Recent years have seen the development of numerous methodologies for reconstructing transmission trees in infectious disease outbreaks from densely sampled whole genome sequence data. However, a fundamental and as of yet poorly addressed limitation of such approaches is the requirement for genetic diversity to arise on epidemiological timescales. Specifically, the position of infected individuals in a transmission tree can only be resolved by genetic data if mutations have accumulated between the sampled pathogen genomes. To quantify and compare the useful genetic diversity expected from genetic data in different pathogen outbreaks, we introduce here the concept of ‘transmission divergence’, defined as the number of mutations separating whole genome sequences sampled from transmission pairs. Using parameter values obtained by literature review, we simulate outbreak scenarios alongside sequence evolution using two models described in the literature to describe transmission divergence of ten major outbreak-causing pathogens. We find that while mean values vary significantly between the pathogens considered, their transmission divergence is generally very low, with many outbreaks characterised by large numbers of genetically identical transmission pairs. We describe the impact of transmission divergence on our ability to reconstruct outbreaks using two outbreak reconstruction tools, the R packages outbreaker and phybreak, and demonstrate that, in agreement with previous observations, genetic sequence data of rapidly evolving pathogens such as RNA viruses can provide valuable information on individual transmission events. Conversely, sequence data of pathogens with lower mean transmission divergence, including Streptococcus pneumoniae, Shigella sonnei and Clostridium difficile, provide little to no information about individual transmission events. Our results highlight the informational limitations of genetic sequence data in certain outbreak scenarios, and demonstrate the need to expand the toolkit of outbreak reconstruction tools to integrate other types of epidemiological data.

Proximal suspensory desmopathy (PSD) is a common cause of hindlimb lameness in sports horses; anecdotally there is an association with straight hock conformation. The objective of this prospective observational study is to describe hindlimb conformation in horses with and without bilateral PSD. Horses examined over one year with a definitive diagnosis for lameness (based on clinical assessment, response to diagnostic anaesthesia, radiography, ultrasonography AE MRI or scintigraphy), were included (n = 193). Markers were placed on predefined landmarks. Lateral photographs were acquired from the left and right sides with the horse standing squarely, using standardised techniques, with each metatarsus perpendicular to the ground, aligned to the tuber ischii marker. Before data acquisition, repeatability studies for marker placement, horse positioning and angle measurements were performed. The tarsal and metatarsophalangeal angles were measured using Image Measurement. Orthopaedic diagnosis, breed, work discipline, weight, height and age were recorded. Z-tests, Fisher's exact tests, Chi-squared tests and multivariable logistic regression were used to determine the associations between diagnosis, tarsal angles and possible confounding variables. Mann Whitney U tests were used to evaluate the relationship between metatarsophalangeal joint angle and suspensory ligament injury. Horses with PSD had larger tarsal angles than controls (P = 0.003). The proportions of Warmblood-type horses and dressage horses with PSD were different to those of other breeds and work disciplines (P = 0.001, 0.02 respectively). A final logistic regression model demonstrated a significant effect of mean tarsal angle on outcome when breed and weight-height product were accounted for. There was a an 11% increase in the odds of PSD for every degree increase in tarsal angle (CI 1.006-1.223, P = 0.04). There was no association between suspensory ligament injury and metatarsophalangeal joint angle. Assessment of tarsal angles at prepurchase examinations and prior to surgical treatment of PSD may be advisable.

An outbreak of equine herpesvirus type 1 (EHV-1) abortions on a UK Thoroughbred stud farm between February 23 and April 2, 2016, is described. The outbreak resulted in the loss of 10 Thoroughbred foals, confirmed pathologically and virologically as EHV-1 infection at postmortem. All aborting mares were vaccinated against EHV-1 according to manufacturer’s recommendations, but had contact with the index aborting mare, either as field companions or housed in the American barn at the time she and subsequent mares aborted. Control measures were implemented in accordance with the Thoroughbred Industry’s Code of Practice on recognising the index case and were maintained until the outbreak had resolved. The report illustrates that prompt investigation and management of this disease outbreak can optimise the safe return of the stud farm to normal breeding operations and highlights EHV-1’s continued potential for multiple late gestation pregnancy losses in mares, despite vaccination.

Transmission EHV-1 is contagious and is spread by direct horse-to-horse contact, indirectly by contaminated hands, equipment and tack, and probably through aerosolisation of the virus within enclosed environments Clinical signs Fever, nasal discharge and coughing in the respiratory form of the disease. Abortion, stillbirth and early neonatal death in pregnant mares. Weakness, incoordination, ataxia, paralysis and difficulty urinating and defaecating may be seen in the neurological form