Bacterial Cell Structure Flashcards

(60 cards)

1
Q

What is the basic structure of a prokaryotic cell?

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2
Q

What is the basic structure of a Eukaryotic Cell?

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3
Q

What are the main differences between Prokaryotic and Eukaryotic Cells?

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4
Q

Define Bactera

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5
Q

What is the Taxonomy of E. Coli?

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6
Q

What are the morphologies of bacterial cells?

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7
Q

What is the bacterial capsule?

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  • Outermost structure of many bacterial cells
  • Made in the cytoplasm, then secreted
  • Mainly polysaccharide but can also be polypeptide or glycoprotein. (except Bacillus anthracis - poly - gamma - glutamate)
  • Most are acidic (polysaccahrides), negatively charged.
  • Visualisation: stain background with acidic stain (congo red) and stain cell with basic stain (violet, safranin)
  • The virulence factor -transforming principle - is realted to the bacteria’s capsule
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8
Q

What is the Quellung Reaction?

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In this method two dyes, crystal violet and india ink are used. The capsule is seen as a clear halo around the microorganism against the black background.

  • Gold standard technique for serotyping Streptococcus pneumoniae (pneumococcus)

Anticapsular antibodies present in the serum reacts with carbohydrate material of the pneumococcal capsule, causing a microprecipitin reaction on the surface of theStreptococcus pneumoniae.This antigen-antibody reaction causes a change in the refractive index of the capsule so that it appears “swollen” and more visible.

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9
Q

What are Pili?

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Hair like filaments (polymer of proteins [pilins])
Extends from cell membrane to the outside
Up to 2um length
Two types: Sex pili (long), common pili (short)[fimbriae]
Common pili (adhesins) – allow attachment to eukaryotic cell surface - resist flushing and evade immune systemTip structure at end corresponds to cell receptor.
Sex pili (conjugation tube) – facilitate the transfer of DNA between donor and recipient bacteria
Motility – twitching, gliding

  • Found mostly in Gram-negative bacteria
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10
Q

Bacterial Cell Wall

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Outer layer present in bacteria, mainly composed of peptidoglycan but also:
* Teichoic acid
* Lipoteichoic acid
* Polysaccharides

Peptidoglycan:
* N-acetylmuramic acid (NAM)
* N-acetylglucosamine (NAG)
* Amino acid crosslinks (lysine, alanine, glucosamine)

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11
Q

What is Techoic acid?

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Glycopolymer embedded in peptidoglycan
Covalently linked to peptidoglycan
Linked to cell membrane through lipid anchor (lipotechoic acid)
Roles:
Contributes to cell wall rigidity
Maintain net negative charge – proton motive force
Resistance – B-lactam abx (antibiotics), high temperature, high salt concentration

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12
Q

What is the mycobacterium: Cell Wall

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No outer membrane.
Peptidoglycan present but thinner than gram +ve
Arabinogalactan – sugars (D-arabinose, D-galactose). Found between peptidoglycan and lipid layer.
Outer lipid layer – primarily composed of mycolic acids (long chained fatty acids, covalently linked to arabinogalactan)
Low permeability, resistant to drying and chemicals
Glycolipids – interact with host cell receptors
Porins – movement of molecules through lipid layer.
Can’t be stained using standard means due to lipid layer.

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13
Q

Plasma/Cell Membrane

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Cell membrane:
Phospholipid bilayer

Outer membrane (Gram -ve):
Phospholipid
Lipopolysaccharide (O-antigen, core polysaccharide, lipid A)

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14
Q

What are Flagella?

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  • Long projection used for motility
    Main components: filament, hook, motor

Filament: composed of protein flagellin
Hook: Curved attachment of filament to motor
Basal body (motor): anchors flagellum to cell membrane and cell wall. (300 RPS)

  • Stator
    Rotor – proton motive force, Mot A/B
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15
Q

What are spores?

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Formed by some gram positive organisms
Primarily for reproduction and dispersal
Form under specific conditions ()
Useful in identification
Resistant to enzymes, heat, radiation (endospores)
Can survive for long periods.

Bacteria produce a thick protective wall around them in adverse conditions.
The walls break when fovaourable conditons return.

Eg. Bacilli and Clostridium.

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16
Q

How do bacteria grow?

