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Final Year > Infectious Diseases > Flashcards

Infectious Diseases Flashcards

1
Q

What is malaria?

A

Infectious disease caused by Plasmodium of protozoan parasites (single-celled organisms)

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2
Q

What is the most severe and dangerous type of malaria?

A

Plasmodium falciparum- Accounts for 80% of malaria causes in the UK

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3
Q

How is malaria transmitted?

A

Through bites from female Anopheles mosquitoes that carry the disease
Not transmitted in the UK- Is associated with travel to areas where malaria is present

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4
Q

List types of malaria

A

Plasmodium falciparum (most common and severe form)
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae
Plasmodium knowlesi

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5
Q

Outline the life cycle of malaria

A

Usually spread at night
Feeding mosquito sucks up infected blood- Parasites reproduce in mosquito’s gut, producing sporozoites
Mosquito bites someone, sporozoites are injected- Travel to liver of newly infected person- P. vivax and P. ovale can lie dormant for months or years before reactivating
Parasites mature in liver into merozoites- Enter blood and infect RBCs- Merozoites reproduce, RBCs rupture, releasing merozoites into blood and causing haemolytic anaemia
In P. vivax and P. ovale- Rupture and release of merozoites occurs every 48h, causing fever spike every other day
P. falciparum- Fever spikes more frequently
P. malariae- Fever spikes every 72h

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6
Q

Outline presentation of malaria

A

Fever (up to 41 degrees C) with sweats and rigors
Fatigue
Myalgia (muscle aches and pains)
Headache
Nausea
Vomiting

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7
Q

What are the signs of malaria on examination?

A

Pallor due to anaemia
Hepatosplenomegaly
Jaundice (bilirubin released during rupture of RBCs)

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8
Q

What is the most characteristic symptom of malaria?

A

Fever which spikes very high every 48h
Exposure can be from several years ago

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9
Q

How is malaria diagnosed?

A

Malaria blood film- Sent in EDTA bottle
3 negative samples taken over 3 consecutive days required to exclude malaria

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10
Q

Outline management of falciparum malaria

A

Admit

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11
Q

Outline oral management of uncomplicated malaria

A

Artemether with lumefantrine (Riamet)- 1st choice
Quinine plus doxycycline
Quinine plus clindamycin
Quinine plus clindamycin
Proguanil with atovaquone (Malarone)
Chloroquine (increasing rates of resistance to chloroquine)
Primaquine (can cause severe haemolysis in patients with G6PD deficiency)

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12
Q

Outline IV management of severe or complicated malaria

A

Admission to HDU or ICU
Artesunate 1st choice (haemolysis common SE)
Quinine dihydrochloride

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13
Q

List complications of P. falciparum malaria

A

Cerebral malaria
Seizures
Reduced consciousness
AKI
Pulmonary oedema
Disseminated intravascular coagulopathy (DIC)
Severe haemolytic anaemia
Multi-organ failure and death

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14
Q

Outline prophylaxis for preventing malaria when travelling to endemic areas

A

No method 100% effective alone
Use mosquito spray (eg: 50% DEET spray)
Use mosquito nets and barriers in sleeping areas
Seek medical advice if symptoms develop
Take antimalarial medication as recommended

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15
Q

What are the main antimalarial medication options?

A

Not 100% effective
Proguanil with atovaquone (malarone)- Take from 2d before until 7d after travel to endemic area
Doxycycline- Taken 2d before until 4wks after travel to endemic area
Mefloquine (risk of psychiatric SEs)- Taken wkly from 2wks before to 4wks after travel to endemic area
Chloroquine with proguanil (less often used due to high resistance)

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16
Q

Outline HIV

A

RNA retrovirus
HIV-1 is most common type
HIV2 mainly found in West Africa
Virus enters and destroys CD4 T-helper cells
Initial seroconversion flu-like illness occurs within few wks of infection- Then asymptomatic until condition progresses to immunodeficiency- May occur yrs after initial infection

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17
Q

Outline transmission of HIV

A

Unprotected anal, vaginal or oral sexual activity
Mother to child- At any stage of pregnancy, birth or breastfeeding- Vertical transmission
Mucous membrane, blood, or open wound exposure to infected blood/bodily fluids- eg: Sharing needles, needle-stick injuries, blood splashed in eye

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18
Q

List AIDS-defining illnesses

A

CD4 count dropped to level that allows for unusual opportunistic infections and malignancies

Kaposi’s sarcoma
Pneumocystis jirovecii pneumonia (PCP)
CMV
Candidiasis (oesophageal or bronchial)
Lymphomas
TB

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19
Q

Outline HIV screening

A

Low threshold for testing
Patients with RFs tested
All patients accessing sexual health/antenatal/substance misuse services offered testing
Verbal consent should be documented

Checks ABs to HIV and p24 antigen
Window period of 45d- Can take up to 45d for +ve test to show
Point of care test- HIV ABs- Give result within mins, have 90d window period
Self-sampling kits- Posted to lab- ABs and p24 antigen

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20
Q

Outline monitoring of HIV

A

Test CD4 count gives number of CD4 cells in blood- Lower count gives higher risk of infection
500-1200 cells/mm3= Normal
<200 cells/mm3= High risk opportunistic infections

Testing for HIV RNA/ml of blood indicates viral load
Undetectable viral load means level below recordable range (20 copies/ml)

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21
Q

Outline treatment of HIV

A

Combination of antiretroviral therapy (ART)- Offered to everyone diagnosed with HIV, irrespective of viral load or CD4 count
Genotypic resistance testing- Establish resistance of each HIV strain to different meds to guide treatment
Aims to achieve normal CD4 count and undetectable viral load

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22
Q

List classes of antiretroviral therapy meds

A

Protease inhibitors (PI)
Integrase inhibitors (II)
Nucleoside reverse transcriptase inhibitors (NRTI)
Non-nucleoside reverse transcriptase inhibitors (NNRTI)
Entry inhibitors (EI)

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23
Q

What is the usual starting regime for antiretroviral therapy?

