Rabies as a threat to wildlife.

The impact of infectious disease may become progressively more harmful to a species' survival as a wild population approaches an 'extinction vortex'. This risk is especially relevant for pathogens that spread rapidly and result in high mortality rates. Rabies, a virus that infects many mammalian species, can be efficiently transmitted through infected saliva, and is fatal without prior vaccination or rapid post-exposure prophylaxis (in humans). The authors conducted an extensive literature review to identify all wild mammal species reported to have been infected with rabies virus. They found reports of infection in 190 mammalian species, including 16 with elevated risk of extinction and two for which rabies is a direct conservation threat: the Ethiopian wolf (Canis simensis) and the African wild dog (Lycaon pictus). This paper discusses selected examples in which rabies has contributed to the population decline of a species of conservation concern. In addition, the authors note the importance of the transmission of rabies virus (RABV) from domestic dogs to wildlife, and the many challenges associated with the vaccination of wild animals. With this in mind, they present potential solutions to reduce the burden of rabies on wildlife. Once stable control of RABV is achieved in domestic dogs, remaining rabies threats to wildlife conservation can be addressed more effectively.

L'impact des maladies infectieuses peut constituer une menace croissante pour la survie d'espèces animales sauvages dès lors que leurs populations sont entraînées dans la « spirale de l'extinction ¼. Ce risque se pose plus particulièrement lorsqu'il s'agit d'agents pathogènes qui se propagent rapidement et induisent un taux de mortalité élevé. Le virus de la rage affecte un grand nombre d'espèces de mammifères et se transmet facilement par contact avec de la salive infectée ; l'infection virale entraîne la mort en l'absence d'une vaccination préalable ou, chez l'être humain, d'une prophylaxie post-exposition administrée rapidement. Les auteurs ont procédé à un examen exhaustif de la littérature afin d'inventorier les espèces de mammifères sauvages chez qui l'infection rabique a été rapportée. Des cas ont été notifiés chez 190 espèces de mammifères, dont 16 présentant un risque élevé d'extinction et deux directement menacées d'extinction en raison de la rage : le loup d'Abyssinie (Canis simensis) et le lycaon (Lycaon pictus). Les auteurs apportent des précisions sur un nombre choisi d'espèces vulnérables ou en danger dont le déclin des populations est en partie imputé à la rage. En outre, ils soulignent l'importance de la transmission du virus de la rage des chiens domestiques aux animaux sauvages et décrivent les nombreuses difficultés liées à la vaccination de la faune sauvage. Ces éléments établis, ils présentent quelques solutions envisageables pour réduire le fardeau de la rage dans la faune sauvage. Une fois le virus de la rage contrôlé de manière pérenne chez le chien domestique il sera possible de lutter plus efficacement contre les autres menaces que la rage fait peser sur la conservation de la faune.

Una enfermedad infecciosa puede tener efectos cada vez más dañinos en la supervivencia de una especie a medida que una población silvestre se va aproximando a un «vórtice de extinción¼. Este riesgo tiene especial importancia en el caso de patógenos que se propagan con rapidez y causan elevadas tasas de mortalidad. La rabia, enfermedad provocada por un virus que infecta a muchas especies de mamíferos y puede transmitirse eficazmente a través de saliva infectada, resulta letal en ausencia de vacunación previa o de rápidas medidas de profilaxis tras la exposición (en el ser humano). Los autores realizaron un amplio estudio bibliográfico para determinar todas aquellas especies de mamíferos silvestres en que se hubiera descrito una infección por el virus de la rabia. Encontraron infecciones descritas en 190 especies de mamíferos, de las que 16 presentan un elevado riesgo de extinción y dos cuya conservación se ve directamente amenazada por la rabia: el lobo etíope (Canis simensis) y el licaón, o perro salvaje africano (Lycaon pictus). Los autores exponen una serie de ejemplos en los que la rabia ha contribuido al declive demográfico de una especie cuya pervivencia está en mayor o menor peligro. Los autores señalan además la importancia que reviste la transmisión del virus de la rabia de los perros domésticos a la fauna silvestre y los numerosos problemas que presenta la vacunación de los animales silvestres. Teniendo presente esta dificultad, exponen posibles soluciones para reducir la carga de rabia en la fauna silvestre. Una vez se logre estabilizar el control del virus rábico en el perro doméstico, será posible combatir más eficazmente la amenaza que representa para la conservación de las especies silvestres.

