FLUKES IN RUMINANTS IN SOUTH AFRICA

Introduction
Flukes, also called trematodes, any member of the invertebrate class Trematoda
(phylum Platyhelminthes), a group of parasitic flatworms that probably evolved from
free-living forms millions of years ago. The symmetrical body of a fluke is covered with
a non-cellular cuticle. Most are flattened and leaf-like or ribbon-like, although some
are stout and circular in cross section. Muscle suckers on the ventral (lower) surface,
hooks and spikes are used for attachment. The body is solid and filled with a spongy
connective tissue (mesenchyme) that surrounds all body organs. A circulatory system
is absent. The digestive system consists of a simple sac with a mouth either at the
anterior end or in the middle of the ventral surface. An anus is usually absent, but
some species have one or two anal pores. The nervous system consists of a pair of
anterior ganglia, or nerve centres, and usually three pairs of lengthwise nerve cords.

Most species are hermaphrodite, i.e. functional reproductive organs of both sexes
occur in the same individual. However, in some, the sexes are separated. Most
species go through egg, larval, and mature stages.

We focused mainly on three (3) flukes that are found in Ruminants in South Africa. 1st
there a blood fluke, Schistosoma spp., which occurs in most vertebrates, and have
three species that attacks humans; the urinary blood fluke (Schistosoma
haematobium), the intestinal blood fluke (S. mansoni), and the Oriental blood fluke (S.
japonicum). The human diseases caused by them are known as schistosomiasis
(bilharziasis). 2nd is the fluke of adverse economic importance to humans, which
includes the widespread giant bovine liver fluke (Fasciola hepatica). Fasciola hepatica
causes the highly destructive liver rot in sheep and other domestic animals. Man can
be afflicted with this accident by eating uncooked vegetables. And thirdly there’s the
conical fluke, Paramphistomum spp. and Calicophoron spp. All these flukes are
discussed in detail
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Schistosomiasis (Blood fluke)

Schistosomiasis is a common parasitic infection in cattle and rarely in other domestic
animals in Africa and Asia. Although schistosomes may act as important pathogens
under rare conditions favouring intensive transmission, most infections in endemic
areas are subclinical (Merck and Dohm, 2010). Schistosomiasis is a chronic
debilitating infection of humans and animals caused by different species of
schistosomes and hence the disease is of public health importance. Schistosoma
bovis, the cause of bovine Schistosomiasis, is one of the major veterinary problems in
many Mediterranean and African countries (Parija, 2004).

Classification:
Phylum: Platyhelminthes
Class: Trematoda
Order: Diplostomida
Family: Schistosomatidae
Genus: Schistosoma
Species: bovis
Species: mattheei

Hosts:
Intermediate hosts are various species of freshwater snails.

Signs:
In cattle the clinical sign exhibited emaciation marked diarrhea, mixed with blood or
mucous, dehydration pale of mucous membrane, marked weight loss, decreased
production, rough hair coat, anaemia, hypoalbuminemia, hyperglobulinemia and
severe eosinophilia that develop after the onset of egg excretion. Severely affected
animals deteriorate rapidly and usually die within a few months of infection, while those
less heavily infected develop chronic disease with growth retardation (Merck and
Dhome, 2010). Hemorrhagic enteritis, anaemia and emaciation which develop after
the onset of eggs excretion, are major clinical signs associated with the intestinal and
hepatic form schistosomiosis in ruminants severely affected animals deteriorate
rapidly and usually die within a few months of infection (Charles and Robinson, 2004).

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Diagnosis:
Examination of stool and/or urine for ova is the primary methods of diagnosis for
suspected schistosome infections. The choice of sample to diagnose schistosomiasis
depends on the species of parasite likely causing the infection. Adult stages of S.
mansoni, S. japonicum, S. mekongi, and S. intercalatum reside in the mesenteric
venous plexus of infected hosts and eggs are shed in faeces; S. haematobium adult
worms are found in the venous plexus of the lower urinary tract and eggs are shed in
urine (CDC, 2012).

