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Host and Defense > Week 5 > Flashcards

Week 5 Flashcards

1
Q

Which layer of the epidermis prevents water loss and chemical entry?

A

Stratum corneum

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2
Q

____ is a critical component in diagnosis of skin diseases

A

Histology

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3
Q

Of the cutaneous infections we need to know. Name the four bacterial infections

A

Impetigo

Cellulitis

Folliculitis

Infectious fasciitis

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4
Q

Name the three viral cutaneous infections we need to know

A

Herpes virus

Molluscum contagiosum

Verruca vulgaris

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5
Q

Name the three fungal cutaneous infections we need to know

A

Tinea versicolor

Tinea corporis

Deep fungal infection

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6
Q

Name the two cutaneous infestations we need to know of

A

Scabies

Myiasis

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7
Q

Describe the normal skin flora

A

Aerobic cocci

Aerobic and anaerobic coryneform bacteria

Gram negative bacteria

Yeast

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8
Q

How does the skin flora prevent bacterial infections?

A

Skin flora provides ecological competition for pathogenic microbes

Hydrolyzes lipids of sebum to produce free fatty acids, which are toxic to many other types of bacteria

Note that ~20% of dermatology visits are due to bacterial infections

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9
Q 
Where in the integumentary system do the following conditions occur?   
Impetigo
Cellulitis 
Folliculitis 
Infectious fasciitis
A

Impetigo - epidermis

Cellulitis - dermis

Folliculitis - appendages (hair follicles)

Infectious fasciitis - hypodermis/fascia

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10
Q

Most cutaneous infections are caused by ____

A

Staphylococcus aureus

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11
Q

Scales and crusts (specifically honey-yellow crusts) will often result in neutrophils beneath the ____ in the epidermis. This condition is most likely ___

A

Stratum corneum

Impetigo

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12
Q

50-70% of impetigo cases are due to ____. They may also be due to ___ and ___

A

Staphylococcal

Streptococcal

Mixed infections

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13
Q

Describe the symptoms of impetigo, where they are likely to be found, and what the treatment is

A

Discrete, thin-walled vesicles that become pustular and rupture.

Thin, straw colored discharge noted which dries to form golden-yellow crusts

Most likely to be found on exposed areas of the face, hands, neck, and extremities.

Treatment: antibiotic ointment, sometimes with systemic antibiotic

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14
Q

Describe folliculitis, what causes it, and how to treat it

A

Inflammation of the hair follicle. Dome-shaped pustules around hair follicles

Bacterial infections Most often due to staph aureus

Treatment: decrease bacterial load with antibacterial soap, use topical or systemic antibiotics

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15
Q 
Which of the following viruses are DNA and RNA viruses? 
Herpes virus
Pox virus
Retroviruses (HIV)
Papovavirus
A

DNA: herpes virus, poxvirus, papovavirus (infect keratinocytes)

RNA: retrovirus (HIV, HTLV) (infect CD4 T cells)

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16
Q 
Describe where each virus infects..
Molluscum contagiosum
Herpes virus
Verruca
Folliculitis - herpes virus
A

Epidermis: molluscum contagiosum, herpes virus, verruca

Appendages: folliculitis - herpes virus

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17
Q

Name some features of a cutaneous herpes virus infection

A

Grouped papulovesicles on an erythematous base (typically doesn’t cross the midline)

Pain with no rash, then rash develops a few days later

Typically restrained to a single dermatome, unilaterally

Keratinocytes lose their connections (desmosomes) with other keratinocytes (acampolysis)

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18
Q

What does a positive Tznack smear indicate?

A

This is a herpes/chicken pox skin test

multinucleate giant keratinocytes

Peripheral marginization of chromatin (ground-glass appearance)

A negative interpretation is problematic in clinical situations in which a herpes virus infection is likely - you must go back and scrape another lesion.

Tzanck smear has high sensitivity and specificity

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19
Q

Why is it that herpes zoster (AKA varicella, AKA, shingles, AKA reactivated chicken pox) affects dermatomes?

A

The virus resides in dorsal root ganglia

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20
Q

What are adnexa?

