VETERINARY HELMINTHOLOGY

Veterinary helminthology is concerned with the study of helminths or

parasitic worms.

Helminths are trophoblastic metazoans (multi-cellular organisms).

Helminths are among the common parasitic causes of animal suffering.

They are the cause of high morbidity and mortality of animals worldwide.

They cause different diseases in animals, but few helminthic infections

cause life- threatening diseases. They cause anaemia and malnutrition and
economic loss as a result of infections of domestic animals.

The sources of the parasites are different. Exposure of animals to the

parasites may occur in one of the following ways:

1. Contaminated soil (Geo-helminths), water (cercariae of blood flukes) and

food (Taenia in raw meat).

2. Blood sucking insects or arthropods (as in filarial worms).

3. Domestic or wild animals harboring the parasite (as in echinococcus in

dogs).

4. Animal to animal contact

5. Oneself (auto-infection) as in lungworms.

They enter the body through different routes including: mouth, skin and
the respiratory tract by means of inhalation of airborne eggs.

Helminth parasites are Classified into 3 classes;

➢ Nemathelminthes (roundworms)
➢ Platyhelminthes (flatworms)

➢ Acanthocephala (thorny-headed worms)

DIFFERENT TYPES OF HOSTS (COULD BE ANIMALS OR HUMANS) OF

PARASITES

. Final (definite) hosts - hosting the sexual stages of the parasite

. Intermediate hosts - hosting asexually reproducing stages of the

parasite

. Transitory/accidental/paratenic hosts - hosting parasitic stages

without further reproduction

. Vectors - representing bloodsucking parasites such as arthropods, worms

or leeches which transmit other pathogens and/or parasites during their
blood meal.

GENERAL POINTS.

▪ Helminths are parasites which are multicellular and often big enough to be
seen by naked eye ie macroscopic.

▪ The drugs used to reduce their burden in domestic animals are called
Anthelmintics (note absence of “i” between t and h.

▪ Administering anthelmintics is also referred to as “deworming”

▪ It is not practically possible to eliminate all worms in domestic animals and

the more practical approach is to keep the worm burden low enough not to
cause clinical signs in the host.
▪ For every helminth covered one should know:-

Morphology

These are the physical characteristics that enable one to recognize and
distinguish one worm from others

Life cycle

This refers to the stage by stage development of the helminth from the egg
stage to the adult(s) that can reproduce. It is important to note the both
the internal and external environment of each stage, the infective stage,
whether there is any migration and the stage that causes most harm to the
host

Effects on hosts

Some of these are general to all worms and parasites in general (see
Parasitology I notes) but one should note also those that are characteristic
to the particular worms

Diagnosis

Making a statement that the animal is adversely affected by a particular

worm

Control

Means of preventing infestation and infection especially to the extent of

showing clinical disease.

Treatment of Disease caused

Which dewormer to use, when, the dosage and the route of administration,
usually oral.
 The information about dosage, route and various precautions is usually
provided in the instructions for use. Broad spectrum anthelmintics are often
used because livestock often host more than one species of helminths.
There are, however those helminthes that are unique and require unique
anthelminthes. For cost effectiveness, practice of tactical and strategic
deworming is often recommended in control of helminths.

NEMATODES

Nematodes are also called round worms

GENERAL POINTS ON NEMATODES

▪ They are cylindrical and unsegmented

▪ Both ends are usually (but not always) somewhat pointed

▪ They have a cuticle that usually looks smooth to the unaided eye but show
various cuticular structures on magnification. These are either circular
annulations or longitudinal striations.

▪ The males have on the posterior extremity the genital papillae, mostly
paired supporting the caudal alae or the copulatory bursa used for
mating. They also have one or two pairs of spicules for either attachment
during mating or expanding the female worm’s cloaca

▪ There are separate male and female worms, the male being smaller

▪ They have either direct or indirect life cycles

▪ Some nematode females are oviparous, others ovoviviparous or viviparous.

The eggs greatly vary and are used for diagnosis by fecal examination.
 Females are very prolific in egg laying and can lay as many as several
thousand eggs per day.

▪ Gastrointestinal nematodes may disturb the normal functions of the

gastrointestinal tract. Gut disorders lead to a disease syndrome involving
diarrhea, weight loss, anemia (loss of blood and plasma proteins),
mucoid hyperplasia, disorder of pepsinogen production, and other
functional and intestinal disorders such as depressed levels of
minerals and depressed activity of some other intestinal enzymes.

▪ The effects of nematode parasitism on production are well known and will
remain one of the major factors limiting animal productivity on farms that
rely on grazing animals on pasture. Economic loss may be due to the
reduced skeletal growth (mineral deficiencies), to reduced weight gains
(reduced incorporation of amino acids into muscle protein), or to
suppressed wool production and reduced wool quality (e.g., break in wool
growth due to reduced incorporation of amino acids into protein in hair
follicles). Clinical parasitism markedly affects milk production in dairy cows,
and sub clinical parasitism appears to be of economic importance, as it will
also reduce animal productivity. Knowledge of the epizootiology of the
parasites permits strategic timing of drug treatments.

