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Human infections caused by the Raccoon roundworm, Baylisascaris procyonis
Clinical Microbiology Newsletter January 1,2002
Vol. 24, No. 1
Human Infections Caused by the Raccoon Roundworm, Buylisascaris procyonis William J. Murray, DVM, Associate Professor of Microbiology,
San Jest State University, San Jo&, CA
Abstract Raccoons are the natural host of the roundworm, Baylisascaris procyonis, a zoonotic nematode parasite capable of causing severe human ocular and neurologic disease. Although a rare human infection, baylisascariasis is increasingly being recognized as a significant public health problem, especially in young children less than 4 years old. Large numbers of raccoons are frequently found living in urban and suburban environments, where they thrive because of easily accessible food and shelter. Transmission of the parasite occurs through the inadvertent ingestion of B. procyonis eggs, which are shed in the feces of infected raccoons. Groups of raccoons typically defecate in common areas called latrines, where large numbers of environmentally resistant eggs accumulate. Once released in the intestinal tract, ‘B.procyonis larvae migrate extensively and aggressively in tissues, causing an intense eosinophilic infl a~ato~ reaction. The larvae have a noted tendency to invade the eye (causing ocular larva migrans [OLM], spinal cord, and brain (causing neural larva migrans BLM]). Infections in humans can be difficult to cot&-m, and diagnosis is typically arrived at by exclusion of other known causes of OLM and NLM. There is no effective cure for human infection. Steroids and anthelmintic agents are usually employed for symptomatic treatment , but their efficacy is controversial. Preventing the establishment of raccoon latrine sites in areas where humans live is of paramount public health importance.
Introduction For the majority of the public, the “masked bandit” appearance of the raccoon conjures up an image of an appealing, clever, and mischievous animal that symbolizes wildlife and the beauty of nature. Despite this appearance, raccoons are among a fast-growing list of problem wildlife nationwide ( l-3). There are numerous reasons for this, including a reduction in trapping and hunting activities, human movement into formerly rural areas by housing expansion, lack of comprehensive wildlife control programs in many areas. and feeding of wildlife by wellintentioned but seriously misinformed and misguided individuals. All animals, including pets, can harbor zoonotic pathogens, but the case of Mnifing nddress: Department of Biological Sciences, San Jo.& State University, San Jo.@, CA 9~i92-010~. Phone: 408-9244856. Fax: 408-924-4840. E-mail: mrlrra.v(~emai(.sjslr.edu.
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raccoons is unusual. Few other species of wildlife have the propensity to interact with and live freely in such close association with humans. Raccoons harbor a number of zoonotic parasites, including the common raccoon roundworm, B. procyonis. Human disease caused by B. procyonis is among the most severe of all known helminthic zoonoses. Even with treatment, human baylisascariasis carries a universally poor prognosis, often resulting in permanent neurologic damage, blindness, or death. Although baylisascariasis is a rare human infection, the growing number of cases reported in the United States suggests strongly that physicians and clinical laboratory technologists should be aware of the possibility of infection with this parasite (45).
North America wherever raccoons are found (5). Other species of Baylisascaris are found in various other North American mammals. Their zoonotic significance is not known but presumably is possible. B. procyonis biologically and morphologically resembles the intestinal roundworm (Toxocara canis) of dogs (6) (Fig. 1). In its natural host, the parasite causes no disease unless there is an unusually heavy infestation in juveniles. Adult female worms in the small intestine of raccoons collectively produce millions of eggs per day, which are shed in the feces of infected raccoons (7). Depending on environmental conditions, the
Life Cycle and Biology of B. proqonis
In This Issue
Raccoons are the natural host of B. procyonis. Except for the deep south, the parasite is common throughout
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eggs continue to develop, eventually resulting in formation of an infective larva within the egg in about 2 to 4 weeks. Like other ascarid eggs, the eggs of B. procyonis are very resistant to degradation in the environment and can survive for years under appropriate conditions (8). Like most other ascarids, B. procyonis has a typical direct life cycle; that is, it has no obligatory intermediate host. Raccoons become infected in one of two ways (Fig. 2). Generally, young raccoons become infected by ingesting the eggs during feeding and grooming activities. Alternatively, a large variety of other mammals and birds (in which the parasite often causes severe central nervous system [CNS] disease) can become infected with B. procyonis, and adult raccoons can become infected by ingesting the larva-containing flesh of these affected animals (5). &mans become infected with B. procyonis just as these other animals do and become aberrant intermediate hosts following inadvertent ingestion of eggs containing infective larvae.
Figure /. Ad& B. procyonis nematodes remwed,from rhe small itllestine of a raccoon. Female on lefr; male shown on r&hr. Adult,females are ahow 24 cm long, whereas the smallei males are about I2 cm long.
Transmission and Epidemiology off?. pracyonis Of great importance to understanding the transmission of B. procyonis to non-natural hosts is the behavior of raccoons. Groups of raccoons typically defecate in common areas called latrines. Although the motivation for this behavior is uncertain, it is thought that it has to do with territorial marking or group socialization. In rural or wilderness areas, raccoon latrines are typically found off the ground in downed timber, rocky outcroppings, and tree cavities (9). In urban and suburban environments, latrines are commonly found directly on the ground, on lawns. at the bases of trees, along and on tops of fences, on roofs, in outbuildings, on stored firewood, and in other locations (Fig. 3). Womeowners are frequently
unaware that there are large latrines on roofs or elsewhere on their property, and thus, the risk of exposure to raccoon feces is increased. Despite claims by some that the placement of moth balls, cayenne pepper, and liquid ammonia (or other repellents such as “bobcat,” “coyote,” or “mountain lion” urine sold in some pet or garden stores) are effective deterrents to latrining behavior, there is no evidence that these work under any circumstances. The long-term viability of B. procyonis eggs and the tremendous numbers of them that are deposited in the environment by raccoons are key factors in understanding how the parasite is transmitted. On average, infected
raccoons shed over 20,000 eggs per gram of feces and have been reported to produce as many as 256,700 eggs per gram of feces (7). Thus, both actively used and abandoned latrines become focal accumulations of large numbers of the environmentally resistant eggs, which remain viable, and thus infective, for years. The eggs also possess a sticky surface coating that makes them adherent to objects they come into contact with, including human hands, toys, garden tools, and the like. The eggs can be inactivated only by incineration or soaking with volatile solvents. such as mixtures of xylene and acetone; the latter method obviously is impractical for use on latrines. Mixtures of boiling
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water and bleach are sometimes also recommended, especially for the decontamination of roofs, wooden patios, and decks, but it is important to realize that these methods may only remove the outer sticky coating of the egg, leaving a viable larva still protected within. Nonetheless, such action will reduce infectivity. Populations of raccoons are substantially greater in urban and suburban areas than in rural or wilderness habitats (3,10,1 I). This is due primarily to abundant sources of food, water, and shelter afforded by areas of human habitation. Humans frequently exacerbate this situation further by inadvertently leaving pet food outdoors or, in some cases, purposefully feeding raccoons, usually with large amounts of dog food. A substantial risk factor for human infection with B. procyonis is the presence of raccoon latrines around areas of human habitation. Transmission occurs in humans via geophagia or pica. Young children (less than 4 years old) are at greatest risk of infection because of their propensity to readily explore the environment, handle and mouth objects they find interesting, and their poor hygienic habits. Most baylisascariasis cases reported in the iitera~re involve young children. In those cases in which a field investigation was done to try to locate the source of infection, evidence of raccoon activity, latrines, or raccoon feces were found in areas that the children were known to frequent. Incidents of older children or adults becoming infected typically involve developmentally delayed individuals with pica. Seven cases of severe neurologic disease or death caused by B. procyonis have been reported in the medical literature (10). Other suspect cases are known or are currently being investigated. The prevalence of sub-clinical cases is unknown, but these are likely to occur given the close association of raccoons with areas of human habitation. Also of great concern are reports of dogs developing patent B. procyonis infections, which results in adult worms shedding viable eggs in the dog’s feces (7,12). Presumably, dogs become infected either by consuming infected small animals or ingesting raccoon feces at latrine sites. The prevalence of canine 3. procyonis infections is
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1 I. in
EQgS s?led in feces
rei \ Vi-30 days to infective stag0 in environment Infected animals c.onsllmed by raccoon
Eggs hatch
\ CNS Disease IngestIon by yo6ng raccoons
Leon by other vedbrate hosts, rodents, bird& 4tc.
