Congenital Defects in Northern Elephant Seals Stranded Along the Central California Coast

Trupkiewicz, John G.; Gulland, Frances M. D.; Lowenstine, Linda J.

doi:10.7589/0090-3558-33.2.220

Cited by 29 publications

(27 citation statements)

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“…Leipold (1980) published a list of 145 congenital anomalies from wild and zoological mammals, of which seven were from marine mammals including one fur seal (ectrodactyly-lack of all or parts of the digits). Additionally, two nonfatal anomalies were reported in California sea lions (Zalophus californianus; Sweeney and Gilmartin, 1974) and 17 congenital anomalies were reported in phocids (Csordas, 1966;Griner, 1983;Baker, 1984;Suzuki et al, 1992;Trupkiewicz et al, 1997). The types of congenital anomalies found during this investigation varied from year to year with no specific pattern observed.…”

Section: Northern Fur Seal Pupsmentioning

confidence: 75%

Causes of Mortality in Northern Fur Seals (Callorhinus Ursinus), St. Paul Island, Pribilof Islands, Alaska, 1986–2006

Spraker

Lander

2010

Journal of Wildlife Diseases

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ABSTRACT:To determine whether infectious diseases might have contributed to the present-day decline of northern fur seals (Callorhinus ursinus), preweaned pups (n52,735), subadult males (n598), and adults (n5179) were examined postmortem from 1986 to 2006 on St. Paul Island, Alaska. Gross necropsy findings and histologic lesions were used to determine causes of death. Five general categories of mortality were identified for pups: emaciation (1,454 pups, 53%), trauma (497 pups, 18%), perinatal mortality (516 pups, 19%), infectious diseases (82 pups, 3%), and miscellaneous causes (186 pups, 7%). A condition of unknown etiology characterized by multifocal necrotizing myopathy and cardiomyopathy was found in 92 pups. Thirty-three congenital anomalies were identified in 49 pups, including a rare multicentric ganglioneuroblastoma. General linear models were used to examine change in pup mortality and condition (i.e., pup mass) over time. The prevalence of perinatal mortality appeared to increase during the study and relative to past reports. Trauma and infectious conditions appeared to decrease slightly from 1986 to 2006. Although relatively stable during this investigation, emaciation was greater than that reported for past studies. Emaciated pups weighed less than expected during 1988, 1996, and 2004 and more than expected during 1987, 1989, 1990, and 1994 (P#0.003). Average annual weights for all other categories of mortality did not change significantly from 1986 to 2006. Fatal conditions for subadult males included hyperthermia, blunt trauma, entanglement, and bite wounds; nonfatal conditions included seizures, orange discoloration of the blubber, neoplasia, and parasitism. Causes of mortality for most adults included bite wounds with cellulitis and secondary infections, pulmonary edema, dystocia, blunt trauma, and neoplasia. We found no evidence to implicate infectious diseases as a cause in the recent decline of northern fur seals.

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Section: Northern Fur Seal Pupsmentioning

confidence: 75%

Causes of Mortality in Northern Fur Seals (Callorhinus Ursinus), St. Paul Island, Pribilof Islands, Alaska, 1986–2006

Spraker

Lander

2010

Journal of Wildlife Diseases

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“…Four cases of VSD in northern elephant seal have been reported, and at least one other congenital abnormality was identified in every case, including hydrocephalus, patent ductus arteriosus (PDA) (Colegrove et al 2005), partial aortic coarctation and pulmonary arterial aplasia with right ventricular hypoplasia (Trupkiewicz et al 1997). Other published cardiovascular congenital anomalies in marine mammal species describe lesions that have been identified during necropsy examination, and these include a persistent right aortic arch (PRAA) in a northern elephant seal (MacLean et al 2008), an atrial septal defect (ASD) in a common dolphin Delphinus delphis (Jepson et al 2005) and multiple abnormalities, including VSD, ASD, mitral valve and pulmonary artery hypoplasia with associated secondary changes, in a bottlenose dolphin Tursiops truncatus (Powell et al 2009).…”

Section: Bpm Range 80 To 95 Bpm)mentioning

confidence: 99%

Antemortem diagnosis of a ventricular septal defect in a California sea lion Zalophus californianus

Dennison¹,

Bonn²,

Boor³

et al. 2011

Dis. Aquat. Org.

