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Milk sickness, also known as tremetol vomiting or, in animals, as trembles, is a kind of poisoning, characterized by trembling, vomiting, and severe intestinal pain, that affects individuals who ingest milk, other dairy products, or meat from a cow that has fed on white snakeroot plant, which contains the poison tremetol.
Although very rare today, milk sickness claimed thousands of lives among migrants to the Midwest in the early 19th century in the United States, especially in frontier areas along the Ohio River Valley and its tributaries where white snakeroot was prevalent. New settlers were unfamiliar with the plant and its properties. A notable victim was Nancy Hanks Lincoln, the mother of Abraham Lincoln, who died in 1818. Nursing calves and lambs may have died from their mothers' milk contaminated with snakeroot, although the adult cows and sheep showed no signs of poisoning. Cattle, horses, and sheep are the animals most often poisoned.
Anna Pierce Hobbs Bixby, called Dr. Anna on the frontier, is credited today by the American medical community with having identified white snakeroot as the cause of the illness. Told about the plant's properties by an elderly Shawnee woman she befriended, Bixby did testing to observe and document evidence. She wrote up her findings to share the discovery in the medical world. The Shawnee woman's name has been lost to history.
Human milk sickness is uncommon today in the United States. Current practices of animal husbandry generally control the pastures and feed of cattle, and the pooling of milk from many producers lowers the risk of tremetol present in dangerous amounts. The poison tremetol is not inactivated by pasteurization. Although extremely rare, milk sickness can occur if a person drinks contaminated milk or eats dairy products gathered from a single cow or from a smaller herd that has fed on the white snakeroot plant. There is no cure, but treatment is available.
The Coggins test (agar immunodiffusion) is a sensitive diagnostic test for equine infectious anemia developed by Dr. Leroy Coggins in the 1970s.
Currently, the US does not have an eradication program due to the low rate of incidence. However, many states require a negative Coggins test for interstate travel. In addition, most horse shows and events require a negative Coggins test. Most countries require a negative test result before allowing an imported horse into the country.
Horse owners should verify that all the horses at a breeding farm and or boarding facility have a negative Coggins test before using the services of the facility. A Coggins test should be done on an annual basis. Tests every 6 months are recommended if there is increased traveling.
Sweating sickness, also known as "English sweating sickness" or "English sweate" (), was a mysterious and highly contagious disease that struck England, and later continental Europe, in a series of epidemics beginning in 1485. The last outbreak occurred in 1551, after which the disease apparently vanished. The onset of symptoms was dramatic and sudden, death often occurring within hours. Although its cause remains unknown, it has been suggested that an unknown species of hantavirus was responsible for the outbreak.
Travelers who are susceptible to motion sickness can minimize symptoms by:
- Choosing a window seat with a view of the ground or of lower clouds, such that motion can be detected. This will not work if the plane is flown in the clouds for a long duration.
- Choosing seats with the smoothest ride in regards to pitch (the seats over the wings in an airplane). (This may not be sufficient for sensitive individuals who need to see ground movement)
- Sitting facing forward while focusing on distant objects rather than trying to read or look at something inside the airplane.
- Eating dry crackers, olives or suck on a lemon, to dry out the mouth, lessening nausea.
- Drinking a carbonated beverage.
The cause is the most mysterious aspect of the disease. Commentators then and now put much blame on the generally poor sanitation, sewage and contaminated water supplies of the time, which might have harboured the source of infection. The first outbreak at the end of the Wars of the Roses means that it may have been brought over from France by the French mercenaries whom Henry VII used to gain the English throne. However, the "Croyland Chronicle" mentions that Thomas Stanley, 1st Earl of Derby used the "sweating sickness" as an excuse not to join with Richard III's army prior to the Battle of Bosworth.
Relapsing fever has been proposed as a possible cause. This disease, which is spread by ticks and lice, occurs most often during the summer months, as did the original sweating sickness. However, relapsing fever is marked by a prominent black scab at the site of the tick bite and a subsequent skin rash.
