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Infections
58問 • 2年前
  • Two Clean Queens
  • 通報

    問題一覧

  • 1

    The time during which an infectious agent may be transferred directly or indirectly (infectious period)

    Communicability

  • 2

    The ability to produce or transmit infection (contagious period)

    Infectivity

  • 3

    The ability of a foreign substance, such as an antigen, to provoke an immune response in the body

    Immunogenicity

  • 4

    The ability of a MO to produce a toxin that contributes to the development of disease

    Toxigenicity

  • 5

    The ability of an MO to cause disease (harm the host)

    Pathogenicity

  • 6

    The degree of pathology caused by the MO; it is usually correlated with the ability of the pathogen to multiply within the host but may be affected by other factors

    Virulence

  • 7

    The way a pathogen enters a susceptible host

    Portal or entry

  • 8

    A disease or condition regularly found among particular people or in a certain area

    Endemic

  • 9

    A Disease that affects a large number of people within a community, population, or region.

    Epidemic

  • 10

    An epidemic that’s spread over multiple countries or continents

    Pandemic

  • 11

    A greater-than-anticipated increase in the number of endemic cases. It can also be a single case in a new area. If it’s not quickly controlled, an outbreak can become an epidemic.

    An outbreak

  • 12

    Introduction of a disease-causing agent(s) into the body tissues (avoids immune system defense, triggers inflammatory response)

    Invasion

  • 13

    Period of rapid cell growth and division (occurs before the immune system responds)

    Multiplication

  • 14

    Local or disseminated presence of disease-causing agent

    Spread

  • 15

    The presence of bacteria on a body surface (skin, mouth, intestines, or airway) without causing disease in the person

    Colonization

  • 16

    Shapes of bacteria

    Cocci, Bacilli, and Spiral

  • 17

    Pilus, plasmid, ribosome, cytoplasm, cytoplasmic membrane, cell wall, capsule, nucleoid, and flagellum

    Structral components of bacteria

  • 18

    Thin cell wall but duplicate cell walls (more resistant). Release endotoxins from cell wall with lysis. Endotoxin release causes fever, hypotension, DIC, and septic shock

    Gram Negative

  • 19

    Single cell wall. Release exotoxins. Type I; proinflammatory cytokines. Type II: damage cell membrane. Type III: enter cells and cause damage.

    Gram Positive

  • 20

    Very thick cell wall. Slow growing due to lack of nutrient penetration of cell wall. Long time to positive cultures and long duration of abx treatment.

    Acid Fast Bacilli

  • 21

    Must have oxygen to maintain metabolic process

    Aerobic MO

  • 22

    Do not grow in presence of oxygen

    Anaerobic MO

  • 23

    Grow in either (with or without oxygen), prefer aerobic

    Facultative Anaerobes

  • 24

    Common flora of skin and nasal passages. Adheres via surface proteins->connective tissue and endothelium. Develop protective capsule, produce proteins that inhibit complement activation, resistant to intracellular oxidative lysis. Resistant forms exist. Community and hospital acquired strains.

    Staph Aureus

  • 25

    Normal flora of GI. Various strains (HUS, UTIs, travelers diarrhea). Commonly found in biofilm of Foley catheters. Resistant forms exist.

    E Coli

  • 26

    Survives and grows within macrophages; phagolysosomes. Develop a capsule that prevents phagocytosis. Induce anergy; suppress host response. Forms granuloma->tubercle->caseates->collagen scar->immune response->dormant. Contagious, opportunistic, resistant, and can be active or latent.

    M Tuberculosis

  • 27

    Ability of MO to adapt genetically to antibiotics due to inappropriate use and/or farming practices

    Antibiotic Resistance

  • 28

    Inactivate the antibiotic (beta-lactam resistance). Modify antibiotic target molecule (AZT-resistant reverse transcriptase). Change metabolic pathways to be less sensitive->resistant (sulfa drugs). Multi-drug transporters prevent entrance of or incre efflux of antibiotics (aminoglycosides)

    Mechanisms of Resistance

  • 29

    A 10% decrease in appropriate prescribing = 17% decrease in resistance. Use guidelines and antibiograms to help you prescribe. If you culture, follow cultures and change/stop antibiotics. I’d you prescribe abx, intentional about duration, and follow for C diff (increasing abx resistance)

    Antibiotic Stewardship

  • 30

    Timing (hospital acquired if less than 14 days after discharge, more than 4 days since admission, any time in a long-term care setting). Common infections:(CLABSI, CAUTI, VAP, SSI). Not reimbursed conditions - considerable attention focused on preventing. Different typical pathogens, need for empiric antibiotic coverage and duration of therapy.

