Complementary sex determination, inbreeding depression and inbreeding avoidance in a gregarious sawfly.

Although most Hymenoptera reproduce via arrhenotokous haplodiploidy, the underlying genetic mechanisms vary. Of these, the most widespread mechanism appears to be single-locus complementary sex determination (sl-CSD), in which individuals that are diploid and heterozygous at a sex-determining locus are female, and individuals that are homozygous or hemizygous are male. Because inbreeding increases the probability of producing diploid males, which are often sterile or inviable, sl-CSD can generate substantial inbreeding depression. To counteract this, Hymenoptera with traits that promote inbreeding, such as gregariousness, may evolve one or more of the following: inbreeding avoidance, functional diploid males or alternative sex determination mechanisms. Here, we investigate sex determination, inbreeding depression and inbreeding avoidance in Neodiprion lecontei, a gregarious, pine-feeding sawfly in the family Diprionidae. First, via inbreeding experiments and flow cytometry, we demonstrate that this species has CSD. By modeling expected sex ratios under different conditions, we also show that our data are consistent with sl-CSD. Second, via tracking survival in inbred and outbred families, we demonstrate that inbred families have reduced larval survival and that this mortality is partly attributable to the death of diploid males. Third, using a no-choice mating assay, we demonstrate that females are less willing to mate with siblings than nonsiblings. Together, these results suggest that inbreeding depression stemming from CSD has shaped mating behavior in N. lecontei. These results also set the stage for future comparative work that will investigate the interplay between sex determination, ecology and behavior in additional diprionid species that vary in larval gregariousness.

Magnetic resonance imaging in dogs with neurologic impairment due to acute thoracic and lumbar intervertebral disk herniation.

BACKGROUND: Magnetic resonance imaging (MRI) is a correlate to physical examination in various myelopathies and a predictor of functional outcome. OBJECTIVES: To describe associations among MRI features, neurological dysfunction before MRI, and functional outcome in dogs with disk herniation. ANIMALS: One hundred and fifty-nine dogs with acute thoracolumbar disk herniation. METHODS: Retrospective case series. Signalment, initial neurological function as assessed by a modified Frankel score (MFS), and ambulatory outcome at hospital discharge and >3 months (long-term) follow-up were recorded from medical records and telephone interview of owners. Associations were estimated between these parameters and MRI signal and morphometric data. RESULTS: Dogs with intramedullary T2W hyperintensity had more severe pre-MRI MFS (median 2, range 0-4) and lower ambulatory proportion at long-term follow-up (0.76) than those dogs lacking hyperintensity (median MFS 3, range 0-5; ambulatory proportion, 0.93) (P=.001 and .013, respectively). Each unit of T2W length ratio was associated with a 1.9 times lower odds of long-term ambulation when adjusted for pre-MRI MFS (95% confidence interval 1.0-3.52, P=.05). Dogs with a compressive length ratio >1.31 (which was the median ratio within this population) had more severe pre-MRI MFS (median 3, range 0-5) compared with those with ratios < or =1.31 (median MFS 3, range 0-4; P=.006). CONCLUSIONS AND CLINICAL IMPORTANCE: MRI features were associated with initial injury severity in dogs with thoracolumbar disk herniation. Based on results of this study, the T2W length ratio and presence of T2W intramedullary hyperintensity appear to be predictive of long-term ambulatory status.

Pneumonia after intracranial surgery in dogs.

