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Pharmacology III > Exam 3 > Flashcards

Exam 3 Flashcards

1
Q

how many human cells in body vs microbial cells?

what % of cells in human are microbial?

A
  • 10^14 human cells
  • 10^13 microbial cells
  • 90% of cells in the human body are microbial
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2
Q

What determines if an organism is a pathogen?

A
  • characteristic of virulence (ability to cause infection)
  • non-pathogens = avirulent
  • can have different strands of same organism that are virulent or avirulent (ex. TB H37Rv is virulent, TB H37Ra is avirulent)
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3
Q

Types of host-bacterial interactions (4)

A
  • infestation: distinct from bacterial infections - animal parasites such as worms
  • infectious disease: manifestations of the fight due to pathogenic origins
  • mutualism: relation between two different organisms in which both benefit
  • opportunist: pathogens that attack persons with a compromised immune system
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4
Q

Who do opportunistic pathogens usually attack?

A
  • those on immunosuppressants or immunocompromised
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5
Q

Commensal Microbiota

A
  • makeup of microbiota depends on various factors: environment, nutrition, stress, age, etc
  • normal microbiota are important
  • microbiota varies depending on anatomic sites
  • contributes to immune defense
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6
Q

Difference between a pathogen and commensal

A
  • pathogens can establish in areas devoid of commensal populations
  • pathogens possess inherent ability to cross barriers and evade hosts defenses
  • pathogenic characteristics are genetically encoded
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7
Q

Innate immunity

A
  • early response: recognition and pro-inflammatory response
  • non-clonal distribution, all cells of a class are identical
  • perfect self-nonself discrimination
  • recognition in conserved molecular patterns (LPS, glycans, mannans)
  • response is co-stimulatory molecs, cytokines (IL-1b, IL-6), chemokines (IL-8)
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8
Q

Adaptive Immunity

A
  • later response: elimination of pathogens in late phase
  • very specific recognition
  • clonal distribution, all cells of a class are distinct
  • imperfect self-nonself discrimination (selected in individual somatic cells)
  • recognition in detailed molecular structure (proteins, peptides, carbohydrates)
  • response is clonal expansion, IL-2, effector cytokines (IL-4, IFNgamma)
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9
Q

Timeline for Innate, Early induced innate, and adaptive immune responses

A
  • innate immunity: immediate, 0-4 hours
  • Early induced innate response: early, 4-96 hours
  • Adaptive immune response: late, >96 hours
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10
Q

Innate Immunity: Physical Barriers

A
  • Barriers to infection –> skin (pH 5-6)
  • tight junctions between cells
  • mucus lining interior epithelial surface (coated with Mucin and other glycoproteins reduces ability of microbes to stick)
  • Antimicrobial peptides
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11
Q

Antimicrobial peptides also called what and what it do

A
  • defensins

- can create holes in membrane of bacteria

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12
Q

Places where epithelial surfaces provide first line of defense (4)

A
  • Skin
  • Gut
  • Lungs
  • Eyes/Nose/Oral cavity
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13
Q

Phagocytic cells (overview)

A
  • macrophages long lived and abundant in areas where infection likely to occur (among first cells to encounter invading microbes)
  • Neutrophils are most abundant white blood cell (short lived and not present in normal healthy tissue)
  • both unleash weapons once they phagocytose the pathogen (NADPH oxidase complex which kills pathogen but is also highly toxic)
  • key is pathogens need to be recognized for this to happen
  • production of these toxic compounds leads to a respiratory burst (increased O2 consumption)
  • macrophages survive this but neutrophils usually die.. major component of pus in wounds
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14
Q

Neutrophils sense ____ of pathogenic DNA

A
  • CpG tracts
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15
Q

Innate immunity: conserved pathogenic features

A
  • human cells recognize conserved pathogenic features (Pathogen-associated molecular patterns –>PAMPS)
  • recognition of these triggers innate immune response
  • inflammatory responses
  • apoptosis of autophagy of infected cell
  • phagocytosis by cells such as neutrophils and macrophages
  • complement action
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16
Q

