Migratory Pneumonia

 

Migratory Pneumonia

PKGhatak,MD

Migratory pneumonia is a group of pulmonary conditions having one common finding in all. In migratory pneumonia, different parts of the lung are infected repeatedly by the same agent. The diagnosis is based on a radiological finding of pulmonary infiltrations located at different lobes or sub-lobes.

There are many and varied causes of migratory pneumonia.

Loffler's syndrome due to visceral larva migration is one of the three top causes of Migratory pneumonia when all the cases are taken together worldwide. Migratory pneumonia results from the migration of larvae of Ascaris lumbricoides, Strongyloides stercoralis, Wuchereria bancrofti, Dirofilaria immitis and Trichinella spiralis. As the larva migrates through the lung an intense eosinophilic inflammation takes place. The patients complain of wheezing, cough, fever, and shortness of breath. Sometimes streaks of blood are present in the coughed-up sputum. Sputum contains many eosinophils. Blood eosinophil count reaches 400 to 800/ul. Chest x-ray shows patchy localized infiltrate one day, in another spot another day if the x-ray is repeated. Other parasites known to produce a similar picture are Toxocara, Schistosomiasis, Paragonimus, and Fasciola hepatica.

In western countries, old people residing in nursing homes often develop this migratory pneumonia from repeated aspiration. Asthmatic bronchopulmonary aspergillosis may produce a similar picture. Cystic fibrosis patients have frequent pneumonia episodes.

Common medications are known to produce migratory pneumonia. These drugs are Penicillin, sulfonamides, Aspirin, and Nitrofurantoin.

Fumes of metals like Nickel Zinc Chloride, Beryllium may present with migratory pulmonary infiltrates.

Primary lung diseases like Alveolar cell carcinoma, alveolar proteinosis, bronchiectasis, and Cystic fibrosis, have these characteristics.

Bronchiolitis obliterans with organizing pneumonia (BOOP) is a special serious infectious disease in children.

Certain diseases caused by auto-antibodies are well-known for these migratory pulmonary infiltrates. These are Goodpasture syndrome, Churg-Straus syndrome, Pulmonary fibrosis in Rheumatoid arthritis, Systemic Lupus erythematosus and polyarteritis nodosa may have a similar pulmonary presentation.

Lastly, an obscure entity known as Cryptogenic organizing pneumonia and small vessel angiitis also have this migratory presentation.

The clinical picture of one entity of Migratory pneumonia varies considerably from the others because of the various nature of etiology. In parasitic diseases and drug induced migratory pneumonia resolves easily when proper medical attention is given. Aspiration pneumonia is a preventable disease but is difficult to achieve because of a shortage of trained manpower. Exposure to metal fumes can be controlled by local ordinances and EPA's efforts.

Migratory pneumonia due to autoimmune diseases takes course according to the response obtained by specific treatment of autoimmune pathology.

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CAP and Walking Pneumonia

 

Community acquired pneumonia (CAP) and Walking pneumonia

                                 PKGhatak,MD

Pneumonia is an inflammatory condition of the lungs. The name pneumonia has to be qualified further to define it narrowly like viral pneumonia, mycoplasma pneumonia, bronchopneumonia, etc. Infectious agents like viruses, bacteria, and fungus are the most common causes of pneumonia. Other agents like toxic fumes, aspirated stomach acids, drowning, medications, radiation, etc. may also cause pneumonia.

Not all pneumonia is life threatening. Based on the degree of severity of pneumonia, and where the infection is acquired, pneumonia can be put in two separate entities.

 1. Community acquired.

 2. Hospital-acquired pneumonia.

When an otherwise healthy person develops pneumonia, the disease is called Community acquired. Whereas, those patients admitted to hospital for conditions other than pneumonia, subsequently get infected while in hospital, the resulting pneumonia is called hospital acquired pneumonia. Hospital bacteria are generally gram negative and resistant to multiple antibiotics and produce serious complications and deaths.

Walking pneumonia:

Community acquired pneumonia when mild, most patients can be effectively treated outside the hospital with oral antibiotics and common over the counter cold & cough medications. These patients are free to walk around and are not bed confined.

So, doctors have coined this term as walking pneumonia to eliminate fear and concerns of people because in the past, pneumonia was akin to a death sentence, days prior to the availability of sulfonamides and penicillin, like we had experienced with HIV/AIDS before retrovirus medications.

