Brainscape's Knowledge GenomeTM

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


See full index

MicroBio > Dr. Zhou - Lecture 19 > Flashcards

Dr. Zhou - Lecture 19 Flashcards

1
Q

What is Medical Parasitology

A
  • Study of eukaryotic parasites
  • 7/8 tropical diseases
  • Easily spread: travel
  • Common property: CANNOT live outside host
  • 2 major categories of studying infections and diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What are the 2 major categories of studies of infections + diseases?

A
  • Protozoa: small, single-celled

- Helminth worms: small to very big (10m)

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

What causes sleeping sickness?
A. Plasmodium
B. Trypanosomes

A

Trypanosomes

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

Protozoa

A
  • Kingdom: Protista (algae + protozoa)
  • Single celled, animal-like: Amoebas, Ciliates, Flagellates, Sporozoans
  • Structure:
    Cytoplasmic membrane
    Cytoplasm
    Usually w/ flagellum
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What are the 4 kingdoms?

A
  • Protista
  • Plants
  • Animals
  • Fungi
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Sporozoan parasite structure:

A
  • Cytostome (mouth)
  • ER (makes protein)
  • Nucleus
  • Food vacuole
  • Mito (energy)
  • Membrane
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Protozoan Life Processes

A
  • Aquatic
  • Obligate parasites (have to live inside host)
  • Chronic or acute diseases
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

What are the chronic and acute diseases of protozoa, and what are they caused by?

A
  • Amebiasis (amebic dysentery): bacteria and stomach aches; Entamoeba
  • Sleeping sickness (caused by brain damage): Trypanosoma bruci
  • Chagas disease (severe tissue damage): Trypanosoma cruzi
    STD: Trichomonas vaginalis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Life Cycle - Reproduction

A
  • Asexual: binary fission

- Sexual: Conjugate; exchange DNA; segregate

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

How many and what are the major phases in protozoan life cycle?

A
  • Reproduction

- Encystment

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

Life Cycle - Encystment

A
  • Cyst formation under adverse conditions:
    • Round w/ protective coating
    • Survive w/o food, water, and at high temp
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

What are the 4 phyla of protozoans?

A

Amoebas
Ciliates
Flagellates
Sporozoan

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

Infective Amoebas: General Properties

A
  • Pseudopodia (fake foot)
  • Trophozoite (actively growing)
  • ONLY binary fission
  • Form cysts
  • Major diseases (most NOT pathogenic):
    • Amoebiasis: diarrhea + blood stool; Entamoeba histolytica
    • Brain infection: naegleria, acanthamoeba
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Amoebiasis

A
  • Caused by Entamoeba histolytica
  • Intestinal disease (100,000 deaths/yr)
  • Sign of infection: intestinal mucosa
  • Symptoms: Mostly diarrhea, dysentery (blood stool), abdominal pain, fever, fatigue, weight loss
  • Tissue damage: cell ingestion (enzymes dissolving tissue, ulcerations)
  • Severe cases: extra-intestinal infections
    • Liver: amoebic hepatitis
    • Lung: pulm amoebiasis
    • Less frequent: spleen, adrenals, kidney, skin brain
      * 10% fatality rate
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Epidemiology of Amoebiasis:

A
  • Tropical + subtropical disease (US: 0.1-0.5% infection rate; tropical: 5-8% - raw sewage = fertilizer)
  • Spread by asymptomatic chronic carriers
  • Healthy carriers: cyst formation
  • Unhealthy carriers: active dysentery: NOT infectious –> cysts CANNOT form
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Entamoeba Histolytica life cycle

A
  • Metacysts: each cell in the cyst
  • Mature cyst –> excystment –> metacysts –> metacysts are released into environ–> grow into trophozoite –> new cyst formation
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Amoebiasis: Diagnosis

A
  • Based on stool exams
  • Symptoms
    Parasites have:
  • Ingested RBCs
  • 4 nuclei in cysts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Amoebiasis: Treatmetn

A
  • Drugs targeting parasites in both stool + tissues
  • Iodoquinol
  • metronizazole
  • Dehydroemetine
  • Chloroquine
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Amoebic brain infections

A
  • Caused by N. fowleri and Acantheomoeba
  • Common, free-living protozoans
  • Accidental parasites
  • Live in lakes, hot springs, swimming pools, hot tubs, moist soil
  • CAN survive w/o hosts
  • Primary amoebic meningoencephalitis (N. fowleri) - invades nasal mucosa
  • Granulomatous amoebic encephalitis (acantheomoeba) - invades broken skin; conjunctiva, lung, eye
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Amoebic infections of Brain: Pathogenesis

