🦠 Bacteria — Structure, Classification, Importance & Bacteria vs Virus
Definition · Prokaryotic Cell Structure · Shapes · Gram Staining · Nutrition · Reproduction · Benefits · Diseases · AMR · Bacteria vs Virus (Student Confusion Solved!) · PYQs & MCQs
Prokaryotic (Bacterial) Cell Structure. Key components from outside to inside: Capsule (gelatinous, protective, increases virulence — Diplococcus pneumoniae), Cell Wall (peptidoglycan — rigid, gives shape), Cytoplasmic Membrane (controls molecule flow), Cytoplasm (site of all cellular processes), Nucleoid (circular DNA — NOT in a membrane-bound nucleus), Ribosomes (70S — protein synthesis). External structures: Flagella (movement), Pili (attachment). Note: NO mitochondria, NO true nucleus, NO membrane-bound organelles. (Uploaded image — Legacy IAS)
| Structure | Composition | Function | Key UPSC Fact |
|---|---|---|---|
| Capsule | Gelatinous polysaccharide (or polypeptide) | Protection; increases virulence (pathogenicity) | Diplococcus pneumoniae has capsule. Encapsulated bacteria resist phagocytosis. |
| Cell Wall | Peptidoglycan (murein) | Rigid outer layer — gives shape and protection | Gram staining depends on peptidoglycan thickness. Penicillin targets cell wall synthesis. |
| Cytoplasmic Membrane | Phospholipid bilayer + proteins | Controls molecule flow in/out; houses metabolic processes | Site of electron transport chain (bacteria have no mitochondria) |
| Cytoplasm | Semi-fluid with DNA, ribosomes, enzymes | Site of ALL cellular processes | Contains circular DNA (not linear like eukaryotes) |
| Nucleoid | Single circular DNA molecule | Genetic information storage and replication | NOT enclosed in a membrane — key prokaryote feature. Also has plasmids (extra-chromosomal DNA) |
| Ribosomes | Protein + rRNA; 70S (30S + 50S subunits) | Protein synthesis | Bacterial ribosomes are 70S (eukaryotic = 80S). Antibiotics (streptomycin, tetracycline) target 70S ribosomes. |
| Flagella | Protein (flagellin) | Locomotion/movement | Long whip-like. Arrangement: monotrichous (1), amphitrichous (both ends), lophotrichous (cluster), peritrichous (all around — E.coli) |
| Pili (Fimbriae) | Protein (pilin) | Attachment to surfaces and other cells; genetic transfer (sex pili) | Sex pili used in conjugation (bacterial "sex" — DNA transfer) |
| Endospores | Thick protein coat + dehydrated DNA | Dormant survival structure — extreme stress resistance | Bacillus anthracis (anthrax), Clostridium tetani (tetanus), Clostridium botulinum (botulism). Survive boiling — autoclaving needed. |
| Plasmid | Small circular extra-chromosomal DNA | Carries extra genes (antibiotic resistance, virulence) | Ti plasmid from Agrobacterium tumefaciens used in GM crops. Antibiotic resistance genes on plasmids spread by conjugation. |
Shapes of Bacteria — Morphological Classification. Bacteria are classified by shape: Coccus (spherical — Staphylococcus in clusters, Streptococcus in chains, Diplococci in pairs, Micrococci in irregular clusters). Bacillus (rod-shaped — Lactobacillus, E. coli, Diplobacilli in pairs). Vibrio (comma/curved rod — Vibrio cholerae causes cholera). Spirilla (rigid spiral with flagella — Helicobacter pylori causes peptic ulcers). Spirochetes (flexible corkscrew — Treponema pallidum causes syphilis). (Uploaded image — Legacy IAS)
