Brainscape's Knowledge GenomeTM


Top Flashcards (Certified)
All Flashcards

Pathology > Infectious Disease > Flashcards

Infectious Disease Flashcards

(83 cards)

Start Studying
1
Q

Chlamydia, Rickettsia, Mycoplasma

A

Simple treatment-Doxycycline.

Obligate intracellular organisms.

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Factors that influence bacterial infections (4)

A
  1. Site of propagation
  2. Immune response
  3. Virulence factors
  4. Resistance of host
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Bacteria Virulence 4 Factors

A
  1. Adherence to host cell
  2. Intracellular survival
  3. Invasion
  4. Toxin production
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

types of bacterial infections

A

Superficial or deep

Externally acquired pathogen or derived from flora

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Mycobacterium Tuberculosis can be detected by

A

NAT on sputum.

–Rapid diagnosis, guides therapy

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Bordetella pertussis

A

NAT on respiratory secretions

–most sensitive method

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Chlamydia trachomatis

A

NAT-most sensitive method of diagnosis

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

serology

A

indirect evidence of infection

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

antibacterial agents 3 types

A

cell wall agents
ribosomal agents
inhibitors of replication

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Examples of cell wall agents

A

beta lactams, glycopeptides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Examples of ribosomal agents

A

macrolides, aminoglycosides

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Examples of replication

A

fluoroquinolones

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Antibiotic resistance mechanisms

A
  1. altered target
  2. efflux pump
  3. inactivation of drug (enzymes)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Resistance gene

A
  • develops in presence of antibiotic pressure

- may be passed between bacteria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

MIC

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

resistance testing

A

molecular detection of resistance genes

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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!

