Distribution of the misfolded isoform of the prion protein in peripheral tissues and spinal cord of Rocky Mountain elk (Cervus elaphus nelsoni) with naturally occurring chronic wasting disease.

Chronic wasting disease (CWD) is an infectious transmissible spongiform encephalopathy of cervids associated with the presence of a misfolded prion protein (PrPCWD). Progression of PrPCWD distribution has been described using immunohistochemistry and histologic changes in a single section of brain stem at the level of the obex resulting in scores from 0 (early) to 10 (terminal) in elk with naturally occurring CWD. Here we describe the spread and distribution of PrPCWD in peripheral tissues and spinal cord in 16 wild and 17 farmed Rocky Mountain elk (Cervus elaphus nelsoni) with naturally occurring CWD and correlate these findings with obex scores. Spinal cord and approximately 110 peripheral tissues were collected, processed, stained with hematoxylin and eosin, and immunolabeled with the anti-prion protein monoclonal antibody F99/97.6.1. The medial retropharyngeal and tracheobronchial lymph nodes were the first tissues to accumulate PrPCWD, followed by other lymphoid tissues, myenteric plexus, spinal cord, and finally tissues outside of the lymphatic and neural systems. However, the only significant histological lesion observed was mild spongiform encephalopathy in the dorsal column of the lower spinal cord in elk with an obex score of ≥9. Initial exposure to CWD prions may be through the respiratory system and spread appears to occur primarily via the autonomic nervous system. Therefore, we suggest using obex scores as a proxy for stage of disease progression and verifying with key peripheral tissues.

Digeneans of northern fur seals Callorhinus ursinus (Pinnipedia: Otariidae) from five subpopulations on St. Paul Island, Alaska.

A parasitological survey of 651 northern fur seals Callorhinus ursinus L. from five subpopulations was conducted on St. Paul Island, Alaska, during July-August 2012-2014. Digenean trematodes were found in 210 of 651 fur seals with a total prevalence of 32.3%. Intensity of infection varied from 1 to 1540 parasites with mean intensity 18.4 ± 111.1 SD and median intensity of 2 specimens per host. Significant differences in prevalence and intensity of infection in northern fur seals between separate rookeries was not observed (Mann-Whitney test; p > 0.05). Four species of digeneans belonging to the families Heterophyidae (Apophallus zalophi Price, 1932, Phocitrema fusiforme Goto and Ozaki, 1930, and Galactosomum ubelakeri (Dailey, 1969)) and Troglotrematidae (Nanophyetus salmincola (Chapin, 1926)) were found. Nanophyetus salmincola is reported from C. ursinus for the first time. We obtained partial 28S rDNA sequences for all digenean species and conducted molecular phylogenetic analysis to demonstrate their phylogenetic relationships.

Shaggy Lame Fox Syndrome in Pribilof Island Arctic Foxes ( Alopex lagopus pribilofensis), Alaska.

A previously unrecognized condition is described in wild free-ranging Pribilof arctic foxes ( Alopex lagopus pribilofensis) from the Pribilof Islands, Alaska, USA. This condition is called shaggy lame fox syndrome (SLFS) denoting the primary clinical signs first observed. Criteria used to suspect SLFS on gross examination included emaciation, failure to shed winter pelage and moderate to severe polyarthritis. Criteria used to confirm SLFS histologically included polyarthritis (characterized by lymphoplasmacytic synovitis, tenosynovitis, bursitis, periosteal bony proliferation, and periarticular lymphoplasmacytic vasculitis) and systemic leukocytoclastic vasculitis. Other histological lesions often found included renal cortical infarcts, myocarditis with myocardial infarcts, lymphoplasmacytic meningitis, lymphoplasmacytic cuffing of meningeal and a few cerebral vessels, and cavitating infarcts of the brainstem and thalamus. The cause of SLFS is not known at this time; however, the gross and histological lesions suggest that the cause of SLFS may be a bacterial polyarthritis with a secondary immune-mediated vasculitis. These lesions are consistent with changes described with Erysipelothrix rhusiopathiae in domestic dogs; E. rhusiopathiae was identified from the synovial membrane of a swollen stifle joint and the kidney from one fox using real-time polymerase chain reaction and with culture from a fox that had gross and histological lesions of SLFS. Therefore, E. rhusiopathiae is a possible etiological agent for SLFS.

Anisakids (Nematoda: Anisakidae) from stomachs of northern fur seals (Callorhinus ursinus) on St. Paul Island, Alaska: parasitological and pathological analysis.

