Clinical ID Flashcards

1
Q

viruses

A
  • 20-30 nm
  • obligate intracellular
  • dependent on host cell metabolism for replication
  • classified by the nucleic acid content of their core and shape of their protein capsid or coat
  • cause acute illnesses
  • capable of lifelong latency and of long term reactivation or of giving rise to chronic disease
  • ex. ebola, herpes
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2
Q

chlamydiae

A
  • 200-100 nm
  • obligate intracellular
  • Can cause GU infections, conjunctivitis, respiratory infections & STDs
  • obligate intracellular pathogens that divide by binary fission, are susceptible to antibiotics, but lack certain cell structures
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3
Q

rickettsiae

A
  • 300-1200 nm
  • obligate intracellular
  • Transmitted by insect vectors (lice, ticks, mites) and can cause Rocky Mountain Spotted Fever, Q Fever, ehrlichiosis &scrub typhus
  • obligate intracellular pathogens that divide by binary fission, are susceptible to antibiotics, but lack certain cell structures
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4
Q

mycoplasmas

A
  • 125-350nm
  • Tiniest free-living organism known and can cause atypical pneumonia & nongonococcal urethritis
  • obligate intracellular pathogens that divide by binary fission, are susceptible to antibiotics, but lack certain cell structures
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5
Q

fungi imperfecti

A

2-200um
-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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6
Q

protozoa

A
  • 1-50 um
  • 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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7
Q

helminths

A
  • 3mm-10m
  • 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
  • 3 classes: roundworms, flatworms, and flukes
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8
Q

prions

A
  • composed of modified host proteins (prion protein)
  • cause transmissible spongiform encephalopathies
  • assoc with neurodegenerative diseases such as kuru, mad cow disease CJD
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9
Q

bacteriophages, plasmids, and transposons

A
  • mobile genetic elements that encode bacterial virulence factors = plasmids and transposons
  • include adhesins, toxins or enzymes that confer antibiotic resistance
  • they can infect bacteria and incorporat themselves into their genome
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10
Q

bacteria

A
  • prokaryotes that lack nuclei and ER
  • capable of synthesizing own DNA, RNA and proteins but rely heavily on host for favorable growth conditions
  • grow both extracellularly and intracellularly
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11
Q

round worms

nematodes

A
  • collagenous tegument and non-segmented structure (hookworms & Trichinella)
  • larvae penetrate skin (often through bare feet), are carried to lungs, go through respiratory tract to mouth, are swallowed, and eventually reach the small intestine. Cycle takes about a week.
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12
Q

flatworms (cestodes)

A
  • gutless worms

- heads sprout a ribbon of flat segments (tapeworms)

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13
Q

flukes (trematodes)

A

-primitive leaflike worms with syncytial integument (schistosomes

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14
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, babesia and ehrlichia while the dog ticks are harmless
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15
Q

breeches to host barriers by commensal bacteria

A
  • skin bacteria can cause infection after etering through cuts
  • GI system- virulent organisms can penetrate the intact mucosal barriers and cause infection
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16
Q

spread and dissemination of mibcrobes

A
  • The major manifestations of infectious disease may arise at sites distant from those of entry (eg. Chickenpox and measles enter through airways but manifest as skin rash
  • Bloodstream invasion is a common event for both non-virulent and virulent microbes.
  • The placental-fetal route is an important mode of transmission.
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17
Q

how microorganisms cause disease

A
  • direct cell death
  • endo/exotoxins
  • secondary response through host immune response
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18
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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19
Q

bacterial virulence

A

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

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20
Q

bacterial adherence

A
  • Adhesins are bacterial surface molecules that bind to host cells
    • lipoteichoic acids, M proteins of S. pyogenes
    • Fimbriae or pili on surface of gram-negative bacteria
  • Entry into macrophages – directed by receptors that recognize antibodies or complement on surface of bacteria
  • Entry into epithelial cells – dependent on interactions between bacterial surface and epithelial cell receptor such as integrins
21
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

22
Q

bacterial exotoxin

A

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

23
Q

immune evasion by microbes

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

24
Q

spectrum of inflammatory responses to infection

A

A. Suppurative (Polymorphonuclear) Inflammation
B. Mononuclear and Granulomatous Inflammation
C. Cytopathic-Cytoproliferative Inflammation
D. Necrotizing Inflammation
E. Chronic Inflammation and Scarring

25
Q

suppurative (polymorphonuclear) inflammation

A
  • Caused by pyogenic bacteria
  • Characterized by increased vascular permeability and leukocytic infiltration by neutrophils
  • Bacteria recruit neutrophils:
  • Directly by release of chemoattractive peptides
  • Indirectly by release of endotoxin which stimulates macrophages to release cytokines that chemoattract neutrophils
26
Q

Mononuclear and Granulomatous Inflammation

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
27
Q

Cytopathic-Cytoproliferative Inflammation

A
  • 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
28
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)
29
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)
30
Q

poliovirus

A

virus
obligate intracellular
= poliomyelitis

31
Q

-Chlamydia trachomatis

A

= trachoma
clamydiae
obligate intracellular

32
Q

-rickettsia prowazekii

A

== typhus fever

obligate intracellular

33
Q

-mycoplasma pneumoniae

A

-extracellular

== atypical pneumonia

34
Q

staphylococcus epidermidis

A

bacteria
= wound infection,
cutaneous

35
Q

vibrio cholerae

A

bacteria
cholera
mucosal

36
Q

streptoccocus pneumoniae

A

bacteria
extracellular
pneumonia

37
Q

mycobacterium tuberculosis

A

bacteria
tuberculosis
facultative intracellular

38
Q

trichophyton sp

A

fungi imperfecti
-cutaneouse
= tinea pedis

39
Q

canadida albicans

A

fungi imperfecta
-mucosal
= thrush

40
Q

sporothrix schenckii

A

fungi imperfecta
-extracellular
= sporotrichosis

41
Q

histoplasma capsulation

A

fungi imperfecta
-facultative intracellular
= histoplasmosis

42
Q

giardia lambi

A

protozoa
-mucosal
= giardiasis

-

43
Q

tyrpanosoma gambiense

A

protozoa
-extracellular
= sleeping sickness

44
Q

trypanosome cruzi

A

protozoa
-facultative intracellular
= chagas disease

45
Q

leishmania donovani

A

protozoa
obligate intracellular
= kala-azar

46
Q

enterobias vermicularis

A

helminths
-mucosal
= oxyuriasis

47
Q

wuchereria bancrofti

A

helminths
-extracellular
= filariasis

48
Q

trichinella spiralis

A

helminths
-intracellular
= trichinosis