Survey of cardiovascular pathology in wild urban Rattus norvegicus and Rattus rattus.

Norway (Rattus norvegicus) and black rats (Rattus rattus) are common commensal pests, yet little is known about the ecology of wild rats, including their natural diseases. We describe microscopic cardiovascular pathology in a subset of a sample of 725 wild urban rats. Changes observed in the pulmonary blood vessels (n = 199) included arteriolar medial hypertrophy (20.1%, n = 40) and blood vessel mineralization (19.1%, n = 38). Microscopic changes in the heart (n = 200) included myocarditis (33.5%, n = 67), fibrosis (6.0%, n = 12), mineralization (9.5%, n = 19), myocardial degeneration (22.0%, n = 44), and right ventricular hypertrophy (4.5%, n = 9). Rats with myocarditis, fibrosis, or myocardial degeneration were grouped into a composite variable: cardiomyopathy. Statistical analysis showed that the odds of being affected by cardiomyopathy were greater in male rats (odds ratio [OR] = 2.49; 95% confidence interval [CI] = 1.12-5.55) and heavier rats (OR = 1.14; 95% CI = 1.09-1.20). The odds of pulmonary arteriolar medial hypertrophy was greater in sexually mature rats (OR = 2.35; 95% CI = 0.75-7.36), while the odds of pulmonary vessel mineralization were greater in heavier rats (OR = 1.07; 95% CI = 1.03-1.11) and in black rats (OR = 5.35; 95% CI = 1.62-17.69) compared to Norway rats. To our knowledge, this is the first detailed description of pathology in the cardiovascular system of wild rats and demonstrates that cardiovascular disease is common. The impact of these lesions on individual and population health remains to be investigated.

Respiratory Pathology and Pathogens in Wild Urban Rats (Rattus norvegicus and Rattus rattus).

Norway (Rattus norvegicus) and black rats (Rattus rattus) are common peridomestic species, yet little is known about wild rat ecology, including their natural diseases. We describe gross and histological lesions in the respiratory tract of a sample of 711 wild urban rats. A subset was examined for 19 distinct categories of histological lesions in the respiratory tract. Testing for known respiratory pathogens included serology and polymerase chain reaction (PCR) of lung samples. Grossly evident lesions were rare (8/711; 1%). Upper respiratory tract inflammation was present in 93 of 107 (87%) rats and included rhinitis, submucosal and periglandular lymphoplasmacytic tracheitis, and/or tracheal intraluminal necrotic debris and was significantly associated (P < .05) with the presence of cilia-associated respiratory bacillus (CARB), Mycoplasma pulmonis, and increased body mass (odds ratio [OR] = 1.09; 95% confidence interval [CI] = 1.05-1.14 per 10 g). Within the lungs, peribronchiolar and/or perivascular lymphoplasmacytic cuffs were present in 152 of 199 rats (76%) and were also significantly associated (P ≤ .02) with CARB, M. pulmonis, and increased body mass (OR = 1.20; 95% CI = 1.14-1.27 per 10 g). Rats were frequently coinfected with M. pulmonis and CARB, and lesions associated with these pathogens were histologically indistinguishable. Pneumocystis sp was detected in 48 of 102 (47%) rats using PCR but was not significantly associated with lesions. This description of pathology in the respiratory system of wild rats demonstrates that respiratory disease is common. Although the impact of these lesions on individual and population health remains to be investigated, respiratory disease may be an important contributor to wild rat morbidity and mortality.

