Postmortem Evaluation Research Articles

Utilizing mobile digital radiography for detection of thoracolumbar vertebrae traits in live donkeys.

It has been well-established that the number of vertebrae is associated with body size and meat productivity. In current study we utilized a digital radiography (DR) technology to detect the number of thoracolumbar vertebrae in live donkeys. For this purpose, we introduced for the first time a groundbreaking device designed by our team for assessing thoracolumbar vertebrae number traits in equids, employing a sample of 1,000 donkeys sourced from five distinct donkey farms. This assessment incorporates a range of crucial body metrics, including body height, length, and various other measurements. Subsequently, our study determined the number of thoracolumbar vertebrae in 112 donkeys, utilizing the DR system. These findings were further validated through post-mortem evaluations conducted by slaughtering the donkeys. Our findings demonstrated a remarkable resemblance between the thoracolumbar vertebrae numbers visualized through the DR system in live donkeys and those obtained via slaughter verification. In conclusion, this research underscores the accuracy and effectiveness of the DR system for the detection of thoracolumbar vertebrae in live donkeys, which might be helpful for assessing the body size and meat productivity. We also recommended the utilization of DR system for counting thoracolumbar vertebrae in other animals in live state and could be a useful addition to livestock business industry for the prediction of body size and meat productivity efficiency.

Anticoagulant Rodenticide Toxicity in Terrestrial Raptors: Tools to Estimate the Impact on Populations in North America and Globally.

Anticoagulant rodenticides (ARs) have caused widespread contamination and poisoning of predators and scavengers. The diagnosis of toxicity proceeds from evidence of hemorrhage, and subsequent detection of residues in liver. Many factors confound the assessment of AR poisoning, particularly exposure dose, timing and frequency of exposure, and individual and taxon-specific variables. There is a need, therefore, for better AR toxicity criteria. To respond, we compiled a database of second-generation anticoagulant rodenticide (SGAR) residues in liver and postmortem evaluations of 951 terrestrial raptor carcasses from Canada and the United States, 1989 to 2021. We developed mixed-effects logistic regression models to produce specific probability curves of the toxicity of ∑SGARs at the taxonomic level of the family, and separately for three SGARs registered in North America, brodifacoum, bromadiolone, and difethialone. The ∑SGAR threshold concentrations for diagnosis of coagulopathy at 0.20 probability of risk were highest for strigid owls (15 ng g-1 ) lower and relatively similar for accipitrid hawks and eagles (8.2 ng g-1 ) and falcons (7.9 ng g-1 ), and much lower for tytonid barn owls (0.32 ng g-1 ). These values are lower than those we found previously, due to compilation and use of a larger database with a mix of species and source locations, and also to refinements in the statistical methods. Our presentation of results on the family taxonomic level should aid in the global applicability of the numbers. We also collated a subset of 440 single-compound exposure events and determined the probability of SGAR-poisoning symptoms as a function of SGAR concentration, which we then used to estimate relative SGAR toxicity and toxic equivalence factors: difethialone, 1, brodifacoum, 0.8, and bromadiolone, 0.5. Environ Toxicol Chem 2024;00:1-11. © 2024 His Majesty the King in Right of Canada and The Authors. Environmental Toxicology and Chemistry published by Wiley Periodicals LLC on behalf of SETAC Reproduced with the permission of the Minister of Environment and Climate Change Canada.

Intravenous Reelin rescues despair-like behavior, Reelin cells in the dentate sub-granular zone, and spleen atrophy in the cyclic corticosterone model of recurring depressive episodes.

