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Host and Defense > Week 6 > Flashcards

Week 6 Flashcards

1
Q

What are the four classic presentations to look for while taking a physical examination?

A

Rubor, calor, tumor, dolor

Redness, heat, swelling, pain

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2
Q

What is crepitus and what causes it?

A

Crunchy sounding due to microbes that produce gas. Clostridium proferengens causes this

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3
Q

What is fluctuance?

A

Fluid filled

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4
Q

What is purpura?

A

Micro-breaks in capillaries that look like bruises

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5
Q

What is bullae?

A

Blisters

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6
Q

Name six other diseases that can mimic SSTI’s

A 
Gout-build up of uric acid
Thrombophlebitis 
Deep vein thrombosis
Contact dermatitis (skin exposed to some kind of chemical it doesn't like(allergy))
Drug eruption
Foreign body reaction
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7
Q

What is folliculitis?

What bacterial are most likely to cause folliculitis?

A

Folliculitis is a minor infection associated with friction and sweat gland activity

Staph aureus 
Pseudomonas aeruginosa (hot tub folliculitis)
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8
Q

What is acne? What bacteria is a common cause?

A

Inflammation of hair follicles with their associated sebaceous glands

Propionibacterium acnes - within sebum, trapped in follicles/glands (S. Aureus is also a common cause)

Hormones and organic acids produced by p. Acnes contributes

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9
Q

What are soft tissue abscesses? What are its symptoms?

A

Any breach in skin

Local superficial cellulitis, bacteria necrose/liquefy tissue, pus formation (cell debris and WBCs)

Fluctuant, tender, erythematous nodule with surrounding erythema

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10
Q

What is the most common cause for soft tissue abscesses? Who is at most risk for polymicrobial infections?

A

Staph. Aureus (including MRSA)

IV drug users, oral, rectal, Volvo-vaginal are often polymicrobial

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11
Q

Why is it that systemic antibiotics aren’t always helpful for the treatment of soft tissue abscesses? What should you do instead?

A

Systemic antibiotics aren’t always helpful because they wont penetrate into the abscess.

Incision and drainage is necessary to get rid of the source of infection

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12
Q

What is a furuncle (AKA boil)? Are furuncles commonly recurrent?

A

Abscess in the area of a hair follicle

These are commonly recurrent

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13
Q

What is the difference between a furuncle and a carbuncle?

A

Carbuncles are a grouping of furuncles and the infection spreads into the subcutaneous tissue

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14
Q

What is the most common cause for necrotizing fasciitis?

A

Group A strep

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15
Q

What is Fournier’s gangrene?

A

Polymicrobial infection causing necrotizing fasciitis of genitals and perinuem 😳😵

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16
Q

What is one of the hallmark symptoms of necrotizing fasciitis?

A

Pain our of proportion to exam findings

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17
Q

Name some examples of dermatophyte fungi

A

Tinea cruris, corporis

Ringworm

Nail infections - onychomycosis

Occurs in keratinized layers of skin/nails

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18
Q

What are the three genera of dermatophyte fungi that cause SSTIs?

A

Trichophyton

Microsporum

Epidermophyton

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19
Q

What is the most common type of fungal infection in humans?

A

Candida albicans

Usually occurs in warm, moist environments. Treatment is topical antifungals, systemic antibiotics if severe

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20
Q

Name three types of infections caused by candida albicans and where they occur

A

Diaper rash

Intertrigo - on skin due to bad hygiene

Thrush - oral cavity

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21
Q

What is erysipelas? What is it caused by?

A

Rapidly spreading infection of group A strep in the deep dermis. Causes rubor, calor, tumor, dolor

Treatment is penicillin

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22
Q

What is cellulitis? What causes it? What is the treatment?

A

Infection of the subcutaneous tissue. Usually due to group A strep, but may also be caused by staph aureus, or gram negatives in immunocompromised individuals

Treatment is systemic antibiotics (cant use topical because its too deep)

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23
Q

What four factors increase the risk of wound infections?

