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SPM (ARSH) > Weeks 9-12 > Flashcards

Weeks 9-12 Flashcards

1
Q

Transmission: Food and water contaminated with cysts

Site of Infection: Small Intestine

Clinical Presentation: Chronic diarrhea, abdominal pain, bloating,

Epidemology: Transmission: daycare center

A

Cryptosporidium parvum

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2
Q
  • What happens in a type I hypersensitivity reaction?
  • What are some common clinical characteristics?
  • What activates this response?
  • What effector cells respond?
  • What are examples of this reaction?
A
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3
Q

What gene is mutated in IPEX and what is the result of this mutation?

A

FoxP3 mutation → few to no Tregs produced → increased immune activity

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4
Q

Spectrum:

  • Gram(+): Staph (including MRSA)
  • Gram(-): E. coli

Clinical:

  • Pneumocystis jirovecii
  • UTIs
  • Staph Soft tissue infection
A

Trimethoprim/sulfamethoxazole

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5
Q

What is the structure of MHC Class I?

  • How many alpha and beta chains?
  • Expressed on what ells?
  • Binds peptides of what size?
A
  • MHC Class I
    • 3 alpha chains and 1 beta chain
    • Expressed on all somatic cells
    • Binds short peptides (8 to 11 AAs)
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6
Q

How does negative feedback of B-cells occur?

  • What cells facilitate this process?
  • What cytokines are released by this cell?
A
  • Negative feedback
    • T regulatory cells release cytokines that deactivate all lymphocytes
    • Cytokine released: IL-10 by T-cells activates ITIM, which blocks signal transduction
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7
Q

Superficial Mycoses

Characterisitics and Examples (4)

Only 1 for SPM exam, 4 total otherwise.

A
  • Characteristics
    • Involves outer keratinized layer and noninvasive
  • Tinea versicolor (caused by Malassezia fufur)
    • Causes hypo/hyper pigmentated lesions
    • Lipophilic and can infect intravenously through IVs
  • NOT REQUIRED FOR SPM EXAM
    • Tinea nigra – caused by Hortaea werneckii and causes lesions
    • Black piedra – caused by Piedraia hortae and causes dark nodules on hair shafts
    • White piedra – caused by Trichosporon genus and causes white growths around hair of groin
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8
Q

Disease: Whooping Cough (Pertussis)

Presentation, Etiology, Treatment?

A

Presentation: 1- to 3-week incubation; dry short coughs followed by inspiratory gasp or “whoop”; lymphocytosis

Etiology: Bordetella pertussis

Treatment: Macrolides (Azithromycin)

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9
Q

Chronic Granulomatous Disease

A

NADPH deficiency leads to macrophage ingesting microorganism without ability to eliminate it

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10
Q

Spectrum:

  • Gram(+): Broad coverage
  • Gram(-): Broad including Pseudomonas

Clinical:

  • Nosocomial aspiration pneumonia (caused by pseudomonas)
A

4th Generation (Cross BBB)

  • Cefeprime
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11
Q

Spectrum:

  • Gram(+): Anaerobes (C. diff)
  • Gram(-):Anaerobes
  • Other: Protozoa

Clinical:

A

Metronidazole

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12
Q

Wiskott-Aldrich Syndrome

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: mutation in WASP
  • Pathophysiology: decreased actin polymerization in cytoskeleton
  • Symptoms: skin bleeding
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13
Q

X-Linked Lymphoproliferative

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: mutation in SLAM, SAP, or XIAP
  • Pathophysiology: decreased NK and T cell activation
  • Diagnostic characteristics: inability Epstein-Barr virus (EBV)
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14
Q

Disease: Common Cold

Presentation, Etiology, Treatment?

A

Presentation: Coryza (runny nose)

Etiology: Rhinovirus or coronavirus

Treatment: Let run natural course

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15
Q

Gram: +

Bacilli

aerobic

A
  • Listeria
  • Bacillus
  • Corynebacterium
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16
Q

Explain the TH1/ TH2 balance

A
  • Th2 cytokines inhibit Th1 immune responses
    • Th1 cytokine promotes macrophages to kill microbials
    • Th2 cytokines inhibit microbial killing
  • Normally, Th1 > Th2
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17
Q

Transmission: Anopholes Mosquitoes

Site of Infection: Hepatocytes → RBCs → lysed RBCs → anemia

Clinical Presentation:

  • Malaria

Epidemology: Africa, South Asia, Tropical Regions

A

Plasmodium

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18
Q

How does ipilmumab work?

A

Anti-CTLA-4 (ipilmumab) blocks downregulation of activated T cells

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19
Q

DNA Virus

Capsid Structure?

Naked or Enveloped?

(NAME EXCEPTIONS TOO)

A
  • DNA Viruses
    • Capsid: icosahedral
      • Exceptions: Pox
    • Envelope: none
      • Exceptions: Hepatitis B., Herpes viruses, and Pox
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20
Q

Gram: -

Baccili

aerobe

Lactase: -

A

P’s and S’s
(PSPSPSPS)
-Psuedoonas
-Proteus
-Providencia
-Salmonella
-Shigella
-Serratia

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21
Q

What happens in a type IVb hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

A
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22
Q
  • Family: Echinocandins
  • Target: Cell wall
  • MOA:
    • Inhibits synthesis of 1,3-beta-D glucan
  • Use:
    • Candida and Aspergillus
  • Clinical:
    • Tx: esophagitis, candidemia

Last line of defense against Aspergillus

A

Caspofungin (IV)

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23
Q

Describe epidemiology of and clinical syndromes from…

Aspergillus - most commonly Aspergillus fumigatus (or Aspergillus-like: Pseudallescheria boydii, Fusarium, Penicllium)

  • mold or yeast or dimorphic?
  • 3 total syndromes?
A
  • Invasive Molds
    • Septated hyphae with 45 degree branching
    • Neutropenia is biggest risk
    • Clinical Syndromes
      • Allergic bronchopulmonary aspergillosis (ABPA) – colonization of airways leads to asthmatic symptoms
        • Responds to steroids
      • Invasive aspergillosis (IA) – prolonged neutropenia and causes infarcts
        • Responds to antifungals
      • Aspergilloma (or fungus ball) – in pre-existing lung cavity
        • Responds to surgery
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24
Q

Spectrum:

  • Gram(+): none
  • Gram(-): none
  • Other: Mycobacteria

Clinical:

  • TB
  • In combo w/ other drugs b/c of development of rapid resistance
  • Accelerates P450 Enzymatic activity of other drugs
A

Rifampin

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25
Q

What bacteria are associated with the following infection?

  • Abdominal Infections (two classes of bacteria)
A
  • Abdominal Infections
    • GNRs AND anaerobes
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26
Q

Hyper-IgE Syndromes (HIES)

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: dominant negative mutation in STAT3 or recessive mutation in DOCK8
  • Symptoms: eczema, eosinophilia, two rows of teeth
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27
Q

Avidity versus Affinity

A
  • Avidity – the strength of all of the antigen binding sites combined
    • Monomers (IgG) have two binding sites while pentamers (IgM) have ten binding sites
  • Affinity – the strength of one antigen binding site
  • Antibodies with low affinity binding sites can have an overall high avidity, depending on the number of these binding sites
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28
Q

What is the best test for assessing a classical complement deficiency?

  • What will the level of this test be if a complement protein is absent?
A
  • CH50 Test
    • If a complement component is absent, the CH50 level will be zero; if one or more components of the classical pathway are decreased, the CH50 will be decreased because lysis in the assay will not occur
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29
Q

Transmission: Food and water contaminated with cysts

Site of Infection: Small Intestine

Clinical Presentation: Chronic diarrhea, abdominal pain, bloating,

Epidemology: Uncommon in USA

A

Cyclospora cayetanensis

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30
Q

What are the 4 modes of genetic exchange and define each one?

