Typhus is any of several similar diseases caused by Rickettsiae.[1] The name comes from the Greek typhos, meaning smoky or hazy, describing the state of mind of those affected with typhus. The causative organism Rickettsia is an obligate parasite and cannot survive for long outside living cells. Typhus should not be confused with typhoid fever which is a completely different disease.

Multiple diseases include the word “typhus” in their description. Types include:

Without treatment the disease can be fatal, particularly the epidemic form. Prompt treatment with antibiotics cures nearly every patient.[3]

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Typhoid fever, also known as enteric fever, or commonly just typhoid,[1] is an illness caused by the bacterium Salmonella enterica serovar Typhi. Common worldwide, it is transmitted by the ingestion of food or water contaminated with feces from an infected person.[2] The bacteria then perforate through the intestinal wall and are phagocytosed by macrophages. Salmonella Typhi then alters its structure to resist destruction and allow them to exist within the macrophage. This renders them resistant to damage by PMN’s, complement and the immune response. The organism is then spread via the lymphatics while inside the macrophages. This gives them access to the reticuloendothelial system and then to the different organs throughout the body. The organism is a Gram-negative short bacillus that is motile due to its peritrichous flagella. The bacteria grows best at 37 °C/99 °F – human body temperature.

Typhoid fever is characterized by a sustained fever as high as 40 °C (104 °F), profuse sweating, gastroenteritis, and nonbloody diarrhea. Less commonly a rash of flat, rose-colored spots may appear.[3]

Classically, the course of untreated typhoid fever is divided into four individual stages, each lasting approximately one week. In the first week, there is a slowly rising temperature with relative bradycardia, malaise, headache and cough. A bloody nose (epistaxis) is seen in a quarter of cases and abdominal pain is also possible. There is leukopenia, a decrease in the number of circulating white blood cells, with eosinopenia and relative lymphocytosis, a positive diazo reaction and blood cultures are positive for Salmonella Typhi or Paratyphi. The classic Widal test is negative in the first week.

In the second week of the infection, the patient lies prostrated with high fever in plateau around 40 °C (104 °F) and bradycardia (Sphygmo-thermic dissociation), classically with a dicrotic pulse wave. Delirium is frequent, frequently calm, but sometimes agitated. This delirium gives to typhoid the nickname of “nervous fever”. Rose spots appear on the lower chest and abdomen in around 1/3 patients. There are rhonchi in lung bases. The abdomen is distended and painful in the right lower quadrant where borborygmi can be heard. Diarrhea can occur in this stage: six to eight stools in a day, green with a characteristic smell, comparable to pea-soup. However, constipation is also frequent. The spleen and liver are enlarged (hepatosplenomegaly) and tender and there is elevation of liver transaminases. The Widal reaction is strongly positive with antiO and antiH antibodies. Blood cultures are sometimes still positive at this stage.

In the third week of typhoid fever a number of complications can occur:

The fever is still very high and oscillates very little over 24 hours. Dehydration ensues and the patient is delirious (typhoid state). By the end of third week the fever has started reducing (defervescence). This carries on into the fourth and final week.

Diagnosis is made by blood, bone marrow or stool cultures and with the Widal test (demonstration of salmonella antibodies against antigens O-somatic and H-flagellar). In epidemics and less wealthy countries, after excluding malaria, dysentery or pneumonia, a therapeutic trial time with chloramphenicol is generally undertaken while awaiting the results of Widal test and blood cultures.[4]

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Turner syndrome or Ullrich-Turner syndrome (also known as “Gonadal dysgenesis”[1]:550 ) encompasses several conditions, of which monosomy X is most common. It is a chromosomal disorder affecting females in which all or part of one of the X chromosomes is absent. Occurring in 1 out of every 2500 girls, the syndrome manifests itself in a number of ways. There are characteristic physical abnormalities, such as short stature, lymphoedema, broad chest, low hairline, low-set ears, and webbed neck. Girls with TS typically experience gonadal dysfunction with subsequent amenorrhea and infertility. Concurrent health concerns are also frequently present, including congenital heart disease, hypothyroidism, ophthalmological problems, and otological concerns. [2] Finally, a specific pattern of cognitive deficits is often observed, with particular difficulties in visuospatial, mathematic, and memory areas.[3]

