Dermatitis, branchitis and mortality in empire gudgeon Hypseleotris compressa exposed naturally to runoff from acid sulfate soils.

Severe dermatitis and branchitis are described in a wild population of empire gudgeon Hypseleotris compressa, an Australian eleotrid, exposed naturally to runoff from acid sulfate soils (ASS) in a drained estuarine embayment in eastern Australia. After at least 2 d exposure to pH < 4, and up to 7 d exposure to pH < 6, approximately 50% of the fish sampled had moderate to severe diffuse epidermal hyperplasia, usually at scale margins, and scattered areas of moderate to severe, focal to locally extensive, subacute, necrotising dermatitis. Saprolegnia spp. had invaded epidermis in some inflamed areas. In gills, there was moderate to severe hyperplasia and necrosis of secondary lamellar epithelium, with fusion of adjacent secondary lamellae. Inorganic monomeric aluminium and calcium concentrations in water at the site during the event were 27.7 and 16.6 mg l(-1), respectively. Large numbers of empire gudgeons at the study site had died after at least 8 d exposure to pH < 4, and up to 13 d exposure to pH < 6. These findings provide clear evidence that acidification of estuarine systems by runoff from ASS has deleterious effects on aquatic biota. Furthermore, study findings suggest a mechanism whereby lesions of epizootic ulcerative syndrome (EUS) may be initiated in estuarine fishes by a combination of sublethal exposure to ASS runoff and Aphanomyces invadans infection, a suggestion consistent with the geographic and temporal distribution of EUS outbreaks in Australian estuaries.

Fatal, virus-associated peripheral neuropathy and retinopathy in farmed Penaeus monodon in eastern Australia. I. Pathology.

Lesions are described in farmed Penaeus monodon affected with a previously unreported, fatal disease, 'peripheral neuropathy and retinopathy' (PNR). Outbreaks, associated with minor to heavy mortalities, occurred in 22 of 25 ponds on a farm in eastern Australia during the mid to late 1998/99 growout period. Moribund prawns, 5 to 26 g mean body weight, gathered at pond edges and were typically reddish in colour, lethargic, with mild to moderate epibiotic fouling and 1 or more partially amputated appendages. Histologically, there was mild to severe, focal to diffuse degeneration and necrosis of axons and their sheaths, together with associated glial cell apoptosis, in peripheral nerve fibres. Of the 3 appendage types examined systematically, these pathognomonic lesions were most common and severe in proximal antennal nerves and less common and severe in distal antennal nerves, antennular nerves and pereiopod nerves. Mild to severe, acute to chronic retinitis, associated with degeneration and necrosis of retinular cells and their axons, was also present in most clinically affected prawns. Transmission electron microscopy revealed moderate to large numbers of intracytoplasmic rod-shaped, helical nucleocapsids and enveloped virions, morphologically consistent with a yellow head-like virus, in putative glial cells in the antennal nerve, in the fasciculated zone of the eye and in putative sensory nerve cells of antennules. Immunohistochemical examination revealed lesions, but not histologically normal tissues, in peripheral nerves, eyes, lymphoid organ and vas deferens that consistently stained positively for a yellow head-related virus. The findings strongly suggest that a yellow head-related virus such as the Australian gill-associated virus (GAV) is causally associated with PNR. It is likely that PNR was not recognised during earlier investigations of mid-crop mortalities of farmed P. monodon in eastern Australia because appropriate peripheral nerves and eyes were not routinely examined histologically.

Fatal, virus-associated peripheral neuropathy and retinopathy in farmed Penaeus monodon in eastern Australia. II. Outbreak descriptions.

