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Esa 3 > Infection > Flashcards

Infection Flashcards

0
Q

How do organisms cause disease?

A

Exposure- Adherence- invasion - multiplication - dissemination
Virulence factors endo and exo toxins
Host inflammatory response, oxidative damage, not oxygen dependent.

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1
Q

Disease determinants

A 
Site of injury 
Size of inoculation
Co morbidities 
Age
Genetics
Immunity
Immune function 
Antibiotic resistance
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2
Q

How so you determine infection

A

History, examination, investigation
Supportive - fbcs, us and es, crp, liver function tests, blood microscopy, imaging, histiopathology
Specific -
Bacteria - stain, microscopy, PCR, antigen/ antibiotic susceptibility, nucleic acid detection.
Virus- antigen, PCR, antibody

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3
Q

Beta lactams

A

Penicillins e.g. Amoxicillin (gram neg), flucloxacillin (staph and strep), penicillin V (most staph)
Cephalosporins e.g. (Broad spec cause C diff, not anaerobes) e.g. Ceftriaxone
Carbrapenems- (broad spec) e.g. Meropenem mostly gneg
Monobactams

Cell wall synthesis

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4
Q

Glycopeptides

A

Cell wall synth
Vancomyosin MRSA
G pos

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5
Q

Macrolides

A

Erythromycin - gram positive e.g. Strep pneumonea and H. Influ (penicillin allergy)
Protein synth

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6
Q

Aminoglycosides

A

Protein synth
Pseudomonas aeoriginosa and other g neg and some mycobacteria e.g. Tobramyosin
Gentamicin - g neg sepsis reserved for

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7
Q

Polymixins

A

Cell membrane function

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8
Q

Quinolones

A

Fluroquinolone
Nucleic acid synth
G neg
Ciprofloxacin

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9
Q

Tetracyclines

A 
Doxycycline
Protein synth
G pos, broad spec I'm penicillin resistance 
Atypical pathogens in pneumonia
Chlamydia and some protozoa
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10
Q

How do bacteria become resistant?

A

Vertical
Horizontal - transformation(from environment), conjugation, transduction (vector).
Mutations

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11
Q

Describe most common pathogen of sepsis and give pathogenesis including multi organ failure

A

Neisseria menigitidis. Gram negative diplococci. Aerobic.
Capsule prevents phagocytosis, promotes adherence and triggers inflammatory response. Cytokines, (IL1 and TNFa) released which cause clotting (more thrombin and less fibrinolysis). Coagulation damaging micro vasculature and leading to organ ischemia.

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12
Q

When is SIRS

A

Systemic inflammatory response syndrome
RR >20
HR >90
Temp >38 12x109/l

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13
Q

Give the history, examination and investigation of Sepsis

A

History- nausea, vomiting, photophobia, fever, malaise, confusion
Examination- hot/ cold, high rr, high BP, purpuric rash (not blanching
Investigations:
Sepsis 6 and
Fbcs
Us and es
Lfts
Crp
Blood culture and stain, PCR, antigen ect.
Possible lumbar puncture for csf
Blood sugar
Clotting study
Blood gas
Sats
Possible complications include: lung failure, renal damage, raised inter cranial pressure, irreversible hypotension, ischeamia of digits

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14
Q

Describe treatment of sepsis

A 
Sepsis 6
IV antibiotics e.g. For N meningitidis then ceftriaxone
Blood culture
Serum lactate 
O2
IV fluids 
Urine output measure

Blood of csf to confirm

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15
Q

Prevention of n menigitidis

A

Prophylactic antibiotics and group C vaccine

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16
Q

Difference between innate and adaptive immunity

A

Constant intensity
Non specific (but recognises groups of pathogens)
No memory
Immediate

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17
Q

Describe the barrier to infection

A

Physical - skin, epithelium, cilia
Chemical - Saliva (lysozyme) tears (IgA) acid in stomach and vagina, gastric acid, pepsin, mucus , beta defensins (epithelium - form pores in cell membranes)
Biological - skin flora and mucosal flora e.g. Lactobacillus spp. Synthesise vit K and vit B12
Physiological - vomiting, sneezing, diarrhoea, coughing, mucocillary escalator?

