Transcript Microbes and diseases: what to study-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?
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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..)
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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
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Staphylococcus: G+ coccus
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• 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.
S. aureus virulence factors & Rx
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• Coagulase, triggers blood clotting.
• Capsules, hyaluronidase, staphylokinase, betalactamases (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 ??
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
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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
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S. pneumoniae
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• 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
Enterococcus
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• 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
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
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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
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Clostridium: G+ rods
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• 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
More clostridia
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• 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
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.
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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
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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.
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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
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M. tuberculosis
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• 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?
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
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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.
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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
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