Trachoma

Trachoma (Ancient Greek: "rough eye") is an infectious eye disease, and the leadingcause of the world's infectious blindness.

Trachoma is caused by the bacterium Chlamydia trachomatis and it is spread by direct contact with eye, nose, and throat secretions from affected individuals, or contact with fomites (inanimate objects), such as towels and/or washcloths, that have had similar contact with these secretions. Untreated, repeated trachoma infections result in a painful form of permanent blindness when the eyelids turn inward, causing the eyelashes to scratch the cornea. Children are the most susceptible to infection, but the blinding effects are often not felt until adulthood.
Blinding endemic trachoma occurs in areas with poor personal and family hygiene. Many factors are indirectly linked to the presence of trachoma including lack of water, absence of latrines or toilets, poverty in general, flies, close proximity to cattle, crowding and so forth.

Prevention
Although trachoma was eliminated from much of the developed world in the last century, this disease persists in many parts of the developing world particularly in communities without adequate access to water and sanitation. In many of these communities, women are three times more likely than men to be blinded by the disease.
Without intervention, trachoma keeps families shackled within a cycle of poverty, as the disease and its long-term effects are passed from one generation to the next.
National governments in collaboration with numerous non-profit organizations implement trachoma control programs using the WHO-recommended SAFE strategy, which includes:
Surgery to correct advanced stages of the disease;
Antibiotics to treat active infection, using Zithromax donated by Pfizer Inc through the International Trachoma Initiative;
Facial cleanliness to reduce disease transmission;
Environmental change to increase access to clean water and improved sanitation.
Surgery: For individuals with trichiasis, a bilamellar tarsal rotation procedure is warranted to direct the lashes away from the globe.Early intervention is beneficial as the rate of recurrence is higher in more advanced disease.

Antibiotic therapy: WHO Guidelines recommend that a region should receive community-based, mass antibiotic treatment when the prevalence of active trachoma among one to nine year-old children is greater than 10 percent. Subsequent annual treatment should be administered for three years, at which time the prevalence should be reassessed. Annual treatment should continue until the prevalence drops below five percent. At lower prevalences, antibiotic treatment should be family-based. Antibiotic selection: WHO recommends azithromycin (single oral dose of 20mg/kg) or topical tetracycline (one percent eye ointment twice a day for six weeks). Azithrtomycin is preferred because it is used as a single oral dose. InitiativeAzithromycin can be used in children from the age of six months and in pregnancy.
Facial cleanliness: Children with grossly visible nasal discharge, ocular discharge, or flies on their faces are at least twice as likely to have active trachoma as children with clean faces Intensive community-based health education programs to promote face-washing can significantly reduce the prevalence of active trachoma, especially intense trachoma (TI).

Environmental improvement: Modifications in water use, fly control, latrine use, health education and proximity to domesticated animals have all been proposed to reduce transmission of C. trachomatis. These changes pose numerous challenges for implementation. It seems likely that these environmental changes ultimately impact on the transmission of ocular infection by means of lack of facial cleanliness. Particular attention is required for environmental factors that limit clean faces.

Symptoms
The bacteria has an incubation period of 5 to 12 days, after which the affected individual experiences symptoms of conjunctivitis, or irritation similar to "pink eye." Blinding endemic trachoma results from multiple episodes of reinfection that maintains the intense inflammation in the conjunctiva. Without reinfection, the inflammation will gradually subside.
The World Health Organization recommends a simplified grading system for trachoma.

The Simplified WHO Grading System is summarized below:
• Trachomatous inflammation, follicular (TF) – Five or more follicles of >0.5mm on the upper tarsal conjunctiva
• Trachomatous inflammation, intense (TI) – Papillary hypertrophy and inflammatory thickening of the upper tarsal conjunctiva obscuring more than half the deep tarsal vessels
• Trachomatous trichiasis (TT) – At least one ingrown eyelash touching the globe, or evidence of epilation (eyelash removal)
• Corneal opacity (CO) – Corneal opacity blurring part of the pupil margin
Further symptoms include:
Eye discharge
Swollen eyelids
Trichiasis (turned-in eyelashes)
Swelling of lymph nodes in front of the ears
Corneal scarring
Further ear, nose and throat complications.

Prognosis
If not treated properly with oral antibiotics, the symptoms may escalate and cause blindness, which is the result of ulceration and consequent scarring of the cornea. Surgery may also be necessary to fix eyelid deformities.