Noting symptom overlap with hantavirus pulmonary syndrome, several scientists proposed an unknown hantavirus as the cause. A critique of this hypothesis included the argument that, whereas sweating sickness was thought to be transmitted from human to human, hantaviruses are rarely spread in this way. However, infection via human-to-human contact has been proven in hantavirus outbreaks in Argentina.
A method to increase pilot resistance to airsickness consists of repetitive exposure to the flying conditions that initially resulted in airsickness. In other words, repeated exposure to the flight environment decreases an individual’s susceptibility to subsequent airsickness. Recently, several devices have been introduced that are intended to reduce motion sickness through stimulation of various body parts (usually the wrist).
As astronauts frequently have motion sickness, NASA has done extensive research on the causes and treatments for motion sickness. One very promising looking treatment is for the person suffering from motion sickness to wear LCD shutter glasses that create a stroboscopic vision of 4 Hz with a dwell of 10 milliseconds.
Diagnosis is based on history given by patient, including recent medications.
Milk allergy is distinct from lactose intolerance, which is a nonallergic food sensitivity, due to the lack of enzyme lactase in the small intestines to break lactose down into glucose and galactose. Lactose intolerance does not cause damage to the gastrointestinal tract. There are four types: primary, secondary, developmental, and congenital. Primary lactose intolerance is when the amount of lactase declines as people age. Secondary lactose intolerance is due to injury to the small intestine such as from infection, celiac disease, inflammatory bowel disease, or other diseases. Developmental lactose intolerance may occur in premature babies and usually improves over a short period of time. Congenital lactose intolerance is an extremely rare genetic disorder in which little or no lactase is made from birth.
Diagnosis is usually based on a medical history, elimination diet, skin prick test, blood tests for food-specific IgE antibodies, or oral food challenge.
- For skin-prick tests, a tiny board with protruding needles is used. The allergens are placed either on the board or directly on the skin. The board is then placed on the skin, to puncture the skin and for the allergens to enter the body. If a hive appears, the person is considered positive for the allergy. This test only works for IgE antibodies. Allergic reactions caused by other antibodies cannot be detected through skin-prick tests.
Skin-prick testing is easy to do and results are available in minutes. Different allergists may use different devices for testing. Some use a "bifurcated needle", which looks like a fork with two prongs. Others use a "multitest", which may look like a small board with several pins sticking out of it. In these tests, a tiny amount of the suspected allergen is put onto the skin or into a testing device, and the device is placed on the skin to prick, or break through, the top layer of skin. This puts a small amount of the allergen under the skin. A hive will form at any spot where the person is allergic. This test generally yields a positive or negative result. It is good for quickly learning if a person is allergic to a particular food or not, because it detects IgE. Skin tests cannot predict if a reaction would occur or what kind of reaction might occur if a person ingests that particular allergen. They can, however, confirm an allergy in light of a patient's history of reactions to a particular food. Non-IgE-mediated allergies cannot be detected by this method.
- Patch testing is used to determine if a specific substance causes allergic inflammation of the skin. It tests for delayed food reactions.
- Blood testing is another way to test for allergies; however, it poses the same disadvantage and only detects IgE allergens and does not work for every possible allergen. Radioallergosorbent testing (RAST) is used to detect IgE antibodies present to a certain allergen. The score taken from the RAST is compared to predictive values, taken from a specific type of RAST. If the score is higher than the predictive values, a great chance the allergy is present in the person exists. One advantage of this test is that it can test many allergens at one time.
A CAP-RAST has greater specificity than RAST; it can show the amount of IgE present to each allergen. Researchers have been able to determine "predictive values" for certain foods, which can be compared to the RAST results. If a person's RAST score is higher than the predictive value for that food, over a 95% chance exists that patients will have an allergic reaction (limited to rash and anaphylaxis reactions) if they ingest that food. Currently, predictive values are available for milk, egg, peanut, fish, soy, and wheat. Blood tests allow for hundreds of allergens to be screened from a single sample, and cover food allergies as well as inhalants. However, non-IgE-mediated allergies cannot be detected by this method. Other widely promoted tests such as the antigen leukocyte cellular antibody test and the food allergy profile are considered unproven methods, the use of which is not advised.