Lipopolysaccharide

A
  • conserved pathogenic feature of gram (-) bacteria

- has lipid component, sugar component, and antigen component

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17
Q

Innate Immunity: Pattern Recognition Receptors (PRRs)

A
  • responsible for detection (binding) of PAMPS
  • Toll-like receptors (TLRs) represent major family and most extensively studied class of PRRs
  • also cytoplasmic PAMP receptors (RLR, NLR) and DNA sensors
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18
Q

Toll-like receptors (TLRs)

A
  • major family of PRRs, 10 primary TLRs
  • abundant on epithelial cells lining lungs and gut
  • abundant on macrophages and neutrophils
  • act as an alarm system for both the innate and adaptive immune systems
  • membrane bound
  • PAMP recognition by leucine-rich repeat on outside of membrane, gives signal to Toll/interleukin-1 receptor (TIR) homology domain
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19
Q

Is there communication between the innate and adaptive immune systems?

A
  • yes
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20
Q

Cytoplasmic PAMP receptors

A
  • RIG-1-like receptors (RLR)
  • NOD-like receptor (NLR)
  • less studied that TLRs
  • responsible for detecting PAMPs inside of cells
  • inside our cells, have the ability to detect DNA and RNA that is non-self
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21
Q

PAMPs and detection by TLRs, RLRs, NLRs, and DNA sensors

A
  • TLRs: viruses, gram (+), gram (-), fungi, protozoa
  • RLRs: just RNA of viruses (primarily good at detecting intracellular RNA)
  • NLRs: DNA, RNA of viruses, DNA and PG of gram (+)s, and DNA, PG, and Flagellin of gram (-)s
  • DNA sensors: DNA of viruses, DNA of gram (-) and gram (+)
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22
Q

Fungi have b-glycan and mannan that are detected by TLRs.. what category are those molecules?

A
  • polysaccharides
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23
Q

TLRs and adaptive immunity

A
  • pathogens that usually cause harm evade the innate immunity
  • pathogen binds to PRR on cell membrane with stimulates release of IL-12 and also stimulates a T-cell to bind
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24
Q

Complement pathway

A
  • non-adaptive immunity pathway
  • 3 distinct pathways (Alternative pathway, lectin pathway, classical pathway) involving 20 interacting proteins
  • binding domains that can tag outside of a pathogen
  • surveillance proteins that see what is tagged and respond through signaling of neutrophils and others
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25
Q

lectins

A
  • proteins that bind sugars
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26
Q

membrane-attack complex

A
  • part of the complement pathway

- make a hole in the pathogen and allows content to escape

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27
Q

engulfment of C3 fragments

A
  • part of the complement pathway

- pathogens are tagged with C3, phagocyte comes and engulfs

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28
Q

Human Health and Gut Microbiota

A
  • 500-1000 different species of bacteria in humans
  • normal gut microbiota helps with digestion and immunity
  • altering microbiota results in disease esp in adults (crohn’s, obesity)
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29
Q

majority of antibiotic resistance found where?

A
  • in hospitals because of the potent antibiotics used there.. pathogens can develop broad-spectrum resistance
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30
Q

What colors do gram (+) vs gram (-) stain?

A
  • Gram (+) : purple, thick wall takes up stain

- Gram (-) : red, stain washes away with alcohol from outer membrane, then perfused with safarin

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31
Q

in general what shapes are gram (+) vs gram (-)s

A
  • gram (+): clusters, grape-like

- gram (-): rod-like, smaller

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32
Q

Which gram-positive bacteria doesn’t stain?

