On chest X-ray and CT, pulmonary aspergillosis classically manifests as a halo sign, and, later, an air crescent sign.

In hematologic patients with invasive aspergillosis, the galactomannan test can make the diagnosis in a noninvasive way. False positive "Aspergillus" galactomannan tests have been found in patients on intravenous treatment with some antibiotics or fluids containing gluconate or citric acid such as some transfusion platelets, parenteral nutrition or PlasmaLyte.

On microscopy, "Aspergillus" species are reliably demonstrated by silver stains, e.g., Gridley stain or Gomori methenamine-silver. These give the fungal walls a gray-black colour. The hyphae of "Aspergillus" species range in diameter from 2.5 to 4.5 µm. They have septate hyphae, but these are not always apparent, and in such cases they may be mistaken for Zygomycota. "Aspergillus" hyphae tend to have dichotomous branching that is progressive and primarily at acute angles of about 45°.

The specific criteria for diagnosis of CPA are:

Chest X-rays showing one or more lung cavities. There may be a fungal ball present or not.

Symptoms lasting more than 3 months, usually including weight loss, fatigue, cough, coughing blood (haemoptysis) and breathlessness

A blood test or tissue fluid test positive for Aspergillus species

Aspergilloma

An aspergilloma is a fungal mass caused by a fungal infection with Aspergillus species that grows in either scarred lungs or in a pre-existing lung cavity, which may have been caused by a previous infection. Patients with a previous history of tuberculosis, sarcoidosis, cystic fibrosis or other lung disease are most susceptible to an aspergilloma. Aspergillomas may have no specific symptoms but in many patients there is some coughing up of blood called haemoptysis - this may be infrequent and in small quantity, but can be severe and then it requires urgent medical help.

Tests used to diagnose an aspergilloma may include:

- Chest X-ray

- Chest CT

- Sputum culture

- Bronchoscopy or bronchoscopy with lavage (BAL)

- Serum precipitins for aspergillus (blood test to detect antibodies to aspergillus)

Almost all aspergillomas are caused by "Aspergillus fumigatus". In diabetic patients it may be caused by "Aspergillus niger". It is very rarely caused by "Aspergillus flavus", "Aspergillus oryzae", "Aspergillus terreus" or "Aspergillus nidulans".

The current medical treatments for aggressive invasive aspergillosis include voriconazole and liposomal amphotericin B in combination with surgical debridement.

For the less aggressive allergic bronchopulmonary aspergillosis findings suggest the use of oral steroids for a prolonged period of time, preferably for 6–9 months in allergic aspergillosis of the lungs. Itraconazole is given with the steroids, as it is considered to have a "steroid sparing" effect, causing the steroids to be more effective, allowing a lower dose.,

Other drugs used, such as amphotericin B, caspofungin (in combination therapy only), flucytosine (in combination therapy only), or itraconazole,

are used to treat this fungal infection. However, a growing proportion of infections are resistant to the triazoles. "A. fumigatus", the most commonly infecting species, is intrinsically resistant to fluconazole.

Culturing fungi from sputum is a supportive test in the diagnosis of ABPA, but is not 100% specific for ABPA as "A. fumigatus" is ubiquitous and commonly isolated from lung expectorant in other diseases. Nevertheless, between 40–60% of patients do have positive cultures depending on the number of samples taken.

Fungal pneumonia can be diagnosed in a number of ways. The simplest and cheapest method is to culture the fungus from a patient's respiratory fluids. However, such tests are not only insensitive but take time to develop which is a major drawback because studies have shown that slow diagnosis of fungal pneumonia is linked to high mortality. Microscopy is another method but is also slow and imprecise. Supplementing these classical methods is the detection of antigens. This technique is significantly faster but can be less sensitive and specific than the classical methods.

A molecular test based on quantitative PCR is also available from Myconostica. Relying on DNA detection, this is the most sensitive and specific test available for fungi but it is limited to detecting only pneumocystis jirovecii and aspergillus.

Consolidation and mucoid impaction are the most commonly described radiological features described in ABPA literature, though much of the evidence for consolidation comes from before the development of computed tomography (CT) scans. Tramline shadowing, finger-in-glove opacities and ‘toothpaste shadows’ are also prevalent findings.

When utilising high resolution CT scans, there can be better assessment of the distribution and pattern of bronchiectasis within the lungs, and hence this is the tool of choice in the radiological diagnosis of ABPA. Central (confined to medial two-thirds of medial half of the lung) bronchiectasis that peripherally tapers bronchi is considered a requirement for ABPA pathophysiology, though in up to 43% of cases there is considerable extension to the periphery of the lung.

Mucoid impaction of the upper and lower airways is a common finding. Plugs are hypodense but appear on CT with high attenuation (over 70 Hounsfield units) in up to 20% of patients. Where present it is a strong diagnostic factor of ABPA and distinguishes symptoms from other causes of bronchiectasis.

CT scans may more rarely reveal mosaic-appearance attenuation, centrilobular nodules, tree-in-bud opacities and pleuropulmonary fibrosis (a finding consistent with CPA, a disease with ABPA as a known precursor). Rarely other manifestations can be seen on CT scans, including military nodular opacities, perihilar opacities (that mimic hilar lymphadenopathy), pleural effusions and pulmonary masses. Cavitation and aspergilloma are rarer findings, not exceeding 20% of patients, and likely represent a shift from ABPA to CPA if accompanied by pleural thickening or fibrocavitary disease.

Patients with single aspergillomas generally do well with surgery to remove the aspergilloma, and are best given pre-and post-operative antifungal drugs. Often, no treatment is necessary. However, if a patient coughs up blood (haemoptysis), treatment may be required (usually angiography and embolisation, surgery or taking tranexamic acid). Angiography (injection of dye into the blood vessels) may be used to find the site of bleeding which may be stopped by shooting tiny pellets into the bleeding vessel.

For chronic cavitary pulmonary aspergillosis and chronic fibrosing pulmonary aspergillosis, lifelong use of antifungal drugs is usual. Itraconazole and voriconazole are first and second-line anti fungal agents respectively. Posaconazole can be used as third-line agent, for patients who are intolerant of or developed resistance to the first and second-line agents. Regular chest X-rays, serological and mycological parameters as well as quality of life questionnaires are used to monitor treatment progress. It is important to monitor the blood levels of antifungals to ensure optimal dosing as individuals vary in their absorption levels of these drugs.

Eosinophilic pneumonia is diagnosed in one of three circumstances: when a complete blood count reveals increased eosinophils and a chest x-ray or computed tomography (CT) identifies abnormalities in the lung, when a biopsy identifies increased eosinophils in lung tissue, or when increased eosinophils are found in fluid obtained by a bronchoscopy (bronchoalveolar lavage [BAL] fluid). Association with medication or cancer is usually apparent after review of a person's medical history. Specific parasitic infections are diagnosed after examining a person's exposure to common parasites and performing laboratory tests to look for likely causes. If no underlying cause is found, a diagnosis of AEP or CEP is made based upon the following criteria. AEP is most likely with respiratory failure after an acute febrile illness of usually less than one week, changes in multiple areas and fluid in the area surrounding the lungs on a chest x-ray, and greater than 25% eosinophils on a BAL. Other typical laboratory abnormalities include an elevated white blood cell count, erythrocyte sedimentation rate, and immunoglobulin G level. Pulmonary function testing usually reveals a restrictive process with reduced diffusion capacity for carbon monoxide. CEP is most likely when the symptoms have been present for more than a month. Laboratory tests typical of CEP include increased blood eosinophils, a high erythrocyte sedimentation rate, iron deficiency anemia, and increased platelets. A chest x-ray can show abnormalities anywhere, but the most specific finding is increased shadow in the periphery of the lung, away from the heart.

