Bacteria Pt 1 Flashcards
What are general characteristics of clostridia pathogens?
Why do we have so much C diff?
Gram positive
spore forming, anaerobic rods
all are obligate anaerobes, but oxygen tolerance varies
- if bug doesn’t make catalase, oxygen is toxic
- if bug doesn’t make superoxide dismutase, very sensitive to superoxide
spore are highly resistant to oxygen, which is reason for so many nosocomial C. diff infections
Which clostridia have neurotoxins and what are their symptoms?
Clostridia tetanii (tetatnospasm)
Clostridia botulinum (flaccid paralysis)
Which clostridia have tissue damaging toxins?
Clostridia perfigens have alpha toxin (causing cell lysis, massive destruction of muscle, soft tissue)
Clostridia difficile toxins cause ulceration of colon
Which clostridia cause pathology from toxins and which cauase pathology from infection?
Clostridia botulinum result from ingestion of toxin, there is no live bacteria consumed
- exception to infant botulism, and wound botulism
clostridia perfinges cause pathology from toxins (alpha toxin)
clostridia dificile produce tissue damaging toxin (pseudomembranous colitis)
Clostridia tetatni causing tetanus and C diff causing pseudomembranous colitis are caused by infections
Clostridia perfringes cause damage via toxin (alpha toxin, theta toxin, enterotoxin)
What is an exotoxin and what is the classic example?
Exotoxins are secreted proteins that directly interact with targets in host tissues to cause loss of function, altered function, or physical damage?
Botulinum toxin is the classic example
Which toxins do not fit the A-B model? Which do?
Do not- Pore forming toxins via assembly of a ring of protein subunits
Lipases that degrade lipids organizing the membrane (Clostridium perfringes)
Do- Botulism toxin, cholera toxin, bordatella pertussis toxin
Clostridium perfringens characteristics- Gram? Spore? Growth? Where is it found?
Gram positive, anaerobic, spore former, invasive,
- more aerotolerant than other clostridial pathogens
capable of VERY rapid growth (10 min generation time)
common in soil and intestines of many mammals
- risk of infection following wound contamination, abdominal surgery
How does Clostridium perfringens cause pathology? What type of pathology does it cause?
Produces many toxins
alpha toxin most important- phospholipase that hydrolyzes cell membrane proteins leading to lysis
q-toxin is a pore forming toxin causing lysis
enterotoxin- important in benign food poisoning
Pathology- anaerobic cellulitis, gas gangrene
What are characteristics of Clostridium dificile? Treatment?
Gram positive, spore former
antibiotic associated pseudomembranous colitis
treat with oral vancomycin or metronidazole
What are characteristics of Clostridium botulinum? Where is it commonly found? Treatment/Prevention?
Gram positive rod, anaerobe, spore-former
Encounter: commonly found in food/honey, and no live bacteria involved in transmission! just toxin
Mech: Has botulinum neruotoxin (AB) which inactivates synaptobrevin, blocks cholinergic synpases of peripheral nerves at motor end plates and cause descending flaccid paralysis (respiratory paralysis can be fatal)
Clinical: Presents with dysphagia
Infants and wound botulinum involve infections
- infant- toxin produced by gut bacteria
- wound- spores germinate in wound and result in similar Sx to botulism toxin
Prevent by heating to 80C before eating, polyvalent antitoxin
Sketch- Robutulism
What are characteristics of Clostridium tetanus?
Gram positive rod, o. anaerobe, spore former, non-invasive, MOTILE
Encounter: Wound contaminated with soil
Mech: TOXIN causes symptoms
Tetanospasm from zinc-dependent protease inactivating synaptobrevin/SNARE, utilizes zinc-dependent protease to move up motor neurons to CNS, prevents release of GABA and Glycine, resulting is spastic paralysis
Clinical: Lockjaw, respiratory paralysis, osiphotonus (back muscle rigidity) and facial muscle rigidity (Risus sardonicus)
Treatment: untreated mortality>50%, antitoxin, DPT vaccine, boosters, antibiotics
Sketchy: Risus Research Revolution
What are characteristics of Corynebacterium diptheriae?
