Cervical vertebral canal endoscopy in the horse: intra- and post operative observations

Reasons for performing study: Despite modern medical diagnostic imaging, it is not possible to identify reliably the exact location of spinal cord compression in horses with cervical vertebral stenotic myelopathy (CVSM). Vertebral canal endoscopy has been successfully used in man and a technique for cervical vertebral canal endoscopy (CVCE) has been described in equine cadavers. Objective: To determine the feasibility and safety of CVCE in healthy mature horses. Methods: Six healthy mature horses were anaesthetised. A flexible videoendoscope was subsequently introduced via the atlanto‐occipital space into the epidural space (epiduroscopy, Horses 1–3) or the subarachnoid space (myeloscopy, Horses 4–6) and advanced to the 8th cervical nerve. Neurological examinations were performed after surgery and lumbosacral cerebrospinal fluid (CSF) analysed in horses that had undergone myeloscopy. Results: All procedures were completed successfully and all horses recovered from anaesthesia. Anatomical structures in the epidural space (including the dura mater, nerve roots, fat and blood vessels) and subarachnoid space (including the spinal cord, blood vessels, arachnoid trabeculations, nerve roots and the external branch of the accessory nerve) were identified. During epiduroscopy, a significant increase in mean arterial pressure was recognised, when repeated injections of electrolyte solution into the epidural space were performed. In one horse of the myeloscopy group, subarachnoid haemorrhage and air occurred, resulting in transient post operative ataxia and muscle fasciculations. No complications during or after myeloscopy were observed in the other horses. CSF analysis indicated mild inflammation on Day 7 with values approaching normal 21 days after surgery. Conclusions: Endoscopic examination of the epidural and subarachnoid space from the atlanto‐occipital space to the 8th cervical nerve is possible and can be safely performed in healthy horses. Potential relevance: Cervical vertebral canal endoscopy might allow accurate identification of the compression site in horses with CVSM and aid diagnosis of other lesions within the cervical vertebral canal.     

Otitis media‐interna and secondary meningitis associated with Corynebacterium pseudotuberculosis infection in a horse

A one‐year‐old Thoroughbred colt was evaluated because of facial nerve paralysis, ataxia and fever. Neurological evaluation found the colt to be obtunded and grade 3/5 ataxic in all 4 limbs. Right‐sided facial nerve paralysis was present and a large, deep corneal ulcer noted in the right eye. Signs of vestibular disease were also present, including circling towards the right and horizontal nystagmus. A complete blood count showed mild leucocytosis, neutrophilia and hyperfibrinogenaemia. A computed tomography (CT) examination of the skull was performed under general anaesthesia and a diagnosis of right sided otitis media‐interna was made. Culture of fluid taken from the middle ear and cerebrospinal fluid collected from the atlanto‐occipital site yielded pure growth of Corynebacterium pseudotuberculosis. Initial therapy consisted of antimicrobial treatment with cefotaxime and anti‐inflammatory treatment with flunixin meglumine. Six days after initiating treatment, the colt developed Clostridium difficile associated colitis. The colitis resolved with supportive care and the colt was discharged from the hospital receiving chloramphenicol. Eight months later, the colt continued to be mildly ataxic (grade 1/5), with a slight head tilt and facial nerve paralysis. To the authors' knowledge, this is the first reported case of otitis media‐interna due to C. pseudotuberculosis in the horse.     

Modulation of formalin‐induced pain‐related behaviour by clonidine and yohimbine in the Speke's hinged tortoise (Kiniskys spekii)

The study was designed to investigate the involvement of noradrenergic and serotonergic receptor systems in the modulation of formalin‐induced pain‐related behaviour in the Speke's hinged tortoise. Intradermal injection of 100 μL of formalin at a dilution of 12.5% caused pain‐related behaviour (hindlimb withdrawal) that lasted for a mean time of 19.28 min (monophasic response). Intrathecal administration of clonidine (α₂‐adrenergic receptor agonist) and yohimbine (α₂‐adrenergic receptor antagonist) at a dose of 40 μg/kg and 37.5 μg/kg or 50 μg/kg, respectively, caused a highly significant reduction in the duration of the formalin‐induced pain‐related behaviour. The effect of clonidine was reversed by intrathecal administration of yohimbine at a dose of 26.7 μg/kg. The effect of yohimbine at a dose of 50 μg/kg was reversed by intrathecal injection of 20 μg/kg of the serotonergic receptor antagonist methysergide maleate. When performing antagonistic reactions, the administration of the antagonist was followed immediately by that of the agonist. The study indicates that for experimental purposes, intrathecal route of drug administration through the atlanto‐occipital joint is effective in tortoises. The data also suggest that testudines have noradrenergic and serotonergic systems that appear to play a role in the modulation of pain in this species.     

