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Phase 3 > Microbiology > Flashcards

Microbiology Flashcards

1
Q

Describe the likely causes of fever in Sub-Saharan Africa

A
  • Malaria: plasmodium falciparum, non-falciparum (P. vivax)
  • Dengue fever
  • Enteric fever
  • Tick typhus
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2
Q

Describe the likely causes of fever in South-Central and South-East Asia

A

South-Central Asia
-Enteric fever
- Dengue
- Plasmodium vivax: non-falciparum malaria

South-East Asia
- Dengue fever
- Falciparum malaria
- Non-falciparum malaria
- Enteric fever

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3
Q

Describe the pathophysiology and diagnosis of malaria

A

Malaria is spread by female anopheles mosquitoes

> Pathophysiology
> Malaria parasites enter the bloodstream and travel to the liver, where they develop: incubation period
> Attach to RBCs, leading to symptoms

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4
Q

Describe the clinical features of malaria

A

Falciparum: features of severe malaria often reflect sludging up of microcirculation (sticky RBCs)

  • Impaired consciousness or seizures
  • Renal impairment: oliguria, high creatinine
  • Acidosis
  • Hypoglycaemia
  • Pulmonary oedema or ARDS (acute respiratory distress syndrome)
  • Hb < 80
  • Spontaneous bleeding / DIC
  • Shock
  • Haemoglobinuria
  • Parasitaemia
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5
Q

Describe the management of non-falciparum malaria

A

> Includes P. vivax, P. ovale, P. malariae, P. knowlsei

> Tend to cause non-severe disease (not benign)
Vivac & ovale can relapse due to hypnozoites

> Oral chloroquine: blood stages
Artemether-containing therapies
Oral primaquine: hypnozoites

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6
Q

Describe the management of falciparum malaria

A

Uncomplicated
- Supportive management
- Oral antimalarials
> Artemether + lumafantrine/Riamet (3 days)
> Quinine + doxycycline (5-7 days)
> Atovaquone + proguanil/Malarone (3 days)

Severe
- Supportive treatment
> Euvolaemia
> Monitoring for hypoglycaemia
> Antibiotics v secondary bacterial infection (algid malaria)
> Haemofiltration if required
> Treatment of seizures

  • Prompt antimalarial therapy
    > Artesunate preferred over quinine
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7
Q

Describe the pathophysiology of enteric fever

A

Ingestion of S. typhi or S. paratyphi from contaminated water
> Organism enters via Peyer’s patches and attacks via reticuloendothelial system (RES)
> Bacteraemia

Incubation period is 5-21 days and this depends on infectious load, age, gastric acidity & immune status

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8
Q

Describe the clinical features and diagnosis of enteric fever

A

Clinical features
- Fever
- Myalgia
- Headache
- Cough
- Abdominal pain
- Constipation
- Diarrhoea
- Septic shock & death

Diagnosis
> Travel history: area visited, food & drink, pre-travel vaccination/advice
> Blood culture
> Stool culture
> Serology

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9
Q

Describe the treatment of enteric fever

A

Quinolones
- Most effective agents but resistance is an issue

Cephalosporins
- Empiric therapy; longer courses (14 days)

Azithromycin
- Good activity with increasing evidence; oral option

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10
Q

Describe the clinical features of dengue

A

Virus spread by Aedes mosquitos

  • Breakbone fever
    > Headache
    > Fever
    > Retro-orbital pain
    > Arthralgia/myalgia
    > Rash
    > Cough
    > Sore throat
    > Nausea
    > Diarrhoea
  • Lab findings:
    > Leucopenia
    > Thrombocytopaenia
    > Transaminitis
  • Dengue haemorrhagic fever: <1% of infections
    > Increased vascular permeability
    > Thrombocytopaenia
    > Fever
    > Bleeding
    > Less likely in travellers
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11
Q

Describe the different causes of viral haemorrhagic fever

A
  • Lassa (spread by rats)
  • Ebola & Marburg viruses (spread by bats)
  • CCHF (Congo Crimean Haemorrhagic Fever - spread by ticks)

Spread by mosquitoes
> SAVHFs: South American Haemorrhagic Fevers
> RVF: Rift Valley Fever
> DHF: Dengue Haemorrhagic Fever
> Yellow fever

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12
Q

Describe the clinical presentation and treatment of viral haemorrhagic fevers

A

Clinical presentation: up to 21 days
> Non-specific febrile illness
> Haemorrhagic manifestations
> Sepsis syndrome / shock
> Death

Treatment
> Supportive
> Correct coagulopathy / anaemia
> Ribavirin
> Ebola antivirals

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13
Q

List the main bacterial, viral and parasitic causes of GI illness

A

Bacteria
> Enterotoxigenic E. coli
> Enteroaggregative E. coli
> Campylobacter species
> Salmonella species
> Shigella species
> C. difficile
> Vibrio species
> Aeromonas
> Plesiomonas shigelloides
> Yersinia enterocolitica

Viruses
> Norovirus
> Rotavirus
> Enteric adenovirus

Parasitic
> Giardia
> Cryptosporidium
> Cyclospora
> Microsporidia
> Isospora
> Entamoeba histolytica

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14
Q

Describe the clinical presentation of GI illnesses

A

Self-limiting diseases, often 1-5 days

Symptoms
> Anorexia
> Malaise
> Abdominal cramps
> Watery diarrhoea (no blood)
> Fever
> Nausea
> Vomiting
> Colitic symptoms - salmonella, shigella

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15
Q

Describe the investigations used in GI illnesses

A
  • Stool culture
    > Microscopy
    > Giardia ELISA/PCR
  • Non-infectious diagnoses
    > TTG
    > Faecal calprotectin (IBD)
  • HIV testing
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16
Q

Describe the management of GI illnesses

A
  • Fluid replacement
  • Antibiotics (usually not indicated, reduce duration by 24h)
    > Quinolones (ciprofloxacin)
    > Azithromycin
  • Antimotility agents (use with caution)
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17
Q

Describe post-infectious irritable bowel syndrome

A
  • 40% of diarrhoea cases lasting more than 2 weeks end up with post-infectious IBS

> Loose stool
Intermittent abdominal discomfort
Bloating

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18
Q

Describe the cause and treatment of cutaneous larva migrans

A

Itchy serpiginous rash caused by the larvae of various nematode parasites of the dog hookworm family
> eggs in dog faeces

Usually present in the feet

Treatment: albendazole

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19
Q

Describe the pathophysiology of schistosomiasis

A

3 major species: S. haematobium, S. mansoni, S. japonicum

  • Snails become infected, cercariae hatch and enter fresh water (NOT saltwater)
    > Swimming, paddling, splashing, washing, showers, drinking
    > To reduce risk: avoid water contact

> Cercariae penetrate skin
Adult, male flatworms (helminth - trematode) live in venules
Produce eggs, which are fertilized and gain the ability to move through tissues

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20
Q

Describe the clinical features of schistosomiasis

A

Clinical features

> Asymptomatic: especially in residents of endemic areas

> Symptomatic infection
> Swimmers itch soon after infection (cercarial dermatitis)
> Katayama fever at least 6 weeks after infection

> Chronic effects
> Liver: pipe stem cirrhosis, portal hypertension
> Bladder: predisposition to cancer, calcification

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21
Q

Describe the diagnosis and treatment of schistosomiasis

A

Diagnosis
> All tests depend upon the presence of eggs
> Need adult worms so will take 6+ weeks to be positive

  • Serology: antibodies to egg antigen (at least 12 weeks)
  • Urine/ stool culture

Treatment
- Praziquantel 40mg/kg on one day
- Side effects very rarely reported
- 80% effective
- Serology remains positive

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22
Q

What is the mechanism of action of beta lactam antibiotics?

A

Beta lactam motif is an analogue of the branching structure of peptidoglycans

> Inhibit cross-linking of cell wall peptidoglycan
Cause lysis of bacteria - bactericidal

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23
Q

Describe the adverse effects associated with beta lactam antibiotic use

A
  • GI toxicity
    > Nausea and vomiting
    > Diarrhoea
    > Cholestasis
  • Infection
    > Candidiasis: oral, vulvovaginal
    > Clostridium difficile infection
    > Selection of resistant bacteria
  • Hypersensitivity

> Type 1: urticarial rash, hives, swelling, anaphylaxis

> Type 4: mild to severe dermatological conditions
> Stevens-Johnson syndrome (SJS)
> Toxic epidermal necrolysis (TEN)
> DRESS syndrome: drug reaction with eosinophilia and systemic symptoms

> Interstitial nephritis
> Especially with flucloxacillin, can lead to renal failure

  • Miscellaneous rare
    > Seizure
    > Haemolysis
    > Leukopaenia
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24
Q

Describe the use of amoxicillin and flucloxacillin

A

Amoxicillin
> Synthetic modification of the original penicillin molecule
> Well absorbed orally
> Prescribed for respiratory tract infections (streptococci)
> Resistance in E. coli & other coliforms is very common so should be avoided in UTI unless organism is sensitive

Flucloxacillin
> Synthetic penicillin modified to overcome the S. aureus beta-lactamase
> Able to be given orally but not as well absorbed as amoxicillin
> Less well tolerated: GI upset, renal & liver dysfunction at high doses
> Gold standard treatment for soft tissue infection & S. aureus when risk of MRSA is low (MSSA)

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25
Q

Describe the use of co-amoxiclav and piperacillin/tazobactam

A

Co-amoxiclav aka amoxicillin-clavulanate
> Amoxicillin + clavulanic acid (beta lactamase inhibitor)
> Expands the spectrum to include S. aureus, more coliforms & anaerobes
> Broadest spectrum beta-lactam available orally
> Cholestasis common

Piperacillin/tazobactam aka Tazocin
> IV route
> Tazobactam is a beta lactamase inhibitor
> Active against pseudomonas
> First line treatment for neutropenic sepsis in severely immunocompromised patients

