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An 18-month-old boy developed a mild respiratory infection with a low-grade fever. Over the next several days, he became increasingly lethargic and was hospitalized.¹ Physical examination revealed mild hepatomegaly and neurologic abnormalities including stupor, vertical nystagmus, and hypertonicity of the right arm. Laboratory investigation revealed a WBC count of 10,000 cells/mm³, with 37% eosinophils; the CSF contained 5 WBC/mm³. Computed tomography, with contrast infusion, revealed ventricular dilatation with periventricular enhancement. Over the next 2 and a half weeks, the boy became comatose with diffuse hypotonia. The WBC count was 9,500 cells/mm³, with 34% eosinophils, and the CSF count increased to 275 WBC/mm³, with 80% eosinophils.

Fungal, bacterial, and mycobacterial organisms could not be isolated from the CSF, and results of serologic tests for trichinosis and systemic fungi were negative. Thiabendazole was administered for presumed Toxocara larva migrans, although the toxocaral IgG antibody titer was less than 1:8. Improvement was not observed, and 3 weeks after hospitalization the boy died. At autopsy, multiple nematode larval granulomas were detected on the pleura, epicardium, and mesentery, and severe pathologic changes were in the brain. Larvae were morphologically identical to raccoon ascarid larvae, Baylisascaris procyonis.^1-4 Subsequent serologic analysis revealed antibodies against Baylisascaris spp in serum and CSF samples.^1,5 Several locations on the midwestern farm where the boy had lived were contaminated with raccoon feces and infective B procyonis eggs. It was believed that the boy had become infected while chewing on bark and wood chips from contaminated firewood brought into the home.¹ The boy's parents asked their veterinarian a number of questions concerning B procyonis and raccoons.

Q: What kind of disease is larva migrans?

A: Larva migrans refers to the prolonged migration and persistence of parasite larvae in the organs and tissues of human beings and animals, similar to that in the natural intermediate or paratenic host(s) of the parasites.⁶ Larva migrans is commonly separated into clinical entities referable to the organ systems involved, namely, visceral and ocular larva migrans and cerebrospinal nematodiasis. A number of nematode species, including Toxocara spp, Baylisascaris spp, other ascarids, gnathostomes, Strongyloides spp, hookworms, and others, are capable of causing larva migrans disease in human beings.⁶ The most common causes of visceral and ocular larva migrans in human beings are Toxocara spp of dogs and cats.^7,8

Q: What is Baylisascaris procyonis?

A: Baylisascaris procyonis (Nematoda, Family Ascarididae) is the common large roundworm parasite in the small intestine of raccoons.⁹ Adult worms are about 12 (male) to 23 (female) cm long, tan, and superficially resemble the dog roundworm, Toxocara canis. Other species of Baylisascaris in North America include B melis in badgers, B columnaris in skunks, B devosi in fishers and martens and B transfuga in bears.⁹

Baylisascaris procyonis is a well-recognized cause of larva migrans in wild and domestic animals in North America.^3,10,11 It is usually associated with the production of clinical CNS disease. The zoonotic potential of B procyonis was demonstrated in experimental infections of subhuman primates, which developed extensive larva migrans and fatal CNS disease.² In the past several years, 2 fatalities in children (including your son) have been attributed to B procyonis.^1,12 In addition, other probable cases of CNS disease in human beings have been discovered,^13,a and the parasite has been implicated as a cause of human ocular larva migrans.^14,15

Q: How is B procyonis transmitted in raccoons and other animals?

A: Adult female worms in the small intestine of raccoons produce eggs, which are shed in the feces (Fig 1, 2).

Figure 1--Baylisascaris procyonis egg from fresh raccoon feces. Bar = 20 µm

View Figure 2--Life cycle of Baylisascaris procyonis.

Under moderate weather conditions, the eggs reach infectivity in about 3 to 4 weeks. Young raccoons become infected by ingesting eggs containing infective larvae,^b whereas older raccoons become infected by ingesting larvae in the tissues of intermediate hosts, such as rodents, rabbits, and birds.^10,11,16,b Susceptibility of young raccoons to infection via eggs^b and age resistance in older animals may explain the higher prevalence of B procyonis in juvenile vs adult raccoons.^10,11 In young raccoons, larvae from eggs enter the wall of the small intestine and develop there before reentering the intestinal lumen to mature; patency is reached in 50 to 76 (mean, 63) days.^b Larvae acquired from intermediate hosts develop to adults in the intestinal lumen, and patency is reached in 32 to 38 (mean, 35) days.^b More extensive migration does not seem to take place in raccoons; transmammary and transplacental infection has not been investigated.¹¹

Intermediate hosts become infected by accidentally ingesting infective B procyonis eggs from environmental areas contaminated by raccoon feces. If their fur has become contaminated, rodents and other animals may also ingest eggs while grooming. After infection, the larvae migrate to various somatic and visceral tissues, where they become encapsulated.^10,16,17 About 5 to 7% of ingested larvae enter the brain of intermediate hosts, and usually cause CNS disease.^11,16 Because these infected animals are then more easily captured by raccoons, transmission of B procyonis back to the definitive host is enhanced.^10,11,16-18 Encapsulated Baylisascaris larvae will also survive for some time in dead intermediate hosts, with the added potential of transmission via scavenging.¹⁹

Occasionally, partial or complete development of Baylisascaris adults takes place in animals other than their normal definitive hosts. How often this happens in nature, the range of hosts involved, and the percentage of worms that so develop are not known. A patent infection developed in a young opossum that was fed mice containing B procyonis larvae,^c and some young adult worms developed in rats and squirrels infected with B columnaris eggs.^d Recently, patent Baylisascaris infections were seen in 2 unrelated young dogs in Iowa.²⁰ How these dogs became infected (whether by ingestion of infective eggs or larvae in intermediate hosts), and how long they maintained patent Baylisascaris infections is not known.

Q: How do human beings become infected with B procyonis?

A: Human beings become interposed in the life cycle of B procyonis, substituting for the natural intermediate hosts of the parasite (Fig 2). Human beings become infected with B procyonis by accidentally ingesting infective eggs from the environment, from raccoon feces, contaminated soil, water, fomites, or via contaminated hands.^10,11 The larvae of B procyonis migrate in human beings as they would in their natural intermediate hosts. Infected raccoons can shed millions of eggs per day, and these eggs can remain viable in the environment for months to years, increasing the likelihood of transmission to human beings and animals.^10,11

Q: How does B procyonis cause disease in human beings and animals?