Novel antidepressants are predominantly evaluated preclinically in rodent models of chronic stress in which animals experience a single prolonged exposure to chronic stress prior to treatment. Rodent models of a single episode of chronic stress translate poorly to human depressive disorders, which are commonly marked by recurring depressive episodes. Intravenous administration of Reelin has previously been shown to resolve immobility in the forced swim test of rats exposed to a single prolonged exposure to chronic stress. To determine whether Reelin has antidepressant-like properties in a model of recurring depressive episodes, Long-Evans rats (N = 57) were exposed to multiple cycles of chronic stress and stress-free periods before the administration of a single injection of Reelin during the final cycle of chronic stress. The animals then performed in the forced swim test and open field test before the post-mortem evaluation of Reelin cell counts in the sub-granular zone of the dentate gyrus to determine the impact of treatment on hippocampal Reelin levels and spleen white pulp to evaluate the role of Reelin treatment in peripheral inflammation. The results show a single Reelin injection reversed elevated levels of immobility in the forced swim test in both male and female subjects exposed to the cyclic chronic stress model of recurring depressive episodes. Treatment with Reelin also restored Reelin-positive cell counts in the dentate gyrus sub-granular zone and reversed atrophy of spleen white pulp. The results shown here indicate that treatment with Reelin could effectively resolve alterations in forced swim test behavior caused by the cyclic corticosterone model of recurring depressive episodes and that Reelin homeostasis is important for regulating stress-related inflammation. Future preclinical antidepressant research should incorporate models of multiple depressive episodes to improve the translation of preclinical rodent research to human depressive disorders.

Fatal leptospirosis in endangered Barbary macaques (Macaca sylvanus) kept in captivity: Assessing the role of sympatric rodents

Between December 2020 and January 2021, an outbreak of acute mortality in endangered Barbary macaques (Macaca sylvanus) kept in captivity was detected in a zoo in Spain. The main findings observed in the two fatally affected animals at post-mortem evaluation were jaundice, renal tubular necrosis and interstitial nephritis. Leptospira spp. infection was confirmed by real time PCR (qPCR) in different tissues in both individuals. Analyses of secY gene from a positive individual showed 100% homology with a previously published sequence corresponding to Leptospira interrogans serovar Copenhageni. Free-living sympatric brown rats (Rattus norvegicus) from the affected zoo were also analyzed, and showed a prevalence and seroprevalence of Leptospira spp. of 18.2% (4/22; 95% CI: 2.1–34.3) and 41.9% (26/62; 95% CI: 29.7–54.2), respectively. We detected seropositive sera to five different serovars of Leptospira spp. (Copenhageni, Grippotyphosa, Pomona, Canicola and Hardjo) in the rodent population, with L. Copenhageni being the predominant one. This study describes for first time an outbreak of fatal leptospirosis in captive non-human primates in Europe. Our results show that Barbary macaques, an endangered species, are highly susceptible to Leptospira spp. infection, with sympatric wild rodents being the most likely reservoir animals involved in transmission in this outbreak. Our results suggest that rodent control could be an effective measure for minimizing exposure to Leptospira spp. in zoological collections. Given the potential implications for conservation, animal and public health, non-human primates and rodents should be included in surveillance programs for Leptospira spp. in zoos.

Association of Antenatal Evaluations with Postmortem and Genetic Findings in the Series of Fetal Osteogenesis Imperfecta

Introduction: Counseling osteogenesis imperfecta (OI) pregnancies is challenging due to the wide range of onsets and clinical severities, from perinatal lethality to milder forms detected later in life. Methods: Thirty-eight individuals from 36 families were diagnosed with OI through prenatal ultrasonography and/or postmortem clinical and radiographic findings. Genetic analysis was conducted on 26 genes associated with OI in these subjects that emerged over the past 20 years; while some genes were examined progressively, all 26 genes were examined in the group where no pathogenic variations were detected. Results: Prenatal and postnatal observations both consistently showed short limbs in 97%, followed by bowing of the long bones in 89%. Among 32 evaluated cases, all exhibited cranial hypomineralization. Fractures were found in 29 (76%) cases, with multiple bones involved in 18 of them. Genetic associations were disclosed in 27 families with 22 (81%) autosomal dominant and five (19%) autosomal recessive forms, revealing 25 variants in six genes (COL1A1, COL1A2, CREB3L1, P3H1, FKBP10, and IFITM5), including nine novels. Postmortem radiological examination showed variability in intrafamily expression of CREBL3- and P3H1-related OI. Conclusion: Prenatal diagnosis for distinguishing OI and its subtypes relies on factors such as family history, timing, ultrasound, genetics, and postmortem evaluation.

Perineuronal net deglycosylation associates with tauopathy-induced gliosis and neurodegeneration.

