I upload part from the book (Essentials of Clinical Infectious Diseases by William F. Wright DO MPH)
not necessarily the presentation should be all from this book but need some from it.
– I upload the rubric and the guideline.
– I uploaded the example
– SHOULD BE LOOK LIKE A STUDENT WHO WROTE IT.
– I need it in PowerPoint.
– 22 to 25 slides.
3
9
HIV and AIDS
Shivakumar Narayanan, MBBS
Guesly Delva, MD
Robert R. Redfield, MD
Bruce L. Gilliam, MD
I. IntroductIon
A. definitions
1. Human immunodeficiency virus (HIV) is a retrovirus that infects humans.
a. The clinically asymptomatic phase can last 3 to 12 years.
b. It eventually leads to symptoms of disease such as opportunistic infec-
tions and other noninfectious diseases that constitute the syndrome
known as acquired immune deficiency syndrome (AIDS).
2. AIDS is defined by the Centers for Disease Control and Prevention (CDC)
as any person with HIV infection and a CD4 lymphocyte count below 200
cells/mcL (or a CD4 count below 14%) or having an AIDS indicator condi-
tion (see Table 39.1).
B. Pathogenesis. The primary route of transmission of the HIV virus is by enter-
ing the mucosal surface (predominantly sexual contact). Following mucosal
entry, the virus binds to peripheral circulating T-cells and macrophages (eg,
dendritic cells) that express the CD4 and CCR5 receptors. As the disease
progresses to later stages after years of infection, the virus uses the CD4 and
CXCR4 receptor to primarily enter T-cells. Hosts with a congenitally deleted
CCR5 receptor generally fail to establish a productive infection. Once the
virus enters the intended target cell, it replicates by converting RNA to DNA
by an RNA-dependent DNA polymerase (reverse transcriptase). This DNA is
integrated in the host genome and leads to the production of new viruses
that result in a burst of HIV viremia and widespread dissemination. HIV
establishes a chronic infection and elicits a robust humoral and cell-mediated
immune response. The infection results in the reduction of CD4 T-cells as the
result of HIV-induced cytolysis and T-cell induced cytolysis. The course of
HIV infection to AIDS parallels the reduction of CD4 T-cells and the amount
of circulating virus in the blood.
c. risk Factors. Risk factors for the transmission of HIV include:
1. Sexual contact, which is the most common mode of transmission. This
includes both heterosexual (most common worldwide) and men who
have sex with men (MSM).
39. HIV and AIDS 27
7
a. Risk per coital (sexual) act:
i. Unprotected receptive anal intercourse (1.4%)
ii. Insertive anal intercourse (0.11%)
iii. Receptive vaginal intercourse (0.08%)
iv. Insertive vaginal intercourse (0.04%)
b. Risk factors associated with increased transmission:
i. In the host transmitting the virus (ie, HIV infected person)
a. High viral load
b. Genital ulcers/sexually transmitted disease
c. Acute HIV infection
d. Advanced disease stage
e. Substance abuse
ii. In the exposed individual (generally non-HIV infected person)
a. Lack of circumcision in men
b. Genital ulcers/sexually transmitted disease
tABle 39.1 ■ AIDS-indicator conditions
Candidiasis of bronchi, trachea, lungs, or
esophagus
Bacterial pneumonia, recurrent
Pneumocystis jiroveci pneumonia (PCP) Mycobacterium tuberculosis, any site
(pulmonary or extrapulmonary)
Salmonella spp bacteremia or sepsis,
recurrent
Mycobacterium spp disease, other species or
unidentified species (disseminated or
extrapulmonary)
Cryptosporidiosis, chronic intestinal (greater
than one month’s duration)
Toxoplasmosis of the brain
Cytomegalovirus retinitis or disease (other
than liver, spleen, or nodes)
Kaposi’s sarcoma
Herpes simplex virus infection; chronic
ulcer(s) (greater than one month’s
duration); or bronchitis, pneumonitis,
esophagitis
Cervical cancer, invasive
Histoplasmosis (disseminated or
extrapulmonary)
Encephalopathy, HIV-related
Isosporiasis, chronic intestinal (greater than
one month’s duration)
Lymphoma, primary of the brain
Mycobacterium avium complex or
Mycobacterium kansasii (disseminated or
extrapulmonary)
Lymphoma (Burkitt, immunoblastic, or
equivalent term)
Coccidioidomycosis (disseminated or
extrapulmonary)
Progressive multifocal leukoencephalopathy
(PML)
Cryptococcosis, extrapulmonary Wasting syndrome due to HIV
278 XII. Approach to Sexually Transmitted Infections
iii. Infected blood and blood products—8% of overall infections, risk
varies.
a. Injection drug use (IDU)/needle sharing (0.67%)
b. Occupational needle-stick exposure (0.3%)
c. Blood and component transfusion including platelets, plasma,
leukocytes (90%)
iv. Infected mothers to infants (intrapartum, peripartal, or postpartum
via breast milk).
a. Risk factors for increased vertical transmission:
1. High maternal HIV viral load
2. Low maternal CD4 count
3. Prolonged interval between membrane rupture and delivery
4. Sexually transmitted diseases
5. Hard drug use
6. Cigarette smoking during pregnancy
7. Preterm delivery
8. Invasive obstetric procedures except for planned or
nonemergent
d. epidemiology
1. HIV-1. Majority of worldwide cases
a. Group M represents 90% of human infections
i. Subtypes: A, B, C, D, F, G, H, J, and K
a. A—Eastern Europe, Central Asia, East and Central Africa
b. B—North America, Western Europe, Australia, Central and South
America, East Asia, Oceania
c. C—Southern/Eastern Africa, India
d. D—Eastern Africa
e. F—South America, Eastern Europe, Central Africa
f. G, H, J, K—Central/West Africa
ii. Circulating recombinant forms (CRFs)—combinations of two
subtypes
a. AE(CRF01)—Southeast Asia
b. AG(CRF02)—West Africa
b. Groups N, O, P—Rare. West/Central Africa/Cameroon
2. HIV-2. Predominantly in West Africa
a. Lower transmission rates than HIV-1, slower disease progression. (This
may be accounted for by lower viral load.)
b. Certain HIV drugs are not active against HIV-2 (eg, NNRTIs and
enfuvirtide).
39. HIV and AIDS 279
II. clInIcAl MAnIFestAtIons oF HIV And AIds
A. Acute HIV Infection
1. Characterized by high viral loads with dissemination and widespread dis-
semination to lymphoid organs.
a. CD4 counts may be depressed in this period and recover once the host
immune response controls viremia.
b. Viral loads drop to their set point following this initial infection with
high viral loads.
2. Acute retroviral syndrome occurs in 50% to 70% of infected individuals
3 to 6 weeks after infection.
a. Patients are highly infectious during this period and often may not
recognize that they are infected.
b. Symptoms are those of a viral-like illness and may occur at frequen-
cies as noted: fever (96%), lymphadenopathy (74%), pharyngitis (70%),
rash (70%), myalgia or arthralgia (54%), diarrhea (32%), headache
(32%), nausea/vomiting (27%), hepatosplenomegaly (14%), weight loss
(13%), thrush (12%), neurologic symptoms (12%).
c. Opportunistic infections may also occur during this time.
d. Differential diagnosis of acute retroviral syndrome includes: Epstein-
Barr virus or cytomegalovirus mononucleosis, primary HSV infection,
influenza, viral hepatitis, rubella, drug reaction, secondary syphilis, and
measles (as these conditions can mimic acute retroviral syndrome).