Walking Pneumonia should not be confused with Migratory Pneumonia. In migratory pneumonia, pneumonia walks from one place to another place in the lungs. In Walking pneumonia, the patient walks.

Infectious agents causing CAP.

In 2020 the covid-19 pandemic has taken 20 million lives,( 7 million by official count) worldwide and sickened hundreds of millions. The influenza pandemic in 1918 took 50 million lives. Virus pneumonia is undoubtedly the worst human pathogen. In this article only bacterial pneumonia will be discussed.

Every year in the USA about 5 million cases of CAP are seen; it is the second most common infection requiring hospitalization, on average 650 per 1000,000 population are admitted with CAP.

The health department of every community in corroboration with the CDC keeps a close eye on the prevalent infectious agents causing CAP. CDC provides weekly notification about the common bacteria, the best possible antibiotic to treat CAP and any emerging bacterial resistance to antibiotics.

The most common bacteria causing CAP is Streptococcus pneumoniae followed by Hemophilus influenzae and Moraxella catarrhalis, Mycoplasma pneumoniae, Klebsiella, E. coli, Group A streptococcus, Staphylococcus auras, Legionella, Chlamydia and Coxiella organisms follow.

The mode of infection is by aerosol and droplet; lung infection also occurs from another infection site. 

The symptoms start as a runny nose and scratchy throat. Headaches and a low-grade fever develop in a day or two. Most cases of URI recover in 5 to 7 days, but some may develop chills and temperature elevation of 101 to 103 F followed by the productive cough of yellow sputum, and occasional blood streaking of sputum is seen. Chest wall pain on coughing and rapid breathing is noted. At this stage, most people seek medical attention and are hospitalized.

Blood count shows neutrophilic leukocytosis in most bacterial pneumonia, in severe cases, immature neutrophils may appear in the peripheral blood. Chest x-rays show the location and severity of lung infiltrates. Pulse oximetry may show under saturation specially in COPD patients.

Sputum culture and blood cultures identify the causative bacteria but the results take several days, so rapid antigen tests are used to identify common bacterial infections.

In hospitalized patients, IV antibiotic is administered initially, often empirically based on the prevalence of CAP causing bacteria, till bacteriological confirmation is available. As the condition of the patient improves antibiotic is switched to orally. In addition, inhalation of bronchodilators, and chest physiotherapy may be required in COPD and feeble elderly patients to help to raise sputum.

Complications are rare with early intervention and proper selection of antimicrobial agents. But some of these complications are anticipated.

Plural effusion.

 In streptococcus pneumonia, a small pleura effusion is seen. In general plural, effusion resolves along with pulmonary infiltrates. Occasionally thoracentesis is required for rapid clearing. At times Empyema develops when the pleural effusion is associated with Pseudomonas and Staphylococcus pneumonia.

Lung abscess.

 Lung abscess is a special concern in patients with bronchial obstruction from lung cancer and bronchiectasis. Lung abscess is often due to staphylococcus pneumonia. Anaerobic bacterial pneumonia from aspiration is another important source of lung abscesses.

Delayed clearing of pulmonary infiltrates.

 Delayed clearing of pneumonia is often due to mistakes made in bacterial identification, and secondary infections - specially by fungus or drug resistant bacteria. Preexisting severe lung diseases like pneumoconiosis, emphysema, post lobectomy for cancer are special concerns.

Myocarditis.

 Myocarditis was a serious problem before the antibiotic area, It should not happen nowadays.

Septicemia and multiorgan failure.

Immunosuppressed patients from any cause are carefully watched and treated properly in anticipation of such complications. Cardiovascular support therapy, renal function preservation and adequate oxygenation in all vital organs and the brain are undertaken early.

Prevention.

The cessation of smoking is very important. Annual influenza vaccination of the elderly and COPD should be mandatory. Pneumonia vaccines are available. All are encouraged to take the pneumonia vaccine.

Community acquired pneumonia is an annual event. The problem is increasing due to emerging drug resistant bacteria, cigarette smoking in teenagers and in women and the gradual deterioration of air quality from pollution. Children living in proximity to chemical plants and landfills are specially venerable. It is also a drain for limited medical facilities in rural areas and a great financial burden for the uninsured.

Updated: March 2023.

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Legionnaires' Disease

 

LEGIONNAIRES' DISEASE

PKGhatak,MD

Legionnaires' disease and Pontiac fever.

In 1968 several workers of the health department of Pontiac, MI came down with a flu like illness. The cause remained unknown at the time. Several years later in 1976, a new disease called Legionnaires' pneumonia was named by the press following an outbreak of a cluster of 182 pneumonia cases in Philadelphia, PA. The cases happened suddenly in a hotel in Philadelphia during an American Legion convention. Pneumonia is caused by a gram negative, facultative intracellular bacteria called Legionnaires pneumophila. Pontiac fever was subsequently found to be caused by the same bacteria.

Characteristics of legionella bacteria.

Legionella bacteria live in nature in the soil and the surface of the water. The bacteria live intracellularly in symbiosis with amoebae. The bacterium is relatively resistant to heat and thrives in temperatures 77 to 113 degrees F. The bacteria are easily killed by chlorine, UV light and copper-silver ions. In nature, the bacteria can be found in water tanks, cooling towers, air conditioning units, water mists and sprays in supermarkets, tap water and hot water baths, swimming pools, streams and lakes, etc. Biofilms made by amoebae harboring legionella bacteria are resistant to elimination by usual disinfectants.

Pathogenic strains of Legionella that cause human illness are L pneumonia, L micdadei, L longbeachae, L feelcii and L anisa. In addition to pneumonia L pneumonia can cause pericarditis, gastroenteritis, hepatitis, systemic infection and death.

Wounds can be infected with Legionella.

The Legionella organism requires amino acid L-cysteine and Ferric iron for growth and is grown in special charcoal agar media. The bacteria derive energy from amino acids rather than carbohydrates. On the surface of the culture media, the bacteria take a filamentous motile form and use a single flagellum. The bacterium is gram negative but stains poorly with safranin.

Human diseases:

Legionella pneumonia.

The elderly, people having chronic obstructive lung disease (COPD), and those immunosuppressed are prone to infection. The mode of infection is by inhalation of water mist contaminated with these bacteria. The use of contaminated nebulizer machines, central air conditioners in closed spaces, polls, and showers are the main sources of infection. Person to person infection does not happen. In the USA 13,000 cases are seen yearly, more cases in summer due to the use of air conditioners.

The incubation period is 2 to 10 days. The initial symptoms are like any URI, followed by cough and high fever. Some develop nausea, vomiting, streaks of blood in sputum, headache, muscle aches, and neuromuscular symptoms.

Clinically two groups are recognized. One with mild symptoms. They usually recover in 2 to 5 days. The other more seriously ill patients develop shortness of breath, and chest tightness, have a high fever and require hospitalization and antibiotics and oxygen therapy.

Unusual characteristics of L.pneumonia.

The bacteria are recognized as invaders by macrophages of lung alveoli and the macrophages engulf the bacteria. But the bacteria not only neutralize the digestive enzymes of the macrophages but multiply rapidly and kill the macrophages, and infect more macrophages. The cytokines released by the dying macrophages attract monocytes and lymphocytes at the site and the inflammation and pneumonia begin. IL- 1 and TNF play a significant role in the genesis of inflammatory reactions. The Legionella spreads to the other areas in the lung by the movement of macrophages, by mucociliary escalator and lymphatics and in rare cases by blood.

There are no clinical or laboratory distinguishing features of L pneumonia. The initial chest x-rays show nodular infiltrates, in 5 days infiltrates spread to the other lung in spite of usual antibiotics. Lower lobes are usually involved in pneumonia but may spread to the middle lobes. Hyponatremia and abnormal liver enzymes, and renal functions may be present. The use of corticosteroids worsens the condition.

Diagnosis is made by the presence of the Legionella antigen in the urine, and L pneumophila growth by sputum culture. No antibody test is possible because of poor antibody response and for the same reason, no vaccine is available. Macrolides antibiotics are usually prescribed and quinolones and tetracyclines are also effective.

The mortality rate was  5 to 30% in earlier days. And inpatient mortality was as high as 28 %.

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Surfactant and Alveolar Proteinosis

 Surfactant and Alveolar Proteinosis

PKGhatak,MD

A Phopholipoprotein compound present in the lung alveoli (air sacs) acts as a Surface Tension Lowering Agent. Alveoli are tiny air sacs, lined by just one layer of pneumocyte type1 cell - inside the sac outside air enters and leaves and outside the alveoli the blood circulates and the exchange of gases takes place. If the surfactant is removed, the wall of the alveoli will come in apposition and will not be separated by the force generated during breathing in the air (inspiration).

