Parasitology Flashcards

You may prefer our related Brainscape-certified flashcards:
1
Q

What does DALY stand for?

A

Disability Affected Life Years

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Name some of the factors that contribute to a parasite being successful.

A
  • Morphological adaptations
  • Biochemical changes
  • Specialized mechanisms for entry
  • complex life cycles and transmission opportunities
  • Mechanisms for immune evasion (ex. antigenic variation )
  • Impact on host vs. impact of host
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What are the two main parasitic groups? How do you distinguish between the two? Give examples.

A

Microparasites (protists) and Macroparasites (Helminths, Arthropods). Microparasites are small unicellular parasites that use the host as the unit of study (ex. kinetoplastea, Ciliophora, Apicomplexa). Macroparasites are larger and visible to the naked eye. The number of parasites present is considered the unit of study because a larger number of parasites translates to greater symptoms and increased morbidity (ex. Platyhelminthes, Nematoda, Arthopoda).

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Which parasitic group often causes acute disease? Chronic?

A

Microparasites often provoke more acute disease whereas macroparasites cause more chronic disease.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

How many micro and macroparsites fall under the category of Neglected Tropical Diseases (NTDs)?

A

There are 17 NTDs. There are 9 microparasites and 8 Macroparasites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What is the total DALY for NTDs?

A

56.6 Million DALYs with 534, 000 deaths

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

According to Cecilia, what are the top 5 parasitic infections in the US?

A

Chagas Disease, Cysticercosis, Toxocariasis, Toxoplasmosis, and Trichomoniasis

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Which parasite is also known as the Guinea worm and how is infection being prevented?

A

Dracunculus medinensis. Infection is being prevented by using a pipe to drink water to prevent ingestion of parasites.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

What causes Toxoplasmosis?

A

Toxoplasma gondii

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Which phylum does toxoplasma gondii fall in?

A

Apicomplexa (aka. Apicomplexia)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is the major factor that makes toxoplasma gondii successful? Explain.

A

It has multiple routes of transmission

  • Ingestion of oocyst (via food, H20, sand or dirt contaminated with cat feces)
  • Ingestion of tissue cysts in undercooked contaminated meat
  • Vertical transmission (Mother with acute tachyzoite infection to fetus)
  • Blood transfusion or organ transplant (rare)
  • Lambing
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Explain the life cycle of Toxoplasma gondii. Include key cell stages.

A

T. gondii primarily exists in three forms: oocysts, tachyzoites, and bradyzoites. Oocysts (encapsulated zygote) are only produced in the definitive host, members of the family Felidae (felines), after they ingest intermediate hosts infected with bradyzoites (slow dividing stage in host tissue to make tissue cysts). Unsporulated oocysts are produced in the definitive host via merogony (asexual reproduction of apicomplexan) followed by gametogony (sexual reproduction) and are then passed in the cat feces. The oocysts then sporulate in the soil forming sporozoites (a spore-like stage in the life cycle that invade intestinal epithelium). When passed in feces and then ingested (via food, H2O, soil etc.), the oocysts can infect humans and other intermediate hosts (pigs, goats, birds, rodents etc). They develop into tachyzoites, which are the rapidly multiplying trophozoite (a growing stage in the life cycle of some sporozoan parasites, when they are absorbing nutrients from the host) form of T. gondii. They divide rapidly in cells, causing tissue destruction and spreading the infection. Tachyzoites can live in macrophages. Tachyzoites in pregnant women are capable of infecting the fetus. Eventually tachyzoites localize to muscle tissues and the CNS where they convert to tissue cysts, or bradyzoites. This is thought to be a response to the host immune reaction. Ingestion of cysts in contaminated meat is also a source of infection, as bradyzoites transform back into tachyzoites upon entering a new host.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

What is a definitive host?

A

The host where sexual reproduction of the parasite occurs.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

What is a tachyzoite? Provide example of parasite

A

The cell stage that is ~rapidly dividing~ in any cell of the intermediate host and in non-intestinal epithelial cells of the definitive host. This is the ~spreading stage~. Example of parasite - T. gondii.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

What is a Bradyzoite? Give example of parasite.

