Respiratory tract infection Flashcards
Compare symptoms of the cold to the flu.
Onset: cold has a slower onset than the flu.
Debilitation: Flu is more debilitating. General greater feeling of ‘illness’.
Affected sites: Cold mainly throat and nose. Flu affects everywhere.
Fever: Flu has onset of fever (greater than 38) whereas the cold does not.
Innate immunity in respiratory tract
Cilia- accompanied with mucus which removes debris and pathogen.
Alveolar macrophages:
- Kills pathogens
- Secrete antibacterial
- Recruit other immune cells
- Antigen presentation on T cells.
Acquired immunity in the respiratory tract
B + T cells: deal with intracellular pathogens.
IgA interferes with viral adherence and viral assembly.
The common cold
Caused commonly by the rhinovirus- 30-50%
More common in preschool children.
Symptoms mainly in throat and nose and have a slow onset.
Main pathogen that causes the common cold
Rhinovirus
30-50% of cases
Transmission of the common cold
Direct or indirect hand contact- individual coughing/sneezing into their hands and touch other surfaces.
Virus can remain on skin for 2 hours and for longer hours on other surfaces.
Incubation period of the common cold
2-3 days
Length of symptoms in individuals with the common cold
3-10 days commonly
Up to 2 weeks in 25% of individuals.
Influenza
Infection that causes the ‘flu’.
Virus: Influenza A or B.
Usually occurs in outbreak and epidemics- mainly in the winter season.
Incubation period of influenza
1-4 days- usually quicker onset than common cold.
Symptoms of influenza
Abrupt onset of fever: 38-41
Headache
Myalgia
Malaise
Coughs, sore throat, nasal discharge.
Complications of influenza
Can primary cause viral pneumonia.
Can cause secondary bacterial pneumonia.
CNS disease
Risk groups for influenza complications
Those with immunosuppressed or chronic conditions.
Women who are pregnant or 2 weeks postpartum.
Age: below 2, above 65
BMI> 40
Influenza virus receptors
Contains haemagglutinin surface protein (H) which binds to sialic acid receptors on respiratory tract cells.
Neuraminidase receptor allows the virus to escape the host cell by cleaving sialic acid.
The gene coding for each receptor are on different segments (of the 8) in the virus. This allows wide variation in virions.
Receptor on influenza that allows it to enter host cells .
Haemagglutinin (H)
This binds to sialic acid on the host cells in the respiratory tract- allowing it to enter the host cell.
Receptor on influenza that allows it to leave host cells .
Neuraminidase (N)
This receptor cleaves sialic acid on host cells, allow it to escape cells- prevents virons from clumping.
Influenza shift
Occurs when RNA segments are exchanged between viral strains in their secondary host.
This provides no cross-protective immunity to virus expressing new haemagglutinin.
This causes an epidemic/ outbreak- where most people are not immune.
Influenza drift
Occurs as a result of point mutation in virus.
Some neutralising antibodies are still able to bind to the virus- majority will be immune.
Pneumonia
Infection of lung parenchyma
This causes alveoli to fill with inflammation contents- pus/ debris/ pathogens
Pneumonia symptoms
Fever- above 38
Breathlessness
Cough- producing sputum
Hypoxia
Tachypnea
Pleuritic chest pain
Sepsis
3 features in pneumonia CXR
- Consolidation
Air bronchograms may be present
Heart/ diaphragm borders obscured. - Interstitial infiltrates
- Cavitation may occur.
Community versus acquired pneumonia
Hospital- acquired >48+ after hospital administration
Community acquired not from hospital.
Helps to narrow down pathogenic cause.
3 main pathogens that cause pneumonia
Streptococcus pneumoniae
Mycoplasma pneumoniae
Legionella pneumophila
Streptococcus pneumoniae
Gram positive bacteria
Primary cause of pneumonia
Usually acquired through nasopharynx region.
Prevention- vaccine
Risk factors of developing Step. pneumoniae pneumonia
Alcoholics
Respiratory disease
Smokers
Hyposplenism
HIV
Diagnosing pneumococcal disease (Strep. pneumoniae)
Sputum culture- easy to grow and diagnose.
