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Transmission of TSEs through ectoparasites i.e. P. tenuis

Subject: Transmission of TSEs through ectoparasites i.e. P. tenuis and CWD
Date: May 3, 2007 at 9:05 am PST

SEAC 97/2
Annex 2

Other organisms

Transmission of TSEs through ectoparasites has been postulated by Lupi5.
Post et al6
fed larvae of meat eating and myiasis causing flies with brain material from
hamsters. Two days after eating infected material, the larvae showed high
amounts of PrPSc by Western blot. In further studies, the inner organs of
larvae, which
had been fed with scrapie brain, were extracted and fed to hamsters. Six out
of eight
hamsters developed scrapie. Two out of four hamsters fed on scrapie infected
subsequently developed scrapie.

I AGAIN raise the possibility of that damn brain eating worm in elk and CWD
transmission via elk, deer, and other critters eating that worm. ...tss

Immunodiagnosis of experimental Parelaphostrongylus tenuis infection in elk
Oladele Ogunremi, Murray Lankester, and Alvin Gajadhar
Centre for Animal Parasitology, Canadian Food Inspection Agency, 116
Veterinary Road, Saskatoon, Saskatchewan S7N 2R3 (Ogunremi, Gajadhar);
Department of Biology, Lakehead University, 955 Oliver Road, Thunder Bay,
Ontario P7B 5E1 (Lankester).

Elk infected with the meningeal worm, Parelaphostrongylus tenuis
(Protostrongylidae), do not consistently excrete larvae in feces, making the
current method of diagnosing live animals using the Baermann fecal technique
unreliable. Serological diagnosis could prove more useful in diagnosing
field-infected animals but depends on the identification and availability of
good quality antigen. To mimic field infections, 2 elk were inoculated with
6 infective L3 larvae of P. tenuis, and another 2 with 20 L3 larvae. Fecal
samples were examined for nematode larvae using the Baermann technique and
serum samples taken were tested for anti-P. tenuis antibody with ELISAs by
using the excretory-secretory (ES) products of L3, and sonicated adult worms
as antigens. One animal passed first-stage larvae in its feces 202 days
postinoculation, but passed none thereafter. The remaining 3 inoculated
animals did not pass larvae. In contrast to parasite detection, antibodies
against larval ES products were detected in all animals starting from 14 to
28 days postinoculation and persisted until the termination of the
experiment on day 243 in 2 animals that harbored adult worms. Antibodies
against somatic antigens of the adult worm were not detected until day 56
but also persisted until the end of the experiment in the animals with adult
worms. In 2 elk that had no adult worms at necropsy, anti-ES antibodies were
detected transiently in both, while anti-adult worm antibodies were present
transiently in one. These findings confirm the superiority of P. tenuis
larval ES products over somatic adult worm antigens as serodiagnostic
antigens, as previously observed in studies of infected white-tailed deer,
and extend the application of the newly developed ELISA test in diagnosing
and monitoring cervids experimentally infected with P. tenuis.

Subject: TSE & insects as a vector of potential transmission
Date: October 26, 2006 at 12:50 pm PST

i try to keep an open mind about any other routes and sources that we may be
overlooking. i mean, there is enough TSE protein in circulation now VIA the
FDA, just in 2006 alone, and the oral route has been proven with BSE, and
the non-forced oral consumption of scrapie to primate, as to not worry about
a natural route of a few worms that have maybe been feasting on a deer
that's brain is infected with CWD, then excreted out, and then passed on to
another worm hungry deer looking for that feast. i suppose maybe just
another potential route and source for a TSE, and possibly even a 'double
dose' so to speak from not only the worm in the feces (maybe triple with
feces), but the soil as well (see soil and prion study as well below)
following that are some other studies that may be of interest ;

Myiasis as a risk factor for prion diseases in humans

Journal of the European Academy of Dermatology and Venereology
Volume 20 Page 1037 - October 2006
Volume 20 Issue 9