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

4 factors that influence fungal infections

A
  1. Site of propagation
  2. Immune response
  3. Virulence factors
  4. Resistance of host
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
How does the resistance of host play part in fungal infections?
Diabetics have compromised neutrophils--don't work correctly | Malnutrition--too weak to mount immune system attack
26
Types of fungal infections
``` Superficial or deep (host-dependent) Skin and soft tissue Upper respiratory tract Lower respiratory tract GI, Urinary tract, Genital, CNS, bloodsream ```
27
Examples of dimorphic fungi (produce sever disseminated infection in compromised hosts)
``` Histoplsam capsulatum. Coccidiodes immitis. Blastomyces dermatiditis. Paracoccidiodides brasiliensis. Penicillium marneffei. ```
28
Fungi Dx methods
``` Direct visualization- cell wall stain, morphology Culture- different media Antigen testing NAT Serology (select-dimorphic) ```
29
Antifungal agents
Cell wall & membrane agents- interfere with integrity 1. polyenes 2. azoles 3. echinocandins 4. others
30
polyenes
bind and disrupt fungal membrane
31
polyenes examples
amphotericin B, nystatin
32
azoles
inhibit synthesis of ergosterol (essential component of fungal membrane)
33
echinocandins examples
caspofungin, micafungin
34
azole examples
fluconazole, voriconazole, others
35
echinocandins
inhibit sythesis of glucans (essential components of fungal cell wall
36
Antifungal resistance is ___common due to ___ evolution and ___ horizontal transfer.
less / slower / less
37
Treatment usually empiric, fungal susceptibility testing less common than bacteria. Why?
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
Candida spp. C. albicans, C. glabrata, C. tropicalis, others
Yeasts-colonizers of oral, resp tract, GI, GU tract Superficial--normal host Deep/disseminated in compromised host Dx: culture, (antigen testing)
39
Cryptococcus neoformans
Yeast; environmental Self-limited -normal host (pumonary) Significant disease-compromised host. Dx: antigen testing (serum, CSF), culture
40
Cryptococcus neoformans in HIV compromised host leads to
meningitis, pulmonary, skin infections
41
Aspergillus spp.
Mould; environmental allergic disease --normal host Severe fatal invasive disease- neutropenic hosts Dx: direct visualization, culture, antigen testing, serology (for allergic disease)
42
Zygomycosis/Mucomycosis
Family related moulds (Rhizopus, Mucor, etc) rarely affect-normal host severe, aggressive disease --compromised host, specially diabetics Dx: Direct visualization, culture
43
Diabetics with Zygomycosis/Mucomycosis infection. What happens?
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
Histoplasmosis, H. capsulatum
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
Coccidiomycosis, Coccidiodes immitis & C.posadasii
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
Coccidiomycosis affects certain races severely. Which ones?
Filipino, Black
47
Viral host cell damage occurs via
- the effects of conscription of cell machinery - other toxic effects - cell lysis
48
Immune-mediated response to viral infection
-cytotoxic T lymphocytes | CD8 try to kill the infected cell
49
Incubation period. Define:
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
Incubation period that can last decades is involved in what infections and why?
HIV--CD8 decline can be slow Hepatitis--liver is hardy TB-long incubation, normal host
51
Viral tropism definition
Propensity of virus to infect certain cell types
52
Viral tropism is important because
it determines the clinical manifestations of the infection
53
Viral tropism example
Rhinovirus-infects nasal mucosal cells
54
clinical manifestations: Rhinovirus-infects nasal mucosal cells
Upper respiratory tract infection, rhinitis
55
Viral tropism example
HBV, HCV--infect hepatocytes
56
clinical manifestations: HBV, HCV--infect hepatocytes
Hepatitis
57
Viral tropism example
Parvovirus B19--infects erythroid precursor cells
58
clinical manifestations: Parvovirus B19--infects erythroid precursor cells
Anemia
59
Viral tropism example
HSV (herpes simplex virus)-infects DRG neurons
60
clinical manifestations: HSV (herpes simplex virus)-infects DRG neurons
Recurrent skin infection in dermatome pattern
61
Direct detection of virus (4)
``` Histology/cytology culture antigen Nucleic Acid detection (PCR) Indirect evidence--Serology ```
62
Histology/cytology
examination of infected cells in tissue, fluids
63
Histology/cytology looks for
Viral cytopathic effect (CPE) - cell damage - viral inclusions (nuclear or cytoplasmic)
64
CPE is specific for some viruses
HSV (PAP smear), CMV (lung)
65
What principles are important in culturing viruses?
Tropism--viruses infect specific tissue Viruses -need mammalian cell to replicate Infection causes cell damage (CPE)
66
Serology: IgM ??
indicates current or recent infection
67
Serology: IgG ??
recent or remote infection (takes time to develop)
68
Serology: 4-fold rise in IgG
diagnostic of infection
69
Serology: detection of IgM
diagnostic of infection
70
Antiviral therapy challenges:
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
High replication and polymerase error rates leads to
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
Potential targets for antivrals:
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
Influenza
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
Anti-influenza drugs
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
Herpes Simplex Virus (HSV)
Enveloped DNA virus Neurotropic--latent in dorsal root ganglia (orolabial, genital, other) Recurs--as skin/mucosal ulcers Dx: DFA, culture, PCR
76
HSV may cause ___, recurring or severe
meningitis
77
anti-HSV drugs
Acyclovir, valacyclovir (nucleoside analog competes with dGTP) Resistance: in mutated viral thymidine kinase or DNA polymerase genes
78
Cytomegalovirus (CMV)
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
anti-CMV drugs
Ganciclovir--nucleoside analog Cidofovir--nucleoside analog Foscarnet--DNApol inhibitor, nonnucleoside Resistance: mutation in viral phosphatransferase (gangciclovir) or DNA polymerase genes (ganciclovir, foscarnet, cidofovir)
80
Human immunodeficiency Virus (HIV)
Retrovirus, Enveloped RNA virus Chronic infection in CD4+ T cells Dx: Serology, (RNA in plasma) Monitoring: viral load, quantitative HIV RNA in plasma
81
HIV: Immunodeficiency occurs when ___ of ___ cell outstrips replenishment
destruction / CD4+
82
anti-HIV drugs
``` NRTI NNRTI Protease inhibitors Fusion inhibitors Integrase inhibitors ```
83
HIV resistance indicated by rise in viral load
Level of replication**error rate of HIV polymerase | Detect by sequencing RT & protease, integrase genes

Pathology (4 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2025 Bold Learning Solutions. Terms and Conditions