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Infection Flashcards

0
Q

Give some examples of pathogens using different routes of infection

A

Self - Escherichia coli - Uti
Direct contact - Herpes Simplex Virus - Cold sore
Vector - Plasmodium vivax - malaria
Faeco-oral (food and water) - Clostridium difficile - c diff
Droplet - Influenza - flu
Aerosol - Mycobacterium tuberculosis - TB
Blood - Hepatitis B - hep B
Vertical transmission - cytomegalovirus (placental), Chlamydia trachomatis (delivery)

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1
Q

Define infection

A

Ann invasion of hosts tissues by microorganisms

Causing disease by microbial multiplication, toxins or host response

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2
Q

Differentiate exo and endo toxins

A

Exo - released by the bacteria usually acting away from the site
Endo - structural components of bacteria

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3
Q

Which types of bacteria are more likely to express endotoxins?

A

Gram -ve

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4
Q

What are the toxins released by c diff

A

type A create pores in enterocytes

type B are cytotoxic

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5
Q

What pathogen and host factors influence disease severity?

A

Pathogen
Virulence of pathogen
Inoculation size
Antimicrobial resistance

Host
Site
Co morbidities
Age

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6
Q

What are the two broad categories of investigations for infection?

A

Supportive (e.g. Cxr, fbc)

Specific (e.g. Micorscopy, culture)

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7
Q

What sorts of viruses are effected by alcohol?

A

Enveloped - disrupts their membrane

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8
Q

Examples of Non enveloped viruses (thus less effected by alcohol)

A 
Paravirus 19 (fifths disease)
HPV (warts)
Enteroviruses (polio)
Noroviruses (D/V)
Rotaviruses (D/V)
Hep A and E
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9
Q

Give some examples of DNA viruses

A

Herpes viruses
HBV
Paravirus 19
HPV

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10
Q

Counterstain in a gram stain?

A

Safranin

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11
Q

Differentiate the types of fungi

A

Yeast - single cell (e.g. Candida, pneumocystis jiroveci)

Mould - multi cell (e.g. Aspergillus, tinia)

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12
Q

Give 3 examples of protazoa and their disease

A

Plasmodium - malaria
Giardia lamblia - giardiasis
Trypanosoma cruzi - chagas

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13
Q

Cause of bilharzia

A

Schistosoma mansoni

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14
Q

What patient factors influence susceptibility to infection?

A

Age (Stis in teens and 20s, varied levels of immunity to meningococcal meningitis)
Gender (uti and anatomy, suppressed immunity in males)
Physiological state (preggers, puberty/menopause)
Pathological state (immunocompromised, low blood flow)
Drugs (PPIs, steroids)
Social (living cramped, damp)
Time (seasonal infections, incubation)
Place (current - e.g. Hospital, recent - e.g. Travel infections)

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15
Q

What are the two main categories of infection treatment? What can be done in each?

A

Specific - abx, surgery

Supportive - fluids, o2, pain relief, immunoglobulins, abx against proteins to reduce exotoxin production

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16
Q

What are the sirs criteria?

A 
2 OF
Temp >38
Pulse >90
Rr >20
WBC 12x10*9
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17
Q

Give some examples of organ dysfunction seen in severe sepsis

A

Hypotension, confusion, decreased urine output, lactic acidosis

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18
Q

Why does sepsis alter coagulation?

What are the consequences

A

Cytokines initiate thrombin production and inhibit thrombolysis
Endothelial damage exposes TF and impairs prostacyclin production
DIC develops and clots can cause gangrene

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19
Q

What are the sepsis 6?

A 
Within one hour:
O2
Bloods for culture
Antibiotics administered
Serum lactate
IV fluids up
Urine output monitored
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20
Q

How is meningococcal meningitis subdivided?

What can we vaccinate against

A

Serogroups a,b, and c

Vaccines for a and c

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21
Q

What sort of a response does innate immunity provide to the body?

A

Fast and non specific

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22
Q

What are the first and second line defences of the innate immune system?

