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A 66-year-old female patient experienced intermittent low-grade fever, cough, shortness of breath and decreased activity endurance in the past 3 months
.
The patient is a farmer by profession and has no history of smoking or chronic lung disease
.
Only type 2 diabetes was reported (no medication), no recent travel, and no bird breeding at home
.
The initial diagnosis of the local hospital showed that the left lower lobe atelectasis was accompanied by a small amount of pleural effusion; the diagnosis of mucormycosis was diagnosed by bronchial biopsy
.
Subsequently, the amphotericin B was injected intravenously and inhaled by aerosol at the same time, and the course of treatment was 15 days
.
However, the symptoms did not improve significantly after treatment, but the symptoms of dyspnea gradually worsened
.
Physical examination after admission: T 36.
8℃, BP128/67 mmHg, P 106 beats/min, R 27 beats/min, air pulse blood oxygen saturation 94%
.
Auscultation revealed that the breath sounds of the left lower lung were weakened
.
The rest of the physical examination results were not significant
.
Laboratory examination: arterial blood gas analysis showed that the pH was 7.
45, PaCO227 mmHg, PaO2 70 mmHg
.
The blood test found that there were leukocytosis (reaching 14,200 WBC/mm3), neutrophils accounted for 84.
2%, lymphocytes accounted for 7.
5%, and monocytes accounted for 7.
7%
.
Hemoglobin and platelet counts are normal
.
HbA1c is 6.
5%
.
Procalcitonin is normal
.
Plasma (1,3)-β-D-glucan, galactomannan and serum Aspergillus IgG antibodies were all negative
.
The serum CD4+ cell count was 581 cells/mL
.
On admission, chest CT showed segmental bronchial occlusion of the left lower lobe with atelectasis and a small amount of pleural effusion (Figure 1A, A and D1B)
.
Lung function tests cannot be performed
.
Bronchoscopy showed that the distal part of the left main bronchus was blocked by white necrosis (Figure 1C)
.
The biopsy was not completed due to concerns about the risk of major bleeding
.
The smear and culture of fungi, acid-fast bacilli and other bacteria in bronchial lavage fluid were all negative
.
Figure 1 Enhanced CT of the chest showed segmental bronchial occlusion of the left lower lobe with atelectasis and a small amount of pleural effusion
.
Bronchoscopy revealed white necrosis on the distal end of the left main bronchus to block part of the lumen
.
The left diagnostic thoracentesis revealed exudative effusion, lactate dehydrogenase was 128 U/L, and the ratio of pleural fluid/serum total protein was 0.
57
.
The pH of the pleural fluid is 7.
31
.
Culture of the pleural effusion and subsequent microscopic examination revealed fungal hyphae
.
Lactofol cotton blue staining revealed transparent septal hyphae with clusters of short conidia (Figure 2A)
.
The immunohistochemical tests of antibodies to Aspergillus and Mucor that were suspected to be diagnosed in previous hospitals were negative (Figures 2B and 2C)
.
Figure 2 A lactophenol cotton blue staining revealed transparent septal hyphae with clusters of short conidia; B immunohistochemistry negative for Aspergillus antibodies; C negative immunohistochemistry for Mucor antibodies followed by next-generation metagenomic sequencing (mNGS) The final diagnosis was an invasive lung infection of Trichoderma longibrachiatum
.
After the susceptibility test of Trichoderma isolated from the pleural fluid, it was found that the minimum inhibitory concentration of each fungal drug was: amphotericin B 2 mg/L, voriconazole 0.
25 mg/L, fluconazole 32 mg/L, and itrax Conazole 0.
5 mg/L, posaconazole 0.
5 mg/L, flucytosine>64 mg/L
.
The patient's fever subsided shortly after receiving treatment, and his dyspnea and cough symptoms gradually improved
.
After 6 months of antifungal treatment, follow-up chest CT scans showed improvement in obstructive pneumonia and pleural effusion (Figure 3)
.
Figure 3 After 6 months of antifungal treatment, the patient’s CT chest scan showed that obstructive pneumonia and pleural effusion were significantly improved.
Discussion Trichoderma is a saprophytic filamentous fungus widely distributed in soil, plants, and rotting Vegetation and wood
.
In the past, several immunocompromised patients were found to have been invasively infected by Trichoderma: such as solid tumors or hematological tumors receiving chemotherapy, bone marrow or solid organ transplant patients taking immunosuppressive agents, and patients receiving peritoneal dialysis.
There are reports of Trichoderma infection
.
Previous studies reported that the mortality rate of Trichoderma infection was as high as 53%
.