A
  • Modes of genetic exchange: can cause antibiotic resistance
    • Transformation – released DNA taken up directly by neighboring cells, integrated by recombination
    • Transduction – phages carry DNA to a new cell, either the bacteriophage or pieces of bacterial chromosome
    • Conjugation – plasmid or chromosomal DNA is transferred to new cell via sex pilus
    • Transposition – gene clusters hop between chromosome, bacteriophage, and plasmid DNAs
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31
Q

Describe epidemiology of and clinical syndromes from…

Mucormycosis – most commonly caused by Mucor (or Zygomyces)

  • mold or yeast or dimorphic?
A
  • Invasive Molds
    • Risk factors: DKA, steroids, neutropenia, iron overload
    • Diagnosis: non-septated hyphae with 90 degree branching
    • Clinical Syndromes
      • Rhinocerebral: black necrotic eschars in nasal passage
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32
Q

Describe the events that occur when T cells are activated.

A
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33
Q

Spectrum:

  • Gram(+): MSSA, beta strep, Strep pneumoniae
  • Gram(-): E. coli

Clinical:

  • Uncomplicated Cellulitis
  • Surgery prophylaxis (heart)
A

1st Generation

  • Cefazolin
  • Cephalexin
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34
Q

Gram: +

Cocci

aerobic

catalase: -
hemolysis: gamma

A

enterococcus

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35
Q
  • Family: DNA Viruses
  • Target: CMV
  • MOA:
    • Triphosphate that inhibits viral DNA synthesis
  • Clinical:
    • IV for therapeutics
    • PO for prophylaxis
    • CMV retinitis
    • Very toxic (bone marrow)
A

Ganciclovir (IV) /Valganciclovir (po)

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36
Q
  • What is a type A drug reaction?
  • Is it predictable?
  • What is it dependent on?
  • How common are these?
A
  • Most adverse reactions
  • Predictable – related to the pharmacological action of drug
  • Dose dependent
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37
Q
  • Family: RNA Viruses
  • Target: Influenza A & B
  • MOA: Neuraminidase Inhibitor – prevents cleavage of HA and sialic acid à blocking release of virus
  • Clinical:
    • Zanamivir – powder (contraindicated in asthma pts)
    • Oseltamivir – oral
A

Zanamivir/Oseltamivir(Tamiflu)

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38
Q
  • What three classes inhibit initiation in protein synthesis?
A
  • Tetracyclines
  • Aminoglycosides
  • Linezolid
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39
Q

Spectrum:

  • Gram(+): MSSA
  • Gram(-): H. flu, legionella, moraxella, chlamydia

Clinical:

  • Community acquired Resp. tract infection (atypical pneumonia)
  • Chlamydia
A

Azithromycin (Z-pack)

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40
Q

X-Linked Hyper-IgM Syndrome

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: mutations in CD40L (CD154) gene
  • Pathophysiology: defect in class-switching; low levels of all Igs except IgM
  • Symptoms: severe and frequent infections
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41
Q

What bacteria are associated with the following infection?

  • Non-purulent cellulitis (just erythematous)
  • Purulent cellulitis (skin abscesses)
A
  • Cellulitis
    • Non-purulent cellulitis (just erythematous)
      • Most likely Strep pyogenes
    • Purulent cellulitis (skin abscesses)
      • Either Staph aureus or Strep pyogenes
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42
Q

Spectrum:

  • Gram(+):MSSA, beta strep, Strep pneumoniae
  • Gram(-): Neisseria meningitidis
  • Other: Borrelia burgforferi (Lyme)

Clinical:

  • Meningitis
  • Lyme Disease
A

3rd Generation (Cross BBB)

  • Ceftriaxone
  • Cefotaxime
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43
Q
  • Family: DNA Viruses
  • Target: Resistant CMV, HSV, VZV
  • MOA:
    • Pyrophosphate analog that inhibits viral DNA synthesis
  • Clinical:
    • CMV retinitis
    • Very toxic (kidney)
A

Foscarnet (IV)

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44
Q

What are the three phases of Signal 1?

A
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45
Q
  • How can bacteria resist vancomycin?
A
  • Caused by a change in the peptide component from ala-ala to ala-lactate, which doesn’t allow the drug to bind
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46
Q

Which antibiotics are bactericidal? There are six main types.

A
  • penicilins
  • cephalosporins
  • vancomycin
  • quinilones
  • metronidazole
  • aminoglycosides
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47
Q

What is the structure of MHC Class II?

  • How many alpha and beta chains?
  • Expressed on what ells?
  • Binds peptides of what size?
A
  • 2 alpha chains and 2 beta chains
  • Expressed only on professional APCs (dendritic, B, and macrophage)
  • Binds long peptides (11 to 30 AAs)
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48
Q

What causes Type III Bare Lymphocyte Syndrome?

A
  • Type III – loss of both I and II
    • Similar to type II
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49
Q

Transmission: Ingestion of undercooked crustaceans

Site of Infection: Migratory from GI to lungs

Clinical Presentation:

  • Egg in sputum sample
  • Acute infection
  • Mimics TB
A

Lung Flukes

  • paragohomus westermari
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50
Q

Describe epidemiology of and clinical syndromes from…

Blastomycosis

  • yeast or mold or dimorphic?
A
  • Endemic Mycoses - DIMORPHIC
    • Epidemiology: Ohio and Mississippi River valleys
    • Transmission: mold grows in soil → grows as yeast in human
      • Patients not contagious in yeast form
    • Symptoms: infects lungs/cutaneous lesions
    • Diagnosis: histology showing broad-based budding during division
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51
Q

Spectrum:

  • Gram(+): staph, strep (MSSA)
  • Gram(-): none

Clinical:

  • Uncomplicated Cellulitis
A

Penicillinase – resistant penicillin (methicillin):

  • Nafcillin
  • Dicloxacillin
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52
Q
  • What is a live, attenuated vaccine?
  • Do they require a booster?
  • What are some examples of this?
A
  • Infectious agents have reduced virulence due to mutations or genetic engineering
  • Give strongest response and longest protection
  • Examples: MMR, chickenpox
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53
Q
  • What is the mechanism of action of fluoroquinolones?
A
  • Inhibits topoisomerase activity of prokaryotes
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54
Q

What happens in a type IVa hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

A
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55
Q

What is Signal 2?

A
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56
Q

Th1 synthesis?

What does it release?

A
  • Synthesis/Differentiation: via IL12/IFN-gamma → activate T-bet
  • Releases cytokine: IFN-gamma
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57
Q

What is the antigen receptor-mediated signal transduction in B lymphocytes?

  • What transcription factors are activated?
A
  • Signal transduction activated via phosphorylation of Ig-alpha and Ig-beta – co-stimulatory motifs
  • Phorsphorylation cascade leads to activation of transcription factors: Myc, NFAT, NF-(kappa)B, and AP-1
  • B-cells can also be activated via toll-like receptors (TLRs) or the complement pathway
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58
Q

Transmission: Undercooked fish

Site of Infection: Small intestines

Clinical Presentation:

  • Prolonged infection → B12 deficiency (megoblastic anemia)
A

Diphyllobatrium latum

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59
Q

What bacteria are associated with the following infection?