A

The cell stage that is ~slowly dividing~ enclosed in the tissue of an intermediate host forming a tissue cyst. Tissue cysts can contain 2 to 100s of bradyzoites in the intermediate host. They can lie dormant in body and contaminated items for many years and be reactivated if the host becomes immunocompromised. Example of parasite - T. gondii.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What is an oocyst?

A

A hardy, thick-walled stage of the life cycle of coccidian parasites (ex. T. gondii). The thick wall encapsulates a zygote. This is the stage that is shed in the feces.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

What happens in rodents infected with toxoplasmosis?

A

They behave differently. They no longer fear cats thus becoming more susceptible to predation.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the symptoms of acquired Toxoplasmosis?

A

Most infections are benign and a large majority of cases are asymptomatic, but some present with mono-like syndrome. Infection remains latent for life and can be activated with immunosupression.
In rare severe infections (immunocompromised) - encephalomyelitis, cerebral mass lesions (cerebral toxoplasmosis), myocarditis, hepatitis, chorioretinitis.

19
Q

What are the symptoms of congenital Toxoplasmosis?

A

Retinochoroiditis, encephalomyelitis, hydocephalus, micocephaly, seizures, blindness or sever visual impairment and/or severe developmental delay

20
Q

What are the CDC criteria for diagnosis of cerebral toxoplasmosis?

A
  • recent onset of focal neurological abnormality consistent with intercranial disease or reduced consciousness
  • Brain imaging of a lesion (CT or MRI)
  • positive serum antibody to T. gondii or response to treatment
21
Q

What are some of the diagnostic tests for toxoplasma?

A
  • Sabin-Feldman dye test (DT)
  • Enzyme Immunoassay for T. gondii specific IgM (EIA)
  • Immunsorbent agglutination assay (ISAGA for IgM)
  • Enzyme Immunoassay for IgG avidity (this is important in pregnancy to determine how long an individual has been infected)
  • Isolation and culture of parasite
  • Direct detection by microscopy and PCR (very sensitive for detection but can’t determine tachy vs bradyzoite)
22
Q

What is the treatment for toxoplasmosis?

A

no treatment for immunocompetent, not prego, no severe organ damage
Pregnancy: spiramycin (US, CAN) or pyrimethamine and trisulfapyrimdines
Clindamycin for encephalitis

23
Q

How does toxoplasmosis relate to psychiatric patients?

A

higher seroprevalence in psych patients – maybe due to high dopamine
Get a decreased density of grey matter in infected brain – see changes in human behaviour and a decreased willingness to follow rules

24
Q

Which parasite(s) cause(s) Malaria in humans

A

Plasmodium Falciparum
Plasmodium Vivax
Plasmodium Malariae
Plasmodium Ovale

25
Q

What is the definitive host for malaria in humans?

A

Female Anopheles mosquito

26
Q

What group does Plasmodium fall into?

A

Apicomplexan

27
Q

Which species of plasmodium is (are) important lab models?

A

Plasmodium Chabaudi

Plasmodium berghei

28
Q

What is the life cycle of plasmodium?

A

Human infection begins with the injection of sporozoites (motile spore-like stage in the life cycle of some parasitic sporozoans, which is typically the infective agent introduced into a host) into the bloodstream by infected female Anopheles mosquitoes during a blood meal. Sporozoites travel to the liver and initially invade hepatocytes and multiply, which is known as pre-erythrocytic development. This is followed by the release of non-motile merozoites (daughter cells that infect RBCs - release of them causes paroxysm) into the bloodstream (erythrocytic development), which initiates the asexual parasite multiplication stage (see the figurehttp://www.nature.com/nrmicro/journal/v12/n12/box/nrmicro3364_BX1.html). The duration of blood-stage infection is highly variable: many infections are cleared at an early stage, whereas others remain for several months. A fraction of merozoites form sexual gametocytes, which is the only parasite form that is capable of transmission from humans to mosquito vectors. Immature gametocytes (those in stages I–IV) are sequestered in the bone marrow and only mature gametocytes (stage V) circulate in peripheral blood. The density of mature gametocytes in peripheral blood is typically less than 100 gametocytes per μl of blood and the vast majority are present at submicroscopic densities. Following ingestion by mosquitoes, each individual gametocyte forms one female macrogamete or up to eight male microgametes. In the mosquito midgut, gamete fusion produces a zygote that develops into a motile ookinete, which can penetrate the midgut wall and form oocysts. Oocyst densities in naturally infected mosquitoes that have fed on either microscopic or submicroscopic parasite carriers are typically in the range of 1–10 oocysts. The oocysts enlarge over time and burst to release sporozoites that migrate to the mosquito salivary gland, from where they can infect humans during the next blood meal. Some sporozoites in P. ovale and P. vivax can also develop into hypnozoites in the human liver which are the dormant phase that cause relapses.

