Pulmonary Infection

ATELECTASIS AND PULMONARY INFECTION Ella C. Lim, M.D., DPSP

ATELECTASIS 

The long of lung volume due to inadequate expansion of the air spaces (collapse).

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Types:  Resorption

Atelectasis  Compression Atelectasis  Atelectasis due to loss of surfactant

ATELECTASIS 

Compression Atelectasis  Air or fluid in the pleural cavity under increased pressure (e.g., tension pneumothorax, effusion) collapses small airways under the pleura.

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Resorption Atelectasis  Airway obstruction prevents air from reaching the alveoli; May

RESORPTION ATELECTASIS 

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Causes of obstruction:  Mucous or mucoplurulent plug  aspiration of foreign material  bronchogenic carcinoma Cause of alveolar collapse:  Lack of air  Distal resorption of preexisting air Most common cause of fever 24-36 hours after surgery – develops into

ATELECTASIS due to Loss of Surfactant  

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Respiratory distress in newborns Causes of decreased surfactant in fetal lungs:  Prematurity  Maternal diabetes  Cesarean section Microscopic findings: collapsed alveoli lined by hyaline membranes derived from necrotic cellular debris

PULMONARY INFECTION   

Tuberculosis Pneumonia Other pulmonary infections

TUBERCULOSIS Epidemiology:  Inhalation of the bacterium (droplet infection) Screening: PPD skin test – does not distinguish active from inactive disease Primary TB  initially localizes in a subpleural location (upper part of the lower lobes or lower part of the upper

TUBERCULOSIS 

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Ghon complex – spread of infection to hilar lymph nodes with caseous necrosis in nodes Usually resolves – calcified granuloma or area of scar tissue (may be a nidus for reactivation TB)

Secondary (reactivation) TB  Cavitary lesion involves one or both apices in the upper lobes 

TUBERCULOSIS Complications of secondary (reactivation) TB:  Miliary spread in lungs – invasion into the bronchus or lymphatics 

Systemic miliary spread – invasion of pulmonary vein; kidneys is the most common extrapulmonary site

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Massive hemoptysis, bronchiectasis,

TUBERCULOSIS 

Most common cause of TB in AIDS patients:

Mycobacterium aviumintracellulare

TUBERCULOSIS 

 

                                                                      

TUBERCULOSIS   

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Ghon complex Calcified lymph nodes Subpleural nodule

CXR & photo: Note a calcified, wellcircumscribed nodule in the left lung an old healed focus of primary tuberculosis; characteristically peripheral in location. Other calcified nodules can be seen in the CXR in the left hilar region where the clavicle appears to touch the arch

TUBERCULOSIS 

The peripheral and mediastinal calcified nodules together form the Ghon complex.

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What are the different stages of pulmonary tuberculosis?

TUBERCULOSIS  Primary pulmonary tuberculosis: residuum of which is the Ghon complex, usually asymptomatic. 

Secondary, or reactivation tuberculosis: occurs years after the primary infection, most commonly involves the apex of the lung - typically causes caseous necrosis and cavitation.

TUBERCULOSIS 

Either of these types of tuberculosis may become progressive, that is, evolve into miliary tuberculosis or tuberculous bronchopneumonia.

TUBERCULOSIS

 

                                                                      

TUBERCULOSIS Cystic cavities  Patchy consolidation Note:  The cavities in the upper lobes pathologic & radiographic findings in secondary, or reactivation tuberculosis.  Patchy consolidation is present in the upper lobe - may represent either superimposed bronchopneumonia or progressive spread of tuberculosis. 

TUBERCULOSIS 

How does the morphology of tuberculosis differ in the immunocompetent vs. the immunosuppressed host?

TUBERCULOSIS Immunosuppressed patients more likely to have disseminated infection involving lymph nodes, blood, central nervous system, and bowel.  Less likely to have well-formed granulomas  More likely to consist of histiocytes and necrosis. 

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TUBERCULOSIS 

 

                                                                      

TUBERCULOSIS 

Caseous necrosis

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Zone of epithelioid cells

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Large central area of caseous necrosis - seen as granular pink structureless material with complete destruction of lung parenchyma

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Caseous material - surrounded by a

TUBERCULOSIS

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What are the causes of caseous necrosis?