Common symptoms of Turner syndrome include:

Other symptoms may include a small lower jaw (micrognathia), cubitus valgus (turned-out elbows), soft upturned nails, palmar crease and drooping eyelids. Less common are pigmented moles, hearing loss, and a high-arch palate (narrow maxilla). Turner syndrome manifests itself differently in each female affected by the condition, and no two individuals will share the same symptoms.

Risk factors for Turner syndrome are not well known. Nondisjunctions increase with maternal age, such as for Down syndrome, but that effect is not clear for Turner syndrome. It is also unknown if there is a genetic predisposition present that causes the abnormality, though most researchers and doctors treating Turners women agree that this is highly unlikely. There is currently no known cause for Turner syndrome, though there are several theories surrounding the subject.

Approximately 98% of all fetuses with Turner syndrome result in miscarriage. Turner syndrome accounts for about 10% of the total number of spontaneous abortions in the United States. The incidence of Turner syndrome in live female births is believed to be 1 in 2500.

The syndrome is named after Henry Turner, an Oklahoma endocrinologist, who described it in 1938.[4] In Europe, it is often called Ullrich-Turner syndrome or even Bonnevie-Ullrich-Turner syndrome to acknowledge that earlier cases had also been described by European doctors. The first published report of a female with a 45,X karyotype was in 1959 by Dr. Charles Ford and colleagues in Harwell, Oxfordshire and Guy’s Hospital in London.[5] It was found in a 14-year-old girl with signs of Turner syndrome.

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Tungiasis is a skin infestation of the Tunga penetrans flea (also known as chigoe flea, jigger, nigua or sand flea), found in the tropical parts of Africa, Caribbean, Central and South America, and India. This disease is endemic in Nigeria and Trinidad and Tobago where in the 1980s the prevalence of tungiasis among children approached 40%. It is rarely found outside these areas.

The first reported case of tungiasis was noted in the 1500s by Gonzalez Fernandez De Oviedo y Valdes, when sailors from the Santa Maria who sailed with Christopher Columbus were shipwrecked on Haiti and became infected. Tungiasis also infected many of the soldiers of the Spanish conquistadores, who also reported that an entire village in Colombia was abandoned because of this disease. The first clinical account of tungiasis was provided by the Portuguese doctor Aleixo de Abreu.

The symptoms of this disease include:

Left untreated, secondary infections such as bacteremia, tetanus, and gangrene can occur.

Because of their limited jumping ability, the most common sites of infection are the soles of the feet, the toe web and toenails. Preventing infection by chigoe flea is easily achieved by wearing shoes when traveling in endemic regions and spraying insecticides on infested soil. Walking barefoot, especially in children, remains the most common reason why tungiasis remains prevalent in poor, rural populations.

Treatment for tungiasis include physical removal of the flea by use of forceps or needles, application of topical anti-parasitic medicine, and surgery to completely remove the nodules. If the flea is discovered in the early stages it can be easily removed, though it is slightly harder without breaking the egg sack. It appears similar to a pustule on the thick skin of the feet or hands.

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Tuberous sclerosis or tuberous sclerosis complex (TSC) is a rare, multi-system genetic disease that causes benign tumours to grow in the brain and on other vital organs such as the kidneys, heart, eyes, lungs, and skin. A combination of symptoms may include seizures, developmental delay, behavioural problems, skin abnormalities, lung and kidney disease. TSC is caused by mutations on either of two genes, TSC1 and TSC2, which encode for the proteins hamartin and tuberin respectively. These proteins act as tumour growth suppressors, agents that regulate cell proliferation and differentiation.[1]

The name, composed of the Latin tuber (swelling) and the Greek skleros (hard), refers to the pathological finding of thick, firm and pale gyri, called “tubers”, in the brains of patients postmortem. These tubers were first described by Désiré-Magloire Bourneville in 1880; the cortical manifestations may sometimes still be known by the eponym Bourneville’s disease.

