1. Dr Dhaher Jameel Salih Al-habbo Department of Medicine.
Pneumonia Lecture No.2
Hospital-acquired pneumonia
Dr Dhaher Jameel Salih Al-habbo
FRCP London UK
Professor of medicine
Department of Medicine.

2. Hospital-acquired pneumonia
Hospital-acquired or nosocomial pneumonia refers to a new episode of pneumonia occurring at least 2 days after admission to hospital.
It is the second most common hospital-acquired infection (HAI) and the leading cause of HAI-associated death.
Older people are particularly at risk, as are patients in intensive care units, especially when mechanically ventilated, in which case the term ventilator-associated pneumonia (VAP) is applied.

3. Hospital-acquired pneumonia
Health care-associated pneumonia (HCAP) refers to the development of pneumonia in a person who has spent at least 2 days in hospital within the last 90 days, attended a haemodialysis unit, received intravenous antibiotics, or been resident in a nursing home or other long-term care facility.

4. Aetiology
When HAP occurs within 4-5 days of admission (early-onset), the organisms involved are similar to those involved in CAP; however, late-onset HAP is more often attributable to Gram-negative bacteria (e.g. Escherichia, Pseudomonas and Klebsiella species), Staph. aureus (including meticillin-resistant Staph. aureus (MRSA)) and anaerobes.

5. Factors predisposing to hospital-acquired pneumonia
Reduced host defences against bacteria
Reduced immune defences (e.g. corticosteroid treatment, diabetes, malignancy)
Reduced cough reflex (e.g. post-operative)
Disordered mucociliary clearance (e.g. anaesthetic agents)
Bulbar or vocal cord palsy

6. Factors predisposing to hospital-acquired pneumonia
Aspiration of nasopharyngeal or gastric secretions
Immobility or reduced conscious level
Vomiting, dysphagia, achalasia or severe reflux
Nasogastric intubation

7. Factors predisposing to hospital-acquired pneumonia
Bacteria introduced into lower respiratory tract
Endotracheal intubation/tracheostomy
Infected ventilators/nebulisers/bronchoscopes
Dental or sinus infection
Bacteraemia
Abdominal sepsis
I.v. cannula infection
Infected emboli

8. Nosocomial Pneumonia (Hospital-Acquired, Ventilator-Associated, and Health Care–Associated) Essentials of Diagnosis
Hospital-acquired pneumonia (HAP) occurs > 48 hours after admission to the hospital or other health care facility and excludes any infection present at the time of admission.
Health care–associated pneumonia (HCAP) occurs in community members whose extensive contact with healthcare has changed their risk for virulent and drug resistant organisms.
At least two of the following: fever, leukocytosis, purulent sputum.
New or progressive parenchymal opacity on chest radiograph.
Especially common in patients requiring intensive care or mechanical ventilation.

9. Clinical features and investigations
Universally agreed diagnostic criteria are lacking;
however, HAP should be considered in any hospitalised or ventilated patient who develops purulent sputum (or endotracheal secretions),
new radiological infiltrates, an otherwise unexplained increase in oxygen requirement,
a core temperature > 38.3°C, and a leucocytosis or leucopenia.

10. Clinical features and investigations
Circulating biomarkers may assist with the diagnosis but are currently non-specific.
Appropriate investigations are similar to those outlined for CAP, although whenever possible, microbiological confirmation should be sought.
In mechanically ventilated patients, bronchoscopy-directed protected brush specimens or bronchoalveolar lavage (BAL) may be performed.
Endotracheal aspirates are easy to obtain but less reliable

11. Management Adequate Gram-negative cover is usually provided by:
A third-generation cephalosporin (e.g. cefotaxime) with an aminoglycoside (e.g. gentamicin)
Meropenem or a monocyclic β-lactam (e.g. aztreonam) and flucloxacillin
MRSA is treated with intravenous vancomycin, but when appropriate, oral therapy may be considered with doxycycline, rifampicin or linezolid.
The nature and severity of most HAPs dictate that these antibiotics are all given intravenously, at least initially. Physiotherapy is important in those who are immobile or old. Adequate oxygen therapy, fluid support and monitoring are essential.

12. Prevention
The mortality from HAP is high at approximately 30%, emphasising the importance of prevention.
Good hygiene is paramount, including both hand washing and equipment.
Steps should be taken to minimise the chances of aspiration and limit the use of stress ulcer prophylaxis with proton pump inhibitors.
Oral antiseptic (chlorhexidine 2%) may be used to decontaminate the upper airway and some intensive care units use selective decontamination of the digestive tract when the anticipated requirement for ventilation will exceed 48 hours.

13. Respiratory infection in old age
Increased risk of and from respiratory infection: because of reduced immune responses, increased closing volumes, reduced respiratory muscle strength and endurance, altered mucus layer, poor nutritional status and the increased prevalence of chronic lung disease.
Predisposing factors: other medical conditions may predispose to infection, e.g. swallowing difficulties due to stroke increase the risk of aspiration pneumonia.
Atypical presentation: older patients often present with, for example, confusion, rather than breathlessness or cough.

14. Respiratory infection in old age
Mortality: the vast majority of deaths from pneumonia in developed countries occur in older people.
Influenza: has a much higher complication rate, morbidity and mortality. Vaccination significantly reduces morbidity and mortality in old age but uptake is poor.
Tuberculosis: most cases in old age represent reactivation of previous, often unrecognised disease and may be precipitated by steroid therapy, diabetes mellitus and the factors above. Cryptic miliary TB is an occasional alternative presentation. Older people more commonly suffer adverse effects from antituberculous chemotherapy and require close monitoring.

15. Suppurative pneumonia, aspiration pneumonia and pulmonary abscess
Suppurative pneumonia is characterised by destruction of the lung parenchyma by the inflammatory process and, although microabscess formation is a characteristic histological feature,
'pulmonary abscess' is usually taken to refer to lesions in which there is a large localised collection of pus, or a cavity lined by chronic inflammatory tissue, from which pus has escaped by rupture into a bronchus.

16. Suppurative pneumonia, aspiration pneumonia and pulmonary abscess
Suppurative pneumonia and pulmonary abscess often develop after the inhalation of septic material during operations on the nose, mouth or throat, under general anaesthesia, or of vomitus during anaesthesia or coma, particularly if oral hygiene is poor.
Additional risk factors for aspiration pneumonia include bulbar or vocal cord palsy, stroke, achalasia or oesophageal reflux, and alcoholism.
Aspiration tends to localise to dependent areas of the lung such as the apical segment of the lower lobe in a supine patient.
Suppurative pneumonia and abscess may also complicate local bronchial obstruction from a neoplasm or foreign body.

17. Suppurative pneumonia, aspiration pneumonia and pulmonary abscess
Infections are usually due to a mixture of anaerobes and aerobes in common with the typical flora encountered in the mouth and upper respiratory tract, and isolates of Bacteroides melaninogenicus, Fusobacterium necrophorum, anaerobic or microaerophilic cocci, and Bacteroides fragilis may be identified. When suppurative pneumonia or pulmonary abscess occurs in a previously healthy lung, the most likely infecting organisms are Staph. aureus or Klebsiella pneumoniae.

18. Suppurative pneumonia, aspiration pneumonia and pulmonary abscess
Bacterial infection of a pulmonary infarct or a collapsed lobe may also produce a suppurative pneumonia or lung abscess.
The organism(s) isolated from the sputum include Strep. pneumoniae, Staph. aureus, Strep. pyogenes, H. influenzae and, in some cases, anaerobic bacteria.
In many cases, however, no pathogen can be isolated, particularly when antibiotics have been given.
Recently, cases of community-acquired MRSA (CA-MRSA) have been reported.
This organism is distinct from MRSA but produces the toxin Panton-Valentine leukocidin, which causes a rapidly progressive severe necrotising pneumonia

19. Suppurative pneumonia, aspiration pneumonia and pulmonary abscess
Lemierre's syndrome is a rare cause of pulmonary abscesses.
The usual causative agent is the anaerobe, Fusobacterium necrophorum. It typically commences as a sore throat, painful swollen neck, fever, rigor, haemoptysis and dyspnoea, and bacterial spread into the jugular veins leads to thrombosis and metastatic spread of the organisms.
A non-infective form of aspiration pneumonia-exogenous lipid pneumonia-may follow the aspiration of animal, vegetable or mineral oils.

20. The clinical features of a suppurative pneumonia
Cough productive of large amounts of sputum which is sometimes fetid and blood-stained
Pleural pain common
Sudden expectoration of copious amounts of foul sputum occurs if abscess ruptures into a bronchus.
Clinical signs
High remittent pyrexia,Profound systemic upset
Digital clubbing may develop quickly (10-14 days)
Chest examination usually reveals signs of consolidation; signs of cavitation rarely found.Pleural rub common.
Rapid deterioration in general health with marked weight loss can occur if disease not adequately treated

21. Investigations
Radiological features of suppurative pneumonia include homogeneous lobar or segmental opacity consistent with consolidation or collapse.
Abscesses are characterised by cavitation and fluid level. Occasionally, a pre-existing emphysematous bulla becomes infected and appears as a cavity containing an air-fluid level. Sputum and blood should be sent for culture.

22. Management
Oral treatment with amoxicillin 500 mg 6-hourly is effective in many patients. Aspiration pneumonia can be treated with co-amoxiclav 1.2 g 8-hourly. If an anaerobic bacterial infection is suspected (e.g. from fetor of the sputum), oral metronidazole 400 mg 8-hourly should be added. Further modification of antibiotics should be informed by clinical response and the microbiological results.

23. Management
CA-MRSA is usually susceptible to a variety of oral non-β-lactam antibiotics, such as trimethoprim/sulfamethoxazole, clindamycin, tetracyclines and linezolid.
Parenteral therapy with vancomycin or daptomycin can also be considered. Fusobacterium necrophorum is highly susceptible to β-lactam antibiotics and to metronidazole, clindamycin and third-generation cephalosporins.
Prolonged treatment for 4-6 weeks may be required in some patients with lung abscess.

24. Management
Physiotherapy is of great value, especially when suppuration is present in the lower lobes or when a large abscess cavity has formed.
In most patients, there is a good response to treatment, and although residual fibrosis and bronchiectasis are common sequelae, these seldom give rise to serious morbidity.
Surgery should be contemplated if no improvement occurs despite optimal medical therapy.
Removal or treatment of any obstructing endobronchial lesion is essential.

25. Pneumonia in the immunocompromised patient
Patients immunocompromised by drugs or disease (particularly HIV) are at high risk of pulmonary infection.
The majority of infections are caused by the same pathogens that cause pneumonia in non-immunocompromised individuals, but in patients with more profound immunosuppression, unusual organisms, or those normally considered to be of low virulence or non-pathogenic, may become 'opportunistic' pathogens .
In addition to the more common agents, the possibility of Gram-negative bacteria, especially Pseudomonas aeruginosa, viral agents, fungi, mycobacteria, and less common organisms such as Nocardia asteroides, must be considered. Infection is often due to more than one organism.

26. Clinical features
Causes of immune suppression-associated lung infection:
Infecting organisms
Defective phagocytic function
Acute leukaemia Cytotoxic drugs Agranulocytosis
Gram-positive bacteria, including Staph. aureus Gram-negative bacteria Fungi, e.g. Candida albicans and Aspergillus fumigatus

27. Clinical features
Causes of immune suppression-associated lung infection:
Infecting organisms
Defects in cell-mediated immunity
Immunosuppressive drugs Cytotoxic chemotherapy Lymphoma Thymic aplasia
Viruses   Cytomegalovirus   Herpesvirus   Adenovirus   Influenza
Fungi   Pneumocystis jirovecii (formerly carinii)   Candida albicans   Aspergillus fumigatus
Defects in antibody production
Multiple myeloma Chronic lymphocytic leukaemia
Haemophilus influenzae Mycoplasma pneumoniae

28. Clinical features
These typically include fever, cough and breathlessness, but are less specific with more profound degrees of immunosuppression.
In general, the onset of symptoms tends to be less rapid when caused by opportunistic organisms such as Pneumocystis jirovecii and in mycobacterial infections, than with bacterial infections.
In P. jirovecii pneumonia, symptoms of cough and breathlessness can be present several days or weeks before the onset of systemic symptoms or the appearance of radiographic abnormality.

29. Diagnosis
The approach to investigation is informed by the clinical context and severity of the illness.
Invasive investigations such as bronchoscopy, BAL, transbronchial biopsy or surgical lung biopsy are often impractical, as many patients are too ill to undergo these safely.
However, 'induced sputum‘ may offer a relatively safe method of obtaining microbiological samples.
HRCT is useful in differentiating the likely cause:Focal unilateral airspace opacification favours bacterial infection, mycobacteria or nocardia.

30. Diagnosis
Bilateral opacification favours P. jirovecii pneumonia, fungi, viruses and unusual bacteria, e.g. nocardia.
Cavitation may be seen with N. asteroides, mycobacteria and fungi.
The presence of a 'halo sign' may suggest Aspergillus.
Pleural effusions suggest a pyogenic bacterial infection and are uncommon in P. jirovecii pneumonia.

31. Management
In theory, treatment should be based on an established aetiological diagnosis;
In practice, the causative agent is frequently unknown and broad-spectrum antibiotic therapy is required, such as:
A third-generation cephalosporin, or a quinolone, plus an antistaphylococcal antibiotic, or
An antipseudomonal penicillin plus an aminoglycoside.

32. Management
Thereafter treatment may be tailored according to the results of investigations and the clinical response.
Depending on the clinical context and response to treatment, antifungal or antiviral therapies may be added.
The management of P. jirovecii infection and that of invasive aspergillosis,need special consideration

33. Management
Mechanical ventilation increases the risk of nosocomial pneumonia and is associated with a greater mortality rate. It may be avoided by the early use of NIV.
The delivery of NIV via a hood is as effective as a face mask and allows the patient to expectorate, communicate and feed.

34. Aspergilloma Antifungal therapy Patient is not a candidate for surgery
Concomitant tissue invasion
Itraconazole with some help
Ampho B for invasive component.
Newer Azoles, Voriconazole , Posaconazole , and Ravuconazole.Their role is not clear.
Antibiotics for bacterial superinfection.