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Phase 2A > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Define pathogen

A

Disease-causing organism

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2
Q

Define commensal

A

Organism which colonises the host but causes no disease in normal circumstances.

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3
Q

Define opportunist pathogen

A

Microbe that only causes disease if host defences are compromised

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4
Q

Define virulence/pathogenicity

A

The degree to which a given organism is pathogenic

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5
Q

Define asymptomatic carriage

A

When a pathogen is carried harmlessly at a tissue site where it causes no disease.

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6
Q

What are the 4 main types of bacteria?

A

Cocci - unicellular, spherical or elliptical shape and either remain single-cellular or aggregate in various configurations
Rods/Bacilli - rod-shaped bacteria which either remain singly or form chains.
Vibrio - curved, comma-shaped single bacteria
Spirochaete - spiral-shaped bacteria with terminal flagella

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7
Q

Define endotoxin

A

component of outer membrane of gram -ve bacteria - lipopolysaccharide.

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8
Q

Define exotoxin

A

secreted proteins of gram +ve and gram -ve bacteria. Can inhibit and stimulate the nervous system.

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9
Q

What are three ways bacteria mutate?

A
  • base substitution
  • deletion
  • transfer
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10
Q

What are 3 ways bacteria undergo gene transfer?

A
  • transformation
  • transduction
  • conjugation
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11
Q

What are the steps of performing a gram stain?

A
  • Apply primary stain such as crystal violet (purple) to heat fixed bacteria
  • Add iodine which binds to crystal violet and helps fix it to the cell wall
  • Decolourise with ethanol or acetone
  • Counterstain with safranin (pink)
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12
Q

What is the result of a gram stain on gram -ve bacteria?

A

Stains pink due to the thin layer of peptidoglycan (high lipid content) in the cell wall.

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13
Q

What is the result of a gram stain on gram +ve bacteria?

A

Gram + ve bacteria retain purple colour of crystal violet due to their cell wall composed of a thick layer of peptidoglycan.

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14
Q

What are the typical features of bacteria?

A
  • outer membrane, inner membrane, chromosomes or nuclear membrane
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15
Q

What environment do bacteria survive in?

A

temp: < -80oC -> 80oC temp
pH: <4-9
water/dessication: 3 hours to 3 months (>50 years for spores)
Light: UV

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16
Q

What are 3 species groups of obligate intracellular bacteria?

A
  • Rickettsia
  • Chlamydia
  • Coxiella
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17
Q

What are the mollicutes?

A

bacteria cultured on artificial media with no cell wall (e.g. mycoplasma pneumoniae, M. hominis, ureaplasma urealyticum)

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18
Q

What are 3 species groups of bacteria that can be grown on artificial media, have a cell wall and grow as filaments?

A
  • Actinomyces
  • Nocardia
  • Streptomyces
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19
Q

What are 3 species groups of spirochaetes (can be grown on artificial media, have a cell wall and grow as single cells)?

A
  • Leptospira
  • Treponema
  • Borrelia
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20
Q

Describe the characteristic features of gram positive bacteria

A
  1. single membrane
  2. large peptidoglycan area
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21
Q

Describe the charateristic features of gram negative bacteria

A
  1. Double membrane
  2. Small peptidoglycan area
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22
Q

What bacterial species are examples of gram negative cocci?

A

Aerobic = veillonella
Anaerobic = neisseria

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23
Q

What bacterial species are examples of aerobic gram positive cocci?

A
  • Staphylococcus
  • Streptococcus (beta-haemolytic, alpha-haemolytic, non-haemolytic, enterococcus)
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24
Q

What bacterial species are examples of anaerobic gram positive cocci?

A

Peptostreptococcus

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25
Q

What are Ziehl-Neelsen stain positive rods?

A

Mycobacteria

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26
Q

What are examples of anaerobic gram positive rods?

A
  • Clostridium
  • Propionibacterium
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27
Q

What species are aerobic gram positive rods?

A
  • Corynebacterium
  • Listeria
  • Bacillus
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28
Q

What species are anaerobic gram negative rods?

A

Bacteriodes

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29
Q

Which species are aerobic gram negative rods?

A

Vibrio
Coliforms (Escherichia, Klebsiella, Enterobacter)

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30
Q

What is the difference between streptococci and staphylococci?

A

Streptococci are organised in chains of bacterial cells and staphylococci are arranged in clusters.

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31
Q

What is the main treatment for staphylococcus aureus infection?

A

Flucloxacillin

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32
Q

Give an example of a slow growing bacteria

A

TB

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33
Q

Give an example of a fast growing bacteria

A

E.coli and S.aureus

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34
Q

Name 5 infections caused by S.pyogenes?

A
  • Tonsilitis
  • Otitis media
  • Impetigo
  • Cellulitis
  • Scarlet fever
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35
Q

Define nosocomial

A

Hospital-aquired

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36
Q

Describe the Ziehl-Neelson stain test.

A

Used to distinguish acid-fast bacilli (e.g. mycobacterium) from non acid-fast bacilli (e.g. E.coli).
Acid-fast bacteria will turn red with ZN stain whereas non acid-fast will turn blue.

