Objective: To determine whether a novel optimized plasmid carrying the porcine growth hormone–releasing hormone (GHRH) wild-type cDNA administered at a lower dose was as effective at eliciting physiologic responses as a commercial GHRH plasmid approved for use in Australia. Animals: 134 gilts. Procedures: Estrus was synchronized and gilts were bred. Pregnant gilts were assigned to 2 treatment groups (40 gilts/group) or 1 untreated control group (24 gilts). Gilts in one of the treatment groups received the commercial GHRH plasmid, whereas gilts in the other treatment group received a novel optimized GHRH plasmid; both plasmids were administered IM in the right hind limb, which was followed by electroporation. Sow and litter performance were monitored for the 3 gestations after treatment. Results: A significant increase in insulin-like growth factor-I concentrations, decrease in perinatal mortality rate, increase in the number of pigs born alive, and increase in the weight and number of pigs weaned were detected for both groups receiving the GHRH-expressing plasmids, compared with values for the control group. Additionally, there was a significant decrease in sow attrition in GHRH-treated females, compared with attrition in the control group, during the 3 gestations after treatment. Conclusions and Clinical Relevance: Both of the GHRH plasmids provided significant benefits for sow performance and baby pig survivability for pregnant and lactating sows and their offspring during the 3 gestations after treatment, compared with results for untreated control gilts. Use of a novel optimized plasmid reduced the effective plasmid dose in these large mammals.

Porcine blood mononuclear cells (BMC) were exposed to prepartum concentration of estrogen in gilts before acquisition (in vivo), and their subsequent reactivity (in vitro) was explored. In a cross-over experimental designed study, 6 ovariectomized gilts were injected once with 3.75 mg of estradiol-17beta benzoate in arachidic oil or with arachidic oil only during 2 experiments. The ability of their BMC to proliferate in response to stimulation with phytohemagglutinin, concanavalin A, and pokeweed mitogen was assayed in cultures of blood and in cultures of purified BMC. After 2 days of mitogen stimulation, activity of accessible interleukin 2 was quantified in supernatants obtained from cultures of purified BMC and supernatants of blood cultures stimulated with pokeweed mitogen. Also, production of immunoglobulins by purified BMC in response to polyclonal stimuli was measured. Three days after treatment with estradiol, the proliferative response was suppressed in blood cultures stimulated with concanavalin A (P < 0.05) and phytohemagglutinin (P < 0.07). Effects of estradiol treatment were not found in any of the assays performed with purified BMC. We, therefore, assumed that in vivo exposure to estradiol can affect the function of porcine BMC; however, this was only evident when the in vitro assays were performed on blood cultures.

Specimens of the uterine tube epithelium (ampulla) were obtained from 20 healthy, prepubertal, ovariohysterectomized gilts. A 2 to 3% proportion of atypical cilia was observed. Of 6,600 transversely sectioned cilia, 122 (1.8%) had microtubular disorganization, whereas 444 of 48,080 totally examined cilia (0.9%) were compound, 104 (0.2%) were swollen, and 44 (0.09%) were intracytoplasmic.

