When Diarrhea Is More Serious Than You Think
Hepatobiliary Clinic
Program Highlights
The University of Alabama at Birmingham (UAB) Liver Transplant faculty have busy elective hepatobiliary practices. Over 150 major liver resections or extrahepatic biliary tree procedures are performed annually. The clinic has a large patient volume of hepatocellular carcinoma, cholangiocarcinoma, benign biliary disorders, and focal hepatic lesions in addition to metastatic disease. All patients with malignancies are discussed at an Interdisciplinary Liver Tumor Board consisting of physicians with clinical expertise in hepatobiliary malignancies including hepatobiliary surgeons, hepatologists, medical oncologists, radiation oncologists, interventional radiologists and liver pathologists. The Interdisciplinary Liver Tumor Board functions in a collaborative effort to best diagnose and treat patients with focal hepatic lesions, hepatocellular carcinoma, hepatic colorectal metastases, and cholangiocarcinoma.
Outcomes
A host of tertiary care treatment options are provided including surgical, interventional, chemotherapy, and radiation approaches. In many cases, multiple treatment modalities are utilized in concert to eradicate hepatic malignancies. The advanced surgical approaches include techniques to facilitate aggressive liver resections when close margins or residual liver function is a concern, such as portal vein embolization, sequential liver resection, and vascular resection/ reconstruction. Liver transplantation is also offered for tumors that meet certain requirements. Approximately 30% of the 100+ liver transplants performed annually are for hepatic malignancies. There is expertise in tumor ablation techniques, transarterial chemoembolization (TACE), and Ytrium90 intra-arterial spheres with approximately 100 patients treated with these interventions annually. UAB also offers novel methods of focal liver tumor irradiation. There are several clinical trials for developing chemotherapy regimens, and chemotherapy-radiation combination protocols. In many cases, chemotherapy and radiation protocols are initiated at UAB and continued locally for patient convenience.
Patient Centered Approach
Patients are contacted directly by the hepatobiliary physician extenders and offered a clinic appointment within a week of referral. We strive to provide excellent communication with referring physicians and compassionate patient care. Every patient is presented at the Interdisciplinary Liver Tumor Board. Health care professionals with interest and expertise in hepatic malignancies including surgeons, hepatologists, medical and radiation oncologists, liver pathologists, and diagnostic and interventional radiologists attend this weekly meeting. All radiographic studies and pathological information is reviewed before a comprehensive treatment plan is recommended. The treatment plan will be clearly communicated to both the patient and the referring physician.
Facilities
Outpatient clinics are located in the Kirklin Clinic, in close proximity to laboratory and radiology services. Liver operations are performed in the new, state-of-the-art operating complex at UAB, and interventional radiology procedures are performed in the Heart and Vascular Institute. Patients are initially cared for in the surgical intensive care unit when appropriate and then transferred to a dedicated liver surgery general ward that is staffed by a dedicated transplant and liver surgery nursing team.
Unraveling The Pathogenesis And Etiology Of Biliary Atresia
Sokol RJ, Mack C, Narkewicz MR, Karrer FM 2003 Pathogenesis and outcome of biliary atresia: current concepts. J Pediatr Gastroenterol Nutr 37: 4–21
Ohi R 2000 Biliary atresia. A surgical perspective. Clin Liver Dis 4: 779–804
Schweizer P 1986 Treatment of extrahepatic biliary atresia: results and long-term prognosis after hepatic portoenterostomy. Pediatr Surg 1: 30–36
