Search

The article describes the possibility for human exposure to Baylisascaris procyonis (BP) infection from pet kinkajous. BP is considered a common roundworm of raccoons. Infected animals can shed millions of BP eggs in their feces every day based on raccoon studies. Disease prevention is based on stopping migration of BP larvae to organs and tissues through postexposure treatment.

Objective: Eosinophil-associated proteins, especially eosinophil-derived neurotoxin, may be important contributors to the neurologic pathology and symptoms caused by Baylisascaris procyonis infection., Methods: Two cases of severe B procyonis encephalitis with evidence of marked eosinophil degranulation in the central nervous system are presented. Serial cerebrospinal fluid (CSF) specimens were collected from each patient during the course of their illness. Antibodies against B procyonis were measured in the patients' serum and CSF. Levels of the eosinophilopoietin interleukin-5 (IL-5) and 2 important eosinophil proteins, eosinophil-derived neurotoxin and major basic protein, were assayed in the CSF., Results: Both patients had rapidly progressive central nervous system disease with evidence of eosinophilic meningoencephalitis. Both tested positive for antibodies to B procyonis in serum and CSF and had progressively worsening deep white matter changes on magnetic resonance images of the brain. CSF levels of IL-5, eosinophil-derived neurotoxin, and major basic protein were markedly elevated over controls., Conclusions: This is the first report of the measurement of IL-5, eosinophil-derived neurotoxin, and major basic protein in human CSF. In addition to traumatic damage and necrosis caused by migrating larvae, eosinophil-derived neurotoxin from associated eosinophilic inflammation may be an important contributory factor in the pathogenesis of B procyonis encephalitis. parasite, eosinophil-derived-neurotoxin, major basic protein, eosinophilia, hypereosinophilia, interleukin-5, encephalitis, child.

Baylisascaris procyonis is a common and widespread parasite of raccoons in the United States and Canada. With large raccoon populations occurring in many areas, the potential risk of human infection with B procyonis is high. We report a case of severe raccoon roundworm (B procyonis) encephalitis in a young child to illustrate the unique clinical, diagnostic, and treatment aspects, as well as public health concerns of B procyonis infection. Acute and convalescent serum and cerebrospinal fluid samples from the patient were tested for antibodies against B procyonis to assist in documenting infection. An extensive field survey of the patient's residence and the surrounding community was performed to investigate raccoon abundance and to determine the extent of raccoon fecal contamination and B procyonis eggs in the environment. The patient evidenced serologic conversion, and the field investigation demonstrated a raccoon population far in excess of anything previously reported. There was abundant evidence of B procyonis eggs associated with numerous sites of raccoon defecation around the patient's residence and elsewhere in the community. Because B procyonis can produce such severe central nervous system disease in young children, it is important that pediatricians are familiar with this infection. The public should be made aware of the hazards associated with raccoons and B procyonis to hopefully prevent future cases of B procyonis infection.

A 13-month-old boy developed eosinophilic meningoencephalitis, retinitis, and a protracted encephalopathy with severe residual deficits. The initial MR examination revealed diffuse periventricular white matter disease, and follow-up images showed atrophy. Brain biopsy, serology, and epidemiologic studies lead to the diagnosis of Baylisascaris procyonis infection, a parasitic disease contracted through exposure to soil contaminated by the eggs of a common raccoon intestinal roundworm. The pathologic, epidemiologic, and imaging features of this disease are herein reviewed.

Raccoons (Procyon lotor) frequently establish defecation sites, termed latrines, on large logs, stumps, rocks, and other horizontally oriented structures/surfaces. These latrines are important foci of infective eggs of Baylisascaris procyonis, a nematode parasite of raccoons which is pathogenic to numerous species of mammals and birds. To examine the role of raccoon latrines in this animal-parasite interaction, we documented animal visitations to raccoon latrines in two large forested tracts and two woodlots in Indiana (USA) during 1994 and 1995. Species richness of vertebrate visitors did not differ between sites or years, but species composition differed by site and year. Fourteen mammal and 15 bird species were documented visiting raccoon latrines. Small granivorous mammals, including white-footed mice (Peromyscus leucopus), eastern chipmunks (Tamias striatus), and tree squirrels (Sciurus carolinensis, S. niger, Tamiasciurus hudsonicus) were the most common visitors to latrine sites. White-footed mice, chipmunks, white-breasted nuthatches (Sitta carolinensis), and opossums (Didelphis virginiana) were photographed foraging on undigested seeds in raccoon feces. Active foraging at latrines also was shown experimentally; seeds embedded in raccoon feces were removed at a greater rate at latrine sites than at nonlatrines. We conclude that raccoon latrines are visited routinely by a variety of vertebrates, especially small granivorous rodents and birds which forage for seeds in raccoon feces, and that raccoon latrines are probable sites of transmission of B. procyonis to susceptible mammals and birds.

In this study, we compared the susceptibility of Peromyscus leucopus (white-footed mouse), a common natural intermediate host, and Mus musculus, a commonly used experimental model, to infection with larvae of the raccoon ascarid, Baylisascaris procyonis. Three groups of 10 mice of each species were given 50, 250, or 500 infective B. procyonis eggs by gavage. The mice were observed daily for clinical signs of central nervous system (CNS) disease and at necropsy the distribution of larvae in 10 body regions and organs was determined and compared. Clinical CNS disease developed in 57% of P. leucopus and 93% of M. musculus. The average clinical incubation period was significantly longer in P. leucopus (20.6 days postinfection [PI]) than in M. musculus (10.7 days PI), and clinical disease progressed slower in P. leucopus. Significantly fewer larvae were recovered from P. leucopus than from M. musculus. Most larvae were recovered from the anterior carcass and viscera of P. leucopus and from the carcass, head, and brain of M. musculus. CNS invasion was dose dependent in M. musculus but not in P. leucopus. Few or no grossly visible larval granulomas were present in P. leucopus but were abundant in M. musculus. We concluded that P. leucopus was less susceptible than M. musculus to B. procyonis infection, based on a decreased intensity of infection, longer clinical incubation period or lack of clinical disease, slower progression of disease, different larval distribution, and lower tissue reactivity to larvae.

Laboratory-reared Aedes aegypti mosquitoes were employed in the successful transmission of Hepatozoon mocassini from a cotton-mouth moccasin (Agkistrodon piscivorus leucostoma) to 3 lizard species (Sceloporus undulatus, Eumeces obsoletus and Sceloporus poinsetti). Marked to severe lethargy and anorexia developed in the S. undulatus, E. obsoletus and S. poinsetti at 15, 38, and 96 days postinfection (PI), respectively. All 3 lizards developed a leukocytosis and had increased plasma aspartate aminotransferase activity (AST) by 14 days PI. Multifocal random hepatocellular necrosis and intrahepatic aggregates of heterophils centered on mature H. mocassini meronts were demonstrated in all 3 lizards. The pulmonary interstitium was multifocally thickened by aggregates of heterophils centered on meronts. No comparable clinical or anatomical pathological changes were demonstrated in naturally infected snakes. The results of this study suggest that H. mocassini is capable of inducing necrotizing inflammatory by lesions in unnatural reptilian hosts.

Baylisascaris larva migrans (LM) has been recognized as a cause of central nervous system (CNS) disease in puppies. A presumptive antemortem diagnosis is based on a history of raccoon exposure, clinical signs, cerebrospinal fluid eosinophilic pleocytosis, and peripheral blood eosinophilia. Early diagnosis is critical for treatment or prevention of disease in other dogs, animals, or humans exposed to the suspected contaminated area. In the present case, an antemortem diagnosis was not made, emphasizing the importance of postmortem examination in cases of CNS disease in puppies.

Four guinea pigs from a colony of approximately 50 animals were examined for progressive neurologic disease of 5 days' duration. Signs of neurologic dysfunction included cachexia, stupor, hyperexcitability, lateral recumbency, and opisthotonos. Results of gross pathologic, microbiologic, and serologic examinations were unremarkable. Histologic examination of cerebral and cerebellar sections revealed multifocal malacia and regions of eosinophilic granulomatous inflammation. Cross-sections of nematode larvae, identified as Baylisascaris sp., most likely B. procyonis, the raccoon ascarid, were seen in the brain of some affected animals. An intact Baylisascaris larva was recovered from a symptomatic animal when cerebral tissue was processed by the Baermann extraction technique. Results of further investigation indicated that wood shavings used for the guinea pigs had been contaminated by raccoon feces, some of which contained numerous B. procyonis eggs. The bedding source for this colony was changed and, to date, no new cases of neurologic disease have been seen. This report emphasizes the potential insidious entrance of B. procyonis into well-managed laboratory animal facilities.

