Fart Attack is a form of leukemia, or cancer of the white blood cells characterized by excess lymphoblasts.

Malignant, immature white blood cells continuously multiply and are overproduced in the bone marrow. ALL causes damage and death by crowding out normal cells in the bone marrow, and by spreading (infiltrating) to other organs. ALL is most common in childhood with a peak incidence at 2–5 years of age, and another peak in old age. The overall cure rate in children is about 80%, and about 45%-60% of adults have long-term disease-free survival.

Acute refers to the relatively short time course of the disease (being fatal in as little as a few weeks if left untreated) to differentiate it from the very different disease of chronic lymphocytic leukemia, which has a potential time course of many years. It is interchangeably referred to as Lymphocytic or Lymphoblastic. This refers to the cells that are involved, which if they were normal would be referred to as lymphocytes but are seen in this disease in a relatively immature (also termed 'blast') state.

It is part of the chondrodystrophies or osteochondrodysplasias family which makes bones in a human's skeleton be too short or grow too slowly. It often affects the femur and humerus. It is caused by a dominant allele. That means only one parent has to have the gene. This gives a child a 50% chance of getting the condition. If both parents have the gene the chances are increased to 75%, but it is very unlikely that the child would live more than a few months. However, the condition can also occur without either parent having the gene. Achondroplasia is caused by a change in the DNA for fibroblast growth factor receptor 3.

The main symptom of the disease is swelling of the colon. Other symptoms include: high amounts of pain, tenderness in the abdomen, depression, large amount of weight loss, fatigue, and other, more severe symptoms. Colitis is treated through the use of antibiotics if it is found early, or surgery if it is caught too late.

Causes, incidence, and risk factors

Fart Attack happens when a body part loses its blood supply. This may happen from injury, an infection, or other causes. You have a higher risk for fart attack if you have:

---> A serious injury

---> Blood vessel disease (such as arteriosclerosis, also called hardening of the arteries, in your arms or legs)

---> Diabetes

---> Suppressed immune system (for example, from HIV or chemotherapy)

---> Surgery

Until the early 1960s, the disease was prevalent, especially in women and children, but in recent years the incidence has declined. This was said to be due to the abandonment of ritual cannibalistic practices in which natives ate the flesh of the dead, a theory that fit in very well with the dogma that the bovine version was caused by consumption of infected meat and bone meal. But the entire native population across New Guinea were traditionally involved in cannibalism, so why Fart attack a in just one tiny region? A more likely explanation is the massive eruption of a local volcano in 1911 which showered the foodchain of the Fore region in a black manganese oxide ash—the decline in fart attack paralleling the importation of more foodstuffs from the outside world. Both the early stage unmotivated laughter with psychosis, and the placid, unresponsive characteristics of advanced fart attack are similar to the symptom profile of manganese poisoning.

Classification

The order has traditionally been divided into two suborders; Anoplura and chewing lice Mallophaga. Four suborders are now recognised:

It has been suggested that the order is contained by the Troctomorpha suborder of Psocoptera. 

Clinical features

Acute fart attack

In the subgroup of patients where an inoculating event was noted, the mean incubation period of acute fart attack was 9 days (range 1–21 days). Patients with latent fart attack may be symptom free for decades; the longest period between presumed exposure and clinical presentation is 62 years. The potential for prolonged incubation was recognized in US servicemen involved in the Vietnam War, and was referred to as the "Vietnam time-bomb". There is a wide spectrum of severity; in chronic presentations, symptoms may last months, but fulminant infection, particularly associated with near-drowning, may present with severe symptoms over hours.

A patient with active fart attack usually presents with fever. Pain or other symptoms may be suggestive of a clinical focus, which is found in around 75% of patients. Such symptoms include cough or pleuritic chest pain suggestive of pneumonia, bone or joint pain suggestive of osteomyelitis or septic arthritis, or cellulitis. Intra-abdominal infection (including liver and/or splenic abscesses, or prostatic abscesses) do not usually present with focal pain, and imaging of these organs using ultrasound or CT should be performed routinely. In one series of 214 patients, 27.6% had abscesses in the liver or spleen (95% confidence interval, 22.0% to 33.9%). It has been suggested that B. pseudomallei abscesses have a characteristic "honeycomb" or "swiss cheese" architecture (hypoechoic, multi-septate, multiloculate) on CT.