B. Asymptomatic stage
1. Lack of clinically evident symptoms despite persistent viremia. Median
duration of this stage in untreated patients is 10 years in the United States
and Europe. Untreated patients follow a course of inexorable viral repli-
cation and immunologic decline with the average rate of CD4 decline of
approximately 50 cells/mL per year.
2. A small subset of untreated patients is able to maintain relatively high
CD4 counts and suppress HIV viremia to low levels without antiretroviral
therapy. These hosts are called long-term nonprogressors, and subsets
of these who have no detectable virus are called elite controllers or nat-
ural viral suppressors.
c. symptomatic disease (AIds)
1. Characterized by clinical symptoms of immune dysfunction or
dysregulation.
a. Opportunistic infections (OI) are the most common reason for the clin-
ical symptoms (see Table 39.2) encountered. Following the introduc-
tion of combination antiretroviral therapy (ART) and widespread use of
guidelines for the prevention of OIs, the incidence of these secondary
infections has decreased dramatically.
2. Non-AIDS defining illnesses. These conditions, such as cancers, cardiovas-
cular, kidney and liver disease, tend to dominate the disease burden in
patients whose disease is controlled on antiretroviral therapy.
(text continues on p. 291)
2
8
0
tABle 39.2 ■ Selected HIV-related diseases and opportunistic infections and their treatment or prophylaxis
Disease/Clinical
Syndrome Signs and Symptoms
Etiologic
Agent
Typical CD4
Count
(copies/mL)
Diagnosis, Lab Results,
or Other Studies
Initial Treatments or
Comments Prophylaxis/Prevention
Dermatologic
Bacillary angiomatosis Red, peduculated, often
friable skin nodules/
lesions, can resemble
KS
Can also have peliosis
hepatis, osteomyelitis,
endocarditis, CNS
disease
Bartonella spp ,50 Biopsy of tissue (H&E,
silver stains)
PCR of tissue
Blood
culture
Doxycycline 100 mg PO BID x at
least 3–4 months
Alternatives:
Erythromycin 500 mg PO q6 hr
or azithromycin 500 mg PO
daily or clarithromycin 500 mg
PO bid
Consider IV therapy with
rifampin in peliosis hepatis,
osteomyelitis, endocarditis,
CNS disease
HAART
; MAC prophylaxis
with clarithromycin or
azithromycin will prevent
Cryptococcosis Can resemble
molluscum; Can also
be pustules, plaques,
etc
Cryptococcus
neoformans
,50 Skin biopsy
Serum Cryptococcal
antigen
Fluconazole 200–400 mg PO daily
if no CNS or disseminated
disease
HAART; continue
fluconazole treatment
until CD4 200 3 6
months
Herpes simplex Vesicular lesions or
ulcers in orolabial or
genital regions;
chronic mucocutane-
ous (MC) disease in
late-stage patients
HSV Any (chronic
MC disease
usually
,100)
Viral culture from Swab
HSV DNA PCR or antigen
Acyclovir 400 mg PO TID
or famciclovir 500 mg PO bid
or valacyclovir 1 g PO bid 3
14 days; severe disease:
acyclovir 5 mg/kg IV q8 hr
until improved then PO
Consider prophylaxis with
one of the 3 drugs for
recurrent or chronic MC
disease;
HAART
Herpes zoster (shingles) Painful/pruritic rash in
dermatomal
distribution
VZV Any Clinical: vesicular rash in
dermatomal distribution
Famciclovir 500 mg PO tid or
valacyclovir 1 g PO TID 3 7–14
days
Alternative: acyclovir 800 mg PO
5 3/day
Varicella immune globulin
with exposure; consider
varicella vaccine in those
with CD4 200
Kaposi’s sarcoma Skin: violaceous or red
skin or oral lesions,
may be raised or flat
Systemic disease: see
below
HHV-8 ,200 but can
occur at
higher if not
on HAART
Skin: clinical appearance,
biopsy
Biopsy: Spindle cells and
endothelial proliferation
seen
Single lesion: HAART
Limited lesions: cryotherapy or
laser ablation, vinblastine
lesions
HAART
2
8
1
Molluscum contagiosum Dome-shaped papules
with central
umbilication
Pox virus Usually
,100
Biopsy: intraepidermal
molluscum bodies
Liquid nitrogen; curettage or
electrosurgery; imiquimod
cream
HAART
Gastrointestinal
Oral lesions: aphthous
ulcers/candidiasis/oral
hairy leukoplakia/
histoplasmosis
Pain in mouth or with
swallowing, may
interfere with eating
(Oral hairy leukopla-
kia is usually without
symptoms)
Aphthous ulcers:
unknown
Candida spp
Oral hairy
leukoplakia:
EBV
,50 for
aphthous
ulcers.
Others:
varies
Aphthous ulcers:
yellow-gray pseudomem-
brane with erythematous
“halo”
Diagnosis of exclusion.
Aphthous ulcers: HAART
Topical: Clobetasol 0.05% or
fluocincide 0.05% ointment in
Orabase
Systemic: prednisone 40–60 mg/
day 3 1–2 weeks then taper or
thalidomide 200 mg PO daily
3 4–6 weeks
HAART
Candidiasis: curdy, white
plaques. May cause
erythematous lesions
Hairy leukoplakia presents
as white frond-like
plaques on lateral surface
of tongue
Candidiasis: topical-clotrimazole
10 mg troche 53 per day for
7–14 days
Alternative: nystatin 100,000 U/
mL: 4–6 ml 43 per day for 7–14
days
Systemic: fluconazole 100–
200 mg per day PO for 7–14
days
Candida esophagitis Dysphagia, odynopha-
gia, retrosternal pain,
usually have thrush as
well
Candida spp ,100 Clinical presentation leads
to empiric treatment with
endoscopy if no response.
Endoscopy reveals white
plaques in esophagus
Fluconazole 400 mg PO
daily 3 14–21 days
HAART; fluconazole 200
mg PO daily for
recurrent disease only
(Continued)
2
8
2
Disease/Clinical
Syndrome Signs and Symptoms
Etiologic
Agent
Typical CD4
Count
(copies/mL)
Diagnosis, Lab Results,
or Other Studies
Initial Treatments or
Comments Prophylaxis/Prevention
CMV esophagitis or colitis Esophagitis:
odynophagia,
retrosternal pain
Colitis: diarrhea, fever,
abdominal pain,
weight loss
CMV ,50 Endoscopy revealing ulcers
Biopsy pathology:
intranuclear and
intracytoplasmic
inclusions
Valganciclovir 900 mg PO BID 3
4 weeks or
ganciclovir 5 mg/kg IV q12 hr 3
4 weeks
HAART
HAART
HSV esophagitis Esophagitis:
odynophagia,
retrosternal pain
HSV ,50 Endoscopy revealing ulcers
Biopsy pathology:
multinucleated giant cells
PCR positive
Acyclovir 5 mg/kg IV q8 hr 3
14 days
Until improvement then acyclovir
400 mg TID or valacyclovir
500 mg PO q12 hr
HAART; acyclovir or
valacyclovir for recurrent
disease
Diarrhea—Bacterial Watery stool, abdominal
pain, nausea, vomiting
Salmonella,
Shigella,
Campylobacter,
Vibrio,
Yersinia,
Escherichia
coli
Clostridium
difficile
Depends on
pathogen
Fecal WBC,
Stool culture
Stool C difficile. toxin/PCR
Blood cultures
Endoscopy with biopsy and
culture
Ciprofloxacin 500–750 mg PO
BID (for 14 days with CD4
200, for 4–6 weeks for CD4 ,
200, for up to 6 months and
start HAART with recurrent
Salmonella)
C difficile: metronidazole 500 mg
PO QID x 10–14 days
HAART
Diarrhea—Parasitic Watery stool, abdominal
pain, nausea, vomiting
Entamoeba,
Giardia, Crypto-
sporidium,
Cyclospora,
Microsporidia,
Isospora
Any Fecal WBC
stool O&P
stool antigen (Giardia),
stool modified acid fast
Entamoeba, Giardia: tinidazole
2 g PO 3 1–5 days or
metronidazole 500–750 mg PO
QID 3 7–14 days or
nitazoxanide 500 mg BID 3 3
days
tABle 39.2 ■ Selected HIV-related diseases and opportunistic infections and their treatment or prophylaxis (Continued)
2
8
3
(Cryptosporidium,
Isospora, Cyclospora)
stain and trichrome stain
(microsporidia),
Endoscopy with biopsy and
culture
Cyclospora, isospora: TMP/SMX
DS PO QID 3 10 days
(continue 3 times/week in
AIDS patients)
Cryptosporidium: nitazoxanide
0.5–1 g PO BID 3 14–30 days
(and HAART)
Microsporidia: HAART and
albendazole 400 mg PO BID 3
3 weeks
Perianal lesions: HPV-
associated warts
Others: mucocutaneous HSV,
Kaposi sarcoma
Mild pruritus,
discomfort. Lesions
can be intra-anal in
MSM. Cauliflower-like
on moist partly
keratinized skin. Can
be popular, flat, or
keratinized
Human
papillomavirus
6, 11 (low
risk), 16, 18,
31, 33, 35
(high risk
oncogenic
types)
Varies Visual inspection; can
confirm with biopsy.