It has been shown that zearalenone disrupts early pregnancy in swine without altering intrauterine content of estradiol 17 beta or progesterone, embryo migration, or estradiol-17 beta thesis by blastocysts. However, serum concentrations of progesterone were reduced 2 to 3 weeks after mating in gilts that ingested zearalenone. Therefore, progesterone was administered to gilts during early pregnancy to determine whether it could counteract the detrimental actions of zearalenone on embryonic development. Thirty-two crossbred gilts (Hampshire X Chester White X Yorkshire X Duroc) were assigned randomly to a 2 X 2 factorial arrangement of treatments: zearalenone (Z); zearalenone plus progesterone (ZP); progesterone (P); or control (C). From postmating days 4 to 15, Z- and ZP-treated gilts were fed 1 mg of Z/kg of body weight, and P-treated and C gilts were fed ethanol as vehicle in a corn-soybean diet. On postmating days 3 to 15, P- and ZP-treated gilts were injected IM with 100 mg of progesterone, and C and Z-treated gilts were injected with progesterone carrier (15% ethanol, 15% benzyl alcohol, 70% propylene glycol). Blood was collected from gilts by puncture of the jugular vein daily from days 3 to 15, on alternate days from days 17 to 31, and then twice weekly until the end of the experiment. Fetal development was assessed in Z and ZP-treated gilts on postmating day 47.6 +/- 2.9 by cesarean section and in P-treated and c gilts at slaughter on postmating days 51.2 +/- 3.2. Serum concentrations of progesterone in P-treated gilts were greater on days 7 to 8, 10 to 15, 17, and 19 than in C gilts. Serum concentrations of progesterone were greater on days 8, 10, and 12 in ZP-treated than in C gilts. However, serum concentrations of progesterone were lower in ZP-treated gilts than in C gilts on postmating days 19 to 31. Serum concentrations of progesterone were lower in Z-treated gilts than C gilts on postmating days 15, 17, and 19. At slaughter or cesarean section, viable fetuses were not found in Z-treated gilts, but 80% of the C and P-treated gilts had viable fetuses. All Z-treated gilts were classified as pseudopregnant because uteri were turgid and the ovaries had functional corpora lutea. Uteri of ZP-treated gilts appeared normal. Corpora lutea of pregnancy had regressed by postmating day 35 in 7 of 8 ZP-treated gilts. Crown-to-rump length was similar between P-treated and C gilts (94 vs 92 mm). Fetal weight was similar between P-treated and C gilts (70 vs 62 g). These data demonstrate that 100 mg of progesterone/d failed to counteract the adverse effects of 1 mg of Z/kg of body weight on early pregnancy in primiparous gilts.

The ability of pseudorabies virus (PRV) to infect and establish latency in pigs with passively acquired (maternal) antibody for PRV was tested by exposing such pigs to the virus and subsequently attempting to reactivate latent virus by administering large doses of dexamethasone. Pigs of each of 4 litters that had nursed gilts with relatively high (512, gilts 1 and 2), moderate (32, gilt 3), and no (less than 2, gilt 4) serum titers of virus-neutralizing (VN) antibodies for PRV were allotted to 3 treatment groups (A, B, C) when they were 2 weeks old. Group-A pigs were separated from littermates and dam and thereafter kept in isolation; group-B pigs were experimentally exposed oronasally to PRV and 1 hour later returned to their dam; group-C pigs were kept with their dam and potentially exposed to PRV by contact with littermates of group B. Sera obtained from pigs at selected intervals until they were 17 weeks old were tested for VN activity and for precipitating activity for radiolabeled viral proteins. All group-A pigs remained clinically normal throughout the experiment. Depending on the initial amount of passively acquired antibody, little or no serum VN or precipitating activity remained by the time these pigs were 17 weeks old. Group-B and -C pigs, with relatively high amounts of passively acquired antibody when exposed to PRV, also remained clinically normal. However, most became latently infected as subsequently evidenced by either dexamethasone-induced or noninduced virus reactivation. Noninduced reactivation may have been initiated by weaning the pigs when they were about 8 weeks old. Group-B and -C pigs with no or moderate amounts of passively acquired antibody when exposed to PRV, had severe clinical signs. These pigs either died or recovered but remained stunted in growth. Virus was reactivated in all of the recovered pigs by treatment with dexamethasone. Quantitative and qualitative changes in serum precipitating activity, especially for viral proteins of relatively low molecular weight (less than 46,000), were a more consistent indication of virus reactivation than were either increased VN titers or virus isolation. Results with litters 1 and 2 clearly indicate that latent infection of young pigs with highly virulent PRV can develop in the absence of clinical signs.

