Experiments were conducted to establish a persistent Salmonella typhimurium infection in convalescent swine, and to determine rate of shedding and distribution of the organism in internal organs. Naturally farrowed Salmonella-free pigs (n = 37) were orally exposed to S typhimurium when 7 to 8 weeks old. Fecal samples, tonsillar scrapings, and rectal swab specimens were examined bacteriologically for S typhimurium at weekly intervals after exposure until necropsy (maximum of 28 weeks after exposure). Necropsies of 1 to 4 randomly selected pigs were conducted at 2, 4, and 7 days and at 2, 4, 6, 8, 12, 16, 20, 24, and 28 weeks after exposure. The following internal organs were examined bacteriologically for S typhimurium: liver, spleen, kidney, gallbladder, heart, lung, and stomach; segments of the intestinal tract with corresponding lymph nodes; lymph nodes from lymphocenters of the head and neck, thoracic and abdominal cavities, pelvic wall, and thoracic and pelvic limbs. Fecal samples were 83 to 100% culture-positive up to postexposure (PE) week 22, then varied from 14 to 67% positive until PE week 28. At least 60% of tonsillar swab specimens and 50% of rectal swab specimens were culture-positive up to PE week 20, after which they varied from 0 to 70% positive until PE week 28. At necropsy, S typhimurium was recovered most freguently from tonsils (93.5% positive), followed by segments of the intestinal tract from caudal portion of jejunum to rectum (71% recovery from cecum), and mandibular (54.8%) and ileocolic (45.2%) lymph nodes. The organism generally did not persist beyond PE week 2 in other lymph nodes of the head and neck, lymph nodes of the abdominal wall, thoracic cavity, or limbs, or in heart, liver, or spleen. The gallbladder, kidney, and lungs of all pigs were culture-negative.

Heifers were inoculated IV with 1 of 4 modified-live bovine herpesvirus-1 vaccinal strains against infectious bovine rhinotracheitis (2 heifers/strain) on postbreeding day (PBD) 14. The effect of infection on fertility was monitored by plasma progesterone assay at 1- to 3-day intervals from the time of virus exposure until PBD 60. Infertility was detected in 4 of 8 inoculated heifers. In 2 heifers, progestrone concentrations decreased to values indicative of estrus within 10 days after inoculation (PBD 24). The 2 other heifers had evidence of embryonic death on PBD 40 and 42. Two control heifers inoculated with culture medium from noninfected cells maintained their pregnancies.

Twenty-nine healthy 17- to 29-day-old unweaned Isaeli-Friesian male calves were each given a single IV or IM injection of 10 or 20 mg of moxalactam disodium/kg of body weight. Serum concentrations were measured serially during a 12-hour period. Serum concentration vs time profiles were analyzed by use of linear least-squares regression analysis and the statistical moment theory. The elimination half-lives after IV administration were 143.7 +/- 30.2 minutes and 155.5 +/- 10.5 minutes (harmonic mean +/ SD) at dosages of 10 and 20 mg of moxalactam/kg of body weight, respectively. Corresponding mean residence time values were 153.1 +/- 26.8 minutes and 169.9 +/- 19.3 minutes (arithmetic mean +/- SD). Mean residence time values after IM administration were 200.4 +/- 17.5 minutes and 198.4 +/- 19.9 minutes at dosages of 10 and 20 mg/kg, respectively. The volumes of distribution at steady state were 0.285 +/- 0.073 L/kg and 0.313 +/- 0.020 L/kg and total body clearance values were 1.96 +/- 0.69 ml/min/kg and 1.86 +/- 0.18 ml/min/kg after administration of dosages of 10 and 20 mg/kg, respectively. Moxalactam was rapidly absorbed from the IM injection site and peak serum concentrations occurred at 1 hour. The estimated bioavailability ranged from 69.8 to 79.1%. The amount of serum protein binding was 53.4, 55.0, and 61.5% when a concentration of moxalactam was at 50, 10, and 2 micrograms/ml respectively. The minimal inhibitory concentrations of moxalactam ranged from 0.01 to 0.2 micrograms/ml against Salmonella and Escherichia coli strains and from 0.005 to 6.25 micrograms/ml against Pasteurella multocida strains.

Sixteen 7-week-old Holstein male calves were inoculated with sporulated oocysts of Eimeria zuernii. Four calves (controls) were euthanatized and necropsied at 14 and 20 days after inoculation (DAI). Two calves were treated with 20 mg of dexamethasone (IM) on 13, 14, and 15 DAI and euthanatized and necropsied 17 DAI and 2 calves were given similar treatments and necropsied 20 DAI. The 8 other calves were euthanatized and necropsied 20 DAI. Two were started on the anticoccidial drug decoquinate in feed 13 DAI; 2 others were given decoquinated on the same schedule plus dexamethasone on 13, 14, and 15 DAI. Two calves were given the antibiotic narasin in feed beginning 13 DAI and 2 calves were given parasin on the same schedule plus dexamethasone on 13, 14, and 15 DAI. All calves, except 2 controls necropsied 14 DAI and 4 calves given decoquinate, discharged moderate-to-large numbers of oocysts in feces and had moderate-to-severe changes in fecal consistency. Histologic examintions revealed large numbers of endogenous stages in tissues of calves treated or not treated with dexamethasone. Few endogenous stages were observed in tissues from calves that were given decoquinate or decoquinate plus dexamethasone. Calves given narasin or narasin plus dexamethasone had moderate-to-large numbers of endogenous stages in the tissues.

