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Tropical Spastic Paraparesis

Tropical spastic paraparesis


Tropical spastic paraparesis (TSP) is a slowly progressive spastic paraparesis caused by the human T-cell lymphotropic virus-1 (HTLV-1), with an insidious onset in adulthood. It has been found all around the world (except in the poles), mainly in tropical and subtropical regions.


For several decades the term tropical spastic paraparesis (TSP) was used to describe a chronic and progressive clinical syndrome that affected adults living in equatorial areas of the world. Neurological and modern epidemiological studies found that in some individuals no one cause could explain the progressive weakness, sensory disturbance, and sphincter dysfunction that affected individuals with TSP. During the mid-1980s, an important association was established between the first human HTLV-1 virus and idiopathic TSP. Since then, this condition has been named HTLV-1 associated myelopathy/tropical spastic paraparesis or HAM/TSP and scientists now understand that it is a condition caused by a retrovirus that results in immune dysfunction. The main neurological features of HAM/TSP consist of spasticity and hyperreflexia (increased reflex action) of the lower extremities, urinary bladder disturbance, lower-extremity muscle weakness, sensory disturbances, and loss of coordination. Patients with HAM/TSP may also exhibit arthritis, lung changes, and inflammation of the skin.

Co-factors that may play a role in transmitting the disorder include being a recipient of transfusion blood products, breast-feeding from an infected mother, intravenous drug use, or being the sexual partner of an infected individual for several years.


Sporadic cases of TSP have been reported in the United States, mostly in immigrants from countries where this disease is endemic (naturally occurring). In the United States, the lifetime risk of an HTLV-1-infected person developing TSP/HAM has been calculated to be 1.77%, similar to that reported for United Kingdom, Africa, and the Caribbean.

The international incidence is difficult to estimate because of the insidious nature of this disease. HAM/TSP is common in regions of endemic HTLV-1, such as the Caribbean, equatorial Africa, Seychelles, southern Japan, and South America. However, it also has been reported from non-endemic areas, such as Europe and the United States. The prevalence in southern Japan is in the range of 8.6128 per 100,000 inhabitants. An estimated 1020 million individuals worldwide are carriers of HTLV-1.

HAM/TSP generally affects women more than men, with a female-to-male ratio of 3:1. This disease may occur at any age, with a peak in the third or fourth decade.

Causes and symptoms

The cause of HAM/TSP is still a matter of debate. Whereas only a small proportion of HTLV-1-infected individuals develop HAM/TSP, the mechanisms responsible for the progression of an HTLV-1 carrier state to clinical disease are not clear. However, three hypotheses are considered by scientists as the most likely cause of TSP: direct toxicity, autoimmunity, and bystander damage. The direct toxicity theory of HAM/TSP pathogenesis suggests that HTLV-1-infected cells are directly damaged by certain white blood cells. The autoimmunity theory postulates that the immune system attacks cells that react to HTLV-1 infected cells. In the bystander damage hypothesis, circulating antivirus-specific cells migrating through the central nervous system produce damage to nearby cells that is directed against the infected cells.

Symptoms may begin years after infection. In response to the infection, the body's immune response may injure nerve tissue, causing symptoms including:

  • spasms and loss of feeling or unpleasant sensations in the lower extremities, accompanied by weakness
  • decreased sense of touch in mid-body areas
  • a vibration sensation, especially in the lower extremities, resulting from spinal cord or peripheral nerve involvement
  • low lumbar pain with irradiation to the legs
  • increased reflexes of the upper extremities
  • increased urinary frequency and associated increased incidence of urinary tract infection

Less frequently observed symptoms include tremors in the upper extremities, optical nerve atrophy, deafness, abnormal eye movements, cranial nerve deficits, and absent or diminished ankle jerk reflex.


During the clinical examination, it is important to exclude other disorders causing progressive spasticity and weakness in the legs. Diagnosis of HAM/TSP criteria typically involve documenting the following:

  • absence of a history of difficulty walking or running during school age
  • within two years of onset: increased urinary frequency, nocturia, or retention, with or without impotence; leg cramps or low back pain ; symmetric weakness of the lower extremities
  • within six months of onset: complaints of numbness or dysesthesias of the legs or feet
  • a clinical examination documenting increased reflexes; spasticity of both legs, abnormal gait (manner of walking), and absence of normal sensory level

Laboratory diagnosis using ELISA (enzyme-linked immunosorbent assay) detects the presence of antibodies against HTLV-1, confirmed by the western blot assay. Electrodiagnostic studies and magnetic resonance imaging may also be helpful to show evidence of active denervation, associated with HTLV-1.