OBJECTIVE: To determine factors associated with the occurrence of pneumonia after intracranial surgery in dogs. STUDY DESIGN: Retrospective cohort study. Animals-Forty-nine client-owned dogs. METHODS: The medical records of 49 dogs with space-occupying intracranial disease that underwent craniotomy were reviewed. Development of pneumonia after surgery was considered highly likely in 12 dogs (affected dogs) based on clinical signs, including acute dyspnea or coughing in association with typical radiographic findings or abnormal transtracheal wash results. Pneumonia was confirmed in 6 dogs based on necropsy findings. Affected dogs were compared with 37 dogs that did not develop pneumonia (unaffected dogs) subsequent to intracranial surgery. Based on the medical records of affected dogs, determinations were made regarding time between development of pneumonia and surgery, surgical procedure, intracranial lesion type, and intracranial lesion location. Risk factors examined for both affected and unaffected dogs included level of consciousness, body position during the postoperative recovery period, duration of anesthesia, occurrence of vomiting or regurgitation, presence of seizures, cranial nerve deficiencies, and the presence of megaesophagus before and after surgery. We also compared the feeding protocol after surgery for each group. RESULTS: Pneumonia typically occurred within the first week after surgery (median, 6.5 days); however, this was variable (range, 1-96 days). Of the factors that were present within 24 hours before the clinical signs of pneumonia, vomiting or regurgitation and megaesophagus were found to be significant risk factors. Dogs that vomited or regurgitated were 2.71 times more likely to develop pneumonia than dogs that did not. Vomiting or regurgitation occurred in 63% of the dogs that developed pneumonia in this cohort. Dogs with megaesophagus were 9.25 times more likely to develop pneumonia than dogs without megaesophagus. Seven dogs with pneumonia died. Five of these 7 dogs appeared to have died as a direct sequel to pneumonia. CONCLUSION: Dogs undergoing craniectomies for space-occupying intracranial disease may be at higher risk for development of pneumonia due to several factors, including vomiting, regurgitation, and megaesophagus.

Magnetic resonance imaging features of equine nigropallidal encephalomalacia.

Magnetic resonance imaging (MR) was used to make a diagnosis of equine nigropallidal encephalomalacia in a horse. Equine nigropallidal encephalomalacia is a neurodegenerative disease that has many characteristics with Parkinson-like diseases in humans. Historically, horses were euthanized based on clinical signs and exposure to the toxic weed, yellow star thistle (Centaurea solstitialis). Previously, the disease has only been confirmed on necropsy. MR imaging can provide accurate and sensitive visualization of typical lesions seen in the brain of horses affected with equine nigropallidal encephalomalacia. Lesions were seen on T1-weighted, T2-weighted and proton density images. There was no contrast enhancement following Gd-DTPA administration. Lesions seen on MR were confirmed at necropsy. Using MR to confirm a diagnosis of equine nigropallidal encephalomalacia will prevent unnecessary suffering of horses and expense to owners that would otherwise incur, while further diagnostics are performed.

Radiographic diagnosis: cartilaginous exostoses in a dog.

A 6 month-old dog was examined for progressive paraparesis. On physical examination bony malformations were palpated over the cranial lumbar vertebral bodies and on the left metatarsal bone. Neuroanatomic lesion localization for the paraparesis was a T3-L3 spinal cord lesion. Radiographs confirmed bony masses at L1-L2 and on the left 3rd metatarsal bone. Magnetic resonance imaging was performed from T3-L3. Severe spinal cord compression was identified at L1-L2. Surgical decompression and biopsy confirmed the mass to be cartilaginous exostoses. This paper is an example of cartilaginous exostoses imaged with MR.

Effects of changes in power setting of an ultrasonic aspirator on amount of damage to the cerebral cortex of healthy dogs.

OBJECTIVE: To determine the minimal ultrasonic aspirator pressure necessary to damage the cerebral cortex of healthy dogs. ANIMALS: 9 mixed-breed dogs. PROCEDURE: The study comprised 2 parts. In part A, 6 dogs were euthanatized immediately prior to the experiment. In part B, 3 dogs were anesthetized for recording of physiologic variables. In both parts, craniectomy and durotomy were performed to bilaterally expose the lateral aspect of the cerebral cortex. An ultrasonic aspirator was placed in contact with various areas of the cerebral cortex, and aspirator power was altered (10, 20, 30, and 40%). Duration of contact at each power was 5 and 10 seconds. Subsequently, gross morphologic and histologic damage was assessed in the cortex. RESULTS: Gross observations for all dogs were similar. At 10% power, visible or histologic damage was not evident in the cortex. At 20% power, the cortex was slightly indented from contact with the hand piece; however, cortical disruption was not evident. Cortical disruption was initially detectable at 30% power in some dogs and was consistently evident at 40% power in both sets of dogs. CONCLUSIONS AND CLINICAL RELEVANCE: Ultrasonic aspirator power of < 20% created minimal acute morphologic damage to the cortex. Power settings between 20 and 30% may superficially damage the cerebral cortex in healthy dogs, whereas 40% power consistently damages the cerebral cortex. Knowledge of the degree of damage to cerebral cortex caused by various amounts of power for ultrasonic aspirators will allow surgeons to avoid damaging normal brain tissues during surgery.

Cerebellar cystic meningioma in a dog.

