Raccoon SNC

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Journal of Veterinary Diagnostic Investigation

23(5) 873 –884

© 2011 The Author(s)

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DOI: 10.1177/1040638711416851

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Review Article

Introduction

In 1981, the article “Neurologic disorders in the raccoon

from northeastern United States” was published,91 which

described viral, toxic, and neoplastic causes that affected the

central nervous system (CNS) of raccoons ( Procyon lotor ).

At that time, the authors were able to describe a total of 8 indi-

vidual conditions in this species that affected the CNS. Since

then, there has been ever-growing new information pub-

lished, predominantly single case reports, on this subject.

Therefore, the aim of the current review is to provide docu-

mentation of diseases and pathological conditions that have

influenced the nervous system of North American raccoonssince the 1980s.

Geographic distribution

Raccoons belong to the family Procyonidae, in which there

are 9 genera and a total of 18 species.28

The genus Procyon has

7 species. Procyon lotor is found over a large geographical

area of North America. It ranges from southern Canada through

most of the continental United States and into Central America.

Raccoons have been introduced in many other parts of the

world from North America. Between 1931 and 1958, over a

thousand raccoons were released in widely scattered areas

of the former USSR for their fur,1 and the 1964 figures

estimated that there were between 40,000 and 45,000 in

that region.1According to a study published in 1966, the intro-

duced animals have lost most of their North American parasites,

but have acquired new species of endoparasites and ectopara-

sites.1 Raccoons were introduced into German forests in the

1930s and today, as many as 1 million raccoons are estimated

to be in that country.24

Since their introduction, raccoons

have moved across the border to infest most of Germany’s

XXX23510.1177/1040638711416851Hami

From the National Animal Disease Center, Agricultural Research

Service, United States Department of Agriculture, Ames, IA.

1Corresponding Author: Amir N. Hamir, Department of Veterinary

Medicine and Surgery–Unit 63, M.D. Anderson Cancer Center, 1515

Holcombe Boulevard, Room 4055C, Houston, TX 77030. ahamir@

mdanderson.org

Pathology of neurologic disorders

of raccoons ( Procyon lotor )

Amir N. Hamir

1

Abstract. The raccoon ( Procyon lotor ) is almost ubiquitous in North America. In recent times, it was introduced in many

parts of the world where it has now become largely feral. Since the outbreak of raccoon rabies epizootic in eastern United States

and Canada, most diagnostic laboratories have had increased numbers of raccoon carcasses or raccoon brain submissions for

diagnosis of rabies. However, since a number of other diseases that affect the central nervous system and have similar clinical

signs as rabies have been documented in this species, the current review attempts to bring together the published information

on neurologic disorders of raccoons.

Key words: Diseases of central nervous system; infectious; neoplastic; pathologic disorders; raccoons ( Procyon lotor );

toxic conditions.

neighbors. Also, starting in the 1970s, raccoons were imported

into Japan as pets.83 Since then, the number of escaped and

abandoned raccoons in that country has increased, and the

animal has become largely feral.83

Raccoons are primarily nocturnal and are most active at

dawn and dusk (unless they suffer from neurologic disorders).

They prefer to make their dens in trees near water. They are

omnivorous and will flourish on a wide variety of feeds but

prefer frogs, mussels, fish, small mammals, invertebrates, and

a wide selection of seeds.28

The breeding season of the raccoon is long (January –June),

and it is not uncommon for females in the southern latitudesto have 2 litters per year.28 The gestation period averages

