Molecular characterization of avian reovirus causing tenosynovitis outbreaks in broiler flocks, Iran.

Avian reoviruses (ARVs) cause arthritis, tenosynovitis, retarded growth, and malabsorption syndrome. After a long time of effective prevention and low rates of viral arthritis/ tenosynovitis in Iran, outbreaks of tenosynovitis in broiler flocks have increased in recent years. Lameness, splay legs, high rate of cull birds, poor performance, uneven birds at harvest, and condemnation at processing cause huge economic losses. In this study, ARVs from the tendons of birds from 23 broiler flocks with marked tenosynovitis were characterized, and their genetic relationship was examined. Analysis of the amino acid sequence of Sigma C protein revealed that all ARVs detected in affected broiler flocks shared genetic homogeneity and this suggests that a single genotype is involved in recent outbreaks. This genotype, so-called "Ardehal strain", is grouped in cluster I with vaccine strains. The amino acid sequence similarity between Ardehal and vaccine strains, including S1133, 1733, and 2408 was less than 80%. As the outbreaks have occurred in progenies of vaccinated flocks, it is proposed here that the difference between vaccine and field strains might contribute to the failure of currently available vaccines to induce protective immunity against Ardehal strain and this led to widespread viral tenosynovitis in Iran.

Caprine herpesvirus 2-associated malignant catarrhal fever of captive sika deer (Cervus nippon) in an intensive management system.

BACKGROUND: Caprine herpesvirus 2 (CpHV-2) infection usually induces chronic malignant catarrhal fever (MCF) in sika deer (Cervus nippon), with the primary signs of weight loss, dermatitis and alopecia. CASE PRESENTATION: Here, we report a case of CpHV-2-associated acute MCF in a sika deer herd raised in an intensive management system distant to the reservoir goats. Affected deer developed clinical signs of high fever (41 °C) followed by nasal discharge and lameness. Severe lesions of hemorrhage, necrosis and infiltration of lymphoid cells could readily be observed in the lung, kidney, heart valves and subcutaneous tissue surrounding a tendon. Etiologically, identical CpHV-2 specific DNA sequences were detected in peripheral blood lymphocyte (PBL) from the affected deer and reservoir goats. CONCLUSION: In summary, domestic goats were the reservoir of the CpHV-2, which is the causative agent of the outbreak of MCF in the three hinds. The disease was probably transmitted via aerosol infection. In addition, necrosis and inflammation in subcutaneous tissue surrounding a tendon was the reason for lameness. Therefore, MCF should be put into a differential diagnostic list when similar disease occurs in sika deer herds.

Prospective case-control study of toe tip necrosis syndrome (TTNS) in western Canadian feedlot cattle.

A case-control study was conducted to investigate potential risk factors for toe tip necrosis syndrome (TTNS) in western Canadian feedlot cattle. Feedlot veterinarians provided hooves from 222 animals that died of either TTNS ("cases") or from all other causes ("controls"). The claws were sectioned by researchers to confirm the diagnoses; there was very good agreement between the practitioners' field diagnosis and that of the researchers (Cohen's kappa = 0.81; P < 0.001). The sole thickness of the apical white line region was thinner (P < 0.001) in the cases (3.74 mm) than the controls (4.72 mm). Claws from cases were 5.0 [95% confidence interval (CI): 1.5 to 8.6; P < 0.001] and 7.3 times (95% CI: 1.5 to 69.3; P < 0.01) more likely than those of controls to yield a heavy growth of Escherichia coli and Trueperella pyogenes, respectively. Cases were 4.4 times (95% CI: 4.4 to 22.9; P < 0.001) more likely to be acutely/transiently infected with bovine viral diarrhea virus than were controls. The findings support the hypothesis that TTNS is initiated by excessive wear along the white line, leading to separation and bacterial colonization of the 3rd phalangeal bone (P3) and associated soft tissues.

