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pathophysiology > lecture 9 pathogenic organisms > Flashcards

lecture 9 pathogenic organisms Flashcards

1
Q

stats

A

-cells:virus:bacteria is 1:1:1
-about 1kg of our body weight
-full body weight in organisms extracted (in feces) in a year
-1400 microbial pathogens (viral, bacterial, fungi, protozoa, parasites) - only 1% of microbes
- many unknown/ yet to be discovered, new ones each year
- 16m die from infectious disease each year worldwide

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2
Q

disease in low-income vs high-income countries

A

low income: infectious diseases are the problem (communicable)

high income: mostly non-infectious diseases (non-communicable) - access to medical care controls, microbial infections

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3
Q

3 types of pathogenic organisms

A

bacteria
viruses
fungi

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4
Q

archea

A
  • similar to bacteria but evolutionarily distinct
  • NO pathogenic members
  • prokaryotes: single-celled microbes, SIMILAR TO BACTERIA, no nucleus, share characteristics with eukaryotes as well as introns
  • important part of human microbiome (in GUT, SKIN, MOUTH)
  • mostly ANAEROBIC (low oxygen environments, hard to culture)
  • many found in EXTREME ENVIRONMENTS (high temp - hot springs, pressure, salt, deep sea - methanogens) - distinct metabolic pathways to survive

compared to bacteria: some pathogenic, cause trouble looking for a place to live, change the environment to suit their growth (endo/ exotoxins, enzymes) H pylori - ulcers

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5
Q

4 characteristic to classify bacteria

A
  1. shape and arrangement
    - coccus, bacillus, spiral
  2. gram stain reaction
    - gram+, gram-
  3. biochemical and growth characteristics
    - anaerobic and aerobic
    - spore formation
    - biochemical profile
  4. antigenic structure
    - antigens in cell body, capsule, flagella (motility)
    - laborious and time consuming but low tech
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6
Q

modern bacteria classification

A
  • modern taxonomy (naming) based on genomic sequence (particularly 16S ribosomal RNA, highly conserved)
    -also based on array of proteins and peptides
  • tests are automated using MALDI-TOF-MS (matrix assisted later desorption/ ionization time of flight mass spectrometry
  • PCR amplification (Viruses)
  • can identify bacteria specific peptide/ protein profiles
  • fast, specific
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7
Q

major classes of pathologic bacteria: coccus
clusters, chains, pairs, kidney bean-shaped pairs

A

COCCUS = SPHERICAL (circular)

clusters = staphylococci
chains = streptococci
pairs = diplococci
kidney bean-shaped in pairs = Neisseriae

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8
Q

major classes of pathologic bacteria: bacillus
square ends, rounded ends, club shaped, comma shaped

A

BACILLUS = ROD-SHAPED

square ends: bacillus anthracis (anthrax)
rounded ends: mycobacterium tuberculosis (TB)
club shaped: corynebacterium (diptheria)
comma shaped: vibrio (cholera)

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9
Q

spiral organisms
tightly coiled, relaxed coil

A

SPIRAL = SPIRAL
tightly coiled: treponema pallidum (syphilis)
relaxed coil: borrelia (lyme)

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10
Q

what is gram staining?

A
  • bacteria are classified as either gram-positive or gram-negative based on ABILITY TO RESIST OR RETAIN CERTAIN DYES
  • based on chemical and physical properties of their CELL WALLS

(gram+ and gram-, shape or chained - does not relate to pathogenicity - wide variety!!)

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11
Q

Gram staining steps and results

A

dried fixed suspension of bacteria prepared on a microscopic slide
1. crystal violet (purple dye) - stains peptidoglycan
2. gram iodine (acts as mordant)
3. alcohol or acetone (rapid decolorization)
4. safranin (red dye) - stains cell membrane

gram positive = purple stain (resists decolorization and retains purple stain)
gram negative = red stain (can be decolorized)

can also be gram variable in bacteria with THIN peptidoglycan layers (clostridium)
not all bacteria can be stained (mycobacterium - no cell wall)

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12
Q

structure of peptidoglycan

A

units of NAG and NAM joined laterally and vertically by amino acids
(carb backbone, amino acid side chain, peptide cross-bridge)

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13
Q

gram positive cell wall

A
  • thick peptidoglycan with multiple layers combined with teichoic acid, susceptible to penicillin
  • no lipopolysaccharide
  • cell wall rigid
  • inner membrane
  • usually produce exotoxins (secreted by cell)
  • show high tolerance towards dryness/ physical stress

*gram+ spore forming clostridium/ bacillus

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14
Q

gram negative cell wall

A
  • thin peptidoglycan with single layer without teichoic acid, protected
  • lipopolysaccharide present
  • less rigid
  • inner/ outer membrane
  • periplasmic regulated
  • produce both exotoxins and endotoxins
  • less tolerance, rarely spore forming
  • lipid A and porins (contribute to resistance to some antimicrobial agents)

*more pathogenic than gram+

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15
Q

extracellular pathogens

A
  • wound infection, pneumonia, UTI
  • use an opening or wound to gain entry but multiply on tissues or intercellular spaces

staphylococcus aureus, streptococcus pyogenes/ pneumoniae, pseudomonas aeruginosa, Escherichia coli, bacillus anthracis, helicobacter pylori

try to find their way in, but don’t enter cells, just want a place to live

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16
Q

intracellular pathogens

A
  • trojan horse - enter cells by PHAGOCYTOSIS and multiply in host cells in phagosomes/ vacuoles or escape into cytosol (macrophages/ dendritic cells, epithelial cells/ hepatocytes)
  • many can then exit and thrive EXTRACELLULARLY as well

listeria monocytogenes, chlamydia trachomatis, mycobacterium tuberculosis, salmonella enterica, legionella

*many viruses also exploit phagocytes as well (measles, yellow fever, small pox, ebola HCV, HIV, Zika)

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17
Q

staphylococci

A

GRAM+ COCCI, grape-like clusters
normal inhabitants:
- skin (staphylococcus epidermidis)
- nasal cavity (staphylococcus aureus)

  • commonly found on skin and in nose of patients and hospital staff
  • normally not pathogenic (skin provide barrier)
  • OPPORTUNISTIC organisms - serious cases can lead to sepsis
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18
Q

staphylococci strains

A

pathogenic strains cause disease by producing TOXINS
- vomiting and diarrhea; toxic shock
- tissue necrosis
- hemolysis

cause disease by causing INFLAMMATION
can be distinguished by CULTURE on blood agar plates

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19
Q

staphylococci infections

A

SKIN: impetigo, boils (furuncles, carbuncles), nail infection (paronychia), cellulitis, surgical wound infection, eye infection, postpartum breast infections (mastitis), abscess

SEPSIS: wounds and IV drug use

ENDOCARDITIS: infection of lining of heart and valves
- normal and prosthetic valves, IV drug use

PNEUMONIA (in lungs)

bacteria produce a range of immune evasion proteins and virulence factors (enable microbial pathogens to colonize, evade or suppress the immune response)
- some strains are highly resistant to antibiotics (methicillin-resistant Staphylococcus AUREUS, or MRSA)
- S. Aureus (a strain of staph) - produces 100s of immune evasion proteins, affecting a wide range of immune cells/ functions

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20
Q

streptococci

A

GRAM+ COCCI, chains or pairs

normal inhabitants:
- skin, mouth, pharynx (streptococcus viridans), GI, female genital tract (peptostreptococci)
- opportunistic organisms

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21
Q

streptococci diseases

A

PYOGENIC: pharyngitis, cellulitis, endocarditis, urinary tract infection
TOXIGENIC: scarlet fever, toxic shock syndrome
IMMUNOLOGIC: rheumatic fever, glomerulonephritis (induce hypersensitivity)

*can survive in anaerobic or aerobic making them more pathogenic than STAPH

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22
Q

streptococci classification

A

based on the type of HEMOLYSIS and differences in carbohydrate antigens in the CELL WALLS or C carbohydrate (Lancefield classification groups A to V)

most important: A,B,D
categorized further based on BLOOD AGAR CULTURE

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23
Q

streptococci beta hemolysis

A

complete lysis of red cells
(different strains of strep to come…)