A

Skin organelles such as hair follicles, sweat glands, etc.

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21
Q

What do you use to stain a tzanck smear?

A

HemaQuick (Dif Quik)

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22
Q

What is herpetic whitlow?

A

Herpes on the digits

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23
Q

True or false.. eczema herpeticum is a rare and sometimes life threatening disease

A

True

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24
Q

Oral hairy leukoplakia is most often seen in patients with ___. True or false.. this is life threatening and must be treated

A

HIV or epstein-barr or other immunocompromising conditions.

One of the most common viral induced oral diseases in HIV

False, it has low morbidity

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25
Q

True or false.. marginization of chromatin occurs in both herpesvirus - EBV, and herpesvirus varicella zoster

A

True

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26
Q

Red umbillicated papules located on the trunk that are scattered and grouped is a characteristic of…

A

Molluscum contagiosum

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27
Q

What causes molluscum contagiosum? Who does it primarily affect? How is it transmitted? What is significant about its histology? Describe its treatment.

A

Caused by poxvirus

Primarily affects young children, sexually active adults, those with systemic T-cell immunosuppresion.

Transmitted by direct skin-to-skin contact especially if skin is wet.

Molluscum bodies (henderson paterson bodies) present in histologic samples

Spontaneous resolution of disease is certain in children within two years

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28
Q

Verrucous epidermal hyperplasia often is associated with a thick granular cell layer with ____. It is often caused by ____

A

Koilocytes

HPV (human papillomavirus)

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29
Q

Define each of the following.. verruca vulgaris, verruca plantaris, verruca plana, verruca condyloma

A

Verruca vulgaris - common wart

Verruca plantaris - wart on foot

Verruca plana - wart on arm?

Verruca condyloma - genital wart

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30
Q

Name the two fungal infections that infect the epidermis?

A

Tinea versicolor

Dermatophytosis

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31
Q

What should you do if the rash is scaly?

A

Do a KOH preparation looking for fungal elements

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32
Q

What does a KOH preparation look like for tinea versicolor?

A

Spaghetti (hyphae) and meatballs (yeast)

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33
Q

What causes tinea versicolor? Describe what this condition looks like

A

Caused by pityrosporum orbiculare. (Part of normal skin flora, normally non pathogenic)

Presents as multiple minimally scaly circular white, tan, or orangish macules or papules that coalesce into patches or plaques

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34
Q

What conditions predisposes you to tinea versicolor? Where is the most likely common site of infection?

A

Excess heat and humidity

Most commonly seen in upper trunk

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35
Q

What layer of the skin does pityrosporum orbiculare usually infect?

A

The stratum corneum

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36
Q

What is the technical name for scaling?

A

Parakeratosis

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37
Q

Why can’t dermatophyte infections survive in the mouth or vagina?

A

This is nonkeratinized tissue so the stratum corneum doesn’t form. Dermatophytes can only survive on dead keratin

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38
Q

What are the three genera that cause dermatophyte infections?

A

Microsporum

Trichophyton

Epidermophyton

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39
Q

What is the most important diagnostic test for dermatophyte infections?

A

KOH preparation

Note that hyphae are present in largest numbers at the advancing annular edge

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40
Q

A fungal infection with an ulcerated, firm plaque with satellite papules, has round cells within multinucleated giant cells, and the fungus cells look like a mariner’s wheel (round cell with multiple buds)… what is this?

A

Paracoccidiodomycosis

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41
Q

True or false… most deep fungal infections are a manifestation of systemic infections. Primary infections are introduced directly into the skin via puncture, abrasion, trauma, etc.

A

Both statements are true

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42
Q

Name 5 types of infections that can be deep fungal infections

A

Coccidioidomycosis (SW US)

Paracoccidiodomycosis (south america)

Histoplasmosis (mississippi river)

North american blastomycosis

Others (sporotrichosis, mycetoma)

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43
Q

Most opportunistic fungal disease is seen in patients with ___ or ___

A

Leukemia

Hematologist neoplasia

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44
Q

____ is the key risk factor for invasive deep fungal infections

A

Neutropenia

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45
Q

Female Scabies mites burrow into what layer of the skin?