Gram positive rod, F anaerobe, non spore former
Encounter: human throat, transmitted oral secretions
Mech: Diptheria toxin (AB), expressed only when organism is infected with a particular bacteriophage! in absence, only pharyngitis
Clinical: sore throat and pharyngitis, pseudomembrane in throat, BULL NECK due to cervical edema and lymphadenitis, asphyxiation, reversible neuro impairment (muscle paralysis)
Treatment: Antitoxin, DPT vaccine
What are characteristics of Bordatella pertussis? What is it commonly called in kids?
Gram negative coccobacillus, non motile, non-invasive fastidious slow grower, aerobe
Encounter: Aerosols, Human only host, colonizes on ciliated respiratory epithelium
Mech: toxin
- Pertussis toxin (AB) exotoxin, causes ADP-ribosylation of G protein, causing increase in cAMP, increased mucosal secretions, high lymphocytosis
- Filamentous hemagluttinin mediates adhesion to increase colonization
- Adenylate cyclase (AB), exotoxin
- Tracheal cytotoxin (TCT), an endotoxin, destroys ciliated epithelial cells
Clinical
- Catarrahl phase (1-2 weeks) with mild fever and dry nonproductive cough, highly infectious
- Paroxysmal phase (2-4 weeks) with explosive cough, danger of secondary pnemonia
- Convalescent phase
Treatment: Antibiotics early- macrolides d
DTap/Tdap with toxoid in it, acellular vaccine
- purified proteins
- D for diptheria and T for tetanus
Sketchy- Disabled GI coughing with bowtie spilling popcorn with tracheal toxin (tractor) which cleaves grass (cilia)
What are the two most pyogenic organisms?
Streptococcus and staphylococcus
What are the classification methods and how can you differentiate different types of streptococcus? Group A specifically?
Hemolytic pattern on a blood agar plate
- alpha hemolytic- partial clearing
- beta hemolytic- complete clearing
- gamma hemolytic- no clearing
For alpha and beta hemolytic streptococci you can use the Lancfield grouping according to major cell-wall carbohydrate antigens
Group A streptococcus has the M antigen, a major virulence protein allowing it to resist phagocytosis
What are the official names for Group A strep and Group B strep? Tests to differentiate the two?
Group A- Streptococcus pyogenes
Group B- Streptococcus agalactiae
Group A- bacitracin sensitive
Group B- Bacitracin resistant
What are characteristics of Streptococcus pyogenes?
Gram positive cocci in pairs or chains Beta hemolytic Group A (Lancfield) Possess M antigen- evading phagocytosis Lots of genetic diversity due to horizontal genetic exchange
Encounter: Human reservoir, may be carried in nasopharynx, skin, GI tract asymptomatically. Air-born and food born, colonized on human skin/mucous membranes. Person to person transmission. Transmitted by M protein adhering to keritinocytes. Lopoteichoic acid binding fibronectin. F protein binding Fibronectin (stimulated by increased O2)
Mech: Enters by adhering to cells (M protein- to keratinocytes or lipoteichoic acid)
- has multiple antiphagocytic mechanisms (M protein binds host complement control factors and has an antibody to M protein which is protective, Hyaluronic acid capsule- anti-phagocytic, diminished chemotaxis via C5a peptidase, kill phagocytes using streptolysin O
- streptolysin O can be used diagnostically to see if we really had a strep infection
- Damage caused by hydrolytic enzymes, inflammatory response, STSS
Clinical: sore throat, person to person transmission
- Asymptomatic carrier
- Suppurative disease
- skin and mucous membrane infections leads to classic strep, impetigo, or erysupelas
- deep tissue and blood leading to pneumonia, cellulitis, necrotizing fasciitis, myositis, puerperal fever
- toxigenic manifestations leading to Scarlet fever with Pastias lines or Streptococcal toxic shock syndrome (TSS)
- Non-suppurative complications
- Acute rheumatic fever (triggered by pharyngitis)
- Glomerulonephritis
- endocarditis
Treatment: Penicillin, amoxicillin and other beta-lactam agents (Nafcillin), If allergic to penicillin use clindamycin, azithromycin, vancomycin if severe
Sketchy- Pie genies shop encapsulated hot apple pies (hyaluronic acid), bacitracin sensitive (basset hound)
What are characteristics of Streptococcus agalactiae (Group B)?
Gram positive cocci in pairs or chains
Beta hemolytic
Encounter: Human reservoir, may be carried in nasopharynx, skin, genital tract asymptomatically.