The physical manifestations of tuberous sclerosis are due to the formation of hamartia (malformed tissue such as the cortical tubers), hamartomas (benign growths such as facial angiofibroma and subependymal nodules) and, very rarely, cancerous hamartoblastomas. The effect of these on the brain leads to neurological symptoms such as seizures, developmental delay and behavioral problems.

About 50% of people with TSC have learning difficulties ranging from mild to profound,[2] and studies have reported that between 25% and 61% of affected individuals meet the diagnostic criteria for autism, with an even higher proportion showing features of a broader pervasive developmental disorder.[3] A 2008 study reported self-injurious behavior in 10% of people with TSC.[4] Other conditions, such as ADHD, aggression, behavioral outbursts and OCD can also occur. Lower IQ is associated with more brain involvement on MRI.

Three type of brain tumours may be associated with TSC: i. Giant cell astrocytoma: (grows and blocks the CSF flow leading to dilatation of ventricles causing headache and vomiting. ii. Cortical tubers: after which the disease is named. iii. Sub-ependymal nodules: form in the walls of ventricles.

Classic intracranial manifestations of tuberous sclerosis include subependymal nodules and cortical/subcortical tubers.[5]

The tubers are typically triangular in configuration, with the apex pointed towards the ventricles, and are thought to represent foci of abnormal neuronal migration. The T2 signal abnormalities may subside in adulthood, but will still be visible on histopathological analysis. On magnetic resonance imaging, TSC patients can exhibit other signs consistent with abnormal neuron migration (radial white matter tracts hyperintense on T2WI, heterotopic gray matter).

Subependymal nodules are composed of abnormal, swollen glial cells and bizarre multinucleated cells which are indeterminate for glial or neuronal origin. There is no interposed neural tissue. These nodules have a tendency to calcify as the patient ages. A nodule that markedly enhances and enlarges over time should be considered suspicious for transformation into a subependymal giant cell astrocytoma (SEGA). A SEGA typically develops in the region of the foramen of Monro, in which case it is at risk of developing an obstructive hydrocephalus.

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Tuberculosis (abbreviated as TB for tubercle bacillus or Tuberculosis) is a common and often deadly infectious disease caused by mycobacteria, mainly Mycobacterium tuberculosis [1]. Tuberculosis usually attacks the lungs (as pulmonary TB) but can also affect the central nervous system, the lymphatic system, the circulatory system, the genitourinary system, the gastrointestinal system, bones, joints, and even the skin. Other mycobacteria such as Mycobacterium bovis, Mycobacterium africanum, Mycobacterium canetti, and Mycobacterium microti also cause tuberculosis, but these species are less common.

The classic symptoms of tuberculosis are a chronic cough with blood-tinged sputum, fever, night sweats, and weight loss. Infection of other organs causes a wide range of symptoms. The diagnosis relies on radiology (commonly chest X-rays), a tuberculin skin test, blood tests, as well as microscopic examination and microbiological culture of bodily fluids. Tuberculosis treatment is difficult and requires long courses of multiple antibiotics. Contacts are also screened and treated if necessary. Antibiotic resistance is a growing problem in (extensively) multi-drug-resistant tuberculosis. Prevention relies on screening programs and vaccination, usually with Bacillus Calmette-Guérin (BCG vaccine).

