, ruvA mutants retained full infectivity, and no vlsE recombination was detected. Our findings reinforce the importance of vlsE variation in immune evasion and persistent infection. Continued