INFECTIONS OF THE RESPIRATORY TREE GENERAL RISK FACTORS

PNEUMONIA v Alcoholism – Immunocompromised

v Infection of the pulmonary parenchyma (alveolar sacs) v Asthma
v Proliferation of microbial pathogens at the alveolar level and the v Immunosuppression
host’s response Ø Extremes of ages
v Cause of significant morbidity and mortality Ø Steroid intake
v Institutionalization
PRESENT CLASSIFICATION v Age > 70 years
v Community-acquired Pneumonia (CAP)
Ø Acquired outside the hospital RISK FACTORS FOR PNEUMOCOCCAL PNEUMONIA
Ø Oral meds and O.P. follow-up v Dementia
Ø No need for confinement unless severe v Seizure disorders
v Health Care-associated Pneumonia (HCAP) v Heart failure
Ø Hospital-acquired Pneumonia (HAP) v Cerebrovascular disease
• More severe than CAP v Smoking
Ø Ventilator-associated Pneumonia (VAP) v COPD
v Alcoholism
MULTIDRUG-RESISTANT (MDR) PATHOGENS v HIV Infection
v Seen over the past 2 decades
v Associated with hospital-acquired pneumonia CLINICAL MANIFESTATIONS
PHYSICAL EXAMINATION FINDINGS
FACTORS TO MDResistance v Fever
v Development and widespread use of potent oral antibiotics Ø Extremes of ages do not usually present with this
v Earlier transfer of pts out of acute-care hospitals to their homes or v Tachycardia
various lower-acuity facilities v Chills and/or sweat
v Increased use of O.P. IV antibiotic therapy v Cough: Productive or Non-productive
v General aging of the population, and more extensive Ø Not all pneumonia have productive cough
immunomodulatory therapies v Dyspnea
v Pleurisy
PATHOPHYSIOLOGY Ø Inflamed pleural cavity = painful
ROUTES OF INFECTION v GI Symptoms: Nausea, Vomiting, Diarrhea
v Aspiration v Constitutional: Myalgia, HA, Fatigue, Arthralgia
Ø Most common Ø Not really sole property of pneumonia
Ø Small volume aspirations during sleep and decreased levels Ø May be seen in other disorders
of sensorium
v Inhalation PHYSICAL FINDINGS
Ø Contaminated droplets Tachypnea
v Hematogenous Spread Ø Impending doom Decreased breath sounds
v Contiguous Spread Ø Must intubate
Use of accessory muscles of
3 FACTORS CRITICAL TO PATHOGENESIS OF VAP Crackles
respiration
1. Colonization of the oropharynx with pathogenic microorganisms Consodilation: increased tactile
2. Aspiration of these organisms from the oropharynx into the lower Bronchial breath sounds
fremitus, dull percussion
respiratory tract Effusion: decreased tactile
3. Compromise of the normal host defense mechanisms Friction rub
fremitus, flat percussion
Hypotension
HOST’S DEFENSES
v Hair and turbinates in the nares DIAGNOSIS
v Branching architecture of the tracheobronchial tree CLINICAL DIAGNOSIS
Ø Mucocillia clearance and local antibacterial factors v Based on history and PE
v Gag and cough v PE: sensitivity = 58%; Specificity = 67%
Ø Without these, aspiration might happen v CXR
v Normal flora in the oropharynx
Ø Steroids – flora might be destroyed = immunocompromised ETIOLOGIC DIAGNOSIS
v Resident alveolar macrophages v Based on laboratory investigations
Ø “Security guards” v Used to guide treatment
Ø Find out what is causing the disease
ETIOLOGY v Sputum gram stain and culture / sensitivity
Ø Culture – grow in another medium
Ø Sensitivity – if drug administered is effective
v Blood CS
v Antigen tests
v Polymerase Chain Reaction
v Serology

OTHER PROCEDURES
v CBC
Ø Investigate presence of inflammation
v ABG
Ø Arterial Blood Gas
Ø To determine levels of O2 and CO2
v CT Scan
v Thoracentesis
Ø Aspiration of fluids in the lungs
 TREATMENT DIAGNOSTIC APPROACH
v Antibiotics
v Other meds
v Hydration
v Oxygenation
v Assisted Ventilation
v Physiotherapy

