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MEDSCI 202 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Extremophiles

A

Live under extreme conditions

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2
Q

Halophiles

A

Need high salt conditions

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3
Q

Thermophiles

A

Can thrive at temperatures betwen 60-120

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4
Q

Cryophiles

A

Grow better at tempartures of 15 or lower

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5
Q

Acidophile

A

Optimum pH level at or below 3

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6
Q

Alkaliphile

A

Optimal growth at pH levels of 9 or above

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7
Q

Xerophile

A

Grow in extremely dry, desiccating conditions

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8
Q

Brightfield Microscopy

A

0.2um resolving power, 1000x,
Mostly used gram staining

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9
Q

Darkfield

A

0.2um, 1000x
Examination of very thing organisms against dark background (spirochetes)

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10
Q

Phase constrast

A

0.2um, 1000x
To observe unstained live organisms

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11
Q

Fluorescence

A

0.2u, 1000x
Mainly for immunodiagnostic fluorescent dye attached to organism

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12
Q

Scanning Electron

A

20nm, 10,000x
Examination of surface feature of cells and viruses, gives illusion of depth (3D)

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13
Q

Transmission electron

A

0.2nm, 200,000x
Examination of cellular and viral ultra structure, reveals internal features

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14
Q

Gram positive vs Gram negative

A

Gram positive = 1 membrane and cell wall is thick
Gram negative = 2 membrane and cell wall is thin

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15
Q

Taxonomic catergories

A

Kingdom, Phylum, Class, Order, Family, Genus, Species

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16
Q

Endospores

A

Endospores are resistant to heat, cold, drying and many chemicals and can survive for many years in soil or dust. The spores germinate after landing on moist, nutrient-rich surface and develop into vegetative state. Important for survival, but not for reproduction (dormant, metabolically active)

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17
Q

Flagella

A

Provide motility, powered by proton-motif force

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18
Q

Fimbriae (pili)

A

Hair-like structures, not associated with motility. Pili often contain an adhesin at tip which is used to bind to host cells (colonisation). Some produce sex pilli for conjugation (exchange of genetic material)

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19
Q

Slime layers

A

Gelatinous material secreted from cells used for gliding and aggregation. Formation of biofilms (dental plaque )

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20
Q

Capsules

A

Firmly attached to the cell surface and usually composed of polysaccharide. Provides protection from desiccation and immune system. Immune evasion factor

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21
Q

Strain

A

Genetic variant of a species (subtype)

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22
Q

Serotype

A

subtype that can defined by using specific antibodes

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23
Q

Pathovar

A

subtype with tissue/host specificity

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24
Q

Isolate

A

Pure microbial sample obtained from an infected individual

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25
Q

Coagulase Test

A

Used for identification of Staph Aureus. Mediates fibrin polymerisation that can be seen as clot in plasma

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26
Q

Oxidase test

A

Some obligate aerobic bacteria produce cytochrome C oxidase as part of the respiratory chain. Incubation of bacteria with oxidase reagent results in dark blue stain. Only use results <20 seconds

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27
Q

Catalase test

A

Use to differentiate between Staph and Strep, both gram positive. Staph will produce catalase producing bubbles.

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28
Q

Microbact strips

A

Reactions are assessed by change of colour, either by the product of pH indicator. Test produces code, which compares to analysis sheet

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29
Q

Antiobiotic Susceptibilty test

A

Differentiate between species with different resistance. Test conducted on lawn agar plates with antibiotic discs.

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30
Q

Selective Agar

A

Contains inhibitors to discourage growth of certain organsism

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31
Q

Differential Agar

A

Contains indicators to differentiate organisms.

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32
Q

Mannitol Salt Agar

A

use to identify Staph aureus. Salt inhibits non-haloduric bacteria, mannitol can be used as a carbon source by Staph aureus, but not by an other Staphylococci. Fermentation of mannitol results in a pH decrease, which is detected by a pH indicator changed from red to yellow

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33
Q

Sabourand agar

A

selective for fungi, as low pH suppresses growth of most bacteria. Non -differential

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34
Q

Eosin-methylene blue agar (EMB)

A

selective for gram-negative bacteria as aniline dyes are toxic for gram positive bacteria. Differential for lactose fermenter. Appearance fo pink colonies indicates lactose fermentation (white = negative)

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35
Q

Blood Agar plate

A

Growth of many fastidious bacteria. Differentiates for haemolytic reactions. alpha = some, beta = all, gamma = none

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36
Q

Cytine-lactose-electrolyte deficient (CLED) agar

A

used for growth of urinary pathogens. Lack of electrolytes inhibits movement of motile organisms. Differentiates lactose fermenters (yellow), blue = negative

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37
Q

Bile-Esculine agar:

A

selective for Enterococci (Group D streptococci). Oxgall inhibits non-enteric bacteria. Esculine hydrolysis results in a dark brown color. Some members of the Enterobacteriaceae family also hydrolyse esculine

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38
Q

Cell aggulination

A

Antibodies recognise component on cell surface resulting in visible clumping (agglutination). Basis of serotyping, where serum is used to distinguish between different types of a given species based on specific antibodies to a variable surface molecule

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39
Q

Latex bead agglutination

A

Antibodies (or antigen) can be bound to latex beads. A positive reaction leads to visible clumping of the latex beads. Used for e.g Lancefield group typing of Streptococci

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40
Q

Western-blot

A

For identification of proteins or antibodes. Proteins are separated on a gel according to their molecular weight and then immobilized by blotting onto a nitrocellulose membrane. Antibodies are added to the membrane and specific binding to protein occurs. A second antibody labeled with an enzyme and with specificity to the Fc region of the first antibody is added. Binding is monitored by adding a substrate that is converted by an enzyme resulting in a detectable protein band

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41
Q

Anti-streptolysin O assay

A

antibodies against steptolysin O are a marker for a recent S. pyogenes infection and important for diagnosis of poststreptococcal diseases such as acute rheumatic fever. Red blood cells are mixed with streptolysin O and patient serum. Lysis of RBC leads to a red solution. If lysis is inhibited by neutralizing ab in the serum. RBC sediment and the solution remians clear

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42
Q

Restriction fragment length polymorphism (RFLP)

A

small mutations on the genome can leda to destruction (or generation) of a recognition sequence for a restriction enzyme (a DNase that cleaves at short specific DNA sequences). This leads to changes in the length of DNA fragments after treatment with the DNase and can be detected after separating the DNA fragments on an agarose gel. Mainly used to epidemiological studies

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43
Q

PCR

A

Uses specific oligo DNA primers and a heat-stable DNA-polymerase to amplify very small amounts of DNA. Important method to identify organisms that cannot be easily grown in culture. Also used to amplify small amounts of DNA.