Anisakid nematodes parasitize the alimentary tracts of aquatic vertebrates, including northern fur seals (Callorhinus ursinus) (NFS). The main purpose of this study was to estimate the prevalence, intensity, and species composition of anisakids in NFSs on St. Paul Island, Alaska, and to analyze changes in NFS infection with these nematodes during the last decades. The study was carried out on St. Paul Island, Alaska, in July-August 2011-2013. Stomachs of 443 humanely harvested NFS males were collected from five separate haul-out areas. A total of 4,460 anisakid specimens were collected and identified by morphological criteria. Gross and histological examinations of stomachs were also performed. The overall prevalence of NFS infection was 91.2%; overall mean intensity 10.9, and overall median intensity 6. Five species, Anisakis simplex s. l., Contracaecum osculatum s. l., Pseudoterranova decipiens s. l., P. azarazi and Phocascaris cystophorae, were found. The prevalence of Anisakis was 46.5%, its intensity 7.5. The prevalence and intensity of Contracaecum, Pseudoterranova, and Phocascaris were 33.6% and 3.5, 81.9% and 6.5, and 5.2% and 1.7, respectively. Significant differences in the prevalence of NFS infection were observed between separate haul-outs. Comparison of the present data with the results of studies performed in the North Pacific in the 1960s, showed a significant decrease in the intensity of NFS infection with anisakids during the last decades. The prevalence of mucosal lesions in NFS stomachs caused by anisakids also decreased from 92 to 20.9%. Possible reasons for the changes in NFS infection with anisakids are discussed.

Oxidative stress and redistribution of glutamine synthetase in California sea lions (Zalophus californianus) with domoic acid toxicosis.

The aim of this study was to test the hypothesis that oxidative stress and glutamine synthetase (GS) redistribution occur in domoic acid (DA) toxicosis in California sea lions (CSLs, Zalophus californianus). Sections of archived hippocampi from seven control and 13 CSLs diagnosed with DA toxicosis were labelled immunohistochemically for GS and for two markers of oxidative stress, malondialdehyde (MDA) and 3-nitrotyrosine (NT). The distribution and intensity of labelling were compared with the pathological changes seen in haematoxylin and eosin-stained sections. Increased expression of MDA and NT occurred in neurons of the hippocampal formation of CSLs with lesions consistent with DA toxicosis. The degree of oxidative stress was not affected significantly by the chronicity or severity of hippocampal damage. In six out of seven CSLs with chronic effects of DA toxicosis, in addition to the normal glial distribution of GS, GS expression was very strong in some neurons of the subiculum. However, neuronal GS labelling was also seen in one control CSL, an effect that may have been due to previous exposure to DA. GS expression in neurons was associated with decreases in GS labelling in neighbouring glial cell processes. DA toxicosis therefore induces increased expression of markers of oxidative stress in neurons consistent with oxidative stress contributing to the initial DA insult and also the epilepsy that often develops in chronic DA toxicosis. GS redistribution occurred primarily in chronic DA toxicosis, perhaps leading to alterations of the glutamine-glutamate-GABA (gamma-aminobutyric acid) cycle and contributing to the excitotoxicity and seizures often seen in DA toxicosis.

Ecological, morphological, and molecular studies of Acanthocheilonema odendhali (Nematoda: Filarioidea) in northern fur seals (Callorhinus ursinus) on St. Paul Island, Alaska.

Studies of northern fur seal (Callorhinus ursinus Linnaeus, 1758) infection by the filariid nematode Acanthocheilonema odendhali were carried out in 2011-2012 on St. Paul Island, Pribilof Archipelago, Alaska. Skins of 502 humanely harvested northern fur seals from haul-out areas of five rookeries, Polovina (n = 122), Morjovi (n = 54), Zapadni (n = 72), Lukanin (n = 109), and Gorbatch (n = 145), were examined. A. odendhali was found in 18% of northern fur seals. The prevalence of infection ranged from 12.5% up to 22.9% on different haul-out areas on the island. The mean intensity of infection was 1.3 (range 1-7). Detailed morphological examination of collected specimens was performed using light microscopy. Several characters were added to the morphological description of the species, among them lateral thickening of the body cuticle, especially prominent in males, variations in number and position of genital papillae in males, transverse striation of the cuticle, and terminal dilation on tail end in microfilariae. The adult specimens studied had a shorter esophagus than type specimens from the California sea lion described by Perry (1967). Comparison of partial sequences of the mitochondrial cox1 gene from specimens collected from five sampling sites on St. Paul Island and a specimen from the type host and territory in California showed no significant differences and strongly supported conspecificity of the material from Alaska with A. odendhali.

