Selenium toxicity in breeding ring-necked pheasants (Phasianus colchicus).

A flock of breeding ring-necked pheasants received feed with a high selenium content. Within 4 days of eating the toxic feed, the rate of egg production began to decrease, and bird aggression increased. Approximately 12% of the hens died within a week. Necropsy of the hens revealed colorless fluid around the heart and a friable, but otherwise normal, liver. The rapid onset of the problem and signs noted at necropsy suggested toxicosis. Based on analysis, the feed contained 9.3 ppm of selenium. Selenium toxicity was consistent with the histologic diagnosis of degenerative cardiomyopathy, vacuolar degeneration of hepatocytes, and centrilobular hepatic necrosis. After 8 days, the toxic feed was removed and replaced with fresh feed. Egg production, which had dropped to 50%, returned to normal within 10 days of feed replacement. Hatchability of eggs laid from days 8 to 14 after delivery of the toxic feed was 35%. Approximately 10% of the chicks that hatched had deformed beaks and abnormal eyes. Many of the chicks that died in the shell had deformities, bringing the total to more than 50% of all embryos that developed. The selenium content of eggs that had no embryonic development was 2.05 ppm. Hatchability of eggs laid from days 21 to 28 after the toxic feed was delivered was almost 80%, which was slightly lower than normal. The selenium content of these eggs was 0.30 ppm. These results show the rapid onset and correction of selenium toxicity and suggest that specific embryologic defects are diagnostic for selenium toxicity.

Toxoplasma gondii isolates from free-ranging chickens from the United States.

Prevalence of Toxoplasma gondii infection in chickens is a good indicator of the strains prevalent in their environment because they feed from ground. The prevalence of T. gondii was determined in 118 free-range chickens from 14 counties in Ohio and in 11 chickens from a pig farm in Massachusetts. Toxoplasma gondii antibodies (> or = 1: 5) were found using the modified agglutination test (MAT) in 20 of 118 chickens from Ohio. Viable T. gondii was recovered from 11 of 20 seropositive chickens by bioassay of their hearts and brains into mice. The parasite was not isolated from tissues of 63 seronegative (< or = 1:5) chickens by bioassay in cats. Hearts, brains, and muscles from legs and breast of the 11 chickens from the pig farm in Massachusetts were fed each to a T. gondii-negative cat. Eight cats fed chicken tissues shed oocysts; the 3 cats that did not shed oocysts were fed tissues of chickens with MAT titers of 1:5 or less. Tachyzoites of 19 isolates of T. gondii from Ohio and Massachusetts were considered avirulent for mice. Of 19 isolates genotyped, 5 isolates were type II and 14 were type III; mixed types and type I isolates were not found.

Prevalence of Salmonella, Campylobacter, and Escherichia coli on ostrich carcasses and the susceptibility of ostrich-origin E. coli isolates to various antibiotics.

There has been limited research on the prevalence of foodborne pathogens such as Escherichia coli O157:H7, Salmonella, and Campylobacter on ostrich carcasses. Likewise, few studies have been done in ostriches to determine the antimicrobial susceptibilities of common bacteria, like E. coli. In this study, ostrich carcasses were sampled from eight slaughterhouses in Ohio and one in Indiana. Although results demonstrated no E. coli O157:H7 from the carcasses sampled, 91% (116/128) of the dressed carcasses sampled had E. coli present. One carcass sample (1/152) was positive for Salmonella. Campylobacter were detected in 10% (19/191) of the carcasses. Antimicrobial susceptibility testing on 93 carcass E. coli isolates showed resistance to erythromycin (99%), neomycin (65%), netilmicin (2%), oxytetracycline (22%), streptomycin (2%), and trimethoprim (3%). All isolates were resistant to bacitracin, lincomycin, penicillin, and vancomycin. For the large intestinal sampling, 149 of the 217 (69%) samples had E. coli present. Fifty of these 149 samples had E. coli levels ranging from 10(2) to 10(5) colony-forming units/g feces. Campylobacter were isolated from 6 of 201 (3%) samples. No Salmonella colony was detected. Antimicrobial susceptibility testing on 131 intestinal E. coli isolates showed resistance to erythromycin (98%), neomycin (66%), netilmicin (34%), oxytetracycline (34%), streptomycin (40%), and trimethoprim (13%). All isolates were resistant to bacitracin, lincomycin, penicillin, and vancomycin.