A
  • Naegleria infection starts at nose –> amoeba burrows in, multiplies –> travels into brain –> primary acute meningoencephalitis

Meningoencephalitis: ; fast, massive destruction of brain + spinal tissues, causing hemorrhage + coma, and eventually death in ~1 wk

Symptoms: hemorrhage + coma, death in 1 wk

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

Ameobic Brain Infections: Treatment

A
  • Naegleria meningoencephalitis advances too fast to have effective treatment
  • Some drugs if started early can work: Amphotericin B, sulfadiazine, tetracycline, ampicillin
  • Acanthamoeba invades broken skin, conjunctiva, lung, and urogenital epithelia
  • Special risks: ppl w/ eye injuries or abrasions from contact lenses
  • Course of infection longer than naegleria - gives time for treatment
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Amoebiasis:
A. Intestinal disease
B. Brain infection

A

Intestinal disease

80% caused by enterotoxigenic E. Coli

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

Intestinal Ciliate Properties

A
  • B. Coli

The Ciliates:

  • Cilia: movement
  • 2 nuclei - macro + micro nucleus
  • Sexual + asexual reproduction
  • Trophozoites and mature cysts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

B. Coli Disease

A

Balantidiosis: infection in intestinal mucosa. Quite widespread

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

B. Coli Natural habitat

A
  • Large intestines of pigs, and other domestic animals

- Primates: cysts in feces

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

Anatomy of B. Coli

A 
Macronucleus
Micronucleus
Vacuole
Cytostome
Cilia tufts
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

B. Coli - infection + symptoms

A
  • Intestinal mucosa
  • Irritation, injury, NV, diarrhea, dysentery, abdominal pain (colic)

Healthy ppl: Resistant; usually NOT pathogenic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

B. Coli treatment

A

PO tetracycline

- If fails: dodoquinol, nitrimidazine, or metronidazole

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

B. Coli Prevention

A

Prevent food or drink contamination w/ pig manure

30
Q

Flagellates

A
  • Mastigophorans

- Common feature: long filamentous flagella

31
Q

Flagellates - diseases

A

Mild diseases:

  • Trichomoniasis
  • Giardiasis

Debilitating:

  • Trypanosomiasis
  • Leismaniasis

Others:

  • T. Vaginalis (STD): urogenital pathogen; vaginal infections. Has flagella + undulating membranes (both used for movement)
  • T. Tena: gingival (rare infection)
  • T. hominis: intestinal species (rare infection). NON-patho
32
Q

Trichomonads (shape, properties, disease, reservoir, mode of transmission)

A
  • Small, pear-shaped protozoa w/ 4 flagella + an undulating membrane
  • No cysts
  • MOST IMPORTANT PATHO: T. Vaginalis - trichomoniasis (STD)
  • Reservoir: human urogenital tract (50% asymptomatic)
  • Mode of transmission: sexual contact, communal bath, public facilities, mother to child
33
Q

Trichomoniasis

A
  • 2nd most prevalent STD
  • Most common in young women
  • Most common: chlamydia (bacterium)
    C. Trachomatis - bacterium that ONLY infects humans
34
Q

Trichomoniasis - Symptoms

A

Females:

  • Foul smelling, green-yellow vaginal discharge
  • Vulvitis
  • Cervicitis
  • urinary frequency + pain

Males:

  • Urethritis
  • Milky discharge
  • Prostate infection
35
Q

Trichomoniasis - Treatment

A
  • PO + vag metronidazole

- BOTH sexual partners have to be treated

36
Q

Trichomoniasis is caused by:
A. an amoeba
B. Flagellate

A

Flagellate

37
Q

Giardia lamblia (G. lamblia) and Giardiasis (definitions, outbreak cause)

A

Giardiasis: infection + disease caused by G. lamblia
- Prominent cause of diarrhea

G. lamblia is most common flagellate isolated in clinical specimens

Outbreaks:

  • Traveler’s diarrhea -
  • Hikers + campers drink from fresh mountain streams
  • Kids in daycare centers
38
Q

Giardiasis Treatment

A
  • Quinacrine

- Metrodinazole

39
Q

Hemoflagellates

A
  • Vector-borne blood parasites (VERY dangerous)
  • Flagellates in blood + tissue
  • 2 major species:
  • Trypanosoma
  • Leishmania
  • Life threatening diseases
  • Spread via blood-sucking insects
  • Complicated life cycles
40
Q

Hemoflagellates: Developmental stages (4)

