Ulcerative Tracheobronchitis Research Articles

An Unusual Case of Invasive Aspergillus Ulcerative Tracheobronchitis Without Involvement of Lung Parenchyma in a Post-Renal Transplant Patient

We present the case of a 54-year-old male, who presented with respiratory complaints four months after he underwent renal transplantation. Bronchoscopy showed ulcerated mucosa of the left main bronchus and computed tomography (CT) of the thorax showed foci of air within the bronchial wall. A biopsy from the lesion showed septate fungal hyphae, dichotomously branching at acute angles. A locally invasive Aspergillus ulcerative tracheobronchitis with no parenchymal involvement is an important cause of tracheobronchitis in post-renal transplant patients. An early diagnosis and institution of appropriate treatment can improve the outcome. A combination treatment of caspofungin and voriconazole can be considered if patient is not responding to voriconazole alone.

STENOSIS OF THE BRONCHIAL TREE DUE TO GRANULOMATOSIS WITH POLYANGIITIS

SESSION TITLE: Medical Student/Resident Pulmonary Manifestations of Systemic Disease 1 SESSION TYPE: Med Student/Res Case Rep Postr PRESENTED ON: 10/09/2018 01:15 PM - 02:15 PM INTRODUCTION: Tracheobronchial tree (TBT) stenosis is a severe complication of Granulomatosis with Polyangiitis (GPA) due to granulomatous lesions along the respiratory tract. There is limited data regarding appropriate therapy for these patients. This is a case of a rare subtype of TBT, bronchial stenosis. CASE PRESENTATION: A 73-year-old woman with a history of rheumatic fever, chronic obstructive pulmonary disease requiring tracheostomy with reversal and residual tracheal stenosis, presented with a productive cough worsening over three months. She had associated chills, fevers, night sweats, dyspnea, and weight loss. Her sputum was brown without hemoptysis. She denied prior tobacco use and had no recent sick contacts or travel. Antibiotic and steroid therapy provided no relief. Chest radiograph showed hyperinflation, bilateral patchy infiltrates, and left lower lobe atelectasis. A computerized-tomography scan showed complete impaction of the left main bronchus with collapse of the left upper and lower lobes, significant bronchiectasis, and mediastinal lymphadenopathy.Bronchoscopy revealed 70% stenosis of the upper trachea, friable respiratory mucosa, and complete occlusion of the left main-stem bronchus. The right main-stem bronchus and the bronchus intermedius were circumferentially narrowed by granulation tissue. Cryoablation of the left main stem occlusion was unsuccessful.Endobronchial biopsy revealed granulation tissue with fibrosis and multi-nucleated giant cells. Her cytoplasmic anti-neutrophil cytoplasmic antibody titer was 1:320. Bronchial washings were negative for bacterial organisms. She was then diagnosed with bilateral bronchial stenosis due to GPA. DISCUSSION: TBT stenosis presents in 12-23% of patients with GPA. The stenosis is due to a non-infectious ulcerative tracheobronchitis caused by an underlying small vessel vasculitis, followed by fibrotic scarring. Symptoms such as cough, hemoptysis, or dyspnea mimic infection or obstructive lung disease.There is no clear consensus on the management of patients with bronchial stenosis. These fibrotic lesions are often refractory to pharmacological management with corticosteroids or immunosuppressive agents alone, and an endoscopic intervention such as cryotherapy, balloon dilation, or stent placement is needed for symptomatic relief. The benefits of endoscopic intervention can be transient due to a high restenosis rate. Comparison of patient outcomes based on the treatment modality of choice would prevent delay in therapy or worsening of disease. CONCLUSIONS: Bronchial stenosis is a complication of GPA that can mimic other common obstructive lung diseases due to the similar pathogenesis of bronchoconstriction. Optimal therapeutic approach for bronchial stenosis is controversial. Literature currently supports a combination of pharmacological and endoscopic therapy. Investigation of patient outcomes based on treatment modality is warranted. Reference #1: Girard et al. Tracheobronchial Stenosis in Granulomatosis With Polyangiitis (Wegner’): A Report on 26 Case. Medicine (Baltimore). 2015 Aug;94(32):e1088. Reference #2: Daum et al. Tracheobronchial Involvement in Wegener’s Granulomatosis. Am J Respir Crit Care Med. 1995 Feb;151(2 Pt 1):522-6. Reference #3: Terrier et al. Granulomatosis with Polyangiitis: Endoscopic Management of Tracheobronchial Stenosis: Results From a Multicenter Experience. Rheumatology (Oxford). 2015 Oct;54(10):1852-7. DISCLOSURES: No relevant relationships by Omar Ibrahim, source=Web Response No relevant relationships by Anil Magge, source=Web Response No relevant relationships by Rahul Mutneja, source=Web Response No relevant relationships by Evan Nadler, source=Web Response No relevant relationships by Aysha Tandon, source=Web Response