Larva migrans CNSdisease
Cgure 2. Life cycle of B. procyonis. (I) Ingestion of infective-stage eggs by young raccoons occurs as a consequence of their close association with infected adults. The eggs hatch in the intestinal lumen, releasing Iurvae that continue to develop as they migrate in the wall of the intestine. They then re-enter the lumen and develop into mating adults; the females begin sheddi~gfertilized eggs. This entire process requires about 60 days f?om the time eggs are ingested, !n the raccoon, there is no e.rtensive somatic larval migration that is typical qf other ascarid l$e cycles. (2) White an intermediate host is not ~q~lired,~~r B. procyonis to complete its l$e cycle, older raccoons typically become infected by consuming any one qf a wide variety of host animals that become infected throaghfeedit~g activities at iatrine sites. The resulting visceral migration by B. procyonis larvae in the somatic tissues of intermediate hosts freql~ently leads to nearal larva migrans and severe central nervous system disease, making them easy prey forforaging raccoons. Once the affected animal b,flesh is irlgested by the raccoon, the infective larvae encysted in the host3 tissues are w/eased in the adult raccoon b intestine, where they develop into adults in abolrf 35 da
unknown. Nonetheless, these reports suggest that given the ubiquitous nature of dog feces in the environment, the potential for exposure to B. procyonis would be increased, especially for children who are very likely to have close contact with pet dogs.
Pathogenesis of Bay~isaseariasis is similar to most other parasites in that the parasite
B. procyonis
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causes no clinical disease in its natural host unless there is an unusually heavy infestation in juvenile raccoons. However, if infective-stage eggs are ingested by non-raccoon hosts, including humans, the eggs hatch in the intestinal tract, releasing the immature larvae, which instead of developing into adults as they do in raccoons, begin to migrate extensively through body tissues, causing
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visceral larva migrans (VLM). The migrating larvae produce damage to tissues directly and by an intense eosinophilic inflammatory reaction along the tract of migration. Unlike the larvae of other helminths that cause VLM (such as I: canis), the larvae of B. pvocyanis exhibit very aggressive tissue migration behavior. They continue to grow and molt during their migration, becoming up to 2 mm long, and do not die readily (5). Eventually, the migrating larvae become encapsulated in eosinophilic granulomas but remain viable. For reasons that are still not entirely clear, the larvae of R. procyonis also have a noted tendency to invade the spinal cord and brain (causing NLM) and the eye (causing OLM). Whereas experimental infections in animals have shown that only a small percentage (5 to 7%) of larvae actually enter the CNS, the damage
they cause is extensive
(13).
Factors influencing the severity of CNS disease in humans (and other animals) include (i) the number of eggs ingested, (ii) the extent and pattern of larva migration in tissues, (iii) the severity of inflammation caused by migrating larvae, (iv) the amount of tissue necrosis, and perhaps (v) how soon after infection treatment is given (see below). Clinical signs of infection may develop as soon as 2 to 4 weeks following ingestion of eggs containing infective larvae and vary depending on the factors mentioned above. Symptoms of baylisascariasis range from clinically inapparent to varying degrees of mild CNS dystinction to signs of severe neurologic deficits, paralysis, coma, blindness, and death (7,lO). Ingestion of large numbers of B. procyonis eggs may produce rapidly fatal NLM. Another factor contributing
to severity of disease is the fact that infection with B. procyonis is often not suspected until late in the diagnostic evaluation of a patient, as the larvae continue to migrate unimpeded in body tissues. Migrating larvae eventually become encapsulated in eosinophilic granulomas but remain viable in the tissues for extended periods (4). Despite treatment, progressive neurologic deterioration often continues. The prognosis for patients with B. procyonis NLM is poor.
Diagnosis of Baylisascariasis in Humans Because of the severe nature and often fulminant course of human infection with B. procyonis, it is important that clinical laboratory personnel be aware of this zoonotic disease so as to properly advise physicians of available diagnostic tests. Humans are dead-end
Figure 3. Typical raccoon latrines found in ciose association with human dwellings. (A) Latrine directly on the ground in a suburban yard adjacent to a stack offirewood. Note evidence of a varied diet, which in this case includes a lot ofpetfood. (6} Latrine at the base of a tree stump in a city park. (C) Large latrine on the roof of a suburban home. The action of weather washes the decomposing feces directly #the roof and dorvn gutters, where B. procyonis eggs can contaminate the surrounding area, including children k tqvs, which was the case at this ho&e. (17) A latrine on the top ofa stone fence in a backyard. Note e-in. ruler in the foreground.