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37
Q

Describe the catalase test

A

Used to differentiate between staphylococci and streptococci.
H2O2 is added to bacteria and a positive reaction results in bubbling.
Staphylococci are catalase positive and streptococci are catalase negative.

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38
Q

Describe the coagulase test.

A

Coagulase is an enzyme produced by staphylococcus aureus that converts soluble fibrinogen in plasma to insoluble fibrin resulting in clumping. All other staphylococci are coagulase negative so do not demonstrate clumping.

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39
Q

Describe the haemolysis test.

A

Used to classify streptococci.
Haemolysis is the ability of bacteria to break down RBCs in blood agar.
Alpha haemolytic bacteria cause partial destruction of red blood cells so the blood agar around the colony becomes a green-brown colour. (e.g. strep. pneumoniae, strep. viridans)
Beta haemolytic bacteria cause complete lysis of RBCs resulting in the agar around the colony becoming clear and colourless. (e.g. strep pyogenes)

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40
Q

How can beta haemolytic bacteria be further distinguished?

A

Lancefield grouping (detection of surface antigens)
A, C, G - tonsilitis + skin infections
B - neonatal sepsis + meningitis
D - urinary tract infection

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41
Q

Describe the optochin test

A

Used to differentiate between streptococci.
Streptococcus pneumoniae is sensitive to optochin and so the test results in a clear zone around the optochin disc.
Viridans streptococci and other alpha haemolytic streptococci are optochin resistant and will grow around the disc.

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42
Q

Describe the oxidase test

A

Used to test whether the micro-organism contains a cytochrome oxidase (an enzyme of the bacterial electron transport chain).
All bacteria that are oxidase positive are aerobic and oxidase negative bacteria could be aerobic or anaerobic.
Oxidase positive bacteria turns blue and oxidase negative bacteria show no change.

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43
Q

Describe the Macconkey agar test.

A

Differentiates between lactose-fermenting and non-lactose fermenting gram negative bacilli.
Lactose-fermenting bacteria will produce lactic acid and turn the indicator in the agar from white/yellow to pink/red. (e.g. E. coli)
Non lactose-fermenting bacilli will not produce acid and appear white/transparent. (e.g. salmonella)

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44
Q

What are 6 infections caused by E.coli?

A
  • Wound infections
  • UTIs
  • Gastroenteritis
  • Traveller’s diarrhoea
  • Bacteraemia
  • Meningitis
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45
Q

Name 3 infections caused by salmonella

A
  • Gastroenteritis
  • Enteric fever (typhoid fever from drinking poor quality water)
  • Bacteraemia
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46
Q

Describe the XLD test.

A

Xylose lysine deoxycholate agar is a very selective gorwth medium used to differentiate Salmonella and Shigella spp. Both colonies are red and can be differentiated by a hydrogen sulphide indicator. Salmonella spp. produce hydrogen sulphide and are initially yellow, then turn pink/red with black centres. Shigella spp. do not and therefore remain pink/red.

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47
Q

What is an API strip?

A

Analytic profile index strips consist of a series of 20 mini test-chambers containing dehydrated media which are used to distinguish enterobacteriaceae.

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48
Q

What are the sterile sites of the body? And examples of infections of these sites

A

Blood (sepsis)
CSF (meningitis)
Pleural fluid (pericarditis, pleural effusion)
Perineum (Spontaneous bacterial peritonitis)
Joints (septic arthritis)
Urinary tract (UTIs)
Lower respiratory tract (TB + pneumonia)

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49
Q

Define virus

A

An infectious, obligate intracellular (cell-dependent) parasite comprising genetic material (DNA or RNA) surrounded by a protein coat and/or a membrane.

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50
Q

Describe how viruses replicate.

A
  1. Receptor binding - virus binds to receptor on host cell
  2. Host cell invasion - viral core carrying nucleic acid and some associated proteins enters host cell
  3. Viral replication - virus interacts with host cell and uses its enzymes, amino acids and nucleotides to replicate and form new virus particles.
  4. New virus release - the new virus particles are then released from the cell causing the cell to die.
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51
Q

What is the humoral response to viruses?

A
  • antibodies (IgG, A, M) - block binding and virus-host cell fusion, also involved in opsonisation
  • IgM antibodies agglutinate viral particles
  • Complement proteins cause opsonisation and lysis of infected cells
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52
Q

What is the cell-mediated response to viral infection?

A
  • IFN from Th or Cytotoxic T cells - block virus replication
  • Cytotoxic T cells can kill infected cells
  • NK cells and macrophages are involved in antibody-dependent cellular cytotoxicity (ADCC)
  • IFN induces anti-viral proteins for bystander cells
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53
Q

Which viruses cause direct cell cytotoxicity and to which cells?

A
  • Influenza/RSV virus - respiratory epithelium
  • Varicella Zoster virus - skin cells
  • Yellow Fever virus - liver cells
  • HIV – Th cells
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54
Q

How do viruses evade the immune system?

