• Shuffle
    Toggle On
    Toggle Off
  • Alphabetize
    Toggle On
    Toggle Off
  • Front First
    Toggle On
    Toggle Off
  • Both Sides
    Toggle On
    Toggle Off
  • Read
    Toggle On
    Toggle Off
Reading...
Front

Card Range To Study

through

image

Play button

image

Play button

image

Progress

1/61

Click to flip

Use LEFT and RIGHT arrow keys to navigate between flashcards;

Use UP and DOWN arrow keys to flip the card;

H to show hint;

A reads text to speech;

61 Cards in this Set

  • Front
  • Back
How many vaccines are there for parasitic diseases?
None. They're developing one for malaria, but it's not even 50% effective.
Top 3 infectious/parasitic diseases in terms of deaths caused?
HIV, TB, malaria
2 big divisions in parasites:
Protozoa (unicellular motile)

Helminths (worms)
2 big divisions of helminths:
Nematodes (roundworms)

Platyhelminths (flat worms)
Two types of nematodes:
Luminal (gut) nematodes

Tissue nematodes
Two divisions of platyhelminths:
Trematodes (flukes; non-segmented)

Cestodes (tapeworms/cysts; segmented)
Two types of cestodes:
Luminal cestodes (tapeworms)

Tissue cestodes (cysts)
List all the categories of parasites!
8 types of protozoa:
Amoeba
Babesia
Giardia
Leishmania
Malaria
Toxoplasma
Trichomonas
Trypanosomes
5 types of luminal nematodes:

5 types of tissue nematodes:
Luminal nematodes:
Ascaris
Hookworm
Pin Worm
Strongyloides
Whip Worm

Tissue nematodes:
Dracunculus
Filaria
Loa Loa
Onchocerciasis
Trichinosis
5 species of trematodes:
Schistosomes
Clonorchis
Fasciola
Opisthorchis
Paragonimus
2 species of luminal cestodes:

2 species of tissue cestodes:
Taenia and Diphyllobothrium

Cysticercosis and Hydatid disease
What are Neglected Tropical Diseases? 4
-Serious bacterial & parasitic diseases that affect > 1 billion people worldwide

-Impair physical & cognitive development

-Cause maternal and child morbidity & mortality

-Impact earning capacity
11 examples of Neglected Tropical Diseases.

How might they be controlled? 2
-African trypanosomiasis (African sleeping sickness)
-Chagas’ disease (American trypanosomiasis)
-cysticercosis
-dracunculiasis (Guinea worm disease)*
-echinococcus
-fascioliasis
-leishmaniasis
-lymphatic filariasis*
-onchocerciasis*
-schistosomiasis*
-soil‐transmitted helminths (ascaris, hookworm, whipworm)*

*Disease is controllable by mass drug administration or effective intervention
Trypanosomiasis:
how widespread?
new and old world carriers?
3 traits
-widespread parasites
-“Old world” (Africa): cattle, sheep, goats, wild game, humans
-New world (S. America): cats, dogs, armadillo, humans

-unifying feature = kinetoplast (mitochondrial DNA)
-flagella
-Giemsa staining
-widespread parasites
-“Old world” (Africa): cattle, sheep, goats, wild game, humans
-New world (S. America): cats, dogs, armadillo, humans

-unifying feature = kinetoplast (mitochondrial DNA)
-flagella
-Giemsa staining
Trypanosomiasis
Trypanosome Distribution:
3
West-African type
East-African type
*distinguised by vectors--the type of flies involved

South American type (Shaggar's disease)
West-African type
East-African type
*distinguised by vectors--the type of flies involved

South American type (Shaggar's disease)
East and West African tsetse flies. Why do we care about them?
East: G. morsitans

West: G. palpalis

*These are the vectors for Trypanosomiasis.
List the human (3) and tsetse fly (5) stages in the life cycle of Trypanosomiasis.
Scientific names for the east and west African variants of Trypanosomiasis:
East is T.b. rhodesiense (think rhodesia)

West is T.b. gambiense (aka sleeping sickness, think The Gambia)
Zoonosis:
Infection that is naturally transferable between animals and humans.
Trypanosomiasis, blood stage.
Trypanosomiasis on EM.
Characteristics of a tsetse bite?

How are they able to serve as vectors?
-Usually painful and can have hypersensitivity.