Prevalence, antigenic specificity, and bactericidal activity of poultry anti-Campylobacter maternal antibodies.

Poultry are considered the major reservoir for Campylobacter jejuni, a leading bacterial cause of human food-borne diarrhea. To understand the ecology of C. jejuni and develop strategies to control C. jejuni infection in the animal reservoir, we initiated studies to examine the potential role of anti-Campylobacter maternal antibodies in protecting young broiler chickens from infection by C. jejuni. Using an enzyme-linked immunosorbent assay (ELISA), the prevalence of anti-C. jejuni antibodies in breeder chickens, egg yolks, and broilers from multiple flocks of different farms were examined. High levels of antibodies to the organism were detected in serum samples of breeder chickens and in egg yolk contents. To determine the dynamics of anti-Campylobacter maternal antibody transferred from yolks to hatchlings, serum samples collected from five broiler flocks at weekly intervals from 1 to 28 or 42 days of age were also examined by ELISA. Sera from the 1-day and 7-day-old chicks showed high titers of antibodies to C. jejuni. Thereafter, antibody titers decreased substantially and were not detected during the third and fourth weeks of age. The disappearance of anti-Campylobacter maternal antibodies during 3 to 4 weeks of age coincides with the appearance of C. jejuni infections observed in many broiler chicken flocks. As shown by immunoblotting, the maternally derived antibodies recognized multiple membrane proteins of C. jejuni ranging from 19 to 107 kDa. Moreover, in vitro serum bactericidal assays showed that anti-Campylobacter maternal antibodies were active in antibody-dependent complement-mediated killing of C. jejuni. Together, these results highlight the widespread presence of functional anti-Campylobacter antibodies in the poultry production system and provide a strong rationale for further investigation of the potential role of anti-C. jejuni maternal antibodies in protecting young chickens from infection by C. jejuni.

Presence and recovery of Ascaridia dissimilis ova on the external shell surface of turkey eggs.

Ascaridia dissimilis, a roundworm in turkeys, has been noted with increased frequency in commercial turkeys. Because infected turkeys can shed A. dissimilis ova in their feces, the potential exists for the external surface of turkey eggshells to be contaminated with A. dissimilis ova. The objectives of this study were to determine the presence of and recover A. dissimilis ova on the external surface of the turkey egg. In Experiment 1, turkey eggs were collected from naturally infected flocks, and eggs were processed by a sodium hydroxide procedure to recover any A. dissimilis ova on the external egg surface. In Experiment 2, the external surface of the turkey eggs was inoculated with 116 A. dissimilis ova/g feces, and eggshells were sampled every 3 days until 28 days of incubation to assess the recovery of A. dissimilis ova from the eggshell. In Experiment 1, of the 36 eggs examined from a flock naturally infected with A. dissimilis, one egg had an A. dissimilis ovum on its external eggshell surface. Experiment 2 demonstrated that A. dissimilis ova can be recovered from the external egg surface after a 28-day incubation period in the incubator. Ova recovery declined from an average of 62 A. dissimilis ova/turkey egg at day 2 of incubation to an average of 3 A. dissimilis ova/turkey egg at day 28 of incubation.

Fecal shedding and antimicrobial susceptibility of selected bacterial pathogens and a survey of intestinal parasites in free-living waterfowl.

Free-living waterfowl residing in metropolitan parks in central Ohio were surveyed for the fecal shedding and antimicrobial susceptibility patterns of Campylobacter jejuni, Escherichia coli, Salmonella spp., and Pasteurella multocida. In addition, a survey for intestinal parasites was also conducted in these same waterfowl to determine parasite burdens in free-living waterfowl. Prevalences of 67%, 50%, and 0.2% of E. coli, C. jejuni, and Salmonella spp., respectively, were observed for all waterfowl species. Pasteurella multocida was not isolated from the sampled population. Salmonella java was isolated from one mallard duck. Statistically, there was a significantly higher E. coli isolation rate for mallard ducks than for Canada geese, but no difference was observed for C. jejuni isolation rates between waterfowl species. Antimicrobial susceptibility testing was conducted via the disk diffusion method and multidrug resistance was exhibited for penicillin G, lincomycin, vancomycin, erythromycin, and bacitracin. In addition, the prevalence of endoparasites in these sampled waterfowl ranged from 5% to 66%. Protozoan oocysts were most prevalent followed by nematode ova. No trematode or cestode ovum was recovered from this sampled population.