Acanthocephalans in northern fur seals (Callorhinus ursinus) and a harbor seal (Phoca vitulina) on St. Paul Island, Alaska: species, prevalence, and biodiversity in four fur seal subpopulations.

Monitoring studies of acanthocephalans in northern fur seals (Callorhinus ursinus Linnaeus, 1758) (NFSs) and a harbor seal (Phoca vitulina Linnaeus, 1758) were performed on St. Paul Island, Alaska, in July-August 2011. Gastrointestinal tracts of 105 humanely harvested NFS subadult males (SAMs) (3-4 years old) were collected during the annual Aleut subsistence harvest at four haul-out areas (HOAS): Lukanin (n = 26 NFSs), Polovina (n = 28), Gorbatch (n = 30), and Morzhovyi (n = 21). One gastrointestinal tract collected from a harbor seal (about 3-4 years old) found dead at Morzhovyi HOAS was also examined. The total prevalence of infection in NFSs with acanthocephalans was 29.52 % with variations from 7.69 % to 47.62 % between the four different HOAS. Eight acanthocephalan species of two genera-Corynosoma Lühe, 1904 (Corynosoma strumosum, Corynosoma alaskensis, Corynosoma cameroni, Corynosoma semerme, Corynosoma similis, Corynosoma validum, and Corynosoma villosum), and Bolbosoma Porta, 1908 (Bolbosoma nipponicum)-were found in the NFSs and a harbor seal. This is a new record of C. alaskensis for the NFSs. Short biological notes of the species found are presented. Differences in species composition as well as in prevalence of acanthocephalans parasitizing NFSs were observed in subpopulations from four different HOAS on St. Paul Island. The highest biodiversity of acanthocephalans and infection were found in subpopulations on Polovina and Morzhovyj HOAS, the lowest was on Lukanin HOAS. From 3.2 % (for C. validum) to 19.4 % (for C. villosum) of NFSs were infected by one acanthocephalan species; two species were found in 22.6 %; three in 9.7 %; and four in 3.2 %. Further studies of NFS parasites are necessary to follow the trends in parasitic infection rates and diversity in NFS population on the Pribilov Islands and for monitoring the influence of various ecological factors on NFS populations in Alaska.

Passive transfer of maternal GnRH antibodies does not affect reproductive development in elk (Cervus elaphus nelsoni) calves.

Gonadotropin-releasing hormone is intermittently released from the hypothalamus in consistent patterns from before birth to final maturation of the hypothalamic-pituitary-gonadal axis at puberty. Disruption of this signaling via GnRH vaccination during the neonatal period can alter reproduction at maturity. The objective of this study was to investigate the long-term effects of GnRH-antibody exposure on reproductive maturation and function in elk calves passively exposed to high concentrations of GnRH antibodies immediately after birth. Fifteen elk calves (eight males and seven females) born to females treated with GnRH vaccine or sham vaccine during midgestation were divided into two groups based on the concentration of serum GnRH antibodies measured during the neonatal period. Those with robust (>15 pmol (125)I-GnRH bound per mL of serum) titers (N = 10; four females and six males) were designated as the exposed group, whereas those with undetectable titers (N = 5; three females and two males) were the unexposed group. Onset of puberty, reproductive development, and endocrine function in antibody-exposed and unexposed male and female elk calves were compared. Neonatal exposure to high concentrations of GnRH antibodies had no effect on body weight (P = 0.968), endocrine profiles (P > 0.05), or gametogenesis in either sex. Likewise, there were no differences between groups in gross or histologic structure of the hypothalamus, pituitary, testes, or ovaries. Pituitary stimulation with a GnRH analog before the second potential reproductive season induced substantial LH secretion in all experimental elk. All females became pregnant during their second reproductive season and all males exhibited similar mature secondary sexual characteristics. There were no differences between exposure groups in hypothalamic GnRH content (P = 0.979), pituitary gonadotropin content (P > 0.05) or gonadal structure. We concluded that suppressing GnRH signaling through immunoneutralization during the neonatal period likely does not alter long-term reproductive function in this species.

Parasitological examination for presence of hookworms (Uncinaria spp.) in northern elephant seals (Mirounga angustirostris) at Año Nuevo State Reserve, California (2012).