Vertigo (medical)

Vertigo, a specific type of dizziness, is a major symptom of a balance disorder. It is the sensation of spinning or swaying while the body is stationary with respect to the earth or surroundings. There are two types of vertigo: subjective and objective. Subjective vertigo is when a person feels a false sensation of movement. Objective vertigo is when the surroundings will appear to move past a person's field of vision.

Causes
Vertigo is usually associated with a problem in the inner ear balance mechanisms (vestibular system), in the brain, or with the nerve connections between these two organs.
The most common cause of vertigo is benign paroxysmal positional vertigo, or BPPV. Vertigo can be a symptom of an inner ear infection. Vertigo can be a symptom of an underlying harmless cause, such as in BPPV or it can suggest more serious problems. These include drug toxicities (specifically gentamicin), strokes or tumors (though these are much less common than BPPV), syphilis

Vertigo can also be brought on suddenly through various actions or incidents, such as skull fractures or brain trauma, sudden changes of blood pressure, or as a symptom of motion sickness while sailing, riding amusement rides, airplanes or in a motor vehicle. Vertigo can also be caused by Carbon Monoxide poisoning. It is also one of the more common symptoms of superior canal dehiscence syndrome and Meniere's disease.Vertigo-like symptoms may also appear as paraneoplastic syndrome (PNS) in the form of opsoclonus myoclonus syndrome, a multi-faceted neurological disorder associated with many forms of incipient cancer lesions or virus.
Vertigo in context with the cervical spine

According to chiropractors, ligamental injuries of the upper cervical spine can result in head-neck-joint instabilities which can cause vertigo.[citation needed] In this view, instabilities of the head neck joint are affected by rupture or overstretching of the alar ligaments and/or capsule structures mostly caused by whiplash or similar biomechanical movements.
Symptoms during damaged alar ligaments besides vertigo often are dizziness; reduced vigilance, such as somnolence; seeing problems, such as seeing "stars", tunnel views or double contures. Some patients tell about unreal feelings that stands in correlation with depersonalization and attentual alterations

Medical doctors (MDs) do not endorse this explanation to vertigo due to a lack of any data to support it, from an anatomical or physiological standpoint. Often the patients who have an odyssey of medical consultations without any clear diagnosis and are sent to a psychiatrist because doctors think about depression or hypochondria. Standard imaging technologies such as CT Scan or MRI are not capable of finding instabilities without taking functional poses
Neurochemistry of vertigo

The neurochemistry of vertigo includes 6 primary neurotransmitters that have been identified between the 3-neuron arc that drives the vestibulo-ocular reflex (VOR). Many others play more minor roles. Three neurotransmitters that work peripherally and centrally include glutamate, acetylcholine, and GABA. Glutamate maintains the resting discharge of the central vestibular neurons, and may modulate synaptic transmission in all 3 neurons of the VOR arc. Acetylcholine appears to function as an excitatory neurotransmitter in both the peripheral and central synapses. GABA is thought to be inhibitory for the commissures of the medial vestibular nucleus, the connections between the cerebellar Purkinje cells and the lateral vestibular nucleus, and the vertical VOR.

Three other neurotransmitters work centrally. Dopamine may accelerate vestibular compensation. Norepinephrine modulates the intensity of central reactions to vestibular stimulation and facilitates compensation. Histamine is present only centrally, but its role is unclear. It is known that centrally acting antihistamines modulate the symptoms of motion sickness.The neurochemistry of emesis overlaps with the neurochemistry of motion sickness and vertigo. Acetylcholinc, histamine, and dopamine are excitatory neurotransmitters, working centrally on the control of emesis. GABA inhibits central emesis reflexes. Serotonin is involved in central and peripheral control of emesis but has little influence on vertigo and motion sickness.

Diagnostic
Tests of vestibular system (balance) function include electronystagmography (ENG), rotation tests, Caloric reflex test, and Computerized Dynamic Posturography (CDP).
Tests of auditory system (hearing) function include pure-tone audiometry, speech audiometry, acoustic-reflex, electrocochleography (ECoG), otoacoustic emissions (OAE), and auditory brainstem response test (ABR; also known as BER, BSER, or BAER). Other diagnostic tests include magnetic resonance imaging (MRI) and computerized axial tomography (CAT, or CT).

