TREMODES & CESTODES

DICROCOELIUM spp, the LANCET FLUKE, parasite of CATTLE,

SHEEP, GOATS, HORSES, DOGS and CATS. Biology, prevention
and control

The trematodes (or flukes) are leaf shaped with an outer cover called the
tegument which may be smooth or spiny. There are two suckers or attachment
organs, an anterior oral sucker and a posterior ventral sucker. The suckers
form a characteristic feature of the group, from which the name Trematode is
derived from the Greek word for hole. They can occur in a variety of host
environments, with the majority being endoparasites but some are found to be
ectoparasitic.
Most trematodes are hermaphroditic and most of the body consists of
reproductive organs and their associated structures. The digestive system is
well developed; they generally feed on intestinal debris, blood, mucus and
other tissues, depending on the host environment.

Dicrocoelium is
a
genus
of flukes with cattle,
sheep,
goats, pigs, and
other wild
animalsas
major
final
hosts.
It
occasionally infests horses, dogs, cats, and also humans. They are
also called lancet flukes or small liver flukes .

There are two major species:

Dicrocoelium dendriticum , (= Dicrocoelium lanceolatum) has a worldwide distribution

but prevalence varies strongly depending on the regions.
Dicrocoelium hospes , found in Africa.

The disease caused by Dicrocoelium is called dicrocoeliosis.

Are animals infected with Dicrocoelium contagious for

humans?
Usually NOT. If livestock is infected with lancet flukes, its is not
directly contagious forhumans, neither through contact, nor when
consuming meat, milk or blood of contaminated animals, nor through
the feces. BUT it cannot be excluded that humans become infected
when consuming raw livers contaminated with juvenile lancet flukes.
The same applies to pets infected with lancet flukes. Normally humans
become infected with lancet flukes through accidental ingestion of
contaminated ants (see below under life cycle), not by ingesting
adult flukes or their eggs.
You can find additional information in this site on the general
biology of parasitic worms and/or flukes.

Final location of Dicrocoelium spp

Predilection sites
the gall bladder.

of Dicrocoelium flukes are

the bile

ducts and

Anatomy of Dicrocoelium spp

Life cycle and biology of Dicrocoelium spp

Lancet flukes have an indirect life

cycle with two intermediate
hosts, a snail and anant. It is one of the most conspicuous life
cycles among the parasitic helminths.
The eggs shed by adult flukes reach the host's gut with the bile and are expelled with the
feces. Once outside the host terrestrial snails ingest the eggs. Several species can act as
intermediate
hosts,
depending
on
the
regions
and
the
environment,
e.g. Thebaspp, Zebrina spp, or Cionella spp for Dicrocoelium dendriticum; Limicolaria spp
orAchatina spp for Dicrocoelium hospes. Inside the snails young miracidia hatch out of the
eggs, penetrate the intestinal wall and develop to sporocysts, which on their turn multiply
asexually, each one producing up to 100 daughter sporocysts. Each daughter sporocyst can
produce up to 60 cercariae in the 3-4 months that it remains inside the snail. The snail
encysts these cercariae and expels them in the form of sticky slime balls that adhere to the
vegetation. Each slime ball can contain up to 100 cercariae.

Several ant species can act as the second

intermediate host, e.g. Formica spp or Lasius spp for Dicrocoelium

dendriticum; Dorylusspp or Cematogaster spp for Dicrocoelium

hospes. These ants eat the slime balls. Inside the ants, most cercariae
continue their developmentto metacercariae that are infective for the
final host (cattle, sheep, goats, humans, etc.). These cercariae remain
in the hemocoele of the ant. But one cercaria migrates to the subesophageal ganglion (a kind of brain) of the ant and manipulates its
behavior by acting on the nerve cells. Towards the evening, instead of
following the rest of the ant colony, the manipulated ant climbs on top
of a blade of grass and remains there the whole night through until
dawn. This increases the chance that a final host swallows it during
early morning grazing. If a final host does not ingest the infected ant,
it climbs down the blade of grass, joins the other ants and behaves
normally until the next evening, when the process starts again.
Otherwise, if it would remain the whole day on top of the blade of
grass it would dry out and die exposed to excessive sun irradiation.
Once a final host ingests the infected ant while grazing, the
metacercariae are released in the gut of the host andmigrate to the
liver through the common bile duct (ductus choledocus), i.e. they do
not migrate through the liver tissues as Fasciola flukes do.
Metacercariae complete the development to adults and start
producing eggs in 8 to 12 weeks (= prepatent period) after being
ingested. The adult flukes feed on bile and not on liver tissues.

Harm
caused by Dicrocoelium infections , symptoms and diagnos
is

Most infections with Dicrocoelium cause no

symptoms or only slight ones. However, in case of heavy infestations
(up to 50,000 flukes in one animal) the bile ducts can be irritated and

become distended. Chronic infestations can turn into cirrhosis. Edema

and blood loss (anemia) can also develop.
Nevertheless, infections with Dicrocoelium no are not as harmful as
those with Fasciola hepatica or Fasciola gigantica and fatalities are
rare. Economic damage is mostly due to condemnation of the livers at
slaughter and to reduced productivity of affected livestock.
Diagnosis is done by egg detection in the feces or by identification of
the flukes after necropsy. However, since the eggs are passed to the
intestine only when the gall bladder is emptied, a negative fecal egg
count is not conclusive, i.e. there can be false negatives.

