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ESA 3 > Infection > Flashcards

Infection Flashcards

1
Q

Define an ‘infection’

A

Invasion of a host’s tissues by a microorganism

Disease/illness that’s caused by toxins, microbial multiplication or by a host response

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2
Q

What are commensals?

A

Microorganisms normally carried on skin and mucosal surfaces. They’re normally harmless and can be beneficial but if they’re transferred to other locations, they can be harmful

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3
Q

What are some examples of horizontal transmission of an infection?

A

Direct contact, inhalation, ingestion

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4
Q

What are some examples of virulence factors?

A

They’re molecules expressed that help cause disease.
Endotoxins or
Exotoxins such as enzymes, antibody toxins and superantigens

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5
Q

What are the disease determinants involved in developing infections, with specific reference to Patient and Pathogen?

A

Patient - co-morbidities and infection site

Pathogen - virulence factors and resistance

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6
Q

What are the most important specific investigations that can be carried out in bacteriology?

A

Microscopy
Culture
Antibiotic susceptibility testing

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7
Q

What are the main functions of the lymphatic system?

A

Immune defecne
Fluid balance
Fat absorption from gut via lacteals in small intestine

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8
Q

What’s the function of lymphatic capillaries and vessels?

A

To circulate excess fluid, away from interstitium and into blood stream.

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9
Q

Briefly describe the structure of lymphatic capillaries

A

Similar to blood capillaries, with one layer of simple squamous epithelium but there is no basement membrane so lymphatics are more permeable than blood vessels.

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10
Q

Briefly describe the structure of lymphatic vessels

A

Similar to small veins. Have one way valves

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11
Q

What forces help promote flow of lymph in the right direction?

A

Valves in vessels but also compression due to skeletal muscle contraction, smooth muscle contraction in walls of lymphatic vessels, and pressure changes due to breathing, in the chest

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12
Q

Where do lymphatic vessels drain into?

A

The right upper limb and the right half of the head, neck and chest drain into the right lymphatic duct which then drains into the right subclavian vein.
The rest of the body’s lymph drains into the thoracic duct which then drains into the left subclavian vein

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13
Q

What are the four main lymphoid organs?

A

Lymph nodes
spleen
tonsils
thymus gland

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14
Q

When is the thymus at its peak size

A

Adolescence/ pre puberty

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15
Q

What are the functions of the spleen?

A

Hold a blood reserve.
Red pulp - removal of old RBCs
White pulp - lymphocyte activation

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16
Q

What is SIRS?

A 
Sytemic Inflammatory Response Syndrome
Patient must have 2 of more of these signs
Heart rate>90 bpm
Temp 38
WBC 12x109
Resp rate >20
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17
Q

What is sepsis?

A

The systemic response to infection

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18
Q

What is classed as severe sepsis?

A

SIRS + either organ dysfunction or hypoperfusion

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19
Q

What is classed as septic shock?

A

Severe sepsis + persistent hypotension, despite IV fluid administration

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20
Q

What is ‘the sepsis six’?

A 
Steps that should be taken in treatment of sepsis
High flow oxygen
cultures
empirical IV antibiotics
Measure serum lactate
IV fluid resuscitation
Urine output measurement
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21
Q

What is the cascade that leads to SIRS?

A

An endotoxin binds to macrophages and macrophages then stimulate the local release of cytokines such as TNF and IL 1. This stimulates an inflammatory response.
There is then systemic release of cytokines into the blood stream, promoting growth factor, macrophages and platelets to try and restore homeostasis.
If this fails, there is vascular damage and activation of humoral cascade - SIRS

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22
Q

What are the most common causative agents of bacterial meningitis in neonates?

A

Group B strep
Listeria
E coli

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23
Q

What are the most common causative agents of bacterial meningitis in under 5s?

A

Neisesseria meningitidis

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24
Q

What are the most common causative agents of bacterial meningitis in the elderly?

