nan Alley

An epidemic of salmonellosis caused by Salmonella Typhimurium DT160 in wild birds and humans in New Zealand

Abstract AIM: This study reports an outbreak of salmonellosis due to S. Typhimurium DT160 which caused extensive mortality in wild birds and enteric disease in humans in New Zealand during the winter and spring months of the year 2000. METHODS: Necropsies were performed and microbiological examinations undertaken on wild birds from populations in which mass mortality was reported, and on captive indigenous birds which died suddenly during the winter and spring of 2000. Affected tissues were examined histologically and isolates of S. Typhimurium were phage typed and examined using pulsed- field gel electrophoresis (PFGE). Isolates of S. Typhimurium obtained from cases of human enteric disease which occurred during these months were phage typed, examined using PFGE and compared with the bird isolates. RESULTS: Central and northern areas of the South Island and the southern North Island were worst affected with die-offs of several hundreds of sparrows and other birds reported in rural areas. Mortalities reached a peak in winter (July–August) 2000 and decreased to small numbers during the spring and early summer. The birds usually died of an acute septicaemia with multifocal necrotising lesions in the liver and spleen. Human cases throughout the country increased gradually over the same period. Isolates from birds, livestock and humans examined using PFGE were indistinguishable from one another. CONCLUSION: This strain of Salmonella has emerged as a major cause of septicaemia in wild birds in New Zealand. Because of the close association between house sparrows (Passer domesticus) and humans, the organism also poses a serious zoonotic risk. The possibility that the infection may spread to involve indigenous species needs investigation.

Concurrent avian malaria and avipox virus infection in translocated South Island saddlebacks (Philesturnus carunculatus carunculatus).

Abstract CASE HISTORY: Outbreaks of mortality in South Island saddlebacks (Philesturnus carunculatus carunculatus) that had been translocated to two offshore islands in the Marlborough Sounds of New Zealand were investigated during the summer of 2002 and 2007. Both outbreaks were associated with a severe decrease in numbers of saddlebacks of up to 60% of approximately 200 birds. CLINICAL AND PATHOLOGICAL FINDINGS: Many of the surviving birds were in poor condition, and had skin lesions on the legs and head. Necropsy showed pale liver and lungs, and a swollen spleen. Histopathology revealed schizonts resembling Plasmodium spp. within the cytoplasm of many hepatocytes and splenic histiocytes. The skin lesions consisted of epithelial proliferations containing numerous Bollinger bodies typical of avipox virus (APV) infection. Two different APV were isolated, using PCR, from two different birds exhibiting skin lesions. Each isolate had 100% sequence homology with APV members from either Clade A or Clade B. In addition, PCR analysis revealed that the Plasmodium elongatum present in infected birdsbelonged to a strain that was endemic in the population of North Island saddlebacks (Philesturnus carunculatus rufusater). DIAGNOSIS: Concurrent infections with Plasmodium spp. haemoparasites and APV were identified as the likely cause of death in the birds examined. CONCLUSIONS AND CLINICAL RELEVANCE: Although the Plasmodium spp. identified is thought to be endemic to saddlebacks in New Zealand, the affected birds were likely to be immunocompromised by concurrent APV infection or through lack of genetic diversity. Both the introduced mosquito Culex quinquefasicatus and the native mosquito Culex pervigilans are likely vectors for both these diseases, and the provision of water supplies less favourable to mosquito-breeding is recommended.

