L 15 clinical ID Flashcards

1
Q

Prions

A

Composed of modified host proteins (prion protein)

Cause transmissible spongiform encephalopathies

Associated with neurodegenerative diseases such as kuru, mad cow disease, Creutzfeldt-Jakob Disease (CJD).

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2
Q

Viruses

A

Obligate intracellular organisms
Dependent on host cell metabolism for replication
Classified by their nucleic acid content of their core and shape of their protein capsid or coat
Cause acute illnesses (colds, influenza)
Capable of lifelong latency and of long-term reactivation or of giving rise to chronic disease

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3
Q

Bacteriophages, Plasmids, Transposons

A

Mobile genetic elements that encode bacterial virulence factors

Include adhesins, toxins or enzymes that confer antibiotic resistance

They can infect bacteria and incorporate themselves into their genome (eg. Toxin genes of Vibrio cholerae and Corynebacterium diphtheriae)

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4
Q

Bacteria

A

Prokaryotes that lack nuclei and endoplasmic reticulum

Capable of synthesizing own DNA, RNA and proteins but rely on host for favorable growth conditions

Grow both extracellularly and intracellularly

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5
Q

characterists of Chlamydiae, Rickettsiae, Mycoplasmas

A

Obligate intracellular pathogens, divide by binary fission, susceptible to antibiotics, but lack certain cell structures

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6
Q

Chlamydiae

A

Can cause GU infections, conjunctivitis, respiratory infections & STDs

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7
Q

Rickettsiae

A

Rickettsiae: Transmitted by insect vectors (lice, ticks, mites) and can cause Rocky Mountain Spotted Fever, Q Fever, ehrlichiosis & scrub typhus

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8
Q

Mycoplasmas

A

Mycoplasmas: Tiniest free-living organism known and can cause atypical pneumonia & nongonococcal urethritis

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9
Q

Fungi

A

Possess thick cell walls
Growth patterns include budding yeast and slender tubes called hyphae
Hyphae produce fruiting bodies called conidia
Infect superficial layers of skin (Tinea)
Deep fungal infections can spread systemically (some species limited to geographic regions eg. Blastomyces, Histoplasma, Coccidioides)
Opportunistic fungi that normally colonize the body may cause disease in immunosuppressed patients such as lethal pneumonia & tissue necrosis

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10
Q

Prozoa

A

Parasitic, single-celled organisms with motility, pliable plasma membranes and complex cytoplasmic organelles

Can be transmitted:
sexually (Trichomonas)
via the fecal-oral route (Giardia)
by blood – sucking insects (Leishmania)
by contact with infected cats or eating cyst ridden, undercooked meat (Toxoplasma gondii)

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11
Q

Helminths

A

Parasitic worms that are highly differentiated multicellular organisms
Complex life cycles
Most are dependent on an intermediary host or vector for asexual reproduction
Disease is often caused by host inflammatory responses (ex. Schistosomiasis) and in proportion to the number of infecting organisms

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12
Q

3 classes of helminths

A
  1. Roundworms (nematodes): collagenous tegument non-segmented structure (hookworms & Trichinella)
  2. Flatworms (cestodes): gutless worms, heads sprout a ribbon of flat segments (tapeworms)
  3. Flukes (trematodes): primitive leaflike worms with syncytial integument (schistosomes)
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13
Q

Ectoparasites

A

Arthropods (lice, ticks, bedbugs, fleas)
Attach and live on skin
May be vectors for other pathogens such as deer ticks transmitting Lyme disease

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14
Q

HOW DO MICROORGANISMS CAUSE DISEASE

A
  • Direct Cell Death
  • Endotoxins/Exotoxins
  • Secondary Through Host Immune Response
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15
Q

