Week 1 Flashcards
(104 cards)
1
Q
Blood agar plates differentiate Streptococci
species based on _______– pattern
- Alpha-hemolytic: _____ hemolysis
- Beta-hemolytic: ________ hemolysis
- Gamma-hemolytic: ____ hemolysis
A
hemolysis
partial
complete
no
2
Q
_________ classification based on cell wall carbohydrate Ags
- Human pathogens largely Groups __ -___
- Group A = _________
A
Lancefield
A-D
S. pyogenes
3
Q
organisms that are alpha hemolytic
A
S. pneumoniae
Viridans
4
Q
Organisms that are B hemolytic
A
S. pyogenes
S. agalactiae
5
Q
organisms that are gamma hemolytic
A
enterococcus
non enterococcus
6
Q
what are the GAS suppurative infections?
what do you see with the second one?
A
Streptococcal pharyngitis
Skin and soft tissue infections
- Impetigo, folliculitis
- Necrotizing fasciitis – Severe; Toxin production
- Cellulitis – Dermis & subcutaneous infection
- Erysipelas – Epidermis only; Painful rash; Fever
7
Q
S pyogens Impetigo characteristics:
age
why does it usually develop
where do you usually see it?
does it show symptoms and is it contagious?
treatment
complications
can also be caused by?
A
2-5years
poor hygeins
skin ulceration on face and lower extremitites: vesicles, pustules, crusted lesion, ulcerations
no systemic symptoms but contagious
local, penicillin
glomerulonephritis (pink foamy urine, hypertension, edema)
Staph Aureus
8
Q
S. pyogenes (GAS) Disease Deep Soft Tissue Infection - Necrotizing Fasciitis “Flesh eating syndrome”
is pathogenesis clear or unclear?
Exotoxins ____ and ____ induce inflammation by activating:
Cysteine protease SpeB degrades:
A
pathogenesis is unclear
SpeA, SpeC, T cells & stimulating inflammatory cytokines
extracellular matrix, cytokines, Igs
9
Q
Orbital Cellulitis:
what is it and where does it come from?
A
Inflammation of eye tissues behind the orbital septum
- Acute spread of infection into the eye socket from either the adjacent sinuses or through the blood
- May also occur after trauma
- usually comes from GAS, but other bacteria can cause it as well
10
Q
What leads to streptococcal toxic shock syndrome?
is it caused more by skin infection or pharyngitis?
blood cultures are often _____
_________ in some
mortality may reach >___
A
when the GAS infection becomes severe to the point of having hypotension and end organ damage
caused more by skin infection
positive
erythematous rash
50%
11
Q
GAS immunologic disease
Acute Rheumatic Fever (ARF)
characteristics?
what symptoms?
______ in nature
ages ____-____ most affected
what areas are effected?
is it rare or prevalent in US? what about other countries?
presents itself ___-___ years after the initial infection
A
multi-organ inflammatory syndrome following untreated GAS pharyngitis
subcutaneous nodules, aschoff bodies, erythema marginatum
autoimmune
5-15
heart, brain, skin, joints
rare in US but one of the most common causes of chronic heart disease in developing countries
10-20
12
Q
GAS Immunologic disease: Post-streptococcal glomerulonephritis (PSGN)
follows ____ or _____ infections
more common in:
symptoms
not reduced by:
good or bad prognosis?
A
skin, pharyngeal
children
dark urine due to hematuria, edema, hypertension from fluid retention
antibiotic therapy
good prognosis
13
Q
infective endocarditis is usually caused by:
A
bacteria
- can also be caused by fungi and viruses
14
Q
what is the most common causes of infective endocarditis?
A
S. aureus
streptococci
enterococci
15
Q
S. aureus Infective Endocarditis
Most common cause of IE in:
Incidence has increased because of?
Infection can occur on previously ______ heart valves
- For prosthetic valve endocarditis, most often the cause is:
Clinical Features:
A
in industrialized countries
because of healthcare-associated infections for older population (younger its ID users)
normal
Staphylococcus aureus and coagulase-negative Staphylococcus epidermidis
- Typically Acute IE
- Fulminant course
- Metastatic spread of infection: e.g., lungs, spleen, bone, etc.
