The mosquito-borne West Nile virus (WNV) is responsible for outbreaks of viral encephalitis in humans and horses with particularly virulent strains causing recent outbreaks in Eastern Europe, the Middle East, and North America. In Australia, a strain of WNV, Kunjin (WNVKUN), is endemic in the north and infection with this virus is generally asymptomatic. However, in early 2011, following extensive flooding, an unprecedented outbreak of WNVKUN encephalitis in horses occurred in South-Eastern Australia, resulting in more than 1,000 cases and a mortality of 10–15%. Despite widespread evidence of equine infections, there was only a single mild human case reported during this outbreak. To understand why clinical disease was seen in horses without similar observations in the human population, a serosurvey was conducted using blood donor samples from areas where equine cases were reported to assess level of flavivirus exposure. The seroprevalence to WNVKUN in humans was low before the outbreak (0.7%), and no significant increase was demonstrated after the outbreak period (0.6%). Due to unusual epidemiological features during this outbreak, a serosurvey was also conducted in rabbits, a potential reservoir host. Out of 675 animals, sampled across Australia between April 2011 and November 2012, 86 (12.7%) were seropositive for WNVKUN, with the highest prevalence during February of 2012 (28/145; 19.3%). As this is the first serological survey for WNVKUN in Australian feral rabbits, it remains to be determined whether wild rabbits are able to develop a high enough viremia to actively participate in WNV transmission in Australia. However, they may constitute a sentinel species for arbovirus activity, and this is the focus of on-going studies. Collectively, this study provides little evidence of human exposure to WNVKUN during the 2011 outbreak and indicates that the Australian population remains susceptible to the emergence of virulent strains of WNV.

Background Gastroesophageal reflux and regurgitation occurs in brachycephalic dogs, but objective assessment is lacking. Objectives Quantify reflux in brachycephalic dogs using an esophageal pH probe and determine the association with scored clinical observations. Animals Fifty‐one brachycephalic dogs. Methods Case review study. Signs of respiratory and gastrointestinal disease severity were graded based on owner assessment. An esophageal pH probe with 2 pH sensors was placed for 18‐24 hours in brachycephalic dogs that presented for upper airway assessment. Proximal and distal reflux were indicated by detection of fluid with a pH ≤4. The median reflux per hour, percentage time pH ≤4, number of refluxes ≥5 minutes and longest reflux event for distal and proximal sensors were recorded. Association of preoperative respiratory and gastrointestinal grade, laryngeal collapse grade, and previous airway surgery with the distal percentage time pH ≤4 was examined using 1‐way ANOVA. Results A total of 43 of 51 dogs (84%; 95% confidence interval 72‐92) displayed abnormal reflux with a median (range) distal percentage time pH ≤4 of 6.4 (2.5‐36.1). There was no significant association between the distal percentage time pH ≤4 and respiratory grade, gastrointestinal grade, laryngeal collapse grade, or previous upper airway surgery. Conclusions and Clinical Importance The occurrence of reflux is not associated with owner‐assessed preoperative respiratory and gastrointestinal grade, laryngeal collapse grade, and previous airway surgery. Esophageal pH measurement provides an objective assessment tool before and after surgery.

Background Swine dysentery (SD) caused by Brachyspira hyodysenteriae is an important disease in Australia. Aim The aim of this study is to evaluate the macrolide antibiotic kitasamycin for use in SD control. Methods The minimum inhibitory concentrations (MICs) of kitasamycin, tylosin and lincomycin for 32 Australian isolates of B. hyodysenteriae were evaluated. Mutations in the 23S rRNA gene were examined. Isolate ‘13’ with a low kitasamycin MIC was used to challenge weaner pigs. Sixty pigs were housed in 20 pens each containing three pigs: pigs in four pens received 2 kg/tonne of a product containing kitasamycin (3.1% active) prophylactically in their food starting 4 days before B. hyodysenteriae challenge (group 1); pigs in four pens were challenged and received the same dose therapeutically once one pig in a pen showed diarrhoea (group 2); four pens were challenged and received 4 kg/tonne of the product therapeutically (group 3); four pens were challenged but not medicated (group 4); two pens were unmedicated and unchallenged (group 5) and two pens received 2 kg/tonne and were unchallenged (group 6). Pigs were monitored for B. hyodysenteriae excretion and disease. Results Macrolide resistance was widespread, and mutations in the 23S rRNA gene were identified in 23 isolates. Four isolates with kitasamycin MICs < 5 μg/mL were considered susceptible. Following experimental challenge, 10 of 12 unmedicated pigs developed SD. No pigs receiving kitasamycin prophylactical or therapeutically developed SD. Medicated pigs shed low numbers of B. hyodysenteriae in their faeces. Conclusions Kitasamycin can help control SD in pigs infected with susceptible isolates of B. hyodysenteriae.

The anaerobic intestinal spirochaete Brachyspira hyodysenteriae colonises the large intestine of pigs and causes swine dysentery (SD), a severe mucohaemorrhagic colitis. SD occurs worldwide, and control is hampered by a lack of vaccines and increasing antimicrobial resistance. B. hyodysenteriae strains typically produce strong beta-haemolysis on blood agar, and the haemolytic activity is thought to contribute to the pathogenesis of SD. Recently, weakly haemolytic variants of B. hyodysenteriae have been identified in Europe and Australia, and weakly haemolytic strain D28 from Belgium failed to cause disease when used experimentally to infect pigs. Moreover, pigs colonised with D28 and then challenged with virulent strongly haemolytic strain B204 showed a delay of 2–4 days in developing SD compared to pigs not exposed to D28. The current study aimed to determine whether Australian weakly haemolytic B. hyodysenteriae strain MU1, which is genetically distinct from D28, could cause disease and whether exposure to it protected pigs from subsequent challenge with strongly haemolytic virulent strains. Three experimental infection studies were undertaken in which no diseases occurred in 34 pigs inoculated with MU1, although mild superficial lesions were found in the colon in 2 pigs in one experiment. In two experiments, significantly fewer pigs exposed to MU1 and then challenged with strongly haemolytic virulent strains of B. hyodysenteriae developed SD compared to control pigs not previously exposed to MU1 ( p = 0.009 and p = 0.0006). These data indicate that MU1 lacks virulence and has potential to be used to help protect pigs from SD. Electronic supplementary material The online version of this article (10.1186/s13567-019-0668-5) contains supplementary material, which is available to authorized users.

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