Imaging diagnosis and clinical presentation of a Chiari malformation in a Thoroughbred foal

A newborn Thoroughbred foal was presented to the clinic with ambiguous neurological deficits, spinal anomalies and a soft tissue swelling dorsal to the lumbar vertebral column. The foal was alert but unable to rise and stand. With radiography, ultrasonography, computed tomography (CT) and magnetic resonance imaging (MRI) a lumbar dysraphic anomaly, cerebellar herniation and coincidental skeletal abnormalities were documented. Finally, a meningomyelocele was defined and, in context with the cerebellar herniation through the foramen magnum, the foal was diagnosed to have a Chiari malformation. The MRI examination corresponded best with the post mortem findings. Although 3‐dimensional imaging methods have been considered superior regarding full and detailed assessment of the congenital malformation, radiography and ultrasonography also provide essential information to diagnose dysraphic lesions at reduced costs and efforts. A Chiari malformation should be considered as a differential diagnosis in foals with neurological deficits.     

Radiographic retrospective study of the caudal cervical articular process joints in the horse

Reasons for performing study: Arthropathy of the caudal cervical articular process joints (APJs) in the horse is documented as a cause of ataxia and paresis secondary to spinal cord compression. Enlargement of the caudal APJs is reported to increase with age, but there are no known associations of any other factors. No association of the degree of APJ enlargement with neurological signs seen has been documented. This study investigated the associations of cervical APJ enlargement at the C5‐C6 and C6‐C7 articulations with case subject details (breed, age, sex, usage) and clinical signs. Objectives: To ascertain if there are of any associations between: the subject details and enlargement of the caudal cervical APJs; and the degree of APJ enlargement and the presence and type of clinical signs. Hypotheses: There would be an effect of age, breed and usage on APJ grade, with no effect of sex. Association between grade and clinical signs seen was also investigated. Materials and methods: The radiographs of 122 horses qualified for inclusion. Horses were excluded if they were known to have a neck lesion cranial to C5‐C6, or if the radiographs were rotated or of poor quality. In order to standardise the interpretation of APJ enlargement, a novel grading system was developed and used. Results: An association was found between age and APJ grade at C5‐C6 but not C6‐C7. There was no association between grade, breed, sex and usage, or clinical signs seen. Data also showed a trend for increasing enlargement the more caudal the APJ. Conclusion and potential relevance: The data in this study support that the size of the caudal cervical APJ at the level of C5‐C6, appear to increase with age, but this enlargement may not be significant. Enlargement cannot be associated with breed, sex or discipline of the horse at present, and specific grades and therefore degree of enlargement, cannot necessarily be assumed to be the cause of neurological deficits.     

Ultrasonographic Percutaneous Anatomy of the Atlanto‐Occipital Region and Indirect Ultrasound‐Guided Cisternal Puncture in the Dog and the Cat

Cisternal puncture in dogs and cats is commonly carried out. This article describes the percutaneous ultrasound anatomy of the cisternal region in the dog and the cat and an indirect technique for ultrasound‐guided cisternal puncture. Ultrasound images obtained ex vivo and in vivo were compared with anatomic sections and used to identify the landmarks for ultrasound‐guided cisternal puncture. The ultrasound‐guided procedure was established in cadavers and then applied in vivo in seven dogs and two cats. The anatomic landmarks for the ultrasound‐guided puncture are the cisterna magna, the spinal cord, the two occipital condyles on transverse images, the external occipital crest and the dorsal arch of the first cervical vertebra on longitudinal images. Using these ultrasound anatomic landmarks, an indirect ultrasound‐guided technique for cisternal puncture is applicable in the dog and the cat.     