Serologic test for syphilis
recommended
HSV: viral culture from
swab, PCR, or antigen
KS: biopsy
Podofilox gel (0.55) BID 3 3
days of a week 3 4 weeks
Imiquimod 5% cream OD at
bedtime 3 times a week for 16
weeks
Cryotherapy with liquid
nitrogen/cryoprobe
Trichloroacetic acid chemical
cautery
Surgical removal of recalcitrant
lesions
HSV: see above
HPV4 vaccine (Gardasil)
between ages 9 to 26.
Protects against HPV
types 6, 11, 16, 18
Neurologic
Cerebral toxoplasmosis Headache, altered
mental status, focal
deficits, seizures, can
have fever but is less
common
Toxoplasma
gondii
,100
(Most cases
occur at
,50)
Compatible clinical
syndrome 1 IgG-positive
serology 1 CT or MRI
imaging with multiple
corticomedulary lesions
Sulfadiazine: 1–1.5 g PO QID 1
pyrimethamine 200 mg PO 3 1
then 50 mg PO daily 1 folinic
acid 10–25 mg PO daily or
TMP/SMX 5 mg/kg IV/PO QID
Primary: TMP/SMX
800/160 mg 1 tablet PO
daily
(Continued)
2
8
4
tABle 39.2 ■ Selected HIV-related diseases and opportunistic infections and their treatment or prophylaxis (Continued)
Disease/Clinical
Syndrome Signs and Symptoms
Etiologic
Agent
Typical CD4
Count
(copies/mL)
Diagnosis, Lab Results,
or Other Studies
Initial Treatments or
Comments Prophylaxis/Prevention
Risk factors include
consumption of
uncooked meat,
handling of cat litter
with edema and contrast
enhancement; PCR-
positive CSF (96%
specificity, 50%
sensitivity)
Definitive diagnosis with
brain biopsy
Alternative: clindamycin 600 mg
PO QID 1 pyrimethamine 1
folinic acid
Alternative: dapsone 50 mg
PO daily 1 pyrimeth-
amine 1 leucovorin
Secondary: continue
treatment until
asymptomatic and CD4
200 3 6 months
Progressive multifocal
leukoencephalopathy
(PML)- or JC-virus
associated encephalopathy
Cognitive dysfunction,
progressive limb
weakness (focal
deficit) and/or sensory
loss, ataxia, speech
and/or visual
disturbances, seizure,
CN deficits
JC virus ,100 MRI usually shows
hyperintense lesions on
T2-weighted and fluid
attenuated inversion
recovery sequences,
hypointense on
T1-weighted sequences,
typically in parietal and
occipital lobes
CSF positive for JC virus;
DNA PCR (sensitivity
76%; specificity 100%)
HAART in treatment-naïve
patients. HAART intensification
in treatment experienced
Prevention of progressive
HIV-related immunosup-
pression with HAART
Cryptococcal meningitis Headache, fever 1/2
meningeal signs,
cranial nerve palsies,
altered mental status,
motor or sensory
deficits, seizures
Immune reconstitution
phenomena are
common with
worsening infection
Cryptococcus
neoformans
,100 Positive CSF 1/2 blood
(75%) cryptococcal
antigen
Abnormal CSF 1/2
elevated opening
pressure on lumbar
puncture
Positive CSF India ink
Basilar contrast
enhancement,
Amphotericin B 0.7 mg/kg IV
daily (or lipid amphotericin
6 mg/kg) 1 flucytosine 100 mg/
kg daily in 4 divided doses for
~2 weeks, then fluconazole 400
mg PO daily for 8 weeks for
maintenance
Alternatives: amphotericin B 1
fluconazole IV/PO 400 mg daily
Primary prophylaxis not
recommended
Secondary: fluconazole 200
mg PO daily until CD4
200 3 6 months
2
8
5
and elevation of
intracranial pressures
when ART is begun
early in meningitis
ventricles enlargement
on CT
or fluconazole (400–800 mg
daily) 1 flucytosine
CMV encephalitis or
polyradiculomyelopathy
Encephalitis:
confusion, lethargy,
cranial nerve palsies,
ataxia
Polyradiculitis:
leg paresis, bowel/
bladder dysfunction
CMV ,50 Positive CSF PCR.
CSF: increased protein,
PMNs or mononuclear
pleocytosis; periventricu-
lar contrast enhancement
Ganciclovir 5 mg/kg IV BID until
symptoms improve then
valganciclovir 900 mg PO daily
Valganciclovir 900 mg PO
daily until CD4 count
100 3 6 months and no
active disease
Tuberculous meningitis Fever, headache,
meningismus,
decreased level of
consciousness, focal
deficits
Mycobacterium
tuberculosis
,350 CT/MRI: may have
intracerebral lesions
CSF: WBC 5–2,000
Protein nl-500
Glucose low
AFB smear positive in 20%
PCR positive; culture
positive
CXR: active TB up to 50%
Isoniazid, rifampin, pyrazin-
amide, ethambutol until
cultures return (~8 weeks)
then, if sensitive, isoniazid and
rifampin for a total of 12
months therapy (See TB
chapter for dosing)
May substitute rifabutin 150 mg
every other day for rifampin if
on boosted PIs
See section on pulmonary
tuberculosis below
Result of HIV Infection
HIV encephalopathy, or
dementia
Evolves to involve both
cognitive and motor
abnormalities
Early: memory,
concentration and
attention decreased
Later: ataxia, coordina-
tion decreased to
paraplegia, dementia
HIV ,200 CSF: increased cells and
protein
MRI: atrophy, increased T2
signal/white matter
hyperintensities
Neuropsychological testing:
dementia
Must rule out other OIs
HAART treatment/intensification
(Continued)
2
8
6
Disease/Clinical
Syndrome Signs and Symptoms
Etiologic
Agent
Typical CD4
Count
(copies/mL)
Diagnosis, Lab Results,
or Other Studies
Initial Treatments or
Comments Prophylaxis/Prevention
Noninfectious /Neoplastic
Primary CNS lymphoma Headache, focal deficits
or nonfocal signs,
altered mental status
with slow onset,
seizures, no fever
EBV 50 MRI-ring enhancing lesions;
less prominent contrast
enhancement as
compared to toxoplasmo-
sis. Carcinomatous
meningitis in CSF in up to
20%
Positive CSF EBV PCR.
