Helminths Lecture
Helminths Lecture
1. Flukes (Trematodes)-digenea
2. Tapeworms (Cestodes)
Adult tapeworms are elongated, segmented, hermaphroditic flatworms that inhabit the
intestinal lumen.
Larval forms, which are cystic or solid, inhabit extraintestinal tissues.
3. Roundworms (Nematodes)
Class Digenea-Flukes
General characteristics
Causes Schistosomiasis
Affects over 500m people almost all of them in the developing countries.
The disease causes anguish, deformity and death
Also causes considerable economic losses
Habitat
Adult: In the mesenteric venous (haemorroidal) plexuses draining the large intestine
(colon and rectum)
Larvae: In fresh water snails.
Egg: In the faeces, and rarely in the urine of man.
Morphology:
There are three main species causing schistosomiasis: S. mansoni, S. japonicum and S.
haematobium
Adult worms are of separate sexes, are small with each varying in length.
Outer integument of female is smooth while that of S. haematobium and S. mansoni
may be covered with minute spines.
The integument of the adult parasite has the ability to withstand immunological attack
of the host.
Adult worms posses an oral sucker opening which leads into the alimentary canal and
there is also a more posteriorly situated ventral sucker used for attachment to the
endothelium of the blood vessel.
The male has a distinct large ventral groove called the gynaecophoral canal which
encloses the female during mating.
LIFE CYCLE
Life Cycle
For pairing male worms form a ventral groove, the gynaecophoric canal, in which the
longer and thinner female resides.
This close and permanent pairing contact can last for many years and is a prerequisite
for sexual maturation of the female and subsequent egg production.
The eggs penetrate the wall of the veins, migrate to the intestinal lumen (S. mansoni,
S. japonicum among others) or the bladder (S. haematobium) of their hosts, and are
released with the faeces (S. mansoni among others) or the urine (S. haematobium).
A multicellular larva develops within the egg, the miracidium, which hatches from
the egg stimulated by phototaxis and water contact.
As the first free-swimming larval stage the miracidium searches a specific water
snail, which serves as intermediate host, and penetrates the snail´s skin.
Within the snail, the miracidium transforms into a mother sporocyst.
By asexual reproduction daughter sporocysts are generated, which finally develop
cercariae, the only infective stage for vertebrate hosts.
The life stage infectious for humans or other vertebrates is the cercaria, which
represents the second free-living larval form of this parasite.
Cercariae are released into the water by schistosome species-specific snails and swim
to get contact to the skin of final hosts, such as humans.
Following penetration through the skin the cercaria transforms into a
schistosomulum, a juvenile form which enters blood capillaries to migrate via lung
and heart to the liver.
Arriving in the liver the worms have reached adulthood and pair.
As paired adults schistosomes finally migrate to their final destination in the
mesenteric veins of the gut, except S. haematobium, which colonizes the bladder.
Pathology of schistosomiasis
Urinary schistosomiasis
Urinary bladder is the most affected
Autopsy reveals multiple lesions, focal granulomas of bean head size on the wall
of bladder
Muscle hypertrophy
Bladder calcification
Cyctic inflammation of the bladder
Haematuria and pain on urination
Intestinal schistosomiasis
Affects the large intestine and rectum
Eggs lodge in venules and submucosa act as foreign bodies
Abdominal pain
Diarrhea with blood/pus
Periportal hepatic fibrosis-hepatomegally
Splenomegally
Cerebral schistosomiasis in S. mansoni eggs lodge in brain
Diagnosis
Worldwide in distribution
Presense of man made lakes
Urbanization
Walking bare feet in water
Occupation-agriculture and mining are at risk of infection
Age-common in children
Control measures
Drainage of marshy areas
Improved sanitation facilities
Observe good personal hygiene
Use of molluscicides to kill snails
Introduce biological control agents
Boil water before drinking and bathing
Wear protective clothing while working under water
Chemotherapy
Paragonimus westermani
Morphology
Occurs in lungs and more rarely in the brain, spinal cord and other organs of man,
pigs, dogs, cats, goats, fox and wild carnivores.
The parasite is reddish brown in colour and the cuticle is covered with spines
It has a ventral sucker situated slightly anterior to the middle.
