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Leishmaniasis cont.

• The mucocutaneous parasites growth at 34 C


• The visceral parasite at 37 C
• The severity of disease is determined by the
leishmania species and the host immune response
• Cell mediated (granulomatous) response (limited
infection with a few parasites)
• Anergic response Macrophages stuffed with
parasites
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Leishmaniasis

• Chronic inflammatory disease of skin .mucous


membranes,or viscera
The etiologic agent is an obligate intracellular
protozoa transmitted by Sandflies (kind of small fly
found in beaches)
• Leishmania Major Cutaneous L. ‫ששנת יריחו‬

• Leishmania Donovani Visceral leishmaniasis


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Leishmania reproduce in macrophages,–
resist lysis and is cleared from the body by
cell mediated immune mechanism

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Leishmaniasis cont.

• Cutaneous L. : relatively mild, localized, single


ulcer on exposed skin. The lesion begins as an
itching papule surrounded by induration changes
into an expanding ulcer with irregular borders and
usually heals by involution within 6 months.
Microscopically granulomatous inflammation with
few parasites

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Cutaneous leishmaniasis

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•Diffuse Cutaneous L. : Begins as single
nodule which continues spreading until the
entire body is covered by bizarre nodular
lesions Keloid like Histologically
•The lesions are of the anergic type

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Leishmaniasis cont/
• Visceral Leishmaniasis: L. Invades macrophages,and
cause severe systemic disease marked by
Hepatosplemomegaly, lymphadenopaty, pancytopenia,
fever and weight loss. The spleen may weigh as 3kgand
the lymph N. may measure 5cm. Phagocytic cells are
enlarged and filled with Leishmania many plasma cells are
present and the normal architecture of the spleen is
obscured. In the late stage the Liver becomes increasingly
fibrotic. Phagocytic cells crowd the B.M. and may be also
found in the Lungs GIT Kidney Pancreas and Testes.
Often there is hyperpigmentation of skin (Kala Azar black
fever) In Kidney Immune-complex mesangioproliferative
GN may be. There is a predisposition to get bacterial
infections
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Liver HE

Viceral leishmaniasis

Bone marrow Giemsa


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Patric Mason Ronald Ross
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Malaria

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Malaria
• Pathogenesis: A- Reed Blood Cells
. B- Circulatory changes
I . C- Immune Phenomena
• A: Anemia: P. Vivax, Ovale Attack only
immature eritrocytes and P. Malariae only
senescent ones for that reason no more than 1-2%
of cells are involved at any one time
P. Falciporum
invades RBC of all ages that’s why there are high
levels of parasitemia
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Malaria cont.
• B: Vasodilatation and vasoconstriction, vessels
are plugged with parasitized RBC causing stasis in
spleen and liver and brain
• C: Immune related thrombocytopenia and
immune complex GN
• PATHOLOGY Splenomegaly with malarian
pigment and eventually rupture , Hepatomegaly
with malarian Pigment , Cerebral malarie (ring
hemorrhages) , Malarian pigment in all organs
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Plasmodium in red blood cells

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Malarial pigment
liver

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Malarial pigment kidney
and muscle

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Toxolpasmosis
• Toxoplasma gondii is an obligate intracellular
protozoa that commonly cause subclinical
infection or mild lymphadenopathy in normal
persons,
• Yet produces severe [opportunistic infection in
infants, in uterus, in immunocompromised patients
• Infects a wide range of animals. Sexual
reproduction occurs only in cats
• Human can be infected either by ingestion of
oocyts from cat feces or by ingestion of
incompletely cooked lamb or pork
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Toxoplasma cont
• Entering through the gut, T. gondii spread
systemically and penetrates any type of host cells
spread from cell to cell until T cell mediated
immunity develops
• Some T. gondii cysts containing bradyzoites may
remain dormant for years in muscle and viceral
cells
• Primary T. inf. to mother during the first
trimester often cause fatal parasitemia in 25% of
fetuses, congenital infection is a frequent cause of
choriorretinitis.
• In immunocomp. reactivation of dormant cyst
cause encephalitisi 26
Toxoplasmosis cont.
• Limphadenopathy
1 follicular hyperplasia
2 monocytoid B cells
hyperplasia 3 Large
aggregates of epithelioid histiocytes not forming
well-demarcate granulomas
• Destructive lesions of the CNS Liver Heart
Lungs And Adrenal
• Chorioretinitis destruction of the retina
accompanied by granulomas in choroid and sclera27
Toxoplasmosis Lymphadenitis

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Ocular
Toxoplasm
is Lesion

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Cerebral toxoplasmosis

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Toxoplasma in Mucle

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Fungal infections

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Candidiasis
• Obiquitus fungi: part of the normal flora of the
skin mouth and GIT is the most frequent cause of
fungal infection
• Immunocompetent : Superficial infection
• Immunocompromised : disseminated infection
• Diabetic patients, burns, wet workers are
suceptibles to soperficial infections
• wide tropism

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Candidiasis pathology
• Macroscopica lession: white patches fluffy
membranes easily detached, living a
reddened irritated underlying surface
• Histologically: Acute and chronic
inflammation ,in chronic stages
granulomatous reaction may develop
• Hyphae pseudohyphae blatoconidiae (yeast)

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pseudohypha

septa
hypha

Blastocyst yeast

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Aspergillosis
• Obiquitous fungi,infective forms Septated
bifurcated hyphae fruiting bodies
• Immunocompetent patients: allergic alveolitis
• Immunocompromised patients:serious destructive
sinusitis pneumonia fungemia
• Toxines:Aflotoxin (carcinogenic) Restrictocin and
mitogillin (inhibit protein synthesis IgE inducer)

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Asperllilosis pathology
• Colonization:growth of fungi within pre-
existing cavities (Tb absces bronchoectasis)
• Invasive: (Lungs, heart-valves, brain,
kindney ) Necrotizing lession (target like)
blood vessels invasion

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Phycomycosis (mucormycosis)
• Mucor, abisidia, rhizopus, cunnighamella
• Ubiquitous fungi
• Opportunistic infection (diabetic and
neutropenic patients)
• No harm to immunocompetent individials
• Nasal sinuses, lungs, GIT orbits brain

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Non septated hipha branching 90o

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schistosoma

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Schistosomal reserborium

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Schistosomiasis in colon

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Liver granulomas

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Liver granulomas
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