    Community and hospital acquired infections

  • 31

    Include mold and yeasts. Highly opportunistic- T-cells important to limit infection and produce cytokines for macrophage activation. Adapt to host environment (change morphology, survive in macrophages, produce immunosuppressive cytokines). Tissue damage (direct - enzyme and toxin secretion; indirect - inflammation)

    Fungal Structure and Success

  • 32

    Part of normal microbiome (skin, GI, mouth, vagina). Opportunistic (antibiotics change normal flora; immunocompromised). Cell wall adhesion molecules (adhere to medial devices). Local or disseminated infections.

    C Albicans

  • 33

    Small pathogens. Capsid coating that protects the nucleic core. Virus cannot replicate without a host (binds to plasma membrane-> inserts into host cell->matures->buds and releases from plasma membrane)

    Virus Structure and Replication

  • 34

    Identified initially in 1960s (100s of strains). Prior severe SARS (2002-2004) and MERS (2012-localized outbreaks). Transmitted via droplet. Mild to moderate URI symptoms.

    Coronavirus

  • 35

    Antigenic Drift

    Accumulation of mutations over time

  • 36

    Antigenic Shift

    Intermixing of RNA between two viruses

  • 37

    Caused by an antigenic shift. Spike proteins allow virus to infect cells. Infectious 2-3 days before symptoms and unto 10 days after developing symptoms. Cormobidites and infection. Protective factors. MIS-C in pediatric patients.

    COVID-19

  • 38

    Family of viruses with different types (A, B, and C). Two surface proteins (hemagglutinin) that bind to receptors on epithelia cells of throat and lungs. Incubation: short, long shedding. Symptoms: fever, ache, and fatigue from release of pro-inflammatory cytokines and chemokines (TNF and interferon) produced by viral cells.

    Influenza

  • 39

    Sheds from point of infection. Activates with fatigue, fever, and stress.

    Herpes Simplex

  • 40

    Oral infection via saliva contact. Infection of epithelia cells. Virus moves along axon ID dorsal root ganglion

    HSV-1

  • 41

    Gential with mucous membrane contact

    HSV-2

  • 42

    VZV is initial infection, zoster is reactivation of earlier acquired infection. Appears as vesicles along dermatomes. Mother can transmit to neonate. Post-herpetic neuralgia with Zoster. Vaccines exist.

    Herpes Varicella and Zoster

  • 43

    RNA paramyxovirus spread via upper respiratory tract. Amplifies in local lymphatic tissue and disseminates. Maculopapular rash: head, trunk, extremities, Koplik spots, and bucal mucosa.

    Rubeola (Classic Measles)

  • 44

    RNA virus spread via upper respiratory tract. Maculopapular rash: head, trunk, and extremities. 1st trimester - congenital rubella syndrome (sensorineural deafness, retinopathy, cataracts, congenital heart disease, PA stenosis)

    Rubella (3-day, German)

  • 45

    Emerged in 1980s, now considered chronic disease, two types (1 &2), transmission blood borne

    HIV

  • 46

    More common and virulent

    HIV-1

  • 47

    less common (west Africa), less virulent and harder to transmit

    HIV-2

  • 48

    Virus binds to CD4->viral RNA injected into cytoplasm->viral RNA is uncoated (capsid removed)->enzyme reverse transcriptase used to make DNA from viral RNA->viral DNA travels to cell nucleus and integrates with host DNA->transcription and translation result in new viral protein production->virus buds through cell membrane and infects more cells. Infected CD4 cells will eventually rupture (apoptosis) or be killed by other T-cells->decreasing total CD4 cells.

