BIOL 2041 Final Exam review

know the way of writing scientific names?

SCIENTIFIC NAMING SYSTEM: called binomial nomenclature (two-name system), developed by Linnaeus

FORMAT RULES:

first name = Genus

second name = species (specific epithet)

example: Homo sapiens

WRITING RULES:

Genus is capitalized

species is lowercase

both are italicized when typed (Homo sapiens)

if handwritten, both parts are underlined separately

ABBREVIATION RULE:

after first full mention, Genus can be shortened

example: Escherichia coli → E. coli

EXAMPLES:

Staphylococcus aureus

Mycobacterium tuberculosis

Canis lupus

KEY EXAM POINTS:

always two words

Genus capital, species lowercase

italicized or underlined

genus can be abbreviated after first use

Which one is species, which one is genus in binomial nomenclature

Genus = the first word (always capitalized)

Species (specific epithet) = the second word (always lowercase)

Why is Koch famous for? What are his postulates, what are the flaws of his postulates

Robert Koch is famous for helping prove that specific microorganisms cause specific diseases—this is the foundation of the germ theory of disease. He also identified the bacteria responsible for tuberculosis (Mycobacterium tuberculosis), cholera (Vibrio cholerae), and anthrax (Bacillus anthracis), and developed key lab techniques for growing microbes.

Koch’s Postulates

These are the criteria he proposed to link a microbe to a disease:

The microorganism must be found in all organisms with the disease, but not in healthy ones.

The microorganism must be isolated and grown in pure culture.

The cultured microorganism should cause the same disease when introduced into a healthy host.

The same microorganism must then be re-isolated from the newly diseased host.

Flaws / Limitations

Koch’s postulates don’t always work perfectly:

Some microbes can’t be grown in culture (e.g., viruses, some bacteria).

Ethical issues: you can’t intentionally infect healthy humans to test disease.

Asymptomatic carriers exist (people can have the microbe but not show disease, like Typhoid Mary).

Some diseases are caused by multiple pathogens, not just one.

Host factors matter (immune system, genetics), so not everyone exposed gets sick.

Viruses require host cells, so they don’t fit the “pure culture” rule.

So, Koch’s work was groundbreaking, but modern microbiology uses more flexible, updated methods (like molecular techniques) to establish disease causation.

Parts of prokaryotic and eukaryotic cells, what are functions of these parts? Which domain has eukaryotic cells and which ones have prokaryotic cells? What is the difference between cells of archaea, bacteria and animal cells, be able to identify the parts

DOMAINS OF LIFE: Bacteria = prokaryotes, Archaea = prokaryotes, Eukarya = eukaryotes (animals, plants, fungi, protists)

PROKARYOTIC CELLS (bacteria + archaea): no nucleus, no membrane-bound organelles, DNA in nucleoid (circular chromosome), 70S ribosomes, small and simple cells

PROKARYOTE STRUCTURES & FUNCTIONS: cell membrane controls entry/exit, cell wall gives shape/protection (bacteria = peptidoglycan, archaea = no peptidoglycan), cytoplasm site of reactions, nucleoid holds DNA, ribosomes make proteins, plasmids extra DNA (antibiotic resistance), flagella movement, pili attachment + DNA transfer (bacteria)

BACTERIA vs ARCHAEA: bacteria have peptidoglycan cell walls and ester-linked membranes, archaea lack peptidoglycan and have ether-linked membranes, archaea often live in extreme environments, bacteria more often pathogenic

EUKARYOTIC CELLS: have nucleus and membrane-bound organelles, larger and more complex, linear DNA in nucleus, 80S ribosomes

EUKARYOTE STRUCTURES & FUNCTIONS: nucleus controls cell and stores DNA, nucleolus makes ribosomes, rough ER makes proteins, smooth ER makes lipids and detoxifies, ribosomes make proteins, Golgi modifies/packages proteins, mitochondria make ATP (energy), lysosomes digest/recycle waste (mainly animals), cytoskeleton gives structure and movement

PLANT CELL SPECIALS: cell wall (cellulose) for structure, chloroplasts for photosynthesis, large central vacuole for water storage and turgor pressure

ANIMAL VS PLANT VS FUNGI: animals = no cell wall, no chloroplasts, small vacuoles; plants = cellulose cell wall, chloroplasts, large vacuole; fungi = chitin cell wall, no chloroplasts, heterotrophic decomposers

FAST IDENTIFICATION RULES: no nucleus = prokaryote, nucleus = eukaryote, peptidoglycan wall = bacteria, ether-linked lipids = archaea, chloroplast = plant, 70S ribosomes = prokaryote, 80S ribosomes = eukaryote

BIG OVERALL DIFFERENCE: prokaryotes are simple and lack nucleus/organelles, eukaryotes are complex with nucleus and specialized organelles

What are the parts of virus, how can they be visible, lysogenic and lytic cycle, mechanism of formation of enveloped virus

PARTS OF A VIRUS: nucleic acid (DNA or RNA = genetic material), capsid (protein coat that protects genetic material), nucleocapsid (capsid + genome together), envelope (lipid membrane in some viruses, derived from host cell), spike proteins (surface proteins used for attachment to host cells), enzymes (sometimes present, e.g., reverse transcriptase in retroviruses)

HOW VIRUSES ARE “VISIBLE”: viruses are too small for light microscopes, so they are seen using electron microscopy; they can also be detected indirectly by observing infected cells, plaque assays (clear zones of cell death in cultures), or molecular methods like PCR

LYTIC CYCLE (active destruction cycle): virus attaches to host cell, injects genetic material, host cell machinery is hijacked to make viral DNA/RNA and viral proteins, new virus particles assemble, host cell lyses (bursts), releasing many new viruses

LYSOGENIC CYCLE (dormant/integrated cycle): virus attaches and injects genetic material, viral DNA integrates into host DNA (called a prophage in bacteria), host cell replicates normally copying viral DNA with it, can stay inactive for long periods, then may switch to lytic cycle when triggered (stress, UV, etc.)

