Internal Parsites
(worms) cause more
goats to die in the
Southeastern U.S.
than the total of
the next three
leading causes of
goat deaths
according to
necropsy records
from Kentucky State
University.
Controlling worms in
goats is much more
complex than
controlling other
goat diseases. Many
other diseases can
be controlled by
simple management
practices and
vaccination. Many
goat producers in
the past have
controlled worms
solely by the use of
dewormers, but now
goats still die due
to the worms
developing
resistance to the
dewormer and some
goat producers in
the humid South have
gone out of the goat
business because no
dewormer was
effective against
the worms in their
goats. Goats have a
lower immune
response to worms
than most other
animals and
therefore have
greater problems
with worms. There
is a lot of
disinformation on
controlling worms
which increases the
problem. Our
knowledge on
controlling worms in
sheep and goats has
quadrupled in the
last decade due to
research in
Australia, New
Zealand and South
Africa and therefore
many animal
professionals may
not be current on
the recent
developments. In
fact, some of our
old good management
practices to control
worms have been
found to not be good
and in some cases
harmful.
This is the first of
a series of articles
which will appear in
the Goat Rancher
over the next
several months. The
articles are written
and reviewed by the
consortium members
which include a
number of
parasitologists with
an interest in small
ruminants and a
number of small
ruminant scientists
so that the articles
contain the most up
to date and accurate
information on
parasites.
This first article
is an introduction
to worms in sheep
and goats. The next
article discusses
the life cycle of a
goat worm and how we
can use that
knowledge reduce
their numbers. The
third article
describes dewormers
and the correct use
of dewormers and
focuses on the
problem of dewormer
resistance and what
can be done. The
fourth article
describes the
FAMACHA system for
reducing dewormer
resistance and
selecting more
resistant animals.
The final article
describes
alternative
(non-chemotherapeutic)
methods for
controlling worms
and what supporting
data is available.
The purpose of this
series of articles
is to teach the
producer to assemble
his or her worm
control program,
using applicable
management practices
as the first line of
defense against
worms and using
dewormers only when
management is not
enough to control
worms. Using this
program, we can
reduce the use of
dewormers, reduce
the rate at which
worms develop
dewormer resistance
and select for
animals which have
genetic resistance
against worms. This
will enable the goat
business to be
sustainable in the
face of dewormer
resistance.
Although there are
more than 15 species
of worms identified
in goats, we will
discuss the most
economically
important worms and
parasites in goats
and list some useful
sources for further
information. The
most common worms in
goats are
gastrointestinal
nematodes because
they are nematodes
which live in the
digestive tract,
predominantly the
stomach and small
intestine. In this
first paper, we
discuss several
other worms
including the
tapeworm, the deer
brain worm as well
as coccidia and
liver flukes which
are other types of
internal parasites
in goats which can
be important at
times.
Worms are a normal
part of the animal=s
ecosystem. A low
level of worms is
desirable to keep
the animal=s
immune system active
against worms.
However, excessive
worms causes
disease. Excessive
worms are caused by
such things as a
depressed immune
system, consuming
too many worm larva,
filth and lack of
sanitation,
rainfall, close
grazing etc. Worms
function in the
ecosystem to keep
animals from
overrunning the
ecosystem when
production
conditions are good
and they also
prevent all animals
from starving when
there is a shortage
of food. One cannot
eradicate worms on
your farm; you have
to learn how to live
with them and use
management to
control them to
levels which do not
harm animal
production.