16
Q
Streptococcal Infective Endocarditis
traditionally the most common cause of:
- still the case for _____ countries and ______ based cohorts
- superseded by:
mainly due to _____ group streptococci, normal inhabitant of the:
- poor ____ a risk factor
occurs in patients with: (examples)
______ presentation and what symptoms?
Is there a higher or lower rate of death than S. aureus IE?
A
IE
- non industrialized, community
- S. aureus
viridans, oral cavity
- dentition
pre-existing valve disease (rheumatic heart disease, mitral valve proplapse, congenital heart disease)
indolent presentation, low grade fevers and non specific symptoms
lower rate of complications and death
17
Q
Enterococcal Infective Endocarditis
____ most commo cause of IE
Typically occurs in:
______ IE
easy or difficult to treat and why?
High or low mortality rate? Why?
A
3rd
older men after genitourinary procedures
young women after uro-gynecologic procedures
subacute (between occute and chronic)
difficult to treat (high resistance to antibiotics)
high mortality rate due to older age of individuals, antibiotic resistance
18
Q
what are some risk factors for endocarditis?
A
prosthetic heart valve, IV drug use, indwelling central venous catheter, poor dentition
19
Q
Myobacterium
No _____________ so most closely related to Gram ______
Gram stain does/does not not penetrate the waxy wall – ________ stain
Both structural components and virulence factors activate or suppress:
A
outer membrane, positive
does not, acid fast
immune responses
20
Q
What are the mycobacteria infecting humans?
A
M. tuberculosis complex (7 species)
- M. tuberculosis
- M. bovis
M. leprae
Non-tuberculous Mycobacteria (NTM)
- Naturally-occurring, found in water & soil
- A person inhales the organism from their environment
- Non-contagious
- Most people do not become ill
21
Q
Transmission of NTM(non tuberculosis myobacterium) vs Mtb
A
NTM:
- aerosolized water droplets
- ingestion
- NOT contagious
Mtb
- aerosolized resp. droplet nuclei
- ingestion
- CONTAGIOUS
22
Q
Reservoir of NTM vs Mtb:
A
NTM
- environemnt
Mtb
- humans
23
Q
Characteristics of NTM vs Mtb
type of pathogen
predisposition?
latency?
Indolent or slowly progressive?
worse in?
A
NTM
- Opportunistic pathogen
- underlying predisposition (lung disease, immunocompromised)
- no latency
- indolent and slowly progressive
- worse in severly immunocompromised
Mtb
- primary pathogen
- predisposition not needed
- latent infection common
- indolent and slowly progressive
- worse in severly immunocompromised
24
Q
what are the 4 immune compartments?
A
1) complement (land mines/waits around until activated and blows up)
2) phagocytes (marines/crawl through and move to site of infection, big appetite)
3) B cells (air force)
4) T cells (generals, assasins, psychologists)
25
**_Complement_**:
Where is it made?
Where does it go?
What does it do?
proteins made in the liver
circulating and at the ready in plasma and lymph, waiting to be triggered
After triggering, several activation events end in an explosion
* **formation of the membrane attack complex**
* cytolysis
* **coats bacteria for phagocytosis (opsonization)**
26
what happens if complement doesn't work?
what are the bacteria you get infected with?
encapsulated bacteria are vulnerable to complement attack --\> infections from encapsulated bacteria due to innefficient opsonization and phagocytosis
* strep. pneumoniae
* hemophilus influenzae
* neisseria meningitidis
27
How do phagocytes (marines) work?
first deployed into battle
crawl through tissues
eat cells
digest what they have eaten then present antigen to T cells
28
Antigen Presentation in MHC:
T cells require _____ to recognize peptides being presented to them
Phagocytes present what they have eaten with the help of \_\_\_\_\_
MHC
29
What happens if the phagocytes don't work?
What disease do you see with this?
soft tissue abscesses or lymphadenitis
susceptible to catalase + organisms (Staph aureus, serratia marcescens, aspergillus)
poor wound healing
**Chronic Granulomatous Disease**
* defective NADPH oxidase
* unable to kill catalase + bacteria
30
What do B cells do?
