Influence of age on surfactant isolated from healthy horses maintained on pasture.

BACKGROUND: Surfactant alterations are described in horses after exercise, anesthesia, and prolonged transport, in horses with recurrent airway obstruction, and in neonatal foals. The effect of horse age or bronchoalveolar lavage fluid (BALF) sample characteristics on surfactant is unknown. OBJECTIVES: To evaluate surfactant phospholipid composition and function in healthy horses, and to investigate the influence of age and BALF sample characteristics on surfactant. ANIMALS: Seventeen healthy horses 6-25 years of age maintained on pasture year-round. METHODS: BALF was collected by standard procedures and was assessed for recovery volume, nucleated cell count (NCC), and cytology. Cell-free BALF was separated into crude surfactant pellet (CSP) and surfactant supernatant (Supe) by ultracentrifugation. Phospholipid and protein content were determined from both fractions. CSP phospholipid composition was analyzed by high-performance liquid chromatography with an evaporative light scatter detector. Surface tension of CSP was evaluated with a pulsating bubble surfactometer. Regression analysis was used to evaluate associations between age, BALF sample characteristics, and surfactant variables. RESULTS: Results and conclusions were derived from 15 horses. Increasing age was associated with decreased phospholipid content in CSP but not Supe. Age did not affect protein content of CSP or Supe, or surfactant phospholipid composition or function. Age-related surfactant changes were unaffected by BALF recovery percentage, NCC, and cytological profile. CONCLUSIONS AND CLINICAL IMPORTANCE: Older horses have decreased surfactant phospholipid content, which might be because of age-related pulmonary changes. Surfactant composition is unaffected by BALF sample characteristics at a BALF recovery percentage of at least 50%.

Ophthalmic examination findings in a colony of Screech owls (Megascops asio).

OBJECTIVE: To report ophthalmic findings in the Screech owl (Megascops asio). Sample population Twenty-three, apparently healthy adult captive Screech owls in Maryland. PROCEDURES: OU of all owls underwent complete ophthalmic examination. One randomly assigned eye of each bird was measured by phenol red thread tear test (PRT), and the other eye by Schirmer tear test (STT). TonoVet rebound tonometry and TonoPen-XL applanation tonometry were performed in each eye to measure IOP. Conjunctival swabs were cultured from one eye of 10 birds, corneal diameter was measured in OU of eight birds, and streak retinoscopy was performed on OU of seven birds. Ten birds were anesthetized, and A-scan ultrasonography using a 15-MHz probe was performed to obtain axial intraocular measurements. RESULTS: Ophthalmic abnormalities were noted in 24/46 (52%) of eyes. Median STT result was < or = 2 mm/min, ranging < or = 2-6 mm/min, and mean +/- SD PRT was 15 +/- 4.3 mm/15 s. Mean +/- SD IOP were 9 +/- 1.8 mmHg TonoVet-P, 14 +/- 2.4 mmHg TonoVet-D, and 11 +/- 1.9 mmHg TonoPen-XL. Coagulase negative staphylococcal organisms were cultured from all conjunctival swabs. Mean +/- SD corneal dimensions were 14.5 +/- 0.5 mm vertically and 15.25 +/- 0.5 mm horizontally. All refracted birds were within one diopter of emmetropia. Mean +/- SD axial distance from the cornea to the anterior lens capsule was 4.03 +/- 0.3 mm, from cornea to the posterior lens capsule was 10.8 +/- 0.5 mm, and from cornea to sclera was 20.33 +/- 0.6 mm. CONCLUSIONS: This study reports ophthalmic examination findings in Screech owls, and provide means and ranges for various ocular measurements. This is the first report of rebound tonometry and PRT in owls.

Curli production and genetic relationships among Escherichia coli from cases of bovine mastitis.

Curli are adhesive surface structures produced by some Escherichia coli and Salmonella strains that bind host proteins and activate inflammatory mediators. In this study, 61 E. coli isolates from 36 clinical cases of bovine mastitis were characterized using enterobacterial repetitive intergenic consensus-PCR and screened for their ability to produce curli. Effect of curli production on case recovery, based on a return to precase milk yield, was investigated for a subset of 43 isolates from 20 quarters of 19 cows. Thirty-five (57%) of 61 isolates were curli positive. Fifty-eight of the 61 isolates clustered into 2 clonal groups at 52% genetic similarity. Genetically diverse E. coli isolates were simultaneously cultured from individual cases. Twenty-three isolates from 13 cows were clustered in clonal group I, of which 5 cases (38%) were curli positive; 35 isolates from 22 cows were clustered in clonal group II, of which 15 cases (68%) were curli positive. No association was found between genetic similarity and phenotypic curli expression of isolates from cows with clinical E. coli mastitis cases. Phenotypic curli expression in isolates did not affect recovery of cows' milk yield to premastitis production levels.

