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Infectious Disease Flashcards

1
Q

Chlamydia, Rickettsia, Mycoplasma

A

Simple treatment-Doxycycline.

Obligate intracellular organisms.

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2
Q

Factors that influence bacterial infections (4)

A
  1. Site of propagation
  2. Immune response
  3. Virulence factors
  4. Resistance of host
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3
Q

Bacteria Virulence 4 Factors

A
  1. Adherence to host cell
  2. Intracellular survival
  3. Invasion
  4. Toxin production
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4
Q

types of bacterial infections

A

Superficial or deep

Externally acquired pathogen or derived from flora

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5
Q

Mycobacterium Tuberculosis can be detected by

A

NAT on sputum.

–Rapid diagnosis, guides therapy

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6
Q

Bordetella pertussis

A

NAT on respiratory secretions

–most sensitive method

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7
Q

Chlamydia trachomatis

A

NAT-most sensitive method of diagnosis

Important to prevent PID (pelvic inflammation disease), which leads to sterility

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8
Q

serology

A

indirect evidence of infection

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9
Q

antibacterial agents 3 types

A

cell wall agents
ribosomal agents
inhibitors of replication

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10
Q

Examples of cell wall agents

A

beta lactams, glycopeptides

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11
Q

Examples of ribosomal agents

A

macrolides, aminoglycosides

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12
Q

Examples of replication

A

fluoroquinolones

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13
Q

Antibiotic resistance mechanisms

A
  1. altered target
  2. efflux pump
  3. inactivation of drug (enzymes)
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14
Q

Resistance gene

A
  • develops in presence of antibiotic pressure

- may be passed between bacteria

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15
Q

MIC

A

Minimum inhibitory concentration-bacteria grown in presence of antibiotic at several concentrations

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16
Q

resistance testing

A

molecular detection of resistance genes

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17
Q

Staphylococcus aureus

A

Gram positive cocci in clusters
Skin & soft tissue infections: pneumonia, endocarditis
MRSA-resistant to b-lactams
Dx:culture, NAT for MRSA

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18
Q

Group A streptococcus / Streptococcus pyogenes

A

Gram positive cocci in chains
Skin & soft tissue infections: pharyngitis, post-infectious complications (rheumatic fever)
Dx: culture, antigen testing, NAT, serology (post-infectious complications)

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19
Q

Neisseria meningitidis

-These patients need drugs imediately or they die!

A

Gram negative diplococci (paired cocci)
Bacterial meningitis
Dx: direct visualization, culture, NAT
These patients need drugs imediately or they die!

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20
Q

E. coli

A

Gram negative rod (enteric-GI tract)
GU, GI infections, abdominal abscesses
Sepsis (bloodstream infections with LPS release)
Dx: Culture, (antigen testing -certain forms: GI)

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21
Q

Pseudomonas aeruginosa

A

Gram negative rod (environmental, colonizer, loves water)
Multiple types infections (esp. nosocomial, cystic fibrosis)
May be highly resistant to antibiotics
Dx: culture

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22
Q

Clostridium difficile

A

Gram postive rod-anaerobic (enteric)-causes diarrhea
antibiotic-associated colitis (toxin producing strains)
Dx: previous antigen testing (for toxins A & B)
Now PCR

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23
Q

Mycobacterium tuberculosis

A

gram positive rod-acid fast (lost of waxy mycolic acids in cell wall)
Tuberculosis (sites of infection: pulmonary, extrapulmonary-bone, GU)
Dx: direct visualization (acid fast stain), NAT, 6 wks to culture

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24
Q

4 factors that influence fungal infections

A
  1. Site of propagation
  2. Immune response
  3. Virulence factors
  4. Resistance of host
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25
Q

How does the resistance of host play part in fungal infections?