63 days in length, but may vary from 60 to 73 days. In each

litter, there are 1–7 kits (average 3–4) that weigh approximately

70 g at birth. The females begin to bear young at 1 year of

age. Although the life expectancy of the raccoon can exceed

10 years in captivity, free-ranging raccoons usually do not sur-

vive beyond 2 years78 because most raccoons do not survive

predation and diseases in the wild.78

Raccoons are highly susceptible to a variety of infectious

diseases, both in free-ranging and under experimental con-

ditions (Fig. 1). Many of these diseases are common to

domestic dogs and cats. Raccoons can also transmit many

diseases to human beings and animals. Since raccoons share

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874 Hamir

our immediate habitat, they have been used as environmen-

tal sentinels.6,40

Diseases

The following brief description of diseases and lesions con-

sisting of various infectious agents (predominantly viral causes),

and other noninfectious conditions such as toxic, neoplastic,

and other incidental but abnormal conditions have been

documented in raccoons. Although many viral diseases of

raccoons have been documented, only a handful of bacterial

diseases, namely leptospirosis,44 tuberculosis,8 campylobac-

teriosis,69 Tyzzer disease,103 nocardiosis,65 listeriosis,51 and

Staphylococcus aureus36 have been reported in this species.

However, none of these bacterial agents appeared to have

caused any neurologic problems in raccoons. Similarly, only

a few fungal infections, namely oral candidiasis51

and pulmo-

nary adiaspiromycosis,35 have been reported in raccoons but

none have involved the CNS.

Rabies

Rabies followed by canine distemper are the 2 most important

diseases that affect the CNS of raccoons. Rabies virus (order

Mononegavirales, family Rhabdoviridae, genus Lyssavirus)causes an acute, progressive polioencephalomyelitis, with a

high mortality. Once the clinical signs of the disease appear,

it is usually considered to be invariably fatal, and only a hand-

ful of clinical cases of rabies have survived the disease.57,102

The epizootic rabies among raccoons was first identified in

Florida in the 1940s, and the area affected gradually expanded

into other southeastern states. In the late 1970s, a second focus

of rabies among raccoons emerged on the border of West

Virginia and Virginia.12,25 Epizootiologic and virologic

investigations indicated that this new focus resulted from

the translocation of raccoons incubating rabies from the

Figure 1. Three experimental raccoon ( Procyon lotor ) kits in

a plastic tunnel (provided for enrichment of their environment) at

the National Animal Disease Center, Ames, Iowa.

southeastern United States and, that for the first time in 1990,

raccoons outnumbered skunks as the primary rabies reser-

voir in the United States. In 2008, there were 6,841 cases of

rabies in animals, of which 2,389 (34.9%) were in raccoons.7

Since 2000, at least 1 case of human rabies has been attrib-

uted to the raccoon Rabies virus variant.7

Rabid raccoons, like other infected animals, exhibit dra-matic neurologic signs. At necropsy, gross lesions are not

seen in the CNS.55,56 For the diagnosis of rabies, a fluorescent

antibody test is used on fresh brain tissue, which is the gold

standard for the confirmation of the disease. Histologically,

severe and extensive histopathologic lesions of nonsuppura-

tive polioencephalomyelitis with marked perivascular cuff-

ing with mononuclear cells (Fig. 2) are commonly seen in

the cerebrum, brainstem, and spinal cord sections of raccoons

that were experimentally infected with the raccoon Rabies

virus strain (Fig. 3). Those infected with a canine strain of

Rabies virus had lesions confined to the brainstem and spinal

cord (Fig. 3), and these raccoons died suddenly without

showing marked neurologic signs.56 Therefore, it appearsthat the distribution of lesions in the brain of a raccoon would

