Avascular necrosis is a disease resulting from the temporary or permanent loss of the blood supply to the bones.[1] Without blood, the bone tissue dies and causes the bone to collapse.[1] If the process involves the bones near a joint, it often leads to collapse of the joint surface. This disease also is known as osteonecrosis, aseptic (bone) necrosis, and ischemic bone necrosis.[1]

There are many theories about what causes avascular necrosis. Proposed risk factors include alcoholism[2], excessive steroid use,[3] post trauma,[4][5] caisson disease (decompression sickness),[6][7] vascular compression,[8] hypertension, vasculitis, thrombosis, damage from radiation, bisphosphonates (particularly the mandible),[9] sickle cell anaemia,[10] and Gaucher’s Disease.[11] In some cases it is idiopathic (no cause is found).[12] Rheumatoid arthritis and lupus are also common causes of AVN.

While it can, by definition, affect any bone, and half of cases show multiple sites of damage, this disease primarily affects the joints at the shoulder, knee, and hip.

Although it can happen in any bone, avascular necrosis most commonly affects the ends (epiphysis) of long bones such as the femur, the bone extending from the knee joint to the hip joint. Other common sites include the humerus (the bone of the upper arm),[13][14] knees,[15][16] shoulders,[13][17] ankles and the jaw.[18] The disease may affect just one bone, more than one bone at the same time, or more than one bone at different times.[19] Avascular necrosis usually affects people between 30 and 50 years of age; about 10,000 to 20,000 people develop avascular necrosis of the head of the femur in the US each year. When it occurs in children at the femoral head, it is known as Legg-Calvé-Perthes syndrome.[20]

Orthopaedic doctors most often diagnose the disease except when it affects the jaws, when it is usually diagnosed and treated by dental and maxillofacial surgeons.

Because early x-rays are usually normal in the early stage of the disease, bone scintigraphy[21] and MRI[22] are the diagnostic modalities of choice since both can detect minimal changes at early stages of the disease. Late radiographic signs include a radiolucency area following the collapse of subchondral bone (crescent sign) and ringed regions of radiodensity resulting from saponification and calcification of marrow fat following medullary infarcts.

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Autism is a brain development disorder characterized by impaired social interaction and communication, and by restricted and repetitive behavior. These signs all begin before a child is three years old.[2] The autism spectrum disorders (ASD) also include related conditions with milder signs and symptoms.[3]

Autism has a strong genetic basis, although the genetics of autism are complex and it is unclear whether ASD is explained more by multigene interactions or by rare mutations.[4] In rare cases, autism is strongly associated with agents that cause birth defects.[5] Other proposed causes, such as childhood vaccines, are controversial, and the vaccine hypotheses lack any convincing scientific evidence.[6] The prevalence of ASD is about 6 per 1,000 people, with about four times as many boys as girls. The number of people known to have autism has increased dramatically since the 1980s, partly due to changes in diagnostic practice; the question of whether actual prevalence has increased is unresolved.[7]

Autism affects many parts of the brain; how this occurs is not understood. Parents usually notice signs in the first two years of their child’s life. Although early behavioral or cognitive intervention can help children gain self-care, social, and communication skills, there is no known cure.[3] Few children with autism live independently after reaching adulthood, but some become successful,[8] and an autistic culture has developed, with some seeking a cure and others believing that autism is a condition rather than a disorder.[9]

Autism is a highly variable brain development disorder[10] that first appears during infancy or childhood, and generally follows a steady course without remission.[11] Symptoms tend to continue through adulthood, although often in more muted form.[12] It is distinguished not by a single symptom, but by a characteristic triad of symptoms: impairments in social interaction; impairments in communication; and restricted interests and repetitive behavior. Other aspects, such as atypical eating, are also common but are not essential for diagnosis.[13] Autism is one of three related autism spectrum disorders (ASD; see Classification). Its individual symptoms occur in the general population and appear not to associate highly, without a sharp line separating pathological severity from common traits.[14]

Social deficits distinguish ASD from other developmental disorders.[12] People with autism have social impairments and often lack the intuition about others that many people take for granted. Noted autistic Temple Grandin described her inability to understand the social communication of neurotypicals, or people with normal neural development, as leaving her feeling “like an anthropologist on Mars”.[15]

