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Y1 - Pathology > 14_Pathology of Infections > Flashcards

14_Pathology of Infections Flashcards

1
Q

what are the attributes of infectious agents?

A
  • can replicate either in the environment or in a host (obligate needs a host)
  • usually provoke a host response
  • may be ACELLULAR, UNICELLULAR, or MULTICELLULAR
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2
Q

vwhat are the 2 acellular infectious agents?

how are they different?

A

Prions and Viruses

  • PRIONS
    • proteinaceous particles resist inactivation by procedures that modify RNA/DNA
    • causes spongiform encephalopathies in humans
    • mech: formation of insoluble aggregates of intracellular protein w/ modified tertiary structure
  • VIRUSES
    • infectious agents that attach to and invade host cells;
    • contain RNA or DNA
    • contain few or no synthetic enzymes or other biochem agents required for replication
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3
Q

prions:

define, and diseases

A
  • infectious proteins that do NOT contain RNA or DNA (resilient in environment)
  • prion protein is a normal protein in brains; but in JC disease – the protein becomes protease-resistant
  • diseases –> resulting in dementia
    • kuru
    • Jakob-Creutzfeld disease
    • bovine spongiform encephalopathy (BSE)
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4
Q

prion protein (PrP):

define

A

protein changes from alpha-helical –> BETA-PLEATED SHEET, which is protease resistant

(prion protein is normal UNTIL interacting w/ infectious prion –> induces the ^conformational change)

(helical - happy

beta-pleated sheet - BAD)

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5
Q

viruses:

define

A
  • contain RNA or DNA; infectious agents that attach to and invade host cells to replicate
  • (*NOT considered prokaryotes NOR eukaryotes)
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6
Q

prokaryotes (bacteria):

define, structure

A
  • def: unicellular organism that lacks a membrane-bound nucleys, mitochondria, or other organelles
  • bacteria are PROKARYOTES
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7
Q

different categories of bacteria, and examples of each

A
  • obligate intracellular bacteria lacking ATP synthesis_:_ CHLAMYDIA, RICKETTSIA
  • lack cell call, bind to resp mucosa by P1 adhesion; (smallest free living organisms): MYCOPLASMA
  • replicate in cytoplasm of endothelial cells (hemorrhagic vasculitis): RICKETTSIA
  • possess lipid coats –> protects against inactivation/clearance by host: mycobacteria
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8
Q

layman’s terms for mycoplasma respiratory disease?

A

walking pneumonia;

tends to cluster in families

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9
Q

which bacteria cause tuberculosis?

A

mycoBACTERIA

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10
Q

eukaryotes:

define, and examples

A
  • def: organisms w/ cells containing well-defined membrane-bound nucleus and organelles
  • ex:
    • humans
    • fungi
    • protozoa
    • algae
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11
Q

best stain to identify fungi?

A

GMS or PAS

  • Grocott’s methenamine silver stain (GMS) is also good for picking up bacteria as well;
  • Periodic acid–Schiff (PAS)
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12
Q

helminths:

define, disease mech, transmission

A
  • define: multicellular pathogens; parasitic worms
  • mech: disease is often from response to pathogen and proportionate to # of organisms
  • tx:
    • arthropods: ectoparasites; incl: lice, bedbugs, fleas, stinging insects, mosquitoes, which may be disease vectors
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13
Q

best way to prevent transmission of malaria?

A

mosquito nets; to protect when sleeping

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14
Q

four diff’t types of host-parasite relationships

A
  • parasitism: interactions that exploit the living environment
  • colonization: proliferation of parasite in host w/o causing disease
  • subclinical infection: host undergoes injury, but remains free of symptoms
  • clinical infection: disease; damage to host
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15
Q

3 key mechanisms of disease by infectious agents?

A
  • directly: contact cell –> causing direct cell death
  • toxic infectious agent component (LPS) - indirectly killing cells at a distance, or releasing enzymes that digest tissue components or damage BVs –> causing ischemic damage
    • either toxic or releases exotoxins
  • induce host immune reponse –> cuase tissue damage (HBV, HCV, or TB)
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16
Q

what are various transmission of infectious agents?

A
  • contact
  • resp droplets
  • fecal-oral (vibrio cholerae)
  • sexual transmission
  • insect/animal vector
  • vertical transmission (from mother to baby)
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17
Q

routes by which host defenses are breached?