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hosts for B. procyonis. Thus, it is important to recognize that B. procyonis eggs or larvae cannot be found in human stool specimens. Therefore, physicians should be advised that ordering ova and parasite (“0 & P”) examinations of a patient’s stool are not useful, although such examination may reveal the presence of human parasites unrelated to the patient’s illness. Results obtained from complete blood count and cerebrospinal fluid (CSF) examinations are usually consistent with a parasitic infection but are non-specific. Peripheral blood and CSF eosinophilia are common but may not be profound (10). It is generally recognized that eosinophilic pleocytosis in the CSF in combination with peripheral blood eosinophilia in patients with progressive neurologic deficits is characteristic of baylisascariasis but is not pathognomonic (5,13). The other major cause of larva migrans in humans, I: canis, can generally be excluded by negative serologic results (4,14). Infections in humans can be difficult to confirm. Diagnosis is typically arrived at by exclusion of other known causes of VLM, OLM, and NLM. The demonstration of characteristic B. proqonis larvae in tissue biopsy specimens is considered to be the “gold standard’ of diagnosis (Fig. 4). However, permission to perform a biopsy (particularly one of the brain) is frequently difficult to obtain, and most consider such an invasive procedure unwarranted (4,10). Even when permission to biopsy is granted, removing tissue from sites where the larvae actually are is problematic, especially if the method used is fine-needle aspiration. In cases of OLM, ophthalmologic examinations revealing chorioretinal lesions, larval tracks, or migrating larvae can support a diagnosis of baylisascariasis (4). This is particularly true if larvae themselves are seen, because of their large size (up to five times larger) relative to that of 7: canis, the most common cause of OLM in humans ( 14,15). Abnormal ocular findings are often the first clue to a helminthic cause for clinical signs in a patient (4,10,14). Furthermore, the larvae of B. procyonis are now recognized as a cause of a condition known as diffuse unilateral subacute neuroretinitis (DUSN) in humans (7:16). DUSN is characterized by unilateral vision loss that presumably Clinml
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Figure 4. Human brain biopsy. Hematoxylin and eosin stain, x200. This fine-needle aspirate was removedfrom the brain ofan adolescent boy with severe central nervous system disease. A B. procyonis larva is clearly visible in cross section (at midbody level) at the edge of the tissue section. B. procyonis larvae can be easily distinguishedfrom the larvae of Ascaris and Toxocara spp., which may also cause larva migrans. In addition to the large size (approximately 70 ,um in diameter) of the larva, conspicuous features are the prominent lateral alae on opposite sides of the cuticle and large excretoty columns adjacent to the centrally located intestinal canal. (Photomicrograph courtesy of DI: Lawrence R. Ash, UCLA School of Public Health).
results from inflammation caused by wandering of the various species of juvenile nematodes in the retina and associated ocular tissues. It is also important to point out that baylisascariasis is not confined to North America; a case of DUSN caused by B. procyonis has been reported from Germany (17). Neuroimaging methods, such as computed tomography scans and magnetic resonance imaging, are also helpful in supporting a diagnosis. In cases where such imaging has been obtained, evidence of ventricular dilatation, periventricular enhancement in contrast studies, and white matter abnormalities are prominent features in infected individuals (7,10,18). Various serologic methods have been developed for baylisascariasis but are not in routine use in clinical laboratories. Serologic testing is currently available on a limited basis from the Department of Veterinary Pathobiology at Purdue University (7). A history of patient exposure to raccoons is obviously helpful, but in many instances, especially in cases of OLM, no patient contact with raccoons or their feces is reported. Nonetheless, additional 8’) 2002 Elsevier Science Inc.
diagnostic support can be obtained by visiting sites suspected to be locations where the patient may have become exposed and searching for evidence of the source of exposure. Careful questioning of parents of young children will often provide a clue as to where their child may have been exposed. Even when a historical report of such contact is obtained, it is important to recall that the vast majority of people cannot correctly identify a raccoon latrine site (or raccoon feces). Often the assistance of wildlife biologists from federal or state agencies or university researchers familiar with the behavior of raccoons and the biology of B. procyonis can be sought. Examination of raccoon stool specimens or soil samples brought to the laboratory can be accomplished using modified flotation assays (19,20). Providing the person collecting the scat samples can confirm they are from a raccoon, such an examination may be warranted to help confirm a diagnosis of baylisascariasis. This would be helpful to determine whether a patient could have been exposed to raccoon feces containing B. procyonis eggs. The 0 I96-4399!00
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examination of samples collected in the field is best accomplished at reference or research laboratories that are skilled in the examination of fecal specimens obtained from veterinary and witdlife sources. The sheer number of different types of eggs. lamae, and artifacts typically found in these specimens may o\~envhelm the technologist accustomed to the examination of human fecal specimens. R. JW~,IWZ~.Seggs have typical ascarid features (Fig. 5). However, because of similarities with other ascarid eggs of domesticated animals and wildlife. it is of paramount importance that specimens be examined by those with the requisite expertise to conclusively identify B. pwqmis eggs. Given the pre\.alence and geographic distribution of the parasite in raccoons, it is best to consider any sample of raccoon feces positive for 3. jmqmis eggs until proven otherwise by microscopic examination.
Treatment of Baylisascariasis There is no effective cure for human infection. Steroids and anthelmintic agents are usually employed for symptomatic treatment, but the efficacy of this therapy is controversial. In any event, no treatment described to date has altered the prognosis (7, IO). A contributing factor to this lack of success is no doubt the fact that the larvae continue to migrate unimpeded in body tissues because infection with B. proqmis is not suspected until late in the course of the disease. Various anthelmintic agents have been employed for treatment. Currently the drug of choice is albendazole, because it has been shown to have good distribution into brain and CSF. especially when used in conjunction with dexamethasone (10.2 1,22). Experimental B. procyonis infections in mice have demonstrated that albendazole and another anthelmintic. diethylcarbamazine, were of prophylactic value in preventing CNS disease when administered 1 to 10 days post-infection ( 10). Furthermore, in several cases when children were observed ingesting raccoon feces, the prompt administration of albendazole is thought to have prevented development of cfinical symptoms of baylisascariasis (7). In light of these facts, the current recommendation is that whenever infection with B. proc:vonis is suspected, treat-
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Figure 5. B. procyonis eggs. Microscopic examination (magnification. X 40) i$twccooi~,feces ,following modijTed_flotation of a fecal specimen,fowd in a latrine in a large plnyKrolrnd sad box in A suburban park. Lej, an embvonated, but non-infective. egg. Right, an infectilae egg containing a.fitlly,formed larva that is clearly i+sible within. B. procyonis eggs can be d@erell~i~te~~~?n other ascarid eggs c~rnrnotl~~,~~l~ti~ in the e~~~,i~~rne~t,strch as those qf Toxocara. Ascaris, and Toxascaris spp., by expert e.~amiFlatiotl. &-&fly. B. procyonis eggs are ellip‘so~~. appro.~itnate~y 7.5 x 60 pm in size, with a dark brawn, granular surface.
ment should be started immediately while diagnostic tests and field investigations to document a source of exposure are carried out. The only successful treatment for human baylisascariasis has been in cases of OLM in which laser photocoagulation was employed in conjunction with treatment with co~icosteroids (7).