A

First - limits entry and growth

Second - contains and clears

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23
Q

What are the four categories of first line innate defences?

A

Physical - eg epithelial barrier, mucus membrane
Physiological - eg d/v coughing, sneezing
Chemical - eg stomach acid, vaginal acid, molecules (lysozymes, IgA, mucous, pepsin)
Biological - normal flora (compete, actively kill)

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24
Q

How does the stomach act as a chemical barrier to infection?

A

Acid

Pepsin

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25
Q

What is involved in second line innate defences?

A

Phagocytes
Chemicals
Inflammation

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26
Q

What do phagocytes use to recognise pathogens?

A

Use pathogen recognition receptors (PRRs) to detect pathogen associated molecular patterns (PAMPs)

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27
Q

Examples of PAMPs with associated bacteria

A

Lipopolysaccerides (gram -ve)
Peptidoglycan (gram +ve)
Flagellin (flagella bacteria)
Mannose rich glycans (mycobacteria)

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28
Q

What can enhance recognition of bacteria by PRRs?

A

Opsinisation with C3b, C4b, IgG, CRP

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29
Q

In which bacteria is opsionisation vital?

A

Encapsulated bacteria - neisseria meningitidis, streptococcus pneumoniae

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30
Q

How does phagocytosis occur?

A 
PRR recognises PAMP
Pseudopods engulph and ingest microbe forming phagosome
Phagosome fuses with lysosome
Microbe digested leaving residual body
Waste discharged from cell
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31
Q

How do phagocytes kill the microbes..

A

Oxidative burst

Lysozymes, lactoferrin, proteolytic enzymes

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32
Q

What chemical pathways are involved in second line innate immunity?

A

Compliment

Cytokines

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33
Q

How is complement activated?

A

Classical pathway - antibody antigen complex
Alternative pathway - cell surface on microbes (e.g. LPS)
Mannose binding lectin - MBL binds to mannose on pathogen

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34
Q

What are the active components of compliment? What do they do?

A

C3a and C5a - chemotaxis
C3b and C4b - opsinisation
C5-C9 - membrane attack complexes

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35
Q

What are the effects of macrophage derived chemical in second line innate immunity?

A 
Increase crp
Chemotaxis
Vasodilation
Increase vascular permiability
Increase body temperature
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36
Q

What chemicials do macrophages release?

A

Tnf alpha
Il-1
Il-6

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37
Q

In what conditions are second line defences of innate immunity compromised?

A 
Asplenia/hyposplenia 
Decreased neutrophils (leukaemia, chemotherapy)
Decreased neutrophil function
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38
Q

Define a healthcare related infection

A

An infection arising from a consequence of healthcare both within and out of hospital

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39
Q

How are hospital acquired infections differentiated form normal infections?

A

An infection that was neither present nor incubating at the time of admission (onset of symptoms >48 hrs after admission

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40
Q

What are the most common categories of healthcare related infections? What is the in hospital prevalence..

A

Gi and utis

8%

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41
Q

What can we do to reduced healthcare related infections regarding patient factors?

A

Screening
Prophylactic treatment
Optimise physical health
Appropriate choice of medications (e.g. Decreased cephalosporins)

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42
Q

What can we do to reduced healthcare related infections regarding place factors?

A

Bed layout with siderooms for high risk patients
Pressure isolation rooms
Sink and toilets accessible and individual in high risk
Sterilisation and decontamination

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43
Q

What can we do to reduced healthcare related infections regarding practice factors?

A

Handwashing
Hospital policies (eg. No relative sitting on beds)
Leadership up to government level - incentives work
Healthcare worker vaccinations
Ppe
Food hygene

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44
Q

What are the subdivisions of streptococcus?