A

2 NRTIs (eg: Tenofovir plus emtricitabine) plus 3rd agent (eg: Bictegravir)

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24
Q

Outline additional management of HIV

A

PCP- Prophylactic co-trimoxazole given to all HIV +ve patients with CD4 count<200/mm3
Increased risk developing CVD- Monitor blood lipids and consider statins
Yrly cervical smears- Increased risk HPV and cervical cancer
Vaccinations- Yrly influenza, pneumococcal, HPV, Hep A and B- Avoid live vaccines

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25
Q

Outline reproductive health and HIV

A

Correct use of condoms
Effective treatment combined with undetectable viral load can prevent spread of HIV

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26
Q

Outline prevention of transmission of HIV during birth

A

Mother’s viral load determines mode of delivery
<50 copies/ml- Normal vaginal delivery
>50 copies/ml- Consider pre-labour C section
>400 copies/ml- Pre-labour C section

IV zidovudine infusion during labour and delivery if viral load unknown/>1000 copies/ml

Prophylaxis given to baby depending on mother’s viral load:
<50 copies/ml- Zidovudine for 2-4wks
High-risk babies- Zidovudine, lamivudine, nevirapine for 4wks

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27
Q

Outline HIV and breastfeeding

A

Can be transmitted during breastfeeding
Risk reduced if mother’s viral load undetectable but not eliminated

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28
Q

Outline post-exposure prophylaxis (PEP) of HIV

A

Post-exposure prophylaxis (PEP)- Used after exposure to reduce risk of transmission- Not 100% effective and must be commenced within <72h
Combination of ART therapy- Emtricitabine/tenofovir (Truvada) and raltegravir for 28d

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29
Q

Outline pre-exposure prophylaxis (PrEP) of HIV

A

Emtricitabine/tenofovir (Truvada)

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30
Q

Outline TB

A

Caused by mycobacterium TB (rod-shaped acid-fast bacillus)- Require Zeihl-Neelsen stain- Turns bright red against blue background

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31
Q

What type of staining is used to diagnose TB?

A

Require Zeihl-Neelsen stain- Turns bright red against blue background

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32
Q

Outline the disease course of TB

A

Mainly spread by inhaling saliva droplets from infected
Several options:
- Immediate clearance (most cases)
- Primary active TB (active infection after exposure)
- Latent TB (Presence of bacteria w/o symptomatic or contagious)
- Secondary TB (reactivation of latent TB to active infection)

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33
Q

What is miliary TB?

A

When immune system can’t control infection
Disseminated and severe disease

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34
Q

Outline latent TB

A

When immune system encapsulates the bacteria and stops progression of the disease
No symptoms and can’t spread the bacteria
Can reactivate, usually due to immunosuppression- Secondary TB

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35
Q

Where is the most common site for TB infection?

A

Lungs

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36
Q

List sites of extrapulmonary TB

A

Lymph nodes
Pleura
CNS
Pericardium
GI system
GU system
Bones and joints
Skin (cutaneous TB)

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37
Q

What is a cold abscess?

A

Firm, painless abscess caused by TB, usually in neck
No inflammation/redness/pain

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38
Q

Outline risk factors for TB

A

Close contact with active TB
Immigrants from areas with high TB prevalence
People with relatives/close contacts from countries with high rate TB
Immunocompromised (eg: HIV or immunosuppressant meds)
Malnutrition, homelessness, drug users, smokers and alcoholics

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39
Q

Outline the BCG vaccine

A

Intradermal injection of live attenuated Mycobacterium bovis
Protects against severe and complicated TB, but less against pulmonary TB
Tested with Mantoux before vaccine

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40
Q

Outline presentation of TB

A

Chronic, gradually worsening symptoms
Most involve pulmonary disease
Cough
Haemoptysis
Lethargy
Fever or night sweats
Weight loss
Lymphadenopathy
Erythema nodosum (tender, red nodules on shins caused by inflammation of SC fat)
Spinal pain in spinal TB (Pott’s disease)

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41
Q

Outline investigations of TB

A

Ziehl-Neelsen stain
2 tests for immune response to TB caused by previous infection/latent TB/active TB- Mantoux test or Interferon-gamma release assay (IGRA)
If disease activity suspected- CXR and cultures

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42
Q

Outline Mantoux test

A

Inject tuberculin into intradermal space on forearm
Doesn’t contain live bacteria
Creates a bleb under skin- Read after 72h- >5mm is +ve

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43
Q

Outline Interferon-Gamma release Assay (IGRA)

A

Mixing a blood sample with antigens from M. TB bacteria
After previous contact- WBCs become sensitised to bacteria antigens- Will release interferon-gamma on further contact
Positive- Interferon-gamma is released during test