Social impairments become apparent early in childhood. Autistic infants show less attention to social stimuli, smile and look at others less often, and respond less to their own name. Autistic toddlers have more striking social deviance; for example, they have less eye contact and anticipatory postures and are more likely to communicate by manipulating another person’s hand.[16] Three- to five-year-old autistic children are less likely to exhibit social understanding, approach others spontaneously, imitate and respond to emotions, communicate nonverbally, and take turns with others. However, they do form attachments to their primary caregivers.[17] They display moderately less attachment security than usual, although this feature disappears in children with higher mental development or less severe ASD.[18] Older children and adults with ASD perform worse on tests of face and emotion recognition.[19]

Contrary to common belief, autistic children do not prefer to be alone. Making and maintaining friendships often proves to be difficult for those with autism. For them, the quality of friendships, not the number of friends, predicts how lonely they feel.[20]

There are many anecdotal reports, but few systematic studies, of aggression and violence in individuals with ASD. The limited data suggest that, in children with mental retardation, autism is associated with aggression, destruction of property, and tantrums. A 2007 study interviewed parents of 67 children with ASD and reported that about two-thirds of the children had periods of severe tantrums and about one-third had a history of aggression, with tantrums significantly more common than in children with a history of language impairment.[21] A 2008 Swedish study found that, of individuals aged 15 or older discharged from hospital with a diagnosis of ASD, those who committed violent crimes were significantly more likely to have other psychopathological conditions such as psychosis.[22]

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Atopic dermatitis (also known as “Atopic eczema,” “Disseminated neurodermatitis,” “Flexural eczema,” “Infantile eczema,” and “Prurigo diathsique”[1]:69 ) is a disease characterized by chronic inflammation of the skin[2] which is atopic, hereditary, and non-contagious.

The skin of a patient with atopic dermatitis reacts abnormally and easily to irritants, food, and environmental allergens and becomes red, flaky and very itchy. It also becomes vulnerable to surface infections caused by bacteria. The skin on the flexural surfaces of the joints (for example inner sides of elbows and knees) are the most commonly affected regions in people.

Atopic dermatitis often occurs together with other atopic diseases like hay fever, asthma and conjunctivitis. It is a familial and chronic disease and its symptoms can increase or disappear over time. Atopic dermatitis in older children and adults is often confused with psoriasis. Atopic dermatitis afflicts humans, particularly young children; it is also a well-characterized disease in domestic dogs.

Although there is no cure for atopic eczema, and its causes not well understood, it can be treated very effectively in the short term through a combination of prevention (learning what triggers the allergic reactions) and drug therapy.

Since the beginning of the twentieth century, many mucosal inflammatory disorders have become dramatically more common; atopic eczema (AE) is a classic example of such a disease. It now affects 10-20% of children and 1-3% of adults in industrialized countries, and its prevalence in the United States alone has nearly tripled in the past thirty to forty years.[3]

Although it is an inherited disease, eczema is primarily aggravated by contact with or intake of allergens. It can also be influenced by other “hidden” factors such as stress or fatigue. Atopic eczema consists of chronic inflammation; it often occurs in people with a history of allergy disorders such as asthma or hay fever. There is no certain cause of atopic dermatitis.

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Atherosclerosis is a disease affecting arterial blood vessels. It is a chronic inflammatory response in the walls of arteries, in large part due to the accumulation of macrophage white blood cells and promoted by low density (especially small particle) lipoproteins (plasma proteins that carry cholesterol and triglycerides) without adequate removal of fats and cholesterol from the macrophages by functional high density lipoproteins (HDL), (see apoA-1 Milano). It is commonly referred to as a “hardening” or “furring” of the arteries. It is caused by the formation of multiple plaques within the arteries.[1]

The atheromatous plaque is divided into three distinct components:

The following terms are similar, yet distinct, in both spelling and meaning, and can be easily confused: arteriosclerosis, arteriolosclerosis, and atherosclerosis. Arteriosclerosis is a general term describing any hardening (and loss of elasticity) of medium or large arteries (from the Greek Arterio, meaning artery, and sclerosis, meaning hardening); arteriolosclerosis is any hardening (and loss of elasticity) of arterioles (small arteries); atherosclerosis is a hardening of an artery specifically due to an atheromatous plaque. Therefore, atherosclerosis is a form of arteriosclerosis.

Atherosclerosis, though typically asymptomatic for decades, eventually produces two main problems: First, the atheromatous plaques, though long compensated for by artery enlargement (see IMT), eventually lead to plaque ruptures and clots inside the artery lumen over the ruptures. The clots heal and usually shrink but leave behind stenosis (narrowing) of the artery (both locally and in smaller downstream branches), or worse, complete closure, and, therefore, an insufficient blood supply to the tissues and organ it feeds. Second, if the compensating artery enlargement process is excessive, then a net aneurysm results.

