Download Respiratory Tract Infections

Respiratory Tract Infections
Dr Lynne Lawrance
2A21
[email protected]
Session Aims
 To give you an overview of a range of respiratory diseases
that are predominantly infectious in nature
 To also link in to other module sessions to look at how
microbes play a role in the pathology of diseases that have a
more multi-factorial pathogenesis
The Respiratory Tract – a
microbiologists perspective!
 Same way in as out
 Has a normal flora in the upper
region
 Many different environmental
niches that different microbes
could find suits their growth
preferences
 Normal flora of one region of the
tract can be a cause of disease if it
gets somewhere else
Public Domain Image from Wikipedia
Some of the conditions with definite or
possible microbial involvements
Rhinitis
Oral and oesophageal thrush
Sinusitis
Common cold
Pharyngitis
Diphtheria
Whooping Cough
Influenza
Tonsillitis
Epiglottitis
Bronchitis
Exacerbation of Cystic Fibrosis or other
structural or mechanical disorders
SARS
Pneumonia
Tuberculosis
Bronchiolitis
Plus the system is also linked to the
ears and eyes and skin with no barriers
 It is suggested that the respiratory tract is the most common
site of microbial infection
 However as there is a huge range of severities of these
infections this almost goes unnoticed – after all just think
how many coughs or mild flu like illnesses you have had!
 Upper respiratory tract infections (which includes most flu,
coughs and colds) are the main reasons for GP visits in the
US and probably in the UK as well
 But why?....
• Several reasons
Air
 It has been estimated that indoors the air contains between 400
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and 900 microbes per cubic metre, outside is less concentrated
This is predominantly made up of non-pathogenic microbes
However with an average ventilation rate of 6L per minute at rest
this means that average person would inhale around 8 microbes
per minute or >10,000 per day
Fortunately the respiratory system is equipped with mechanisms
for removing inhaled particles including microbes
So normally the lungs are “almost sterile” due to the protective
mechanisms
Sneezing and Coughing
 When sneezing you eject around 20 000 water droplets derived
from both the mouth and the nose
 During coughing microbes from the mouth predominate what is
shed, but those from the lungs and the digestive tract can also be
detected
 Larger droplet fall to the ground quite quickly, but smaller
particles can become suspended in the air, almost like birds on
thermal currents. These smaller particles are those we are most
likely to inhale
 Being close to someone coughing and sneezing is recognised as a
risk factor for acquiring the infection from them
Survival of Microbes in the Air
 Some microbes can survive in the air for sometime
 e.g. TB, smallpox virus, foot and mouth virus (foot and mouth can
cross the English Channel!!)
 Other dry out quickly and are inactivated
 e.g. measles, flu, meningococci (require close contact)
 Others fall in between
 e.g. Legionella (about 2km)
 Of course we also deposit these microbes on to tissue, hankies
and hands which adds to transmission
The Normal Flora
 The upper respiratory tract has a complex normal flora that
resides on the many varied surfaces
 Amongst this normal flora a number of potential lower
respiratory tract pathogens reside – especially it seems in the
nasopharyngeal/oropharyngeal area
 Streptococcus pneumonaie, Haemophilus influenzae, Moraxella catarrhalis,
Staphylococcus aureus
 However the normal flora also protect against other potential
upper respiratory tract pathogens
Selected Upper Tract Infections
Whooping Cough - Pertussis
 Caused by Bordetella pertussis infecting the nasopharyngeal area
 Symptoms may start as similar to the common cold
 Starts as an irritating cough which gradually develops into outbursts of
coughing (paroxysms) Spasms frequently followed by vomiting
 Patients often feel like they are choking
 Low grade fever and general fatigue
 Timeline of Illness
 Incubation of 7-10 days
 Spasms can start to occur rapidly, or can take up to 3 weeks to appear
 Cough can then last for several weeks
 In older patients (>15 years) the symptoms are more mild, possibly
due to residual immunity
Complications
 Secondary respiratory infections
 Lung collapse
 Convulsions – half of those who develop convulsions die
 For those who survive convulsions, paralysis, mental retardation
