General Introduction Parasitology

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INTRODUCTION

Medical parasitology deals with the parasites, which cause human infections and the diseases they produce.
 It is broadly divided into two parts:
- Protozoology
- Helminthology.
 The pioneer Dutch microscopist, Antonie 11an Leeuwenhoek of Holland in 1681, first introduced
single lens microscope and observed Giardia in his own stools.
 Louis Pastuer in 1870, first published scientific study on a protozoa( disease leading to its control
and prevention during investigation of an epidemic silk worm disease in South Europe.
 A seminal discovery was made in 1878 by Patrick Manson about the role of mosquitoes in filariasis.
This was the first evidence of vector transmission.
 Afterwards, Laveran in Algeria discovered the malarial parasite (1880), and Ronald Ross in
Secunderabad and Calcuna in India, showed its transmission by mosquitoes (1897). A large nwnber
of vector-borne disease have since then been identified.
 By mid 20th century, with dramatic advances in antibiotics and chemotherapy, insecticides and
antiparasitic drugs, and improved lifestyles, all infectious diseases seemed amenable to control.

PARASITES
Parasites are living organisms, which depend on a living host for their nourishment and survival. They
mulriply or undergo development in the host.
 The term "parasite" is usually applied to Protozoa (unicellular organisms) and Helminths
(multicellular organisms) (Flow chart 1).
 Parasites can also be classified as:
- Ectoparasite: Ectoparasites inhabit only the body surface of the host without penetrating the
tissue. Lice, ticks and mites are examples of ectoparasites. The term infestation is often employed
for parasitization with ectoparasites.
- Endoparasite: A parasite, which lives within the body of the host and is said to cause an infection
is called an endoparasite. Most of the protozoan and helminthic parasites causing human disease
are endoparasites.
- Free-living parasite: It refers to nonparasitic stages of active existence, which live independent of
the host, e.g. cystic stage of Naegleriafowleri.
 Endoparasites can further be classified as:
- Obligate parasite: The parasite, which cannot exist without a host, e.g. Toxoplasma gondii and
Plasmodium.
- Facultative para.site: Organism which may either live as parasitic form or as free-living form,
e.g. Naegleriafowleri.
- Accidental parasites: Parasites, which infect an unusual host are known as accidental parasites.
Echinococcus granulosus infects man accidentally, giving rise to hydatid cysts.
- Aberrant parasites: Parasites, which infect a host where they cannot develop further are known as
aberrant or wandering parasites, e.g. Toxocara canis (dog roundworm) infecting lhwnans.

HOST
Host is defined as an organism, which harbors the parasite and provides nourishment and shelter to
latter and is relatively larger than the parasite.
 The host may be of the following types:
- Definitive host: The host, in which the adult parasite lives and undergoes sexual reproduction is
called the definitive host, e.g. mosquito acts as definitive host in malaria.
- The definitive host may be a human or any other living being. However, in majority of human
parasitic infections, man is the definitive host (e.g. filaria, roundworm, hookworm).
- Intermediate host: The host, in which the larval stage of the parasite lives or asexual
multiplication takes place is called the intermediate host. In some parasites, two different
intermediate hosts may be required to complete different larval stages. These are known as first
and second intermediate hosts, respectively (Box 1).
- Paratenic host: A host, in which larval stage of the parasite remains viable without further
development is referred as a paratenic host. Such host transmits the infection to another host, e.g.
fish for plerocercoid larva of D. lalum. Reservoir host: In an endemic area, a parasitic infection is
continuously kept up by the presence of a host, which harbors the parasite and acts as an
important source of infection to other susceptible hosts, e.g. dog is the reservoir host of hydatid
disease.
- Accidental host: The host, in which the parasite is not usually found, e.g. man is an accidental
host for cystic echinococcosis.

ZOONOSIS
The word zoonosis was introduced by RudolfVirchow in 1880 to include the diseases shared in nature by
man and animals.
 Later, in 1959, the World Health Organization (WHO) defined wonosis as those diseases and
infeclions, which are naturally transmitted between vertebrate animals and man.
 It is of following types:
o Protozoal zoo noses, e.g. toxoplasmosis, leishmaniasis, balanlidiasis and cryptosporidiosis.
o Helminthic zoonoses, e.g. hydatid disease, taeniasis.
o Anthropozoonoses: Infections transmitted to man from lower vertebrate animals, e.g. cystic
echinococcosis.
o Zooanthroponoses: Infections transmitted from man to lower vertebrate animals, e.g. human
n1berculosis to cattle.

