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HIV, the cause of the well-known AIDS, can rightly be included as one of the clinical masquerades of modern medicine. Public health measures in the Western world have limited the spread of the infection. By contrast, the incidence in Africa and Asia continues to rise at an alarming rate. The World Health Organization estimated that in 2010,1 34 million adults and children were living with HIV, including 23 million in sub-Saharan Africa and 25 000 in Australia, with 2.7 million newly infected and increasing, while 1.8 million people with HIV died. However, this figure reduced to 1.1 million in 2015.
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In 2012, the average age of people newly diagnosed with HIV infection was 37 years and about 86% were male; most infections are in men who have sex with men (MSM). The conversion rate of HIV to AIDS has been 33% but it is improving with antiretroviral therapy (ART), which has dramatically changed people’s lives. HIV is now a chronic disease management problem. The introduction of combination treatment with the protease inhibitors in November 1995 changed the previously understood natural history of the disease.
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The benefit of early diagnosis has become even more impressive since the discovery that HIV is not a latent infection throughout most of its course. Soon after initial infection, an explosive replication of HIV occurs, which is brought under control by the immune system in 6 to 8 weeks as the host-versus-virus interaction reaches an active and dynamic equilibrium. This dynamic situation continues throughout a person’s lifetime, with as many as 10 billion new viroids produced and up to 2 billion CD4 T lymphocytes destroyed and replaced daily. Clinical immunodeficiency develops when the body’s ability to replace CD4 cells is finally exhausted, resulting in further uncontrolled viral replication. Viral load assays based on molecular techniques have revolutionised our understanding of the natural history of HIV disease. These advances make it imperative to make the diagnosis early in the course of the disease in order to start combination treatment to lessen the viral load.
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The management of HIV infection is a specialised field but the GP is central in prevention, diagnosis, counselling, monitoring and shared management of HIV disease. The GP must be alert to the benefits of early diagnosis as summarised in TABLE 27.1.
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Key facts and checkpoints
HIV is a retrovirus with two known strains that cause a similar spectrum of syndromes: HIV-1 and HIV-2 (mainly confined to West Africa). It infects T-helper cells bearing the CD4 receptor.
Always consider HIV in those at risk: enquire about history of STIs, injection of illicit drugs, past blood transfusions, sexual activities and partners.
About 50% of patients develop an acute infective illness similar to glandular fever within weeks of acquiring the virus (the HIV seroconversion illness).1 The main features are fever, lymphadenopathy, lethargy and possibly sore throat, and a generalised rash.
If these patients have a negative infectious mononucleosis test, perform an HIV antibody test, which may have to be repeated in 4 weeks or so if negative.
Patients invariably recover to enter a long period of good health for 5 years or more.2
The so-called ‘set point’ is where the plasma viral load drops to a steady level for many years.
Pneumocystis jiroveci (ex carinii) pneumonia (PJP) is the commonest presentation of AIDS.
Approximately 15–40% of HIV-positive children are infected from HIV-infected mothers.3
Infants born to these mothers may develop the disease within a few months, with 30% affected by the age of 18 months.
The time for the onset of AIDS in HIV-affected adults varies from 2 months to 20 years or longer; the median time is around 10 years.
In family practice the most common presentation of HIV-related illness is seen in the skin/oral mucosa, for example, candidiasis and herpes.4
TB is a common, serious but treatable complication of HIV.
HIV antibody testing is a two-stage process: the antigen–antibody test for screening followed by another method (e.g. Western blot) if positive.
New rapid HIV tests or point of care HIV tests will overcome barriers, including delays to diagnosis.
The seroconversion period from acquiring HIV infection to a positive antibody test varies between individuals: this period is known as the ‘window period’.
All HIV-infected patients require regular monitoring for immune function and viral load. The viral load test monitors viral activity.
The level of immune depletion is best measured by the CD4 positive T-lymphocyte (helper T-cell) count—the CD4 cell count. The cut-off points for good health (asymptomatic) and severe disease appear to be 500 cells/μL and 200 cells/μL respectively.2
Most patients with AIDS will need lifelong1 daily medication with a combination of antiretroviral drugs.
Current management focuses on treating HIV as a chronic disease.
A leading concerning cause of death is cardiovascular disease.