A: Baylisascaris procyonis larvae undergo somatic migration in intermediate hosts, including human beings, similar to that of larvae of Toxocara and other carnivore ascarids.^{10,11,16-19,21,22} After ingestion of eggs containing infective larvae, the eggs hatch in the small intestine and the larvae quickly penetrate the intestinal wall and reach the liver via the portal circulation. They then migrate rapidly to the lungs, where most enter the systemic circulation via the pulmonary veins and become distributed to the somatic tissues and viscera.^17,18,21,22 Pulmonary hemorrhages are seen in mice within 12 to 48 hours of infection, and larvae enter the eyes, brain, and somatic tissues of mice as early as 3 days after infection.^11,15,17 Baylisascaris procyonis larvae, unlike Toxocara larvae, molt and grow as they migrate through the tissues, increasing in length from about 300 µm to 1,500 to 1,900 µm.^1,10,11,17 Larvae continue to migrate in the tissues until they become encapsulated within eosinophilic granulomas.^1-3,10

Because of their large size and aggressive migration, B procyonis larvae cause mechanical damage and incite vigorous host inflammatory reactions.^1-3,12,14-16 Such pathologic changes are particularly important in the CNS. Inflammatory reactions appear to be directed against antigenic excretory-secretory products, including enzymes and metabolic wastes released by the larvae during migration.^5,23,24 Eosinophils are a major component of host reactions to B procyonis, and eosinophil granule proteins released in the CNS and other tissues may contribute to the pathologic changes and clinical signs.²⁴

Baylisascaris procyonis causes visceral larva migrans, ocular larva migrans, and cerebrospinal nematodiasis in human beings.^{1,2,10-12,14,15} The extent of disease caused by B procyonis depends on the number of larvae ingested and their location and behavior in the body, especially those migrating in the CNS.^10,11 Clinical CNS disease is the most serious and characteristic form of B procyonis infection; however, when only a few larvae are ingested, infected individuals would probably be asymptomatic because visceral damage would be minor and most larvae would become encapsulated in noncritical locations such as skeletal muscle or connective tissue.^10,17,21 The latter is probably the most frequent form of human infection with B procyonis. Larger numbers of migrating larvae may induce nonspecific symptoms and clinical signs, or more classical visceral larva migrans, with fever, leukocytosis, persistent eosinophilia, hepatomegaly, and pneumonitis.¹ As opposed to Toxocara, if enough B procyonis larvae are ingested to cause clinical visceral larva migrans, CNS disease will probably also develop because of the much greater pathogenicity of B procyonis larvae in CNS tissues.^{1,2,10-13,17,22}

The severity and progression of clinical CNS disease depends on the number of B procyonis larvae entering the brain, the location and extent of migration damage, and the size of the brain.^10,11,16,17 One B procyonis larva in the brain of a mouse or small bird usually is fatal.^10,16-18,d In a much larger animal, such as a human being, one or a few larvae in noncritical areas of the brain would probably cause minor or no clinical problems, which may be slow to develop; however, if enough larvae are ingested, progressive CNS disease can develop rapidly, with severe signs possible within 2 to 4 weeks of infection.^{1,2,10-12,16,17} In such cases, typical clinical signs would include sudden lethargy, loss of muscle coordination, decreased head control, torticollis, ataxia, and nystagmus, progressing to stupor, extensor rigidity or hypotonia, coma, and death.^{1,2,10-12,16,17} The CNS fatalities in children^1,12 seem to represent infections with large numbers of B procyonis larvae. In the case of your son, 3 larvae/g of brain tissue were isolated, which corresponded to a total brain burden of 3,207 larvae, and an oral infecting dose estimated at 46,000 to 64,000 eggs.¹ Although clinically characteristic for B procyonis, and more of a possibility in children, such cases probably do not represent usual human infections with this parasite.

Ocular disease results from larval invasion of the eye via the systemic circulation. Clinical signs of ocular larva migrans include unilateral loss of vision and photophobia, and are related to larval migration damage and inflammatory reactions, usually involving the retina.^14,15 Migration tracks and larvae were seen clinically in the retinas of monkeys as early as 7 days after infection.^14,15 Suspected Baylisascaris-induced ocular larva migrans has been seen in patients without concurrent clinical visceral larva migrans or CNS disease, and probably represents chance migration of larvae into the eye.^14,15 Such cases support the hypothesis that low-level infections with B procyonis are probably the most common form in human beings.

Q: What animal species have been affected by Baylisascaris migration?

A: Baylisascaris procyonis causes larva migrans in a wide range of hosts. In fact, few other parasites are so indiscriminate in their infection of animals. In addition to human beings, larva migrans and CNS disease caused by Baylisascaris has been detected in 19 species of mammals and 13 species of birds, and the list of affected species continues to grow. In only a few cases were Baylisascaris species other than B procyonis determined to be involved. All rodents, birds, and rabbits appear to be susceptible, and compose the natural intermediate hosts for B procyonis. Natural CNS disease has been seen in wild mice, house mice, gray squirrels, fox squirrels, a red squirrel, ground squirrels, chinchillas, prairie dogs, woodchucks, nutria, beavers, a capybara, a cavy, porcupines, cottontail rabbits, domestic rabbits, silver foxes, a dog, marmosets, chickens, quail, partridges, a brush turkey, pheasants, macaws, cockatiels, a robin, pigeons, blue jays, mourning doves, emus, and ostriches.^{d, cited in e,2,3,10,16,25-29}

Species experimentally susceptible to B procyonis-induced CNS disease include some of the aforementioned (wild mice, squirrels, rabbits, woodchucks, chickens, dogs) as well as white laboratory mice and rats, cotton rats, hamsters, guinea pigs, chipmunks, ferrets, weasels, ducks, squirrel monkeys, and cynomolgus monkeys.^{d,cited in 10,11,16,17,25}

Baylisascaris procyonis infections usually are discovered because of clinical CNS disease. Frequently, affected animals such as woodchucks and squirrels are submitted to diagnostic laboratories or health departments as rabies suspects, because of their abnormal behavior and clinical signs^10,11; however, many affected animals, especially smaller rodents, go unnoticed in the environment because of their size and location or because they are eaten by predators. Dr. Jack Tiner, who did pioneering research on B procyonis, estimated that B procyonis causes about 5% of natural rodent mortalities in woodlots where infected raccoons are common.¹⁸ As stated, some cases of infection also exist in which CNS disease doesn't develop because of the localization of larvae in non-CNS tissues.^16,18

A few animal species appear to be only marginally susceptible or resistant to B procyonis larva migrans, as there is little or no migration in these species; such species include opossums, skunks, cats, and large domestic livestock such as swine, sheep, and goats.^10,25,d

Q: How common is B procyonis in raccoons?