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26
Q

Describe the use of ceftriaxone and meropenem

A

Ceftriaxone: cephalosporin
> IV route
> Different affinity for penicillin binding proteins (PBPs) to overcome many beta-lactamases
> Broader spectrum for gram negatives than co-amoxiclav
> Implication in C. diff infection so now largely restricted to CNS infections e.g. bacterial meningitis

Meropenem: carbapenem
> Ultra broad spectrum beta lactam
> IV route
> Active against most common causes of infection except MRSA and some extremely resistant gram negatives
> Substantial ecological impact: thrush, C. diff infections

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27
Q

Describe the mechanisms of resistance against beta lactam antibiotics

A

1) Mutation of antibiotic target site e.g. MRSA
> Mutation of penicillin binding proteins or through gene transfer
> May result in
» Loss of efficacy: antibiotic failure
» Decreased potency: increased dose

2) Production of inactivating enzymes

> Beta-lactamases
> Lyse beta-lactam ring to inactivate the antibiotic
> Common in gram negative bacilli and S. aureus
> Some easy to overcome e.g. S. aureus beta-lactamase, prescribe flucloxacillin
> Some hard to overcome e.g. metallo-beta-lactamase like NDM-1 can lyse almost all beta-lactams

> Extended spectrum beta-lactamases (ESBLs)
> Beta-lactamases able to lyse ceftriaxone and similar antibiotics
> Meropenem generally recommended for severe infection

> Carbapenemases e.g. metallo-beta-lactamases + reduced membrane permeability
> CPEs - carbapenemase producing enterobacteriaceae lead to carbapenem resistance

3) Antibiotic influx/efflux mechanims

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28
Q

Describe the uses and adverse effects of vancomycin

A
  • Ultra broad spectrum Gram positive antibiotic
  • Delivered IV EXCEPT in C. diff infection
  • Less effective than flucloxacillin when managing MSSA
    > Large molecule results in difficult penetration into bacteria
  • Used in MRSA or in patients unable to take flucloxacillin

Adverse effects
> Nephrotoxicity (high doses)
> Red-man syndrome
» Anaphylactoid reaction if infusion is too rapid
> Ototoxicity (rare)

Therapeutic drug monitoring is required due to narrow therapeutic range

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29
Q

Which gene grants S. aureus resistance?

A

MecA gene, derived from S. fleurettii

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30
Q

Describe the mechanism of action of gentamicin

A

Aminoglycoside antibiotic; IV route administration

> Used for gram negative bacteria: management of patients with UTI/intra-abdominal infection

> Reversibly binds to 30S ribosome
> Bacteriostatic; results in prolonged post-antibiotic effect

> Poorly understood action on cell membrane
> Bactericidal
> Prominent at high concentrations
> Rapid killing early in dosing interval

  • Relatively low rates of resistance
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31
Q

Describe the adverse effects of gentamicin

A
  • Nephrotoxicity
  • Ototoxicity
  • Neuromuscular blockade
    > Especially in patients with myasthenia gravis
    > Critical worsening of respiratory function
  • Once-daily dosing
    > High initial dose to take advantage of rapid killing
    > Leave long dosing interval (24-48h) to minimise toxicity
    > 3 days only
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32
Q

List risk factors for antibiotic resistance

A
  • Antibiotic consumption within the last 6 months
  • Overnight stays in hospital
  • Visiting countries with high rates of drug resistance
  • Risk of resistance persists for many months after acquired
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33
Q

Describe the action of macrolides and their adverse effects

A
  • Good spectrum of activity against Gram positives and respiratory Gram negatives
  • Active against atypicals: Legionella, Mycoplasma, Chlamydia

> Excellent oral absorption

  • Adverse effects
    > Diarrhoea & vomiting
    > QT prolongation
    > Hearing loss with long-term use
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34
Q

List significant interactions with macrolides

A
  • Simvastatin
    > Avoid co-prescription
    > Temporarily stop simvastatin
  • Atorvastatin
  • Warfarin
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35
Q

Describe the antibiotics most commonly associated with C. diff infection

A

4 C’s
> Clindamycin
> Co-amoxiclav
> Cephalosporins
> Ciprofloxacin

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36
Q

Describe the action of tetracyclines

A
  • Similar spectrum of activity to macrolides, also active against atypicals
  • Relatively non-toxic
  • Avoid in children and pregnant women due to tooth discolouration and bone abnormalities
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37
Q

Describe the mechanism of action of the quinolones giving 3 examples

A

> Broad spectrum, bactericidal antibiotics
Excellent oral bioavailability
Active against atypicals

  • Ciprofloxacin
    > Broad spectrum antibiotic mainly targeting Gram negative pathogens
    > Useful in UTI / intra-abdominal infection
    >
  • Levofloxacin
  • Rifampicin
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38
Q

Describe the mechanism of action of the quinolones giving 3 examples

A

> Broad spectrum, bactericidal antibiotics
Excellent oral bioavailability
Active against atypicals

  • Ciprofloxacin
    > Broad spectrum antibiotic mainly targeting Gram negative pathogens
    > Useful in UTI / intra-abdominal infection
    > o
  • Levofloxacin
  • Rifampicin
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39
Q

Describe the mechanism of action of the quinolones giving 3 examples

A

> Broad spectrum, bactericidal antibiotics
Excellent oral bioavailability
Active against atypicals

  • Ciprofloxacin
    > Broad spectrum antibiotic
    > Useful in UTI / intra-abdominal infection
    > Only oral antibiotic with good activity against diffcult to treat Gram negatives e.g. pseudomonas
    > Widespread resistance now
  • Levofloxacin
    > Extended spectrum quinolone with increased activity against Gram positive organisms
    > Less activity against Gram negative organisms
    > In practice, used for pneumonia and LRTIs
  • Rifampicin
    > 2 indications: tuberculosis & in addition to another antibiotic in serious Gram positive infection (especially Staph aureus)
    > Drug interactions: potent CYP450 enzyme inducer; most drugs undergoing hepatic metabolism are affected
    > Never prescribe rifampicin monotherapy
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40
Q

List the adverse effects associated with quinolone use

A
  • GI toxicity
  • QT prolongation/arrhythmia
    > Tendonitis, even tendon rupture
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41
Q

Describe the mechanism of action of inhibitors of folate synthesis and give examples

A

> Inhibition of folate metabolism pathway leads to impaired nucleotide synthesis and therefore impaired DNA replication

> Trimethoprim
> Resistance is a major problem
> Used in uncomplicated UTIs

> > Adverse events: elevation of serum creatinine, potassium, rash and GI disturbance

> Co-trimoxazole: trimethoprim + sulphamethoxazole
> Significant additional toxicity - bone marrow suppression & Stevens Johnson syndrome
> Used for uncommon specialists, e.g. pneumocystis jirovecii pneumonia

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42
Q

Describe the scoring system used for sepsis and the choice of empirical antibiotic therapy

A

Sepis refers to life-threatening organ dysfunction occurring as a result of dysregulated host response to infection

> Quantified by Sequential Organ Failure Assessment (SOFA) score of >=2 for the organ in question
> or quick SOFA: confusion or hypotension or tachypnoea

Empirical therapy
> Source unknown: amoxicillin + gentamicin
> If S. aureus is suspected: add flucloxacillin
> If MRSA suspected or true penicillin allergy: vancomycin + gentamicin
> If severe streptococcal infection is suspected, add clindamycin

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43
Q

List conditions which may require IV antibiotic therapy

A
  • Sepsis
  • Infective endocarditis
  • CNS infection
  • Bacteraemia: S. aureus
  • Osteomyelitis (Initially)
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44
Q

Describe contact, droplet and airborne precautions

A

Contact precautions
> Used to prevent and control infections that spread via direct contact
> Wear apron, gloves, fluid resistant surgical mask
> Single side room accommodation (cleaned twice daily)

Droplet precautions
> Used to prevent infections that spread via droplets from respiratory tract of one person to mucosal surfaces of another person
> Wear apron, gloves, fluid resistant surgical mask and eye protection
> Single side room accommodation

Airborne precuations
> Spread via aerosols - small buoyant particles - from the respiratory tract
> Wear gown, gloves, mask (FFP3 respirator)
> Single side room with negative pressure (to ensure infected aerosols stay in room)

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45
Q

Name a common cause of S. aureus bacteraemia and list its complications

A
  • IV access devices as they breach skin’s natural defensive barriers, allowing entry of S. aureus on skin
  • Complications
    > Endocarditis
    > Discitis
    > Metal work-related
    > Vascular graft infections
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46
Q

Describe the symptoms, complications and contact precautions associated with C. diff infection

A
  • Major cause of infectious diarrhoea, predominantly HAI
  • Production of toxins resulting in
    > Watery diarrhoea
    > Nausea
    > Fever
    > Abdominal pain
  • Complications
    > Pseudomembranous colitis
    > Toxic megacolon
    > Recurrent infection
    > Death

Contact precautions, single side room accommodation, soap & water for hand hygiene

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47
Q

List the sources of infection associated with
1) Water
2) Ventilation

A

1)
Water ingress - leaks resulting in wet building material and germination of fungal spores
Supply water - for drinking and patient bathing; can be a source of pathogens like legionella, pseudomonas
Endoscopy rinse water
Hydrotherapy pools
Heater cooler units (devices used in ECMO and cardiac bypass machines)

2)
Theatres - ventilation limits the ingress of organisms from the outside & has high air exchanges to dilute any contamination generated within
Infectious disease isolation rooms: negative pressure + air exchanges
Bone marrow transplant units, assisted conception units, sterile pharmacy units…

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48
Q

Describe the typical causes of community acquired pneumonia (CAP)

