EFFECT OF SEDATION ON CONTRAST‐ENHANCED ULTRASONOGRAPHY OF THE SPLEEN IN HEALTHY DOGS

Contrast‐enhanced ultrasound of the spleen enables the dynamic assessment of the perfusion of this organ, however, both subjective and quantitative evaluation can be strongly influenced by sedative agent administration. The purpose of this prospective, experimental study was to test effects of two sedative agents on splenic perfusion during contrast‐enhanced ultrasound of the spleen in a sample of healthy dogs. Contrast‐enhanced ultrasound of the spleen was repeated in six healthy Beagles following a cross‐over study design comparing three protocols: awake, butorphanol 0.2 mg/Kg intramuscular (IM), and dexmedetomidine 500 μg/m² IM. After intravenous injection of a phospholipid stabilized sulfur hexafluoride microbubble solution (SonoVue®, Bracco Imaging, Milano, Italy), the enhancement intensity and perfusion pattern of the splenic parenchyma were assessed and perfusion parameters were calculated. Normal spleen was slightly heterogeneous in the early phase, but the parenchyma was homogeneous at a later phase. Sedation with butorphanol did not modify perfusion of the spleen. Dexmedetomidine significantly reduced splenic enhancement, providing diffuse parenchymal hypoechogenicity during the entire examination. Measured parameters were significantly modified, with increased arrival time (AT; (< 0.0001) and time to peak (TTP; P < 0.0001), and decreased peak intensity (PI; P = 0.0108), wash‐in (P = 0.0014), and area under the curve (AUC; P = 0.0421). Findings supported the use of butorphanol and contraindicated the use of dexmedetomidine as sedatives for splenic contrast ultrasound procedures in dogs. Short‐term and diffuse heterogeneity of the spleen in the early venous phase was determined to be a normal finding.     

IMAGING DIAGNOSIS—TRAUMATIC ABOMASITIS CAUSED BY FOREIGN BODIES IN A COW

A 2‐year‐old Holstein cow presented with a history of colic signs of 3 days’ duration that had not responded to routine medical therapy. Physical examination findings were consistent with tachycardia and colic. Ultrasonographic examination of the abomasum revealed a thin hyperechoic line producing a cone shadow. Radiography of the cranial abdomen revealed two radiopaque objects within the abomasum. Right paracostal laparotomy and abomasotomy permitted palpation and manual removal of two metallic foreign bodies and a small quantity of gravel. The animal recovered well after surgery and no signs of colic were observed. Her appetite and rumination were also improved.     

Sudden acquired retinal degeneration syndrome (SARDS) – a review and proposed strategies toward a better understanding of pathogenesis,early diagnosis,and therapy

Sudden acquired retinal degeneration syndrome (SARDS) is one of the leading causes of currently incurable canine vision loss diagnosed by veterinary ophthalmologists. The disease is characterized by acute onset of blindness due to loss of photoreceptor function, extinguished electroretinogram with an initially normal appearing ocular fundus, and mydriatic pupils which are slowly responsive to bright white light, unresponsive to red, but responsive to blue light stimulation. In addition to blindness, the majority of affected dogs also show systemic abnormalities suggestive of hyperadrenocorticism, such as polyphagia with resulting obesity, polyuria, polydipsia, and a subclinical hepatopathy. The pathogenesis of SARDS is unknown, but neuroendocrine and autoimmune mechanisms have been suggested. Therapies that target these disease pathways have been proposed to reverse or prevent further vision loss in SARDS‐affected dogs, but these treatments are controversial. In November 2014, the American College of Veterinary Ophthalmologists' Vision for Animals Foundation organized and funded a Think Tank to review the current knowledge and recently proposed ideas about disease mechanisms and treatment of SARDS. These panel discussions resulted in recommendations for future research strategies toward a better understanding of pathogenesis, early diagnosis, and potential therapy for this condition.     

Mycotic proventriculitis in gray partridges (Perdix perdix) on two game bird farms

