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Laboratory Findings in Respiratory Disease
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Croup Pulmonary Embolism or Infarction Bronchiolitis Whooping Cough
Bacterial Pneumonias Mycoplasmal Pneumonia Viral Pneumonias Neoplasms
Legionnaires' Disease Mycrobacterial Diseases other than Tuberculosis Tuberculosis Abscess
Actinomycosis and Nocardiosis Coccidiodomycosis Crytococcosis Lung Abscess
Aspergillosis Blastomycosis Chronic Bronchitis Pulmonary Emphysema
Asthma Fat Embolism Pleural Effusion Bronchiectasis
Pulmonary Edema Pneumoconiosis Pulmonary Embolism and Infarction Sarcoidosis
. . Bronchogenic Carcinoma .
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RESPIRATORY DISEASES

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CROUP

LABORATORY FINDINGS



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BRONCHIOLITIS

LABORATORY FINDINGS



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WHOOPING COUGH

LABORATORY FINDINGS*

*Serologic tests are of little diagnostic value because antibodies appear late.
 

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VIRAL PNEUMONIAS

LABORATORY FINDINGS



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BACTERIAL PNEUMONIAS

LABORATORY FINDINGS

Sputum

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MYCOPLASMAL PNEUMONIA

LABORATORY FINDINGS



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LEGIONNAIRES' DISEASE

LABORATORY FINDINGS



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Infected Lungs
Originating site

M. Tuberculosis (meningitis)
(Link to source file)

TUBERCULOSIS

LABORATORY FINDINGS



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MYCOBACTERIAL DISEASES OTHER THAN TUBERCULOSIS

LABORATORY FINDINGS



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Nocardia
Link to source page
Actinomyces, Nocardia, and Streptomyces.
These organisms have been shown to be higher bacteria, but they were thought to be fungi for many years because they have filamentous forms, 0.5 to 0.8 microns in diameter, which appear to branch. Some species form aerial mycelia in culture. The clinical manifestations of infection are similar to those of a systemic fungal infection. It is now clear that they are not fungi but are closely related to the mycobacteria. Some facts that you should know about these genera are that:

Actinomyces are anaerobic, while Nocardia and Streptomyces are aerobic. 

Nocardia stain partially acid-fast, Actinomyces and Streptomyces are not acid-fast. 

Actinomyces produce granules. Most actinomycetes in tissue do not stain with the H & E stain commonly used for general histopathology. All genera may produce granules; Actinomyces almost always produce granules.


ACTINOMYCOSIS AND NOCARDIOSIS

LABORATORY FINDINGS

Actinomycosis

Nocardiosis

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HISTOPLASMOSIS

Link to image source

The yellow lesion is a severe histoplasmosis scar that involves the macula
The fungal organism has a propensity to result in ocular disease, however, and the macula is the most common site of infection. When macular infection occurs, the patient may experience visual loss due to inflammation and scarring of the macula, and some patients will develop hemorrhage in the macula, due to the growth of vessels beneath the retina (choroidal neovascular membrane). The presence of the macular lesion, and peripheral retinal lesions known to ophthalmologists as "Histo spots," is generally all that is necessary to make the diagnosis. There is no single test that proves the diagnosis, however, and in some cases, blood and skin testing, and a chest x-ray may help confirm the diagnosis.

LABORATORY FINDINGS

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COCCIDIOIDOMYCOSIS

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Etiology
Coccidioidomycosis is caused by Coccidioides immitis, a dimorphic fungus that grows as a mold in the soil. The mold forms arthroconidia within the hypha, a type of conidia formation known as enteroarthric development (Figure 1) (4). C. immitis is the only species within the primary pathogenic fungi that has this type of conidia development. Alternate conidia undergo autolysis, leaving empty spaces between viable arthroconidia. The arthroconidia are released into the atmosphere when the wind ruptures the hypha. C. immitis infects humans and animals almost exclusively by the respiratory route (5). Once inhaled, the arthroconidia cluster in the lungs and undergo a dramatic morphologic change. The round cells, which develop into spherules, undergo repeated internal divisions until they are filled with hundreds to thousands of offspring, termed endospores. This process occurs over 48 to 72 hours (6). When the spherule ruptures, each released endospore has the capacity to develop into a mature spherule

