Lecture 28 - Clinical Infections Respiratory Flashcards
(101 cards)
1
Q
What does the upper respiratory tract consist of?
A
Nose Sinuses Mouth Pharynx Larynx
2
Q
What does the lower respiratory tract consist of?
A
Trachea
Bronchi
Bronchioles
Lungs
3
Q
What is Pharyngitis
A
Inflammation of the back of the throat (pharynx), resulting sore throat and fever
4
Q
Acute tonsillar pharyngitis
A
Symmetrically Inflamed tonsils and pharynx with or without a fever and headache. Patient has marked systemic symptoms of infection and/or unable to swallow
5
Q
Infectious mononucleosis
A
Symmetrically inflamed tonsils/soft palate inflammation and posterior cervical lymphadenopathy
6
Q
Epiglottitis
A
Sudden onset of severe sore throat, no inflammation of the tonsils and/or oropharynx and systemic symptoms/signs of infection
7
Q
What are the key history taking points for causes of an acute sore throat?
A
- Rapidity of onset of sore throat
- Difficulty breathing/speaking
- Ability to eat/drink/swallow
- Associated neck pain/swellings
- Symptoms of systemic infection e.g. fever, chills, rigors, general malaise
- Travel history
8
Q
What are the VIRAL causes of Pharyngitis and tonsillar pharyngitis?
A
- Viruses: Rhinovirus, Coronovirus, Parainfluenza, Influenza (A&B), Adenovirus etc.
9
Q
What are the bacterial causes of pharyngitis and tonsillar pharyngitis?
A
Group A beta-haemolytic Streptococcus (GABHS) is the most common bacterial cause of a sore throat (15-30% of sore throats in children and 10% in adults)
10
Q
What are the rarer causes of pharyngitis and tonsillar pharyngitis?
A
Neisseria gonorrhoeae (Gonococcal pharyngitis) HIV - 1 (can be the first presentation of HIV infection) Corynebacterium diphtheriae (Diptheria)
11
Q
What is the centor criteria?
A
Gives an indication of the likelihood of a sore throat being due to bacterial infection.
12
Q
What are the 4 Centor criteria?
A
- Tonsillar exudate
- Tender anterior cervical lymphadenopathy
- fever over 38 degrees
- Absence of cough
If 3 or 4 criteria are met - positive predictive value is 40% to 60%
The absence of 3 or 4 of the Centor criteria has a fairly negative predictive value of 80%
13
Q
Acute sore throat - investigations
A
Outpatient/ambulatory investigation (non-severe infection): No routine investigations, unless infectious mononucleosis is suspected
Inpatients (severe infection) investigation: Throat swab for culture, blood cultures, (blood tests: Full blood count, urea and electrolytes and liver function tests).
Suspected infectious mononucleosis: blood sample for Monospot or EBV serology
14
Q
Acute sore throat - Management
A
- Oral analgesics (paracetamol, ibuprofen)
- Most acute sore throats do not require antibiotics. Consider antibiotics non severe acute tonsillar pharyngitis, quinsy or epiglottis
15
Q
Infectious mononucleosis/glandular fever/kissing disease?
A
- Epstein-Barr Virus (EBV)
- Teenagers. Often asymptomatic
- Characterised by a triad of symptoms: fever, tonsilar pharyngitis, and cervical lymphadenopathy.
- Complications eg. splenic rupture
- Avoid ampicillin (mac-pap rash, not allergy)
- Blood for Monospot +/- EBV serology
16
Q
What is Epiglottitis
A
Supraglottitis: inflammation of structures above the glottis
17
Q
What is the cause of Epiglottitis?
A
Almost always cause by bacterial infection
Haemophilius influenzae type b was the commonest cause in >90% of paediatric cases but the HIB vaccine has significantly reduced the rate of HIB epiglottis.
Still do see HIb cases in adults and rarely in children
18
Q
What are the other causes of epiglottitis?
A
Other causative organisms include: Streptococcus pneumoniae & Group A Streptococcus
19
Q
What are the investigations for Epiglottitis?
A
Blood cultures and epiglottic swabs
20
Q
Management of Epiglottitis?
A
Acute Epiglottitis and associated upper airway obstruction has significant morbidity and mortalitiy and may cause respiratory arrest and death within 24 hours.
Securing the airway and oxygenation is a priority.
IV antibiotics (usually 3rd generation cephalosporin)
Analgesia
Hib epiglottitis - Inform public health
21
Q
What is otitis externa?
A
The ear canal is the only skin-lined cul-de-ac in the body. OE = inflammation of the externa ear canal presenting with a combination of otalgia (ear pain), pruritis (itching) and non mucoid ear discharge.
Symptoms < 3/52 = acute OE
Symptoms > 3/52 = chronic OE
22
Q
Risk factors for OE
A
Swimming , trauma ( e.g ear scratching, cotton swabs)
Occlusive ear devices (e.g. hearing aids, ear phones), allergic contact dermatitis (e.g. due to shampoos, cosmetics). and dermatologic conditions (e.g. psoriasis).
23
Q
Presentation of an Acute OE
A
Range in severity mild/moderate/severe +necrotising (malignant) OE
Typically unilateral
2% AOE fungal
Diagnosis: history & otoscopic examination
Investigations: Ear swab or pus sample for culture. For necrotising otitis externa: CT temporal bone (and bone biopsy).
Blood cultures (if systemically unwell)
24
Q
What is Acute OE caused by bacterial or viral or fungal
A
90% AOE bacterial (most common: Pseudomonas aerugionosa & Staphylococcus aureus
2% AOE fungal
25
How is Acute OE diagnosed?
History and Otoscopic examination
26
How would you investigate an OE?
Ear swab or pus example for culture. For necrotising otitis externa: CT temporal bone (and bone biopsy). Blood cultures (if systemically unwell)
27
Non-antimicrobial management
Remove/modify precipitating factors
Remove pus and debris from ear canal
Analgesia
28
Antimicrobial management
Topical agents for mild-moderate
| Topical plus systemic antibiotic such as flucloxacillin for severe AOE
29
What is malignant (necrotising) external otitis?
-Malignant (necrotising) external otitis occurs when external otitis spreads to the skull base (soft tissue, cartilage, and bone of the temporal region and skull).
- Can be life threatening
- Most commonly develops in elderly diabetic or other immunocompromised patients
- Severe pain, otorrhoea, granulation tissue in the canal floor, and cranial nerve palsies may be present
- These patients should be promptly referred ENT
30
How is malignant necrotising external otitis treated?
Treat for a minimum of 6 weeks e.g. IV ceftazidime then po ciprofloxacin
31
What is Chronic OE?
- Pruritus, mild discomfort, erythematous external canal that is usually devoid of wax
- Often bilateral
- White keratin debris may fill the ear canal and over time the canal wall skin may become thickened narrowing the external ear canal
- A common cause of chronic OE is allergic contact dermatitis (e.g. from chemicals in cosmetics or shampoos).
- Generalised skin conditions such as atopic dermatitis or psoriasis can also predispose to chronic OE
- Treat underlying cause
32
Otitis media
Middle ear inflammation
Fluid present in middle ear
V. common in children
Uncomplicated acute OM is defined as: mild pain < 72 hours duration and an absence of severe systemic symptoms, with a temperature of less than 39 degrees and no ear discharge
33
Complicated acute OM is defined as the presence of
severe pain, perforated eardrum and/or purulent discharge, bilateral infection, mastoiditis.
34
What are the organisms that cause otitis media?
Viruses! Streptococcus pneumoniae, Haemophilus influenzae & Moroxella catarrhalis
35
What is the treatment for Otitis media?
If not unwell, watch and treat symptomatically (analgesia, decongestant etc.) and review early. if unwell - amoxicillin
36
What is a complication of Otitis media
Mastoiditis
37
What is mastoiditis?
Infection of the mastoid bone and air cells
| The most common complication of AOM - incidence significantly reduced with the use of antibiotics for OM
38
What are the clinical features of Otitis media?
Fever, posterior ear pain and/or local erythema over the mastoid bone, oedema of the pinna, or a posteriorly and downward displaced auricle
39
Investigation of Mastoiditis
CT scan always required
40
Treatment for Mastoiditis
Analgesia. IV antibiotics +/- mastoidectomy
41
What is pinna cellulitis
Associated with trauma (including ear piercing and acupuncture), surgery or burns
42
What is perichondritis?
May be a complication of high ear piercing (puncture through the cartilage of the upper third of the pinna)
43
How to manage pinna cellulitis?
A swab of the area and blood cultures (if in secondary care) should be obtained prior to starting antibiotics
44
Infective agents in auricular perichondritis
Pseudomonas aeruginosa and/or Staphylococcus aureus
45
Treatment for Pinna cellulitis
Ciprofloxacin + Flucloxacillin (or vancomycin if penicillin allergy)
46
What is pneumonia?
Infection affecting the most distal ariways and alveoli
- Formation of inflammatory exudate
47
What are the 2 anatomical patterns of pneumonia?
Bronchopneumonia - characteristic patchy distribution centred on inflamed bronchioles and bronchi then subsequent spread to surrounding alveoli
Lobar pneumonia - Affects a large part, or the entirety of a lobe
90% due to S.pneumoniae
48
What are the different types of Community acquired pneumonia? (CAP)
Hospital acquired pneumonia
Ventilator acquired pneumonia
Aspiration pneumonia
49
What is hospital acquired pneumonia?
- Pneumonia developing after 48 hours of hospital admission
| - Additional causative organisms to CAP, especially if after 5 days after admission: enterobacteriaceae
50
What is ventilator acquired pneumonia?
Subgroup of HAP
Pneumonia developing over 48 hours after ET intubation and ventilation
Pseudomonas spp. may be implicated
51
What is aspiration pneumonia?
- Pneumonia resulting from the abnormal entry of fluids
e. g. food, drinks, stomach contents, etc. into the lower respiratory tract
- Patient usually impairs swallow mechanism
- Anaerobes may be implicated
52
Epidemiology of CAP
Incidence of 1 per 100 people per year
20-40% cases require hospital admission
Peak age 50-70 years
Peak onset midwinter to early spring
53
What organisms cause person to person transmission of CAP
S.pneumoniae, H influenzae
54
What organisms cause transmission of CAP from the environment
L. pneumophilia
55
What organisms cause transmission of CAP from animals
C. psittaci
56
Bacterial causes for CAP can be divided into ?
Typical and atypical
57
What is atypical pneumonia?
Traditionally described cases and no organism could be identified which failed to repsond to penicillin (organisms with atypical or no cell wall)
58
What are atypical organisms?
NO/ATYPICAL CELL WALL
```
Mycoplasma pneumoniae
Legionella pneumophilia
Chlamydophila pneumoniae
Chlamydophila psittaci
Coxiella burnetti
```
59
What are the typical organisms
Have a cell wall
```
Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
Klebsiella pneumoniae
```
60
Symptoms of bacterial pneumonia
```
Usually rapid onset
Fever/chills
Productive cough
Mucopurulent sputum
Pleuritic chest pain
General malaise: fatigue, anorexia
```
61
Signs of bacterial pneumonia
- Tachypnoea, tachycardia, hypotension
- Examination findings consistent with consolidation"
- Dull to percuss
- Reduced air entry, bronchial breathing
62
Mycoplasma pneumoniae
Atypical
```
Autumn epidemics 4-8 years
Commonest in children & young adults
Main symptom is cough
Diagnosis: serology
Rare complications: pericarditis, arthritis
```
Guillain-Barre, peripheral neuropathy
63
Legionella pneumophilia
Atypical
Colonises water piping systems
Outbreaks associated with showers, air conditioning units, humidifiers
HIgh fevers, rigors, cough: dry initially becoming productive, dyspnoea, vomiting, diarrhoae, confusion
- Bloods: deranged LFT's, SIADH (low sodium)
64
Chlamydophila pneumoniae
3-10% of CAP cases in adults
Causes mild pneumonia or bronchitis in adolescents and young adults
Incidence highest in the elderly - may experience more severe disease
65
Chlamydophila psittaci
- Associated with exposure to birds
- Consider in those with pneumonia, splenomegaly &history of bird exposure
- May also have rash, hepatitis, haemolytic anaemia, reactive arthritis
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Assessment of disease severity: CAP
CURB-65 score
```
Confusion
Urea
Respiratory rate >= 30
Blood pressure: systolic < 90 mmHg or
diastolic < = 60 mmHg
```
Age >= 65 years
One point given for each feature present
0- severity - low Home treatment
1- severity - low Home treatment
2 - severity - moderate Hospital treatment
3-5 severity - high - Hospital: assess for ITU admission
67
Investigations for inpatients with CAP
Chest X-ray can take 6 weeks+ for radiological changes to resolve
Recommended for all moderate-severe CAP bases on
CURB65 score > 2 (BTS guideline 2009)
- Sputum culture
- Blood culture
- Pneumococcal urinary antigen
- Legionella urinary antigen
- PCR or serology for:
- Viral pathogens e.g. influenza (PCR of respiratory samples)
- Mycoplasma pneumoniae (PCR of respiratory samples preferable, complement fixation: interpret with caution)
- Chlamydophila sp. (complement fixation test most widely available - on blood)
68
Management: CP/HAP/VAP & Aspiration pneumonia
As with any unwell or septic patient
A = Airway
ensure an open, patent and maintained airway
B= Breathing
Assess respiratory rate and saturations
Provide supplemental oxygen to reach prescribed target
C= Circulation
Assess blood pressure and heart rate
Gain IV access and give IV fluids if haemodynamically unstable
Urinary catheter to monitor urine output
Then: Prompt empirical antibiotic therapy
69
Pneumonia complications
3-5% Pleural effusion: clear fluid +/- pus cells +/- organisms
1% Empyema: pus in the pleural space (loculated)
Lung abcess: suppuration + destruction of lung parenchyma
-single (aspiration) anaerobes, Pseudomonas
-Multiple (metastatic) Staphylococus aureus
70
Viral LRTI - Pneumonia in the normal host
- Adults
Influenza A and B
Adenovirus
Varicella zoster virus (VZV)
-Children
RSV (Respiratory syncytial virus)
Parainfluenza
71
Pneumonia in the immunocompromisd hosts
As for the above plus
- Measles
- Herpes simplex (HSV)
- Varicella zoster virus (VZV)
- HHV-6
72
Clinical presentation - influenza
Usually influenza produces uncomplicated disease:
- Fever, headache, myalgia, dry cough, sore throat
- Convalescence takes 2-3 weeks
73
Primary viral pneumonia
Primary viral pneumonia occurs more commonly in patients with pre-existing cardiac and lung disorders
- Cough, breathlessness, cyanosis
- Secondary bacterial pneumonia then may develop after initial period of improvement
- S. pneumoniae, H. influenzae, S.aureus
- Diagnosis: Viral antigen detection in respiratory samples using PCR
74
Diagnosis of Influenza
Viral antigen detection in respiratory samples using PCR
75
VZV pneumonia
a complication of VZV (chicken pox) infection
- Rare in children, significant morbidity & mortalitiy in adults with varicella
- Those at greatest risk are immunocompromised, adults with chronic lung disease, smokers and pregnant women.
- Insidious onset 1-6 days after the rash has appeared with symptoms of progressive tachypnoea and dry cough
Tests: Chest X-ray typically reveals diffuse bilateral infiltrates
Treatment: Supportive and prompt administration of IV acyclovir
76
Rhinovirus
- Agent responsible for most "common colds'
- Can cause LRTI & trigger exacerbations of asthma
- Tests: PCR on NPA/throat swab
- Treatment: supportive
77
CMV (Cytomegalovirus) pneumonia
- Is rarely described in immunocompetent hosts
- Can cause severe illness in transplant recipients & HIV patients (uncommon)
- Tests: Chest X-ray, broncho-alveolar lavage and viral load PCR
- Treatment : Supportive, anti-viral (e.g. ganciclovir) and consider immunosuppression reduction (transplant pts)
78
LRTI with Bronchiectasis
- Acquired disorder of the major bronchi and bronchioles that is characterised by permanent abnormal dilatation and destruction of the bronchial walls.
- Chronic cough, mucopurulent sputum production and recurrent infections (e.g. S.aureus, H influenzea, Pseudomonas aeruginosa, viruses).
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Exacerbating investigations for bronchiectasis
SpO2, CXR, FBC, U&Es, LFTs, CRP, review
| previous sputum culture
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Treatment for bronchiectasis
Antibiotics are recommended for exacerbations with acute deterioration with worsening symptoms
Non-Antimicrobial Management
- Effective clearance of respiratory secretions
e. g. physiotherapy, postural drainage
- Nutritional support
- Identification and treatment of underlying cause
- Annual influenza vaccination
81
LRTI with cystic fibrosis
An inherited disease caused by a genetic mutation on chromosome 7 resulting in abnormal production and function of the cystic fibrosis transmembrane conductance regulator (CFTR). The defective CFTR chloride channel function results in viscous secretions.
82
Colonising organisms & resistance change over time
- Staphylococcus aureus in childhood
- Pseudomonas aeruginosa in childhood/early adolescence (attempts will be made to eradicate)
- Burkholderia cepacia complex: very resistant & transmissible
- Non tuberculous mycobacteria & Fungi
83
Acute exacerbations:
Use most recent sputum culture results to guide treatment
- Prolonged antibiotics courses (3-4 weeks not uncommon)
- General measures: postural drainage, deep breathing coughing exercise, aerosolised DNAase etc + Influenza and Pneumococcal vaccinations. Lung transplant
84
Method of prevention of LRTIs
Pneumococcal vaccination (S. pneumoniae)
- Patients with chronic heart, lung and kidney disease
- Patients with splenectomy
- Infant vaccination schedule
- May repeat after 5 years in certain populations
Influenza vaccination for vulnerable groups
- 2-1 7 years old
- Over 65s
- Chronic disease, multiple co-morbidities
85
Aspergillosis
- Infection caused by aspergillus, common mold (fungus) that lives indoors and outdoors
- Most people breathe in Aspergillus spores every day without getting sick
- Immunocompromised patients & those with lung disease are at a high risk of developing health problems due to Aspergillus
- The types of health problems caused by Aspergillus include allergic reactions, lung infections, and infections in other organs
86
Allergic bronchopulmonary aspergillosis (ABPA)
- ABPA occurs in people with a background atopy, asthma & cystic fibrosis
- Presents with worsening asthma & lung function
- Diagnostic features include a high total IgE, specific IgE to Aspergillus and positive serum IgG to Aspergillus.
- CT Imaging of the thorax may demonstrate central bronchiectasis
- Treatment of ABPA is with corticosteroids and antifungal therapy
87
Aspergilloma (pulmonary)
```
Mobile mass (of Aspergillus) within a pre-existing lung cavity
Old cavities left by previous TB or sarcoidosis become colonised with Aspergillus spp.
```
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Symptoms of an aspergilloma
Cough, haemoptysis, weight loss, wheeze and clubbing. Some are asymptomatic.
89
Diagnosis for Aspergilloma
Can be demonstrated on either chest X-ray or CT Thorax.
The diagnosis can be confirmed by a positive test for Aspergillus IgG antibody
Sputum culture may be positive for Aspergillus spp.
90
Complication
Massive haemoptysis
91
Treatment for Aspergilloma
10% cases resolve spontaneously, surgical resection, antifungals (injected into the cavity, or orally for symptom relief)
92
PCP: Pneumocystis jiroveci pneumonia
- Is a fungus. But lacks ergosterol in it's cell wall
and is not susceptible to a number of antifungals.
- Ubiquitous is in the environment
- Principle mode of transmission is airborne route
-Pneumonia: insidious onset of fever, dyspnoea, non-productive
cough & reduced exercise tolerance. Exercise induced hypoxia is a
classic finding.
• Specimens: rarely isolated from expectorated sputum, can be found
in induced sputum, broncho-alveolar lavage increases the diagnostic
rate. PCR to detect P.jiroveci DNA has overtaken
immunofluorescence techniques.
• Supportive care, antimicrobials (including co-trimoxazole) and
steroids.
• Some at risk groups including HIV-infected patient with a CD4 count
<200 get primary prophylxis.
93
Nocardia asteroides
Nocardia is a genus of bacteria found in the
environment
• Pulmonary nocardiasis is acquired through inhalation
of the organism
• More common in the immunosuppressed & those
with pre-existing lung disease (esp. alveolar
proteinosis) – but still rare!
• Presentation & clinical/radiological findings are
variable, making diagnosis difficult.
• Lung abscesses can develop
• The most suitable specimens are the sputum, or if
necessary, broncho-alveolar lavage or biopsy.
• Treatment: as with all pneumonic infectionssupportive
Rx (ABC) & then antibiotics (several
months). Co-trimoxazole most commonly used.
94
Mycobacterium tuberculosis
Infects 1/3 of the world’s population & is the most frequent
infectious cause of death worldwide
• Most cases occur in the developing world (but are by no means
limited to there)
• Infection is acquired by inhalation of infected respiratory droplets,
the bacilli lodge in alveoli & multiply, resulting in the formation of a
Ghon focus.
• Depending on the host’s immune response the infection will either
become quiescent or progress and/or disseminate.
95
Symptoms of TB
90% of primary infections are asymptomatic
96
when is risk of disease progression the highest?
At extreme ages and in the immunocompromised (inc. HIV
97
is there risk of reactivation of TB
May occur later in life, particularly in the immunocompromised
98
Presentation of Pulmonary TB
Chronic productive cough, haemoptysis
• Weight loss, fever, night sweats
Can disseminate (miliary TB) or affect almost any other organ
99
Diagnosis of TB
Clinical features + supportive radiology + detection
of acid-fast bacilli or culture of M. tuberculosis from clinical specimens (usually sputum). PCR-based tests may be used to detect MTB in clinical specimens.
Interferon gamma release assays (IGRA) +/- Tuberculin skin
test – Mantoux can be used (do not differentiate active from
latent disease)
100
Treatment for TB
Treatment is with combined chemotherapy for several
| months (usually 6/12)
101
Prevention of the disease and spread of TB
Notifiable disease and contact tracing
Prevention: BCG given to infants and children in high prevalence areas (or parents & grandparents from high prevalence area)
