respiratory tract infections Flashcards

1
Q

what are the the common normal microbiota of the RT?

A

(common >50% of people)
- bacteroides spp.
- Candida albicans
- oral streptococi
- haemophilus influenza

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2
Q

what are the normal microbiota of the RT found in the latent state in in tissues?

A
  • herpes simplex virus type I
  • epstein Barr Virus
  • cytomegalovirus
  • mycobacterium
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3
Q

what are the normal microbiota of the RT that are only occasionally found?

A

(occasional <10% in normal people)
- streptococcus pypgenes
- streptococcus pneumoniae
- neisseria meningiditis

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4
Q

what are the main respiratory tract host defences?

A
  • saliva
  • mucus
  • cilia
  • nasal secretions
  • antimicrobial peptides
  • alveolar macrophages
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5
Q

what are examples of the normal microbiota found in the nasal passages and sinuses?

A
  • fermicutes
  • actin bacteria
  • staphylococcus epidermis
  • haemophilus spp
  • staphylococcus aureus
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6
Q

what are the normal microbiota found in the oral pharynx?

A
  • prevotella
  • fusobacterium
  • candida spp
  • haemophilus
  • neisseria
  • streptococcus
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7
Q

what are the normal microbiota found in the Lower respiratory tract?

A
  • pseudomonas
  • streptococcus
  • prevotella
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8
Q

common cold:
actual name?
tranmission?
causative agents?
seasonal?

A

name = acute coryza

transmission = aerosol, virus- contaminated hands

causative agents = 40% rhinovirus (>100 serotypes)
30% coronaviruses (>3 serotypes)
coxsackie virus A
Echovirus
Parainfluenza

seasonal = early autumn and mid/late spring

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9
Q

why are colds less common in summer?

A

because uV light tends to kill the pathogens.

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10
Q

clinical features of common cold?

A
  • tiredness
  • slight pyrexia
  • malaise
  • sore nose & pharynx
  • profuse, watery nasal discharge
  • sneezing in early stages
  • secondary bacterial infection occurs in minority
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11
Q

describe the pathogenesis of the common cold?

A
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12
Q

what are the viral and bacterial causative agents for acute pharyngitis and tonsillitis?

A

virus:
- Epstein-Barr virus
- cytomegalovirus
- HSV1
- rhinovirus
- coronavirus
- adenovirus

bacteria:
- streptococcus pyogenes
- haemophilus influenza

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13
Q

describe the cytomegalovirus (CMV)

A
  • transmission in body secretions and organ transplants
  • usually asymptomatic
  • virus can reactivate and cause disease when cell-mediated immunity is compromised
  • diagnose secondary infection using IgM in the blood
  • diagnose CMV pneumonitis using CMV Ag in BAL
  • treatment with ganciclovir, foscarnet, cidofovir
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14
Q

describe Epstein- Barr virus?

A
  • replicated specifically in B lymphocytes (CD21)
  • causes glandular fever
  • transmitted by saliva and aerosol
  • usually occurs in 2 peaks:
    1-6 years old
    14-20 years old

incubation period: 4-8 weeks
illness= 4-14 days

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15
Q

clinical features of glandular fever?

A
  • fever
  • headache
  • malaise
  • sore throat
  • anorexia
  • palatal petechiae
  • cervical lyphadenopathy
  • mild hepatitis
  • swollen tonsils
  • white exudate
  • petechiae on the soft palate
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16
Q

tonsilitis:
causes
transmission?
treatment?

A

caused by= streptococcus pyrogenes
tranmission= by airborne droplets and contact

  • confection occurs mainly in children
  • 15-20% become asymptomatic carriers
  • treat with penicillin
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17
Q

what does strep. progenies havee an increasing resistance to in tonsillitis?

A

erythromycin and tetracycline

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18
Q

clinical features of tonsillitis?

A
  • fever
  • pain in throat
  • enlargement of tonsils
  • tonsils lymphadenopathy
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19
Q

streptococcus pyogenes

A
  • group A streptococcus
  • gram positive cocci in chains
  • cultured in blood agar
  • haemolytic activity ue to exotoxin streptomycin
  • susceptible to treatment with penicillin
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20
Q

complications of streptococcus pyogenes ?

A
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20
Q

parotitis?