depend on the source of the infection. Raccoons infected with

the raccoon isolate of Rabies virus show numerous neuronal

inclusions (Negri bodies) in the CNS (Fig. 4) as well as in non-

CNS tissues such as tongue, salivary glands, pancreas, para-

adrenal glands (Fig. 5), and intestines. In the non-CNS organs,

the viral inclusions are present within ganglion cells.55

In

raccoons naturally infected in the raccoon rabies endemic

areas, the immunohistochemical labeling for the antigen was

widely dispersed.99

Canine distemperIn addition to the dog, Canine distemper virus (CDV; order

Mononegavirales, family Paramyxoviridae, subfamily

Paramyxovirinae, genus Morbillivirus) is seen in a variety

of other carnivores and is considered a major disease prob-

lem of raccoons. Natural outbreaks and lesions of the disease

have been documented in raccoons.75,80,86 In most cases, there

is generalized depletion of cells in lymphoid organs (lymph

nodes, spleen, bone marrow, etc.), diffuse interstitial pneumo-

nia, and multifocal areas of cerebellar necrosis (Fig. 6) with

demyelination of the cerebellar white matter.94

Viral inclu-

sions are present in many tissues (Fig. 8). A previous study31

documented the incidence and anatomic locations of distemperinclusions, which include the brain, bronchi, salivary glands,

bile ducts, lymph nodes, spleen, urinary bladder, stomach,

colon, and adrenal glands. Testicular degeneration and min-

eralization of seminiferous tubules has also been described

in raccoons with this infection.59

Since CDV infection pro-

duces immunosuppression in the host, it is susceptible to a

variety of secondary opportunistic infections, and occasional

cases of concurrent infections with rabies, toxoplasmosis,

Tyzzer disease, and neosporosis have been documen

ted.16,32,61,70,87,103

Morphologically, because of the immuno-

suppression caused by canine distemper, there is usually a







Pathology of neurologic disorders of raccoons 875

Figure 2. Top, location of microscopic lesions in brain and anterior cervical spinal cord of raccoon ( Procyon lotor ) experimentally

infected with a raccoon isolate of street Rabies virus. Bottom, location of microscopic lesions in brain and anterior cervical spinal cord

of raccoon experimentally infected with a canine isolate of street Rabies virus. ● = presence of nonsuppurative encephalitis. Figure 3.

Rabies virus –infected raccoon ( Procyon lotor ) brain; cerebrum. There is polioencephalomyelitis characterized by multifocal gliosis and

perivascular cuffing with mononuclear cells. Hematoxylin and eosin. Bar = 200 µm. Figure 4. Rabies virus –infected raccoon ( Procyon

lotor ) brain; cerebellum. One Purkinje cell showing 2 eosinophilic cytoplasmic inclusions (Negri bodies). Hematoxylin and eosin. Bar

= 200 µm. Figure 5. Rabies virus –infected raccoon ( Procyon lotor ); para-adrenal gland ganglion. Numerous eosinophilic cytoplasmic

inclusions are present in the cytoplasm of ganglion cells. Hematoxylin and eosin. Bar = 50 µm.








876 Hamir

Figure 6. Raccoon ( Procyon lotor ) with Canine distemper virus infection; cerebellum. There is a focal area of cerebellar necrosis

involving granular and Purkinje cell layers. Hematoxylin and eosin. Bar = 200 µm. Figure 7. Raccoon ( Procyon lotor ) with Canine

distemper virus infection; cerebellum. Viral antigen is present in the granular, Purkinje cell, and molecular layers. Immunohistochemistry,

immunoperoxidase method, 3,3′-diaminobenzidine with hematoxylin counterstain. Bar = 200 µm. Figure 8. Raccoon ( Procyon lotor )

with Canine distemper virus infection; cerebellum. There is extensive nonsuppurative encephalitis with presence of intranuclear eosinophilic

inclusions (arrows) in many of the glial cells. Hematoxylin and eosin. Bar = 100 µm. Figure 9. Raccoon ( Procyon lotor ) brain; cerebellum.

Molecular layer shows a sarcocyst (arrow) of Sarcocystis kirkpatricki. Note there is no cellular response to the presence of the parasite.