Summary Baylisascariasis is a rare human infection. Despite the rarity of infection, factors that cannot be over-emphasized are the severity of the disease, its inability to be cured, and its potentially fatal outcome, especially in very young children, who are most likely to become infected. Transmission of the parasite occurs through the inadvertent ingestion of B. procyonis eggs, which are shed in the feces of infected raccoons. In any area where raccoons are found, the probability of infection with B. procyonis is likely, and any raccoon should be considered infected unless proven otherwise. Also of concern are reports of patent B. procyonis infections in dogs, which could greatly amplify the likelihood of human exposure to this parasite. B. procyonis infections in humans are difficult to confirm. Because of delays in diagnosis and treatment, most cases present after there has been extensive CNS damage. In the absence
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of a definitive diagnosis (i.e., demonstration of larvae in tissue biopsy specimens or autopsy results), diagnosis in humans is arrived at by a combination of clinical symptoms, patient history, neuroimaging results, documentation of a source of exposure to raccoon feces, and serologic results. Raccoon latrine sites are frequently implicated as the source of human infections. The possibility of inadvertent infection increases with exposure to raccoon feces, which in turn is related to the number of raccoons living in a given area. Under no circumstances should raccoons be purposefully (or inadvertently) fed or otherwise encouraged to take up residence near areas of human habitation. Because the density of raccoon latrines in a given area is proportional to the raccoon population living there, public health officials, physicians, and others involved in health care should be aware of the increased potential for human infection when raccoon densities are high. Natural dispersal of the eggs from latrine sites occurs from the action of weather and other forces, leading to long-term contamination of large areas. Preventing the establis~ent of raccoon latrine sites around areas of human habitation and recreational use is of paramount public health importance.
Acknowledgment
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I thank Darcy Levee for her assistance in preparation of the manuscript.
I. Sharp. D. 2000. Creature discomfort is call to battle in suburbs. USA Today, Aug. 3O:Sect. 4A. 2. McCombie, B. 1999. Those dirty raccoons: how a once revered fur bearer became reduced to cockroach status, Field and Stream, December: 8. -3 Roussere, G.P. et al. 2000. An epidemiologic survey of raccoon (frocyffn lotor) latrine sites and the prevalence of raccoon roundworn (~~~/~sffscarjs procyotris) eggs in Pa&tic Grove and Cannel, CA. Y-4. p.683. In Abstr. 100th Gen. Meet. Am. Sot. Microbial. ASM Press, Washington, DC. 4. Kazacos, K.R. 1997. Visceral, ocular, and neural larva migrans, p. 1459-1473. 1/r D.H. Connor et al. (ed.), Pathology of infectious diseases, vol. II. Appleton & Lange, Stamford, CT. 5. Kazacos. K.R. and W.M. Boyce. 1995. Bqdisnscaris larva migrans, p. 20-30. I/I Zoonosis updates from the Journal of the American Veterinary Medical Association, 2nd ed. American Veterinary Medical Association, S~haumburg, IL. 6. Averbeck, G.A. et al. 1995. Differentiation of &y/isascaris species, Toxocaru carzis and To.vascaris leonina infections in dogs. Compendium of Continuing
Education of the Practicing Veterinarian 17:475-5 11. 7. Kazacos, K.R. 2000. Protecting children from helminthic zoonoses. Contemp. Pediatr. I7(Suppl): l-24. 8. Roberts, L.S. and J. Janovy. 1996. Nematodes: ascardida, intestinal iarge roundwo~s, p. 4 19-43 1. In Gerald D. Schmidt and Larry S. Roberts’ Foundations of parasitology, 5th ed. W.C. Brown, Dubuque, IA. 9. Page, L.K. and R.K. Swihart. 1998. Raccoon latrine structure and its potential role in transmission of Baylisascaris procyonis to vertebrates. Am. Midland Naturalist 140: 180-l 85. IO. Park. S.Y. et al. 2000. Raccoon roundworm (Baylisascaris procyonis) encephalitis: case report and field investigation. Pediatrics 106: l-5. II. Riley, S.P.D., J. Hadidian, and D.A. Manski. 1998. Population density, survival and rabies in raccoons in an urban national park. Can. J. Zool. 16: 11.531164.
migrans. Vet. Clin. N. Am. 17:39-53. 15. Kazacos, K.R. 1991. Visceral and ocular larva migrans. Sem. Vet. Med. Surg. 6:227-235. 16. Goldberg, M.A. et al. 1993. Diffuse unilateral subacute neuroretinitis: morphometric, serologic and epid~iologic support for ~ay~is~~~r~s as a causative agent. Ophthalmology 100: 1695- I70 1. 17. Kuchle, M. et al. 1993. Diffuse unilateral subacute neuroretinitis syndrome in a German most likely caused by the raccoon roundworm, Bayhascaris procyonis. Graefe’s Arch. Clin. Exp. Ophthalmol. 23 1:48-5I. 18. Rowley, H.A. et al. 2000. Radiologicpathologic findings in raccoon roundworm (Baylisascaris procyonis) encephalitis. Am. J. Neuroradiol. 21:415-420. 19. Sloss, M.W., R.L. Kemp, and A.M. Zajac. 1994. Veterinary clinical parasitology, 6th ed., p. 3-8. Iowa State University Press, Ames, IA.
12. Greve, J.H. and S.E. O’Brien. 1989. Adult Baylisascaris infections in two dogs. Companion Anim. Pratt. l9:4 1” 43.
20. Kazacos, K.R. 1983. Improved method for recovering ascarid and other helminth eggs from soil associated with epizootics and during survey studies. Am. J. Vet. Res. 44:896-900.
13. Kazacos, K.R. 1996. Baylisascariasis, p. 716-7 17. In A.M. Rudolph (ed.), Rudolph’s Pediatrics, 20th ed. Appleton & Lange, Stamford, CT.
21. de Silva, N., H. Guyatt, and D. Bundy. 1997. Anthelminti~s: a compamtive review of their clinical pharmacology. Drugs 53:769-788.
