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pathogenics exam 3 > patho exam 3 > Flashcards

patho exam 3 Flashcards

1
Q

bacteria strategies for evading or surviving host defense systems.

A

Man and animals have evolved many strategies for defending themselves against bacterial invation. Battle of evolution, as bacteria develop methods to overcome these defenses.

Most of these strategies can be thought of as those aslo suited to a natural enviroments.

i.e. properties such as adherence can be just as useful in staying close to a nutrient source as bacteria sicking to teeth or heart valves ect.

Defenses against protozoa are akin to avoid phagocytosis involved in the immune system.

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2
Q

virulence factors?

A

the properties (gene products) that enable a microorganism to establish itself on or within a host and enhance its potential to cause disease.

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3
Q

samonella

A

gram negative

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4
Q

pathogencic interations

A
  1. enter the body, attach to host cells for colonization
  2. evade the host innate and adaptive immune systems and persist in the immuno-evasion or immuno-suppression.
  3. Obtain nutrients and other requirements susch as iron
  4. Disseminate (sprad) within the host, replication and travel to other hosts.
  5. these may result in symptoms from the bacteria/ bacterial products ( i.e. toxins)
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5
Q

Preinfection

factors to consider?

A

Survival in the External Enviroment Reservoir?

Must be able to survive in the enviroment but also adapt to rapid changes?

  • production of endospores to survive harsh enviroments
  • Gram +ve walls to help reduce dehydration and protein oxidation

* Animal—animal—human—-human-human

* Enviroment to human

  • Gene expression of new proteins
  • Production of secondary metbolites - acids, antibiotics, bacterocins, antimicroial products, biofils
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6
Q

Most frequent Entry Portals

A
  • skin
  • Intestinal tract
  • Respiratory tract
  • Genitourinary tract

and many others

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7
Q

medical and dental related entry portals

A
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8
Q

preferred portals of entry

A
  • many microbs have to enter in a specific manner and in a specific place to cause disease.
  • ex vibrio cholerae infects the GI tract therefore, rubbing and infected oyster on a wound of the skin will not caused cholera.
  • cross referance modes of transmission in section 2
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9
Q

Penetration of Skin or Epithelial Layer

A
  • Skin -normal does a good job of preventing entry but can be breached
  • surgery, catheters, trama, burns
  • Biting arthropods?
  • Tick,mouse,deer interations
  • Borrelia burgdoferi- lyme disease

-

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10
Q

pareternal infections

-by some rout other than through the alimentary canal, such as by subcutaneeous, intramuscular or intravenous injection.

A

Microorganisms are depositied into the tissues below the skin or mucous membranes

  • Puntures
  • Injections
  • bites
  • scratches
  • surgery
  • splitting of skin due to swelling or dryness.
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11
Q

skin

A

when intact - it is normally impentrable

  • when integrity lost then it becomes portal for entry
  • hair folicles and Sweat gland ducts ( many have antimicrobial oils for production)
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12
Q

colonization and invation of host

A

it has been proposed that the reason the skin and immune systems are so effectiv e for the great majority of organisums is that the host-microbe relationship maybe viewed as somewhat short( evolutionary time).

No bacterium can borrow or penetrate skin alone with so form of breach.

-But there aer many virulence factors that have evolved that promote colonization and survival.

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13
Q

first steps

A
  • penetration of skin
  • penetration of the Epithelial and Mucin Layers
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14
Q

Rickettsial Diseases

A

Rickettsias are small bacteria,

  • gram negative
  • non-sporeforming
  • strictily obligate
  • intracellular
  • in vertebrates - associated with/ fleas, lice or ticks.
  • not cultured in laboratory media

– only in lab animals, mammalian tissue culture and yolk sac of chick embryos.

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15
Q

Rickettsia prowazekii-

A

common body or head louse, causes

  • Typhus
  • 3 million death in WW1 among troops, unsanitary conditions, caused more deaths than combate.
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16
Q

Human Louse

A

Rickettia prowazekii-typus

Borrelia recurrents- relapsing fever

Bartonella quintana-trench fever

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17
Q

Pool feeding

A

bite of louse puntures skin

  • makes a trough
  • blood pools and the bacterium enters from louse fecal matter which is aided by scratching
  • Bacteria multiply in the cells lining blood vessles that eventually lyse resulting in the skin rash.
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18
Q

Penetration of Epithelial or Mucin Layers

Respiratory tract

A
  • easiest portal to enter and most commonly infected
  • Many microbs travel in aerosols which we breath
  • ex. cold, TB, influenza,smallpox,Pneumonia
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19
Q

Penetration of the Epithelial or Mucin Layers.

Gastrointestianl tract

A
  • Through food, water and dirty fingers
  • Must overcome low pH of the gut
  • Ex. Amobic dysentary, Hepatitis, Shigellosis
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20
Q

Penetration of the Epitelial or Mucin Layers

Genitourinary tract

A
  • for STDs
  • Broken (parentral route) or unbroken membranes ( depends on the microb
  • Ex. HIV, Genital warts, Herpes, Syphillis
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21
Q

Epithelial Layer

-Nesseria gonorrhoeae

A

-STD attaches to urogenital epithelia more tightly than other tissue via

–Protiein Opa (opacity associated protein).

  • Opa binds specifically to host cells processing the protein
  • CD66- only found on human epithelial cells.
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22
Q

epithelial Layer

-Evolutionary pressure have made this organism host specific

A
  • behavior of host- transmission, reproductive process?
  • procreation (reproduction) vs Recreation
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23
Q

what is Mucin?

A

Network of protein and polysaccharide

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24
Q

what does Mucin do?

general and specialized functions

A
  • prevent bacteria reaching mucosal cells
  • Gi and vaginal tracts act as lubricats
  • Goblet cells
  • Respiratory tract- ciliated cells expel bacteria caught in mucin
  • secoundary infections with colds and flu?
  • Mucus is expelled in long streams that forms a network of tangled strands
  • however pathogens have sought out weaknesses.
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25
Q

cholera outbreak in Yemen

A

worlds worst cholera outbreak

2000 people have died, a quarter of them children

more than half a million suspected cases

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26
Q

some bacteria can cross the Mucosal layer?

A

this is an active system in the bodies immune system.

Antibodies are produced against ingested organisums some of which are termed Secretory and released back into the Lumen t attach incoming organisms.

Preemptive strike!

Mycobacterium tuberculosis is an intercellular pathogen that infects macrophages.

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27
Q

Scanning EM of Mouse Peyers’ Patches

A

pic a-m- cell

pic b- infected by Y. pseudotuberculosis.

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28
Q

once organisums penetrate the host what are important virulence fcactors?

A

motility and methods to stick to cells

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29
Q

Motility, chemotaxis and Adherence

A

mouth, small intestin, bladder?

  • mucsal surfaces are washed by fluids. Bacteria capable of adhearing to a surface have a selective advantage.
  • many pathogens have mechanisms of attaching themselves to host epithelial cells.
  • Specific receptors , diffrent parts of the body infected. Also host specific human strains of the particular bacterial species may not adhere to epithelial cells of an animal and vice-versa.
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30
Q

motility

A

addvantage to be able to move towards a nutrient source or away from an unfavorable enviroment.

  • Flagella- ae specialized structures that provide motility
  • Fimbrie/pill- can be involved in motility
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31
Q

chemotaxis

A

Directe movement of an organism toward ( positive) or away from ( negative ) a chemical gradient.