Delayed onset vagus nerve paralysis after occipital condyle fracture in a horse

Occipital condylar fractures (OCFs) causing delayed onset lower cranial nerve paralysis (LCNPs) are rare. We present a 7‐year‐old Friesian horse with delayed onset dysphagia caused by vagus nerve (CNX) paralysis and suspicion of glossopharyngeal nerve (CNIX) paralysis developed several days after a minor head injury. Endoscopic examination revealed right laryngeal hemiplegia and intermittent dorsal displacement of the soft palate. An area of submucosal hemorrhage and bulging was appreciated over the dorsal aspect of the medial compartment of the right guttural pouch. Radiological examination of the proximal cervical region showed rotation of the atlas and the presence of a large bone fragment dorsal to the guttural pouches. Occipital condyle fracture with delayed onset cranial nerve paralysis was diagnosed. Delayed onset cranial nerve paralysis causing dysphagia might be a distinguishable sign of OCF in horses. Delayed onset dysphagia after head injury should prompt equine clinicians to evaluate the condition of the atlanto‐occipital articulation and skull base.     

Intracranial botryomycosis in a mature horse

This case report describes an unusual diagnosis of central nervous system botryomycosis in a horse. A 16‐year‐old Welsh Section D gelding was evaluated for acute onset of hypermetric ataxia, leaning to the left and head tilt to the right. Based on the neurological signs, a cerebellar lesion with accompanying vestibular disease was suspected and supportive therapy consisting of antimicrobial and glucocorticosteroid drugs and hypertonic saline was instituted. This resulted in marked clinical improvement over a 48 h period. Computed tomography performed in the standing, sedated horse following initial stabilisation identified extensive sclerosis and lysis of the right temporal and occipital bones, consistent with an infectious or neoplastic process. Based on the grave prognosis for survival despite the clinical improvement, euthanasia was undertaken. Post mortem magnetic resonance imaging identified a mass lesion impinging on the right cerebellar hemisphere, sclerosis of the temporal and occipital bones lateral and ventral to the mass, as well as destruction of the temporal bone between the inner ear and the cerebellum. These changes corresponded to the presence of a mass within the right dorsal temporal bone, extending into the right lateral temporal bone. The mass extended to compress and adhere to the right lateral hemisphere of the cerebellum. A histopathological diagnosis of botryomycosis was made, affecting the temporal and occipital bones and compressing the cerebellum.     

COMPARISON OF CLOSURE TIMES FOR CRANIAL BASE SYNCHONDROSES IN MESATICEPHALIC,BRACHYCEPHALIC, AND CAVALIER KING CHARLES SPANIEL DOGS

Premature closure of cranial base synchondroses has been proposed as the mechanism for brachycephaly in dogs and caudal occipital malformation syndrome (COMS) in Cavalier King Charles Spaniels. The purpose of this retrospective study was to compare times of closure for cranial base synchondroses in mesaticephalic, brachycephalic, and Cavalier King Charles Spaniel dogs. Cranial magnetic resonance imaging studies were retrieved for client‐owned dogs less than 18 months of age. Breed, age, skull conformation, and the open or closed state of cranial base synchondroses were independently recorded by two observers. For dogs with a unanimous observer agreement, regression analysis was used to test effects of age and gender on the open or closed status of synchondroses and differences between groups. A total of 174 dogs were included in MRI interpretations and 165 dogs were included in the regression analysis. Statistically significant differences in closure time of the spheno‐occipital synchondrosis were identified between brachycephalic and mesaticephalic dogs (P = 0.016), Cavalier King Charles Spaniels and mesaticephalic dogs (P < 0.0001), and Cavalier King Charles Spaniels and brachycephalic dogs (P = 0.014). Findings from the current study supported the theory that morphological changes leading to the skull phenotype of the Cavalier King Charles Spaniels could be due to an earlier closure of the spheno‐occipital synchondrosis.     

Ataxia and weakness as uncommon primary manifestations of hepatic encephalopathy in a 15‐year‐old trotter gelding

