I.

Definition
AIDS (Acquired Immunodeficiency Syndrome) is a recently recognized condition characterized by a defect in
natural immunity against disease. Acquired refers to the fact that the disease is not inherited or genetic but
develops as result of a virus. Immuno refers to the bodys immunologic system and deficiencyindicates that the
immune system is underfuctioning resulting in a group of signs and symptoms that occur together called
syndrome.

II. Overview
AIDS
-first recognized in US in 1981
Unexplained occurrence of Pneumocystis carinii pneumonia in 5 homosexual men in Los Angeles,
California
Kaposis sarcoma (KS) = 26 healthy homosexual men in New York and Los Angeles
-months after that
Recognized in male and female injection drug users (IDUs) and blood transfusions recipients and
hemophiliacs
-1983, Human Immunodeficiency Virus (HIV) was isolated
-By 1984, demonstrated HIV as the causative agent of AIDS
-1985, Enzyme-Linked Immunosorbent Assay (ELISA) was developed
Appreciate the scope and evolution of HIV epidemic

III. Etiology
Human Immunodeficiency Virus
-family of human retroviruses (Retroviridae)
Subfamily of lentiviruses
-RNA virus
Hallmark: reverse transcription of genomic RNA to DNA by enzyme reverse transcrptase
2 distinct species:
HIV-1
-originated from Pan troglodytestroglodytes, a specie of chimpanzee
-classic AIDS virus
-most common type
Divided into 3 subgroups:
Group M (major): most infections in the world
Group O (outlier): rare viral formfound originally in Cameroon, Gabon and France
Group N: 1st in Cameroonian women with AIDS; only a few cases documented
HIV-2
-similar to Simian Immunodeficiency Virus (SIV) found in Sooty Mangabeys
-lower progression and transmission to AIDS
-localized in West Africa
-Both are zoonotic infections
HIV Transmission
A. Both heterosexual and homosexual contact
i. Sexual Transmission
-predominantly considered as a STD
-In US:
42% transmitted homosexually (men to men)
33% heterosexually
-Worldwide (esp developing countries):
Heterosexual transmission
-virus concentratein the seminal fluid esp in genital inflammatory states
E.g. urethritis, epididymitis and other STDs
-strongly related with receptive anal intercourse
Due to thin, fragile rectal mucosal membrane
-provides at least two modalities of infection:
 Direct inoculation into blood due to traumatic tears in the rectal mucosa
Infection of susceptible target cells (Langerhans cells) in the mucosal layer of rectum
History of Sexually Transmitted Disease
-strongly associated with HIV transmission
-close linked with genital ulcerations and transmission
Treponemapallidum, haemophilusducreyi and Herpes Simplex virus: important causes of genital
ulcerations
-Nonulcerative inflammatory STD:
Chlamydia trachomatis, Neisseria gonorrhoeae and Trochomatisvaginalis
-Bacterial vaginosis
Also linked to increased risk of transmission
Treatment of STDs and genital tract syndromes help prevent transmission
ii. Lack of Circumcision : strongly associated with higher risk of HIV infection
Increased susceptibility to ulcerative STDs
Inner foreskin tissue has density of Langerhans cells, increased CD4 T cells, macrophages
Moist environment under foreskin promote presence or persistence of microbial flora
iii. Oral Contraceptive Drugs (OCD)
Increases incidence HIV infection over and above expected than using a condom
Oral sex
-less efficient mode of transmission
-(+) transmission result from receptive fellatioandinsertive cunnilingus
iv. Alcohol consumption and illicit drug use with unsafe sexual behavior also increases risk
B. Transmission by Blood and Blood Products
-by receiving HIV-tainted blood transfusions, blood products or transpalted tissue
-Intravenous Drug Use
Sharing needle, syringes and water drugs in which are mixed or in cotton
-also via subcutaneous (skin popping) or intramuscular (muscling injections)
Counter measures used:
Screening of all blood for transfusions
Self-deferral of donor with risky behavior
Screening out HIV-negative individuals with positive surrogate laboratory parameters of HIV
infection (Hepatitis B and C)
Serologic testing for syphilis
C. Occupational Transmission of HIV
-small but definite risk of HIV transmission
-in health care workers stuck with needles or other sharp medical instruments
-transmission may occur via non-intact skin exposure
-transmission through intact skin has not been documented
D. Maternal-Fetal/Infant Transmission
-transmission from mother to her fetus via:
During pregnancy
During delivery
By breast-feeding
-majority of transmission occurs perinatal period
E. Transmission by other Body Fluids
-HIV can be isolated from saliva
No convincing evidence can transmit infection either through kissing or other exposures
-transmission by human can occur but rare
-no evidence of transmission via exposure to tears, sweat and urine

