OVERVIEW
Spliceomycosis is an acute, subacute and chronic conditioned infection caused by pathogenic bacteria belonging to the phylum Spliceomycetes. Spliceomycetes belong to the phylum Spliceomycetes, a group of relatively primitive, fast-growing, and widely distributed terrestrial fungi, most of which are found in plant spoilage and soil.
Spliceomycetes includes 7 orders and 30 families. However, only the Trichoderma and the Wormy Molds are of medical importance. Trichoderma pathogens include a wide range of fungi in the Trichoderma genera Rhizoctonia, Ploughshares, Rhizophora, Trichoderma, and Cystotrichum, as well as in the families Ginkhaniaceae, Tetrasporaceae, Bottle Molds, Symphylloctococcaceae, and Dendrobacteriaceae. The pathogenic fungi in the order of entomopathogenic molds include frog fecal mold in the family of frog fecal mold, and entomopathogenic streptomycetes in the family of crown otoliths and heterosporous otoliths.
The disease has a worldwide distribution. The incidence of the disease has increased significantly in recent years with the expansion of the immunodeficiency population.
Causes
Spliceomycosis is toxic to humans and animals. In general, the organism is not virulent, and infection occurs in patients with severe underlying diseases. Splice bacillosis attacks blood vessels and tends to form thrombi in the lumen, causing local tissue necrosis.
Symptoms
1. Trichoderma infections
Clinical features are rapid onset of fever and tissue necrosis. Different clinical types are often related to the underlying disease of the patient. The prognosis of the disease is related to the underlying disease, the type of infection and whether it is diagnosed and treated early. It is most often seen with diabetes, starvation, severe burns, intravenous drug use and other illnesses such as leukemia, lymphoma, immunosuppressive treatments with cytotoxic drugs or corticosteroids, treatment with desferrioxamine (a type of iron chelator used to treat iron overload), and severe trauma. The incidence of co-infections in human immunodeficiency virus (HIV)-positive patients is gradually increasing.
(1) Nasal-cerebral splicing mycobacteriosis In the early stages, it is similar to chronic rhinitis, such as nasal congestion and headache. In the early stage, it is similar to chronic rhinitis, such as nasal congestion, headache, etc. Later, dark red bloody secretion may flow from the nasal cavity, and necrotic granuloma may be formed in the nasal cavity and sinuses. Invasion of the eye can cause eyelid edema, eye muscle paralysis, eyeball protrusion, pupil fixation, vision loss and even blindness. Once invading the skull, meningitis, encephalitis and other corresponding symptoms can appear rapidly, and cerebral nerves are often involved, especially V, VII cranial nerve dysfunction. Facial pain, paralysis and other symptoms can occur, with the progression of the disease, the pathogenic bacteria invade the larger cerebral blood vessels, causing embolism and necrosis, advanced patients can appear intracranial hypertension and cerebral hernia, most of which lead to death.
(2) pulmonary junction mycobacteriosis Pathogenic bacteria include the root mold (the most common). Due to the pathogenic bacteria through the respiratory tract invasion of the lungs, a few due to inhalation of nasoencephalic splicing bacteria secretion secondary. Persistent fever and rapidly progressive pulmonary infiltrates are common. Most present with nonspecific bronchopneumonia. When invasion of the pulmonary artery produces thrombosis and necrosis, chest pain, coughing up bloody sputum and hemoptysis appear.
(3) Gastrointestinal tract succubiosis Pathogenic bacteria include Mycobacterium umbelliferum (the most common). Lesions to the stomach, duodenum for the most, accounting for the majority of the type, chronic peptic ulcer is an important underlying disease. The duration of the disease ranges from 4 months to 30 years, and the most common symptom is epigastric pain, which may be accompanied by nausea and vomiting. Secondary to ulcers, the pattern, degree and frequency of abdominal pain change, according to ulcer treatment is not effective.
