Joint Pathology Center

Veterinary Pathology Services

Wednesday Slide Conference


Conference 3

4 September, 2019


Conference Moderator:

Dr. Corrie Brown, DVM, PhD, Diplomate ACVP

Josiah Meigs Distinguished Teaching Professor
University Professor

Department of Pathology
University of Georgia College of Veterinary Medicine
2200 College Station Road Athens, GA, 30602


CASE I: W343-12 (JPC 4020435).


Signalment: Pigeon (Columba livia), age and sex unknown


History: An onset of high mortality affecting pigeons occurred in Victoria (Australia) in 2011. Clinical presentations in affected birds were lethargy, sudden death or neurological signs not further specified. Hundreds of birds were subsequently investigated, including racing pigeons, feral pigeons, domestic and commercial poultry and native birds of many species.


Gross Pathology: All the affected pigeons had diffuse pale and enlarged kidneys. The majority of birds also had enlarged spleens and grey mottled discoloration of the pancreas.


Laboratory results: Initial PCR testing for Newcastle Disease (APMV-1) was positive. Virus isolation and sequencing showed the virus to be the virulent strain of APMV-1. lmmunohistochemistry for paramyxovirus showed widespread immunoreactivity in the kidneys and in many cases pancreatic and splenic positivity were also observed.


Microscopic Description:

Pancreas: Multifocally and randomly distributed throughout the parenchyma there are numerous variably sized necrotic areas, characterized by disruption of normal architecture and stromal collapse, loss of cellular detail and accumulation of amorphous necrotic material, cellular debris and fibrin. There are scattered lymphocytes and plasma cells within the necrotic areas.


Small intestine: in the lamina propria of the mucosa there are small numbers of inflammatory cells, predominantly composed of lymphocytes and plasma cells. Not all slides: in the intestinal lumen there are few cross and longitudinal sections of nematode parasites, characterized by external cuticle, digestive tract, reproductive tract containing eggs with bipolar plugs, and hypodermal bacillary bands (consistent with Capillaria sp.).


Contributor Morphologic Diagnoses:
1. Pancreatic necrosis, multifocal, acute, severe, pancreas, pigeon (Columba livia)

2. Mild, chronic, diffuse lymphoplasmacytic enteritis with intraluminal nematode parasites, consistent with Capillaria sp., small intestine, pigeon (Columba livia)



Contributor Comment: The clinical, pathological and laboratory findings in this case are consistent with infection with avian paramyxovirus 1 (APMV-1). APVM-1 or Newcastle Disease Virus (NDV) belongs to the family of Paramyxoviridae, genus Avulavirus [1]

Different strains and isolates of NOV cause quite distinct clinical signs and severity of disease, even in the same host species. Based on the disease produced in chickens under laboratory conditions, NOV isolates have been placed in five pathotypes:

·       viscerotropic velogenic, NOV strains that cause a highly virulent form of disease in which hemorrhagic lesions are characteristically present in the intestinal tract;

·       neurotropic velogenic, NOV strains that cause high mortality following respiratory and nervous signs;

·       mesogenic, NOV strains that cause respiratory and sometimes nervous signs with low mortality;

·       lentogenic, NOV strains that cause mild or unapparent respiratory infections;

·       asymptomatic enteric, NOV strains that cause unapparent enteric infections.


However, such groups should be regarded only as a guide because there is always some degree of overlap and some viruses are not easily placed in a specific pathotype.8


Newcastle Disease (ND) is mainly a disease of poultry but NDV infections have been established in at least 241 species from 27 of the 50 orders of birds. All birds are probably susceptible to the infection, but the disease observed with any given virus may vary enormously from one species to another. Infection with NDV has been reported to infect animals other than birds, ranging from reptiles to humans.1 APVM-1 has been responsible for outbreaks in pigeons in Africa, Middle East, Europe, Japan Canada and United States.1 The variant nature of the virus enabled unequivocal demonstration of infection with this strain and for pragmatic purposes it became known as PPMV-1, although if this virus infects poultry, including pigeons reared for food, it fulfills the definitions of notifiable ND currently in use by the OIE.2 Infection of feral and domestic pigeons with APMV-1 has been reported for the first time in Australia in August 2011.