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32
Q

flagellum

A
  • same basic structure shared between Bacteria and Archaea.
  • flagella genes are highly conserved across these 2 domains sugetting motility has Depp evolutionary Roots.
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33
Q

phylogenetic Tree of life

A

Bacteria- Green filamentous bacteria

gram positives

spirochetes

proteobacteria

cyanobacteria

Planctomyces

Bacteroides Cytophaga

Themotoga

Aqyifex

-Archaea

halophiles

methanosarcina

methanobacterium

methanococcus

T.celer

Themoproteus

Pyrodicticum

-Eukaryota

Entamoebae

slime molds

animals

fungi

plants

ciliates

flagellates

Trichomonads

Microsporidia

Diplomonads

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34
Q

flagella arrangments

A

polar

lophotrichous

peritrichous

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35
Q

speed of bacteria

A
  • some can move at 60 cell length /sec
  • cheetah only 25 lengths /sec
  • Polar flagellated organisms -rapid , spinning motion
  • Peritrichously and lophotrichous flagellated organisms move in a straight line

-

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36
Q

Approx. 40 genes are involed in flagella

A
  • Regulation genes- for synthesis and control
  • structural proteins- make up flagella itself
  • Chaperones proteins- mediate export of flagella proteins through cytoplasmic membrane to the outside of the cell to construct the flagellum itself.
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37
Q

the flagella consists of several components

A
  • Base and Filament
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38
Q

gram- ve flagella

A

several “rings” make the basal body

-an outer L in LPS, P in Peptidoglycan, MS and C rings ar3e located in cytoplasmic Membrane and Cytoplasm.

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39
Q

Gram +ve

A

lack outer membrane and so no outer L Ring

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40
Q

flagella pic

A
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41
Q

flagella base

A

1000-1200 protons/ revolution

  • protons flowing through channels exert electrostatic forces on helically arranged charges on the rotor proteins.
  • Attractions between + and -ve ions cause the base to rotate 1200 protons/revolution
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42
Q

flagella structre

A
  • at the base the motor that rotates the flagella is anchored in the cytoplasmic membrane and cell wall.
  • Acchored int eh cytoplasm membrane ar ethe Mot and Fil proteins acting as the motor and switching ( reverse) mechanisms.

-Motion from te basal body- Proton Motive Force,- protons move across the cytoplasmic membrane through the Mot complex (1000-1200 ions per revolution)

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43
Q

articles on flagella

A

many belive the flagella is not evolution but intelligent design

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44
Q

chemotaxis

A

prokaryotes are too small to sense a gradient along the single cell insted sense what they passed through a few secounds before movement /direction therefor apper a little erratic

  • without a gradient, cells move in a random fashion
  • -Smooth “runs” swimming forward and ” tumbles” where cell stops and jigs about, changes direction then “runs” in a new direction.
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45
Q

flagella attraction

A
  • in gradient, fewer tublems and more runs and bacteria moves towards attractant or way from a repellant.
  • Anticlockwise forward motion, clockwise the bundle of flagella pushes apart, foward motion cease and cells tumble.
  • Polar flagellated cells, reverse direction of rotation results in backward motion.
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46
Q

chemoreceptores

A

sensory proteins in the cytoplasmic membran sense the chemical gradients

  • changes in the enviroment are sensed at both genetic and biochemical levels.
  • Interact with cytoplasmic proteins to affect flagellar motor direction.
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47
Q

Adhesion

surface structures?

A

surface structures

  • Fibriae
  • Pilli
  • Capsules
  • Slime layers
  • Specialized proteins
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48
Q

Fimbriae and Pili

A

Rod shaped protein structures, adhesins that diffre in thickness and length ( often on Gr -ve organisms)

-Fimbriae- shorter, thinner structures

-Pili- longer, thicker structures

-orderly array of single subunits called Pilin packed in a helical way to form a cylindrical structure.

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49
Q

Pili Adhesins

A

-many pathogens have a two- step process of the pili making initial contact. The pile retract and “pull” the bacteria close to the host cell where the adhesins take over and the pili depolymerize to make a much more strong bond.

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50
Q

Signal transduction-

A

-once thought that pili were metabolically inert. Now it appers that the attachment of Pili envokes a whole range of “gene switching” of virulence genes. The action may take the form of conformational changes in the pili tips upon binding (proteins E,F,G).

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51
Q

flagella

fimbriae

A

flagella- long tails

fimbriae- smaller hairs

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52
Q

assembly of Pili is undertaken in the periplasmic space.

A
  • additional proteins -ushers interact with chapreons and guide the subunits to the cell surface.
  • present in the periplasm , prevent the pili from folding into their final configuration until ready to be extruded from the out membrane
  • this is called the Chaperone Usher system
  • finally a periplamic Protein H signals the end of the extrusion process.

how the bacteria mesures the length of decided what the final should be is not yet known.

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53
Q

chaperone- usher sytem

steps

A
  1. secrection and Specialized tip proteins (E,F,G) cross the inner membrane and into the periplasmic space.
  2. in addition to the actual pilus proteins there are a number of proteins that help in construction of the pilus.
    - Usher

-scaffold structure C

-Chaperones

-the main shaft is assembled from Protein (A)

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54
Q

classes of fimbriae /pili are known.

functions:

A

Twitching motility. - rapid extension/ reaction enables the cell to “crawl” along the surface.

Key colonization factor-in Nesseria menigitidis ( bacterial meningitis) and Vibrio Cholerae ( cholera)

Avoid host defenses . -Pili break easily when bound by host aantibodies can break away (E,F and G protiens). Also Once the body recognizes the pili another type of pili with a diffrent tip is produced by the bacteria.

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55
Q

Pili (fimbriae) of Gram+ve bacteria

A

-oral strains able to adhere and form biofilms

strep, salvivarius, Strep, gordonii, Strep. oralis, Strep. Parasaguis and Actinomyces naeslundii.

  • short, thin, rod- like fimbriae.
  • covalent attachment of sbunits to each other and to peptidoglycan cell wall.
  • Biofils can be thought of as a virulence factor.
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56
Q

biofilms

A

are matrices of organisms where gradients of nutrients exist.

-homoserine lactones-involves communication between cells- Quorum sensing

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57
Q

biofils

quorum sensing

properties and benifits

A
  • reduced metabolic levels
  • resistance to antibiotics
  • reduction to predation
  • pseudomonas aeruginosa
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58
Q

biofilms

exapmles:

A
  • important in pre-infection and establishing colonization/ disease.
  • Pseudomonas aeruginosa - in cystic fibrosis

-Legionella pneumophillia in Legionnaire’s disease

-Streptococcus, Bacteroides, Fusobacterium in dental plaque (endocarditis)

-S.epidermidis, Enterococcus facalis, E. coli, Proteus mirablis, P. aeruginosa

-K. pneumoniae- medical catheters.

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59
Q

during _________ organisums must evade or have counter measures to the host immune system.

A

colonization organisms.

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60
Q

complement system

A
  • is part of the immune system that helps (complements) the ability of antibotics and phagocytic cells to clear microbes and damaged cells from the host organisum Promotes inflamation
  • 3 patheays involved but all lead to the formation of the Membrane Attack Complex (MAC)
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61
Q

calassical pathway

A

antibody controlled

-host may produce antibodies that bind capsule providing sites both for phagocyte binding and activation of complement.

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62
Q

classic pathway

antibody controlled

A

-IgG and IgM antibodies bind antigens that become cross-linkage by multiprotein C1.

- this antiody -antigen complex leads to C2 and C4 binding at an adjacent membrane.

-

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63
Q

alternative Pathway

A
  • controlled by serum protein
  • Serum protein Properdin binds to bacterial cell surface.
  • this membrane bound complex binds C3 and protein factor B
  • catalyzes the formation of C5-9MAC leading to cell destruction as demonstrated in the classical pathway.
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64
Q

the 3rd pathway is initiated by?

A

Mannose Binding Lectins present on the cell walls of bacteria.

