Swine brucellosis

Brucella suis
Brucella suis culture
Scientific classification
Kingdom: Bacteria
Phylum: Proteobacteria
Class: Alpha Proteobacteria
Order: Rhizobiales
Family: Brucellaceae
Genus: Brucella
Species: B. suis
Binomial name
Brucella suis

     Absent

     Serologic evidence
     Confirmed infections

Swine brucellosis is a zoonosis affecting pigs, caused by the bacteria Brucella suis. The disease typically causes chronic inflammatory lesions in the reproductive organs of susceptible animals or orchitis and may even affect joints and other organs.[1] The most common symptom is abortion in pregnant susceptible hosts at any stage of gestation.[2] Other manifestations are temporary or permanent sterility, lameness, posterior paralysis, spondylitis, and abscess formation. It is transmitted mainly by ingestion of infected tissues or fluids, semen during breeding, and suckling infected animals.[3] In humans, it can cause undulant fever.[4]

Since brucellosis threatens food supply and cause undulant fever, Brucella suis and other Brucella species (B. melitensis, B. abortis, B. ovis, B. canis) are recognized as potential agricultural, civilian, and military bioterrorism agents.[5]

Contents

Etiology

B. suis are gram-negative, facultative intracellular coccobacilli and therefore are capable of growing and reproducing inside of host cells, specifically phagocytic cells.[6] They are also non-spore-forming, non-capsulated, and non-motile.[7] Flagellar genes, however, are present in the B. suis genome, but thought to be cryptic remnants because some were truncated and others were missing crucial components of the flagellar apparatus.[8][9] Interestingly, in mouse models, studies have shown that the flagellum is essential for a normal infectious cycle, where the inability to assemble a complete flagellum leads to severe attenuation of the bacteria.[10]

Brucella suis are differentiated into five biovars (strains), where bv. 1-3 infect boars and pigs and bv.1 and 3 may cause severe diseases in humans.[11] In contrast, bv. 2 found in wild boars in Europe show mild or no clinical signs and cannot infect healthy humans, but do infect pigs and hares.[12]

Pathogenesis

Phagocytes are an essential component of the host’s innate immune system with various anti-microbial defense mechanisms to clear pathogens via oxidative burst, acidificiation of phagosomes, and fusion of the phagosome and lysosome. B. suis, in retun, have developed ways to counteract the host cell defense to survive in the macrophage and to deter host immune responses.

Brucella suis possess smooth lipopolysaccharide (LPS), which have a full length O-chain, as opposed to rough LPS, which have a truncated or no O-chain.[13] This structural characteristic allows for B. suis to interact with lipid rafts on the surface of macrophages to be internalized, and the formed lipid rich phagosome is able to avoid fusion with lysosomes through this endocytic pathway.[14] In addition, this furtive entry into the macrophage does not affect the cell’s normal trafficking.[15] The smooth LPS also inhibits host cell apoptosis via O-polysaccharides through a TNF-alpha independent mechanism, which allows for B. suis to avoid the activation of the host immune system.[16]

Once inside the macrophage, B. suis are able to endure the rapid acidificiation in the phagosome to pH 4.0-4.5 [17] by expressing metabolism genes mainly for amino acid synthesis.[18] The acidic pH is actually essential for replication of the bacteria by inducing major virulence genes of the virB operon [19] and the synthesis of DnaK chaperones.[20] DnaK is part of the heat shock protein 70 family and aids in the correct synthesis and activation of certain virulence factors.[21]

In addition, the B. suis gene for nickel transport, nikA, is activated by metal ion deficiency and is expressed once in the phagosome.[22] Nickel is essential for many enzymatic reactions including ureolysis to produce ammonia which in turn may neutralize acidic pH.[23] It is suggested that since B. suis is unable to grow in strongly acidic medium, it could be protected from acidification by the ammonia.

Summary:

Symptoms

The most frequent clinical sign following Brucella suis infection is abortion in pregnant females, reduced milk production, and infertility.[24] Cattle can also be transiently infected when they share pasture or facilities with infected pigs and B. suis can be transmitted by cow’s milk.[25][26]

Swine also develop orchitis (swelling of the testicles), lameness (movement disability), hind limb paralysis, or spondylitis (inflammation in joints).[27]

Treatment

Because Brucella suis are facultative intracellular and are able to adapt to environmental conditions in the macrophage, treatment failure and relapse rates are high.[28] The only effective way to control and eradicate zoonosis is by vaccination of all susceptible hosts and elmination of infected animals.[29] The Brucella abortus (rough LPS Brucella) vaccine, developed for bovine brucellosis is licensed by the USDA Animal Plant Health Inspection Service, has shown protection for some swine and is also effective against B. suis infection, however, there is currently no approved vaccine for swine brucellosis.[30]

Biological warfare

In the United States, Brucella suis was the first biological agent weaponized in 1952 and was field-tested with B. suis-filled bombs called M33 cluster bomb.[31] It is, however, considered to be one of the agents of lesser threat because many infections are asymptomatic and the mortality is low,[32] but it is used more as an incapacitating agent.

