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this series of cluster headaches

and insane migraines and sweating

the bed, completely drenched two,
three nights in a row, that I was
emergency hospitalized
thought I had a brain tumor. I

thought it was over. After a battery of

tests and spinal taps, all that crap,
they walked in the room and said,
'Boom. Here's what's going on.' It's a
hard three letters to absorb," he
"I'm here to admit that I am in fact
HIV-positive," the 50-year-old star


Dennis went to the clinic after he had

been suffering with the worst strep
throat and mouth ulcers for ten days.
They gave him an antibiotic and the
strep throat went away, three days
later his lymph nodes swelled to golf
ball size. When Dennis went back to
the clinic, they told him that they had
run the HIV test on him (without his
knowledge) and he was positive. He
had no idea he was going to be finding
out the results that day.



Human Immunodeficiency Virus (HIV) is the

causative agent of Acquired Immune Deficiency
Syndrome (AIDS).

HIV-1 was isolated in 1983 in France and

HIV-2 was isolated in 1986 in West Africa

Belong to the Lentivirus subfamily of the

Enveloped RNA virus, 120nm in diameter

The AIDS Epidemic

S/S associated with decreased immune function were first
recognized in homosexual men in 1981
Although initially thought to affect the gay male population specifically, AIDS cases
began to be diagnosed in the following high risk groups:
IV drug users
Blood transfusion recipients
High risk heterosexuals

As a result of HIV infection, the bodys immune system begins to progressively

fail making the infected person more susceptible to infections that are normally
harmless to the body (Opportunistic infections)


Sexual Contact = 0.1 -1.0 %
Transfusion of blood and
blood products = > 90%
Tissues and organ donation = 50 -90%
Injections and injuries, unsterile needles = 0.5 -1.0%
Mother to baby (transplacental) = 30%

Pathophysiology and Clinical


2 forms of HIV

Most associated with AIDS in the US, Europe, and Central Africa
Prevalent in West Africa
Spreads more slowly in comparison to HIV 1
Causes disease more slowly in comparison to HIV 1

Cells attacked by HIV

CD4+ T lymphocytes
Dendritic cells: specialized protective cells found in tissues where antigens enter the body

Phases of HIV
3 phases which occur over 8 to 12 years
Primary Infection phase:
Signs and symptoms appear 2 to 4 weeks after exposure lasting a few
days to 2 weeks
Patient has fever, fatigue, myalgia, sore throat, night sweats, GI
problems, lymphadenopathy, maculopapular rash, and headache.
During this phase there is a high amount of viral replication
(up to 1 million/ml) and a decreasing amount of CD4+
After a few weeks the immune system catches up controlling viral
replication where it remains for several years.
If diagnosed in this stage and therapy is started treatment may reduce the
number of long-living CD4+ infected cells

Chronic Asymptomatic (Latency Phase)

Patient has no signs or symptoms of illness
On average this phase lasts 10 years
There is a decreasing amount of CD4+ cells down to 200 per
microliter or lower.
AIDS Phase
Occurs when the CD4+ cell count falls less than 200/microliter
Patient is susceptible to opportunistic infections
Without antiretroviral therapy this phase can lead to death within 2
to 3 years

Classification of HIV
3 Categories relating to the amount of CD4+ cells per microliter of
blood (normal is 800 to 1000 cells/microliter)
Category 1: >500 cells/microliter
Category 2: 200 to 499 cells/mircroliter
Category 3: <200 cells/microliter.
The clinical staging and case definition of HIV for resource-constrained
settings were developed by the WHO in 1990 and revised in 2007.
Staging is based on clinical findings that guide the diagnosis, evaluation,
and management of HIV/AIDS, and it does not require a CD4 cell count.
This staging system is used in many countries to determine eligibility for
antiretroviral therapy, particularly in settings in which CD4 testing is not

These stages are defined by specific clinical conditions or

symptoms. For the purpose
of the WHO staging system, adolescents and adults are
defined as individuals aged 15 years
4 Clinical categories based on symptoms:
Clinical Category 1: persons who are asymptomatic or have
persistent generalized lymphadenopathy, or symptoms of primary
Clinical Category 2: person has symptoms of immune
deficiency, however, not severe enough to be AIDS
Clinical Category 3 and 4: person has AIDS defining
illnesses such as pneumocystis carinii pneumonia.