We encountered two cases of human intraocular infection with mesocercariae of Alaria (Trematoda), involving unrelated Asian men who had unilateral decreased vision. Both patients had pigmentary tracks in the retina, areas of active or healed retinitis, or both, and other signs of diffuse unilateral subacute neuroretinitis. Similar, nonnematode worms were seen in the patients' retinas and vitreous, respectively, several years after apparent infection. The worm in Case 1 was analyzed from projected fundus photographs and diagnosed as an Alaria mesocercaria on the basis of its shape, size (500 x 150 microns), and movement; it was successfully killed with laser. The worm in Case 2 was removed surgically from the vitreous and identified as A. mesocercaria, 555 x 190 microns, most likely A. americana. The probable source of infection in the patients was ingestion, in local restaurants, of undercooked frogs' legs containing A. mesocercaria. In addition to causing prolonged intraocular infection, A. mesocercaria was found to be a cause of diffuse unilateral subacute neuroretinitis, a condition previously attributed only to intraocular nematode larvae.

A 56-d growth study compared the effects of lasalocid and decoquinate, or a combination of the two, on rate of gain and control of naturally occurring coccidiosis in weaned Holstein calves. Sixty-four calves (mean BW of 188 kg; age 16 wk) were blocked by BW and degree of oocyst shedding and assigned randomly to one of four treatments with 4 calves per pen and 4 pens per treatment. Treatment groups included an unmedicated control group, lasalocid at 1 mg/kg of BW, decoquinate at .5 mg/kg of BW, or lasalocid plus decoquinate. For the combination treatment, decoquinate was fed at the recommended rate for 28 d, followed by lasalocid for the remaining 28 d of the study. Diets were based on dry-rolled corn and haylage and were fed once daily for ad libitum feed consumption. Calves were weighed weekly, and feces were collected for quantitation of oocyst shedding. Oocyst shedding was low, and clinical coccidiosis was not observed. However, unmedicated calves shed oocysts at a higher rate than medicated calves. Small differences were found among treatments on overall rate of gain and gain efficiency. There was little advantage in gain or performance when calves with subclinical coccidiosis were medicated with anticoccidial agents.

Purpose: Several nematodes have been postulated as etiologic agents in diffuse unilateral subacute neuroretinitis (DUSN), but the cause of this condition remains uncertain. The authors report the first case of DUSN from the western United States (northern California), along with morphometric, serologic, and epidemiologic evidence supporting Baylisascaris procyonis as its cause., Methods: One patient was examined and evaluated for disc edema and transient obscurations of vision. A diagnosis of DUSN was confirmed when a motile nematode was identified within the substance of the patient's retina. Morphometric analysis of the nematode was done from projected fundus photographs. Serologic evidence of Baylisascaris infection was suggested by Western blot analysis. A necropsy was done on 12 raccoons from the area. They were examined for evidence of Baylisascaris infection, previously believed to be nonendemic in the region., Results: The intraocular nematode measured 1727 x 67 microns, most consistent with Baylisascaris. The patient had considerable exposure to raccoons, and was seropositive for B. procyonis infection on Western blot analysis. Necropsy evaluation showed B. procyonis infection in 8 of 12 raccoons examined from the area., Conclusions: The morphometric, serologic, and epidemiologic findings in this case provide evidence that the raccoon ascarid, B. procyonis, is a cause of the large nematode variant of DUSN.

Echinococcus multilocularis was identified in a coyote in Indiana in January 1990. Subsequently, 300 wild canids (red foxes, gray foxes, coyotes) were collected from Indiana, Ohio, Illinois, Michigan, and Kentucky and examined for this parasite. Of these, 41 (13.7%) were infected with E. multilocularis. Infected animals were from northern and central Indiana, northwestern Ohio, and east-central Illinois. Twenty-nine of 162 (17.9%) animals from northern and central Indiana were positive, versus 0 of 83 from southern Indiana. Infected animals from northern and central Indiana included 16 of 71 (22.5%) red foxes and 13 of 70 (18.6%) coyotes. In Ohio, 6 of 22 (27.3%) red foxes were infected, and in Illinois, 6 of 17 (35.3%) coyotes were positive. Mean intensity of infection for red foxes was 372 worms (range, 2-3, 640), and for coyotes, 6,579 worms (range, 1-52,000). These findings constitute new state and distribution records for E. multilocularis and a significant range extension for this parasite species in central North America.

