Chapter 15:Lung: Pulmonary Infections Flashcards

1
Q

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 _____________, but bacterial, viral, mycoplasmal, and fungal infections of the lung (pneumonia) still account for an enormous
amount of morbidity and are responsible for one sixth of all deaths in the United States. [121]
Pneumonia can be very broadly defined as any infection of the lung parenchyma.

A

upper
respiratory tract infections caused by viruses (common cold, pharyngitis)

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2
Q

Pulmonary defense mechanisms are described in Chapter 8 .

Pneumonia can result whenever
these 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:

A
  • 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 bynalcohol, tobacco smoke, anoxia, or oxygen intoxication
  • • Pulmonary congestion and edema
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3
Q

Defects in innate immunity (including neutrophil and complement defects) and humoral
immunodeficiency typically lead to an increased incidence of infections with____________

A

pyogenic bacteria.

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4
Q

On the other hand, cell-mediated immune defects (congenital and acquired) lead to increased
infections with intracellular microbes such as ______________

A

mycobacteria and herpesviruses as well as with
microorganisms of very low virulence, such as Pneumocystis jiroveci.

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5
Q

Several other points should be emphasized.

First, one type of pneumonia sometimes
predisposes to another, especially in debilitated patients. For example, the most common cause
of death in viral influenza epidemics is superimposed bacterial pneumonia.

Second, although
the portal of entry for most pneumonias is the respiratory tract, hematogenous spread from one
organ to other organs can occur , and secondary seeding of the lungs may be difficult to
distinguish from primary pneumonia.

Finally, many patients with chronic diseases acquire
terminal pneumonias while hospitalized (nosocomial infection).

Bacteria common to the hospital
environment may have acquired resistance to antibiotics; opportunities for spread are
increased; invasive procedures, such as intubations and injections, are common; and bacteria
may contaminate equipment used in respiratory care units.

A
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6
Q

Pneumonias are classified by the specific etiologic agent, which determines the treatment, or, if
no pathogen can be isolated, by the clinical setting in which the infection occurs.

The latter
considerably narrows the list of suspected pathogens for administering empirical antimicrobial
therapy.

As Table 15-8 indicates, pneumonia can arise in seven distinct clinical settings
(“pneumonia syndromes”), and the implicated pathogens are reasonably specific to each
category

A

TABLE 15-8 – The Pneumonia Syndromes

  • COMMUNITY-ACQUIRED ACUTE PNEUMONIA
  • COMMUNITY-ACQUIRED ATYPICAL PNEUMONIA
  • HOSPITAL-ACQUIRED PNEUMONIA
  • ASPIRATION PNEUMONIA
  • CHRONIC PNEUMONIA
  • NECROTIZING PNEUMONIA AND LUNG ABSCESS
  • PNEUMONIA IN THE IMMUNOCOMPROMISED HOST
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7
Q

COMMUNITY-ACQUIRED ACUTE PNEUMONIA

A
  • Streptococcus pneumoniae
  • Haemophilus influenzae
  • Moraxella catarrhalis
  • Staphylococcus aureus
  • Legionella pneumophila
  • Enterobacteriaceae (Klebsiella pneumoniae) and
  • Pseudomonas spp.
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8
Q

COMMUNITY-ACQUIRED ATYPICAL PNEUMONIA

A
  • 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
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9
Q

HOSPITAL-ACQUIRED PNEUMONIA

A
  • Gram-negative rods, Enterobacteriaceae (Klebsiella spp., Serratia marcescens,
  • Escherichia coli) and Pseudomonas spp.
  • Staphylococcus aureus (usually penicillin resistant)
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10
Q

ASPIRATION PNEUMONIA

A
  • Anaerobic oral flora (Bacteroides, Prevotella, Fusobacterium, Peptostreptococcus), admixed with
  • aerobic bacteria (Streptococcus pneumoniae, Staphylococcus aureus, Haemophilus influenzae, and Pseudomonas aeruginosa)
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11
Q

CHRONIC PNEUMONIA

A
  • Nocardia
  • Actinomyces
  • Granulomatous: Mycobacterium tuberculosis and atypical mycobacteria, Histoplasma capsulatum, Coccidioides immitis, Blastomyces dermatitidis
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12
Q

NECROTIZING PNEUMONIA AND LUNG ABSCESS

A
  • Anaerobic bacteria (extremely common), with or without mixed aerobic infection
  • Staphylococcus aureus, Klebsiella pneumoniae, Streptococcus pyogenes, and type 3
  • pneumococcus (uncommon)
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13
Q

PNEUMONIA IN THE IMMUNOCOMPROMISED HOST

A
  • Cytomegalovirus
  • Pneumocystis jiroveci
  • Mycobacterium avium-intracellulare
  • Invasive aspergillosis
  • Invasive candidiasis
  • “Usual” bacterial, viral, and fungal organisms (listed
  • above)
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14
Q

Community-acquired pneumonias may be bacterial or viral.