▪ A number of strategies have been suggested to limit the development of

drug-resistant nematodes but any strategy must fit the particular
characteristics (parasite and host biology, epizootiology, etc.) of the target
population within a certain region, and hence, strategy will vary
considerably between different regions. Therefore, efficient control
programs for grazing ruminants (cattle and sheep) are based on seasonal
fluctuations of L3 on pasture. In temperate countries (e.g., Europe)
sufficient L3 may overwinter on pasture to infect susceptible animals next
spring. However, the numbers of larvae, which are acquired in spring are
 seldom sufficient to produce clinical signs. Non ingested overwintered L3
may die off in early summer, and L3 that are found in midsummer stem
primarily from hatching of eggs deposited the same year. Thus, young
cattle should be treated with anthelmintics after they start spring grazing.
Removal of cattle to “clean” pastures may allow treatment to be delayed
until early summer, and in general there will be no requirement for further
treatments during the grazing season.

HEMONCHUS (BARBER’S POLE WORM)

Two common species are Haemonchus contortus and Haemonchus

placei

Common names:

Barber’s pole worm, Wire worm of ruminants, Twisted worm,

stomach worm, bankrupt worm.

Basically this is a blood sucking worm that causes haemorhagic anaemia

Morphology

▪ Small buccal cavity

▪ Both male and female worm have a slender tooth or lancet used for
piercing and sucking blood

▪ Prominent cervical papillae

▪ Large bursa

Life cycle
 Direct: Embryonated eggs, yellow in colour are laid, hatch into L1 during
warm wet season, develop into L2 and finally infective L3. This is ingested
and pass into rumen , then reticulum, omasum of host animal unharmed
and finally reach abomasum and develop into L4 and L5 both of which are
immature adults. L5 then matures into adult worms, mating occurs and the
female worm starts to lay eggs. This completes the cycle

Effects on hosts

1. Haemonchus suck blood resulting in haemorrhagic anaemia which on the

live animal is manifested clinically as pale mucous membranes

2. Anaemia makes the animal to have an increased heart and pulse rate

3. The anemia also leads to an increased respiratory rate

4. Chronic haemomchosis leads to development of sub-mandibular

oedema. This is what is called poverty jaw or bottleneck jaw This
condition arises from hypophosphatemia i.e. loss of protein especially in the
blood. Consequently water escapes the blood stream into the tissues of the
body leading to oedema. In sheep the oedema may be present in the belly
area (anarsaca)

5. Diarrhoea

Diagnosis

This is done by :-

1. faecal examination to demonstrate the strongyle eggs of haemonchus

2. Clinical signs, especially sub-mandibular oedema

Treatment of Disease caused

Treatment using broad spectrum anthelmintics like Albendazole

Control

1 Strategic deworming

2 tactical deworming

Short notes on Strategic Deworming

This general phrase is used to denote a way of deworming to control a variety of worms. It
takes into account when and how to maximize benefits of the exercise in terms of reducing
the worm burden and keeping the animals healthy for the longest period of time.

For this reason deworming is done bearing in mind the season when the larvae population
on the pastures (being ingested by host animals) is highest and just before the worm burden
reaches a level that causes clinical disease in the host animal. In our local circumstances the
animals are dewormed during the warm period following the rains (about 2-3 weeks)

Short notes on Tactical Deworming

This term is used for the type of deworming that takes into account special circumstances
like

▪ Introduction of new animal into a herd or flock

▪ Change in the nutritional status of individual host animals
▪ Change in the immune status of individual host animals

SELF-CURE PHENOMENON

This is an immune reaction whereby an infected animal has both L3 and adult worms in the
abomasums but due to previous exposure of the abomasums to antigenic fluid of L3 the
abomasal wall has become hypersensitive (by release of a lot of antihistamines), making it
impossible for the worms to attach. As a result of this the worms are expelled. In other
words the host animal will be ingesting the infective L3 but they come out without causing
any harm to the animal.

This phenomenon is seen in a several genera of worms, including Haemonchus and

Oesophagostomum . It is the same phenomenon that makes adult animal more resistant to
worms (having been exposed earlier) and young animals more affected by worms (having
had no previous exposure)
 OSTERTAGIA

Ostertagiasis is the infestation of the abomasums by Ostertagia genus of

nematodes:

▪ Ostertagia ostertagi – cattle

▪ Ostertagia circumcincta - sheep

Common name: medium stomach worm

Morphology

▪ Both male and female about 10-12 mm in length

▪ Male worms have a bursa and spicule

Life cycle

Direct: Embryonated eggs, yellow in colour are laid, hatch into L1 during
warm wet season, develop into L2 and finally infective L3. This is ingested
and passes into rumen , then reticulum, omasum of host animal unharmed
and finally reach abomasum and develop into L4 and L5 both of which are
immature adults.L5 then matures into adult worms, mating occurs and the
female worm starts to lay eggs. This completes the cycle

L3 stages of Ostertagia spp. ingested may have their development arrested

at the L4 stage, primarily in the abomasums when circumstances are not
favourable. To prevent type II ostertagiasis, susceptible cattle should be
treated with an effective drug against these stages. Lack of treatment leads
larvae to resume their development next favorable time, causing severe
damage of abomasal mucosa.

Effects on hosts

There are two types of Ostertagiasis: TYPE I OSTERTAGIOSIS and TYPE II

OSTERTAGIASIS

Type I occurs when L3 and L4 stay in the mucosa of the abomasums for a
few (1-2) weeks and are then expelled. During this time they cause a
watery diarrhea.

Type II ostertagiasis:

After ingestion of the infective L3 these invade the glandular epithelium of

the abomasal mucosa and remain there for 6 months to 1 year interfering
with production of HCl that converts pepsinogen to pepsin As a result, the
abomasal ph remains alkaline and pepsinogen leaks into circulation There is
also actual loss of blood protein like albumin and destruction of glandular
mucosa Hypoprotaenemia results and also accumulation of bacteria. A
variety of diseases could then result. There is greenish diarrhea and
formation of nodules on the abomasal mucosa Submandibular eodema is
also often observed.

