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Concern with Communicable (Infectious)
Diseases of Raccoons


1 Communicable (Infectious) Diseases of Raccoons
Raccoons are part of urban and suburban areas and are commonly seen or encountered by people in parks, neighborhoods or yards.  Raccoons are susceptible
to a large number of different infectious agents including bacteria, viruses, and parasites. Several of these infectious diseases are zoonotic; that is, diseases that
can be spread to people and pets.  Veterinarians involved with the diagnosis and treatment of wildlife, including raccoons, and need to make the correct
diagnosis understand the potential hazards associated with exposure to raccoons.  People who may come in contact with racoons should be aware of the
potential hazards associated with exposure to raccoons (Common Infectious Diseases of Raccoons, Raymond and White, 1997).  The disease pathogen that
presents the most serious risk to human health of all the above and the disease that is most difficult to clean up and to kill of all the above is a round worm
parasite found in the raccoon named Baylisascaris procyonis.

2 Baylisascaris procyonis Overview
Baylisascaris procyonis is a round worm parasite found in the raccoon.  Raccoons are well-known reservoirs of a large number of zoonotic (disease causing in
humans) viral, bacterial, protozoal (ameba), and helminth (worm) pathogens, including Salmonella, Baylisascaris, and rabies (Murray and Kazacos, 2004, Gavin,
et al 2005).  B. procyonis is a recognized cause of visceral (organ), ocular (eye), and neural (nervous tissue) larva migrans in humans and other animals
(Kazacos and Boyce, 1995, Kazacos, 2001, Kazacos, 2000).  Larva migrans occurs when the larva from eggs in the intestine penetrate the intestinal wall and
migrate to other tissues in the body.  B. procyonis larva migrate to the viscera (organs), eyes, brain, and central nervous tissue of humans and other animals.  
Fatal or severe central nervous system disease from B. procyonis has been reported in more than 90 species of birds and mammals (Kazacos, 2001).  Fifteen
known or suspected cases of neural larva migrans have been reported in humans, primarily in children <2 years of age, and developmentally disabled persons
(Gavin, Kazacos, and Shulman, 2005).  In the spring of 2009, the New York City Department of Health and Mental Hygiene reported that two cases of
Baylisascaris procyonis infection were identified in children from Brooklyn, both with serious pathological effects.  An infant with encephalitis from neural larva
migrans caused severe permanent brain damage, and a teenager with ocular larva migrans resulted in loss of vision in one eye (Slavinski, and Fine, 2009).

3 Epidemiology of Baylisascaris procyonis in Raccoons
Raccoons may have a high B. procyonis parasite burden, averaging 43 to 52 worms per raccoon.  Young raccoons have a significantly higher prevalence of
infection  (93.5%) than adults.  Adult raccoons have infection prevalences of 72% to 82% in the mid-west, northeast, and the west coast and 0% to 22% in the
southeast (Snyder and Fitzgerald. 1985).  In raccoons, a Baylisascaris procyonis infection is usually subclinical (none or few signs and symptoms) and adult
worms remain in the small intestine (Kazacos, 2001).  The adult B. procyonis worm is large, and tan-colored.  The female worm is about twice as large (20 to 22
cm (9 inches) long) as the male worm (9 to 11 cm) (Kazacos, 2001).  In the raccoon intestine, the adult female worm produces between 115,000 and 179,000
eggs per worm per day (Kazacos, 2001). In nature, infected raccoons shed about 20,000 to 26,000 eggs per gram of feces, however, this value can reach
250,000 eggs per gram of feces (Kazacos, 2001).  With this generation of eggs per day, infected raccoons can shed millions of B. procyonis eggs daily.

4 Baylisascaris procyonis Eggs
Baylisascaris procyonis eggs are ellipsoidal, dark brown, and measure from 63 to 88 um long by 50 to 70 um wide and are extremely difficult to destroy (Kazacos,
2001).  Similar to other Ascaris species, the eggs have a 3-4 um thick four-layer protective shell that consists of: 1) an inner lipoprotein layer (ascaroside layer),
2) a thicker chitin/protein layer, 3) a lipoprotein vitelline layer, and,  4) an outer acid mucopolysaccharide/protein uterine layer (Murray, 2002).  The inner
lipoprotein layer consists of 25% protein and 75% lipid-containing ascarosides, and provides the impermeability of the shell (Murray, 2002.) The chitinous layer
gives the egg structural strength through chitin spindles in a protein matrix (Gamble et al. 1995).  The vitelline and the uterine layers contain protein but their
structure and function are not completely understood (Murray, 2002.).  Soaking the eggs in a solution of hypochlorite will remove the outer three layers while the
inner lipoprotein ascaroside layer remains (Barrett, 1976., Kennedy, and Qureshi, 1986).

