Reading material for Basic Mechanisms of Diseases/S.

Wahyuni/Department of Parasitology/
Medical Faculty, Hasanuddin University/2009

HOST PARASITE RELATIONSHIP

A parasite may live in or on the tissues of its host without causing evident harm, and in some
instances the relationship may be mutually advantageous; but in a majority of cases the parasite
has the capacity to produce damage. Tissue repair may take place as rapidly as its destruction, in
which circumstance the host is referred to as a carrier , at times without demonstrable symptoms.
Under other conditions, and invariably in some parasitoses, the damage is considerable, resulting
in varying degrees of disease. The parasite is then designated as a pathogen.
The dynamics of any disease process is its pathogenesis. The lesion may be localized at
the site where the parasite has become established or it may extend to distant parts of the host's
body. The ways in which damage may be produced include the following: trauma or physical
damage, lytic necrosis, stimulation of host-tissue reactions, toxic and allergic phenomena, and
the opening of pathways for entry of other pathogens into the tissues.
Traumatic Damage
This occurs when the parasite invades the skin, as in the case of the scabic mite (Sarcoptes
scabiei) and of several species of fly maggots, or even as a result of the puncture wound made
by a tick. Relatively slight physical damage is produced by entry of hookworm or blood-fluke
larvas into the skin, or the usually minute skin lesion made by a mosquito. Internally, during the
migration of larval stages of several helminths through the lungs there is rupture of the pulmonary
capillaries, which may cause appreciable extravasation of blood if many organisms are in
migration simultaneously. Similar damage in the cerebral, retinal or renal capillaries may
precipitate serious, even fatal damage. Eggs of Schistosoma spp. cause extensive trauma with
hemorrhage as they escape from mesenteric or vesical venules, respectively, into the intestinal
canal or the lumen of the urinary bladder. Moreover, the attachment of hookworms to the
intestinal wall invariably results in traumatic destruction of the villi. Large worms such as Ascaris
or Tania saginata may produce acute intestinal obstruction, while Ascaris may occlude the lumen
of the appendix, the common bile duct, may cause perforation of the intestinal wall or may
penetrate into the parenchyma of the liver and even of the lungs.
Lytic Necrosis.
Enzymes elaborated by many parasites make it possible for them to digest available food in the
immediate environment and to transform this nutriment into their own protoplasm or to store it for
the production of energy. One of the most striking examples of tissue digestion and necrosis is
that of Entamoeba histolytica, which not only lyses tissues for nutritional needs but also as a
means of penetration into tissues of the colon and extra-intestinal viscera. Several species of
protozoa which are obligate intracellular parasites (e.g., plasmodia, leishmanias, Trypanosoma
cruzi, Toxoplasma gondii) cause necrosis of the parasitized host cells during the parasite's
growth and multiplication. And the sheep liver fluke (Fasciola hepatica) causes extensive necrosis
("liver rot") during its migration as an immature worm through the hepatic parenchyma to the
proximal bile ducts.
Stimulation of Host Tissue Reaction
With a few exceptions all animal parasites provoke host tissue reaction. This may consist of
cellular proliferation and infiltration at the site of the parasite, and it may involve systemic increase
in certain types of cells, especially those circulating in the blood. Characteristically in many
parasitoses an attempt is made by the host to destroy the parasite or to wall it off by fibrous

Reading material for Basic Mechanisms of Diseases/S. Wahyuni/Department of Parasitology/

