Vol 39 # 2 June 2007 - Kma.org.kw

186Aspergillus Pseudomembranous Tracheobronchitis Complicating Treatment of COPD Exacerbation June 2007DISCUSSIONAspergillus tracheobronchitis is an uncommonmanifestation of acute a s p e rg i l l u sinfection occurring inless than 7% of cases of pulmonary aspergillosis [1] .Infection is confined to the larger airways, often withthe formation of inflammatory pseudomembranes [ 2 ] .The disease has several morphological forms [3] . Thefirst consists of intraluminal growth of the fungusinvolving more or less the entire circumference ofthe airway wall. Grossly, such disease may take theform of psuedomembranes lining and partiallyo b s t ructing the airway lumen or completelyocclusive mucus / fungus plugs. The infection isoften confined to the mucosa and extension beyondthe bronchial wall is unusual. Depending on theextent and location of airway disease, aff e c t e dpatients may be asymptomatic or complain ofvariable degrees of dyspnea and hemoptysis. Bothpatients in our report had this form of aspergillust r a c h e o b ro-nchitis, probably with an additionalcomponent of aspergillus bronchopneumonia.A second morphological variety of aspergillustracheobronchitis consists of one or more discreteplaques limited to a relatively small area of theairway wall. Such infection can remain localized tothat site and grow within the lumen to form ano b s t ructing mass. More commonly, the fungusinvades the trachea or bronchial wall and extendsinto adjacent tissue. Complications include fistulaformation between the airway and mediastinum,esophagus or pleura, and pulmonary arteryinvasion with pleural hemorrhage.The final form of tracheobronchial aspergillosisis the least common and is seen predominantly inthe smaller bronchi and bronchioles. Histologically,the abnormality is characterized by bronchocentricgranulomatosis.Unlike angioinvasive aspergillosis whichtypically afflicts patients who are pro f o u n d l yimmunocompromised, it has been suggested thatAspergillus tracheobronchitis is more common inmild to moderately immunocompromised patients,which may explain the endobronchial localization [ 4 ] .N e u t ropenia was the underlying factor in 55p e rcent of patients presenting with a s p e rg i l l u stracheobronchitis [1] . It has also been suggested thatT-cell abnormalities, such as those occurringfollowing influenza A infection, may contribute tothis form of aspergillosis [5] . Boots et al reported acase of aspergillus tracheobronchitis in a healthypatient following influenza A i n f e c t i o n [ 5 ] . Thatpatient had a persistent lymphopenia involving Tcells and NK cells associated with cutaneousa n e rg y. The disease has also been reported inpatients with no known risk factors [ 1 ] .Tracheobronchial aspergillosis has been reported inCOPD patients [ 6 - 8 ] . Many of these patients hadreceived corticosteroids or bro a d - s p e c t ru mantibiotics [2] . It was found in a case control studythat invasive aspergillosis, although rare in COPD,was associated with the use of high doses ofc o r t i c o s t e roids and multiple broad spectru mantibiotics [9] . It is possible that an alteration in themicrobial flora in the airways of these patients as aconsequence of broad spectrum antibiotic therapy,coupled with the immunosuppressive effects ofhigh dose corticosteroids, predisposed tocolonization and infection of their airways bya s p e rg i l l u s. Our patients were receiving bothcorticosteroids and broad spectrum antibiotics tot reat their COPD exacerbations. Patient 1 alsoreceived a short course of oral steroids one yearprior to presentation but there is no record of thesecond patient having received corticostero i d sprior to presentation. Viral infections are a commonprecipitant of COPD exacerbations, but we do notknow whether either of our patients had influenzaor another viral respiratory tract infection as theprecipitating cause of their acute illness.Patients with aspergillus tracheobronchitis can beasymptomatic. The most common pre s e n t i n gcomplaints are cough, fever, dyspnea, chest painand hemoptysis [1,2] . They occasionally expectorateintraluminal mucus plugs [2] . These mucus plugs canbe filled with fungal hyphae [2] and are usuallyculture positive for aspergillus. In our report, bothpatients complained of dyspnea and were febrile.Patient No.1 also had a history of coughing up at r a c h e o b ronchial cast that contained A s p e rg i l l u s,many weeks after initial presentation.The diagnosis of aspergillus tracheobronchitis istypically delayed because of the insidious onset,nonspecific signs and symptoms and lack ofradiographic abnormalities. The radiologic picturemay show only slight changes since the infection ismainly limited to the trachea and bronchi. Theradiological findings range from normal to bilateralc o n s o l i d a t i o n [ 10 ] . High resolution CT characteristicallyshows centrilobular nodules and branching linearopacities giving a pattern known as “tre e - i n -bud” [11] . Both of our patients also had bronchial wallthickening.Treatment of A s p e rg i l l u s t r a c h e o b ronchitis issimilar to that of the other forms of invasiveaspergillosis. Amphotericin B is the treatment ofchoice. Itraconazole has also been successfullyused. Nebulized Amphotericin B can also be added.Systemic steroids have no role in the treatment ofAspergillus tracheobronchitis. Rather steroids are arisk factor for the disease [9] . The mortality rate ishigh with 43 percent patients dying despitetreatment and cure achieved in only 21 percent [1] .Our patients died of their disease, with patient No.1improving initially but succumbing later during a