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Ron Hines DVM PhD Dear Viewer, If you keep a pet racoon or you are helping one out, this is an article you should read. This is not to say you should not keep the critter. But you should know the risks. Recently, a very sensititive PCR test became available to detect Baylisascaris. All raccoon owners should have their animals tested.
Emerging
Infectious Diseases Journal Atlanta, GA Vol. 8, No. 4 Synopsis Authors: Frank Sorvillo, Lawrence
R. Ash,* O.G.W. Berlin, JoAnne Yatabe, Chris Degiorgio, and Stephen
A. Morse Baylisascaris procyonis, a roundworm infection of raccoons, is emerging as an important helminthic zoonosis, principally affecting young children. Raccoons have increasingly become peridomestic animals living in close proximity to human residences. When B. procyonis eggs are ingested by a host other than a raccoon, migration of larvae through tissue, termed larval migrans, ensues. This larval infection can invade the brain and eye, causing severe disease and death. The prevalence of B. procyonis infection in raccoons is often high, and infected animals can shed enormous numbers of eggs in their feces. These eggs can survive in the environment for extended periods of time, and the infectious dose of B. procyonis is relatively low. Therefore, the risk for human exposure and infection may be greater than is currently recognized. Baylisascaris procyonis, a ubiquitous roundworm infection of raccoons (Procyon lotor), is increasingly being recognized as a cause of severe human disease (1,2). B. procyonis has a widespread geographic distribution, with infection rates as high as 70% in adult raccoons and exceeding 90% in juvenile raccoons (3). As with other ascarids, eggs are excreted in feces and must develop externally, typically in soil, to become infectious. When raccoons ingest infective eggs, larvae will hatch, enter the wall of the small intestine, and subsequently develop to adult worms in the small bowel. However, ingestion of eggs by other host animals, especially rodents and other small mammals, results in extraintestinal migration of larvae (4); an estimated 5%-7% of larvae invade the brain (5). The migration of helminth larvae through tissue in suboptimal hosts is termed larva migrans and may affect the viscera (visceral larva migrans [VLM]), the eye (ocular larva migrans [OLM]), or the nervous system (neural larva migrans [NLM] (6). Raccoons may also become infected when they eat larvae that have become encapsulated in the tissues of rodents and other animals (3). More than 90 species of wild and domesticated animals have been identified as infected with B. procyonis larvae (3). Outbreaks of fatal central nervous system disease caused by B. procyonis have occurred on farms and in zoos and research animal colonies and have affected commercial chickens, bobwhite quail, guinea pigs, commercial pheasants, and domestic rabbits (7-11). Natural infections have also been recognized in dogs, rodents, porcupines, chinchillas, prairie dogs, primates, woodchucks, emus, foxes, and weasels (12-16). Experimental infection of a variety of nonhuman primates has also been reported (17). Human Infection B. procyonis infection of humans
typically results in fatal disease or severe sequelae (1,2,18-24;
pers. comm., W. Murray). Clinical manifestations include eosinophilic
encephalitis, ocular disease, and esoinophilic cardiac pseudotumor.
Elevated peripheral cerebrospinal fluid eosinophilia can be detected
in cases of meningoencephalitis. Eleven recognized human cases,
four of them fatal, have been reported (Table). The first human
case was reported in 1984 in a 10-month-old infant with fatal eosinophilic
meningoencephalitis (18). At autopsy, numerous granulomas containing
larvae of B. procyonis were observed in several organs and tissues
(18). The brain was the most heavily affected, with granulomas concentrated
in the periventricular white matter, around the dentate nuclei,
and along the cerebral and cerebellar cortices. Numerous granulomas
and larvae were also found in the mesentery and cardiac tissue.
The infant’s family lived in a rural, wooded area of Pennsylvania,
and raccoons were nesting in unused chimneys at the time infection
was acquired. No effective therapy exists for the visceral form of B. procyonis larval infection. In an experimental model, mice treated with albendazole and diethylcarbamezine within 10 days after infection were protected from CNS disease (25); however, several anthelminthic agents have been used to treat human cases without success. Laser photocoagulation has been successful in treating ocular infection (26). Because the disease is transmitted
by the fecal-oral route, human cases of B. procyonis infection typically
occur in younger age groups, mainly infants, who often engage in
oral exploration of their environment and are therefore more likely
to be exposed to B. procyonis eggs. Raccoon activity near the patient’s
residence is often described. All but one of the reported patients
to date have been male; however; there is no reason to believe that
females are less susceptible to infection. Diagnosis of B. procyonis infection is typically done through morphologic identification of larvae in tissue sections (27). However, accurate diagnosis requires experience in recognizing larval morphologic characteristics and differentiating among a number of possible larval nematode agents, including Toxocara canis, T. cati, Ascaris lumbricoides, and species of Gnathastoma, Angiostrongylus, and Ancylostoma, as well as larval cestode infections such as cysticercosis and echinococcosis (6,27). Characteristic features of B. procyonis larvae in tissue include its relatively large size (60 µ) and prominent single lateral alae (27) (Figure 2). While serologic testing has been performed in some cases as supportive diagnostic evidence, no commercial serologic test is currently available (28,29). However, a presumptive diagnosis can be made on the basis of clinical (meningoencephalitis, diffuse unilateral subacute neuroretinitis [DUSN], pseudotumor), epidemiologic (raccoon exposure), radiologic (white matter disease), and laboratory results (blood and CNS eosinophilia). Human baylisascariasis is probably
underrecognized, and the full spectrum of clinical illness is unclear.
