Term
| Describe the bacteria cell wall. |
|
Definition
o Peptidoglycan
• sugar backbone with peptide side chains cross-linked
• rigid support, protect v osmotic pressure, site of PCN action
o Outer membrane of gram-neg
• Lipid A (puts toxin in endotoxin)
• Polysaccharide (Ag for lab dx)
o Surface fibers of gram-pos
• Teichoic acid (rarely used for dx) |
|
|
Term
| Describe the bacteria cytoplasm. |
|
Definition
o Lipoproteins and sterols
o Site of oxidative and transport enzymes |
|
|
Term
| What to bacteria ribosomes do? |
|
Definition
o RNA, protein
o Protein synthesis
o Sites of action of aminoglycosides, erythromycin, tetracyclins, chloramphenicol
- Nucleoid (DNA) |
|
|
Term
|
Definition
o Invagination of plasma membrane
o Division/secretion |
|
|
Term
|
Definition
o Space between plasma membrane and outer membrane
o Contains many hydrolytic enzymes |
|
|
Term
|
Definition
- Not all microorganisms have them, but many medically important ones do (in order to survive bloodstream)
- Hydrophilic gel-like substance
- Usually made of polysacharrides
- Completely surrounds the cell
- Impedes phagocytosis, penetration of toxins (including antibiotics)
- Picture fresh tomato seeds
- Loose Slime is the same material may amorphously surround the cell |
|
|
Term
| What are pilli or fimbria? |
|
Definition
o Glycoprotein
o (1) Mediate attachment to cells
o (2) Mediate attachment for sex |
|
|
Term
|
Definition
- Not all have them
- Require ATP
- Various types: monotrichus |
|
|
Term
| What is in a Gram + call wall? |
|
Definition
- 40-80% peptidoglycan
- Contains compounds not found elsewhere in nature
- Mammalian enzymes can’t break them down well (except for lysosome, which isn’t very effective)
- Microbial products will break these down
- Penicillin (product of fungi) will disrupt wall production and induce hydrolase that will lyse wall
- Teichloic acids – function as adhesins, antigenic determinants |
|
|
Term
| What is in a gram - cell wall? |
|
Definition
- Minimal layer (10%) peptidoglycan
- Periplasmic space
o Where hydrolytic enzymes and antibiotic inactivating enzymes are stored
- Outer wall with Lipopolysaccharide
o AKA Endotoxin
o Provides permeability membrane barrier
- Porins
o Can genetically change porin size to disallow movement of antibiotics in and out |
|
|
Term
| What is the function of the bacteria cell membrane? |
|
Definition
- Site of all secretion (exotoxins)
- Cell wall synthesis
- DNA synthesis
- ATP production (like eukaryotic mitochondria)
- Permeability |
|
|
Term
| What is a bacteria nucleiod? |
|
Definition
o Single chromosome (4K genes)
• Huge: 1mm uncoiled (1,000 times larger than cell it comes from)
• Gyrase (enzyme) super-coils chr (targets of quinilone drugs)
o No Introns |
|
|
Term
|
Definition
o Extra-chromosomal DNA
o Replicate autonomously
o Unique features: enzymes that protect v. toxins, heavy metals; antibiotic resistence genes (beta-lactimase snips PCN) |
|
|
Term
| What are the six ways bacteria are transmitted? |
|
Definition
1.transformation
2. conugation
3.transduction
4. Plasmids
5.transposition
6. spores |
|
|
Term
|
Definition
| one cell lyses, releases DNA bits, which are incorporated into new host (introducing new function) |
|
|
Term
|
Definition
| donor DNA crosses cytoplasm bridge and integrates into recipiant DNA |
|
|
Term
|
Definition
| the exchange of genetic info between bacteria as moderated by a transducing bacterial virus |
|
|
Term
|
Definition
| Transposons (jumping genes) can exist on a plasmid, then jump to chromosome, and back – important for variation |
|
|
Term
|
Definition
| usually produced in response to nutrient deficiencies; very resistant to environmental changes |
|
|
Term
| What are the 5 steps to establishing a bacterial infection? |
|
Definition
1. Entry
2. Adhesion, Colonization
3. Toxin/Enzyme Production
4. Evasion of Cell-Mediated and Humoral Immune Systems
5. Antibiotic Resistance
- host vs bacterial-mediated pathogenesis |
|
|
Term
|
Definition
- When treated with formaldehyde, acid or heat, they form toxoids (lose toxicity, retain antigenicity) – vaccines
- Spreading factors
- Hyaluronidase snips a certain point so organism can move into new space
- DNAase breaks through viscous DNA
- Streptokinase breaks through post-derived fibrin clots so bacteria can escape wound site
- Membrane disrupting
- Hemolysins break open and spill RBCs
- Leukocydins
- Protein synthesis inhibition
- Diptheria
- Activation of second messenger
- Cholera, E. coli ST/LT
- Cholera produces choeragin which causes unregulated production of cAMP, flooding enteric cells, causing chloride release, ion flush, secretory diarrhea, massive dehydration
- Proteases
- Clip specific proteins, especially synaptobrevins (which are responsible for NT release and inhibition)
- Tetanus/botulism
- Immune response activators (superantigens)
- Presence hyperstimulates cytokine release
- Toxic shock syndrome
- Type III secretion system – like needle injection |
|
|
Term
|
Definition
- Alarm Reactions
- Fever
- Complement activation
- Macrophage activation
- B-lymphocyte stimulation
- Hypoglycemia
- Circulatory effects (increased permeability of capillaries, vasodilation)
- Shock, DIC (Disseminated intravascular coagulation)
- No toxoids can be produced; endotoxins not used as antigens in any available vaccine
* Cytokine-mediated reaction may also cause premature labor and spontaneous abortion (Cuidado con UTI in pregos)
*Gram positives have NO endotoxins but they do have other cell wall fragments that can stimulate the immune system |
|
|
Term
| What are bacterial invasive factors? |
