Article 3: Introduction to Clinical Parasitology Flashcards Preview

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Flashcards in Article 3: Introduction to Clinical Parasitology Deck (38)
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1
Q

Symbiosis vs. Commensalism vs. Parasitism

A

Symbiosis (Mutualism): both partners benefit

Commensalism: one partner benefits; the other is unaffected

Parasitism: one partner benefits at the EXPENSE of the other. All infectious agents causing illness belong to this category.

2
Q

Ectoparasite

A

Live ON SURFACE of host. Usually arthorpods (e.g. ticks and mites)

3
Q

Endoparasite

A

Live WITHIN the body of host. Mostly protozoa and helminths

4
Q

Obligate Parasites (Majority)

A

Must spend at least part of their life cycle in association with a host (e.g. Schistosoma (trematode) and Filaria (nematodes))

5
Q

Facultate Parasites

A

Capable of leading both a free and parasitic existence. (e.g. Naegleria (ameba) and Strongyloides (nematode))

6
Q

Vector

A

insect that transmits infectious agent from one host to the next

7
Q

Protozoa

A

unicellular eukaryotic microbe

8
Q

Helminth

A

worm

9
Q

Nematode

A

roundworm

10
Q

Cestode

A

tapeworm

11
Q

Trematode

A

fluke (complex flatworms)

12
Q

Parasitic infections currently account for _____ compared to other infectious agents, worldwide

A

greater morbidity and mortality

***Uncommon in the US, however, those who are immunosuppressed or immunocompromised are at increased risk

13
Q

Definitive Host

A

Species in which the parasite reproduces SEXUALLY and reaches sexually maturity (adulthood) (in parasites that have a life cycle involving more than one host)

14
Q

Intermediate Host

A

Species in which the parasite reproduces ASEXUALLY or larval stages of development occur (in parasites that have a life cycle involving more than one host)

15
Q

In general, the more complicated an organism’s life cycle, the ___ likely change of survival it has

A

Less

16
Q

How do parasitic disease occur in non-endemic countries?

A

Travel to endemic countries, immigration (e.g. malaria)

17
Q

Reservoir

A

Animal (definitive host) that serves to maintain the parasite’s life cycle in the environment

18
Q

What three types of parasites does medical parasitology concern itself with?

A

Protozoa, Helminths, and (to a lesser extent) Arthropods

19
Q

Trophozoite

A

Metabolically active, motile, “feeding stage” of a Protozoa

20
Q

Protozoa

A

Single celled eukaryotes with a nucleus and cell organelles

  • Many can form a cyst (protects against environment)
  • Those that don’t form cysts will be transmitted via an insect vector
21
Q

Protozoa Classes

A
  1. Ameba (locomotion: pseudopodia)
  2. Flagellates (locomotion: flagella)
  3. Sporozoa (locomotion: gliding)
  4. Ciliates (locomotion: cilia)
22
Q

Schizogony

A

A type of ASEXUAL reproduction performed by Sporozoans and some Amoebas

-Multiple intracellular nuclear divisions (mitosis) that precede cytoplasmic division

23
Q

Sporogony

A

A type of SEXUAL reproduction that entails multiple nuclear divisions (meiosis) followed by cytokinesis after zygote formation

24
Q

Helminths

A

Multicellular organisms with an elongated appearance

  • Can vary from a few mm to over 40 feet
  • Thick membranous coat known as a CUTICLE
  • Have hooks or suckers to aid in attachment
  • Two classes: Roundworms (nematodes) and Flatworms (cestodes and trematodes)
25
Q

Transmission of Parasitic Diseases involves what three factors?

A
  1. The source of infection
  2. The mode of transmission
  3. The presence of a susceptible host
26
Q

Name the 5 mechanisms of transmission:

A
  1. Ingestion: consumption of food/water with parasitic eggs (helminths) or cyst (protozoa); usually involves fecal contamination
  2. Penetration/Inoculation: larval forms of some helminths have develops the ability to directly penetrate the skin (hookworms or schistosomes); also can occur via insect bite (e.g. malaria or trypanosomes)
  3. Direct transmission: Trichomonas vaginalis, causative agent of a common STD, is transmitted through SEXUAL CONTACT
  4. Congenital transmission: mother to infant (e.g. toxoplasmosis and malaria)
  5. Transfusion and Transplantation: potentially any blood or tissue dwelling parasite. Most frequently observed with malaria and American trypanosomes (Trypanosoma cruzi)
27
Q

What are the two mechanisms by which parasites produce pathology?