**Air force** of the immune system
make and deploy **antibodies**
deploy antibodies at or **near** the site of inflammation or can be **distant**
31
What happens if B cells and antibodies don't work?
recurrent bacterial sinopulmonary infections (Sinusitis, Ear Infections, Bronchitis, Pneumonias) with bacteria including Streptococcus pneumoniae, Hemophilus influenzae, Moraxella catarrhalis
32
What are the 3 types of T cells and what do they do?
**CD4** - Helper T cells direct immune responses (where to go and what to do)
**CD8** - Cytotoxic T cells **kill** cells infected with intracellular pathogens like viruses, fungi, etc.
**Regulatory T cells** control & modulate immune responses (psychologist)
33
What happens if T cells don't work?
inability to generate effective antibody responses
severe viral infections (**CMV, EBV**)
severe fungal infections
autoimmunity
34
What are the Innate compartments of the immune system?
complement and phagocytes
35
what are the adaptive immunity compartments of the immune system?
B cells and T cells
36
which bacteria have one celll membrane surrounded by a thick cell wall?
gram positive
37
which bacteria has an additional outer membrane but no thick cell wall?
gram negative
38
\_\_\_\_\_\_\_\_ structure determines the gram stain
cell envelope
39
cell wall assembly is an important __________ agent
antibiotic agent
40
what is on the outer membrane of gram negative bacteria?
What recognizes this in the body?
It is also known as:
It is a type of:
LPL (sugar chains on lipids of the outer membrane)
recognized by the innate immune system and can lead to shock
endotoxin
pathogen associated molecular pattern (PAMP)
41
What are the 3 main pathways of the complement system and what do they all lead to?
classical, lectin, alternative
lead to the productino of the **membrane attack complex**
42
what activates the classical pathway?
immune complexes (antibody/antigen complex)
43
what activates the lectin pathway?
pathogen oligosaccharides
44
what activates the alternative pathway?
pathogen surfaces (spontaneous activation)
45
what are the major roles of complement and how do they work?
1) opsonizatioin
* the most important role of coplement
* Binds to the surface of encapsulated, slippery, slimy bacteria to provide handles for phagocytes to bind and ingest them
2) Cytolysis
* Forms the MAC and directly destroys bacteria
3) promotes antibody production by B cells
4) chemotaxis
5) removal of immune complexes and apoptotic cells
46
Classical Pathway:
initiated by binding of the _____ complex to _____ complexes
only ____ and _____ can activate complement
C1, Ab-Ag
IgM, IgG
47
4 steps of how your body recognnizes and deals with invading pathogens:
1) sensor
2) alarm
3) resident
4) recruit
48
Innate immunity recognition:
Distinguishes between _________ by looking for:
There are certain signals that the body uses as a sensor, what are they?
self & non-self, molecular patterns that are present on pathogens but not in us
**DAMPs** and **PAMPs**
DAMPs
* HSPs induced by heat, toxins, oxidants; Reduce denaturation or enhance renaturation to regain correct tertiary structure
* HMGB1 released by necrotic cells can mediate inflammation in CNS & peripheral tissues
* **MSU crystals precipitate within joints & soft tissues (Inflammation, Gout)**
49
What PAMP targets microbial carbs in bacterial, viral, and fungal cell membranes?
C-type lectin receptors
50
what does TLR2 recognize?
molecular specificity
cell surface
peptidoglycan
51
what does TLR4 recognise?
molecular specificity
cell surface
LPS
52
What does TLR5 recognize?
molecular speceficity?
cell surface
flagellin
53
what does TLR9 recognize?
molecular speceficity
endosomal
unmethylated CpG DNA
54
What are NOD like receptors?
What do they sense?
Family of more than 20 different **cytosolic** proteins
Sense cytoplasmic **PAMPs** and **DAMPs, recognize both gram + and - bacteria,** V**arious ligands from microbial pathogens**
Lead to inflammatory reactions (NLRs signal through inflammasomes which activate capsases)
55
what do innate alarm signals do?
what do they include?
induce local and systemic effects
cytokines
chemokines
leukotrienes and prostaglandins
acute phase reactants
56
what are 3 major inflammatory cytokines and what are their **LOCAL** effects?
