Download Theme: "Medical Helminthology. Phylum Nemathelminthes " Plan of

Theme: "Medical Helminthology. Phylum Nemathelminthes "
Plan of the lecture:
1. General characteristics and classification of type Roundworms.
2. The most important representatives of class Roundworms - human
pathogens (Ascaris, toxocara, whipworm, intestinal, threadworm,
Trichinella).
PHYLUM NEMATHELMINTHES. CLASS NEMATODA. Nematodes may
actually be second only to arthropods in number of species ~25,000 known
species. specialists estimate that only ~20% of existing species have been
studied and described so far, there may be over 100,000 living species, occur
in virtually all habitats from arctic to tropics; marine, freshwaters, and
especially in soil. ~60% of all known nematode species are parasitic. In type
Nemathelminthes medical importance has only Nematoda class - actually
roundworms.
General Characters1 . The nematodes are unsegmented, elongated and
cylindrical or filiform in appearance; both ends are often pointed.2. The sizes
show a great variation, most are very small 0.5-1.0mm (100th of an inch to
1/5th inch) the smallest (T. spiralis and S. stercoralis) measures less than 5
mm and the largest (D . medinensis) measures up to 1 metre. most are
colorless and transparent or with whitish or yellowish tint 3. The body is
covered with a tough cuticle. Tube within a tube’ body plan: allows an
increase in size allows more elaborate lengthening and coiling of internal
organs allows circulation of gasses, food and wastes in the absence of a
circulatory system provides hydrostatic skeleton 2 major kinds of body
cavities: pseudocoelom and true coelom both have: three embryonic tissue
layers: ectoderm - skin, nervous system, mesoderm- muscles, bones, circ sys,
endoderm -dig and resp tracts. secretes tough, flexible cuticle containing
collagen - protects worms parasites from digestive enzymes.( their cuticle is
highly resistant to fairly extreme environments and conditions ! some can
survive pH’s from 1.5-11.5 ! some can survive mercuric chloride solutions that
would kill most other animals ! only living organisms to survive a space
shuttle explosion) pseudocoelom important as a transport medium for
oxygen, foods and wastes ! pressure created by tough cuticle and muscle layer
creates hydrostatic skeleton 4. The worm possesses a body cavity in which the
various organs, such as the digestive and genital systems, float. Excretory and
nervous systems are rudimentary. Nervous System “brain” = nerve ring with
ganglia around pharynx dorsal and ventral nerve cords. Senses especially
chemoreceptors sometimes in head or tail. unique excretory system: excretory
system a series of canals or tubules or interconnected glandular cells (=renette
cells) sometimes with protonephridia tubules form lateral line along sides of
animal visible from the outside empties through excretory pore near front of
animal no circulatory or respiratory system pseudocoelom fluids circulate
nutrients, oxygen and wastes
5. The alimentary canal is complete, consisting of an oral aperture, mouth
cavity, oesophagus, intestine and a subterminal anus. The mouth cavity, when
present, may have teeth or cutting plates; in other cases, where the mouth
cavity is absent, the oral aperture is directly continuous with the oesophagus.
6. The nematodes of man all sexes are separate. most with internal
fertilization after mating, females lay 100,000 eggs/day eggs often extremely
resistant to environmental extremes. (some can enter a state of arrested
activity = cryptobiosis ! makes them successful in seemingly unfavorable
environments eg. some have been dried for several years then rehydrated eg.
some have been placed in liquid air (-194ºC (= -317ºF)) and revived
afterwards).The male is generally smaller than the female and its posterior
end is curved or coiled ventrally. The male genital system consists of a long
convoluted tube which can be differentiated into testis, vas deferens, seminal
vesicle and ejaculatory duct. The genital duct forms a common passage with
the intestine and is known as cloaca. Accessory copulatory organs such as
spicule and gubernaculum, are also present. The female genital system
consists of a single or double convoluted tubes. Each part of the tube is
differentiated into ovary, oviduct, seminal receptacle, uterus, vagina and
vulva. The female nematodes may be divided as follows: (1) Viviparous, giving
birth to larvae;(examples are D. medinensis, W. bancrofti, B. malayi and T.
spiralis). (2) Oviparous, laying eggs; examples are A. lumbricoides, T.
trichiura (laying unsegmented eggs), A. duodenale and N. americanus (laying
eggs with segmented ovum), E. vermicularis (laying eggs containing larvae).