|
Definition
1. Adhesins
2. Iron Aquisition
3.Subvert Humoral Immune Response
4.Subvert Cell Mediated (Phagocytic) Response |
|
|
Term
| What is meant by Iron Acquisition? |
|
Definition
o Require millions more times amount of iron for metabolic processes than eukaryotes
o Specialized ligands sequester and store iron:
o Seiderophores, Hemolysins |
|
|
Term
| What is meant by Subvert Humoral Immune Response? |
|
Definition
o Antibody cleavage – directed at mucosa
o Antibody shedding – organisms liberate bits off own Ag, letting them bind to some other surface and attracting Ab (distraction)
o Antigenic variation – organisms genetically modify surface proteins, altering genetic fingerprint (nicera gonorrhea)
o Immunosupression – chemicals produced which depress immune response |
|
|
Term
| What is meant by subvert cell mediated (phagocytic) immune response? |
|
Definition
o Kill phagocytes (including apotosis proteins)
o Depress normal function (chemically)
o Inhibit phagocyte chemotaxis
o Inhibit ingestion of microbe
o Intracellular growth
o Inhibit phagosome-lysosome fusion (prevent products of oxidative burst that kill pathogen; use residence in phagocyte to reproduce)
o Neutralize oxidative products
o Caveoli – cave-like structures found on Mast cells where bacteria hide and avoid exposure to IS and antibiotics; from there they can enter cells via endocytosis (E.coli)
o Inhibit cell:cell communication – prevent IS communication |
|
|
Term
| What are the typical ID stages? |
|
Definition
1. Incubation (between infection and symptoms)
2. Prodrome (nonspecific malaise, fever, anorexia)
3. Specific-illness (characteristic overt disease)
4. Recovery (illness abates) |
|
|
Term
|
Definition
| toxins in bloodstream (cultures negative) |
|
|
Term
|
Definition
| bacteria in bloodstream (cultures positive) |
|
|
Term
|
Definition
- 85 % of deaths in ICU; tenth leading cause of death in U.S. – and the numbers are rising
o Immune compromise due to chemotherapy, transplants, and AIDS
o Indiscriminant use of antibiotics
o Older population
- Up to 1 million people a year get severe sepsis
- More deadly than top five cancers combined
- Billions spent on it each year. |
|
|
Term
|
Definition
| (aka microbemia) organisms in blood |
|
|
Term
|
Definition
Systemic inflammatory response syndrome - response to infectious/non-infectious insult – at least two defined conditions:
o High or low temperature
o Tachychardia
o Tachypnea or hyperventilation
o WBC elevated (above 1200) or decreased (below 400)
o Hemoglobin greater than 12 or less than 4 |
|
|
Term
|
Definition
help differentiate between infectious and non-infectious causes of SIRS:
o C reactive protein (released in response to infection)
o Procalcitonin (only released in pts with systemic infections) |
|
|
Term
|
Definition
| of classifying patients: Predisposition, Infection, host Response, Organ dysfunction |
|
|
Term
|
Definition
(sepsis syndrome): sepsis with at least 1 organ dysfunction (increasing mortality rates by 20% with each organ involved)
o MODS multiple organ dysfunction syndrome. Respiratory is the usual starting point. Then renal, liver, CV. |
|
|
Term
| What is refractory septic shock? |
|
Definition
| patient unresponsive to fluid therapy for longer than one hour |
|
|
Term
| What is the mechanism of sepsis? |
|
Definition
- Inflammation, coagulation intended to isolate pathogen. In sepsis, the regulators aren’t working, so there is over-inflammation and coagulation of endothelial cells, which then triggers a second wave of the same, as well as the release of tissue factor, releasing thrombin, which causes clotting
- Low APC: Activated Protein C is a controller of inflammation and a supporter of fibrinolysis. When it’s low, you get tiny little clots all over, causing blockage and tissue/organ death |
|
|
Term
| What is the biophasic sequence of sepsis? |
|
Definition
1. Overwhelming pro-inflammatory response
a. TNF, IL1, IL2, IL6, IFN gamma
b. This stimulates damage, which then stimulates more inflammation
2. Attempt to regulate
a. Synthesis of anti-inflammatories (IL 10)
b. State of immunosuppression, increasing ability to get subsequent infections
*As a result of this balance between inflammation and anti-inflammation, you have coagulation, microvascular thrombosis, ischemia, shock, MODS, death |
|
|
Term
| What are the common source sites of sepsis? |
|
Definition
1. CNS
2. Pnemonia
3. Skin (cellulites, wounds)
4. Appendix/intestine
5. Liver
6. IV catheters
7. UTIs – especially in elderly
30% have unidentified source of sepsis.
Preceding viral infection may predispose to bacterial sepsis. |
|
|
Term
| What are the Signs and Symptoms due NOT to infecting organism but rather to immune response of sepsis? |
|
Definition
- Initial: Peripheral vasodilation, increased cardiac output, early direct effects on lungs, migration of neutrophils to pulmonary endothelial cells (local inflammation and fluid leakage) leading to Adult Respiratory Distress Syndrome Chills, fever, nausea, vomiting, diarrhea, decreased urine output, tachycardia, hyporthermia, hyperventilation (for metabolic acidosis),
- Later: Signs consistant with specific organ failure
- Dx requires high index of suspicion, and tests for the infectious agent and MODS |
|
|
Term
| What are the management strategies for sepsis? |
|
Definition
- Treat fast with broad-spectrum antibiotics, then tailor later if you know what pathogen it is
o Clindomycin and linzaloid that may suppress exotoxins as well as bacteria
- Source control: Look for abcesses in lungs and sinuses, look for UTIs, etc.