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44
Q

Fluorescene in situ hybridisation

A

Cytogenetic method that uses fluorescent probes specific to certain DNA or RNA sequences

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45
Q

Organic antibiotics

A

isolated from bacteria or fungi

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46
Q

Semi-synthetic antibiotic

A

further derivisation of organic compound for greater efficacy, ampicilin, methicillin, oxacillin

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47
Q

Synthetic

A

generated in the lab

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48
Q

Antibacterial spectrum

A

gives the range of activity against bacteria. e.g broad or narrow. A narrow antibiotic is only effective against a limited variety of bacteria. A broad-spectrum antibiotic works against a larger variety of bacteria

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49
Q

Bacteriostatic activity

A

is the level of antimicrobial activity that inhibits growth of an organism

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50
Q

Bactericidal activity

A

is the level of antimicrobial activity that kills the organism

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51
Q

Antibiotic combination

A

different antibiotics are sometimes combined to broaden the antimicrobial spectrum, to treat polymicrobial infections

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52
Q

Antibiotic synergism

A

enhanced antimicrobial activity of combined drugs compared to activity of each individual antibiotics

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53
Q

Antibiotic antagonism

A

activity of one antibiotic interferes with activity of other, so the sum of activity is less than most active individual drug

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54
Q

Minimum inhibitory concentration

A

minimum concentration of an antibiotic to inhibit growth of a given bacterium

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55
Q

Minimum Bactericidal concentration

A

minimum concentration of an antibiotic to kill a given bacterium. MBC is reached when colony forming units (CFU) are reduced by 99.9% below control

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56
Q

Antibiogram

A

this shows the sensitiviy of an isolated strain to a certain antibiotic. The semi-quantative method is based on diffusion of the antibiotic from a filter disc on an agar plate producing a concentration gradient around the disc. the MIC can be calculated from the diameter

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57
Q

Drugs that block cell water synthesis: B-lactam antibiotics

A

inhibit peptidoglycan synthesis by irreversible inhibition of transpeptidase (=penicillin binding protein PBP), the enzyme that catalyse the peptide-cross links. Eg. penicillin. These antibiotics are bactericidal

B-lactams include penicillin, cephalosporins, carbapenems

Gram negative bacteria are resistant to penicllin, does not pass through outer membrane porins, however extended spectrum penicillins (amoxicillin, ampicillin) can

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58
Q

Drugs that block cell wall synthesis: Glycopeptides

A

which inhibits PG synthesis by binding to the petides of the peptidoglycan monomers. Drug of last resort for MRSA. eg vancomysin

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59
Q

Inhibitors of RNA transcription: Rifamycins

A

inhibit bacterical RNA polymerase. typically used against Myobacteria. Rifamysins are bactericidal.

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60
Q

Inhibitors of nucleic acid synthesis: Quinolones and Fluoroquinones

A

bind DNA topoisomerases and prevent DNA replication. They are broad spectrum, bactericidal and coomnly used against urinnary tract infection. They can enter host cells, which makes them useful against intracellular bacteria. Due to increased resistance, quinolones have been replaced with fluroquinolones which are more active.

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61
Q

Antimetabolites: Sulfonamides and diaminopyrimidines

A

prevent the synthesis of tetrahydrofolic acid from PABA. Tetrrahydrofolic acid is a cofactor needed to synthesise nucleic acids and methionine. Mammalian cells depends on external folate. These antibiotics are bacteriostatic and useuful against urinary tract infection and Shigellosis

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62
Q

Antibiotics: Inhibition of protein synthesis

A

Antibiotics that can bind to the 2 different subunits of the ribosomes, some targeted to the 50s and others to the 80s.

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63
Q

Binding to the 30s subunit: Aminoglycosides

A

freeze the 30s initiation complex resulting in misreading (induce frameshift) of DNA. They are mostly effective against aerobic, gram negative bacteria and are bactericidal and synergistic with penicillin.

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64
Q

Binding to the 30s subunit: Tetracyclines

A

inhibit binding of aminoacyl-t-RNA to the acceptor site on the ribosome. They have broad-spectrum activity, are bacteriostatic and used against many different bacterial infections.

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65
Q

Binding to the 50s subunit: Macrolides

A

inhibit translocation of the peptidyl transferase activity. from the A to the P site. They are bacteriostatic and active against Gram-positives and Mycoplasma

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66
Q

Binding to the 50s subunit: Lincosamides

A

inhibit peptidyl transferase activity. They have broad-spectrum activity and are bacteriostatic

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67
Q

Binding to the 50s subunit: Chloramphenicol

A

is a broad-spectrum, bacteriostatic antibiotic. Only used in certain cases such as bacterial meningitis, due to strong side-effects

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68
Q

Antibiotic resistance mechanisms

A

Exclusion of antibiotic from site of action - outer membrane of Gram-negatives often impermeable

New or modified antibiotic insensitive target - MRSA produces PBP2a (altered transpeptidase) with reduced affinity for penicillin

Efflux pump for the antibiotic removal from site of action - specific transport out of the cell e.g tetracylclin, macrolides, fluroquinolones

Enzymatic modification or degradation of the antibiotic - some bacteria produce B-lactamase, which breaks the B-lactam ring. Some B-lactamases are specific for certain B-lactams, while others inactivate a wide range of B-lactams.

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69
Q

Antibiotic resistance (genetic vs non-genetic)

A

Non-genetic (intrinsic drug resistance

  • metabolic inactivity
  • lack of target structure, mycoplasmas (lack cell wall)
  • exclusion, antibiotic can’t enter cell

Genetic resistance

  • Chromosomal resistance- spontaneous mutation n a gene encoding a target receptor
  • Acquired resistance - conjugation (plasmid transmid)
  • Transformation (transfer of free DNA)
  • Transduction (Transfer by viral DNA)
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70
Q

MRSA

A

Methicillin resistant S-aureus, carry Staph cassette chromosome mec (SCCmec)
integrated in bacterial genome
SCCmecII: mainly in hospital MRSA strains, also encodes resistance
SCCmecIV: mainly in community acquired MRSA

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71
Q

Staph aureus: general info

A

Gram postiive-spherical cocci, found in irregular grape-like cluters. Non-motile. Halodurent

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72
Q

Staph aureus: location

A

mosit skin folds, oropharynx, GI tract and urogentical tract. 15%

of people are persistant nasopharyngeal carriers.

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73
Q

Staph aureus: resistance

A

has b-lactamase gene. MRSA and vancoymcin resistnat strains have emerged too

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74
Q

S.aureus: catalase test

A

Postive

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75
Q

S.aureus: coagulase test

A

Positive

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76
Q

S.aureus: Adhesins

A

MSCRAMMS (Microbial surface components recognizing adhesive matrix molecules) - cell wall atttached proteins found in gram positive bacteria. They specifcally bind to host extracellular matrix proteins, fibronectin, elastin, laminin, vitronectin and collage. Important for tissue colonisation

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77
Q

S.aureus: factors that damage host cell

A

Cytolysins - alpha toxin form membrane pores. Beta toxin hydrolyses membrane phospholipids. Gamma tozin are pore forming toxins. Toxic to leukocytes, erythrocytes and tissue cells

Exfoliative toxins - serine proteases that split intercellular bridges (desmosomes) in stratum granulosum, resulting in peeling.

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78
Q

S.aureus: Spreading factors

A

Lipases: hydrolyse lipids for invasion of cutaneous tissues

Nucleases - hydrolyses DNA, decrease viscocity of pus

Hyaluronidase: hydrolyses hyaluronic acid in connective tissue

Proteases - serine protease, aureolysin

Staphylokinase (fibrolysin) - causes fibrolysis

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79
Q

S.aureus: Superantigens

A

Toxic shock syndrome toxin , Staphylococcal enterotoxins

The staphylococcal SAgs are struturally and functionally related to the streptococcal superantigens. SAgs trigger massive release of pro-inflammatory cytokins and over-stimulation of the host immune response, resulting in system inflamation. Some of them can also cause food poisoning.

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80
Q

S.aureus: Immune evasion factors

A

Capsule - a dense polysaccharide coast that prevents oponisation with ab and complement. It also contains water which protects bacteria against desiccaiton

Slime layer - loose-boudn water-soluble film (biofilm) made from polysaccharides, which protects from immune factors and antiobiotics

Catalase: detoxifies peroxide produced by macrophages and neutrophils. The catalase test is used to distinguish staphylococci from streptococci

Clumping factor (CIF-A) bound coagulase - binds fibrinogen and converts it to insoluble fibrin. Fibrin deposition of cell surface prevents oponisation and phagocytosis. CIF-A also promotes cell aggregation (clumping). The coagulase test is used to identify S.aureus, as it is not produced by any other staphylococci

Protein A: found on the surface of most S.aureus strains. It binds IgG in wrong orientation thereby preventing oponisation and phagocytosis

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81
Q

S.aureus - Superficial skin disease

A

Impetigo - localised cutaneous infection with pus-filled vesicles. Primarily young children

Folliculitis - impetigo involving hair follicles

Furuncles or boils: painful pus-filled cutaneous nodules

Carbuncles: coalescence of furnuncles, extenstions into subcutaneous tissue that can lead to bacteremia and systemic disease

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82
Q

S.aureus - Disease 2

A

Osteomyelitis - can occur after hematogenous dissemination of bacteria to bone or by a secondary infection from trauma. Usually involves metaphyseal area of long bones. The cure rate is good, if treated with appropriate antibiotics

Septic arthritis - mainly found in children and young adults receiving intra-articular injections or caused by hematogenous spread from a localised focus. Characterised by painful erythematous joint and purulent material (pus) in joint space

Staphylococcal Scaled Skin Syndrome (SSSS) - cutaneous blisters followed by desquamation of epithelum caused by action of exfoliative toxins. affects mainly neonates and young children. Mortaility usually low

Bacteremia and endocarditis - spread of bacteria into the blood from a focus on infection (bacteremia). More than 50% of cases are hospital acquired (surgery, contaminated catheters). Bacteria can then spread to other organs, particular the heart leading to endocarditis S.aureus endocarditis has a mortality rate of nearly 50%. Bacterial endocarditis results in damage to the endothelial lining of the heart. The infected heart valaved is often coated with bacteria, platelets and cellular debris. Perofration of heart valve can occur mainly by secreted enzymes. Flushing of the debris into the blood can lead to septic emboli.

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83
Q

S.aureus - Disease 3

A

Pneumonia - can occur after aspiration of oral secretion or by hematgenous spread resulting in consolidation and abscess formation in lung. Cytolytic toxins are believed to play a role

Staphylococcal food poisoning - contamination of food by human carrier and improper food handling. Not infection. Mediated by heat stable enterotoxins (SEA and SEB..) that cause sever vomiting, diarrhea, abdominal pain, nausea, sweating headache. It has a rapid onset (hours), and generally doesn’t last long

TSS - caused by superantigen producing strains.

Menstrual TSS - growth of TSST-producing strain in vagina (TSST is the only superantigen that can penetrate mucosal bacteria) caused by prolonged use of expandable tampons.

Non-menstrual - grwoth of superantigen producing strain in wound. Toxins are released into the bblood and can cause systemic disease with fever, hypotension, erythematous rash and multiple organ failure. 30-40% mortality rate.

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84
Q

S.aureus - susceptible patientsq

A

infants

children with poor hygiene

mentruating women

patient with intravascular catheers

patients with compromised pulmonary function

immunocompromised patients

diabetes

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85
Q

Streptococci: general info

A

Gram positive cocci, grow in chains. Susceptible to penicillin

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86
Q

Streptococcus: Classification

A

A: S.pyogenes

B: S.agalactiae

C: S.disgalactiae, S.equi

D: S.bovis, Enterococcus spp

Group F: S.intermedius

No lancefield antigen: S.pneumoniae, viridan group

(write down on sheet)

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87
Q

S.aureus - risk factors

A

presence of foreign body

previous surgical procedure

poor hygiene of hospital staff

lack of antibodies

use of antibiotics that supress microbial flora

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88
Q

Streptococcus: where and how is it transmitted

A

Upper respiratory tract and respiratory droplets

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89
Q

Streptococcus Virulence Factors: Adhesins

A

MSCRAMMS: same as Staph.aureus

Pilli:

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90
Q

Streptococcus: Factors that damage the host cell

A

Cytolysins:

Streptolysin O (SLO): oxygen-labile cytolysin that forms pores in host cell membrane

Streptolysin S: (SLS): oxygen stable cytolysin that lyses leucocytes,erys and platelets

Completely lyses red blood cells

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91
Q

Streptococcus: spreading factors

A

Lipases: hydrolyse lipids, for invasion of cutaneous tissues

Nucleases: hydrolyses DNA, decrease viscosity of pus

Hyaluronidase: hydrolyses hyaluronic acid in connective tissue

Proteases: streptococcal cysteine protease (SCP) with wide substrate spectrum

Streptokinase (fibrolysin): causes fibrinolysis (dissolves clots)

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92
Q

Streptococcus: Superantigens

A

Streptococcal pyogenic exotosins, Streptococcal mitogenic exotoxin Z (SMEZ) :

Structurally and functionally related to the Staph superantigens, but they don’t cause food poisoning. trigger massive release of pro-inflammatory cytokines and over stimulation of the host immune response, resulting in system inflammation

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93
Q

Streptococcus: Immune evasion factors

A

Capsule: a dense hylauronic acid coat that prevents oponisation with ab and complement (inhibits phagocytosis). Only is some strains. Camoflauge effect.