A
  • Influenza - changes coat antigen
  • Rhinovirus, HIV - show antigenic variation
  • Mumps, measles, EBV, HIV, CMV - cause immune suppression by altering or destroying lymphocytes/macrophages
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55
Q

How does the influenza virus evade the immune system?

A

Changes in the glycoprotein projections haemagglutinin (HA) and neuraminidase (NA) result in coat variability

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56
Q

Define antigenic drift

A

spotaneous mutations which occur gradually resulting in minor changes in HA (haemagglutinin) and NA (neuraminidase). (epidemics)

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57
Q

Define antigenic shift

A

sudden emergence of a new subtype different to that of preceding virus (pandemics)

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58
Q

What are mycobacteria?

A

Aerobic, non-spore forming, non-motile bacilli with high lipid content and myolic acids in cell wall which makes them gram stain resistant.

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59
Q

What are 5 diseases and the mycobacterial species that cause them?

A

Tuberculosis (TB) - M. tuberculosis
Leprosy - M. leprae
Chronic lung infection - M. kansasii
Disseminated infection in AIDS, chronic lung infection - M. avium complex (MAC)
Buruli ulcer - M. ulcerans

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60
Q

Why are mycobacteria difficult to treat with antibiotics?

A

They are slow growing and have lipid rich cell walls and have multiple drug resistance mechanisms.

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61
Q

What are the 5 stages of rash evolution in chickenpox?

A

Macule - flat reddened area of skin
Papule - raised area of skin
Vesicle - raised spot filled with blister fluid
Pustule - pus filled spot
Crust - spot covered with hardened layer

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62
Q

What are the 2 main approaches to viral diagnosis?

A
  • Viral detection (e- microscopy, PCR)
  • Serology (ELISA, immunofluorescence, complement fixation test)
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63
Q

What is shingles (herpes zoster)?

A

Red, painful rash that is confined to a single dermatome. Caused by reactivation of the varicocella-zoster virus (chickenpox virus)

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64
Q

What is EBV?

A

Epstein-Barr virus is the cause of infectious mononucleosis (glandular fever).
Presents with white/yellowish purulent lining over the tonsils (DDx = s.pyogenes throat infection), cough, fever and splenomegaly.
Diagnosed using blood test (atypical lymphocytes), serology (ELISA test)

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65
Q

How is Eptein Barr virus treated?

A

Fluids and analgesia, avoid contact sports for 6 weeks to prevent splenic rupture.

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66
Q

What is CMV?

A

Cytomegalovirus causes CMV colitis which is gastrointestinal inflammation. It can also cause eye and lung infections or infect the foetus while it’s in the womb.
It is an AIDS defining virus and presents with characteristic owl eye inclusion under the microscope.
Treated with IV ganciclovir (antiviral)

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67
Q

What are protozoa?

A

Single-celled, nucleated organisms of over 30000 species.

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68
Q

What are the 5 major groups of protozoa?

A
  • Flagellates (e.g. Trypanosoma spp)
  • Amoebae (e.g. Entamoeba histolytica)
  • Sporozoa (Toxoplasma gondii)
  • Cilliates (Balantidium coli)
  • Microsporidia
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69
Q

What is malaria?

A

A potentially life-threatening parasitic infection transmitted by female anopheles mosquitos which causes a variety of symptoms.

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70
Q

What are the 5 sporozoite species that cause malaria?

A
  • Plasmodium falciparum (most common, high mortality)
  • Plamodium ovale
  • Plasmodium vivax
  • Plasmodium malariae
  • Plasmodium knowlesi
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71
Q

What are the symptoms of malaria?

A

FEVER
Chills
Headaches
Myalgia
Fatigue
D+V
Abdo pain

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72
Q

What are signs of malaria

A

Anaemia, Jaundice, Hepatosplenomegaly, ‘Black Water Fever’(very dark urine)
*patients will not always “look sick”

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73
Q

What are the steps in the development of malarial infection? (Exo-erythrocytic and erythrocytic cycles)

A
  1. Mosquito bite
    - Sporozoites are injected into blood as mosquito takes up blood
  2. Abdo pain
    - The sporozoites are carried in the blood to liver cells where they enter and form schizonts which rupture forming merozoites which enter the blood stream .
  3. Cyclical fever
    - Merozoites infect erythrocytes and multiply forming schizonts again so the process repeats.
    - This causes death of erthyrocytes and anaemia, jaundice and haemoglobinuria as a result.
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74
Q

How does malaria spread? (sporogonic cycle)

A
  • When an Anopheles mosquito takes a blood meal from a person infected with malaria, gametocytes formed from sporozoites will be ingested.
  • Once in the mosquito’s stomach, the microgametes (male gametocytes) penetrate the macrogametes (female gametocytes) generating zygotes.
  • The zygotes in turn become motile and elongated (ookinetes) which invade the midgut wall of the mosquito where they develop into oocysts.
  • The oocysts grow, rupture, and release sporozoites, which make their way to the mosquito’s salivary glands.
  • These are then injected into the blood of humans bitten by the mosquito.
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75
Q

What are the symptoms of complicated malaria?