TUBERCULOSIS 

Causes of Caseous Necrosis:  Tuberculosis  Leprosy  Fungal infections

FUNGAL PULMONARY INFECTION 

The differential diagnosis of granuloma formation includes histoplasmosis, blastomycosis, and coccidioidomycosis.

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Special stains for these organisms help differentiate the cause of the granulomatous inflammation.

TUBERCULOSIS

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How does caseous necrosis differ from coagulative necrosis under the microscope?

TUBERCULOSIS 

In caseous necrosis, there is total loss of tissue structure.

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In coagulative necrosis, cell outlines are retained.

TUBERCULOSIS 

 

                                                                      

TUBERCULOSIS 

Caseous necrosis

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Zone of epithelioid cells

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Langhan’s Type Giant cell

TUBERCULOSIS 

Caseous necrosis - seen as pink granular structureless material that has destroyed the lung alveoli.

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Epithelioid cells - surrounding the caseous material are elongated cells with indistinct cell boundaries.

TUBERCULOSIS

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What is the origin of epithelioid cells?

TUBERCULOSIS

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They are transformed macrophages.

TUBERCULOSIS

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Is this lesion an example of granulomatous inflammation or granulation tissue?

TUBERCULOSIS

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This lesion is granulomatous inflammation.

TUBERCULOSIS 

 

                                                                      

TUBERCULOSIS 

Reddish rods = acid-fast bacteria (Mycobacterium tuberculosis) seen within an area of caseous necrosis.

TUBERCULOSIS CASE 

A 68-year-old man presented with weight loss over a four-month period and the recent onset of fever and chills at night.

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Admission chest x-ray revealed an irregular opacity of the right lung with pleural effusion.

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Thoracocentesis was performed, and cytologic examination of the pleural

TUBERCULOSIS CASE 

Abdominal CT revealed hepatomegaly and diffuse lymphadenopathy.

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The patient was treated with multiple broad-spectrum antibiotics, but his fever did not respond.

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His hospital course was also notable for electrolyte imbalances, including hyperkalemia and hyponatremia.

TUBERCULOSIS CASE 

Despite supportive care, the patient expired on the fourth hospital day, and an autopsy was performed.

TUBERCULOSIS 

Why do you think this patient developed tuberculosis?

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Can this explain the other clinical features in this patient?

TUBERCULOSIS 

Cancer patients are often immunosuppressed. Most likely, immunosuppression allowed reactivation of some old focus of TB in this patient after he developed cancer.

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Disseminated TB could cause lymphadenopathy and hepatomegaly. Destruction of the adrenal cortex by tuberculosis is

PNEUMONIA CASE 

A 45/M was found wandering downtown with an alcohol breath and coughing up thin, rusty sputum.

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He was brought to ER and said he was fine the day before but that morning he had begun to shake uncontrollably and felt alternately cold then hot and sweaty. He said his chest hurt when he breathed and

PNEUMONIA CASE 

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The patient’s past medical history included a hospital admission for tuberculosis 10 years ago. Physical examination revealed a thin male who was anxious and mildly cyanotic. Other abnormal physical findings included tachypnea and chest splinting, accompanied by fine rales and decreased breath sounds by auscultation over the right lower

PNEUMONIA CASE 

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His temperature was 39.2°C, but his pulse was normal. WBC count was 16 x 103/µL (ref. range 4.1-10.9 x 103/µL) with 70% polys, 18% bands, and 12% lymphocytes. Blood gases demonstrated hypoxia and respiratory alkalosis. Sputum was collected for smear and culture. A gram stain of the sputum showed lancet-shaped, gram-positive

PNEUMONIA CASE 

The patient was admitted and promptly begun on antibiotics and oxygen therapy.

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However, he became progressively more hypoxic, was placed in the ICU on increasing concentrations of oxygen, and expired 24 hours after admission.

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During this time, both of the blood

PNEUMONIA What predisposed this patient to get pneumonia?