Northern elephant seals (Mirounga angustirostris Gill, 1866), inhabiting rookeries on the mainland of Año Nuevo State Reserve in central California, were investigated in 2012 for presence of hookworms (Uncinaria spp.). Material collected and examined for hookworms included: blubber (n = 15), stomach and intestines (n = 21) from dead pups; feces from the rectum of weaned pups (n = 23); sand containing apparent feces in areas of weaned pups (n = 28) and sand without apparent feces in areas of weaned pups (n = 54); milk from females (n =23) at 5 days and about 23 to 26 days postpartum; and placenta from one female. Evidence of hookworm presence was not detected in any of the samples examined. Possible reasons why hookworms were not found in northern elephant seals on the mainland of Año Nuevo State Reserve are discussed.

Neurolymphomatosis in a dog with B-cell lymphoma.

Lymphoma in the left femoral nerve of a 10-year-old English Cocker Spaniel caused complete paralysis of the affected limb. Neoplastic cells were immunopositive for CD79a and Pax5 and negative for CD3. Neoplastic cells were in multiple lymph nodes and one kidney but spared bone marrow. The clinical and histologic features in this case resemble those of the rare human condition of neurolymphomatosis.

Clinical and pathologic responses of American crows (Corvus brachyrhynchos) and fish crows (C ossifragus) to experimental West Nile virus infection.

West Nile virus (WNV)-associated disease has a range of clinical manifestations among avian taxa, the reasons for which are not known. Species susceptibility varies within the avian family Corvidae, with estimated mortality rates ranging from 50 to 100%. We examined and compared virologic, immunologic, pathologic, and clinical responses in 2 corvid species, the American crow (Corvus brachyrhynchos) and the fish crow (C ossifragus), following experimental WNV inoculation. Unlike fish crows, which remained clinically normal throughout the study, American crows succumbed to WNV infection subsequent to dehydration, electrolyte and pH imbalances, and delayed or depressed humoral immune responses concurrent with marked, widespread virus replication. Viral titers were approximately 3,000 times greater in blood and 30,000 to 50,000 times greater in other tissues (eg, pancreas and small intestine) in American crows versus fish crows. Histologic lesion patterns and antigen deposition supported the differing clinical outcomes, with greater severity and distribution of lesions and WNV antigen in American crows. Both crow species had multiorgan necrosis and inflammation, although lesions were more frequent, severe, and widespread in American crows, in which the most commonly affected tissues were small intestine, spleen, and liver. American crows also had inflammation of vessels and nerves in multiple tissues, including heart, kidney, and the gastrointestinal tract. WNV antigen was most commonly observed within monocytes, macrophages, and other cells of the reticuloendothelial system of affected tissues. Collectively, the data support that WNV-infected American crows experience uncontrolled systemic infection leading to multiorgan failure and rapid death.

Paranasal sinus masses of Rocky Mountain bighorn sheep (Ovis canadensis canadensis).

This article describes 10 cases of paranasal sinus masses in Rocky Mountain bighorn sheep (Ovis canadensis canadensis). Among 21 bighorns that were examined from 11 herds in Colorado, 10 individuals (48%) from 4 herds (36%) had masses arising from the paranasal sinuses. Affected animals included 9 of 17 females (53%) and 1 of 4 males (25%), ranging in age from approximately 2 years to greater than 10 years. Defining gross features of these masses included unilateral or bilateral diffuse thickening of the respiratory lining of the maxillary and/or frontal sinuses, with abundant seromucinous exudate in the affected sinus cavities. Defining histologic features of these masses included chronic inflammation and proliferation of mesenchymal and epithelial cells of the mucosa and submucosa. Epithelial changes included hyperplasia of mucosal epithelium, hyperplasia of submucosal glands and ducts, and neoplasia (adenocarcinoma). Mesenchymal changes included submucosal myxedema, submucosal fibroplasia/fibrosis, bone destruction, and neoplasia (myxomatous fibroma). Specific immunohistochemistry and polymerase chain reaction for Jaagsiekte sheep retrovirus and enzootic nasal tumor virus were performed with negative results.

Detection of the abnormal isoform of the prion protein associated with chronic wasting disease in the optic pathways of the brain and retina of Rocky Mountain elk (Cervus elaphus nelsoni).

