Botulism in a California Condor (Gymnogyps californianus)
American Association of Zoo Veterinarians Conference 2002
Kathy Orr, DVM
The Phoenix Zoo, Phoenix, AZ, USA


On August 12, 1999, a female California condor (#84), that had hatched in 1998 at the Peregrine Fund facility in Boise, Idaho and had been released in November of 1998 at the Hurricane Cliffs in Arizona, was presented to The Phoenix Zoo for evaluation and treatment. The bird was one of four that had been recaptured and had been in a holding cage for 2.5 weeks. A field technician noticed abnormal behavior that deteriorated throughout the day before presentation. The bird was weak but still standing when caught from the cage that evening. She was transported to the closest cooperating veterinarian in Page, Arizona for radiographs and emergency treatment. By the time the bird reached the veterinarian, she could no longer stand. When the condor arrived in Phoenix, approximately 5–6 hours later, she was totally flaccid and nonresponsive. There was no pupillary light response or corneal reflex. Heart rate and respirations were normal. The bird weighed 6.36 kg.

Eight ml of blood was drawn from the brachial vein and put into tubes with lithium heparin prior to instituting therapy. Emergency treatment was started and consisted of 0.63 mg/kg dexamethasone, (Dexamethasone Solution, Phoenix Scientific Inc., St. Joseph, MO, USA) IV, 6 ml 50% dextrose (Dextrose Solution 50%, Phoenix Pharmaceutical Inc., St. Joseph, MO, USA) IV, 9.4 ml/kg lactated Ringer’s solution (LRS) IV, 0.06 ml/kg vitamin B complex (Vitamin B Complex, Veterinary Laboratories Inc., Lenexa, KS, USA) IV, 5.35 mg/kg enrofloxacin (Baytril, Bayer Corporation, Agriculture Division, Animal Health, Shawnee Mission, KS, USA) IM BID, 2.36 mg/kg ceftiofur sodium (Naxcel, manufactured for Pharmacia and Upjohn Co., Kalamazoo, MI, USA by SmithKline Beecham Corp., Philadelphia, PA, USA) IM BID for 12 days, 35 mg/kg Ca EDTA (Calcium Disodium Versenate, manufactured for 3M Pharmaceuticals, Northridge, CA, USA by Abbott Laboratories, North Chicago, IL, USA) IM once, 0.042 mg/kg atropine (Atropine Sulfate 1/120, VEDCO Inc., St. Joseph, MO, USA) IM, 70 mg/kg potassium chloride (Abbott Laboratories, North Chicago, IL, USA) PO via gavage and 20 ml of activated charcoal suspension (ToxiBan, Vet-A-Mix, Shenandoah, IA, USA) PO via gavage. An IV catheter was placed in the metatarsal vein for administration of IV fluids. At one point the first day, oxygen was given via face mask when respirations slowed almost to a stop. Metoclopramide (Metoclopramide Injection, USP, manufactured for Faulding Pharmaceutical Co., Elizabeth, NJ, USA by Faulding Puerto Rico Inc., Aguadilla, Puerto Rico) was added to the treatment regimen at a dose of 0.39 mg/kg IV three times per day, because the crop was not emptying.

Blood collected prior to treatment was submitted to various laboratories for complete blood count (CBC), plasma chemistry panel, blood lead, and barbiturate drug screen. All tests were normal. Plasma was banked for further diagnostic testing. Botulism was considered, but rejected as a diagnosis initially, because vultures are thought to be resistant to botulinum toxin. Plasma saved from the first day was sent to the National Wildlife Health Center (NWHC, Madison, WI, USA; 608-270-2400) on day 5 for botulinum toxin type C testing. Meanwhile, treatment was started on day 4 using antitoxin (frozen rabbit-origin botulinum type C produced in Aug 1991 by T. Rocke at NWHC) obtained from the San Diego Wild Animal Park. The antitoxin is not commercially available. It has been produced for experimental use in migratory waterfowl. The NWHC can be contacted for information on current availability of the antitoxin.

The NWHC performs the mouse inoculation test for botulinum toxin type C. Briefly, one mouse is given antitoxin and the other receives none. Both mice are then injected with serum or plasma from the animal being tested. In this case, the unprotected mouse died so quickly that the laboratory personnel were unsure if it was an accurate test. Plasma saved from the second day was submitted, and it produced the same results. The lab diluted the condor plasma from the second day by four times before a response similar to what would be typical in a duck positive for botulism was noted. It was concluded that the condor had botulinum type C toxin in her plasma at a concentration four times higher than the amount that is lethal in ducks.

The condor slowly improved with continued supportive care which included IV fluid therapy (11.8 ml/kg LRS with 2.5% dextrose and 1 ml vitamin B complex/L added of fluids) TID, metoclopramide IV TID, water PO via gavage, force feeding of whole mice and bird-of-prey diet, and continued antibiotics [enrofloxacin was discontinued after 4 days and gentamicin sulfate (Gentocin, Schering-Plough Animal Health, Kenilworth, NJ, USA) was added at a dose of 4.7 mg/kg BID for 8 days]. The flaccid paralysis (which included eyelids, striated muscle in the iris, and crop muscles) improved gradually over 8 days. A timeline is included in Table 1. Although the bird improved slowly with the initial supportive care, the improvement was more rapid after antitoxin administration. The first antitoxin dose of 0.5 ml was administered via the metatarsal IV catheter on the third day after presentation. Three additional 0.5 ml doses were given IV the next day approximately every 8 hours. The last two doses were given on the third day. Two days later (8 days after initial presentation), the condor progressed from interest in water and food, which she could not pick up or swallow in the morning, to eating and drinking that afternoon.