Treatment
Treatment is specific for underlying disorder of vertigo.Vestibular rehabilitation; anticholinergics; antihistamines; benzodiazepines; calcium channel antagonists, specifically Verapamil and Nimodipine; GABA modulators, specifically gabapentin and baclofen; Neurotransmitter reuptake inhibitors such as SSRI's, SNRI's and Tricyclics

Toxoplasmosis

Toxoplasmosis is very daunted disease by pregnant mother because can cause the miscarriage and handicapped at they child. this disease represent the contagious disease from animal or zoonosis Toxoplasmosis is a parasitic disease caused by the protozoan Toxoplasma gondii. The parasite infects most warm-blooded animals, including humans, but the primary host is the felid (cat) family. Animals are infected by eating infected meat, by ingestion of faeces of a cat that has itself recently been infected, or by transmission from mother to fetus. Cats have been shown as a major reservoir of this infection.

In United States as determined with specimens collected by the third National Health and Nutritional Assessment Survey (NHANES III) between 1988 and 1994 was found to be 22.5%, with seroprevalence among women of childbearing age (15 to 44 years) of 15%.People with a weakened immune system, such as those infected with HIV, and fetuses, may become seriously ill, and it can occasionally be fatal. The parasite can cause encephalitis (inflammation of the brain) and neurologic diseases and can affect the heart, liver, and eyes (chorioretinitis).

Transmission
Ingestion of raw or partly cooked meat, especially pork, lamb, or venison containing Toxoplasma cysts. Infection prevalence in countries where undercooked meat is traditionally eaten, such as France, has been related to this transmission method. Oocysts may also be ingested during hand-to-mouth contact after handling undercooked meat, or from using knives, utensils, or cutting boards contaminated by raw meat. Ingestion of contaminated cat faeces. This can occur through hand-to-mouth contact following gardening, cleaning a cat's litter box, contact with children's sandpits, or touching anything that has come into contact with cat faeces.
Drinking water contaminated with Toxoplasma.

Transplacental infection in utero.

Receiving an infected organ transplant or blood transfusion, although this is extremely rare.
The cyst form of the parasite is extremely hardy, capable of surviving exposure to freezing down to −12 degrees Celsius (10 degrees Fahrenheit), moderate temperatures and chemical disinfectants such as bleach, and can survive in the environment for over a year. It is, however, susceptible to high temperatures—above 66 degrees Celsius (150 degrees Fahrenheit), and is thus killed by thorough cooking, and would be killed by 24 hours in a typical domestic freezer.
Cats excrete the pathogen in their faeces for a number of weeks after contracting the disease, generally by eating an infected rodent. Even then, cat faeces are not generally contagious for the first day or two after excretion, after which the cyst 'ripens' and becomes potentially pathogenic. Studies have shown that only about 2% of cats are shedding oocysts at any one time, and that oocyst shedding does not recur even after repeated exposure to the parasite. Although the pathogen has been detected on the fur of cats, it has not been found in an infectious form, and direct infection from handling cats is generally believed to be very rare.

Pregnancy precautions
Congenital toxoplasmosis is a special form in which an unborn child is infected via the placenta. A positive antibody titer indicates previous exposure and immunity and largely ensures the unborn baby's safety. A simple blood draw at the first pre-natal doctor visit can determine whether or not the woman has had previous exposure and therefore whether or not she is at risk. If a woman receives her first exposure to toxoplasmosis while pregnant, the baby is at particular risk. A woman with no previous exposure should avoid handling raw meat, exposure to cat feces, and gardening (cat feces are common in garden soil). Most cats are not actively shedding oocysts and so are not a danger, but the risk may be reduced further by having the litterbox emptied daily (oocysts require longer than a single day to become infective), and by having someone else empty the litterbox. However, while risks can be minimized, they cannot be eliminated. For pregnant women with negative antibody titer, indicating no previous exposure to T. gondii, as frequent as monthly serology testing is advisable as treatment during pregnancy for those women exposed to T. gondii for the first time decreases dramatically the risk of passing the parasite to the fetus.