A

Streptococcus pneomoniae

Listeria

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25
Q

What is found in CSF of patients with bacterial meningitis?

A

Low glucose
High protein
High neutrophils

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26
Q

Why is a Meningitis B vaccine not used?

A

Group B meningitis agent is too similar to neural tissue so extremely difficult to develop a safe vaccine for use

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27
Q

Where are beta-defensins found?

A

Epithelia where they’re toxic to microbes

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28
Q

Where are lysozymes found as a chemical barrier?

A

Sebum, perspiration, urine, where they make holes in cell walls

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29
Q

Why is normal flora an effective biological barrier against infection?

A

Compete with pathogens for binding sites and other resources
Produce antimicrobial chemicals
Synthesise vitamins, especially B and K

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30
Q

What are the main functions of the immune system?

A

Minimisation of host damage
Containing and removing infection
Recognition of pathogens
Memory to prevent recurrence

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31
Q

Describe the process of phagocytosis

A

Innate cells recognise microbes via PAMPs. Microbe is opsonised and then zippered up into phagocyte to form phagosome. This fuses with lysosome to form a phagolysosome. Phagocyte then kills microbe either by enzymatic digestion or oxidative burst

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32
Q

What are the most common opsonins of the innate immune system?

A

C3a/C5a

CRP

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33
Q

How does the complement cascade result in killing of a microbe?

A

Forms a membrane attack complex in microbe wall which causes cell lysis

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34
Q

How can the 4 Ps of infection prevention be applied to healthcare infections?

A

Patient - COnsider patient interactions e.g. with other patients, staff or visitors
Pathogen - consider virulence factors and antibiotic resistance/ interactions
Practice - initiatives and policies, activities of healthcare workers and organisational structure

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35
Q

What patient interventions can be made in infection control?

A

Optimise patient’s condition and use antibiotic prophylaxis. Halt patient to patient transmission through isolation/protection

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36
Q

What healthcare worker interventions can be made in infection control?

A

Ensure staff are disease free and vaccinated.

Ensure good sterile clinical techniques are carried out and that personal protective equipment is used

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37
Q

What environmental interventions can be made in infection control?

A

Try to ensure toilets are well distributed and clean
Consider use of easy-clean furnishings and rooms with positive/negative pressure
Ensure medical devices are sterilised/decontaminated and single use

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38
Q

Describe the characteristics of Clostridium difficile

A

It’s a gram positive, anaerobic, spore formind bacilli.

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39
Q

What can cause C diff infection?

A

Antibiotic use diminishing normal gut flora so c diff is allowed to proliferate

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40
Q

How does C diff cause its symptoms?

A

Releases toxins a and b which inactivate gtpases and reduce amount of actin in cytoskeletons to increase permeability of cell membranes so water leaks out - diarrhoea

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41
Q

What are the characteristics of staphylococcus aureus?

A

Gram positive cocci

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42
Q

How does staph aureus cause infection?

A

Produces cell surface toxins that bind to and inactivate antibodies

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43
Q

What are the main species of malaria parasite?

A

Plasmodium falciparum, vivax, ovale and malariae

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44
Q

What causes enteric fever?

A

Salmonella enterica - a gram -ve enterobacteriaceae that’s aerobic,a rod and a non-lactose fermenter

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45
Q

What are the symptoms and signs of enteric fever?

A

Fever, headache, abdominal discomfort, dry cough, rash, hepatosplenomegaly, bradycardia, constipation. Maybe be intestinal perforation and haemorrhage

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46
Q

What abnormalities would be found in an FBC of a patient with enteric fever?

A

Anaemia and decreased lymphocytes

47
Q

How is enteric fever treated?

A

With ceftriaxone of azithromycin for milder cases, for 7-14 days

48
Q

How should malaria be treated?

A

Depends on species.
P. Falciparum should be treated with quinine or artemisinin
Other types should be treated with chloroquinine and/or primaquine

49
Q

What tests should be done to confirm diagnosis of malaria?