A history of One Health.

One Health is not a new concept. It can be demonstrated that its origins and development literally run the gamut from A to Z, that is to say, from Aristotle to Zoobiquity. Indeed, the consequences of the interaction that occurs between ecosystems, animals and people have shaped, and continue to shape, the course of human events and history. A reasoned and evidence-based assessment of the history of One Health must first be founded on an agreed definition of the term, but, given the many disciplines and sciences involved, finding such a definition is no easy task. Furthermore, there is an extensive and growing list of visionary individuals who have, over the centuries, attempted to promote awareness and advance the conceptto improve the management of the risks and consequences that arise at the interface between animal, human and ecosystem health. The One Health ideas of the 21st Century constitute a re-conceptualisation of health management in response to the accelerating environmental changes of the past 100 years, changes that are associated with the parallel exponential growth and concentration of the global human population. Consequently, the concept of One Health must recognise the constantly evolving relationship between animals and humans and the planet they share.

A feasibility study for the establishment of a national wildlife health centre in Sri Lanka.

Sri Lanka is a tropical nation within a zoogeographic zone that is at high risk for infectious disease emergence. In 2010, a study was conducted on the feasibility of enhancing capacity in Sri Lanka to manage wildlife diseases through the establishment of a national wildlife health centre. The Canadian Cooperative Wildlife Health Centre was assessed as a potential model for adaptation in Sri Lanka. Interviews and group meetings were conducted with potential key participants from the Sri Lankan Departments of Wildlife Conservation and Animal Production and Health, and the Faculty of Veterinary Medicine and Animal Science of the University of Peradeniya. In addition, site visits were made to potentially participating facilities and the literature on best practices in building scientific capacity was consulted. With strategic enhancements in education and training, additional personnel, improvements in transportation and diagnostic facilities, and central coordination, Sri Lanka appears very well positioned to establish a sustainable wildlife health centre and programme.

Heinz-body hemolytic anemia from the ingestion of crude oil: a primary toxic effect in marine birds.

Hemolytic anemia developed in young herring gulls and Atlantic puffins given daily oral doses of a Prudhoe Bay crude oil. Anemia developed 4 to 5 days after the initiation of oil ingestion and was accompanied by Heinz-body formation and a strong regenerative response. The data evince a toxic effect on circulating red blood cells involving an oxidative biochemical mechanism and the first clear evidence of a primary mechanism of toxicity from the ingestion of crude oil by birds.

Evidence of exposure to Brucella sp. in harbor porpoises (Phocoena phocoena) from the Bay of Fundy, Canada.

Novel strains of Brucella recently have been discovered in marine mammals. To investigate Brucella exposure and infection in a general population of cetaceans, blood and tissue samples were collected and analyzed from wild harbor porpoises (Phocoena phocoena) incidentally caught in fishing gear in the Bay of Fundy, Canada. Two of 170 (1.2%) animals had detectable antibodies against Brucella, but no organisms were isolated from genital swabs or tissues from 22 and 8 porpoises, respectively. Genetic analysis of inflamed testes from 20 animals yielded no amplification of Brucella DNA. This is the first evidence of exposure to Brucella in porpoises from the western North Atlantic, and the prevalence is much lower than documented for conspecifics from the eastern North Atlantic.

[Wildlife and emerging diseases]. / La faune sauvage et les maladies émergentes.

This article reviews the conditions that allow an infectious or parasitic pathogen to migrate from a wild reservoir to domestic animals and/or humans, and examines the possibility of a new disease emerging as a result. The review presents epidemiological mechanisms grouped into three principal models, illustrating them with examples: the intentional or accidental release of the reservoir host or pathogen; the exceeding of a numerical, ecological or behavioural threshold in the host populations and/or increased exposure of humans and domestic animals due to changes in behaviour; and lastly, an "adaptive" leap that ensures that a new host species finally succumbs to the pathogen and that it spreads among the conquered population. The authors examine the lessons to be drawn from such occurrences in terms of surveillance, prophylaxis and prevention.