-Tsetse are “pool feeders” (lacerate skin and suck up blood in lesion).
-Metacyclic trypomastigotes in saliva enter bite wound
Acute symptoms and Blood Stage of African Trypanosomiasis:
-incubation period
-characteristic mark
-symptoms?
-∆ between rhodesiense and gambiense
-1-3 week asymptomatic incubation period
sometimes local inflammation
-'trypanosomal chancre'
-parasite replication at bite site
-invasion of blood is characterized by irregular fever and headache
*T. rhodesiense can quickly develop into fulminating infection
*T. gambiense can be self-limiting or slowly progressing to more serious disease
Trypanosomal chancre
Describe the Lymphatic Stage of Trypanosomiasis:
-Disease progression often involves invasion of lymphatics
*Winterbottom’s sign (cervical adenopathy)
*fever, continued febrile attacks
itching
edema
weight loss (cachexia)
weakness
Winterbottom’s sign (cervical adenopathy) in Trypanosomiasis, lymphatic stage.
Describe the CNS disease course and symptoms in African Trypanosomiasis:

∆ b/t East and West African types?
-parasites cross blood-brain barrier
*meningoencephalitis
-increased apathy and fatigue
-confusion and somnolence
-motor changes --> tics, slurred speech, incoordination
-convulsions, coma
-progression to CNS involvement is rapid (weeks) in East African type and slow (6-12 months) in West African type
-death results from disease (eg., convulsions, hyperpyrexia) or other infections
Describe the course of fevers in Trypanosomiasis:
-parasitemia fluctuates

-peak parasitemia usually associated with intermittent fever or other symptoms

-parasites from peaks are antigenically distinct  i.e. variant antigenic types which produce variant surface glycoproteins (VSG; the basis for the
-parasitemia fluctuates

-peak parasitemia usually associated with intermittent fever or other symptoms

-parasites from peaks are antigenically distinct i.e. variant antigenic types which produce variant surface glycoproteins (VSG; the basis for the high spiking fevers)
VSG:
general description:
genetic traits:
-Variant Surface Glycoprotein
-uniformly cover surface of parasite
-form electron dense surface coat

-100’s of VSG genes
-they have conserved regions
-Mutation rate = 10^-3 to 10^-5 per generation
*they mutate a lot; that's the point.
-Variant Surface Glycoprotein
-uniformly cover surface of parasite
-form electron dense surface coat

-100’s of VSG genes
-they have conserved regions
-Mutation rate = 10^-3 to 10^-5 per generation
*they mutate a lot; that's the point.
What's the significance of VSG mutation in Trypanosomiasis?
-VSG is immunogenic and host response clears parasites
-some trypanosomes will change VSG coat because of mutations
-this population expands until host develops immunity against new VSG
How do you diagnose Trypanosomiasis?
clinically 6
what lab tests do you run? 2
Clinical Features:
-travel or residence in endemic area
-history or scar of 'trypanosomal chancre'
-irregular fever, enlarged lymph nodes (esp. posterior cervical), loss of weight
-behavioral changes/mental symptoms

Laboratory Diagnosis:
serological tests
microscopy trypanosomes in blood or CSF (especially during fever)
*blood smear is key
How do you go about detecting African Trypanosomes in a blood smear?
5
-examine on several days
-stained thin or thick smears (thick is best)
-fresh (characteristic movement)
-buffy coat (microhematocrit)
-[inoculate rats or mice, xenodiagnosis, not often done]
Describe other ways to detect African Trypanosomes besides a blood smear: 2
1) Lymph node aspirate- fresh or stained.

2) CSF- examine sediment; increased cells and PRO could indicate infection. Can also stain to see trypanosomes.
Describe early stage treatment of African Trypanosomiasis: 2
Early Stage--no CNS involvement

-suramin
-pentamidine

*excellent prognosis if caught early
Describe late stage treatment of African Trypanosomiasis: 3
Late Stage--CNS involvement

-Melarsoprol
*arsenic based drug; highly toxic (4-12% mortality)

-Eflornithine (DFMO) ± nifurtimox
*expensive; 14 consecutive daily injections
*oral formulation in phase 3 trials
Describe Prophylaxis and Control techniques for African Trypanosomiasis: 5

What's contraindicated? Why
-insect repellants
-protective clothing
-surveillance and treatment
-traps, insecticides placed near livestock
-habitat alteration

drugs are contraindicated (mask infections, toxicity)
-insect repellants
-protective clothing
-surveillance and treatment
-traps, insecticides placed near livestock
-habitat alteration

drugs are contraindicated (mask infections, toxicity)
Describe Trypanosoma cruzi:
what does it cause?
epidemiological info?
-causes Chagas disease
-16-18 million infected
-100 million at risk
-50,000 deaths annually
-leading cause of cardiac disease in S. and Central America
Talk about the bug that spreads Trypanosoma cruzi:
what is the bite like?
what names is it known by?
-painless bite
-called triatomine bugs
AKA reduviid bugs
assassin bugs
kissing bugs
conenose bugs
-painless bite, often around lips or face. The bugs defecate, and the feces gets into the skin via the bite.

