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Baylisascariasis

[Baylisascaris procyonis]

Causal Agents

Human baylisascariasis is caused by larvae of Baylisascaris procyonis, an intestinal nematode of raccoons.

Life Cycle

lifecycle

Baylisascaris procyonis completes its life cycle in raccoons, with humans acquiring the infection as accidental hosts (dogs serve as alternate definitive hosts, as they can harbor patent and shed eggs). Unembryonated eggs are shed in the environment The Number 1, where they take 2-4 weeks to embryonate and become infective The Number 2. Raccoons can be infected by ingesting embryonated eggs from the environment The Number 3. Additionally, over 100 species of birds and mammals (especially rodents) can act as paratenic hosts The Number 4 for this parasite: eggs ingested by these hosts hatch and larvae penetrate the gut wall and migrate into various tissues where they encyst The Number 5. The life cycle is completed when raccoons eat these hosts The Number 6. The larvae develop into egg-laying adult worms in the small intestine The Number 7 and eggs are eliminated in raccoon feces. Humans become accidentally infected when they ingest infective eggs from the environment; typically this occurs in young children playing in the dirt The Number 8. Migration of the larvae through a wide variety of tissues (liver, heart, lungs, brain, eyes) results in VLM and OLM syndromes, similar to toxocariasis The Number 9. In contrast to Toxocara larvae, Baylisascaris larvae continue to grow during their time in the human host. Tissue damage and the signs and symptoms of baylisascariasis are often severe because of the size of Baylisascaris larvae, their tendency to wander widely, and the fact that they do not readily die. Diagnosis is usually made by serology, or by identifying larvae in biopsy or autopsy specimens.

Geographic Distribution

Raccoons infected with Baylisascaris procyonis appear to be common in the Middle Atlantic, Midwest, and Northeast regions of the United States and are well documented in California and Georgia. Proven human cases have been reported in California, Oregon, New York, Pennsylvania, Illinois, Michigan, and Minnesota, with a suspected case in Missouri.

Clinical Presentation

Human infections can be asymptomatic. However, because these larvae continue to grow and wander in the human host, infections often result in severe disease manifestations. Much like toxocariasis, infection with Baylisascaris can result in visceral larva migrans (VLM) or ocular larva migrans (OLM) syndromes. The larvae of B. procyonis have a tendency to invade the spinal cord, brain, and eye of humans, resulting in permanent neurologic damage, blindness, or death. Human infection with Baylisascaris appears to be rare. To date, 13 well documented Baylisascaris encephalitis cases, and 1 suspected case in a young girl with CNS larva migrans, have been reported. The prevalence of subclinical cases is unknown. Because there is no widely available definitive diagnostic test for humans infected with this parasite, many cases are not diagnosed initially.

Baylisascaris procyonis eggs.

 

Baylisascaris procyonis eggs are 80-85 µm by 65-70 µm in size, thick-shelled, and usually slightly oval in shape. They have a similar morphology to fertile eggs of Ascaris lumbricoides, although eggs of A. lumbricoides are smaller (55-75 µm by 35-50 µm). The definitive host for B. procyonis is the raccoon, although dogs may also serve as definitive hosts.  As humans do not serve as definitive hosts for B. procyonis, eggs are not considered a diagnostic finding and are not excreted in human feces. The following images show larval development within the eggs, from a freshly-shed unembryonated egg to eggs containing L1 larvae. The images are all courtesy of Dr. Cheryl Davis, Western Kentucky University, KY.
	Figure A

Figure A: Unembryonated egg of B. procyonis

	Figure B

Figure B: Egg of B. procyonis. In this specimen, the developing embryo has started to divide.

	Figure C

Figure C: Eggs of B. procyonis in a further state of cleavage.

	Figure D

Figure D: Eggs of B. procyonis in a further state of cleavage.

	Figure E

Figure E: Embryonated eggs of B. procyonis, showing the developing larva inside.

	Figure F

Figure F: Embryonated eggs of B. procyonis, showing the developing larva inside.

Baylisascaris procyonis hatching larvae.

	Figure A

Figure A: Larva of B. procyonis hatching from an egg.

Viable B. procyonis egg in formalin, recovered from a raccoon.

	Figure A

Figure A: Egg of B. procyonis in formalin-fixed stool from a raccoon. Animated image contributed by the Oregon State Public Health Laboratory.

Larvae of Baylisascaris spp. in tissue.
B procyonis adults.
	Figure A

Figure A: Cross-sections of larvae of B. columnaris in the brain of a laboratory-infected mouse. The larval morphology and microscopic manifestations would be similar with B. procyonis in human tissue.Image taken at 400x magnification.

	Figure B

Figure B: Higher magnification (1000x oil) of a cross-section of B. columnaris from the same specimen as Figure A. Notice the prominent alae (green arrows), excretory columns (red arrows) and multinucleate intestinal cells (blue arrow).

	Figure C

Figure C: Cross-sections of larvae of B. columnaris in muscle of a laboratory-infected mouse. The larval morphology and microscopic manifestations would be similar with B. procyonis in human tissue. Image taken at 400x magnification.