A
  • Streptococcus pneumoniae
    > Gram positive diplococci
    > Colony morphology - Draughtsman colonies
    > Risk factors: alcohol abuse, smoking, asthma, HIV, co-infection with viruses e.g. influenza
    >Treatment:
    » Penicillin
    » If penicillin resistant: vancomycin, rifampicin
    > If penicillin allergic: clarithromycin (macrolide), doxycycline (tetracycline)
  • Haemophilus influenzae
    > Gram positive coccobacilli
    > Often identified on chocolate agar (requires growth factors X and V to grow)
    > Common in older people or patients with underlying lung disease
    > Colonisation of upper respiratory tract, ears, eyes, lungs…
    > Risk of beta-lactamase: treatment with co-amoxiclav, macrolides or tetracyclines
  • Moraxella catharralis
    > Gram negative coccobacilli
    > Movable colonies
    > Frequent cause of infective exacerbations of COPD
    > Risk of beta-lactamase: treatment with co-amoxiclav, macrolides or tetracyclines
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49
Q

Describe atypical causes of pneumonia

A
  • Mycoplasma pneumoniae
    > Smallest free-living bacterium
    > Lack of cell wall
    > Very difficult to grow

> Symptoms
> Extra-respiratory manifestations
» Haemolysis:
» Guillain-Barré
» Erythema multiforme
» Cardiac
» Arthritis, arthralgia

> > Respiratory symptoms

> Diagnosis: serology, PCR: sputum/throat swab
Treatment: clarithromycin, doxycycline, ciprofloxacin

  • Legionella pneumophila
    > Associated with exposure of aerosols from water e.g. air conditioning

> Symptoms: extra-respiratory manifestations + respiratory symptoms

> Diagnosis: culture, serology, urinary antigen test

  • Chlamydophila pneumoniae
  • Chlamydophila psittaci
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50
Q

Describe the common causes of hospital-acquired pneumonia (HAP)

A
  • Bacterial species
    > Enterobacterales (oxidase negative)
    » Klebsiella
    » E. coli
    » Enterobacter

> Pseudomonas aeruginosa (oxidase positive)

> Staphylococcus aureus

> Acinetobacter

> Stenotrophomonas

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51
Q

List the clinical features of pneumonia

A

> Fever
Cough / sputum
Chest pain
Insidious/abrupt onset
Non-respiratory symptoms

> Signs: dull percussion, coarse crepitations, increased vocal resonance

> Past medical history: underlying lung disease, immunosuppression

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52
Q

Describe the scores used to assess the severity of pneumonia

A

CURB65 score
> Confusion
> Urea > 7
> Respiratory rate > 30
> BP < 60/90
> Age over 65

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53
Q

Describe the investigations used for pneumonia

A
  • Blood tests
    > FBC
    > U&Es
    > ABG / oxygen sats
  • Microbiology
    > Blood culture
    > Sputum culture
    > Throat swab
    > Urine Legionella antigen
    > Viral or bacterial PCR
  • Investigations
    > Chest X-ray
    » Severe infection: multilobar consolidation, patchy opacities bilaterally
    > ECG
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54
Q

Describe the bacterium which causes tuberculosis

A
  • Mycobacterium tuberculosis is a weakly gram positive bacterium (acid-alcohol fast bacilli)
  • Complex lipid laden structure containing mycolic acids
  • Slow growing organisms, form white or buff coloured colonies (appear on solid LJ culture media within 6-8 weeks)
    > Faster isolation can be achieved in liquid MGIT culture
    > Molecular tests - Gene Xpert - can identify TB direct from samples
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55
Q

Describe how populations of M. tuberculosis behave

A
  • Patients often harbour heterogeneous populations, usually 4
    > Actively growing organisms - killed by isoniazid
    > Semi-dormant organisms inhibited by an acid environment - killed by pyrazinamide
    > Semi-dormant organisms with spurts of active metabolism - killed by rifampicin
    > Completely dormant organisms - not killed by standard rugs
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56
Q

Describe the pathophysiology of TB

A
  • Cough produces droplets containing M. tb which can infect others:
    > 90-95% of infected individuals
    » Contain bacteria & can be reactived later in life

> 5-10% of infected individuals develop primary active TB

Immune response: cell-mediated immunity
> Dendritic cells process TB antigens and present them via MHC-II
> Drain to lymph nodes where they encounter and activate naive CD4+ T cells
> CD4+ T cells produce interferon gamma - Th1 response - which activates macrophages (also TNF alpha)
> Surround activatedd macrophages forming a granuloma

> Granuloma consists of compact organised aggregates of epithelioid cells
Macrophages undergo specialised transformation, become multinucleated giant cells which contain TB bacteria but do not kill it
Central caseous necrosis
Ghon complex on CXR

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57
Q

Describe the clinical features of TB

A
  • Constitutional symptoms
    > Fever + chills
    > Night sweats
    > Fatigue
    > Loss of appetite, weight loss
    > Lymphadenopathy
  • CNS: meningitis - neck stifffness, headaches, photophobia
  • Eyes: choroiditis - blurred vision, red eyes
  • CVS: constrictive pericarditis, chest pain, shortness of breath
  • Renal: dysuria, haematuria (sterile pyuria)

> GI - ileocaecal: abdominal pain, mass in RIF; peritoneal: distended abdomen and ascites

> Skeletal: arthritis, osteomyelitis

> Skin: lupus vulgaris - brown plaques which can ulcerate and occur at mucocutaneous junction

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58
Q

List 5 risk factors for TB

A
  • HIV/AIDS
  • Transplantation
  • Chronic renal failure
  • TNF-alpha inhibitors
  • Diabetes
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59
Q

Describe the tests used to detect TB

A
  • Mantoux test
    > Inject small amount of purified protein derivative from M. tb under surface of skin
    > Previous exposure/active TB: circular area several cm in diameter (delayed hypersensitivity reaction)
  • Interferon Gamma Release Assays
    > T-spot TB
    » White cell preparation from patient put into well with anti-interferon-gamma antibodies
    » Activate it with highly purified recombinant TB proteins, which are taken up by APCs
    » T cells activated, secrete interferon-gamma, captured by antibody
    » Colour change produced (blue spot)
  • Quantiferon
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60
Q

Describe how TB is diagnosed

A
  • Identification of acid-alcohol fast bacilli in respiratory or other sample: microbiology, histopathology
  • M. tuberculosis growth in culture (solid LJ or liquid MGIT culture media)
  • Clinical and/or radiological diagnosis
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61
Q

Describe the treatment of latent TB

A
  • Isoniazid monotherapy: 6 months
  • Rifampicin + isoniazid: daily for 3 months
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62
Q

Describe the treatment for active TB

A

Total 6 months: 2 RHEZ / 4RH

> Intensive phase treatment - 2 months
> Rifampicin, isoniazid, ethambutol and pyrazinamide

> Continuation phase - 4 months
> Rifampicin and isoniazid

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63
Q

Describe the drug interactions and adverse events associated with TB treatment

A
  • Rifampicin
    > Enzyme inducer
    > Turns bodily secretions orange
    > Flu-like illness
  • Isoniazid
    > Liver injury
    > Drug-induced lupus erythematosus (DILE)
  • Ethambutol
    > Toxic optic neuropathy - monitor vision
  • Pyrazinamide
    > Liver injury
    > Raised lactate
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64
Q

Describe the treatment for multiple drug resistant TB

A
  • Resistance to both rifampicin and isoniazid
  • May be detected rapidly using molecular testing - gene Xpert
  • Extended second and third line sensitivity testing is complex
  • Current strategy
    > 18 months-2 years of treatment
    > Drugs associated with significant adverse event profiles
    > Injectable agents with risk of HIV and BBV transmission
  • Pyrazinamide + 4 second-line agents during intensive phase (>8 months)
    > Fluoroquinolone
    > 2nd line injectable
    > Ethionamide or prothionamide
    > Cycloserine or p-aminosalicylic acid
  • Total duration >20 months if not previously treated for MDR TB
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65
Q

Describe XDR TB

A

MDR TB + additional resistance to fluoroquinolone and one of the injectables (amikacin, kanamycin, capreomycin)

> No standard treatments
Consider surgical interventions

New drugs in trials: BDQ, delamanid, pretomanid

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66
Q

What is the “Sepsis 6”?

A

3 investigations
- Blood cultures
- Urine output
- Lactate

3 treatments
- Oxygen
- IV antibiotics
- IV fluids

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67
Q

What is the antibiotic of choice for meningitis?

A

IV ceftriaxone

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68
Q

Describe the body’s barriers to infection

A
  • Mouth: lysozyme
  • Stomach: acid pH
  • Small intestine:
    > Mucus
    > Bile
    > Secretory IgA
    > Peyer’s patches
    > Epithelial turnover
    > Normal flora
  • Large intestine
    > Epithelial turnover
    > Normal flora - gut microbiome
    » 99% anaerobes
    » Enterobacteriales e.g. E. coli, proteus species
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69
Q

Describe the general mechanisms of transmission of GI infection

A

3 F’s

> Food
> Contamination: farm to fork
> Cross-contamination: distribution chain, domestic kitchen

> Fluids
> Water, contaminated juices

> Fingers
> Importance of washing hands after toileting (faecal-oral) and before/after preparing food/drink

Person-to-person spread depends on the infectious dose & environmental setting

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70
Q

Describe the investigations and diagnosis of GI infetions

A
  • History: nature of diarrhoea, timing (acute v chronic), food history, recent antibiotic usage, foreign travel
  • Examination:
    > Febrile, shock, systemically unwell
    > Wasting: chronic change
    > Neurological changes e.g. Clostridium botulism
  • Investigations:
    > Blood tests: FBC, U&Es, blood film
    > Sigmoidoscopy
    > Abdo X-ray, CT
  • Lab:
    > Enrichment broth
    > Selective & differential media
71
Q

Describe the differences between selective and differential media

A
  • Selective media suppresses the growth of background flora while allowing the growth of the pathogen
  • Differential media e.g. MacConkey’s agar
    > Distinguishes mixed organisms on the same plate
    > Uses biochemical characteristics of microorganisms growing in the presence of specific nutrients combined with an indicator which changes colour
    » E.g. salmonella & shigella - non-lactose fermenters (NLFs)
    » Lactose fermenting colonies (E. coli) are pink
    » Non-lactose fermenting colonies (Shigella) are colourless
72
Q