- Fluid resuscitation in conjunction with vasopressors to normalize the intravasculature
- Other supportive care: mechanical intervention for organs, corticosteroid therapy for hemodynamics, high caloric diet, close monitoring of blood glucose (sepsis can lead to insulin receptor resistence) |
|
|
Term
| What are the principle pathogens of Staphylococcus? |
|
Definition
S. aureus
S. epidermis
S. saporphyticus |
|
|
Term
| What are the general characteristics of Staphylococcus? |
|
Definition
- Relatively resistant to heat
- Resistant to desiccation
- Tolerate of salt
- Present in normal human flora and therefore found on everything humans touch
- There are hundreds of types |
|
|
Term
| What are the typical transmissions of Staphylococcus? |
|
Definition
o Direct contact
o Fomites |
|
|
Term
| What is the microbiology of Staphylococcus? |
|
Definition
- Grape-like clusters, 1 micrometer diameter
- Non-motile
- Don’t produce spores
- Have capsule (evade phagocytosis)
- ALL are catalase positive |
|
|
Term
| What are the general characteristics of S. aureus? |
|
Definition
- Most virulent, causes most severe infections
- Can infect from any place once skin barrier is breached; can set up metastatic sites of infection throughout body
- Can produce sepsis |
|
|
Term
| What are the predisposing factors of S. aureus? |
|
Definition
- WBC chemotaxis defect
o Trisomy 21
o Diabetics
o Rheumatoid arthritis
- Antibody opsonization defect
o Complement deficiency
- Intracellular killing defect
o Following phagocytosis, the inability to mount the oxidative burst of H2O2 to kill bacteria
o Lukemia, granulomatous diseases
- Severe skin trauma
o Recent burns, incisions
o Foreign bodies – IV lines, sutures, caths, prosthetic devices
- Prior infections
o Reduced granulocytes
- Chronic underlying disease
o Malignancy, alcoholism
- Recent administration of antibiotics |
|
|
Term
| What are the Pathogenicity factors of S. aureus? |
|
Definition
1. Catalase
2. Coagulase
3. Hyaluronidase
4.Staphylokinase
5. Beta-lactamase
6. Protein A
7. Peptidoglycan |
|
|
Term
|
Definition
enzyme which splits H2O2 (used by phagocytes to kill bacteria) – neutralizes it to water and oxygen
o All Staph are catalase positive! |
|
|
Term
|
Definition
allows conversion of host fibrinogen to fibrin, which then coats bacteria (hiding!)
o Only S. aureus produces this |
|
|
Term
|
Definition
| dissolves host-derived fibrin clots, so host can’t wall off the bacteria |
|
|
Term
|
Definition
| dissolves host-derived fibrin clots, so host can’t wall off the bacteria |
|
|
Term
|
Definition
| components of wall can have endotoxin-like attributes |
|
|
Term
| What are the cytolytic toxins of S. aureus? |
|
Definition
o Alpha, Beta, Gamma, Delta
o Aka Hemolysins
o Formerly thought to lyse RBCs exclusively, now known to have more general actions
o Pore-forming protein complex & membrane damaging toxins
o Produce classic abscesses
• Pus, erythema |
|
|
Term
| What are the pyrogenic toxin superantigens of S. aureus? |
|
Definition
o Solely products of S. aureus
o Very similar to strep STEs |
|
|
Term
| What are the exfoliative toxins of S. aureus? |
|
Definition
o Impetigo bullus
o Staph scalded skin syndrome
• Intraepidermal blisters |
|
|
Term
| What is TSST 1 & 2 of S. aureus? |
|
Definition
o Toxic Shock syndrome
o Directly related to a group of enterotoxins
o Produced by some s. aureus
o Both 1&2 are superantigens
o Have direct effects on endothelial cells, causing leakage, edema, shock
o Rash in both males and females
o Most common associated with tampons |
|
|
Term
| What are the lab identifications of S. aureus? |
|
Definition
- Gram (+) coccus (+)
- Catalase (+)
- Coagulase (+) – only S. aureus
- Mannitol fermentation (+) – only S. aureus
- DNAase (+)
- Novobiocin sensitive (+)
- S. epi (=), S. sapro (-) |
|
|
Term
| What are the common manifestations of S. aureus? |
|
Definition
1. Skin - impetigo, furuncle, carbuncle, cellulites, mastitits, necrotizing fasciitis
2. Toxin-mediated – bullus impetigo, SSSS, TSS
3. Deep Infection - endocarditis |
|
|
Term
| What are the coagulase negative staphyolococci? |
|
Definition
S. epidermidis
S. saprophyticus |
|
|
Term
| What are the S. epidermidis pathogenic factors? |
|
Definition
1. PS/A – capsular lysaccharide/adhesin
2.PIA – polysaccaride intracellular adhesions
3.Fibrinogen Binding Protein
4.Fatty acid modifying enzyme
5.Lipase
6. Ab Resistance – MRSE, VRSE
Produces almost nothing for toxins |
|
|
Term
| What is PS/A – capsular polysaccharide/adhesin ? |
|
Definition
| used to stick to host cell, and can also stick to various plastics (catheters, IV lines |
|
|
Term
| PIA – polysaccaride intracellular adhesions ? |
|
Definition
| used to stick bacteria together and also to stick to RBCs |
|
|
Term
| What is Fibrinogen Binding Protein ? |
|
Definition
| allows interaction between organism and collagen/fibronectin of host cells (when you live on the skin, you need a way to hold on) |
|
|
Term
| What is Fatty acid modifying enzyme ? |
|
Definition
| inactivates FAs produced by host cells to inactivate bacteria – allows for long-term colonization of epithelial cells |
|
|
Term
|
Definition
| primarily for colonization, and maybe for initiating infections |
|
|
Term
| What does S. saprophyticus affect? |