Karrer FM, Bensard DD 2000 Neonatal cholestasis. Semin Pediatr Surg 9: 166–169
Chardot C, Carton M, Spire-Bendelac N, Le Pommelet C, Golmard JL, Auvert B 1999 Epidemiology of biliary atresia in France: a national study 1986–96. J Hepatol 31: 1006–1013
Karrer FM, Price MR, Bensard DD, Sokol RJ, Narkewicz MR, Smith DJ, Lilly JR 1996 Long-term results with the Kasai operation for biliary atresia. Arch Surg 131: 493–496
Perlmutter DH, Shepherd RW 2002 Extrahepatic biliary atresia: a disease or a phenotype?. Hepatology 35: 1297–1304
Yoon PW, Bresee JS, Olney RS, James LM, Khoury MJ 1997 Epidemiology of biliary atresia: a population-based study. Pediatrics 99: 376–382
Strickland AD, Shannon K 1982 Studies in the etiology of extrahepatic biliary atresia: time-space clustering. J Pediatr 100: 749–753
Caton AR, Druschel CM, McNutt LA 2004 The epidemiology of extrahepatic biliary atresia in New York State, 1983–98. Paediatr Perinat Epidemiol 18: 97–105
Fischler B, Haglund B, Hjern A 2002 A population-based study on the incidence and possible pre- and perinatal etiologic risk factors of biliary atresia. J Pediatr 141: 217–222
Bangaru B, Morecki R, Glaser JH, Gartner LM, Horwitz MS 1980 Comparative studies of biliary atresia in the human newborn and reovirus-induced cholangitis in weanling mice. Lab Invest 43: 456–462
Morecki R, Glaser JH, Cho S, Balistreri WF, Horwitz MS 1982 Biliary atresia and reovirus type 3 infection. N Engl J Med 307: 481–484
Glaser JH, Balistreri WF, Morecki R 1984 Role of reovirus type 3 in persistent infantile cholestasis. J Pediatr 105: 912–915
Brown WR, Sokol RJ, Levin MJ, Silverman A, Tamaru T, Lilly JR, Hall RJ, Cheney M 1988 Lack of correlation between infection with reovirus 3 and extrahepatic biliary atresia or neonatal hepatitis. J Pediatr 113: 670–676
Dussaix E, Hadchouel M, Tardieu M, Alagille D 1984 Biliary atresia and reovirus type 3 infection. N Engl J Med 310: 658
Rosenberg DP, Morecki R, Lollini LO, Glaser J, Cornelius CE 1983 Extrahepatic biliary atresia in a rhesus monkey (Macaca mulatta). Hepatology 3: 577–580
Morecki R, Glaser JH, Johnson AB, Kress Y 1984 Detection of reovirus type 3 in the porta hepatis of an infant with extrahepatic biliary atresia: ultrastructural and immunocytochemical study. Hepatology 4: 1137–1142
Steele MI, Marshall CM, Lloyd RE, Randolph VE 1995 Reovirus 3 not detected by reverse transcriptase-mediated polymerase chain reaction analysis of preserved tissue from infants with cholestatic liver disease. Hepatology 21: 697–702
Saito T, Shinozaki K, Matsunaga T, Ogawa T, Etoh T, Muramatsu T, Kawamura K, Yoshida H, Ohnuma N, Shirasawa H 2004 Lack of evidence for reovirus infection in tissues from patients with biliary atresia and congenital dilatation of the bile duct. J Hepatol 40: 203–211
Tyler KL, Sokol RJ, Oberhaus SM, Le M, Karrer FM, Narkewicz MR, Tyson RW, Murphy JR, Low R, Brown WR 1998 Detection of reovirus RNA in hepatobiliary tissues from patients with extrahepatic biliary atresia and choledochal cysts. Hepatology 27: 1475–1482
Riepenhoff-Talty M, Gouvea V, Evans MJ, Svensson L, Hoffenberg E, Sokol RJ, Uhnoo I, Greenberg SJ, Schakel K, Zhaori G, Fitzgerald J, Chong S, el-Yousef M, Nemeth A, Brown M, Piccoli D, Hyams J, Ruffin D, Rossi T 1996 Detection of group C rotavirus in infants with extrahepatic biliary atresia. J Infect Dis 174: 8–15
Bobo L, Ojeh C, Chiu D, Machado A, Colombani P, Schwarz K 1997 Lack of evidence for rotavirus by polymerase chain reaction/enzyme immunoassay of hepatobiliary samples from children with biliary atresia. Pediatr Res 41: 229–234
Riepenhoff-Talty M, Schaekel K, Clark HF, Mueller W, Uhnoo I, Rossi T, Fisher J, Ogra PL 1993 Group A rotaviruses produce extrahepatic biliary obstruction in orally inoculated newborn mice. Pediatr Res 33: 394–399
