Food Microbiology

0 · Exam Blueprintread first

FOOD90023 is 70% written exam: a 1-hr mid-semester exam (20%, closed book · calculators only, SAQ + MCQ) and a 2-hr final (50%, ~7 short-answer/essay Qs). Plus 6 fortnightly quizzes (10%) + a 1000-word practical report (20%).

SAQs reward full sentences + a named example + a number. The MCQ section mirrors the quizzes. The coordinator recycles questions across the MTE and final.

Guaranteed-recurring SAQs: bacteriophages (define + lytic/lysogenic + food uses); the swollen-can scenario; infection vs intoxication + exotoxin classes; bacterial vs fungal spores; 3 gene-transfer mechanisms; malolactic fermentation + its inhibitors; the growth-maths calc N=N₀·e^(µt); conventional-ID limitations; validation vs evaluation.

1 · Classification & TaxonomyLec 2

Taxonomy = classification (grouping by similarity/phylogeny) + nomenclature (naming) + identification (placing a new isolate). Hierarchy: Domain > Kingdom > Phylum > Class > Order > Family > Genus > Species > Strain.

Binomial (Linnaeus): Genus (cap) + epithet (lower), italic; e.g. Staphylococcus aureus → S. aureus. Strains carry the safety load: E. coli O157:H7 (O=cell-wall, H=flagellar antigen) is a pathogen; most E. coli are harmless.

Prokaryote (Bacteria, Archaea): no nuclear membrane, single circular chromosome, 70S ribosomes, no organelles. Eukaryote (fungi, protozoa): true nucleus, organelles, 80S.

Trap: classification = the scheme; identification = the process. Archaea ARE prokaryotes but lack peptidoglycan & their transcription resembles eukaryotes.

1b · Microbial Groups in Foodname one each

Trap (MTE): "classes of disease-causing microbes" → list across ALL groups, not just bacteria.

1c · Strain & Specieswhy it matters

A species is a group of strains sharing many stable properties; a strain is a subset differing by minor traits. The strain carries the food-safety load — E. coli O157:H7 is pathogenic, most E. coli are harmless. Modern classification uses 16S rRNA for phylogenetic relatedness, not morphology alone.

2 · The Bacterial CellLec 3 · anatomy

Shapes: cocci (spheres), bacilli (rods), spiral (spirilla/vibrio/spirochaetes); 1–10 µm. Arrangements: diplo-, strepto- (chains), staphylo- (clusters), tetrad, sarcina.

Trap: pili = long & few (conjugation); fimbriae = short & many (attachment). Plasmids are NOT in the nucleoid & replicate independently.

3 · Gram +ve vs −ve Envelope★ Lec 2/3

The Gram stain: crystal violet → iodine → alcohol decolourise → safranin. G+ retain violet (purple); G− stain pink/red.

Alcohol dehydrates the thick G+ wall (traps dye); it dissolves the G− outer membrane (dye washes out). LPS (lipid A) = endotoxin → fever/septic shock on lysis. The G− outer membrane gives bile/detergent tolerance (basis of selective media) + antibiotic resistance.

Trap: teichoic acid = G+ only; LPS/outer membrane = G− only.

3b · Reading the Gram Stainprac P4

1. Crystal violet — all cells stain purple
2. Iodine (mordant) — fixes the CV–iodine complex in the wall
3. Alcohol/acetone — the decolouriser; the critical step
4. Safranin — counterstain (pink)

G+ thick wall dehydrates & traps the complex → stays purple; G− thin wall + dissolved outer membrane loses it → goes pink. Over-decolourising turns G+ cells falsely G− — the classic prac error. Old/dead G+ cells can also stain unevenly (gram-variable), so always use a fresh log-phase culture.

Endotoxin (LPS, structural, heat-stable, G−) vs exotoxin (secreted protein, often heat-labile, G+ and G−) — see side 2. The G− outer membrane is also why those organisms tolerate bile & detergents, the basis of selective enrichment media for gut pathogens.

4 · Endospores★ MTE Q6

A dormant, highly resistant survival structure formed inside Gram-positive Bacillus (aerobic) & Clostridium (anaerobic). One cell → one spore (NOT reproduction).