Étude prospective de cas-témoins du syndrome de la nécrose du bout des orteils dans un parc d'engraissement de l'Ouest canadien. Une étude de cas-témoins a été réalisée pour investiguer les facteurs de risques potentiels pour le syndrome de la nécrose du bout des orteils (SNBO) chez le bétail des parcs d'engraissement de l'Ouest canadien. Les vétérinaires des parcs d'engraissement ont fourni des sabots provenant de 222 animaux qui sont morts soit du SNBO («cas¼) ou d'autres causes («témoins¼). Les ongles ont été sectionnés par les chercheurs pour confirmer les diagnostics; il y avait une très bonne concordance entre le diagnostic sur le terrain des praticiens et celui des chercheurs (Kappa de Cohen = 0,81; P < 0,001). L'épaisseur de la sole dans la région de la ligne blanche atypique était plus mince (P < 0,001) dans les cas (3,74 mm) que dans les témoins (4,72 mm). Il était 5,0 fois (IC de 95 % de 1,5 à 8,6; P < 0,001) et 7,3 fois (IC de 95 % de 1,5 à 69,3; P < 0,01) plus probable que les ongles des cas donnent une croissance importante d'Escherichia coli et de Trueperella pyogenes, respectivement. Il était 4,4 fois (IC de 95 % de 4,4 à 22,9; P < 0,001) plus probable que les cas soient infectés de manière aiguë ou transitoire par le virus de la diarrhée virale des bovins comparativement aux témoins. Les résultats appuient l'hypothèse que le SNBO est amorcé par une usure excessive le long de la ligne blanche, ce qui entraîne une séparation et la colonisation bactérienne de l'os de la troisième phalange (P3) et des tissus mous connexes.(Traduit par Isabelle Vallières).

Neonatal Mortality, Vesicular Lesions and Lameness Associated with Senecavirus A in a U.S. Sow Farm.

A 300-sow farrow-to-finish swine operation in the United States experienced a sudden and severe increase in mortality in neonatal piglets with high morbidity followed by vesicular lesions on the snout and feet of adult females and males. Affected live piglets were submitted for diagnostic investigation. Samples tested polymerase chain reaction (PCR) negative for foot-and-mouth disease virus, porcine delta coronavirus, porcine epidemic diarrhoea virus, porcine rotavirus types A, B and C, transmissible gastroenteritis virus, and porcine reproductive and respiratory syndrome virus. Senecavirus A (SV-A) formerly known as Seneca Valley virus was detected by real-time reverse-transcription polymerase chain reaction (rRT-PCR) from serum, skin and faeces of piglets and from serum and faeces of sows. SV-A was isolated in cell culture from piglet samples. SV-A VP1 gene region sequencing from piglet tissues was also successful. A biosecurity and disease entry evaluation was conducted and identified potential biosecurity risks factors for the entry of new pathogens into the operation. This is the first case report in the United States associating SV-A with a clinical course of severe but transient neonatal morbidity and mortality followed by vesicular lesions in breeding stock animals. Veterinarians and animal caretakers must remain vigilant for vesicular foreign animal diseases and report suspicious clinical signs and lesions to state animal health authorities for diagnostic testing and further investigation.

Detection of antibodies against Theiler's murine encephalomyelitis virus GDVII strain in experimental guinea pigs.

A disease affecting guinea pigs called 'guinea pig lameness' characterized by clinical signs of depression, lameness of limbs, flaccid paralysis, weight loss and death within a few weeks was first described by Römer in 1911. After a research group in our facility kept laboratory guinea pigs from two different origins together in one room, lameness was observed in two animals. Further investigations revealed a serological immune response against Theiler's murine encephalomyelitis virus (TMEV; GDVII strain) in these animals. Histopathology of the lumbar spinal cord of these animals showed mononuclear cell infiltration and necrotic neurons in the anterior horn. Therefore, all guinea pigs from this contaminated animal unit, from other units in our facility, as well as from different European institutions and breeding centres were screened for antibodies directed against GDVII. Our investigations showed that approximately 80% of all guinea pigs from the contaminated animal unit were seropositive for GDVII, whereas animals from other separate units were completely negative. In addition, 43% of tested sera from the different European institutions and breeding centres contained antibodies against GDVII. The present data confirm that an unknown viral infection causes an immune response in experimental guinea pigs leading to seroconversion against GDVII and that guinea pigs from a commercial breeder are the source of the infection.