These complications of advanced atherosclerosis are chronic, slowly progressive and cumulative. Most commonly, soft plaque suddenly ruptures (see vulnerable plaque), causing the formation of a thrombus that will rapidly slow or stop blood flow, leading to death of the tissues fed by the artery in approximately 5 minutes. This catastrophic event is called an infarction. One of the most common recognized scenarios is called coronary thrombosis of a coronary artery, causing myocardial infarction (a heart attack). Even worse is the same process in an artery to the brain, commonly called stroke. Another common scenario in very advanced disease is claudication from insufficient blood supply to the legs, typically due to a combination of both stenosis and aneurysmal segments narrowed with clots. Since atherosclerosis is a body-wide process, similar events occur also in the arteries to the brain, intestines, kidneys, legs, etc.

Yet, many infarctions involve only very small amounts of tissue and are termed clinically silent, because the person having the infarction does not notice the problem, does not seek medical help or when they do, physicians do not recognize what has happened.

Atherosclerosis develops from low-density lipoprotein molecules (LDL) becoming oxidized (ldl-ox) by free radicals, particularly oxygen free radicals (ROS). Blood in arteries contains plenty of oxygen and is where atherosclerosis develops. Blood in veins contains little oxygen where atherosclerosis rarely develops. When oxidized LDL comes in contact with an artery wall, a series of reactions occurs to repair the damage to the artery wall caused by oxidized LDL. The LDL molecule is globular shaped with a hollow core for carrying cholesterol throughout the body for making brain tissue, vitamin D, etc. Cholesterol does not dissolve in water. Blood is 70% water. The only way cholesterol can move in the bloodstream is to be carried by LDL.

The body’s immune system responds to the damage to the artery wall caused by oxidized LDL by sending specialized white blood cells (macrophages and T-lymphocytes) to absorb the oxidized-LDL. Unfortunately, these white blood cells are not able to process the oxidized-LDL, and ultimately grow then rupture, depositing a greater amount of oxidized cholesterol into the artery wall. This triggers more white blood cells, continuing the cycle.

Eventually, the artery becomes inflamed. The cholesterol plaque causes the muscle cells to enlarge and form a hard cover over the affected area. This hard cover is what causes a narrowing of the artery, reduces the blood flow and increases blood pressure.

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Astrocytomas are primary central nervous system tumors that arise primarily in and rarely spread away from the CNS parenchyma contained within the cranial vault. Astrocytomas “are CNS neoplasms in which the predominant cell type is derived from an immortalized[1] astrocyte and account for roughly 75% of neuroepithelial tumors. In 1993 the World Health Organization (WHO) established a four-tiered histologic grading guideline for astrocytomas in an effort to eliminate confusion regarding diagnoses. The low grade astrocytomas (I & II) are among the least common of all reported brain tumors, less than 6%, while the highest grade (IV), also known as glioblastoma multiforme (GBM), is the most common primary CNS malignancy and second most frequent brain tumor. Despite the comparatively low incidence of astrocytomas to other human cancers, the higher grades (III & IV) represent disparate mortality rates. Median survival of GBM victims who forgo treatment is approximately 90 days, and even with aggressive surgical, radio- and chemo- therapies is only extended to about twelve months, while long term survival (at least five years) falls under 3%.[2][3]

A Computed Tomography (CT) or Magnetic Resonance Imaging (MRI) scan is necessary to characterize the extent of these tumors (size, location, consistency). CT will usually show distortion of third and lateral ventricles with displacement of anterior and middle cerebral arteries. Histologic analysis is necessary for grading diagnosis.

In the first stage of diagnosis the doctor will take a history of symptoms and perform a basic neurological exam, including an eye exam and tests of vision, balance, coordination and mental status. The doctor will then require a computerized tomography (CT) scan and magnetic resonance imaging (MRI) of the patient’s brain. During a CT scan, x rays of the patient’s brain are taken from many different directions; these are combined by a computer, producing a cross-sectional image of the brain. For an MRI, the patient relaxes in a tunnel-like instrument while the brain is subjected to changes of magnetic field. An image is produced based on the behavior of the brain’s water molecules in response to the magnetic fields. A special dye may be injected into a vein before these scans to provide contrast and make tumors easier to identify.

