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    Parasite Infections

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    Abdullah Alkhars
    This document provides a summary of common parasitic infections including amoebiasis and giardiasis. It discusses the pathogenesis and clinical presentation of Entamoeba histolytica, including the production of cytotoxins, tissue destruction in the colon, and extraintestinal spread to the liver and lungs. Giardia lamblia is described as a non-invasive intestinal parasite that can cause asymptomatic or symptomatic infections characterized by diarrhea. The life cycle and transmission of Toxoplasma gondii is outlined, and it is noted that toxoplasmosis is an opportunistic infection that can manifest as congenital or acquired disease.

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    Parasite Infections

    Uploaded by

    Abdullah Alkhars
    25 views45 pages
    This document provides a summary of common parasitic infections including amoebiasis and giardiasis. It discusses the pathogenesis and clinical presentation of Entamoeba histolytica, including the production of cytotoxins, tissue destruction in the colon, and extraintestinal spread to the liver and lungs. Giardia lamblia is described as a non-invasive intestinal parasite that can cause asymptomatic or symptomatic infections characterized by diarrhea. The life cycle and transmission of Toxoplasma gondii is outlined, and it is noted that toxoplasmosis is an opportunistic infection that can manifest as congenital or acquired disease.

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    This document provides a summary of common parasitic infections including amoebiasis and giardiasis. It discusses the pathogenesis and clinical presentation of Entamoeba histolytica, including the production of cytotoxins, tissue destruction in the colon, and extraintestinal spread to the liver and lungs. Giardia lamblia is described as a non-invasive intestinal parasite that can cause asymptomatic or symptomatic infections characterized by diarrhea. The life cycle and transmission of Toxoplasma gondii is outlined, and it is noted that toxoplasmosis is an opportunistic infection that can manifest as congenital or acquired disease.

    Copyright:

    © All Rights Reserved
    Download as PDF, TXT or read online from Scribd
    Download as pdf or txt
    25 views45 pages

    Parasite Infections

    Uploaded by

    Abdullah Alkhars
    This document provides a summary of common parasitic infections including amoebiasis and giardiasis. It discusses the pathogenesis and clinical presentation of Entamoeba histolytica, including the production of cytotoxins, tissue destruction in the colon, and extraintestinal spread to the liver and lungs. Giardia lamblia is described as a non-invasive intestinal parasite that can cause asymptomatic or symptomatic infections characterized by diarrhea. The life cycle and transmission of Toxoplasma gondii is outlined, and it is noted that toxoplasmosis is an opportunistic infection that can manifest as congenital or acquired disease.

    Copyright:

    © All Rights Reserved
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    of 45

    Common Parasitic

    Lecture outline
    infections
    Discuss factors important for parasite
    pathogenecity.

    Give the most common modes of entry of


    parasites in the human host.

    Describe 3 pathologic mechanisms important


    in parasitic diseases.

    Sonia Allam
    Professor of Medical Parasitology
    Lecture outline

    What is the difference between diarrhea and


    dysentery & responsible protozoa?

    What is the pathogenesis of intestinal and


    extraintestinal amoebiasis.

    What is meant by the amoebic carrier and its


    management?

    What is the main clinical syndromes of


    intestinal giardiasis?
    Lecture outline

    Describe the mode of infection in human


    toxoplasmosis

    What is the clinical presentation of


    toxoplasmosis in man.

    Why Toxoplasma gondii is considered an


    opportunistic parasite?
    Pathogenesis of Amoebiasis

    Pass out in Binucleate Uninucleate Enter with


    stool cyst cyst Precyst food

    In the lumen Quadrinucleate


    Attached cyst
    to colonic Binary fission Trophozoite
    mucosa Lectin

    Mucosa of large intestine


    Pathogenesis of Amoebiasis
    Pathogenesis of Amoebiasis

    • ‘Flasked-shaped ulcer’
    • Trophozoites at
    boundary of necrotic
    and healthy tissue
    • Trophozoites ingesting
    host cells
    • Dysentry (blood and
    mucus in feces)
    Pathogenesis of amoebiasis
    Production of cytotoxin Attachment of trophozoites
    Lysis of colon epithelial cells, neutrophils, lymphocytes
    and monocytes Alteration of host cell permeability

    Irreversible increase of intracellular Ca levels


    Release of toxic neutrophil constituents

    Tissue destruction
    Pathogenesis of amoebiasis
    Markers to identify invasive strains are:
    - Lectin binding
    - Zymodeme analysis
    - Genome DNA
    - Staining with monoclonal antibodies
    Pathogenic Entamoeba histolytica is similar
    morphologically to non pathogenic E. dispar,
    E. moshkovoskii and E. bangladeshi
    Pathogenesis of amoebiasis
    Amoeboma Bacterial infection