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44
Q

Outline CXR of TB

A

Primary TB- Patchy consolidation, pleural effusions and hilar lymphadenopathy
Reactivated TB- Patchy or nodular consolidation with cavitation (gas-filled spaces), typically in upper zones
Disseminated miliary TB- Millet seeds uniformly distributed across lung fields

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45
Q

Outline cultures of TB

A

Can take several mths
Sputum cultures (3 separate collected)
Mycobacterium blood cultures
Lymph node aspiration or biopsy

If not producing enough sputum:
Sputum induction with nebulised hypertonic saline
Bronchoscopy and bronchoalveolar lavage (saline used to wash airways and collect a sample)

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46
Q

Outline Nucleic Acid Amplification Tests (NAAT)

A

Assesses genetic material of a pathogen
Detects TB DNA
Faster than traditional culture
Used for- Diagnosing TB in patients with HIV or <16y or RFs for multidrug resistance

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47
Q

Outline treatment of latent TB

A

Isoniazid and rifampicin for 3mths
Isoniazid for 6mths

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48
Q

Outline treatment of active TB

A

R- Rifampicin for 6mths
I- Isoniazid for 6mths
P- Pyrazinamide for 2mths
E- Ethambutol for 2mths

Co-prescribe pyridoxine (Vit B6) to prevent peripheral neuropathy caused by isoniazid

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49
Q

What is the main SE of isoniazid and how is this managed?

A

Peripheral neuropathy
Give pyridoxine (Vit B6)

Other SE- Hepatotoxicity

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50
Q

Outline other management options for TB

A

Test for other infectious disease (HIV/Hep B/Hep C)
Contact tracing
Isolate patients with active TB (at least 2wks)
Negative pressure rooms in hospitals used to prevent airborne spread

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51
Q

What are the SEs of rifampicin?

A

Red/orange discolouration of secretions- Urine and tears
Potent inducer of cytochrome P450 enzymes- Reduces effects of drugs metabolised by this system (eg: combined contraceptive)
Hepatotoxicity

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52
Q

What are the SEs of Pyrazinamide?

A

Hyperuricaemia (high uric acid levels)- Results in gout and kidney stones
Hepatotoxicity

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53
Q

What are the SEs of Ethambutol?

A

Colour blindness and reduced visual acuity

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54
Q

What is meningitis?

A

Inflammation of meninges usually due to infection
Meninges- Lining of brain and spinal cord
CSF is contained within meninges (in subarachnoid space)

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55
Q

List the causes of bacterial meningitis

A

Neisseria meningitidis
Streptococcus pneumoniae (pneumococcus)
Haemophilus influenzae
Group B Streptococcus (GBS)- Particularly in neonates
Listeria monocytogenes- Particularly in neonates

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56
Q

Outline Neisseria meningitidis

A

Gram-negative diplococcus bacteria
Typically known as meningococcus
Most common cause of bacterial meningitis

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57
Q

Outline Meningococcal meningitis

A

Bacteria infects meninges and CSF

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58
Q

Outline Meningococcal speticaemia

A

Meningococcus bacterial infection in bloodstream
Causes non-blanching rash

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59
Q

What are the most common causes of viral meningitis?

A

Enteroviruses (eg: Coxsackie virus)
Herpes simplex virus (HSV)
Varicella zoster virus (VZV)

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60
Q

How is viral meningitis diagnosed?

A

Viral PCR testing on CSF sample

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61
Q

How is viral meningitis managed?

A

Aciclovir- Used to treat HSV and VZV

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62
Q

Outline presentation of meningitis

A

Fever
Neck stiffness
Vomiting
Headache
Photophobia
Altered consciousness
Seizures

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63
Q

Outline presentation of meningitis in neonates and babies

A

Non-specific signs and symptoms
Hypotonia
Poor feeding
Lethargy
Hypothermia
Bulging fontanelle

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64
Q

What are the NICE guidelines for investigations of children with suspected sepsis?

A

Lumbar puncture
Under 1mth, presenting with fever
1-3mths and are unwell/have low or high WBC count

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65
Q

What are the special tests to perform to look for meningeal irritation?

A

Kernig’s test
Brudzinski’s test

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66
Q

What is Kernig’s test?

A

Lie patient on back, flex one hip and knee to 90 degrees, slowly straighten knee whilst keeping hip flexed at 90 degrees
Creates stretch in meninges
If meningitis- Produce spinal pain or resistance to movement

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67
Q

What is Brudzinski’s test

A

Lie patient flat on back and use hands to lift their head and neck off bed, flexing chin to their chest
Positive test for meningitis- Causes patient to flex their hips and knees involuntarily

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68
Q

Outline the lumbar puncture result of bacterial meningitis

A

Cloudy
High protein
Low glucose
High WCC (neutrophils)
Bacteria on culture

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69
Q

Outline the lumbar puncture result of viral meningitis

A

Clear
Mildly raised/normal protein
Normal glucose
High WCC (lymphocytes)
Negative culture

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70
Q

Outline the procedure of a lumbar puncture

A

Insert needle into L3-L4 or L4/L5 intervertebral space
Spinal cord ends at L1-L2

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71
Q

Outline management of bacterial meningitis

A

MEDICAL EMERGENCY
Children in primary care with suspected meningitis and non-blanching rash- Urgent benzylpenicillin (IM or IV)
Blood cultures and LP before starting ABs- Meningococcal PCR (gives faster result than blood cultures and still positive after treated with ABs)

<3mths- Cefotaxime plus amoxicillin
>3mths- Ceftriaxone

Aciclovir added if viral meningitis suspected
Vancomycin added if risk of penicillin-resistant pneumococcal infection (recent foreign travel or prolonged AB exposure)
Steroids (dexamethasone) in bacterial meningitis- Reduce frequency and severity of hearing loss and neuro complications

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72
Q

What is used to reduce frequency of hearing loss and neurological complications in meningitis?