Eosinophilic pneumonia due to cancer or parasitic infection carries a prognosis related to the underlying illness. AEP and CEP, however, have very little associated mortality as long as intensive care is available and treatment with corticosteroids is given. CEP often relapses when prednisone is discontinued; therefore, some people with CEP require lifelong therapy. Chronic prednisone is associated with many side effects, including increased infections, weakened bones, stomach ulcers, and changes in appearance.

The diagnosis of plastic bronchitis is confirmed by recovery of casts that have been coughed up or visualized during a bronchoscopy. There is no specific cytologic, pathologic or laboratory test that is diagnostic for casts due to lymphatic PB.

X-rays can be used to examine the lung tissue, however it can not be used to positively diagnose geotrichosis. X-rays may show cavitation that is located the walls of the lungs tissues. The lung tissue resemble the early signs of tuberculosis. The results of an x-ray examination of pulmonary geotrichosis presents smooth, dense patchy infiltrations and some cavities. Bronchial geotrichosis shows peribronchial thickening with fine mottling may be present on middle or basilar pulmonary fields. Bronchial geotrichosis usually present itself as non-specific diffuse peribronchical infiltration.

Simple chest roentenograms may reveal collapse due to airway obstruction. The contralateral lung may be hyperinflated. Casts can be visualized within the major airways using computerized axial tomography scans.

Heavy T2-weighted MRI, and, as appropriate, intranodal lymphangiogram and/or dynamic contrast-enhanced MR lymphangiography may be useful for identifying pathological lymphatic tissue and/or lymphatic flow.

Fungal pneumonia can be treated with antifungal drugs and sometimes by surgical debridement.

The diagnoses of geotrichosis cannot be determined without using culture or microscopic measurements. The laboratory diagnosis of geotrichosis involves collected fungi samples areas of infections without contamination. Scraping of the mouth lesions and the ulcers can provide a sample of "G. candidum." Samples can also be collected from pus and mucus can be obtained from the feces. Sputum can be searched for the mucoid-like white flakes for further examination. Culturing the cylindrical barrel-shaped or elliptical fungi in considerable numbers in oral lesions is an indicator that a patient may have geotrichosis. Under the microscope the fungi appears yeast-like and septate branching hyphae that can be broken down into chains or individual arthrospores. Arthrospores appear rectangular with flat or rounded ends. Under the microscope the arthroconidia size range from 6-12μm x 3-6μm. Arthroconidia and coarse true hyphae can be observed can be observed under the microscope. Another identification method for "G. candidum" is selective isolation method. A selection isolation method based on the fungi tolerance to novobiocin and carbon dioxide can determine if "G. candidum" is the cause of illness.

Bronchiectasis may be diagnosed clinically or on review of imaging. The British Thoracic Society recommends all non-cystic-fibrosis-related bronchiectasis be confirmed by CT. CT may reveal tree-in-bud abnormalities, dilated bronchi, and cysts with defined borders.

Other investigations typically performed at diagnosis include blood tests, sputum cultures, and sometimes tests for specific genetic disorders.

Airway obstruction may cause obstructive pneumonitis or post-obstructive pneumonitis.

In order to prevent bronchiectasis, children should be immunized against measles, pertussis, pneumonia, and other acute respiratory infections of childhood. While smoking has not been found to be a direct cause of bronchiectasis, it is certainly an irritant that all patients should avoid in order to prevent the development of infections (such as bronchitis) and further complications.

Treatments to slow down the progression of this chronic disease include keeping bronchial airways clear and secretions weakened through various forms of pneumotherapy. Aggressively treating bronchial infections with antibiotics to prevent the destructive cycle of infection, damage to bronchial tubes, and more infection is also standard treatment. Regular vaccination against pneumonia, influenza and pertussis are generally advised. A healthy body mass index and regular doctor visits may have beneficial effects on the prevention of progressing bronchiectasis. The presence of hypoxemia, hypercapnia, dyspnea level and radiographic extent can greatly affect the mortality rate from this disease.