  • Hospital-Acquired Pneumonia (HAP) - 2 types
A
  • Hospital-Acquired Pneumonia (HAP)
    • GNRs (Pseudomonas), Staph aureus
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60
Q

Cutaneous Mycoses

Characterisitics and Examples (5)

A
  • Characteristics
    • Involves keratinized layer → inflammation of epidermis and upper dermis
    • Referred to as tinea and named by location on body (not an organism!)
  • Caused by molds called Dermatophytes
    • Itchy, flakey, red lesions
    • Referred to as ringworm
  • tinea pedis – foot (athlete’s foot)
    • Provides portal of entry for Group A Beta Strep (cellulitis)
  • tinea cruris – groin (jock itch)
  • tinea corporis – general body (classic Ringworm)
  • tinua capitis – scalp
  • tinea unguium – nails (called onychomycosis)
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61
Q

Describe epidemiology of and clinical syndromes from (3 total syndromes)

Candida (i.e. C. albicans, C. glabrata, C. krusei)

  • Yeast or mold or dimorphic?
A
  • (YEAST)
    • Part of normal flora
    • Pathogenicity occurs endogenously
    • Syndromes
      • Mucosal: thrush – cottage cheese-like coating of mouth
      • Cutaneous: intertrigo – red rash in between skin folds
      • Candidemia: retinitis – fungus in bloodstream seeds in retina (via IV)
      • IMPORTANT: positive respiratory samples never indicate pneumonia
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62
Q

Describe epidemiology of and clinical syndromes from…

Pneumocystis (fungi but treated as a protozoan)

A

Lacks ergosterol and does not respond to anti-fungals

Strictly opportunistic pathogen seen predominately in AIDS

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63
Q

Non-invasive Molds

A

Dermatophytes (see above)

Trichophyton, Microsporum

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64
Q

Describe epidemiology of and clinical syndromes from…

Cryptococcus (i.e. C. neoformans)

  • yeast or mold or dimorphic?
A
  • (YEAST)
    • Prominent capsule that is identified with India Ink
    • Strictly opportunistic pathogen seen predominately in AIDS
    • Bird feces → lungs → brain
    • Syndromes
      • Cryptococcal Meningitis
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65
Q

Gram: -

Baccili

anaerobe

A

B. fragilis

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66
Q

Explain how the TH1/ TH2 balance contributes to different outcomes of a Mycobacterium leprae infection.

A
  • Mycobacterium leprae → Leprosy
    • Th2 > Th1 → unable to eradicate infection → lepromatous leprosy (destructive lesions)

Th1 > Th2 → activation of T cells and macrophages → tuberculoid leprosy (less destruction form)

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67
Q

Transmission: Sexual Intercourse

Site of Infection: Vagina, urethra

Clinical Presentation: Usually Asymptomatic, Dysuria from urethritis

Epidemology: Worldwide

A

Trichomonas vaginalis

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68
Q

Disease: CAP

Presentation, Etiology, Treatment?

A

Presentation: Fever; cough; sputum; X-ray consolidation

Etiology:

  • Normal anaerobes from aspiration
  • Typical: Strep pneumoniae
  • Atypical: Mycoplasma pneumoniae, Legionella pneumophila, Chlamydophila pneumoniae

Treatment: Sputum sent for Gram stain and culture

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69
Q

Spectrum:

  • Gram(+): cocci
  • Gram(-): none

Clinical:

  • Reserved for VRE & MRSA
A

Linezolid

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70
Q
  • Family: misc.
  • Target: n/a
  • MOA:
    • interferes with nucleic acid synthesis
  • Use:
    • Candida, Cryptococcal,
  • Clinical:
    • In meningitis: used with amphotericin initially → fluconazole
    • Toxic to bone marrow
A

Flucytosine (PO)

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71
Q

What happens in a type II hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

A
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72
Q
  • Family: Azole
  • Target: Cell membrane
  • MOA:
    • inhibits ergosterol synthesis
  • Use:
    • Aspergillus & Mucormycosis
  • Clinical:
    • New drug: expanding role
A

Isavuconazole

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73
Q

What are the 3 immune mechanisms involved in the response to cancer?

A
  • CD8+ T cell-mediated killing of tumor cells
    • Tumor presents MHC I + peptide
    • Binding stimulates secretion of IFN-gamma (to block tumor proliferation) and perforin/granzymes (apoptosis)
  • CD4+ T-cell mediated control of tumor cells
    • Macrophage presents MHC II + peptide
    • Binding activates macrophage and releases IFN-gamma
  • NK cell-mediated killing of tumor cells
    • Loss of inhibitory receptor triggers tumor-killing
    • Antibody-mediated response to tumor cells
      • AB binds tumor proteins → apoptosis
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74
Q

Virus-Cell Interactions (5 TYPES)

A
  • Lytic infection – virus production with cell death
  • Abortive infection – infection of non-permissive cells with no infectious virus production
  • Persistent infection – long-term virus-cell association with cell survival
    • Chronic: virus replicates
    • Latent: no replication but some viral gene expression
  • Recurrent infection: has latent and lytic periods
  • Transformation: oncogenic conversion caused directly by viral gene activities
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75
Q

What is passive therapy underlying immunotherapeutic strategies for cancer?

A
  • Passive therapy – temporary effect (you stop treatment, you stop response)
    • Antibody mediated
      • Antibodies which lead directly to cell death (trastuzumab)
      • Engineered antibodies
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76
Q

X-Linked Gamma Agammaglobulinemia

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: mutations in Bruton Tyrosine Kinase
  • Pathophysiology: failure of B cell maturation past pre-B
  • Diagnostic characteristic: no germinal centers in lymph nodes
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77
Q
  • Family: Polyenes
  • Target: Cell membrane
  • MOA:
    • Lipophilic molecule that binds to ergosterol
  • Use:
    • Candida, Cryptococcal,
    • Mucormycosis (drug of choice)
    • EXCEPT: Pseudallescheria
  • Clinical:
    • Tx: Meningitis, Neutropenia
    • HIGH nephrotoxicity
    • Less toxic versions available (Lipid versions)
A

Amphotercin (IV)

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78
Q

What happens in AERD?

A

Aspirin Exacerbated Respiratory Disease (AERD)

  • If you take aspirin, you get COX blocks → inhibition of PGE2 → increased release of LTs from mast cells → increased inflammatory response
  • Diagnostic characteristics: acute dyspnea, nasal polyps and nasal inflammation
  • Treatment: aspirin desensitization and “–lukast” drugs (leukotriene modifiers)
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79
Q

Chronic Granulomatous Disease

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

Diagnosis

A
  • Etiology: mutations in phagocyte oxidase (NADPH Burst)
  • Pathophysiology: inability to kill phagocytosed microbes
  • Symptoms: recurrent infections
  • Diagnosis: NBT Tests (histological view of macrophage activity)
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80
Q

Spectrum:

  • Gram(+): none
  • Gram(-): broad including multi-drug resistance bacteria (Pseudomonas & Klebsiella)

Clinical:

  • LAST RESORT DRUG
  • Hearing loss & vertigo
A

Aminoglycosides

  • Gentamicin
  • Tobramycin
  • Amikacin
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81
Q

Can you mix 2 or 3 antifungals?

A

Mix 2 or 3 of these Antifungals → Extra toxicity and possible antagonism of MOAs

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82
Q

Gram: +

Cocci

aerobic

catalase: +
coagulase: +

A

S. aureus

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83
Q

Gram: -

Cocci

aerobic

(5)

A
  • Neisseria gonorrhoeae (diplocooci)
  • Neisseria meningitidis (diplococci)
  • Haemophilus influenzae
  • Bordetella pertussis

-Moraxella catarrhalis

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84
Q

What bacteria are associated with the following infection?

  • Community Acquired Pneumonia (CAP)
    • generalized pneumonia (1 type)
    • atypical pneumonia (3 types)
    • post-influenza pneumonia (1 type)
A
  • Community Acquired Pneumonia (CAP)
    • Strep pneumoniae
    • “Atypical” pneumonias
      • Mycoplasma pneumoniae
      • Legionella pneumophila
      • Chlamydophila pneumoniae
    • Staph aureus (post-influenza)
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85
Q

Leukocyte Adhesion Defects (LAD) (3 types)

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Overall pathophysiology: failure to recruit leukocytes to sites of infection
  • Symptoms: leukocytosis and recurrent infections early in life
  • Types
    • Type I
      • Etiology: mutation in CD18 gene → defect in integrin
      • Diagnostic characteristics: delayed umbilical cord separation
    • Type II
      • Etiology: abnormality in fucosylation (glycosylation of sialyl Lewis X) → defect in sialyl Lewis X → required for leukocyte-endothelium binding
      • Diagnostic characteristics: severe mental/growth retardation
    • Type III
      • Etiology: mutation in KINDLIN-3 gene → defective platelet aggregation
      • Diagnostic characteristic: excessive bleeding
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86
Q

What is the alternate pathway and how is it initiated?

A
  • Alternative pathway
    • Initiated via C3 convertase formation in addition to Factor B and D binding
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87
Q

Transmission: Insect bite, Swallowing crustaceans

Site of Infection: Blood and Tissue

Clinical Presentation:

  • Incubated for one year, then NVD
  • Blister formation
A

Dracunculiasis

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88
Q

Late defects in the complement pathway predispose to:

A
  • Predisposition to Neisseria
    • Types of Neisseria
      • Meningococcal Meningitis
    • Defects in Complement Pathway
      • C5b, C6, C7, C8, C9 (any component in MAC)
    • Patients with these defects often have reoccurrences because they are unable to use complement pathways to lyse bacteria
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89
Q

Cold sores/blisters on the genitals or mouth

A

Herpes Simplex virus

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90
Q

Gram: +

Bacilli

anaerobe

A

Clostridium difficile/perfringens

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91
Q

What is the Granule Mech?

A
  • Granule contain Granzyme B and Perforin
    • Perforin – perforates transmembrane on target cell
    • Granzyme B – cleaves and activates caspases → triggers apoptosis → degrades viral DNA via apoptotic nucleases
92
Q

Transmission: Ingestion via anthropods

Site of Infection: GI

Clinical Presentation:

  • Nonspecific
  • Nasuea, weakness, abdominal pain, loss of appetite
A

Hymenolepis nana

93
Q

Gram: +

Cocci

aerobic

catalase: -
hemolysis: alpha

A

Strep peneumonia

94
Q

Effector CD4+ T cell: Helper T cell (2) functions

A
  • Cell mediated immunity
    • CD40:CD40L binding → macrophage activation → kill phagocytosed microbes
  • Humoral immunity
    • CD40:CD40L binding → antibody hypermutation and class switching
95
Q

Describe mechanisms used by CD8+ T cells to kill infected cells.

A
  • After antigen-binding to effector cytotoxic T cells, prepackaged cytolytic granules are released towards target cell
    • Granules are not cell specific, close junction between target cell and T cell reduce effects on endogenous non-harmful molecules
96
Q

Transmission: Flies

Site of Infection: Skin

Clinical Presentation:

  • swelling of skin
A

Filaria: Loiasis (Loa loa)

97
Q

Th17 synthesis?

What does it release?

A
  • Synthesis/Differentiation: via IL6/IL23/TGF-beta → activate ROR-gamma-t
  • Release cytokines: IL17,22
98
Q

Gram: +

Cocci

aerobic

catalase: +
coagulase: -

A

S. epidermidis

99
Q

Function of IL4?

A
  • Stimulates production of IgE
    • IgE → mast cells → histamines → allergic reaction
    • Stimulate B cells → production of antibodies (IgE) against helminth worms
100
Q

Spectrum:

  • Gram(+):Broad including MRSA and VRE
  • Gram(-): none

Clinical:

  • VRE
A

Daptomycin

101
Q

Transmission: penetration of skin

Site of Infection: Migratory

  • In small intestine

Clinical Presentation:

  • Pruritic rash at site of penetration
  • Pulmonary sx
  • Autoinfection
A

Strongyloides

102
Q

RNA Virus

Capsid Structure?

Naked or Enveloped?

(NAME EXCEPTIONS TOO)

A
  • Capsid: icosahedral or helical
  • Envelope
    • Icosahedral: all naked
      • Exceptions: Togaviruses and Flaviviruses
    • Helical: all enveloped
      • Exceptions: none
  • Retroviruses have complex capsid and are enveloped
103
Q

Transmission: Sand flies

Site of Infection: Visceral and cutaneous tissues

Clinical Presentation:

  • Visceral/cutaneous disease of Kala-azar
  • Skin ulcers

Epidemology: Worldwide except for Australia/Antartica

A

Leishmania

104
Q

Describe the differences between a B cell receptor and a T cell receptor.

A
  • BCRs have antibodies that can be membrane bound or secreted while TCRs are membrane bound
  • BCRs recognize both linear epitopes and conformational epitopes
  • BCRs bind free antigens while TCRs bind peptides associated with MHC
  • BCRs facilitate signal transduction with Ig-alpha and Ig-beta proteins while TCRs use CD3s and Zeta proteins
  • TCRs don’t undergo class switching or affinity maturation (somatic hypermutations)
105
Q

Describe epidemiology of and clinical syndromes from…

Histoplasmosis

  • Mold or yeast or dimorphic
A
  • Endemic Mycoses - DIMORPHIC
    • Epidemiology: Ohio and Mississippi River valleys
    • Transmission: mold grows in soil → infects macrophages → grows as yeast in human
      • Patients not contagious in yeast form
    • Symptoms: infects lungs
    • Diagnosis: histology showing macrophages with many small intracellular yeast
106
Q

Define biofilm and Quorum sensing.

A
  • Biofilm – multi-species population enmeshed in a matrix of protein and polysaccharide
    • Growth on teeth (dental plaque) and steel
  • Quorum sensing – bacteria sense each other’s presence to regulate group behaviors needed for biofilm formation and/or coordinated production of virulence factors
107
Q

Transmission: Food and water contaminated with cysts

Site of Infection: Small Intestine

Clinical Presentation: Chronic diarrhea, abdominal pain, bloating, foul smelling stool

Epidemology: Most common parasitic illness in USA, Transmission: person-person, daycare centers

A

Giardia lamblia,

  • duodenalis
  • intesitnalis
108
Q

Transmission: Tsetse flies

Site of Infection: Extracellular

Clinical Presentation:

  • Lymphadenopathy (Winterbottom’s sign)
  • Encephalopathy/ coma
  • Chancre: shallow ulcer
  • Sleeping sickness

Epidemology: Africa, Antigenic Variation of parasite

A

Trypanosomiasis brucei (African)

109
Q

What is the classical pathway initiated by?

A
  • Classical pathway
    • Initiated via antigen-antibody binding
    • C1 binds to antibody at the Fc region
110
Q

What are three mechanisms of evasion of humoral immunity by microbes?