A

Alpha haemolytic - pneumoniae and viridans
Beta haemolytic - pyrogenes
Non haemolytic - enterococcus

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45
Q

Diseases from strep viridans

A

Endocarditis

Dental caries

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46
Q

Diseases from strep pyogenes

A

Necrotising fascitis
Impertigo
Tonsilitis
Scarlet fever

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47
Q

Diseases from strep pneumoniae

A

Pneumonia

Meningitis

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48
Q

Diseases from staphylococcus

A

Boils
Carbuncles
Impertigo
Wound infection

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49
Q

Treatment options for staphylococcus infection

A

Flucloxacillin

Co-amoxiclav

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50
Q

Treatments for necrotising fasciitis

A

Initial broad spectrum like tazocin (pipperacillin and tazobactam)
Once id as strep pyogenes swich to ben pen
Large dose immunoglobulins to neutralise toxins
Antiprotein abx like clindamycin to decrease toxins
Debridment and amputation

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51
Q

Why is travel history important?

A 
Different diseases
Different strains (resistance change and change in detecting)
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52
Q

What do you need to know about in a travel hx

A 
Where
When
Via anywhere
Doing what
Staying where
Specific risks (sex, animals, swimming)
Preventative measures taken (prophylaxis, vaccinations, bite prevention)
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53
Q

What should you do with a suspected travel related infection?

A

Isolate until you know what it is!

Flag as high risk for lab

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54
Q

What are the causes of malaria?

A

P vivax
P falciparum
P ovale
P malariae

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55
Q

What is the characteristic fever of malaria? Which subtype differs?

A

3 day cycling, malariae is 4 day cycling

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56
Q

Symptoms of malaria

A 
Fever 3 day cycling
Headache
Cough
Fatigue
Malaise
Arthralgia
Myalgia
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57
Q

What is the usual incubation period for malaria?

A

1-3 weeks

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58
Q

What are the methods of transmission of malaria?

A

Vector - anaphalies mosquito in endemic region
Cryptic - mosi on a plane arriving at non endemic airport
Haematogenous
Iatrogenic - infected equipment

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59
Q

What investigations would you perform in malaria?

A 
Blood smear
Fbc
U and e
Lft 
Glucose
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60
Q

What are the causative organisms of enteric fever?

A

Salmonella enterica typhi

Salmonella enterica paratyphi

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61
Q

How are Salmonella enterica typhi/paratyphi spread?

How can you reduce your risk?

A

Faeco oral

Hand hygiene, safe food, vaccination

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62
Q

What treatments are effective in enteric fever?

A

Ceftrioxone

Azithromycin

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63
Q

Signs and symptoms of enteric fever

A 
Abdo discomfort
Cough
Constipation or diarrheoa
High fever
Relative bradycardia
Hepatosplenomegally 
Intestinal haemorrhage and perforation
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64
Q

Investigations in suspected enteric fever

A

Fbc
Lft
Stool and blood cultures

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65
Q

How do salmonella enterica typhi/paratyphi cause illness?

A

Fibriae adhere to epithelium over peyers patches
Invasin allows intracellular growth
As gram -ve have endotoxins

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66
Q

How can salmonella enterica typhi/paratyphi be distinguished in culture from escherichia coli?

A

They. Are non lactose fermenters

Otherwis both gram neg aerobic bacilli

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67
Q

What travel related infection is present in southern Europe?what is the causative organism?

A

Brucellosis

Brucella abortus/melitensis

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68
Q

How does brucellosis spread?

A

Zoonosis (cattle)
Spread via breaks in the skin and via the. Gi tract (e.g. Unpasturised milk)
Very rare person to person direct contact spread

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69
Q

How does brucellosis present?

A 
Non specific flu like febrile illness
Bone and joint involvement
Epididymitis 
Weight loss
PROLONGED SYMPTOMS
Long term complication endocarditis
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70
Q

How is brucellosis treated?

A

Doxycycline

Rifampicin

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71
Q

What are the two main components of adaptive immunity?

A

Cellular

Humoural

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72
Q

How is mhc adapted to a generalist presenting role?