Hematoxylin and eosin. Bar = 400 µm. Figure 10. Raccoon ( Procyon lotor ) adrenal gland with ganglioneuroma. There is a lobulated

nodular mass consisting of ganglion cells attached to the adrenal gland (A). Hematoxylin and eosin. Bar = 500 µm.









paucity of host cellular inflammatory infiltrate that is directed

at the opportunistic pathogen. The CDV antigen (Fig. 7), how-

ever, can be demonstrated in the brains of these raccoons.61,70

Pseudorabies and herpesvirus encephalitis

Although since 2003 no commercially produced pig herdshave been found to be infected with Pseudorabies virus,

sporadic infections have been found in feral pigs. Prior to

1981, there had been 2 reports of herpesviral infection in

raccoons.91,97

Although the affected raccoon tissues were

examined by electron microscopy, the tissues were not tested

for the presence of pseudorabies. The disease can infect many

mammalian species and, on the basis of experimental

evidence, the raccoon is considered a major reservoir of

Pseudorabies virus.104 Microscopically, pseudorabies cases

involve the brain and show herpes-like viral lesions in neu-

ronal and non-neuronal tissues.30 A non-pseudorabies her-

pesviral disease has also been described in a raccoon with

lesions in non-neuronal tissues.60 The only documentedcase of herpesvirus encephalitis was described in 1981.91 The

encephalitis was characterized by perivascular cuffing,

choroiditis, and presence of magenta-colored intranuclear

inclusions in choroid plexus and adrenal medulla.91 As indi-

cated previously, the case was not differentiated from pseu-

dorabies.

Other viral diseases

Encephalomyocarditis virus (order Picornavirales, family

Picornaviridae, genus Cardiovirus) was isolated from a rac-

coon in Florida,26 and an experimental transmission study

has been documented.105 However, although some of the

raccoons in the study seroconverted, no clinical signs or

lesions were observed in the experimental raccoons.105 In

addition to the above-mentioned diseases that affect the ner-

vous system, raccoons have been shown to have evidence

(serology, polymerase chain reaction, Western blot, etc.) of

other viruses such as Venezuelan equine encephalitis virus5

and West Nile virus.29 However, clinical cases of these dis-

eases have not been documented in raccoons.

Prion diseases

Although naturally occurring transmissible spongiform enceph-alopathies (TSEs) have not been reported in the raccoon,

reports of successful experimental transmission of similar

spongiform diseases, transmissible encephalopathy of mink

(TME) and sheep scrapie, have been documented in this spe-

cies21,49,52,53

by intracerebral (IC) and oral inoculations.21

In

the IC-infected route, the raccoons were administered TME

and developed a rapidly progressive disease within 190 days,

whereas the orally infected raccoon developed neurologic

signs after 306 days, which included weakness, behavior

change, and incoordination. Scrapie-infected raccoons required

a 2-year period to develop the disease when inoculated by the

IC route.49,52,53 Microscopically, the lesions were identical in

both groups (TME and scrapie) and consisted of widespread

vacuolar changes, neuronal degeneration, and astrocytosis in

the brain (except in cerebellum). Neuronal vacuolar changes,

although described in scrapie and related diseases including

naturally occurring TME, were rare.49,52,53

According to some researchers, Spiroplasma mirum is

the causative agent of animal TSEs.3,4 However, when

this organism was inoculated intracerebrally into raccoons,

they did not succumb to any form of disease, and neither

lesions nor abnormal prion protein of TSE was detected in

the brains of these animals when necropsied at 30 months

postinoculation.42

Toxoplasmosis

Various surveys indicate a high prevalence of Toxoplasma

gondii antibodies in U.S. raccoon populatiotns,9,16,77 and, in

1992, a case of clinical toxoplasmosis with presence of theorganism in liver and brain was reported.16 In the 1992 case,

the raccoon was also found to have co-infection with CDV.16

Experimental transmission of the organism has also been

shown in the raccoon.18

Neospora caninum

Antibodies to Neospora caninum were demonstrated in approx-

imately 10% of raccoons from the eastern United States88 and,

to date, only 1 naturally occurring case in a juvenile rac-

coon has been documented.87 This raccoon also had con-

current CDV infection. Thus, the findings of necrotizing

encephalitis in the raccoon were largely due to the viral

infection.87

Sarcocystis neurona encephalitis

Sarcocystis neurona is the etiological agent of equine protozoal

myeloencephalitis (EPM), which has resulted in the deaths

of large numbers of horses in North America. Sarcocystis

neurona has also been reported in the raccoon, skunk, mink,

and cat.15,17,20 In a retrospective survey of 84 adult raccoons,

2 raccoons were found with S. neurona– associated granulo-

matous encephalitis.38 Both raccoons also had extensive non-

suppurative myocarditis and 1 raccoon revealed S. neurona in the myocardium by immunohistochemistry. The CNS