Prevention and control of Dicrocoelium spp

The most important preventative measure is to keep the snail population as low as
possible. The snails that act as intermediate hosts are terrestrial, but need humidity
for development and survival. Effective drainage or anything else that keeps the pastures
dry will reduce the snail population.
A few anthelmintics may have a label claim against Dicrocoelium spp on livestock. There are
reports on effective control with albendazole (1x15 mg/kg or 2x7.5 mg/kg for on consecutive
days for sheep and cattle, 10 mg/kg for cattle), triclabendazole, netobimin (20 mg/kg)
and praziquantel (20 mg/kg 2 days).
Neither macrocyclic
lancet flukes.

lactones (e.g. ivermectin)

nor levamisole are

effective

against

There are very few commercial flukicides approved for use on pig, horses, dogs and cats,
simply because flukesare seldom a problem for them.
Chemical control of the snails with molluscicides (i.e. snail killers) such as copper
sulphate, sodium pentachlorophenate, niclosamide, etc. can make sense for very specific
purposes, e.g. for treating places where livestock congregates (water holes, feeding areas,
salt licks, shade trees, etc) to keep them free of snails. However,trying to eradicate snails
from a property is hopeless and useless. It is virtually impossible to treat every place
where they can survive and they reproduce extremely quickly. Cleaned pastures would
become re-infested very fast. In addition it would be also very harmful for the environment. In
fact, such molluscicides (mainly niclosamide) are approved only in a few countries as an aid in
the prevention of human schistosomiasis (also called bilharziosis or snail fever).
For similar reasons, trying to eliminate the ants that act as intermediate hosts
of Dicrocoelium is not advisable either. Using insecticides for this purpose is not indicated,
both for economic and ecologic reasons. Whatever insecticide spread on the pastures would
kill numerous beneficial arthropods as well.

There are so far no vaccines against lancet flukes. To learn more about vaccines against
parasites of livestock and pets click here.
Biological control of lancet flukes (i.e. using their natural enemies) is so far not feasible.
You may be interested in an article in this site on medicinal plants against external and
internal parasites.

LIVER FLUKE, FASCIOLA HEPATICA, parasite of CATTLE,

SHEEP, GOATS, HORSES, DOGS, and CATS. Biology, prevention
and control
Fasciola hepatica (= Distomum hepaticum ), the common liver
fluke (also called the sheep liver fluke) is a flatworm belonging to the
Trematodes. Its final hosts are sheep, goats, cattle and other domestic
and wild mammals, including horses, dogs, cats and humans.

The common liver fluke occurs worldwide but is particularly abundant

in humid regions with temperate climate where it can be endemic.

It is one of the most abundant and damaging helminth parasites

of grazing ruminants(sheep, goats, cattle). In endemic regions 100%
of the animals can be infected. It is particularly harmful, even fatal for
sheep. Prevalence and incidence in a particular region depends
strongly on ecologic and climatic conditions (e.g. habitats for
intermediate hosts and wild mammals, overwintering of the parasites
in the environment, etc.) and on livestock management practices
(stock density, grazing patterns, etc.).
Horses and pigs kept
outdoors
can
also
be
liver flukes are usually not a problem in housed pigs.

affected,

but

Horses, dogs and cats can be occasionally infected, especially in

rural environments, but liver fluke is usually not an issue for these
animals.
The
disease
caused
by
liver flukes is
called fasciolosis, fasciolasis, distomatosis or liver rot.

Are animals infected with Fasciola hepatica contagious for

humans?
Usually NOT. If livestock is infected with liver flukes, it is not directly
contagious for humans, neither through contact, nor when consuming
meat, milk or blood of contaminated animals, nor through the
feces. BUTexperimental studies suggest that humans may be infected
when consuming raw livers contaminated with juvenile liver flukes.
The same applies to pets infected with liver flukes. Normally humans
become infected through ingestion of water contaminated with

infective cercariae (see below under life cycle), not by ingesting

adult flukesor their eggs.
You can find additional information in this site on the general
biology of parasitic worms and/or flukes.

Final location of Fasciola hepatica

Predilection sites of Fasciola hepatica are the biliary ducts in the
liver and the gall bladder.

Anatomy of Fasciola hepatica

Adult liver flukes have a flat body, an oval shape, and are rather large:
up to 30 mm long and 15 mm wide. The have a pink-grayish to dark red
color. Liver flukes have two suckers, both in the ventral side. The body
surface is covered with numerous spines. Liver flukes have no
external signs of segmentation. The mouth ends in thepharynx, a
muscular tube that allows sucking. The digestive system is blind (i.e.
without anus: the only opening is the mouth) and not linear, as in most
animals, but branched, ending in several blind ducts (called coeca).
Liverflukes are simultaneous hermaphrodites, i.e. they have both
male and female reproductive organs.
The eggs of liver flukes are about 80x140 micrometers, with an oval form, operculated (i.e.
with a cap-like cover) and of a yellowish to greenish color derived from the host's bile.

Life cycle and biology of Fasciola hepatica

Fasciola
hepatica has
an indirect
life
cycle with amphibious snails asintermediate hosts, typically from
the genus Lymnaea .
Adult flukes produce eggs in the biliary ducts of their hosts. These
eggs reach the gall bladder and are passed to the host's gut when the
gall bladder is emptied. They are passively transported to the anus
and are expelled with the feces. A single liver fluke can produce up to
25'000 eggs a day!
Once outside the host, the larvae called miracidia hatch out of the
eggs in 7 to 15 days. These larvae can survive for weeks off a host
provided there is enough humidity. They die quickly in a dry
environment. Miracidia can swim and penetrate actively into the snails
where they remain for 4 to 8 weeks and develop successively
to sporocysts, rediae and cercariae, the usual larval stages of most
fluke species. A single miracidium can asexually produce up to 600
cercariae.
Mature cercariae leave the snail, attach to the vegetation, lose their
tail and produce cysts of about 0.2 mm, the so-called metacercariae,
which are infective for the final host. Such cysts can survive for
months in the vegetation, even under dry conditions, even in hay!
Livestock becomes infected by grazing contaminated pastures or hay,
i.e. animals kept indoors can also become infected if they are fed
contaminated hay.

