Lung Disease in Whales and Dolphins
IAAAM 1968
Daniel F. Cowan, MD, CM
Assistant Professor of Pathology, College of Human Medicine and College of Veterinary Medicine, Michigan State University, East Lansing, MI

Many anatomic and physiologic adjustments are necessary for a mammal to be able to live in the sea. Among the most striking of these are the modifications found in the respiratory tract. Whales and dolphins must be able to retain relatively large volumes of air in physiologically useful places in the lung when diving, and in so doing must avoid the diver's "squeeze" effect. That is, they must be able to adjust pressures in the lung so that the hydrostatic pressures found at depths are not able to force blood out of small vessels into air spaces. Whales and dolphins must be able to exchange large volumes of air in the very short time that the blow-hole is clear of the water as the animal surfaces. Slijper states that a large rorqual, for example, may exchange 1,500 liters of air in 1.5-2 seconds. Cetaceans therefore require some mechanism to keep airways from collapsing under the effects of great swings of pressure.

Land animals have requirements of a different nature. In their environment they must be able to cope with inhaled dust, pollen, bacteria, and other air-borne pollutants. Their adaptive mechanisms, the cough reflex, mucous glands, and well developed lymphatic tissues are protective and are designed to clear the passages. Marine mammals do not need protection against inhaled particles, and are without cough reflex, mucous glands, and significant pulmonary lymphoid apparatus. Their adaptive mechanisms are designed to retain air in the alveoli and to allow rapid, high-pressure exchange of air.

The anatomical adaptive changes in cetacean lungs have been described elsewhere, 1-3 but as they are critical to the understanding of lung diseases in these animals, it is appropriate to summarize them here. The lungs are un-lobed, covered with a dense, elastic opaque pleura and, in some species at least, connected anteriorly at their bases by a lymphoid mass. The trachea and large bronchi are fenestrated cylinders made of fused rings of cartilage. The cartilage extends the length of the bronchi and bronchioles as rings and bars to the origin of the alveolar sac.* (With one known exception, a Berardius, in which it stops higher up).The cells of the bronchial mucosa have well developed cilia, and most secrete mucus (in the Pilot whale and in the California grey whale, at least). There is a series of muscular sphincters in the bronchioles, extending to the opening of the acinus. The alveolar orifice is ringed with a musculo-elastic sphincter. The alveolar septae are double. Each alveolar septum is made of the walls of adjacent alveoli, with an intervening loose connective tissue. These structural peculiarities are generally conceded to be modifications required to cope with marked intra-alveolar pressure changes associated with diving. In general, these adaptive modifications work very well, but under certain circumstances they are detrimental to the animal.

Non-parasitic diseases of the whale lung are considered to be very rare in nature. Pneumonia was first discovered and reported from a Fin whale as late as 1959.1 Cockrill4 examined thousands of carcasses on factory ships in the Antarctic without finding evidence of bacterial lung disease, although he did find lesions that he attributed to hematogenous spread of parasites. Uys and Best5 do not mention the lungs at all in their report of lesions found in more than 2,000 whale carcasses examined in South Africa. However, in a study of the naturally occurring diseases of the North Atlantic Pilot whale,2 lung diseases was found to be the most important abnormality.

The discrepancies in these observations do not need to be explained on the basis of species differences. Detection of lung disease depends, to a great extent, on selection of specimens and technique of examination. Most of the whales included in pathological studies were killed by pelagic whalers. Animals in these circumstances are generally healthy and can be expected to show no more disease than would be found in any random sampling of a wild population. Also, the use of explosive harpoons often results in destruction of the lungs. In otherwise healthy animals, lesions present are likely to be small, and any examination less than gross serial slicing of the lung will not show them. External inspection is not reliable, as the pleura is very dense and opaque. In the Pilot whale, it has been shown that lung weight is not a reliable indicator of disease, contrary to expectation, as the lungs are normally so heavy that any pathological alteration severe enough to produce a significant alteration in weight would likely be catastrophic and the animal would die at sea.6