lesions were characterized by perivascular infiltration with

mononuclear cells and presence of randomly distributed

glial nodules. The organisms were observed in the inflamma-

tory foci.38

The life cycle of S. neurona is not fully under-

stood. The opossum is recognized as a definite host, and horses

and other susceptible animals are considered as aberrant

hosts. Susceptible animals become infected by ingesting S.

neurona sporocysts, which get excreted in feces of infected

opossums.19








878 Hamir

Other Sarcocystis species in brain

Four species of Sarcocystis have been reported in striated

muscles of raccoons.81,98

However, in North America, only

Sarcocystis kirkpatricki has been documented in the muscles

of raccoons. Although the prevalence of infection of this para-

site appears to be variable, up to 50% of raccoons in a studyfrom the northeastern United States were found to be infected

in the heart, tongue, diaphragm, masseter muscle, or the

esophagus.81 A previous study98 designated this organism

S. kirkpatricki and reported a prevalence of 66% in raccoons

from Illinois. Neither of these studies reported Sarcocystis in

the brain of these raccoons. Subsequently, there has been a

single report of S. kirkpatricki in the cerebellum (Fig. 9)

of a raccoon with dual infections of T. gondii and CDV.16

Also, a retrospective survey of 760 raccoons revealed 9 ani-

mals with sarcocysts of S. kirkpatricki in the brains.39 Seven

of the raccoons had concurrent viral diseases (canine distem-

per or rabies), suggesting that concurrent viral infections

in raccoons may facilitate infection of brain tissue withS. kirkpatricki.39

Eosinophilic meningitis and encephalitis

In normal free-ranging raccoons, eosinophilia of cerebrospi-

nal fluid appears to be a common finding.71 A case of gener-

alized eosinophilic myositis with eosinophilia of blood and

cerebrospinal fluid has been described in a raccoon,66 which

was presumed to be due to immune-mediated causes. Also,

a raccoon with experimental canine Rabies virus infection

has been documented with eosinophilic polioencephalomy-

elitis.62 However, that raccoon did not show eosinophilia of

the blood.

Neural and visceral larva migrans

Neural and visceral larva migrans have been documented in

a large number of domestic and wild animal species (Snyder

DE: 1983, The prevalence, cross-transmissibility to domes-

tic animals and adult structure of Baylisascaris procyonis

(Nematoda) from Illinois raccoons ( Procyon lotor ). PhD diss.

University of Illinois, Urbana, IL).79 The common round

worm, Baylisascaris procyonis, found in raccoons, appears

to be a frequent etiologic agent that is responsible for severe

CNS disease in these parantenic hosts. However, viscerallarva migrans due to B. procyonis has not been documented

in raccoons. Other nematode species known to cause neu-

ral and visceral larva migrans include Toxocara spp.,

Angiostrongylus spp., and Strongyloides spp.

In raccoons, a form of visceral larva migrans associated

with a trematode ( Phagicola sp.) has been described.67

However, these parasites did not migrate into neuronal tissues.

A case of verminous encephalitis associated with an ascarid

larval nematode in a raccoon has been described.68 Although

the morphologic characteristics indicated that the nema-

tode was an ascarid larva, it was smaller than the larva of

Baylisascaris sp. This appears to be the first documented

case of cerebral larva migrans in a raccoon.68

Neoplasms

Neoplastic lesions have infrequently been documented in the

family Procyonidae. With the exception of thyroid adeno-

mas76,85 and adrenal gland adenomas,64 neoplasia appears to

be rather rare in raccoons, and only infrequent case reports

have been documented. In a retrospective survey of over

400 raccoon necropsies,13

only 1 astrocytoma of the brain

was found. Since that time, 1 additional astrocytoma involving

the brain, cervical spinal cord, and spinal nerves has been

documented.58 In both cases, the characteristics of the neo-

plasm were similar to that published in other species. Also,

a ganglioneuroma involving an adrenal gland has been seen

(Fig. 10; Hamir AN, personal observation).

