30: Human immunodeficiency virus infection, AIDS and infections in compromised patients

Chapter 30 Human immunodeficiency virus infection, AIDS and infections in compromised patients

Human immunodeficiency virus infection and acquired immune deficiency syndrome

By the end of 2008, an estimated 33.4 million people worldwide were living with human immunodeficiency virus (HIV) infection. That same year, some 2 million people died of acquired immune deficiency syndrome (AIDS)-related illnesses, and in total, 20 million globally have died of AIDS and related illnesses thus far. Globally, less than one person in five at risk of HIV has access to basic HIV prevention services. Only 36% of people who needed HIV treatment had access to it by the end of 2009.

Although HIV infection is now a global pandemic, AIDS was only described in 1981, in young homosexual men in the USA. However, the disease appears to have originated in Africa, where cases have been revealed from as long ago as 1959. The virus causes depletion of CD4+ T-helper lymphocytes over many years; as a consequence of which, patients succumb to opportunistic infections, particularly Pneumocystis carinii pneumonia (PCP) and oral candidiasis, and neoplasms, especially Kaposi’s sarcoma.

After infection with HIV, there is a prolonged asymptomatic period that may last up to 10 years, but the risk of developing severe immunodeficiency and AIDS increases with time. Thus, the clinical spectrum of HIV infection is broad, ranging from asymptomatic or mild infection to severe clinical illness and profound immunodeficiency. The variety of clinical manifestations seen in AIDS has spawned a number of definitions of the disease. However, the US Centers for Disease Control and Prevention has rationalized and revised these to include all patients with CD4+ cell counts of less than 200 per microlitre.

The battle to conquer HIV infection and AIDS is fought on many fronts, consuming millions of dollars, and thus far all efforts at producing a preventive vaccine have failed. However, the introduction of new antiviral regimens such as highly active antiretroviral therapy (HAART) has increased life expectancy in HIV infection and dramatically reduced complications, suppressing viral replication to undetectable levels.

The impact of HIV and AIDS on the practice of clinical dentistry has been enormous; first, because of the regimentation in infection control it has spawned throughout the profession, and second, because of the many oral manifestations and their management, of which the practising dentist has to be aware.

Definitions

• HIV infection: infection with the HIV – an RNA retrovirus.
• HIV disease: the resulting immunodeficiency and the appearance of attendant diseases (i.e. not all HIV-infected persons will have symptomatic disease).
• AIDS: a term given to a group of disorders characterized by a profound cell-mediated immunodeficiency consequential to irreversible suppression of T lymphocytes by the HIV. These disorders are called AIDS-defining illnesses and include parameters such as CD4 lymphocyte count below 200 × 106/l, oropharyngeal candidiasis, hairy leukoplakia, etc. (Table 30.1).

Table 30.1 Centers for Disease Control classification of HIV infection

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Retroviridae

HIV is a lymphotrophic virus that belongs to the family Retroviridae. The latter RNA viruses comprise a single taxonomic group made up of three subfamilies:

• Lentiviruses cause slowly progressive disease and are cytopathic in nature; they include HIV-1 and HIV-2.
• Oncoviruses include those that cause tumours: human T cell leukaemia virus type I (HTLV-I) that causes adult T cell leukaemia–lymphoma (ATLL); and HTLV-II, associated with hairy cell leukaemia.
• Spumaviruses are not recognized human pathogens.

Human immunodeficiency virus

The virus has a diameter of 100 nm, and its structure is described below. There are two types: HIV-1 is the most prevalent; HIV-2 is a variant that originated in West Africa and has spread to Central Africa, Europe and South America. Type 1 is classified into two major groups: M, containing 10 genetically distinct subtypes (A–J), and O, containing a heterogeneous collection of viruses. Type 2 HIV, except for its antigenic and nucleic acid profile, has similar biological properties to HIV-1.

The structure of HIV is shown in Figure 30.1. It consists of:

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Fig. 30.1 Human immunodeficiency virus. (A) Structure; (B) scanning electron micrograph of virions showing the pyramid-shaped central core.

1. an envelope containing virus-specific ‘coat’ proteins (e.g. glycoproteins gp41 and gp120), which can act as antigens. Glycoprotein gp120 has a ‘rugger-ball’ configuration and plays an important role in the initial events leading to infection. These coat proteins undergo almost continuous structural changes, which hamper the development of effective vaccines
2. three core proteins, of which p24 is especially antigenic: antibodies to this form the basis of most serological testing (the HIV test)
3. a genome of RNA comprising two identical molecules of single-stranded RNA
4. two molecules of an enzyme, reverse transcriptase (an RNA-dependent DNA polymerase), essential for transcribing the RNA code of the virus to a DNA code during viral multiplication (so that it may integrate into the host cell DNA).

