Intro to Protozoans pt1 Flashcards
slides 2 to 23
INTRODUCTION TO PARASITES
Protozoa
(unicellular animal-like microorganisms)
INTRODUCTION TO PARASITES
Helminths
(parasitic worms)
IMPORTANCE OF PARASITES
Read over slide
Simple
PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL
Pathogenesis of parasitic disease is
highly variable.
PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL
The organisms themselves are
not highly virulent.
PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL
Some are ____ to replicate within the host.
unable
PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL
Parasitic infections are often , _____ lasting months to years.
chronic
PATHOGENESIS OF PARASITIC INFECTIONS IN GENERAL
Parasites are almost always exogenous to the human host and must enter the body through ___
ingestion or direct penetration of anatomic barriers
LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS
what type of smear and how many?
3-4 blood smears
LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS
Routine microscopic examination of stool for ____ is useful for detecting
ova and parasites (O&P)
LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS
ova
(of worms)
LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS
cysts
(of protozoa)
LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS
Concentration of specimens by sedimentation or flotation techniques may be required to detect
to detect low numbers of ova (of worms) or cysts (of protozoa) in fecal specimens.
LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS
Immunoassays can be utilized for
Giardia
LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS
Where can you easily see Giardia at?
Can be seen in stool samples
LABORATORY DIAGNOSIS OF PARASITIC INFECTIONS
Look over powerpoint slide 5
BIOLOGIC, MORPHOLOGIC, AND PHYSIOLOGIC CHARACTERISTICS OF PATHOGENIC PROTOZOA
look over powerpoint
ROLE OF PROTOZOANS IN DISEASE
Trypanosoma cruzi
Chagas disease
ROLE OF PROTOZOANS IN DISEASE
Trypanosoma brucei (gambiense & rhodesiense
trybass
African sleeping sickness
ROLE OF PROTOZOANS IN DISEASE
Plasmodium spp. (P. vivax, P. falciparum)
Malaria
ROLE OF PROTOZOANS IN DISEASE
Entamoeba histolytica
Amebiasis
ROLE OF PROTOZOANS IN DISEASE
Giardia lamblia
Giardiasis
CHARACTERISTICS OF TRYPANOSOMA SPP
hemoflagellates
parastic protozoan flagellates that are found in the blood
CHARACTERISTICS OF TRYPANOSOMA SPP
vector borne means
carried by an insect
transmitted to humans
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
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
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
Life Cycle :TRYPANOSOMA BRUCEI
trypomastigotes in blood
stage 5:tsete fly takes
Life Cycle :TRYPANOSOMA BRUCEI
a blood meal
bloodstream trypomastigotes transform into
stage 6
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
Life Cycle :TRYPANOSOMA BRUCEI
transform into epimastigotes
epimastigotes multiply in ____. They transform into ____ trypomastigotes
stage 8
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
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 ____
T. BRUCEI GAMBIENSE CLINICAL FEATURES
malaria or pneumonia.
Swelling of the posterior cervical lymph nodes is characteristic of Gambian disease and is
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.
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.
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
- Immunofluorescence
- ELISA
- precipitin
- 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
-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
- passes metacyclic trypomastigotes in feces
- 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
Stage 2 : Human stage
amastigotes
Life Cycle: Chagas disease
amastigotes multiply by ______ in cells of infected tissues
Stage 3: Human stage
binary fission
Life Cycle: Chagas disease
intracellular amastigotes transform into ____ then burst out of the cell and enter the _____
Stage 4: Human stage
- trypomastigotes
- bloodstream
wont replicate
Life Cycle: Chagas disease
trypomastigotes can infect other cells and tranform into
human stage inbetween
intracellular amastigotes in new infection sites.
Clinical manifestations can result from this infective stage.
Life Cycle: Chagas disease
triatomine bug takes
stage 5
a blood meal (trypomastigotes ingested)
Life Cycle: Chagas disease
Stages 6, 7, and 8
- epimastigotes in midgut
- multiply in midgut
- metacyclic trypomastigotes in hindgut
T. CRUZI VIRULENCE FACTORS
Intracellular location
If in muscle, immune cant find you
Chagas disease may be _____ , _____ , or _____
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
T. CRUZI DIAGNOSIS
In endemic areas, xenodiagnoses is widely used
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
T. CRUZI
transfusion therapy
what protozoa?
Notorious for biting, feeding on blood and tissue juices and then defecating into the wound
TRYPANOSOMA CRUZI