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Microbio Ex 1 > EX 1 - Biology of Infectious Agents 2- Igboin > Flashcards

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
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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)

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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

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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

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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
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6
Q

Intra-abdominal infections typically result in ____ disease

A

bisphasic

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7
Q

What is the most common bacterial species isolated from abcesses?

A

B. fagilis

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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
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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
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10
Q

How can abscesses be diagnosed?

A
  • CAT scan

- Culture abscess fluid drained under anaerobic conditions

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11
Q

How are abscesses treated?

A
  • Combined surgical -medical therapy

- Drain abscesses, surgically repair, antibiotics

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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

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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

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14
Q

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

A

Bacteremia

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15
Q

T/F Sepsis does not = bacteremia

A

True

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16
Q

What microbial components trigger sepsis?

A
  • LPS- gram -ve

- Peptidoglycan- gram +ve

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17
Q

What are the primary cytokine mediators of sepsis?

A

Proinflammatory cytokines

  • IL-1
  • TNF-a
  • -released by macrophages
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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
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19
Q

What is the damage caused by sepsis?

A
  • Hemodynamic derangement
  • Multi-organ dysfunction syndrome (MODS)
  • Shock phase
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20
Q

What is the treatment for sepsis?

A
  • Ventilator (high O2)
  • IV fluids ( inc bp volume/bp)
  • Adrenergic drugs ( inc tissue perfusion)
  • Antibiotics
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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 _____

A

syphilis

24
Q

What are the 2 modes of T.pallidum transmission?

A
  1. Sexual (mucous membranes- skin abrasions)

2. Transplacental

25
Q

What happens in the initial stages of syphillis infection?

A
  • Extracellular replication in subepithelia tissues

- Systemic spread via lymphatic system (almost immediately)

26
Q

What are the 3 stages of sexually transmitted syphillis?

A
  • Primary
  • Secondary
  • Tertiary
27
Q

What is the primary characteristic of primary syphilis?

A

syphilitic chancre

28
Q

A lesion formed by WBCs battling replicating spirochetes at the initial area of inoculation

A

syphilitic chancre

29
Q

Where does the bacterium replicate in Secondary Syphilis?

A

Lumph nodes, liver, jints, muscles, skin, and mucous membranes

30
Q

Many variable symptoms associated with secondary syphilis so it is termed the _________
-lesions

A

“Great Imitator”

31
Q

Where can lesions occur on the body during secondary syphilis?

A

One or more places, even on the palms and soles of feet

32
Q

The reaction is due to penicillin therapy of secondary syphilis that can result in fever and sometimes shock

A

Jarisch-Herxhemer rxn

33
Q

1/3 of ppl bacterium resolves without treatment, other 2/3 bacterium becomes _____

A

latent, tertiary stage can develop

34
Q

What mediates the tertiary stage of syphilis?

A

Treponemal antigens

35
Q

Treponemal antigens cause ______ due to chronic inflammation and vasculitis

A

destruction of host tissues

36
Q

Gummas

A

Lesions (few treponemes + inflammatory cells) that appear in tertiary syphilis and destroy soft tissue and bone

37
Q

What are the CNS symptoms of Tertiary Syphilis?

A
  • ataxic gait
  • general paresis
  • death
38
Q

How is syphilis diagnosed?

A

Detecting antibodies against the bacterium

39
Q

How is syphilis treated?

A

Penicillin, all stages

40
Q

What is the mode of B. burgdorferi transmission?

A

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
Q

What is the potential importance of plasminogen/plasmin to B. burgorferi?

A
  • spread facilitated by ability to bind human plasminogen and convert to plamin- protease that my promote tissue invasion
42
Q

How many stages are in lyme’s disease?

A

3

43
Q

Stage 1 of lyme’s disease is characterized by?

A
  • Localized infection at site of bite (bacterial multiplication)
  • Erythema migrans- lesion
44
Q

Stage 2 of lyme’s disease is characterized by?

A
  • Disseminate infection (spread throughout body)
45
Q

What is the mechanism of damage in stage 2 lyme’s disease?

A
  • Hosts rxn (proinflammatory cytokines IL-1 and TNF-a) to presence of bacteria
46
Q

Stage 3 of lyme’s disease is characterized by?

A
  • Arthritis
  • CNS (memory, mood, sleep)
  • Skin- lesions that lead to atrophy of skin (Acrodermatisis chronica atrophicans)
47
Q

How is lyme’s disease diagnosed?

A

Detecting antibodies against bacterium (ELISAs and Western Blots)

48
Q

What is not effective against lyme’s disease?

A

penicillin

49
Q

How is lyme’s disease treated for patients w/ arthritis?

A
  • doxycycline or amoxicillin
50
Q

How is lyme’s disease treated for patients w/ neurologic symptoms?

A

Cephalosporin drugs intravenously

Microbio Ex 1 (18 decks)

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