PATHOGENESIS

OF PARASITIC
INFECTIONS
 Introduction
• The pathogenic effects of parasites are many
and varied.
• To discussed the pathogenic effects of parasitic
infection under the headings of :
1. Trauma.
2. Nutrition robbing.
3. Toxin production.
4. Interactions of the host immune responses
and inflammatory responses.
continue 2
 just for EXAMPLE
1. Trauma:-
• Physical trauma, or destruction of cells, tissues, or
organs by mechanical or chemical means.
• Ex: Ascaris or hookworm penetrates a lung
capillary to enter an air space, it damages the
blood vessel and causes hemorrhage and possible
infection by bacteria that may have been inhaled.
• EX: Entamoeba histolytica digests away the
mucosa of the large intestine, forming ulcers and
abscessed pockets that can cause severe disease.
3
 Just for EXAMPLE
2. Nutrition robbing:-
• EX: D. latum has such strong affinity for vitamin B12
that it absorbs large amounts from the intestinal
wall and contents of its host since B12 is necessary
for erythrocyte production, a severe anaemia may
result.
• Ex: Giardia robs by it is concave on its ventral
surface and applies this suction cup to the surface of
an intestinal epithelial cell. When many of these
parasites are present, they cover so much intestinal
absorptive surface which interfere with the host’s
absorption of nutrients.
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 just for EXAMPLE
3. Toxin production:-
• Ex: Malaria parasites produce hemozoin which is
the insoluble waste product, Macrophages and
other phagocytes engulf particles of hemozoin
but, because it is insoluble, they cannot digest it,
and it remains unchanged in their cytoplasm.
That reduces their capacity to perform further
phagocytosis.
• Ex: Excretory/secretory (ES) antigens produced
by Helminths.
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 just for EXAMPLE
4. Interactions of the host immune responses and
inflammatory responses:-
• Ex: T.cruzi develops clusters of cells in the smooth
and cardiac muscle cells ,the inflammatory response
damages the supporting cells of the nerve ganglia
that control peristalsis and heart contraction and
parasite antigens on the host’s own cells,
particularly in the endocardium, cause autoimmune
reactions attacked as foreign by the immune system.
• Ex: The blood flow carries many of the Schistosomes
eggs to the liver where they lodge, leaking antigen
and causing a chronic DTH reaction). The formation
of granulomas around the eggs eventually impedes
blood flow through the liver, resulting in cirrhosis
and portal hypertension. 6
PATHOGENESIS
OF PROTOZOAN
INFECTIONS
7
1-Direct damage due to parasite activity

• May occur as the result of :-

1. The blockage of internal organs.

2. The pressure effects exerted by growing parasites.
3. Physical and chemical damage.
4. Immunopathologic response.

8
 i- The blockage of internal organs
• As in
Obstruction of hepatobiliary system by Gairdia
which represented as biliary colic, cholecystitis , acute
cholangitis or hepatic abscess.
Sequestration and Cytoadherence of the RBCs due
to Malaria or Trypanosomes lead to decreased
microcirculation which results in complete or
partial obstruction in small capillaries ,tissue
hypoxia, ischaemia and edema .
Enlargement of the liver is due to hyperplasia of
Kupffer cells which are packed with Amastigotes.
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 ii- The pressure effects
• As in :-
Regional lymphadenopathy at one side of the
face. Unilateral edema(upper and lower eyelid)
in addition to Conjunctivitis, and this is known as
Romanas' sign or in case of chronic infection in
American Trypanosome lead to Megaesophagus
and Megacolon .

10
Romanas' sign

11
Enlargement of the internal organ

12
 iii- Physical and chemical damage
• As in:-
Flask shaped ulcers and abscessed pockets that
can cause severe disease due to E.histolytica
digests away the mucosa of the large intestine.
Other pathological changes may occur as in
kidneys may show pathological changes
secondary to deposition of certain immune
complexes as occur in Nephrotic Syndrome

continue 13
 Flask shaped ulcer

14
Nephrotic
Syndrome

15
• Ulceration of skin occur during infection of Cutaneous
Leishmaniasis produce diffused cutaneous Leishmaniasis ,
Leishmania Recidiva or Mucocutaneous Leishmaniasis.

• Acute American trypansomaisis cause serious damage to

the heart and other complications leading to death.

• Stage II & III African trypansomaisis is represented as

Lymphatic swollen , Meningo-encephalitis, confusion,
apathy and excessive sleeping due to C.N.S damage.

16
 vi- Immunopathologic response
• Tropical Splenomegaly Syndrome is Splenomegaly of
unknown cause in tropical malarious area which
present high IgM lead to Chronic Splenomegaly in
addition to Black water fever in non-immunized pt.
• Post Kala-azar Dermal Leishmaniais (PKDL)In some
post treated individuals in tropical endemic area
present high IgG level. PKDL occur in face , trunk or
extremities.
• Repeated abortion caused by T.gondii due to the
rejection of the infected fetus by mode of IgG of the
per-infected woman.
• Hypersensitive response and Anergic response occur
during Cutaneous Leishmaniasis produce diffused
cutaneous Leishmaniasis , Leishmaniasis Recidiva
continue 17
Tropical Splenomegaly Syndrome