Prevalence and characteristics of Pasteurella multocida in commercial turkeys.

The oropharyngeal regions of 680 meat turkeys and 55 breeder turkeys from nine outbreak farms, three history-outbreak farms, and 19 nonoutbreak farms in Ohio, Indiana, and Pennsylvania were cultured to determine the prevalence of Pasteurella multocida in turkeys. Pasteurella multocida was recovered from 32 out of 105 turkeys belonging to outbreak farms. Pasteurella multocida was not recovered from either history-outbreak or nonoutbreak farms. Characterization via capsular and somatic serotyping, biotyping, restriction endonuclease analysis, and antimicrobial susceptibility testing was performed on all recovered P. multocida isolates. Pasteurella multocida serotype A:1 and somatic serotype 1 with an un-typable capsular serogroup (UT:1) were the most common serogroups found. All isolates belonged to biotype P. multocida ssp. multocida. EcoRI, HpaII, and HindIII restriction enzyme digestions identified three, five, and five restriction fragment length polymorphism profiles, respectively. A majority of the isolates were susceptible to amikacin, ampicillin, ceftiofur, cephalothin, enrofloxacin, florfenicol, gentamicin, neomycin, novobiocin, oxacillin with 2% NaCl, sarafloxacin, tilmicosin, and trimethoprim with sulphadiazine and resistant to clindamicin, penicillin, tiamulin, and tylosin.

Characterization of nine Pasteurella multocida isolates from avian cholera outbreaks in Indonesia.

Avian cholera outbreaks have been identified in Indonesia in recent years. Despite vaccination programs, outbreaks continue to occur. To date, there has been a lack of information on the characteristics of Pasteurella multocida isolates involved in these outbreaks. Hence, the objective of this study was to characterize Indonesian P. multocida isolates in poultry. During 1998-99, 20 field outbreaks were reported in Indonesia. Nine isolates of P. multocida were recovered from these field outbreaks. The isolates were compared with four vaccine strains that were used in Indonesia and designated PM-V1, PM-V2, PM-V3, and PM-V4. The isolates were characterized by biotype, capsular type, somatic serotype, restriction endonuclease analysis, plasmid presence, and antimicrobial susceptibility patterns. Of the nine Indonesian isolates, three were of capsular type A (A:1,3,13; A:1,3; and A:8). One isolate was of type B:2,3 and one isolate was of capsular type F. For three isolates, the capsular serogroup could not be identified. Plasmids the size of 2.3 kbp were present in three of the field isolates and two of the vaccine strains. One plasmid less than 2 kbp was isolated from the vaccine strain PM-V4. Eight distinct DNA profiles were obtained from digestion with the restriction endonuclease EcoRI, and seven distinct DNA profiles were obtained from digestion with the restriction endonuclease HindIII. All of the isolates were resistant to lincomycin and sulfadiazine and were susceptible to ampicillin and trimethoprim. Of the nine isolates, seven (78%) were susceptible to doxycycline and gentamicin and six (67%) were susceptible to enrofloxacin.

Evaluation of avian-specific probiotic and Salmonella enteritidis-, Salmonella typhimurium-, and Salmonella heidelberg-specific antibodies on cecal colonization and organ invasion of Salmonella enteritidis in broilers.