The most common worm
(especially in the
Southeastern US)
that causes the
majority of deaths
as well as depressed
animal performance
is the Barber pole
worm (scientific
name Haemonchus
contortus). In
figure 1 is a
picture of a fresh
barberpole worm with
red and white
stripes like a
barber pole. The
red stripe is the
gut which is filled
with blood which he
has sucked from the
animal that he
infects. The white
stripe is the uterus
which contains
eggs. This pretty
well describes the
barber pole worm; he
is a blood
sucking-egg laying
machine. He sucks
about half to one
drop of blood per
day and produces
1,000-6,000 eggs per
day. The barberpole
worm can multiply
rapidly under good
conditions because
of the large number
of eggs that they
lay. Since he
sucks a half to one
drops of blood per
day, 1000 worms can
suck two ounces of
blood per day, two
quarts in a month,
which is why your
goat will die from a
heavy infection. The
goat can make blood
fast enough to
replace that
consumed by a low
level of barberpole
worm infection, but
as the infection
gets worse, the goat
is unable to make
components (red
blood cells and
blood protein) of
blood fast enough to
replace lost blood
and the goat starts
getting low on blood
components. A low
level of red blood
cells (a component
of blood) is called
anemia ( a thin
layer of blood is
pale because of the
loss of red blood
cells). The
percent red blood
cells in the blood
can be measured in
the laboratory to
determine the extent
of anemia. You can
determine if an
animal has anemia by
looking at the color
of the mucous
membranes of the
animal. Mucous
membranes are areas
of tissue where the
capillaries are
close to the surface
of the skin and the
color of the skin
reflects the color
of a thin layer of
blood. When an
animal becomes
anemic these mucous
membranes change
from a healthy pink
to a lighter pink
and then if the
anemia is severe,
the mucous membranes
will be white as a
sheet of paper. When
mucous membranes
become white, the
animal is critically
low on blood and
needs dewormed
immediately. It
must be remembered
that other
conditions that
cause blood loss
such as liver flukes
or lice can also
cause anemia.
Mucous membranes
that are easily
observed are located
on the inside of the
lower eyelid
(touching the
eyeball), the gums
(hard to see in
animals with
pigmentation in the
mouth) and inside
the vulva (often
checked at goat
dairies). A low
level of blood
protein also causes
edema, due to a
shortage of blood
proteins to pull
fluid back into the
circulatory system.
Edema is often seen
as a pouch of fluid
under the lower
jaw. Angora goats
may also get edema
on the floor of the
chest. When an
animal gets edema,
he is severely low
on blood components
and needs dewormed
promptly.
The barber pole worm
is a tropical worm;
he likes a warm
climate and
therefore,
predominates in the
South, although he
can cause major
problems in northern
areas, but for a
shorter period of
time. These worms
require rain to
infect small
ruminants and
therefore are much
less of a problem in
the West or any
location where there
is less than 25" of
rain per year. The
barber pole worm
also has a short
generation interval,
being able to
complete a
generation as quick
as 4 weeks which
enables him to
develop dewormer
resistance quicker
than for most other
worms.
The barber pole worm
is relatively large,
and can easily be
seen with the naked
eye. He is about
the diameter of
paper clip wire and
about an inch long.
The barberpole worm
pierces the stomach
lining and
establishes
connections to small
blood vessels to
suck blood. If you
open up the true
stomach (abomasum)
of a goat that has
died from worms, you
will see some
floating free, but
most are attached to
the stomach and they
may look like hair
growing on the
inside of the
stomach. The
barberpole worm will
lose its coloration
as it is exposed to
air. The average
lifespan of a worm
in the stomach is 6
months, but they can
live longer than a
year. The animal=s
immune system is
constantly fighting
against the worms
and may suppress egg
production of the
worm or cause it to
die prematurely.
The immune system on
some occasions may
have a hyperimmune
response and
eliminate most of
the worms in the
animal. There are
barber pole worms in
sheep and cattle.
But the strain in
cattle will not
infect sheep or
goats (and vice
versa) except under
unusual
circumstances.
There are two
temperate species
gastrointestinal
nematodes which are
important in goats
and sheep. These
are the Bankrupt
worm (scientific
name
Trichostrongylus
colubriformis) and
Brown stomach worm
(scientific name
Telodorsagia
circumcincta
formerly known as
Ostertagia).