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24
Q

streptococci beta hemolysis: group A

A

(over 200 unknown types): many pathogenic strains

(streptococcus pyogenes): causes pharyngitis, strep throat, tissue infections (necrotizing fasciitis, gangrene)

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25
Q

streptococci beta hemolysis: group B

A

(streptococcus agalactiae): Commonly in the anal/ genital tract, neonatal transmission risk, meningitis, sepsis

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26
Q

streptococci beta hemolysis: group D

A

(enterococcus faecalis, streptococcus bovis): urinary, biliary, cardiovascular infections
- difficult to treat and Ab RESISTANT!

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27
Q

streptococci non-beta hemolysis

A

ALPHA HEMOLYSIS: incomplete lysis of red cells (streptococcus pneumoniae, strep mutans (tooth decay)

GAMMA HEMOLYSIS: nonhemolytic, no lysis!

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28
Q

Pneumococci (streptococcus pneumoniae) still strep

A

GRAM+, grow in pairs and short chains
- common cause of bacterial pneumonia, ear infections
- one of the MOST COMMON infections in humans
- childhood vaccination important

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29
Q

gram- cocci

A
  • most are nonpathogenic members of the genus NEISSERIA

2 pathogenic members:
MENINGOCOCCUS
- causes meningitis (inflammation of membranes surrounding brain and spinal cord)
- vaccination important for protection (12y)
GONOCOCCUS
- causes gonorrhea (STI)

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30
Q

gram+ bacilli

A

make of several important groups
-characterized based on OXYGEN REQUIREMENTS and SPORE FORMING

  • corynebacteria, listeria, bacilli, clostridia
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30
Q

spore forming vs non spore forming

A

spore forming: bacteria can go into dormant state if there is a lack of nutrients or abx that are killing them
- they can stay in this form until they get more nutrients and then they can come back (this is very problematic for abx)

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31
Q

aerobic non-spore forming gram+ organisms (most are pathogenic)

corynebacteria

A
  • NONPATHOGENIC inhabitants of the SKIN and SQUAMOUS body surfaces with the exception of C. diphtheriae (ulcerative inflammation of throat and injure to heart and nerve tissues)
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32
Q

aerobic non-spore forming gram+ organisms (most are pathogenic)

listeria monocytogenes

A
  • FOOD contaminant found widely in nature (soil, plants, intestinal tract)

*both: can cause systematic illness leading to meningitis, brain abscess and serious complications to fetus by transmission through placenta

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33
Q

aerobic spore-forming gram+ organisms

bacillus

A
  • ONLY 1 pathogenic member (bacillus anthracis: ANTHRAX)
  • inhalation of spores (can survive forever as spores) germinate and spread rapidly in alveoli
    -facultative anaerobe (makes ATP by aerobic respiration if oxygen is present, but is capable of switching to fermentation if oxygen is absent)
  • lung macrophages ingest spores and carry to LN for germination
  • produce toxins - tissue destruction leading to severe pulmonary and systemic infection
  • fever, chest pain, SOB, 20% fatality without treatment in days
  • bioweapon capability (storage - contaminant)
  • requires long course AB tx - spores not susceptible
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34
Q

aerobic spore-forming gram+ organisms

clostridia

A

tend to produce potent toxins found in soil and the environment

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35
Q

aerobic spore-forming gram+ organisms

clostridia: gas gangrene

A

clostridium perfringens

  • contaminate wounds, proliferate in dead/ necrotic muscle tissue (ferment necrotic tissue)
  • release tissue destroying toxins with systemic effects (sepsis)
  • toxins also cause neutrophil lysis
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36
Q

aerobic spore-forming gram+ organisms

clostridia: tetanus

A

C. tetani
- produces neurotoxin that causes sustained muscular contractions (bone fractures)
- symptoms days to weeks after exposure
- fatal due to effect on respiratory muscles
(very dangerous if not treated early)

37
Q

aerobic spore-forming gram+ organisms

clostridia: botulism

A

C. botulinum
- food poisoning from toxin ingestion of improperly cooked/ stored food
- infants particularly susceptible
- highly toxic (400g of toxin would kill every person on the planet)
- produces neuroparalytic toxins - pathology not caused by infection