Inside the final host young immature flukes hatch out

of the cysts and within a few hours they cross the intestinal wall and
get into the peritoneal cavity where they migrate towards the liver,
which they reach in about 3 weeks. To reach the biliary ducts they
have to cross the hepatic tissue, a particularly harmful process for the
host that lasts 6 to 8 weeks. Once in the biliary ducts they complete
theirdevelopment to adult flukes and start producing eggs.
The prepatent period of Fasciola hepatica is 9 to 15 weeks,
depending on the host and other factors. The entire life cycle can be
completed in a minimum of 16 weeks. Left untreated liver flukes can
live up to 20 years on sheep, usually not more than one year in cattle.
Livestock grazing in regions with a high water table or frequently
flooded are at high risk of becoming infected with liver fluke. The
reason
is
that
the
snails
acting
as
intermediate
hosts
areamphibious and need humid habitats that are periodically
submerged or flooded. Relatively small humid habitats (e.g. irrigation
channels, ditches,
ponds,
watering
holes, etc.)
offer
suitable
conditions for the development of such snails and keep the
surrounding pastures infected. Permanently stabled livestock can also
become infected through contaminated hay.
Humans and carnivores such as dogs and cats are infected mainly
ingesting aquatic plants or drinking water contaminated with
cercariae. There is also evidence that consumption of raw liver
contaminated with juvenileflukes can be contagious for humans.

Harm caused by Fasciola hepatica

Liver flukes are very

harmful for
their
hosts,
particularly for sheep. Young immatureflukes migrating through the
liver tissues and crossing the wall of the bile ducts cause the major
harm. This process destroys the tissues and causes bleeding. The
spines in the surface of the flukes irritate the tissues that become
inflamed. All this leads to cell death and fibrosis, i.e. the formation of
excessive connective tissue that replaces the dead liver cells, which
impairs the normal functioning of the liver. Affected livers increase in
size and become fragile. Some flukes can become encapsulated in the
liver tissues and build cysts as large as walnuts. The bile ducts are
also damaged: they become thickened and can be calcified and even
obstructed. Infections with secondary bacteria can also happen,
mainly due to the general weakness of the host that debilitates its
own immune system. In addition, flukesproduce own toxins that impair
the normal function of the liver.
The bottom line is that the numerous vital physiological processes
that run in the liver are disturbed and the affected animals become
sick in a degree that depends on the number of flukes that infect them.
Infections with liver flukes are usually more harming for sheep
(fatalities are not rare) than for cattle and other livestock. Besides
fatalities the major economic damage is the consequence of reduced
weight gains of young animals (up to 30% less, even after slight
infections) and the condemnation of livers at slaughter. Light
infection can already reduce milk production in dairy cattle.
Worlwide annual economic loss due to fasciolosis has been estimated
to be over US$ 3 billion!

Symptoms and diagnosis of Fasciola hepatica infections

There are no really typical and easily recognizable symptoms of a liver

fluke infection in livestock or other animals. The major symptoms are
related with the inflammation of the liver (hepatitis) and of the bile
ducts (cholangitis) that can be also due to other disorders. Other vital
organs are usually not affected. Infections with a few dozen
adult flukes may not cause clinical signs other than general weakness
and reduced productivity.
Chronic fasciolosis is the more common form in sheep, goats and
cattle. It develops along the gradual establishment of adult flukes in
the bile ducts. It is characterized by the progressive development of
such
symptoms
as anemia (reduced
number
of
red
blood
cells), edema (local swellings due to excess fluid) often as "bottle
jaw",digestive
disturbances (diarrhea,
constipation
etc.),
and cachexia (wasting, i.e. weight loss, fatigue, weakness, loss of
appetite, etc.).
Acute fasciolosis is seldom in cattle but can occur in sheep. It is
caused by the sudden migration of many immature flukes through the
liver, which leads to complete organ failure. It can develop in healthy
animals that may be killed in a few days.
Detection of eggs in the feces confirms the diagnosis. However, since
the eggs are passed to the intestine only when the gall bladder is
emptied, a negative fecal egg count is not conclusive, i.e. there can be
false negatives. It is also important to distinguish Fasciola eggs
from Paramphistomum eggs that have a similar aspect.

Prevention and non-chemical control of Fasciola

hepatica infections

Fasciola hepatica can infect virtually all

mammal
species,
wild
and
domestic.
Consequently
it
is
almost impossible to eradicate it from a given property in endemic
regions with favorable conditions. Therefore, where it is known to
occur, preventive measures are a must to reduce the snail populations,
the infection of pastures with infective stages, or the access to
livestock to highly infested pastures.
Vector snails are amphibious and live both in water (e.g. streams,
lakes, pools, swamps, marshes, irrigation channels, ditches, ponds,
watering holes, etc.) as well in the humid vegetation around such
places. These snails are enormously prolific: a single snail can
produce more than 100'000 snails within one year.
Whatever measures help keeping
encouraged, e.g.:

the

pastures

Ensuring an adequate drainage.

Building watering points on solid ground, without puddles.

dry have to be

Make unavoidable ditches or channels less attractive to the snails: make the borders
steeper and/or cover them with concrete, eliminate the surrounding vegetation, drying
them completely out periodically, etc.

