Rhabdomyolysis, myoglobinuric nephrosis, and crystalline nephropathy in a captive bottlenose dolphin.

A 5-y-old female bottlenose dolphin (Tursiops truncatus) from an aquarium in Japan had clinical signs of anorexia, vomiting, and bradykinesia. Enrofloxacin and lactated Ringer solution were administered for treatment of bacterial infection and for rehydration. Elevations of creatine kinase and aspartate aminotransferase activities were detected on day 4 of treatment, indicating that rhabdomyolysis had developed on day 3. On day 5, serum creatinine and urea concentrations increased and remained high throughout the remaining treatment; the dolphin died on day 16. Postmortem examination revealed massive necrosis of the longissimus dorsi muscles. Histologic examination revealed extensive necrosis of skeletal myofibers, multifocal renal tubular necrosis with intratubular casts and crystals, and suppurative bronchopneumonia. The renal casts labeled positively with anti-myoglobin antibody; expression of aquaporin-1 was decreased in renal tubules compared to normal kidney tissue. To our knowledge, this description of clinicopathologic findings of rhabdomyolysis leading to acute kidney injury with concomitant crystalline nephropathy has not been reported previously in a bottlenose dolphin.

Histological survey for oxalate nephrosis in Victorian koalas (Phascolarctos cinereus).

The Mount Lofty Ranges koala (Phascolarctos cinereus) population in South Australia has a high prevalence of the renal disease oxalate nephrosis, for which an underlying genetic cause is suspected. South Australian koalas primarily originate from those in French Island, Victoria; however, oxalate nephrosis has not previously been reported in Victorian koalas. Examination of kidney tissue sections from 63 koalas across Victoria found that nine koalas were affected by oxalate nephrosis (14.3%). These included 2/5 koalas from French Island (40%), 4/14 koalas from the western regions (29%), 2/11 Raymond Island koalas (18%), and 1/13 Cape Otway koalas (8%). There were no cases of oxalate nephrosis identified in the Strzelecki koalas (n = 12). These findings suggest that oxalate nephrosis occurs in koalas from French Island and populations that have received significant influx of koalas from French Island, but not in the Strzelecki region, which has little to no French Island input. This lends support to the theory that an inherited abnormality of oxalate metabolism could underlie the high prevalence of oxalate nephrosis in the Mount Lofty Ranges koala population, and molecular investigations are currently underway to investigate a genetic cause.

Symmetric dimethylarginine values in koalas (Phascolarctos cinereus) based on oxalate nephrosis status.

Oxalate nephrosis is a prevalent renal disease in koalas (Phascolarctos cinereus) of the Mount Lofty Ranges population in South Australia. The symmetric dimethylarginine (SDMA) assay is widely used in companion animals to diagnose renal disease, particularly in the early stages. This study aimed to determine: (1) reference intervals for SDMA in koalas and (2) SDMA values of koalas with oxalate nephrosis. Blood samples were collected from 41 Mount Lofty Ranges koalas euthanased on welfare grounds. Koalas were necropsied and, based on renal histopathology, were classified as unaffected (n = 22) or affected (n = 19) by oxalate nephrosis. Serum or plasma samples were analysed for creatinine, urea and SDMA and urine samples for urine specific gravity (USG). The reference interval for SDMA in unaffected koalas was 2.4-22.9 µg/dL. In koalas with oxalate nephrosis, SDMA was elevated in 74% of cases above the upper limit of the confidence interval. SDMA was elevated in three affected koalas with normal creatinine values. A positive correlation was found between SDMA and creatinine (R = 0.775, P < 0.001) and SDMA and urea (R = 0.580, P < 0.001) and a negative correlation between SDMA and USG (R = -0.495, P = 0.027). In conclusion, SDMA correlates well with other commonly used tests of renal function in koalas and should be included as part of the standard diagnostic process to increase the accuracy of oxalate nephrosis diagnosis in koalas.