PREVENTION
v Good hygiene
v Vaccination
v Smoking Cessation

TREATMENT
1. Treatment of infection
COMPLICATIONS 2. Improved clearance of tracheobronchial secretions
v Respiratory failure 3. Reduction of inflammation
v Shock and multi-organ failure 4. Treatment of an identifiable underlying problem
v Bleeding diathesis
Ø Disseminated Intravascular Coagulation (DIC) might use PULMONARY TUBERCULOSIS
up all coagulate ® after clotting, pt bleeds v One of the oldest disease known to affect humans
v Exacerbation of comorbid illnesses v Major cause of death worldwide
v Metastatic infection v Mycobacterium tuberculosis complex
v Lung abscess v Usually affects the lungs
rd
v Pleural effusion v Other organs are involved in up to 1/3 of cases
v Bronchiectasis v If properly treated, tuberculosis caused by drug-susceptible strains
v Prolonged hospital stay is curable in virtually all cases
v Muscle loss and general debilitation v If untreated, the disease may be fatal within 5 years in 50 – 65%
v Death of cases
v Airborne spread of droplet nuclei
BRONCHIECTASIS
v Abnormal and permanent dilatation of bronchi EPIDEMIOLOGY
v Focal – Involves a limited region of lung parenchyma v 2005 WHO
v Diffuse – More widespread distribution Ø 8.8 million new cases of tuberculosis occurred worldwide in
v In older individuals 2005
v F>M • 95% in developing countries of Asia (4.9 million), Africa
(2.6 million), Middle East (0.6 million), and Latin America
PATHOLOGY (0.4 million)
v Destructive and inflammatory changes in the walls of medium- Ø 1.6 million deaths from tuberculosis
sized airways • 95% in developing countries
v Neutrophils, elastase and matrix metalloproteinases
v Fibrosis, emphysema, atelectasis, ulcerations, squamous FROM EXPOSURE TO INFECTION
metaplasia, glandular hyperplasia v Most commonly
v Pools of thick purulent material in dilated airways transmitted from
v Peripheral airways are often occluded by secretions or obliterated a person with
and replaced by fibrous tissue infectious
v Increased vascularity, AV anastomoses pulmonary
tuberculosis to
ETIOLOGY AND PATHOGENESIS others by
v Consequence of inflammation and destruction of the structural droplet nuclei
components of the bronchial wall v Tiny droplets dry
Ø With destruction = more bacteria = more infection = more rapidly
destruction v Smallest (<5 –
v Infection is the usual cause of the inflammation 10 µm in
v As protection against infection is compromised, the dilated airways diameter) may
become more susceptible to colonization and growth of bacteria remain
suspended in
CLINICAL MANIFESTATIONS the air for
v Persistent or recurrent cough several hours and may reach terminal air passages when inhaled
v Purulent Sputum production v As many as 3000 infectious nuclei per cough
v Repeated, purulent respiratory tract infections should raise clinical
suspicion of bronchiectasis DETERMINANTS OF TRANSMISSION
v Hemoptysis occurs in 50 – 70% of cases v Probability of contact with a person who has an infectious form of
v Systemic symptoms tuberculosis
Ø Fever v Intimacy and duration of that contact
Ø Fatigue v Degree of infectiousness of the case
Ø Weight loss v Shared environment in which the contact takes place
Ø Myalgias
v Dyspnea or wheezing generally reflects either widespread
bronchiectasis or underlying COPD
INFECTIOUS PATIENTS WITH PTB v Cough
v AFB-positive sputum v Hemoptysis
Ø AFB = Acid-Fast Bacilli v Pleuritic Chest Pain
v Cavitary pulmonary disease v Dyspnea
5 7
v Laryngeal tuberculosis with 10 – 10 AFB/mL

NON-INFECTIOUS PATIENTS WITH PTB

v Sputum smear-negative / Culture-positive tuberculosis
v Culture-negative pulmonary disease
v Extrapulmonary tuberculosis

RISK OF DEVELOPING DISEASE

v Largely on endogenous factors:
Ø Individual’s innate immunologic and non-immunologic
defenses
Ø Level of function of cell-mediated immunity

PRIMARY PTB
v Clinical illness directly following infection
v Common among
Ø Children up to 4 y/o – may be from adults
Ø Immunocompromised persons
v May be severe and disseminated
v Not generally associated with high-level transmissibility

POST-PRIMARY PTB
v Usually in adults
EXTRAPULMONARY TB
v Dormant bacilli persist for years before reactivating
v Tuberculosis Lymphadenitis
v More often infectious than primary disease
v Pleural TB
v 10% of infected persons will eventually develop disease in their
Ø Not considered pulmonary TB
lifetime
Ø Not contagious
v The risk is much higher among HIV-infected persons
v Upper Airway TB
v Reinfection favors development of disease
v GUT TB
v Skeletal TB
NATURAL HISTORY
v CNS TB
PRE-TREATMENT ERA
v GIT TB
v 1/3 of pts died within 1 year after diagnosis
v Tuberculous Pericarditis
v ½ died within 5 years
v Miliary / Disseminated TB
v The 5-year mortality rate among sputum smear-positive cases was
65%
DIAGNOSIS
v Of the survivors at 5 years
v AFB Microscopy
Ø ~ 60% had undergone spontaneous remission
v Mycobacterial Culture
Ø ~ 40% were still secreting tubercle bacilli
v Nucleic Acid Amplification
v Radiography
“With effective, timely, and proper chemotherapy, patients have a
v Tuberculin Skin Testing
very high chance of being cured”
v Others
“Improper use of anti-TB drugs, while reducing mortality rates,
TREATMENT
may also result in large numbers of chronic infectious cases,
v First Line of Drugs
often with drug-resistant bacilli.”
Ø Rifampicin
Ø Isoniazid
CLINICAL MANIFESTATION
Ø Pyrizanamide
PRIMARY PTB
Ø Ethambutol
v Middle and lower lung zones
Ø Streptmycin
v A small calcified nodule (Ghon Lesion)
v Pleural effusion
v Cavitation (Progressive PTB)
v Almost invariably accompanied by hilar or mediastinal
lymphadenopathy
v Obstruction and subsequent segmental or lobar collapse
v Metastasis

POST-PRIMARY PTB
v Usually apical and posterior segments of upper lobes and
superior segments of the lower lobes
v Small infiltrates to extensive cavitary disease
v Tuberculous pneumonia
v 1/3 of untreated pts reportedly die of severe PTB within a few
weeks or months after onset
v Some have spontaneous remission or proceed along a chronic,
progressively debilitating course

SIGNS AND SYMPTOMS

v Fever and night sweats
v Weight loss
v Anorexia
v General malaise
v Weakness