Zoonotic Nematodes

By
Dr. Abdou K. Sillah
• Trichinella
• Capillaria
• Oesophagostomum
• Toxocara
• Angiostrongylus
• Anisakis
• Gnathostoma
 ZOONOTIC NEMATODES WHICH DEVELOP FULLY IN HUMANS.

TRICHINELLA spp.
• Disease: Trichinosis

• Currently 7 species shown to

infect humans: T. spiralis, T.
britovi, T. nativa, T. nelsoni,
T.murrelli, T. pseudospiralis, and
T. Papuae

• (distinguised by molecular
typing, differential resistance to
freezing and host infectivity).
• DISTRIBUTION
• Throughout the world from Arctic to tropics (not Antarctica).

• LIFE CYCLE
• Trichinella is transmitted by eating infected meat and is predominantly a parasite
of carnivores, cannibalistic animals and carrion feeders.

• The infective cysts survive decomposition for around 10 days after death.

• Humans become infected when they consume raw or undercooked infected

meat from animals in the zoonotic cycle.

• In humans parasite development is complete and similar to that in the zoonotic

hosts but humans are dead-end hosts
• Adult females (2-4 mm in length) and males (~1mm) live buried in the mucosa in the intestine (duodenum and
jejunum) where they copulate.

• They only live for a few weeks but in that time the female may produce up to 1000 1st stage larvae (100μm)
which invade the intestinal wall and travel via the lymphatics and blood to reach the skeletal muscles where
they penetrate into a muscle cell and grow (1mm).

• Most species induce the host cell to develop into a “nurse cell” or cyst (T. pseudospiralis, does not form a cyst).

• These cysts calcify within 18 months but the larvae will remain alive and infective for years.

• So an animal only has to eat one meal to be infective for life.

• When infected meat is eaten the cyst wall is digested in the stomach and the larvae emerge in the duodenum,
invade the mucosa and develop via additional moults into adults which start producing larvae within 5 days of
ingestion of cysts.

• A variety of different animal species are involved in differing ecological situations:-

• Domestic pigs provide the main source of human Trichinella infection
in all parts of the world except the Arctic and East and West Africa.

• Pigs are usually infected through being fed infected uncooked

garbage or slaughterhouse scraps containing pork.

• The habit of chewing each others tails may contribute.

• Ingestion of infected dead rats and mice may also occur.

• Rats and mice can ingest infected meat

Lifecycle
 CLINCAL EFFECTS AND PATHOGENESIS

• Trichinosis mimics almost everything clinically and has often been

misdiagnosed as influenza but it frequently goes unrecognised especially in
light infections.

• The severity depends on the number of cysts ingested

• A heavy infection of adult worms in the bowel may cause diarrhoea.

• The main symptoms are due to the acute inflammatory reaction to the
migration of the larvae and their settling in the striated muscles
• causing myositis

• Typically the diaphragm, eyelids and tongue are particularly infected.

• Classical symptoms include fever, myalgia (muscle tenderness), peripheral and
peri-orbital oedema, rash, myocarditis

• Lungs – dyspnoea, cough, chest pain, pulmonary oedema with disseminated

haemorrhages, eosinophilic abscesses – indicative of an allergic response;

• Nervous system - larvae may be in CSF and meninges where they induce punctate
haemorrhages and microscopic nodules with clear area of necrosis around the
larvae.

• Many people only have an influenza-like infection but often with swollen eyelids.

• In very heavy infections death can occur from exhaustion, pneumonia or cardiac
failure.
 DIAGNOSIS

• 1) Clinical picture is often confusing but eosinophilia, fever, painful muscles and swollen eyelids are
the first typical signs.

• 2) Elevation of muscle enzyme concentration (lactate dehydrogenase, creatine

• phosphokinase) in blood.

• 3) Electromyogram may be abnormal.

• 4) Dietary history. Infection often occurs in community epidemics associated, for example,
• with attending a particular feast.

• 5) Parasitological: Adult worms live for only 1-2 months and so may have gone by the time a patient is
seen.

• Definitive diagnosis is by finding the characteristic coiled larvae in muscle biopsy

• 6) Serology. ELISA using crude larval antigen is very sensitive.

