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Zoonotic Nematodes
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
• (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.
• 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.
• 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.
• 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
• 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.
• 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.
• Mebendazole (200mg for 5 days), albendazole (400mg for 3 days) or pyrantel (10mg/kg for 5 days).
• 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).
• 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
CONTROL
• Adequate cooking of freshwater fish would
prevent the disease.
OESOPHAGOSTOMUM spp.
DISTRIBUTION
• Until the early 1990s Oesophagostomum in humans was considered a rare zoonotic
infection.
• Apparent absence of a likely zoonotic reservoir host suggests transmission in this large
focus is now maintained by humans.
• 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.
Eggs are shed in the feces of the definitive host , and may be
indistinguishable from the eggs of Necator and Ancylostoma.
In the environment, the larvae will undergo two molts and become
infective filariform (L3) larvae .
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”).
TREATMENT
• Albendazole reduces number, size and speed of resolution of the ultrasound-visible nodules,
EPIDEMIOLOGY
• Prevalences of 30-60% occur in some villages.
DISTRIBUTION
• T.canis is a very common ascarid of dogs in many part of the temperate and tropical world
• 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.
• 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).
• Seroprevalence rates in children in UK, USA and France are around 3-5%.
CLINICAL EFFECTS AND PATHOGENESIS
• Larval migration in liver, lungs or brain may cause eosinophilic tracks and when
they die, eosonophilic granulomas.
• 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
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.
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
DISTRIBUTION
• Particularly in Japan (e.g sushi) and
Netherlands (pickled herring).
LIFE CYCLE
• 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).
• 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.
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.
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
• 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.
TREATMENT
• Prolonged albendazole or Ivermectin treatment.
CONTROL
• Discourage eating of uncooked, pickled or marinated fish/shellfish/poultry in endemic regions.