Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

POD Test 3 > Bacterial/Parastitic Lecture > Flashcards

Bacterial/Parastitic Lecture Flashcards

(66 cards)

Start Studying
1
Q

Prokaryotes

A

No membrane bound nucleus

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

Gram staining

A

Gram positive: thick cell wall of peptidoglycan

Gram negative: peptidoglycan sandwiched between two membranes

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

Classification

A

Shape

Anerobic/anaerobic

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

Mechanisms of bacterial injury

A

Adhere to host cells, invade or deliver toxins
Virulence genes confer these properties
- Pathogenicity island (genes are bound together)

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

Biofilms

A

Within extracellular polysaccharides that adhere to host tissues or devices as catheters
Makes them inaccessible to immune systems

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Adhesins

A

Surface molecules on bacteria that bind to host cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Entry into host?

A

Opsonization (coated with antibody and taken in) and phagocytosisinto macrophages

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Inside the host?

A

Replicate, inhibit host protein synthesis, lyse hotst cells

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Bacterial toxins?

A

Endotoxins (components of bacterial cells):
Lipopolysaccharids (gram - bacteria) which activate protective immunity but can cause septic shock
- Exotoxins (secreted by bacteria): enzymes, intracellular toxins and neurotoxins (superantigens)

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

Injurious effects of host immunity?

A

Granulomatous reaction in TB (tries to engulf the bacteria but it is hypersensitive so you have huge influx of macrophages that form granulomas)
Antibodies react against strept proteins begin to act against heart
Poststrep glomerulonephritis
— Type 3 hypersensitivity (lots of antibody/antigen complexes forming) deposit in the joints

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

Gram Positive Bacterial Infections

A 
Diptheria
Listeriosis
Anthrax
Streptococcal infection
Staphylococcal Infections
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Diptheria

A

corynebacterium diptheriae

  • Produce toxin that blocks host cell protein synthesis
  • Immunization: protects against leathal effects of toxin
  • EF2 (elongation factor): conversion from RNA to protein is blocked
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Listeriosis

A

Listeria monocytogenes
Food borne
Causes menigitis
ACTA: allows it to escape the lysosomes and move to adjacent cells
IFN-gamma activates macrophages to phagocytose and kill bacteria
- Internalins + E-cadherins: internalization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Anthrax

A

Bacillus anthracis
Has a polyglutamyl capsule: prevent anthrax toxins
Two parts: can’t act without B
Heptamer: interacts with edema factor or lethal factor –» forms an acidic pH
Edema fact: interacts with calmodulin convert AMP to cAMP causing water efflux leading to edema
Lethal factor: protease that works on MAPK and causes cell death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Steptococcal infections

A

Rheumatic fever, glomerulonephritis
Pneumonia and meningitis
Dental caries

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Rheumatic fever, glomerulonephritis

A

S. pyogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Pneumonia and meningitis

A

S. pneymoniae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Dental caries

A

S. mutans

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Staphylococcal infections

A

Multiple toxins and enzymes
Superantigens
Antibiotic resistance

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Multiple toxins and enzymes

A

S. aureus

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

Superantigens

A

Huge release of antigens causing shock

S. aureus and S. pyogenes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Antibiotic resistance

A

MRSA

Methicillin resistance

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

Gram negative bacterial infections

A 
Neisserial Infections
Whooping Cough
Pseudomonas Infections
Plague
Chancroid
Granuloma Inguinale (donovanosis)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Neisserial Infections