M-protein: in addiotn to its function as an adhesin, M protein prevents complement factor C3b from oponising

C5a peptidase: a proteae that cleaves complement factor C5a prevent neutrophil migration to the site of infection

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94
Q

S.pyogenes non invasive diseases

A

Impetigo - same as Staph aureus

Pharyngitis: develops 2-4 days after exposure to S.pyogenes. Symptoms includes sore throat, fever, reddened pharynx, tonsillitis

Scarlet fever: a complication of pharyngitis that can develop into serious systemic disease. Epidemic outbreaks with high mortality rates in the 19th century. Caused by strains that produce the superantigen pyrogenic exotoxin A (SPE-A) = “scarlet fever toxin”

Cellulitis: infection of skin that involves subcutaneous tissue. An acute and rapidly spreading infection

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95
Q

S.pyogenes invasive diseases

A

Necrotising fasciitis: a deep infection of the skin that involves destruction of muscles. S.pyogenes is introduced through e.g minor cuts, trauma, burn, surgery or vesicular viral infection. The deep tissue infection is supported by spreading factors, such as DNAses, proteases and hyaluronidase. NF often develops into sever systemic disease with high mortaility (TSS)

Streptococcal toxic shock syndrome (STSS): often follows necrotising facsciitis and sepsis. STSS, mortality rate 30-70% (more severe than staphylococcal TS). Massive release of pro-inflammatory cytokines occurs in response to superantigen secretion. Systemic inflammation, symptoms includes fever, headache, multiorgan failure and shock.

Rheumatic fever and rheumatic heart disease - connected to pharyngitis and tonsilitis. Develops after untreated/chronic sore throats due to S.pyogenes. Inflammation of endocardium, myocardium, pericardium results in thickened and deformed heart valves and granulomas in myocardium. The disease often starts with inflammatory changes in joints.

ARF (acute renal failure) is an autoimmune disease, NOT an infection. It is triggered by molecular mimcry an antibody cross infection where antibodies generated against the M protein also bind to host proteins (cardiac myosin, collagen). Triggers a type 2 hypersensitivity immune response

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96
Q

S.agalactiae

A

Gram positive, long chains, either B or non haemolytic, lancefield B group carbohydrate. Resides in upper respiratory and genitourinary tract.

Neonatal disease: pneumonia, bacteremia, sepsis, meningitis

Infections in pregnant women: UTI, bacteremia

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97
Q

Viridans Streptococci

A

Alpha haemolytic

Oropharynx, gastrointestinal tract and genitourinary tract. Commensales of mouth flora.

Virulance factors: some carry adhesins/pilli for binding to teeth, biofilm

Disease: dental caries, bacterial endocarditis, septic shock in immunocompromised patients

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98
Q

Streptococcus pneumoniae

A

Diplococci or short chains, most strains have outer capsule.

Pharynx -> lungs -> sinuses, ears

conditions that interfere with bacterial interference at risk

capsule, and pneumolysin - destroys ciliated epithelial cells

Disease: pneumonia, menigitis, bacteremia, sinusitis and otitis media

Alpha haemolysis

Infiltration of neutrophils and macrophages

Symptoms: Fever, yellowish sputum, chest pain

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99
Q

Cholera: vibrio cholerae

general info

A

Gram negative: comma shaped rod

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100
Q

Cholera: Source

A

Source: contaminated water, contaminated by faeces

Reservoir = shellfish in coastal water

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101
Q

Cholera: Route of transmission

A

Route of transmission: drinking water contaminated by faeces of infected individuals. Other contact with faeces of infected.

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102
Q

Cholera: risk factors for infection

A

Risk factors for infection: poor hygiene and sanitation

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103
Q

Cholera: key virulence factors

A

Key virulence factors:

Colonisation: Flagellum, Type 4 pilus

Damage: Cholera Toxin

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104
Q

Cholera: progression of symptoms

A

Progression of symtoms: Vomiting then profuse watery diarrhoea

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105
Q

Cholera: Identification and diagnosis

A

Sample tested: stool

Microscopy: Gram negative comma shaped rod

Culture: yellow coloured (sucrose fermenting) colonies of Thiosulfate-citrate bile salts sucrose (TCBS) agar

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106
Q

Cholera: treatment options

A

Oral rehydration (salt,sugar water) or IV fluids if serious

Antibiotics: Doxycycline (cheap), reduces shedding. Not a huge effect on symptoms and duration of disease

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107
Q

Cholera: prevention options

A

Provide clean water and effective sanitation. Antiobiotics may reduce bacterial shedding. There is a vaccine, variants of the inactivated oral vaccine are currently in use. live attenuated vaccine also approved

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108
Q

Campylobacteriosis: causative agent

A

Campylobacter jejuni

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109
Q

Campylobacteriosis: source

A

Gut bacteria found in faeces from farm animals and birds. Most commonly attributed source is chicken

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110
Q

Campylobacteriosis: route of transmission

A

faecal/oral route

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111
Q

Campylobacteriosis: Risk factors for infection

A

eating undercooked chicken and other contaminated food or water. Immune deficiencies for more serious invasive diseases.

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112
Q

Campylobacteriosis: key virulence factors

A

Colonisiation: flagellae, outer membrane adhesins

Immune evasion: Lipooligosaccharide mimicking our molecules

Damage: cytolethal distending toxin increases water secretion, cholera-like toxin leads to cell death

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113
Q

Campylobacteriosis: progression of symptoms

A

Intestinal colonisation, leading to diarrhoea, inflammation and abdominal pain.

Sequellae: molecular mimicry can lead to immune cross-reactivity at joints (reactive arthritis) and nerves (Guillain Barre syndrome)

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114
Q

Campylobacteriosis: sample tested

A

Stool, blood in rare cases of invasive diseases

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115
Q

Campylobacteriosis: microscopy

A

Gram-negative rod, seagull shape

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116
Q

Campylobacteriosis: Culture

A

CAMPY agar, blood agar base with antiobiotics to inhibit other faecal bacteria. Incubate in microaerophilic conditions

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117
Q

tCampylobacteriosis: Treatment options

A

Keep hydrated, pain relief

Antiobiotics: yes , severe ,azithromycin, erythormyin especially if prolonged or at risk of invasive disease

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118
Q

Campylobacteriosis: prevention options

A

Cook food properly, control carriage in farm animals. No vaccine

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119
Q

Clostridioides difficile: causative agent

A

Clostridium difficile

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120
Q

Clostridioides difficile: general info

A

endospore forming, anaerobic, gram positive rod. Primarily problem in hospital patients

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121
Q

Clostridioides difficile: source

A

Human gut flora

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122
Q

Clostridioides difficile: route of transmission

A

Faecal/oral route between people

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123
Q

Clostridioides difficile: risk factors for infection

A

Broad spectrum antibiotics and other treatments that disrupt the gut flora

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124
Q

Clostridioides difficile: virulence factors

A

Colonisation: endospores

Damage: two similar c.difficile toxins

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125
Q

Clostridioides difficile: progression of symptoms

A

Watery diarrhoea, pseudomembranous colitis, then toxic megacolon in worst cases

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126
Q

Clostridioides difficile: sample tested

A

stool

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127
Q

Clostridioides difficile: microscopy and culture

A

Not useful as people can be colonised without infection

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128
Q

Clostridioides difficile: toxin testing

A

Immunodiffusion test for toxin in stool, sometimes immunodiffusion for cell antigens and PCR for toxin genes

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129
Q

Clostridioides difficile: treatment options

A

Rehydration and pain relief

Antiobiotics: discontinue precipitating antiobiotics. Treat Cd with metronidazole or vancomycin.

