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Bacteriology and Mycology > Bacterial Pathogenesis and Immunology I > Flashcards

Bacterial Pathogenesis and Immunology I Flashcards

1
Q

Bacterial-host interaction

A
  • Normal flora (normal microbiota) - expected to be present; do not cause disease under normal circumstances
  • -Skin; mucous membranes; digestive tract
  • Pathogen
  • -Opportunistic - normally does not cause disease; can cause disease when host defenses are breached
  • -Obligate (frank) - must cause disease in order to survive and be transmitted to another host
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2
Q

Basic steps in pathogenesis

A
  1. Attachment/entry
  2. Evasion of host defenses
  3. Multiplication/spread
  4. Damage
  5. Transmission
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3
Q

Entry - Transmission Routes

A
  • Ingestion
  • Inhalation
  • Breach of physical barrier: mucosal, ocular, cutaneous
  • Vector borne: mechanical or biological vectors
  • Transplacental
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4
Q

Breach of barriers

A
  1. Tissue injury; release of chemical signals
  2. Dilation and increased permeability of capillary
  3. Phagocytosis of pathogens
    Ex: cutaneous, ocular, or mucosal membranes
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5
Q

Entry - traumatic

A

-Ex: foxtails and Actinomyces sp. –> draining tracts

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6
Q

Entry - iatrogenic

A
  • Surgical site infection
  • Injection site infection
  • -Joint infection in horses (need to ensure proper preparation of skin site)
  • Iatrogenic = relating to illness caused by medical examination or treatment
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7
Q

Hand washing

A
  • Single most effective method of decreasing transmission of pathogens (hands can serve as fomites)
  • Most germs located under fingernails
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8
Q

Entry - vector borne

A
  1. Mechanical vector = transfers the pathogen like a fomite
    - Fomite = An inanimate object that can carry an infectious agent from host to host
    - Flies and Moraxella bovis (pink eye; infectious bovine keratoconjunctivitis)
    - Face fly (musca autumnalis), house fly (Musca domestica), stable fly (Stomaxys calictrans)
  2. Biological vector = the pathogen undergoes a biological change within the vector that is required for transmission
    - A vector in which the pathogen undergoes a change that renders it capable of infecting a susceptible host
    - Ixodid ticks and Anaplasma marginale
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9
Q

Entry - attachment

A
  1. Agent’s adhesins interact with host’s receptors
  2. Extracellular colonization or internalization of the pathogen
    - Variation of host cell receptors may explain host or organ specifically of infection
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10
Q

Entry - ingestion –> attachment

A
  • Enterotoxigenic E. coli (ETEC)
  • -Bovine (ETEC K99 (F5) fimbriae
  • -Porcine (ETEC F18 fimbriae)
  • Nothing for it to bind to in the older calf or weaned pig so it cannot cause disease
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11
Q

Entry - ascending into the bladder –> attachment

A
  • Uropathogenic E. coli (UPEC): P-fimbriae facilitate attachment
  • Proanthocyanidins (PACs) found in cranberries help prevent UTIs by blocking uropathogenic bacteria from adhering to the uroepithelium
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12
Q

Entry - Ingestion –> attachment

A
  • Enteropathogenic E. coli (EPEC)
  • -Bacterial surface protein: intimin
  • -Protein receptor on host cell surface: Tir (translocated intimin receptor)
  • –The bacteria puts it there
  • -Pedestal formation and effacement microvilli
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13
Q

Evasion of host defenses

A
  1. Defense against innate immune mechanisms

2. Defense against adaptive immune mechanisms

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14
Q

Breaching the cornea

A
  • Pseudomonas aeruginosa –> equine corneal ulcers
  • -Pili and LPS - adherence to epithelial cells and mucin
  • -Protease (Phospholipase C) - tissue damage allowing entry
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15
Q

Evasion of innate immunity

A
  • Antimicrobial peptides (AMP)
  • -AKA host defense peptides
  • -Non-specific
  • -Found in vertebrates and invertebrates
  • -Active against bacteria, fungi, and many viruses
  • -Ex: defensins and cathelicidins
  • Repulsion of AMPs by reducing the net negative charge of the bacterial cell envelope
  • Expelling AMPs through energy dependent pumps
  • Cleaving AMPs wit proteases
  • Decrease expression
  • Ex: S. aureus
  • -Staphylokinase binds and neutralizes defensins
  • -Aureolysin detroys cathelicidins
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16
Q

Evasion - innate immunity toll-like receptors (TLRs)