Diagnosis

This is done by:-

1. faecal examination to demonstrate the strongyle eggs of ostertagia

 2. Clinical signs

Treatment of Disease caused

Give:

▪ Broad spectrum anthelmintics

▪ Kaolin because of diarrhea

▪ Protein supplements and multivitamins

Control

▪ Strategic deworming

▪ Tactical deworming

▪ (Optional) antibiotics

TRICHOSTRONGYLUS

Common name –small stomach worm, stomach hair worm

These worms are capable of hypobiosis, just like some species of

Ostertagia, Haemonchus, Cooperia, Nematoduirus, Dirifilaria and
Ancylostoma.

Hypobiosis is a temporary cessation of development of nematodes at a

precise point in early parasite and serves to synchronize the development
of the parasite with events in the host and environment.
 Trichostrongylus spp live in the abomasum of cattle, sheep, and goats and
some in the intestines. In ruminants, T. axei infections are usually part of a
mixed abomasal helminthosis and its effects cannot be dissociated from
those of other worm species. The worm is rarely a pathogen on its own, as
most infections are mild.

Life cycle

Eggs passed in feaces → LI →L2 →L3 (infective) ingested together with

herbage → abomasum → intestines L4 → L5 → adult worm → mating
and subsequent laying of eggs by female worms

Effects on hosts

The clinical signs include diarrhoea, anorexia, progressive emaciation,

listlessness, and weakness.

Diagnosis

Make a faecal culture and demonstrate the infective larvae

Treatment of Disease caused

Broad spectrum anhelmintics

Control

▪ Strategic deworming

▪ Tactical deworming

▪ (Optional) antibiotics

Examples of Trichostrongylus spp

▪ Trichostrongylus axei

▪ Trichostrongylus colubriformis

COOPERIA

Genus Cooperia belongs to the same family with Haemonchus, Ostertagia,

Trichostronylus and Nematodirus. They are usually found in the small
intestines and rarely in the abomasums of ruminants.

Morphology

They are relatively small worms of reddish colour when fresh.

The adult worms (male 5–8 mm, female 8–11 mm) are often spiral-
shaped.

The cuticle of the anterior extremity frequently forms a cephalic swelling

and the rest of the body cuticle bears longitudinal ridges which are
transversally striated The male bursa has a small dorsal lobe and rays.
They have spicules. The males have vulva which may be covered by a flap
situated behind the middle of the body.

Important/common species are:-

▪ Cooperia curtcei – sheep, rarely cattle

▪ Cooperia punctata – cattle, rarely sheep

▪ Cooperia pectinata – cattle, rarely sheep

▪ Cooperia oncophora – primarily in cattle but also in sheep

The rest of the information about Cooperia spp is more or less as for other
trichostrongylidae

ASCARIDS

Adult ascarids live in the lumen of the small intestine.

They are typically between 5 and 40 cm long (depending on species, sex
and stage of development) and pinkish-white or ivory-white in
colour.
The females are very prolific, each producing hundreds of thousands of
eggs per day. The eggs are almost spherical, so they appear round when
seen under the microscope.
Ascarid eggs are un-embryonated when passed into the environment. If
conditions are favorable, an infective larva will develop inside each. The
egg does not hatch until swallowed by a host.
 Three ascarid worms and their hosts

- Toxascaris leonina affects dogs and cats

- Toxocara canis affects dogs

- Toxascaris cati affects cats

These worms occur in the dog and cats

GENERAL ASCARIASIS

Young puppies and kitten are affected more than the adults

General Clinical signs

They show pot belly, diarrhea (alternating with constipation at times),

wasting, vomiting and anaemia, nervous symptoms like rabies(when larvae
 migrate to the CNS), coughing and migration into the lungs where they
cause pneumonia, Jaundice or icterus when they invade bile ducts.

General Diagnosis for ascariasis , like many nematodes

▪ depend on clinical signs and

▪ egg demonstration in faeces

General Treatment of ascariasis

Use mebendazole

General control of ascariasis

▪ Proper kennel hygiene

▪ Regular treatment

Toxocara canis

Morphology

The female is about 17 cm (quite long) and has large alae

Life cycle

The eggs are passed out in faeces

They become infective 15 days later

After ingestion they hatch in the intestines and migrate in the body and
finally settle in the lungs, liver, kidney and other tissues. They may even
enter the liver of fetuses in pregnant bitches or even infect successive
pregnancies

Effects on hosts, diagnosis, treatment and Control; See above

 Toxocara cati

This worm has two life cycles :

▪ one with migration of larvae to the liver and lungs → liver and lungs →
trachea → pharynx → stomach → intestines, just like toxocara canis

▪ second one with eggs first being eaten by mice, the larvae migrating in the
tissues and when the mice are eaten by the cats they are released to
develop into adults in the digestive tract without migration

Effects on hosts, diagnosis, treatment and Control; See above

Ascaris suum

Ascaris suum is a very common parasite of pigs. Its importance is related

both to the sometimes very significant lesions caused by larvae during
migration through the liver and lungs, and to the effects of adult worms in
the small intestine. In the liver, the traveling larva causes intralobular
necrosis and a granulation reaction known as “milk spots.” However, these
lesions are not associated with symptoms. In the ordinary

moderate infections, adults have no defined pathogenesis. In heavy

infection, there is experimental evidence of reduction in growth rate,
diarrhoea, and ill thriving. Intestinal obstruction is rare.

