Biology:Swine brucellosis

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Swine brucellosis
Brucella suis culture.jpg
Brucella suis culture
Scientific classification edit
Domain: Bacteria
Phylum: Pseudomonadota
Class: Alphaproteobacteria
Order: Hyphomicrobiales
Family: Brucellaceae
Genus: Brucella
Species:
B. suis
Binomial name
Brucella suis
Huddleson, 1929
Brucellosis in Wild Swine, distribution in USA.svg

   Absent
   Serologic evidence
   Confirmed infections

Swine brucellosis is a zoonosis affecting pigs, caused by the bacterium 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 sows 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]

Since brucellosis threatens the food supply and causes undulant fever,[4] 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]

Cause

B. suis is a Gram-negative, facultative, intracellular coccobacillus, capable of growing and reproducing inside of host cells, specifically phagocytic cells.[6] They are also not spore-forming, capsulated, or motile.[6] Flagellar genes, however, are present in the B. suis genome, but are thought to be cryptic remnants because some were truncated and others were[6] missing crucial components of the flagellar apparatus.[7][8] In mouse models, the flagellum is essential for a normal infectious cycle, where the inability to assemble a complete flagellum leads to severe attenuation of the bacteria.[9]

B. suis is differentiated into five biovars (strains), where biovars 1-3 infect wild boar and domestic pigs, and biovars 1 and 3 may cause severe diseases in humans.[1] In contrast, biovar 2 found in wild boars in Europe shows mild or no clinical signs and cannot infect healthy humans, but does infect pigs and hares.[10]

Pathogenesis

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

B. suis possesses smooth lipopolysaccharide (LPS), which has a full-length O-chain, as opposed to rough LPS, which has a truncated or no O-chain.[11] 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.[12] In addition, this furtive entry into macrophages does not affect the cell’s normal trafficking.[13] The smooth LPS also inhibits host cell apoptosis by O-polysaccharides through a TNF-alpha-independent mechanism, which allows for B. suis to avoid the activation of the host immune system.[11]

Once inside macrophages, B. suis is able to endure the rapid acidificiation in the phagosome to pH 4.0-4.5[14] by expressing metabolism genes mainly for amino acid synthesis.[13] The acidic pH is actually essential for replication of the bacteria by inducing major virulence genes of the virB operon[15] and the synthesis of DnaK chaperones.[14] DnaK is part of the heat shock protein 70 family, and aids in the correct synthesis and activation of certain virulence factors.[13]

In addition, the B. suis gene for nickel transport, nikA, is activated by metal ion deficiency and is expressed once in the phagosome.[16] Nickel is essential for many enzymatic reactions, including ureolysis to produce ammonia which in turn may neutralize acidic pH.[13] Since B. suis is unable to grow in a strongly acidic medium, it could be protected from acidification by the ammonia.

Summary:

  • B. suis encounters a macrophage, but no oxidative burst occurs.
  • Lipid rafts are necessary for macrophage penetration.
  • The phagosome rapidly acidifies, creating a stressful environment for bacteria, which triggers activation of virulence genes.
  • Lipid rafts on phagosomes prevent lysosomal fusion, and normal cell trafficking is unaffected.

Symptoms

The most frequent clinical sign following B. suis infection is abortion in pregnant females, reduced milk production, and infertility.[17] 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.[17][18]

Swine also develop orchitis (swelling of the testicles), lameness (movement disability), hind limb paralysis, or spondylitis (inflammation in joints).[18]

Treatment

Because B. suis is facultative and intracellular, and is able to adapt to environmental conditions in macrophages, treatment failure and relapse rates are high.[18] The only effective way to control and eradicate zoonosis is by vaccination of all susceptible hosts and elimination of infected animals.[19] The Brucella abortus (rough LPS Brucella) vaccine, developed for bovine brucellosis and licensed by the USDA Animal Plant Health Inspection Service, has shown protection for some swine and is also effective against B. suis infection, but there is currently no approved vaccine for swine brucellosis.[20]

Biological warfare

In the United States, B. suis was the first biological agent weaponized in 1952, and was field-tested with B. suis-filled bombs called M33 cluster bombs.[21] It is, however, considered to be one of the agents of lesser threat because many infections are asymptomatic and the mortality is low,[22] but it is used more as an incapacitating agent.