14. Glickman, LT. and F.S. Shofer. 1987. Zoonotic visceral and ocular larva
22. Venkatesan, P. 1998. Albendazole. J. Antimicrob. Chemother. 4 I : l45- 147.
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Vol. 24, No. 1
Human Infections Caused by the Raccoon Roundworm, Buylisascaris procyonis William J. Murray, DVM, Associate Professor of Microbiology,
San Jest State University, San Jo&, CA
Abstract Raccoons are the natural host of the roundworm, Baylisascaris procyonis, a zoonotic nematode parasite capable of causing severe human ocular and neurologic disease. Although a rare human infection, baylisascariasis is increasingly being recognized as a significant public health problem, especially in young children less than 4 years old. Large numbers of raccoons are frequently found living in urban and suburban environments, where they thrive because of easily accessible food and shelter. Transmission of the parasite occurs through the inadvertent ingestion of B. procyonis eggs, which are shed in the feces of infected raccoons. Groups of raccoons typically defecate in common areas called latrines, where large numbers of environmentally resistant eggs accumulate. Once released in the intestinal tract, ‘B.procyonis larvae migrate extensively and aggressively in tissues, causing an intense eosinophilic infl a~ato~ reaction. The larvae have a noted tendency to invade the eye (causing ocular larva migrans [OLM], spinal cord, and brain (causing neural larva migrans BLM]). Infections in humans can be difficult to cot&-m, and diagnosis is typically arrived at by exclusion of other known causes of OLM and NLM. There is no effective cure for human infection. Steroids and anthelmintic agents are usually employed for symptomatic treatment , but their efficacy is controversial. Preventing the establishment of raccoon latrine sites in areas where humans live is of paramount public health importance.
Introduction For the majority of the public, the “masked bandit” appearance of the raccoon conjures up an image of an appealing, clever, and mischievous animal that symbolizes wildlife and the beauty of nature. Despite this appearance, raccoons are among a fast-growing list of problem wildlife nationwide ( l-3). There are numerous reasons for this, including a reduction in trapping and hunting activities, human movement into formerly rural areas by housing expansion, lack of comprehensive wildlife control programs in many areas. and feeding of wildlife by wellintentioned but seriously misinformed and misguided individuals. All animals, including pets, can harbor zoonotic pathogens, but the case of Mnifing nddress: Department of Biological Sciences, San Jo.& State University, San Jo.@, CA 9~i92-010~. Phone: 408-9244856. Fax: 408-924-4840. E-mail: mrlrra.v(~emai(.sjslr.edu.
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raccoons is unusual. Few other species of wildlife have the propensity to interact with and live freely in such close association with humans. Raccoons harbor a number of zoonotic parasites, including the common raccoon roundworm, B. procyonis. Human disease caused by B. procyonis is among the most severe of all known helminthic zoonoses. Even with treatment, human baylisascariasis carries a universally poor prognosis, often resulting in permanent neurologic damage, blindness, or death. Although baylisascariasis is a rare human infection, the growing number of cases reported in the United States suggests strongly that physicians and clinical laboratory technologists should be aware of the possibility of infection with this parasite (45).
North America wherever raccoons are found (5). Other species of Baylisascaris are found in various other North American mammals. Their zoonotic significance is not known but presumably is possible. B. procyonis biologically and morphologically resembles the intestinal roundworm (Toxocara canis) of dogs (6) (Fig. 1). In its natural host, the parasite causes no disease unless there is an unusually heavy infestation in juveniles. Adult female worms in the small intestine of raccoons collectively produce millions of eggs per day, which are shed in the feces of infected raccoons (7). Depending on environmental conditions, the
Life Cycle and Biology of B. proqonis
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Raccoons are the natural host of B. procyonis. Except for the deep south, the parasite is common throughout
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eggs continue to develop, eventually resulting in formation of an infective larva within the egg in about 2 to 4 weeks. Like other ascarid eggs, the eggs of B. procyonis are very resistant to degradation in the environment and can survive for years under appropriate conditions (8). Like most other ascarids, B. procyonis has a typical direct life cycle; that is, it has no obligatory intermediate host. Raccoons become infected in one of two ways (Fig. 2). Generally, young raccoons become infected by ingesting the eggs during feeding and grooming activities. Alternatively, a large variety of other mammals and birds (in which the parasite often causes severe central nervous system [CNS] disease) can become infected with B. procyonis, and adult raccoons can become infected by ingesting the larva-containing flesh of these affected animals (5). &mans become infected with B. procyonis just as these other animals do and become aberrant intermediate hosts following inadvertent ingestion of eggs containing infective larvae.
Figure /. Ad& B. procyonis nematodes remwed,from rhe small itllestine of a raccoon. Female on lefr; male shown on r&hr. Adult,females are ahow 24 cm long, whereas the smallei males are about I2 cm long.
Transmission and Epidemiology off?. pracyonis Of great importance to understanding the transmission of B. procyonis to non-natural hosts is the behavior of raccoons. Groups of raccoons typically defecate in common areas called latrines. Although the motivation for this behavior is uncertain, it is thought that it has to do with territorial marking or group socialization. In rural or wilderness areas, raccoon latrines are typically found off the ground in downed timber, rocky outcroppings, and tree cavities (9). In urban and suburban environments, latrines are commonly found directly on the ground, on lawns. at the bases of trees, along and on tops of fences, on roofs, in outbuildings, on stored firewood, and in other locations (Fig. 3). Womeowners are frequently
unaware that there are large latrines on roofs or elsewhere on their property, and thus, the risk of exposure to raccoon feces is increased. Despite claims by some that the placement of moth balls, cayenne pepper, and liquid ammonia (or other repellents such as “bobcat,” “coyote,” or “mountain lion” urine sold in some pet or garden stores) are effective deterrents to latrining behavior, there is no evidence that these work under any circumstances. The long-term viability of B. procyonis eggs and the tremendous numbers of them that are deposited in the environment by raccoons are key factors in understanding how the parasite is transmitted. On average, infected
raccoons shed over 20,000 eggs per gram of feces and have been reported to produce as many as 256,700 eggs per gram of feces (7). Thus, both actively used and abandoned latrines become focal accumulations of large numbers of the environmentally resistant eggs, which remain viable, and thus infective, for years. The eggs also possess a sticky surface coating that makes them adherent to objects they come into contact with, including human hands, toys, garden tools, and the like. The eggs can be inactivated only by incineration or soaking with volatile solvents. such as mixtures of xylene and acetone; the latter method obviously is impractical for use on latrines. Mixtures of boiling
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water and bleach are sometimes also recommended, especially for the decontamination of roofs, wooden patios, and decks, but it is important to realize that these methods may only remove the outer sticky coating of the egg, leaving a viable larva still protected within. Nonetheless, such action will reduce infectivity. Populations of raccoons are substantially greater in urban and suburban areas than in rural or wilderness habitats (3,10,1 I). This is due primarily to abundant sources of food, water, and shelter afforded by areas of human habitation. Humans frequently exacerbate this situation further by inadvertently leaving pet food outdoors or, in some cases, purposefully feeding raccoons, usually with large amounts of dog food. A substantial risk factor for human infection with B. procyonis is the presence of raccoon latrines around areas of human habitation. Transmission occurs in humans via geophagia or pica. Young children (less than 4 years old) are at greatest risk of infection because of their propensity to readily explore the environment, handle and mouth objects they find interesting, and their poor hygienic habits. Most baylisascariasis cases reported in the iitera~re involve young children. In those cases in which a field investigation was done to try to locate the source of infection, evidence of raccoon activity, latrines, or raccoon feces were found in areas that the children were known to frequent. Incidents of older children or adults becoming infected typically involve developmentally delayed individuals with pica. Seven cases of severe neurologic disease or death caused by B. procyonis have been reported in the medical literature (10). Other suspect cases are known or are currently being investigated. The prevalence of sub-clinical cases is unknown, but these are likely to occur given the close association of raccoons with areas of human habitation. Also of great concern are reports of dogs developing patent B. procyonis infections, which results in adult worms shedding viable eggs in the dog’s feces (7,12). Presumably, dogs become infected either by consuming infected small animals or ingesting raccoon feces at latrine sites. The prevalence of canine 3. procyonis infections is
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EQgS s?led in feces
rei \ Vi-30 days to infective stag0 in environment Infected animals c.onsllmed by raccoon
Eggs hatch
\ CNS Disease IngestIon by yo6ng raccoons
Leon by other vedbrate hosts, rodents, bird& 4tc.