Describe the general treatment of GI infections

A
  • Many are mild & self-limiting
  • Supportive management: fluid resuscitation
  • Antibiotic treatment is often contraindicated (unless severe or prolonged symptoms)
    » Antibiotic therapy may prolong symptom duration or exacerbate them (STEC infection)
73
Q

Describe measures which are put in place to control GI infections

A
  • Control depends on breaking the chain of infection

> Adequate public health measures
> Provision of safe, clean drinking water
> Proper sewage disposal

> Education in hygienic food preparation
> Hand hygiene
> Avoid cross contamination (especially raw & cooked food)
> Cook foods properly

> Pasteurisation of milk & dairy production

> Sensible travel food practices

74
Q

Describe the pathogenesis, clinical features and treatment of Salmonella infection

A

Pathogenesis
- Diarrhoea due to invasion of epithelial cells in the distal small intestine & subsequent inflammation
- Bacteraemia can occur: extremes of age, immunocompromised
- Distant organs may become seeded to establish metastatic foci of infection e.g. osteomyelitis, septic arthritis, meningitis…

Clinical features
- Incubation 12-72h
- Watery diarrhoea
- Vomiting
- Fever (more invasive disease)
- Duration 2-7 days

Treatment
- Fluid replacement
- Antibiotics if severe infection/bacteraemia
» Beta-lactams, quinolones or aminoglycosides
» Antibiotics & antimotility agents prolong excretion of salmonellae in the faeces

75
Q

Describe the microbiology and epidemiology of Campylobacter

A

Microbiology
> Curved gram negative bacilli (seagull shaped)
> Microaerophilic & thermophilic (42ºC)
> Culture on Campylobacter selective agar
> C. jejuni most important species

Epidemiology
> Associated with food-borne infection e.g. poultry
> Transmitted via contaminated food, milk or water

76
Q

Describe the pathogenesis, clinical features and treatment of Campylobacter infection

A

Pathogenesis
- Inflammation, ulceration & bleeding in small & large bowel due to bacterial invasion
- Bacteraemia can occur (extremes of age, immunocompromised)
- Rarely causes post-infectious demyelination syndrome (Guillain-Barré syndrome)

Clinical features
- Incubation 2-5 days
- Bloody diarrhoea
- Cramping abdominal pain
- Fever
- Vomiting uncommon
- Duration 2-10 days

Treatment
- Fluid replacement
- Clarithromycin/erythromycin for severe/persistent disease
- Quinolone e.g. ciprofloxacin or aminoglycoside e.g. gentamicin for invasive disease

77
Q

List the different pathogenic types of E. coli and give general microbiological information about this bacterium

A

E. coli is a gram negative bacilli of the enterobacteriales family; it is a normal part of gut flora

  • 6 pathogenic types
    > Enteropathogenic E. coli (EPEC)
    > Enterotoxigenic E. coli (ETEC)
    > Enterohaemorrhagic E. coli (EHEC)
    > Enteroinvasive E. coli (EIEC)
    > Enteroaggregative E. coli (EAEC)
    > Diffuse aggregative e. coli (DAEC)
78
Q

Describe the microbiology, pathogenesis & clinical features of enteropathogenic E. coli (EPEC)

A

Microbiology
> No differential media available
> Test slection of colonies using polyvalent antisera for common EPEC “O” types

Pathogenesis
> Initial adherence via pili
> Followed by formation of characteristic “attaching & effacing” lesion mediated by intimin protein & Tir (transolated intimin receptor) with disruption of intestinal microvilli

Clinical features
> Incubation 1-2 days
> Duration 1-several weeks
> Watery diarrhoea with abdominal pain & vomiting, often with fever

79
Q

Describe the microbiology, epidemiology, pathogenesis & clinical features of enterotoxigenic E. coli (ETEC)

A

Microbiology: no differential media available; test liquid cultures for production of toxins by immunoassays

Epidemiology: major cause of travellers’ diarrhoea & diarrhoea in infants and children in the developing world

Pathogenesis: diarrhoea due to action of 1 or 2 plasmid-encoded toxins
> Heat-labile (LT): structural and functional analogue of cholera toxin
> Heat-stable (ST): produced in addition to or instead of LT

Clinical features
> Incubation period 1-7 days
> Duration 2-6 days
> Watery diarrhoea with abdominal pain & vomiting
> No associated fever

80
Q

Describe the epidemiology and pathogenesis of enterohaemorrhagic E. coli (EHEC)

A

> Specifically E. coli O157:H7 (non-sorbitol fermenter)

Epidemiology
> Large animal reservoirs, especially sheep & cattle
> Consumption of contaminated food, water & dairy products
> Direct environmental contact with animal faeces e.g. petting zoos
> Secondary person-to-person spread is important

Pathogenesis
> Attaching and effacing lesion, similar to EPEC
> Production of Shiga-like toxins: structural & functional analogue of Shigella dysenteriae toxin

81
Q

Describe the clinical features and treatment of Enterohaemorrhagic E. coli (EHEC)

A

Clinical features
> Incubation 1-7 days; duration 5-10 days
> Bloody diarrhoea with abdominal pain & vomiting
> Haemolytic uraemic syndrome (HUS)
» Microangiopathic haemolytic anaemia
» Thrombocytopaenia
» Acute renal failure

Treatment
> Adequate rehydration
> Antibiotics not indicated (increased risk of HUS)

82
Q

Describe the GI manifestations of a Staphylococcus aureus infection

A
  • Food poisoning/gastroenteritis is caused by ingestion of a S. aureus enterotoxin that acts as a superantigen within the GI tract
  • Stimulates the release of large amounts of interleukins (IL-1, IL-2) from macrophages & T helper cells
  • Toxic shock syndrome (TSS) is caused by toxic shock syndrome toxin-1 (TSST-1)
    > Hyperstimulates the release of interleukins
    > Clinical features: fever, hypotension, skin manifestations e.g. diffuse erythroderma
83
Q

Describe the structure and transmission of norovirus

A

Norovirus is a non-enveloped single-stranded RNA virus
> Very stable, remains viable for long periods of time in the environment
> 24-48h incubation period
> Can shed virus for up to 3 weeks after incubation

10 geno-groups (G1-GX), only 3 affect humans: commonly GII-4 strain

Transmission
> Person-to-person: faecal-oral or aerosolised e.g. toilet flush
> Food-borne: shellfish
> Water
> Low infectious dose & infects all ages

84
Q

Describe clinical features, complications and the immunity associated with norovirus

A

Clinical features
> Asymptomatic
> Vomiting
> Non-bloody diarrhoea
> Low grade fever
> Dehydration
> Nausea
> Abdominal cramps
> Headaches, muscle aches

Complications (solid organ and bone marrow transplant patients)
> Chronic diarrhoea and virus shedding

Immunity
> Antibodies last 6-14 weeks
> Link between expression of human histo-blood group antigens (HBGAs) & susceptibility to norovirus

85
Q

Describe the structure and clinical features of rotavirus

A

> Affects mainly children under 2, elderly & immunocompromised

> Reoviridae family: double-stranded non-enveloped RNA virus

> > 5 predominant strains: G1-G4, G9
> G1 accounts for most infections

  • Clinical features
    > Incubation period 1-3 days
    > Clinical manifestation depends on if it is the first infection (more severe) or reinfection

> Symptoms
> Watery diarrhoea
> Abdominal pain
> Vomiting
> Loss of electrolytes leading to dehydration

> Complications
> Severe chronic disease
> Dehydration
> Electrolyte imbalance
> Metabolic acidosis

> Immunity
> Antibodies against VP7 and VP4 and secretory IgA
> Rotavirus vaccine given to children under 2

86
Q

Describe the structural and clinical features of adenovirus

A

> Affects mainly children under 2, elderly & immunocompromised

> Family: adenoviridae - double-stranded DNA virus
> more than 50 serotypes; adenovirus 40 & 41 cause gastroenteritis

> Symptoms
> Fever, watery diarrhoea

87
Q

Describe the structure and clinical features of astrovirus

A
  • Family: astroviridae - single-stranded, non-enveloped RNA virus
  • Causes less severe gastroenteritis than other enteric pathogens
  • Infection is usually sporadic, but can be outbreaks in children

> Affects mainly children under 2, elderly and immunocompromised

88
Q

Discuss the diagnosis of viral gastroenteritis

A
  • Cannot be cultured
  • Previously EM
  • All these viruses are detected using PCR which detctes the DNA or RNA
  • Sample: vomit or stool
89
Q

Describe impetigo including its causative agents and treatments

A
  • Golden encrusted skin lesions with inflammation localised to the dermis
  • Contagious - outbreaks in nurseries
  • Caused by Staphylococcus aureus & Group A strep
  • Treatment: topical fusidic acid or systemic antibiotics
90
Q

Describe tinea including causative agents, diagnosis and treatment

A

Tinea refers to a superficial fungal infection of the skin or nails, e.g. athlete’s foot

Causes: microsporum, epidermophyton, trichophyton

Diagnosis: skin scrapings

Treatment
> Topical therapy: non-severe
» Clotrimazole cream
» Terbinafine cream

> Systemic therapy (severe, involving hair/nails)
> Oral antifungals: terbinafine, itraconazole

91
Q

Describe soft tissue abscesses and their treatment

A
  • Infection within the dermis or fat layers - development of walled off infection & pooled pus
  • Limited antibiotic penetration into abscess
    > Antibiotics not usually required if abscess fully drained & no surrounding cellulitis

Best treatment is surgical drainage

92
Q

Describe cellulitis, including causes

A
  • Bacterial infection involving dermis
  • Most commonly begins on the lower limbs
  • Can track through lymphatic system and may involve localised lymph nodes
  • May be associated with systemic upset although bacteraemia is uncommon

Causes: staphylococcus aureus, beta-haemolytic streptococci (Group A strep most common)