Environmental toxins

Lead

Lead is an environmental toxin with multisystemic toxic

effects.31,34 A clinical case showing neurologic abnormalities

in a free-ranging raccoon has been documented,14

and also

high levels of tissue lead levels have been reported from dif-

ferent areas of the United States.14,39 In the reported case,14

the CNS lesions were subtle and consisted of mild endothe-

lial hyperplasia and scattered neuronophagia. In experimental

animals, administration of inorganic lead may lead to the

impairment of immune functions, resulting in increased sus-

ceptibility to infectious agents.74,84,90

Although neurologic

manifestations of lead toxicosis has been reported in a rac-

coon,14

experimental administration of oral lead acetate did

not succeed in producing neurologic signs when the com-

pound was administered over an 8-week period.50

Ethylene glycol

Neurologic signs of ethylene glycol (antifreeze) toxicity include

depression, ataxia, seizures, and coma,22

and since these signs

can be confused with other disorders in this species, clinical

differential diagnosis of this condition is rather difficult. Adiagnosis of ethylene glycol toxicosis is rarely reported in

free-ranging wildlife;2 however, morphologic lesions of this

toxicity are often seen in diagnostic cases. There has been

only 1 reported case of ethylene glycol poisoning in a free-

ranging raccoon.22

Since antifreeze is commonly found in

the environment, and cases of this toxicity are frequently

seen in domestic animals, it may be assumed that cases of

ethylene glycol toxicity are being overlooked in free-ranging

wildlife.









Figure 11. Raccoon ( Procyon lotor ) brain. Coronal sections of cerebrum showing a unilateral area devoid of brain parenchyma due

to chronic ischemia. Figure 12. Raccoon ( Procyon lotor ) brain; globus pallidus. There is multifocal mineralization in the wall of blood

vessels. Hematoxylin and eosin. Bar = 200 µm. Figure 13. Raccoon ( Procyon lotor ) brain; choroid plexus. Four small blood vessels

show concentric mineralized foci (psommoma bodies). Hematoxylin and eosin. Bar = 200 µm. Figure 14. Raccoon ( Procyon lotor ) brain;

dorsal medulla oblongata. Foci of neuroaxonal degeneration with presence of vacuolar change and hypereosinophilic spheroids in the area

of nucleus gracilis. Hematoxylin and eosin. Bar = 400 µm. Figure 15. Raccoon ( Procyon lotor ) brain. Brainstem showing aggregates of

magenta-colored polyglucosan inclusions (Lafora bodies) in the neuropil. Periodic acid–Schiff. Bar = 200 µm.








880 Hamir

Trauma

It has been the author’s experience that during routine nec-

ropsy of free-ranging raccoons (>500) from the eastern and

northwestern United States,55 minor abrasions and/or trauma

to the skin was a common finding in these animals. Fighting

among males appeared to be the main reason for these skinlesions (Hamir AN, personal observation). Physical trauma

due to gunshot wounds, collisions with automobiles, and

falls from heights (in raccoons with neurologic abnormalities)

were frequently observed in field specimens. In the latter

cases, the animals had usually some preexisting neurological

abnormalities. One raccoon with neurologic signs was observed

to have a piece of porcupine quill logged in the brain tissue

(Hamir AN, personal observation).

Miscellaneous conditions of unknown etiology

Ischemic encephalopathy

One acute and 1 chronic case of cerebral infarction syndrome

has been described in a free-ranging and a laboratory-

confined raccoon, respectively.63 Both were mature adults.

