Thank you, Stuart. I really do appreciate your (and everyone's) input on my little Ask the Vet questions. I will include a sample of my "scientific" writing, just so you can see the style I am more at ease with.

You will probably be more comfortable if you enlarge the field to see the text. Don't feel you must read it. Just sample a line or two to understand my difficulty in writing for the lay public.

You know, as I read through my little case report, I realize I LIKE THIS STUFF! It is more enjoyable when "we" are successful, but telling all my fellow avian practitioners about this case is fun! I like my job. Writing this case report was NOT fun. I agonized over this paper for months! As John was committing matrimony, I was checking the format for references (yes, on Sunday morning). I guess the point I am trying to make is that not everything about one's job is "fun", but when there are things (like this paper for me) that make you feel good, as though you have really contributed, it makes the job worth going to. RIGHT?!

SEPTIC THROMBOSIS IN A GREAT CURASSOW (CRAX RUBRA)

Drury R., DVM
Avian Medical Center of Sacramento
and California Avian Laboratory

Abstract

A severe vegetative endocarditis of the left atrioventricular valves and septic thrombus of the left brachial arteries were diagnosed in a six-year-old male Great Curassow (Crax rubra). The bird presented with an edematous, cool left wing, previous history of lameness, elevations in several biochemical enzymes, and a leukocytosis. Therapy was ineffective. Diagnosis was made on necropsy findings.

History

The Great Curassow (Crax rubra) or Pavo del Monte as they are known in their native lands, are medium to large size gallinaceous birds. Members of this group belong to the Cracidae family, which includes guans and chachalacas. Cracidae and Hoatzin are the only arboreal Galliformes. The Great Curassow inhabits the lowland jungles from southern Mexico to Columbia and Ecuador. The largest of the cracids, this species weighs in at an average of 4.0 kg. Prized by humans as a game bird, the hunting of the Great Curassow contributes to their decreasing numbers in the wild^1,2.

A six-year-old, 3.0 kg male Great Curassow was presented with a two-day history of being unable to lift the left wing and a recent change in the knob on the cere, which became pale and wrinkled. One week earlier the owner noted that the bird was weight-bearing lame on the left leg, which resolved. Housed with a mate in an enclosed outdoor aviary, the birds had been together for three years, without engaging in breeding behavior or egg laying. The diet consisted of a commercial game bird feed, fruit, and a vitamin/mineral supplement.

Physical Examination and Laboratory Findings

The curassow was alert and active at examination. However, it could not raise the left wing. The tissue, from the proximal humerus to the wing tip was slightly edematous and cool to the touch. The nasal knob on the cere was wrinkled, shrunken, and a pale yellow color. The bird felt thin with a moderately prominent sternum. Droppings had scant fecal material with brown urates.

Blood for a complete blood count and serum biochemistries was collected via a clean toe nail clip. The white blood cell count was significantly elevated, 60,000 (86% heterophils, 14% lymphocytes). The heterophils were toxic. The serum was yellow in color. The aspartate aminotransferase (SGOT, AST,524 IU/l), lactate dehydrogenase (LDH, 4108 IU/l) and creatinine phosphokinase (CPK, >6,692 IU/l) were all elevated. An acid fast stain of the feces for mycobacterium was negative. Whole body radiographs demonstrated a slightly enlarged cardiac silhouette and increased prominence to the brachiocephalic vessels. The radiograph of the left wing revealed no significant findings.

Treatment commenced with supportive care of parenteral piperacillin (100mg/kg q 12 hours) and subcutaneous lactated Ringer's solution (40ml/kg/day). Eighteen hours after admission the bird suddenly seizured and died before emergency treatment could be administered.

Pathology

Necropsy revealed thickening of the artrioventricular valves as well as a firm, organized blood clot adhered to one of the valves. The left brachial plexus at the level of the axillary artery was grossly thickened, white, and firm. The muscles, spleen, heart, liver, intestines, and lungs appeared grossly normal. Histopathologically, the lesions in the heart were described as a severe vegetative valvular endocarditis associated with numerous staphylococcal-type bacteria. The lesion at the level of the axillary artery was a septic thrombus. An incidental finding was a multifocal mild nephrocalcinosis. Aerobic bacterial cultures of the liver and lung were negative. Heart and blood cultures were not collected.

Discussion

Vegetative endocarditis is not a common disorder in birds^3-7. It has been described at necropsy examinations of the chicken^3,4,6,8,9, turkey^8,16, swan^10,11, emu¹², and Bald Eagle¹³. The aortic and left atrioventricular valves are more commonly affected^3,5,8,9. Vegetative endocarditis is less commonly found on the right atrioventricular and pulmonary valves^5,8. This trend also appears in dogs, horses, and man^14,17. These lesions seem to be more common in adult birds^3,5,9.