and epilepsy are common
 Hernias, urinary tract problems, fractured ribs can be caused by
the severity of the coughing
 The parents of a sick child will find they suffer severe sleep
deprivation
Transmission
 Inhalation of droplets from infected patients
 The bacteria do not survive long in the environment
 They are rarely isolated from the nasopharynx of healthy
subjects
 They may be intracellular in carriers but this has not yet been
proven
 No animal reservoirs have been identified
 Highly contagious in non-immune populations with an attack
rate of ~90% in close contact groups such as a family
Treatment and Prevention
 Vaccine preventable – part of UK routine vaccine schedule
 Antibiotic therapy may reduce the duration of the disease, but
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recovery is still quite slow
Erythromycin is the drug of choice, with chloramphenicol
sometimes used
Unvaccinated close contacts of patients will be offered erythromycin
prophylaxis
Some resistance to erythromycin has been seen
In moderate to severe cases hospitalisation may be required to
protect the airway and monitor seizures
Vaccination and Infection in the UK
70000
100
90
60000
Data from HPA – no
longer accessible
80
Notification
Vaccine Coverage
70
60
cases
40000
50
30000
40
vaccine coverage (%)
50000
30
20000
20
10000
10
0
0
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2007
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2004
2003
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2001
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1970
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Prior to vaccination ~10,000 children died of pertussis in the UK each year
Vaccination introduced in the late 1950s
Vaccine uptake levels in the early 1970s reached about 80%
Press coverage of side effects caused a dip in uptake to as low as 30%
The resultant epidemic in 1982 meant >100,000 children developed whooping cough and 36 children died, and permanent
brain damage occurred in a significant number of survivors
Current vaccine coverage is around 94% and disease incidence is low
However, in 2011 numbers started rising again – then in late 2012 maternal vaccination was introduced to protect newborn
children – reasons for this are not yet clear – but the data may also be “skewed”
https://www.gov.uk/government/collections/pertussis-guidance-data-and-analysis
https://www.gov.uk/government/publications/whooping-cough-pertussis-statistics
Respiratory Diphtheria
 Signs and Symptoms
 Sore throat
 Low grade fever
 Membrane formed across tonsils
 Swollen neck glands
 Incubation period of 5-9 days
 Symptoms are toxin mediated, and the toxin can go systemic
causing complication in the circulatory system and the CNS
 Non toxigenic strains can cause a localised pharyngitis
Epidemiology - basics
 Pre the introduction of mass immunisation 5-10% of cases of
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respiratory diphtheria died
In the US there was 100-200 cases per 100,000 population in the 1920s
(thus around 5 per 100,000 population died of diphtheria per year – at
the time the population of the US was ~100,000,000 therefore ~ 5000
people per year died in the US of the disease
In the post-vaccination era infections and subsequent deaths are rare
Currently the infection level is just 0.001 per 100,000 and deaths are
now very rare
This picture is mirrored in the UK
The disease is endemic in many countries where vaccination is not in
place, and outbreaks have been reported in several of the former Soviet
states- in these outbreaks, adults have been the predominantly affected
group
Image from the CDC PHIL
Influenza (the proper “flu”)
 Enveloped, Single-stranded RNA virus
 First identified in 1933, but existed long before
 Three types A, B, & C
 B & C appear restricted to man – but C is less common
 A found in wide range of species including pigs and poultry as
well as man
 Type A appears to be responsible for more severe disease
 Generally considered an infection of the bronchi
 That is to say influenza is effectively a form of bronchitis – i.e. it
causes inflammation of the bronchi in the same way chemicals and
other noxious agents can
Influenza basics
 Transmission by aerosols
 Incubation ~2 days
 Contagious during first 3-5days of illness
 Symptoms – fever, myalgia, headache, dry cough, sore throat,
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hoarseness
Recovery ~7-10 days for most
Complications – most frequent secondary bacterial pneumonia,
rarely viral pneumonia, myocarditis, encephalitis
No specific treatment
Vaccination for high risk groups including the elderly, health
care workers, those with underlying respiratory conditions…
 With the recent interest in influenza the PHE have been trying to
raise awareness that there are different “types” of “flu”
 Avian
 The main reservoir is wildfowl that are resistant to the disease
 Avian flu viruses do not usually affect animals other than poultry and
pigs
 However some transfer events occur
 Seasonal
 Incidence highest in winter, peaking December to March
 Strains vary from year to year
 Pandemic
 Can be caused by any strain that has not been seen in the human
population for some time
 We are effectively due a large pandemic
Pandemic Influenza
 New strains evade the herd immunity that exists to previously
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encountered strains
1918 /19 –( Spanish) estimated 40-50 million deaths worldwide
1957 – Influenza A/H1N1 (Asian)
1968 – Influenza A/H3N2 (Hong Kong)
Pandemics occur at long, unpredictable intervals (decades), when a
strain emerges to which the population have little or no immunity
Is not seasonal in nature – pandemics will run “all year round” – for
example the 1918/19 pandemic took just 2 or 3 months to
circumnavigate the world but then stayed around for two years
Eventually the virus runs out of susceptible hosts and the epidemic
fizzles out
Predicting Pandemics
 Experts generally agree a pandemic is inevitable, and may be imminent –
maybe we have had some minor pandemics
 16000 confirmed H1N1 deaths in 2009 affecting over 200 countries
 Consensus is that the prompt action of the Hong Kong authorities probably
prevented a pandemic in 1997
 The prediction is scary!
 For industrialised countries they predict
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57-132 million GP visits
1.0 – 2.3 million hospitalisations
280,000-650,000 deaths
All in a two year time frame
 A network of 112 centres monitor flu isolates to identify unusual strains that
can then be examined further
 The WHO has a Pandemic Preparedness Plan in place
 http://www.who.int/influenza/preparedness/pandemic/en/
Diagnosis
 Generally based on GP diagnosis
 Virus isolation / virus demonstration from nasopharyngeal
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secretions during acute phase
Demonstration of viral antigen in secretions
Antibody rise using paired sera ( 1st sample taken between days 13 of illness, 2nd taken around day 12 of illness) by
haemagglutination inhibition or complement fixation test
Molecular methods evolving rapidly – in particular in response to
the recent epidemic/pandemic strains emerging
A range of respiratory illnesses have the same symptoms, only
laboratory testing can confirm the aetiological agent
Treatment & Therapy
 In the UK NICE argue that immunisation against predicted strains is the best form of defence –
traditionally focused on the elderly and those with underlying lung problems, but recently
started rolling out a childhood vaccine (nasal spray)
 http://www.nhs.uk/conditions/vaccinations/pages/child-flu-vaccine.aspx
 Vaccines generally based on the H & N surface structures which mutate, however hopes of an
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M protein based vaccine which will give longer lasting protection raised recently
In general they advise against the use of antivirals in otherwise healthy people (also that
amantadine should not be used at all).
However when the incidence of flu-like illness reaches a certain level then zanamivir and
oseltamivir should be used in those considered high risk for the development of complications
– PROVIDED THAT TREATMENT IS STARTED WITHIN 48 HOURS OF ONSET OF
SYMPTOMS
Zanamivir should not be used in children
Under certain circumstances NICE approve the use of antivirals as prophylaxis post exposure
in high risk people
Resistance is becoming an issue
 Reference: NICE (2009) - https://www.nice.org.uk/guidance/ta168
Pneumonias and other selected
Lower Tract Infections
Pneumonia – a leading cause of death
 “Pneumonia is called the old man's friend because, left
untreated, the sufferer often lapses into a state of reduced
consciousness, slipping peacefully away in their sleep, giving
a dignified end to a period of often considerable suffering.”