A

Stratum corneum

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46
Q

What does a scabies infestation look like?

A

Intense itching

Pruritic papular lesions, excoriations, burrows

Sites of predilection include finger webs, wrists and hands, groins - the circle of Hebra

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47
Q

How is scabies transmitted? How is it treated?

A

Contracted by close personal contact, contaminated lenins.

Treatment with permethrin 5% cream, oral ivermectin

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48
Q

What is myiasis?

A

Infestation of human tissue by fly larvae

Human botfly, dermatobia hominis is a common cause

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49
Q

How is myiasis contracted?

A

Female botfly glues its eggs to the body of a mosquito, stablefly, or tick

When the vector punctures the skin, the egg enters the wound

Painful furuncle develops

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50
Q

How are maggots of myiasis removed?

A

Injection of local anesthetic or occlusion of breathing pre with petrolatum

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51
Q

Name two bacterial DNA replication enzymes that are targeted by antimicrobials

A

Topoisomerase 2 (DNA gyrase)

Topoisomerase 4

There are structural differences between bacterial topoisomerase and human topoisomerases that make this possible

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52
Q

What is the role of DNA polymerase 1?

A

Removes RNA primers from DNA and puts in DNA nucleotides

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53
Q

What is the difference between the roles of topoisomerase 2 (DNA gyrase) and topoisomerase 4?

A

DNA Gyrase - reduces supercoiling of DNA

Topoisomerase 4 - facilitates bacterial cell division by unblinking DNA following DNA replication

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54
Q

What is the only CNS penetrant fluoroquinolone?

A

Oxyfloxacin

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55
Q

Quinolone/fluoroquinolones bactericidal or bacterostatic? Narrow spectrum or broad spectrum?

A

Bactericidal

Broad spectrum

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56
Q

How does quinolones work? What is the difference between targeting gram - and gram + positive microbes?

A

Block DNA gyrase (topoisomerase 2) and topoisomerase 4

DNA gyrase for gram -

Topoisomerase 4 for Gram +

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57
Q

What is the trend as you go down quinolone generations?

A

First generations inhibit DNA gyrase only (gram -)

Subsequent generations broaden gram - coverage and/or add topoisomerase 4 inhibitions to also give them gram + coverage

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58
Q

What are the names of the second, third, and fourth generation quinolones?

A

2nd: ciprofloxacin
3rd: levofloxacin AND oxflaxacin
4th: moxifloxacin

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59
Q

Which is the best quinolone for treating pseudomonas?

A

Ciprofloxacin

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60
Q

Which quinolone isn’t the first choice for any infection but is a good alternative for gonorrhea, anthrax, strep. Pneumonia, or H. Influenzae infections when resistant to B-lactams?

A

Levofloxacin (3rd generation)

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61
Q

Which quinolone is effective in treating systemic gram - infections such as traveller’s diarrhea?

A

Ciprofloxacin

-acts synergistically if given with B-lactams

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62
Q

Which quinolone is conserved the best respiratory fluoroquinolone?

A

Moxifloxacin

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63
Q

What is the drug of choice for prophylaxis or treatment of Anthrax?

A

Ciprofloxacin

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64
Q

Which quinolone is good at treating chronic bone infections (osteomyelitis) due to enterobaceriacaie?

A

Ciprofloxacin

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65
Q

True or false… Moxifloxacin is good at treating pseudomonas Aeruginosa.

A

False.. ciprofloxacin is the best at treating pseudomonas aeruginosa

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66
Q

Which quinolone has excellen anaerobic activity and enhanced gram + S. Pneumoniae activity

A

Moxifloxacin

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67
Q

True or false ciprofloxacin is good at treating pneumonia or sinusitis

A

False… because ciprofloxacin has weak activity against streptococcus pneumoniae

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68
Q

True or false… fluoroquinolones is readily absorbed orally, and should be taken with food

A

The first part of this statement is true… however, fluoroquinolones should not be taken with food because Al and Mg antacids or Fe or An will interfere with oral adsorption

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69
Q

Although quinolones are distributed through all tissues and body fluid, which organ has quinolone levels that actually exceed those levels detected in the serum?

