General Introduction
General Introduction
General Introduction
College of Medicine
Department of Microbiology and Parasitology
2021-2022
Dr. Rasha Khalil Abd Aljalil
Ph.D. Parasitology Lecture: 1
General Introduction
The earliest agents of human infection to have been observed were helminthic parasite
Whip worm eggs were identified in the colonic contents.
In more recent times,parasites have figured in various milestones along the stor of infectious
disease. The first description of a human pathogenic microbe was given by the pioneer
microscopist Leeuwenhoek in 1681, when he observed Giardia in his own stools and
communicated to the Royal Society of London,
With the coming of colonialism, interest in parasitic diseases suddenly soared as many of the
tropical countries could be penetrated only after controlling parasitic infections like malaria,
kala-azar, amoebiasis, trypanosomiasis and schistosomiasis.
Their aetiological agents were identified and control measures introduced.
discovery was made in 1878 by Patrick Manson about the role of mosquitoes in filariasis.
This was the first evidence of vector transmission.
Soon afterwards, Laveran in Algeria discovered the malarial parasite (1880) and Ronald
Ross in India showed its transmission by mosquitoes (1897). A large number of vector
borne diseases have since been identified.
This provided a new approach to disease control, by targeting the vectors.
Many parasitic infections are associated with overcrowding, poor sanitation, contaminated
food and water, under nutrition and other poverty-related factors.
A major drawback in the fight against parasitic diseases is the inability to prevent
them by immunisation. No effective vaccine is currently available against any parasitic
disease. However, host immunity is decisive in determining the course of many parasitic
infections.
Parasitology :The science which deals with the study of parasites .
The parasites : An organism which lives in or on another organism( host ) .
The host : The organism which harbours the parasite .
Symbioses : Is the relationship between the host and the parasite .
Types of symbiosis:
1-Mutualism:close relationship in which the parasite and the host depend on each other to
survive.
It's beneficial for both of them. E.g: termites, wood roaches.
2-Commensalism: it's beneficial for the parasite, at the same time it's harmless for the host.
E.g.:E.coli(in large intestine).
3-Parasitism: the parasite harmful to the host. E.g.: E. histolytica.
Form the medical point of view the parasites are classified into four major phylum:
1-protozoa 2-Helminths 3-Arthropods 4-Snails
PARASITISM
Medical parasitology deals with the parasites which cause human infections and the
diseases they produce.
They multiply or undergo development in the host. Parasitism arose early in the course of
biological evolution. Some organisms, instead of remaining as free-living forms deriving
nourishment from raw materials in the environment,
learned to use the bodies of other organisms as readymade food. One manner of
achieving this is by predation, where larger animals prey on smaller ones which they
kill and eat.
Parasitism is a more durable and intimate association in which the parasite establishes itself
in or on the living body of the host, being physically and physiologically dependent on it for
at least part of its life cycle.
This may or may not lead to disease in the host. Parasites which live in complete harmony
with the host, without causing any damage to it are called commensals, while those which
cause disease are called pathogens. This distinction is however not absolute, as many
commensals can act as facultative or opportunist pathogens when the host resistance is
lowered.
Rarely, even free-living organisms may become pathogenic under special circumstances.
The discipline of parasitology, by tradition deals only with parasites belonging
to the animal kingdom. Though bacteria, fungi and viruses are also parasitic, they are
excluded from the purview of ‘parasitology.’ Human parasites may be either
unicellular microbes (protozoa), or larger organisms (metazoa), some of which may
be many metres in size.
Parasites may pass their life cycles in more than one host. The host in which the adult stage
lives or the sexual mode of reproduction takes place is called the definitive host.
The species in which the larval stage of the parasite lives or the asexual multiplication takes
place is called the intermediate host.
A vertebrate host in which a parasite merely remains viable without development or
multiplication is called a paratenic host.
Parasitic infections which humans acquire from animals are known as zoonotic
infections or zoonoses. In most of these, the parasite lives normally in cycles involving
domestic or wild animals, domestic zoonoses and feral or sylvatic zoonoses respectively
without affecting humans.
The term anthroponoses has been applied for infections with parasitic species that
are maintained in humans alone. Malaria and filariasis are exampIes. The term
zooanthroponoses refers to infections in which human is not merely an incidental host, but
an essential link in the life cycle of the parasite. Beef and pork tapeworms are examples of
zooanthroponoses.
Modes of Infection
Oral Transmission
The most common method of transmission is oral, through contaminated food, water,
soiled fingers or fomites. Many intestinal parasites enter the body in this manner,
the infective stages being cysts, embryonated eggs or larval forms. Infection with
Entamoeba histolytica and other intestinal protozoa occurs when the infective cysts
are swallowed. In most intestinal nematodes, such as the roundworm. whipworm
or pinworm, the embryonated egg which is the infective form is swallowed. In trichinellosis
and in beef, pork and fish tapeworm, infection occurs by ingestion of flesh containing
the mature larval stages. Infection with the tissue nematode guinea worm follows
consumption of water containing its arthropod host cyclops carrying infective larvae.
Skin Transmission
Entry through skin is another important mode of transmission. Hookworm infection
is acquired when the larvae enter the skin of persons walking barefooted on contaminated
soil. Schistosomiasis is acquired when the cercarial larvae in water penetrate
the skin. Many parasitic diseases, including malaria and filariasis are transmitted
by blood sucking arthropods. Arthropods which transmit infection are called vectors.
Vector Transmission
Parasites undergo development or multiplication in the body of true vectors, which
are called biological vectors. Some arthropods may transmit infective parasites
mechanically
or passively without the parasites multiplying or undergoing development in them.
