Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0152031 (swollen joints)
 535 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Blood samples from Wisconsin horses and cows suspected of having clinical disease due to Borrelia burgdorferi infection were submitted by veterinary practitioners. All serum, milk, colostrum, and synovial samples were tested for B. burgdorferi antibodies by immunofluorescence. Whole blood, milk, colostrum, and synovial fluid samples were cultured for B. burgdorferi. Records were kept on the clinical signs of antibody-positive animals, date of sample, and location of the animal by county. Of the samples tested for antibodies 282/430 cow sera, 118/190 horse sera, 5/10 cow synovial fluids, 3/6 horse synovial fluids, 2/3 cow colostrums, 0/44 cow milk samples and 1 aborted fetus serum were antibody positive at a titer of 1:128 or greater. Of samples cultured 7/156 cow bloods, 2/35 horse bloods, 1/14 cow synovial fluids, 0/4 synovial fluids, 1/3 cow colostrums, 0/44 cow milk, and 2/10 cow urine samples were B. burgdorferi culture positive. For both cows and horses October and May were the two peak months for the number of antibody-positive samples. The most frequent clinical signs in antibody-positive horses and cows were lameness and swollen joints, but many also had stiffness, laminitis, abortions, and fevers. Not all antibody-positive animals showed clinical signs. These findings show that B. burgdorferi infection occurs in horses and cows and can cause clinical illness in some but not all animals. Infection in cows and horses occurs most frequently 1 month after the emergence of adult I. dammini. Because spirochetes could be isolated from blood, synovial fluid, colostrum, and urine, these animals could be important in providing an infected blood meal for ticks and bringing B. burgdorferi in direct contact with humans.
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PMID:Borrelia burgdorferi infection in Wisconsin horses and cows. 319 95

Infection with helminth parasites triggers strong and stereotypic immune responses in humans and mice, which can protect against specific experimentally-induced autoimmune diseases. We have shown that infection with the rat tapeworm, Hymenolepis diminuta, confers a protective effect on FCA-induced joint inflammation. Here, we investigated the effect of a prophylactic infection with H. diminuta on the K/BxN-serum model of polyarthritis in BALB/c mice. Mice were infected with 10 cysticercoids of H. diminuta by oral gavage and 8 days later arthritis was induced by i.p. injection of K/BxN arthritogenic serum. Joint swelling and pain measurements were recorded throughout a 13 day time course. At necropsy, joints and blood serum were collected. K/BxN-treated mice developed joint inflammation in the front paws, hind paws and knees as shown by increased swelling, mechanical allodynia and myeloperoxidase activity. Mice infected with H. diminuta had more severe disease, with increased eosinophil peroxidase activity in their paws and greater inflammatory infiltrate and synovitis in the knee joints. Hymenolepis diminuta-infected mice displayed significant increases in serum levels of C5a and mast cell protease-1 compared with K/BxN-serum only treatment, the latter being indicative of mast cell activation. In contrast to the protective effect of infection with H. diminuta in FCA-induced monoarthritis, infection with this helminth exacerbated K/BxN serum-induced polyarthritis in BALB/c mice. This correlated with increases in C5a and mast cell activation: factors critical in the development of K/BxN-induced arthritis. Thus, while data accumulate from animal models showing that infection with helminth parasites may be beneficial for a variety of auto-inflammatory diseases, our findings demonstrate the potential for helminths to exacerbate disease. Hence care is needed when helminth therapy is translated into a clinical setting.
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PMID:Murine autoimmune arthritis is exaggerated by infection with the rat tapeworm, Hymenolepis diminuta. 2358 16