Alzheimer's disease (AD) is a progressive neurodegenerative disorder characterized by clinical symptoms of memory and cognitive deficiencies. Postmortem evaluation of AD brain tissue shows proteinopathy that closely associate with the progression of this dementing disorder, including the accumulation of extracellular beta amyloid (Aβ) and intracellular hyperphosphorylated tau (pTau) with neurofibrillary tangles (NFTs). Current therapies targeting Aβ have limited clinical efficacy and life-threatening side effects and highlight the need for alternative treatments targeting pTau and other pathophysiologic mechanisms driving AD pathogenesis. The brain's extracellular matrices (ECM), particularly perineuronal nets (PNNs), play a crucial role in brain functioning and neurocircuit stability, and reorganization of these unique PNN matrices has been associated with the progression of AD and accumulation of pTau in humans. We hypothesize that AD-associated changes in PNNs may in part be driven by the accumulation of pTau within the brain. In this work, we investigated whether the presence of pTau influenced PNN structural integrity and PNN chondroitin sulfate-glycosaminoglycan (CS-GAG) compositional changes in two transgenic mouse models expressing tauopathy-related AD pathology, PS19 (P301S) and Tau4RTg2652 mice. We show that PS19 mice exhibit an age-dependent loss of hippocampal PNN CS-GAGs, but not the underlying aggrecan core protein structures, in association with pTau accumulation, gliosis, and neurodegeneration. The loss of PNN CS-GAGs were linked to shifts in CS-GAG sulfation patterns to favor the neuroregenerative isomer, 2S6S-CS. Conversely, Tau4RTg2652 mice exhibit stable PNN structures and normal CS-GAG isomer composition despite robust pTau accumulation, suggesting a critical interaction between neuronal PNN glycan integrity and neighboring glial cell activation. Overall, our findings provide insights into the complex relationship between PNN CS-GAGs, pTau pathology, gliosis, and neurodegeneration in mouse models of tauopathy, and offer new therapeutic insights and targets for AD treatment.

Clinical and molecular characteristics of 26 fetuses with lethal multiple congenital contractures.

Multiple congenital contractures (MCC) due to fetal akinesia manifest across a broad spectrum of diseases, ranging from mild distal arthrogryposis to lethal fetal akinesia deformation sequence. We hereby present a series of 26 fetuses displaying severe MCC phenotypes from 18 families and describe detailed prenatal ultrasound findings, postmortem clinical evaluations, and genetic investigations. Most common prenatal findings were abnormal facial profile (65%), central nervous system abnormalities (62%), polyhydramnios (50%), increased nuchal translucency (50%), and fetal hydrops (35%). Postmortem examinations unveiled additional anomalies including facial dysmorphisms, dysplastic skeletal changes, ichthyosis, multiple pterygia, and myopathy, allowing preliminary diagnosis of particular Mendelian disorders in multiple patients. Evaluation of the parents revealed maternal grip myotonia in one family. By exome sequencing and targeted testing, we identified causative variants in ACTC1, CHST14, COG6, DMPK, DOK7, HSPG2, KLHL7, KLHL40, KIAA1109, NEB, PSAT1, RAPSN, USP14, and WASHC5 in 15 families, and one patient with a plausible diagnosis associated with biallelic NEB variants. Three patients received a dual diagnosis. Pathogenic alterations in newly discovered genes or in previously known genes recently linked to new MCC phenotypes were observed in 44% of the cohort. Our results provide new insights into the clinical and molecular landscape of lethal MCC phenotypes.

Stress relaxation cracking susceptibility evaluation in 347H stainless steel welds

AbstractStress relaxation cracking (SRC) has been reported as a dominant failure mechanism for 347H stainless steel welds at elevated service temperatures, occurring in either the heat-affected zone (HAZ) or fusion zone (FZ). In this study, SRC susceptibility of physically simulated HAZ and cross-welded E347-347H stainless steel welds was studied using a four-step accelerated SRC test with a thermomechanical physical simulator. The stress and temperature range studied represents weld-induced residual stress at 150–600 MPa and post-weld heat treatment temperatures between 800 and 1050 °C. For all temperature conditions, the cross-welded samples failed at a lower critical stress threshold than the simulated HAZ. A finite element model of a 50.8-mm-thick single-V groove weld was used to generate the residual stress maps induced by a 40-pass welding procedure, which in combination with the experimental threshold stress map predicted potential SRC failure locations. Postmortem microstructural evaluations were performed to identify contributing characteristics to SRC. It was found that HAZ samples exhibited a combination of creep void development, secondary cracks with intergranular fracture near grain boundary carbides, and eutectic phases. FZ samples showed brittle fracture with cracks propagating along straight, non-tortuous interdendritic grain boundaries.