If very severe, may need surgery to remove colon

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130
Q

Clostridioides difficile: prevention options

A

Good hygiene, especially patient toilets, restrict risk antiobiotics. No vaccine

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131
Q

Clostridioides difficile: why relapse

A

endospores not killed by antibiotics, can lie dormant.

Prevented by restoring normal gut flora. e.g using transplant of gut bacteria from healthy individuals

132
Q

Most common cause of microbial cause of diarrhoea in NZ

A

Camplybacteriosis

133
Q

Clostridioides difficile: mutation

A

Europe, australia. Resistant to fluoroquionlones, produces more toxins A and B because of a mutation in a toxin repressor gene and exhibits a higher rate of sporulation

134
Q

Major causes of community acquired UTIs

A

E.coli most common. Proteus mirabilis, Klebsiella pneumoniae and Staphlococcus saprophyticus

135
Q

Major causes of hospital acquired UTIs

A

E.coli, Enteric bacteria (Klebsiella) , Proteus, Staphylococci, Pseudomonas, Enterococci

136
Q

UPEC: general info

A

Uropathogenic Escherichia coli (UPEC). Oxidase negative, gram negative rod.

137
Q

UPEC: source

A

Colonic flora of patient

138
Q

UPEC: route of transmission

A

Faecal matter to vagina/urethra

139
Q

UPEC: risk factors for infection

A

Being female, (shorter route), previous UTI, antibiotics that deplete competitive vaginal flora, poor hygiene, anatomical conditions

140
Q

UPEC: virulence factors

A

Colonisation: pilli, type 1, for colonisation of bladder, pap pilli for kidneys

Immune evasion: invasion of bladder mucosa

Proliferation: Siderophores for iron acquisition

Damage: LPS for inflammation, toxins, (Cytolysins, contribute to immune cell killing)

Progression of symptoms: Cystitis (urinary bladder infection, urgerncy, frequency, hesitation, dysuria), maybe blood in urine. Pyelonephritis (more serious kideny infection) key new symptom of flank pain (pain higher up)

141
Q

UPEC: identification and diagnosis of cystitis

sample tested

A

urine

142
Q

UPEC: identification and diagnosis of cystitis

Microscopy

A

G-rods, neutrophils

143
Q

UPEC: identification and diagnosis of cystitis

Culture:

A

CLED agar (yellow colonies); MacConkey agar red colonies with zone of precipitations > 105 CFU/ml

144
Q

UPEC: identification and diagnosis of cystitis

Further tests:

A

MALDI-TOF (biochemical tests to distinguish from other lactose fermenters). Urine dipstick Nitrite (bacteria in urine). Leukocyte esterase (WBC in urine)

145
Q

UPEC: cystits

How can we treat the symptoms

A

Fluids, pain relief

146
Q

UPEC: Cystitis

Antibiotics:

A

Probably, but if mild may not be needed. Trimethoprim, Sulfamethoxazole and Trimethoproim, fluroquinolones

147
Q

UPEC: Cystitis

Options in most severe cases

A

Fluids, pain relief, antibiotics

148
Q

UPEC: cystitis

Prevention options

A

Fluids, go to toilet, good hygiene, various remedies that work some people

149
Q

UPEC: pyelonephritis

Sample tested:

A

Add blood to samples tested

150
Q

UPEC: pyelonephritis

Microscopy: Culture: Further tests:

A

As cystitis

151
Q

UPEC: pyelonephritis

Antibiotics

A

Yes, need to kill infecting bacteria before do damage to kidenys

152
Q

UPEC: pyelonephritis

Prevention options

A

Effective treatment of cystitis

153
Q

Hospital acquired UPEC

Source:

A

Patients colonic flora

154
Q

Hospital acquired UPEC

Route of transmission

A

Bacteria from faecal matter travels via catheter to bladder

155
Q

Hospital acquired UPEC: Risk factors for infection

A

Urinary catheter, with risk increasing each day

156
Q

Hospital acquired UPEC: key virulence factors

A

As cystitis

colonisation: biofilm forms on catheter

157
Q

Hospital acquired UPEC:

Progression of symptoms

A

As cystitis, but patient may be less likely to notice as not going to toilet. Bad and urine collected will be cloudy

158
Q

Hospital acquired UPEC: sample tested

A

Urine collected, catheter tip, blood

159
Q

Hospital acquired UPEC: Treatment options

A

Remove catheter, fluids, pain relief

160
Q

Hospital acquired UPEC: antibiotics

A

Yes

161
Q

Hospital acquired UPEC: Prevention options

A

Remove catheter when not needed

162
Q

Mutations: E. coli UTI

A

E.coli and other members of the enterobacteriaciae carry plasmids with antibiotic resistance specifically to penicllin, cephalosporin and in some carbapenemases. Some hospitals have a large problem with these bacteria, and screen patients on admision so colonised patients, can be segregated from uncolonised patients. Treat with polymyxin B or E.

Monitor renal toxicitiy to polymyxin.

163
Q

How does Ebola work?

A
  1. Attachment of glycoprotein to TIM-1 receptor on epithelial cells lining respiratory tract, conjuctiva around eyes, skin or body.
  2. Pentration: Viral envelope fuses with host cell, passes into cytoplasm
  3. Uncoating: Viral envelope releases nucleic acid. Polymerase protein turns negative-sense RNA into postive sense mRNA template.
  4. Translation: mRNA uses host-cell systems to replciate viral RNA
164
Q

Ebola: source

A

From bats to animals to humans

165
Q

Ebola: symptoms

A

Fever, headache, weakness, sore throat, joint and muscle pains

followed by vomiting, diarrhoea, stomach pain, impaired kidney and liver function

sometimes: both internaly and external bleeding, sometimes rash, red eyes and hiccups.