A 21-kg, seven-year-old, male, mixed-breed Labrador retriever was admitted for incoordination and a head tilt of approximately three months' duration. Ataxia was noted of the trunk and limbs, and there was a head tilt to the right side. Conscious proprioceptive deficits were present in the left thoracic and pelvic limbs (i.e., hemiparesis). These abnormalities were consistent with paradoxical vestibular syndrome and a lesion involving the caudal cerebellar peduncle. A mass lesion consisting primarily of fluid was present on magnetic resonance imaging and at craniectomy. Histopathological diagnosis was a cystic meningioma. Based upon previous reports and experience, the location of this tumor was unusual.

Spinal fracture or luxation.

Spinal trauma is a common cause of spinal cord dysfunction in dogs and cats. When the spine is injured by exogenous injury, the impact often results in vertebral fracture or luxation. As each injury is unique, treatment guidelines have to be individualized to the animal. This article reviews the clinical management including surgical and nonsurgical treatments for animals with vertebral fracture/luxation.

Magnetic resonance imaging features of tumors of the spine and spinal cord in dogs.

Twenty-one dogs with confirmed tumors of the spinal cord or paraspinal tissues were imaged with magnetic resonance (MR) imaging. Anatomical location, location in relation to the dura and the medulla (spinal cord), and bone infiltration were assessed on the MR images and compared to findings at surgery or necropsy. Localization of tumors in the intradural-extramedullary compartment was not always possible. Bone infiltration was correctly assessed in all but one dog, and the anatomical locations involved were accurately determined in all dogs. Sagittal T2-weighted images were helpful to determine the anatomical location. Transverse T1-weighted images pre and post Gd-DTPA administration were helpful for additional localization and definition of tumor extension.

Clinical signs associated with brain tumors in dogs: 97 cases (1992-1997).

OBJECTIVE: To determine the prevalence of various clinical signs in dogs with brain tumors. DESIGN: Retrospective study. ANIMALS: 97 dogs with brain tumors. PROCEDURE: Medical records were reviewed for signalment, tumor type and location, and clinical signs. RESULTS: 33 breeds were represented; Golden Retrievers were most commonly affected. Most dogs were older (median age, 9 years); 95% of dogs were > or = 5 years old. Seventy-six percent of dogs had tumors in the supratentorial region. Seizures were the most common clinical sign at initial examination, with lower prevalence for circling, ataxia, and head tilt. Meningioma was the most common tumor. CONCLUSIONS AND CLINICAL RELEVANCE: Brain tumors develop most often in dogs > or = 5 years old and are uncommon in dogs < 5 years old. Seizures are a common clinical sign, and a brain tumor should be considered in dogs that have their first seizure after they are 4 years old.

Contribution of plasmid DNA to inflammation in the lung after administration of cationic lipid:pDNA complexes.

Cationic lipid-mediated gene transfer to the mouse lung induces a dose-dependent inflammatory response that is characterized by an influx of leukocytes and elevated levels of the cytokines interleukin 6 (IL-6), tumor necrosis factor alpha (TNF-alpha), and interferon gamma (IFN-gamma). We have examined the contribution of plasmid DNA (pDNA) to this observed toxicity, specifically the role of unmethylated CpG dinucleotides, which have been previously shown to be immunostimulatory. We report here that complexes of cationic lipid GL-67 and unmethylated pDNA (pCF1-CAT) instilled into the lungs of BALB/c mice induced highly elevated levels of the cytokines TNF-alpha, IFN-gamma, IL-6, and IL-12 in the bronchoalveolar lavage fluids (BALF). In contrast, BALF of animals administered either GL-67 alone or GL-67 complexed with SssI-methylated pDNA contained low levels of these cytokines. Similar results were observed using a plasmid (pCF1-null) that does not express a transgene, demonstrating that expression of chloramphenicol acetyltransferase (CAT) was not responsible for the observed inflammation. The response observed was dose dependent, with animals receiving increasingly higher amounts of unmethylated pDNA exhibiting progressively higher levels of the cytokines. Concomitant with this increase in cytokine levels were also elevated numbers of neutrophils in the BALF, suggesting a possible cause- and-effect relationship between neutrophil influx and generation of cytokines. Consistent with this proposal is the observation that reduction of neutrophils in the lung by administration of antibodies against Mac-1alpha and LFA-1 also diminished cytokine levels. This reduction in cytokine levels in the BALF was accompanied by an increase in transgene expression. In an attempt to abate the inflammatory response, sequences in the pDNA encoding the motif RRCGYY, shown to be most immunostimulatory, were selectively mutagenized. However, instillation of a plasmid in which 14 of the 17 CpG sites were altered into BALF/c mice did not reduce the levels of cytokines in the BALF compared with the unmodified vector. This suggests that other unmethylated motifs, in addition to RRCGYY, may also contribute to the inflammatory response. Together, these findings indicate that unmethylated CpG residues in pDNA are a major contributor to the induction of specific proinflammatory cytokines associated with instillation of cationic lipid:pDNA complexes into the lung. Strategies to abate this response are warranted to improve the efficacy of this nonviral gene delivery vector system for the treatment of chronic diseases.

