11. Parasitic Diseases Flashcards

1
Q

What is a parasite?

A
  • An organism that lives upon or within another living organism at whose expensive it gains some advantage
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2
Q

What is an ectoparasite?

A
  • Parasite that lives on surface of host

e. g. ticks, louse, scabies

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3
Q

What is an endoparasite?

A
  • Parasitic organism that lives within the host
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4
Q

What are parasitic diseases?

A
  • Can be caused by many organisms including:
  • Viruses
  • Bacteria
  • Fungi/yeast/algi
  • protozoa
  • helminths
  • anthropods
  • Particularly prevalent in developing countries
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5
Q

What are protozoa?

A
  • Single-celled eukaryotes
  • Have different modes of transmission
    e. g. Plasmodium- malaria
    e. g. Toxoplasma- toxoplasmosis
    e. g. trypanosoma- African sleeping sickness
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6
Q

What are zoonoses?

A
  • Animal diseases that are transmissible to humans
  • Transfer can be direct or indirect
  • Natural reservoir of the infectious agent is an animal
  • 70% of pathogens that affect humans are zoonotic
    e. g. protozoa and helminths
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7
Q

What is malaria?

A
  • Arguably most important parasitic pathogen: kills many children
  • Caused by protozoan parasites of the genus Plasmodium
  • Class: apicomplexa- specialised for invasion and intracellular growth (in this case invasion of liver and red blood cells)
  • Limited drugs and no vaccine
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8
Q

What is toxoplasmosis?

A
  • Disease caused by protozoan parasite: Toxoplasma gondii (a type of Apicomplexa)
  • One of the most common infections in the world (but few infected people are symptomatic)
  • Primary host (species in which the adult (sexual) for or parasite occurs) is the cat
  • Transmission:
    Primary host: cats spread oocytes into environment through feces
    Intermediate host: pigs, sheep goat etc. eat from soil and ingest oocytes where they mature and form cysts
    Humans: ingest cysts from infected meat or through ingestion of cat feces
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9
Q

What is the pathogenesis of Toxoplasmosis?

A

Process:

  • Ingestion of cycts
  • Cysts activated in gut and penetrate intestinal epithelium
  • Toxoplasma invade multiple cell types including phagocytes and other tissue cells
  • Develop into tissue cysts to avoid immune recognition/clearance
  • Can cross placenta to fetus

Symptoms:

Healthy individuals:

  • Acute systemic inflammatory response involving flu like symptoms but often no symptoms at all
  • Chronic: due to tissue cysts
  • Possbily linked to psychiatric disorders

Immunocomprimisied/pregnant individuals:

  • severe pathogenic consequences
  • fetal abnormalities
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10
Q

How is Toxoplasmosis diagnosed?

A
  • Serology (testing for toxoplasmosa antibodies)
  • PCR
  • Blood test
  • Histology (detection of tissue cysts)
  • Difficult to determine if infections are acute or chronic
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11
Q

What is the treatment and prevention for toxoplasmosis?

A
Treatment: 
Healthy people: 
- usually none 
Pregnant/immunocomprimised: 
- antibiotics 

Prevention:

  • gloves when gardening
  • hygiene around cats
  • washing hands properly
  • cooking meat thoroughly
  • no vaccine
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12
Q

What are trypanosomes?

A
  • A type of protozoan parasite
  • Class: kinetoplastida
  • Transmitted by insect vectors
  • Causes:
    African trypanosomiasis (ASS)- African sleeping sickness: T. brucei
    American Chagas’ disease: T. cruzi
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13
Q

Describe African Trypanosomiasis

A
  • Caused by 3 species of Trypanosoma brucei
  • These protozoa have a kinetoplast which is a DNA containing granule located in base of flagella
    1. T. b. brucei (doesn’t infect humans)
    2. T. b. gambiense (causes West African sleeping sickness)
    3. T. b. rhodesiense (causes East African sleeping sickness)

Transmission:

  • All forms transmitted via Tsetese flies
  • Primary host: Tsetse fly; they reproduce in gut of fly and enter saliva and are transmitted to humans via bites
  • They replicate extracellularly (different from apicomplexa which are intracellular)
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14
Q

What are the stages of ASS pathogenesis?