If a tumor is found it will be necessary for a neurosurgeon to perform a biopsy on it. This simply involves the removal of a small amount of tumor tissue, which is then sent to a neuropathologist for examination and staging. The biopsy may take place before surgical removal of the tumor or the sample may be taken during surgery. Staging of the tumor sample is a method of classification that helps the doctor to determine the severity of the astrocytoma and to decide on the best treatment options. The neuropathologist stages the tumor by looking for atypical cells, the growth of new blood vessels, and for indicators of cell division called mitotic figures.

For low grade astrocytomas, removal of the tumor will generally allow functional survival for many years. In some reports, the 5 year survival has been over 90% with well resected tumors. Indeed, broad intervention of low grade conditions is a contested matter. In particular, pilocytic astrocytomas are commonly indolent bodies that may permit normal neurologic function. However, left unattended these tumors may eventually undergo neoplastic transformation. To date, complete resection of high grade astrocytomas is impossible because of the diffuse infiltration of tumor cells into normal parenchyma. Thus, high grade astrocytomas inevitably recur after initial surgery/therapy and are usually treated similarly as the initial tumor. Despite decades of therapeutic research, curative intervention is still nonexistent for high grade astrocytomas; patient care ultimately focuses on palliative management.

The cause of astrocytoma is not known. It has been speculated that electromagnetic waves emitted from high-tension wires or even cell phones may increase the risk of developing brain tumors, but, to date, there is no scientific evidence supporting this theory.[4]

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Asthma is a very common chronic disease involving the respiratory system in which the airways constrict, become inflamed, and are lined with excessive amounts of mucus, often in response to one or more triggers.[1] These episodes may be triggered by such things as exposure to an environmental stimulant such as an allergen, environmental tobacco smoke, cold or warm air, perfume, pet dander, moist air, exercise or exertion, or emotional stress. In children, the most common triggers are viral illnesses such as those that cause the common cold.[2] This airway narrowing causes symptoms such as wheezing, shortness of breath, chest tightness, and coughing. The airway constriction responds to bronchodilators. Between episodes, most patients feel well but can have mild symptoms and they may remain short of breath after exercise for longer periods of time than the unaffected individual. The symptoms of asthma, which can range from mild to life threatening, can usually be controlled with a combination of drugs and environmental changes.

Public attention in the developed world has recently focused on asthma because of its rapidly increasing prevalence, affecting up to one in four urban children.[3]

Asthma is classified according to the frequency of symptoms, FEV1 and peak expiratory flow rate.[4]

In some individuals asthma is characterized by chronic respiratory impairment. In others it is an intermittent illness marked by episodic symptoms that may result from a number of triggering events, including upper respiratory infection, stress, airborne allergens, air pollutants (such as smoke or traffic fumes), or exercise. Some or all of the following symptoms may be present in those with asthma: dyspnea, wheezing, stridor, coughing, a tightness and itching of the chest or an inability for physical exertion. Some asthmatics who have severe shortness of breath and tightening of the lungs never wheeze or have stridor and their symptoms may be confused with a COPD-type disease.

An acute exacerbation of asthma is commonly referred to as an asthma attack. The clinical hallmarks of an attack are shortness of breath (dyspnea) and either wheezing or stridor.[5] Although the former is “often regarded as the sine qua non of asthma”,[5] some patients present primarily with coughing, and in the late stages of an attack, air motion may be so impaired that no wheezing may be heard. When present the cough may sometimes produce clear sputum. The onset may be sudden, with a sense of constriction in the chest, breathing becomes difficult, and wheezing occurs (primarily upon expiration, but can be in both respiratory phases).

Signs of an asthmatic episode include wheezing, prolonged expiration, a rapid heart rate (tachycardia), rhonchous lung sounds (audible through a stethoscope), the presence of a paradoxical pulse (a pulse that is weaker during inhalation and stronger during exhalation), and over-inflation of the chest. During a serious asthma attack, the accessory muscles of respiration (sternocleidomastoid and scalene muscles of the neck) may be used, shown as in-drawing of tissues between the ribs and above the sternum and clavicles.

During very severe attacks, an asthma sufferer can turn blue from lack of oxygen (so-called blue bloaters), and can experience chest pain or even loss of consciousness. Just before loss of consciousness, there is a chance that the patient will feel numbness in the limbs and palms may start to sweat. The person’s feet may become icy cold. Severe asthma attacks, which may not be responsive to standard treatments (status asthmaticus), are life-threatening and may lead to respiratory arrest and death. Despite the severity of symptoms during an asthmatic episode, between attacks an asthmatic may show few or even no signs of the disease.[6]

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Aspiration pneumonia is bronchopneumonia that develops due to the entrance of foreign materials that enter the bronchial tree,[1] usually oral or gastric contents (including food, saliva, or nasal secretions). Depending on the acidity of the aspirate, a chemical pneumonitis can develop, and bacterial pathogens (particularly anaerobic bacteria) may add to the inflammation.