Tuberculosis is spread through the air, when people who have the disease cough, sneeze, or spit. One third of the world’s current population has been infected with M. tuberculosis, and new infections occur at a rate of one per second.[2] However, most of these cases will not develop the full-blown disease; asymptomatic, latent infection is most common. About one in ten of these latent infections will eventually progress to active disease, which, if left untreated, kills more than half of its victims. In 2004, mortality and morbidity statistics included 14.6 million chronic active cases, 8.9 million new cases, and 1.6 million deaths, mostly in developing countries.[2] In addition, a rising number of people in the developed world are contracting tuberculosis because their immune systems are compromised by immunosuppressive drugs, substance abuse, or AIDS. The distribution of tuberculosis is not uniform across the globe with about 80% of the population in many Asian and African countries testing positive in tuberculin tests, while only 5-10% of the US population test positive.[1] It is estimated that the US has 25,000 new cases of tuberculosis each year, 40% of which occur in immigrants from countries where tuberculosis is endemic.[1]

In the past, tuberculosis has been called consumption, because it seemed to consume people from within, with a bloody cough, fever, pallor, and long relentless wasting. Other names included phthisis (Greek for consumption) and phthisis pulmonalis; scrofula (in adults), affecting the lymphatic system and resulting in swollen neck glands; tabes mesenterica, TB of the abdomen and lupus vulgaris, TB of the skin; wasting disease; white plague, because sufferers appear markedly pale; king’s evil, because it was believed that a king’s touch would heal scrofula; and Pott’s disease, or gibbus of the spine and joints.[3][4] Miliary tuberculosis—now commonly known as disseminated TB—occurs when the infection invades the circulatory system resulting in lesions which have the appearance of millet seeds on X-ray.[3][5] TB is also called Koch’s disease after the scientist Robert Koch.[6]

When the disease becomes active, 75% of the cases are pulmonary TB. Symptoms include chest pain, coughing up blood, and a productive, prolonged cough for more than three weeks. Systemic symptoms include fever, chills, night sweats, appetite loss, weight loss, pallor, and often a tendency to fatigue very easily.[2]

In the other 25% of active cases, the infection moves from the lungs, causing other kinds of TB, collectively denoted extrapulmonary tuberculosis[7]. This occurs more commonly in immunosuppressed persons and young children. Extrapulmonary infection sites include the pleura in tuberculosis pleurisy, the central nervous system in meningitis, the lymphatic system in scrofula of the neck, the genitourinary system in urogenital tuberculosis, and bones and joints in Pott’s disease of the spine. An especially serious form is disseminated TB, more commonly known as miliary tuberculosis. Although extrapulmonary TB is not contagious, it may co-exist with pulmonary TB, which is contagious.[8]

The primary cause of TB, Mycobacterium tuberculosis, is an aerobic bacterium that divides every 16 to 20 hours, an extremely slow rate compared with other bacteria, which usually divide in less than an hour.[9] (For example, one of the fastest-growing bacteria is a strain of E. coli that can divide roughly every 20 minutes.) Since MTB has a cell wall but lacks a phospholipid outer membrane, it is classified as a Gram-positive bacterium. However, if a Gram stain is performed, MTB either stains very weakly Gram-positive or does not retain dye due to the high lipid & mycolic acid content of its cell wall.[10] MTB is a small rod-like bacillus that can withstand weak disinfectants and survive in a dry state for weeks. In nature, the bacterium can grow only within the cells of a host organism, but M. tuberculosis can be cultured in vitro.[11]

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A trisomy is a form of aneuploidy with the presence of three copies, instead of the normal two, of a particular chromosome.[1] The presence of an extra chromosome 21, which is found in Down syndrome, is called trisomy 21.

Full trisomy of an individual occurs due to non-disjunction when the cells are dividing (meiosis I or II) to form egg and sperm cells (gametogenesis). This can result in an extra or missing chromosome (either 24 or 22 chromosomes instead of the typical 23) in a sperm or egg cell. After fertilization, the resulting fetus has 47 chromosomes instead of the typical 46.

A partial trisomy occurs when part of an extra chromosome is attached to one of the other chromosomes, or if one of the chromosomes has two copies of part of its chromosome. A mosaic trisomy is a condition where extra chromosomal material exists in only some of the organism’s cells.

