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Flashcards in Bacteriology Deck (160)
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1

What are mechanisms that bacteria or pathogens use to cause disease?

Invasion - The process of microorganisms entering body tissue or host cells, surviving & spreading in the body. Toxigenicity - Production of microbial toxins that damage the host but aid in microorganism's survival. Immunopathology - Host's immune response causes damage to the host itself.

2

Give an example of a bacteria that uses toxigenicity to cause disease.

Clostridium tetani - Causes tetanus by production of tetanospasmin toxin, which causes muscle spasms. Prevents neurons from releasing inhibitory neurotransmitters GABA & glycine by degrading protein synaptobrevin. Results in FAILED INHIBITION of motor reflexes by sensory stimuli. Gram+ rod, anaerobic, spore-forming, found in soil & faeces.

3

Give an example of a bacteria that uses invasion to cause disease.

Brucella abortus - Causes Brucellosis in cattle by invading host cells. Gram (-), non-spore-forming, facultatively intracellular.

4

Give an example of a bacteria that uses immunopathology to cause disease.

Mycobacterium bovis or M. tuberculosis - Causes granulomatous response that damages lung tissue. Gram+ rod, aerobic, non-motile; replicates in alveoli of host.

5

What is pathogenicity?

The ability of an infectious agent to cause disease.

6

What is virulence?

The measure of a pathogen's ability to cause disease; how pathogenic something is.

7

What is pathogenesis?

The process of disease progression.

8

What is an opportunistic pathogen?

A pathogen only capable of causing disease when allowed to do so through particular circumstances of the host.

9

What is a commensal?

A microorganism that naturally resides on the body, causing no harm. In some cases, when immunity in the host is suppressed or compromised or ends up in the wrong area, a commensal can become pathogenic. Eg., E. coli is a commensal of the colon but becomes pathogenic if it gets into the urinary tract. Eg. Staphylococci is a commensal of the skin but can cause infection if skin is broken.

10

What is nosocomial infection?

Hospital-acquired infection. Eg., Bacteria tend to become more pathogenic in hospitals where a lot of antibiotics are used, resulting in resistant microorganisms.

11

What are the differences between Gram (+) & Gram (-) bacteria?

The distinction depends on the microorganism's response to Gram stain with crystal violet. Gram (+) bacteria stain purple because they have a thick peptidoglycan wall that absorbs and reacts with the stain. Gram (-) bacteria stain pink with counterstain because they have outer & inner membranes that sandwich the thin peptidoglycan cell wall, which doesn't pick up the crystal violet.

12

What are the main mechanisms employed by Gram+ bacterial exotoxins?

1. Digest surroundings / break down host tissue so bacteria can extract needed nutrients for survival and replication. 2. Damage host's immune system using neurotoxin or biological toxin.

13

Give some examples of exotoxins that are enzymes.

1. Phospholipase 2. Protease 3. Collagenase 4. Hyaluronidase - digests host proteins

14

Give some examples of Gram+ exotoxins that are neurotoxins/biological toxins and explain how they work.

1. Botulinum - produced by Clostridium botulinum; causes botulism. Prevents vesicles in neuromuscular junction from anchoring to neuron cell-membrane to release acetylcholine. Inhibition of Ach release at synapse results in FLACCID PARALYSIS. 2. Tetanus, aka tetanospasmin: produced by C. tetani; prevents affected neurons from releasing inhibitory neurotransmitters GABA & glycine, so muscles respond to just tiny sensory stimuli, tetanic spasms.

15

Give some examples of exotoxins that damage the host's immune system.

1. Leucocidins: kill white blood cells such as neutrophils, basophils, eosinophils, monocytes, lymphocytes, etc. These are produced by Staphylococcus & Streptococcus spp. 2. Antichemotaxins: Inhibit chemotaxis of neutrophils to site of infection. Eg., Chemotaxis Inhibiting Protein of S. Aureus (CHIPS) 3. C5a Protease: Cleaves potent neutrophil chemotaxin called C5a, which is produced by complement system. C5a peptidase, produced by Streptococcal progenes, is necessary to minimuse influx of neutrophils.

16

What are endotoxins and what type of bacteria produce them?

They are lipopolysaccharides (LPS) in the bacterial cell's outer membrane that don't do damage themselves but ignite host immune response (mainly cytokine response). They are kept "within" the bacteria cell membrane & only released after destruction of the bacteria cell wall, e.g. via detergent. The lipid part of cell membrane is the "endotoxin" & the hydrophilic"polysaccharide O side-chain" makes up the "O-antigen". Gram (-) bacteria ONLY are associated with endotoxins.

17

What mechanisms of pathogenicity do Gram (-) bacteria employ?

1. Adhesion 2. Exotoxins 3. Endotoxins (lipopolysaccharides) 4. Cell-host interaction 5. Capsular polysaccharide 6. Iron acquisition 7. Evasion of host immune system

18

How do Gram (-) bacteria use adhesion as a mechanism of pathogenicity?

