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Microbiology > Intro to Protozoans pt1 > Flashcards

Intro to Protozoans pt1 Flashcards

slides 2 to 23

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1
Q

INTRODUCTION TO PARASITES

Protozoa

A

(unicellular animal-like microorganisms)

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2
Q

INTRODUCTION TO PARASITES

Helminths

A

(parasitic worms)

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3
Q

IMPORTANCE OF PARASITES

Read over slide

A

Simple

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4
Q

PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL

Pathogenesis of parasitic disease is

A

highly variable.

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5
Q

PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL

The organisms themselves are

A

not highly virulent.

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6
Q

PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL

Some are ____ to replicate within the host.

A

unable

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7
Q

PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL

Parasitic infections are often , _____ lasting months to years.

A

chronic

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8
Q

PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL

Parasites are almost always exogenous to the human host and must enter the body through ___

A

ingestion or direct penetration of anatomic barriers

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9
Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

what type of smear and how many?

A

3-4 blood smears

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10
Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

Routine microscopic examination of stool for ____ is useful for detecting

A

ova and parasites (O&P)

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11
Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

ova

A

(of worms)

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12
Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

cysts

A

(of protozoa)

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13
Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

Concentration of specimens by sedimentation or flotation techniques may be required to detect

A

to detect low numbers of ova (of worms) or cysts (of protozoa) in fecal specimens.

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14
Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

Immunoassays can be utilized for

A

Giardia

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15
Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

Where can you easily see Giardia at?

A

Can be seen in stool samples

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16
Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

A

Look over powerpoint slide 5

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17
Q

BIOLOGIC, MORPHOLOGIC, AND PHYSIOLOGIC CHARACTERISTICS OF PATHOGENIC PROTOZOA

A

look over powerpoint

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18
Q

ROLE OF PROTOZOANS IN DISEASE

Trypanosoma cruzi

A

Chagas disease

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19
Q

ROLE OF PROTOZOANS IN DISEASE

Trypanosoma brucei (gambiense & rhodesiense

A

trybass

African sleeping sickness

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20
Q

ROLE OF PROTOZOANS IN DISEASE

Plasmodium spp. (P. vivax, P. falciparum)

A

Malaria

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21
Q

ROLE OF PROTOZOANS IN DISEASE

Entamoeba histolytica

A

Amebiasis

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22
Q

ROLE OF PROTOZOANS IN DISEASE

Giardia lamblia

A

Giardiasis

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23
Q

CHARACTERISTICS OF TRYPANOSOMA SPP

hemoflagellates

A

parastic protozoan flagellates that are found in the blood

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24
Q

CHARACTERISTICS OF TRYPANOSOMA SPP

vector borne means

A

carried by an insect

transmitted to humans

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25
Q

CHARACTERISTICS OF TRYPANOSOMA SPP.

Trypomastigote

A

: large, fully formed stage

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26
Q

CHARACTERISTICS OF TRYPANOSOMA SPP.

Epimastigote

A

: the flagellate stage

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27
Q

CHARACTERISTICS OF TRYPANOSOMA SPP.

Promastigote

A

: the stage bearing a single, anterior flagellum

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28
Q

CHARACTERISTICS OF TRYPANOSOMA SPP

Obligate parasites that live in

A

blood and tissues of human host

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29
Q

CHARACTERISTICS OF TRYPANOSOMA SPP

trypanosoma causes

A

life-threatening and debilitating zoonoses

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30
Q

CHARACTERISTICS OF TRYPANOSOMA SPP

Spread in specific tropical regions by

A

blood-sucking insects that serve as intermediate hosts

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31
Q

CHARACTERISTICS OF TRYPANOSOMA SPP.

Amastigote

A

: the form lacking a free flagellum

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32
Q

CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES

Trypanosoma brucei, Amastigote

A

Does not occur

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33
Q

CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES

Trypanosoma brucei: Promastigote

A

Does not occur

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34
Q

CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES

Trypanosoma brucei: Epimastigote

A

Present in salivary gland of tsetse fly

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35
Q

CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES

Trypanosoma brucei: Trypomastigote

A

In biting mouthparts of tsetse fly; infective to humans

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36
Q

CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES

Trypanosoma cruzi: Amastigote

A

Intracellular in human macrophages, liver, heart, spleen

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37
Q

CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES

Trypanosoma cruzi: Promastigote

A

Does not occur

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38
Q

CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES

Trypanosoma cruzi: Epimastigote

A

Present in gut of reduviid (kissing) bug

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39
Q

CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES

Trypanosoma cruzi: Trypomastigote

A

In feces of reduviid bug; transferred to humans

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40
Q

TRYPANOSOMA BRUCEI

T.b. rhodesiense reservoir hosts:

A

cattle, sheep, wild game
(antelope)

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41
Q

TRYPANOSOMA BRUCEI causes

TRYPANOSOMA BRUCEI

A

African sleeping sickness (African
Trypanosomiasis)

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42
Q

TRYPANOSOMA BRUCEI

Spread by

A

tsetse flies

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43
Q

TRYPANOSOMA BRUCEI

T.b. gambiense –

A

Gambian strain; West & Central
Africa

Camerron,Congo, Angola

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44
Q

TRYPANOSOMA BRUCEI

T.b. rhodesiense

A

– Rhodesian strain; East Africa

uganda,kenya, zim

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45
Q

Life Cycle : TRYPANOSOMA BRUCEI

Biting of tsetse fly inoculates skin with trypomastigotes, which

A

multiplies in blood and damages spleen, lymph nodes, and brain

46
Q

Life Cycle :TRYPANOSOMA BRUCEI

The entire life cycle of African trypanosomes is represented by

A

extracellular stages

47
Q

Life Cycle :TRYPANOSOMA BRUCEI

stage 1: infective stage: tsetse fly takes

A

tsetse fly takes a blood meal

48
Q

Life Cycle :TRYPANOSOMA BRUCEI

injected metacyclic trypomastigotes transform into

Stage 2

A

bloodstreams trypomastigotes, which are carried to other sites

49
Q

Life Cycle :TRYPANOSOMA BRUCEI

trypomastigotes multiply

stage 3

A

by binary fission in various body fluids, e.g. blood, lymph, and spinal fluid

50
Q

stage 4 : diagnostic stage

Life Cycle :TRYPANOSOMA BRUCEI

A

trypomastigotes in blood

51
Q

stage 5:tsete fly takes

Life Cycle :TRYPANOSOMA BRUCEI

A

a blood meal

52
Q

bloodstream trypomastigotes transform into

stage 6

Life Cycle :TRYPANOSOMA BRUCEI

A

procyclic trypomastigotes in tsets fly’s midgut. Procyclic trypomastigotes multiply by binary fission

53
Q

procyclic trypomastigotes leave the midgut and

stage 7

Life Cycle :TRYPANOSOMA BRUCEI

A

transform into epimastigotes

54
Q

epimastigotes multiply in ____. They transform into ____ trypomastigotes

stage 8

Life Cycle :TRYPANOSOMA BRUCEI

A
  • salivary gland
  • metacyclic
55
Q

TRYPANOSOME VIRULENCE FACTORS

Indole catabolites (immunosuppression)

A

○ Toxic byproducts of organisms: decreases glycolysis with macrophages which inhibits them and helps in immunovasion
○ Inhibits the proinflammatory cytokine IL-1Beta

56
Q

TRYPANOSOME VIRULENCE FACTORS

Failure to display microbial antigen on host cell surface

A

○ Evade antibody responses (MHC molecules and on themselves) - hard to have vaccines for them

57
Q

TRYPANOSOME VIRULENCE FACTORS

Suppression of parasite-specific

A

B-cell and T-cell responses

58
Q

TRYPANOSOME VIRULENCE FACTORS

enzymes involved

A

Hydrolytic enzymes, proteinases, collagenase, elastase

59
Q

TRYPANOSOME VIRULENCE FACTORS

Antigenic variation of its Variable Surface Glycoprotein (VSG) coat

A

○ Evade antibody responses

60
Q

T. BRUCEI GAMBIENSE CLINICAL FEATURES

T. b. gambiense produces ____ , often ending fatally, with ___ involvement after several years’ duration

A
  • chronic disease
  • CNS
61
Q

T. BRUCEI GAMBIENSE CLINICAL FEATURES

One of the earliest signs of disease is an occasional

A

ulcer at the site of the fly bite.

62
Q

Chronic disease symptoms are

T. BRUCEI GAMBIENSE CLINICAL FEATURES

A

sleep disturbances, tremors, paralysis, and coma

63
Q

What protozoa is this?