A
  • Mycoplasma
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33
Q

Antibiotic resistant Threat levels criteria

A

how much infection they cause in US and world and what are the antibiotic resistance patterns that makes it a problem

  • ranges from concerning to serious to urgent
  • few gram + in urgent, many in serious
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34
Q

Microbial Resistance Evolution

A
  • WT, Multidrug resistant (MDR), extremely drug resistant (XDR, resistant to >3 antibiotic categories)
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35
Q

Staphylococci

A
  • Gram positive cocci in CLUSTERS
  • coagulase negative except for S. aureus which is coagulase positive
  • colonize skin, nose, axilla, groin
  • range from benign to pathogenic
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36
Q

what does coagulase +/- tell us?

A

-differentiates whether to treat and what to treat with

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37
Q

primary pathogen

A
  • causes infection in patients w/ and w/o risk factors
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38
Q

Staphylococcus Aureus

A
  • numerous infections
  • # 1 cause of bloodstream infections in US
  • multi-drug resistance
  • high morbidity and mortality
  • MRSA (methicillin-resistant staph aureus)
  • classified as “serious”
  • 11,000 deaths/year, 80k severe infections/yr
39
Q

Pathogenicity of Staphyloccus Aureus

A
  • can cause toxic shock syndrome

- can attach to many surfaces: joints, valves

40
Q

Pathogenicity of Staphylococci

A
  • toxin production
  • TSST-1, Panton Valentine Leukocidin (PVL) Superantigen toxins, alpha-cytotoxins
  • accessory gene regulator
  • microcapsule (ghost capsule) can live with or without a capsule
  • slime-adhesion (biofilm) production
41
Q

S. aureus virulence factors (5 main categories) and notes about resistance

A
  • Attachment, persistence, evading/destroying host defenses, tissue invasion/penetration, toxin-mediated disease and/or sepsis
  • very tolerant to antibiotic therapy
  • many antibiotics have been tried, the S. aureus becomes resistant
42
Q

MRSA encodes resistance to ____ which is the backbone to antibiotics

A
  • b-lactam
43
Q

Vancomycin-resistant S. aureus

A
  • threat level concerning
  • plasmid with resistance: not common, but multiple types
  • only 13 cases in 10 years in US
  • leaves little to no treatment options
44
Q

Hospital associated S. aureus epidemiology

A
  • MRSA, multi-drug resistant
  • variety of infection types
  • invades pop at risk
  • reduces fitness of the pathogen (not rapidly aggressive)
  • less common virulence factors
45
Q

Community associated S. aureus epidemiology

A
  • susceptible to many non b-lactams
  • variety of infection types but most commonly in skin infections
  • invades normal healthy people
  • increased fitness (not harboring as much resistance in genome, can be more fit)
  • more common virulence factors
46
Q

S. epidermis

A
  • not really a pathogen, will infect when on things
  • collinizer
  • often a contaminant when found in culture
  • adheres to prostetic surfaces (biofilm formation)
  • prosthetic joints, IV catheters, surgical site infections examples of where it harbors
  • biofilm leads to antibiotic resistance that’s hard to treat
47
Q

Streptococcus species (2 main groups)

A
  • b-hemolytic and a-hemolytic
  • b-hemolytic has group A, B, and C
  • a-hemolytic has s. pneumoniae and viridans streptococci which has group D
48
Q

Streptococci features

A
  • classification on how they lyse RBCs (A,B,C,D,G,H,K)
  • Toxin production (scarlet fever, “flesh eating bacteria”)
  • often found in normal flora
  • infection types: cellulitis, abscess, URI, LRI, bacteremia, endocarditis, septic arthritis, neonatal sepsis
49
Q

S. pneumonia

A
  • a-hemolytic
  • virulent and pathogenic diplococci
  • major cause of meningitis, CAP, otitis media, other URI
  • also colonizer of mouth nasopharynx
  • encapsulated (polysaccharide capsule) with over 90 serotypes
  • target for vaccine (adults 25 valent vaccine, 9 in children, 13 in children since 2010)
  • reduced susceptibility to penicillins, macrolides, fluoroquinolones becoming a concern
  • drug resistant s. pneumonia
  • threat level serious
  • PCN and erythromycin resistant
  • 1.2 mil infections/yr, 7k deaths
50
Q

