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Clinical Pathology > Lecture 28 - Clinical Infections Respiratory > Flashcards

Lecture 28 - Clinical Infections Respiratory Flashcards

1
Q

What does the upper respiratory tract consist of?

A 
Nose
Sinuses
Mouth
Pharynx
Larynx
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2
Q

What does the lower respiratory tract consist of?

A

Trachea
Bronchi
Bronchioles
Lungs

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3
Q

What is Pharyngitis

A

Inflammation of the back of the throat (pharynx), resulting sore throat and fever

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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

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5
Q

Infectious mononucleosis

A

Symmetrically inflamed tonsils/soft palate inflammation and posterior cervical lymphadenopathy

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6
Q

Epiglottitis

A

Sudden onset of severe sore throat, no inflammation of the tonsils and/or oropharynx and systemic symptoms/signs of infection

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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
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8
Q

What are the VIRAL causes of Pharyngitis and tonsillar pharyngitis?

A
  • Viruses: Rhinovirus, Coronovirus, Parainfluenza, Influenza (A&B), Adenovirus etc.
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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)

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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)
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11
Q

What is the centor criteria?

A

Gives an indication of the likelihood of a sore throat being due to bacterial infection.

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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%

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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

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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
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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
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16
Q

What is Epiglottitis

A

Supraglottitis: inflammation of structures above the glottis

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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

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18
Q

What are the other causes of epiglottitis?

A

Other causative organisms include: Streptococcus pneumoniae & Group A Streptococcus

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19
Q

What are the investigations for Epiglottitis?

A

Blood cultures and epiglottic swabs

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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

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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

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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).

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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)

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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

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25
Q

How is Acute OE diagnosed?

A

History and Otoscopic examination

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26
Q

How would you investigate an OE?

A

Ear swab or pus example for culture. For necrotising otitis externa: CT temporal bone (and bone biopsy). Blood cultures (if systemically unwell)

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27
Q

Non-antimicrobial management

A

Remove/modify precipitating factors
Remove pus and debris from ear canal
Analgesia

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28
Q

Antimicrobial management

A

Topical agents for mild-moderate

Topical plus systemic antibiotic such as flucloxacillin for severe AOE

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29
Q

What is malignant (necrotising) external otitis?

A

-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
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30
Q

How is malignant necrotising external otitis treated?

A

Treat for a minimum of 6 weeks e.g. IV ceftazidime then po ciprofloxacin

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31
Q

What is Chronic OE?

A
  • 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
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32
Q

Otitis media

A

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

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33
Q

Complicated acute OM is defined as the presence of

A

severe pain, perforated eardrum and/or purulent discharge, bilateral infection, mastoiditis.

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34
Q

What are the organisms that cause otitis media?

A

Viruses! Streptococcus pneumoniae, Haemophilus influenzae & Moroxella catarrhalis

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35
Q

What is the treatment for Otitis media?

A

If not unwell, watch and treat symptomatically (analgesia, decongestant etc.) and review early. if unwell - amoxicillin

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36
Q

What is a complication of Otitis media

A

Mastoiditis

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37
Q

What is mastoiditis?

A

Infection of the mastoid bone and air cells

The most common complication of AOM - incidence significantly reduced with the use of antibiotics for OM

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38
Q

What are the clinical features of Otitis media?

A

Fever, posterior ear pain and/or local erythema over the mastoid bone, oedema of the pinna, or a posteriorly and downward displaced auricle

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39
Q

Investigation of Mastoiditis

A

CT scan always required

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40
Q

Treatment for Mastoiditis

A

Analgesia. IV antibiotics +/- mastoidectomy

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41
Q

What is pinna cellulitis

A

Associated with trauma (including ear piercing and acupuncture), surgery or burns

42
Q

What is perichondritis?

A

May be a complication of high ear piercing (puncture through the cartilage of the upper third of the pinna)

43
Q

How to manage pinna cellulitis?

A

A swab of the area and blood cultures (if in secondary care) should be obtained prior to starting antibiotics

44
Q

Infective agents in auricular perichondritis

A

Pseudomonas aeruginosa and/or Staphylococcus aureus

45
Q

Treatment for Pinna cellulitis

A

Ciprofloxacin + Flucloxacillin (or vancomycin if penicillin allergy)

46
Q

What is pneumonia?

A

Infection affecting the most distal ariways and alveoli

  • Formation of inflammatory exudate
47
Q

What are the 2 anatomical patterns of pneumonia?

A

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
Q

What are the different types of Community acquired pneumonia? (CAP)

A

Hospital acquired pneumonia
Ventilator acquired pneumonia
Aspiration pneumonia

49
Q

What is hospital acquired pneumonia?

A
  • Pneumonia developing after 48 hours of hospital admission

- Additional causative organisms to CAP, especially if after 5 days after admission: enterobacteriaceae

50
Q

What is ventilator acquired pneumonia?

A

Subgroup of HAP
Pneumonia developing over 48 hours after ET intubation and ventilation
Pseudomonas spp. may be implicated

51
Q

What is aspiration pneumonia?

A
  • 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
Q

Epidemiology of CAP

A

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
Q

What organisms cause person to person transmission of CAP

A

S.pneumoniae, H influenzae

54
Q

What organisms cause transmission of CAP from the environment

A

L. pneumophilia

55
Q

What organisms cause transmission of CAP from animals

A

C. psittaci

56
Q

Bacterial causes for CAP can be divided into ?

A

Typical and atypical

57
Q

What is atypical pneumonia?

A

Traditionally described cases and no organism could be identified which failed to repsond to penicillin (organisms with atypical or no cell wall)

58
Q

What are atypical organisms?

A

NO/ATYPICAL CELL WALL

Mycoplasma pneumoniae
Legionella pneumophilia
Chlamydophila pneumoniae
Chlamydophila psittaci
Coxiella burnetti
59
Q

What are the typical organisms

A

Have a cell wall

Streptococcus pneumoniae
Haemophilus influenzae
Moraxella catarrhalis
Staphylococcus aureus
Klebsiella pneumoniae
60
Q

Symptoms of bacterial pneumonia

A 
Usually rapid onset
Fever/chills
Productive cough
Mucopurulent sputum
Pleuritic chest pain
General malaise: fatigue, anorexia
61
Q

Signs of bacterial pneumonia

A
  • Tachypnoea, tachycardia, hypotension
  • Examination findings consistent with consolidation”
    • Dull to percuss
    • Reduced air entry, bronchial breathing
62
Q

Mycoplasma pneumoniae

A

Atypical

Autumn epidemics 4-8 years
Commonest in children &amp; young adults
Main symptom is cough
Diagnosis: serology 
Rare complications: pericarditis, arthritis

Guillain-Barre, peripheral neuropathy

63
Q

Legionella pneumophilia

A

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
Q

Chlamydophila pneumoniae

A

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
Q

Chlamydophila psittaci

A
  • Associated with exposure to birds
  • Consider in those with pneumonia, splenomegaly &history of bird exposure
  • May also have rash, hepatitis, haemolytic anaemia, reactive arthritis
66
Q

Assessment of disease severity: CAP

A

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
Q

Investigations for inpatients with CAP

A

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
Q

Management: CP/HAP/VAP & Aspiration pneumonia

A

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
Q

Pneumonia complications

A

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
Q

Viral LRTI - Pneumonia in the normal host

A
  • Adults
    Influenza A and B
    Adenovirus
    Varicella zoster virus (VZV)

-Children
RSV (Respiratory syncytial virus)
Parainfluenza

71
Q

Pneumonia in the immunocompromisd hosts

A

As for the above plus

  • Measles
  • Herpes simplex (HSV)
  • Varicella zoster virus (VZV)
  • HHV-6
72
Q

Clinical presentation - influenza

A

Usually influenza produces uncomplicated disease:

  • Fever, headache, myalgia, dry cough, sore throat
  • Convalescence takes 2-3 weeks
73
Q

Primary viral pneumonia

A

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
Q

Diagnosis of Influenza

A

Viral antigen detection in respiratory samples using PCR

75
Q

VZV pneumonia

A

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
Q

Rhinovirus

A
  • Agent responsible for most “common colds’
  • Can cause LRTI & trigger exacerbations of asthma
  • Tests: PCR on NPA/throat swab
  • Treatment: supportive
77
Q

CMV (Cytomegalovirus) pneumonia

A
  • 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
Q

LRTI with Bronchiectasis

A
  • 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).
79
Q

Exacerbating investigations for bronchiectasis

A

SpO2, CXR, FBC, U&Es, LFTs, CRP, review

previous sputum culture

80
Q

Treatment for bronchiectasis

A

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
Q

LRTI with cystic fibrosis

A

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
Q

Colonising organisms & resistance change over time

A
  • 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
Q

Acute exacerbations:

A

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
Q

Method of prevention of LRTIs

A

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
Q

Aspergillosis

A
  • 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
Q

Allergic bronchopulmonary aspergillosis (ABPA)

A
  • 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
Q

Aspergilloma (pulmonary)

A 
Mobile mass (of Aspergillus) within a pre-existing lung cavity
Old cavities left by previous TB or sarcoidosis become colonised with Aspergillus spp.
88
Q

Symptoms of an aspergilloma

A

Cough, haemoptysis, weight loss, wheeze and clubbing. Some are asymptomatic.

89
Q

Diagnosis for Aspergilloma

A

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
Q

Complication

A

Massive haemoptysis

91
Q

Treatment for Aspergilloma

A

10% cases resolve spontaneously, surgical resection, antifungals (injected into the cavity, or orally for symptom relief)

92
Q

PCP: Pneumocystis jiroveci pneumonia

A
  • 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
Q

Nocardia asteroides

A

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
Q

Mycobacterium tuberculosis

A

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
Q

Symptoms of TB

A

90% of primary infections are asymptomatic

96
Q

when is risk of disease progression the highest?

A

At extreme ages and in the immunocompromised (inc. HIV

97
Q

is there risk of reactivation of TB

A

May occur later in life, particularly in the immunocompromised

98
Q

Presentation of Pulmonary TB

A

Chronic productive cough, haemoptysis
• Weight loss, fever, night sweats

Can disseminate (miliary TB) or affect almost any other organ

99
Q

Diagnosis of TB

A

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
Q

Treatment for TB

A

Treatment is with combined chemotherapy for several

months (usually 6/12)

101
Q

Prevention of the disease and spread of TB

A

Notifiable disease and contact tracing

Prevention: BCG given to infants and children in high prevalence areas (or parents & grandparents from high prevalence area)

Clinical Pathology (16 decks)

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