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2A Medicine Sam > Microbiology > Flashcards

Microbiology Flashcards

1
Q

What five categories can bacteria fall into

A

They can be categorised into aerobic and anaerobic, gram positive and gram negative and atypical bacteria.

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2
Q

Difference between Gram negative and Gram positive bacteria

A

Gram positive bacteria have a thick peptidoglycan cell wall that stains with crystal violet stain. Gram negative bacteria don’t have this thick peptidoglycan cell wall and don’t stain with crystal violet stain but will stain with other stains

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3
Q

What are the two shapes of bacteria

A

Cocci (circular) or Bacilli (rods)

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4
Q

Pathway to create folic acid inside the bacterial cell

A

PABA is absorbed across the cell membrane and is then converted to DHFA which is then converted to THFA and then to folic acid

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5
Q

Explain gram staining

A

Add a crystal violet stain which binds to molecules in the thick peptidoglycan cell wall in gram positive bacteria turning them violet.

Then add a counterstain (such as safranin) which binds to the cell membrane in bacteria that don’t have a cell wall (gram negative bacteria) turning them red/pink.

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6
Q

Name three Gram positive Cocci

A

Staphylococcus, Streptococcus and Enterococcus

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7
Q

Name the Gram-Positive Rods

A

Use the mnemonic “corney Mike’s list of basic cars”:

Corney – Corneybacteria
Mike’s – Mycobacteria
List of – Listeria
Basic – Bacillus
Cars – Nocardia

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8
Q

Name the four Gram positive Anaerobes

A

Use the mnemonic “CLAP”:

C – Clostridium
L – Lactobacillus
A – Actinomyces
P – Propionibacterium

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9
Q

Name 5 Gram negative bacteria

A

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

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10
Q

Define atypical bacteria

A

The definition of atypical bacteria is that they cannot be cultured in the normal way or detected using a gram stain. Atypical bacteria are most often implicated in pneumonia.

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11
Q

Name the atypical bacteria

A

The atypical bacteria that cause atypical pneumonia can be remembered using the mnemonic “legions of psittaci MCQs”:

Legions – Legionella pneumophila
Psittaci – Chlamydia psittaci
M – Mycoplasma pneumoniae
C – Chlamydydophila pneumoniae
Qs – Q fever (coxiella burneti)

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12
Q

What does MRSA stand for

A

Methicillin-Resistant Staphylococcus Aureus

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13
Q

What has MRSA become resistant to

A

resistant to beta-lactam antibiotics such as penicillins, cephalosporins and carbapenems

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14
Q

What can be used to eradicate MRSA in hospital to stop its spread

A

Chlorhexidine body washes and antibacterial nasal creams

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15
Q

Name 3 antibiotic options for MRSA

A

Doxycycline
Clindamycin
Vancomycin
Teicoplanin
Linezolid

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16
Q

What are ESBL’s

A

Extended Spectrum Beta Lactamase bacteria

ESBLs are bacteria that have developed resistance to beta-lactam antibiotics. They produce beta lactamase enzymes that destroy the beta-lactam ring on the antibiotic. They can be resistant to a very broad range of antibiotics

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17
Q

What bacteria tend to be ESBL’s

A

E.coli and Klebsiella - tend to cause UTI’s but can also cause other infections such as pneumonia

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18
Q

What would you use to treat ESBL’s

A

They are usually sensitive to carbapenems such as meropenem or imipenem.

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19
Q

What are the two ways Antibiotics can work?

A

They work in various ways to either stop the reproduction and growth of bacteria (bacteriostatic) or kill the bacteria directly (bactericidal)

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20
Q

What antibiotics attack the bacteria cell wall

A

Penicillin, Carbapenems (e.g. imipenem), vancomycin, Teicoplanin and Cephalosporins (e.g. cephalexin, cefuroxime or ceftriaxone)

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21
Q

What antibiotic inhibits the conversion of DHFA to THFA

A

Trimethoprim

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22
Q

What antibiotic inhibits the conversion of PABA to DHFA

A

Sulfamethoxazole

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23
Q

What antibiotics inhibit protein synthesis by targeting ribosomes

A

Macrolides such as erythromycin, clarithromycin and azithromycin
Clindamycin
Tetracyclines such as doxycycline
Gentamicin
Chloramphenicol

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24
Q

What type of bacteria can metronidazole treat and why?

A

The reduction of metronidazole into its active form only occurs in anaerobic cells. When partially reduced metronidazole inhibits nucleic acid synthesis. This is why metronidazole is effective against anaerobes and not aerobes.

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25
Q

Which antibiotics have beta-lactam rings vs w/o

A

Antibiotics with a beta-lactam ring:
Penicillin
Carbapenems such as meropenem
Cephalosporins

Antibiotics without a beta-lactam ring:
Vancomycin
Teicoplanin

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26
Q

What antibiotic is a combination of Trimethoprim and Sulfamethoxazole?

A

Co-trimoxazole

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27
Q

Stepwise escalation of antibiotic prescribing

A

Start with amoxicillin which covers streptococcus, listeria and enterococcus

Switch to co-amoxiclav to additionally cover staphylococcus, haemophilus and e. coli

Switch to tazocin to additionally cover pseudomonas

Switch to meropenem to additionally cover ESBLs

Add teicoplanin or vancomycin to cover MRSA

Add clarithromycin or doxycycline to cover atypical bacteria

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28
Q

What antibiotics are considered to be broad spectrum?

A

Co-amoxiclav and Doxycycline

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29
Q

What can amoxicillin treat?