93
Q

Explain the classification system used in cellulitis

A

Eron classification

  • Class I: no signs of systemic toxicity/uncontrolled comorbidities
    > Oral antibiotics for 7 days in primary care: flucloxacillin OR doxycyline, clarithromycin, clindamycin

> IV therapy in ambulatory care: flucloxacillin OR vancomycin

  • Class II: person systemically well/unwell but with a comorbidity
    > Short-term hospitalisastion & discharge on OPAT
  • Class III: significant systemic upset, unstable comorbidities, limb-threatening infection due to vascular compromise
    > Urgent admission to hospital
  • Class IV: sepsis / severe life-threatening infection e.g. necrotising fasciitis
    > Urgent admission to hospital and surgical management
94
Q

Describe streptococcal toxic shock including treatment

A
  • Caused by toxin producing Group A streptococcus
    > Primary infection: throat or skin/soft tissue
  • Clinical features
    > Localised infection
    > Fever
    > Shock
    > Diffuse, faint rash overy body/limbs

Treatment
> Surgery: aggressively seek out abscesses for drainage

> Antibiotics: penicillin + clindamycin

> Pooled human immunoglobulin (severe cases)

95
Q

Describe necrotising fasciitis including the different types and treatments

A
  • Immediately life-threatening soft tissue infection with deep tissue involvement
    > Demarcate with pen and assess spread
    > Rapidly progressive with extensive tissue damage requiring extensive surgical debridement (surgical emergency)
  • Signs and symptoms
    > Pain out of proportion with appearance
    > Severe systemic upset
    > Rapidly progressive
  • 2 types
    > Type 1: polymicrobial
    » Complicates existing wounds including surgical wounds
    » Microbiology: mix of Gram positives, Gram negatives & anaerobes

> Type 2: Group A streptococcus (usually streptococcus pyogenes)
> Occurs in previously healthy tissue, typically on the limbs
May follow a minor injury such as a scratch/sprain

Treatment: broad spectrum antibiotic therapy + surgical intervention
> Flucloxacillin
> Benzylpenicillin
> Gentamicin
> Clindamycin
> Metronidazole

96
Q

Describe the mechanism of action of gentamicin

A

Disrupts peptide elongation by binding to the 16S ribosomal RNA

97
Q

Describe the skin lesions caused by herpes simplex virus including treatment

A

HSV 1 - cold sores

> Vesicular, may be painful
Recurrent: virus may be latent in sensory nerve ganglia

> Diagnosis
> Clinical
> Blood or vesicle fluid for PCR
> Serology sometimes helpful

Treatment: aciclovir (topical, oral, IV)

98
Q

Describe the skin lesions caused by varicella zoster virus

A

> Highly infectious self-limiting childhood infection
Contagious from day 8-21 (before symptoms begin on day 10)
Congenital abnormalities if acquired during pregnancy

Diagnosis: PCR of vesicle fluid (or serology)

Problematic in adults - can cause pneumonitis (treat with aciclovir)

Shingles: reactivation of dormant VZV in dorsal root ganglia
> Dermatomal distribution
> Transmissible - isolate until last crop of vesicles is crusted
> May be very painful: pain management with NSAIDs, gabapentin
> Treat only high risk patients with aciclovir

99
Q

Discuss how burns may predispose patients to infection including the typical causative agents

A

> Microbial colonisation can occur due to the loss of the main protective barrier and commensal organisms

> Burns have 3 distinct zones: zone of coagulation, stasis, hyperaema

Causes of infection
> Group A strep
> Staph aureus
» TSS

> Opportunistic infection: pseudomonas, enterococcus, bacillus

100
Q

Discuss the main considerations in bite injuries and their treatment

A

2 main considerations
> Penetrating injuries involving vulnerable structures e.g. hands

> Altered microbiology of wounds
> Staphylococci & streptococci
> Anaerobic organisms
> Pasteurella & capnocytophagia from mammal bites

Treatments
1st line - co-amoxiclav
2nd line - doxycyline & metronidazole

Surgical debridement & exploration

Prophylaxis: antibiotics, vaccination (tetanus, rabies)

101
Q

Discuss PVL staphylococcus including treatment

A

PVL staphylococcus or Panton-Valentine Leucocidin is a virulence factor carried by some Staph aureus
> Cytotoxin that causes leukocyte destruction & tissue necrosis

Associated with recurrent soft tissue boils (furunculosis) and abscesses over months or years; necrotising chest infections

Transmissible - outbreaks in families and others living close together e.g. universities

Treatment
> Surgical drainage of abscess

> Antibiotics e.g. clindamycin - reduces toxin production as it is a protein synthesis inhibitor

> Decolonisation therapy (patient & household contacts): topical chlorhexidine for skin and hair, nasal muciprocin ointment, washing of sheets/towels

102
Q

Describe the clinical features of adenovirus infection

A
  • Rhinorrhoea
  • Pharyngitis
  • Pharyngoconjunctival fever
  • Children - otitis media
  • Tracheitis
  • Pneumonia
  • Non-respiratory infections
    > Hepatitis
    > Immunocompromise
    > Diarrhoea
103
Q

Describe the main symptoms of common cold coronaviruses in children & the elderly, compare to MERS-CoV & SARS-CoV

A

> OC43, 229E, NL63, HKU1

Children
- URTI
- Croup
- Otitis media
- Pneumonia with wheeze
- Diarrhoea and necrotising enterocolitis in infants

Elderly
- Flu-like illness
- Pneumonia
- IECOPD

MERS-CoV: reservoir in dromedary camels, endemic in the middle east, similar clinical syndrome to other coronaviruses but pneumonia is much more frequent

SARS-CoV: similar clinical syndrome to other coronaviruses but pneumonia is much more frequent

104
Q

Describe the symptoms of rhinovirus in children

A
  • URTI
  • Bronchiolitis - children < 5y/o: alone or in combination with respiratory syncytial virus
  • Pneumonia: children < 5y/o and older adults
  • IECOPD
105
Q

Describe the clinical syndrome associated with influenza including risk factors for severe disease and complications

A
  • Systemic features
    > Fever
    > Myalgia
    > GI disturbance
  • URTI symptoms often predominate after 3 days of systemic features
  • Risk factors for severe disease
    > Pregnancy, extremes of age, T2DM, immunosuppression, morbid obesity
  • Complications
    > Meningoencephalitis, pneumonia, secondary bacterial infection, Guillain-Barré syndrome
106
Q

Describe the 3 different types of influenza

A
  • Influenza A
    > 8 RNA segments; mutates rapidly via antigenic drift, causes pandemics (surface proteins e.g. haemagglutinin can change quickly)
    > Infects horses, pigs, birds & marine ammals
  • Influenza B
    > 8 RNA segments
    > Mutates rapidly, causes epidemics & infects marine mammals
  • Influenza C
    > 7 RNA segments
    > Minor outbreaks, causes mild disease and infects pigs
107
Q

Describe avian influenza

A
  • Human strain receptor = sialic acid (2-6) galactose (URTI)
  • Avian strain receptor = sialic acid (2-3) galactose (in humans - terminal bronchi & alveoli)
  • Currently circulating non-avian strains: H1N1, H3N2
  • Avian strains
    > H5N1:
    » Case fatality rate 52.8%
    » Backyard poultry; limited human to human transmission

> H7N9: causes milder disease in poultry; in humans, case fatality rate is 39%

108
Q

Describe the symptoms of parainfluenza

A
  • Otitis media
  • Croup (HPIV 1 and 2)
    > Croupy cough
    > Inspiratory stridor
    > Hoarse voice
    > Difficulty during inspiration and in-drawing of the chest wall in the subcostal, intercostal or supraclavicular areas
    > Rhonchi
    > Hospitalisation usual in 3-24h after symptom onset, improvement 1-2 days after
  • Bronchiolitis (HIPV3)
  • Children 6 months-5 years & adults: URTI & pharyngitis (HIPV1 & 2)
109
Q

Describe the manifestations of metapneumovirus & respiratory syncytial virus (RSV)

A
  • First infection is always symptomatic
  • Manifestations

> Bronchiolitis (children < 3y/o)
> Proliferation and necrosis of bronchial epithelium followed by sloughing, air trapping & hyperinflation
When air absorbed: atelectasis

> Tracheobronchitis
Croup
Rhinitis
Otitis media with fever

110
Q

Describe the treatments used for viral respiratory illness

A

Mostly supportive: steroids usually not helpful (& lack of evidence), antivirals used for some infections in immunocompromised

> Influenza-specific
> Amantadine: do not use
Baloxavir: single dose; inhibits cap snatching
Ribavirin, favipiravir, laminamivir - research use only

> NA inhibitors e.g. oseltamivir
> Sialic acid analogues - bind to neuraminidase & prevent virus from detaching from the host cell
> Use within 48h of symptom onset (36h for zanamivir in children)
> Toxicity: well-tolerated but can cause GI upset or neuropsychiatric symptoms

111
Q

Describe the cause and clinical features of COVID-19

A

COVID-19 is caused by SARS-CoV-2, a coronavirus - crown-like appearance due to spike proteins

Clinical features
> Fever
> Cough
> Shortness of breath
> Myalgia
> Diarrhoea
> Headache
> Confusion
> Loss of smell/taste
> Chest pain

Incubation period is 5-6 days; period of infectivity usually 5-10 days
> Infectivity starts 24-36h before symptom onset, important in transmission

112
Q

Describe how the manifestation of COVID-19 has changed in new variants

A

> Alpha

> Delta

> Omicron - BA5 now dominant
> Sore throat without coryza
> Cough/fever
> Myalgia, fatigue, recession of loss of taste/smell

Complications
- Increasing oxygen requirement - need for intensive care
- Progressive patchy infiltrates on CXR
- Single organ failure
- Abnormal LFTs
- Low lymphocytes
- GI presentation: anorexia, abdominal pain
- Elderly: delirium, extreme fatigue
- CPR & D dimer highly elevated: thrombosis/PE in severe disease
- Troponins elevated but no evidence of myocardial dysfunction

