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MMMD 1 - QH > Micro: Intro & Bacteria & others > Flashcards

Micro: Intro & Bacteria & others Flashcards

1
Q

Staphylococcus?
ex?
what is coagulase-negative staph?

A 
gram+ve
cocci
aerobe
clusters
-normal flora:
ex: 
-Staphylococcus aureus = MRSA

Coagulase-negative: have proteins that coagulate in plasma = form fibrin clot around bacteria to hide
-S. epidermidis, S.lugdunensis (bacteremia, endocarditis), S.saprophyticus (UTI)

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2
Q

Streptococcus?
ex?
alpha vs beta hemolytic?

A 
gram+ve
cocci
aerobe
chains
-normal flora:
ex: 
Beta-hemolytic: hemolysis through culture
-S. pyogenes (Group A streptococci)
-S. agalactiae (Group B strepto)

Alpha-hemolytic: cells look green
-S. pneumoniae: **gram+ve DIPLOCCI!

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3
Q

Enterococcus?

causes»

A 
gram+ve, cocci, aerobe, chains
-normal flora:
ex:
-E faecium, E. faecalis
-VRE

-GI tract, GU tract normal flora
-contact transmission
-virulence: adhesin, hemolysin
» UTI, abdo

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4
Q

Corynebacterium?

A 
gram+ve
baccilli
aerobe
(look like zigzag Vs)
-normal flora:
ex: C. jeikeium, C. urealyticum, C. diphtheriae
causes: UTI
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5
Q

Bacillus?

A 
gram+ve
baccilli
aerobe
-forms spores
-normal flora: skin
ex: B. anthracis
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6
Q

Ecoli

A

gram-ve, baccilli, aerobe
-normal flora: GI
-contact
virulence: fimbriae, hemolysin, flagella, cytoxin, enterotoxin
» UTI, hospital-ac pneumonia, abdo, gastroenteritis

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7
Q

Haemophilus?

A

gram-ve
coccobacilli
aerobe
-normal flora: oropharynx

H.influenzae
-contact, droplet
virulence: capsule IgA protease
»pneumonia, sinusitis, otitis media, meningitis

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8
Q

Neisseria?

A 
gram-ve
diplococci
aerobe
-normal flora:
ex: N. meningitidis, N. gonorrhea
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9
Q

Clostridium?

A 
gram+ve
baccilli
ANerobe
-soil, hospital, GI tract
-contact
-virulence: spores, exotoxins
ex:
Cdiff, C. tetani, C.botulinum, C.perfringens

> > tetanus, botulism, gas gangrene, diarrhea

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10
Q

Bacteroides?

A 
gram-ve
baccilli
ANerobe
-normal flora: GI
virulence: lipase, protease, capsule
>>intraabdo abscesses, bacteremia
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11
Q

Gram Staining procedure?

A
  • get sample
  • assess adequacy (too much squamous epithelial cells = reject), identify any non-bacteria present
  • smear (from specimen or from grown culture), fix smear
    1. Crystal violet - stains purple
    2. Idodine - set stain
    3. Wash with alcohol, water - thick stays purple; thin washs off
    4. Safranin - dye pink. thick stays purple, thin pink.

see under microscope:
purple = gram +ve (thick peptigoglycan wall)
pink = gram -ve (thin wall)

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12
Q

Why does gram staining work?

A
  1. peptidoglycan layer: thick crosslinkage resistat alcohol decolourization
  2. magnesium ribonucleate in gram +ve wall: affinity for crystal violet-iodine
  3. cell wall permeability: gram +ve less lipid = less effect of decolourizer
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13
Q

Yeast?

ex?

A

-fungi
-single eukaryotic, ovoid/spherical
-rigid cell wall
-budding
fuzzy, hyphae
ex: Candida

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14
Q

Chlamydia trachomatis?