A

Gram positive bacteria such as Streptococcus, listeria and enterococcus

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30
Q

What can Clarithromycin treat

A

Gram positive and atypical bacteria

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31
Q

What can Clindamycin treat

A

Gram positive and Anaerobe

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32
Q

What can Gentamycin treat

A

Gram negative

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33
Q

What can Ciprofloxacin treat

A

Gram negative and Atypical

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34
Q

What can Metronidazole treat

A

Anaerobe

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35
Q

What can vancomycin treat

A

Gram positive resistant e.g. MRSA

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36
Q

How to treat vancomycin resistant enterococcus

A

Linezolid and daptomycin

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37
Q

What do macrophages, lymphocytes and mast cells release in response to the presence of bacteria or other pathogens?

A

Cytokines such as interleukins and tumor necrosis factor

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38
Q

What does cytokine immune activation lead to

A

Release of nitrous oxide which causes vasodilation

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39
Q

Pathophysiology of sepsis

A

cytokines cause the endothelial lining of blood vessels to become more permeable. This causes fluid to leak out of the blood and in to the extracellular space leading to oedema and a reduction in intravascular volume. The oedema around blood vessels creates a space between the blood and the tissues reducing the amount of oxygen that reaches the tissues.

Activation of the coagulation system leads to deposition of fibrin throughout the circulation further compromising organ and tissue perfusion. It also leads to consumption of platelets and clotting factors as they are being used up to form the clots within the circulatory system. This leads to thrombocytopenia, haemorrhages and an inability to form clots and stop bleeding. This is called disseminated intravascular coagulopathy (DIC).

Blood lactate rises due to hypoperfusion of tissues that starves the tissues of oxygen causing them to switch to anaerobic respiration. A waste product of anaerobic respiration is lactate

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40
Q

How to measure septic shock

A

Systolic BP: less than 90 despite fluid resuscitation

Hyperlactaemia: (lactate > 4 mmol/L)

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41
Q

How to treat septic shock

A

This should be treated aggressively with IV fluids to improve the blood pressure and the tissue perfusion. If IV fluid boluses don’t improve the blood pressure and lactate level then they should be escalated to high dependency or intensive care where they can use medication called inotropes (such as noradrenalin) that help stimulate the cardiovascular system and improve blood pressure and tissue perfusion.

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42
Q

What is severe sepsis

A

Severe sepsis is defined when sepsis is present and results in organ dysfunction, for example:

Hypoxia
Oliguria
Acute Kidney Injury
Thrombocytopenia
Coagulation dysfunction
Hypotension
Hyperlactaemia (> 2 mmol/L)

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43
Q

RF for Sepsis

A

Any condition that impacts the immune system or makes the patient more frail or prone to infection is a risk factor for developing sepsis:

Very young or old patients (under 1 or over 75 years)
Chronic conditions such as COPD and diabetes
Chemotherapy, immunosuppressants or steroids
Surgery or recent trauma or burns
Pregnancy or peripartum
Indwelling medical devices such as catheters or central lines

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44
Q

Presentation of sepsis

A

The National Early Warning Score (NEWS) is used in the UK to pick up the signs of sepsis. This involves checking physical observations and their consciousness level:

Temperature
Heart rate
Respiratory rate
Oxygen saturations
Blood pressure
Consciousness level
Other signs on examination:

Signs of potential sources such as cellulitis, discharge from a wound, cough or dysuria
Non-blanching rash can indicate meningococcal septicaemia
Reduced urine output
Mottled skin
Cyanosis
Arrhythmias such as new onset atrial fibrillation
There are a few key points worth being aware of:

High respiratory rate (tachypnoea) is often the first sign of sepsis
Elderly patients often present with confusion or drowsiness or simply “off legs”
Neutropenic or immunosuppressed patients may have normal observations and temperature despite being life threatening unwell

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45
Q

Investigations for sepsis

A

Arrange blood tests for patients with suspected sepsis:

  • Full blood count to assess cell count including white cells and neutrophils
  • U&Es to assess kidney function and for acute kidney injury
  • LFTs to assess liver function and for possible source of infection
  • CRP to assess inflammation
  • Clotting to assess for disseminated intravascular coagulopathy (DIC)
  • Blood cultures to assess for bacteraemia
  • Blood gas to assess lactate, pH and glucose
    Additional investigations can be helpful in locating the source of the infection:

Urine dipstick and culture
- Chest xray
- CT scan if intra-abdominal infection or abscess is suspected
- Lumbar puncture for meningitis or encephalitis

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46
Q

What are the ‘Sepsis Six’

A

Three Tests:
- Blood lactate level
- Blood cultures
- Urine output

Three Treatments:
- Oxygen to maintain oxygen saturations 94-98% (or 88-92% in COPD)
- Empirical broad spectrum antibiotics
- IV fluids

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47
Q

What is neutropenic sepsis

A

Neutropenic sepsis is a very important medical emergency. It is sepsis in a patient with a low neutrophil count of less than 1 x 109/L.

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48
Q

What medications cause neutropenia

A

Anti-cancer chemotherapy
Clozapine (schizophrenia)
Hydroxychloroquine (rheumatoid arthritis)
Methotrexate (rheumatoid arthritis)
Sulfasalazine (rheumatoid arthritis)
Carbimazole (hyperthyroidism)
Quinine (malaria)
Infliximab (monoclonal antibody use for immunosuppression)
Rituximab (monoclonal antibody use for immunosuppression)

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49
Q

Management of neutropenic sepsis

A

Broad spectrum antibiotic e.g. Tazocin

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50
Q

What do chest infections typically present with?

