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Med > Y2C1-Mümtaz Güran-Microbiology Blood Tissue And Protozoa > Flashcards

Y2C1-Mümtaz Güran-Microbiology Blood Tissue And Protozoa Flashcards

1
Q

What are the organisms and vector of Trypanosomiasis?

A

Organisms: Trypanosoma gambiense, T.rhodiense (vector: Tse-tse fly)
Organism: T.cruzi (vector: Triatomine bugs)

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2
Q

What are the organism and vector of Leishmaniasis?

A

Organism: Leishmania
Vector: Sand flies

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3
Q

What are the organism and vector of Malaria?

A

Organism: Plasmodium
Vector: Malaria

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4
Q

What are the organism and vector of Babesiosis?

A

Organism: Babesia
Vector: Ticks

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5
Q

What are the organism and vector of Toxoplasmosis?

A

Organism: Toxoplasma Gondii
Vector: Ticks

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6
Q

In Malaria, what are the roles of female anopheles and humans?

A

Female anopheles: definitive host
Humans: intermediate host

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7
Q

Which spp of plasmodium is more dominant in Africa and which is in Asia?

A

In Africa: P.falciparum
In Asia: P.vivax

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8
Q

Life cycle of plasmodium vivax.

A

1.) Mosquito injects sporozoites
2.) Sporozoites infect liver cell
3.) Schiozont formation
4.) Schiozont ruptures, merozoites released
5.) Merozoites invade RBC
6.) Early trophozoite formation
7.) Late trophozoite formation
8.) Schiozont maturation
9.) Mature schizont burst releasing merozoites
10.) Gametogony occurs in which merozoites seperate into male and female.

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9
Q

There are no symptoms of malaria during the schizont formation AKA the liver stage. But there are sym0toms after that, what are they?

A

Malaise, fatigue, fever (uptk 40.6 C), myalgia, arthralgia, dry cough and anorexia.

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10
Q

What is the other saying of acute febrile attacks?

A

Malarial paroxsyms; periodic episodes of fever alternating with symptom-free episodes.

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11
Q

Explain the prodrome stage of Malarial paroxsym.

A

-Symptoms are malaise, fever, fatigue, muscle pains, nausea, anorexia.
-It can be mistaken for influenza or gastrointestinal infection.
-Slight fever may worsen just prior to paroxysm.

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12
Q

Explain the paroxysm stage of Malarial paroxysm.

A

-Cold stage - rigors
-Hot stage - Max temperature can reach 40-41°C, SPLENOMEGALY IS EASILY PALPABLE.
-Sweating stage
-Lasts 8-12 hours, starts between midnight and midday.

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13
Q

How is the clinical diagnosis taken?

A

By looking at the; travel history, symptoms and blood smear.

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14
Q

What are examined in microscopy and what do they mean?

A

Thick and thin blood films are examined with respect to gold standard. Thick film shows the presenceor qbswence of the parasite, the thin one shows the morphology/species of the parasite.

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15
Q

With which four main factors should the malaria treatment be guided?

A

1.) Infecting Plasmodium species
2.) Clinical status of the patient
3.) Expected drug susceptibility
4.) Previous use of antimalarials

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16
Q

How should severe malaria be treated?

A

It should be treated aggresively with parental antimalarial therapy.

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17
Q

How to prevent Malaria?

A

1.) Inhibit mosquito breeding
2.) Kill adult mosquitoes in order to reduce survival rate (and hence vectorial capacity) of adult mosquito population
3.) Isolate humans from biting of vector mosquitoes
4.) Reduce malaria infection and morbidity in humans

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18
Q

The definitive host of babesiosis is _____.

A

Ixodid ticks

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19
Q

What are the 3 important species of babesiosis?

A

-B.microti from rodents
-B.clivergens from cattles
-B.bovis from cattles

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20
Q

What are the clinical features of human babesiosis infection?

A
  • NO MALARİA-LİKE PAROXYSM
  • Mild chills and fever
  • Hemolytic anemia
  • Jaundice
  • Hepatomegaly
21
Q

What are the risk factors of severe babesiosis?

A

Asplenia, advanced age >50, impaired immune function.

22
Q

Why is toxoplasmosis a threat to immunosuppressed and unborn people?

A

Infected pregnant women can pass tachyzoites to fetus via bloodstream.

23
Q

What are the 3 infective forms of toxoplasmosis?

A
  • Schizogenic stages (asexual)
    • Trophozoite
    • Tissue cyst
  • Gametogenic stages (sexual)
    •Oocyst
    -Domestic cats and felines are main reservoirs
24
Q

What are the ways of toxoplasmosis transmission?

A
  • İngestion of undercooked meat & Toxoplasma cyst
  • İngestion of the oocyst from fecally contaminated hands or food
  • Organ transplantation or blood transfusion
  • Transplacental transmission
  • Accidental inoculation of tachyzoites
25
Q

What is the lifecycle of Toxoplasmosis oocyst?

A
  • Both oocyst and tissue cysts transform into tachyzoites shortly after ingestion.
  • Tachyzoites localize in neural and muscle tissue and develop into tissue cyst bradyzoites.
  • If a pregnant woman becomes infected, tachyzoites can infect the fetus via the bloodstream.
26
Q

What are the prenatal symptoms of Toxoplasmosis?

A

Serious brain and eye damage, less serious visual and mental problems, late visual and mental problems.

