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The correct diagnosis was in fact Napthalene Poisoning. Napthalene is a gas, a fat soluable gas. It's released by termites to protect thier nest, which we can assume was somewhere in the boy's house. Most likely in the walls of his room, as he seems to be the only one affected by it, other than his cat of course. When he breathed the gas in, it was storded in his fat cells. Becasue of the car crash, he was admitted to hospital. Due to a sudden change in diet, going from his fathers home cooking to hospital food, his body started to burn fat in order to gain energy. Thus, the flood gates opened (metaphorically) and the poison flooded his system. The longer the boy stayed in hospital the worse he would obviously get.
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A ganglion is a pseudocysts that occurs when synovial fluid leaks from and accumulates near a joint. They often fluctuate in size, and the radial aspect of the wrist, both dorsal and volar, is a common location. They also occur on the dorsal aspect of IP joints and the volar aspect of MCP joints. Treatment is excision.
Epidermal inclusion cysts more commonly appear on volar surfaces, typically the pads of fingers. These, lipomas, and giant cell tumors typically do not fluctuate in size.
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Source: http://www.cdc.gov/ncidod/dvrd/qfever/
Signs and Symptoms in Humans
Only about one-half of all people infected with C. burnetii show signs of clinical illness. Most acute cases of Q fever begin with sudden onset of one or more of the following: high fevers (up to 104-105° F), severe headache, general malaise, myalgia, confusion, sore throat, chills, sweats, non-productive cough, nausea, vomiting, diarrhea, abdominal pain, and chest pain. Fever usually lasts for 1 to 2 weeks. Weight loss can occur and persist for some time. Thirty to fifty percent of patients with a symptomatic infection will develop pneumonia. Additionally, a majority of patients have abnormal results on liver function tests and some will develop hepatitis. In general, most patients will recover to good health within several months without any treatment. Only 1%-2% of people with acute Q fever die of the disease.
Chronic Q fever, characterized by infection that persists for more than 6 months is uncommon but is a much more serious disease. Patients who have had acute Q fever may develop the chronic form as soon as 1 year or as long as 20 years after initial infection. A serious complication of chronic Q fever is endocarditis, generally involving the aortic heart valves, less commonly the mitral valve. Most patients who develop chronic Q fever have pre-existing valvular heart disease or have a history of vascular graft. Transplant recipients, patients with cancer, and those with chronic kidney disease are also at risk of developing chronic Q fever. As many as 65% of persons with chronic Q fever may die of the disease.
The incubation period for Q fever varies depending on the number of organisms that initially infect the patient. Infection with greater numbers of organisms will result in shorter incubation periods. Most patients become ill within 2-3 weeks after exposure. Those who recover fully from infection may possess lifelong immunity against re-infection.
Diagnosis
Because the signs and symptoms of Q fever are not specific to this disease, it is difficult to make an accurate diagnosis without appropriate laboratory testing. Results from some types of routine laboratory tests in the appropriate clinical and epidemiologic settings may suggest a diagnosis of Q fever. For example, a platelet count may be suggestive because persons with Q fever may show a transient thrombocytopenia. Confirming a diagnosis of Q fever requires serologic testing to detect the presence of antibodies to Coxiella burnetii antigens. In most laboratories, the indirect immunofluorescence assay (IFA) is the most dependable and widely used method. Coxiella burnetii may also be identified in infected tissues by using immunohistochemical staining and DNA detection methods.
Coxiella burnetii exists in two antigenic phases called phase I and phase II. This antigenic difference is important in diagnosis. In acute cases of Q fever, the antibody level to phase II is usually higher than that to phase I, often by several orders of magnitude, and generally is first detected during the second week of illness. In chronic Q fever, the reverse situation is true. Antibodies to phase I antigens of C. burnetii generally require longer to appear and indicate continued exposure to the bacteria. Thus, high levels of antibody to phase I in later specimens in combination with constant or falling levels of phase II antibodies and other signs of inflammatory disease suggest chronic Q fever. Antibodies to phase I and II antigens have been known to persist for months or years after initial infection.
Recent studies have shown that greater accuracy in the diagnosis of Q fever can be achieved by looking at specific levels of classes of antibodies other than IgG, namely IgA and IgM. Combined detection of IgM and IgA in addition to IgG improves the specificity of the assays and provides better accuracy in diagnosis. IgM levels are helpful in the determination of a recent infection. In acute Q fever, patients will have IgG antibodies to phase II and IgM antibodies to phases I and II. Increased IgG and IgA antibodies to phase I are often indicative of Q fever endocarditis.
Treatment
Doxycycline is the treatment of choice for acute Q fever. Antibiotic treatment is most effective when initiated within the first 3 days of illness. A dose of 100 mg of doxycycline taken orally twice daily for 15-21 days is a frequently prescribed therapy. Quinolone antibiotics have demonstrated good in vitro activity against C. burnetii and may be considered by the physician. Therapy should be started again if the disease relapses.
Chronic Q fever endocarditis is much more difficult to treat effectively and often requires the use of multiple drugs. Two different treatment protocols have been evaluated: 1) doxycycline in combination with quinolones for at least 4 years and 2) doxycycline in combination with hydroxychloroquine for 1.5 to 3 years. The second therapy leads to fewer relapses, but requires routine eye exams to detect accumulation of chloroquine. Surgery to remove damaged valves may be required for some cases of C. burnetii endocarditis.