Treatment is very important for recently infected pregnant women, to prevent infection of the fetus. Since a baby's immune system does not develop fully for the first year of life, and the resilient cysts that form throughout the body are very difficult to eradicate with anti-protozoans, an infection can be very serious in the young. Transplacental transmission:(a) infection in 1st trimester - incidence of transplacental infection is low (15%) but disease in neonate is most severe. (b) infection in 3rd trimester - incidence of transplacental infection is high (65%) but infant is usually asymptomatic at birth.[citation needed]

Infection has two stages:
Acute
During acute toxoplasmosis, symptoms are often influenza-like: swollen lymph nodes, or muscle aches and pains that last for a month or more. Rarely, a patient with a fully functioning immune system may develop eye damage from toxoplasmosis. Young children and immunocompromised patients, such as those with HIV/AIDS, those taking certain types of chemotherapy, or those who have recently received an organ transplant, may develop severe toxoplasmosis. This can cause damage to the brain or the eyes. Only a small percentage of infected newborn babies have serious eye or brain damage at birth.

Latent
Most patients who become infected with Toxoplasma gondii and develop toxoplasmosis do not know it. In most immunocompetent patients, the infection enters a latent phase, during which only bradyzoites are present, forming cysts in nervous and muscle tissue. Most infants who are infected while in the womb have no symptoms at birth but may develop symptoms later in life.

Anemia

Anemia (AmE) or anæmia/anaemia (BrE), from the Greek meaning "without blood," is defined as a qualitative or quantitative deficiency of hemoglobin, a molecule inside red blood cells (RBCs). As hemoglobin carries oxygen from the lungs to the tissues, anemia leads to hypoxia (lack of oxygen) in organs. Since all human cells depend on oxygen for survival, varying degrees of anemia can have a wide range of clinical consequences.
The three main classes of anemia include excessive blood loss (acutely such as a hemorrhage or chronically through low-volume loss), excessive blood cell destruction (hemolysis) or deficient red blood cell production (ineffective hematopoiesis). Anemia can be classified in a variety of ways, based on the morphology of RBCs, underlying etiologic mechanisms, and discernible clinical spectra, to mention a few. There are two major approaches of classifying anemias, the "kinetic" approach which involves evaluating production, destruction and loss, and the "morphologic" approach which groups anemia by red blood cell size. The morphologic approach uses a quickly available and cheap lab test as its starting point (the MCV).Most commonly, people with anemia report a feeling of weakness or fatigue in general or during exercise, general malaise and sometimes poor concentration. People with more severe anemia often report dyspnea (shortness of breath) on exertion. Very severe anemia prompts the body to compensate by increasing cardiac output, leading to palpitations and sweatiness, and to heart failure. Pallor (pale skin, mucosal linings and nail beds) is often a useful diagnostic sign in moderate or severe anemia, but it is not always apparent. Other useful signs are cheilosis and koilonychia. Pica, the consumption of non-food such as dirt, paper, wax, grass and hair, may be a symptom of iron deficiency, although it occurs often in those who have normal levels of hemoglobin. Chronic anemia may result in behavioral disturbances in children as a direct result of impaired neurological development in infants, and reduced scholastic performance in children of school age. Behavioral disturbances may even surface as an attention deficit disorder.
DiagnosisGenerally, clinicians request complete blood counts in the first batch of blood tests in the diagnosis of an anemia. Apart from reporting the number of red blood cells and the hemoglobin level, the automatic counters also measure the size of the red blood cells by flow cytometry, which is an important tool in distinguishing between the causes of anemia. Examination of a stained blood smear using a microscope can also be helpful, and is sometimes a necessity in regions of the world where automated analysis is less accessible.In modern counters, four parameters (RBC count, hemoglobin concentration, MCV and RDW) are measured, allowing others (hematocrit, MCH and MCHC) to be calculated, and compared to values adjusted for age and sex. Some counters estimate hematocrit from direct measurements. For adult men, a hemoglobin level less than 13.0 g/dl is diagnostic of anemia, and for adult women, the diagnostic threshold is below 12.0 g/dl.Reticulocyte counts, and the "kinetic" approach to anemia, have become more common than in the past in the large medical centers of the United States and some other wealthy nations, in part because some automatic counters now have the capacity to include reticulocyte counts. A reticulocyte count is a quantitative measure of the bone marrow's production of new red blood cells. The reticulocyte production index is a calculation of the ratio between the level of anemia and the extent to which the reticulocyte count has risen in response. If the degree of anemia is significant, even a "normal" reticulocyte count actually may reflect an inadequate response. If an automated count is not available, a reticulocyte count can be done manually following special staining of the blood film. In manual examination, activity of the bone marrow can also be gauged qualitatively by subtle changes in the numbers and the morphology of young RBCs by examination under a microscope. Newly formed RBCs are usually slightly larger than older RBCs and show polychromasia. Even where the source of blood loss is obvious, evaluation of erythropoiesis can help assess whether the bone marrow will be able to compensate for the loss, and at what rate. When the cause is not obvious, clinicians use other tests: ESR, ferritin, serum iron, transferrin, RBC folate level, serum vitamin B12, hemoglobin electrophoresis, renal function tests (e.g. serum creatinine). When the diagnosis remains difficult, a bone marrow examination allows direct examination of the precursors to red cells.Anemia diminishes the capability of individuals who are affected to perform physical activities. This is a result of one's muscles being forced to depend on anaerobic metabolism. The lack of iron associated with anemia can cause many complications, including hypoxemia, brittle or rigid fingernails, cold intolerance, and possible behavioral disturbances in children. Hypoxemia resulting from anemia can worsen the cardio-pulmonary status of patients with pre-existing chronic pulmonary disease. Cold intolerance occurs in one in five patients with iron deficiency anemia, and becomes visible through numbness and tinglingAnemia during pregnancyAnemia affects 20% of all females of childbearing age in the United States. Because of the subtlety of the symptoms, women are often unaware that they have this disorder, as they attribute the symptoms to the stresses of their daily lives. Possible problems for the fetus include increased risk of growth retardation, prematurity, intrauterine death, rupture of the amnion and infection. During pregnancy, women should be especially aware of the symptoms of anemia, as an adult female loses an average of two milligrams of iron daily. Therefore, she must intake a similar quantity of iron in order to make up for this loss. Additionally, a woman loses approximately 500 milligrams of iron with each pregnancy, compared to a loss of 4-100 milligrams of iron with each period. Possible consequences for the mother include cardiovascular symptoms, reduced physical and mental performance, reduced immune function, tiredness, reduced peripartal blood reserves and increased need for blood transfusion in the postpartum period.