A: The prevalence of B procyonis in raccoons varies among the geographic regions of the United States. Prevalence may also vary according to season, although less is known about this aspect.^d,f The infection is most common in the northern temperate regions of the midwestern and northeastern United States, although it usually can be found to some extent in other areas where raccoons exist. In Indiana and Illinois, 72% of 1,425 and 82% of 310 raccoons, respectively, were found to be infected, with much higher prevalence in juveniles (92 to 94%) than in adults (37 to 55%).^30,d Baylisascaris procyonis was found in 51% of 213 Wisconsin raccoons (70% of juveniles, 19% of adults), and the prevalence decreased from the southern (77%) to the northern (18%) part of the state.^g In western New York, 68% of 429 raccoons were infected, including 91% of juveniles and 38% of adults.³¹

The prevalence of B procyonis decreases from northern to southern states, so that it is either less common or absent in raccoons from areas in the Deep South. Baylisascaris procyonis has been found in 30% of 70 raccoons in western Kentucky,³² 26% of 72 raccoons from Virginia,³³ 7.5% of 253 raccoons from Tennessee,³⁴ 1 of 110 (0.9%) raccoons in northern Georgia,^c and was not detected in raccoons from North Carolina (225), South Carolina (64), Alabama (371), Georgia (149), Florida (70), and Texas (37).^35-38 Recently, however, B procyonis was detected in 23% of 62 raccoons in east Texas, indicating that local prevalences may vary.^h In the Southeast, the parasite appears to be found primarily in mountainous areas.^33,34,38 In the West, B procyonis has been reported at low frequency in Washington (3.5% of 29 raccoons)³⁹ and twice from California.^40,41 The translocation of raccoons practiced by hunting clubs and others has the potential of introducing this parasite into areas where it is not presently located.³⁸ Its establishment in such areas could pose a threat to indigenous mammals and birds.^18,38

Q: Does B procyonis cause disease in raccoons?

A: For the most part, adult B procyonis in the small intestine of raccoons appear to be well tolerated causing few obvious problems. Most infected raccoons are normal appearing and have no outward signs of infection. In areas where the parasite is common, average parasite intensity ranges from 43 to 52 worms, with higher average burdens in juveniles (48 to 62 worms) than adults (12 to 14 worms) and maximal intensities of 241 to 328 worms.^30,31,d,g Whether the parasite in large numbers causes subtle or direct effects on growth and vitality of raccoons is unknown, but might be expected. In heavily infected raccoons (primarily juveniles), B procyonis has caused intestinal obstruction resulting in emaciation and starvation; in 3 such cases, worm burdens of 141, 636, and 1,321 were reported.^42,43

Q: How common is B procyonis infection in human beings?

A: The prevalence of B procyonis in human beings is unknown, but there is little question that it is more common than the number of documented cases suggests. On the basis of the ubiquity of infected raccoons and the likelihood of human contact with raccoons and their feces, the potential for human infection with B procyonis is high, although probably not as high as that for Toxocara infection. Human disease from B procyonis infection has only recently been documented,^1,12,15 and the medical community is not always familiar with this parasite or its potential health effects. Therefore, B procyonis may be considered less often in the differential diagnosis of human disease, including visceral larva migrans and CNS disease. This will continue to be a problem until there is general awareness of B procyonis among physicians and public health personnel. In addition, subclinical or mild infections would probably be missed, also contributing to underdiagnosis. General infection rates in human beings can only be determined seroepidemiologically, such as has been done for Toxocara.^7,8 This would involve the widespread application of specific immunodiagnostic tests for Baylisascaris, which are presently being developed and evaluated.^1,5,12,23,44 Until this is done, and based on what is presently known, it would be unwise to categorize human infection with B procyonis as rare or uncommon.

At present, in addition to your son, there has been one other confirmed fatality related to B procyonis, which involved a 10-month-old boy from Pennsylvania, who also died from extensive infection and rapidly progressive CNS disease.^1,12 A third probable, but unconfirmed, case of Baylisascaris infection involved an 18-month-old Missouri girl with nonfatal CNS disease, and CSF as well as serum antibody titers to Ascaris.¹³ Because somatic migration and CNS invasion are not characteristic of Ascaris,^21,22 the investigators astutely suggested infection by some animal ascarid species other than T canis, which is more closely related antigenically to A lumbricoides.¹³ Baylisascaris is such a parasite,^5,44,i with a propensity for causing clinical CNS disease. A fourth case of CNS disease involved a 21-year-old man from Oregon who was seropositive for B procyonis and had compatible migratory lesions in brain tissue.^a About a dozen suspected human cases of Baylisascaris-induced ocular larva migrans are known, most being from the Midwest.^14,15,d In one of those cases, a 13-year-old girl from Kentucky developed ocular larva migrans 6 weeks after acquiring a pet raccoon, and measurements of the intraocular larva were compatible with B procyonis.^14,15

Q: Who is at greatest risk of infection with B procyonis?

A: Seroprevalence studies have not been done for B procyonis as they have for Toxocara^7,8; therefore, whether age, race, or socioeconomic patterns exist for B procyonis infection is unknown. It is logical to assume that those people who have increased contact with raccoons and their feces would be at a greater risk of infection. This would include people who keep raccoons as pets and those who raise them for other purposes, such as wildlife rehabilitators. In such situations, environmental contamination with B procyonis eggs can be quite heavy in areas routinely frequented by human beings.¹⁰ Whether more casual contact with raccoons, such as by raccoon hunters, trappers, taxidermists, or others would also result in increased infection rates is not known.

