Infectious diseases Flashcards
Explain the immune system
Protects the body from pathogens
Can be specific
Has memory
Mobile and fast acting
Flexible (can attack foreign entities)
What are the non-specific lines of defense?
Physical barriers (skin)
Chemical barriers (stomach acid)
Mucus and cilia protect our respiratory tract
Urine flushes out the bacteria from our urinary tract
Enzymes in our tears (high salt content) and our tears
Bacteria on our skin and digestive tract
*Weakened primary defenses increase likelihood for infection
What are the components of the innate immune system and what do they rely on?
Macrophages, neutrophils (PMNs), monocytes, natural killer cells and eosinophils
Mast cells and basophiles - phagocytize and release inflammatory mediators
Complements - lyse pathogens, coat pathogens, call for backup
Chemokines - act as traffic controllers for WBCs
They rely on receptors on the pathogens or surface components such as antibodies and complements
Explain the components of the innate cells in more detail
macrophages and monocytes - antigen presenting cells and serveillance
neutrophils - defense against bacteria and fungus
eosinophils - defense against parasites and respond to allergies
basophils - respond to allergies
True of false: the innate and adaptive immune system work together to fight invading pathogens
True
Explain the adaptive immune system
Involve B and T lymphocytes
They are very specific and have the ability to remember
Two parts:
Humoral mediated - w/in the serum
Cellular mediated - w/in the cells
How are T-lymphocytes activated
Activated by an antigen presenting cell
What do T cells do?
They secrete IL-2, which can stimulate the production of more activated T cells
What can activated T-cells turn into/be
Helper T cells (CD4+) - secrete IL’s and interferons, stimulate CD8+ cells, and stimulates production of antibodies
Cytotoxic cells (CD8+) - kill cells recognized as foreign
Regulating cell - regulates the T cell response
How are B-lymphocytes activated?
After they recognize anitgens
What do activated B cells become?
Plasma cells that secrete antibodies
Memory cells that are important for future attacks
How to antibodies work?
They bind to antigens and they may trap antigens, clump together, and/or increase the attack of immune cells
What do cytokines do? Provide examples
Soluble factors excreted by cells
Can activate cells, call for back-up, etc
ex) IL’s, TNF, IFN, etc
What are inflammatory mediators?
Any soluble factor that causes inflammation
Usually secretes by various cells
Ex) histamine, PGs, etc
What is infection?
Get a response of host systems and the person gets ill
Signs and symptoms present
What is sub-clinical infection?
Specific response in the body is evoked (i.e AB production), but the person is not ill
The body is able to fight off due to previous exposure
ex) influenza, EBV, SARS-CoV-2
What is Colonization?
Presence of organism at a body site without production of disease
We don’t treat these ones!
ex) skin wounds with staph
What are the two things that cause a disease?
Invasion of microorganism (breach host defense)
Toxins - bacteria produce toxins that can damage cells
ex) botulism, cholera, tetanus, staph aureus (food poisoning)
*we give antitoxins in these cases
Normal microbiota (won’t cause disease in healthy patients) of the skin
Diphtheroid
Propionibacteria
Staphylococci
Streptococci
Normal microbiota of the GI tract
Bacteroides sp
Clostridium sp
Diptheroids
Enterobacteriaceae (E. coli, Klebsiella sp.)
Fusobacterium sp
Streptococci (anaerobic)
Normal microbiota of the upper respiratory tract
Bacteroides sp.
Haemophilus sp.
Neisseria sp.
Streptococci
Normal microbiota of the genital tract
Corynebacterium sp.
Enterobacteriaceae sp.
Lactobacillus sp.
Mycoplasma sp.
Staphylococci
Streptococci
True or false: antibiotics always cure an infection
False. May require:
Drainage of abscess
Removal of dead tissue (no blood supply + can’t get to site)
Removal of foreign bodies or prosthetic device (biofilm on the devices that prevent AB penetration)
Decrease in immune suppression (in organ transplant need to turn down to accept)
What are the factors that affect host defenses?
Malnutrition –> affect WBC fxn
Extreme ages
Immune globulin deficiencies
Deficiencies in cellular immunity
Alcoholism
Diabetes
Immunisuppresive therapy
Invasive procedures - breach the host defense barriers
What are examples of drugs that suppress the immune system
Anti-cancer medications, corticosteroids (prednisone), organ transplant dugs, drugs for autoimmune diseases
What are the non-specific clinical manifestations for infection?
Malaise, listlessness, loss of appetite, headache, myalgias, arthralgias, etc
What are some specific clinical manifestations for infection?