HOST-PARASITE RELATIONSHIPS
Host-parasite relationships are o f following types (Flow chart 2):
 Symbiosis
 Commensalism
 Parasitism.

LIFE CYCLE OF PARASITES


 Direct life cycle: When a parasite requires only single host to complete its development, it is called
as direct life cycle, e.g. Entamoeba histolytica requires only a human host to complete its life cycle
(Table 1).
 Indirect life cycle: When a parasite requires two or more species of host to complete its development,
the life cycle is called as indirect life cycle, e.g. malarial parasite requires both human host and
mosquito to complete its life cycle (Tables 2 and 3).

SOURCES OF INFECTION
 Contaminated soil and water:
- Soil polluted with embryonated eggs (roundworm, whipworm) may be ingested or infected
larvae in soil, may penetrate exposed skin (hookworm).
- lnfeclive forms of parasites present in water may be ingested (cyst of ameba and Giardia).
- Water containing the intermediate host may be swallowed (cyclops containing guinea worm
larva).
- Infected larvae in water may enter by penetrating exposed skin (cercariae of schisotosomes).
- Free-living parasites in water may directly enter through vulnerable sites (Naegleria may enter
through nasopharynx).
 Food:
- Ingestion of contaminated food or vegetables conraining infeclive stage of parasite (amebic cysts,
Toxoplasma oocysts, Echinococcus eggs).
- Ingestion of raw or undercooked meat harboring infeclive larvae (measly pork containing
cysticercus cellulosae, the larval stage of Taenia solium).
 Vectors:
A vector is an agent, usually an arthropod that transmits an infection from man to man or from other
animals to man, e.g. female Anopheles is the vector of malarial parasite. Vectors can be:
o Biological vectors: The term biological vector refers to a vector, which not only assists in the
transfer of parasites but the parasites undergo development or multiplicaLion in their body as
well. They are also called as true vectors. Example of true vectors are:
• Mosquito: Malaria, filariasis
• Sandflies: Kala-azar
• Tsetse flies: Sleeping sickness
• Reduviicl bugs: Chagas disease
• Ticks: Babesiosis.
o Mechanical vectors: The term mechanical vector refers to a vector, which assists in the
transfer of parasitic form between hosts but is not essential in the life cycle of the parasite.
Example of mechanical vectors is:
• Housefly: Amebiasis
In 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
infecLion only after the parasite multiplies to a certain level or undergoes a
developmental process in its body. This interval between the entry of the parasite into
the vector and the Lime it takes to become capable of transmitting the infection is
called the extrinsic incubation period.
• Animals:
 Domestic:
o Cow, e.g. T. saginata, Sarcocystis
o Pig, e.g. T. solium, Trichinella spiralis
o Dog, e.g. Echinococcus granulosus
o Cat, e.g. Toxoplasma, Opisthorchis.
Wild:
o Wild game animals, e.g. trypanosomiasis
o Wild felines, e.g. Paragonimus westermani
o Fish, e.g. fish tapeworm
o Molluscs, e.g. liver flukes
o Copepods, e.g. guinea worm.
• Carrier: A person who is infected with parasite without any clinical or subclinical
disease is known as carrier. He can transmit parasite to others. For example, all
anthroponotic infections, vertical transmission of congenital infections.
• Self(autoinfection) (Box 2): Finger-to-mouth transmission, e.g. pinworm Internal
reinfection, e.g. Strongyloides.
MODES OF INFECTION
 Oral transmission: The most common method of transmission is through oral route by 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 E. histolytica and
other intestinal protozoa occurs when the infective cysts are swallowed.
 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.
 Vector transmission: Many parasitic diseases are transmitted by insect bite, e.g. malaria is
transmitted by bite offemale Anopheles mosquito, filariasis is transmitted by bite of Culex mosquito.
A vector could be a biological vector or a mechanical vector.
 Direct transmission: Parasitic infection may be transmitted by person-to-person contact in some
cases, e.g. by kissing in the case of gingivaJ amebae and by sexual intercourse in trichomoniasis.
 Vertical transmission: Mother to fetus transmission may take place in malaria and toxoplasmosis.
 Iatrogenic transmission: It is seen in case of transfusion malaria and toxoplasmosis after organ
transplantation.

