EX 1 - Biology of Infectious Agents 2- Igboin Flashcards

1
Q

Bacterioides

A
  • Gram -ve rods
  • Strict anaerobes but tolerate short exposure to O2
  • Vertebrate intestinal flora (B. fragilis)
  • metabolize complex carbs
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

How can bacteriodes tolerate short exposure to oxygen?

A

Secrete superoxide dismutase (SOD) and catalase (enzymes) that detoxify and breakdown reactive oxygen species (ROS)

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

Fluid filled space btw the organs contained in the abdomen. Susceptible to contamination more than any other place in body

A

Peritoneal Cavity

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

How can the peritoneal cavity become infected?

A

Spillage of intestinal material (ruptured bowel, appendix, abdominal surgery) into cavity can be catastrophic
- few mls of intestinal fluid: billions of bacterial cells, 100s of differentspecies

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

What are the characteristics of infections of peritoneal cavity?

A
  • Results in bisphasic disease- acute inflammation leads to localized abscess
  • Few species predominate in these abscesses, although 100s introduced into PC
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Intra-abdominal infections typically result in ____ disease

A

bisphasic

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

What is the most common bacterial species isolated from abcesses?

A

B. fagilis

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

Why is B. fragilis the predominant species in intra-abdominal abscesses?

A
  1. Evades phagocytosis (caspule)
  2. Tolerates initail oxygenated environment (tolerant anaerobe)
  3. Thrives once environment becomes anaerobic
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

How are abscesses harmful to the host?

A
  • Reservoir for bacteria to enter blood causing secondary infections (sepsis/septic shock)
  • can extend to nearby sites and cause tissue necrosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

How can abscesses be diagnosed?

A
  • CAT scan

- Culture abscess fluid drained under anaerobic conditions

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

How are abscesses treated?

A
  • Combined surgical -medical therapy

- Drain abscesses, surgically repair, antibiotics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Severe systemic illness characterized by hemodynamic derangement and multiple organ malfunction, brough about by interaction of microbial products w/ host reticuloendothelial cells (macrophages)

A

Sepsis

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

What is it called when the circulatory system goes ape:

  • high cardiac output
  • low bp
  • inadequate perfusion of organs (kidney, liver, gut)
A

Hemodynamic derangement- causes organ failure

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

___________ is the presence of bacteria in the blood, with or without the presence of blood

A

Bacteremia

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

T/F Sepsis does not = bacteremia

A

True

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

What microbial components trigger sepsis?

A
  • LPS- gram -ve

- Peptidoglycan- gram +ve

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

What are the primary cytokine mediators of sepsis?

A

Proinflammatory cytokines

  • IL-1
  • TNF-a
  • -released by macrophages
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

What are the effects of IL-1 and TNF-a on the vasuclature?

A
  • Vasodilation- dec bp
  • Vascular lekeage: edema
  • Intravascular coagulation (blood clots): impedes blood flow, consumes clotting molecules, inc bleeding
  • Inc expression of neutrophil adhesion molecules: degranulation in tissue (ROS + degradative enzymes) + tissue damage
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is the damage caused by sepsis?

A
  • Hemodynamic derangement
  • Multi-organ dysfunction syndrome (MODS)
  • Shock phase
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

What is the treatment for sepsis?

A
  • Ventilator (high O2)
  • IV fluids ( inc bp volume/bp)
  • Adrenergic drugs ( inc tissue perfusion)
  • Antibiotics
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Without ___ a patient will die from sepsis

A

antibiotics

- even w/ treatment sepsis at shock phase has > 50 % mortality

22
Q

What are the general characteristics of Treponemes?

A
  • Helical shape

- Corkscrew-like movement mediated by periplasmic flagella

23
Q

T. pallidum causes _____

24
Q

What are the 2 modes of T.pallidum transmission?

A
  1. Sexual (mucous membranes- skin abrasions)

2. Transplacental

25
What happens in the initial stages of syphillis infection?
- Extracellular replication in subepithelia tissues | - Systemic spread via lymphatic system (almost immediately)
26
What are the 3 stages of sexually transmitted syphillis?
- Primary - Secondary - Tertiary
27
What is the primary characteristic of primary syphilis?
syphilitic chancre
28
A lesion formed by WBCs battling replicating spirochetes at the initial area of inoculation
syphilitic chancre
29
Where does the bacterium replicate in Secondary Syphilis?
Lumph nodes, liver, jints, muscles, skin, and mucous membranes
30
Many variable symptoms associated with secondary syphilis so it is termed the _________ -lesions
"Great Imitator"
31
Where can lesions occur on the body during secondary syphilis?
One or more places, even on the palms and soles of feet
32
The reaction is due to penicillin therapy of secondary syphilis that can result in fever and sometimes shock
Jarisch-Herxhemer rxn
33
1/3 of ppl bacterium resolves without treatment, other 2/3 bacterium becomes _____
latent, tertiary stage can develop
34
What mediates the tertiary stage of syphilis?
Treponemal antigens
35
Treponemal antigens cause ______ due to chronic inflammation and vasculitis
destruction of host tissues
36
Gummas
Lesions (few treponemes + inflammatory cells) that appear in tertiary syphilis and destroy soft tissue and bone
37
What are the CNS symptoms of Tertiary Syphilis?
- ataxic gait - general paresis - death
38
How is syphilis diagnosed?
Detecting antibodies against the bacterium
39
How is syphilis treated?
Penicillin, all stages
40
What is the mode of B. burgdorferi transmission?
Animal Vector- Ticks that normally feed on deer and mice have it dormant in gut. - Mammalian blood triggers spirochetes to replicate and migrate to salivary glands - Inject it into the skin of mammals (while they're feeding) from their salivatory glands
41
What is the potential importance of plasminogen/plasmin to B. burgorferi?
- spread facilitated by ability to bind human plasminogen and convert to plamin- protease that my promote tissue invasion
42
How many stages are in lyme's disease?
3
43
Stage 1 of lyme's disease is characterized by?
- Localized infection at site of bite (bacterial multiplication) - Erythema migrans- lesion
44
Stage 2 of lyme's disease is characterized by?
- Disseminate infection (spread throughout body)
45
What is the mechanism of damage in stage 2 lyme's disease?
- Hosts rxn (proinflammatory cytokines IL-1 and TNF-a) to presence of bacteria
46
Stage 3 of lyme's disease is characterized by?
- Arthritis - CNS (memory, mood, sleep) - Skin- lesions that lead to atrophy of skin (Acrodermatisis chronica atrophicans)
47
How is lyme's disease diagnosed?
Detecting antibodies against bacterium (ELISAs and Western Blots)
48
What is not effective against lyme's disease?
penicillin
49
How is lyme's disease treated for patients w/ arthritis?
- doxycycline or amoxicillin
50
How is lyme's disease treated for patients w/ neurologic symptoms?
Cephalosporin drugs intravenously