|
Definition
Primary cause of UTIs in young females
- Endogenous in colon |
|
|
Term
| Diseases commonly associated with coag-neg Staph: ? |
|
Definition
-S. epi – endocarditis, iv/renal catheter infection, burns, prosthetic joints
- S. sap - UTI/urethritis/cysticit, young women, urethral syndrome |
|
|
Term
| What are hte characteristics of genus stroptococcus? |
|
Definition
- Form chains (only divide in one plane)
- Approximately same size as Staph (1 micrometer)
- Don’t form spores
- Not motile
- ALL catalase (-)
- Some of the most important clinically
- Vary in hemolytic qualities |
|
|
Term
| What are the characteristics of GROUP A STREP – S. Pyrogenes? |
|
Definition
- Ubiquitous, most important, most successful
- Bacterial pharyngitis to cutaneous infections, to systemic infections, with many post-infxn sequellae |
|
|
Term
| What are the toxic factors of Group A Strep? |
|
Definition
- Capsule of hyaluronic acid
o Retards phagocytosis,
o Acts as binding protein for epithelial cells
o Has little immunogenicity (looks like human HA)
- M-protein on fibrils – outermost structure
o Major virulence and resistance factor
o Avoids phagocytosis and binds to fibrinogin
o May initiate hallmark shock
o Produce post-infxn sequellae
o More than 100 kinds
- Lipotychoic acids
o Used to bind to other cells
o One group focuses on pharyngeal epithelia |
|
|
Term
| What are the extracellular products of Group A Strep? |
|
Definition
- Strep pyrogenic exotoxins (STE)
o A and C are superantigens, stimulate hyperimmune response
- Erythrogenic Toxin
o Repsonsible for rash, strawberry tongue of scarlet fever
o Only produced by GAS that are themselves infected with a virus!
- Hemolysins
o Streptolysin O – breaks down in presence of oxygen; antigenic (produces Ab response)
• Presence of ASO is used in Dx
o Streptolysin S – oxygen Stable
- DNAses (streptodornase)
o Helps them move through pus, which is viscous because of DNA of dead WBCs
- Hyaluronidase
- C5a Peptidase – cleaves C5a component – stops recruitment of phagocytes
- Streptokinase – fibrinolysin used to break down clots – a spreading factor |
|
|
Term
| What is the Presumptive Dx of Group A Strep? |
|
Definition
1. Gram (+)
2. Catalase (-)
3. Hemolysis on SRBC – B-hemolytic
4. Bacitracin - sensitive |
|
|
Term
| What are the characterisitcs of GROUP B STREP – S. agalactiae? |
|
Definition
- Gram positive
- Catalase negative
- Less pathogenic than GAS
- Leading cause of sepsis and meningitis in neonates
- Normal flora in lower GI – spreads easily
- 10-30% of women have vaginal carriage of GBS |
|
|
Term
| What are the virulence factors of Group B Strep? |
|
Definition
1. Polysaccharide capsule
2. C5a peptidase
a. Disrupts complement
3. B-hemolysin (sometimes) / cytolysin
a. Can lyse epi and endo thelium
4. LIpoteichoic acid (all gram + have it)
a. Specifically cytotoixc for embryonic brain cells
5. C-antigen
a. Helps internalize organism inside cervical epithelial cells
6. Hyaluronic acid lyase
a. Breaks down high concentrations of H. acid which occur in placenta and fetus – used as a spreading factor in these tissues. |
|
|
Term
| How is Group B Strep transmitted? |
|
Definition
- Vertical – infect baby in utero via amniotic fluid or ruptured membranes
o Much higher risk of GAB infection in premature births
o Infection can also occur during birth process
o Results in early-onset infection (within 1st week of life), manifesting as bacteremia, pnemonia or meningitis – 20% mortality
- Horizontal
o Between care-givers (especially of infants)
o 7 days to 3 months – bacteremia and meningitis
o ***GBS is the most common agent of meningitis in neonates, followed by E. coli |
|
|
Term
| What are the commmon manifestations of Group B Strep? |
|
Definition
1. Neonatal: meningitis, pnemonia, sepsis
2. Adult: pnemonia, soft tissue infection |
|
|
Term
| What are the characteristics of GROUP C STREP – S. dysgalactiae? |
|
Definition
- Occur in patients with chronic underlying disease
- HIV, ETOH, IV drug use
- Usual manifestations from pharyngitis to sepsis |
|
|
Term
| What are the characteristics of Streptococcus pneumoniae? |
|
Definition
- Kind of a wimp, but a major pathogen
- Worldwide distribution
- ***Most important cause of CAP (community acquired pnemonia)***
- Primarily occurs in children under 2 and the elderly
- Gram positive cocci, catalase negative (all strep)
- 20% healthy adults, 40% healthy kids carry it asymptomatically |
|
|
Term
| What are the virulence factors of Strep. pneumoniae? |
|
Definition
- Strongly alpha-hemolytic
- All pathogenic strains are encapsulated (128 different serotypes based on capsule antigens)
o No virulence sans capsule
- Pneumolysin
o Inhibits and kills PMNs
o Interferes with normal function of ciliated upper respiratory cells
o Stimulates cytokines, complement
- Autolysin – causes disintigration of own cell wall
o At end of cell life, it allows splitting
o Further stimulates inflammatory response
- Hyaluronidase |
|
|
Term
| What is the pathology of Strep pneumoniae? |
|
Definition
- Humans are the only host
- Doesn’t last long on surfaces, heat, cold, etc
- Direct contact/aerosols spread it
- The problem comes when they move into an area they can’t be cleared from because of a predisposing factor . . .