References

  1. ↑ 1.0 1.1 Fretin, D; Whatmore, AM; Al Dahouk, S; Neubauer, H; Garin-Bastuji, B; Albert, D; Van Hessche, M; Ménart, M et al. (15 October 2008). "Brucella suis identification and biovar typing by real-time PCR". Veterinary microbiology 131 (3-4): 376–85. doi:10.1016/j.vetmic.2008.04.003. PMID 18499359. 
  2. ↑ Godfroid, J; Cloeckaert, A; Liautard, JP; Kohler, S; Fretin, D; Walravens, K; Garin-Bastuji, B; Letesson, JJ (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 (3): 313–26. doi:10.1051/vetres:2005003. PMID 15845228. open access
  3. ↑ Nicoletti, P (2016). "Brucellosis in Pigs - Reproductive System". http://www.merckvetmanual.com/reproductive-system/brucellosis-in-large-animals/brucellosis-in-pigs. Retrieved 2017-04-29. 
  4. ↑ Wilson, G. S. (1955). Topley and Wilson’s principles of bacteriology and immunity. London, England: Edward Arnold Publishers Ltd.
  5. ↑ Halling, SM; Peterson-Burch, BD; Bricker, BJ; Zuerner, RL; Qing, Z; Li, LL; Kapur, V; Alt, DP et al. (April 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 (8): 2715–26. doi:10.1128/jb.187.8.2715-2726.2005. PMID 15805518. 
  6. ↑ 6.0 6.1 6.2 Liautard, JP; Gross, A; Dornand, J; Köhler, S (June 1996). "Interactions between professional phagocytes and Brucella spp". Microbiología 12 (2): 197–206. PMID 8767704. 
  7. ↑ DelVecchio, VG; Kapatral, V; Elzer, P; Patra, G; Mujer, CV (20 December 2002). "The genome of Brucella melitensis". Veterinary microbiology 90 (1-4): 587–92. doi:10.1016/S0378-1135(02)00238-9. PMID 12414174. 
  8. ↑ Moreno, E; Moriyon, I (8 January 2002). "Brucella melitensis: a nasty bug with hidden credentials for virulence". Proceedings of the National Academy of Sciences of the United States of America 99 (1): 1–3. doi:10.1073/pnas.022622699. PMID 11782541. 
  9. ↑ Fretin, D; Fauconnier, A; Köhler, S; Halling, S; Léonard, S; Nijskens, C; Ferooz, J; Lestrate, P et al. (May 2005). "The sheathed flagellum of Brucella melitensis is involved in persistence in a murine model of infection". Cellular microbiology 7 (5): 687–98. doi:10.1111/j.1462-5822.2005.00502.x. PMID 15839898. 
  10. ↑ Lagier, A; Brown, S; Soualah, A; Julier, I; Tourrand, B; Albert, D; Reyes, J; Garin-Bastuji, B (2005). "Brucellose aiguë à Brucella suis biovar 2 chez un chasseur de sanglier" (in fr). Médecine et Maladies Infectieuses 35: 185. 
  11. ↑ 11.0 11.1 Seleem, MN; Boyle, SM; Sriranganathan, N (25 May 2008). "Brucella: a pathogen without classic virulence genes.". Veterinary microbiology 129 (1-2): 1–14. doi:10.1016/j.vetmic.2007.11.023. PMID 18226477. 
  12. ↑ Lapaque, N., Moriyon, I., Moreno, E., Gorvel, J.P. "Brucella lipopolysaccharide acts as a virulence factor." Curr. Opin. Microbio 8 (2005): 60-66.
  13. ↑ 13.0 13.1 13.2 13.3 Köhler, S; Porte, F; Jubier-Maurin, V; Ouahrani-Bettache, S; Teyssier, J; Liautard, JP (20 December 2002). "The intramacrophagic environment of Brucella suis and bacterial response". Veterinary microbiology 90 (1-4): 299–309. doi:10.1016/S0378-1135(02)00215-8. PMID 12414150. 
  14. ↑ 14.0 14.1 Porte, F; Liautard, JP; Köhler, S (August 1999). "Early acidification of phagosomes containing Brucella suis is essential for intracellular survival in murine macrophages". Infection and Immunity 67 (8): 4041–7. PMID 10417172. 
  15. ↑ Boschiroli, ML; Ouahrani-Bettache, S; Foulongne, V; Michaux-Charachon, S; Bourg, G; Allardet-Servent, A; Cazevieille, C; Liautard, JP et al. (5 February 2002). "The Brucella suis virB operon is induced intracellularly in macrophages.". Proceedings of the National Academy of Sciences of the United States of America 99 (3): 1544–9. doi:10.1073/pnas.032514299. PMID 11830669. 
  16. ↑ Jubier-Maurin, V; Rodrigue, A; Ouahrani-Bettache, S; Layssac, M; Mandrand-Berthelot, MA; Köhler, S; Liautard, JP (January 2001). "Identification of the nik gene cluster of Brucella suis: regulation and contribution to urease activity". Journal of Bacteriology 183 (2): 426–34. doi:10.1128/jb.183.2.426-434.2001. PMID 11133934. 
  17. ↑ 17.0 17.1 Acha, PN; Szyfres, B, eds (2003). "Brucellosis". Zoonoses and communicable diseases common to man and animals. Volume 1 (3rd ed.). Washington, DC: Pan American Health Organization. pp. 40–66. ISBN 9275119910. http://www1.paho.org/hq/dmdocuments/2010/ZoonosesVol-1.pdf. 
  18. ↑ 18.0 18.1 18.2 Seleem, MN; Boyle, SM; Sriranganathan, N (27 January 2010). "Brucellosis: a re-emerging zoonosis.". Veterinary microbiology 140 (3-4): 392–8. doi:10.1016/j.vetmic.2009.06.021. PMID 19604656. 
  19. ↑ 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.
  20. ↑ 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.
  21. ↑ 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.
  22. ↑ 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.

Wikidata ☰ Q836301 entry




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