In the final stages of chronic disease, convulsions, hemiplegia, and incontinence occur, and the patient becomes difficult to arouse or evoke a response, eventually progressing to a comatose state.

A

T. BRUCEI GAMBIENSE CLINICAL FEATURES

64
Q

Death is the result of CNS damage and other infections such as ____ or ____

T. BRUCEI GAMBIENSE CLINICAL FEATURES

A

malaria or pneumonia.

65
Q

Swelling of the posterior cervical lymph nodes is characteristic of Gambian disease and is

T. BRUCEI GAMBIENSE CLINICAL FEATURES

A

Winterbottom sign. Patients in this acute phase often exhibit hyperactivity.

66
Q

As reproduction of organisms continues, the lymph nodes are invaded, and fever, myalgia,arthralgia, and ____ result.

T. BRUCEI GAMBIENSE CLINICAL FEATURES

A

lymph node enlargement (lymphadenopathy)

67
Q

T. BRUCEI RHODESIENSE CLINICAL FEATURES

The incubation period for T. b. ____ is shorter than that for T. b. ____

A
  • rhodesiense
  • gambiense
68
Q

T. BRUCEI RHODESIENSE CLINICAL FEATURES

________ disease (fever, rigors, and myalgia) occurs more rapidly and progresses to a fulminating, rapidly fatal illness.

A

Acute

69
Q

This more virulent organism also develops in ____ numbers in the blood.

T. BRUCEI RHODESIENSE CLINICAL FEATURES

A

greater

70
Q

T. BRUCEI RHODESIENSE CLINICAL FEATURES

Lymphadenopathy is uncommon, and CNS invasion occurs ____ in the infection, with lethargy, anorexia, and mental disturbance

A

early

71
Q

chronic stages for T. b. gambiense leads to an organism produces _______ & ______ leading to death.

A

kidney damage and myocarditis

72
Q

T. BRUCEI DIAGNOSIS: BLOOD SMEARS

features of the organism

A
  • sea horse shape
  • smaller eye
  • larger than a red blood cell
73
Q

T. BRUCEI DIAGNOSIS: BLOOD SMEARS

serological test are

A
  1. Immunofluorescence
  2. ELISA
  3. precipitin
  4. agglutination methods
74
Q

TRYPANOSOMA CRUZI

A

Causes Chagas Disease (American Trypanosomiasis)

75
Q

TRYPANOSOMA CRUZI

Spread by

A

Reduviid bug (kissing bug or assassin bug)

76
Q

TRYPANOSOMA CRUZI

Also spread by blood transfusion, placental transfer, organ transplant, and accidental ingestion of ____

A

parasitized reduviid bugs or their feces in food or drink

77
Q

what bug and diease?

  • Central and South America
  • Mexico and southern parts of the U.S.
  • Texas (up and coming)
A

Reduviid bug , (TRYPANOSOMA CRUZI

78
Q

What disease?

  • Human disease is found most often among children in south and central america
A

CHAGAS DISEASE

79
Q

Direct correlation between infected wild animal reservoir hosts and the presence of infected bugs whose nests are found in human homes
○ Chagas prefer to nest in

A

animal burrows

80
Q

Oral transmission of acute Chagas disease caused by fruit juices contaminated with the reduviid vector or feces containing the ________

A

infective metacyclic trypomastigotes

-been documented in south america and may be more common than previously thought

81
Q

Life Cycle: Chagas disease

Infection occurs when bug feces are inoculated into the site of the ______ releasing ____

A

bite wound releasing trypomastigotes

82
Q

Life Cycle: Chagas disease

Bloodstream trypomastigotes do
not

A

replicate

83
Q

Life Cycle: Chagas disease

Mechanism of Attachment and Receptor:

A

penetrin, fibronectin, and fibronectin receptor

84
Q

What diease has these symptoms?