A

Lung

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70
Q

What is the only fluoroquinolone that can reach the CSF in clinically-active levels?

A

Oxfloxacin

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71
Q

How are quinolones eliminated from the body?

A

Excreted by kidneys

72
Q

Why is it that the respiratory quinolones like levofloxacin and moxifloxacin only need to be taken once daily?

A

They have long half-lives and accumulate in the lung

73
Q

What drug is the most common cause of a C. Difficile super infection?

A

Ciprofloxacin

74
Q

What are some adverse effects of quinolones?

A

GI upset

CNS problems (headache, dizziness)

Photosensitivity

Prolongation of QT interval

Connective tissue problems

75
Q

True or false… quinolones should be used with caution with patients with epilepsy. Why?

A

True because it may provoke seizures

76
Q

How is it that ciprofloxacin should be used with caution with asthma patients?

A

It interferes with the metabolism of theophylline inhalers, and can produce toxic doses that may provoke seizures

77
Q

Fluoroquinolones taken with ____ can increase the risks of CNS stimulation and convulsions

A

NSAIDs

78
Q

Which quinolone is known to prolong the QT interval?

A

Moxifloxacin

79
Q

The use of quinolones is contraindicated in what kind of patients to prevent connective tissue problems?

A

Pregnant, nursing mothers, children

Patients with myasthenia gravis

Patients with tendinitis (can lead to ruptured tendons)

80
Q

Quinolones have what known drug interaction?

A

Antacids - decreases food absorption

Inhibits drug metabolism of theophylline*** warfine, caffeine and cyclosporine

81
Q

Name three non-quinolone drugs that disrupt nucleic acid synthesis

A

Metronidazole

Rifampin

Nitrofurantoin

82
Q

Which non-quinolone drug is the drug of choic for diarrhea due to superinfection of pseudomembranous colitis?

A

Metronidazole

83
Q

Which non-quinolone is the drug of choice for tetanus?

A

Metronidazole

84
Q

What is the mechanism and spectrum of metronidazole?

A

Mechanism - inhibits DNA replication

Spectrum - anaerobes, trichomonas vaginalis, entamoeba histolytica, C. Difficile

85
Q

What are the adverse effects of metronidazole? What is a contraindication?

A

Metallic taste, GI disturbance

CNS (dizziness, vertigo, headache, depression)

Dark urine

Contraindications - do not take with alcohol… disulfuram like reaction

86
Q

If drugs that cause a disulfuram-like reaction are taken within ___ hours of drinking alcohol, an “instant hangover” is produced due to a build-up of ___

A

72

Acetaldehyde

87
Q

Name 8 drugs that have disulfuram-like reactions

A 
Beta-lactams
Cephalosporins
Chloramphenicol
Isoniazid
Ketoconazole
Metronidazole
Nitrofurantion
Sulfonamides
88
Q

What is the mechanism and spectrum of rifampin?

A

Mechanism: inhibits DNA-dependent bacterial RNA polymerase

Broad spectrum (gram +, - and mycobacteria)

89
Q

What are the clinical uses of rifampin?

A

Treatment of mycobacteria

Prevention of haemophilus influenzae type B and meningococcal disease

90
Q

True or false… rifampin is absorbed well orally, penetrates the CNS and is excreted in saliva, tears, sweat, urine, and feces

A

True

91
Q

What are some adverse effects of rifampin?

A

Turns urine, sweat, and tears to a reddish-orange color

Dose-dependent hepatotoxicity risk

CYP450 inducer (increases metabolism of other drugs)

92
Q

What is the mechanism of nitrofurantoin? How is it selective for bacteria?

A

Forms highly-reactive intermediates that attack bacterial ribosomal proteins, DNA, and other macromolecules

Bacterial cells reduce the drug more rapidly than the host

93
Q

What are the clinical uses for nitrofurantoin?