A

cough and sputum production, shortness of breath, fever, lethargy and crackles on the chest

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51
Q

What does viral bronchitis present with in addition to typical symptoms

A

Productive cough

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52
Q

Most common causes of chest infection

A

Streptococcus pneumoniae (50%)
Haemophilus influenzae (20%)

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53
Q

Other causes and assocations for chest infections

A
  • Moraxella catarrhalis in immunocompromised patients or those with chronic pulmonary disease
  • Pseudomonas aeruginosa in patients with cystic fibrosis or bronchiectasis
  • Staphylococcus aureus in patients with cystic fibrosis
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54
Q

What are the five causes of atypical pneumonia

A

Legions – Legionella pneumophila
Psittaci – Chlamydia psittaci
M – Mycoplasma pneumoniae
C – Chlamydydophila pneumoniae
Qs – Q fever (coxiella burnetii)

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55
Q

What would be the initial antibiotic of choice in the community be for a chest infection?

A

Amoxicillin

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56
Q

Alternatives to amoxicillin for chest infections?

A

Eruthromycin/clarithromycin or Doxycycline

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57
Q

How to treat atypical bacteria in regards to chest infections

A

Macrolides such as clarithromycin

Quinolones such as levofloxacin

Tetracycline such as doxycycline

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58
Q

Most common bacteria involved in UTI’s?

A

E.Coli

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59
Q

Common reasons for UTI

A

Sexual activity spreading faecal matter around the perineum, hygiene problems and urinary catherters (harder to trear)

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60
Q

LUT infection presentation

A
  • Dysuria (pain, stinging or burning when passing urine)
  • Suprapubic pain or discomfort
  • Frequency
  • Urgency
  • Incontinence
  • Confusion is commonly the only symptom in older more frail patients
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61
Q

Pyelonephritis presentation

A
  • Fever is a more prominent feature than lower urinary tract infections.
  • Loin, suprapubic or back pain. This may be bilateral or unilateral.
  • Looking and feeling generally unwell
  • Vomiting
  • Loss of appetite
  • Haematuria
  • Renal angle tenderness on examination
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62
Q

What two things are you looking for on a urine dipstick for suspected UTI

A

Nitrites and Leukocyte esterase

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63
Q

Why does increased nitrites suggest infection?

A

Gram negative bacteria (such as E. coli) breakdown nitrates, a normal waste product in urine, into nitrites. The presence of nitrites suggest bacteria presence

64
Q

Are nitrites or leukocytes a better indicator of UTI, why?

A

Nitrites are a better indication of infection than leukocytes. If both are present then the patient should be treated as a UTI. If only nitrites are present then it is worth treating as a UTI however if only leukocytes are present then the patient should not be treated as a UTI unless there is clinical evidence that they have a UTI.

If nitrites or leukocytes are present the urine should be sent to the microbiology lab. If neither are present the patient is unlikely to have a UTI

65
Q

Other causes of UTI

A
  • Klebsiella pneumoniae (gram-negative anaerobic rod)
  • Enterococcus
  • Pseudomonas aeruginosa
  • Staphylococcus saprophyticus
  • Candida albicans (fungal)
66
Q

Duration of antibiotic treatment

A
  • 3 days of antibiotics for a simple lower urinary tract infection in women
  • 5-10 days of antibiotics for women that are immunosuppressed, have abnormal anatomy or impaired kidney function
  • 7 days of antibiotics for men, pregnant women or catheter related UTIs
67
Q

Antibiotics of choice in community for UTI

A

Trimethroprim or Nitrofurantoin

68
Q

Alternative antibiotic options for UTI

A

Pivmecillinam, Amoxicillin, Cefalexin

69
Q

When to avoid Nitrofurantoin

A

Avoid in third trimester of pregnancy as linked with haemolytic anaemia

70
Q

Management of Pyelonephritis

A

Referral to hospital if there are features of sepsis.

NICE recommend the following first line antibiotics for 7-10 days when treating pyelonephritis in the community:

Cefalexin
Co-amoxiclav
Trimethoprim
Ciprofloxacin

71
Q

Name 5 intra-abdominal infections

A

Acute diverticulitis
Cholecystitis (with secondary infection)
Ascending cholangitis
Appendicitis
Spontaneous bacterial peritonitis
Intra-abdominal abscess

72
Q

Common causes of Intra-abdominal infections

A
  • Anaerobes (e.g. bacteroides and clostridium)
  • E. coli
  • Klebsiella
  • Enterococcus
  • Streptococcus
73
Q

General antibiotic management for intra-abdominal infection

A

Broad-spectrum antibiotic such as Co-Amoxiclav

74
Q

Specific antibiotic management for intra-abdominal infection

A

Co-amoxiclav - good for gram positive, gram negative and anaerobic. Does not cover pseudomonas or atypical bacteria

Quinolones - Ciprofloxacin and Levofloxacin provide reasonable Gram neg and pos cover and also cover atypical but don’t cover anaerobes so is usually paired with metronidazole

Metronidazole - Exceptional anaerobic coverage but no cover against aerobic

Gentamicin - Good gram negative cover with some gram positive cover (particularly against staph) and its bactericidal

Vancomycin - V good gram positive cover including MRSA, often combined with Gentamicin to cover gram negatives and metronidazole to cover anaerobes in patients with Penicillin allergies

Cephalosporins - Good broad spectrum cover against gram positive and gram negative but not v effective against anaerobes - avoided due to risk of C.diff infection

Tazocin/Meropenem - heavy hitters that cover gram positive, negative and anerobes. They don’t cover atypical or MRSA and tazocin doesnt cover ESBL’s but covers almost everything else - usuallt reserved for very unwell patients that are not responding to other antibiotics

75
Q

Give 4 common regimes for intra-abdominal infection

A
  • Co-amoxiclav alone
  • Amoxicillin plus gentamicin plus metronidazole
  • Ciprofloxacin plus metronidazole (penicillin allergy)
  • Vancomycin plus gentamicin plus metronidazole (penicillin allergy)
76
Q

When is gentamicin added to an intra-abdominal infection regime?