**1) TNF alpha**
* induced by TLRs, NLRs, and RLRs **through NFkB**
**2) Interleukin-1 (IL-1)**
**3) Interleukin-6 (IL-6)**
* Stimulates neutrophil production in bone marrow
**Activate endothelial cells to express selectin ligands, cell adhesion molecules, and chemokines**
**Activate resident immune cells**
**Stimulate phagocytosis, production of oxidants for microbe killing, and production of prostaglandins**
57
what are the systemic effects of major inflammatory cytokines?
Specifically for TNF alpha?
* Act on the hypothalamus as endogenous pyrogens
* Induce hepatocytes to express acute-phase reactants (C-reactive protein, Fibrinogen, Complement)
* **TNFa** inhibits myocardial contractility and vascular smooth muscle tone --\> Hypotension
* **TNFa** causes intravascular thrombosis
* Prolonged production of **TNFa** causes wasting of muscle and fat cells --\> Cachexia
58
What causes massive release of inflammatory cytokines?
Results in?
What happens in SIRS (systemic inflammatory response syndrome)
caused by bacterial sepsis (septic shock), toxic shock, and largescale lymphocyte activation
cytokine storm
* Vascular collapse
* Disseminated intravascular coagulation
* Severe metabolic disturbances
59
horizontal vs vertical approaches
horizontal: prevents infection from many organisms (surveillance, disinfection, hand hygeine)
vertical: Prevents one specific infection (Isolation precautions)
60
how do we prevent infections?
Helpful to have a working knowledge of common infections and mechanisms of transmission
Skills to provide safe care
Have systems and cultures in place that prioritize safety!
61
**Hand hygeine for dental settings:**
when to perform hand hygeine:
Use soap and water when hands are: other wise, ______ may be used
1) when hands are visibly soiled
2) after barehanded touching of intruments, equipment, materials, and other objects likely to be contaminated by blood, saliva, or resp. secretions
3) before and after treating each patient
4) before putting on gloves and again immediatley after removing gloves
visibly soiled, alcohol based hand rub
62
hepatitis C infectivity
3%
63
HIV infectivity
0.3
Risk of HIV after a mucous membrane exposure \<0.1%
64
Safe use and disposal of sharps
Keep handling to a minimum
Do NOT recap needles
Discard each needle into a sharps container at point of use
Do NOT overload bin
65
# define standard precautions
examples
The minimum infection prevention practices that apply to all patient care, regardless of suspected or confirmed infection status of the patient
* Hand hygiene
* PPE (gloves, mask, eyewear) if appropriate
* Sharps safety
* Safe injection practices (aseptic technique for medications)
* Sterile instruments and devices
* Clean and disinfected environmental surfaces
66
Standard precautions in dental settings
Gloves & barrier protection when there is possible contact with blood or body fluids, mucous membranes, non-intact skin
Use of protective clothing during procedures or activities where contact with blood or body fluids is anticipated.
Use of mouth, nose, and eye protection during procedures that are likely to generate splashes or sprays of blood or other body fluids
67
Lipid Inflammatory mediators are derived from:
2 maine pathways:
**arachidonic acid**
**Cyclooxygenase pathway Prostaglandins**
* Vasodilation/vascular permeability; Inflammatory pain; Hyperalgesia; Fever
**Lipoxygenase pathway Leukotrienes**
* Mediators of allergic rx & inflammation
68
What are chemokines?
What do they form?
Can be presented on:
Stimulate:
Tell ______ where to go
chemotactic cytokines
* large family of small secreted proteins
Form chemotactic gradients, lead immune cells & WBCs to an infection site
Can be presented on the surface of endothelium
Stimulate leukocyte migration & leukocyte integrins
Tell white blood cells where to go
69
What are the 2 main types of chemokines and what do they each recruit?
**IL-8 (CXCL8)**
* Recruiter of **neutrophils** to site of acute inflammation
**Monocyte Chemoattractant Protein (MCP-1, CCL2)**
* Recruiter of **monocytes** to sites of inflammation
70
What are the 4 resident innate immune cells?
1) mast cells
2) macrophages
3) dendritic cells
4) innate like lymphocytes
71
Where are mast cells located?
what are type of defense are they involved in?
What activates Mast cells? What happens next?
what are 3 things mast cells produce when activated? what does this lead to?