Eyes and nuclei of the visual pathways in the brain were examined in 30 Rocky Mountain elk (Cervus elaphus nelsoni) representing 3 genotypes of the prion protein gene PRNP (codon 132: MM, ML, or LL). Tissues were examined for the presence of the abnormal isoform of the prion protein associated with chronic wasting disease (PrP(CWD)). Nuclei and axonal tracts from a single section of brain stem at the level of the dorsal motor nucleus of the vagus nerve were scored for intensity and distribution of PrP(CWD) immunoreactivity and degree of spongiform degeneration. This obex scoring ranged from 0 (elk with no PrP(CWD) in the brain stem) to 10 (representing elk in terminal stage of disease). PrP(CWD) was detected in the retina of 16 of 18 (89%) elk with an obex score of > 7. PrP(CWD) was not detected in the retina of the 3 chronic wasting disease-negative elk and 9 elk with an obex score of < 6. PrP(CWD) was found in the nuclei of the visual pathways in the brain before it was found in the retina. Within the retina, PrP(CWD) was first found in the inner plexiform layer, followed by the outer plexiform layer. Intracytoplasmic accumulation of PrP(CWD) was found in a few neurons in the ganglion cell layer in the PRNP 132ML elk but was a prominent feature in the PRNP 132LL elk. Small aggregates of PrP(CWD) were present on the inner surface of the outer limiting membrane in PRNP 132LL elk but not in PRNP 132MM or 132ML elk. This study demonstrates PrP(CWD) accumulation in nuclei of the visual pathways of the brain, followed by PrP(CWD) in the retina.

Emergence of diseases from wildlife reservoirs.

Interest in the epidemiology of emerging diseases of humans and livestock as they relate to wildlife has increased greatly over the past several decades. Many factors, most anthropogenic, have facilitated the emergence of diseases from wildlife. Some livestock diseases have "spilled over" to wildlife and then "spilled back" to livestock. When a population is exposed to an infectious agent, depending on an interaction of factors involving the host, agent, and environment, the population may be resistant to infection or may become a dead-end host, a spillover host, or a maintenance host. Each exposure is unique; the same species of host and agent may respond differently in different situations. Management actions that affect the environment and behavior of a potential host animal may allow the emergence of a new or as yet undetected disease. There are many barriers in preventing, detecting, monitoring and managing wildlife diseases. These may include political and legal hurdles, lack of knowledge about many diseases of wildlife, the absence of basic data on wildlife populations, difficulties with surveillance, and logistical constraints. Increasing interaction between wildlife and humans or domestic animals may lead to disease emergence and require innovative methods and strategies for disease surveillance and management in wildlife.

Generalized nodular dermatofibrosis in the absence of renal neoplasia in an Australian Cattle Dog.

A 13-year-old, spayed, female Australian Cattle Dog had at least a 10-year history of numerous subcutaneous nodules for which fine-needle aspiration and cytologic evaluation were nondiagnostic. Abdominal ultrasound 3.5 months before necropsy detected a small left kidney but no cysts or neoplasms. At gross necropsy, innumerable, firm, round to oval, white, 0.25 to 2 cm masses were detected throughout the subcutaneous tissues of the axial and appendicular skeleton, epimysium of numerous muscles, and parietal peritoneum of the lateral abdominal body wall. The left kidney was approximately half the size of the right, and there was severe bilateral renal medullary (papillary) necrosis. Histologically, the subcutaneous nodules were well-demarcated masses of mature, hypocellular collagen that were consistent with previous reports of nodular dermatofibrosis and renal cystadenomas or cystadenocarcinomas. In addition to diffuse acute medullary necrosis, both kidneys were affected by severe chronic lymphoplasmacytic interstitial nephritis. This is the first known report of nodular dermatofibrosis in a dog without renal cysts, cystadenoma, or cystadenocarcinoma.

Hookworms (Uncinaria lucasi) and acanthocephalans (Corynosoma spp. and Bolbosoma spp.) found in dead northern fur seals (Callorhinus ursinus) on St. Paul Island, Alaska in 2007.

Intestines of dead northern fur seals (Callorhinus ursinus) on St. Paul Island (SPI), Alaska were inspected for specific internal parasites (hookworms and acanthocephalans) in July and August, 2007. Pups (n=64) were examined for adult hookworms (Uncinaria lucasi) and four (6.25%) were infected. The number of specimens per infected pup was 1, 2, 2, or 408. Low prevalence was similar to that determined in the last investigation (2001) in dead fur seal pups on SPI by two of the present authors (Lyons and Spraker). Subadult males (SAMS-3-4 years old, n=115) were examined for acanthocephalans and 25 (21.7.0%) were infected. Adult Corynosoma (C. obtuscens, C. strumosum, and C. validum) (n=56) and immature Bolbosoma spp. (n=4) were found. Apparently, this is a new host record for C. obtuscens and C. validum. Notes were made on finding tapeworms. in 114 of the 115 SAMs. Examination of some specimens revealed scolices characteristic of Diphyllobothrium spp.