Seizures as a complication of brain tumors in dogs.

Seizures are a common reflection of a variety of intracranial physiologic abnormalities in dogs. In dogs with brain tumors, seizures often provide the clinical clue to the existence of an underlying structural brain disease. The majority of brain tumors that result in seizures affect the supratentorial nervous system, especially the olfactory and frontal lobes. Diagnosis requires advanced imaging such as computed tomography (CT) or magnetic resonance imaging (MRI) to establish the presence of a structural abnormality. Therapy is directed both at tumor and seizure control to afford the best chance of successful management of dogs with brain tumors.

Realignment of a seventh lumbar vertebral fracture/luxation using a Senn retractor in two puppies.

Two puppies, each with fractures of the seventh lumbar (L7) vertebra, had their vertebral canals aligned surgically with the aid of a Senn retractor. The retractor was used to provide leverage during vertebral manipulations. Surgical fixation was achieved using Steinmann pins and polymethylmethacrylate. Both puppies were improved immediately after surgery and were clinically normal six months after surgery.

Clinical features of trigeminal nerve-sheath tumor in 10 dogs.

Nerve-sheath tumor was diagnosed in 10 dogs with clinical signs of unilateral trigeminal nerve dysfunction. Unilateral temporalis and masseter muscle atrophy were present in all cases. An enlarged foramen and distorted rostral petrous temporal bone were seen with computed tomography imaging in one case. Magnetic resonance imaging was used to identify the lesion accurately in seven cases. Surgery was performed for biopsy and lesion removal in three cases. Cases not treated had a progressive course eventually resulting in euthanasia or death. Of the cases treated surgically, one case is alive without disease progression 27 months after surgery. Survival times of the nontreated cases ranged from five to 21 months.

Scoliosis and associated cystic spinal cord lesion in a dog.

A 7-month-old female Mastiff was admitted for weakness in the hind limbs and an abnormal gait. There was an obvious scoliosis in the midlumbar region. Using electromyography, fibrillation potentials and positive sharp waves were found in the epaxial musculature of the vertebral column lateral to the spinous processes of Tl3-L4 on the right (convex) side of the body. On myelographic evaluation, contrast medium irregularly filled the subdural and epidural space of Tl1-L3. On surgical examination, the dog had a cystic lesion of the spinal cord that correlated with myelographic findings. This lesion was incised and drained. The scoliotic defect was surgically straightened, and the affected vertebrae were fused. Six months after surgery, the vertebral column continued to be straight and the paraparesis had resolved.

Idiopathic polyneuropathy in Alaskan malamutes.

Clinical and morphologic features of a progressive polyneuropathy in young mature Alaskan Malamutes are described. Clinical signs included progressive paraparesis, synchronous pelvic limb gait, exercise intolerance, hyperesthesia, hyporeflexia, muscle atrophy, and tetraplegia. Electromyographic testing revealed diffuse fibrillation potentials and positive sharp waves in limb muscles, especially in muscles below the elbow and stifle. Pathologic findings in skeletal muscles and peripheral nerves included neurogenic muscle atrophy, focal or diffuse loss of myelinated nerve fibers, myelinoaxonal necrosis, and variable demyelination or remyelination. Ultrastructural changes included axonal degeneration, presence of numerous Büngner bands, and denervated Schwann cell subunits. The nature and distribution of abnormal electrophysiologic and pathologic findings were suggestive of a distal sensorimotor polyneuropathy, which we have termed idiopathic polyneuropathy of Alaskan Malamutes to distinguish this condition from hereditary polyneuropathy of Norwegian Alaskan Malamutes, last described in 1982.