A

Blood smear using giemsa stain to detect parasite
FBC
U and Es
LFTs
Glucose test as metabolism can be affected

50
Q

What kind of virus is the HIV virus?

A

Single stranded RNA

51
Q

What symptoms are there in the primary infection of HIV?

A 
Flu like illness
fever
pharyngitis
weight loss
general lymphadenopathy
52
Q

How does HIV exert its effect?

A

Attaches to host CD4 cells and then use reverse transcriptase to convert its genome to DNA, which integrates into the host nucleus. Then replicates viral components which assemble and released. As virus attaches to CD4 signals, it stimulates an immune response against CD4 cells, causing CD4 levels to drop and viral load to increase so becomes symptomatic

53
Q

How is HIV treated?

A

With Highly Active Antiretroviral Therapy which act to increase CD4 levels and decrease viral load

54
Q

What investigations should be done in investigating HIV?

A 
Blood test
Immunoblot
Resistance profile
Viral load
CD4 levels
55
Q

What kind of virus is Hep B?

A

Double stranded DNA

56
Q

What are the different outcomes of an initial infection with hep b?

A

Can be acute whereby viral load increases and immune response causes symptoms but immune system clears infection.
Can be chronic where immune system can’t clear infection so causes inflammation and cirrhosis

57
Q

What are the signs and symptoms of chronic hep B?

A

Jaundice
ascites
caput medusa
clubbing (signs of liver disease)

58
Q

What kind of virus is hep c?

A

Single stranded RNA

59
Q

What’s the classification of lymphoid organs?

A

Primary organs that produce mature lymphocytes. i.e. bone marrow and thymus
Secondary organs where lymphocyte activation takes place

60
Q

What is meant by co-stimulation in T cell activation?

A

Ensures only harmful antigens are responded to and not self-antigens. Antigen presenting cells containing harmful antigen express a B7 molecule on their surface to bind to CD28 molecule on a T cell which signals that it requires a response. If this doesn’t happen, T cell becomes ‘anergised’

61
Q

What are the 2 main steps of T cell maturation?

A

Positive selection - cells that bind to foreign antigens survive and replicate
Negative selection - cells that bind to self-tissues are deleted

62
Q

What are the 2 types of MHCs and what do they present?

A

Class 1 MHCs present intracellular pathogens to CD8 cytotoxic cells, via exogenous pathway
Class 2 MHCs present extracellular pathogens to CD4 cells, via endogenous pathway

63
Q

What type of antibody is found in breast milk?

A

IgA

64
Q

What type of antibody can cross the placenta?

A

IgG

65
Q

What type of antibody is responsible for primary response to an antigen?

A

IgM

66
Q

What type of antibody is involved in allergic responses?

A

IgE

67
Q

How do CD8 T cells exert their cytotoxic effect?

A

Release perforins which make a pore in the cell membrane then release granzymes which enter through this pore and stimulate apoptosis

68
Q

How can commensals cause infection?

A

Through migration, inoculation, invasion and through blood stream

69
Q

What is qurum sensing?

A

Process by which bacteria monitor local population. Uses signalling molecules called autoinducers, cell surface and cytoplasmic receptors and gene expression to increase autoinducer formation and control behaviour of bacteriae

70
Q

What’s difficult about treating surface infections?

A

Biofilms are difficult to penetrate with antimicrobials and then microorganisms aren’t very metabolically active so don’t take up drugs quickly so drugs are inneffective.
resection of infection is also risky due to risks of surgery

71
Q

What causes rhesus disease?

A

When mother is eg rhesus negative and foetus is rhesus positive. If small amount of blood passes from foetal - maternal circulation (ie through small haemorrhage) then foetal Rh stimulates inflammatory response in mother and IgM - IgG are produced. IgG then crosses placenta and causes haemolytic anaemia in foetus.

72
Q

How is rhesus disease treated?

A

Give anti-RhD antibodies to mother

73
Q

Why do primary immunodeficiencies tend to present roughly 1 month after birth?

