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Micro Biology > Chapter 22 > Flashcards

Chapter 22 Flashcards

1
Q

A) What two layers compose the skin? What are they composed of? [Figure 22.1]

A

Epidermis: surface layer. made of multiple layers of flat cells. outermost is made of dead cells filled with Keratin
Dermis: underlayer. vessels and nerves inervate. has ct wich binds to fat and other cells of subcutaneuos layer

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2
Q

B) What is subcutaneous tissue and where is it located?

A

it is under dermis and it supports layers of the skin

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3
Q

C) What type of bacteria are commonly found on the skin? [Table 22.1]

A

diptheroids: non motile gram pos rods of corynbacterium and propionibacterium

Staphylococci. gram pos cocci. coagulase neg

Fungi: sm yeasts of Massezia

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4
Q

A) What are the symptoms of acne vulgaris? What causes it? What does it do to the skin?
1) How can it be treated?

A

enlarged subcuatneous glands and increase secretion of sebum. “back heads and white heads”
Where hair follicle epithelium thickens and sloughs off in lumps gradually blocking sebum from working to the surface.

Cause: propionibacterium acnes.They eat sebum and to get more sebum they grow in to trap the sebum to eat. This attracts neutrophils whose enzymes damage the walls of the follicle.

Treated: limiting with benzoyl peroxide, Acutane reduce sebum production ( for more serious acne)

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5
Q

2) What is an abscess?

A

When neutrophils attracted to infected site release their enzymes which damage the walls of the follicle causing it to burst and releases it’s contents into surrounding tissue.

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6
Q

B) What are the symptoms of a hair follicle infection? What causes them? By what mechanism do they affect the skin? [Figure 22.2, 22.3 and Table 22.3]

A

inflamation of hair follicles
Cause: staph areus
Attatches to cells of follicle multiplies and spreads to the sebaceous gland. Producing inflamatory response frorming absesses.

  • Some produce polysacharide capsule, or a protiens to prevent phagocytosis.
  • Coagulase: activates blood protien prothrombrin to make thrombrin which is converted ot fibrin which forms protiens that make a weblike clot. The bact gets covered in the fibrin allowing it to hide.
  • Hylurindase: degrades hyluronic acid which holds host cells together.
  • Proteases: degrades collegen
  • Lipase: degrades lipids to proved a food source
  • Alpha toxin: kills hosts cells by making holes in their membranes.
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7
Q

1) What are the differences between folliculitis, furuncles, and carbuncles?

A

Folliculitis: inflamation of one or more hair follicles causing red bumps or pimples.
Furuncles: infection goes from folicle to other cells and caused lovalized swelling. This is a boil.
Carbuncles: a large area of redness and pain with several sites of drainng pus. rever can be present

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8
Q

What does protein A do?

A

cell wall component which messes with phagocytosis.

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9
Q

folicle infections 4 How do you get these types of infections? How are they treated?

A

Typically live in moist areas like nose and then gets transfered

Treated: with draining pus and oral antibiotics for carbuncles.

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10
Q

5) What type of resistance has S. aureus developed?

A

resistant to penicillin MRSA
vancoycin VRSA
ha= hospital aquired
ca= community aquired

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11
Q

C) What are the symptoms of SSSS? What causes it? By what mechanism does it affect the skin? [Figure 22.4 and Table 22.4]

		2) What is the most common age group affected? How do you get it?
		3) How is it treated?
A

Staphylococcal scalded skin syndrom: redness of skin, malaise, fever. whithin 48 hrs skinbecomes wrinkled and blisters formed and easily peel.
Affect:
-Exfoliatin: destroys material and binds together outer layers of epidermis
– splits under layer of epidermis and so it enters blood stream.
Common among infants.
Spread: from person to person
Treatment: methicillin and dead skin is removes.