who statistics of 2014epidemiology

Since the beginning of the epidemic, almost 78 million people have been
infected with the HIV virus and about 39 million people have died of HIV.
Globally, 35.0 million [33.237.2 million] people were living with HIV at the
end of 2013. An estimated 0.8% of adults aged 1549 years worldwide are
living with HIV, although the burden of the epidemic continues to vary
considerably between countries and regions. Sub-Saharan Africa remains
most severely affected, with nearly 1 in every 20 adults living with HIV and
accounting for nearly 71% of the people living with HIV worldwide.

why ent physician should be

aware of hiv?
About 80% of patients with HIV infections present with otolaryngological
symptoms. Often, the otolaryngologist is the primary physician who
diagnoses the HIV infection. He should be aware and vigilant for its
symptoms and unusual presentations

ent manifestations of hiv

a study was conducted at kasturba medical college,mangalore from 1996 to
2004 on ent manifestations of HIV among 968 diagnosed patients.
In their study, otolaryngological findings were noted in 79% of
individuals. Oropharyngeal findings, which were the commonest, were
seen in 59%, followed by cervical lymphadenopathy in 42% of patients.
Oral candidiasis was the commonest oropharyngeal finding, seen in 39%
of patients. Among nasal complaints, rhinosinusitis was the commonest,
found in 17% of patients. Otological manifestations were seen in 20%, of
which chronic suppurative otitis media was the commonest, seen in 13%
of patients. Routine investigations were found to suffice for diagnosis. Of
419 patients who were followed up, the 5-year survival rate was 73%.

ent manifestation of aids

They are caused by opportunistic infections due to viruses,bacteria, fungi and
protozoa and due to activation of theneoplastic process, e.g. Kapos i's
sarcoma and non-Hodgkin's lymphoma.More than 50% of the patients with
AIDS present with symptoms or signs in the head an neck region.

Otitis media
Kaposi's sarcoma of pinna
Sensorineural hearing loss (usually due to cytomegalovirus
affecting inner ear or CN Vlll)
Facial paralysis (viral origin)
Sinusitis (due to both aerobic and anaerobic
Fungal sinusitis due to aspergillus or mucormycosis.
It is rapidly invasive and extends intracranially
Oral cavity:
Candida infection
Angular cheilitis
Recurrent aphthous ulcers

Hairy leukoplakia (it is caused by E.B. virus and

appears as white patches on the lateral border of
tongue. Occurs early in HIV infection)
Kaposi's sarcoma (can occur anywhere in the oral
cavity but is most common in the pa late)
Non-Hodgkin's lymphoma
Parotid cysts and parotitis
Candida infection of oesophagus causing severe
Cervical lymphadenopathy. It can be secondary
infection, lymphoma, tuberculosis or carcinoma or
Kaposi's sarcoma.

kaposis sarcoma
The most common malignancy associated with HIV disease is KS, an idiopathic multiple sarcoma
of the skin. KS occurs in 43% of homosexual or bisexual men with advanced HIV disease, only
4% of injection drug users, and essentially no hemophiliacs.(1) Although considered an
opportunistic neoplasm, KS can manifest early in the patient's course with HIV infection, and may
be the first clinical manifestation of their immunodeficiency.It is a multicentric neoplasm which
may involve skin,mucosa or viscera. There is excessive proliferation of spindle cells of vascular
origin. It is non-invasive and respects the fascial planes. In the oral cavity, Kaposi's sarcoma is
mostly seen in the palate, but may occur on the tongue or gingiva or the posterior wall of pharynx.
I t appears purplish in colour and may need to be differentiated from angioma or pyogenic
granuloma. It can occur at any stage of HIV infection, even in those with normal CD4 counts.
Size of the tumour may vary from a few mm to several centimetres. Diagnosis is based on biopsy
which may show proliferation of spindle cells, endothelial cells,extravasation of red blood cells
and haemosiderin laden macrophages.Methods of treatment include local or systemic
chemotherapy and radiation therapy. Cure is not a realistic goal; therefore, extensive surgical
procedures, such as maxillectomy or lymphadenectomy, are not indicated given the systemic
nature of this malignancy. The goals of therapy are to relieve symptoms .

non hodgkins lymphoma

NHL is the second most common malignancy associated with HIV disease. Most patients have
fever, night sweats, and significant weight loss.(3) NHL appears late in the course of HIV disease,
often after KS and opportunistic infections. Fine-needle aspiration biopsy (FNAB) can lead to the
diagnosis of lymphoma, but evaluation of cell architecture and immunohistochemical analysis
often require open biopsy. NHL frequently can present in the background of benign follicular
hyperplasia, as seen in HIV lymphadenopathy; thus, diagnosis may require multiple FNABs. The
histopathologic findings are variable, but the majority of these lymphomas are high grade.
Treatment consists of aggressive systemic chemotherapy. HIV-infected patients with advanced
disease have little tolerance for radiation therapy and often develop severe refractory mucositis
even following small radiation doses to the upper aerodigestive tract.

