An Aboriginal Community-Controlled Health Organization model of service delivery: qualitative process evaluation of the Tulku wan Wininn mobile clinic

BACKGROUND: Mobile clinics have been implemented in diverse clinical and geographical settings to provide proximal health care for specific populations. Primary health care mobile clinics have been implemented widely for Indigenous populations, with a paucity of research evaluations around service delivery models internationally. To redress factors impeding service accessibility for Aboriginal and Torres Strait Islander Peoples, Budja Budja Aboriginal Cooperative (Aboriginal Community Controlled Health Organisation located in a small rural town in Victoria, Australia), developed and implemented the Tulku wan Wininn primary health mobile clinic. METHODS: A qualitative process evaluation methodology was used to explore contextual factors mediating the implementation of the mobile clinic, including the acceptability of the service to health service personnel, external key informants, and Aboriginal and/or Torres Strait Islander clients. A synthesis of international ethical guidelines, (Consolidated Criteria for strengthening reporting of health research involving Indigenous peoples (CONSIDER statement), was prospectively applied to shape the study design and research process. Semi-structured interviews were conducted with participants. Data collection occurred from July 2019 to October 2021. Inductive thematic data analysis was undertaken concurrently with data collection. RESULTS: Data was collected from 19 participants which included 12 health service personnel and key informants, and 7 Aboriginal clients. In total, data from 22 interviews were included as interviews with three clients were undertaken twice. Four themes were developed: considerations for early implementation, maintaining face-to-face services during COVID-19, acceptability as a model of service delivery, and maintaining the mobile clinic as a service delivery model. CONCLUSION: Evidence supporting the acceptability of a primary health care mobile clinic for Aboriginal Peoples residing in rural Victoria is provided. Despite the experience of early implementation challenges and adaptations, the mobile clinic addressed known transport and cultural barriers to accessing primary health care services. In the context of COVID-19 lockdowns, the mobile clinic was valued for the provision of face-to-face care for Aboriginal clients. Key issues for maintaining the mobile clinic include health workforce and funding. Findings are of value to other organizations seeking to implement a primary health mobile clinic service delivery model to redress barriers to accessibility experienced by the communities they serve.

Effect of simulated stages of the canine oestrous cycle on Escherichia coli binding to canine endometrium.

Pyometra, a prevalent infectious uterine disease that affects intact middle-aged bitches, is typically associated with Escherichia coli. Our hypotheses were (i) that bacterial adhesion to canine endometrium differs between different stages of the oestrous cycle and (ii) that the adhesin FimH facilitates this adhesion. Twelve post-pubertal, ovariectomized greyhound bitches were treated with exogenous hormones to simulate different stages of the oestrous cycle. Tissue samples from each uterus were incubated with a pathogenic E. coli strain carrying the fimH gene, but no other adhesin genes (P4-wt)--or an E. coli strain in which fimH was insertionally inactivated (P4-∆fimH::kan)--or with phosphate-buffered saline as a negative control. After washing, tissue samples were homogenized for quantification of adherent bacteria. The differences in binding to canine endometrium at different stages of the oestrous cycle were not significant. However, the mean difference in binding of the P4-wt and the P4-∆fimH::kan across all stages of the simulated oestrous cycle was significant (p < 0.001 by paired t-test on geometric means). Individual differences in numbers of P4-wt bacteria bound between dogs might suggest genetic variations or epigenetic differences in FimH receptor expression by the endometrium, unrelated to the stage of the oestrous cycle.

Use of transcolonic portal scintigraphy to evaluate efficacy of cellophane banding of congenital extrahepatic portosystemic shunts in 16 dogs.