    HIV Pathogenesis

  • 49

    Syndrome that occurs after initial infection. Occurs in 40-90% of persons infected. Timing 1-6 weeks after exposure. FLI that lasts 3-14 days. Common symptoms: fever, lymphadenopathy, pharyngitis, rash, myalgias, diarrhea, H/A, N/V, heptaosplenomegaly, weight loss, thrush.

    Acute HIV infection

  • 50

    Gold standard Ab/Ag test. Possible test results: if the antigen results is negative and the person is unlikely to have an infection then the person is negative; is antigen result is positive, then a HIV-1/HIV-2 Ab differentiation immunoassay should be done; if antigen result is positive and the HIV-/HIV-2 Ab differentiation immunoassay is negative and indeterminate, then HIV viral load should be done to confirm diagnosis.

    HIV Testing

  • 51

    CD4 >/= 200 and absences of AIDS defining illness or history of one

    HIV

  • 52

    CD4 <200 (even once, even if transient) and/or an AIDS defining illness

    AIDS

  • 53

    Thrush, cervical dysplasia, cervical carcinoma in situ, Fever 38.5C or higher x 1 month, oral hairy leukoplakia, Herpes Zoster, ITP, PID, peripheral neuropathy, persistent vaginal yeast infections, Karposi Sarcoma, presence of any opportunistic infections.

    Signs of HIV Immunocompromise

  • 54

    PJP, Toxoplasmosis, progressive multi focal leukencephalopathy, MAC, Kaposi’s sarcoma, lymphoma, TB, esophageal or tracheal candida infection, invasive cervical cancer, CMV infection, Histoplasmosis

    AIDS Defining Illness

  • 55

    Neonates are infected by their mother with HIV via ___.

    placenta

  • 56

    To diagnose HIV in children in post-natal period use ____.

    HIV viral load

  • 57

    2 negative HIV viral load tests at 2 weeks and 4 weeks of life, is presumptive uninfected state. 2 negative HIV viral tests at 1-4 months is a definitive uninfective state

    Diagnosis of HIV in post-natal period

  • 58

    Symptoms begin within 6 months of life. Opportunistic infection within 1st year of life. Life expectancy is typically no more than 3 years

    HIV without prenatal

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    問題一覧

  • 1

    The time during which an infectious agent may be transferred directly or indirectly (infectious period)

    Communicability

  • 2

    The ability to produce or transmit infection (contagious period)

    Infectivity

  • 3

    The ability of a foreign substance, such as an antigen, to provoke an immune response in the body

    Immunogenicity

  • 4

    The ability of a MO to produce a toxin that contributes to the development of disease

    Toxigenicity

  • 5

    The ability of an MO to cause disease (harm the host)

    Pathogenicity

  • 6

    The degree of pathology caused by the MO; it is usually correlated with the ability of the pathogen to multiply within the host but may be affected by other factors

    Virulence

  • 7

    The way a pathogen enters a susceptible host

    Portal or entry

  • 8

    A disease or condition regularly found among particular people or in a certain area

    Endemic

  • 9

    A Disease that affects a large number of people within a community, population, or region.

    Epidemic

  • 10

    An epidemic that’s spread over multiple countries or continents

    Pandemic

  • 11

    A greater-than-anticipated increase in the number of endemic cases. It can also be a single case in a new area. If it’s not quickly controlled, an outbreak can become an epidemic.

    An outbreak

  • 12

    Introduction of a disease-causing agent(s) into the body tissues (avoids immune system defense, triggers inflammatory response)

    Invasion

  • 13

    Period of rapid cell growth and division (occurs before the immune system responds)

    Multiplication

  • 14

    Local or disseminated presence of disease-causing agent

    Spread

  • 15

    The presence of bacteria on a body surface (skin, mouth, intestines, or airway) without causing disease in the person

    Colonization

  • 16

    Shapes of bacteria

    Cocci, Bacilli, and Spiral

  • 17

    Pilus, plasmid, ribosome, cytoplasm, cytoplasmic membrane, cell wall, capsule, nucleoid, and flagellum

    Structral components of bacteria

  • 18

    Thin cell wall but duplicate cell walls (more resistant). Release endotoxins from cell wall with lysis. Endotoxin release causes fever, hypotension, DIC, and septic shock

    Gram Negative

  • 19

    Single cell wall. Release exotoxins. Type I; proinflammatory cytokines. Type II: damage cell membrane. Type III: enter cells and cause damage.

    Gram Positive

  • 20

    Very thick cell wall. Slow growing due to lack of nutrient penetration of cell wall. Long time to positive cultures and long duration of abx treatment.

    Acid Fast Bacilli

  • 21

    Must have oxygen to maintain metabolic process

    Aerobic MO

  • 22

    Do not grow in presence of oxygen

    Anaerobic MO

  • 23

    Grow in either (with or without oxygen), prefer aerobic

    Facultative Anaerobes

  • 24

    Common flora of skin and nasal passages. Adheres via surface proteins->connective tissue and endothelium. Develop protective capsule, produce proteins that inhibit complement activation, resistant to intracellular oxidative lysis. Resistant forms exist. Community and hospital acquired strains.

    Staph Aureus

  • 25

    Normal flora of GI. Various strains (HUS, UTIs, travelers diarrhea). Commonly found in biofilm of Foley catheters. Resistant forms exist.

    E Coli

  • 26

    Survives and grows within macrophages; phagolysosomes. Develop a capsule that prevents phagocytosis. Induce anergy; suppress host response. Forms granuloma->tubercle->caseates->collagen scar->immune response->dormant. Contagious, opportunistic, resistant, and can be active or latent.

    M Tuberculosis

  • 27

    Ability of MO to adapt genetically to antibiotics due to inappropriate use and/or farming practices

    Antibiotic Resistance

  • 28

    Inactivate the antibiotic (beta-lactam resistance). Modify antibiotic target molecule (AZT-resistant reverse transcriptase). Change metabolic pathways to be less sensitive->resistant (sulfa drugs). Multi-drug transporters prevent entrance of or incre efflux of antibiotics (aminoglycosides)

    Mechanisms of Resistance

  • 29

    A 10% decrease in appropriate prescribing = 17% decrease in resistance. Use guidelines and antibiograms to help you prescribe. If you culture, follow cultures and change/stop antibiotics. I’d you prescribe abx, intentional about duration, and follow for C diff (increasing abx resistance)

    Antibiotic Stewardship

  • 30

    Timing (hospital acquired if less than 14 days after discharge, more than 4 days since admission, any time in a long-term care setting). Common infections:(CLABSI, CAUTI, VAP, SSI). Not reimbursed conditions - considerable attention focused on preventing. Different typical pathogens, need for empiric antibiotic coverage and duration of therapy.

    Community and hospital acquired infections

  • 31

    Include mold and yeasts. Highly opportunistic- T-cells important to limit infection and produce cytokines for macrophage activation. Adapt to host environment (change morphology, survive in macrophages, produce immunosuppressive cytokines). Tissue damage (direct - enzyme and toxin secretion; indirect - inflammation)

    Fungal Structure and Success

  • 32

    Part of normal microbiome (skin, GI, mouth, vagina). Opportunistic (antibiotics change normal flora; immunocompromised). Cell wall adhesion molecules (adhere to medial devices). Local or disseminated infections.

    C Albicans

  • 33

    Small pathogens. Capsid coating that protects the nucleic core. Virus cannot replicate without a host (binds to plasma membrane-> inserts into host cell->matures->buds and releases from plasma membrane)

    Virus Structure and Replication

  • 34

    Identified initially in 1960s (100s of strains). Prior severe SARS (2002-2004) and MERS (2012-localized outbreaks). Transmitted via droplet. Mild to moderate URI symptoms.

    Coronavirus

  • 35

    Antigenic Drift

    Accumulation of mutations over time

  • 36

    Antigenic Shift

    Intermixing of RNA between two viruses

  • 37

    Caused by an antigenic shift. Spike proteins allow virus to infect cells. Infectious 2-3 days before symptoms and unto 10 days after developing symptoms. Cormobidites and infection. Protective factors. MIS-C in pediatric patients.

    COVID-19

  • 38

    Family of viruses with different types (A, B, and C). Two surface proteins (hemagglutinin) that bind to receptors on epithelia cells of throat and lungs. Incubation: short, long shedding. Symptoms: fever, ache, and fatigue from release of pro-inflammatory cytokines and chemokines (TNF and interferon) produced by viral cells.