In general when schistosomiasis is suspected, diagnosis is best confirmed by detailed

post mortem examination, which reveal lesion and if mesentery is stretched the
presentence of typical lesion in the skin that come in contact with pond, lake, and
stream or ocean water containing infective cercaria from the snail intermediate hosts.
Faecal examination is most useful in early infection, because egg production decline
as infection progresses. Eggs don’t have an operculum and most are spindling shaped
(Bowman et al., 2003).

Morphology:
Blood flukes form five different developmental stages: eggs, miracidia, sporocysts,
cercariae and adult worms. Eggs are round to oval in shape, operculate (hinged at
one end) and contain a developing embryonic larva (miracidium). Differences in egg
morphology can be used to distinguish between Schistosoma species means
differentiate in their position of spine (Springer, 2001).

Eggs of some species are armed with spine when discharged in the feces (S. mansoni
and S. japonicum) and in urine (S. haematobium). The eggs of Hetrobiliharzia
americana are rather spherical and possess only a slight bump on one side rather than
a spine as seen in S. haematobium and S. mansoni (Bowman et al., 2003). Generally
the eggs have typical morphological features. Relatively larger, slender (spindle)
shaped and have lateral of terminal spine (pointed at both ends) (Urquhart et al.,
2003).

Miracidia are elliptical free-swimming larval stages (~200µm long) covered with cilia.
Sporocysts appear as pleomorphic sac-like bodies which contain developing

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cercariae. Mature cercariae are elongate free- swimming larval stages (400-600µm
long) consisting of a tapering head (with prominent penetration glands) and a forked
tail. Adult flukes are elongate tubular worms (10 – 20 mm long), with rudimentary oral
and ventral suckers. Males are shorter and stouter than females, and they have a
longitudinal cleft (gynecophoral canal or schist) in which the longer slender female lies
folded (Springer, 2001).

Figure 4: Egg of S. bovis https://www.msdvetmanual.com/digestive-system/fluke-

infections-in-ruminants/fasciola-hepatica-in-ruminants

Life cycle:
Schistosomes have a typical trematode vertebrate- invertebrate life cycle (Laurant,
2013). Schistosomes live in the mesenteric and hepatic veins of the host (except for
S. nasale, which lives in the nasal veins), where they feed on blood and produce eggs
with a characteristic terminal or lateral spine (Merck and Dhome, 2010).

Parasite eggs are released into the environment from infected individuals, hatching on
contact with fresh water to release the free-swimming miracidium. Miracidia infect
freshwater snails by penetrating the snail's foot. After infection, close to the site of
penetration, the miracidium transforms into a primary (mother) sporocyst (Laurant,
2013). Germ cells within the primary sporocyst will then begin dividing to produce
secondary (daughter) sporocysts, which migrate to the snail's hepatopancreas. Once
at the hepatopancreas, germ cells within the secondary sporocyst begin to divide
again, this time producing thousands of new parasites, known as cercariae, which are
the larvae capable of infecting mammals (Laurant, 2013).

Cercariae emerge daily from the snail host in a circadian rhythm, dependent on
ambient temperature and light. Young cercariae are highly mobile, alternating between

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vigorous upward movements and sinking to maintain their position in the water.
Cercarial activity is particularly stimulated by water turbulence, by shadows and by
chemicals found on human skin (Fenwick, 2012). Detailed schematic presentation of
the life cycle of schistosomiasis is indicated in Figure 5 below.

Figure 5: Life cycle of schistosomes. Source: (CDC, 2011).