The eggs are yellowish brown and are provided with an operculum with the shell
thickened at the opposite side.
Life cycle
The eggs are laid in the cysts in which the worms live and escape through the
connecting channels into the bronchi.
Then they pass up from the lungs with mucus and may be found in the sputum which
has a characteristic plastic colour.
Animals usually swallow the sputum so that eggs are found in the faces.
After development for 2-7 weeks, the larvae called miracidium escapes and penetrates
into a snail of genus Melania or Ampullaria or pomatiopsis in which the usual further
development takes place including sporocysts, rediae and cercariae. The germ layer of
sporocysts give rise to a second larval stage called radiae.
This develops into a third larval stage called cercaria
Cercaria escapes from the snail and swim about in the water, then they enter a second
intermediate host which could be a crayfish or crab in which they encyst to form a
stage called metacercaria
The final host (man, pig, goat etc) becomes infected by eating the infected crustacean
or by drinking water in which metacercaria occur after they have escaped from the
second intermediate host.
The metacercaria escape from the crustacean when these cercariae are injured and
they may live in water for 3 weeks.
When the final host ingests the metacercaria, they excyst in the small intestines
liberating young flukes and these penetrate the intestinal mucosa and then they
wander through the body cavity and diaphragm entering the lungs from the pleural
cavity.
They may also enter other organs e.g. brain, spinal cord and other organs. Then they
arrive in the bronchioles where they form a cyst wall around themselves and grow
into adults. Others mate, females producing eggs within the cyst.
Pathogenicity
It causes a disease called pargonimiasis and there are several types of this disease i.e.
lung and cerebral paragonimiasis
Lung paragonimiasis is not of much medical importance (no clinical signs).
In lungs paragonimus causes congestion and haemorrhages called pneumonitis.
Cerebral paragonimiasis-when the parasites are lodged in the brain causing epileptic
convulsions which may lead to coma and death
They may also cause ulcers in bile ducts and intestines
Diagnosis
Bithionol
Emetine hydrochloride
Control and prophylaxis
Measures 30-50mm in length of which the thread like oesophageal region occupies
two thirds.
Mouth has no lips but has a minute spear
Males a little smaller than females but they are distinguished from females by having
a curled tail
Eggs are barrel shaped
Life cycle and epidemiology
Has a very simple life cycle
Eggs develop slowly and are less resistant to dessication and epidemiological
evidence shows that a high incidences of Trichiuris infection is always associated
with an abundance of moisture in the soil which may be due to heay and well
distributed rainfall or dense shade.
Infection may result from polluted moist soil. When embryonated eggs are
swallowed, they hatch near the caecum and the embryos burrow into the villi for afew
days then take their residence into the caecum, appendix and rectum where they
mature in about a month.
After mating, females start to produce eggs which are voided along with faeces.
Pathology
If only a few worms are present, it does not produce pathological effects.
Under heavy infestation, it results in hookworm disease which is characterized by :
Loss of appetite
Nausea
Diarrhea
Blood streaked stool
Weakness
Loss of weight
Anaemia
Eosinophilia-increased white blood cells in circulation
Abdominal discomfort
Emaciation and sometimes fever
In chronic cases, there is prolapse of rectum
Diagnosis
Trichiuris trichiura is difficult to eliminate because of its remote position in the caecum
which is far from either the mouth or anus. Therefore, most antihelminthics are not effective
but the following can be used:
Latex
Enema
Dithiazanine
After ingesting infected meat, the capsule of the encysted larvae is digested by gastric juice,
and the larvae are released in the duodenum or jejunum where they molt four times to
become adult worm. After mating, the male worm dies and the female worm begins to deliver
the embryos 4-7 days after the infection. The larvae penetrate the intestinal wall and migrate
through the lymphatic vessels to the blood stream, which carries them to various organs.
Skeletal muscles and diaphragm are most frequently parasitized. Others include the tongue,
masseter and ocular muscles.
Clinical features
There are two clinical phases.
1. The intestinal phase: lasting 1-7 days - asymptomatic; sometimes cause nausea, vomiting,
diarrhea, constipation, pain, etc,
2. The muscle phase: which causes myalgia, palpabral edema, eosinophilia, fever,
myocarditis, meningitis, bronchopneumonia etc.