- When they start growing, they produce no reactive toxins, but do produce a nasty host inflammatory response |
|
|
Term
| What are the predisposing factors for Strep pneumoniae? |
|
Definition
- Myriad. Most everyone.
- Any condition causing defective Ab
- Senescence
- Immunosupression
- Prior respiratory infection
- Anything that hinders respiratory clearance (tobacco, mines, dust, bronchitis, asthma, etc) |
|
|
Term
| How do you Lab ID Strep pneumoniae? |
|
Definition
- Gram (+) cocci
- Catalase (-)
- Alpha hemolytic
- Optochin sensitive
- Quellung reaction (+)
o Specific antiserum to pneumococci, which causes swelling of capsule |
|
|
Term
| What are the common manifestations of Strep pneumoniae? |
|
Definition
- *Leading cuase of Otitis media and sinusitis
- Leading bacterial cause of meningitis (espec elderly)
- Leading cause of community ac pnemonia
- Sepsis |
|
|
Term
| What are the characteristics of ENTEROCOCCUS and non-GAS strep? |
|
Definition
- Live in GI tract, normal flora
- Acquire resistance very quickly
o VRE – vancomycin resistant enterococcin
o VDE – vancomycin dependent enterococcin
- Problems mostly in hospitals:
o Very common cause of nosocomial UTI
o Ditto for nosocomial bacteremia |
|
|
Term
| What are the virulence factors for Enterococcus and Non-GAS Strep? |
|
Definition
1. Cytolysin/hemolysisn
2. Aggregation Substance
a. Allow for gene exchange
b. Some part of endocarditis
3. Extracellular surface protein (Esp) |
|
|
Term
| How do you differentiated Enterococcus and Non-GAS strep from other cocci? |
|
Definition
- Gram (+)
- Catalase (-)
- Hemolysis – alpha or gamma
- Bacitracin – resistant
- Optochin/Bile salt resistant
- Esculin hydrolysis (+) |
|
|
Term
| What are the comman manifestations of enterococcus and non-GAS strep? |
|
Definition
- Primarily Nosocomial
o UTI, soft tissue, intra abdominal, endocarditis, bacteremia |
|
|
Term
| What are the characteristics of Viridians Strep? |
|
Definition
.) Virulence
b.) Lab ID
c.) Common manifestations
- endocarditis
- dental caries |
|
|
Term
| What are the pathogenic Gram - Cocci? |
|
Definition
1. NEISSERIA
a. N. gonorrhea
b. N. meningiditis
2. MORAXELLA
a. M. catarrhalis
3. ACINETOBACTER
a. A. baumanni
b. A. lwoffii |
|
|
Term
|
Definition
- N. gonorrhea, N. meningiditis
- Distinguished: gonorrhea only grows on “chocolate” blood agar; meningiditis grows on any blood agar
- For more on N. gonorrhea, see STD lecture |
|
|
Term
|
Definition
- Like ticks, serves no purpose
- If it becomes systemic it can lead to death in hours
- Among the leading causes of bacterial meningitis, especially in the 12-25 year old group |
|
|
Term
| What are the virulence factors for Gram - cocci? |
|
Definition
- Polysaccharide capsule
- LOS (lipooligosaccharide)
o Strong burst in cytokine activity
- Pili (for attachment and causing inflammation)
- OMP (outer membrane proteins)
o For adherence
- IgA1 protease
o splits secretory IgA (takes down the first line of defense)
- Antibiotic Resistance |
|
|
Term
| What is the pathology of Gram - cocci? |
|
Definition
- Asymptomy to sepsis to death
- US incidence: 3-5/100K
o Higher incidence in 15-24 year olds, especially males, otherwise healthy, more likely to be fatal – college freshman
- 10-15% healthy individuals carry it in nasopharyngeal area
o Presence isn’t a good predictor of infectious risk – carriers may never get disease but can transmit
- Don’t like hot/cold/environment
- Major worldwide health threat
- Exclusively human pathogen
- See meningitis lecture for more details |
|
|
Term
| What are the common illnesses associated with Gram - cocci? |
|
Definition
1. Meningococcemia
2. Menintigits |
|
|
Term
|
Definition
- Easily mistaken for Neisseria
Common Manifestations of M. catarrhalis:
- 3rd leading cause of Community Ac pnemonia
- Otitis, sinusitis, bronchitis – children
- High colonization in asthmatic children |
|
|
Term
|
Definition
- Like surfaces that are constantly wet
- Preference for UR tract
- Usually infections in immunocompromised and hospitalized people
- UTI, pnemonia, soft tissue |
|
|
Term
| What are the general characteristics of Gram - Rods? |
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Definition
- Soil, animals, human flora; free-living and endogenous
- Very diverse
- Being gram negative, they can cause sepsis when they gain access to blood
- Can set up metastatic sites of infection
- 1-2micrometers in length, usually motor (shigella, chicken salmonella), usually polar or peritrichisly (covered in flagella) motile
- All ferment glucose (not all lactose)
- Non-spore forming
- Oxidase negative, most reduce nitrate
- Tons of UTIs and diarrheas
o UTIs – opportunistic pathogens, usually from colon
o Diarrheas – cytotoxic and invasive, causing inflammatory response, or cause watery diarrhea |
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Term
| What is the Antigenisticity for Enterobacteriaceae? |
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Definition
o O (somatic) Antigens – comprise outer wall (LPS)
o H Antigens – associated with flagella
o K Antigens – capsular |
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Term
| What are the virulence factors for Enterobacteriaceae? |
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Definition
o Enterotoxins
o LPS
o Capsules
o ß-lactamase |
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Term
| What are the general characteristics of Escherichia coli ? |
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Definition
- Most common species seen in clinical labs
- Can infect almost anywhere
- *Lactose-positive (fermentor) helps to distinguish b/t shigella, samonella
- GI, UTI mainly and other factors (3rd cause of neonatal meningitis, pneumonia, skin infections) |
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Term
| What are the uropathogenic strains of Escherichia coli? |
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Definition
80-90 % UTIs,
- All endogenous
- Contain specific absorptive pilli that allow them to attach to uroepithelial cells
o Not just any E. coli can give you a UTI
o Type 1 fimbriae – allow attachment specifically for bladder
o PAP (P fimbriae) for binding to renal epithelial cells as opposed to other ecoli
-tend to be opportunistic (come from enteric and then get into sterile area) |
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Term
| What are the pathogens of enteric pathogens of Escherichia coli? |