A

Higher number of organisms

Higher virulence of organisms

Poor circulation near wound

Poor general health

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24
Q

True or false… nearly all of the population are carriers for staph aureus

A

False. About 10-30% of the population carries staph aureus, especially in the anterior nares

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25
Q

Staphylococcus aureus can secrete ___ toxin into ____ tissue to cause scolded skin syndrome (usually in ___)

A

alpha

Subcutaneous

Infants

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26
Q

Staph aureus can also cause exfoliatin, which is…

A

Bullous impetigo

Yellow blisters over extremities and/or face

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27
Q

What is staph toxic shock syndrome (TSST-1)? What causes it?

A

Causes desquamation of the skin (peeling)

Can be caused by super absorbent tampons or excessive gauze post surgery

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28
Q

What does the staph toxin, enterotoxin do?

A

Causes food poisoning (diarrhea, vomiting)

Note that the toxin just has to be present in the food, not necessarily the microbe, in order to cause food poisoning

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29
Q 
What does each staphylococcal toxin cause?   
Alpha toxin
Exfoliatin
TSST-1
Enterotoxin
A

Alpha toxin - scolded skin

Exfoliatin - bullous impetigo

TSST-1 - toxic shock syndrome

enterotoxin - food poisoning

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30
Q

MRSA strains acquire the ___ gene which…

A

MecA

Makes new penicillin binding proteins with reduced affinity for b-lactams

Makes it resistant to ALL B-lactams

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31
Q

What are the drugs of choice for MSSA?

A

Anti-staphylococcal penicillins such as nafcillin and oxacillin

Cephalosporins

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32
Q

What are four risk factors for getting MRSA? What is the treatment?

A

Close skin-skin contact
Crowded living conditions
Poor hygiene
IV drug use

Treatment: trimethoprim-sulfa, doxycycline, vancomycin, linezolid, daptomycin

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33
Q

What are some complications post-group a strep infection?

A

Strep A primes our immune system against certain antigens that resemble antigens on our heart valves and other locations, causing autoimmune disorders. It can lead to rheumatic fever or glomerulonephritis

Differences in the M protein

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34
Q

Name the two streptolysins and what they do?

A

O and S

cytotoxic

Lyse leukocytes, tissue cells, and platelets (which helps the microbe evade the immune system)

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35
Q

Name the two pyrogenic exotoxins of group a strep and what they do

A

A and B

These are “superantigens”

These hijack a normal APCs reaction to stimulate a large number of T cells, causes massive dysregulatd cytokine respone, and causes severe systemic illness (shock)

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36
Q

Name three inflammatory enzymes of group a strep and what they do.

A

Streptokinase: a protease

Hyaluronidase: degrades carbohydrates and breaks down CT

DNAse - degrades DNA

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37
Q

Describe clostridium perfringens

A

Anaerobic, spore-forming, gram positive rods

Found in soil and human colon

Produces hydrogen and CO2 gas to cause gas gangrene***

Has multiple exotoxins (neurolytic toxin destroys WBCs)

Rapidly fatal

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38
Q

What is pasteurella multocida?

A

Gram negative rod

Transmitted through animal bites

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39
Q

Describe pseudomonas aeruginosa

A

Gram negative rod

Prototypical non fermenter

Can cause hot tub folliculitis, secondary infection after burns*, necrotizing fasciitis.

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40
Q

Describe vibrio vulnificus

A

Gram negative rod

Found in salt water environments (colonizes shell fish)

Causes fever, sepsis, hemorrhagic bullae

Associated with iron overload and cirrhosis

Somewhat rare. Infection spreads rapidly. Can cause liver damage

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41
Q

What is mycetoma?

A

Madura’s foot

Bacterial infection often due to actinomyces or nocardia or fungal infection due to lots of different types of molds

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42
Q

What causes sporotrichosis?