1. Fimbriae, villi-like extensions on cell wall made of pili protein units that act as antigens. Eg., K88 aka F4 help E. Coli stick to mucosal surfaces / enterocytes in colon. P. fimbriae help E. Coli stick to epithelium of urinary tract, causing infection. 2. Filamentous haemagglutinin helps Bordatella bronchisepta to stick to canine ciliated tracheal epithelium, avoiding muco-ciliary escalator. 3. Polar fimbriae help Dichelobacter nodosus to stick to keratinised tissues in hoof of sheep, leading to footrot.

19

Give examples of exotoxins used by Gram (-) bacteria.

1. Cholera toxin - Activates adenylate cyclase; increased level of intracellular cAMP promote secretion of fluid and electrolytes in intestinal epithelium leading to diarrhea 2. Heat-labile LT toxin - released by E. Coli; similar or identical to cholera toxin 3. Heat-stable ST toxin - released by E. Coli; binding of ST enterotoxins to a guanylate cyclase receptor results in an increase in cyclic GMP (cGMP) that adversely effects electrolyte flux. Promotes secretion of water and electrolytes from intestinal epithelium leading to diarrhea 4. Shiga-like toxin - released by E. coli; cleaves rRNA resulting in inhibition of protein synthesis in susceptible cells. Results in diarrhea & hemorrhagic colitis. 5. Osteolytic toxin of Pasteurella multocida 6. Leucotoxin of Mycobacterium haemolytic 7. Exotoxin A of Pseudomonas aeruginosa 8. Keratinase of Dichelobacter nodosus

20

What is meant by cell-host interaction employed by Gram (-) bacteria?

Bacteria that are either commensal and/or opportunistic.

21

What is a Gram (-) bacteria's capsular polysaccaride (capsule) and how does it work?

A thick, mucous-like, layer of polysaccharide. This "capsule" cloaks antigenic proteins on the bacterial surface that would otherwise provoke an immune response - phagocytosis by neutrophils and opsonophagocytosis by macrophages -- & thereby lead to the destruction of the bacteria. Capsular polysaccharides are water soluble, commonly acidic & linear.

22

What is LPS and what role does Lipid A play in LPS's role as Gram (-) endotoxin?

LPS is a three-part structure in Gram (-) outer membrane. The innermost, hydrophobic portion is Lipid A, which anchors the LPS molecule, comprised of Lipid A, core polysaccharide & O-side chains, aka O-antigen, to the outer membrane. When released from the bacterial cell well, Lipid A activates macrophages and causes IL-1 & TNFalpha release, stimulating a strong immune response. Clinically, the response can range from fever, thrombosis, DIC, leucopenia to complement, hypotension, circulatory collapse, shock & death.

23

How does iron acquisition aid in a Gram (-) bacteria's pathogenicity?

Since no bacteria can synthesize iron, Gram (-) bacteria scavenge or harvest it to grow using: 1. Siderophores: High-affinity chelating compounds put out by Gram (-) bacteria into environment that scavenge iron & bring back. 2. Transferrin-binding protiens - Proteins that hold iron, like Hb, that bacteria can clutch onto & steal from. Eg. S. aureus possess transferrin-binding proteins in cell wall.

24

What are three ways in which the cell membrane & capsule of the Gram (-) bacteria help the pathogen evade the host immune system?

1. Evade phagocytosis by innate immune system: use hydrophilic capsule or LPS outer membrane; 2. Resist complement & lysozyme: same non-stabilising capsule & LPS helps avoid opsonisation with C3b (alternative pathway); 3. Use of molecular mimicry to avoid antibody-mediated opsonophagocytosis ie., host recognises surface components as "self antigens", thus no antibody not produced. Eg., K1 antigen (sialic acid) of E. coli, hyaluronic-acid capsule of beta-haemolytic streptococci & K5 antigen (desulfoheparin) of E. coli.

25

What are some diseases caused by bacterial use of adhesion, ie., fimbriae or filamentous haemagglutinin?

Kennel cough (Bordatella bronchisepta) Pink Eye / New Forest Eye (Moraxella bovis) Diarrhoea (E. coli) Footrot (Dichelobacter nodosus)

26

How do obligate & facultative intracellular pathogens hide from the host's immune defences?

1. Inhibit phagosome & lysosome fusion (evading macrophages); 2. Lyse phagosomal membranes to escape into cytoplasm 3. Resist killing by lysosomal killing mechanisms

27

Which of the following are extracellular pathogens? More than one. A. Escherichia coli B. Chlamydia C. Rickettsia D. Streptococci

A & D Chlamydia & Rickettsia are obligate intracelluar bacteria.

28

Salmonella, Listeria, Mycobacterium and Brucella are: A. Extracellular pathogens B. Obligate intracellular pathogens C. Facultative intracellular pathogens D. None of the above

C

29

Fimbriae that bind mannose are non-pathogenic except for assisting in bladder colonisation & infection. True or False?

True. Mannose sugar binds to fimbriae, thus blocking it from binding to enterocytes. But mannose-resistant fimbriae, such as K88 aka F4 on E. coli are highly pathogenic.

30

Which type of bacteria, Gram (+) or Gram (-), staphylococci or bacilli, can form spores?

Gram (+) bacilli only.

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