The role of bile salt in biliary lipid excretion was studied in 3 healthy ponies with chronic external biliary fistulas. After endogenous bile salt pool depletion, micelle-forming taurocholate or taurochenodeoxycholate was infused to replace excreted bile salt. Enterohepatic circulations were held open (total biliary diversion) throughout each study. Results indicated that biliary lipid excretion in ponies (113 +/- 21 nmol/in/kg of body weight) is approximately 10 times less than that reported in rodents. Although the lipid composition (4.4% cholesterol, 5.6% phospholipid, and 90% bile salt) was within the predicted range for a single phase of micellar (or vesicular) liquid in solution, it was supersaturated with cholesterol because of low absolute concentrations of bile salt and phospholipid. Ponies, like guinea pigs, were determined to have a high bile salt-independent secretion of biliary lipid with little (or no) coupling to endogenous bile salt output. However, bile salt excretion induced by higher taurocholate infusion rates (ie, those greater than the physiologic range of 61 to 125 nmol/min/kg) was positively correlated with an increase in biliary phospholipid excretion, but not cholesterol excretion, thus indicating that a threshold intracellular bile salt concentration may be associated with enchanced biliary phospholipid excretion in ponies. The apparent cholerectic effects of endogenous bile salts, taurocholate, and taurochenodenoxycholate (that is, the increment in bile flow per increment in bile salt recovered) were greater in ponies than reported for any other mammal.

The effects of prolonged plasmapheresis of cattle on total and antigen-specific immunoglobulin production were evaluated. Five adult cows were hyperimmunized by repeated IV administration of live, logarithmic-phase Pasteurella haemolytica A1 organisms. Three of the cows underwent plasmapheresis daily for 3 weeks. From 2 cows, serum was only obtained periodically. Anti-P haemolytica antibody was assayed by indirect hemagglutination and a kinetic-augmented, antigen-capture ELISA for capsular polysaccharide and lipopolysaccharide/outer membrane protein antigens. Total serum immunoglobulin concentration was determined for IgM, IgG1, and IgG2 by primary radial immunodiffusion. Anti-P haemolytica A1 activity increased rapidly after immunization. After beginning plasmapheresis, the antigen-specific antibody activities remained nearly constant. In general, antilipopolysaccharide/outer membrane protein activity (in terms of concentration) was higher than anti-capsular polysaccharide activity and was not affected as much by the plasmapheresis. Total serum Ig concentration decreased transiently by a small amount after beginning plasmapheresis.

Liposomes with entrapped gentamicin were used to treat mice with infection attributable to Brucella melitensis. Liposomes bearing positive charge and formed by egg yolk lecithin, cholesterol, and stearylamine were effective in the elimination of B melitensis residing in liver and spleen. Negatively charged liposomes, formed by egg yolk lecithin, cholesterol, and dicetyl phosphate were also effective in suppression of the infection in liver, but were less so in suppression of the infection in the spleen. Free gentamicin was less effective than the encapsulated antibiotic. At 20 hours after administration of gentamicin encapsulated in liposomes, the gentamicin concentrations in liver and spleen were similar, regardless of the charge of the liposomes--neutral, positive, or negative. However, positively charged liposomes were more efficient than were other liposome types for the treatment of brucellosis caused by B melitensis.

The detection of volatile fatty acids (VFA) by gas chromatography of 85 purulent specimens from abscesses or pyogenic infections in cats, dogs, rodents, and ruminants was compared with the results of bacteriologic culturing, and proved to be a rapid means of presumptively diagnosing anaerobic infections. Of 83 bacteriologically positive specimens, 52 (61%) yielded obligate anaerobes and in 50 specimens, 1 or more VFA (butyric acid, isobutyric acid, valeric acid, isovaleric acid, caproic acid, or isocaproic acid) was detected. Forty-six specimens were positive for culturing of anaerobes and for detection of 1 or more of these VFA. By contrast, pus from infections caused by (facultative) aerobic microorganisms contained no VFA or only acetic and/or propionic acid.

Four groups of 8 horses each had 1 midcarpal joint injected with 33 colony-forming units (CFU) of viable Staphylococcus aureus plus: 1 ml of saline solution (group 1, control), 250 mg of polysulfated glycosaminoglycan (PSGAG, group 2), 100 mg of methylprednisolone acetate (group 3), or 20 mg of sodium hyaulronate (group 4). Horses were euthanatized, and samples were obtained on the basis of clinical signs of septic arthritis that were nonresponsive to phenylbutazone administration. One group-1 horse, all 8 group-2 horses, 3 group-3 horses, and 4 group-horses 4 were culture-positive for S aureus and had clinical signs, results of synovial fluid analysis, and histopathologic findings that were consistent with sepsis. The addition of 250 mg of PSGAG increased the development of sepsis significantly (P = 0.001), compared with results in control horses. Differences in the development of sepsis between horses injected with methylprednisolone acetate or sodium hyaluronate and control horses were not significant.

Serum concentrations of iodine were determined after cattle were given ethylenediamine dihydriodide (EDDI) orally at dosages ranging from 0.0 (placebo) to 0.77 mg/kg of body weight/day. The serum iodine concentration was correlated with the dosage of EDDI. A rate of 0.11 mg EDDI/kg/day was correlated with serum iodine concentrations (20 to 80 micrograms/dl) previously found to be effective in preventing foot rot in cattle. A linear dose-response curve that was generated could be helpful in predicting dosage of EDDI if the serum iodine concentration is known.