Sporulation (triggered by starvation): DNA replicates → axial filament → septum near a pole → engulfment of forespore → cortex + germ wall → accumulate Ca²⁺ + dipicolinic acid (DPA) → spore coat → core dehydrates → mother cell lyses, spore freed. Germination returns it to a vegetative cell when conditions favour growth.

Resistance basis: (a) dehydrated core, (b) Ca-dipicolinate stabilises macromolecules, (c) thermal adaptation + tough coats/SASPs protecting DNA. Resists heat, irradiation, desiccation, chemicals, time.

Significance: survive cooking & pasteurisation → demand commercial sterility (121 °C botulinum cook). C. botulinum in canned/anaerobic foods, B. cereus in rice, C. perfringens in warm-held meats.

5 · Yeasts & MouldsLec 4 · fungi

Eukaryotes, chitin wall (not cellulose, not peptidoglycan), absorptive/heterotrophic (no photosynthesis). Modes: saprophytic, parasitic, symbiotic.

Moulds — multicellular; hyphae (septate or coenocytic) form a mycelium; spores on conidiophores; colonise food surfaces. Groups: Zygomycetes (Rhizopus), Ascomycetes (Aspergillus, Penicillium), Deuteromycetes (asexual only). Mycotoxins: aflatoxin (A. flavus, carcinogen), patulin, ochratoxin.

Yeasts — unicellular ~10–20 µm; reproduce mainly by budding; in the depth of liquid foods. S. cerevisiae: bread/beer/wine; meiosis → 4 ascospores under stress.

Single Cell Protein (SCP): microbial biomass (30–50% protein) from algae/fungi/yeast/bacteria on cheap substrates.

Trap: fungal spores = reproduction (contrast endospore); a fungus reproducing only asexually = Deuteromycetes.

5b · Bacterial vs Fungal Spore★ the comparison

Yeasts & moulds also de-acidify wine: acid-reducing yeasts (Schizosaccharomyces pombe) metabolise malic acid → ethanol + CO₂ (compare MLF on side 2).

5c · Yeast Life Cycle & SCPLec 4

S. cerevisiae alternates haploid and diploid vegetative states; starvation → ascus → meiosis → 4 haploid ascospores; opposite mating types fuse to restore diploidy. Osmotolerant/fermentative yeasts (Zygosaccharomyces, Candida) spoil high-sugar/brined foods (gas, films).

SCP advantages: short generation time, easy genetic modification, grows on cheap/waste substrates, continuous culture; rich in lysine/threonine + B-vitamins. Sources = algae, fungi, yeasts AND bacteria.

6 · Bacteriophages★★ MTE+Final Q1

A phage = a virus that infects bacteria; an obligate intracellular parasite, non-living outside a host. Structure: icosahedral head (genome) + contractile sheath/tail + baseplate + tail fibres.

Genome: ssDNA, dsDNA, ssRNA or dsRNA — "DNA or RNA, never both." Host-specific via tail fibres recognising receptors (LPS in G−, teichoic acid in G+). A phage infects to reproduce, not to sicken.

Lytic (virulent)

Adsorption → Penetration (inject) → Biosynthesis → Maturation/Assembly → Lysis & Release. Seen as plaques on a lawn. Biosynthesis comes BEFORE maturation.

Lysogenic (temperate)

Adsorb → penetrate → integrate as a prophage in the host chromosome → replicated passively each generation → induced later to go lytic. Can carry toxin genes (lysogenic conversion).

Trap: integrated genome = prophage; phages CAN survive pasteurisation/freezing/drying but NOT without a host.

6b · Phages in FoodSAQ structure

Negative (headline): phages lyse LAB dairy starters (Lactococcus lactis, Strep. thermophilus, Leuconostoc, Lactobacillus) → fermentation fails, big financial loss. Sources: raw milk, whey, starter cultures; survive pasteurisation.

Positive uses: biocontrol/biopreservation (anti-Listeria phage on RTE meat), biosanitisation (clear biofilms), phage therapy (AMR alternative).