A

Dexamethasone

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73
Q

List complications of hearing loss

A

Hearing loss
Seizures and epilepsy
Cognitive impairment and learning disability
Memory loss
Focal neurological deficits- Limb weakness or spasticity

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74
Q

Outline post-exposure prophylaxis of meningitis

A

Risk highest with close prolonged contact within 7d before onset of illness
Single dose of ciprofloxacin given as soon as possible after diagnosis

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75
Q

Outline Clostridium difficile

A

Gram positive, rod-shaped, anaerobic bacteria
Infection associated with repeated use of ABs/PPIs/healthcare settings
Spores released in faeces
May colonise intestines w/o causing any symptoms or issues
Produces Toxin A (enterotoxin) and Toxin B (cytotoxin)

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76
Q

List ABs most associated with C. difficile

A

Clindamycin
Ciprofloxacin (and other fluoroquinolones)
Cephalosporin
Carbapenems (eg: Meropenem)

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77
Q

Outline presentation of C. difficile

A

Colonisation usually asymptomatic
Infection- Diarrhoea, nausea and abdo pain
Severe infection with colitis- Dehydration, systemic symptoms (eg: Fever, tachycardia, hypotension)

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78
Q

Outline diagnosis of C. difficile

A

Stool tests:
C. difficile antigen (specifically glutamate dehydrogenase)
A and B toxins (by PCR or enzyme immunoassay)

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79
Q

Outline management of C. difficile

A

Supportive care and oral ABs
1st line- Oral vancomycin
2nd line- Oral fidaxomicin

Isolate until 48h after last episode of diarrhoea- High recurrence rate
Recurrent cases- Faecal microbiota transplantation

80
Q

List complications of C. difficile

A

Pseudomembranous colitis
Toxic megacolon
Bowel perforation
Sepsis

81
Q

What is Pseudomembranous colitis?

A

Inflammation of large intestine
Yellow/white plaques form pseudomembranes on inner surface bowel wall
Seen during colonoscopy and confirmed on biopsy

82
Q

What is Toxic megacolon?

A

Complication of severe inflammation in large intestine and involves dilation of colon
High risk of bowel rupture

83
Q

List some post-gastroenteritis complications

A

Lactose intolerance
IBS
Reactive arthritis
Guillain-Barre syndrome
HUS

84
Q

Outline general management of Gastroenteritis

A

Food poisoning- NOTIFIABLE DISEASE
Isolate- Barrier nursing and infection control- 48h after symptoms resolve
Faeces sample- Microscopy, culture and sensitivities
Dehydration- Assess whether need for admission for IV fluids
Oral rehydration salt solution
Antidiarrhoeal drugs- Avoid
Antibiotics- If risk of complications
Oral intake tolerated- Light diet with bland foods

85
Q

What is oral rehydration salt solution?

A

Dioralyte sachets mixed with water
Replace losses in risk of dehydration
Contains glucose, potassium and sodium

86
Q

Outline giardiasis

A

Parasite in small intestines of mammals- Releases cysts in faeces- May contaminate food/water
Faecal-oral transmission
May cause chronic diarrhoea
Diagnosis- Stool test (NAAT or EIA)
Treat- Tinidazole or metronidazole

87
Q

Outline staphylococcal aureus as a cause of gastroenteritis

A

Can produce enterotoxins growing on food (eggs/dairy/meat)
Cause inflammation in intestines
Symptoms- Diarrhoea, vomiting, abdo cramps, fever- Start within hrs of ingestion and settle within 12-24h

88
Q

Outline Yersinia Enterocolitica

A

Gram negative bacillus
Pigs are key carriers (raw pork) and contact with infected humans/animals and faeces
Typically affects children- Watery/bloody diarrhoea, abdo pain and fever
Incubation 4-7d- Symptoms last >3wks
Older children/adults present with R sided abdo pain due to mesenteric lymphadenitis (inflammation in intestinal lymph nodes) and fever- Can impersonate appendicitis

89
Q

Outline Yersinia pestis

A

Spread through rat flea bites
Causes plague

90
Q

Outline Bacillus Cereus

A

Gram positive rod
Spread through contaminated cooked foods- Fried rice/cooked pasta left at room temperature
Toxin cereulide causes abdo cramping and vomiting within 5h of ingestion
Reheating food can kill bacteria but doesn’t destroy the cereulide toxin- Watery diarrhoea
Vomiting within 5h, diarrhoea >8h after ingestion- Symptoms resolve within 24h

Can also occur with infective endocarditis in IV drug users, where heroin is contaminated

91
Q

What is the most common cause of infective endocarditis in IV drug users?