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65
Q

pore formation

A
  • membrane damage and cell lysis
  • recruits the C6-C9 proteins
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66
Q

capsule and slime layers

A
  • many prokaryotes secrete a loose, unstructured network of polysaccharide/protein-carbohydrate.
  • may be rigd (capsule) or flexible (slime) thick or thin.
  • Evade complement and phagocyte- mediated killing.
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67
Q

types of slime and capsules

A
  • enteropathic (disease of the intestine) e. coli
  • extracellular polysaccharide
  • Mucoid colonies
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68
Q

functions of capsules and slime layers

A
  • protect from host inflammatory response (complement activation and phagocyte-mediated killing)
  • Interferes in “alternative pathway”?
  • can prevent binding of the B protein and activation of the C3 complement and the MAC ( membrane Attack Complex)
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69
Q

Alternative pathway

A
  1. Serum protein -Properdin binds to cell surface. This membrane bound complex binds C3 and Protein factor B
  2. -catalyzes the formation of C5-9MAC leading to cell destruction as demonstrated in the classical pathway.
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70
Q

Bacteria not killed by MAC are called?

A

Serum resistant

  • although some C3b (opsonizing) can attach under the loose capsule, the capsule can prevent contact with phagocyte receptors.
  • MAC may form too far way from membrane due to capsule that forms a physical barrier and therefore no bactericidal effect.
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71
Q

capsular material

A
  • in some instances, proteins can diffuse through the capsule layer and still cause complement activation
  • so just having a capsule or slime layer dosent protect pathogens ompletely.
  • can be used for vaccines and have been very successful against a number of pathogens.
    ex. Haemophilus influenzae type b
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72
Q

Bacterial meningitis

A

meningitis is an infection of the fluid of a persons spinal cord and the fluid that surrounds the brain.

  • Viral meningitis is generally less severe and resolves without specific treatment, while bacterial meningitis can be quite severe and may result in brain damage, hearing loss, learning disabilities and death.
  • Before the 1990’s Haemophilus influenzae type b was the leading cause of bacterial meningitis, but new vaccins being given to all children as part of thier routine immunizations have reudced the occurrence of invasive disease due to H. influenzae.

-leading causes are Streptococcus pneumoniae and Neisseria meningitis are leading causes of bacterial meningitis.

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73
Q

bacteria can produce _____ that resemble or mimicks host polysaccharides.

A

-non immunogenic or autoimmune problems

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74
Q

some organisum can attach host substances to thier cell walls to evade host immune system.

A

S.pyogenes- Hyaluronic acid (mammalian polysaccharide)

Neisseria meningitdis-Sialic acid (SA) (mammalin glycoprotein)

Attachment of sialic acid ( and othr substances) to LPS O-antigen prevents formation of C3 convertase.

-SA- can also hide mannose antigens on the surface of host cells or bacteria from mannose- binding lectian ( 3rd pathway of complement system) of host immune cells.

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75
Q

______ prevent effective MAC formation.

A

changes in the length of the LPS-O antigen side chains

this mechanism is not well understood.

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76
Q

what Bacteria can coat themselves with antibotics using immune cells receptors on thier cell surfaces.

A

s.aureus-protein A

Step. pyogenes- protein G

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77
Q

optimization-

A

making the bacteria more sticky.

so phagocytes get trapped and kill the cell

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78
Q

IGg

A

singal monomer

complement binding site

phagocyte receptor binging site

binds to antigen on forgin materia

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79
Q

IGM

A

5 monomers=10 binding sites

more efficent

cause clumping action-easier for macro phages to degrade bacteria

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80
Q

S. aureus

A

IgG

clumping factor binds fibrogen

collegen binding protein

attachment to extracellular matrix proteins

fibrogen binding protein

capsule

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81
Q

Phagocytic process is ______ and a further ______

A

enhanced 10-fold by antibody binding

10-fold by c3b fixation.

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82
Q

the body can be dampened down the bodys response by

A

produce enzymes that specifically degrads C5a found in gram +ve’s

-produce toxins that kill ohagocytes inhibit migration or reduce the oxidative burst

,odification of LPS so the immune response is not activated

-H. Pylori

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83
Q

pyogenic

A

pus forming bacteria

dead phagocytes make up large part of pus

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84
Q

Sty. aureus

A

produces pigmented compounds called Carotenoids neutralized the “oxidative burst”

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85
Q

Mycobacterium tuberculosis

A

intercellular pathogen uses cell wall Glycolipids to scavenge toxic oxygen compounds, remove hydroxyl radicals and superoxide anions.

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86
Q

Leukocidins

A

cytotoxin

produced by some intracellular pathogens such as Stap.aureus and Strep. pyogenes

-organisums are ingested but then released as phagocytes are killed

dead phagocytes make up a large part of pus

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87
Q

capsule

A

polysaccharide/protein coating

-Encapsulated bacteria aqre often highly resistat to phagocytosis

prevents adherence of phagocyte to the bacteial cell killing action of the MAC

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88
Q

Strep pnemoniae

A

capsule

10 cells can kill a mouse in a few days

non- encapulated strains are a virulent.

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89
Q

PMN’s release lysosomal granules that causes more tissue
damage as well as killing themselves, Pus is mainly
composed of DNA from these two sources.
•Close control of this system is essential

A

cytokines /chemokines and complement guide the
phagocytes to the infection
-prime these cells for activation only at the site of infection.
118

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90
Q

cytokines

A

involved in cell signaling

cytokines -include chemokines, interferons, interleukins, lymphokines, tumor necrosis factor.

-produced by a broad range of cells including immune cells like macrophages, B lymphocytes, Tlymphocytes and mast cells as well as endothelial cells and fibroblast.

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91
Q

Nitric oxide (NO)

A

free radical

during infection cytokines trigger monocytes and macrophages to produce Nitric Oxide.

  • attacks bacterial metalloenzymes, proteins and DNA
  • NO also combines withsuperoxide the synergy is more reactivve =Peroxynitrite - that oxidizes amino acids causing protiens to denature

NO- is toxic to both bacteria and human cells

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92
Q

Inflammation

A
  • a non specific reaction to noxious stimuli such as toxins and pathogens -redness, sweling and pain
  • mediated by Cytokines

-an bnormal upward deviation from 37C

  • may be caused by externally induced pyrogenic agents from bacteria (LPS) (fever inducing/heat generating) or Endogenous Pyrogens-released from leukocytes
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93
Q

Interlukins

A

are a group of cytokines

interlukins lL-1,IL-6, Tumor Necrosis Factor (TNF-a)

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94
Q

pryogenic

A

fever/heat generating

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95
Q

types of fever

A

continuous fever

inter mittent fever

relapsing fever

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96
Q

countinuous fever

A

body temperature remains elevated over 24 hour period; <1 C variation

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97
Q

intermittent fever

A

body temperature shifts between normal and raised throught 24 hour period; period characteristic of most infectious diseases

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98
Q

relapsing fever

A

fever returning after an infection is reestablished.

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99
Q

signs of inflammation

A

swelling

redness

pain

heat

loss of function

these signs are due to the changes in blood vessel function

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100
Q

goal of inflammation

A

to bring phagocytes to the injered area to

isolate destroy inactivate the invader

remove debris

prepare subsequent healing

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101
Q

stages of inflammation

A

phagocytosis by macrophages

dilation an incread permeability

Containment of bacteria nad forign matter

leukocyte proliferation and migration

continued activity of recruited leukocytes.

102
Q

specific Cytikines are produced that _______

A

up regulate host responses

103
Q

cytokines -Il-1,Il-6, Tumor Necrosis Factor (TNF-a)

A

stimulate the killing active of PMNs

104
Q

Granulocyte-Macrophage Colony-Stimulating Factor (GMCSF)
and interleukin 3 (IL-3) trigger the

A

trigger the release of
monocytes and PMNs (Polymorphonuclear leukocytes
/neutrophiles) from the bone marrow onto circulation.

105
Q

Pmn’s move rapidly through the blood vessles via a

A

rolling motion

106
Q

IL-1, interferon and TNF-a

A

stimulate endothelial cells to
produce selectins that bind loosely to the surface of PMNs
and other cells causing them to slow.