Myiasis as a risk factor for prion diseases in humans
O Lupi *


Prion diseases are transmissible spongiform encephalopathies of humans and
animals. The oral route is clearly associated with some prion diseases,
according to the dissemination of bovine spongiform encephalopathy (BSE or
mad cow disease) in cattle and kuru in humans. However, other prion diseases
such as scrapie (in sheep) and chronic wasting disease (CWD) (in cervids)
cannot be explained in this way and are probably more associated with a
pattern of horizontal transmission in both domestic and wild animals. The
skin and mucous membranes are a potential target for prion infections
because keratinocytes and lymphocytes are susceptible to the abnormal
infective isoform of the prion protein. Iatrogenic transmission of
Creutzfeldt–Jakob disease (CJD) was also recognized after corneal
transplants in humans and scrapie was successfully transmitted to mice after
ocular instillation of infected brain tissue, confirming that these new
routes could also be important in prion infections. Some ectoparasites have
been proven to harbour prion rods in laboratory experiments. Prion rods were
identified in both fly larvae and pupae; adult flies are also able to
express prion proteins. The most common causes of myiasis in cattle and
sheep, closely related animals with previous prion infections, are Hypoderma
bovis and Oestrus ovis, respectively. Both species of flies present a life
cycle very different from human myiasis, as they have a long contact with
neurological structures, such as spinal canal and epidural fat, which are
potentially rich in prion rods. Ophthalmomyiases in humans is commonly
caused by both species of fly larvae worldwide, providing almost direct
contact with the central nervous system (CNS). The high expression of the
prion protein on the skin and mucosa and the severity of the inflammatory
response to the larvae could readily increase the efficiency of transmission
of prions in both animals and humans.

International Journal of Dermatology
Volume 42 Page 425 - June 2003
Volume 42 Issue 6

Could ectoparasites act as vectors for prion diseases?
Omar Lupi, MD, PhD

Prion diseases are rare neurodegenerative diseases of humans and animals
with a lethal evolution. Several cell types found on the human skin,
including keratinocytes, fibroblasts and lymphocytes, are susceptible to the
abnormal infective isoform of the prion protein, which transforms the skin
to produce a potential target for prion infection. Iatrogenic transmission
of Creutzfeldt-Jakob disease was also recognized after corneal transplants
in humans, and scrapie was successfully transmitted to mice after ocular
instillation of infected brain tissue, confirming that these new routes, as
well as cerebral inoculation and oral ingestion, could be important in prion
infections. Animal prion infections, such as scrapie (sheep) and "mad cow
disease" (cattle), have shown a pattern of horizontal transmission in farm
conditions and several ectoparasites have been shown to harbor prion rods in
laboratory experiments. Fly larvae and mites were exposed to brain-infected
material and were readily able to transmit scrapie to hamsters. New lines of
evidence have confirmed that adult flies are also able to express prion
proteins. Because ocular and cerebral myiases and mite infestation are not
rare worldwide, and most cases are caused by fly larvae or hay mites that
usually affect sheep and cattle, it is important to discuss the possibility
that these ectoparasites could eventually act as reservoirs and/or vectors
for prion diseases.

P. tenuis – The White-tailed Deer Parasite

“Brain worms” (meningeal worms) can affect sheep, goats, llamas, alpacas,
moose and other exotic small ruminants

M. Kopcha, D.V.M., M.S., J. S. Rook, D.V.M. & D. Hostetler, D.V.M

MSU Extension & Ag. Experiment Station

Michigan State University

College of Veterinary Medicine

Many livestock producers are familiar with internal parasites that invade
the digestive system (the abomasum, small or large

intestines), liver, and lungs. An internal parasite which may not be so
well-recognized is one that invades the central nervous system

(brain and spinal cord). Commonly called the “brain worm” or meningeal worm
(the meninges are a thin membrane that covers the

brain and spinal column), the scientific name for this parasite is
Parelaphostroneylus tenuis (P. tenuis), and its natural host is the

White-tailed deer. Usually, P. tenuis completes its life cycle in

the deer (Figure 1) without causing noticeable problems.

However, when P. tenuis is ingested by unnatural, or aberrant

hosts such as, llamas, sheep, goats, moose, elk, caribou, and

other susceptible ruminants, the parasite moves into the brain

and/or spinal cord, damaging delicate nervous tissue.

Neurologic problems result.

White-tailed deer may he parasitized by P. tenuis year-round.

However, the neurologic disease seen in aberrant hosts has a

seasonal occurrence that starts in the late summer and continues

until a hard freeze occurs. A cool, moist summer and/or a mild

winter may extend the period during which the disease occurs.

How does it occur?

To understand this disease and how to prevent or minimize its

occurrence, it is important to understand the life cycle of P.

tenuis in the White-tailed deer and what happens when the

parasite is ingested by susceptible ruminants. The life cycle is

as follows (Figure 1): adult meningeal worms live in the deer's

central nervous system (brain and spinal cord) and produce

eggs which hatch into larvae. The larvae migrate from the deer's

central nervous system to the lungs, where they are coughed

into the mouth, swallowed and passed from the intestinal tract

with the manure. This portion of the life cycle takes

approximately three months (Figure 1 - numbers 1 and 2).