Table 1. Condor #84 treatment and response timeline during 1999

August 11

Condor #84 noticed sick—transported to veterinarian in Page, AZ, then to Phoenix.

August 12

To Phoenix Zoo by 7:00 a.m.; bird flat out and non-responsive. Received fluids IV, dextrose, antibiotics, dexamethasone. Blood drawn. Treated for lead poisoning, organophosphates. Some struggling movements by 9:00 p.m. Weight 6.36 kg.

August 13

Continued supportive care. By 10:00 p.m., could sit up on her hocks and hold her head up some. Eyelids closed and no pupillary light response.

August 14

Continued supportive care. Some eyelid movement. Standing up on hocks longer. Some mouth movement. By 11:00 p.m., stood up on feet briefly for the first time.

August 15

Continued supportive care. Up on hocks. Slight opening of eyes. Started antitoxin IV at 3:00 p.m. (two doses).

August 16

Stood on hocks and turned around when disturbed. Three doses of antitoxin given. Attempted to preen. Opened eyes well in afternoon and eyes open most of the time. Struggled a lot. Grabbed with beak.

August 17

Two doses of antitoxin given. Sat on hocks during part of a.m. treatment. At noon, stood on table and walked. Walked across floor and jumped into cage after treatment. Same behavior at p.m. treatment.

August 18

Eyes open, yawning, trying to bite, trying to preen, and interested in water, but not able to swallow. Taking treatment on hocks and standing.

August 19

Interested in water and a mouse, but not able to pick up mouse or swallow in a.m. By 3:45 p.m., eating and drinking.

August 20

Drinking a lot and preened. Went back into cage on her own. No food offered because crop not empty.

August 21

Ate again. Last IV treatment given.

August 22

Ate eagerly.

August 23

Last antibiotic treatment.

August 24

Took a bath, and threatened keeper.

August 25

Started treatment with itraconazole for Candida.

August 27

Flying onto shelf while recovering in the isolation ward.

August 30

Moved to outside pen.

September 10

Picked up for transport back to Vermillion Cliffs, AZ.

September 26

Released back into the wild. Weight 7.5 kg.


A Candida infection, probably secondary to antibiotic therapy, was detected by cloacal culture. It was treated successfully with 7.86 mg/kg itraconazole (Itraconazole 50 mg capsules compounded by Pet Health Pharmacy, Youngtown, AZ, USA) PO BID for 6 days. The bird made a complete and uneventful recovery and was released 5 weeks after presentation.

This case demonstrated that California condors, and probably other vultures, are susceptible to poisoning by Clostridium botulinum toxin type C. However, this condor survived a concentration of toxin four times greater than that which is lethal to a duck. Captive-reared condors may be more susceptible to the toxin than those found in the wild, because they are rarely exposed to contaminated food.

The source of the toxin in this case was not determined. Three other young condors in the same holding cage did not develop clinical signs. The birds had been held for approximately 2.5 weeks and were fed dairy calves and road-killed animals such as rabbits. The cage was not cleaned in order to prevent the birds from becoming too habituated to humans. Food items were placed in the cage after dark so the birds would not associate food with people. As soon as we suspected toxicity, the cage was cleaned completely to prevent the problem in the other three birds. Unfortunately, no food items were available for toxin testing. The sick condor did regurgitate some maggots; thus, it was likely that she had eaten something fairly decomposed.


I want to sincerely thank all the people who helped make this case a success. They are Kirk Stodola, the observant and gutsy field technician who recognized the condor was in trouble and took the initiative to transport her to appropriate facilities without waiting for approval from his supervisor who was unreachable out in the field; Jerry Roundtree and Jim Baker, veterinarians in Page and Phoenix who assisted with diagnostic and supportive treatment for the condor on her way to us; all the cooperating Condor Recovery Team veterinarians at San Diego Zoo and Wild Animal Park , Los Angeles Zoo and Minnesota Raptor Center who let me call them for advice day and night throughout this case (Phil Ensley, Jeff Zuba, Cynthia Stringfield, and Pat Redig); the diagnosticians (especially Lynn Creekmore) at National Wildlife Health Center who tested and retested until we were all satisfied with the unexpected diagnosis; Tony Rocke for having made some botulism type C antitoxin, and Jeff Zuba for sending the antitoxin via Federal Express to Phoenix from San Diego; and last but not least, my Phoenix Zoo hospital staff who helped in every way possible to provide the technical and nursing care that was required to save such a special bird (Linda Ambrose, Gregg Goldschlager).


Speaker Information
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Kathy Orr, DVM
Phoenix Zoo
Phoenix, AZ, USA

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