The four layer shell system protects Ascaris eggs so that they are more resistant to different types of water treatment inactivation techniques than most other
water borne pathogens (Feachem et al. 1980).  Ascaris eggs are more resistant to high temperatures.  They can survive for more than one year at 40oC.  
Temperature of above 60oC will inactivate Ascaris eggs.  Chlorine at the commonly applied water disinfection dose does not kill the eggs (Krishnaswami, and
Post. 1968).  The inner lipoprotein layer (ascaroside layer) protects the eggs from strong acids, strong bases, oxidants, reductants, protein disrupting agents and
surface -active agents (Barrett, 1976).

Baylisascaris procyonis eggs are not immediately infective after shedding.  Under suitable environmental temperature and humidity, B. procyonis eggs develop
into infective second-stage larvae in 2 to 4 weeks.  In nature, B. procyonis eggs resist decontamination and environmental degradation and remain viable and
infective in moist soil for years (Kazacos, 2001).  Inactivation of infective eggs will occur under conditions of high ambient temperatures and extreme dryness.  
Examples of high ambient temperatures and extreme dryness include direct sunlight, hot dry attics, and haylofts. (Kazacos, 2001).

5 Epidemiology of Baylisascaris procyonis Raccoons to Humans
The epidemiology of Baylisascaris procyonis infection is associated with the defecation habit of racoons.  Racoons usually defecate in specific areas called
“latrines” (Kazacos, 2001, Roussere et al. 2003, Page et al.1999).  Large amounts of racoons feces and B. procyonis eggs are amassed here.  Raccoon latrines
are located at the base of trees, tree branch crotches, on wood piles, along fences, on top of fences, on decks, on roofs, in buildings, attics, and haylofts.

The most significant risk factors for human infection with B. procyonis are contact with raccoon feces, soil ingestion, age of less than 4 years, male gender, and
intellectual development delay (Kazacos, 2000, Kazacos, 2001, Fox, et al, 1985, Cunningham, Kazacos et al. 1994, CDC 2000, Gavin et al. 2002).  Adults who
have pica, ingest soil, or have hand to mouth activity are at risk for infection.  Adults with intellectual development delay have been infected with B. procyonis
resulting in severe or fatal CNS disease (Kazacos, 2000, Cunningham, Kazacos et al. 1994, CDC 2000).  Accidental contact and low level infection can occur in
persons with seropositivity without overt clinical signs and symptoms (Kazacos, 2000, Kazacos, 2001, Cunningham, Kazacos et al. 1994, Brinkman et al 2003).  
Additionally, accidental contact and low level infection can result in persons developing ocular larval migrans without overt clinical signs and symptoms (Kazacos
et al. 1985, Goldberg et al, 1993, Kazacos, 1997).  Young children and toddlers appear to be more likely than adults to ingest the eggs due to their hand to
mouth behavior of putting dirt and other objects into their mouths.  There are a very small number of reported raccoon roundworm infections in humans, despite
the large number of raccoons living in close association with humans.  This suggests that the risk of B. procyonis infection in humans is rare.

6 Baylisascaris procyonis Persistence in the Environment
B. procyonis eggs have a long life (years) and a significant resistance to disinfection that makes successful environmental cleanup difficult.  Heating and or drying
the egg is the best method of killing B. procyonis eggs (Kazacos, 2001).  Boiling water, flaming, or fire are very effective methods for decontamination of large or
small areas.  The use of direct flames from a propane flame-gun is a recommended outdoor treatment technique (Kazacos, 2001).  For heavily contaminated
outdoor areas removal and disposal of the top few inches of surface soil with flaming is effective.  Persons cleaning contaminated areas should wear personal
protective equipment including; respirators, disposable coveralls, gloves, and eye protection.  All potentially contaminated material removed from these sites,
including used protective clothing, should be incinerated.  Indoors the cleaning of eggs from contaminated surfaces is extremely difficult because of their
significant resistance to many chemicals and disinfection.  Some contaminated indoor surfaces have been adequately cleaned with a xylene-ethanol mixture, after
the solid waste has been removed.  However, chemical disinfection, in general, is rarely effective and usually not practical for large areas.  Eggs are resistant to
most common chemicals and disinfectants.  A 20% bleach solution (1% sodium hypochlorite) will wash away the sticky eggs but does not kill the eggs (Kazacos,
2001).

Charles E. Gilbert, Ph.D., M.S.,

Toxicologist & Epidemiologist                     


7                References
Barrett, J.  1976. Studies on the induction of permeability in Ascaris lumbricoides eggs. Parasitology 73:109-121.