A
  • caused by mumps virus
  • paramyxovirus family
  • transmission by droplet spread and fomites
  • communicable in 2 days before disease onset
  • diagnosis is based on clinical features - IgM serology can be performed in doubtful cases from saliva, CSF or urine.
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20
Q

who does parotitis normally effect?
clinical features?

A
  • primarily effects school aged children and young adults
  • clinical features:
  • fever
  • malaise
  • headache
  • anorexia
  • trismus
  • severe pain and swelling of parotid glands
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21
Q

parotits:
treatment?
prevention?
complications?

A

treatment:
- mouth care
- nutritional
- analgesia

prevention:
- active immunisation
- measles mumps rubella vaccine (MMR)

complications:
- CNS involvement
- epididymo orchitis

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22
Q

acute epiglottis?

A
  • caused by haemophilus influenza
  • most often seen in young children
  • 88% reduction in England and Wales since advent of Hib vaccine in 1992
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23
Q

clinical features of acute epiglottis?

A
  • high fever
  • massive oedema of the epiglottis
  • severe airflow obstruction resulting on breathing difficulties
  • bacteraemia
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24
Q

haemophilus influenza

A
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25
Q

how to diagnose acute epiglottisis

A
  • do not examine throat or take throat swabs as this will precipitate obstruction of airway
  • blood cultures to isolate H influenza
26
Q

treatment of acute epiglottis?

A
  • life threatening emergency
  • requires urgent endotracheal intubation
  • intravenous antibiotics (ceftriiaxone or chloramphenicol)
27
Q

diphtheria?

A
  • rare in developed countries as a result of vaccination
  • usually a childhood disease
  • may affect adults in countries where childhood vaccination uptake is poor
  • present in 3-5% of healthy throats
  • incubation 2-7 days
28
Q

clinical diphtheria?

A
  • sore throat
  • fever
  • formation of pseudomembrane
  • lymphadenopathy
  • oedema of anterior cervical tissue (bull neck)
29
Q

diphtheria?
diagnosis:
treatment:
prevention:

A

diagnosis= made on clinical ground as therapy is usually urgently required

treatment=
- prompt anti-toxin therapy administered intramusculary
- concurrent antibiotics
- strict isolation

prevention:
- childhood immunisation with toxoid vaccine
- booster dose given if travelling to endemic area if > 10 years have elapsed since primary vaccine

30
Q

corynebacterium diptheriae?

A

-

31
Q

what are the 2 subunit toxins of corynebacterium diphtheria?

A

Subunit A = ACTIVE, responsible for clinical toxicity

Subunit B = (Binding), transports toxin to receptors on myocardial and peripheral nerve cells

32
Q

laryngitis and tracheitis:
- where may these infections spread down from?
-what are its usual origins?
- what will it cause in adults?
- what will it cause in children?

A
33
Q

what bacteria will cause whooping cough?

A

bordetella pertussis

34
Q

what is the spread of whooping cough like?

A
  • 90% cases in children <5 years old
  • > 50 million cases worldwide annually
  • 600,000 deaths world wide annually
  • uncommon in developing countries
35
Q

how is whooping cough spread and what is the incubation period?

A

transmission is by airborne droplets
incubation period is 1-3 weeks

36
Q

clinical features of whooping cough?
2 stages?

A
  • catarrhal stage (1 weeks)
  • paroxysmal stage (1-4weeks)

catarrhal stage:
- highly contagious
- malaise
- mucoid rhinorrhoea
- conjunctivitis

37
Q

PARYOXYSMAL STAGE OF WHOOPING COUGH?

A

1-4 weeks
- paroxysms of coughing with a classic inspiratory “whoop”
- lumen of respiratory tract is compromised by mucus secretion and mucosal edema.

38
Q

Diagnosis of whooping cough?

A
  • clinically by characteristics”whoop”
  • bacterial isolation from nasopharyngeal swabs
  • nucleic acid amplification tests (NAATs)
39
Q

treatment and prevention of whooping cough?

A

treatment:
- in catarrhal stage can be treated with erythromycin
- in paroxysmal stage, antibiotics have no effect
- isolation
- supportive care.

prevention:
- vaccination (whole cell vaccine)

40
Q

bordetella pertussis

A
  • gram negative aerobic coccobacillus
  • human pathogen
  • attaches to and replicated in the ciliated respiratory epithelium
  • does not invade deeper structures
  • specific attachment is due to surface components
41
Q

what are toxic factors if the bordetella pertussis?

