Microbiology - Test 2

Front 1

3 phylum of fungi

Back 1

Ascomycota
Basidiomycota
Zygomycota

Front 2

examples of Ascomycota

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sac fungi, yeast

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examples of Basidiomycota

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mushroom, rusts, smuts

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examples of Zygomycota

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bread molds, Phizopus, Mucor

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cell wall of fungi include?

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mannan, glucan, chitin

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are fungi motile?

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no

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Fungi are divided into 2 categories

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yeasts and molds

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mature supragingival plaque:dental caries and gingivitis

subgingival plaque:______

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periodontitis

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define gingivitis

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inflammation of gingiva

Front 10

define periodontitis

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inflammation and destruction of the attachment apparatus

Front 11

3 components of attachment apparatus

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alveolar bone
cementum
periodontal ligament

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nonspecific plaque hypothesis

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Non-specific overgrowth of any or all bacteria results in gingivitis.

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specific plaque hypothesis

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Limited overgrowth of a unique organism (or group of organisms) causes gingivitis.

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6 problems with Koch's postulates concerning perio

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1. technical difficulty in isolation and characterization of organisms
2. gingival microbiota composed of a complex mixture of organisms derived form over 500 species of bacteria previously isolated from the oral cavity
3. the existence of multiple forms of "periodontal" disease
4. presence of putative pathogens isolated from both diseased and healthy individuals
5. unclear as to whether the presence of the organism actually causes the disease or is simply the result of favorable environmental conditions induced by the disease
6. lack of an animal model that accurately depicts the human condition

Front 15

Sigmund Socransky's modification of Koch's Postulates (4)

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1. the putative pathogen should be found at higher number in disease-active sites relative to inactive sites.
2. the elimination of the organism should arrest the progression of the disease
3. the organism should exhibit virulence factors relevant to the initiation and progression of the disease
4. the cellular/humoral immune responses to the organism should be suggestive of its unique role in the pathogenesis of the disease

Front 16

evidence supporting specific plaque hypothesis (3)

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1. clinical observations
2. longitudinal microbiologic studiesq
3. associations btw the presence of specific bacterial organisms and the incidence of unique forms of disease

Front 17

longitudinal microbiologic studies utilized what kind of model. This model indicate the

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experimental gingivitis model

Front 18

Necrotizing Ulcerative gingivitis is associated with what kinds of bacteria? (4)

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spirochetes, Fusobacteria species, Selenomonas species, Prevotella intermedia

Front 19

Localized Aggressive Periodontitis is caused by what bacteria?

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Aggregatibacter actinomycetemcomitans (AA)

Front 20

Aggregatibacter actinomycetemcomitans (AA) is
Gram ___
shape
respiration
capsule or noncapsulate?
motile or non-motile?

Back 20

Gram -, coccobacillus, microaerophilic (capnophilic), non-encapsulated, non-motile

Front 21

Chronic periodontitis is associated with what bacteria

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Porphyromonas gingivalis, Tannerella forsythesis, AA, Treponema denticola

Front 22

P. gingivalis are
G ____
shape
respiration requirement
capsulated or non
motile or nonmotie

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G-, coccobacillus, obligate anaerobe, encapsulated, non-motile

Front 23

bacterial virulence factors are molecules produced by bacterial organisms that enable them to: (4)

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colonize specific niches
invade tissues
obtain nutrients
immune evasion/suppresion

Front 24

key virulence factor of AA (3)

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1. leukotoxin
2. cytolethal distension toxin
3. endotoxin LPS

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function of leukotoxin

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kills neutrophils and lymphocytes. toxin inserts and pokes holes on cell membranes. the mechanism may be apoptosis in low amount of leukotoxin.

Front 26

function of Cytolethal Distending Toxin (CD

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cells become distended; toxin arrests cells in the cell cycle such that they stop function. Epithelial cells appear to be most susceptible; breaks down epithelial cells at junctional epithelium.

Front 27

function of endotoxin

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found on the surface of bacterial cell. It induces the inflammatory rx that leads to destruction of bone in people who have periodontal disease

Front 28

2 important virulence factors of P. gingivalis

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LPS (endotoxin) and gingipain

Front 29

functions of Gingipain

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Proteases that activate and inactivate human proteins. not found in AA, maybe a major virulence factors associated with P. gingivalis

Front 30

Can P. gingivalis invade human cells?

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Yes

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3 bacteria that are primary cause of periodontitis

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P. gingivalis, T. forsythia, T. denticola

Front 32

Hypothesis that best explains the occurrence of periodontitus

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Ecologic plaque hypothesis - P.D. Marsh

Front 33

Define Ecologic Plaque Hypothesis

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The ecologic plaque hypothesis predicts that “pathogens” are part of the normal oral flora but at levels too low to cause disease. Changes in ecologic conditions favor the outgrowth of these organisms beyond a threshold number that leads to disease.

Front 34

Risk factors of developing perio (3)

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smoking, diabetes, and genetics

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caries is chronic endogenous infection that's caused by members of normal oral flora.

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T

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Classification of caries are dependent upon (4)

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tooth types
anatomic location
hard tissue
others

Front 37

Theory of caries pathogenesis

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Chemoparasitic Thoery

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Define Chemoparasitic Theory

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Mineral phase of teeth is dissolved by acid of metabolism produced by bacteria. In the second phase, the organic phase (enamel and dentin) is broken down.

Front 39

major etiology of caries is what bacteria?