A

Stage 1:

  • Trypanosomes multiply in tissue around bite causing inflammation
  • Trypanosomes enter blood stream and lymphatic system
  • Causes low grade fever, swollen lymph nodes and toxic symptoms (at this stage T. b, rhodesiense has more severe symptoms)

Stage 2:

  • Characterised by progressive anemia and kachexia (wasting of the body)
  • Due to extremely high levels of TNF-a

Stage 3:

  • Trypanosomes infect CNS (still are extracellular)
  • Causes sleeping sickness and severe dementia
  • Stage 3 occurs much easlier in EASS (T. b. Rhodesciense
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15
Q

Why is African sleeping sickness so deadly?

A
  • They are extracellular pathogens and produce a strong antibody response but constantly undergo antigenic variation of surface coats
  • This occurs through the expression of different VSGs (variant surface glycoproteins)
  • They switch VSG expression and thus surface protein coat under immune pressure
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16
Q

How is African trypanosomiasis diagnosed?

  • Possible treatments?
A
Direct: 
- In blood samples 
- In CSF (lumbar punctures) 
- In skin and lumph node biopsies 
Indirect: 
- ELISA (hindered by antigenic switching) 
- card agglutination tests 

Treatments:

  • drugs (all very toxic)
  • early treatment is important
  • mainly just prevention by avoiding fly bites
17
Q

What is American Trypanosomiasis?

A
  • Cause of Chagas disease
  • Parasite: Trypanosoma cruzi
  • A zoonosis
  • Transmitted via Rduviid bug (feces from bug rubbed into bite/wound/mouth) this occurs when the Reduviid bug has taken a blood meal from an infected mammal and then takes a blood meal from them
  • Romana’s sign:
  • Unilateral conjuctivitis and oedema
  • Acute marker of Chagas disease
18
Q

Does trypanosoma cruzi (American trypanosoma) invade intracellularly?

A
  • Yes, it invades multiple cell types

- Invasion is by receptor mediated endocytosis (note- not true invasion which apicomplexans do)

19
Q

What are the symptoms of American Trypanosomiasis?

A

2 phases of disease:

Acute:

  • lasts for weeks to months
  • often asymptomatic or mild
  • Romana’s sign
  • Faitgue, fever, swelling of lymph nodes
  • Can severe in immuno-comprimised people

Chronic:

  • infection may remain silent (asymptomatic for decades)
  • Chronically infected people are at a greater risk of cardiac complications and intestinal complications
20
Q

How does Trypanosoma avoid the immune response?

A
  • T. cruzi has a different mechanism for surviving the immune system than T. bruchei (cause of African Trypanosomiasis) because it doesn’t spend as much time extracellularly
  • Rather than having a mosaic antigen coat T. cruzi have a mosaic coat of mucins
  • These are O-glycosylated glycoproteins
21
Q

How is American Trypanosomasis (T. cruzi) diagnosed and treated?

A

Diagnosis:
- Checks for presence of parasite in various samples such as blood smears (for acute phase) and muscle/bowel biopsies

Treatment:

  • difficult to treat chronic infection
  • best to treat acute infection with anti-parasitic drugs
  • also prevention: avoid vector bites
22
Q

What is Leishmaniasis?

A
  • Disease that occurs in under resourced countries and in tropical and sub-tropical regions
  • Has two forms: new world (Americas) and old world *other continent except Australia)
  • It is caused by a protozoan parasite that is a member of the Kinetoplastida family: Leishmania
  • It is transmitted in bites of female sandfly
  • Obligate intracellular pathogen: ‘invasion’ is by phagocytosis thus replicates inside macrophages
23
Q

What is the pathogenesis of Leishmaniasis?

A
  • Parasite replicates intracellularly insidde macrophages
  • 3 types:
    1. Cutaneous: involving skin at site of sandfly bite- a skin ulcer develops
    2. Visceral: lymphatics, liver and spleen- causes fever and is fatal without treatment
    3. Mucocutaneous: mucosal membranes (nose, throat, mouth) after spread from cutaneous lesion

Avoidance of immune system:
- Modifying coat to appear like host to survive in macrophages

Treated:

  • with drugs
  • no vaccine
  • avoid bites