Intro to Protozoans pt1 Flashcards by Medically Makk

Q

INTRODUCTION TO PARASITES

Protozoa

A

(unicellular animal-like microorganisms)

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Q

INTRODUCTION TO PARASITES

Helminths

A

(parasitic worms)

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Q

IMPORTANCE OF PARASITES

Read over slide

A

Simple

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Q

PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL

Pathogenesis of parasitic disease is

A

highly variable.

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Q

PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL

The organisms themselves are

A

not highly virulent.

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Q

PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL

Some are ____ to replicate within the host.

A

unable

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Q

PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL

Parasitic infections are often , _____ lasting months to years.

A

chronic

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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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Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

what type of smear and how many?

A

3-4 blood smears

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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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Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

ova

A

(of worms)

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Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

cysts

A

(of protozoa)

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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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Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

Immunoassays can be utilized for

A

Giardia

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Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

Where can you easily see Giardia at?

A

Can be seen in stool samples

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Q

LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS

A

Look over powerpoint slide 5

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Q

BIOLOGIC, MORPHOLOGIC, AND PHYSIOLOGIC CHARACTERISTICS OF PATHOGENIC PROTOZOA

A

look over powerpoint

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Q

ROLE OF PROTOZOANS IN DISEASE

Trypanosoma cruzi

A

Chagas disease

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Q

ROLE OF PROTOZOANS IN DISEASE

Trypanosoma brucei (gambiense & rhodesiense

A

trybass

African sleeping sickness

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Q

ROLE OF PROTOZOANS IN DISEASE

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

A

Malaria

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Q

ROLE OF PROTOZOANS IN DISEASE

Entamoeba histolytica

A

Amebiasis

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Q

ROLE OF PROTOZOANS IN DISEASE

Giardia lamblia

A

Giardiasis

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Q

CHARACTERISTICS OF TRYPANOSOMA SPP

hemoflagellates

A

parastic protozoan flagellates that are found in the blood

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Q

CHARACTERISTICS OF TRYPANOSOMA SPP

vector borne means

A

carried by an insect

transmitted to humans

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# CHARACTERISTICS OF TRYPANOSOMA SPP. Trypomastigote

: large, fully formed stage

# CHARACTERISTICS OF TRYPANOSOMA SPP. Epimastigote

: the flagellate stage

# CHARACTERISTICS OF TRYPANOSOMA SPP. Promastigote

: the stage bearing a single, anterior flagellum

# CHARACTERISTICS OF TRYPANOSOMA SPP Obligate parasites that live in

blood and tissues of human host

# CHARACTERISTICS OF TRYPANOSOMA SPP trypanosoma causes

life-threatening and debilitating zoonoses

# CHARACTERISTICS OF TRYPANOSOMA SPP Spread in specific tropical regions by

blood-sucking insects that serve as intermediate hosts

# CHARACTERISTICS OF TRYPANOSOMA SPP. Amastigote

: the form lacking a free flagellum

# CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES Trypanosoma brucei, Amastigote

Does not occur

# CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES Trypanosoma brucei: Promastigote

Does not occur

# CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES Trypanosoma brucei: Epimastigote

Present in salivary gland of tsetse fly

# CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES Trypanosoma brucei: Trypomastigote

In biting mouthparts of tsetse fly; infective to humans

# CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES Trypanosoma cruzi: Amastigote

Intracellular in human macrophages, liver, heart, spleen

# CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES Trypanosoma cruzi: Promastigote

Does not occur

# CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES Trypanosoma cruzi: Epimastigote

Present in gut of reduviid (kissing) bug

# CELLULAR AND INFECTIVE STAGES OF TRYPANOSOMES Trypanosoma cruzi: Trypomastigote

In feces of reduviid bug; transferred to humans

# TRYPANOSOMA BRUCEI T.b. rhodesiense reservoir hosts:

cattle, sheep, wild game (antelope)

TRYPANOSOMA BRUCEI causes ## Footnote TRYPANOSOMA BRUCEI

African sleeping sickness (African Trypanosomiasis)