S. pneumoniae reasons why differences in vaccine coverage

A
  • different strands affect different age groups
  • younger children: PCV7 more likely
  • as age, PPV23 more likely
51
Q

S. Pyogenes

A
  • Group A strep
  • virulent and pathogenic
  • common cause of strep throat, impetigo, cellulitis, necrotizing faciitis, toxic shock syndrome
  • most common in children and elderly
  • still highly sensitive to penicillin
  • erythromycin-resistant subset
  • threat level concerning
  • 1300 infections/yr, 160 deaths
52
Q

S. algalactiae

A
  • Group B strep
  • normal vaginal flora in up to 40% of women
  • if (+) treat continuously during delivery
  • infection types:
  • Children: #1 neonatal sepsis
  • immunocompromised adults: pneumonia, bacteremia, endocarditis, UTI, SSTI
  • PCN treatment still most effective
  • can be resistant to Clindamycin
  • threat level concerning
  • 7600 cases, 440 deaths
53
Q

Enterococcus species

A
  • Gram-positive cocci in chains
  • normal flora of GI, mouth, female genital tract
  • not very pathogenic but highly drug resistant
  • associated infections: bacteremia, IE, UTI, wounds
  • organisms: E faecalis and E faecium
  • vancomycin resistant enterococci (VRE) continues to increase
  • serious threat level
  • 20,000 infections and 1300 deaths/yr
54
Q

Gram Pos Anaerobes

A
  • Normal flora of mouth, URT, GI, skin, and female genitourinary tract
  • commonly occur as polymicrobial infections
  • infections: aspiration pneumonia, GI, SSTI
  • cocci and bacilli
55
Q

E faecalis

A
  • enterococcus species
  • common
  • more antibiotic susceptible
56
Q

E faecium

A
  • enterococcus species

- nosocomial, antibiotic resistant (aminoglycosides, b-lactams, glcopeptides)

57
Q

gram pos cocci (anaerobes) (2 and where located)

A
  • mouth
  • peptococcus, peptostreptococcus
  • mostly PCN and clyndamycin suceptible
58
Q

gram pos bacilli (anaerobes) (4) and where located

A
  • lower gi
  • clostridium, propionibacterium, lactobacillus, actinomyces
  • suceptibility varies by organism
59
Q

Clostridium species (2)

A
  • c. perfingens

- c. difficile

60
Q

c. perfringens

A
  • Clostridium species
  • gas gangrene
  • produces toxins and acidic enzymes that cause tissue necrosis
  • rapidly progressive, high mortality rate
  • may involve other Clostridium species
61
Q

c. difficile

A
  • cause of antibiotic associated pseudomembranous colitis
  • spore form difficult to eradicate
  • produces A/B toxin causing GI tissue destruction and necrosis
  • threat level urgent
  • causes life-threatening diarrhea
  • 250,000 infections per year
  • 14,000 deaths
  • 1 BILLION in excess medical costs / year
62
Q

Corynebacterium species (diptheriae)

A
  • corynebacterium diptheriae
  • produces a deadly toxin resulting in organ failure and death
  • PCN and erythromycin are generally recommended
  • vaccination for this
63
Q

Corynebacterium and actinomyces

A
  • widely distributed in the environment as normal inhabitants of soil and water
  • common colonizing organisms
  • indicated in multiple infection types
64
Q

Bacillus spp

A
  • bacillus anthracis
  • gram-positive rod from soil
  • non-anthrax species are normally contaminants of human cultures
65
Q

Anthrax (bacillus anthracis)

A
  • 3 routes of exposure:
  • cutaneous: naturally occurring, 95% of all anthrax cases
  • GI: associated within 1-5 days after eating undercooked meat
  • inhalational: bioterrorism route: universally fatal w/o antibiotics
  • many antibiotic options for treatment!
66
Q

