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N. J. Thomas

Publications and source records attributed to N. J. Thomas.

At least 37 records · Page 2Linked to original sources

Fatal spirochetosis due to a relapsing fever-like Borrelia sp. in northern spotted owl

Acute septicemic spirochetosis was diagnosed in an adult male northern spotted owl (Strix occidentalis caurina) found dead in Kittitas County, Washington, USA. Gross necropsy findings included marked enlargement of the liver and spleen and serofibrinous deposits on the serous membranes lining the body cavities and the pericardial and perihepatic sacs. Microscopic observations included macrophage infiltration in the liver and spleen with mild thrombosis and multifocal necrosis, as well as hemorrhage and acute inflammation in the choroid plexus of the brain. No viruses or pathogenic bacteria were isolated from brain, liver, or spleen, and no parasites were found in blood smears or impression smears of the liver. Chlamydial culture attempts were unsuccessful and no chlamydial antibodies were detected in serum. In silver-stained microscopic sections and by transmission electron microscopy of liver, numerous long, thin, spiral-shaped bacteria were seen in the liver, spleen, cerebral ventricles, and within blood vessels in many organs. The organism was identified as a member of the Borrelia genus by sequence analysis of the PCR-amplified 16S rRNA gene. The most closely related species is B. hermsii, an agent of relapsing fever in humans in the western United States. This is the first report of a relapsing fever-related Borrelia in a wild bird.

Washington↗

Epizootiologic studies of avian vacuolar myelinopathy in waterbirds

Epizootic avian vacuolar myelinopathy (AVM) was first recognized as a neurologic disease in bald eagles (Haliaeetus leucocephalus) and American coots (Fulica americana) in Arkansas, USA in 1994 and 1996, respectively, but attempts to identify the etiology of the disease have been unsuccessful to date. Between 1998 and 2001, wing clipped sentinel birds (wild American coots and game farm mallards [Anas platyrhynchos]) were released at Lake Surf, North Carolina, a lake with recurrent outbreaks of AVM, in order to gain a better understanding of the epizootiology of the disease. As early as 5-7 days post-release, sentinel coots and mallards showed neurologic signs of disease and were confirmed with AVM upon histologic examination of their brains. Serial releases of sentinel mallards during the summer, fall, and winter of 2000-01 demonstrated that exposure to the causative agent at a threshold sufficient to manifest disease was seasonal and occurred over about a 2 mo period, during November and December. Our findings that disease onset can be very rapid (5-7 days) and that exposure to the causative agent of AVM is site-specific, seasonal (late fall to early winter), and occurs over a relatively short duration (several months) supports the hypothesis that the disease is caused by a chemical substance, most likely of natural origin.

North Carolina↗

Sarcocystis neurona infections in sea otter (Enhydra lutris): Evidence for natural infections with sarcocysts and transmission of infection to opossums (Didelphis virginiana)

Although Sarcocystis neurona has been identified in an array of terrestrial vertebrates, recent recognition of its capacity to infect marine mammals was unexpected. Here, sarcocysts from 2 naturally infected sea otters (Enhydra lutris) were characterized biologically, ultrastructurally, and genetically. DNA was extracted from frozen muscle of the first of these sea otters and was characterized as S. neurona by polymerase chain reation (PCR) amplification followed by restriction fragment length polymorphism analysis and sequencing. Sarcocysts from sea otter no. 1 were up to 350 I?m long, and the villar protrusions on the sarcocyst wall were up to 1.3 I?m long and up to 0.25 I?m wide. The villar protrusions were tapered towards the villar tip. Ultrastructurally, sarcocysts were similar to S. neurona sarcocysts from the muscles of cats experimentally infected with S. neurona sporocysts. Skeletal muscles from a second sea otter failed to support PCR amplification of markers considered diagnostic for S. neurona but did induce the shedding of sporocysts when fed to a laboratory-raised opossum (Didelphis virginiana). Such sporocysts were subsequently fed to knockout mice for the interferon-gamma gene, resulting in infections with an agent identified as S. neurona on the basis of immunohistochemistry, serum antibodies, and diagnostic sequence detection. Thus, sea otters exposed to S. neurona may support the development of mature sarcocysts that are infectious to competent definitive hosts.