Outbreaks of 'peripheral neuropathy and retinopathy' (PNR) occurring during 2 consecutive growout periods (typically October-April) are described for an intensive Penaeus monodon farm in eastern Australia. In the 1998/99 growout period, outbreaks graded minor to severe occurred in 22 of 25 ponds, 12 to 25 wk post-stocking. In the severely affected index pond, harvested 8 wk after outbreak recognition in mid-January, estimated survival for the period late December to harvest was 50%. Minor to moderate losses could be attributed to PNR in the other ponds. Mean survival over the same period for the 14 ponds harvested within 5 wk of outbreak recognition was 93% (83 to 100%); for the 7 ponds harvested 5 to 8 wk after outbreak recognition was 79% (67 to 92%) and for the 3 unaffected ponds was 90% (86 to 95%). Analysis indicated a significantly lower risk (Fisher's exact p = 0.016) of an outbreak in the 2 ponds stocked only with postlarvae from one hatchery (D) versus the 18 ponds stocked only with postlarvae from 3 other hatcheries (A, B and C). In the 1999/2000 growout period, minor to severe PNR outbreaks occurred in all 26 ponds, each stocked with postlarvae from the same hatchery (E), 19 to 21 wk post-stocking. Stocking date in 1999/2000 appeared to influence PNR outbreak severity; for ponds stocked on 2 of the 7 stocking dates versus those stocked on remaining dates, the crude relative risks (CRR) of a severe outbreak, or either a moderate or severe outbreak, were 11.25 (1.55 < CRR < 81.40) and 2.63 (1.30 < CRR < 5.31), respectively. Although inconclusive, study findings are consistent with the hypothesis that 'gill-associated virus' (GAV), the putative causal pathogen identified in a separate pathological study, entered ponds via postlarvae, and that prevalence and/or severity of infection within postlarval batches influenced outbreak severity. The generally high survival in ponds harvested soon after outbreak recognition, together with PNR prevalence of approximately 50% in prawns collected from 4 ponds 7 wk before those ponds were recognised as affected, also suggest that GAV is highly infectious and that PNR has a relatively long incubation period and/or clinical course.

Further observations on the epidemiology and spread of epizootic haematopoietic necrosis virus (EHNV) in farmed rainbow trout Oncorhynchus mykiss in southeastern Australia and a recommended sampling strategy for surveillance.

Epizootic haematopoietic necrosis virus (EHNV) is an iridovirus confined to Australia and is known only from rainbow trout Oncorhynchus mykiss and redfin perch Perca fluviatilis. Outbreaks of disease caused by EHNV in trout populations have invariably been of low severity, affecting only 0+ post-hatchery phase fingerlings < 125 mm in length. To date the virus has been demonstrated in very few live in-contact fish, and anti-EHNV antibodies have not been found in survivors of outbreaks, suggesting low infectivity but high case fatality rates in trout. During an on-going study on an endemically infected farm (Farm A) in the Murrumbidgee River catchment of southeastern New South Wales, EHNV infection was demonstrated in 4 to 6 wk old trout fingerlings in the hatchery as well as in 1+ to 2+ grower fish. During a separate investigation of mortalities in 1+ to 2+ trout on Farm B in the Shoalhaven River catchment in southeastern New South Wales, EHNV infection was demonstrated in both fingerlings and adult fish in association with nocardiosis. A 0.7% prevalence of antibodies against EHNV was detected by ELISA in the serum of grower fish at this time, providing the first evidence that EHNV might not kill all infected trout. EHNV infection on Farm B occurred after transfer of fingerlings from Farm C in the Murrumbidgee river catchment. When investigated, there were no obvious signs of diseases on Farm C. 'Routine' mortalities were collected over 10 d on Farm C and EHNV was detected in 2.1% of 190 fish. Tracing investigations of sources of supply of fingerlings to Farm B also led to investigation of Farm D in Victoria, where the prevalence of anti-EHNV antibodies in 3+ to 4+ fish was 1.3%. The results of this study indicate that EHNV may be found in trout in all age classes, need not be associated with clinically detectable disease in the population, can be transferred with shipments of live fish, can be detected in a small proportion of 'routine' mortalities and may be associated with specific antibodies in a small proportion of older fish. Sampling to detect EHNV for certification purposes should be based on examination of 'routine' mortalities rather than random samples of live fish. Antigen-capture ELISA can be used as a cost effective screening test to detect EHNV on a farm provided that sampling rates conform with statistical principles.

