Microbes and diseases: what to study-1
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Transcript of Microbes and diseases: what to study-1
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.– 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.
5S. 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 ??
6Streptococci: 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
7Virulence 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
8S. 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
9Enterococcus
• 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
10Bacillus: 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
11Bacillus: 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
12Clostridium: 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
13More 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
14More 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.
15Listeria: 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
16Corynebacterium: 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.
17Mycobacterium: 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
18M. 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?
19M. 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
20Other 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.
21Other 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