Morphology
Males measure 15-25 cm and females up to 41 cm

Life cycle

Eggs are laid by a mated female, about 200,000 per day (a claim of 2
million has been made) → development into infective stage (L3) →
swallowing by pig → burrow wall of gut → enter peritoneal cavity → enter
liver via the hepato-portal blood stream → heart → lungs and other
organs →bronchial tree → pharynx → in intestines after swallowing →
development to L4, L5 and adult ascaris

Effects on hosts

Piglets show pneumonia, and get stunted growth. Adults show milk spots
at PM

Diagnosis

Demonstration of eggs and at PM

Treatment of Disease caused

Broad spectrum Anthelmintics

Control.

Deworming and hygiene at pig houses

HOOK WORMS
Members of this superfamily have a head equipped with a large buccal
cavity armed with teeth and/or cutting plates, and is bent dorsally – hence
the name ‘hookworm’.

They all live in the small intestine. Many are blood-suckers with big
appetites and are therefore capable of causing anaemia if present in large
numbers.

The L3 can enter the host either by ingestion or by skin penetration. In the
latter case, it proceeds to its predilection site via the lymphatics and blood-
stream. The larvae of some species can become arrested in their
development in subcutaneous tissues.

Ancylostoma caninum
A. caninum has three teeth on either side of its mouth as well as teeth in
the buccal cavity. It uses these to bite deeply into the intestinal mucosa so
the pharynx can pump copious volumes (0.1 ml/worm/day) of arterial
blood through its body.

The prepatent period is 2–3 weeks and female worms produce large
numbers of eggs. The hatched larvae can develop to the L3 stage in 5 days
under optimal conditions.

Bunostomum

Important/common species:-

Bunostomum phlebotomum for cattle

Bunostomum trigonocephalum for sheep and goats

Morphology

These hookworms belong to the same family Ancylomastidae

They have bursae and spicules, and females lay strongyle eggs

The anterior parts are well developed for identification

The bursal rays are hooked

They have teeth

Are commonly found in large and small intestines.

Life cycle

Adults → eggs → L1 → L2 → L3 (infective) ingested or enters through

the skin
▪ If through skin → venous system →lungs →trachea and pharynx
→swalled into the gut →L4 → L5 → mature worm in intestines

▪ If through the mouth direct to small intestines → L4 → L5 → Adult

hookworm

Effects on hosts

Sucking of blood leading to Anaemia, Hypoalbuminaemia, Pepsinogen

Increase, Pale Mucosa and also Anorexia, Diarrhoea, Oedema (ascites),
Dehydration Productivity Loss, itching at site of skin penetration, feet
stamping and possible Death

Young animals are affected most.

Diagnosis

▪ By clinical signs (especially diarrhoea, anaemia and submandibular

oedema)

▪ demonstration of eggs in faeces

Treatment of Disease caused

Broad spectrum Anthelmintics

Control

▪ Avoid dump areas and moist pastures

▪ Rotational grazing

▪ Strategic deworming
TRICHURIS (WHIP WORMS)

Common name: whip worms because they have are have a long , slender
anterior hart , the posterior part much thicker and the hind end is also
curled.

Morphology

The anterior part is long and slender while the posterior part is much
thicker. The male has a twisted hind part with one spicule and a spicule
sheath but no bursa while the female has a vulva with flaps at the
beginning of the thick part

Life cycle

Adult worms in the caecum and colon, embedded in the mucosa mate and
the female lay eggs. The eggs are passed into the environment with faeces
 where, under favourable weather they become embryonated and develop
into L1, then L2 and L2. The host swallows the eggs with L2 or L3 (infective
stages) which then hatch in the large intestines but mature into adults in
the caecum.

Five species of Trichuris and their host animals

▪ Trichuris ovis - Sheep, cattle, goats

▪ Trichuris globulosa - Sheep, cattle, goats

▪ Trichuris vulpis - dogs

▪ Trichuris suis - pigs

Effects on hosts

a Clinical signs and pathology:

▪ Weight Loss;

▪ Anorexia;,

▪ Diarrhoea;

▪ Dehydration

▪ In severe cases the faeces may be speckled with fresh blood. The lesions
are caused by the adult worms boring tunnels into the mucosa of the large
intestine.

▪ Anaemia;
 It has been shown that concurrent infections with T. suis enhances the
ability of opportunistic bacteria to multiply and cause disease and
pathology.

Diagnosis

By clinical signs and demonstration of eggs in faeces

Treatment of Disease caused

For dogs – whipcide

For pigs – Trichlorophon

For ruminants - promintic

(Genus)Oesophagostomum

Common name: nodular worms

Morphology

▪ The anterior part is well developed

▪ The worms may or may not have teeth

▪ The worms have a leaf crown called corona radiate

▪ Males have a bursa and spicules while females have vulva flaps

▪ Their bursal capsule have cephalic vescicles

 These worms infest the large intestines where the cause formation of
nodules and a pimply gut

Life cycle

Egg → L1 → L2 →L3 (infective and swallowed) → large intestines → L4

→ L5 → Adult which mat and female starts to lay eggs

The L4 is the one that forms nodules on the wall of the large intestines and
caecum to give rise to the so called pimply gut