Macrophage inhibitory factor-A3 derived from Mycobacterium avium serovar 2 inhibits candidacidal activity of murine peritoneal macrophages.

Macrophage inhibitory factor-A3 (MIF-A3), a fraction derived from Mycobacterium avium serovar 2 inhibited candidacidal activity in macrophages from C57BL/6, C57BL/10, C3H/HeJ and A/J strains of mice. Inhibition of candidacidal activity was demonstrated at MIF-A3 concentrations ranging from 100-400 micrograms/ml in macrophages without additional stimulators (exception C3H/HeJ macrophages) and in macrophages additionally stimulated with 200 U/ml interferon-gamma, 100 ng/ml phorbol myristate acetate and 0.4 ng/ml E. coli lipopolysaccharide from all mouse strains tested. The decreased candidacidal effect produced by MIF-A3 was dose-dependent and appeared greatest in macrophages treated with phorbol myristate acetate and lipopolysaccharide. This effect was neutralized by the addition of goat anti-MIF-A3 antiserum. Macrophages from the Bcgs mouse strains (C57BL/6 and C57Bl/100 were more sensitive to the effect(s) of MIF-A3 than macrophages from the Bcgr mouse strains (C3H/HeJ and A/J).

Protection of pigs by vaccination of pregnant sows against eastern equine encephalomyelitis virus.

Serum-virus neutralizing antibodies were detected in serum and colostrum of sows vaccinated during pregnancy with commercially available vaccines against eastern equine encephalomyelitis virus (EEEV), and antibodies were detected in serum from nearly all pigs from vaccinated sows following colostrum uptake. Serum-virus neutralizing antibody (SVN) test titers were measured in colostrum and pigs at the next farrowing, and additional vaccination of sows prior to the third farrowing led to elevated SVN titers in serum, colostrum and all pigs. Six pigs from vaccinated sows challenged at 8 to 9 days of age with 1 x 10(6) TCID50 EEEV did not develop the high temperatures or signs of central nervous system disease that 6 pigs from non-vaccinated sows developed. Virus was isolate from blood and oropharyngeal swabs from all pigs from non-vaccinated sows with blood virus titers as high as 9.3 x 10(4) TCID50, while only low levels of virus were detected in blood and oropharyngeal swabs from pigs from vaccinated sows. Virus was also isolated from tonsils collected at necropsy from 3 pigs from non-vaccinated and 1 pig from vaccinated sows. Vaccination of pregnant sows leads to development of maternal antibodies that are transmitted via colostrum to pigs and are protective against clinical EEEV related disease after experimental challenge with EEEV. In addition, vaccination prevents amplification of virus in infected pigs and could result in protection of animals and farm labor in the environment of infected pigs.

Antibody titers to pseudorabies virus in piglets immunized with gIII deleted pseudorabies vaccine in a pseudorabies infected herd.

The decrease in titer of PRV antibodies in serum was evaluated at 10, 37, 67, 109 and 173 days of age in 16 non-vaccinated pigs and 43 pigs vaccinated at 3, 67 and 80 days of age with a modified live TK/gIII gene deleted pseudorabies virus (PRV) vaccine. Serum samples were analyzed for antibodies to PRV by the serum-virus neutralization test (SN), a commercial competitive ELISA (CELISA), and the CELISA OMNIMARK PRV differential (OMD) diagnostic kit. At 10 days of age, all pigs had SN titers > or = 1:4 and were CELISA+/OMD+, indicating circulating antibodies to field strains of PRV. At 109 days, all non-vaccinated pigs had SN titers < 1:4. Forty-five percent of vaccinated pigs had SN titers > or = 1:4, 56% were CELISA positive and most were CELISA+/OMD-, indicating antibodies due to vaccination. At 24 weeks of age, all pigs had SN titers > or = 1:4 and were CELISA+/OMD+ due to exposure to field strains. Although circulating maternal antibodies interfere with the development of active immunity, vaccination at 3 days of age resulted in detectable antibodies by 67 days of age, and a limited immune response could be measured at 109 days of age.

