Description of a presumptive hepatopancreatic reovirus, and a putative gill parvovirus, in the freshwater crayfish Cherax quadricarinatus

The redclaw freshwater crayfish Cherax quadricarinatus has a reputation for being hardy and resistant to handling stress. However, in recent years, possibly since 1996, C. quadricarinatus farmers in northern Queensland have noted a decrease in stress resistance in their stock. A presumptive reovirus in the hepatopancreas, and a putative parvovirus in the gills, were associated with chronic mortalities in C. quadricarinatus at one northern Queensland farm. Hypertrophic nuclei with marginated chromatin were observed in gill epithelium in moribund crayfish which had recently been relocated to a laboratory from the holding tank facility on the farm. Affected nuclei appeared to be vacant or contained a faint granular basophilia in H&E stained sections. However, toluidine blue staining revealed a homogeneously granular appearance of the nuclei. Transmission electron microscopy revealed approximately 20 nm diameter virus-like particles within the nucleus. Eosinophilic, Feulgen-negative, cytoplasmic inclusions were observed in distal hepatopancreatocytes in 1 moribund C. quadricarinatus collected from the same on-farm holding tank approximately 6 mo later. This crayfish did not display the gill lesions. Transmission electron microscopy showed that the inclusions contained icosahedral virus particles 35 to 40 nm in diameter. The histopathology and preliminary virus morphology of the presumptive hepatopancreatic reovirus, and the histopathology, ultrastructural pathology and preliminary virus morphology of the putative gill parvovirus, are reported herein

A compendium of idiopathic lesions observed in redclaw freshwater crayfish, Cherax quadricarinatus (von Martens)

Idiopathic lesions observed in redclaw freshwater crayfish, Cherax quadricarinatus (von Martens), from farms in northern Queensland, Australia, over a 4-year period are described. Various idiopathic lesions were observed in the exoskeleton, antennal gland, mandibular organ, haemolymph vessel endothelium and enteric tissues of C. quadricarinatus collected for histopathological surveys, investigations of chronic mortalities or during other activities. The need for an increased use of histopathology in crayfish disease diagnosis is highlighted

Susceptibility of the Australian freshwater crayfish Cherax destructor albidus to white spot syndrome virus (WSSV)

Cherax destructor occurs naturally and/or is farmed in all Australian mainland states and territories and is of major cultural, economical and conservation significance. The aim of this study was to determine susceptibility of the commercially important subspecies C. destructor albidus to white spot syndrome virus (WSSV), a hazard to crustaceans and currently considered to be exotic to Australia. In challenge tests by intramuscular injection, C. destructor albidus displayed a similar level of susceptibility to white spot disease (WSD) as Penaeus monodon (i.e. 100% mortality in 3 d). In one oral challenge test where C. destructor albidus was subjected to significant temperature stress, over 50% died of severe WSD within 14 d post challenge. All dead and moribund crayfish displayed histopathological lesions typical for WSD and gave positive results for WSSV in DNA dot blot hybridization tests. Survivors to 30 d (n = 3) showed no lesions and gave negative dot blot test results. In a second oral challenge test without temperature stress, mortality was delayed but reached 75% by 30 d. However, no typical WSD lesions were observed in the dead, dying or surviving crayfish and dot blot test results were negative. The results suggested that C. destructor albidus would be less susceptible than P. monodon to WSSV exposure via natural routes of infection in farms and in the wild. This information may be useful for disease import risk analysis for WSSV

Understanding the causes of disease in European freshwater crayfish

Native European freshwater crayfish (Astacida, Decapoda) are under severe pressure from habitat alteration, the introduction of nonindigenous species, and epizootic disease. Crayfish plague, an acute disease of freshwater crayfish caused by the fungus-like agent Aphanomyces astaci, was introduced into Europe in the mid-nineteenth century and is responsible for ongoing widespread epizootic mortality in native European populations. We reviewed recent developments and current practices in the field of crayfish pathology. The severity of crayfish plague has resulted in an overemphasis on it. Diagnostic methods for detecting fungi and fungal-like agents, and sometimes culturing them, are frequently the sole techniques used to investigate disease outbreaks in European freshwater crayfish. Consequently, the causes of a significant proportion of outbreaks are undetermined. Pathogen groups well known for causing disease in other crustaceans, such as viruses and rickettsia-like organisms, are poorly understood or unknown in European freshwater crayfish. Moreover, the pathogenic significance of some long-known pathogens of European freshwater crayfish remains obscure. For effective management of this culturally significant and threatened resource, there is an urgent need for researchers, diagnosticians, and resource managers to address the issue of disease in European freshwater crayfish from a broader perspective than has been applied previously

An Intensive Locomotor Training Paradigm Improves Neuropathic Pain following Spinal Cord Compression Injury in Rats

Spinal cord injury (SCI) is often associated with both locomotor deficits and sensory dysfunction, including debilitating neuropathic pain. Unfortunately, current conventional pharmacological, physiological, or psychological treatments provide only marginal relief for more than two-thirds of patients, highlighting the need for improved treatment options. Locomotor training is often prescribed as an adjunct therapy for peripheral neuropathic pain but is rarely used to treat central neuropathic pain. The goal of this study was to evaluate the potential anti-nociceptive benefits of intensive locomotor training (ILT) on neuropathic pain consequent to traumatic SCI. Using a rodent SCI model for central neuropathic pain, ILT was initiated either 5 d after injury prior to development of neuropathic pain symptoms (the "prevention" group) or delayed until pain symptoms fully developed (∼3 weeks post-injury, the "reversal" group). The training protocol consisted of 5 d/week of a ramping protocol that started with 11 m/min for 5 min and increased in speed (+1 m/min/week) and time (1-4 minutes/week) to a maximum of two 20-min sessions/d at 15 m/min by the fourth week of training. ILT prevented and reversed the development of heat hyperalgesia and cold allodynia, as well as reversed developed tactile allodynia, suggesting analgesic benefits not seen with moderate levels of locomotor training. Further, the analgesic benefits of ILT persisted for several weeks once training had been stopped. The unique ability of an ILT protocol to produce robust and sustained anti-nociceptive effects, as assessed by three distinct outcome measures for below-level SCI neuropathic pain, suggests that this adjunct therapeutic approach has great promise in a comprehensive treatment strategy for SCI pain