The epidemiology of Baylisascaris closely parallels that of Toxocara.^7,8,10,11 It can thus be predicted that children 1 to 4 years old are at the greatest risk of infection with B procyonis, because of their poorer hygienic habits and their propensity for placing soil and other materials into the mouth. The risk of infection for young children would be increased when raccoons are kept in the home environment, or if the children otherwise have access to areas or materials contaminated by raccoon feces.^1,12 In 3 of the 4 known or suspected cases of B procyonis-induced CNS disease in human beings, a history of pica was evident.^1,13,a

Q: How are infections with B procyonis diagnosed and treated in human beings?

A: Because neither eggs nor larvae are in fecal or blood samples from infected human beings, antemortem diagnosis of Baylisascaris larva migrans must be made on history clinical findings and serologic testing.^1,10-12,44 A history of actual or possible exposure to raccoons or their feces is important, and the extent of such exposure should be evaluated.^1,10-12 Clinical findings of visceral larva migrans include leukocytosis, persistent eosinophilia, hypergammaglobulinemia, hepatomegaly, and pneumonitis.^1,7,8,13 Of importance in Baylisascaris infections is the sudden onset and/or progressive development of CNS disease in the presence of peripheral eosinophilia and eosinophilic pleocytosis of the CSF. The latter is an important diagnostic finding in Baylisascaris-induced CNS disease in human beings and animals.^{1,2,10,12,13,d} Ocular larva migrans caused by Baylisascaris is diagnosed by ophthalmologic examination, which would reveal inflammatory migration tracks in the retina as well as inflammation of the vitreous and the choroid.^14,15 Baylisascaris larvae may be seen in the retina and are much larger than Toxocara larvae; they are in the size range of 31 to 75 x 625 to 1,900 µm, with a final size of 50 to 75 x 1,500 to 1,900 µm.^{1,4,11,14,15,17,d} A specific diagnosis is made by morphologic identification of larvae recovered from tissues or in histopathologic sections.^1-4

Serologic tests currently being developed and evaluated for Baylisascaris larva migrans include indirect immunofluorescence methods, using B procyonis larvae, and protein immunoblotting and ELISA methods, using larval excretory-secretory antigens.^{1,5,12,23,44,a} Baylisascaris is more closely related antigenically to Ascaris than to Toxocara,^44,i so separation of Baylisascaris and Toxocara larva migrans appears possible. All 4 people with known or suspected B procyonis-induced CNS disease^1,12,13,a were serologically negative for Toxocara and positive for B procyonis or, in one case, Ascaris.

An important problem concerning B procyonis infections is that effective anthelmintic treatments currently do not exist for visceral or ocular larva migrans or CNS disease caused by this parasite. Empirical treatment of suspected infections in birds and mammals (including human beings) with thiabendazole, fenbendazole, levamisole, and ivermectin were not effective, and living larvae were later recovered from the brain.^1,29,45,d,e Even if effective larvicides were available, clinical cerebrospinal nematodiasis caused by B procyonis would still have a poor prognosis, as this infection is not usually considered or diagnosed until CNS signs are pronounced, and considerable CNS damage has already developed.^10,11 Baylisascaris larvae can enter the brain within the first week of infection,^{10,11,15,17,21,22,d} and thus pathologic changes far precede the development of recognizable signs. Additionally, killing the larvae at this time might exacerbate inflammatory responses in the CNS, because of the sudden release of larval antigens. It is apparent that any empirical treatments for Baylisascaris larva migrans should be started as soon as possible after suspected infection.

Patients with ocular larva migrans caused by B procyonis have a better prognosis if recognized early and if larvae can be located and visualized in the eye. These patients have been successfully treated by use of a laser to destroy the intraretinal larvae, thus preventing further migratory damage.^14,15 Eyesight may or may not improve after treatment, depending on the location and extent of ocular damage and inflammation.

Considering the potential seriousness of this infection as well as the limitations in effective treatment, prevention of human infection with B procyonis is of considerable importance.

Q: What situations have led to human and animal infections with B procyonis?

A: Infection of human beings and animals with B procyonis is possible in urban and rural settings, from free-ranging as well as captive raccoons. Infection involves the special circumstances of exposure to contaminated areas and accidental ingestion of infective B procyonis eggs.^10,11 Free-ranging raccoons typically defecate in favored areas, termed latrines, which are commonly found in wooded areas at the bases of trees, in the raised forks of trees, and on fallen logs, large rocks, and other raised horizontal surfaces.^d,j Studies in an urban park have shown that these latrine sites represent hot-spots of contamination where many B procyonis eggs will be concentrated.^j There seems to be little leaching and dispersal of B procyonis eggs from these areas.^j Contact with these latrine sites, particularly by young children, could result in infection if eggs are accidentally ingested. Undigested seeds in raccoon feces/latrines are attractive food items for birds and rodents and probably serve as a vehicle for B procyonis eggs.

Other common latrine sites near human beings include woodpiles and decks, and accessible areas of buildings such as attics, garages, chimneys, and the straw and haylofts of barns.^1,3,10 When used as bedding or feed, contaminated straw or hay from barns is an important potential source of infection for animals, and has been linked to a number of episodes of B procyonis-induced CNS disease.^3,10,11 Fatal infection of a Pennsylvania child was believed to have occurred from open fireplaces in the home, which were contaminated with raccoon feces from raccoons dwelling in the chimneys.¹²

Raccoons kept as pets or for other purposes pose a more direct threat of infection because of localized fecal contamination and the increased possibility of human contact with infective B procyonis eggs.^10,11 Large numbers of B procyonis eggs may build up in and around enclosures, cages, and other areas where raccoons are kept.¹⁰ A number of cases of fatal B procyonis infection in animals have been directly linked to the use of cages or enclosures that had previously housed raccoons.^{d,cited in 2,3,10,16,25-29} Some of these cages had been washed or otherwise cleaned, but not decontaminated in a manner known to kill B procyonis eggs. These cases included deaths in other pets, animals raised or kept in wildlife rehabilitation centers, humane societies, and zoos, and animals temporarily housed while awaiting shipment for research purposes. The recent acute fatality of a young hunting dog was associated with keeping a caged raccoon for training purposes.²⁷ The raccoon had been passing large numbers of B procyonis worms in its feces, thus was heavily infected and had been contaminating the home environment for weeks.²⁷ The maturation of Baylisascaris in dogs²⁰ increases the zoonotic potential of this parasite, as the dogs could also contaminate the home environment with eggs.

