Exam 2 materials Flashcards
What are the advantages to using molecular techniques for analysis of infectious agents?
The three S’s: Sensitivity, Safety and speed.
Better, faster, safer”—on a whole we don’t do a bunch of things to get bacteria because it is cumbersome and not very safe or fast; so we’ve developed “quick tests” (also, we don’t want to grow scary bacteria in our labs)
Describe how PCR works for identifying bacteria?
a copy machine for DNA—you can do PCR because of heat stable enzymes from BACTERIA (use an enzyme called tack)
- DNA fingerprinting:
- the enzymes we use to cut DNA are “restriction enzymes” which also come from bacteria
- but this can be dangerous to bacteria, the fact that it can be so flexible with genome
- bacteria have a primitive immune system which consist of “restriction enzymes”—if you inject DNA into bacteria, they have molecular scissors that cut things up at different points—can order the enzymes based on what things they cut
How does RFLP work for identifying bacteria?
RFLP – restriction fragment length polymorphism “fingerprinting”
-can detect bacteria out on STRAIN level; can tell them apart;
-“lane” 1 and 12 are what we call “markers”—can buy DNA and they give us a standard size
-lanes 2 and 11 are two unrelated strings of bug in
(also had 500kb and arrow pointing to middle of left side)
-common source is lane 10—the bug in question that was isolated from hospital with contaminated AIR FILTER; so “common source” fingerprint
-the rest-restriction fragment polyphorism—the when you cut DNA, the fragments have different shapes
-so in some cases, will see DNA fingerprinting to see if strains are the same;
How does DNA hybridization work for identifying bacteria?
look directly at a sample to detect pathogen DNA in the sample; at a quick glance
- can the probe anneal? if yes, then you have the pathogen - so a STRAIN can be ID’ed or verified by DNA hybridization - you can also verify presence or absence of a bacteria
How does in site hybridization work for identifying bacteria?
use probes to look for pathogen DNA in fixed sample
How do do we use monoclonal antibodies in Flow cytometry, ELISA, RIA, and Western Blot?
Flow Cytometry– use antibodies to look for markers on cells/separate cells
ELISA – use antibodies to detect antigen!!!
RIA – similar to ELISA but uses radiation
Western blot – identify protein or antibodies to a protein
Define idiopathic and iatrogenic diseases.
Idiopathic – unknown cause
Iatrogenic - disease contracted from a health care setting
What is the MIC?
MIC - antimicrobial susceptibility tests (Minimum Inhibitory Concentration)
- take some test tubes; cultures of bacteria—these are bacterial cultures - and then add diluted antibiotic—looking for the minimal inhibitory concentration
Describe the most important mechanism explaining how bacteria become antibiotic resistant. Describe at least one other mechanism of antibiotic resistance.
The most important mechanism - passing R plasmids
Other mechanisms include biofilm formation, phage genes for resistance, mutation, enzymes to modify bugs, metabolic pathway changes
State where antibiotics were first isolated from and how semi-synthetic and synthetic agents improve on these antibiotics.
Antibiotics isolated from bacteria and fungi
Semi-synthetic antibiotics increase spectrum and decrease breakdown
Differentiate between chemotherapeutic agents and antiseptics, disinfectants, and sterilants.
chemotherapeutic agents can be used internally – like antibiotics
Antiseptics – used externally to prevent infections - mouthwash
Disinfectants – not usually used on patient
Sterilants – never ever on patients – remove all life including spores
Describe the MIC test. Is a higher or a lower MIC test desirable? How does this compare with an agar diffusion method? The MBC test? Differentiate between empirical and rational antibiotic therapy.
MIC (minimum inhibitory concentration) determines which drug will stop bacterial GROWTH at the LOWEST concentration
Can also test drug susceptibility using an agar diffusion/Kirby-Bauer
MBC – (minimum bactericidal concentration) determines the smallest amount to kill bacteria
Empirical antibiotic therapy - ‘best-guess’
Rational antibiotic therapy – antibiotic selected based on sensitivity
If a patient is immunosuppressed, do you want a bacteriocidal or bacteriostatic antibiotic?
Bactericidal
What do beta-lactams do and give an example of two regular beta lactase and two types that are beta lactase inhibitors.