A

Treatment of uncomplicated UTIs and prophylaxis against UTIs in people prone to recurrent UTIs

94
Q

Nitrofurantoin contraindications

A

Patients with decreased renal function

Patients in the last 4 weeks of pregnancy or in neonates up to one month (it can cause hemolytic anemia)

95
Q

True or false.. nitrofurantoin is absorbed orally and tissue penetration outside the urinary tract is negligible

A

True

96
Q

What is PABA (para-aminobenzoic acid)?

A

PABA is a key intermediate in the synthesis of dihydrofolic acid, which is then converted to folic acid (tetrahydrofolic acid)

97
Q

What does the dihydropteroate synthetase enzyme do?

What does dihydrofolate reductase do?

A

Converts PABA to dihydropteroic acid

Converts dihydrofolic acid to folic acid

98
Q

How does sulfamethoxazole work?

A

Structurally similar to PABA to compete for and inhibit dihydropterate synthetase

99
Q

How does trimethoprim work?

A

Inhibits dihydrofolate reductase (second step for the production of folic acid)

100
Q

Why are the sulfamethoxazole and trimethoprim so selective?

A

Humans lack the enzymes needed to convert PABA to folic acid

Humans get folate through dietary resources instead

Bacterial growth is selectively inhibited by folate deficiencies

101
Q

Which sulfonamide antibiotic is used systemically, and is rapidly absorbed, and intermediate acting?

A

Sulfamethoxazole

102
Q

What sulfonamide antibiotic is used topically only and used specifically for skin burns

A

Silver sulfadiaxine

103
Q

How does sulfamethoxazole work? Is it bacetiocidal or bacteriostatic?

A

Competitive inhibitor of dihydropteroate synthetase

Bacteriostatic

No longer used clinically as a monotherapy

104
Q

True or false… sulfadiazine is used as an oral monotherapy for UTIs and burns. Is it bacterostatic or bacterocidal

A

True

Bacterostatic

105
Q

Is silver sulfadiazne use topically or orally? What is it used to treat?

A

Topically

It is used for prevention and treatment of infections relating to skin burns and superficial wounds

106
Q

Name some adverse effects of sulfadiazine and silver sulfadiazine

A

Sulfa-hypersensitivity and photosensitivity. Allergic patients usually have cross sensitivity to all sulfa containing drugs

Accumulation in at risk patients can result in…
Hemolytic anemia
Nephrotoxicity
Kernicterus in infants (brain damage due to excessive billireubin in blood and brain)

107
Q

Trimethoprim is bacterostatic and ___ as potent than sulfonamides alone

A

20-50x more

108
Q

Describe the mechanism of trimethoprim

A

Binds to and inhibits dihydrofolate reductase, preventing the conversion of dihydrofolic acid to folic acid

Trimethoprim’ selectivity comes from its greater affinity from bacterial dihydrofolate reductase than the hosts

109
Q

What are the adverse effects of trimethoprim?

A

Pseudomembranous colitis

Hematological disorders including bone marrow suppression (TMP-treats marrow poorly)

110
Q

What is cotrimoxazole?

A

trimethoprim + sulfamethoxazole

Synergistic relationship

111
Q

Describe the spectrum of cotrimoxazole

A

Broad spectrum. Gram + and - aerobic bacteria

No anaerobic coverage!

112
Q

Is cotrimoxazole bactericidal or bacterostatic?

A

Time-dependent bactericidal

Combination provides 2 step blockade of folate synthesis, inhibiting bacterial DNA synthesis

113
Q

What are the clinical uses for cotrimoxazole?

A

Drug of choice for treatment of pneumocystis jiroveci pneumonia

Gram + aerobes (recurrent UTIs)

Haemophilus influenzae (respiratory tract infections and otitis)

114
Q

What was the 1937 elixir sulfanilamide tragedy?

A

Sulfanilamide was solublized in diethylene glycol to give it a sweeter taste, but resulted in the most consequential mass poisoning in the US in the 20th century

115
Q

What are the components of the immediate innate immune system?