38
Q

aerobic spore-forming gram+ organisms

clostridia: intestinal infection

A

C. Diff
- antibiotic-associated colitis
- broad spectrum Ab use
- GI tract issue
(kills bacteria you want but also goes into gut and destroys gut floor, since spore-forming it can go into dormant state)

39
Q

gram- pathogens (really dangerous)
list all 9 BACILLI

A
  1. hemophilus influenzae
  2. Yersinia pestis (plague)
  3. salmonella
  4. shigella
  5. campylobacter
  6. legionella
  7. vibrio cholerae (cholera)
  8. helicobacter pylori
  9. E.coli
40
Q

gram- pathogens: 1. hemophilus influenzae

A

lung infections, CNS, skin, blood

41
Q

gram- pathogens: 2. Yersinia pestis (plague)

A

plague
PNS degradation
lack of sensation leads to injury/ limb loss

42
Q

gram- pathogens: 3. salmonella

A

food poisoning, GI infection

43
Q

gram- pathogens: 4. shigella

A

food poisoning, GI infection

44
Q

gram- pathogens: 5. campylobacter

A

food poisoning, GI infection

45
Q

gram- pathogens: 6. legionella

A

severe pneumonia
inhaled from contaminated water (infects alveolar macrophages)

46
Q

gram- pathogens: 7. vibrio cholerae (cholera)

A

severe, acute, watery diarrhea
(significant mortality in developing places)

47
Q

gram- pathogens: 8. helicobacter pylori

A

stomach inflammation - ulcers

48
Q

gram- pathogens: 9. E.coli

A

GI tract resident
some strains- ingested raw/ uncooked animal products (typically develop toxic effects like inflammation, anemia, bloody diarrhea, abdominal pain)

49
Q

pathogenic organisms - spiral (2 main ones)

A

syphilis (treponema pallidium)
lyme disease (borrelia burgdorferi)

50
Q

lyme disease (spiral)

A

Borrelia burgdorferi
- transmitted through infected tick bit to spread throughout body

STAGE 1: circular bulls eye rash, flu symptoms
STAGE 2: cardio (heart palpitations), neuro (meningitis, facial paralysis) and joint pain
STAGE 3: chronic arthritis and neuro deficits (memory, fatigue, insomnia)

51
Q

acid-fast bacteria (2 main ones)

A

waxy coat, difficult to stain (stain can’t penetrate)
- causes granulomatus inflammation (macrophage infection)

tuberculosis (mycobacterium TB)
leprosy (mycobacterium leprae)

52
Q

acid-fast bacteria: Tuberculosis

A

tuberculosis (mycobacterium TB)
- lungs, (airborne, highly contagious)
- most show no symptoms (latent) 10% progress (increased in immunodeficient)
- chronic cough (blood in the septum), fever, weight loss “consumption”

53
Q

acid-fast bacteria: Leprosy

A

mycobacterium leprae
- leads to skin lesions/ peripheral damage (lack of sensation, muscle weakness, vision loss)
- low infectivity and pathogenicity (95% do not progress to disease - often slow (up to 20y) to develop)
- binds to SCHWANN CELLS - chronic inflammation causes most/ all damage

54
Q

Chlamydiae

A

gram-
non-motile bacteria
deficient in enzyme production and can only live as parasite of infected cell

over 100 million new infections/ year (most common ID in US/ Canada)
- OBLIGATE INTRACELLULAR PARASITES
- form inclusion bodies in infected cells after they are phagocytosed
- rigid cell wall and reproduce by a distinct intracellular cycle
- susceptible to tetracycline and erythromycin it responds to abx)
- no vaccine!!

(viral-like properties, it can’t live outside of a cell or produce on their own, they need our cells!!)

55
Q

the infection cycle of chamydia

A

(attachment and entry of elementary body to target cell) - “like” a virus!