They destroy the cell wall by stopping peptidoglycan linkage by inhibiting transpeptidases
Penicillins
Cephalosporins
Beta-lactamase inhibitors (clavulanic acid)-these stop it
Carbapenems – imipenem, meropenem
Monobactams – aztreonam- narrow spectrum (Gram -) – not widely used
What are four non-beta lactic cell wall inhibitor antibiotics?
- Isoniazid – cell wall of Mycobacteria
- Vancomycin – used if bacteria have B-lactamase
- Bacitracin –used on skin; effective against Gram positive organisms
- Cycloserine – seromycin – second line against Mycobacterium TB (drug resistant) – technically an oxazolidinone because it inhibits protein synthesis.
What are some antibiotics that interfere with cell membranes?
These are BROAD spectrum
Lipopeptides - Daptomycin- Gram positive only – drug resistant Staph, Strep, Enterococcus.
Topical only - polymyxins – detergent action – skin and eye infections
What are some antibiotics that are nucleic acid inhibitors?
Quinolones – nalidixic acid – narrow spectrum – inhibits DNA gyrase/topoisomerase
Flouroquinolone – broad spectrum - modified quinolones –ciprofloxacin- damage growing bone
Rifamycin – hepatotoxic – used for Mycobacterium tuberculosis
What are some antibiotics that are translation inhibitors?
- Aminoglycosides – bind to ribosomes - streptomycin, kanamycin, gentamicin, neomycin - ototoxic and nephrotoxic
- Macrolides
Erythromycin – binds to prokaryotic ribosomes - targets Gram positive bacteria - used when patient is penicillin allergic
Dificid – first new abx for C. diff in 30 years. Macrocyclic abx that is not absorbed so works locally in GI tract. - Lincosamides – clindamycin – binds ribosomes – pseudomembranous colitis risk
- Tetracyclines – broad spectrum - translation inhibitor
- Glycyclines – tigecycline – broad spectrum- IV for MRSA and VRE – 2010 FDA warning increased mortality with serious infection
- Oxazolidinone – Zyvox and Sivextro (2014) – Gram positive drug resistant infections – MRSA and VRE
- Streptogramins – quinupristin-dalfopristin. Gram positive bacteria, MRSA and VRE
What do metabolic inhibitors do and name an example for an antibiotic?
sulfonamides – stop folate synthesis
What’s the difference in Penicillin G and V in terms of giving it to the patient?
G is IV/intravenous and V is oral form.
What are semi-synethetic antibiotics and give some examples?
Semi-synthetic penicillins – broader spectrum and can be given orally. Not susceptible to the enzyme penicillinase
Methicillin – much narrower spectrum - IV only
Ampicillin – broad spectrum – works on Gram negative , too. Beta lactam
Amoxicillin - helps prevent of infective endocarditis
Describe the beta lactam, cephalosporin vs. penicillin.
also broader spectrum – Gram negative, too (WARNING: up to 10% of penicillin allergic patients are also allergic to cephalosporins)
Compare/contrast carbapenom an monobactem with penicillin
All are beta-lactams but carbapenom and monobactem are resistant to beta-lactamase
Carbapenem broad spectrum – but enteric bacteria becoming resistant
Monobactam – narrow spectrum – Gram negative only
Compare the Isoniazid with penicillin.
It is cell wall inhibitor of mycolic acid - acid fast Mycobacteria only –hepatotoxic
Classify the mode of action of vancomycin and contrast with bacitracin and penicillin.
Vancomycin - cell wall synthesis inhibitor, but non beta-lactam – Gram positive only
Bacitracin is used on the skin for Gram positive bacteria – cell wall synthesis inhibitor - non beta lactam
Penicillin – beta lactam cell wall synthesis inhibitor
What is the mechanism of action of polymyxin? What is the significant risk of polymyxin use? What do we use polymyxin for?
Used externally for Gram negative infection – detergent action used for skin and eye infection – neurotoxic, nephrotoxic and not stable in GI tract
What is the mechanism of action of clindamycin? What is the risk?
Clindamycin – translation inhibitor – reserved for serious anaerobic infection –
Risk pseudomembranous colitis - C. difficile superinfection
What are the risks of tetracycline use?