Epidemiology:
It is almost similar to Fasciola gigantica and Paramphistomum. Schistosoma requires
water for hatching of the eggs. Eggs can hatch in slightly acidic pH. Shedding of
cercariae is temperature dependent. Long time is required for development of
Schistosoma in snail high rainfall is good predisposing factor for occurrence of these
parasites (Mandal, 2012). Epidemiological studies on bovine schistosomiasis are
suggestive of the endemicity of the disease particularly in areas with large permanent
water bodies and marshy pasture areas. In Ethiopia, the optimum range for distribution
of S. mansoni has been reported as 1500 to 2000 meter above sea level (Gashaw,
2010).
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Pathogenesis:
Schistosomiasis (or bilharziasis) is unusual amongst helminth diseases for two
reasons: much of the pathogenesis is due to the eggs (rather than larvae or adults);
and most of the pathology is caused by host immune responses (delayed-type
hypersensitivity and granulomatous reactions) (Olivier et al., 2004). The course of
infection is often divided into three phases: migratory, acute and chronic. The
migratory phase occurs when cercariae penetrate and migrate through the skin. This
is often asymptomatic, but in sensitized patients, it may cause transient dermatitis
(‘swimmers itch’), and occasionally pulmonary lesions and pneumonitis (Olivier et al.,
2004).

Eggs released into the bloodstream by adult worms can invade local tissues, where
they release toxins and enzymes and provoke a TH-2-mediated immune response
(Coutinho et al., 2007). Inflammation and granuloma formation occurs around
deposited eggs, which can lead to fibrosis and scarring of affected tissues, if the
burden of eggs is heavy (Cheever et al., 2000). Eggs tend to either penetrate the bowel
(adjacent to the mesenteric vessels in which the adult worms are residing) or travel
via the portal venous system to the liver. In the bowel, granulomatous inflammation
around the invading eggs can result in intestinal schistosomiasis characterized by
ulceration and scarring (Friedman et al., 2007).

The migration of the eggs may cause mechanical damage and lesions. Moreover
Schistosoma eggs trapped in the tissue elicit granulomatous reaction that is mounted
to destruct the eggs. These granulomas consist of several cell types, mainly
eosinophils, macrophages and lymphocytes. In the chronic stages of the disease the
pathology is associated with collagen deposition and fibrosis, resulting in organ
damage and dysfunction (Koqulan and Lucely, 2005).

Treatment:
Infections with all major Schistosoma species can be treated with praziquantel. The
timing of treatment is important since praziquantel is most effective against the adult
worm and requires the presence of a mature antibody response to the parasite (CDC,
2012). Over the years, different drugs with known schistosomocidal but also toxic

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effects such as antimonials, trichlorphon or nequvon have been tested against visceral
schistosoma infection in cattle (Reinecke, 1997).

Distribution:
Schistosoma bovis infects snails in southern Africa and North Africa, Europe (Sardinia,
Corsica, Spain) and the Middle East as far as Iraq (Mahmoud, 2001). Schistosoma
bovis-haematobium hybrids have been reported first in Senegal in the early 1990s,
and then an outbreak in 2013 in Corsica (Dec, 1987).

Control and Prevention:

The most effective way to control cattle schistosomiasis in endemic areas is to prevent
contact between the animals and the parasite by fencing of dangerous waters
and supplying clean water. Unfortunately, this is not always possible in parts of the
world where nomadic conditions of management prevail. Other methods of control
include destruction of the snail intermediate host population at transmission sites,
either by chemical or biological methods, or their removal by mechanical barriers or
snail traps (Merck and Dohme, 2010).

In humans, the most effective way of controlling Schistosomosis are the provision of
sanitary facilities and the provision of piped water since, it reduces human contact with
contaminated water (Mohammad and Waqtola, 2006).

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Paramphistomum and Calicophoron (Conical fluke)

Stomach fluke Calicophoron calicophorum is the most commonly found stomach fluke
in cattle. They cause sporadic disease in young cattle 6-18 months in age. The cattle
becomes infected by grazing fluke contaminated green-pick in dry winters following an
unseasonably wet summer that enabled enormous explosions of snail numbers.
During dry spells, snails can survive by burrowing into the mud where they can remain
dormant until the rains return. Infective metacercariae encysted on herbage are also
tolerant of dry conditions and survive long after the season has dried out. Most cattle
carry small numbers of stomach fluke without any signs of infection or loss of
productivity. By contrast, disease may occur in previously non immune adult cattle
moved from farms outside the endemic stomach fluke region, to farm where stomach
fluke is endemic. Cattle rapidly develop a strong resistance to reinfection with this
parasite. Adult stomach fluke have fleshy pear shaped body 5-12 mm long by 2-4 mm
in diameter in the lower body and are pink or light red.