A

Sporothrix schenckii

*rose gardeners disease

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43
Q

True or false.. one of the best strategies to diagnose SSTIs is through pus

A

True

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44
Q

Hemotogenous, monomicrobial osteomyelitis is often due to what kind of bacteria?

A

Staphylococcus aureus

Coagulase negative staphylococci

Gram-negative rods

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45
Q

Bone infections due to periodontal issues are ____ spread

A

Contiguous

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46
Q

Name the three sources for osteomyelitis

A

Hemotogenous (through the blood stream) - typically monomicrobial

Contiguous spread (prolonged exposure nearby) - typically polymicrobial

Direct inoculation (result of trauma)

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47
Q

Where is hemotogenous osteomyelitis most likely to occur in children and adults?

A

Children - long bones

Adults - vertebrae

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48
Q

What is sequestra?

A

Separated dead bone

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49
Q

In hematogenous osteomyelitis, the infection lands in the _____, then spreads to the _____, which can result in ____

A

Inter-medullary canal

Cortical bone

Lifting of the periosteum

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50
Q

What is an involucrum?

A

When the infection in a bone pushes the periosteum out and causes NEW BONE to form between the periosteum and the old bone

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51
Q

Name the four stages of the anatomical classification of osteomyelitis

A

Stage 1 - medullary osteomyelitis. confined to the medullary cavity

Stage 2 - Superficial osteomyelitis. Involves only the cortical bone

Stage 3 - localized osteomyelitis. Involves both cortical and medullary bone but does not involve the enter

Stage 4 - diffuse osteomyelitis. Involves the interest thickness of the bone, with loss of stability

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52
Q

Why is it that you can treat stage 1 osteomyelitis with antibiotics but not stage 2, 3, or 4?

A

In stages 2, 3, and 4, a biofilm forms and requires physical removal. Also, in stage 3 and 4, the infection cuts off the blood supply so it is difficult to get the antibiotics to the site.

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53
Q

What are the differences between the acute and chronic classifications of osteomyelitis?

A

Acute - infection prior to development of sequestra. Usually less than 2 weeks

Chronic - infection after sequestra have formed. Involves Formation of involucrum, bone loss, and sinus tract formation

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54
Q

What are the clinical presentations acute osteomyelitis?

A

gradual onset over several days

Dull pain/local tenderness

Warmth, erythema, swelling

Can present as septic arthritis (bacterial infection in a joint coming from the bone (common on the superior tibia)

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55
Q

What are the clinical presentations of chronic osteomyelitis?

A

Mild pain over several weeks

May have localized swelling or erythema

Draining sinus tract

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56
Q

What are some characteristics that help in the diagnosis of chronic osteomyelitis?

A

Suspected based on chronic, poorly healing wounds, DM, vascular disease, decubitus ulcers, or in the presence of underlying hardware

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57
Q

Typically, radiographs/MRIs only help so much in the diagnosis of osteomyelitis. Laboratory tests such as WBC count, ESR/C-reactive protein, blood cultures are nonspecific. What is the best way to specifically diagnose osteomyelitis?

A

Culture of bacteria from bone.

Biopsy+pathology with inflammation and osteonecrosis.

However… note that if you are somehow able to diagnose the disease without culture, there is no need for biopsy

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58
Q

True or false… intravenous antibiotic administration is the best way to treat acute osteomyelitis

A

False… both intravenous and oral therapy work equally well. (However you should consider the oral bioavailability of the antibiotic and its ability to penetrate bone)

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59
Q

What is the treatment for acute osteomyelitis?

A

3-6 week treatment with antibiotics. (Surgery may or may not be indicated)

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60
Q

What is the treatment for chronic osteomyelitis?

A

3-6 week treatment of antibiotics + surgery

Greater role for surgery due to necrotic bone and the lack of antibiotic penetration to devascularized bone

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61
Q

Odontogenic infections can spread ____ to the jaw (oral aerobes and anaerobes)

A

Contiguously (not hematogenously)

This is relatively rare

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62
Q

Which is more susceptible to osteomyelitis, the mandible or maxilla? Why?

