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1
Q

60-80% of microbial infections caused by

A

biofilm bacteria

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2
Q

Formation of biofilms

A

Reversible adsorption of bacteria
(sec.)
Irreversible attachment. “Sessile” (sec.-min.)
Attached bacteria multiply, microcolonies: recruitment of other bacteria (hrs.-days)
Exopolymer production by microcolonies, biofilm establishment (quorum sensing) (hrs.-days)
Incorporation of other bacteria into the growing biofilm. Other materials depending on environment e.g. leaf litter, silt (days-months)


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3
Q

Attachment

A

Surface conditioning of clean surfaces necessary for biofilm formation

  • Deposition of organic molecules onto a clean surface (sec.) - salivary proteins on tooth enamel
  • fibronectin, fibrin on vascular catheters
  • Bacteria attach to conditioning film, NOT directly to surface
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4
Q

Adhesion molecules:

A

bacterial cell surface proteins, mediate attachment to surfaces/other cells (other bacteria, host)
Binding to other cells mediated by adhesion molecule/receptor interactions: highly specific, lock-and-key

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5
Q

Formation of biofilms

A

Secondary colonizers bind to 1°s, co-aggregation (adhesion molecule/ receptor)
- 3°and later colonizers become associated with the growing microcolony
- F. nucleatum “bridge
species”
- Bacteria co-aggregate into cooperative consortia based on most important needs

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6
Q

Physical

A

Anchorage to surface via binding to other species

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7
Q

Nutritional

A

By-products of metabolism of 1 sp. = food for other e.g lactic acid
Enzymes to degrade carb chains off host glycoproteins = food Proteins to scavenge iron = available to other species

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8
Q

Respiratory

A

Anaerobes co-aggregate with facultative anaerobes, lower O2

tension

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9
Q

Structure of a mature biofilm

A

Biofilm microcolonies are made up microbes surrounded by a “spiders web” of extracellular polymers
- Volume: 75-95% extracellular polymer, 5-25% bacteria

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10
Q

Biofilm dispersal

A

Release of bacteria from the mature biofilm

  • Active, enzyme degradation of polysacch. matrix - Passive, fluid flow, collision
  • New pioneer cells
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11
Q

Light production in the squid

A

Lux I: autoinducer synthase, makes signaling molecule/autoinducer Lux R: receptor AND response regulator/transcription activator, turns on expression of genes including luciferase ( makes light)

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12
Q

Light pro

A

A threshold concentration of inducer is needed to stimulate light production

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13
Q

A general mechanism of QS (Gram–ve bacteria)

A 
LuxI/LuxR quorum sensing circuit
2 main components:
- Signal mol: autoinducer (AHL), made by LuxI
- Receptor/Response regulator: LuxR
*Species-specific
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14
Q

Oligopeptide mediated quorum sensing circuit

A

3 main components:
- Signal mol: Oligopeptide - Receptor (R)
- Response regulator/ transcription activator (RR)
*Species-specific
transporter
R
RR

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15
Q

3rd general mechanism of quorum sensing

A

LuxS/AI-2 based quorum sensing

  • Signaling molecule: autoinducer-2 (AI-2), made by LuxS
  • Made by >30 different G+ and G- species
  • Proposed interspecies communication
  • Not as well studied
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16
Q

3 classes of signaling molecules

A
  1. Acyl homoserine 2. Oligopeptides, 3. AI-2, multi lactone (AHL), Gram-ve Gram+ve species
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17
Q

Motility

A
  • Flagellum gene expression by quorum sensing
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18
Q

QS can trigger

A

Quorum sensing can trigger the expression of virulance genes

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19
Q

Quorum sensing can trigger biofilm formation

A

Necessary to initiate exopolysaccharide production - Block QS, inhibit biofilm formation

20
Q

Bacteroides

A

Gram-ve rods
• Strict anaerobes, can’t grow in O2, tolerate
short exposure
• Normal residents of vertebrate intestinal
and oral microbiomes
• One of the most dominant genera in the
large intestine of vertebrates • >1011 per gram of feces
• Nutrition: metabolize complex carbohydrates