Aspiration pneumonia is often caused by an incompetent swallowing mechanism, such as occurs in some forms of neurological disease (a common cause being strokes) or while a person is intoxicated. An iatrogenic cause is during general anaesthesia for an operation and patients are therefore instructed to be nil per os (NPO) (aka Nil By Mouth) for at least four hours before surgery.

Whether aspiration pneumonia represents a true bacterial infection or a chemical inflammatory process remains the subject of significant controversy. Both causes may present with similar symptoms.

When bacteria are implicated, they are usually of the anaerobic oral flora:

They may also be admixed with aerobic bacteria:

The location is often gravity dependent, and depends on the patient position. Generally the right middle and lower lung lobes are the most common sites of infiltrate formation due to the larger caliber and more vertical orientation of the right mainstem bronchus. Patients who aspirate while standing can have bilateral lower lung lobe infiltrates. The right upper lobe is a common area of consolidation in alcoholics who aspirate in the prone position.[3]

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Aspergillosis is the name given to a wide variety of diseases caused by fungi of the genus Aspergillus. The most common forms are allergic bronchopulmonary aspergillosis, pulmonary aspergilloma and invasive aspergillosis. Most humans inhale Aspergillus spores every day; aspergillosis develops mainly in immunocompromised individuals. The most common cause is Aspergillus fumigatus.

A fungus ball in the lungs may cause no symptoms and may be discovered only with a chest x-ray. Or it may cause repeated coughing up of blood and occasionally severe, even fatal, bleeding. A rapidly invasive Aspergillus infection in the lungs often causes cough, fever, chest pain, and difficulty breathing.

Aspergillosis affecting the deeper tissues makes a person very ill. Symptoms include fever, chills, shock, delirium, and blood clots. The person may develop kidney failure, liver failure (causing jaundice), and breathing difficulties. Death can occur quickly.

Aspergillosis of the ear canal causes itching and occasionally pain. Fluid draining overnight from the ear may leave a stain on the pillow. Aspergillosis of the sinuses causes a feeling of congestion and sometimes pain or discharge.

In addition to the symptoms, an x-ray or computerised tomography (CT) scan of the infected area provides clues for making the diagnosis. Whenever possible, a doctor sends a sample of infected material to a laboratory to confirm identification of the fungus.

On chest X-ray and computed tomography pulmonary aspergillosis classically manifests as an air crescent sign.[1] In hematologic patients with invasive aspergillosis the galactomannan test can make the diagnosis in a noninvasive way.

The drugs amphotericin B, caspofungin, flucytosine, itraconazole, voriconazole [2] are used to treat this fungal infection. For severe cases of invasive aspergillosis a combination therapy of voriconazole and caspofungin is suggested as a first line treatment.

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In medicine (gastroenterology), ascites (also known as peritoneal cavity fluid, peritoneal fluid excess, hydroperitoneum or more archaically as abdominal dropsy) is an accumulation of fluid in the peritoneal cavity. Although most commonly due to cirrhosis and severe liver disease, its presence can portend other significant medical problems. Diagnosis of the cause is usually with blood tests, an ultrasound scan of the abdomen and direct removal of the fluid by needle or paracentesis (which may also be therapeutic). Treatment may be with medication (diuretics), paracentesis or other treatments directed at the cause.

Mild ascites is hard to notice, but severe ascites leads to abdominal distension. Patients with ascites generally will complain of progressive abdominal heaviness and pressure as well as shortness of breath due to mechanical impingement on the diaphragm.

Ascites is detected on physical examination of the abdomen by visible bulging of the flanks in the reclining patient (“flank bulging”), “shifting dullness” (difference in percussion note in the flanks that shifts when the patient is turned on the side) or in massive ascites with a “fluid thrill” or “fluid wave” (tapping or pushing on one side will generate a wave-like effect through the fluid that can be felt in the opposite side of the abdomen).

Other signs of ascites may be present due to its underlying etiology. For instance, in portal hypertension (perhaps due to cirrhosis or fibrosis of the liver) patients may also complain of leg swelling, bruising, gynecomastia, hematemesis, or mental changes due to encephalopathy. Those with ascites due to cancer (peritoneal carcinomatosis) may complain of chronic fatigue or weight loss. Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and exercise intolerance.