Washington↗

Dual Sarcocystis neurona and Toxoplasma gondii infection in a northern sea otter from Washington state, USA

Dual Sarcocystis neurona and Toxoplasma gondii infection was observed in a Northern sea otter from Washington, USA. The animal was found stranded, convulsed, and died shortly thereafter. Encephalitis caused by both S. neurona and T. gondii was demonstrated in histological sections of brain. Immunohistochemical examination of sections with S. neurona specific antisera demonstrated developmental stages that divided by endopolygeny and produced numerous merozoites. PCR of brain tissue from the sea otter using primer pairs JNB33/JNB54 resulted in amplification of a 1100 bp product. This PCR product was cut in to 884 and 216 bp products by Dra I but was not cut by Hinf I indicating that it was S. neurona [J. Parasitol. 85 (1999) 221]. No PCR product was detected in the brain of a sea otter which had no lesions of encephalitis. Examination of brain sections using T. gondii specific antisera demonstrated tachyzoites and tissue cysts of T. gondii. The lesions induced by T. gondii suggested that the sea otter was suffering from reactivated toxoplasmosis. T. gondii was isolated in mice inoculated with brain tissue. A cat that was fed infected mouse brain tissue excreted T. gondii oocysts which were infective for mice. This is apparently the first report of dual S. neurona and T. gondii in a marine mammal.

Washington↗

Minimum survival rates for Mississippi sandhill cranes: a comparison of hand-rearing and parent-rearing

Hand-reared (56) and parent-reared (76) juvenile Mississippi sandhill cranes (Grus canadensis pulla) were produced at the Patuxent Wildlife Research Center (Patuxent), Laurel, Maryland over a 4-year period (1989-92) and released at the Mississippi Sandhill Crane National Wildlife Refuge (Refuge), Gautier, Mississippi in a controlled experiment. Hand-reared survival rates proved higher than for parent-reared survival for each time category: 6 months, 86% versus 75%; 1 year, 77% versus 68%; 2 years 66% versus 53%; 3 years, 55% versus 43%: partial data for fourth and filth years were 57% versus 31% and 48% versus 37%.

Maryland, Mississippi↗

Biological characterisation of Sarcocystis neurona isolated from a Southern sea otter (Enhydra lutris nereis)

Sarcocystis neurona was isolated from the brain of a juvenile, male southern sea otter ( Enhydra lutris nereis ) suffering from CNS disease. Schizonts and merozoites in tissue sections of the otter’s brain reacted with anti- S. neurona antiserum immunohistochemically. Development in cell culture was by endopolyogeny and mature schizonts were first observed at 3 days postinoculation. PCR of merozoite DNA using primer pairs JNB33/JNB54 and restriction enzyme digestion of the 1100 bp product with Dra I indicated the organism was S. neurona . Four of four interferon-γ gene knockout mice inoculated with merozoites developed S. neurona -associated encephalitis. Antibodies to S. neurona but not Sarcocystis falcatula , Toxoplasma gondii , or Neospora caninum were present in the serum of inoculated mice. This is the first isolation of S. neurona from the brain of a non-equine host.

International Journal for Parasitology↗

Biological and molecular characterizations of Toxoplasma gondii strains obtained from Southern sea otters (Enhydra lutris nereis)

Toxoplasma gondii was isolated from brain or heart tissue from 15 southern sea otters ( Enhydra lutris nereis ) in cell cultures. These strains were used to infect mice that developed antibodies to T. gondii as detected in the modified direct agglutination test and had T. gondii tissue cysts in their brains at necropsy. Mouse brains containing tissue cysts from 4 of the strains were fed to 4 cats. Two of the cats excreted T. gondii oocysts in their feces that were infectious for mice. Molecular analyses of 13 strains indicated that they were all type II strains, but that they were genetically distinct from one another.