IF IN BLOOD:
There is a higher chance of mortality and other extrapulmonary disease
Occurs when alcohol intake is high
Only <1% of patients show positive result in blood.
Mycoplasma pneumoniae
Bacteria that causes pneumonia- most common bacteria that causes atypical pneumonia.
Usually in young patients and lasts for several weeks
Symptoms of Mycoplasma pneumonia
Non specific:
Malaise
Headache
Arthralgia
Extrapulmonary very common:
- Skin: rashes
- CNS: aseptic meningitis, cerebellar ataxia
- Heart: pericarditis, myocarditis
The infection can spread bilaterally- into both lungs.
Diagnosing Mycoplasma pneumonia
PCR of throat walls- VTS
Mycoplasma lacks cell wall so cannot grow in normal lab plates.
Treating mycoplasma pneumonia
Due to lack of cell wall, cannot be treated with penicillin.
Drugs: macrolides or tetracyclines
Typical pneumonia
Pneumonia causes by the ‘typical’ microorganisms:
- Strep.pneumoniae
- Haemophilus influenzae
- Moraxella catarrhalis
Atypical pneumonia
Pneumonia caused by microorganisms that are not:
- Strep.pneumoniae
- Haemophilus influenzae
- Moraxella catarrhalis
Mycoplasma pneumoniae is the most common atypical bacteria that causes pneumonia.
Legionella pneumophilia
A rare cause of pneumonia- accounts for 2-9% of community acquired pneumonia (CAP).
Can occurs from outbreak from contaminated water source.
Can cause severe and life-threatening infections
Symptoms of legionella pneumophilia
Initially starts with a mild headache
Escalates to: High fever Myalgia Dyspnoea Confusion Dry cough GI upset
Further extrapulmonary complications
Extrapulmonary complications of Legionella pneumophila
Lymphopenia
Low Na
Diagnosis of L.pneumophila
Not grow in culture as it requires very special conditions and takes a long time.
Urinary legionella antigen is used to diagnosis.
Treatment of Legionella pneumophila
Macrolides
Quinolones
Hospital acquired pneumonia
Occurs when patients get pneumonia >48 hours after admission.
This is due to patients getting colonised with hospital bacteria.
Therefore: bacteria can acquired resistance mechanism or be intrinsically resistant to antibiotic.
This causes a broader spectrum of antibiotics being used.
Local complications of pneumonia
Parapneumonic effusion
Empyema- collection of pus in pleural cavity caused by microorganism
Lung abscess
Collapsed lung
Post-infection bronchiectasis
Bronchiectasis
Permanent enlargement of the lung airway.
This is a complication after pneumonia infection.
TB pathology
Caused by aerobic bacillus (mycobacterium tuberculosis), which divide very slowly- takes 56 days to culture
Bacillus is acid fast- AFB
Cell wall lack outer membrane- poor stain, so it weakly positive
Special stains for TB
Ziehl-Neelsen
Auramine-rhodamine
Transmission of TB
TB is acquired by inhaling aerosol droplets.
Pathogenesis of TB
After inhaling aerosol droplet containing TB- innate immune system recognises and recruit inflammatory cells to lungs.
Bacteria spread and causes dendritic cells to present their antigens to T cells.
T cells that are antigen-specific to TB expand as a result of dendritic presentation and are recruited to the lungs.
Granulomas form as a result of recruited T, B and macrophages- forms miliary spots in CXR
Latent TB
Occurs in 95% if TB infections
After TB infections and cause parenchymal + lung node caseation, TB becomes dormant.
Patients will be asymptomatic until activation
Dormant TB is reactivated and proliferate- causes disease again
Progressive primary TB
Occurs after primary infection of TB the infection progresses:
Haematogenous spread
Miliary TB
Cavitation
Healed lesion TB
- Aerosol droplet containing TB is inhaled and deposited in terminal airspaces.
- Macrophages ingest bacilli but bacteria replicate in endosome.
- Macrophage with ingested bacilli are transported to lymph node to be killed.
This forms scar/ calcification.
Diagnosing Latent TB
Identify immune response to TB proteins or TB-specific antigens