The agent is unknown to most clinicians and typically is not considered
in a differential diagnosis. In addition, confirming the diagnosis
requires an effective biopsy specimen that must contain an adequate
cross-section of a larva. Since small numbers of larvae can cause
severe disease and larvae occur sporadically in tissue, a biopsy
may frequently fail to include larvae; such a specimen will result
in a negative finding. Moreover, larval morphologic characteristics
may not be recognized or may be misidentified. The accurate diagnosis
of parasites in tissues can be difficult even for trained microscopists,
and mistaken identification, particularly of helminth larvae, is
not uncommon (27). Finally, no commercial serologic test exists
for the diagnosis of B. procyonis infection, and the sensitivity,
specificity, and predictive value of available serologic tests are
unknown. Evidence for underrecognition of larval B. procyonis infection
can be found in several reported cases of DUSN caused by larvae
compatible with B. procyonis and a case of eosinophilic meningoencephalitis
reported in an infant in 1975 (26,30,31). Although relatively few human cases of baylisascariasis have been reported, several factors suggest that the likelihood of exposure and infection may be greater than is currently recognized. Raccoons have a widespread geographic distribution, and infection with B. procyonisis common in raccoon populations, with typically high prevalence rates observed.An infected raccoon can harbor numerous adult worms and may excrete large numbers of eggs. A single adult female worm may produce an estimated 115,000 to 877,000 eggs per day, and an infected raccoon can shed as many as 45,000,000 eggs daily (3,4,32). In light of the relatively low infectious dose of B. procyonis (estimated to be < 5,000 eggs) and the viability of the eggs in the environment for months to years, the infection potential is not insubstantial. Raccoons have increasingly become peridomestic animals living in close proximity to human residences and are among the fastest growing wildlife populations nationwide. These animals benefit from feeding on abundant pet food left accessible, either accidentally or intentionally, and their populations can thrive under such conditions. In one suburban area near the residence of a recent patient in northern California, the raccoon population was measured at 30 animals per quarter acre. Areas frequented by raccoons and used for defecation were found in close proximity to human dwellings, and B. procyonis eggs are routinely recovered from these areas (1). Children, particularly toddlers, may be at particular risk of exposure. Although baylisascariasis may
indeed be underdiagnosed, asymptomatic human infection may be the
typical response, and the limited number of cases reported may indicate
that an unrecognized immune defect is necessary for severe infection
to occur. The prevalence of asymptomatic infection in human populations
has yet to be determined. In an era of increasing concern
about bioterrorism (33), certain characteristics of B. procyonis
make it a feasible bioterrorist agent. The organism is ubiquitous
in raccoon populations and therefore easy to acquire. Enormous numbers
of eggs can be readily obtained, and these eggs can survive in an
infectious form for prolonged periods of time. As with other ascarids,
the eggs can remain viable in a dilute (0.5%-2%) formalin solution
for an indefinite period of time, and animal studies suggest that
B. procyonis has a relatively small infectious dose. Moreover, the
organism causes a severe, frequently fatal infection in humans,
and no effective therapy or vaccine exists. Introduction of sufficient
quantities of B. procyonis eggs into a water system or selected
food products could potentially result in outbreaks of the infection.
A similar agent, Ascaris suum, a roundworm of pigs, was used to
intentionally infect four university students who required hospitalization
after eating a meal that had been deliberately contaminated with
a massive dose of eggs (34). Contamination of community water sources
would be difficult since the eggs of B. procyonis are relatively
large (80 µm long by 65 µm wide) and would be readily
removed by standard filtration methods or the flocculation and sedimentation
techniques used by municipal water systems in the United States.
However, posttreatment contamination or targeting of smaller systems
could be possible. Baylisascariasis is an emerging
helminthic zoonosis with the potential for severe infection that
may be a more important public health problem than is currently
recognized. Educating the medical community is of paramount importance
in helping to define the extent of infection. Physicians should
consider B. procyonis infection in the differential diagnosis of
patients with eosinophilic meningoencephalitis, DUSN, and eosinophilic
pseudotumor. While infants and children have a higher probability
of infection, all age groups are at risk. The public should be made
aware of the potential risks of exposure to raccoons and raccoon
feces. Raccoons should be discouraged as pets or should be routinely
evaluated for B. procyonis infection and treated. However, screening
and treatment may not be sufficient to prevent exposure, since the
likelihood of reinfection is high. The public should be discouraged
from feeding raccoons and should ensure that possible food sources
(such as pet food, water, and garbage) are protected from raccoon
access. Further study of the impact of larval B. procyonis infection
on human health is warranted. Development of a standardized serologic
test for B. procyonis would allow epidemiologic studies of its prevalence
and incidence and help determine factors associated with infection.
A sensitive and specific test would also provide a noninvasive method
of diagnosis. Finally, a better understanding of the pathogenesis
of B. procyonis infection and efforts to develop effective treatment
approaches are warranted. The authors thank Howard A. Rowley for graciously providing the images Dr. Sorvillo is Associate Professor, Department of Epidemiology, UCLA School of Public Health. His research interests include the epidemiology and control of infectious diseases, particularly parasitic agents. Address for correspondence:
Frank Sorvillo, UCLA School of Public Health, Box 951772, Los Angeles,
CA 90024, USA; fax: 714-816-9099; e-mail: fsorvill@ucla.edu |