LYTIC vs LYSOGENIC KEY DIFFERENCE: lytic = immediate replication + cell death, lysogenic = dormant integration + delayed activation

MECHANISM OF ENVELOPED VIRUS FORMATION: after replication inside host cell, viral proteins (especially spike proteins) are inserted into host cell membrane, viral nucleocapsid moves to membrane, virus buds out of the host cell taking part of the host’s lipid membrane with it, this stolen membrane becomes the viral envelope, virus leaves without immediately killing the cell (in many cases), examples include influenza and HIV

Cell morphology and their arrangement

CELL MORPHOLOGY (BACTERIAL SHAPES): cocci = spherical cells, bacilli = rod-shaped cells, spirilla = spiral/helical shaped cells, vibrio = comma-shaped curved rods, coccobacilli = short oval rods (between cocci and bacilli), pleomorphic = variable shape (no fixed form, e.g., some bacteria like Mycoplasma)

ARRANGEMENT OF COCCI (SPHERICAL BACTERIA): diplococci = pairs of cocci, streptococci = chains of cocci, staphylococci = grape-like clusters, tetrads = groups of four cocci, sarcinae = cube-like packets of eight cocci

ARRANGEMENT OF BACILLI (ROD-SHAPED BACTERIA): single bacillus = single rod, diplobacilli = pairs of rods, streptobacilli = chains of rods, palisades = rods lined up side-by-side like a fence

ARRANGEMENT OF OTHER SHAPES: spirilla and vibrios are usually single cells and do not form complex arrangements like cocci or bacilli

HOW TO IDENTIFY ON EXAMS: clusters = staphylococcus, chains = streptococcus, pairs = diplo-, rods = bacilli, curved rods = vibrio, spiral = spirilla, no fixed shape = pleomorphic

KEY IDEA: morphology = shape, arrangement = how cells group after division (useful for bacterial identification in lab tests)

Difference between gram positive and gram-negative bacteria, who produces exotoxin and which one produces endotoxin? What is the function of endotoxin?

GRAM-POSITIVE BACTERIA: thick peptidoglycan cell wall, no outer membrane, retain crystal violet stain → appear purple in Gram stain, contain teichoic acids in the cell wall, generally more sensitive to antibiotics that target cell wall synthesis

GRAM-NEGATIVE BACTERIA: thin peptidoglycan layer, have an outer membrane containing lipopolysaccharide (LPS), do not retain crystal violet → appear pink/red in Gram stain, more resistant to antibiotics due to outer membrane barrier, periplasmic space present between membranes

EXOTOXINS: produced mainly by both Gram-positive and Gram-negative bacteria, but especially common and potent in Gram-positive bacteria (also some Gram-negatives)

ENDOTOXIN: produced ONLY by Gram-negative bacteria (it is the LPS component of the outer membrane, specifically the lipid A portion)

FUNCTION OF ENDOTOXIN (LPS): not “designed” as a toxin for attack but is a structural part of the bacterial outer membrane; when released (especially when bacteria die or divide), lipid A triggers a strong immune response in the host → causes fever, inflammation, low blood pressure (septic shock in severe cases), activation of immune cells and cytokine release

KEY DIFFERENCE SUMMARY:

Gram-positive = thick peptidoglycan, no outer membrane, no endotoxin, often strong exotoxin producers

Gram-negative = thin peptidoglycan + outer membrane (LPS), endotoxin present, can also produce exotoxins

Exotoxin = secreted protein toxin (very potent, specific effects)

Endotoxin = structural LPS (causes generalized inflammatory response when released)

Different transport systems in the cells, how they work and what happens to each cells in different solution dependent on tonicity?

CELL TRANSPORT SYSTEMS: passive transport (no ATP), active transport (uses ATP), vesicular/bulk transport (uses vesicles)

PASSIVE TRANSPORT: movement from high → low concentration, includes simple diffusion (small nonpolar molecules like O₂, CO₂), facilitated diffusion (uses channel/carrier proteins like glucose, ions), osmosis (water movement across membrane via aquaporins)

ACTIVE TRANSPORT: movement from low → high concentration (against gradient), requires ATP, uses protein pumps (e.g., sodium-potassium pump), includes co-transport (symport = same direction, antiport = opposite direction)

VESICULAR TRANSPORT: movement of large materials using vesicles, includes endocytosis (cell takes in material: phagocytosis = solids, pinocytosis = fluids, receptor-mediated = specific molecules) and exocytosis (cell releases materials like hormones, enzymes, waste)

ISOTONIC SOLUTION: equal solute inside and outside cell, no net water movement, cell stays normal size

HYPOTONIC SOLUTION: lower solute outside than inside, water moves into cell, animal cells swell and may burst (lysis), plant cells become turgid

HYPERTONIC SOLUTION: higher solute outside than inside, water moves out of cell, animal cells shrink (crenation), plant cells undergo plasmolysis (membrane pulls away from cell wall)

KEY RULES: water moves toward higher solute concentration, animal cells lack cell wall so they are more sensitive to tonicity changes, plant cells have cell wall so they don’t burst but can lose turgor pressure

Glycolysis, Kreb cycle, oxidative phosphorylation, how many ATPs produce in each, products, How many ATPs are produced as a whole after aerobic respiration

GLYCOLYSIS (cytoplasm): glucose → 2 pyruvate + 2 NADH + 2 ATP (net gain = 2 ATP)

PYRUVATE OXIDATION (link reaction, mitochondria): 2 pyruvate → 2 acetyl-CoA + 2 CO₂ + 2 NADH