Advantages: natural, safe to eukaryotes, highly specific (spare commensals), no sensory change. Disadvantages: contaminate fermentations, narrow host range (need a cocktail), resistance evolves, regulatory hurdles.

6c · Phage Structure · Label ItTut 5

• Head / capsid — icosahedral; holds the nucleic acid
• Collar / fibritins — between head & tail
• Contractile sheath — around the hollow core/tail tube; contracts to inject
• Baseplate (hub) — anchors the tail to the host
• Tail fibres — recognise host surface receptors (specificity)

Defence: bacteria resist phages via restriction–modification systems (cut foreign DNA, methylate self).

6d · Virus vs Prion vs Virionterms

Virion = a complete infectious virus particle (coat + genome). Virus = the agent/type. Prion = an infectious protein with no nucleic acid (BSE/CJD). A phage is a virus of bacteria; outside a host it is an inert virion.

6e · Lytic-Cycle Order TrapTut 5 Q11

The lysing enzyme/protein is expressed late, after the genome is replicated. The correct order is adsorption → injection → biosynthesis → maturation → lysis — biosynthesis BEFORE maturation/assembly. A common MCQ swaps these or asks "when is substance X (lysozyme) made?" → answer: late. Temperate phages can also convert the host: a prophage may carry a toxin gene the host then expresses (a food-safety link to §13 exotoxins).

7 · Microbial MetabolismLec 7

Catabolism breaks down → releases energy (→ ATP); anabolism builds up → consumes energy. Coupled by ATP & NAD(P)H.

Glycolysis (EMP): glucose → 2 pyruvate, net 2 ATP + 2 NADH; universal, cytoplasmic, anaerobic first stage. Aerobic resp. then adds the TCA cycle + ETC/oxidative phosphorylation for the big yield.

Trap: fermentation = organic final acceptor + substrate-level ATP only, NOT merely "no oxygen." Respiration uses an ETC. Glycolysis alone nets only 2 ATP; the big yield is downstream ETC/oxidative phosphorylation, only when O₂ is present.

7b · Fermentation ProductsLec 7 · MLF

• Lactic — pyruvate → lactic acid; homo- (mostly lactate) vs hetero- (lactate + ethanol/acetate + CO₂). LAB: Lactobacillus, Lactococcus, Leuconostoc. Yoghurt, cheese, sauerkraut.
• Alcoholic — pyruvate → acetaldehyde → ethanol + CO₂ (yeast); beer, wine, bread.
• Propionic (Swiss-cheese eyes), acetic (vinegar, Acetobacter).

Malolactic fermentation (MLF) — Final Q6: LAB (Oenococcus oeni) decarboxylate harsh L-malic acid → softer L-lactic acid + CO₂ in wine. De-acidifies, raises pH, softens mouthfeel, stabilises. Inhibited by: pH <3.1, high SO₂, low T, high ethanol, nutrient limit, lysozyme, low cell count.

Trap: MLF is decarboxylation (de-acidification), NOT alcoholic fermentation — give the definition AND the inhibitors.

7c · Oxygen / Redox Classesswollen-can clue

Vacuum/canned/MAP → low Eh favours anaerobes → gas + spoilage.

7d · Spoilage ↔ Fermentationsame logic

The same metabolic chemistry drives both spoilage (unwanted gas/acid/off-odour) and desirable fermentation (controlled, beneficial). Aerobic spoilers (Pseudomonas) dominate in air; anaerobes/fermenters dominate in vacuum packs, cans & the gut. Gas (CO₂/H₂) production is what blows a can. "Fermentative microbes are found wherever electron acceptors run short."

Why anaerobes make fewer ATP: with no O₂ (or other terminal acceptor) feeding an ETC, NADH can only be re-oxidised by dumping electrons onto an organic molecule — so the cell harvests just the 2 substrate-level ATP of glycolysis and discards most of the glucose's energy in the fermentation product — which is exactly the acid/alcohol/gas we exploit in fermented foods.