Nine species of Trichoderma have been reported as potential human pathogens (including: Trichoderma dark green, Trichoderma citrinum, Trichoderma harzianum, Trichoderma konsi, Trichoderma longibrachia, Trichoderma orientale, Trichoderma pseudokonsi, Trichoderma reesei and Trichoderma viride), among which Trichoderma longiflorum is the most common
.
The first confirmed case of lung infection with Trichoderma longibrachiatum was an invasive lung infection in a leukemia patient with neutropenia in 2002
.
The diagnosis of Trichoderma longibrachiatum invasive lung infection is based on clinical symptoms, imaging and microbiology
.
Diagnosis should meet the following criteria: (1) High-risk patients with persistent fever >96h are ineffective for appropriate broad-spectrum antimicrobial treatment; (2) There are special X-ray signs on CT images; (3) Fungal hyphae are directly detected by microscopy, Or respiratory secretions or body fluids cultured with Trichoderma longibrachiatum; the common X-ray manifestations of Trichoderma longiflora infection include multiple nodules with halo or air crescent sign, focal compaction, pleural effusion, and even pericardium The effusion has imaging features similar to invasive aspergillosis
.
There are many ways to treat Trichoderma longibrachia infections, including surgical resection plus amphotericin B, amphotericin B alone, surgical debridement alone, or the use of other antifungal drugs, including itraconazole, caspofencin, and voriconazole
.
Trichoderma longibrachiatum is highly resistant to amphotericin B, partly due to poor tissue permeability
.
Voriconazole is an alternative to amphotericin B for the treatment of invasive Trichoderma infections because of its lower minimum inhibitory concentration (MIC) value, fewer side effects, and higher penetration rate
.
Clinical points ➤ Trichoderma is a saprophytic filamentous fungus, and infection with Trichoderma is easily confused with mucor
.
Trichoderma infection can occur in a host with a normal immune function or a host with a weakened immune function
.
➤If untreated or improperly treated, the mortality rate of patients with Trichoderma infection is close to 50%
.
➤Treatment methods for Trichoderma infection include surgical resection and antifungal treatment.
Antifungal drugs such as amphotericin B and voriconazole should be used according to the severity of the disease, the minimum inhibitory concentration and the degree of invasive damage
.
Trichoderma has low toxicity, but it is highly resistant to antifungal drugs; in some cases, combination therapy can be considered
.
Reference: Yu Q, et al.
Chest.
2021 Aug;160(2):e177-e180.
.
The patient is a farmer by profession and has no history of smoking or chronic lung disease
.
Only type 2 diabetes was reported (no medication), no recent travel, and no bird breeding at home
.
The initial diagnosis of the local hospital showed that the left lower lobe atelectasis was accompanied by a small amount of pleural effusion; the diagnosis of mucormycosis was diagnosed by bronchial biopsy
.
Subsequently, the amphotericin B was injected intravenously and inhaled by aerosol at the same time, and the course of treatment was 15 days
.
However, the symptoms did not improve significantly after treatment, but the symptoms of dyspnea gradually worsened
.
Physical examination after admission: T 36.
8℃, BP128/67 mmHg, P 106 beats/min, R 27 beats/min, air pulse blood oxygen saturation 94%
.
Auscultation revealed that the breath sounds of the left lower lung were weakened
.
The rest of the physical examination results were not significant
.
Laboratory examination: arterial blood gas analysis showed that the pH was 7.
45, PaCO227 mmHg, PaO2 70 mmHg
.
The blood test found that there were leukocytosis (reaching 14,200 WBC/mm3), neutrophils accounted for 84.
2%, lymphocytes accounted for 7.
5%, and monocytes accounted for 7.
7%
.
Hemoglobin and platelet counts are normal
.
HbA1c is 6.
5%
.
Procalcitonin is normal
.
Plasma (1,3)-β-D-glucan, galactomannan and serum Aspergillus IgG antibodies were all negative
.
The serum CD4+ cell count was 581 cells/mL
.
On admission, chest CT showed segmental bronchial occlusion of the left lower lobe with atelectasis and a small amount of pleural effusion (Figure 1A, A and D1B)
.
Lung function tests cannot be performed
.
Bronchoscopy showed that the distal part of the left main bronchus was blocked by white necrosis (Figure 1C)
.
The biopsy was not completed due to concerns about the risk of major bleeding
.
The smear and culture of fungi, acid-fast bacilli and other bacteria in bronchial lavage fluid were all negative
.
Figure 1 Enhanced CT of the chest showed segmental bronchial occlusion of the left lower lobe with atelectasis and a small amount of pleural effusion
.
Bronchoscopy revealed white necrosis on the distal end of the left main bronchus to block part of the lumen
.