Lower airway obstruction is mainly caused by increased resistance in the bronchioles (usually from a decreased radius of the bronchioles) that reduces the amount of air inhaled in each breath and the oxygen that reaches the pulmonary arteries. It is different from airway restriction (which prevents air from diffusing into the pulmonary arteries because of some kind of blockage in the lungs). Diseases that cause lower airway obstruction are termed obstructive lung diseases.

Lower airway obstruction can be measured using spirometry. A decreased FEV1/FVC ratio (versus the normal of about 80%) is indicative of an airway obstruction, as the normal amount of air can no longer be exhaled in the first second of expiration. An airway restriction would not produce a reduced FEV1/FVC ratio, but would reduce the vital capacity. The ventilation is therefore affected leading to a ventilation perfusion mismatch and hypoxia.

In more severe cases, it is treated by administering intravenous antibiotics and may require admission to an intensive care unit (ICU) for intubation and supportive ventilation if the airway swelling is severe. During an intensive care admission, various methods of invasive and non-invasive monitoring may be required, which may include ECG monitoring, oxygen saturation, capnography and arterial blood pressure monitoring.

Treatment for fungal sinusitis can include surgical debridement; helps by slowing progression of disease thus allowing time for recovery additionally we see the options below:

- In the case of invasive fungal sinusitis, echinocandins, voriconazole, and amphoterecin (via IV) may be used

- For allergic fungal sinusitis, systemic corticosteroids like prednisolone, methylprednisolone are added for their anti-inflammatory effect, bronchodilators and expectorants help to clear secretions in the sinuses.

As of tissue or discharge are generally unreliable, the diagnosis of mucormycosis tends to be established with a biopsy specimen of the involved tissue.

Tracheitis is an inflammation of the trachea.

Although the trachea is usually considered part of the lower respiratory tract, in ICD-10 tracheitis is classified under "acute upper respiratory infections".

Usually the sequestration is removed after birth via surgery. In most cases this surgery is safe and effective; the child will grow up to have normal lung function.

In a few instances, fetuses with sequestrations develop problematic fluid collections in the chest cavity. In these situations a Harrison catheter shunt can be used to drain the chest fluid into the amniotic fluid.

In rare instances where the fetus has a very large lesion, resuscitation after delivery can be dangerous. In these situations a specialized delivery for management of the airway compression can be planned called the EXIT procedure, or a fetal laser ablation procedure can be performed. During this minimally invasive fetal intervention, a small needle is inserted into the sequestration, and a laser fiber is targeted at the abnormal blood vessel going to the sequestration. The goal of the operation is to use laser energy to stop the blood flow to the sequestration, causing it to stop growing. Ideally, after the surgery, the sequestration steals less blood flow from the fetus, and the heart and lungs start growing more normally as the sequestration shrinks in size and the pleural effusion goes away.

The treatment for this is a wedge resection, segmentectomy, or lobectomy via a VATS procedure or thoracotomy.

Pulmonary sequestrations usually get their blood supply from the thoracic aorta.

In terms of diagnosis, the clinical examination gives an idea about fungal sinusitis, as well as:

Bronchopulmonary sequestration (BPS) is a rare congenital malformation of the lower respiratory tract.

It consists of a nonfunctioning mass of normal lung tissue that lacks normal communication with the tracheobronchial tree, and that receives its arterial blood supply from the systemic circulation.

BPS is estimated to comprise 0.15 to 6.4 percent of all congenital pulmonary malformations, making it an extremely rare disorder.

Sequestrations are classified anatomically.

Intralobar sequestration (ILS) in which the lesion is located within a normal lobe and lacks its own visceral pleura.

Extralobar sequestration (ELS) in which the mass is located outside the normal lung and has its own visceral pleura

The blood supply of 75% of pulmonary sequestrations is derived from the thoracic or abdominal aorta.

The remaining 25% of sequestrations receive their blood flow from the subclavian, intercostal, pulmonary, pericardiophrenic, innominate, internal mammary, celiac, splenic, or renal arteries.