Demographic features of Bartonella infections in Richardson's ground squirrels (Spermophilus richardsonii).

The epidemiology of Bartonella infections in Richardson's ground squirrels (Spermophilus richardsonii) was studied at multiple sites in Saskatchewan, Canada, from 2002 to 2004. The overall prevalence of Bartonella infection was 48%. Juvenile squirrels were significantly more likely to be infected with Bartonella than were adults (58% and 37%, respectively), and juvenile animals also were significantly more likely to have high levels of bacteremia compared to adult animals. Prevalence of Bartonella infection appeared to decrease with age; only 24% of animals known to be > or = 2 yr old were infected with Bartonella. Prevalence of infection was lowest in May (27%) and highest in late summer and early autumn (71%). The prevalence of fleas also varied seasonally, and animals were more likely to have fleas in the late summer and early autumn than in early summer. We found no relationship between Bartonella prevalence and host density or flea prevalence.

Effect of experimental ectoparasite control on bartonella infections in wild Richardson's ground squirrels.

The purpose of this study was to investigate the role of ectoparasites in transmitting Bartonella infections in wild Richardson's ground squirrels (Spermophilus richardsonii). Richardson's ground squirrels were trapped, examined for fleas, and tested for Bartonella bacteremia once monthly, at six sites, from April to September 2004. After the initial trapping session in April, burrows at three sites were treated with deltamethrin insecticide. Richardson's ground squirrels trapped on treated sites were less likely to have fleas and had fewer fleas than squirrels on control sites in all months following treatment. We found no difference in the prevalence of Bartonella infections on control and treated sites in May, immediately following treatment; however, significantly fewer squirrels were infected with Bartonella on treated sites in June and July. We conclude that ectoparasites are a main route of transmission for Bartonella infections in Richardson's ground squirrels.

Assessment of biological effects of chlorinated hydrocarbons in osprey chicks.

Osprey (Pandion haliaetus) eggs were collected during 1995 and 1996 at seven sites along the Fraser and Columbia River systems of British Columbia, Canada, and Washington and Oregon, USA. Fifty-four eggs were placed into a laboratory incubator. Thirty-eight of the hatched chicks were sacrificed within 24 h. Hatching success did not differ among sites and therefore between treatment and reference areas. Residual yolk sacs of eggs collected downstream of the large bleached-kraft pulp mill at Castlegar contained greater mean concentrations of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD, 2,930 ng/kg lipid) compared with reference sites such as the Nechako River, an upper tributary of the Fraser system (33.7 ng/kg). Total polychlorinated biphenyls (PCBs) in yolk sacs were also higher at Castlegar and in samples from the Columbia River downstream of Portland, Oregon, compared with those from the Nechako River. Concentrations of measured chemicals, including TCDD toxic equivalents (TEQs), total PCBs, p,p'-dichlorodiphenylethylene (p,p'-DDE), and other organochlorines were not different in eggs that failed to hatch compared with calculated whole-egg values for hatched eggs. There were significant biochemical responses; a hepatic cytochrome P4501A (CYP1A) cross-reactive protein was detected in all samples tested and correlated positively with ethoxyresorufin o-deethylase (EROD) activity and yolk sac concentrations of TEQs and total PCBs. Tissue concentrations of vitamin A compounds varied among sites and correlated positively with yolk sac concentrations of TEQs and PCBs. Morphological, histological, and other physiological parameters, including chick growth, edema, deformities, and hepatic and renal porphyrin concentrations, neither varied among sites nor showed concentration-related effects.

A serological survey of rural dogs and cats on the southwestern Canadian prairie for zoonotic pathogens.