 Dr John Pillinger
http://www.netdoctor.co.uk/ate/cancer/202478.html
Intro to pneumonia
 Pneumonia is a major cause of morbidity and mortality worldwide
 It is 6th in the list of causes of death in the USA
 It is also economically costly in terms of antibiotics, time off work,
hospitalisation
 In half the cases the cause is not identified
 In those where a cause is identified, S. pneumoniae is the most
common cause
 The reservoir is usually humans (oneself or a contact) and spread is
through respiratory droplets
Pneumonia intro continued
 Community acquired
 Main causes: Streptococcus pneumoniae, Haemophilus influenzae,
Moraxella catarrhalis, Mycoplasma pneumoniae, Chlamydia pneumoniae
 Noscomial
 Main causes: Enterobacteriaceae, Staphylococcus aureus, Anaerobes,
Pseudomonas aeruginosa
 Many patients have an underlying condition, e.g. bronchitis,
asthma, a viral infection, tumours
 Characterised by the alveolar sacs filling up with pus, giving rise
to a purulent sputum
 Results in chest tightness or pain, difficulty in breathing, fever,
reduced blood oxygen, coughing to clear mucus, chest will
sound “dull” when tapped
Pneumonia Pathogenesis
 Causative agents can enter the lungs through 5 possible routes
 Inhalation (most common?), aspiration, spread across mucous
membrane (some viruses), haematogenous spread (occasionally, e.g. IV
drug users with S. aureus septicaemia) and penetrating injury (rare)
 Immune response is triggered in the lung and there are local defence
factors in the respiratory secretions
 Cilia if functioning will move material up the respiratory tract, but if
damaged this physical defence is impaired
 The lungs also have a resident macrophage population (alveolar
macrophages) but they are of limited use against several respiratory
pathogens that possess a capsule
 some organisms can even replicate in these cells
Pathogenesis cont.
 Damage to the lung is caused by the microbes and the immune
response
 Enzymes released by the bacteria
 Factors released by immune cells that cause local irritation and cell
apoptosis
 Systemic manifestations follow
 Oxygen deprivation – thickening of the membranes reduces
transfer
 Systemic shock – especially with Gram-negative bacilli such as
Haemophilus influenzae
Pneumonia classification and risks
 Pneumonia is subdivided in a number of ways that are relevant to
patient management even before a pathogen is identified
 Acute v Chronic
 Community Acquired v Nosocomial
 Typical v Atypical
 Patient risk factors can also help suggest possible causative agents
whilst waiting for laboratory confirmation
 Animal or environmental exposure (Chlamydia psittiaci, Yersinia pestis,
Bacillus anthracis, Legionella pneumophila)
 Some pastimes expose you to specific risks – for example some of
the unusual fungal agents are associated with pastimes that disturb
soil and expose you to animal droppings
 Immunocompromised state - much higher risk of Mycobacteria and
fungi
Diagnosis & Treatment
 Diagnosis
 X-ray showing infiltrates
 Elevated temperature
 Changes in WBC counts
 Culture confirmation
 Treatment
 May require supportive therapy even to ITU level
 Tailored antimicrobials if possible – limited options for viruses
Atypical pneumonia
 Patients present with less obvious symptoms –
 Dryish, non-productive cough, slightly raised temperature,
drowsiness, nasal discharge – i.e. almost “flu-like” symptoms
 Causative organisms include Legionella pneumophila, Mycoplamsa
pneumoniae, Chlamydiae pneumoniae, Coxiella burnetti and various
viruses
Legionellosis – atypical pneumonia
 Legionellosis is the collective term for diseases caused by members of
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the family such as Legionnaires’ disease and Pontiac fever
48 species and >60 serogroups in the Legionellaceae family, although
infections in man usually caused by L. pneumophila
First reported outbreak in 1976 – identified as an outbreak of
pneumonia at a conference in Philadelphia (The American Legion
Convention). 221 cases 34 deaths
Transmission by inhalation of aerosols
The pneumonia ranges from mild to life-threatening
Incubation 2-10 days
Abrupt onset with rapid development of symptoms including fever,
muscle aches, headache and dry cough. Diarrhoea may also be observed.
Pontiac fever is a milder form that resembles flu – diagnosis is
serological or by antigen as the microbe is not recovered from
respiratory samples in these cases
UK Epidemiology of Legionellosis
600
Total Cases
Male Cases
Female Cases
500
Deaths
Travel Associated
400
300
200
100
0
2006
2005
2004
2003
2002
2001
2000
1999
1998
1997
1996
1995
1994
1993
1992
1991
1990
1989
1988
1987
1986
1985
1984
1983
1982
1981
1980
Data from HPA – no longer accessible
Image from the CDC PHIL
SARS and MERS
 Sudden Acute Respiratory Syndrome
 Viral infection – Coronavirus
 Recognised cause of acute URTI, first identified in humans in late 1960’s
through work at the common cold unit in Salisbury – but really emerged in
2002-3
 Stable in the environment for
 36 hours on paper, formica, plaster
 72 hours on plastic and steel
 96 hours on glass
 In Canada, evidence of environmental contamination was found including
walls and the ventilation system
 MERS: a newer Coronavirus
 http://www.nhs.uk/news/2012/09september/pages/new-sars-like-virus-
detected.aspx
 http://www.nhs.uk/news/2014/07July/Pages/Deadly-MERS-camel-flu-maynow-be-airborne.aspx
SARS continued
 Incubation period ~4-6 days but up to 14 days reported
 Transmission from an infected patient appears greatest from the
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most severely ill and those undergoing dramatic deterioration
The virus is shed in faeces (peaking at day 12-14) as well as nasal
secretions (peaking at day 9-11)
The case fatality ratio on average was 15%, however it varied
greatly with age group – most fatalities were in the elderly,
diabetes also appears a possible factor for increased mortality
There is limited evidence that the disease killed proportionally
more men then women, but numbers are too small for certainty
A number of domestic pets were found to carry the virus
Focal points for transmission included a hotel and an aeroplane
A modern day pandemic
Mid-Nov 2002 – first cases in Guangdong Province, China
28th Feb 2003 – first case in Vietnam by 11th of March ~30 cases in the cluster
12th March 2003 –WHO issue global alert
14th March 2003 – Canadian cluster reported
15th March 2003 – Case in Singapore
15th March 2003 –WHO issue global travel alert due to spread
17th April 2003 – the identity of the virus confirmed
April and May –WHO restates the travel advisory notices
4th May 2003 – preliminary research on stability in the environment
15th June 2003 – last confirmed case in China
5th July 2003 –WHO issue statement that the first global epidemic of SARS had been
contained
 8th Sept 2003 – isolated case in a researcher – no spread from index observed
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 >4000 cases and 813 deaths
 21% of cases were amongst health care workers
 May 2004 WHO declare end of emergency with chain of transmission from last
cases now broken
SARS main centres of the pandemic
6000
5000
4000
Total
3000
Number of
deaths
2000
Number of
HCW affected
1000
0
Canada
China
Hong Kong
Taiwan
Data from WHO website
Singapore
Other “affected” areas
70
Total
Number of deaths
60
Number of HCW affected
50
40
30
20
10
0
Viet Nam
United States
United Kingdom
Thailand
Switzerland
Sweden
Spain
South Africa
Russian Fed
Romania
Korea
Eire
Philippines
New Zealand
Mongolia
Malaysia
Kuwait
Italy
Indonesia
India
Germany
France
Macao
Australia
Data from WHO website
Aspiration pneumonia
 Occurs when the stomach contents, saliva, oral debris etc get into
the lungs
 Can cause chemical pneumonitis
 Can deliver “unusual” pathogens into the respiratory tract
 e.g. anaerobes
 Can occur with some neurological conditions, in those with
swallowing problems, during anaesthesia (hence nil by mouth preop) or when drunk!!