Trisomies can occur with any chromosome, but often result in miscarriage. For example, Trisomy 16 is the most common trisomy in humans, occurring in more than 1% of pregnancies. This condition, however, usually results in spontaneous miscarriage in the first trimester. The most common types of trisomy that survive to birth in humans are:

The most common forms of autosomal trisomy are trisomy of chromosome 21 which results in Down syndrome and trisomy of chromosome 18 which results in Edwards syndrome. In rare cases, a fetus with trisomy of chromosome 13 can survive, giving rise to Patau syndrome. Autosomal trisomy can be associated with birth defects, mental retardation and shortened life expectancy.

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Trimethylaminuria (TMAU), also known as fish odor syndrome or fish malodor syndrome[1], is a rare metabolic disorder that causes a defect in the normal production of the enzyme Flavin containing monooxygenase 3 (FMO3).[2][3] When FMO3 is not working correctly or if not enough enzyme is produced, the body loses the ability to properly breakdown trimethylamine (TMA) from precursor compounds in food into trimethylamine oxide (TMAO) through a process called N-oxygenation. Trimethylamine then builds up and is released in the person’s sweat, urine, and breath, giving off a strong fishy odor.

The first clinical case of TMAU was described in 1970 in the medical journal The Lancet,[4] but literary references go back more than a thousand years. Shakespeare’s Tempest describes the outcast Caliban, “He smells like a fish; a very ancient and fish-like smell…”. Hindu folklore mentions in the epic Mahabharata (compiled around 400 AD) a maiden who “grew to be comely and fair, but a fishy odor ever clung to her.”

Trimethylamine builds up in the body of patients with trimethylaminuria. The trimethylamine gets released in the person’s sweat, urine, reproductive fluids, and breath, giving off a strong fishy odor. Some people with trimethylaminuria have a strong odor all the time, but most have a moderate smell that varies in intensity over time. Individuals with this condition do not have any physical symptoms, and typically appear healthy.[5]

The condition seems to be more common in women than men, but scientists don’t know why. Scientists suspect that female sex hormones, such as progesterone and/or estrogen, aggravate symptoms. There are several reports that the condition worsens around puberty. In women, symptoms can worsen just before and during menstrual periods, after taking oral contraceptives, and around menopause.[5]

This odor varies depending on many known factors, including diet, hormonal changes, other odors in the space, and individual sense of smell.

TMAU is a life-disruptive disorder caused by both genetic and environmental factors. Living with TMAU is challenging, and it can adversely affect the livelihood of adults who have it and their families. Children with the condition could face rejection or a lack of understanding from peers during school or at play. There are various online support groups that have been created to help those in with malodor issues such as TMAU. The Yahoo TMAU support group [1] is listed in the National Institute of Healths publication “Learning About Trimethylaminuria” [2].

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Trigeminal neuralgia (TN) or tic doloureux (also known as prosopalgia) is a neuropathic disorder of the trigeminal nerve that causes episodes of intense pain in the eyes, lips, nose, scalp, forehead, and jaw.[1] It is estimated that 1 in 15,000 people suffer from trigeminal neuralgia, although those numbers may be significantly higher due to frequent misdiagnosis. TN usually develops after the age of 50, more commonly in females,for reasons we can not explain, although there have been cases with patients being as young as three years of age [2].

The condition can bring about stabbing, mind-numbing, electric shock-like pain from just a finger’s glance of the cheek.

The most common forms of TN affect 1 in 15,000 to 20,000, but 1 in 5,000 are thought to suffer from some type of facial pain.