Clinical: Neonatal meningitis and sepsis, from mom during delivery, pneumonia
meningitidis bacteremia in adults
CAMP Test Positive
Sketchy- Space galactic baby (new born serious infections) with hippo stuffed animal, bacitracin resistant, with space camp and a space ship with pencil legs
What causes acute rheumatic fever and what is its presentation?
Group A streptococcus (S pyogenes)
- Triggered by pharyngitis and is delayed for weaks after strep throat
- Often recurs, and predisposes one to endocarditis due to heart valve damage
- Presents clinically with carditis, erytheema marginata
- Caused by a specific subset of Group A strep, and it is decreasing in incidence
- It is immune mediated, and treated with aspirin acutely and long term penicillin prophylaxis
What causes of acute glomerulonephritis and what is its presentation/pathogenesis?
Caused by Streptococcus pyogenes
Associated with a few M types, and follows pharyngitis OR impetigo
- spread via immune complexes of IgG and complement in the glomerular basement membrane of the kidney
What are characteristics of Enterococci, or Group D streptococci?
Gram positive cocci in pairs and short chains, catalase negative
Encounter: Normal fecal flora of humans/animals, has extended survival on surfacecs, resistant to cephalosporins, inhibited but not killed by vancomycin, often spread by healthcare workers
Mech: resistant to multiple antibiotics
Clinical: can cause UTI, endocarditis, bacteremia, catheter related infections, intra-abdominal/pelvic infections
Treatment: Not unless causing major infection
- intravascular infection requires bactericidal, synergistic therapy (ampicillin and gentamicin) with a cell wall agent and an aminoglycoside
- VRE are becoming a problem in hospitals
What are common noscomial infections?
Enterococcus faecalis
- in pts treated with broad spectrum antibiotics or immunocompromised patients
- leads to same types of infections of enterococci (UTI, endocardits, bacteremia, etc)
What are the characteristics of Streptococcal pneumoniae?
Gram positive diplococci, alpha hemolytic, positive P test (optochin sensitivity) and bile solubility, fastidious growth (difficult to grow), opaque and transparent colony morphologies
Encounter: Asymptomatic carriers, Air borne (preschool!) colonized in the nasopharynx
Mech: Acute inflammatory response, Cell wall components induce cytokines IL-1 and TNF, resulting in systemic manifestation
- IgA Protease cleaves IgA antibodies from immune response
- Capsule diminishes complement help, phagocytosis when capsule specific antibody is produced
- Pneumolysin- pore forming toxin causes damage and may impair mucociliary clearance from lower respiratory tract, promotes auto lysis due “Autolysin” production
- Subject to PHASE VARIATION
- Spreads to lower respiratory tract due to loss of conscioussness, preceding viral infection, or immune defects
Clinical: MOPS- meningits, otitis media, pneumonia, strep throat, Fever and chills, pleuritic chest pain, crackles, productive cough, dullness at lung bases, egophony
- complications include pleural effusion, recurrent otitis media, septic shock/death, meningitis, bacteremia with seeding or pericardial or peritoneal spaces
- 5% fatality, 25% fatality for bacteremia, higher mortality for splenectomized individuals
Treatment: PCN resistant, need multivallent vaccine based on capsular polysaccharide, can use ceftriaxone
What are the clinical phases of pneumococcal pneuonia?
Exudative phase
- alveoli fill in with exudate, bacteria–> lobar pneumonia
Early consolidation
- Chemotaxis causes infiltrate of RBC and PMNs into alveoli
Hepatization
- lung looks like liver
Resolution
- macrophages clear debris, lung architecture restored
What are Koch’s postulates?
The microorganism must be found in abundance in all organisms suffering from the disease, but should not be found in healthy organisms.
The microorganism must be isolated from a diseased organism and grown in pure culture.
The cultured microorganism should cause disease when introduced into a healthy organism.
The microorganism must be reisolated from the inoculated, diseased experimental host and identified as being identical to the original specific causative agent.
What was the first organism for transformation to be demonstrated in?
Streptococcal pneumoniae
Virdans streptocci
alpha hemolytic
colonizes the orapharynx (normal flora)
low virulence
can cause subacute bacterial endocarditis, on the teeth
What is a special part about streptococcus pneumoniae cell wall? What are some of the proteins that interact with this cell wall component?