Repair of Tracheal Aspergillosis Perforation Causing Tension Pneumothorax

Tracheobronchial aspergillosis is a rare entity mainly observed in immune-compromised patients or those who have undergone transplantation. It may cause airway ulcerations or bleeding. We report the case ofa 17-year-old patient receiving chemotherapy foracute lymphoblastic leukemia who presented withright-sided tension pneumothorax. Chest tube drainage revealed a massive air leak without reexpansion of the lung, and bronchoscopy showed a15-× 15-mm defect of the distal trachea related to aspergillosis infection. The defect was closed by an intrathoracic transposition of a pedicled latissimus dorsi muscle flap, which was sutured into the debrided defect followed by temporary endotracheal stenting and antifungal medication.

Ulcerative Tracheobronchitis Due to Aspergillus

Aspergillus ulcerative tracheobronchitis is a life-threatening form of invasive aspergillosis and is seldom seen in patients without underlying an immunocompromised state. Bronchoscopists must be familiar with this entity and consider Aspergillus ulcerative tracheobronchitis whenever mucosal erosions are seen, especially when unconventional risk factors such as intensive care unit admission and short-term glucocorticoid therapy are present. We present a case of invasive Aspergillus causing widespread ulcerative tracheobronchitis in a 39-year-old man with an asthma exacerbation requiring intensive care unit admission.

A Remedy for Hoarseness in a Patient With Granulomatosis With Polyangiitis

A Remedy for Hoarseness in a Patient With Granulomatosis With Polyangiitis

Feasibility, tolerability, and outcomes of nebulized liposomal amphotericin B for Aspergillus infection prevention in lung transplantation

Nebulized amphotericin B deoxycholate (n-ABD) is used to prevent Aspergillus infection in lung transplantation. Nebulized liposomal amphotericin B (n-LAB) is another option; however, no clinical data are available on the results of n-LAB for this purpose. In an observational study performed in 2 centers to assess the feasibility, tolerability, and outcomes of n-LAB prophylaxis, 104 consecutive patients undergoing prophylaxis with n-LAB were compared with 49 historical controls who received n-ABD. Patient follow-up lasted 12 months. The n-LAB prophylaxis regimen was 25 mg thrice weekly starting on the first post-operative day and continuing to 60 days, 25 mg once weekly from 60 to 180 days, and the same dose once every 2 weeks thereafter. Aspergillus infection developed in 8 of 104 patients (7.7%) with n-LAB prophylaxis (5 colonization, 1 simple tracheobronchitis, 1 ulcerative tracheobronchitis, and 1 invasive pulmonary infection). Ulcerative tracheobronchitis and invasive pulmonary aspergillosis were regarded as invasive disease; hence, the rate of invasive disease was 1.9% (2 patients). The control group had similar rates of Aspergillus infection (10.2%; p = 0.6) and invasive disease (4.1%; p = 0.43). In 3 patients (2.9%), n-LAB was withdrawn due to bronchospasm in 2 and nausea in 1. In the control group, prophylaxis was stopped in 2 patients (4.1%) because of bronchospasm (p = 0.7). At the dose and frequency described, n-LAB seems effective, safe, and convenient for the prevention of Aspergillus infection in lung transplant patients.

