MEDICINE 2 – [INFECTIOUS DISEASES]: GENERAL LECTURE

AY 21-22

25 OCT 21
John S. Delgado, MD
TABLE OF CONTENTS C. PANDRUG-RESISTANT ORGANISMS (XDRO)
I. DEFINITION .............................................................................. 1 ● Resistance to all agents in all antimicrobial classes
A. MULTIDRUG-RESISTANT ORGANISM (MDRO)……………1 → Example:
B. EXTENSIVELY DRUG-RESISTANT ORGANISM (XDRO)…1
→ Isolate: Pseudomonas aeruginosa
C. PANDRUG-RESISTANT ORGANISMS (XDRO)……...……..1
→ Sensitive: none
II. FACTORS CONTRIBUTING TO ANTIBIOTIC RESISTANCE ... 1
III. MECHANISMS OF ANTIBIOTIC RESISTANCE ........................ 1 → Intermediate: none
A. INACTIVATION BY ENZYMES………………….……………..2 → Resistant: Amikacin, Aztreonam, Ceftazidime, Cefepime,
B. MODIFIED DRUG TARGET…..………………………………..2 Ciprofloxacin, Colistin, Imipenem, Meropenem, Piperacillin-
C. INHIBITION OF DRUG UPTAKE……………………..………..2 tazobactam
D. EFFLUX PUMP…………………………………………………..2 II. FACTORS CONTRIBUTING TO ANTIBIOTIC RESISTANCE
IV. ANTIBIOTIC MISUSE................................................................ 2
V. MULTIDRUG-RESISTANT GRAM-NEGATIVE ORGANISMS ... 2 ● Improper use of antibiotics (human and animals)
A. EXTENDED-SPECTRUM BETA-LACTAMASES (ESBLs)….2 → Giving antibiotics for the wrong indication
B. CARBAPENEMASES…………………….……………………..3 ■ Example: antibiotics for asymptomatic COVID patients,
C. METALLO-β-LACTAMASES……………………..…………….3 Antibiotic overuse for animals develop antibiotic resistance
D. COLISTIN RESISTANCE…………………………………..…..3 (food source infected), Colistin sulphate mixed in Chicken
E. ANTIBIOTIC RESISTANCE SURVEILLANCE PROGRAM..3 feeds
VI. MULTIDRUG-RESISTANT GRAM-POSITIVE ORGANISMS..... 4 ● Patient movement within and among medical institutions
A. METHICILLIN-RESISTANT S. AUREUS (MRSA)…………...4 ● Example: Patients from provinces being transferred to referral
B. VANCOMYCIN-RESISTANT S. AUREUS (VRSA)……….….4 centers (MDR pathogen can be spread)
C. VANCOMYCIN-INTERMEDIATE S. AUREUS (VRSA)…..…4 ● Lack of implementation of infection control measures
D. COMMUNITY-ACQUIRED AND HOSPITAL-ACQUIRED
MRSA ………………………………………………………………..…..4
E. LIVESTOCK-ASSOCIATED MRSA……………….…………...5
VII. IMPACT OF MULTIDRUG-RESISTANT ORGANISMS ............. 5
VIII. ANTIBIOTIC STEWARDSHIP ................................................... 5
VII. IMPACT OF THE COVID-19 PANDEMIC ON ANTIBIOTIC
STEWARDSHIP.................................................................................. 5
IX. Q&A .......................................................................................... 6
REFERENCES ................................................................................... 6