A

N. menigitidis and V gonorrheae

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Whooping cough
Bordetella pertussis Inspiratory whoop PCR Infects bronchial epithelium and macrophages Pertussis toxin- paralyzes the respiratory cilia --> inactivates G proteins
26
Whooping Cough mechanism
Virulence factors: BVGS is activated and phosphorylates BVGA | BVGA regulates transcription of mRNA for adhesions and toxins
27
Necrotizing pneumonia
Pseudomonas aeruginosa
28
Plague from human by fleabites
Yersinia pestis
29
Chancroid: acute sexually transmitted ulcerative infection
Hemophilus ducreyi
30
Granuloma Inguinale (Donovanosis): inflammatory disease
Klebsiella granulomaris/calymmato-bacterium donovant
31
Myobacterial Infections
Slender aerobic rods Mycolic acid in cell wall- acid fast (retains even with acid or alcohol) TB Leprosy
32
Tuberculosis
``` TB Mycobacterium TB Myobacterium bovis HIV = immunocompromised Infection: leads to delayed hypersensitivity to M tuberculosis antigens TB skin test ```
33
TB skin test
Won't work 0-3 weeks | 3+ weeks: IFN-gamma works on activated macrophages and breaks down bacterial genomes; creates TNF which works against TB
34
Leprosy
Mycobacterium leprae - Obligate intracellular bacteria - Two forms: tuberculoid and lepromatous/anergic (severe) - - People with robuts Th1 response (tuberculoid) - - Lepromatous leprosy -- weak Th1 response
35
Spirochete infections
Syphilis and lyme's disease
36
Syphilis
``` Treponema pallidum subsp. Pallidum Sexual contact Congenital syphilis (transplacental) Immune response to the spirochete - controls it but accounts for pathology - Jerisch-Herxheimer reaction ```
37
Herisch-Herxheimer reaction
You give antibiotics to a patient with high bacterial contents, you have high flow of exotoxins with will release a lot of cytokines leading to shock
38
Lyme disease
Borrelia burgdorferi | Transmitted by ixodes deer ticks
39
Stages of Lyme disease
Stage 1: acute illness- tick bite Stage 2: dissemination - demyelination, heart block Stage 3: late chronic form - arthritis
40
Anaerobic bacterial infections
Can cause abscessess - Head and neck with facultative aerobic bacteria Closterdial infections
41
C perfringens and C speticum
cellulitis and myonecrosis of woulds
42
C. botulinum
Blocks neuromuscular transmission by blocking release of ACh- sever paralysis
43
C. tetani
tetanus | Violent spastic paralysis -- block GABA release
44
C. difficile
colitisis
45
Obligate intraceullular bacterial infections
Proliferate only within host cells | Chlamydial Infections
46
Chlamydia trachomatis
``` Elementary body (inactive) Reticulate body (active) ```
47
Genital infection
STD with gonorrohoea
48
Riskettsia prowazekii
epidemic typhus
49
Orienta tsutsugamushi
scrub typhys
50
Rickettsia tickettsii
Spotted fever
51
Ehrlichia ewingii
Infect neutrophils
52
Ehlichia chaffeenis
Infect macrophages
53
Richettsial infections
Enter and lyse the endothelial cells- hypovolemic shock, edema - Mediated by NK cells and CTLs
54
Protozoal infections
``` Unicellular eukaryotic organisms Microscopic exams Malaria Leishmaniasis African Trypanosomiasis Chagas Disease ```
55
Malaria
``` Plasmodium falciparum Mosquito Anemia Cerebral malaria RBCs clump causing ischemia --> cerebral malaria ```
56
Leishmaniasis
Chronic inflammation Promastigote (extracellular) and amastigote (macrophages) Promastigotes injected by bite, phagocytosed by macrophages and the acidity of the phagosomes convert them to amastigotes Amastigotes multiple and are released from macrophages --> infect more
57
Promastigotes
for virulence: lipophosphoglycan and gp63 - Lipophosphoglycan: activates and inhibits complement GP63: promotes promastigote adhesion to macrophages --- Parasite specific CD4 response (AIDS)
58
African trypanosomiasis
Trypanosoma brucei rhodesiense | Trypanosoma brucei gambiense
59
Chagas disease
Trypanosoma cruzi Brief exposure to acidic phagolysosome to develop into the amastigotes - Amastigotes develop flagella, lyse host cells, enter bloodstream and penetrate smooth, skeletal and heart muscles -- Cardiac damage, inflammation
60
Chagas autoimmune mechanism?
Cross react with host cells and extracellular proteins such as laminin
61
Metazoal infections
Multicellular eukaryotic organisms Microscopic examination of tissue and serology Schistosomiasis Lymphatic filariasis
62
Schistosomiasis
Schistosoma mansoni, S. Japonicum, S. mekongi Snails Eggs in circulation cause inflammation --> granuloma formation and hepatic fibrosis TH1 and TH2 mediated immune response --- excessive immune response
63
Lymphatic filariasis
Mosquitos | Wucheria bancorfti and brugia malayi
64
Category A
Highest risk, person to person, high mortality | Small pox, anthrax
65
Category B
Moderate morbidity, low mortality | Typhys fever
66
Category C
Engineered pathogens for mass dissemination High damage potenial Nipah virus and hantavirus

POD Test 3 (10 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions