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SPM (ARSH) > Weeks 9-12 > Flashcards

Weeks 9-12 Flashcards

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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
What bacteria are associated with the following infection? * Abdominal Infections (two classes of bacteria)
* Abdominal Infections * GNRs AND anaerobes
26
**Hyper-IgE Syndromes (HIES)** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs
* Etiology: dominant negative mutation in STAT3 or recessive mutation in DOCK8 * Symptoms: eczema, eosinophilia, two rows of teeth
27
Avidity versus Affinity
* 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
28
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?
* 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
29
**Transmission:** Food and water contaminated with cysts **Site of Infection:** Small Intestine **Clinical Presentation:** Chronic diarrhea, abdominal pain, bloating, **Epidemology:** Uncommon in USA
Cyclospora cayetanensis
30
What are the 4 modes of genetic exchange and define each one?
* 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
31
Describe epidemiology of and clinical syndromes from… Mucormycosis – most commonly caused by Mucor (or Zygomyces) * mold or yeast or dimorphic?
* ***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
32
Describe the events that occur when T cells are activated.
33
Spectrum: * Gram(+): MSSA, beta strep, Strep pneumoniae * Gram(-): E. coli Clinical: * Uncomplicated Cellulitis * Surgery prophylaxis (heart)
1st Generation * Cefazolin * Cephalexin
34
Gram: + Cocci aerobic catalase: - hemolysis: gamma
enterococcus
35
* 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)
Ganciclovir (IV) /Valganciclovir (po)
36
* What is a type A drug reaction? * Is it predictable? * What is it dependent on? * How common are these?
* Most adverse reactions * Predictable – related to the pharmacological action of drug * Dose dependent
37
* 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
Zanamivir/Oseltamivir(Tamiflu)
38
* What **three** classes inhibit initiation in protein synthesis?
* Tetracyclines * Aminoglycosides * Linezolid
39
Spectrum: * Gram(+): MSSA * Gram(-): H. flu, legionella, moraxella, chlamydia Clinical: * Community acquired Resp. tract infection (atypical pneumonia) * Chlamydia
Azithromycin (Z-pack)
40
**X-Linked Hyper-IgM Syndrome** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs
* Etiology: mutations in CD40L (CD154) gene * Pathophysiology: defect in class-switching; low levels of all Igs except IgM * Symptoms: severe and frequent infections
41
What bacteria are associated with the following infection? * Non-purulent cellulitis (just erythematous) * Purulent cellulitis (skin abscesses)
* Cellulitis * Non-purulent cellulitis (just erythematous) * Most likely *Strep pyogenes* * Purulent cellulitis (skin abscesses) * Either *Staph aureus* or *Strep pyogenes*
42
Spectrum: * Gram(+):MSSA, beta strep, Strep pneumoniae * Gram(-): Neisseria meningitidis * Other: Borrelia burgforferi (Lyme) Clinical: * Meningitis * Lyme Disease
3rd Generation (Cross BBB) * Ceftriaxone * Cefotaxime
43
* Family: DNA Viruses * Target: Resistant CMV, HSV, VZV * MOA: * Pyrophosphate analog that inhibits viral DNA synthesis * Clinical: * CMV retinitis * Very toxic (kidney)
Foscarnet (IV)
44
What are the three phases of Signal 1?
45
* How can bacteria resist vancomycin?
* Caused by a change in the peptide component from ala-ala to ala-lactate, which doesn’t allow the drug to bind
46
Which antibiotics are bactericidal? There are six main types.
* penicilins * cephalosporins * vancomycin * quinilones * metronidazole * aminoglycosides
47
What is the structure of MHC Class II? * How many alpha and beta chains? * Expressed on what ells? * Binds peptides of what size?
* 2 alpha chains and 2 beta chains * Expressed only on professional APCs (dendritic, B, and macrophage) * Binds long peptides (11 to 30 AAs)
48
What causes Type III Bare Lymphocyte Syndrome?