A survey for antibodies against agents of plague, tularemia, and Rocky Mountain spotted fever (RMSF), and against Sin Nombre hantavirus (SNV), Bartonella henselae and B. clarridgeiae was conducted in the summer of 1995 using serum from rural dogs and cats living in the vicinity of four public parks in southeastern Alberta and southwestern Saskatchewan. Antibodies to all pathogens were detected in all survey areas. Overall prevalence rates were 0.075 for Yersinia pestis, 0.089 for Francisella tularensis, 0.025 for Rickettsia rickettsii (dogs only), and 0.029, 0.178 and 0.186 for SNV, B. henselae and B. clarridgeiae, respectively (cats only). This serological survey of rural dogs and cats was more sensitive and efficient than previous surveys based on collection and culture of rodents and ectoparasites. All six pathogens appear endemic to the region. Surveillance for plague, tularemia, RMSF and SNV, and management of associated public risks should be done in endemic regions.

Health risk assessment of the translocation of wild animals.

Potential health risks are always associated with the translocation of wild animals. A formal assessment of these health risks should be conducted in advance of each translocation, and the results of the risk assessment should be incorporated into decisions as to whether or not the translocation should occur or whether changes in the translocation protocol could substantially reduce health risks inherent in the translocation. Credible health risk assessments can be performed by individuals without extensive previous experience, given the necessary background in animal health and wildlife biology and access to sufficient valid information. Assessment of health risks should not be performed or influenced by those who will use the results to make decisions or those with vested interests in a particular outcome. The assessment process itself must be transparent, and the final risk assessment report must clearly present each step taken, all available information and all reasoning. Health risk assessment is a rigorous application of common sense to evaluate whether or not important health-related risks are associated with a proposed activity. The level of health risk inherent in a planned translocation is determined by identifying the full range of possible health hazards that might be associated with that translocation, identifying from among these a subset of potential hazards that require complete assessment, and for each hazard thus selected, evaluating the probability that the hazardous event will occur and the magnitude of negative consequences if it does occur. The combination of probability of occurrence and magnitude of consequences constitutes the risk posed by a potential health hazard, and the combined risk for each assessed health hazard constitutes the overall health risk estimate for the translocation. A valid numerical (quantitative) health risk assessment for wild animals is rarely possible because the available information on which the assessment must be based is too approximate and imprecise. Qualitative health risk assessments for wild animal translocations are usually of equal or greater value than numerical assessments and can be of enormous importance to wildlife conservation, domestic animal health and public health.

The role of wildlife in emerging and re-emerging zoonoses.

There are huge numbers of wild animals distributed throughout the world and the diversity of wildlife species is immense. Each landscape and habitat has a kaleidoscope of niches supporting an enormous variety of vertebrate and invertebrate species, and each species or taxon supports an even more impressive array of macro- and micro-parasites. Infectious pathogens that originate in wild animals have become increasingly important throughout the world in recent decades, as they have had substantial impacts on human health, agricultural production, wildlife-based economies and wildlife conservation. The emergence of these pathogens as significant health issues is associated with a range of causal factors, most of them linked to the sharp and exponential rise of global human activity. Among these causal factors are the burgeoning human population, the increased frequency and speed of local and international travel, the increase in human-assisted movement of animals and animal products, changing agricultural practices that favour the transfer of pathogens between wild and domestic animals, and a range of environmental changes that alter the distribution of wild hosts and vectors and thus facilitate the transmission of infectious agents. Two different patterns of transmission of pathogens from wild animals to humans are evident among these emerging zoonotic diseases. In one pattern, actual transmission of the pathogen to humans is a rare event but, once it has occurred, human-to-human transmission maintains the infection for some period of time or permanently. Some examples of pathogens with this pattern of transmission are human immunodeficiency virus/acquired immune deficiency syndrome, influenza A, Ebola virus and severe acute respiratory syndrome. In the second pattern, direct or vector-mediated animal-to-human transmission is the usual source of human infection. Wild animal populations are the principal reservoirs of the pathogen and human-to-human disease transmission is rare. Examples of pathogens with this pattern of transmission include rabies and other lyssaviruses, Nipah virus, West Nile virus, Hantavirus, and the agents of Lyme borreliosis, plague, tularemia, leptospirosis and ehrlichiosis. These zoonotic diseases from wild animal sources all have trends that are rising sharply upwards. In this paper, the authors discuss the causal factors associated with the emergence or re-emergence of these zoonoses, and highlight a selection to provide a composite view of their range, variety and origins. However, most of these diseases are covered in more detail in dedicated papers elsewhere in this Review.