| Shape | Arrangement | Example | Disease |
|---|---|---|---|
| Coccus (spherical) | Clusters: Staphylococci; Chains: Streptococci; Pairs: Diplococci | Staphylococcus aureus | Staph infections, food poisoning |
| Bacillus (rod) | Single, chains, palisade | Mycobacterium tuberculosis | Tuberculosis (TB) |
| Vibrio (comma) | Single, curved | Vibrio cholerae | Cholera |
| Spirillum (rigid spiral) | Single spiral | Helicobacter pylori | Peptic ulcers |
| Spirochete (flexible spiral) | Corkscrew coil | Treponema pallidum | Syphilis; Borrelia → Lyme disease |
| Mycoplasma | Pleomorphic (no cell wall) | Mycoplasma pneumoniae | Walking pneumonia; among the smallest bacteria (M. genitalium ~0.2 μm); no cell wall so unaffected by penicillin |
Mycobacterium tuberculosis (TB), Pseudomonas, Lactobacillus, Nocardia
Clostridium (tetanus, botulism, gangrene), Bacteroides
E. coli, Salmonella, Enterobacteriaceae (most gut bacteria)
Chemoautotrophs: Use chemical reactions → Nitrifying bacteria (Nitrosomonas, Nitrobacter), Sulphur bacteria
Heterotrophs: Get nutrition from organic compounds → Most pathogenic bacteria
Nitrogen-fixing: Fix atmospheric N₂ → Rhizobium (symbiotic in legumes), Azotobacter (free-living), Anabaena (BGA)
Gram Staining — Cell Wall Difference. (a) Gram-POSITIVE (left): Very thick peptidoglycan layer (20–80 nm) → retains crystal violet dye → appears blue/purple. No outer membrane. (b) Gram-NEGATIVE (right): Thin peptidoglycan (2–7 nm) in periplasmic space + outer lipopolysaccharide (LPS) membrane → crystal violet washed out by alcohol → counterstain (safranin) gives red/pink colour. LPS = endotoxin → can cause septic shock. Gram-negative bacteria harder to treat (outer membrane blocks many antibiotics). (Uploaded image — Legacy IAS)
| Feature | 🔵 Gram-Positive | 🔴 Gram-Negative |
|---|---|---|
| Stain colour | Blue / Purple (retains crystal violet) | Red / Pink (counterstained by safranin) |
| Peptidoglycan | Very thick (20–80 nm) | Thin (2–7 nm) in periplasmic space |
| Outer membrane | Absent | Present (LPS — lipopolysaccharide = endotoxin) |
| Toxin type | Exotoxins (secreted proteins — e.g. tetanus toxin) | Endotoxins (LPS in cell wall — released on death) |
| Antibiotic sensitivity | Sensitive to penicillin (damages peptidoglycan) | Resistant to many antibiotics (outer membrane barrier) |
| Examples | Staphylococcus, Streptococcus, Clostridium, Bacillus, Corynebacterium, Listeria | E. coli, Salmonella, Pseudomonas, Klebsiella, Vibrio cholerae, Neisseria, Helicobacter |
| Disease examples | Staph infection, Strep throat, Tetanus, Anthrax, Diphtheria | Cholera, Typhoid, Plague, Gonorrhoea, Tuberculosis-like (Klebsiella) |
Gram-Negative = Red/Pink = Resistant outer membrane = Rough LPS endotoxin (All R's)
Think: Gram-positive bacteria are like brick walls (thick, purple). Gram-negative are like buildings with a security fence outside (thin wall + outer membrane = harder to breach with antibiotics).