Experimental chronic wasting disease (CWD) in the ferret.

Chronic wasting disease (CWD), a prion disease of North American deer, elk and moose, affects both free-ranging and captive cervids. The potential host range for CWD remains uncertain. The susceptibility of the ferret to CWD was examined experimentally by administering infectious brain material by the intracerebral (IC) or oral (PO) route. Between 15 and 20 months after IC inoculation, ferrets developed neurological signs consistent with prion disease, including polyphagia, somnolence, piloerection, lordosis and ataxia. Upon first sub-passage of ferret-adapted CWD, the incubation period decreased to 5 months. Spongiform change in the neuropil was most marked in the basal ganglia, thalamus, midbrain and pons. The deposition of PrP(CWD) was granular and was occasionally closely associated with, or localized within, neurons. There were no plaque-like or perivascular PrP aggregates as seen in CWD-infected cervids. In western blots, the PrP(CWD) glycoform profile resembled that of CWD in deer, typified by a dominant diglycosylated glycoform. CWD disease in ferrets followed IC but not PO inoculation, even after 31 months of observation. These findings indicate that CWD-infected ferrets share microscopical and biochemical features of CWD in cervids, but appear to be relatively resistant to oral infection by primary CWD inoculum of deer origin.

Locoweed (Oxytropis sericea)-induced lesions in mule deer (Odocoileius hemionus).

Locoweed poisoning has been reported in wildlife, but it is unknown whether mule deer (Odocoileius hemionus) are susceptible. In areas that are heavily infested with locoweed, deer and elk (Cervus elaphus nelsoni) have developed a spongiform encephalopathy, chronic wasting disease (CWD). Although these are distinct diseases, no good comparisons are available. The purpose of this study was to induce and describe chronic locoweed poisoning in deer and compare it with the lesions of CWD. Two groups of four mule deer were fed either a complete pelleted ration or a similar ration containing 15% locoweed (Oxytropis sericea). Poisoned deer lost weight and developed a scruffy, dull coat. They developed reluctance to move, and movement produced subtle intention tremors. Poisoned deer had extensive vacuolation of visceral tissues, which was most severe in the exocrine pancreas. Thyroid follicular epithelium, renal tubular epithelium, and macrophages in many tissues were mildly vacuolated. The exposed deer also had mild neuronal swelling and cytoplasmic vacuolation that was most obvious in Purkinje cells. Axonal swelling and dystrophy was found in many white tracts, but it was most severe in the cerebellar peduncles and the gracilis and cuneate fasciculi. These findings indicate that deer are susceptible to locoweed poisoning, but the lesions differ in severity and distribution from those of other species. The histologic changes of locoweed poisoning are distinct from those of CWD in deer; however, the clinical presentation of locoweed poisoning in deer is similar. Histologic and immunohistochemical studies are required for a definitive diagnosis.

Seasonal prevalence and intensity of hookworms (Uncinaria spp.) in California sea lion (Zalophus californianus) pups born in 2002 on San Miguel Island, California.

Intestines of California sea lion (Zalophus californianus) pups (n= 204), born in 2002 on San Miguel Island, California, were examined for hookworms (Uncinaria spp.) as part of a seasonal mortality study from June through December 2002 and January 2003. The investigation was planned to coincide with most of the previously established hookworm infection period of the pups. Prevalence of hookworms in dead pups was 100% for each month of the study. The geometric mean intensity of infections per month was: 94.03 (n=30) for June, 629.09 (n=50) for July, 319.90 (n=31) for August, 159.90 (n=30) for October, 109.03 (n=30) for November, 37.84 (n=24) for December 2002 and 11.05 (n=9) for January 2003. In addition to the temporal pattern, the infection intensity was higher for pups in good condition and for male pups. An inter-year comparison of hookworm counts from dead pups collected in July of 1996, 2000, and 2002 also demonstrated higher intensity in pups in better condition but sex-differences in intensity were inconsistent across years. The inter-year comparison also demonstrated higher intensities in dead pups collected from portions of the rookery with sandy substrate versus rocky substrate. No annual differences in intensity were found after adjusting for substrate and condition.