Pulmonary Infections-Part Two

Assistant Professor Dr. Ahmed Hamdi

M.B.Ch.B F.I.B.M.S-Pathology
Community-Acquired Viral Pneumonia
Common viral infections include influenza virus types A and B,
respiratory syncytial viruses, human metapneumovirus, adenovirus,
rhinoviruses, rubeola, and varicella viruses.
Any of these agents can cause a relatively mild upper respiratory tract
infection, recognized as the common cold, or a more severe lower
respiratory tract infection.
Factors that favor extension of the infection to the lung include extremes
of age, malnutrition, alcoholism, and underlying debilitating illnesses.
Human Coronaviruses
Coronaviruses are enveloped, positive-sense RNA viruses that infect humans
and several other vertebrate species.
Weakly pathogenic coronaviruses cause mild cold-like upper respiratory tract
infections, while highly pathogenic ones may cause severe, often fatal
pneumonia. An example of a highly pathogenic type is SARS-CoV-2, a strain
that emerged in late 2019 in China that is producing a still evolving pandemic
as of early 2020.
Highly pathogenic coronaviruses like SARS-CoV-2 bind the ACE2 protein on
the surface of pulmonary alveolar epithelial cells (SARS-CoV-2 uses the
human angiotensin-converting enzyme 2 (ACE2) to bind to host cells and to
mediate membrane fusion.), explaining the tropism of these viruses for the
lung. With highly pathogenic forms in susceptible hosts, typically older
individuals with morbid conditions, the host immune response and locally
released cytokines often produce acute lung injury and ARDS.
Aspiration Pneumonia
Aspiration pneumonia occurs in markedly ill patients or those who
aspirate gastric contents either while unconscious (e.g., after a stroke) or
during repeated vomiting.
These patients have abnormal gag and swallowing reflexes that
predispose to aspiration. The resultant pneumonia is partly chemical due
to the irritating effects of gastric acid and partly bacterial (from the oral
flora).
Typically, more than one organism is found on culture, aerobes being
more common than anaerobes.
This type of pneumonia is often necrotizing, results in a severe clinical
course, and is a frequent cause of death. In patients who survive, lung
abscess is a common complication.