A

Staph aureus

92
Q

Outline salmonella

A

Spread by eating raw eggs/poultry/food contaminated with infected faeces of small animals
Incubation 12h-3d- Symptoms resolve within 1wk
Symptoms- Watery diarrhoea (may have mucous/blood), abdo pain, vomiting
ABs only necessary in severe cases- Guided by stool culture and sensitivities (eg: Ciprofloxacin)

93
Q

Outline Shigella

A

Spread via faeces
Either person-person or through contaminated drinking water/food
Incubation period 1-2d- Symptoms resolve within 1wk
Symptoms- Bloody diarrhoea, abdo cramps, fever
Can produce Shiga toxin- Can cause Haemolytic Uraemic Syndrome
Treat severe cases- Azithromycin or ciprofloxacin

94
Q

Outline Campylobacter Jejuni

A

Traveller’s diarrhoea
Gram negative bacteria
Spread- Raw poultry, untreated water, unpasteurised milk
Incubation 2-5d- Symptoms resolve 3-6d
Symptoms- Abdo cramps, diarrhoea with blood, vomiting, fever
ABs considered if severe symptoms or other RFs (HIV or HF)- Clarithromycin (1st line), azithromycin, ciprofloxacin

95
Q

Outline E. coli

A

E. coli is normal intestinal bacteria
Spread through contact with infected faeces/unwashed salad/contaminated water
Produces Shiga toxin- Increased risk HUS- Avoid ABs

96
Q

Outline viral gastroenteritis

A

Common and highly contagious
Rotavirus
Norovirus
Adenovirus (tends to cause respiratory symptoms)

97
Q

What is acute gastritis?

A

Stomach inflammation
Presents with epigastric discomfort, nausea and vomiting

98
Q

What is enteritis?

A

Inflammation of intestines
Presents with abdo pain and diarrhoea

99
Q

What is gastroenteritis?

A

Inflammation from stomach to intestines
Presents with pain, nausea, vomiting and diarrhoea

100
Q

What is the most common cause of gastroenteritis?

A

Virus
Easily spread
Isolate in a healthcare environment

101
Q

What is the prognosis of gastroenteritis?

A

Most people recover well
Can rarely be fatal- Especially in very young or old patients, or those with other health conditions

102
Q

Outline influenza virus

A

RNA
3 types- A, B, and C
A and B most common
Outbreaks typically occur in winter

103
Q

Outline influenza vaccination

A

Yearly required in:
>65y
Young children
Pregnant women
Chronic health conditions- Asthma, COPD, HF, diabetes
Healthcare workers and carers

104
Q

Outline presentation of influenza

A

Fever
Lethargy and fatigue
Anorexia (loss of appetite)
Muscle and joint aches
Headache
Dry cough
Sore throat
Coryzal symptoms

105
Q

What is the typical difference in features between cold and flu?

A

Flu- Abrupt onset, fever, ‘wiped out’ with muscle aches and lethargy
Common cold- Gradual onset

106
Q

Outline testing of influenza

A

Point-of-care tests- Swabs- Detect viral antigens
Viral nasal or throat swabs- PCR analysis

107
Q

Outline management of influenza

A

If risk of complications- Oral oseltamivir (twice daily for 5d), inhaled zanamivir (twice daily for 5d)
Treatment needs to be started within 48h of onset of symptoms

108
Q

Outline criteria for receiving post-exposure prophylaxis of influenza

A

Started within 48h of close contact with influenza
Increased risk (eg: Chronic disease or immunosuppression)
Not protected by vaccination (eg: <14d since vaccinated)

109
Q

What are the options for post exposure prophylaxis for influenza?

A

Oral osetamivir 75mg once daily for 10d
Inhaled zanamivir 10mg once daily for 10d

110
Q

List complications of influenza

A

Otitis media, sinusitis and bronchitis
Viral pneumonia
Secondary bacteria pneumonia
Worsening chronic health conditions- COPD and HF
Febrile convulsions (young children)
Encephalitis

111
Q

What is septic arthritis?

A

MEDICAL EMERGENCY
Infection in joint
Can occur in original joint or prosthetic joint replacement

112
Q

Outline presentation of septic arthritis

A

Usually affects single joint
Rapid onset
Hot, red, swollen and painful
Stiffness and reduced range of motion
Systemic symptoms- Fever, lethargy and sepsis

113
Q

What is the most common cause of septic arthritis?

A

Staph aureus

114
Q

What are the less common causes of septic arthritis?

A

Neisseria gonorrhoea (gonococcus)- In sexually active individuals- Typically a young patient with single acutely swollen joint- Gram negative diplococcus
Group A strep
Haemophilus influenza
E. coli

115
Q

What is the difference between Septic arthritis and reactive arthritis?

A

Disclude septic arthritis first
Reactive arthritis- Urinary or genital symptoms- Typically triggered by urethritis or gastroenteritis and associated with conjunctivitis

116
Q

What is the difference between Septic arthritis and gout?

A

Gout- Joint fluid shows urate crystals that are negatively birefringent of polarised light

117
Q

What is the difference between Septic arthritis and pseudogout?

A

Pseudogout- Joint fluid shows rod-shaped calcium pyrophosphate crystals that are positively birefringent

118
Q

What is the difference between Septic arthritis and haemarthrosis?

A

Bleeding into joint, usually after trauma

119
Q

Outline management of septic arthritis

A

Joint aspiration before starting ABs
Sample sent for gram staining, crystal microscopy, culture and AB sensitivities- Joint fluid may be purulent (pus)
Empirical IV ABs continued for 4-6wks

120
Q

Outline the AB choices for septic arthritis

A

1st line- Flucloxacillin
Penicillin allergy- Clindamycin
MRSA suspected- Vancomycin
Ceftriaxone- Neisseria gonorrhoea

121
Q

List possible intra-abdominal infections

A

Acute diverticulitis- Infection in intestinal diverticula
Acute cholecystitis- With secondary infection in gallbladder
Ascending cholangitis- Infection in bile ducts
Appendicitis
Spontaneous bacterial peritonitis- Infection in fluid in peritoneal cavity

122
Q

What type of bacteria is E. coli?

A

Gram-negative

123
Q

What type of bacteria is Klebsiella?

A

Gram-negative

124
Q

What type of bacteria is Enterocolitis?

A

Gram-positive

125
Q

What type of bacteria is Streptococcus?

A

Gram-positive

126
Q

Which bacteria does Co-amoxiclav cover?

A

Gram +ve
Gram -ve
Anaerobes

127
Q

Name types of anaerobic bacteria

A

Bacteroides
Clostridium

128
Q

Outline the coverage of amoxicillin plus gentamicin plus metronidazole

A

Amoxicillin- Gram +ve
Gentamicin- Gram -ve
Metronidazole- Anaerobes

129
Q

Outline the coverage of ciprofloxacin plus metronidazole

A

Ciprofloxacin- Gram +ve, Gram -ve
Metronidazole- Anaerobes

130
Q

Outline coverage of vancomycin plus gentamicin plus metronidazole

A

Vancomycin- Gram +ve
Gentamicin- Gram -ve
Metronidazole- Anaerobes

131
Q

Outline Co-amoxiclav

A

Covers gram +ve, gram -ve, anaerobes
Doesn’t cover pseudomonas or atypical bacteria

132
Q

Outline quinolones

A

Ciprofloxacin and levofloxacin
Covers gram +ve, gram -ve, atypical
Don’t cover anaerobes
Usually paired with metronidazole

133
Q

Outline metronidazole

A

Anaerobic cover
Inhibits metronidazole
Bactericidal

134
Q

Outline gentamicin

A

Covers gram -ve bacteria and some gram +ve cover (staph)
Bactericidal

135
Q

Outline vancomycin

A

Gram +ve cover, including MRSA
Combine with gentamicin (gram -ve) and metronidazole (anaerobe cover) in patients with penicillin allergy

136
Q

Outline cephalosporins

A

Broad-spectrum cover against gram +ve and gram -ve bacteria
Often avoided due to risk of C. diff infection

137
Q

Outline Piperacillin with tazobactam and meropenem

A

Cover gram +ve, gram -ve and anaerobic bacteria
Don’t cover atypical bacteria or MRSA
Usually reserved for very unwell patients and those not responding to other ABs

138
Q

What is cellulitis?

A

Infection of skin and soft tissues underneath
May be due to skin trauma, eczema, fungal nail infections or ulcers

139
Q

Outline presentation of cellulitis

A

Erythema
Warm/hot to touch
Tense
Thickened
Oedematous
Bullae (fluid filled blisters)
Golden-yellow crust indicates Staph aureus
May be systemically unwell- Sepsis

140
Q

What are the most common causes of cellulitis?

A

Staph aureus
Group A strep
Group C strep

MRSA should be considered- Repeated hospital admissions and ABs

141
Q

Outline Eron classification

A

Severity of cellulitis
Class 1- No systemic toxicity or comorbidity
Class 2- Systemic toxicity or comorbidity
Class 3- Significant systemic toxicity or significant comorbidity
Class 4- Sepsis or life-threatening infection

142
Q

Outline management of cellulitis

A

Class 3 and 4 cellulitis requires admission for IV ABs
1st line- Flucloxacillin- Effective against Staph aureus
Alternatives- Clarithromycin, clindamycin, Co-amoxiclav (1st line for cellulitis near eyes or nose)

143
Q

What are Lower UTIs?

A

Infection in bladder
Causing cystitis (inflammation of bladder)

144
Q

What is pyelonephritis?

A

Inflammation of kidney resulting from bacterial infection
Affects kidney tissue (parenchyma) and renal pelvis (ureter joins kidney)

145
Q

Outline UTIs

A

More common in women- Urethra is shorter
Primary source is faeces
Urinary catheters are a possible source of infection- More challenging to treat

146
Q

Outline presentation of Lower UTIs

A

Dysuria (pain, stinging or burning when passing urine)
Suprapubic pain or discomfort
Frequency
Urgency
Incontinence
Haematuria
Cloudy or foul-smelling urine
Confusion- Commonly only symptom in older and frail patients

147
Q

Outline presentation of pyelonephritis

A

Fever
Loin or back pain (bilateral or unilateral)
Nausea or vomiting
Systemic illness
Loss of appetite
Haematuria
Renal angle tenderness

148
Q

Outline management of UTIs in pregnancy

A

7d ABs
MSU and MC&S
Nitrofurantoin (avoid in 3rd trimester)
Amoxicillin (only after sensitivities known)
Cefalexin (typical choice)

149
Q

Why is nitrofurantoin avoided in 3rd trimester of pregnancy?

A

Risk of neonatal haemolysis

150
Q

Why is trimethoprim avoided in 1st trimester of pregnancy?