After excreted in the manure, larvae must continue their

development in an intermediate host (certain land-dwelling

snails and slugs) for another three to four weeks until they reach

their infective stage (Figure 1 - numbers 3 and 4).

White-tailed deer become infested with P. tenuis by eating

these snails or slugs that contain the infective stage of the larvae

(Figure 1 - number 5). Once ingested, the larvae migrate

through the deer’s gut and eventually move into their central

nervous system where they mature into adults, produce eggs,

Figure 2 The Angora goat in the

center of the picture had a mild

lameness in its left forelimb

(arrow). The presumptive

diagnosis was meningeal worm

infestation. Mild cases such as

this one may recover


Figure 3 This Angora goat was

probably affected with

meningeal worms and was able

to use its hindlimbs, but was

unable to rise onto its


Figure 4 This alpaca had been

paralyzed by meningeal worms.

Notice that despite the paralysis,

the animal appears alert. This is

typical for a brain worm

infestation that affects the spinal

cord and not the brain.

Figure 6: This Suffolk sheep was one of several

sheep from a flock that were affected with

Parelaphostrongylus tenuis. The posture that this

animal is displaying is referred to as a

“dogsitting” position.

Figure 5: This alpaca

displayed weakness in both

hindlimbs and was unable to

stand without assistance. The

presumptive diagnosis was

brain worm infestation. This

animal eventually recovered.

and the cycle begins again.

When P. tenuis-infected snails and slugs are ingested by aberrant hosts, the
larvae migrate into the brain and/or spinal cord, but

do not mature into adults. Instead, these immature larvae wander through the
central nervous system causing inflammation and

swelling which damages sensitive nervous tissue producing a variety of
neurologic signs. Because these larvae do not mature into

adults in aberrant hosts, they cannot produce eggs that would mature into
larvae which would then pass outside the animal with the

feces. This is why sheep, goats, llamas and other unnatural hosts are
considered dead-end hosts for P. tenuis. Dead end hosts

infected with P. tenuis larva cannot spread the disease to other aberrant
hosts or back to deer - i.e. infected sheep or

goats can not bring the disease to your flock or herd.

The neurologic signs observed in infected llamas,

sheep, goats and others depend upon the number of

larvae present in the nervous tissue and the specific

portion of the brain or spinal cord that has been

affected. For example - a mild infestation in a very

local area may produce a slight limp (Figure 2)) or

weakness in one or more legs (Figure 3,4,5, & 6). A

more severe infestation may cause an animal to

become partially or completely paralyzed. If the

parasites are located only in the spinal cord, an

affected animal will appear bright and alert, and have

a normal appetite, despite the altered gait or

paralysis. When larvae migrate through the brain, they

may cause blindness, a head tilt, circling, disinterest in

or inability to eat, or other signs that can mimic brain

diseases caused by bacteria, viruses, nutritional

deficiencies, trauma, or toxins. Table I lists some of

the diseases that P. tenuis can mimic when the

parasites migrate through nervous tissue.

Table 1_Included in this table are various diseases that can look similar to

“brain worm” infestation. Also listed are the target species that are

susceptible to each of the diseases.


Disease Llamas and


Sheep Goats

Listeriosis X X X

Caprine Arthritis-



Scrapie X Rare*

Rabies X X X

Trauma X X X

Copper Deficiency X X X

Vitamin E/Selenium



Spinal Cord or Brain



Polioencephalomalacia X X X

Could it happen on my farm?

Animals pastured in lowland areas frequented by infected White-tailed deer
are prime candidates for exposure to snails containing

P. tenuis larvae. When such animals develop neurological problems during the
late summer through early winter in the Upper

Midwest (the season for exposure may be longer in other parts of the
country), “brain worms” are a likely possibility.

Presently there is no definitive test

that can be performed on a live

animal to confirm P. tenuis

infestation. Since the larvae do not

mature to adulthood in aberrant

hosts, and therefore, cannot

produce eggs or pass larvae in the

feces, a fecal examination is not

useful. Also, these parasites cannot

be detected by blood testing.

A test that can help support

suspicions of brain worm infestation

is evaluation of cerebrospinal fluid

(CSF), which is the fluid that

bathes the brain and spinal cord.