Salmonella Enteritidis colonizes the intestinal tract of poultry and causes foodborne illness in humans. Reduction of Salmonella Enteritidis colonization in the intestinal tract of poultry reduces potential carcass contamination during slaughter. The purpose of this study was to determine the effect of an avian-specific probiotic combined with Salmonella Enteritidis-, Salmonella Typhimurium-, and Salmonella Heidelberg-specific antibodies on the cecal colonization and organ invasion of Salmonella Enteritidis in broiler as well as on body weights. The treatment group was defined as chicks spray-vaccinated with Avian Pac Plus at the hatchery and given Avian Pac Plus for the first 3 days after placement. An intermediate treatment was given at 10 and 14 days, 2 days prior to vaccination and 2 days postvaccination. All birds were vaccinated with Newcastle disease vaccine, La Sota virus (one drop/eye) at 12 days of age. A final treatment was given 3 days preslaughter. The control group was defined as chicks not given Avian Pac Plus at any time. Six hours after oral administration of the probiotic suspension (treatment group) or water (control group) at placement, the chicks were challenged with Salmonella Enteritidis. All chickens were orally inoculated with 0.25 ml of Salmonella Enteritidis that contained 4 x 10(7) CFU/1.0 ml. Cecal colonization and organ invasion were evaluated for Salmonella Enteritidis on days 0, 1, 3, 7, 10, 17, 24, 31, 38, and 41. The probiotic-treated group had a significantly lower concentration of Salmonella Enteritidis cecal colonization at days 3, 7, 10, 17, 24, 31, 38, and 41 when compared to the nontreated, control group (P < 0.05). Similarly, there was a significant difference (P < 0.05) in the isolation of Salmonella Enteritidis from the internal organs (liver and spleen) when probiotic-treated and nonprobiotic-treated groups were compared. There was no significant difference (P > 0.05) in the mean body weight between the two experimental groups at each collection period. These results indicated that a combination of Lactobacillus acidophilus, Streptococcus faecium, and Salmonella Enteritidis, Salmonella Typhimurium, and Salmonella Heidelberg-Specific antibodies have a beneficial effect in reducing the colonization of Salmonella Enteritidis in market-aged broilers.

Induction of vitamin A deficiency in turkeys.

The objective of this study was to determine the relationship between the hepatic vitamin A (VitA) level and the pathologic changes in the oropharynx and esophagus of VitA-deficient turkeys. Study turkeys were provided with a diet sufficient (11,000 IU/kg) or deficient (2750 IU/kg) in VitA from 4 to 17 wk of age. Body weight, bacterial culture, and tissues from internal organs were collected at weekly intervals. VitA deficiency causes epithelial tissue damage in poultry. This epithelial damage was seen grossly as white plaques in the oropharynx and esophagus and histologically as squamous metaplasia of mucosal glands and keratinization of epithelium. No significant difference in body weights was seen among the groups. Moreover, no pathogenic bacteria was isolated during sampling periods. Liver VitA levels declined significantly after consumption of low VitA diet for 3 wk and were depleted after 5 wk. Squamous metaplasia due to VitA deficiency developed in the esophagus after 3 wk and in the oropharynx after 4 wk of consuming a VitA-deficient diet.

The effect of hypovitaminosis A on the pathogenesis of Pasteurella multocida in turkeys.

It has been proposed that Pasteurella multocida can invade the host tissues via the mucous membrane. Vitamin A (VitA) deficiency has been associated with mucous membrane damage, such as squamous metaplasia. The objective of this study was to determine the early stages in the pathogenesis of P. multocida in VitA-deficient turkeys and clinically healthy turkeys. Fifteen-week-old VitA-deficient and clinically healthy turkeys were inoculated with P. multocida P-1059, a virulent strain, and the portal of entry, invasion, and localization of P. multocida were studied by microbial examination of the trachea, liver, and lung and histologic examinations of internal organs. Higher mortality was found in VitA-deficient turkeys. Pasteurella multocida was first reisolated from the trachea, secondarily from the liver and blood, and finally from the lung in both groups. Invasion of P. multocida into tissues occurred between 3 hr and 24 hr postinoculation in both groups. Our findings suggest that altered membrane integrity in VitA-deficient birds did not appear to change the time course of the systemic spread of P. multocida infection in turkeys and that the increased mortality seen in the VitA-deficient turkeys may be associated with immune system impairment.

Serologic survey of slaughter-age ostriches (Struthio camelus) for antibodies to selected avian pathogens.

Serum samples from 163 slaughter-age ostriches (Struthio camelus) in Ohio and Indiana were tested for antibodies to avian influenza virus (AIV), Newcastle disease virus (NDV), paramyxovirus (PMV) 2, PMV3, PMV7, infectious bursal disease virus (IBDV), Bordetella avium, Mycoplasma synoviae, Mycoplasma gallisepticum, Ornithobacterium rhinotracheale, Salmonella pullorum, Salmonella gallinarum, and Salmonella typhimurium. One ostrich had antibodies to AIV H5N9, 57% of the ostriches had antibodies to NDV, four ostriches had antibodies to both NDV and PMV2, and one ostrich had antibodies to NDV, PMV2, PMV3, and PMV7. None of the ostriches had antibodies to IBDV, B. avium, M. synoviae, M. gallisepticum, O. rhinotracheale, S. pullorum, S. gallinarum, and S. typhimurium. This is the first report of antibodies to avian influenza and PMV7 in ostriches in the United States.