A

Mandible

Because it has thinner cortical plates and is less vascularized

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63
Q

What portion of the mandible is most susceptible to developing osteomyelitis? How is it developed?

A

Lingual aspect in the molar region

Periosteum is penetrated with chronic infection with the formation of mucosal or cutaneous abscesses and fistulae

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64
Q

What are some risk factors for osteomyelitis of the jaw?

A

Dental infection, compound fracture, malignancy, irradiation, DM, steroid use

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65
Q

What are the symptoms of osteomyelitis of the jaw? What is the treatment?

A

Mandibular pain, anesthesia or parasthesia on affected side. Lymphadenopathy, can progress to trismus (locked-jaw)

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66
Q

What is the leading cause of arthroplasty failure? (Joint replacements)

A

Prosthetic joint infections

Failure rate is 10-20%

PJIs lead to need for more surgery, antimicrobials, more rehab, etc.

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67
Q

What is the biggest risk factor for PJIs?

A

Surgical site infection not involving joint prosthesis

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68
Q

What type of bacteria are the most likely culprits of PJIs?

A

Gram positive cocci (65%)

This includes…

Staph aureus
Streptococcus spp.
Enterococcus spp.

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69
Q

Aerobic gram negative bacilli cause about ___% of PJIs. Name two species that are likely culprits

A

6

Enterobacteriaceae

Pseudomonas aeruginosa

70
Q

Describe the pathogenesis of PJIs

A

Skin organisms inoculate at time of implantation

Some seed in the blood, but more importantly, a small number adheres to the implant forming a protective biofilm that evades immune system and antimicrobials

71
Q

If a PJI occurs within the first __ months of surgery, the infection was most likely introduced during surgery

A

3

72
Q

Late PJIs occur > ____ years after surgery and are due to…

A

1-2 years

Hematogenous seeding or late manifestation of surgical infection

73
Q

What is the treatment for PJIs?

A

SURGERY + antimicrobials

74
Q

Name 5 surgical management options for PJIs

A

Debridement and retention

Two stage exchange

One stage exchange (during a single procedure, everything is taken out then new stuff is put back in)

Resection arthroplasty with arthodesis (fusion)

Amputation

75
Q

What antimicrobial is recommended for either a 1 stage exchange or debridement and retention?

A

Rifampin (for 2-6 weeks)

76
Q

Why is rifampin not recommended in a 2 stage exchange? How long should you wait for re-implantation?

A

Rifampin is not recommended because the prosthetic material is removed in this method

6 weeks - 3 months

77
Q

True or false… prophylactic antibiotics are recommended for dental procedures in patients with prosthetic joints

A

False! Dental procedures do not cause PJIs and prophylactic antibiotics don’t prevent it

78
Q

Prophylactic antibiotics are indicated for patients who have prosthetic joints and ____

A

Are severely immunocomprimised or have a history of PJIs

79
Q

What mycobacteria defenses make it exceptionally difficult for antimicrobials to do their jobs?

A

Cell wall is thick, hydrophobic, and rich in mycolic acid

Cell membrane has efflux pumps that pumps out harmful chemicals such as antibiotics

Some species can hid inside host cells

80
Q

True or false… TB is the 2nd leading killer of adults in the world with 2 million TB deaths a year

A

True

81
Q

What is the prophylactic treatment of choice for a latent/asymptomatic primary TB infection?

A

Isoniazid for 9 months

82
Q

What is the treatment of choice for an overt/active TB infection?

A

2 with 4, then 4 with 2

2 months treatment with combination of (RIPE) rifampin, isoniazid, pyrazinamide, ethambutol

Then 4 months with rifampin and isoniazid

83
Q

How do you treat an overt active TB infection that is an intracellular organism?

A

Treat with RIPE for 12 months + azithromycin

**restrict the use of pyrazinamide to only the first two months because it is hepatotoxic

84
Q

Reactivated (resistant) TB is a greater risk in hat kinds of patients?

