Download Ascaris lumbricoides

Lac.4
biology 1 stage
The Round worm (nematodes)
The nematodes characteristics:
1- The nematodes are cylindrical shape hence the common name round
2- The body wall is consist of three layer: outer cuticle, thin hypodermis
musculature.
worm.
and
3- The cuticle in some species has longitudinal modifications called alae
4- The alimentary canal of round worm is complete, with both mouth and
mouth is surrounded by lips bearing sensory papillae.
anus.The
5- Nematodes are usually bisexual. Males are usually smaller than
females.
The males have a curved posterior end, and posses (in some
species) copulatory
structures, such as spicules (usually two) and
bursa, or both.
Genus:Ascaris
Ascaris lumbricoides
Ascaris lumbricoides , common saying “round worm of man”, is the largest of the
intestinal nematodes parasitizing humans. It is the most common worm found in
human. It is worldwide in distribution and most prevalent through out the tropics, subtropics and more prevalent in the countryside than in the city
Morphology:
1. Adult: The adults are cylindrical in shape, creamy-white or pinkish in color.
The female averages 20-35cm in length, the largest 49cm. The male is smaller,
averaging 15-31cm in length and distinctly more slender than the female.
2. The lips of Ascaris lumbricoides:
The three lips are seen at the anterior end. The margin of each lip is lined with
minute teeth.
Egg: There are three kinds of the eggs. They are fertilized eggs, unfertilized
eggs and decorticated eggs. We usually describe an egg in 5 aspects: size,
color, shape, shell and content.
a. Fertilized eggs: broad oval in shape, brown in color, an average size 60×
45µm. The shell is thicker and consists of ascaroside, chitinous layer,
fertilizing membrane and mammillated albuminous coat stained brown by
bile. The content is a fertilized ovum. There is a new-moon(crescent) shaped
clear space at the each end inside the shell.
b. Unfertilized egg: Longer and slender than a fertilized egg. The chitinous layer
and albuminous coat are thinner than those of the fertilized eggs without ascaroside
and fertilizing membrane. The content is made of many refractable granules various
in size.
c. Decorticated eggs: Both fertilized and unfertilized eggs sometimes may lack
their outer albuminous coats and are colorless which are not visible at this
magnification.
Life Cycle:
 Site of inhabitation: small intestine
2. Infetive stage: embryonated eggs
3. Route of infection: by mouth
4. No intermediate and reservoir hosts
5. Life span of the adult: about 1 year
This worm lives in the lumen of small intestine, feeding on the intestinal
contents, where the fertilized female lays eggs. An adult female can produce
approximately 240,000 eggs per day, which are passed in feces. When passed, the
eggs are unsegmented and require outside development of about three weeks until a
motile embryo is formed within the egg.
After the ingestion of embryonated eggs in contaminated food or drink or from
contaminated fingers, host digestive juices acts on the egg shell and liberate the larva
into the small intestine. These larvae penetrate the intestinal mucosa and enter
lymphatics and mesenteric vessels. They are carried by circulation to the liver, right
heart and finally to the lungs where they penetrate the capillaries into the alveoli in
which they molt twice and stay for 10-14days and then they are carried, or migrate, up
the bronchioles, bronchi, and trachea to the epiglottis. When swallowed, the larvae
pass down into the small intestine where they develop into adults. The time from the
ingestion of embryonated eggs to oviposition by the females is about 60-75 days. The
adult worms live for about one year. The ascarid life cycle is as the following
diagram.
Pathogenesis:
There are two phase in ascariasis:
1. The blood-lung migration phase of the larvae: During the migration through
the lungs, the larvae may cause a pneumonia. The symptoms of the pneumonia are
low fever, cough, blood-tinged sputum, asthma. Large numbers of worms may give
rise to allergic symptoms. Eosionophilia is generally present. These clinical
manifestation is also called Loeffler’s syndrome.