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Binary Fission – (asexual)
Growth curve

Growth factors:
Temperature
pH
Nutrient availability
* Generation time: time taken for population to double

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17
Q

Describe the 4 stages of the growth curve

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Lag phase:
Adaptation to new environment
Variable (bacteria vs environment)
RNA, enzyme synthesis

Log phase:
Doubling of population
Optimal conditions – faster growth (steeper curve)

Generation time (doubling time)

Stationary phase:
New cells = dying cells, growth halt
Lack of nutrients
Physical space
Waste products inhibiting growth

Decline phase:
Exponential decrease
No growth on fresh medium

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18
Q

How does temperature affect bacterial growth?

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Enzymes: heat denatured, cold – slowed metabolism
Optimal, minimum and maximum temp
Thermophiles (heat loving): 45-80C (60)
Hyperthermophiles: 65-120C (88-106)
Mesophiles: 20-45C (37) [human pathogens]
Psychrophiles (cold loving): -20-20C (15)
Psychrotophs (cold tolerant): 0-35C (16)

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19
Q

How deos ph affect Bacterial growth?

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Neutrophiles – pH (5.5 – 8)
Acidophiles – pH (0 – 5.5)
Alkaliphiles – pH (8 – 11.5)

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20
Q

How does O2 conc affect bacterial growth?

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Obligate aerobes require the presence of atmospheric oxygen (20%) for their metabolism.

Microaerophiles require oxygen, but at a lower level than normal atmospheric levels – they only grow at levels of 2-10%.

Organisms that can grow in the absence of oxygen are referred to as anaerobes

facultative anaerobes are the most versatile, being able to grow in the presence
or absence of oxygen by switching their metabolism to match their environment.

Aerotolerant anaerobes can also grow in the presence or absence
of oxygen, exhibiting no preference.

Obligate anaerobes can only grow in the absence of oxygen and
find an oxygenated environment to be toxic.

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21
Q

How do bacterial genes differ from eukaryotic genes?

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22
Q

Which antibiotics make the bacterial DNA supercoil and how?

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There are some antibiotics whose MOA is to inhibit bacterial type II topoisomerases:

Fluoroquinolones (Ciprofloxacin, Levofloxacin, Moxifloxacin)
inhibit type II topoisomerases (DNA gyrase and topoisomerase IV).

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23
Q

Which antibiotics inhibit ribosomal function and how?

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There are some antibiotics whose MOA is to inhibit ribosomal function:

Aminoglycosides and Tetracycline
Inhibit by binding the small subunit.

Macrolides and Lincosamides
Inhibit by binding the large subunit.

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24
Q

What are the causes of genetic mutations?

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Chemical agents; Three classes:
Nucleotide base analogues – lead to mispairing and DNA replication mistakes.

Frameshift mutagens – These changes cause addition or deletion of a single base also lead to replication mistakes.

DNA-reactive chemicals – These act directly on the DNA changing the chemical structure directly at the base. These abnormal bases may pair abnormally or not at all. Such a base may be removed from the backbone of the DNA.