A
  • pertussis toxin
  • adenylate cyclase toxin
  • tracheal cytotoxin
  • endotoxin
42
Q

describe the incidence of whooping cough?

A
  • whole heat killed vaccine introduced in 1958
  • epidemics at approx 4 year intervals
  • concern over vaccine side effects led to reduced vaccine uptake and large epidemic in 1978-9.
43
Q

acute bronchitis?
due to what infections?
due to what secondary infections?

A
  • inflammation of the trachaebronchial tree
  • usually due to infection:
    rhinovirus
    coronavirus
    adenovirus
    mycoplasma pneumoniae

secondary infection:
- streptococcus pneumoniae
- haemophilus influenza

44
Q

what is chronic bronchitis characterised by?

A
  • characterised by a cough and excessive mucus secretion in tracheobronchial tree
  • not attributed to a specific disease such as TB, bronchiectasis, asthma.
  • anatomical disturbances of the respiratory system:
  • immune deficit- SCID
  • ciliary deficit: kartegener syndrome, smoking
  • excessively thick mucus: cf
45
Q

bronchiolitis

A
  • restricted to children to <2 years
  • bronchioles have such a fine bore
  • infection may lead to epithelial cell necrosis
  • mainly caused by RSV (75%)
46
Q

what bacteria will cause pneumonia?

A

streptococcus pneumoniae

47
Q

pneumonia?

A

inflammation of the substance of the lungs

48
Q

describe the characteristics on pneumonia ?

A
  • confirmed on chest radiograph
  • most common cause of infection related death in the Uk and USA
  • caused by a wide range of micro organisms
  • indistinguishable symptoms.
  • laboratory identification of microbial cause is challenging
  • access to LRT by inhalation of aerosolised microbes or by aspiration of normal flora of the URT
49
Q

describe the difference in pneumonia is children and adults?

A

children:
- mainly viral
- notates may develop pneumonia cause by chlamydia trachomatis acquired Fromm mother during brith

adults:
- mainly bacterial
- aetiology varies with age, underlying disease, occupational and geographic risk.

50
Q

aetiology classification:
viral pneumonia, common causes?

A
51
Q

aetiology classification:
bacterial pneumonia- common causes?

A
52
Q

what are bacteria associated with atypical pneumonia- variants that fail to respond to treatment with penicillin?

A
53
Q

anatomical classification of pneumonia?

A
  • lobar pneumonia:
    involvement of distinct region of the lung

bronchopneumonia:
- diffuse, patchy consolidation
- associated with bronchi and bronchioles

interstitial pneumonia:
- invasion of lung interstium
- usually characteristic of viral infection

necrotising pneumonia:
- lung abscesses and destruction of parenchyma

54
Q

streptococcus pneumonia clinical features:
initially?
followed by?

A

initially=
- abrupt onset
- rigors
- fever
- malaise
- tachycardia
- dry cough

followed by=
- productive cough with rust sputum
- spiky temp
- lobular consolidation

55
Q

clinical features of mycoplasma pneumonia?

A
  • fever
  • dry cough
  • dyspnoea
  • lymphadenopathy
56
Q

haemophilus influenza clinical features

A
  • mainly occurs in children
  • consolidation or patchy bronchopneumonia
  • persistent purulent sputum and malaise
57
Q

legionella pneumophila:
cause
clinical features

A
58
Q

laboratory diagnosis of legionnaires disease?

A
59
Q

measles
- clinical features

A
  • one of the leading causes of death globally

clinical features:
- fever
- runny nose
- koplik’s spots
- characteristic rash

  • may result in neurological complications
  • can cause giant cell (Hecht’s) pneumonia in the immunocompromised - usually fatal
60
Q

measles virus

A
  • paramyxovirus
  • spread via aerosol
  • multisyetm infection
  • replicates in LRT
  • incubation 10-14 days
61
Q

measles:
diagnosis
treatment
prevention

A

diagnosis =
serology for measles specific IgM
- virus isolation
- viral RNA detection

treatment:
- if severe, ribavirin treatment
- antibiotics for secondary bacterial infections

prevention:
- immunisation with highly effective, live, attenuated MMR vaccine

62
Q

3 types of influenza

A
63
Q

endemic
epidemic
pandemic

A
64
Q

what are the genetic changes that influenza will undergo during the

A