Bacterial repsiratory Infections

Question 1

The natural microflora of URT

Answer 1

Densely populated. Provides colonisation resistance. Source of opportunistic pathogens

Question 2

The natural microflora of LRT

Answer 2

Anexic- free of permanent colonisation, some transient microbial presence

Question 3

How does depth of infection change respiratory infection

Answer 3

Worsen infection. Infection in bottom of lung can spread via blood dissemination and systemic infection

Question 4

Examples of bacterial respiratory infectionsA

Answer 4

Tuberculosis
Diphtheria (corynebacterium diphtheria)
Whooping Cough (bordatella pertussis)
Cystic fibrosis (pseudomonas aeruginosa)
Legionnaires disease (legionella pneumphila

Question 5

Define a professional invader

Answer 5

Infect a healthy respiratory tract

Question 6

Define secondary invader

Answer 6

Infect when host defences are impaired

Question 7

Requirements of Professional Invaders

Answer 7

Adhese to normal mucosa( in spite of mucocilliary system

Interfere with cilia

Resist destruction in alveolar macrophage

Ability to damage local tissue( mucosal and sub mucosal tissue

Question 8

Requirements of Secondary Invader

Answer 8

Initial infection and damage by respiratory virus

Impair local defences

Chronic bronchitis

Depresse immune system

Question 9

Describe M.tuberculosis

Answer 9

Rod shaped
Symptoms: cough, chest pain, fever, weight loss, fatigue, bloody sputum

Not diagnostic common to other LRT infections

Question 10

Epidemiology of Tuberculosis

Answer 10

Majority of cases infection does not hold.
Goes through phases of latency and activity

Forms granulomas composed of mainlu immune cells in attempt to wall of infection

1/3rd of world population latently infected
1/10 of latent infections become active diseases

Question 11

Countries where tuberculosis is problem

Answer 11

South African countries
Papa New Guinea
Burma

Question 12

Percentage of people untreated tuberculosis kills

Answer 12

Untreated 50%
25% remain I’ll
25% recover

Question 13

How is Tuberculosis diagnosed

Answer 13

Clinical symptoms is helpful, bloody sputum. Coughing, fever

No culturing as takes 6 weeks

Chest radiography to view granulomas in lung

Microscopic detection of acid fast rods in sputum is diagnostic

Question 14

Antibacterial chemotherapy for Tuberculosis is?

Answer 14

3 or more drugs for at least 6 months. Can be up 18-24 months

Rifampicin, Isoniazid and ethambutol is most often used combination.

Drugs often switched out to prevent resistance

Question 15

Reasons for Difficulty in clearing tuberculosis

Answer 15

M.tb is able to hide from immune system in macrophages

Shows long term survival in bone marrow stem cells

Slow growth and persistence limits efficacy of Antibiotics used

Question 16

3 classes of drug resistant M.tb

Answer 16

Multi-DR MDR - resistant to first line agents (rifampicin+isoniazid)

Extensively-DR XDR - MDR Resistance + resistance to quinolones + second line injectables (kanamycin ,capreomycin,amikacin)

Totally-DR TDR - XDR + resistance to all common second line agents

Question 17

Most common cause of Bacterial pneumonia

Answer 17

Commensal of the URT S.pneumoniae

Question 18

Epidemiology of Bacterial Pneumonia

Answer 18

Leading cause of death in resource limited settings

High prevalence in males and winter

More common in those with lung conditions or compromised immune system

Question 19

Prevention of Pneumonia

And vaccines

Answer 19

Immunisation decreases incidence of pneumonia by 50%

2 pneumococcal vaccines;
Pneumococcal conjugate vaccine PCV, childhood vaccine protects against 13 common strains
Conjugated to diphtheria toxin

Pneumococcal polysaccharide vaccine PPV, adult vaccine
Protects against 23 common strains
70% more effective

Question 20

Diagnosis of Pneumonia

Answer 20

Clinical presentations:
Raised respiratory rate, fever, chest signs, confusion in over 65s

Sputum not useful, hard to produce when infected and many LRT caused by commensals

Chest X-ray

CURBAge
Confusion, Urea, Respiratory rate, blood pressure, age

Question 21

Pneumonia treatment problems

Answer 21

Disease progression is fast.
Doctor must achieve diagnosis, decide on cause and treatment regimen, then treat as soon as possible

High mortality rate

Question 22

What is cystic fibrosis?

Answer 22

Most common lethal genetic disorder

Defect in cystic fibrosis transmembrane conductance regulator (CFTR)
Chloride transporter In epithelial cells.
Defect means reduced chloride transport therefore secretions lack water and are more viscous

Lungs fill with thick mucus prevent cilia cells moving mucus out of kings

Increase risk opportunistic infection
Immune system mediated damage to lungs

Question 23

Life expectancy in U.K. With Cystic fibrosis

Answer 23

40-50

Question 24

Treatment of Cystic Fibrosis

Answer 24

Airway clearance techniques- chest precision/excel uses

Bronchodilator use

Aerosolised recombinant Dnase1/hypertonic saline/ steroids inhalation

Oral/aerosolise Antibiotics - macrolodes- fluoroquinolones, aminoglycosides

Question 25

Benefits of aersolisation

Answer 25

Increases exposure to lungs and not rest of body

Question 26

Troubles treating CF-associated Respiratory Tracy infections

Answer 26

Chronic infections persist
Late colonisers tend to be gram negative which have more intrinsic resistance to Antibiotics

Biofilm formation makes harder to treat

• matrix hampers Ab and phagocytes access to bacteria cells
• reduced metabolism/ persistence cells
• transient hypermutuation

Question 27

What’s is synergy between Viral and Bacterial disease

Example

Answer 27

Major cause of human death

Question 28

What improvements are helping Bacterial respiratory tract infection treatment

Answer 28

Improved rapid diagnostics

Better access to Antibiotics and vaccines

Question 29

What improvements can be made for Cystic Fibrosis, TB, Pneumonia treatment

Answer 29

New Antibiotics that
Kill rapidly
Killing of persistent and biofilm-associated cells
Eradication with limited immune system support
Low resistance potential

Genetic manipulation to prevent CF in first place