A
  • Antigenic variation – mutation of antigen-specific sites or variants of surface proteins
  • Inhibition of complement pathway – complement-binding proteins expressed by bacteria
  • Cell-surface structure for blocking – structures that prevent antibodies from binding (i.e. hyaluronic acid capsules)
111
Q

Severe Combined Immunodeficiencies (SCID)

(4 Types)

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Pathophysiology: impaired T cell development with or without impaired B cell or NK cell development
  • Symptoms:
    • Infections by live attenuated vaccines (chicken pox, MMR)
    • Skin rash via maternal graft (graft-versus-host reaction)
  • Diagnosis: TREC Assay (absence of TREC = absence of T cells = SCID)
  • Types
    • DiGeorge Syndrome
      • Etiology: 22q11 deletion
      • Diagnostic characteristics: defective parathyroid glands/thymus and facial deformities
    • ADA Deficiency (adenosine deaminase)
      • Etiology: mutation in adenosine deaminase (purine salvage pathway)
      • Diagnostic characteristics: reduction of lymphocyte numbers
    • X-linked SCID
      • Etiology: mutations in interleukins
    • Absence of V(D)J Recombination
      • Etiology: mutations in NHEJ pathway → lack of specificity for epitopes
112
Q

HIV

Etiology

Pathophysiology

Symptoms

A
  • Etiology: virus that interacts with chemokine receptors of CD4+ T Cells
  • Pathophysiology: reduction of CD4+ T cell counts
    • Acute Phase: momentary spike in viral load and reduction of CD4+ cells
    • Chronic Phase: clinical latency and asymptomatic
    • AIDs: CD4+ cells less than 200 cells/mm3
  • Symptoms: tumors and opportunistic infections
113
Q

Defects in TLR Pathways

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • TLR3 mutations →→ herpes simplex encephalitis
  • NEMO (NF-kB Essential Modulator) → ectoderm defects → lack of sweating
114
Q

What is adoptive therapy underlying immunotherapeutic strategies for cancer?

How does this solve issues with patients who do not have tumor reactive cells?

A
  • Adoptive therapy – transfer of autologous (self) or allogenic (donor) immune cells (can be durable) with anti-tumor activity
115
Q

Disease: Pharyngitis / Tonsillitis / Laryngitis

Presentation, Etiology, Treatment?

A

Presentation: Inflammation of pharynx, tonsils, larynx

Etiology: Viral, usually part of common cold or flu

Treatment: Make sure it’s not bacterial

116
Q

Spectrum:

  • Gram(+): strep, staph
  • Gram(-): Excellent!

Clinical:

  • Only oral drug for pseudomonas
  • High Risk Pneumonia
  • Complex UTI
  • Too strong for most Gram (+)’s
A

Levofloxacin

117
Q

Function of IFN-gamma? (2)

A
  • Activates macrophages → microbial killing via ROS
    • CD40L needed for activation of macrophage
      • CD40L not always present on Thl surface. It is upregulated when Th1 binds to MHC II complex.
  • Activates B cell proliferation / Antibody production
    • Upregulation of complement binding and opsonizination (when antigens bind IgG triggering phagocytosis)
118
Q
  • What are potential adverse effects of aminoglycosides?
A
  • Ototoxicity (vertigo or hearing loss)
  • Nephrotoxicity
119
Q
  • Family: Azole
  • Target: Cell membrane
  • MOA:
    • inhibits ergosterol synthesis
  • Use:
    • Mucormycosis (not used clinically)
  • Clinical:
    • Prophylaxis
A

Posaconazole

120
Q

Disease: Sinusitis / Otitis Media / Mastoiditis

Presentation, Etiology, Treatment?

A

Presentation: Inflammation of ear drum, sinuses

Etiology: Assumed to be bacterial: Strep pneumonia, H. flu, or Moraxella catarrhalis

Treatment: Amoxicillin

121
Q

What are cephalosporin toxicities?

A

Type I hypersensitivity reaction including rash or anaphylaxis

122
Q

Disease: Post-influenza Pneumonia

Presentation, Etiology, Treatment?

A

Presentation: Fever; cough; sputum; X-ray consolidation

Etiology: Staph aureus

Treatment: Sputum sent for Gram stain and culture

123
Q

Mechanism of Extraversion

Difference between Naive and effector?

A
  1. Selectin (T cell) to Selectin ligand (endothelium) binding → weak adhesion between T cell and endothelium
  2. Integrin (T cell) to Integrin ligand (endothelium) binding → stabilizes adhesion between T cell and endothelium
    1. LFA-1 (naïve T cell) to ICAM (endothelium)
    2. VLA-4/ LFA-1 (effector T cell) to VCAM/ ICAM (endothelium)
  3. Chemokine Receptor to chemokine binding → activation of integrin and chemotaxis towards lymph cortex or site of infection
    1. CCR7 (naïve T cell) to CCL19/21 (endothelium)
    2. CXCR3 (effector T cell) to CXCL10 (endothelium)
124
Q

What are natural killer cells?

MOA?

What do they release?

A
  • Normal Cell: has activating receptor and inhibitory (self-MHC I receptor) → NK Cell binds but not activated → no cell killing
  • Virus-Infected Cell: only has activating receptor and absence of inhibitory receptor (self-MHC I)→ NK Cell activated → cytotoxic granules induce apoptosis
  • Produce IFN-gamma (interferon gamma) to induce macrophage killing
    • Macrophages release IL-12, IL-15 → recruits NK cells to area
125
Q

What is the role of these complement pathway proteins?

  • C3b
  • C5b6789
  • C5a
  • C3a, C4a, C5a
A
  • C3b activates macrophages for phagocytosis and opsonization (ROS – NADPH Burst)
  • Membrane attack complex (C5b6789) triggers cell lysis by puncturing plasma membrane
  • C5a is a chemokine that attracts macrophages and neutrophils to site of infection (follows gradient)
  • C3a, C4a, C5a activates basophils and mast cells to release histamine and serotonin → inflammatory response
126
Q

Transmission:

  • Foodborne (poorly cooked meat)
  • Handling of cat feces
  • Congenital Transmission
  • Organ Transplantation

Site of Infection: Tissue cysts in any tissue

Clinical Presentation:

  • Asymptomatic/limited flu sx in healthy people
  • Retinochoroiditis

Epidemology: HIV patients can have reactivation

A

Toxoplasma gondii

127
Q

Disease: Epiglottitis (Supraglottitis)

Presentation, Etiology, Treatment?

A

Presentation: In children: cellulitis of supraglottic region (vocal cords); fever; sore throat; drooling

Etiology: Haemophilus influenzae type b

Treatment: Beta-lactamase resistant antibiotic (Cefatriaxone)

128
Q
  • What two classes inhibit elongation in protein synthesis?
A
  • Macrolides (azithromycin, clarithromycin)
  • Clindamycin
129
Q

What is Immunodominance?

A

Immunodominance – most expanded T cells clones recognizes only a few peptides of a given microbe

130
Q

Transmission: Food and water contaminated with cysts

Site of Infection: Colon, Metastatic Liver infection

Clinical Presentation: Amebic dysentery: fever, abdominal pain, cramps, bloody stools (RBCs engulfed)

Epidemology: N/A

A

Entamoeba histolytica

131
Q

Which antibiotics are bacteriostatic? There are three main types.

A
  • tetracyclines
  • macrolides
  • clindamycin
132
Q

What are the general steps of virus life cycle?