A
  1. Amastigote: no free flagellum (round cell no flagella)
  2. Promastigote: w/ 1 free anterior flagellum
  3. Epimastigote: flagellate stage, w/ both flagellum + undulating membrane
  4. Trypomastigote: large, fully formed stage of Trypanosoma

BUT: NOT ALL HEMOFLAGELLATES HAVE ALL STAGES

41
Q

Leishmania stages

A
  1. Amastigote (intracellular in human MPs)

2. Promastigote (found in sand fly gut; INFECTIVE to humans)

42
Q

T. Brucei stages

A
  1. Epimastigote (in salivary gland of tsetse fly)

4. Trypomastigote (in biting mouthparts of tsetse fly; INFECTIVE to humans)

43
Q

T. Cruzi stages

A
  1. Amastigote (intracellular in human MPs, liver, heart, spleen
  2. Promastigote
  3. Epimastigote (in gut of reduviid (kissing) bug)
  4. Trypomastigote (in feces of reduviid bug; TRANSFERRED to humans)
44
Q

Trypanosoma and Trypanosomiasis

A

2 major typanosoma species:

  • T. brucei: African sleeping sickness
  • T. cruzi: Chagas disease
45
Q

T. brucei disease, species, and principle vector

A

Disease: sleeping sickness
2 subspecies:
- T. b. gamibense: West Africa
T. b. rhodesiense: East Africa

Principle vector: tsetse flies

46
Q

T. brucei infection pathogenesis

A
  • Tsetse flies get infected by feeding on infected rservoir hosts (antelope, lion, cow, goat, human) –> trypanosomes multiply in fly gut –> migrates to salivary glands –> develop into infectious stage –> transfers into bite wounds on new hosts to lymphatics + blood

T. b. gamibense: chronic, may not affect brain for several years

T. b. rhodesiense: acute, affects brain in 3-4 wks

47
Q

Patho of sleeping sickness

A
  • Intermittent fever
  • Enlarged spleen
  • Swollen lymph nodes
  • Joint pain
  • Personality change, sleep disturbances (sleepy during the day, sleepless at night)
  • Advance neuro disorders:
  • Muscular tremors, shuffling gait, slurred speech, epileptic seizures, paralysis
  • Death: coma, 2ndary infections, heart damage
48
Q

Sleeping sickness: Treatment + Prevention

A

Treatment:

  • Chemo: successful if admin before brain
  • Treating brain infections: expensive - melarsoprol-toxic arsenic-based drug (one of most ancient potent poisons, death dose is 0.1-0.2g) OR DFMO (less toxic)

Control tsetse pop:
- Insecticides (difficult since some are resistant)

Sudan and Zaire: 20-40% of pop infected

49
Q

Why Can’t the immune system defeat Trypanosome?

A
  • Trypanosomes make a large # of surface antigen in succession
  • Antibodies made by host fail to stop bugs w/ new antigen
  • Eventually overwhelms host
  • Hard to immunize bc there’s >100 diff antigenic variations
50
Q

Chagas disease

A
  • Disease causing heart damage (enlarged heart filled w/ amastigotes of T. cruzi)
  • Caused by T. cruzi
  • Millions of cases, thousands of deaths in Latin America
51
Q

T. Cruzi infection

A

Insect host: kissing bugs w/ trypanosomes in hind gut; discharge it in feces
- Found in Central + South America: share habitat w/ humans
So parasite is well adapted to habits of both kissing bugs + hosts

Infection happens when bug poops near bite wounds, and inoculation by rubbing bug feces into wounds

52
Q

Chagas Disease: patho

A

Major patho:

  • Fever
  • Swelling lymph nodes, spleen, and liver
  • Favored targets: heart muscle + large intestine
  • Heart enlargement + death in 2 yrs
53
Q

Chagas Disease: Treatment

A
  • Nifurtimox + benzonidazole for early treatment

- Damaging ADRs (protozoans are also eukaryotic, so similar physiology to human cells = toxicity to human cells)

54
Q

Leishmaniasis

A
  • Caused by Leishmania
  • Cutaneous leishmaniasis: capillary infections = extensive tissue damage
  • Tranmitted among mammals by phlebotomine flies (sand flies)
  • Endemic to equatorial regions
  • Special risks: Travelers + immigrants
  • Death by tissue destruction
55
Q

Leishmania Life Cycle:

A

Infected sand fly has promastigotes in gut –> bite/inoculate parasite into new host (human, other mammal) –> migrates to spleen + RBCs –> free + intracellular amastigotes in spleen + RBCs taken up by another sand fly