(4) skin junction mycosis Pathogenic bacteria for the tiny root hairy mold (the most common). Primary infection is often caused by trauma, surgery, etc., the damage pattern is diverse, with erythema, papules, plaques, pustules, ulcers, necrosis, etc.. The course of the disease is 2 months to 24 years, generally not spread by blood, the prognosis is better. Secondary infection is mostly from the nose, brain, lung or other parts of the hairy mold dissemination, the beginning of the skin lesions for painful or painless erythema, nodules, gradually expanding, and later the central ulceration, crusting and dry necrosis, the periphery is grayish-white, the outermost periphery of the edematous erythema, and gradually expanding outward. The course of the disease is short and the prognosis is poor.
(5) Neonatal succubus disease varies depending on the site of infection. Vomiting, abdominal distension and bloody stools can be seen when the intestines are invaded. If the brain, lungs, liver and so on are invaded, poor response, dyspnea, jaundice and other non-specific symptoms of the corresponding parts appear. Hepatic necrosis from umbilical trauma is a characteristic of neonatal infections. The mortality rate is extremely high.
(6) Others: Kidney and uterus can also be invaded.
2. Infections caused by mycobacteria
Mostly chronic inflammatory or granulomatous disease. Mainly in male children. Damage begins as a subcutaneous nodule that enlarges, hardens, sclerotizes, and swells painlessly, moving freely over the affected muscle but adhering to the skin, without ulceration but with hyperpigmentation. Systemic damage is rare and includes ulceration causing penetration of the patient’s hard palate, gastrointestinal and muscular infections.
Ear mold infections are mainly confined to the submucosa of the nose and are characterized by polyps or clearly palpable, confined granulomas. The vast majority are seen in adult males. The infection usually begins unilaterally in the nasal mucosa, and symptoms include nasal congestion, excessive discharge, and pain in the sinus area. Formation of subcutaneous nodules in the nasal or perinasal area may result in extensive facial swelling.
Examination
1. Direct microscopic examination
Broad, overwhelmingly nonseptate, thin-walled hyphae, often with focal bulbous swelling and irregular branching, are seen in clinical specimens. Scrapings, sputum and substaining observations. Direct microscopic detection of Trichoderma from necrotic tissue, sputum, or clinical specimens of bronchoalveolar lavage fluid is more meaningful than culture isolation. Microscopically the fungus is easily distinguished from other fungi, such as Aspergillus spp.
2. Fungal culture
Trichoderma spp. have no special requirements for nutrition, and can be grown on conventional fungal culture medium without actinomycetone.
3.Histopathology
The histopathology of Trichoderma infections has no obvious specificity, often with edema and neutrophilic infiltration, and rarely with strong inflammatory reaction.
Diagnosis
Diagnosis is mainly based on mycological examination and histopathological examination. This type of fungus is a common saprophytic fungus, and if Trichoderma is isolated from necrotic tissue, sputum, or bronchoalveolar lavage fluid by culture, it should be considered with caution. However, if the patient is diabetic or immunosuppressed, a positive culture is important for the diagnosis.
Treatment
1. Treatment of Trichophyton rubrum infection
The principles include control of the underlying disease, removal of infected necrotic tissue, and prompt administration of amphotericin B. Immunosuppressive drugs should be reduced or discontinued without jeopardizing patient safety.
(1) Systemic treatment Amphotericin B. If the infection cannot be controlled, consider switching to liposomal amphotericin B, and use it continuously until the patient returns to normal, or use it for at least 2 weeks, then switch to generic amphotericin B. Treatment of Trichophyton mentagrophytes with fluconazole and itraconazole can be successful, but due to the very small number of cases, its exact clinical efficacy is difficult to determine.
(2) Localized treatment If the infection is confined to a certain area of the lung and amphotericin B treatment is ineffective within 48 to 72 hours, surgical resection should be considered. Sometimes wedge resection can achieve the purpose, but often need to do the whole lung lobe or segmental resection. However, it is not suitable for more extensive infections. For patients with infections caused by Trichophyton mentagrophytes, excision of necrotic skin lesions and surrounding infected tissues is the most important and effective means of treatment, and skin grafting is required after surgical excision.
2. Frog fecal mold infection treatment
Saturated potassium iodide solution is effective, and oral ketoconazole can also be used. Amphotericin B is rarely used. surgical excision is not curative. Surgical excision is not curative. Ear mold infections are mainly treated by surgical excision. Sometimes there may be a therapeutic response to iodine preparations and oral azoles. Mycobacteria and ashwagandha are ineffective.