A key feature in the epidemiology and transmission of B procyonis is that infection can only be acquired by the ingestion of eggs containing infective larvae. Freshly deposited raccoon feces contain undeveloped eggs (Fig 1) and, therefore, do not pose a direct threat of infection; it takes 3 to 4 weeks for B procyonis eggs to reach the infective stage, at which time raccoon feces become dangerous.

Q: What precautions should be taken by people who raise or keep raccoons, such as wildlife rehabilitators?

A: If effective preventive measures are taken, the chances of spreading B procyonis or becoming infected with the parasite can be limited. The most important points are to prevent egg shedding and contamination by raccoons, and to limit contact of human beings and animals with contaminated areas. Raccoons should be quarantined away from other animals, in cages or enclosures that could be decontaminated if necessary. All raccoons should be on a strict treatment program to eliminate B procyonis intestinal infections. Young raccoons should not be placed into egg-contaminated cages or enclosures, as they may become (re)infected with B procyonis.^b Similarly, raccoons should not be fed uncooked wild meat from rodents, rabbits, or birds, because encysted larvae in such animals could also lead to (re)infection with B procyonis.^10,16,b,d

Access by people, especially children, to known or potentially contaminated areas should be restricted. Feces should be removed and disposed of, at least weekly, in a manner that prevents their contact by human beings and animals; feces from infected raccoons should be destroyed. Contaminated areas, cages, or traps that have held infected raccoons should be decontaminated. Cages and enclosures used for raccoons should not be used for other species. All personnel involved with maintenance of raccoons should wear gloves, rubber boots, and wash with hot soapy water. A set of boots dedicated to the raccoon pens is a good idea, and/or a foot bath containing bleach and a scrub-brush should be used. Coveralls and clothing should be washed in near-boiling water with bleach added.

Any people having contact with raccoons or raccoon feces who develop visual or CNS disturbances should be examined immediately by a physician, who should be alerted to the possibility of B procyonis infection. Similarly, animals that have been in contact with raccoon feces and that develop CNS disease should be submitted to a diagnostic laboratory for necropsy examination with the suggestion that Baylisascaris migration may be involved.

Q: How are B procyonis infections diagnosed and treated in raccoons?

A: Baylisascaris procyonis infections are diagnosed in raccoons by finding eggs in the feces or by finding worms in feces or vomitus or in the small intestine at necropsy.^10,11 The eggs are similar in size and shape to those of other ascaridoid nematodes; they are rounded-oval, golden-brown, average 65.5 x 54.7 µm in size (range, 62.5 to 70.0 µm x 52.5 to 57.5 µm), and have a finely granulated surface (Fig 1).^2,11 If in the feces, B procyonis eggs can be readily detected by standard fecal flotation techniques.

In the wild, most raccoons probably become infected with B procyonis between 2 and 4 months old, although earlier infection is also possible.^b,f In young raccoons, B procyonis undergoes a prolonged developmental period of about 2 months in the intestine, during which time eggs will not be found in the feces.^10,b Such raccoons pose real problems for diagnosis and control, because they will repeatedly have false-negative results on fecal examination, then can suddenly begin shedding large numbers of eggs.

All captive raccoons should be regularly examined and treated for B procyonis. Newly acquired raccoons should be quarantined and treated immediately to prevent contamination of the environment with eggs.¹⁰ Initially, they should be treated weekly or biweekly for 3 to 4 treatments, despite negative fecal examination results, because they may be harboring developing worms. This is especially important for young raccoons, which should be treated for at least 2.5 months.^b Treatment can probably be started at about 7 to 8 weeks old.

Any of the common anthelmintics used to treat ascarids in dogs and cats, including piperazine, pyrantel pamoate, fenbendazole, mebendazole, and dichlorvos, should be effective against adult B procyonis in raccoons.^8,10,11,46 The efficacy of ivermectin is unknown, but judging from studies on Toxocara, dosages greater than 200 µg/kg of body weight may be necessary.⁴⁶ Liquid preparations such as pyrantel pamoate are generally easier to administer to raccoons than are tablets or capsules. If the drugs are mixed with food, the raccoons should be fed separately to ensure administration of the full dose. Daily administration of pyrantel salts prevented B procyonis infection in mice,⁴⁷ and could prove useful as a preventive for captive young raccoons. After anthelmintic treatment, feces should be examined for expelled roundworms which should be flushed down a toilet or destroyed by burning.^8,10

Q: What can be done to clean up areas that are contaminated with B procyonis eggs?

A: The eggs of B procyonis, like those of other ascaridoid nematodes, are resistant to environmental conditions.¹⁰ With adequate moisture and humidity, embryonated eggs will survive for years in the soil, such as in dirt-floored enclosures or in yards.^10,11 Under conditions of extreme dryness, such as in barn lofts or attics, dessication will kill the eggs,¹ but the amount of time needed is unknown. Some eggs must survive for weeks in such areas, because they reach infectivity and become a source of infection for animals.^3,10,11

Baylisascaris procyonis eggs are resistant to all common disinfectants, although certain solvent mixtures will kill them.^10,48 Thus, small areas of contamination on resistant surfaces can be treated with a 1:1 mixture of xylene:ethanol after most organic debris has been removed.^10,48 Treatment with sodium hypochlorite (bleach) will remove the outer protein coat; this makes the eggs nonadherent, but does not kill them.^2,8,46 Large areas of contaminated soil or concrete, and metal cages or enclosures are best decontaminated by thorough flaming, using a portable propane torch (flame gun) or other means.^10,49 Surface soil can be turned over and broken up several times with a rake or shovel and reflamed each time. It may also be desirable to remove and bury the surface soil from heavily contaminated areas, depending on the circumstances. Techniques have been developed for assessing the presence of B procyonis eggs in the soil and the effectiveness of their destruction or removal.⁵⁰ Autoclaving is effective and useful for decontaminating small cages and other items.¹⁰

Appropriate precautions should be taken when removing raccoon feces from contaminated attics, lofts, fireplaces, and other areas. One should wear old disposable clothes, disposable gloves, and a dust mask, such as those used by painters, to prevent the inhalation-ingestion of any eggs stirred up in dust. Dry feces and other contaminated material should be carefully removed and properly disposed of. Residual material can then be removed, using a vacuum cleaner that contains a disposable filter bag. Raccoon feces, contaminated hay, straw, or other materials should be burned, if possible, burned, or sent to a landfill. Raccoon feces and contaminated straw should never be used as fertilizer or mulch on vegetable or flower gardens. After removing accessible debris, contaminated fireplaces and chimneys can be decontaminated by building a roaring fire in the fireplace. Chimney caps and other means should be used to prevent raccoons from gaining access to human habitations and outbuildings.