Tetracyclines – broad spectrum - translation inhibitor
Risks – superinfections, hepatotoxicity. May effect bone growth and stain developing teeth
What are three typical gram positive strains?
staphylococcus, streptococcus, enterococcus
What are three atypical gram positive strains?
Actinomyces
Nocardia
Streptomyces
What are spore forming gram positive bacteria?
Bacillus
Clostridium
What is a typical gram negative family?
Enterobacteriacea family
What are atypical gram negative bacteria?
Chlamydia
Rickettsiae
What are odd cell wall bacteria?
Acid Fast – waxy cell wall
Mycobacterium -stains weakly Gram positive
What has NO cell wall?
Mycoplasma
What are the oxygen needs of staphylococcus?
facultative anaerobes
What bacteria is catalase positive?
Staphylococccus
What bacteria is coagulase positive?
Staph. Aureus and Yersinia pestic
Differentiate between infections caused by exotoxin release and organ invasion.
Exotoxin can make you sick in absence of bacteria. Food “intoxication”
Invasion means the bug GOT IN to your body and is growing
How does cutaneous S. aureus differ from Staphylococcal food poisoning?
Food poisoning is caused by an enterotoxin/exotoxin
Cutaneous S. aureus is a colonization
What does S. Aureus slime layer and capsule help with?
Slime layer – helps bugs stick to catheters, valves, joints, etc.
Capsule – polysaccharide layer – stops phagocytosis
What are S. Aureus cell wall components?
Peptidoglycan
Teichoic acids – helps ID species and strain
Protein A
Coagulase
What are the cytolytic toxins that S. aureus has?
Alpha – cell lysis – tissue damage Beta – cell lysis – tissue destruction Gamma – rbc lysis Delta – acts as a detergent on rbc’s and other cells PV – leukocidin
What are some enzymes that S. aureus has?
Coagulase (S. aureus) - clot formation
Catalase-H2O2 breakdown ALL Staphylococcus– not Streptococcus
Hyaluronidase -spreading in connective tissue
Staphylokinase -(fibrinolysin) - dissolves clots
Penicillinase
What are the names of the two most prevalent species of coagulase negative Staphylococci? What infections do coagulase negative Staphylococci commonly cause?
S. lugdunensis, S. epidermis
Both infect prosthetic valves and less common native valves
Also infect catheters and joints
What are some things R-plasmids can do to resist antibiotics?
Pump—> Pump drug out
Enzyme—> break down the drug
What are some reasons for making semi-synthetic bacteria?
1) Increase its spectrum (range)
2) to have a decreased breakdown in the body
What does the Kirby Bauer test do?
- if you don’t know what anti-biotic, take a plate with a “lawn” of bacteria
- and then disc with different antibiotics
- see different reactions
- TELLS US how susceptible our bacteria is to a given antibiotic
What are the different “generations” of cell wall inhibitors?
e.g. cephalosporin
“first generation”—> S. aureus & group A strep
“second gen”—> adds some gram negative coverage
“third gen”—> Good against gram negative
“fourth gen”—> Very good from gram negative, drug of choice
for pseudonomas (gram negative rod)
What does clindamycin do?
It is a translation inhibitor but watch out for C. Diff; so then switch to Dificid.
What does tetracycline affect?
Liver, bones, teeth.
Acronym for staph. infections
“SOFT PAINS” skin infections (LO9) osteomycitis food poisiting (LO 10) toxic shock syndrome (LO11) pneumonia acute endocarditis infective endocarditis nectrotizing fascitis sepsis
What is the main gram positive that causes the cutaneous infections?
Staph. Aureus.
Describe the three classification schemes used to classify Streptococci
A. Serological groupings – aka Lancefield groups
1) looks at carbs on cell surface
2) GAS, GBS, GCS, GDS
B. Hemolytic patterns – based on rbc breakdown
C. Location - for us the most important is VIRIDANS
1) viridans = green because alpha-hemolytic – partial hemolysis
2) NO Lancefield groupings in this system – viridans/non-viridans only
What diseases does Strep. pyogenes cause?