In pigeons, neurological signs, such as torticollis, disturbed equilibrium, pecking aside seeds, paresis of wings or feet, and digestive symptoms (watery to hemorrhagic diarrhea) are frequently observed but respiratory signs are usually absent. Atypical digestive forms are being seen increasingly frequently and consist of persistent diarrhea without neurological signs.1 The major clinical presentation in pigeons from the Australian outbreak were sudden death or neurological signs not further specified. Some of the birds submitted alive for euthanasia and autopsy had head tilt and/or ataxia.


Histologically, the main lesions were in the pancreas and kidney. Pancreatic necrosis was invariably present in all the pigeons examined, occasionally associated with a lymphoplasmacytic infiltrate. Renal lesions were characterized by acute tubular necrosis, sometimes associated with a lymphoplasmacytic inflammation. Although behavioral and neurological disease was usually the presenting sign where sudden death had not intervened, histological lesions in the brain were rare and, where present, mild, limited to a mild lymphocytic infiltrate in the meninges. Similar lesions were described in the outbreaks previously reported in pigeons in Canada, United States and Europe; the lesions most commonly encountered were focal non-suppurative meningoencephalitis, lymphoplasmacytic infiltration in liver, pancreas and lung, multifocal hepatic necrosis, pulmonary congestion, piecemeal pancreatic necrosis, interstitial lymphoplasmacytic nephritis and tubular necrosis.3,6


In pigeons, experimental inoculation with the pigeon variant of PPMV-1 produced histological changes consistent with those we found in naturally infected pigeons, including pancreatic necrosis as well as necrotizing enterocolitis, necrotizing hepatitis with periportal hepatitis, pulmonary hemorrhage, tracheitis, and perivascular cuffing in the brain.8


The cases of PMV-1 infection in pigeons documented in the present report were not linked to any known Newcastle disease outbreaks in commercial poultry. The source of infection is not known, but in the previous European and Californian outbreaks the racing activities were the main means of transmission.2,3


Contributing Institution:

Faculty of Veterinary Science, University of Melbourne, Australia

Diagnosis: 1. Pancreas: Pancreatitis, necrotizing, random, multifocal to coalescing, moderate.

2. Small intestine, lumen: Few adult nematode parasites.


JPC Comment: Newcastle disease is a constant threat to the poultry industry worldwide, and the importance of not only recognizing its clinical signs, but also the pathogenesis and infection kinetics of this virus cannot be overestimated. This Tier 1 USDA Select agent has been reclassified from its previous genus Rubulavirus to a new genus of Avulavirus (which includes the previous rubulaviruses which infect birds). OIE reporting is required for velogenic and mesogenic viruses, and these strains are endemic in Asia, Africa, the Middle East and parts of Central and South America. An ongoing outbreak continues in California arising from backyard flocks (a similar outbreak spilled over into commercial poultry in California in 2003, resulting in losses of over three million birds and a cost of over $120 million).4


In addition to the infectious threat posed by illegal importation of backyard fowl in the US, several wild bird species pose a reservoir threat for virulent strains, including pigeons and doves, and waterfowl such as double-crested cormorants and swans, and upland game birds (pheasants and partridges)5. Most cases of Newcastle disease in pigeons are the result of pigeon-specific strains, denoted as pigeon paramyxovirus-1 (in order to differentiate them from the rest of the avulaviruses that infect birds.5 Pet psittacines, including parrots, conures, budgerigars, and conures also develop neurologic disease after NDV infection, and a psittacine isolate was responsible for an outbreak of NDV in California in 1971.5


Strains of NDV virus have also been identified in wild anseriformes, shorebirds, and gulls, but virulent fusion protein sequences have not been identified.4 Interestingly, bird surveys in many countries have found vaccine strain virus (lentogenic forms of the virus are often used in vaccination programs), which leads to concern that passaging through wild bird species may result in reversion to a more virulent strain. This particular event has occurred in poultry resulting in a 1998 outbreak in Australia, but not yet in wild birds.4

Backyard fowl are a special problem to the biosecurity of our nation’s poultry as a result of poor vaccination practices as well as their mobility. While all most all birds produced by the commercial industry receive one or more NDV vaccines during their lifetime (more long-lived birds like broiler-breeders may receive 3 or more vaccinations), estimates are that less than 10% of backyard birds are vaccinated,4 and their exposure to other unvaccinated birds and potential wild reservoir birds makes the potential for an outbreak of mesogenic or velogenic NDV highly likely in this country.