    Influenza

  • 39

    Sheds from point of infection. Activates with fatigue, fever, and stress.

    Herpes Simplex

  • 40

    Oral infection via saliva contact. Infection of epithelia cells. Virus moves along axon ID dorsal root ganglion

    HSV-1

  • 41

    Gential with mucous membrane contact

    HSV-2

  • 42

    VZV is initial infection, zoster is reactivation of earlier acquired infection. Appears as vesicles along dermatomes. Mother can transmit to neonate. Post-herpetic neuralgia with Zoster. Vaccines exist.

    Herpes Varicella and Zoster

  • 43

    RNA paramyxovirus spread via upper respiratory tract. Amplifies in local lymphatic tissue and disseminates. Maculopapular rash: head, trunk, extremities, Koplik spots, and bucal mucosa.

    Rubeola (Classic Measles)

  • 44

    RNA virus spread via upper respiratory tract. Maculopapular rash: head, trunk, and extremities. 1st trimester - congenital rubella syndrome (sensorineural deafness, retinopathy, cataracts, congenital heart disease, PA stenosis)

    Rubella (3-day, German)

  • 45

    Emerged in 1980s, now considered chronic disease, two types (1 &2), transmission blood borne

    HIV

  • 46

    More common and virulent

    HIV-1

  • 47

    less common (west Africa), less virulent and harder to transmit

    HIV-2

  • 48

    Virus binds to CD4->viral RNA injected into cytoplasm->viral RNA is uncoated (capsid removed)->enzyme reverse transcriptase used to make DNA from viral RNA->viral DNA travels to cell nucleus and integrates with host DNA->transcription and translation result in new viral protein production->virus buds through cell membrane and infects more cells. Infected CD4 cells will eventually rupture (apoptosis) or be killed by other T-cells->decreasing total CD4 cells.

    HIV Pathogenesis

  • 49

    Syndrome that occurs after initial infection. Occurs in 40-90% of persons infected. Timing 1-6 weeks after exposure. FLI that lasts 3-14 days. Common symptoms: fever, lymphadenopathy, pharyngitis, rash, myalgias, diarrhea, H/A, N/V, heptaosplenomegaly, weight loss, thrush.

    Acute HIV infection

  • 50

    Gold standard Ab/Ag test. Possible test results: if the antigen results is negative and the person is unlikely to have an infection then the person is negative; is antigen result is positive, then a HIV-1/HIV-2 Ab differentiation immunoassay should be done; if antigen result is positive and the HIV-/HIV-2 Ab differentiation immunoassay is negative and indeterminate, then HIV viral load should be done to confirm diagnosis.

    HIV Testing

  • 51

    CD4 >/= 200 and absences of AIDS defining illness or history of one

    HIV

  • 52

    CD4 <200 (even once, even if transient) and/or an AIDS defining illness

    AIDS

  • 53

    Thrush, cervical dysplasia, cervical carcinoma in situ, Fever 38.5C or higher x 1 month, oral hairy leukoplakia, Herpes Zoster, ITP, PID, peripheral neuropathy, persistent vaginal yeast infections, Karposi Sarcoma, presence of any opportunistic infections.

    Signs of HIV Immunocompromise

  • 54

    PJP, Toxoplasmosis, progressive multi focal leukencephalopathy, MAC, Kaposi’s sarcoma, lymphoma, TB, esophageal or tracheal candida infection, invasive cervical cancer, CMV infection, Histoplasmosis

    AIDS Defining Illness

  • 55

    Neonates are infected by their mother with HIV via ___.

    placenta

  • 56

    To diagnose HIV in children in post-natal period use ____.

    HIV viral load

  • 57

    2 negative HIV viral load tests at 2 weeks and 4 weeks of life, is presumptive uninfected state. 2 negative HIV viral tests at 1-4 months is a definitive uninfective state

    Diagnosis of HIV in post-natal period

  • 58

    Symptoms begin within 6 months of life. Opportunistic infection within 1st year of life. Life expectancy is typically no more than 3 years

    HIV without prenatal