A

Barriers and soluble effectors

Barriers include mechanical, chemical, and microbiological

Soluble effectors include complement and antimicrobial peptides

116
Q

What does the induced innate immune system consist of?

A

Cells (neutrophils, macrophages, etc.)

Cytokines (interleukins, chemokines, growth factors)

117
Q

About how long does the immediate innate immune response last before the early induced innate response kicks in?

A

0-4 hours

118
Q

The innate immune system is a system of pattern recognition. Name the two classes of molecular patterns, recognized by this system?

A

PAMPs (pathogen-associated molecular patterns)

DAMPs (damage-associated molecular patterns)

119
Q

Name four types of pathogen associated molecular patterns

A

Lipopolysacharides (LPS)
Flagellin
Mannose sugars
Unmethylated cpG DNA

120
Q

Name three types of damage associated molecular patterns

A

Heat shock proteins

Fibronectin

Chromatin

(Note that these all elicit different immune responses)

121
Q

Name and define the three types of barriers pathogens must overcome in order to infect a host

A

Mechanical - such as epithelial cells preventing entry, flow of air or fluid, cilia (lungs)

Chemical - fatty acids on the skin, defensins in skin gut lungs (big role in oral cavity, and low pH in stomach

Microbiological - normal microbiota

122
Q

Mechanical barriers are not passive. What does this mean?

A

The barriers are also constantly producing antimicrobial peptides and stuff

123
Q

Explain how specialized immune tissues are integrated into barriers

A

Lymph tissue (simpler than lymph nodes) resides just beneath barriers such as payers patches in the gut (gut associated lymphoid tissue)

This is where localized B and T cell activation takes place

124
Q

How do chemical barriers act on pathogens? Give examples

A

Isolation and physical removal… every mucosal tissue secretes a fluid (mucus) to trap the pathogen, then removes the pathogen. (Mucus and cilia in lungs)

Targeted destruction (lysozyme cleaves peptidoglycan.. only works on gram + cause it cannot penetrate the outer membrane of gram - )

125
Q

Name 7 protein/peptides that are used as chemical barriers and some are especially important in the oral cavity.

A 
Lysozyme
Lactoferrin
Defensins
Cathelicidin
Surfactant proteins
Secretory leukocyte protease inhibitor
S100 proteins (calprotectin and psoriasin)
126
Q

What does lysozyme do?

A

Cleaves glycosidic bonds in peptidoglycan to lyse bacterial cells

127
Q

What does lactoferrin do?

A

Binds and sequesters iron to limit growth and disrupt membranes

128
Q

What do psoriasin and calprotectin do?

A

Disrupts membranes

Binds and sequesters divalent cations to limit growth

129
Q

What do defensins do?

A

Disrupt membranes and has intracellular toxicity

130
Q

Where are alpha defensins produced? What about beta?

A

Alpha - mostly neutrophils (some paneth cells) (HNP=human neutrophil peptide)

Beta - most mucosal cells (contiguously)

Some are constitutive and some are induced

131
Q

Describe how defensins disrupt pathogen membranes. How is it selective?

A

Defensins are positively charged which integrate into the negatively charged membrane. Then the positive charge of the defensins repel each other to form pores in the membrane

It is selective because eukaryotic cells have more proteins in their membrane which are positively charged and repel the defensins

Note that defensins must have access to membrane in order to be effective, so lysozyme must cleave peptidoglycan first

132
Q

What are some other things defensins can do besides disrupting pathogen membranes?

A

Signaling function to drive inflammatory response

Induce chemotaxis

Cause histamine release

Cause wound repair and cell migration

Interacts with complement and opsonization

133
Q

Neutrophils ____ secrete __-defensins into GCF while stratified oral epithelim ____ secrete __-defensins

A

Are induced to

Alpha

Contitutively

Beta

134
Q

What are some ways that mutualistic and commensal bacteria form barriers?

A

Protective functions by pathogen displacement, nutrient competition, receptor competition, and production of antibiotics

135
Q

What are some other functions that mutualistic/commensal bacteria have?