Positive cytology rare
Radiotherapy 1/2 chemotherapy
with rituximab-based regimens
Patients should be treated with
HAART
Ophthalmologic
CMV Retinitis Asymptomatic or can
have decreased acuity,
field deficits, floaters,
scotomata
CMV ,50 Fundoscopic exam by
ophthalmologist:
yellow-white perivascular
infiltrates hemorrhages
Valganciclovir 900 mg PO BID 3
14–21 days or ganciclovir 5 mg/
kg IV q12 hrs. 3 14-21 days or
foscarnet 60 mg/kg IV q8 hr 3
14–21 days
Secondary: 900 mg PO
daily until disease
inactive and CD4 100
3 6 months
Alternative: ganciclovir
5 mg/kg IV daily or
foscarnet 90 mg IV once
daily
Acute retinal necrosis (ARN)
or progressive outer retinal
necrosis (PORN)
ARN: Ocular or
periorbital pain,
floaters, blurred vision
PORN: floaters,
decreased vision,
decreased visual fields
VZV PORN:
,50
ARN: Any
Often have history of
cutaneous herpes zoster;
may occur bilaterally in
2/3
Fundoscopic exam by
ophthalmologist
ARN: vasculitis
ARN: acyclovir 10 mg/kg IV q8
hr 3 10–14 days followed by
oral therapy for up to 14
weeks
PORN: acyclovir 10 mg/kg IV q8
hr or ganciclovir 5 mg/kg IV
q12 hr or foscarnet 60 mg/kg
IV q8 hr. May need lifelong
maintenance with IV
HAART
tABle 39.2 ■ Selected HIV-related diseases and opportunistic infections and their treatment or prophylaxis (Continued)
2
8
7
Pulmonary
Bacterial pneumonia Acute fevers, chills,
rigors, chest pain,
cough productive of
purulent sputum, and
dyspnea as in
non-HIV infected
individuals
Mainly
Streptococcus
pneumoniae,
Hemophilus spp
Any Positive sputum and/or
blood culture, chest
radiography: lobar
infiltrate
Depends on organisms (please
see related chapters in this
book)
Pneumococcal and
influenza vaccine
recommended for HIV
patients
Pneumocystis jiroveci
pneumonia (PCP)
Subacute, progressive
dyspnea; fever,
nonproductive cough
Pneumocystis
jiroveci
,200 Hypoxemia,
elevated LDH,
demonstration of
organisms in tissue,
bronchoalveolar lavage
fluid, or induced sputum
CXR: normal to diffuse
ground glass opacities,
CT chest: ground glass
opacities and cysts
Trimethoprim-sulfamethoxazole
800/160 mg PO/IV q8 for 21
days
Add steroids if severe illness
(pO2,70)
Alternatives: dapsone 100 mg PO
daily 1 trimethoprim 5 mg/kg/
day q8 or primaquine 15–30 mg
PO daily 1 clindamycin
600–900 mg IV q6–8 or
300–450 mg PO q6–8 or
atovaquone 750 mg PO BID
Trimethoprim-
sulfamethoxazole
800/160 mg one tablet
PO daily or 400/80 mg
one tablet daily until
CD4 count 200 3 6
months
Alternatives: dapsone
100 mg PO daily or
dapsone 50 mg PO daily
1 pyrimethamine 50 mg
PO weekly leucovorin 25
mg PO weekly or
aerosolized pentamidine
300 mg monthly or
atovaquone 1500 mg PO
daily
Pulmonary tuberculosis Fever—subacute to
acute, productive
cough, night sweats,
weight loss,
lymphadenopathy
Mycobacterium
tuberculosis
Any (higher
risk as CD4
declines)
Latent TB infection (LTBI):
diagnosed with
tuberculin skin test or
interferon gamma release
assay (IGRA).
Active disease:
Sputum smear AFB positive
or sputum culture
DOT is recommended for all
patients with HIV-related TB
Rifampin 600 mg PO daily 1
isoniazid 300 mg PO daily 1
ethambutol 15–25 mg/kg/day
and pyrazinamide 15–25 mg/
kg/day(max dose 2000 mg)
PO daily.
Primary: LTBI treatment is
isoniazid 300 mg PO
daily 1 pyridoxine 50 mg
PO daily for 9 months
(Continued)
2
8
8
Disease/Clinical
Syndrome Signs and Symptoms
Etiologic
Agent
Typical CD4
Count
(copies/mL)
Diagnosis, Lab Results,
or Other Studies
Initial Treatments or
Comments Prophylaxis/Prevention
positive or nucleic acid
amplification test of
sputum positive
CXR: infiltrate, cavity,
effusion in higher CD4;
may have infiltrate/
effusion only in low CD4
May substitute rifabutin 150 mg
every other day for rifampin
when the patient is given with
boosted PIs
Disseminated Disease
Mycobacterium avium
complex disease
Fever, diarrhea, weight
loss, night sweats,
abdominal pain.
Mycobacterium
avium
complex
,50 Blood or bone marrow
culture (85% positive
with disseminated
disease)
Anemia, elevated alkaline
phosphatase, low albumin
Endoscopy with biopsy
Lymphadenopathy on CT
abdomen in disseminated
disease
Clarithromycin 500 mg PO bid or
azithromycin 600 mg PO daily
1 ethambutol 15 mg/kg daily
third agent (rifabutin 300 mg
PO daily (adjust dose with PIs)
or quinolones)
HAART
Primary (CD4 , 50):
azithromycin 1200 mg
PO once weekly or
clarithromycin 500 mg
PO bid
Secondary: continue
treatment 3 12 months
and until CD4 100 3 6
months
Disseminated
cryptococcosis
Cough, fever, malaise,
dyspnea, pleuritic pain
Cryptococcus
neoformans
,100 Positive blood or
respiratory culture;
positive serum cryptococ-
cal antigen
Amphotericin B 0.7 mg/kg IV
daily (or lipid amphotericin
6 mg/kg) 1 flucytosine 100 mg/
kg daily in four divided doses
for ~2 weeks, then
fluconazole 400 mg daily for 8
weeks for maintenance
Primary prophylaxis not
recommended
Secondary: fluconazole
200 mg PO
tABle 39.2 ■ Selected HIV-related diseases and opportunistic infections and their treatment or prophylaxis (Continued)
2
8
9
CXR: nodules or focal
infiltrate
Alternatives: amphotericin B 1
fluconazole IV/PO 400 mg daily
or fluconazole (400–800 mg
daily) 1 flucytosine
daily until CD4 200 3
6 months
Disseminated
histoplasmosis
Fever, fatigue, weight
loss, hepatospleno-
megaly, and
lymphadenopathy.
Cough, chest pain, and
dyspnea occur in
approximately 50% of
patients.
Histoplasma
capsulatum
150 for
dissemi-
nated; ,300
for
pulmonary
alone
Histoplasma antigen in
blood or urine is sensitive
for disseminated disease
(85–95%) but insensitive
for pulmonary infection.