-called triatomine bugs
AKA reduviid bugs
assassin bugs
kissing bugs
conenose bugs
-called triatomine bugs
AKA reduviid bugs
assassin bugs
kissing bugs
conenose bugs

-painless bite!
What's a simple intervention to reduce the number of triatomine bugs?
-Replace thatch dwellings with another material. They live in thatch.
Discuss the life cycle of Trypanosoma cruzi:
-Have predilection for the heart
-Called amastigotes in heart because they will replicate there.
-Have predilection for the heart
-Called amastigotes in heart because they will replicate there.
What stain do we use to find trypanosomes in a blood smear?

Can you distinguish b/t the African and S. American type?
-Giemsa stain
-We won't be able to tell. Experts can.
-Giemsa stain
-We won't be able to tell. Experts can.
What factors make triatomine bugs good transmitters of Trypanosoma cruzi? 4
-defecation during triatomine feeding (their bite)
-colonization of human habitats
*adobe walls
*thatched roofs
-para-domiciliary cycles
*animal stalls adjacent to homes (live near livestock, which live near humans)
-proximity to sylvatic cycle (live in the woods, which people go into)
triatomine bug
Describe the Clinical Course of Chagas Disease:
Acute phase
Indeterminate phase
Chronic Phase
-Acute Phase
*active infection (1-2 week incubation)
*1-4 months duration
*most are asymptomatic (children most likely to be symptomatic)

-Indeterminate Phase
*10-30 years of latency
*relatively asymptomatic with no detectable parasitemia
*seropositive

-Chronic Phase
*10-30% of infected exhibit cardiomyopathy or megacolon, -esophagus
*This is the dangerous part!
Why is Chagas disease hard to diagnose and treat?
-It's often asymptomatic at first
-Once it gets to the chronic phase it's hard to treat.
-To identify
-what do they become?
-what are they spread by?
-To identify
-what do they become?
-what are they spread by?
-Amastigotes in heart muscle
-Will divide and become trypomastigotes once again in the blood.
-Spread by triatomine bugs
Describe the acute phase of Chagas Disease:
-1-2 week incubation period
-local inflammation
-Romaña’s sign
-chagoma (similar to African type)

-symptoms: fever, malaise, lymphadenopathy, hepatosplenomegaly, nausea, diarrhea

-acute, often fatal, myocarditis develops in a FEW individuals (uncommon)
-Romaña's sign and chagoma in Chagas disease.
Describe Chronic Chagas' Cardiomyopathy:
clinical presentations? 3
-long latency characterized by seropositivity and no parasitemia

-progressive development of abnormalities

-clinical presentations include:
*Arrhythmias; heart block; conduction defects
*congestive heart failure
*thromboembolic phenomenon
What does this indicate?
What does this indicate?
-Cardiomegaly, hypertrophy
-indicative of Chagas disease
List pathologies involved in Chagas Disease: 5
cardiomegaly
apical aneurysm (left ventricle)
extensive fibrosis
hypertrophy
± cellular infiltration
Describe Megaviscerae in Chagas Disease:
-which organs most commonly affected? 2
-what signs/symptoms are involved? 3
-what happens to PS ganglia?
-colon and esophagus most frequently affected

-megaesophagus --> painful swallowing, regurgitation

-megacolon --> severe constipation

*loss of parasympathetic ganglia
Megaviscerae in Chagas Disease.
What's the basis of the Pathogenesis of Chagas Disease?
-Autoimmunity vs. Parasite-mediated destruction
-Not quite clear.

-There IS an altered immune response; there's a Th1 to Th2 switch that happens.

-No chagasic toxin has been identified.
How do you diagnose Chagas Disease?
3 broad methods
-parasite detection
*direct examination
*stained blood smears
*in vitro culture
*xenodiagnosis (not routinely done)

-PCR

-serological tests
*hemagglutination
*immunofluorescence
*ELISA
Treatment in Chagas Disease:
acute (3 drugs) and chronic stages
-acute stage
*nifurtimox
*benznidazole
*azole antifungal agents (experimental)

-chronic stage
*treat the symptoms; it's not going to get cured.
-Possible benefits of Chagas disease drugs?
-Cons of Chagas drugs?
-One study showed good ECG ∆s, no worsening of clinical condition, and sero-negative conversion.

-Another study showed no benefits.

-There are severe side effects of nitroderivatives and concomitant compliance issues.
What interventions can help control Chagas? 5
-improvement of human dwellings
-separation of animal stalls from house
-health education
-insecticides
-screen blood supply (it can be transmitted by transfusion)