# TRYPANOSOMA BRUCEI Spread by

tsetse flies

# TRYPANOSOMA BRUCEI T.b. gambiense –

Gambian strain; West & Central Africa | Camerron,Congo, Angola

# TRYPANOSOMA BRUCEI T.b. rhodesiense

– Rhodesian strain; East Africa | uganda,kenya, zim

# Life Cycle : TRYPANOSOMA BRUCEI Biting of tsetse fly inoculates skin with trypomastigotes, which

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

# Life Cycle :TRYPANOSOMA BRUCEI The entire life cycle of African trypanosomes is represented by

extracellular stages

# Life Cycle :TRYPANOSOMA BRUCEI stage 1: infective stage: tsetse fly takes

tsetse fly takes a blood meal

# Life Cycle :TRYPANOSOMA BRUCEI injected metacyclic trypomastigotes transform into ## Footnote Stage 2

bloodstreams trypomastigotes, which are carried to other sites

# Life Cycle :TRYPANOSOMA BRUCEI trypomastigotes multiply | stage 3

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

stage 4 : diagnostic stage ## Footnote Life Cycle :TRYPANOSOMA BRUCEI

trypomastigotes in blood

stage 5:tsete fly takes ## Footnote Life Cycle :TRYPANOSOMA BRUCEI

a blood meal

bloodstream trypomastigotes transform into | stage 6 ## Footnote Life Cycle :TRYPANOSOMA BRUCEI

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

procyclic trypomastigotes leave the midgut and | stage 7 ## Footnote Life Cycle :TRYPANOSOMA BRUCEI

transform into epimastigotes

epimastigotes multiply in ____. They transform into ____ trypomastigotes | stage 8 ## Footnote Life Cycle :TRYPANOSOMA BRUCEI

* salivary gland * metacyclic

# TRYPANOSOME VIRULENCE FACTORS Indole catabolites (immunosuppression)

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

# TRYPANOSOME VIRULENCE FACTORS Failure to display microbial antigen on host cell surface

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

# TRYPANOSOME VIRULENCE FACTORS Suppression of parasite-specific

B-cell and T-cell responses

# TRYPANOSOME VIRULENCE FACTORS enzymes involved

Hydrolytic enzymes, proteinases, collagenase, elastase

# TRYPANOSOME VIRULENCE FACTORS Antigenic variation of its Variable Surface Glycoprotein (VSG) coat

○ Evade antibody responses

# T. BRUCEI GAMBIENSE CLINICAL FEATURES T. b. gambiense produces ____ , often ending fatally, with ___ involvement after several years’ duration

* chronic disease * CNS

# T. BRUCEI GAMBIENSE CLINICAL FEATURES One of the earliest signs of disease is an occasional

ulcer at the site of the fly bite.

Chronic disease symptoms are ## Footnote T. BRUCEI GAMBIENSE CLINICAL FEATURES

sleep disturbances, tremors, paralysis, and coma

# 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.

T. BRUCEI GAMBIENSE CLINICAL FEATURES

Death is the result of CNS damage and other infections such as ____ or ____ ## Footnote T. BRUCEI GAMBIENSE CLINICAL FEATURES

malaria or pneumonia.

Swelling of the posterior cervical lymph nodes is characteristic of Gambian disease and is ## Footnote T. BRUCEI GAMBIENSE CLINICAL FEATURES

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

As reproduction of organisms continues, the lymph nodes are invaded, and fever, myalgia,arthralgia, and ____ result. ## Footnote T. BRUCEI GAMBIENSE CLINICAL FEATURES

lymph node enlargement (lymphadenopathy)

# T. BRUCEI RHODESIENSE CLINICAL FEATURES The incubation period for T. b. ____ is shorter than that for T. b. ____

* rhodesiense * gambiense

# T. BRUCEI RHODESIENSE CLINICAL FEATURES ________ disease (fever, rigors, and myalgia) occurs more rapidly and progresses to a fulminating, rapidly fatal illness.

Acute

This more virulent organism also develops in ____ numbers in the blood. ## Footnote T. BRUCEI RHODESIENSE CLINICAL FEATURES

greater

# T. BRUCEI RHODESIENSE CLINICAL FEATURES Lymphadenopathy is uncommon, and CNS invasion occurs ____ in the infection, with lethargy, anorexia, and mental disturbance

early

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

kidney damage and myocarditis

# T. BRUCEI DIAGNOSIS: BLOOD SMEARS features of the organism

* sea horse shape * smaller eye * larger than a red blood cell

# T. BRUCEI DIAGNOSIS: BLOOD SMEARS serological test are

1. Immunofluorescence 2. ELISA 3. precipitin 4. agglutination methods

TRYPANOSOMA CRUZI

Causes Chagas Disease (American Trypanosomiasis)

