Weeks 9-12 Flashcards

Question

What bacteria are associated with the following infection? * Abdominal Infections (two classes of bacteria)

Answer 1

* Abdominal Infections * GNRs AND anaerobes

Answer 2

* Etiology: dominant negative mutation in STAT3 or recessive mutation in DOCK8 * Symptoms: eczema, eosinophilia, two rows of teeth

Answer 3

* 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

Answer 4

* 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

Answer 5

Cyclospora cayetanensis

Answer 6

* 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

Answer 7

* ***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

Answer 8

1st Generation * Cefazolin * Cephalexin

Answer 9

enterococcus

Answer 10

Ganciclovir (IV) /Valganciclovir (po)

Answer 11

* Most adverse reactions * Predictable – related to the pharmacological action of drug * Dose dependent

Answer 12

Zanamivir/Oseltamivir(Tamiflu)

Answer 13

* Tetracyclines * Aminoglycosides * Linezolid

Answer 14

Azithromycin (Z-pack)

Answer 15

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

Answer 16

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

Answer 17

3rd Generation (Cross BBB) * Ceftriaxone * Cefotaxime

Answer 18

Foscarnet (IV)

Answer 19

* Caused by a change in the peptide component from ala-ala to ala-lactate, which doesn’t allow the drug to bind

Answer 20

* penicilins * cephalosporins * vancomycin * quinilones * metronidazole * aminoglycosides

Answer 21

* 2 alpha chains and 2 beta chains * Expressed only on professional APCs (dendritic, B, and macrophage) * Binds long peptides (11 to 30 AAs)

Answer 22

* Type III – loss of both I and II * Similar to type II

Answer 23

Lung Flukes * paragohomus westermari

Answer 24

* **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

Answer 25

Penicillinase – resistant penicillin (methicillin): * Nafcillin * Dicloxacillin

Answer 26

* Infectious agents have reduced virulence due to mutations or genetic engineering * Give strongest response and longest protection * Examples: MMR, chickenpox

Answer 27

* Inhibits topoisomerase activity of prokaryotes

Answer 28

* Synthesis/Differentiation: via IL12/IFN-gamma → activate T-bet * Releases cytokine: IFN-gamma

Answer 29

* 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

Answer 30

Diphyllobatrium latum

Answer 31

* Hospital-Acquired Pneumonia (HAP) * GNRs (*Pseudomonas)*, *Staph aureus*

Answer 32

* 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)

Answer 33

* *(**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

Answer 34

Lacks ergosterol and does not respond to anti-fungals Strictly opportunistic pathogen seen predominately in AIDS

Answer 35

Dermatophytes (see above) Trichophyton, Microsporum

Answer 36

* *(**YEAST**)* * Prominent capsule that is identified with **India Ink** * Strictly opportunistic pathogen seen predominately in AIDS * Bird feces → lungs → brain * Syndromes * **Cryptococcal Meningitis**

Answer 37

B. fragilis

Answer 38

* 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)

Answer 39

Trichomonas vaginalis

Answer 40

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

Answer 41

Flucytosine (PO)

Answer 42

Isavuconazole

Answer 43

* 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

Answer 44

* 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

Answer 45

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

Answer 46

* Etiology: mutations in Bruton Tyrosine Kinase * Pathophysiology: failure of B cell maturation past pre-B * Diagnostic characteristic: no germinal centers in lymph nodes

Answer 47

Amphotercin (IV)

Answer 48

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)

Answer 49

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

Answer 50

Aminoglycosides * Gentamicin * Tobramycin * Amikacin

Answer 51

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

Answer 52

- Neisseria gonorrhoeae (diplocooci) - Neisseria meningitidis (diplococci) - Haemophilus influenzae - Bordetella pertussis -Moraxella catarrhalis

Answer 53

* Community Acquired Pneumonia (CAP) * *Strep pneumoniae* * “Atypical” pneumonias * *Mycoplasma pneumoniae* * *Legionella pneumophila* * *Chlamydophila pneumoniae* * *Staph aureus* (post-influenza)

Answer 54

* 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

Answer 55

* Alternative pathway * Initiated via C3 convertase formation in addition to Factor B and D binding

