Abstract

Introduction

Baylisascaris sp., the common roundworm of raccoons and skunks, can cause devastating disease in many captive species of animals due to abnormal parasitic migration.^{1-5,8,9,11-14} Baylisascaris is not only a concern for a zoo’s animals, but it is a zoonosis, especially dangerous in a zoo/park setting where children abound.^6,7,9,10 In the past 3 years at the Los Angeles Zoo, we have seen numerous cases of central nervous system disease secondary to Baylisascaris. Major management changes and aggressive action has brought this disease under control at our zoo.

Case Reports

Affected animals were primarily from four exhibits in the zoo and included six species:

1.  A family of 2.1 golden-headed lion tamarins (Leontopithecus rosalia chrysomelas). The two wild-caught adults survived, but their 2-year-old male offspring was euthanatized.

2.  A 12-year-old female Indian fruit bat (Pteropus giganteus), which was euthanatized.

3.  1.1 juvenile yellow-footed rock wallabies (Petrogale xanthopus), which both survived.

4.  An 8-year-old male red-tailed black cockatoo (Calyptorhynchus magnificus), which survived.

5.  A 7-year-old male thick-billed parrot (Rhynchopsitta pachyrhyncha), which survived.

6.  0.3 young adult rose-breasted cockatoos (Eolophus roseicapullus), which were euthanatized.

In addition, multiple necropsies have demonstrated Baylisascaris in the wild fox squirrel (Sciurus niger) population at the zoo. All affected animals showed neurologic impairment consistent with brain dysfunction (ataxia, head tilt, intention tremors, circling). In surviving animals, the diagnosis was based on clinical signs, the elimination of other differential diagnoses, and gradual improvement. Unfortunately, no ante-mortem diagnostic test is available for this disease in animals.

Management Problems

The Los Angeles Zoo sits in the middle of Griffith Park, which is a large wild area. Previous non-management of pests had allowed the zoo to become overrun with these animals, and problems had reached epidemic proportions in 1995. Coyotes living in the zoo were hunting gerenuk and flamingos, skunks were everywhere, and raccoons had free-roam of the zoo.

Common problem areas included “roundhouse” exhibits with wire tops which were the staple of 1960s design in our zoo. Raccoons and skunks traveled over the tops of these roundhouses and defecated into the exhibit. Even worse, feces could remain undetected on the top of the exhibit where they would dry up, crumble, and fall into the exhibit. Large wire mesh allowed skunks to run in and out of exhibits at will. A large overgrown botanical collection provided perfect hiding areas and pathways over the roundhouses. Garbage bin tops were broken or missing completely, allowing free access to unwanted visitors.

Management Response

With a change in zoo management came an immediate and aggressive response to this problem. A multi-faceted approach was taken as described below.

1.  Current population of resident wildlife were removed. Working with an outside agency, we trapped and eliminated skunks, coyotes, and raccoons from the zoo.

2.  Access by future inhabitants was prevented by repairing gaps in the perimeter fence.

3.  Tree-trimming and foliage pruning were instituted to eliminate overhead pathways and hiding areas.

4.  Animals were prevented from getting into exhibits. Small gauge mesh along bottoms of large gauge mesh exhibits was installed in heavily trafficked areas.

5.  Animals were prevented from having easy access to garbage bins containing thrown away food by repairing lids and educating keepers to keep them closed.

6.  Infected exhibits were rehabilitated. As much dirt as possible and all foliage were removed and replaced. A protocol for clean-up was issued to involved personnel and incorporated into the zoo’s procedure manual. Personnel cleaning exhibits were required to wear face mask filters capable of filtering ova larger than 53 microns,9 disposable coveralls, gloves, and shoe-covers or boots. All disposable and organic materials were incinerated. No ground-eating or foraging species were put in these exhibits after rehabilitation.

7.  Control measures were instituted. Animal care staff was instructed to check exhibit tops and nooks and crannies routinely for feces or debris. Staff was educated about the importance of removing feces immediately since feces are not infective until 3–4 weeks later when the eggs embryonate.⁹ Keeper education was paramount to the success in getting them to report raccoons and skunks in the area and maintenance of routine monitoring and trapping.

Conclusion

The tasks outlined above were mammoth but were successful in preventing additional clinical cases. Community and staff education and cooperation were challenging, but were the key to the implementation of the above steps. Political issues regarding control of wildlife at the zoo had to be overcome, including animal rights objections and the refusal of outside agencies to help. While native wildlife cannot be completely eliminated, the population can be controlled by continual trapping and surveillance. Through education of personnel regarding the effects of this parasite, and aggressive, thorough, and continual action, zoological parks can conquer Baylisascaris.

Addendum: Baylisascaris - Everything a Keeper Should Know

What Is It?

Baylisascaris is a nematode parasite, a roundworm that is carried commonly by raccoons, as well as by badgers, skunks, fishers and martens, and bears (different species for each).

Why Should It Be a Problem for the Animals We Care For?

In its normal host, this parasite is just a GI parasite like any others. The problem lies when the eggs are ingested by an “intermediate host.” The larvae mature and start to migrate through this unfortunate animal’s body, eventually encysting wherever they end up (approx. 5–7% of these are in the brain).

How Would I as a Keeper Come Into Contact With This Parasite?