Clinical signs

▪ Diarrhoea

▪ Anorexia

▪ Abdominal pain and grinding of teeth due to the pain

▪ Emaciation

▪ Anaemia

▪ oedema

▪ pimply gut at PM

Diagnosis

▪ By clinical signs and demonstration of eggs in faeces

▪ Nodules in the large intestines at PM

Treatment

Broad spectrum anthelmintics

Control

Strategic deworming

LUNGWORMS

Dictyocaulus filaria These are the lungworms that infect sheep and goats

Dictyocaulus viviparus are the lungworms that infect cattle

General Information

The adult worms of D. viviparus, which reach as females a length of 70 mm

and 40 mm as males and live in the trachea and bronchial cavities of cattle.
Similar species D. filaria/sheep/goat, D. arnfieldi/ horses/donkeys) are
found in other hosts in identical habitats. The females lay thin shelled eggs
which contain already the L1. This stage is set free inside the host, so that
the larvae are found in the faeces. Within 1 week the sheathed infectious
L3 develops in the faeces (if there is a temperature higher than 16° C).
After oral uptake the L3 enters the mesenterial lymph nodes, where the L4
is

formed. By lymph and blood transport the L4 reaches the lung beginning at
the end of the 7th p.i. Within 21–25 days maturity is reached and after this
prepatent period eggs/larvae can be found. The larval excretion extends
over a period of only 5–6 weeks.

Clinical signs

Bronchitis and Pneumonia leading to

▪ Rapid breathing

▪ Coughing

▪ Exercise intolerance

Diagnosis

▪ By clinical signs (especially coughing) and demonstration of eggs in faeces

▪ History of recent introduction to pastures

Treatment

Broad spectrum anthelmintics

Control

Grazing management, giving regard to young and animals not previously

exposed
Thelazia rhodesii

Common name of Thelazia :

Bovine eye worms because they located in the eyes of bovine

Intermediate hosts of Thelazia rhodesii: Flies of the genus Musca

Morphology

These worms are milky white in colour and specifically found in the
conjuctival fold, third eye-lid and in the lachrymal duct of the bovine eyes

The male is 8-12 mm long and the female 12-18 mm long

Life cycle

The Transmission occurs by means of flies of the genus Musca that take up
larvae 1 from the conjunctiva and introduce finally larvae 3. The mass of
larvae 1 block the excretion of the lachrymal fluid.

Five clinical signs of infection by Thelazia rhodesii

- eye inflammation

- Running eyes (excessive lacrimation)

- conjuctivitis

- corneal opacity

- photophobia,

- oedematous eyelids,

- mild or ulcerative keratitis

- predispose to bacterial and viral

infections
 Diagnosis

By demonstration of the worms in the eyes and the clinical signs seen
therein

Treatment of infection by Thelazia rhodesii

▪ Oral drench of levamisole

▪ sub-conjuctival injection of levamisole

Control

Treat clinical cases and control flies of genus musca which are the
intermediate hosts

DIROFILARIA IMMITIS

Common name heartworm of dogs

DIROFILARIASIS

The common heartworm of dogs and other carnivores, Dirofilaria immitis

(adults, about 12–30 cm long, slender and white, live in arteries of the
lungs and right ventricle of heart), is primarily a problem of warm countries
where the mosquito intermediate host abounds.
Canine Heart worm (Dirofilaria immitis)

Life cycle

The male and female mate in the dog after which the female lay
microfilaria into the blood stream. These are picked by mosquitoes and
other biting insects which then bite dogs and fransmit the same L3 to dogs

Effects on hosts

Anterior uveitis, iritis, blindness and very heavy infestations may lead to
heart failure

Treatment of Disease caused

Give adulticide and microfilaricid

Control
 Keep dogs housed and prevent infection by giving antihelmintic like
arsenical thiacetisemide for six months

TRICHINELLA SPIRALIS

This worm occurs in the small intestines of man, pigs and other mammals

Morphology

Males are 1.4 -1.6 mm long and female 3-4 mm long

Life cycle

The cycle is initiated when encysted muscle larvae are ingested with meat
and are liberated by the digestive process. Three moults takes two days in
the small intestines. Within 4 days adults mate and start laying eggs. The
males die after mating but the females penetrate the mucosa, reaches the
lymph spaces where they produce more eggs. The L1 enter the lymph
vessels and pass into the thoracic duct to the left superior vena cava, reach
the blood stream for distribution throughout the body. They invade muscles
and some encyst there ready to be eaten by humans

Effects on hosts

▪ Enteritis with diarrhea

▪ Fever

▪ Stiffness and pain of muscles

▪ respiratory problems.

▪ Oedema of the face

 Treatment of Disease caused

In man- give mebendazole

Control

Avoid eating raw pork

Heterakis gallinarum

This a nematode found in the caecum of poultry and is commonest in

turkey

Morphology

Male is 7-13 mm long and the female is 10-15 mm long

The eggs are thick with smooth shells and unsegmented

Life cycle

Eggs develop in the open and reach infective L2, are swallowed and from
the stomach migrate to the caecal mucosa and become L3 then L4 and
reach maturity. The earthworm acts as the transport host L5

Effects on hosts

• Hemorrhage at the caecum

• Diarrhoea

• Wasting

• Emaciation
• death

Economic importance

This worm is the vector of a protozoa Histomonas meliagradis that

causes blackhead or entero-hepatitis in turkey

Treatment of Disease caused

Phenothiazine

Piperazzine mixture of the two above

menbebdazole

Control

Strict sanitation of poultry houses

SYNGAMUS TRACHEA

This is a roundworm of birds (poultry) found in the trachea and is most

common in Turkey but also in geese and guinea fowl

Common names:

▪ Gape worm

▪ Red worm (because the female worm is bright red in colour)

▪ Y-worm

Morphology
Syngamus trachea (= red worm, gapeworm); males (6 mm) and females
(20 mm) suck blood in the trachea of poultry and are permanently attached
to each other, thus giving a Y-shape to the pair.