* Type III – loss of both I and II * Similar to type II
49
**Transmission:** Ingestion of undercooked crustaceans **Site of Infection:** Migratory from GI to lungs **Clinical Presentation:** * Egg in sputum sample * Acute infection * Mimics TB
Lung Flukes * paragohomus westermari
50
Describe epidemiology of and clinical syndromes from… Blastomycosis * yeast or mold or dimorphic?
* **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
51
Spectrum: * Gram(+): staph, strep (MSSA) * Gram(-): none Clinical: * Uncomplicated Cellulitis
Penicillinase – resistant penicillin (methicillin): * Nafcillin * Dicloxacillin
52
* What is a live, attenuated vaccine? * Do they require a booster? * What are some examples of this?
* Infectious agents have reduced virulence due to mutations or genetic engineering * Give strongest response and longest protection * Examples: MMR, chickenpox
53
* What is the mechanism of action of fluoroquinolones?
* Inhibits topoisomerase activity of prokaryotes
54
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?
55
What is Signal 2?
56
Th1 synthesis? What does it release?
* Synthesis/Differentiation: via IL12/IFN-gamma → activate T-bet * Releases cytokine: IFN-gamma
57
What is the antigen receptor-mediated signal transduction in B lymphocytes? * What transcription factors are activated?
* 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
58
**Transmission:** Undercooked fish **Site of Infection:** Small intestines **Clinical Presentation:** * Prolonged infection → B12 deficiency (megoblastic anemia)
Diphyllobatrium latum
59
What bacteria are associated with the following infection? * Hospital-Acquired Pneumonia (HAP) - 2 types
* Hospital-Acquired Pneumonia (HAP) * GNRs (*Pseudomonas)*, *Staph aureus*
60
Cutaneous Mycoses Characterisitics and Examples (5)
* 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 * **t****inea 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)
61
Describe epidemiology of and clinical syndromes from (3 total syndromes) Candida (i.e. C. albicans, C. glabrata, C. krusei) * Yeast or mold or dimorphic?
* *(**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
62
Describe epidemiology of and clinical syndromes from… Pneumocystis (fungi but treated as a protozoan)
Lacks ergosterol and does not respond to anti-fungals Strictly opportunistic pathogen seen predominately in AIDS
63
Non-invasive Molds
Dermatophytes (see above) Trichophyton, Microsporum
64
Describe epidemiology of and clinical syndromes from… Cryptococcus (i.e. C. neoformans) * yeast or mold or dimorphic?
* *(**YEAST**)* * Prominent capsule that is identified with **India Ink** * Strictly opportunistic pathogen seen predominately in AIDS * Bird feces → lungs → brain * Syndromes * **Cryptococcal Meningitis**
65
Gram: - Baccili anaerobe
B. fragilis
66
Explain how the TH1/ TH2 balance contributes to different outcomes of a Mycobacterium leprae infection.
* 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)
67
**Transmission:** Sexual Intercourse **Site of Infection:** Vagina, urethra **Clinical Presentation:** Usually Asymptomatic, Dysuria from urethritis **Epidemology:** Worldwide
Trichomonas vaginalis
68
Disease: CAP Presentation, Etiology, Treatment?
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
69
Spectrum: * Gram(+): cocci * Gram(-): none Clinical: * Reserved for VRE & MRSA
Linezolid
70
* 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
Flucytosine (PO)
71
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?
72
* Family: Azole * Target: Cell membrane * MOA: * inhibits ergosterol synthesis * Use: * Aspergillus & Mucormycosis * Clinical: * New drug: expanding role
Isavuconazole
73
What are the 3 immune mechanisms involved in the response to cancer?
* 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
74
Virus-Cell Interactions (5 TYPES)
* 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
75
What is passive therapy underlying immunotherapeutic strategies for cancer?