A

Co dominant expression giving range of different subgroups

Peptide binding clefts very polymorphic

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73
Q

What is the difference in structure of mhc class 1 and class 2?

A

Class one - three alpha and one beta units
Class two - two alpha and two beta units
Note that the alpha and beta units are located on separate polypeptide chains.

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74
Q

What mhc molecule is active in cellular immunity? Which in humoural immunity?

A

Cellular - mhc 1 on most cells, both on apcs

Humoural - mhc 2 on apcs

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75
Q

How are cytotoxic t cells activated?

A

CD8 binds to MHC1 on an antigen presenting cell - presenting antigen recognised by t cell receptor
T cell binds to antigen on MHC1 on infected cell
Costimulation from IL2 produced by activated CD4 TH1 t cells

76
Q

How do activated cd8 t cells kill the cell?

A 
Release granzymes (protein digesting enzymes that trigger apoptosis) 
Release granulysin and perforin (create channels in plasma membrane)
77
Q

How does a t cell bind to a antigen presenting cell?

A

CD4/8 recognises MHC2/1. T cell receptor detects antigen in the MHC

78
Q

How is an antigen attached to MHC1?

A 
Sampling of cytosol 
Proteins broken down by proteasome
Fragments released into ER
Fragment attached to MHC1
MHC1 moves to cell surface
79
Q

How is an antigen attached to MHC2?

A

Pathogen phagocytosed by APC
Pathogen broken down by low pH and proteolysis
Vesicle of fragments merges with vesicle containing MHC2
Fragments load onto MHC2 and are moved to cell membrane

80
Q

How are cd4 t cells activated?

A

Recognise and bind MHC2 on APC

Co stimulated by IL2 from APC

81
Q

What do activated CD4 T cells do once activated?

A

TH1 - release IL 2 costimulating CD8 cells
TH2- costimulate b cells causing them to differentiate into plasma cells. Also activates eosinophils and mast cells
TH17 - activate neutrophils

82
Q

What are the different antibodies?

What do they do?

A

G - opsinisation
A - mucosal immunity decreasing aggregation
M - initial response to novel antigen
E - on mast and basophils involved in allergic reaction/parasites
D - B cell receptor

83
Q

What are the main functions of antibodies

A

Enhancing phagocytosis by opsionisation
Neutralisation of toxins
Complement activation (classical pathway)

84
Q

In an infection what is the first antibody released? What is released on reinfection? What is different?

A

IgM

IgG much faster stronger and longer with a higher affinity

85
Q

What are clinical uses of antibodies?

A 
Vaccinations
Active immunisations (e.g. Rabies)
Immunoglobulin therapy 
Immediate protection (e.g. Post exposure hep b)
Diagnostic testing
86
Q

What would make a hiv patient a slow progressor?

A

MHC configured to present antigens of the virus that cannot be altered by the virus, thus the virus cant mutate and avoid being expressed.

87
Q

What is the difference between HLA and MHC

A

MHC is the protein

HLA is the locus on the genome

88
Q

How can HIV be subclassified generally? What is the epidemiology?
Clinical relevance?

A

Hiv 1 - most common, nearly all western cases
Hiv 2 - confined to west africa, more indolent course
Different tx

89
Q

How is hiv 1 divided into groups?

A

M - major
N - new
O - outlier
P

90
Q

How is group M of HIV 1 subclassified!!?

What is the clinical relevance?

A

A-K - CRF (circulating recombinant forms on co-infection)
West mainly B
Same tx but different response

91
Q

What is the histological structure of the hiv virus?

A

Enveloped

SsRNA with reverse transcriptase

92
Q

What is the lifecycle of HiV

A

Gp120 binds to CD4
Virus fuses with plasma expelling contents
Reverse transcriptase converts rna to dna
Dna intergrates into host genome
Production of viral mrna and proteins
Caspid assemble and buds from cell

93
Q

At what point is a hiv infection irreversible?

A

Once the dna intergrates into the host genome

94
Q

How long is the incubation period for HiV

What happens at the end of it?