Pathogenesis of porcine Actinobacillus pleuropneumonia: Part I. Effects of surface components of Actinobacillus pleuropneumoniae in vitro and in vivo.

To understand the role of non-secreted components of Actinobacillus pleuropneumoniae in virulence, we investigated in vitro cytotoxicity and in vivo pulmonary changes in pigs due to various A. pleuropneumoniae (serotype 1) fractions. Following 1.5 h incubation, lipopolysaccharide (LPS), 2 crude extracts and bacterial culture supernatant (BCS) at high concentrations were cytotoxic to porcine pulmonary alveolar macrophages (PAM), peripheral blood mononuclear leucocytes, neutrophils and a cultured porcine bone marrow cell line. Heat-killed bacteria were cytotoxic to PAM after 24 h incubation. The 2 crude extracts were prepared by shaking either intact bacteria after removing culture supernatants (crude surface extract, CSE), or whole bacterial culture (crude surface plus culture supernatant extract, CSSE) with glass beads in saline at 60 degrees C. Further experiments showed that proteins from the bacterial membrane were partially involved in cytotoxicities of these 2 extracts. Both BCS and CSSE caused multivocal hemorrhage and neutrophil infiltration when inoculated into porcine lungs, but CSE did not. The lung:whole body weight ratios of the pigs treated with CSSE were significantly higher (P < 0.05) than those of pigs treated with BCS, CSE, or control solution. It is concluded that beside the secreted proteins, bacterial surface components including LPS and non-secreted proteins were cytotoxic in vitro; and secreted and non-secreted components act synergistically to cause lung lesions.

Pathogenesis of porcine Actinobacillus pleuropneumonia, part II: roles of proinflammatory cytokines.

The in vitro production of proinflammatory cytokines after stimulation with Actinobacillus pleuropneumoniae and the relation of these cytokines in vivo with the disease caused by A. pleuropneumoniae were investigated. Within 24 h, in vitro stimulation by A. pleuropneumoniae (serotype 1) preparations, including killed bacteria, bacterial culture supernatant, lipopolysaccharide, and bacterial extracts, porcine pulmonary alveolar macrophages (PAM) produced significant (P < 0.05) amounts of tumor necrosis factor-alpha (TNF-alpha) and interleukin-1 (IL-1) as measured by bioassays. The supernatants containing interleukin-8 from PAM after stimulation by bacterial preparations showed significant neutrophil chemotaxis, while bacterial preparations alone did not. After in vivo infection with A. pleuropneumoniae, the mean levels of TNF-alpha and IL-1 in serum, as measured by bioassays, were elevated 37- to 27836-fold for TNF-alpha and 11- to 5941-fold higher for IL-1 within 4 d post-infection, depending on the treatments, and remained elevated up to Day 7. Both cytokines were also detected in porcine lungs by bioassays and immunocytochemistry. The results indicated that both secreted and surface components of A. pleuropneumoniae can stimulate PAM to produce proinflammatory mediators. Neutrophil chemoattractants rather than bacterial components are the major factor causing acute lung inflammation. The elevation of TNF-alpha and IL-1 in pigs occurred coincident with the onset of acute clinical disease.

Parallel measurement of brain acetylcholinesterase and the muscarinic cholinergic receptor in the diagnosis of acute, lethal poisoning by anti-cholinesterase pesticides.