    Peritonitis Perforation

    Appendicitis Extension

    Hemorrhage Erosion
    Emboli

    Portal Systemic

    skin liver Brain


    Lung
    Pathogenesis of Extraintestinal
    Amoebiasis
    Pathogenesis of Extraintestinal
    Amoebiasis
    Amoebic Liver Abscess
    Chocolate-colored
    necrotic tissue
    (leucocytes & RBC)

    Trophozoites
    found only in
    the wall.
    Pathogenesis of Extraintestinal
    Amoebiasis
    Pulmonary Amoebiasis
    Rupture of liver abscess Cutaneous Amoebiasis
    through diaphragm

    Amoebic pericarditis
    Pericardial effusion ( fatal)
    Management of Amoebic carrier

    • 80-90% of cases are asymptomatic Cyst Passers


    (Carriers)
    • They must be detected and treated
    • Danger : Transmit infection ( food handler).
    May develop complications later on.
    Management of Amoebic carrier
    (Chronic non dysentric colitis)

    C.P.
    • vague abdominal discomfort.
    • Distension of colon
    • + Diarrhea alternating with constipation.
    D.D.
    • Giardia, Cryptosporidia, Cyclospora
    Management of Amoebic carrier
    (Diagnosis)

    Stool Examination Serology

    Well formed
    Cyst wall, refractile spheres IHAT
    ELISA
    Yellow cytoplasm 4 nuclei
    IFAT
    Management of Amoebic carrier

    Luminal (Local) Tissue ( Systemic)

    • Iodoquinol • Flagyl
    (Diloxanide furoate) ( Metronidazole)
    500 mg tds 10 days 750 mg tds 10 days
    Suitable for carrier state Not suitable for carrier state
    Giardia lamblia
    Antony van Leeuwenhoek (1632-1723)

    In fact, he is the first


    one to discover and
    describe Giardia in
    1681in his own stool
    with its characteristic
    movement using his
    newly invented
    microscope.
    Two hundred years after van
    Leeuwenhoek, in 1859, a
    Czech physician named
    Vilem Lambl observed G.
    intestinalis in the stools of
    children with diarrhea, but
    believed the protozoa to be
    commensal and not
    responsible for the pathology
    The species was then named
    Giardia lamblia in his name. Vilem Lambl
    Giardia duodenalis: Clinical syndromes

    mucosa
    Cyst
    Binary fission
    Pass in stool Enter with
    Trophozoite food
    taglin
    GLAM-1
    Giardia duodenalis
    Clinical syndromes

    Giardia is a non-invasive parasite


    1- Asymptomatic
    2- Symptomatic (IP 1 – 4 weeks).
    Dyspepsia, epigastric pain, nausea,
    flatulence
    Sudden onset of explosive, watery, foul-
    smelling diarrhea.
    Giardia duodenalis
    Clinical syndromes

    In severe infection

    Malabsorption of protines,carbohydrates,
    fatty acids, vitamin B12 ( pernicious anaemia)

    Fatty diarrhea ( steatorrhoea)


    Giardia duodenalis
    Clinical syndromes

    - Within 10 to 14 days spontaneous recovery


    occurs
    - Sometimes a more chronic disease with
    multiple relapses may develop.
    This occurs commonly with patients with
    Ig A deficiency.
    Protozoa inhabiting human intestine
    • Entamoeba histolytica (large intestine).
    • Balantidium coli (large intestine). Pathogenic
    • Giardia lamblia (small intestine). protozoa

    • Cryptosporidium parvum (small intestine).


    • Cyclospora cayetanensis (small intestine).
    Opportunistic
    protozoa
    In large intestine: dysentry.
    Painful frequent evacuation of small quantities of stool
    containing mucus tinged with blood and tenesmus
    In small intestine: diarrhoea.
    Increase in frequency, fluidity or volume of bowel motions
    Toxoplasmosis
    Life Cycle of Toxoplasma
    Toxoplasma gondii Toxoplasmosis
    Geog. Distribution: worldwide
    Toxoplasma attacks man, animals (cats) and cattle
    II Unsporulated
    Pseudocyst oocyst in cat’s
    (tachyzoites) intestine
    I Develops on the ground
    Tachyzoites III IV
    Tissue cyst 4 sporozoites
    (bradyzoites) Sporulated oocyst

    Stages I to IV are infective stages to man


    Epidemiology
    • Oocysts are shed in faeces of infected cats in large
    numbers, remain viable and infective for long
    periods.