Oxalate-degrading bacteria, including Oxalobacter formigenes, colonise the gastrointestinal tract of healthy koalas (Phascolarctos cinereus) and those with oxalate nephrosis.

BACKGROUND: Koalas in the Mount Lofty Ranges, South Australia, have a high prevalence of oxalate nephrosis, or calcium oxalate kidney crystals. Gastrointestinal tract oxalate-degrading bacteria, particularly Oxalobacter formigenes, have been identified in other animal species and humans, and their absence or low abundance is postulated to increase the risk of renal oxalate diseases. This study aimed to identify oxalate-degrading bacteria in the gastrointestinal tract of koalas and determine their association with oxalate nephrosis. METHODS: Caecal and faecal samples were collected at necropsy from 22 Mount Lofty Ranges koalas that had been euthanased on welfare grounds, with 8 koalas found to have oxalate nephrosis by renal histopathology. Samples were analysed by PCR for the oxc gene, which encodes oxalyl-CoA decarboxylase, and also by Illumina sequencing of the V3-V4 region of the bacterial 16S rRNA gene. RESULTS: The oxc gene was detected in 100% of koala samples, regardless of oxalate nephrosis status. Oxalobacter formigenes was detected in all but one faecal sample, with no difference in abundance between koalas affected and unaffected by oxalate nephrosis. Other species of known oxalate-degrading bacteria were infrequently detected. CONCLUSION: This is the first study to identify Oxalobacter and other oxalate-degrading bacterial species in koalas, but an association with oxalate nephrosis and absence or low abundance of Oxalobacter was not found. This suggests other mechanisms underlie the risk of oxalate nephrosis in koalas.

Necropsy findings of koalas from the Mount Lofty Ranges population in South Australia.

OBJECTIVE: This study reports necropsy findings of koalas from the Mount Lofty Ranges region in order to identify health threats to this mainland South Australian population. METHODS: Koalas from the Mount Lofty Ranges region (n = 85) that had died or been euthanased on welfare grounds were examined at necropsy during 2012-13 at the School of Animal and Veterinary Sciences, University of Adelaide. Disease findings, approximate age, sex and body condition of koalas were recorded. Histopathological examination was undertaken on gross lesions and in suspect cases, skin scrapings taken for microscopy and PCR performed for Chlamydia pecorum detection. RESULTS: Traumatic injury was the most common necropsy finding (48/85; 57%), caused by motor vehicle accidents (35/48; 73%), canine attacks (11/48; 23%) or bushfire burns (2/48; 4%). Oxalate nephrosis (27/85; 32%) was also more common than other conditions. Infectious diseases included chlamydiosis (10/85; 12%) and sarcoptic mange (7/85; 8%). Marked testis asymmetry was evident in 11% (6/56) of males, with histopathology suggestive of atrophic change in four animals. Other pathological conditions included gastrointestinal disease (7/85; 8%) and respiratory disease (3/85; 4%). Almost half of the koalas (38/85; 45%) were found to have two or more abnormalities at necropsy. CONCLUSION: This study found trauma, mainly from motor vehicle accidents, and oxalate nephrosis to be the predominant causes of death and/or disease in koalas from the Mount Lofty Ranges region. Recent emergence of both clinical chlamydiosis and sarcoptic mange has also occurred, providing insight into the health status and causes of disease or injury in this South Australian mainland koala population.

Pathological and molecular studies of the renal trematode Paratanaisia bragai in Indian peafowls (Pavo cristatus).