Often, the bacterial infection follows
an upper respiratory tract viral infection.

A
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15
Q

What is consolidation?

A

Bacterial invasion of the lung parenchyma causes the
alveoli to be filled with an inflammatory exudate, thus causing consolidation (“solidification”) of
the pulmonary tissue.

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16
Q

Many variables, such as the ______________ determine the precise form of pneumonia.

A

specific etiologic agent, the host reaction,
and the extent of involvement
,

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17
Q

Predisposing
conditions include :

A
  • extremes of age,
  • chronic diseases (congestive heart failure, COPD, and diabetes),
  • congenital or acquired immune deficiencies, and
  • decreased or absent splenic function (sickle cell disease or post-splenectomy, which puts the patient at risk for infection with encapsulated bacteria such as pneumococcus).
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18
Q

What is most common cause of communityacquired
acute pneumonia?

A
  • *Streptococcus pneumoniae, or pneumococcus**, is the most common cause of communityacquired
  • *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

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19
Q

Describe Haemophilis influenzae?

A

Haemophilus influenzae is a pleomorphic, gram-negative organism that is a major cause of lifethreatening
acute lower respiratory tract infections and meningitis in young children
.

In adults it
is a very common cause of community-acquired acute pneumonia. [122]

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20
Q

Haemophilis influenzae is a
ubiquitous colonizer of the pharynx, where it exists in two forms:

A
  • encapsulated (5%) and
  • unencapsulated (95%).
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21
Q

Describe the encapsulated form of H.inluenzae?

A

Typically, the encapsulated form dominates the unencapsulated forms
by secreting an antibiotic called haemocin that kills the unencapsulated H. influenzae. [123]

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22
Q

Although there are six serotypes of the encapsulated form of H. influenzae (types a to f), what is the most frequent cause of severe invasive disease?

A
  • *type b**, which has a
  • *polyribosephosphate capsule**, used to be the most frequent cause of severe invasive disease.

With routine use of H. influenzae conjugate vaccines, the incidence of disease caused by the b
serotype has declined significantly.

By contrast, infections with nonencapsulated forms are
increasing. Also called nontypeable forms, they spread along the surface of the upper
respiratory tract and produce otitis media (infection of the middle ear), sinusitis, and
bronchopneumonia.

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23
Q

What mediate adherence of the H. influenzae organisms to the respiratory

epithelium. [124]

A
  • *Pili on the surface of H. influenzae** mediate adherence of the organisms to the respiratory
    epithelium. [124]
In addition, **H. influenzae secretes a factor** that **disorganizes ciliary beating**
and a **protease that degrades IgA,** the **major class of antibody secreted into the airways.**
24
Q

Survival of H. influenzae in the bloodstream correlates with the presence of the

A

Survival of H. influenzae in the bloodstream correlates with the presence of the capsule, which,
like that of pneumococcus, prevents opsonization by complement and phagocytosis by host
cells.

Antibodies against the capsule protect the host from H. influenzae infection; hence the
capsular polysaccharide b is incorporated in the vaccine against H. influenzae used for
children

25
Q

What orgasnim which may follow a viral respiratory infection, is a pediatric emergency
and has a high mortality rate
.

A

H. influenzae pneumonia, which may follow a viral respiratory infection, is a pediatric emergency
and has a high mortality rate
.

Descending laryngotracheobronchitis results in airway obstruction
as the smaller bronchi are plugged by dense, fibrin-rich exudate of polymorphonuclear cells,
similar to that seen in pneumococcal pneumonias.

Pulmonary consolidation is usually lobular
and patchy but may be confluent and involve the entire lung lobe.

Before a vaccine became
widely available, H. influenzae was a common cause of suppurative meningitis in children up to
5 years of age. H. influenzae also causes an acute, purulent conjunctivitis (pink eye) in children
and, in predisposed older patients, may cause septicemia, endocarditis, pyelonephritis,
cholecystitis, and suppurative arthritis.

26
Q

What is the most common bacterial cause of acute exacerbation of COPD.

A

H. influenzae

27
Q

What is Moraxella catarrhalis?

A
  • *Moraxella catarrhalis is being increasingly recognized** as a cause of bacterial pneumonia,
  • *especially in the elderly**.