  1. target cell nucleus
  2. formation of reticulate body
  3. binary fission of reticulate bodies
  4. reorganization of reticulate bodies into elementary bodies (elementary bodies in large cytoplasmic inclusion)
  5. multiplication ceases
  6. release of elementary bodies
  7. infectious elementary body

targets cell nucleus, multiply in there, release as infectious

56
Q

chlamydial diseases: psittacosis (pneumonia)

A

inhalation of dried bird feces

57
Q

chlamydial diseases: trachoma (trachomatis A,B,C)

A

chronic conjunctivitis
blindness

58
Q

chlamydial diseases: nongonococcal urethritis

A

(men)
spread to other areas

59
Q

chlamydial diseases: cervicitis

A

(women)
lead to salpingitis (inflamed fallopian)
pelvic inflammatory disease
infertility
ectopic pregnancy (egg in fallopian)

60
Q

chlamydial diseases: neonatal inclusion conjunctivitis

A

newborn from infected mother

61
Q

Rickettsiae and Ehrlichiae

A

OBLIGATE INTRACELLULAR PARASITES (typically endothelial cells)
need our cells to reproduce

transmission: insect bites
- lack of genes for glycolysis or biosynthesis of a.a./ nucleosides
- both respond to some abx

62
Q

Rickettsiae diseases

A

infects, proliferates, endothelial cells in SMALL BLOOD VESSELS OF SKIN
- causing damage, leakage of blood into surrounding tissues (rash and edema)

  1. rocky mountain spotted fever (ticks)
    - east coast spring and early summer (flu-like)
    - rash after 2-6 days, hands and feet then trunk, affects CNS
  2. rickettsia pox (mites from mice)
    - flu-like
    - full body rash
  3. typhus
    - flu-like
    - rash (epidemic: lice, endemic: fleas, mites)
63
Q

Ehrlichiosis

A
  • susceptible to tetracycline or chloramphenicol (abx)
  • transmitted via bite of an arthropod vector (ticks, mites, lice, fleas)
  • infect and multiply in neutrophils or monocytes
  • cause febrile-like flu (muscle aches, chills) with skin rash
  • transmission enhanced by poor hygiene, overcrowding, wars, poverty
  • member of the family is similar to possible mitochondria descendent (similar to mitochondria)
64
Q

mycoplasma

A

primary atypical pneumonia: mycoplasma pneumoniae
- most common in winter, young adults, outbreaks in groups
- cough, sore throat, fever, headache, malaise (unhappiness), myalgia (muscle aches)
- resolves spontaneously in 10 to 14 days

smallest, NO CELL WALL, free-living bacteria
- about the size of a virus (0.3 micrometer)

simple CELL MEMBRANE (cholesterol), but no cell wall
- medical implications: stains poorly
- penicillin and cephalosporin are not effective - but do respond to some abx (tetracycline, erythromycin)
- can reproduce OUTSIDE living cells, can grow on artificial media

65
Q

viruses classification

A

all obligatory intracellular parasites

nucleic acid structure: DNA or RNA (ss,ds,+/-ve), enclosed in a CAPSID with OUTER ENVELOPE made of LIPOPROTEIN (often from host cell)

size and complexity of genome: varies 9-400 genes, HIV, HSV

smaller than cells: 20-300 nm diameter

cannot be seen under a light microscope

also have glycoproteins

66
Q

viruses: nucleiod

A

genetic material, DNA or RNA, NOT BOTH

67
Q

viruses: capsid

A

protective protein membrane surrounding genetic material

68
Q

viruses: coat/ envelope

A

combination of host membrane and viral proteins (retrovirus)
- also non-enveloped viruses (adenovirus)

69
Q

main point about viruses

A

very specific in their target cells (always! one specific receptor, they have a main effect)

detected through DNA isolation and other ways, needs to be sequenced

70
Q

viruses as obligate intracellular parasites

A
  • must reproduce or replicate within cells
  • LACK METABOLIC ENZYMES, rely on host’s metabolic processes for survival
  • DO NOT have nucleus, ribosomes, mitochondria, and lysosomes, cannot synthesize proteins or generate energy
  • DO NOT multiply by binary fission or mitosis

(but adenoviruses enter as a whole)

71
Q

modes of action of viruses

A

invasion of susceptible cell leads to:

  • asymptomatic latent viral infection (HSV, VZV: herpes zoster/ shingles) - dormant in neural cells
  • acute cell necrosis and degeneration (ebola)
  • cell hyperplasia and proliferation (HPV)
  • slowly progressive cell injury (HCV) - injury caused by constant immune activation
  • neoplasia (HPV)
  • destruction of immune system (HIV)

formulation of INCLUSION BODIES (protein aggregates) from prolific viral replication resulting in cellular toxicity (smallpox, rabies)

72
Q

fungi

A

plantlike organisms without chlorophyll
- most are obligate AEROBES

2 main types:
- yeasts (small ovoid/ spherical)
-molds (branching and filamentous)

cell wall: chitin (not peptidoglycan)

cell membrane: ergosterol and zymosterol (not cholesterol)

growth factors: high humidity (moist), heat, dark areas with oxygen supply

other fungi: bread, cheese, wine, beer production
- frequently associated with decaying matter
- molds: spoilage of foods (fruit, grains, veg, jams) - don’t cause pathogenic issues
- and athletes foot

Young and healthy? you don’t have to worry about fungi?

73
Q

fungi causing infections in presence of certain conditions

A

most are present everywhere in our natural habitat/ environment

may cause INFECTION in the presence of certain CONDITIONS:
- chronic disease
- immunocompromised (opportunistic) HIV, Cancer tx (chemo is toxic to WBCs)
- loss of regular bacterial flora (competition) antibiotics
- lack of hygiene - superficial skin infections (dermatophytes)

74
Q

fungi treatment

A

antifungal drugs
topical treatment in mild cases
(usually very easy to treat)

75
Q

fungal infections

A

most are pathogens of low virulence (low damage to host) which only become life threatening in susceptible (from coinfection or chronic disease), IMMUNOCOMPROMISED (like HIV)

  1. superficial fungal infections (skin)
  2. mucous membranes (Candida albicans): common in immunocompromised patient with infection on TONGUE, MOUTH, ESOPHAGUS (thrush)
  3. aspergillus fumigatus (spores from decaying plant matter)
    - can result in severe PULMONARY and SYSTEMIC disease in immunocompromised
    - contributes and exacerbates allergic asthma development
  4. histoplasmosis, coccidioidomycosis, blastomycosis, cryptococcosis
    - inhaled sores in DUST
    - usually acute, self-limited respiratory function
    - in severe cases, if they can invade blood vessels - they can cause widespread systemic disease
76
Q

4 types of antimicrobials

A

medicines used to PREVENT and TREAT infections caused by microorganisms in humans, animals and plants (works against only ONE type of organism)

  1. antibiotics (antibacterials)
    - cellulitis, urinary tract infection, TB, STIs like gonorrhea
  2. antivirals
    - colds, flu, chickenpox/ shingles, COVID, HIV!!!!
  3. antifungals
    - thrush, ring worm, athletes foot
  4. antiparasitics
    - malaria, threadworm and headlice (immune system used a lot here)
77
Q

antimicrobial resistance

A

when the microorganisms change or mutate over time and get to a point where they no longer respond to medicines previously used to treat them

78
Q

viruses - defences

A

bodily defenses against viral infections
- (innate/ adaptive) formation of interferons: broad spectrum antiviral agent, inhibits viral replication (non-specific), activates immune cells
- cell-mediated immunity (CD4/ CD8 T cells-specific)
- humoral defenses (B-cell -Ab production)
- cell-mediated (against infected cells) often SUPERIOR to Humoral

treatment with antiviral agents
- block viral replication (HIV/HCV)
- prevent virus from invading cell (HIV)
- limited application (toxicity and limited effectiveness - why hard to kill? not alive)
- symptomatic, supportive

*best defense for most viral infections: VACCINATION PREVENTIVE/ THERAPEUTIC COMMUNITY vs personal immunity

*Overall, antivirals aren’t very impressive; they don’t do much for the most part, and we rely on the immune system (viruses aren’t alive) - antivirals are more for SYMPTOMATIC TX AND SUPPORT