A

A stat dose of gentamicin is often added to regimes not including gentamicin if the patient is severely septic to provide initial strong bactericidal gram negative action.

77
Q

How to treat spontaneous bacterial peritonitis

A
  • Piperacillin/Tazobactam (Tazocin) is often first line
  • Cephalosporins such as cefotaxime are also often used
  • Levofloxacin plus metronidazole is an common alternative in penicillin allergy
78
Q

What is septic arthritis

A

Septic arthritis is where an infection occurs within a joint

79
Q

Presentation of septic arthritis

A
  • Hot, red, swollen and painful joint
  • Stiffness and reduced range of motion
  • Systemic symptoms such as fever, lethargy and sepsis
80
Q

Most common cause of septic arthritis

A

Staph aureus

81
Q

Other causes of septic arthritis

A
  • Neisseria gonorrhoea (gonococcus) in sexually active individuals
  • Group A Streptococcus (most commonly Streptococcus pyogenes)
  • Haemophilus influenza
  • Escherichia coli (E. coli)
82
Q

Differentials for septic arthritis

A
  • Gout (fluid shows urate crystals that are negatively birefringent of polarised light)
  • Pseudogout (fluid shows calcium pyrophosphate crystals that are rod-shaped intracellular crystals positively birefringent of polarised light)
  • Reactive arthritis typically triggered by urethritis or gastroenteritis and associated with conjunctivitis
  • Haemarthrosis (bleeding into the joint)
83
Q

Management for septic arthritis

A

Have a low threshold for treatment

Aspirate the joint prior to antibiotics and send the sample for gram staining, crystal microscopy, culture and antibiotic sensitivities. The joint fluid may be purulent (full of pus). The gram stain will come back quite quickly and may give a clue about the organism. The full culture will take longer

Empirical IV antibiotics should be given until the sensitivities are known. Antibiotics are usually continued for 3 – 6 weeks in total. Choice of antibiotic depends on the local guidelines.

Example regimes are:
- Flucloxacillin plus rifampicin is often first line
- Vancomycin plus rifampicin for penicillin allergy, MRSA or prosthetic joint
- Clindamycin is an alternative

84
Q

Define and overview of Infuenza

A

The influenza virus is an RNA virus. There are three types: A, B and C, of which A and B are the most common. The A type has different H and N subtypes and you may hear about different strains, for example H1N1 (swine flu) and H5N1 (avian flu). Outbreaks typically occur during the winter

85
Q

Presentation of influenza

A
  • Fever
  • Coryzal symptoms
  • Lethargy and fatigue
  • Anorexia (loss of appetite)
  • Muscle and joint aches
  • Headache
  • Dry cough
  • Sore throat
86
Q

Diagnosis of Influenza

A

Treatment is usually started based on the history, risk factors and clinical presentation.

Viral nasal or throat swabs can be sent to the local virology lab for polymerase chain reaction (PCR) analysis. This will confirm the diagnosis and also provide data to public health so that they can monitor the number of cases of influenza

87
Q

Management options for patients with influenza who are at high risk of complications

A
  • Oral oseltamivir 75mg twice daily for 5 days
  • Inhaled zanamivir 10mg twice daily for 5 days

Treatment needs to be started within 48 hours of the onset of symptoms to be effective.

Post-exposure prophylaxis can be given to higher risk patients such as those with chronic diseases or immunosuppression within 48 hours of close contact with influenza. This aims to minimise the risk of developing flu and complications.

  • Oral oseltamivir 75mg once daily for 10 days
  • Inhaled zanamivir 10mg once daily for 10 days
88
Q

Complications of influenza

A

Otitis media, sinusitis and bronchitis
Viral pneumonia
Secondary bacteria pneumonia
Worsening of chronic health conditions such as COPD and heart failure
Febrile convulsions (young children)
Encephalitis

89
Q

Acute Gastritis vs Enteritis vs Gastroenteritis

A

Acute gastritis is inflammation of the stomach and presents with nausea and vomiting. Enteritis is inflammation of the intestines and presents with diarrhoea. Gastroenteritis is inflammation all the way from the stomach to the intestines and presents with nausea, vomiting and diarrhoea.

90
Q

Most common cause of gastroenteritis

A

Viral

91
Q

Three viral causes of gastroenteritis

A
  • Rotavirus
  • Norovirus
  • Adenovirus is a less common cause and presents with a more subacute diarrhoea
92
Q

How can E.Coli cause the symptoms of Gastroenteritis

A

Produces Shiga toxin which causes abdo cramps, bloody diarrhoea and vomiting and it destroys blood cells leading to HUS

93
Q

How is Campylobacter spread

A

Raw or improperly cooked poultry, Untreated water and unpasteurised milk

94
Q

Symptoms of Gastroenteritis that is causes by Campylobacter Jejuni

A

Abdominal cramps
Diarrhoea often with blood
Vomiting
Fever

95
Q

When should antibiotics be considered for Gastroenteritis causes by campylobacter and which antibiotics are indicated?

A

Azithromycin and Ciprofloxacin

96
Q

Overview of Shigella including spread, symptoms and treatment

A

Shigella is spread by faeces contaminating drinking water, swimming pools and food. The incubation period is 1-2 days and symptoms usually resolve within 1 week without treatment. It causes bloody diarrhoea, abdominal cramps and fever. Shigella can produce the Shiga toxin and cause haemolytic uraemic syndrome. Treatment of severe cases is with azithromycin or ciprofloxacin

97
Q

Overview of Salmonella including spread, symptoms and treatment

A

Salmonella is spread by eating raw eggs or poultry and food contaminated with infected faeces of small animals. Incubation is 12 hours to 3 days and symptoms usually resolve within 1 week. Symptoms are watery diarrhoea that can be associated with mucus or blood, abdominal pain and vomiting. Antibiotics are only necessary in severe cases and guided by stool culture and sensitivities.