Petersen C, Biermanns D, Kuske M, Schakel K, Meyer-Junghanel L, Mildenberger H 1997 New aspects in a murine model for extrahepatic biliary atresia. J Pediatr Surg 32: 1190–1195
Czech-Schmidt G, Verhagen W, Szavay P, Leonhardt J, Petersen C 2001 Immunological gap in the infectious animal model for biliary atresia. J Surg Res 101: 62–67
Tarr PI, Haas JE, Christie DL 1996 Biliary atresia, cytomegalovirus, and age at referral. Pediatrics 97: 828–831
Oliveira NL, Kanawaty FR, Costa SC, Hessel G 2002 Infection by cytomegalovirus in patients with neonatal cholestasis. Ar Qgastroenterol 39: 132–136
Fischler B, Ehrnst A, Forsgren M, Orvell C, Nemeth A 1998 The viral association of neonatal cholestasis in Sweden: a possible link between cytomegalovirus infection and extrahepatic biliary atresia. J Pediatr Gastroenterol Nutr 27: 57–64
Jevon GP, Dimmick JE 1999 Biliary atresia and cytomegalovirus infection: a DNA study. Pediatr Dev Pathol 2: 11–14
Drut R, Drut RM, Gomez MA, Cueto Rua E, Lojo MM 1998 Presence of human papillomavirus in extrahepatic biliary atresia. J Pediatr Gastroenterol Nutr 27: 530–535
Domiati-Saad R, Dawson DB, Margraf LR, Finegold MJ, Weinberg AG, Rogers BB 2000 Cytomegalovirus and human herpesvirus 6, but not human papillomavirus, are present in neonatal giant cell hepatitis and extrahepatic biliary atresia. Pediatr Dev Pathol 3: 367–373
Tracy TF Jr, Dillon P, Fox ES, Minnick K, Vogler C 1996 The inflammatory response in pediatric biliary disease: macrophage phenotype and distribution. J Pediatr Surg 1: 121–125
Ahmed AF, Nio M, Ohtani H, Nagura H, Ohi R 2001 In situ CD14 expression in biliary atresia: comparison between early and late stages. J Pediatr Surg 36: 240–243
Gosseye S, Otte JB, De Meyer R, Maldague P 1977 A histological study of extrahepatic biliary atresia. Acta Paediatr Belg 30: 85–90
Bill AH, Haas JE, Foster GL 1977 Biliary Atresia: histopathologic observations and reflections upon its natural history. J Pediatr Surg 12: 977–982
Ohya T, Fujimoto T, Shimomura H, Miyano T 1995 Degeneration of intrahepatic bile duct with lymphocyte infiltration into biliary epithelial cells in biliary atresia. J Pediatr Surg 30: 515–518
Dillon PW, Belchis D, Minnick K, Tracy T 1997 Differential expression of the major histocompatibility antigens and ICAM-1 on bile duct epithelial cells in biliary atresia. Tohoku J Exp Med 181: 33–40
Broome U, Nemeth A, Hultcrantz R, Scheynius A 1997 Different expression of HLA-DR and ICAM-1 in livers from patients with biliary atresia and Byler's disease. J Hepatol 26: 857–862
Davenport M, Gonde C, Redkar R, Koukoulis G, Tredger M, Mieli-Vergani G, Portmann B, Howard ER 2001 Immunohistochemistry of the liver and biliary tree in extrahepatic biliary atresia. J Pediatr Surg 36: 1017–1025
Ahmed AF, Ohtani H, Nio M, Funaki N, Shimaoka S, Nagura H, Ohi R 2001 CD8+ T cells infiltrating into bile ducts in biliary atresia do not appear to function as cytotoxic T cells: a clinicopathological analysis. J Pathol 193: 383–389
Mack CL, Tucker RM, Sokol RJ, Karrer FM, Kotzin BL, Whitington PF, Miller SD 2004 Biliary atresia is associated with CD4+ Th1 cell-mediated portal tract inflammation. Pediatr Res 56: 79–87
Dillon P, Belchis D, Tracy T, Cilley R, Hafer L, Krummel T 1994 Increased expression of intercellular adhesion molecules in biliary atresia. Am J Pathol 145: 263–267
Bezerra JA, Tiao G, Ryckman FC, Alonso M, Sabla GE, Shneider B, Sokol RJ, Aronow BJ 2002 Genetic induction of proinflammatory immunity in children with biliary atresia. Lancet 360: 1653–1659
Shivakumar P, Campbell KM, Sabla GE, Miethke A, Tiao G, McNeal MM, Ward RL, Bezerra JA 2004 Obstruction of extrahepatic bile ducts by lymphocytes is regulated by IFN-gamma in experimental biliary atresia. J Clin Invest 114: 322–329
Abbas AK, Lichtman AH, Pober JS 2000 Cellular and Molecular Immunology. WB Saunders, Philadelphia, pp vii, 553
Kobayashi H, Puri P, O'Briain DS, Surana R, Miyano T 1997 Hepatic overexpression of MHC class II antigens and macrophage-associated antigens (CD68) in patients with biliary atresia of poor prognosis. J Pediatr Surg 32: 590–593
Kobayashi H, Li Z, Yamataka A, Lane GJ, Miyano T 2003 Role of immunologic costimulatory factors in the pathogenesis of biliary atresia. J Pediatr Surg 38: 892–896
Tracy TF Jr, Dillon P, Fox ES, Minnick K, Vogler C 1996 The inflammatory response in pediatric biliary disease: macrophage phenotype and distribution. J Pediatr Surg 31: 121–126
Urushihara N, Iwagaki H, Yagi T, Kohka H, Kobashi K, Morimoto Y, Yoshino T, Tanimoto T, Kurimoto M, Tanaka N 2000 Elevation of serum interleukin-18 levels and activation of Kupffer cells in biliary atresia. J Pediatr Surg 35: 446–449
Funaki N, Sasano H, Shizawa S, Nio M, Iwami D, Ohi R, Nagura H 1998 Apoptosis and cell proliferation in biliary atresia. J Pathol 186: 429–433
Liu C, Chiu JH, Chin T, Wang LS, Li AF, Chow KC, Wei C 2000 Expression of fas ligand on bile ductule epithelium in biliary atresia—a poor prognostic factor. J Pediatr Surg 35: 1591–1596
Schreiber RA, Kleinman RE 1993 Genetics, immunology, and biliary atresia: an opening or a diversion?. J Pediatr Gastroenterol Nutr 16: 111–113
Sokol RJ, Mack C 2001 Etiopathogenesis of biliary atresia. Semin Liver Dis 21: 517–524
Eagar T, Tompkins S, Miller S 2001 Helper T-cell subsets and control of the inflammatory response. In: Rich R, Fleisher T, Shearer W, Kotzin B, Schroeder H Jr (eds) Clinical Immunology Principles and Practice. Mosby, London, pp 16.11–16.12
Rose NR, Bona C 1993 Defining criteria for autoimmune diseases (Witebsky's postulates revisited). Immunol Today 14: 426–430
Vasiliauskas E, Targan S, Cobb L, Vidrich A, Rosenthal P 1995 Biliary atresia—an autoimmune disorder?. Hepatology 22: 87
Burch J, Sokol RJ, Narkewicz MR, Reichlin M, Frank B, Marchbank A, Lee L 2000 The Role of maternal antibodies in cholestatic liver disease in infants: a new isolated finding in neonatal lupus?. J Pediatr Gastroenterol Nutr 31( suppl 2): S108
Kerkar N, Hadzic N, Davies ET, Portmann B, Donaldson PT, Rela M, Heaton ND, Vergani D, Mieli-Vergani G 1998 De-novo autoimmune hepatitis after liver transplantation. Lancet 351: 409–413
Hernandez HM, Kovarik P, Whitington PF, Alonso EM 2001 Autoimmune hepatitis as a late complication of liver transplantation. J Pediatr Gastroenterol Nutr 32: 131–136
Chapman RW 1991 Role of immune factors in the pathogenesis of primary sclerosing cholangitis. Semin Liver Dis 11: 1–4
Donaldson PT, Manns MP 1999 Immunogenetics of liver disease. In: Benhamou J-P, McIntyre N, Rizetto M, Rodes J (eds) Oxford Textbook of Clinical Hepatology. Oxford University Press, Oxford, pp 173–188
Manabe K, Donaldson PT, Underhill JA, Doherty DG, Mieli-Vergani G, McFarlane IG, Eddleston AL, Williams R 1993 Human leukocyte antigen A1–B8-DR3-DQ2-DPB1*0401 extended haplotype in autoimmune hepatitis. Hepatology 18: 1334–1337
Rosenthal P, Woolf GM, Tyan DB 1995 A striking association between HLA-C and biliary atresia. Gastroenterology 108: A1158
Silveira TR, Salzano FM, Donaldson PT, Mieli-Vergani G, Howard ER, Mowat AP 1993 Association between HLA and extrahepatic biliary atresia. J Pediatr Gastroenterol Nutr 16: 114–117
A-Kader HH, El-Ayyouti M, Hawas S, Abdalla A, Al-Tonbary Y, Bassiouny M, Boneberg A, El-Sallab S 2002 HLA in Egyptian children with biliary atresia. J Pediatr 141: 432–433
Donaldson PT, Clare M, Constantini PK, Hadzic N, Mieli-Vergani G, Howard E, Kelley D 2002 HLA and cytokine gene polymorphisms in biliary atresia. Liver 22: 213–219
Mazziotti MV, Willis LK, Heuckeroth RO, LaRegina MC, Swanson PE, Overbeek PA, Perlmutter DH 1999 Anomalous development of the hepatobiliary system in the Inv mouse. Hepatology 30: 372–378
Yokoyama T, Copeland NG, Jenkins NA, Montgomery CA, Elder FF, Overbeek PA 1993 Reversal of left-right asymmetry: a situs inversus mutation. Science 260: 679–682
Schon P, Tsuchiya K, Lenoir D, Mochizuki T, Guichard C, Takai S, Maiti AK, Nihei H, Weil J, Yokoyama T, Bouvagnet P 2002 Identification, genomic organization, chromosomal mapping and mutation analysis of the human INV gene, the ortholog of a murine gene implicated in left-right axis development and biliary atresia. Hum Genet 110: 157–165
Otto EA, Schermer B, Obara T, O'Toole JF, Hiller KS, Mueller AM, Ruf RG, Hoefele J, Beekmann F, Landau D, Foreman JW, Goodship JA, Strachan T, Kispert A, Wolf MT, Gagnadoux MF, Nivet H, Antignac C, Walz G, Drummond IA, Benzing T, Hildebrandt F 2003 Mutations in INVS encoding inversin cause nephronophthisis type 2, linking renal cystic disease to the function of primary cilia and left-right axis determination. Nat Genet 34: 413–420
Johnson CA, Gissen P, Sergi C 2003 Molecular pathology and genetics of congenital hepatorenal fibrocystic syndromes. J Med Genet 40: 311–319
Low Y, Vijayan V, Tan CE 2001 The prognostic value of ductal plate malformation and other histologic parameters in biliary atresia: an immunohistochemical study. J Pediatr 139: 320–322
Bamford RN, Roessler E, Burdine RD, Saplakoglu U, dela Cruz J, Splitt M, Goodship JA, Towbin J, Bowers P, Ferrero GB, Marino B, Schier AF, Shen MM, Muenke M, Casey B 2000 Loss-of-function mutations in the EGF-CFC gene CFC1 are associated with human left-right laterality defects. Nat Genet 26: 365–369
Jacquemin E, Cresteil D, Raynaud N, Hadchouel M 2002 CFCI gene mutation and biliary atresia with polysplenia syndrome. J Pediatr Gastroenterol Nutr 34: 326–327
Ware SM, Peng J, Zhu L, Fernbach S, Colicos S, Casey B, Towbin J, Belmont JW 2004 Identification and functional analysis of ZIC3 mutations in heterotaxy and related congenital heart defects. Am J Hum Genet 74: 93–105
Zhang DY, Sabla G, Shivakumar P, Tiao G, Sokol RJ, Mack C, Shneider BL, Aronow B, Bezerra JA 2004 Coordinate expression of regulatory genes differentiates embryonic and perinatal forms of biliary atresia. Hepatology 39: 954–62
Vijayan V, Tan CE 1997 Developing human biliary system in three dimension. Anat Rec 249: 389–398
Lemaigre FP 2003 Development of the biliary tract. Mech Dev 120: 81–87
Clotman F, Lannoy VJ, Reber M, Cereghini S, Cassiman D, Jacquemin P, Roskams T, Rousseau GG, Lemaigre FP 2002 The onecut transcription factor HNF6 is required for normal development of the biliary tract. Development 129: 1819–1828
Coffinier C, Gresh L, Fiette L, Tronche F, Schutz G, Babinet C, Pontoglio M, Yaniv M, Barra J 2002 Bile system morphogenesis defects and liver dysfunction upon targeted deletion of HNF1beta. Development 129: 1829–1838
Clotman F, Libbrecht L, Gresh L, Yaniv M, Roskams T, Rousseau GG, Lemaigre FP 2003 Hepatic artery malformations associated with a primary defect in intrahepatic bile duct development. J Hepatol 39: 686–692
Kohsaka T, Yuan ZR, Guo SX, Tagawa M, Nakamura A, Nakano M, Kawasasaki H, Inomata Y, Tanaka K, Miyauchi J 2002 The significance of human jagged 1 mutations detected in severe cases of extrahepatic biliary atresia. Hepatology 36: 904–912
Tan CE, Moscoso GJ 1994 The developing human biliary system at the porta hepatis level between 11 and 25 weeks of gestation: a way to understanding biliary atresia. Part 2. Pathol Int 44: 600–610
Rolleston HD, Hayne LB 1901 A case of congenital hepatic cirrhosis with obliterative cholangitis (congenital obliteration of the bile ducts). BMJ 1: 758–760
An Introduction To The Boxelder Tree
Boxelder trees, also known as ash-leaved maples, are one of the most common and adaptable urban trees in North America—though they also may be the "messiest" from a visual perspective. The boxelder is very commonly seen in treeless plains and flanking the streets west of the Mississippi River.
It seems that the tree takes on positive characteristics not seen in the eastern half of North America in its western habitat. California interior boxelders take on yellow and red colors in autumn that rival eastern maple. Its drought tolerance makes the tree great for dry country landscapes and very easy on limited water resources. The best thing about it is that it's comfortable on poor sites where more desirable trees cannot maintain adequate health for a long life.
Learn more about the ubiquitous boxelder, including how to identify it, how to grow and maintain it, and problems that could come up.
About the Boxelder undefined undefined / Getty Images The boxelder (Acer negundo) also goes by ashleaf maple, Manitoba maple, and poison ivy tree. It's a member of the plant family Aceraceae. Although considered a "maple outcast" by many, it is indeed in the maple family and the only native maple with more than one blade or leaflet on a single leaf stalk. Boxelder is native to North America and grows in USDA Plant Hardiness Zones 3 through 8. It's very common throughout the western U.S. The tree is crafted into bonsai specimens and used as a screen or windbreak and for land reclamation. Boxelders often have multiple furrowed trunks or very squat single trunks. It grows rapidly and large (25 to 50 feet). One of the tallest ever measured had a recorded height of 110 feet. The tree's crown spread is 25 to 45 feet, and the crown is typically broad and ragged or disheveled. For this reason—and its proneness to breakage—it's not recommended to plant one in your yard. Flowers are without petals, dioecious, and yellowish-green, and the female tassels are very conspicuous. The very maple-looking seeds, called samaras, hang in long, profuse clusters and stay on the tree throughout winter. Nearly every seed is viable and will cover up a disturbed area with seedlings. The boxelder is a very prolific seeder. Boxelder Leaf Botanics Leaf arrangement: Opposite/subopposite Leaf type: Odd pinnately compound Leaflet margin: Lobed; serrate Leaflet shape: Lanceolate; ovate Leaflet venation: Pinnate; reticulate Leaf type and persistence: Deciduous Leaflet blade length: 2 to 4 inches Leaf color: Green Fall color: Orange; yellow Fall characteristic: Showy Boxelder Cultivars Nahhan / Getty Images There are several attractive cultivars of boxelder including "Aureo-Variegata," "Flamingo," and "Auratum." The cultivar Acer negundo, "Aureo-Variegata," is noted for its leaves bordered in gold. Acer negundo, "Flamingo," has variegated leaves with pink margins and is somewhat available at local nurseries. Acer negundo, "Auratum," has abundant gold leaves but is a little harder to find. Even though these cultivars are ornamental, they still share the original boxelder tree's undesirable characteristics, including unattractive female fruit and breakage. The chances of the tree's early removal are still high because of its quick growth. Problems With Boxelder Robert_schafer_photography / Getty Images Boxelder is a rather unattractive tree when limbs break and create a landscape maintenance nightmare. The fruit droops in clusters, which some describe as looking like "dirty brown socks." And the boxelder bug makes things even worse. The Boxelder Bug The boxelder bug (Leptocoris trivittatus) loves the boxelder tree. This half-inch red-striped insect is a true pest during winter. Adults even multiply and invade homes near where boxelder trees grow, making it one of the most common household pests in the U.S. The bug emits a foul odor, stains fabric, and can cause asthmatic reactions. Despite the havoc it could wreak in your home, it does not harm its host tree. Pruning Boxelder Nahhan / Getty Images You will have to prune this tree regularly. Boxelder branches droop as the tree grows and will require pruning if you have consistent walking and vehicular traffic under the canopy. The tree form is not particularly showy and should be grown with one single trunk to maturity. The tree is susceptible to breakage that can occur either at the crotch due to poor collar formation or where the wood itself is weak. Boxelder Trees The boxelder, also known as ash-leaved maple, is a common urban tree in North America known for its adaptability, drought tolerance, and vibrant autumn colors in the western half of the continent. Despite its quick growth and drought resistance, boxelder is often considered undesirable due to its messy appearance, prolific seeding, and susceptibility to breakage. Boxelder trees attract boxelder bugs, which can become household pests during winter but don't harm the tree itself.
Comments
Post a Comment