Culture: blood, bone
marrow, respiratory
secretions, or other
involved sites (1 in 85%
of patients with AIDS)
CXR: infiltrates, cavities,
mediastinal/hilar
lymphadenopathy
Lipid formulation of amphoteri-
cin B 3 mg/kg IV (6 mg/kg if
CNS disease) for 2 weeks (or
until clinical improvement)
then oral itraconazole 200 mg
tid for 3 days and then 200 mg
bid for a total of 12 months
Itraconazole 200 mg daily
can be considered for
patients with CD41
counts ,150 cells/mcL
and are at high risk due
to occupational exposure
or presence in an
hyperendemic area for
histoplasmosis (10
cases/100 patient-years)
Coccidioidomycosis Cough, fever, dyspnea,
weight loss, night
sweats
CNS: headache, altered
mental status
Coccidioides
immitis
200 focal
pneumonia;
dissemi-
nated:
usually ,50
CXR: focal or diffuse
nodular infiltrate
Sputum: stain or culture
positive
Blood: positive serology
CSF: low glucose, elevated
protein, mononuclear
pleocytosis, eosinophils,
positive antibody/culture
Focal pneumonia:
Fluconazole 400 mg PO daily
(Itraconazole and posaconazole
have also been used.)
Diffuse pneumonia: amphoteri-
cin B 1 mg/kg/day IV daily
until improvement then
fluconazole
Meningitis: fluconazole
400–800 mg PO daily
(alternative intrathecal
amphotericin B)
Secondary: fluconazole
400 mg PO daily
(Continued)
2
9
0
Disease/Clinical
Syndrome Signs and Symptoms
Etiologic
Agent
Typical CD4
Count
(copies/mL)
Diagnosis, Lab Results,
or Other Studies
Initial Treatments or
Comments Prophylaxis/Prevention
Neoplastic
Visceral Kaposi’s sarcoma Pulmonary: subacute or
chronic dyspnea,
cough, hemoptysis
GI: bleeding, dysphagia,
pain
Lymphadenopathy
Human herpes
virus-8
(HHV-8) or
Kaposi
sarcoma–asso-
ciated virus
(KSHV)
Any Pulmonary: perihilar
nodular infiltrate on chest
radiograph or CT,
bronchoscopy with
biopsy
GI: endoscopy with biopsy
Systemic: liposomal doxorubicin
or daunorubicin, paclitaxel
HAART
Non-Hodgkin lymphoma Lymph node swelling,
fevers/night sweats/
weight loss (B
symptoms),
hepatosplenomegaly,
anemia, bruising
EBV-diffuse
large B cell,
Burkitts,
primary CNS
HHV8: body
cavity
lymphoma/
plasmacytic
oral cavity
lymphoma
,200 Blood: anemia, elevated
LDH
CT imaging: mediastinal
and abdominal
lymphadenopathy,
hepatosplenomegaly
Lymph node biopsy
Rituximab-based chemotherapy
Abbreviations: AIDS, acquired immune deficiency syndrome; ART, antiretroviral treatment; bid, twice daily; CMV, cytomegalovirus; CN, cranial nerves; CNS, central nervous system; CSF,
cerebrospinal fluid; CT, computed tomography; CXR, chest radiography; EBV, Ebstein-Barr virus; H&E, hematoxilin and eosin; HAART, highly active anti-retroviral therapy; HHV8,
human herpesvirus 8; HIV, human immunodeficiency virus; HSV, herpes simplex virus; IV, intravenous; KS, Kaposi sarcoma; MAC, Mycobacterium avium complex; MRI, magnetic
resonance imaging; MSM, men having sex with men; O&P, ova and parasites; OI, opportunistic infections; PCR, polymerase chain reaction; PO, per os; QD, daily; tid, 3 times per day;
TM/SMX, trimethoprim sulfamethoxazole; WBC, white blood cells.
tABle 39.2 ■ Selected HIV-related diseases and opportunistic infections and their treatment or prophylaxis (Continued)
39. HIV and AIDS 291
III. APProAcH to tHe PAtIent
A. History. Whether caring for a newly HIV-infected patient or an ART
treatment–experienced infected patient, a thorough comprehensive history
should be taken at the initial assessment. It should include date of diagno-
sis, nadir (the lowest) CD4 count, and past HIV-related conditions. The
duration of HIV infection based on the dates of previous negative serologies,
high-risk exposures (see risk factors above), and acute illnesses suggestive of
the acute retroviral syndrome can be valuable in understanding the state of
the patient’s disease. Knowledge of the source of the infection may be helpful
in determining a possible infection with drug-resistant viruses.
Chronic medical conditions such as hepatitis, cardiovascular disease,
renal disease, and gastro-esophageal reflux disease likely to have an impact
on the choice or efficacy of anti-HIV therapy should also be obtained. Social
history and family history may also have an impact on when to start and the
choice of ART.
B. Physical examination. A comprehensive physical examination should be
performed on initial evaluation including a careful eye, skin, and rectal exam-
ination. This can help to diagnose conditions that may indicate advanced HIV
disease or AIDS. Areas to focus include:
1. HEENT examination. Fundoscopic examination may suggest findings of
CMV retinitis. Oral cavity lesions may suggest thrush, oral hairy leukopla-
kia, HSV (more commonly located on the vermillion border of the lip), or
Kaposi sarcoma.
2. Dermatologic examination. Many skin conditions can occur with
advancing HIV disease; however, the most common ones to evaluate for
are Kaposi’s sarcoma lesions, cutaneous candidiasis, scabies, seborrheic
dermatitis, molluscum contagiosum, and paronychia.
3. Gastrointestinal examination. Hepatomegaly, splenomegaly, and hepa-
tosplenomegaly can give clues to systemic comorbid infections.
4. Genitourinary examination. A detailed anogenital inspection and exami-
nation can help uncover other sexually transmitted diseases such as HPV
and HSV infections (see Chapter 38, Sexually Transmitted Diseases).
5. Lymph node examination. Lymphadenopathy, localized or generalized,
can help strengthen suspicions of opportunistic infections.
6. Neurologic examination. Level cognitive function and peripheral neuro-
logical status should be determined.
c. laboratory studies
1. Diagnosis. The CDC recommends a policy of performing HIV testing rou-
tinely for everyone between ages 13 and 64 in health care settings.
a. Enzyme Immune Assay (EIA) is most commonly used and has a
reported sensitivity and specificity of over 99%.
i. Positive or indeterminate EIA results must be confirmed with a
more specific assay such as the Western blot (WB).
ii. False-positive results can occur with recent immunization (HBV,
influenza), autoimmune diseases (SLE), pregnancy (due to antibodies
to HLA antigens), multiple myeloma, and end-stage renal disease.
292 XII. Approach to Sexually Transmitted Infections
iii. False-negative results can occur during acute HIV infection prior
to antibody development (this can range from 12 to 22 days);
this period is otherwise known as the window phase. False-
negative results may also occur in cases of infection with cer-
tain genetic variants (HIV-2 or N and O group infections), and
hypogammaglobulinemia.
iv. The most recent EIA tests combine detection of antibodies with
HIV p24 antigen to allow earlier diagnosis.
v. Point of care rapid screening tests are available to screen in appro-
priate clinical situations (eg, patient in labor, source of needlestick
injury, acutely ill patient with possible Pneumocystis pneumonia,
where the acuity of the condition warrants emergent diagnosis and
treatment, or concern for lack of follow up) with results available
in 30 to 60 minutes. A positive EIA test still needs confirmation
with a Western blot.
b. Western blot (WB): This is essentially an EIA test to detect specific
HIV proteins after they are subject to electrophoresis with separation
on a membrane. The false-positive rate without EIA is estimated at 2%.
i. Positive WB is defined as reactive to gp 120/160 and either p24,
gp 41, or both.
ii. Indeterminate WB is common and can occur in as many as 15% to
20% of serum from patients without HIV infection. Indeterminate
WB can also occur with very early or far-advanced HIV infection.
An indeterminate WB is defined as the presence of one or more
bands that do not meet the criteria for being positive. This is one of
the major reasons why the WB alone is not suitable as a screen-
ing test. Indeterminate WB results should always be repeated.
c. p24 Antigen capture assay. Detects HIV-1 p24 protein in an EIA-
based format. Only 30% to 90% sensitive.
d. Direct detection of HIV virus. Three molecular techniques are avail-
able and include: reverse transcriptase polymerase chain reaction
(PCR), branched DNA (bDNA), and nucleic acid sequence-based ampli-
fication (NASBA).
i. Can be used in making a diagnosis of primary HIV infection espe-
cially in window period.
ii. These tests are more useful in monitoring the effects of therapy
(see below).
2. Immunologic monitoring
a. CD4 T lymphocyte counts are commonly determined by flow cytom-
etry are useful to stage disease, assess risk for OIs, diagnose AIDS, and
monitor immunologic response to therapy. It’s commonly measured at
the time of diagnosis and every 3 to 6 months thereafter.
3. Virologic monitoring
a. Standard assays use molecular methods and can detect as few as 20 to
40 copies of HIV RNA per milliliter of plasma.
39. HIV and AIDS 293
b. Measure approximately 2 to 8 weeks after initiation of ART and
then every 3 to 6 months to evaluate continued effectiveness. In most
instances HIV RNA will drop to less than 50 copies per milliliter within
six months after the initiation of antiretroviral treatment.
4. Resistance testing
a. Usually performed at baseline HIV evaluation (due to the frequency
of transmission of resistant viruses) and in cases of virologic failure
(persistent viral detection on a seemingly adequate regimen).
b. Generally must have a viral load greater than 1000 copies/mL to
obtain an accurate result.
c. Assay subtypes:
i. Genotypic assays: reports the genomic sequence of the HIV
obtained from patient’s serum:
a. Must be interpreted by an experienced HIV provider.
b. Results come back faster, and the test is less expensive than the
phenotypic assays.
ii. Phenotypic assays: detects growth of viral isolates obtained
from the patient and is then compared to reference strains of
the virus in the presence or absence of different antiretroviral
medications.
a. Reports fold change of the virus (similar to minimal inhibitory
concentration for bacteria).
b. Easy to determine if drug is sensitive/resistant.
iii. Virtual phenotype: Uses a database of matched genotypes and phe-
notypes to determine report from patient’s genotype:
a. Easier to interpret.
b. The number of matches in the database determine how useful.
Of limited utility with new drugs or patients with rare mutation
patterns.
c. More expensive than genotype but cheaper than phenotype.
5. Labs prior to use of certain medications:
a. Co-receptor tropism assays: for the potential use of the CCR5-antagonists
maraviroc.
i. Assess which co-receptor the infecting virus uses to enter into CD4
positive cells. Maraviroc is only active when the virus is predomi-
nantly CCR5-tropic.
a. CCR5-tropic viruses predominate in early infection.
b. CXCR4-tropic viruses predominate later in disease.
b. HLA B5701 testing: for the potential use of abacavir (ABC).
i. With positive test, there is higher incidence of hypersensitivity
reaction to ABC.
ii. With negative test, risk of hypersensitivity extremely low.
294 XII. Approach to Sexually Transmitted Infections
c. Glucose-6-phosphate dehydrogenase (G6PD): for the potential use of
dapsone. (Deficiency can be associated with increased risk of hemo-
lytic anemia with dapsone.)
6. Other baseline labs or screening tests:
a. CBC with differential: baseline and every 3 to 4 months in those on
ART.
b. Complete metabolic and cholesterol panel (includes glucose, renal, liver,
and lipid profiles): baseline and every 3 to 4 months in those on ART.
c. Syphilis serology (i.e., RPR): baseline and every 6 to 12 months.
d. Gonorrhea and chlamydia screen: annually (see Chapter 38, Sexually
Transmitted Diseases for testing).
e. Papanicolau smear should be performed for both men and women and
includes the following:
i. Vaginal/cervical: at baseline for all female patients. Repeat at
6 months, then annually if normal.
ii. Anal: recommended by some experts in high-risk populations.
Needs high resolution anoscopy if abnormal.
f. Purified protein derivative (PPD) or interferon-gamma release assay
(IGRA): usually measured at baseline then repeated following CD4
recovery for those whose tests were performed when the patient’s ini-
tial CD4 count was below 200; repeat annually for high-risk popula-
tions (see Chapter 13, Tuberculosis).
g. Hepatitis serology (A, B, and C): usually measured at baseline and
annually in high risk populations who have not been vaccinated (see
hepatitis chapters).
h. Urinalysis (dipstick and microscopic).
d. radiography studies. Chest plain-film radiology is sometimes recom-
mended at baseline in patients with certain risk factors for asymptomatic
Mycobacterium tuberculosis (TB).
IV. MAnAgeMent oF HIV/AIds
A. treatment of HIV. The treatment for HIV consists of using a combination
of antiretroviral agents (usually a combination of 3 agents) with the goals of
suppressing viral replication to undetectable levels, reducing HIV-associated
morbidity, and prolonging the duration and the quality of the patient’s life.
The restoration and the preservation of the host immunologic functions as
well as the prevention of HIV transmission by achieving a durable and opti-
mal viral suppression are also goals of the treatment of HIV according to
the most recent guidelines. Recommended antiretroviral treatment regimens
have comparable efficacy; however, a regimen choice tailored to the patient
and based on expected side effects, convenience, comorbidities, interactions
with concomitant medications, and results of pretreatment genotypic drug-
resistance testing among other factors offers the best chance of a durable
regimen. Adherence counseling is a major prerequisite of starting HIV
treatment. Usually, a physician trained in HIV care is consulted when ART is
being started or changed.
39. HIV and AIDS 295
B. Indications for starting Art
1. Prior to initiating any antiretroviral regimen, each patient’s barriers to
adherence including medical and social issues must be addressed.
2. The U.S. Department of Health and Human Services (DHHS) Guidelines
a. The DHHS recommends treatment in the following patients:
i. Symptomatic disease
ii. Pregnant women
iii. HIV-associated nephropathy (HIVAN), hepatitis B co-infection, and
patients at risk of transmitting HIV
iv. Asymptomatic patients with CD4 less than 500 cells/mL3 (strong
recommendation)
v. Asymptomatic patients with CD4 greater than 500 cells/mL3 (mod-
erate recommendation)
b. Suggest that those with or having risk of cardiovascular disease be con-
sidered for treatment
3. Other guidelines similarly recommend treatment for symptomatic disease
and comorbid conditions but vary on the CD4 count to start from less than
350 cells/mL3 in the British guidelines to less than 500 cells/mL3 in the
International Antiviral Society-USA guidelines due to different interpreta-
tions of the incremental benefit of earlier treatment.
a. Overall, the trend of most experts and guidelines is to treat patients
earlier to minimize the risk of complications of HIV including cardio-
vascular disease and cancer and to reduce transmission.
c. Art regimens (in treatment-naïve patients). All the guidelines make rec-
ommendations based on available evidence, expert opinion, and toxicity.