 TREATMENT

• Mebendazole (200mg for 5 days), albendazole (400mg for 3 days) or pyrantel (10mg/kg for 5 days).

• Large doses of corticosteroids (prednisolone) may be needed

• to alleviate allegic and inflammatory symptoms

• CONTROL

• Improved animal husbandry. Never feed pork (or meat from wild carnivores) to a pig (unless
• heat to 60oC).

• For human consumption heat pork to at least 55oC or freeze to –15oC for 20 days to kill
• larvae.

• Identification of cysts in infected pork in abbatoirs is not easy (cysts only 0.4 x0.25mm).

• Trichinoscope, which projects an image of squashed muscle from tongue to identify cysts has been used in
some endemic countries.
 AONCHOCERCA (formerly CAPILLARIA) PHILIPPINENSIS

DISEASE:
Intestinal capillariasis, a cause of “non-vibrio cholera”

• Presumed to be a zoonotic infection but the major natural reservoir for this parasite is
uncertain.

• Fish-eating birds are naturally infected and so migratory fish-eating birds are potential
natural hosts having intestinal adult worms and producing eggs in their stools which can
infect fish.

• Human infection arises from eating raw or undercooked fish harbouring the larval stages

DISTRIBUTION
• Endemic in Philippines and southern Thailand (few cases elsewhere: Taiwan, Japan, Egypt
and Iran).
 LIFE CYCLE

• The adult male and female worms are slender, 3-5 mm in length and are found in
the upper small intestine of humans (jejunum) where they may occur in
enormous numbers (10,000-200,000 in autopsy cases).

• They produce eggs which appear in the stool.

• If appropriate fish are fed embryonated eggs they develop infective larvae which
arrest in the gut

• if such uncooked fish are fed to animals such as monkeys, and fish-eating birds
adult worms develop on average 6 weeks later.

• Humans are infected by eating fresh water fish such as Ambassis commersoni
which are commonly eaten raw.
Lifecycle
 CLINICAL EFFECTS AND PATHOGENICITY

• Adults and larvae are found embedded in the mucosa and

submucosa of the small intestine causing inflammation, flattening of
the villi and sloughing of the mucosa.

• This leads to enteritis with malabsorption and a protein losing

enteropathy.

• Patients have intermittent diarrhoea, voluminous stools, recurrent

abdominal pain and severe weight loss.

• If not treated the infection can become overwhelming and cause

death within 4 weeks
 DIAGNOSIS

• Clinical presentation is often abdominal pain, diarrhoea, borborygmus

(gurgling).

• Pronounced eosinophilia is not a common feature.

• Parasitological diagnosis is by finding the characteristic thick-walled eggs in

stool ( 40 X 20μm with flattened polar plugs).

• In biopsy specimens the adults can be distinguished from Strongyloides

which only has female worms and has a double uterus and thin walled
eggs.

• After treatment Capillaria adults can be found in stool.

TREATMENT
• Treatment with mebendazole or albendazole
needs to be prolonged as the larvae in the mucosa
may be resistant.

CONTROL
• Adequate cooking of freshwater fish would
prevent the disease.
 OESOPHAGOSTOMUM spp.

• Oesophagostomum spp. are normally parasites of ruminants, primates and swine.

DISTRIBUTION
• Until the early 1990s Oesophagostomum in humans was considered a rare zoonotic
infection.

• Polderman et al (1991) reported O. bifurcum is, in fact, a common infection in northern

Togo and Ghana infecting an estimated 250,000 people.

• Apparent absence of a likely zoonotic reservoir host suggests transmission in this large
focus is now maintained by humans.

DISEASE: Oesophagostomiasis, “Tumeur do Dapaong” (Dapaong = town in northern Togo)

 LIFE CYCLE

• Infection arises by oral ingestion of larvae from the soil.

• These burrow into the walls of the intestine where they form nodules in
which they develop.

• The adults (10-15mm long) emerge to live within the lumen of the large
intestine.

• These produce eggs which are passed in the faeces.

• Eggs hatch and develop into infective L3.

• The same pattern of infection occurs in humans.

Lifecycle
Common livestock such as sheep, goats, and swine, as well as non-
human primates, are the usual definitive hosts for Oesophagostomum
spp., but other animals, including humans and cattle, may also serve
as definitive hosts.