Larva migrans CNSdisease
Cgure 2. Life cycle of B. procyonis. (I) Ingestion of infective-stage eggs by young raccoons occurs as a consequence of their close association with infected adults. The eggs hatch in the intestinal lumen, releasing Iurvae that continue to develop as they migrate in the wall of the intestine. They then re-enter the lumen and develop into mating adults; the females begin sheddi~gfertilized eggs. This entire process requires about 60 days f?om the time eggs are ingested, !n the raccoon, there is no e.rtensive somatic larval migration that is typical qf other ascarid l$e cycles. (2) White an intermediate host is not ~q~lired,~~r B. procyonis to complete its l$e cycle, older raccoons typically become infected by consuming any one qf a wide variety of host animals that become infected throaghfeedit~g activities at iatrine sites. The resulting visceral migration by B. procyonis larvae in the somatic tissues of intermediate hosts freql~ently leads to nearal larva migrans and severe central nervous system disease, making them easy prey forforaging raccoons. Once the affected animal b,flesh is irlgested by the raccoon, the infective larvae encysted in the host3 tissues are w/eased in the adult raccoon b intestine, where they develop into adults in abolrf 35 da
unknown. Nonetheless, these reports suggest that given the ubiquitous nature of dog feces in the environment, the potential for exposure to B. procyonis would be increased, especially for children who are very likely to have close contact with pet dogs.
Pathogenesis of Bay~isaseariasis is similar to most other parasites in that the parasite
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causes no clinical disease in its natural host unless there is an unusually heavy infestation in juvenile raccoons. However, if infective-stage eggs are ingested by non-raccoon hosts, including humans, the eggs hatch in the intestinal tract, releasing the immature larvae, which instead of developing into adults as they do in raccoons, begin to migrate extensively through body tissues, causing
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visceral larva migrans (VLM). The migrating larvae produce damage to tissues directly and by an intense eosinophilic inflammatory reaction along the tract of migration. Unlike the larvae of other helminths that cause VLM (such as I: canis), the larvae of B. pvocyanis exhibit very aggressive tissue migration behavior. They continue to grow and molt during their migration, becoming up to 2 mm long, and do not die readily (5). Eventually, the migrating larvae become encapsulated in eosinophilic granulomas but remain viable. For reasons that are still not entirely clear, the larvae of R. procyonis also have a noted tendency to invade the spinal cord and brain (causing NLM) and the eye (causing OLM). Whereas experimental infections in animals have shown that only a small percentage (5 to 7%) of larvae actually enter the CNS, the damage
they cause is extensive
(13).
Factors influencing the severity of CNS disease in humans (and other animals) include (i) the number of eggs ingested, (ii) the extent and pattern of larva migration in tissues, (iii) the severity of inflammation caused by migrating larvae, (iv) the amount of tissue necrosis, and perhaps (v) how soon after infection treatment is given (see below). Clinical signs of infection may develop as soon as 2 to 4 weeks following ingestion of eggs containing infective larvae and vary depending on the factors mentioned above. Symptoms of baylisascariasis range from clinically inapparent to varying degrees of mild CNS dystinction to signs of severe neurologic deficits, paralysis, coma, blindness, and death (7,lO). Ingestion of large numbers of B. procyonis eggs may produce rapidly fatal NLM. Another factor contributing
to severity of disease is the fact that infection with B. procyonis is often not suspected until late in the diagnostic evaluation of a patient, as the larvae continue to migrate unimpeded in body tissues. Migrating larvae eventually become encapsulated in eosinophilic granulomas but remain viable in the tissues for extended periods (4). Despite treatment, progressive neurologic deterioration often continues. The prognosis for patients with B. procyonis NLM is poor.
Diagnosis of Baylisascariasis in Humans Because of the severe nature and often fulminant course of human infection with B. procyonis, it is important that clinical laboratory personnel be aware of this zoonotic disease so as to properly advise physicians of available diagnostic tests. Humans are dead-end
Figure 3. Typical raccoon latrines found in ciose association with human dwellings. (A) Latrine directly on the ground in a suburban yard adjacent to a stack offirewood. Note evidence of a varied diet, which in this case includes a lot ofpetfood. (6} Latrine at the base of a tree stump in a city park. (C) Large latrine on the roof of a suburban home. The action of weather washes the decomposing feces directly #the roof and dorvn gutters, where B. procyonis eggs can contaminate the surrounding area, including children k tqvs, which was the case at this ho&e. (17) A latrine on the top ofa stone fence in a backyard. Note e-in. ruler in the foreground.
