All Posts Tagged With: "protozoa"

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.

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