Ulcerative and pseudomembranous Aspergillus tracheobronchitis in a patient with acute myeloid leukemia

Ulcerative and pseudomembranous Aspergillus tracheobronchitis are rare, invasive forms of tracheobronchial aspergillosis. The typical focal ulcerative tracheobronchitis has been recognized in patients with AIDS and heart and/or lung transplant recipients, while pseudomembranous forms have usually been found in severely immunocompromised hosts with hematologic malignancies [1].

Health care-acquired aspergillosis and air conditioning systems.

Aspergillus species (Fig. 1) are conidia-forming fungi that are responsible for a wide spectrum of human illnesses. About 19 species of Aspergillus have been documented as agents of human disease, but the majority of infections are caused by Aspergillus fumigates (Fresenius, 1850), Aspergillus flavus (Link,1809), Aspergillus niger (Van Tieghem, 1867), and Aspergillus terreus (Thom, 1918) [1, 2]. Clinical syndromes and diseases associated to Aspergillus spp. can be: “cutaneous” (primary skin and burnwound infections, especially in neonates and children); “hypersensity” (allergic bronchopulmonary aspergillosis); “acute invasive” (pneumonia, ulcerative tracheobronchitis, osteomyelitis,..);“chronic invasive” (chronic pneumonitis) [3-5]. The primary route of acquiring Aspergillus infections is by the inhalation of conidia [6]. The respiratory tract is therefore the most common portal of entry of Aspergillus spp. conidia [7]. Conidia of the most commonly involved pathogenic Aspergillus spp. are relatively small, with sizes ranging from 2 to 5 μm [8, 9]. The small size of conidia permits them to deposit deep into the lung after inhalation and to reach the pulmonary alveolar spaces, where they may germinate to form hyphae. Humans inhale approximately 200 conidia of filamentous fungi per day, 7 of which reach the alveoli. These conidia are phagocytosed by the alveolar macrophages and destroyed [10]. The outcome of infection depends more on host factors than on the virulence of the individual Aspergillus species [2, 4, 11]. Therefore, host immunity plays a major role in determining who may be at risk of developing invasive aspergillosis (IA). The principal host defences against invasive Aspergillus infection are alveolar macrophages, which target inhaled conidia, and neutrophils, which target the hyphal stage [12-14]. Immunocompromised patients are extremely susceptible to local invasion of respiratory tissues by deposited conidia, resulting in invasive aspergillosis [12, 15]. Most cases of health care-acquired invasive aspergillosis present with pneumonia [8]. However, while invasive aspergillosis occurs typically in severely immunocompromised patients, cases of surgical site infection have been reported in immunocompetent individuals [8, 16].

Nontraumatic Disruption of the Fibrocartilaginous Trachea: Causes and Clinical Outcomes

<h3>Background</h3> Nontraumatic disruption of the fibrocartilaginous trachea is rare, and the appropriate management of this condition is not well-characterized. <h3>Methods</h3> Retrospective analysis of the clinical features, causes, and outcomes with surgical and nonsurgical management in nine adult patients with nontraumatic fibrocartilaginous tracheal disruption identified by bronchoscopy from January 1, 1975, to December 31, 2004, at a single institution. <h3>Results</h3> The most common cause was external beam radiotherapy (RT) in five patients. Other causes included postoperative complications of cervical and superior mediastinal operations in three patients and <i>Aspergillus fumigatus-</i>induced ulcerative tracheobronchitis in one patient post-lung transplantation. Four patients were treated surgically; three because of significant pneumomediastinum and one because the size of the tracheal defect made spontaneous healing seem unlikely. A silicone stent was placed in one patient for concomitant tracheal narrowing, and one patient was treated medically with antifungal agents. The remaining three patients were followed up serially without any intervention. With these treatments, only one patient died as a consequence of tracheal disruption. Repeat bronchoscopies were performed in seven of the remaining eight patients and confirmed healing of the necrotic defect in all. <h3>Conclusion</h3> Nontraumatic disruption of the fibrocartilaginous trachea occurs most commonly as a consequence of external beam RT. It can also occur as a complication of cervical and superior mediastinal operations or from <i>A fumigatus</i>-induced ulcerative tracheobronchitis post-lung transplantation. Although surgical treatment has been generally recommended for patients with this condition, patients with contained disruptions without evidence of pneumomediastinum may be managed nonoperatively.

2-CHLORODEOXYADENOSINE TREATMENT IN PULMONARY LESIONS OF LCH

Nontraumatic disruption of the fibrocartilaginous trachea is rare, and the appropriate management of this condition is not well-characterized.Retrospective analysis of the clinical features, causes, and outcomes with surgical and nonsurgical management in nine adult patients with nontraumatic fibrocartilaginous tracheal disruption identified by bronchoscopy from January 1, 1975, to December 31, 2004, at a single institution.The most common cause was external beam radiotherapy (RT) in five patients. Other causes included postoperative complications of cervical and superior mediastinal operations in three patients and Aspergillus fumigatus-induced ulcerative tracheobronchitis in one patient post-lung transplantation. Four patients were treated surgically; three because of significant pneumomediastinum and one because the size of the tracheal defect made spontaneous healing seem unlikely. A silicone stent was placed in one patient for concomitant tracheal narrowing, and one patient was treated medically with antifungal agents. The remaining three patients were followed up serially without any intervention. With these treatments, only one patient died as a consequence of tracheal disruption. Repeat bronchoscopies were performed in seven of the remaining eight patients and confirmed healing of the necrotic defect in all.Nontraumatic disruption of the fibrocartilaginous trachea occurs most commonly as a consequence of external beam RT. It can also occur as a complication of cervical and superior mediastinal operations or from A fumigatus-induced ulcerative tracheobronchitis post-lung transplantation. Although surgical treatment has been generally recommended for patients with this condition, patients with contained disruptions without evidence of pneumomediastinum may be managed nonoperatively.

Active Endobronchial Wegener??s Granulomatosis

A 47-year-old woman presented with symptoms of cough, streaky hemoptysis, and shortness of breath of 4 weeks' duration. A high-resolution computed tomography of the chest revealed cavitating nodular lesions. Her antinuclear cytoplasmic antibody (cANCA) was positive. She underwent flexible bronchoscopy, which revealed inflammation and ulceration of the arytenoids and epiglottis of the larynx (Fig. 1), along with multiple ulcerative lesions of the tracheal and the left main bronchus (“ulcerative tracheobronchitis”) (Fig. 2). Her transbronchial biopsy revealed necrotizing granulomatosis with capillaritis. This pathologic finding along with the radiologic and laboratory reports led to the diagnosis of Wegener's granulomatosis (WG).FIGURE 1: Inflammation and ulceration of the arytenoids and the epiglottis.FIGURE 2: Ulcerative tracheobronchitis of the posterior wall of the trachea and left main bronchus.DISCUSSION Wegener's granulomatosis is a multisystemic, idiopathic, necrotizing granulomatous vasculitis, which mostly involves the upper and lower airways, lungs, and the kidneys.1-5 Other sites that are also involved are the joints, eyes, skin, and the nervous system.1 When the condition is restricted to the respiratory system without the involvement of the renal system, it is referred as limited Wegener's granulomatosis, which is seen in 25% of patients.1,5,7,8 The lung is the most frequent and sometimes only organ involved. Approximately 85% of patients develop lung development during the course of the disease, and 45% have lung involvement at presentation.6,10,11 Endobronchial involvement occurs in up to 55% of the patients.4,13 Hoffman et al in his series of 158 patients found 73% of the patients had presented with upper airway involvement and 92% during the course of the disease. Lower airway involvement present in 48% of the patients at the time of presentation and 85% during the course of the disease.1 The endobronchial involvement could be in the form of active inflammation and ulceration of the mucosa called “ulcerating tracheobronchitis.” This is the most common presentation seen in up to 55% of the patients along with inflammatory pseudotumor and cobblestoning of the mucosa. The late complications include subglottic stenosis, tracheal stenosis, bronchial stenosis, and tracheobronchomalacia.1,2,4,7,13-16,22,24 There has been anecdotal case reports of main bronchus necrosis with WG.23 The etiology and pathogenesis of endobronchial involvement in WG remains uncertain. Feinberg had proposed the initial fibrinoid degeneration of collagen at sites where there is extensive deposition such as tracheal and nasal cartilage, eliciting a granulomatous immune response.19,20 This could cause inflammation and edema leading to stenosis and later organizing to form fibrotic stenosis or give rise to tracheobronchomalacia. The lower airway symptoms of WG consist of cough being the most common, followed by dyspnea, hemoptysis, chest pain, and stridor.13 The upper airway symptoms consist of sinusitis, rhinitis, otitis, and epistaxis; occasionally, one can get perforation of the nasal septum and saddle nose deformity resulting from destruction of the nasal cartilage.9 The radiologic features vary depending on activity of WG from masses, cavitating nodules, parenchymal bands, septal thickenings, parenchymal opacification, centrilobular nodules, interstitial thickening, and diffuse alveolar shadows in alveolar hemorrhage.1,9 Cavitating nodules and masses are predominantly seen in active diseases. Antineutrophil cytoplasm antibodies (cANCA) have been found positive in 70% to 90% of patients with active WG and has a sensitivity of up to 92%.21,25-27 The renal system involvement presents with abnormal laboratory findings like proteinuria, active urine sediment with microscopic hematuria to red cell casts, and in case of severe glomerulonephritis, it can be seen with decline of renal function as seen by an increase of serum creatinine and decreased creatinine clearance.5 The American College of Rheumatology has published the criteria for diagnosis of WG from other vasculitis condition, which include nasal or oral inflammation, abnormal chest radiograph, urinary sediment, and granulomatous inflammation on biopsy. Any 2 or more criteria present are suggestive of WG and has a sensitivity of 88.2% and specificity of 92%. The most common indications for flexible bronchoscopy include hemoptysis followed by dyspnea on exertion, stridor or wheezing, persistent cough, hoarseness of voice, biopsy of masses, and nodules or new infiltrates on immunosuppressive therapy to rule out opportunistic infections.3,9,13,18 Therapeutic procedures such as removal of pseudotumors by biopsy forceps, laser and electrocautery along with balloon dilatation in tracheal and bronchial stenosis can also be carried out with flexible bronchoscope.12,13,14,17,22 Untreated WG has a poor outcome with a median survival time of 5 months. Glucocorticosteroids have been the mainstay of treatment of WG, and the combination of cyclophosphamide and glucocorticosteroids has been the best in the treatment of WG.9 Recognition of the early spectrum of the endobronchial involvement is essential to ensure early therapy that may prevent irreversible organ damage. Active ulcerating tracheobronchitis in a case of WG which, if not diagnosed or treated, can progress into late endobronchial complication of subglottic stenosis, tracheal, or bronchial stenosis.13,24