2. The intestinal phase of the adults. The presence of a few adult worms in the lumen
of the small intestine usually produces no symptoms, but may give rise to vague
abdominal pains or intermittent colic, especially in children. A heavy worm burden
can result in malnutrition. More serious manifestations have been observed.
Wandering adults may block the appendical lumen or the common bile duct and even
perforate the intestinal wall. Thus complications of ascariasis, such as intestinal
obstruction, appendicitis, biliary ascariasis, perforation of the intestine, cholecystitis,
pancreatitis and peritonitis, etc., may occur, in which biliary ascariasis is the most
common complication
Diagnosis:
 The symptoms and signs are for reference only. The confirmative diagnosis
depends on the recovery and identification of the worm or its egg.
1. Ascaris pneumonitis: examination of sputum for Ascaris larvae is sometimes
successful.
2. Intestinal ascariasis: feces are examined for the ascaris eggs.
(1) direct fecal film: it is simple and effective. The eggs are easily found using
this way due to a large number of the female oviposition, approximately 240,000 eggs
per worm per day. So this method is the first choice.
(2) brine-floatation method:
(3) recovery of adult worms: when adults or adolescents are found in feces or
vomit and tissues and organs from the human infected with ascarids , the diagnosis
may be defined.
Epidemiology:
 World wide distribution, very common in China, especially in the
countryside.
Factors favoring the spread of the transmission:
1. Simple life cycle.
2. Enormous egg production ( 240,000 eggs/ day/ female ).
3. These eggs are highly resistant to ordinary
The eggs may remain viable for several years.
disinfectants( due to the ascroside).
4. Social customs and living habits.
5. Disposal of feces is unsuitable.
Prevention and Treatment:
1.Treatment to ascariasis:Mebendazole, Albendazole and Levamizole are
effective.
2.Sanitary disposal of feces.
3.Hygienic habits such as cleaning of hands before meals.
4.Health education.
Genus: Ancylostoma
Ancylostoma caninum
Ancylostoma caninum is a species of nematode which principally infects the small
intestine of dogs. The result of A. caninum infection ranges from asymptomatic cases
to death of the dog; better nourishment, increasing age, prior A. caninum exposure
or vaccination are all linked to improved survival. Other hosts include carnivores such
as wolves, foxes and cats with a small number of cases having been reported in
humans.
Morphology:
A. caninum females are typically longer the males. On males a copulatory
bursa exists which, during copulation, attaches the female via ~0.9 mm long spinelike spicules positioned on three muscular rays. As with other nematodes, the sperm
lack flagella. The copulatory bursa is a unique feature of Strongylida members, thus
making it a useful means for identifying members of this suborder; it is also used to
distinguish members within the suborder due to differences in bursa appearance
between species. The vulva of A. caninum females is located at the boundary of the
second and final thirds of the body.
The teeth of A. caninum are found in the buccal capsule and divided into three
sets. Two ventral sets form a lower-jaw equivalent, while a further set projects from
the dorsal side and loosely equates to an upper-jaw. Each ventral set has three points
with those furthest to the sides being the largest. While the ventral sets are prominent,
the dorsal set is hidden deeper in the buccal capsule.
Eggs are laid by the females typically when at the 8-cell stage. Eggs are thin walls.
Life Cycle:
Transmission via the Environment
Eggs are excreted from host in the feces and typically hatch within a day on moist,
warm soil giving larvae with a non-living cuticle layer. By four or five days the larvae
havemoulted twice and are now able to infect a host. Migration occurs from the faeces
into the surrounding soil. Two routes of infection from the environment exist. The
first route involves penetration of skin at hair follicles or sweat glands, especially
between the footpads where contact with soil is frequent and the skin is thinner than
otherwise. Secretion of a protease by A. caninum is thought to aid this process. The
larvae then migrate through the dermis of the skin, enter the circulatory system and
are carried to the lungs. A. caninum larvae exit the blood at the lungs, move from
the alveoli up through the trachea and are swallowed to end up in the intestine.