First-litter commerical cross-bred gilts were treated with levamisole (1.5, 2.5, or 3.5 mg/kg of body weight) weekly during the last 4 weeks of gestation, because similar treatment of dairy heifers had improved postpartum maternal health and neonatal survival. In the gilts, differences in reproductive performance were not found on the basis of pig survival at birth, pig survival at weaning, birth weight, or weaning weight. Also differences between treated and control gilts were not found in response of circulating lymphocytes to mitogen stimulation (phytohemagglutinin A, concanavalin A, and pokeweed mitogen). In all gilts, the lymphocyte response to mitogen stimulation was decreased during the first week after farrowing.

Porcine infectious anemia caused by Mycoplasma suis is a global disease and results in serious economic losses. To determine the prevalence of M. suis infection in eastern China, a cross-sectional serologic study was conducted with 3458 porcine serum samples randomly obtained from January 2014 to August 2016. The samples were tested with a blocking enzyme-linked immunosorbent assay developed in our laboratory. The seroprevalence was 33.3% in the complete sample set and was 25.9%, 37.8%, and 37.8% in 2014, 2015, and 2016, respectively. The seroprevalence was distinctly higher in summer (39.9%) and autumn (42.0%) than in spring (28.9%) and winter (23.3%). Shanghai was the region with the highest seroprevalence (54.2%) and Jiangsu the region with the lowest (23.0%). The seroprevalence was markedly higher in boars (47.1%), multiparous sows (47.0%), and replacement gilts (39.2%) than in piglets (24.2%), fattening pigs (17.2%), and nursery pigs (12.5%). These data demonstrate that the prevalence of M. suis infection is increasing yearly in eastern China.

The objective of this study was to determine the effect of additional human chorionic gonadotrophin (hCG) on the ovarian response of gilts previously treated with 200 IU hCG combined with 400 IU equine chorionic gonadotrophin (eCG) (eCG/hCG). Seventy-one prepuberal gilts (105 ± 7.5 kg) were assigned to groups: i) eCG/hCG (hCG-0; n = 25); ii) eCG/hCG followed by 100 IU of hCG at 24 h (hCG-100; n = 24); iii) eCG/hCG followed by 200 IU hCG at 24 h (hCG-200; n = 10); and iv) controls (CON; n = 12). Ovulation response was assessed by ovarian dissection or real-time ultrasonography. Additional hCG did not significantly improve numbers of gilts ovulating. Numbers of corpora lutea increased with hCG, and was higher in hCG-200 (P < 0.01). Compared to hCG-0, the frequency of cysts in gilts was higher in hCG-100 (P < 0.05) and further increased in hCG-200 (P < 0.01). The number of cysts per gilt was dose-dependently increased by additional hCG. We conclude that supplemental hCG will increase the number of corpora lutea but will be associated with follicular cyst development in a dose dependent manner.

Objective-To use mathematical modeling to assess the effectiveness of control strategies for porcine reproductive and respiratory syndrome (PRRS) virus on a swine farm. Sample-A hypothetical small, medium, or large farrow-to-weaning swine farm in the Midwestern United States. Procedures-Stochastic models were formulated to simulate an outbreak of PRRS on a farm. Control strategies assessed in those models included none (baseline) and various combinations of mass immunization, herd closure, and gilt acclimatization. Nine different models resulting from the combination of low, moderate, or high PRRS virus virulence and small, medium, or large herd size were simulated. A stabilized status, the outcome of interest, was defined as the absence of positive PCR assay results for PRRS virus in 3-week-old piglets. For each scenario, the percentage of simulations with a stabilized status was used as a proxy for the probability of disease control. Results-Increasing PRRS virus virulence and herd size were negatively associated with the probability of achieving a stabilized status. Repeated mass immunization with herd closure or gilt acclimitization was a better alternative than was single mass immunization for disease control within a farm. Conclusions and Clinical Relevance-Repeated mass immunization with a PRRS modified-live virus vaccine with herd closure or gilt acclimitization was the scenario most likely to achieve a stabilized status. Estimation of the cost of various PRRS control strategies is necessary.