Effects of dietary protein on restrict-fed broiler breeder pullets during a coccidial challenge.

In each of two experiments with young, feed-restricted broiler breeder pullets, the effects of differences in dietary protein intake on intestinal development and growth were studied. All pullets were restrict-fed either a 15 or 19% CP diet to see whether differences in dietary protein would influence intestinal growth in the face of controlled exposure to coccidiosis. In each experiment, pullets were vaccinated with one of three dilutions of Coccivac (control, 1X, 4X), each level representing a different proportion of the manufacturers' suggested dosage level. Experiment 1 was conducted in battery cages with wire floors, and no infection was established, most likely because of a lack of oocyst recycling. The pullets that were restrict-fed the 19% CP diet had a significantly heavier Pectoralis major breast muscle weight at 14 and 21 d postvaccination (PV) and heavier BW at 21 d PV. Experiment 2 was conducted in floor pens with litter. In this experiment, coccidiosis was successfully established as coccidial oocysts invaded the mucosal cells of the villi in the upper small intestine. Pullets fed the 19% CP diet had significantly heavier BW at 14, 28, and 35 d of age. There were, however, no significant effects caused by level of dietary protein or vaccination dose on intestinal development (villus height and crypt depth). In conclusion, mild coccidial infections induced via the administration of commercial anticoccidial vaccines do not warrant changes in dietary protein during the onset of feed restriction in young broiler breeder pullets.

Survey of pathogens and blood parasites in free-living passerines.

To determine the disease prevalence of free-living passerines, 1709 passerines were sampled from 38 different field sites in Ohio. Choanal and cloacal swabs were collected from each bird and cultured for the presence of Pasteurella multocida, Salmonella spp., and Escherichia coli by standard microbiologic techniques. In addition, the serum from each bird was analyzed for the presence of antibodies to Mycoplasma gallisepticum, Mycoplasma synoviae, Newcastle disease virus, and avian influenza virus. A blood smear was also made to examine for the presence of blood parasites. Results indicated that the isolation of E. coli varied with bird species, with the European starling having a higher (21.4%) isolation of E. coli. Salmonella spp. were also isolated from these free-living passerines. Pasteurella multocida was not isolated from any of the sampled passerines. These birds did not have antibodies to M. gallisepticum, M. synoviae, Newcastle disease virus, or avian influenza virus. Blood parasites were not detected in any of the birds sampled.

Virulence of raptor-origin Pasteurella multocida in domestic chickens.

Pasteurella multocida belonging to somatic serotype 1 and capsular type A has been known to cause avian cholera in domestic poultry. Pasteurella multocida serotype 1 has also been isolated from raptorial birds. However, the capsular type for these raptorial isolates remains unknown. Moreover, the virulence of these raptorial isolates for domestic poultry has not been determined. The objectives of this study were to determine the capsular type of raptorial P. multocida serotype 1 isolates and to determine if these isolates were virulent for domestic chickens. Study chickens were inoculated with one of three P. multocida isolates. Isolate WESO-1 was obtained from a western screech owl (Otus kennicottii) and isolates RTHA-2 and RTHA-4 were isolated from two red-tailed hawks (Buteo jamaicensis). These isolates were given by either the oral, intravenous, or intraocular route. Control birds were given brain-heart infusion broth. The capsular serotypes of three isolates were also determined. The RTHA-2 and RTHA-4 isolates belonged to P. multocida capsular type A. The WESO-1 isolate belonged to capsular type F. Results also demonstrated that, for the isolates examined, the intraocular route did not cause mortality in chickens. There was mortality in all groups for the intravenous route. However, various mortality patterns were observed when P. multocida was given orally for the three different isolates. The RTHA-4 isolate (serotype 1:A) was the most virulent for domestic chickens. The WESO-1 isolate (serotype 1:F) was the least virulent for chickens among the raptorial isolates examined.

The effect of route of inoculation on the virulence of raptorial Pasteurella multocida isolates in Pekin ducks (Anas platyrhynchos).

