Proventricular nematodiasis is one of the most common forms of gastrointestinal parasitism in avian collections, and in many cases, it can directly or indirectly result in mortality. There are a number of different nematodes that have been reported to infect the proventriculus. Tetrameres striata has been reported to cause chronic proventriculitis in ducks.1 Proventricular spiruridiasis has been reported to cause mortality in African jacanas and California quail.3,4 The death of large numbers of herons has been attributed to Eustrongylides ignotus infection of the proventriculus. Proventricular nodules have been observed in ducks infected with Echinuria uncinata and Hystrichis tricolor. We report on a condition in birds associated with proventricular nematodiasis referred to as adenomatous proliferative proventriculitis (APP).
From 1995 through 2001, 24 birds from five orders [Galliformes (eight birds), Passeriformes (eight birds), Psittaciformes (four birds), Anseriformes (two birds), and Gruiformes (two birds)] submitted to Northwest ZooPath were diagnosed with APP. All birds resided in captivity in 14 zoological parks located throughout North America. Twelve birds were female and eight were male (four had undetermined gender). Most birds with APP were adult (age range of 1.5 months to 15.75 years old). Many of the birds were found dead with no premonitory clinical signs. Two birds were noted to have weight loss prior to death. One bird was reported to be weak and another had diarrhea.
Grossly, the proventriculus in most birds was distended and had single to multiple, sometimes coalescing masses that thickened and raised the mucosa. In a few cases, the thickening of the mucosa was diffuse and nodular. A few birds also had mucus and blood on the mucosa. Two birds had ulcers associated with the masses. Twenty of 24 birds had nematodes noted in the proventriculus either at necropsy and/or histologically. Nematodes identified in some cases were Dispharynx spiralis, Dispharynx nasuta, and Capillaria spp.
Histologically, all cases were characterized by discrete to confluent, polypoid, adenomatous masses of hyperplastic mucosal epithelium that formed papilliferous projections and glandular structures lined by pseudostratified epithelium and hyperplastic goblet cells overlying a fibrous connective tissue stroma. There was infiltration of the masses by variable numbers of heterophils, lymphocytes, plasma cells, and macrophages. Two cases had progressed to proventricular adenocarcinoma. The adenocarcinoma in both cases infiltrated into the underlying submucosa and muscularis externa.
Common concurrent lesions in birds with APP were fat atrophy (eight cases), pneumonia (six cases), renal gout (six cases), ventriculitis (five cases), sepsis (four cases), enteritis (four cases), and amyloidosis (two cases). The systemic fat atrophy was attributed directly to the proventriculitis in all cases. Six birds with APP had pneumonia. In most of these cases, there was foreign material within inflamed airways, which would be supportive of aspiration pneumonia. There was most likely abnormal regurgitation and subsequent aspiration of feed material because of the proventriculitis. Sepsis was another very common problem in birds with APP. Several birds with APP had concurrent bacterial infections of the proventriculus. The damage to the normal mucosal protective barrier likely caused sepsis in these cases. Proventricular damage from Geopetitia aspiculata infection in zebra finches reportedly rendered them more susceptible to secondary bacterial infection.2 The renal gout noted in six cases was most likely due to dehydration secondary to the proventriculitis. Enteritis, as noted in four cases, may have been from microfloral imbalances in the gastrointestinal tract secondary to the proventriculitis. Amyloidosis was only noted in two birds with APP and was secondary to the chronic inflammation in the proventriculus.
Adenomatous proliferative proventriculitis is a serious and sometimes lethal morphologic manifestation of proventricular nematodiasis that occurs in various species of birds. APP underscores the importance of parasite detection and treatment in captive avian populations.
This work would not be possible without the technical experience of Roy Brown (Histology Consultation Service), administrative work of Jamie Kinion (Northwest ZooPath), and case contributions from Drs. Wynona Shellabarger, Enrique Rodrigues, Jan Ramer, Freeland Dunker, Scott Gearhart, Karen Emanuelson, Jeff Proudfoot, Mary Denver, Nancy Lung, Gary Riggs, Roberto Aguilar, Tim Reichard, Kathryn Gamble, Allan Prowten, Vicky Haines, Robin Radcliffe, Elizabeth Hammond, Gary West, and Genny Dumonceaux.
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2. French, R., K. Todd, T. Meehan, and J. Zachary. 1994. Parasitology and pathogenesis of Geopetitia aspiculata in zebra finches (Taeniopygia guttata): Experimental infection and new host records. J. Zoo. Wildl. Med. 25(3): 403–422.
3. Moore, J., M. Freehling, J. Crawford, and P. Cole. 1988. Dispharynx nasuta in California quail (Callipepla californica) in western Oregon. J. Wildl. Dis. 24: 564–567.
4. Schulman, F. Y., R. J. Montali, and S. B. Citino. 1992. Pathology, diagnosis, and treatment of Synhimantus nasuta infection in African jacanas (Actophilornis africana). J. Zoo Wildl. Med. 23(3): 313–317.