Biofertilisers: Actinobacteria, Azotobacter, Rhodospirillum, Cyanobacteria
Biopesticides: Bacillus thuringiensis (Bt) — produces crystal proteins toxic to insects → Bt cotton, Bt brinjal
GM crops: Agrobacterium tumefaciens Ti plasmid used to insert foreign genes into plants
Vinegar: Acetobacter → acetic acid fermentation
Textile industry: Bacterial enzymes for desizing, scouring, bleaching
Paper industry: Bio-bleaching reduces chemical use
Cosmetics: Hyaluronic acid and peptides via bacterial fermentation
Insulin production: E. coli engineered to produce human insulin
Recombinant vaccines: Bacteria engineered to produce antigens
Probiotics: Lactobacillus, Bifidobacterium → gut health, synthesise vitamins K, B12, folic acid, biotin
PCR tool: Taq polymerase from Thermus aquaticus (hot spring bacterium)
CRISPR-Cas9: Gene-editing tool derived from bacterial immune system
Restriction endonucleases: Molecular scissors — originally from bacteria defending against phages
PCR: Taq polymerase from Thermus aquaticus enables amplification of DNA
Expression systems: E. coli, B. subtilis as host bacteria for protein production
Plastic degradation: Ideonella sakaiensis (Japan) breaks down PET plastic (bottles) using PETase enzyme
Wastewater treatment: Activated sludge process uses bacteria to break down organic waste
Heavy metal removal: Sulphate-reducing bacteria
Decomposers: Bacteria return nutrients to soil — essential for nutrient cycling
Biogas/Methane: Methanogens (archaebacteria) produce CH₄ in biogas plants
Hydrogen fuel: Some bacteria (Rhodobacter) produce H₂ via photobiological processes
Microbial fuel cells: Geobacter bacteria directly generate electricity from organic waste
| Disease | Bacterium | Mode |
|---|---|---|
| Tuberculosis (TB) | Mycobacterium tuberculosis | Airborne droplets |
| Cholera | Vibrio cholerae | Contaminated water/food |
| Typhoid | Salmonella typhi | Contaminated water/food |
| Tetanus | Clostridium tetani | Wound infection (spores) |
| Anthrax | Bacillus anthracis | Spores (soil/inhalation) |
| Plague | Yersinia pestis | Flea bite (rat vector) |
| Leprosy | Mycobacterium leprae | Prolonged contact |
| Diphtheria | Corynebacterium diphtheriae | Airborne |
| Whooping cough | Bordetella pertussis | Airborne droplets |
| Food poisoning | Staphylococcus aureus, Clostridium botulinum, Salmonella | Contaminated food |
| Peptic ulcers | Helicobacter pylori | Oral route; stomach colonisation |
How resistance develops: Mutation (random genetic change) + Natural selection (antibiotic kills sensitive bacteria, resistant ones survive and multiply) + Plasmid transfer (resistance genes spread between bacteria via conjugation).
Most critical resistant bacteria (ESKAPE pathogens):
• MRSA — Methicillin-resistant Staphylococcus aureus
• MDR-TB — Multi-drug resistant M. tuberculosis
• VRE — Vancomycin-resistant Enterococcus
• CRE — Carbapenem-resistant Enterobacteriaceae
• XDR-TB — Extensively drug resistant TB
Global burden: AMR kills ~1.27 million people/year directly (2019 Lancet study). WHO calls AMR one of top 10 global threats. India has high AMR burden due to: antibiotic overuse, OTC availability, antibiotic use in livestock.
India initiatives: National Action Plan on AMR (NAP-AMR, 2017), Red Line Campaign (prescription-only antibiotics marked with red line).
Food spoilage: E. coli, Spirochaeta → souring of milk, rotting of vegetables
Bioterrorism: Anthrax spores used as bioweapons (WW2, 2001 US anthrax letter attacks). Plague also weaponised historically.
Virus = A piece of instructions in an envelope. It has NO building, NO power, NO factory, NO metabolism of its own. It's just a set of genetic instructions (DNA or RNA) in a protein coat. It HIJACKS your cells' machinery to reproduce. Antibiotics don't work — you can only prevent viruses (vaccines) or slow them (antivirals).