Pathogenic and fecal Escherichia coil strains from turkeys in a commercial operation.

The biochemical phenotypes and antimicrobial susceptibility patterns of 105 clinical Escherichia coli isolates from flocks with colibacillosis in a turkey operation were compared with 1104 fecal E. coli isolates from 20 flocks in that operation. Clinical isolates and 194 fecal isolates with biochemical phenotypes or minimum inhibitory concentrations for gentamicin and sulfamethoxazole similar to clinical isolates were tested for somatic antigens and the potential virulence genes hylE, iss, tsh, and K1. The predominant biochemical phenotype of clinical isolates contained 21 isolates including 14 isolates belonging to serogroup 078 with barely detectable beta-D-glucuronidase activity. Thirty-five fecal isolates had biochemical phenotypes matching common phenotypes of clinical isolates. Sixty-six (63%) clinical isolates exhibited intermediate susceptibility or resistance to gentamicin and sulfamethoxazole compared with 265 (24%) fecal isolates (P < 0.001). Seventy-seven clinical isolates reacted with O-antisera, of which 51 (66%) belonged to the following serogroups: O1, O2, O8, O25, O78, O114, and O119. In comparison, 8 of 35 (23%) fecal isolates subtyped on the basis of biochemical phenotype belonged to these serogroups and four of 167 (2%) fecal isolates subtyped on the basis of their antimicrobial resistance patterns belonged to these serogroups. Iss, K1, and tsh genes were detected more often among clinical isolates than these fecal isolates (P < 0.05). In summary, a small subgroup of E. coli strains caused most colibacillosis infections in this operation. These strains existed at low concentration in normal fecal flora of healthy turkeys in intensively raised flocks. The data suggest that colibacillosis in turkey operations may be due to endogenous infections caused by specialized pathogens.

Exposure of swine to Trichinella spiralis antigen as determined by consecutive ELISAs and western blot.

Exposure of swine to Trichinella spiralis was evaluated using a combination of 3 consecutive enzyme-linked immunosorbent assays (ELISAs) based on larval T. spiralis excretory-secretory antigen as screening test and western blot analysis as confirmatory test. Ninety-three of 32,693 domestic swine sera collected in Georgia over a 5-yr period contained antibodies specific to T. spiralis (prevalence of exposure = 0.28%). The highest prevalence (0.52%) of exposure to T. spiralis was in samples from stockyards and salebarns. Prevalence of exposure in samples from cull sows from 1 slaughter house was 0.38% compared with 0.17% in samples obtained from farms. Pepsin-HCl digestion of diaphragms from 49 swine from 6 seropositive farms revealed 0.01 larvae/g in 4 swine from 3 farms. Determination of T. spiralis infection status of farms appears to be accurately determined with this combination of exploratory ELISAs and confirmatory western blot analysis.

Ataxia and paresis with equine herpesvirus type 1 infection in a herd of riding school horses.

An outbreak of neurologic disease associated with serologic evidence of equine herpesvirus type 1 (EHV-1) infection occurred in a herd of 46 riding school horses. Ataxia and paresis were observed in 14 geldings and 5 barren mares. Eight affected horses had distal limb edema, 1 horse had a head tilt, and 3 others had urinary incontinence. Other clinical signs included fever, depression, and inappetance in 30 horses. Seven horses with neurologic signs were treated with acyclovir. Serum neutralizing antibody titers against EHV-1 increased 4-fold between acute and convalescent samples or exceeded 1:256 in 19 of 44 horses, confirming recent infection. A significantly greater proportion of horses that seroconverted were mares (P = .014). Of the 19 horses exhibiting ataxia and paresis, 17 made a complete recovery, 1 made a partial recovery, and 1 was euthanized.

Effects of feeding supplemental fat to beef cows on cold tolerance in newborn calves.