Fever
WBC counts (elevated when there is an infection)
- normal range is 5-10 x10^9/L
- elevated in pt with leuk. and Rheumatoid arthritis and pt taking Li or corticosteroids
- elderly or less severe infxn features lower counts
Increased HR
Anxiety
Confusion
List the percentage of WBC in the body from highest to lowest
Neutrophils, segmented neutrophils, bands, lymphocytes, monocytes, eosinophils, basophils.
What is a segmented neutrophil?
mature neutrophil w/ segmented nucleus
What is a band?
an immature neutrophil (nucleus is smooth and parallel)
What are two other non-specific manifestations?
Anemia - especially with chronic infxn
Increased erythrocyte sedimentation rate (ESR) and C-reactive protein (CRP)
These are both markers of inflammation too
Explain septic shock
Another clinical manifestation of infection
Lots of body system malfxn
Decreased BP, then decreased CO
Decrease in renal fxn
Hepatic dysfunction (increase in bilirubin)
Decreased oxygenation (due to decrease lung perforation)
Disseminated intravascular coagulation (DIC)
*** Eventually leads to multiple organ failure and antibiotics won’t even help
What are the steps for infection diagnosis?
History
Physical examination
Laboratory
Laboratory with microbiology, gram stain, culture, and sensitivity testing
What are considerations of history for infxn diagnosis?
Pt signs and symptoms and its severity
The source of the infection such as trauma or contact with a person
- We must try to determine which organism is the most likely cause
What is the goal of physical examination?
To localize the infxn, this will be different for each infection
ex) meningitis - neck stiffness
ex) pneumonia - cough and sputum production; chest sounds
ex) measles - characteristic rash
What is the goal of the laboratory in terms of microbiology? What can we do to achieve this?
To determine the invading pathogen(s), so that the proper AB can be used
We can achieve this through gram staining, culturing, and sensitivity testing
What does a gram stain tell us?
it gives us an idea of the organism
Gram +ve vs -ve
cocci vs bacillus
presence of WBC (WBC can stain too)
if the infxn is bacterial (viral don’t stain)
What are the sp. of gram +ve cocci clusters?
Staphylococci
Coagulase +ve:
Staph aureus
coagulase -ve:
staph epidermidis
staph saprophyticus
staph hominis
staph hemolyticus
staph warneri
What are the sp. of gram +ve cocci pairs (diplococci)?
Pneumococci
Steph pneumoniae
What are the sp. of gram +ve chains
steptococci
B-hemolytic:
Strep pyrogenes (group A strep)
Strep agalactiae (group B strep)
Groups C,F,G
a-hemolytic:
Viridans streptococci
Strep pneumoniae
What are the sp. of gram +ve bacilli?
Small
Listeria
Cutibacterium
Corynebacterium
Gardnerella
Large
Spore forming:
Clostridium
Bacillus
Nonspore-forming:
Lactobacillus
What are the sp. of gram +ve branching or filamentous bacilli?
Nocardia
Actinomyces
Erysipelothrix
What are the sp of gram -ve cocci?
Neisseria meningitidis
Neisseria gonorrhoeae
Veillonella
What are the sp of gram negative bacilli (Lactose fermenter)?
Lactose fermenter
oxidase +ve:
Aeromonas
Pasteurella
Vibrio
oxidase -ve:
Escherichia coli
Klebsiella spp.
Enterobacter spp.
Citrobacter spp.
What are the sp of gram negative bacilli (Non-lactose fermenter)?
Non-lactose fermenter
oxidase +ve:
Pseudomonas spp.
Flavobacterium spp.
Alcaligenes spp.
Achromobacter spp.
Moraxella spp.
oxidase -ve:
Proteus spp.
Proficendia spp.
Serratia spp.
Morganella spp.
Salmonella spp.
Shigella spp.
Stenotrophomonas
Acinetobacter spp. (coccobacilli)
What are the gram -ve coccobacilli?
Haemophilus influenzae
Moraxella catarrhalis
What is culturing?
Taking the specimen and inoculating it on an agar plate
BEST METHOD FOR REVEALING ORGANISM
Organism growth and biochemical profile is determined thru testing
Some organisms may grow some not at all (aerobes vs anaerobes)
Potential contamination is possible
Explain MALDI-TOF MS
Matrix-assisted laser desorption/ionization time of flight mass spectrometry
Sample is growing, then vaporize bacterial sample with a laser. This ionized proteins and other macromolecules
Cloud is created and the analyte is separated by mass and charge
Then a detector detects the organism’s fingerprint, which then gets compared to a database to ID the microorg
What is sensitivity testing?