Infection with Baylisascaris procyonis, the common roundworm of raccoons, was found to be the cause of an epizootic of fatal CNS disease in domestic rabbits (Oryctolagus cuniculus). Clinical signs included torticollis, ataxia, tremors, and falling. Gross lesions were limited to white, raised nodules (1 to 1.5 mm) on the epicardium, endocardium, and liver serosa, and they were found to be larval granulomas. Microscopic lesions included multifocal myocarditis, multifocal hemorrhagic tracks and associated necrosis and inflammation in the liver, multifocal eosinophilic myositis, focal nephritis, and mild interstitial pneumonia; larval granulomas were seen in the heart, liver, lung, and mandibular salivary gland. Lesions in the brain consisted of multifocal areas of necrosis and inflammation in the cerebrum, cerebellum, midbrain, and medulla, with accompanying perivascular leukocyte aggregates and neuronal and axonal degeneration. Large numbers of large ascarid larvae were seen in the brain. Epidemiologically, infection was linked to the use of contaminated straw from a barn used by raccoons. On the basis of this study as well as that of similar studies, it was concluded that barn use and contamination by raccoons may be an important source of infection of animals and possibly man with this parasite.

Two noncentrifugal and 5 centrifugal flotation methods for the recovery of infective Baylisascaris procyonis eggs from contaminated soil were evaluated after an epizootic of fatal cerebrospinal nematodiasis in bobwhites. All involved the use of inexpensive, readily available materials and routine procedures. In all but 1 of the methods, sizes of the soil samples were 30 g; in 1 centrifugal method, the sample size was 1 g. The centrifugal methods included various combinations of (i) anionic detergent (Tween) pretreatment of the soil, (ii) 3 X washing of the sediment, (iii) NaNO3 or ZnSO4 flotation solution, and (iv) resuspension and reexamination of the sediment. By the 30-g sample centrifugal methods, significantly more eggs (av 251 to 448) were recovered than by the noncentrifugal methods (av 7 and 12) or the 1-g sample method (av 44). In the most efficacious method, the combination of Tween pretreatment, washed sediment, NaNO3 flotation solution, and resuspension/reexamination of the sediment was used. This method was tested against the 1-g sample method on soil from a naturally occurring infection of Toxocara cati visceral larva migrans in a child. On initial examination of 5 areas, 3 to 10 eggs were recovered by the 30-g sample method vs 0 eggs by the 1-g sample method. Using sandbox soil and 10 replicates each, recoveries by the 30-g sample method averaged 9.2 eggs/replicate (range 5 to 12) and those by the 1-g sample method, 0.1 eggs (range 0 to 1).

Baylisascaris procyonis, the ascarid of raccoons, causes a characteristic, rapidly fatal eosinophilic meningoencephalitis with ocular involvement in many naturally and experimentally infected aberrant hosts, including monkeys. Warnings that humans are potentially susceptible to the devastating infection have been issued, but an instance in humans has not been recognized. This report describes a boy who died from an eosinophilic meningoencephalitis, which mimicked B. procyonis infection in monkeys. The causative agent was not identified during life. Autopsy showed a systemic larval ascarid infection with massive involvement of the brain. The size and anatomy of the larvae in histologic sections were identical to those recorded for B. procyonis. The larvae were indistinguishable from the B. procyonis larvae observed in histologic sections of experimentally infected monkeys. An indirect immunofluorescence test was positive for B. procyonis. Exposure to raccoon feces was highly likely. The evidence suggests that this is the first recognized B. procyonis infection in humans. Prudent avoidance of exposure to raccoon feces is indicated.

Following vaccination for distemper, using a modified live-virus vaccine developed for dogs, 2 young kinkajous (Potos flavus) developed diarrhea, then central nervous system disease. Clinical signs included myoclonus, head trembling, loss of muscular coordination, and convulsions. One kinkajou gradually recovered; the other seemed to recover, then relapsed and was euthanatized. Microscopic lesions included those of interstitial pneumonia and enteritis and multifocal lymphocytic inflammation, gliosis, spongiosis, and swollen and degenerating axons in the cerebral, cerebellar, and brain stem white matter. Similar lesions were found at all caudally, as exemplified by complete destruction of the dorsal funiculi and dorsal horns of the gray matter of the upper sacral cord segments. Eosinophilic intranuclear inclusions were seen histologically in the glia in the spinal cord, midbrain, and cerebellum, and were confirmed as canine distemper viral inclusions by the fluorescent antibody method. It was concluded that modified live canine distemper virus vaccines should be used with caution or not at all in kinkajous.

