The preferred antitubercular regimen in susceptible cases consists of an initial 2-month treatment with four drugs (isoniazid, rifampin, pyrazinamide, and either ethambutol or streptomycin) followed by a 4-month phase of isoniazid and rifampin. Total treatment time is typically 6 months. If the local prevalence of isoniazid resistance is less than 4%, and the patient is not from an area with a high prevalence of drug resistance, then ethambutol (or streptomycin) may be withheld from the first phase. If cultures show that the organism is fully drug susceptible, then the ethambutol (or streptomycin) may be discontinued.Prior to the initiation of therapy, patients should have sufficient material obtained for culture to particularly ensure that susceptibility testing can be undertaken. In addition, baseline laboratory studies should be performed, including measurement of liver-associated enzymes, total bilirubin, and a complete blood cell count. All patients diagnosed with tuberculosis should be offered HIV testing. If treatment with pyrazinamide is considered, a baseline uric acid level should be obtained, and if ethambutol is to be used, both visual acuity and color perception should be evaluated.
Directly Observed TherapyStudies have shown that clinicians are unable to predict patient compliance. Patient compliance is one of the key factors in treatment success and in the prevention of drug resistance. Directly observed therapy implies that a health care provider is present when the patient takes the medications. Although labor intensive, directly observed therapy is effective, especially when intermittent dosing regimens are chosen. It may take place in an office or clinic setting, or may consist of outreach workers who travel to the patient’s residence. If the patient remains noncompliant with therapy, the local health department should be contacted to mobilize additional resources.
HIV InfectionTreatment of tuberculosis in the HIV-infected patient is complicated by drug interactions, particularly for patients on antiretroviral therapy. The administration of rifampin with certain protease inhibitors and non-nucleoside reverse transcriptase inhibitors can cause elevations in levels of rifampin, and sub-therapeutic levels of the antiretroviral agents. One should not discontinue antiretroviral therapy so that rifampin can be used to treat tuberculosis. Instead, rifabutin can be substituted for rifampin and used in combination with the protease inhibitors indinavir or nelfinavir as well as most available non-nucleoside reverse transcriptase inhibitors. Rifabutin should not be used with the protease inhibitor ritonavir or the non-nucleoside reverse transcriptase inhibitor delavirdine. If a regimen that does not contain rifabutin or rifampin is desired, a regimen consisting of isoniazid, pyrazinamide, and streptomycin for 9 months, with ethambutol added for the first 2 months, is recommended. Given the complexities of antiretroviral therapy and the potential for drug interactions, patients with HIV infection and tuberculosis should be referred to clinicians who are experienced in the treatment of both infections.
PregnancyPregnant women diagnosed with tuberculosis should be treated promptly. The preferred initial regimen is isoniazid, rifampin, and ethambutol. Streptomycin should not be used because of known teratogenic effects. The safety of pyrazinamide in pregnancy is unknown, and this drug should be avoided. Once the organism is known to be susceptible, ethambutol can be discontinued. The duration of treatment with regimens without pyranzinamide is typically 9 months.*62/348/5*
Archive for the ‘Anti-Infectives’ Category
The viruses that cause influenza are genetically unstable. They change both gradually and abruptly, and each change may enable the virus to skirt around previously acquired immunity, invade the respiratory tract, and cause the flu. This genetic instability is why people can get influenza over and over again, why they get it some years and not others, why some attacks make them much sicker than others, and why it’s necessary to get a new flu shot every year for maximum protection.
The gradual changes in the virus, called antigenic drift, may or may not be enough to override most people’s immunity to it. But when the abrupt changes known as antigenic shift occur, large numbers of people—and sometimes the entire population—have no protection. Such shifts usually result in worldwide epidemics, or pandemics, and, when they involve type A flu viruses, they are often highly lethal.
Type A flu viruses have two major antigens on their surface called H and N (the “H” stands for hemagglutinin and the “N” for neuraminidase). When they encounter a person’s immune system, these antigens trigger the production of antibodies that protect the person against the viral infection. When major changes occur in H and/or N, most people have no preexisting antibody protection, and so they are susceptible to an invasion by the new form of the virus. The following table shows the major shifts that have occurred in the type A influenza virus during this century. The pandemics are usually named for the area where the virus was first isolated.
