Identification of pathogenic Leptospira strains in tissues of a premature foal by use of polymerase chain reaction analysis.

Studies were carried out to determine the cause of death in a prematurely born Thoroughbred foal that died 24 hours after birth. Necropsy revealed gross lesions suggestive of septicemia. A commercial Leptospira polymerase chain reaction (PCR) assay designed to specifically amplify the hemolysis-associated protein 1 (hap1) gene present only in pathogenic Leptospira strains detected the presence of Leptospira DNA in various tissues of the foal. Histologic examination of lung, liver, kidney, and myocardium revealed numerous spirochetes in Warthin-Starry-stained tissue sections. Results of PCR analysis and histologic examination suggested a leptospiral infection in the newborn foal. At the moment of death, the infection coexisted with a streptococcal-associated aspiration bronchopneumonia and postpartum septicemia. These findings indicate that the PCR assay based on the amplification of the hap1 gene represents a useful tool for specific detection of pathogenic leptospira in field samples taken from horses.     

Evaluation of biomarkers of kidney injury following 4% succinylated gelatin and 6% hydroxyethyl starch 130/0.4 administration in a canine hemorrhagic shock model

Objective : To investigate the association between synthetic colloids and biomarkers of acute kidney injury (AKI) in dogs with hemorrhagic shock. Design : Experimental interventional study. Setting : University. Animals : Twenty‐four healthy ex‐racing Greyhounds. Interventions : Anesthetized Greyhounds subjected to hemorrhage for 60 min were resuscitated with 20 mL/kg of fresh whole blood (FWB), 6% hydroxyethyl starch (HES) 130/0.4, 4% succinylated gelatin (GELO), or 80 mL/kg of isotonic crystalloid (CRYST) over 20 min (n = 6 per treatment). Concentrations of biomarkers of AKI were measured at baseline, end of hemorrhage, and at 40 (T60), 100 (T120), and 160 (T180) min after fluid bolus. Biomarkers included neutrophil gelatinase‐associated lipocalin in urine and serum (uNGAL; sNGAL), and urine cystatin C (uCYSC), kidney injury molecule‐1 (uKIM), clusterin (uCLUST), osteopontin, gamma‐glutamyl transferase, monocyte chemoattractant protein‐1 (uMCP), interleukin‐6, interleukin‐8, protein (uPROT), hyaluronan, and F₂‐isoprostanes. Renal histology was scored for tubular injury and microvesiculation. Biomarker fold‐change from baseline was compared between groups using mixed effects models (Bonferroni–Holm corrected P<0.05). Frequencies of histology scores were compared by Fisher's exact test. Measurements and main results : In dogs treated with GELO, uNGAL fold‐change was markedly greater compared with all other groups at T60, T120, and T180 (all P<0.001), and uCYSC was greater at T60 compared with CRYST (P<0.001), and at T120 and T180 compared with all other groups (all P<0.001). Smaller, albeit significant, between‐group differences in uKIM, uCLUST, uMCP, and urine protein concentration were observed across the FWB, GELO, and HES groups, compared with CRYST. The GELO group more frequently had marked tubular microvesiculation than the other groups (P = 0.015) although tubular injury scores were comparable. Conclusion : In dogs with hemorrhagic shock, GELO was associated with greater magnitude increases in urine biomarkers of AKI and more frequent marked tubular microvesiculation, compared with FWB, CRYST, and HES.     

Ultrasound findings in horses with severe eyelid swelling, and recognition of acute dacryoadenitis: 10 cases (2004-2010)

Objective To report the sonographic findings, treatment, and outcome of horses with severe eyelid swelling, to describe the sonographic appearance of enlarged lacrimal glands, and to describe the clinical features of acute dacryoadenitis. Materials and methods Medical records of all horses with severe eyelid swelling that underwent an ultrasound evaluation of the globe and periorbital structures from 2004–2010 were examined. Cases were limited to those in which the eyelid swelling was so severe that the globe could not be visualized. Results Ten horses met the criteria for inclusion in the study. All cases were unilateral and acute. Marked enlargement of the lacrimal gland was found in five cases, and supported the diagnosis of acute dacryoadenitis. Eyelid abscessation was found in three horses, accompanied by mild to moderate lacrimal gland enlargement in two of the three. Enlarged lacrimal glands were slightly heterogeneous in appearance and could be differentiated from an abscess by imaging the protrusion of the gland from beneath the supraorbital rim. Only two cases of severe eyelid swelling were soley traumatic. Conclusions Severe eyelid swelling was often associated with dacryoadenitis and/or eyelid abscessation. The detection of marked lacrimal gland enlargement in horses with an acute onset of severe painful eyelid swelling is consistent with a diagnosis of acute dacryoadenitis. Ultrasonographic evaluation of eyelid swelling of any degree is warranted to determine if enlargement of the lacrimal gland, etiology notwithstanding, is an underlying or contributing cause.     