* Passive therapy – temporary effect (you stop treatment, you stop response) * Antibody mediated * Antibodies which lead directly to cell death (trastuzumab) * Engineered antibodies
76
**X-Linked Gamma Agammaglobulinemia** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs
* Etiology: mutations in Bruton Tyrosine Kinase * Pathophysiology: failure of B cell maturation past pre-B * Diagnostic characteristic: no germinal centers in lymph nodes
77
* 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)
Amphotercin (IV)
78
What happens in AERD?
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)
79
**Chronic Granulomatous Disease** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs Diagnosis
* Etiology: mutations in phagocyte oxidase (NADPH Burst) * Pathophysiology: inability to kill phagocytosed microbes * Symptoms: recurrent infections * Diagnosis: NBT Tests (histological view of macrophage activity)
80
Spectrum: * Gram(+): none * Gram(-): broad including multi-drug resistance bacteria (Pseudomonas & Klebsiella) Clinical: * LAST RESORT DRUG * Hearing loss & vertigo
Aminoglycosides * Gentamicin * Tobramycin * Amikacin
81
Can you mix 2 or 3 antifungals?
Mix 2 or 3 of these Antifungals → Extra toxicity and possible antagonism of MOAs
82
Gram: + Cocci aerobic catalase: + coagulase: +
S. aureus
83
Gram: - Cocci aerobic (5)
- Neisseria gonorrhoeae (diplocooci) - Neisseria meningitidis (diplococci) - Haemophilus influenzae - Bordetella pertussis -Moraxella catarrhalis
84
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)
* Community Acquired Pneumonia (CAP) * *Strep pneumoniae* * “Atypical” pneumonias * *Mycoplasma pneumoniae* * *Legionella pneumophila* * *Chlamydophila pneumoniae* * *Staph aureus* (post-influenza)
85
**Leukocyte Adhesion Defects (LAD) (3 types)** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs
* 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
86
What is the alternate pathway and how is it initiated?
* Alternative pathway * Initiated via C3 convertase formation in addition to Factor B and D binding
87
**Transmission:** Insect bite, Swallowing crustaceans **Site of Infection:** Blood and Tissue **Clinical Presentation:** * Incubated for one year, then NVD * Blister formation
Dracunculiasis
88
Late defects in the complement pathway predispose to:
* 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
89
Cold sores/blisters on the genitals or mouth
Herpes Simplex virus
90
Gram: + Bacilli anaerobe
Clostridium difficile/perfringens
91
What is the Granule Mech?
* 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
**Transmission:** Ingestion via anthropods **Site of Infection:** GI **Clinical Presentation:** * Nonspecific * Nasuea, weakness, abdominal pain, loss of appetite
Hymenolepis nana
93
Gram: + Cocci aerobic catalase: - hemolysis: alpha
Strep peneumonia
94
Effector CD4+ T cell: Helper T cell (2) functions
* Cell mediated immunity * CD40:CD40L binding → macrophage activation → kill phagocytosed microbes * Humoral immunity * CD40:CD40L binding → antibody hypermutation and class switching
95
Describe mechanisms used by CD8+ T cells to kill infected cells.
* 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
**Transmission:** Flies **Site of Infection:** Skin **Clinical Presentation:** * swelling of skin
Filaria: Loiasis (Loa loa)
97
Th17 synthesis? What does it release?
* Synthesis/Differentiation: via IL6/IL23/TGF-beta → activate ROR-gamma-t * Release cytokines: IL17,22
98
Gram: + Cocci aerobic catalase: + coagulase: -
S. epidermidis
99
Function of IL4?
* Stimulates production of IgE * IgE → mast cells → histamines → allergic reaction * Stimulate B cells → production of antibodies (IgE) against helminth worms
100
Spectrum: * Gram(+):Broad including MRSA and VRE * Gram(-): none Clinical: * VRE
Daptomycin
101
**Transmission:** penetration of skin **Site of Infection:** Migratory * In small intestine **Clinical Presentation:** * Pruritic rash at site of penetration * Pulmonary sx * Autoinfection
Strongyloides
102
RNA Virus Capsid Structure? Naked or Enveloped? (NAME EXCEPTIONS TOO)
* 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
**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
Leishmania
104
Describe the **differences** between a B cell receptor and a T cell receptor.