LABORATORY FINDINGS



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BLASTOMYCOSIS


Link to source

Link to source

Same source as adjacent image
Each yeast is multinucleate with 2-5 nuclei per cell. The mechanism for the phase transition is unknown, but the reason for the transition is quite clear, as described below.
The fungus can also form a sexual state; the so-called teleomorph form is Ajellomyces dermatitidis, which forms a gymnothecium. The gymnothecium is kind of like a cleistothecium (closed ascocarp) as found in powdery mildews or Aspergillus. The gymnothecium, however, has an outer covering that is more loosely woven, so that ascospores can fall out without having the covering degraded by other microbes.
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Blastomycosis starts out as a lung infection caused by inhalation of the conidia. The conidia transform into the yeast form, The transformation into a yeast involves many physiological and biochemical changes, having the effect of "buying some time" for the fungus to become established. The fungus evades the body's immune system by changing its surface antigens. Once established, the infection progresses as an occult, insidious (hidden and sneaky) process or as a chronic, expanding, and eventually systemic infection. The patient may have severe presenting symptoms or may be inapparent infection that resolves spontaneously or disseminates to another location. If symptoms do appear, the incubation period may be long - 21 to 106 days. It starts with mild progressive respiratory infection with a dry cough, some pleuritic pain, hoarseness, and a low grade fever, symptoms that overlap many other diseases, such as tuberculosis or chronic histoplasmosis. If the primary pulmonary infection does not resolve, severe progressive blastomycosis can result. It can sometimes be fatal. Sometimes the disease spreads to the skin (cutaneous blastomycosis, as shown to the right), the bones (osseous blastomycosis), the urogenital tract, or the central nervous system. The tissue response is variable, but organism shows up as big blue broad based budding yeast. An unequivocal diagnosis cannot be made unless this form is seen. A diagnosis may also involve isolating the fungus and growing it at room temperature and body temperature. LABORATORY FINDINGS
  • Identification of organism by direct or phase-contrast microscopy of sputum, pus, or tissue
  • Isolation of organism by culture of sputum, pus, or tissue is required for definitive diagnosis.
  • Complement-fixing antibodies may be positive or negative with systemic infection.  Cross-reaction with H. capsulatum further detracts from the diagnostic usefulness of this test.
  • The immunodiffusion test for blastomycosis is specific and has a sensitivity of approximately 80% Negative tests, therefore, do not exclude the diagnosis.
  • Leukocytosis and increased sedimentation rate occur in active disease.


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CRYPTOCOCCOSIS

Link to source

Link to source

LABORATORY FINDINGS



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ASPERGILLOSIS

Link to source

LABORATORY FINDINGS

  • Identification of organism on smear;  culture of organism from sputum or lung tissue;  because the organisms are usually saprophytes their isolation is not diagnostic but must be correlated with clinical information.  Diagnosis requires demonstrating the fungus in tissues.
  • Immunodiffusion test for antibody, when used with reference sera, is 100% specific.  Conversion of the immunodiffusion antibody test from negative to positive is diagnostic of infection.  Demonstration of one or more precipitating antibodies indicates infection, fungus ball formation, or allergy due to an Aspergillus species.
  • Laboratory findings of an underlying disease, such as tuberculosis, asthma, bronchiectasis, or bronchogenic carcinoma


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CHRONIC BRONCHITIS

LABORATORY FINDINGS



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PULMONARY EMPHYSEMA

LABORATORY FINDINGS



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ASTHMA

LABORATORY FINDINGS



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BRONCHIECTASIS

LABORATORY FINDINGS



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PNEUMOCONIOSIS

LABORATORY FINDINGS



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SARCOIDOSIS

Link to source
LABORATORY FINDINGS
  • Increased serum angiotensin-converting enzyme - this enzyme converts angiotensin I to angiotensin II and normally occurs within the pulmonary capillary endothelial cells.  Increased activity of this enzyme in sarcoidosis is believed to be the result of an increased rate of enzyme synthesis by epithelioid cells of the carcoid granulomas and of release of the enzyme into the bloodstream.  In a recent report, 83% of patients with active disease had elevated enzyme levels. 10 The enzyme level tends to fall during spontaneous or steroid-induced remission of the disease.
  • Increased sedimentation rate and serum fibrinogen indicate active disease.
  • Decreased serum albumin reflects chronic disease.
  • Increased serum globulins;  stepwise increase of Alpha2-,  Beta-, and y-globulins, especially IgG;  this reflects humoral immunologic response of chronic inflammation
  • Leukopenia (<5,000/ul) in 40% of patients
  • Mild normocytic anaemia - chronic-disease type
  • Decreased lymphocytes
  • Increased serum uric acid
  • Increased urine calcium as a result of increased intestinal absorption due to increased sensitivity to vitamin D.
  • Laboratory findings reflecting specific organ involvement of lungs, liver, spleen, central nervous system, pituitary, or kidneys


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PLEURAL EFFUSION

LABORATORY FINDINGS

1.    A pleural fluid-serum ratio of total protein of 0.5 or greater
2.    A pleural fluid lactate dehydrogenase (LDH) of 20 IU or greater
3.    A pleural fluid-serum ratio of LDH of 0.6 or greater