18
Post Kala-azar Dermal Leishmaniais
(PKDL)

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2- Indirect Damage from Host Response
• As with all infectious organisms, it is impossible to
separate the pathogenic effects caused strictly by
mechanical or chemical tissue damage from those
caused by the immune response to the parasite.
• All protozoa are “foreign bodies” not only in large
numbers and invasive but also in the immunologic
sense: they are antigenic and therefore stimulate
immunity.
• An excellent illustration of this interrelation between
direct and indirect damage is seen in the pathology
associated with Malaria and T.cruzii infections.
• The severity of these indirect changes is a result of
the chronic nature of the infection. 20
 Pathology
&
Pathogenesis of
Parasitic
Helminth
 Introduction
• The majority of individuals infected with parasitic
worms experience relatively minor symptoms and
small percentage suffer severe life-threatening
consequences.
• Many of them have multistage within their
mammalian hosts they often undergo extensive
growth and differentiation that resulted a different
pathological damages.
• This damage may be from:-
1. Direct damage from worm activity.
2. Indirect damage from host response.
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1-Direct damage due to parasite activity

• May occur as the result of :-

1. The blockage of internal organs.

2. The pressure effects exerted by growing parasites.
3. Physical and chemical damage.
4. Immunopathologic response.

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 i- The blockage of internal organs
• As in
– Large Ascaris or tapeworms can physically block the
intestine or by migrating Ascaris may also block the bile
duct.
– Granulomas that form around Schistosome eggs may
block the flow of blood through the liver.
– Obstruction of the genital organs may result in
hydrocoele formation and scrotal
lymphoedema.(W.bancrofti)
– Obstruction of the retroperitoneal lymphatics may
cause the renal lymphatics to rupture into the urinary
tract producing chyluria .(W.bancrofti).
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 ii- The pressure effects
• As in :-
– The pressure atrophy of larval hydatid cyst
(E.granulosus) where the parasite grows as a large
fluid-filled cyst in the liver, brain, lungs, or body
cavity.
– The hydatid cysts caused by E.multilocularis have
a different growth form, metastasizing within
organs and causing necrosis.
– Cysticercosis develop in CNS and eyes produce
some neurological symptoms.
– Ectopic Cerebral infection (P.westermani)
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 iii- Physical and chemical damage
• As in:-
– The anticoagulants secreted by Hook worms cause
the wounds to bleed for prolonged periods, resulting
in considerable blood loss .
– Chronic destruction of the epithelial lining of the bile
ducts leads to thickening of the walls (C.sinensis)”
– Septicemia in Disseminated Strongyloidiasis

continue 26
• Chronic inflammatory changes around parasites
have been linked with neoplasia (Schistosoma
egg).
• There is a loss of elastic fibres resulting in hanging
groin, hernias and elephantiasis of the scrotum.
Finally atrophy of the skin resulting in loss of
elasticity. also mottled depigmentation of the skin
(‘leopard skin’) caused by O.volvulus.

continue 27
A case of ‘hanging groin’
with loss of elasticity in the
skin. There is also leopard
skin

28
 vi- Immunopathologic response
• Pulmonary symptoms (Loeffler’s syndrome) during
pulmonary migration of the filari-form larvae.
• Tropical pulmonary eosinophilia (W.bancrofti)
• Calabar swellings are inflammatory swellings resulting
in a localized subcutaneous edema (L.loa)
• Allergic nasopharyngitis and itching in the throat
(Halzoun -Marrara Synedrom- due to F.hepatica).
• Migrations of adult or Laravae through body tissues
initiate hypersensitivity reactions . While skin, lungs,
liver, and intestines are the organs most affected.
• The immunopathologic changes that lead to loss of
vision.(O.volvulus)
continue 29
 In Schistosomiasis

• Skin dermatitis occur in secondary exposure

• Acute Schitosomiasis or Katayama syndrome .
• Chronic inflammatory changes around parasites (for
example, the granulomas around schistosome eggs in
the bladder wall).
• The clinical features resulted from : -
1. Type 1 hypersensitivity ( Urticaria & angiodema ) .
2. Circulating immune complexes (glomerulonephritis )
3. Cell mediated immunity ( tissues damages ) as portal
fibrosis and pulmonary hypertension .
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2- Indirect Damage from Host Response
• As with all infectious organisms, it is impossible to
separate the pathogenic effects caused strictly by
mechanical or chemical tissue damage from those
caused by the immune response to the parasite.
• All helminthes are “foreign bodies” not only in the
large and invasive but also in the immunologic
sense: they are antigenic and therefore stimulate
immunity.
• An excellent illustration of this interrelation between
direct and indirect damage is seen in the pathology
associated with Schistosome infections
• The severity of these indirect changes is a result of
the chronic nature of the infection. continue
31
• Hypersensitivity-based granulomatous responses
to eggs trapped in the liver cause a physical
obstruction to blood flow, which leads to liver
pathology.
• Hypersensitivity-based inflammatory changes
probably contribute to the lymphatic blockage
associated with filarial infections (Brugia,
Wuchereria).
• Immune-mediated inflammatory changes occur in
the skin, lungs, liver, intestine, CNS, and eyes as
worms migrate through these structures. Systemic
changes such as eosinophilia, edema, and joint
pain reflect local allergic responses to parasites.
continue 32
• Worms are extremely long-lived means that
many inflammatory changes become irreversible,
producing functional changes in tissues.
• examples are :
1. Hyperplasia of bile ducts in long-term liver fluke
infections.
2. Extensive fibrosis associated with chronic
Schistosomiasis.
3. Skin atrophy associated with Onchocerciasis.
4. Infection with O. volvulus leads to blindness due
to the immuno-pathologic changes that lead to
loss of vision . 33
 ‫هي اقىال سيدًا على ابي ابى طالب كرم اهلل‬
‫وجهه‪( :‬راحة الجسن فى قلة الطعام‪ ،‬و راحة‬
‫الٌفس فى قلة اآلثام‪ ،‬و راحة القلب فى قلة‬
‫اإلهتوام‪ ،‬و راحة اللساى فى قلة الكالم)‪.‬‬