Avoid even very small water points that support the snails, e.g. hardened footprints (of
shoes or car tires).

If permanent humid environments cannot be eliminated, they have to

be fenced to prevent livestock from grazing there.

Rotational grazing is highly recommended to diminish fluke infestations. Simultaneous

grazing of sheep and cattle is not advisable. Alternate grazing (e.g. sheep and cattle, sheep
and horses, etc.) won't help, because liver flukes can infest all livestock.
Livestock infected with liver flukes can develop a certain level of natural immunity and
become resistant, especially cattle. Animals with chronic fasciolosis may recover
spontaneously. However, such natural resistance is usually associated with hepatic fibrosis,
i.e. a partial impairment of the liver function that will certainly result in a reduced
productivity.
Keeping livestock healthy and well fed diminishes the harm caused by liver flukes and favors
the development of the previously mentioned natural immunity.
There are so far no vaccines against the common liver
about vaccines against parasites of livestock and pets click here.

fluke.

To

learn

more

Biological control of liver flukes (i.e. using their natural enemies) is so far not feasible.

You may be interested in an article in this site on medicinal

plants against external and internal parasites.

Chemical control of Fasciola hepatica infections

Active
ingredients with
efficacy
against
flukes
are
usually
called flukicides or fasciolicides. The following anthelmintics are
used nowadays against liver flukes:

Albendazole (benzimidazole), broad-spectrum anthelmintic. Effective also

against most roundworms andtapeworms.
Clorsulon (benzenesulphonamide), narrow-spectrum flukicide.
Closantel (salicylanilide), medium-spectrum anthelmintic. Effective also against some
gastrointestinalroundworms.

Nitroxinil (halogenated phenol), medium-spectrum anthelmintic. Effective also against

some gastrointestinalroundworms.
Oxyclozanide (salicylanilide), narrow-spectrum flukicide.
Rafoxanide (salicylanilide), medium-spectrum anthelmintic. Effective also against
some gastrointestinalroundworms.
Triclabendazole (benzimidazole), narrow-spectrum flukicide.

As previously mentioned migrating immature flukes are the most

harmful, therefore efficacy against these stages is essential. Products
without efficacy against immature flukes will not protect livestock
from migrating flukes and need to be administered more
frequently. The tables below summarize the efficacy of these
flukicidal active ingredients (at their usual therapeutic doses) against
the various stages of Fasciola hepatica in sheep and cattle.

SCHISTOSOMA spp, BLOOD FLUKES, parasites of CATTLE,

SHEEP, GOATS, HORSES, CATS and other domestic animals.
Biology, prevention and control.
Schistosoma, also called blood flukes, is a genus of flatworms that
has cattle, sheep andgoats, as final hosts, but also other wild and
domestic ruminants, horses, cats, andhumans as well. They are
found mainly in tropical and subtropical Asia and Africa, but also in
South America and parts of Southern Europe. Abattoir studies in
Tanzania showed up to 34% of investigates cattle to be infected.
Another study in Ethiopia showed that up to 17% of the investigated
cattle shed eggs of these worms.

The
most
relevant
species
for livestock and horses are: Schistosoma
bovis ,Schistosoma
matthei , Schistosoma indicum , Schistosoma curassoni. Cats are
affected by Schistosoma japonicum and Schistosoma reflexum.

The
disease
caused
by Schistosoma spp
is
called schistosomiasis, bilharziosis orsnail
fever.
It
is
also
a serious human disease in endemic regions of Asia, Africa and
South America. It is estimated that close to 200 million people are
infected worldwide, mainly in Africa.

Are animals infected with Schistosoma species contagiousfor

humans?
NO. If livestock is infected with blood flukes, they are not directly
contagious forhumans, neither through contact, nor when consuming
meat, milk or blood of contaminated animals, nor through the feces.
The same applies to pets infected with blood flukes. Humans acquire
schistosomiasis
through
exposure
or
ingestion
toinfective
cercariae (see below under life cycle), not by ingesting adult flukes or
their eggs. Most blood fluke species that infect livestock are not
human parasites. However, aquatic immature stages (= cercariae, see
life cycle below)of other Schistosoma species that are not pathogenic
for humans can nevertheless penetrate the human skin and cause
a skin inflammation (dermatitis) known as swimmer's itch, lake
itch or cercarial dermatitis, which is a benign dermatitis: it will
spontaneously recede about a week after infection.

Final location of Schistosoma spp

Predilection sites of blood flukes are the blood vessels, especially
the portal and mesenteric veins.

Anatomy of Schistosoma spp

Blood flukes do not resemble most other fluke species. Instead of
being flat and with an oval shape, they look very much like "normal"
worms. Also
unlike
most
other
flukes Schistosoma is
not
hermaphroditic but bisexual, and males and females show a different
form (sexual dimorphism). Males are about 10 to 20 mm long and 1 to
2 mm thick, whereas females are 20 to 30 mm long and <1 mm thick,
i.e. significantly longer and thinner than males. The oral and

ventral suckers are rather small. Each male has a special structure
along tits body, the gynacophoriccanal, where the adult female
resides permanently. In fact it seems that females cannot mature in
absence of the males. As in other flukes the digestive system
of Schistosoma is blind, i.e. it has no anus but ends in a blindbranch,
the cecum.

Schistosoma eggs have

species-specific
sizes
(130-300x40-90
micrometers) and are oval to spindle-shaped, with or without spines.

