Clinical and Ecological Bacteria Summaries

Overview

These notes summarize multiple student presentations on clinically and ecologically important bacteria, focusing on morphology, metabolism, interactions, disease roles, and applications.

Lactobacillus acidophilus

• Gram-positive, rod-shaped lactic acid bacterium; appears as single rods or short chains; non-sporeforming.
• Thick peptidoglycan cell wall typical of gram-positive bacteria; increases structural strength and stress resistance.
• Many strains have an S-layer (protein coat) plus surface proteins that aid adhesion to mucus and epithelial cells.
• Lives in human GI tract, mouth, vagina, and fermented foods such as yogurt and cheese.

Phylogeny and relatives

• Belongs to Lactobacillus genus, in the Lactobacillus acidophilus group.
• Close relatives: L. johnsonii, L. gasseri, L. helveticus, L. crispatus, L. amylovorus.
• Group members share preference for carbohydrate fermentation to lactic acid and similar niches (gut, fermented foods).

Metabolism and growth

• Homofermentative: mainly ferments sugars (e.g., glucose, lactose) to lactic acid.
• Nutritionally demanding; requires external amino acids, vitamins, nucleotides, and metal ions.
• Thrives in nutrient-rich, low pH environments (milk, human gut); highly acid tolerant.
• Adjusts gene expression based on available nutrients, allowing metabolic flexibility.

Ecological and host interactions

• Competes with pathogens for nutrients and attachment sites on gut and vaginal mucosa.
• Produces lactic acid, hydrogen peroxide, and bacteriocins that inhibit pathogens (e.g., E. coli, Clostridium perfringens, Staphylococcus aureus, Salmonella).
• Forms clusters and biofilm-like assemblies with itself and other commensals, helping block pathogen attachment.
• Supports epithelial barrier, modulates immune signaling, and promotes microbiome balance.

Roles in health and industry

• Symbiont that supports immune regulation, reduces inflammation, and enhances colonization resistance.
• Lactic acid production lowers local pH, making conditions unfavorable for many pathogens.
• Rarely pathogenic; loss of L. acidophilus (e.g., after antibiotics) can reduce colonization resistance.
• Widely used in food fermentation, improving safety, flavor, and shelf life of fermented products.

Salmonella enterica

• Gram-negative, rod-shaped bacterium (~2 μm), facultative anaerobe.
• Peritrichous flagella for motility; covered in fimbriae (short hair-like structures) important for virulence and adhesion.
• Adheres to host cells and to environmental surfaces such as food and stainless steel.

Habitat, phylogeny, and evolution

• Natural habitat: intestinal tracts of animals and humans.
• Major subtype: Salmonella enterica, leading cause of bacterial foodborne illness worldwide and in the US.
• Evolved from E. coli via point mutations, horizontal gene transfer, and acquisition of virulence factors.
• Intermediate form: S. bongori, restricted to cold-blooded animals.

Metabolism and growth

• Facultative pathogen; survives in intestinal tracts but also many external environments.
• Uses carbohydrates and some amino acids (e.g., aspartate) as nutrients.
• Does not ferment lactose.
• Multiplies by binary fission after ingestion and invades host cells.
• Tolerates broad ranges of temperature, pH, and oxygen.

Interactions, transmission, and disease

• Competitive and manipulative with other microbes; competes for iron and uses inflammatory environments to access nutrients.
• Carried by many animals; spreads via fecal contamination of water, plants, animal skin, and environments.
• Persists on plants, inorganic surfaces, and in or on livestock (e.g., chickens).
• Transmitted to humans through undercooked animal products and contaminated produce (e.g., spinach).
• Proper cooking kills Salmonella in animal products; harder to remove from raw vegetables when internalized.
• Causes gastroenteritis: severe stomach pain, diarrhea, fever within 12–36 hours; can require hospitalization or be fatal.
• Typical “food poisoning” (salmonellosis) lasts 4–7 days; diarrhea may last up to 10 days; hydration is critical.

Prevention

• Handwashing before and after food preparation.
• Thorough cooking of animal products; careful rinsing of raw vegetables.
• Avoiding consumption of raw or undercooked eggs and poultry.

Azospirillum (plant-associated nitrogen fixer)

• Genus of Gram-negative, rod-shaped (often slightly curved) bacteria.
• Has outer membrane, thin peptidoglycan layer, and periplasmic space.
• Possesses polar flagellum for swimming and multiple lateral flagella for movement along plant roots.