It is the second most common bacterial cause of acute exacerbation of
COPD.

28
Q

What are the three
most common causes of otitis media in children.

A

Along with S. pneumoniae and H. influenzae, M. catarrhalis constitutes one of the three
most common causes of otitis media in children.

29
Q

Describe Staphylococcus aureus in line with pneumonia.

A

Staphylococcus aureus is an important cause of secondary bacterial pneumonia in children and
healthy adults following viral respiratory illnesses (e.g., measles in children and influenza in
both children and adults).

Staphylococcal pneumonia is associated with a high incidence of complications, such as lung abscess and empyema.

Intravenous drug abusers are at high risk
of developing staphylococcal pneumonia
in association with endocarditis. It is also an important
cause of hospital-acquired pneumonia, as will be discussed later

30
Q

What is the most frequent cause of gram-negative bacterial pneumonia.

A

Klebsiella pneumoniae is the most frequent cause of gram-negative bacterial pneumonia.

It commonly afflicts debilitated and malnourished people, particularly chronic alcoholics.

Thick
and gelatinous sputum is characteristic, because the organism produces an abundant viscid
capsular polysaccharide, which the patient may have difficulty expectorating.

31
Q

Which organism is common in patients with cystic fibrosis?

A

Although Pseudomonas aeruginosa most commonly causes hospital-acquired infections, it is
mentioned here because of its occurrence in cystic fibrosis patients. It is common in patients
who are neutropenic and it has a propensity to invade blood vessels with consequent
extrapulmonary spread.

Pseudomonas septicemia is a very fulminant disease.

32
Q

What is the Legionnaires’ disease?

A

Legionella pneumophila is the agent of Legionnaires’ disease, an eponym for the epidemic and
sporadic forms of pneumonia caused by this organism.

33
Q

What is Pontiac fever?

A

Legionnella pneumophilia also causes Pontiac fever, a related
self-limited upper respiratory tract infection.

34
Q

Where can you find Legionnella pneumophilia?

A

This organism flourishes in artificial aquatic

  • *environments, such as water-cooling towers and within the tubing system of domestic (potable)**
  • *water supplies.**

The mode of transmission is either inhalation of aerosolized organisms or
aspiration of contaminated drinking water.

Legionella pneumonia is common in individuals with
some predisposing condition such as cardiac, renal, immunological, or hematologic disease.
Organ transplant recipients are particularly susceptible . It can be quite severe, frequently
requiring hospitalization, and immunosuppressed patients may have fatality rates of up to 50%.
Rapid diagnosis is facilitated by demonstration of Legionella antigens in the urine or by a
positive fluorescent antibody test on sputum samples; culture remains the gold standard of
diagnosis.

35
Q

Bacterial pneumonia has two patterns of anatomic distribution:.

A
  • lobular bronchopneumonia and
  • lobar pneumonia ( Fig. 15-31 )
36
Q

What is the dominant characteristic of bronchopneumonia?

A

Patchy consolidation of the lung is
the dominant characteristic of bronchopneumonia ( Fig. 15-32 ),

37
Q

while _____________of a large portion of a lobe or of an entire lobe defines lobar pneumonia ( Fig.
15-33 ).

These anatomic but still classic categorizations are often difficult to apply in individual
cases because patterns overlap.

The patchy involvement may become confluent, producing virtually total lobar consolidation; in contrast, effective antibiotic therapy for any form of
pneumonia may limit involvement to a subtotal consolidation.

Moreover, the same organisms
may produce either pattern depending on patient susceptibility

. Most important from the
clinical standpoint are identification of the causative agent and determination of the
extent of disease.

A

fibrinosuppurative
consolidation

38
Q

In lobar pneumonia, four stages of the inflammatory response have classically been
described:

A
  • congestion
  • , red hepatization,
  • gray hepatization,
  • and resolution
39
Q

In the first stage of congestion
the lung is :

A

heavy, boggy, and red.

It is characterized by vascular engorgement, intra-alveolar fluid with few neutrophils, and often the presence of numerous bacteria.

40
Q

The stage of red
hepatization that follows is characterized by :

A
  • *massive confluent exudation with neutrophils,**
  • *red cells,** and fibrin filling the alveolar spaces ( Fig. 15-34A ).

On gross examination, the lobe
now appears distinctly red, firm, and airless, with a liver-like consistency, hence the term
hepatization.

41
Q

The stage of gray hepatization follows with:

A

progressive disintegration ofred
cells and the persistence of a fibrinosuppurative exudate ( Fig. 15-34B ), giving the gross
appearance of a grayish brown, dry surface.

