The influence of immunosuppression by T-2 mycotoxin on the fungal disease aspergillosis was investigated in rabbits. Four groups of rabbits (groups 1A, 1B, 3A, and 3B) were given 0.5 mg of T-2 toxin/kg of body weight/day, PO; in addition, rabbits of groups 3A and 3B were exposed to aerosols of Aspergillus fumigatus conidia from days 7 through 16. Rabbits of groups 2A and 2B were exposed to A fumigatus aerosols, but were not given T-2 toxin, and rabbits of group 0 served as controls. Two rabbits of group 1A, 1 rabbit of group 1B, and 1 rabbit of group 3A died before scheduled necropsy. Rabbits of groups 1A, 2A and 3A were killed and necropsied on day 17, and the remaining rabbits (groups 0, 1B, 2B, and 3B) were killed and necropsied on day 28. Changes caused by T-2 toxin included leukopenia, marginal anemia, and increased number of and morphologic changes in nucleated erythrocytes by day 21, followed by a regenerative hematologic response. Serum alkaline phosphatase and sorbitol dehydrogenase activities and antibody response to A fumigatus (as measuredby an indirect hemagglutination test) were decreased by T-2 toxin ingestion. Rabbits with aspergillosis had leukocytosis, increased PCV, and increased antibody response to A fumigatus. Histologic lesions consisting of centrilobular hepatocellular swelling, portal and periportal fibrosis, and lymphocyte necrosis and/or depletion within secondary lymphoid tissue were observed in most rabbits treated with T-2 toxin. Normal defense mechanisms against A fumigatus infection were compromised by T-2 treatment, as evidenced by the severity and extent of lung lesions, greater number of hyphal elements observed, and greater number of colonies of A fumigatus isolated from rabbits of groups 3A and 3B. There were no significant changes in group-0 rabbits.

To study communications and boundaries of the middle carpal and carpometacarpal joints of the horse, 50 forelimbs were obtained from fresh cadaver specimens. Blue latex solution (20 +/- 2.5 ml) was injected into the middle carpal joint, and the specimens were frozen in extension. Frozen specimens were cut into 1-cm sagittal sections from the middle of the radius to the middle of the metacarpus. The communications between the middle carpal and carpometacarpal joints and the presence, length, and position of the distopalmar outpouchings of the carpometacarpal joint were recorded. The middle carpal and carpometacarpal joints always communicated between os carpale III (C3) and os carpale IV (C4). An additional communication between the joints existed in 17 (34%) of the specimens, 10 on the palmar aspect of C4, and 3 on the palmar aspect of os carpale II (C2). When os carpale 1 (C1) was present (n = 5), communication between C1 and C2 was observed in 4 of the 5 specimens. In all specimens, medial and lateral distopalmar outpouchings of the carpometacarpal joint were observed and were located between the axial surface of os metacarpale II (MC2) and os metacarpale IV (MC4) and the abaxial surface of the suspensory ligament. There was no significant difference between the lengths of the lateral (2.3 +/- 0.54 cm) or medial (2.6 +/- 0.75 cm) distopalmar outpouchings. Small extensions from the distopalmar outpouchings were seen and extended axially into the fibers of the suspensory ligament or between the suspensory ligament and the distal accessory ligament of the deep digital flexor tendon. In one carpus, the middle carpal joint communicated with the antebrachiocarpal joint between the articulation of the os carpi intermedium (Ci) and the os carpi ulnare (Cu).

Fischer-344 rats were exposed for 4 hours to 0, 14, 280, or 560 mg of hydrogen sulfide.m-3 and killed 1, 18, or 44 hours later. We evaluated the nasal epithelial cells and determined the anatomic distribution of lesions. Inhalation of 560 mg of hydrogen sulfide.m-3 induced necrosis and exfoliation of respiratory and olfactory mucosal cells, but not squamous epithelial cells. The anatomic distribution of lesions was midway along the nasal passages involving nasal and maxillary conchae, but not ethmoidal conchae. Injured respiratory mucosa repaired rapidly, whereas olfactory mucosa continued to exfoliate at 44 hours after exposure.

On each day of feeding on susceptible calves, salivary glands obtained from groups of adult ticks that transmitted Anaplasma marginale were examined for A marginale colonies by use of light microscopy and transmission electron microscopy. On day 8 of feeding, salivary glands were examined, using fluorescein-labeled antibody and methyl green-pyronine stain. Use of fluorescein-labeled antibody consistently revealed small numbers of fluorescent foci in salivary gland acinar cells obtained from ticks that had fed for 8 days. Colonies of A marginale were seen by transmission electron microscopy only in salivary gland acini of male ticks; these colonies could not be identified, using light microscopy, in companion 1-micron plastic sections stained with Mallory stain. Methyl green-pyronine stain, used commonly to detect theilerial parasites in tick salivary glands, did not differentiate A marginale from cytoplasmic inclusions normally found in salivary gland acinar cells.

Parasite-free, 4-month-old-calves were inoculated with Ostertagia ostertagi and/or Trichostrongylus axei, followed 6 weeks later by inoculation with increasing doses of O ostertagi for 8 weeks in the 2 groups (n = 9) of calves that had been given O ostertagi. Gastrin immunoreactivity concentration in serum was measured before and after infection and was correlated with changes in mucosal thickness. Gastrin immunoreactivity concentration in preinoculation control sera ranged from 95.2 to 287.1 pg/ml, and increased values were measured in all parasitized calves after 15 weeks. Significantly (P < 0.05) increased serum gastrin immunoreactivity concentration compared with the preinfection value, was found in calves infected with O ostertagi or T axei, and highly significant (P < 0.01) values were observed in calves infected with both parasites. Abomasal mucosal hyperplasia was observed in all parasitized calves; increased mucosal thickness and mucosal cross-sectional area were most prominent in calves infected with O ostertagi and T axei.

