Microbes and diseases: what to study-1

1. Microbes and diseases: what to study-1 • 1. Causative microbe: name, morphology (shape, size, Gram stain, etc.), physiology (aerobe, anaerobe, etc) and some info on classification (what's it related to?) • 2. Pathogenesis and clinical disease:  what disease does it cause (signs and symptoms) and how does it do it (capsule, toxins..)? • 3. Transmission and epidemiology: how do you get the disease?

2. Microbes and diseases: what to study-2 • 4. Diagnosis: How does the lab usually identify the causative agent? • 5. Treatment: antibiotics prescribed (or not- no cell wall, no penicillin) or other treatment (oral rehydration therapy for cholera). • 6. Prevention and control (stop the spread; condoms, kill urban rats..)

3. Pathogenic Bacteria • Gram positive rods and cocci • Pyogenic cocci: Staph and Strep • Gram positive rods: Bacillus to Actinomycetes • Gram negative cocci and bacilli • Gram negative cocci: Neisseria • The Enteric bacteria • Aerobic & Anaerobic Gram negative bacteria • Miscellaneous pathogens • Mycoplasmas to Helicobacter; Gram -, but odd

4. Staphylococcus: G+ coccus • S. aureus and S. epidermidis. • S. aureus much worse, S. epi an opportunist. • Sturdy, salt tolerant, fac anaerobes; clusters • S. epidermidis common on skin, S. aureus less. • Diseases of S. aureus • Food poisoning, skin diseases (impetigo, folliculitis, furuncles & carbuncles, scalded skin syndrome), systemic diseases (TSS, bacteremia, heart, lung, and bone infections) • Diseases spread by fomites and direct contact.

5. S. aureus virulence factors & Rx • Coagulase, triggers blood clotting. • Capsules, hyaluronidase, staphylokinase, beta-lactamases (destroy penicillins) • Toxins: various, including TSS toxin, exfoliatin, and enterotoxins (heat stable) • 95% resistant to penicillin, but now many resistant to methicillin, and now vancomycin leaving ??

6. Streptococci: G+ cocci • Genera: Steptococcus and Enterococcus • Aerotolerant anaerobes, catalase negative • Grow in chains, pairs • Strep: Lancefield groups, viridans, S. pneumoniae • Group A strep: S. pyogenes • Pharyngitis, scarlet fever, pyoderma, erysipelas, TSS, necrotizing fasciitis • Sequelae: rheumatic fever and glomerulonephritis • Group B strep: S. agalactiae • Infects newborns during birth, various illnesses

7. Virulence factors, etc. • S. pyogenes (“pus-producing”) • M protein and capsule: avoids phagocytosis • Streptokinase, streptolysins for escape & attack • Pyrogenic erythrotoxins (SPEs) 3 different types • Cause scarlet fever: fever, rash • Beta hemolytic on blood agar • Viridans group: greenish alpha hemolysis • Common in throat, mouth, but can be opportunists • S. mutans associated w/ dental caries

8. S. pneumoniae • Gram + coccus in pairs, alpha hemolytic • Pneumonia, sinusitis, otitis media, meningitis • Major virulence factor is a capsule • Other unrelated bacteria also have capsules, cause meningitis • Also, get phagocytized by “non-professionals”, spread • Carried in URT by 75% of population • Disease greatest in children and elderly

9. Enterococcus • Formerly part of Group D Strep • Grow under conditions (e.g. high salt) that Strep do not tolerate. • E. faecium, E. faecalis found in GI tract • Opportunists • Cause of nosocomial, wound infections • Resistant to most antibiotics • Plasmids transfer resistance to others

10. Bacillus: G+ rods-1 • Bacillus species very common and numerous • Present in soil, most non-pathogenic • All form endospores when nutrient limited • Bacillus cereus: cause of GI distress • Emetic and diarrheal toxins; bad rice http://biochem.ultraevil.com/bio/Images/bioloskoorozje/anthrax/BacillusAnthrax.jpg

11. Bacillus: G+ rods-2 • Bacillus anthracis: cause of anthrax • Anti-phagocytic capsule of glutamic acid • 3 protein toxin that is lethal • Zoonotic: primarily disease of livestock • Ingestion, inhalation, and cutaneous forms • Black eschar characteristic of cutaneous form • Not hemolytic; antibiotics, vaccine effective