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A yearling California sea lion Zalophus californianus stranded in poor body condition, and on physical examination a heart murmur was audible bilaterally. The sea lion was diagnosed with a left-to-right shunting membranous ventricular septal defect (VSD) using B-mode, color-flow Doppler and continuous-wave Doppler echocardiography. A left-to-right intracardiac shunting lesion was confirmed during cardiac angiographic computed tomography. The VSD defect was verified during the necropsy examination. On histologic examination concurrent mild multifocal myocarditis with focal mild ventricular free-wall myocardial necrosis were identified. A specific cause for the myocarditis and myocardial necrosis was not found, and association with the VSD and resultant myocardial dysfunction was presumed. This is the first report of the antemortem diagnosis of a VSD in a marine mammal and the first report of a VSD in a California sea lion. KEY WORDS: Echocardiography · Congenital defect · Cardiac disease · Heart disease · Ultrasound Resale or republication not permitted without written consent of the publisherDis Aquat Org 94: [83][84][85][86][87][88] 2011 to be left-to-right using color-flow Doppler ( Fig. 1) and continuous-wave Doppler. Both ventricles were subjectively dilated. Other cardiac structures were considered normal. Fractional shortening was calculated as 14.5% and ejection fraction as 31%. Heart rate was considered normal at 90 beats per minute (bpm). Published normal cardiac values for fractional shortening and ejection fraction for this species have not been published to the authors' knowledge.On observation of those echocardiogram findings, we obtained right lateral and ventro-dorsal radiographs of the thorax. Radiographs showed an enlarged cardiac silhouette with a calculated vertebral heart score (VHS) from the lateral radiographic view of 10.5 compared to the previously reported mean VHS of 8.65 (Dennison et al. 2009), and increased width on the ventro-dorsal view with the cardiac silhouette occupying 78% compared to the previous mean normal reported as 66% (Dennison et al. 2009). The pulmonary arteries and veins were symmetrical and enlarged compared to radiographs of other animals without evidence of cardiovascular disease, consistent with pulmonary over-circulation. A mixed bronchointerstitial to alveolar pattern was identified in all lung fields and was more apparent ventrally. These radiographic findings were most consistent with a left-toright shunting VSD and concurrent pneumonia and/or early cardiogenic pulmonary edema. The ventral distribution and lack of pulmonary venous distension was more consistent with pneumonia (aspiration, verminous or bacterial).Recovery from anesthesia was uneventful. Therapy for verminous pneumonia was started; it consisted of penicillin G procaine/penicillin G benzathine 1 ml per 10 kg intramuscular (i.m.) every other day (150 000 units of both penicillin forms in suspension; Pen BP-48, IVX Animal Health), carprofen 4.4 mg kg -1 once daily orally (100 mg chewab...

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“…Congenital anomalies reported in juvenile northern elephant seals (Mirounga angustirostris; NES) have been reviewed recently (Trupkiewicz et al, 1997), and they include hydrocephalus, severe cardiac anomalies, hydronephrosis, focal pulmonary dysplasia, and congenital epidermal angiomatosis. In this article, we report a persistent right aortic arch (PRAA) anomaly and aplasia of the right cribiform plate in a juvenile NES, and we provide an update on congenital defects noted in this species at The Marine Mammal Center (TMMC; Marin Headlands, Sausalito, California, USA) between January 1996 and December 2003.…”

mentioning

confidence: 99%

“…In humans, the defect has been associated with a deletion on chromosome 22 (Momma et al, 1999). Some researchers have speculated that congenital defects in the NES may be caused by the severe genetic bottleneck of perhaps less than 10 individuals that occurred in the late 1800s after heavy hunting pressure (Trupkiewicz et al, 1997;Hoelzel et al, 2002). Studies of NES genetic material from both before and after the bottleneck have indeed shown a historic loss in diversity in both allelic and mitochondrial DNA (Weber et al, 2000;Hoelzel et al, 2002).…”

mentioning

confidence: 99%

“…Congenital viruses, such as bovine viral diarrhea virus, can also cause central nervous system defects (Jubb and Huxtable, 1993). In the previous report on NES anomalies, it was noted that six animals over 2 mo of age were observed with a patent ductus arteriosus, suggesting that closure of this vessel may be delayed normally in marine mammals compared with terrestrial species (Trupkiewicz et al, 1997). An examination of 111 necropsy records at the TMMC between January 1996 and December 2003, where the status of the ductus arteriosus was recorded, revealed 10 animals, averaging 4 mo of age (range 3-6 mo), that had either an open (n54) or a partially closed (n56) ductus with no other vascular abnormalities noted.…”

mentioning

confidence: 99%

See 1 more Smart Citation

Persistent Right Aortic Arch and Cribiform Plate Aplasia in a Northern Elephant Seal (Mirounga angustirostris)

MacLean

Imai

Dold

et al. 2008

Journal of Wildlife Diseases

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Congenital Defects in Northern Elephant Seals Stranded Along the Central California Coast

Cited by 29 publications

References 0 publications

Causes of Mortality in Northern Fur Seals (Callorhinus Ursinus), St. Paul Island, Pribilof Islands, Alaska, 1986–2006

Causes of Mortality in Northern Fur Seals (Callorhinus Ursinus), St. Paul Island, Pribilof Islands, Alaska, 1986–2006

Antemortem diagnosis of a ventricular septal defect in a California sea lion Zalophus californianus

Persistent Right Aortic Arch and Cribiform Plate Aplasia in a Northern Elephant Seal (Mirounga angustirostris)

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