Ascites exists in three grades:[1]

Routine complete blood count (CBC), basic metabolic profile, liver enzymes, and coagulation should be performed. Most experts recommend a diagnostic paracentesis be performed if the ascites is new or if the patient with ascites is being admitted to the hospital. The fluid is then reviewed for its gross appearance, protein level, albumin, and cell counts (red and white). Additional tests will be performed if indicated such as Gram stain and cytology.[2]

The Serum-ascites albumin gradient (SAAG) is probably a better discriminant than older measures (transudate versus exudate) for the causes of ascites.[3] A high gradient (> 1.1 g/dL) indicates the ascites is due to portal hypertension. A low gradient (< 1.1 g/dL) indicates ascites of non-portal hypertensive etiology.

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Ascariasis is a human disease caused by the parasitic roundworm Ascaris lumbricoides. Perhaps as many as one quarter of the world’s people are infected[1], and ascariasis is particularly prevalent in tropical regions and in areas of poor hygiene. Other species of the genus Ascaris are parasitic and can cause disease in domestic animals.

Infection occurs through ingestion of food contaminated with feces containing Ascaris eggs. The larvae hatch, burrow through the intestine, reach the lungs, and finally migrate up the respiratory tract. From there they are then reswallowed and mature in the intestine, growing up to 30 cm (12 in.) in length and anchoring themselves to the intestinal wall.

Infections are usually asymptomatic, especially if the number of worms is small. They may however be accompanied by inflammation, fever, and diarrhea, and serious problems may develop if the worms migrate to other parts of the body.

Roughly 1.5 billion individuals are infected with this worm, primarily in Africa and Asia.[2][1] Ascariasis is endemic in the United States including Gulf Coast; in Nigeria and in Southeast Asia. One study indicated that the prevalence of ascariasis in the United States at about 4 million (2%) [8]. In a survey of a rural Nova Scotia community, 28.1% of 431 individuals tested were positive for Ascaris, all of them being under age 20, while all 276 tested in metropolitan Halifax were negative[3]. Deposition of ova (eggs) in sewage hints at the degree of ascariasis incidence. A 1978 study showed about 75% of all sewage sludge samples sampled in United States urban catchments contained Ascaris ova, with rates as high as 5 to 100 eggs per litre[citation needed]. In Frankfort, Indiana, 87.5% of the sludge samples were positive with Ascaris, Toxocara, Trichuris, and hookworm[citation needed]. In Macon, Georgia, one of the 13 soil samples tested positive for Ascaris[citation needed]. Municipal wastewater in Riyadh, Saudi Arabia detected over 100 eggs per litre of wastewater [4] and in Czechoslovakia was as high as 240-1050 eggs per litre [5].

Ascariasis can often be measured by examining food for ova. In one field study in Marrakech, Morocco, where raw sewage is used to fertilize crop fields, Ascaris eggs were detected at the rate of 0.18 eggs/kg in potatoes, 0.27 eggs/kg in turnip, 4.63 eggs/kg in mint, 0.7 eggs/kg in carrots, and 1.64 eggs/kg in radish[6]. A similar study in the same area showed that 73% of children working on these farms were infected with helminths, particularly Ascaris, probably as a result of exposure to the raw sewage.

First appearance of eggs in stools is 60-70 days. In larval ascariasis, symptoms occur 4-16 days after infection. The final symptoms are gastrointestinal discomfort, colic and vomiting, fever; observation of live worms in stools. Some patients may have pulmonary symptoms or neurological disorders during migration of the larvae. However there are generally few or no symptoms. A bolus of worms may obstruct the intestine; migrating larvae may cause pneumonitis and eosinophilia.

The source of transmission is from soil and vegetation on which fecal matter containing eggs has been deposited. Ingestion of infective eggs from soil contaminated with human feces or transmission and contaminated vegetables and water is the primary route of infection. Intimate contact with pets which have been in contact with contaminated soil may result in infection, while pets which are infested themselves by a different type of roundworm can cause infection with that type of worm (Toxocara canis, etc) as occasionally occurs with groomers.

Transmission also comes through municipal recycling of wastewater into crop fields. This is quite common in emerging industrial economies, and poses serious risks for not only local crop sales but also exports of contaminated vegetables. A 1986 outbreak of ascariasis in Italy was traced to irresponsible wastewater recycling used to grow Balkan vegetable exports[7] .

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