Habitat and lifestyle

• Lives externally along plant roots (rhizosphere), not in root nodules.
• Forms biofilms on root surfaces, gaining protection and stability.
• Rhizosphere: active soil zone around roots with dynamic oxygen and plant-derived chemicals.

Phylogeny and genetics

• Belongs to Alphaproteobacteria.
• Important species include A. brasilense and A. lipoferum.
• Have circular chromosomes and plasmids carrying nitrogen fixation genes.

Nitrogen fixation and metabolism

• Performs nitrogen fixation: converts atmospheric N₂ to ammonia usable by plants.
• Uses nitrogenase enzyme (two-protein complex using ATP and electrons to break N≡N bonds).
• Nitrogenase functions only in low-oxygen conditions; Azospirillum creates microaerophilic pockets along roots and lowers oxygen via respiration.
• Released ammonia enters the rhizosphere, used by roots, soil, and other microbes.

Plant growth promotion

• Produces auxin (indole-3-acetic acid) to increase root branching and number of roots.
• Produces cytokinins and gibberellins that promote cell division and shoot development.
• Produces ACC deaminase, reducing ethylene levels and enhancing plant stress tolerance.
• Results in larger, stronger root systems with improved water and nutrient uptake.

Microbial and agricultural roles

• Contributes to nutrient cycling by releasing ammonia; sometimes competes for nutrients but also coexists in root biofilms with decomposers.
• Used as biofertilizer: applied as seed coating or soil inoculant in crops (corn, wheat, rice, sugarcane, grasses).
• Increases plant growth, nutrient uptake, and yields.
• Allows reduction of synthetic nitrogen fertilizers, lowering costs and environmental pollution.
• Does not require specific host or nodules, enabling large-scale, flexible use in sustainable farming.

Streptococcus thermophilus

• Gram-positive, nonmotile, non-sporeforming coccus; appears as spheroidal/ovoid cells in pairs or short chains.
• Cell diameter ~0.7–0.9 μm with thick peptidoglycan cell wall for rigidity and osmotic protection.
• Some strains produce exopolysaccharides forming capsules or slime layers, increasing viscosity of dairy products and stress tolerance.
• Lacks many virulence-associated surface proteins of pathogenic streptococci.

Phylogeny and evolution

• Kingdom Bacteria; phylum Bacillota; class Bacilli; order Lactobacillales; family Streptococcaceae; genus Streptococcus.
• Member of Streptococcus salivarius group (with S. salivarius, S. vestibularis).
• Diverged from S. salivarius after adaptation to milk, with genome reduction and specialization for dairy.
• Genomic features: many pseudogenes; loss of genes for commensal/pathogenic lifestyles; retention of dairy-beneficial traits.
• Acquired traits (e.g., bacteriocin production, oxygen tolerance) from other lactic acid bacteria via horizontal gene transfer.
• Forms distinct evolutionary branch separate from pathogenic S. pyogenes and S. pneumoniae.

Metabolism and physiology

• Homofermentative lactic acid bacterium; major organism in cheese and yogurt fermentation.
• Thermophilic: optimal growth 40–42 °C; can tolerate 60 °C for under 30 minutes.
• Auxotrophic for several amino acids; relies on peptides and amino acids (especially from casein breakdown).
• Possesses proteases and transporters for peptide uptake; strains lacking protease depend on Lactobacillus delbrueckii subsp. bulgaricus to supply peptides.
• Uses lactose as primary carbon source:
  • Lactose transported by lactose permease.
  • Cleaved by β-galactosidase into glucose and galactose.
  • Glucose enters glycolysis, converted to pyruvate then lactic acid via lactate dehydrogenase.
• Some strains metabolize galactose; others excrete it.
• Produces lactic acid, exopolysaccharides, and flavor compounds (e.g., acetaldehyde, formate).
• Stress responses: tolerates acid, heat, oxidation via membrane changes and regulatory proteins maintaining homeostasis.

Interactions and industrial importance

• Key dairy symbiont; especially in yogurt with L. delbrueckii subsp. bulgaricus:
  • S. thermophilus rapidly ferments lactose to lactic acid and formate, stimulating L. bulgaricus.
  • L. bulgaricus breaks down milk proteins, releasing peptides and amino acids used by S. thermophilus.
  • Cooperation accelerates acidification and improves texture and flavor (e.g., acetaldehyde production).
• Produces bacteriocins (e.g., thermophilins) that inhibit pathogens such as Listeria and Bacillus cereus.
• Exopolysaccharides protect cells and improve thickness and smoothness of fermented milk.
• Economically, the second most important lactic acid bacterium, with large global market value.