Life cycle and biology of Schistosoma spp

Blood flukes have an indirect life cycle with freshwater snails as

theintermediate hosts, mainly of the genus Bulinus .
The adult females lay eggs in the capillaries of the intestinal wall. The
egg masses form abscesses that finally burst and release the eggs
into the gut, which are transported outside with the host's feces. The
abscesses usually heal spontaneously.
Once outside and in contact with water the eggs release small
swimming larvae, the miracidia, which find a suitable snail and
penetrate into its body. Inside the snail miracidia develop further
during 1 to 4 months through two generations ofsporocysts to
asexually produce dozens of cercariae. Mature infective cercariae
leave the snail through its respiratory hole. A single snail can release
up to 3'000 cercariae.

Free-swimming cercariae actively search a final host. Their survival in

the environment is limited to a few days. These infective cercariae
actively penetrate through the skin of the host, or are ingested with
contaminated water when grazing in marshes, swamps, and otherwise
humid vegetation. Ingested cercariae penetrate the rumen. Once
inside the host's body they get into a blood vessel and start a speciesspecific migration (often passively transported with the blood)
through various organs until they reach their preferred final locations
where they complete development to adult flukes, copulate and start
producing eggs. During this time they feed on red blood cells.
The prepatent period (i.e. time between infection with cercariae and
start of egg production) is species-specific, e.g. about 7 weeks
for Schistosoma matthei.

Harm caused
by Schistosoma species, symptoms and diagnosis
Blood flukes are not excessively harmful for livestock. Most damage is
due to the immature stages that penetrate the skin, or to the bursting
of the egg filled abscesses in the gut. Immature flukes in the blood
vessels feeding in red blood cells can cause anemia and compete for
nutrients with the host's own tissues. They can also cause blood
poisoning. Schistosoma bovis can also damage the gall bladder.
Most Schistosoma infections of livestock produce no clinical signs,
even heavy infections. Intermittent diarrhea is sometimes observed,
occasionally with blood and mucus. Constipation, anemia, weight loss
and progressive weakness can happen as well.
In horses most infections remain asymptomatic.
occasionaly occur in case of heavy burdens.

Problems

may

Diagnosis is confirmed through fecal examination for the presence of eggs, for some species
also in urine.

Prevention and non-chemical control of Schistosoma infections

Where blood flukes are endemic, preventive measures are highlyrecommended to reduce the
snail populations, the infection of pastures with infective stages, or the access to livestock to
highly infested pastures.
Vector snails are aquatic and live in water (e.g. streams, lakes, pools, swamps, marshes,
irrigation channels, ditches, ponds, watering holes, etc.) and are highly prolific. Whatever
measures help keeping the pastures dry have to be encouraged to reduce the snail
population e.g.:

Ensuring an adequate drainage

Building watering points on solid ground, without puddles

Make unavoidable ditches or channels less attractive to the snails: making the borders
steeper and/or cover them with concrete, eliminate the surrounding vegetation, drying
them completely out periodically, etc.

If permanent humid environments cannot be eliminated, they have to be fenced to prevent

livestock from grazing there.

In endemic regions preventative measures must include providing

livestock with snail-free drinking water. These measures will prevent
infections with other parasites that may appear at the same time,
e.g. liver flukes (Fasciola hepatica, Fasciola gigantica) or stomach
flukes (Paramphistomum spp).
There
are
so
far no
vaccines
against
blood
more about vaccines against parasites of livestock and pets click here.

flukes.

To learn

Biological control of blood flukes (i.e. using their natural enemies) is so far not feasible.
You may be interested in an article in this site on medicinal plants against external and
internal parasites.

Chemical control of Schistosoma infections

Chemical control of blood flukes in livestock is not easy and mostly
uneconomic, because damage is usually not substantial.
The most effective anthelmintic is praziquantel, but this drug is often
not available for use on livestock in many countries. However, sudden
death of many flukes in the blood vessels can cause thrombosis in the
hepatic vein, which can be fatal for the host. Therefore whatever
anthelmintic treatment must aim at killing the flukes slowly.
Many other classic flukicides do not control rumen flukes,
e.g. albendazole, clorsulon, netobimin, nitroxinil andtriclabendazole.
Neither macrocyclic
lactones (e.g. ivermectin)
nor levamisole are
effective against any kind of flukes either.
Chemical control of the snails with molluscicides (i.e. snail killers) such as copper
sulphate, sodium pentachlorophenate, niclosamide, etc. can make sense for very specific
purposes, e.g. for treating places where livestock congregates (water holes, feeding areas,
salt licks, shade trees, etc) to keep them free of snails, or if the drinking water is already
contaminated with snails. But trying to eradicate snails from a property is hopeless and
useless. It is virtually impossible to treat every place where they can survive and they
reproduce extremely quickly. Cleaned pastures would become re-infested very fast. In
addition, it would be too expensive and very harmful for the environment. In fact, such
molluscicides are not approved in most countries.

CYSTICERCUS OVIS, sheep measles, parasitic tapeworm of

SHEEP and GOATS. Biology, prevention and control
Cysticercus ovis is the larval stage (cysticercoid, metacestode)
of Taenia ovis , atapeworm parasite of dogs and other canids
(coyotes, wolves, foxes, very occasionallycats, etc.), that has sheep
and goats as well as various wild ruminants as intermediate hosts.

Cysticercus
ovis occurs worldwide,
mainly in rural areas of countries with large sheep populations.
Regional incidence varies a lot. Unexpected outbreaks can happen due
to climatic conditions that favor the survival of eggs in pastures or the
activity of wild canids that carry the disease.
The
disease
caused
by
this
and
other
cysticercoids
is
calledcysticercosis. In this particular case it is also called sheep
measles.