(3) Ovo-viviparous, laying eggs containing larvae which are immediately
hatched out; example is S. stercoralis.
Life Cycle. Man is the optimum host for all the nematode parasites. They pass
their life cycle in one host except the superfamilies Filarioidea and
Dracunculoidea, where two hosts are required. In Filarioidea, the second host
is an insect vector in which the larval development takes place. In
Dracunculoidea, cyclops constitutes the second host for the growth of its
larva. In cases where the nematodes choose one host, they localise in the
intestinal tract and start developing. The eggs in these cases come out of the
body and undergo certain developmental changes before they can enter a new
host. In the case of T. spiralis, pig is the optimum host and man represents the
alternative host but the worm passes both its adult and larval stages in the
same host.
Modes of Infection of Nematode Parasites 1. By ingestion of: (a)
Embryonated eggs contaminating food and drink, as in A. lumbricoides, E.
vermicularis and T. trichiura. (b) Growing embryos in an intermediate host
(infected cyclops), as in D. medinensis. (c) Encysted embryos in infected pig’s
flesh, as in T. spiralis. 2. By penetration of the skin: The filariform larvae
boring through the skin, as in A. duodenale, N. americanus and S. stercoralis.
3: By blood-sucking insects, as in the parasites belonging to the superfamily
Filarioidea. 4. By inhalation of infected dust containing embryonated eggs, as
in A. lumbricoides and E. vermicularis.
Question 2
HUMAN roundworm (Ascaris lumbricoides) - true, obligate, intracavitary
entozoon, geohelminthes. It causes ascariasis - invasive disease anthroponosis.
Ascariasis is widespread, except the areas of tundra and dry desert, where
there are only imported cases this geohelminthiasis. The largest human
nematode parasites; ~ 10 - 12” (up to 30 cm) long found exclusively in humans
1 Billion people in world are infected common in tropics; in some countries
over 50% of children are infected even in US infections are not uncommon
main cause of infection is fecally contaminated food Ascaris eggs are resistant
to concentrated bleach and formalin they are also coated with an extremely
sticky coating to adhere to almost anything egg can survive >7 yrs after any
trace of feces is gone after ingestion the juvenile burrows into blood/lymph
vessels ! circulates into lungs arrives in lungs ~2 months after initial infection !
enters alveoli and ascends trachea or is coughed up and reswallowed become
adults in the intestine adult worms can survive for 25 years.
Life cycle. A. lumbricoides, infects humans when an ingested fertilised egg
becomes a larval worm (calledrhabditiform larva) that penetrates the wall of
the duodenum and enters the blood stream. From there, it is carried to
the liver and heart, and enters pulmonary circulation to break free in
the alveoli, where it grows and molts. In three weeks, the larva passes from
the respiratory system to be coughed up, swallowed, and thus returned to the
small intestine, where it matures to an adult male or female
worm. Fertilization can now occur and the female produces as many as
200,000 eggs per day for a year. These fertilized eggs become infectious after
two weeks in soil; they can persist in soil for 10 years or more.The eggs have
a lipid layer which makes them resistant to the effects of acids and alkalis, as
well as other chemicals. This resilience helps to explain why this nematode is
such a ubiquitous parasite.
Incubation Period. In man it takes 60 to 75 days from the time of exposure to
infection, for the mature female to lay eggs and that is the period when the
symptoms are manifested.
Symptoms
Often, no symptoms are seen with an A. lumbricoides infection. However, in
the case of a particularly bad infection, symptoms may include bloody
sputum, cough, fever, abdominal discomfort, intestinal ulcer, passing worms,
etc. Accompanying symptoms include pulmonary infiltration, eosinophilia.