Clostridium botulinum

• Gram-positive, rod-shaped (bacillus), often with peritrichous flagella for motility.
• Obligate anaerobe; thrives in dark, oxygen-free environments.
• Forms endospores under stress, making it highly resistant and hard to destroy in food.

Ecology and phylogeny

• Ubiquitous in soil worldwide; spores can contaminate many environments and foods.
• Member of genus Clostridium (family Clostridiaceae) with other anaerobic pathogens:
  • C. difficile (diarrhea),
  • C. tetani (tetanus), among others.
• “Clostridium botulinum” is used as a functional group name for at least four closely related but phylogenetically distinct species that produce botulinum neurotoxin; some species cause human disease.

Metabolism and virulence

• Produces botulinum neurotoxin (BoNT), the most lethal known human poison.
• Neurotoxin blocks neuromuscular transmission, leading to flaccid paralysis and potentially respiratory failure.
• Likely evolved neurotoxin to secure a large food resource (a corpse) for future bacterial generations.
• Secretes tissue-degrading enzymes (for complex proteins and chitin), aiding decomposition.
• Ferments sugars, amino acids, and peptides as energy sources.

Forms of botulism

• Foodborne botulism:
  • Caused by ingestion of pre-formed toxin in improperly processed foods (e.g., home-canned vegetables, sausages).
  • Endospores survive and germinate in anaerobic foods; toxin is heat-labile, destroyed by sufficient cooking, but spores survive typical cooking.
• Infant botulism:
  • Occurs when spores germinate in underdeveloped infant gut microbiota, leading to toxin production in situ.
• Wound botulism:
  • Spores germinate in anaerobic wound environments; historically associated with intramuscular heroin injection contaminated with soil.

Microbial interactions and control

• Clostridial spores are widespread; contamination of airtight jars, sausages, and fermented foods can occur easily.
• Certain probiotics can outcompete C. botulinum, acidifying environments, releasing bacteriocins, and preventing spore germination and vegetative growth.
• Botulinum toxin has been repurposed for medical and cosmetic use (e.g., Botox for wrinkle reduction, migraine treatment).

Rickettsia (genus Rickettsia)

• Small Gram-negative, rod-shaped to very small spherical bacteria.
• Nonmotile, obligate intracellular parasites.
• Outer membrane contains lipopolysaccharide with endotoxin activity.
• Order Rickettsiales, class Alphaproteobacteria, phylum Proteobacteria.

Transmission and intracellular lifestyle

• Maintained in arthropod vectors (ticks, lice, fleas, mites).
• Arthropods acquire infection and then transmit to humans (e.g., via bites), breaching skin barrier.
• Once inside, Rickettsia enter host cells (especially endothelial/smooth muscle cells) and replicate in cytosol.
• Obtain ATP via ATP/ADP translocase, exchanging host ATP for bacterial ADP.
• Utilize host NAD+ and perform β-oxidation and electron transport chain coupled to oxidative phosphorylation.
• Cannot use glucose; oxidize amino acids and citric acid cycle intermediates.
• Reproduce by binary fission in cytosol, causing significant host-cell damage.

Entry mechanisms and immune evasion

• Use “zipper” and “trigger” mechanisms to enter target cells.
• Must evade innate immune defenses to colonize host.

Major diseases (rickettsioses)

• Cause acute febrile illnesses collectively called rickettsioses.
• Rocky Mountain spotted fever:
  • Caused by Rickettsia rickettsii; transmitted by hard ticks among rodents and to humans.
  • Symptoms: fever, headache, chills; potentially severe.
• Epidemic typhus (louse-borne typhus):
  • Caused by Rickettsia prowazekii; transmitted by human body lice.
  • Symptoms: high fever, depression, rash.
• Murine typhus:
  • Caused by Rickettsia typhi; rodents as main reservoir.
  • Transmitted by rat flea; symptoms include abrupt fever, headache, chills.

Public health importance

• Significant causes of severe human disease.
• Prevention involves vector control and protection in tick- and lice-endemic areas.

Akkermansia (Akkermansia species)

• Rod-shaped, Gram-negative, nonmotile, non-sporeforming, obligate anaerobes.
• Prefer mucosal environments and coexist with other gut bacteria.
• Common in adult humans; found in ~90% of adults.