The left diagnostic thoracentesis revealed exudative effusion, lactate dehydrogenase was 128 U/L, and the ratio of pleural fluid/serum total protein was 0.
57
.
The pH of the pleural fluid is 7.
31
.
Culture of the pleural effusion and subsequent microscopic examination revealed fungal hyphae
.
Lactofol cotton blue staining revealed transparent septal hyphae with clusters of short conidia (Figure 2A)
.
The immunohistochemical tests of antibodies to Aspergillus and Mucor that were suspected to be diagnosed in previous hospitals were negative (Figures 2B and 2C)
.
Figure 2 A lactophenol cotton blue staining revealed transparent septal hyphae with clusters of short conidia; B immunohistochemistry negative for Aspergillus antibodies; C negative immunohistochemistry for Mucor antibodies followed by next-generation metagenomic sequencing (mNGS) The final diagnosis was an invasive lung infection of Trichoderma longibrachiatum
.
After the susceptibility test of Trichoderma isolated from the pleural fluid, it was found that the minimum inhibitory concentration of each fungal drug was: amphotericin B 2 mg/L, voriconazole 0.
25 mg/L, fluconazole 32 mg/L, and itrax Conazole 0.
5 mg/L, posaconazole 0.
5 mg/L, flucytosine>64 mg/L
.
The patient's fever subsided shortly after receiving treatment, and his dyspnea and cough symptoms gradually improved
.
After 6 months of antifungal treatment, follow-up chest CT scans showed improvement in obstructive pneumonia and pleural effusion (Figure 3)
.
Figure 3 After 6 months of antifungal treatment, the patient’s CT chest scan showed that obstructive pneumonia and pleural effusion were significantly improved.
Discussion Trichoderma is a saprophytic filamentous fungus widely distributed in soil, plants, and rotting Vegetation and wood
.
In the past, several immunocompromised patients were found to have been invasively infected by Trichoderma: such as solid tumors or hematological tumors receiving chemotherapy, bone marrow or solid organ transplant patients taking immunosuppressive agents, and patients receiving peritoneal dialysis.
There are reports of Trichoderma infection
.
Previous studies reported that the mortality rate of Trichoderma infection was as high as 53%
.
Nine species of Trichoderma have been reported as potential human pathogens (including: Trichoderma dark green, Trichoderma citrinum, Trichoderma harzianum, Trichoderma konsi, Trichoderma longibrachia, Trichoderma orientale, Trichoderma pseudokonsi, Trichoderma reesei and Trichoderma viride), among which Trichoderma longiflorum is the most common
.
The first confirmed case of lung infection with Trichoderma longibrachiatum was an invasive lung infection in a leukemia patient with neutropenia in 2002
.
The diagnosis of Trichoderma longibrachiatum invasive lung infection is based on clinical symptoms, imaging and microbiology
.
Diagnosis should meet the following criteria: (1) High-risk patients with persistent fever >96h are ineffective for appropriate broad-spectrum antimicrobial treatment; (2) There are special X-ray signs on CT images; (3) Fungal hyphae are directly detected by microscopy, Or respiratory secretions or body fluids cultured with Trichoderma longibrachiatum; the common X-ray manifestations of Trichoderma longiflora infection include multiple nodules with halo or air crescent sign, focal compaction, pleural effusion, and even pericardium The effusion has imaging features similar to invasive aspergillosis
.
There are many ways to treat Trichoderma longibrachia infections, including surgical resection plus amphotericin B, amphotericin B alone, surgical debridement alone, or the use of other antifungal drugs, including itraconazole, caspofencin, and voriconazole
.
Trichoderma longibrachiatum is highly resistant to amphotericin B, partly due to poor tissue permeability
.
Voriconazole is an alternative to amphotericin B for the treatment of invasive Trichoderma infections because of its lower minimum inhibitory concentration (MIC) value, fewer side effects, and higher penetration rate
.
Clinical points ➤ Trichoderma is a saprophytic filamentous fungus, and infection with Trichoderma is easily confused with mucor
.
Trichoderma infection can occur in a host with a normal immune function or a host with a weakened immune function
.
➤If untreated or improperly treated, the mortality rate of patients with Trichoderma infection is close to 50%
.
➤Treatment methods for Trichoderma infection include surgical resection and antifungal treatment.
Antifungal drugs such as amphotericin B and voriconazole should be used according to the severity of the disease, the minimum inhibitory concentration and the degree of invasive damage
.
Trichoderma has low toxicity, but it is highly resistant to antifungal drugs; in some cases, combination therapy can be considered
.
Reference: Yu Q, et al.
Chest.
2021 Aug;160(2):e177-e180.