1) Strep throat/pharyngitis – kids/ young adults with tonsils – fall/winter
2) Scarlet fever – rash and then skin peeling
3) Rheumatic fever – AFTER effect - cross-reactive antibody
4) Necrotizing fasciitis – SUPERANTIGENS – deeper infection
5) Pyoderma/impetigo – purulent skin infection – hot climates, young kids
6) Erysipelas– acute skin infection – larger area
7) Cellulitis – deeper skin infection
8) Toxic Shock syndrome – from superantigens – usually bacteremic
9) Endocarditis – infection of a heart valve
10) Post-streptococcal glomerulonephritis (from antibodies to streptococcus clogging kidneys)
What are virulence factors of strep. pyogenes?
1) Capsule
2) Adhesins
a) Lipoteichoic acid
b) M-protein family
c) F-protein – binds epithelial cells
What are toxins of strep. pyogenes?
Lots of things to lyse our cells!
Pyrogenic exotoxins - mitogens for T-cells/inflamm – rash, fever – pus –
2) Streptolysin S – lyses wbc’s, platelets and rbc’s
3) Streptolysin O – lyses wbc’s, platelets and rbc’s
4) Streptokinase – lyses blood clots and allows spread
5) Hyaluronidase – spreading
6) DNase - streptodornase
7) C5a peptidase
How are the strep. pyogenes toxins spread between the bacteria?
Phage conversion- pyrogenic toxins passed between bacteria by phage
Name the suppurative streptococcal diseases and know what part of the body they infect.
A. Pharyngitis – throat
B. Pyoderma/impetigo – skin (impetigo involves Staph and Strep)
C. Erysipelas– skin
D. Cellulitis – skin/connective tissue
E. Necrotizing fascitis – fascia – underlying tissue
F. Toxic shock syndrome - systemic
G. Endocarditis – heart
- Name the two post-streptococcal diseases. What causes each?
A. Rheumatic Fever – antibodies cross react with myocardium
B. Acute glomerulonephritis – antibody/antigen complexes in kidney
- How is Streptococcus pyogenes diagnosed and treated?
A. Diagnosed – rapid test followed by culture
B. Rheumatic fever or acute glomerulonephritis- ASO test
What is the most disease of neonates?
S. agalactiae is GBS – most serious disease of neonate – screen moms
What causes a bug for 15% of colon cancer patients?
S. bovis is a mystery- 15% of colon cancer patients have this bug.
Describe the arrangement,of S. pneumonia. What diseases are caused by S. pneumoniae? Give this organism’s common name. What is the role of the capsule for this organism? What treatment strategies are effective (drug and vaccine)?
A. diplo-strepto cocci
common name pneumococcus
B. Lung infections and pneumonia -can spread to sinuses, ear and meninges
C. Capsule – HUGE – resist phagocytosis
D. Other virulence factors: proteases to break down IgA and pnuemolysin
E. Diagnosis
1) Elevated CRP
2) Lyse rapidly with bile (other Streptococci don’t)
F. Treatment:
1) Drugs – becoming penicillin resistant
2) Vaccine
What are some highlights of Enterococcus?
few virulence factors but SUPER DRUG RESISTANT
- related to streptococcus
- in GUT
- salt and drying tolerant; found in water
- Bacteremia, UTI, abdominal abscess, diverticulum, endocarditis
What shape are most pathogenic gram negative bacteria?
rods – family Enterobacteriaceae.
1) Other Gram negative pathogens – Neisseria- diplococcus; Treponema and Borrelia are spirochetes.
2) Atypical Gram negatives - Chlamydia and Rickettsiae- obligate intracellular parasites.
State the Gram status, shape, arrangement, and oxygen preferences of Bacillus anthracis. What virulence factors does B. anthracis have?
facultative aerobic Gram positive strepto/diplo
B. Virulence factors 1) Capsule 2) Spores 3) Toxins – all three on one plasmid (PA, EF and LF)
Describe how Bacillus anthracis causes damage to a host. Include cutaneous, gastrointestinal anthrax, and inhalation anthrax.
Cutaneous anthrax – majority of cases – contact with spores – may develop eschar - septicemia
Inhalation anthrax– before weaponized anthrax this was called wool-sorters disease – goat hair
GI anthrax – rare in humans – common in grazing animals – mortality nearly 100%
How is anthrax treated?