A
  • Virus Attachment Protein (VAP) binds to non-suspecting receptor on host PM
    • Capsomere on naked virus
    • Glycoprotein spike on envelope virus
  • Virus penetration: release of nucleocapsid is dependent on pH changes → conformational change
    • Endocytosis
    • Fusion
  • Uncoating of genome: release of genome from capsid
  • Cellular Sites of Replication
133
Q

Spectrum:

  • Gram(+):Broad including MRSA, Enterococcus
  • Gram(-): none

Clinical:

  • MRSA
A

Vancomycin

134
Q

Transmission: Solium: Undercooked pork/beef

Site of Infection: Migratory tissue cysts from small intestines to bloodstream

Clinical Presentation:

  • Cysticercosis (formation of cysts)
135
Q

Transmission: Undercooked fish/watercrests (water plants)

Site of Infection: Small intestine → biliary system

Clinical Presentation:

  • GI problems
  • Biliary obstruction
  • RUQ pain
A

Liver Flukes

  • Clonorchis
  • Fasciola
136
Q

Function of IL22?

A

Act on tissues cells → increased barrier function/wound healing

137
Q

Disease: Laryngotracheobronchitis (Croup)

Presentation, Etiology, Treatment?

A

Presentation: In children: inflammation of subglottic region (below vocal cords); barking cough; stridor; hoarseness

Etiology: Parainfluenza virus

Treatment: n/a

138
Q

What is the end result of signal transduction?

A

End result of T cell signal transduction is the activation of transcription receptors including NFAT and NF-kB and activates mTOR protein à increases protein synthesis

139
Q

Disease: HAP

Presentation, Etiology, Treatment?

A

Presentation: Fever; cough; sputum; X-ray consolidation

Etiology: Pseudomonas (nosocomial)

Treatment: Sputum sent for Gram stain and culture

140
Q

What is paroxysmal nocturnal hemoglobinuria?

A
  • complement-mediated intravascular RBC lysis
  • patients may report red or pink urine (from hemoglobinuria)
  • Treatment: eculizumab (terminal complement

inhibitor)

141
Q

Spectrum:

  • Gram(+): Broad coverage
  • Gram(-): Broad including Pseudomonas

Clinical:

  • Good for people w/ penicillin allergy
142
Q

Gram: indeterminate

Baccili

aerobe

Acid Fast: +

A

Mycobacterium tuberculosis

(bacillus)

143
Q

Ataxia-Telangiectasia

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: defect in ATM (DNA repair protein)
  • Symptoms: abnormal gait and neurological deficits
144
Q

What genes have mutations in Autoimmune Lymphoproliferative Syndrome?

A

Mutations in genes associated with apoptosis (caspases, Fas)

145
Q

NAME EACH TYPE

146
Q
  • What are conjugate vaccines?
  • Do they require a booster?
  • What are some examples?
A
  • Vaccine against encapsulated bacteria – conjugates polysaccharide + protein carrier (protein carrier is needed to act as peptide in MHC complex because when bacteria is broken down, this protein subunit can be used as peptide)
  • Safe because it lacks infectious agent
  • Examples: Neisseria meningitidis, H. flu, and streptococcus pneumoniae
147
Q

Disease: Tracheobronchitis / Bronchitis

Presentation, Etiology, Treatment?

A

Presentation: Cough

Etiology: Virus

Treatment: Make sure it’s not pneumonia

148
Q

Transmission: Ingestion of water plants

Site of Infection: Intestines

Clinical Presentation:

  • Asymptomatic
  • Can lead to infection
A

Intestinal Flukes

  • Fasciolopsis buski
149
Q
  • Family: Azole
  • Target: Cell membrane
  • MOA:
    • inhibits ergosterol synthesis
  • Use:
    • Sporotrichosis
    • Histo & Blasto
  • Clinical:
    • Pulse therapy for onychomycosis
A

Intraconazole

150
Q

A depressed alternative pathway predisposes to:

A
  • Sepsis
    • Defects in C3 ALSO predispose to sepsis
151
Q

Function of IL13?

A
  • In intestines: stimulates mucus secretion and peristalsis → inhibits worm entry and promotes worm expulsion
  • Activates alternative macrophages (M2 macrophages) → tissue repair

**** Works with IL4

152
Q

Transmission: ingestion

Site of Infection: non-Migratory

  • colon/cecum

Clinical Presentation:

  • Painful passage of stool (blood, mucus)
  • Rectal prolapse
A

Trichuris (whipform)

153
Q

Chediack-Higashi Syndrome

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Etiology: mutation in LYST gene
  • Pathophysiology: defective phagosome-lysosome fusion
  • Symptoms: recurrent infections and giant lysosomes in leukocytes
  • Diagnostic characteristic: albinism
154
Q
  • Family: Azole
  • Target: Cell membrane
  • MOA:
    • inhibits ergosterol synthesis
  • Use:
    • Aspergillus (drug of choice)
  • Clinical:
    • Visual disturbances
A

Voriconazole

155
Q

What causes Type II Bare Lymphocyte Syndrome?

A
  • Type II – loss of MHC class II expression
    • Reduced number of T helper cells
    • Much more detrimental
156
Q

Flu-like symptoms (fever, coughing, chills, myalgia)

157
Q

Function of IL5?

A
  • Activate eosinophils → bind to IgE (from IL4) → eosinophils release lytic granules → kill worms
158
Q

What are the 5 vaccination types and what are their forms of protection?

A
  • Attenuated pathogens
    • Antibody response
  • Subunit vaccines
    • Antibody response
  • Conjugate vaccines
    • Helper T – Cell dependent antibody response
  • Synthetic vaccines
    • Antibody Response
  • Recombinant viruses and bacteria
    • Cell-mediated and humoral immune responses
159
Q

What are the two pathways of antigen presentation for MHC Class I and Class II (picture)?

160
Q

Spectrum:

  • Gram(+): staph, streph, Enterococcus faecalis
  • Gram(-): Broad
  • Other: Anaerobes

Clinical:

  • (Broadest Antibiotic)
  • Doesn’t treat MRSA
161
Q

For Hereditary Angioedema (HAE),

  • What is the Etiology?
  • A decrease in what complement protein is seen?
  • What sympyoms are seen?
  • What is the pathophysiology?
  • What is the treatment?
A
  • HAE
    • Etiology: decreased C1esterase inhibitor
    • Diagnosis: depressed C4 levels
    • Systemic swelling
    • Contact Pathway: Factor 12 →→→→ bradykinin (all steps are inhibited by C1esterase Inhibitor)
      • Increase in bradykinin → vasculature permeability (NO and PGI2) → angioedema
    • Treatment: C1esterase Inhibitor
      • Epinephrine can only be used histamine-induced angioedema
162
Q

Spectrum:

  • Gram(+): Staph (including MRSA)
  • Gram(-): Broad

Clinical:

  • THINK TICKS (Rickettsia, Lyme)
  • Staph Soft tissue infection
  • Chlamydia
A

Doxycycline

163
Q

Define exotoxins.

  • What roles do the “B” and “A” subunit play here?
  • What 4 bacteria have an exotoxin function and how do they each work and what occurs as a result of each one?
A
  • Exotoxins – proteins secreted by bacteria that cause direct cellular and tissue injury (B subunit binds to cell and A subunit causes toxic effect)
    • C. diptheriae
      • Diphtheria toxin blocks EF2, inhibiting protein synthesis
    • V. cholerae
      • Cholera toxin increases cAMP → loss of electrolytes and water → diarrhea
    • C. tetani
      • Blocks end plate inhibitor → continuous stimulation → spastic paralysis
    • C. botulinum
      • Blacks release of ACh vesicle → stimulation blocked → flaccid paralysis
164
Q
  • Family:RNA Viruses
  • Target:Influenza A
  • MOA:M2 inhibitors
  • Clinical:Not used clinically
A

Amantadine/Rimantadine

165
Q

Transmission: Water exposure → penetration of skin

Site of Infection: Mesenteric/urogenital veins and super-migratory

Clinical Presentation:

  • inflammatory reaction
A

Schistosomes

  • hematobium: pelvic vein - hematuria
  • mansoni: liver/spleen enlargement, portal hypertension
166
Q

What is Tacrolimus?