Metabolism and niche

• Specializes in degrading mucin (major component of mucus) as source of carbon, nitrogen, and energy.
• Produces metabolites including short-chain fatty acids, ketone, and polyamines.
• These metabolites:
  • Support glucose homeostasis and balanced host metabolism.
  • Nourish intestinal wall cells and broader bacterial community.
• By degrading mucin, helps maintain and renew the mucosal layer, strengthening barrier against pathogens.

Health roles

• Anti-inflammatory and protective against bone loss, making it relevant to periodontal disease (a leading cause of adult bone loss).
• Strain Akkermansia muciniphila is well-studied:
  • Abundant in gut; synthesizes vitamin B12 and choline, important co-factors for many coenzymes.
  • Further supports microbial community, reinforcing its symbiotic role.
• Considered a “next-generation” microbe for probiotic development.
• Does not directly modulate all gut microbes but creates conditions favorable to beneficial communities and host health.

Promotion and potential therapy

• Probiotic supplements are being developed.
• Diets rich in healthy fats, fruits, berries, legumes, and leafy greens and low in sugar substitutes and ultra-processed foods support its presence.
• Oral health practices (e.g., regular dental hygiene care) indirectly support mucosal health where such organisms contribute.

Cyanobacteria

• Ancient photosynthetic bacteria; Gram-negative cell envelope, often with mucilaginous sheaths.
• Internal thylakoid-like membrane networks capture sunlight.
• Exhibit diverse morphologies: solitary cells, colonies, filaments; can form visible mats on water surfaces.

Habitats and adaptations

• Ubiquitous: hot springs, deserts, polar ice, oceans, freshwater, and many illuminated environments.
• Possess protective pigments and robust sheaths against intense sunlight, desiccation, and oxidative stress.
• Belong to phylum Cyanobacteria; often called “blue-green algae” but are true bacteria.

Metabolism and global cycles

• Perform oxygenic photosynthesis:
  • Use light to convert CO₂ into organic matter, releasing O₂.
• Many fix atmospheric nitrogen at night (nitrogen fixation), converting N₂ to biologically usable forms.
• Together, daytime photosynthesis and nighttime nitrogen fixation drive global carbon and nitrogen cycles.

Evolutionary significance

• Ancestors of plant chloroplasts: an ancient cyanobacterium entered a eukaryotic cell and became the chloroplast.
• Responsible for a large share of global carbon fixation and oxygen production.

Ecological roles and interactions

• Form base of many aquatic food webs.
• In lichens, cyanobacteria provide photosynthate to fungal partners, receiving shelter and structure in return.
• In biofilms, exchange nutrients, signals, and genes with neighboring microbes, forming adaptable microbial networks.

Human uses and impacts

• Cultivated for biofuels, carotenoids, and carbon capture technologies, exploiting their ability to convert sunlight and CO₂.
• Under nutrient-rich conditions, can form harmful algal blooms producing toxins that harm ecosystems and human health.

Vibrio parahaemolyticus

• Gram-negative, slightly curved rod (bacillus), facultative anaerobe, halophile.
• Possesses flagella:
  • Swimmer cells: single polar flagellum for swimming in water.
  • Swarmer cells: multiple lateral flagella for movement in viscous substrates.
• Belongs to family Vibrionaceae; genus Vibrio includes ~40 species (e.g., V. cholerae, V. vulnificus).

Habitat and preferences

• Natural environment: marine and estuarine waters.
• Halophilic: prefers higher salinity (≈20–25 parts per thousand) and warmer waters.
• Commonly associated with shellfish (e.g., oysters); leading bacterial cause of seafood-related gastroenteritis.

Virulence factors

• Multivalent adhesion molecule 7 (MAM7):
  • Mediates adhesion to host cells and surfaces; important for biofilm formation and infection.
• Type III secretion systems (T3SS):
  • Needle-like structures that inject effector proteins into host cells, disrupting host energy production and viability.
• Toxins:
  • Thermostable direct hemolysin (TDH) and TDH-related hemolysin (TRH):
    • TDH: pore-forming protein that disrupts mitochondrial membrane pores, impairing energy production.
    • TRH: alters host cell morphology, including nucleus, cytoplasm, and microvilli.
• Biofilm formation:
  • MAM7 and other factors allow persistent colonization of surfaces and hosts.
• Antibiotic resistance:
  • Many environmental strains resistant to multiple antibiotics due to misuse in humans and aquaculture.
  • Can transfer resistance genes to other human pathogens.