The effect of T-2 toxin, a radiomimetic immunosuppressive agent, on resistance to the facultative intracellular bacterial pathogens Listeria monocytogenes (strain EGD), Mycobacterium bovis (BCG Copenhagen 1331), and Salmonella typhimurium was determined. Female Swiss ICR mice were given a single dose of T-2 toxin (4 mg/kg of body weight) by gastric gavage. On the seventh day after toxin administration, the mice were infected by intraperitoneal inoculation with L monocytogenes, S typhimurium, or M bovis. Mice given the toxin also were exposed to respirable droplet nuclei containing L monocytogenes or M bovis. The effect of the toxin on the course of infection was monitored by observing mortality or by enumeration of bacteria in te spleen or lungs of infected mice. The toxin increased resistance to infection with L monocytogenes initiated by intraperitoneal inoculation, but reduced resistance to M bovis infection initiated by intraperitoneal inoculation. The toxin had no appreciable effect on the course of salmonellosis or on resistance to infection initiated by inhalation of L monocytogenes or M bovis aerosols. Therefore, it was concluded that T-2 toxin does not necessarily reduce resistance to infection in mice. The toxin's effect on the course of in vivo bacterial infections depends on the nature of the infective agent and the route of inoculation.

Hybridomas were selected for secretion of monoclonal antibodies directed against pseudorabies virus (PRV) glycoproteins. Each monoclonal antibody was capable of neutralizing PRV in vitro in the presence of complement. This panel of antibodies was used in passive immunization studies to protect mice and swine from PRV-induced mortality. The most protective antibody in mice was 3A4, specific for PRV glycoprotein gp50, which afforded as high as 100% protection. Although antibody 3A4 was partially protective in swine, antibody 3D11, which is specific for PRV glycoprotein gIII, afforded greater protection-83% protection when ascitic fluid was used and 100% protection when immunoglobulin concentrated from cell cultures was used at a dose of 150 mg/pig. These studies demonstrated that monoclonal antibodies may be useful for short-term prophylaxis against PRV-induced disease and that antibody directed against either PRV gylcoprotein gIII or gp50 is sufficient to protect animals from PRV-induced mortality.

Angora goats heavily infested with Chorioptes bovis were dipped one time in either 0.05% amitraz, 0.27% coumaphos, 0.05% fenvalerate, or 0.03% lindane, Control of the mites by the single dips was evaluated for 21 days. Amitraz caused 98% mortality of the mites initially. Both coumaphos and lindane caused greater than 85% mortality at 3 days, but mite numbers increased rapidly thereafter. Only fenvalerate killed all of the mites.

Eighteen 4-day-old gnotobiotic pigs were orally inoculated with porcine enteric calicivirus-like virus (C strain). Seven additional gnotobiotic pigs served as noninoculated controls. Mild diarrhea developed in all inoculated pigs by postinoculation day (PID) 3 and persisted for 3 to 7 days. Severe diarrhea developed in 2 inoculated pigs between PID 4 and 5. Twelve inoculated and 7 control pigs were euthanatized over a 7-day period. Small intestinal mucosal smears were stained with a fluorescein-conjugated anti-porcine enteric calicivirus-like virus serum. Immunofluorescence was observed in villous epithelial cells (primarily in the duodenum or jejunum) of all inoculated pigs, except for 1 pig euthanatized at PID 7. Villus length was determined in histologic sections of the small intestinal specimens from control and inoculated pigs. Statistically significant (P less than 0.01) villus atrophy was found in the duodenum and/or jejunum of inoculated pigs at PID 3 to 7. These observations were confirmed by scanning electron microscopy, which revealed shortening, blunting, fusion, or absence of villi in the duodenum and jejunum of inoculated pigs at PID 3 to 7. Lesions were not seen in control pigs. Calicivirus-like particles were detected by immune electron microscopy in the large intestinal contents and feces of inoculated pigs from PID 1 to 7.

Three experiments were conducted to investigate experimentally the occurrence of periparturient nematode egg rise in ewes and the hormonal modulation of Haemonchus contortus infections. In the first experiment, fall-bred and winter-bred pregnant (n = 4 and 14, respectively) and nonpregnant (n = 5 and 29, respectively) ewes were treated with anthelmintic and were pastured together on fields that were contaminated with H contortus. Three weeks before lambing, all ewes were placed in concrete pens; fecal egg counts for the winter-bred group were obtained on alternate days. Pregnant and lactating ewes had significantly larger numbers (P < 0.01) of H contortus eggs than did the nonpregnant controls 1 week before and after lambing. Lactating, fall-bred ewes had significantly (P < 0.01) more adult worms in their abomasum through natural acquisition than the nonpregnant controls. In the second experiment, fall-bred and winter-bred helminth-free, pregnant (n = 4 and 8, respectively) and nonpregnant (n = 3 and 15, respectively) ewes were inoculated on 5 alternate days, beginning 70 days after breeding with 20,000 infective H contortus larvae. The ewes were maintained on concrete pens throughout pregnancy. Fecal egg counts were significantly (P < 0.05) greater in pregnant ewes, beginning 1 week before lambing until 1 week after lambing. Abomasums of lactating ewes from both lambing seasons yielded significantly (P < 0.01) more adult worms at necropsy than nonpregnant ewes. In the third experiment, ewes were ovariectomized (n = 15) or sham-operated (n = 9); half of the control ewes were bred. Beginning on day 70 of pregnancy, all ewes were inoculated orally with 20,000 infective H contortus larvae on 5 alternative days. Abomasums were removed from all ewes after lambing, and adult worms were recovered. Pregnant ewes and half of the ovariectomized ewes had significantly (P < 0.05) more worms than did the sham-operated ewes.