Is livestock infected with Cysticercus oviscontagious for

humans?
NO. The reason is that Taenia ovis is not a human parasite. See the life cycle below.
You can find additional information in
worms and/or tapeworms.

this

site

on

the general

biology of parasitic

Final location of Cysticercus ovis

Cysticercoids of Taenia ovis are found mainly in the muscles of sheep
and goats. The predilection site of adulttapeworms in their final host
(dogs and other canids) is the small intestine.

Anatomy of Cysticercus ovis

In sheep and goats Cysticercus ovis cysticercoids appear as small
whitish cysts filled with fluid that contain an immature worm. They
have the size of a grain rice (~4 to 9 mm). Infected meat can have
dozens of such cysts. They are found mainly in the skeletal muscles
and those of the heart, the diaphragm, and the jaws. Several months
after infection the cysts die and become calcified.

Visit the page on Taenia species for

the anatomy of adult Taenia tapeworms.

additional information of

Life cycle and biology of Cysticercus ovis

As
all tapeworms, Taenia
ovis has
an indirect life
cycle,
with dogs and
other
canids
(foxes,
wolves,
coyotes,
very
occasionally cats)
as final
hosts,
and sheep
and
goats as intermediate hosts.
Sheep and goats become infested when ingesting food or water
contaminated with eggs or gravid segments of Taenia ovis through
herbage or stored feed. A single gravid segment can have uo to 75,000
eggs! Contamination of sheep feed can occur through contamination
with dog feces. The eggs can remain infective for up to 12 months.
Intrauterine infection of unborn lambs has been also reported.
Once ingested by sheep or goats the young larvae hatch out of the
eggs in the gut, go through the intestinal wall, reach the blood stream
and migrate to a muscle, where they encyst. The cysts need 10 to 12
weeks to completedevelopment. The cysts may remain infective for
dogs for up to one year.
Dogs and other canids become infected when eating insufficiently
cooked meat contaminated with cysts. Once in the dog's gut, the cysts
release the young tapeworms, which attach to the gut's wall and start
producing
segments.
Within
5
to
8
weeks (prepatent
period) the tapeworms mature and start shedding eggs.

Harm caused by Cysticercus ovis, symptoms and diagnosis

Cysticercus ovis is not pathogenic for sheep or goats and usually the
infection causes no clinical signs, unless a vital organ (e.g. the heart)
is massively infected, which is very unsusual. However, infections
have a substantial economic impact because the whole carcass is
condemned at slaughter. An epidemic outbreak can beeconomically
devastating.

So far diagnosis on sheep or goats is only possible post-mortem after

carcass examination.
Infection of dogs with Taenia ovis are usually benign as well. They can
cause diarrhea and loss of appetite, but they often cause no clinical
signs.

Prevention and control of Cysticercus ovis

Although sheep measles is not harmful the intermediate hosts and not
contagious for humans, the FAO recommends condemnation of heavily
infected carcasses, and this is usually followed worldwide.
Best prevention consists in avoiding the contamination of sheep feed
(fresh pasture as well as hay, silage, and other stored feed) or water
with dog feces that may contain tapeworm eggs. It must be
considered that the eggs may remain infective in the feed after silage
or other processing of hey or fodder (pelletizing, fermentation, etc.).
At the same time dog scavenging on potentially contamined cadavers
or offal has to be avoided. If this cannot be avoided,
in endemic regions
is
is
advisable
to regularly
deworm
dogs (particularly working and guard dogs) at least 3 to 4 times a
year, especially if sheep measles has been found in the region. There
are numerous dog anthelmintic products that control such infections.
They contain active ingredients with broad-spectrum anthelmintic
efficacy
such
as benzimidazoles (e.g. fenbendazole, febantel, mebendazole) or
specific taenicides such as praziquantel and epsiprantel, the latter
often in combination with nematicides (e.g. levamisole, milbemycin
oxime, pyrantel, etc.) to cover a broader spectrum of worms.
Scavenging on potentially infected
Most of these dog dewormers are available in formulations for oral delivery either as solids
(tablets, pills, etc.) or as liquids (drenches, suspensions, etc.). There are also a
few injectable taenicides in some countries (mainly with praziquantel).
So far there are no antiparasitic medicines for external use (spot-on - squeeze-on pipettes, shampoos, soaps, sprays, powders, insecticide-impregnated collars, etc.) that
control established tapeworm infections on dogs.

The regular use of anthelmintics is usually not indicated for preventing sheep or
goat infections with Cysticercus ovis. There are reports that praziquantel is effective, but
results can be unreliable.
Several
classic
anthelmintics
such
as macrocyclic
lactones (e.g. ivermectin, doramectin, selamectin,etc.), levamisole, tetrahydropyrimidines (e.g
. pyrantel, morantel) and piperazine derivatives are not effective at all against Cysticercus
ovis or whatever adult tapeworm or cysticercoid, neither on dogs, nor on sheep, goats or
otherlivestock.
There are so far no vaccines that would protect sheep or goats against Cysticercus ovis. A
lot of research is being done in the development of a vaccine against sheep measles, but so
far
there
are
no
commercial
vaccines
in
most
countries. To
learn
more
about vaccines against parasites of livestock and pets
Biological control of Taenia tapeworms respectively Cysticercus ovis (i.e. using its natural
enemies) is so far not feasible.
You may be interested in an article in this site on medicinal plants against external and
internal parasites.