KREBS CYCLE / CITRIC ACID CYCLE (mitochondrial matrix): per glucose (2 turns): 4 CO₂ + 6 NADH + 2 FADH₂ + 2 ATP (or GTP) → 2 ATP total

OXIDATIVE PHOSPHORYLATION (electron transport chain + chemiosmosis): NADH and FADH₂ donate electrons → proton gradient → ATP synthase makes ATP → produces about 26–28 ATP per glucose (varies by cell type and shuttle system)

TOTAL ATP FROM AEROBIC RESPIRATION (per glucose):

Glycolysis = 2 ATP

Krebs cycle = 2 ATP

Oxidative phosphorylation = ~26–28 ATP

TOTAL = ~30–32 ATP per glucose molecule

KEY PRODUCTS SUMMARY:

Glycolysis → ATP, NADH, pyruvate

Krebs cycle → CO₂, ATP, NADH, FADH₂

ETC → H₂O + large ATP production (uses O₂ as final electron acceptor)

IMPORTANT EXAM POINT: most ATP comes from oxidative phosphorylation, not glycolysis or Krebs cycle.

Classification of organism depending on temperature and oxygen

CLASSIFICATION BASED ON TEMPERATURE (THERMAL REQUIREMENTS):

Psychrophiles: grow in cold temperatures (~0–20°C), thrive in ice, deep oceans, glaciers

Psychrotrophs: can grow in cold (refrigeration) but prefer moderate temps (~20–30°C), important in food spoilage

Mesophiles: moderate temperatures (~20–45°C), include most human pathogens and human-associated microbes

Thermophiles: high temperatures (~45–80°C), found in hot springs and compost

Hyperthermophiles: extremely high temperatures (~80–121°C), found in hydrothermal vents, archaea are common

CLASSIFICATION BASED ON OXYGEN REQUIREMENTS:

Obligate aerobes: require oxygen to survive (use aerobic respiration)

Obligate anaerobes: oxygen is toxic to them, grow only without oxygen

Facultative anaerobes: can use oxygen if present but can also grow without it (switch between aerobic respiration and fermentation)

Aerotolerant anaerobes: do not use oxygen but are not harmed by it (always ferment)

Microaerophiles: require low oxygen levels (less than atmospheric oxygen)

KEY EXAM RULES:

Oxygen requirement is about energy metabolism and toxicity of O₂

Temperature classification is about enzyme stability and protein function

Mesophiles include most human disease-causing bacteria

Obligate anaerobes are often found in deep tissues or oxygen-free environments

What are the biosafety levels of organisms and what is available in each level, and which one is most dangerous, at which level, extreme measures are taken

BIOSAFETY LEVELS (BSL 1–4): classification based on how dangerous organisms are and what containment is needed

BSL-1 (LOWEST RISK):

Organisms: non-pathogenic or very low-risk microbes (e.g., E. coli K-12)

Lab practices: basic lab safety, no special containment

Equipment: open bench work, standard lab coat/gloves

Risk: minimal to humans and environment

BSL-2 (MODERATE RISK):

Organisms: cause mild disease in humans (e.g., Staphylococcus aureus, influenza virus, Salmonella)

Lab practices: restricted access, biohazard signs, careful handling of sharps

Equipment: biosafety cabinet for aerosol-producing work, PPE (gloves, lab coat, eye protection)

Risk: moderate human infection risk but treatable/preventable

BSL-3 (HIGH RISK):

Organisms: serious or potentially lethal diseases via inhalation (e.g., Mycobacterium tuberculosis, anthrax)

Lab practices: controlled access, negative air pressure rooms, all work done in biosafety cabinets

Equipment: respirators, sealed environments, specialized ventilation systems

Risk: high danger to individuals, limited treatments available

BSL-4 (HIGHEST RISK / EXTREME CONTAINMENT):

Organisms: deadly, often untreatable diseases (e.g., Ebola virus, Marburg virus)

Lab practices: maximum containment, isolated facilities, full-body positive-pressure suits, decontamination showers

Equipment: completely sealed lab systems, airlocks, independent air supply

Risk: extreme lethality and no widely available treatment or vaccine

MOST DANGEROUS LEVEL: BSL-4

EXTREME MEASURES ARE TAKEN AT: BSL-4 (highest containment, full isolation, advanced protective suits, strict decontamination procedures)

KEY EXAM SUMMARY:

BSL-1 = safe/basic teaching labs

BSL-2 = common pathogens, moderate precautions

BSL-3 = airborne serious diseases, high containment

BSL-4 = deadly viruses, maximum containment and isolation

Bacterial cell division name and process, yeast cell division name

BACTERIAL CELL DIVISION: Binary fission

Process:

DNA (single circular chromosome) replicates

Cell elongates and copies DNA separates to opposite ends

Cell membrane and wall grow inward

Septum forms in the middle

Cell splits into two genetically identical daughter cells

YEAST CELL DIVISION: Budding (asexual reproduction)

Process:

Small outgrowth (bud) forms on parent cell

Nucleus divides by mitosis

One nucleus moves into the bud

Bud grows and eventually separates from parent

Produces a genetically identical daughter cell (usually smaller initially)

KEY DIFFERENCE:

Bacteria → binary fission (equal division)

Yeast → budding (unequal division, one small bud forms)

Different phases of bacterial growth and what happens in each

BACTERIAL GROWTH PHASES (in a closed system/batch culture):

1. LAG PHASE: bacteria are metabolically active but not dividing rapidly, cells adapt to new environment, enzyme production increases, little to no increase in cell number

2. LOG (EXPONENTIAL) PHASE: rapid binary fission, bacteria multiply at maximum rate, population doubles at regular intervals, highest metabolic activity, most sensitive to antibiotics

3. STATIONARY PHASE: nutrients become limited and waste builds up, rate of cell division equals rate of cell death, population size remains stable, stress responses and secondary metabolite production may occur (e.g., toxins, antibiotics)