8 · Gene Transfer★ Final Q5

Three horizontal mechanisms — name each with its agent:

• Transformation — uptake of naked/free DNA by a competent cell.
• Transduction — DNA moved by a bacteriophage (ties to lysogeny).
• Conjugation — cell-to-cell transfer (often a plasmid) via a sex pilus; donor F⁺/Hfr → recipient.

Significance: spreads antibiotic-resistance & toxin/virulence genes through food & gut bacteria (AMR).

9 · Conventional IDLec 10 · phenotype

Microscopy/morphology: shape, arrangement, Gram stain, spore stain, motility, capsule. Cultural: selective/differential media, colony form, haemolysis. Biochemical: O₂ need, catalase, oxidase, glucose fermentation, sugar use (API). Serological: O & H antigens.

The ID tree: Enterobacteriaceae = G− oxidase−ve fermenters; Pseudomonas = G− oxidase+ve non-fermenter; Campylobacter = G− catalase+/oxidase+ curved rod.

Molecular: PCR/qPCR (toxin genes), 16S rRNA sequencing (gold standard ID/phylogeny), PFGE, MALDI-TOF, ELISA. Faster, more specific, detect VBNC/unculturable cells.

9b · Conventional Limits★ MTE Q5 / Final Q4

Why phenotype-based ID fails: slow (days); many organisms unculturable/VBNC; phenotype varies with conditions; subjective; poor strain-level discrimination; overlapping biochemical profiles. → Molecular (16S rRNA) gives true phylogenetic relatedness.

9c · Validation vs EvaluationMTE Q2

Validation = does the method measure what it claims, reliably/reproducibly? (sensitivity, specificity, accuracy, detection limit vs a reference). Evaluation = is it fit for purpose? (cost, speed, ease, robustness). e.g. a rapid PCR kit validated against standard plate count, then evaluated for routine use.

9d · Microbial MediaLec 6 · pracs

Defined (synthetic) vs complex (undefined). By function:

• Selective — suppress unwanted flora (bile salts for G−, MacConkey)
• Differential — distinguish by appearance (MacConkey; MRS for LAB; OGYE for yeasts/moulds)
• Enrichment — favour a target organism

Plate counts: dilute, plate, count colonies (30–300), CFU/mL = colonies × dilution factor.

Side 1 · Quick Trapsmemorise

G+ = thick peptidoglycan + teichoic, no OM
G− = thin PG + outer membrane + LPS
Endospore = survival (1); fungal = repro (many)
Phage genome = DNA OR RNA, never both
Ferment = organic acceptor, ~2 ATP only
Pili long&few · fimbriae short&many

10 · The Growth Curve★ Lec 8

Bacteria divide by binary fission (1 → 2) → exponential growth. Four batch-culture phases:

Trap: generation time is defined in the LOG phase; lag length depends on inoculum history, not a fixed value.

10b · Growth Maths★ Final Q7

Exponential growthN = N₀·2ⁿ · N = N₀·e^(µt)
g (doubling) = t/n · µ = ln2/g = 0.693/g
n = (log N − log N₀)/log 2 = 3.3(log N − log N₀)

Worked: N₀ = 100, g = 20 min, t = 5 h ⇒ n = 300/20 = 15 generations. N = 100·2¹⁵ ≈ 3.3 × 10⁶. µ = 0.693/0.333 h = 2.08 h⁻¹.

Doubling N₀ only doubles the result; raising µ or t multiplies it by orders of magnitude — so time–temperature control beats lowering initial load.

10c · Counting Generationslog method

To get n from counts: n = 3.3·(log N − log N₀). e.g. 10³ → 10⁹ CFU/mL is 6 logs ⇒ n = 3.3 × 6 ≈ 20 generations; if that took 4 h, g = 240/20 = 12 min.

Why preservation targets time & temperature: extending lag (chilling, hurdles) and preventing log-phase growth limits both n and µ — the levers the exponent multiplies.