- Food challenges test for allergens other than those caused by IgE allergens. The allergen is given to the person in the form of a pill, so the person can ingest the allergen directly. The person is watched for signs and symptoms. The problem with food challenges is that they must be performed in the hospital under careful watch, due to the possibility of anaphylaxis.
Food challenges, especially double-blind, placebo-controlled food challenges, are the gold standard for diagnosis of food allergies, including most non-IgE-mediated reactions. Blind food challenges involve packaging the suspected allergen into a capsule, giving it to the patient, and observing the patient for signs or symptoms of an allergic reaction.
The best method for diagnosing food allergy is to be assessed by an allergist. The allergist will review the patient's history and the symptoms or reactions that have been noted after food ingestion. If the allergist feels the symptoms or reactions are consistent with food allergy, he/she will perform allergy tests. Additional diagnostic tools for evaluation of eosinophilic or non-IgE mediated reactions include endoscopy, colonoscopy, and biopsy.
Over-the-counter and prescription medications are readily available, such as dimenhydrinate, scopolamine, meclizine, promethazine, cyclizine, and cinnarizine. Cinnarizine is not available in the United States, as it is not approved by the FDA. As these medications often have side effects, anyone involved in high-risk activities while at sea (such as SCUBA divers) must evaluate the risks versus the benefits. Promethazine is especially known to cause drowsiness, which is often counteracted by ephedrine in a combination known as "the Coast Guard cocktail.". There are special considerations to be aware of when the common anti-motion sickness medications are used in the military setting where performance must be maintained at a high level.
Scopolamine is effective and is sometimes used in the form of transdermal patches (1.5 mg) or as a newer tablet form (0.4 mg). The selection of a transdermal patch or scopolamine tablet is determined by a doctor after consideration of the patient's age, weight, and length of treatment time required.
Many pharmacological treatments which are effective for nausea and vomiting in some medical conditions may not be effective for motion sickness. For example, metoclopramide and prochlorperazine, although widely used for nausea, are ineffective for motion-sickness prevention and treatment. This is due to the physiology of the CNS vomiting centre and its inputs from the chemoreceptor trigger zone versus the inner ear. Sedating anti-histamine medications such as promethazine work quite well for motion sickness, although they can cause significant drowsiness.
Ginger root is commonly thought to be an effective anti-emetic, but it is ineffective in treating motion sickness.
The gold standard for diagnosis is identification of trypanosomes in a patient sample by microscopic examination. Patient samples that can be used for diagnosis include chancre fluid, lymph node aspirates, blood, bone marrow, and, during the neurological stage, cerebrospinal fluid. Detection of trypanosome-specific antibodies can be used for diagnosis, but the sensitivity and specificity of these methods are too variable to be used alone for clinical diagnosis. Further, seroconversion occurs after the onset of clinical symptoms during a "T. b. rhodesiense" infection, so is of limited diagnostic use.
Trypanosomes can be detected from patient samples using two different preparations. A wet preparation can be used to look for the motile trypanosomes. Alternatively, a fixed (dried) smear can be stained using Giemsa's or Field's technique and examined under a microscope. Often, the parasite is in relatively low abundance in the sample, so techniques to concentrate the parasites can be used prior to microscopic examination. For blood samples, these include centrifugation followed by examination of the buffy coat; mini anion-exchange/centrifugation; and the quantitative buffy coat (QBC) technique. For other samples, such as spinal fluid, concentration techniques include centrifugation followed by examination of the sediment.
Three serological tests are also available for detection of the parasite: the micro-CATT, wb-CATT, and wb-LATEX. The first uses dried blood, while the other two use whole blood samples. A 2002 study found the wb-CATT to be the most efficient for diagnosis, while the wb-LATEX is a better exam for situations where greater sensitivity is required.
