Enterococcus cecorum, a normal intestinal inhabitant, is increasingly responsible for outbreaks of arthritis and osteomyelitis in chickens worldwide. Enterococcal spondylitis (ES) is a specific manifestation of E. cecorum-associated disease in which increased flock morbidity and mortality result from chronic infection involving the free thoracic vertebra. In this study the genetic relatedness and antimicrobial resistance of isolates recovered from ES-affected flocks in the southeastern United States were determined. ES outbreaks from 2007 to 2011 were investigated in North Carolina (15 flocks, 13 farms, four integrators), South Carolina (one flock, one farm, one integrator) and Alabama (six flocks, six farms, one integrator). From these 22 epidemiologically distinct outbreaks, 326 isolates of E. cecorum were recovered. Isolates from spinal lesions and caeca of affected birds (cases) and caeca of unaffected birds (controls) were genotyped using pulsed-field gel electrophoresis; phenotyped using both GenIII MicroPlate TM (Biolog; Hayward, CA, USA) microbial identification plates and antimicrobial sensitivity testing; and compared with each other. Isolates from spinal lesions were incapable of mannitol metabolism and the majority of these isolates were genetically clonal. In contrast, caecal isolates from control birds varied in their ability to metabolize mannitol and were genetically diverse. Isolates from both case and control birds had high levels of antimicrobial resistance. These findings indicate that the increase in E. cecorum-associated disease in the southeast United States is due to the emergence of new clones with increased pathogenicity and multidrug resistance.

Enterococcus cecorum was isolated from spondylitis lesions in broilers from two flocks in North Carolina that were experiencing increased mortality. Affected birds showed paresis and paralysis, clinical signs characteristic of enterococcal spondylitis (ES). Affected birds rested on their hocks and caudal abdomens with legs extended forward and were unable to stand or walk. Necropsy examination of affected birds revealed firm to hard inflammatory masses involving the vertebral bodies at the level of the free thoracic vertebra that bulged dorsally and compressed the spinal cord. When opened, lesions contained pale, tan to yellow caseonecrotic material. Microscopically, necrosis and fibrinoheterophilic spondylitis with intralesional gram-positive bacteria were seen. Heavy growth of E. cecorum recovered from vertebral lesions confirmed the diagnosis of ES. To investigate possible sources of the organism for one of the flocks bacterial cultures were made from the environment, water lines, mice trapped on the farm, cecal/cloacal swabs from one of the parent broiler breeder flocks, egg residue, hatching eggs, and the hatchery environment. Except for cecal/cloacal swabs from the breeders, E. cecorum was not isolated from any of these samples. When compared phenotypically and genotypically, cecal/cloacal isolates of E. cecorum from the breeders differed from isolates from spondylitis lesions in the broilers. The source of E. cecorum for the broiler flocks was not determined, but vertical transmission appears unlikely.

Periodic monitoring of poultry flocks in the United States via molecular diagnostic methods has revealed a number of potential enteric viral pathogens in continuous circulation in turkeys and chickens. Recently turkey integrators in the Southeastern United States and Arkansas experienced an outbreak of moderate to severe enteritis associated with turkey enteric coronavirus (TCoV), and numerous enteric samples collected from turkey flocks in these areas tested positive for TCoV via real-time reverse-transcriptase PCR (RRT-PCR). This report details the subsequent sequence and phylogenetic analysis of the TCoV spike glycoprotein and the comparison of outbreak-associated isolates to sequences in the public database. TCoVs investigated during the present outbreak grouped geographically based upon state of origin, and the RRT-PCR assay was a good indicator of subsequent seroconversion by TCoV-positive turkey flocks.

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An outbreak of ascaridiasis occurred in 10-wk-old guinea fowl (Numida meleagris) on a commercial farm. Birds had exhibited elevated mortality (11.66%) in the previous week, as well as increased water consumption, weakness, anorexia, and stunted growth. Numerous nematodes, occasionally occluding the intestinal lumen, were present in the jejunum and ileum and were identified as Ascaridia numidae based on microscopic morphology. Ribosomal DNA 18S and 28S D3 sequences of the nematode were deposited into GenBank and found to be most similar to Ascaridia galli and Toxocara vitulorum, respectively; sequences for A. numidae had not been previously reported. Treatment with piperazine sulfate significantly reduced the number of adult worms in the intestines, greatly decreased eggs per gram of feces, relieved clinical signs in the flock, and returned the flock mortality back to expected levels. All findings implicate A. numidae as the cause of elevated mortality in this flock.