Mechanisms of Viral Injury

A
  1. Viruses inhibit host cell DNA, RNA or protein
    synthesis.
  2. Viral proteins insert into host cell’s plasma
    membrane.
  3. Viruses replicate efficiently and lyse host cells.
  4. Viral proteins on the surface of the host cells are
    recognized by immune systems and host
    lymphocytes attack the viral infected cells.
  5. Viruses damage cells involved in secondary
    infections.
  6. Viral killing of one cell type causes the death
    of another.
  7. Slow virus infection and latency.
  8. In addition to causing injury, viruses induce cell
    proliferation and transformation which can lead
    to neoplasms.
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16
Q

Mechanisms of Bacteria-Induced Injury

A
  1. Bacterial Virulence
  2. Bacterial Adherence
  3. Bacterial Endotoxin
  4. Bacterial Exotoxins
17
Q

Bacterial Adherence

A

a. Adhesins are bacterial surface molecules that bind to host cells (Fig. 8-2)
lipoteichoic acids, M proteins of S. pyogenes
Fimbriae or pili on surface of gram-negative bacteria
b. Entry into macrophages – directed by receptors that recognize antibodies or complement on surface of bacteria
c. Entry into epithelial cells – dependent on interactions between bacterial surface and epithelial cell receptor such as integrins

18
Q

Bacterial Endotoxin

A

Lipopolysaccharide (LPS): structural component of outer cell wall in gram negative bacteria; induces host cytokine release to cause fever, activate macrophages & B cells

19
Q

Bacterial Exotoxins

A

Toxins released by bacteria that interfere with cellular metabolism & allow bacteria to outgrow competing bacteria (ex. Diphtheria toxin, Vibrio cholera toxin, anthrax toxin)

20
Q

Bacterial Virulence depends on

A

ability of bacteria to adhere, invade, & deliver toxic moieties

21
Q

Ways microbes evade the immune system

A
  1. Being inaccessible to the immune response
  2. Resisting complement-mediated lysis and phagocytosis
  3. Varying or shedding antigens
  4. Causing specific & non-specific immuosuppression
22
Q

types of inflammatory responses to infections

A

A. Suppurative (Polymorphonuclear) Inflammation

B. Mononuclear and Granulomatous Inflammation

C. Cytopathic-Cytoproliferative Inflammation

D. Necrotizing Inflammation

E. Chronic Inflammation and Scarring

23
Q

Suppurative (Polymorphonuclear) Inflammation

A

Caused by pyogenic bacteria
Characterized by increased vascular permeability and leukocytic infiltration by neutrophils
Bacteria recruit neutrophils:
1. Directly by release of chemoattractive peptides
2. Indirectly by release of endotoxin which stimulates macrophages to release cytokines that chemoattract neutrophils

24
Q

Mononuclear and Granulomatous Inflammati

A

Diffuse, predominantly mononuclear interstitial infiltrates form in response to pathogens

Include lymphocytes (syphilis chancres) and macrophages (mycobacterium granulomas) depending on the pathogen and host responses

Granulomatous inflammation occurs when aggregates of altered macrophages form or fuse to form giant cells

25
Q

Cytopathic-Cytoproliferative Inflammation

A

Cytopathic-Cytoproliferative Inflammation

Reactions characteristic of virus-mediated damage to individual host cells in the absence of host inflammatory responses

Result in:
Inclusion bodies (CMV)
Polykaryons following cell fusion (measles)
Blisters due to cell damage (Herpesvirus)
Morphologic lesions (venereal warts/HPV)
Dysplastic changes & cancers

26
Q

Necrotizing Inflammation

A

Rapid and severe tissue damage with predominant cell death in the absence of inflammatory infiltrates

Caused by uncontrolled viral infections, secreted bacterial toxins or cytolysis of host cells in protozoa infections (eg. Necrotizing fasciitis caused by Group A streptococcus)

27
Q

Chronic Inflammation and Scarring

A

Chronic inflammation can lead to either complete healing or to extensive scarring

Several inert organism cause damage by the scarring response (ex. schistosome eggs)