Experimentally induced lameness in turkeys inoculated with a newly emergent turkey reovirus.

Newly emergent turkey arthritis reoviruses (TARVs) have been isolated from cases of lameness in male turkeys over 10 weeks of age. In a previous study, experimental inoculation of TARV in one-week-old turkey poults produced lymphocytic tenosynovitis at four weeks post inoculation but without causing clinical lameness. This study was undertaken to determine if TARV infection at an early age can lead to clinical lameness in birds as they age. One-week-old male turkeys were inoculated orally with a TARV (strain TARV-O'Neil) and monitored for the development of gait defects until 16 weeks of age. At 4, 8, 12 and 16 weeks of age, a subset of birds was euthanized followed by the collection of gastrocnemius tendon, digital flexor tendon, and intestines for virus detection by rRT-PCR and for histologic inflammation scoring. Clinical lameness was first displayed in TARV-infected turkeys at 8 weeks of age and ruptured gastrocnemius tendons with progressive lameness were also seen at 12-16 weeks of age. The virus was detected in gastrocnemius tendon of 4- 8- and 12-week-old turkeys but not in 16-week-old turkeys. Histologic inflammation scores of tendons at each of the four time points were significantly higher in the virus-inoculated group than in the control group (p < 0.01). Lesions began as lymphocytic tenosynovitis with mild synoviocyte hyperplasia at four weeks of age and progressed to fibrosis as the birds aged. These results demonstrate the potential of TARV to infect young turkeys and to produce subclinical tenosynovitis that becomes clinically demonstrable as the turkeys age.

Prepulse inhibition in HIV-1 gp120 transgenic mice after withdrawal from chronic methamphetamine.

HIV infection is frequently comorbid with methamphetamine (METH) dependence. Both factors are associated with impairment in inhibitory function that continues even after abstinence from the drug. Deficits in prepulse inhibition (PPI), a measure of sensorimotor gating, are induced by acute stimulant administration, but the combined effect of HIV and chronic METH exposure on PPI is not well characterized. We quantified baseline acoustic startle and PPI in mice expressing the HIV-1 gp120 envelope protein (gp120tg) and in wild-type (WT) littermates; thereafter, we administered a chronic regimen of METH or vehicle and tested startle and PPI after 7 days of drug withdrawal. We hypothesized that METH-treated gp120tg mice would exhibit PPI deficits compared with vehicle-treated WT or gp120tg animals. Before METH administration, drug-naive female gp120tg mice exhibited decreased PPI compared with female WT mice, whereas male gp120tg mice exhibited increased startle compared with other groups. After drug withdrawal, no consistent genotype effect was observed, but METH-treated mice exhibited increased PPI compared with vehicle, in contrast to previous reports of acute METH-induced PPI deficits. In summary, PPI impairment in HIV could depend on factors such as sex, whereas changes in PPI following METH withdrawal may depend on the quantity and duration of drug exposure.

Isolation and characterization of a turkey arthritis reovirus.

