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. 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. 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. 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. 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. 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. 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. 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. 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. 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/anth rax/BacillusAnthrax.jpg

11. 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. 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. 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. 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. 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. 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. 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. 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. 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. 20 Other Gram positive rods Propionibacterium –Ferments, produces propionic acid and CO 2 –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. 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