Ecological interactions

• Commensal association with zooplankton:
  • V. parahaemolyticus gains protection and transport through water; zooplankton largely unaffected.
• Prey of Halobacteriovorax:
  • Predatory bacterium enters periplasmic space, consumes cytoplasm, and lyses the host.
  • Being explored as a biocontrol agent to reduce V. parahaemolyticus populations.

Disease and transmission

• Major cause of acute gastroenteritis associated with consumption of raw or undercooked shellfish.
• Symptoms include diarrhea, abdominal cramps, nausea, vomiting, and fever.

Neisseria gonorrhoeae

• Gram-negative diplococcus; obligate human pathogen.
• Obligate aerobe: requires oxygen.
• Prefers warm, moist mucosal surfaces at ~37 °C (98.6 °F).

Nutritional requirements

• Requires enriched media in lab (blood agar, chocolate agar).
• Needs glucose, glutamine, thiamine, phosphate, iron, and CO₂ for growth.

Phylogeny and relatives

• Genus Neisseria; includes N. meningitidis (leading cause of bacterial meningitis) and other mucosal species.
• Only N. gonorrhoeae and N. meningitidis are major human pathogens.

Transmission and colonization

• Transmitted via sexual contact.
• Colonizes mucosal epithelium of throat, cervix/vagina, urethra, or rectum.
• Binds to epithelial cells using surface structures and adhesins.

Immune evasion and resource acquisition

• In cervix, binds factor H, a host regulatory protein, disguising itself to avoid complement attack.
• Uses outer-membrane proteins (including TBDT-like transporters) to capture nutrients (e.g., iron) from host and competing microbes.
• Forms biofilms; uses pili to exchange genes (horizontal gene transfer), building antibiotic resistance.
• Shares resistance information among strains, contributing to “superbug” status.

Infection course and clinical impact

• Highly prevalent; tens of millions of new infections annually worldwide.
• After infection, contagious about one week post-exposure; tests may remain negative early on.
• Often asymptomatic in females; commonly detected by routine screening.
• In males, can cause urethral discharge and other symptoms.
• Untreated infection in females:
  • ~20% develop pelvic inflammatory disease, with scarring and potential infertility; requires prolonged therapy.
• In pregnancy:
  • Can infect newborns during birth, causing neonatal conjunctivitis, blindness, corneal scarring, and ulcers.

Staphylococcus species (S. aureus, S. epidermidis, S. saprophyticus)

• Gram-positive, spherical (coccus) bacteria that form grape-like clusters.
• Size ~0.5–1 μm.
• Nonmotile, non-sporeforming, facultative anaerobes.
• Normal colonizers of human skin, nasal cavity, body creases, and other sites.

Common pathogenic species

• Staphylococcus aureus:
  • Often in skin and nose; major pathogen.
• Staphylococcus epidermidis:
  • Common skin commensal; frequent healthcare-associated pathogen.
• Staphylococcus saprophyticus:
  • Colonizes perineum, rectum, urethra, cervix, GI tract; causes urinary tract infections (especially in sexually active females).

Basic differentiation tests

• All three are catalase positive.
• Coagulase test:
  • S. aureus: coagulase positive.
  • S. epidermidis and S. saprophyticus: coagulase negative.
• Novobiocin susceptibility:
  • Novobiocin sensitive: S. epidermidis.
  • Novobiocin resistant: S. saprophyticus.

S. aureus diseases and toxins

• Skin infections: boils, folliculitis, cellulitis, impetigo.
• Toxins:
  • Hemolysin: pore-forming toxin that destroys erythrocytes.
  • Leukotoxin: targets leukocytes, inducing necrosis and tissue destruction, potentially leading to organ failure.
  • Exfoliative toxin: causes staphylococcal scalded skin syndrome.
  • Enterotoxins: produced in food; heat-stable, can cause food poisoning even after bacteria are killed.
  • TSST-1 (toxic shock syndrome toxin): superantigen causing fever, rash, hypotension, organ failure, and potentially death.

S. epidermidis and S. saprophyticus infections

• S. epidermidis:
  • Common nosocomial bloodstream infection.
  • Associated with prosthetic valves, cardiac devices, catheters, and IV drug use.
• S. saprophyticus:
  • Common cause of UTIs in sexually active young women.