The prevalence of beak and feather disease virus infection in wild populations of parrots and cockatoos in New Zealand

Abstract The prevalence of beak and feather disease virus infection in wild populations of parrots and cockatoos in New Zealand METHODS: Eastern rosellas (Platycercus eximius, n=162) were caught from Te Puke, Wellington and Dunedin, using mistnets, between April 2004 and February 2006, and sulphurcrested cockatoos (Cacatua galerita, n=255) were captured for pet-trading from November 2001 to September 2004. Feathers from both species were tested for BFDV, using an established polymerase chain reaction (PCR) test. Post-mortem examinations were conducted on some of the eastern rosellas, and selected tissues from 24 birds positive for BFDV were examined using routine histological methods for the presence of characteristic inclusion bodies. RESULTS: Of the eastern rosellas, 24/162 (14.8%) were positive for BFDV, and the 95% confidence interval (CI) for true prevalence was estimated as 8.6–20.4%, which varied between regions. Eastern rosellas that were positive for BFDV showed no clinical or histological signs of disease or inclusion bodies. Of the sulphur-crested cockatoos, 70/255 (28%) were positive for BFDV, and the 95% CI for true prevalence was calculated as 22–33%. CONCLUSIONS: The surprisingly high prevalence of BFDV in wild eastern rosellas and sulphur-crested cockatoos has serious implications for the conservation of native parrots and the export of wild-trapped parrots and cockatoos from New Zealand. Serological studies for BFDV in wild exotic parrots, and molecular studies of virus genotype, are recommended to further characterise the origin and epidemiology of the disease in populations of wild exotic parrots and cockatoos in New Zealand.

Avian malaria in New Zealand

Avian malaria parasites of the genus Plasmodium have the ability to cause morbidity and mortality in naïve hosts, and their impact on the native biodiversity is potentially serious. Over the last decade, avian malaria has aroused increasing interest as an emerging disease in New Zealand with some endemic avian species, such as the endangered mohua (Mohua ochrocephala), thought to be particularly susceptible. To date, avian malaria parasites have been found in 35 different bird species in New Zealand and have been diagnosed as causing death in threatened species such as dotterel (Charadrius obscurus), South Island saddleback (Philesturnus carunculatus carunculatus), mohua, hihi (Notiomystis cincta) and two species of kiwi (Apteryx spp.). Introduced blackbirds (Turdus merula) have been found to be carriers of at least three strains of Plasmodium spp. and because they are very commonly infected, they are likely sources of infection for many of New Zealands endemic birds. The spread and abundance of introduced and endemic mosquitoes as the result of climate change is also likely to be an important factor in the high prevalence of infection in some regions and at certain times of the year. Although still limited, there is a growing understanding of the ecology and epidemiology of Plasmodium spp. in New Zealand. Molecular biology has played an important part in this process and has markedly improved our understanding of the taxonomy of the genus Plasmodium. This review presents our current state of knowledge, discusses the possible infection and disease outcomes, the implications for host behaviour and reproduction, methods of diagnosis of infection, and the possible vectors for transmission of the disease in New Zealand.

Infectivity and persistence of an outbreak strain of Salmonella enterica serotype Typhimurium DT160 for house sparrows (Passer domesticus) in New Zealand

Abstract AIM: To examine the infective dose, incubation period and disease progression of an isolate of Salmonella enterica serotype Typhimurium definitive type 160 (DT160) originating from a naturally-infected house sparrow (Passer domesticus) during an outbreak of the disease in New Zealand. METHODS: Thirty-six house sparrows captured from the wild and free of Salmonella spp were divided into six groups of six birds, housed individually, and inoculated orally with phosphate buffered saline (PBS) or 101, 102, 103, 105, 2 × 108 colony forming units (cfu) of the outbreak strain of S. Typhimurium DT160. The birds were observed for 10 days for clinical signs and/or mortality, and faecal samples were collected to determine excretion of S. Typhimurium. The birds were eutha- nised 11 days post-inoculation (p.i.) and a wide range of tissue samples were collected for histopathological examination, and culture and typing of Salmonella spp. Macro-restriction profiling by pulsed-field gel electrophoresis (PFGE) using XbaI was performed for the epidemiological typing of S. Typhimurium DT160 isolates. RESULTS: Mortality in house sparrows inoculated with S. Typhimurium DT160 was dose-dependent, and 2/6 birds inoculated with 105 cfu and all six birds inoculated with 2 × 108 cfu died during the study. Infected sparrows displayed few clinical signs, apart from diarrhoea and/or polyuria, fluffed plumage, and sitting on the floor of the cage. Faecal excretion of DT160 occurred briefly in two birds inoculated with 102 cfu and four birds inoculated with 103 cfu, on most days in five birds inoculated with 105 cfu, and continuously in six birds inoculated with 2 × 108 cfu. DT160 was isolated from the livers of three birds which received 103 cfu, five birds dosed with 105 cfu, and all six birds given 2 × 108 cfu. Following necropsy, histopathological lesions similar to those seen in the natural disease were observed in the liver or spleen of three birds which received 103 cfu, and all birds dosed with ≥105 cfu. CONCLUSION: The results indicate that an isolate of S. Typhimurium DT60 originating from house sparrows in New Zealand is pathogenic to these birds and that the response is dose- dependent. The persistence and excretion of the pathogen may last for at least 10 days. This confirms that sparrows infected with DT160 could be a source of infection to humans and other in-contact animals.