The activity of acetylcholinesterase (AChE) and the density of muscarinic cholinergic binding receptors (mCBR) were measured in brains from normal Japanese quail (Coturnix coturnix japonica) and from quail after lethal intoxication with diazinon. These were measured in brains from whole heads held at 25 C for 0 to 8 days after death. The maximum relative loss of activity due to post mortem decomposition alone during 8 days was 13% and 10% for AChE and mCBR, respectively. During post mortem decomposition, the ratio of AChE: mCBR activities remained constant at approximately 1.3:1 in normal brains while it was always less than or equal to 0.5:1 after intoxication with diazinon. Normal AChE activity could be estimated from mCBR density. Parallel measurement of AChE and mCBR may assist in the post mortem diagnosis of death due to acute poisoning with anti-cholinesterase pesticides when control specimens are not available.

Eimeria fraterculae sp. n. in the kidneys of Atlantic puffins (Fratercula arctica) from Newfoundland, Canada: species description and lesions.

Renal coccidiosis is reported for the first time in an auk (Alcidae). Infection was detected in seven of 50 nestling Atlantic puffins (Fratercula arctica) and a new species of coccidia, Eimeria fraterculae sp. n., is described. The structure and sporulation of oocysts are characterized. Meronts, gamonts, and developing oocysts were present in collecting duct epithelium of medullary cones. The predominant host response was hypertrophy of infected cells, tubule dilation, and a mild localized peritubular infiltration with mononuclear inflammatory cells.

Effects of Prudhoe Bay crude oil on hatching success and associated changes in pipping muscles in embryos of domestic chickens (Gallus gallus).

Fertile white leghorn chicken eggs were exposed to 0, 1, 2, 4, 6, 8 or 16 microliters of Prudhoe Bay Crude oil (PBCO) on day 9 of incubation. The effects of oil on pipping and hatching success, body weight gain after hatching, serum creatine kinase levels, and pathological changes in organ systems were assessed in embryos that had survived acute toxic effects and were alive on day 18 of incubation. Exposure to oil greatly reduced pipping and hatching success. Severe edema and hemorrhage in the pipping muscle, multifocal subcapsular hepatic necrosis, marked depletion of lymphocytes in the bursa of Fabricius with infiltration by heterophils, and occasional dorso-caudal subcutaneous edema were observed in treated embryos. Pipping muscles were heavier in oil-exposed embryos. Embryos exposed to 4 microliters of PBCO had significantly reduced gain in body weight post-hatching. Serum creatine kinase levels were significantly elevated in the oil-exposed embryos only at the time of hatching. There was no evidence that exposure to oil caused degenerative changes in pipping muscle cells.

Further studies of brain cholinesterase: cholinergic receptor ratios in the diagnosis of acute lethal poisoning of birds by anticholinesterase pesticides.

Cholinesterase (ChE) and the muscarinic (mAChR) and nicotinic (nAChR) cholinergic receptors were measured in the brains of 86 birds of 20 different species collected in Saskatchewan, Canada during 1991 and 1992. There was a strong correlation between ChE and mAChR, and the ratio of ChE: mAChR was 38% less variable than was ChE alone. In a hypothetical test for minimal acute lethal poisoning of all birds based on a reduction by 50% of the normal ChE measured in each, the use of a single diagnostic threshold value of the ChE: mAChR ratio had a diagnostic sensitivity of 98% and a specificity of 99%, thus making theoretically possible the diagnosis of acute lethal poisoning by anticholinesterase chemicals without the use of reference control values for ChE. Both ChE and mAChR were highly stable during 12 days of postmortem decomposition under several different daily temperature regimes. Substantial changes in these molecules occurred only under conditions of constant high temperature (36 C). Acute lethal poisoning by the organophosphate chlorpyrifos did not affect the density of mAChR. Postmortem decomposition did not appear to be an important confounding factor in the diagnostic interpretation of either ChE or the ChE: mAChR ratio except under hot climatic conditions.