10d · The Four Phases · Detailwhat happens

• Lag — adaptation; enzyme/RNA synthesis; cells viable but not dividing
• Log — constant max µ, balanced growth; cells most sensitive to heat/antimicrobials
• Stationary — growth = death; nutrients depleted, waste & space limit; sporulation + secondary metabolites begin
• Death — viable count falls exponentially

Predictive models (col 5) fit these phases as λ (lag), µ_max (slope) & N_max (asymptote). The log phase is the danger window: cells divide fastest, so spoilage and pathogen risk climb most steeply here. Growth is "balanced" in log phase, and cells are also most heat- and antimicrobial-sensitive then — the best moment for a kill step.

11 · Factors · Temperatureextrinsic · master

Every microbe has min/optimum/max ("cardinal") temps; classed by optimum:

Danger zone ≈ 4–60 °C. Trap: refrigeration only slows mesophiles — it does NOT stop psychrotrophs like Listeria; refrigeration is not a kill step. Thermoduric organisms survive (but don't grow at) pasteurisation temps; thermophilic spore-formers cause flat-sour spoilage in canned goods held warm.

11b · Factors · pH & Water Activityintrinsic

pH — most bacteria optimum near neutral; pathogens generally need pH > 4.6 (the basis of "low-acid foods" needing the botulinum cook). Yeasts/moulds tolerate lower pH; pH 4.6 = the C. botulinum safety threshold.

Water activity (aₓ) — available water, 0–1; lowered by salt/sugar/drying:

Other intrinsic factors: nutrients, redox (Eh)/O₂, natural antimicrobials (lysozyme), physical barriers. Trap: dried foods spoil by mould, not bacteria; S. aureus is unusually salt/low-aₓ tolerant — so it grows in cured meats & salty foods that exclude most competitors.

11c · Hurdle Conceptsynergy

Combine several sub-lethal factors — mild heat + low pH + low aₓ + preservative + low T + MAP — so no single hurdle is harsh but together they prevent growth while preserving quality.

e.g. fermented sausage = aₓ↓ + pH↓ + nitrite + smoke. Trap: hurdle = synergy of mild factors, NOT one strong treatment. Each hurdle stresses the cell's homeostasis; combined, they overwhelm its repair/repair-energy budget before any single one would, so milder individual treatments keep the food fresher.

11d · Intrinsic vs Extrinsicclassify

Intrinsic = properties of the food itself: pH, aₓ, nutrients, redox/O₂, natural antimicrobials (lysozyme in egg, eugenol, allicin), physical barriers (rind, shell).

Extrinsic = the storage environment: temperature (master variable), relative humidity (sets surface aₓ), and gas atmosphere (O₂/CO₂/N₂). MAP/vacuum suppresses aerobes but can select anaerobes (Clostridium) and psychrotrophs.

Trap: know which factor is intrinsic vs extrinsic — temperature & atmosphere are extrinsic; pH & aₓ are intrinsic. Implicit factors (a third group) cover microbe-microbe interactions: competition, synergy & antagonism between the resident flora — the basis of protective cultures.

12 · Hazards · Types★ Lec 9

Spoilage organisms reduce quality (odour, gas, slime) but usually aren't dangerous (Pseudomonas, yeasts/moulds). Pathogens cause disease, often without altering smell/look — the danger. Indicators signal poor hygiene: coliforms/E. coli (faecal), total viable count.

Trap: a food can be spoiled but safe, or unspoiled but dangerous. An indicator's presence ≠ a pathogen, but raises suspicion.

13 · Infection vs Intoxication★ guaranteed

Toxico-infection = organism ingested, makes toxin in situ in the gut (C. perfringens, B. cereus diarrhoeal, ETEC) — a hybrid: live cells needed, but a toxin does the damage. B. cereus uniquely causes both forms: a heat-stable emetic toxin (intoxication, classically reheated rice) and a diarrhoeal toxin made in the gut (toxico-infection).

Trap: intoxication can occur even after reheating kills the microbe, if the toxin is heat-stable. Incubation time is the classic discriminator: minutes-to-hours = pre-formed toxin; many hours-to-days + fever = the organism is multiplying inside you.