Our objectives were to examine the effects of added fat in late-gestation cow diets on neonatal response to cold. In Exp. 1, pregnant fall-calving heifers received control (n = 5), safflower seed (n = 5), or whole cottonseed (n = 5) diets. The hay-based, isonitrogenous, and isocaloric diets, fed for 47 d prepartum, contained 1.5, 4.0, and 5.0% fat for control, safflower, and whole cottonseed diets, respectively. At calving, calf BW and vigor score, as well as fat, lactose, and IgG in colostrum were not affected (P > 0.30) by diet. Heifers fed the safflower diet tended to have greater colostral solids (P < 0.10) than heifers fed the control or whole cottonseed diets. At 6.5 h of age, calves were placed in a 5 degrees C cold room for 90 min. Calf vigor, shivering, body temperature, and blood samples were taken every 15 min. During cold stress, calf body temperature decreased 0.7 degrees C (P < 0.03). Across all diets, shivering and serum glucose concentrations increased (P < 0.05), whereas calf vigor and cortisol concentrations decreased (P < 0.02) during cold exposure. In Exp. 2, pregnant spring-calving cows (n = 98) received a control (n = 47) or whole cottonseed (n = 51) supplement. Hay-based diets fed for 68 d prepartum contained 2.0 and 5.0% fat for control and whole cottonseed diets, respectively. Calf BW, vigor, shivering, dystocia score, time to stand, time to nurse, serum glucose concentrations, and serum IgG were not affected (P > 0.50) by diet. Between 30 and 180 min, body temperature of calves from dams fed the whole cottonseed supplement decreased (P < 0.05) more than calves from dams fed the control supplement. Serum glucose concentrations in calves were not affected by diet (P > 0.30). Serum cortisol concentrations tended (P < 0.09) to be greater for calves from dams fed whole cottonseed than control calves. When ambient temperature was < 6 degrees C, calves born to dams fed whole cottonseed had greater (P < 0.05) BW, tended (P < 0.1) to stand earlier, and had greater serum IgG concentrations. We conclude that calves from dams fed high-fat diets containing safflower or whole cottonseed respond similarly to cold stress, but these responses may not be consistent with greater cold resistance. In addition, high-fat dietary supplementation of late-gestation cows may only be beneficial during calving seasons with prolonged cold weather.

Modulation of function of bovine polymorphonuclear leukocytes and lymphocytes by high temperature in vitro and in vivo.

Function of polymorphonuclear leukocytes (PMNL) and proliferation of lymphocytes after stimulation with mitogens were evaluated in vitro at incubation temperatures of 38.5 and 42 C, and after in vivo heat stress of lactating Holstein cows. Cytochrome-c reduction and random migration of PMNL were reduced when cells were preincubated or incubated at 42 C, but high incubation temperature had little or no effect on phagocytosis and killing of Escherichia coli. Proliferation of lymphocytes was reduced when cells were incubated for 60 hours at 42 C after stimulation with phytohemagglutinin, pokeweed mitogen, or concanavalin A. After stimulation with phytohemagglutinin, lymphocytes were most sensitive to high temperature during the first 24 hours of the 60-hour culture period. High incubation temperature had little effect on viability of cells. In vivo heat stress had no significant effect on responses of PMNL in vitro, but the decrease in proliferation of lymphocytes in vitro at high temperature was less when cells were obtained from heat-stressed cows. Total leukocyte counts in blood and somatic cell counts in milk were higher in heat-stressed cows. Results indicate that: exposure to high temperature in vitro can depress responses of PMNL and lymphocytes; apparent adaptive mechanisms induced by in vivo heat stress provide protection from effects of high temperature seen in vitro; and evidence could not be found to support the hypothesis that reduction in immune function is the basis for increases in the incidence of mastitis during the summer.

Mycoplasmal mastitis in a dairy herd.