Medical Faculty, Hasanuddin University/2009
encapsulation. If the parasite lives normally in the bile ducts, as is the case with Fasciola hepatica
and Clonorchis sinensis, the first host reaction is a hyperplasia of the biliary epithelium, then an
enveloping fibrosis of the ducts. In infection with the filaria worm, Wuchereria bancrofti, in the
lymphatic vessels retrograde to lymph nodes, there is hyperplasia of the endothelial lining of the
vessels, cellular infiltration into their lumens and perilymphatic fibrosis, together with
lymphadenitis, leading to temporary or permanent sequestration of the worms. During the
biological incubation period of blood flukes in the intrahepatic portal veins there is an acute
hepatitis. Later, after the worms have migrated into mesenteric or vesical venules, have matured
and the females are ovipositing, a pseudotubercle is formed around each egg which becomes
lodged for any length of time in the perivascular tissues.
The leishmanias and Toxoplasma live in cells of the reticuloendothelial system. Here they
multiply, destroy the host cells and after temporary extra cellular existence are engulfed by other
macrophages which un- successfully attempt to destroy the parasites. This produces increasing
local granulomatous growth and in visceral leishmaniasis a marked increase in the mononuclear
leukocytes, with compensatory decrease in the production of polymorphonuclear leukocytes and
later of the erythrocytes.
In metazoan parasitoses, but seldom if ever in protozoan infections, there is a moderate
to notable eosinophilia, most often observed in infec- tions with helminths which have an intimate
host-tissue association, as, for example, in trichinosis, strongyloidiasis, ascariasis and
schistosomiasis. However, arthropod infestation may likewise be responsible for marked
eosinophilia.
To a certain degree increased erythropoiesis may be stimulated in infections which cause
mechanical loss or destruction of the erythrocytes. This may be observed following deep
extensive amebic invasion of the colon or attachment of hookworms to the intestinal wall,
although it will not com- pensate for prolonged extensive hemorrhage. In malaria, with the
destruction of the red blood cells by the plasmodia, there is evidence of increased red blood cell
production, but this is frequently not sufficient to replace the cells which are being destroyed.
Thus anemia is commonly associated with chronic hookworm disease, malaria and a number of
other parasitoses. .
The only infection in which almost no host-cell stimulation is produced is uncomplicated
amebic colitis.
Mention should be made at this point of the potential relationship to neoplastic growth as
a result of the irritation of animal parasites to host tissues. Cases of carcinoma of the colon have
been reported in amebic granulomas. This relatively rare type of lesion may develop at any level
of the large intestine which has been invaded by Entamoeba histolytica. The tumor (the so-called
ameboma) may be polypoid with undamaged surface, or ulcerative; it may be bacterially sterile or
invaded by pyogenic bacteria. It consists of an internal zone of cytolyzed debris, an intermediate
zone of granulation containing neutrophils, eosinophils, plasma cells, fibroblasts, newly-formed
blood vessels and active amebic trophozoites, an outer fibrous coat, and usually a covering of
intestinal epithelium.
In visceral leishmaniasis (kala-azar) the etiologic agent (Leishmania donovani)
parasitizes fixed macrophages in the spleen, liver, bone marrow and visceral lymph nodes. In
these organs it stimulates a remarkable increment of the reticuloendothelium comparable
perhaps in degree to leukemia, but completely different in its prognosis, since specific drugs
administered to kill the protozoan agent will provide a gradual return to the normal cytological
picture.
More frequently attention in the pathological literature has been focused on parasitic
worms as causative agents of neoplastic growths in the digestive tract, liver and urinary bladder.

Reading material for Basic Mechanisms of Diseases/S. Wahyuni/Department of Parasitology/