A

atypical bacteria: inracellular

  • GU tract
  • contact
    virulence: intracellular

> > UTI, pelvic inflammatory disease

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15
Q 
Staphylococcus aureus?
morph:
resevoir:
transmission: 
virulence factors:
causes>
A 
-gram+ cocci, aerobe, clusters
Resevoir: skin, nares
transmission: contact, fomites
virulence factors:
-adhesin - stick
-Protein A - disable Ab
-capsule - prevent phago
-leukocidin
-hemolysin - break down RBC, WBC
-catalase - break down phago
-DNAase
-exotoxins > Toxic Shock Syndrome, Exfoliatin, Enterotoxin

causes> lots

  • skin infections > abscess
  • bacteremia
  • endocarditis
  • pneumonia
  • food poisoning
  • toxic shock
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16
Q

What is Protein A?

M protein

A

A; binds Ab to prevent action
M: prevents phagocytosis
-virulence factor for bacteria

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17
Q

Virulence Factors are based on 2 things?

A
  • invasion

- host damage

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18
Q

Staphylococcus epidermidis?

A
  • gram+ cocci, aerobe, clusters
  • skin
  • contact
    virulence: adhesins, capsule, biolfilm
  • less virulent than S.aureus
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19
Q

What is group A strep?

A

-Streptococcus pyogenes
-gram+, cocci, chains, aerobe
-in skin, pharynx
-contact, droplet
virulence factors = adhesins, M protein, capsule, hemolysins, enzymes
-SPExotoxin = superantigen

causes>

  • pharyngitis
  • impetigo - skin-skin lesion
  • necrotizing fasciitis
  • bacteremia
  • toxic shock
  • septic arthitis, rheumatic fever, glomerulopnerphritis)
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20
Q

Streptococcus pneumoniae?

A

-gram+, DIPLOCOCCI, aerobe
-normal flora: oropharynx
-droplet, contact
-virulence: capsule, autolysin, pneumolysin, protein A
» pneumonia, sinusitis, otitis media, meningitis, bacteremia

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21
Q

What are enteric pathogens?

A

GI: gram-ve bacilli

ex: ecoli, salmonella, shigella, campylobacter
virulence: enterotoxin, cytotoxin

> > gastroenteritis: diarrhea, hemolytic uremic syndrome, bacteremia

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22
Q

Neisseria meningiditis?

A
  • gram-ve DIPLOCCI, aerobe
  • oropharynx
  • contact, droplet
  • virulence: capsule, IgA protease, endotoxin

> > meningitis, meningococcemia

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23
Q

Neisseria gonorrhoeae

A
  • gram-ve DIPLOCCI, aerobe
  • GU tract
  • contact
  • virulence: pili, antigenic variation, IgA protease

> > UTI, pelvic inflammatory disease, gonoccocemia

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24
Q

What are atypical bacteria?

ex?

A
  • intracellular (chlamydia)
  • lack rigid cell wall (mycoplasma)
  • acid fast bacilli (mycobacterium)
  • partial acid fast (nocardia)
  • spirochetes (treponema pallidum)
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25
Q 
Strict Aerobes
Facultatie anaerobes
microaerophilic
aerotolerant
strict anaerobes
A
  • need O2 else dies
  • can do both but prefers O2
  • depends on O2 but die if too high
  • use anerobic fermentation but can survive in O2
  • dies in O2
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26
Q

Types of virulence factors: invasion (5)

A
  • portal of entry: skin, tracts, transplantattion/transfusion
  • surface colonization: adhesins, use host receptors
  • surviving host defences: Protein A, viral latency, Ab proteases, changing surface antigens, immunosuppression by depleting T cells or messing it up via superantigen, biolfim, intracellular passage, capsules, exotoxins that kill immune cells, adhesins
  • portal of exit: skin, tracts, transplantattion/transfusion
  • transmission
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27
Q

Routes of transmission? (5)

ex:

A
  • contact: direct (mucosa, skin); indirect (hands, fomites), faecal-oral
    ex: HIV, herpes, cdiff
  • droplet: large (>=5microm) propelled 2m through air, land on nasal/oral mucosa
    ex: influenza, resp, neisseria meningtidis
  • airborne: small droplets or skin squams (<5microm) - remain suspended
    ex: TB, measles, varicella zoster
  • vector borne: carried by insects, ticks, mosqu
    ex: west nile, malaria
  • common vehicle: single contaminated item, food
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28
Q

Types of virulence factors: host damage (4)

A
  • damage due to host response (inflammation, loss of func, septic shock)
  • toxins: endo vs exo
  • apoptosis: triggers (HIV, herpes) or block (HPV)
  • mechanical : ex - helminths obstruction
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29
Q

Endotoxins vs exotoxins?

ex?