A

Immunosuppressed, HIV-positive, other “high risk patients

85
Q

What is the rule of 5s for TB?

A

In otherwise healthy patients infected with TB…

5% risk of reactivation in first 2 years

Then a 5% lifetime risk of reactivation

High risk patients have a 5% + 5% risk of reactivation each year

86
Q

True or false… secondary tuberculosis always reactivates in the lungs

A

False… it may also reactivate in lymph nodes, joints, kidney, CNS..

87
Q

What is the treatment of choice for secondary TB?

A

RIPES

2 months treatment with combo of rifampin, isoniazid, pyranzinamide, and STREPTOMYCIN

Then 4 months with rifampin and isoniazid

88
Q

Second line drugs such as ___ can be added to overcome drug resistance when treating secondary TB

A

Bedaquiline

89
Q

What are the clinical uses for Isoniazid?

A

Prophylaxis of TB

Effective in combo for treating TB

90
Q

What is Isoniazid’s mechanism?

A

Decreases mycolic acid synthesis

It is a prodrug that must be activated by the bacterial enzyme, Kat G.

Then, an activated complex is formed that blocks a key substrate and enzyme in mycolic acid synthesis

**KatG activation of isoniazid also produces free radicals such as NO

91
Q

Name three adverse effects of isoniazid.

A

Hepatotoxicity

INH can cause a pyridoxine deficeincy so always administer with vitamin B6 to maintain heme synthesis and prevent neurotoxicity

Disulfuram-like reaction (avoid alcohol 72 hours before and after use)

92
Q

What is the clinical use of pyrazinoamide? True or false.. it is also a prodrug

A

Treatment of ACTIVE TB

True, pyrazinamide is a prodrug

93
Q

What is the mechanism of pyrazinamide?

A

Inhibits mycolic acid synthesis

Net effect is that pyrazinoic acid accumulates inside the granulomas

Bacterostatic

94
Q

Pyrazinamide requires a ___ pH to be activated. Pyrazinamide is an essential part of the treatment of TB ___

A

Acidic

Meningitis

95
Q

What are some adverse effects of pyrazinamide?

A

Hepatotoxicity (if used for longer than two months).

Increases uric acid (gout)

Rash

Contraindicated in pregnancy - can cause fetal harm and infertility in nonpregnant patients

96
Q

What is the clinical use for ethambutal?

A

Treatment of ACTIVE TB

97
Q

What is the mechanism of ethambutal?

A

Obstructs the mycobacteria cell wall formation

Decreases carbohydrate polymerization by inhibiting aribinosol transferase

98
Q

True or false… ethambutal crosses the blood brain barrier

A

True

99
Q

Name three adverse effects of ethambutal

A

Ocular toxicity

Color blindness

Ocular neuritis (swelling of optic nerve leading to blindness)

100
Q

What are some adverse effects of streptomycin?

A

Ototoxic

Nephrotoxic

Avoid during pregnancy

101
Q

Azithromycin should be added to the combo treatment in cases of ___

A

Mycobacterium avium

102
Q

What is the clinical use for bedaquiline?

A

Multi-drug resistant TB

103
Q

What is the mechanism of bedaquiline?

A

Inhibits mycobacterial ATP synthase

Long half life

104
Q

What are two adverse effects of bedaquiline?

A

Common side effects include nausea, vomiting, arthralgias (joint pain), and headache

** can cause prolonged QT syndrome, so be very careful with patients with arrhythmias

105
Q

What is the drug of choice for treatment of both TB and leprosy?

A

Rifampin

106
Q

What is the drug of choice for prophylaxis of leprosy? (Can also be used for prophylaxis of pneumocystis jiroveci)

A

Dapsone

107
Q

What is the mechanism of Dapsone?

A

Competes with PABA to inhibit dihydrofolate synthesis in bacteria

108
Q

What are three adverse effects of Dapsone?