Classification:
Phylum: Platyhelmintes
Class: Trematoda
Subclass: Digenea
Order: Echinostomata
Family: Paramphistomidae
Genus: Calicophoron
Genus: Paramphistomum

Intermediate hosts:
In the form of water snails, including planorbid snails of the sub – family Buliniae. The
immature parasites are found in the duodenum from where they migrate towards the
rumen and reticulum where the adults are situated. The adult parasite is distinctly
visible in the forestomaches of ruminants. In South Africa, P. microbothrium seems to
be the most important fluke in domestic ruminants. Adult stomach fluke inhabit the
rumen and sometimes the reticulum of cattle. Juvenile fluke are found in the upper
small intestine.

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Signs:
Moderate infections may produce reduced weight gains or milk production, intermittent
diarrhoeas or ill–thrift. Acute infections may develop rapidly in young susceptible
yearling calves due to massive number of pre-adult fluke developing in the small
intestine. Signs include a loss of appetite, lethargy and weight loss. A profuse fetid
diarrhoea containing immature fluke and dehydration may start 2 to 4 weeks after
calves have been exposed to contaminated pastures and can cause death.

Diagnosis:
The clinical diagnosis of Paramphistomosis remains challenging as immunological
techniques and serum antibody detection is usually not conclusive. Therefore, a
diagnosis in live animals still depends on faecal detection of eggs, in conjunction with
a typical clinical history and clinical signs. Eggs of the stomach fluke are detected
during laboratory analysis of dung samples for the liver fluke. Eggs only appear in the
faeces of the host 10-12 weeks after infection.

Morphology:
Calicophoron adults are conical rather than flat shaped ,they are small 1 cm long ,they
have a large ventral sucker in sub terminal position ,their gut is simple with two
branches, two testes are lobed situated in tandem in midbody, the ovary is sub-
spherical, post-testicular and pre-acetabular, eggs are operculate, unembryonated
and clear light brown in colour. Paramphistomum was pear-shaped, slightly concave
ventrally and convex dorsally. The fluke was of about 5.50 - 5.53 mm in length (Daves,
1962). Mouth was terminal funnel shaped, widened posteriorly. Posterior sucker was
sub-terminal, about one–fourth to one-fifth of body length. Clusters of vitelline glands
were extended from the pharynx to the posterior sacker and lie between the caeca
and lateral margins of the body. The uterus was wavy and runs dorsally to the testes
(Gupta, 1977).

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Figure 6: Showing the development of Calicophoron daubneyi.

Figure 7: Showing the egg of Paramphistomum

https://www.msdvetmanual.com/digestive-system/fluke-infections-in-ruminants/fasciola-
hepatica-in-ruminants

They are hermaphrodites with a common genital pore through which they release eggs
directly into the rumen. The eggs are large (130-180 x 76-95 µm), operculate and
morphologically similar to eggs of Fasciola hepatica but are colourless and not bile-
stained yellow in colour.