California↗

Miscellaneous diseases

This concluding chapter is intended to further inform the reader of the broad spectrum of causes affecting the health of wild birds by illustrating a variety of disease conditions that are not described elsewhere in this Manual. The information in this chapter is not intended to represent a comprehensive description of other causes for ill-health and death in wild birds. Instead, examples are provided of some less commonly reported conditions that, in some instances, illustrate larger health issues. Too little is known about these conditions to currently assess their biological significance as mortality factors in wild birds.

Information and Technology Report↗

Barbiturates

Barbiturate products are commonly used to euthanize domestic animals. The primary active component in euthanasia solutions is sodium pentobarbital, but some products also contain other minor ingredients (Fig. 48.1). Euthanasia solutions are generally injected intravenously in domestic animals; therefore, after death, the solutions will be most concentrated in the blood and the highly vascularized organs, such as the liver or spleen, of the euthanized animal. Euthanized carcasses that are available as carrion pose a hazard to scavenging birds and mammals. Large domestic animal carcasses, such as horses, that are not used for food or rendering but that are sufficiently valuable (monetarily or psychologically) to warrant veterinary services and euthanasia drugs are the most common sources of barbiturate poisoning in scavengers. In one instance in British Columbia, a single cow carcass was responsible for poisoning 29 bald eagles. Circumstances that interfere with burial, such as frozen winter soil or bulky carcasses, result in euthanized carcasses being available for scavenger species. This problem could increase in the future if more stringent air-quality standards restrict carcass incineration.

Information and Technology Report↗

Electrocution

Power lines and power poles present a potential electrocution hazard to wild birds. Many birds, especially raptors, select power poles for perching, and, sometimes, for nesting (Figs. 50.1–3). If a bird’s appendages bridge the gap between two energized parts or between an energized and a grounded metal part, electricity flows through the “bridge” that is filling the gap and the bird is electrocuted. Most commonly, birds are electrocuted where conducting wires (conductors) are placed closer together than the wingspan of birds that frequent the poles (Fig. 50.2). Feathers are poor electrical conductors, but if contact is made between points on the skin, talons, or beak, or if the feathers are wet, conduction can occur. Common anatomical sites of contact include conduction between the wrists of each wing or between the skin of one wing and a foot or leg. The resulting shock causes severe, usually fatal, cardiovascular injury. Because conductors on distribution lines are placed closer together than high voltage transmission lines, birds are more frequently electrocuted on distribution lines despite their lower voltage. In addition to one to three conductors, power poles may also carry ground wires, transformers, or grounded metal crossarm braces. Complicated wiring configurations that put multiple energized and grounded metal parts near attractive perching or nesting sites are the most hazardous configurations (Fig. 50.3).

Information and Technology Report↗

Poisoning of raptors with organophosphorus and carbamate pesticides with emphasis on Canada, U.S. and U.K.

We reviewed cases of raptor mortality resulting from cholinesterase-inhibiting pesticides. We compiled records from the U.S., U.K. and Canada for the period 1985-95 (520 incidents) and surveyed the relevant literature to identify the main routes of exposure and those products that led to the greatest number of poisoning cases. A high proportion of cases in the U.K. resulted from abusive uses of pesticides (willful poisoning). The proportion was smaller in North America where problems with labeled uses of pesticides were as frequent as abuse cases. Poisoning resulting from labeled use was possible with a large number of granular pesticides and some seed treatments through secondary poisoning or through the ingestion of contaminated invertebrates, notably earthworms. With the more toxic products, residue levels in freshly-sprayed insects were high enough to cause mortality. The use of organophosphorus products as avicides and for the topical treatment of livestock appeared to be common routes of intoxication. The use of insecticides in dormant oils also gave rise to exposure that can be lethal or which can debilitate birds and increase their vulnerability. A few pesticides of high toxicity were responsible for the bulk of poisoning cases. Based on limited information, raptors appeared to be more sensitive than other bird species to organophosphorus and carbamate pesticides. Some of the more significant risk factors that resulted in raptor poisonings were: insectivory and vermivory; opportunistic taking of debilitated prey; scavenging, especially if the gastrointestinal tracts are consumed; presence in agricultural areas; perceived status as pest species; and flocking or other gregarious behavior at some part of their life cycle. Lethal or sublethal poisoning should always be considered in the diagnosis of dead or debilitated raptors even when another diagnosis (e.g., electrocution, car or building strike) is apparent. Many cases of poisoning are not currently diagnosed as such and, even when diagnosed, the information is often not made available to regulatory authorities. The importance of pesticide intoxications relative to other sources of mortality is highly variable in time and place; on a regional level, the increased mortality of raptors resulting from cholinesterase-inhibiting pesticides can be significant, especially in the case of rare species.