Another area of concern is the minimal mutation required for transformation of an avirulent NDV into one of high virulence. The NDV genome encodes for 6 structural proteins - nucleocapsid protein, phosphoprotein, a matrix protein, a fusion protein, a hemagglutinin-neuroaminidase protein, and an RNA polymerase. Virulence has been attributed to amino acids at the cleavage site on the fusion protein, with three or more lysine or arginine residues starting at position 133 and a phenylalanine residue at 117 are common to all virulent strains of the virus. Hence, mutations resulting in this particular lineup of amino acid residues in the fusion protein may potentially give rise to new and virulent strains of the virus.4


On a somewhat lighter note, Newcastle disease received its name from the second documented outbreak of Newcastle disease which occurred in Newcastle-on-Tyne, England in 1927. A previous outbreak in Java (the Dutch East Indies at the time) did not result in the disease being called "Dutch East Indies chicken fever¨ or some other appellation, presumably as public relations experts were not in great numbers in Indonesia at the time. It has been theorized that an even earlier outbreak of Newcastle Disease may have occurred in South Uist on the Outer Hebrides islands (where cormorants are occasionally shot and consumed by the inhabitants - with the offal presumably tossed out on the ground). An outbreak of this type was memorialized in the Gaelic poem "Call nan Cearc" (The Loss of the Hens) written by John Campbell in 1898.7


The moderator reviewed the disease causes by pigeon paramyxovirus, an avuloviral disease first identified in the 1980s which has spread around the world, largely as a result of racing pigeon enthusiasts and the mobility of their charges. The virus, belonging to the same family as NDV is not particularly pathogenic for poultry, although if it has a high intracerebral pathogeneicity index (a measurement of pathogenicity for NDV), it can halt trade.


The moderator also perfomed an immunohistochemical study on the stlide, using an anti-NDV antibody. The amount of staining within small intestinal villi was surprising, as attendees obviously misinterpreted much of the necrosis in this tissue as autolysis.


As a final note, the class Aphasmidia (to which Capillaria belongs), has recently been renamed Adenophorasda.



1.   Alexander DJ. Newcastle Disease and other avian Paramyxoviruses, Rev Sci Tech Off Int Epiz 19(2): 443-462, 2000

2.   Alexander DJ: Newcastle disease in the European Union 2000 to 2009. Avian Pathol 40:547-58, 2011

3.   Barton JT, Bickford AA, Cooper GL, Charlton BR, Cardona CJ: Avian Paramyxovirus Type 1 Infections in Racing Pigeons in California. I. Clinical Signs, Pathology, and Serology. Avian Dis Apr-36(2):463-8, 1992.

4.   Brown VR, Bevins SN. A review of virulent Newcastle disease viruses in the United States and the ole of wild birds in viral persistence and spread. Vet Research 2017; 48:68-83.

5.   Cattoli G, Susta L, Terregino C, Brown C. Newcastle disease: a review of field recognition and current methods of laboratory detection. J Vet Diagn Invest 2011, 23(4): 637-656.

6.   Johnston KM and Key WO. Paramyxovirus infection in feral pigeons (Columba livia) in Ontario. Can Vet J 33: 796-800, 1992

7.   MacPherson L.W. Some observation on the epizootiology of Newcastle DiseaseCan J Comp Med 1956; 20(5):155-168.

8.   Pearson JE, Senne DA, Alexander DJ, Taylor WO, Peterson LA, Russell PH: Characterization of Newcastle disease virus (avian para-myxovirus-1) isolated from pigeons. Avian Dis. 31: 105-111, 1987.


Click the slide to view.

01-1. Pancreas and intestine, pigeon.

01-2. Pancreas, pigeon.

01-3. Pancreas, pigeon.

01-4. Pancreas, pigeon.

01-5. Intestine, pigeon.

01-6. Pancreas, pigeon.

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