A
  • Cerebral - drowsiness, increased ICP, seizures and coma
  • ARDS/Pulmonary oedema - SOB, hypoxia and pulmonary oedema
  • Renal failure - proteinuria, fatigue and haematuria
  • Sepsis
  • Bleeding/Anaemia - epitaxis, abnormal bleeding and worsening anaemia
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76
Q

How is P.falciparum malarial infection different?

A

It causes red blood cells to become more “sticky” and adhere to capillary endothelial walls - this causes obstructed microcirculation which leads to “complicated malaria”

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77
Q

What are the sites of entry for bacterial infection?

A
  • respiratory tract
  • gastrointestinal tract
  • genitourinary tract
  • skin/mucous membrane break
78
Q

What kind of immune response do bacteria induce?

A

A humoral response unless intracellular bacteria which elicits cell-mediated immunity.

79
Q

How does the number of organisms and their virulence determine the defence mechanism which responds?

A

Low number or virulence – phagocytes active
High number or virulence – immune response

80
Q

How do bacteria survive inside the human body?

A
  • Use host nutrients
  • Use novel metabolic pathways
  • Out-compete other microorganisms
81
Q

What is regulated as a result of the ‘two component sensor-kinase’ systems sensing environmental changes and altering gene transcription?

A
  • virulence factors
  • competence to exchange genetic material
  • biofilm formation
  • production of bacteriocins/toxins (to kill other bacteria)
82
Q

How are bacterial toxins classfied?

A
  • Tissue target
  • Molecular action
  • Biological effect
  • Contribution to disease process
83
Q

What is the function of adhesins?

A

Help bacteria to bind to mucosal surfaces

84
Q

What are 4 types of adhesins?

A
  • Fimbriae and pili filamentous proteins e.g. Neisseria gonorrhoeae
  • Non-fimbrial proteins e.g. Fibronectin binding protein of Treponema pallidum
  • Lipid e.g. lipid teichoic acid of Streptococcus pyogenes
  • Glycosaminoglycans of Chlamydia sp.
85
Q

What are biofilms and their function?

A

Extracellular polymeric substances made up of proteins, polysaccharides and DNA. They enable bacteria to stick together on a surface and help protect against antimicrobials.

86
Q

What are the examples of host responses to bacterial infection?

A
  • Block attachment to host cells - IgA
  • Opsonisation, prevents proliferation - Ab C3b
  • Cell lysis, prevents proliferation - complement system
  • Neutralise toxins -
87
Q

What are the stages of the immune response to bacterial infection?

A
  • Sensitisation (1-2 weeks)
  • Th cell activation (DTH*)
  • Second contact – effector phase
  • T(DTH) cells secrete IFN, TNF, IL2
  • Macrophage recruitment
    *Delayed-type hypersensitivity
88
Q

What is delayed-type hypersensitivity?

A

An immune response that occurs through direct action of sensitised T cells when stimulated by contact with antigens.

89
Q

What are 6 ways in which bacteria evade the immune system?

A
  • Secrete protease lyses IgA(s) (Neisseria, HI)
  • Pilli, Antigenic variation (N.gonorrhoea)
  • Secrete adhesion molecules (B.pertussis)
  • Polysaccharide capsule (84 serotypes) prevents phagocytosis (S.pneumoniae)
  • Coagulase, forms fibrin coat around organism (staphylococci)
  • Escape from phagolysosome and can live in cytoplasm (mycobacterium)
90
Q

How does the body respond to protozoan infection?

A
  • IgE elicits an immune response by binding to Fc receptors on mast cells, eosinophils, and basophils, causing degranulation and cytokine release
  • Excessive production of cytokines (TNF) may cause some of symptoms associated with malaria
  • Antibody produced against sporozoites – generates a poor response as sporozoites only present in blood for short time
91
Q

How do protozoa evade the immune system?

A
  • Surface antigen variation (trypanosomes)
  • Intracellular phase
  • Outer coat sloughing
92
Q

How does the body respond to helminth infections?

A

Poor response to helminths:
- IgE reponse by binding to Fc receptors on mast cells, eosinophils and basophils, causing degranulation and cytokine release but not sufficient to kill
- Eosinophil basic proteins are toxic to worms

93
Q

How do helminths evade the immune system?

A

They can establish hyporesponsiveness
- mediated by immunosuppressive T-reg cells
- decreased antigen expression by adult - shielding
- glycolipid/glycoprotein coat (host derived)

94
Q

What are antibiotics?

A

Molecules that work by binding a target site on a bacteria to destroy it or prevent it’s growth.

95
Q

Define antimicrobial

A

Molecules that work by binding a target site on a microorganism (worm, virus, fungus, protozoan, bacterium) to destroy it or prevent further growth.

96
Q

Define bacteriocidal antibiotics

A

Kill bacteria by inhibiting cell wall synthesis, kill >99.9% in 18-24hrs
- useful if poor penetration (endocarditis), difficult to treat infections or if infection needs to be eradicated quickly (meningitis)

97
Q

Define bacteriostatic antibiotics

A

Inhibits the growth of bacteria by inhibition of protein synthesis, DNA replication or metabolism.
Reduce toxin production and Endotoxin surge less likely
Kill >90% in 18-24hrs
Defined as ratio of Minimum Bactericidal Concentration (MBC) to Minimum Inhibitory Concentration (MIC) of >4

98
Q

What are the mechanisms of antibiotic action?