The most common bacterial isolates are Streptococcus, Staphylococcus, Pasteurella, and Erysipelothrix^{3,5,7,9,12,15,16}. Antecedent events to vegetative endocarditis include ventricular septal defect¹⁰, extracardiac chronic infection (e.g. bumblefoot, hepatitis, salpingitis)⁴, social stress⁷, and frostbite or cold stress¹¹. It is interesting to note that curassows are "sensitive to cold" and breeders recommend providing heated shelters for birds maintained in cold climates1. Most often, the cause of vegetative endocarditis goes unidentified.

Thromboembolism associated with vegetative valvular lesions has been described. In birds, emboli have been lodged in the liver, central nervous system, spleen, heart, lung, kidneys, and left external iliac and ischiatic arteries^{5,6,8,9,12,13}.

The disease's early stage is seldom observed clinically in birds^3,4,8,9,10. In turkeys and chickens with experimentally induced vegetative endocarditis a continuous bacteremia, increased heterophil count and a drop in blood pressure can be detected^5,8. Clinical signs including gradual emaciation, abnormal heart sounds, weakness, lameness, depression, pale and shrunken combs and wattles and sudden death occur later^5,7,12,16. Echocardiography was found to be a valuable tool for antemortem diagnosis in several species (avian, dog, man, horse)^12,14,17,18. Blood cultures should be attempted in order to initiate the appropriate antibiotic therapy. Bacteremia is usually of low magnitude but is continuous in bacterial endocarditis^7,19,20,21.

Treatment should be aggressive and long term. A combination of therapy employing antibiotics, coronary vasodilators, aspirin, sodium heparin, and surgery to remove infarcted organs was successful in a dog¹⁷.

I hope this report stimulates the high index of suspicion required to diagnose this disorder.

a) Piperacil, Lederle, Carolina, Puerto Rico.

References

1. OLLSON M: Captive propagation of cracids. The AFA Watchbird 17 (3):36-37, 1990.
2. WEYER D: The bird that sounds like a jaguar. The AFA Watchbird 9 (4):18-21, 1982.
3. RANDALL CJ: A Colour Atlas of Diseases of the Domestic Fowl & Turkey. Ames, Iowa State University Press, 1985, pp 20.
4. POVAR ML, BROWNSTEIN B: Valvular endocarditis in the fowl. Cornell Vet 37:49-54, 1947.
5. GROSS WB, DOMERMUTH CH: Bacterial endocarditis of poultry. Am J Vet Res 23:320-329, 1962.
6. NAYAK BC, MISRA B, BISWAL G: Histopathology of vegetative endocarditis in the chicken. Indian Vet J 44:837-841, 1967.
7. GROSS WB: Miscellaneous bacterial diseases, bacterial endocarditis. In Hofstad MS (ed): Diseases of Poultry, 7th ed. Ames, Iowa State University Press, 1978, pp 319-320.
8. WAGES DP: Streptococcosis. In Calnek BW, et al (ed): Diseases of Poultry, 9th ed. Ames, Iowa State University Press, 1991, pp 299-304.
9. JORTNER BS, HELMBOLDT CF: Streptococcal bacterial endocarditis in chickens. Vet Pathol 8:54-62, 1971.
10. HARARI J, MILLER D: Ventricular septal defect and bacterial endocarditis in a whistling swan. J Am Vet Med Assoc 183 (11):1296-1297, 1983.
11. WALLACH JD, FLIEG GM: Frostbite and its sequelae in captive exotic birds. J Am Vet Med Assoc 155 (7):1035-1038, 1969.
12. RANDOLPH JF, et al: Bacterial endocarditis and thromboembolism of a pelvic limb in an emu. J Am Vet Med Assoc 185 (11):1409-1410, 1984.
13. JESSUP DA: Valvular endocarditis and bacteremia in a bald eagle. Mod Vet Prac 61:49-51, 1980.
14. DEDRICK P, et al: Treatment of bacterial endocarditis in a horse. J Am Vet Med Assoc 193 (3):339-342, 1988.
15. Miscellaneous bacterial diseases. In Calnek BW, et al (ed): Diseases of Poultry, 9th ed. Ames, Iowa State University Press, 1991, pp 289-304.
16. BRINKER JM, SAIF YM: Erysipelas. In Calnek BW, et al (ed): Diseases of Poultry, 9th ed. Ames, Iowa State University Press, 1991, pp 247-256.
17. ELLISON GW, et al: Medical and surgical management of multiple organ infarctions secondary to bacterial endocarditis in a dog. J Am Vet Med Assoc 193(10):1289-1291, 1988.
18. CALVERT CA, GREENE CE: Cardiovascular infections. In Greene CE (ed): Clinical Microbiology and Infectious Diseases of the Dog and Cat, Philadelphia, WB Saunders Co, 1984, pp 220-236.
19. HIRSH DC, JANG SS, BIBERSTEIN EL: Blood culture of the canine patient. J Am Vet Med Assoc 184 (2):175-178, 1984.
20. DOW SW, JONES RL : Bacteremia: Pathogenesis and diagnosis. Comp Cont Ed 11 (4):432-444, 1989.
21. WERNER AS, et al: Studies on the bacteremia of bacterial endocarditis. J Am Med Assoc 202 (3):199-203, 1967.