A survey of bovine leukemia virus resistant bovine leukocyte antigen (BoLA)-DRB3*009:02 allele-carrying Japanese Black cattle in two prefectures in Japan

The bovine leukocyte antigen (BoLA) DRB3*009:02 allele is strongly associated with a low/undetectable bovine leukemia virus (BLV) proviral load. Understanding the status of cattle possessing DRB3*009:02 allele is key for BLV control by breeding. We performed a survey of DRB3*009:02-carrying cattle in two prefectures in Japan using a TaqMan assay developed previously. The allele was found in 3.8% (confidence interval (CI): 3.3–4.3) of 6020 Japanese Black female cattle. A prefecture-level difference was found: the allele was observed in 8.6% CI: 7.5–9.9) of 2242 cattle of the birth prefecture B in Kyushu/Okinawa region, and this percentage was significantly higher than those of prefecture C in Kyushu/Okinawa region (1.3% (CI: 0.4–3.4) of 319) and prefecture A in Chugoku region (0.9% (CI: 0.6–1.4) of 2741), respectively. Consideration on the difference in possession of DRB3*009:02 allele is needed to establish the more efficient control strategy of BLV infection in Japanese Black cattle.     

An ovine hepatotoxicosis caused by the plant Pteronia pallens (Asteraceae) L.f

The hepatotoxicity of Pteronia pallens was demonstrated in 5 sheep which developed lesions that ranged from centrilobular necrosis to diffuse hepatocellular degeneration. Botanical, clinical and pathological data are given and the lesions are briefly compared with those caused by other hepatotoxic plants in South Africa.     

The potential of organoids in toxicologic pathology: role of toxicologic pathologists in in vitro chemical hepatotoxicity assessment

The development of in vitro toxicity assessment methods using cultured cells has gained popularity for promoting animal welfare in animal experiments. Herein, we briefly discuss the current status of hepatoxicity assessment using human- and rat-derived hepatocytes; we focus on the liver organoid method, which has been extensively studied in recent years, and discuss how toxicologic pathologists can use their knowledge and experience to contribute to the development of in vitro chemical hepatotoxicity assessment methods for drugs, pesticides, and chemicals. We also propose how toxicological pathologists should assess toxicity regarding the putative distribution of undifferentiated and differentiated cells in the organoid when liver organoids are observed in hematoxylin and eosin–stained specimens. This was done while considering the usefulness and limitations of in vitro studies for toxicologic pathology assessment.     

Causes of death in beef cattle in southern Brazil

We determined the prevalence of diseases and pathogens associated with mortality in beef cattle in the State of Rio Grande do Sul, Brazil, based on pathology laboratory submissions. Postmortem examinations were conducted on 1,277 beef cattle that died between 2008 and 2018. Information regarding age, time of the year, breed, and regional location were analyzed statistically. Most cattle were from the surrounding region of Porto Alegre, and 78.7% of the analyzed cases had diagnostic value. The diagnostic category with most cases was infectious and/or parasitic diseases (60%), followed by toxic and toxicoinfectious (25%). Most cases occurred in the fall. Major disease conditions identified included hemoprotozoal infection (18.2%), rabies (8.2%), and plant intoxications by Senecio spp. (8.5%) and Pteridium arachnoideum (4.6%). Hemoprotozoal infection occurred at a higher frequency in young cattle, mainly in animals up to 1 y old. Intoxication by Senecio spp. was more frequent in cattle 2–3 y old.     

Trema micrantha toxicity in horses in Brazil

After ingesting green leaves of T. micrantha, 2 horses showed apathy, locomotor deficit, blindness, recumbency, paddling, coma and death. The main gross findings were scattered haemorrhages, enhanced lobular pattern of the liver, and cerebral oedema. Histological changes included disseminated haemorrhages, massive hepatocellular necrosis, neuronal degeneration, Alzheimer type II astrocytes and cerebral perivascular oedema. Clinicopathological findings which were comparable with those observed in Trema micrantha poisoned ruminants, associated with epidemiological evidence suggested the diagnosis.Trema micrantha poisoning should be evaluated as a possible cause in the diagnosis of equine hepatopathy and occasional secondary encephalopathy.     