Immunology. A partial immunity may be acquired by man, induced by the
migrating larvae. Antigens are liberated during the moulting period of the
larvae and produce protective antibodies which lower the worm burden and
play a part in the immune response. A severe allergic reaction (urticaria and
fall of blood pressure) occurs when the larvae reach the small intestine for the
second time. Eosinophilic count is increased at the time of tissue invasion.
Specific antibodies (complement-fixing and precipitating) can be
demonstrated in Ascaris infection. Hypersensitivity to Ascaris is determined
by skin test.
Pathogenesis. Mostly related to the gastro-intestinal tract. (1) s p o l i a t i v e a
c t i o n : By robbing the host of its nutrition (protein and vitamin content of
the worm is high). Ascaris infection may cause vitamin A deficiency (night
blindness).
(2) “ t o x i c ” a c t i o n : The body fluid of Ascaris when absorbed is toxic
and may give rise to typhoid-like fever; also responsible for various allergic
manifestations .
(3 ) m e c h a n i c a l effects: The presence of A. lumbricoides has led to the
occurrence of intussusception it may penetrate through the ulcers of the
alimentary canal
Wandering Ascaris may enter the lumen of an appendix, causing appendicitis.
Laboratory Diagnosis. This may be described under two heads: Direct
evidences and indirect evidences.
I . D ir ect E v id en c e s: (a) Finding o f Adult Worms
(1) in th e s t o o l or v o m it . The adult worm may pass out spontaneously in
the stool or per anum between stools,or be vomited.
(2) x - ray d ia g n o s is . The presence of A. lumbricoides has been
demonstrated by radiography with barium emulsion,
which being ingested by the worm within 4 to 6 hours, casts an opaque
shadow (string-like shadow).
(b) Finding o f Eggs
(1) in t h e s t o o l . As the Ascaris eggs are passed in the stool in enormous
numbers, it should be easy to detect the
infected persons by a direct microscopical examination of a saline emulsion of
the stool. Concentration by floatation
method may be employed for the detection of eggs in the stool. It is to be noted
that unfertilised eggs do not float in
salt solution. If the patient harbours a solitary male Ascaris, eggs are not
found in the stool. *
(2) in t h e b il e . Microscopical examination of the bile obtained by duodenal
intubation may reveal Ascaris eggs.
I I . I n d ir e c t E v id e n c e s: Blood Examination. Eosinophilia is present
only at the early stage of invasion, but if present in the intestinal phase
suggests associated strongyloidiasis or toxocariasis.
Dermal Reaction (Allergic). “Scratch test” with powdered Ascaris Antigen has
often been found to be positive but the results are variable. Serological tests
are useful in diagnosis of extraintestinal ascariasis (Loeffler’s syndrome).
Note: Larvae may be found in the sputum during the stage of migration.
Treatment. Drugs which are known to have specific action on Ascaris include
the following: pyrantel pamoate (a
single dose of 10 mg/kg. maximum 1 gm), thiabendazole and mebendazole
(100 mg twice daily for three days),
albendazole (a single dose of 400 mg).
Prophylaxis. The measures should consist of'(i) proper disposal of human
faeces, (ii) treatment of parasitised
individuals, and (iii) education of children in schools on sanitary laws and
hygiene.
Superfamily RHABDITOIDEA. A number o f small worms with a peculiar
life cycle, having parasitic and free-living existence. The oesophagus of
parasitic
female is a long cylindrical muscular tube with a posterior bulb containing
valves; also possesses a prebulbar swelling. Females
are ovo-viviparous.
G e n u s s t r o n g y lo id e s G r a s s i, 1879. Species S. stercoralis.
Geographical Distribution. World-wide. Common in Brazil, Far East
(Cochin-China and Philippines) andAfrica.
Habitat. The parasitic females live in the wall (mucous membrane) of the
small intestine of man, especially in the
duodenum and jejunum. They can be demonstrated post-mortem by
examining scrapings of the mucosa, under low
power of the microscope.
Morphology. A d u l t W o rm . In the parasitic phase, the females are readily
discovered but not the males.The parasitic females are hardly visible to the
naked eye; they measure 2.5 mm in length by 40 to 50 um in
breadth. The cylindrical muscular oesophagus extends through the anterior
third of the body and the intestine extends through the posterior two-thirds.