A

Hepatotoxicity

Hemolysis

Cross-sensitivity if allergic to sulfonamides

109
Q

Most of traveller’s diarrhea is caused by ___ and is treated by ___

A

E. Coli

Rifaximin is the drug of choice for treating traveller’s diarrhea due to E.coli

110
Q

Ciprofloxacin is the drug of choice in treating traveller’s diarrhea due to…

A

Campylobacter jejuni

Salmonella

Shigella

111
Q

What is the drug of choice for treating pseudomembranous colitis?

A

Metronidazole

112
Q

How long does the induced innate immune response last?

A

Hours to days

113
Q

True or false… dendritic cells, neutrophils, and macrophages can do phagocytosis. However only macrophages and dendritic cells are APCs

A

True

114
Q

True or false.. neutrophils die after phagocytosis

A

True

115
Q

What three innate immune cells respond to parasites such as helminths and are also involved in allergic responses?

A

Mast cell

Eosinophil

Basophil

116
Q

What are two ways in which cells communicate that they are infected, damaged, or diseased?

A

Interferon response

Altered MHC expression

117
Q

What are three pro-inflammatory signaling mechanisms?

A

Cytokines

Eicosanoids

Acute phase response

118
Q

Most tissues have resident macrophages. Name the resident macrophages of the following tissues…

Brain
Bone
Liver
Skin

A

Brain: microglia

Bone: osteoclasts

Liver: kupffer cells

Skin: langerhans cells

119
Q

What are the effector mechanisms of macrophages?

A

Phagocytosis

Cytokine release

Degranulation

Antigen presentation

120
Q

How does intracellular recognition work with NK cells?

A

Recognizes changes at the surface of human cells that are caused by viral infection

121
Q

Most of the macrophage receptors are involved in phagocytosis. Except for ___ which can be involved in phagocytosis but function mainly in signaling and driving the inflammatory response

A

TLR (toll-like receptors)

122
Q

What ligands do the lipopolysaccharide receptors bind?

A

LPS!!! (And some other stuff like peptidoglycan)

123
Q

What ligand binds to the mannose receptor?

A

LPS, CPs and ManLam

124
Q

What are the similar agents in phagolysosomes and granules in macrophages and neutrophils

A

Both macrophage and neutrophil phagolysosomes have…

Low pH, superoxide, hydrogen peroxide, NO, lysozyme, cathelicidin

125
Q

What are some differences between the produce of phagolysosomes between macrophages and neutrophils?

A

Macrophages: macrophage elastase-derived peptide

Neutrophils: alpha defensins, lactoferrin, bacterial permeability inducing protein.

Note that macrophages do not have any “competitors” like neutrophils do

126
Q

Name the external and internal TLRs

A

External: 1, 2, 4, 5, 6

Internal: 3, 7, 8, 9

127
Q 
Name what TLRs read each of the following extracellular antigens...
Diacyl lipopeptides
Triacyl lipopeptides
Flagellin
LPS
A

Diacyl lipopeptides - 2, 6

Triacyl lipopeptides - 1, 2

Flagellin - 5

LPS - 4

128
Q

What TLRs detect the following antigens internally?

DsRNA
SsRNA
CpG DNA

A

DsRNA - 3

SsRNA - 7

CpGDNA - 9

129
Q

TLR10 homerdimerizes and heterodimerizes with ___ and ____

A

TLR 1 and 2

130
Q

What antigen does TLR-9 detect? Is this bacterial or viral?

A

TLR-9 detects CpG DNA, which is bacterial DNA or DNA viruses

131
Q

TLR activation requires ____

A

Dimerization. (Like tyrosine receptor kinase)

Dimerization will allow signal transduction to occur

132
Q

In the Nf-kb pathway, a complex of ___, ___, ___, and ____ is assembled on the macrophage surface

A

TLR4
MD2
CD14
LPS

133
Q

Once the complex is assembled on the macrophage surface, ____ binds to TLR4 and activates ___ to phosphorylate ____ which leads to the phosphorylation and activation of ___

A

MyD88

IRAK4

TRAF6

IKK

134
Q

IKK phosphorylates ___, leading to its degradation and the release of ____, which enters the nucleus

A

IkB

NF-kB

135
Q

Upon entering the nucleus, NF-kB activates transcription genes for…

A

Inflammatory cytokines which are synthesized in the cytoplasm and secreted via the ER

136
Q

What are NOD receptors?