Salmonella in animals in New Zealand: the past to the future

Abstract Extract In New Zealand, salmonellosis was first reported in pigs in 1934 when Bacillus suipestifer (Salmonella enterica serovar Cholerae-suis) infection was recognised as a common cause of mortality in young pigs raised in unsanitary conditions in the Waikato district (Marshall 1934). A few years later, mild forms of Pullorum disease were reported in young chickens (Bobby 1946) and a blood-testing programme involving 700 birds revealed a prevalence of 23.3% (Bobby 1941). A 5-year survey by the Animal Research Station at Wallaceville (1941-45) found that Pullorum was the most common disease of poultry, but by 1945, when 110,000 birds were tested, the prevalence had reduced to 9.08%. Over the next 10 years a test and slaughter programme succeeded in reducing the prevalence to 0.39% (Salisbury 1958), but isolated pockets of infection still persisted; it was a further 10 years before the disease was eradicated from commercial flocks (Russell and Kicks 1964).

Avian polyomavirus identified in a nestling Gouldian finch (Erythrura gouldiae) in New Zealand.

Abstract CASE HISTORY: Four 4–5-month-old nestlings and one adult in a commercial aviary of 53 Gouldian finches (Erythrura gouldiae) died over a 2-week period in July 2000. PATHOLOGICAL FINDINGS: One nestling was necropsied and showed bronze-tinged skeletal muscles, a swollen liver with haemorrhagic margins and numerous haemorrhages on serosal surfaces. The histological lesions included multifocal hepatic necrosis and haemorrhage associated with the presence of large clear or basophilic intranuclear inclusions in hepatocytes and Kupffer cells suggestive of avian polyomavirus infection. Similar inclusion bodies were present in splenic histiocytes. MOLECULAR BIOLOGY: DNA was subsequently extracted from archived portions of liver, spleen, gizzard, heart, lung and kidney. A broad spectrum nested PCR was used to detect polyomavirus which sequence analysis confirmed as finch polyomavirus. DIAGNOSIS: Avian polyomavirus. CLINICAL RELEVANCE: Avian virus infections such as polyomavirus should be suspected in cases of sudden death in nestlings, particularly in susceptible species such as psittacine and passerine birds. The archiving of tissues from unconfirmed disease outbreaks provides a valuable resource for retrospective investigations.