98
Q

Overview of Bacillus Cereus including shape, spread, toxin, symptoms and treatment

A

Bacillus cereus is a gram positive rod that is spread through inadequately cooked food. It grows well on food not immediately refrigerated after cooking. The typical food is fried rice left out at room temperature.

Whilst growing on the food it produces a toxin called cereulide that causes abdominal cramping and vomiting within 5 hours of ingestion. When it arrives in the intestines it produces different toxins that cause a watery diarrhoea. This occurs more than 8 hours after ingestion. All of the symptoms usually resolves within 24 hours.

Therefore the typical course is vomiting within 5 hours, then diarrhoea after 8 hours, then resolution within 24 hours

Typical exam presentation: Patient eats leftover fried rice

99
Q

Overview of Yersinia Enterocolitica including shape, spread, symptoms and treatment

A

Yersinia is a gram-negative bacillus. Pigs are key carriers of Yersinia and eating raw or undercooked pork can cause infection. It is also spread through contamination with the urine or faeces of other mammal such as rat and rabbits.

Yersinia most frequently affects children causing watery or bloody diarrhoea, abdominal pain, fever and lymphadenopathy. Incubation is 4-7 days and the illness can last longer than other causes of enteritis with symptoms lasting 3 weeks or more. Older children or adults can present with right-sided abdominal pain due to mesenteric lymphadenitis (inflammation in the intestinal lymph nodes) and fever which can give the impression of appendicitis.

Antibiotics are only necessary in severe cases and guided by stool culture and sensitivities.

100
Q

Overview of Giardiasis including appearance, spread, symptoms, diagnosis and management

A

Giardia lamblia is a type of microscopic parasite. It lives in the small intestines of mammals. These mammals may be pets, farmyard animals or humans. It releases cysts in the stools of infected mammals. These cysts then contaminate food or water and are eaten to infect a new host. This is called faecal-oral transmission.

Infection may not cause any symptoms or it may cause chronic diarrhoea. Diagnosis is made by stool microscopy. Treatment is with metronidazole.

101
Q

Principles of Gastroenteritis management

A

Good hygiene, immediately isolate patient to prevent spread, test faeces with microscopy, culture and sensitivities to establish cause, attempt a fluid challenge to see if they can tolerate oral fluid and then give rehydration solutions (e.g. dioralyte), slowly introduce light diet in small quantities once oral intake is tolerated, antibiotics only used in patients at risk of complications and once causative organism is found

102
Q

Post-gastroenteritis complications

A
  • Lactose intolerance
  • Irritable bowel syndrome
  • Reactive arthritis
  • Guillain–Barré syndrome
103
Q

Common bacterial cause of meningitis

A

Neisseria meningitidis is a gram negative diploccous bacteria. They are circular bacteria (“-cocci”) that occur in pairs (“diplo-”). It is commonly known as meningococcus

104
Q

What is Meningococcal septicaemia

A

Meningococcal septicaemia is when the meningococcus bacterial infection is in the bloodstream

Meningococcal septicaemia is the cause of the classic “non-blanching rash” that everybody worries about as it indicates the infection has caused disseminated intravascular coagulopathy (DIC) and subcutaneous haemorrhages

105
Q

What is Meningococcal meningitis

A

Meningococcal meningitis is when the bacteria is infecting the meninges and the cerebrospinal fluid around the brain and spinal cord

106
Q

What are some other causes of Bacterial meningitis

A

Streptococcus pneumoniae (pneumococcus).

In neonates the most common cause is Group B Streptococcus (GBS). GBS is usually contracted during birth from the GBS bacteria that can often live harmlessly in the mothers vagina

107
Q

Typical presentation of meningitis

A

Typical symptoms of meningitis are fever, neck stiffness, vomiting, headache, photophobia, altered consciousness and seizures. Where there is meningococcal septicaemia children can present with a non-blanching rash. Other causes of bacterial meningitis do not usually cause the non-blanching rash

108
Q

What are Kernig’s and Brudzinski’s tests?

A

Kernig’s test involves lying the patient on their back, flexing one hip and knee to 90 degrees and then slowly straightening the knee whilst keeping the hip flexed at 90 degrees. This creates a slight stretch in the meninges and where there is meningitis will produce spinal pain or resistance to this movement.

Brudzinski’s test involves lying the patient flat on their back and gently using your hands to lift their head and neck off the bed and flex their chin to their chest. A positive test is when this causes the patient to involuntarily flex their hips and knees.

109
Q

Management of meningitis in the community

A

Meningococcal septicaemia and bacterial meningitis are medical emergencies and should be treated immediately.

Community

Children seen in the primary care setting with suspected meningitis AND a non blanching rash should receive an urgent stat injection (IM or IV) of benzylpenicillin prior to transfer to hospital as time is so important:

< 1 year – 300mg
1-9 years – 600mg
> 10 years and adults – 1200mg
This shouldn’t delay transfer. Where there is a true penicillin allergy transfer should be the priority rather than other antibiotics.

110
Q

Hospital investigations for meningitis

A

Ideally a blood culture and a lumbar puncture for cerebrospinal fluid (CSF) should be performed prior to starting antibiotics however if the patient is acutely unwell antibiotics should not be delayed.

Send blood tests for meningococcal PCR if meningococcal disease is suspected. This tests directly for the meningococcal DNA. It can give a result quicker than blood culture depending on local services and will still be positive after the bacteria has been treated with antibiotics.

