Antimicrobials are sometimes given to food animals at low doses in order to promote faster growth. However, the mechanisms by which those drugs improve performance are not fully understood. This study aimed to investigate the impact of zinc bacitracin (55g/ton), enramycin (10g/ton); halquinol® (30g/ton); virginiamycin (16,5g/ton) and avilamycin (10g/ton) on the cecal microbiota of broiler chicken, compared to a control group. Six hundred and twenty four chicks (Cobb 500) arriving to an experimental unit were randomly assigned into each treatment with four repetitions per treatment. The cecal content of 16 animals per treatment (n = 96) was used for DNA extraction and sequencing of the V4 region of the 16S rRNA gene using Illumina technology. The use of antimicrobials induced significant changes in membership but not in structure of the cecal microbiota compared to the control group, suggesting a greater impact on the less abundant species of bacteria present in that environment. Halquinol was the only drug that did not affect microbial membership. Firmicutes comprised the major bacterial phylum present in the cecum of all groups. There was no statistical difference in relative abundances of the main phyla between treated animals and the control group (all P>0.05). Treatment with enramycin was associated with decreased richness and with lower relative abundance of unclassified Firmicutes, Clostridium XI, unclassified Peptostreptococcaceae (all P<0.001) and greater abundance of Clostridium XIVb (P = 0.004) and Anaerosporobacter spp. (P = 0.015), and treatment with bacitracin with greater relative abundance of Bilophila spp. (P = 0.004). Several bacterial genera were identified as representative of usage of each drug. This study used high throughput sequencing to characterize the impact of several antimicrobials in broiler chicken under controlled conditions and add new insights to the current knowledge on how AGPs affect the cecal microbiota of chicken.
BackgroundDiarrhea associated with parvovirus infection is common in dogs. Supportive care is the mainstay of treatment, but recovery may be prolonged and mortality rate can be high. Modification of the intestinal bacterial microbiota has been promising in human and veterinary medicine as an adjunctive treatment of various enteric diseases.ObjectivesTo investigate the safety and efficacy of fecal microbiota transplantation (FMT) on the clinical recovery of puppies with acute hemorrhagic diarrhea syndrome.AnimalsSixty‐six puppies with parvovirus infection were evaluated at 2 veterinary hospitals.MethodsRandomized clinical trial. Puppies were randomly distributed into 2 groups: standard treatment (STD) and standard treatment + FMT (STD + FMT). The STD puppies (n = 33) received only treatment with IV fluids and antimicrobials and the STD + FMT puppies (n = 33) received FMT in addition to standard treatment. For FMT, 10 g of feces from a healthy dog diluted in 10 mL of saline were administered rectally 6‐12 hours post‐admission.ResultsAmong survivors, treatment with FMT was associated with faster resolution of diarrhea (P < .001) and shorter hospitalization time (P = .001; median, 3 days in STD + FMT; median, 6 days in STD) compared to standard treatment. Mortality in STD was 36.4% (12/33) as compared to 21.2% (7/33) in puppies treated with FMT, but there was no statistical difference between groups (P = .174). Polymerase chain reaction indicated that all animals carried canine parvovirus, strain CPV‐2b.ConclusionsFecal microbiota transplantation in parvovirus‐infected puppies was associated with faster resolution of diarrhea.
The concomitant infections of Canine distemper virus (CDV), Canine adenovirus A types 1 (CAdV-1) and 2 (CAdV-2), Canine parvovirus type 2 (CPV-2), and Toxoplasma gondii are described in a 43-day-old mixed-breed puppy. Clinically, there were convulsions and blindness with spontaneous death; 14 siblings of this puppy, born to a 10-month-old dam, which was seropositive (titer: 1,024) for T. gondii, also died. Necropsy revealed unilateral corneal edema (blue eye), depletion of intestinal lymphoid tissue, non-collapsible lungs, congestion of meningeal vessels, and a pale area in the myocardium. Histopathology demonstrated necrotizing myocarditis associated with intralesional apicomplexan protozoa; necrotizing and chronic hepatitis associated with rare intranuclear inclusion bodies within hepatocytes; necrotizing bronchitis and bronchiolitis; interstitial pneumonia associated with eosinophilic intracytoplasmic inclusion bodies within epithelial cells; atrophy and fusion of intestinal villi with cryptal necrosis; and white matter demyelination of the cerebrum and cerebellum associated with intranuclear inclusion bodies within astrocytes. Polymerase chain reaction (PCR) amplified the partial fragments (bp) of the CDV N gene (290 bp), CPV-2c VP2 capsid protein gene (583 bp), and CAdV-1 (508 bp) and CAdV-2 (1,030 bp) E gene from urine and tissue samples. The PCR assays demonstrated that the apicomplexan protozoa observed within several organs contained DNA specific for T. gondii; genotyping revealed T. gondii type III. The findings support the characterization of concomitant infections of CDV, CAdV-1, CAdV-2, CPV-2, and T. gondii in this puppy. Further, seroreactivity to T. gondii of the dam in association with the systemic disease observed in the puppy described herein is suggestive of congenital toxoplasmosis.
Senecavirus A (SVA) is a positive-sense single-stranded RNA virus that belongs to the Senecavirus genus within the Picornaviridae family. The virus has been silently circulating in pig herds of the USA since 1988. However, cases of senecavirus-associated vesicular disease were reported in Canada in 2007 and in the USA in 2012. Since late 2014 and early 2015, an increasing number of senecavirus outbreaks have been reported in pigs in different producing categories, with this virus being detected in Brazil, China, and Thailand. Considering the novel available data on senecavirus infection and disease, 2015 may be a divisor in the epidemiology of the virus. Among the aspects that reinforce this hypothesis are the geographical distribution of the virus, the affected pig-producing categories, clinical signs associated with the infection, and disease severity. This review presents the current knowledge regarding the senecavirus infection and disease, especially in the last two years. Senecavirus epidemiology, pathogenic potential, host immunological response, diagnosis, and prophylaxis and control measures are addressed. Perspectives are focused on the need for complete evolutionary, epidemiological and pathogenic data and the capability for an immediate diagnosis of senecavirus infection. The health risks inherent in the swine industry cannot be neglected.
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