How to recognize pulmonary trichomycosis

  Pulmonary mucormycosis (pulmonary mucormycosis), also known as pulmonary mucormycosis, is a serious infection of the lungs caused by Trichoderma spp. and Rhizopus spp. in the order Trichoderma. Clinically caused by the infection is more common, Trichoderma infection in addition to frequent involvement of the lungs, but also often invade the nose, sinuses, orbits, brain and gastrointestinal tract, both can be disseminated to the whole body through the bloodstream to cause disseminated trichinosis. This disease is rare, but in recent years, with the widespread use of broad-spectrum antibiotics, antineoplastic drugs, corticosteroids and organ transplantation, the incidence of the trend has increased. The disease is not easily diagnosed before birth, and the death rate is extremely high. According to foreign reports, the death rate is 80% for untreated cases, 65% for lesions confined to the lungs, and up to 96% for disseminated cases. In cases diagnosed prenatally, timely medical treatment can reduce the mortality rate to 50%, and surgical resection combined with medical treatment may further reduce it to about 10%. Therefore, it is important to improve the prognosis of this disease by raising awareness, timely diagnosis and treatment.  Since 1885, when Paltauf first discovered and reported pulmonary trichinosis in autopsy, it has been reported all over the world, and 13 cases have been reported in China so far. Trichoderma belongs to the subclass of the algae class of jointed bacteria, widely distributed in the soil, decaying organic matter and air. Trichoderma spp. (rhizopus), Trichoderma spp. (mucor) and Plasmodium spp. (absidia) have a strong pathogenicity, Trichoderma spp. to invade the lungs mainly, Rhizopus often invade the nose, sinuses, orbits, brain and digestive tract. Trichoderma spp. can grow rapidly on Sabo medium, forming mycelial colonies. Mycelium is broader (6 to 25 mm in diameter), rarely separated, with irregular or right-angled branches, the end of the sporangia filled with ellipsoidal spores. Pulmonary trichinosis is caused by inhalation of spores. Healthy human alveolar macrophages can remove inhaled spores, so the disease occurs mostly in those with severe underlying disease and predisposing factors. Leukocyte deficiency, impaired phagocytosis, and acidosis are three important factors in susceptibility to this disease. Leukemia and solid tumor patients with primary or post-radiotherapy leukocyte deficiency and dysfunction, diabetes, especially in ketoacidosis, the body’s high-glucose acidic environment and leukocyte chemotaxis is weakened, all contribute to the growth and reproduction of Trichophyton. Other underlying diseases are still aplastic anemia, severe malnutrition, organ transplantation and the use of a large number of immunosuppressive agents. A small number of often exposed to spores healthy people (such as farmers) can develop the disease. After inhalation of spores through the nose, most often cause paranasal sinus and orbital infections, which can then invade the cranial brain causing meningitis and frontal lobe abscesses, pulmonary trichinosis is second only to the nasal brain type of infection. In addition, can also be caused by injection of contaminated spores of drugs and blood-borne infections. After Trichoderma enters the respiratory tract of susceptible individuals, mycelium can penetrate the walls of small bronchi and invade the walls and lumina of blood vessels, forming thrombi and emboli, leading to tissue ischemia, hemorrhagic infarction and necrotizing inflammation. Pathologic histology shows more extensive arterial tether formation, thrombus containing a large number of neutrophils, surrounding tissues with hemorrhage, edema and neutrophil-dominated purulent inflammation, extensive tissue necrosis, multiple abscess formation, rarely granuloma formation, and Trichoderma mycelium visible in the lumen and tissue. Vascular infarction and tissue necrosis are the characteristics of the disease.  [Clinical symptoms include cough, sputum, fever, dyspnea and chest pain, etc. There is no obvious difference with general bacterial pneumonia. Because Trichoderma is easy to invade the blood vessel wall, coughing blood is more common, and a few patients can have a large cough of blood. Physical examination has fever (mostly high fever), accelerated respiration, solid lung signs and dry and wet rales, pleural grating sounds can be heard when the pleura is involved. The disease is rapidly progressive and severe and can lead to death within a few days. Chronic limited pulmonary trichomycosis is seen only in healthy individuals. Routine blood tests may increase total white blood cells and neutrophils and decrease in severe infections or with immunosuppressive drugs. Chest x-ray shows an exudative solid shadow, which may involve the entire lobe of the lung, and a soft tissue-dense mass shadow, which is sometimes difficult to distinguish from a lung tumor. There are often multiple irregular cavity formation in the shadow, and pleural effusion signs can be seen, and all lung lobes can be involved. Early chest radiographs may show no abnormal findings. In the literature, the halo sign (halo sign), a circular hypodense area around the infiltrative shadow in chest computed tomography (CT) films, and the gas crescent sign, a crescent-shaped gas-containing sign between the lesion and normal tissue after vascular invasion, are typically seen. These signs can also be seen in lung abscesses, tuberculomas, hematomas, and lung cancer with cavities, but fungal infections should be highly guarded in immunocompromised individuals. The pathogenic fungus of nasal cerebral trichinosis invades the palate, paranasal sinuses, orbits and frontal lobes of the brain via the nasal cavity, causing necrotizing inflammation and abscess formation. Clinical symptoms include nasal congestion, nasal discharge with pus and blood, headache and vomiting, in addition to severe systemic symptoms. CT and magnetic resonance examination shows brain abscess and abscess formation. Trichoderma can also be disseminated hematologically to the lungs, gastrointestinal tract, kidneys, bladder, uterus and bilateral cerebral hemispheres, causing disseminated trichomycosis.  Patients with severe underlying disease and predisposing factors presenting with the above clinical manifestations should consider pulmonary trichomycosis, and a history of extensive spore exposure is also a clue to the proposed diagnosis of the disease. Definitive diagnosis depends on tissue biopsy to find Trichoderma filaments and pathological changes characterized by thrombosis and tissue necrosis, or the detection of Trichoderma in secretions from the lesion. Trichophyton examination includes direct microscopy and culture. The former sputum, pus, biopsy lung tissue and autopsy specimens made of smears and sections, hematoxylin eosin (HE) and periodic acid – Siff (PAS) staining can be found short thick non-separated into right-angle branching mycelium; the latter will be specimens in the sandburg medium or other acidic medium containing glucose culture, colonies began to white woolly, then gray and or yellow. Negative cultures cannot exclude Trichoderma infection. The authors reviewed 93 cases of pulmonary trichinosis diagnosed during life, of which 40 cases were confirmed by fiberoptic bronchoscopic lung biopsy, 30 cases by open chest exploration and lung biopsy, 12 cases by positive sputum bacteria, 6 cases by needle aspiration lung biopsy through the chest wall and 5 cases by bronchoalveolar lavage fluid culture.  [Treatment] Because of the pathological characteristics of vascular obstruction and tissue necrosis, it is difficult for drugs to reach the core of the lesion, and the efficacy of medical treatment is poor, so surgical excision or drainage should be considered for isolated lesions with surgical conditions, regardless of whether they are confined to the lung or not. Aggressive antifungal therapy is administered before and after surgery. The surgical approach includes lobectomy or segmental resection, wedge resection, or irregular resection. The authors treated a case of pulmonary trichomycosis with double upper lung giant mass shadow with multiple cavities, which was cured by successive lobectomy of both upper lungs and treatment with antifungal drugs, similar cases have not been reported and can be used as clinical reference. For those who do not have surgical conditions, antifungal drug therapy should be administered as early as possible. At the same time, actively control the underlying disease and remove the causative factors. The antifungal drug with positive efficacy is amphotericin B. The first dose of 1 mg/d for adults is increased by 2-5 mg daily to 30-50 mg/d for 1 to 2 months or longer. The efficacy of pyrrole antifungal drugs for trichinosis has not been clearly evaluated, some authors believe that Trichinella is naturally resistant to pyrrole antifungal drugs, but in recent years there are reports of fluconazole curing pulmonary trichinosis at home and abroad, worth further research and verification.