Dynamics of African swine fever virus shedding and excretion in domestic pigs infected by intramuscular inoculation and contact transmission

African swine fever virus (ASFV) is a highly virulent swine pathogen that has spread across Eastern Europe since 2007 and for which there is no effective vaccine or treatment available. The dynamics of shedding and excretion is not well known for this currently circulating ASFV strain. Therefore, susceptible pigs were exposed to pigs intramuscularly infected with the Georgia 2007/1 ASFV strain to measure those dynamics through within- and between-pen transmission scenarios. Blood, oral, nasal and rectal fluid samples were tested for the presence of ASFV by virus titration (VT) and quantitative real-time polymerase chain reaction (qPCR). Serum was tested for the presence of ASFV-specific antibodies. Both intramuscular inoculation and contact transmission resulted in development of acute disease in all pigs although the experiments indicated that the pathogenesis of the disease might be different, depending on the route of infection. Infectious ASFV was first isolated in blood among the inoculated pigs by day 3, and then chronologically among the direct and indirect contact pigs, by day 10 and 13, respectively. Close to the onset of clinical signs, higher ASFV titres were found in blood compared with nasal and rectal fluid samples among all pigs. No infectious ASFV was isolated in oral fluid samples although ASFV genome copies were detected. Only one animal developed antibodies starting after 12 days post-inoculation. The results provide quantitative data on shedding and excretion of the Georgia 2007/1 ASFV strain among domestic pigs and suggest a limited potential of this isolate to cause persistent infection.     

The Blonde d’Aquitaine T3811>G3811 mutation in the myostatin gene: association with growth,carcass, and muscle phenotypes in veal calves

The mutation T3811 → G3811 (TG3811) discovered in the myostatin gene of the Blonde d’Aquitaine breed is suspected of contributing to the outstanding muscularity of this breed. An experiment was designed to estimate the effect of this mutation in an F2 and back-cross Blonde d’Aquitaine × Holstein population. By genotyping all known mutations in the myostatin gene, it was ensured that the TG3811 mutation was indeed the only known mutation segregating in this population. Fifty-six calves (43 F2, 13 back-cross) were intensively fattened and slaughtered at 24.0 ± 1.4 wk of age. The effects of the mutation were estimated by comparing the calves with the [T/T] (n = 18), [T/G] (n = 30), and [G/G] (n = 8) genotypes. Highly significant substitution effects (P < 0.001), above + 1.2 phenotypic SD, were shown on carcass yield and muscularity scores. Birth weight (P < 0.001) was positively affected by the mutation (+0.8 SD) but not growth rate (P = 0.97), while carcass length (P = 0.03), and fatness (P ≤ 0.03) were negatively affected (–0.5 to –0.7 SD). The characteristics of the Triceps brachii muscle were affected by the mutation (P < 0.001), with lower ICDH activity (oxidative) and a higher proportion of myosin type 2X muscle fibers (fast twitch). The effects of the TG3811 mutation were similar to those of other known myostatin mutations, although the Blonde d’Aquitaine animals, which are predominantly [G/G] homozygous, do not exhibit extreme double muscling.     

A Necropsy Survey of Neurologic Diseases in 4,319 Horses Examined in Normandy (France) from 1986 to 2006

The frequencies of neurologic diseases and various corresponding causes were analyzed in 4,319 Norman horses examined by autopsy between 1986 and 2006. Five hundred forty-three cases of nervous system disorders were detected, or a total prevalence of 12.6%. One hundred eighty-seven of the 543 horses (34.4%) exhibited lesions of a traumatic origin affecting the skull or the vertebral column at different levels. Their frequency was less in foals younger than 1 month of age and higher in horses aged 6 months to 2 years. Eighty-three cases of cervical vertebral compressive myelopathy (CVCM) (15.3%) were identified. Males and geldings were more often affected than females. CVCM was diagnosed mostly in animals aged 6 months to 2 years. Horses affected with lesions in the mid-cervical region (region C3–C5) were significantly younger than those exhibiting more caudal lesions (region C5–C7). Neonatal maladjustment syndrome was diagnosed in 62 foals younger than 3.5 days (4.8% of the causes of death between birth and 1 month) by using clinical or lesional criteria. The prevalence was higher in Thoroughbreds as well as in the miscellaneous breed category and less in French Standardbreds. Bacterial meningoencephalomyelitis and meningitis represented 9.6% of nervous system disorders (52 cases) and most often affected foals aged 1 to 6 months. The main bacteria identified were beta-hemolytic Streptococci , Escherichia coli, Listeria monocytogenes, Staphylococcus aureus, and Actinobacillus sp. The other causes diagnosed were, in decreasing order of frequency: grass sickness or equine dysautonomia (6.3% of neurologic diseases), hepatic encephalopathy syndrome (5.2%), septic vertebral arthritis or osteitis mainly caused by Rhodococcus equi (2.6%), congenital defects of the nervous system (2.4%), equine herpesvirus 1 myeloencephalopathy (2.2%), botulism (2.2%), malformations of the vertebral column other than CVCM (2%), and neighboring polyneuritis associated with guttural pouch mycosis (1.5%).     