Gape worm (Syngamus trachea)

Life cycle

Eggs are mainly passed in feces of final hosts usually Turkey but can also
be other poultry.

On the soil (during moist conditions) the eggs embryonate, leading to a

first stage larva (L1). development proceeds until the L3 is formed inside
the egg, Intermediate hosts may ingest the eggs thus initiating the
development of infectious larvae (L3), which may become accumulated in
considerable numbers.

Infection of the final hosts always occurs via the oral route. This can be:
directly by ingestion of eggs containing a third-stage larva indirectly by
ingestion of intermediate hosts (earth worm, snails, flies and other
arthropods) containing infectious third-stage larvae. The L3 migrate via
 lungs(causing pneumonia) and then to the bronchi by whose time it is
mature and mating occurs. Soon the female worm starts to lay eggs.

Effects on hosts especially turkey i.e clinical signs of a turkey infected by

Syngamus trachea

▪ inflammation of lungs ie pneumonia

▪ leading to respiratory complications due to secondary bacterial infection

▪ Frothing in the mouth

▪ Gaping posture head shaking,

▪ coughing

▪ emaciation

▪ asphyxia and death

Diagnosis is done from

▪ gape appearance,

▪ PM demonstration of worms and

▪ demonstration of eggs in faeces

Treatment of and Control

Six control measures for gape worm infection in poultry

- isolate and treat affected birds using Thiabendazole

 - destroy infected birds (may slaughter but throw away heads and
necks)

- move affected birds to fresh dry ground

- house birds so tat they do not eat earthworms (transport host)

- buy new birds from clean flocks

- Do not mix other birds with turkeys

TREMATODES also called flat worms

Fasciola

GENERAL CHARACTERISTICS OF THE GENUS FASCIOLA

▪ They are flattened dors-ventrally

▪ Are leaf-like and broad anteriorly

▪ These are endoparasites

▪ They require an intermediate host for their life cycle, the snail

▪ They have 2 suckers, both anterior and posterior the anterior one encircling
the mouth
 A typical trematode (Fasciola hepatica).

Life cycle of Fasciola hepatica and Fasciola gigantica

Egg (passed out in faeces and hatch in wet environment) → miracidium

(which enter the intermediate host –snail) → sporocyst → redia I → redia
II → cercaria- tadpole-like (which leave the intermediate host and lodge on
water plants) → metacercaria (which enter the final/definitive host)→ adult
worm in the liver, especially the bile ducts after passing through the gut,
penetrate through the intestinal wall, and into the abdominal cavity)
The life-cycle of a digenean trematode, Fasciola hepatica: a – egg voided in
faeces; b – miracidium develops and hatches; c – miracidium seeks snail
intermediate host; d – three phases of asexual reproduction produce
sporocysts, rediae, then cercariae; e – cercariae leave snail; f-
metacercariae form on vegetation; g – metacercaria eaten by final host; h
– fluke migrates to its predilection site and matures

Fasciola hepatica is found in temperate countries (not Africa) and causes

hepatic necrosis and hemorrhages during migration, and erosions of the
biliary mucosa when it reaches the bile duct.

F. gigantica, the larger liver fluke, occurs in the tropics (including Africa).
It occurs mainly in sheep and cattle, but a patent infection can develop in
goats, horses, pigs, wild animals, and in humans. The pathogenesis of
fasciolosis is attributable in part to the invasive stages in the liver and in
 part to the blood feeding by the adults in the bile ducts. When fresh they
are brown in colour. Its eggs are passed from the bile ducts into the
duodenum then the faeces

The aquatic snails involved as intermediate hosts belong to the genus

Lymnea.

Fascioliasis may be acute, sub-acute or chronic.

At post mortem the abdominal cavity fluid is found to be blood stained, in

case of acute fascioliasis. In the other two forms there is a hemorrhagic
and friable liver, sometimes cirrhotic and enlarged (and seen especially at
meat inspection) with flukes in the bile ducts sometimes blocking them.
Ascites may also be encountered even on a live animal which also has sub-
mandibular oedema, is emaciated and anemic.

Treatment for Fascioliasis is by use of flukicides e.g;

▪ Carbon tetrachloride drench

▪ Hexachloroethane (cooaphene)

▪ Oxyclozinide (zanil)

▪ Rafoxanide (flukanide)

▪ Nitroxynil (trodax injectable)

▪ Meniclopholan (bilevon)

Control of fascioliasis
- Use flukicides to deworm the host animals thus reduce pasture
contamination

- Improve drainage to destroy habitat of snails (intermediate hosts)

- Use molluscicides to reduce/eliminate snail population in

- Fence off wet marshy areas

- Avoid low lying pastures during wet seasons

Post mortem findings of a sheep that has died of infection by Fasciola

hepatica

1 Emaciated carcass

2 Enlarged bile ducts in the liver

3 Enlarged liver (hepatomegally) often cirrhotic

4 Presence of flukes in the ducts when incised

5 ascites

6 blood stained abdominal fluid

7 pale mucous membranes

 Schistosomes

The disease caused, Schistosomiasis is also known as Bilharzia occurring in

humans and ruminants. Their eggs can be identified easily because they
are yellow when fresh, and elongated.

In Africa, Schistosoma bovis, S. mattheei, and S. curassoni occur

commonly in ruminants, and S. rhodhaini has been reported to infect dogs.

