In 1986 the U S. Centers for Disease Control and Prevention (CDC) introduced, mainly for epidemiologic and clinical reporting purposes, a system for classifying HfV-induced disease into four major categories: I, acute infection; II, asymptomatic infection; III, persistent generalized lymphadenopathy (PGL); IV, other disease. Only certain listed clinical conditions within group IV qualified to establish the diagnosis of AIDS; groups I, II, and III were regarded as pre-AIDS conditions which may or may not progress to AIDS. Recently, the CDC expanded its definition of AIDS to include HIV-infected persons with CD4+ lymphocyte counts of less than 200 per (jlI. This reflects the reality that most HIV-infected individuals whose CD4+ cell numbers have dropped below 200 per pjul are already showing clinical abnormalities resulting from this degree of immunosuppression and will go on to develop clinical AIDS within the next 2 years. Advancing the diagnosis enables more realistic case recording and early commencement of treatment.
Two to three weeks after infection there is often a brief illness similar to but distinguishable from "mononucleosis. Features include acute-onset fever with or without night sweats, myalgia, arthralgia, lethargy, malaise, diarrhea, depression, lymphadenopathy, sore throat, skin rash and mucocutaneous ulceration, and sometimes neurologic manifestations, often presenting clinically as headache, photophobia, and retroorbital pain. Examination of the blood reveals a temporary reduction in CD4V (and CD8+) T cell count, followed by a predominantly CD8+ lymphocytosis. This illness is often disregarded or misdiagnosed; a high level of clinical suspicion should be triggered if there are relevant lifestyle considerations. Virus, viral nucleic acid, or viral p24 antigen may be detectable during the illness. Seroconversion (development of antibodies) coincides with resolution of the illness or follows shortly thereafter.
With few exceptions, the patient recovers from the primary (seroconversion) illness within 2-3 weeks, and the majority go on to enjoy at least 5 years of relatively good health. PGL, otherwise known as lymphadenopathy syndrome (LAS), may or may not become apparent toward the end of this period but does not have any clear prognostic relevance. Reflecting the polyclonal activation of the immune system, autoimmune conditions may occur during this period. They include the Guillain-Barre syndrome, chronic demyelinat-ing neuropathy, idiopathic thrombocytopenia, Reiter's syndrome, polymyositis, cranial nerve palsy, and Sjogren's syndrome.
When the CD44 T-cell count falls below about 400 per (xl the patient may develop a constellation of constitutional symptoms (fever, night sweats, oral candidiasis, diarrhea, and weight loss) which used to be known as AIDS-related complex (ARC). Early opportunistic infections begin to be seen. At this intermediate stage of immune depletion these infections are generally not life-threatening. They particularly include infections of the skin and mucous membranes such as tinea, seborrheic dermatitis, bacterial folliculitis, warts, molluscum contagiosum, gingivitis, oral and esophageal candidiasis, oral hairy leukoplakia (Fig. 35-10D), and chronic sinusitis. Reactivation of latent herpesviruses, particularly herpes simplex and zoster, also occurs (see Chapter 20). Gastrointestinal infections, caused by any of a wide vanety of organisms, including the yeast Candida albicans and parasites such as Cryptosporidia, are common. Mycobacterial infections are also common in these patients, and this has led to an alarming resurgence of tuberculosis in some countries such as the United States.
When CD4+ T cells drop below 200 per jut,] their numbers generally begin to decline at an accelerated rate, the titer of virus in the blood increases markedly, and the tempo of progression of the illness increases. This stage of HIV infection is associated with more severe opportunistic infections. Particular infections tend to appear at a relatively predictable level of CD44 T cells
(Fig. 35-9). By far the commonest of these opportunistic infections (in the absence of chemoprophylaxis) is pneumonia caused by Pneumocystis carinii, an organism rarely encountered in immunocompetent people (Fig 35-10A). Others include EBV-associated interstitial pneumonitis (particularly in pediatric AIDS), esophageal candidiasis, Cryptosporidia! and microsporidial enteritis, infections with members of the Mycobacterium avium complex, cytomegalovirus retinitis (Fig. 35-10C), enteritis, or encephalitis, and infections of the brain with Toxoplasma gondii or Cryptococcus neoformans.
Malignant tumors may also appear as CD4 cell counts decline. The most common of these, seen mainly in male homosexuals and therefore thought perhaps to be caused by an unknown sexually transmitted agent, is Kaposi's sarcoma (Fig. 35-1 OB). Previously known best as a relatively harmless collection of indolent skin tumors in old people of Mediterranean descent, Kaposi's sarcoma presents in young gay HIV-infected males in a more invasive but slowly progressive form, often quite early in the symptomatic phase of AIDS. Other types of malignancy, notably aggressive B-cell lymphoma or non-Hodgkin's lymphoma, may develop in patients with very low CD4 cell counts; genital cancers are also being increasingly recorded.
Neurologic disease is now recognized to be an extremely common and sometimes the first observed manifestation of HIV infection. The spectrum of HIV-associated neurologic disease includes dementia and its early forms, a severe encephalopathy (especially in children), myelopathy, and motor dysfunction. The patients may notice diminished concentration and memory, together with motor disturbances such as action tremor and loss of balance, as in Parkinson's disease. They often also display signs of coexistent myelopathy and peripheral neuropathy (e.g., ataxia and parasthesia). Other CNS manifestations include cerebral toxoplasmosis, cryptococcal meningitis, primary CNS lymphoma, CMV-associated encephalomyelitis, and progressive multifocal leukoencephalopathy (see Fig. 18-4).
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