Antibiotic Resistance: How Bacteria Adapt Cell Wall Repair
Why in the news
Research from CCMB Hyderabad explained how bacteria keep dividing and surviving even when key cell-wall enzymes are missing, making resistance harder to beat and new antibiotics more urgent.
Key facts
- Burden: about 1.2 million deaths in 2021 were linked to antimicrobial resistance worldwide; hospital surveys in India show around 13% mortality from drug-resistant infections.
- Definition: resistance occurs when bacteria change and survive drugs that once treated them.
- Spread of resistance: bacteria adapt over time and can pass resistance genes on through horizontal gene transfer.
- Where it spreads: hospitals, farms, communities and the environment; travel and trade carry it across borders.
- Patient impact: longer stays, costlier care, more follow-ups, and sometimes death.
- Prevention: use antibiotics only when needed and follow hygiene and sanitation.
Cell wall science
| Item | Detail |
|---|---|
| Bacterial wall | Peptidoglycan, absent in human cells |
| Backbone | Glycan chains of NAG and NAM sugars |
| Lattice | Peptides crosslink the NAM sugars |
| Penicillin action | Disrupts crosslinks, weakening the wall so the cell bursts (lysis) |
| Resistance routes | Enzymes that degrade penicillins; altered target that blocks binding |
Research insight
- To divide, bacteria extend the wall by selectively breaking and rebuilding bonds.
- Endopeptidases cut the peptide crosslinks; lytic transglycosylases (LTs) cut the sugar chains.
- Dr. Manjula Reddy’s team at CCMB Hyderabad showed bacteria can make up for lost endopeptidases by overproducing LTs and keep remodelling their walls.
- This flexibility helps bacteria withstand antibiotics and complicates resistance.
Exam angle
- Institute: CCMB, Hyderabad; scientist: Dr. Manjula Reddy.
- Terms: peptidoglycan, horizontal gene transfer, endopeptidase, lytic transglycosylase.