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Lung Abscess
The term pulmonary abscess describes a local suppurative process that
produces necrosis of lung tissue.
Oropharyngeal surgical or dental procedures, sinobronchial infections, and
bronchiectasis play important roles in their development.
Etiology and Pathogenesis
Under appropriate circumstances any bacterial pathogen can produce an
abscess; those that do so most commonly include aerobic and anaerobic
streptococci, S. aureus, and a host of gram-negative organisms.
Mixed infections often occur because of the important causal role played by
inhalation of foreign material.
Anaerobic organisms normally found in the oral cavity, including members of
the Bacteroides, Fusobacterium, and Peptococcus genera, are the exclusive
isolates in about 60% of cases. The causative organisms are introduced by the
following mechanisms:
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1. Aspiration of infective material (the most frequent cause).
Risk factors include suppressed cough reflexes (e.g., acute alcohol intoxication, opioid abuse, coma,
anesthesia, seizure disorders), severe dysphagia (e.g., neurologic deficits, esophageal disease),
protracted vomiting, and poor dental hygiene. Aspiration first causes pneumonia, which progresses to
tissue necrosis and formation of lung abscess.
2. Antecedent primary lung infection.
Postpneumonic abscess formations are usually associated with S. aureus, K. pneumoniae, and
pneumococcus. Posttransplant or otherwise immunosuppressed individuals are at special risk.
3. Septic embolism
Infected emboli may arise from thrombophlebitis in any portion of the systemic venous circulation or
from the vegetations of infective bacterial endocarditis on the right side of the heart and lodge in the
lung.
4. Neoplasia
Secondary infection is particularly common in bronchopulmonary segments obstructed by a primary or
secondary malignancy (postobstructive pneumonia).
5. Miscellaneous
Traumatic penetrations of the lungs; direct extension of suppurative infections from the esophagus,
spine or pleural cavity; and hematogenous seeding of the lung by pyogenic organisms all may lead to
lung abscess formation.
When all these causes are excluded, there are still cases in which no discernible basis for the abscess
formation can be identified. These are referred to as primary cryptogenic lung abscesses.
Chronic Pneumonia
Chronic pneumonia is most often a localized lesion in the immunocompetent patient, with or without regional
lymph node involvement.
Typically the inflammatory reaction is granulomatous and is caused by bacteria (e.g., Mycobacterium
tuberculosis) or fungi (e.g., Histoplasma capsulatum).
Histoplasmosis
H. capsulatum infection is acquired by inhalation of dust particles from soil contaminated with bird or bat
droppings that contain small spores (microconidia), the infectious form of the fungus.
Like M. tuberculosis, H. capsulatum is an intracellular pathogen that is found mainly in phagocytes. The clinical
presentations and morphologic lesions of histoplasmosis bear a striking resemblance to those of tuberculosis,
including
1. Self-limited and often latent primary pulmonary involvement, which may result in coin lesions on chest
radiography
2. Chronic, progressive, secondary lung disease, which is localized to the lung apices and causes cough, fever,
and night sweats.
3. Spread to extrapulmonary sites, including mediastinum, adrenal glands, liver, or meninges; and
4. Widely disseminated disease in immunocompromised patients.
Histoplasmosis can occur in immunocompetent individuals but as per usual is more severe in those with
depressed cell mediated immunity.
Tuberculosis
Tuberculosis is a chronic pulmonary and systemic disease caused most often by
(Mycobacterium) M. tuberculosis, and the leading infectious cause of death worldwide.
The source of transmission is humans with active tuberculosis who release
mycobacteria into the sputum. Oropharyngeal and intestinal tuberculosis contracted by
drinking milk contaminated with Mycobacterium bovis is rare in countries where milk
is routinely pasteurized, but it is still seen in countries that have tuberculous dairy cows
and unpasteurized milk.
It is important that infection with M. tuberculosis be differentiated from active disease.
Infection refers to the presence of bacteria in the body, which may be symptomatic
(active disease) or not (latent infection).
Most infections are acquired by person-to-person transmission of airborne organisms
from an active case to a susceptible host.
In most healthy people primary tuberculosis is asymptomatic, although it may cause
fever and pleural effusion. Generally, the only evidence of infection, if any remains, is a
tiny, fibrocalcific pulmonary nodule at the site of the infection.
Viable organisms may remain dormant in such lesions for decades. If immune defenses
are lowered, the infection may be reactivated, producing communicable and potentially
life-threatening disease.
Immunity to M. tuberculosis is primarily mediated by Th1 cells, which stimulate
macrophages to kill the bacteria. This immune response, although largely effective,
comes at the cost of accompanying tissue destruction.
Reactivation of the infection or re-exposure to the bacilli in a previously sensitized
host results in rapid mobilization of a defensive reaction but also increased tissue
necrosis.
Clinical Features
Clinical tuberculosis is separated into two important types that differ in
pathophysiology: primary tuberculosis, which occurs with the first infection, and
secondary tuberculosis, which occurs in an individual who has been previously
infected by M. tuberculosis.
Primary tuberculosis is the form of disease that develops in a previously unexposed
and therefore unsensitized person.
With primary tuberculosis, the source of the organism is exogenous. In most people,
the primary infection is contained, but in others, primary tuberculosis is progressive
and more often resembles an acute bacterial pneumonia with consolidation of the
lobe, hilar lymphadenopathy, and pleural effusion.
Lymphatic and hematogenous dissemination following primary infection may result
in the development of tuberculous meningitis and miliary tuberculosis.
Secondary tuberculosis is the pattern of disease that arises in a previously sensitized
host. It may follow shortly after primary tuberculosis, but more commonly it appears
months to years after the initial infection, usually when host resistance is weakened.
It most commonly arises from reactivation of a latent infection, but may also result
from exogenous reinfection in the case of weaking host immunity or when a large
dose of virulent bacilli overwhelms the host immune system.
Secondary pulmonary tuberculosis classically involves the apex of the upper lobes of
one or both lungs.
Because of the preexistence of hypersensitivity, the bacilli induce a prompt and
marked tissue response that tends to wall off the focus of infection. As a result, the
regional lymph nodes are less prominently involved early in secondary disease than
they are in primary tuberculosis. On the other hand, cavitation occurs readily in the
secondary form.
Miliary tuberculosis: Type of tuberculosis that occurs when a large number of the
bacteria travel through the bloodstream and spread throughout the body

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Morphology
• Hallmark is necrotizing granulomatous inflammation, composed of
central necrotic zone surrounded by epithelioid histiocytes with varied
number of multinucleated giant cells and lymphocytes
• Multinucleated giant cells may contain Langhans type giant cells
(nuclei arranged in a horseshoe shaped pattern at the periphery of the
cell) but Langhans type giant cells are not specific for TB infection
• Organisms are usually present within the central zone of necrosis, seen
on special stains (in some cases)
• Nonnecrotizing granulomas can be present as well