Treatment

• Mild skin infections: topical antibiotics.
• Boils/abscesses: may require drainage by clinicians.
• Invasive infections: systemic therapy with oral or IV antibiotics, depending on severity and resistance profile.

Yersinia pestis

• Gram-negative, rod-shaped bacterium in family Enterobacteriaceae.
• Outer membrane protein Ail (Attachment-Invasion Locus) aids adhesion and immune evasion.

Evolution and phylogeny

• Closely related to Yersinia pseudotuberculosis, diverging ~1,500–2,000 years ago.
• Y. pseudotuberculosis: mild gastrointestinal disease.
• Y. pestis: evolved to cycle between mammals and fleas, becoming highly virulent and pandemic-capable.

Metabolism and survival

• Facultative anaerobe; grows with or without oxygen.
• Possesses specialized iron acquisition systems to survive in iron-poor environments such as bloodstream.
• Able to persist in flea gut, rodent tissues, and human hosts.

Transmission cycle

• Maintained in rodent populations, transmitted by flea vectors.
• In fleas:
  • Forms biofilm in digestive tract, blocking feeding.
  • Starving fleas bite more aggressively and regurgitate bacteria into mammalian hosts.
• Affects rodent populations (e.g., prairie dogs in South Dakota), altering predator–prey dynamics.
• Control strategies focus on flea control and rodent monitoring.

Plague forms in humans

• Bubonic plague:
  • Infection of lymph nodes; causes painful swollen “buboes.”
  • Mortality 30–75% untreated.
• Pneumonic plague:
  • Infection of lungs; highly transmissible via respiratory droplets; rapidly fatal if untreated.
• Septicemic plague:
  • Bloodstream infection; rare but nearly always fatal without treatment.
• Prompt antibiotic therapy is life-saving.

Virulence factors and history

• Ail protein: resists serum killing and promotes adhesion.
• Plasminogen activator (Pla): breaks down host tissues, aiding rapid spread.
• Historically caused pandemics (e.g., Black Death, killing ~25 million in Europe).
• Still endemic in some regions with occasional outbreaks; ongoing surveillance is required.

Shigella (general)

• Gram-negative, non-sporeforming, nonmotile, rod-shaped bacterium.
• Chemoorganotroph; facultative anaerobe.
• Commonly cultured on MacConkey agar:
  • Does not ferment lactose, helping distinguish it from lactose-fermenting E. coli.

Virulence mechanisms

• Uses Type III Secretion System (T3SS):
  • Injects effector proteins into host cells via translocon pore in host membrane.
  • Facilitates invasion and intracellular survival.
• Often acquires multidrug resistance via horizontal gene transfer, including quinolone resistance.

Transmission and public health

• Spread via contaminated water, hand-to-mouth contact, and improper food handling.
• Contamination often linked to poor sanitation and hygiene.
• Control requires:
  • Improved water sanitation,
  • Monitoring antibiotic resistance,
  • Strengthening public health infrastructure to prevent and manage outbreaks.

Mycobacterium tuberculosis (MTB)

• Acid-fast, Gram-positive bacillus; obligate aerobe.
• Cell wall contains mycolic acids and lipoarabinomannan, forming a waxy, damage-resistant coat.

Historical context

• Detected in ancient remains (Egyptian and Peruvian mummies).
• Known historically as phthisis (Greek), scrofula (Roman), and mentioned in ancient Hindu texts.
• In 19th century called “consumption”; associated with deaths of notable figures (e.g., Keats, Chopin, Charlotte Brontë).
• Widely represented in art and literature.

Infection phases

• Primary infection:
  • Spread via inhaled droplets; alveolar macrophages phagocytose MTB.
  • MTB releases factors that destroy macrophages and enzymes that damage lung tissue, forming tubercles.
  • Immune response usually contains infection; tubercles heal in many cases.
• Latent infection:
  • MTB can persist in a dormant state in lungs, awaiting immunosuppression.
• Reactivation (pulmonary TB):
  • Occurs when immunity wanes; lungs fill with tubercles.
  • Symptoms: chronic cough, fever, weight loss, bloody sputum.
  • Untreated, often fatal within 2–5 years.

Treatment and resistance

• First effective antibiotic: streptomycin (discovered 1943; first cure in 1945).
• MTB rapidly evolved antibiotic resistance.
• Standard therapy: long multi-drug regimens; shortest noted ~4-month combination therapy.
• Rise of multidrug-resistant (MDR) and totally drug-resistant TB strains.