Can tolerate short exposure to air
•  Enzymes to detoxify and breakdown reactive
oxygen species (ROS)
21
Q

B. fragilis (Bf) virulence

A

B. fragilis clinically important Bacteroides • Polysaccharide capsule: anti-phagocytic
• Neuraminidase-cleaves sialic acid from host
carbohydrates, use carbs as energy source • Catalase and SOD: oxygen tolerant
**Most dominant species cultured from intra- abdominal abscesses that result from intestinal spillage into peritoneal cavity

22
Q

Bacteroides The peritoneal cavity (PC)

A

Fluid filled space between the organs contained in the abdomen, usually sterile
• More susceptible to contamination that any other place in the body
• Spillage of intestinal material into cavity can be catastrophic
• Few mls of intestinal fluid: billions of bacterial cells, 100s of different species
• Sources of spillage:
• Ruptured bowel
• Ruptured appendix • Abdominal surgery

23
Q

biphasic diseases

A

Intra-abdominal infections typically result in this

Acute inflammation localized abcesses
• Few species predominate in the abcesses
although 100s introduced into PC
• B. fragilis, most common species isolated from
abcesses
• B. fragilis, is not the most common Bacteroides
in the intestine normally (~1%)

24
Q

Damage caused by intra-abdominal abscesses

A

Can extend to nearby sites, tissue necrosis
• Serve as reservoirs for bacteria to enter the blood: secondary infections
sepsis/septic shock