There is evidence that during the last decade of the nineteenth century, a type A virus very similar to the H2N2 Asian flu virus prevailed, and that during the first seventeen years of the twentieth century a virus similar to the H3N2 Hong Kong virus was the primary troublemaker.
The Spanish flu A-H1N1 virus that first appeared in 1918 lingered in the population until 1957, when the Asian virus, A-H2N2, emerged and supplanted it. However, in 1977 a virus reappeared that was virtually identical to the A-H1N1 that had circulated at least until 1950. Most people born before 1950 had immunity to the 1977 virus, but those who were younger or who had missed being exposed to the original cause of Spanish flu had no natural protection, and many became very ill.
In 1992, the type A virus genetically rearranged some of its attire, but did not do a total costume switch. A variant known as Beijing arose, an A-H3N2 virus that was a kissing cousin of the A-H3N2 virus that caused the Hong Kong flu in 1968. Thus, many people had at least a partial immunity to it because they had encountered its close relative in the past. In the 1994-95 flu season, yet another A-H3N2 virus called Shandong was a leading troublemaker.
What will come along next is anybody’s guess. But the nation’s flu watchers are always on guard, and as soon as any new variant arises that causes a significant outbreak of influenza anywhere in the world, the manufacturers of flu vaccine will be ready to add it to their mix.
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The clinical hallmarks of acute viral encephalitis include fever, headache, and an altered level of consciousness. Other common clinical findings include behavioral changes, speech disturbances, and focal or diffuse neurologic signs such as seizure or hemiparesis.
Establishing a diagnosis of viral encephalitis may be difficult, so clinicians should inquire about certain epidemiologic features:
- Season of the year
- Prevalent diseases within the community
- History of travel
- Recreational activities
- Occupational exposures
- Animal contacts (insects or animal bites)
The use of neurodiagnostic tests, including electroencephalogram
(EEG), computed tomographic scan, and magnetic resonance imaging (MRI), can provide useful information in the evaluation of encephalitis. Although only herpes simplex encephalitis has specific treatment, the confirmation of other viral causes can provide helpful prognostic information and minimize unnecessary and ineffective therapies. Evaluation and management of acute viral encephalitis can be complex, and practitioners should seek consultation with an infectious diseases specialist for assistance.
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In everyday life, perhaps no ailment is as bothersome as the common cold, with its irritating symptoms of runny nose, itchy eyes, and generally uncomfortable sensations. Colds are responsible for more days lost from work and more uncomfortable days spent at work than any other ailment.
Caused by any number of viruses (some experts claim there may be over 100 different viruses responsible for the common cold), colds are endemic (always present to some degree) among peoples throughout the world. Current research indicates that otherwise healthy people carry cold viruses in their noses and throats most of the time. These viruses are held in check until the host’s resistance is lowered. In the true sense of the word, it is possible to “catch” a cold – from the airborne droplets of another person’s sneeze or from skin-to-skin or mucous membrane contact – though recent studies indicate that the hands may be the greatest avenue of colds and transmission of other viruses. Obviously, then, covering your mouth with a tissue or handkerchief when sneezing is better than covering it with your bare hand, particularly if you next use your hand to touch food in a restaurant, shake your friend’s hand, or open the door.
Although numerous theories exist concerning how to “cure” the common cold, including the ingestion of mega-doses of vitamin C, little hard evidence supports any of them. The best rule of thumb is to keep your resistance level high. Sound nutrition, adequate rest, stress reduction, and regular exercise appear to be the best bets in helping fight off infection. Also, avoiding people with newly developed colds (colds appear to be most contagious during the first 24 hours of onset) is advisable. Once you contract a cold, bed rest, plenty of fluids and aspirin for relief of pain and discomfort are the tried-and-true remedies for adults. Children should not be given aspirin for colds or the flu because of the possibility that this may lead to a potentially fatal disease known as Reye’s syndrome. Several over-the-counter preparations have proved effective for alleviating certain cold symptoms.
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