R.O Lecture 8&9 Flashcards

1
Q

Virulence Factors

A

Specialised structures or characteristics that improve the ability of an organism to cause infection and disease.

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2
Q

Adherence

A

Attachment to host cell’s surfaces; important tool for initiation of infection

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3
Q

Adhesins

A
  • proteins/glycoproteins that bind to complementary surface receptors (usually glyoproteins/sugars) on host cells.
  • Found on surfaces of bacterial attachment pili or glycocalyx
  • Adhere to membranes of specific cell types
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4
Q

Is aderence alone sufficient to cause infection?

A
  • No, adherence alone is not sufficient to cause infection.
  • Microbes must be able to colonise the tissue surface or penetrate it
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5
Q

Types of identified adhesions and their targets

A

Refer to slide 3

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6
Q

Action of Hyaluronidase in bacterial invasion

A
  • Enzyme that digests hyaluronic acid (a glue-like substance that holds cells together in some tissues)
  • Produced by some pneumococci and streptococci species
  • Enables passage through the epithelium to deeper tissues
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7
Q

Coagulase

A
  • Enzyme that causes blood clotting; can aid infection by some bacterial species like Staphylococcus aureus; protects them from immune defenses
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8
Q

Streptokinase

A

Enzyme that dissolves blood clots; allows bacteria trapped within a clot to free themselves and spread the infection

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9
Q

Can organisms such as Mycobacterium tuberculosis and Neisseria gonorrhoeae survive within host cells?

A

Organisms such as Mycobacterium tuberculosis and Neisseria gonorrhoeaecan survive within host cells –escape destruction and are transported to other tissues

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10
Q

Toxin

A

A toxin is any substance that is poisonous to other organisms

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11
Q

Toxigenicity

A
  • The capacity of microbes to produce toxins.
  • Can produce fever, cardiovascular disturbances, diarrhoea, destroy blood cells/vessels, disrupt the nervous system, inhibit protein synthesis, damage cell membranes etc.
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12
Q

Endotoxins

A
  • Part of the outer membrane of Gram-negative bacteria; released into host tissue when bacteria die or divide.
  • Consist of Lipid A portion of Lipopolysaccharide (LPS) complexes
  • Relatively weak unless released in large doses
  • Non-specific effects: Fever, sudden drop in blood pressure (endotoxic shock)
  • Produced by species including Salmonella typhi, Neisseria meningitidis
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13
Q

Exotoxins

A
  • Soluble substances produced by Gram-positive and Gram-negative bacteria that are secretedinto the host tissues
  • Produced by species of Clostridium, Bacillus, Staphylococcus, Streptococcus etc.
  • Most are polypeptides; some are enzymes.
  • Most genes for exotoxins are carried on plasmids/phages
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14
Q

Cytotoxins

A

Kill host cells/inhibit their functions

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15
Q

Neurotoxins

A

Interfere with nerve impulse transmission

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16
Q

Enterotoxins

A
  • Affect cells lining the GI tract
  • Includes cholera toxin (Vibrio cholerae), heat-labile enterotoxin (E. coli) and Staphylococcal enterotoxin (S. aureus)
  • Can cause symptoms by attaching to GI cell membranes and causing them to release fluids, disturbing the electrolyte balance and affecting muscle contractions
  • Diarrhea, vomiting
17
Q

Hemolysins

A

Lyse red blood cells; produced by Strepto-and Staphylococci; release iron.

  • α-hemolysin - Partially break down hemoglobin
  • β-hemolysin - Completelybreak down hemoglobin
18
Q

Botulisim neurotoxin (BoNT)

A
  • Botulism neurotoxin (BoNT) blocks acetylcholine (neurotransmitter) release from excitatory neurons at neuromuscular junctions, preventing muscle contraction (botulism).
19
Q

Tetanus neurotoxin (TeNT)

A

blocks acetylcholine (neurotransmitter) release from inhibitory neurons, preventing muscle relaxation (tetanus).