Schistosomes live within the mesenteric blood vessels and hepatic portal
veins of ruminants. Although Schistosoma infections in ruminants are
highly prevalent in certain regions, the general level of infestation is often
too low to cause clinical disease or losses in productivity.

Levels sufficiently high to cause outbreaks of clinical schistosomosis do

occur occasionally and infestation Alimentary System Diseases, Ruminants
becomes manifest either as an intestinal syndrome which is usually self-
limiting, or as a chronic hepatic syndrome, which is usually progressive
(Schistosomiasis, Animals).

The intestinal syndrome is caused by the deposition of large numbers of

eggs in the intestinal wall and usually follows a heavy infestation in a
susceptible animal, i.e., an animal in which the capacity of the host to
suppress the egg laying of the parasite has not been stimulated by
previous infestations. This has been reported among cattle, sheep, and
goats infected with either S. bovis or by S. mattheei. As the faecal egg
counts rise sharply with the onset of egg production the animal develops a
mucoid and then haemorrhagic diarrhoea, accompanied by anorexia, loss of
condition, general weakness and dullness, roughness of coat,
hypoalbuminaemia, and paleness of mucous membranes.
Death may occur 1 or 2 months after the onset of clinical signs. In most
cases, the animal makes a spontaneous but slow recovery. The primary
cause of the diarrhoea is the passage of large numbers of eggs through the
wall of the intestine. The anaemia is usually due to an increased rate of red
cell removal from the circulation; while haemodilution and the inability to
mount a sufficiently effective erythropoietic responseare of secondary
importance. The underlying cause of the hypoalbuminaemia is
hypercatabolism of albumin due to substantial loss of protein in the
gastrointestinal tract.

There is no easily available treatment for Schistosomiasis in animals but

control is as for Fasciola

Paramphistomes

Paramphistomes, also called stomach flukes or conical flukes are located

in the rumen. As the name suggests they are conical in shape.

The incidence in Kenya is as high as 80%. The life cycle is as for Fasciola
and the intermediate host (snail) belong to Bolinus genus.

Young paramphistomes are deeply embedded into the mucosa of the small
intestine causing mechanical damage of the epithelial cells by their large
posterior (ventral) sucker.

Adult Paramphistomum living in the fore stomachs of ruminants may

produce only slight clinical signs i.e. they act as commensals.

During the migration phase in the duodenal wall and abomasum wall the
young rumen flukes are highly pathogenic to young, naive (previously
uninfected) sheep and cattle, and large numbers of larval stages can cause
clinical signs, such as loss of appetite (anorexia), diarrhea (dehydration),
anemia (loss of protein), retarded growth, and even mortality. As a rule,
susceptible calves, and lambs should not be grazed together with adult
animals, as these are chronically infected in most cases.

Treatment and control is as for fasciola

CESTODES also called tape worms

GENERAL CHARACTERISTICS OF TAPE WORMS (morphology)

➢ They are elongated

➢ They are segmented into proglottids

➢ They are dorsal-ventrally flattened (making some authorities to

also call them flat worms together with flukes) except at the scolex

➢ They are hermaphrodites (have both male and female sexual

apparatus on the same worm)

➢ The sexually mature worms are found in small intestines and

(occasionally) stomach diverticulum of the definitive hosts

➢ Have three main parts: scolex or “head”, neck and strobilla or “body”

➢ The scolex is the organ for attachment to the host and is equipped
with hold-fast organs like suckers, hooks, grooves, rostellum,
acetabula, bothria

➢ When hooked the suckers are said to be “armed”

➢ The strobilla has segments formed from the neck the through a
process called strobilation. Just behind the neck proglottids are
immature, then further posterior there are proglottids with mature
male organs, then those with mature female organs, and finally those
whose uterus contains fertilized eggs; the latter proglottids are thus
described as gravid. Copulation (mating) occurs before egg
formation; a given proglottid can copulate with itself, with others in
the same strobila, or with those in other worms. When a gravid
proglottid reaches the end of a strobila, it detaches and passes out
intact with the feces or partly disintegrates before reaching the anus.

➢ In cases where the uterus has an opening, the proglottids release the
eggs and become detached when exhausted

➢ In some tapeworms the neck is not easily distinguishable from the

other parts

Typical tapeworm (Taenia saginata)

A typical tapeworm (Taenia): a – scolex with hooks and suckers; b
– neck; c – immature segments; d – mature segments; e – gravid
segments.

General Life Cycle of Cestodes

Eggs in the gravid proglottid passed out in faeces → metacestodes (larval

forms) which are eaten by the intermediate hosts → oncospheres which
migrate to their predilection site → various types of cysts which depend on
specific cestode and were given name different from the name of the
original cestode → eaten by the definitive host (usually humans) →
maturation into adult tapeworm inside the definitive hosts, complete with a
scolex, neck and strobila.
Types of cysts of tape worms in the intermediate hosts

Type of cyst Cestode (s) Intermediate host and habitat Name of the cyst Definitive/
final host

Cysticercus Taenia saginata Cattle in active muscles like tongue, heart, fore Cysticercus bovis Humans
(most mature worm 6–15 leg and thigh muscles
common) meters long

Cysticercus Taenia solium 1. Pigs in active muscles like tongue, heart, fore Cysticercus humans
(most mature worm 2–7 leg and thigh muscles cellulosae
common) meters in length
2. humans (rarely), cysticercus raccemosus