Tracheobronchial Aspergillosis

CASE A 20-year-old student with a history of acute myeloid leukemia 2 years after allogeneic bone marrow transplant was admitted from the outpatient clinic for evaluation of chronic diarrhea due to suspected graft-versus-host disease of the gastrointestinal tract. He first presented more than 2 years ago with severe anemia (presenting hemoglobin level was 7.3 g/dL) and was diagnosed to have acute myeloid leukemia. He underwent chemotherapy (with a regimen including cyclophosphamide) and total body irradiation before undergoing bone marrow transplantation 2 years ago. About 20 months post-transplant, the patient developed exertional dyspnea (his hemoglobin then was 14 g/dL), and spirometry showed severe airway obstruction with a forced expiratory volume in 1 second (FEV1) of 1.66 L (37.2% of predicted). His pretransplant spirometry was normal. High-resolution computed tomographic scan of the thorax showed hyperinflated lungs with bilateral perihilar bronchial thickening. He was treated with inhaled bronchodilators, and his immunosuppressive agents were adjusted for possible graft-versus-host disease of the lung. He was also admitted about a month before his present admission for an episode of spontaneous pneumomediastinum. This had resolved with conservative management. Seven days after his present admission, the patient developed acute dyspnea. He was tachypneic at rest with subcutaneous emphysema, and auscultation showed poor air entry bilaterally with expiratory wheeze. Chest radiograph showed pneumomediastinum with subcutaneous emphysema. Hours later, the patient developed acute respiratory failure and required emergent bilateral tube thoracostomies, endotracheal intubation, and mechanical ventilation. Bronchoscopy performed in the intensive care unit showed an extensive cream-colored pseudomembrane in the tracheobronchial tree (Fig. 1), and careful bronchial biopsies as well as bronchial aspirates confirmed the diagnosis of pseudomembranous tracheobronchial aspergillosis. The patient died from progressive respiratory failure 6 days after endotracheal intubation despite therapy with intravenous amphotericin B.FIG. 1.: (A) Distal trachea and right mainstem bronchus showing extensive cream-colored irregular pseudomembrane especially involving the posterior wall. (B) Left mainstem bronchus showing pseudomembrane involving the origins of bronchi to left upper and lower lobes. (C) Extensive coating of segmental bronchi to right upper lobe with pseudomembrane.Figure 1: ContinuedFigure 1: ContinuedDISCUSSION Invasive pulmonary aspergillosis occurs in up to 15%1 of bone marrow transplant patients, and it can either have a tracheobronchial distribution or be localized within the lung parenchyma. Aspergillus tracheobronchitis occurs most often in patients with acquired immunodeficiency syndrome and in lung transplant recipients. Three different forms of Aspergillus tracheobronchitis have been described: obstructive bronchial aspergillosis, where thick mucous plugs filled with the fungus are found in the airways, but causing little mucosal inflammation and invasion; ulcerative tracheobronchitis, where there is focal invasion of the tracheobronchial mucosa and/or cartilage; and finally, pseudomembranous tracheobronchitis, where there is extensive inflammation and invasion of the tracheobronchial tree with the formation of a pseudomembrane composed mainly of fungal hyphae and necrotic debris. 2 Up to 80% of patients may be symptomatic, although these symptoms may be attributed to other causes such as was the case here. Patients with Aspergillus tracheobronchitis may exhibit signs of airway obstruction such as localized wheezing or stridor. The chest radiograph may be normal with tracheobronchial involvement or show areas of atelectasis and parenchymal infiltrates. Computed tomography findings are nonspecific and include peribronchial consolidation and centrilobular nodules. 3 Bronchoscopy is diagnostic, and endobronchial biopsy may be hazardous because of possible transmural and vascular invasion. The prognosis is poor, and the majority of patients progress to respiratory failure and death. Perforation of the tracheobronchial tree is also a known complication.

Invasive Bronchopulmonary Aspergillosis Presenting as an Ulcerative Tracheobronchitis and Endobronchial Aspergilloma

Invasive Bronchopulmonary Aspergillosis Presenting as an Ulcerative Tracheobronchitis and Endobronchial Aspergilloma

Ulcerative Tracheobronchitis Years After Colectomy for Ulcerative Colitis

Two men with severe ulcerative colitis developed ulcerative tracheobronchitis 4 and 8 years after total colectomy. Intense plasma cell infiltration of tracheal mucosa and submucosa and destruction of mucous glands occurred, with partial relief of symptoms with corticosteroids. We compare them with the only other case reported, also years after colectomy.

Ulcerative and Plaque-Like Tracheobronchitis Due to Infection with Aspergillus in Patients with AIDS

Tracheobronchitis is an uncommon manifestation of infection due to Aspergillus species, occurring in < 7% of cases of pulmonary aspergillosis. At least 58 cases of invasive aspergillus tracheobronchitis have been described since 1962. We describe four patients with AIDS, all of whom were severely immunocompromised, who had ulcerative tracheobronchitis due to Aspergillus species demonstrated histologically. Three patients had received corticosteroids or were neutropenic at presentation. At bronchoscopy, three patients had some degree of diffuse tracheobronchitis, multiple ulcerative or "plaque-like" inflammatory lesions, and occasionally nodules involving the mainstem and segmental bronchi. The remaining patient had a single deep ulceration of the proximal trachea. Aspergillus was isolated from biopsy specimens from all four patients. There were varied degrees of invasion of the mucosa, submucosa, and cartilage on histological examination in three patients, one of whom had evidence of disseminated aspergillosis. Two patients subsequently developed pulmonary parenchymal disease due to Aspergillus. A review of aspergillus tracheobronchitis, including a discussion of airway disease in patients infected with human immunodeficiency virus, is presented.