Global impact

• Estimated up to one-third of people infected with MTB.
• HIV and COVID increase TB susceptibility.
• Causes ~1.5 million deaths annually, the leading cause of death by a single infectious agent.
• Leading cause of death among people with HIV.
• Major contributor to global antibiotic resistance burden.

Helicobacter pylori

• Gram-negative, nonfermenting, non-sporeforming, microaerophilic bacterium.
• Helical shape, ~2–4 μm long, 0.5–1 μm diameter.
• Possesses 2–7 lophotrichous flagella at one pole; helical shape and flagella facilitate burrowing through mucus.

Phylogeny and diversity

• Domain Bacteria; belongs to a defined phylum, class, order, family, genus Helicobacter; species H. pylori.
• Very prevalent: up to ~two-thirds of global population infected at some point; higher in developing regions.
• Extensive strain diversity within and between hosts.
• Genus has >20 recognized species; others await description; related species inhabit other mammals’ stomachs.

Metabolism and survival in the stomach

• Microaerophilic: requires low oxygen.
• Uses hydrogenase to oxidize environmental hydrogen for energy.
• Produces oxidase, catalase, and urease.
• Urease hydrolyzes urea into ammonia and CO₂:
  • Ammonia locally raises pH, creating a less acidic microenvironment around the bacterium.
  • This allows survival in otherwise highly acidic gastric lumen.

Colonization and pathogenesis

• Uses helical shape and flagella to penetrate gastric mucus and reach epithelial surface.
• Produces adhesins to attach to epithelial cells and resist mechanical clearance.
• Ammonia and altered pH damage epithelial cells; triggers inflammation and increased acid exposure.
• Leads to chronic gastritis, peptic ulcers, and can contribute to gastroesophageal reflux disease.
• Strongly linked to gastric cancer:
  • Associated with ~89% of gastric cancers and ~5.5% of all cancers worldwide.
  • Only known bacterium directly linked to cancer development at this scale.

Microbiome effects and transmission

• Can comprise 40–90% of stomach microbiota when present, reducing microbial diversity.
• Changes in pH disrupt other gastric microbes.
• Eradication regimens (antibiotics, proton pump inhibitors, bismuth salts) may further disrupt microbiome.
• Found in saliva, gastric mucus, dental plaque, and feces.
• Transmitted via oral–oral or fecal–oral routes.
• No vaccine; prevention relies on hygiene and clean water.
• Symptoms: abdominal pain, nausea, heartburn, belching, bad taste; evaluation recommended when persistent.

Treponema pallidum

• Gram-negative spirochete; causes syphilis.
• Highly motile via endoflagella (axial filaments) enabling corkscrew movement (counterclockwise and clockwise).
• Microaerophilic: needs low oxygen; cannot survive outside human host.

Evolution and origin hypotheses

• Exact origin unclear; syphilis incidence is rapidly rising.
• Pre-Columbian hypothesis:
  • Suggests treponemal diseases evolved and manifested differently as environments changed (e.g., climate).
• Columbian hypothesis:
  • Links spread to voyages of Christopher Columbus.
  • Based on physician reports from the era and skeletal remains with syphilitic lesions.
  • Proposes introduction into Europe from the Americas.

Stages of syphilis

• Primary stage:
  • Painless lesion (chancre) at site of inoculation (genital, oral, anal).
  • Enlarged regional lymph nodes.
• Secondary stage:
  • Systemic symptoms; characteristic rash on palms and soles; associated with fever.
• Latent stage:
  • Asymptomatic; infection persists.
  • Congenital syphilis risk: pregnant individuals can transmit to fetus, leading to infected newborn.
• Tertiary stage:
  • Late complications with neurological damage and possible involvement of other organs.
• Penicillin is effective, but late-stage damage often irreversible; infection may persist despite therapy in advanced stages.

Ethics and historical impact

• Tuskegee Syphilis Study (1932–1972):
  • 600 African American men (≈400 with syphilis, 200 controls) in Alabama.
  • Men were misled to believe they were treated; therapy was withheld to study natural disease course.
  • Grossly unethical; catalyzed major reforms in human-subject research ethics and protections, now central in medical ethics education.

Escherichia coli (E. coli)

• Gram-negative, rod-shaped, non-sporeforming; may appear singly or in pairs.
• Often motile with peritrichous flagella.
• Facultative anaerobe; highly metabolically flexible.