Medical Faculty, Hasanuddin University/2009
In the area of comparative parasitology one finds that the spiruroid nematode of rodents,
Gongylonema neoplasticum, provokes malignant gastric tumors in rats which have been
experimentally inoculated with the larval stage of this worm, and that Cysticercus fasciolaris, the
larval stage of the cat tapeworm, Taenia crassicollis, stimulates the development of metastasizing
sarcoma in the liver of the rodent intermediate host.
Although no such oncogenic association of nematodes or tapeworms has been
demonstrated for man, several species of trematodes have reportedly been involved in the
development of carcinoma, Among these are Fasciola hepatica, Clonorchis sinensis and
Opisthorchis felineus, which inhabit the biliary tract, and species of Schistosoma, or blood flukes,
which live in mesenteric-portal and vesical venous blood vessels.
The flukes in the bile ducts provoke hyperplasia of the biliary epithelium, formation of new
ducts and periductal fibrosis, with progressive hepatic cirrhosis in heavy infections. Occasionally
adenocarcinoma and solid primary carcinoma of the liver have been found at postmortem of
these cases. In blood fluke infections involving primarily the mesenteric-portal system, extensive
perivascular infiltration of eggs in the wall of the large intestine and the liver has been found to be
associated at times with colonic, rectal and hepatic carcinoma. Moreover, in adult male farmers of
Lower Egypt the statitical relationship of Schistosoma haematobium eggs trapped in the bladder
wall to vesical carcinoroa involving the male and female genitalia haye been diagnosed in
persons with blood-fluke involvement of these organs.
Toxic and Allergic Phenomena
Several of the arthropods harmful to roan introduce toxins into the skin, inducing host reaction.
The volume of the toxin may be minute and the potency hardly meeasurable, as in the case of
some of the smaaller insects; or the amount may be appreciable with varying degrees of potency.
Spiders and ticks introduce venom when they insert their mouth parts into the skin; scorpions,
bees, wasps and ants have their venom apparatus at the caudal end of the body. Many species
of caterpillars elaborate toxins in glands at the base of delicate hollow hairs, which become filled
with the secretions; in contact with human skin or mucous membranes the hairs break off,
introducing the toxin. Jelly fishes (Colenterata) are provided with roultiple stinging cells, each
containing a nematocyst. When these cells touch the skin the nematocysts re exploded, causing
a painful nettling dermatitis of the contact area and occasionally systeroic reaction. Blister beetles
have a vesicating fluid which produces painful blisters if the fluid is discharged on body surfaces.
When protein or at times other metabolites of the parasite are introduced into the skin in
minute drops of an arthropod's saliva or from active penetration of a living helrointh larva,
sensitization to the foreign substance is initiated. Similarly, when an active helminth larva makes
intimate contact with the host's viscera, it stimulates production of antibody. Wherever migration
through the tissues normally occurs following active entry of a parasite through the skin or after its
peroral introduction, the relatively prolonged association of the parasite with the host increases
the probability of specific antibody response to introduction of the foreign antigen. Moreover,
superinfection with the same agent at times causes hypersensitization, as in ascariasis in
children, and in some instances anaphylactic shock, as in bee sting. Likewise, the sudden release
of the foreign protein in the host's body may precipitate anaphylaxis, as when a gravid female
Dracunculus medinensis begins to migrate from the viscera to the skin or hydatid fluid is released
from the rupture of an Echinococcus cyst in a body cavity. Cumulative evidence indicates that a
greater degree of intolerance may result from entry into the tissues of a host by a parasite not
adapted to that particular species of host than occurs under circurostances in which there is
parasite-host compatibility. Two particular examples in human parasitology support this concept :
(1) schistosome dermatitis caused by percutaneous entry of the cercarial larvas of non-human

Reading material for Basic Mechanisms of Diseases/S. Wahyuni/Department of Parasitology/

Medical Faculty, Hasanuddin University/2009
blood flukes , and (2) visceral larva migrans due to migration through the tissues of the larvas of
the dog ascarid, Toxocara canis.
Secondary Invaders
In assessing the overall damage produced in parasitic diseases, it must be borne in mind that
entry of an animal parasite may open pathways in the skin or the intestinal tract for invasion by
other pathogenic microorganisms. "Ground itch" in the skin at sites where hookworm larvas have
penetrated is characteristically complicated by pyogenic bacteria. Similarly, in chronic amebic
colitis and in balantidiasis the architecture of the enlarged ulcer and its histologic appearance
indicate that enteric bacteria have entered the lesion and have altered the picture, with dense
infiltration of neutrophilic leukocytes and fibroblasts around the 1argins of the lesion. Irrespective
of the actual site of entry of the parasite into the tissues, whether by the skin or the intestinal
mucosa, it is probably the exception rather than the rule that bacteria reach the deeper visceral
organs via pathways produced by the parasites. However, recent investigations suggest that
viruses may be introduced into the viscera by invading and migrating animal parasites.
Finally, in communities where conditions are favorable for high prevalence of parasites in
the population, several species of protozoa and helminths are usually found together in a majority
of the individuals. Under these circumstances the pathologic effect of the multiple infections
(polyparasitism) is the sum of the individual effects, to which an under lying state of malnutrition
must frequently be added as an important contributor to the total disease picture.