Answer 56

Dracunculiasis

Answer 57

* 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

Answer 58

Herpes Simplex virus

Answer 59

Clostridium difficile/perfringens

Answer 60

* 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

Answer 61

Hymenolepis nana

Answer 62

Strep peneumonia

Answer 63

* Cell mediated immunity * CD40:CD40L binding → macrophage activation → kill phagocytosed microbes * Humoral immunity * CD40:CD40L binding → antibody hypermutation and class switching

Answer 64

* 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

Answer 65

Filaria: Loiasis (Loa loa)

Answer 66

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

Answer 67

S. epidermidis

Answer 68

* Stimulates production of IgE * IgE → mast cells → histamines → allergic reaction * Stimulate B cells → production of antibodies (IgE) against helminth worms

Answer 69

Daptomycin

Answer 70

Strongyloides

Answer 71

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

Answer 72

Leishmania

Answer 73

* 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)

Answer 74

* **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**

Answer 75

* 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

Answer 76

Giardia lamblia, * duodenalis * intesitnalis

Answer 77

Trypanosomiasis brucei (African)

Answer 78

* Classical pathway * Initiated via antigen-antibody binding * C1 binds to antibody at the Fc region

Answer 79

* **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)

Answer 80

* 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

Answer 81

* 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

Answer 82

* TLR3 mutations →→ herpes simplex encephalitis * NEMO (NF-kB Essential Modulator) → ectoderm defects → lack of sweating

Answer 83

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

Answer 84

Presentation: Inflammation of pharynx, tonsils, larynx Etiology: Viral, usually part of common cold or flu Treatment: Make sure it’s not bacterial

Answer 85

Levofloxacin

Answer 86

* 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)

Answer 87

* Ototoxicity (vertigo or hearing loss) * Nephrotoxicity

Answer 88

Posaconazole

Answer 89

Presentation: Inflammation of ear drum, sinuses Etiology: Assumed to be bacterial: Strep pneumonia, H. flu, or Moraxella catarrhalis Treatment: Amoxicillin

Answer 90

Type I hypersensitivity reaction including rash or anaphylaxis

Answer 91

Presentation: Fever; cough; sputum; X-ray consolidation Etiology: Staph aureus Treatment: Sputum sent for Gram stain and culture

Answer 92

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)

Answer 93

* 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

Answer 94

* 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

Answer 95

Toxoplasma gondii

Answer 96

Presentation: In children: cellulitis of supraglottic region (vocal cords); fever; sore throat; drooling Etiology: Haemophilus influenzae type b Treatment: Beta-lactamase resistant antibiotic (Cefatriaxone)

Answer 97

* Macrolides (azithromycin, clarithromycin) * Clindamycin

Answer 98

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

Answer 99

Entamoeba histolytica

Answer 100

* tetracyclines * macrolides * clindamycin

Answer 101

* 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

Answer 102

Vancomycin

Answer 103

Liver Flukes * Clonorchis * Fasciola

Answer 104

Act on tissues cells → increased barrier function/wound healing

Answer 105

Presentation: In children: inflammation of subglottic region (below vocal cords); barking cough; stridor; hoarseness Etiology: Parainfluenza virus Treatment: n/a

Answer 106

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

Answer 107

Presentation: Fever; cough; sputum; X-ray consolidation Etiology: Pseudomonas (nosocomial) Treatment: Sputum sent for Gram stain and culture

Answer 108

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

Answer 109

Mycobacterium tuberculosis | (bacillus)

Answer 110

* Etiology: defect in ATM (DNA repair protein) * Symptoms: abnormal gait and neurological deficits

Answer 111

Mutations in genes associated with apoptosis (caspases, Fas)

Answer 112

* 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

Answer 113

Presentation: Cough Etiology: Virus Treatment: Make sure it’s not pneumonia

Answer 114

Intestinal Flukes * Fasciolopsis buski

Answer 115

Intraconazole

Answer 116

* Sepsis * Defects in C3 ALSO predispose to sepsis

Answer 117

* In intestines: stimulates mucus secretion and peristalsis → inhibits worm entry and promotes worm expulsion * Activates alternative macrophages (M2 macrophages) → tissue repair \*\*\*\* Works with IL4

Answer 118

Trichuris (whipform)