166
Q

Ebola: mortality rate

A

25-100%

167
Q

Ebola treatment:

A

Monoclonal antibodies, fluids and electrolytes, support other infections and symptoms

Vaccination but not that effective

168
Q

Main cellular properties of yeasts

A

Germ tube, pseudohypa, hypa

Germ tube forms in less that 2hrs in serum broth for candida albicans

169
Q

Main cellular properties of moulds

A

Conidia used in asexual reproduction

Ascophore used in sexual reproduction

170
Q

Skin infections associated with yeasts and moulds

A

Ringworm and tinea

Dermatophytes: microsporum, trichophyton, epidermophyton

171
Q

Mucosal infections associated with yeasts and moulds

A

Thrush

Candida albicans

172
Q

Invasive infections associated with yeasts and moulds

A

Sepsis, meningitis, pneuomonia

(SiMP)

Candida, Cryptococcus, Aspergillus

173
Q

Yeasts and moulds associated with exacerbation of asthma

A

Penicllium, Aspergillus, Cladosporium

174
Q

Mechanism of the antifungal drug Azole

A

FLU inhibits ergosterol biosynthesis resulting in depletion of this sterol in the cell membrane

175
Q

Mechanism of the antifungal Polyene

A

Pore/channel fomred in Arn8 results in cell death

176
Q

Mechanism of the antifungal Candins

A

Candin inhibits fungal glucan synthase

177
Q

Mechanism of antifungal 5-Fluorocytosine

A

Inhibition of protein and DNA synthesis

178
Q

Cutaneous mycoses (Fungal): source

A

Humans (trichophyton and epidermophyton) and Animals, esp Pets (Microsporum)

179
Q

Cutaneous mycoses (Fungal): route of transmision

A

direct contact, sometimes via fomties

180
Q

Cutaneous mycoses (Fungal): risk factors

A

small abrasions, humidity, diabetes

181
Q

Cutaneous mycoses (Fungal): symptoms

A

Itchiness, distinctive appearance

182
Q

Cutaneous mycoses (Fungal): identification and diagnosis

A

Microscopy and agar growth. May fluorescence under black light (UV-A)

183
Q

Cutaneous mycoses (Fungal): sample tested

A

hairs, skin scraping from infected areas

184
Q

Cutaneous mycoses (Fungal): treatment options

A

Antifungal creams and systemic treatment for severe cases or onychomycosis (nail infection). Imidazoles and synthetic allyamines

185
Q

Cutaneous mycoses (Fungal): prevention options

A

Infection can be avoided by lifestyle and hygiene modifications such as avoiding walking barefoot on damp floors particularly in communal areas. Avoid contact. Dry between toes. Treat ringworm in pets and avoid contact. Avoid or prevent chaffing.

186
Q

Candidiasis/thrush (Fungal mucosal infection): source

A

mucosal flora

187
Q

Candidiasis/thrush (Fungal mucosal infection): route of transmission

A

contact with carrier (overgrowth, a dysbiosis)

188
Q

Candidiasis/thrush (Fungal mucosal infection): risk factors

A

antibiotic use depleting competitive flora, immunosupression

189
Q

Candidiasis/thrush (Fungal mucosal infection): identification and diagnosis

A

microscopy (germ tube/ hypae); selective agars, e.g CHROMagar Candida (green/blue colonies)

190
Q

Candidiasis/thrush (Fungal mucosal infection): sample tested

A

Swab/scrape

191
Q

Candidiasis/thrush (Fungal mucosal infection): Treatment options

A

Nystatin (oral suspension); Imidazole (lozenge, suppository, pessary); fluconzaole (DiFlucan)

192
Q

Candidiasis/thrush (Fungal mucosal infection): prevention options

A

Prophylactic drug, espeically if in risk group/recurrent

193
Q

Invasive aspergillosis (Fungal systemic): source

A

soil, compost, built environment growth of mould

194
Q

Invasive aspergillosis (Fungal systemic): route of transmission

A

airborne conidia

195
Q

Invasive aspergillosis (Fungal systemic): Risk factors

A

Previous lung infection, immunosuppression (transplant, HIV cancer treatment)

196
Q

Invasive aspergillosis (Fungal systemic): symptoms

A

lung infection, possible spread to other organs (pain and loss function effects)

197
Q

Invasive aspergillosis (Fungal systemic): identification and diagnosis

A

Microscopy, culture, PCR, Galactomannan EIA

198
Q

Invasive aspergillosis (Fungal systemic): Sample tested

A

Biopsy

199
Q

Invasive aspergillosis (Fungal systemic): Treatment options

A

IV imidazoles (voriconazole)

200
Q

Invasive Candida (Fungal systemic): source

A

mucosal infection, injected drugs

201
Q

Invasive Candida (Fungal systemic): Route of transmission

A

penetrate weakened mucosal defences, injected

202
Q

Invasive Candida (Fungal systemic): Risk factors

A

Immunosuppresion, IV drug use (can also cause damage for yeast to easily colonise)

203
Q

Invasive Candida (Fungal systemic): symptoms

A

Sepsis

204
Q

Invasive Candida (Fungal systemic): Sample tested

A

Blood/biopsy

205
Q

Invasive Candida (Fungal systemic): Treatment options

A

Fluconazole, alternative is echinocandin

206
Q

Invasive Candida (Fungal systemic): Prevention options

A

Treat mucosal infection, discourage drug use

207
Q

Crytococcal meningitits (Fungal systemic): source

A

basidospores in bird (pigeon) faeces

208
Q

Crytococcal meningitits (Fungal systemic): Route of transmission

A

aerolised basidospores

209
Q

Crytococcal meningitits (Fungal systemic): Risk factors

A

contact with source, immunosuppresion

210
Q

Crytococcal meningitits (Fungal systemic): Identification and diagnosis

A

microscopy (encapsulated yeast), culture, crypotococcal antigen test (EIA)

211
Q

Crytococcal meningitits (Fungal systemic): Sample tested

A

Sputum for lung colonisation, CSF (meningitis)

212
Q

Crytococcal meningitits (Fungal systemic): Treatment options

A

Amphotericin B (intrathecal), 5-flurocytosine (IV or oral) but may be toxicity issues

213
Q

Crytococcal meningitits (Fungal systemic): Prevention options

A

avoid contact with source

214
Q

Exacerbation of conditions Asthma: Source, aeitology, prevention options

A

Growth in homes, allergic reaction to inhaled conidia, good quality housing

215
Q

General STI transmission

A

Require intimiate contact for transmission

Require persistent infection to allow for occasional opportunites for transmission

May remain as local infection or may disseminate

May be an important cause of neonatal disease

216
Q

Important bacterial STIs

A

Chlamydia, Gonorrhoea, Syphillis

217
Q

Important Viral STIs

A

Human papilloma virus, Herpes simplex, HIV

218
Q

Important fungal STIs

A

Candidiasis

219
Q

Important Protozoal STIs

A

Trichomonas

220
Q

Urethritis

A

Inflammation of urethra, can be purulent

221
Q

Cervicitis

A

Inflammation of cervix, can be purulent

222
Q

Epididymis complications

A

Inflammation of epididymis, chronic pain, infertility, hypogonadism, defective hormone production

223
Q

Pelvic inflammatory disease

A

Inflammation of uterus, fallopian tubes, ovaries

Chronic pelvic pain, ectopic pregnancy, infertility

224
Q

Gonorrhoea: causative agent

A

Neisseria gonorrhoeae, second most prevalent bacterial STI

225
Q

Gonorrhoea: transmission

A

Transmitted during vagina, oral and anal sex

Female to male = 20% / episode

Male to female = 50% episode

Can be passed to baby during childbirth

226
Q

Gonorrhoea: asymptomatic

A

>50% woman

~5% men

227
Q

Gonorrhoea: symptoms

A

Pain and inflammation/burning during urination

If untreated can lead to systemic dissemination

Skin pustules

Septic arthritis

Meningitis

Endocarditis

Pelvic inflammatory disease

Septic abortion
Infertility

228
Q

Gonorrhoea: is it notifiable?

