Pseudorabies is a porcine herpesvirus of major importance in the swine industry. Isoprinosine is an immunomodulating drug that has been shown to be beneficial in treating herpesvirus infections. Twenty-four 7-week-old pigs were allotted within litters to 1 of 4 groups: control, isoprinosine (ISO), pseudorabies virus (PRV), or isoprinosine and pseudorabies virus (ISO-PRV). Isoprinosine was administered daily for 16 days to the ISO and ISO-PRV groups (75 mg/kg of body weight/day, PO). Immunity in pigs in the PRV and ISO-PRV groups was challenged with pseudorabies virus (10(5) TCID50 units) on day 4. Rectal temperatures and viral excretion were monitored daily; total and differential leukocyte counts, lymphocyte response to mitogens, and interleukin-2 production were monitored every 4 days. Pigs challenge-inoculated with pseudorabies virus became ill, with the ISO-PRV group most severely affected. Rectal temperatures were high (P less than 0.05) in virally challenged pigs on days 5 to 12 and 14 to 16; isoprinosine did not alter this effect. Pseudorabies virus-infected pigs had leukocytosis (P less than 0.05) on days 12 and 16, primarily caused by neutrophilia. Concanavalin A-stimulated lymphocyte proliferation was decreased (P less than 0.06) in both PRV and ISO-PRV groups on day 12, compared with control pigs, but only in the PRV group on day 16. Pokeweed mitogen-stimulated lymphocyte proliferation was decreased (P less than 0.02) in ISO-PRV pigs on day 8 of the experiment. Interleukin-2 concentrations, pooled over all sampling days, were decreased (P less than 0.03) in pseudorabies virus-infected pigs. Viral excretion was not altered by isoprinosine treatment. These data suggest that pseudorabies virus infection decreased lymphocyte proliferative responses and interleukin-2 prodcution in pigs, and that isoprinosine did not mitigate these effects.

A study was performed to assess the effect of xylazine HCl (0.1 mg/kg of body weight, IV) in heifers maintained at thermoneutrality (18 C, 42% humidity) or under heat stress (33 C, 63% humidity) conditions. Xylazine caused 50 and 70% decreases in serum insulin concentrations in the thermoneutral and heat-stressed heifers, respectively. Xylazine-induced hypoinsulinemia was associated with hyperglycemia. In the thermoneutral group, serum glucose concentrations increased from a basal concentration of 75 mg/dl to 150 mg/dl after 15 minutes. In the heat stress group, the serum glucose concentration increased from 65 mg/dl to 105 mg/dl. Hyperglycemia peaked at 2 hours and remained high for 6 hours after xylazine administration. Heat-stressed heifers took a longer time (107 minutes) to stand than did heifers under thermoneutral conditions (41 minutes). The time to regain sensation to pain was significantly prolonged in heat-stressed heifers. Xylazine had no effect on body temperature and respiration rate in heifers under the thermoneutral conditions, whereas it markedly induced hyperthermia and suppressed respiration rate in the heat-stressed heifers. Furthermore, the pulse rate was slightly decreased in thermoneutral heifers and was markedly decreased in the heat-stressed heifers.

Sensory nerve conduction velocity was measured in the lateral palmar nerve of 8 horses. The limb temperature was manipulated by external means and monitored. Alterations in the nerve conduction velocity related to limb temperature variation were identified at both increased and decreased temperatures. These were quantified and a mean value of 2.15 +/- 0.2 m/s/degree Celsius was determined. The effect of altered limb temperature should be considered in nerve conduction velocity determinations.

To evaluate the relationship between pneumonic lesions and distribution of bacteria, lungs from calves inoculated with Pasteurella multocida were examined histologically by use of immunoperoxidase technique. Pneumonic lesions fundamentally consisted of bronchopneumonia with fibrinopurulent pleuritis. The lesions were confirmed to be associated with inoculated P multocida, using the immunoperoxidase technique. The P multocida antigen was detected not only in the bacterial clusters in the lesions, but also in the cytoplasm of infiltrating neutrophils and macrophages. Further, immunoelectron microscopy indicated that the inoculated bacteria generally were phagocytosed and digested by neutrophils.

Colostrum-deprived lambs (10 to 20 days old) were inoculated with either ovine adenovirus type 6 (OAV-6; n = 6), Pasteurella haemolytica type A1 (n = 6), or OAV-6 followed by P haemolytica 5 days later (n = 10). Another group (n = 3) served as sham-inoculated controls. Lambs inoculated with OAV-6 or P haemolytica developed mild and moderate respiratory tract disease of 6 and 3 days' duration, respectively. Lambs inoculated with virus and bacteria developed clinical signs of respiratory tract disease of greater intensity and duration (9 days) than with either agent alone. Within 3 hours of bacterial inoculation, all lambs that received P haemolytica were anorectic, listless, and febrile, and had hyperpnea and dyspnea. Ovine adenovirus type 6 was isolated from all virus-inoculated lambs. Although P haemolytica was not recovered from all bacteria-inoculated lambs, it was recovered for a longer period in the group that received both agents. Antibody to OAV-6 was detected in virus-inoculated lambs as early as day 6 after inoculation. The control lambs remained clinically normal and neither virus nor bacteria were recovered at necropsy.

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.