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hosts for B. procyonis. Thus, it is important to recognize that B. procyonis eggs or larvae cannot be found in human stool specimens. Therefore, physicians should be advised that ordering ova and parasite (“0 & P”) examinations of a patient’s stool are not useful, although such examination may reveal the presence of human parasites unrelated to the patient’s illness. Results obtained from complete blood count and cerebrospinal fluid (CSF) examinations are usually consistent with a parasitic infection but are non-specific. Peripheral blood and CSF eosinophilia are common but may not be profound (10). It is generally recognized that eosinophilic pleocytosis in the CSF in combination with peripheral blood eosinophilia in patients with progressive neurologic deficits is characteristic of baylisascariasis but is not pathognomonic (5,13). The other major cause of larva migrans in humans, I: canis, can generally be excluded by negative serologic results (4,14). Infections in humans can be difficult to confirm. Diagnosis is typically arrived at by exclusion of other known causes of VLM, OLM, and NLM. The demonstration of characteristic B. proqonis larvae in tissue biopsy specimens is considered to be the “gold standard’ of diagnosis (Fig. 4). However, permission to perform a biopsy (particularly one of the brain) is frequently difficult to obtain, and most consider such an invasive procedure unwarranted (4,10). Even when permission to biopsy is granted, removing tissue from sites where the larvae actually are is problematic, especially if the method used is fine-needle aspiration. In cases of OLM, ophthalmologic examinations revealing chorioretinal lesions, larval tracks, or migrating larvae can support a diagnosis of baylisascariasis (4). This is particularly true if larvae themselves are seen, because of their large size (up to five times larger) relative to that of 7: canis, the most common cause of OLM in humans ( 14,15). Abnormal ocular findings are often the first clue to a helminthic cause for clinical signs in a patient (4,10,14). Furthermore, the larvae of B. procyonis are now recognized as a cause of a condition known as diffuse unilateral subacute neuroretinitis (DUSN) in humans (7:16). DUSN is characterized by unilateral vision loss that presumably Clinml
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Figure 4. Human brain biopsy. Hematoxylin and eosin stain, x200. This fine-needle aspirate was removedfrom the brain ofan adolescent boy with severe central nervous system disease. A B. procyonis larva is clearly visible in cross section (at midbody level) at the edge of the tissue section. B. procyonis larvae can be easily distinguishedfrom the larvae of Ascaris and Toxocara spp., which may also cause larva migrans. In addition to the large size (approximately 70 ,um in diameter) of the larva, conspicuous features are the prominent lateral alae on opposite sides of the cuticle and large excretoty columns adjacent to the centrally located intestinal canal. (Photomicrograph courtesy of DI: Lawrence R. Ash, UCLA School of Public Health).
results from inflammation caused by wandering of the various species of juvenile nematodes in the retina and associated ocular tissues. It is also important to point out that baylisascariasis is not confined to North America; a case of DUSN caused by B. procyonis has been reported from Germany (17). Neuroimaging methods, such as computed tomography scans and magnetic resonance imaging, are also helpful in supporting a diagnosis. In cases where such imaging has been obtained, evidence of ventricular dilatation, periventricular enhancement in contrast studies, and white matter abnormalities are prominent features in infected individuals (7,10,18). Various serologic methods have been developed for baylisascariasis but are not in routine use in clinical laboratories. Serologic testing is currently available on a limited basis from the Department of Veterinary Pathobiology at Purdue University (7). A history of patient exposure to raccoons is obviously helpful, but in many instances, especially in cases of OLM, no patient contact with raccoons or their feces is reported. Nonetheless, additional 8’) 2002 Elsevier Science Inc.
diagnostic support can be obtained by visiting sites suspected to be locations where the patient may have become exposed and searching for evidence of the source of exposure. Careful questioning of parents of young children will often provide a clue as to where their child may have been exposed. Even when a historical report of such contact is obtained, it is important to recall that the vast majority of people cannot correctly identify a raccoon latrine site (or raccoon feces). Often the assistance of wildlife biologists from federal or state agencies or university researchers familiar with the behavior of raccoons and the biology of B. procyonis can be sought. Examination of raccoon stool specimens or soil samples brought to the laboratory can be accomplished using modified flotation assays (19,20). Providing the person collecting the scat samples can confirm they are from a raccoon, such an examination may be warranted to help confirm a diagnosis of baylisascariasis. This would be helpful to determine whether a patient could have been exposed to raccoon feces containing B. procyonis eggs. The 0 I96-4399!00
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examination of samples collected in the field is best accomplished at reference or research laboratories that are skilled in the examination of fecal specimens obtained from veterinary and witdlife sources. The sheer number of different types of eggs. lamae, and artifacts typically found in these specimens may o\~envhelm the technologist accustomed to the examination of human fecal specimens. R. JW~,IWZ~.Seggs have typical ascarid features (Fig. 5). However, because of similarities with other ascarid eggs of domesticated animals and wildlife. it is of paramount importance that specimens be examined by those with the requisite expertise to conclusively identify B. pwqmis eggs. Given the pre\.alence and geographic distribution of the parasite in raccoons, it is best to consider any sample of raccoon feces positive for 3. jmqmis eggs until proven otherwise by microscopic examination.
Treatment of Baylisascariasis There is no effective cure for human infection. Steroids and anthelmintic agents are usually employed for symptomatic treatment, but the efficacy of this therapy is controversial. In any event, no treatment described to date has altered the prognosis (7, IO). A contributing factor to this lack of success is no doubt the fact that the larvae continue to migrate unimpeded in body tissues because infection with B. proqmis is not suspected until late in the course of the disease. Various anthelmintic agents have been employed for treatment. Currently the drug of choice is albendazole, because it has been shown to have good distribution into brain and CSF. especially when used in conjunction with dexamethasone (10.2 1,22). Experimental B. procyonis infections in mice have demonstrated that albendazole and another anthelmintic. diethylcarbamazine, were of prophylactic value in preventing CNS disease when administered 1 to 10 days post-infection ( 10). Furthermore, in several cases when children were observed ingesting raccoon feces, the prompt administration of albendazole is thought to have prevented development of cfinical symptoms of baylisascariasis (7). In light of these facts, the current recommendation is that whenever infection with B. proc:vonis is suspected, treat-
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Figure 5. B. procyonis eggs. Microscopic examination (magnification. X 40) i$twccooi~,feces ,following modijTed_flotation of a fecal specimen,fowd in a latrine in a large plnyKrolrnd sad box in A suburban park. Lej, an embvonated, but non-infective. egg. Right, an infectilae egg containing a.fitlly,formed larva that is clearly i+sible within. B. procyonis eggs can be d@erell~i~te~~~?n other ascarid eggs c~rnrnotl~~,~~l~ti~ in the e~~~,i~~rne~t,strch as those qf Toxocara. Ascaris, and Toxascaris spp., by expert e.~amiFlatiotl. &-&fly. B. procyonis eggs are ellip‘so~~. appro.~itnate~y 7.5 x 60 pm in size, with a dark brawn, granular surface.
ment should be started immediately while diagnostic tests and field investigations to document a source of exposure are carried out. The only successful treatment for human baylisascariasis has been in cases of OLM in which laser photocoagulation was employed in conjunction with treatment with co~icosteroids (7).