MUST KNOW BOOK PREVIOUS TRANS

  
New notes from Dr. Delgado’s lecture with C2023 in blue.
Prophetic Warning…
“The time may come when penicillin can be bought by anyone in the shops.
Then there is the danger that the ignorant man may easily underdose himself
Figure 1. How Antibiotic Resistance spreads. A screencap from the lecture
and by exposing his microbes to non-lethal quantities of the drug make them
RESISTANT.” No ESKAPE (common MDROs in clinical practice)
- Sir Alexander Fleming
The Discoverer of Penicillin ● E: Enterococcus faecium (Gram +)
Nobel Lecture, December 11, 1945 ● S: Staphylococcus aureus (Gram +)
● K: Klebsiella pneumoniae (in Europe and Asia-Pacific); (Gram -)
I. DEFINITION → C: Clostridioides difficile (in USA)
● A: Acinetobacter baumannii (Gram -)
A. MULTIDRUG-RESISTANT ORGANISM (MDRO)
● P: Pseudomonas aeruginosa (Gram -)
● Resistance to at least 1 agent in ≥3 antimicrobial classes ● E: Enterobacter spp. (Enterobacterales) (Gram -)
● Example:
→ Isolate: Pseudomonas aeruginosa III. MECHANISMS OF ANTIBIOTIC RESISTANCE
→ Sensitive: Aztreonam, Colistin, Imipenem, Meropenem
→ Intermediate: none
→ Resistant: Amikacin, Ceftazidime, Cefepime, Ciprofloxacin,
Piperacillin-tazobactam (4 classes)
B. EXTENSIVELY DRUG-RESISTANT ORGANISM (XDRO)
● Resistance to at least 1 agent in all but ≤ 2 antimicrobial classes
● Example:
→ Isolate: Pseudomonas aeruginosa
→ Sensitive: Colistin (1 class)
→ Intermediate: none
→ Resistant: Amikacin, Aztreonam, Ceftazidime, Cefepime,
Ciprofloxacin, Imipenem, Meropenem, Piperacillin-
tazobactam
Figure 2. Examples of Mechanisms of antibiotic resistance. A screencap from
the lecture
Torres, CD | Funelas, JN; Sabulao, JVN; San JoSy, DG; Tagupa, EA Revised by: Perez, J. Page 1 of 6
 [MED 2-IR] L3 – MDR Organisms and Antibiotic Stewardship (24 OCTOBER 2021) Page 2 of 6

A. INACTIVATION BY ENZYMES MDR Gram-negative organisms (new definition) | 

● Most common mechanism of antibiotic resistance Table 2. History of MDR Gram-negative organisms and revised definition
→ e.g. Beta lactamases destroying antibiotics 1965 Extended spectrum Resistance to all penicillins
■ Beta lactamase hydrolyze the beta lactam ring, that will beta-lactamases (ESBLs) and cephalosporins (except
render the antibiotic ineffective cephamycins and new
■ Penicillin Binding Proteins (PBP) produce transpeptidase cephalosporins) and
responsible for cross-linking of the cell wall (makes it rigid) monobactam AND EXCEPT
■ Beta-lactam inhibits transpeptidation, but beta-lactamases repurposed beta-lactams
attack the antibiotic before it reaches the target site 1981 AmpC beta-lactamases Resistance to all
(ESBL-like) beta-lactams except
carbapenems and
repurposed beta-lactams
1996 Klebsiella pneumoniae Resistance to all
carbapenemases (KPC) beta-lactams except
repurposed formulations
2008 New Delhi Resistance to all antibiotics
metallo-beta-lactamases except tigecycline and
(NDM-1) polymyxins*, and
repurposed beta-lactams
*2 polymyxin preparation available in the market: polymyxin B and polymyxin E
(colistin)