Candida albicans infection in free-living populations of hihi (stitchbird; Notiomystis cincta)

Abstract AIM: To describe the occurrence of candidiasis in hihi (stitch-bird; Notiomystis cincta) nestlings, and investigate the carriage and impact of Candida albicans infection in a free-living population of hihi. METHODS: Mortality of nestlings was investigated in a reintroduced population of the endangered, endemic hihi at Zealandia: Karori Sanctuary, Wellington, New Zealand. Oral and faecal samples were collected from live hihi nestlings, for microbiological examination, between October 2008 and April 2009. All hihi that died and could be recovered were submitted to the New Zealand Wildlife Health Centre (NZWHC) at Massey University, for post-mortem examination. The results were compared with data obtained retrospectively from the National Wildlife Mortality (NWM) database for two other reintroduced populations of hihi on Mokoia and Tiritiri Matangi Islands. RESULTS: Fifty chicks fledged from 82 eggs hatched during the 2008–2009 breeding season at Zealandia: Karori Sanctuary. Thirty-four live nestlings were sampled from 11 nests, and C. albicans was isolated from gastrointestinal swabs of 13 live nestlings from four nest sites. Eight (62%) of those nestlings survived to fledge, compared with 17/21 (81%) of those that tested negative (p=0.254; Fishers exact test). Of the 32 hihi nestlings that died during the period of the study, 25 were recovered for necropsy. Histopathological examination revealed candidiasis was a factor in the deaths of four nestlings. An adult hihi that died during the period of the study at Zealandia: Karori Sanctuary was also found to have candidiasis. Retrospective analysis of data from the NWM database revealed candidiasis was also a factor in the deaths of five nestlings aged between 1 and 10 days from Mokoia Island, and of three nestlings <5 days old and one adult from Tiritiri Matangi Island. CONCLUSIONS: Candida albicans was isolated from 38% of hihi nestlings sampled in this study, and vertical transmission of this organism from parent to offspring is likely to occur. Some colonised nestlings developed ventriculitis associated with Candida spp., but survival to fledging was not significantly different between nestlings that tested positive or negative, although the fate of birds following fledging was unknown.

Causes of mortality in a nestling population of free-living hihi (stitchbird—Notiomystis cincta)

The hihi is an endangered New Zealand species and its survival depends on the health of translocated populations. Low nestling survival was detected at Zealandia–Karori Sanctuary (KS) during the 2008–09 breeding season with 34% of eggs surviving to fledge. Samples obtained from live and dead hihi nestlings showed that several disease syndromes contributed to nestling deaths. Cause of death was diagnosed by necropsy and histopathology for 25 nestlings. Mortality was highest (60%) in nestlings ≤7 days old and was associated with seasonally low minimum daily temperatures (<11°C). Deaths in this age group were most commonly attributed to poor pulmonary aeration and starvation. Ventriculitis was associated with mortality in eight 6–19-day-old nestlings with no indication that weather was implicated. The remaining deaths were from a variety of unrelated events or causes. Candida albicans, Aspergillus sp. and an unidentified haemoparasite were found among the nestling population. There was no evidence of coccidia or other intestinal parasite infections. In contrast to translocated populations at other sites, nesting material recovered from nest boxes contained low densities of tropical fowl mites (Ornithonyssus bursa). To improve survival for nestlings up to 7 days old, extra food provisioning and nest box weather protection during inclement weather is suggested.

Fatal levamisole toxicosis of captive kiwi (Apteryx mantelli)

Abstract CASE HISTORY: Nine of 24 captive kiwi treated with oral levamisole at a dose between 25–43 mg/kg showed signs of respiratory distress. Six died within 4 h of treatment and the remaining three made a full recovery within 24 h. CLINICAL AND PATHOLOGICAL FINDINGS: Within 3–4 h of treatment, the affected birds had an elevated respiratory rate, mucoid nasal discharge and rapidly became comatose. Post mortem examination revealed accumulation of thick mucus in the oral cavity and trachea. There was severe pulmonary congestion and oedema and early bronchopneumonia in the lungs of five of the birds. In two birds, there was acute hepatic degeneration and necrosis and one bird had acute pancreatic degeneration and necrosis. DIAGNOSIS: Acute levamisole toxicity. CLINICAL RELEVANCE: Kiwi were acutely sensitive to levamisole toxicity at doses that are well within the safe range for domestic poultry. Levamisole should not be used as an anthelmintic in kiwi.