IMMUNITY TO PARASITE
In animal parasitoses is rarely solid as it is in some of the viral diseases like measles and yellow
fever. A notable exception is found in cutaneous leishmaniasis, in which a natural infection
followed by spontaneous cure appears to confer immunity for life against subsequent attack.
Possibly this is also true for toxoplasmosis but the evidence is still far from convincing. In
trichinosis light exposure in experimental animals prevents infection of clinical grade when a large
inoculum is administered later. There is similar suggestive information with respect to hookworm
infection, blood-fluke infection and infestation with the fly maggot, Cordylobia anthropophaga.
In malaria there is substantial evidence concerning human immunity or susceptibility to
different strains of the same species of plasmodium and to different species of plasmodia.
Individuals who have had malaria are highly resistant to the homologous strain of the parasite,
less so to heterlogous strains of the same species, and demonstrate little or no resistance to
other species of plasmodia which are infective for man. In infection with Entamoeba histolytica
immunologic diagnostic tests are more satisctory when strain specific antigen is employed.

SYMPTOMATOLOGY
The response of the host is a protective reaction against a harmful stimulus, and the local
or general signs and symptoms are manifestations of the deranged functions of the affected
organs. The location of the parasite in a vital organ, its toxic action, and the intensity of the
infection determine the presence, time of appearance, and severity of the local and systemic
symptoms. Such a symptomatic response results in a typical clinical case; when the
maladjustment between parasite and host is less marked, mild or atypical cases are produced;
and when there is an equilibrium, a carrier state with slight or no clinical evidence of disease is
created.
Parasitic infections produce a wide range of clinical symptoms, depending upon the
species of the parasite, the condition of the host, the organs affected, and the number of

Reading material for Basic Mechanisms of Diseases/S. Wahyuni/Department of Parasitology/

Medical Faculty, Hasanuddin University/2009
parasites. Likewise, symptoms may be induced by supersensitiveness of the host to the parasite
or its products; an infection that normally calls forth no response may result in a pronounced
reaction in a sensitized host. For concise tabular presentation it has been necessary to group the
numerous symptoms into several categories rather than to attempt to list them in detail.
Systemic Symptoms
1. Fever (chills)
2. Headache
3. Muscle and joint pains
4. Lymphangitis and lymphadenitis
5. Weakness (fatigue, languor, prostration, neurasthenia, syncope)
6. Debility (loss of weight, malnutrition, cachexia)
Gastrointestinal Symptoms
1. Mild (irregular or loss of appetite, hunger or gnawing sensations, vague abdominal
discomfort)
2. Moderate (anorexia, nausea, vomiting, abdominal discomfort, diarrhea or con- stipation)
3. Severe (diarrhea or dysentery, epigastric, hypochondric or other abdominal pains and
cramps)
Nervous Symptoms
1. Psychic
a. Mild (confusion, irritability, insomnia)
b. Severe (instability or incoordination, altered personality, hallucinations, mental
deterioration)
2. Neurologic
a. Intracranial pressure (headache, vertigo, vomiting, convulsions, optic neuritis and
retinitis, and other symptoms of brain tumor )
b. Parasthesia and amnesia
c. Encephalitis
d. Epilepsy
e. Paralyses
Allergic Symptoms
1. Gastrointestinal ( anorexia, nausea, vomiting, diarrhea, abdominal pain and cramps)
2. Cutaneous and subcutaneous (pruritus, erythematous, macular, papular, purpuric and
eczematous rashes, urticaria, edema and calabar swellings, lymphangitis)
3. Pulmonary (coughing, sneezing, dyspnea, slight hemoptysis, transient thoracic pain,
asthma)
4. Systemic (fever, headache, sweating, polyarthritis, photophobia, languor, signs of
collapse)

DIAGNOSIS
The clinical manifestations of parasitic diseases are so general that in most instances diagnosis
based upon symptomatology alone is inadequate. Although the experienced clinician may
recognize the characteristic signs and symptoms of certain parasitic diseases, particularly those
that. involve the multiplication of the parasite or its larvae in the host, the symptoms in atypical
cases may be so confusing that no clear clinical picture is presented. Likewise, many diseases,
chiefly of helminthic origin, give few and indefinite symptoms, and often are clinically

Reading material for Basic Mechanisms of Diseases/S. Wahyuni/Department of Parasitology/