Journal of Raptor Research↗

Epizootic vacuolar myelinopathy of the central nervous system of bald eagles ( Haliaeetus leucocephalus ) and American coots ( Fulica americana )

Unprecedented mortality occurred in bald eagles ( Haliaeetus leucocephalus ) at DeGray Lake, Arkansas, during the winters of 1994-1995 and 1996-1997. The first eagles were found dead during November, soon after arrival from fall migration, and deaths continued into January during both episodes. In total, 29 eagles died at or near DeGray Lake in the winter of 1994-1995 and 26 died in the winter of 1996-1997; no eagle mortality was noted during the same months of the intervening winter or in the earlier history of the lake. During the mortality events, sick eagles were observed overflying perches or colliding with rock walls. Signs of incoordination and limb paresis were also observed in American coots ( Fulica americana ) during the episodes of eagle mortality, but mortality in coots was minimal. No consistent abnormalities were seen on gross necropsy of either species. No microscopic findings in organs other than the central nervous system (CNS) could explain the cause of death. By light microscopy, all 26 eagles examined and 62/77 (81%) coots had striking, diffuse, spongy degeneration of the white matter of the CNS. Vacuolation occurred in all myelinated CNS tissue, including the cerebellar folia and medulla oblongata, but was most prominent in the optic tectum. In the spinal cord, vacuoles were concentrated near the gray matter, and occasional swollen axons were seen. Vacuoles were uniformly present in optic nerves but were not evident in the retina or peripheral or autonomic nerves. Cellular inflammatory response to the lesion was distinctly lacking. Vacuoles were 8-50 microns in diameter and occurred individually, in clusters, or in rows. In sections stained by luxol fast blue/periodic acid-Schiff stain, the vacuoles were delimited and transected by myelin strands. Transmission electron microscopy revealed intramyelinic vacuoles formed in the myelin sheaths by splitting of one or more myelin lamellae at the intraperiodic line. This lesion is characteristic of toxicity from hexachlorophene, triethyltin, bromethalin, isonicotinic acid hydrazide, and certain exotic plant toxins; however, despite exhaustive testing, no etiology was determined for the DeGray Lake mortality events. This is the first report of vacuolar myelinopathy associated with spontaneous mortality in wild birds.

Arkansas↗

Accumulation pattern of organochlorine pesticides and polychlorinated biphenyls in southern sea otters (Enhydra lutris nereis) found stranded along coastal California, USA

Concentrations of PCBs, DDTs ( p,p' -DDE, p,p' -DDD and p,p' -DDT), HCHs (α-, β-, γ-isomers), chlordanes ( trans -chlordane, cis -chlordane, trans -nonachlor, cis -nonachlor and oxychlordane) and HCB (hexachlorobenzene were measured in liver, kidney and brain tissues of adult southern sea otters ( Enhydra lutris nereis ) found stranded along coastal California, USA, during 1992–96. The contamination pattern of organochlorines in sea otters from several locations was in the order of DDTs>PCBs>>CHLs>HCHs>>HCB, whereas those from Monterey Harbor contained greater concentrations of PCBs than of DDTs. Hepatic concentrations of PCBs and DDTs were in the ranges of 58–8700 and 280–5900 ng/g, wet weight, respectively, which varied depending on the geographic location. Sea otters collected from Monterey Harbor contained the greatest concentrations of PCBs and DDTs. In general, accumulation of DDTs, CHLs and PCBs was greater in kidney than in liver, whereas that of HCHs was similar in both the tissues. The gender difference in organochlorine concentrations was less than those reported in cetaceans. The composition of DDTs, HCHs and CHLs compounds in sea otter tissues indicated no recent inputs of these compounds in coastal California. Sea otters that died from infectious diseases, neoplasia and emaciation contained higher concentrations of DDTs than those that died from trauma.