A
  1. Physical presence of parasite or its products

2. Immunopathology caused by the host’s response to infection

28
Q

Mechanical Damage

A

Caused by physical presence of parasite or parasite movement within the host. Examples of this type of pathology include obstruction of the intestine by high worm burdens (Ascaris), blockage of the lymphatics by filarial worms, damaged caused by the migration of helminth larvae through tissues, and lysis of RBC by malaria parasites.

29
Q

Damage caused by Parasite Products

A

Numerous parasites, particularly helminths and intestinal protozoa, produce products that aid in the establishment and persistence of infections. Often these products cause severe damage to host tissues and organs, and include hydrolytic enzymes such as proteases, phospolipases, collagenases and hyaluronidases.

30
Q

Immunopathology

A

The response of the host to parasitic infection can often result in or contribute to pathology

(e.g. Schistosome eggs (granuloma formation), Trypanosoma cruzi (Chagas disease–>myocarditis and neuropathy caused by autimmune response)

31
Q

Immune Responses to Protozoal Infection

A
  1. ) neutralizing antibody. e.g. block entry of parasite into host cells
  2. ) antibody + complement. e.g. lysis of blood dwelling parasites
  3. ) antibody/complement opsonization (plus neutrophils or macrophages) e.g. phagocytosis and clearance of pathogens
  4. ) Activated macrophages. e.g. destruction of intracellular protozoa such as Leishmania, Toxoplasma, and Trypanosoma cruzi
  5. ) CD8+ cytotoxic T cells. e.g. lysis of parasite infected host cells
32
Q

Immune Responses to Helminthic Infections

A

Appears to be mediated by IgE and eosinophils (Hallmark of helminthic infections)

IgE Abs bind to the surface of the worm, are recognized, and are bound by Fc receptors on eosinophils, which then dump their cytotoxic granules onto the parasite

33
Q

Two problems for the immune system posed by Helminthic Infections

A
  1. Too big to be phagocytosed

2. They are often covered with a protective cuticle or sheath that protects them from complement-mediated lysis

34
Q

What are the eight ways in which parasites avoid immune destruction?

A
  1. Size (large size makes phagocytosis unlikely)
  2. Anatomical location (i.e. in the gut; makes it difficult for immune system to reach them)
  3. Intracellular sequestration (within the host cell)
  4. Formation of cysts
  5. Avoidance of phago-lysosomal destruction (survive and replicate within macrophages)
  6. Antigenic variation
    - Two classic examples (1. Malaria parasites have man different life cycle stages, each with a unique antigen; 2. African trypanosomes present successive “waves of infection” so that the immune system is constantly trying to “catch-up”)
  7. Antigenic masking (Helminths coat themselves with host cellular or serum proteins, “masking” their own antigens”)
  8. Immuno-suppression (thought to involve the production of immunosuppressive cytokines by macrophages and T-cells in response to parasitic antigens or infections; host is susceptible to SECONDARY INFECTIONS)
35
Q

What is the main challenge in treating parasitic infections?

A

They are EUKARYOTIC cells, so treating these infections often results in a fair amount of TOXICITY TO THE HOST

36
Q

How is differential toxicity commonly achieved?

A

By 1) preferential uptake of drug by the parasite, 2) metabolic alteration of the drug by the parasite, or 3) differences in the susceptibility of functionally equivalent sites in the parasite and the host.

37
Q

Anti-protozoals

A

Generally, target RAPIDLY PROLIFERATING, METABOLICALLY ACTIVE cells

Mnemonic: “Anti-PROtozoals treat rapidly PROliferating cells”

38
Q

Anti-helminthics

A

Generally, targeted at non-proliferating adult helminthes. Most affect the neuromuscular system, carbohydrate metabolism, or egg (larvae) production of adult worms.