A

endo: LPS on cell wall is toxic

exo: bacteria treat to help spread or lyse host cells: block protein synthesis, affect cell func, block nerve fnc
-ex:
Tetanus toxin: CNS GABA> stiffness
Botulism: PNS Ach> paralysis, floppy

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30
Q

Normal flora:

skin, oropharynx, colon, GU?

A
  • skin: staphylococcus, corynebaceterium, bacillus
  • oropharynx: streptocci, neisseria, harmophilus, candida
  • colon: enterococcus, ecoli, bacteriodes, clostridium, candida
  • GU: streptococci, candida
31
Q

Benefits vs harm of normal flora

A

Benefits:

  • helps train immune system
  • infection prevention
  • nutrition
  • digestion

Harms:

  • opportunistic infections
  • contaminations
32
Q

Define virulence factors? pathogenicity?

A

vf = traits that make organism pathogenic

p=ability to cause disease

33
Q

Define resevoir. ex?

A
  • living/nonliving thing on which organism lives

ex: human, animal, soil, objects

34
Q

Define incubation period?

A

-time of entry > first sign/symptoms

35
Q

Define period of communicability?

A

-time agent able to be transmitted

36
Q

What are control measures?

A
  • to reduce transmission

- public health, hospital infection control

37
Q

What are public health control measures? (6)

A
  • vaccination
  • post-exposure prophalyxis
  • reporting systems to surveillance
  • contact tracing
  • quarantine
  • outbreak investigation
38
Q

What are infecton control measures? (6)

A
  • surveillance
  • routine practice: washing, ppe, sharps, housekeeping
  • additional precautions: contact, droplets, airborne
  • decolonization: drugs
  • post-exposure prophalyxis: drugs, vaccines
  • outbreak investigation
39
Q

(7) steps of outbreak investigation?

A
  1. confirm outbreak
  2. define cases
  3. epicurve, line listing
  4. assemble team
  5. control measures
  6. evaluate
  7. decide when its over
40
Q

Approach to CXR?

A

-name
-L/R markers
-assess of rotation: clavicle ant; spinous = post
-penetration: should see verterbral body of spine
-degree of inspiration: count ribs - 6th ant; 10th post
if expiration: bigger heart, bigger mediastinum, less ribs

41
Q

What is spine sign?
silhoutte sign?
bronchograms?

A
  • normally: post lung gets darker lower down
  • abnormal: loss of borders bt structures b/c density contrast loss
  • abnormal: see broncho. usually airways same as lung so don’t see. suspect consolidation
42
Q

Chest Xray - what’s white and black?

A 
higher density = white
bone
soft tissue/water
blood
air=black
43
Q

airspace disease (Consolidation) vs instititial disease (edema)

A

c: white lungs, see airways, loss of borders
institial: see thick white borders

44
Q

Atypical signs:
cavitations
miliary
ex:

A

cavitations: black holes with air in lung
ex: pneumonia, TB, fungal

miliary: dissemination > white tiny dots everywhere
ex: TB, fungal

45
Q

Signs of edema on CXR?

A
  • instititial disease
  • cardiomegaly
  • see extra lines: kerly B, thicker fissures, thickened bronchioles (cuffing), “butterfly” (borders are spared)
46
Q

pathogenesis of pneumonia (3 mech)

A
  1. Aspiration - normal flora down resp, inhalation from vomiting, those on ventilation
  2. Inhalation- inhale aerosols with streptrococci pneum
  3. Hematogenous-
47
Q

community vs hosp acquired pneumonia organisms

A 
CAP:
S. pneumoniae
H.influenzae
viruses
*children: more viruses

HAP:
gram-ve bacilli: Ecoli, klebsiella, p.aeruginosa, S.aureus

48
Q

What is pneumonia?