107
Q

IL8-

A 
(cytokine) –stimulate PMNs to produce integrins that
in turn stimulate more cytokines called intracellular
adhesion molecules (ICAMS) to generate a tighter
attachment of above cells (Margination).
108
Q

PMNs stop and flatten against the vessel wall and force
themselves between the endothelial cells

A 
(Transmigration) assisted by platelet-endothelial cell
adhesion molecule (PECAM).
109
Q

once PMN’s have moved out of the blood vessel into the tissue they follow a gradient of _______to the site of infection

A

C5a

110
Q

IL-1, IL-8, (TNF-a) and platelet activating factor (PAF)

A

activate the
PMNs oxidative burst so enabling the full killing capacity of the cell.

111
Q

Platelet Activation Factor

A

also triggers mast cells to produce
additional vasoactive compounds ?

112
Q

margination

A

slowing and stopping of polymorphonuculear leukocytes (PMNs)

113
Q

Transmigration

A

PMNs cross the endothelial wall into the deeper tissue.

114
Q

how is inflammation a defense mechanism?

A
  1. expansion of capilaries to increase blood flow
  2. incr3ease in permeability of the micovascular structure to allow escape of fluid
  3. exit of leukocytes from the capillaries and response to infection (pus)
115
Q

Gram negativ e bacteria

A

pattern of recognition molecules are toll like receptors TLRs

These receptors recognize structures on bacteria -pathogen associated molecular patterns

-LBP-Lipopolsaccaride binding protien-produces by hepatocyte intestinal epihelial cells- ciculates in serum

116
Q

Down regulation of this sytem

A

when the phagocytes are sucessful in eliminating the invading bacterium, a second set of cytokines begin to predominate.

117
Q

IL-4, IL-10 and IL-13

A

down regulate production of TNF-a and reduce the kiling activities of phagocytes and returning the sytem to its normal inactive level.

118
Q

proinflammaotry cytokines

A

IL-1, IL6, IL-8, platelet activating factor (PAF)
and TNF-a (killing action of phagocytes)

119
Q

Anti-inflammaotry cytokines

A

IL-4, IL-10, and IL13

120
Q

sptic shock

A

the inflammatory processes fails to localize the pathogen and reaction becomes widespread.

121
Q

most ocmmon causes of sptic shoke

A
  • gr -ve’s Salmonella or E.coli- ruptured or leaking boel releasinf organisms into the intra peritoneal cavity or the bloodstream
  • gr- +ve’s Staphlococcus aureus and Streptococcus pyogenes-burns
  • production of endotoxins
122
Q

4 stages of septic shock

A
  1. systemaic inflammation response syndrom (SIRS):- temos over 38C higher and respitoratory rates. Unusally high or low neutrophile count
  2. sepsis- organ dysfunction and very low blood pressure.

severe sepsis- organ dysfunction and very low blood pressure

  1. septic shock - very low blood pressure despite fluid administration.
123
Q

sptic shock leads to

A
  • vascular resistance and blood pressure drop despite normal or high cardiac output.
  • essential organs denied oxygen and nutrients.
  • resulting failure of the kidneys , heart , brain, and lungs is the cause of death- multipe organ dysfunction (failure)
124
Q

sepsis statistics

A
  • More than 1.5 million people get sepsis each year in the U.S
  • About 250,000 Americans die from sepsis each year
  • One in three patients who die in a hospital have sepsis
125
Q

out of control inflammation—- due to-

A
  • LPS
  • Inflammatory cytokines
  • prostaglandins
126
Q

cell lysis of gr -ve organisums release LPS causing _____

A

sepsis

127
Q

There are currently ten known _________ on
various cell types

A

prostaglandin receptors

128
Q

prostaglandins act
on an array of cells and have a wide variety of effects:

A

* constriction or dilation in vascular smooth muscle cells
* aggregation or disaggregation of platelets
* sensitize spinal neurons to pain
* regulate inflammatory mediation
* control cell growth
* control hormone regulation

129
Q

Bacteria or their products reach high enough levels to trigger
complement, cytokine release and the____________of the blood in many parts of the body.
•

A

Coagulation Cascade
System

-This depletes the blood of essential clotting factors and leading
to small hemorrhages (?) in many parts of the body adding to
hypotension and organ damage.

-clots plug capiillaries—-> blackish or reddish skin lesions.—>DIC_ disseminated intravascular coagulation.

130
Q

_______is often more dangouse than the origianal infection when organs start to fail it is virtually impossible to treat and death rate exceeds 70%

A
131
Q

treatment for septic shock.

A

past treatment centered on glucocorticoid treatment (corticosteroids-steroid
hormones (down regulate cytokines)- not effective.
•Antibodies and compounds active against TNF-a are being tested, not
promising.
•Anti-cytokine agents may be more promising.
•Early antibiotic treatment
- expensive tests, take time, delays leads permanent damage to vital organs.
•Many types of bacteria can cause septic shock -no single antibiotic / or test
is effective.
-require more tests to identify specific pathogen, but costs $$$

132
Q

At present there is no agent that can reverse the established
organ failure….

treatment primarily consists of the following:-

A
  1. Oxygen administration and airway support.
  2. Volume resuscitation (serum /plasma /artificial blood).
  3. Early antibiotic administration.
  4. Rapid source identification and control.
  5. Support of major organ dysfunction.
133
Q

intracellular pathogens

A

very specialized group of pathogens, some are obligately parasitic ( i.e cannot survive outside the host)

  • normally functional genes are not required as host cell provide all nutrients ect.

reduction in genome size.

134
Q

e. coli

A

4 million base apirs with about 3000 genes

135
Q
A
136
Q

non phagocytic cells

A

Bacterial surface proteins called invasins causes polymerization
and depolymerization of actin that form and mediate the
cytoskeleton producing pseudopodia-like structures that mediate
engulfment of the bacterium forming a vacuole.

137
Q

entry into phagocytes.

bacteria are ingested and form the phagosome, however the fusion with lysome is blocked.

A

Legionella pneumophila,
Mycobacterium tuberculosis, and
Salmonella typhimurium.

138
Q

onece bacteria are inside the cell

A

• disrupt the surrounding vacuole membrane and escape into
the cytoplasm
• multiply and move about by directing local actin
polymerization at one end of the bacterium, a process called
‘actin-based motility’.

—Listeria monocytogenes,
Rickettsia,
Shigella.

139
Q

shigella

A

causes bacillary dysentery ( sever bloody and muscous diarrhea) or water. the bacteria are highly infectios since as few as 10 tp 100 microorganisms are sufficient to cause disease

-unlike many pathogens have no adheareence factors

- in the colon and rectum- shigella translocate through the epithelial barrier via M cells invading the resident macrophages, escape from the phagosomes into the cytoplasm where they multiply and induce rapid cell death.

140
Q

released from the dead macrophages______ then infect other epithelial cells using a “ trigger mechanism of entry”

  • when Shigella comes into contact with epithelial cells, the Tpe III SECRETION systems (TTSS) is stimulated and delivers Effectors (IcsB) into the host cells which play roles in camouflage against phagocytic recognition. Focus of both Genomic and Protemics research
A

Shigella-

when Shigella comes into contact with epithelial cells, the Tpe III SECRETION systems (TTSS) is stimulated and delivers Effectors (IcsB) into the host cells which play roles in camouflage against phagocytic recognition. Focus of both Genomic and Protemics research

141
Q

toxins cause tremendous damage and can lead to death but what is the mode of action/targets?

A
  • Protein synthesis stopped
  • Cell wall integrity affected
  • Nerve impulses interrupted
142
Q

Some toxins have obvious functions

A

Kill neutrophils and macrophages
kill host cells to release iron stores or carbon (nutritional)
sources.

143
Q

C. botulinum -

A

toxin produced when in food prior to ingestion.