1) Ciprofloxacin - for cutaneous
2) Could use penicillin and doxycycline but penicillin resistance has been reported
3) Cipro or doxycycline for inhalation
4) Prevent with vaccine – available for military
What is bacillus cereus and it’s three different forms?
causes food poisoning and occasionally eye infections
1) Emetic form – intoxication – heat stable enterotoxin – rice is common source
2) Diarrheal form – longer reaction time – infection NOT intoxication - heat labile enterotoxin – common source is meat or veggies
3) Ocular form – less common – secondary to traumatic eye injury
What is bacillus stearothermophilus?
autoclave indicator organism
State the Gram status, shape, and oxygen preferences of Listeria monocytogenes. Why is cellular immunity important for Listeria infections?
aerobic or facultative anaerobic Gram positive rod (cocco-bacilli)
-Facultative intracellular pathogen – can form “actin rockets” and go directly from one cell into the next without being exposed to the immune system
What diseases are caused by Listeria? How are these diseases treated?
Causes food poisoning – 20-30% mortality
1) Populations at risk include pregnant women, newborns, elderly and those with CMI defects
2) Risky foods deli meats, soft cheeses, unpasteurized milk ice cream, raw veggies
B. Treat with penicillin OR gentamicin + penicillin or ampicillin for serious infection.
C. Serious infections in patients with organ transplant, cancer, and pregnant women. Higher mortality and meningitis in these populations
State the shape of gram status/shape of Corynebacterium. Where can you find these organisms?
Gram positive rods (called coryneform or club shaped)
1) Many are part of your normal flora – respiratory, GI, urogenital tracts and skin
2) Can be opportunistic pathogens but few are true pathogens
Discuss Corynebacterium diphtheriae
1) Worldwide distribution and asymptomatic carriers
2) Causes respiratory disease - pseudo-membrane in throat
3) Cardiac and neurologic complications from A-B exotoxin
4) Mortality 5-10% BUT 20% mortality for kids under 5 and adults over 40
5) Also cutaneous form – toxin can then go systemic
Describe the mechanism of action of diphtheria toxin. What type of a toxin does this represent?
A-B toxin
1) Two part exotoxin (A for Action, B for Binding)
o B subunit binds to the cell - specific for heart and nerve cells
o A subunit goes into the cell and causes damage by stopping translation
What are the treatment strategies for diphtheria?
A. Antitoxin neutralizes exotoxin
B. At the same time give penicillin or erythromycin to remove bacteria
C. Vaccine is a toxoid vaccine – inactivated toxin
What is clostridium perfringens?
1) Wound infection/gas gangrene or gastroenteritis
2) Wound infection is more severe than gastroenteritis – necrosis, myonecrosis, ischemia
3) Treat with wound care and penicillin
4) High mortality for would infections because more than 12 toxins
What is the most important toxin with clostridium perfringens?
Lecithinase –aka alpha toxin –histotoxin – hydrolyzes host cell membranes (rbc, wbc, platelets and endothelial cells). Mediates massive hemolysis, increased vascular permeability and bleeding, tissue destruction, hepatic toxicity, and myocardial dysfunction.
Discuss Clostridium tetani and its two powerful toxins. What is the best treatment?
Causes tetanus
-Found in soil and GI tracts – ubiquitous
-- Two important toxins o Tetanolysin - hemolysin o Tetanospasmin - A-B toxin - neurotoxin --) Treatment o Debride wound o Metronidazole o Antitoxin
What causes the neurotoxins in C. botulism?
Exotoxins – most potent toxins known!
o Botulinum toxin - A-B toxin that blocks acetylcholine release – inability to stimulate muscles – don’t have to have live organisms – toxin in food
Discuss C. botulism
1) Food poisoning, wound botulism and infant botulism
2) Exotoxins are neurotoxins – most potent toxins
o Botulinum toxin - A-B toxin that blocks acetylcholine release – inability to stimulate muscles – don’t need live organisms – toxin in food
3) Treatment – remove organism if in GI tract – metronidazole or penicillin – use antitoxin
4) Prevention
o Destroy spores in food
o Prevent germination – cold or acid
o Destroy toxin – 60 degrees for 10 minutes
Discuss Clostridium difficile and treatment.