Diagnosis
Muscle Biopsy
Detection of larvae in blood or CSF
Detection of larvae and adult worms in stool (rare).
ELISA
Treatment - Thiabendazol
Prevention
Cooking of all meat before consumption
Inspection of pigs
Pork must be stored at -150C for 20 days.
HOOK WORMS
There are two species of hookworm:
1. Ancylostoma duodenale
2. Necator americanus
The adults are found in the small intestines of man.
Ancylostoma duodenale
Grayish-white in color. The body is slightly ventrally curved. The anterior end follows the
body curvature. The buccal cavity is provided ventrally with pairs of teeth and dorsally with a
notched dental plate.
Distribution: This species is found in the northern part of the world including China, Japan,
Europe, North Africa and Ethiopia.
Morphology
Male: The male measures 10 cm in length. The posterior end is broadened into a
membraneous copulatory bursa that is provided with two long spicules.
Female: The female measures 12 cm in length. The posterior end is straight.
Life cycle
Eggs are passed in the stool, and under favorable conditions (moisture,
warmth, shade),
larvae hatch in 1 to 2 days.
The released rhabditiform larvae grow in the feces and/or the soil,
after 5 to 10 days (and two molts) they become filariform (third-stage) larvae
that are infective.
These infective larvae can survive 3 to 4 weeks in favorable environmental
conditions.
On contact with the human host, the larvae penetrate the skin and are carried
through the blood vessels to the heart and then to the lungs.
They penetrate into the pulmonary alveoli, ascend the bronchial tree to the
pharynx, and are swallowed.
The larvae reach the small intestine, where they reside and mature into adults.
Adult worms live in the lumen of the small intestine, where they attach to the
intestinal wall with resultant blood loss by the host.
Most adult worms are eliminated in 1 to 2 years, but the longevity may reach
several years.
Pathogenesis:
A.duodenale (third-stage) larvae follow thermal gradients and are guided by
heat to human skin where they may irritate or invade the skin.
A pruritic, erythematous, papular rash develops and produces what is known
as “ground itch” around penetration sites of the infective larvae, usually on the
hands and feet.
Invasive infection occurs when larvae enter the bloodstream and are carried to
the lungs.
A mild cough and pharyngeal irritation may occur during larval migration in
the airways; however, passage through the lungs is usually asymptomatic.
The larvae are swallowed down the oesophagus and migrate to the
gastrointestinal tract.
Larvae then hook onto the intestinal mucosa where they mature into adult
hookworms by feeding on blood.
The major-hookworm related injury occurs due to intestinal blood loss, which
can lead to iron-deficiency anaemia in moderate to heavy infections.
In the gut, adult worms may produce epigastric pain and abnormal peristalsis.
Clinical features are highly dependent on worm burden and dietary iron levels.
In children this condition may precipitate heart failure or kwashiorkor.
Retardation of mental, sexual, and physical development has also been noted
in children.
Intrauterine growth retardation, prematurity and low birth weight among
newborns born to infected mothers has been noted.
Acute/heavy infections may result in fatigue, weakness, abdominal pain, and
diarrhea with blood loss.
Adult’s lifespan in human intestine is 1-2 years but can be as long as 10-12
years
Epidemiology
Environmental factors influence the amount of hookworm infection in a community
Temperature is a prime controlling factor
Rainfall is also fundamental: when soils dry up after a shower or as faeces dry up,
some of the larvae escape desiccation b y going down the surface
Clay or sandy soil is bad for survival of hookworm larvae but humus soil is favorable.
Soil impregnation by salt is injurious to the larvae
Excessive rainfall is also not favorable but moderate rainfall
Vegetation and dense shade are favorable for larvae survival
Animals which feed on faces are injurious to larvae
Age and sex of man; youngones are more susceptible than adults because of soft skins
and habit of playing with soil; females are more susceptible than females
Occupation: mining and agriculture are more susceptible
Wearing of shoes
Poor sanitation
Expectoration habits:
Diagnosis: Examination of stool by direct saline smear to detect the eggs.