12. Clostridium: G+ rods • Strict anaerobes! Endospore formers. Toxigenic • Common in soil, sewage animal GI tracts • Produce neurotoxins, enterotoxins, histolytic toxins • Four important species: C. perfringens, C. botulinum, C. tetani, and C. difficile. • C. perfringens • Food poisoning: cramps and diarrhea • From injury: myonecrosis to gas gangrene • Fermentation in tissues, killing of tissues and spread of cells into anaerobic areas. • Oxygen treatment, debridement, amputation

13. More clostridia • C. difficile: normal GI microbiota • Cause of pseudomembranous colitis, resulting from overgrowth following broad spectrum anitbiotics • Damage to GI wall can lead to serious illness • Nosocomial infection, easily transmitted • C.botulinum: cause of botulism • Usually acquired by ingestion: intoxication • Food borne, infant (no honey), wound • Produces neurotoxin, inhibits acetylcholine release • Flaccid paralysis; Botox: deadly poison / beauty • Mouse bioassay; administer antitoxin

14. More clostridia-2 • C. tetani: cause of tetanus • Growth in anaerobic wounds, makes tetanus toxin • Toxin prevents action of inhibitory neurons • Opposing muscle pairs both contract • Spastic paralysis, leading to death. • Recommendation is booster shot every 10 years • Toxoid vaccine, with diphtheria toxin • No natural immunity: you die first.

15. Listeria: Gram + rod • L. monocytogenes, non-spore forming coccobacillus • Common in many environments • Portal of entry is food or drink • Esp. meat, dairy products. Check for recalls. • Is psychrotrophic. • Escapes into cytoplasm during phagocytosis • Lives intracellularly, moves cell to cell • Severe infections in: pregnant women/fetuses, newborns, elderly, immunocompromised

16. Corynebacterium: G+ rod • Found on humans, animals, plants • Normal microbiota and opportunists • C. diphtheriae: cause of disease diphtheria • Colonizes the throat, inflammation, fever, and pseudomembrane, release of toxin • Pseudomembrane can block throat • Toxin inhibits protein synthesis, kills cells locally • Toxin diffuses, kills heart and nerve cells • Antitoxin, antibiotic treatment • Vaccination (DPT); humans are only host.

17. Mycobacterium: G+ rods • Many non-pathogenic species, most disease: M. tuberculosis and M. leprae • M. avium-intracellulare: environmental source of lung disease (like TB) in AIDS patients • Mycolic acids as part of complex cell wall • Protects against dessication • Protects against destruction by phagocytes • Requires acid-fast staining • Generally grow very slowly (chronic illnesses) • Can grow intracellularly

18. M. tuberculosis • Causes disease tuberculosis, mostly lung dis. • Cord factor: cell wall factor that connects cells, resists phagocytosis, toxic to host cells • Disease: cells enter lungs, infect macrophages • Cell mediated immunity fights back, walls off infection; forms tubercle (caseous necrosis occurs) • Disease remains controlled, cured, or returns • Disseminated TB: spreads thru body • Worldwide problem; lowered immunity=risk • Skin test, chest x-ray, drug treatment, vaccine?

19. M. leprae • Cause of Hansen’s disease, aka leprosy • Slow growing, likes it cool; armadillos as model • Grows in peripheral nerve and skin cells • Numbness is characteristic of disease • Tuberculoid vs. lepromatous leprosy • Mild, severe, respectively, depending on cell mediated immune response. • Numbness vs tissue destruction • Spread mostly by direct contact • Treatable with antibiotics, but long term

20. Other Gram positive rods • Propionibacterium • Ferments, produces propionic acid and CO2 • makes Swiss cheese • P. acnes: causes inflammation of sebaceous glands: acne. Bacterial growth stimulated by excessive oil production. • Diphtheroids • Bacteria resembling Corynebacterium diphtheriae as normal microbiota on skin.

21. Other G+ -2 • Partially to totally filamentous bacteria • Nocardia asteroides • Causes skin and lung disease • Filamentous cells with pus, draining • Acid fast • Actinomycetes • Large group of filamentous bacteria • Mostly environmental, source of geosmin, antibiotics • Some species do cause infections • abscesses