25
Treatment of intra-abdominal abscesses
Combined surgical and pharmacologic approach • Drainage of abcesses, surgical repair of source of infection • Combined antibiotic therapy needed, polymicrobial abscesses • B. frag resistant to many antibiotics, excellent results with: Metronidazole b-lactam-b-lactamase inhibitor combinations Carbapenems
26
Sepsis/Septic shock
Sepsis ≠ bacteremia • Bacteremia is the presence of bacteria in the blood, with or without the presence of an illness e.g. brushing • Sepsis is a severe systemic illness characterized by hemodynamic derangement and multiple organ malfunction, brought about by interaction of microbial components with host macrophages. Begins with bacteremia • “Hemodynamic derangement”: high cardiac output yet low bp and inadequate perfusion of organs (kidney, liver, gut)
27
Mediators of sepsis
• Thehost’sownmoleculescausethedamage(the body self destructs) Primarily proinflammatory cytokines (IL-1 and TNF-α) released from macrophages that have detected specific microbial components • Microbial components: G-ve bacteria: LPS, G+ve bacteria: peptidoglycan, lipoteichoic acid • Pathogen associated molecular patterns (PAMPs) recognized by pattern recognition receptors (PRRs)
28
Damage - sepsis
Hemodynamic derangement due to effects of IL-1 and TNFα ( blood pressure, increased cardiac output, low organ perfusion) causes multi-organ failure • Multi-organ dysfunction syndrome (MODS) • “Shock” phase
29
Treatment for sepsis
Administer high O2 air (ventilator), IV fluids ( blood volume/bp), vasopressors (vasoconstriction, tissue perfusion) Antibiotics (broad spectrum) must be used, however... Killing bacteria releases additional molecules that stimulate Mφ; may cause an initial detrimental effect to the patient w/o antibiotics, the patient will die Even with treatment, sepsis at “shock” phase has >50% mortality rate
30
Spirochetes
Helical/corkscrew shaped, slender, long cells • Widespread in nature, species are divese: free-living/ parasitic, aerobic/anaerobic • Some are important symbionts ruminant stomach and termite gut. Breakdown difficult to digest plant polysaccharise e.g. cellulose • Large numbers in subgingival plaque, some species asso. with periodontal disease e.g T. denticola • Cause few diseases in humans, primarily Syphilis (Treponema pallidum) and Lyme disease (Borrelia burgdorferi)
31
Treponema pallidum
Causes syphilis Limited knowledge of virulence mechanisms 1. Inability to culture in a lab setting 2. Lack of an animal model Enters through mucous membranes, minute skin abrasions that occur during sex Enters subepithelial tissues, extracellular replication Carried through lymphatic channels to systemic circulation, becomes systemic almost immediately 3 stages of sexually transmitted syphilis: primary, secondary, tertiary
32
Primary syphilis
Host white blood cells (neutrophils, macrophages, lymphocytes) battle replicating spirochetes @ site of initial inoculation, forming a lesion, syphilitic chancre • Syphilitic chancre asso. with increased risk of acquiring HIV infection, 3-5 fold • Painless, heal spontaneously (26 weeks), but infection has already become systemic • Secondary stage occurs 3-6 weeks after the chancres heal, but only in ~50% of people (who don’t receive treatment)
33
Secondary syphilis
Results from systemic spread of the bacteria, lasts weeks-months • Replicate in the lymph nodes, liver, joints, muscles, skin, and mucous membranes • Patient develops rash on one or more places on the body, even palms and soles of feet • Many additional variable symptoms asso. with 2° stage, “Great Imitator” • Symptoms can resolve with or without treatment - Spontaneously resolves in 1/3 of people, bacterium no longer detected - Unlucky 2/3, bacterium persists, no symptoms (latent syphilis), up to decades after initial infection
34
Tertiary Syphilis
Characterized by renewed multiplication of T. pallidum, destruction of host tissues by the host’s immune response to detection of bacterial antigens • Development of lesions, that destroy soft tissue and bone, sometimes organs - gummas (few treponemes + inflammatory cells) • Patientssufferfromchronicinflammationand vasculitis (inflammation of blood vessels), aneurysms • Neurosyphilis (CNS), bacterial invasion of brain or vasculitis, causes staggering (ataxic gait), dementia and loss of motor function (general paresis) • Can eventually cause death
35
Syphilis | Diagnosis
Involves detecting antibodies against the bacterium
36
Congenital syphilis
Manifests as premature birth, intrauterine growth retardation, multiple organ failure • Other manifestations evident around age 2, facial and tooth deformities, deafness, arthritis • 100% preventable if the pregnant mother takes penicillin
37
SpirochetesBorrelia burgdorferi
Causes Lyme disease
38
burgdorferiEncounter and Entry
Spread by bite from infected deer tick Bacteria lie dormant in the midgut of ticks Tick feeds on mammalian blood, triggers the spirochetes to replicate and migrate to tick’s salivary glands (2-7 days) Injected into the skin of the mammal from salivary glands
39
burgdorferiSpread and Multiplication
Initially multiplies at site of the bite, causes a localized infection • Spreads within the skin then disseminates systemically particularly to nervous sys, heart, joints, eyes • Spread facilitated by it’s ability to bind human plasmin, a protease which may promote tissue invasion • Cancanliedormantforyears • Causes Lyme disease in 3 stages
40
Lyme disease Stage 1
Involves a localized skin infection due to infiltration of host white blood cells to combat replicating bacteria at tick bite site • Forms a lesion, erythema migrans
41
diseaseLyme disease Stage 2
Disseminated infection • CNS, joints, eyes, heart primarily affected • Symptoms: - Muscle pain/stiffness, excrutiatingheadaches -S econdary skin lesions -N eurological abnormalities e.g. meningitis -Eye abnormalities e.g. conjunctivitis • Damage mediated by host’s response to bacterial antigens, involves IL-1 and TNFα • Can remain latent for 6 mo.-30yrs.
42
Lyme disease Stage 3
Occurs months to years after initial infection • Most common symptom= repeated episodes of arthritis in infected joints • Antibiotictherapycuresarthritisinmost patients • Arthritiscancontinueevenafterbacterial eradication. • Post-treatmentLymediseasesyndrome.Bb infection of joints triggers autoimmunity, presence of bacterial antigens cross reactive with human proteins
43
Lyme encephalopathy:
CNS Lyme encephalopathy: memory, sleep, speech affected
44
Acrodermatitis chronica atrophicans
Skin begins as lesions that gradually lead to atrophy of the skin, takes yrs-decades
45
Diagnosis & Treatment Lyme disease
Detecting antibodies against the bacterium: ELISAs, Western blots • Penicillin not very effective • Doxycycline or amoxicillin most common, good outcomes for patients with arthritis • 3rd gen. cephalosporin drugs, delivered i.v., good outcomes for patients with neurologic symptoms

Micro (14 decks)

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