A

Induction of IgA

Apical tightening of tight juncitons

Immune system development

Synthesize vitamins such as biotin and folate**

136
Q

What role do antimicrobial peptides have in the mucosal flora? What other ways does our body interact with the mucosal flora?

A

They dictate the composition of the local gut flora (Note that commensal bacteria induce IgA and antimicrobial peptide secretion)

Dendritic cells constantly browse mucosal flora

Pattern recognition receptors detect commensal bacteria and prevent inflammation

137
Q

What is the complement system and what four things does it do?

A

The complement system is an immune surveillance system of plasma proteins that act in cascades to selectively kill extracellular pathogens and diseased tissue, promote inflammation, clear tissue damage, and regulate tissue homeostasis

138
Q

What are the three pathways of the complement system? Name them in the order in which they activate and describe how each is initiated.

A

Alternate - C3, properdin

Lectin - mannose - binding lectins

Classical - antibody/C1q complexes

139
Q

Where is most of the complement produced?

A

Liver

Note that 15% of plasma globulin protein is complement

140
Q

Name 7 components of the complement system

A

Initiators - initiate the complement pathways
Convertase activators - form convertases which labelantigens with C3b and C5b
Opsonins - coat pathogens to target them for phagocytosis
Anaphylotoxins - initiate and promote inflammation
Membrane attack complexes - form the MAC pore
Complement receptors - initiate signaling
Regulators - restrict or halt complement activity

141
Q

What are some differences between the a and b complement fragments? Which complement is the exception?

A

A: small, no enzyme activity, anaphylotoxin, signalling activity

B: large, enzyme activty, opsonin, signaling activity

C2 is the exception to this rule

142
Q

What initiates the alternative pathway?

A

Pathogen surface creates local environment conductive to complement activation

143
Q

What initiates the lectin pathway?

A

Mannose-binding lectin binds to pathogen surface

144
Q

How is the classical pathway activated?

A

C-reactive protein or antibody binds to specific antigen on pathogen surface

145
Q

____ initiates the classical pathway by binding to the ___ portion of ___. Attached to C1q are ___ and ___, which have a ___ activity, thus initiating the complement cascade

A

C1q

Conservative portion of antibodies

C1r and C1s

Proteolytic

146
Q

True or false… a single plasma cell can produce both IgG and IgM antibodies, as long as they have the same variable region. The first antibody that they typically produce is IgM

A

True

147
Q

True or false.. C1q only needs to bind to one IgM or IgG

A

False.. although it must only bind to one IgM molecule, it must bind to multiple IgG

148
Q

Once C1q binds to antibodies and recruits 2 C1r and 2 C1s, the complex is called ___. This complex cleaves ___ into ___ and ___

A

C1qr2s2

C4

C4a

C4b

149
Q

Once C4 is cleaved into C4a and C4b by c1qr2s2, ___ stays on the surface of the pathogen to recruit ___ which is cleaved by ____ to form ___ (___).

A

C4b

C2

C1qr2s2

C4b2a (C3 convertase)

Note that this complex is made up of C4b and C2a

150
Q

C4b2a will cleave ___ into ___ and ____. ____ remains attached to the complex to become ____ (____).

A

C3

C3a

C3b

C4b2a3b

Note that C3b opsonizes the pathogen too

151
Q

C4b2a3b (C5 convertase) cleaves ___ into ____ and ____. ___ functions to opsonizes the pathogen

A

C5

C5a
C5b

C5b

152
Q

Name the order of complexes of the classical pathway

A

C1qr2s2

C4b2a (C3 convertase)

C4b2a3b (C5 convertase)

153
Q

The lectin pathway is initiated by the binding of two different proteins, ___ and ____

A

Mannose binding lectins

Ficolins

154
Q

What are MASP-1 and MASP-2? They cleave ___

A

MBL(Mannose binding lectin) associated serine proteases

They cleave C4

155
Q

MASP-2 cleaves ___ into ___ and ____. ___ stays on the pathogen surface. Then, MASP-2 also cleaves ____ into ___ and ____. ____ binds to ____ forming ___ (____)

A

C4
C4a
C4b

C2
C2a
C2b

C2a binds to C4b forming C4b2a (C3 convertase)

156
Q

In the lectin pathway, C4b2a cleaves ___ into ___ and ___ which can bind to ____ or ____.