PATHOGENESIS
Parasitic infections may remain inapparcnt or give rise to clinical disease. A few organisms, such as E.
histolytica may live as surface cornmensals, without invading the tissue.
 Clinical infection produced by parasite may take many forms: acute, subacute, chronic, latent, or
recurrent.
 Pathogenic mechanisms, which can occur in parasitic infections are:
- Lytic necrosis: Enzymes produced by some parasite can cause lyric necrosis. E. histolylica
lyses intestinal cells and produces amebic ulcers.
- Trauma: Attachment of hookworms on jejunal mucosa leads to traumatic damage of villi and
bleeding at the site of attachment.
- Allergic manifestations: Clinical illness may be caused by host immune response to parasitic
infection, e.g. eosinophilic pneumonia in Ascaris infection and anaphylactic shock in rupture
ofhydatid cyst.
- Physical obstruction: Masses of roundworm cause intestinal obstruction. Plasmodium
falciparum malaria may produce blockage of brain capillaries in cerebral malaria.
- inflammatory reaction: Clinical illness may be caused by inflammatory changes and
consequent fibrosis, e.g. lymphadenitis in filariasis and urinary bladder granuloma in
Schistosoma haemalobium infection.
- Neoplasia: A few parasitic infection have been shown to lead to malignancy. The liver fluke,
Clonorchis may induce bile duct carcinoma, and S. haematobium may cause urinary bladder
cancer.
- Space occupying lesions: Some parasites produce cystic lesion that may compress the
surrounding tissue or organ, e.g. hydatid cyst.

IMMUNITY IN PARASITIC INFECTION


Like other infectious agents, parasites also elicit immunoresponses in the host, both humoral as well
as cellular (Fig. 1). But immunological protection against parasitic infections is much less efficient, than it is
against bacterial or viral infections. Several factors may contribute LO this:
 Compared to bacteria and viruses, parasites are enormously larger or more complex structurally and
antigenically, so that immune system may not be able to focus attack on the protective anrigens.
 Many protozoan parasites arc intracellular in location, and this protects them from immunological
attack. Several protozoa and helminths live inside body cavities. 1h.is location limits the efficiency
of immunological attack.
 Once the parasitic infection is completely eliminated, the host becomes again susceptible to
reinfection. This type of immunity to reinfection is dependent on the continued presence ofresidual
parasite population and is known as "premunition".
 Antibodies belonging to different immunoglobulin classes are produced in response to parasitic
infections. Selective tests for immunoglobulin M (IgM) are helpful in differentiating current
infections from old infections. Excessive IgE response occurs in helminthiasis. A characteristic
cellular response in helminth parasite is eosinophilia both local and systemic {Fig. 1).
 Parasites have evolved to be closely adapted to the host and most parasitic infections are chronic and
show a degree of host specificity. For example, malarial parasites of human, bird and rodents are
confined to their own particular species.
 Parasites like trypanosomes exhibit antigenic variation within the host. This genetic switch protects
them from antibodies. Similar mechanism may be operative in the recrudescences in human malaria
(Box 3).
 Some parasites adopt antigenic disguise. Their surface antigens are so closely similar to host
components that they are not recognized as foreign by the immune system.
 Some infections may produce immunodeficiency due to extensive damage to the reticuloendothelial
system, as in case of visceral leishmaniasis.
The fact that immunity normally plays an important role in the containment of parasitic infections is
illustrated by the florid manifestations caused by opportunistic parasites such as Pneumocystis jirovecii and
T. gondii, when the immune response is inadequate as in acquired immunodeficiency syndrome (AIDS) and
other immunodeficiencies.

IMMUNE EVASION
All animal pathogens, including parasitic protozoa and worms have evolved effective mechanism to avoid
elimination by the host defense system as described in Table 4.

VACCINATION
No effective vaccine for humans has so far been developed against parasites due to their complex life cycles,
adaptive responses and antigenic variation, great progress has been