The purpose of this study was to determine the virulence of raptorial Pasteurella multocida for ducks and the effect of various routes of inoculation on virulence. Four-week-old Pekin ducks (Anas platyrhynchos) were challenged with one of three raptorial isolates (RTHA-2, RTHA-4, or WESO-1) by one of five inoculation routes (intranasal, intraocular, intravenous, oral, and subcutaneous). Ducks were monitored daily for mortality until 2 wk postchallenge. Results indicated that the intravenous route caused the most mortality for all isolates and that significant variation existed in the virulence among the sources of P. multocida, with WESO-1 causing the least mortality of the isolates tested.

Crop impaction resulting from feather ball formation in caged layers.

Abnormal behaviors in commercial poultry, including feather pulling and pica, have been known to occur when birds are exposed to an unfamiliar environment. We report here the development of crop impactions resulting from feather ball formation. Twelve specific-pathogen-free (SPF) chickens were placed in one of three cages housed among a commercial layer flock in three different buildings on a farm site. Three weeks after placement, the birds were removed from the cages and given a physical exam. Chickens were thin, and one bird in each of the three caged groups had a palpable mass at the level of the thoracic inlet. At necropsy, a mass was noted in the crop. Upon further dissection, a wet, foul-smelling mass consisting of feathers and feed debris was recovered. Results from our case indicate that unfamiliar surroundings can cause pica in birds. Hence, avian researchers and veterinarians planning to introduce new birds into a flock, i.e., SPF birds, should consider the birds' previous environmental conditions prior to placement because sudden placement in unfamiliar surroundings can result in pica.

Clinical assessment of gallinaceous birds and waterfowl in backyard flocks.

Obtaining a complete history and performing a physical examination are key steps in any clinical assessment. In addition, being familiar with common clinical signs helps in the formulation of a differential diagnosis. Once a definitive diagnosis is made, it is important to follow up each case with client education as well as the development of preventive medicine programs for avian patients.

Encephalomalacia associated with vitamin E deficiency in commercially raised emus.

Thirteen of 64 emus on a commercial emu farm in Ohio exhibited neurological signs that included backward staggering, incoordination, generalized weakness, and sitting on their hocks with head retracted backward. Eight of the birds showing such signs were found dead. Two of these emus were necropsied, and no significant gross lesions were observed. Major histopathological lesions were found in the cerebellum and included multiple malacic foci in association with neuropil rarefaction and astrogliosis within the white matter of folia. In addition, the hepatic vitamin E level of one emu was determined at the Michigan State University Animal Health Diagnostic Laboratory (MSU-AHDL) to be 14.61 micrograms/g dry weight. This vitamin E level was in the lower percentile (35%) of 30 emu liver samples examined at MSU-AHDL. A diagnosis of vitamin E-associated encephalomalacia was made based on clinical signs, gross and histological lesions, and liver vitamin E levels.

Evaluation of an avian-specific probiotic and Salmonella typhimurium-Specific antibodies on the colonization of Salmonella typhimurium in broilers.

Salmonella typhimurium colonizes the intestinal tract of poultry and causes food-borne illness in humans. Reduction of S. typhimurium colonization in the intestinal tract of poultry reduces potential carcass contamination during slaughter. The purpose of this study was to determine the effect of an avian-specific probiotic and S. typhimurium-specific antibodies on the colonization of S. typhimurium in broilers and on body weights. Broiler chicks were spray-vaccinated at the hatchery with the commercial product. Avian Pac Plus, which contains Lactobacillus acidophilus, Streptococcus faecium, ad S. typhimurium-specific antibodies. At placement, these chicks were administered Avian Pac plus in the water. Six hours postplacement, chicks were orally challenged with 1.8 x 10 (7) CFU of S. typhimurium. Chicks were administered Avian Pac Plus for two additional days postchallenge. Chicks were evaluated for S. typhimurium colonization and shedding every 3 to 4 days for the first 2 weeks and every 7 days for 6 weeks. The mean cecal and colonic concentration of S. typhimurium from the Avian Pac Plus-treated group was significantly lower at day 31 (P = 0.0001), day 38 (P = 0.0005), and day 43 (P = 0.0001) than the nontreated control group. These results indicated that a combination of Lactobacillus acidophilus, Streptococcus faecium, and S typhimurium-specific antibodies have a beneficial effect in reducing the colonization of S. typhimurium in market-aged broilers.