13b · Toxins★ Final Q3

Exotoxins — secreted proteins (mostly G+, also G−); potent; usually heat-labile (botulinum/staph exceptions); antigenic → toxoids. Classes:

• Neurotoxins — nerves (C. botulinum, C. tetani)
• Enterotoxins — gut (S. aureus, V. cholerae, ETEC)
• Cytotoxins — kill cells (Shiga toxin of O157, diphtheria)

Endotoxins = LPS (lipid A) of the G− outer membrane; structural, heat-stable, released on lysis; fever/septic shock; not toxoids.

13c · Exo vs Endo · Compare★ table

Define toxins first (microbial products that harm the host), then classify exotoxins as neuro-/entero-/cytotoxin with an example each — the full-marks structure for Final Q3.

Two exotoxins break the "heat-labile" rule and matter most in food: staphylococcal enterotoxin (survives boiling → vomiting even from reheated food) and botulinum neurotoxin (denatures at boiling, but the spore that makes it does not). This is why intoxication can defeat a cook step.

14 · Key Foodborne Pathogensprofiles

Trap: Listeria at fridge temps defeats "just refrigerate it"; spore-formers survive cooking; O157/Campylobacter need a very low infective dose. Match each organism to its control gap: chill fails for Listeria, cooking fails for pre-formed staph toxin, and only a full botulinum cook clears C. botulinum spores. That organism-specific gap is the heart of the hazard SAQ.

15 · The Swollen-Can Scenario★★ MTE Q4 / Final Q2

Reasoning: a low-acid canned meat with a bad smell + gas on opening = under-processing or post-process leakage let spore-forming anaerobes survive/grow. Gas + odour ⇒ gas-producing anaerobes — Clostridium spp. (incl. the safety-critical C. botulinum making neurotoxin; or C. sporogenes causing putrefactive "swell"). Spores survived an inadequate botulinum cook; the anaerobic interior favours germination → fermentation/putrefaction → gas (CO₂/H₂) + H₂S/amines.

Isolate/identify: aseptic sample → anaerobic culture on selective media → Gram + spore stain (expect G+ rods with spores) → biochemical (catalase−, anaerobic) → confirm toxin by ELISA/immunoassay (or PCR for toxin genes). Prevention = 121 °C / 12-D botulinum cook.

Trap: don't say "bacteria" — name spore-forming anaerobic Clostridium AND explain why.

15b · Spoilage Diagnosis Cuesread the can

Always pair the observation (gas/odour/pH) with the organism + its O₂ class and spore status — that is what the SAQ marks.

15c · Indicators & Countshygiene proxies

Indicator organisms flag probable contamination rather than being the hazard: coliforms / E. coli (faecal), Enterobacteriaceae, total viable / aerobic plate count (general hygiene), Enterococcus. An indicator's presence ≠ a pathogen, but signals poor process control — the basis of the standard plate-count enumeration in the report.

16 · Predictive MicrobiologyLec 11 · ILO 5

Quantitative microbiology: capture growth/survival/death responses to environment as mathematical models, to predict behaviour without testing every product. Three levels:

• Primary — microbial number vs time at fixed conditions (Gompertz, Baranyi); gives µ, lag, N_max.
• Secondary — how those params change with environment (T, pH, aₓ) — square-root/Ratkowsky, Arrhenius.
• Tertiary — software combining both (ComBase, Pathogen Modeling Program).

Uses: shelf-life & risk prediction, HACCP critical limits, product design, "what-if" scenarios, fewer challenge tests, objective decisions. Limits: valid only within the range used to build them (no extrapolation); assume homogeneous conditions; lab broth ≠ real food matrix/competition; need validation in the actual product. The Ratkowsky square-root model is the classic secondary form linking µ to temperature.

Trap: know primary/secondary/tertiary + one example each; never extrapolate beyond the validated boundaries. Validation checks the model's bias (does it over- or under-predict?) and accuracy against real observed counts — predictive ≠ a replacement for verification.

17 · Thermal Death Kinetics★ Lec 12 · D/z/F

At a lethal temperature, death is first-order/exponential — a constant fraction dies per unit time, so survivors fall log-linearly. Implication: you reach probabilities, never true zero → "commercial sterility."