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Definition
- All exogenous
- 6 varieties of enteric ecolis (EECs – enterovirulent e. coli) All cause some kind of gastric upset, but in slightly different ways
- Enterotoxigenic (watery diarrhea), enteropathogenic, enteroinvasive(inflammatory diarrhea-mucus/blood/white cells), enteroaggressive, enterohemorrhagic EHEC gets all the press! (in capibable of fermemeting sorbital-also not self limiting like others)-danger of dehydration and assoc. emerhagic colitis-facillatied by toxin(shigatoxins), LT, ST toxins
o diffusely adherent |
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Term
| What are the clinical presentations of Escherichia coli? |
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Definition
- Usually 1-5 days incubation
o Abrupt onset
o Vomiting, diarrhea, fever x 24 hours
o Only diarrhea after first day
o Self-limiting, except enterhemorrhagic
• E.H. can’t ferment sorbitol |
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Term
| What is the diagnosis of Escherichia coli ? |
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Definition
lots of examples – see lab
Look for lactose positive gram neg rods
- Variety of toxins are species-specific |
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Term
| What are the common diseases caused by Escherichia coli? |
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Definition
UTI, diarrhea, neonatal meningitis
- 90% of UTIs are caused by these bugs
- Diarrhea-producing E. coli also have attachment pilli that help attach them to enterocytes |
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Term
| What are the general characteristics of Klebsiella? |
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Definition
- Heavily encapsulated
- Not particularly pathogenic, but they do have associations with UTIs and pneumonia
o Hemorrhagic pneumonia: blood mixed with thick gooey capsules – “current jelly sputum”
- Rarely, if ever, associated with diarrhea
- Primarily in alcoholics, immunecompromised
- Quellun Reaction: used for organisms with heavy capsules (klebsiella and strep pnemoniae) |
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Term
| what are the general characteristics of Proteus (mirabilis)? |
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Definition
- Lactose-negative, Gram negative, low pathogenic potential
- Important as agent of UTI in men
o Usually associated with blockage (stones)
o Produces urease,(also H.pylori) which causes production of ammonia, raising pH, yielding alkaline stones |
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Term
| What are the general characteristics of Salmonella enterica (and subspecies)? |
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Definition
- Gram negative rods, unable to ferment lactose (big difference between this and e. coli), produces H2S (hydrogen sulfide positive- only in certain medias) (whereas shigella is H2S neg. and nonmotile)
- Live in intestines of warm and cold blooded animals
- Most are motile, like water
- Classification is very complicated – more than 2400 different serotypes!
o Species name, with serotype name after (Salmonella enterica typhi)
- Predominantly industrialized society diseases: in mass-production, we contaminate food, food at rest., sewage contamination
- Disseminated in environment via water, soil, plants, human and animal excretion (but don’t multiple, but survive here)
- Food (eggs, ice-cream, mayo, meats (contim by shit), veggies, rec. drugs,) pets or water (main source of wide epi)
- Usual entrance: oral ingestion |
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Term
| What is Salmonella Disease? |
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Definition
1. Acute gastroenteritis
2. Blood infection: enteric fever (tyhoid fever-not common) |
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Term
| What are the toxins the Salmonella preoduces? |
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Definition
Enterotoxin: causes watery diarrhea – like cholera toxin and e. coli LT (but binds in different place)
Cytotoxin: inhibits protein synthesis – also contributes to diarrheal symptoms, necrosis |
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Term
| What is the pathogenesis of the GI salmonella strains? |
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Definition
- Infect gut epithelium
- Digest mucosal glycocalyx
- Invade enterocytes in large or small bowel
- Pro-inflammatory cytokines production is stimulated
- Diarrhea results from inflammation short-term
- Long term: destruction of mucosa, ulcers |
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Term
| What is the pathogenesis of the typhoid salmonella? |
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Definition
- Few GI symptoms
o Brief prodrome of GI in some cases
- Organisms attract phagocytes from Peyer’s patches, then prevent phag-lys marriage, grow in phagocyte, release into lymphoidal tissue, then to blood
- Can infect many tissues – espec gallbladder, liver
- Associated with fever (“enteric fever” “typhoid fever”)
- Can persist for years |
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Term
| How do you ID Salmonella? |
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Definition
Gram (-) rods
- Lactose (-)
- Usually motile, produce Hydrogen Sulfide |
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Term
| What are the general charcteristics of Shingella? |
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Definition
*Like Salmonella, do not produce Lactose
- All non-motile, all non-H2S producers
Humans are primary reservoir
Usually fecal-oral route via water supplies
Transmission: Flies, Food, Feces, Fomites |
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Term
| What are the 4 types of Shingella? |
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Definition
1. Shigella dysenteriae (A)
2. Shigella flexneri (B)
3. Shigella boydii (C)
4. Shigella sonnei (D) ((90% of cases in this country) |
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Term
| What is the pathogenesis of Shingella? |
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Definition
- Bloody diarrhea with mucoid stools
- Invade mucus cells/aggressive/invasive, inflammation, possible colitis, ulcers, bloodmuscoid cells
- Fever sometimes (from inflammatory response, not systemic infxn)
- Endotoxin contributing to diarrhea? This is suggested by some studies, but unimportant.