Determines which AB the org is susceptible to
Based on the minimal inhibitory conc (MIC) = the lowest antimicrobial conc that prevents growth after 24 hrs of incubation
Must take into account the site of infxn and penetration of the AB (look for ZOI)
S- sensitive
R-resistant
I-intermediate … against the AB
What is an E-test?
Single antibiotic against a patient’s specific cultured org
There is a strip that assesses the amount of AB inhibition
What is immunologic testing or serology?
It is a lab test that is useful if an organism cannot be cultured or tx has already begun.
ex) penumoniae - won’t grow and won’t stain. It needs a special media, so do serology
What is antibody testing?
It detects the presence of antibodies directed against the pathogen
various methods used
What is antigen detection?
Detects the presence of an antigen in the serum, urine, CSF, etc
Bacterial, fungal, or viral
Various methods used
What is Polymerase chain rxn (PCR)?
Detects v. low amounts of specific DNA in clinical specimens
What is used in the lab to see viruses?
Electron microscopy is used as viruses don’t stain
What is the empiric antibiotic choice?
Empirical -> it is an educated guess on what the pathogen is based on host and drug factors and what antibiotic to use against it
we don’t necessarily know for sure what it is
What are the reasons that an antibiotic may be used?
Prophylaxis, empiric therapy, specific therapy
What is prophylaxis?
To prevent an infxn
This is not a good therapy because it drives resistance
Inappropriate use -> physician prescribes an antibiotic for a pt with a viral infxn “just in case”
Appropriate -> Rheumatic heart disease or surgical prophylaxis (before a surgery to prevent infxn)
What is empiric therapy
…
What is specific therapy?
Treating directly
If a pt has a UTI, we treat with UTI ABs
What are the questions that we should ask before choosing an antibiotic?
- Is the AB indicated?
Penumonia, wound infxn, UTI are examples where AB’s are needed
bacterial infxn with fever and no local findings are a red flag
Consider age, illness, travel history,etc
Consider the urgency of AB tx (acute endocardidits is urgent)
Consider likelihood of viral infxn
Examine the possibility that symptoms could mean something else - Have the appropriate specimens been obtained?
- gram stain is cheap, fast, and easy
- cultures first, then AB (need it first because AB may remove the org)
- follow-up cultures only if pt not getting better - What are the most likely orgs?
- gram stain gives us clues
- environment where the org was acquired matters (some orgs are in hospital only vs community)
- take into account regional data such as resistance in geographic regions
- also some patients tx may vary based on their age
What is an antibiogram?
The lab takes info and the put this info into a chart or data set that shows the statistics.
For example the percent susceptible of gram negative rods against a variety of antibiotics in a given area
What are the questions to ask after Q3?
Which drug is best?
1st line drugs, penetration ability, and the location of the infection (ex. the stomach may alter ab effect)
Side effects must be considered, allergies, bacteriostatic vs cidal (cidal would be used for life-threatening or immunocompromised), frequency of admin, route of admin, monitoring?
narrow vs broad spectrum
Cost
What is Q5?
Is combination therapy appropriate
Normally one agent for one org
Sometimes multiple orgs -> intraabdominal abscess with gram -ve and bacilli
Using two agents can limit resistance
Two agents also for synergism -> penicillin + clavulanic acid
What are some disadvantages of using multiple AB?
increased risk of tox
increased risk of colonization with Resistant orgs
higher costs
false sense of security
What is Q6?
What are the important host factors?
Renal or hepatic fxn (low clearance = tox risk increases)
immunosuppressed (need cidal)
Prosthetic devices -> low blood supply hard to eradicate
Age
Drug interactions
Pt preference -> macrolides with GI upset
Adherence
What is safe, caution, and avoid in pregnant patients?
Safe: penicillin, cephalosporins, erythromycin base
Caution: AMG, vancomycin, clindamycin, trimethoprim, nitrofurantoin
Avoid: tetracycline, FQ, TMP-SMX, erythromycin estolate, sulfonamides (in last trimester)
What is Q7?
Best route of administration?
More for hospital
Mainly oral for outpatients
Serious infections require parenteral use (can step down to oral AB; need adequate blood levels)
What is Q8?
What is the right dose and duration?
highly dependent on the infxn in question
ex) meningitis vs pneumonia
can be individualized based on pt factors
What are the reasons for AB failure?
Pt not improving
Noncompliance
Under dosing
inaccessible site (abscess)
Prosthetic material
resistance
Superinfection -> second infxn develops from treating the first one ex) UTI develops into yeast infxn; thrush -> fungal infxn