* 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
Describe epidemiology of and clinical syndromes from… Histoplasmosis * Mold or yeast or dimorphic
* **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
Define biofilm and Quorum sensing.
* 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
**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
Giardia lamblia, * duodenalis * intesitnalis
108
**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
Trypanosomiasis brucei (African)
109
What is the classical pathway initiated by?
* Classical pathway * Initiated via antigen-antibody binding * C1 binds to antibody at the Fc region
110
What are three mechanisms of evasion of humoral immunity by microbes?
* **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
**Severe Combined Immunodeficiencies (SCID)** **(4 Types)** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs
* 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
**HIV** Etiology Pathophysiology Symptoms
* 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
**Defects in TLR Pathways** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs
* TLR3 mutations →→ herpes simplex encephalitis * NEMO (NF-kB Essential Modulator) → ectoderm defects → lack of sweating
114
What is adoptive therapy underlying immunotherapeutic strategies for cancer? How does this solve issues with patients who do not have tumor reactive cells?
* Adoptive therapy – transfer of autologous (self) or allogenic (donor) immune cells (can be durable) with anti-tumor activity
115
Disease: Pharyngitis / Tonsillitis / Laryngitis Presentation, Etiology, Treatment?
Presentation: Inflammation of pharynx, tonsils, larynx Etiology: Viral, usually part of common cold or flu Treatment: Make sure it’s not bacterial
116
Spectrum: * Gram(+): strep, staph * Gram(-): Excellent! Clinical: * Only oral drug for pseudomonas * High Risk Pneumonia * Complex UTI * Too strong for most Gram (+)’s
Levofloxacin
117
Function of IFN-gamma? (2)
* 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
* What are potential adverse effects of aminoglycosides?
* Ototoxicity (vertigo or hearing loss) * Nephrotoxicity
119
* Family: Azole * Target: Cell membrane * MOA: * inhibits ergosterol synthesis * Use: * Mucormycosis (not used clinically) * Clinical: * Prophylaxis
Posaconazole
120
Disease: Sinusitis / Otitis Media / Mastoiditis Presentation, Etiology, Treatment?
Presentation: Inflammation of ear drum, sinuses Etiology: Assumed to be bacterial: Strep pneumonia, H. flu, or Moraxella catarrhalis Treatment: Amoxicillin
121
What are cephalosporin toxicities?
Type I hypersensitivity reaction including rash or anaphylaxis
122
Disease: Post-influenza Pneumonia Presentation, Etiology, Treatment?
Presentation: Fever; cough; sputum; X-ray consolidation Etiology: Staph aureus Treatment: Sputum sent for Gram stain and culture
123
Mechanism of Extraversion Difference between Naive and effector?
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
What are natural killer cells? MOA? What do they release?
* 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
What is the role of these complement pathway proteins? * C3b * C5b6789 * C5a * C3a, C4a, C5a
* 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
**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
Toxoplasma gondii
127
Disease: Epiglottitis (Supraglottitis) Presentation, Etiology, Treatment?
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
* What **two** classes inhibit elongation in protein synthesis?
* Macrolides (azithromycin, clarithromycin) * Clindamycin
129
What is Immunodominance?
Immunodominance – most expanded T cells clones recognizes only a few peptides of a given microbe
130
**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
Entamoeba histolytica
131
Which antibiotics are bacteriostatic? There are three main types.
* tetracyclines * macrolides * clindamycin
132
What are the general steps of virus life cycle?
* 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
Spectrum: * Gram(+):Broad including MRSA, Enterococcus * Gram(-): none Clinical: * MRSA
Vancomycin
134
**Transmission:** Solium: Undercooked pork/beef **Site of Infection:** Migratory tissue cysts from small intestines to bloodstream **Clinical Presentation:** * Cysticercosis (formation of cysts)
Taeniasis
135
**Transmission:** Undercooked fish/watercrests (water plants) **Site of Infection:** Small intestine → biliary system **Clinical Presentation:** * GI problems * Biliary obstruction * RUQ pain
Liver Flukes * Clonorchis * Fasciola
136
Function of IL22?