The anus opens mid-ventrally, a short distance in front of the caudal tip. The
posterior
extremity is pointed. The vulval opening is at the junction of the middle and
posterior thirds of the body. The paired genitalia extend at right angles from
the vulva, one set being disposed anteriorly and the other set posteriorly.
The females are ovo-viviparous.
The parasitic males, as described by Kreis, are shorter and broader than the
females. They resemble the males of free-living sexual generation, except for
their conspicuous buccal cavity. They have no penetrating power and remain
parasitic in the lumen of the bowel. The parasitic males were discovered only
by Kreis (1932) but others have so far failed to demonstrate them.
Eggs. In the gravid female, the eggs are conspicuous within its body, lying
antero-posteriorly in a single file (5 to10 eggs in each uterus). The eggs
measure about 55 (nm in length by 30 in breadth; they are thin-shelled,
transparent and oval. They contain larvae ready to hatch. As soon as the eggs
are laid, the rhabditiform larvae start hatching and bore their way out of the
mucous membrane into the lumen from where they are passed in the faeces.
Hence, it is the larvae and not the eggs which are found in the human faeces.
Larvae. Two types of larvae are found:
(a) rhabditiform larvae and (b) filariform larvae. Rhabditiform Larvae. These
are developed directly from the gravid females and are found in the lumen of
the bowel. They measure 200 to 250 fim in length by 16 jam in breadth; they
have short mouth and double-bulb oesophagus. The course of development of
these larvae are as follows:(i) While in the lumen of the bowel, they are
metamorphosed into filariform larvae (often facilitated by steroid therapy).
These may penetrate the intestinal epithelium, thus providing internal
reinfection. If the larvae are carried
down the bowel, they may be voided with the faeces and during transit some
may penetrate the perianal and perineal skin without leaving the host and
going through a soil phase again, thus providing a source of autoinfection(hyperinfection). This explains the heavy worm loads in some
individuals and also the persistence of infection (20 to 30 years) in persons
who have left endemic areas.
(ii) The rhabditiform larvae may be voided with the faeces and may undergo
development in the soil—Direct (host-soil-host) and Indirect cycle.
(a) I n d i r e c t ( h e t e r o g f . n k t ic ) D e v e lo p m e n t. The rhabditiform
larvae mature in course of 2 4 to 30 hours into free-living sexual generations,
males (0 .7 mm) and females (1 mm). Copulation between the sexes takes
place, resulting in the production of a second batch of rhabditiform larvae
which are indistinguishable from those produced by the parasitic females. In 3
to 4 days’ time, they are transformed into filariform larvae. Each pair from
the first batch o f rhabditiform larvae gives rise to 30 filariform larvae.
(b) D i r e c t D e v e lo pm e n t. In this type, the rhabditiform larvae directly
metamorphose, in 3 to 4 days’ time, into filariform larvae, the sexual phase
being omitted. In this cycle, each rhabditiform larva gives rise to only one
filariform larva. Filariform Larvae. These are longer and more slender than
the rhabditiform larvae. They have short mouths and cylindrical oesophagus.
They constitute the infective stage and enter the body of the human host
through the skin, in the same manner as ancylostomes. As already stated they
are developed in the following ways:(i) Metamorphosed in the human bowel
from the first batch o f rhabditiform larvae.(ii) Rhabditiform larvae voided
with the faeces directly metamorphosed into filariform larvae in the soil. It
occurs intemperate climates.
(iii) Rhabditiform larvae voided with faeces pass a sexual phase in the soil,
giving rise to a second batch of rhabditiform larvae from which filariform
larvae are developed. It occurs in moist tropical climates.
Life Cycle. No intermediate host is required. The worm passes its life cycle in
one host and unlike other nematodes, a change of host is not essential as it
undergoes a hyperinfective form of development. Man is the optimum host.
Mode o f Infection (Entrance into the Host). This occurs when a man walks
bare-foot on the faecally contaminated soil. The filariform larvae penetrate
directly through the skin coming in contact with the soil. Infecting Agent—
Filariform larvae. Portal of Entry—Skin. Site o f Localisation—Lungs,
intestine.