Ulcerative tracheobronchitis after lung transplantation. A new form of invasive aspergillosis.

Invasive aspergillosis is frequently a fatal disease in the setting of immunosuppression, including organ transplant recipients. The fungus usually affects lung parenchyma and may disseminate from there. We have recently noted tracheobronchitis in six patients with heart-lung and lung transplants, three of whom had deep mucosal ulceration and histologic evidence of invasive aspergillosis. This apparently new form of invasive disease is initially limited to the anastomosis site and large airways. Ulceration, necrosis, cartilage invasion, and formation of a pseudomembrane are the pathologic features. In two patients subsequent disseminated aspergillosis occurred with a fatal outcome. In the two single-lung recipients, disease was limited to the transplanted side emphasizing the importance of abnormal local defense mechanisms in the airways of lung transplant recipients. Routine bronchoscopic examination of the airways is important in early detection of this complication. Oral therapy with the new, antifungal agent itraconazole was successful in five of the six patients, with fatal relapse in one. A classification of the various forms of saprophytic, allergic, and invasive forms of aspergillus tracheobronchitis, to include this new entity, is proposed.

The pathology of infection of chickens with the lentogenic V4 strain of Newcastle disease virus

Seven-week-old chickens infected oro-nasally with the lentogenic V4 strain of Newcastle disease virus showed no clinical signs and minimal gross pathology. There was slight ulcerative tracheobronchitis but the main system response was a rapid and progressive lymphoproliferative hyperplasia in the respiratory system, gastrointestinal tract, bursa and spleen which tended to peak after three weeks. By using an indirect immunoperoxidase technique with antibody prepared against homologous virus, viral antigen was localised chiefly in the cytoplasm of lymphoreticular cells, persisting for at least 28 days in the caecal tonsil. Positive cells were not seen in the bursa or brain.

Fatal chlorine poisoning: report of two cases with clinicopathologic correlation.

Two healthy adults died 25 and 76 hours, respectively, after being exposed to gaseous chlorine. Clinically, each had severe hypoxemia and metabolic acidosis. At autopsy, both patients had severe pulmonary edema with superimposed pneumonia, prominent hyaline membrane formation, multiple recent pulmonary thromboses, and ulcerative tracheobronchitis. The kidneys of the longer-surviving victim were the seat of glomerular capillary thromboses, and the white matter of her brain was studded with focal and confluent destructive hemorrhages. The pulmonary and airway damage in chlorine poisoning are produced by the strong oxidizing action created by the interaction of the toxic gas with water, which results in the liberation of nascent oxygen, a potent protoplasmic poison. Because lungs traumatized by the irritant effect of chlorine may be abnormally vulnerable to the toxic effect of oxygen, it is probable that at least some of the pulmonary damage observed in both victims was created by the deleterious effects of high pressure therapy with this gas.

ULCERATIVE TRACHEOBRONCHITIS FOLLOWING ATYPICAL PNEUMONIA

It is no longer felt that atypical (viral) pneumonia is always as innocuous as it was originally described. Many patients have experienced recurring episodes of this disease over a period of several years. In some the symptoms have continued unabated; a productive cough has developed, and the presence of bronchiectasis has been confirmed by bronchographic examination. Other patients have had residual ulcerative tracheobronchitis associated with hemoptysis and production of sputum. These patients may show roentgenographic evidence of bronchial and bronchiolar dilatation and occlusion, atelectasis or obstructive emphysema. In others the convalescence has been prolonged and characterized by neurasthenia, chronic cough, production of sputum, pain in the chest, generalized weakness, easy fatigability, occasional hemoptysis, loss of weight or failure to regain previous weight lost, elevated sedimentation rate and low grade fever. Twenty-nine of 150 patients having bronchoscopic examinations during the first six months of 1944 were found to have ulcerative lesions