A

Nucleotide-binding oligomerization domain

Recognize degraded intracellular PAMPs and DAMPs (microbial toxins, viruses, cell stress proteins) (often from phagocytosis)

137
Q

What happens upon activation of NOD receptors?

A

They induce cytokine expression and release

Form inflammasome

Cooperate with TLRs

138
Q

What is an inflammasome?

A

They activate and promote cytokine release

Have proteolytic activity to cleave procytokines into their fully functional form.

Enhance other inflammatory signals

Has a checkpoint function

139
Q

True or false… cytokines are mostly soluble, have mostly paracrine and autocrine signaling functions, consist of interleukins, chemokines, and others

A

True

140
Q

What are the six families of cytokines based on receptor morphology?

A 
Class 1
Class 2
Interleukin 1
Interleukin 17
TNF (tumor necrosis factor) 
Chemokines
141
Q

True or false… cytokines only affect immune tissues

A

False.. they also affect non-immune tissues

142
Q

What are some common intracellular signaling pathways induced by cytokines?

A

JAK-STAT (most common)
MAPK
NF-kB

143
Q

Name 5 proinflammatory cytokines that macrophages release

A

Il-1B

TNF-a

IL-6

CXCL8

IL-12

144
Q

What are the local and systemic effects of IL-1B?

A

Allows cells to enter diseased area by activating vascular endothelium, increasing access of effector cells, causing local tissue destruction, and also activates lymphocytes

Systemic: fever and causes production of IL-6

145
Q

What are the local and systemic effects of TNF-alpha?

A

Activates vascular endothelium, increases vascular permeability to allow increased entry of igG, complement, and cells, and allow fluid drainage to lymph nodes

Systemic: fever, mobilization of metabolites, septic shock syndrome

146
Q

What are the systemic and local effects of IL-6?

A

Local: lymphocyte activation, increased antibody production

Systemic: fever, induces acute-phase protein production

147
Q

What are the local effects of CXCL8?

A

Chemotactic factor recruits neutrophils, basophils, and T cells to site of infection

148
Q

What are the local effects of IL-12?

A

Activates NK cells, induces the differenation of T cells into T helper cells

149
Q

Inflammatory cytokines have systemic effects? What are these effects and where do they occur?

A

Liver: activation of complement

Bone marrow: neutrophil mobilization

Hypothalamus: increased body temp.

Fat/muscle: protein and energy mobilization to increase body temp.

Dendritic cells: TNF-alpha stimulates them to migrate to lymph nodes and activate the adaptive immune system

150
Q

What does Il-6 signaling do to the liver?

A

Stimulates the liver to increase its production of induced innate immune system proteins, like complement

151
Q

Describe the process once leukocytes are initiated by cytokines to get to the tissues

A

Cytokines cause dilation of blood vessels

Endothelium expresses adhesion molecules which stick to leukocytes

Leukocytes extravasated to site of infection

Blood clotting occurs in the vessel

152
Q

Extravasation depends on ___, ____, and ____. Describe what each does.

A

Chemokines: chemoattractants

Adhesion molecules: teather leukocytes to endothelium of vessel. Upon binding, proteases are released

Proteases: opens basement membranes with MMPs and Elastases

153
Q

Excessive plasma TNF-a can cause ____. What is this?

A

Septic shock syndrome

This causes all of the vasculature in the body to become leaky

Often initiated by blood borne infection

Systemic extravasation and neutrophil invasion

Vascular collapse

Rapid, multi-organ failure

154
Q

What are the effector mechanisms of neutrophils?