Increased water intake may also help in acclimatization to replace the fluids lost through heavier breathing in the thin, dry air found at altitude, although consuming excessive quantities ("over-hydration") has no benefits and may cause dangerous hyponatremia.
Diagnosis of milk allergy is based on the person's history of allergic reactions, skin prick test (SPT), patch test and measurement of milk protein specific serum immunoglobulin E (IgE or sIgE). A negative IgE test does not rule out non-IgE mediated allergy, also described as cell-mediated allergy. Confirmation is by double-blind, placebo-controlled food challenges, conducted by an allergy specialist. SPT and sIgE have sensitivity around 88% but specificity of 68% and 48%, respectively, meaning these tests will probably detect a milk sensitivity but will also be positive for other allergens.
Attempts have been made to identify SPT and sIgE responses accurate enough to avoid the need for a confirming oral food challenge. A systematic review stated that for children younger than two years, cut-offs for specific IgE or SPT seem to be more homogeneous and may be proposed. For older children the tests were less consistent. It concluded "None of the cut-offs proposed in the literature can be used to definitely confirm cow's milk allergy diagnosis, either to fresh pasteurized or to baked milk."
Important differential diagnoses are:
- Lactose intolerance generally develops later in life, but can present in young patients in severe cases. It is due to an enzyme deficiency (lactase) and not allergy, and occurs in many non-Western people.
- Celiac disease is an autoimmune disorder triggered by gluten proteins such as gliadin (present in wheat, rye, and barley). It is a non-IgE-mediated food allergy by definition.
- Irritable bowel syndrome
- C1 Esterase inhibitor deficiency (hereditary angioedema), a rare disease, generally causes attacks of angioedema, but can present solely with abdominal pain and occasional diarrhea.
A vaccine is available, called "Chinese Live Attenuated EIA vaccine", developed in China and widely used there since 1983. Another attenuated live virus vaccine is in development in the United States.
Reuse of syringes and needles is a risk factor for transfer of the disease. Currently in the United States, all horses that test positive must be reported to federal authorities by the testing laboratory. EIA-positive horses are infected for life. Options for the horse include sending the horse to a recognized research facility, branding the horse and quarantining it at least 200 yards from other horses for the rest of its life, and euthanizing the horse. Very few quarantine facilities exist, which usually leads to the option of euthanizing the horse. The Florida Research Institute for Equine Nurturing, Development and Safety (a.k.a. F.R.I.E.N.D.S.) is one of the largest such quarantine facilities and is located in south Florida.
The horse industry and the veterinary industry strongly suggest that the risks posed by infected horses, even if they are not showing any clinical signs, are enough of a reason to impose such stringent rules. The precise impacts of the disease on the horse industry are unknown.
Presumptive diagnosis is made by characteristic clinical signs, post mortem lesions, and presence of competent vectors. Laboratory confirmation is by viral isolation, with such techniques as quantitative PCR for detecting viral RNA, antigen capture (ELISA), and immunofluorescence of infected tissues. Serological tests are only useful for detecting recovered animals, as sick animals die before they are able to mount effective immune responses.
In high-altitude conditions, oxygen enrichment can counteract the hypoxia related effects of altitude sickness. A small amount of supplemental oxygen reduces the equivalent altitude in climate-controlled rooms. At (), raising the oxygen concentration level by 5% via an oxygen concentrator and an existing ventilation system provides an effective altitude of (), which is more tolerable for those unaccustomed to high altitudes.
Oxygen from gas bottles or liquid containers can be applied directly via a nasal cannula or mask. Oxygen concentrators based upon pressure swing adsorption (PSA), VSA, or vacuum-pressure swing adsorption (VPSA) can be used to generate the oxygen if electricity is available. Stationary oxygen concentrators typically use PSA technology, which has performance degradations at the lower barometric pressures at high altitudes. One way to compensate for the performance degradation is to utilize a concentrator with more flow capacity. There are also portable oxygen concentrators that can be used on vehicular DC power or on internal batteries, and at least one system commercially available measures and compensates for the altitude effect on its performance up to . The application of high-purity oxygen from one of these methods increases the partial pressure of oxygen by raising the FiO (fraction of inspired oxygen).