B. procyonis adults.

 

Baylisascaris procyonis adults are found only in the definitive host, the raccoon. They have the typical form of ascarid worms. Males measure 60-80 mm in length and demonstrate the curved posterior end similar to Ascaris. Females measure 80-120 mm in length.
	Figure A

Figure A: Several adults of B. procyonis from a raccoon

Laboratory Diagnosis

Human infections are difficult to diagnose, and often the diagnosis is by exclusion of other causes. Results from complete blood count (CBC) and cerebrospinal fluid (CSF) examination would be consistent with parasitic infection, but tend to be nonspecific. Examination of tissue biopsies can be extremely helpful if a section of larva is contained, but removing an appropriate piece of tissue where the larva is actually present can be problematic. Ocular examinations revealing a migrating larva, larval tracks, or lesions consistent with a nematode larva are often the most significant clue to infection with Baylisascaris. Serologic testing can be extremely helpful in suspected cases; however, tests are not routinely in use nor widely available.

Treatment Information

In cases where suspicion of exposure is high, immediate treatment with albendazole (25-50 mg/kg per day by mouth for 10 – 20 days) may be appropriate. Treatment is successful when administered soon after exposure to abort the migration of larvae. Indications for immediate treatment may include known oral exposure to raccoon feces, presence of Baylisascaris eggs in the feces of the implicated animal or animals, and suspected oral exposure to raccoon feces in an area where the prevalence of raccoon infection is known to be high. Treatment should be initiated as soon as possible after ingestion of infectious material, ideally within three days. If albendazole is not immediately available, mebendazole or ivermectin may be used in the interim.

For clinical baylisascariasis, treatment with albendazole, at the dose given above, with concurrent corticosteroids to help reduce the inflammatory reaction is indicated to attempt to control the disease.

Albendazole

Oral albendazole is available for human use in the United States.

Albendazole is pregnancy category C. Data on the use of albendazole in pregnant women are limited, though the available evidence suggests no difference in congenital abnormalities in the children of women who were accidentally treated with albendazole during mass prevention campaigns compared with those who were not. In mass prevention campaigns for which the World Health Organization (WHO) has determined that the benefit of treatment outweighs the risk, WHO allows use of albendazole in the 2nd and 3rd trimesters of pregnancy. However, the risk of treatment in pregnant women who are known to have an infection needs to be balanced with the risk of disease progression in the absence of treatment.

Pregnancy Category C: Either studies in animals have revealed adverse effects on the fetus (teratogenic or embryocidal, or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the fetus.

It is not known whether albendazole is excreted in human milk. Albendazole should be used with caution in breastfeeding women.

 

The safety of albendazole in children less than 6 years old is not certain. Studies of the use of albendazole in children as young as one year old suggest that its use is safe. According to WHO guidelines for mass prevention campaigns, albendazole can be used in children as young as 1 year old. Many children less than 6 years old have been treated in these campaigns with albendazole, albeit at a reduced dose.

Mebendazole

Mebendazole is available in the United States only through compounding pharmacies.

Mebendazole is in pregnancy category C. Data on the use of mebendazole in pregnant women are limited. The available evidence suggests no difference in congenital anomalies in the children of women who were treated with mebendazole during mass treatment programs compared with those who were not. In mass treatment programs for which the World Health Organization (WHO) has determined that the benefit of treatment outweighs the risk, WHO allows use of mebendazole in the 2nd and 3rd trimesters of pregnancy. The risk of treatment in pregnant women who are known to have an infection needs to be balanced with the risk of disease progression in the absence of treatment.

Pregnancy Category C: Either studies in animals have revealed adverse effects on the fetus (teratogenic or embryocidal, or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the fetus.

It is not known whether mebendazole is excreted in breast milk. The WHO classifies mebendazole as compatible with breastfeeding and allows the use of mebendazole in lactating women.

The safety of mebendazole in children has not been established. There is limited data in children age 2 years and younger. Mebendazole is listed as an intestinal antihelminthic medicine on the WHO Model List of Essential Medicines for Children, intended for the use of children up to 12 years of age.

Ivermectin

Oral ivermectin is available for human use in the United States.

Ivermectin is pregnancy category C. Data on the use of ivermectin in pregnant women are limited, though the available evidence suggests no difference in congenital abnormalities in the children of women who were accidentally treated during mass prevention campaigns with ivermectin compared with those who were not. The World Health Organization (WHO) excludes pregnant women from mass prevention campaigns that use ivermectin. However, the risk of treatment in pregnant women who are known to have an infection needs to be balanced with the risk of disease progression in the absence of treatment.

Pregnancy Category C: Either studies in animals have revealed adverse effects on the fetus (teratogenic or embryocidal, or other) and there are no controlled studies in women or studies in women and animals are not available. Drugs should be given only if the potential benefit justifies the potential risk to the fetus.

Ivermectin is excreted in low concentrations in human milk. Ivermectin should be used in breast-feeding women only when the risk to the infant is outweighed by the risk of disease progress in the mother in the absence of treatment.

The safety of ivermectin in children who weigh less than 15kg has not been demonstrated. According to the WHO guidelines for mass prevention campaigns, children who are at least 90 cm tall can be treated safely with ivermectin. The WHO growth standard curves show that this height is reached by 50% of boys by the time they are 28 months old and by 50% of girls by the time they are 30 months old, many children less than 3 years old been safely treated with ivermectin in mass prevention campaigns, albeit at a reduced dose.

 

DPDx is an education resource designed for health professionals and laboratory scientists. For an overview including prevention and control visit www.cdc.gov/parasites/.

  • Page last reviewed: May 3, 2016
  • Page last updated: May 3, 2016
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