A 15‐year‐old trotter gelding was evaluated because of an acute onset of ataxia in all 4 limbs. There was no known history of trauma. The gelding showed grade 2/5 ataxia in all 4 limbs, which was localised after clinical neurological examination to the cervical vertebral spinal cord. Initial therapy consisted of oral anti‐inflammatory doses of prednisolone and antimicrobial treatment with potentiated sulphonamides. The ataxia progressed to grade 3/5 at Day 10 of hospitalisation. Additionally, the horse was slightly depressed and showed spontaneous yawning during examination. Facial sensation was blunted. Blood chemistry revealed a marked elevation of liver specific enzymes and blood ammonia levels. Transcutaneous abdominal ultrasonography revealed hepatomegaly. Due to a guarded prognosis, the horse was subjected to euthanasia. At necropsy the left lateral liver lobe was markedly enlarged and showed a firm texture, whereas the cranial part and the right and quadratic liver lobe displayed a severe and diffuse atrophy. Histopathologically, the left lateral liver lobe revealed a moderate to severe cirrhosis with a severe, diffuse hepatocellular iron‐accumulation. Increased numbers of Alzheimer type II astrocytes in the cerebral cortex and cerebral white matter vacuolisation were indicative for encephalopathy. These findings were interpreted as haemosiderosis and cirrhosis of the liver with consecutive hepatic encephalopathy. Aetiologically, haemosiderosis should be considered as a cause of liver cirrhosis with consecutive hepatic encephalopathy. Although hepatic encephalopathy in horses usually presents with predominating cerebral signs, it has to be taken into account as a differential diagnosis in cases of acute onset generalised ataxia.     

CLINICAL,IMAGING, AND PATHOLOGIC CHARACTERISTICS OF GURLTIA PARALYSANS MYELOPATHY IN DOMESTIC CATS FROM CHILE

Gurltia paralysans is a rare metastrongylid nematode of domestic cats that is found mainly in the veins of the spinal cord subarachnoid space and parenchyma. Endemic regions for G. paralysans mainly include Chile and Argentina. The ante mortem diagnosis of gurltiosis is difficult and based primarily on neurological signs, epidemiological factors, and the exclusion of other causes of feline myelopathies. The purpose of this retrospective case series was to describe clinical, imaging, and pathologic characteristics in nine domestic cats naturally infected with G. paralysans. Imaging tests included radiography, myelography, computed tomographic myelography (myelo‐CT), and magnetic resonance imaging (MRI). Neurological signs included paraparesis, paraplegia, pelvic limb ataxia and proprioceptive deficits, pelvic limb tremors, lumbosacral hyperesthesia, and tail trembling or atony. Complete blood count findings included a decrease in the mean corpuscular hemoglobin concentration value in eight cats. Eosinophilia in peripheral blood was observed in three cats, and thrombocytopenia was observed in three cats. Cerebrospinal fluid analysis revealed mononuclear pleocytosis in five cases. Myelo‐CT showed diffuse enlargement of the spinal cord at the midthoracic, lumbar, and sacral regions in all cats. Magnetic resonance image findings in the thoracic and lumbar region demonstrated multiple small nodular areas of T2 hyperintensity in the periphery of the spinal cord parenchyma. Localized intraparenchymal areas of increased T2 intensity were also observed in the thoracolumbar spinal cord and lumbosacral conus medullaris. In conclusion, G. paralysans should be considered as a differential diagnosis for domestic cats in endemic regions that have this combination of clinical and imaging characteristics.     

Chiari‐like malformation in two cats

Two male, neutered, domestic, shorthaired cats were evaluated for progressive paresis and ataxia. Neurological examinations suggested a spinal cord lesion in each case. Complete blood examination and cerebrospinal fluid analysis were unremarkable in both cats. MRI revealed malformation of the occipital bone with herniation of the cerebellar vermis through the foramen magnum but without syringomyelia. Chiari‐like malformation was suspected in both patients. MRI repeated one year later in both cats because of progression of clinical signs yielded the same findings as the initial scans. Foramen magnum decompression in one cat was associated with resolution of clinical signs.     

Brain penetration of emodepside is increased in P‐glycoprotein‐deficient mice and leads to neurotoxicosis

The antiparasitic drug emodepside (EMO) is a substrate of the P‐glycoprotein multidrug efflux carrier (P‐gp; syn. MDR1, ABCB1), which has an important function in protecting the brain from potentially toxic compounds by functional drug efflux at the blood–brain barrier (BBB). Many dogs of the Collie breed and even dogs of many other breeds have a loss‐of‐function 4‐bp deletion mutation in the MDR1 gene. In these dogs, brain penetration of many P‐gp‐transported drugs is increased and so their therapeutic usage is restricted. To elucidate the role of P‐gp at the BBB for the brain penetration of EMO, we applied EMO at 1 mg/kg to mdr1‐deficient (PGP^mut) and mdr1‐intact (PGP^WT) CF1 mice. Whereas in the brain of the PGP^WT mice, EMO was below the detection level of 10 ng/g, its concentration was at 43.7 ng/g in the PGP^mut mice. Furthermore, appearance of neurological toxicity was analyzed in these mice after application of 1 mg/kg EMO using a rotarod setup. In all PGP^mut mice, but not in the PGP^WT mice, the walking performance on the rotarod was impaired by EMO with clear differences in the degree and duration of neurological toxicity. Some of the mice were completely unable to walk on the rotarod already at 2 h after drug application and showed long‐lasting ataxia over >24 h. Others even showed significantly reduced walking performance, but completely recovered within 1 day. In conclusion, P‐gp restricts brain penetration of EMO and prevents neurological toxicity of this drug in mice.     

