Necropsy Reports of Bird Deaths at Parrot Depot
When birds die at an aviary/farm, it is standard procedure to send the carcass for analysis. By law,
any bird found dead must be assumed to have died from disease. Aviaries/farms would normally have necropsies
done for all deaths to insure that there is no contagious disease present; in the case of contagious diseases,
treatment and quarantine would need to be put into effect immediately.
- absence of adipose stores—the bird has metabolized all its fat and is nothing but skin, muscle, and bone; see
also serous atrophy of fat below as an early stage; synonym: starvation
- antibiotic sensitivity testing—Sensitive = bacteria are sensitive to antibiotic
and are killed; "I"ntermediate sensitivity indicates some are sensitive (killed), some are resistant; "R"
indicates resistant (antibiotic is not effective)
- macaw wasting disease (PDD)—proventricular dilatation disease, caused by a
virus that progressively destroys the nerve supply to the
proventriculus (forestomach), ventriculus (gizzard), and portions of the small
intestines; as a result of the damage, birds are unable to digest their food properly and starve to
death; there is no cure and the disease is contagious, although the exact
mechanism is unknown; early detection and quarantine is the only means for preventing its spread
- serous atrophy of fat—aka mucoid atrophy of fat, refers to a reduction in
the amount of fat in the body's fat stores; when inadequate nutrition persists,
the fat throughout the body is mobilized and utilized for nutrients; in this situation,
the adipose tissue throughout the body becomes gelatinous in consistency
- unknown cause—when there is no "histopathalogic" cause identified,
it simply means evidence of disease (lesions, hemorrhages, inflamation/infection, etc.) was not present; identifying causes of death
such as environmental factors, toxins, and so on is not part of the post-mortem analysis unless specifically
Macaw wasting disease (PDD), Martha Scudder
has testified, "But I have never had one, to my knowledge, die
out and out of any of those diseases. It has all been
pending [in terms of any definitive final answer]." In arriving at a diagnosis of PDD, the
necropsies do cite specific findings
consistent with PDD and do differentiate cases where PDD is the diagnosed cause
versus being the "likely" cause.
The summaries are of the necropsy contents; where we have added
explanations for clarity, those are enclosed in [brackets]. Arranged chronologically—we are
continuing to add necropsies; there are over 100 total.
- Case 98-600510, April 10, 1998 (baby chicks dying, 2 submitted, "5-6" reported), one bird has omphalitis [inflamation of umbilicus and surrounding parts], livers of both were yellowish; no other significant leasions in second bird; no bacterial growth from first chick; Streptococcus (liver, yolk sac) and Saphylococcus (lung) from second
- Case 98-600522, April 13, 1998 (an Amazon originally caught wild, age unknown), an Amazon originally caught wild, age unknown multi-organ adhesions and severe airsacculitis possibly from rupture of intestines; pneumonia; extensive inflammation throughout lungs, air sacs, intestines and reproductive tract suggestive of bacterial infection; E.coli in lung, kidney, intestine
- Case 98-600570, April 20, 1998, possibly neoplasia [form of cancer]; congestive heart failure; Streptococcus in liver, lung, kidney, heart sac; recurrent bacterial infections and chlamydiosis would be the primary considerations (testing for chlamydia could be pursued)—we should note that although the necropsist indicated that chlamydial (="psittacosis") infection might be a "prime consideration" in the sudden, unexplained death of a bird who was in contact with other birds in the aviary, we can find no record that Martha Scudder took the common sense step to have any further testing done
- Case 98-600937, June 22, 1998, possibly PDD; "The changes seen in sections of brain and spinal chord were of Macaw Wasting Disease."
- Case 99-600439, March 17, 1999, airsacculitis and peritonitis; suggestive of proventricular dilation [PDD]/ganglieneuritis syndrome (no section of proventriculus examined)
- Case 99-601333, August 3, 1999, acute hepatic necrosis; multiple possible causes (additional testing for viral agents can be pursued at additional charge if desired) multi-drug resistant Enterobacter aerogenes in intestine (including resistant to Baytril)
- Case 99-601656, September 13, 1999, occluded inflamed trachea, severe airsacculitis multi-drug resistant Enterobacter cloacae (including resistant to Baytril, with which Scudders had treated this bird)
- Case 99-602012, November 5, 1999, bird with history of unthriftyness [failure to grow or gain weight at a normal rate]; gross findings: severely emaciated with severe airsacculitis; tissues not collected for histopathology considering chronic disease condition
- Case 00-1242, July 7, 2000 (three macaws), confirmed positive for Pachecos; "You may ask a question, 'How come only a few birds have died?' It is likely there are some birds that are carriers and they are passing on the infection to those birds. Please use Novacin for an extended period of time to contain this disease."