111
Q

Antibiotic treatment for meningitis

A

< 3 months – cefotaxime plus amoxicillin (the amoxicillin is to cover listeria contracted during pregnancy from the mother)
> 3 months – ceftriaxone

Add Vancomycin if theres a risk of penicillin resistant infection

Steroids are used to reduce frequency and severity of hearing loss and neurological damage. Dexamethasone is given 4 times daily for 4 days to children over 3 months

Inform public healt

112
Q

Antibiotic treatment for meningitis

A

< 3 months – cefotaxime plus amoxicillin (the amoxicillin is to cover listeria contracted during pregnancy from the mother)
> 3 months – ceftriaxone

Add Vancomycin if theres a risk of penicillin resistant infection

Steroids are used to reduce frequency and severity of hearing loss and neurological damage. Dexamethasone is given 4 times daily for 4 days to children over 3 months

Inform public health

113
Q

Most common causes of viral meningitis

A

The most common causes of viral meningitis are herpes simplex virus (HSV), enterovirus and varicella zoster virus (VZV). A sample of the CSF from the lumbar puncture should be sent for viral PCR testing.

114
Q

Management for viral meningitis

A

Viral meningitis tends to be milder than bacterial and often only requires supportive treatment. Aciclovir can be used to treat suspected or confirmed HSV meningitis.

115
Q

Complications of meningitis

A
  • Hearing loss is a key complication
  • Seizures and epilepsy
  • Cognitive impairment and learning disability
  • Memory loss
  • Focal neurological deficits such as limb weakness or spasticity
116
Q

What bacteria causes Tuberculosis, explain its shape, staining and test results

A

Mycobacterium Tuberculosis. It is a small rod shaped bacteria (a bacillus). It has a waxy coating that makes gram staining ineffective. They are resistant to the acids used in the staining procedure. This property is called acid-fastness. Therefore, the TB bacteria are described as acid-fast bacilli. They require a special staining technique using the Zeihl-Neelsen stain. This turns TB bacteria bright red against a blue background.

117
Q

Epidemiology of TB

A

TB is more prevalent in non-UK born patients (i.e. from South Asia), those who are immunocompromised (i.e. HIV) and those with close contacts with TB. Multi-Drug Resistant TB (MDR TB) are strains that are resistant to more than one TB drug making them very difficult to treat

118
Q

Spread of TB

A

The TB bacteria are very slow dividing with high oxygen demands and this makes them difficult to culture and treat. It is mostly spread by inhaling saliva droplets from infected people. It then spreads through the lymphatics and blood. Granulomas containing the bacteria form around the body

119
Q

What is Active TB

A

Active TB is where there is active infection in various areas within the body

120
Q

What is latent TB

A

The immune system may encapsulate sites of infection and stop the progression of the disease and this is referred to as latent TB

121
Q

What is secondary TB

A

When latent TB reactivates this is known as secondary TB

122
Q

What is miliary TB

A

When the immune system is unable to control the disease this causes a disseminated, severe disease and is referred to as miliary TB

123
Q

What other areas beside the lungs can become infected with TB

A
  • Lymph nodes. A “cold abscess” is a firm painless abscess caused by TB, usually in the neck. They do not have the inflammation, redness and pain you would expect from an acutely infected abscess.
  • Pleura
  • Central nervous system
  • Pericardium
  • Gastrointestinal system
  • Genitourinary system
  • Bones and joints
  • Cutaneous TB affecting the skin
124
Q

RF for TB

A

Known contact with active TB
Immigrants from areas of high TB prevalence
People with relatives or close contacts from countries with a high rate of TB
Immunosuppression due to conditions like HIV or immunosuppressant medications
Homeless people, drug users or alcoholics

125
Q

What vaccine is given for TB?

A

BCG

126
Q

Explain the BCG vaccine including what it is, who is offered it and what it is effective against

A

The BCG vaccine involves an intradermal infection of live attenuated (weakened) TB. It offers protection against severe and complicated TB but is less effective at protecting against pulmonary TB.

Prior to the vaccine patients are tested with the Mantoux test and given the vaccine only if this test is negative. They are also assessed for the possibility of immunosuppression and HIV due to the risks related to a live vaccine.

BCG vaccine is offered to patients that are at higher risk of contact with TB:

  • Neonates born in areas of the UK with high rates of TB
  • Neonates with relatives from countries with a high rate of TB
  • Neonates with a family history of TB
  • Unvaccinated older children and young adults (< 35) who have close contact with TB
  • Unvaccinated children or young adults that recently arrived from a country with a high rate of TB
  • Healthcare workers
127
Q

Presentation of TB

A

Tuberculosis usually presents with a history of chronic, gradually worsening symptoms. Most cases are of pulmonary TB (around 70%) but they often have systemic symptoms.

Typical signs and symptoms of TB include:

  • Lethargy
  • Fever or night sweats
  • Weight loss
  • Cough with or without haemoptysis
  • Lymphadenopathy
  • Erythema nodosum
  • Spinal pain in spinal TB (also known as Pott’s disease of the spine)
128
Q

Investigations for TB

A

Tuberculosis can be very difficult to diagnose. The bacteria grows very slowly in a culture compared with other bacteria. It also can’t be stained with traditional gram stains and requires specialist stains like the Ziehl-Neelsen stain.

There are two tests for an immune response to TB caused by previous, latent or active TB. These are the Mantoux test and interferon‑gamma release assay. In patients where the active disease is suspected a chest xray and cultures are used to support the diagnosis

129
Q

Explain the Mantoux test

A

The Mantoux test is used to look for a previous immune response to TB. This indicates possible previous vaccination, latent or active TB.

This involves injecting tuberculin into the intradermal space on the forearm. Tuberculin is a collection of tuberculosis proteins that have been isolated from the bacteria. The infection does not contain any live bacteria.