Migration and Localisation. The filariform larvae invade the tissues,
penetrate into the venous circulation and are carried "by the blood stream to
the right heart and then to the lungs. They leave the pulmonary capillaries
and enter the lung alveoli; they then migrate to the bronchi, trachea, larynx
and epiglottis, are swallowed back and enter the intestinal tract. On arrival
into the duodenum and jejunum, they develop into parasitic females and
possibly males. The parasitic females then burrow into the mucous membrane
and begin to oviposit in the tissues. The rhabditiform larvae hatch out
immediately and enter into lumen of the bowel. Parasitic males do not invade
the tissues and are therefore eliminated in the faeces. A parasitic female,
before penetrating, may possibly be fertilised by a parasitic male but as there
is no general agreement about the existence of parasitic males, the parasitic
females are considered to be parthenogenetic Immunology. After the first
primary infection an immunity develops which prevents reinfection and the
Strongyloides larvae and adult worms remain confined to the intestine and
tissue invasion is prevented. The immunity may be diminished in immunosuppressive states which reduce the resistance of the body, leading to an
extensive tissue
invasion by the adult worm. An infected individual when exposed to
reinfection responds by tissue hypersensitivity with eosinophilia and giant
urticaria. Serum antibody develops in strongyloidiasis and gives a cross
reaction with filarial complement fixation test. Pathogenicity. Infection with S.
stercoralis is known as strongyloidiasis. The following lesions may be
observed:1. Skin Lesions (2 types). An urticarial rash at the site of entry and a
linear, erythematous urticarial wheal around the anus caused by migrating
filariform larvae.
2. Pulmonary Lesions. Haemorrhages in the lung alveoli and
bronchopneumonia. These develop during migration of filariform larvae
through the lungs and form an avenue of escape into the alveoli. These areas
are often infiltrated with eosinophil cells.
3. Intestinal Lesions. Intractable diarrhoea with blood and mucus, produced
by the mechanical movements of the female parasites. Microscopically small
tunnels through which parasitic females have burrowed their ways may be
seen; congestion haemorrhages, round cell infiltration and desquamation of
epithelial cells are observed.
4. Blood Changes. A marked eosinophilia and a moderate leucocytosis during
the invasive stage. Note, Patients with Strongyloides infection when on
steroids or in immunosuppressive states (in AIDS patients) may develop
massive strongyloidiasis (hyperinfective syndrome) which then becomes a real
danger. Severe diarrhoea, malabsorption, paralytic ileus, peritonitis,
meningitis, brain abscess may occur in this hyperinfective condition.
Excessive internal reinfection may lead to increase in number of worms in the
intestine and lung and larvae in various tissues. Filariform larvae may act as
vehicles of microbial infection leading to Gram-negative bacteriaemia
(Woodruff, 1968). Effective prompt management with albendazole and other
measures may save the life of the patient.
Diagnosis. A specific diagnosis is based upon the finding of the typical
rhabditiform larvae in freshly passed stool. A high eosinophilia is often a
feature of strongyloidiasis. In pulmonary infection examination of the sputum
will
demonstrate the presence of rhabditiform larvae. In case of scanty larvae in
faeces, culture of faeces is helpful. Microscopical examination of duodenal
washing and material obtained from jejunal biopsies may reveal larvae of 5
stercoralis. C.F.T., I.H.A. & ELISA (75% positive) tests are used for diagnosis
of the disease.
Treatment. The specific anthelmintics for strongyloidiasis are thiabendazole,
albendazole, mebendazole'and ivermectin.
Prophylaxis. Same as those for hookworm infection.
Superfamily STRONGYLOIDEA. The peculiarities are as follows:
(i) Possesses a well developed mouth cavity (buccal capsule); may contain
teeth or cutting organs.
(ii) Male possesses a bursa (bursa copulatrix) which surrounds the cloaca.
(iii) Egg possesses a transparent shell and is hatched in a segmented condition.
The larva develops in moist earth.
The superfamily Strongyloidea is divided as follows.