Phylogeny and commensal role

• Family Enterobacteriaceae; related to Shigella, Salmonella, and Yersinia pestis.
• Most studied bacterium; nearly 1,000 strains known and still counting.
• Commensal strains inhabit GI tract, often ~1% of gut microbiota.
• Occupy niches that could otherwise be taken by pathogens (including pathogenic E. coli strains).

Metabolism and environment

• Acid tolerant; can survive several hours in stomach acid on way to intestines.
• Metabolic pathways include glycolysis, pentose phosphate pathway, TCA cycle, and fermentation.
• Nutrient sources for commensals in biofilms:
  • Shed epithelial cells,
  • Dietary fiber,
  • Mucosal polysaccharides.
• Different pathotypes adapt to specific nutrient conditions of their niches.

Genetic exchange

• Conjugation:
  • Uses pili to connect to other bacteria and transfer plasmid DNA.
• Transduction:
  • Most frequent gene exchange via bacteriophages that infect E. coli.
• Frequent horizontal gene transfer leads to rapid evolution of virulence and resistance.

Major pathogenic pathotypes

• Enterohemorrhagic E. coli (EHEC):
  • Produces Shiga toxin.
  • Highly acid resistant, surviving saliva and stomach acid.
  • Causes bloody diarrhea, renal failure, dehydration, fever, and fatigue.
• Enteropathogenic E. coli (EPEC):
  • Does not produce Shiga toxin.
  • Attaches and effaces microvilli, disrupting intestinal absorptive surface.
  • Causes persistent diarrhea; leading cause of infant mortality in developing countries.
• Enterotoxigenic E. coli (ETEC):
  • Produces enterotoxins that induce watery diarrhea.
• Enteroinvasive E. coli (EIEC):
  • Similar to Shigella; invades intestinal epithelium.
  • Causes severe watery diarrhea, fever, cramps; can spread systemically.

Transmission and control

• Found in feces of animals and humans.
• Transmission routes:
  • Fecal contamination of food and water,
  • Irrigation water contaminated by sewage or manure,
  • Contaminated recreational waters and beaches.
• Commonly contaminated foods:
  • Fresh produce, raw milk/dairy, undercooked beef.
• USDA and FDA mitigate risk via facility inspections and food testing.

Beneficial uses

• E. coli has been a central model organism since the 1940s.
• Fundamental microbiology, genetics, and molecular biology advances rely heavily on E. coli research.

Summary Table of Selected Bacteria

Key Terms & Definitions

• Gram-positive / Gram-negative: Bacterial cell wall types distinguished by Gram staining; Gram+ have thick peptidoglycan, Gram− have thin peptidoglycan and outer membrane.
• Homofermentative: Fermentation pathway that mainly produces a single end product, typically lactic acid.
• Facultative anaerobe: Can grow with or without oxygen.
• Obligate anaerobe: Cannot tolerate oxygen; grows only in its absence.
• Microaerophilic: Requires low levels of oxygen.
• Endospore: Highly resistant dormant structure formed by some Gram-positive bacteria.
• Biofilm: Community of microorganisms attached to a surface, embedded in extracellular matrix.
• S-layer: Crystalline protein layer on outer surface of some bacteria.
• Nitrogen fixation: Conversion of atmospheric N₂ into ammonia by nitrogenase.
• Type III Secretion System (T3SS): Needle-like protein complex used by Gram-negative bacteria to inject effectors into host cells.
• Bacteriocin: Antimicrobial peptide produced by bacteria against closely related species.
• Virulence factor: Molecule or structure that enables a microorganism to cause disease.
• Plasmid: Small, circular DNA molecule independent of the chromosome.
• Horizontal gene transfer: Movement of genetic material between organisms other than by descent.
• Latent infection: Persistent infection without active disease, with potential for reactivation.

Action Items / Next Steps

• Review morphology, Gram status, and oxygen requirements for each organism to aid identification questions.
• Practice matching key virulence factors (e.g., T3SS, toxins, urease, nitrogenase) with their corresponding bacteria.
• Create comparison charts focusing on:
  • Foodborne pathogens (Salmonella, C. botulinum, Vibrio, Shigella, E. coli).
  • Gut commensals/probiotics (L. acidophilus, Akkermansia, E. coli).
  • Vector-borne pathogens (Rickettsia, Yersinia pestis).
• Use these notes to prepare for exam essays on:
  • Microbe–host interactions,
  • Microbes in food fermentation,
  • Historical and ethical case studies (TB, syphilis, plague).