The raccoon with the acute form of the condition had abnor-

mal neurologic signs whereas the raccoon with the chronic

lesion did not. In the chronic case, the lesion was present

unilaterally (Fig. 11) and since only one-half of the brain

was available for examination in the acute case, it was not

possible to determine if there were multiple lesions. In both

cases, the nature and distribution of the lesions was compat-

ible with an ischemic etiology, although vascular lesions

were not observed.63

Cerebrovascular mineralization

A case of cerebrovascular mineralization in an aged (>10

years old) female with uremia associated with polycystic

kidney disease has been reported in a raccoon.47 The vascu-

lar lesions were bilateral and consisted of multifocal miner-

alized foci in the walls of blood vessels in globus pallidus

(Fig. 12). The affected vessels were patent, and there was no

inflammatory cellular response to the mineralized foci.

Morphologically, this lesion appeared to be similar to a non-

symptomatic condition that has been documented in other

species.

27

Neuronal lipid vacuolation

Spongiform changes affecting the neuropil as well as neuro-

nal cell bodies have been described in a newborn calf,43

in

experimental and natural cases of rabies in skunks,11 foxes11

and in a heifer.23 Neuronal perikaryonic vacuolation is also

seen in scrapie and related spongiform encephalopathes,33

and in lysosomal and acquired storage diseases of various

animals.100

Naturally occurring TSE and storage diseases

have not been documented in raccoons. Rabies, on the other

hand, is commonly encountered in raccoons of the eastern

United States. However, vacuolation of either the neurons or

the neuropil has not been reported in raccoons with naturally

acquired rabies, or in raccoons experimentally infected with

either a dog or a raccoon isolate of Rabies virus.55

During a 2-year period, clear vacuoles were morphologi-cally detected in neurons of 42% of raccoon brains exam-

ined in Oregon.41,46 Neither age nor sex predisposition was

apparent in this population. Microscopically, the vacuoles

were variable in size, were in the perikarya, and were con-

sistently present in pontine nuclei. Brain tissues were neg-

ative for Rabies virus antigen by fluorescent antibody test

and for the protease-resistant protein (PrP) prion by immu-

nohistochemistry. Electron microscopic examination of the

brainstem of selected cases revealed accumulation of elec-

tron-dense material within neuronal perikarya.41 Based

on light and electron microscopic findings, the accumu-

lated intracellular material appeared to have a high lipid

content. These lesions indicate a form of neuronal storagecondition.

Mineralized foci (psammoma bodies) in meninges

and choroid plexus

With advancing age, the human brain shows increased pres-

ence of focal mineralized foci.10

Often referred to as psam-

moma bodies, such mineralized foci are small, hardened

bodies composed of concentric rings of calcium carbonate

and calcium and magnesium phosphate.10

Microscopic evidence of multifocal mineralizations (psam-

moma bodies) were seen in the brain of 62% of raccoons

necropsied on Parramore Island, Virginia.45 The mineralized

foci revealed concentric laminations and were present in

small capillaries of meninges of the brain, choroid plexus

(Fig. 13), or at both these sites. In 2 raccoons, the lesions

were confined to the meninges of the proximal cervical spi-

nal cord. In most cases, the affected vessels appeared to have

been completely occluded. However, no evidence of ischemic

changes in the brain parenchyma was seen, and none of the

raccoons showed abnormal neurologic signs prior to eutha-

nasia. The condition appears to be a common incidental his-

topathological finding in raccoons from the eastern United

States.45 It is speculated that mineralization and subsequent

occlusion of larger blood vessels may result in cerebral isch-emia. Although the exact cause of this condition is not known,

a primary vascular insult with resultant dystrophic mineral-

ization of the affected vessels is suspected.45

Neuroaxonal dystrophy

During a 12-month period, microscopic evidence of neuroax-

onal dystrophy was seen in 12 out of 29 raccoons from Iowa.54

In the affected animals, clinical signs were not apparent.