Injecting the tuberculin creates a bleb under the skin. After 72 hours the test is “read”. This involves measuring the induration of the skin at the site of the injection. NICE suggest considering an induration of 5mm or more a positive result. After a positive result they should be assessed for active disease.

130
Q

Explain the Interferon-Gamma Release Assay (IGRA)

A

This test involves taking a sample of blood and mixing it with antigens from the TB bacteria. In a person that has had previous contact with TB the white blood cells have become sensitised to those antigens and they will release interferon-gamma as part of an immune response. If interferon-gamma is released from the white blood cells then this is considered a positive result.

The IGRA test is used in patients that do not have features of active TB but do have a positive Mantoux test to confirm a diagnosis of latent TB.

131
Q

CXR findings for TB

A
  • Primary TB may show patchy consolidation, pleural effusions and hilar lymphadenopathy
  • Reactivated TB may show patchy or nodular consolidation with cavitation (gas filled spaces in the lungs) typically in the upper zones
  • Disseminated Miliary TB give a picture of “millet seeds” uniformly distributed throughout the lung fields
132
Q

Management of Latent TB

A

Otherwise healthy patients do not necessarily need treatment for latent TB. Patients at risk of reactivation of latent TB can be treated with either:

Isoniazid and rifampicin for 3 months
Isoniazid for 6 months

133
Q

Management of Acute Pulmonary TB

A

Management of active TB is coordinated by a specialist TB service with an MDT approach.

RIPE is the mnemonic used to remember the treatment for TB. It involves a combination of 4 drugs used at the same time:

R – Rifampicin for 6 months
I – Isoniazid for 6 months
P – Pyrazinamide for 2 months
E – Ethambutol for 2 months

134
Q

Other management considerations for TB

A
  • Test for other infections
  • Test contact for TB
  • Notify Public health
  • Isolate patient
  • Specialist MDT management and follow up
  • Different drug regime for multidrug-resistant TB
135
Q

Side effects of TB treatment

A
  • Rifampicin can cause red/orange discolouration of secretions like urine and tears. It is a potent inducer of cytochrome P450 enzymes therefore reduces the effect of drugs metabolised by this system. This is important for medications such as the contraceptive pill.
  • Isoniazid can cause peripheral neuropathy. Pyridoxine (vitamin B6) is usually co-prescribed prophylactically to reduce the risk of peripheral neuropathy.
  • Pyrazinamide can cause hyperuricaemia (high uric acid levels) resulting in gout.
  • Ethambutol can cause colour blindness and reduced visual acuity.
  • Rifampicin, isoniazid and pyrazinamide are all associated with hepatotoxicity
136
Q

HIV vs AIDS

A

HIV – Human Immunodeficiency Virus
AIDS – Acquired Immunodeficiency Syndrome
AIDS is usually referred to in the UK as Late-Stage HIV

137
Q

Basics of HIV

A

HIV is an RNA retrovirus. HIV-1 is the most common type. HIV-2 is rare outside West Africa.

The virus enters and destroys the CD4 T helper cells.

An initial seroconversion flu-like illness occurs within a few weeks of infection. The infection is then asymptomatic until it progresses and the patient becomes immunocompromised and develops AIDS-defining illnesses and opportunistic infections potentially years later.

138
Q

Transmission of HIV

A

HIV can’t spread through normal day to day activities including kissing. It is spread through:

  • Unprotected anal, vaginal or oral sexual activity.
  • Mother to child at any stage of pregnancy, birth or breastfeeding. This is referred to as vertical transmission.
  • Mucous membrane, blood or open wound exposure to infected blood or bodily fluids such as through sharing needles, needle-stick injuries or blood splashed in an eye.
139
Q

AIDS-Defining Illnesses

A

There is a long list of AIDS-defining illnesses associated with end-stage HIV infection where the CD4 count has dropped to a level that allows for unusual opportunistic infections and malignancies to appear. Some examples are:

  • Kaposi’s sarcoma
  • Pneumocystis jirovecii pneumonia (PCP)
  • Cytomegalovirus infection
  • Candidiasis (oesophageal or bronchial)
  • Lymphomas
  • Tuberculosis
140
Q

Screening for HIV

A

HIV is a treatable condition and most patients are fit and healthy on treatment. There are many people that have HIV that do not know the diagnosis and these patients are at risk of the complications and spreading the disease. Generally the earlier a patient is diagnosed the better the outcome.

We should test practically everyone admitted to hospital with an infectious disease regardless of their risk factors. Patients with any risk factors should be tested. Antibody tests can be negative for 3 months following exposure so repeat testing is necessary if an initial test is negative within 3 months of a potential exposure.

Patients need to give consent for a test. Verbal consent should be documented prior to a test. Consent only needs to be as simple as “are you happy for us to test you for HIV?” Patients no longer require formal counselling or education prior to a test.

141
Q

What antigen is looked for in a HIV antibody blood test

A

p24 antigen

142
Q

What test gives the viral load count for HIV

A

PCR testing

143
Q

Monitoring for HIV

A

CD4 count

This is a count of the number of CD4 cells in the blood. These are the cells destroyed by the HIV virus. The lower the count the higher the risk of opportunistic infection.

500-1200 cells/mm3 is the normal range
Under 200 cells/mm3 is considered end stage HIV / AIDS and puts the patient at high risk of opportunistic infections

Viral Load (VL)

Viral load is the number of copies of HIV RNA per ml of blood. “Undetectable” refers to a viral load below the labs recordable range (usually 50 – 100 copies/ml). The viral load can be in the hundreds of thousands in untreated HIV.