Disease that occurs in these areas

may cause changes in the CSF

detectable by various tests.

Normal CSF contains very few

cells and little protein. An animal

that has parasites migrating in the

brain or spinal cord, often will have

a larger number of cells, especially

a certain type of cell called an

eosinophil. Also, the protein

concentration may be increased.

Therefore, finding eosinophils in a

CSF tap taken from an animal with

neurologic abnormalities is very supportive evidence for “brain worm”
infestation. If eosinophils are not found, this does not rule

out the possibility of a “brain worm” problem. Currently, the only way to
confirm this diagnosis is by finding the parasite in the

nervous system, which requires a necropsy examination.

Obtaining CSF from sheep, goats, and llamas is somewhat more involved than
obtaining a blood sample. Two areas used most often

for CSF collection are just behind the poll or over the hips, in the area
called the lumbosacral junction. We prefer the lumbosacral

site because the test can be performed using local anesthetic only (rarely
would a tranquilizer be required), and the animal can be

standing or lying down, whichever is most comfortable. The head site usually
requires that the animal be heavily tranquilized or


The procedure can be performed in a hospital setting or on the farm, and
must be done in a sterile manner. This includes removal

of the hair or wool from a small area where the puncture will be made,
scrubbing the site with surgical disinfectant and rinsing with

alcohol. Sterile gloves and equipment are used.

After the site has been scrubbed, an injection of a local anesthetic is
placed under the skin and into the deeper tissues where the

spinal needle will be placed. The needle is inserted through the
anesthetized area. The animal may notice slight discomfort when the

needle enters the spinal canal. However, having a quiet person at the
animal's head (in some cases the best person is the owner or

handler) will provide a calming effect. The needle does not penetrate the
spinal cord. In many animals, the cord ends just ahead of

where the needle is placed. Once fluid has been obtained, the needle is
withdrawn. The amount of fluid collected depends on the

animal's size. Usually, 5 to 8 cc's are withdrawn and submitted to a
clinical laboratory for analysis. This is a very safe procedure

if performed properly.

What about treatment?

Many different drugs including thiabendazole, levamisole, fenbendazole,
albendazole, and ivermectin have been used in an attempt

to treat “brain worm” infestation. However, to date, no controlled studies
have confirmed or refuted the efficacy of various treatment

recommendations. Some anthelmintics can kill P. tenuis larvae while they
migrate from the stomach to the brain or spinal cord, but

are unable to enter the central nervous system because of a structure called
the blood-brain barrier. Therefore, they do not have

an effect on parasitic larvae once the parasite has migrated across the
blood-brain barrier and is in the central nervous system. Other

anthelmintics may be able to kill the larvae regardless of their location in
the body. An important point to remember is that once the

parasite begins to migrate within the nervous tissue, damage occurs that is
usually irreversible. Although some drugs may kill the

worms, thus pre venting further damage, treatment does not repair nervous
tissue. Some animals with mild clinical signs may recover

without treatment. At this time, the best recommendation for treatment is
"do no harm." Perhaps some medications are helpful,

however, remember that drugs used at higher-than-usual levels or more
frequently than usual may cause toxicity problems.

The best approach to “brain worm” infestation is prevention. This s achieved
by keeping the life cycle in mind. Animals kept in

pastures that have wetlands and White-tailed deer should be removed from
these pastures in the late summer and until the first hard

freeze. If this is not possible, strategic deworming is the second best
approach. This would involve either continuously providing

an anthelmintic in feed or mineral mix throughout the “brain worm” season,
or deworming with an oral or injectable product every

10 to 14 days - starting in late summer and continuing through early to
mid-winter, depending on the severity of the freezing


The 10- to 14-day schedule recommendation is based on experimental evidence
that demonstrated the parasites' ability to reach

the brain and/or spinal cord in this amount of time after an animal eats the
snails containing P. tenuis larvae. Thus, this is a "window

of opportunity" to kill the worms before they enter the central nervous
system where they may be "safe" or protected from the killing

effect of drugs that cannot cross the blood-brain barrier.

While clinical cases of meningeal worm infestation are rare, “brain worms”
could affect your animals if they have access to wetlands

harboring P. tenuis-infected White-tailed deer. Wetlands contain a
population of snails and slugs needed to complete the parasite's

life cycle if it is the season when P. tenuis infestation occurs. Remember:
the success of treatment is variable - prevention is the best

means of control.