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18
Q

When can biological barriers become damage routs

A

Transfer to sterile environment e.g. Bladder or surgery.
Antibiotics e.g. C diff
Affected immune system e.g. DM leading to overgrown flora
Poor dental work - bacteraemia especially with altered spleen function.

Skin - staph aureus, epididymis, strep pyrogens, Candida albicans, clostridium perfingens
Nasopharynx - haemophilus influenzae, neisseria meningitidis and strep pneumonea

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19
Q

Describe cells of the innate immune system

A

Macrophage- PRRs (pathogen recognition receptor) recognise PAMPs (pathogen associated molecular patterns) on bacteria. Phagocytose. Kill via O2 dependent and independent e.g. Lysozyme, lactoferrinor transferrin, Cationic proteins, and proteolytic/ hydrolytic enzymes.
Monocytes
Basophils
Eosinophils

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20
Q

Describe the complement system

A

Activated via alternate pathway- cell surface constituents on microbes, or via MBL pathway binding to mannose residues of proteins.
C3a and 5a are chemoattractants for phagocytes
C3b and 4b opsonise
C5-9 form membrane attack complex

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21
Q

Decribe the roles of TNFa, il1 and il6 released from macrophages

A

Stimulate neutrophil production and migration from bone marrow.
Dilate vessels, increase blood flow and make more permeable.
Increase body temp (hypothalamus)
CRP and MBL from liver

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22
Q

Describe malaria and it’s pathogenesis and investigations

A

Female anopheles mosquito carries- hepatocytes- RBC
4 types plasmodium falciparum, ovalae, malariae, vivax.
1-3 week incubation
Falciparumw causes RBCs to become sticky
Causes fever, arthralgia, myalgia, headache, chills, fatigue, cough
Possible splenomegaly, cerebral features e.g. Coma, respiratory distress

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23
Q

Treatment for malaria

A 
ID physician
Can be seen under microscopy
If CNS then do a head CT
If falciparum then quinine or artemisinin
If other then chloroquine or primaquine
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24
Q

Pathogenesis enteric fever

A

Typhoid or paratyphoid caused by salmonella enterica subspecies. G neg bacilli
Faecal oral route
Use fimbriae to cover and adhere to epithelium over ilieal lymphoid tissue causing payers patches. Invasion allows intracellular invasion. Endotoxins antigen VI

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25
Q

Symptoms enteric fever

A 
Fever
Malaise
Abdo pain
Constipation 
Hepatospenomegaly 
Dry cough 
Bradycardia
Intestinal haemorrhage/ perforation
Occasional rash
- paratyphoid not as bad
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26
Q

Investigation of enteric fever

A

Anaemia
Feacal/ blood culture
Raised LFTs
Relative lymphopenia

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27
Q

Treatment of enteric fever

A

Ceftriaxone or azithromyosin (macrolide)
Typhoid vaccine to VI antigen or a live attenuated vaccine but not 100%
Also s typhimurium or enteritidis

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28
Q

Briefly describe brucellosis

A

From animals, milk or cut, gram neg bacilli (Brucella)
Fever non specif symptoms, myalgia, arthralgia and epidydimitis
Doxy or rifam
Isolation required

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29
Q

Understand where and how to look up information on travel related infections

A

CDC - centres for disease control

WHO

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30
Q

Describe influenza virus and it’s transmission and management

A

Aerosol
Influenza A -ss RNA
Fluids and painkiller

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31
Q

Describe legionella pneumophila and an example of its clinical importance.

A 
Water Bourne amoebae.
Legionella pneumophila g neg bacilli
Multiply inside macrophage
Fever, diarrhoea, chills, cough, muscle ache, tiredness, loss of appetite.
Affected liver function
Similar to pneumonia
May develop potanic fever similar to flu
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32
Q

Difference between antigenic drift and antigenic shift

A

Antigenic drift - mutations in antigens

Antigenic shift- combination of different strains

33
Q

Describe features of an APC

A

Found in a variety of places - SALT, MALT, lymphoid organs, blood stream.
Phagocytose of micropinocytosis (soluble particles from pathogen)