Physical agents:
Heat, UV light,

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25
What are the types of genetic mutations that can occur in bacteria?
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What are terms used in bacterial genetics?
27
3 mechanisms of horizontal gene transfer?
May occur via one of three mechanisms: Conjugation Transformation (COMPETENCE) Transduction * Resistance genes may be shared in the above ways
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What is Conjugation?
The ability to conjugate is conferred by the F plasmid (fertility factor) Bacterial cells that contain an F plasmid are called “F+”. Bacteria that don’t have an F plasmid are called “F-”. F+ cells grow special tubes called “sex pilli” from their bodies. When an F+ cell bumps into an F- cell, the sex pilli hold them together, and a copy of the F plasmid is transferred from the F+ to the F-. Now both cells are F+. F plasmids can be spontaneously lost.
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What is Transformation?
Competent cell takes up naked DNA from the environment Source of DNA from lysed donor cell DNA transported into cell through transmembrane channel using DNA translocase DNA incorporated into bacterial chromosome by RecA protein
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What is Transduction?
Generalized: Caused by lytic phages (bacteriophage). Any genes from the host chromosome may be incorporated into future cells by bacteriphages Specialized: Caused by lsogeny phages. Genes close to the prophage insertion site may be transduced
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What is Recombination?
The means by which transferred DNA is incorporated into the bacteria’s chromosomal DNA. Can be classified as: * Homologous (legitimate) recombination Occurs between closely related DNA sequences and generally substitutes one sequence for another. * Non-homologous (illegitimate) recombination. These generally occur between dissimilar sequences and generally produces insertions, deletions or both. These usually require special enzymes such as those produced by transposons and lysogenic bacteriophages.
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What are Transposons?
Conjugative Transposons are self-transmissible - have all genes necessary to connect and transmit themselves to other bactera. Mobile sections of DNA that can move within or between genomes. (cut & paste model, conservative replication). Alternatively, it can be copied, with the copy being inserted at a second site, in a process known as replicative transposition.
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What are constitutive and adaptive genes?
* Constitutive Genes: Always active (expressed continuously). Necessary for basic cellular functions (e.g., metabolism, protein synthesis). Examples: Genes for ribosomal RNA, ATP synthesis * Adaptive Genes: Expressed in response to environmental changes or specific signals. Enable the cell to adapt to changing conditions (e.g., stress, nutrient availability). Expression is regulated (turned on/off as needed). Examples: Heat shock proteins, lactose operon in E. coli.
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What are Inducible and Repressible genes?
* Inducible Genes Activated (turned on) in response to specific environmental stimuli. Typically off but can be induced when a substrate or condition is present. Allow the organism to conserve resources by producing enzymes or proteins only when needed. Example: Lac operon in E. coli, activated by the presence of lactose * Repressible Genes Turned off when the end product or specific condition reaches a certain level. Typically on, but repressed when sufficient levels of a substance (usually a product of a biosynthetic pathway) are available. Helps to prevent overproduction of a substance. Example: Trp operon in E. coli, repressed when tryptophan levels are high.
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What are Promoters and Operons?
Promoters and Operators These are nucleotide sequences that control the expression of a gene by influencing which sequences will be transcribed into mRNA. Operans Groups of one or more structural genes, expressed from a particular promoter and ending at a transcriptional terminator. E.g.. The E. coli lac operan includes all the genes necessary for lactose metabolism.
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How does the Lac operon work?
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Difference between normal flora, opportunistic pathogens and frank pathogens
* Normal flora - microbes that colonize the body and usually do not cause disease * Opportunistic pathogens – generally don’t cause disease, but may under certain circumstances. * Frank pathogens - always cause disease.
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How are normal flora acquired?
* First introduction of human microbiome occurs at birth (a fetus in utero should be microbe-free) * Typically, from the mother’s vaginal flora * Infants born by caesarean section have significantly different microbiota than those born vaginally. Infants born by caesarean section tend to have a high proportion of bacteria normally found on the skin
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What are the normal flora of the skin?
