Respiratory infections Flashcards
State 3 common lung bugs
Streptococcus pneumoniae
Mycobacterium tuberculosis
Legionella Pneumoniae
Influenze Rhinovirus Aspergillus fumigateurs SARS Pneumocystis jirovecis
What is the difference between an upper respiratory tract infection and a Lower respiratory tract infection?
URTI affects nasal cavity, pharynx and larynx
LRTI affects trachea, bronchi, bronchioles and alveoli
Describe the pathogenesis of infection in lung.
Lungs constantly exposed to particulate material and microbes from upper airway
Lower airways usually devoid of conventional pathogens, in infection this is untrue
How does the innate immunity and acquired immunity keep the lower tract sterile?
INNATE
- Cilia- mucocilary escalator removes debris and pathogens
- Alveolar macrophages secrete antimicrobials; engulf and kill pathogens; recruit other WBCs; process and present antigens to T cells
ACQUIRED
- B/T cell responses- essential for intracellular pathogens inc. mycobacterium, viruses and fungi
- IgA secreted by plasma cells interferes with adherence and viral assembly
Explain the role of IgA in preventing respiratory infections in the lungs.
Forms additional epithelial protective barrier which prevent microbial adherence to epithelial surface and inhibits viral infections (influenza) by interfering assembly processes
Also binds pathogens for phagocytosis and antibody-dependent cell-mediated cytotoxicity
In response to infection, inflammation occurs. How does this occur and what are the cardinal signs?
Give an example of an inflammatory condition in both the upper and lower respiratory tract.
Redness, heat, loss of function, pain, swelling
- Vasodilation
- Increased vascular permeability
- inflammatory cells infiltrate area
URT: Rhinitus, sinusitis, pharyngitis, tonsillitis, laryngitis
LRT: Bronchitis, Bronchiolitis, Pneumonia, P.tuberculosis, P.abscesses, Empyema
Describe the common cold(URTI) in terms of epidemiology, aetiology and transmission
Recurs 5/7x in preschool kids; 2/3x per year in adulthood
Accounts for 40% of workdays lost
> 200 viruses cause it with commonest being rhinovirus (30-50%)
Transmission:
- Hand contact- direct/indirect . Viable on skin <2hrs, longer on surfaces
- Droplet
Infectious period: 2/3 days
Symptomatic period: 3-10 days - 2 weeks in 25% of ppl
How does the cold compare to the flu?
ONSET: Cold appears gradually, Flu quickly within hours
TARGET: Cold mainly nose and throat, Flu more than just nose and throat (systemic)
EFFECT: Cold no fever and ill but functional, Flu is exhausted and unwell (non functional),high fever.
Describe the aetiology and epidemiology of influenza
What does uncomplicated influenza look like?
Caused by influenza A or B
Occurs in outbreaks and epidemics worldwide- in winter (so swaps hemispheres over the course of the year)
Infectious period: 1-4 days
Abrupt onset of fever (38-41), headache, myalgia, malaise, cough, sore throat, nasal debilitating
ACUTELY DEBILITATING
What can cause influenza to become complicated?
Which groups of people are at risk of this?
- Primary viral pneumonia
- Secondary bacterial pneumonia
- CNS disease
Those on immunosuppressants or with chronic illness
Pregnancy (or 2 weeks postpartum)
<2y/o or >65
BMI >40
Briefly outline how viruses replicate
Attachment Penetration Synthesis of new components Assembly Release
Viruses must be able to replicate inside a cell, move from one infected cell to another and new host, as well as develop mechanisms to evade host defences
Describe how an influenza viron enters a host cell
Express hemogglutinin surface protein (H) which bind to sialic acid receptor on host cell in respiratory tract
This binding allows the iron entry into the cell
The iron also expresses neuraminidase (N) which allows it to escape host cell by cleaving silica acid bonds- otherwise the escaping irons all clump together
Suggest a target for treatment of influenza
Immunisation against Hemogglutinin surface protein (H) and Neurominidase (N)
Tamiflu = osel tamivir= (N) inhibitor
In terms of influenza, describe viral SHIFT
The influenza virus has a segmented genomes (8 parts) so in the case where a cell is co-infected by 2 or more different viruses they can reassort themselves which leads to viral diversity which is important in the evolution of influenza virus
This only occurs in influenza A as it can infect different species of animals. When viruses infect different species they adapt, by chance if one of reassorted viruses is infectious in humans –> swine flu e.g.