- Case 00-1249, July 10, 2000, "The changes seen are suggestive of a viral infection and on examination of previous birds from this facility have been confirmed (using in-situ hybridization test) as having Pachecos virus infection. Please use cautionary measures as discussed."
- Case 99-601657, September 13, 2000, cause of death not evident from sections; peracute [resulting from disease] or environmental causes of death may not leave lesions
- Case 00-2020, November 15, 2000, 8 week old macaw; cause of death not readily evident; final diagnosis hepatitis
- Case 01-358, March 7, 2001, only 10-15% of liver appeared as liver tissue; severe airsacculitis; most likely neoplasia [form of cancerous growth]; liver showed multi-drug resistant E.coli (including resistant to Baytril)
- Cases 01-642 and 01-643, May 1, 2001 (two birds), both showed histopathalogical changes consistent with Macaw Wasting Disease; final histopathology pending with Macaw wasting disease noted as possible for one bird
- Case 01-667 (submitted with 01-668), May 7, 2001, severe atrophy adipose tissue consistent with cachexia, postventriculus not identified in submitted tissues; possible macaw wasting disease
- Case 01-668 (submitted with 01-667), May 7, 2001, accumulations of sloughed cells and remnants of urate deposits, may reflect dehydration; suggestive of cardiac arrest; slightly enlarged postventriculus
- Case 01-1397, November 6, 2001 (eight-week old baby Macaw), severe gout, urate deposits in heart sac and liver; kidneys twice normal size and containing urates; potentially related to high protein intake or low vitamin A [urate buildup is also indicative of dehydration]
- Case 02-04, January 2, 2002 (two birds), cause of death of one bird suspected to be chronic debilitation (atrophy of adipose stores noted); PDD the most likely cause of death of second bird
- Case 02-104, Februrary 2, 2002 (27 birds, 17 more not necropsied—44 birds total), ...a common cause of death is not evident. Absence of adipose stores is a notable finding in all examined birds and may indicate chronic poor nutritional status or debilitating disease. Presence of yellow brown pigment in the gastrointestinal contents is suggestive of melena or hematochezia [both types of gastrointestinal bleeding]...; rodenticide was suspected by the Scudders but was not found; numerous birds had urate deposits in their ureters, an indicator of dehydration
- Case 02-1747, July 8, 2002 (a bird Martha had for two months), macaw wasting disease (PDD)
- Case 02-1008, September 12, 2002 (tumor from live hen submitted for analysis), tuberculosis; Incidence of tuberculosis to human beings are rare, however, immunocompromised people can be infected with M. avium and M. genavense.
- Case 02-1009, September 12, 2002 (chick), peritonitis, airsacculitis and enlarged proventriculus; E. coli present; strain partially to fully resistant to several antibiotics (including partially resistant to Baytril)
- Case 02-1030 (two birds), macaw wasting disease (PDD) in one bird; no histopathologic evidence in second bird (unknown)
- Case 02-1271, November 18, 2002, no evidence found of infectious or inflammatory disease, cause unknown
- Case 02-1304, November 27, 2002, intestinal hemorrhage; cancer of kidney also present
- Case 03-57, January 17, 2003 (Martha's grandson's pet, a Mexican red head), necrosis of the liver, heart; kidney necrosis and urates; lung hemorrhage—results of follow-on immunochemistry analysis not available (to rule out West Nile virus and Chlamydophila); kidney urates a common finding typically associated with dehydration
- Case 03-285, March 7, 2003,, macaw wasting disease (PDD)
- Case 03-1103, September 25, 2003,, mild hepatitis and chronic steatitis
- Case 03-1127, October 10, 2003, septicemia; traumatic injury caused by another aggressive bird resulted in this condition
- Case 03-1144, October 6, 2003, emaciation with liver atrophy and severe serous fat atrophy; Changes in the liver and pericardial fat are indicative of emaciation. Evaluation of diet and housing conditions in this flock are warranted.
- Case 03-1307, November 17, 2003 (two conures belonging to Robin and Bill Scudder), macaw wasting disease (PDD) in one bird, moderate epicarditis in the other bird, indicative of PDD; both suffered from severe loss of body fat
- Case 03-1463, December 24, 2003, cause of emaciation and death not apparent, possible enteritis (Martha Scudder had purchased the bird two weeks prior)
- Case 04-38, January 14, 2004, nephritis
- Case 04-175, February 12, 2004, cause of death not apparent from histology; serous atrophy of fatevidence of long-standing negative energy balance; [in the absence of disease lesions, death could be the result of environmental factors, toxins, or starvation]
- Case 04-395, April 2, 2004, possible hypovitaminosis A deficiency
- Case 04-596, May 18, 2004, severely decomposed, histopathology not possible; macaw hatchling treated with Nystatin and Baytril for three days before death