Treatment team

Persons with TPS have multiple needs and the team should include a neurologist and a physical therapist. An occupational therapist can prescribe exercises designed to develop fine coordination or compensate for tremor or weakness, or suggest assistive devices. More advanced patients require continual nursing assistance.


The US Food and Drug Administration (FDA) has not officially approved any drug for the specific treatment of HAM/TSP in the United States. Many patients benefit from oral prednisolone or equivalent glucocorticoid therapy. A response rate of up to 91% has been reported in less advanced cases. Oral treatment with methylprednisolone may produce excellent to moderate responses in around 70% of patients. Plasmapheresis, interferon, oral azathiaprine, danazol, and vitamin C have been tried and also show transient effects. None of these treatments has been systematically studied in a controlled clinical trial. Antiviral drugs like AZT would be expected to help in reducing viral replication and associated direct cell injury.

Patients with HAM/TSP sometimes report neuropathic pain. Useful drugs include antiepileptics (e.g., carbamazepine , phenytoin, gabapentin , topiramate ), baclofen, and tricyclic antidepressants. The dosages used usually are well below those used in the treatment of epilepsy . Physical therapy is commonly used in combination with medication for nerve pain.

Recovery and rehabilitation

The goal of a rehabilitation program for a person affected with HAM/TSP is to restore functions essential to daily living in individuals who have lost these capacities through injury or illness. Most rehabilitation programs are comprehensive in nature and have several different aspects.

Physical therapy is designed to help restore and maintain useful movements or functions and prevent complications such as frozen joints, contractures, or bedsores. Examples of physical therapy include:

  • stretching and range of motion exercises
  • exercises to develop trunk control and upper arm muscles
  • training in walking and appropriate use of assistive devices, such as ambulatory aids, braces, and wheelchairs
  • training in how to get from one spot to another, such as from the bed to a wheelchair or from a wheelchair to the car
  • training in how to fall safely in order to cause the least possible damage

Occupational therapy focuses on specific activities of daily living that primarily involve the arms and hands. Examples include grooming, dressing, eating, handwriting, and driving.

Some rehabilitation centers have innovative programs designed to help people compensate for loss of memory or slowed learning ability. Rehabilitation may be carried out in a residential or an outpatient setting.

Clinical trials

In 2004 there were some open clinical trials for the study and treatment of TSP, including:

  • "Evaluation of Patients with HAM/TSP," "Phase I/II Study of HTLV-I-Associated Myelopathy/Tropical Spastic Paraparesis (HAM/TSP) Using the Humanized MiK-beta-1 Monoclonal Antibody," and "Assessment of Patients with Multiple Sclerosis," sponsored by National Institute of Neurological Disorders and Stroke (NINDS).
  • "Phase I Study of T Cell Large Granular Lymphocytic Leukemia in Humanized MiK-Beta-1 Monoclonal Antibody Directed Toward the IL-2R/IL-15R Subunit (CD122)," sponsored by National Cancer Institute (NCI).

Further updated information on these clinical trials can be found at the National Institutes of Health website for clinical trials at <>.


HAM/TSP is usually a progressive neurological disorder, but it is rarely fatal. Most patients live for several decades after the diagnosis. Their prognosis improves if they take steps to prevent urinary tract infection and skin sore formation, and if they enroll in physical and occupational therapy programs.

Special concerns

An important component in the care of patients with TSP is the prevention of infections with the HTLV-1 virus. Several studies indicate that transmission of the HTLV-1 virus occurs through sexual or other intimate contact, intrauterine exposure, newborn exposure via breast milk, sharing of needles by drug abusers, and blood transfusion from infected persons. Transfusion of HTLV-1 antibody-positive blood causes infection in about 60% of recipients. Breastfeeding is contraindicated for mothers who are carriers of HTLV-1.



Parker, James N., and Philip M. Parker. The Official Patient's Sourcebook on Tropical Spastic Paraparesis. San Diego: Icon Group International, 2002.


Mora, Carlos A., et al. "Human T-lymphotropic Virus Type I-associated Myelopathy/Tropical Spastic Paraparesis: Therapeutic Approach." Current Treatment Options in Infectious Diseases 5 (2003): 443455.


"NINDS Tropical Spastic Paraparesis Information Page." National Institute of Neurological Disorders and Stroke. (April 20, 2004). <>.

"Tropical spastic paraparesis." Dr. Joseph F. Smith Medical Library. Thompson Corporation. (April 20, 2004). <>.


National Organization for Rare Disorders (NORD). P.O. Box 1968 (55 Kenosia Avenue), Danbury, CT 06813-1968. (203) 744-0100 or (800) 999-NORD (6673); Fax: (203) 798-2291. <>.

National Institute of Allergy and Infectious Diseases (NIAID). 31 Center Drive, Rm. 7A50 MSC 2520, Bethesda, MD 20892-2520. (301) 496-5717. <>.

Francisco de Paula Careta

Iuri Drumond Louro

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Disease, Tropical

Disease, Tropical. Tropical disease has plagued American forces from the colonial period to modern times. Malaria, dysentery, dengue, and yellow fever (all endemic to the United States), as well as schistosomiasis, yaws, leishmaniasis, filariasis, and scrub typhus (all from other areas), have decimated garrisons and overwhelmed combat troops. To conquer or contain tropical disease, the U.S. military, sometimes cooperating with civilian scientists, developed preventive techniques, therapies, and cures. Collaborative research controlled and even vanquished most tropical diseases except for malaria, whose parasite became immune to traditional antimalarials, and whose prevention and cure remain elusive.

The military historically follows standard civilian practice regarding contagion, diagnosis, and treatment. Before the Civil War, physicians did not suspect mosquitoes as transmitters, blamed fever on the climate or air, and often could not distinguish one fever from another, treating them with emetics, chinchona bark, bleeding, mercury, wine, aromatics, snakeroot, or arsenic compounds. During the Mexican War, physicians at the Veracruz hospital treated yellow fever with quinine sulfate, first extracted from chinchona bark in 1820, to reduce the fever; mustard plasters and baths to help the circulation; and mercurials to evacuate the bowels. About 28 percent of victims died in the spring and summer of 1847. More prevalent was diarrhea or dysentery, which accounted for one‐third of all hospital admissions. Quinine proved highly beneficial in treating malaria. During the Civil War, the Union army had plenty of quinine, but the disease scourged the Confederate army, which occupied infested areas and had limited supplies. Better sanitation in the post–Civil War period helped curtail communicable disease among troops.

The Spanish‐American War (1898) forced the U.S. Army to lead a fight against tropical disease. American forces could not garrison the islands they had won without controlling yellow fever, typhoid, malaria, and dengue. The work of Maj. William C. Gorgas of the Medical Corps in Havana (1899) and (as colonel) in Panama (1904–06) in preventive medicine halted epidemics of typhoid, dysentery, and yellow fever, and made possible construction of the Panama Canal. Maj. Walter Reed and the Army Medical Board in the autumn and winter of 1900–1901 proved scientifically that the mosquito served as intermediate host for the yellow fever parasite. Reed was indebted to Dr. Carlos Finlay of Cuba, Sir Patrick Manson of Britain, and Maj. Ronald Ross of the British army, each of whom had helped prove that the mosquito was the carrier of disease. Their research pioneered the science of tropical medicine. During the early twentieth century, army medical research boards, such as the Philippine Tropical Disease Board, conducted investigations and began control measures that drastically reduced disease around U.S. bases at home and overseas.

By World War II, the development of vaccines, due largely to support from the Rockefeller Foundation, had eliminated yellow fever and typhus. Improvement of field sanitation controlled the dysenteries. Wartime research under the aegis of the National Research Council improved chemotherapy for the prevention and treatment of malaria and secured development of a powerful insecticide: DDT. Those advances, plus the work of army and navy malaria control units, and the enforcement of malaria discipline by personnel (taking atabrine tablets and wearing protective clothing) reduced incidence to historic lows. In the Southwest Pacific, monthly rates fell from 251 per 1,000 in December 1943 to 62 per 1,000 in November 1944: malaria no longer impeded campaigns.

