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ACQUIRED IMMUNODEFICIENCY SYNDROME
Human immunodeficiency virus (HIV) infection is the virus that causes acquired immunodeficiency syndrome (AIDS). Although characterized by gradual destruction of cell-mediated (T-cell) immunity, AIDS also affects humoral immunity and even autoimmunity through the central role of the CD4+ (helper) T lymphocyte in all immune reactions. The resulting immunodeficiency makes the patient susceptible to opportunistic infections, cancers, and other abnormalities that define AIDS.
There are two species of HIV: HIV-1 and HIV-2. HIV-1 is the most common of the two. HIV-1 and HIV-2 retrovirus are transmitted by contact with infected blood or body fluids (semen, breast milk, rectal, or vaginal fluids), although HIV-2 has a slightly lower risk of transmission and typically progresses slower.
Homosexual or bisexual men
I.V. drug users
Neonates of infected women
Recipients of contaminated blood or blood products
Heterosexual partners of persons in high-risk groups
The natural history of AIDS begins with infection by the HIV retrovirus, which is detectable only by laboratory tests, and ends with death. The HIV virus may enter the body by any of several routes involving the transmission of blood or body fluids, for example:
direct inoculation during intimate unprotected sexual contact
transfusion of contaminated blood or blood products
use of contaminated needles
transplacental or postpartum transmission.
HIV strikes helper T cells bearing the CD4+ antigen. Normally a receptor for major histocompatibility complex molecules, the antigen serves as a receptor for the retrovirus and allows it to enter the cell. Viral binding also requires the presence of a coreceptor on the cell surface (CCR5, CXCR4, or both).
Like other retroviruses, HIV copies its genetic material in a reverse manner compared with other viruses and cells. Through the action of reverse transcriptase, HIV produces deoxyribonucleic acid (DNA) from its viral ribonucleic acid (RNA). Transcription is often poor, leading to mutations, some of which make HIV resistant to antiviral drugs. The viral DNA enters the nucleus of the cell and is incorporated into the host cell’s DNA, where it’s transcribed into more viral RNA. If the host cell reproduces, it duplicates the HIV DNA along with its own and passes it on to the daughter cells. Thus, the host cell carries this information and, if activated, replicates the virus. Viral enzymes and proteases arrange the structural components and RNA into viral particles that move to the periphery of the host cell, where the virus buds and emerges from the host cell — free to infect other cells. Reservoirs of HIV include gut-associated lymphoid tissue (GALT) and peripheral lymphoid tissues. The reproductive tract, bone marrow, reticuloendothelial system, peripheral blood dendritic cells, and microglial cells of the central nervous system are sites that are believed to be reservoirs of HIV.
HIV replication may lead to cell death or the virus may become latent. HIV infection leads to profound pathology, either directly through destruction of CD4+ cells, other immune cells, and neuroglial cells or indirectly through the secondary effects of CD4+ T-cell dysfunction and resulting immunosuppression.
Acute Retroviral Syndrome
Over 50% of those infected with HIV develop a mononucleosislike syndrome, which may be attributed to flu or another virus and which occurs 1 to 6 weeks post exposure; may remain asymptomatic for years
During this time period, which can last for a decade or more, the virus is replicating at low levels, but people are often asymptomatic. People who are taking antiretroviral therapy can remain in this phase for decades.
Persistent generalized lymphadenopathy
Nonspecific symptoms, including weight loss, fatigue, and night sweats
Fevers related to altered function of CD4+ cells, immunodeficiency, and infection of other CD4+ antigen-bearing cells
Diagnostic Test Results
Laboratory studies reveal CD4+ T-cell count less than 200 cells/µL and the presence of HIV antibodies.
Human granulocyte colony-stimulating growth factor
Anti-infective and antineoplastic agents
Supportive therapy, including nutritional support, fluid and electrolyte replacement therapy, pain relief, and psychological support
Prevention and treatment of opportunistic infections
Allergic rhinitis is a reaction to airborne (inhaled) allergens. Depending on the allergen, the resulting rhinitis and conjunctivitis may occur seasonally (hay fever) or year-round (perennial allergic rhinitis). Allergic rhinitis is the most common atopic allergic reaction, affecting over 20 million US residents.
Immunoglobulin (Ig) E-mediated type I hypersensitivity response to an environmental antigen (allergen) in a genetically susceptible person
Spring — oak, elm, maple, alder, birch, and cottonwood
Summer — grasses, sheep sorrel, and English plantain
Autumn — ragweed and other weeds
Perennial allergens and irritants:
Dust mite excreta, fungal spores, and molds
During primary exposure to an allergen, T cells recognize the foreign allergens and release chemicals that instruct B cells to produce specific antibodies called IgE. IgE antibodies attach themselves to mast cells. Mast cells with attached IgE can remain in the body for years, ready to react when they next encounter the same allergen.
The second time the allergen enters the body, it comes into direct contact with the IgE antibodies attached to the mast cells. This stimulates the mast cells to release chemicals, such as histamine, which initiate a response that causes tightening of the smooth muscles in the airways, dilation of small blood vessels, increased mucus secretion in the nasal cavity and airways, and itching.
Signs and Symptoms
Seasonal Allergic Rhinitis
Profuse watery rhinorrhea; nasal obstruction or congestion
Pruritus of nose and eyes
Pale, cyanotic, edematous nasal mucosa
Red, edematous eyelids and conjunctivae
Headache or sinus pain
Itching of the throat
Perennial Allergic Rhinitis
Chronic nasal obstruction, commonly extending to eustachian tube
Conjunctivitis and other extranasal effects rare
Diagnostic Test Results
A definitive diagnosis is based on the patient’s personal and family history of allergies as well as physical findings during a symptomatic phase.
Microscopic examination of sputum and nasal secretions reveals large numbers of eosinophils.
Blood chemistry shows normal or elevated IgE.
Skin testing paired with tested responses to environmental stimuli pinpoints the responsible allergens given the patient’s history.
Anaphylaxis is an acute, potentially life-threatening type I (immediate) hypersensitivity reaction marked by sudden onset of rapidly progressive urticaria (vascular swelling in skin, accompanied by itching) and respiratory distress. With prompt recognition and treatment, prognosis is good. Typically occurring within minutes, the reaction can occur up to 1 hour after reexposure to an antigen.
Ingestion of or other systemic exposure to sensitizing drugs or other substances, such as:
serums (usually horse serum), vaccines, and allergen extracts
diagnostic chemicals, such as sulfobromophthalein, sodium dehydrocholate, and radiographic contrast media
enzymes such as L-asparaginase in chemotherapeutic regimens
hormones such as insulin
penicillin or other antibiotic and sulfonamides
food proteins, as in legumes, nuts, berries, seafood, and egg albumin
sulfite food additives, common in dried fruits and vegetables and salad bars
nonimmunologic triggers such as cold air or water, heat, exercise, and ethanol
Latex allergy is a hypersensitivity reaction to products that contain natural latex derived from the sap of a rubber tree, not synthetic latex. Natural latex is increasingly present in products in the home and workplace. Hypersensitivity reactions can range from local dermatitis to a life-threatening anaphylactic reaction.
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