In October 1985, mycoplasmas were isolated from bulk tank milk samples in a large Florida dairy (greater than 1,400 lactating cows). At that time, measures to isolate and control the spread of infection were instituted. In an initial screening test, Mycoplasma bovis was isolated from 21 of 153 milking string samples (milk from all quarters of 10 cows/string). Composite quarter milk samples from all quarters of every individual lactating cow in the herd were obtained for culture in November 1985 and December 1985. In October, 88 of 1,535 (5.7%) cows were identified as Mycoplasma-positive. An additional 31 Mycoplasma-infected cows were identified in December. The dairy elected to maintain the infected cows in a separate Mycoplasma-positive subherd, which would be milked at the end of each milking session. Seven additional Mycoplasma-positive cows were identified at initiation of lactation. All newly identified infected cows were transferred to the Mycoplasma-positive subherd. After segregation of Mycoplasma-positive cows, bulk tank milk samples obtained routinely from the main herd remained culture negative throughout the study. From February 1986 to October 1986, quarter milk samples were obtained monthly from cows in the Mycoplasma-positive subherd. Any cow that developed clinical mastitis or substantial decrease in milk production was, at the discretion of the herdsman, culled. Of the 126 cows in the subherd, 22 (17.5%) were culled for mastitis, 35 (27.8%) were culled for low production, and 9 (7.1%) were culled for other reasons. Of the remaining 60 cows, 16 (12.7% of the 126 cows) were Mycoplasma-positive on the basis of results from one or more samples obtained after February 1986.(ABSTRACT TRUNCATED AT 250 WORDS)

Eastern equine encephalomyelitis virus infection in swine.

In 1 of 2 outbreaks of eastern equine encephalomyelitis virus (EEEV) infection in swine, 280 of 350 pigs died. Histopathologic findings in the brain were typical of EEEV infection. In addition, multifocal necrosis and inflammation were seen in the myocardium. Follow-up investigation in 1 of the herds revealed antibody response to EEEV in surviving pigs and in adult swine. Growth retardation was noticed in surviving pigs. Histologic examination revealed mild lesions in the brain of the survivors.

Adiposity, plasma insulin, leptin, lipids, and oxidative stress in mature light breed horses.

BACKGROUND: Increased blood insulin levels are associated with an increased risk of pasture-associated laminitis in equids. OBJECTIVE: To determine the relationship between plasma insulin, leptin, and lipid levels, and measures of oxidative stress with adiposity in mature light breed horses. ANIMALS: 300 randomly selected light breed horses, aged 4-20 years. METHODS: A random sample of horses (140 mares, 151 geldings, and 9 stallions) was drawn from the VMRCVM Equine Field Service practice client list. Evaluations occurred June 15 - August 15, 2006, with all sampling performed between 0600 and 1200 hours. Concentrate feed was withheld for at least 10 hours before sampling. Plasma was analyzed for insulin, glucose, leptin, triglycerides, nonesterified fatty acids, and measures of oxidative stress. Body condition score was determined as the average of 2 independent investigators. RESULTS: Overconditioned and obese horses had higher plasma insulin (P < .001) and leptin (P < .01) levels than optimally conditioned horses. Obese horses had higher triglyceride levels (P = .006) and lower red blood cell gluthathione peroxidase activities (P = .001) than optimally conditioned horses. CONCLUSIONS AND CLINICAL IMPORTANCE: Maintaining horses at a BCS <7 might be important for decreasing the risk of pasture-associated laminitis.

Prevalence of overconditioning in mature horses in southwest Virginia during the summer.

BACKGROUND: The prevalence of obesity in horses in the eastern United States is not well documented. OBJECTIVE: To determine body condition and risk factors for obesity in horses in Southwest Virginia during summer. ANIMALS: A sample of 300 mature (4-20 years old), light breed horses (140 mares, 151 geldings, and 9 stallions) from the VMRCVM Equine Field Service practice equine database. The horses were from 114 farms and 138 owners. METHODS: Horses were evaluated over a 60-day period in this cross-sectional, prospective study. A questionnaire was completed for each horse. Body condition score (BCS) was assigned using a scale of 1 (emaciated) to 9 (obese) by 2 independent scorers. Morphometric measurements included average neck circumference (ANC), girth, body length, and height at the withers. Horses were categorized based on BCS as underconditioned (BCS < 4), optimal condition (BCS 4-6), overconditioned (BCS 7), and obese condition (BCS 8-9). RESULTS: Five horses (1.7%) were underconditioned, 142 horses (47.3%) were optimally conditioned, 97 horses (32.3%) were overconditioned, and 56 (18.7%) were obese. Estimated body weight (EBW) (r = 0.14, P = .015), body mass index (BMI) (r = 0.46, P < .001), and neck circumference to height ratio (NCHR) (r = 0.50, P = .001) increased with increasing BCS. CONCLUSIONS AND CLINICAL IMPORTANCE: The prevalence of overconditioned and obese horses in this population was higher than reported in previous studies and indicates that obesity might be an emerging problem in horses.