OBJECTIVE: To evaluate the efficacy of cellophane banding of single congenital extrahepatic portosystemic shunts in dogs using transcolonic portal scintigraphy. To investigate the portal circulation of those dogs with elevated postoperative shunt fractions to determine the cause of the persistent shunting. Further, to evaluate whether presenting signs, clinical pathology findings and liver histopathology are predictive of outcome. DESIGN: Prospective study of 16 dogs presenting with single congenital extrahepatic portosystemic shunts. PROCEDURE: Dogs with single extrahepatic portosystemic shunts attenuated by cellophane banding underwent portal scintigraphy and bile acids tolerance testing pre- and post-operatively. Dogs identified with elevated shunt fractions at 10 weeks post-operatively underwent mesenteric portovenography. Qualitative hepatic histopathology from all dogs was reviewed by a veterinary pathologist and assigned a semi-quantitative score to identify any abnormalities that may predict surgical outcome. RESULTS: At 10 weeks post cellophane banding, 10 of 16 cases (63%) had normal shunt fractions, whilst six dogs (37%) had increased shunt fractions and seven dogs (44%) had increased serum bile acids. Of these dogs, mesenteric portovenography revealed incomplete closure of the shunt in three dogs (18.6%) and multiple acquired shunts in three dogs (18.6%). Liver histopathology findings were similar for all dogs, regardless of outcome. CONCLUSIONS: Cellophane banding is an efficacious method for complete gradual occlusion of single extrahepatic shunts when the shunt vessel is attenuated to < or = 3 mm. Transcolonic portal scintigraphy is a reliable method for assessment of shunt attenuation and, unlike serum bile acids, is not influenced by other causes of liver dysfunction.

Eimeria taggarti N. Sp., a Novel Coccidian (Apicomplexa: Eimeriorina) in the Prostate of an Antechinus flavipes.

A novel coccidian species was discovered in the prostate of an Antechinus flavipes (yellow-footed antechinus) in South Australia during the period of postmating male antechinus immunosuppression and mortality. This novel coccidian is unusual because it develops extraintestinally and sporulates endogenously within the prostate gland of its mammalian host. Histological examination of prostatic tissue revealed dense aggregations of spherical and thin-walled tetrasporocystic, dizoic, sporulated coccidian oocysts within tubular lumina, with unsporulated oocysts and gamogonic stages within the cytoplasm of glandular epithelial cells. This coccidian was observed occurring concurrently with dasyurid gammaherpesvirus 1 infection of the antechinus' prostate. Eimeria-specific 18S small-subunit ribosomal (r)DNA polymerase chain reaction amplification was used to obtain a partial 18S rDNA nucleotide sequence from the antechinus coccidian. Bayesian phylogenetic analysis based on 18S rDNA gene sequences revealed that the novel coccidian clusters with reptile-host coccidians, forming an ancestral basal lineage of the eimeriid clade. The species has been named Eimeria taggarti n. sp. on the basis of both sporulated oocyst morphology and molecular characterization. It is suspected that E. taggarti is sexually transmitted via excretion of sporulated oocysts or free sporocysts with prostatic secretions in semen.

Risk factors for Thoroughbred racehorse fatality in jump starts in Victoria, Australia (1989-2004).

REASONS FOR PERFORMING STUDY: The risk of fatality is greater in jump than in flat racing in Victoria, Australia. This is the first study to identify risk factors specific to jump starts in Victoria. OBJECTIVE: To identify risk factors for fatality of Thoroughbred racehorses in jump starts on all racecourses in Victoria, Australia between 1989 and 2004. METHODS: Fatalities comprised all horses that died during or immediately after a jump (hurdle or steeplechase) race or official jump trial and all horses that were subjected to euthanasia within 24 h of an event in which an injury was sustained. The retrospective study involved 191 case starts and 2324 control starts. Univariable and multivariable backward stepwise logistic regression was used to identify risk factors for fatality at any one start. A multiple level model was used with racecourse included as a random effect. RESULTS: In the final multivariable model, the duration of the racing career of the horse, the number of flat, hurdle and steeple starts accumulated in the 60 days prior to the case or control start, the number of flat and jump starts accumulated over the racing career, if the horse had had a start between 1 and 14 days prior to the case or control start, the type of jump race (hurdle or steeple), the calendar year of the start and the location of the racecourse were associated with fatality. CONCLUSIONS: The findings highlight the need to investigate further the differences between hurdle and steeplechase events and the adverse effect of prolonged prior flat racing careers on the risk of fatality in jump starts. POTENTIAL RELEVANCE: This is the first study to examine risk factors for fatality in jump starts in Victoria. The results should shape the development of interventions to reduce the risk in jump starts in the future.

