Pathology in Practice

Veronica M. Rolim Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA 30602.

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Monique Franca Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA 30602.

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Holly M. Brown Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA 30602.

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Elizabeth A. Driskell Department of Pathology, College of Veterinary Medicine, University of Georgia, Athens, GA 30602.

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History

A 5-month-old neutered male domestic shorthair cat was submitted to the Athens Veterinary Diagnostic Laboratory for necropsy. This kitten was part of a managed colony of feral cats on campus at the University of Georgia, Athens, Ga. The managed feral cat colony included cats that were trapped, spayed or castrated, and vaccinated against rabies; after veterinary care, these cats were either adopted or returned to their campus territories. The kitten was found alone in an area not commonly frequented by these cats but appeared in good health. The kitten was taken home by a member of the managed cat colony program, but during the next 2 days, the kitten developed labored breathing and died.

Clinical and Gross Findings

At necropsy, the cat was in good body condition with adequate subcutaneous and abdominal adipose tissues and the mucous membranes were pale. There was abundant frothy fluid in the lumens of the trachea and primary bronchi. All lung lobes were firm, noncollapsing, and covered by multifocal to coalescing, tan to white nodules that ranged from pinpoint in size to approximately 1 cm in diameter and extended into the parenchyma (Figure 1). The bronchiolar lumens exuded copious catarrhal, opaque material when cut. There was ingesta in the stomach and feces in the colon.

Figure 1—
Figure 1—

Photograph of the lungs of a feral 5-month-old cat that had developed labored breathing and died. Notice that all lung lobes are diffusely firm and noncollapsing and have multifocal to coalescing, tan to white nodules that range from pinpoint to approximately 1 cm in diameter.

Citation: Journal of the American Veterinary Medical Association 241, 12; 10.2460/javma.241.12.1587

Histopathologic and Cytologic Findings

Results of fluorescent antibody testing of lung tissue indicated that the cat was negative for feline infectious rhinotracheitis virus, and fluorescent antibody testing of specimens of spleen and bone marrow indicated that the cat was negative for FeLV infection. At necropsy, major organs were examined. Impression smears were made from the cut surface of a lung lobe and stained with Wright-Giemsa stain. Microscopic examination of the impression smears revealed abundant columnar and cuboidal epithelial cells admixed with alveolar macrophages, infrequent multinucleated giant cells, rare neutrophils, and scattered nematode larvae and embryonated eggs (Figure 2).

Figure 2—
Figure 2—

Photomicrograph of an impression smear made from the cut surface of affected lung tissue from the cat in Figure 1. Nematode larvae (arrow) and embryonated eggs (arrowhead) are surrounded by columnar and cuboidal epithelial cells, alveolar macrophages, and rare neutrophils. Wright-Giemsa stain; bar = 50 μm.

Citation: Journal of the American Veterinary Medical Association 241, 12; 10.2460/javma.241.12.1587

Lung, liver, kidney, heart, and spleen tissue samples were fixed in neutral-buffered 10% formalin and processed for histologic examination. Microscopic examination of lung tissue sections revealed that the tissue was diffusely effaced with large numbers of macrophages, many multinucleated Langhans and foreign body–type giant macrophages, fewer collections of plasma cells and lymphocytes, and rare neutrophils that filled nearly all of the bronchioles and alveoli. Also within alveoli were myriad nematode larvae (15 to 20 μm in diameter) and eggs (approx 20 to 30 μm in diameter) that were embryonated or morulated with 5 to 20 blastomeres (Figure 3). Occasionally, multinucleated giant macrophages with phagocytosed larvae were detected. There were small numbers of larvae and eggs in bronchiolar lumens. Edema was admixed with the inflammatory cells in the airway lumens and moderately expanded the interstitium. The alveoli were occasionally lined by hyperplastic type II pneumocytes, and multifocal alveoli were dilated and had disrupted alveolar septa. The bronchi had moderate hyperplasia of submucosal glands. Multifocal vessels were surrounded by moderate numbers of plasma cells and lymphocytes. There was multi-focal moderate hypertrophy of smooth muscle cells of the tunica media of the vessels. In the liver, there was mild degeneration of centrilobular hepatocytes. There were no notable lesions in the kidneys, heart, or spleen.

Figure 3—
Figure 3—

Photomicrograph of a section of affected lung tissue from the cat in Figure 1. Notice that the lumens of the pulmonary alveoli are filled with numerous macrophages and many multinucleated giant cells with fewer plasma cells and lymphocytes. Multifocal alveoli also contain nematode larvae (arrows), a morulated egg (arrowhead), and embryonated eggs (asterisk). H&E stain; bar = 50 μm.