  • commen in canning proccess
    •Bacteria form spores, pass through the GI tract and do not colonize the
    GI tract or enter tissue.
    •Toxin attacks neurons causing paralysis and death (collapse of respiratory
    system).
144
Q

some toxin genes are not normal components of the bacterial
genome.
Carried on lysogenic bacteriophage or plamids

A

C. botulinum (C & D)
Corynebacterium diphtheriae

-The example of Botulinum toxins suggests this is not the complete
story and toxins may have other physiological role in the
bacterium……….
- Regulation of cellular or phage function
- cell-cell signaling

145
Q

“exotoxin” used for many years as a generic term, now falling
out of use

A

Some toxins are not excreted
- rather accumulate and released on cell lysis
- or injected directly into host cells therefore bypassing
extracellular phase

146
Q

naming systems based on a number of criteria

A
  1. Cytotoxins:
  • can have a more general action and attack a variety of cells
    2. From disease or bacteria:
  • cholera, shiga, diptheria, tetanus
    3. Type of cell or organ affected:

-neurotoxin, leukotoxin, hepatotoxin, cardiotoxin
brain leuckocytes liver heart

147
Q

Naming systems: based on a number of criteria

activity

A
  • adenylate cyclase, (Bordetella pertussis –whooping cough)
  • lecithinase (Clostridium perfringens –gangrene)
148
Q

Naming systems: based on a number of criteria

Immunological cross-reactivity

A
  • Botulinum – A-G
149
Q

Naming systems: based on a number of criteria

Letter designation:

A

-Exotoxin A (Peudomonas aeruginosa)

150
Q

Naming systems: based on a number of criteria

A
  • E.coli 0157:H7 –shiga-like, verotoxin (culture cells)

O157 means that this was the 157th different kind of O antigen found in E. coli.
The antigens on the tail, or flagella are called H antigens. H7 means that this was the 7.
Most E. coli strains harmlessly colonize the gastrointestinal tract of humans and
animals as a normal flora. However, there are some strains that have evolved into
pathogenic E. coli by acquiring virulence factors through plasmids, transposons,
bacteriophages, and/or pathogenicity islands.
These pathogenic E. coli can be categorized based on serogroups, pathogenicity
mechanisms, clinical symptoms, or virulence factors. Among them,
enterohemorrhagic E. coli (EHEC) is defined as pathogenic E. coli strains that produce
Shiga toxins and cause hemorrhagic colitis (HC) and the life-threatening sequelae
hemolytic uremic syndrome (HUS) in humans.
E. coli O157:H7 is the most frequently isolated serotype of EHEC from ill persons in
the United States, Japan, and the United Kingdom.

151
Q

Endotoxin/entortoxin

A

endotoxin-LPS

  • structure of Gr-ve cell wall, recognized by the ummune system
  • entrotoxin used specifically for toxins in the small intestin producing diarrhea or vomiting

enteric symptoms

  • food posing
  • e.g. Sty. aureus, C. perfringens, B. cereus, Camp. jejuni
  • intestinal pathogens
  • ibrio cholera, E. coli, Salmonella enteritidis
152
Q

O antigen

A

A repetiitive glycan polymer - contained within an LPS is referered to as the O antigen, O polysaccharide or O side chain of the bacteria

153
Q

O antigen

A

is exposed on the very outer surface of the bacterial cell,
and, as a consequence, is a target for recognition by host antibodies.

154
Q

core

A

the core domain always contains an oligosaccharide componet that attaches directly to Lipid A and Commonly contains sugars.

155
Q

Lipid A

A

is a phosphorylated glucosamine disaccharide decorated with multiple fatty acids.
These hydrophobic fatty acid chains anchor the LPS into the bacterial membrane,
and the rest of the LPS projects from the cell surface. The lipid A domain is responsible
for much of the toxicity of Gram-negative bacteria. When bacterial cells are lysed by
the immune system, fragments of membrane containing lipid A are released into
the circulation, causing fever, diarrhea, and possible fatal endotoxic shock (also
called septic shock). The Lipid A moiety is a very conserved component of the LPS

156
Q

camoylobacter

A

the leading cause of bacterial food poisoning, caused by an Campylobacter jejuni, most
often spread by contact with raw or undercooked poultry.

-Campylobacteriosis. Low
multiplicity number

— diarrhea, fever, abdominal pain, cramping, nausea and vomiting – but with
campylobacter, fever is typical and the diarrhea is often bloody.

157
Q

virulence facotrs of C. jejuni.

A

Flagella

Mucin has been found to be a positive chemotaxin for C. jejuni which is compatible
with the bacteria’s colonization of the intestine where there is abundant mucus.

-Adhesion and invasion are important virulence factors for colonizing the host’s
intestinal cells.

-C. jejuni also contains lipopolysaccharides (LPS) in their outer membrane.

158
Q

1 type 1 toxin - superantigens

A

bind to host surface but are not translocated into the cell

159
Q

superantigens bind to

A

macrophages and T-cells and stimulate large amounts of toxic cytokines.

160
Q

Over-secretion of cytokines can trigger a dangerous syndrome known as a _________

A

cytikine storm

-cell singlaing protiens that are secreaed by numous cells and are a catagorey of sinalikng molecules used extensively in intercellular communication.

161
Q

___________ also were the main cause of death in the 1918 “Spanish Flu”

A

Cytokine stoms-

pandemic. Deaths were weighted more heavily towards people with healthy
immune systems, due to its ability to produce stronger immune responses, like
increasing cytokine levels.
• Nausea, vomiting, malaise, and fever
Staphylococcus aureus (enterotoxin) and Streptococcal infections
200

162
Q
  1. Type II Toxins - Cytolytic or Membrane disrupting

2 types.

A
  1. Proteins that form channels in the membrane

-Osmotic strength of the cytoplasm is higher than the environment
- breach in membrane causes water to rush in and the cell swells
and ruptures.
202

163
Q

Streptococcal- Streptolysin O

A

Streptococcal Streptolysin O
-affects the sterols of the host cytoplasmic membrane

164
Q

Staphylococcal Leukocidins

A

-lyse white blood cells

165
Q

Staphylococcal a-toxin

A

-disrupts smooth muscle in blood vessels but also
toxic to many cell types

166
Q
  1. Enzymes that disrupt the membrane phospholipid

rather than make “holes” some enzymes just__________ group of the lipid portion of the molecule that normally acts
to stabilize the lipid bilayer of the cytoplasmic membrane – cell
lysis.

A

remove the charged
head

167
Q

Phospholipases

A

cleave at other sites again to destabilize the cell
membrane.

  • ex Eg. Phopholipase, hemolysin, cytotoxin.
168
Q

what augar is used to test for toxins that use phospholipase

A

hemolysis cytotoxin phopholipase

blood agar assay-

C. perfringens a-toxin
Toxin can enter bloodstream and damage the kidneys

gas gangren

169
Q
  1. Type III Toxins (A-B)
    * *-Protein Inhibitor Toxins**

-these toxins consist of two components:-

A

Active (enzymatic) (A) and Binding (B) portions.
• Simple (single polypeptide) or compound (multiple subunits).
proteolytic cleavage occurs when the A portion is internalized and
activated when the disulphide bonds are broken.
(B) portion is very specific
-Binds to carbohydrate moiety of a host cell glycoprotein or
glycolipid
(A) portion is less specific and can kill several types of cell if it can
gain entry into the cytoplasm.

170
Q

Protein Inhibition

A

• Binding of B – leads to A and B being translocated through host
membrane into the cytoplasm via Endocytosis or direct translocation
forming a vesicle.
• Acidification of the vesicle results in A becoming disassociated from B,
entering the cytoplasm and traveling to the target and exerting its toxic
effect.
Although different cells may be attacked the mode of action of the toxin is
the same.

171
Q

scalded skin syndrome

A

Characterized by peeling skin, staphylococcal infection.
begins with a fever and redness of the skin, followed by the formation of a fluid-filled blister that ruptures
easily.
Eventually, the top layer of skin may begin to peel off in sheets.
Staphylococcal scalded skin syndrome mostly affects infants, young children and individuals with a
depressed immune system or renal insufficiency.
The disease can be life threatening. Treatment usually requires hospitalization, often in the burn unit of the
hospital

172
Q

scaled skin mode of action

A

Protein synthesis is inhibited.
• ADP-ribosylation of host cell proteins
ADP-ribosyl group is removed from NAD and covalently
attaches to the host protein inactivating it or causing it to
behave abnormally.

173
Q

• Diptheria toxin

A

Acts on elongation factor-2 –which normally brings an amino charged tRNA to
the ribosome for incorporation into a peptide
-prevents protein synthesis

174
Q

cholera toxin (enterotoxin)

acts specifically on the GI tract

A 
ADP-ribosylates an enzyme that controls AMP and ion flow leading to massive
water loss (diarrhea)
175
Q

Shiga toxin

A

A) subunit cleaves a host cell rRNA molecule, which prevents
the ribosome carrying out translocation of proteins.
-Protein synthesis is terminated

176
Q

Non-protein Toxins:
1. Endotoxins

A

• part of the outer portion of the cell wall of Gram negative bacteria
• endotoxin consists of polysaccharide (immunogenic) and lipid part of
the LPS, is Lipid A which is the toxic component
• released upon cell lysis and cell multiplication

•LPS binds to LPS-binding protein and interacts with Toll-like
receptors (TLRs)
• Stimulate macrophages to release pro-inflammatory cytokines in
very high concentrations

177
Q

Cytokine Storm

A

chills, fever, weakness, endotoxic /septic shock and even
death

178
Q

Cytokines can also induce the Alternative Complement and
Coagulation systems

-activate blood - clotting protiens - _______ leads to blood clots in small blood vessles

A

-Factor XII

-Disseminated intravascular coagulation (DIC)
results in lower blood pressure and blood supply to vital organs and
accumulation of fluid in the lungs
Acute respiratory distress syndrome

179
Q

Membrane Blebs

A

Bordetella pertussis -Whooping Cough
Bordetella Tracheal Cytotoxin (TCT)
-small molecular weight glycopeptide part of its PG,
- Ciliostasis ?
- Release of cytokine Iinterlukin-1
-arrest of ciliary movement
Without ciliary movement, coughing becomes the only way to clear
the airways of mucus, bacteria and inflammatory debris
-triggers violent coughing
-susceptible to secondary infections and can lead to death.

180
Q

Bordetella tracheal cytotoxin (TCT) has stimulating effects on the immune system.

A

Cellular damage associated with TCT is thought to be a result of increased levels of
nitric oxide (NO) secretion by mucosal cells as part of an innate defense.
In humans, peptidoglycan recognition proteins appear to bind with TCT and
consequently induce the Tumor Necrosis Factor Receptor (TNFR) pathway.
- cytokine secretion
- acts as a pyrogen

-a substance, typically produced by a bacterium, that produces fever when introduced or
released into the blood.

181
Q
  1. Mycolactone Toxins
A

Lipid-like toxin –cytotoxic and immunosuppressive properties
Mycobacterium ulcerans
Emerging human pathogen
Reservoir – aquatic insects
Buruli Ulcer –
Destructive effects on the skin, soft tissues and bones.
–Central/West Africa, Central and South America, Asia and
Australia.
237

182
Q

Buruli Ulcer

A

such as a small scratch in water or insect bite.
-toxin is secreted in vesicles
-inhibits uptake by phagocytes but can survive if phagocytized
M. ulcerans turns off the mycolactone synthesis during the
intramacrophage growth.
Can cover up to 15% of the body if untreated
Even in advanced stages there is little inflammation and
pain!
-lifelong disability

-cluster of 3 giant biosynthetic genes-polyketide synthases
infection of subcutaneous fat, resulting in a focus of necrotic
(dead) fat containing mycobacteria in characteristic spherules
formed within the dead fat cells.
Skin ulceration is a secondary event.

183
Q

toxin mediated Diseases

Diptheria-III A-B toxin

A

terium diphtheriae, Gr. +ve, non-sporeforming, nonmotile,
aerobic, club-shaped rod.

-Epidemiology and Pathology:
Severe respiratory condition that usually infects children. But
due to immunizations now shifted towards the elderly.
BUT Preventable and treatable

184
Q

Diphtheria

A

Humans only
known reservoir.
• Diphtheria is a serious disease, with fatality rates between 5% and 10%.
• In children under 5 years and adults over 40 years, the fatality rate may be
as much as 20%
247
George Washington is thought to have died of this at the age of 67

185
Q

How common is diphtheria in the United States?

A

Diphtheria was once a greatly feared illness in the United States.
1920s, there were 200,000 cases of diphtheria each year with approx. 15,000 deaths.
Because of widespread immunization and better living conditions, diphtheria is now rare in
the United States (during 1998-2004, seven cases of respiratory diphtheria were reported to
CDC).

However, surveys have found that immunity decreases with age, and only 30% of U.S. adults
age 60-69 years are protected against diphtheria. This is a concern because the disease
continues to occur in other parts of the world
• 1980 and 2000 - US. 52 reported cases of diphtheria between
•Diphtheria–Pertussis–Tetanus (DPT) vaccine is recommended for all school-age
children

186
Q

Consequences of non-vaccination!

A

After the breakup of the former Soviet Union, vaccination rates fell, and large
outbreaks of diphtheria began in 1990 in the Newly Independent States.
From 1990 to 1998, more than 150,000 people got sick from diphtheria and more
than 5,000 people died.

187
Q

how does diptheria start?

A

-colonization of throat and tonsils. Inhalation of airborne
droplets.

Grayish membrane called the pseudomembrane (fibrin (protein
involved in blood clotting), dead host cells, inflammatory cells and
bacteria) forms in the throat extending to the lungs.

• Pseudomembrane may block the passage of air, death is from
combination of partial suffocation and tissue destruction by the
toxin.

188
Q

diptheria

A

club shaped rods

  • swollen or bull neck
  • also present as a skin disease

• Toxin enters the bloodstream, but bacteria remain in the throat.

• Untreated – irregular heartbeat, difficulty in swallowing, stupor, coma
indicative of internal damage to organs.
• toxin causes systemic damage to the heart, kidneys, liver and adrenal
glands.

-

189
Q

A-B Toxin protein consists of 3 functional regions

A

B - consists of two subunits
Receptor binding region
Translocation region
A - Catalytic region

• Toxin B subunit binds to host cell receptor identified as heparinbinding
epidermal growth factor (HB-EGF) and taken up in an
endocytic vesicle.
• Epidermal growth factors are important to may cell types
(particularly heart and nerve) as signals for growth and
differentiation.
• toxin comprises 5% of total protein!

190
Q

_____ is an important step in toxin activation?

A

endocytosis

-pH drops to 5 and amino acids are protonated making them less
hydrophilic.
• Conformational change, partial unfolding of the A-B chains
exposing hydrophobic regions. Insertion into vesicle membrane.

191
Q

Reduction of disulphide bonds releases (A) chain into cytoplasm
– action?

A

Acts on elongation factor-2 –protein synthesis

-Turnover of EF-2 is very slow and only 1 molecule per
ribosome…
Extremely potent, 1 toxin molecule can kill a host cell.

192
Q

iditarode race

A

20 dog team to deliver diptheria antitoxin

-1,049 miles in 9–15 days from Anchorage to Nome.

193
Q

blood agar

A

use for C. diphteheria

  • Loefflers medium- selective-
194
Q

dipthiera vaccine

A

antitoxins can be used to neutralize the toxin (passive
immunization)
- derived from horse serum

195
Q

Vaccines

A

Highly effective vaccine DTaP (diphtheria, tetanus, acelluar pertussis).
• Made by treating the exotoxin with formalin yielding an
immunogenic toxoid preparation.
• However it is not the active component that is targeted……

Binding of antibodies that bind (B) and physically interferes with
binding to host cell hence preventing internalization of the (A) chain
that leads to toxic effect.