Although these worms
do not kill as many
goats as the
barberpole worm,
under some
circumstances they
can cause important
production losses as
well as death of the
goat. Many of the
management practices
which suppress the
barberpole worm will
also suppress these
worms. Since these
worms are best
adapted to temperate
conditions, they are
more of a problem in
the fall and winter
as compared to the
barber pole worm
which dominates in
the summer. The
main symptoms of a
bankrupt worm or
brown stomach worm
infection is
diarrhea , a slow
growing animal, a
rough haircoat and
an unthrifty
animal. In the next
article in this
series, we will be
discussing the life
cycle of the
gastrointestinal
nematodes mentioned
above with emphasis
on management
techniques that can
be utilized to help
control the
parasites.
The tapeworm is
another worm that
causes goat
problems. It seldom
kills goats, but
causes poor
performance,
especially among
young animals and
may give them a
pot-bellied
appearance.
Occasionally
diarrhea is a
symptom of
tapeworms. Tapeworm
segments can be
readily observed in
feces as they look
like grains of rice
making this parasite
easy to diagnose.
The general
tapeworms that
infect goats will
infect sheep and
occasionally
cattle. Tapeworms
are located in the
small intestine and
can grow to be
several feet long.
Tapeworms absorb
nutrients from the
digestive tract and
therefore decrease
nutrition available
for the goat. The
immune system of
mature animals
usually keeps the
tapeworm suppressed.
The tapeworm eggs
are consumed by a
grass mite (like a
chigger) and the egg
develops to an
infective stage in
the body cavity of
the mite over a 1 to
4 month period. The
goat then eats grass
on which the mite is
crawling and becomes
infected. It takes
40 days from the
time a goat consumes
infected grass mites
until the tape worm
segments appear in
feces. Pasture
areas that are
infected usually
remain infected for
some time although
the mites may be
killed by winter
weather. Tapeworms
are more of a
problem under
intensive production
systems. If young
animals get infected
in a pasture, the
general
recommendation for
cleaning the pasture
up is to not graze a
pasture for a year
(make hay or graze
with another species
of animal).
Tapeworms are not
killed by all
dewormers, but is
controlled by the
Benzamidole group of
dewormers.
Valbazen is one of
the more popular
dewormers used for
tapeworm control.
Coccidiosis is a
common goat parasite
that appears when
animals are stressed
or sanitation is
lacking. It mainly
causes diarrhea, but
unlike cattle, blood
is seldom seen in
the feces. Coccidia
are normally present
at low numbers in
the digestive tract
of the animal, but
the infection level
is low and the
immune system is
able to prevent them
from causing
disease.
Coccidiosis is a
disease of stress
and filth. The main
route of infection
is the consumption
of feces due to
uncleanliness. The
animal is usually
stressed, depressing
the immune system.
Coccidiosis is most
commonly seen in
just weaned kids due
to stress, lack of
a mature immune
system and fecal
contamination.
Stressing animals by
shipping is also a
major cause
coccidiosis.
Animals often
consume the
infective stage
coccidia from feces,
such as fecal
contamination in the
feed trough or water
trough. Moisture
whether by rain or
humidity increases
the time that
infective coccidia
live. Therefore,
keeping the goat=s
environment clean
and dry will help
prevent coccidiosis.
During times of
stress, a medicated
feed containing
Rumensin or Deccox
can be fed which is
quite effective at
preventing
coccidiosis.
Occasionally
coccidiosis will
still occur despite
feeding medicated
feed, but fewer
animals will be
affected. Animals
should be treated
when diarrhea first
starts if
coccidiosis is
suspected ( history
of stress) because
delaying treatment
can result in
scarring of the
intestine and an
poor-doing animal
for life. Coccidia
are not observed
when feces are
examined under a
microscope in early
stages of disease,
but they are very
numerous later on.
Coccidiosis may be
treated with Corid (Amprolium)
or Albon (Sulfadimethoxine).
If Corid is used at
too high a dose, or
for too long a time,
animals may develop
a thiamine
deficiency called
polioencephalomalacia
(animals behave like
they are drunk)
which can be readily
treated with
thiamine and removal
of the Corid
treatment.