42
Q

What happens in the final stage, the resolution?

A

In the final stage of resolution the consolidated
exudate within the alveolar spaces undergoes progressive enzymatic digestion to produce
granular, semifluid debris that is resorbed, ingested by macrophages, expectorated, or
organized by fibroblasts growing into it ( Fig. 15-34C ).

Pleural fibrinous reaction to the
underlying inflammation, often present in the early stages if the consolidation extends to the
surface (pleuritis), may similarly resolve.

More often it undergoes organization, leaving
fibrous thickening or permanent adhesions.

43
Q

Describe the foci of bronchopneumonia.www.w

A

Foci of 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.

Well-developed lesions are slightly elevated, dry, granular, gray-red to yellow, and poorly
delimited at their margins (see Fig. 15-32 ).

Histologically, the reaction usually elicits a
suppurative, neutrophil-rich exudate that fills the bronchi, bronchioles, and adjacent alveolar
spaces

44
Q

Complications of pneumonia include

A
  • (1) tissue destruction and necrosis, causing abscess formation (particularly common with type 3 pneumococci or Klebsiella infections);
  • (2) spread of infection to the pleural cavity, causing the intrapleural fibrinosuppurative reaction known as empyema; and
  • (3) bacteremic dissemination to the heart valves, pericardium, brain, kidneys, spleen, or joints, causing metastatic abscesses, endocarditis, meningitis, or suppurative arthritis
45
Q
A

FIGURE 15-31 Comparison of bronchopneumonia and lobar pneumonia.

46
Q
A

FIGURE 15-32 Bronchopneumonia. Gross section of lung showing patches of
consolidation (arrows).

47
Q
A

FIGURE 15-33 Lobar pneumonia—gray hepatization, gross photograph. The lower lobe is
uniformly consolidated

48
Q

The major symptoms of community-acquired acute pneumonia are

A

abrupt onset of high fever,
shaking chills, and cough productive of mucopurulent sputum; occasional patients may have
hemoptysis.

When fibrinosuppurative pleuritis is present it is accompanied by pleuritic pain and
pleural friction rub.

The whole lobe is radiopaque in lobar pneumonia, whereas there are focal
opacities in bronchopneumonia.

49
Q

The clinical picture is markedly modified by the administration of antibiotics.

Treated patients
may be relatively afebrile with few clinical signs 48 to 72 hours after the initiation of antibiotics.
The identification of the organism and the determination of its antibiotic sensitivity are the
keystones to appropriate therapy. Fewer than 10% of patients with pneumonia severe enough

A
50
Q

What is primary atypical pneumonia?

A

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**.
51
Q

The pneumonitis of atypical pneumonia is caused by a variety of organisms, the most common being _______________.

A

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).

Other etiologic agents are viruses,
including influenza virus types A and B, the respiratory syncytial viruses, human
metapneumovirus, adenovirus, rhinoviruses, rubeola, and varicella viruses; Chlamydia

pneumoniae; and Coxiella burnetii (Q fever). [124,] [125]

In some cases the cause cannot be
determined.

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, and
underlying debilitating illnesses.

52
Q

What is the common pathogenic mechanism in atypical pneumonia?

A

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 infections

53
Q

All causal agents in atypical pneumonia produce essentially similar morphologic patterns.

T or F

A

T

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.

54
Q

The histologic patter atypical pneumonia depends on the severity of the disease.

Wnat is the predominat feature?

A

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 (see Fig. 15-3 )

. Eradication of the infection is followed by reconstitution of
the normal architecture of the lung.

55
Q

Superimposed bacterial infection modifies the histologic picture by causing :

A

ulcerative
bronchitis, bronchiolitis, and bacterial pneumonia. Some viruses, such as herpes simplex,
varicella, and adenovirus, may be associated with necrosis of bronchial and alveolar
epithelium and acute inflammation.

Characteristic viral cytopathic changes are described in
Chapter 8 .

56
Q

The clinical course of atypical pneumonia s extremely varied.

A

Many cases masquerade as severe upper respiratory
tract infections or as chest colds .

Even individuals with welldeveloped 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. The edema and exudation are both strategically located to cause mismatching of ventilation and blood flow and thus evoke
symptoms out of proportion to the scanty physical findings.

The ordinary sporadic form of the disease is usually mild with a low mortality rate, below 1%.
Interstitial pneumonia, however, may assume epidemic proportions with intensified severity and
greater mortality, as documented in the devastating influenzal pandemics of 1915 and 1918 and
the many smaller epidemics since then. Secondary bacterial infection by staphylococci or
streptococci is common in such circumstances.

57
Q
A