Q: Are there any other species of Baylisascaris capable of causing human or animal disease?

A: Several other species of Baylisascaris, including B melis of badgers, B columnaris of skunks, B devosi of fishers and martens, and B transfuga of bears⁹ are potentially capable of causing human or animal disease if enough of the eggs are ingested. All 4 species undergo somatic migration in rodents, but with variations in growth, migratory behavior, and distribution of larvae to somatic and visceral tissues.^16-19,21,22 Similar to B procyonis, B melis and B columnaris larvae grow considerably and, in addition to entering other tissues and organs, enter the brain to cause cerebrospinal nematodiasis. Under experimental conditions, B melis caused clinical CNS disease in mice, ground squirrels, and rabbits, and B columnaris caused CNS disease in mice, hamsters, woodchucks, and rabbits.^{3,10,16,17,22,44,d} Larvae of both species can also enter the eyes to cause ocular larva migrans.^3,10,d In some animal species, B melis appears to be as pathogenic as B procyonis,^16,17,44,d whereas B columnaris is less pathogenic, requiring more infective eggs and more larvae in the brain to cause the same effects.^16,17,22,d Nonetheless naturally developing CNS disease caused by B columnaris has been reported in marmosets^e and is suspected in emus.³ The larvae of B devosi and B transfuga are smaller and/or grow more slowly, and are distributed primarily to the skeletal musculature and intestinal viscera, respectively, of mice.^19,21,22 Although a few larvae also entered the brain, CNS disease was absent or rare with B devosi and was not caused by B transfuga.^21,22

Clinical visceral larva migrans in human beings could be caused by any of these 4 Baylisascaris species if enough infective eggs were ingested. Baylisascaris melis and B columnaris, however would have a greater likelihood of causing clinical CNS disease or ocular larva migrans, because their migratory behavior more closely resembles that of B procyonis. Precautions similar to those described for raccoons and B procyonis should be taken around carnivores infected with these other Baylisascaris species, especially badgers infected with B melis and skunks infected with B columnaris.

Discussion

Raccoons are common North American mammals, and are well-adapted to coexistence with human beings in both urban and rural environments. Their numbers can be quite high in suburban residential areas, particularly in and around wooded parks.^51,j Because of their many engaging qualities, raccoons are often encouraged through feeding to frequent peoples' yards and homes. They are also frequently kept by people as pets and during wildlife rehabilitation. Consequently, the potential for human contact and infection with Baylisascaris is high. The actual risk of zoonotic infection with this parasite will depend on peoples' exposure to contaminated areas and their chance of ingesting infective eggs.

In general, the pet-owning public tends to be unaware of zoonotic diseases associated with pets and wildlife, except for rabies.⁸ The key to preventing human infections with Baylisascaris will be education of the public about this parasite and its potential health effects. Veterinarians are in an important position to do this, because of their contact with pet owners and other people interested in animals. By providing the public with accurate information, veterinarians can play a key role in the prevention of zoonotic diseases, including human infections caused by Baylisascaris.

Footnotes

(a) Lahr M, Medical Department, Fairview Training Center Jansen RD, Capitol Medical Laboratories, Salem, OR: Personal communication, 1986.

(b) Kazacos KR. Life cycle studies on Baylisascaris procyonis in raccoons (abstr), in Proceedings. 64th Annu Meet Conf Res Work Anim Dis 1983; 24.

(c) Nettles VF, Southeastern Cooperative Wildlife Disease Study. University of Georgia, Athens: Personal communication, 1985.

(d) Kazacos KR, Purdue University: Information on file.

(e) Huntress SL, Spraker T. Baylisascaris infection in the marmoset (abstr), in Proceedings. Annu Meet Am Assoc Zoo Vet 1985; 78.

(f) Schultz AL. A survey of parasites of the raccoon (Procyon lotor) in southeastern Michigan. MS Thesis, University of Michigan, Ann Arbor, 1962.

(g) Amundson T, Marcquenski S. Baylisascaris procyonis in Wisconsin raccoons. Wisconsin Department of Natural Resources, Madison, WI, 1986.

(h) Waring SC, Dingley DD, Texas Department of Health, Tyler: Personal communication, 1989.

(i) Little AS. Immunological comparison of larval Baylisascaris procyonis, Toxocara canis, and Ascaris suum using immunodiffusion. MS Thesis, Purdue University, West Lafayette, IN, 1987.

(j) Cooney TA. Environmental contamination with Baylisascaris procyonis in an urban park. MS Thesis, Purdue University West Lafayette. IN, 1989.

References

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2. 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.

3. Kazacos KR, Reed WM, Kazacos EA, et al. Fatal cerebrospinal disease caused by Baylisascaris procyonis in domestic rabbits. J Am Vet Med Assoc 1983; 183: 967-971.

4. Bowman DD. Diagnostic morphology of four larval ascaridoid nematodes that may cause visceral larva migrans: Toxascaris leonina, Baylisascaris procyonis, Lagochilascaris sprenti, and Hexametra leidyi. J Parasitol 1987; 73: 1198-1215.

5. Boyce WM, Asai DJ, Wilder JK, et al. Physicochemical characterization and monoclonal and polyclonal antibody recognition of Baylisascaris procyonis larval excretory-secretory antigens. J Parasitol 1989; 75:540-548.

6. Beaver PC. The nature of visceral larva migrans. J Parasitol 1969; 55:3-12.

7. Glickman LT, Schantz PM. Epidemiology and pathogenesis of zoonotic toxocariasis. Epidemiol Rev 1981; 3:230-250.

8. Schantz PM, Stehr-Green JK. Toxocaral larva migrans. J Am Vet Med Assoc 1988; 192:28-32.

9. Sprent JFA. Notes on Ascaris and Toxascaris, with a definition of Baylisascaris gen. nov. Parasitology 1968; 58:185-198.