56
Q

Sporozoans

A
  • Aka Apicomplexan parasites
  • No locomotor organells in mature stage
  • Sexual + asexual reproduction
57
Q

Most human patho sporozoans:

A

2 most important:

  • Plasmodium: malaria
  • Toxoplasma: toxoplasmosis
  • Cryptosporidium: cryptosporidiosis (no severe issues)
58
Q

Malaria

A
  • Dominant protozoan disease for centuries
  • Caused by plasmodium
  • Italian: mal = bad; aria = air
  • Exposure to bad air from swamps: lots of mosquitos
  • Most common in Africa
  • = or > serious than COVID
59
Q

Malaria symptoms:

A
  • Chills + fever at regular intervals followed by sweating: 48-72 hrs bc of synchronous rupturing of RBCs
  • Anemia in young kids; organ rupture from accumulated cell debris (spleen, liver, kidneys)
  • Long recovery: up to 5 yrs
60
Q

Plasmodium

A
  • Obligate intracellular sporozoan

4 species:

  • P. malariae
  • P. vivax
  • P. falciparum
  • P. ovale

Most severe malaria caused by P. falciparum (P. falc). Causes:

  • Persistent fever
  • Rapid pulse
  • Cough
  • Weakness for wks w/o relief
  • Acute phase: High death rate
61
Q

Plasmodium Transmission:

A
  • Mostly by female Anopheles mosquitoes
  • Occasionally by sharing needles
  • Blood transfusions
  • Mother to child through umbilical cord blood
62
Q

Plasmodium Complex life Cycle

A

2 distinct phases:

  • Asexual (happens in human host)
  • Sexual
63
Q

Plasmodium Complex Life Cycle - Asexual phase

A

Asexual phase 1: exoerythrocytic development (happens in liver)

  • Starts from outside RBC
  • Start: mosquito injects anticoagulant saliva into capillary –> asexual plasmodium cells (sporozoites) get injected –> sporozoites reach liver –> undergo schizogony (asexual division), making many daughter parasites, merozoites –> liver cells erupt –> releases numerous mature merozoites into circulation
  • 5-16 days

Asexual phase 2: Erythrocytic development
- Released merozoites invade RBCs –> feed on Hb, making schizonts cells (cells filled w/ merozoites) –> RBCs bursts (start of symptoms (chills, fever) when large # bursts)–> releases more merozoites –> merozoites turn into macrogametocytes (female) + microgametocytes (male)

64
Q

Plasmodium Complex Life Cycle - Sexual phase

A

Mosquitos bring gametes into stomach –> fertilization –> diploid cells (oocyst) implants into stomach wall –> undergo multiple mitotic divisions, releasing sporozoites –> sporozoites migrate to salivary glands and available for next infection

65
Q

Malaria - Genetic Change

A
  • Changed human genetics protects against malaria
  • Certain mutations in Hb, HbS gives protection
  • Hb-C: protection w/o fitness cost (3% pop)
  • Hb-S: protection w/ cost - sickle cell anemia in s/s pts (homo recessive)
  • Hetero mutation (S/s): better survival than no mutations, no sickle cell anemia
  • Large % of Africans carry Hb S mutations: 20% pop
66
Q

Malaria - Diagnosis + Control

A 
Diagnosis:
(Best - first 2)
- Stained blood smear
- Antibodies
- DNA-PCR analysis

Control:

  • Pesticides: DTT (best)
  • ISSUE: Pesticide resistant mosquitos
67
Q

Malaria - Treatment:

A

Non-resistant strains: Chloroquine - less toxic ADRs

Resistant strains: use mefloquine or quinine

Eliminating parasites from liver: primaquine or proguenil

68
Q

Toxoplasma gondii (T. gondii) and Toxoplasmosis

A
  • Exposure rate: 90% (very common pathogen)

Most cases:

  • Mild
  • Sore throat
  • Lymph node enlargement
  • Low grade fever

Immunodeficient pts:

  • Brain lesions
  • Fetal disruption of heart + lungs
69
Q

Toxoplasmosis in pregnant women:

A
  • 33% (1/3) chance fetus transmission
  • Pregnant women can be infected through contact w/ infected pets or undercooked meat
    Causes:
  • Still birth
  • Liver failure
  • Hydrocephalus
  • Convulsions
  • Retina damage + blindness
70
Q

Why is it so hard to control trypanosome infections?
A. they replicate fast
B. antigenic changes

A

Antigenic changes

MicroBio (3 decks)

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