During the spring and summer of 2011, the Minnesota Veterinary Diagnostic Laboratory at the University of Minnesota received 14 submissions of 15-to-18-week-old tom turkeys that were recumbent with wing tip bruises ("wing walkers") and uni- or bilateral swelling of the hock (tibiotarsal) joints. Gastrocnemius or digital flexor tendons were occasionally ruptured. A total of five turkey arthritis reoviruses (TARV-MN1 through TARV-MN5) were isolated in specific-pathogen-free embryonated chicken eggs and QT-35 cells. The identity of the isolates was confirmed by electron microscopy, reverse transcription-polymerase chain reaction, and gene sequence analysis. BLAST analysis on the basis of a 880 bp nucleotide sequence of the S4 gene confirmed all isolates as a reovirus. Phylogenetic analysis divided the five isolates into two subgroups: subgroup I containing TARV-MN1, -2, -3, and -5, and the other subgroup containing TARV-MN4. Isolates in subgroup I had a similarity of 97%-100% with each other, while subgroup II (TARV-MN4) had a similarity of only 89.2% with subgroup I viruses. This isolate showed 90%-93% similarity with turkey enteric reoviruses in the United States, while the other four isolates in subgroup I had 89%-97.6% similarity. These results indicate divergence within TARVs as well as from enteric viruses, which needs to be confirmed by complete genome sequence analysis. Further experimental studies are planned to determine the role of these isolates in turkey arthritis and to compare them with classical chicken reovirus.

Neurobehavioral performance in feline immunodeficiency virus infection: integrated analysis of viral burden, neuroinflammation, and neuronal injury in cortex.

Human immunodeficiency virus (HIV) infection causes motor and neurocognitive abnormalities affecting >50% of children and 20% of adults with HIV/AIDS (acquired immunodeficiency syndrome). The closely related lentivirus, feline immunodeficiency virus (FIV), also causes neurobehavioral deficits. Herein, we investigated the extent to which FIV infection affected specific motor and cognitive tasks in conjunction with viral burden and immune responses within the brain. Neonatal animals were infected with a neurovirulent FIV strain (FIV-Ch) and assessed in terms of systemic immune parameters, viral burden, neurobehavioral performance, and neuropathological features. FIV-infected animals displayed less weight gain and lower blood CD4(+) T-cell levels than mock-infected animals (p < 0.05). Gait analyses disclosed greater gait width with increased variation in FIV-infected animals (p < 0.05). Maze performance showed that FIV-infected animals were slower and made more navigational errors than mock-infected animals (p < 0.05). In the object memory test, the FIV-infected group exhibited fewer successful steps with more trajectory errors compared with the mock-infected group (p < 0.05). Performance on the gait, maze, and object memory tests was inversely correlated with F4/80 and CD3 epsilon expression (p < 0.05) and with viral burden in parietal cortex (p < 0.05). Amino acid analysis in cortex showed that D-serine levels were reduced in FIV-infected animals, which was accompanied by diminished kainate and AMPA receptor subunit expression (p < 0.05). The neurobehavioral findings in FIV-infected animals were associated with increased gliosis and reduced cortical neuronal counts (p < 0.05). The present studies indicated that specific motor and neurocognitive abilities were impaired in FIV infection and that these effects were closely coupled with viral burden, neuroinflammation, and neuronal loss.

Assessment of hindlimb gait as a powerful indicator of axonal loss in a murine model of progressive CNS demyelination.

Identifying the role of axonal injury in the development of permanent, irreversible neurologic disability is important to the study of central nervous system (CNS) demyelinating diseases. Our understanding of neurologic dysfunction in demyelinating diseases and the ability to assess therapeutic interventions depends on the development of objective functional assays that can non-invasively measure axonal loss. In this study, we demonstrate in a murine model of progressive CNS demyelination that assessment of the hindlimb width of stride provides a powerful indicator of axonal loss and can dissociate between deficits induced by demyelination versus axonal loss.

Comparison of the primary signs induced by experimental exposure to either a pneumotrophic or a 'limping' strain of feline calicivirus.

Two strains of feline calicivirus, one reportedly pneumotrophic (FPV 255) and the other associated with a limping syndrome (2280) were compared with respect to the signs induced in kittens after oronasal exposure. Neither strain induced severe upper respiratory symptoms, and both caused oral ulcers and lameness. However oral ulcers were more prevalent, and lameness and depression were more pronounced in the kittens which received strain 2280. Kittens which exhibited lameness also had elevated blood levels of alpha 1-acid glycoprotein. A decline in lymphocyte count was noted only in kittens which received strain 2280. These data demonstrate that despite reported antigenic and genetic differences between these strains, no distinct differences in pathogenicity could be determined.