At mucosal surfaces of the gut and lungs, skin, around blood vessels
Located at the boundaries between tissues and the external environment
Defense to parasitic infection and in allergic reactions
IgE. --\> granulation
1. biogenic amines (histamine) --\> vasodilation, vascular leak
2. cytokines (TNF) --\> inflammation
3. enzymes (tryptase) --\> tissue damage
72
Macrophages:
Invlved in \_\_\_\_\_\_
release ______ and \_\_\_\_\_\_
\_\_\_\_ and ____ to kill phagocytosed bacteria
repair _______ tissues by stimulating _______ and \_\_\_\_\_\_
Phagocytosis
Release cytokines & growth factors
ROS & NO to kill phagocytosed bacteria
Repair damaged tissues by stimulating angiogenesis & fibrosis
73
Phagocytosis and its outcome involve three distinct steps
1. Recognition and attachment
2. Engulfment and fusion of phagosome and lysosome
3. Killing and degradation of ingested material
74
Dendritic cells:
Acts as a:
\_\_\_\_\_ presenting cells
capture and process \_\_\_\_, converting _____ to _____ that are presented on MHC molecules recognized by T cells
Mediator between innate and adaptive immunity
Antigen
Capture and process Ags, converting proteins to peptides that are presented on MHC molecules recognized by T cells
75
What are Innate Like Lymphocytes?
found in:
atypical lymphocytes that perform innate functions
Found in the intestinal mucosa, skin, lungs
76
What are the 5 types of recruited inflammatory cells
1. neutrophils
2. monocytes --\> macrophages
3. natural killer cells
4. eosinophils
5. basophils
77
What do Neutrophils do?
Produce:
when do they arrive at inflammatory sites?
Phagocytosis & ROS killing
Production of antimicrobial peptides - Human Neutrophil Peptides (HNPs)/α-defensins
First to arrive at inflammatory sites - Most active in extracellular bacterial infections
78
Monocytes:
**short/long** lasting
most active against:
eat _____ and _______ - responsible for:
produce:
as infection resolves, produce:
long lasting
intracellular bacteria and viruses
dead and dying: responsible for cleanup
large amounts of chemokines and cytokines to promote further inflammation
proteases and growth factors to mediate tissue repair
79
what do natural killer T cells do?
express perforin to:
exress FasL and Granzyme B to:
Express FcR to:
Kill infected cells and activate macrophages to destroy phagocytosed microbes
Express Perforin to make holes in target cell membrane
Express FasL & Granzyme B to kill cells
Express FcR to stimulate Antibody-Dependent Cellular Cytotoxicity (ADCC)
80
Eosinophils are specialized to fight _____ infections
Active in _______ responses
parasitic
allergic
81
basophils are structurally and functionally similar to:
infiltrate:
release:
Structurally and functionally similar to Mast cells
Infiltrate sites of allergic inflammation
release mediators & cytokines
82
primary pathology of anaerobic infection:
anaerobic infections are often **one microbe/polymicrobial**
anaerobic infection treatment:
pus/abscess formation
polymicrobial
surgical drainage and antibiotics
83
Bacteroides:
Is it commensal or pathogenic?
where does it reside?
what happens when there is a break in the mucosal surface?
most frequent cause of:
B. fragilis is ressistant to:
commensal
gut flora
turns from friend to foe
anaerobic infections
beta lactamase confer resistance to penicillin
84
**Clostridium**
\_\_\_\_\_\_ forming
* allows organism to withstand:
* can quickly _______ and produce \_\_\_\_\_\_
Commonly found in:
has many different ______ factors including ,able to evade immune system via:
spore
* harsh conditions
* proliferate in an ideal environment and produce toxin
GI tract and soil
virulence, enzymes
85
**C. perfringens** causes:
toxin:
Gas gangrene (tissue death)
alpha toxin
86
C. difficile causes:
toxin:
inflammation in the colon (pseudomembranous collitis)
* antibiotic associated diarrhea
toxin A and B
87
C. tetani causes, how does it work?:
toxin:
where is it found?
enters the body through:
another way of transmission?
Is there an immunization?
tetanus
* Blocks the release of inhibitory neurotransmitters, resulting in constant muscle contraction (spasms and/or spastic paralysis)
neurotoxin
In soil, dust, manure
deep cut
neonatal via contaminated umbilicus
Immunization combined with diphtheria toxoid and pertussis – Tdap, Td (booster)
88
**C. botulinum** does what?
most potent \_\_\_\_\_\_\_
what 3 kinds of botulism are there?