Resistance of Taenia spp to anthelmintics

So far there are no reports on resistance of Taenia spp, respectively Cysticercus ovis to
anthelmintics.
This means that if an anthelmintic fails to achieve the expected efficacy, chance is very high
that either the product was unsuited for the control of Cysticercus ovis, or it was used
incorrectly.

ECHINOCOCCUS GRANULOSUS, the hydatid tapeworm,

parasite of DOGS, HORSES, CATTLE, SHEEP, GOATS, PIGS and
other LIVESTOCK. Biology, prevention and control.
Echinococcus granulosus (= Echinococcus unilocularis) is a parasitic tapeworm that
hasdogs and other canids (e.g. foxes, wolves, coyotes, etc.) as final hosts. It is also called
thehydatid worm and the dog tapeworm (not to be confused with Dipylidium caninum).

But it infects many other domestic and wild mammals (mainly ungulates,
but
also
rodents)
that
act
as intermediate
hosts,
including cattle, sheep, goats, pigs, horses,dromedaries, South American camelids, deer,
kangaroos, etc. where it causes a disease called cystic echinococcosis or hydatid
disease. Humans can also act as intermediate hosts. There are a few reports that cats can
acts as intermediate hosts as well.

Echinococcus granulosus is found worldwide, but the prevalence varies a lot. It is generally
more abundant in rural regions with abundant livestock and wildlife together with poor
sanitary conditions.
Echinococcus multilocularis is a related species that affects dogs, cats, and humans but not
livestock.

Are dogs, horses or livestock infected with Echinococcus

granulosus contagious for humans?

YES. The worm eggs shed with the feces of dogs can contaminate food and drinking
water and are infective for humans as well as other animals. Contact with contaminated
dogs can also be contagious, because their hair coat can carry such eggs as well. See the
life cycle below. Intermediate hosts (horses, livestock, etc.) contaminated
with Echinococcus granulosus, i.e. suffering of cystic echinococcosis (= hydatid disease)
are not contagious for humans.

You can find additional

worms and/or tapeworms.

information in

this

site

on

the general

Final location of Echinococcus granulosus

biology of parasitic

Predilection site of adult Echinococcus granulosus worms is the small intestine.

Thy hydatid cysts on intermediate hosts (cattle, sheep, pigs, etc.) develop mainly in
the liver and the lungs but can affect other organs, e.g. the brain.

Anatomy of Echinococcus granulosus

Adult Echinococcus granulosus worms are rather small, not longer than 7 mm. They have only
4 segments, the last one being the largest and gravid, i.e. filled with eggs. The head (scolex)
has 4 suckers and numerous hooksfor attaching to the gut's wall. Otherwise, as other
tapeworms, Echinococcus
granulosus has neither
a
digestivetube,
nor circulatory or respiratory systems. It doesn't need them because each proglottid
absorbs what it needs directly through its tegument. Each proglottid has its own reproductive
organs of both sexes (i.e. they are hermaphroditic) and excretory cells known as flame
cells (protonephridia). The reproductive organs in each proglottid have a common opening
called the genital pore. In young proglottids all these organs are still rudimentary. They
develop progressively, which increases the size of the proglottid as it moves towards the tail.
Mature gravid proglottids are full of eggs and detach from the strobila (the chain of segments)
to be shed outside the host with its feces.
The eggs are have an ovoid to spherical shape, are rather small (~30 micrometers). They are
embryonated (i.e. contain already developed larvae called oncospheres or hexacanths) with
a thick capsule radially striated.
Thy hydatid cysts (also known as metacestodes or bladder worms) develop in various
organs of the intermediate hosts, are oval to spherical in shape and grow slowly but steadily.
Eight weeks after infection the cysts can reach about 2.5 mm in diameter, three months later
about 2 cm. Hydatid cysts found in slaughterhouses can reach the size of an orange (5 to 10
cm). Infected organs can have dozens of cysts. Each cyst is filled with liquid and contains
several heads of the parasite (protoscolices) produced through asexual multiplication.

Life cycle and biology of Echinococcus granulosus

Echinococcus granulosus has an indirect life cycle with dogs (and other canids) as final
hosts, and numerousdomestic and wild mammals, including humans as intermediate
hosts.
Gravid segments filled with eggs are shed with the dog's feces hosts. Each adult worm
deposits one gravid segment aprox. every two weeks, and each gravid segment contains
several hundred eggs. Once in the environment, survival of the eggs depends strongly on the
climatic conditions and is lower by warm and dry weather. Infectivity decreases with time.

Intermediate hosts ingest such eggs through contaminated

food (both fresh herbage and hey) or water. Inside the intermediate host, the eggs release the
hexacanths (larvae) in the intestine. They go through the intestinal wall, get into the portal
vein and are transported to the liver. The capillaries in the liver act like a filter that retains
numerous hexacanths, which develop to cysticercoids and produce the hydatid cysts. The
blood stream can transport hexacanths to other organs too, e.g. to the lungs or the brain,
where the respective capillary networksretain the hexacanths that produce the cysts. Such a
cyst can rupture and the immature worms are transported further to other organs. The hydatid
cysts in intermediate hosts can contain hundreds if not thousands of infective larvae.
The immature worms in the hydatid cysts do not complete development to adults there. They
do it only once they get into a final host that has fed on a prey infected with hydatid cysts. In
this case the young worms (protoscolices) are released after digestion of the cysts, attach to
the gut's wall, complete their development to mature adults and start producing eggs.
The prepatent period (time between infection and recovery of first eggs in the feces) is 6 to 7
weeks.