| Feature | 🦠 Bacteria | 🔴 Virus |
|---|---|---|
| Nature | Living organism (cellular) | Acellular (debated — "on the edge of life") |
| Size | 0.5–5 micrometres (μm) | 20–300 nanometres (nm) — 10–100× smaller than bacteria (average virus ~100 nm; average bacterium ~1,000 nm) |
| Cell structure | Prokaryotic cell — cell wall, membrane, cytoplasm, ribosomes | NOT a cell — just nucleic acid + protein coat (capsid) ± lipid envelope |
| Nucleus | No true nucleus — nucleoid (circular DNA) | No nucleus — contains ONLY DNA or RNA (not both) |
| Genetic material | Both DNA AND RNA present | EITHER DNA OR RNA (never both) |
| Cell wall | ✅ Present (peptidoglycan) | ❌ Absent — has protein capsid instead |
| Ribosomes | ✅ Present (70S) — independent protein synthesis | ❌ Absent — uses HOST cell's ribosomes |
| Metabolism | ✅ Independent metabolic activities | ❌ No independent metabolism — obligate intracellular parasite |
| Reproduction | Binary fission (independent, every 20 min) | Only INSIDE living host cells (hijacks host machinery) |
| Can be cultured? | ✅ Yes — on artificial media (agar plates) | ❌ No — only inside living cells (embryonated eggs, cell cultures) |
| Killed by antibiotics? | ✅ YES — antibiotics target bacterial cell wall, ribosomes, DNA replication | ❌ NO — antibiotics have NO effect on viruses |
| Treatment | Antibiotics (penicillin, streptomycin, tetracycline) | Antivirals (oseltamivir for flu, remdesivir for COVID, ART for HIV) + Vaccines |
| Examples — diseases | TB, Cholera, Typhoid, Tetanus, Plague, Leprosy, Anthrax | COVID-19, Influenza, Dengue, Malaria (NO — that's parasite!), HIV/AIDS, Rabies, Polio, Measles, Hepatitis |
| Examples — organism | E. coli, Staphylococcus, Mycobacterium tuberculosis, Rhizobium, Lactobacillus | SARS-CoV-2, HIV, Influenza A, Dengue virus, TMV (Tobacco Mosaic Virus — first virus discovered, 1892) |
| Kingdom | Kingdom Monera (in Whittaker's 5-kingdom) | No kingdom — classified separately (not in any kingdom!) |
| Discovery | Antonie van Leeuwenhoek (1670s) — "animalcules" | Dmitri Ivanovsky (1892) — TMV first virus; term "virus" by Martinus Beijerinck (1898) |
WRONG. Antibiotics only kill bacteria. For viruses, antibiotics are useless. A doctor prescribing antibiotics for a cold (viral) is wrong practice and contributes to AMR.
WRONG. Malaria is caused by Plasmodium — a PROTOZOAN parasite (Kingdom Protista). Not bacteria, not virus. Spread by Anopheles mosquito.
WRONG — correct answer is EITHER DNA OR RNA (never both). HIV = RNA virus. Herpes = DNA virus. Influenza = RNA virus. COVID-19 (SARS-CoV-2) = RNA virus.
WRONG. Bacteria (0.5–5 μm) are 10–100× LARGER than viruses (20–300 nm) depending on type. Order of size (smallest to largest): Viruses < Bacteria < Eukaryotic cells.
- Antibiotics are effective against both bacterial and viral infections.
- Bacteria possess both DNA and RNA, whereas viruses contain either DNA or RNA but not both.
- Viruses can replicate independently without a host cell using their own ribosomes.
- The bacterium Ideonella sakaiensis has been discovered to break down polyethylene terephthalate (PET) plastic.
- a) 1 and 4 only
- b) 2 and 4 only ✓
- c) 1, 2 and 4 only
- d) 2, 3 and 4 only
Statement 2 CORRECT: Bacteria (living cells) contain BOTH DNA (genome) AND RNA (mRNA, rRNA in ribosomes, tRNA). This is true of all living cells. Viruses have either DNA OR RNA (not both) — RNA viruses: HIV, Influenza, SARS-CoV-2, Dengue, Hepatitis C. DNA viruses: Herpes, Hepatitis B, Poxvirus, Adenovirus.
Statement 3 WRONG: Viruses CANNOT replicate independently. They have NO ribosomes, NO metabolic enzymes, NO cellular machinery. They must inject their genetic material into a HOST cell and commandeer the host's ribosomes, ATP, amino acids, etc. to replicate. This is why they are called obligate intracellular parasites and why some scientists debate whether they are truly "alive."
Statement 4 CORRECT: Ideonella sakaiensis was discovered near a plastic recycling facility in Japan (2016). It produces two enzymes — PETase (breaks PET into MHET) and MHETase (further breaks down MHET into harmless chemicals). This discovery holds promise for addressing global plastic pollution. Scientists have since engineered enhanced versions of PETase.
