Pulmonary Infections pdf - سرى سلمان

د. سرى سلمان عجام

Respiratory diseases

Pulmonary Infections

Respiratory tract infections are more frequent than infections of any other
organ and account for the largest number of workdays lost in the general
population. The vast majority are upper respiratory tract infections caused
by viruses (common cold, pharyngitis), but bacterial, viral, mycoplasmal,
and fungal infections of the lung (pneumonia) still account for an
enormous amount of morbidity

Pneumonia can be very broadly defined as any infection of the lung

parenchyma

Pneumonia can result whenever the local defense mechanisms are
impaired or the systemic resistance of the host is lowered. Factors that
affect resistance in general include chronic diseases, immunological
deficiency, treatment with immunosuppressive agents, and leukopenia.

The local defense mechanisms of the lung can be interfered with by many
factors, such as the following:

• Loss or suppression of the cough reflex, as a result of coma,
anesthesia, neuromuscular disorders, drugs, or chest pain (may lead to

aspiration of gastric contents

)

•

Injury to the mucociliary apparatus, by either impairment of ciliary
function or destruction of ciliated epithelium, due to cigarette smoke,
inhalation of hot or corrosive gases, viral diseases, or genetic defects of

ciliary function (e.g., the immotile cilia syndrome

)

•

Accumulation of secretions in conditions such as cystic fibrosis and
bronchial obstruction

•

Interference with the phagocytic or bactericidal action of alveolar
macrophages by alcohol, tobacco smoke, anoxia, or oxygen intoxication

• Pulmonary congestion and edema

The Pneumonia Syndromes

COMMUNITY-ACQUIRED ACUTE PNEUMONIA

Streptococcus pneumoniae

Haemophilus influenzae

Moraxella catarrhalis

Staphylococcus aureus

Legionella pneumophila

Enterobacteriaceae (Klebsiella pneumoniae) and Pseudomonas spp

COMMUNITY-ACQUIRED ATYPICAL PNEUMONIA

Mycoplasma pneumoniae

Chlamydia spp. (C. pneumoniae, C. psittaci, C. trachomatis

)

Coxiella burnetii (Q fever

)

Viruses: respiratory syncytial virus, parainfluenza virus (children);
influenza A and B (adults); adenovirus (military recruits); SARS virus

HOSPITAL-ACQUIRED PNEUMONIA

Gram-negative rods, Enterobacteriaceae (Klebsiella spp., Serratia

marcescens, Escherichia coli) and Pseudomonas spp

Staphylococcus aureus (usually penicillin resistant

)

ASPIRATION PNEUMONIA

Anaerobic oral flora (Bacteroides, Prevotella, Fusobacterium,
Peptostreptococcus), admixed with aerobic bacteria (Streptococcus
pneumoniae, Staphylococcus aureus, Haemophilus influenzae, and

Pseudomonas aeruginosa

)

CHRONIC PNEUMONIA

Nocardia

Actinomyces

Granulomatous: Mycobacterium tuberculosis and atypical
mycobacteria, Histoplasma capsulatum, Coccidioides immitis,
Blastomyces dermatitidis

NECROTIZING PNEUMONIA AND LUNG ABSCESS

Anaerobic bacteria (extremely common), with or without mixed
aerobic infection

Staphylococcus aureus, Klebsiella pneumoniae, Streptococcus

pyogenes, and type 3 pneumococcus (uncommon

)

PNEUMONIA IN THE IMMUNOCOMPROMISED HOST

Cytomegalovirus

Pneumocystis jiroveci

Mycobacterium avium-intracellulare

Invasive aspergillosis

Invasive candidiasis

SARS, severe acute respiratory syndrome

Streptococcus pneumoniae

Streptococcus pneumoniae, or pneumococcus, is the most common cause of
community-acquired acute pneumonia. Examination of Gram-stained sputum is an
important step in the diagnosis of acute pneumonia. The presence of numerous
neutrophils containing the typical gram-positive, lancet-shaped diplococci supports
the diagnosis of pneumococcal pneumonia, but it must be remembered that S.
pneumoniae is a part of the endogenous flora in 20% of adults, and therefore false-
positive results may be obtained. Isolation of pneumococcifrom blood cultures is
more specific but less sensitive (in the early phase of illness, only 20% to 30% of
patients have positive blood cultures). Pneumococcal vaccines containing capsular
polysaccharides from the common serotypes are used in patients at high risk.

Clinical Features

The onset is usually abrupt, with high fever , shaking chills ,
pleuritic chest pain, and productive mucopurulent cough .
occasional patients may have heamoptysis

Morphology:

There are 2 morphological pattern:-

a- labor pneumonia .

b- Bronchopneumonia. (is much more prevalent at extremes age) .