Local lesion, fever, and swelling of lymph nodes, spleen, and liver

A

Chagas disease

Life Cycle: Chagas disease

85
Q

Life Cycle: Chagas disease

Heart muscle and large intestine harbor masses

A

harbor masses of amastigotes

86
Q

Life Cycle: Chagas disease

Chronic inflammation occurs in the

A

organs (especially heart and brain)

87
Q

Life Cycle: Chagas disease

triatomine bug takes a blood meal. how do they enter ? (2 ways)

Stage 1

A
  1. passes metacyclic trypomastigotes in feces
  2. trypomastigotes enter bite wound or muscoal membranes, such as conjuctiva
88
Q

Life Cycle: Chagas disease

Metacyclic trypomastigotes penetrate various cells at bite wound site. Inside cells they transform into

Stage 2 : Human stage

A

amastigotes

89
Q

Life Cycle: Chagas disease

amastigotes multiply by ______ in cells of infected tissues

Stage 3: Human stage

A

binary fission

90
Q

Life Cycle: Chagas disease

intracellular amastigotes transform into ____ then burst out of the cell and enter the _____

Stage 4: Human stage

A
  • trypomastigotes
  • bloodstream

wont replicate

91
Q

Life Cycle: Chagas disease

trypomastigotes can infect other cells and tranform into

human stage inbetween

A

intracellular amastigotes in new infection sites.

Clinical manifestations can result from this infective stage.

92
Q

Life Cycle: Chagas disease

triatomine bug takes

stage 5

A

a blood meal (trypomastigotes ingested)

93
Q

Life Cycle: Chagas disease

Stages 6, 7, and 8

A
  1. epimastigotes in midgut
  2. multiply in midgut
  3. metacyclic trypomastigotes in hindgut
94
Q

T. CRUZI VIRULENCE FACTORS

Intracellular location

A

If in muscle, immune cant find you

95
Q

Chagas disease may be _____ , _____ , or _____

T. CRUZI CLINICAL FEATURES

A

asymptomatic, acute, or chronic

96
Q

T. CRUZI VIRULENCE FACTORS

Escape from phagosome into

A

cytoplasm, with subsequent replication

97
Q

T. CRUZI VIRULENCE FACTORS

A

Look over slide and read in the book

98
Q

T. CRUZI CLINICAL FEATURES

One of the earliest signs is development of an erythematous and indurated area, called a

A

chagoma, at the site of the bug bite.

99
Q

T. CRUZI CLINICAL FEATURES

a rash and edema around the eyes and face

what is it called?

A

(Romaña sign).

100
Q

T. CRUZI CLINICAL FEATURES

The disease is most severe in children younger than 5 years and frequently is seen as an ___

A

acute process with CNS involvement.

101
Q

T. CRUZI CLINICAL FEATURES

Acute infection is characterized by _____. (What symptoms?) Parasites may be present in the blood during the acute phase; however, they are sparse in patients older than 1 year.

A

fever, chills, malaise, myalgia, and fatigue.

102
Q

T. CRUZI CLINICAL FEATURES

Death may ensue a few weeks after an acute attack, the patient may recover, or the patient may enter the chronic phase as organisms proliferate and enter ____

A

the heart, liver, spleen, brain, and lymph nodes.

103
Q

what diease is this?

is characterized by hepatosplenomegaly, myocarditis, and enlargement of the esophagus (megaesophagus) and colon (megacolon) as a result of the destruction of nerve cells (e.g., Auerbach plexus) and other tissues that control the growth of these organs.

A

Chronic Chagas disease

104
Q

T. CRUZI CLINICAL FEATURES

Megacardia and electrocardiographic changes are commonly seen in chronic disease. Involvement of the CNS may produce granulomas in the brain, with ______ and _______.

A

cyst formation and a meningoencephalitis.

105
Q

T. CRUZI CLINICAL FEATURES

Death from chronic Chagas disease results from tissue destruction in the many areas invaded by the organisms, and sudden death results from _____ and _____

A

complete heart block and brain damage.

106
Q

T. CRUZI DIAGNOSIS

Culture of blood or inoculation into laboratory animals may be useful when the

A

parasitemia is low

107
Q

diagnosis for ?

Thick and thin blood films or concentrated anticoagulated blood early in the acute stage

A

chagas diease, TRYPANOSOMA CRUZI

T. CRUZI DIAGNOSIS

108
Q

In endemic areas, xenodiagnoses is widely used

T. CRUZI DIAGNOSIS

A

Uninfected kissing bugs are allowed to feed on infected patients then dissect gut of the bug

109
Q

Screening of blood donors form endemic areas that would otherwise be associated with

T. CRUZI

A

transfusion therapy

110
Q

what protozoa?

Notorious for biting, feeding on blood and tissue juices and then defecating into the wound

A

TRYPANOSOMA CRUZI

Microbiology (21 decks)

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