The comparative pathology of enterocolitis caused by Clostridium perfringens type C,Clostridioides difficile, Paeniclostridium sordellii,Salmonella enterica subspecies enterica serovar Typhimurium,and nonsteroidal anti-inflammatory drugs in horses

To determine if there were significant differences produced by 5 of the most prevalent causes of equine enterocolitis, we studied retrospectively the gross and microscopic pathology of 90 cases of enterocolitis submitted to the San Bernardino laboratory of the California Animal Health and Food Safety Laboratory. Included were cases caused by Clostridium perfringens type C (CP; n = 20), Clostridioides difficile (CD; n = 20), Paeniclostridium sordellii (PS; n = 15), Salmonella enterica subspecies enterica serovar Typhimurium (ST; n = 20), and NSAID intoxication (NS; n = 15). Grossly, necrotizing hemorrhagic typhlocolitis was seen most frequently in cases of CD, ST, and NS disease. Cases of CP and PS had enteritis or colitis in similar percentages. Congestion, hemorrhage, and pleocellular inflammatory infiltrates followed by mucosal and submucosal necrosis were the main lesions found in horses with enteritis or colitis produced by any of the etiologic agents investigated. Severe lesions were more frequent in cases of CD and CP than in cases associated with any of the other 3 etiologies. Pseudomembranes were observed with similar prevalence in the small intestine and colon affected by all agents studied. Thrombosis of the lamina propria and/or submucosa was observed in ~50% of the cases of enteritis and colitis by all etiologies, except for PS, in which the majority of the cases had thrombosis. Gross and microscopic lesions of enterocolitis were not sufficiently specific for any of these etiologic agents to enable these enteritides to be distinguished by gross and/or histologic examination.     

Genetic and antigenic analysis of Chlamydia pecorum strains isolated from calves with diarrhea

Chlamydia pecorum (designated 22–58) was isolated in 2010 in HmLu-1 cells from the jejunum of a calf which died of necrotizing enterocolitis in Yamaguchi Prefecture, Japan. Immunohistochemical staining identified C. pecorum positive reactions in the jejunal villi. C. pecorum, designated 24–100, was isolated from the feces of a calf with diarrhea in another farm in Yamaguchi Prefecture in 2012. A significant increase in neutralizing antibody titers against C. pecorum was confirmed in paired sera. Nucleotide sequence identities of omp1 genes of the 2 isolates were 100%. The isolates were genetically and antigenically more closely related to C. pecorum Bo/Yokohama strain isolated from cattle with enteritis in Japan than to the other prototype strains, Bo/Maeda isolated from cattle with pneumonia and Ov/IPA isolated from sheep with polyarthritis. These results indicate that C. pecorum strains similar to 22–58 and 24–100 might be endemic in Yamaguchi Prefecture and cause enteric disease in cattle.     

Clinical and pathologic features of acute bovine liver disease in Australia

Acute bovine liver disease (ABLD) is a sporadic hepatic disease affecting cattle in southern Australia, characterized histologically by striking periportal hepatocellular necrosis. The cause of ABLD is unknown; however, the seasonality and acute presentation of outbreaks suggest mycotoxin involvement. We describe here the clinical and pathologic findings of ABLD in 45 naturally affected cattle from 13 outbreaks occurring from 2010 to 2019 in Victoria, Australia. Outbreaks occurred in herds located along the southern coastal plain of Victoria and were observed most frequently in lactating dairy cattle. Clinical signs commonly included a combination of mild photosensitization, progressive neurologic signs, and hypogalactia, which preceded death by ≤ 48 h. All affected animals had marked elevations in activities of glutamate dehydrogenase, aspartate aminotransferase, and gamma-glutamyl transferase. At autopsy, the most common lesions were serosal petechiae and/or gastrointestinal hemorrhage, and hepatomegaly with a pronounced hepatic reticular pattern. The principal histologic lesion was widespread—severe periportal hepatocellular coagulative necrosis and erythrocyte pooling—which often extended to massive necrosis. Lesions in other organs were uncommon. Our study of ABLD suggests involvement of a potent hepatotoxin that is either directly cytopathic or requires bioactivation by periportal-specific enzymes.     