Citation: Journal of the American Veterinary Medical Association 241, 12; 10.2460/javma.241.12.1587

Morphologic Diagnosis and Case Summary

Morphologic diagnosis: severe multifocal to coalescing granulomatous pneumonia with myriad intralesional metastrongylid nematode larvae and eggs consistent with Aelurostrongylus abstrusus.

Case summary: Aelurostrongylus pneumonia in a cat.

Comments

The kitten of the present report had severe pneumonia attributable to infection with A abstrusus (phylum, Nematoda; superfamily, Metatastrongyloidea). This nematode is the most important lungworm that infects domestic cats.1 Lungworm infection is not uncommon in cats, but the severe clinical signs and extensive pulmonary involvement observed in this kitten infrequently develop in infected cats. Bronchiolitis and interstitial pneumonia are caused by the presence of adult lungworms in the terminal and respiratory bronchioles and eggs and first-stage larvae in the alveoli. Aelurostrongylus abstrusus has an indirect life cycle. The third-stage larvae are ingested with the intermediate (snails and slugs) or paratenic (birds, rodents, frogs, and lizards) hosts and migrate from the gastrointestinal tract to the lungs.1,2 Adults develop and then deposit eggs; after hatching, the first-stage larvae are coughed up from the lungs, swallowed, and passed in the feces to infect an intermediate host.1,3 Aelurostrongylus abstrusus has a 5- to 10-week prepatent period. Although this parasite is usually observed only in lung tissues, first-stage larvae have been detected in the colonic glands of 2 cats that had pulmonary aelurostrongylosis.4

Aelurostrongylus abstrusus infection is more prevalent in cats that are free-ranging,5,6 as was the cat of the present report. Lungworm infections in cats are considered to be an emerging problem in several regions around the world and have acquired increased clinical importance.7 However, there are some difficulties in the diagnosis of aelurostrongylosis in living animals. The Baermann migration method is considered the gold standard test for clinical diagnosis of aelurostrongylosis, and the disease may be undetected if less sensitive methods of direct fecal smear or fecal floatation are used. A nested PCR assay performed on fecal samples or pharyngeal swabs is an efficient means of disease detection (assay specificity, 100%; assay sensitivity, 80% to 96.6%).8

Aelurostrongylosis may induce either subclinical or clinical disease depending on the parasite burden, age, and immune response of the cat.9 Young cats are more susceptible to aelurostrongylosis,9 as illustrated by the case described in the present report. More severe infections are characterized by mild to intense cough, sneezing, mucopurulent nasal discharge, severe dyspnea, and even death.10 The cat of the present report had severe clinical signs including dyspnea, which was explained by the severe pulmonary lesions observed at necropsy. Grossly, aelurostrongylosis is characterized by multifocal to coalescing 1- to 10-mm-diameter white foci or firm, yellow protruding nodules and multifocal areas of hemorrhage in the lungs. In severe infections, the nodules may coalesce to form confluent areas of consolidation.2 In the cat of the present report, the lesions observed were characteristic of severe disease, with nearly the entire field of all lung lobes affected. Differential diagnoses for this gross lesion would include other causes of granulomatous pneumonia, particularly systemic fungal diseases associated with dimorphic fungi (eg, Histoplasma capsulatum), depending upon geographic location of the cat. Typically, an inflammatory infiltrate predominantly composed of mononuclear inflammatory cells and multinucleated giant cells is present in the lumens of the airways and surrounds the nematode larvae and eggs, similar to the lesions in the case described in the present report. Adult A abstrusus were not observed microscopically in tissue sections from this cat; however, adult A abstrusus can be identified in histologic sections by the presence of a thin cuticle, coelomyarian-polymyarian musculature, and a pseudocoelom containing intestines composed of few multinucleate cells occasionally containing birefringent yellow-brown pigment. Eosinophilic and neutrophilic infiltrations may also be observed and are usually more predominant in the early stages of the disease. Smooth muscle hyperplasia and hypertrophy are also commonly detected in the walls of the bronchioles and in the alveolar septae.2

Affected cats may develop severe and permanent pulmonary lesions when a diagnosis is not made and they are not treated for aelurostrongylosis early in the disease process.7 Antiparasitic topical spot-on treatment with 10% imidacloprid plus 1% moxidectin or oral treatment with 18.75% fenbendazole is effective in the control of aelurostrongylosis in cats.5,11 Ivermectin lacks efficacy to eliminate lungworm infections in cats.5 One study11 in cats revealed that spot-on administration of a single dose of 10% imidacloprid with 1% moxidectin was slightly superior in treatment efficacy, compared with oral treatment with 18.75% fenbendazole (50 mg/kg, q 24 h) for 3 consecutive days (percentage reduction in parasite load in 26 to 30 days [in terms of mean larvae count/g of feces], 100% vs 99.29% respectively).

References

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