Eggs are shed in the feces of the definitive host , and may be
indistinguishable from the eggs of Necator and Ancylostoma.

Eggs hatch into rhabditiform (L1) larvae in the environment , given

appropriate temperature and level of humidity.

In the environment, the larvae will undergo two molts and become
infective filariform (L3) larvae .

Definitive hosts become infected after ingesting infective L3 larvae .

After ingestion, L3 larvae burrow into the submucosa of the large or

small intestine and induce cysts.

Within these cysts, the larvae molt and become L4 larvae. These L4
larvae migrate back to the lumen of the large intestine, where they
molt into adults .

Eggs appear in the feces of the definitive host about a month after
ingestion of infective L3 larvae.
 CLINICAL FEATURES AND PATHOGENESIS

• The colonic wall nodules and the extensive adhesions they provoke cause
multinodular disease which may lead to intestinal blockage.

• The large masses can adhere to and rupture the abdominal wall
appearing as absceses or tumours on the abdomen (“Tumeur do
Dapaong”).

• Major symptoms leading to surgery are intestinal obstruction and/or

disfiguring or painful abdominal mass.

• Around 2% of infected individuals progress to clinical oesophagostomiasis

if untreated
DIAGNOSIS
• Eggs indistinguishable from hookworms.

• Stool is cultured for L3 larvae which can be distinguished.

• The adults can be expelled with anthelminthic treatment.

• Nodules can be seen on ultrasound.

TREATMENT
• Albendazole reduces number, size and speed of resolution of the ultrasound-visible nodules,

• stops egg excretion.

EPIDEMIOLOGY
• Prevalences of 30-60% occur in some villages.

• Reasons for the limited distribution are not cleared

 ZOONOTIC NEMATODES WHICH ARREST AT THE LARVAL STAGE IN
HUMANS

VISCERAL LARVA MIGRANS

• The condition resulting from the ingestion of eggs or larvae of animal
parasites

• leading to the presence of wandering larvae in the deep organs of the

human body.

• Nematode species which may be involved include: Toxocara canis, T. cati,

Gnathosotoma spinigerum, Angiostrongylus cantonensis, Anisakis spp.

• Other nematodes are occasionally involved as are parasites of other phyla

e.g. Spirometra. N.B. the adult forms of these larvae occur in animals.
 TOXOCARA spp
DISEASE
• Toxocariasis. A common and important cause of visceral larva migrans

• May be caused by a variety of species (Toxocara canis, T. cati, Toxascaris leonina).

• T. Canis of dogs is the most common and important.

DISTRIBUTION
• T.canis is a very common ascarid of dogs in many part of the temperate and tropical world

• but more common in hot wet regions than in drier areas.

• In 1980s the prevalence in dogs: 21% London, 40% Ibadan, 70% New York. No recent
surveys in UK.
 LIFE CYCLE

• In the dog adult worms are somewhat smaller than human Ascaris and have characteristic cervical alae.

• Worms in the dog’s intestine pass eggs which embryonate in soil in 2-4 weeks at 15-35C.

• On ingestion larvae penetrate the wall of the small intestine and undergo a somatic migration through blood to
liver, kidneys and lung.

• During lung migration the larvae may be coughed up and swallowed leading to development of adults in the gut.

• This adult phase occurs mainly in younger dogs (<6months).

• Following oral infection of older dogs larval development is arrested at the L2 stage which become dormant in the
tissues.

• In pregnant bitches the larvae are activated and migrate transplacentally to infect the puppies shortly before
birth.

• So it is the puppies which contribute most to contamination of the environment with eggs.
Lifecycle
 Lifecycle ctd
• In humans infection is by ingestion of embryonated eggs from soil (not
from dog faeces in which the eggs will not have matured).

• L2 larvae migrate in a similar somatic way as in dogs although they do

not mature and may reach the CNS and the eye.

• Eventually they die.

• Infection usually occurs in children close to pets or those who frequent

parks.

• Seroprevalence rates in children in UK, USA and France are around 3-5%.
 CLINICAL EFFECTS AND PATHOGENESIS

• Larval migration can continue for months or years.

• Larval migration in liver, lungs or brain may cause eosinophilic tracks and when
they die, eosonophilic granulomas.