10. Kazacos KR. Raccoon roundworms (Baylisascaris procyonis). A cause of animal and human disease. Bulletin No. 422. West Lafayette, IN: Purdue University Agricultural Experiment Station, 1983; 1-25.

11. Kazacos KR. Raccoon ascarids as a cause of larva migrans. Parasitol Today 1986; 2:253-255.

12. Huff DS, Neafie RC, Binder MJ, et al. The first fatal Baylisascaris infection in humans: an infant with eosinophilic meningoencephalitis. Pediatr Pathol 1984; 2:345-352.

13. Anderson DC, Greenwood R, Fishman M, et al. Acute infantile hemiplegia with cerebrospinal fluid eosinophilic pleocytosis; an unusual case of visceral larva migrans. J Pediatr 1975; 86:247-249.

14. Kazacos KR, Vestre WA, Kazacos EA. Raccoon ascarid larvae (Baylisascaris procyonis) as a cause of ocular larva migrans. Invest Ophthalmol Vis Sci 1984; 25:1177-1183.

15. Kazacos KR, Raymond LA, Kazacos EA, et al. The raccoon ascarid. A probable cause of human ocular larva migrans. Ophthalmology 1985; 92:1735-1743.

16. Tiner JD. Fatalities in rodents caused by larval Ascaris in the central nervous system. J Mammal 1953; 34:153-167.

17. Tiner JD. The migration, distribution in the brain, and growth of ascarid larvae in rodents. J Infect Dis 1953; 92:105-113.

18. Tiner JD. The fraction of Peromyscus leucopus fatalities caused by raccoon ascarid larvae. J Mammal 1954; 35:589-592.

19. Sprent JFA. On the migratory behavior of the larvae of various Ascaris species in white mice. II. Longevity of encapsulated larvae and their resistance to freezing and putrefaction. J Infect Dis 1953; 92:114-117.

20. Greve JH, O'Brien SE. Adult Baylisascaris infections in two dogs. Compan Anim Pract 1989; 19:41-43.

21. Sprent JFA. On the migratory behavior of the larvae of various Ascaris species in white mice. I. Distribution of larvae in tissues. J Infect Dis 1952; 90:165-176.

22. Sprent JFA. On the invasion of the central nervous system by nematodes. II. Invasion of the nervous system in ascariasis. Parasitology 1955; 45:41-55.

23. Boyce WM, Branstetter BA, Kazacos KR. In vitro culture of Baylisascaris procyonis and initial analysis of larval excretory-secretory antigens. Proc Helminthol Soc Wash 1988; 55:15-18.

24. Hamann KJ, Kephart GM, Kazacos KR, et al. Immunofluorescent localization of eosinophil granule major basic protein in fatal human cases of Baylisascaris procyonis infection. Am J Trop Med Hyg 1989; 40:291-297.

25. Kazacos KR, Kazacos EA. Experimental infection of domestic swine with Baylisascaris procyonis from raccoons. Am J Vet Res 1984; 45:1114-1121.

26. Dixon D, Reinhard GR, Kazacos KR, et al. Cerebrospinal nematodiasis in prairie dogs from a research facility. J Am Vet Med Assoc 1988; 193:251-253.

27. Thomas JS. Encephalomyelitis in a dog caused by Baylisascaris infection. Vet Pathol 1988; 25:94-95.

28. Medway W, Skand DL, Sarver CF. Neurologic signs in American porcupines (Erethizon dorsatum) infected with Baylisascaris and Toxoplasma. J Zoo Wildl Med 1989; 20:207-211.

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

30. Snyder DE, Fitzgerald PR. The relationship of Baylisascaris procyonis to Illinois raccoons (Procyon lotor). J Parasitol 1985; 71:596-598.

31. Ermer EM, Fodge JA. Occurrence of the raccoon roundworm in raccoons in western New York. NY Eish Game J 1986; 33:58-61.

32. Cole RA, Shoop WL. Helminths of the raccoon (Procyon lotor) in western Kentucky. J Parasitol 1987; 73:762-768.

33. Jones EJ, McGinnes BS. Distribution of adult Baylisascaris procyonis in raccoons from Virginia. J Parasitol 1983; 69:653.

34. Bafundo KW, Wilhelm WE, Kennedy ML. Geographic variation in helminth parasites from the digestive tract of Tennessee raccoons, Procyon lotor.J Parasitol 1980; 66:134-139.

35. Jordan HE, Hayes FA. Gastrointestinal helminths of raccoons (Procyon lotor) from Ossabaw Island, Georgia. J Parasitol 1959; 45:249-252.

36. Harkema R, Miller GC. Helminth parasites of the raccoon, Procyon lotor, in the southeastern United States. J Parasitol 1964; 50:60-66.

37. Johnson SA. Biology of the raccoon (Procyon lotor varius), Nelson and Goldman in Alabama. Bulletin No. 402. Auburn University, Al: Agricultural Experiment Station, Auburn University, 1970; 1-148.

38. Schaffer GD, Davidson WR, Nettles VF, et al. Helminth parasites of translocated raccoons (Procyon lotor) in the southeastern United States. J Wildl Dis 1981; 17:217-227.

39. McNeil CW, Krogsdale JT. Parasites of raccoons in southwest Washington. J Mammal 1953; 34:123-124.

40. Voge M. A list of nematode parasites from California mammals. Am Midl Nat 1956; 56:423-429.

41. Overstreet RM. Baylisascaris procyonis (Stefanski and Zarnowski,1951) from the kinkajou, Potosflavus, in Colombia. Proc Helminthol Soc Wash 1970; 37:192-195.

42. Stone WB. Intestinal obstruction in raccoons caused by the ascarid Baylisascaris procyonis. NY Fish Game J 1983; 30:117-118.

43. Carlson MS, Nielsen SW. Jejunal obstruction due to Baylisascaris procyonis in a raccoon. J Am Vet Med Assoc 1984; 185:1396-1397.

44. Boyce WM, Branstetter BA, Kazacos KR. Comparative analysis of larval excretory-secretory antigens of Baylisascaris procyonis, Toxocara canis and Ascaris suum by western blotting and enzyme immunoassay. Int J Parasitol 1988; 18:109-113.