HIV lymphadenopathy
HIV Lymphadenopathy

The terms "persistent generalized lymphadenopathy" and "HIV lymphadenopathy" describe the
syndrome of unexplained diffuse lymphadenopathy involving two or more extrainguinal sites for longer
than 3 months. Up to 70% of patients infected with HIV will develop this syndrome within the first few
months after seroconversion, long before any other symptoms of HIV infection appear.(8)
The lymph nodes in HIV lymphadenopathy are soft and symmetrically distributed and can range from
1 to 5 cm.(9) Such findings are common in the head and neck locations, especially the posterior

sensorineural hearing loss

Sensorineural hearing loss, both unilateral and bilateral, occurs in 21 to 49% of HIV-infected
patients. A possible etiology is a primary infection by HIV of either the central nervous system
(CNS) or peripheral auditory nerve. Increased latencies on auditory brain stem testing suggest
central demyelination consistent with a viral infection. A recent study suggested that the
abnormality is in the upper brain stem. One report also described sudden sensorineural hearing
loss with no clear cause in HIV-infected patients. The incidence of sudden hearing loss does not
seem to be increased in HIV-infected patients when compared to non-HIV-infected patients.
Clinicians should consider other causes of the sensorineural hearing loss in HIV-infected
patients, such as CNS infections, neoplasms, and past medications, particularly ototoxic agents.
The diagnostic work-up should include a complete audiogram with impedance audiometry and
auditory brain stem response testing, and a routine laboratory evaluation with serologic testing for
syphilis. A thorough neurologic examination is mandatory for patients with a suspected CNS
process, and clinicians should perform a lumbar puncture with associated chemistries, cytology,
and cultures, and obtain CT or MRI scans of the brain. Aural rehabilitation with hearing aids
should be considered for HIV-infected patients with no identified cause for hearing loss.(16) Use
of any ototoxic medications such as furosemide and aminoglycosides should be avoided in
patients with sensorineural hearing loss.

facial nerve paralysis and bells palsy

Facial nerve paralysis is more common in the HIV-infected patient than in the immunocompetent
patient. According to one report, up to 7.2% of patients with HIV disease will have either unilateral
or bilateral facial paralysis.(18) In the majority of these patients, CNS processes are the cause of
the facial paralysis; CNS toxoplasmosis is the most common identifiable cause, followed by HIV
encephalitis and CNS lymphoma.
Idiopathic facial nerve palsy, or Bell's palsy, is the single most common diagnosis given for HIVinfected patients with seventh nerve paralysis. The leading theory for the cause of Bell's palsy is
an infection of the facial nerve by herpes simplex virus (HSV). Researchers believe that the
immunocompromisation caused by the HIV infection allows greater incidence of viral infection
and associated facial paralysis. The outcome in this patient group, like that in the general
population, is excellent. The nerve usually recovers completely in 3 weeks to 3 months.(30,31).

Rhinitis and sinusitis

although depressed cellular immunity results in decreased total lymphocyte and helper Tlymphocyte counts (CD4 counts), polyclonal B-cell activation produces increased circulating
immune complexes with increased production of IgA, IgG, and IgE. This excessive IgE production
is associated with increased IgE-mediated allergic symptoms, including allergic rhinitis
Rhinosinusitis is common in HIV-infected patients, with a reported prevalence of between 20 and
68% and reason is thought to be impaired mucociliary clearance leading on to recurrent
infections with staph aureus and pseudomonas aeruginosa predominantly.When patients are in
the late stages of HIV infection, atypical opportunistic infections can occur in the nose or
paranasal sinuses. Reports have described fungal sinusitis with Alternaria alternata, Aspergillus,
Pseudallescheria boydii, Cryptococcus, and Candida albicans.
Clinicians must rigorously employ a dual approach, which includes an antibiotic as well as
decongestant. Amoxicillin (500 mg 3 times a day) or sulfamethoxazole-trimethoprim (400 mg 2 times
a day) may be used for primary treatment; however, amoxicillin with clavulanate (Augmentin) (875 mg
2 times a day) or an oral cephalosporin, such as cefuroxime axetil (Ceftin) (250 mg 2 times a day), is
often more effective. Oral antibiotic therapy should continue for a minimum of 3 weeks. In patients
resistant to therapy or with evidence of actual or impending extrasinus complications, hospital
admission for intravenous antibiotics, surgical drainage, or both is imperative.(61)
Decongestant therapy is as important as antibiotic management. Systemic decongestants (usually
pseudoephedrine, 120 mg every 12 hours) should be continued throughout the 3 weeks of therapy.