Getting clues from nature: the impact of grass hay on suckling piglets' gastrointestinal growth and colonic microbiota.

The effect of dietary fiber on pig production has been extensively evaluated. Inspired by observations of the diet of wild, young piglets, this study aimed to examine the possibility of feeding grass hay to suckling piglets besides concentrated creep feed. The sow-nursed piglets in this study were divided into two groups based on balanced sow parities. The control group (CON, n = 7 sows) only received a regular, concentrated creep feed, while the treatment piglets (GH, n = 8 sows) were also provided with chopped grass hay from 2 days of age until weaning (28 days). At weaning, one piglet with a median weight was selected from each litter for post-mortem evaluation. Subsequently, six pigs around median weight per sow were grouped into nursery pens and monitored for their feed intake and body weight gain until 9 weeks of age. Piglets in GH consumed, on average, 57 g of grass hay per piglet during the entire lactation period. The emptied weight of the small and large intestine was significantly greater in GH (280 vs. 228 g, 88.8 vs. 79.3 g, respectively, p < 0.05), and the length of the large intestine was stimulated by the grass hay (164 vs. 150 cm, p < 0.05). Morphologically, the villus height in the jejunum was higher in GH (p < 0.05). In the large intestine, the crypt depth of the mid-colon was lower in GH. Moreover, the short-chain fatty acid (SCFA) concentrations in the cecum were increased in GH compared to CON (1,179 vs. 948 µmol/g dry matter, p < 0.05), whereas in the colon, SCFA concentrations were lower in CON (341 vs. 278 µmol/g dry matter, p < 0.05). There was no major impact of grass hay inclusion on the colonic microbiota composition. Only a trend was observed for a lower inverse of the classical Simpson (InvSimpon) index and a higher abundance of Lactobacillus genera in GH. After weaning, no significant differences in feed intake and body weight gain were observed. Inconclusion, supplementing the grass hay to suckling piglets led to alterations in intestinal morphology, increased SCFA fermentation in proximal sections of large intestine, stimulation of gastrointestinal tract growth, and subtle modifications in colonic microbiota.

In vivo exposure of the bladder using a non-invasive high intensity focused ultrasound toroidal transducer

A toroidal high-intensity focused ultrasound (HIFU) transducer was used to expose normal bladder wall tissues non-invasively in vivo in a porcine model in order to investigate the potential to treat bladder tumors. The transducer was divided into 32 concentric rings with equal surface areas, operating at 2.5 MHz. Eight animals were split into two groups of 4. In the first group, post-mortem evaluation was performed immediately after ultrasound exposure. In the second group, animals survived for up to seven days before post-mortem evaluation. The ultrasound imaging guided HIFU device was hand-held during the procedure using optical tracking to ensure correct targeting. One thermal lesion in each animal was created using a 40 s exposure at 80 acoustic Watts (free-field) in the trigone region of the bladder wall. The average (±Standard Deviation) abdominal wall and bladder wall thicknesses were 10.3 ± 1.4 mm and 1.1 ± 0.4 mm respectively. The longest and shortest axes of the HIFU ablations were 7.7 ± 2.9 mm and 6.0 ± 1.8 mm, respectively, resulting in an ablation of the whole thickness of the bladder wall in most cases. Ablation were performed at an average depth (distance from the skin surface to the centre of the HIFU lesion) of 42.5 ± 3.8 mm and extended throughout the thickness of the bladder. There were two cases of injury to tissues immediately adjacent to the bladder wall but without signs of perforation, as confirmed by histological analysis. Non-invasive HIFU ablation using a hand-held toroidal transducer was successfully performed to destroy regions of the bladder wall in vivo.

A pilot study of antimicrobial effects and ototoxicity of a Norway spruce (Picea abies) resin-based canine otic rinse product.

Norway spruce (Picea abies) resin-based products are used in human medicine. A resin-based otic rinse also could be useful in supportive care of canine otitis externa (COE), yet information on its antimicrobial effect against canine pathogens or ototoxicity is lacking. To investigate the antimicrobial properties and ototoxicity of a commercial resin-based otic product. Antimicrobial effect was evaluated using a standardised challenge test on Staphylococcus pseudintermedius, Corynebacterium auriscanis, Pseudomonas aeruginosa, Escherichia coli, Malassezia pachydermatis, and Streptococcus halichoeri strains to measure reduction in growth after 24 h exposure to the product. Effect on cell morphology was investigated by exposing S. pseudintermedius, C. auriscanis, P. aeruginosa and M. pachydermatis to the product in 20% and 100% (v/v) concentrations for 6, 24 and 48 h, and evaluating cells by transmission (TEM) and scanning (SEM) electron microscopy. An invitro microbial kill-rate assay also was performed. Auditory brain stem response test, clinical evaluation and postmortem histological evaluation of ear canals were undertaken on experimental guinea pigs treated with the test product or saline controls. The product showed >log 5 growth reduction for all strains in the challenge test. TEM and SEM images showed clear changes in the cells' inner structures and deterioration of cells, and 100% (v/v) test product exposure induced microbial killing in 1-2 h. Ototoxicity was not detected in guinea pigs. The product may be an option in supportive care of COE because of antimicrobial effects and lack of ototoxic properties in a guinea pig model.

Evaluation of microglia activation related markers following a clinical course of TBS: A non-human primate study.

While the applicability and popularity of theta burst stimulation (TBS) paradigms remain, current knowledge of their neurobiological effects is still limited, especially with respect to their impact on glial cells and neuroinflammatory processes. We used a multimodal imaging approach to assess the effects of a clinical course of TBS on markers for microglia activation and tissue injury as an indirect assessment of neuroinflammatory processes. Healthy non-human primates received continuous TBS (cTBS), intermittent TBS (iTBS), or sham stimulation over the motor cortex at 90% of resting motor threshold. Stimulation was delivered to the awake subjects 5 times a week for 3-4 weeks. Translocator protein (TSPO) expression was evaluated using Positron Emission Tomography and [11C]PBR28, and myo-inositol (mI) and N-acetyl-aspartate (NAA) concentrations were assessed with Magnetic Resonance Spectroscopy. Animals were then euthanized, and immunofluorescence staining was performed using antibodies against TSPO. Paired t-tests showed no significant changes in [11C]PBR28 measurements after stimulation. Similarly, no significant changes in mI and NAA concentrations were found. Post-mortem TSPO evaluation showed comparable mean immunofluorescence intensity after active TBS and sham delivery. The current study suggests that in healthy brains a clinical course of TBS, as evaluated with in-vivo imaging techniques (PET and MRS), did not measurably modulate the expression of glia related markers and metabolite associated with neural viability.

Pneumonia, aerossaculite e osteomilelite por Aspergillus fumigatus em um papagaio-cinzento (Psittacus erithacus) - relato de caso

ABSTRACT Aspergillosis is a fungal disease with high morbidity and mortality in wild and exotic bird species. The aim of this report is to describe a case of acute aspergillosis caused by Aspergillus fumigatus in a young African grey parrot (Psittacus erithacus). A three-month-old male African grey parrot from a commercial breeding site presented serous nasal discharge, inappetence, and wheezing on pulmonary auscultation. The parrot died three days after the onset of clinical signs. Postmortem evaluation demonstrated multiple smooth gray plaques in air sacs and left lung with dark red areas and adhesions to the ribs. Microscopically, there were intralesional hyphae and conidiophores in the lungs, air sacs, and ribs, which were associated with pneumonia, airsacculitis, and osteomyelitis, respectively. DNA samples were extracted from paraffinized tissues and subjected to PCR targeting the ITS-2 region, followed by sequencing, which yielded a sequence with 100% coverage and 100% identity to Aspergillus fumigatus sequences. Although A. fumigatus infection is quite common in birds, a particular aspect of interest in this case was the finding of conidiophores in the bone marrow, which may occur in birds due to air circulation through pneumatic bones.

Quantification of cytosine modifications in the aged mouse brain.