Tuberculosis
The Genus – Mycobacterium
 The genus Mycobacterium are
 Aerobic bacilli
 0.2 – 0.6μm wide x 1 - 10 μm long
 Non-motile
 They have a lipid rich cell wall,
 That differs from “standard” bacterial cell walls
 That increases their resistance to disinfectants
 That makes them nutritionally fastidious (fussy)
 That means they grow and divide slowly (12-24hours)
Mycobacteria and disease
 There are at least 70 species in the genus
 They have animal and/or environmental reservoirs
 A number of have been associated with human disease including
 However, 95% of mycobacterial infections are caused by
 M. tuberculosis, M. avium-intracellulare, M. kansasii, M. fortuitum, M.
chelonae, and M. leprae.
 Of these all but M. leprae cause respiratory infections
 They are a major cause of morbidity and mortality in the
developing world, and also in immunocompromised patients in the
developed
TB has a long history
 Reports of disease that are almost certainly TB can be seen in historic
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texts (particularly those of Greek scholars) dating back centuries
As recently as the 1800s TB was endemic in the UK (and Europe and
the US)
The annual death toll at this time was approaching 1% of the
population of major cities
As living standards improved, the incidence of TB declined without any
specific action against it
Vaccination was introduced in the UK in the 1950s and this resulted in
a further substantial decline in infection
Illustrious victims include – Orwell, Austen, Moliere, Keats and of
course Satine in Moulin Rouge!
Pathogenesis aspects
 Spread is via the respiratory route – it is estimated that each person
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with active TB will infect 10-15 others
TB can evade the immune response by “hiding” inside pulmonary
macrophages
T cells and macrophages combine to try and prevent spread of
infection by “walling off ” the bacteria – this lesion (called a tubercule)
becomes hardened
Much of the damage in the lung is caused by the phagocytes trying to
kill the bacteria and releasing enzymes etc in to the environment
The walled off lesions contain live bacteria, which grow and multiply.
The bacteria alter the nature of the lesion over time, from caseous to
liquefied. Once the lesion is liquefied both aerosol transmission
(spread) and dissemination through the host become more likely
Signs, symptoms and diagnosis
 Signs and symptoms
 Coughing – often producing bloodstained sputum
 Fever
Image from CDC PHIL
resource
 Weight loss
 Loss of energy (malaise)
 Night sweats
 Swollen glands in the neck
 Diagnosis
 Shadow infiltrate on lung x-ray
 Possible positive tuberculin test (care in interpretation needed)
 Laboratory culture or molecular detection
Treatment
 There are a number of antibiotics that are either
 Specifically active against mycobacteria
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or
 On a restricted use list to preserve their effect
 Acute TB treatment in UK is usually based around Rifampicin and Isoniazid
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(for 6 months) with Ethambutol and Pyrazinamide (for the first 2 months).
Streptomycin can also be used
Latent TB may be left untreated in over 35s as the risk of the medications
causing liver damage rises such that the risks of treatment may outweigh the
benefits – patients will be monitored for reactivation and then treated at that
point.
Resistance occurs at a relatively high frequency, so even in a patient with no
evidence of resistance or history of previous treatment it is usual to prescribe
a dual or triple therapy approach
Treatment takes around 6 months, and is a relatively complex regime for the
patient to follow. Non-compliance is therefore a major problem.
Prevention - vaccination
 BCG is the currently used vaccine. This is an attenuated live vaccine
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strain of Mycobacterium bovis (a close relative of M. tuberculosis)
Billions of doses has been given worldwide and very few ill-effects
have been reported (making it one of the safest vaccines known)
However, its effectiveness is controversial.
The vaccine prevents children form getting the disease but does not
protect adults from reactivation of latent infections.