oral candidiasis
Oral candidiasis (thrush) is by far the most common oral condition in this population. Even for
patients with CD4 counts from 200 to 500 mm3, thrush often is a recurring problem. This
infection typically presents as tender, white, pseudomembranous or plaque-like lesions with
underlying erosive erythematous mucosal surfaces; however, the less typical atrophic or chronic
hypertrophic form is also often encountered. Another common form of oral candidiasis is angular
cheilitis, which typically presents as a clinically obvious, nonhealing fissure at the oral
commissure (the corners of the mouth). In atypical cases, a potassium hydroxide preparation of
scrapings from these lesions is usually diagnostic

diagnostic tests for hiv

1. ELISA test (Enzyme-linked immunosorbent assay ):
It is a screening test with high sensitivity of 99.9%.When positive, it is confirmed by Western blot
2. Western blot test: Confirmation test for HIV infection. The specificity of positive results by ELISA
and Western blot reaches 100%.
3. Blood tests: May indicate anaemia, leukopenia especially lymphopenia and thrombocytopenia in
advanced disease.
4. CD4 T-cell count: Normal count 600-1500/mm3.Falling counts indicate progression of disease.
Count < 200/mm3 indicates risk of AIDS.
CD4lymphocyte percentage is more reliable thanCD-4 count. Risk of progression to AIDS is high
with count of <20%.
5. beta 2 Microglobulin level: It is indicative of macrophagemonocytestimulation. Levels of this
protein rise at seroconversion and continue to rise with progressioof disease. This test is useful
for prognosis.

6. P-24 antigen: P-24 is core protein of the AIDS virus. Presence of this antigen indicates active
HIV replication. Test is positive even prior to seroconversion.
7. pCR (polymerase chain reaction): It is a quantitative test which measures viral load and thus
correlates with progression of disease
Biosensor is the most recent advance in the field of diagnosis.though not commericially
available,its has more specificity and sensitivity, helps in early diagnosis ,rapid and would be
cheap on availability.

hiv infection and health care workers

Doctors, particularly the surgeons, nurses and laboratory staff handling the blood, blood-stained
body fluids and other secretions may contract the disease as occupational hazard. They should
follow the universal precautions considering that every sample they handle is potentially infected.
The risk is due to:
1. Needle-stick injury. Hollow needle (e.g. injectionneedle) is more dangerous than solid needle
(e.g.suture needle). The risk is 1:250.
2. Cuts with contaminated knife or other sharp instruments.
3. Exposure of open wound to infected blood or bodyfluid. Entry of virus can also occur through an
areaof dermatitis.
4. Large mucous membrrane exposure, e.g. by splatter of blood, amniotic fluid, etc.
5. Exposure of skin to infected blood and body fluids.
Use of gloves and gown/coat is protective.

management after needle stick injury

In case of needle-stick injury or cut, wash the area thoroughly with water and apply an antiseptic.
ELISA test is done as soon as possible to establish negative baseline for worker's compensation.
Test should be repeated at 6 weeks, 3 months and 6 months for any seroconversion. Zidovudine
therapy for 6 weeks as soon as possible after exposure can be offered. It is shown to.decrease
the rate of seroconversion after needle-stick injury. However, the side effects of drug and also
the fact that seroconversion can srill occur in spite of drug therapy, should be borne in mind.

universal precautions for hiv

Universal Precautions
Wash hands before and after patient or specimen contact.
Handle the blood of all patients as potentially infectious.
Wear gloves for potential contact with blood and body fluids.
Place used syringes immediately in nearby impermeable container; DO NOT recap or manipulate
needle in any way
Wear protective eyewear and mask if splatter withblood or body fluids is possible (e.g.
bronchoscopy,ora l surgery).
Wear gowns when splash with blood or body fluids is antic ipated.
Handle all linen soiled with blood and/or body secretions as potentially infectious.
Process all laboratory specimens as potentially infectious.
Wear mask for TB and other respiratory organisms
(HIV is not airborne).

Antiretroviral Drugs
(a) Nucleoside analogues
Zidovudine (AZT)
Didanosine (ddI)
Zalcitabine (ddC)
. Stavudine (d4T)
Lamivudine (3TC) (reverse transcriptase inhibitor)
(b) Protease inhibitors
(c) Combination of drugs

recent advances
claw gene therapy?