1) Obligate anaerobe
2) Component of normal flora for 5% of population
3) Causes pseudomembranous colitis - clindamycin is a cause because it wipes out normal flora
4) Treatment – stop abx. and stay hydrated – switch to C. diff safe abx -metronidazole or vancomycin
Discuss nocardia and why it was originally confused with fungi.
- Gram + aerobe – related to Mycobacterium
- Originally classified as a fungi because of branching
- Immunocompromised patients are at risk for bronchopulmonary disease and cutaneous infection – ubiquitous organism
- treat with wound care and sulfonamide
Why is nocardia of interest to dentists?
Nocardia is found in gingival pockets with Actinomyces but the role is unknown
Discuss lactobacillus and its role in caries.
Gram positive, rod shaped aerotolerant anaerobe found in mouth, stomach, intestines and genitourinary tract.
- Role in dental caries because it is acidogenic and acidouric
1) Lactobacillus are important in pit and fissure caries
2) Lactobacillus often a late colonizer (after S. mutans)
Discuss Actinomyces and its role in caries.
-Gram positive facultative anaerobe or strict anaerobes
1) Filamentous hyphae
2) May have role in caries at enamel/dentin surface
3) A. israelii is part of normal flora but opportunistic pathogen
o Find in plaque, gingivitis and granulomatous lesions
o See sulfur granules
o May see post-surgical Actinomycosis – after craniofacial surgery on lower jaw – hyphae (unique)
4) Treat by removing infected tissue and penicillin
What is the gram status and oxygen and shape of Mycobacterium and how would you test for it?
A. Gram stains weakly positive or not at all because of waxy cell wall - aerobic acid-fast rods
B. Staining test – acid fast stain
C. Clinical diagnostic test = PPD test (aka Mantoux test). Newer Quantiferon-TB gold blood test
Does mycobacterium have any exotoxins? How is the damage accomplished?
D. FEW if any exotoxins – the damage is from YOUR immune response – forming granulomas
1) Primary infection – droplet/aerosolized transmission - taken up by macrophage - Ghon’s complex formed – inflammation – wbc’s and tissue destruction
2) Secondary infection - reactivation of infection - pulmonary TB or miliary TB (spreading), granulomas – inflammation – chronic fever, night sweats, weight loss, cough
How do you treat mycobacterium?
Treatment is difficult and long term
1) Rifamycins – inhibit transcription – liver damage
2) Isoniazid – cell wall synthesis inhibitor – mycolic acid – liver toxicity
3) Pyrazinamide – unclear mode
- prevent with BCG vaccine
“RIP” up those granulomas!
What organism causes leprosy? What type of immunity is necessary to fight this infection? Be familiar with the different forms of leprosy.
Mycobacterium leprae - intracellular bacteria, therefore cell mediated immunity B. Two forms of leprosy 1) Lepromatous leprosy – most severe form – Hansen’s disease a) Highly infectious b) Lack of CMI c) Skin destruction d) Takes at least a year of treatment 2) Tuberculoid leprosy –milder form a) Hypopigmented skin lesions b) Nerve damage c) Low infectivity
Describe the epidemiology of Mycobacterium avium.
Pulmonary disease or disseminated disease, especially in immunocompromised individuals
Treat:
1) Prophylaxis in HIV patients – azithromycin
2) Treat infections with rifampin or isoniazid
What are most gram negative bacteria shapes? What are the exceptions?
Most are RODS except neisseria (diplococcus) and treponema and barrel (spirochetes)
What is an endotoxin in gram negative cell walls?
Lipopolysacchardie (LPS)–it is realized with bacteria lyse and die–since it is part of its cell wall, it is an endotoxin
What does endotoxin do to cause an infection?
Reacts with macrophages and causes endotoxic shock–it interacts through TLR and stimulates the macs to release cytokines
How do we test drugs for endotoxins?
We put drugs into a horseshoe crab WBC to look for a change to see if there are endotoxins–ALL DRUGS MUST BE TESTED FOR THIS
Where does bacterial meningitis come from for newborns?
- Listeria; 2. E.coli; 3. Strep. agalactiae (LES)
Where does meningitis come from if you are over 6 months?