Quantifying cytosine modifications in various brain regions provides important insights into the gene expression regulation and pathophysiology of neuropsychiatric disorders. In this study, we quantified 5-methylcytosine (5-mC), 5-hydroxymethylation (5-hmC), and 5-formylcytosine (5-fC) levels in five brain regions (the frontal lobe, cerebral cortical region without frontal lobe, hippocampus, basal ganglia, and the cerebellum) and the heart at three developmental periods (12, 48, and 101 weeks). We observed significant regional variations in cytosine modification. Notably, regional variations were generally maintained throughout development, suggesting that epigenetic regulation is unique to each brain region and remains relatively stable with age. The 5-mC and 5-hmC levels were positively correlated, although the extent of the correlations seemed to differ in different brain regions. On the contrary, 5-fC levels did not correlate with 5-mC or 5-hmC levels. Additionally, we observed an age-dependent decrease in 5-fC levels in the basal ganglia, suggesting a unique epigenetic regulation mechanism. Further high-resolution studies using animal models of neuropsychiatric disorders as well as postmortem brain evaluation are warranted.

Comparison of clinicopathologic features of Limbic and Diffuse Transactive Response DNA‐binding Protein 43 pathology in Alzheimer’s disease neuropathologic spectrum

AbstractBackgroundIncreasing evidence suggests that transactive response DNA‐binding protein 43 (TDP‐43) pathology in Alzheimer’s Disease (AD), or AD‐TDP, can be diffuse or limbic‐predominant. Understanding whether diffuse AD‐TDP has genetic, clinical, and pathological features that differ from limbic AD‐TDP could have clinical and research implications. We aimed to better characterize the clinicopathologic features of diffuse AD‐TDP and differentiate it from limbic‐predominant AD‐TDP pathology.MethodThree hundred sixty‐three participants were prospectively recruited and followed in the Mayo Clinic Study of Aging, Alzheimer’s Disease Research Center, and Neurodegenerative Research Group and died between May 1999 and August 2021. All underwent genetic, clinical, neuropsychologic, and neuropathologic evaluations. At postmortem evaluation, they showed Alzheimer’s disease neuropathologic changes and TDP‐43‐immunoreactive inclusions. The distribution of TDP‐43 pathology was assessed using the Josephs 6‐stage scheme. Participants with TDP‐43 stages 1‐3 were classified as Limbic, while those with stages 4‐6 were classified as Diffuse. Neuropathologically defined frontotemporal lobar degeneration cases were excluded. Multivariable logistic regression was used to identify clinicopathological features that predicted diffuse TDP‐43 pathology at postmortem. We hypothesized that the Diffuse group would show impairment in cognitive domains beyond episodic memory and more hippocampal sclerosis.ResultsThe cohort was 61% female and old at onset (median:76 years [IQR:70‐82]) and death (median:88 years [IQR:82‐92]). Fifty‐four percent (n = 197) were classified as Limbic and 46% (n = 166) as Diffuse. A “clinical” multivariate logistic regression fit to 85 participants with all clinical variables of interest showed that later age at onset (OR:1.09, 95%CI:1.01‐1.19;P = 0.03), longer disease duration (OR:1.17, 95%CI:1.02‐1.36;P = 0.03) and higher Neuropsychiatric Inventory scores (OR:1.14, 95%CI:1.01‐1.28;P = 0.03) all independently increased the odds of being Diffuse, while higher Trails Making Test‐B (OR:0.99, 95%CI:0.98‐0.99;P = 0.02) and Block Design Test scores (OR:0.91, 95%CI:0.85‐0.99;P = 0.023) independently decreased the odds of being Diffuse. A “pathology” multivariate logistic regression fit to 233 cases with all neuropathological data revealed that widespread amyloid‐β pathology corresponding to Thal phases 3‐5 all significantly decreased the odds of diffuse pathology by 80‐90%, while hippocampal sclerosis increased it sixfold (OR:6.18, 95% CI:2.93‐13.03;P&lt;0.001).ConclusionsDiffuse AD‐TDP shows clinicopathological features that differ from Limbic AD‐TDP, which could have public health implications relating to treatment and research on AD and dementia.