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LUNG ABSCESS

LABORATORY FINDINGS



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ALLERGIC PULMONARY PARENCHYMAL DISEASES

LABORATORY FINDINGS



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PULMONARY OEDEMA

LABORATORY FINDINGS



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PULMONARY EMBOLISM AND INFARCTION

LABORATORY FINDINGS



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FAT EMBOLISM

LABORATORY FINDINGS



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RESPIRATORY DISTRESS SYNDROME

LABORATORY FINDINGS

RDS

Determination of lecithin and sphingomyelin in amniotic fluid is the single most accurate test of foetal lung maturity.  The lecithin - sphingomyelin ratio (L/S ratio) is lower in prematurity than at maturity.  RDS is unlikely when the ratio is high, indicating lung maturity.  When a mixture of amniotic fluid and ethanol is shaken, the mixture will produce foam if an adequate amount of surfactant is present.  If amniotic fluid is not available, the L/S ratio may be determined through analysis of the gastric aspirate of the infant.

RDS and ARDS

The following are cumulative findings occurring in order of increasing severity of pulmonary insufficiency:



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RESPIRATORY FAILURE

LABORATORY FINDINGS

Arterial P02 and PC02 are the only clinical laboratory indicators of pulmonary function.  (pH is altered with changes in PC02, but this reflects changes in bicarbonate.)  Decreased arterial P02 is an early and sensitive indicator of respiratory insufficiency.  Hypoxema occurs in the following circumstances:
 

Hypoventilation:  impaired movement of air in and out of the lungs.  This may be seen following sedative or narcotic drug depression of respiration;  impaired cerebral control of respiration due to stroke, brain tumour, or injury;  weakness of respiratory muscles; or obesity.

Diffusion abnormality:  impaired exchange of 02 and C02 between alveoli and pulmonary capillaries.  This may occur owing to injury to the alveolar membranes, such as following prolonged use of certain cytotoxic drugs.

Ventilation - perfusion abnormality:  diminished ventilation to areas of the lung that continue to receive normal blood flow.  Associated with this abnormality are many forms of lung disease, including pulmonary oedema, viral pneumonia, pulmonary embolism, and RDS.

Right-to-left shunt:  flow of venous blood through portions of the lungs that are completely unventilated.  This could occur with lung collapse (atelectasis);  extensive filling of the lungs with oedema fluid, pus, blood, or inflammatory cells as in pneumonia;  or with accumulation of air or fluid in the pleural cavity.
 

The four abnormalities that cause hypoxemia may be differentiated by determining the patient's arterial PC02 and P02 while he is breathing room air and again while he is breathing room air and again while he is breathing 100% oxygen.  The basis for this differentiation is shown in Table 2-1.

Arterial PC02 is the single most important measurement of alveolar ventilation.  C02 retention (hypercapnia) occurs less frequently than does hypoxemia and indicates a serious ventilatory problem.  Hypercapnia is accompanied by acidosis and hypoxemia unless the patient is receiving oxygen.  This occurs acutely following sudden airway obstruction, pulmonary oedema, sedative overdose, or cardiac arrest.  This also may occur following long-standing severe pulmonary or alveolar hypoventilation, as seen in emphysema and chronic bronchitis.

Decreased PC02 (hypocapnia) is due to hyperventilation and occurs more frequently than does hypercapnia.  Hypocapnia is accompanied by alkalosis.  Hyperventilation is seen as a response to hypoxemia in many pulmonary diseases including pneumonia, atelectasis, pulmonary embolism, and acute RDS.

Table 2-1.  Pulmonary Causes of Hypoxemia and Their Differentiation

ABNORMALITY ARTERIAL PC02 ARTERIAL P02 (ROOM AIR) ARTERIAL P02 (100% 02)
Hypoventilation Increased Decreased Normal
Diffusion abnormality Normal or decreased* Normal at rest:  decreased during exercise Normal
Ventilation-perfusion abnormality Normal, increased, or decreased Decreased Normal
Right-to-left shunt Normal or decreased* Decreased Low
Fall in cardiac output in patient with right-to-left shunt Normal, increased, or decreased Decreased Low

*Attributable to hyperventilation from secondary causes
(Adapted from Hyde RW:  Clinical interpretation of arterial oxygen measurements.  Med. Clin. North Am 54:617-629, 1970)
 



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BRONCHOGENIC CARCINOMA

LABORATORY FINDINGS
 

Laboratory Findings of Ectopic Hormone Formation by Oat Cell Carcinomas
 
 

 
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