- Some cytotoxin
- The diarrhea is mostly cytokine-mediated inflammation
- Cell death and necrosis in epithelium, resulting in more colitis, diarrhea, abcesses
- Spread via Actin Rocket (like Listeria) within colonic mucosa
- Some potential for extra-intestinal infection (UTI in young females, systemic infection in immunocompromised, sexual transmission) |
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Term
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Definition
- Suspect when you see inflammatory diarrhea
- Gram (-) rods
- Lactose (-)
- H2S (-)
- Non-motile |
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Term
| What are the Non-Enterobacteriaceae Enteric Bacteria? |
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Definition
1. Vibrio
2.Campylobacter (Spirillaceae)
3.Helicobacter (Spirillaceae) - H. pylori |
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Term
| What are the Vibrio species? |
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Definition
- V. cholera,
- V. parahemolyticus,
- V. vulnificus (most impt. In US) |
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Term
| What diseases does vibrio cause? |
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Definition
| Common diseases: cholera, gastroenteritis, wound infection/cellulitis, sepsis |
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Term
| What are the clinical presentations of vibrio? |
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Definition
| RICE WATER STOOL, RICE WATER STOOL! Mostly mucus and water, not much stool |
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Term
| What are the species of Campylobacter (Spirillaceae) |
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Definition
- C. jejuni
- C. fetus
- C. coli
- 14 others that cause infections in humans |
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Term
| How do you ID Campylobacter (Spirillaceae)? |
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Definition
- Gull-wing shape
- Motile via single polar flagella (salmonella and ecoli which have peritryious-lots of flagella)
-campy plates can be used to indentify using |
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Term
| What is the pathogensis of Campylobacter (Spirillaceae) |
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Definition
-Oral and then colonization of enteric mucousal cells (unknown if toxin) ranges from
- Chicken is most common source for human infxn
- Use quirky, darty motility to get into host cells
- Most common clinical result is acute inflammatory diarrhea – not as perfuse as dysentery or EIAC
- Between 3 and 4 million cases per year in US
- Also can cause sepsis, GB Syndrome
- Highest rates in infants and elderly – more likely to see invasive disease in elderly, IC
- Exact mechanism for diarrhea not known, but it is inflammatory and non-perfuse |
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Term
| How does H. pylori cause disease? |
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Definition
urease (break down urea to make ammonia, higher pH so they can prosper-alter local environment)
- Proteus also produces urease |
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Term
| What are the common diseases of H. pylori? |
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Definition
| Type B gastritis, gastric ulcer, gastric carcinoma |
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Term
| What are the virulence factors of H. pylori? |
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Definition
- Urease – breaks down urea, producing ammonia, neutralizing the acid of the stomach so it can live
o Creation of slightly higher pH zone stimulates stomach to produce overall hyperacidity – this can aggravate ulcers
- Mucinase/motility – for spreading (can “swim” to less acidic areas) use flagella to migrate and then push into mucosal cells
- Vac A toxin – intercytoplasmic vaccule inducing toxin which causes apoptosis, blocks production of T cells, and may help induce ulceration
- Adhesins- like pilli – aid attachment so they can hold on in movement-filled stomach
- CAG proteins |
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Term
| What is the pathogenesis of H. pylori? |
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Definition
- thought to be in 50-60% adults in developed countries, 100% in undeveloped, people to people transmission or fecal/oral, lasts forever in you if not cured
- They are the most common cause of gastritis (type B), gastric ulcers, adenocarcinoma of stomach
- Colonize underneath mucosal layer and begin producing proteins (CAG proteins associated with adenocarcinoma) that induce an inflammatory response (ulcers first) |
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Term
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Definition
- Endoscopy with biopsy and culture of the gastric mucosa
- High end urease production (watch out for p.mirabilis)
- Directly look for ureases in biopsy
- Non-invasive: C-13 breath test (for urease production after drinking urea)
- EIAs for antibodies in serum or feces
- H.pylori MAY decrease asthma. |
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Term
| What are the Non-Enteric Gram (-) Rods? |
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Definition
1. Pseudonomas
2.Burkholderia
3.Legionella |
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Term
| What are the general characteristics of Pseudonomas? |
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Definition
- P. aeruginosa is most important
- Strictly aerobic, curved gram (-) rods
- Ubiquitous – found everywhere – very resistant-need lots of antibiotics-FOUND IN FLOWERS GOING TO HOSPITAL PATIENTS!