Regardless the morphologic pattern , the lower lobes or the right middle
lobe are most frequently involved.

which is most frequent is caused by streptococcus

lobar pneumonia

a
Pneumoniae, It involve the entire lobe. Consolidation can be seen by X-
ray .

Microscopically + grossly

in preantibiotic era, it evolved through 4 stages:-

1-congestion: - The affected lobe is heavy, red and baggy .

histologically: - vascular congestion can be seen, with proteinaceous
Fluid, scattered neutrophils and many bacteria in the alveoli

2-Red hepatization: - in which the lung has a liver like consistency, the
alveolar spaces are packed with neutrophils, red cells and fibrin and the
pleura shows fibrino or fibrinopurulent exudate

3-Grey hepatization; - the lung is dry, gray and firm because the
red cells become lysed while fibrinous exudate persists within
alveoli .

4- resolution: follows in uncomplicated cases, as exudates within
the alveoli are enzymatically digested and either resorbed or
expectorated leaving basic architecture intact. the pleural
reaction, leaving fibrous thickening or permanent adhesion

bronchopneumonia are consolidated areas of acute suppurative
inflammation. The consolidation may be patchy through one lobe
but is more often multilobar and frequently bilateral and basal
because of the tendency of secretions to gravitate into the lower
lobes

Histologically : the reaction consist of focal Suppurative
exudate that fills the bronchi, bronchioles and adjacent alveolar

spaces

With appropriate therapy, complete restitution of lung is the

rule for both forms of pneumonia

COMMUNITY-ACQUIRED
ATYPICAL (VIRAL AND MYCOPLASMAL) PNEUMONIAS

Definition

The term primary atypical pneumonia was initially applied to an
acute febrile respiratory disease characterized by patchy
inflammatory changes in the lungs, largely confined to the
alveolar septa and pulmonary interstitium.

The term atypical (denotes the moderate amount of sputum, no
physical findings of consolidation, only moderate elevation of
white cell count, and lack of alveolar exudate.)

Causative agents

The pneumonitis is caused by a variety of organisms,

1- the most common being Mycoplasma pneumoniae. Mycoplasma
infections are particularly common among children and young
adults. They occur sporadically or as local epidemics in closed
communities (schools, military camps, and prisons).

2- viruses, including influenza virus types A and B, the respiratory
syncytial viruses, human metapneumovirus, adenovirus,
rhinoviruses, rubeola, and varicella viruses;

3-Chlamydia pneumoniae; and Coxiella burnetii (Q fever).

Any one of these agents can cause merely an upper respiratory
tract infection, recognized as the common cold, or a more severe
lower respiratory tract infection.

Factors that favor such extension of the infection include

extremes of age,

malnutrition,

alcoholism,

underlying debilitating illnesses

The common pathogenetic mechanism

is attachment of the organisms to the upper respiratory tract
epithelium followed by necrosis of the cells and an inflammatory response.
When the process extends to the alveoli there is usually interstitial
inflammation, but there may also be some outpouring of fluid into alveolar
spaces, so that on chest x-ray the changes may mimic bacterial pneumonia.
Damage to and denudation of the respiratory epithelium inhibit mucociliary
clearance and predispose to secondary bacterial infection

Morphology. All causal agents produce essentially similar morphologic
patterns. The lung involvement may be quite patchy or may involve whole
lobes bilaterally or unilaterally. The affected areas are red-blue and
congested. The pleura is smooth, and pleuritis or pleural effusions are
infrequent.

The histologic pattern depends on the severity of the disease.
Predominant is the interstitial nature of the inflammatory reaction,
virtually localized within the walls of the alveoli. The alveolar septa are
widened and edematous and usually have a mononuclear inflammatory
infiltrate of lymphocytes, macrophages, and occasionally plasma cells. In
acute cases neutrophils may also be present. The alveoli may be free from
exudate, but in many patients there is intra-alveolar proteinaceous material
and a cellular exudate. When complicated by ARDS, characteristically pink
hyaline membranes lining the alveolar walls are present Eradication of the
infection is followed by reconstitution of the normal architecture of the lung.

ClinicalCourse.

The clinical course is extremely varied. Many cases masquerade as severe
upper respiratory tract infections or as chest colds. Even individuals with
well developed atypical pneumonia have few localizing symptoms. Cough
may be absent, and the major manifestations may consist only of fever,
headache, muscle aches, and pains in the legs.

Tuberculosis (TB)

TB is a communicable chronic granulomatous disease caused by
Mycobacterium tuberculosis it usually involves the lungs but may affect any
organ or tissue .

((Immune Mechanisms in pathogenesis of TB.)):

a- the organism are ingested by macrophages which process the
bacterial antigens for presentation to CD4 TH1 T cells in the
context of class II MHC molecules

b- The CD4+ T cells proliferate and secrete cytokines , attracting
lymphocytes and macrophages.