A

Diabetics have compromised neutrophils–don’t work correctly

Malnutrition–too weak to mount immune system attack

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26
Q

Types of fungal infections

A 
Superficial or deep (host-dependent)
Skin and soft tissue
Upper respiratory tract
Lower respiratory tract
GI, Urinary tract, Genital,
CNS, bloodsream
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27
Q

Examples of dimorphic fungi (produce sever disseminated infection in compromised hosts)

A 
Histoplsam capsulatum.
Coccidiodes immitis.
Blastomyces dermatiditis.
Paracoccidiodides brasiliensis.
Penicillium marneffei.
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28
Q

Fungi Dx methods

A 
Direct visualization- cell wall stain, morphology
Culture- different media
Antigen testing
NAT
Serology (select-dimorphic)
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29
Q

Antifungal agents

A

Cell wall & membrane agents- interfere with integrity

  1. polyenes
  2. azoles
  3. echinocandins
  4. others
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30
Q

polyenes

A

bind and disrupt fungal membrane

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31
Q

polyenes examples

A

amphotericin B, nystatin

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32
Q

azoles

A

inhibit synthesis of ergosterol (essential component of fungal membrane)

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33
Q

echinocandins examples

A

caspofungin, micafungin

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34
Q

azole examples

A

fluconazole, voriconazole, others

35
Q

echinocandins

A

inhibit sythesis of glucans (essential components of fungal cell wall

36
Q

Antifungal resistance is ___common due to ___ evolution and ___ horizontal transfer.

A

less / slower / less

37
Q

Treatment usually empiric, fungal susceptibility testing less common than bacteria. Why?

A

Not automatically done on all isolates. Slow growing, different medias–usually use CDC guidelines for geographical regions and identify to ID major resistance of strains–then prescribe and empirically determine any drug resistance.

38
Q

Candida spp. C. albicans, C. glabrata, C. tropicalis, others

A

Yeasts-colonizers of oral, resp tract, GI, GU tract
Superficial–normal host
Deep/disseminated in compromised host
Dx: culture, (antigen testing)

39
Q

Cryptococcus neoformans

A

Yeast; environmental
Self-limited -normal host (pumonary)
Significant disease-compromised host.
Dx: antigen testing (serum, CSF), culture

40
Q

Cryptococcus neoformans in HIV compromised host leads to

A

meningitis, pulmonary, skin infections

41
Q

Aspergillus spp.

A

Mould; environmental
allergic disease –normal host
Severe fatal invasive disease- neutropenic hosts
Dx: direct visualization, culture, antigen testing, serology (for allergic disease)

42
Q

Zygomycosis/Mucomycosis

A

Family related moulds (Rhizopus, Mucor, etc)
rarely affect-normal host
severe, aggressive disease –compromised host, specially diabetics
Dx: Direct visualization, culture

43
Q

Diabetics with Zygomycosis/Mucomycosis infection. What happens?

A

Predilection for CNS/brain (sinusitis extension)
Fungal sinusitis will lead to death in a few hours–strictly for diabetics
Must be treated immediately or patient dies

44
Q

Histoplasmosis, H. capsulatum

A

Dimorphic fungus, yeast at 37C, filamentous at 25C
Enviromental.
Self-limiting pulmonary infection- normal host
Disseminated infection in compromised host
Dx: antigen testing (immunocompromised), serology (immunocompetent), culture

45
Q

Coccidiomycosis, Coccidiodes immitis & C.posadasii

A

Dimorphic fungus, spherule at 37C, filamentous at 25C
Environmental-SW
Self-limiting pulmonary infection–normal host
Severe/disseminated infection in certain races–Filipino, Afr.-Am
Dx: direct visualization, culture

46
Q

Coccidiomycosis affects certain races severely. Which ones?

A

Filipino, Black

47
Q

Viral host cell damage occurs via

A
  • the effects of conscription of cell machinery
  • other toxic effects
  • cell lysis
48
Q

Immune-mediated response to viral infection

A

-cytotoxic T lymphocytes

CD8 try to kill the infected cell

49
Q

Incubation period. Define:

A

Period of time between infectious agent’s entry and the appearance of the first signs of symptoms.
Can range from 1 day to decades.

50
Q

Incubation period that can last decades is involved in what infections and why?

A

HIV–CD8 decline can be slow
Hepatitis–liver is hardy
TB-long incubation, normal host

51
Q

Viral tropism definition

A

Propensity of virus to infect certain cell types

52
Q

Viral tropism is important because

A

it determines the clinical manifestations of the infection

53
Q

Viral tropism example

A

Rhinovirus-infects nasal mucosal cells

54
Q

clinical manifestations: Rhinovirus-infects nasal mucosal cells

A

Upper respiratory tract infection, rhinitis

55
Q

Viral tropism example

A

HBV, HCV–infect hepatocytes

56
Q

clinical manifestations: HBV, HCV–infect hepatocytes

57
Q

Viral tropism example

A

Parvovirus B19–infects erythroid precursor cells

58
Q

clinical manifestations: Parvovirus B19–infects erythroid precursor cells

59
Q

Viral tropism example

A

HSV (herpes simplex virus)-infects DRG neurons

60
Q

clinical manifestations: HSV (herpes simplex virus)-infects DRG neurons

A

Recurrent skin infection in dermatome pattern

61
Q

Direct detection of virus (4)

