Mycobacterium avium infection and AIDS: a therapeutic dilemma in rapid evolution

Article Abstract:

Mycobacterium avium (M. avium) is a bacteria that causes a lung disease that is similar to tuberculosis. It is one of the most common types of bacterial infection in patients with AIDS, and it has been reported to cause death in some of these patients. It is estimated that 18 to 27 percent of the patients infected with the human immunodeficiency virus (HIV, which causes AIDS) are also infected with M. avium. Studies that have examined AIDS patients after they have died have reported that almost 50 percent of the patients had infections due to M. avium. This infection can spread to many different parts of the body including the liver, kidneys, spleen, bone marrow, lymph glands, stomach, intestines, muscles and brain. The most common symptoms of infection are fever, sweating, loss of appetite, weight loss and weakness. Infection with M. avium is diagnosed by testing blood samples for the presence of the bacteria. To determine if the infection is spreading throughout the body, tissue samples are taken from the lymph nodes, bone marrow and liver for further examination. Antibiotic drugs used to treat infections caused by M. avium include isoniazid, clofazimine, ciprofloxacin, ethambutol, amikacin, rifabutin and rifampin. It is common practice to treat infected patients with three or more of these drugs simultaneously because none of the drugs is effective when given alone. A recent study reported improvement in 19 of 20 AIDS patients with M. avium infections who were treated with a combination of amikacin, ciprofloxacin, ethambutol, rifampin, and clofazimine. The use of more than one drug reduces the required dose of each drug, minimizes the severity of side effects, and reduces the chance that the bacteria will become resistant to (not killed by) the drugs. (Consumer Summary produced by Reliance Medical Information, Inc.)

Risk factors, Mycobacterial infections, Mycobacterium infections, Mycobacterium avium

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Successful foscarnet therapy for cytomegalovirus retinitis in an AIDS patient undergoing hemodialysis: rationale for empirical dosing and plasma level monitoring

Article Abstract:

The virus that causes AIDS attacks and destroys cells in the immune system, the body's natural defense system for fighting infection. This explains why patients with AIDS are so susceptible to infections. Cytomegalovirus (CMV) retinitis (inflammation of the retina) is a type of eye infection that is estimated to occur in five percent of patients with AIDS. Ganciclovir has been reported to be effective in treating CMV retinitis in 81 to 97 percent of the AIDS patients. However, many patients suffer a relapse within eight weeks and others develop neutropenia (abnormally low number of white blood cells) as a result of ganciclovir treatment. Foscarnet is another antiviral drug that may be useful for treating CMV retinitis, but it is toxic to the kidneys; it is estimated to cause kidney damage in 20 to 50 percent of patients. In addition, foscarnet can cause anemia (abnormally low number of red blood cells), muscle twitching and nausea. However, foscarnet may be useful for treating AIDS patients who already have advanced stage kidney disease and can not be treated with ganciclovir. This article describes the case of a 32-year-old black man with AIDS who developed kidney failure. As a result, the patient was dependent on hemodialysis. Two years after beginning dialysis treatment he developed CMV retinitis. The retinitis stabilized during 14 weeks of foscarnet therapy. However, the patient developed several other AIDS-related complications during that period and died. The authors suggest that foscarnet may be a useful alternative for treating CMV retinitis in AIDS patients who are receiving hemodialysis. (Consumer Summary produced by Reliance Medical Information, Inc.)

Infection, Cytomegalovirus infections, Eye

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Altered sensitivity to antiviral drugs of herpes simplex virus isolates from a patient with the acquired immunodeficiency syndrome

Article Abstract:

Human immunodeficiency virus (HIV) is the causative agent of AIDS. Individuals with HIV infection have suppressed immune systems and are at greater risk for developing opportunistic infections. Herpes simplex virus (HSV) is a common infection among patients with HIV, and acyclovir is the usual treatment for HSV infection in these patients. For acyclovir to work, it must be activated by an enzyme called thymidine kinase (TK), which is present in the virus. However, some mutant strains of HSV lack the TK enzyme, and thus are not killed by acyclovir. These strains of HSV are called acyclovir-resistant. Acyclovir-resistant HSV type 2 (HSV-2) was isolated from a 24-year-old female patient with AIDS. The patient had no prior history of intravenous drug use, blood transfusions or herpes genitalis (genital herpes). She was treated with acyclovir, intermittently, for five months. During the initial stages of acyclovir therapy the genital lesions responded to the treatment, but did not heal completely. When HSV-2 was isolated from the patient and grown in culture, the combination of acyclovir and interferon reduced viral replication by greater than 97 percent. However, when administered to the patient, the combination of acyclovir and interferon only resulted in partial clinical improvement. Intravenous treatment with foscarnet for 10 to 12 days controlled severe ulceration of the lesions, but clinical improvement only lasted for 6 months. When HSV-2 infection recurred, the HSV-2 was resistant to both acyclovir and foscarnet. (Consumer Summary produced by Reliance Medical Information, Inc.)

Case studies, Genetic aspects, Drug resistance in microorganisms, Microbial drug resistance, Herpes genitalis, Genital herpes, Acyclovir, Herpesviruses

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