Para Flashcards

1
Q

What is a parasite?

A

→parasite is an organism that lives on or in a host organism and gets its food from or at the expense of its host

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2
Q

What are the three main classes of parasite?

A

→Protozoa

→Helminths

→Ectoparasites

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3
Q

What are protozoa?

A

→microscopic, single-celled organisms that can be free- living

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4
Q

How are protozoa living in the intestine transmitted?

A

→ can be transmitted by the faecal-oral route

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5
Q

How are protozoa living in blood transmitted?

A

→transmitted by an arthropod vector

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6
Q

How are protozoa classified?

A

→by mode of movement

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7
Q

What are 4 types of protozoa?

A

→Amoeba, e.g. Entamoeba

→Flagellates, e.g. Giardia, Leishmania

→Ciliates e.g. Balantidium

→Sporozoa – organisms whose adult stage is not motile
e.g. Plasmodium, Cryptosporidium

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8
Q

Name some medically important protozoa infections

A

→Entamoeba histolytica- amoebic dysentery- forms ulcers in the large intestines
→Trichomonas vaginalis- STD
→Malaria (Plasmodium spp.)

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9
Q

What are helminths?

A

→large, multicellular organisms (worms)

→visible to the naked eye in their adult stages

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10
Q

When can helminths not multiply?

A

→adult form

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11
Q

What are the three groups of helminths?

A

→Nematodes (roundworms)

→Trematodes (flukes)

→Cestodes (tapeworms)

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12
Q

What are the three types of medically important nematodes?

A

→Soil-transmitted helminths
→Filarial parasites
→Others

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13
Q

Give an example of soil transmitted nematode

A

→Hookworm spp.- small intestines

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14
Q

What is the difference between Taenia saginata and Taenia solium?

A

→Taenia solium is shorter than saginata

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15
Q

Where can Taenia solium larvae migrate to?

A

→brain

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16
Q

What are ectoparasites?

A

→Blood-sucking arthropods such as ticks, fleas, lice, and mites

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17
Q

How long do ectoparasites remain in the skin?

A

→weeks to months

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18
Q

What are the 4 types of ectoparasites?

A

→mites
→ticks
→lice
→flies

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19
Q

What are the 2 types of hosts of parasites?

A

→Intermediate – host in which larval or asexual stages develop eg shictoma uses snail

Definitive – host in which adult or sexual stage occurs

20
Q

What are the types of vectors?

A

→Mechanical when no development of parasite in vector

→Biological when some stages of life cycle occur

21
Q

What is a primary determinant of distributions of parasite infections in the humans?

A

→Relative wealth

22
Q

What are other determinants of parasite infections?

A

→Government resources and level of human development/per capita income
→Education
→Country-level and regional control programmes
→Availability of cheap and efficacious treatments
→Construction and building regulations (eg Chagas)
→Urban vs. rural residence
→Environmental sanitation

23
Q

Describe the life cycle of Trypansoma cruzi(Chagas)

A

→triatomine bug takes a blood meal
→metacyle trypomastigotes penetrate various cells at bite wound
→amastigotes multiply by binary fission
→intracellular amastigotes transform into trypomastigotes
→they burst out of cells and enter blood stream
→epimastigotes in midgut multiply

24
Q

Where is Chagas endemic to?

A

→South America

25
Q

What are the phases of disease?

A

→acute
→intermediate chronic
→determinate chronic

26
Q

Describe the acute phase of Chagas disease

A

→Incubation 1-2 wks after bite

→Up to months after transfusion

→Trypanosomes in blood

27
Q

Describe the intermediate phase of Chagas

A

→Lifelong infection

→trypanosomes not detectable but often positive for parasite DNA

→Seropositive
→60-70%
→Normal ECG and X rays

28
Q

Describe the determinate phase of chronic disease

A

→Seropositive

29
Q

Describe the symptoms of acute Chagas

A

→Local swelling (Romaña)

→Nodule or chagoma

→Fever

→Anorexia

→Lymphadenopathy

30
Q

How long do symptoms last in Chagas?

A

→8-10 wks

31
Q

What are rare effects of Chagas?

A

→Hepatopsplenomegaly

→Acute myocarditis

→Meningoencephalitis

→fatal

32
Q

What is Chagas effect on the heart?

A

→damage to Purkinje fibres
→thin heart muscles
→aneurysms of the muscle

33
Q

What parts of the digestive tract does chronic commonly Chagas affect?

A

→Esophagus,
→rectum,
→sigmoid
→colon

34
Q

What is the main presentation for chronic Chagas affect on the colon?

A

→megacolon

→constipation

35
Q

What are the complications of a megacolon?

A

→Faecaloma

→Obstruction

→Sigmoid volvulus

→Ulceration

→Perforation

36
Q

Describe acute immune response to Chagas pathogenesis

A

→Tissue damage caused by inflammatory response
→Parasite killing by antibodies
→Th1 pro- inflammatory cytokines

37
Q

Describe immediate immune response to Chagas pathogenesis

A

→characterized by IL-10 and IL-17

38
Q

Describe chronic immune response to Chagas pathogenesis

A

→Predominance of Th1 cytokines and CD8+ T cells

→Autoimmune mechanisms

39
Q

What is the difference between Old World and New World cutaneous leishmaniasis?

A

→Old World- Mediterranean/Middle East

→New world- Central and South America

40
Q

Describe the life cycle of leismaniasis

A

→sandfly bites skin
→promastigote engulfed by histocyte
→binary fission
→amastigotes in histocytes infect other cells
→amastigotes released and taken up by sandfly

41
Q

What is the vector of leismaniasis?

A

→sandfly

→feed on chicken

42
Q

What are the clinical features of cutaneous leishmaniasis?

A

→purple colouring
→plaques
→ulcer

43
Q

What can happen in the most serious cases of leishmaniasis?

A

→uncontrolled proliferation of parasites on skin

44
Q

Describe chronic leishmaniasis pathogenesis

A

→Mucocutaneous disease associated with strong but inadequate inflammatory response to parasites that have metastasized to mucosa

→Diffuse cutaneous leishmaniasis associated with uncontrolled parasite replication.

→Recividans – recurrence of lesions at old ulcer site

→alteration in immune reponse

45
Q

Describe latent leishmaniasis pathogenesis

A

→characterized by balance of Th1 and anti-inflammatory responses
→use of steroids

46
Q

Describe acute leishmaniasis pathogenesis

A

→Parasite killing by Th1 pro-inflammatory responses

→Tissue damage caused by inflammatory response