A
  • Disruption of cell membrane function (polymyxins, polyenes)
  • Inhibition of RNA and DNA synthesis (Rifamycin, quinolones, nalidixic acid
  • Inhibition of folic acid metabolism (sulfonamides, trimethoprim)
  • Inhibition of protein synthesis (50S ribosomes - erythromycin, chloramphenicol. 30S ribosomes - tetracyclines, streptamycin, gentamycin)
  • Inhibition of cell wall synthesis (penicillins, cephalosporins, vanomycin, bacitracin)
99
Q

What are the 5 groups of beta lactam antibiotics?

A
  • Penicillins (Penicillin V, Flucloxacillin, Amoxicillin)
  • Cephalosporins (Cefalexin, Ceftriaxone)
  • Carbapenems (Meropenem, Ertapenem, Imipenem)
  • Monobactams (Aztreonam)
  • Glycopeptides (Vancomycin, Teicoplanin)
100
Q

What is the antibiotic action of beta lactams ?

A

They diffuse through the cell wall and bind covalently and irreversibly to the Penicillin Binding Proteins of the cell wall causing disruption of peptidoglycan production and lysis. This results in a hypo-osmotic or iso-osmotic environment.
*Beta lactams are only active against rapidly multiplying organisms

101
Q

Which gram bacteria are more susceptible to B-lactams and why?

A

Gram-negative bacteria are usually less susceptible due to the extra lipopolysaccharide layer that decreases antibiotic penetration of the cell wall.

102
Q

What causes differences in the spectrum and activity of B-lactam antibiotics?

A

They have different relative affinities for different penicillin binding proteins.

103
Q

Why are B-lactams ineffective in the treatment of intracellular pathogens?

A

They poorly penetrate mammalian cells.

104
Q

What are the main antibiotics which inhibit DNA and RNA synthesis?

A

Metronidazole, Ciproflaxin

105
Q

What are the main antibiotics which inhibit the 30S subunit in protein synthesis?

A

Gentamycin, Doxycycline

106
Q

What is the main antibiotic which inhibits the 50S subunit in protein synthesis?

A

Clarithromycin

107
Q

What are the main antibiotics which inhibit folate synthesis?

A

Trimethoprim, Co-trimoxazole

108
Q

What is the aim of antibiotic treatment?

A

To give the body time and support for the immune system to deal with an infection.

109
Q

What is the bacterial agenda?

A
  1. Attach and enter
  2. Local spread
  3. Multiply
  4. Evade host defences
  5. Shed from body
110
Q

What are the consequences of bacterial infection?

A

Direct - destroy phagocytes or cells in which bacteria replicate
Indirect - inflammation (e.g. necrotic cells), immune-pathology (e.g. antibody release)
Toxins - (exotoxin - protein production, endotoxin - gram negative)
Diarrhoea

111
Q

What are the two major determinants of anti-bacterial effects?

A
  • Concentration of antibiotic
  • Time that the antibiotic remains on these binding sites
112
Q

What is the MIC?

A

Mininum Inhibitory Concentration, the lowest concentration (in μg/mL) of an antibiotic that inhibits the growth of a given strain of bacteria.

113
Q

What is the key parameter in time-dependent killing? Give examples of antibiotics which carry out time-dependent killing.

A

The time that the serum concentration is above the MIC during the dosing interval.
- beta-lactams
- clindamycin
- macrolides
- oxazolidinones

114
Q

What is the key parameter in concentration-dependent killing? Give examples of antibiotics which carry out concentration-dependent killing.

A

How high the concentration of antibiotic is above the MIC.
- aminoglycosides
- quinolones

115
Q

How do bacteria resist antibiotics?

A
  • Change antibiotic target
  • Destroy antibiotic
  • Prevent antibiotic access
  • Remove antibiotic from bacteria
116
Q

What are 3 examples of antibiotic resistance by change or masking of the molecular binding site?

A
  1. Flucoxacillin/Methicillin is no longer able to bind the PBP of Staphylococci (MRSA)
  2. Wall components change in enterococci and reduce vancomycin binding (VRE)
  3. Rifampicin activity reduced by changes to RNA polymerase in MTB (Multi Drug Resistant TB)
117
Q

What are 3 examples of antibiotic resistance by destruction of the antibiotic?

A
  1. Beta lactam ring of Penicillins and Cephalosporins hydrolysed by bacterial enzyme ‘Beta lactamase’ - now unable to bind PBP
  2. Staphylococci produce ‘penicillinase’ so penicillin but not flucoxacillin inactivated
  3. Gram -ve bacteria phosphorylate and acetylate aminoglycosides (gentamycin)
118
Q

What are 2 examples of antibiotic resistance by preventing antibiotic access?