A

As until then, they still have some maternal immunity via IgG which crosses the placenta. After that’s gone - present with immune problems

74
Q

What is the mechanisms behind Common Variable Immunodeficiency?

A

Failure of B cells to mature into plasma cells so there’s low IgG, IgA and IgM

75
Q

What is Bruton’s disease?

A

X-linked agammaglobulinaemia. There’s no tyrosine kinase so B cells can’t mature. There’s low IgG and undetectable IgA
Causes failure to thrive and recurrent bacterial respiratory infections and diarrhoea which can be fatal. Also undetectable tonsils and adenoids

76
Q

What is chronic granulomatous disease?

A

Neutrophils fail to make oxygen radicals so ixidative burst fails in killing of bacteria. Therefore many granulomas form (frustrated phagocytosis)
There’s failure to thrive and increase in deep seated infections, especially staph aureus infections of the skin that need surgical removal.

77
Q

What is DiGeorge syndrome?

A

T cell CATCH 22 disease. With cardiac abnormalities, abnormal facies, tymus aplasia, cleft palate and hypocalcaemia/ hypoparathyroidism, due to defect on 22nd chromosome. There’s failure of 3rd and 4 th pharyngeal arch development. Thymus aplasia means T cells can’t mature so there’s increased susceptibility to infection

78
Q

What is Severe Combined Immunodeficiency?

A

Deficiency in T and B cells so cellular and humoral components of adaptive immune system are absent. There are recurrent severe respiratory infections and diarrhoea after first month of life and can be fatal if untreated. (boy in bubble syndrome)

79
Q

How is SCID treated?

A

Reverse barrier nursing
Prophylactic antibiotics
IV immunoglobulins
Potentially bone marrow transplant

80
Q

When does neutropenic sepsis normally occur?

A

In cytotoxic chemotherapy. Kills neutrophils. Neutropenia leads to increased susceptibility to infection so can be sepsis.

81
Q

What is a ‘dead end infection’?

A

One that spreads from non-human source to human but can’t pass between humans

82
Q

What can cause an outbreak/epidemic/pandemic?

A

Pathogen that’s either never been around before or that has new characteristics such as virulence factors, antibacterial resistanceor antigens
Host that’s either never been seen in that location before or host that used to be immune but isn’t anymore
New practice - either social or healthcare related

83
Q

What is basic reproduction number?

A

Average number of cases of disease that one original case causes in an otherwise non-infected non-immune population

84
Q

What are some disadvantages of infection control?

A

Decreased exposure decreases immunity so outbreaks on re-exposure are more common
Also an increase in average exposure age can increase the severity upon infectionsuch as in chickenpox

85
Q

What are some common adverse effects of antibiotic use?

A 
GI upsets
Allergies/skin rashes
Organ toxicity
Super infections
Haematological disturbances
86
Q

How do beta lactams exert their effects?

A

By inhibiting peptidoglycan cross-linkages in bacterial cell walls.

87
Q

What are penicillins active against?

A

Penicillin - streptococci
Amoxicillin - Streptococci and gram negatives
Flucloxacillin - Streptococci and staphylococci

88
Q

What are cephalosporins active against?

A

Made in generations.
Increasingly active against gram negative and decreasingly active against gram positives. Not effective against anaerobes.
Ceftriaxone has good CSF action

89
Q

What are carbopenems active against?

A

Very broad but predominantly anaerobes and gram negatives. Can be safe in mild penicillin allergies

90
Q

What are beta-lactamase inhibitor combinations used for?

A

Coamoxiclav used for streptococci, staphylococci, gram negative and anaerobes
Piperacillin/Tazobactam used for streptococci, staphylococci, anaerobes and more gram negatives, including pseudomonas

91
Q

How do glycopeptides exert their effects?

A

Inhibit peptidoglycan cross-linking in gram positive organisms.

92
Q

Which antibacterials affect protein synthesis?