A
  • Tacrolimus – Calcineurin inhibitor
    • Prevents rejection of allograft organs
167
Q

Spectrum:

  • Gram(+): Strep, Enterococcus, mouth flora (methicillin-sensitive staph)
  • Gram(-): E.coli, Proteus, H. influenza, (B. fragilis)

Clinical:

  • Simple community acquired Gram (-)
A

Ampicillin/(sulbactam) [iv]

Amoxicillin/(clavulanate) [po]

168
Q

Transmission: Midges and flies

Site of Infection: Skin

Clinical Presentation:

  • dermatitis
A

Filaria: Mansonellosis

169
Q

Transmission: Pork, wild animals

Site of Infection: Muscle Tissue

Clinical Presentation:

  • muscle inflammation
A

Trichinellosis

170
Q

Chicken pox: red sores all over the skin

Shingles: painful rash on half the body (neural)

A
  • Varicella-zoster virus
    • Varicella – Chicken pox: red sores all over the skin
    • Zoster – Shingles: painful rash on half the body (neural)
171
Q

Transmission: ingestion

Site of Infection: non-Migratory

  • colon/rectum

Clinical Presentation:

  • Perianal itch
  • Most common worm infection is USA
  • Insomnia
A

Enterobius (pinworm)

172
Q

Subcutaneous Mycoses

Characterisitics and Examples (3)?

A
  • Characteristics
    • Infection of dermis and subcutaneous tissue
    • Develops at site of trauma (i.e. rosebush thorn prick)
  • Sporotrichosis (Rose gardener’s disease)
    • Caused by Sporothrix schenckii (dimorphic)
    • Presents as lymphocutaneous nodules/legions following site of trauma up lymph
      • Similar presentation caused by Mycobacterium marinum (from fish tanks)
  • Chromoblastomycosis
    • Due to various pigmented molds
    • Presents as slow growing cauliflower-like nodules
  • Eumycotic mycetoma – seen in tropics (swelling)
173
Q

NFAT pathway?

A

Ca++ enters cells → binds calmodulin → which binds calcineurin (a phosphatase) → dephosphorylates NFAT → NFAT acts as a transcription factor → transcribes IL2 → T cell clonal expansion

174
Q

What is the lectin pathway initiated by?

A
  • Lectin pathway
    • Initiated via lectin binding mannose residues on foreign cells
175
Q

What happens in a type III hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

176
Q

What are the 3 ways tumors escape the immune system?

Name examples of each way.

A
  1. Tumor Directly Escapes
    1. Antigen loss
    2. MHC Class I Loss
    3. Production of Inhibitory Receptors
    4. Production of Immunosuppressive Cytokines (IL-10 and TGF-B)
  2. Active Suppression
    1. Regulatory T cells block effector T cell activation
    2. Myeloid cells (leukocytes) downregulate T cell response
  3. Problems with Effector T Cells
    1. T cell exhaustion
    2. T cell apoptosis
177
Q

What happens in a type IVc hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

178
Q

Gram: -

Baccili

aerobe

Lactase: +

A

EEK

  • Escherichia coli
  • Enterobacter
  • Klebsiella
179
Q

Retinitis – inflammation of the eye

A

Cytomegalovirus

180
Q

Spectrum:

  • Gram(+): Strep, Enterococcus, mouth flora
  • Gram(-): none
  • Other: Spirochetes (Syphilis)

Clinical:

  • Strep. Pyogenes (Group A)
  • Dental Infection
A

Natural Penicillin (IV or PO)

181
Q

Papain vs. Pepsin

A

Papain is an enzyme that cleaves the Fab and Fc above the hinge

Pepsin is an enzyme that cleaves the Fab and Fc below the hinge

182
Q

Transmission: Flies (Simulium)

Site of Infection: Cornea

Clinical Presentation:

  • River blindness, dermatitis
A

Filaria: onchocerca volvulus

183
Q
  • What are carbapenem toxicities?
A
  • Seizures
  • Type I hypersensitivity reaction
184
Q

Signal 3?

185
Q
  • Family: DNA Viruses
  • Target: HSV, VZV
    • (EBV – oral hairy leukoplakia in AIDs)
  • MOA:
    • DNA homolog: Acts as a DNA chain terminator
    • Prodrug → active drug via viral thymidine kinase (TK)
  • Clinical:
    • Resistance via TK mutations
    • Drug of choice for HSV encephalitis
A

Acyclovir (IV)

186
Q

Spectrum:

  • Gram(+): oral anaerobes, some MRSA
  • Gram(-): none

Clinical:

  • Oral infection if penicillin allergic
A

Clindamycin

187
Q

Spectrum:

  • Gram(+): strep, staph
  • Gram(-): Excellent!
  • Other: Anerobes

Clinical:

  • Only oral drug for pseudomonas
  • High Risk Pneumonia
  • Complex UTI
  • Too strong for most Gram (+)’s
A

Moxifloxacin

188
Q

What bacteria are associated with the following infection?

  • Otitis Media (ear infection) - 3 types
A

Strep pneumoniae, H. flu, Moraxella catarrhalis

189
Q

Selective IgA Deficiency

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Pathophysiology: IgA deficiency (important in mucosal regions)
  • Symptoms: increased incidence of respiratory and GI infections
190
Q

How do Chimeric Antigen Receptor (CAR) Expressing T Cells work?

What can it treat?

A
  • Building a T cell receptor signaling motif with an antibody specific binding domain
  • Combines power of signals with specificity of antibody
  • Treats Acute Lymphoblastic Leukemia (ALL)
191
Q

Transmission: Triatomine bugs (kissing bugs)

Site of Infection: Intracellularly muscle and nerves

Clinical Presentation:

  • Organomegaly (i.e. cardiomyopathy, megacolon)
  • Romaña’s Sign: swelling of eyelid
  • Chagoma: ulcer at bite site

Epidemology: The Americas (south of the USA)

A

Trypanosomiasis cruzi (Americas) – Chagas

192
Q

List some noninfectious medical problems from fungi.

A
  • Allergies – hypersensitivity to fungi
  • Mycotoxins
    • Aflatoxins – Aspergillus flavus in grain storage
    • Amatoxins/phallotoxins – poisonous mushrooms produce alpha-amanitin, which inhibits RNA Pol II (mRNA)
193
Q
  • What are penicillin toxicities?
A
  • Type I hypersensitivity reaction including mild rash or anaphylaxis
194
Q

Disease: Bronchiolitis

Presentation, Etiology, Treatment?

A

Presentation: Occurs in first two years of life; wheezing; hyperaeration of lungs (air trapping)

Etiology: Respiratory Syncytial Virus (RSV), especially during winter

Treatment: Let run natural course

195
Q

Transmission: Sheep (Humans accidental)

Site of Infection: Lung and liver

Clinical Presentation:

  • Asymptomatic, nonspecific
  • Anaphylaxis
A

Echinococcus

196
Q

What is active therapy underlying immunotherapeutic strategies for cancer?

A
  • Active therapy – induced within the host, durable response
    • In situ immunization – activates the immune system against endogenous tumor
197
Q
  • What is a type B reaction?
  • Is it predictable?
  • How common are they?
  • What are three types of type B reactions?
A
  • Unpredictable – unrelated to known pharmacological action of drugs
  • Types of type B reaction
    • Intolerance – known side effect at lower dose than expected
    • Idiosyncratic – based on how patient metabolizes drug
    • Hypersensitivity/allergy/immune mechanisms
198
Q

Relate the leukotriene and prostaglandin pathway to hypersensitivity reactions.