The pathology of canine mammary candidiasis with embolic dissemination in a dog

Candidiasis is a fungal disease caused by Candida albicans or other members of the genus Candida. Descriptions of candidiasis are comparatively reduced in veterinary relative to human medicine, with no cases of mammary candidiasis being identified in pet animals. This report presents the cytological, pathological, and molecular findings of mammary candidiasis with embolic dissemination in a postpartum dog. A 1-year-old, female Shih-tzu dog that had recently given birth was admitted to a veterinary teaching hospital in Southern Brazil after repeated episodes of intermittent mammary disease and a neurological syndrome. The dog was euthanized due to worsened clinical status and poor prognosis despite adequate clinical therapy and was submitted for routine post-mortem evaluation to determine the cause of the neurological manifestations. Cytological analysis of purulent mastitis identified intralesional fungal hyphae. Gross evaluation revealed multiple masses within the kidneys, liver, myocardium, pancreas, and brain. Routine histopathology and histochemistry identified fungal nephritis, hepatitis, myocarditis, pancreatitis, and encephalitis associated with intralesional fungal hyphae, frequently with fungal emboli and vasculitis. Pure cultures of C. albicans were obtained from fragments of the masses observed at the myocardium and kidneys, with the typical germ tube of C. albicans being identified by microscopic evaluation. A PCR assay that targeted the ITS1 and 4 generic regions of fungi, amplified the desired amplicon, and direct sequencing confirmed C. albicans. Immunohistochemical and molecular assays designed to identify common infectious disease pathogens of dogs did not confirm the participation of canine distemper virus, canine parvovirus, or canine adenovirus in the target tissues of this dog. These findings suggest that this dog suffered an initial cutaneous lesion, that probably served as portal of entry to the mammary gland, resulting in mammary candidiasis with subsequent embolic dissemination to multiple organs. This report represent the first description of mammary candidiasis in pet animals and probably one of the few pathological descriptions of mammary candidiasis in domestic animals. In this case, the cause of the fungal infection was probably associated with factors intrinsic to abdominal surgery, pregnancy, and the utilization of antibiotics.

A Systematic Approach to Evaluate Sudden Unexplained Death in Children

To evaluate in the Netherlands the national outcomes in providing cause of and insights into sudden and unexplained child deaths among children via the Postmortem Evaluation of Sudden Unexplained Death in Children (PESUDY) procedure. Suddenly deceased children aged 0-18 years in the Netherlands were included in the PESUDY procedure if their death was unexplained and their parents gave consent. The PESUDY procedure consists of pediatric and forensic examination, biochemical, and microbiological tests; radiological imaging; autopsy; and multidisciplinary discussion. Data on history, modifiable factors, prior symptoms, performed diagnostics, and cause of death were collected between October 2016 and December 2021. 212 cases (median age 11 months, 56% boys, 33% comorbidity) were included. Microbiological, toxicological, and metabolic testing was performed in 93%, 34% and 32% of cases. In 95% a CT scan or MRI was done and in 62% an autopsy was performed. The cause of death was explained in 58% of cases and a plausible cause was identified in an additional 13%. Most children died from infectious diseases. Non-infectious cardiac causes were the second leading cause of death found. Modifiable factors were identified in 24% of non-SIDS/USID cases and mostly involved overlooked alarming symptoms. The PESUDY procedure is valuable and effective for determining the cause of death in children with sudden unexplained deaths and for providing answers to grieving parents and involved health care professionals.

APOE-ε4 and BIN1 increase risk of Alzheimer’s disease pathology but not specifically of Lewy body pathology