113
Q

Describe the viral life cycle

A

Viral entry
- Binding to receptor
- Internalised and taken into endosome
- Release of contents

Processing of nucleic acid
- Error prone DNA/RNA viral polymerases

Viral release from cell

114
Q

Describe the mechanism of action and toxicity associated with aciclovir

A
  • Guanosine analogue
  • Aciclovir is activated by viral thymidine kinase in infected cell
  • Inserted into replicating viral DNA sequence, but virus cannot replicate as it is not actually guanosine > termination of viral DNA replication
  • Principally active against HSV & VZV

Toxicity
> Low dose used for most patients; relatively little toxicity, generally well tolerated
> High doses: encephalitis, renal tubular crystalosis, seizures

115
Q

List the normal flora found in different areas of the body

A

Nasopharynx
- Streptococci
- Haemophilus
- Neisseria
- Mixed anaerobes
- Candida
- Actinomyces

Skin
- Staphylococci
- Streptococci
- Corynebacteria
- Proprionibacteria
- Yeasts

Upper bowel
- Enterobacteriaceae
- Enterococci
- Candida

Lower bowel
- Bacteroides
- Bifidobacteria
- Clostridium
- Peptostreptococci

Vagina
- Lactobacilli
- Streptococci
- Corynebacteria
- Candida
- Actinomyces
- Mycoplasma hominis

116
Q

List 3 primary immunodeficiency disorders

A
  • Chronic Granulomatous Disease (CGD)
    > X-linked inheritance
    > Defect in gene coding for NADPH oxidase
    » Deficient production of oxygen radicals
    » Defective intracellular killng

> Recurrent bacterial & fungal infections: abscesses in the lung, lymph nodes, skin

> Inflammatory responses with widespread granuloma formation

> Pulmonary infection: aspergillus species, staph aureus, nocardia species

  • Bruton’s agammaglobulinaemia: no antibody production
  • DiGeorge syndrome: suppression of cellular immunity
117
Q

Describe how organ dysfunction can lead to secondary immunocompromise

A
  • Tumours can cause blockage: e.g. in bile duct, causes ascending cholangitis leading to sepsis
  • Lung cancer can lead to obstruction of cilia (also seen in CF) leading to respiratory infections
  • CNS tumours / spinal cord compression: loss of cough or swallowing reflex, incomplete bladder emptying
  • Lymphoproliferative disorders: antibody production decreases in CLL, multiple myeloma
  • Malignant lymphoma suppresses cellular immunity
118
Q

Describe how neutropaenia can lead to secondary immunocompromise

A
  • Cytotoxic chemotherapy or therapeutic irradiation can suppress humoral and cellular immunity
  • Leads to reduction in proliferation of haemopoietic progenitor cells: depletion of marrow reserves
  • Neutropaenia leads to decreased chemotaxis, phagocytic activity and intracellular killing
  • Pathogens
    > Gram positive cocci: staph aureus, coagulase negative staphylococci, viridans streptococci (mitis, oralis), enterococci (faecalis, faecium)
    > Anaerobes: bacteroides and clostridia species
    > Gram negative bacilli: E. coli, pseudomonas aeruginosa, Klebsiella pneumoniae, Enterobacter species
    > Fungi: candida and aspergillus species

Treatment of neutropaenic sepsis: IV meropenem, amikacin & vancomycin

if chemotherapy patient but no sepsis: IV piperacillin/tazobactam, gentamicin & vancomycin (sub piperacillin/tazobactam with ciprofloxacin if penicillin allergic)

119
Q

Describe how chemotherapy and radiation can lead to mucosal barrier injury

A
  • High mitotic index of GI epithelium is affected by chemo and radiation
    > GI lymphoid tissue responds with inflammatory response
    > Leads to mucositis: presents with dysphagia, xerostomia, ulceration
    > Impairment of GI function & alterations in permeability
    > Altered nutritional status
120
Q

List the treatments for disease which can lead to secondary immunocompromise

A
  • Antibiotics, H2 antagonists, PPIs: altered microbiome
  • Immunosuppressive drugs: corticosteroids, cyclosporin, tacrolimus, alemtuzumab, rituximab, purine analogues
  • Allogeneic stem cell transplantation
  • Solid organ transplant
121
Q

Describe the infections which may arise in solid organ transplant patients

A
  • Community acquired pathogens:
    > Pneumococcus, listeria, salmonella, legionella
    > Viruses: influenza, parainfluenza,RSV
  • Nosocomial infecftions
    > Resistant gram positive and gram negative bacteria, fungi
  • Pre-emptive therapy required for CMV, fungal infection
  • Donor-derived infections
    > Latent: TB, syphilis, viruses (HIV, Hep B, CMV)
    > Active bloodstream infection at procurement: staphylococci, pneumococci, salmonella, E. coli
  • Reactivation of infections. TB, HSV, VZV, CMV
  • Opportunistic infections: aspergillus, pneumocystis
122
Q

Describe the standard STI screen including samples

A
  • Chlamydia and gonorrhoea: nucleic acid amplification test (NAAT)
  • Syphilis and HIV: blood test (EDTA bottle)

Samples
> Females: self-taken vulvovaginal swabs, urine, throat swab & self-taken rectal swabs
> Males: urine, throat swab & self-taken rectal swabs

123
Q

Describe the microbiology of gonorrhoea including the structures which it infects & high risk groups

A
  • Intracellular gram negative diplococci - Neisseria gonorrhoea
  • Infects mucous membranes of
    > Urethra
    > Endocervix
    > Rectum
    > Pharynx
    > Conjunctiva
  • Higher risk groups
    > Men who have sex with men
    > Afro-Caribbean
    > Urban areas with deprivation
    > Women < 25 years
124
Q

Describe the diagnosis of gonorrhoea, including tests, signs & symptoms, treatment

A

Signs and symptoms

> Penile urethra: urethral discharge (profuse yellow/green discharge), dysuria

> Vaginal (endocervix/urethra): change in discharge, abdominal/pelvic pain, dysuria, altered bleeding

> Pharynx: asymptomatic

> Rectum: usually asymptomatic but can present with proctitis (anal discharge, pain or discomfort)

Diagnosis
> NAAT testing
> Urethral sample microscopy
> Culture plate: widespread drug resistance

Treatment = IM ceftriaxone

125
Q

List the treatment and complications of gonorrhoea

A

Treatment: ceftriaxone 1g IM stat (or ciprofloxacin if sensitive); repeat test after 2 weeks to ensure cure

Complications
- Epididymo-orchitis
- Prostatitis
- PID
- Disseminated gonococcal infection (rare, affects skin & joints)
- Resistance

126
Q

Describe the signs and symptoms of chlamydia

A

Penile urethra
> Majority asymptomatic but can include discharge/dysuria/meatal discomfort

Vaginal
> Most asymptomatic
> Intermenstrual or PC bleeding
> Cervicitis or contact bleeding
> Change in discharge
> Pelvic pain

Pharynx: asymptomatic

Rectum
> Asymptomatic
> Proctitis: rectal pain, PR, discharge, rectal bleeding, tenesmus, constipation
> Lymphogranuloma venereum (LGV) subtype often presents as proctitis: can have lymphadenopathy/ulcer disease

127
Q

Describe the diagnosis, treatment and complications of chlamydia

A
  • Diagnosis: NAAT testing
  • Treatment: doxycycline 100mg BD 7/7
  • Complications
    > PID: pelvic pain, fever, dyspareunia
    > Tubal infertility
    > Ectopic pregnancy
    > Fitz-Hugh-Curtis syndrome (peri-hepatitis)

> Epididymo-orchitis: male infertility associated

128
Q

Describe the pathophysiology of mycoplasma genitalium

A
  • Bacteria
  • Some people get symptoms of urethritis / PID

Treatment not indicated unless symptomatic

Diagnosis via NAAT

129
Q

Describe the pathophysiology of Trichomonas vaginalis

A
  • Protozoa with flagella
  • Often asymptomatic
  • Vaginal: frothy yellow discharge with intense itch; strawberry cervix in 2%
  • Penile: asymptomatic or urethritis
  • Diagnosis: microscopy/culture
  • Treatment: metronidazole
130
Q

Describe the mechanism of action of metronidazole

A

Prodrug that undergoes reductive activation in anaerobic bacteria

Forms free radicals and cytotoxic intermediate products

131
Q

Describe the pathophysiology of syphilis

A
  • Caused by a gram negative spirochete - Treponema pallidum
  • Normally transmitted sexually: more common in MSM
  • Presentation
    > Chancre: single, painless ulcer with clear fluid
    > Presents 9-90 days after inoculation; can be in genitals, perianal area or mouth

Secondary syphilis: 3 months-2 years after infection
> Generalised rash affecting palms and soles
> Muco-cutaneous lesions, condylomata lata (wart lesions), lymphadenopathy, fever

> Less commonly: anterior uveitis, hearing loss, patchy alopecia, meningitis, cranial nerve palsies, hepatitis, splenomegaly, arthritis, glomerulonephritis

Tertiary syphilis
> Neurosyphilis: many variations of neurological symptoms including cognitive
> Cardiovascular syphilis: aortic valve disease, aortic aneurysm, aortitis
> Gummatous syphilis: punched out lesions

132
Q

Describe the diagnosis and treatment for syphilis

A

Diagnosis
> If chancre: dark ground microscopy / viral PCR swab
> Bloods for antibody (3 month window period, stays positive even after treatment)
> Rapid plasma reagin: quantitative marker

Treatment: IM benzathine penicillin

133
Q

Describe the cause, symptoms and treatment of anogenital warts

A
  • Caused by human papillomavirus (HPV)
    > Most common types causing warts are HPV 6, HPV 11
    > 89-99% protection with quadrivalent vaccine (6, 11, 16, 18) - Gardasil
  • Symptoms: itch, aesthetic problems

Treatment:
> Cryotherapy
> Topical treatments: podophyllotoxin / imiquimod
> Surgical excision

134
Q

Describe the diagnosis, complications and treatment of herpes simplex virus (HSV)

A

First outbreak flu-like presentation, usually further episodes are less severe

Diagnosis: viral PCR swab

Advice: high prevalence, possible future recurrence, condoms reduce transmission

Complications
> CNS infection
> Balanitis, proctitis
> Urinary retention
> If first episode in pregnancy: risk of neonatal infection

Treatment with aciclovir

135
Q

Describe the pathophysiology of scabies, including treatment

A

Scabies causes itching, especially at night

Scabies is caused by mite excrement which triggers hypersensitivity reaction
> Burrows classically in web spaces, wrist, elbows, nipples

Treatment
> Permethrin 5% or malathion 0.5% - wash off after 24h
> Wash contaminated clothes at 50ºC

136
Q

Describe the pathophysiology and treatment of phthirus pubis

A

Pubic lice - transmitted by close bodily contact
Live on course body hair

Incidence decreasing due to hair removal fashion

Treatment: malathion 0.5% or permethrin 1% cream

137
Q

Describe HIV transmission

A

HIV enters the body via
- Cuts, sores or breaks in the skin
- Mucous membranes e.g. anus or vagina
- Direct injection

Activities that allow HIV transmission
> Anal or vaginal intercourse
> Injecting drugs
> Mother-to-child transmission: before/during birth or through breast milk
> Transmission in healthcare settings
> Transmission via donated blood or blood clotting factors

138
Q

Describe the pathophysiology of HIV

A
  • HIV infects T helper cells, macrophages & dendritic cells
    > HIV infects T cells via high-affinity interactions between virion envelope glycoprotein gp120 and CD4 molecule
  • HIV infection causes depletion of CD4+ T helper cells by:
    > Direct viral killing of cells
    > Apoptosis of uninfected bystander cells
    > CD8+ cytotoxic T cell killing of infected CD4+ T cells
  • Abnormal B cell activation results in inappropriate immunoglobulin production
  • Once CD4+ T cell count falls below 200 (normal range 450-1660), person is at risk of opportunistic infections & some cancers
139
Q

List the opportunistic infections an individual with HIV may contract

A
  • Kaposi’s sarcoma
    > Caused by HHV-8 infection (human herpesvirus 8 - same family as EBV)
    > Presents as brown lesions on skin
  • Oesophageal candida
    > White spots; difficulty swallowing
  • Pneumocystis carinii pneumonia (PCP)
    > Fungal infection causing extensive infiltrate in both lungs
  • Cytomegalovirus retinitis
    > Inflammation of retina, can lead to blindness
  • Epstein-Barr virus
    > Raised white lesions of oral mucosa
  • Cryptosporidiosis
    > Protozoa causing watery diarrhoea
  • Tuberculosis
140
Q

Describe the structure of the HIV virus and how it replicates within cells

A
  • HIV is a retrovirus with 2 strands of ss+ viral RNA
  • 3 key enzymes: integrase, reverse transcriptase & protease
  • Surface glycoproteins
    > Gp120: docking glycoprotein
    > Gp41: transmembrane glycoprotein

After binding, nucleocapsids containing viral genome and enzymes enter target cell & are released

Viral reverse transcriptase catalyses reverse transcription of ssRNA, producing viral double-stranded DNA which is integrated into the host genome by viral integrase

Host cell ribosome catalyses synthesis of viral precursor proteins, which are cleaved into viral proteins by viral proteases

Mature virion buds from plasma membrane & infects another cell

141
Q

Describe HIV testing

A
  • Universal testing: antenatal, GUM, drug addiction
  • Higher risk testing
    > Sub-Saharan Africa, especially Southern Africa
    > Men who have male sexual partners
    > Children of people living with HIV
    > People who inject drugs
    > People who have transactional sex
  • 4th generation testing: purple EDTA bottle
    > Tests p24 antigen / HIV antibody
    > Window period for 99% certainty: 45 days
  • Confirmatory test: different assay
142
Q

Describe primary HIV infection

A
  • Systemic: fever, weight loss
  • Central: malaise, headache, neuropathy
  • Mouth: sores (oesophagus too), thrush, pharyngitis
  • Gastric: nausea, vomiting
  • Myalgia
  • Hepatomegaly, splenomegaly
  • Lymphadenopathy
  • Widespread maculopapular rash
    > DDX: infectious mononucleosis, secondary syphilis, drug rash, other viral infections like CMV or influenza
143
Q

List HIV indicator conditions

A
  • Respiratory: bacterial pneumonia
  • Neurology: dementia, recurrent shingles
  • GI: weight loss, recurrent diarrhoea
  • Unexplained lymphadenopathy
  • Unexplained retinopathy
  • Gynaecology: CIN2 or above
144
Q

Describe the blood markers used in HIV assessment

A
  • HIV viral load
    > Can be up to >10 million
    > Aim is to maintain an undetectable viral load
    > Undetectable means below 200 copies/ml
  • CD4
    > Calculated from total lymphocyte count
    > HIV negative: 400-1600; risk of opportunistic infection increases below 200
    > If VL <200 for >6 months, no risk of onward transmission
145
Q

Describe HIV treatment

A

Aim of treatment is VL suppression & CD4 recovery

Highly active antiretroviral treatment (HAART)

> Triple therapy: 2 nucleoside reverse transcriptase inhibitors + 1 drug from another class (usually integrase inhibitor)

Classes of ARVs
> Nucleoside reverse transcriptase inhibitors e.g. abacavir, tenofovir disoproxil
> Non-nucleoside reverse transcription inhibitors e.g. nevirapine, efavirenz
> Integrase inhibitors e.g. raltegravir
> Protease inhibitors e.g. ritonavir
> Others e.g. CCR5 entry inhibitor

146
Q

Describe the side-effects associated with anti-retroviral treatment

A

Short-term side effects
- Rash
- Hypersensitivity: abacavir & nevirapine
- CNS side effects e.g. Efavirenz - sleep disturbance, vivid dreams, mood
- GI, renal and hepatic

Long-term toxicities
- Body shape changes: lipoatrophy/lipodystrophy, weight gain
- Renal: tenofovir disoproxil
- Hepatic
- Lipid
- Bone

Drug-drug interactions
- Often class-specific and mediated by CYP450: induction/inhibition e.g. PPIs, statins, antipsychotics

147
Q

Describe the differences between active & passive HIV vaccination, and why live attenuated vaccines are not tested

A
  • Active vaccination: aims to induce immune response against HIV
  • Passive vaccination: preformed antibodies against HIV are administered
  • Live attenuated vaccines not tested due to concern about reversion to live virus
148
Q

Describe the methods used in HIV prevention

A
  • Condoms
  • Treatment as prevention (TasP)
  • Pre-exposure prophylaxis (PrEP)
    > Tenofovir disoproxil emtricitabine
    > For people at higher risk of HIV through sexual transmission
    > Long term: caution renal/bone
  • Post-exposure prophylaxis (PEP)
    > 2 NRTIs + integrase inhibitor
    > Take within 72h; take for 28 days
    > Based on exposure type & risk of contact, available from sexual heatlh and A&E
  • Prevention of mother to child transmission (PMTCT)
  • Harm reduction measures e.g. needle exchange
149
Q

Describe the origins of HIV

A

2 distinct viruses: HIV-1 & HIV-2

HIV-1: related to viruses called Simian immunodeficiency virus (SIV) found in chimpanzees & gorillas in West Africa
HIV-2 is related to SIV in another primate: Sooty Mangabey

HIV viruses are thought to have crossed species from primates to humans in Africa in the late 19th/early 20th century

> Bush meat theory: a hunter was bitten/cut while butchering an animal

> Other factors triggered an epidemic of transmission: social changes & urbanisation, unsterile injections, genital ulcer diseases & sexual promiscuity

150
Q

Describe the signs and symptoms of septic arthritis

A
  • New onset joint pain - atraumatic
  • Hot red swollen joint - effusion
  • Reduced range of movement
  • Sepsis
151
Q

List the causes of septic arthritis

A
  • Haematogenous
    > Infective endocarditis
    > Skin infection
    > Respiratory tract infection
    > Urinary tract infection
    > Dental infection
  • Direct inoculation
    > Following arthroscopy / intra-articular injection / trauma / bite
  • Contiguous spread
    > Osteomyelitis
    > Bursitis
    > Cellulitis
    > Soft tissue abscess
152
Q

List the causative microorganisms of septic arthritis in adults & children

A

Adults
- Staphylococcus aureus
- Streptococci
- Enterobacteriacaeae or “coliforms”
- Mycobacterium tuberculosis
- Neisseria gonorrhoeae

Children
- Streptococcus pneumoniae
- Kingella kingae
- Haemophilus influenzae type B

153
Q

Describe the investigations used in septic arthritis

A

Blood cultures + microscopy
> Gram stain procedure, agar plates, coagulase plates

Bloods
> FBC, CRP, ESR, U&Es, LFTs

Joint aspirate

> Synovial white cell count (WCC)
> High WCC count may indicate septic arthritis but also occur with crystal-induced arthritis or inflammatory arthritis
> Low synovial WCC: early infections / immunocompromised / prior antibiotics / low virulence organisms

> Synovial fluid microscopy
> Gram stain and culture (septic arthritis is not excluded by negative microscopy & culture)
> Synovial fluid usually appears turbid

> Synovial fluid examination
> Polarised light used to look for crystals (urate/calcium)

154
Q

Describe additional investigations used to determine the causative microorganism

A

Staphylococcus aureus
- Source: skin, send swabs for culture / infective endocarditis
- Blood cultures / echocardiogram (TTE) if positive cultures

Viridans streptococci (streptococcus mitis/oralis)
- Source: mouth or infective endocarditis
- BCs / TTE if positive BCs

Enterobacteriaceae / enterococci
> Source: abdomen / urogenital tract (+ infective endocarditis for enterococci)
> Urine culture / imaging of abdomen & pelvis

Gonococcal infection
> Men: PCR first catch urine, rectal and throat swab
> Women: vaginal, rectal and throat swab

TB or fungal infection - synovial biopsy for culture + synovial fluid

Lyme arthritis (Borrelia burgorferi) - diagnose by serum antibody testing
> If positive, PCR synovial fluid / tissue

155
Q

What are the differential diagnoses for septic arthritis?

A
  • Rheumatoid arthritis
  • Psoriatic arthritis
  • Crystal induced arthritis
  • Trauma
  • Haemarthrosis
  • Extra-articular infection - cellulitis / bursitis
156
Q

Describe the treatment for septic arthritis

A
  • Repeat joint aspiration as often as required (open washout maybe)
  • Start empirical antibiotics as per local guidelines
    > IV, bactericidal

> Staphylococcus aureus
> MSSA: IV flucloxacillin
> MRSA: IV vancomycin

> Streptococcus species: IV benzylpenicillin / IV ceftriaxone / IV vancomycin (if beta lactam allergy)

> Enterococcus species: IV amoxicillin / vancomycin

> Enterobacteriaceae: IV ceftriaxone / meropenem if ESBL producing organism / gentamicin if beta lactam allergy

> Pseudomonas aeruginosa: IV piperacillin/tazobactam

> Neisseria gonorrhoea: IV ceftriaxone

Duration of antibiotic treatment is prolonged: 4-6 weeks

157
Q

Describe the pathogenesis of periprosthetic joint infection (PJI)

A

Microorganisms adhere to surface & secrete extracellular substances to form a complex glycocalyx structure

Microorganisms within biofilm are slowly dividing: evade host defence systems and are more resistant to antimicrobial therapy

Located at bone-prosthesis
> Eradication of infection may not be possible without removal of the prosthesis / biofilm

158
Q

Describe the timing of periprosthetic joint infection (PJI)

A

Early: within 4 weeks of implantation
> Virulent pathogens: staph aureus, streptococci, aerobic gram negative rods

Delayed: 3 months to 3 years following implantation
> Low viruelnce organisms: CoNS, cultibacterium acnes (shoulder joints)
> Joint pain/loosening

Haematogenous seeding to an implant from a distant focus can also occur

Contiguous infection from a nearby source e.g. soft tissue abscess/osteomyelitis can also occur

159
Q

How are periprosthetic joint infections classified?

A

Acute: immature biofilm
> Red, hot, painful joint
> Fever / sepsis
> Prolonged leaking wound post-operatively (>7-10 days)

Chronic: mature biofilm
> Pain, stiffness
> Loosening of prosthesis on X-ray
> +/- mildly raised inflammatory markers

160
Q

How is periprosthetic joint infection diagnosed?

A

Acute presentation / sepsis
- Joint aspirate % PMNs: WCC, microscopy (gram stain) and culture
- Blood cultures

Chronic presentation
- Sinus tract communicating with prosthesis
- Pre-operative joint aspirate: WCC / % PMNs, culture, biomarkers e.g. alfa-defensin

Acute & chronic presentations: intraoperative samples
> Microbiology: >=2 intraoperative samples with the same microorganisms
> Histopathology: >=5 neutrophils per high power field

Biofilm disruption (sessile biofilm rather than planktonic which is loose in joint fluid)

> Beadmill processing
> Shaking with glass beads to disrupt the biofilm and dissociate bacteria from biofilm

> Sonication of explanted prosthesis
> Low intensity ultrasound to disintegrate biofilm

Laboratory process
> Direct & enrichment culture
» Tissue sample + broth

> Antibiotic sensitivity testing
> Disc diffusion agar plate
> Antibiotic impregnated discs
> Zone of inhibition indicates activity

161
Q

Outline the management of periprosthetic joint infection

A

Surgical strategies

> DAIR: Debridement, Antibiotics & Implant Retention
> Radical debridement, thorough joint washout, exchange of polyethylene liners

> Complete removal of prosthesis

> Resection without reimplantation

> Amputation

Antimicrobial management
> Empirical therapy: IV vancomycin + gentamicin
> Pathogen-directed IV or oral therapy

162
Q

Describe the classification systems used in osteomyelitis & host physiology

A
  • Cierny-Mader Classification
  • Anatomical type
    > Stage 1: medullary
    > Stage 2: superficial
    > Stage 3: localised
    > Stage 4: diffuse
  • Host physiology
    > Category A: no systemic or local compromising factors
    > Category B: systemic or local compromising factors
    > Category C: severely compromised / not a surgical candidate

Waldvogel Classification

> Duration of symptoms
> Acute: days or weeks
> Chronic: months or years, persistence of infection, low grade inflammation, sequestrum, fistulous tracts

> Pathogenesis
> Haematogenous
> Contiguous: trauma, surgery, prosthetic material
> Presence of vascular insufficiency: diabetic foot infection, peripheral vascular disease

163
Q

Describe the pathogenesis of osteomyelitis

A

S. aureus virulence factors

> Bacterial adhesins - promote attachment to ECM proteins

> Protein A, some toxins, capsular polysaccharides - promote evasion from host defences

> Tissue invasion: attacking host cells - exotoxins - or degrading components of extracellular matrix (hydrolases)

> S. aureus can invade cells allowing it to colonise tissues & persist after bacteraemia

> S. aureus & staphylococcus epidermis can form biofilms, allowing escape from immune response & resistance to antibiotics

164
Q

Describe the signs and symptoms of osteomyelitis

A
  • Wound over open fracture
  • Draining sinus / fistula
  • Probe to bone test
  • No wound but swelling & bone tenderness
  • Fever
  • Rigors
  • Sepsis
165
Q

What investigations are used in the diagnosis of osteomyelitis?

A
  • Blood cultures
  • Image guided bone biopsy
    > Microbiology: aerobic & anaerobic culture, myocbacterial/fungal culture

> Histopathology: >=5 neutrophils per high power field, presence of granulomas, consider mycobacterial infection

  • Bloods: CRP / ESR
  • X-ray: bone changes seen usually after 7-10 days from symptom onset, when 30-50% of bone mass has been lost
  • MRI: high diagnostic accuracy
166
Q

List the 3 main types of osteomyelitis

A
  • Acute contiguous osteomyelitis
  • Acute haematogenous osteomyelitis
  • Native vertebral osteomyelitis
167
Q

Describe the pathophysiology of acute contiguous myelitis

A

> Route of organism entry to bone: trauma, surgery, adjacent focus of infection e.g. soft tissue abscess

> Without vascular insufficiency
> Puncture wounds through footwear (pseudomonas aeruginosa)
> Following bites (anaerobes, streptococci, Eikenella corrodens, Pasteurella multocida)

> With vascular insufficiency
> Diabetic foot infection
> Acute infection usually monomicrobial e.g. S. aureus / beta-haemolytic streptococci
> Chronic infections; polymicrobial involving gram negative & gram positive organisms; enterococci, enterobacteriaceae, anaerobes, P. aeruginosa

168
Q

Describe the pathophysiology of acute haematogenous osteomyelitis

A

Site of infection
> Adults: vertebral bodies
> Children: growing ends of long bones or “metaphyses”

Micoorganisms (staph aureus in all age groups)

> Neonates: group B strep / Staph aureus / E. coli
Children <5: S. aureus / Kingella kingae / Group A streptococcus
Children >5: S. aureus / group A strep
Adults: S. aureus
Elderly: S. aureus / gram negative rods

> IV drug users: S. aureus / pseudomonas aeruginosa, Candida species
Sickle cell disease: S. aureus / salmonella species
Intravascular deivcs/lines
Consider Brucella & dimorphic fungi in endemic areas

169
Q

Describe the pathophysiology of native vertebral osteomyelitis

A

Clinical presentation
> Back pain
> Fever
> Raised inflammatory markers
> Bloodstream infection or infective endocarditis
> New neurological symptoms

Causes
> Haematogenous seeding
> Microorganisms: S. aureus, gram negative rods, TB…

170
Q

Describe the treatment of osteomyelitis

A

Duration of antibiotics is 6 weeks - 3 months for Brucella

Empirical antibiotics: cover S. aureus, streptococci, aerobic gram negative rods
> Flucloxacillin + gentamicin / ciprofloxacin
> Ceftriaxone + vancomycin

Indications for surgery
> Progressive neurological deficit
> Progressive deformity
> Spinal instability

171
Q

Describe diabetic foot infection

A
  • Not all foot ulcers are infected: microorganisms isolated from superficial swabs may represent commensal flora

Sepsis/fever - send blood cultures prior to starting antibiotics

Superficial infection
> Pus from ulcer bed
> Surrounding skin: erythema / heat / swelling +/- pain

Osteomyelitis: probe going through ulcer reaching bone

Antibiotic duration is 6 weeks (or longer if no surgical resection)
> Empirical guidelines
» Acute: IV flucloxacillin
» + clindamycin if moderate
» + gentamicin if severe

> > Non-acute: clindamycin + ciprofloxacin

172
Q

Describe the pathophysiology and testing of eczema

A
  • Leaky skin barrier allows entry of food, pollen, allergens
  • Presents in children before school (often before first birthday)

> Mainly affects antecubital fossa, popliteal fossa, ankles, wrists…

> Testing: skin prick testing and blood testing can be used in atopic eczema

173
Q

Describe the treatment of eczema

A

Moisturiser (emollients) - very mild eczema

Combination of emollients & steroids - multiple times a day

Antihistamines - treat itchy skin

Antibiotics - in case of infection

Antifungals - in case of infection

Tacrolimus - immunosuppressant, used as an alternative to steroid cream

174
Q

Give a mild and a potent steroid used in the treatment of eczema

A

Very potent: clobetasol propionate 0.05% (Dermovate)

Mild: hydrocortisone 1%

Phase 3 (14 decks)

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