Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

Microbiology Final > Blood-borne Parasitic Diseases > Flashcards

Blood-borne Parasitic Diseases Flashcards

You may prefer our related Brainscape-certified flashcards:
Biology 101 flashcards
1
Q

Malaria vector

A

Anopheles mosquito

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

Malaria species

A 
Plasmodium vivax
P. falciparum
P. malariae
P. ovale
P. knowlesi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Malaria life cycle

A
  • SPOROZOITES from mosquito saliva
  • SCHIZOGONY cycle begins in liver
  • MEROZOITES released from the liver
  • Merozoites become uninucleate RING TROPHOZOITE
  • Trophozoites age and can develop into AMOEBOID trophozoites or become MULTINUCLEATED SCHIZONT
  • Erythrocytic schizonts can produce erythrocytic MEROZOITES
  • RBC ruptures and they invade new cells
  • Schizogony begins again or GAMETOGONY is initiated
  • Mosquito feeds and takes in GAMETOCYTES that lead to sexual reproduction in the mosquito

Cycle starts over in new host

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

Motile form of plasmodium

A

Sporozoites

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

Cycle that takes place in the liver

A

Schizogony

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

Released from the liver

A

Merozoites

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

Cycle that takes place in the RBC

A

Erythrocytic cycle

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

Differentiation in RBC to…

A

Ring trophozoite

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

Uninucleated plasmodium in the RBC

A

Ring trophozoite

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

Mature ring trophozoite

A

Amoeboid trophozoite

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

Multinucleated trophozoite

A

Schizont

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Erythrocytic schizonts can produce…

A

Erythrocytic merozoites OR

Gametocytes

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

Sexual cycle of plasmodium

A

Gametogony

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

Sexual form of plasmodium

A

Gametocytes (male or female)

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

Plasmodium that do not rupture erythrocyte

A

Gametocytes

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

Pathogenicity of Malaria

A
  • Consumes hemoglobin & destroys RBCs
  • Fever and chills from PYROGENIC waste
  • TNF intensifies symptoms
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Other signs of Malaria

A

Anemia
Hypotension
GI, HA, myalgia

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

Host resistance to malaria

A
  • Sickle cell = FALCIPARUM

- Duffy gene off (black people) = VIVAX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Malaria reservoirs

A

Humans

Simians

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Infects YOUNG erythrocytes

A

P. pivax

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

P. vivax key points

A
  • Seldom fatal
  • Young erythrocytes
  • Caribbean, Latin America
  • Primates are NOT reservoirs
  • Sickle cell affords natural protection
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Liver hypnozoites

A

Dormant (3-5 years) form of VIVAX

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

P. vivax locations

A

Caribbean
Latin America
**Rare in US and West Africa

24
Q

P. vivax diagnosis

A

GIEMSA STAIN

  • Enlarged infected RBCs with SCHUFFNER’s DOTS (surface invaginations and stipling)
  • Few infected cells
25
Q

Schuffner’s dots

A

P. vivax

26
Q

Blackwater fever

A

Result of P. falciparum:

  • High levels of free hemoglobin in urine
  • Leads to autoimmune reaction in which host destroys kidney
  • Chills, fever, rigor, dark to black urine
27
Q

P. falciparum key points

A
  • HIGH GRADE PARASITEMIA (all RBCs can be infected)
  • Multiples rapidly
  • High fever
  • NO hypnozoite stage (non relapsing)
28
Q

P. falciparum complications

A
  • Black water fever
  • Cerebral malaria
  • Gastric falciparum malaria
  • Algid malaria
29
Q

Cerebral malaria

A

Occlusion of capillaries results in necrosis, hemorrhages, extreme fever, mania, convulsions, and death

30
Q

Gastric falciparum malaria

A

Frequent vomiting in addition to other symptoms

31
Q

Algid malaria

A

Skin is cold but internal temp is high

32
Q

P. falciparum diagnosis

A

Erythrocytes with:

  • Double or multiple ring stages
  • Crescent shaped gametocyte
  • MAURER’S CLEFTS
  • Many infected cells

Young trophozoites and gametocytes (but NOT schizonts) observed in the periphery

33
Q

Older erythrocytes

A

P. malariae

34
Q

P. malariae key notes

A
  • Older erythrocytes
  • Paroxysms every 4th day
  • Zoonotic from primate reservoir
  • Basket and band shaped trophozoites
  • Rosette shaped schizonts
35
Q

P. ovale key points

A
  • Similar to P. vivax
  • Relapses common
  • Common to west coast of Africa
36
Q

P. knowlesi

A
  • Zoonotic
  • Maybe life-threatening if a heavy parasite burden
  • Usually found in Southeast Asia
37
Q

Relapses common

A

Vivax

Ovale

38
Q

Resistance mechanism of malaria species

A

Efflux pumps

39
Q

Nantucket Island Fever (Babesiosis) cause

A

Babesia microti

40
Q

Vector for babesiosis

A

Deer tick

41
Q

Babesiosis clinical manifestations

A

Similar to malaria:

  • Fever, chills, HA, anemia
  • Small pinpoint lesions (no significant rash)
  • Ranges from asymptomatic to life-threatening
42
Q

Risk fo life-threatening babesiosis

A
  • Immunocompromised
  • Asplenic
  • 50% mortality rate in Europe
43
Q

Coinfection with babesiosis

A

Lyme Disease

44
Q

Babesiosis morphology

A

“Cross-like” morphology in RBCs

45
Q

Preventing babesiosis

A

Insect repellant

46
Q

African sleeping sickness cause

A

Trypanosoma brucei

47
Q

Chagas disease cause

A

Trypanosoma cruzi

48
Q

Chaga’s vector

A
  • Triamtomine bugs (“Kissing bug”)***
  • Blood transfusions
  • Organ tranpslants
  • Congenital
49
Q

T. cruzi life cycle

A
  • TRYPOMASTIGOTES passed in feces of tiatomine bug at site of bite
  • Trypomastigotes enter cells near inoculation site and differentiate into AMASTIGOTES
  • Amastigotes replicate by binary fission in cells and differentiate into trypomastigotes
  • Host cell ruptures and trypomastigotes released into circulation
  • Ingested during bloodmeal by tiatomine bug and cycle starts over
50
Q

Romana’s sign

A

Swelling of the eyelid near the parasite entry site

51
Q

2 stages of Chaga’s Disease

A

Acute

Chronic

52
Q

Acute Chaga’s

A
  • Asymptomatic to mild manifestation
  • Non-specific signs/symptoms
  • CHAGOMA
  • ROMANA’S SIGN (most characteristic)

*Upon waning of signs and symptoms, organism persists

53
Q

Chronic Chaga’s

A
  • Infection may be asymptomatic for years (even for life)
  • Pseudocysts of amastigotes in cells (preferentially in muscle and nerves - degeneration and necrosis)
  • Chronic inflammation of organs (enlarged organs)
54
Q

Complications of chronic chaga’s

A
  • Cardiac: Cardiomyopathy, HF, arrhythmia, cardiac arrest

- Intestinal: Enlarged esophagus and colon

55
Q

Chaga’s diagnosis

A

Observe parasite on microscopy:

  • Blood smear (acute phases): Trypomastigotes
  • Biopsy (chronic cases): Amastigotes

Serologic tests
PCR test available

56
Q

Chaga’s prevention

A
  • Vaccine being developed
  • Spray houses with insecticides in endemic areas
  • Bed nets
  • Screen blood, organ, and tissue donors
  • Screen newborns of infected mothers

Microbiology Final (8 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions