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Chisholm Trail
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For other uses, see Chisholm Trail (disambiguation).
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1873 Map of Chisholm Trail with Subsidiary Trails in Texas (from Kansas Historical Society)
The Chisholm Trail was a trail used in the post-Civil War era to drive cattle overland from ranches in Texas to Kansas railheads. The portion of the trail marked by Jesse Chisholm went from his southern trading post near the Red River to his northern trading post near Kansas City, Kansas.
Contents
1 Overview
2 Business aspects
3 Route
3.1 Northern end of trail
3.2 Southern start of trail
4 Challenges
5 Legacy
6 Further reading
7 References
8 External links
Overview[edit]
Texas ranchers using the Chisholm Trail started on the route from either the Rio Grande or San Antonio, joined the Chisholm Trail at the Red River of the South at the border between Texas and Oklahoma, and continued to the railhead of the Kansas Pacific Railway in Abilene, Kansas, where the cattle would be sold and shipped eastward. The trail is named for Jesse Chisholm, a half-Cherokee trader from Tennessee, who originally created the trail as a means to transport his goods from one trading post to another.[1]
Business aspects[edit]
By 1853, Texas cattle were being driven into Missouri, where local farmers began blocking herds and turning them back because the Texas Longhorns carried ticks that caused diseases in other types of cattle. Violence, vigilante groups, and cattle rustling caused further problems for the drovers. By 1859, the driving of cattle was outlawed in many Missouri jurisdictions. By the end of the Civil War, most cattle were being moved up the western branch of trail at Red River Station in Montague County, Texas.
In 1866, cattle in Texas were worth only $4 per head, compared to over $40 per head in the North and East, because lack of market access during the American Civil War had led to over stock of cattle in Texas. In 1867, Joseph G. McCoy built stockyards in Abilene, Kansas. He encouraged Texas cattlemen to drive their herds to his stockyards. The stockyards shipped 35,000 head that year and became the largest stockyards west of Kansas City, Kansas.
That same year, O. W. Wheeler answered McCoy's call, and he along with partners used the Chisholm Trail to bring a herd of 2,400 steers from Texas to Abilene. This herd was the first of an estimated 5,000,000 head of Texas cattle to reach Kansas over the Chisholm Trail.[2][3]
The construction of the Union Pacific Railway through Nebraska eventually offered a cattle drive destination which was an attractive alternative to the Kansas Pacific Railroad, and the Texas Trail emerged as an alternative to the Chisholm Trail. Some cattle drives in 1876 and up to 1884 went along the Texas Trail instead of the Chisholm Trail.[4]
Route[edit]
Chisholm Trail crossing through modern-day Duncan, Oklahoma
Chisholm Trail historical marker in Kingfisher, Oklahoma
In Texas, hundreds of feeder trails headed north to one of the main cattle trails. In the early 1840s, most cattle were driven up the Shawnee Trail. The Chisholm Trail was previously used by Indian hunting and raiding parties; the trail crossed into Indian Territory (present-day west-central Oklahoma) near Red River Station (in present-day Montague County, Texas) and entered Kansas near Caldwell. Through Oklahoma, the Chisholm Trail generally follows the route of US Highway 81 through present-day towns of El Reno, Duncan, Chickasha, and Enid.[5]
Northern end of trail[edit]
From 1867 to 1871, the trail ended in Abilene, Kansas, but as railroads incrementally built southward, the end of the trail moved to other cities. The end of the trail moved to Newton, Kansas then soon afterward moved to Wichita, Kansas. From 1883 to 1887, the end of the trail was Caldwell, Kansas. Ellsworth, Kansas, is also considered a major influence of the trail.[citation needed]
Southern start of trail[edit]
Historians consider the Chisholm Trail to have started either at Donna, Texas or San Antonio, Texas.[citation needed] In 1931, George W. Saunders, then president of the Old Trail Drivers Association and an authority on Texas livestock history wrote: "The famed Chisholm Trail, about which more has been written than any other Southwestern Trail, cannot be traced in Texas for the reason that it never existed in this State." It was always understood by pioneer cattlemen that they would strike the Chisholm Trail at Red River Station, at the mouth of Salt Creek in Montague County, where they left Texas and crossed into the Indian Territory.[citation needed]
Challenges[edit]
See also: Cattle drives in the United States
On the long trips—up to two months—the cattlemen faced many difficulties. They had to cross major rivers such as the Arkansas River and the Red River, and innumerable smaller creeks, plus the topographic challenges of canyons, badlands and low mountain ranges. The weather was less than ideal but the major drives typically needed to start in the spring after the rains brought green grasses for the grazing cattle. The spring drives, with those rains and higher water levels with the runoff, always meant more danger for bridgeless river crossings. The days of longest sunlight, near mid-June, were also an important consideration in the timing of drives. In addition to natural dangers, rustlers and occasional conflicts with Native Americans erupted. The latter demanded that drovers, the trail bosses, pay a toll of 10 cents a head to local tribes for the right to cross Indian lands (Oklahoma at that time was Indian Territory, governed from Fort Smith, Arkansas). The half-wild Texas Longhorn cattle were contrary and prone to stampede with little provocation.
Legacy[edit]
At least 27 movies have depicted fictional accounts of the first drive along the Chisholm Trail, including The Texans (1938), directed by James P. Hogan and starring Randolph Scott and Joan Bennett, and Red River (1948), directed by Howard Hawks and starring John Wayne and Montgomery Clift. Walter Brennan co-starred in both films in his usual grizzled-old-coot role.
The trail is the subject of at least two pop songs: "The Last Cowboy Song" written and recorded by Ed Bruce, also performed by The Highwaymen, and the song "The Old Chisholm Trail." Among those who have covered the song are Gene Autry, Girls of the Golden West, Woody Guthrie, Michael Martin Murphey, Tex Ritter, Roy Rogers, and Lead Belly (Huddie Ledbetter), although his version was titled "When I Was A Cowboy".
In 1964, Texas rancher Charles Schreiner, III, founded the Texas Longhorn Breeders Association of America. The next year, he conducted a cattle drive from San Antonio to Dodge City with a stop at the LBJ Ranch in Gillespie County, home of then U.S. President Lyndon B. Johnson. The drive was promoted as a centennial commemoration of the original Chisholm Trail drives.[6]
Many schools have been named after the Chisholm Trail, including:
Chisholm Trail High School in Fort Worth, Texas
Chisholm Trail Middle School in Olathe, Kansas[7]
Chisholm Trail Middle School in Round Rock, Texas
Chisholm Trail Middle School in Rhome, Texas[8]
Chisholm Trail Elementary School in Park City, Kansas[9]
Chisholm Middle School in Newton, Kansas
Chisholm Trail intermediate school in Keller, Texas
Chisholm High School in Enid, Oklahoma
Chisholm Elementary School in Edmond, Oklahoma
Chisholm Trail Heritage Center, located in Duncan, Oklahoma, is an interactive museum dedicated to the history of the trail. It has a large monument depicting a scene from the Chisholm Trail cattle drive, as well as a trail walkway.[10]
On the second weekend of June, Lockhart in Caldwell County holds a four-day festival to celebrate its place on the Chisholm Trail. Newton, Kansas also holds a three- to four-day Chisholm Trail Festival, combining it with the annual Fourth of July celebration.
On September 26, 2009, a historical marker on the Chisholm Trail was unveiled at the site of Red River Station in Montague County. The 5.5-foot concrete marker is the last of 12 erected in Montague County as part of a joint project of the Texas Lakes and Trails and the Montague County Historical Commission to outline the Chisholm Trail (as said in Wichita Falls Times Record News).
In 2014, the North Texas Tollway Authority constructed a 26-mile-long toll road named after the trail, the Chisholm Trail Parkway connecting downtown Fort Worth to the nearby city of Cleburne in Johnson County.
In 2017, the Texas Historical Commission released The Chisholm Trail: Exploring the Folklore and Legacy, an online tour and mobile app.[11] The tour includes audio tracks and short videos that retell the history of communities and local heritage in towns and cities that line the route of the former Chisholm Trail.
Further reading[edit]
Library resources about
Chisholm Trail
Online books
Resources in your library
Resources in other libraries
Guide Map of the Best and Shortest Cattle Trail to the Kansas Pacific Railway; Kansas Pacific Railway Company; 1875. (Read Online)(Map)
Morality and Money: A Look at how the Respectable Community Battled the Sporting Community over Prostitution in Kansas Cowtowns, 1867-1885; Jessica Smith; Kansas State University; 2013. Read Online
References[edit]
Jump up ^ C., RICHARDSON, T. (12 June 2010). "CHISHOLM, JESSE". tshaonline.org. Retrieved 4 April 2018.
Jump up ^ Worcester, Donald E.: "Chisholm Trail" from the Handbook of Texas Online. Retrieved December 23, 2008.
Jump up ^ Dortch, Steven D. "Chisholm Trail". Encyclopedia of Oklahoma History and Culture - Oklahoma Historical Society. Retrieved November 11, 2012.
Jump up ^ "The Texas Trail".
Jump up ^ Oklahoma Map of Chisholm Trail Oklahoma State University Digital Library Collections
Jump up ^ Douglas Martin (April 29, 2001). "Charles Schreiner III, 74, Dies; Colorful Texas Rancher Fought to Save Longhorn". The New York Times. Retrieved October 16, 2015.
Jump up ^ "Chisholm Trail Middle School". schools.olathe.k12.ks.us. Retrieved 4 April 2018.
Jump up ^ "Home - Northwest Independent School District". www.nisdtx.org. Retrieved 4 April 2018.
Jump up ^ "Chisholm Trail Elementary / Homepage". chisholmtrail.usd259.org. Retrieved 4 April 2018.
Jump up ^ Chisholm Trail Heritage Center Chisholm Trail art, culture, and history - Duncan, Oklahoma
Jump up ^ "The Chisholm Trail: Exploring the Folklore and Legacy". Texas Travel. Retrieved 4 April 2018.
External links[edit]
Wikimedia Commons has media related to Chisholm Trail.
The Texas Historical Commission Chisholm Trail mobile tour
History on the trail from the "Kansas Heritage Group"
Up the Chisholm Trail by the Williamson County Historical Commission
Along the Chisholm Trail Web site with maps, history, monuments, and guides for visiting.
The Chisholm Trail Heritage Museum Texas cowboy and Longhorn cattle drive history - Cuero, Texas
On the Chisholm Trail Heritage Museum Chisholm Trail history and settlement of the Southern Great Plains of the US. - Duncan, Oklahoma
Maps
Simplified map of the trail
1873 map of the main trail and subsidiary trails
Detailed map of the trail through Oklahoma
Detailed map of the trail through Kansas
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text:
Hemolytic anemia
From Wikipedia, the free encyclopedia
Jump to: navigation, search
Hemolytic anemia
Classification and external resources
Specialty
Hematology
ICD-10
D55-D59
ICD-9-CM
282, 283, 773
DiseasesDB
5534
MedlinePlus
000571
eMedicine
med/979
MeSH
D000743
[edit on Wikidata]
Hemolytic anemia or haemolytic anaemia is a form of anemia due to hemolysis, the abnormal breakdown of red blood cells (RBCs), either in the blood vessels (intravascular hemolysis) or elsewhere in the human body (extravascular, but usually in the spleen). It has numerous possible consequences, ranging from relatively harmless to life-threatening. The general classification of hemolytic anemia is either inherited or acquired. Treatment depends on the cause and nature of the breakdown.
Symptoms of hemolytic anemia are similar to other forms of anemia (fatigue and shortness of breath), but in addition, the breakdown of red cells leads to jaundice and increases the risk of particular long-term complications, such as gallstones and pulmonary hypertension.[citation needed]
Contents
[hide]
1 Signs and symptoms
2 Causes
2.1 Intrinsic causes
2.2 Extrinsic causes
3 Mechanism
4 Diagnosis
5 Treatment
6 Animals
7 References
Signs and symptoms[edit]
In general, signs of anemia (pallor, fatigue, shortness of breath, and potential for heart failure) are present. In small children, failure to thrive may occur in any form of anemia. Certain aspects of the medical history can suggest a cause for hemolysis, such as drugs, consumption of fava beans due to Favism, the presence of prosthetic heart valve, or other medical illness.
Chronic hemolysis leads to an increased excretion of bilirubin into the biliary tract, which in turn may lead to gallstones. The continuous release of free hemoglobin has been linked with the development of pulmonary hypertension (increased pressure over the pulmonary artery); this, in turn, leads to episodes of syncope (fainting), chest pain, and progressive breathlessness. Pulmonary hypertension eventually causes right ventricular heart failure, the symptoms of which are peripheral edema (fluid accumulation in the skin of the legs) and ascites (fluid accumulation in the abdominal cavity).
Causes[edit]
Main articles: Congenital hemolytic anemia and Acquired hemolytic anemia
They may be classified according to the means of hemolysis, being either intrinsic in cases where the cause is related to the red blood cell (RBC) itself, or extrinsic in cases where factors external to the RBC dominate.[1] Intrinsic effects may include problems with RBC proteins or oxidative stress handling, whereas external factors include immune attack and microvascular angiopathies (RBCs are mechanically damaged in circulation).
Intrinsic causes[edit]
Hereditary (inherited) hemolytic anemia can be due to :
Defects of red blood cell membrane production (as in hereditary spherocytosis and hereditary elliptocytosis)
Defects in hemoglobin production (as in thalassemia, sickle-cell disease and congenital dyserythropoietic anemia)
Defective red cell metabolism (as in glucose-6-phosphate dehydrogenase deficiency and pyruvate kinase deficiency)
Paroxysmal nocturnal hemoglobinuria (PNH), sometimes referred to as Marchiafava-Micheli syndrome, is a rare, acquired, potentially life-threatening disease of the blood characterized by complement-induced intravascular hemolytic anemia.
Extrinsic causes[edit]
Acquired hemolytic anemia may be caused by immune-mediated causes, drugs and other miscellaneous causes.
Immune-mediated causes could include transient factors as in Mycoplasma pneumoniae infection (cold agglutinin disease) or permanent factors as in autoimmune diseases like autoimmune hemolytic anemia (itself more common in diseases such as systemic lupus erythematosus, rheumatoid arthritis, Hodgkin's lymphoma, and chronic lymphocytic leukemia).
Spur cell hemolytic anemia
Any of the causes of hypersplenism (increased activity of the spleen), such as portal hypertension.
Acquired hemolytic anemia is also encountered in burns and as a result of certain infections (e.g. malaria).
Lead poisoning resulting from the environment causes non-immune hemolytic anemia.
Similarly, poisoning by arsine or stibine also causes hemolytic anemia.
Runners can suffer hemolytic anemia due to "footstrike hemolysis", owing to the destruction of red blood cells in feet at foot impact.[2][3]
Low-grade hemolytic anemia occurs in 70% of prosthetic heart valve recipients, and severe hemolytic anemia occurs in 3%.[4]
Mechanism[edit]
Hemolytic anemia involves the following:
Abnormal and accelerated destruction of red cells and, in some anemias, their precursors
Increased breakdown of hemoglobin, which may result in:
increased bilirubin level (mainly indirect-reacting) with jaundice
increased fecal and urinary urobilinogen
Hemoglobinemia, methemalbuminemia, hemoglobinuria and hemosiderinuria (where there is significant intravascular hemolysis).
Bone marrow compensatory reaction:
Erythroid hyperplasia with accelerated production of red cells, reflected by reticulocytosis, and slight macrocytosis in peripheral blood
Expansion of bone marrow in infants and children with severe chronic hemolysis - changes in bone configuration visible on X-ray
The balance between red cell destruction and marrow compensation determines the severity of anemias.
In a healthy person, a red blood cell survives 90 to 120 days in the circulation, so about 1% of human red blood cells break down each day[citation needed]. The spleen (part of the reticulo-endothelial system) is the main organ that removes old and damaged RBCs from the circulation. In healthy individuals, the breakdown and removal of RBCs from the circulation is matched by the production of new RBCs in the bone marrow.
In conditions where the rate of RBC breakdown is increased, the body initially compensates by producing more RBCs; however, breakdown of RBCs can exceed the rate that the body can make RBCs, and so anemia can develop. Bilirubin, a breakdown product of hemoglobin, can accumulate in the blood, causing jaundice.
In general, hemolytic anemia occurs as a modification of the RBC life cycle. That is, instead of being collected at the end of its useful life and disposed of normally, the RBC disintegrates in a manner allowing free iron-containing molecules to reach the blood. With their complete lack of mitochondria, RBCs rely on glycolysis for the materials needed to reduce oxidative damage. Any limitations of glycolysis can result in more susceptibility to oxidative damage and a short or abnormal lifecycle. If the cell is unable to signal to the reticuloendothelial phagocytes by externalizing phosphatidylserine, it is likely to lyse through uncontrolled means.[5][6][7]
The distinguishing feature of intravascular hemolysis is the release of RBC contents into the blood stream. The metabolism and elimination of these products, largely iron-containing compounds capable of doing damage through Fenton reactions, is an important part of the condition. Several reference texts exist on the elimination pathways, for example.[8][9] Free hemoglobin can bind to haptoglobin, and the complex is cleared from the circulation; thus, a decrease in haptoglobin can support a diagnosis of hemolytic anemia. Alternatively, hemoglobin may oxidize and release the heme group that is able to bind to either albumin or hemopexin. The heme is ultimately converted to bilirubin and removed in stool and urine.[8] Hemoglobin may be cleared directly by the kidneys resulting in fast clearance of free hemoglobin but causing the continued loss of hemosiderin loaded renal tubular cells for many days.
Additional effects of free hemoglobin seem to be due to specific reactions with NO.[10]
Diagnosis[edit]
The diagnosis of hemolytic anemia can be suspected on the basis of a constellation of symptoms and is largely based on the presence of anemia, an increased proportion of immature red cells (reticulocytes) and a decrease in the level of haptoglobin, a protein that binds free hemoglobin. Examination of a peripheral blood smear and some other laboratory studies can contribute to the diagnosis. Symptoms of hemolytic anemia include those that can occur in all anemias as well as the specific consequences of hemolysis. All anemias can cause fatigue, shortness of breath, decreased ability to exercise when severe. Symptoms specifically related to hemolysis include jaundice and dark colored urine due to the presence of hemoglobin (hemaglobinuria). When restricted to the morning hemaglobinuria may suggest paroxysmal nocturnal haemoglobinuria. Direct examination of blood under a microscope in a peripheral blood smear may demonstrate red blood cell fragments called schistocytes, red blood cells that look like spheres (spherocytes), and/or red blood cells missing small pieces (bite cells). An increased number of newly made red blood cells (reticulocytes) may also be a sign of bone marrow compensation for anemia. Laboratory studies commonly used to investigate hemolytic anemia include blood tests for breakdown products of red blood cells, bilirubin and lactate dehydrogenase, a test for the free hemoglobin binding protein haptoglobin, and the direct Coombs test to evaluate antibody binding to red blood cells suggesting autoimmune hemolytic anemia.
Treatment[edit]
This section needs expansion. You can help by adding to it. (March 2010)
Definitive therapy depends on the cause:
Symptomatic treatment can be given by blood transfusion, if there is marked anemia. A positive Coombs test is a relative contraindication to transfuse the patient. In cold hemolytic anemia there is advantage in transfuse warmed blood
In severe immune-related hemolytic anemia, steroid therapy is sometimes necessary.
In steroid resistant cases, consideration can be given to rituximab or addition of an immunosuppressant ( azathioprine, cyclophosphamide)
Association of methylprednisolone and intravenous immunoglobulin can control hemolysis in acute severe cases
Sometimes splenectomy can be helpful where extravascular hemolysis, or hereditary spherocytosis, is predominant (i.e., most of the red blood cells are being removed by the spleen).[11]
Animals[edit]
Hemolytic anemia affects nonhuman species as well as humans. It has been found, in a number of animal species, to result from specific triggers.[12]
Some notable cases include hemolytic anemia found in black rhinos kept in captivity, with the disease, in one instance, affecting 20% of captive rhinos at a specific facility.[13][14][15] The disease is also found in wild rhinos.[16]
Dogs and cats differ slightly from humans in some details of their RBC composition and have altered susceptibility to damage, notably, increased susceptibility to oxidative damage from consumption of onion. Garlic is less toxic to dogs than onion.[17]
References[edit]
Jump up ^ Current Medical Diagnosis and Treatment 2009 By Stephen J. McPhee, Maxine A. Papadakis page 436 https://books.google.com/books?id=zQlH4mXSziYC&pg=PT454&dq=hemoglobin+hemosiderin+hemolysis+bilirubin&ei=Z2P_SuzwA6D2ygT9vOz3Dg#v=onepage&q=hemoglobin%20hemosiderin%20hemolysis%20bilirubin&f=false
Jump up ^ Telford RD, Sly GJ, Hahn AG, Cunningham RB, Bryant C, Smith JA (January 2003). "Footstrike is the major cause of hemolysis during running". J. Appl. Physiol. 94 (1): 38–42. doi:10.1152/japplphysiol.00631.2001. PMID 12391035.
Jump up ^ Lippi G, Schena F, Salvagno GL, Aloe R, Banfi G, Guidi GC (July 2012). "Foot-strike haemolysis after a 60-km ultramarathon". Blood Transfus. 10 (3): 377–383. doi:10.2450/2012.0167-11. PMC 3417738  . PMID 22682343.
Jump up ^ Wise, Donald Lee (2000). "Biomaterials Engineering and Devices: Orthopedic, dental, and bone graft applications". ISBN 978-0-89603-859-2.
Jump up ^ Kolb S, Vranckx R, Huisse MG, Michel JB, Meilhac O (July 2007). "The phosphatidylserine receptor mediates phagocytosis by vascular smooth muscle cells". The Journal of Pathology. 212 (3): 249–59. doi:10.1002/path.2190. PMID 17534843.
Jump up ^ Bosman GJ, Willekens FL, Werre JM (2005). "Erythrocyte aging: a more than superficial resemblance to apoptosis?". Cellular Physiology and Biochemistry. 16 (1–3): 1–8. doi:10.1159/000087725. PMID 16121027.
Jump up ^ Bratosin D, Mazurier J, Tissier JP, et al. (February 1998). "Cellular and molecular mechanisms of senescent erythrocyte phagocytosis by macrophages. A review". Biochimie. 80 (2): 173–95. doi:10.1016/S0300-9084(98)80024-2. PMID 9587675.
^ Jump up to: a b Hematology in clinical practice: a guide to diagnosis and management By Robert S. Hillman, Kenneth A. Ault, Henry M. Rinder page 136-139 https://books.google.com/books?id=NJs1VpA8SEoC&pg=PA138&dq=hemoglobin+hemosiderin+hemolysis+bilirubin&ei=Z2P_SuzwA6D2ygT9vOz3Dg#v=onepage&q=hemoglobin%20hemosiderin%20hemolysis%20bilirubin&f=false
Jump up ^ Wintrobe's Clinical Hematology, Volume 1 By John P. Greer https://books.google.com/books?id=68enzUD7BVgC&pg=PA161&dq=hemoglobin+hemosiderin+hemolysis+bilirubin&ei=Z2P_SuzwA6D2ygT9vOz3Dg#v=onepage&q=hemoglobin%20hemosiderin%20hemolysis%20bilirubin&f=false page 160
Jump up ^ Boretti FS, Buehler PW, D'Agnillo F, et al. (August 2009). "Sequestration of extracellular hemoglobin within a haptoglobin complex decreases its hypertensive and oxidative effects in dogs and guinea pigs". The Journal of Clinical Investigation. 119 (8): 2271–80. doi:10.1172/JCI39115. PMC 2719941  . PMID 19620788.
Jump up ^ "Hemolytic Anemias, F. Spherocytosis". http://MedicalAssistantOnlinePrograms.org/. Retrieved 6 November 2013. External link in |website= (help)
Jump up ^ Mary Anna Thrall, Dale C. Baker, E. Duane Lassen, Veterinary hematology and clinical chemistry, ISBN 0-7817-6850-0, 2004.
Jump up ^ Edward F. Gibbons, Barbara Susan Durrant, Jack Demarest, Conservation of endangered species in captivity: an interdisciplinary approach, page 324, 2005, ISBN 0-7914-1911-8
Jump up ^ Oliver A. Ryder, Zoological Society of San Diego, Rhinoceros biology and conservation, Zoological Society of San Diego, 1993, page 312, 335.
Jump up ^ Texas Monthly, Oct 1992, Vol. 20, No. 10, ISSN 0148-7736, page 98-100.
Jump up ^ Jutta Meister, ed. Catharine E. Bell, Encyclopedia of the world's zoos, Volume 3, page 1008, ISBN 1-57958-174-9, 2001.
Jump up ^ Kovalkovičová N, Sutiaková I, Pistl J, Sutiak V (2009). "Some food toxic for pets". Interdisciplinary Toxicology. 2 (3): 169–76. doi:10.2478/v10102-009-0012-4. PMC 2984110  . PMID 21217849.
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