79
Q

antibiotics: penicillins and cephalosporins (and vancomycin and bacitracin)

A
  • inhibits synthesis of bacterial cell wall
  • leads to swelling-rupture and cell membrane injury-death
80
Q

antibiotics: chloramphenicol, tetracycline, macrolide, and “mycins” (not vancomycin)

A
  • inhibits synthesis of microbial proteins, ribosomal subunits
  • targets DNA synthesis, replication
    (inhibits bacterial protein synthesis - translation)
81
Q

antibiotics: sulfonamides, trimethoprim

A
  • inhibits folic acid synthesis
  • inhibits bacterial metabolic functions (loss of metabolic functions)
82
Q

antibiotics: ciprofloxacin, norfloxacin, ofloxacin (quinolones)

A
  • inhibits bacterial DNA synthesis
83
Q

antibiotics things to consider…

A

route and delivery
ex. vancomycin (blocks cell wall synthesis):
- only effective against gram+
- not absorbed through intestine if taking orally (good for C.diff) - this is good so it can stay there and do its job
- must be IV if you want it for systemic use (ex. for widespread diseases ex. sepsis)

84
Q

antibiotics more…

A

SEE LECTURE NOTES FOR COMPLETE LIST OF DRUGS AND IMAGES OF THEIR ORGANIZATION

85
Q

antibiotics: adverse effects

A
  • toxicity - kidney injury, other tissues
  • hypersensitivity - penicillin allergy/ anaphylaxis
  • alteration of normal bacterial flora - C. diff
  • development of resistant strains (spontaneous mutation, plasmid-acquired resistance)
    • bacteria is good at acquiring resistance (can gain resistance by presenting over and over in small amounts)
86
Q

mechanisms for circumventing (avoid) effects of antibiotics

A
  • develop antibiotic enzymes (penicillinase)
  • change cell wall structure (repel Ab)
  • change internal metabolic machinery (Ab loses functioning binding)
87
Q

antibiotic sensitivity tests (tests to see how resistant the antibiotic is - to see if that bacteria will respond to a certain antibiotic, it it’s sensitive it will treat the bacteria and you can use it)

A
  • tube dilation (measures highest dilution that inhibits growth in test tube)
  • disk method (inhibition of growth around disk indicated sensitivity to antibiotic)
  • MALDI-TOF-MS identification of strains with known abx-resistance characteristics
  • also need to consider patient allergy/ resistance, organ function and ability of Ab to access infection site
  • tetracycline levels - kidney function
  • need to consider route of administration/ delivery
88
Q

causes of abx resistance

A
  • over prescribing
  • poor infection control in hospitals and clinics
  • lack of hygiene and poor sanitation
  • patients not finishing their treatment
  • over-use of antibiotics in livestock and fish farming
  • lack of new antibiotics being developed

growing issue!
- penicillin first known to be resistant, before it was used!! (bacterial strains were already resistant to it before it was used

89
Q

abx pictures and stats (bacterias that are getting more resistant)

A

SEE SLIDES

90
Q

phage therapy

A

(attach, inject, destroy)

  • therapeutic approach from 1917 but was replaced by abx by 1940s with the introduction of PENICILLIN
  • resurgence in last 10-15 years to treat RESISTANT STRAINS OF BACTERIA (MRSA) - experimental/ clinical trials now
  • bacteriophages “phages”, virus that attach to bacterial cells and inject their genome into the cell to kill or inhibit bacterial function - HALTING INFECTION

advantages: much more specific than abx
- reduced side effects
- reduced risk of bacterium developing resistance
- won’t impact beneficial bacteria (host biome) or host cells

disadvantages: difficulty of FINDING an EFFECTIVE PHAGE for a particular infection

!!!phage therapy is particularly effective over abx at PENETRATING the BIOFILM generated by ANTIBIOTIC-RESISTANT BACTERIA
(viruses for bacteria, this is coming back)

91
Q

abx resistance over time

A

number of abx was decreasing and we thought we were running out of abx due to resistance but now there are more approvals coming out to treat resistant strains TREAT RESISTANT STRAINS (starting 2013 good)

pathophysiology (10 decks)

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