Endoparasitic diseases are commonly encountered in free-ranging birds. Although not all endoparasites cause disease, persistent infection with large numbers of parasites almost always affects normal physiological functions, leading to deleterious effects on the host. This paper describes the anatomopathological alterations caused by the renal trematode Paratanaisia bragai in Indian peafowl (n = 3) and examines the phylogeny of these and related parasites. Peafowl from forests in and around the Bareilly region, Uttar Pradesh, India, were necropsied, and microscopic and molecular investigations were performed. The peafowl were confirmed to be infected with P. bragai. Significant gross pathological lesions suggested nephrosis, and microscopic findings indicated a mild-to-moderate degree of nephrosis caused by the parasites in the tissue. The parasites were identified as P. bragai by histomorphological analysis of adult and eggs in the ureters, and the identification was confirmed by PCR and phylogenetic analysis. Nucleotide sequencing of the PCR products from the renal trematodes recovered from Indian peafowl revealed a close association with P. bragai from Columbiformes in the United Kingdom and Spain. The pathology and molecular epidemiology of parasitic diseases affecting peafowl is not well understood in India. This is the first report from India and the second report worldwide to document P. bragai infection in peafowl.

Pathology and Epidemiology of Oxalate Nephrosis in Cheetahs.

To investigate cases of acute oxalate nephrosis without evidence of ethylene glycol exposure, archived data and tissues from cheetahs ( Acinonyx jubatus) from North America ( n = 297), southern Africa ( n = 257), and France ( n = 40) were evaluated. Renal and gastrointestinal tract lesions were characterized in a subset of animals with ( n = 100) and without ( n = 165) oxalate crystals at death. Crystals were confirmed as calcium oxalate by Raman spectroscopy in 45 of 47 cheetahs tested. Crystals were present in cheetahs from 3.7 months to 15.9 years old. Cheetahs younger than 1.5 years were less likely to have oxalates than older cheetahs ( P = .034), but young cheetahs with oxalates had more oxalate crystals than older cheetahs ( P < .001). Cheetahs with oxalate crystals were more likely to have renal amyloidosis, interstitial nephritis, or colitis and less likely to have glomerular loop thickening or gastritis than those without oxalates. Crystal number was positively associated with renal tubular necrosis ( P ≤ .001), regeneration ( P = .015), and casts ( P ≤ .001) but inversely associated with glomerulosclerosis, renal amyloidosis, and interstitial nephritis. Crystal number was unrelated to the presence or absence of colitis and was lower in southern African than American and European animals ( P = .01). This study found no evidence that coexisting chronic renal disease (amyloidosis, interstitial nephritis, or glomerulosclerosis), veno-occlusive disease, gastritis, or enterocolitis contributed significantly to oxalate nephrosis. Oxalate-related renal disease should be considered as a potential cause of acute renal failure, especially in young captive cheetahs. The role of location, diet, stress, and genetic predisposition in the pathogenesis of oxalate nephrosis in cheetahs warrants further study.

Clinico-pathological findings in a striped dolphin (Stenella coeruleoalba) affected by rhabdomyolysis and myoglobinuric nephrosis (capture myopathy).

A striped dolphin (Stenella coeruleoalba) calf stranded alive because of a Salter-Harris fracture type 1 of a caudal vertebra and remained in a provisional rehabilitation facility for 3 days where the fracture stabilization was attempted, but he died the day after bandaging. Serum and urine samples were collected during hospitalization (days 1, 2 and 3 serum and day 2 urine). Serum analysis showed increased urea, alanine transaminase, aspartate transaminase, and serum amyloid A values, while creatinine was below the lower limit. Urine analysis showed urinary protein-to-creatinine ratio of 5.3 with glomerular proteinuria. Postmortem analyses demonstrated a severe rhabdomyolysis and myoglobinuric nephrosis, suggestive of capture myopathy syndrome. We report, for the first time, the clinico-pathological changes during this condition in a striped dolphin.