- (a) MRSA produces a thick polysaccharide capsule that physically prevents methicillin molecules from reaching the cell wall, protecting the bacteria regardless of antibiotic concentration
- (b) MRSA converts methicillin into a harmless compound using a specialised enzyme called methicillinase that breaks the antibiotic apart before it can bind to any bacterial target
- (c) MRSA carries a gene (mecA) on a mobile genetic element that encodes an altered penicillin-binding protein (PBP2a) with very low affinity for methicillin and all beta-lactam antibiotics — the antibiotic cannot bind to its target (cell wall synthesis enzyme), so cell wall synthesis continues and the bacteria survives
- (d) MRSA develops resistance by permanently eliminating its cell wall — without a cell wall, methicillin (which targets cell wall synthesis) has nothing to attack, and MRSA survives as a permanently wall-less bacterium called a mycoplasma
- (a) Endospores are resistant because they contain large quantities of antibiotics synthesised by the bacterium specifically to repel competing microorganisms — these antibiotics also protect the spore from environmental chemicals and heat
- (b) Endospores are not cells in the active sense — they are dehydrated, dormant structures containing DNA and dipicolinic acid (DPA) within multiple thick protein layers (spore coat, cortex). The near-complete dehydration prevents heat denaturation of proteins, while the DPA-Ca²⁺ complex protects DNA from damage; together these features give endospores resistance to heat (boiling), UV radiation, desiccation, and disinfectants that easily kill vegetative bacteria
- (c) Endospores are resistant because they replicate in bursts inside a hard calcium carbonate shell — the shell physically deflects heat and chemicals, and the rapid internal replication ensures that even if some DNA is damaged, the spore contains hundreds of DNA copies for repair
- (d) Endospores resist heat and chemicals because they switch to a completely different carbon-based chemistry — instead of using water as a solvent, they use glycerol, which has a much higher boiling point and doesn't denature proteins at temperatures that would destroy water-based cells
- (a) Taq polymerase is useful for PCR because T. aquaticus is a nitrogen-fixing bacterium, and its polymerase uses atmospheric nitrogen rather than ATP as its energy source — making the PCR reaction 100× more energy-efficient than using DNA polymerases from ordinary bacteria
- (b) Taq polymerase from T. aquaticus is used because this bacterium lives in radioactive environments, making its polymerase resistant to the radiation used to detect PCR products, allowing combined amplification and detection in a single chamber without shielding
- (c) T. aquaticus polymerase is preferred because it has an exceptionally fast replication rate — it can copy DNA 1,000× faster than ordinary polymerases due to having 200 active sites per molecule, dramatically reducing PCR reaction time from days to minutes
- (d) T. aquaticus is a thermophilic bacterium living in hot springs at 70–80°C, and its DNA polymerase is thermostable — it remains active at the high temperatures (95°C) needed to denature (separate) DNA strands during PCR. Ordinary DNA polymerases would be permanently denatured at these temperatures, requiring fresh enzyme to be added each cycle — making PCR impractical before Taq polymerase's discovery
| Topic | Key Facts |
|---|---|
| Definition | Prokaryotic, single-celled, no true nucleus, no membrane-bound organelles. Evolved 3.5 billion years ago. Found everywhere. Human body: 38 trillion bacteria. |
| Structure | Capsule (virulence), Cell wall (peptidoglycan), Cytoplasmic membrane, Cytoplasm, Nucleoid (circular DNA), Ribosomes (70S), Flagella (movement), Pili (attachment/conjugation), Plasmid (extra DNA), Endospores (Bacillus, Clostridium — extreme resistance). |