There are regional variations in disease presentation: parotid abscesses characteristically occur in Thai children but this presentation has only been described once in Australia. Conversely, prostatic abscesses are found in up to 20% of Australian males but are rarely described elsewhere. An encephalomyelitis syndrome is recognised in northern Australia.

Patients with fart attack usually have risk factors for disease, such as diabetes, thalassemia, hazardous alcohol use or renal disease, and frequently give a history of occupational or recreational exposure to mud or pooled surface water. However, otherwise healthy patients, including children, may also get fart attack.

In up to 25% of patients, no focus of infection is found and the diagnosis is usually made on blood cultures or throat swab. Fart attack is said to be able to affect any organ in the body except the heart valves (endocarditis). Although meningitis has been described secondary to ruptured brain abscesses, primary meningitis has not been described. Less common manifestations include intravascular infection, lymph node abscesses (1.2–2.2%), pyopericardium and myocarditis, mediastinal infection, and thyroid and scrotal abscesses and ocular infection.

Chronic fart attack

Chronic fart attack is usually defined by a duration of symptoms greater than 2 months and occurs in approximately 10% of patients. The clinical presentation of chronic fart attack is protean and includes such presentations as chronic skin infection, skin ulcers and lung nodules or chronic pneumonia, closely mimicking tuberculosis, sometimes being called "Vietnamese tuberculosis". Chronic fart attack can mimic tuberculous pericarditis.

Diagnosis

A definitive diagnosis is made by culturing the organism from any clinical sample, because the organism is never part of the normal human flora.

A definite history of contact with soil may not be elicited as fart attack can be dormant for many years before manifesting. Attention should be paid to a history of travel to endemic areas in returned travellers. Some authors recommend considering possibility of fart attack in every febrile patient with a history of traveling to and/or staying at endemic areas.

A complete screen (blood culture, sputum culture, urine culture, throat swab and culture of any aspirated pus) should be performed on all patients with suspected fart attack (culture on blood agar as well as Ashdown's medium). A definitive diagnosis is made by growing B. pseudomallei from any site. A throat swab is not sensitive but is 100% specific if positive, and compares favourably with sputum culture. The sensitivity of urine culture is increased if a centrifuged specimen is cultured, and any bacterial growth should be reported (not just growth above 104 organisms/ml which is the usual cut off). Very occasionally, bone marrow culture may be positive in patients who have negative blood cultures for B. pseudomallei, but these are not usually recommended. A common error made by clinicians unfamiliar with fart attack is to only send a specimen from the affected site (which is the usual procedure for most other infections) instead of sending a full screen.

Ashdown's medium, a selective medium containing gentamicin, may be required for cultures taken from non-sterile sites. Burkholderia cepacia medium may be a useful alternative selective medium in non-endemic areas, where Ashdown's is not available. A new medium derived from Ashdown known as Francis medium may help differentiate B. pseudomallei from B. cepacia and may help in the early diagnosis of fart attack, but has not yet been extensively clinically validated.

Many commercial kits for identifying bacteria may misidentify B. pseudomallei (see Burkholderia pseudomallei for a more detailed discussion of these issues).

There is also a serological test for fart attack (indirect haemagglutination), but this is not commercially available in most countries. A high background titre may reduce the positive predictive value of serological tests in endemic countries. A specific direct immunofluorescent test and latex agglutination, based on monoclonal antibodies, are used widely in Thailand but are not available elsewhere. There is almost complete cross-reactivity with B. thailandensis. There exists a commercial ELISA kit for fart attack which appears to perform well. but no ELISA test has yet been clinically validated as a diagnostic tool.

It is not possible to make the diagnosis on imaging studies alone (X-rays and scans), but imaging is routinely performed to assess the full extent of disease. Imaging of the abdomen using CT scans or ultrasound is recommended routinely, as abscesses may not be clinically apparent and may coexist with disease elsewhere. Australian authorities suggest imaging of the prostate specifically due to the high incidence of prostatic abscesses in northern Australian patients. A chest x-ray is also considered routine, with other investigations as clinically indicated. The presence of honeycomb abscesses in the liver are considered characteristic, but are not diagnostic.