If you take two glass sides and put a drop of water on one slide then place the other slide over it; then try to separate those glass slides by pulling them apart, no matter how strong your hands are, you will not able to separate the slides. Now repeat the same experiment with one drop of soap water. The slides will come apart easily. Soap is a surface tension lowering agent. That is the reason the doctors are asking you to wash your hands with soap water as soon as possible in order to minimize covid infection if you were out.

A surfactant molecule has two ends, one end is a Hydrophobic end the other is a Hydrophilic end. The hydrophobic end is turned toward the air, and the other end towards the blood. Thereby keeping air and blood separate.

The Alveolar type 2 cells secrete surfactant. The surfactant molecules inside the cells are called laminar bodies and the extracellular surfactant is chemically the same. Chemically the surfactant is Dipalmitoylphosphatidylcholine. Surfactant is also present in the intestine and inner ear.

There is a balance between surfactant production and removal from the alveoli. Alveolar type 2 cells play a major role in both the formation and removal of the surfactant. In addition, several other factors are also involved in the removal of the surfactant from the lung. The alveolar macrophages, airway epithelial cells and ciliary escalator effect and reabsorption in blood in airways, breakdown of surfactant to its constituents by enzymes- lipid and protein components are all thought to be involved in this process. Granulocyte-Macrophage  stimulating factor plays a crucial role by increasing the production of Macrophages which engulf surfactants.

Group B streptococcus can degrade surfactants, pulmonary infections, pulmonary edema fluid and serum protein also destroy surfactants.

Chromosome 10 carries two genes that code the four proteins that are parts of the surfactant molecule. The deficiency of these genes is inherited as autosomal dominant and also as recessive modes. Congenital absence of surfactant is not compatible with life. In the fetal lung, surfactants are present in small amounts. Maturation of Alveolar type 2 cells correlated with the capacity to generate an adequate amount of surfactant. This becomes a crucial point in the survival of preterm infants with Acute Respiratory Syndrome.

Alveolar Proteinosis:

 

 Alveolar proteinosis:

When the balance between production and removal of surfactant is disrupted and removal grossly lags behind the accumulated surfactant in the alveoli completely fills up the alveolar space; the exchange of gases is markedly impaired and hypoxemia develops. The patients become short of breath, complain of tightness of the chest, and develop fever and marked hypoxemia.

Pulmonary alveolar proteinosis is a rare disease. The incidence is 1:000,000 population, higher in males and high in the age group 30 to 60 years.

The causes of alveolar proteinosis are three. Congenital, Autoimmune and Secondary.

Congenital alveolar proteinosis.

The granulocyte-macrophage colony stimulating factor (GM-CSF) deficiency impairs the clearing of surfactant from alveoli. The disease is inherited as an Autosomal recessive mode. The GM-MSF gene is located in the 5q 3.1 location on chromosome 5.

Autoimmune alveolar proteinosis.

Autoimmune proteinosis accounts for 90 % of all cases. Antibodies to GM-CSF are demonstrated in some cases but not all instances. The response to the removal of antibodies by plasmapheresis and IV therapy; and also Rituximab, a monoclonal antibody to phospholipids and also decreases the lymphocyte B 20 activities, results in the improved outcome, support this theory.

Secondary alveolar proteinosis.

The clinical picture develops the following conditions - cancers like Chronic Myeloid Leukemia, post exposure to inhaled toxic gases, exposure to a toxic level of Nickle.

Laboratory findings and diagnosis.

Hypoxemia is generally severe - often below 87%, with a low PaO2 when on oxygen at 100 %. Clubbing of fingers is present; evidence of weight loss is common. Chest X-ray shows lower and middle lobe dense consolidation, more centrally located giving an appearance of "Bat Wings". Bronchoscopy shows frothy, profuse secretion filling the airways and lung parenchyma. Fluid obtained from bronchoalveolar lavage fluid shows Periodic Acid Schiff (PAS) positive proteinous materials is diagnostic.

Treatment. Maintaining a near normal PaO2 by any means is essential including intubation and mechanical ventilation.

GM -CSF delivered by inhalation is most commonly employed, it may also be given IV. Plasmapheresis can also be undertaken. Bronchoalveolar lavage was a standard mode of treatment until GM-CSF therapy became available.

In resistant cases, Lung Transplantation is the only option that remains.

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