29
Q

Which human malaria causing agent is the most predominant?

A

Plasmodium vivax

30
Q

Which malaria causing agents can have relapses?

A

Plasmodium Ovale and Plasmodium vivax

31
Q

Describe the fever cycles of the malaria species?

A

Vivax - Benign tertian (tertian =48 hours)
Ovale - Ovale tertian
Malariae - Quartan (=72 hrs)
Falciparum - Malignant tertian

32
Q

What are the different methods of diagnosing malaria?

A

Microscopy –>Blood smears (thin and thick)
Malaria rapid diagnostic tests (RDTs)
Serology, Gene amplification (mostly for research)

33
Q

What are the disadvantages of microscopy?

A

need skilled technicians
time consuming
require expensive materials –> microscopes, clean slides, and reagents

34
Q

Compare the incubation periods of the 4 types of malaria.

A

Vivax - 10-17d (sometimes prolonged months to years)
Ovale - 10-17d (sometimes prolonged months to years)
Malariae - 18-40d (sometimes prolonged months to years)
Falciparum - 8-11d

35
Q

Compare the periodicity for the types of malaria.

A

vivax- 44-48h
Ovale - 48-50h
Malariae - 72h
Falciparum 36-48h

36
Q

Compare the duration of untreated primary attack for the types of malaria.

A

Vivax 3-8+wks
Ovale 2-3wks
Malariae 3-24wks
Falciparum 2-3wks

37
Q

What are the different durations of untreated infection for the types of Malaria?

A

Vivax 5-8yrs with relapses
Ovale 12-20mo with relapses
Malariae 20-50yrs with recrudescences
Falciparum 6-17mo

38
Q

What are some complications of malaria and which type are they associated with?

A

Cerebral Malaria - Falciparum
Anemia - Malariae (b/c in RBCs causing damage)
Renal Disease - Malariae
Blackwater fever aka Malarial hemoglobinuria (large amounts of dark urine because of excreted damaged RBCs)
Dysenteric Malaria
Algid Malaria (lack of vascular perfusion- hypotension and go into shock) - falciparum
Hyper-reactive malarial splenomegaly (excessive IgM production)

39
Q

What are some things that cause pathogenesis of plasmodium species?

A
  • Sequestration and cytoadherence - the plasmodium matures in the RBC and may cause the RBC to stick to endothelium and uninfected RBCs
  • Host secreted proteins - cytokines TNF and interleukins
  • Differential ability to infect RBCs
  • RBC recognition and invasion
  • Paroxysm
40
Q

What are the 2 ways someone can have innate resistance to malaria?

A
  • Red blood cell defects - ex Sickle cell anemia (can’t survive in the cells)
  • Immunity - species and stage specific, its incomplete and wanes rapidly making it difficult to develop prevention and control
41
Q

How do you treat malaria?

A

Chloroquine for ovale, malariae and sensitive trains of falciparum and vivax

42
Q

What are some preventative and control measures for malaria?

A
  • early Dx and Tx
  • Prevention against parasite and vector
  • detect and contain epidemics
  • regularly reassess malaria situation
43
Q

What was found in the malaria vaccine trial?

A

the vaccine is a antisporozoite protein (RTS,S/AS01)
tested children and infants
greater impact in children vs infants (VE 46%, 27%)