A. EXTENDED-SPECTRUM BETA-LACTAMASES (ESBLs)

● Resistant to all penicillins, cephalosporins (except cephamycins)
and monobactams, and except repurposed beta-lactams
Figure 3. Inactivation by Beta-lactamase. A screencap from the lecture (2020) → new cephalosporins mentioned here are ceftazidime-
B. MODIFIED DRUG TARGET avibactam and ceftolozane-tazobactam which only have a
coverage for ESBL and MDR pathogens. They are not
● The antibiotic can enter the cell, but the receptor has been altered
considered 5th generation cephalosporins because of lack of
(antibiotic shaped as a circle; target site is triangular) leaving the
MRSA coverage and pseudomonal coverage. Ceftaroline only
antibiotic unable to bind to the original target site
has coverage for MRSA but not pseudomonas.
● This is the mechanism in MRSA
● Conferred by the resistance genes: TEM, SHV, CTX-M. Bacteria
C. INHIBITION OF DRUG UPTAKE with resistance genes leads to survival of some bacteria that will
● The antibiotic is unable to enter the cell due to closure of porin multiply pass on the resistance to antibiotics to the subsequent
channels. generations.
● Genes are located on the same plasmids that carry resistance
D. EFFLUX PUMP genes for aminoglycosides, chloramphenicol, co-trimoxazole,
● The drug enters the cell, only to be pumped out. fluoroquinolones, and tetracycline
→ In other words, since the plasmid contains resistance genes
IV. ANTIBIOTIC MISUSE for those other drug classes as well, then the drug of choice
● Antibiotic misuse contributes to antibiotic resistance should not belong to the above classes. Do not give these
● ~50% of prescribed antibiotics are inappropriate. Meaning, they drugs anymore for ESBLs!
are given for wrong indication like giving antibiotics for colds or ● DOC: Carbapenems | 
mild covid. → Not hydrolyzed by ESBLs
● ~30% of antibiotics are unnecessary ● Alternative agents: ceftazidime-avibactam, ceftolozane-
→ Excessive duration tazobactam, polymyxins, tigecycline, fosfomycin IV (fosfomycin
→ Non-infectious etiology not available in the Philippines), cefepime-enmetazobactam
→ Colonizers or contaminants → Side note: tigecycline is bacteriostatic. Bacteriostatic agents
→ Redundant coverage are not used for septic patients.
■ In treating intra-abdominal infections, there is no need to → Ceftazidime-avibactam and cefepime-enmetazobactam
give metronidazole if you already gave piperacillin- ■ Called “repurposed beta-lactams”
tazobactam. ■ Old drug: cefepime/ceftazidime – no coverage for ESBL
→ Failure to de-escalate − Added a beta-lactamase inhibitor
enmetazobactam/avibactam (makes it very useful for
V. MULTIDRUG-RESISTANT GRAM-NEGATIVE ORGANISMS ESBLs
MDR Gram-negative organisms (old definition) Risk Factors for the Development of MDROs | 
● DO NOT use narrow-spectrum antibiotics if one of these is
Table 1. History of MDR Gram-negative organisms and Old definition
1965 Extended spectrum Resistance to all penicillins
present. Start broad.
beta-lactamases (ESBLs) and cephalosporins (except → Antimicrobial therapy within the last 90 days (especially if 3 rd
cephamycins*) and or 4th generation cephalosporins or quinolones like
monobactam ciprofloxacin were used. These antibiotics increase ESBL risk)
1981 AmpC beta-lactamases Resistance to all ■ Always ask about history of antibiotic use
(ESBL-like) beta-lactams except → Current hospitalization of ≥ 5 days or hospitalization lasting ≥
carbapenem 2 days in the last 90 days
1996 Klebsiella pneumoniae Resistance to all → High frequency of antibiotic resistance in the community or in
carbapenemases (KPC) beta-lactams the specific hospital unit (e.g., ICU)
2008 New Delhi Resistance to all antibiotics ■ Most patients in the ICU have pneumonia, so they received
metallo-beta-lactamases except tigecycline and antibiotics
(NDM-1) colistin → Residence in a nursing home or extended care facility
*Cephamycins are cephalosporin-like (2nd generation cephalosporins) antibiotics → Chronic dialysis within 30 days
which are also used for infections caused by anaerobic organisms. Examples are → Home infusion therapy (including antibiotics)
cefoxitin and cefotetan.
 [MED 2-IR] L3 – MDR Organisms and Antibiotic Stewardship (24 OCTOBER 2021)
→ Home wound care
■ In the Philippine setting, some patients crush amoxicillin