PNEUMONIA 

This patient is a chronic alcoholic, probably malnourished and somewhat immunosuppressed.

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Alcoholics are also prone to aspirate bacteria-laden secretions from the upper respiratory tract during an alcoholic bout.

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Impaired mucociliary clearance and defective phagocytic functions of

PNEUMONIA 

What accounts for the rusty sputum in this case?

PNEUMONIA 

The sputum is composed of the exudate in the alveoli; it is rusty because of the red cells in the exudate.

PNEUMONIA 

Community Acquired Pneumonia (CAP)  Typical  Atypical

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Nosocomial Pneumonia (hospitalacquired)

TCA PNEUMONIA 

Risk factors:  Splenic dysfunction  Immunodeficiency (old age, AIDS)

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BRONCHOPNEUMONIA

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LOBAR PNEUMONIA

PNEUMONIA

What is the most common pathogen causing typical community-acquired pneumonia?

PNEUMONIA  Streptococcus

pneumoniae

PNEUMONIA 

What are the complications of pneumonia?

Complications of PNEUMONIA Abscess formation  Empyema  organization with subsequent fibrosis (excessive scar tissue)  bacteremic dissemination (sepsis) 

PNEUMONIA CLINICAL FINDINGS:  Sudden onset of symptoms: high fever w/ productive cough  Signs of consolidation (alveolar infiltrate): dullness to percussion ; increased vocal tactile fremitus LABORATORY FINDINGS:  Positive gram stain, neutrophilic leukocytosis

PNEUMONIA 

 

                                                                      

PNEUMONIA Cardiac silhouette  Infiltrate  Note: The usual angle between the right heart border and the right diaphragm has been lost.  Diffuse infiltrate extends to the fissure between the right middle and right lower lobes.  This is a lobar pneumonic 

PNEUMONIA

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What would bronchopneumonia look like radiographically?

PNEUMONIA 

Bronchopneumonia tends to be patchy, although, if severe, even bronchopneumonia may become confluent and involve an entire lobe of lung.

BRONCHOPNEUMONIA

 

                                                                      

BRONCHOPNEUMONIA Bronchopneumonia  Abscess 

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There is extensive involvement of the anterior aspect of the lung by bronchopneumonia. Bronchopneumonia - patchy consolidation and follows the distribution of the bronchi and bronchioles.

BRONCHOPNEUMONIA 

Begins as ACUTE BRONCHITIS and spreads locally into the lungs

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Usually involves the LOWER LOBES or RIGHT MIDDLE LOBE

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Microabscesses in areas of consolidation

BRONCHOPNEUMONIA 

What organisms are particularly associated with abscess formation?

BRONCHOPNEUMONIA Staphylococcus aureus  Klebsiella pneumoniae  type 3 Pneumococcus. 

BRONCHOPNEUMONIA

 

                                                                      

BRONCHOPNEUMONIA  

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Bronchopneumonia Normal Lung Note: the focal distribution of the inflammatory process in bronchopneumonia. The inflammation is in a bronchiolar distribution - there is abundant inflammation within and surrounding the bronchioles. Some normal areas

Lungs, LOBAR PNEUMONIA 

 

                                                                      

PNEUMONIA  

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Bronchopneumonia is patchy Lobar pneumonia is diffuse, complete or almost complete consolidation of a lung lobe See contrast between the stages of red hepatization (right) and gray hepatization (left). The lower lobes are expanded Red hepatization stage - the gross appearance reflects the microscopic features of congestion and

PNEUMONIA 

Gray hepatization stage congestion becomes less prominent and red blood cells that have exited into the alveoli lyse, leaving behind the fibrinosuppurative exudate.

LOBAR PNEUMONIA

 

                                                                      

LOBAR PNEUMONIA  

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Congested alveolar septa Interstitial pneumonitis The alveolar spaces are filled with neutrophils (PMNs) and a fibrinous exudate. The alveolar septa are easily demarcated because of congestion with red cells. Because of the alveolar exudate, the lung becomes airless (solid). This is called consolidation.

INTERSTITIAL PNEUMONITIS 

Interstitial pneumonitis - the typical inflammatory response to viruses and mycoplasma, is very different from acute bacterial pneumonia.