The second and more common route to the small intestine is by direct ingestion of A.
caninum by the host, but the subsequent process is identical in either case. It is during
this third stage of the larva that male or female reproductive organs become
established. Larvae of this stage have been shown to secrete a molecule (Ac-asp-2)
related tovenom allergens in response to host-specific signals; this is thought to have a
possible role in helping with the infection process. A third and final moulting occurs
to give the mature form of A. caninum which then feeds on mucosa and blood of the
small intestine wall. The trigger of feeding is understood to be a receptor-mediated
response, however the detail of this process has yet to be established. Sexual
reproduction also occurs in the intestine to give a further round of eggs to complete
the cycle. Females are thought to produce a pheromone which attracts males and are
able to produce approximately 10,000 eggs per day.
Direct transmission
It is also possible for direct transmission between hosts. Larvae having accessed
through the skin may avoid exit via the lungs and remain in circulation for transport
around the body. At the uterine artery of a pregnant female the larvae are able to cross
the placenta to cause pre-natal infection of foetuses. Larvae of an infected foetus will
move to theliver until birth at which point migration continues with movement to the
intestine via the circulation and lungs as previously described. Alternatively A.
caninum larvae evading exit from the circulation at the lungs may instead be carried
to the mammary glands and transmitted from the mother in her colostrum or milk to
her pups; infection then proceeds in an identical manner to infection by ingestion
from the environment. Infected bitches have been found to only rarely give prenatal
transmission to pups while the likelihood of nursing of pups causing transmission (via
the lactational route) is much higher.
Pathogenesis:
1. Damage during migration to intestine
Ancylostomum caninum larvae cause damage to the host at the point of entry through
the skin leaving a wound vulnerable to secondary infections. As the larvae migrate
through the skin an inflammatory response, dermatitis, is often stimulated which can
be exacerbated in hosts which give hypersensitive responses. Further damage is
caused when the larvae leave the circulation and enter the lung with the amount of
damage dependent on the extent of the infection; pneumonia and coughing are
common consequences.
2. Damage once in intestine
Once in the gut A. caninum attaches to and ingests the mucosal lining along with
some consumption of blood. In a 24hr period A. caninum typically feeds from six
sites. This damage to the mucosa compromises the body’s defences and can result in
secondary infections by microbes. A group of anticoagulant proteins called AcAPs (A.
caninum anticoagulant proteins) which inhibit a range of blood coagulation
factors such as Xa are utilised by A. caninum to help in the feeding process by
preventing clotting and increasing blood loss. These AcAPs are among the most
powerful natural anticoagulants that exist and are a key reason for anemia being
caused and blood being observed in the faeces of infected hosts. Blood losses peak
just prior to egg production by the females because this is when their requirements for
food are greatest; the amount that they are eating is also peaking and so maximal
damage to the intestine is being caused.
Diagnosis
1. Analysis of faeces is the definitive method by which a suspected A.
caninum infection is confirmed. The faeces are sampled and the characteristic
ovular, thin-shelled eggs ofA. caninum looked for. Absence of eggs in faeces
does not rule out infection; a significant delay of at least 5 weeks exists
between initial infection and excretion of eggs in the faeces (larvae must fully
mature and reproduce before eggs can be laid).
2. Signs and symptoms expected to be observed together with A. caninum eggs
in the faeces are lethargy, weight loss, weakness, roughness of the hair coat
and pale mucous membranes indicative of anemia. Well-fed, older dogs with
smaller infestations may present few or even none of these
symptoms. Diarrhoea is rare but stools are typically black due to the bloodderived haemoglobin present in them.
Prevention and Control
1. A clean environment minimises the risk of A. caninum infection; this can
include regularly washed concrete or gravel in kennels instead of soil.
2.
Bitches are typically checked prior to using them for breeding purposes for
nematodes such as A. caninum and birth and sucklingcan be restricted to
sanitised areas to lower the risk of health complications to the pups.
3. When
infection
of
a
pregnant
bitch
is
known
or
suspected fenbendazole or ivermectin can be administered to the bitch to help
avoid transmission to the pups.