4. DEATH (DECLINE) PHASE: nutrients are depleted and toxic waste increases, cell death exceeds cell division, exponential decrease in viable bacteria, cells may lyse

KEY EXAM POINTS:

log phase = fastest growth and best antibiotic effectiveness

stationary phase = survival mode (no net growth)

death phase = population decline due to harsh conditions

lag phase = adjustment period, no significant growth yet

What happens with bacteriostatic, bactericidal, fungicide, sterilant

BACTERIOSTATIC: stops bacteria from growing and multiplying, but does not kill them, immune system is needed to clear infection

BACTERICIDAL: kills bacteria directly, causes cell death (often by damaging cell wall, DNA, or essential enzymes)

FUNGICIDAL: kills fungi (yeasts and molds), destroys fungal cells completely rather than just stopping growth

STERILANT: destroys or removes ALL forms of microbial life, including bacteria, fungi, viruses, and spores, results in complete sterilization (no living microorganisms remain)

KEY DIFFERENCE SUMMARY:

bacteriostatic = stops growth

bactericidal = kills bacteria

fungicidal = kills fungi

sterilant = kills everything (including spores)

Autoclaving, iodophor, peroxide

AUTOCLAVING: uses pressurized steam (moist heat), typically 121°C at 15 psi for ~15–20 minutes, kills all microorganisms including endospores, used for sterilization of surgical tools, media, and lab waste, works by denaturing proteins and destroying cell structures

IODOPHOR (e.g., povidone-iodine): iodine-based antiseptic/disinfectant, slowly releases iodine which penetrates microbial cells and oxidizes proteins, enzymes, and nucleic acids, effective against bacteria, fungi, and some viruses, commonly used on skin before surgery, not always fully sporicidal at low concentrations

HYDROGEN PEROXIDE (H₂O₂): oxidizing agent disinfectant/antiseptic, produces reactive oxygen species that damage proteins, lipids, and DNA, effective against bacteria, viruses, fungi; at higher concentrations or special formulations it can act as a sterilant, decomposes into water and oxygen so it is environmentally safe

KEY DIFFERENCES:

autoclaving = physical sterilization (heat + pressure, kills everything including spores)

iodophor = chemical antiseptic/disinfectant (oxidation via iodine)

peroxide = chemical oxidizer (reactive oxygen damage, can disinfect or sterilize at high strength)

Function of penicillin, cephalosporin, aminoglycosides, streptomycin, polymyxin B

PENICILLIN (β-lactam antibiotic): inhibits bacterial cell wall synthesis by blocking peptidoglycan cross-linking (binds PBPs), causes cell lysis; mainly effective against Gram-positive bacteria

CEPHALOSPORINS (β-lactam antibiotics): also inhibit cell wall synthesis (same PBP mechanism as penicillin), but broader spectrum depending on generation, often more resistant to β-lactamase enzymes

AMINOGLYCOSIDES (class): inhibit bacterial protein synthesis by binding to the 30S ribosomal subunit, causing misreading of mRNA and faulty proteins; usually bactericidal and effective against many Gram-negative bacteria

STREPTOMYCIN (aminoglycoside): specifically binds 30S ribosome, blocks initiation of protein synthesis and causes misreading of genetic code; used historically against tuberculosis and plague

POLYMYXIN B: targets bacterial cell membrane (Gram-negative outer membrane) by binding to lipopolysaccharides (LPS), disrupts membrane integrity causing leakage and cell death; mainly used for Gram-negative infections, can be toxic to human cells at high doses

KEY EXAM SUMMARY:

penicillin + cephalosporin → cell wall inhibitors (β-lactams)

aminoglycosides + streptomycin → protein synthesis inhibitors (30S)

polymyxin B → membrane disruptor (Gram-negative outer membrane)

Why fungus and helminths are difficult to treat in human

FUNGUS AND HELMINTHS ARE DIFFICULT TO TREAT BECAUSE THEY ARE EUKARYOTES (like human cells), so their cell structures are very similar to ours, making it hard to target them without harming the host

FUNGUS DIFFICULTY: fungal cells are eukaryotic, have sterols (ergosterol) in membranes instead of cholesterol, but still very similar overall to human cells; fewer safe drug targets exist, and antifungal drugs often have more side effects because they can affect human cell processes

HELMINTH (WORM) DIFFICULTY: helminths are multicellular parasites with complex tissues, large size makes them harder to kill with drugs, they have protective outer layers (cuticle) that resist drugs and immune attack, and they often evade the immune system by hiding or modulating host responses

KEY COMPARISON:

bacteria = prokaryotes → many unique drug targets (easy to treat)

fungi + helminths = eukaryotes → similar to humans (harder to target safely)

EXAM SUMMARY: harder to treat because there is less difference between pathogen and human cells, so drugs must be more selective to avoid damaging the host organism

What is serological testing, ELISA (EIA), western blot and southern blot, NAAT

SEROLOGICAL TESTING: testing blood serum for antibodies (immune response) or antigens (parts of pathogen), used to detect past or present infection, relies on antigen–antibody binding reactions

ELISA (Enzyme-Linked Immunosorbent Assay / EIA): detects antibodies or antigens using enzyme-linked antibodies that produce a color change when a reaction occurs, highly sensitive and commonly used for infections (HIV, COVID, etc.), positive result = color change indicating antigen–antibody binding

WESTERN BLOT: detects specific proteins (antigens or antibodies), proteins are separated by gel electrophoresis, transferred to a membrane, and identified using labeled antibodies, used as a confirmatory test (e.g., confirming HIV after ELISA)

SOUTHERN BLOT: detects specific DNA sequences, DNA is cut, separated by gel electrophoresis, transferred to a membrane, and probed with labeled DNA probes, used for identifying genes or mutations