Risk factors for Thoroughbred racehorse fatality in flat starts in Victoria, Australia (1989-2004).

REASONS FOR PERFORMING STUDY: Research into risk factors specific for fatality in flat racing should be focused at a regional level as the risk factors may differ among countries and even regions within countries. OBJECTIVE: To identify risk factors for fatality of Thoroughbred racehorses in flat starts on all racecourses in Victoria, Australia between 1989 and 2004. METHODS: Fatalities comprised all horses that died during or immediately after a flat race or official flat trial, and all horses that were subjected to euthanasia within 24 h of an event in which an injury was sustained. The retrospective study involved 283 case starts and 3307 control starts. Univariable and multivariable backward stepwise logistic regression was used to identify risk factors for fatality at any one start. RESULTS: In the final multivariable model, horse gender, prior racing history, race length, racing year, racecourse location and track rating were associated with fatality. CONCLUSIONS: This study identified specific risk factors for fatality. The findings are consistent with the hypothesis that horses accumulating high speed exercise are predisposed to catastrophic injury. The study has also highlighted the need to investigate further the adverse effects of different track ratings on the incidence of injury and subsequent fatality. RELEVANCE: The results will facilitate the development of effective strategies to improve overall safety of horses and jockeys in flat racing in Victoria, Australia.

Recurrent rectal prolapse caused by colonic duplication in a dog.

A 9-month-old female Shar Pei cross-bred dog was presented with a history of recurrent rectal prolapse over 7 months. Repeated reduction and anal purse string sutures and subsequent incisional colopexy failed to prevent recurrent rectal prolapse. Digital rectal examination following reduction of the prolapse identified a faeces-filled sac within the ventral wall of the rectum and an orifice in the ventral colonic wall, cranial to the pubic brim. A ventral, communicating tubular colonic duplication was diagnosed by means of a barium enema. Surgical excision of the duplicated colonic tube was performed via a caudal ventral midline laparotomy. At 20 weeks post-operation, there has been no recurrence of rectal prolapse.

Risk of fatality and causes of death of Thoroughbred horses associated with racing in Victoria, Australia: 1989-2004.

REASONS FOR PERFORMING STUDY: Determining the risk of fatality of Thoroughbred horses while racing is essential to assess the impact of intervention measures designed to minimise such fatalities. OBJECTIVES: To measure the risk of racehorse fatality in jump and flat starts on racecourses in Victoria, Australia, over a 15 year period and to determine proportional mortality rates for specific causes of death. METHODS: All fatalities of Thoroughbred horses that occurred during or within 24 h of a race were identified from a database. The risk of a start resulting in a racehorse fatality in all races and within flat and jump races, proportional mortality rates, population attributable risk, population attributable fraction and risk ratios were calculated along with 95% confidence intervals. Poisson regression was also performed to estimate risk ratios. RESULTS: There were 514 fatalities over the 15 year period; 316 in flat races and 198 in jump races. The risk of fatality was 0.44 per 1000 flat starts and 8.3 per 1000 jump starts (18.9 x greater). The risk of fatality on city tracks was 1.1 per 1000 starts whereas on country tracks it was 0.57 per 1000 starts. Of the 316 fatalities in flat races, 73.4% were due to limb injury, 2.5% to cranial or vertebral injury and 19.0% were sudden deaths. Of the 198 fatalities in jump races, 68.7% were due to limb injury, 16.2% to cranial or vertebral injury and 3.5% were sudden deaths. The risk of fatality in flat starts increased between 1989 and 2004 but the risk in jump starts remained unchanged over the 15 year period. CONCLUSIONS: The risk of fatality in flat starts was lower in Victoria than North America and the UK but the risk in jump starts was greater. Catastrophic limb injury was the major reason for racehorse fatality in Victoria but there was a larger percentage of sudden deaths than has been reported overseas. The risk of fatality in jump starts remained constant over the study period despite jump racing reviews that recommended changes to hurdle and steeple races to improve safety. POTENTIAL RELEVANCE: This study provides important benchmarks for the racing industry to monitor racetrack fatalities and evaluate intervention strategies.