Summary Baylisascariasis is a rare human infection. Despite the rarity of infection, factors that cannot be over-emphasized are the severity of the disease, its inability to be cured, and its potentially fatal outcome, especially in very young children, who are most likely to become infected. Transmission of the parasite occurs through the inadvertent ingestion of B. procyonis eggs, which are shed in the feces of infected raccoons. In any area where raccoons are found, the probability of infection with B. procyonis is likely, and any raccoon should be considered infected unless proven otherwise. Also of concern are reports of patent B. procyonis infections in dogs, which could greatly amplify the likelihood of human exposure to this parasite. B. procyonis infections in humans are difficult to confirm. Because of delays in diagnosis and treatment, most cases present after there has been extensive CNS damage. In the absence
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of a definitive diagnosis (i.e., demonstration of larvae in tissue biopsy specimens or autopsy results), diagnosis in humans is arrived at by a combination of clinical symptoms, patient history, neuroimaging results, documentation of a source of exposure to raccoon feces, and serologic results. Raccoon latrine sites are frequently implicated as the source of human infections. The possibility of inadvertent infection increases with exposure to raccoon feces, which in turn is related to the number of raccoons living in a given area. Under no circumstances should raccoons be purposefully (or inadvertently) fed or otherwise encouraged to take up residence near areas of human habitation. Because the density of raccoon latrines in a given area is proportional to the raccoon population living there, public health officials, physicians, and others involved in health care should be aware of the increased potential for human infection when raccoon densities are high. Natural dispersal of the eggs from latrine sites occurs from the action of weather and other forces, leading to long-term contamination of large areas. Preventing the establis~ent of raccoon latrine sites around areas of human habitation and recreational use is of paramount public health importance.
Acknowledgment
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I thank Darcy Levee for her assistance in preparation of the manuscript.
I. Sharp. D. 2000. Creature discomfort is call to battle in suburbs. USA Today, Aug. 3O:Sect. 4A. 2. McCombie, B. 1999. Those dirty raccoons: how a once revered fur bearer became reduced to cockroach status, Field and Stream, December: 8. -3 Roussere, G.P. et al. 2000. An epidemiologic survey of raccoon (frocyffn lotor) latrine sites and the prevalence of raccoon roundworn (~~~/~sffscarjs procyotris) eggs in Pa&tic Grove and Cannel, CA. Y-4. p.683. In Abstr. 100th Gen. Meet. Am. Sot. Microbial. ASM Press, Washington, DC. 4. Kazacos, K.R. 1997. Visceral, ocular, and neural larva migrans, p. 1459-1473. 1/r D.H. Connor et al. (ed.), Pathology of infectious diseases, vol. II. Appleton & Lange, Stamford, CT. 5. Kazacos. K.R. and W.M. Boyce. 1995. Bqdisnscaris larva migrans, p. 20-30. I/I Zoonosis updates from the Journal of the American Veterinary Medical Association, 2nd ed. American Veterinary Medical Association, S~haumburg, IL. 6. Averbeck, G.A. et al. 1995. Differentiation of &y/isascaris species, Toxocaru carzis and To.vascaris leonina infections in dogs. Compendium of Continuing
Education of the Practicing Veterinarian 17:475-5 11. 7. Kazacos, K.R. 2000. Protecting children from helminthic zoonoses. Contemp. Pediatr. I7(Suppl): l-24. 8. Roberts, L.S. and J. Janovy. 1996. Nematodes: ascardida, intestinal iarge roundwo~s, p. 4 19-43 1. In Gerald D. Schmidt and Larry S. Roberts’ Foundations of parasitology, 5th ed. W.C. Brown, Dubuque, IA. 9. Page, L.K. and R.K. Swihart. 1998. Raccoon latrine structure and its potential role in transmission of Baylisascaris procyonis to vertebrates. Am. Midland Naturalist 140: 180-l 85. IO. Park. S.Y. et al. 2000. Raccoon roundworm (Baylisascaris procyonis) encephalitis: case report and field investigation. Pediatrics 106: l-5. II. Riley, S.P.D., J. Hadidian, and D.A. Manski. 1998. Population density, survival and rabies in raccoons in an urban national park. Can. J. Zool. 16: 11.531164.
migrans. Vet. Clin. N. Am. 17:39-53. 15. Kazacos, K.R. 1991. Visceral and ocular larva migrans. Sem. Vet. Med. Surg. 6:227-235. 16. Goldberg, M.A. et al. 1993. Diffuse unilateral subacute neuroretinitis: morphometric, serologic and epid~iologic support for ~ay~is~~~r~s as a causative agent. Ophthalmology 100: 1695- I70 1. 17. Kuchle, M. et al. 1993. Diffuse unilateral subacute neuroretinitis syndrome in a German most likely caused by the raccoon roundworm, Bayhascaris procyonis. Graefe’s Arch. Clin. Exp. Ophthalmol. 23 1:48-5I. 18. Rowley, H.A. et al. 2000. Radiologicpathologic findings in raccoon roundworm (Baylisascaris procyonis) encephalitis. Am. J. Neuroradiol. 21:415-420. 19. Sloss, M.W., R.L. Kemp, and A.M. Zajac. 1994. Veterinary clinical parasitology, 6th ed., p. 3-8. Iowa State University Press, Ames, IA.
12. Greve, J.H. and S.E. O’Brien. 1989. Adult Baylisascaris infections in two dogs. Companion Anim. Pratt. l9:4 1” 43.
20. Kazacos, K.R. 1983. Improved method for recovering ascarid and other helminth eggs from soil associated with epizootics and during survey studies. Am. J. Vet. Res. 44:896-900.
13. Kazacos, K.R. 1996. Baylisascariasis, p. 716-7 17. In A.M. Rudolph (ed.), Rudolph’s Pediatrics, 20th ed. Appleton & Lange, Stamford, CT.
21. de Silva, N., H. Guyatt, and D. Bundy. 1997. Anthelminti~s: a compamtive review of their clinical pharmacology. Drugs 53:769-788.
14. Glickman, LT. and F.S. Shofer. 1987. Zoonotic visceral and ocular larva
22. Venkatesan, P. 1998. Albendazole. J. Antimicrob. Chemother. 4 I : l45- 147.
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