Eggs are shed in feces and an intermediate host (animal or human) becomes infected by ingesting eggs from environmental areas that have become contaminated by these eggs.

What Symptoms Would Be Seen With an Abnormal Parasite Migration?

Three syndromes are seen: visceral, ocular, and CNS migration, depending on the number of larvae ingested, and their location and behavior in the body. CNS disease (incoordination, head tilt, decreased head control, loss of balance, etc.) is the most serious and characteristic form of infection, however, disease can manifest itself in the retina or other tissues of the body. Clinical signs may never show in a mild infection of muscle, connective tissue, or other noncrucial parts of the body.

How Common Is Human Infection?

This is difficult to say, as the disease has been documented only relatively recently. Thus far only four CNS cases, two of which were fatal, and about a dozen cases of ocular disease are known.

How Is This Disease Diagnosed and Treated?

Unfortunately, there is no good test for animals. In people, blood tests are available. There is no treatment for CNS disease. In ocular disease, laser therapy of the retina is a potential treatment.

How Can We Prevent Exposure to This Parasite?

Foremost in importance is proper sanitation. The eggs are only infective after 3–4 weeks of sitting in the feces. Prompt cleanup of feces eliminates this problem. As with any infectious disease, careful sanitation habits will prevent transmission. Wash hands frequently, and always wash before eating, smoking, etc. Avoid putting your hands in your mouth (biting fingernails, etc.) during work. Showering and changing of clothes before leaving the zoo is ideal. Animals that have become clinically infected with CNS disease from migration are not infective to you. The larvae have encysted in the brain and thus they are not shedding eggs in their feces. The other form of control is eliminating the animals that are shedding these eggs. Feral animals must be prevented from entering captive animals’ enclosures.

How Do We Clean up Chronically Infected Areas?

Unfortunately, there is no easy way. The eggs are resistant to all common disinfectants and most environmental conditions. Large areas of contaminated soil or concrete must be flamed. Topsoil can be removed and buried. Autoclaving and use of a 1:1 mixture of xylene:ethanol can be used for certain surfaces or small cages. Personnel should wear disposable clothes, gloves, a dust mask, and rubber boots that should be washed in hot soapy water to clean organic debris, then rinsed with a foot bath containing bleach.

For further questions, discuss this topic with your veterinarian. Information for this article was taken from, Zoonosis update: Baylisascaris larva migrans. J Am Vet Med Assoc. 1989;195:7.

Literature Cited

1.  Armstrong DL, Montali RJ, Doster AR, et al. Cerebrospinal nematodiasis in macaws due to Baylisascaris procyonis. J Zoo Wildl Med. 1989;20:354–359.

2.  Ball RL, Wilson S, Dryden M, Veatch J. Cerebrospinal nematodiasis in a white-handed gibbon due to Baylisascaris procyonis. In: Proceedings of the American Association of Zoo Veterinarians. 1995:354–355.

3.  Dixon D, Reinhard GR, Kazacos KR, Arriaga C. Cerebrospinal nematodiasis in prairie dogs from a research facility. J Am Vet Med Assoc. 1988;193:251–256.

4.  Fox AS, Kazacos KR, Gould NS, Heydemann PT, Thomas C, Boyer KM. Fatal eosinophilic meningoencephalitis and visceral larval migrans caused by the raccoon ascarid Baylisascaris procyonis. New Engl J Med. 1985;312:1619–1623.

5.  Garlick KS, Marcus LC, Pokras M, Schelling SH. Baylisascaris larva migrans in a spider monkey. J Med Primatol. 1996;25:133–136.

6.  Goldberg MA, Kazacos KR, Bouce WM, Ai E, Katz B. Diffuse unilateral subacute neuroretinitis: Morphometric, serologic, and epidemiologic support for Baylisascaris as a causative agent. Ophthalmology. 1993;100:1695–1701.

7.  Huff DS, Neafie RC, Binder MJ, De Leon GA, Brown LW, Kazacos KR. Case 4. The first fatal Baylisascaris infection in humans: An infant with eosinophilic meningoencephalitis. Ped Pathol. 1984;2:345–352.

8.  Huntress SL, Spraker T. Baylisascaris infection in the marmoset. In: Proceedings of the American Association of Zoo Veterinarians. 1985:78.

9.  Kazacos KR, Boyce WM. Baylisascaris larva migrans. J Am Vet Med Assoc. 1989;195:894–903.

10.  Kazacos KR, Raymond LA, Kazacos EA, Vestre WA. The raccoon ascarid: A probable cause of human ocular larva migrans. Ophthalmology. 1985;92:1735–1744.

11.  Kazacos KR, Reed WM, Kazacos EA, Thacker HL. Fatal cerebrospinal disease caused by Baylisascaris procyonis in domestic rabbits. J Am Vet Med Assoc. 1983;183:967–971.

12.  Kazacos KR, Reed WM, Thacker HL. Cerebrospinal nematodiasis in pheasants. J Am Vet Med Assoc. 1986;189:1353–1354.

13.  Kazacos KR, Wirtz WL, Burger PP, et al. Raccoon ascarid larvae as a cause of fatal central nervous system disease in subhuman primates. J Am Vet Med Assoc. 1981;179:1089–1094.

14.  Myers RK, Monroe WE, Greve JH. Cerebrospinal nematodiasis in a cockatiel. J Am Vet Med Assoc. 1983;183:1089–1090.