Explian each normal pathway and the end result of each pathway..

A
  • PM FAs → arachidonic acid → PGH2 → PGE2 → PGE2 binds to EP-Rs on mast cells and eosinophils → inhibits inflammatory response
    • COX1/COX2 are needed for AA to PGH2
  • PM FAs → arachidonic acid → LTX4 (variants of leukotrienes) → inflammation
199
Q

How do Toll-Like Receptors Promote Inflammation?

(2) Pathways

A
  • Activation of NF-kB (cytokines) – acute inflammation
  • Activation of IFNs (interferons) – resistance to viral infection
    • Plasmacytoid dendritic cells produce type I IFNs → expression of interferon stimulated genes → inhibition of viral RNA replication and activation of immune response
    • Act in an autocrine and paracrine manner to protect uninfected cells
200
Q

How doees Provenge work?

A

Provenge – antigen from cancer is fused with growth factor to trigger prostate specific T cell response

201
Q

Common Variable Immunodeficiency (CVID)

Etiology

Pathphysiology

Symptoms/Clinical Charcaterisitcs

A
  • Pathophysiology: low IgG, IgA, IgM
  • Diagnostic characteristics: low IgG leads to impaired antibody response to vaccines
202
Q
  • What are subunit vaccines?
  • Do they require boosters?
  • What are two examples?
A
  • Contain only a “subunit” or portion of an organism
  • Requires boosters
  • HPV and HepB
203
Q
  • What is an inactivated vaccine?
  • Do they require boosters?
  • What is an example?
A
  • Infectious agents have been killed by fixatives or chemicals so they cannot produce proteins or replicate in cells
  • Requires boosters
  • Safer than attenuated
  • Examples: seasonal influenza vaccines
204
Q
  • What is the role of adjuvants in the success of vaccines?
  • What do they activate?
  • What are some examples?
A
  • Adjuvant: any substance that enhances the immune response to an antigen with which it is mixed
    • Aluminum salts/gels
    • Monophosphoryl lipid A
  • Activate PRRs (TLRs, NODs)
205
Q

Transmission: Anopholes Mosquitos

Site of Infection: Lymphatic

Clinical Presentation:

  • Elephantitis
A

Filaria: wuchreria bancrofti

206
Q

Transmission: Ingestion/penetration of skin

Site of Infection: Migratory

  • In small intestine
  • Travels to bile duct or pancreas

Clinical Presentation:

  • Intestinal obstruction
  • Pulmonary sx
A

Ascaris lumbricoides

207
Q

How do Anti-PD-1 drugs work?

A
  • Normally, PD-1 in T cell can bind PD-L1 in tumor and APCs, blocking effector functions
  • With treatment, AB is used to block binding, therefore restoring T cell effector function (allows signaling cascade to occur)
  • Good for metastatic cancers
208
Q

Gram: +

Cocci

aerobic

catalase: -
hemolysis: beta

A

Strep pyogenes

209
Q

Describe epidemiology of and clinical syndromes from…

Coccidioidomycosis

  • yeast or mold or dimorphic?
A
  • Endemic Mycoses - DIMORPHIC
    • Epidemiology: arid Southwestern States (AZ and CA)
    • Transmission: mold grows in soil → inhalation of spores → yeast grows in lungs
    • Symptoms: asymptomatic but disseminated disease is lethal (skin/lung)
    • Diagnosis: large spherules containing endospores
210
Q

What are some other pathways to activate apoptosis by killer T cells?

A

Fas/Fas Ligand

TRAIL/TRAIL Receptors

211
Q

Th2 synthesis?

What does it release?

A
  • Synthesis/Differentiation: via IL4 → activate GATA-3
  • Releases cytokine: IL4, IL5, IL13
212
Q

Function of IL17?

A
  • Act on leukocytes and tissues cells → produces cytokine and chemokines → recruit neutrophils → inflammation
    • Good if against bacterial/fungal extracellular infection
    • Bad if against endogenous extracellular molecules (i.e. MS, IBD)
213
Q

What bacteria are associated with the following infection?

  • Bacterial Meningitis - 4 types
A
  • Bacterial Meningitis
    • Strep pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Listeria monocytogenes
214
Q

Transmission: penetration of skin

Site of Infection: Migratory

  • In small intestine

Clinical Presentation:

  • Ground itch
  • Anemia (attaches to epithelium and sucks blood)
  • Bloody stools
  • Transient pneumonitis​
A

Hookworm

  • Necator americanus
  • Ancylostoma
215
Q
  • Family: Azole
  • Target: Cell membrane
  • MOA:
    • inhibits ergosterol synthesis
  • Use:
    • Candida albicans, Cryptococcal
    • NOT MOLDS
  • Clinical:
    • Candida krusei & glabrata are resistant
    • Tx: esophagitis, candidemia
A

Fluconazole

216
Q

Transmission: Ticks

Site of Infection: RBCs (tetrads form)

Clinical Presentation:

  • Asymptomatic/flu-like sx
  • Immunocompromised: anemia

Epidemology: Northeast/Midwest USA

217
Q
  • Family: DNA Viruses
  • Target: HSV, VZV
  • MOA:
    • Prodrug of Acyclovir that are activated in intestinal wall or liver
    • More bioavailable form of Acyclovir
  • Clinical:
    • More Bioavailable than acyclovir in oral form
    • Used for herpes labialis before symptom appear
A

Valacyclovir/Famciclovir (PO)

218
Q

Spectrum:

  • Gram(+): none
  • Gram(-): Excellent!

Clinical:

  • Only oral drug for pseudomonas
  • Complex UTI
  • Too strong for most Gram (+)’s
A

Ciprofloxacin

219
Q
  • What are potential adverse effects of tetracyclines?
A
  • Chelates to bone (teeth staining)
  • Phototoxicity
220
Q

Early defects in the complement system predispose a patient to:

A

ICX (immune complex) disease

  • Example: Depressed C3 is seen in active Lupus (SLE)
221
Q

What causes Type I Bare Lymphocyte Syndrome?

A
  • Type I – loss of MHC class I expression
    • Mutations in TAP
222
Q

Spectrum:

  • Gram(+): Strep, Enterococcus, mouth flora (methicillin-sensitive staph)
  • Gram(-): Pseudomonas, Enterobacter, Acinetobacter, (B. fragilis)

Clinical:

  • Hospital acquired Gram (-)
  • Nosocomial aspiration pneumonia (caused by pseudomonas)
A

Piperacillin/(tazobactam) [iv]

223
Q
  • What is a potential adverse effect of fluoroquinolones?
A
  • Tendon rupture
224
Q

What happens in a type IVd hypersensitivity reaction?

What are some common clinical characteristics?

What activates this response?

What effector cells respond?

What are examples of this reaction?

225
Q
  • Oral hairy leukoplakia in AIDs
    • White rash on edge of the tongue
A

Epstein-Barr Virus

226
Q

Describe the NLRP-3 Inflammasome Pathway?

A
  • Phagocytosis by macrophages → recognition of PAMPS/DAMPS → NLRP-3 trimerization with adaptor protein and caspase-1 → cleavage and activation of caspase-1 → caspase-1 cleaves pro-IL-1B → active IL-1B → secretion → fever/acute inflammation
  • Can cause auto-inflammatory syndromes, kidney diseases, and gout (by urate crystals)

SPM (ARSH) (5 decks)

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