Prevalence of and factors associated with Brucella sero-positivity in cattle in urban and peri-urban Gulu and Soroti towns of Uganda

Brucellosis is a key zoonosis of major public health, animal welfare and economic significance, and is endemic in livestock in Uganda. A cross-sectional epidemiological study was carried out to estimate the sero-prevalence of brucellosis and identify factors associated with sero-positivity in cattle in urban and peri-urban Gulu and Soroti towns of Northern and Eastern Uganda, respectively. A total of 1007 sera and data on biologically plausible risk factors from 166 herds and their spatial locations, were collected from cattle reared in urban and peri-urban Gulu and Soroti towns of Uganda. The sera were analyzed using indirect ELISA and sero-positive reactors confirmed by competitive ELISA. Multivariable models were used to investigate for risk factors. The overall animal-level and herd-level sero-prevalence was 7.5% (76/1007, 95% Confidence Interval (CI): 6.15–9.4%) and 27.1% (45/166, 95% CI: 20.9–34.3%), respectively. Herd-level sero-prevalence was significantly (P<0.001) higher in Soroti than Gulu. In Gulu town, sero-positivity increased with an increase in herd size (P=0.03) and age (P=0.002), and was higher in cattle brought in from western Uganda (P<0.0001). In Soroti town, introduction of new cattle into a herd was significantly (P=0.027) associated with herd sero-positivity. There was a geographically differential risk (clustering) of Brucella sero- positivity in herds in Soroti, while sero-positivity was homogeneously distributed in Gulu. The data highlight brucellosis occurrence and major risk factors for its transmission in cattle in urban and peri-urban areas.     

Acute hepatic necrosis and death in a subadult southern white rhinoceros (Ceratotherium simum) associated with exposure to sterigmatocystin in forage contaminated with Aspergillus nidulans

A young male southern white rhinoceros (Ceratotherium simum), which was resident in a zoo as part of a multi‐rhinoceros group, died suddenly. Necropsy and histopathological findings supported a diagnosis of death from acute hepatic necrosis. The microscopic distribution of liver lesions was suggestive of hepatotoxicosis. Further investigation revealed potential exposure to a mycotoxin, sterigmatocystin, present in spoiled lucerne hay contaminated with Aspergillus nidulans. It was concluded that mycotoxicosis was the likely cause of the hepatic necrosis and death in this animal.     

Experimental Alkylmercurial Poisoning in Swine. Lesions in the Peripheral and Central Nervous Systems

The effects of alkylmercurial poisoning were studied in 16 pigs poisoned with daily oral doses of a fungicide containing methylmercury 2, 3-dihydroxy propyl mercaptide and methylmercury acetate. Clinical signs included weakness, wobbling gait, blindness, recumbency and death. Microscopic studies of the peripheral nervous system revealed Wallerian degeneration in sensory fibers and neuronal degeneration in dorsal root ganglia. In the central nervous system, there were neuronal degeneration of ischemic type, glial degeneration, gliosis and necrosis of the media of meningeal arterioles. The last mentioned lesion was not extensive.

The sequential development o lesions and the absence of segmental demyelination suggest that the primary lesion in the peripheral nervous system was neuronal-axonal degeneration rather than degeneration of the Schwann cell and myelin sheath.

     

Relationship of bovine NOS2 gene polymorphisms to the risk of bovine tuberculosis in Holstein cattle

Many studies suggest significant genetic variation in the resistance of cattle and humans to infection with Mycobacterium bovis, the causative agent of zoonotic tuberculosis. The inducible nitric oxide synthase (iNOS which is encoded by the NOS2 gene) plays a key role in the immunological control of a broad spectrum of infectious agents. This study aimed to investigate the influence of genetic variations in the promoter of the NOS2 gene on bovine tuberculosis (bTB) susceptibility. In this study, the NOS2 genes of 74 bTB-infected Holstein cows and 90 healthy controls were genotyped using PCR followed by nucleotide sequencing. Polymorphisms at rs207692718, rs109279434, rs209895548, rs385993919, rs433717754, rs383366213, rs466730386, rs715225976, rs525673647, rs720757654 and g.19958101T>G in the promoter region of the NOS2 gene were detected. The g.19958101T>G SNP produced two different conformation patterns (TT and TG) and the TG genotype was over-represented in the bTB group (20.27%) compared with the control group (2.22%). The TG genotype frequency of the g.19958101T>G variant was significantly higher in bTB cattle than in healthy controls (OR, 11.19; 95% CI, 2.47–50.73; P=0.0002). The G allele of the g.19958101T>G polymorphism was more frequent in bTB group when compared to control group (10.14% versus 1.11%). Furthermore, the G allele was a risk factor for bTB susceptibility (OR, 10.04; 95% CI, 2.26–44.65; P=0.0002). In conclusion, the g.19958101T>G polymorphism of the NOS2 gene may contribute to the susceptibility of Holstein cattle to bTB.     