A 
Histology/cytology
culture
antigen
Nucleic Acid detection (PCR)
Indirect evidence--Serology
62
Q

Histology/cytology

A

examination of infected cells in tissue, fluids

63
Q

Histology/cytology looks for

A

Viral cytopathic effect (CPE)

  • cell damage
  • viral inclusions (nuclear or cytoplasmic)
64
Q

CPE is specific for some viruses

A

HSV (PAP smear), CMV (lung)

65
Q

What principles are important in culturing viruses?

A

Tropism–viruses infect specific tissue
Viruses -need mammalian cell to replicate
Infection causes cell damage (CPE)

66
Q

Serology: IgM ??

A

indicates current or recent infection

67
Q

Serology: IgG ??

A

recent or remote infection (takes time to develop)

68
Q

Serology: 4-fold rise in IgG

A

diagnostic of infection

69
Q

Serology: detection of IgM

A

diagnostic of infection

70
Q

Antiviral therapy challenges:

A
  1. In host cell using the host’s cell machinery.
  2. Difficult to target therapeutic agents without undue toxicity to human cells.
  3. High replication and polymerase error rates
71
Q

High replication and polymerase error rates leads to

A
  1. Rapid development of resistance in some targets
    - -error prone polymerases can lead to mutations in each gene, w/c leads to rapid emergence of resistance
  2. Need for careful selection of target of agent (needs to be a conserved, vital function)
72
Q

Potential targets for antivrals:

A
  1. Attachment–will interrupt infection of next cell
  2. Penetration, uncoating
  3. Viral polymerases (replication)–minimize effect of human polymerases
  4. Viral enzymes (proteases) vital for viral protein processing/packaging
73
Q

Influenza

A

Enveloped, segmented RNA virus.
-Types A & B
-animal & human reservoirs
-antigenic shift, antigenic drift
Cause respiratory infections, infect nasopharyingeal musosal cells
Dx: DFA (rapid antigen tests), (culture), PCR

74
Q

Anti-influenza drugs

A

Amantidine, rimantidine (anti M2 protein- prevents viral uncoating); works only on type A
Oseltamivir, zanavir: inhibition of neuroaminadase (stops release from infected cells); works against Type A & B

75
Q

Herpes Simplex Virus (HSV)

A

Enveloped DNA virus
Neurotropic–latent in dorsal root ganglia (orolabial, genital, other)
Recurs–as skin/mucosal ulcers
Dx: DFA, culture, PCR

76
Q

HSV may cause ___, recurring or severe

A

meningitis

77
Q

anti-HSV drugs

A

Acyclovir, valacyclovir (nucleoside analog competes with dGTP)
Resistance: in mutated viral thymidine kinase or DNA polymerase genes

78
Q

Cytomegalovirus (CMV)

A

Enveloped DNA virus
Latent in leukocytes* but replicates in many cell types, especially endothelial cells.
Self-limited viral syndrome
Dx: serology, qPCR, antigenemia, (culture)
Severe in Immunocompromised

79
Q

anti-CMV drugs

A

Ganciclovir–nucleoside analog
Cidofovir–nucleoside analog
Foscarnet–DNApol inhibitor, nonnucleoside

Resistance: mutation in viral phosphatransferase (gangciclovir) or DNA polymerase genes (ganciclovir, foscarnet, cidofovir)

80
Q

Human immunodeficiency Virus (HIV)

A

Retrovirus, Enveloped RNA virus
Chronic infection in CD4+ T cells
Dx: Serology, (RNA in plasma)
Monitoring: viral load, quantitative HIV RNA in plasma

81
Q

HIV: Immunodeficiency occurs when ___ of ___ cell outstrips replenishment

A

destruction / CD4+

82
Q

anti-HIV drugs

A 
NRTI
NNRTI
Protease inhibitors
Fusion inhibitors
Integrase inhibitors
83
Q

HIV resistance indicated by rise in viral load

A

Level of replication**error rate of HIV polymerase

Detect by sequencing RT & protease, integrase genes

Pathology (4 decks)

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