- Strep Pneumonia; 2) Neisseria meningitides; 3) Haemophilis infulenzia (SNH)
What is a common name for neisseria meningitides
meningococcus
How do people contract N. meningitides?
Close contact with secretions; then bacteria engulfed by epithelial cells and eventually cross the blood-brain barrier
How do we treat N. Meningitides?
Spinal tap, penicillin
There is a vaccine available
For chemoprophylactis, use rifampin, ciprofloxin, tetracyclin
Describe the risks for contracting N. meningitides
Children and young adults at most risk–esp. in institututions
- it has a low infection rate but 100% mortality if not treated in 12-24 hours
- 10-20% have a long term cognitive impairment
What are the virulence factors of N. meningitides?
Capsule, endotoxin (LPS), pili, adjesings, IgA protease, tranfsferring binding proteins, LOS
What diseases does N. gonorrhoeae cause?
Pelvic inflammatory disease (PID) or septic arthritis
Conjunctivitis/blindness in newborns
How do you get N. gonorrhoeae and what are the symptoms?
Sexual transmission; 2-7 days incubation with painful urination, puss or NOTHING; then maybe 2 years later you have PID or can’t conceive
What is the most prevalent and second most prevalent STD?
Most is chlymidia, second most is N. gonorrhoeae
Stages of N. gonorrhoeae ubfectuib
Direct contact; attach to epithelial with finbriae, pili and Opa protein; invade the underlying connective tissue
-this stimulates complement but provides NO LONG-LASTING immunity
How do you diagnose and treat N. gonorrhoeae?
Diagnose form exudate, treat with cephalosporin (PENICILLIN RESISTANT)
What are the virulence factors of N. gonorrhoeae?
NO CAPSULE but fimbriae, pili and Opa protein; IgA protease; B-lactamase, por protein, endotoxins, and others
How do we classify the different enterobacteriace?
By metabolism
Remember, enterobacteriaceae are CATALISE NEG. AND OXIDASE NEG
What are the rapid vs. slow lactose fermenters for Enterobacteriacae?
Raid: Escherichia, Klebsiella, Enterobacter, Citrobacter, and serratis
Slow or Non: Proteus, Salmonella, Shigella, Yersinia (PSSY)
Are enterobacterioceae resistance to bile salts?
Yes
What are common disease of enterobacterioceae?
Mostly GI tract but can go elsewhere 1. CNS 2. Lower resp. tract 3. Blood stream 4. Urinary tract Diagnose with kit/tube that runs 10-20 metabolic tests and computer analysis; TEST YOUR POOP
Describe salmonella in general?
Facultative anaerobes, in animals and animal by-products,
Transmitted from host to fecal/oral
NOT PART OF NATURAL FLORA
-enteritis and systemeic
Describe salmonella typhi. Is it the most severe form of salmonella?
Yes, it is
Typhoid fever; severe diarrhea
The dose to get is is SMALL (Only 1000 bacteria)
asymptomatic carriers
treat with CHLORAMPHENICOL–binds ribosomes to stop translation
Vaccines give short-term protection
Salmonella typhimuniam–what is it?
milder salmonella then type; it causes enterocolitis/diarrhea
-you get it form uncooked poultry/eggs
Toxins include: enterotoxins, cytotoxin, type III secretion system
Virulence factors—toxins, fimbriae, and IT CAN LIVE INTRACELLULAR
-antigenic–often changes its surface coat
-drug resistance
Describe some features of E. Coli
Facultive anaerobe
FLAGELLA
normal gut but can cause GI problems
Often cause of UTI infections but 15-20% of infants die if they have it; also causes traveler’s diarrhea
What is the source of the most common gram negative sepsis?
E. Coli
What are the enterotoxins from E. COlo?
ETEC-Enterotoxin–heat stable and labile–heat kills the bug but not the toxin
EHEC-enterohemorrhagic–0157:h7; large intestine–shiga toxin, BLOODY POOP; from beef but also passes from person to person!
Do we normally have ETEC/EHEC strains of E. Coli in our gut?
No, we have E. Coli in our gut but not those kinds.
What types of shigella are there and how do you spread it?
