ANTIMICROBIAL

RESISTANCE MECHANISM
WHAT IS WOUND HEALING
BY: MUNAWER ALSAEED (20201416)
TRIGGER 4

• 3 days later the mother brought her son to the health center. He was afebrile and pain in
his foot had subsided. After the doctor looked at the results of the lab tests (see below),
He asked the mother to continue with the drugs for further 4 days and to report to the
center after 2-3 weeks.
TRIGGER 5

• Three weeks later the mother brought her boy to the clinic for follow up. He was walking
normally and had no complaints. The wound had healed completely leaving a clean scar
without any complication. The doctor advised the mother that her child should always
wear shoes when playing football.
ANTIMICROBIAL RESISTANCE:

• Antimicrobial resistance is the ability of microbes to resist the effects of drugs .

• Thereafter, the germs are not killed, and their growth is not stopped.
ANTIMICROBIAL RESISTANCE:

Antimicrobial resistance is a global problem faced today in the treatment of infectious

diseases.

Resistance to antimicrobials is more prevalent in hospitals especially in intensive care units

due to the higher use.

Resistance to antimicrobial agents is of tow categories either intrinsic or acquired.

INTRINSIC (NATURAL) RESISTANCE:

• This type of resistance refers to bacteria that are insensitive, in their natural state, to an
antibiotic without the acquisition of any resistance factors. It is consistent and can be
expected:
1. An organism e.g. Streptomycetes has a gene that protects it from the antibiotics it
produces
2. Gram-negative cell membrane has pores too small to allow large antibiotic molecules,
e.g. nafcillin, to penetrate.
ACQUIRED RESISTANCE:

• It results from changes in the organism.

• It is inconsistent and unpredictable.

• The unpredictable nature of this resistance is the 1ry reason why laboratory

methods to detect resistance are necessary.

ANTIMICROBIAL RESISTANCE MECHANISMS 1

A- Altered permeability

• Decreased influx
 Reduction of permeability of the outer membrane by modification or
loss of porin (a hollow membrane protein) required for entry of the
antibiotic molecules, e.g. imipenem resistance in Pseudomonas.

 Reduction of uptake across the cytoplasmic membrane, e.g.

aminoglycosides resistance in Staphylococcus aureus.
ANTIMICROBIAL RESISTANCE MECHANISMS 2

• Efflux pumps:

The antibiotic is pumped out across the cytoplasmic membrane faster than it can
diffuse in, so the concentration of antibiotic remains too low to be effective.

This mechanism plays a role in the resistance to many antibiotics including

macrolides, tetracycline, quinolones and β-lactams by organisms such as
Escherichia coli, Shigella, Staphylococcus aureus and Pseudomonas aeruginosa.
 ANTIMICROBIAL RESISTANCE MECHANISMS 3

B. Inactivation of the antimicrobial (enzymatic), e.g.:

• Production of β-lactamases leads to hydrolysis of the β-lactam ring,

thus inactivating penicillins and cephalosporins.
• Production of acetyl transferase results in chloramphenicol resistance.
• Production of aminoglycosides modifying enzymes.
ANTIMICROBIAL RESISTANCE MECHANISMS 4

C. Target (site) modification:

• Modification of the penicillin-binding proteins (PBPs) is a primary mode of resistance to penicillin

in pneumococci and to all β-lactam antibiotics in methicillin-resistant S. aureus (MRSA).

• Alteration of the 50S ribosomal subunit reduces the affinity of macrolides, linezolid and
streptogramins for the ribosome.

• Alteration of the 30S ribosomal subunit for aminoglycosides

ANTIMICROBIAL RESISTANCE MECHANISMS 5

D. Target elimination by developing new metabolic pathways: These bacteria have the ability to
create new metabolic pathways that bypass the original target, e.g. Staphylococcus aureus can
bypass the drug effects of trimethoprim i.e. resistance to trimethoprim.

E. Target overproduction: In this mechanism, the bacteria counteract by increasing the production
of the antibiotic target with the objective of overwhelming the antibiotic by increasing the amount
of targets available (relative insufficiency of the antibiotic). This may be the mechanism used by
S. aureus strains with intermediate susceptibility to vancomycin (VISA). Similarly,
overproduction of PABA contributes to resistance to both sulfonamides and trimethoprim.
WOUND HEALING:

• Wound healing refers to a living organism's replacement of destroyed or damaged tissue

by newly produced tissue.
MECHANISM OF WOUND HEALING:

• Hemostasis Phase: Hemostasis is the process of the wound being closed by clotting.
Hemostasis starts when blood leaks out of the body. 

• Inflammatory Phase: is the second stage of wound healing and begins right after the
injury when the injured blood vessels leak transudate (made of water, salt, and protein)
causing localized swelling. Inflammation both controls bleeding and prevents infection.
MECHANISM OF WOUND HEALING:

• Proliferative Phase: The phase of wound healing is when the wound is rebuilt with new
tissue made up of collagen and extracellular matrix.

• Maturation Phase: Also called the remodeling stage of wound healing. Is when collagen is
remodeled from type III to type I and the wound fully closes. The cells that had been used
to repair the wound but which are no longer needed are removed by apoptosis, or
programmed cell death.
GRANULOMA:

• A granuloma is a small area of inflammation. Often found incidentally on an X-ray or

other imaging test done for a different reason. Typically, granulomas are noncancerous.
Frequently occur in the lungs, but can occur in other parts of the body and head as well.

• Granulomas seem to be a defensive mechanism that triggers the body to "wall off"
foreign invaders such as bacteria or fungi to keep them from spreading.
TYPES OF GRANULOMA:

• Foreign body granulomas: This type of granuloma develops when the body's immune
system reacts to an object or irritant that penetrates the skin, eye or body. 

• Skin granulomas: Several types of granuloma can affect the skin. The most common is 
granuloma annulare, a harmless skin condition that causes raised pink or flesh-coloured
bumps under the skin. 
COMPLICATIONS OF WOUND HEALING:

1. INFECTION

• 2. OSTEOMYELITIS: attacks a bone by traveling through the bloodstream or

spreading from nearby tissue 
COMPLICATIONS OF WOUND HEALING:

• 3. GANGRENE: can occur anytime there is a loss of blood supply to a certain area of
the body, usually the extremities such as the hands or feet.

• 4. PERIWOUND EDEMA: Another complication affecting the periwound area is

edema, swelling caused by excess fluid trapped within the body's tissues.
RESOURCES:

• Gyton and Hall

• https://www.bandgrip.com/blog/7-wound-care-complications-you-should-be-aware-of
• WHO: https://www.who.int/news-room/fact-sheets/detail/antimicrobial-resistance
 •The end!!!
•Any questions??