Answer 119

* Etiology: mutation in LYST gene * Pathophysiology: defective phagosome-lysosome fusion * Symptoms: recurrent infections and giant lysosomes in leukocytes * Diagnostic characteristic: albinism

Answer 120

Voriconazole

Answer 121

* Type II – loss of MHC class II expression * Reduced number of T helper cells * Much more detrimental

Answer 122

* Activate eosinophils → bind to IgE (from IL4) → eosinophils release lytic granules → kill worms

Answer 123

* 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

Answer 124

* 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

Answer 125

Doxycycline

Answer 126

* 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

Answer 127

Amantadine/Rimantadine

Answer 128

Schistosomes * hematobium: pelvic vein - hematuria * mansoni: liver/spleen enlargement, portal hypertension

Answer 129

* Tacrolimus – Calcineurin inhibitor * Prevents rejection of allograft organs

Answer 130

Ampicillin/(sulbactam) [iv] Amoxicillin/(clavulanate) [po]

Answer 131

Filaria: Mansonellosis

Answer 132

Trichinellosis

Answer 133

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

Answer 134

Enterobius (pinworm)

Answer 135

* 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)

Answer 136

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

Answer 137

* Lectin pathway * Initiated via lectin binding mannose residues on foreign cells

Answer 138

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

Answer 139

EEK - Escherichia coli - Enterobacter - Klebsiella

Answer 140

Cytomegalovirus

Answer 141

Natural Penicillin (IV or PO)

Answer 142

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

Answer 143

Filaria: onchocerca volvulus

Answer 144

* Seizures * Type I hypersensitivity reaction

Answer 145

Acyclovir (IV)

Answer 146

Clindamycin

Answer 147

Moxifloxacin

Answer 148

*Strep pneumoniae, H. flu, Moraxella catarrhalis*

Answer 149

* Pathophysiology: IgA deficiency (important in mucosal regions) * Symptoms: increased incidence of respiratory and GI infections

Answer 150

* 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)

Answer 151

Trypanosomiasis cruzi (Americas) – Chagas

Answer 152

* Allergies – hypersensitivity to fungi * Mycotoxins * Aflatoxins – *Aspergillus flavus* in grain storage * Amatoxins/phallotoxins – poisonous mushrooms produce alpha-amanitin, which inhibits RNA Pol II (mRNA)

Answer 153

* Type I hypersensitivity reaction including mild rash or anaphylaxis

Answer 154

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

Answer 155

Echinococcus

Answer 156

* Active therapy – induced within the host, durable response * In situ immunization – activates the immune system against endogenous tumor

Answer 157

* 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

Answer 158

* 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

Answer 159

* 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

Answer 160

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

Answer 161

* Pathophysiology: low IgG, IgA, IgM * Diagnostic characteristics: low IgG leads to impaired antibody response to vaccines

Answer 162

* Contain only a “subunit” or portion of an organism * Requires boosters * HPV and HepB

Answer 163

* 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

Answer 164

* 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)

Answer 165

Filaria: wuchreria bancrofti

Answer 166

Ascaris lumbricoides

Answer 167

* 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

Answer 168

Strep pyogenes

Answer 169

* **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**

Answer 170

Fas/Fas Ligand TRAIL/TRAIL Receptors

Answer 171

* Synthesis/Differentiation: via IL4 → activate GATA-3 * Releases cytokine: IL4, IL5, IL13

Answer 172

* 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)

Answer 173

* Bacterial Meningitis * *Strep pneumoniae, Neisseria meningitidis, Haemophilus influenzae, Listeria monocytogenes*

Answer 174

Hookworm * Necator americanus * Ancylostoma

Answer 175

Fluconazole

Answer 176

Valacyclovir/Famciclovir (PO)

Answer 177

Ciprofloxacin

Answer 178

* Chelates to bone (teeth staining) * Phototoxicity

Answer 179

ICX (immune complex) disease * Example: Depressed C3 is seen in active Lupus (SLE)

Answer 180

* Type I – loss of MHC class I expression * Mutations in TAP

Answer 181

Piperacillin/(tazobactam) [iv]

Answer 182

* Tendon rupture

Answer 183

Epstein-Barr Virus

Answer 184

* 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)

Weeks 9-12 Flashcards

(226 cards)