A

2-6 weeks

Seroconversion

95
Q

How does hiv seroconversion present?

A

Only 25% ill enough to attend hcp

Non specific illness, fever, rash, sore throat, lymphadonopathy, headache

96
Q

How many hiv infected people get seroconversion? What does it mean prognostically?

A

50-75%

May be at risk of more accelerated disease course.

97
Q

What is the term for the period between seroconversion and symptomatic hiv? What may be present?

A

Latent period

Lymphadenopathy

98
Q

What may be detectable in a hiv pt undergoing a seroconversion reaction?

A

Lymphopdnia
Low cd4;cd8 ratio
Circulating viral rna
Viral p24 antigen

99
Q

What causes symptomatic hiv?

How does it present?

A

Neurotoxins from hiv, cytokine abnormalities, low immunity

Aseptic meningitis, dementia, polyneuropathy, puritis, anaemia, anorexia, diarrhoea, weight loss ,

100
Q

What are aids defining illnesses?

A 
Candida of lower airways/oesophagus
Karposi's sarcoma
Tb
Pneumocystis jiroveci
Cmv retinitis
Hiv encephalitis
101
Q

What is the hiv core antigen?

A

P24

102
Q

What blood test will first show hiv?

When?

A

Viral p24 antigen

2 to 8 weeks

103
Q

What IgG tests can be used to detect hiv?

A

IgG to envelope - takes 3 months to build

IgG to core (p24) - detectible after weeks but lost as disease progresses

104
Q

How are hiv antigens detected and assessed?

A

Elisa followed by western blotting

105
Q

How would you not hiv test a baby of a infected mother?

A

Using IgG - it crosses the placenta so all babies will be positive

106
Q

What are the general classes of antiretrovirals?

What is the term for the combination used in. hiv?

A

Reverse transcriptase inhibitors
Protease inhibitors
Fusion inhibitors

107
Q

What are the subtype of reverse transcriptase inhibitors?

A

Nucleoside (NRTISs)
Nucleotide (NtRTIs)
Non-nucleoside (NNRTIs)

Highly active antiretroviral therapy (haart)

108
Q

What is a big side effect associated with NRTIs?

A

Effect mitochondria so lactic acidosis

109
Q

What is the lifecycle of HBV?

A

Attaches to and enters hepatocyte
Looses coat and core enters nucleus
Processing of dna with reverse transcriptase
New virons enter blood

110
Q

How is hepatic damage caused in hbv?

A

Immune response against virus

111
Q

What are the immediate outcomes post infection with HBv? What percentage of patients do which?

A

Acute infections - clear (89%)
Acute infection - death (1%)
Acute infection - chronic infections (10%

112
Q

What are the symptoms of acute hbv infection?

A 
Malaise
Jaundice
Nausea/vomiting
Weight loss
Diarrheoa
113
Q

What causes death in acute hbv infection?

A

Fulminant hepatic failure

114
Q

What age group is more likely to develop a chronic hbv infection?

A

Children (esp infants)

115
Q

How can chronic hbv present?

A

Progressive - cirrhosis - risk of liver carcinoma

Non-progressive

116
Q

How do hbv antibodies change over the course of a disease with recovery?

A

Initial rise in HBs antigen and HBc IgG
HBs antigen falls
HBs IgG rises

117
Q

How do hbv antibodies change in a chronic disease?

A

Rise and maintainance of HBc IgG and HBc antigen

118
Q

If someone is vaccinated against hbv what antibody would you expect to be high? What would indicate that they had been infected?

A

HBs IgG

If infected HBc antigen and IgG

119
Q

How can HBV be prevented?

A

Lifestyle changes/PPE
HBs antigen vaccination
PEP with immunoglobulin

120
Q

Which infection can only occur alongside HBV? In what ways? What is different about the two ways of dual infection?

A

HDV
Coinfection - severe acute disease with low risk of chronic
Superinfection - reactivation of HBV with high risk of chronic

121
Q

Why does HDV need HBV?

