It broadly specifies the term in which microbes evolve mechanisms that protect them from the action of antimicrobials, which are used to treat Infections, making them difficult to treat. Bacteria, viruses, fungi, and parasites evolve to resist the drugs that are used to kill them.

MECHANISM OF RESISTANCE

DRUG INACTIVATION: A perfect example includes the breakdown of β-lactam antibiotics by β-lactamase enzymes. Microbes produce enzymes that chemically alter or destroy the drug, which has an antimicrobial property, rendering it ineffective.

TARGET MODIFICATION:  microbes change or modify the structure of the part of the cell target site that the drug normally attacks. For example, resistance can develop by altering ribosomes or other target proteins.

REDUCED DRUG ACCESS: Two mechanisms can explain this;

• Decreased uptake: changes in cell membrane permeability can prevent the drug from entering, hence hindering its action. Usually, this is observed in Gram-negative bacteria, which can alter their outer membrane to limit drug penetration.
• Active efflux: microbes can use efflux pumps to actively transport the antimicrobial drug out of the cell before it can accumulate to a lethal level.

BYPASS METABOLIC PATHWAYS: Bacteria can develop new metabolic pathways that allow them to bypass the step that the drug would normally inhibit.

TARGET MIMICRY: Some microbes produce proteins that mimic drug targets, binding the drug and sequestering it before it can reach its actual target site.

HOW DOES RESISTANCE DEVELOP?

Main reasons:

• Intrinsic resistance: Some bacteria naturally have certain characteristics, like lacking a target for a specific antibiotic, that make them inherently resistant. It is due to genes that they have natural, pre-existing resistance encoded in their chromosomes. For example, E. coli isnaturally resistant to vancomycin.
• Extrinsic resistance: resistance that’s developed over time due to exposure to antimicrobials and environmental pressures. Mechanism usually includes HGT, horizontal gene transfer between bacteria via conjugation, transduction, and transformation. Secondly, it can be done by random mutations during DNA replication.

SUB MECHANISM

• Natural selection: during an infection, antimicrobials kill susceptible microbes, but microbes that have random genetic mutations resist the drug survive and multiply.
• Environmental spread: release of antimicrobials and resistant bacteria in the environment through waste.
• Gene transfer: bacteria can share resistance genes, spreading them to even different kinds of bacteria.
• Exposure: frequent exposure to antimicrobials, both in humans and animals, provides the selective pressure that drives the development and spread of resistance.

FACTORS CONTRIBUTING TO AMR:

• Overprescription: Doctors prescribe antibiotics for viral infections or for too long periods.
• Misuse: Antibiotic course not finished for the given period.
• Agricultural use: Using antimicrobials for growth promotion or disease prevention in livestock.
• Poor infection control: Inadequate hygiene in healthcare settings and the community that allows resistant microbes to spread.
• Lack of new drugs: The slow pace of developing new antimicrobial drugs.

WHAT ARE THE IMPLICATIONS?

• INCREASED MORTALITY: AMR is the leading cause of death globally, threatening to reverse decades of medical progress.
  • LIMITED TREATMENT OPTIONS: very few effective treatment options are available for some infections, and some treatments, including carbapenem antibiotics, may be given through injection.

TREATMENT OF ANTIMICROBIAL RESISTANCE

Treatment involves using more distinguishable and powerful drugs, combination therapies, or newer treatments like phage therapy and antimicrobial peptides.

CURRENT TREATMENT STRATEGIES

• SPECIALIZED AND COMBINATION THERAPIES: Doctors should prescribe antibiotics that are effective against the resistant strain or combine different drugs to fight the infection.
• SECOND & THIRD LINE TREATMENT: In some cases, powerful and less common medicines like carbapenems, tigecycline, or polymyxin B may be necessary for particular resistant infections.
• OTHER ANTIBIOTICS: Older antibiotics may still be effective against certain resistant antibiotic strains, and new ones are being discovered.

EMERGING AND EXPERIMENTAL TREATMENTS

PHAGE THERAPY: Use of bacteriophages –viruses that infect bacteria to specifically target and kill resistant bacterial strains.

ANTIMICROBIAL PEPTIDES [AMPS]: These are a part of the body’s defense mechanism and can be used as a treatment as they are resistant to antimicrobial resistance.

ANTIBIOTIC RESISTANCE GENE INHIBITORS: These drugs work by silencing genes that give bacteria resistance or by targeting mechanisms like ribosomal subunits or efflux pumps.

PROBIOTICS: These introduce beneficial bacteria to outcompete and inhibit harmful strains.

SEPSIS

A term for an immune system’s dangerous reaction to an infection, which causes extensive inflammation throughout the body that can lead to tissue damage, organ failure, and even death.

SYMPTOMS

• Septicemia
• Sepsis rash
• Urinary issues
• Low energy
• Fast heart rate
• Low blood pressure
• Hypothermia
• Shaking and chills
• Sweaty skin
• Hyperventilation \shortness of breath
• Extreme pain
• Dementia

CAUSES OF SEPSIS

Any type of infection can lead to sepsis. This includes bacterial, viral, or fungal infections. Those that more commonly cause sepsis include infections of:

• Lungs, such as pneumonia.
• Kidney, bladder, and other parts of the urinary system.
• Digestive system.
• Bloodstream.
• Catheter sites.
• Wounds or burns.

HOW ANTIMICROBIAL RESISTANCE COMPLICATES SEPSIS

• Infections become difficult to treat: the pathogens causing sepsis are no longer susceptible to common antibiotics, making it challenging to control the original infection.
• Sepsis can escalate: without effective treatment to clear infection, the body’s inflammatory response to the infection can injure its own tissues and organs, leading to septic shock and organ failure.
• Limited treatment options: as resistance becomes stronger with time, the number of effective antimicrobial drugs decreases, forcing the use of second and third-line treatments that can have severe side effects and take a longer duration to work.
• Long-term and adverse outcomes: patients with AMR infections may have prolonged hospital stays and are greater risk of serious complications like organ failure.
• Increased mortality: sepsis has high and rising rates of mortality due to the inability to effectively treat infection due to resistance contributes significantly.

CONCLUSION

Below are some of the takeaways to be noted.

• The importance of prevention
• Vaccinations can prevent infections that might require antibiotics, such as pneumococcal for bacterial infections.
• Proper antimicrobial use is only when necessary and as prescribed in critical situations only.
• Key factors and solutions
• Need for rapid response with prompt recognition is crucial for treatment.

Addressing AMR to the public is essential to improve sepsis outcomes, and this includes responsible use of antibiotics and research into new treatments.

FAQs

1. What are superbugs?

They are bacteria that have become resistant to multiple antibiotics typically used to treat them.

2. Is it a new pandemic?

With each year, it is dangerously emerging as a global health issue.

3. What is antibiotic stewardship?

It is the process to improve the use of antibiotics while effectively treating infections.

4. Do antibiotic works in the common cold and flu?

No, it only works for bacterial infections. These infections, like the common cold, improve with time.

5. How is it detected that and infection is resistant?

A sample taken from a sick person is sent to a lab, where it is tested to see whether the given bacteria are treated with an antibiotic or not.