**Blocks** release of acetylcholine; Paralysis of the cranial nerves (“Botox”); Infant botulism (Floppy baby syndrome)
natural toxin known
**'Food’ ‘Wound’** & ‘**Infant**’ botulism
89
**Actinomyces:**
what does it look like?
**A. sraelii & A. naeslundii**
part of the \_\_\_\_\_\_
becomes pathogenic after \_\_\_\_\_\_\_\_
**Cervicofacial actinomycosis**
pyogenic \_\_\_\_
\_\_\_\_\_\_\_\_ may form
incidents i**nclining/declinging** due to:
**Abdominal actinomycosis**
due to:
**Treatment for actinomyces:**
long branching filaments
normal oral flora
after trauma (extraction, disruptino of mucosal surfaces)
abscesses
sulfur granules
declining, improved oral hygeine
perforation of intestinal mucosa, e.g., perforated ulcer, ruptured appendix
Surgical drainage + penicillin/ampicillin
90
**N. meningitidis**
Entry:
disease:
Gram ____ \_\_\_\_\_\_\_\_\_
most species are:
fermentation:
resp tract, blood, neurotopic
Meningococcemia Meningitis
negative diplococci
non pathogenic
ferments maltose and glucose
91
**N. gonorrhoeae**
Entry:
disease:
Gram ____ \_\_\_\_\_\_\_\_\_
most species are:
fermentation:
GU tract, blood (uncommon)
Cervicitis/urethritis, Conjunctivitis, Tenosynovitis
negative diplococci
non pathogenic
glucose
92
How does **N. meningitidis** evade the immune system?
How does **N. meningitidis** overstimulate the immune system?
**IgA protease, Polysaccharide capsule** (invisibility cloke)
Lipooligosaccharide **(overproduction of immune components)**
93
What is the pathogenesis of **Neisseria meningitidis? (2)**
evasion of the immune system
overstimulation of the immune system
94
What is the pathogenesis of **N. gonorrhoeae?**
1) attach to mucosa via pili
2) evade the immune system via IgA protease
95
How do bacteria get into the CSF?
**Hematogenous**
* **colonization** - Pili
* **Invasion** - IgA Protease
* **Blood stream survival** - Evasion of complement pathway by capsular polysaccharide
* **Meningeal invasion** – Cross the BBB (Invade CSF, Multiply, Meningitis)
**Direct spread** (via surgery)
96
What are the signs and symptoms of meningeal inflammation?
What is Kernig's sign?
What is Brudzinski’s sign?
* Headache/Jolt accentuation of headache
* Neck stiffness
* Photophobia
* Severe stiffness of the hamstrings I
* nability to straighten the leg when the hip is flexed to 90 degrees
* Severe neck stiffness
* Hips and knees flex when the neck is flexed
97
**Diagnositc testing for Meningeal Inflammation**
Direct sampling of:
CSF sent for:
CSF
* Cell count - WBC **increases**
* Protein **increases**
* Glucose **decreases**
* Gram stain
* Bacterial culture
98
Meningitis Counts:
Bacterial vs. Viral vs. Chronic Table
99
**Strep pneumoniae** and **Neisseria meningitidis** are responsible for Meningitis in what age groups?
children
young adults
adults \>50
100
Listeria monocytogenes are responsible for meningitis in what age groups?
Neonates
adults \>50
101
Haemophilus influenzae affects what age groups?
children
102
What are the top 5 HAI?
pneumonia
surgical site infection
clostridium difficile colitis
UTI
catheter related blood infection
103
Hierarchy of Risk Controls
**MOST EFFECTIVE** Elimination - **(physically remove hazard)** triage patients prior to hospital entrance, screening at entrances, visitor policy, physical distancing, tlehelath, vaccines
substitution - **replace the hazard**
engineering controls - **(isolate people from the hazard)** platic barriers, ventilation, negative pressure rooms
administrative controls - **(change the way people work)** employee attestation, patient triage process
**LEAST EFFECTIVE** PPE - universal masking, face sheilds, goggles, HH
104