Has a c- cell wall susbtance
- the polysaccharide residue of teichoic acid has a phosphorylcholine residue
- the choline anchors certain proteins important in pathogenesis like autolysins, PspA, CbpA
- – PspA- decreases complement activation, binds lactoferrin
- choline can bind to C-reactive protein and activate complement
What is the main pathogenic mechanism of S pneumoniae?
Capsular polysaccharide- 90 different types
What are examples of pneumococcal phase variation?
Opaque colonies have:
low peptidoglycan/choline
high capsule
invade blood stream
Transparent colonies have:
high phosphoryl choline
low capsule
colonize nasopharynx better
What is phase variation and how is it useful for microbes? Mechanisms of phase variation include…
Phase variation results in phenotypic heterogeneity in an organism to evade host defenses
- can take on a capsule to get into blood, but has difficulty attaching to endothelial cells with capsule
- uncapsulated bugs establish niches in nasopharynx better in S pneumo, N meningitidis and H influenzae
Mechanisms:
Slipped strain mispairing
Site specific homologous recombination
Epigenetic regulation mediated by DNA methylation
What are characteristics of haemophilus influenzae?
Small pleomorphic, gram negative rods, can be encapsulated or nonencapsulated, encodes pili for adhesion and flagellae for movement
- encapsulated– Hib
- nonencapsulated- common cause of otitis media in kids
Encounter: human only known host, mucosal colonization in the nasopharynx (Attachment, IgA protease, LPS), areosol spread
Spread: Local or Systemic (invasion into blood, polysaccharide capsule promotes systemic infection)
Mech: damage caused by LPS (endotoxin) and is proinflammatory and causes endothelial leakage
Clinical: Subdural effusion due to H. flu meningitis (capsular type B)
Epiglotitis (drooling and inspiratory stridor)
Otitis media
Treatment: Anticapsular antibodies
- polysaccharide antigen requires a T-INDEPENDENT response
- 3 m to 3 y/o major vulnerability
- ceftriaxone
- rifampin propylaxes
Sketchy- Phylises chocolate (agar) covered cherries (cherry red tounge) with kid screaming with huge epiglottis
What are pneumococcal vaccines targetting?
Polysaccharide capsule (23-valent vaccine with no t-cell memory and limited efficacy, then a 7 valent conjugate vaccine for kids, and now a 13 valent conjugate vaccine),
What are similarities between encapsulated pneumococcus and haemophilus?
Humans are only host and asymptomatic carriers are key to transmission
Nasopharyngeal colonization
- IgA protease, phosphoryl choline
Invasive disease due to capsule
Anti-capsular antibody critical for protection
Underlying conditions that diminish bloodstream clearance increase risk for infection
What are the characteristis of Clostridum difficile?
Gram + anaerobe, spore former
Colonizes the intestinal flora
Antibiotic-associated pseudomembranous colitis
Relapse common
Stop antibiotics, treat with oral vancomycin or metronidazole
What are some differences between Strep pneumo and Strep viridans?
Both are alpha hemolytic
Pneumo- optochin sensitive, bile soluble, capsule
Viridans- optochin resistant, bile insoluble, no capsule
What type of organisms and why are some individuals more susceptible to infection if they have had a splenectomy?
Encapsulated organisms, spleen plays a major role in removing encapsulated organisms from the body (sickle cell patients)
What are major characteristics of Streptococcus viridans?
alpha hemolytic, colonizes the oropharynx (normal flora), low virulence, and commony associated with dental carries and subacute bacterial endocarditis
What are Klebsiellae characteristics?
Gram - rods, important cause of nosocomial infections, lactose fermenter (like E. coli), capsule, grow pink on McConkey Agar, immotile, urease positive
3 As of Klebsiellae-alcoholics, abcesses, aspiration
Encounter: colonize GI tract, skin, pharynx (which serve as important pathogenic reservoirs)
Risk: diminished host immune defense AND/OR antibiotic use (Klebsiellae are often resistant to multiple antibiotics)
Virulence: K antigen- prominent polysaccharide capsule which is antiphagocytic and antigenically diverse
Clinical Presentation:
- Respiratory infection, introduced potentially via respiratory support equipment, causes lobar pneumonia with destructive changes (necrosis, inflammation, hemorrhage within lung tissue sometimes producing a thick, bloody, mucoid sputum- Currant jelly sputum)
- UTIs, risk factor if using urinary catheter
Treatment: Carbapenem
