Equine gastrointestinal nematodes (GINs) have been the subject of intermittent studies in Australia over the past few decades. However, comprehensive information on the epidemiology of equine GINs, the efficacy of available anthelmintic drugs and the prevalence of anthelmintic resistance (AR) in Australasia is lacking. Herein, we have systematically reviewed existing knowledge on the horse GINs recorded in Australia, and main aspects of their pathogeneses, epidemiology, diagnoses, treatment and control. Six electronic databases were searched for publications on GINs of Australian horses that met our inclusion criteria for the systematic review. Subsets of publications were subjected to review epidemiology, diagnoses, pathogeneses, treatment and control of GINs of horses from Australia. A total of 51 articles published between 1950 to 2018 were included. The main GINs reported in Australian horses were cyathostomins (at least 28 species), Draschia megastoma, Habronema muscae, H. majus, Oxyuris equi, Parascaris equorum, Strongyloides westeri and Trichostrongylus axei across different climatic regions of Queensland, New South Wales, Victoria, and Western Australia. Nematodes are diagnosed based on the traditional McMaster egg counting technique, though molecular markers to characterise common GINs of equines were characterised in 1990s. The use of anthelmintic drugs remains the most widely-used strategy for controlling equine GIN parasites in Australia; however, the threshold of faecal egg count that should trigger treatment in horses, remains controversial. Furthermore, anthelmintic resistance within GIN population of horses is becoming a common problem in Australia. Although GINs infecting Australian horses have been the subject of occasional studies over the past few decades, the effective control of GIN infections is hampered by a generalised lack of knowledge in various disciplines of equine parasitology. Therefore, coordinated and focused research is required to fill our knowledge gaps in these areas to maximise equine health and minimise economic losses associated with the parasitic infections in Australia.

Purpose: Pet animals have been considered a potential carrier of clinically important multidrug-resistant Escherichia coli. However, little is known about the role of pets as reservoirs of extended-spectrum β-lactamase (ESBL) producing E. coli in Pakistan. This study was designed to determine the prevalence and genetic relatedness of ESBL-producing multidrug-resistant E. coli in pets, their owners, and veterinary professionals. Methods: A total of 105 fecal samples were collected from dogs, cats, their owners, and veterinary professionals from veterinary clinics. Isolates of ESBL-producing E. coli were subjected to antimicrobial susceptibility testing. The presence of bla _CTX-M genes and CTX-M groups I and II in multidrug-resistant E. coli was detected using PCR. Clonal diversity was checked using BOX-PCR. Results: Of the 105 fecal samples screened, 73 (69.5%) were found to contain ESBL-producing E. coli. The percentage of ESBL-producing E. coli isolates in dogs and dog owners was found to be 81.8% (18/22) and 59% (13/22), respectively. In cats, this percentage was 73.9% (17/23) and in cat owners, 56.5% (13/23). Furthermore, 80% (12/15) of E. coli isolates in veterinary professionals were ESBL producers. Of these 73 ESBL-producing E. coli isolates, 23 isolates exhibited a multidrug-resistant phenotype. The most prevalent multidrug-resistant pattern (17.4%) identified was resistant to ampicillin, cefotaxime, ciprofloxacin, and nitrofurantoin. In the multidrug-resistant E. coli, bla _CTX-M was identified as the most common ESBL-producing genotype (19/23), with bla _CTX-M-1 dominating in all 19 isolates. Furthermore, BOX-PCR analysis exhibited genetically diverse clonal groups among isolates of the CTX-M-1 group. Conclusion: Our results provide important baseline information on the potential burden of multidrug-resistant E. coli among companion animals in Pakistan. Further studies are needed to understand the drivers of antimicrobial resistance at human–animal–environmental intersections.

ImportanceWe sought to unravel the genetic cause in a consanguineous Pakistani family with a complex neurological phenotype.ObservationsNeurological and ophthalmological examination, including videotaping and fundoscopy, and genetic investigations, including homozygosity mapping and exome sequencing, were performed at the University of the Punjab and the University of Lübeck. Participants included 2 severely affected cousins from consanguineous parents, 10 of their reportedly unaffected relatives, and 342 Pakistani controls. Motor symptoms in the 2 patients started at the age of 3 to 4 years and included chorea, cerebellar ataxia, dystonia, and pyramidal tract signs. Genome-wide genotyping delineated 2 regions of homozygosity on chromosomes 13q12.11 to 13q12.13 and 19q12 to 19q13.41. Exome sequencing revealed 2 rare, homozygous variants (c.32 T>A [p.L11Q] in OPA3 and c.941 C>G [p.A314G] in TSHZ3) that segregated with the disease. Only the OPA3 variant was absent in the control subjects and predicted to be damaging. Subsequent ophthalmological assessment revealed bilateral optic atrophy in both patients.Conclusions and RelevanceMutations in OPA3 have been reported in Costeff optic atrophy syndrome. We identify a novel missense mutation in OPA3 as the cause of a complex neurological disorder, expanding the OPA3 -linked phenotype by early-onset pyramidal tract signs and marked lower limb dystonia. Investigation of optic atrophy was initiated only after genetic analysis, a phenomenon referred to as reverse phenotyping.

The present study aimed to evaluate the immunopotentiating effect of plant-derived soyasaponin and its immunogenicity in chickens challenged with Newcastle disease virus (NDV). Soyasaponin was extracted from soybean seeds and detected using the phytochemical tests, followed by quantification through the dry-weight method. One-day-old broiler chicks (n = 90) were divided into 3 groups, named as A, B, and C. Group A birds were orally administrated with soyasaponin (5 mg/kg), followed by immunization with inactivated ND vaccine intramuscularly (IM), whereas group B birds were vaccinated with inactivated ND vaccine alone. Group C birds were kept unvaccinated. A booster dose on day 21 was also administered IM to group A and B birds. At day 35, all 3 groups were challenged with NDV. To determine the immunogenicity potential of soyasaponin, antibody titer was measured using the hemagglutination inhibition test before and after the NDV challenge. Histochemical examination was performed to determine the pathological changes associated with NDV infection. Foam formation and hemolytic activity confirmed the presence of saponin in soya bean extract. Group A birds showed a higher antibody response compared with group B and C birds. The disease challenge study showed that soyasaponin-adjuvanted NDV vaccine provided complete protection to group A birds against ND. Moreover, no side effects of soyasaponin were observed on the growth performance of birds during the experiment. Therefore, we can conclude that soyasaponin is a potential immunogenic agent and therefore could be a promising candidate to launch a protective humoral response against ND in chickens.