Management of Respiratory Infectious - Reid - 13-08-03

PNEUMONIA

Types / Setting: Community acquired (strep, h. influenzae, influenzae virus), Hospital acquired (mainly in ICU, proteus, E coli, pseudomonas aeruginosa, k. pneumoniae), Immunocompromised Pt ( normal organisms cause it, and then opportunistic pathogens: HSV, CMV, pneumocystis carinii, aspergillus, toxoplasmosis). 

Clinical features: SOB, cough (sputum/blood), fevers/chills/rigors, pleuritic chest pain

Clinical signs: Inspection: febrile, Palpation: reduced chest expansion, increased fremitus, Percussion: dull on affected side, stony dull if pleural effusion, Auscultation: pan inspiratory crackles (liquefaction of alveolar exudate). 

Investigations: 
Radiology: homogenous opacity of affected lobe (lobar pneumonia) or patchy opacity (bronchopneumonia). Pleural effusions can be identified. 

Sputum ( Gram stain, ZN stain) / Blood culture ( pneumococcal pneumonia) / Serology (influenzae virus, mycoplasma, legionella, chlamydia)

Markers of severity (any two or more of the following):
RR >= 30, diastolic BP <=60, serum urea >= 7mmol/L, confusion 

DDx: pulmonary oedema, pulmonary infarction, pulmonary TB

Management: 

Community acquired pneumonia: mild (amoxycillin, roxithromycin, doxycycline), moderate (benzylpenicillin - think COPD), severe (erythromycin, benzylpenicillin, gentamicin)
Hospital acquired: 3rd generation cephalosporin, gentamicin
Immunocompromised: 3rd generation cephalosporin, clavulanic acid. 

INFLUENZAE
This is a orthomyxovirus and there are three types: A, B, C. The viruses contain haemaggluttins & neuraminidases that are the antigens. A affects many animals and, unlike B & C, it can change its antigenic components. It can undergo antigenic drift (point mutations in the haemoaggluttin genes) & antigenic shift (acquisition of new HA &/or NA genes).  It is the antigenic shift that can produce a totally new human virus which goes on to become a PANDEMIC. There have been 4 in the 20th century, but usually they come up with a vaccine as protection.

Vaccinations is recommended in elderly, immunocompromised, health workers and in children. There are 110 cities in 80 countries that monitor the progress of this virus each year. 

Clinical features: The virus is transmitted by respiratory droplets. Patients present with fever, headaches, myalgias, athralgias, runny nose, and dry cough (A&B). C is usually just upper respiratory infections. 

BRONCHIECTASIS
What is it?: This disease is characterised by abnormal dilatation of the bronchi. It can be acquired or congenital. 
Aetiology: Congenital: primary ciliary dyskinesia, congenital hypogammaglobulinaemia, Acquired (children): pneumonia, measles, whopping cough, TB, Acquired (adults): pneumonia, TB, bronchial tumours, allergic bronchopulmonary aspergiollis. 

Pathology: The pathological dilatation is usually 2nd to childhood infection, that produces copious amounts of mucous which accumulates distal to the bronchus obstruction (tumour, lymphadenopathy etc). Rarely congenital causes are identified. 

Clinical features: chronic cough with production of copious sputum, fever/chills/rigors, haemopytsis. 

Clinical signs: digital clubbing, sinusitis (70%), coarse pan/late inspiratory crackles. 

Investigations:
Bacteriological & mycological assessment of sputum sample
CXR: doesnt really show up bronchiectasis but can show up complications (effusions, pneumonia etc). 
CT: very accurate in diagnosis of bronchiectasis. 

Management:
Acute: IV antibiotics to treat the superlying infection. Staph aureus: beta-lactam penicillins, H. inf: penicillin, Pseudomonas: gentamicin etc. 
Chronic: postural drainage of lungs (assume drainage position 5-10mins / day), physiotherapy, surgical resection, monitoring for complications. 

TUBERCULOSIS
Aetiology: mycobacteria (tuberculosis, bovis etc)
Types: Primary, Progressive Pulmonary TB (when primary does not heal and it progresses to more serious disease), Post-primary TB (reactivation of incompletely healed TB). 
Risk factors: nutrition, race, socioeconomic status, smoking, silicosis

Pathology: Primary (Ghon complex: caseating necrosis with hilar lymphadenopathy) --> may compress bronchus and cause lobar collapse, erythema nodosum is important association (rare), Post-primary: caseating necrosis that causes large 'hole' in lung. 

Clinical features (should make you suspicious): haemoptysis, chronic cough, weight loss, night sweats, malaise

Management:
Prevention: bCG, Mantoux (+ve if after 72 hrs there is >=5mm induration surrounded by erythema)
Treatment: chemotherapy ( 1st 2 months: rifampicin, pyrazinamide, isoniazid, ethambutol, then 4 months: rifampicin, isoniazid).