Animals dying in captivity are much more likely to have some form of lung disease, as they are subjected to a great variety of environmental contaminants, and are much more likely to aspirate dirty water. They are likely to come into contact with new parasites that may affect the respiratory system. Captive cetaceans are usually small species, such as the dolphins, and are more easily handled. Complete examination of all organ systems under controlled conditions may be expected. Technique of examination is very important. Autopsy must be done immediately after death, as autolysis progresses very rapidly, and agonal aspiration of water introduces contaminants. An animal frozen for storage and thawed before autopsy is a useless specimen for the study of disease. A suggested procedure for examination of the respiratory tract of a dolphin is appended.

Nearly all cases of lung diseases in whales and dolphins reported were found in the North Atlantic Pilot whale. Most cases were caused by lung worms, but segmental bronchitis not associated with worms and lipid pneumonias were also found. Whales captured under adverse conditions, aspirating dirty water, rapidly developed acute necrotizing pneumonia and died.

In this series, it was found that the peculiar anatomy of the lung contributed greatly to the development of disease, whatever the cause, but also tended to keep the disease process localized. Intraluminal particles, rather than being rapidly expelled by coughing, etc., as would happen in land animals, tended to be trapped and retained by the sphincter mechanism. Edema and cellular infiltration of the bronchial mucosa confined by the cartilage rings and bars, very rapidly caused obstruction of the air passages. This retention of foreign material, inflammatory and mucous exudates and debris caused rapid development of abscesses and necrosis of segments of the lung. In land animals, this kind of destructive process would spread throughout adjacent regions of the lung. In the Pilot whale, however, the dense connective tissue of the bronchi and alveolar walls confined the disease to small segments. The end result of lung inflammations was either dense fibrous nodule or scar formation, or a localized form of scarred, destructive secondary "emphysema". In several older animals, accumulation and confluence of scars had produced extensive of functional destruction of the lungs.

Examination of tissues from both odontocetes and Mysticetes, including the Pilot whale, Pygmy sperm whale, Beluga, Fin whale, California grey whale, and the dolphins Delphinus, Lagenorhyncus, Stenella, and Tursiops, indicates that these mechanisms are probably universal among the Cetacea.

There is insufficient data to attempt a systematic description of the pathologic conditions that can affect the whale lung. However, there are certain lesions that can be recognized with no difficulty, and it is worthwhile to describe a few of these.


Scars are found frequently. These may be seen as small nodules, up to a centimeter or more in diameter, often under the pleura, or as larger, "honeycomb" cavitated and fibrous regions. Histologically, these are inactive, and show only fibrosis, with no clear evidence of the causative agent. Some lungs may have fibrous regions of much greater extent; most of the lung may be involved, as in an extreme case found in a Pilot whale. The dominant change in that animal was fibrosis rather than necrosis or cavitation. The specimen showed changes that were best explained by the presence of some form of oil in the lung.2


Parasites may cause a particularly violent reaction. There is an initial acute inflammatory reaction that soon becomes associated with fibrosis and granuloma formation. The worm is gradually broken down and removed by phagocytosis. The residual change is production of a dense fibrous mass. Larval forms have been found in a dolphin in association with marked, heavily proteinaceous, poorly cellular exudation. This may be merely the initial stage of a reaction like that produced by adult worms. it is worth noting that this exudate contains apparently more protein than edema from other causes such as respiratory distress caused by beaching.


Aspiration of dirty water produces acute pneumonia very quickly. This is much like pneumonia in land animals, with the exception that it tends to remain localized. Occlusion of the bronchi by mucosal swelling is a prominent feature.


The finding of a large pseudocyst in the lung of a Pilot whale has been mentioned elsewhere.2 This probably resulted from an old focus of inflammation. This kind of lesion is probably very rare.