# TRYPANOSOMA CRUZI Spread by

Reduviid bug (kissing bug or assassin bug)

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

parasitized reduviid bugs or their feces in food or drink

# what bug and diease? * Central and South America * Mexico and southern parts of the U.S. * Texas (up and coming)

Reduviid bug , (TRYPANOSOMA CRUZI

# What disease? - Human disease is found most often among children in south and central america

CHAGAS DISEASE

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

animal burrows

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

infective metacyclic trypomastigotes ## Footnote -been documented in south america and may be more common than previously thought

# Life Cycle: Chagas disease Infection occurs when bug feces are inoculated into the site of the ______ releasing ____

bite wound releasing trypomastigotes

# Life Cycle: Chagas disease Bloodstream trypomastigotes do not

replicate

# Life Cycle: Chagas disease Mechanism of Attachment and Receptor:

penetrin, fibronectin, and fibronectin receptor

# What diease has these symptoms? Local lesion, fever, and swelling of lymph nodes, spleen, and liver

Chagas disease | Life Cycle: Chagas disease

# Life Cycle: Chagas disease Heart muscle and large intestine harbor masses

harbor masses of amastigotes

# Life Cycle: Chagas disease Chronic inflammation occurs in the

organs (especially heart and brain)

# Life Cycle: Chagas disease triatomine bug takes a blood meal. how do they enter ? (2 ways) | Stage 1

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

# Life Cycle: Chagas disease Metacyclic trypomastigotes penetrate various cells at bite wound site. Inside cells they transform into ## Footnote Stage 2 : Human stage

amastigotes

# Life Cycle: Chagas disease amastigotes multiply by ______ in cells of infected tissues ## Footnote Stage 3: Human stage

binary fission

# Life Cycle: Chagas disease intracellular amastigotes transform into ____ then burst out of the cell and enter the _____ ## Footnote Stage 4: Human stage

* trypomastigotes * bloodstream | wont replicate

# Life Cycle: Chagas disease trypomastigotes can infect other cells and tranform into ## Footnote human stage inbetween

intracellular amastigotes in new infection sites. ## Footnote Clinical manifestations can result from this infective stage.

# Life Cycle: Chagas disease triatomine bug takes ## Footnote stage 5

a blood meal (trypomastigotes ingested)

# Life Cycle: Chagas disease Stages 6, 7, and 8

6. epimastigotes in midgut 7. multiply in midgut 8. metacyclic trypomastigotes in hindgut

# T. CRUZI VIRULENCE FACTORS Intracellular location

If in muscle, immune cant find you

Chagas disease may be _____ , _____ , or _____ ## Footnote T. CRUZI CLINICAL FEATURES

asymptomatic, acute, or chronic

# T. CRUZI VIRULENCE FACTORS Escape from phagosome into

cytoplasm, with subsequent replication

T. CRUZI VIRULENCE FACTORS

Look over slide and read in the book

# T. CRUZI CLINICAL FEATURES One of the earliest signs is development of an erythematous and indurated area, called a

chagoma, at the site of the bug bite.

# T. CRUZI CLINICAL FEATURES a rash and edema around the eyes and face | what is it called?

(Romaña sign).

# T. CRUZI CLINICAL FEATURES The disease is most severe in children younger than 5 years and frequently is seen as an ___

acute process with CNS involvement.

# 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.

fever, chills, malaise, myalgia, and fatigue.

# 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 ____

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

# 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.

Chronic Chagas disease

# 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 _______.

cyst formation and a meningoencephalitis.

# 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 _____

complete heart block and brain damage.

# T. CRUZI DIAGNOSIS Culture of blood or inoculation into laboratory animals may be useful when the

parasitemia is low

# diagnosis for ? Thick and thin blood films or concentrated anticoagulated blood early in the acute stage

chagas diease, TRYPANOSOMA CRUZI ## Footnote T. CRUZI DIAGNOSIS

In endemic areas, xenodiagnoses is widely used ## Footnote T. CRUZI DIAGNOSIS

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

Screening of blood donors form endemic areas that would otherwise be associated with ## Footnote T. CRUZI

transfusion therapy

# what protozoa? Notorious for biting, feeding on blood and tissue juices and then defecating into the wound

TRYPANOSOMA CRUZI