Twenty-six of 97 (27%) scats from raccoons (Procyon lotor) in an urban area and 37 of 121 (31%) scats from raccoons collected in a rural area of Indiana during October and November of 1980 contained eggs of Baylisascaris procyonis, an ascarid of animal health significance. Raccoons that were livetrapped from the same areas had similar prevalences of B. procyonis eggs in their feces. Therefore, monitoring the prevalence of B. procyonis in raccoon populations by analyzing scats appeared to be feasible.

Baylisascaris spp larvae were determined to cause CNS disease in 3 prairie dogs maintained at a research facility. Clinical signs consisted of ataxia, stumbling, and head tilt, which progressed to severe torticollis, paddling in lateral recumbency, and loss of the righting reflex. Gross lesions were not found at necropsy. Microscopically, the cerebellar white matter and medulla oblongata were most severely affected and had numerous sections of large ascarid larvae. Our findings indicated that natural infections of Baylisacaris spp larvae can cause CNS disease in prairie dogs. Also, Baylisascaris spp larval infection should be considered in differential diagnoses of CNS disease in prairie dogs.

Genetic relationships of 20 Trichinella isolates from Indiana wildlife were assessed and compared to Trichinella isolated from an infected swine herd. Trichinella larvae were isolated from coyotes, mink, raccoons, and red foxes. The larvae were maintained and amplified in white mice (ICR) and wild mice (Peromyscus leucopus). Differences in phenotypic characters of sylvatic isolates in the 2 laboratory hosts included an approximately 10-30-fold increase in parasite fecundity in wild mice. DNA for each isolate was extracted from Trichinella larvae and analyzed by dot-blot hybridization using a repetitive DNA probe pBP2 that recognizes DNA sequences specific for swine Trichinella. The probe hybridized only to Trichinella from swine and a single coyote isolate. Restriction endonucleases were used to digest DNA and the resulting fragments were separated by gel electrophoresis. Based on the presence of repetitive DNA sequences in the Trichinella genome, distinctive banding patterns were seen among the isolates. Trichinella isolated from swine had a pattern distinct from all sylvatic isolates except 1 from a coyote. Because this coyote was from the same general locality as the swine Trichinella outbreak, it was concluded that the isolate represents transmission of swine trichinellosis to the wildlife population. Further analysis using the enzyme Cla I identified unique banding patterns for wild isolates, suggesting that the sylvatic group is a genetically heterogeneous complex.

Renal styphlodoriasis was diagnosed in a 2 1/2-year-old male boa constrictor (Constrictor constrictor). The snake had been anorexic for 6 months prior to its death. Necropsy revealed numerous hard, white foci of mineralization in the kidneys. Histologic examination revealed distorted renal tubules containing cross sections of trematodes or mineralized debris, tubular epithelial hyperplasia, and chronic interstitial nephritis. Several adult trematodes were recovered and identified as Styphlodora horrida.

Larvae of the common raccoon roundworm, Baylisascaris procyonis, are known causes of visceral larva migrans and CNS disease in animals and human beings. In the present experiments we examined the ability of B. procyonis to cause ocular larva migrans (OLM) in subhuman primates, as an indication of its possible ocular zoonotic importance. Squirrel monkeys given 5,000 or 10,000 infective B. procyonis eggs per os and cynomolgus monkeys given 20,000 eggs had clinical and histologic evidence of OLM, beginning 7 days after inoculation. Clinically, multifocal retinal hemorrhages, white spots, chorioretinitis, inflammatory tracks, vascular sheathing, diffuse retinal degeneration, and motile intraretinal larvae were seen. Histologically, primarily subretinal larvae caused varying degrees of retinal disruption, degeneration and necrosis, retinitis, vasculitis, and perivascular sheathing, primarily with eosinophils. Larvae were also present in choroidal granulomas. It was concluded that B. procyonis larvae have marked ability to produce OLM in subhuman primates following oral infection and should be considered as a possible etiology in human ocular disease.