Transient renal tubulopathy in a racing Greyhound.

A 2-year-old female Greyhound was presented for inappetence and lethargy. On referral, results of diagnostic tests indicated renal glucosuria, increased excretion of selected amino acids and abnormal fractional excretion of electrolytes consistent with renal tubular dysfunction. Systemic blood pressure was elevated. Renal biopsy revealed mild proximal renal tubular damage consistent with a subacute toxic or hypoxic insult. Systemic hypertension, renal glucosuria and altered fractional excretion of electrolytes resolved during the 7 day period of hospital treatment. The Greyhound resumed training without recurrence of renal dysfunction.

Lymphoma(s) showing epitheliotropism and diffuse skeletal muscle involvement presenting as a polymyopathy in a young dog.

A 3-year-old dog presented with a severe polymyopathy and subsequently developed nodular skin lesions. The disease in this dog was caused by lymphoma, showing cutaneous epitheliotropism as well as infiltration of skeletal muscle in conjunction with polymyositis.

Cerebral cryptococcal granuloma in a cat.

A 7-year-old cat was presented for seizures. Cerebrospinal fluid cytology and serology were consistent with a diagnosis of toxoplasmosis. The cat was treated with clindamycin but seizures continued and additional neurological signs developed over 6 months. A mass lesion was identified in the left cerebral hemisphere using magnetic resonance imaging (MRI). The lesion enhanced after gadolidium and a tumour was considered likely. Histologically, the lesion proved to be a cryptococcal granuloma and retrospective serology confirmed that the cat had cryptococcosis at its initial presentation. This report provides the first description in the veterinary literature of the MRI appearance of a cerebral cryptococcoma and emphasises the importance of performing cryptococcal antigen determination in cats with signs of intracranial disease.

Akabane virus.

Akabane virus, an arthropod-borne Bunyavirus, is the major cause of epizootics of congenital malformations in ruminants in Australia, Japan, Korea, and Israel, and is suspected to be a cause of sporadic outbreaks elsewhere. Blood-sucking insects, such as biting midges, transmit the virus horizontally to vertebrates. Climatic factors influence the seasonal activity and geographic range of the vector population and, therefore, occurrence of related disease. Inoculated ruminants seroconvert rapidly after a short subclinical viremia. Infection is of consequence only if ruminants are pregnant and not protected by adequate specific neutralizing antibodies. In naive pregnant animals, virus may spread hematogenously to replicate and persist in trophoblastic cells of placental cotyledons and subsequently invade the fetus. A distinct tropism for immature rapidly dividing cells of the fetal central nervous system and skeletal muscle results in direct virus-induced necrotizing encephalomyelitis and polymyositis. If fetuses survive, such injury may manifest as arthrogryposis, hydranencephaly, porencephaly, microencephaly, hydrocephalus, or encephalomyelitis at term. The earlier in gestation that fetal infection occurs, the more severe the lesions, reflecting the large population of vulnerable cells and lack of fetal immunocompetency at earlier stages of pregnancy. Injury during the period of critical cell migration and differentiation in organogenesis may substantially disrupt structural development in target organs. Late gestational infections cause nonsuppurative inflammation in the brain and spinal cord, premature birth, or fetal death with stillbirth or abortion. Affected neonates are nonviable. Control is by vaccination but is not always justified economically. Akabane viral infections must be differentiated from infections with other teratogenic viruses (including related Bunyaviruses), inherited conditions, and maternal intoxications. Diagnosis is made by serology and viral isolation.

Outbreak of equine herpesvirus type 1 myeloencephalitis: new insights from virus identification by PCR and the application of an EHV-1-specific antibody detection ELISA.