A

Phagocytosis

Degranulation

Extracellular traps***

Cytokine release

155
Q

Granules serve to functions, what are they? What are the four neutrophil granule types? Which is released first?

A

Phagocytosis and degranulation

Azurophil granules -released first

Specific granules

Gelatinase granules

Secretory granules (these are released to damage the pathogen)

156
Q

Other than granules, what is another way that the pathogen is killed within the phagosome of neutrophils?

A

Oxidative burst and pH dropping

157
Q

What are the three types of neutrophil extracellular traps?

A

Non lytic (by release by mitochondrial DNA)

Non-lytic (by vesicular mechanism)

Lytic

**note that the non-lytic traps are mobile

*also note that traps are important in the vascular, to keep the infection from spreading

158
Q

Natural killer cells are large cytotoxic lymphocytes that kill ____ by responding to ___, ___, and ___. Unlike neutrophils, NK cells go through bone marrow education for functional receptor patterns and do not die after killing.

A

Diseased self cells

Interferons, MHC class 1, and unique stress ligands

159
Q

Altered or absent ___ on self cell surface will stimulate a negative signal, leading to granule release and death of the cell

A

MHC class 1

160
Q

Virus-infected cells will ___ their interferon release, which will cause what three things?

A

Increase

Induce resistance to viral replication in all cells

Increase expression of ligands for receptors on NK cells

Activate NK cells to kill virus-infected cells

161
Q

TLR-3 in endosome binds ___ and signals via __ to induce____ gene expression

A

DsRNA

TRIF

IFN (interferon)

162
Q

TLR-7 in endosome binds ___ and signals via ___ to induce ___ expression

A

SsRNA

MyD88

IFN

163
Q

Describe how cells detect viral infections

A

Viral replication in cytoplasm produces uncapped RNA

RLR (retinoic acid inducable gene -like receptor) binds to viral RNA and induces MAV (mitochondrial antiviral signaling protein) and dimierizes

Dimerization initiates signaling pathways that activate IRF3 and NF-kB

IRF3 causes synthesis and secretion of type 1 interferons
NF-kB causes synthesis and secretion of inflammatory cytokines

164
Q

Interferons are cytokines that can do what four things? They are released by what cells?

A

Reduce viral replication
Prevent cell division
Induce apoptosis
Activate NK cells, T cells, and macrophages

Released by diseased/stressed cells such as intracellular infection or cancer. Also released by leukocytes

165
Q

Describe how interferons activate NK cells, and what the NK cells do.

A

Virus infection of cells triggers interferon response

Type 1 interferon drives the proliferation of NK cells, then differentiation into cytotoxic effector cells

NK cells then signal the affected cells to undergo apoptosis

166
Q

Explain how macrophage and NK cells are bidirectionally regulated

A

Macrophage activated by virus recruits NK cells

NK cells synapse with the macrophage

Nk cells proliferate and differentiate.

NK cells tell the macrophage to continue phagocytosis

167
Q

Explain how NK cells regulate DC recruitment of adaptive immunity

A

Dendritic cells locally activate NK cells. This also acts as a checkpoint on adaptive immune function

  • large NK response = DC presentation limited (DC cells actually killed)
  • small NK response = DC are activated to initiate adaptive immune system
168
Q

True or false… granulcytes such as mast cells, eosinophils, and basophils are predominant in tissues but rare in the blood. They degranulate when activated. Responsible for initiating type 1 hypersensitivity (allergic response)

A

True

Also note that the first time you are exposed to an antigen, mast cells dont do anything. They become more sensitive over time

169
Q

What is a onychomycosis?

A

Fungal infection of the nails

170
Q

Once staph is on the skin how may it access deeper tissues in the skin?

A

Through skin appendages or trauma

171
Q

Which drug used to treat TB revs up cyp450? Why is this significant?

A

Rifampin

This will increase the metabolism of drugs such as oral contraceptives. …May result in pregnancy… whoops!

Host and Defense (17 decks)

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