34
Q

Describe extracellular PAMPs and how they are identified

A

Phagocytosed by APC.
Phagosome fuses with vesicle containing MHC class II, antigen bound to MHC.
CD4 T cell binds to the MHC with TCR and CD28-B7.
This activates TH2 - activates B cells, eosinophils and mast cells.
It activates TH17 - neutrophils - phagocytosis.
Extracellular = humeral immunity
Pathogens= bacteria, parasites, fungi

35
Q

Describe intracellular PAMPs and how they are identified

A

Antigen enters ER, binds to MHC1. On membrane MHC1 binds to CD8 (not also found MHC2).
MHC 2 binds to CD4- TH1 which activates CD8 on MHC1. CD8 activates CTL which use perform and granzymes after binding to MHC1.
TH1 activates B cells and macrophages
Cellular immunity
Pathogens- virus and bacteria

36
Q

Properties of MHC

A

Co dominant
Polymorphic binding clefts
Must be able to fit/ match antigen for it to express
E.g. Some can’t express gp120 so have rapid progression.
Can cause organ rejectin
Some hLA (form of MHC) varient cause autoimmune disease.

37
Q

T cells and cytokines?

A

TH1 - TNFa, IFN gamma
Th2- Il4,5,10
TH17- Il17

38
Q

Apply the infection model to a patient with HIV

A 
Pathogen
Ss +RNA
Gp120 binds to enter
Reverse transcriptase and integrase
Sex, blood vertically
Incubation 1-3 weeks. Seroconversion long.
Infection- chronic, suppresses immune system so pneumonia, meningitis, encephalopathy, peripheral neuropathy
Acute - presents as cold/ flu with rash
Detected by PCR and p24 antigen via ELISA- 6 months to be sure.
Treatment HAART:
Nucleoside reverse transcriptase inhibitors
Non nucleoside rti
Integrase invibitors
Protease inhibitors
Fusion inhibitors
Co receptor entry inhibitor
39
Q

Apply the infection model to Hep B

A

Pathogen replicates in hepatocytes
Blood Bourne, sex
Chronic affects children, symptomatic in adults
Different antigens screened
Jaundice, liver failure, cirrhsis and liver cancer
Acutely- fever malaise and jaundice around 2-6 months
Vaccination not 100%
Made worse by HepD

40
Q

Understand the concept of microbiota

A

Commensal bacteria both symbiotic and pathogenic that live on a body surface.

41
Q

Appreciate the range of normal microbiota

A 
HPV and herpes simplex
GP:
Staph aureus
Coag neg staph aureus e.g. Epidermidis
Viridens strep
Group b haemolytic strep
Corynebacterium (rods) 
GN:
Enterobacteriacae 
Fungi and yeasts - dermatophytes athletes foot
42
Q

Describe pathogenesis of infections at a surface

A

Adherence to prosthetic surface via pili or frimbriae
Invasion and multiplication
Formation of biofilm/ slime
Bacteria produce matrix and nutrient diffuse.
Quorum sensing - uses signals, auto inducers, receptors and gene expression to regulate sporulation, biofilm formation and virulence factor secretion.
Host response is pyrogens or granulomatous

43
Q

Describe the management of infected sites

A

Diagnose with blood culture, sonication.
ntibacterials
Surgery to respect
Prevent by maintaining surface integrity and prevent colonisation
Prosthetic- prevent contamination, inhibit e.g. Silver.

44
Q

Describe the range and origins of surface infections on both natural and prosthetic surfaces

A

Strep throat - strep pyrogens pharyngitis
UTI- candida
Inoculation- coag neg staph and prosthetic
Uaem
Haematogenous- viridens from teeth/ mouth
Empyema- pleural cavity
Vasculitis- pleural cavity
Native vales- viridens, enterococcus faecalis, HACEK, candida. Turbulence
Prosthetic less than 1 year then coag neg.
Prosthetic:
IV lines
Catheter
Joints
Valves
Pacing wires

45
Q

Describe the different types of hypersensitivity reactions

A

Type 1- IgE mediated, non infectious allergens, less than 30 mins
Type 2 - IgG/M mediated, non soluble antigen 5-12 hour
Type 2- IgG/M mediated antibody complex, soluble antigen 3-8 hour
Type 4- cell mediated, environmental infectious agents and self. 24-48 hour