A

HDV uses envelope of HBV

122
Q

In what ways can pathogens infect the internal surface of the body or prothesis?
Examples of each

A

Migration - Escherichia coli - UTI
Invasion - Streptococcus pyogenes - necrotising fasciitis
Haematogenous - streptococcus viridans - infective endocarditis
Innoculation - coag -ve staphylococcus - prothesis infection

123
Q

What are the varying causes of infective endocarditis in native and prosthetic valves?

A

Native and >1 yr prosthetics - Strep. viridans, Staph. aureus, Candida
<1 yr prosthetics - coag -ve staphylococcus

124
Q

What are the stages involved in the infection of a prothetic joint? How are bacteria adapted for this?

A

Adherence - pili/fimbriae
Biofilm formation - ecf production, quorum sensing (signalling for neighbours to produce ecf)
Invasion and multiplication

125
Q

How do biofilms aid bacteria?

A

Protection from immune system
Protection from abx
Nutrients
Chemically favourable environment

126
Q

What are the clinical problems regarding biofilms?

A

Poor abx penetration

Hard to grow as must shake loose first

127
Q

Define hypersensitivity reactions

A

Antigen specific
Immune response
Inappropriate or excessive
Harm the host

128
Q

What are the four types of hypersensitivity reaction?

A

Type 1 - antigen interacts with IgE on MAST cells triggering mediators inc. histamine release
Type 2 - drug attaches to cell membrane of RBC becoming a hapten then bound by antibodies activating complement causing cell lysis
Type 3 - antibody antigen complex not removed from blood by phagocytosis so keeps activating complement causing endothelial damage - can be especially bad if trapped in endothelium
Type 4 - activation t cells by hapten protein complex, causes skin inflammation and rash

129
Q

What is the prevalence of allergy?
What is the most common?
How common is it?

A

About 50%
Peanut
1:50

130
Q

What is the hygiene hypothesis?

A

Low pathogen exposure (clean living, small family, increased abx, low dirt)
Favours increased th2 cd4 t cells which instigate second phase of an allergic reaction

131
Q

What do mast cells release? What do they do?

A

Histamine - smooth muscle dilation (arterioles) and constriction (bronchioles)
Cytokines - stimulate CD4 TH2, promote eosinophils and inflammation
Chemokines - attract inflammatory cells
Leukotrines - increase vascular permeability

132
Q

How can a diagnosis of allergy be made?

A

Skin prick testing
Blood test for allergen specific IgE
Allergy challenge

133
Q

What controls are used in skin prick testing?

Where does it test for reaction

A

Heparin and saline

Epidermis

134
Q

What are the signs of epidermal allergy, dermis allergy?

A

Urticaria

Angioedema

135
Q

Management of allergy

A 
Allergen avoidance!
Education to recognise and get help
Epipen
Medialert
Desensitisation therapy 
Emergency anaphylaxis tx.
136
Q

What levels of disease can transmissable infection cause?

A

Endemic disease - normal background rate
Outbreak - 2 or more cases linked in time and place
Epidemic - a rate of infection greater that background rate
Pandemic - very high rate of infection across many countries and continents

137
Q

How can we classify if a disease is going to increase in cases, remain constant or decrease in cases?

A

R0 number - the number of people one case infects
If more than 1 then numbers will increase
If 1 numbers will be constant
If less than 1 numbers will decrease

138
Q

What could lead to an new increase in number of infections?

A

New pathogens - e.g. Mutation, spread
New person - e.g. Migration, newborn baby
New practice - e.g. Air conditioning

139
Q

How do the general pattern of cases in epidemics and outbreaks differ?

A

Epidemics tend to follow a bell curve distribution of incidence against time
Outbreaks tend to follow a much more random distribution - they can be large with excellent control or small with non. This can lead to the false belief a certain intervention is effective even when it isn’t

140
Q

What is a paradox in polio control regarding immunisation? How can this paradox be applied to a western disease?