196
Q

cholera

A

vibero cholerae- Gram Neg curved rod

  • sever diarreal disease
  • Contaminated water, raw shellfish and raw vegetables

-Blood, Na+, K+ HCO-3
(electrolytes)
and V. colerae

-

197
Q

Cholera

Diagnosis and Prevention

A

Adequate water treatment / safe drinking water

198
Q

cholera

treatment

A

Electrolyte replacement therapy
Simple, effective and inexpensive
Intravenous or oral liquid
Glucose, NaCl, KCl, NaHCO3 – mortality down to 1%.

199
Q

Botulism(III-A-B)

Organism:

A

Clostridium botulinum, Gr. +ve, sporeforming, obligative anaerobic
rod.
• Normally found in soil and lake sediments
• cause death in humans in doses as small as 0.05–0.1 μg

200
Q

Botulism(III-A-B)

Epidemiology and Pathology:

A

-Severe food poisoning, often fatal due to paralysis of lungs
(suffocation) and heart muscle.
Not an infection as more intoxication ?
Preformed, toxin-mediated, so more of a chemical attack not by the
presence of the actual organism

toxin is so deadly, in fact, that simply sniffing it at a dose of 13-billionths of a gram can be
lethal.Worse,an injection of only 2-billionths of a gram can kill. For comparison, arsenic, one
of the most popular fatal poisons, is lethal at only one-tenth of a gram!!

201
Q

How common is botulism?

A

In the United States, an average of 145 cases are reported each year.
Of these, approximately 15% are foodborne, 65% are infant botulism, and 20%
are wound.

202
Q

Botulism

A

ingestion of foods not cooked correctly
after processing
- canning, plastic vacuum packed meats/fish, honey etc
• If the food is cooked correctly, boiling 10-15 mins inactivates
toxin.
• Toxin absorbed from the intestines into the bloodstream.
• Specific for neurons attacking peripheral nerve endings.

203
Q

bothulisum

diagnosis

A

Clinical observations, localized paralysis (impaired sight and
speech), neurological problems- within 4-36hrs after ingestion

204
Q

boulisum

prevention and treatment

A

•Prevention- correct preparation of food
•Controls over canning and preservation methods
–especially in rural communities (home canning!).
•Early diagnosis – antitoxin can prevent the disorder from
worsening, but recovery still takes many weeks
286

205
Q

2 forms of botulism that do involve the organism

A

Transient colonization:
Infant Botulism:

The infant intestinal tract often lacks both the protective bacterial flora and the clostridiuminhibiting
bile acids found in normal adult intestinal tract.Consequently the infant intestinal tract
is more susceptible to colonization by toxin producing Clostridium botulinum species.
Spores ingested -growth of bacteria in GI tract
Nausea and vomiting not seen but constipation seen.
Absorption is slower from colon but death can occur.
288

206
Q

Wound Botulism:

A

deep wounds can provide an anaerobic environment, due to tissue
damage that cuts off the bloodstream.
Enables the growth of the organism prior to toxin production.

207
Q

Botulisum

treatment

A

Botulism can be treated with an antitoxin which blocks the action of toxin circulating in the
blood.
Antitoxin for infants is available from the California Department of Public Health, and antitoxin for
older children and adults is available through CDC.If given before paralysis is complete, antitoxin can
prevent worsening and shorten recovery time. Physicians may try to remove contaminated food still
in the gut by inducing vomiting or by using enemas.

-Wounds should be treated, usually surgically, to remove the source of the toxin-producing
bacteria followed by administration of appropriate antibiotics. Good supportive care in a hospital
is the mainstay of therapy for all forms of botulism.

-Respiratory failure and paralysis that occur with severe botulism may require a patient to be on a
breathing machine (ventilator) for weeks or months and may require intensive medical and
nursing care.

-After several weeks, the paralysis slowly improves as axons in the nerves are regenerated.

208
Q 
Botulinum Toxin (III -A-B)
•
A

-8 related toxins A-H most potent biological toxin known. Types A and B cause
most infections.

-1mg can kill 1million guinea pigs.
death in humans in doses as small as 0.05–0.1 μg
• At least two coded by lysogenic phages, C & D.
• Type G may be plasmid borne.
294

209
Q

3 components produced

botulisum

A
  • Botulinum toxin (Botox)-neurotoxin,
  • C2 and C3 toxins (ADP-ribosylation) – protein synthesis.
210
Q

Botulinum toxin, protein complex called progenitor toxin, once
processed the toxin is called _______ consists of “heavy”
and “light” chains.

A

derivative toxin-

• Activation by proteolytic cleavage by either protease produced by
the clostridia or gastric proteases.
• Amino terminus of the “H” chain causes formation of a endocytic
vesicle in the neuronal membrane allowing the “light chain” to enter
the cell.

211
Q

action of botulisum

A

-nerve pulse to the muscle is through acetylcholine interaction
with receptor.

Toxin binds to presynaptic membranes on the termini of the
stimulatory motor neurone at the neuromuscular junction,
blocking release of Acetylcholine (Neurotransmitter).
• Nerve receives excitatory signal but contraction is prevented,
causing flaccid paralysis.

212
Q

nerotrasmitters

A

are chemicals that are used to relay, amplify and modulate electical signals between a neron and another cell.

213
Q

Tetanus:

organism

A

Organism:
Clostridium tetani, Gr. +ve, motile, spore-forming, anaerobic rod.
Found in soil (and GI tract of animals).
Epidemiology and Pathology:
Serious life threatening, but preventable by immunization. (last
decade 473 US cases / 68 deaths)

214
Q

tetnas

diagnosis

A

Diagnosis based on exposure, clinical symptoms. Culture of
organism is variable.
• muscles of face and jaw first affected, diagnostic trait ?
• Death results from respiratory failure.
Lockjaw

215
Q

tetunas

preventan and treatment

A

Treatment of cuts and punctures, “booster” tetanus shot. Antitoxin
made in horses, neutralizes toxin as it is released. Penicillin, sedation.
• Effect of toxin is not reversible, recovery depends on whether new
axonal terminals form. Significant mortality.
Prevention and Treatment:
• Toxoid vaccine, very effective.

216
Q

tetnus

A

Major killer worldwide in developing countries.
• Infant tetanus in the top 15 of top killers
Local customs contribute
e.g. packing of umbilical cord with cattle dung.

217
Q

tetnus

toxin

A

Opposite to botulism rather than flaccid, a rigid or “spastic” paralysis
ensues.
Contracted muscles cannot relax.
2 toxins combined
- oxygen labile hemolysin (tetanolysin)
- plasmid borne, heat labile neurotoxin (tetanospasmin).

218
Q

tetnus

A

On contact with CNS, toxin is transported through the motor neurons
back to the spinal cord.
• Binds to ganglioside lipids at the terminus of the inhibitory
interneurons,
• Cleaves synaptobrevin, blocks release of glycine.
• Inhibitory neurotransmitter (glycine),binds to receptors on the
motor neurons and allows relaxation of muscle.

219
Q

Clostridium perfringens

A

Gramstain-positive, rod-shaped, anaerobic.•Spore forming.

Commonly found in the intestinal tracts of

humans and animals.

Ubiquitous in nature.

Produces

Clostridium

perfringens

enterotoxin

(CPE).

220
Q

Clostridium perfringens

A

•

Major cause of food poisoning

in the United

States and Great Britain.

Spores are extremely resistant to heat and

other means of food preservation.

•

cpe

encoded chromosomally.

•

CPE released upon cell

lysis

in the final stage of sporulation

221
Q

Clostridium perfringens

A

-causes 80-95% of cases of gas gangrene.
Mortality from traumatic gas gangrene is 25%,
mortality from non-traumatic gas gangrene caused by the more aerotolerant organism
Clostridium septicum ranges from 67-100%.
Gangrene shows the full potency of a virulence factor !!

222
Q

C. perfringens is anaerobic but C. septicum

A

is aerotolerant and infects normal, healthy
tissue (unlike C. perfringens) and therefore may be the deadlier of the two Clostridia.