A
  1. Pseudomonas aeruginosa modifies the bacterial membrane porin channels so Imipenem is unable to enter
  2. Gram -ve bacteria modify the bacterial membrane porin channels so Aminoglycosides cannot enter
119
Q

What are 2 examples of antibiotic resistance by removal of antibiotic from bacteria?

A
  1. S. aureus or S. pneumoniae have proteins in bacterial membranes which export fluoroquinolones
  2. Enterobacteria have proteins in their membranes which export tetracyclines
120
Q

What is intrinsic antibiotic resistance? Give examples

A

Natural resistance in which all subpopulations of a species will be equally resistant.
- aerobic bacteria are unable to reduce metronidazole to its active form
- vancomycin cannot penetrate outer membrane of gram -ve bacteria

121
Q

What is acquired antibiotic resistance?

A

A bacterium which was previously susceptible obtains the ability to resist the activity of a particular antibiotic. Only certain strains or subpopulations of a species will be resistant.
Occurs by spontaneous gene mutation or horizontal gene transfer.

122
Q

What are the 4 ways in which spontaneous gene mutation comes about?

A
  • new nucleotide base pair
  • change in amino acid sequence
  • change to enzyme or cell structure
  • reduced affinity or activity of antibiotic
123
Q

What are the 3 methods of horizontal gene transfer?

A

Conjugation - sharing of extra chromosomal DNA plasmids
Transduction - insertion of DNA by bacteriophages (viruses that infect bacteria)
Transformation - picking up of naked DNA

124
Q

What is MRSA?

A

Methicillin Resistant Staphylococcus aureus

125
Q

How does S. aureus become MRSA?

A
  • Bacteriophages infect bacteria with Staphylococcal cassette chromosome mec (SCCmec)
  • This contains resistance gene mecA which encodes penicillin-binding protein 2a (PBP2a)
  • MecA confers resistance to all B-lactam antibiotics in addition to methicillin
126
Q

What is VRE?

A

Vancomycin resistant enterococci

127
Q

How do enterococci become vancomycin-resistant?

A
  • Plasma mediated acquisition of gene encoding altered amino acid on peptide chain preventing vancomycin binding
  • Promoted by cephalosporin use
128
Q

What is ESBL?

A

Extended Spectrum Beta Lactamase is an enzyme found in some gram -ve bacterial strains which inhibits antibiotic action by hydrolysing oxyamino side chains of cephalosporins and monobactams.

129
Q

What is AmpC B-lactamase resistance?

A
  • Broad-spectrum penicillin, cephalosporin and monobactam resistance
  • encoded on the chromosome in bacteria such as Citrobacter spp., Serratia marascens, Enterbacter spp.
  • B-lactamase inhibitor resistant!
  • Inducible expression (gene only turned on by antibiotic)
130
Q

What are carbapenems?

A

B-lactam antibiotics which are highly resistant to degradation by B-lactamases or cephalosporinases
- They are often the last resort antibitoics to treat infections by ESBL or AmpC producing organisms of the Enterobacteriacae family

131
Q

Which factors need to be considered when deciding if its safe to prescribe an antibiotic?

A
  • Intolerance, allergy and anaphylaxis
  • Side effects
  • Age
  • Renal and Liver function
  • Pregnancy and breast feeding
  • Drug interactions
  • Risk of Clostridium difficile
132
Q

What are CPEs?

A

Carbapenemase producing Enterobacteriaceae
- most common causes of UTI, intra-abdominal infection.

133
Q

What is Norovirus?

A

Virus affecting the GI tract that causes diarrhoea and vomiting. Is highly contagious with a low infecting dose. Puts patients and staff at risk and is able to persist in the environment.

134
Q

What is Clostridium difficile?

A

A bacterium thats causes chronic diarrhoea and colitis. It produces bacterial spores which can survive outside the host.

135
Q

What is Clostridium difficile?

A

A bacterium thats causes chronic diarrhoea and colitis. It produces bacterial spores which can survive outside the host.

136
Q

What are endogenous infections?

A

Infections caused by patients own bacterial flora.
Important in hospitalised patients, especially those with invasive devices or surgical patients.

137
Q

What are fungi?

A

Eukaryotic, heterotrophic organisms which “move” by means of growth or through the generation of spores (conidia) carried through air or water.

138
Q

What are yeasts?

A

Small, single celled fungi that divide by budding (<1%of fungal species).

139
Q

What are moulds?

A

Fungi that form multicellular hyphae (branching filaments) and spores.

140
Q

What is a dimorphic fungus?

A

A fungus that can switch between being yeast and mould depending on conditions.

141
Q

Why are very few of the millions of fungal species able to cause human infection?

A
  • Inability to grow at 37 degrees
  • Fungi cannot evade innate and adaptive immune responses
142
Q

What are the main genera of human mycoses (fungi)?

A
  • Ascomycota - Aspergillus, Pneumocystis, Candida, Fusarium, Scedosporium
  • Basidiomycota - Cryptococcus, Trichosporon
  • Mucormycota - aka zygomycetes
143
Q

What are the most commonly seen fungal infections?