LABORATORY DIAGNOSIS
Most of the parasitic infection cannot be conclusively diagnosed. On the basis of clinical features and
physical examination laboratory diagnosis depends upon:
 Microscopy
 Culture
 Serological test
 Skin test
 Molecular method
 Animal inocuJation
 Xenodiagnosis
 Imaging . Hematology
Microscopy
An appropriate clinical specimen should be collected for definitive diagnosis of parasitic infections.
 Following specimens are usually examined to establish a diagnosis: Stool Blood Urine Sputum
Cerebrospinal fluid (CSF) Tissue and aspirates
- Stool
- Blood
- Urine
- Sputum
- Cerebrospinal fluid (CSF)
- Tissue and aspirates
- Genital specimens.
Stool Examination
Examination of stool is very important for the detection of intestinal infections like Giardia, Enlamoeba,
Ascaris, Ancylostoma, etc. Cysts and lrophozoites of E. histolytica, C. lamblia can be demonstrated in feces.
Eggs of roundworm and tapeworm are also found in stool. The larvae are found in the feces in S. slercoralis
infection (Table 5). For further details, refer to Chapter 23.
Blood Examination
Examination of blood is of vital importance for demonstrating parasites which circuJate in blood vessels
(Table 6). Malarial parasite is confirmed by demonstration of its morphological stages in the blood.
Urine Examination
The characteristic lateral-spined eggs of S. haematobium and trophozoites of T. vagina/is can be detected in
urine. Microfilaria of W bancrofti are often demonstrated in the chylous urine (Box 4).
Sputum Examination
lhe eggs of P. westermani are commonly demonstrated in the sputum specimen. Occasionally, larvaJ stages
of S. s/ercoralis and A. lumbricoides may also be found in sputum.
Cerebrospinal Fluid Examination
Some protozoa like T. brucei, Naegleria, Acanthamoeba, Balamulhia and Angiostrongylus can be
demonslrated in the CSF.
Tissue and Aspirates Examination
The larvae of Trichinella and eggs of Schistosoma can be demonstrated in the muscle biopsy specimens. By
histopathological examination of brain, Naegleria and Acanthamoeba can be detected. In kala-azar,
LeishmanDonovan (LO) bodies can be demonstrated in spleen and bone marrow aspirate. Trophozoites of
Giardia can be demonstrated in intestinal aspirates. Trophozoites of E. histolytica can be detected in liver
pus in cases of amebic liver abscess.
Genital Specimen Examination
Trophozoites of T. vagina.Lis are found in the vaginal and urethral discharge. Eggs of E. vermicularis are
found in anal swabs.
Culture
Some parasites like Leishmania, Entamoeba and Trypanosoma can be cultured in L he laboratory in various
axenic and polyxenic media.
Serological Tests
Serological tests are helpful for the detection and surveillance of many protozoa! and helminthic infections.
These tests are basically of two types:
 Tests for antigen detection
Malaria antigen like P. falciparum lactate dehydrogenase (pLDI I) and histidine-rich protein 2 (HRP-
2) are detected by rapid immunochromatographic test. Filarial antigens are detected in current
infection by enzyme-linked immunosorbcnt assay (ELISA) (Table 7).
 Tests for antibody detection.
The following antibody detection procedures are useful in detecting various parasitic infections like
amebiasis, echinococcosis and leishmaniasis in man:
- Complement fixation test ( CFT)
- Indirect hemagglutination (IHA)
- Indirect immunofluoresccnt antibody (IFA) test
- Rapid immunochromatographic test (ICT)
- Enzyme-linked immunosorbent assay test (ELISA).
Skin Test
Skin tests are performed by injecting parasitic an tigen intradermally and observing the reaction. In
immediate hypersensitivity reaction, wheal and flare response is seen within 30 minutes of infection,
whereas erythema and in duration seen after 48 hours of injection is called as delayed hypersensitivity
reaction (Box 5).
Molecular Diagnosis
Molecular methods most frequently used to diagnose human parasitic infection are deoxyribonucleic acid
(ONA) probes, polymerase chain reaction (PCR) and microarray technique. 1hese tests are very sensitive
and specific.
Animal Inoculation
It is useful for the detection of Toxoplasma, Trypanosoma and Babesia from the blood and other specimens.
Xenodiagnosis
Some parasitic infection like Chagas disease caused by T. cruzi can be diagnosed by feeding the larvae of
reduviid bugs with patient's blood and then detection of amastigotes of T. cruzi in their feces.
Imaging
Imaging procedures like X-ray, ulcrasonography (USG), computed tomography (CT) scan and magnetic
resonance imaging (MRI) are now being extensively used for diagnosing various parasitic infections like
neurocysticercosis and hydatid cyst disease.
Hematology
Anemia is frequently seen in hookworm infection and malaria. Eosinophilia is frequently present in
helminthic infections. HypergammaglobuJinemia occurs in visceral leishmaniasis. Leukocytosis is seen in
am ebic liver abscess.

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