Occurrence of cutaneous infections of Myxobolus episquamalis (Myxozoa:Myxobolidae) in sea mullet, Mugil cephalus L, in Australia.

OBJECTIVE: To report the occurrence of Myxobolus episquamalis in sea mullet, Mugil cephalus L, caught in estuaries in eastern and western Australia. DESIGN: A prospective study of commercial catches of mullet in the Clarence River of NSW and individual cases from other areas. RESULTS: The organism caused pale, white to pink, raised lesions on the scales and fins of sea mullet. Occurrence of infection was highest in spring and in a marine (down-river) environment compared to a brackish environment. Up to 6% of fish were affected in commercial catches. CONCLUSION: The infection is widespread in Australian mullet, but rarely causes significant economic loss.

Enterocolitis in cattle associated with Yersinia pseudotuberculosis infection.

A syndrome in cattle of diarrhoea and death associated with enteric Yersinia pseudotuberculosis infection is described. Outbreaks occurred during winter and early spring in adult cattle grazing pastures waterlogged by recent flooding or persistent heavy rain. Antibiotic therapy was effective early in the course of the syndrome. At necropsy there was severe acute enterocolitis, and bacteria consistent with Y. pseudotuberculosis were observed in the lesions. This organism could usually be isolated from the intestines of affected animals but was recovered less often from other organs. Representative isolates were identified as Y. pseudotuberculosis serotype III. The association of this syndrome with waterlogged pastures and low temperatures suggests that these conditions favour transmission of Y. pseudotuberculosis infection in cattle. The role of Y. pseudotuberculosis as primary pathogen requires confirmation.

Mortalities associated with herpesvirus infection in captive macropods.

Fatal cases of herpesvirus infection in a quokka (Setonix brachyurus), eight grey dorcopsis wallabies (Dorcopsis muelleri luctuosa) in two separate outbreaks, as well as presumptive fatal herpesvirus infection in a western grey kangaroo (Macropus fuliginosus) are described. All were captive animals and deaths were preceded by a period of stress. Lesions occurred most often in alimentary tract epithelium, respiratory tract, skin, genital epithelium, conjunctivae, liver and adrenal cortex. Herpesviruses were recovered from the quokka and a grey dorcopsis wallaby from each outbreaks. The implications, particularly concerning certain apparently susceptible species, for those responsible for the health of macropod collections are discussed.

An outbreak of disease in pigeons associated with a herpesvirus.

An outbreak of disease in young pigeons associated with a herpesvirus is reported. The clinical history, macroscopic and microscopic appearance of lesions and virus isolation are described. Most affected birds showed lesions in the upper alimentary tract epithelium as well as in skin, nasal mucosa and salivary glands. Lesions in liver, spleen and pancreas were uncommon. A herpesvirus capable of producing CPE on tissue culture and lesions on chorioallantoic membrane of developing chicken embryos was isolated and described. Inoculation of experimental pigeons with the virus failed to reproduce the disease.

Haemophilus parasuis infection in swine.

Septicemic disease occurred in 49 of 126 pigs several days after being transported 80 km. All affected pigs died. The main changes in acutely affected pigs were skin discoloration, pulmonary edema, arthritis, meningitis, and renal glomerular thrombosis. In peracute cases, gross findings were minimal. Haemophilus parasuis was isolated from multiple organ sites in most affected pigs. Haemophilus parasuis was isolated from nasal swab specimens from 17 of 20 clinically normal pigs on the farm of origin. Fatal acute septicemia was reproduced in 2 pigs by intravenous or intratracheal exposure to an isolant of H parasuis obtained from 1 of of the 49 fatally affected pigs. Aerosol exposure of 5 pigs resulted in mild pneumonia in 4 pigs and severe pneumonia, pleurisy, pericarditis, and terminal septicemia in 1 pig.