Five of 10 pregnant, lactating mares, each with a foal at foot, developed neurological disease. Three of them became recumbent, developed complications and were euthanased; of the two that survived, one aborted an equine herpesvirus type 1 (EHV-1)-positive fetus 68 days after the first signs were observed in the index case and the other gave birth to a healthy foal on day 283 but remained ataxic and incontinent. The diagnosis of EHV-1 myeloencephalitis was supported by postmortem findings, PCR identification of the virus and by serological tests with an EHV-1-specific ELISA. At the time of the index case, the 10 foals all had a heavy mucopurulent nasal discharge, and PCR and the ELISA were used to detect and monitor EHV-1 infection in them. The status of EHV-1 infection in the five in-contact mares was similarly monitored. Sera from three of the affected mares, taken seven days after the index case were negative or had borderline EHV-1-specific antibody titres. In later serum samples there was an increase in the titres of EHV-1-specific antibody in two of the affected mares. In contrast, sera from the five unaffected in-contact mares were all EHV-1-antibody positive when they were first tested seven or 13 days after the index case.

Effect of oral ursodeoxycholic acid on bile acids tolerance tests in healthy dogs.

OBJECTIVE: To determine whether oral administration of ursodeoxycholic acid (UDCA) to healthy dogs alters the results of the bile acids tolerance test. METHODS: UDCA (15 mg/kg once daily) was administered to 16 healthy dogs for 7 days. Health of the dogs was assessed by clinical examination, haematology, serum biochemistry and a bile acids tolerance test. Normal liver structure was confirmed by histopathology at the end of the study. Bile acids tolerance tests were performed before and at the end of the treatment period, with each dog serving as its own control. For the posttreatment bile acids tolerance test, UDCA was administered at the time of feeding. RESULTS: Pretreatment, the fasted serum total bile acid concentrations ranged between 0 and 9 micromol/L. In the majority of dogs, the postprandial total bile acid concentration was greater than the preprandial value, with a range of 0 to 16 micromol/L. The fasted total bile acid concentration was 0 micromol/L in most dogs (93.75%) after treatment with UDCA. Postprandial serum bile acids also remained within the reference range for the majority of dogs (93.75%) after UDCA treatment. A single dog had a postprandial bile acid concentration above the reference range, but the concentration was within the reference range when the assay was repeated the following day without concurrent administration of UDCA. The pre- and postprandial total serum bile acid concentrations were not significantly affected by UDCA treatment. CONCLUSION: The administration of UDCA does not alter the bile acids tolerance test of normal healthy dogs.

Fasciola hepatica infection in farmed emus (Dromaius novaehollandiae).

OBJECTIVE: To describe two cases of infection with Fasciola hepatica in young farmed emus, subacute and chronic fasciolosis and a response to treatment of the flock with albendazole. PROCEDURE: Gross lesions were found at necropsy and hepatic lesions in microscopic examination. The parasite recovered from one emu was identified by its morphological characteristics and an egg count reduction test was carried out after treatment of the flock with albendazole. RESULTS: Hepatic lesions resembling subacute and chronic fasciolosis of ruminants were identified. An adult fluke was recovered from the liver of one of the birds and was identified as F hepatica. The eggs of the fluke were irregular in shape and size. No fluke eggs were identifiable in faeces of live emus 10 days after treatment of the flock with albendazole at a dose of 10 mg/kg. CONCLUSIONS: This is the first reported case of infection with F hepatica in farmed emus and the first report of the occurrence of Fasciola infection is the class Aves. The irregular shape and size of the eggs may be attributable to infection of an aberrant host. Treatment with albendazole eliminated eggs from the faeces of the flock.

Feline inductive odontogenic tumour in a Burmese cat.

A 7-month-old, male, Burmese cat was presented with an oral mass that had rapidly regrown following excisional biopsy 3 weeks earlier. The tumour was identified by histological examination as a feline inductive odontogenic tumour. A unilateral segmental mandibulectomy was performed. Although dental malocclusion resulted from mandibular drift to the operated side, the cat displayed minimal dysphagia post-operatively and there was no evidence of tumour regrowth 8 months after surgery. Feline inductive odontogenic tumour is a rare dental tumour described exclusively in cats under 3-years-of-age. Although histopathologically benign, feline inductive odontogenic tumour grows by expansion and can infiltrate underlying bone to cause considerable local destruction. This article is intended to increase awareness of this unusual tumour which, with complete surgical excision, carries a good prognosis. It also emphasises the importance of obtaining a histological diagnosis from oral mass lesions to direct appropriate therapy and to provide an accurate prognosis.