* CoNs (S. epidermidis) - major inhabitant of the skin More than 90 percent of the resident aerobic flora in some areas. * Staphylococcus aureus - nose and perineum are the most common sites for S. aureus colonization Also prevalent (67 percent) on vulvar skin S. aureus is extremely common (80 to 100 percent) on the skin of patients with certain dermatologic diseases such as atopic dermatitis. Reason for this finding is unclear * Micrococci - not as common as staphylococci and diphtheroids; However, frequently present on normal skin. Mainly Micrococcus luteus, (20 to 80 percent of the micrococci) from the skin * Diphtheroids (Coryneforms) Denotes bacteria belonging to the genus Corynebacterium. Corynebacterium acnes - originally used to describe skin anaerobic diphtheroids: * Re-classified as Propionibacterium acnes and as P. granulosum P. acnes 8x more frequent than P. granulosum in acne Possibly involved in acne pathogenesis Children <10 years :- rarely colonized with P. acnes.
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What are the normal oral flora?
* Many variations in oral flora, based on: Time, individual, oral cavity site Healthy oral cavity (human): * Gram positive Cocci – Abiotrophia, Peptostreptococcus, Streptococcus, Stomatococcus Rods – Actinomyces, Bifidobacterium, Corynebacterium, Eubacterium, Lactobacillus , Propionibacterium, Pseudoramibacter, Rothia * Gram negative Cocci – Moraxella, Neisseria, Veillonella Rods – Campylobacter, Capnocytophaga, Desulfobacter, Desulfovibrio, Eikenella, Fusobacterium, Hemophilus, Leptotrichia, Prevotella, Selemonas, Simonsiella, Treponema, Wolinella Non-bacteria Oral cavity contains diverse forms of microbes such as protozoa, fungi and viruses Protozoa (commonly seen) Entamoeba gingivalis and Trichomonas tenax Fungi (Candida most common) Candida, Cladosporium, Aureobasidium, Saccharomycetales, Aspergillus, Fusarium and Cryptococcus Histatins - antimicrobial peptides secreted by salivary glands.
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What are the normal repiratory flora?
Pharynx and trachea contain bacterial genera commonly found in the oral cavity. * Common organisms: α- and β-hemolytic streptococci, anaerobes, staphylococci, neisseriae, diphtheroids. * Potential Pathogens present in the pharynx: Haemophilus spp. Mycoplasmas Pneumococci * Upper respiratory tract is often the first site of colonization for pathogens like: Neisseria meningitidis Corynebacterium diphtheriae Bordetella pertussis Lower Respiratory Tract (small bronchi and alveoli) is typically sterile
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What are the normal GI tract flora?
* Duodenum and Jejunum: Low bacterial levels (approximately 10³ organisms/ml) Streptococci, lactobacilli, and Bacteroides. * Ileum: Bacterial populations increase at the ileocecal junction to around 10⁶ to 10⁸ organisms/ml. * Common bacteria: Streptococci, lactobacilli, Bacteroides, and bifidobacteria. * Colon and Faeces: Highest bacterial concentrations (10⁹ to 10¹¹ organisms/g), with over 400 species identified. -Anaerobes: Bacteroides, Bifidobacterium, Clostridium, and others.
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What is Normal Flora of the Urogenital Tract?
* The composition of vaginal flora varies based on age, pH, and hormonal levels of the host. Yeasts (e.g., Candida) are occasionally present in the vagina (10-30% of women). - Yeast overgrowth can cause vaginitis. * Anterior Urethra Flora: Common bacteria: S. epidermidis, Enterococci, Diphtheroids. Occasionally present: E. coli, Proteus, Nonpathogenic Neisseria (10-30%). * Clinical Relevance: Urine cultures may contain these organisms if a midstream (clean-catch) sample is not obtained, leading to potential contamination.
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What are Normal Flora for the Conjunctiva?
Conjunctival flora is sparse. Tears may have a role in spare flora Corynebacteria, Neisseriae, and Moraxellae have been cultured. Staphylococci and streptococci also present.
44
Which concentration of alcohol is best for use as a disinfectant?
Believed that isopropyl alcohol dehydrates the bacterial cell and denatures its proteins Concentration difference of water and alcohol on either side of the cell wall 70% alcohol enters the cell to denature both enzymatic and structural proteins * 99% isopropanol evaporates very quickly and results in almost immediate coagulation of surface or cell wall proteins, preventing penetration of cell walls and killing bacteria
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Define infectivity, pathogenicity, parasitism, commensalism, symbiosis, opportunistic pathogen and obligate pathogen?
1. Infectivity: The organism's ability to invade, survive within, multiply, and spread in the host. 2. Pathogenicity: The ability of a microorganism to cause disease in a host. Parasitism: A relationship where one organism lives on or within another. Different types of host-parasite interactions exist. - Commensalism: The parasite resides in or on the host without causing harm or disease. - - Symbiosis: A mutually beneficial relationship between two organisms. 3. Opportunistic Pathogen: Normally harmless, but can cause disease when it enters different tissues or sites. 4. Obligate Pathogen: Always causes disease when present in a host.
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What is Pathogen Transmission?
Infection begins with exposure to a pathogen from its natural reservoir, which can be either animate (humans or animals) or inanimate (water, soil, food). Carriers may spread pathogens without showing symptoms. Zoonosis: Diseases transmitted from animals to humans. Nosocomial Infection: Infections acquired in hospitals.