Part of enterobacteriacea family;
S. Sonnei (u.s.); S. flexneri (developing countries); s. dysenteriae (most severe)
What does shigella cause?
gastroenteritis; dairrhea, cramps, bloodystool
Infects large intestine (but not as invasive as salmonella)
What are toxins that shigella has?
Endotoxin, shiga toxins, plasmids with other toxins, and move cell to cell (like listeria; so it can be hard to get rid of)
How is shigella transmitted?
The four Fs: Food, fingers, flies, fomites
Describe Yersinia generally
Facultative anerobic rods that cause zoonotic disease–diarrhea or the plague
What causes bubonic and pneumonic plague?
Y. pestis
Describe bubponic plague
Non-enteric Rats are reservoir; fleas are vector can go septic=lack death gut swelling in lymph--a bubo virulence factors cause coagulation, hemorrhage, necrosis 75% mortality ofo not treated Vaccine for military/vets
Describe pneumonic plague
Y. pestis AEROSOL--infection in lungs person to person spread 90% mortality of untreated they have CAPSULES--ability to grow in macs coagulase, endotoxin
What does Y. enterocolitica do?
reservoirs are pigs, rodents, rabbits, horses, sheep, cattle cats, and dogs
acute gastroenteritis-may mistake for appendicitis
-invades small intestine and survive intracellularly in phagocytes
What does Y. pseudotuberculosis do?
reservoirs are same dogs, carts, farm animals–similar to Y. enterocolitica but more benign
often self-limiting
What does klebsiella pneumoniae do?
Causes pneumonia but also wound and soft tissue infections as well as UTIs
Proteus mirabilis–what does it cause and what protein does it have?
UTI’s–has urease which increases virulence
Urease splits CO2 and ammonia; raises urine pH and ultimately cause kidney stones
What shape is vibrio cholera and what does it cause?
curved rod; infets GI tract and causes diarrhea (cholera)
death is from dehydration (20L/day)
profure watery diarrhea resulting in hypovolemic shock
What are the toxin/virulence factors of V. cholera?
AB toxin–interferes with cAMP which causes water poops–sodium absorpotion stops so water rushes out of cells to dilute sodium
pili, LPS, neuraminidase
How is cholera transmitted and treated?
transmitted via water or shellfish
10millino bacteria are an infectious dose (but less if on drugs)
have oral vaccine for travelers with multiple doses
but HYGIENE IS KEY
national disasters
Relative virulence for vibrio cholerae, salmonella, shigella, streptococcus and yersinia
- Vibrio and salmonella–imilar in virulence–100,000 (ID5)
- Shigella-100
- Strep pneumoniae 50
- Yersinia pestis-10 (crazy!)
Campylobacter in general
vibrio or spiral shaped microaerophilic gram negative bacteria
hard to see in scope
What are the two types of campylobacter that cause gastroenteritis in the US?
C. Jejuni
C. Coli
Describe C. jejuni
One of major causes of food borne illness in developed countries–high inf. dose unless not good stomach acid
- zoonotic–carried by sheep/chickens (NOT person to person)
- water, milk, meat and chicken
- rehydration is often a sufficient way to treat
Describe C. Coli
2-5% of campybacter gastritis cases
associated with PORK and also bottled water in Europe
-possible association with Guillian-Barre syndrome (autoimmune reactive arthritis)
Describe helicobacter
pleomorphic rod fecal oral or oral oral transmission; flies can also be vectors Humans MAIN reservoir zoonotic from cats/dogs/other mammals treat with abx. clarithromycin and PPIs chronic damage may increase cancer Produce urease-protect from stomach acid most people with gastritis or peptic ulcers (duodenum) have this; also gastric ulcers and duodenal ulcers
Describe Pseudomonas aeruginoisa
Obligate aerobe rods; ubiquitous; form biofilms, fluorescent pigments–greenish, sweet swelling infections resistant to abx. and disinfectants
- pneumonia, osteomyelitis, sepsis, wound infections in burn patients, etc. NOT NORMAL FLORA
- cytic fibrosis get it in lungs and can’t get rid of it
What are the virulence factors of Pseudomonas
capsule (mucoid/not), pili, LPS, exotoxins, elastase, hemolysins and abx. resistance