Listeria monocytogenesis

A
  • aka listeria
  • uncommon cause of illness in the general population
  • specific groups are susceptible: neonates, pregnant women, elderly, transplant, and others with impaired cell-mediated immunity
  • mostly foodborne transmission
  • intracellular and able to move from cell to cell without being exposed to antibodies, complement, or neutrophils
  • manifestations: CNS meningitis, endocarditis, bloodstream infection, septic emboli, febrile gastroenteritis
  • treatment: beta-lactam plus aminoglycoside
67
Q

Atypical Bacteria: 3 categories

A
  • Mycoplasma
  • Ureaplasma
  • Mycobacteria
68
Q

Mycobacterium

A
  • Gram (+) “ghosts”, acid fast +
  • commonly found in water and soil
  • infections: lung, skin and soft tissue, lymph nodes, GI tract, other
  • M. tuberculosis and nontuberculous mycobacteria
69
Q

Myobacterium Tuberculosis (Mtb)

A
  • Aerobic, non-spore forming, non-motiile bacillus
  • high cell wall lipid content
  • slow growing 15-20 / hour turnover
  • carried in airborne particles
  • 10% infection risk with + PPV (vaccine)
  • Multi-drug resistance prevlant
  • historically significant pathogen
  • humans only reservoir for species
  • started germ theory
70
Q

M. tuberculosis worldwide

A
  • 1/3 world’s population infected with TB
  • leading killer of people living with HIV
  • much eradication in US
71
Q

Risks for antibiotic resistance in TB

A
  • exposure to a person who has known-antibiotic resistant TB
  • exposure to person with active TB who has had prior treatment for TB and whose susceptibility tests unknown
  • exposure to person with active TB from areas in which drug-resistant TB is prevalent
  • exposure to person who continues to have positive sputum smears after 2 months of combo chemotherapy
  • travel in an area of high prevalence drug resistance
72
Q

M. Tuberculosis identification

A
  • culture is gold standard
  • may take weeks to grow
  • Acid-fast bacilli = mycobacteria
  • Mtb can be detected in any biological fluid
  • QuanterFERON gold: detection of latent and active TB (blood test)
73
Q

Latent vs active TB: Latent

A
  • infected (alive bacteria, not active)
  • skin or blood test positive
  • normal chest x-ray or sputum, no symptoms, not contagious
  • requires single drug treatment, 3-5% risk active Mtb in year 1, 5% lifetime risk thereafter
  • treatment lowers to <1%
74
Q

Latent vs active TB: Active

A
  • infected (alive and active bacteria)
  • skin or blood test positive
  • abnormal chest x-ray or sputum
  • symptoms of disease, coughing, fever
  • contagious
  • requires multi-year treatment
75
Q

TB vaccine

A
  • Bacillus Calmette- Guerin (BCG) vaccine
  • live- attenuated strain of M. bovis
  • often used in young children throughout much of the world with high TB prevalence
  • 60-80% decrease in disease
  • does not prevent infection, but does often prevent progression to clinical disease
  • effectively prevents disseminated disease in young children
  • increases likelihood of positive PPD
76
Q

Non-tuberculosis mycobacteria (1)

A
  • Mycobacterium Avium-intracellulare (MAI)
  • primarily disease of HIV/AIDS
  • many others
77
Q

Drug-resistant TB threat level

A
  • threat level serious
78
Q

Antibiotic Targets and resistance in Mtb

A
  • inhibit cell wall synthesis (isonazid, ethambutol)
  • inhibit RNA synth (Rifampin)
  • disrupt energy metabolism and plasma membrane (pyranzinamide)
  • COME BACK TO THIS
79
Q

Nontuberculosis Mycobacteria

A
  • M. avium-intracellulare (MAI)
  • environmental organism, relatively avirulent in the normal host
  • infection: pulmonary, systemic, and lymphadenitis (children), other sites less common
  • Prevention: 1 antibiotic; treatment: multiple
  • More than 120 species of Nontuberculous Mycobacteria (NMT)
  • environmental organism, common water source
  • M. Fortuitum and M. abscessus common in skin/soft tissue, bone, and resp infections
  • treatment often complicated and long
80
Q