Stability of HIV

The survival of HIV under varying conditions has been investigated.

• HIV is destroyed by heat (autoclave and hot-air oven); the virus is inactivated by a factor of 100-fold each hour at a temperature over 60°C.
• The virus may survive up to 15 days at room temperature and at body temperature (37°C).
• HIV is totally inactivated (>105 units of infectivity) by exposure for 10 min at room temperature to the following disinfectants: 2% glutaraldehyde, sodium hypochlorite (10 000 ppm available chlorine, equivalent to 1 : 10 dilution of domestic bleach), 50% ethanol, 35% isopropanol or 0.3% hydrogen peroxide.
• When HIV is present in clotted blood in a syringe or other material, exposure to undiluted bleach for at least 30 s is necessary for its inactivation.

Important: the above figures indicate the limits of survival at very high starting concentrations of HIV (up to 1000 times more than the levels found in the blood of patients) under experimental conditions. Also, the efficacy of the mentioned disinfectants is affected by a variety of factors such as the associated organic bioburden. Hence, care and strict adherence to protocols are essential when dealing with HIV.

Viral replication

See Chapter 10.

Transmission of HIV

The virus is most commonly acquired by having sex with an infected partner. The virus can enter the body through the lining of the vagina, vulva, penis, rectum or mouth during sex. The infection can also be transmitted by exchange of infected blood, or other body fluids such as breast milk, and is not transmitted by social or casual, non-sexual contact. Currently, heterosexual sex is the major mode of transmission worldwide. Other notable transmission modes include sharing of needles, vertical transmission in utero, breast-feeding and transfusion of infected blood or blood products (factor VIII concentrate). Occasional cases of HIV infection result from needlestick injuries in health care settings. The question of HIV transmission among health care workers, including dentists, is addressed at the end of this chapter.

Saliva and HIV transmission

There is only a very slim possibility that HIV may be transmitted by saliva, for the following reasons.

1. Only a small minority of HIV-infected individuals harbour the virus in whole saliva (e.g. in one study, HIV was detected in mixed saliva of 5% of infected individuals and in only 1 of 15 parotid saliva samples). In any case, HIV virions cannot exist in a cell-free state in saliva, and estimates are that there is less than one infectious particle of HIV per millilitre of mixed saliva.
2. Saliva contains immunoglobulin A (IgA) group antibodies to HIV proteins (p24, gp120, gp160), which may neutralize the infectivity of the virus and are the basis of salivary kits used for HIV-testing in epidemiological studies.
3. Other HIV-inhibitory factors in saliva include high-molecular-weight mucins thought to entrap the virus, proline-rich proteins and a serine protease inhibitor termed salivary leukocyte protease inhibitor (SLPI). SLPI possibly blocks cell surface receptors needed for entry of HIV into cells.
4. The virus loses its infectivity when exposed to mixed saliva for 30 min.
5. Animal studies have shown that it is not possible to transmit HIV by surface application of the virus on the oral mucosa, although it was transmitted in this manner through vaginal mucosa.
6. The dose of HIV required for infection is far higher than that for hepatitis B virus (the risk of acquiring hepatitis B infection from a contaminated needlestick injury is 6–30%, compared with a 0.4% risk of contracting HIV infection).

Epidemiology

The main groups of individuals affected are:

• promiscuous individuals, both homosexuals and heterosexuals: 75% of all infection has been acquired through sexual intercourse; the current male-to-female ratio is 3 : 2 (infections in homosexuals were levelling off due to increased awareness of the disease and safe sex practices, but a recent increase has been reported)
• injecting drug abusers: some 10% of infection globally; 26% in the USA
• persons receiving blood or blood products: about 1% globally (mainly a problem of the developed world)
• offspring of infected mothers: varying transmission rates reported, 10–50%; most infection acquired at birth, with a few in utero and breast-feeding accounting for the rest.

The global pandemic

As mentioned above, by the end of 2008, an estimated 33.4 million people worldwide were living with HIV, and some 20 million have died of HIV infection or related illnesses since the beginning of the epidemic: one person is infected with HIV every 6.4 s. Of those succumbing to AIDS, 90% are living in developing countries, especially in Asia and Africa. The estimated annual increase worldwide is about 20%, but this varies widely in different geographic locales. For instance, the annual increase is about 11% in the Americas, 26% in Africa and 167% in Asia, indicating the staggering explosion of the disease in the latter region. India is the new epicentre of the disease, and it is estimated that by 2010, some 20 million Indians will be infected with HIV. This reflects to a great extent the close link between the disease and the economic, social and cultural issues and taboos in each region.

