1Microbes 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?

2Microbes 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..)

3Pathogenic 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

4Staphylococcus: G+ coccus

• S. aureus and S. epidermidis (and 21 others).– 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– Invasive: skin diseases (rashes, abscesses)

• systemic diseases (bacteremia, organ and bone infections)

– Toxin: toxic shock syndrome, scalded skin syndrome, food poisoning

– Diseases spread by fomites and direct contact.

5Characteristics of S. aureus infections

tray.dermatology.uiowa.edu/ DIB/SSSS-002.htm www.omv.lu.se/.../ rorelse/popup/01d1x.htm

6S. aureus virulence factors & Rx

• Capsules, hyaluronidase, staphylokinase, beta-lactamases (destroy penicillins), leukocidins

• Toxins: various, including TSS toxin, exfoliatin, and enterotoxins (heat stable)

• 95% resistant to penicillin, but now many resistant to methicillin, oxacillin. Treatment usually clindamycin (oral) or vancomycin (IV).

• http://www.textbookofbacteriology.net/staph.html

7Streptococci: G+ cocci

• Genera: Streptococcus 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, major neonatal dis.

8Characteristics of Streptococcal infections

http://euclid.dne.wvfibernet.net/~jvg/Bio208/resp_pix/scarlet-fever.jpg

http://textbookofbacteriology.net/vvpath.jpeg

9Virulence factors, etc.

• S. pyogenes (“pus-producing”)– M protein and capsule: avoids phagocytosis– Streptokinase, streptolysins for escape & attack– Pyrogenic erythrotoxins (SPEs)

• at least 3 different types• Cause scarlet fever: fever, rash; toxic shock

– Beta hemolytic on blood agar• Viridans group: greenish alpha hemolysis

– Common in throat, mouth, but can be opportunists– S. mutans associated w/ dental caries

10Viridans and pneumoniae

faculty.mc3.edu/ jearl/ML/ml-11.htm www.ulb.ac.be/sciences/ biodic/ImBacterie2.html

11S. 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– Protection from Pneumovax vaccine

12Enterococcus

• 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– Dangerous to old, immunocompromised

• Resistant to most antibiotics– Plasmids transfer resistance to others

13Bacillus: 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

14Bacillus: 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

http://www.bt.cdc.gov/agent/anthrax/anthrax-images/images/22-black_eschar.jpg

15Clostridium: 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

16More clostridia• C. difficile: normal GI microbiota

– Cause of pseudomembranous colitis, resulting from overgrowth following broad spectrum antibiotics• 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

17Opposing muscle groups

http://upload.wikimedia.org/wikipedia/sv/thumb/d/dd/185px-Muscles_biceps_triceps.jpg

When biceps contracts, triceps relaxes.

When triceps contracts, biceps relaxes.

Excitatory neurons send signal to contract, inhibitory neurons send signal to NOT contract.

18Function of nerves

http://www.people.virginia.edu/~dp5m/phys_304/figures/motor_unit.jpg

http://upload.wikimedia.org/wikipedia/fr/thumb/e/e4/200px-Synapse.png

19More 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 toxoid• No natural immunity: you would die first.

20Listeria: Gram + rod• L. monocytogenes, non-spore forming rod

– Common in many environments• Portal of entry is food or drink

–Esp. meat, dairy products. Check for recalls.– http://www.fda.gov/ora/compliance_ref/recalls/listeria.htm

–Is psychrotrophic.– Escapes into cytoplasm during phagocytosis

• Lives intracellularly, moves cell to cell– Severe infections in: pregnant women/fetuses,

newborns, elderly, immunocompromised

21October 27, 2006 | Pritzker |Ruohonen Listeria Recall: Ballard's Farm

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with Listeria monocytogenes.

http://biology.kenyon.edu/Microbial_Biorealm/bacteria/gram-positive/listeria/20229A.jpg

Law firm

22Corynebacterium: G+ rod

• Found on humans, animals, plants– Normal microbiota, opportunists,& pathogens

• 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.

23Mycobacterium: 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 desiccation• Protects against destruction by phagocytes• Requires acid-fast staining

– Generally grow very slowly (chronic illnesses)– Can grow intracellularly

24Acid Fast stain of Mycobacteria

http://www.md.huji.ac.il/mirror/webpath/AIDS071.jpg

25M. 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?

26M. 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

27Other 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.

28Other 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

–abscesseswww.reefkeeping.com/ issues/2004-06/eb/