• Most patients infected with Toxocara (judged by seroconversion) have mild,

transient or no symptoms.

• The major clincal syndrome is visceral larva migrans characterised by fever,

malaise, cough, brochospasm (like Loeffler’s syndrome), hepatosplenomegaly
and lymphadenopathy.

• In 80% of cases there is eosinophilia, 50-60% hepatomegaly and 50% coughing

and pulmonary symptoms of Loeffler’s syndrome
• The most common serious complication is if a larva is trapped in the retina.

• The resulting inflammation may cause chronic granulomatous endophthalmitis or

peripheral retinitis resulting in significant loss of vision.

• Once scar tissue has developed little can be done.

• The resulting tumour-like mass can be confused with retinoblastoma and the eye
removed.

• But Toxocara lesions are always raised and invariably unilateral (~98%).

• Larvae are known to die in the brain and behavioural disorders have been reported
in infants infected with Toxocara.
DIAGNOSIS
• Hepatomegaly with eosinophilia (may rise above 50%) and raised gamma-globulin levels is suggestive
especially in a child with history of exposure to a young dog or potentially contaminated soil .

• Definitive diagnosis can be made by tissue biopsy but such material is rarely available.

• Serum ELISA with E/S products of L2 larvae cultured in vitro is sensitive and specific.

TREATMENT
• A three week dose of diethylcarbamazine kills the larvae and can stop the disease but established
pathology is irreversible.

• To suppress allergic and inflammatory reactions steroid treatment (prednisolone) should be given.

• Albendazole plus steroid treatment has been reported to be effective in preventing uveitis
(inflammation of the middle layers of the eye) due to ocular larva migrans.
 PREVENTION AND CONTROL

• Eggs commonly contaminate parks and play areas

and can remain infective in soil for two years.

• Control is by deworming of animals (“Panacure”

fenbendazole –kills larvae and adults),

• Restriction of defecation sites of pets especially in

relation to children’s play areas.
 ANGIOSTRONGYLUS CANTONENSIS

DISEASE: Eosinophilic meningitis

• Humans infected with larvae by ingestion of raw or undercooked

land snails,

• slugs or vegetables contaminated with small molluscs (slugs or

snails). Adults in pulmonary arteries
• of rats and bandicoots.

DISTRIBUTION:
• South Asia, Pacific. (associated with the habit of eating raw snails).
Lifecycle
 LIFE CYCLE:

• Eggs hatch in the lungs of infected rats and the larvae are coughed up,
swallowed and passed in the faeces.

• The L1 larvae are ingested by snails and slugs and develop to L3 larvae
and remain coiled in the muscle.

• When ingested by a rat or by humans the larvae penetrate the gut wall
and are carried by the blood (via liver, heart and lungs to the main
circulation) to the meninges of the brain where they develop into L4
larvae.

• In rats they proceed to develop into pre-adult worms and then migrate
to the pulmonary arteries where they mature.
 CLINICAL SIGNS AND PATHOGENESIS

• Infection in humans is generally benign and self limiting but can be fatal.

• The larvae or preadult worms die and may provoke an inflammatory

granulomatous response and focal necrosis in the brain or the anterior
chamber of the eye.

• Symptoms of eosinophilic meningitis or meningoencephalitis including

severe headache, back and neck stiffness, vomiting and parasthesia (of face
and/or trunk) may occur.

• Eye invasion causes visual impairment.

• Symptoms generally last for two weeks but may persist.

DIAGNOSIS
• Signs of meningitis. History of eating snails.

• Blood eosinophilia is common. There is a raised cell count

(pleocytosis) in the CSF with >25% eosinophils and occasionally larvae.

• Otherwise parasitological diagnosis is not possible.

TREATMENT
• Symptomatic treatment until spontaneous recovery is recommended
as anthelminthic treatment, although effective in animals, may
provoke severe inflammation to the dying larvae.
 ANISAKIS spp
• DISEASE: Anisakiasis

• Human infection with larval stages is caused by

ingestion of uncooked marine fish carrying the
infective larvae of a number of different
species of nematodes of the family Anisakidae

• (e.g. Anisakis spp. Pseudoterranova spp.).