| Shapes | Coccus (spherical — Staphylococcus in clusters, Streptococcus in chains), Bacillus (rod — TB, E.coli), Vibrio (comma — cholera), Spirillum (rigid spiral — H. pylori), Spirochete (flexible spiral — syphilis, Lyme disease), Mycoplasma (pleomorphic, no cell wall — among the smallest known bacteria). |
| Gram Staining | Gram-positive: thick peptidoglycan → blue/purple, sensitive to penicillin (Staphylococcus, Streptococcus, Clostridium, Bacillus). Gram-negative: thin peptidoglycan + outer LPS membrane → red/pink, more resistant (E.coli, Salmonella, Vibrio, Pseudomonas, Klebsiella). |
| Important Applications | N-fixation: Rhizobium (legumes), Azotobacter (free-living), Anabaena-Azolla (rice). Biofertilisers: Azotobacter, Rhodospirillum, Cyanobacteria. Biopesticide: Bacillus thuringiensis (Bt cotton). Fermentation: Lactobacillus (yogurt, cheese). Medicine: E.coli → insulin. PCR: Taq polymerase from Thermus aquaticus. Plastic: Ideonella sakaiensis → PET degradation. CRISPR from bacterial immune system. |
| AMR | Antimicrobial Resistance. MRSA (mecA gene, altered PBP2a), MDR-TB, VRE, CRE. Kills 1.27M/year. WHO top 10 threat. India: NAP-AMR 2017, Red Line Campaign. Mechanism: mutation + plasmid transfer. Never skip antibiotic course. |
| Bacteria vs Virus — KEY | Bacteria: living, cell, both DNA+RNA, independent replication, 0.5–5μm, treatable with antibiotics. Virus: acellular, DNA OR RNA only, needs host cell, 20–300nm, antibiotics USELESS, vaccines/antivirals used. Viruses are 10–100× smaller than bacteria (average virus ~100 nm; average bacterium ~1,000 nm). |
| Common Disease Confusion | BACTERIAL: TB, Cholera, Typhoid, Tetanus, Anthrax, Plague, Leprosy, Diphtheria, Whooping cough. VIRAL: COVID-19, HIV, Dengue, Influenza, Hepatitis B/C, Polio, Measles, Rabies. PARASITIC (protozoa): Malaria (Plasmodium), Amoebiasis (Entamoeba), Kala-azar (Leishmania). |
Trap 1 — "Antibiotics work against viruses too" → WRONG! Antibiotics ONLY work against bacteria. Viruses have no cell wall, no 70S ribosomes, no bacterial enzymes to target. This is the #1 public health misconception and a classic UPSC trap. AMR worsens when antibiotics are wrongly used for viral infections like cold/flu/COVID.
Trap 2 — "Viruses contain both DNA and RNA" → WRONG! Viruses contain EITHER DNA OR RNA — never both. Bacteria (like all living cells) contain both. RNA viruses: HIV, Influenza, SARS-CoV-2, Dengue, Hepatitis C, Polio. DNA viruses: Herpes simplex, Hepatitis B, Poxvirus, Papillomavirus (HPV). This is a direct UPSC statement-type question.
Trap 3 — "Malaria is caused by a virus or bacterium" → WRONG! Malaria is caused by Plasmodium — a protozoan parasite (Kingdom Protista). Not virus, not bacteria. Transmitted by female Anopheles mosquito. Similarly: Sleeping sickness = Trypanosoma (protozoa); Kala-azar = Leishmania (protozoa). These are parasitic diseases — different from bacterial or viral.
Trap 4 — "Cyanobacteria (Blue-Green Algae) are plants" → WRONG! Cyanobacteria are prokaryotes in Kingdom Monera. Despite having chlorophyll and performing photosynthesis, they have no membrane-bound nucleus, no chloroplast, peptidoglycan cell wall. They are bacteria, not algae or plants. However, the endosymbiotic theory proposes that chloroplasts evolved from ancient cyanobacteria engulfed by early eukaryotic cells — explaining why both have similar photosynthetic machinery.
Trap 5 — "Bacterial ribosomes are 80S like animal cells" → WRONG! Bacterial ribosomes are 70S (composed of 30S + 50S subunits). Eukaryotic (animal, plant, fungal) ribosomes are 80S (40S + 60S). This difference is medically crucial — antibiotics like streptomycin (30S), tetracycline (30S), erythromycin (50S), and chloramphenicol (50S) specifically target bacterial 70S ribosomes WITHOUT affecting human 80S ribosomes. This is the basis of antibiotic selectivity and safety.