During the Vietnam War, however, despite research to find better antimalarial drugs or a vaccine, chloroquine‐resistent falciparum malaria from Southeast Asia threatened the U.S. armed forces. Drug‐resistant malaria continues to be the most important military medical problem of the tropics.
[See also Caribbean and Latin America, U.S. Military Involvement in the; Casualties.]


E. C. Andrus et al., eds., Advances in Military Medicine Made by American Investigators Working Under the Sponsorsphip of the Committee on Medical Research, 1948.
John Z. Bowers and Elizabeth F. Purcell, eds., Advances in American Medicine: Essays at the Bicentennial, vols. 1, and 2, 1976.
François Delaporte , The History of Yellow Fever. An Essay on the Birth of Tropical Medicine, 1991.
Mary Ellen Condon‐Rall and and Albert E. Cowdrey , The Medical Department: Medical Service in the War Against Japan, 1998.

Mary Ellen Condon‐Rall

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"Disease, Tropical." The Oxford Companion to American Military History. . 15 Dec. 2017 <>.

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Tropical Spastic Paraparesis

Tropical Spastic Paraparesis


Tropical spastic paraparesis (TSP) is an incurable viral infection of the spinal cord that causes weakness in the legs. It is caused by the human T-cell lymphotropic virus-1 (HTLV-1) retrovirus.


As the name implies, tropical spastic paraparesis usually occurs in tropical locales. Although isolated cases have been diagnosed in the southeastern United States and other places in the United States, TSP is most frequently found in:

TSP usually affects adults between the ages of 30 and 40, and is far more common in women than in men.

The disease may remain undetected for years after infection is contracted. When the immune system's response to the virus causes nerve damage, the legs gradually lose strength and flexibility.

Causes and symptoms

TSP is caused by the HTLV-1 virus, which also causes leukemia. The virus can be spread through the placenta, and also through blood transfusions, breast-feeding, contaminated needles, and sexual contact.

Symptoms may begin years after infection. In response to the infection, the body's immune response may injure nerve tissue, causing symptoms that include bladder abnormalities, leg pain, loss of feeling in the feet, tingling sensations, and unpleasant sensations when the skin is touched.

As many as 20% of patients with TSP may also experience:

  • deafness
  • double vision
  • the tendency to incorrectly estimate the amount of motion necessary to accomplish a specific task (dysmetria)
  • exaggerated reflexes
  • facial paralysis
  • tremor.


Infectious disease specialists use blood tests and magnetic resonance imaging (MRI) of the spinal cord to diagnose this condition.


While the disease is incurable, significant improvement has been reported in the condition of TSP patients treated with corticosteroids. These drugs are believed to alleviate symptoms by suppressing the immune system's response to the virus that causes them.

Plasmapheresis, a dialysis-like procedure in which symptom-producing antibodies are removed from the blood, also provides temporary relief.


As noted, TSP cannot be cured.


The United States Food and Drug Administration (FDA) has approved screening procedures developed to detect HTLV-1 in donated blood and blood products designated for transfusion. These procedures, which can also be used to diagnose patients with TSP, are designed to prevent the spread of the disease.



"Current Trends Licensure of Screening Tests for Antibody to Human T-Lymphotropic Virus Type I." Centers for Disease Control. May 27, 1998.


Retrovirus A family of RNA viruses containing a reverse transcriptase enzyme which allows the viruses' genetic information to become part of the genetic information of the host cell upon replication.

Virus A microorganism, smaller than bacteria, which can only replicate within the a cell of a living plant or animal. The virus provides the genetic code and the host cell provides the energy and raw materials for replication.

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tropical diseases

tropical diseases Any of a number of diseases predominantly associated with tropical climates. Major ones are malaria, leishmaniasis, sleeping sickness, filariasis, and schistosomiasis (bilharzia). The infectious agents of tropical diseases include viruses, bacteria, protozoa, fungi, and worms of various kinds. Many of these disease microbes are spread by insect vectors such as mosquitoes.

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