Intra‐uterine Infection with Babesia bovis in a 2‐day‐old Calf

Infection with Babesia bovis was diagnosed in a 2‐day‐old female calf apparently transmitted in utero. The calf was born as the second calving to a cross‐bred beef cow permanently on pasture. Diagnosis was based upon identification of B. bovis in peripheral blood smears and clinical signs which included fever, jaundice, pale mucous membranes and convulsions. Anaemia, leucocytosis, thrombocytopenia and lymphocytosis were noted at the febrile acute stage of the disease. The blood smears revealed evidence of regeneration of toxic neutrophils with a left shift, severe spherocytosis and high degree of basophilic stippling. Elevated concentration of aspartate aminotransferase, lactate dehydrogenase, and creatine kinase were also noted, and were probably the result of haemolysis, dehydration and muscle damage because of recumbancy. Elevated total bilirubin concentration following haemolysis resulted in jaundice. The neurological symptoms observed were probably caused by sludging of parasitized erythrocytes in the brain capillaries. The calf recovered following treatment with diminazene aceturate and the recovery was followed up clinically, haematologically and biochemically.     

Cerebrospinal Fluid Myelin Basic Protein as a Prognostic Biomarker in Dogs with Thoracolumbar Intervertebral Disk Herniation

Background: Release of myelin basic protein (MBP) into the cerebrospinal fluid (CSF) is associated with active demyelination and correlates with outcome in various neurological diseases. Hypothesis/Objectives: To describe associations among CSF MBP concentration, initial neurological dysfunction, and long‐term ambulatory outcome in dogs with acute thoracolumbar intervertebral disk herniation (IVDH). Animals: Five hundred and seventy‐four dogs with acute thoracolumbar IVDH and 16 clinically normal dogs. Methods: Prospective case series clinical study. Signalment, initial neurological dysfunction as determined by a modified Frankel score (MFS), and ambulatory outcome at >3‐month follow‐up were recorded. Cisternal CSF MBP concentration was determined by an ELISA. Associations were estimated between CSF MBP concentration and various clinical parameters. Results: Dogs with thoracolumbar IVDH that did not ambulate at follow‐up had a higher CSF MBP concentration (median, 3.56 ng/mL; range, 0.59–51.2 ng/mL) compared with control dogs (median, 2.22 ng/mL; range, 0–3.82 ng/mL) (P= .032). A CSF MBP concentration of ≥3 ng/mL had a sensitivity of 78% and specificity of 76% to predict an unsuccessful outcome based on receiver‐operating characteristics curve analysis (area under the curve =0.688, P= .079). Affected dogs with a CSF MBP concentration ≥3 ng/mL had 0.09 times the odds of ambulation at follow‐up compared with affected dogs with CSF MBP concentration <3 ng/mL when adjusted for initial MFS (95% confidence interval 0.01–0.66, P= .018). Conclusions and Clinical Importance: These results would suggest that CSF MBP concentration may be useful as an independent prognostic indicator in dogs with thoracolumbar IVDH.     

Paraparesis as initial manifestation of a Prototheca zopfii infection in a dog

A case of protothecosis causing non‐ambulatory paraparesis in a dog without clinical evidence of disseminated infection is described. A five‐year‐old female Labrador retriever was referred with a 10‐day history of progressive non‐ambulatory paraparesis and lumbar pain as the only physical and neurological abnormalities. Lumbar myelography revealed severe extradural spinal cord compression extending from L4 to L7 vertebrae, and a right hemilaminectomy was performed. Surgical findings included an adherent whitish hard ill‐defined mass. Cytology and biopsy results disclosed the presence of algae enclosed in a matrix of chronic inflammatory infiltrate. Culture confirmed the presence of Prototheca species. Neurological improvement occurred within a month, and the dog received antifungal treatment without evidence of clinical disseminated disease for 6 months, but died after a generalised tonic–clonic seizure. Post‐mortem examination revealed multiple foci of inflammatory granulomatous infiltrate and algae‐like structures in the brain, lumbar intumescence and cauda equina. Prototheca zopfii was identified using molecular biology methods.     