46
Q

Understand the pathophysiology behind the type I hypersensitivity reaction

A

First antigen contact- IgE produced
Second contact- antigen binds to IgE on mast cell or activates it directly via C3a and 5a.
Mast cell releases chemoattractants, cytokines, histamines causing exudation, dilation and vascular leakage.
Location differs the effects:
Epidermis- urticaria
Dermis- angioedema can be fatal in URT
Systemic- anaphylaxis, hypotension, CVS collapse, urticaria, wheezing

47
Q

Treatment of type I anaphylaxis

A

Adrenaline

Monitor EXG, BP, pulse and oximetry

48
Q

Management of type 1

A

Education e.g. Epipen
Avoid allergens
Sensitivity testing, graded exposure
Manage with antihistamines, steroids, anti IgE

49
Q

Apply the infection model to a patient presenting with a hospital aquired infection

A

Within 48 hours of admission including visitors and HCW

50
Q

Practice and place health care infections

A

Practice- activities of HCA, organisation structure and engagement, leadership, government iniative
Place- healthcare environment, fixed features and variable features

51
Q

Understand the range of hospital acquired infections

A 
Ventilator pneumonia
Mrsa
Candida albicans
Pseudomonas aeruginosa 
Clostridium difficile 
TB
Legionaries
UTI
52
Q

Describe the use of personal protective equipment with regard to a hospital setting

A

Vomiting/ diarrhoea then gloves and apon

Full Ppe suit for highly contagious diseases such as Ebola.

53
Q

Pathogenesis of C. difficile

A

Gram neg spore forming aerobic bacillus.
Occurs with antibiotics. (Normally b lactams)
ToxinA (endotoxin) and toxin B (cytotoxin) affect actin production and Rho GTPases.
Check with stools and Elisa

54
Q

Management of C. difficile

A

Metronidazole
Vancomyosin
Often stopping causative antibiotic will sort it out.

55
Q

Characteristics of staph aureus with regard to hospital aquired infections and drug resistance

A

Some resistant to most B lactams antibiotics, eg. Methicillin. Gentimicin some resistance. Vancomyosin little resistance

56
Q

Characteristics of norovirus

A

Aerosol
Winter vomiting disease
+ssRNA non enveloped
Bleach and disinfectants, isolation to prevent spread

57
Q

Significance of reproduction number (Ro) and levels of outbreak

A

Reproduction number (Ro) = average number of cases each new case/infected individual causes
Endemic- normal background rate
Epidemic- greater than normal
Pandemic- much greater than normal

58
Q

Consider the principles of infection prevention

A

Pathogen- avoid/ kill, elimate breeding sites
Patient- keep healthy, immunisations
Practice- behaviour, geography or action to prevent contact between pathogen and patient
Place - environmental engineering, good design ect.

59
Q

Appreciate the consequences of antibiotic resistance

A

MDR! XDR, PDR
Treatment failure
Prophylactic failure - surgery
Economic cost of ITU

60
Q

Principles of anti microbial stewardship

A 
Appropriate use of antibiotics
Minimise adverse effects and toxicity
Maximise optimal clinical outcome
Reduce cost of infectiom
Limit the selection for anti microbial strains
61
Q

What does anti microbial stewardship require?

A

Multidisciplinary team
Leadership to challenge
Interventions- persuasive, restrictive or structural
Surveillance
Leadership and support
Integrate into patient safety
Process measures (use and adherence) vs outcome measures (resistance and patient outcomes)

62
Q

Describe the diversity of chronic infections

A 
Vascular
Infection
Trauma
Autoimmune
Metabolic
Inflammatory
Neoplasm
Congenital
Degenerative
Environmental
Idiopathic
63
Q

Describe CF and infection

A 
Autosomal recessive delta f508
Thickened mucus
Often H influenzae infections
Later staph aureus
Then atypical mycobacteria, candida, aspergillus, pseudomonas aeruginosa
Eventually COPD 
Increased mucus
Acute exacerbation with HI, PA or RSV
64
Q