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12
Q

D) What are the symptoms of impetigo? What causes it? By what mechanism does it affect the skin? [Figure 22.5 and Table 22.6]

A

pyoderma: infection characterized by pus prod.
inflamation in patches just beneath dead layer of skin. Thin walled blisters develop then break and ooze, yellowish crusts and plana. enlarged lyph nodes, fever. Result from damage to skin ie bug bites, burns, scrapes

Cause: Strep pyogenes

Affects: hyluranic acid capsule to to conceal it.
M protien which interferes with phagocytosis
and enzymes preoteases, nucleases, and hyaluronidase.

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13
Q

2) Where is impetigo mostly found? How does it spread?

A

poor kids in hot humid areas. ‘fomites and person to person

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14
Q

3) What are the differences between S. pyogenes and S. aureus? [Table 22.5]

A

virulance factors

pg 529

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15
Q

4) How can impetigo be treated?

A

penicillin

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16
Q

E) What are the symptoms of Rocky Mountain Spotted Fever? What causes it? By what mechanism does it affect the skin? [Figure 22.6, 22.7 and Table 22.7]

A

headache, m, joint pain, fever. Then rash with pink spots start on palms wrists ankles and soles of feet then spreads.

Cause: Rickettsia rickettsii. spread from ticks, lice, mites

Affects:

  • force endothelial engulf them. Once inside they multiply and coat themselve in hose actin and use this proteins to move into adjacent host cells. eventually the membrane is so damaged it ruptures, and it goes into blood stream. Infect sm vessels leading to clotting and small areas of necrosis causing the hemmoratic rash. and can also damage kidneys and heart.
  • lipopollysacharide endotoxin: in blood leads to shock and bleeding
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17
Q

1) How did RMSF get it’s name?

A

It was first recocnised in the rock mountain of the US

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18
Q

2) Where are the highest incidents of RMSF? [Figure 22.8]

A

in the summer. atlantic and south central states.

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19
Q

3) Which types of ticks are known to transmit it? [Figure 22.9] RMSF

A

wood ticks

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20
Q

4) How can RMSF be treated and prevented?

A

doxycycline and cloraphenicol

avoid ticks

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21
Q

F) What is lyme disease? What causes it? By what mechanism does it affect the skin? [Figure 22.11 and Table 22.8]

A

Cause: Borellia burgdorferi (gram neg spirochete)
Affect: multiply and migrate in a circular fashion.
-lipopollysacharide: initiates inflamatory response. Host immune system in suppressed so it can multiply. Then it goes into blood stream.

22
Q

1) What are the three stages of lyme disease? [Figure 22.10]

A

–Early localized infection: afew days-weeks. enlargement of mearby lymphnodes, and a circular skin rash (erythema Migrans) Site of bite redness surrounds about 6 inches. “bulls eye mark)
–Early dessiminated infection:
2-8 weeks after first sign. effects the nervous system. messes with hr, can cause paralysis, headache, pain when moving eye
–Late persistent infection:6 months after rash. joint pain, swelling

23
Q

2) Where is lyme disease common? [Figure 22.12]

A

eastern us

24
Q

3) What is the most important vector? Which stage in the life cycle is responsible for transmission? [Figure 22.13, 22.14]

A

Deer ticks

in nymph cycle or sexually mature

25
Q

4) How can lyme disease be treated and prevented?

A

tick prevention.

antibiotics

26
Q

A) What are the symptoms of varicella (chickenpox)? What causes it? By what mechanism does it affect the skin? [Figure 22.15, 22.17 and Table 22.9]

A

red spots (macules) that progress to bumps (papules) then to blisters (vesicles).

Causes: s pyoenes, or s. aureus.

Affect

27
Q

1) What is the mortality rate?

A

in babies 30%

28
Q

2) What are shingles? [Figure 22.16]

A

when you get chicken pox again in your adult years. Is connected with a sensory nerve. rash is limited to where the nerve is. rash will subside within a week but the pain will continue for weeks-months.

29
Q

3) What is Reye’s syndrome? What age group does it affect?

A

2-12 days of infection begin vomitting and then slips into a coma. in kids 5-15 yrs old
liver, brain damage 30% fatality rate

30
Q

4) Infected cells show intranuclear inclusion bodies, what are these?

A

pink bodies in the nucleus. where virus reproduces.