NAAT (Nucleic Acid Amplification Test): detects pathogen DNA or RNA directly, amplifies genetic material (e.g., PCR), very sensitive and fast, used for diagnosing infections like COVID-19, chlamydia, tuberculosis

KEY DIFFERENCE SUMMARY:

serology = detects antibodies/antigens (immune response)

ELISA = quick antigen/antibody screening test

Western blot = protein confirmation test

Southern blot = DNA detection

NAAT = detects and amplifies pathogen genetic material directly (most sensitive modern method)

Organisms (characteristics, disease, symptom, treatment, diagnosis): Mycoplasma, E. coli (2 chapters), Borrelia, Burkholderia, Salmonella, Shigella, Neisseria meningitidis, N. gonorrhea, prions, Clostridium tetani, C. botulinum, Bordetella pertussis, Corynebacterium diphtheriae, Mycobacterium tuberculosis, Streptococcus pyogenes, rhinovirus, influenza, Vibrio cholerae, Helicobacter pylori, Hepatitis A and B, Arboviruses, Dane particle

Mycoplasma: no cell wall, smallest bacteria; causes atypical pneumonia (walking pneumonia); dry cough, mild fever; diagnosed by PCR; treated with macrolides or doxycycline

E. coli: Gram-negative rod, normal gut flora; causes UTIs, diarrhea, sepsis; symptoms include burning urination or (EHEC) bloody diarrhea; diagnosed by culture/PCR; treated with antibiotics for UTIs (EHEC usually supportive care only)

Borrelia burgdorferi: spirochete, tick-borne; causes Lyme disease; bull’s-eye rash, joint pain, neurological symptoms; diagnosed by ELISA + Western blot; treated with doxycycline

Burkholderia: Gram-negative environmental bacteria; causes pneumonia and melioidosis; fever, lung infection, sepsis; diagnosed by culture; treated with ceftazidime or carbapenems

Salmonella: Gram-negative rod; causes food poisoning and typhoid fever; diarrhea, fever, cramps; diagnosed by stool culture; treated with fluids ± antibiotics

Shigella: Gram-negative, very low infectious dose; causes dysentery; bloody diarrhea, fever, cramps; diagnosed by stool culture; treated with antibiotics and fluids

Neisseria meningitidis: Gram-negative diplococcus with capsule; causes meningitis and septicemia; fever, stiff neck, petechial rash; diagnosed by CSF culture; treated with ceftriaxone + vaccine prevention

Neisseria gonorrhoeae: Gram-negative diplococcus; causes gonorrhea; painful urination, discharge; diagnosed by NAAT; treated with ceftriaxone + azithromycin

Prions: misfolded proteins with no DNA/RNA; cause brain diseases (CJD, mad cow); symptoms include dementia and neurodegeneration; no treatment; diagnosed post-mortem

Clostridium tetani: Gram-positive anaerobic spore former; causes tetanus; muscle spasms, lockjaw; toxin blocks inhibitory neurons; treated with antitoxin, antibiotics, vaccine

Clostridium botulinum: Gram-positive anaerobic spore former; causes botulism; flaccid paralysis, vision problems; toxin blocks acetylcholine release; treated with antitoxin and supportive care

Bordetella pertussis: Gram-negative coccobacillus; causes whooping cough; severe coughing fits with “whoop”; diagnosed by PCR; treated with macrolides

Corynebacterium diphtheriae: Gram-positive rod; causes diphtheria; sore throat, gray pseudomembrane; toxin inhibits protein synthesis; treated with antitoxin + antibiotics

Mycobacterium tuberculosis: acid-fast bacterium; causes tuberculosis; chronic cough, weight loss, night sweats; diagnosed by TB test and sputum culture; treated with RIPE therapy

Streptococcus pyogenes: Gram-positive cocci in chains; causes strep throat, scarlet fever, necrotizing fasciitis; sore throat, fever, rash; diagnosed by rapid strep test; treated with penicillin

Rhinovirus: causes common cold; runny nose, sore throat; diagnosed clinically; treated with supportive care

Influenza virus: causes flu; fever, body aches, cough; diagnosed by rapid test; treated with antivirals (oseltamivir) + vaccines

Vibrio cholerae: Gram-negative curved rod; causes cholera; “rice water” diarrhea, dehydration; diagnosed by stool culture; treated with rehydration ± antibiotics

Helicobacter pylori: Gram-negative spiral bacteria; causes ulcers and gastritis; stomach pain, nausea; diagnosed by urea breath test; treated with antibiotics + PPIs

Hepatitis A: fecal-oral transmission; causes acute liver infection; jaundice, fatigue; diagnosed by blood tests; treatment is supportive, vaccine available

Hepatitis B: blood/sexual transmission; causes chronic liver disease and cancer risk; jaundice, fatigue; diagnosed by serology; treated with antivirals + vaccine available

Arboviruses: mosquito-borne viruses (dengue, Zika, West Nile); cause fever, rash, neurological symptoms; diagnosed by PCR/serology; treated with supportive care

Dane particle: complete infectious form of Hepatitis B virus; contains envelope, core, and DNA; represents fully formed HBV virion

Parts of digestive tract

Mouth (oral cavity): ingestion of food, mechanical digestion (chewing), saliva starts chemical digestion (amylase breaks starch)

Pharynx (throat): passageway for food from mouth to esophagus, swallowing occurs

Esophagus: muscular tube that moves food to stomach by peristalsis

Stomach: stores and mixes food, chemical digestion of proteins using acid (HCl) and enzymes (pepsin), turns food into chyme

Small intestine (duodenum, jejunum, ileum): main site of digestion and nutrient absorption, receives enzymes from pancreas and bile from liver/gallbladder

Large intestine (colon): absorbs water and electrolytes, forms feces, houses gut bacteria