The role of neighboring infected cattle in bovine leukemia virus transmission risk

A cohort study was conducted to evaluate the risk of bovine leukemia virus (BLV) transmission to uninfected cattle by adjacent infected cattle in 6 dairy farms. Animals were initially tested in 2010–2011 using a commercial ELISA kit. Uninfected cattle were repeatedly tested every 4 to 6 months until fall of 2012. The Cox proportional hazard model with frailty showed that uninfected cattle neighboring to infected cattle (n=53) had a significant higher risk of seroconversion than those without any infected neighbors (n=81) (hazard ratio: 12.4, P=0.001), implying that neighboring infected cattle were a significant risk factor for BLV transmission. This finding provides scientific support for animal health authorities and farmers to segregate infected cattle on farms to prevent spread of BLV.     

The pathology of acute Nolletia gariepina poisoning of cattle

Toxicity in cattle by the shrub Nolletia gariepina was induced experimentally by intraruminal administration of 3 g/kg dried, milled plant material as a single dose. The animals had to be starved for 24 hours before dosing, as dosing on a full rumen did not induce any signs of toxicity during 5 days of observation and clinical pathology monitoring. Clinical signs were not specific and varied according to the duration (acute versus subacute) of the toxicological process. Clinical pathological parameters indicated renal and to a lesser extent hepatic damage, with raised serum concentrations of urea, creatinine, aspartate aminotransferase (AST) and gamma glutamyl transferase (GGT). Increased urinary sodium and potassium concentration and GGT activity, as well as proteinuria, were evident. Histological and electron microscopic examinations revealed acute renal tubular epithelial cell degeneration and necrosis, especially of the proximal convoluted tubules. Mild hepatocellular degeneration was also noticeable.     

Cestrum parqui (green cestrum) poisoning in cattle

SUMMARY Naturally occurring cases of poisoning of cattle by Cestrum parqui were characterised by ataxia, depression, recumbency, convulsions and death. Three cattle were dosed experimentally by intrarumenal administration of fresh plant material. One calf died 48 h after receiving 30 g (wet weight) of plant /kg body weight. Doses of 11 and 17 g/kg caused only mild intoxication, with dullness and anorexia lasting 2 days. In natural and experimental cases the main lesion was hepatic periacinar necrosis. Elevated levels of plasma aspartate transaminase and prolonged prothrombin times were demonstrated in experimental cases. Haemorrhage beneath the serosa and into the intestinal lumen occurred in field cases, but not in the experimental. It is concluded that C. parqui poisoning in cattle is a primary hepatotoxicity.     

Effects of Intermittent Positive Pressure Ventilation on Cardiopulmonary Function in Horses Anesthetized with Total Intravenous Anesthesia Using Combination of Medetomidine,Lidocaine, Butorphanol and Propofol (MLBP-TIVA)

Effects of intermittent positive pressure ventilation (IPPV) on cardiopulmonary function were evaluated in horses anesthetized with total intravenous anesthesia using constant rate infusions of medetomidine (3.5 µg/kg/hr), lidocaine (3 mg/kg/hr), butorphanol (24 µg/kg/hr) and propofol (0.1 mg/kg/min) (MLBP-TIVA). Five horses were anesthetized twice using MLBP-TIVA with or without IPPV at 4-week interval (crossover study). In each occasion, the horses breathed 100% oxygen with spontaneous ventilation (SB-group, n=5) or with IPPV (CV-group, n=5), and changes in cardiopulmonary parameters were observed for 120 min. In the SB-group, cardiovascular parameters were maintained within acceptable ranges (heart rate: 33–35 beats/min, cardiac output: 27–30 l/min, mean arterial blood pressure [MABP]: 114–123 mmHg, mean pulmonary arterial pressure [MPAP]: 28–29 mmHg and mean right atrial pressure [MRAP]: 19–21 mmHg), but severe hypercapnea and insufficient oxygenation were observed (arterial CO₂ pressure [PaCO₂]: 84–103 mmHg and arterial O₂ pressure [PaO₂]: 155–172 mmHg). In the CV-group, normocapnea (PaCO₂: 42–50 mmHg) and good oxygenation (PaO₂: 395–419 mmHg) were achieved by the IPPV without apparent cardiovascular depression (heart rate: 29–31 beats/min, cardiac output: 17–21 l /min, MABP: 111–123 mmHg, MPAP: 27–30 mmHg and MRAP: 15–16 mmHg). MLBP-TIVA preserved cardiovascular function even in horses artificially ventilated.     