A

Folate antagonist- Folate essential in early pregnancy for normal development of fetus
Can cause congenital malformations- Neural tube defects (spina bifida)

151
Q

Outline UTIs and pregnancy

A

Increased risk of pyelonephritis, premature rupture of membranes and pre-term labour

152
Q

Outline management of Pyelonephritis

A

Refer to hospital if features of sepsis
7-10d ABs
Cefalexin
Co-amoxiclav (if culture results available)
Trimethoprim (if culture results available)
Ciprofloxacin (keep tendon damage and lower seizure threshold in mind)

153
Q

What should you consider if pyelonephritis is not responding to treatment?

A

Renal abscess
Kidney stone obstructing ureter- Causing pyelonephritis

154
Q

Outline management of Lower UTIs

A

Nitrofurantoin- Avoid in patients with eGFR <45
Trimethoprim- Associated with high rates bacterial resistance

Alternatives- Pivmecillinam, amoxicillin, cefalexin

Typical duration:
3d ABs- Simple lower UTIs in women
5-10d ABs- Immunosuppressed women/abnormal anatomy/impaired kidney function
7d ABs- Men/pregnant women/catheter-related UTIs

155
Q

Outline causes of UTIs

A

E. coli- Most common
Klebsiella pneumoniae
Enterococcus
Pseudomonas aeruginosa
Staph saprophyticus
Candida albicans (fungal)

156
Q

Outline investigations of UTIs

A

Urine dipstick- Nitrites (bacteria in urine), leukocytes (can be infection), RBCs (microscopic/macroscopic haematuria, common sign of infection/bladder cancer/nephritis)
Nitrites better indication of infection than leukocytes
UTI- Nitrites or leukocytes plus RBCs
Dipstick result less reliable in catheterised patients or women >65y
MSU- MC&S

157
Q

When is an MSU done?

A

Pregnant patients
Patients with recurrent UTIs
Atypical symptoms
When symptoms don’t improve with ABs

158
Q

What is sepsis?

A

Body launches large immune response to infection, causing systemic inflammation and organ dysfunction

159
Q

Outline pathophysiology of sepsis

A

Macrophages, lymphocytes and mast cells recognise pathogens- Release cytokines (IL and TNF) that activate immune system- Leads to systemic inflammation and release of NO (causing vasodilation)
Cytokines cause endothelial lining of blood vessels to become more permeable- Fluid leaks out of blood into ECS, resulting in oedema and reduced intravascular volume- Increased gap between blood and tissues- Reduced amount of oxygen that reaches tissue
Activation coagulation system- Deposition of fibrin and formation of thrombi- Compromised organ and tissue perfusion- Consumes platelets and clotting factors- Leads to thrombocytopenia (low platelets) and uncontrolled haemorrhage- DIC
Anaerobic respiration- Raised serum lactate and metabolic acidosis

160
Q

Outline pathophysiology of disseminated intravascular coagulopathy

A

Activation of immune system and systemic inflammation
Release of cytokines and increased oedema- Reduced O2 reaching tissues
Activation of coagulation system- Fibrin deposition- Formation of thrombi- Compromised organ and tissue perfusion
Blood clots consume platelets and clotting factors- Thrombocytopenia (low platelets) and uncontrolled haemorrhage

161
Q

What is seen on an ABG in sepsis?

A

Raised serum lactate and metabolic acidosis

162
Q

Outline septic shock

A

Occurs when arterial BP drops despite adequate fluid resuscitation- Results in organ hypoperfusion
Anaerobic respiration begins and serum lactate level rises

163
Q

Outline diagnosis of septic shock

A

Low mean arterial pressure (<65 mmHg) despite fluid resuscitation (requiring vasopressors)
Raised serum lactate (>2mmol/L)

164
Q

How is septic shock managed?

A

Aggressive treatment with IV fluids to improve BP and tissue perfusion
High dependency or intensive care
Vasopressors (noradrenaline)- Cause vasoconstriction and increase systemic vascular resistance and MAP- Improves tissue perfusion

165
Q

Outline sepsis-related organ failure assessment

A

Assess severity of organ dysfunction- Takes into account signs of organ dysfunction
Hypoxia
Increased oxygen requirements
Requiring mechanical ventilation
Low platelets (thrombocytopenia)
Reduce GCS
Raised bilirubin
Reduce BP
Raised creatinine

166
Q

List risk factors for sepsis

A

Any condition causing immune dysfunction/frailty/predisposition to infection
Very young/old patients (<1y or >75y)
Chronic conditions- COPD and diabetes
Chemotherapy, immunosuppressants, steroids
Surgery, recent trauma, burns
Pregnancy and childbirth
Indwelling medical devices, catheters, central lines

167
Q

Outline presentation of sepsis

A

NEWS2
Temperature
Heart rate
Respiratory rate
Oxygen sats
Blood pressure
Consciousness level

Additional signs of infection:
Signs of potential sources- Cellulitis, discharge from wound, cough, dysuria
Reduced urine output
Mottled skin
Cyanosis
Arrhythmias (new-onset AF)
A non-blanching rash (meningococcal septicaemia)

Raised RR- Sign of early sepsis
Elderly- Non-specific findings- Confusion, drowsiness, ‘off legs’
Neutropenic/immunocompromised- May have normal obs despite being life-threatening

168
Q

Outline investigations of sepsis

A

FBC- WCC and neutrophils
U&Es- Kidney function and AKI
LFTs- Liver function and source of infection
CRP- Assess for inflammation
Blood glucose- Hyperglycaemia and hypoglycaemia
Clotting- Assess for DIC
Blood cultures- Assess for bacteraemia
Blood gas- Lactate, pH, glucose
Urine dipstick and culture
CXR
CT if intra-abdo infection or abscess suspected
LP- Meningitis or encephalitis

169
Q

Outline management of sepsis

A

Sepsis protocol and pathway
Assess and start treatment within 1h of presenting
Sepsis 6

170
Q

Outline sepsis 6

A

Take:
Serum lactate
Blood cultures
Urine output
Give:
O2- Maintain 94-98% (88-92% in COPD)
Empirical broad-spectrum ABs
IV fluids

171
Q

What is neutropenic sepsis?