and put it on their wounds
→ Family member with a MDRO
→ Immunosuppressive disease or therapy
■ e.g. lupus
● Don’t wait for the patient to deteriorate. Start with an appropriate
broad-spectrum antibiotic, get the culture, then either narrow
down the antibiotics or step-up treatment.
B. CARBAPENEMASES
● Organisms include Carbapenem-resistant Enterobacterales
(CREs) (e.g. KPC – Klebsiella pneumoniae carbapenemase)
● Resistant to all beta-lactams except repurposed
formulations
● Conferred by the resistance genes: KPC, VIM, IMP, NDM-1,
OXA-181, and -48
● Drug of choice: colistin (polymyxin E) + carbapenem OR
polymyxin B + carbapenem | 
→ Why give a carbapenem when we are dealing with
carbapenemases?
■ Polymyxin-Carbapenem combination gives a synergistic or
additive effect (still under debate)
■ Polymyxins disrupt the bacterial outer membrane and
increase its permeability to carbapenems
■ On the other hand, the carbapenems delay bacterial
resistance toward polymyxins
− Polymyxins are not used as monotherapy because
resistance develops very fast
− We are conserving the power or polymyxins as they are
considered one of the end-line drugs for gram-negative
organisms
Figure 4. Crystal Structure of Carbapenemase. A screencap from Doc Delgado’s
2023 lecture. KPC-2 (green) is the beta-lactamase located in the periplasmic
space. MexA-MexB OprM (center) - efflux pump. OprD (purple, upper left) –
mutation in porin expression. PBP3 (red, right) – penicillin-binding proteins.
Carbapenemases use 3 out of 4 mechanisms of drug resistance mentioned
previously.
● Alternative agents: (available in the Philippines)
→ For carbapenem-resistant Enterobacterales: tigecycline,
fosfomycin (IV), plazomicin, cefiderocol, eravacycline
■ KPC only: ceftazidime-avibactam, meropenem-
vaborbactam, imipinem-relebactam, cefepime-zidebactam,
cefepime-taniborbactam,
cefepime/aztreonam/meropenem-nacubactam
− should not be used for Enterobacter and E. coli
→ For carbapenem-resistant Acinetobacter spp.: tigecycline,
cefiderocol, eravacycline
■ Tigecycline – only static; cannot be used for bacteremic
patients
→ For carbapenem-resistant Pseudomonas spp.: ceftolozane-
tazobactam, cefiderocol, fosfomycin (IV),
cefepime/piperacillin-nacubactam
Page 3 of 6
C. METALLO-β-LACTAMASES
● NDMs (New Delhi Metallo-beta-lactamases)
● Resistance to ALL antibiotics except tigecycline, polymyxins,
and repurposed beta-lactams
● Due to resistance genes: VIM, IMP, NDM-1, SPM, SIM, GIM,
FIM. AIM, DIM, POM
● Drug of choice: colistin + carbapenem, or polymyxin B +
carbapenem
→ Treatment failure is more common as compared to CREs
● Alternative agents:
→ For NDM Enterobacterales: tigecycline, ceftazidime
avibactam + aztreonam, cefiderocol, aztreonam-avibactam,
cefepime-taniborbactam, aztreonam-nacubactam
→ For NDM Acinetobacter spp.: durlobactam-sulfabactam
■ Novel treatment as it combines two beta-lactamase
inhibitor without a beta-lactam backbone
→ For NDM Pseudomonas spp.: cefepime/piperacillin-
nacubactam
D. COLISTIN RESISTANCE
● Colistin is still the backbone treatment for carbapenemases and
MBLs
● However, resistance has been discovered in food animals and
retail meat in Eastern and Southern China (2011)
● Due to resistance genes: MCR-1 (now, up to MCR-5)
● Risk Factors:
→ Frequent healthcare exposure
→ Handling of contaminated food animals
● Drug of choice: not established
E. ANTIBIOTIC RESISTANCE SURVEILLANCE PROGRAM
● Published yearly
● USTH is one of the sentinel sites in this program
→ All specimens reported with drug resistance are retested and
reported to contribute to the national data
● Generally speaking, resistance rate of > 20% is considered
HIGH.
→ An antibiotic with resistance rate > 20% CANNOT be used for
empiric therapy.
Figure 5. Resistance of E. coli to various antibiotics based on the Antimicrobial
Resistance Surveillance Program in 2020. Taken from the lecture slides
● For E. coli, the most common cause of UTI in the Philippines,
almost all antibiotics are already > 20% resistant (see the graph
above)
→ We are left with IV antibiotics like carbapenems, amikacin, and
piperacillin-tazobactam
→ We might need to admit almost all patients with simple
infections because our oral antibiotics may not work
 [MED 2-IR] L3 – MDR Organisms and Antibiotic Stewardship (24 OCTOBER 2021) Page 4 of 6