Medical Faculty, Hasanuddin University/2009
indistinguishable. Final diagnosis and proper methods of treatment require the identification of the
parasite in the laboratory. Hence, the diagnostician who is proficient in both laboratory and clinical
methods has a decided advantage over one who relies solely upon clinical diagnosis.
Successful laboratory diagnosis requires a knowledge of certain fundamental laboratory
procedures, such as microscopic technic, preparation of material for examination from the feces,
blood, lymph, tissues, urine, sputum, and secretions. It also requires familiarity with the salient
characteristics that permit identification of the adult parasites, ova, or larvae.
TREATMENT
Prompt and adequate treatment of infected individuals, mass therapy to eliminate unrecognized
sources of infection, and preventive or suppressive chemoprophylaxis constitute an essential part
of any program for the prevention of parasitic diseases. The successful treatment of the infected
patient includes medical and surgical measures, a hygienic regimen to build up general
resistance, and specific chemotherapy. Intelligent treatment requires a knowledge of the parasite,
its pathogenic action, the intensity of the infection, and the physical condition of the patient. The
physician should also be familiar with the patient's ability to cooperate intelligently, the sanitary
environment, the epidemiology of the disease, and the best methods of controlling the spread of
the infection. No efficient antiparasitic drug is entirely nontoxic to man. Successful chemotherapy
depends upon the use of a drug that has a minimal toxic effect upon the tissues of the host and a
lethal action upon the parasite. Its success depends not only upon the choice of the drug but also
upon the condition and response of the patient, the method of administration, the dosage, the
auxiliary therapeutic preparation and aftercare of the patient, and additional procedures to
prevent reinfection. New chemotherapeutic agents, largely synthetic, are being constantly
developed, and therapeutic methods are continually undergoing revision.
PREVENTION
The prevention of parasitic diseases depends upon the erection of barriers to the spread of
parasites through the practical application of biologic and epidemiologic knowledge. Almost every
parasite at some time in its life cycle is susceptible to special exterminative measures. Thus,
barriers may be established by breaking such weak links in the life cycle as may exist at the
departure of the parasite from its source, during its extracorporeal existence, or at the time of its
invasion of man. The control of parasitic diseases includes the following procedures:
1. reduction of the sources of infection in man by therapeutic measures
2. education in personal prophylaxis to prevent dissemination of infection and to reduce
opportunities for exposures
3. sanitary control of water, food, living and working conditions, and waste disposal
4. destruction or control of reservoir hosts and vectors
5. erection of biologic barriers to the transmission of parasites.
The therapeutic reduction of human sources of infection is a practical measure, but it is not
applicable to animal reservoir hosts. Education of the general public in personal prophylaxis and
knowledge of the precautions necessary to escape infection and to prevent its transmission to
others is an effective means of combating parasitic diseases. Public health education, however, is
a slow process, particularly in countries with limited educational facilities. Sanitary measures of
waste disposal include the establishment of sewage systems, the installation of screened sanitary
latrines, and the prohibition of untreated night soil as garden fertilizer. Food handlers, who may
be carriers, require careful supervision and training in personal hygiene. The elimination or
reduction in number of intermediate hosts or vectors has made possible the control of many
parasitic diseases. Insect vectors may be controlled by the destruction of their breeding grounds,

Reading material for Basic Mechanisms of Diseases/S. Wahyuni/Department of Parasitology/

Medical Faculty, Hasanuddin University/2009
the application of insecticides, and the protection of the susceptible host by screens and
repellants. Snails, the intermediate hosts of trematodes, may be destroyed, if sufficiently
segregated, by chemical and physical agents, but the destruction of such intermediate hosts as
mammals and fishes is usually impractical.

References :
CLINICAL PARASITOLOGY
By Faust and Russel ( 1st edition since 1937)
Published by Lea & Febiger (Library of Congress Card Number 57-7440)
BASIC CLINICAL PARASITOLOGY
st
By David L. Belding (1 edition since 1958)
Published by Appleton Century Croft, Inc ( Library of Congress Card Number 58-6554)
HUMAN PARASITOLOGY
By Bogitsh, B (Copyright 1998)
Published by Academic Press, Incorporated (ISBN 0121108708)
OXFORD HANDBOOK OF TROPICAL MEDICINE
By Eddleston, M (1999)
Published by Oxford University Press, Incorporated (ISBN 0192627724)