Lewy body (LB) pathology commonly occurs in individuals with Alzheimer’s disease (AD) pathology. However, it remains unclear which genetic risk factors underlie AD pathology, LB pathology, or AD-LB co-pathology. Notably, whether APOE-ε4 affects risk of LB pathology independently from AD pathology is controversial. We adapted criteria from the literature to classify 4,985 subjects from the National Alzheimer’s Coordinating Center (NACC) and the Rush University Medical Center as AD-LB co-pathology (AD+LB+), sole AD pathology (AD+LB–), sole LB pathology (AD–LB+), or no pathology (AD–LB–). We performed a meta-analysis of a genome-wide association study (GWAS) per subpopulation (NACC/Rush) for each disease phenotype compared to the control group (AD–LB–), and compared the AD+LB+ to AD+LB– groups. APOE-ε4 was significantly associated with risk of AD+LB– and AD+LB+ compared to AD–LB–. However, APOE-ε4 was not associated with risk of AD–LB+ compared to AD–LB– or risk of AD+LB+ compared to AD+LB–. Associations at the BIN1 locus exhibited qualitatively similar results. These results suggest that APOE-ε4 is a risk factor for AD pathology, but not for LB pathology when decoupled from AD pathology. The same holds for BIN1 risk variants. These findings, in the largest AD-LB neuropathology GWAS to date, distinguish the genetic risk factors for sole and dual AD-LB pathology phenotypes. Our GWAS meta-analysis summary statistics, derived from phenotypes based on postmortem pathologic evaluation, may provide more accurate disease-specific polygenic risk scores compared to GWAS based on clinical diagnoses, which are likely confounded by undetected dual pathology and clinical misdiagnoses of dementia type.

Assessment of Frequency, Patterns, and Causes of Blunt Abdominal Trauma in a North Indian Cohort: An Autopsy-Based Study.

Introduction The abdomen is one of the most frequently damaged areas in trauma patients and is commonly encountered in road traffic accidents (RTAs). The present study evaluates the frequency, etiology, causation, and form of injuryin blunt abdominal trauma (BAT) cases who had autopsies. Method An autopsy-based observational prospective study was conducted at the Department of Forensic Medicine and Toxicology, Nalanda Medical College and Hospital Patna, India, during the period from October 2018 to September 2020, which included a total of 940 autopsy cases showing blunt abdominal injuries. A predesigned proforma for the postmortem evaluation of BAT victims was used to collect the required information on the cases. Descriptive statistics were performed, and the data were presented as frequency (%) and mean±SD. Chi-square tests were performed to compare categorical variables between groups. Results BAT accounted for 120 (12.76%) cases of all autopsies performed. The majority of victims were male(92.48%). Victims aged 21-30 years (31, 25.83%) were the ones most usually engaged in BAT cases. Among the mechanisms accountable for BAT, RTAs were the most common (99, 82.50%), followed by assault (16, 13.30%). In most of the cases, the liver was injured (107, 89.16%), followed by the spleen (60, 50.00%) and kidney (24, 20.00%). The majority of blunt abdominal injury-related deaths were accidental (100, 83.33%), followed by homicidal (15, 12.5%) and suicidal cases (5, 4.17%). Hemorrhage and neurogenic shock were the most prevalent causes of mortality, particularly if the individual died within a few hours. Conclusion RTAs are the most frequent cause of BAT in autopsy cases, and the liver is the most affected organ. The majority of deaths occur within the first 24 hours of injury. Since blunt abdominal injuries have the propensity to increase morbidity and mortality, appropriate emphasis on their precise diagnosis and satisfactory therapy is mandated.

Eight-Year Study of Haemogregarina stepanowi Infection in Poached European Pond Turtles (Emys orbicularis) Held in Belgrade Zoo Quarantine.

The eight-year study (2015-2023) was performed on a large sample of poached European pond turtles infected with Haemogregarina stepanowi and held in a pond that belongs to a quarantine section of Belgrade Zoo. The protected species of European pond turtles have been found in poor health, with general weakness, anorexia, and low motility. Comprehensive cytological, hematological, molecular, and postmortem evaluations have been performed. Initially, Diff Quick staining of the blood smears revealed rounded or elongated erythrocytes, often bearing premeront or U-shaped gamont of the hemogregarines inside. The reduced erythrocyte numbers, hemoglobin, and hematocrit values found in the examined population of infected turtles indicated anemia. Macroscopically, shell necrosis and massive skin hemorrhages were the most prominent findings observed in diseased turtles. Microscopically, the lungs, liver, kidneys, and spleen revealed hyperemia, hemorrhages, and the presence of parasitic stages in tissue samples in 31 of 40 necropsied turtles. Cytological and microscopic examination of the samples proved to be sufficient for establishing the infection, but molecular analyses of the 18S sequence were used for phylogenetic studies. Over the years, the number of diseased and dead turtles has decreased, which could be hypothetically attributed to the elimination of leeches as the definitive host.