With discontinuation of offending agent, symptoms usually disappear within 4–5 days.
Corticosteroids, antihistamines, and analgesics are the main line of treatment. The choice depends on the severity of the reaction.
Use of plasmapheresis has also been described.
Decompression sickness should be suspected if any of the symptoms associated with the condition occurs following a drop in pressure, in particular, within 24 hours of diving. In 1995, 95% of all cases reported to Divers Alert Network had shown symptoms within 24 hours. An alternative diagnosis should be suspected if severe symptoms begin more than six hours following decompression without an altitude exposure or if any symptom occurs more than 24 hours after surfacing. The diagnosis is confirmed if the symptoms are relieved by recompression. Although MRI or CT can frequently identify bubbles in DCS, they are not as good at determining the diagnosis as a proper history of the event and description of the symptoms.
Immediate treatment with 100% oxygen, followed by recompression in a hyperbaric chamber, will in most cases result in no long-term effects. However, permanent long-term injury from DCS is possible. Three-month follow-ups on diving accidents reported to DAN in 1987 showed 14.3% of the 268 divers surveyed had ongoing symptoms of Type II DCS, and 7% from Type I DCS. Long-term follow-ups showed similar results, with 16% having permanent neurological sequelae.
There is a lack of good evidence to support the use of any particular intervention for morning sickness.
In a hydrogen breath test, the most accurate lactose intolerance test, after an overnight fast, 25 grams of lactose (in a solution with water) are swallowed. If the lactose cannot be digested, enteric bacteria metabolize it and produce hydrogen, which, along with methane, if produced, can be detected on the patient's breath by a clinical gas chromatograph or compact solid-state detector. The test takes about 2.5 hours to complete. If the hydrogen levels in the patient's breath are high, they may have lactose intolerance. This test is not usually done on babies and very young children, because it can cause severe diarrhea.
Currently there are few medically related prevention options for African Trypanosomiasis (i.e. no vaccine exists for immunity). Although the risk of infection from a tsetse fly bite is minor (estimated at less than 0.1%), the use of insect repellants, wearing long-sleeved clothing, avoiding tsetse-dense areas, implementing bush clearance methods and wild game culling are the best options to avoid infection available for local residents of affected areas.
At the 25th ISCTRC (International Scientific Council for Trypanosomiasis Research and Control) in Mombasa, Kenya, in October 1999, the idea of an African-wide initiative to control tsetse and trypanosomiasis populations was discussed. During the 36th summit of the Organization for African Unity in Lome, Togo, in July 2000, a resolution was passed to form the Pan African Tsetse and Trypanosomiasis Eradication Campaign (PATTEC). The campaign works to eradicate the tsetse vector population levels and subsequently the protozoan disease, by use of insecticide-impregnated targets, fly traps, insecticide-treated cattle, ultra-low dose aerial/ground spraying (SAT) of tsetse resting sites and the sterile insect technique (SIT). The use of SIT in Zanzibar proved effective in eliminating the entire population of tsetse flies but was expensive and is relatively impractical to use in many of the endemic countries afflicted with African trypanosomiasis.
Regular active surveillance, involving detection and prompt treatment of new infections, and tsetse fly control is the backbone of the strategy used to control sleeping sickness. Systematic screening of at-risk communities is the best approach, because case-by-case screening is not practical in endemic regions. Systematic screening may be in the form of mobile clinics or fixed screening centres where teams travel daily to areas of high infection rates. Such screening efforts are important because early symptoms are not evident or serious enough to warrant patients with gambiense disease to seek medical attention, particularly in very remote areas. Also, diagnosis of the disease is difficult and health workers may not associate such general symptoms with trypanosomiasis. Systematic screening allows early-stage disease to be detected and treated before the disease progresses, and removes the potential human reservoir. A single case of sexual transmission of West African sleeping sickness has been reported.