A
  • A type of pattern recognition receptors (PRRs)
  • -Bind pathogen-associated molecular patterns (PAMPs)
  • Found on many cell types
  • PAMP binds corresponding TLR –> signals passed to the cell –> pro-inflammatory molecules (cytokines) are produced by the cell
  • Bacterial LPS binds TLR4 on stem cells in bone marrow –> stimulates increased leukocyte production
  • This is why an increased leukocyte count is a consistent feature of bacterial infections
  • Interference with TLR signaling pathways:
  • -Modified PAMPs that will not trigger TLRs
  • -Blockage of TLR signaling pathways
  • -Accelerated destruction of intermediate signaling molecuels
  • -Destruction of NF-kB
  • -Misdirection towards anti-inflammatory pathways
17
Q

Phagocytosis

A
  1. Chemotaxis and adherence of microbe to phagocyte
  2. Ingestion of microbe by phagocyte
  3. Formation of a phagosome
  4. Fusion of the phagosome with a lysosome to form a phagolysosome
  5. Digestion of ingested microbe by enzymes
  6. Formation of residual body containing indigestible material
  7. Discharge of waste materials
18
Q

Evasion - chemotaxis

A
  • Both microbes and damages tissues release specific chemical substances (chemoattractant)
  • Movement of phagocytes toward stimulus
  • Phagocyte already at the infection sites will release cytokines that attract additional phagocytes to the site of infection
  • Bacteria can suppress chemotaxis of phagocytes:
  • -Alginate - Pseudomonas aeruginosa (also important in biofilm formation)
19
Q

Evasion - opsonization

A
  • Opsonins bind to and coat the surface of the pathogen
  • -Complement (innate) or antibodies (adaptive)
  • The ligand binds the receptor –> phagocytosis
  • -Antibody receptor = CD32 –> type 1 phagocytosis
  • -Complement receptor = CD35 –> type 2 phagocytosis
  • Avoiding opsonization: Protein A produced by Staphylococcus aureus attaches to the Fc region of IgG and blocks the cytophilic (cell-binding) domain of the Ab
  • The biofilm matrix inhibits opsonic killing
20
Q

Ingestion

A
  • Adherence of the bacterium to the phagocyte causes the membrane of the phagocytes to move around the microbe, forming pseudopods
  • Pseudopods fuse and enclose the microbe within cytoplasmic vacuole called phagosome
  • Avoiding ingestion:
  • -Polysaccharide capsules of S. pneumoniae, Haemophilus influenzae, Treponema pallidum, and Klebsiella pneumoniae (difficult to phagocytose)
  • -Alginate of Psedomonas aeruginosa
21
Q

Digestion

A
  • Phagosome fuses with lysosome (full of destructive hydrolytic enzymes) to form a phagolysosome
  • The bacterium is digested, and any undigested material within the residual body is excreted from the cell
22
Q

Evading intracellular destruction

A
  • Escape from phagosome into the cytoplasm
  • -Listeriolysin O (Listeria sp.)
  • Prevention of phago-lysosomal fusion
  • -Mycobacterium sp., Aspergilus flavus, B. abortus, Chlamydia psittaci
  • Resistance to lysosomal enzymes
  • -Mycobacterium sp. (mycolic acid)
  • -Yersinia sp. (capsule)
23
Q

Respiratory burst

A
  • Macrophages use oxygen to form:
  • -Hydrogen peroxide
  • -Superoxide anion
  • -Hypochlorite ions
  • -Nitric oxide
  • Survival strategies:
  • -Carotenoid pigments as antioxidants (S. aureus)
  • -Salmonella Typhimurium can downregulate host NOS2 activity
  • -Pasteurella multiocida and Histophilus somni can inhibit the respiratory burst
  • -Catalase (Staphylococcus sp.) breaks down H2O2
24
Q

Iron sequestration

A
  • Iron is an important micronutrient and is a cofactor for many metalloproteases needed for bacterial growth and survival
  • Sequestering iron is a key defense against microbial invaders
  • Vertebrates use iron-binding proteins: transferrin, lactoferrin, haemoglobin
  • Siderophores (iron producing)
  • -Produced by bacteria in iron poor conditions
  • -Bind iron ions and cell receptor –> ferrisiderophore complex is transported into the cell
25
Q

Evasion - adaptive immunity

A
  • Antigenic variation

- Antibody destruction

26
Q

Adaptive immunity - antigenic variation

A

-The process by which an organism changes its surface antigens (proteins, carbohydrates, etc.) and thereby avoids destruction by the host immune response
-Campylobacter fetus ssp. venerealis
-Anaplasma marginale
(lifelong infection)

27
Q

Adaptive immunity - proteases

A
  • Some bacteria secrete proteases that can destroy immunoglobulins or cytokines
  • IgA proteases (Neisseria gonorrhoeae, Haemophilus influenzae, Histophilus somnus, Strep. pneumoniae) –> prevent opsonization and Fc receptor-mediated phagocytosis

Bacteriology and Mycology (6 decks)

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