223
Q

clostridium perfringens

A

t least 7 toxins produced

224
Q

Causes a spectrum of diseases, self-limiting gastroenteritis to
lethal to gas gangrene (clostridial myconecrosis).

A

-high mortality even with early treatment.
Toxins disrupt membranes causing cell lysis ….?
1. releasing nutrients for the bacteria to utilize
2. creates larger area of dead tissue that becomes anoxic (anaerobic) for the
growth of this organism.
324

225
Q

c perfringens

food poisoning

A

Growth of vegetative cells, alkaline conditions of small intestine
stimulates Sporulation, triggering production of the enterotoxin.
Toxin also kills cells producing anaerobic condition
to allow spores to germinate

226
Q

c. perfnges

sporulation and PH

A

• Improperly prepared/stored food.
• Short doubling time (10-15 mins) –
rapidly reaches pathogenic levels.
• A few survive stomach acid inside food
particles.
• Enter small intestine.
• Sporulation -> release of CPE -> food
poisoning.

227
Q

c perfringes treatment

A

Isolation of organism from the GI tract (stools), or direct enzymelinked
immunosorbant assy (ELISA) to detect enterotoxin in stools
(feces).
Self limiting, treatment with antibiotics is not usually
required.
Correct treatment of food, refrigerate food as quickly as possible, low
temps inhibit C. perfringens.
330

228
Q

Gas Gangrene (Clostridial myconecrosis).

A

Develops within a week of trauma or surgery
• Shows full virulence potential of toxins
• life-threatening
• Muscle necrosis, shock, renal failure and death within 2 dys of
initial onset!
• High mortality rate

229
Q

treatmnet of gangrean

A

debridment - removal of dead tissue with maggot therapy

-and hyberic oxygen treatment.

230
Q

Gangrene -

A

Organism?
Clostridium perfringens
Gas gangrene also known as “Clostridial myonecrosis”, is a bacterial infection that
produces gas in tissues -it is a medical emergency.

231
Q

maggot therapy

A

-Use of maggots that eat only dead tissue
leaving alone healthy tissues.

-military surgeons noted that soldiers whose wounds became
infested with maggots often survived than soldiers with similar
wounds not infested!

232
Q

leeches in medicane

A

attach to human or animal through suckers at each end of its body and then eats its host blood

  • eat 10-15x thier body weight and do not need to eat again for a year
  • Hirudotherapy,

-venous congestion
due to inefficient venous drainage
- If this congestion is not cleared up quickly, the blood will
clot and arteries that bring the tissues their necessary
nourishment will become plugged and the tissues will die.

233
Q

Leeches themselves are used to help promote circulation after reconstructive and
microsurgery for two reasons:

A

Leeches can decompress tissues engorged from bleeding or poor venous
circulation
• They can remove hematomas (collections of blood)
• Once detached, the bite sites continue to bleed, which can promote circulation of
the affected tissue.
reducing the swelling in the tissues and promoting healing by allowing
fresh, oxygenated blood to reach the area until normal circulation can be
restored.

234
Q

leech saliva

A

calle hirudin contains a number of chmical compounds useful in medicine

-local anesthetic prevents heart attacks and strokes

the hindin compound used to prevent blood cloots

-bacterium aeromonas hydrophilla aids in the digestion of ingested blood and produces antibiotic that kills tother bacteriqa qnd may cauwse purifacation

235
Q

Hirudotherapy

A

has proven to be useful for a number of other
conditions including cardiovascular disease, ophthalmology,
osteoarthritis and dermatology. Hirudin is also used in the
treatment of inflammation of the middle ear.

-secretion of a local anesthetic by the leech makes the
procedure painless except for the initial attachment phase.
They fall off promptly after they have completed feeding.
• The hazards include infection, excess blood loss that may
require blood transfusion, allergic reactions and…..
•

236
Q

Alternative Therapy:

A

Bacteriophages and Viruses
• Target individual bacterial species and not wide spectrum
• 1920s fist used as anti-bacterial agents
• 1930s Eli Lilly (US) marketed 7 phages –Staphylococcus, Streptococcus
and E.coli.

237
Q

age of antibiotics

A

1940

-new impetus to look for alternative antimicobials

238
Q

Why Bacteriophage ?

A

Every bacteria known – complementary phage
• Extremely specific for individual bacterial species
– no cross-reaction, do not infect animal / human cells
– resident flora
• Self limiting, continue to kill bacteria until all are removed, action
ceases and dormant phage are dispersed.

239
Q

bacteria phage

A

Grow exponentially- single dose
–phage self replicating while bacteria are present.
Antibiotics become diluted and excreted from the body
– multiple does long term therapy.
• Production simple and relatively inexpensive
- under-privileged populations may be served better !?
• No allergic reaction known, omnipresent
- soil, water, plants and humans
387

240
Q

bacterial hage application

A

Phage / virus therapy holds great promise not only for killing bacteria but as
vehicles for drug delivery systems to eukaryotic cells in place of chemotherapy
eg. cancer patients etc. –specific cells affected

241
Q

Use of phage enzymes.

A

Lysins -lyse Gr. +ve cell walls. ?

digest the bacterial cell wall for bacteriophage progeny release

242
Q

Problems with phage therapy:

A

High specificity – need to identify bacterial infection prior to treatment.
•Bacterial subgroups -antibiotic wide spectrum, phages extremely narrow. “phage
cocktails”?
•Gene transfer – phages are used to transfer genetic material
-antibiotic resistance.
•Overcome public concerns of taking “viruses”, past conditioning teaches us that
viruses are dangerous in the extreme.
-However –probiotic bacteria have led the way to reduce these
concerns of taking live organisms.

243
Q

Bacteriocins
•

A

Protein-based anti microbial substances produced by bacteria
•Ribosomally synthesized peptides
•differ from traditional antibiotics in one critical way:
They have a relatively narrow killing spectrum and are only toxic to bacteria closely
related to the producing strain.

244
Q

Alternative therapy: Designer drugs?

A

Given the diversity of bacteriocins produced in nature, it is a relatively simple task to find
bacteriocins active against specific human pathogens

245
Q

Reduction on pressure for antibiotic resistance.

A

a reduction in antibiotic use should lead to a slow down in the spread of antibiotic
resistance.

246
Q

Bacteriocins and Food Preservation

A

produced by Lactic Acid Bacteria used in the production of fermented foods. Because LAB
have been used for centuries to ferment foods, they enjoy GRAS (Generally Regarded As
Safe) status by the U.S. Food and Drug Administration (FDA). ?

247
Q

nisin

A
  • was the first bacteriocin to be isolated and approved for use in foods, specifically to prevent the
    growth of Clostridium botulinum in cheese in England. By 1988, the FDA had approved its use as a
    biopreservative for a narrow range of foods, including pasteurized egg products.
    Today, used as a safe food preservative by over 45 countries, and it is the most widely used commercial
    bacteriocin and it remains the only bacteriocin that may be added to U.S. foods.
248
Q

Predatory Bacteria:
Bdellvibrio bacteriovorus

A

Bdellovibrio bacteriovorus
• Gram-negative curved rod
• Present in all environments
• obligate aerobe
• Optimal growth at 28-30 C
• Large genome (3.85M bp)
• Distinct “attack” phase

249
Q

gram negative bacteria

A

gram negaticve bacteria digest nutrients in the periplasm prior to the transport of nutrients onto the cytoplasmBdellovibrio dependent on prey to
complete lifecycle
• Can attack biofilms
• Often studied attacking E. coli or
Pseudomonas

-

250
Q

take away points

1. Transmission strategies developed
- how affective are organism in colonizing a host.
- use of transmission vectors / vehicles
- some pathogens have found human as ideal hosts.
2. Virulence Factors
• Toolbox of properties
- toxins targeted towards essential components within the host cell or immune
system.
3. Constant battle between host and pathogen

A
251
Q
A

pathogenics exam 3 (3 decks)

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