Pulmonary infection with fungus has not been previously reported from wild whales or dolphins. A small mass collected from the lung of a Pygmy sperm whale killed near Japan proved to be a fungus infection morphologically indistinguishable from actinomycosis of cattle. Colonies of fungal mycelium ("sulfur granules") were found in the lesion associated with large amounts of pus and fibrous tissue. As the tissue had been fixed in formalin, culture was not possible, but on morphologic grounds alone the organism could be placed in the Actinomyces-Nocardia group.

Comment and Summary

Lung diseases are most likely to be found in captive animals. These animals are most likely to be adequately examined, and they are also more likely to become infected than wild animals. Captivity exposes an animal to unnatural conditions, increasing its liability to infection. Unfamiliar pathogens may be encountered, to which the animal has relatively little resistance. Unless conditions are ideal, the water in which the animals are kept is likely to contain large amounts of fecal matter. Aspiration of dirty water may be facilitated by manipulations of the animal for training or for research.

Careful attention to dead as well as living animals is essential to the understanding of disease processes, and by extension, to the intelligent management of healthy animals and proper treatment of sick ones.


Examination of the respiratory tract begins at the blow-hole. This is inspected for the presence of parasites and foreign material, as well as for abnormalities of the walls.

The lower passages and the lungs are removed as a unit. The larynx is examined for obstruction caused by swelling of the tissues or by foreign material. The larynx and trachea are opened longitudinally and the mucosal surfaces examined for signs of inflammation, bits of foreign matter, parasites and abnormalities of the wall. Foam or water may be present in the trachea. This must be interpreted in the light of the circumstances of death.

Each lung is detached from the trachea in turn, and the bronchi are opened longitudinally as far down the passages as practicable. Parasites may be found (particularly in the Pilot whale, which in the wild may carry large numbers of Stenurus). The presence of foam or bits of foreign matter, pus, or blood may be rioted. A long, slender knife has been found most satisfactory for opening the air passages. Scissors tend to crush and squeeze tissues, producing considerable distortion.

Opening the bronchi -in the manner described above will expose a large surface of the respiratory tissue. Since the texture of the normal lung is rough and dense, color change is the most reliable indicator of abnormality. Scars are pale. Inflammation may be pale or dark. Cysts and other masses, such as tumors or granulomas, are easily recognized. Cuts in the respiratory tissue should be made at about one-inch intervals.

The blood vessels not already opened are slit along their long axes. Clots or thrombus may be found.

Specimens for microscopic examination should be taken from both abnormal and apparently normal areas. They should be cut about 5 mm. thick. Specimens are usually fixed in 10% formalin solution. If the specimens are to be sent away for examination, a note outlining the appearance of the fresh tissue should be included.


Many of the specimens described were kindly supplied by Robert L. Brownell, Jr., Los Angeles County Museum, California, and Dr. Edward Mitchell, Arctic Biological Station, Ste. Anne de Bellevue, P.Q. Canada


  1. Slijper, E. J. Whales. 475 pp. Basic Books, Inc., 1962.
  2. Cowan, D. F.: Pathology of the Pilot Whale. Globicephala melaena. Arch.Path., 82: 178-189, 1966.
  3. Engel, S.: The Respiratory Tissue of the Blue Whale and the Fin Whale.Acta. Anat., 65: 381-390, 1966.
  4. Cockrill, W. R.: Pathology of the Cetacea. A Veterinary Study on Whales. Brit. Vet. J., 116: 133-144, 175-190.
  5. Uys, C. J. and Best, P. B.: Pathology of Lesions Observed in Whales Flensed at Saldanha Bay, South Africa. J. Comp. Path., 76: 407-412, 1966.
  6. Cowan, D. F.: Observations on the Pilot Whale Globicephala melaena. Organ Weight and Growth. Anat. Rec., 155: 623-628, 1966.

Speaker Information
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Daniel F. Cowan, MD, CM
Department of Pathology, University of Texas Medical Branch
Galveston, TX, USA
Texas Marine Mammal Stranding Network

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