Currently, HIV infection is the leading cause of death in US men aged 25–44 year. In some countries, such as the Ivory Coast, HIV/AIDS is the leading cause of death; and in Uganda, it causes 80% of deaths in adults aged 20–39 years.

Acquired immune deficiency syndrome

Natural history of the disease

AIDS is an insidious disease, characterized by opportunistic infections (fungal, viral and mycobacterial), malignancies (especially Kaposi’s sarcoma and lymphomas that may be virally induced) and autoimmune disorders (Fig. 30.2).

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Fig. 30.2 Key events in HIV infection. PGL, persistent generalized lymphadenopathy.

The average time to development of AIDS is 8–11 years in most adults in the developed world, and much less in the developing world due to aggravating cofactors such as malnutrition and intercurrent infection (e.g. malaria). A few individuals (some 2%) have not developed AIDS despite antibody positivity. Overall, almost half of those diagnosed with AIDS will die. Untreated, the median survival is about 1 year from the time of diagnosis, and 95% will die within 5 years.

Mean time for seroconversion after exposure to HIV is 3–4 weeks, with the onset of an acute seroconversion illness similar to glandular fever. Most will have antibodies within 6–12 weeks after infection and virtually all will be positive within 6 months. Symptoms of such seroconversion include fever, malaise, rash, oral ulceration and, occasionally, encephalitis and meningitis. In some, the disease may then become quiescent and asymptomatic for several years (range 1–15 years or more) for reasons yet unknown. Some of them may have persistent generalized lymphadenopathy (PGL), where the enlarged lymph nodes are painless and asymmetrical in distribution and involve submandibular and neck nodes. In the HIV disease classification, patients with these symptoms are categorized as group A (Table 30.1).

Progressive disease leads to other features, including fatigue, fever, weight loss, candidiasis, diarrhoea, hairy leukoplakia, herpes zoster and perianal herpes, and these illnesses are sometimes referred to as the AIDS-defining complex. Patients with these symptoms and signs of progressive illness are categorized as group B.

Finally, a percentage of HIV-infected individuals develop full-blown AIDS (50–70% depending on drug therapy and other associated cofactors; median life expectancy is 18 months). These individuals are in group C. The AIDS-defining conditions are subdivided into opportunistic infections and secondary neoplasms, and include Kaposi’s sarcoma, PCP and many other exotic infections (Table 30.2).

Table 30.2 Opportunistic infections, neoplasms and miscellaneous complications of HIV disease

Opportunistic infections  
Mucocutaneous Human herpesviruses
  1, 2, 3, 4, 5, 8
  Human papillomaviruses
  Molluscum contagiosum
  Non-tuberculous mycobacteria
  Candida albicans
  Staphylococcus aureus
  Histoplasmosis
Gastrointestinal Cryptosporidiosis
  Microsporidiosis
  Isosporiasis
  Giardiasis
Respiratory Pneumocystis carinii
  Aspergillosis
  Candidosis
  Cryptococcosis
  Histoplasmosis
  Zygomycosis (mucormycosis)
  Strongyloidosis
  Mycobacteria, including tuberculosis
  Staphylococcus aureus
  Streptococcus pneumoniae
  Haemophilus influenzae
  Toxoplasmosis
  Cytomegalovirus (CMV)
Meningitis Creutzfeldt–Jakob agent
Encephalitis Papovaviruses
  Cryptococcus neoformans
  Toxoplasma gondii
Neoplasms  
  Kaposi’s sarcoma
  Lymphoma
  Squamous cell carcinoma
  Leukaemia
Miscellaneous  
  Encephalopathy
  Thrombocytopenic purpura
  Lupus erythematosus
  Seborrhoeic dermatitis

The Centers for Disease Control disease classification also incorporates blood CD4 lymphocyte count, as a decrease in the latter is associated with adverse prognosis (Table 30.1).

Opportunistic infections and neoplasms in AIDS

The opportunistic infections, neoplasms and other features of AIDS and its prodrome are listed in Table 30.2.

Pneumocystis carinii pneumonia

This pneumonia is caused by an extracellular protozoan, P. carinii, which grows slowly in its trophozoite and cyst forms within the lung alveoli. Seen in 80% of patients, it is the immediate cause of death in 20% of those dying with AIDS. It is treated with aerosolized pentamidine.

Toxoplasmosis

Protozoal infection with Toxoplasma gondii is seen in 15% of AIDS patients, affecting especially the central nervous system.

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Jan 4, 2015 | Posted by in General Dentistry | Comments Off on 30: Human immunodeficiency virus infection, AIDS and infections in compromised patients

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