Three of the animals were kits (<3 months), and none








revealed lesions. The brain did not show any gross lesions.

Microscopically, the lesions were confined to the dorsal

caudal medulla where certain nuclei (predominantly gracilis

and cuneate) were affected. The lesions consisted of eosino-

philic axonal spheroids (Fig. 14) with presence of ampho-

philic periodic acid–Schiff-positive granular material within

some of the degenerate neurons and axones. In a few cases,the latter had completely disappeared leaving behind clear

areas in the neuropil (vacuolar degeneration). None of the

affected cases revealed any appreciable numbers of inflam-

matory cells within the areas of degeneration. Neuroaxonal

dystrophy has been observed in human beings and in various

animals, and these changes have been associated with advanc-

ing age. Although none of the 3 raccoons examined in the

study were old, it was presumed that since the lesions were not

present in kits, the findings may be age-related. Subsequently,

it was shown that severe neuroaxonal dystrophy was present

in old (>7 years of age) raccoons.37

Lafora bodies (polyglucosan inclusions)

Polyglucosan inclusions or Lafora bodies are inclusions of

complex glycoprotein polymers in tissues.100 Although not

reported often in wild animals, Lafora bodies have frequently

been reported in dogs and in a few other domestic animals.

These inclusions are age-related and may or may not be

associated with abnormal neurologic signs.100

There has been

only 1 reported occurrence of Lafora bodies in the brain

(Fig. 15) of a raccoon, which did not show any overt abnormal

neurologic signs.37

AmyloidosisAmyloidosis has been documented in both free-ranging and

captive raccoons.48 It is predominantly seen in the pancreas

where it is deposited in the islets of Langerhans. Although

not reported in the brain, a single case of amyloidosis in cho-

roid plexus of an aged raccoon has been observed (Hamir AN

et al., unpublished data). Amyloid accumulation was associ-

ated with multifocal lymphocytic cell infiltrations. The rac-

coon did not show any neurologic signs.

Congenital conditions

Although albinism is not uncommon in raccoons,

89

only afew other congenital lesions have been reported in this species.

Individual case reports of congenital amelia of forelimbs,73

lack of tail,73

raccoon with 2 tails,101

congenital diaphragmatic

hernia,96 renal hypoplasia,92 dental anomalities,82 and other

skeletal anomalies93

have been reported.

Congenital abnormalities affecting the nervous system or

other body systems that can cause adverse effect on the ner-

vous system are rare, and only 1 documentation of a report of

ocular and nasomaxillary anomalies with neural defects has

been published.95

However, during a field safety trial of the

vaccinia-rabies glycoprotein (V-RG) vaccine,72 a raccoon

with a unilateral micro-ophthalmia was observed (Hamir AN

et al., unpublished data).

Conclusion

Raccoons are almost ubiquitous in North America. Since the1980s, a large number of diseases and lesions, many involv-

ing the nervous system, have been documented in this spe-

cies. As a fair number of these have been individual case

reports, it is difficult to access the general importance of

these conditions on the local populations of raccoons. Also,

some of the described conditions appear not to have been of

immediate severe consequence to the raccoons. However,

such reports are scientifically useful in recognizing patho-

logical conditions that exist at a given time and are also

useful for future disease investigations. Furthermore, since

raccoons are no longer confined to North America, it would

be of interest to compare disease prevalence and pathology

in different raccoon populations of the world with conditionsthat are reported in the current review.

Acknowledgements

The author would like to thank Dr. Charles E. Rupprecht,

now at Centers for Disease Control and Prevention,

Atlanta, GA, for the opportunity to examine and learn

from a large number of raccoon necropsies from his project

of vaccinia-rabies glycoprotein (V-RG) vaccine develop-

ment during the 1980s.

Declaration of conflicting interests

The authors declared no potential conflicts of interest with

respect to the research, authorship, and/or publication of

this article.

Funding

The authors received no financial support for the research,

authorship, and/or publication of this article.

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