Act on tissues cells → increased barrier function/wound healing
137
Disease: Laryngotracheobronchitis (Croup) Presentation, Etiology, Treatment?
Presentation: In children: inflammation of subglottic region (below vocal cords); barking cough; stridor; hoarseness Etiology: Parainfluenza virus Treatment: n/a
138
What is the end result of signal transduction?
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
Disease: HAP Presentation, Etiology, Treatment?
Presentation: Fever; cough; sputum; X-ray consolidation Etiology: Pseudomonas (nosocomial) Treatment: Sputum sent for Gram stain and culture
140
What is paroxysmal nocturnal hemoglobinuria?
* complement-mediated intravascular RBC lysis * patients may report red or pink urine (from hemoglobinuria) * Treatment: eculizumab (terminal complement inhibitor)
141
Spectrum: * Gram(+): Broad coverage * Gram(-): Broad including Pseudomonas Clinical: * Good for people w/ penicillin allergy
Aztreonam
142
Gram: indeterminate Baccili aerobe Acid Fast: +
Mycobacterium tuberculosis | (bacillus)
143
**Ataxia-Telangiectasia** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs
* Etiology: defect in ATM (DNA repair protein) * Symptoms: abnormal gait and neurological deficits
144
What genes have mutations in Autoimmune Lymphoproliferative Syndrome?
Mutations in genes associated with apoptosis (caspases, Fas)
145
NAME EACH TYPE
146
* What are conjugate vaccines? * Do they require a booster? * What are some examples?
* 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
Disease: Tracheobronchitis / Bronchitis Presentation, Etiology, Treatment?
Presentation: Cough Etiology: Virus Treatment: Make sure it’s not pneumonia
148
**Transmission:** Ingestion of water plants **Site of Infection:** Intestines **Clinical Presentation:** * Asymptomatic * Can lead to infection
Intestinal Flukes * Fasciolopsis buski
149
* Family: Azole * Target: Cell membrane * MOA: * inhibits ergosterol synthesis * Use: * Sporotrichosis * Histo & Blasto * Clinical: * Pulse therapy for onychomycosis
Intraconazole
150
A depressed alternative pathway predisposes to:
* Sepsis * Defects in C3 ALSO predispose to sepsis
151
Function of IL13?
* 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
**Transmission:** ingestion **Site of Infection:** non-Migratory * colon/cecum **Clinical Presentation:** * Painful passage of stool (blood, mucus) * Rectal prolapse
Trichuris (whipform)
153
**Chediack-Higashi Syndrome** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs
* Etiology: mutation in LYST gene * Pathophysiology: defective phagosome-lysosome fusion * Symptoms: recurrent infections and giant lysosomes in leukocytes * Diagnostic characteristic: albinism
154
* Family: Azole * Target: Cell membrane * MOA: * inhibits ergosterol synthesis * Use: * Aspergillus (drug of choice) * Clinical: * Visual disturbances
Voriconazole
155
What causes Type II Bare Lymphocyte Syndrome?
* Type II – loss of MHC class II expression * Reduced number of T helper cells * Much more detrimental
156
Flu-like symptoms (fever, coughing, chills, myalgia)
Influenza
157
Function of IL5?
* Activate eosinophils → bind to IgE (from IL4) → eosinophils release lytic granules → kill worms
158
What are the 5 vaccination types and what are their forms of protection?
* 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
What are the two pathways of antigen presentation for MHC Class I and Class II (picture)?
160
Spectrum: * Gram(+): staph, streph, Enterococcus faecalis * Gram(-): Broad * Other: Anaerobes Clinical: * (Broadest Antibiotic) * Doesn’t treat MRSA
Meropenem
161
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?