This fact accounts for some of the variation seen. Alternative and acceptable
agents may be used when the patient’s individual situation warrants
1. DHHS-recommended regimens:
a. Efavirenz/tenofovir/emtricitabine (EFV/TDF/FTC)
b. Ritonavir-boosted atazanavir 1 tenofovir/emtricitabine (ATV/r 1 TDF/
FTC)
c. Ritonavir-boosted darunavir 1 tenofovir/emtricitabine (DRV/r 1 TDF/
FTC)
d. Raltegravir + tenofovir/emtricitabine (RAL 1 TDF/FTC)
2. DHHS alternative agents:
a. Abacavir/lamivudine (ABC/3TC)
b. Rilpivirine (RPV)
c. Ritonavir-boosted Lopinavir (LPV/r) or Fosamprenavir (FPV/r)
d. Elvitegravir/cobicistat/tenofovir/emtricitabine (in patients with CrCl
70 mL/min)
3. DHHS acceptable agents:
a. Zidovudine/lamivudine (ZDV/3TC)
296 XII. Approach to Sexually Transmitted Infections
b. Nevirapine (NVP)
c. Maraviroc (MVC)
d. HIV treatment Failure
1. Virologic failure: failure of viral suppression with initial therapy or detect-
able viral load after achieving viral suppression
a. Confirm with second assay to ensure detectable viral load after viral
suppression was acheived is not a blip or a lab error
b. Assess adherence and address potential barriers to adherence
c. Obtain a viral resistance assay if viral load 1,000 copies per milliliter
d. Work with an HIV expert to develop a new regimen once barriers that
led to failure have been addressed
2. Immunologic failure: persistent decline in CD4 count with concomitant
decline in CD4 percentage and detectable viral load.
3. Clinical failure: development of OI/HIV disease progression. Regimen
changes should be based on viral load information because an Immune
Reconstitution Inflammatory Syndrome (IRIS) due to a undiagnosed OI or
another condition can mimic virologic failure.
4. Discontinuing or briefly interrupting therapy should be avoided if pos-
sible in a patient with HIV viremia because it may lead to a rapid increase
in HIV RNA, a decrease in CD4 cell count, and increases the risk of clinical
progression.
e. treatment of opportunistic Infections (Table 39.2)
1. The risk of an OI is usually assessed by the patient’s CD4 count with
certain OIs occurring at very low counts (Mycobacterium avium com-
plex, cytomegalovirus, Cryptococcus, [progressive multifocal leukoen-
cephalopathy]), while others may occur at any CD4 count (TB, bacterial
pneumonia).
2. OIs may also occur during an acute HIV infection.
3. Prophylaxis for OIs is important for prevention (Table 39.2) especially for
PCP, Toxoplasmosis, MAC, and TB.
F. Immunizations
1. Live virus vaccines should not be given to HIV-infected patients with a
CD4 count of less than 200 cells/mL.
2. Recommended vaccines for routine care includes:
a. Hepatitis A vaccine: provided in high-risk groups (MSM, IDU, HBV,
HCV, liver disease)
b. Hepatitis B: in those without past or present hepatitis B infection
c. Influenza: provided annually
d. Pneumococcal vaccine: vaccinate when CD4 is greater than 200 cells/
mL; consider booster 5 years after initial immunization
e. Tetanus toxoid: provided every 10 years
39. HIV and AIDS 297
BIBlIogrAPHy
Aberg JA, Kaplan JE, Libman H, et al. Primary care guidelines for the management of per-
sons infected with human immunodeficiency virus: 2009 update by the HIV Medicine
Association of the Infectious Diseases Society of America. Clin Infect Dis. 2009 Sep
1;49(5):651–681.
Bartlett JG, Gallant JE, Pham PA. Medical management of HIV infection 2012. Knowledge
Source Solutions. Durham, NC. 2012 edition.
Kaplan JE, Benson C, Holmes KH, et al. Guidelines for prevention and treatment of opportu-
nistic infections in HIV-infected adults and adolescents: recommendations from CDC,
the National Institutes of Health, and the HIV Medicine Association of the Infectious
Diseases Society of America. MMWR Recomm Rep. 2009 Apr 10;58(RR-4):1–207.
Panel on Antiretroviral Guidelines for Adults and Adolescents. Guidelines for the use of
antiretroviral agents in HIV-1-infected adults and adolescents. Department of Health
and Human Services. 1–239. Available at http://www.aidsinfo.nih.gov/ContentFiles/
AdultandAdolescentGL . Accessed 4/21/2012.
http://www.aidsinfo.nih.gov/ContentFiles/AdultandAdolescentGL
http://www.aidsinfo.nih.gov/ContentFiles/AdultandAdolescentGL
- Part XII. Approach to Sexually
Transmitted Infections
39.HIV and AIDS
I. Introduction
II. Clinical Manifestations of HIV and AIDS
III. Approach to the Patient
IV. Management of HIV/AIDS
Bibliography
Kingdom of Saudi Arabia
Ministry of Education
University of Hail
College of Nursing
المملكة العربية السعودية
وزارة التعليم
جامـعـة حـائل
كلية التمريض
Master of Science in Nursing
Clinical infectious diseases – NURS 529
Rubric for Oral /written Presentation & Guided Class Discussion
2nd term 2021/2022
Page 1 of 3
Accredited University by the ASIC on
March 27, 2017
Accredited BSN Program by
AHPGS on February 15, 2018
Students learn through participation and positive involvement in-class activities.
Student(s) will be assigned a topic for a chosen week at the beginning of the semester.
The assigned student(s) for a given week is expected to come prepared to guide class
discussion.
The guided class discussion should focus on presenting the assigned readings provided
by the instructor a week ahead.
Presentations should include visual aids and focus on the topic at the conceptual level.
The assigned student(s) expected to present external readings and research findings
on the topic that are evidence-based (e.g. Latest Advancements in Risk Screening,
Assessment Techniques of infectious diseases, or Diagnostic studies). The group
must provide the instructor with these external readings at least three days before the
presentation.
It is the responsibility of the assigned student(s) to guide the discussion in class. The
instructor will evaluate the group for their contribution, and the rest of the class for
their participation and involvement.
Presentations should include the following:
▪ Cover page with “Title, Name of presenter, ID, Instructor name, university
Badge, college of the nursing badge”
▪ Outlines and objectives
▪ Introduction to the topic
▪ Body of the topic (definition, High-risk’ patients for developing the disease,
Clinical Manifestations)
▪ Control and screening of the disease.
▪ Treatment of Disease and infection.
▪ Discharge protocol.
▪ Clinical practice points related to the disease
▪ Summary and key points.
▪ References.
Kingdom of Saudi Arabia
Ministry of Education
University of Hail
College of Nursing
المملكة العربية السعودية
وزارة التعليم
جامـعـة حـائل
كلية التمريض
Master of Science in Nursing
Clinical infectious diseases – NURS 529
Rubric for Oral /written Presentation & Guided Class Discussion
2nd term 2021/2022
Page 2 of 3
Accredited University by the ASIC on
March 27, 2017
Accredited BSN Program by
AHPGS on February 15, 2018
Assessment Task Assessment Score
□ Oral / written Presentation & Guided Class Discussion 30%
Student Name:
Evaluator Name:
Student ID:
Evaluator Signature:
Date of submission:
Date of presentation:
Assigned Topic:
Overall Given Mark: /30
Assessment Rubric for presentation:
#
POOR
1
ACCEPTABLE
2
IDEAL
3
GIVEN
MARK
1.
Speak unclearly, no eye contact
without holding attention
Speaks clearly, with minimal
making eye contact with the
audience, and holds attention.