IV. Epidemiology

V. Pathophysiology

Hallmark of HIV Disease: Profound Immunodeficiency (quantitative and qualitative decrease of CD4+
Tlymphocyte; normal is 700 1400/mL).
 VARIOUS STAGES OF HIV DISEASE TYPICAL COURSE OF AN HIV-INFECTED INDIVIDUAL
(PATHOGENIC EVENT)

Primary infection

Virus enters directly Virus enters locally

Virus has been introduced to the dendritic cells then

goes to the circulation

I. EARLY ASYMPTOMATIC STAGE CD4+ T-lymphocytes / helper cells (1st target / destroyed)
(>500/mL CD4+ T-lymphocytes)

Drain to the lymphoid organs

Initial viremia

ACUTE HIV SYNDROME (3 6 weeks)

*HIV-specific immune response + trapping of

folliculo-dendritic cells

Humeral immune response - Increase in

circulating antibodies (1 2 months)

Cellular immune response - Increase of

cytotoxic / suppressor cells + natural killer cells in the
body

Decreased viremia

II. INTERMEDIATE STAGE ASYMPTOMATIC STAGE CLINICAL LATENCY (~ 10 years)

(200-500/mL CD4+ T-lymphocytes) Increase of the virus in the lymph node

Progressive decrease of CD4+ T-cells

Architecture of folliculo-dendritic cells

show disruption and decreased trapping efficiency

III. ADVANCED STAGE ADVANCED STAGE

(0-200/mL CD4+ T-lymphocytes
*Complete disruption of folliculo-dendritic cells with
dissociation

(-) Trapping Function

Virus spills over to circulation *At this point the

cytotoxic / suppressor cells and natural killer cells are
outnumbered by the HIV virus (>200/mL CD4+
Tlymphocytes)

Opportunistic infection

DEATH
Clinical Manifestations
i. The Acute HIV Syndrome
-CD4 T cell count falls below a critical level (200/L0 and patient becomes highly susceptible to opportunistic
disease abruptly
-may or may not experience constitutional signs and symptoms
-develop opportunistic disease abruptly
-50 to 70% experience acute clinical syndrome 3 to 6 weeks after primary infection
Clinical Findings:
 General Neurologic
Fever Meningitis
Pharyngitis Encephalitis
Lymphadenopathies Peripheral neuropathy
Headache/Retroorbital pain Myelopathy
Arthralgias/Myalgias Dermatologic
Lethargy/Malaise Erythematous maculopapular rash
Anorexia/ weight loss Mucocutaneous ulceration
Nausea/ vomiting/diarrhea
ii. Asymptomatic Stage Clinical Latency
-duartion is median of 10 years
-rate of disease progression is directly correlated with HIV RNA levels (higher=faster)
-average rate of CD4 T cell decline = 50/L per year
iii. Symptomatic Stage
-appear any time during the course of HIV infection
-severe and life threatening complications occur when CD4 T cells count <200/L
-approximately 60% deaths are a direct result of infection other than HIV (P. carinii, viral hepatitis and non-
AIDS defining bacteria)
A. Respiratory manifestations

B. Cardiovascular manifestations
C. Oropharyngeal manifestations
D. Gastrointestinal manifestations
E. Hepatobiliary manifestations
F. Kidney and GU System manifestation
G. Dermatologic manifestations
-Seborrheic dermatitis
50% cases with HIV
Aggaravated by co-infection with Pityrosporum
-Eosinophilicpustular folliculitis
Rare dermatologic condition but commin in HIV
Multiple, urticarial perifollicular papules that may coalesce into plaquelike lesions
-Reactivation herpes zoster (shingles)
Occurs in 10 to 20% of patients
A reactivation syndrome of varicella zoster virus
-Herpes simples virus
Reactivation due to recurrent orolabial, genital and perianal lesions
Appear as beefy red, exquisitely painful lesions that commonly occur high in the gluteal cleft
H. Neurologic manifestations
-CrytococcusNeoformans Meningitis:
Leading infectious cause of meningitis
Manifest as fever, nausea, vomiting, altered mental status, headache and menigeal signs
Diagnosis:
-(+) organisms in CSF with India ink staining
-CSF detection of cryptococcal antigen
I. Neoplasms
 -Kaposis sarcoma
Multicentric neoplasm consisting of multiple vascular nodes on skin, mucous membrane and viscera
Initial skin lesions are small, raised reddish-purple nodule on sun exposed skin or a discoloration on
the oral mucosa or a swollen lymph node