Describe DM and infections

A

Hyperglycaemia and acidosis affects humoral immunity (antibodies) and neutrophil and lymphocyte functioning.
Damage to vasculature means poor perfusion and decreased host response
Neuropathy - diminished sensations.
More susceptible to:
net e.g. Otis externa- external auditory canal soft stis sues, pain and discharge (otorrhea).
Rhinocerbral mucormycosis- mould infection of sinuses in DKA, soft tissue necrosis and bony erosion.
UTIs common

65
Q

Down’s syndrome and infection

A

More susceptible to viral infection in earlier years. Mucus? Structure?
Humoral:
Affected immunoglobulin production. Decreased neutrophil and monocyte functioning (chemo taxis)
Cellular:
Altered T cell function and distribution, cytokines production and nK cell function

66
Q

The role of pseudomonas aeruginosa in CF

A

Highly resistant
Forms biofilms (mucoid)
G neg aerobic bacillus

67
Q

Typical patient in an immunocompromising host

A

Male

Most diagnosed over 18 but 7-9 years between onset and diagnosis

68
Q

Symptoms of an immunocompromised host

A

Severe
Persistent
Unusual
Recurrent

69
Q

Investigating immunodeficiencies

A 
History - family (X), viral and fungal ingestion Then T cell? Bacterial and fungal then B cell?
IgG IgA IgM
IgG to specific antigen
Immunisation testing
Neutrophil function
Individual complement components
Adhesion molecule expression (LAD
T cell test in vireo
Lymphocyte subset analysis
Test immunisation with antibody
Definitive test e.g. Molecule re and genetic
70
Q

B cell deficiencies

A 
CVID - inability of B cells to mature, presents at any point
IgA deficiency
IgG subclass deficiency- but total IgG fine
bruton's (problem in B cell development- X linked)
Hyper IgM syndrome- cannot switch to IgG
71
Q

Phagocyte deficiencies

A

Cyclic neutropenia - unknown
Leukocyte adhesion deficiency (LAD)
Chronic granulomatous disease- failure of oxidative burst/ killing
Chediak-higashi syndrome- failure of phagocytosis

72
Q

Describe T cell deficiencies

A

Di George- catch 22, cardia, abnormal faeces, thymus hypoplasia, cleft palate, hypocalcaemia- surgey, antibiotics, calcium, bone marrow transplant, X irradiated and cmv- blood, no live vaccine
SCID- stem cell defect or death of tymocytes
Omenns disease/ SCID- defective T cell development

73
Q

Discuss causes of secondary immuno deficiency

A 
Loss of immune components:
Infection e.g. HIV
Malnutrition
Liver disease 
Lymphoproliferative disease
A splenic patients 
Neutropenia:
Drug induced e.g. Alcohol, 
chemotherapy, 
organophosphate, benzene
Autoimmune
Bone marrow malignancy
Aplastic anaemia
Vitamins B12, folate or iron deficiency
Radiotherapy
74
Q

Discuss a splenic patients

A

More susceptible to encapsulated bacteria e.g. H influenzae strep pneumoniae and n meningitidis.
Prophylactic penicillin, immunisations, medical alert bracelet
OPSI- overwhelming sepsis and meningitis

75
Q

Role of the spleen

A

Removes encapsulated bacteria, synthesises antibodies, macrophages to remove opsonised bacteria and immune complexes.

76
Q

Consequences of a primary antibody deficiency and treatment

A 
Resp bacterial infections
GI complications
Lymphoma, gastric carcinoma
Arthropathies
Autoimmune disease.
Management:
Prophylaxis
Immunoglobulin replacement for cvid, bruton's, hyper IgA
Management of resp function
Avoid exposure to radiation
77
Q

Phagocytes deficiency presentation and management

A 
Ulcers
Osteomyelitis
Deep abcesses
Staphylococcal 
Invasive aspergillus
Inflam proba.
Prophylactic
Suregry
Interferon-g (CGD)
Steroids (CGD)
Stem cell transplant
78
Q

SCID presentation

A 
Failure to thrive
Long term Atb therapy
Deep abcesses 
Low lymphocyte
Viral and fungal infections
79
Q

Management of SCID

A 
No live vaccine
Irradiated cmv- blood
Aggressive treatment for infections
Prevention of infection
Bone marrow/ stem cells
Gene therapy

Esa 3 (5 decks)

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