Inheritance, mode of inheritance, and candidate genes for primary hyperparathyroidism in Keeshonden

BACKGROUND: Primary hyperparathyroidism (PHPT) is caused by inappropriate secretion of parathyroid hormone (PTH) by autonomously functioning neoplastic or hyperplastic parathyroid "chief" cells. Keeshonden are thought to be over-represented in studies on canine PHPT, but no proof of heritability or mode of inheritance has been published. The canine disease clinically resembles human familial isolated hyperparathyroidism (FIHP). HYPOTHESIS: Primary hyperparathyroidism in Keeshonden is genetically transmitted and is caused by a mutation in 1 of 4 genes implicated in human FIHP: MEN1, CASR, HRPT2, or RET. ANIMALS: Pedigrees consisting of 1647 Keeshonden were created including 219 Keeshonden with known PHPT phenotypes (69 positive). DNA samples were obtained from 176 of the 219 Keeshonden (34 positive). METHODS: Heritability and mode of inheritance were determined by segregation analysis. Canine homologs to the human genes were identified. Exons and surrounding intron regions were sequenced and scanned for sense-altering polymorphisms or polymorphisms that segregated with the disease. Messenger RNA from a parathyroid tumor of an affected Keeshond was analyzed for polymorphisms and splice alterations. RESULTS: PHPT follows an autosomal dominant mode of inheritance in Keeshonden with possible age-dependent penetrance. No polymorphisms identified in the genes analyzed were associated with a change in predicted protein or in hypothesized splice sites. CONCLUSIONS AND CLINICAL IMPORTANCE: PHPT is an autosomal dominant, genetically transmitted disease in Keeshonden. Once the mutation locus is identified, genetic testing should quickly decrease the incidence of PHPT in this breed. It is unlikely that mutations in MEN1, CASR, HRPT2, or RET cause PHPT in Keeshonden.     

ULTRASONOGRAPHIC CHARACTERISTICS OF THE ABDOMINAL ESOPHAGUS AND CARDIA IN DOGS

Differential diagnoses for regurgitation and vomiting in dogs include diseases of the gastroesophageal junction. The purpose of this cross‐sectional study was to describe ultrasonographic characteristics of the abdominal esophagus and gastric cardia in normal dogs and dogs with clinical disease involving this region. A total of 126 dogs with no clinical signs of gastrointestinal disease and six dogs with clinical diseases involving the gastroesophageal junction were included. For seven euthanized dogs, ultrasonographic features were also compared with gross pathology and histopathology. Cardial and abdominal esophageal wall thicknesses were measured ultrasonographically for all normal dogs and effects of weight, sex, age, and stomach filling were tested. Five layers could be identified in normal esophageal and cardial walls. The inner esophageal layer was echogenic, corresponding to the cornified mucosa and glandular portion of the submucosa. The cardia was characterized by a thick muscularis, and a transitional zone between echogenic esophageal and hypoechoic gastric mucosal layers. Mean (±SD) cardial wall thicknesses for normal dogs were 7.6 mm (±1.6), 9.7 mm (±1.8), 10.8 mm (±1.6), 13.3 mm (±2.5) for dogs in the <10 kg, 10–19.9 kg, 20–29.9 kg and ≥30 kg weight groups, respectively. Mean (±SD) esophageal wall thicknesses were: 4.1 mm (±0.6), 5.1 mm (±1.3), 5.6 mm (±1), and 6.4 mm (±1.1) for the same weight groups, respectively. Measurements of wall thickness were significantly correlated with dog weight group. Ultrasonography assisted diagnosis in all six clinically affected dogs. Findings supported the use of transabdominal ultrasonography as a diagnostic test for dogs with suspected gastroesophageal disease.