VI. Complications

VII. Diagnostic Procedures

CBC: Anemia, Neutropenia and Thrombocytopenia
ESR elevated
Hypergammaglobinemia
Hypercholesterolemia
Enzyme-Linked Immunosorbent Assay (ELISA)
-screening test for HIV infection, 99.9% sensitive
-50% are positive within 22 days after exposure
-95% positive 6 weeks after transmission
Western Blot
-confirmatory test for HIV
-detect antibodies against envelope glycoproteins
Absolute CD4+ Lymphocyte count
-most widely use predictor of disease progression
HIV Viral Load Test
-measures amount of actively replicating HIV virus
-correlates with disease progression and response to treatment
-best test to diagnose acute HIV infection
Viral Culture
-done as part of phenotypic drug resistance testing

VIII. PT Evaluation
Assess the general condition of the patient. Usual assessment of the patient includes:
1) Pulmonary test
2) UE and LE instability test
3) ROM
4) MMT
5) Motor and sensory tests
Usual problems:
1) Impaired mobility
2) Difficult with self-care
3) Impaired cognition
4) Uncontrolled pain
Check for deconditioning problems:
1) Contracture
2) Adhesions
3) Atrophy
 4) LOM
5) Weakness
6) Instabilities
7) Edem/swelling
IX. Medical Management
A. Medical Management
Management is usually supportive because there is no known cure for AIDS.
B. Pharmacological Management The corner stone of pharmacological management of HIV infection is
ANTIRETROVIRAL therapy.
1. Nucleoside Analog Reverse Transcriptase Inhibitors (NARTI):
Zidovudine (AZT)
Zalcitabine (ddC)
Lamivudine (3TC)
Didanosine (ddl)
Stavudine (d4T)
2. Protease Inhibitors
Saquinavir
Ritonavir
Indinavir
3. Non-nucleoside Reverse Transcriptase Inhibitor:
Acvirapine
For acute exposure to the infected products of an HIV-infected person, prophylaxis may be given. One
may take these drugs simultaneously:

AZT (Zidovudine) at 200mg 3x/day

Lamivudine 150mg 2x/day

Indivar 800mg 3x/day

These must be taken within 24 hours upon exposure preferably within the first 2 4 hrs.Then take CBC count
and use CD4+ as a baseline and repeat the test every 2 wks.

C. Surgical Management When surgery is planned, preparations for postoperative rehab can be made in
advance. Orthotic and prosthetic appliances also can be planned in advance and prosthetic fitting can even
take place in the operating room. The need for pretreatment interventions in the patient undergoing
radiation therapy is equally important. The institution of a vigorous stretching program can help to prevent
contractures and deformity that otherwise would occur as a result of radiation fibrosis. Training in skin care
and the proper use of moisturizing creams can help to prevent breakdown or infection.
X. PT Management
Most important aspect of rehabilitation is to keep the patient as mobile as possible to prevent the complications
often associated with prolonged bed rest
A. To improve function:
Gait and functional retraining
Prevention of effects of deconditioning
Use of adaptive equipment and strategies
 B. For impaired mobility, difficulty with self-care, impaired cognition, and uncontrolled pain:
Therapeutic exercises
Gait aids
Bathroom and safety equipment
Orthosis
Pain management
Whirlpool treatment
Assistance especially in areas of stair climbing, ambulation, bowel management, and LE dressing

C.For cancer pain and pain in patients with HIV:

Heat modalities (Caution: may increase circulation to the involved area, possibly increasing the
potential for metastatic spread.)

US over malignant tissues is contraindicated

Therapeutic heat and cold are used on non-cancer patients

TENS for reducing the dependence on opioid medications particularly in phantom pain, radiculopathy
and incisional pain (Conventional high frequency setting is most effective)

D. Prognosis
From the time of seroconversion, 10-20% of HIV-infected individuals will progress to AIDS in 3 6 years. 5 -
Once the patient has constitutional symptoms, herpes zoster, thrush or a lowered CD4+ lymphocyte count,
chances are >40% of progressing to AIDS after 3 years of follow-up and >50% after 5 years. - Prognosis can
be modified by antiretroviral therapy and general medical support.