IFN- γ released by CD4 + T cell is critical in activating
macrophages

c- Activated Macrophages release a variety of mediators:

1-TNF is responsible for recruitment of monocytes which in turn
undergo activation and differentiation into epithelioid histiocytes

2- IFN- γ in conjunction with TNF result in increased level of nitric
oxide at site of infection , Nitric oxide is a powerful oxidizing
agent and results in generation of free radicals capable of
destruction of several Mycobacterial constituents.

d- CD4 T cells facilitate the development of CD8 cytotoxic T cells
and kill TB infected macrophages.

e- Delayed hypersensitivity is marked by a positive tuberculin skin
test result. The test result is positive in both primary and secondary
infect on represents hypersensitivity and relative immunity and
usually remains positive throughout life.

Types of TB:

1° (Primary) TB

is the form of disease that develops in a previously unexposed,
Elderly and profoundly immunosuppressed persons may lose their
sensitivity to tubercles and so may develop tuberculosis more than
once.

With primary TB source of organism is exogenous, 5% only
develop significant disease

Morphology:

Gross:

primary TB almost always begins in lungs. Typically the inhaled
bacilli in distal airways of lower part of upper lobes or upper part
of lower lobes. Gray white consolidation emerges which called
Ghon focus, this focus undergoes caseous necrosis. The TB bacilli
either free or within phagocytes drain to regional LN which is also

caseate → Ghon focus + Regional LN complex = (Ghon complex).
Which is a characteristic of primary TB.

Ghon complex undergoes fibrosis + calcification that can be
detected by X-ray (Ranke complex)

Microscopically

granulomatous inflammatory reaction that forms both caseating
and non caseating tubercles the granulomas are usually enclosed
within a fibroblastic rim punctuated by lymphocytes

Multinucleated giant cells are present in granuloma .

Fate of primary TB

1- induce hypersensitivity and increased resistance

2- The foci of scarring may harbor viable bacilli for years perhaps
for life.

3- Uncommonly the disease may progress without interruption into
so called progressive TB because of well-defined disease such as
AIDS.

Diagnosis of PPTB in adult is difficult. PPTB resembles
pneumonia

lymphatohaematogenous dissemination may develop → TB
meningitis and miliary TB

Secondary TB (reactivation TB)

Is the pattern of disease that arises in previously sensitized host, it
may follow shortly after 1°TB, but more commonly it arises from
reactivation of dormant 1° lesions many decades after initial
infection when host resistance is weakened or it may results from
exogenous reinfection.

2° TB is classically localized to the apex of one or both upper lobes
, this is may be due to high oxygen tension

because of preexisting hypersensitivity, the bacilli excite a prompt
and marked tissue response that tends to wall off the focus so
there's no LN involvement

Cavitation occurs resulting in dissemination along airways in
neglected 2° TB . So the erosion along the airway is an important
source of infectivity because the patient raises sputum containing
bacilli.

Morphology:

a- localized lesions usually in the apical or posterior segments of
upper lobes.

b- Tubercle formation:-The lesions frequently coalesce and rupture
into the bronchi

The Caseous content may liquefy and be expelled resulting in
cavitory lesions . Cavitations is a characteristic of 2° TB (not 1°
TB).

c- Scarring and calcification

nd TB:

Spread of disease of

which is seeding of distal organs with innumerable small

Miliary TB

1
millet seed like lesions by lymphatic and haematogenous routes, this is
may be pulmonary miliary TB or systemic.

develop either by

Endobronchial, endotracheal and laryngeal TB

2
spread of infective material through lymphatic channels or from
expectorated infectious material.

Isolated organ TB:

This is occur by haematogenous spread to any organ and may the
presenting feature, most common sites meninges, kidneys, adrenals, bone,
Para spinal abscess or Pott disease, and fallopian tube.

especially cervical LN

Lymphadenitis

lymph adenopathy is unifocal and the patient don't have the ongoing
disease.

Intestinal TB:

due to ingestion of contaminated milk or secondary to swallowing of
coughed up infective materials in 2° TB .Typically the organisms are
trapped in mucosal lymphoid aggregations of the small and large bowel

which undergo inflammatory enlargement and ulceration especially in the
ileum

Clinical Features

Localized secondary TB may be asymptomatic when manifestation
appear they are usually insidious. There are :

1- systemic symptoms related to (TNF and IL1)

Malaise, anorexia, weight loss and fever (remittent low grade) and night
sweat.

2- localized symptoms (with progressive pulmonary TB)

- increase amount of sputum first mucoid then purulent.

- Haemoptysis (in 1/2 of patients).

- Pleuritic chest pain

in extrapulmonary TB the symptoms depend on the organ that is involved

E.g.: Fallopian tube → infertility

meninges → neurologic deficit.