12-D botulinum cook (F₀ ≈ 3 min) = a 12-log reduction of C. botulinum spores for low-acid canned foods.

Trap: D is for ONE temperature; z links D across temperatures; F is total process time. Death is log-linear → sterility is statistical.

17b · Worked · D/zshow it

If D₁₂₁ = 0.25 min for C. botulinum, a 12-D cook needs 12 × 0.25 = 3 min at 121 °C (= F₀ ≈ 3). With z = 10 °C, dropping to 111 °C makes D ten-fold larger (2.5 min) → the same 12-log kill now needs ~30 min.

To cut a population from 10⁶ to 10⁰ (6 logs) at a D of 1.5 min ⇒ 6 × 1.5 = 9 min. Process time = (logs to kill) × D. Spores have far higher D than vegetative cells — which is exactly why pasteurisation (a short, mild process) clears the latter but not the former, and why low-acid canning must reach the harsh 121 °C cook.

17c · Logarithmic Deathwhy "commercial"

Because a constant fraction (not number) dies each interval, the survivor curve never hits zero — only smaller probabilities. So canning aims for commercial sterility (a defined low probability of a surviving spore, e.g. 12-D ⇒ a 1-in-10¹² chance per can), not absolute sterility. This is also why D/z/F feed directly into HACCP critical limits.

18 · Pasteurisation vs Sterilisation★ Lec 12

Pasteurisation — mild heat killing vegetative pathogens & most spoilers + reducing numbers, NOT spores. Milk: LTLT 63 °C/30 min, HTST 72 °C/15 s, UHT 135–150 °C/few s. Targets the most heat-resistant non-spore pathogen.

Sterilisation — destruction of ALL microbes incl. spores. Commercial sterility = practical absence of organisms able to grow in normal storage (canning, 121 °C); autoclave = 121 °C, 15 psi, 15 min.

Trap: pasteurisation does NOT kill spores or all microbes — spores & phages survive pasteurisation. "Commercial sterility" ≠ absolute sterility.

19 · Other Inactivationnon-thermal · chemical

• Irradiation (gamma, e-beam, UV) — damages DNA; cold pasteurisation
• HPP — high pressure disrupts membranes/proteins, minimal heat damage
• Pulsed electric field, ultrasound, cold plasma — emerging
• Chemical: organic acids, nitrite (anti-Clostridium in cured meat), SO₂, bacteriocins (nisin), smoke
• Drying/salting (↓aₓ); chilling/freezing = static, not lethal; fermentation

Trap: freezing/chilling & low aₓ inhibit but don't reliably kill (esp. spores); Listeria still grows when chilled.

20 · Preservation Logicrecap

Four levers: (1) prevent contamination (hygiene, asepsis); (2) inhibit growth (chill, ↓aₓ, ↓pH, MAP, preservatives — the hurdle set); (3) inactivate/kill (heat, irradiation, HPP); (4) limit access (packaging). Choose by target organism, matrix, shelf-life & quality — most real products stack several (hurdle technology) rather than relying on one.

21 · HACCP (Applied Thread)where it all feeds

Hazard Analysis and Critical Control Points — a preventive system controlling biological/chemical/physical hazards through the process, not by end-product testing. The 7 principles: (1) hazard analysis → (2) determine CCPs → (3) set critical limits (core ≥ 72 °C, pH ≤ 4.6, aₓ ≤ 0.85) → (4) monitor → (5) corrective action → (6) verification → (7) records.

Predictive models & D/z/F values set the critical limits at the CCPs. A CCP is a step where control is essential & can be applied — not every control step is a CCP. HACCP sits on prerequisite GMP/GHP programs and is regulator-required; it controls hazards in-process rather than relying on testing the finished product.

Side 2 · Quick Trapsmemorise

N = N₀·e^(µt) — µ & t dominate over N₀
D = 1-log time · z = °C for 10× D · F = total
pasteurise ≠ sterilise (spores/phages survive)
Infection = live cells · intoxication = pre-toxin
endotoxin = LPS, G−, heat-stable
pH 4.6 = C. botulinum line · danger zone 4–60 °C