Systematic Bacteriology 1 Flashcards

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1
Q

Give the grammar used for bacteria

A

Singular - us ending
Plural - i ending
sp. - 1 species
spp. - more than 1 species

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2
Q

What are the gram positive cocci?

A

Streptococcus (chains)
Enterococcus
Staphylococcus spp. (grape-like clusters)

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3
Q

What are the similar features of Streptococcus and Enterococcus?

A

Grow best aerobically but can grow anaerobically (FACULTATIVELY ANAEROBIC)

Gram positive cocci in CHAINS (streptococci come in STRIPS)

Initially differentiated by type of haemolysis (rupture/destruction of blood vessels) seen when grown on blood agar.

However, haemolysis is ONLY important for classifying Streptococci

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4
Q

What are the types of haemolysis?

A

α (partial) haemolysis
β (complete) haemolysis
Non-haemolytic strains (γ)

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5
Q

Describe α (partial) haemolysis and how does it appear

A

Enzymes DENATURE haemoglobin inside rbcs causing greenish discolouration round colony

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6
Q

Describe β haemolysis and how it appears

A

Most aggressive and virulent organisms

Enzymes LYSE rbcs, causing complete clearing round colony.

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7
Q

Describe γ haemolysis

A

No haemolysis

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8
Q

What are the α-haemolytic Streptococci and how are they recognised?

A

Cause partial haemolysis on blood agar

Streptococcus pneumoniae
Streptococcus “viridians” group

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9
Q

Describe the structure, region and antibiotic sensitivity of Streptococcus pneuomiae?

A

AKA pneumococcus
Gram positive cocci in short chains/pairs
Part of normal upper respiratory tract flora in many people (can do harm if it enters lungs)
Majority of UK strains still sensitive to penicillin

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10
Q

Describe Streptococcus “viridians”, regions and an infection they cause

A

Gram positive cocci in chains, under microscope

Not an actual species but a group of many.

Common COMMENSALS of upper respiratory tract, bowel, vagina.

Cause infection if in a normally sterile site:

Endocarditis - infection of heart valves may be caused by these organisms

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11
Q

What are the β-haemolytic Streptococci and how are they grouped?

A

Cause complete haemolysis of blood (produce exotoxins that lyse rbcs)

Subdivided into groups based on cell wall antigenic structure:

Group A Strep (Strep. pyogenes)
Group B Strep

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12
Q

What are the Group A Streptococcus, how do they functions and what infections do they cause?

A

AKA Strep. pyogenes
Most pathogenic of Streptococci
Produce powerful exotoxins that lyse cells

Cause:
Streptococcal sore throat (tonsillitis) - if rash is present, scarlet fever
Skin and soft tissue infection
Perperal sepsis - life threatening infection in pregnant/recently post-natal women

All strains still sensitive to penicillin

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13
Q

What are the γ-haemolytic bacteria, regions and antibiotic sensitivity?

A
Enterococci (most important group):
Enterococcus faecalis (most strains sensitive to amoxicillin - not penicillin)
Enterococcus faecium (some very antibiotic resistant strains can cause hospital outbreaks, like vancomycin resistant Enterococci - VRE)

Part of normal bowel flora and not really pathogenic but can cause problems if in normally sterile site, like UTIs.

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14
Q

Describe Staphyococci structure, atmosphere and testing ?

A

Gram positive cocci (grape-like clusters)
Grown best aerobically; can grow anaerobically

Coagulase test distinguishes the most common pathogen, Staph. aureus (coagulase positive - gold colonies), from all other Staphylococci (coagulase negative - white)

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15
Q

What are the Staphylococci, other than Staph. aureus, termed?

A

Coagulase negative Staphylococci

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16
Q

How does the coagulase test work?

A

If plasma becomes clotted, it is coagulase positive (gold Staph. aureus)

If plasma runs freely, coagulase negative (white)

17
Q

What are the coagulase negative Staphylococci? What infections do they cause?

A

Common skin commensals that do not cause harm generally

Do not produce toxins but do produce surface
polysaccharide “SLIME” that allows sticking to plastic/artificial materials in body

Cause prosthetic joint/heart valve infection and intravenous catheter/”line” infection - all hard to treat with antibiotics

18
Q

Describe Staphylococcus aureus regions, functions, and antibiotic sensitivity and resistance?

A

Colonise nose and URT in 30% of people (not harmful) but some strains produced exotoxins that damage cells, e.g: TSST (Toxic Shock Syndrome) and PVL (Panton-Valentine leukocidin - damages wbcs)

Some strains produced enterotoxins (act on gut in food poisoning)

MSSA (methicillin sensitive Staph. aureus) to flucoxacillin

MRSA - resistant to all penicillins and all cephalosporins and others

19
Q

Describe the spread of bacterial infection

A

Multiplies at acquisition site and causes local infection and inflammation, like abscess (in many healthy people, bursts without spreading as self-limiting)

Gets in bloodstream and disseminated to distant body sites

May cause abscesses in spleen, liver, kidney, etc

20
Q

What is bacteraemia, how does it occur and what results?

A

Bacteria in bloodstream (Staph. aureus is a common cause, as are infected intravenous catheters)

Patient may become septic and infection can spread to other sites (disseminated infection and inflammation)

21
Q

Meanings of -itis, pyrexia and rigor?

A

Inflammation at site (-itis)
Fever (pyrexia)
“Shivering attack” as raised temp falls (rigor - sign of pyrexia)

22
Q

Steps in diagnosis of infection?

A

Clinical history
Examination
Non-specific tests (wbc count)
Specific microbiology tests

23
Q

What are examples of specific microbiology tests for infection?

A

Blood, urine and faeces cultures
Swab of pus
Specimens for PCR
Blood for serology (check antibodies/antigens)

24
Q

What is a fever, why is it beneficial and how can it be harmful?

A

Fever - adaptive response beneficial in fighting infection.
Can result in febrile convulsions (fits) in young children

Normal temp = 37C (most human pathogens grow optimally)
Fever = >38C (human pathogen growth slows)

25
Q

What is the mechanism of fever production?

A

Antigen or lipopolysaccharide (endotoxin) interact with macrophages (wbc)

Macrophages released cytokines into blood, which travel to hypothalamus (also stimulate adverse effects of sepsis)

Prostaglandin E released, increase body temp

Body perceives it is cold and “shivers” (fever)

Increased survival from infection after fever

26
Q

How does sepsis result?

A

Small blood vessels become “leaky” (fluid goes into tissues)
Lower blood volume makes heart heart rate increase, to oxygenate tissues
Poor tissue oxygen perfusion means blood supply to less essential organs is shut down to maintain blood supply to brain
Blood clotting system activates, causing blood clots in tiny blood vessels
Uses all clotting factors
Increased haemorrhage risk

27
Q

How do hosts respond to infection in order of increasing severity?

A

Infection
Sepsis
Severe sepsis
Septic shock