* 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
Spectrum: * Gram(+): Staph (including MRSA) * Gram(-): Broad Clinical: * THINK TICKS (Rickettsia, Lyme) * Staph Soft tissue infection * Chlamydia
Doxycycline
163
# 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?
* 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
* Family:RNA Viruses * Target:Influenza A * MOA:M2 inhibitors * Clinical:Not used clinically
Amantadine/Rimantadine
165
**Transmission:** Water exposure → penetration of skin **Site of Infection:** Mesenteric/urogenital veins and super-migratory **Clinical Presentation:** * inflammatory reaction
Schistosomes * hematobium: pelvic vein - hematuria * mansoni: liver/spleen enlargement, portal hypertension
166
What is Tacrolimus?
* Tacrolimus – Calcineurin inhibitor * Prevents rejection of allograft organs
167
Spectrum: * Gram(+): Strep, Enterococcus, mouth flora (methicillin-sensitive staph) * Gram(-): E.coli, Proteus, H. influenza, (B. fragilis) Clinical: * Simple community acquired Gram (-)
Ampicillin/(sulbactam) [iv] Amoxicillin/(clavulanate) [po]
168
**Transmission:** Midges and flies **Site of Infection:** Skin **Clinical Presentation:** * dermatitis
Filaria: Mansonellosis
169
**Transmission:** Pork, wild animals **Site of Infection:** Muscle Tissue **Clinical Presentation:** * muscle inflammation
Trichinellosis
170
Chicken pox: red sores all over the skin Shingles: painful rash on half the body (neural)
* Varicella-zoster virus * Varicella – Chicken pox: red sores all over the skin * Zoster – Shingles: painful rash on half the body (neural)
171
**Transmission:** ingestion **Site of Infection:** non-Migratory * colon/rectum **Clinical Presentation:** * Perianal itch * Most common worm infection is USA * Insomnia
Enterobius (pinworm)
172
Subcutaneous Mycoses Characterisitics and Examples (3)?
* 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
NFAT pathway?
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
What is the lectin pathway initiated by?
* Lectin pathway * Initiated via lectin binding mannose residues on foreign cells
175
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
What are the 3 ways tumors escape the immune system? Name examples of each way.
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
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
Gram: - Baccili aerobe Lactase: +
EEK - Escherichia coli - Enterobacter - Klebsiella
179
Retinitis – inflammation of the eye
Cytomegalovirus
180
Spectrum: * Gram(+): Strep, Enterococcus, mouth flora * Gram(-): none * Other: Spirochetes (Syphilis) Clinical: * Strep. Pyogenes (Group A) * Dental Infection
Natural Penicillin (IV or PO)
181
Papain vs. Pepsin
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
**Transmission:** Flies (Simulium) **Site of Infection:** Cornea **Clinical Presentation:** * River blindness, dermatitis
Filaria: onchocerca volvulus
183
* What are carbapenem toxicities?
* Seizures * Type I hypersensitivity reaction
184
Signal 3?
185
* 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
Acyclovir (IV)
186
Spectrum: * Gram(+): oral anaerobes, some MRSA * Gram(-): none Clinical: * Oral infection if penicillin allergic
Clindamycin
187
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
Moxifloxacin
188
What bacteria are associated with the following infection? * Otitis Media (ear infection) - 3 types
*Strep pneumoniae, H. flu, Moraxella catarrhalis*
189
**Selective IgA Deficiency** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs
* Pathophysiology: IgA deficiency (important in mucosal regions) * Symptoms: increased incidence of respiratory and GI infections
190
How do Chimeric Antigen Receptor (CAR) Expressing T Cells work? What can it treat?
* 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
**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)
Trypanosomiasis cruzi (Americas) – Chagas
192
List some noninfectious medical problems from fungi.
* 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
* What are penicillin toxicities?
* Type I hypersensitivity reaction including mild rash or anaphylaxis
194
Disease: Bronchiolitis Presentation, Etiology, Treatment?
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
**Transmission:** Sheep (Humans accidental) **Site of Infection:** Lung and liver **Clinical Presentation:** * Asymptomatic, nonspecific * Anaphylaxis
Echinococcus
196
What is active therapy underlying immunotherapeutic strategies for cancer?