California↗

Butyltin residues in southern sea otters (Enhydra lutris nereis) found dead along California coastal waters

Tributyltin (TBT) and its degradation products, mono- (MBT) and dibutyltin (DBT), were determined in liver, kidney, and brain tissues of adult southern sea otters (Enhydra lutris nereis) found dead along the coast of California during 1992a??1996. Hepatic concentrations of butyltin compounds (BTs = MBT + DBT + TBT) ranged from 40 to 9200 ng/g wet wt, which varied depending on the sampling location and gender. Concentrations of BTs in sea otters were comparable to those reported in stranded bottlenose dolphins from the U.S. Atlantic Coast during 1989a??1994. Greater accumulation of butyltins in sea otters was explained by their bottom-feeding habit and the diet that consists exclusively of invertebrates such as mollusks and gastropods. Livers of female sea otters contained approximately 2-fold greater concentrations of BTs than did those of males. The composition of butyltin compounds in sea otter tissues was predominated by TBT in most cases and suggestive of recent exposure. Large harbors such as Monterey Harbor that handle ships legally painted with TBT-containing antifouling paints continued to experience ecotoxicologically significant butyltin contamination. Sea otters, which were affected by infectious diseases, contained greater concentrations of BTs in their tissues than those that died from trauma and other unknown causes.

Californnia↗

DDE poisoning in an adult bald eagle

A 12-year-old female bald eagle ( Haliaeetus leucocephalus ) was found in May 1993 on Santa Catalina Island, California (USA), in a debilitated condition, exhibiting ataxia and tremors; it died within hours. On necropsy, the bird was emaciated but had no evidence of disease or physical injury. Chemical analyses were negative for organophosphorus pesticides and lead poisoning. High concentrations of DDE (wet weight basis) were found in the brain (212 ppm), liver (838 ppm), and serum (53 ppm). Mobilization of DDE, from depleted fat deposits, probably resulted in the lethal concentration in the eagle's brain.

California↗

Hypopi (Acari: Hypoderatidae) of the wood stork (Aves: Ciconiiformes: Ciconiidae)

A new species is described and additional host records are presented for 2 other species of deutonymphs of the family Hypoderatidae from the subcutaneous adipose tissues of the wood stork, Mycteria americana L. Phalacrodectes (Phalacrodectes) mycteria n. sp. appears to share affinities with species from both pelicaniform and ciconiiform hosts, but it most closely resembles P. (P.) punctatissimus (Černý) Pence & Courtney from pelicans in idiosomal chaetotaxy, cutdcular sclerotization, and posteriorly divergent, widely separated genital openings. The new species differs from this and other species of the genus by its small size, the degree of separation of the genital openings with papillae, no secondary sclerotization in the perigenital area or surrounding the genital openings, and the long filiform setae s and w on genu III. There was a mixed infection of Neottialges kutzeri Fain and N. mycteriae Pence in all of 7 wood storks examined from Florida and Georgia; P. (P) mycteria was found in 4 of these hosts. This is the 7th species described as a deutonymph in the genus Phalacrodectes . The apparent close affinity of P. (P.) mycteria with P. (P.) punctatissimus and allied species from pelicaniform versus ciconiiform birds appears to be inconsistent with the established host-parasite relationships based on classical avian taxonomic relationships. However, this apparent affinity may be more reflective of the close relationships between the families of pelicans, ibises and spoonbills, and storks as recently proposed by DNA–DNA hybridization studies.

Florida, Georgia↗