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What are the modes of Pathogen Transmission?
1. Direct Contact: Transmission through person-to-person contact (e.g., kissing, sexual intercourse), or from mother to child during pregnancy or birth. 2. Droplet Transmission: Spread through respiratory droplets from coughing or sneezing, typically over short distances. 3. Indirect Contact: Pathogens transferred via contaminated objects (fomites) or by healthcare workers between patients. 4. Airborne Transmission: Pathogens carried in small particles over long distances (e.g., fungal spores in the air).Fecal-Oral Transmission: Pathogens in contaminated food or water are consumed by the next host. 5. Vectorborne Transmission: Arthropod vectors (e.g., mosquitoes, ticks) spread pathogens by biting infected hosts and transferring the agent to others.
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What are the portals of entry for bacteria?
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What is Virulence?
A measure of an organism's ability to cause disease; the degree of pathogenicity. It is often used to compare the disease-causing potential between different strains of the same species. LD50: Lethal dose required to kill 50% of inoculated hosts. ID50: Infectious dose required to infect 50% of inoculated hosts.
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What are Virulence factors?
Molecules produced by microorganisms that cause harm to the host. These factors assist pathogens in: 1. Invading the host 2. Causing disease 3. Evading host defenses
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What are the types of virulence factors?
1. Factors promoting bacterial colonization: -Adherence factors -Invasion or spreading factors -Nutrient competition (e.g., iron) -Evasion of immune responses 2. Factors causing damage to the host: - Exotoxins - Endotoxins
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What are Biofilms?
Biofilms: Bacteria within a sticky polysaccharide web, binding cells together and to surfaces (e.g., surgical implants, catheters). -Facilitates colonization -Biofilm production requires adequate numbers of bacteria (quorum). Example: Pseudomonas aeruginosa produces a biofilm once the bacterial colony size is large enough. Example: Dental plaque is another form of biofilm. Biofilm Advantages: Protects bacteria from host defenses and antibiotics, promoting persistence in the host.
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Bacterial Toxins
Bacteria pathogens must survive and multiply in the host There are two main types of toxins: - Endotoxins - Exotoxins
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What are Endotoxins?
* Lipopolysaccharides (LPS) in the outer membrane of Gram-negative bacteria. Released when bacterial cells die or lyse, usually in the late growth stages. * Toxic Effects: Only occur after endotoxins are released into the medium. * Effects of LPS-Endotoxins - Fever and Inflammation - Tissue Destruction and Respiratory Distress - Capillary Damage: Leading to petechial rash, capillary leakage, and hypovolemia.
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What are Exotoxins?
Heat-sensitive soluble proteins secreted by living bacteria. - Highly potent and can cause damage distant from the original infection site. - Associated with specific diseases, with toxin genes often carried on plasmids or prophages. - Examples of exotoxin-related diseases: Botulism, Tetanus, Diphtheria.
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What are the types of Exotoxins?
Type I: Cell surface-active toxins. Bind to cell receptors and stimulate cell responses. Example: Superantigens – Stimulate T cells excessively, causing massive inflammation and tissue damage. Type II: Membrane-damaging toxins. Form pores in the host cell membrane, leading to cell lysis and loss of osmotic balance. Type III: Intracellular toxins. Enter the host cell and disrupt internal processes. Example: AB toxins – The B subunit binds to the cell, and the A subunit disrupts cell function (e.g., Tetanus toxin).
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What are Superantigens?
Superantigens: - Stimulate T cells to produce excessive cytokines (IL-1; TNF), leading to massive immune responses. - Trigger systemic effects such as Toxic Shock Syndrome (S. aureus, Group A Streptococci). - Cause symptoms like inflammation, shock, diarrhea, and vomiting when ingested in contaminated food. Superantigens can bind without processing to MHCII receptors on APC's. Superantigens acts as polyclonal stimulators of T cells.
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What are Membrane-active Exotoxins?
Target host cell membranes, forming pores that cause cell lysis. Example: Clostridium perfringens alpha-toxin, a lecithinase that causes red blood cell (RBC) hemolysis. Commonly observed in aggressive pathogens (S. aureus, Group A Streptococcus, E. coli).
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What are Ab Toxins?
AB Toxins: Composed of two subunits: - B subunit: Binds to specific host cell receptors (determines host cell specificity). - A subunit: Enters the cell and modifies target proteins through enzymatic reactions. Common reaction: ADP-ribosylation, where ADP-ribose is attached to a target protein, inhibiting its function. Example: Cholera toxin inactivates G proteins in intestinal cells, causing hypersecretion of electrolytes and diarrhea. Tetanus toxin cleaves synaptobrevin in neurons, leading to reduced neurotransmitter release and spastic paralysis