Effects of porcine circovirus type 2 (PCV2) maternal antibodies on experimental infection of piglets with PCV2.

To determine the effects of porcine circovirus type 2 (PCV2) maternal antibodies on and response to experimental PCV2 infection, 24 piglets were divided into four groups on the basis of the enzyme-linked immunosorbent assay titers of PCV2 maternal antibodies: group A (n = 6; sample/positive [S/P] ratio, <0.2), group B (n = 5; S/P ratio, >0.2 to <0.5), and groups C (n = 8) and D (n = 5) (S/P ratio, >0.5). Piglets in groups A, B, and C were inoculated with PCV2 at day 0 and challenged with PCV2 at day 42. Group D piglets were not exposed to PCV2 at day 0 but were challenged at day 42. Before challenge, seroconversion to PCV2 antibodies occurred in five of six group A piglets, and the antibody level rose above the cutoff level in one of five group B piglets. Viremia was detected in five of six, four of five, and two of eight pigs in groups A, B, and C, respectively. After challenge, PCV2 DNA was detectable from 7 to 21 days postchallenge in the sera from six of six, four of five, three of eight, and five of five pigs in groups A, B, C, and D, respectively. The results indicated that protection against PCV2 infection conferred by maternal antibodies is titer dependent: higher titers are generally protective, but low titers are not.

Systematic pathogenesis and replication of avian hepatitis E virus in specific-pathogen-free adult chickens.

Hepatitis E virus (HEV) is an important human pathogen. Due to the lack of a cell culture system and a practical animal model for HEV, little is known about its pathogenesis and replication. The discovery of a strain of HEV in chickens, designated avian HEV, prompted us to evaluate chickens as a model for the study of HEV. Eighty-five 60-week-old specific-pathogen-free chickens were randomly divided into three groups. Group 1 chickens (n=28) were each inoculated with 5 x 10(4.5) 50% chicken infectious doses of avian HEV by the oronasal route, group 2 chickens (n=29) were each inoculated with the same dose by the intravenous (i.v.) route, and group 3 chickens (n=28) were not inoculated and were used as controls. Two chickens from each group were necropsied at 1, 3, 5, 7, 10, 13, 16, 20, 24, 28, 35, and 42 days postinoculation (dpi), and the remaining chickens were necropsied at 56 dpi. Serum, fecal, and various tissue samples, including liver and spleen samples, were collected at each necropsy for pathological and virological testing. By 21 dpi, all oronasally and i.v. inoculated chickens had seroconverted. Fecal virus shedding was detected variably from 1 to 20 dpi for the i.v. group and from 10 to 56 dpi for the oronasal group. Avian HEV RNA was detected in serum, bile, and liver samples from both i.v. and oronasally inoculated chickens. Gross liver lesions, characterized by subcapsular hemorrhages or enlargement of the right intermediate lobe, were observed in 7 of 28 oronasally and 7 of 29 i.v. inoculated chickens. Microscopic liver lesions were mainly lymphocytic periphlebitis and phlebitis. The lesion scores were higher for oronasal (P=0.0008) and i.v. (P=0.0029) group birds than for control birds. Slight elevations of the plasma liver enzyme lactate dehydrogenase were observed in infected chickens. The results indicated that chickens are a useful model for studying HEV replication and pathogenesis. This is the first report of HEV transmission via its natural route in a homologous animal model.

Interactions of heat stress and bovine somatotropin affecting physiology and immunology of lactating cows.

During summer, 34 cows received daily injections of placebo or 25 mg of bST and were placed in a thermoregulated or a heat stress environment. Heat stress increased rectal temperatures, respiration rates, and plasma cortisol concentrations and decreased milk yield. Four of 9 bST-treated cows and none of 8 control cows became atactic on the 1st d of heat stress. When exposed to heat stress, cows treated with bST experienced higher rectal temperatures throughout the trials than cows treated with placebo. Nonetheless, bST increased milk yields in both environments. The major effect of heat stress on immune function was decreased migration of leukocytes to the mammary gland after chemotactic challenge. This effect of heat stress was not altered by bST. In summary, hyperthermia induced by heat stress and associated changes were greater for cows treated with bST. Detected effects of heat stress on the immune system were few and were not alleviated by bST. Use of bST during summer in subtropical climate zones requires careful management to avoid overexposure of bST-treated cows to heat stress.