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Occurrence and transmission
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HIV can be isolated from blood, tissues, semen, saliva, breast milk, cervical and vaginal secretions and tears of infected persons. HIV is transmitted in semen, blood and vaginal fluids, transplanted organs and breast milk through:
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unprotected sexual intercourse (anal or vaginal) and in rare cases oral sex with an infected person
infected blood entering the body (through blood transfusion or by IV drug users sharing needles/syringes)
needle-stick injury
artificial insemination, organ transplantation
infected mothers (to babies during pregnancy, at birth or in breast milk)
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Infection with HIV can occur via the vagina, rectum or open cuts and sores, including any on the lips or in the mouth. Social (non-sexual) contact and insect vectors have not been implicated in transmission.
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The clinical stages of HIV disease are summarised in TABLE 27.2.6
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Acute (seroconversion) illness
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At least 50% of patients have an acute illness associated with seroconversion. The illness usually occurs within 6 weeks of infection and is characterised by fever, night sweats, malaise, severe lethargy, anorexia, nausea, myalgia, arthralgia, headache, photophobia, sore throat, diarrhoea, lymphadenopathy, generalised maculoerythematous rash and thrombocytopenia. The main symptoms are headache, photophobia and malaise/fatigue. Neurological manifestations, including meningoencephalitis and peripheral neuritis, can occur. Acute HIV infection should be considered in the differential diagnosis of illnesses resembling glandular fever. This illness, which resembles infectious mononucleosis, is self-limiting and usually resolves within 1 to 3 weeks. However, chronic lethargy, depression and irritability may persist after the acute illness. Non-specific viraemic sequelae such as mucosal ulceration, desquamation, exacerbation of seborrhoea and recurrences of herpes simplex may occur (see FIG. 27.1).
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Acute illness may be accompanied by neutropenia, lymphopenia, thrombocytopenia, and mildly elevated ESR and serum transaminases. During recovery lymphocytosis may occur with appearance of atypical mononuclear cells and an inversion of the CD4+:CD8+ ratio due to elevation of CD8+ cells. It is seronegative for EBV.
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Differential diagnoses are given in TABLE 27.3.
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DxT fever + severe malaise + lymphadenopathy ➜ acute HIV
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After the acute illness, HIV disease passes into an asymptomatic stage of variable length, up to several years, but 30% have persistent generalised lympathenopathy.
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Later constitutional symptoms develop along with minor opportunistic infections such as oral candidiasis, herpes simplex and herpes zoster. This early symptomatic stage is referred to as AIDS-related complex and is regarded as a prodromal to AIDS.
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AIDS-defining conditions
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The original US Centers for Disease Control (CDC) classification has been modified with time to provide a more simplified scheme for defining AIDS. The HIV/AIDS case surveillance system simply specifies a list of clinical conditions associated with the late stages of HIV infection as being ‘AIDS-defining’.7
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The AIDS-defining conditions are:
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candidiasis of bronchi, trachea or lungs
candidiasis, oesophageal
cervical cancer, invasive
coccidioidomycosis, disseminated or extrapulmonary
cryptococcosis, extrapulmonary
cryptosporidiosis, chronic intestinal (>1 month’s duration)
cytomegalovirus (CMV) disease (other than liver, spleen or nodes)
CMV retinitis (with loss of vision)
encephalopathy, HIV-related
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herpes simplex virus (HSV): chronic ulcer(s) (>1 month’s duration); or bronchitis, pneumonitis or oesophagitis
histoplasmosis, disseminated or extrapulmonary
isosporiasis, chronic intestinal (>1 month’s duration)
Kaposi sarcoma
lymphoma, Burkitt (or equivalent term)
lymphoma, immunoblastic (or equivalent term)
lymphoma, primary, of brain
Mycobacterium avium complex of M. kansasii, disseminated or extrapulmonary
Mycobacterium tuberculosis, any site (pulmonary or extrapulmonary)
Mycobacterium, other species or unidentified species, disseminated or extrapulmonary
Pneumocystis jiroveci pneumonia (PJP)
Salmonella septicaemia, recurrent
toxoplasmosis of brain
wasting syndrome due to HIV
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The Australian AIDS surveillance case definition does not refer to the CD4 cell count although in the US AIDS is also defined by a CD4 cell count of <200/μL, regardless of clinical condition. At levels below this, people will become increasingly vulnerable to AIDS-defining conditions.