Hemi-Cerebral Agenesis in a Stranded Pacific Harbor Seal (Phoca vitulina richardsi)
IAAAM Archive
Christy A. McKnight1; Martin Haulena1; Frances M.D. Gulland1; Taylor L. Reynolds2
1The Marine Mammal Center, Sausalito, CA, USA; 2Department of Microbiology, Parasitology and Pathology, North Carolina State University, College of Veterinary Medicine, Raleigh, NC, USA


Congenital defects are physiological or structural abnormalities developing at or before birth. They are usually thought to be a result of faulty development, infection, heredity or injury. While congenital defects are commonly seen in terrestrial mammals, very little is known about congenital defects in marine mammals. Identified congenital neurological abnormalities in marine mammals include cerebellar hypoplasia in the California sea lion (Zalophus californianus), hydrocephalus in the northern fur seal (Callorhinus ursinus), spina bifida in a fossil mysticete, and hydrocephalus in the northern elephant seal, (Mirounga angustirostris).1 Congential defects identified in Pacific harbor seals (Phoca vitulina richardsi) include cleft palate, ectrodactyly, abnormal tooth number, alopecia, dental aplasia and penile deviation.1 This is the first report of neurological agenesis in a marine mammal.

A five-month-old, female Pacific harbor seal (Phoca vitulina richardsi) stranded and was admitted to The Marine Mammal Center on July 29, 2002. Initial exam findings included tachypneia and diminished lung sounds on chest auscultation. The animal was treated for a suspected verminous pneumonia caused by Otostrongylus sp. On August 12, 2002, the animal was discovered in severe respiratory distress, shaking and non-responsive. Despite treatment, the animal died and a necropsy was performed. Gross necropsy examination revealed a severe obstructive verminous pneumonia and pulmonary arteritis associated with large numbers of nematodes identified as Otostrongylus sp. In addition, the right cerebral lobe was absent with concurrent malformation of the right supraoccipital bone. Histopathologic findings included multifocal thrombosis of pulmonary arteries consistent with nematode infection and vacuolation of the sub-ependymal white matter in the third ventricle, possibly representing dilation or swelling of myelin sheaths and edema. Results of histopathologic study concluded no evidence for hydrocephalic pressure atrophy, which supports a diagnosis of cerebral agenesis. No neurological abnormalities were noted in previous clinical evaluations, and the animal had normal locomotive, feeding and behavioral responses when compared to other stranded animals of the same age group. To our knowledge, there are no previous reports of hemi-cerebral agenesis in any species other than in feti.

The case is somewhat complicated by the apparent lack of clinical neurological abnormalities. However, it has been reported in humans that it is possible for one cerebral lobe to take over function of contralateral organs. A case of a six-year-old boy with unilateral cortical malformation had MRI findings that revealed the unaffected hemisphere retained motor control of both hands.2 It is likely that neuronal and axonal development in this animal during fetal growth allowed for similar cortical representation, resulting in apparently normal clinical neurological function.


The authors wish to thank the staff and volunteers of The Marine Mammal Center for their skill and support in the care of stranded marine mammals, and the pathology department at North Carolina State University College of Veterinary Medicine for their guidance and assistance.


1.  Gulland FMD, LJ Lowenstine, TR Spraker. 2001. Non-infectious diseases: congenital defects. In CRC Handbook of Marine Mammal Medicine, 2nd ed. L.A. Dierauf and F.M.D. Gulland (eds.). CRC Press LLC, Boca Raton, Florida, pp. 521-524.

2.  Staudt M, T Pieper, W Grodd, P Winkler, H Holthausen, I Krageloh-Mann. 2001. Functional MRI in a 6-year-old boy with unilateral cortical malformation: concordant representation of both hands in the unaffected hemisphere. Neuropediatrics 32(3): 159-161.

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Christy A. McKnight

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