In terms of influenza, describe viral DRIFT
This can occur in influenza A or B
They have some of their own synthesis machinery- RNA dependent RNA polymerase. This isn’t very good at its job=mistakes=point mutations
These point mutations accumulate and change the shape of hemogglutinin surface proteins and/or neuraminidase such that it is no longer detected by the bodies pre-made antibodies
Describe pneumonia in terms of its aetiology, symptoms, diagnosis and classification
Infection of lung parenchyma (FUNCTIONAL PART)
Alveoli full of inflammation blocks O2 transfer
Symptoms: fever, dyspnoea, cough, sputum, hypoxia, increased respiratory rate, pleuritic pain, sepsis
Diagnosis requires infiltrates on CXR with symptoms
Classification:
- Typical/atypical - not useful
- Lobar/broncho - descriptive, not useful
- Community/hospital acquired- pathogens differ, % contribution differ, useful
Which pathogens causes pneumonia?
Streptococcus pneumoniae
Legionella pneumoniae
Mycoplasma pneumoniae
Haemophilus influenza Resp viruses (1/3) Staphylococcus aureus Pneumocystis jirovecii (in cell-mediated immunodeficiency) Aspergillus fumigatus
Describe pneumonia caused by Strept pneumoniae
COMMONEST Gram +ve Risk factors: alcoholics, respiratory disease, smokers, hyposplenism, HIV Acquired in nasopharynx Asymptomatic in 40-50% Prevention:vaccine Easy to culture
Describe pneumonia caused by Mycoplasma pneumoniae
Commonest ambulatory pneumonia
Young people
Extrapulmonary symptoms - skin, heart, CNS
No cell wall (resistant to PENICILLIN + can’t culture in lab)
Diagnosis: PCR throat swab
Treat: macrolides/tetracyclines
Describe pneumonia caused by Legionella pneumoniae
2-9% of cases (More common in UK than rest of Europe)
Sporadic or outbreaks from outbreak from contaminated water supply
SEVERE LIFE THREATENING
Initially: mild headache then high fever, myalgia, dyspnoea, confusion, dry cough, GI upset EXTRA PULMONARY COMPLICATIONS
Diagnosis: Urinary legionella antigen
Treat: Macrolides/quinolones
Describe hospital acquired pneumonia
Include general and local complications
ONSET: >48 hrs since admission
Caused by host bacterial:
- E.coli
- Klebsiella pneumoniae
- Pseudomonsas aeruginosa
- Stapholococcus aureus
- Streptococcus pneumoniae
Hops pathogens intrinsically more resistant or have acquired resistance. BROAD SPECTRUM ANTIBOTICS
General: Sepsis, resp failure
Local: Pleural effusion, empyema (pus in cavity), lung abscess, collapse, post-injection bonchectasis (abnormal widening)
Describe the epidemiology of tuberculosis
global (although 64% in 2016 cases in 3rd world)
1/4 of population has latent TB
45% of HIV negative will die from it but almost ALL HIV positive will die from it without treatment
Describe the pathology of tuberculosis
Aerobic bacillus
Divides very 16/20 hours (slow)
Cells wall (although lacks phospholipid outer membrane) This makes it weakly gram +ve and it retains stain after treatment with acid (called ACID FAST BACILLUS)
Special stain: Ziehl-Neelson or auramine-rhodamine
Describe the pathophysiology of tuberculosis
Inhalation of mycobacterium tuberculosis
Innate immune response (involved macrophages)
Recruitment of inflammatory cells to lungs (neutrophils)
Bacterial dissemination to draining lymph node
Dendritic cell presents bacterial antigen to T cell thus priming it and causing expansion of antigen-specific T cells which are recruited to lung
Recruitment of T cells/B cells as well as activated macrophage/ other leukocytes leads to the establishment of granulomas
Describe the outcomes of TB
Outcomes after primary infection:
1. Healed lesion( scar, calcification)- nonviable organism
- 95%: Latent lesion. 5% (20x mom in HIV +) will go on to develop post primary TB which leads to cavitation and fibrosis, caseation, military, scarring
- 5%: Progressive primary TB- haemotogenous spread, miliary TB
What does TB diagnosis involve?
- Active TB: Identify area, isolate organism and identify antibacterial susceptibility
- Latent TB: Identify immune response to TB proteins/antigens
How is TB managed?
Cure active disease, reduce spread and prevent reactivation by:
- Prompt and adequate treatments
- Appropiate source isolation
- Contact tracing
