Chronic Fungal Tracheitis with Stenosis in an Atlantic Bottlenose Dolphin (Tursiops truncatus)
IAAAM 2005
Michael J. Kinsel1; Michael B. Briggs2
1University of Illinois Zoological Pathology Program, LUMC, Maywood, IL, USA; 2APCRO, Bolingbrook, IL, USA


An approximately 200 kilogram, adult, male, Atlantic bottlenose dolphin died suddenly. Prior to rapid decline this animal had an approximately 5-year history of increased to harsh respiratory sounds and variable exercise intolerance. Respiratory sounds were expiratory and described as "goose-honking," and often when most severe, were associated with moderate elevations in WBC and/or ESR. During one symptomatic episode diagnostic radiographs were obtained. The dolphin exhibited excessive resistance to being removed from the water, and elevated stress during the procedure. An area of increased density was observed in the laryngeal region, and was interpreted as a poorly defined abscess. This area was not examined with a bronchoscope due to the animal's violent reaction to be pulled from the water. Episodic treatment with a variety of antibiotics and antifungals, based on culture and sensitivity as well as respiratory cytology was employed. At times when respiratory noise was worst or associated with increased respiratory effort, the use of anti-inflammatories generally mitigated symptoms.

At necropsy, the skin had several, randomly distributed, 1-3 cm, round, raised, red regions. Bilaterally the fluke had 8 cm irregular ulcers affecting the dorsal and ventral surfaces, merging at the caudal margin (consistent with infarction). The right cerebral hemisphere at the level of the caudate had a 5x4x2 cm area of hemorrhagic necrosis (infarct). Diffusely the wall of the trachea was up to 2 cm thick (0.4 cm in a normal, age and sex-matched control), mottled yellow/brown to off-white, and firm, with lumenal diameter reduced to an average 1.7 cm versus an estimated original diameter of 4.2 cm. The tracheal mucosal was occasionally ulcerated. The visceral pleura had few, up to 4 mm raised, soft, dark red to black foci. The caudal one-third of both lungs palpated firm. On section there were several, up to 4 cm, irregular pale brown regions. Bronchial lymph nodes were markedly enlarged and mottled pale red to off-white on section. The cranial pole of the left testis had a 4 cm irregular dark red, firm region.

Histologically the cerebrum had a regionally extensive zone of necrosis that was sharply demarcated from surrounding viable parenchyma by an extensive, linear accumulation of neutrophils and admixed erythrocytes. The region of inflammation and immediately adjacent necrotic neuropil contained numerous 4-9 um, irregular, non-parallel walled, aseptate, acute to right angle branching fungal hyphae (zygomycete). Many hyphae extended deep into the viable parenchyma from the zone of inflammation. An adjacent large artery had an extensive lumenal accumulation of neutrophils and fungal hyphae (septic thrombus). Similar septic thrombi with associated necrotizing vasculitis, infarction, and/or regional inflammation were noted in the skin, lung, and left testis.

There was massive distortion of normal tracheal architecture due to vast, diffuse mural fibrosis and large numbers of variably-sized granulomas which appeared to vary greatly in age. Some granulomas contained few central fungal hyphae. Granulomas deep in the wall were often centered on large islands of necrotic hyaline cartilage occasionally containing few fungal hyphae and rare mineralized and necrotic hyphae. In distal sections of trachea all remaining cartilage was incorporated into granulomas. Tracheal mucosal had few, variably-sized ulcers, as well as large regions of squamous metaplasia.

The pulmonary interstitium had multifocal mild to moderate accumulations of fibrous tissue and admixed moderate numbers of lymphocytes, occasionally forming follicular aggregates. There were frequent discrete peribronchiolar accumulations of fibrous tissue. Bronchioles also occasionally had mild to rarely severe submucosal fibrosis, also with moderate numbers of lymphocytes. Bronchiolar lumens contained abundant mucus and small numbers of foamy macrophages. Alveolar ducts and adjacent alveoli were often markedly dilated, and contained copious mucus, occasional cholesterol clefts, few to abundant foamy macrophages, and few neutrophils. Multifocal small clusters of atelectatic alveoli were observed. A few small regions of acute necrosis with accumulations of neutrophils and admixed fungal hyphae, often centered on vascular remnants, were also noted.

Hepatic centrilobular congestion and hemosiderosis were consistent with chronic passive congestion.

Death was attributed to cerebral infarction secondary to fungal sepsis. Cutaneous and testicular infarction and interstitial pneumonia were related. Fungal culture of lung and skin was attempted but no organism was isolated. While sepsis and cerebral infarction were acute sequela of chronic tracheitis, progressive tracheal stenosis and pulmonary consequences led to long-standing clinical signs. From clinical history it was suspected that tracheitis existed for years, with occasional recurrence of acute disease leading to episodic increases in WBC and ESR. Periodic treatment with itraconazole may have mitigated these "flare-ups" but did not eliminate the fungus. Granulomas ranging from quiescent to those appearing only weeks old were also suggestive of periodic recrudescence. One feature of concern was occasional cartilage fragments containing fungal hyphae. This may represent a reservoir of organisms that could be difficult to clear with current antifungal therapeutics as the triazole antifungal drugs are highly lipophilic (and thus hydrophobic) and cartilage matrix is primarily water. In some areas, particularly the distal trachea, granulomas were centered on necrotic cartilage with no evidence of fungal invasion. Perhaps inflammatory response to necrotic cartilage, essentially a foreign body reaction, also contributed to lesion progression.

Tracheal stenosis led to a profound alteration of air flow. Stenosis resulted in an estimated 92-fold increase in resistance. The situation is akin to the use of an undersized endotracheal tube during an anesthetic procedure. In this instance the slowly progressive nature of the lesion likely allowed for partial adaptation via compensatory mechanisms, though clearly respiratory effort was greatly increased. Changes in the lung were considered secondary to tracheitis and stenosis. Clinical signs of exercise intolerance, expiratory wheeze and intermittent cough were consistent with a chronic obstructive disorder. In chronic obstructive pulmonary disease (COPD) of humans and domestic animals, most primary pathologic alterations occur at the level of the small airway.1,2 Chronic bronchiolitis with peribronchiolar fibrosis and mucus plugging in this case were similar to hallmark features of COPD in humans and horses, however tracheal stenosis was the primary obstructive lesion in this case. Interstitial fibrosis and alveolar dilatation were most consistent with restrictive disease. Progression to mixed disease is not uncommon in other species with COPD.1,2 Emphysematous change typical of other mammalian species, with rupture and fibrosis of alveolar septa, was not observed but this may have been a function of the rather robust nature of the alveolar septa of cetaceans. Fibrosis presumably resulted from alveolar accumulation of debris, inflammation, and damage to alveolar walls. Pulmonary hypertension and subsequent impaired right heart function is a common sequela to obstructive and restrictive pulmonary diseases,1,2 and hepatic chronic passive congestion in this dolphin was indicative of right heart compromise.


The authors thank Jane Chladny and histology laboratory of the University of Illinois Veterinary Diagnostic Laboratory for excellent technical assistance.


1.  Dungworth DL. 1993. The Respiratory System. In: Jubb, K.V.F., P.C. Kennedy, and N. Palmer. Pathology of Domestic Animals, 4th ed. Academic Press, San Diego, California. Pp. 539-698.

2.  Kobzik L. 1999. The Lung. In: Cotran, R.S., V. Kumar, and T. Collins. Pathologic Basis of Disease, 6th ed. W.B. Saunders Company, Philadelphia, Pennsylvania. Pp. 697-755.

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Michael B. Briggs

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