• The adults live in the GI tract of marine

mammals (seals, sea lions, whales and
dolphins).

DISTRIBUTION
• Particularly in Japan (e.g sushi) and
Netherlands (pickled herring).
 LIFE CYCLE

• Eggs are passed in the faeces of marine mammals.

• Hatched larvae infect marine crustaceans and develop to L3.

• If eaten by marine fish or squid the larvae will survive in muscle or body cavity.

• Infected fish act as a “paratenic” host and can infect a subsequent host if the fish is eaten (a paratenic host
is one in which there is no parasite development but the larvae survive and so are transported around).

• If eaten by a larger fish this also becomes a paratenic host.

• When the fish is eaten by a marine mammal the larvae will develop into adults.

• If a human eats the uncooked fish, however, the larvae do not develop but behave as in a further
paratenic host.

• Anisakis spp are usually found in herring and mackerel and salmon in north America.
Lifecycle
 CLINCAL EFFECTS AND PATHOGENSIS

• The larvae which may reach 50mm in length, invade the gastric or intestinal
mucosa and cause ulceration at the point of attachment.

• At 1-5 days after eating raw fish there may be abdominal pain which in
heavy infections can simulate appendicitis, nausea, vomiting and diarrhoea.

• Occasionally the larvae can penetrate the bowel wall causing an extra-
intestinal, eosinophilic inflammatory mass.

• Gastric invasion causes severe epigastric pain, nausea and vomiting which
may occur within hours of ingestion.

• In many cases the disease is self-limiting

DIAGNOSIS
• Clinical signs plus history of eating fish. Sometimes larvae are vomited.

• Definitive diagnosis is often following gastroscopy or exploratory

laparotomy during which the embedded larvae can be removed.

TREATMENT
• Anthelminthic treatment is rarely necessary.

CONTROL
• Larvae killed by: Freezing at –20oC for 5 days. Smoking if the
temperature reaches 65oC.
 GNATHOSTOMA SPINIGERUM

DISEASE: Gnathosotomiasis.
• Humans are infected with the larval stages by eating raw fish,
shellfish or poultry.

• Adult worms live embedded in the wall of the alimentary tract

(often stomach) of carnivores, notably members of the cat and
dog families.

DISTRIBUTION
• Japan, Thailand, China, Indonesia, Malaysia, Central and South
America, especially Mexico.
 LIFE CYCLE

• Eggs from carnivore faeces hatch in water and the 1st stage larva infects the 1st intermediate
host, a copepod (e.g. Cyclops) in which the L2 larva develops.

• When eaten by a 2nd intermediate host e.g. fish, shrimp, frog or snake the L2 migrates into
the flesh and develops into the L3.

• The 2nd intermediate host may also be ingested by a variety of paratenic (transport) hosts
e.g. birds (including poultry) in which the L3 will similarly encyst in the muscle.

• When ingested by a definitive host e.g. tiger the L3 develops into the adult parasites which
live in a tumour induced in the stomach wall.

• Humans are similarly infected by eating undercooked fish or poultry containing L3 larvae or
(reportedly) by ingestion of L2 larvae within Cyclops taken in with drinking water.

• In humans the L3 larvae do not develop into adults but migrate around the body.
Lifecycle
 CLINICAL EFFECTS AND PATHOGENESIS

• The larvae which have a characteristic head bulb covered with

spines burrow through the intestinal wall into the abdominal cavity

• This may cause epigastric pain, fever, vomiting.

• The larvae then migrate to the subcutaneous tissues through which

they move at around 1cm/hr giving a characteristic slow moving
oedematous reaction lasting for a few days

• They may also undergo migration through the visceral organs and
cases of invasion of the CNS and eye have been reported
DIAGNOSIS
• Clinical signs and food history.

• High eosinophilia (up to 90%) 1-2 days after eating raw fish.

• Differential diagnosis cutaneous paragonimiasis (immunodiagnosis distinguishes).

• Definitive diagnosis is by surgical recovery of the worm from subcutaneous site.

TREATMENT
• Prolonged albendazole or Ivermectin treatment.

• Surgical removal of cutaneous larvae.

CONTROL
• Discourage eating of uncooked, pickled or marinated fish/shellfish/poultry in endemic regions.