45. Dade AW, Williams JF, Whitenack DL, et al. An epizootic of cerebral nematodiasis in rabbits due to Ascaris columnaris. Lab Anim Sci 1975; 25:65-69.

46. Georgi JR. Parasitology for veterinarians. 4th ed. Philadelphia: WB Saunders Co, 1985.

47. Lindquist WD. Baylisascaris procyonis for testing anthelmintics against migratory ascarids. Am J Vet Res 1978; 39:1868-1869.

48. Lehnert JP. New Ascaris laboratory ovicides. J Parasitol 1972; 58:364.

49. Pegg EJ. A new approach to the control of Toxocara canis and other parasitic ova on concrete-floored kennel runs. Br Vet J 1977; 133:427-431.

50. Kazacos KR. Improved method for recovering ascarid and other helminth eggs from soil associated with epizootics and during survey studies. Am J Vet Res 1983; 44:896-900.

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Figure 1--Baylisascaris procyonis egg from fresh raccoon feces. Bar = 20 5m.

Figure 2--Life cycle of Baylisascaris procyonis.

Addendum (1995)

Since the original report was published, a number of additional cases of fatal or severe neurologic disease (neural larva migrans, NLM) attributable to Baylisascaris in animals and human beings have been documented, all from North America. These include cases in porcupines,¹ chinchillas,² rabbits,³ guinea pigs,^4,5 dogs,⁶ ostriches,⁷ emus,^7-9 and children.¹⁰ We are also aware of additional unpublished cases involving children, lemurs, gibbons, spider monkeys, marmosets, kangaroos, eastern woodrats, peacocks, macaws, and other species (Kazacos KR, information on file). These cases involved animals kept as pets, in laboratory animal colonies, in zoo collections, raised for commercial production, and in the wild. In some instances, losses were extensive; for example, 100 chinchillas on 3 commercial ranches in Ontario² and 30 of 50 guinea pigs in a university breeding colony died because of NLM caused by baylisascariasis.⁴ In all instances, in which specific associations could be made, the parasite was identified as B procyonis from raccoons. Infection of these animals and children involved ingestion of infective B procyonis eggs in food, bedding, soil, or other materials contaminated with the feces of infected feral or pet raccoons.

Baylisascaris procyonis is presently gaining increased recognition and importance as a pathogen in commercial ratite production. As ratite farming has increased substantially, there has been a corresponding increase in the diagnosis of Baylisascaris-induced NLM in emus and ostriches in many parts of North America.^7-9 On ratite farms where B procyonis is a problem, infection appears to be a direct result of animal husbandry and management practices (ie, exposure of the birds to areas or materials contaminated by resident feral raccoons). Preventive measures as outlined in the original report continue to be important for use on such farms. In addition, we have been recommending extralabel use of pyrantel pamoate^a or pyrantel tartrate^b as a top-dressing or premix, respectively, in ratite feed, to prevent birds from becoming infected with B procyonis where it is an established problem.⁹

On the basis of present information, B procyonis from raccoons is considered to be the most common cause of clinical larva migrans disease in animals, and poses a significant health threat to human beings. Nearly 50 species of mammals and birds have now been documented to be susceptible to clinical NLM caused by larvae of this parasite. Groups at particular risk include rodents, lagomorphs, birds, primates, and Australian marsupials, although cases may also be seen in other species. Nearly all cases have been identified in North America, where raccoons and B procyonis are most common.

As a zoonosis, Baylisascaris-induced visceral (VLM) and neural larva migrans continues to be of concern, particularly for children; however, zoonotic ocular larva migrans (OLM) caused by Baylisascaris is actually more common and is being diagnosed with increasing frequency. Baylisascaris procyonis has been identified as the primary cause of the large nematode variant of the ocular syndrome, diffuse unilateral subacute neuroretinitis (DUSN).^11-13 This variant syndrome is a type of OLM in which visual loss appears to be a sequela to parasite-induced inflammation of the retina, associated vessels, and optic nerve head.¹² It may be caused by a number of nematode species, including Baylisascaris and Toxocara, as well as some other helminths.^11-14 Baylisascaris also has been incriminated in a number of human cases of OLM in which retinal migration tracks or posterior pole granulomas were the primary lesions seen.

Baylisascaris procyonis continues to be identified in raccoon populations in various areas of the United States, including recently in California¹² and Washington.³ It was also recently identified as a common parasite of wild raccoons in Germany, after identification of the first human of DUSN attributable to B procyonis in that country.¹³ Raccoons and B procyonis have apparently been present and spreading in Europe for decades. The parasite was responsible for a large episode of clinical NLM in captive-bred nutria in Germany in the late 1970s¹⁵ and is the most likely cause of a human case of OLM reported from Austria in the early 1960s.¹⁶ Baylisascaris procyonis was also identified recently in wild raccoons in Japan,¹⁷ but so far, no animal or human cases of larva migrans have been reported from there. As the worldwide distribution of B procyonis is further delineated, it can be anticipated that additional cases of animal and human disease attributable to this parasite will be reported from these other areas. As pointed out in the original report and reviewed elsewhere,¹⁸ additional species of Baylisascaris, related ascarids, and other helminths from a variety of lower animals are also potential causes of zoonotic larva migrans.

There is also growing evidence that young dogs can become infected with adult B procyonis worms in the small intestine, with subsequent shedding of eggs in their feces.^6,19 This is a cause for concern because it would increase the potential for animal and human transmission of this parasite, particularly in domestic environments where raccoon contact is not present or obvious. Veterinarians need to be aware of this possibility and to accurately diagnose and treat these patent infections in dogs, to prevent domestic contamination with B procyonis eggs. This can be accomplished through periodic fecal examination of dogs and use of anthelmintics to remove intestinal ascarids. Various anthelmintics used to treat intestinal Toxocara infections in dogs (eg, piperazine, fenbendazole, mebendazole, pyrantel, dichlorvos) would also be effective against B procyonis. Because there is no effective treatment for neural larva migrans caused by B procyonis, prevention of infection continues to be of utmost importance. Veterinarians will continue to have a key role in prevention of this infection in animals and human beings, providing accurate information concerning Baylisascaris to their clients and the general public.

Footnotes

(a)Strongid C, Pfizer, Lee's Summit, Mo.

(b)Banminth Medicated Premix-48, Pfizer, Lee's Summit, Mo.

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