31
Q

5) How do chickenpox spread?

A

from lesions or respiratory secretions.

32
Q

6) How can it be treated and prevented?

A

antiviral med acyclovir and famiciclovir.

33
Q

B) What are the symptoms of rubeola (measles)? What causes it? By what mechanism does it affect the skin? [Figure 22.18 and Table 22.10]

A

“hard/red measles”: fever runny nose cough swollen and weepy eyes. then a rash will appear on forehead and spreads outward over the rest of the body.
cause: rubeola virus (enveloped single stranded)
Affects: makes people more susceptible to other infection. latent tb will activate, cold sores etc.
-hemagglutination: attach to host cells
-fusion proteins: cause adjacent hot cells to join together forming multi-nucleated giant cells!

34
Q

1) What is SSPE?

A

Subacute Schlerosis panecephalitis- cause slow degeneration of the brain. and death within 2 year. occurs 2-10 years after measles.

35
Q

2) What are Koplik spots? [Figure 22.19]

A

looks like grains of salt on the mucous membranes located on back of mouth

36
Q

3) What is the mortality rate?

A

15% but with secondary 85%

37
Q

4) How can it be prevented?

A

yes vaccines

38
Q

C) What are the symptoms of rubella? What causes it? By what mechanism does it affect the skin? [Figure 22.20 and Table 22.11]

A

“greman/ 3day measles”
slight fever, mild cold symptoms, lymphnodes swelling, faint rash of pink spots on face, stomach, and chest. adults may develop pain in joints. significance is that it is a threat to fetuses.

Cause: rubella virus (enveloped single stranded)
Affects:
enters resp. tract and multipies in the nasopharynx and enters blood.
if early pregnancy: can go through placenta and kill/ impair chromosomes of fetuses cells leading to birth defects esp within first 6 weeks

39
Q

2) How has vaccination helped? [Figure 22.21]

A

it has eliminated the CRS and almost all rubella.

40
Q

D) What group has 50 member associated with skin lesions?

A

entroviruses

41
Q

E) In the early 1900’s what were the 6 possibilities for childhood rashes?

A
  1. rubeola
  2. scarlet fever
  3. dukes disease
  4. Duke’s disease
  5. erythema infectosum
  6. exanthem subitum
42
Q

F) What is erythema infectiosum? What are the symptoms? What causes it? [Figure 22.22]

A

5th disease :kids and young adults. fever, malaise, head and m aches.
diffuse redness on cheeks making it look slapped and lacy patterned rash lasts 2 weeks. young adultsmay have joint pains
huge threat to those with anemias because it infects bone marrow crlls. and they stop producing blood cells
cause: parvovirus B-19

43
Q

G) What are the symptoms of roseola? What age group does it affect?

A

common in kids 6m-3yrs.
startw with abruptly high fever that results in and convulsions. after fever short red rash apears and can last hrs to days.
cause: herpes virus 6

44
Q

H) What are warts? How are they treated?

A

papilloma viruses. infect skin through minor abraisons.

treat: freese, burn or surgically removint then

45
Q

A) What are dermatophytes and what can they do to the body?

A

molds that invade hair nostirls, and keratinized portion of cells. cause athletes foot, ring worm, and tinea’s
cause itching bad odor or rashes

46
Q

1) What are the symptoms of this type of infection?

A

d

47
Q

2) Which genera include skin-invading molds? [Figure 22.4]

A

epidermophyton, microsporum, and thrichophyton.

48
Q

3) How do they infect the skin?

A

some produce keritinase that breaks it down allowing them to enter. hair is invaded at the moist follicle

49
Q

4) How does an individual acquire this type of infection?

A

excessove moisture

50
Q

5) How can it be treated and prevented?

A

cleanliness, maintiness, moisture control

over the counter drugs, if under nail have to get nail removed

51
Q

B) What does Malassezia furfur cause? What groups of people are at risk? [Figure 22.5]

A

scaley face rash, dandruff

with immunodeficiencies

52
Q

C) What can Candida albicans cause? [Figure 22.26]

A

diaper rash

Micro Biology (25 decks)

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