Ultrasonographic anatomy of the atlanto‐occipital region and ultrasound‐guided cerebrospinal fluid collection in rabbits (Oryctolagus cuniculus)

Cerebrospinal fluid analyses are important for diagnosis of neurologic problems in rabbits and for translational research projects using rabbits as models. Blind puncture of the cisterna magna is the current standard technique for sampling cerebrospinal fluid in this species. However, the complexity and small size of the cisterna magna and surrounding structures are limitations of this technique. Aims of this prospective, anatomic, pilot study were to (1) describe the normal anatomy of the atlanto‐occipital region, (2) describe ultrasonographic anatomic landmarks, and (3) develop and evaluate a technique for ultrasound‐guided puncture of the cisterna magna for cerebrospinal fluid sampling in rabbits. Thirty healthy rabbits were included and the study was conducted in three stages. Three rabbit cadavers were used for the first stage of the study. Then, the second stage was completed using 13 rabbit cadavers. Finally, the third stage was completed in 14 live rabbits. The ultrasound‐guided puncture performed in 13 cadavers was successful at the first attempt in 10 cases, and at the second attempt in the remaining three cases. In the in vivo study, the ultrasound‐guided puncture was successful in all 14 cases, without signs of complications. Findings supported the use of ultrasound‐guided puncture of the cisterna magna as a safe technique that may be used routinely or when the sample of cerebrospinal fluid cannot be obtained with the blind technique in rabbits.     

An unprecedented cluster of Australian bat lyssavirus in Pteropus conspicillatus indicates pre‐flight flying fox pups are at risk of mass infection

In November 2017, two groups of P. conspicillatus pups from separate locations in Far North Queensland presented with neurological signs consistent with Australian bat lyssavirus (ABLV) infection. These pups (n = 11) died over an 11‐day period and were submitted to a government laboratory for testing where ABLV infection was confirmed. Over the next several weeks, additional ABLV cases in flying foxes in Queensland were also detected. Brain tissue from ABLV‐infected flying foxes during this period, as well as archived brain tissue, was selected for next‐generation sequencing. Phylogenetic analysis suggests that the two groups of pups were each infected from single sources. They were likely exposed while in crèche at night as their dams foraged. This study identifies crèche‐age pups at a potentially heightened risk for mass ABLV infection.     

Effects of high‐sulphur water on hepatic gene expression of steers fed fibre‐based diets

Sulphur‐induced polioencephalomalacia (sPEM), a neurological disorder affecting ruminants, is frequently associated with the consumption of high‐sulphur (S) water and subsequent poor performance. Currently, there is no economical method for S removal from surface water sources, and alternative water sources are typically neither readily available nor cost‐effective. Determination of genes differentially expressed in response to high‐S water consumption may provide a better understanding of the physiology corresponding to high dietary S and ultimately lead to the development of treatment and prevention strategies. The objective of this study was to determine changes in gene expression in the liver, an organ important for S metabolism, of fibre‐fed steers consuming high‐S water. For this study, liver tissues were collected on the final day of a trial from yearling steers randomly assigned to low‐S water control (566 mg/kg SO₄; n = 24), high‐S water (3651 mg/kg SO₄; n = 24) or high‐S water plus clinoptilolite supplemented at either 2.5% (n = 24) or 5.0% (n = 24) of diet dry matter (DM). Microarray analyses on randomly selected healthy low‐S control (n = 4) and high‐S (n = 4; no clinoptilolite) steers using the Affymetrix GeneChip Bovine Genome Array revealed 488 genes upregulated (p < 0.05) and 154 genes downregulated (p < 0.05) in response to the high‐ vs. low‐S water consumption. Real‐time RT‐PCR confirmed the upregulation (p < 0.10) of seven genes involved in inflammatory response and immune functions. Changes in such genes suggest that ruminant animals administered high‐S water may be undergoing an inflammation or immune response, even if signs of sPEM or compromised health are not readily observed. Further study of these, and other affected genes, may deliver new insights into the physiology underlying the response to high dietary S, ultimately leading to the development of treatments for high S–affected ruminant livestock.