Androgen insensitivity syndrome

What is androgen insensitivity syndrome?
Androgen insensitivity syndrome is a condition that affects sexual development before birth and during puberty. People with this condition are genetically male, with one X and one Y chromosome. Because their bodies are unable to respond to certain hormones (called androgens), they may have mostly female sexual characteristics or signs of both male and female sexual development (hermaphroditism).

Complete androgen insensitivity syndrome occurs when the body cannot use androgens at all. Partial or mild androgen insensitivity syndrome results when tissues are partially sensitive to the effects of androgens. People with partial androgen insensitivity (also called Reifenstein syndrome) can have normal female sexual characteristics, both male and female sexual characteristics, or normal male sexual characteristics. People with mild androgen insensitivity appear male, but are often infertile and tend to develop female breasts at puberty.

How common is androgen insensitivity syndrome?
Complete androgen insensitivity syndrome affects 2 to 5 per 100,000 live male births. Partial androgen insensitivity is at least as common as complete androgen insensitivity. Mild androgen insensitivity is much less common.

What genes are related to androgen insensitivity syndrome?
Mutations in the AR gene cause androgen insensitivity syndrome.
The AR gene provides instructions to make a protein called an androgen receptor. This protein allows cells to respond to androgens, which are hormones (such as testosterone) that direct male sexual development. Androgens and androgen receptors also have other important functions in both males and females, such as regulating hair growth and sex drive. Mutations in the AR gene prevent the androgen receptor from working properly, which makes cells less responsive to androgens or prevents cells from using these hormones at all. Depending on the level of androgen insensitivity, an affected person's sexual characteristics can vary from mostly female to mostly male.
Read more about the AR gene.

How do people inherit androgen insensitivity syndrome?
This condition is inherited in an X-linked recessive pattern. A condition is considered X-linked if the mutated gene that causes the disorder is located on the X chromosome, one of the two sex chromosomes. In males (who have only one X chromosome) one altered copy of the gene in each cell is sufficient to cause the condition. Males are affected by X-linked recessive disorders much more frequently than females. A striking characteristic of X-linked inheritance is that fathers cannot pass X-linked traits to their sons.
About two-thirds of cases are inherited from mothers who carry an altered copy of the AR gene on one of their two X chromosomes. The remaining cases result from a new mutation in a mother's egg cell before the child is conceived.