Rectum: stores feces before elimination

Anus: opening for defecation, controlled by sphincter muscles

Accessory organs (not part of food pathway but essential):

Salivary glands: produce saliva

Liver: produces bile (fat digestion)

Gallbladder: stores bile

Pancreas: releases digestive enzymes and bicarbonate

KEY FLOW: mouth → pharynx → esophagus → stomach → small intestine → large intestine → rectum → anus

Disease (cause, symptoms, treatment): rabies, meningitis, leprosy, RSV, Mumps, measles, Rubella, warts, chancroid, syphilis, PID, cystitis, pyelonephritis, urethritis, uteritis, candidiasis, encephalitis, genital herpes, trichomoniasis, most prominent cause of UTI, traveler’s diarrhea

RABIES: cause = rabies virus (animal bite, saliva); symptoms = fever → agitation, hydrophobia, paralysis; treatment = post-exposure vaccine + rabies immunoglobulin (before symptoms = effective, after symptoms = usually fatal)

MENINGITIS: cause = bacteria (Neisseria meningitidis), viruses; symptoms = fever, stiff neck, headache, confusion; treatment = antibiotics (bacterial), supportive care (viral)

LEPROSY (Hansen’s disease): cause = Mycobacterium leprae; symptoms = skin lesions, nerve damage, numbness; treatment = multidrug antibiotics (rifampin, dapsone, clofazimine)

RSV: cause = respiratory syncytial virus; symptoms = bronchiolitis, cough, wheezing in infants; treatment = supportive care (oxygen, fluids)

MUMPS: cause = mumps virus; symptoms = swollen salivary glands, fever; treatment = supportive care, vaccine (MMR)

MEASLES: cause = measles virus; symptoms = high fever, rash, Koplik spots; treatment = supportive care, vaccine (MMR)

RUBELLA: cause = rubella virus; symptoms = mild rash, fever; dangerous in pregnancy (birth defects); treatment = supportive, vaccine (MMR)

WARTS: cause = HPV (human papillomavirus); symptoms = skin growths; treatment = removal, cryotherapy, vaccine prevention

CHANCROID: cause = Haemophilus ducreyi; symptoms = painful genital ulcers; treatment = azithromycin or ceftriaxone

SYPHILIS: cause = Treponema pallidum; symptoms = stages: sore → rash → neurological damage; treatment = penicillin

PID (pelvic inflammatory disease): cause = Chlamydia or Gonorrhea; symptoms = pelvic pain, fever, infertility risk; treatment = broad-spectrum antibiotics

CYSTITIS: cause = E. coli (most common UTI); symptoms = burning urination, frequent urination; treatment = antibiotics

PYELONEPHRITIS: cause = ascending UTI (usually E. coli); symptoms = fever, flank pain, nausea; treatment = antibiotics

URETHRITIS: cause = Gonorrhea or Chlamydia; symptoms = painful urination, discharge; treatment = antibiotics

UTERITIS (endometritis): cause = bacterial infection (often postpartum or STI-related); symptoms = pelvic pain, fever, discharge; treatment = antibiotics

CANDIDIASIS: cause = Candida albicans (fungus); symptoms = yeast infection (itching, discharge); treatment = antifungal drugs (fluconazole)

ENCEPHALITIS: cause = viruses (HSV, arboviruses); symptoms = brain inflammation, confusion, seizures; treatment = antivirals + supportive care

GENITAL HERPES: cause = HSV-2 (or HSV-1); symptoms = painful genital blisters, recurring outbreaks; treatment = antivirals (acyclovir)

TRICHOMONIASIS: cause = Trichomonas vaginalis (protozoan); symptoms = frothy discharge, itching; treatment = metronidazole

MOST PROMINENT CAUSE OF UTI: Escherichia coli (E. coli) from intestinal flora

TRAVELER’S DIARRHEA: cause = ETEC (enterotoxigenic E. coli) most common; symptoms = watery diarrhea, cramps; treatment = hydration ± antibiotics in severe cases

Karyogamy and plasmogamy and meiosis in fungus

PLASMOGAMY (fungi): fusion of cytoplasm from two compatible fungal mating types, nuclei remain separate (n + n condition = heterokaryotic or dikaryotic stage)

KARYOGAMY: fusion of the two haploid nuclei after plasmogamy, forming a diploid nucleus (2n), usually occurs later in fungal life cycle

MEIOSIS IN FUNGI: diploid nucleus formed after karyogamy undergoes meiosis to produce haploid spores, restoring haploid state and generating genetic variation

KEY SEQUENCE IN FUNGI: plasmogamy → dikaryotic stage (n + n) → karyogamy (2n) → meiosis → haploid spores

IMPORTANT POINT: in many fungi, plasmogamy and karyogamy are separated in time, creating a prolonged dikaryotic stage (especially in basidiomycetes like mushrooms)

Conidiospore, ascospore, microsporidia, basidiomycetes, zygomycetes, ascomycetes

CONIDIOSPORES (conidia): asexual spores produced externally on specialized hyphae called conidiophores; common in fungi like Aspergillus and Penicillium; used for rapid asexual reproduction and dispersal

ASCOSPORES: sexual spores produced inside a sac-like structure called an ascus; typically formed after meiosis in ascomycetes; usually 8 spores per ascus after mitosis; found in yeasts and molds like Saccharomyces

MICROSPORIDIA: obligate intracellular parasitic fungi (or fungus-like organisms); infect animals and humans; produce very small spores; lack typical mitochondria (reduced organelles); cause disease mainly in immunocompromised patients

BASIDIOMYCETES: fungi that produce sexual spores called basidiospores on a club-shaped structure called a basidium; includes mushrooms, puffballs, rusts, and smuts; long-lived dikaryotic stage (n + n) before karyogamy and meiosis

