Acute invasive pulmonary aspergillosis

　　Invasive aspergillosis is caused by the invasion of endoaspiromycetes (mainly Aspergillus fumigatus) into tissues. Phagocytes, as one of the host's defense mechanisms, play an important role in the pathogenesis of acute invasive pulmonary aspergillosis in terms of their quantity and function. Lymphocyte-mediated cell immunity is also important. Experimental studies have shown that neutrophils can prevent the formation of aspergillus hyphae, while monocytes mainly affect the conidia. This is consistent with the clinical observation that this disease often occurs in patients with granulocytopenia and impaired cell immunity. The role of humoral immunity in the pathogenesis of the disease is unclear. There is no increase in the incidence of the disease in patients with deficient or dysfunctional gamma globulin, suggesting that humoral immunity does not play a major role. The pathological manifestations are mainly acute necrotic hemorrhagic pneumonia, inflammatory infiltration, suppuration, and eventually granuloma formation. Hyphae proliferate and invade blood vessels in the lungs, causing necrotizing vasculitis, leading to thrombosis or septic embolism, causing hemoptysis and hematogenous dissemination, and causing aspergillosis in organs such as the brain, liver, kidney, and heart. Hematogenous dissemination of pulmonary abscesses and thrombi can also sometimes cause lung lesions.

　　This disease is likely to lead to respiratory failure, with clinical manifestations such as dyspnea, cyanosis, and mental and neurological symptoms, and when complicated with pulmonary encephalopathy, there may be conjunctival congestion, papilledema, flapping tremors, and disturbance of consciousness, etc. Severe cases may have gastrointestinal bleeding.

　　The typical symptoms of this disease are granulocytopenia or fever that cannot be explained during the process of receiving broad-spectrum antibiotics, immunosuppressants, and corticosteroids. Chest symptoms are most common with dry cough and chest pain. Hemoptysis is not as common as the first two symptoms but is very important and has diagnostic value. When the lung lesions are extensive, dyspnea and even respiratory failure may occur. In addition, gastrointestinal bleeding and various central nervous system symptoms may also occur. The physical signs of the lungs depend on the nature and extent of the lesions; when the pleura is involved, there may be pleural friction or rub.

　　To prevent the occurrence of acute invasive pulmonary aspergillosis, everyone should pay attention to the following points:

　　1. Treat the primary disease to eliminate or shorten the high-risk period of the patient.

　　2. Prevent or reduce contact between susceptible patients and aspergillus spores.

　　3. Prophylactic use of amphotericin B intravenously has a high toxicity and is not suitable as prophylactic treatment. A nasal spray containing amphotericin B has some preventive effect. Other antifungal drugs have no significant preventive effect. In high-risk patients with fever that is not responsive to antibiotic treatment, amphotericin B can be used early on an empirical basis, usually starting treatment after 7 days of fever.

　　To diagnose acute invasive pulmonary aspergillosis, the following examinations need to be performed:

　　1. Routine blood test

　　Blood routine examination mainly shows an increase in eosinophils, with more than 90% of IgG precipitins positive, and a significant increase in serum total IgE.

　　2. Chest X-ray

　　X-ray manifestations include different forms of lung infiltration, with bronchopneumonia being the most common. Multiple focal infiltrations often occur in the peripheral lung fields, and some cases may present similarly to pulmonary embolism or infarction. Lobar consolidation and granulomatous lesions are also seen. With the progression of the lesion, lung cavities often appear, and acute aspergilloma may also form. When pleural effusion occurs, corresponding X-ray signs are seen.

　　Patients with this disease should pay attention to light diet, limit or avoid eating fish, shrimp, crab, lamb, and other pungent and irritating foods, poultry such as chickens, ducks, and geese, and刺激性食物 such as scallions, ginger, garlic, chili, coriander, and alcohol, as well as difficult-to-digest foods such as fried foods.

　　The treatment of acute invasive pulmonary aspergillosis is首选 with amphotericin B, with a recommended dose of 0.6mg/kg per day for adults, gradually increasing the dose after 2-3 days until 1.0mg/kg per day. Empirical use of amphotericin B in highly suspected but undiagnosed cases should be stopped if there is no efficacy by the 7th day of the course.

　　Flucytosine (5-fluorocytosine) usually has a low antibacterial activity against pulmonary aspergillosis, but it has a synergistic effect with amphotericin B and can be used in combination in patients with severe infections. Its adverse reactions, especially bone marrow suppression, limit its application.

　　Laboratory data shows that rifampicin and amphotericin B have synergistic antibacterial activity against Aspergillus, but their hepatotoxicity and immunosuppressive effects also limit their application. Itraconazole has good antibacterial activity against Aspergillus, and there have been reports of successful treatment of pulmonary aspergillosis. Acute pulmonary aspergilloma sometimes breaks down and causes severe systemic dissemination, so it is advocated that those who are suitable for surgery should undergo surgical resection. In patients with granulocytopenia complicated by pulmonary aspergillosis, the infusion of granulocytes as adjuvant therapy has a certain effect, but there are reports that the combination of amphotericin B with granulocyte transfusion increases pulmonary toxicity, and it must be very cautious. There are some reports that high-dose amphotericin B (1.0mg/kg daily) combined with flucytosine (5-fluorocytosine) before the start of anticancer chemotherapy has been successful in preventing the onset of aspergillosis pneumonia.