A

Those not immunised are exposed later in life and thus experience more severe disease (increased paralysis)
More adult chickenpox and thus increased infertility

141
Q

What are problems with antibiotic resistance generally?

A

Resistance is irreversible
Development has stalled
Use causes resistance even if appropriate

142
Q

What are the problems with abx resistance?

A

Treatment failure
More severe treatments required
More expensive treatments required
Prophylaxis failure

143
Q

What are the different classifications of resistance to abx?

A 
Resistant - 1 or more agents in 1or 2 classes 
Multi drug (MDR) - 1 or more agents in 3 or more classes
Extensively drug (XDR) - more than 1 agent in all but 2 classes
Pan drug (PDR) - all agents in all classes
144
Q

What is the aim of abx stewardship?

A 
Improve appropriate abx use
Achieve optimal clinical outcome
Minimise toxicity 
Reduce cost
Limit resistance
145
Q

What clinicians are involved in ABX stewardship?

A 
Medical microbiologist
Infectious diseases physician
Antimicrobial pharmacist
Infection control nurse
Hospital epidemiologist
146
Q

What types of intervention are there for antimicrobial stewardship?

A

Persuasive - education, consensus between clinicians, reminders, audits, feedback
Restrictive - limit abx on susceptability report, restrict formulary, require authorisation,
Structural - rapid lab tests to avoid general administration, computerised records

147
Q

What type of abx stewardship intervention is most efficacious?

A

Initially restrictive but after several months both restrictive and persuasive

148
Q

What are the outcomes seen from abx stewardship?

A

Non significant reduction in death rate
Significant reduction in length of stay
Significant increase in readmission (why!)

149
Q

What is the pattern of infection seen in CF patients?

A

Birth - 3m = haemophillus influenzae
3m - 3y = staphylococcus aureus
3y - teens = pseudomonas aeruginosa
teens - 30s = atypical mycobacteria, candida, aspergillus

150
Q

Why are cf patients more at risk of infection?

A

Lack of mucous clearence
Lung damage (bronchiectasis)
Steroid treatment

151
Q

Why should cf cf contact be reduced?

A

Environmental psuedomonas tx is amenable to ABX but given time in a cf pt it develops ability to produce biofilm becoming much harder to treat - this can be spread to other cf patients

152
Q

What pathogens are associated with copd exacerbations?

A

Haemophilus influenzae, pseudomonas aeruginosa, respiratory syncytial virus, parainfluenza virus, influenza A

153
Q

Why are poorly controlled diabetics more at risk of infection?

A

Impaired humoural, neutrophil and lymphocyte function
Microvascular damage = poor tissue perfusion = damage
Neuronal damage = not noticing stimuli = damage
Sugar in urine = food for uti

154
Q

What specific infections are associated with diabetes?

A

Malignant otitis externa
Rhinocerebral mucormycosis
Utis
Ulceration

155
Q

What are risk factors for uti in diabetics?

A

Increases glucose in urine

Neurogenic bladder that doesn’t empty fully

156
Q

What pathogens are prone to infecting diabetic foot ulcers?

A 
Staphylococcus aureus 
Streptococcus pyrogenes (beta haemolytic)
157
Q

What is malignant otitis externa?

A

Otitis externa with psuedomonas aerugenosa that can spread to neighbouring soft tissue and bone

158
Q

What is rhinocerebral mucormycosis?

A

Mold fungi like aspergillus effecting paranasal sinuses invading blood vessels

159
Q

Does downs syndrome effect risk of infection?

A

Yes - higher risk of urtis and lrtis due to altered structure of mouth and airways

160
Q

What is an immunodeficiency?

A

A state in which the immune system is unable to respond appropriately and effectively to infectious microorganisms

161
Q

What immune system deficites (generally) can cause immunodeficiencey

A

Quantitative

Qualitative

162
Q

What about an infection should make a clinician consider immunodeficiency?