A

C3
C3a
C3b

C3b can bind to the microbial surface (opsonization) or the convertase itself to become a C5 convertase, coating the cell with C5b

157
Q

What three things can activate the alternative pathway?

A

Spontaneous C3 hydrolysis

Properdin-pathogen binding and C3 recruitment

Proteolytic C3 cleavage (thrombin and clotting cascade proteases)

158
Q

C3, while floating around the bond will spontaneously expose its ___ bond to allow attack by ___ to cleave C3 into ___ and ___

A

Thioester

Water

C3a

C3b

159
Q

Once C3 is spontaneously cleaved into C3a and C3b, C3b has two different fates. What are they?

A

It can turn into iC3b (inactive C3b) or it can label the surface of pathogen and self cells

160
Q

Once C3 is spontaneously cleaved, ____ can bind to iC3b. Then ___ can cleave ___ to form ____

A

Factor B

Factor D can cleave factor B to form iC3Bb

161
Q

IC3Bb functions as a ____ to ____

A

Soluble C3 convertase

Initiate the alternative pathway by cleaving C3 to C3a and C3b.. C3b will bind to cell membranes

162
Q

Describe the formation of the alternative C3 convertase (C3bBb) on a pathogen membrane

A

Factor B binds to C3b (already located on pathogen membrane). Then Factor D cleaves factor B to form the C3 convertase, C3bBb . C3bBb then continues to cleave C3, depositing more and more C3b on the membrane (opsonization)

163
Q

What does properdin do?

A

Stabilizes the C3 convertase C3bBb on a pathogen and recruits additional C3b

164
Q

C3bBb will recruit another C3b to form the ____

A

Alternative C5 convertase

C5 is cleaved by this to form C5a and C5b. When C5b accumulates on membrane, it forms pores

165
Q

The Ca’s are the ____. These function on the ____ and surrounding cells to cause ____

A

Anaphylotoxins

Vasculature

Permeability to allow extravesation of inflammatory cells. The Ca’s also induce the immune cells.

166
Q

How do C3a and C5a influence immune cells?

A

Anaphylotoxins interact with discrete receptors on innate immune cells to Cause chemotaxis, degranulation, and phagocytosis

167
Q

True or false.. in order for phagocytosis to occur, the phagocyte must have its CR1 receptor bound to C3b and its C5a receptor bound to C5a

A

True.

This is important so you dont destroy things you aren’t supposed to.

168
Q

How does complement work with blood borne pathogens?

A

Antibodies bind to pathogen. C3b binds to these antibodies. Erythrocytes bind to the complement. This whole structure is sent to a macrophage where phagocytosis occurs

169
Q

What are the three ways in which complement eliminates pathogens?

A

Anaphylotoxins recruit inflammatory cells

Opsonization of pathogen, targeting for phagocytosis

Formation of pores to lyse bacteria

170
Q

Describe the formation of membrane attack complexes

A

Once C5b is on pathogen, it will recruit C6, then C7, the C8.

This complex then recruits the last complement, C9 which forms the pore

171
Q

How can healthy self-cells block the formation of membrane attach complexes?

A

CD59 blocks C5b678 to prevent it from recruiting C9

172
Q

What are the roles of factor H, I, DAF, and MCP?

A

Leads to complement depletion

DAF-decay accelerating factor
MCP-membrane co-factor protein

173
Q

What is the significance of P. Gingivalis and complement?

A

It hijacks the complement system to create the anaphylotoxins to cause recurrent inflammation to use the inflammatory cells as a food source. Also to disregulate the toll-like receptor to tone down the direct killing of p. Gingivalis

174
Q

Molluscum contagiosum is caused by ____

A

The pox virus

175
Q

Describe the alternate C5 convertase

A

C3b2Bb. The C3bBb cleaves a C3 and the C3b remains attached

Host and Defense (17 decks)

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