Bacterial/Parastitic Lecture Flashcards

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
Q

Whooping cough

A

Bordetella pertussis
Inspiratory whoop
PCR
Infects bronchial epithelium and macrophages
Pertussis toxin- paralyzes the respiratory cilia –> inactivates G proteins

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

Whooping Cough mechanism

A

Virulence factors: BVGS is activated and phosphorylates BVGA

BVGA regulates transcription of mRNA for adhesions and toxins

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

Necrotizing pneumonia

A

Pseudomonas aeruginosa

28
Q

Plague from human by fleabites

A

Yersinia pestis

29
Q

Chancroid: acute sexually transmitted ulcerative infection

A

Hemophilus ducreyi

30
Q

Granuloma Inguinale (Donovanosis): inflammatory disease

A

Klebsiella granulomaris/calymmato-bacterium donovant

31
Q

Myobacterial Infections

A

Slender aerobic rods
Mycolic acid in cell wall- acid fast (retains even with acid or alcohol)
TB
Leprosy

32
Q

Tuberculosis

A
TB Mycobacterium TB
Myobacterium bovis
HIV = immunocompromised
Infection: leads to delayed hypersensitivity to M tuberculosis antigens
TB skin test
33
Q

TB skin test

A

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
Q

Leprosy

A

Mycobacterium leprae

  • Obligate intracellular bacteria
  • Two forms: tuberculoid and lepromatous/anergic (severe)
    • People with robuts Th1 response (tuberculoid)
    • Lepromatous leprosy – weak Th1 response
35
Q

Spirochete infections

A

Syphilis and lyme’s disease

36
Q

Syphilis

A
Treponema pallidum subsp. Pallidum
Sexual contact
Congenital syphilis (transplacental)
Immune response to the spirochete - controls it but accounts for pathology
- Jerisch-Herxheimer reaction
37
Q

Herisch-Herxheimer reaction

A

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
Q

Lyme disease

A

Borrelia burgdorferi

Transmitted by ixodes deer ticks

39
Q

Stages of Lyme disease

A

Stage 1: acute illness- tick bite
Stage 2: dissemination - demyelination, heart block
Stage 3: late chronic form - arthritis

40
Q

Anaerobic bacterial infections

A

Can cause abscessess
- Head and neck with facultative aerobic bacteria
Closterdial infections

41
Q

C perfringens and C speticum

A

cellulitis and myonecrosis of woulds

42
Q

C. botulinum

A

Blocks neuromuscular transmission by blocking release of ACh- sever paralysis

43
Q

C. tetani

A

tetanus

Violent spastic paralysis – block GABA release

44
Q

C. difficile

A

colitisis

45
Q

Obligate intraceullular bacterial infections

A

Proliferate only within host cells

Chlamydial Infections

46
Q

Chlamydia trachomatis

A
Elementary body (inactive)
Reticulate body (active)
47
Q

Genital infection

A

STD with gonorrohoea

48
Q

Riskettsia prowazekii

A

epidemic typhus

49
Q

Orienta tsutsugamushi

A

scrub typhys

50
Q

Rickettsia tickettsii

A

Spotted fever

51
Q

Ehrlichia ewingii

A

Infect neutrophils

52
Q

Ehlichia chaffeenis

A

Infect macrophages

53
Q

Richettsial infections

A

Enter and lyse the endothelial cells- hypovolemic shock, edema
- Mediated by NK cells and CTLs

54
Q

Protozoal infections

A
Unicellular eukaryotic organisms
Microscopic exams
Malaria
Leishmaniasis
African Trypanosomiasis
Chagas Disease
55
Q

Malaria

A
Plasmodium falciparum
Mosquito
Anemia
Cerebral malaria
RBCs clump causing ischemia --> cerebral malaria
56
Q

Leishmaniasis

A

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
Q

Promastigotes

A

for virulence: lipophosphoglycan and gp63
- Lipophosphoglycan: activates and inhibits complement
GP63: promotes promastigote adhesion to macrophages
— Parasite specific CD4 response (AIDS)

58
Q

African trypanosomiasis

A

Trypanosoma brucei rhodesiense

Trypanosoma brucei gambiense

59
Q

Chagas disease

A

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
Q

Chagas autoimmune mechanism?

A

Cross react with host cells and extracellular proteins such as laminin

61
Q

Metazoal infections

A

Multicellular eukaryotic organisms
Microscopic examination of tissue and serology
Schistosomiasis
Lymphatic filariasis

62
Q

Schistosomiasis

A

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
Q

Lymphatic filariasis

A

Mosquitos

Wucheria bancorfti and brugia malayi

64
Q

Category A

A

Highest risk, person to person, high mortality

Small pox, anthrax

65
Q

Category B

A

Moderate morbidity, low mortality

Typhys fever

66
Q

Category C

A

Engineered pathogens for mass dissemination
High damage potenial
Nipah virus and hantavirus