Protection rates vary widely from trial to trial – possibly due to the
genetic differences between trial populations
Vaccination in the UK is now reserved for high risk individuals – e.g.
children of migrants from endemic countries and those in high risk
occupations
Global picture
 Worldwide, TB kills approximately 2 million people each year
 The WHO state that the “epidemic is growing and becoming more
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dangerous”
The breakdown of health services in a number of countries, the spread
of AIDS and the emergence of multi-drug resistant strains are adding to
the problem
In 1993, the WHO declared TB a global emergency and they predict
that between 2002 and 2020, approx 36 million people will die of TB,
and a further 150 million will suffer infection
WHO recently estimated that 2 billion people worldwide are infected
with M. tuberculosis (~1/3rd of the population)
In Eastern Europe and Africa, TB is on the rise after 40 years of decline
The highest burden of TB currently is in Asia – with nearly ½ of all
deaths happening there
Trends in Europe
Data from EuroTB.org (no
longer accessible)
Data from EuroTB.org – no longer accessible
In the UK
 Predominately an imported condition – diagnosed within set
period of arriving in the UK
 Major urban centres highest levels
 Age profile in first generation migrants is different to that seen
in established populations
Exacerbations of other lung
pathologies
Exacerbation of Bronchitis
 Bronchitis is production of excess sputum on most days for 3
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consecutive months with more than one “bout” of illness
Microbes can both cause bronchitis and exacerbate bronchitis
caused by other conditions
Many possible causes, microbial causes tend to be acute, whilst
environmental causes are more likely to cause chronic illness
Much more common in smokers
Bacterial causes include all the possible causes of “simple”
pneumonia, and viral causes as we have seen include influenza
viruses – these can all also exacerbate.
Treatment against cause, plus sufferer will be recommended to
have the flu and pneumococcus jabs
Exacerbation of bronchiectasis
 Bronchiectasis is chronic inflammation or degenerative condition
of the bronchi, in which the bronchi and/or the bronchioles
become distended and lack elasticity – including post-TB scarring
 Leads to excess production of secretions that must be cleared,
through physio or postural drainage
 Sufferers prone to bacterial infection which also must be cleared
as and when it arises – can be caused by many organisms we have
talked about already
Exacerbation of COPD
(link to DL’s lectures)
 Chronic bronchitis and emphysema combined
 Infectious exacerbations are common and can be either mono-
agent or multi-agent – about ¼ of infectious exacerbation will
have both a bacterium and a virus present
 Any of the agents of bronchitis or pneumonia can be implicated
 Patients with COPD should receive the pneumococcal vaccine
and the seasonal flu jab
Exacerbation of Cystic Fibrosis (CF)
 CF is a genetic disease where a chloride channel protein is
mutated – leads to altered secretions at a range of body sites
including the lung
 Major pathogens of concern
 Staphylococcus aureus, Haemophilus influenzae, Pseudomonas aeruginosa,
Burkholderia cepecia
 Other respiratory pathogens also need to be watched out for,
although their role is less well defined
Exacerbations of Asthma
 Viral infections in childhood can increase the risk of
developing asthma
 Viruses and bacteria can also cause acute exacerbations of
asthma
 Many asthmatics are also at increased risk of getting
pneumonia and other infectious diseases
 Moderate – severe asthmatics should consider the flu jab and
also possibly the pneumococcal jab
Conclusion
 Wide range of possible infections are associated with the
respiratory tract
 Wide range of infections can cause each of the different types
of infection
 Patients with underlying lung pathology are at increased risk
of infections and any infections are likely to cause an
exacerbation of their underlying disease
Recommended Additional Reading
 These URLs should take you to free access versions of these papers that show
how any agent that causes infection of the middle and lower respiratory tracts
can exacerbate pre-existing respiratory conditions
 Infectious Etiology of Acute Exacerbations of Chronic bronchitis – by Sethi
 http://journal.publications.chestnet.org/data/Journals/CHEST/21947/380S.pdf

Exacerbations: etiology and pathophysiologic mechanisms – by
Wedzicha
 http://journal.publications.chestnet.org/data/Journals/CHEST/21978/136S.pdf

Bacterial infection in COPD in 2000: a state of the art review – Sethi &
Murphy
 http://www.ncbi.nlm.nih.gov/pmc/articles/PMC88978/?tool=pubmed