    • Hot and humid atmosphere helps infection.


    • Eating undercooked infected meat helps infection.
    • Congenital infection occurs when mother acquires
    primary infection during pregnancy.
    Mode of Infection with Toxoplasma
    1- Oral route (ingestion):
    Contaminated food or drink
    Handling cat excreta Sporulated
    Infected undercooked meat oocyst
    Tissue cyst Pseudocyst

    2- Organ transplantation

    Tachyzoites
    3- Blood transfusion

    4- Transplacental route
    Mode of Infection with Toxoplasma

    5- Contamination of mucous
    membrane & skin abrasion
    (in research workers & butchers)

    Tachyzoites
    Development of Toxoplasma in the infected human
    Ingested Sporulated oocyst Tissue cyst
    containing containing
    sporozoites bradyzoites
    Transform into
    Villi of small intestine tachyzoites
    Tachyzoites penetrate the
    lamina propria of small
    intestine then to the circulation Lamina propria
    Blood vessels

    Parentral Tachyzoites pass to the circulation


    From circulation, Tachyzoites reach the viscera
    especially brain , eye, skeletal muscles and heart
    and form tissue cysts (persists for host’s life)
    Development of Toxoplasma in Cat Intestines
    Sporulated oocyst Sporozoite, bradyzoites
    & tissue cyst attack epithelial cells
    Infective stages
    Unsporulated oocyst
    Pass in stool
    of the cat
    Zygote
    ♂

    ♀ merozoites
    gametocyte

    Sexual cycle: Cat is the definitive host


    Pathogenesis and Clinical Picture
    Toxoplasmosis is considered an opportunistic
    infection
    Congenital infection:
    Congenital toxoplasmosis

    Acquired infection:
    Acquired toxoplasmosis

    Recrudescence:
    Toxoplasmosis in immunocompromized patients
    Congenital toxoplasmosis
    Depends on :
    1- Protective immunity of the mother
    2- Age of the foetus at the time of infection

    Loss of the foetus: (abortion or still birth)


    Early neonatal manifestations:
    CNS affection, eye affection, systemic manifestations
    Late manifestations:
    Complications due to CNS involvement
    Eye affection in adolescence or adulthood
    Congenital toxoplasmosis

    Late manifestations:
    Hydrocephalus, microcephaly, spasticity,
    convulsions.
    Retinochoroiditis
    Fever, pneumonitis, hepatomegaly, jaundice,
    lymphadenitis.
    CNS affection

    Hydrocephalus Microcephaly

    Convulsions
    Acquired Toxoplasmosis
    Depends on :
    1- Immune status of infected person
    2- Age of infected person
    3- Virulence of infecting strain of Toxoplasma
     Asymptomatic (tissue cysts are present)
    Occurs in the majority of cases

     Lymphadenitis, fever, headache,


    myalgia, skin rash & splenomegaly

     Retinochoroiditis in adolescence
    & adult hood
    This may result in blindness
    Toxoplasma Retinochoroiditis

    Healed
    Toxoplasmosis in the immunocompromized

    • Encephalitis leading to death. It is due to


    reactivation of latent cerebral cysts

    • Organ transplant patients develop acute


    disseminated toxoplasmosis
    Diagnosis
    1- Clinical
    Various clinical manifestations

    2- Imaging
    X-ray: calcification
    Diagnosis
    3- Laboratory diagnosis
    - Serology:
    Detection of IgM in patient’s blood indicates
    active infection.
    Detection of IgG (rising titre) indicates
    active infection.

    - Molecular techniques:
    Detection of Parasite DNA in patients serum.
    Laboratory Diagnosis of Congenital Toxoplasmosis
    Detection of IgM in baby’s blood indicates
    foetal infection.
    Maternal IgM does not cross the placenta

    Detection of parasite DNA in infant’s urine or


    amniotic fluid by PCR

    Treatment
    Pyrimethamine + Trisulphapyrimidine

    Spiramycin (to infected pregnant women)


    Case
    A newly born baby was born with microcephaly,
    convulsions and fever. His mother gave a history
    of having a cat at home.
    a- What is your diagnosis?
    Congenital toxoplasmosis.
    b- How was the baby infected?
    Tachyzoites from infected mother crossed the
    placenta and infected the foetus.
    c- How can you confirm your diagnosis?
    By serology: Detection of anti toxoplasma IgM
    antibodies in baby’s blood.

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