The meningeal worm
or deer brain worm
causes partial
paralysis in goats,
sheep and llamas
that are exposed to
the parasite by
deer. The parasite
occurs in deer and
does not cause
clinical symptoms as
it does in goats.
The larvae are
passed in deer feces
and are ingested by
a variety of snails
and slugs where they
develop into
infective larvae
over a 3-4 week
period. The snails
or slugs are
consumed by grazing
goats. Inside the
goat, the larvae
penetrate the
intestine and
migrate to the
spinal cord through
the abdominal cavity
over a 10 day
period. The larva
gets lost in
migrating from the
spinal cord to the
brain because the
goat anatomy is
different from the
deer. They end up
destroying brain
tissue causing
differing degrees of
paralysis. Symptoms
of the brain worm
include paralysis of
one or more limbs,
excessive tail
twitching, circling,
abnormal head
position,
blindness,
inability to get up,
toe dragging, being
in a dog-sitting
position or
difficulty or
exaggerated movement
of limbs when
walking. The
disease usually
occurs in the fall
and winter. There
is no treatment for
the brain worm that
is very effective.
Sometimes it is
treated with high
doses of various
dewormers (fenbendazole
and ivomec) and
steriods, but
treatment is often
not effective.
Since the parasite
is carried by deer
and uses a snails or
slugs as the
infective
intermediate host,
prevention consists
of discouraging deer
from using the
pasture and making
the environment
unfavorable for
snails and slugs.
As goats clear the
cover from an area,
deer will visit that
area less
frequently. Guard
dogs may chase deer
away from pastures.
A number of snails
may serve as
intermediate host
and some may be so
small (1/4") as to
be overlooked.
Snails prefer water,
and so swampy areas
are good habitat for
snails. Therefore,
fencing goats out of
areas that often
have water can help
on prevention.
Slugs and some
snails prefer
organic matter, leaf
piles and compost.
These areas may be
cleaned up if the
area is not
extensive. Guinea
hens and Muscovy
ducks are reputed to
be effective at
controlling snails
and slugs and may
aid in prevention of
the deerworm. Some
producers deworm
goats every 30 days
from 30 days after
the grazing season
until a hard freeze
to prevent the
deerworm. Ivomec and
fenbendazole
(Safeguard, Panacur)
are the most common
dewormers used for
this purpose. This
will likely create
dewormer resistance,
but for many people,
these dewormers do
not work for
roundworms. One
producer used a low
dose of Rumatel fed
every day in a
minimal amount of
corn and appeared to
be effective.
Liver flukes may be
caused by the common
liver fluke and less
commonly by the
large American liver
fluke (also called
the deer fluke).
The flukes invade
the liver and cause
internal bleeding. A
goat with high
numbers of flukes
will have an acute
infection, where the
animal stops eating,
has pale mucous
membranes, gradually
does not get up and
often dies within
days. With fewer
numbers of flukes,
the symptoms may be
milder and is called
a chronic
infection. The
animal will have a
poor appetite, lose
weight for longer
than a month, poor
body condition,
rough hair coat,
rapid heartbeat,
pale mucous
membranes and
sometimes edema,
especially bottle
jaw.
Liver flukes can
infect wildlife,
cattle sheep and
goats and even man.
The fluke lays eggs
in the bile duct of
the animal it
infects and the eggs
end up in the
feces. The
infective larva
develop inside the
egg over a 2-3 week
period which then
infect snails.
These are the common
pond snails which
are in or around
water and may range
form 1/4" to nearly
3" in length. The
larvae further
develops in the
snail over 5-7 days
and then becomes a
true infective
larvae which leaves
the snail and
attaches to grass
where the goats may
consume it. Once
consumed, the fluke
further develops and
penetrates the
intestine on its way
through the
abdominal cavity to
the liver. Once in
the liver, it starts
consuming the liver.
Prevention includes
fencing off ponds or
marshy areas in the
pasture. Muscovy
ducks and guinea
hens may be used to
control snails.