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Vaccination against paratuberculosis, a chronic disease of ruminants caused by Mycobacterium avium subsp. paratuberculosis (Map), has been considered as the most effective control method. However, protection is incomplete, and the mechanisms operating in the response of the animals to vaccination are not fully understood. Therefore, this study analyzed the immune response and the effects on protection against Map infection, elicited by paratuberculosis (Silirum®) and tuberculosis (heat-inactivated M. bovis [HIMB]) vaccines and their components in a caprine experimental model. Fifty goat kids were divided into 10 groups (n = 5) according to their vaccination (Silirum®, HIMB and nonvaccinated), immunization (inactivated bacteria or adjuvant), and/or infection. Oral challenge with Map was performed 45 days postvaccination/immunization (dpv), and animals were euthanized at 190 dpv. Peripheral immune response and proportion of lymphocyte subpopulations were assessed monthly by enzyme-linked immunosorbent assay and flow cytometry analysis, respectively. Local immune response, proportion of tissue lymphocyte subpopulations, Map detection (polymerase chain reaction), and histological examination were conducted in gut-associated lymphoid tissues. All infected groups developed paratuberculosis granulomatous lesions despite vaccination or immunization. The Silirum® and HIMB-vaccinated groups showed a considerable lesion reduction consistent with a significant peripheral cellular and humoral immune response. Besides, a lower number of granulomas were observed in groups immunized with inactivated bacteria and adjuvants in comparison to nonvaccinated and infected group. However, despite not being significant, this reduction was even higher in adjuvant immunized groups, which developed milder granulomatous lesion with no detectable peripheral immune responses associated with immunization. No changes in the peripheral and local proportion of lymphocyte subsets or local immune respo

Ovine enzootic abortion (OEA), caused by Chlamydia abortus, is an economically important disease in many countries. Inactivated vaccines have been used for many years as they induce immunity in sheep, although outbreaks of abortions have been described in vaccinated flocks. In addition, there is a commercially available live attenuated vaccine that provides good protective results. Recently however, reports question the attenuation of this vaccine and associate it with the appearance of outbreaks of OEA in vaccinated flocks. In the present study, a recently commercialized inactivated vaccine (INMEVA®; Laboratorios Hipra S.A., Amer, Spain) has been evaluated using mouse and sheep experimental models. In the mouse models (non-pregnant and pregnant models), the efficacy of INMEVA vaccine has been compared to an unvaccinated control group and to an experimental inactivated vaccine considered as a positive protection control (UMU vaccine). In the non- pregnant model, the UMU vaccine was more effective than the INMEVA vaccine regarding the impact on body weight or the presence of C. abortus in the liver, but both vaccinated groups (UMU and INMEVA) had significantly lower C. abortus in the liver compared to the control group. In the pregnant model in terms of reproductive failures, pups per mouse or the presence of C. abortus in the liver or uterus, no significant differences were found between both vaccines, inducing protection compared to the control group. In the ovine pregnant model, where INMEVA vaccine was compared only to an unvaccinated group, the results indicate that this new commercial vaccine is safe and provides a suitable level of protection against an experimental challenge with C. abortus. A 75% reduction in reproductive disorders, 55% reduction in animals with C. abortus shedding on day of parturition/abortion, and a significant reduction of the average amount of chlamydial shedding from parturition/abortion over the next 21 days was observed, in relation

Toxoplasma gondii is an apicomplexan parasite that infects almost all warm-blooded animals. Little is known about how the parasite virulence in mice extrapolates to other relevant hosts. In the current study, in vitro phenotype and in vivo behavior in mice and sheep of a type II T. gondii isolate (TgShSp1) were compared with the reference type II T. gondii isolate (TgME49). The results of in vitro assays and the intraperitoneal inoculation of tachyzoites in mice indicated an enhanced virulence for the laboratory isolate, TgME49, compared to the recently obtained TgShSp1 isolate. TgShSp1 proliferated at a slower rate and had delayed lysis plaque formation compared to TgME49, but it formed more cyst-like structures in vitro. No mortality was observed in adult mice after infection with 1–105 tachyzoites intraperitoneally or with 25–2,000 oocysts orally of TgShSp1. In sheep orally challenged with oocysts, TgME49 infection resulted in sporadically higher rectal temperatures and higher parasite load in cotyledons from ewes that gave birth and brain tissues of the respective lambs, but no differences between these two isolates were found on fetal/lamb mortality or lesions and number of T. gondii-positive lambs. The congenital infection after challenge at mid-pregnancy with TgShSp1, measured as offspring mortality and vertical transmission, was different depending on the challenged host. In mice, mortality in 50% of the pups was observed when a dam was challenged with a high oocyst dose (500 TgShSp1 oocysts), whereas in sheep infected with the same dose of oocysts, mortality occurred in all fetuses. Likewise, mortality of 9 and 27% of the pups was observed in mice after infection with 100 and 25 TgShSp1 oocysts, respectively, while in sheep, infection with 50 and 10 TgShSp1 oocysts triggered mortality in 68 and 66% of the fetuses/lambs. Differences in vertical transmission in the surviving offspring were only found with the lower oocyst doses (100% after infection with 10 T