144
Q

Treatment for HIV

A

All patients started on an Antiretroviral therapy (ART) regardless of Viral load of CD4 count

BHIVA guidelines recommend a starting regime of 2 x Nucelotide Reverse Transcriptase Inhibitors (NRTI) e.g. tenofovir and emtricitabine plus a third agent

145
Q

Aim of HIV treatment

A

The aim of treatment is to achieve a normal CD4 count and undetectable viral load. As a general rule when a patient has normal CD4 and undetectable VL on ART treat their physical health problems (e.g. routine chest infections) as you would an HIV -ve patient. When prescribing be aware and check interactions any medication might have with the HIV therapy

146
Q

Name 3 Highly Active Anti-retrovirus therapy (HAART) Medication classes

A
  • Protease Inhibitors (PIs)
  • Integrase Inhibitors (IIs)
  • Nucleoside Reverse Transcriptase Inhibitors (NRTIs)
  • Non-Nucleoside Reverse Transcriptase Inhibitors (NNRTIs)
  • Entry Inhibitors (EIs)
147
Q

Additional management for HIV

A

Prophylactic co-trimoxazole (Septrin) is given to patients with CD4 < 200/mm3 to protect against pneumocystis jirovecii pneumonia (PCP).

HIV infection increases the risk of developing cardiovascular disease. Patients with HIV have close monitoring of cardiovascular risk factors and blood lipids and appropriate treatment (such as statins) to reduce their risk of developing cardiovascular disease.

Yearly cervical smears are required for women. HIV predisposes to developing cervical human papillomavirus (HPV) infection and cervical cancer so female patients need close monitoring to ensure early detection of these complications.

Vaccinations should be up to date including annual influenza, pneumococcal (every 5-10 years), hepatitis A and B, tetanus, diphtheria and polio. Patients should avoid live vaccines

148
Q

Explain Post Exposure Prophylaxis

A

Post exposure prophylaxis can be used after exposure to HIV to reduce the risk of transmission. It is not 100% effective and must be commenced within a short period (less than 72 hours). The sooner it is started the better. A risk assessment about the probability of developing HIV should be balanced against the side effects of post exposure prophylaxis.

It involves a combination of ART therapy. The current regime is Truvada (emtricitabine / tenofovir) and raltegravir for 28 days.

HIV tests should be done initially but also a minimum of 3 months after exposure to confirm a negative status. Individuals should abstain from unprotected activity for a minimum of 3 months until confirmed negative

149
Q

Overview of Malaria

A

Malaria is an infectious disease caused by members of the Plasmodium family of protozoan parasites. Protozoa are single celled organisms.

The most severe and dangerous member of the family is Plasmodium falciparum. This accounts for about 75% of the cases of malaria in the UK.

Malaria is spread through bites from the female Anopheles mosquitoes that carry the disease. It commonly occurs in travellers to areas where malaria is known to be present

150
Q

Types of malaria parasite

A

Plasmodium falciparum is the most severe and dangerous form
Plasmodium vivax
Plasmodium ovale
Plasmodium malariae

151
Q

Life cycle for Malaria

A

Malaria is spread by female Anopheles mosquitoes, most commonly at night time. Infected blood is sucked up by feeding mosquito. The malaria in the blood reproduces in the gut of the mosquito producing thousands of sporozoites (malaria spores).

When that mosquito bites another human or animal the sporozoites are injected by the mosquito. These sporozoites travel to the liver of the newly infected person. They can lie dormant as hypnozoites for several years in P. vivax and P. ovale.

They mature in the liver into merozoites which enter the blood and infect red blood cells. In red blood cells the merozoites reproduce over 48 hours, after which the red blood cells rupture releasing loads more merozoites into the blood and causing a haemolytic anaemia. This is why people infected with malaria have high fever spikes every 48 hours.

152
Q

Presentation of malaria

A

Suspected malaria in someone who lives or has travelled to an area of malaria. The incubation period is 1-4 weeks after infection with malaria although it can lie dormant for years.

Non-specific Symptoms
- Fever, sweats and rigors
- Malaise
- Myalgia
- Headache
- Vomiting

Signs
- Pallor due to the anaemia
- Hepatosplenomegaly
- Jaundice as bilirubin is released during the rupture of red blood cells

153
Q

Diagnosis of Malaria

A

A diagnosis can be made using a malaria blood film. This is sent in an EDTA bottle (the red top bottle used for a FBC). Examining the malaria blood film will show the parasites, the concentration and also what type they are.

3 samples are sent over 3 consecutive days to exclude malaria. This is due to the 48 hour cycle of malaria being released into the blood from red blood cells. The sample may be negative on days where the parasite is not released but becomes positive a day or two later when they are released from the RBCs.

154
Q

Management of Malaria

A

Discuss patients with the local infectious diseases unit for advice on management. All patients with falciparum malaria should be admitted for treatment as they can deteriorate quite quickly.

Oral options in uncomplicated malaria:
Artemether with lumefantrine (Riamet)
Proguanil and atovaquone (Malarone)
Quinine sulphate
Doxycycline

Intravenous options in severe or complicated malaria:

Artesunate. This is the most effective treatment but is not licensed.
Quinine dihydrochloride

155
Q

Falciparum complications

A
  • Cerebral malaria
  • Seizures
  • Reduced consciousness
  • Acute kidney injury
  • Pulmonary oedema
  • Disseminated intravascular coagulopathy (DIC)
  • Severe haemolytic anaemia
  • Multi-organ failure and death
156
Q

Malaria Prophylaxis

A

General advice:

  • Be aware of locations that are high risk
  • No method is 100% effective alone
  • Use mosquito spray (e.g. 50% DEET spray) in mosquito exposed areas
  • Use mosquito nets and barriers in sleeping areas
  • Seek medical advice if symptoms develop
  • Take antimalarial medication as recommended
157
Q

Name the three most common antimalarial medications

A

Proguanil and Atovaquone (Malarone), Mefloquine and Doxycycline

2A Medicine Sam (12 decks)

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