A

Sepsis with neutrophil count <1x10^9/L
Usually consequence of anti-cancer or immunosuppressant treatment

172
Q

List medications that may cause neutropenia

A

Chemotherapy
Clozapine- Schizophrenia
Hydroxychloroquine- RA
Methotrexate- RA
Sulfasalazine- RA
Carbimazole- Hyperthyroidism
Quinine- Malaria
Infliximab- Monoclonal antibody used for various AI conditions
Rituximab- Monoclonal antibody used for various AI conditions and cancers

173
Q

Outline management of neutropenic sepsis

A

Low threshold for suspecting neutropenic sepsis in chemotherapy or meds that may cause neutropenia
Any temperature >38 degrees C treated as neutropenic sepsis until proven otherwise
Emergency admission
Neutropenic sepsis policy
Immediate broad-spectrum ABs- Piperacillin with tazobactam

174
Q

What is the prognosis of septic arthritis?

A

Mortality of approx. 10%

175
Q

In OSCEs, treating infections which antibiotic would you give?

A

Antibiotics according to local antibiotic policy

176
Q

Which antibiotics inhibit cell wall synthesis?

A

Antibiotics with beta-lactam ring:
Penicillin
Carbapenems (meropenem)
Cephalosporins

Antibiotics w/o beta-lactam ring:
Vancomycin
Teicoplanin

177
Q

Which ABs inhibit folic acid metabolism?

A

Sulfamethoxazole
Trimethoprim
Co-trimoxazole (bactericidal)- Combination sulfamethoxazole and trimethoprim (bacteriostatic)

178
Q

List ABs that target ribosomes

A

Inhibit protein synthesis
Macrolides (erythromycin, clarithromycin, azithromycin)
Clindamycin
Tetracyclines (eg: Doxycycline)
Gentamicin
Chloramphenicol

179
Q

Outline nitrofurantoin

A

Exclusively used to treat lower UTIs
Bactericidal
Not used to treat pyelonephritis- Only achieves adequate conc. in urine

179
Q

Outline coverage of amoxicillin

A

Gram +ve
Strep, listeria, enterococci

179
Q

Outline coverage of Co-amoxiclav

A

Gram +ve, gram -ve, anaerobes
Staph, Haemophilus, E. coli

179
Q

Outline coverage of clarithromycin

A

Gram +ve, atypicals

179
Q

Outline coverage of clindamycin

A

Gram +ve, anaerobes

180
Q

Outline coverage of gentamicin

A

Gram -ve

180
Q

Outline coverage of ciprofloxacin

A

Gram -ve, atypicals

181
Q

Outline coverage of metronidazole

A

Anaerobes

182
Q

Outline coverage of doxycycline

A

Gram +ve, Gram -ve, anaerobes, atypicals

183
Q

Outline coverage of vancomycin

A

Gram +ve
MRSA

184
Q

Outline gram stain

A

Crystal violet stain- Binds to gram +ve- Turns violet
Counterstain- Binds to cell membrane of gram -ve- Turns red/pink

185
Q

List gram +ve cocci

A

Staphylococcus
Streptococcus
Enterococcus

186
Q

List gram +ve rods

A

Corneybacteria
Mycobacteria
Listeria
Bacillus
Nocardia

187
Q

List gram +ve anaerobes

A

Clostridium
Lactobacillus
Actinomyces
Propionibacterium

188
Q

List positive gram -ve bacteria

A

Neisseria meningitidis
Neisseria gonorrhoea
Haemophilia influenza
E. coli
Klebsiella
Pseudomonas aeruginosa
Moraxella catarrhalis

189
Q

List 5 causes of atypical pneumonia

A

Legionella pneumophilia
Chlamydia psittaci
Mycoplasma pneumoniae
Chlamydophila pneumoniae
Q fever

190
Q

Outline Methicillin-Resistant Staphylococcus Aureus (MRSA)

A

Staph aureus bacteria resistant to beta-lactam ABs (eg: Penicillin, cephalosporin, carbapenems)
Hard to treat
Eradication of MRSA on skin- Chlorhexidine
ABs used to treat- Doxycycline, clindamycin, vancomycin, teicoplanin, linezolid

191
Q

Outline Extended-Spectrum Beta-Lactamase Bacteria

A

Developed resistance to beta-lactam ABs (penicillins, cephalosporins, carbapenems)
Produce beta-lactamase enzymes that destroy beta-lactam ring on AB
ESBLs tend to be E. coli or Klebsiella and cause UTIs
Can cause other type of infections such as pneumonia and septicaemia
Usual treatment:
Nitrofurantoin
Fosfomycin
Carbapenems

Final Year (14 decks)

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