A
  • Nappy rash
  • Vulvovaginal candidasis (yeast infection)
  • Tinea pedia (athlete’s foot)
  • Onychomycosis (fungal nail infection)
  • Otitis externa (outer ear infection)
  • Fungal asthma
  • Tinea capitis (ringworm on the scalp)
  • Fungal keratitis (corneal fungal infection)
144
Q

What invasive fungal diseases are seen in immunocompromised people?

A
  • Candida line infections (eg yeast infection)
  • Invasive aspergillosis (respiratory disease caused by mould)
  • Pneomocystis (fungal pneumonia)
  • Cryptococcosis
  • Mucomycosis (black fungus)
145
Q

What methods are used to diagnose fungal disease?

A
  • Radiology
  • Microscopy
  • Culture
  • Molecular (PCR and antigen tests)
146
Q

What is the aim of antimicrobial drug therapy?

A

To achieve inhibitory levels of agent at the site of infection without host cell toxicity.

147
Q

What are the requirements for selective toxicity for anti-fungal drugs?

A
  • Target does not exist in humans
  • Target is significantly different to human analogue
  • Drug is concentrated in organism cell with respect to humans
  • Organism has an increased permeability to the compound
  • Human cells are ‘rescued’ from toxicity by alternative metabolic
    pathways
148
Q

What drug targets DNA and RNA synthesis of fungi?

A

Flucytosine

149
Q

What drugs target the cell walls of fungi?

A

Echinocandins

150
Q

Which drugs target the cell membrane of fungi?

A

Amphotericin, Azoles and Terbinafine

151
Q

What are the side effects of Azole treatments?

A

All associated with transaminitis and GI side effects
- Rare severe hepatitis
- Alopecia (long-term fluconazole)
- Severe GI symptoms (with Itraconazole)
- Reversible visual disturbance (in 30 % of pts treated with Voriconazole)
- Photosensitivity in 1-2% of pts receiving voriconazole

152
Q

What are the routes of transmission of HIV?

A
  • Sexual
  • Vertical (in the womb, breast-feeding)
  • Blood
153
Q

What is U=U?

A

It stands for Undetectable=Untransmittable. U=U is a campaign to inform the public of research proving that HIV positive individuals who receive effective antiretroviral therapy and have achieved and maintained an undetectable viral load cannot transmit the virus to a sexual partner.

154
Q

What are PrEP and PEP?

A

Pre- and Post-exposure prophylaxis is medication taken before and after possible HIV exposure (sex, injection) to protect against HIV infection. PEP is not as effective as PrEP and must be commensed within 72 hrs of exposure.

155
Q

What are the benefits of knowing HIV status?

A
  • Access to appropriate treatment and care
  • Reduction in morbidity and mortality
  • Reduction of vertical transmission
  • Reduction of sexual transmission
  • Public health/partner notification
  • Cost-effective
156
Q

What are 5 scenarios when HIV testing takes place?

A
  • Clinician indicated diagnostic testing
  • Routine screening in high prevalence locations
  • Antenatal screening
  • Screening in high risk groups
  • Patient initiated requests for testing
157
Q

What symptoms indicate risk of HIV infection?

A

With any recurrent, severe or unexplained medical condition HIV should be considered.
Common examples:
- multi-dermatomal shingles
- unexplained lymphadenopathy
- unexplained weight loss or diarrhoea, night sweats, pyrexia
- oral/oesophageal candidasis or hairy leukoplakia
- flu-like illness, rash, meningitis
- unexplained blood dyscrasias (disorders)

158
Q

What is a normal CD4 count?

A

> 500

159
Q

What is a concerning CD4, at risk of AIDS?

A

<200

160
Q

What is the 90/90/90 goal?

A

Global target for 90% of people living with HIV being diagnosed, 90% of diagnosed ppl on ART, 90% viral suppression for those on ART by 2020

161
Q

What is the mechanism of HIV viral replication?

A
  • Glycoproteins on the HIV molecule (gP160 made of gP120 and gP 41) allow it to dock and fuse onto the CD4 and CCR5 receptors
  • The viral capsid the enters the cell and enzymes and nucleic acid are released
  • Using reverse transcriptase single stranded RNA is converted into double stranded DNA
    Viral DNA then is integrated into the cells own DNA by integrase enzyme
  • When the infected cell divides the viral DNA is read and long chains of viral proteins are made
    Assembly the viral protein chains are cleaved and reassembled
  • Budding here immature virus pushes out of the cell taking with it some cell membrane
    Immature virus breaks free to undergo more maturation
  • Maturation protein chains in the new viral particle are cut by the protease enzyme into individual proteins that combine to form a working virus
162
Q

What are the targets for antiviral therapy?

A
  • Integrase inhibition
  • Protease inhibition
  • Reverse transcriptase inhibition
  • Fusion/entry inhibition
163
Q

What is HIV?

A

Human Immunodeficiency virus, a lentivirus which uses reverse transcriptase to replicate. (retrovirus) Decimates the CD4 cell population over time causing immunodeficiency and viral load increases over time.

164
Q

How long does it usually take to develop symptoms of HIV from the point of infection with acute HIV syndrome?