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Life cycle:
This is a two host indirect life cycle similar to that of the liver fluke, except that adult
flukes live in the rumen of cattle not in the bile duct, and the immature life stages
develop in freshwater planorbid snails not lymnaeid snails. Planorbid snails are 2-5
mm in diameter and are commonly called the red rams head snail.
Adult flukes in the rumen and reticulum pass eggs in dung (faeces), eggs hatch in
water when the temperatures reach 24 to 320 Celsius. After being freed from the
faeces, the miracidia hatch from the eggs in water within 12 to 16 days and penetrate
the intermediate host. Released free swimming miracidia invade a fresh water snail
and undergo further development and multiplications, which encyst, on water plants
to be ingested by the ruminant concerned. Cercariae encyst on grass at the water
surface and, if they are kept moist and cool, they may survive for two months but
metacercariae die off if they become desiccated or completely submerged in water.
Young flukes leave the metacercaria in the duodenum (usually within the first 3 meters
of the duodenum) and attach to the mucous membrane of the intestine with their
posterior sucker. Immature worms migrate back to the rumen from day 15 to 57. Adults
will start passing eggs after metacercariae have been dosed in calves at day 56, and
in sheep at day 70. The entire life cycle, from egg to egg, takes a minimum of 110
days in sheep and 132 days in cattle.

Figure 8: Life cycle of Paramphistomum. Source: CDC

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Epidemiology:
Parasites may survive up to years providing a virtually constant source of infestation
for successive generations of snails. The intermediate hosts are extremely adaptable
and prolific breeders, which ensure a widespread availability of the snails within
infested areas. Asexual multiplication of the parasites in infested snails and the
survival of snails for several months in suitable environments may result in the
shedding of large numbers of cercariae.

Reyneke (1983) reports that cattle develop a strong immunity to P. microbothrium,

which may be dependent on the presence of adult parasites in the rumen. Sheep were
reported to be less resistant after attempts to immunise them by artificial infestation.
While cattle, sheep, goats and horses may be the definitive hosts of intestinal or live
flukes. Conradie (2008) reported infestations of Paramphistomum spp. in impala,
Amphistome in kudu, Calicophoron and Cotylophoron spp in nyala, Calicophoron in
blue wildebeest, Paramphistomum spp. in gemsbuck and Cotylophoron and
Paramphisomum spp in waterbuck in the Limpopo Province.

Planorbid snails are aquatic and adaptable and therefore occupy far more diverse
habitats than lymnaeid snails (intermediate hosts for Fasciola spp.). Endemic areas
for intestinal paramphistomosis and hepatic fasciolosis therefore do not necessarily
coincide. Planorbid snails multiply very rapidly in warm, watery environments and can
be found on pastures prone to flooding, on herbage in and around ponds, streams and
other water sources.

Pathogenesis:
Immature worms attach themselves intimately to the intestinal mucosa and may even
penetrate as far as the intestinal muscular layer. A plug of mucosa becomes drawn
into their acetabula, with strangulation and necrosis of the mucosa as consequence.
The extent of damage is related to the number of migrating flukes. Lesions may vary
in severity from mild localized enteritis, to areas of villous atrophy to severe destruction
of the mucosa. Plasma albumin is probably directly lost through the eroded and
compromised small intestinal mucosa. Plasma calcium levels also drops, most likely
due to the loss of the albumin bound calcium.

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Clinical and production effects are dependent upon the extent of the lesions as some
compensation for functional deficiency can take place in the undamaged lower small
intestine. The presence of mature flukes in the rumen does not usually elicit a
significant response but in massive infestations papillae are short and red, becoming
fused into aggregations with rumenal contents adhering firmly to the surface.

Distribution in South Africa:

Over 40 species have been identified in Africa for Paramphistomum and only 10
amphistome species from the genera Calicophoron also Paramphistomum and are
regarded as the most common species infecting domestic ruminants.

Control:
Effective control of most trematode infestations is based on the strategic use of
effective chemotherapy. Farm management is critical in limiting the contact between
intermediate and final hosts thus controlling infestations. Fencing to restrict access to
wet snail habitat with aid in control.

The important management methods of controlling fluke infestations are:

(a) To prevent snail habitats from developing by regular clearing of drainage channels
of vegetation which provide suitable sites for snail development. Good drainage and
the building of dams at appropriate sites in marshy and low lying areas may reduce
the snail problem.
(b) To keep livestock away from pastures contaminated with metacercariae. This may
only be possible when the number of animals involved is small.
(c) Establish proper watering facilities to prevent animals from drinking from lakes,
ponds and streams.

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