A
  • infectio of lungs > proliferation of organism in alveoli > inflammation.
  • lower resp tract
49
Q

Symptoms of Pneumonia: typical vs atypical?

A
  • fever, chills, cough, sputum, pleuritic chest pain, dyspnea, tachy
  • consolidation on CXR

atypical: dry cough, maybe fever, CXR may not show

50
Q

Complications of pneumonia

A
  • lung abscess
  • empyema - pus in pleural space
  • PEffusion
  • bacteremia
  • metastatic infection
51
Q

Work up of pneumonia:

A 
hx
pe
CXR
arterial blood gas
CBC
blood culture
sputum gram stain and culture

-sometimes: urine antigen for Legionella, serology, pleural fluid culture, sputum for acid fast bacilli (TB)

52
Q

Tx for pneumonia

A
  • Supportive: oxygentation, hydration
  • antimicrobial drugs

prevention: flu vaccine, pneumococcal vaccine

53
Q 
Describe common cold
cause:
symptoms:
dx
tx
A
  • viruses: rhinoviruses, coronaviruses, parainfluenza viruses, adenoviruses…
  • URI: mild resp infection: sore throat, malaise, fever, muscle aches maybe, nasal congestion, rhinorrhea, cough
  • peak 3-4 days; lasts up to 10
    tx: nasal decongestants

**No antibiotics, no antivirals, antihistamines vit C questionable

54
Q 
Describe ACUTE SINUSITIS (rhinosinusitis)
cause:
symptoms:
dx
tx
A

-usually viral
-bacteria: Strep pneumoniea, H.influenzae, S. aureus
-URI + longer 7 days or worsen after 5 days
-bloody nasal discharge, sinus pain, tenderness, toothache, fever, cough
»osteitis, meningitis, brain abscess, venous infection
-last less than 4 wks
-dx: Xray/CT to see inflammation
tx: nothing or antibiotic if bacterial and worsening; inhale steam, irrigation of nasal

55
Q

PHARYNGITIS - common causes

A
  • usually viral - EBV (mono)
  • bacteria: Group A strepto, chlamydia, mycoplasma pneumoniae
  • candida : oral thrush
56
Q

Pharyngitis - Streptococcal

A

-sore throat, fever, abdo, nausea, vomiting, tonsils, lymphnodes, erythema in oral
-self limiting: 3-4days
-antibiotic if risk for rheumatic fever, peritonsillar abscess, worse complications
Dx: throat swab, culture, rapid antigen detection tests
Tx: Penicillin V, amoxicillin
if allergic: Macrolide
if allergic: Clindamycin

57
Q

Pharyngitis - EBV

A

-Mono
-in teens
-sore throat, fever, lymphnodes
-MonoSpot Test: positive for IgM; CBC
»can cause neuro issue, spleen rupture, obstruct airway
-Tx: prednisone

58
Q

What are symptoms of laryngotracheitis?

A

CROUP:
-horse voice, barking cough, inspriatory stridor, possible resp distress
causes: parainfluenza virus, influenza A/B, adenovirus
*agitated children
Tx: IV fluids, oxygen, dexamethasone, epinephrine
-no antibiotics

59
Q

What are symptoms for epiglottitis? causes?

A
  • symptoms: fever, sorethroat, stridor, chills, cyanosis, drooling, breathing diff, swallowing diff, hoarseness
  • Chest Xray - see inflammed epiglottis = thumb sign
  • Tx: support airway, antibiotics
60
Q

What is acute bronchitis?

A

-cough, with/wihtout phlegm, up to 3 weeks
-usually viruses: influenza A, B, parainflu, resp syncytial virus, corona, rhino
-bacteria: mycoplasma, chlamydia pneumoniae, pertussis
dx: CXR
-rule out asthma, COPD
tx: salbutamol puffer
no antibiotics

61
Q

What is influenza?