A

Yes, rates higher than UK and Australia

229
Q

Gonorrhoea: treatment

A

Penicillin initially very effective (MIC < 0.01mg/L)

Accumulation of mutations in porins, acquisition of gene for new transpeptidase made it resistant

Plasmid with gene for beta lactamase too

Ciprofloxacin treatment initally very effective

Recommended treatmnet = Intramuscular ceftriaxone with oral azithromycin

230
Q

Gonorrhoea: coinfection

A

20% of heterosexual men also have chlamydia

40% of heterosexual women also have chlamydia

231
Q

Syphilis: causative agent

A

Treponema pallidum

232
Q

Syphilis: is it notifiable

A

Yes

233
Q

Syphilis: initial infection

A

Chancre (painless ulcer that heals spontaneously)

234
Q

Syphilis: secondary disease

A

If untreated develop secondary disease in 2-8 weeks. Bacteraemic dissemination = widespread rash

Rash, fever, malaise, aseptic meningitis, hepatitis, etc

Relapses then “recovery” over 1-4 years

If untreated 1/3 develop tertiary disease years later, small vessel vasculitis = inflammation of blood vessels affecting brain and aorta

235
Q

Syphillis: pregnancy

A

Untreated syphilis during pregnancy always results in foetal infection. Half of pregnancies will end in miscarriage or stillbirth

236
Q

Syphilis: treatment

A

Penicillin - no resistance

Effective blood level required for at least 7 days

Intramuscular benzathine penicillin

Penicillin G IV for 10 days

237
Q

Chlamydia: causative agent

A

Chlamydia trachomatis

238
Q

Chlamydia: two diffferent classification

A

A-K serovars classified by prominent outer membrane protein ompA

Occulogenital strains infect epithelial cells of either genital tract or inner eyelids

239
Q

Chlamydia: LGV

A

Lymphgranuloma venereum (LGV) - infect macrophages, spread through lymph nodes. Predominantly gay sex, buboes in groin. Protocolitis (inflammation) of colon and rectum

240
Q

Chlamydia: Genital serovars

A

Transmitted through vaginal, oral and anal sex. Can be passed during childbirth.

>70% of women asymptomatic

~25% of men asymptomatic

241
Q

Chlamydia: treatment

A

Single dose of azithromycin, or doxycycline 100mg twice daily for 7 days

242
Q

Chlamydia: untreated women

A

If untreated can lead to pelvic inflammatory disease in ~50% of asymptomatic women. = infection of uterus, fallopian tubes, ovaries, chronic pelvic pain, ectopic pregnancy, infertility

243
Q

Chlamydia: untreated neonates

A

Conjunctivitis and potentially blindness and pneumonia in babies born vaginally to infected women

244
Q

Chlamydia: untreated men

A

Pain, swelling, inflammation of epididymis and testes, urethritis, reactive arthritis and infertility

245
Q

Chlamydia: elementary body

A

metabolically inactive but highly infectious

246
Q

Chlamydia: reticulate body

A

metabolically active and replicative form

247
Q

Chlamydia: cycle of bodies

A

Reticulate body begins to divide, T3SS needles penetrate inclusion membrane to secrete effectors. Infectious elemenary boides escape by cell lysis or extrusion to initiate new infection. Reticulate bodies diffrentiate back into elementary bodies

248
Q

Tuberculosis: causative agent

A

Mycobacterium tuberculosis

249
Q

Tuberculosis: most commonly presents

A

Most commonly presents as a lung disease but can become disseminiated throughout the body

250
Q

Tuberculosis: General information

A

Complex lipid-rich cell wall

Acid fast bacilli (AFBs)

Grows very slowly

Resistant to common antibiotics

Lives inside macrophges

251
Q

Tuberculosis: transmission

A

Bacilli inhaled as droplets

droplets survive for hours

Infectious dose is <5 bacilli

Droplets settle in alveolus

252
Q

Tuberculosis: Granulomas

A

Bacilli are engulfed by alveolar macrophges. Infected macrophages recruit additional macrophages and other immune cells to form organised structures called granulomas. Believed to require adaptive immunity.

253
Q

Tuberculosis: Why are granulomas important?

A

For restricting bacterial expansion

254
Q

Tuberculosis: what happens?

A

Most infections are asymptomatic

10% lead to active disease

Actove disease is when bacteria are infectious

If untreated death rate is 50%

255
Q

Tuberculosis: Symptoms

A

Quartet of symptoms: weight loss, night sweats, fever, malaise

(We never fuck mums)

256
Q

Tuberculosis: Who gets the disease?

A

2 billion people infected

>10 million active cases

>9 million new cases/year

>1.3million deaths/year

257
Q

Tuberculosis: HIV

A

20x more likely to get TB, 10% of TB cases are HIV+.

Major benefits of Anti Retroviral Therapy (ART) in terms of TB risk and mortality

258
Q

Tuberculosis: Risk factors

A

Born outside NZ, reside with someone who was born outside NZ

259
Q

Tuberculosis: Vaccination

A

M. bovis Bacille Calmette Guerin (BCG)

Derived from virulent isolate of bovine tuberculosis

Lost important virulence factors

Efficacy ranges 0-80%,

only effective during childhood

Risk of disseminated infection in HIV+ infants (BCGosis)

260
Q

Tuberculosis: Diagnosis, Chest x-ray

A

Cloudiness (granulomas) and caving formation seen

Cheap but can’t tell if they’re infectious

261
Q

Tuberculosis: Diagnosis, microscopy

A

Ziehl-Neelsen sputum stain

262
Q

Tuberculosis: Diagnosis, Gene Xpert

A

PCR based, Detects organism in sputum, detects resistance markers

263
Q

Tuberculois: interferon testing

A

Detect release of interferon by lymphocytes in reponse to mycobacterial antigens. Can’t distinguish between latent infection and disease

264
Q

Tuberculosis: Mantoux test

A

Tuberculin, purified protein derivative, cell wall extract of Mtb

Lymphocytes in person previously exposed will migrate causing lump.