A

S - severe
P - persistent
U - unusual
R - recurrent

163
Q

Other than infection what are other issues with immunodeficiency?

A

Linked to autoimmune disease and malignancy

164
Q

What are the categories of primary immunodeficiency? What are each group vulnerable too?

A

B cell - bacterial infection
T cell - viral (and fungal) infection
Complement - bacterial infection
Phagocyte - bacterial and fungal infection

165
Q

What are the main B cell deficiencies?

A 
Common variable immune deficiency
IgA deficiency 
IgG subclass deficiency 
Bruton's disease
166
Q

What is CVID?

A

Common variable immunodeficiency
Inability of B cells to mature into plasma cells
Low igg

167
Q

What is brutons disease?

A

X linked agammagloblinaemia

Impaired b cell development with low igg and iga

168
Q

Hw do b cell deficiencies present?

A

Recurrent bacterial urti and lrti
Gi infections
Autoimmune disease
Lyphatic and gastric cancers

169
Q

How do you treat b cell deficiencies

A

Prophylactic ABX
Ig replacement
Symptomatic management
Avoidance of unnecessary radiation due to cancer risk

170
Q

Give two t cell deficiencies

A

De georges syndrome

Severe combined immunodeficiency (SCID)

171
Q

What are the problems in de georges syndrome

A 
C - cardiac abnormalities
A - abnormal facies
T - thymic hypoplasia 
C - cleft palate
H - hypocalcaemia
172
Q

Tx of de georges syndrome

A

Cardiac surgery
Calcium
Prophylactic ABX
Bone marrow transplant

173
Q

How do SCID diseases present?

A

Failure to thrive
Viral and fungal infections (PCP, CMV, VZV, EBV)
Skin and organ abcesses
Low t lymphocytes and decreased b activation so low ig

174
Q

How do you treat SCID?

A

Reverse barrier nursing
Abx
Bone marrow transplant
Gene therapy

175
Q

How do complement deficiencies present?

A 
Hereditory angioedema (C1 inhibitor deficiency)
Recurrent bacterial infections (C3 deficiency)
Neiserria infection (C5-7 deficiency)
176
Q

What are the phagocyte deficiencies?

A

Cyclic neutropenia
Leukocyte adhesion deficiency
Chronic granulomatous disease
Failure of phagosome formation

177
Q

What is chronic granulomatous disease?

A

Lack of respiratory burst

178
Q

How do phagocyte deficiencies present?

A

Bacterial and fungal infections of the skin, mucous membranes and lungs

179
Q

How are phagocyte deficiencies treated?

A

Prophylactic ABX
Steroid/interferon gamma (chronic granulomatous disease)
Stem cell transplant

180
Q

A young patient presents with a large number of persistent bacterial skin abscesses, what primary immunodeficiencies may he have? What tests would you like?

A

Phagocyte deficiency
T cell deficiency

FBC, lymphocyte subset analysis, adhesion molecule expression, neutrophil function tests, IgG levels

181
Q

What can cause primary immunodeficiencies?

A

Single gene disorders
Polygenetic disorders
Hla polymorphism

182
Q

What two general categories of secondary immunodeficiency are there? Examples?

A

Decreased production of immune component
- HIV, splenectomy, liver disease, malnutrition

Increased loss of immune components
- nephropathy, burns, enteropathy

183
Q

What drugs can cause neutropenia?

A

Pheytoin, alcohol, chemotherapy, immunosuppressants

184
Q

What diseases can cause neutropenia?

A

HIV, EBV, HBV, vit b deficiency, bone marrow cancer

185
Q

Why might the spleen need removing?

A

Infarction
Trauma
Immune haemolytic disease
Tumour

186
Q

What disease can cause splenic atrophy?

A

Coeliac disease

187
Q

What happens after the spleen is removed?

A

Decreased IgG production
Thus decreased opsinisation
Thus increased risk of encapsulated bacteria (neiserria meningitidis, haemophillus influenzae, strep. pneumoniae

PPE (12 decks)

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