The relationships between Brucella melitensis predilection sites, bacterial loads in vivo, and the agglutinating antibody response in experimentally infected sheep
F?or exploring Brucella melitensis survival in in vivo predilection sites and the relationship between bacterial loads and the detection of antibody titers in experimentally subcutaneously infected sheep with B.1397645907melitensis 16M, ten rams and ten ewes were used. One ram and one ewe were euthanized at 7, 15, 30, 60, 90, 120, and 180 days post inoculation (dpi). Bacteriological results showed that tissue isolation rates and bacterial loads peaked from 7 dpi to 30 dpi and then cleared until 120 dpi. In in situ hybridization trials the strongest signals for B.1397645907melitensis were detected at 7 dpi and 15 dpi, and then they gradually cleared. Monitoring results of agglutinating antibodies showed that anti-Brucella antibodies began to be produced at 7 dpi, peaked at 15 dpi, and gradually declined until lower detection levels than the threshold were being detected at 180 dpi. Thus, we found that the more Brucella bacterial loads there were in vivo, the higher the antibody titers were in sera, which suggested that detection of the agglutinating antibody titers might be used as an indicator of a Brucella carrier in infected animals.
The relationships between Brucella melitensis predilection sites, bacterial loads in vivo, and the agglutinating antibody response in experimentally infected sheep
F?or exploring Brucella melitensis survival in in vivo predilection sites and the relationship between bacterial loads and the detection of antibody titers in experimentally subcutaneously infected sheep with B.1397645907melitensis 16M, ten rams and ten ewes were used. One ram and one ewe were euthanized at 7, 15, 30, 60, 90, 120, and 180 days post inoculation (dpi). Bacteriological results showed that tissue isolation rates and bacterial loads peaked from 7 dpi to 30 dpi and then cleared until 120 dpi. In in situ hybridization trials the strongest signals for B.1397645907melitensis were detected at 7 dpi and 15 dpi, and then they gradually cleared. Monitoring results of agglutinating antibodies showed that anti-Brucella antibodies began to be produced at 7 dpi, peaked at 15 dpi, and gradually declined until lower detection levels than the threshold were being detected at 180 dpi. Thus, we found that the more Brucella bacterial loads there were in vivo, the higher the antibody titers were in sera, which suggested that detection of the agglutinating antibody titers might be used as an indicator of a Brucella carrier in infected animals.
___
- Enright FM. The pathogenesis and pathobiology of Brucella infection in domestic animals. In: Mielsen K, Duncan JR, editors. Animal Brucellosis. Boca Raton, FL, USA: CRC Press; 1990. pp. 301–320.
- Chand P, Sadana JR, Malhotra AK. Epididymo-orchitis caused by Brucella melitensis in breeding rams in India. Vet Rec 2002; 150: 84–85.
- Payne JM. The pathogenesis of experimental brucellosis in virgin heifers with and without continuous progesterone treatment. J Endocrinol 1960; 20: 345–354.
- Suraud V, Jacques I, Olivier M, Guilloteau LA. Acute infection by conjunctival route with Brucella melitensis induces IgG+ cells and IFN-gamma producing cells in peripheral and mucosal lymph nodes in sheep. Microbes Infect 2008; 10: 1370–1378.
- Durán-Ferrer M, Léon L, Nielsen K, Caporale V, Mendoza J, Osuna A, Perales A, Smith P, De-Frutos C, Gómez-Martín B et al. Antibody response and antigen-specific gamma interferon profiles of vaccinated and unvaccinated pregnant sheep experimentally infected with Brucella melitensis. Vet Microbiol 2004; 100: 219–231.
- Mense MG, Van De Verg LL, Bhattacharjee AK, Garrett JL, Hart JA, Lindler LE, Hadfield TL, Hoover DL. Bacteriologic and histologic features in mice after intranasal inoculation of Brucella melitensis. Am J Vet Res 2001; 62: 398–405.
- Hamdy ME, Amin AS. Detection of Brucella species in the milk of infected cattle, sheep, goats and camels by PCR. Vet J 2002; 163: 299–305.
- Ramin B, Macpherson P. Human brucellosis. BMJ 2010; 341: c4545.
- Adams LG. The pathology of brucellosis reflects the outcome of the battle between the host genome and the Brucella genome. Vet Microbiol 2002; 90: 553–561.
- Alton GG, Jones LM, Pietz DE. Laboratory Techniques in Brucellosis. Geneva, Switzerland: World Health Organization; 1975.
- Elfaki MG, Al-Hokail AA, Nakeeb SM, Al-Rabiah FA. Evaluation of culture, tube agglutination, and PCR methods for the diagnosis of brucellosis in humans. Med Sci Monit 2005; 11: MT69–MT74.
- Wellinghausen N, Nöckler K, Sigge A, Bartel M, Essig A, Poppert S. Rapid detection of Brucella spp. in blood cultures by fluorescence in situ hybridization. J Clin Microbiol 2006; 44: 1828–1830.
- Cheville NF, Olsen SC, Jensen AE, Stevens MG, Florance AM, Houng HS, Drazek ES, Warren RL, Hadfield TL, Hoover DL. Bacterial persistence and immunity in goats vaccinated with a purE deletion mutant or the parental 16M strain of Brucella melitensis. Infect Immun 1996; 64: 2431–2439.
- Bricker BJ, Halling SM. Differentiation of Brucella abortus bv. 1, 2, and 4, Brucella melitensis, Brucella ovis, and Brucella suis bv. 1 by PCR. J Clin Microbiol 1994; 32: 2660–2666.
- Muñoz PM, de Miguel MJ, Grilló MJ, Marín CM, Barberán M, Blasco JM. Immunopathological responses and kinetics of Brucella melitensis Rev 1 infection after subcutaneous or conjunctival vaccination in rams. Vaccine 2008; 26: 2562–2569.
- Elzer PH, Hagius SD, Davis DS, DelVecchio VG, Enright FM. Characterization of the caprine model for ruminant brucellosis. Vet Microbiol 2002; 90: 425–431.
- Bellaire BH, Elzer PH, Baldwin CL, Roop RM. Production of the siderophore 2,3-dihydroxybenzoic acid is required for wild-type growth of Brucella abortus in the presence of erythritol under low-iron conditions in vitro. Infect Immun 2003; 71: 2927–2832.
- Ko J, Splitter GA. Molecular host-pathogen interaction in brucellosis: current understanding and future approaches to vaccine development for mice and humans. Clin Microbiol Rev 2003; 16: 65–78.