- Clinically significant as opportunistic infection – very common nosocomial pathogen
Leukemia, burns, CF, IV drug users, transplant recipients
- Usually does not cause infections in healthy individuals. Maybe swimmers ear
- *Non-fermentative!!!
- Use cytochrome oxidase, usually encapsulated
- Produce water-soluble pigments – most common is pyocyanin pigment (blue-green pus!)
o Also have “fruity” odor (grape-like?)
- Porin structure in outer wall – highly adaptive to living environments |
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Term
| What are the toxins/invasive factors of Pseudonomas? |
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Definition
- Adhesins
- Endotoxins
- Motility – especially in burns and wounds
- Exotoxin A – protein-synthesis blocker, unique to P.
- Exoenzyme S – also unique
- Elastase – degrades elastin layer in blood vessels – particularly useful in lung tissue (extensive damage and hemorrhagic lesions), also debilitates immune cells
- Pyocyanin – blue pigment and toxic factor because it causes host cell to produce H2O2, disrupts ciliary action in respiratory tissue, stops growth of other bacteria
- Alginate – found in capsule of some of them – used as adhesin for binding to lung epithelium – also forms “biofilm” which protects organism
- Enterotoxin – occasional diarrhea
- Antibiotic resistance – inherently resist most of the usual Abx |
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Term
| What is the pathogenesis of Psuedonomas? |
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Definition
1. Attachment and colonization
2. Local invasion
3. Disseminated and systemic disease |
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Term
| What are the common diseases caused by Pseudonomas? |
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Definition
- Pnemonia
- Folliculitis
- UTI
- Burn Infection
- Otitis Externa
- Keratinitis (contact lenses)
- Endocarditis
- Sepsis
- *Especially a problem in CF patients! |
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Term
| What are the genreal characterisitcs of Legionella? |
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Definition
L. pnemophilia
- 90% of all legionella infections in humans involve this member of the legionella family, mostly serogroups 1, 3, 6
- Very hardy (0-60 degrees C; pH 5-8.5; need very little O2)
- Become attached to surfaces in aquatic environments and form biofilm for attachment
o Biofilm then acts as protection
- Naturally distributed in all sorts of water: lakes, ponds, water tanks, swimming pools (can survive chlorination), air conditioners
- These are naturally parasites of aquatic ameba |
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Term
| What is the pathology of Legionella? |
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Definition
- Transmitted when water source becomes infected with amebas, then aerosols are produced from water source (shower heads, air conditioners, mist-ers)
- Inhalation allows for delivery deep into respiratory system.
- Infection begins in respiratory tract, macrophage engulfs (and this is just like natural habitat), multiply, block oxidative burst
- Growth of bacteria activates Complement, dying macrophages cause influx of PMNs
- Leakage of capillaries, deposit of fibrin, etc – this is pnemonia! – quite destructive
- NOT very transmissible between humans (we don’t aerosolize with such tiny particles)
- Mostly affects immunocompomised |
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Term
| How do you ID Legionella? |
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Definition
- Presents like other kinds of pnemonia
- Poorly stain G (-) or don’t stain at all – don’t ID with Gram stain
- Rod-like or coccobaccillari (long cocci or short rods)
- Have to use specific plate to culture: BCYE |
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Term
| What are the Coccobacilli? |
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Definition
1.Hemophilus – “blood-loving”
2.Bordetella |
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Term
| What are the general characterisitics of hemophilus? |
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Definition
| - Small, non-spore, non-motile, coccobacilli |
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Term
| What are the virulence factors of Hemophilus? |
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Definition
- PRP Capsule – avoids complement, phagocytosis
- Adhesins – promote adherence to respiratory cells
- IgA protease – degrades the primary defense of respiratory mucosa and aids in attachment
- Hemocin, a bacteriocin which inhibits competing bacteria |
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Term
| What are the types of hemophilus? |
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Definition
- Six serological types (A-F), based on capsule antigens
- Type B was the most important – especially prevalent in kids under 6
o Has declined in importance since vaccine
- *Atypical unencapsulating strains – have not been typed
o Growing in importance of human disease agents |
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Term
| What are the common dieases caused by hemophylis? |
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Definition
- H. influenzae b - pneumonia, acute epiglottitis, meningiti otitis, sinusitis, sepsis ;
- H. parainfluenzae - endocarditis |
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Term
| What are the speceis of Bordetella? |
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Definition
- B. pertussis – whooping cough, child & adult
- B. parapertussis – “pertussis like”
- B. bronchiseptica – kennel cough |
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Term
| What are the general characteristics of Bordetella? |
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Definition
Gram (-)
Grows on a special medium – not cultured in typical lab
VERY contagious – aerosols direct and indirect |
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Term
| How do you Dx Bordetella? |
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Definition
| clinical suspicion, PCR, Flourescent Ab, |
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Term
| What are the virulence factors of Bordetella? |
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Definition
- Pertussis toxin – works just like diptheria toxin
- Adenylate cyclase toxin – inhibits nutrophil chemotaxis (prevents signal transduction)
- Tracheal cytotoxin – probably a fragment of cell wall, kills ciliated tracheal epithelia cells (preventing their antibiotic sweeping), contributing to special kind of cough
- Filamentous hemagglutinin (Fha) – attachment to respiratory epithelium
- Highly infectious but not highly invasive – stay in upper respiratory tract
- Elaborate various toxins, causing reactions of: irritation, secretion, whooping cough |
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