A

Tetracyclines, aminoglycosides and macrolides

93
Q

How do tetracyclines work and what are they used for?

A

Bind to 30S ribosomal subunit to block aminoacyl tRNA and prevent protein transcription.
Used especially in penicillin allergies against gram positive organisms. Also active in chlamydia and atypical pneumonia

94
Q

What are aminoglycosides used for?

A

e.g gentamycin. Mostly reserved for gram negative sepsis as they are potentially nephrotoxic and ototoxic and so need therapeutic drug monitoring.

95
Q

What are macrolides used for?

A

eg erythromycin.
Used against gram positive cocci, anaerobes (not bacteroides), mycoplasma, chlamydia and atypical respiratory infections. Can be used as penicillin alternative in gram positive infection.

96
Q

What antibacterial affect nucleic acid synthesis?

A

Quinolones, eg ciprofloxacin

Sulphonamids and trimethprim eg nitrofurantoin

97
Q

How do quinolones work?

A

Inhibit DNA gyrase. Highly active against gram negatives and atypical pathogens but have C. difficile association

98
Q

How do sulphonamides work?

A

Inhibit folic acid synthesis by inhibiting tetrahydrofolate. Can be combined with sulphamethoxazole to give co-trimoxazole, used in PCP and MRSA

99
Q

How does aciclovir work?

A

By inhibiting DNA polymerase. Used to treat herpes simplex virus and varicella zoster

100
Q

What is metronidazole used for?

A

As an antibacterial against anaerobes and as an antiviral.
Effective against amoebae, such as those that cause dysentery, giardia that cause diarrhoea and against trichomas that causes vaginitis.

101
Q

What is a common antifungal agent?

A

Azoles such as fluconazole inhibits cell membrane synthesis so used in candida infections

102
Q

How can problems with antibiotic resistance be reduced?

A

Antimicrobial stewardship which involves antimicrobials are taken correctly
Infection control involving reducing exposure of bacteria to antibiotics and preventing spread of resistant bacteria

103
Q

What is the role of disc sensitivity testing and E tests.

A

Discs analyse what antibiotics a certain bacteria is resistant to and then E tests analyse the extent of susceptibility/resistance so at what concentration is a bacteria resistant

104
Q

What are the differences in cell wall structure of gram negative and gram positive organisms?

A

Gram negative have plasma membrane, periplasmic surface, thin peptidoglycan wall, another periplasmic surface and a lipopolysaccharide protien layer.
Gram positive bacteria have cell membrane, periplasmic surface and a thick peptidoglycan layer?

105
Q

How does cell wall structure effect gram staining result?

A

Gram staining involves adding crystal violet and iodine. This complex is retained by the peptidoglycan layer. There is then decolourisation by alcohol/acetone. This only works in gram negative bacteria as their peptidoglycan layer is thinner so doesn’t retain the crystal violet/iodine. Then red dye is added. This dyes the uncoloured gram negative bacteria red but gram positive stay blue/purple

106
Q

What kind of bacteria is E coli?

A

Gram negative bacilli

107
Q

How is E coli treated?

A

If UTI - nitrofurantoin and trimethoprim

In general, Cephalosporin or Co-amoxiclav

108
Q

What does staph aureus look like under a microscope?

A

Purple/blue if gram stained. Forms grape like clusters

109
Q

How is staph aureus treated?

A

Methicillin/ flucoxacillin

If MRSA, use vancomycin/teicoplanin

110
Q

How is strep pneumoniae treated?

A

Preferably penicillin

If resistant, use vancomycin

111
Q

How is C diff infection treated?

A

Fluids and remove causative antibiotics if possible.

Can also use Oral metronidazole/vancomycin

112
Q

What kind of bacteria is haemohilus influenzae?

A

Gram negative coccobacilli. Facultative anaerobe

113
Q

How is H. influenzae treated?

A

Co amoxiclav

ESA 3 (5 decks)

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