Brinkman, W.B., K.R. Kazacos, P.J., Gavin et al.  2003. Seroprevalence of Baylisascaria procyonis (raccoon roundworm ) in Chicago area children [abstract 1872]
. In: Program and abstracts of the 2003 annual meeting of the Pediatric Academic Societies (Seattle, WA).

Centers for Disease Control.  2004. Raccoon roundworm encephalitis Chicago, Illinois, and Los Angeles, California, 2000. MMWR Morb MortalWkly Rep 2002; 50:
1153-5. Available at:  Accessed 25 October 2004.

Cunningham, C. K., K. R. Kazacos, J. A. McMillian, et. al.  1994.  Diagnosis and management of Baylisascaris procyonis infection in an infant with nonfatal
meningoencephalitis. Clin Infect Dis 1994; 18:868-72.

de Silva, N., H. Guyatt, and D. Bundy. 1997. Anthelmintics Drugs 53:769-788.

Feachem, R. G., D. J. Bradley, H. Garelick, and D. D. Mara. 1980. Appropriate technology for water supply and sanitation: health aspects of excreta and sullage
management a state-of-the-art review, vol. 3. The World Bank, Washington, D.C.

Fox, A. S., K. R. Kazacos, N. S. Gould, P. T. Heydemann, C. Thomas, and K. M. Boyer.  1985.  Fatal eosinophilic meningoencephalitis and visceral larva migrans
caused by the raccoon ascarid Baylisascaris procyonis. N Engl J Med 1985; 312:1619-23.

Gamble, H. R., R. H. Fetterer, J. J. F. Urban. 1995. Reproduction and development in helminths, p. 289-305. In J. J. Marr and M. Muller (ed.), Biochemistry and
molecular biology of parasites. Academic Press, London, United Kingdom.

Gavin P. J., K.R. Kazacos, T. Q. Tan, et al. 2002.  Neural larva migrans caused by the raccoon roundworm Baylisascaris procyonis. Pediatr Infect Dis J; 21:971-5.

Gavin P.J., K.R. Kazacos, and Shulman S.T.  2005.,  Baylisascariasis. Clinical Microbiology Reviews, Oct 2005, p. 703-718.

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

Kazacos KR.  1997. Visceral, ocular, and neural larva migrans. In: Connor DH, Chandler FW, Schwartz DA, et al, eds. Pathology of Infectious Diseases. Stamford,
CT: Appleton and Lange; 1997:1459-1473.

Kazacos, K. R. 2001. Baylisascaris procyonis and related species, p. 301-41. In W. M. Samuels, M. J. Pybus, and A. A. Kocans (ed.), Parasitic diseases of wild
animals, 2nd ed. Iowa State University Press, Ames, Iowa.

Kazacos KR, Raymond LA, Kazacos EA, Vestre WA.  1985. The raccoon ascarid: a probable cause of human ocular larva migrans. Ophthalmology 1985; 92:
1735-1743.

Kazacos, K. R. 2000. Protecting children from helminthic zoonoses. Contemp. Pediatr. 17(Suppl):1-24.

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Schaumburg (IL): American Veterinary Medical Association; 1995. p. 20–30.

Kennedy, M. W., and F. Qureshi. 1986. Stage-specific secreted antigens of the parasitic larval stages of the nematode Ascaris. Immunology 58:515-522.

Krishnaswami, S. K., and F. J. Post. 1968. Effect of chlorine on Ascaris (Nematoda) eggs. Health Lab. Sci. 5:225-232.

Murray, W. J. 2002. Human infections caused by the raccoon roundworm, Baylisascaris procyonis. Clin. Microbiol. News 24:1-7.

Murray, W. J., and K. R. Kazacos. 2004. Raccoon roundworm encephalitis. Clin. Infect. Dis. 39:1484-1492.

O’Lorcain, P., and C. V. Holland. 2000. The public health importance of Ascaris lumbricoides. Parasitology 121:S51-S71.

Page L.K., R.K., Swihart, and K. R. Kazacos. 1999. Implications of raccoon latrines in the epizootiology of baylisascariasis.  J Wildl Dis 1999:;35:474-80.

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Roussere, G.P., W.J., Murray, C.B. Raudenbush, M.J., Kutilek, D.J., Levee and K. R. Kazacos.  2003.. Racoon round worm eggs near homes and risk for larva
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Slavinski, S., and Fine, A. 2009.  Health Advisory #08: Baylisascariasis (Raccoon Roundworm) Infection with Severe Outcome Identified in Two New York City
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