See also

References

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  2. ^ Godfroid, J. A.-B. (2005). From the discovery of the Malta fever's agent to the discovery of a marine mammal reservoir, brucellosis has continuously been a re-emerging zoonosis. Veterinary Research , 36, 313-326.
  3. ^ The Merck Veterinary Manual. (2011). Brucellosis in Pigs. Retrieved 4 20, 2011, from http://www.merckvetmanual.com/mvm/index.jsp?cfile=htm/bc/110505.htm
  4. ^ Wilson, G. S. (1955). Topley and Wilson’s principles of bacteriology and immunity. London, England: Edward Arnold Publishers Ltd.
  5. ^ Halling, S. M.-B.-L. (2005). Completion of the Genome Sequence of Brucella abortus and Comparison to the Highly Similar Genomes of Brucella melitensis and Brucella Suis. Journal of Bacteriology , 187, 2715-2726.
  6. ^ Liautard, J. P., A. Gross, J. Dornand, and S. Kohler. "Interactions between professional phagocytes and Brucella spp." Microbiologia 12 (1996): 197-206.
  7. ^ Liautard, J. P., A. Gross, J. Dornand, and S. Kohler. "Interactions between professional phagocytes and Brucella spp." Microbiologia 12 (1996): 197-206.
  8. ^ DelVecchio, V.G., Kapatral, V., Elzer, P., Patra, G., and. "The genome of Brucella melitensis." Veterinary Microbiology 90 (2002): 587-592.
  9. ^ Moreno, E., and Moriyon, I. "Brucella melitensis: a nasty bug with hidden credentials for virulence." Proceedings of the National Academy of Science of USA 99 (2002): 1-3.
  10. ^ Fretin, D., A. Fauconnier, S. Kohler, S. Halling, S. Leonard, C. Nijskens, J. Ferooz, P. Lestrate, R.-M. Delrue, I. Danese, J. Vandenhaute, A. Tibor, X. DeBolle and J.-J. Letesson. "The sheathed flagellum of Brucella melitensis is involved in persistence in a murine model of infection." Cellular Microbiology 7.5 (2005): 687-698.
  11. ^ Fretin, D., A. M. Whatmore, S. A. Dahouk, H. Neubauer, B. Garin-Bastuji, D. Albert, M. Van Hessche, M. Menart, J. Godfroid, K. Walravens, P. Wattiau. "Brucella suis identification and biovar typing by real-time PCR." Veterinary Microbiology 131.2-4 (2008): 376-385.
  12. ^ Lagier, A., S. Brown, A. Soualah, I. Julier, B. Tourrand, D. Albert, J. Reynes and B. Garin-Bastuji. "Brucellose aigue a B. suis biovar 2 chez un chasseur de sanglier." Med. Mal. Infect 35 (2005): 185.
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  16. ^ Seleem, Mohamed N., Boyle, Stephen M. and Sriranganathan, Nammalwar. "Brucella: a pathogen without classic virulence genes." Veterinary Microbiology 129 (2008): 1-14.
  17. ^ Porte, F., Liautard J.P., Kohler, S. "Early acidification of phagosomes containing Brucella suis is essential for intracellular survival in murine macrophage." Infectious Immunology 67 (1999): 4041-4047.
  18. ^ Kohler, S., Porte, F., Jubier-Maurin, V., Ouahrani-Bettache, S., Teyssier, J., Liautard, J.P. "The intramacrophagic environment of Brucella suis and bacterial response." Veterinary Microbiology 90.1-4 (2002): 299-309.
  19. ^ Boschiroli, M. L., S. Ouahrani-Bettache, V. Foulongne, S. Michaux-Charachon, G. Bourg, A. Allardet-Servent, C. Cazevieille, J.P. Liautard, M. Ramuz and D. O’Callaghan. "The Brucella suis virB operon is induced intracellularly in macrophages." Proceedings of the National Academy of Science of USA 99 (2002): 1544-1549.
  20. ^ Porte, F., Liautard J.P., Kohler, S. "Early acidification of phagosomes containing Brucella suis is essential for intracellular survival in murine macrophage." Infectious Immunology 67 (1999): 4041-4047.
  21. ^ Kohler, S., Porte, F., Jubier-Maurin, V., Ouahrani-Bettache, S., Teyssier, J., Liautard, J.P. "The intramacrophagic environment of Brucella suis and bacterial response." Veterinary Microbiology 90.1-4 (2002): 299-309.
  22. ^ Jubier-Maurin, V, A. Rodrigue, S. Ouahrani-Bettache, M. Layssac, M.A. Mandrand-Berthelot, S. Köhler et al., Identification of the nik gene cluster of Brucella suis: regulation and contribution to urease activity. J. Bacteriol. 183 (2001), pp. 426–434.
  23. ^ Kohler, S., Porte, F., Jubier-Maurin, V., Ouahrani-Bettache, S., Teyssier, J., Liautard, J.P. "The intramacrophagic environment of Brucella suis and bacterial response." Veterinary Microbiology 90.1-4 (2002): 299-309.
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  29. ^ Briones, G., N. Inon de Iannino, M. Roset, A. Vigliocco, P.S. Paulo and R.A. Ugalde. "Brucella abortus cyclic beta-1,2-glucan mutants have reduced virulence in mice and are defective in intracellular replication in HeLa cells." Infectious immunity 69 (2001): 4528-4535.
  30. ^ Kemp, Jeffrey M. and Miller, Lowell A. "Oral vaccination and immunocontraception of feral swine using brucella suis with multimeric gnrh protein expression." Proc. 23rd vertebr. Pest Conf. (2008): 250-252.
  31. ^ Christopher, G. W., Again, M. B., Cieslak, T. J. and Olson, P.E. "History of U. S. military contributions to the study of bacterial zoonoses." Military Medicine 170 (2005): 39-48.
  32. ^ Bossi, P., Tegnell, A., Baka, A, Van Loock, F., Hendriks, J., Werner, A., Maidhof, H., Gouvras, G. "Bichat guidelines for the clinical management of brucellosis and bioterrorism-related brucellosis." Eurosurveillance 9 (2004): 1-5.