Harm caused by Echinococcus

granulosus infections, symptoms anddiagnosis
For dogs and other final hosts Echinococcus granulosus infections are benign, mostly
without clinical signs, unless in case of very heavy infections, which are unusual.
For livestock and other intermediate hosts such as horses, the development of hydatid
cysts is mostly asymptomatic, unless the organs are heavily affected, which is usually due to
the growing cysts pressuring the organ tissues. Parts of the tissue die, which impairs the
functioning of the affected organ. The clinical signs depend on the affected organs. Digestive
disturbances, cough and difficult breathing (dispnea) have been described. The major damage
for livestock is organ condemnation at slaughter.
For humans as intermediate hosts, hydatid cysts can be a serious disease. The problem is
that they develop very slowly over years and without symptoms. They are often discovered too
late. If vital organs (e.g. brain, heart) are affected harm is often irreparable and fatalities are
possible. Rupture of the cysts can also cause stronganaphylactic reactions.

Diagnosis in dogs cannot

be
based
on
egg
identification
in
the
feces,
because Echinococcus eggs are undistinguishable from Taenia spp eggs. ELISA tests based
on egg antigens in the feces are very reliable but not available in some countries.
Newer PCR (Polymerase Chain Reaction) tests based on DNA from egg in the feces have also
been developed.
Diagnosis in livestock or other intermediate hosts is usually made after slaughter or
necropsy. So far there are no reliable biochemical tests for early detection.

Prevention and control of Echinococcus granulosus infections

In dogs
In
endemic
regions
it
is
advisable
to
reduce
the
number
of stray dogs. Domestic and working dogs must be kept away from contaminated offal. They
can be preventatively treated with approved taenicides. These products contain mainly broadspectrum anthelmintic active
ingredients such
as benzimidazoles (e.g. fenbendazole,febantel, mebendazole) or
specific
taenicides
such
as praziquantel and epsiprantel, the
latter
often
in
combination
with
nematicides
(e.g. levamisole, milbemycin oxime, pyrantel, etc.) to cover a broader spectrum of worms.
These preventative measures are highly recommended also for urban dogs in endemic areas,
in order to prevent transmission of echinococcosis to humans.
Most of these pet wormers are available in formulations for oral delivery either
as solids (tablets, pills, etc.) or asliquids (drenches, suspensions, etc.). There are also a
few injectable and spot-on (= squeeze-on = pipettes) taenicides in some countries (mainly
with praziquantel).
Most wormers kill the worms shortly after treatment and are metabolized and/or excreted
within a few hours or days. This means that they have a short residual effect, or no residual
effect at all. As a consequence treated animals are cured from worms but do not remain
protected against new infections. To ensure that they remain worm-free the pets have to be
dewormed periodically, depending on age and the local epidemiological, ecological and
climatic conditions.
Other
classic
livestock anthelmintics such
as macrocyclic
lactones (e.g. ivermectin, selamectin,etc.), levamisole, tetrahydropyrimidines (e.g. pyrantel, m
orantel) and piperazine derivatives are not effective at all against Echinococcus species or
whatever tapeworms.
So far there are no antiparasitic medicines for external use such as shampoos, soaps, sprays,
powders, insecticide-impregnated collars, etc. that control established tapeworm infections.

In livestock and horses

Best prevention of Echinococcus infections in livestock and horse farms is to keep dogs
away from feeding contaminated organs, especially working dogs. To achieve it is
essential to thoroughly cook whatever offal they get, or to feed them on commercial dog food.
Wild rodents (rats, mice, squirrels, etc.) can also be intermediate hosts of Echinococcus
granulosus and dogs can become infected if they eat such infected preys. If this is not
possible, working dogs should be regularly treated with taenicides as previously mentioned

A true vaccine against livestock echinococcosis caused byEchinococcus granulosus is

now available in several countries. The commercial brand is called PROVIDEAN HIDATIL EG
95 and was introduced in 2011 in Argentina by a company called TECNOVAX. It is approved
for use on cattle, sheep, goats and South American camelids. It is based on the EG95
antigen obtained from Echinococcus granulosus eggs. One dose provides up to 82%
protection, two doses up to 97% and three doses 100% protection. Hopefully this powerful
weapon will soon become available in other endemic regions.
The use of anthelmintics against hydatid cysts is usually not indicated in livestock, neither
therapeutically (i.e. to cure already established hydatid cysts) nor prophylactically (i.e. to
prevent the development of hydatid cysts). Mostactive ingredients with efficacy against
tapeworms such
as
broadspectrum benzimidazoles (e.g. albendazole,fenbendazole, febantel, mebendazole) or
specific
taenicides such as praziquantel are ineffective againstEchnicoccus granulosus hydatid
cysts at the usual therapeutic dose and have to be administered at significantly higher
doses and repeatedly to achieve only partial control. This is either too expensive, or not well
tolerated by livestock, or both.
Other
classic
livestock
anthelmintics
such
as macrocyclic
lactones (e.g. ivermectin, doramectin, moxidectin,
etc.), levamisole, tetrahydropyrimidines (e.g. pyrantel, morantel)
and piperazine
derivatives are not effective at all against hydatid cysts caused by Echinococcus granulosus.
Biological control of Echinococcus granulosus (i.e. using its natural enemies) is so far not
feasible.
You may be interested in an article in this site on medicinal plants against external and
internal parasites.

Resistance of Echinococcus granulosus to anthelmintics

So far there are no reports on resistance of Echinococcus granulosus to anthelmintics in dogs
or cats.
This means that if an anthelmintic fails to achieve the expected efficacy, chance is very high
that either the product was unsuited for the control of Echinococcus granulosus, or it was
used incorrectly.