27
Q

What are the normal adult symptoms of Toxoplasmosis?

A

Flu-like

28
Q

What are the immuno-compromised symptoms of Toxoplasmosis?

A

Parasitemia, cysts in visceral organs (eyes and CNS, often fatal)

29
Q

How to prevent and treat Toxoplasmosis?

A
  • Pregnant women who are in a risk group, should avoid contact with cat and cat faeces.
  • Congenital toxoplasmosis: Oral pyrimethamine (1mg/kg) with folinic acid.
  • Adults don’t require a specific therapy.
  • Immuno-compromised patients:
    • Trimethoprim - sulfamethoxazole
    • Dapsone - pyrimethamine
30
Q

For Leishmaniasis; what are the focal distribution, what is the type of the sand fly, and where does the parasite replicate?

A
  • New world: Southern Texas to Northern Argentina, Lutzomyia
  • Old world: Asia, Africa, Middle East, Mediterrenean, Phlebotomus
  • Replicates within the macrophages of vertebrate host
31
Q

What are the types of Leishmaniasis?

A
  • Cutaneous Leismaniasis (CL)
  • Mucocutaneous Leishmaniasis (MCL)
  • Visceral Leishmaniasis (VL)
32
Q

What is the life cycle of Leishmaniasis?

A

1.) Sandfly injects promastigote stage into the skin via bloodmeal.
2.) Promastigotes are phagocytized by macrophages or other types of mononuclear phagocytic cells.
3.) Promastigotes transform into amastigotes.
4.) Amastigotes multiply in cells of various tissues and infect other cells
5.) Sandfly ingests parasitized macrophages infected with amastigotes via bloodmeal.
6.) Amastigotes transform into premastigote in the gut.
7.) Then these promastigotes divide in the gut and migrate to proboscis.

33
Q

What are the decisions and the regimens that should be considered?

A
  • Drug resistance
  • The patient’s age
  • Clinical status
  • Immunocompetence
  • Splenic function
  • Comorbidities
  • Pregnancy status
  • Other medications
  • Allergies
34
Q

What are the medications for Leishmaniasis?

A
  • Pentavalent antimonials
  • Amphotericin B
  • Miltefosine
  • Paromomycin
  • Pentamidine
35
Q

What are the parasites and the vector of African Trypanosomiasis (Sleeping Sickness)?

A
  • T.brucei rhodiense
  • T.brucei gambiense
  • Vector: tse-tse flies
36
Q

What are the parasites and the vector of American Trypanosomiasis (Chagas disease)?

A
  • T.cruzi
  • Vector: Triatomine (reduviids, kissing bugs)
37
Q

What are seen in the acute stage of African T?

A

Irregular fever and headache.

38
Q

For African T; The initial _____ stage followed by a _____ stage after the trypanasomes invade the CNS. T._____ can be self-limiting or progressing to a more serious disease (chronic), includes invasion of _____ and _____.

A

Haemolymphatic, meningoencephalitic, gambiense, lymphatics, CNS.

39
Q

For African T; Parasites crossing BBB result in _____ involvement and _____. Resulting in 1.)_____, 2.)_____, 3.)_____, 4.)_____, 5.)_____.

A

CNS, Nervous impairment.
1.) Meningoencephalitis
2.) Increased apathy and fatigue
3.) Confusion and somnolence
4.) Tics, slurred speech, incoordination
5.) Convulsions, coma, death

40
Q

Clinical features of African T?

A
  • Travel or residence in endemic area
  • Irregular fever and enlarged lymph nodes
  • Behavioral changes/mental symptoms
41
Q

Laboratory Diagnosis of African T?

A
  • Serological tests
  • Demonstration of trypanosomes in blood, lymph node aspirates, cerebral spinal fluid
42
Q

Treatment of African T?

A

First stage: Pentamidine, Suramin
Second Stage: Nifurtimox-eflornithine combination therapy (NECT)

43
Q

The life cycle of African Trypanosomiasis?

A

1.) Tse-tse fly injects metacyclic trypomastigotes during a blood meal.
2.) These trypomastigotes transform into bloodstream trypomastigotes, which are carried to other sites.
3.) They multiply by binary fission in blood, lymph, and spinal fluid.
4.) Trypomastigotes circulate in blood during acute phase and usually undetectable in latent phase.
5.) Trypomastigotes are digested during bloodmeal.
6.) They transform into procyclic trypomastigotes in the vector midgut. Then the procyclic ones multiply by binary fission.
7.) They leave the midgut and transform into epimastigotes.
8.) Epimastigotes multiply in salivary gland. They transform into metacyclic trypomastigotes.
9.) The cycle repeats.

44
Q

How does American T. Transmit?

A
  • Kissing bugs (parasite in faeces of bugs)
  • Blood transmission
  • Transplacental route
45
Q

How is American T. treated?

A

With Benznidazol or Nifurtimox.

46
Q

Acute phase of American T.

A
  • Active infection (1-4 months)
  • Most are asymptomatic (children most likely to be symptomatic)
47
Q

Indeterminate phase of American T.

A

-10-30 years of latency
- Seropositive with no detectable parasitemia

48
Q

Chronic phase of American T.

A

-10-30% of infected exhibit cardiomyopathy
- Arrythmias and conduction defects
- Congestive heart failure
- Thromboembolic phenomenon

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