A
  • influenza A & B
  • symptoms: fever, myalgia, headache, rhinitis, malaise, cough, sore throat
    dx: antigen testing
    tx: supportive care; antivirals: AMANTIDINE, ASELTAMIVIR
62
Q

normal body temp?
Febrile neutropenia?
Fever of unknown origin?

A
  • 37.8-37.9degrees C ; abnormal >=38
  • FN: >=38.3 or greater than 38 for >=1hr.
  • FUO >=38.3 over 3 weeks; no causes found after initial, standard investigations - pt otherwise well.
63
Q

Pathophysiology of fever?

A

-microbe products > activate leukocytes > IL1, TNF, IFN, IL6 > increase PGE2 > increase hypothalamic set point range
-HYPOTHALAMUS RESETS set point at higher T- thinks we’re cold so need heat
-low > heat: shivering, decrease cutaneous blood flow
=CHILLS, FEVER
-common pathway in inflammation
(-high > cooling: increase blood flow, sweating, decrease blood flow)

64
Q

Ddx of fever

A 
Infectious
Noninfectious (autoimmunity; increased IL1)
Malignancy
Vascular - thrombosis, dvt
endo/metabolic (ex: thyroid)
drugs (malignant hyperthermia)
65
Q

Meds for fever. How do antipyretics work?

A

*TREAT UNDERLYING CAUSE! not just treat fever alone.
-antipyretics > block COX > decrease PGE2 > block the reset on hypothalamus > block fever changes
ex:
ASA
Acetaminophen -prefered
NSAIDS
-corticosteroids has effects on fever but a lot others too - avoid!

66
Q

adv and disadv of fever?

A

adv: survival to kill microbes?
disadv: symptoms - chills, sweats, tachy, tachypnea, delirium, myalgia
kids: FEBRILE SEIZURES (T>=39)

67
Q

When is elevated T NOT fever?

tx?

A

EMERGENCIES!

  • Hyperthermia - setpoint unchanged, T goes up because body can’t lose heat
  • tx: cooling, specific therapy. NOT antpyretics.
    ex: heat stroke, malignant hyperthermia, neuroleptic malignant syndrome
  • Hyperpyrexia (T>41)
    ex: CNS hemorrhage
  • tx: cooling and antipyretics
68
Q

What are common causes of FUO

A
  • changes with time - before infection > malignancy>inflammatory.
  • now don’t know since we are pretty good at diagnosing the others.
  • hx, pe
  • usually outcome ok
69
Q

SIRS?
def
causes

A

systemic inflammatory response syndrome
Need at least 2:
-T>38 or 90
-RR>20 or PaCOs 1200 or <4000 or immature bands
*Causes: INFECTION!
-pancreatitis, burns, trauma, ischemia, hemorrhagic shock

70
Q

Sepsis

A

=SIRS due to INFECTION

71
Q

Severe Sepsis

A

-sepsis with organ dysfnc, hypotension, hypoperfusion

>ICU

72
Q

Septic Shock

A

-severe sepsis with hypotension that DOESN”T respond to fluid resuscitation and requires pressors

73
Q

Pathogenesis of sepsis?

A

-host response to infection becomes self-perp, unregulated, adn systemic!
normal inflammation >cytokines > vascular perm, blood flow, cell activation
-too much inflammation > pro-inflamm cells and components spread to non-infected tissues > hypotension, ARDS, thrombosis, hypoxia of tissue, immunosuppression

74
Q

Management of sepsis?

A
  1. treat underlying cause EARLY!
    - broad-spectrum antibiotics > narrow spectrum once organism detected
    - SOURCE CONTROL: remove lines, brain abscesses, remove blockages, repair ruptured that is causing infection source
  2. Goal-directed therapy: Ensure perfusion; resusciate; IV fluids
  3. Adjunctive therapy:
    - Corticosteroids if septic shock persists even after using IV fluids and vasopressins
    - treat to get normal glucose
    - enteral nutrition within ~48hrs

MMMD 1 - QH (7 decks)

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