20
Q

Bacterial Meningitis

A
  • Inflammation of the meninges (membranes covering CNS)
  • Causes necrosis, clogging of blood vessels, increased intracranial pressure, decreased CSF flow, impaired CNS function.
  • Toxins (pneumolysin) produced by S. pneumonia contribute to disease (cytotoxins)
  • Most cases are acute but some can be chronic
21
Q

Hansen’s disease (leprosy)

A
  • Caused by Mycobacterium leprae.
  • Disfiguring chronic disease.
22
Q

Tetanus

A
  • Severe muscle spasms; caused by Clostridium tetani.
  • Tetanus toxin (neurotoxin): affects central nervous system, blocking neurotransmitter release from inhibitory neurons leading to lock jaw, muscle rigidity and muscular spasms.
23
Q

Botulism

A
  • Botulism-severe muscle relaxation; caused by Clostridium botulinum.
  • Neurotoxin blocks the release of acetylcholine at the junction between neurons and muscle cells; thusmuscle stimulation does not occur
24
Q

What are the three forms of botulism?

A
  • Foodborne (intoxication)
  • Infant
  • Wound (infection and intoxication)
25
Q

Erysipelas

A

lesions form on skin and spread. Caused by haemolytic streptococci

26
Q

Impetigo

A
  • Highly contagious and caused by staphylococci and/or streptococci.
  • Treated with penicillin.
  • Almost exclusive to children
27
Q

Acne

A
  • Affects 80% of teenagers and many adults.
  • Propionibacteriumacnes responsible for severe cases
  • Feeds on sebum produced by sebaceous glands in skin (overproduction can be hormone stimulated)
28
Q

Burn infections

A
  • Severe burns can remove much of the body’s protective barrier
  • Pseudomonas aeruginosais prime cause of infections
  • Treatment difficulties such as antibiotic access issues (topical treatments or debridement) and antimicrobial resistance

Refer to slide 16

29
Q

Explain the function of lysozyme in tears

A
  • Antimicrobial effect of tears on M. luteus
  • Tears also contain other antimicrobial agents. e.g. lipocalin, lactoferrin, sIgA
30
Q

Ophthalmia neonatorum

A
  • Bacterial eye disease
  • Conjunctivitis of the newborn
  • Caused by Neisseria gonorrhoeaeand Chlamydia trachomatis (birth canal)
  • Can cause inflammation of the cornea (keratitis)
31
Q

Bacterial conjuctivitis (pink eye)

A
  • Extremely contagious
  • Caused by S. aureus, Neisseria gonorrhoeaeand Pseudomonas spp.
  • Causes inflammation of the conjunctiva
32
Q

Trachoma

A
  • Bactieral eye Disease
  • Caused by Chlamydia trachomatis
  • Infection and destruction of conjuctivia; cause of preventable blindness
33
Q

Gas gangrene

A
  • In body regions where oxygen concentration is low, spores germinate, multiply, and produce toxins (alpha toxin: cytotoxin) and enzymes.
  • As the organisms divide they ferment muscle carbohydrates and produce hydrogen gas.
  • These gas bubbles distort and destroy tissue.
  • Produces blackening of tissue
34
Q

Upper respiratory tract infections

A
  • Pharyngitis - sore throat - S.pyrogenes
  • Laryngitis - infection of the larynx, loss of voice
  • Epiglottitis - infection of the epiglottis
  • Sinusitis, bronchitis, tonsillitis

Last 3 - S.pneumoniae and H.influenzae

35
Q

Name diseases of the lower respiratory tract

A
  • whopping cough (pertussis)
  • Pneumonia
  • Tuberculosis
36
Q

Whooping cough (pertussis)

A
  • Main causative agent is Bordetellapertussis (aerobic, encapsulated, Gram negative coccobacillus)
  • Inhaled organisms colonise the cilia lining the respiratory tract; produces endotoxin, exotoxins (cytotoxins: pertussis toxin, tracheal toxin) and hemagglutinins (adhesins)
  • Disease causes mucus and masses of bacteria to fill the airway leading to violent coughing
37
Q

Pneumonia

A
  • Inflammation of lung tissue (children and older adults have higher risk)
  • Can be caused by bacteria, viruses, fungi, inorganic sources
  • Main causative agent is Streptococcus pneumoniae (pneumococcus); can cause fibrin deposits leading to blockage (consolidation) of air spaces and pleurisy
  • Disease causes violent chills, fever, chest pain, cough, and sputum-containing blood.
38
Q

Tuberculosis

A
  • Caused by bacteria from the Mycobacterium tuberculosis complex; aerobic, rod-shaped, long doubling time; replicate inside phagocytes (e.g. neutrophils, macrophages); elicit acute inflammatory response and can produce lesions
  • Prior to 1900, one-third of adults died of TB before reaching old age
  • BCG vaccine (M. bovis strain)
  • Treatment of latent infection with extended course of antibiotics