Coenurus Taenia multiceps Sheep, humans/Brain Coenurus Dogs, foxes

In sheep there is invasion of the brain by the cerebralis

cysts leading to a “turning sickness” where the
(multiple
animal moves in cirles, carries the head
abnormally and loses balance often. The invaginated scoleces
disease is also called “true gid” or sturdy or
stug into a bladder),
Hydatid Echinococcus Ruminants, humans/ Echinococcus Dogs, foxes

granulosus Liver, lungs , brain etc. hydatidosus

Cysticercoid Davainea proglottina Snails/Tissues Cysticercoid Chickens

Mature worm about

1–4 mm long

Cysticercoid Dipylidium caninum Fleas/Body cavity Cysticercoid Dogs, foxes,

Mature worm about
Cats
0.2–0.8 m long

Cysticercoid Stilesia sp. Mites (Oribatids)/Body cavity Cysticercoid Ruminants

 T. saginata cysticercus (circled) in a joint of beef

Taenia multiceps metacestode (coenurus) on brain of sheep (upper right).

Clusters of tapeworm heads appear as white dots on the cyst wall
Hydatid cyst in horse liver: the liver and cyst have been cut to reveal the
thickness of the wall and the appearance of the internal surface.

NB

✓ Today there are no effective drugs, which may be used economically

in the treatment of metacestode infections in livestock. Preventive
measures should therefore always involve treatment of infected
persons (using Niclosamide) and management adjustments such as
proper meat inspection.

✓ Bovine cysticercosis is also called beef measles, just live Porcine

cysticercosis is also called pig measles.

✓ Bovine cysticercosis and Porcine cysticercosis will lead to infection in

humans

✓ when they eat raw or undercooked beef and pork respectively.

✓ When humans defaecate on pastures they maintain the life cycle of

the tapeworms. For the same reason, use of improperly treated
sewage on pastures should be avoided. Infections can also be
brought by birds and immigrants
✓ One can differentiate whole wduld tape worm of T. solium from T.
saginata because the latter’s scolex is not armed

✓ If a carcass has 0-5 cysts during meat inspection, the whole carcass
should be kept at -10 degrees for 10 days before the meat can be
used for human consumption. For 6-20 cysts after keeping if to 10
days at -10 degrees, it can only be released to institutions like
colleges and prison (where meat is cooked thoroughly). For over 20
cysts the whole carcass is completely destroyed.

✓ CYSTIC HYDATID DISEASE (Hydatidosis, or cystic Echinococcosis):

Echinococcus granulosus larva-type is a unilocular hydatid cyst
infection of intermediate host (usually sheep, other herbivores as
cattle, horse, and occasionally man) is due to close contact with dogs
and other canids (definitive hosts), which may be infected with large
numbers of adult worms (3–6 mm long, with a single gravid
proglottid that is longer than wide; it contains typical Taenia-like
eggs); feces of dogs contain embryonated eggs infective to potential
intermediate hosts (occasionally humans); cestode larval stage in
human tissues is characterized by multiple daughter bladders or
“brood capsules” with multiple invaginated protoscolices budding from
their walls (inner layer of germinal epithelium of cystic cavity); cyst
content (materials) consisting of degenerated scolexes and debris in
milky fluid of parent cyst is referred to as hydatid sand. This condition
is common in Turkana are of Kenya

✓ Hydatidosis can be controlled by breaking the cycle by treating dogs

with Praziquantel and arecolin hydrochlomide. Also, dogs should not
be allowed to eat infected meat. Personal hygiene is also important.
Children especially should be prevented from playing with dog and
their faeces. Echinococcus in dogs does not show any clinical sign and
diagnosis is only observation of proglottids in faeces
 General Diagnosis of Tape worm infection

Proglottids may be seen in feces of final hosts and fecal examination of the
material will also reveal the eggs.

Post mortem examination of muscles of carcasses will show the cysts of

Cysticercus cellulosae in pigs and Cysticercus bovis in cattle

▪ Taenia solium - see notes above

▪ Taenia saginata - see notes above

▪ Echinococcus granulosus - see notes above

STILESIA

Stilesia hepatica is a tapeworm found in the bile ducts of ruminants They

have suckers on the scolex the former being quite prominent. The proglottids
are short.

The effect on the animal is that the liver becomes fibrotic due to cirrhosis. This
leads to the condemnation of the liver at meat inspection.

CAUTION. Do not confuse this tape worm with the liver fluke Fasciola hepatica
because of its second name but note that they are found in the same organ

MONIEZA

Monieza expansa and Monieza benedeni is also a tape worm found in

small intestines of ruminants.

They also have prominent suckers on the scolex but have no hooks. The
proglottids are also broader than they are long.
The segments are passed in feces and ingested by birds which also help to
disseminate them to far areas.

Mites are the intermediate hosts.

These tape worms, if massive in the intestines, can cause obstruction,

sometimes diarrhea and un-thriftiness.

The segments of this tapeworm in feces resemble cooked rice. Diagnosis is

also done at PM when the animal dies of other causes.

Treatment is done using copper sulphate mixed with phenothiazine. Control is

by reducing pasture contamination by ploughing or resting them for at least
one year.

DIPHYLIDIUM

Diphylidium caninum is also called double-pored tapeworm of the dog.

The adult worm is found in small intestines of dogs and occasionally humans.

The scolex has hooks in 3-4 rows and is the commonest tapeworm of the dog.

The intermediate hosts are the fleas (Ctenocephalides canis and Pulex
irritans) and the dog louse. Dogs get infected when they swallow these
intermediate hosts during grooming.

The gravid proglottids migrate to the anal area and cause so much itching and
irritation that the dog has a queer habit of pressing the anus to the ground
and dragging (scooting)