Intoxicação por Metternichia princeps (Solanaceae) em caprinos no estado da Bahia / Poisoning by Metternichia princeps (Solanaceae) in goats in the state of Bahia, Brazil

Descreve-se um surto de intoxicação por Metternichia princepsem caprinos no Estado da Bahia. De oito caprinos, três morreram, dos quais dois foram necropsiados; cinco não adoeceram. Os principais sinais clínicos caracterizaram-se por secreção nasal mucosa, emagrecimento, diarreia, apatia, debilidade leve, andar cambaleante, flexão dos membros torácicos e pélvicos, decúbito esterno-abdominal e decúbito lateral, seguidos de morte após aproximadamente dois dias de evolução clínica. Na necropsia foi observado edema pulmonar, hidrotórax, hidropericárdio, ascite, rins pálidos, edema perirrenal e hemorragias no tecido subcutâneo. Microscopicamente nos rins havia acentuada necrose de coagulação do epitélio tubular e túbulos com regeneração do epitélio. No pulmão havia acentuada congestão associada a edema interalveolar e interseptal. Na bioquímica sanguínea observou-se aumento na ureia, creatinina e creatinina fosfoquinase.

An outbreak of poisoning by Metternichia princepsis reported in goats from the State of Bahia. Out of eight goats three showed symptoms of poisoning and died; on two of them post-mortem examinations were performed. The main clinical signs were nasal mucous secretion, weight loss, diarrhea, lethargy, mild weakness, staggering gait, flexion of the fore and hind limbs, sternal recumbence, and lateral recumbence followed by death after approximately two days of clinical manifestations. The serum concentration of urea and creatinine and the serum activities of creatine phosphokinase were increased. At necropsy pulmonary edema, hydrothorax, hydropericardium, ascites, pale kidneys, perirenal edema and hemorrhages in the subcutaneous tissue were observed. Microscopically the kidneys showed accentuated coagulation necrosis of the tubular epithelium and tubules and epithelial regeneration. In the lungs there was accentuated congestion associated with interalveolar and interseptal edema.

Spontaneous glomerular mesangial lesions in common marmoset monkeys (Callithrix jacchus): a benign non-progressive glomerulopathy.

BACKGROUND: Common marmosets are known to develop an IgM glomerulopathy, which has been linked with 'wasting marmoset' syndrome. This study investigated renal pathology in a colony of marmosets, with and without weight loss. METHODS: Renal histology, immunofluorescence, and electron microscopy were performed on marmosets euthanized for research or for weight loss. Serum and urine biochemistry were measured during life and at euthanasia. RESULTS: Histology from 25 adult marmosets (19 research and 6 weight loss) showed mesangial expansion in the majority of glomeruli. Mesangial changes correlated with electron-dense deposits and IgM deposition by immunofluorescence; negligible other pathology was seen. Glomerular basement membrane thickness appeared increased compared to reported human measurements. Low-grade proteinuria was present in all animals, but did not progress. Renal function was normal in all animals. CONCLUSIONS: Marmosets develop a glomerulopathy characterized by mesangial expansion, IgM deposition, and proteinuria. This is a benign occurrence and not specifically associated with weight loss.

Plasma biochemistry and urinalysis variables of koalas (Phascolarctos cinereus) with and without oxalate nephrosis.

BACKGROUND: Oxalate nephrosis is a highly prevalent disease in the Mount Lofty Ranges koala population in South Australia, but associated clinicopathologic findings remain undescribed. OBJECTIVES: The aims of this study were to determine plasma biochemical and urinalysis variables, particularly for renal function and urinary crystal morphology and composition, in koalas with oxalate nephrosis. METHODS: Blood and urine samples from Mount Lofty Ranges koalas with oxalate nephrosis were compared with those unaffected by renal oxalate crystal deposition from Mount Lofty and Kangaroo Island, South Australia and Moggill, Queensland. Plasma and urine biochemistry variables were analyzed using a Cobas Bio analyzer, and urinary oxalate by high-performance liquid chromatography. Urinary crystal composition was determined by infrared spectroscopy and energy dispersive X-ray analysis. RESULTS: Azotemia (urea > 6.6 mmol/L, creatinine > 150 µmol/L) was found in 93% of koalas with oxalate nephrosis (n = 15). All azotemic animals had renal insufficiency (urine specific gravity [USG] < 1.035), and in 83%, USG was < 1.030. Koalas with oxalate nephrosis were hyperoxaluric compared with Queensland koalas (P < .01). Urinary crystals from koalas with oxalate nephrosis had atypical morphology and were composed of calcium oxalate. Mount Lofty Ranges koalas unaffected by renal oxalate crystal deposition had renal insufficiency (43%), although only 14% had USG < 1.030 (n = 7). Unaffected Mount Lofty Ranges and Kangaroo Island koalas were hyperoxaluric compared with Queensland koalas (P < .01). CONCLUSIONS: Koalas with oxalate nephrosis from the Mount Lofty Ranges had renal insufficiency, hyperoxaluria, and pathognomonic urinary crystals. The findings of this study will aid veterinary diagnosis of this disease.