A
  • SKIN: wound or burn; low pH, fatty acids
  • RESP TRACT: mucociliary clearance, IgA, alveolar macrophages
  • GI TRACT: gastric acidity, bile IgA, gut flora
  • GU TRACT: flushing, acid from vaginal flora
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18
Q

mechanism of toxin elaboration (by vibrio cholerae)

A
  • V. cholerae elaborates a toxin in the intestine –> causes diarrhea (but does not actually invade the tissue)
    • toxin consists of subunit A (enzymatic) and subunit B (binding)
    • subunit A manipulates the host –> affects adenylate cyclase so NaCl goes into the gut lumen –> clears out the sodium –> causing electrolyte imbalance
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19
Q

vibrio cholerae:

sxs, transmission, tx, outbreaks

A
  • sxs: often fatal, diarrheal disease –> dehydration and electrolyte imbalace
  • transm: fecal-oral
  • tx: electrolyte replacement therapy
  • outbreaks:
    • often erupts following large scale tragedies e.g. earthquake in Haiti 2010
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20
Q

prior to discovering the true mechanism of Vibrio cholerae, what was thought to be the cause (historically)?

A

MIASMA THEORY: diseases—such as cholera, chlamydia, or the Black Death—were caused by a miasma, a noxious form of “bad air”, also known as night air. The theory held that the origin of epidemics was due to a miasma, emanating from rotting organic matter

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21
Q

how does a nucleid acid w/in a capsid –> enter the cell?

A
  1. adhere to cell membrane
  2. engulfed by cell membrane
  3. w/in the cell in a vesicle
  4. intracellular release to escape vesicle
22
Q

how does an enveloped helical nucleocapsid enter the cell?

A
  1. adhere to cell membrane
  2. fusion of envelope w/ cell membrane
  3. intracellular release of nucleocapsid into cell
23
Q

diff’t mechanisms of immune evasion by infective agents?

A
  • antigenic variation (flu)
  • inactivation of host antibodies/complement
  • resist phagocytosis –> produces a capsule (tuberculosis)
  • suppress immune response
    • e.g. inhibiting MHC expression and Ag presentation (antigen presentation)
24
Q

what are the diff’t ways by which host develops RESISTANCE TO INFECTIONS?

(host-parasite relationships)

A
  • neutralize/inactivate toxins by antibodies
  • cytotoxic/cytolytic rxns directed against infectious organisms
  • delayed hypersensitivity –> results in mobilization of phagocytes to the infection site
  • granulomas localize toxic material and organisms
25
Q

which types of organisms are known for causing granulomas to localize toxic materal and organisms (in host-parasite resistance to infections)?

A

MYCOBACTERIA (tuberculosis)

and fungal infections

26
Q

list the factors that affect resistance?

A
  • **immune system deficiencies:
    • immune globulin deficiency, defect in lysosome fxn, thymic aplasia, leukocyte adhesion deficiency, neutrophil oxidative burst deficiency
  • hormonal factors (steroids)
  • aging
  • nutritional status
27
Q

key immune defense mechanisms for:

bacterial infections

A
  • antibody (B-lymphocyte, immune complex)
  • lysis by complement
  • inflammatory response
28
Q

key immune defense mechanisms for:

viral infections

A
  • antibody (immune complex)
  • T-lymphocytes
29
Q

key immune defense mechanisms for:

mycobacterium

A
  • T lymphocytes (DTH)
  • granulomatous
30
Q

key immune defense mechanisms for:

protozoa

helminths

fungi

A
  • protozoa: *antibody; T-lymphocytes
  • helminths: *antibody; granulomatous
  • fungi: T-lymphocytes; granulomatous
31
Q

what are the key hematologic effects of infection?

A
  • “shift to the left” –> leukocytosis (inc. in neutrophils and bands)
  • anemia; assoc. w/ chronic disease
  • **erythrocyte sedimentation rate
    • spec gravity of RBC: 1.09
    • spec grav of plasma: 1.03
    • inc. rouleaux formation
  • **C reactive protein (CRP) –> elevated and indicates infxn
  • coagulation (fibrinogen can be acute phase protein)
32
Q

acute phase response to infxn INCREASES WHICH MARKERS?

A
  • increase in:
    • cytokines
    • complement (C3)
    • C-reactive protein; opsonins
    • Fibrinogen
    • ceruloplasmin (elaborated by liver)
33
Q

EFFECTS OF INFECTION

(symptoms)

A
  • fever, caused by pyrogens
  • cardiovascular
    • inc. in HR
    • dec in BP; (hypotension)
    • **SHOCK (if severe)
  • renal
    • inc excretion of protein and glucose in urine
    • retenion of BUN/creatinine (azotemia)
    • low urine output(oligouria)
  • hepatic
    • inc. protein synthesis (hypergammaglobulinemia)
34
Q

what are the 6 major patterns of host response to infectious agents?

how is this helpful?

