opportunistic infection

Opportunistic infections

When someone living with HIV has a weakened immune system (shown by a low CD4 count), they are at risk of other illnesses. These are known as ‘opportunistic infections’ because they take the opportunity of the immune system being weak.

Opportunistic infections include:

• cryptococcal meningitis

• Tuberculosis

• toxoplasmosis

• PCP, a type of pneumonia

• esophageal candidiasis

• Certain cancers, including Kaposi’s sarcoma.

Tuberculosis:

Mycobacterium tuberculosis tends to occur in injection drug users and other groups with a preexisting high prevalence of tuberculosis (TB) infection. Unlike other OIs, TB tends to occur early in the course of HIV infection, usually preceding the diagnosis of AIDS. This early occurrence is associated with the development of caseating granulomas (dry, cheeselike masses of granulation tissue), which should raise the suspicion of TB. At this stage, TB responds well to antituberculosis therapy. TB that occurs late in HIV infection is characterized by absence of an immune response to a tuberculin skin test response. This is known as anergy and results because the compromised immune system can no longer respond to the TB antigen. In the later stages of HIV infection, TB is associated with dissemination to extrapulmonary sites such as the CNS, bone, pericardium, stomach, peritoneum, and scrotum. Multiple drug-resistant strains of the bacillus have emerged and are often associated with noncompliance with antituberculosis therapy.

Oral Candidiasis

 Candidiasis, a fungal infection, occurs in nearly all patients with AIDS and AIDS-related conditions. Commonly preceding other life-threatening infections, it is characterized by creamy-white patches in the oral cavity. Untreated, oral candidiasis progresses to involve the esophagus and stomach. Associated signs and symptoms include difficult and painful swallowing and retrosternal pain. Some patients also develop ulcerating oral lesions and are particularly susceptible to dissemination of candidiasis to other body systems.

Kaposi’s Sarcoma.

 Kaposi’s sarcoma (KS), the most common HIV-related malignancy, is a disease involving the endothelial layer of blood and lymphatic vessels. It is associated with human herpes virus 8 (HHV-8) transmissions (USPHS/IDSA, 2002). When first noted in 1872 by Dr. Moritz Kaposi, KS characteristically presented as lower-extremity skin lesions in elderly men of Eastern European ancestry. This form, referred to as classic Kaposi’s sarcoma, was slow to progress and easily treated. An endemic form of KS, found in children and young men in equatorial Africa, is more virulent than the classic form. Acquired KS occurs in patients who are treated with immunosuppressive agents and commonly occurs in patients who have undergone organ transplantation. In such patients, acquired KS usually resolves once the dose of the immunosuppressive medication is decreased or discontinued. 

In people with AIDS, epidemic KS is most often seen in male homosexuals and bisexuals. Although the histopathology of all forms of KS is virtually identical, the clinical manifestations differ: AIDS-related KS exhibits a more variable and aggressive course, ranging from localized cutaneous lesions to disseminated disease involving multiple organ systems. Cutaneous signs may be the first manifestations of HIV, appearing in more than 90% of HIV-infected patients as immune function deteriorates. These skin signs correlate to low CD4 counts. Some disorders, such as Kaposi’s sarcoma, oral hairy leukoplakia, facial molluscum contagiosum, dry skin, and oral candidiasis, indicate CD4 counts at or below 200 to 300.

Cutaneous lesions appearing anywhere on the body are usually brownish pink to deep purple. They may be flat or raised and surrounded by ecchymoses (hemorrhagic patches) and edema. Rapid development of lesions involving large areas of skin is associated with extensive disfigurement. The location and size of some lesions can lead to venous stasis, lymphedema, and pain. Ulcerative lesions disrupt skin integrity and increase discomfort and susceptibility to infection. The most common sites of visceral involvement include the lymph nodes, GI tract, and lungs. Involvement of internal organs may eventually lead to organ failure, hemorrhage, infection, and death. Diagnosis of KS is confirmed by biopsy of suspected lesions. Prognosis depends on the extent of the tumor, presence of constitutional symptoms, and CD4 count. Death may result from tumor progression. More often, however, it results from other complications of HIV infection.

 Management of KS is usually difficult because of the variability of symptoms and the organ systems involved. KS is rarely life-threatening except when there is pulmonary or GI involvement. The treatment goal is reduction of symptoms by decreasing the size of the skin lesions, reducing discomfort associated with edema and ulcerations, and controlling symptoms associated with mucosal or visceral involvement. No one treatment has been shown to increase survival. Localized treatment includes surgical excision of the lesions or application of liquid nitrogen to local skin lesions and injections of intraoral lesions with dilute vinblastine. Injection of intraoral lesions has been associated with local pain and skin irritation. Radiation therapy is effective as a palliative measure to relieve localized pain due to tumor mass (especially in the legs) or for KS lesions that are in sites such as the oral mucosa, conjunctiva, face, and soles of the feet. Interferon is known for its antiviral and antitumor effects. Patients with cutaneous KS treated with alpha-interferon have experienced tumor regression and improved immune system function. Positive responses have been observed in 30% to 50% of patients, with the best responses seen in those with limited disease and no OIs. Alpha-interferon is administered by the IV, intramuscular, or subcutaneous route. Patients may self-administer interferon at home or receive it in an outpatient setting.

Mycobacterium avium Complex. 

Mycobacterium avium complex (MAC) disease is a leading OI in people with AIDS. Organisms belonging to MAC include M. avium, M. intracellulare, and M. scrofulaceum. MAC, comprising a group of acid-fast bacilli, usually causes respiratory infection but is also commonly found in the GI tract, lymph nodes, and bone marrow. Most patients with AIDS who have T-cell counts less than 100 have widespread disease at diagnosis and are usually debilitated. MAC infections are associated with rising mortality rates.

Wasting Syndrome. 

Wasting syndrome is part of the category C case definition for AIDS. Diagnostic criteria include profound involuntary weight loss exceeding 10% of baseline body weight and either chronic diarrhea for more than 30 days or chronic weakness and documented intermittent or constant fever in the absence of any concurrent illness that could explain these findings. This protein-energy malnutrition is multifactorial. In some AIDS-associated illnesses, patients experience hypermetabolic state in which excessive calories are burned and lean body mass is lost. This state is similar to that seen in sepsis and trauma and can lead to organ failure. A distinction between cachexia (wasting) and malnutrition or between cachexia and simple weight loss is important because the metabolic derangement seen in wasting syndrome may not be modified by nutritional support alone.

Anorexia, diarrhea, GI malabsorption, and lack of nutrition in chronic disease all contribute to wasting syndrome. Progressive tissue wasting, however, may occur with only modest GI involvement and without diarrhea. Tumor necrosis factor (TNF) and interleukin-1 (IL-1) are cytokines that play important roles in AIDS-related wasting syndrome. Both act directly on the hypothalamus to cause anorexia. Cytokine-induced fever accelerates the body’s metabolism by 14% for every 1°F increase in temperature. TNF causes inefficient use of lipids by reducing enzymes that are needed for fat metabolism, whereas IL-1 triggers the release of amino acids from muscle tissue. People with AIDS generally experience increased protein metabolism in relation to fat metabolism, which results in significant decreases in lean body mass due to muscle and protein breakdown. Hypertriglyceridemia, seen in people with AIDS and attributed to chronically elevated cytokine levels, can persist in people