A

2-4 weeks

165
Q

Which cell types is the primary receptor for HIV?

A

CD4+ cells

166
Q

What are the targets for anti-retroviral therapy within CD4+ cells?

A

fusion/entry inhibitors
reverse transcriptase inhibitors
integrase inhibitors
protease inhibitors

167
Q

Which dermatological malignancy is an AIDs defining condition for adults?

A

Kaposi’s sarcoma (disease in which cancer cells are found throughout the GI tract and presents with purple patches on the skin)

168
Q

What is seroconversion?

A

The development of specific antibodies in the blood serum as a result of infection or immunisation. A sign that the immune system is reacting to the presence of the virus in the body.

169
Q

What is PCP (Pneumocystis pneumonia) treated with?

A

Co-trimoxazole

170
Q

What is Kaposi’s sarcome?

A

Human herpesvirus 8, usually associated with HIV.
Present as single or multiple lesions on the skin.
Treated with HAART and chemo/radiotherapy

171
Q

When is the viral load counted as undetectable?

A

<50 copies/mL

172
Q

What characteristics of HIV mean that it develops drug resistance?

A
  • 1 mutation in every 2 new viruses produced
  • 1-10 billion new virus particles each day
  • 1-5 billion mutations per day
173
Q

What results in HIV drug resistance?

A
  • Non-adherence
  • Drug-drug interactions
174
Q

What are the 3 groups of helminths?

A
  1. Nematodes (round worms)
  2. Trematodes (flatworms, flukes)
  3. Cestodes (tapeworms)
175
Q

How are intestinal nematodes spread?

A
  • faecal-oral spread
  • between humans via eggs or larvae
  • the egg or larvae is not usually infectious when first passed and undergoes a period of development in the soil
176
Q

What is ascaris lumbricodes?

A

Large roundworm found worldwide but mainly tropics
- can present with symptoms similar to respiratory infection due to the larval migration through lungs
- can survive for 5-10 years in the body

177
Q

What is the hookworm?

A

Small white worm, 1cm in length
2 species: Ancyclostoma duodenale (W/SE Asia, Mediterranean, Middle East), Necator americanus (USA, Central/South America, Central Africa, India)
Symptoms: ground itch (worms enter though soles of feet), pulmonary symptoms, iron-deficiency anaemia

178
Q

What is enterobius vermicularis?

A

Pinworm or threadworm
Very common in the UK
5-10cm long and lives for 56 days
Oral-faecal spread

179
Q

What is a trichuris trichiura?

A

Whipworm
Found world wide, especially in the tropics
2-5cm, 1 yr lifespan
Resides partly buried in the mucosa of the large bowel
Often asymptomatic but patients can have bloody diarrhoea, rectal prolapse, anaemia

180
Q

What is strongyloides stercoralis?

A

Causes strongyloidiasis
Found worldwide
2mm long and lies buried in the small intestinal mucosa
Can last 40-50 years
Symptoms: pulmonary symptoms, pruritis at site of larval entry

181
Q

What is visceral larva migrans?

A

Caused by Toxocara canis (dog roundworm) and T. cati (cat roundworm)
Rare but can cause severe disease in children which can resemble leukemia

182
Q

What is cutaneous larva migrans?

A

Creeping itchy skin eruption due to ancyclostoma caninum (dog hookworms)
Due to contact with dog faeces
lesions at sites where the larvae penetrate e.g. buttocks, feet

183
Q

What is draculunus medinensis?

A

The Guinea worm or Medina worm - adult is up to 100cm long and lives for one year subcutaneously
Diagnosed by drop of water on blister which causes egg release
Symptoms: localised pain and urticaria at site of worm protusion, blister formation with bursting, tetanus

184
Q

What is wuchereria bancroftii?

A

A tapeworm that causes elephantiasis.
Endemic in the tropics
insect borne
Live in the lymphatic system and can survive for 30 yrs

185
Q

What is loa loa?

A

Causes loiasis or African eye worm
Passed onto humans through the repeated bites of deerflies.
Symptoms: calabar swellings, eye worm (visible movement of worm across surface of the eye), full body itching, hives, muscle and joint pains

186
Q

What is brugia malayi?

A

Nematode causing lymphatic filariasis in South East Asia.
Transmitted via mosquitos.
Symptoms: often asymptomatic, fever, lymphangitis and lymphadenitis

187
Q

What is onchocerca volvulus?

A

Nematode causing onchcerciasis.
transmitted via blackflies
Symptoms: pruritis, dermatitis, onchocercomata (subcutaneous nodules) and lymphadenopathies

188
Q

What is the PPP?

A

Pre-patent period = time from onset of infection to appearance of eggs in stool

189
Q

What is campylobacter CSM agar used for?

A

The campylobacter charcoal-based selective medium agar is a selective medium for the primary isolation of campylobacter species from human faecal specimens.
Campylobacter jejuni typically appears as small, grayish mucoid colonies on the black agar.

190
Q

What is the pre-patent period?

A

interval between infection + appearance of eggs/larvae

Phase 2A (18 decks)

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