● Acinetobacter – all antibiotics except colistin has > 20%

resistance rate
→ This alarming as Acinetobacter baumannii is one of the top 3
pathogens of hospital acquired pneumonia since 2013 in
USTH
→ When we suspect this type of infection, we use dual therapy
VI. MULTIDRUG-RESISTANT GRAM-POSITIVE ORGANISMS
Table 3. History of MDR Gram-positive Organisms
Year Organism
1950 Penicillin-resistant Staphylococcus aureus
1961 Methicillin-resistant S. aureus (MRSA)
1987 Vancomycin-resistant S. aureus (VRSA)
1996 Vancomycin-intermediate S. aureus (VISA)
Glycopeptide-intermediate S. aureus (GISA)
Mechanism of Action of Penicillin
● Penicillin Binding Protein (PBP) produces transpeptidase
→ Transpeptidase – responsible for cell wall cross-linking
Figure 6. Resistance of K. pneumoniae to various antibiotics based on the
→ Penicillin inhibits transpeptidase
Antimicrobial Resistance Surveillance Program in 2020. Taken from the lecture
slides
A. METHICILLIN-RESISTANT S. AUREUS (MRSA)
● B-lactam antibiotics cannot bind to PBP (altered PBP)
● Klebsiella pneumoniae – most common cause of pneumonia for → mecA gene produces PBP2a
patients with comorbid conditions ■ Penicillin is not made to bind to PBP2a (only to PBP)
→ We are left with IV antibiotics as all oral antibiotics are > 20% ● DOC for most MRSA infections: Vancomycin
resistant → Though also a cell wall active antibiotic, Vancomycin does
→ Even IV penicillins and cephalosporins are resistant not target the PBP
→ It binds to D-Ala-D-Ala terminus to help break cell wall
B. VANCOMYCIN-RESISTANT S. AUREUS (VRSA)
● Recall: Vancomycin targets the D-Ala-D-Ala terminus
● VanA gene – modified terminus (from D-Ala-D-Ala to D-Ala-D-
Lac) therefore vancomycin cannot bind to the cell wall
→ Modified drug target mechanism of antibiotic resistance
● DOC: daptomycin, linezolid
C. VANCOMYCIN-INTERMEDIATE S. AUREUS (VRSA)
● Vancomycin cannot reach the target site due to thick
peptidoglycan layer that are less completely cross-linked
together
→ “trapping” the vancomycin in the cell wall
● Treated with daptomycin, linezolid, quinupristine-dalfopristine
D. COMMUNITY-ACQUIRED AND HOSPITAL-ACQUIRED
MRSA
Table 4. Community and Hospital-acquired MRSA
Figure 7. Resistance of Pseudomonas aeruginosa to various antibiotics based Community-acquired Hospital-acquired
on the Antimicrobial Resistance Surveillance Program in 2020. Taken from the MRSA MRSA
lecture slides Risk ● Participating in ● Current hospitalization
Factors contact sports ● Residing in long term
● For P. aeruginosa, most antibiotics are still < 20% resistant.
● Crowded/unsanitary facility
conditions (e.g., ● Presence of invasive
prison) device
● Skin trauma ● Recent surgery
● Previous antibiotic ● Chronic dialysis
use
DOC Clindamycin Vancomycin
(bacteriostatic only; use
Vancomycin if patient
is septic or bactermic
as it is bactericidal)
Alternative TMP-SMX Ceftaroline*
Agents Doxycycline Teicoplanin
Dalbavancin
Telavancin
Daptomycin
Tigecycline
Quinopristin-dalfopristin
Linezolid
Figure 8. Resistance of Acinetobacter spp. to various antibiotics based on the Tedizolid
Antimicrobial Resistance Surveillance Program in 2020. Taken from the lecture *only cephalosporin with
slides MRSA coverage
 [MED 2-IR] L3 – MDR Organisms and Antibiotic Stewardship (24 OCTOBER 2021) Page 5 of 6