ZYGOMYCETES: fungi that form sexual spores called zygospores after fusion of hyphae; typically fast-growing molds like Rhizopus (bread mold); produce a thick-walled resistant zygospore during sexual reproduction

ASCOMYCETES: “sac fungi”; produce ascospores inside asci during sexual reproduction; also reproduce asexually via conidia; includes yeasts, molds, and morels; largest fungal group

KEY DIFFERENCES:

conidiospores = asexual external spores

ascospores = sexual spores inside asci (Ascomycetes)

basidiomycetes = mushrooms, basidiospores on basidia

zygomycetes = zygospores from fusion of hyphae

microsporidia = parasitic, reduced fungi-like organisms

QUICK ID RULE:

sac (ascus) → Ascomycetes

club (basidium) → Basidiomycetes

zygospore → Zygomycetes

tiny parasite spores → Microsporidia

external asexual spores → conidia

Process of replication, transcription and translation with enzymes involved, what are the products formed in each

DNA REPLICATION (DNA → DNA): occurs in nucleus (eukaryotes) or cytoplasm (prokaryotes), semi-conservative (each new DNA has one old strand + one new strand)

Enzymes: helicase (unzips DNA), DNA polymerase (adds nucleotides 5’→3’), primase (lays RNA primers), ligase (joins Okazaki fragments), topoisomerase (relieves tension)

Product: 2 identical DNA molecules (each = original strand + new strand)

TRANSCRIPTION (DNA → mRNA): occurs in nucleus (eukaryotes) or cytoplasm (prokaryotes)

Enzymes: RNA polymerase (main enzyme that builds RNA), transcription factors (help initiation), helicase-like unwinding of DNA region

Process: RNA polymerase reads DNA template strand and builds complementary mRNA

Product: pre-mRNA (eukaryotes → then processed to mature mRNA)

TRANSLATION (mRNA → protein): occurs at ribosomes (cytoplasm or rough ER)

Structures/enzymes: ribosome (rRNA + proteins), tRNA (brings amino acids), aminoacyl-tRNA synthetase (charges tRNA), initiation/elongation/release factors

Process: ribosome reads codons on mRNA, tRNA brings amino acids, peptide bonds form

Product: polypeptide chain (protein)

KEY FLOW (CENTRAL DOGMA):

DNA → RNA → Protein

FINAL PRODUCTS SUMMARY:

Replication → DNA

Transcription → mRNA

Translation → protein (polypeptide)

HIGH-YIELD EXAM POINTS:

DNA polymerase builds DNA

RNA polymerase builds RNA

Ribosome builds protein

tRNA = adapter molecule (codon ↔ amino acid matching)

What are DNA and RNA made of and what are differences in their structures

DNA (deoxyribonucleic acid) is made of nucleotides, and each nucleotide has: phosphate group + deoxyribose sugar + nitrogenous base (A, T, C, G)

RNA (ribonucleic acid) is made of nucleotides, and each nucleotide has: phosphate group + ribose sugar + nitrogenous base (A, U, C, G)

STRUCTURAL DIFFERENCES:

DNA is double-stranded (double helix), RNA is usually single-stranded

DNA contains deoxyribose sugar (no oxygen at 2’ carbon), RNA contains ribose sugar (has OH group at 2’ carbon)

DNA bases: A, T, C, G; RNA bases: A, U, C, G (uracil replaces thymine)

DNA is more stable and long-term genetic storage; RNA is less stable and used for short-term information transfer

FUNCTIONAL DIFFERENCES:

DNA stores genetic information

RNA helps express genetic information (mRNA, tRNA, rRNA)

KEY EXAM SUMMARY:

DNA = deoxyribose + thymine + double strand + long-term storage

RNA = ribose + uracil + single strand + protein synthesis roles

Resident and Normal microbiota difference

NORMAL MICROBIOTA: all microorganisms (bacteria, fungi, viruses, protozoa) that are normally found in or on the human body without necessarily causing disease; includes both harmless and potentially opportunistic microbes

RESIDENT MICROBIOTA: the part of normal microbiota that permanently lives in a specific body site (stable population), does not usually get removed by cleaning, and often provides benefits like protection against pathogens

KEY DIFFERENCE:

normal microbiota = broad term (all microbes normally present)

resident microbiota = permanent, stable members of normal microbiota

ADDITIONAL TYPE (for exams):

Transient microbiota: temporary microbes that are picked up from environment and stay for a short time, usually removed by immune system or hygiene

EXAM SUMMARY:

resident = long-term, stable colonizers

transient = short-term visitors

normal microbiota = includes both groups + all normal microbes in body

Definition: Focal, local and systemic infections, sepsis, bacteremia, septicemia, bacteremia, fomite, zoonotic, subacute, latent, acute, pharyngitis, laryngitis, epiglottitis, otitis media, otitis externa

FOCAL INFECTION: infection localized to one area that can spread to other parts of the body (e.g., tooth abscess leading to infection elsewhere)

LOCAL INFECTION: infection restricted to one specific area of the body (e.g., skin infection, wound infection)

SYSTEMIC INFECTION: infection that spreads throughout the body via blood or lymph, affecting multiple organs

BACTEREMIA: presence of bacteria in the bloodstream (can be temporary or mild)

SEPTICEMIA: active multiplication of bacteria in the blood with toxins causing illness (serious systemic infection; often used interchangeably with sepsis in older texts)

SEPSIS: life-threatening systemic inflammatory response to infection causing organ dysfunction

FOMITE: inanimate object that can transmit infectious agents (e.g., doorknob, towel, phone)

ZOONOTIC DISEASE: infection transmitted from animals to humans (e.g., rabies, Lyme disease)

ACUTE INFECTION: rapid onset, short duration, severe symptoms (e.g., flu)

SUBACUTE INFECTION: develops more slowly than acute, lasts longer, moderate severity