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Clinical presentation of IP nonproductive cough, fever, and malaise. Pathologically, there is a lymphoplasmacytic infiltrate in the alveolar septa. Note the absence of inflammatory cells in the alveolar

LOBAR PNEUMONIA What are the components of the inflammatory reaction to bacteria?

LOBAR PNEUMONIA 

Bacteria typically cause acute inflammation, characterized by congestion, formation of an exudate, and a polymorphonuclear infiltrate.

LOBAR PNEUMONIA 

While viral pneumonitis is usually self-limited, some patients develop pulmonary complications secondary to viral pneumonitis. What are these?

LOBAR PNEUMONIA 

The most common complications of viral pneumonitis are:  secondary bacterial pneumonia and  diffuse alveolar damage

ATYPICAL COMMUNITYACQUIRED PNEUMONIA 

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Usually involves school-age children & young adults Occurs in crowded conditions (school, prison, slums) Most often caused by Mycoplasma pneumoniae Other pathogens: Chlamydia pneumoniae, C. trachomatis, RSV, Influenza viruses, adenovirus

ATYPICAL COMMUNITYACQUIRED PNEUMONIA 

Patchy interstitial pneumonia – mononuclear infiltrate; alveolar spaces usually free of exudate (no signs of consolidation)

CLINICAL FINDINGS:  Insidious onset with low grade fever  Flu-like symptoms – pharyngitis, laryngitis, mildly productive cough

HOSPITAL-ACQUIRED PNEUMONIA 

Associated with severe underlying disease, antibiotic therapy, immunosuppression, respirators, and indwelling venous catheters

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Gram-negative bacteria (e.g., E. coli, Pseudomonas aeruginosa) & grampositive bacteria (e.g., Staphylococcus aureus)

PNEUMONIA in the IMMUNOCOMPROMISED 

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Usually in AIDS patients and in bone marrow transplantation Common opportunistic infections: CMV, Pneumocystis carinii

SYSTEMIC FUNGAL RESPIRATORY INFECTIONS 

Usually produces a granulomatous inflammatory reaction with or without caseation

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Most common systemic fungal infection – Histoplasma capsulatum

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Fungal respiratory pathogens: Candida albicans, Aspergillus fumigatus, Coccidioides immitis,

FUNGAL PNEUMONIA

 

                                                                                         

FUNGAL PNEUMONIA

Right middle lobe  Intravascular thrombi  Infarct w/ hyperemic border 

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Diffuse consolidation and vascular thrombosis with infarction of surrounding parenchyma of the right middle lobe of the lung.

FUNGAL PNEUMONIA What are the mechanisms of pulmonary damage in immunocompromised patients with fungal infection?

FUNGAL PNEUMONIA 

Patients with fungal pneumonia may have pulmonary damage from vascular occlusion by the fungus, resulting in ischemic necrosis, or from direct invasion by and host reaction to the organism.

FUNGAL PNEUMONIA

 

                                                                      

FUNGAL PNEUMONIA  

Pulmonary arterial wall Fungal hyphae

This fungus is causing pulmonary damage by occluding a major arterial branch, resulting in a surrounding infarct.  Aspergillus and fungi of the Mucorales group are the most likely to produce this type of 

FUNGAL PNEUMONIA Aside from the lungs, what are the other two sites in the body frequently infected by Mucor?

FUNGAL PNEUMONIA Paranasal sinuses with extension to the brain (rhinocerebral Mucor).

LUNG ABSCESS Etiology:  Aspiration of oropharyngeal material (e.g., carious teeth, infected sinus or tonsillar material)  Complication of bacterial pneumonia Gross findings:  Vary in size and location  Those due to aspiration are primarily on the RIGHT side of the lung  Most common aspiration site –

LUNG ABSCESS Clinical Findings:  Spiking fever with productive cough – foul smelling sputum due to anaerobes (e.g., Fusobacterium)  CXR – cavitation with air-fluid level Aspiration sites in the lungs:  Standing or sitting position – posterobasal segment of the right lower lobe (RLL)

The End