A
  • patterns
    1. suppuration (abscess)
    2. mononuclear and granulomatous inflammation
    3. cytopathic effect and proliferative rxn (CPE)
    4. tissue necrosis
    5. chronic inflammation and scarring
    6. neoplasia
  • helpful bc infectious agent may be inferred from the pattern
35
Q

suppuration

define, sxs, examples

A
  • response to infxn –> inc in neutrophils
    • inc vascular permeability
    • leukocytic (neutrophilic infiltration)
    • causes tissue destruction
  • forms abscess: from accumulation of pus (from accumulation of neutrophils) in a confined space; usually occurs w/ deep seating of pyogenic bacteria in tissue
  • ex:
    • staphylococcus
    • streptococcus (rheumatic fever - image)
36
Q

mononuclear inflammation:

define, cause

A
  • def: Mononuclear cell infiltrates are characteristic of inflammatory lesions, where white blood cells, mainly macrophages and lymphocytes, collect at the site of injury to help clear away the debris
    • results in mixture of host cells: lymphocytes, plasma cells, macrophages
    • but proportion of inflammatory cells may depend on the pathogen
  • causes:
    • viruses
    • intracellular bacteria
    • intracellular parasites
    • helminths
37
Q

a lot of plasma cells in mononuclear inflammation is indicative of what?

A

treponemes;

syphilis infection

38
Q

granulomatous inflammation:

define, mech, cause

A
  • def: small nodules comprised of macrophages of epithelioid appearance, and giant cells mixed w/ lymphocytes, plasma cells, and PMNs
  • mech: formed by host cells reacting to poorly-digested foreign antigens –> to isolate the foreign antigens
  • causes
    • bacteria: tuberculosis, leprosy, syphilis
    • dusts and metals: silicosis, berylliosis
    • fungi and parasites: histoplasmosis and schistosomiasis

sarcoidosis in image

39
Q

cytopathic effect (CPE):

define, mech, cause

A
  • def: formation of blisters by viral infxn and damage to epithelial cells
  • mech: may result in formation of viral aggregates visible as inclusion bodies by light microscopy
  • cause: viral-mediated cell injury
40
Q

neoplasia:

define, causes

A
  • def: inducing the growth of warts and/or cancer
  • causes:
    • viruses such as HPV
41
Q

which are the key HPV variants that cause cancer?

A

16, 18, and 45

42
Q

angioinvasion:

def, sxs

A
  • def: colonization of blood vessels
  • sxs:
    • can cause thrombosis;
    • or cause infarction of tissue supplied by infected vessel
43
Q

necrotizing inflammation:

def, mech, sxs, cause

A
  • def: severe tissue damage
  • mech: caused by powerful toxins (characterized by few inflammatory cells)
  • sxs: resembles infarction or ischemic injury
  • causes:
    • *clostridium perfringens - a gram positive rod –> causes gas gangrene w/ extensive necrosis of skeletal muscle, gas production and sparse inflammation
    • (or any clostridium)
44
Q

which type of inflammation is characterized by sparse/or few inflammatory cells?

A

necrotizing inflammation

(characterized by few inflammatory cells)

45
Q

why is Clostridium difficult to contain, esp in hospital setting?

A
  • due to SPORE formation and transport
  • (bc spores are not killed by alcohol; very difficult to kill)

need to wash hands to prevent spread

46
Q

pseudomembranous inflammation:

def, mech, cause, risk factor

A
  • def: yellow and white exudate (up to 20 mm thick) distributed on surface of the colon –> forming pseudomembrane
    • mech: **NOT ACTUALLY INVADING THE TISSUE; psudomembrane (coating) formed from mucin & neutrophils –> assoc. w/ damage of crypt epithelial cells
  • cause: Clostridium difficile (gram POSITIVE rod; obligate anaerobe) - produces 2 diff’t toxins –> cuase pseudomembranous colitis
  • risk factors:
    • antiobiotic use
    • advanced patient age
47
Q

which infectious diseases cause the most worldwide deaths every year?

A
  1. Tuberculosis - ~1.2M deaths/yr
  2. HIV/AIDs - ~1M deaths/yr
  3. Malaria - ~400,000 deaths/yr

(could also include influenza)

48
Q

tuberculosis:

sxs, frequency

A
  • sxs: image
    • productive cough
    • night sweats
    • fever
    • weight loss
  • frequency
    • 1/3 of world population is affected (90% latent, 10% active)
    • mostly developing countries
    • in 2012 - 8.6 M chronic cases; in 2010 - 1.2-1.4M deaths
49
Q

HIV/AIDS:

sxs, frequency

A
  • sxs: image
    • central, eyes, lungs, skin, GI
  • frequency:
    • second most WW deaths annually
    • global pandemic (36.7M people had HIV WW, w/ 1.8M new infections per year)
    • sl over 1/2 of infected are women, and ~2M are children
    • caused 1M deaths in 2016 (peak in 2005 - 1.9M deaths)
50
Q

malaria:

sxs, frequency

A
  • sxs: image
    • **fever is most known manifestation of malaria
    • spread by mosquitoes
  • frequency:
    • 3rd most deadly infectious disease;
    • WHO estimated 214 M new cases in 2015 –> 438,000 deaths
    • other estimates are 350-550 M cases of falciparum malaria

Y1 - Pathology (14 decks)

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