Mycobacterium Leprae

A
  • armadillos (WATCH SLIDE)
81
Q

MAC/MAI

A
  • Mycobacterium avium and mycobacterium intracellulare (MAI) –> MA complex (MAC)
  • found in water, soil, and animals, not spread from person to person
  • causes pulmonary disesase, lymphadenitis, and disseminated disease
  • lymphadenitis mostly children
  • pulmonary disease mostly older patients with COPD
  • disseminated disease: patients with AIDS with CD4 cell count < 50/mm
82
Q

Clinical Manifestations and Diagnosis of MAC

A
  • WATCH
83
Q

What other two atypicals make up 25% of community acquired pneumonia (CAP) besides mycoplasma pneumoniae?

A
  • Legionella pneumoniae

- Chlamydophila pneumoniae

84
Q

Legionella Pneumoniae

A
  • Legionnaires Disease
  • widespread in water
  • actually a gram (-) rod, not a true atypical
  • treatment options: fluorquinolones, macrolides, tetracyclines
85
Q

Chlamydia Pneumoniae

A
  • Often causes mild RTIs
  • actually a gram (-) rod, not a true atypical
  • obligate intracellular pathogen
  • causes epidemics of CAP (military bases, schools, nursing homes)
  • often cannot be differentiated from other CAP organisms
  • detected in clinic by: Serologic testing to identify anti-C. pneumoniae immunoglobulin G (IgG), IgA, and IgM antibodies… also PCR testing and other rapid testing
  • treatment options: fluoroquinolones, macrolides, tetracyclines
86
Q

Mycoplasma spp

A
  • prokaryotes lacking a cell wall = no gram-stain
  • smallest known free living organism
  • intracellular and extracellular pathogen
  • M. pneumoniae, M. penetrans, M. genitalium, M. fermantans, and M. hominis
  • outbreaks in perosns with close contact and commonly described for pneumonia
  • no cell wall and therefore susceptible to non-cell wall active antibiotics
  • fluoroquinolones, macrolides, tetracyclines
87
Q

Ureaplasma

A
  • 7 species identified
  • Ureaplasmas and highly prevalent in the genital tracts of healthy sexually active women, with infection rates of 60-70% (10-20% for males)
  • U. parvum strains account for 70% of ureaplasms; 30% U. urealyticum
  • opportunists of the lower genital tract
88
Q

U. urealyticum clinical implications

A
  • associated with adverse pregnancy outcome including chorioamionitis, intrauterine infection, and premature birth
  • supperative arthritis in patients with hypogammaglobulinemia
  • neonatal disease: pneumonia, meningitis, sepsis
  • low birthweight babies (<1 kg) at increased risk
  • non-cell wall active antibiotics required for treatment
89
Q

how many organisms are listed as urgent, serious, or concerning? (how many gram pos vs gram neg)

A
  • 18

- 50% are gram negative

90
Q

why has antibiotic discovery gone down?

A
  • no incentive for companies to produce antibiotics
91
Q

Gram negative membrane makeup?

A
  • two cell membranes, (balloon within a balloon) thin cell wall between membranes
  • surface protein on cell wall: lipopolysaccharide (LPS)
92
Q

2013-2015: how many new FDA approved antibiotics? how many gram negative ones?

A
  • 5 new antibiotics

- 2 activity against gram negatives

93
Q

newer antibacterial agents incorporate which types of inhibitors?

A
  • beta lactamase
94
Q

Pathogenic features of gram negatives

A
  • infections
  • endotoxin- lipopolysaccharide on cell wall
  • intrinsic resistance mechanisms exist in some species
  • Enterotoxins
  • community and nosocomial (hospital) acquisitions

Pharmacology III (18 decks)

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