Proventriculitis and chronic respiratory disease were diagnosed in two flocks of gray partridges (Perdix perdix) on unrelated Swedish game bird farms. Affected birds showed loss of condition, respiratory signs, and flock mortality rates of 50 and 98%, respectively. The proventricular lesions were associated closely with fungal organisms that were microscopically indistinguishable from the ascomycetous yeast Macrorhabdus ornithogaster (former provisional name "megabacterium"). At necropsy, the proventriculi were swollen and hyperemic, and viscous mucus adhered to the mucosa. Proventricular hemorrhages were commonly detected, and one bird had proventricular rupture and peritonitis. Microscopically, mild to severe subacute to chronic lymphoplasmacytic proventriculitis, microabscesses, necrosis, epithelial metaplasia, disrupted koilin, ulcers, and hemorrhages were observed. Transmission electron microscopy of the proventricular microorganisms revealed a membrane-bound nucleus, vacuoles, ribosomes, microtubules in parallel arrays, and a two-layered cell wall but no mitochondria. Scanning electron microscopy of the proventricular epithelium demonstrated masses of organisms with occasional constrictions in parallel arrangement. Many of the birds also suffered from concurrent respiratory bacterial infections and/or gastrointestinal candidiasis. The clinical course and gross and microscopic proventricular lesions were similar to those described in psittacine and passerine pet birds colonized by M. ornithogaster-like microorganisms but differed from published case reports and experimental infections of chickens in which the clinical signs and lesions have been considerably milder. The findings presented in this paper suggest that mycotic proventriculitis, presumably associated with M. ornithogaster, may be a serious but possibly opportunistic, although unusual, disease problem in gray partridges on game farms.     

A comparison of equine and bovine sera as sources of lipopolysaccharide-binding protein activity in equine monocytes incubated with lipopolysaccharide

Lipopolysaccharide-binding protein (LBP) is an acute phase protein that binds the lipid A moiety of lipopolysaccharide (LPS) and transfers LPS monomers to soluble CD14 in plasma or membrane bound CD14 on mononuclear phagocytes. The result of these interactions is activation of the TLR4 receptor complex, and the synthesis and release of inflammatory mediators. Inclusion of LBP in cellular assays increases the sensitivity of cells expressing CD14 to LPS. Therefore, the objectives of this study were to (1) compare differentially treated sera from cattle and horses as sources of LBP activity using LPS-induced expression of procoagulant activity (PCA) by equine monocytes as a readout and (2) evaluate the use of commercial equine serum as a source of LBP activity using LPS concentration response and time course studies to validate the response. Monocytes were isolated from eight horses and incubated with five different serum preparations in the presence or absence of Escherichia coli LPS. The sera tested were heat-inactivated fetal bovine serum (HI-FBS), pooled commercial equine serum (CES), heat-inactivated pooled commercial equine serum (HI-CES), autologous equine serum (AES), and heat-inactivated autologous equine serum (HI-AES). In the absence of LPS, monocytes from half of the horses in the study had increased expression of PCA when incubated with HI-FBS alone; PCA was unaffected by incubation with the other sera. There was a four-fold increase in PCA when monocytes were incubated with LPS in the presence of CES, HI-CES or AES compared to LPS without serum. The combination of HI-FBS and LPS increased PCA 20-fold compared to LPS without serum. The HI-AES serum lacked significant LBP activity. Whereas maximal expression of PCA was induced by 1ng/ml of LPS in the absence of serum, inclusion of 1% CES reduced the LPS concentration required for maximal PCA to 30pg/ml. Monocytes incubated with LPS in the presence of CES had increased PCA at 3h and peaked at 6h. In conclusion, monocytes from many horses are directly stimulated by HI-FBS, suggesting that HI-FBS is not an optimal source of LBP for in vitro studies of LPS with equine monocytes. In contrast, CES and AES are effective sources of LBP activity for such studies, as they do not directly induce activation. Although the heat inactivation process did not affect the LBP activity in CES, it ablated LBP activity in AES. Consequently, investigators are advised to utilize either CES or AES in future studies, but not heat-inactivated AES.     

Escherichia coli inoculation of porcine mammary glands affects local mRNA expression of Toll-like receptors and regulatory cytokines

The expression of mRNAs for the Toll-like receptors (TLRs) TLR2 and TLR4, pro- and anti inflammatory cytokines and their receptors was evaluated in mammary gland biopsy material collected from sows intramammarily inoculated with Escherichia coli strain O127 at parturition. Quantitative real-time RT-PCR analysis showed increased mRNA levels for TLR2, the proinflammatory cytokines interleukin IL-1beta and tumor necrosis factor-alpha TNF-alpha, and the anti-inflammatory cytokine IL-10 in the inoculated mammary glands 24h after inoculation. Increased mRNA levels of the proinflammatory cytokine IL-6 were only observed in the inoculated mammary glands of sows that developed clinical signs of mastitis. In contrast, the expression of the anti-inflammatory cytokine, transforming growth factor-beta 1 (TGF-beta1) mRNA was unaltered, as was mRNA expression for the IL-1 receptor type I (IL-1R1). Furthermore, IL-1beta and IL-10 mRNA expression was higher in the inoculated mammary glands of sows that developed clinical signs of mastitis compared with sows that remained clinically healthy. Notably, sows that developed clinical signs of mastitis had significantly lower pre-inoculation levels of IL-1beta mRNA than sows that remained clinically healthy. These findings suggest that development of coliform mastitis is associated with the level of local expression of regulatory cytokines in response to intramammary E. coli inoculation and infection.