>5mm = +

Can’t distinguish between vaccination and infection

265
Q

Tuberculosis: Quantiferon Gold testing

A

Tube with Mtb specific antigen, add patient blood, lymphocytes previously exposed to Mtb will release interferon. Can’t distinguish between latent and old infection

266
Q

Tuberculosis: Treatment

A

Multidrug regiments for 6 months to stop resistance emerging

Two month intensive phase:

Isoniazid, Rifampicin, Pyrazinamide, Ethambutol

(I really pluck eggs)

Four month continuation phase:

Insoniazid, Rifampicin

267
Q

Tuberculosis: MDR

A

Resistant to isoniazid and rifampicin, mainly from India, China and Russia

268
Q

Tuberculosis: MDR treatments

A

Group A first, then B, then C

269
Q

Tuberculosis: XDR TB

A

Pre-XDR-TB = resistant to rifampicin and any fluroquinolone

XDR-TB = resistant to rifampicin, any fluroquinolone, and at least one of bedaquiline or linezolid

270
Q

Tuberculosis: Control

A

Eliminate poverty, control animal TB, isolation of infectious patients, Better diagnosis, faster drug treatment with more tolerable drugs

271
Q

Tuberculosis: COVID

A

TB decreased since COVID pandemic

272
Q

Louis Pasteur

A

Pasteur was able to show that air contained spores of living organims

When placed into nutrient broth the organisms reproduced

When he now boiled the broth in a special swan necked contained that allowed air but kept dust out the broth remained free of organisms

This simple experiment helped disproved the theory of spontaneous generation

273
Q

Bacterial growth Kinetics

A

Check image on desktop

274
Q

Obligate aerobes

A

Required O2, no fermentation, e.g mycobacterium tuberculosis

275
Q

Obligate anaerobes

A

cannt survive in presence of oxygen (e.g clostridium tetani)

276
Q

Facultative anaerobes

A

can metabolise energy aerobically (respiration) or anaerobically (fermentation). Prefer O2 as more ATP is produced, e.g E.coli

277
Q

Microaerophiles

A

Require oxygen (no fermentation), but cannot survive in higher concentrations of O2 (e.g Helicobacter pylori)

278
Q

Aerotolerant bacteria

A

cannot ulilise O2 (fermentation only) but are not harmed

279
Q

Cell wall morphology

A

Check images

280
Q

Indigenous microflora

A

All micobes (bacteria, fungi, protozoa) that reside on or within a person

A fetus has no indigenous microflora

281
Q

Bacteria on our skin

A

1 trillion

most common: Staphylococcus, Streptococcus and Corynebacterium

Metabolise sweat to produce body odor

282
Q

Oral streptococci

A

Biofilms of bacteria 300 to 500 cells thick on surface teeth

Dental plaque (mostly Streptococcus sanguis and S.mutans)

283
Q

Firmicutes and Bacteroidetes in the gut

A

>>500 species of bacteria, weighing about 3.3 pounds

They break down carbohydrates, make essential nutrients like

vitamins K & B12 and crowd out harmful bacteria

284
Q

Vaginal flora

A

beneficial bacteria (Lactobacillus family)

Secrete lactic acid (protect against hostile invaders like the pathogenic yeast Candida albicans (vaginal thrush)

285
Q

HPV

A

Persistent (latent) virus infections

virus lies dormant within the cell

>100 types can infect humans, causing a variety of warts

other viruses, herpes virus, chickenpox virus

286
Q

Fossil viruses

A

about 1/12 of our genome consists of stretches of DNA from viruses that infected our ancestors millions of years ago

287
Q

Symbiosis

A

organsims in live together in close association

288
Q

Mutualism

A

beneficial to both symbionts

289
Q

Neutralism

A

neither symbiont is affected by relationship

290
Q

Commensalism

A

beneficial to only one symbiont

291
Q

Parasitism

A

harmful to one symbiont (host), beneficial to other symbiont (parasite)

292
Q

Synergism

A

two or more microorganisms “team up” to cause disease. Synergisitic or polymicrobial infection

293
Q

Pathogen

A

Microorganism that cause disease <3%

294
Q

Opportunistic pathogen

A

has the potential to cause disease

295
Q

Bacterial portals of entry

A

See folder

296
Q

Koch’s postulates

A

The microorganism must always be found in similarly diseased animals but not in healthy ones

The microorganism must be isolated from a diseased animal and grown in pure culture

The isolated microorganism must cause the original disease when inoculated in a susceptible host

The microorganisms must be re-isolated from the experimentally infected animals

297
Q

Koch’s postulate - revised

A

Original postulates were based on cholera and TB

P1: should be abandoned, as some organisms can be carried asymptomatically

P2: some organisms cannot be grown in culture

P3: ‘must’ is replaced by ‘should’ as infection by certain organism does not always cause disease

298
Q

Incubation period

A

time between infection and onset of symptoms

299
Q

Prodomal period

A

Patient feels out of sorts, but no disease symptoms

300
Q

Illness

A

Experience of symptoms associated with disease

301
Q

Convalescent period:

A

time during which patient recovers

302
Q

Passive carrier

A

Never had the disease

303
Q

Incubatory carrier

A

during incubation period

304
Q

Convalescent carrier

A

recovering from disease

305
Q

Active carrier

A

completely recovered

306
Q

Localised infection:

A

pathogens are contained at site of infection (e.g abscess)

307
Q

Systemic infection:

A

pathogen spreads throughout the body

308
Q

Acute infection

A

rapid onset and rapid recovery

309
Q

Chronic infection

A

slow onset and slow recovery

310
Q

Latent infection:

A

Pathogen not completely eradicated after recovery and can cause symptoms in future

(ex. herpes, chickenpox, tuberculosis,…)

311
Q

Secondary infection:

A

Disease that follows primary infection (ex pneumonia after mild respiratory infection)

312
Q

Infectious disease vs microbial intoxication

A

Check folder

313
Q

Staphylococcus aureus: Treatment

A

Penicillin/amoxicillin - work well against Streptococcus pyogenes, but most S.aureus are resistant

Augmentin - amoxicillin plus B-lactamase inhibitor

Flucloxacillin - B lactamase resistant penicillin, works well against S.pyogenes and S.aureus except MRSA

Vancomysin: used against MRSA (avoid use against MSSA to prevent development of resistant strains (‘last resort drug’)

314
Q

Invasin

A

intracellular growth

resistance to antiobiotics

protection from immune system

315
Q

Cytolysins

A

Destroy ery, leukocytes and tissue cells

access to nutrients

immune evasion

bacterial spreading

316
Q

B-lactamase resistant penicillins

A

Methicillin, oxacillin, flucoxacillin

Cluvanic acid: B-lactamase inhibitor

Augementin = amoxicillin + clavulanic acid

317
Q

S.aureus: Corneal ulcer

A

Deep infection of the cornea

Usually after abrasion e.g contact lenses

Can be caused by S.aureus, but also several other bacteria, viruses and fungi

318
Q

Outbreak

A

sudden increase in occurence

319
Q

Pandemic

A

Outbreak that has spread across a wide region

320
Q

Endemic

A

Cases at a baseline level in a geographic area

321
Q

R0

A

Infectiousness, determined by organism, dose, route of tranmission

322
Q

Reff

A

Effective R, take into account public health measures like vaccination

323
Q

Infection fatality rate

A

Estimated deaths as a proportion of all infected

324
Q

Case fatality rate

A

Death as a proportion of confirmed cases

325
Q

How is Ebola spread?

A

Bodily fluids of a person who is sick or has died from Ebola

Objects contaminated with the virus

Infected animals

MEDSCI 202 (3 decks)

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