* Active therapy – induced within the host, durable response * In situ immunization – activates the immune system against endogenous tumor
197
* What is a type B reaction? * Is it predictable? * How common are they? * What are three types of type B reactions?
* 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
Relate the leukotriene and prostaglandin pathway to hypersensitivity reactions. Explian each normal pathway and the end result of each pathway..
* 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
How do Toll-Like Receptors Promote Inflammation? (2) Pathways
* 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
How doees Provenge work?
Provenge – antigen from cancer is fused with growth factor to trigger prostate specific T cell response
201
**Common Variable Immunodeficiency (CVID)** Etiology Pathphysiology Symptoms/Clinical Charcaterisitcs
* Pathophysiology: low IgG, IgA, IgM * Diagnostic characteristics: low IgG leads to impaired antibody response to vaccines
202
* What are subunit vaccines? * Do they require boosters? * What are two examples?
* Contain only a “subunit” or portion of an organism * Requires boosters * HPV and HepB
203
* What is an inactivated vaccine? * Do they require boosters? * What is an example?
* 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
* What is the role of adjuvants in the success of vaccines? * What do they activate? * What are some examples?
* 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
**Transmission:** Anopholes Mosquitos **Site of Infection:** Lymphatic **Clinical Presentation:** * Elephantitis
Filaria: wuchreria bancrofti
206
**Transmission:** Ingestion/penetration of skin **Site of Infection:** Migratory * In small intestine * Travels to bile duct or pancreas **Clinical Presentation:** * Intestinal obstruction * Pulmonary sx
Ascaris lumbricoides
207
How do Anti-PD-1 drugs work?
* 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
Gram: + Cocci aerobic catalase: - hemolysis: beta
Strep pyogenes
209
Describe epidemiology of and clinical syndromes from… Coccidioidomycosis * yeast or mold or dimorphic?
* **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
What are some other pathways to activate apoptosis by killer T cells?
Fas/Fas Ligand TRAIL/TRAIL Receptors
211
Th2 synthesis? What does it release?
* Synthesis/Differentiation: via IL4 → activate GATA-3 * Releases cytokine: IL4, IL5, IL13
212
Function of IL17?
* 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
What bacteria are associated with the following infection? * Bacterial Meningitis - 4 types
* Bacterial Meningitis * *Strep pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Listeria monocytogenes*
214
**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​
Hookworm * Necator americanus * Ancylostoma
215
* Family: Azole * Target: Cell membrane * MOA: * inhibits ergosterol synthesis * Use: * Candida albicans, Cryptococcal * NOT MOLDS * Clinical: * Candida krusei & glabrata are resistant * Tx: esophagitis, candidemia
Fluconazole
216
**Transmission:** Ticks **Site of Infection:** RBCs (tetrads form) **Clinical Presentation:** * Asymptomatic/flu-like sx * Immunocompromised: anemia **Epidemology:** Northeast/Midwest USA
Babesia
217
* 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
Valacyclovir/Famciclovir (PO)
218
Spectrum: * Gram(+): none * Gram(-): Excellent! Clinical: * Only oral drug for pseudomonas * Complex UTI * Too strong for most Gram (+)’s
Ciprofloxacin
219
* What are potential adverse effects of tetracyclines?
* Chelates to bone (teeth staining) * Phototoxicity
220
Early defects in the complement system predispose a patient to:
ICX (immune complex) disease * Example: Depressed C3 is seen in active Lupus (SLE)
221
What causes Type I Bare Lymphocyte Syndrome?
* Type I – loss of MHC class I expression * Mutations in TAP
222
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)
Piperacillin/(tazobactam) [iv]
223
* What is a potential adverse effect of fluoroquinolones?
* Tendon rupture
224
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
* Oral hairy leukoplakia in AIDs * White rash on edge of the tongue
Epstein-Barr Virus
226
Describe the NLRP-3 Inflammasome Pathway?
* 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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