E. LIVESTOCK-ASSOCIATED MRSA Table 5. New Antibiotics for Resistant Gram-Positive and Negative Organisms
For Resistant Gram (+) For Resistant Gram (-)
● Emerged in humans exposed to livestock Oxazolidinones (NEW class) Tetracyclines (old class)
● Risk Factor: handling of contaminated meat products -Linezolid -Tigecycline (glycylcycline)
● Resistance genes: -Tedizolid -Eravacycline (fluorocycline)**
→ ST398 (America and Europe)
→ CC9 (Asia) Lipopeptide (NEW class) Phosphonic acid (old class)
● Treatment is not yet established -Daptomycin (for relaunching) -Fosfomycin IV

Streptogramins (NEW class) Carbapenems (old class)

-Quinupristin -Meropenem-vaborbactam
-Dalfopristin -Imipenem-relebactam*

Lipoglycopeptides (old class) Cephalosporin (old class)

- Teicoplanin -Ceftolozane-tazobactam
-Telavancin -Ceftazidime-avibactam
-Oritavancin/Dalbavancin (launched July 2020)
-Cefiderocol**
Cephalosporin (old class)
-Ceftaroline (launched June Aminoglycoside (old class)
2018) -Plazomicin*
*Pending FDA approval
**Phase III clinical trials
Figure 9. Resistance of S, aureus to various antibiotics based on the Drugs available in the Philippines are underlined
Antimicrobial Resistance Surveillance Program in 2020. Taken from the lecture
slides VIII. ANTIBIOTIC STEWARDSHIP
● In the Philippines: ● Goals:
→ MRSA rate (resistance to Oxacillin): 47.6% (lower compared → Optimize clinical outcomes
to 2019 data) → Minimize unintended consequences of antibiotic use
■ Still high and problematic: 5 out of 10 patients with S. ■ Reduce toxicity and selection of pathogenic organisms
aureus is likely due to MRSA such as C. difficile
→ Some parts of the country have MRSA rates reaching 91 to ■ Emergence of antibiotic resistance to other classes of
antibiotics that may share a plasmid (collateral damage)
100% (9 or 10 out of 10 patients) ☹
● Strategies of antibiotic stewardship:
VII. IMPACT OF MULTIDRUG-RESISTANT ORGANISMS → Limit unnecessary antibiotic use
● Increases morbidity and mortality ■ Reassess diagnosis and response to treatment after 48-72
● Increases healthcare cost hours
→ Prolonged hospital stay ■ De-escalate based on culture results to safely narrow down
→ Need for more expensive drugs therapy
● Pneumonia due to P. aeruginosa ■ Use shortest duration necessary
→ Fully susceptible − Low risk Community-acquired Pneumonia: 7 days
■ Piperacillin-tazobactam (3 days) - Php 13,860 − Early onset Ventilator-acquired Pneumonia:
■ Ciprofloxacin (11 days) - Php 1,320 ○ 7 days if non-Pseudomonal
→ Multidrug-resistant ○ 14 days if Pseudomonal
■ Meropenem (14 days) - Php 139,230 − Uncomplicated UTI: 7 days
− Cellulitis:
○ 7 days if non-MRSA
○ 14 days if MRSA
− Sepsis: 14 days
■ Follow local guidelines for optimal treatment
● Right drug for the right bug (determined by culture), right time and
the right dose for the right duration
→ Make sure that we do not undertreat as it will also contribute
to resistance (not too short, not too long)

VII. IMPACT OF THE COVID-19 PANDEMIC ON ANTIBIOTIC

STEWARDSHIP

Figure 10. Current Challenges. A screencap from batch 2022 lecture

● Antibiotic Armageddon: Steep rise in resistance rates with very
few new antibiotics in the pipeline
→ Most of the new formulations are only repurposed or modified
from old antibiotic classes
■ May pose a major problem as we expect fast development
of drug resistance
■ New antibiotics should have new mechanism of action,
not just modified
→ In the Philippines, very few agents are available
● This table summarizes the different new antibiotics for Gram (+)
and (-). Old classes are only modified, hence, there is fast
development of resistance. Those underlined are available in the
PH. Figure 11. Antibiotic Usage During the COVID-19 Pandemic. A screencap from
batch 2023 lecture
 [MED 2-IR] L3 – MDR Organisms and Antibiotic Stewardship (24 OCTOBER 2021) Page 6 of 6

