i bc27f85be50b71b1 (196 page)

INFEcnOU5 DISEASES 631

Transmission of these organisms is usually through the ingestion of

contaminated food, water, or both or by direct and indirect fecal-oral

transmission.

The primary manifestations of any form of gastroenteritis are

crampy abdominal pain, nausea, and diarrhea, all of which vary in

severity and durarion according to the type of infection. Gastroenteritis is generally a self-limiting infection, with resolution occurring in 3-4 days. However, patients in the hospital setting with reduced immunity can have longer periods of recovery, with dehydration being a primary concern.ll.JI.44

Management of acute gastroenteritis may consist of the

foliowing'2.JL

• Anti-infective agents

• i.v. fluid and electrolyte replacement

• Antiemetic agents (if nausea and vomiting occur)

Clinical Tip

Strict cOntact and enteric precautions should be observed

with patients who have a diagnosis of C. dif{icile infection.

Immune System Infections

Human Immunodeficiency Vints /"fection

Two types of HN exist: HN-I and HIV-2, with HN-J being the more

prevalent and the one discussed here. It is a retrovirus, occurring in

pandemic proportions, that primarily affects the function of the

immune system. Eventually, howeve� all systems of the body become

affected directly, such as the immune system, or indirectly, as in the cardiac system, or through both methods, as occurs in the nervous system.

The virus is transmirccd in blood, semen, vaginal secretions, and

breast milk through sexual, perinatal, and blood or blood product

contact. Proteins on the surface of the virus attach to CD4+ receptors, found primarily on T4 lymphocytes·' Other types of cells found to house the virus include monocytes, macrophages, uterine

cervical cells, epithelial cells of the gastrointestinal tract, and

microglia cells."

632 AClJfE CARE HANDBOOK FOR PHYSICAL THERAPISTS

On entering the cell, the viral and cellular DNA combine, making

the virus a part of the cell. The exact pathogenesis of cellular destruction caused by HIV is not completely understood, and several methods of destruction may be entailed. It is known that immediately after initial infection, HIV enters a latent period, or asymptomatic stage, in

which viral replication is minimal, but CD4' T cell counts begin to

decline.45 Continued reduction results in decreasing immunity, eventually leading to symptomatic HN, in which diseases associated with the virus begin to appear.4S This eventually leads to the onset of AIDS,

which the CDC defines as occurring when the CD4' T-Iymphocyte

COunt falls below 200 cells/Ill (normal, 650-1,200 cellS/ill) or below

14%, when 1 of 26 specific AIDS defining disorders is contracted, or

a combination of these factors.46

Five laboratory tests are available to detect HIV infection47•48:

1.

Enzyme-linked immunosorbent assay or enzyme immunoas-

say test. This procedure tests for the presence of antibodies [0 HN

proteins in the patient's serum. A sample of the patient's blood is

exposed to H1V antigens in the test reagent. If HIV antibodies are

identified, it is inferred that the virus is present within the patient.

2.

Western blot test. This test detects the presence of antibod-

ies in the blood to twO types of HIV viral proteins and is, therefore,

a more specific HIV test. It is an expensive test to perform and is

used as a confirmatory tool for a positive enzyme-linked immunosorbent assay test.

3.

Immunofluorescence assay. In this test, the patient's blood

is diluted and placed on a slide containing HIV antigens. The slide

is then treated with anti-human globulin mixed with a fluorescent

dye that will bind to antigen-antibody complexes. If a fluorescence

is seen when the specimen is placed under a microscope, then HIV

antibodies are present in the patient'S blood.

4.

p24 Antigen assay. This test analyzes blood cells for the

presence of the p24 antigen located on HN virions. It can be used

to diagnose acute infection, to screen blood for HIV antigens, to

determine HIV infection in difficult diagnostic cases, or to evaluate

the treatment effects of antiviral agents.

5.

Polymerase chain reaction for HIV nucleic acid. This highly

specific and extremely sensitive test detects the viral DNA molecule

INFECfIOUS DISEASES

633

in lymphocyte nuclei by amplifying the viral DNA. It is used to

deteer HfY in neonates and when antibody tests arc inconclusive.

Once HIV has been detected, it can be classified in a number of

ways. The Walter Reed staging system has six categories grouped

according to the quantity of helper T cells and characteristic signs,

such as the presence of an HIV antigen or antibody.·9 However, a

more commonly used classification system was devised by the CDC

and was last updated in 1993. In this system, infection is divided into

three categories, depending on CD4' T-Iymphocyte counts:

I.

Category I consists of CD4' T-Iymphocyte counts greater

than or equal to 500 cellsl�1.

2.

Category 2 consists of counts ranging between 200 and

499 cells/�1.

3.

Category 3 contains cell counts less than 200 cells/�1.

These groups are then subdivided intO A, B, and C, according to the

presence of specific diseases.4•

Advancement in the medical treatment of HfV, in the form of antiretroviral therapy, has recently been made. This therapy consists of three types of medications'9:

1.

Nucleoside analog reverse transcriptase inhibitOrs, otherwise

known as nucleoside analogs. These include zidovlldine, didanosine,

zalcitabine, stavlldine, and lamivudine.

2.

Protease inhibitOrs, including saqllinavir, indinavir, rironavir,

and nelfinavir.

3.

Non-nucleoside reverse transcriprase inhibitors, including

delavirdine and nevi rapine.

Each of these therapies assists in limiting HIV progression by helping to prevent viral replication. This prevention is furrher increased when the drugs are used in combination in a treatment technique

termed highly active alltiretroviral therapy or HAART.'9

As HIV progresses and immunity decreases, the risk for and severity of infections not normally seen in healthy immune systems increase. These opporruilistic infections, combined with disorders

634

AClITE CARE HANDBOOK FOR I'HYSICAL THERAI'ISTS

that result directly from the virus, often result in multiple diagnoses

and medically complex patients. These manifestations of HIV can

affect every system of the body and present with a wide array of signs

and symptoms, many of which are appropriate for physical therapy

intervention. Table 10-5 lists common manifestations and com plicarions of HIV and AIDS and the medications generally used in their management.

Disorders affecting rhe nervous sysrem include HIV-associared

dementia complex, progressive multi focal leukoencephalopathy, primary central nervous system lymphoma, toxoplasmosis, and neuropathies. These manifestations may cause paresis, decreased sensation, ataxia, aphagia, spasticity, altered mental status, and

visual deficits 50 In the pulmonary system, TB, cytomegalovirus

(CMV), and pneumonia can result in cough, dyspnea, sputum production, and wheezing.51 In the cardiac system, cardiomyopathy, arrhythmias, and congestive heart failure can cause chest pain,

dyspnea, tachycardia, tachypnea, hypotension, fatigue, peripheral

edema, syncope, dizziness, and palpitations.52

Physical therapy intervention can assist in minimizing the effect of

these deficits on functional ability, therefore helping to maximize the

independence and quality of life of the individual. However, the course

of rehabilitation in HIV-affected individuals can often be difficult

owing to coinciding opportunistic infections, an often-rapid downhill

disease course, low energy states, and frequent hospitalizations.

Mononucleosis

Mononucleosis is an acute viral disease that has been primarily linked

to the Epstein-Barr virus and less commonly to CMV. Mononucleosis

is transmitted generally through saliva from symptomatic or asymptomatic carriers (the Epstein-Barr virus can remain infective for 18

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