For example, the housefly may passively carry amoebic cysts from faeces
to food. Such vectors which act only as passive transmitters are called mechanical
vectors. In the case of a mechanical vector there need be no delay between picking
up a parasite and transferring it to a host. A housefly picking up amoebic cysts from
feces can within seconds transfer the cysts by landing on food being eaten by a person,
who may thereby get infected. But in the case of biological vectors. A certain
period has to elapse after the parasite enters the vector before it becomes infective.
This is necessary because the vector can transmit the infection only after the parasite
multiplies to a certain level or undergoes a developmental process in its body.
Direct Transmission
Parasitic infection may be transmitted by person-to-person contact in some cases;
by kissing in the case of Amoebae gingivaly and by sexual intercourse in trichomoniasis.
Inhalation of air-borne eggs may be one of the methods of transmission of pinworm
infection. Congenital infection (vertical transmission) may take place in malaria and
toxoplasmosis. Iatrogenic infection may occur as in transfusion malaria and toxoplasmosis
after organ transplantation.
Course of Infection
Following its establishment in the host, the parasite has to multiply or undergo
development before the infection is manifested either biologically or clinically. The
interval of time between the initial infection and the earliest appearance of the parasite
or its products in the blood or secretions is called the biological incubation period or
prepatent period. The prepatent period in malaria is about a week; in filariasis it is
a year or more. When the parasite becomes demonstrable and the host is potentially
infectious to others, the infection is said to be patent. Clinical incubation period,which
is the interval between the initial infection and the onset of the first evidence of
clinical disease is usually longer than the biological incubation period.
PATHOGENESIS
Parasitic infections may remain inapparent or give rise to clinical disease. A few,
such as Entamoeba histolytica may live as surface commensals, multiplying in the 1umen
of the gut for long periods without invading the tissues. Some parasites may lead
to completely asymptomatic infection even though they live inside tissues. Many
persons with filarial infection may not develop any clinical illness though microfilariae
are demonstrable in their blood. Clinical infection produced by parasites may take
many forms—acute, subacute, chronic, latent or recurrent. Some of the pathogenic
mechanisms in parasitic infections are as follows:
Intracellular protozoa can damage and destroy the cells in which they multiply.
Malarial parasites rupture the infected erythrocytes causing anaemia as a long-term
effect and fever as the immediate response.
Enzymes produced by some parasites can induce lytic necrosis. E. histolytica lyses
intestinal cells, enabling it to penetrate the gut wall and produce abscesses and ulcers.
Damage may be due to physical obstruction. Masses of roundworms cause intestinal
obstruction. Even a single worm can cause damage when it blocks the appendix or bile duct.
Hydatid cysts cause illness due to pressure on surrounding tissues.
Parasites in vulnerable sites such as brain and eyes may produce serious damage bypressure.
Physical obstruction may sometimes cause severe secondary effects.
Falciparum malaria may produce blockage of brain capillaries leading to fatal
cerebral malaria.
Clinical disease may sometimes be due to trauma inflicted by parasites.
Hookworms feeding on jejunal mucosa leave numerous bleeding points which ultimately
lead to anaemia. Migration of helminth larvae through the lungs may rupture many
pulmonary capillaries and cause considerable extravasation of blood.
Schistosome eggs with their hooks tear vesical blood vessels and produce haematuria.
Roundworms may perforate the intestine and cause peritonitis.
Clinical illness may be caused by host response to parasitic infection. This may be due to
inflammatory changes and consequent fibrosis, as in the case of filariasis
in which it leads ultimately to lymphatic obstruction and oedema. Host response may also be
hypersensitive or allergic. Fatal anaphylactic shock may occasionally be caused by escape of
hydatid fluid from the cyst.
A few parasitic infections have been shown to lead to malignancy. The liver flukes
Clonorchis and Opisthorchis may induce bile duct carcinoma and Schistosoma
haematobium may pave the way for bladder cancer.
IMMUNITY IN PARASITIC INFECTIONS
Like other infectious agents, parasites also elicit immune responses in the host, both
Humoral as well as cellular. But immunological protection against parasitic infections
is much less efficient than it is against bacterial and viral infections.
Several factors may contribute to this. Compared to bacteria and viruses, parasites are
enormously larger and more complex structurally and antigenically so that the immune
system may not be able to focus attack on the protective antigens.
Many protozoan parasites are intracellular in location and this protects them from
immunological attack. Several parasites, both protozoa and helminths live inside body
cavities as in the intestines. This location limits the efficiency of immunological attack and
also facilitates dispersal of the infective forms.
Secretory IgA which is so effective against luminal virus infections does not appear to play
an important role in defence against parasites.
Some parasites live within cysts whose capsules are partly composed of host tissues. In this
location they are safe from immunological attack.
Trypanosomes causing sleeping sickness exhibit antigenic variation within the host.
When antibody response to one antigenic form reaches high levels, a genetic switch causes a
new set of antigens to appear, which are unaffected by the antibodies present.
This enables the prolonged persistence of the parasites in the host. A similar mechanism may
be operative in the recrudescences in human malaria.
Some parasites adopt antigenic disguise. Their surface antigens are so closely similar to
some host components that they are not recognised as foreign by the immune system.
Many nematodes have a cuticle which is antigenically inert and evokes little immune
response. Immunological tolerance is established in some parasitic infections. Some
infections may produce immunodeficiency due to extensive damage to the reticulo
endothelial system, as for example in visceral leishmaniasis.
Unlike in other microbial infections, complete elimination of the infecting agent
followed by immunity to reinfection is seldom seen in parasitic infections.
Though no vaccine is as yet available for any parasitic disease.