Hemihyperaesthesia and hyperresponsiveness resembling central pain syndrome in a dog with a forebrain oligodendroglioma.

A 4-year-old male Boxer was presented with neurological signs referable to a right forebrain lesion that was confirmed with computed tomography. Whilst characteristic signs of a unilateral forebrain lesion were observed, the dominant and striking finding was a right-sided hemisensory disturbance characterised by hyperaesthesia and hyperresponsiveness. Necropsy revealed a gelatinous mass confined to the right forebrain that was identified histologically as an oligodendroglioma. The lesion was centred on the internal capsule and involved ventral frontal and temporal lobes and the ventrolateral thalamus, including lateral and medial parts of the ventrocaudal nuclear region (ventrobasilar complex) of the thalamus. On clinical and neuroanatomical grounds, the case exhibited features in common with central pain syndrome in human patients with thalamic lesions. These included a somatosensory disorder of hyperaesthesia affecting an entire side of the head and body, behavioural manifestations consistent with spontaneous pain and a lesion involving the ventrobasilar complex. Of interest, the hemisensory abnormality was ipsilateral to the lesion, contrasting with central pain in humans, in which clinical signs are contralateral to analogous lesions. It is suggested that species-specific differences in spinal cord organisation of pain pathways, particularly the greater bilateral projection of nociceptive afferents to thalamic relay nuclei in carnivores, may account for this disparity. Notably, central pain is rare in human patients with brain tumours, even those affecting the thalamus, and this may also be the case in dogs.

Treatment of an acromegalic cat with the dopamine agonist L-deprenyl.

Acromegaly was diagnosed in a 14-year-old domestic short hair cat presented for investigation and management of apparently insulin-resistant diabetes mellitus. Treatment with L-deprenyl and high doses of insulin was commenced. The L-deprenyl did not reduce the requirement for high doses of insulin and did not appear to reduce the clinical signs associated with the disease. The cat was euthanased one year after initial presentation.

Diagnosis of sciatic nerve tumour in two dogs by electromyography and magnetic resonance imaging.

Sciatic nerve tumour was diagnosed in a Staffordshire Bull Terrier cross-bred and a Bichon Frise, both presenting with chronic left hind limb lameness. Neurological examination in each case was consistent with left sciatic nerve deficits and this was confirmed by EMG studies. Rectal examination of both dogs revealed a palpable intrapelvic mass that was not apparent on survey radiographs. A sciatic nerve tumour was identified using MRI in each case. Histological examination of tissue taken from the Staffordshire Bull Terrier cross-bred was consistent with a malignant peripheral nerve sheath tumour.

The role of Type 1, P and S fimbriae in binding of Escherichia coli to the canine endometrium.

Escherichia coli (E. coli) is the most commonly isolated infectious agent causing pyometra in bitches. Many E. coli strains isolated from the uteri of infected dogs carry several adhesin genes (fimH, papGIII and sfa). The objective of this study was to investigate the role of each adhesin gene product, acting alone or expressed in combination, in the bacterial binding to canine endometrium. E. coli strain P3, which was isolated from a uterus of a bitch naturally affected with pyometra, was shown by PCR to carry all three known fimbrial adhesin genes fimH, papGIII and sfa. Knockout (KO) mutants of this wildtype (P3-wt) strain were generated using insertional inactivation. Adhesion assays on anoestrous uteri of three post-pubertal bitches were undertaken. Overall, the number of bacteria adhering to canine endometrial biopsies was comparable between strains and no significant difference in the number of bound bacteria was found between the P3-wt strain and the single or double KO-strains. However, the triple knockout strain displayed less binding to the canine endometrium compared with the P3-wt strain. This study shows that a pathogenic E. coli strain (P3) isolated from the uterus of a bitch with pyometra was able to fully compensate for the loss of two of its three known adhesin genes. It was necessary to inactivate all three known adhesin genes in order to see a significant decrease in binding to canine endometrium.