Diagnostic exercise: hemolysis and sudden death in lambs.

Within a 24-hour period, 7 out of 200 three- to four-week-old pastured Katahdin lambs died after showing clinical signs of hemoglobinuria, red-tinged feces, weakness, and recumbency. One of the lambs that was examined clinically before natural death also had abdominal pain, trembling, tachycardia, and severe anemia with a packed cell volume of 4%. Pathologic findings included icterus, hemoglobinuric nephrosis, dark red urine, pulmonary edema, hydrothorax, splenomegaly, and acute centrilobular to midzonal hepatocellular degeneration and necrosis with cholestasis. The differential diagnoses and diagnostic workup to achieve the diagnosis are briefly discussed.

Pathological features of oxalate nephrosis in a population of koalas (Phascolarctos cinereus) in South Australia.

The wild and captive koala population of the Mt Lofty Ranges in South Australia has a high level of renal dysfunction in which crystals consistent with calcium oxalate have been observed in the kidneys. This study aimed to describe the pathological features of the renal disease in this population, confirm the composition of renal crystals as calcium oxalate, and determine whether any age or sex predispositions exist for this disease. A total of 51 koalas (28 wild rescues, 23 captive) were examined at necropsy, of which 28 (55%) were found to have gross and/or histological evidence of oxalate nephrosis. Histopathological features included intratubular and interstitial inflammation, tubule dilation, glomerular atrophy, tubule loss, and cortical fibrosis. Calcium oxalate crystals were demonstrated using a combination of polarization microscopy, alizarin red S staining, infrared spectroscopy, and energy-dispersive X-ray analysis with scanning electron microscopy. Uric acid and phosphate deposits were also shown to be present but were associated with minimal histopathological changes. No significant differences were found between the numbers of affected captive and wild rescued koalas; also, there were no sex or age predispositions identified, but it was found that oxalate nephrosis may affect koalas <2 years of age. The findings of this study suggest that oxalate nephrosis is a leading disease in this koala population. Possible causes of this disease are currently under investigation.

Suspected poisoning of cattle by scarlet pimpernel (Lysimachia arvensis L.).

The ingestion of scarlet pimpernel (Lysimachia arvensis L.), also known as red chickweed, has been reported as a cause of death of cattle in Uruguay, and as the suspected cause of deaths of sheep in Australia. It has not previously been reported in association with deaths of cattle in Australia. We report the clinical and pathological findings from four cattle in western Victoria that died with a nephrosis suspected to be secondary to intoxication with scarlet pimpernel.

Nephritis associated with infectious bronchitis virus Cal99 variant in game chickens.