● Steep increase in antibiotic use from January to March because about the duration. There will be more room for resistance if you
are not able to kill the organisms. This will result in the
doctors did not know how to treat COVID-19 yet.
mutations, rather than the prolonged intake of the antibiotic.
● By April, there is a decline in antibiotic usage
Learn to balance the pros and cons. Look at the indications and
→ As toxicity in COVID-19 was discovered to be due to the benefits and prioritize the most pressing indication (ie. Most
thrombosis and cytokine storm and not superimposed life threatening)
bacterial infection
7. How is antibiotic stewardship being practiced in USTH?
● Bacterial Co-Infection in COVID-19
Residents need to receive defend and get approval from the ID
→ Bacterial co-infection (on presentation) was identified in 3.5% specialists if they are to prescribe broad spectrum antibiotics.
of cases Additionally, there is an “antibiotic stop policy” where you are
→ Secondary bacterial infection was identified in 14.3% of only given antibiotics for 7 days. This will force you to have to
cases check on the patient (although you have to do this daily anyway)
→ The overall proportion of COVID-19 patients with and review whether the indication for the antibiotic is still
bacterial infection was 6.9% present. If the indication is still there, you will have to reorder the
→ Bacterial infection was more common in critically ill patients antibiotic.
(8.1%)
→ Most patients with COVID-19 received antibacterial agents END OF TRANSCRIPT
(71.9%)
IX. Q&A
1. Do we still need to request for culture before prescribing the
right antibiotic as out-patient?
Yes. if you have specimen that qualify for culture, then do so.
For uncomplicated UTI, no need to request for culture.
2. At what level of pus cells in the urine do we usually give
antibiotic right away?
We do not depend on the pus cells. Remember there is a
condition called sterile pyuria. Not all pus cells in the urine
should be treated as UTI. Clinical symptoms must be matched
with laboratory results. Remember: you do not treat the
laboratory results, treat the patient. Corelate everything you see
in the laboratory with the clinical condition of the patient. If the
patient is asymptomatic and has pyuria, investigate why the
patient has pyuria. For example, asymptomatic bacteriuria
cases should only be treated in pregnant, patients with
uncontrolled diabetes, unsteady creatinine, or in patients who REFERENCES
will undergo genitourinary manipulation, and post-transplant
Delgado, J. (2021), MDR Organisms and Antibiotic Stewardship [PowerPoint
patients.
Presentation]. Manila, Philippines: Faculty of Medicine and Surgery,
3. What is the DOC for MRSA patients with sepsis? University of Santo Tomas, MED 2
You will never go wrong with vancomycin. Next alternative is
Jameson J.L, Kasper, D.L., Longo, D.L., Fauci, A.S., Hauser, S.L.,
daptomycin except if the patient has pneumonia because the Loscalzo, J. (2018). Harrison’s Principles of Internal Medicine. USA:
surfactant of the lungs destroys daptomycin. McGraw-Hill Education.
Questions from the previous trans:
4. How do you treat pandrug resistant organisms knowing they
do not respond to any antibiotics?
If there is true pandrug resistance, the patient will succumb to
the organism. It is possible that there is in vitro resistance
(carbapenemase resistance) but may work in vivo, so you still
give your antibiotics such as polymyxin + carbapenem and
ceftazidime avibactam. So far, the slides that show patients with
pandrug resistance improved after being given antibiotics.
5. Regarding the role of veterinarians in the development of
antibiotic resistance: are the feeds/treatment of the
livestock currently being regulated by the FDA to prevent
antibiotic resistance?
It should be. This should be heavily regulated by the
government. However, it is not sure whether the people who run
the farms follow as there are other ways to get these
medicines/feeds (ie. Black market drugs). Medicines that you
also cannot read (eg. medicines where the whole package is in
another language) should not be made available to the public
because they do not understand the contents of the medication.
6. What is the maximum number of days an antibiotic (eg.
carbapenems and polymixins) can be administered for
patients with extensively resistant organisms? Will
prolonged use put these patients at risk for developing
resistance to these drugs?
Generally, 14 days minimum for XDROs but maximum is
variable. The goal is to kill off all the organisms. Don’t worry