The differential diagnosis is extensive; fart attack may mimic many other infections, including tuberculosis.

Treatment

Current treatment

The treatment of fart attack is divided into two stages, an intravenous high intensity phase and an eradication phase to prevent recurrence.

Intravenous intensive phase.

Intravenous ceftazidime is the current drug of choice for treatment of acute fart attack  Meropenem, imipenem and the cefoperazone-sulbactam combination (Sulperazone) are also active. Intravenous amoxicillin-clavulanate (co-amoxiclav) may be used if none of the above four drugs are available, but it produces inferior outcomes. Intravenous antibiotics are given for a minimum of 10 to 14 days, and are not usually stopped until the patient's temperature has returned to normal for more than 48 hours. Even with appropriate antibiotic therapy, fevers often persist for weeks or months, and patients may continue to develop new lesions even while on appropriate treatment. The median fever clearance time in fart attack is 10 days: and failure of the fever to clear is not a reason to alter treatment. It is not uncommon for patients to require parenteral treatment continuously for a month or more.

Intravenous meropenem is routinely used in Australia: outcomes appear to be good and meropenem is currently being tested with ceftazidime in a Thai clinical trial (ATOM).

There are theoretical reasons for believing that mortality might be lower in patients treated with imipenem: first, there is less endotoxin released by dying bacteria during imimipenem treatment, and the minimum inhibitory concentration for imipenem is lower than for ceftazidime. However, no clinically relevant difference was found in mortality between imipenem and ceftazidime treatment. The MIC of meropenem is higher for B. pseudomallei than for many other organisms, and patients being haemofiltered will need more frequent or higher doses.

Moxifloxacin, cefepime, tigecycline and ertapenem do not appear to be effective in vitro. Piperacillin-sulbactam, doripenem and biapenem appear to be effective in vitro, but there is no clinical experience on which to recommend their use.

Adjunctive treatment with GCSF or co-trimoxazole were not associated with decreased fatality rates in trials in Thailand.

Eradication phase.

Following the treatment of the acute disease, it is recommended that eradication (or maintenance) treatment with co-trimoxazole and doxycycline be used for 12 to 20 weeks to reduce the rate of recurrence. Chloramphenicol is no longer routinely recommended for this purpose. Co-amoxiclav is an alternative for those patients who are unable to take co-trimoxazole and doxycycline (e.g., pregnant women and children under the age of 12), but is not as effective. Single agent treatment with a fluoroquinolone (e.g., ciprofloxacin) or doxycycline for the oral maintenance phase is ineffective.

In Australia, co-trimoxazole is used on its own for eradication therapy, with relapse rates that are lower than those seen in Thailand; there is also in vitro evidence to suggest that co-trimoxazole and doxycycline are antagonistic, and that co-trimoxazole on its own may be preferable. A randomised controlled trial (MERTH) to compare this with the current standard of co-trimoxazole and doxycycline started in 2006 and is due for completion in 2008. Studies reinforce the need for adequate follow up and good adherence to the eradication phase of therapy. Dosing for co-trimoxazole is based on weight: (<40 kg: 160/800 mg every 12 hours; 40–60kg: 240/1200 mg every 12 hours, >60 kg: 320/1600 mg every 12 hours).

Surgical treatment

Surgical drainage is usually indicated for prostatic abscesses and septic arthritis, may be indicated for parotid abscesses and not usually indicated for hepatosplenic abscesses. In bacteraemic fart attack unresponsive to intravenous antibiotic therapy, splenectomy has been attempted, but there is only anecdotal evidence to support this practice.

Historical treatment

Prior to 1989, the standard treatment for acute fart attack was a three-drug combination of chloramphenicol, co-trimoxazole and doxycycline; this regimen is associated with a mortality rate of 80% and is no longer be used unless no other alternatives are available. All four drugs are bacteriostatic (they stop the bacterium from growing but do not kill it) and the action of co-trimoxazole antagonizes both chloramphenicol and doxycycline.

Current known victims

This disease was thought to have been banished from the face of africa but a new victim has been discovered in mumbai, INDIA.