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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
Pathogenesis enteric fever
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
25
Symptoms enteric fever
``` Fever Malaise Abdo pain Constipation Hepatospenomegaly Dry cough Bradycardia Intestinal haemorrhage/ perforation Occasional rash - paratyphoid not as bad ```
26
Investigation of enteric fever
Anaemia Feacal/ blood culture Raised LFTs Relative lymphopenia
27
Treatment of enteric fever
Ceftriaxone or azithromyosin (macrolide) Typhoid vaccine to VI antigen or a live attenuated vaccine but not 100% Also s typhimurium or enteritidis
28
Briefly describe brucellosis
From animals, milk or cut, gram neg bacilli (Brucella) Fever non specif symptoms, myalgia, arthralgia and epidydimitis Doxy or rifam Isolation required
29
Understand where and how to look up information on travel related infections
CDC - centres for disease control | WHO
30
Describe influenza virus and it's transmission and management
Aerosol Influenza A -ss RNA Fluids and painkiller
31
Describe legionella pneumophila and an example of its clinical importance.
``` 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 ```
32
Difference between antigenic drift and antigenic shift
Antigenic drift - mutations in antigens | Antigenic shift- combination of different strains
33
Describe features of an APC
Found in a variety of places - SALT, MALT, lymphoid organs, blood stream. Phagocytose of micropinocytosis (soluble particles from pathogen)
34
Describe extracellular PAMPs and how they are identified
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
Describe intracellular PAMPs and how they are identified
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
Properties of MHC
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
T cells and cytokines?
TH1 - TNFa, IFN gamma Th2- Il4,5,10 TH17- Il17
38
Apply the infection model to a patient with HIV
``` 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
Apply the infection model to Hep B
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
Understand the concept of microbiota
Commensal bacteria both symbiotic and pathogenic that live on a body surface.
41
Appreciate the range of normal microbiota
``` 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
Describe pathogenesis of infections at a surface
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
Describe the management of infected sites
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
Describe the range and origins of surface infections on both natural and prosthetic surfaces
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
Describe the different types of hypersensitivity reactions
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
Understand the pathophysiology behind the type I hypersensitivity reaction
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
Treatment of type I anaphylaxis
Adrenaline | Monitor EXG, BP, pulse and oximetry
48
Management of type 1
Education e.g. Epipen Avoid allergens Sensitivity testing, graded exposure Manage with antihistamines, steroids, anti IgE
49
Apply the infection model to a patient presenting with a hospital aquired infection
Within 48 hours of admission including visitors and HCW
50
Practice and place health care infections
Practice- activities of HCA, organisation structure and engagement, leadership, government iniative Place- healthcare environment, fixed features and variable features
51
Understand the range of hospital acquired infections
``` Ventilator pneumonia Mrsa Candida albicans Pseudomonas aeruginosa Clostridium difficile TB Legionaries UTI ```
52
Describe the use of personal protective equipment with regard to a hospital setting
Vomiting/ diarrhoea then gloves and apon | Full Ppe suit for highly contagious diseases such as Ebola.
53
Pathogenesis of C. difficile
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
Management of C. difficile
Metronidazole Vancomyosin Often stopping causative antibiotic will sort it out.
55
Characteristics of staph aureus with regard to hospital aquired infections and drug resistance
Some resistant to most B lactams antibiotics, eg. Methicillin. Gentimicin some resistance. Vancomyosin little resistance
56
Characteristics of norovirus
Aerosol Winter vomiting disease +ssRNA non enveloped Bleach and disinfectants, isolation to prevent spread
57
Significance of reproduction number (Ro) and levels of outbreak
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
Consider the principles of infection prevention
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
Appreciate the consequences of antibiotic resistance
MDR! XDR, PDR Treatment failure Prophylactic failure - surgery Economic cost of ITU
60
Principles of anti microbial stewardship
``` 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
What does anti microbial stewardship require?
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
Describe the diversity of chronic infections
``` Vascular Infection Trauma Autoimmune Metabolic Inflammatory Neoplasm Congenital Degenerative Environmental Idiopathic ```
63
Describe CF and infection
``` 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
Describe DM and infections
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
Down's syndrome and infection
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
The role of pseudomonas aeruginosa in CF
Highly resistant Forms biofilms (mucoid) G neg aerobic bacillus
67
Typical patient in an immunocompromising host
Male | Most diagnosed over 18 but 7-9 years between onset and diagnosis
68
Symptoms of an immunocompromised host
Severe Persistent Unusual Recurrent
69
Investigating immunodeficiencies
``` 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
B cell deficiencies
``` 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
Phagocyte deficiencies
Cyclic neutropenia - unknown Leukocyte adhesion deficiency (LAD) Chronic granulomatous disease- failure of oxidative burst/ killing Chediak-higashi syndrome- failure of phagocytosis
72
Describe T cell deficiencies
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
Discuss causes of secondary immuno deficiency
``` 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
Discuss a splenic patients
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
Role of the spleen
Removes encapsulated bacteria, synthesises antibodies, macrophages to remove opsonised bacteria and immune complexes.
76
Consequences of a primary antibody deficiency and treatment
``` 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
Phagocytes deficiency presentation and management
``` Ulcers Osteomyelitis Deep abcesses Staphylococcal Invasive aspergillus Inflam proba. ``` ``` Prophylactic Suregry Interferon-g (CGD) Steroids (CGD) Stem cell transplant ```
78
SCID presentation
``` Failure to thrive Long term Atb therapy Deep abcesses Low lymphocyte Viral and fungal infections ```
79
Management of SCID
``` 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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