Respiratory Tract Infections Flashcards
Lung bugs
Streptococcus pneumoniae
Mycobacterium tuberculosis
Legionella pneumophila
Lower airway usually devoid of conventional pathogens
Innate immunity
Cilia – mucociliary escalator removing debris and pathogens
Alveolar macrophages secrete antimicrobials engulf and kill pathogens recruit other immune cells process and present antigens to T cells
Acquired immunity
B cell/T cell responses – essential for intracellular pathogens, inc mycobacteria, viruses and fungi
IgA secreted by plasma cells interferes with adherence and viral assembly
IgA forms an additional epithelial protective barrier, which prevents microbial adherence to the epithelial surface and inhibits certain viral infections (influenza) by interfering with their assembling processes
Response to infection
Inflammation
Macro - redness, swelling, heat, pain and loss of function
Micro = vasodilation, increased vascular permeability and inflammatory cell infiltration
Respiratory tract infections
Rhinitis Sinusitis Pharyngitis Tonsillitis Laryngitis
Bronchitis Bronchiolitis Pneumonia Pulmonary tuberculosis Pulmonary abscesses Empyema
URTIs - transmission
hand contact (direct or indirect)
droplet transmission from sneezing / coughing
remain viable for up to 2 hours on skin or several hours on surfaces
URTIs
> 200 viral subtypes associated
Rhinovirus = most common
Cold
Appears gradually
Affects mainly your nose and throat
Makes you feel unwell but you’re okay to carry on as normal – for example, go to work
Usually no fever
Flu
Appears quickly within a few hours
Affects more than just your nose and throat
Makes you feel exhausted and too unwell to carry on as normal
High fevers
Influenza
Caused by Influenza A or B virus.
Occurs in outbreaks and epidemics worldwide; usually in winter season, so swaps hemispheres over the course of the year.
Uncomplicated influenza
IP 1-4 days
Abrupt onset of fever, headache, myalgia and malaise.
+ cough, sore throat, nasal discharge
Acutely debilitating.
Fever 38-41OC; otherwise examination often unremarkable
Influenza complications
Primary viral pneumonia
Secondary bacterial pneumonia
CNS disease
Risk groups for complications
Immunosuppression or chronic medical conditions
Pregnancy or 2 weeks postpartum
Age <2y or >65y
BMI >40
3 problems facing virus
It must know how to replicate inside a cell
It must move from one infected cell to a new cell (and a new host) in order to persist in nature
It must develop mechanisms to evade host defences
Influenza virus
Hemogglutinin surface protein (H) binds sialic acid receptors on host cells in the respiratory tract. This allows the influenza virus to enter the cell.
The neuraminidase (N) on the surface of the virus allows the virus to escape by cleaving sialic acid bonds – otherwise the escaping virions all clump together.
The influenza virus has a segmented genome (8 parts) so can reassort if 2 different viruses infect the same cell.
Pneumonia
infection of the lung parenchyma
Alveoli inflammation blocks oxygen transfer
Pneumonia symptoms
Fever, breathlessness, cough, sputum production;
Hypoxia, increased respiratory rate;
Pleuritic chest pain
Sepsis
Pneumonia radiology
Consolidation
May see air bronchograms
Heart borders or diaphragm obscured due to loss of solid-gas interface
Interstitial infiltrates
± cavitation
Classifications
Typical versus atypical – but not very helpful, as there is no feature in an individual patient that helps distinguish between them.
Community versus hospital acquired = much more useful, as the pathogens involved differ in their % contribution
Lobar versus bronchopneumonia – also not very helpful; descriptive, but doesn’t help managment
Pneumonia pathogens
Streptococcus pneumoniae Haemophilus influenzae Mycoplasma pneumoniae Legionella pneumophila Staphylococcus aureus Respiratory viruses probably responsible for ~1/3 Pneumocystis jirovecii in cell mediated immunodeficiency Aspergillus fumigatus
Streptococcus pneumoniae
Gram positive cocci
RFs
Alcoholics, respiratory disease, smokers, hyposplenism
HIV – 50- to 100-fold increase in invasive pneumococcal disease in HIV+
Acquired in nasopharynx
Asymptomatic carriage in 40-50%
smokers>non-smokers
Prevention – vaccine
Pneumococcal disease diagnosis
Easy to grow in lab from sputum cultures
Blood cultures: (<1% patients +ve) Higher mortality Extra-pulmonary disease Meningitis Septic arthritis Empyema ↑alcohol intake
Mycoplasma pneumoniae
Commonest cause of ambulatory ‘atypical pneumonia’
Classically young patient, vague constitutional upset, several weeks
Extrapulmonary symptoms very common
Skin, CNS and heart
Lacks cell wall
resistant to penicillins
cannot grow on normal lab plates
Mycoplasma pneumoniae diagnosis
Diagnosis by PCR of throat swab (VTS)
Treatment: macrolides or tetracyclines
Legionella pneumophila
2-9% CAP (more common in UK than Europe)
Cigarettes and chronic lung disease
Can occur as sporadic infection or cause outbreaks associated with a contaminated water source
Can cause severe, life threatening infection
Initial mild headache, then high fevers, myalgia, dyspnoea, confusion, dry cough and GI upset
Extra-pulmonary complications ++ inc lymphopenia and low Na
Legionella pneumophila - diagnosis
Don’t grow on routine culture – need special conditions, and longer
Urinary legionella antigen
Treatment: macrolides or quinolones
Hospital acquired pneumonia
New onset at least >48 hours since admission.
Hospitalised patients become colonised
with hospital bacteria
These may either be intrinsically more resistant to antibiotics, or have acquired resistance mechanisms.
Either way, broader spectrum antibiotics are used empirically.
Pneumonia complications - general
Sepsis (Multi organ failure)
Respiratory failure
Pneumonia complications - local
Pleural effusion Emphysema ? Lung abscess Collapse Post infection bronchiectasis
Pathology of pneumonia
Aerobic bacillus
Divides every 16-20 hours (slow) – lab extends culture to 56 days
Cell wall, but lacks phospholipid outer membrane
Does not stain strongly with Gram stain (weakly positive)
Retains stains after treatment with acids
Referred to as acid fast bacillus (AFB)
Special stains – Ziehl-Neelsen or auramine-rhodamine
Diagnosis of TB
Active TB
Identify the infected area
Isolate the organism
Obtain information regarding susceptibility to antibacterials
Latent infection
Identify immune response to TB proteins or TB-specific antigens
TB step by step
Infection is initiated by the inhalation of aerosol droplets that contain bacteria.
The initial stages of infection are characterized by innate immune responses that involve the recruitment of inflammatory cells to the lung.
Following bacterial dissemination to the draining lymph node, dendritic cell presentation of bacterial antigens leads to T cell priming and triggers an expansion of antigen-specific T cells, which are recruited to the lung.
The recruitment of T cells, B cells, activated macrophages and other leukocytes leads to the establishment of granulomas, which can contain Mycobacterium tuberculosis
TB management
Cure active disease
Reduce spread
Prevent reactivation
By… 1. prompt and adequate treatment;
2. appropriate source isolation;
3. by contact tracing