LATENT INFECTION: pathogen remains inactive in body with no symptoms but can reactivate later (e.g., herpes virus)

PHARYNGITIS: inflammation of the pharynx (sore throat), usually viral or bacterial (strep throat)

LARYNGITIS: inflammation of the larynx (voice box), causes hoarseness or loss of voice

EPIGLOTTITIS: inflammation of epiglottis, can block airway; medical emergency (often bacterial)

OTITIS MEDIA: infection/inflammation of middle ear (behind eardrum), common in children, ear pain, fever

OTITIS EXTERNA: infection of outer ear canal (“swimmer’s ear”), pain, itching, discharge

BACTEREMIA vs SEPTICEMIA vs SEPSIS (KEY):

bacteremia = bacteria in blood

septicemia = bacteria multiplying in blood + toxins

sepsis = body’s dangerous inflammatory response to infection

Symptom vs signs, what are stages of disease and what happens in each stage

Symptoms: subjective changes experienced and reported by the patient (e.g., pain, fatigue, nausea, headache); cannot be directly measured by a clinician

Signs: objective, observable, or measurable indicators of disease (e.g., fever, rash, swelling, abnormal lab results, elevated heart rate)

Stages of Disease

Incubation period: time between infection and appearance of symptoms; pathogen is multiplying but no symptoms are present; individual may still be infectious

Prodromal period: early stage with mild, non-specific symptoms (e.g., slight fever, fatigue, malaise); immune system is beginning to respond

Illness (acute) period: full development of disease; most severe symptoms occur; pathogen is actively replicating at high levels

Decline period: symptoms begin to decrease; immune system or treatment is effectively reducing pathogen levels

Convalescence period: recovery phase; symptoms disappear and the body repairs damage, though full strength may not yet be restored

Key summary: symptoms = felt, signs = observed; incubation = no symptoms; prodromal = early mild symptoms; illness = peak severity; decline = recovery begins; convalescence = healing completed or nearly completed

Normal microbiota in vagina

NORMAL VAGINAL MICROBIOTA: mainly dominated by Lactobacillus species

Lactobacillus (key dominant genus):

produces lactic acid → maintains acidic pH (~3.5–4.5)

helps prevent growth of harmful pathogens

produces hydrogen peroxide and bacteriocins (antimicrobial substances)

Other possible normal residents (lower numbers):

Gardnerella (small amounts in healthy state)

Streptococcus

Staphylococcus

Candida (fungus, usually kept in check by Lactobacillus)

KEY FUNCTION OF VAGINAL MICROBIOTA:

maintains acidic environment

protects against infections by outcompeting pathogens

supports reproductive tract health

IMPORTANT EXAM POINT: decrease in Lactobacillus can lead to overgrowth of pathogens → bacterial vaginosis or yeast infections

Characteristics of algae and fungus

ALGAE:

mostly aquatic organisms (freshwater or marine)

eukaryotic

photosynthetic (contain chlorophyll and other pigments)

autotrophic (make their own food using sunlight)

cell walls usually made of cellulose (in many groups)

can be unicellular (e.g., Chlorella) or multicellular (e.g., seaweed)

produce oxygen as a byproduct of photosynthesis

reproduce sexually and asexually (fragmentation, spores)

FUNGI:

eukaryotic organisms

heterotrophic (absorb nutrients; do not photosynthesize)

cell walls made of chitin

mostly multicellular (except yeast, which is unicellular)

composed of hyphae forming a network called mycelium

obtain nutrients by decomposition, parasitism, or mutualism

reproduce by spores (sexual and asexual)

thrive in moist environments

KEY DIFFERENCES:

algae = autotrophic, photosynthetic, produce oxygen

fungi = heterotrophic, absorptive feeders, decomposers

algae cell wall = cellulose; fungi cell wall = chitin

algae contain chloroplasts; fungi do not

Structure of a tapeworm

TAPEWORM (Cestode) STRUCTURE: flat, segmented parasitic worm with no digestive system

Scolex (head): attachment organ, contains suckers and sometimes hooks (rostellum) used to attach to intestinal wall of host

Neck: region just behind scolex; growth zone where new segments are produced

Proglottids: body segments that form a chain (strobila)

immature proglottids (near neck) = not fully developed reproductive organs

mature proglottids = contain both male and female reproductive organs (hermaphroditic)

gravid proglottids = filled with fertilized eggs, detach and are released in feces

Body (strobila): entire chain of proglottids forming the main body of the worm

Digestive system: absent; nutrients are absorbed directly through the body surface (tegument)

Tegument: outer protective covering that absorbs nutrients and protects against host enzymes

KEY EXAM POINTS:

scolex = attachment

neck = growth zone

proglottids = reproduction

no mouth or digestive tract

absorbs nutrients through skin-like surface

Lac operon and trp operon

OPERON: cluster of genes in prokaryotes controlled by a single promoter and operator, transcribed together into one mRNA

LAC OPERON (inducible, breaks down lactose)

Function: lactose metabolism (catabolic pathway)

Default state: OFF (repressor bound to operator)

Lactose absent: repressor active → blocks transcription

Lactose present (allolactose): binds repressor → inactivates it → transcription ON

Produces enzymes: lacZ, lacY, lacA for lactose uptake and breakdown

Key idea: lactose turns genes ON

TRP OPERON (repressible, makes tryptophan)

Function: tryptophan synthesis (anabolic pathway)

Default state: ON (repressor inactive)

Low tryptophan: genes transcribed → tryptophan produced

High tryptophan: tryptophan acts as corepressor → activates repressor → transcription OFF

Key idea: tryptophan turns genes OFF

KEY DIFFERENCES

lac operon = inducible, usually OFF → ON when substrate present

trp operon = repressible, usually ON → OFF when end product present

lac = breaks down lactose

trp = synthesizes tryptophan