Detection of Mycobacterium tuberculosis complex antibodies in free-ranged wild boar and wild macaques in selected districts in Selangor and reevaluation of tuberculosis serodetection in captive Asian elephants in Pahang,Peninsular Malaysia

Tuberculosis (TB) is a chronic inflammatory and zoonotic disease caused by Mycobacterium tuberculosis complex (MTBC) members, affecting several domestic animals, wildlife species and humans. The preliminary investigation was aimed to detect antibody against MTBC among indigenous wildlife which are free-ranged wild boar, free-ranged wild macaques and captive Asian elephants in selected areas of Selangor and elephant conservation centre in Pahang, respectively. The results indicate that MTBC serodetection rate in wild boar was 16.7% (7.3–33.5 at 95% confidence interval (CI)) using an in-house ELISA bPPD IgG and 10% (3.5–25.6 at 95% CI) by DPP^®VetTB assay, while the wild macaques and Asian elephant were seronegative. The univariate analysis indicates no statistically significant difference in risk factors for sex and age of wild boar but there was a significant positive correlation (P<0.05) between bovine TB in dairy cattle and wild boar seropositivity in the Sepang district.     

Prevalence and risk factor investigation of Campylobacter species in beef cattle feces from seven large commercial feedlots in Alberta,Canada

This fecal prevalence study targeted cattle from 7 large (10 000 to > 40 000 head) commercial feedlots in Alberta as a means of establishing Campylobacter levels in cattle just prior to animals entering the food chain. Overall, 87% [95% confidence interval (CI) = 86–88] of 2776 fresh pen-floor fecal samples were culture positive for Campylobacter species, with prevalences ranging from 76% to 95% among the 7 feedlots. Campylobacter spp. prevalence was 88% (95% CI = 86–90) in the summer (n = 1376) and 86% (95% CI = 85–88) in the winter (n = 1400). In addition, 69% (95% CI = 66–71) of 1486 Campylobacter spp. positive samples were identified as Campylobacter jejuni using hippurate hydrolysis testing. Of those, 64% (95% CI = 58–70) of 277 and 70% (95% CI = 67–72) of 1209 Campylobacter isolates were identified as C. jejuni in winter and summer, respectively. After accounting for clustering within pen and feedlot, feedlot size and the number of days on feed were associated with Campylobacter spp. isolation rates. The high isolation rates of Campylobacter spp. and C. jejuni in feedlot cattle feces in this study suggest a potential role for feedlot cattle in the complex epidemiology of campylobacters in Alberta.     

Thioacetamide-induced Hepatocellular Necrosis Is Attenuated in Diet-induced Obese Mice

To assess modification of thioacetamide-induced hepatotoxicity in mice fed a high-fat diet, male C57BL/6J mice were fed a normal rodent diet or a high-fat diet for 8 weeks and then treated once intraperitoneally with thioacetamide at 50 mg/kg body weight. At 24 and 48 hours after administration, massive centrilobular hepatocellular necrosis was observed in mice fed the normal rodent diet, while the necrosis was less severe in mice fed the high-fat diet. In contrast, severe swelling of hepatocytes was observed in mice fed the high-fat diet. In addition, mice fed the high-fat diet displayed more than a 4-fold higher number of BrdU-positive hepatocytes compared with mice fed the normal rodent diet at 48 hours after thioacetamide treatment. To clarify the mechanisms by which the hepatic necrosis was attenuated, we investigated exposure to thioacetamide and one of its metabolites, the expression of CYP2E1, which converts thioacetamide to reactive metabolites, and the content of glutathione S-transferases in the liver. However, the reduced hepatocellular necrosis noted in mice fed the high-fat diet could not be explained by the differences in exposure to thioacetamide or thioacetamide sulfoxide or by differences in the expression of drug-metabolizing enzymes. On the other hand, at 8 hours after thioacetamide administration, hepatic total glutathione in mice fed the high-fat diet was significantly lower than that in mice fed the normal diet. Hence, decreased hepatic glutathione amount is a candidate for the mechanism of the attenuated necrosis. In conclusion, this study revealed that thioacetamide-induced hepatic necrosis was attenuated in mice fed the high-fat diet.