Infectious bronchitis virus (IBV) Cal99 variant was isolated from the kidneys of seven 2-5-mo-old game chickens with nephritis and respiratory disease. IBV Cal99 variant is usually associated with respiratory disease in broiler chickens in California. Macroscopically, the majority of the birds had moderately to severely enlarged and mottled pale kidneys, with increased urates in the ureters. Microscopically, most of the birds had acute nephrosis and interstitial nephritis. The birds also had sinusitis, tracheitis, bronchopneumonia, airsacculitis, salivary gland adenitis, and lymphoid depletion in the thymus and bursa of Fabricius. Immunohistochemistry was strongly positive for IBV antigen in the cytoplasm of tubular epithelial cells in the kidneys and also in the epithelium of the respiratory tract, salivary glands, proventriculus, intestine, and bursa of Fabricius. Infectious bronchitis virus was isolated from the trachea, lungs, kidneys, and cecal tonsils. Sequencing of the hypervariable region of the S1 gene of the kidney IBV isolate, designated IBV/CA99variant/07, revealed that the virus was 98% homologous to the Cal99 serotype of IBV.

Acute oxalate intoxication associated to ingestion of eshnan (Seidlitzia rosmarinus) in sheep.

An outbreak of acute oxalate intoxication in a sheep flock was associated to Seidlitzia rosmarinus (Chenopodiaceae) with a mortality rate of about 19%. Affected sheep showed marked azotemia and hypocalcemia. Post-mortem findings included congestion and hemorrhage in visceral organs, ruminitis frequently associated with precipitation of birefringent calcium oxalate crystals, and acute nephrosis with numerous birefringent calcium oxalate crystals in renal tubules. This is the first report of oxalate poisoning due to ingestion of S. rosmarinus in sheep.

Putative Aspergillus niger-induced oxalate nephrosis in sheep.

A sheep farmer provided a maize-based brewer's grain (mieliemaroek) and bales of Eragrostis curvula hay to ewes and their lambs, kept on zero-grazing in pens. The 'mieliemaroek' was visibly mouldy. After 14 days in the feedlot, clinical signs, including generalised weakness, ataxia of the hind limbs, tremors and recumbency, were noticed. Six ewes died within a period of 7 days. A post mortem examination was performed on 1 ewe. The carcass appeared to be cachectic with mild effusions into the body cavities; mild lung congestion and pallor of the kidneys were observed. Microscopical evaluation revealed nephrosis and birefringent oxalate crystals in the renal tubules when viewed under polarised light. A provisional diagnosis of oxalate nephrosis with subsequent kidney failure was made. Amongst other fungi, Aspergillus niger was isolated from 'mieliemaroek' samples submitted for fungal culture and identification. As A. niger is known to synthesise oxalates, a qualitative screen to detect oxalic acid in the mieliemaroek and purified A. niger isolates was performed using high-performance liquid chromatography (HPLC). Oxalic acid was detected, which supported a diagnosis of soluble oxalate-induced nephropathy.

Copper toxicosis with hemolysis and hemoglobinuric nephrosis in three adult Boer goats.

Acute and, particularly, chronic copper exposures, along with defects in hepatic copper metabolism, altered excretion of copper, and/or nutritional imbalances between copper and other trace elements, can lead to hepatic accumulation of copper and primary copper toxicosis. There is interspecies variation in susceptibility to copper toxicosis, with sheep being the species most likely to develop this condition. Adult dairy goats and Boer crosses are generally considered resistant to chronic copper toxicosis, especially the hemolytic stage of this disease. The current report is rather unusual in that it describes instances of naturally occurring copper toxicosis with hemolysis and hemoglobinuric nephrosis in 3 adult Boer goats. In 2 of these goats, a possible source of excessive dietary copper was investigated but not definitively identified. In the third goat, the etiologic factors associated with the copper toxicosis were not determined. It appears that mature Boer goats are susceptible to the hemolytic stage of chronic copper toxicosis, which was not observed in a recent, large-scale copper intoxication involving lactating dairy goats. Copper analyses on both liver and kidney samples were necessary to confirm the diagnosis of copper toxicosis in all 3 goats. All feedstuffs associated with instances of copper toxicosis should be analyzed for iron, molybdenum, sulphur, and zinc as well as copper to determine what nutritional factors are contributing to the pathogenesis of this disease. Consideration also should be given to the ingestion of hepatotoxic plants and other toxic exposures, which could predispose an animal to secondary chronic copper toxicosis.