The pain of trigeminal neuralgia is often falsely attributed to a pathology of dental origin. “Rarely do patients come to the surgeon without having many removed, and not infrequently all, teeth on the affected side or both sides.” [3] Extractions do not help. The pain is originating in the mongorians and not in an individual nerve of a tooth. Because of this difficulty, many patients may go untreated for long periods of time before a correct diagnosis is made. The trigeminal nerve is the fifth cranial nerve, a mixed cranial nerve responsible for sensory data such as tactition (pressure), thermoception (temperature), and nociception (pain) originating from the face above the jawline; it is also responsible for the motor function of the muscles of mastication, the muscles involved in chewing but not facial expression. Several theories exist to explain the possible causes of this pain syndrome. Leading research indicates that it is a blood vessel compressing the trigeminal nerve near its connection with the pons. The superior cerebellar artery. Such a compression can injure the nerve’s protective myelin sheath and cause erratic and hyperactive functioning of the nerve. This can lead to pain attacks at the slightest stimulation of any area served by the nerve as well as hinder the nerve’s ability to shut off the pain signals after the stimulation ends. This type of injury may rarely be caused by an aneurysm (an outpouching of a blood vessel); by a tumor; by an arachnoid cyst in the cerebellopontine angle[4]; or by a traumatic event such as a car accident or even a tongue piercing. [1] Two to four percent of patients with TN, usually younger, have evidence of multiple sclerosis, which may damage either the trigeminal nerve or other related parts of the brain. When there is no structural cause, the syndrome is called idiopathic. Postherpetic Neuralgia, which occurs after shingles, may cause similar symptoms if the trigeminal nerve is affected.

People with the condition “are begging to be killed,” said Kim Burchiel, M.D., professor and chairman of neurological surgery at the Oregon Health & Science University School of Medicine who sees several new TN cases a week. “I’m telling you, it’s total agony.” The episodes of pain may occur paroxysmally. To describe the pain sensation, patients may describe a trigger area on the face, so sensitive that touching or even air currents can trigger an episode of pain. It affects lifestyle as it can be triggered by common activities in a patient’s daily life, such as eating, talking, shaving and toothbrushing. The attacks are said to feel like stabbing electric shocks, burning, pressing, crushing or shooting pain that becomes intractable. Individual attacks affect one side of the face at a time, last several seconds, hours or longer, and repeat up to hundreds of times throughout the day. The pain also tends to occur in cycles with complete remissions lasting months or even years. 10-12% of cases are bilateral, or occurring on both sides. This normally indicates problems with both trigeminal nerves since one serves strictly the left side of the face and the other serves the right side. Pain attacks typically worsen in frequency or severity over time. A great deal of patients develop the pain in one branch, then over years the pain will travel through the other nerve branches.

Signs of this can be seen in males who may deliberately miss an area of their face when shaving, in order to avoid triggering an episode. Successive recurrences may be incapacitating, and the fear of provoking an attack may make sufferers reluctant to engage in normal activities.

There is a variant of trigeminal neuralgia called atypical trigeminal neuralgia. In some cases of atypical trigeminal neuralgia, the sufferer experiences a severe, relentless underlying pain similar to a migraine in addition to the stabbing pains. This variant is sometimes called “trigeminal neuralgia, type 2″[5], based on a recent classification of facial pain[6]. In other cases, the pain is stabbing and intense, but may feel like burning or prickling, rather than a shock. Sometimes, the pain is a combination of shock-like sensations, migraine-like pain, and burning or prickling pain. It can also feel as if a boring piercing pain is unrelenting. Some recent studies suggest that ATN may be an early development of Trigeminal Neuralgia.

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Tricuspid atresia is a form of congenital heart disease whereby there is a complete absence of the tricuspid valve. Therefore, there is an absence of right atrioventricular connection. This leads to a hypoplastic or an absence of the right ventricle. This defect is contracted during prenatal development, when the heart does not finish developing. It causes the heart to be unable to properly oxygenate the rest of the blood in the body. Because of this, the body does not have enough oxygen to live, and steps must be taken to keep the child alive. Because of the lack of an A-V connection, an atrial septal defect (ASD) must be present to maintain blood flow. Also, since there is a lack of a right ventricle there must be a way to pump blood into the pulmonary arteries, and this is accomplished by a ventricular septal defect (VSD).

Blood is mixed in the left atrium. Because the only way the pulmonary circulation receives blood is through the VSD, a patent ductus arteriosus is usually also formed to increase pulmonary flow.

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