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S. mutans

Front 40

Evidence supporting the bacterial etiology of dental caries (animal studies)

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1. Hamster experiment
2. Gnotobiotic Rat Experiments
3. Specific pathogen-free rat experiments
4. Transmission of caries to animals via human isolates of S. mutans

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Gnotobiotic Rat Experiments results showed that what bacteria cause caries? (severe to little, and cervical caries)

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severe caries: S. mutans, lactobacilli
moderate caries: Enterococci
little caries: S. salivarius
cervical caries: Actinomyces viscosus

Front 42

The following microorganisms cause what kinds of caries:
Actinomyces viscosus, Actinomyces naeslundii, Lactobacilli, Enterococci

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Actinomyces viscosus: strong association with root surface
Actinomyces naeslundii: no association
Lactobacilli: weak association w/ smooth surface caries, pit and fissure caries but strong w/ root surface caries
Enterococci: weak association with pit and fissure caries

Front 43

The following microorganisms cause what kinds of caries: Mutans Streptococci (S. mutans, S. sobrinus, S. rattus, S. cricetus), S. sanguis, S. mitis

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Streptococci (S. mutans, S. sobrinus, S. rattus, S. cricetus): strong association w/ smooth surface caries, pit and fissure caries and root surface caries.
S. sanguis: weak w/ pit and fissure caries.
S. mitis: weak w/ pit and fissure caries.

Front 44

Is Mutans Streptococci important in caries to develop?

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No

Front 45

virulence factors of S. mutans

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Glucosyltransferases (Gtfs)
Fructosyltransferase (Ftf)
Glucan Binding Proteins (GBPs)
Dextranase
Fructanase
Antigen I/II

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aciduricity

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Capacity to maintain sugar metabolism under extreme environmental conditions such as low pH

Front 47

organic components of extracellular matrix of plaque

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1. salivary/serum proteins and glycoproteins
2. lipids (derived from disrupted bacterial and/or host cells)bacterial 3. polysaccharides (glucans and fructans)

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Glucan Binding Proteins (GBPs)

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bind to extracellular glucan and help tightly adhere plaque matrix to the surface of the tooth, crosslink S. mutan to one another

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Antigen I/II

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allow S. mutans to bind to acquired pellicle.

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dental caries is multifactorial disease which include 5 factors, they are

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1. plaque bacteria
2. saliva flow and composition
3. minerals and F- status
4. nutrients and food components
5. host factors: genetics, race, age and behavior

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Streptococci and Staphylococci are
shape
Gram ___

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round
Gram + cocci

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Streptococci grow in chain or grape-like?

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in chain

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Staphylococci grow in chain or grape-like?

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grape-like

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staphylococci are catalase + or -?

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catalase +

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streptococci is catalase + or -

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catalse -

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coagulase test distinguishes which species of Staphylococci?

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S. aureus

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what color is S. aureus colonies? why?

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golden, b/c of carotenoid pigments

Front 58

what's the rx of coagulase + S. aureus when human plasma are added?

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S. aureus cells clumps into large aggregation

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3 toxin related disease caused by staphylococci

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Staphylococcal Scaled Skin Syndrom (SSSS)
Toxin Shock syndrome (TSS)
Staphylococcal Food Poisoning

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SSSS is caused by what bacterial toxin?

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exfoliatin

Front 61

TSS is caused by what bacterial toxin?

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tampon

Front 62

Strep. Pneumoniae: how it is clustered?

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diplococci

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Strep. Pneumoniae cause what kinds of infection? (2)

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middle ear infection (otitis media)
bacterial meningitis

Front 64

What happens when Strep. Pneumoniae is exposed to bile?

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Bile activate autolysin enzyme of the bacteria, and the bacterial become soluble.

Front 65

quelling test is used to identify what bacteria? Its mechanism

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Strep. pneumoniae.
Ab to capsular Ag of Strep pneumoniae cause the capsule to swell, which can be viewed under the microscope.

Front 66

progression of Strep. Pneumoniae

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1. colonization of nasopharyx by S. pneumoniae. bacterial adhesin binds to N-acetylhexosamine-glycolipid. sLgA protease helps bacteria avoid trapping in mucus and expulsion from the airway.
2. To colonization of lungs. Pneumolysin kills off ciliated cells.
3. After reaching the lungs. capsule prevents phagocytosis of the bacteria by the alveolar macrophages.

Front 67

how does Strep. Pneumoniae cause meningitis?

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the bacteria penetrate the BBB by causing inflammation of endothelial cells due to the effects of IL-1 and TNF alpha

Front 68

2 types of bacterial adherence mechanisms

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pili or fimbriae
afimbrial adhesins

Front 69

ETEC adhere to epithelial cells by pili that are also called?

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colonization factor antigens (CFAs)

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receptors for pili are

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glycolipids or glycoproteins

Front 71

afimbrial adhesin mediate what kind of interaction between bacteria and host, and it always follow what binding?

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tighter binding
follows binding via pili

Front 72

pili that the following have
1. All E. coli strains
2. Enterotoxigenic E. coli
3. Uropathogenic E. coli

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1. common pili
2. type I pili, colonization factor antigens I and II (CFA I and II)
3. P pili

Front 73

CFA is important for colonization of were?

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small intestine

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P pili is responsible for colonization of where? it recognize what surface Ag?

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urinary tract
recognize P blood surface Ag

Front 75

facultative intracellular bacteria include. the adhesins that these bacteria produce are called?

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Salmonella, Shigella and M. tuberculosis

invasins

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invasive bacteria gain accesses to cells in 2 ways

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1. internalization as a result of highly affinity interaction btw bacteria ligand and host receptor
2) signaling and modulating host cell cytoskeleton components

Front 77

adhesins produced by B. pertussis (2)

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Filamentous hemagglutinin (Fha)
Pertussis toxin (Ptx)