Speaks clearly, makes eye
contact with the audience,
and holds attention.
2.
Don’t Engage the audience, or
encourage, students to participation
Engages audience, encourage
most of the students’
participation
Engages audience, grasp the
attention of all students for
participation
3.
Use inappropriate audiovisual
materials, unclear layout, colors
hinder readability and slides
designed without interesting format
Use appropriate audiovisual
materials, clear simple layout,
colors that enhance readability,
and slides designed without
interesting format
Use appropriate audiovisual
materials, a clear simple
layout, colors that enhance
readability, and slides
designed in an interesting
format
4.
The presentation has four or more
spelling and/or grammatical errors.
The presentation has no more
than three misspellings and/or
grammatical errors.
The presentation has no
misspellings or grammatical
errors.
Course Learning Outcomes (CLOs)
5
1.1
Inaccurate and incomplete
discussion of the contemporary
communicable diseases and related
healthcare-associated infections at a
global, regional, national, and local level
For the most part, an accurate
and complete discussion of the
contemporary communicable
diseases and related healthcare-
associated infections at a global,
regional, national, and local level
Accurate and complete
Discussion of the
contemporary communicable
diseases and related
healthcare-associated
infections at a global, regional,
national, and local level
6
1.2
Incorrectly Explore the association
between the
science of infection and
infectious diseases in
the clinical context
Correctly differentiate most of
the association between the
science of infection and
infectious diseases in
the clinical context.
Correctly differentiate all
the associations between the
science of infection and
infectious diseases in
the clinical context
7
1.3
Inappropriate Explain the nurse’s role
in prevention, control, and
management of infectious diseases.
Reasonable Explain the nurse’s
role in the prevention, control,
and management of
infectious
diseases.
Critically and
appropriately Explain the
nurse’s role in prevention,
control, and management of
infectious diseases.
Kingdom of Saudi Arabia
Ministry of Education
University of Hail
College of Nursing
المملكة العربية السعودية
وزارة التعليم
جامـعـة حـائل
كلية التمريض
Master of Science in Nursing
Clinical infectious diseases – NURS 529
Rubric for Oral /written Presentation & Guided Class Discussion
2nd term 2021/2022
Page 3 of 3
Accredited University by the ASIC on
March 27, 2017
Accredited BSN Program by
AHPGS on February 15, 2018
8
2.1
Presents little or no knowledge of
the etiology, natural history,
epidemiology,
diagnosis, transmission,
monitoring, and treatment of classic
and
contemporary infectious
diseases across the lifespan
Presents most etiology, natural
history, epidemiology, diagnosis,
transmission, monitoring, and
treatment of classic and
contemporary infectious
diseases across the lifespan.
Presents complete etiology,
natural history, epidemiology,
diagnosis, transmission,
monitoring, and treatment of
classic and contemporary
infectious
diseases across the lifespan
9
2.2
Unable to demonstrate knowledge of
the scientific
and clinical principles
that underpin the identification,
management, prevention, and control
of
infectious disease in both the
community and in healthcare
settings
Demonstrate most knowledge
of the scientific and clinical
principles that underpin the
identification, management,
prevention, and control of
infectious disease in both the
community and in healthcare
settings
Demonstrate complete
knowledge of the scientific
and clinical principles
that underpin the
identification, management,
prevention, and control of
infectious disease in both the
community and in healthcare
settings
10
2.3
Inappropriately Implement
knowledge of contemporary issues and
topics in infectious diseases including
global health, pandemics, bioterrorism,
and outbreak response
Somewhat appropriately
Implement knowledge of
contemporary issues and topics in
infectious diseases including
global health, pandemics,
bioterrorism, and outbreak
response.
Appropriately Implement
knowledge of contemporary
issues and topics in infectious
diseases including global
health, pandemics,
bioterrorism, and outbreak
response.
Total ( /30)
Evaluator Name:
Evaluator Signature:
HIV AND AIDS
TITLE
Prepared by:
Teacher :
OUTLINE:
Introduction
Pathogenesis
Risk factors
Clinical Manifestation
Diagnosis
History taking
Physical examination
Laboratory studies
VI. Infection control Policies
VII. Nursing Diagnosis And Intervention
VIII. Summary
OBJECTIVES:
At the end of this lecture, students will be able to:
1. Know and understand what is HIV AND AIDS.
2. Understand the process how disease develop.
3. Practice how to deal and take care a patient according to infection control sets of guidelines.
4. Identify Nursing diagnosis and make interventions that help promote patient care and comfort.
INTRODUCTION
The human immunodeficiency virus (HIV) targets the immune system and weakens people’s defense against many infections and some types of cancer that people with healthy immune systems can fight off. As the virus destroys and impairs the function of immune cells, infected individuals gradually become immunodeficient. Immune function is typically measured by CD4 cell count.
The most advanced stage of HIV infection is acquired immunodeficiency syndrome (AIDS), which can take many years to develop if not treated, depending on the individual. AIDS is defined by the development of certain cancers, infections or other severe long-term clinical manifestations.
Since HIV was first identified almost 30 years ago, remarkable progress has been made in improving the quality and duration of life for people living with HIV disease.
HIV or human immunodeficiency virus and acquired immunodeficiency syndrome is a chronic condition that requires daily medication.
HIV- 1 is a retrovirus isolated and recognized as the etiologic agent of AIDS.
HIV-2 is a retrovirus identified in 1986 in AIDS patients in West
HIV
AIDS
is defined by the Centers for Disease Control and Prevention (CDC) as any person with HIV infection and a CD4 lymphocyte count below 200 cells/mcL (or a CD4 count below 14%) or having an AIDS-indicator condition
The primary route of transmission of the HIV virus is by entering the mucosal surface (predominantly sexual contact).
Following mucosal entry, the virus binds to peripheral circulating T cells and macrophages (e.g., dendritic cells) that express the CD4 and CCR5 receptors.
As the disease progresses to later stages after years of infection, the virus uses the CD4 and CXCR4 receptor to primarily enter T cells.
Hosts with a congenitally deleted CCR5 receptor generally fail to establish a productive infection.
Once the virus enters the intended target cell, it replicates by converting RNA to DNA by RNA-dependent DNA polymerase (reverse transcriptase).
Pathogenesis.
This DNA is integrated in the host genome and leads to the production of new viruses that result in a burst of HIV viremia and widespread dissemination.
HIV establishes a chronic infection and elicits a robust humoral and cell-mediated immune response.
The infection results in the reduction of CD4 T cells as the result of HIV-induced cytolysis and T-cell-induced cytolysis.
The course of HIV infection to AIDS parallels the reduction of CD4 T cells and the amount of circulating
virus in the blood.
RISK FACTORS
Behaviours and conditions that put individuals at greater risk of contracting HIV include:
having unprotected anal or vaginal sex;
having another sexually transmitted infection (STI) such as syphilis, herpes, chlamydia, gonorrhoea and bacterial vaginosis;
sharing contaminated needles, syringes and other injecting equipment and drug solutions when injecting drugs;
receiving unsafe injections, blood transfusions and tissue transplantation, and medical procedures that involve unsterile cutting or piercing; and
experiencing accidental needle stick injuries, including among health workers
APPROACH TO THE PATIENT
date of diagnosis, nadir(the lowest) CD4 count, and past HIV-related conditions
The duration of HIV
source of the infection
Chronic medical conditions Social history and family history
HEALTH HISTORY
Whether caring for a newly HIV-infected patient or an ART treatment–experienced infected patient, a thorough comprehensive history should
be taken at the initial assessment
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Physical Examination
This can help to diagnose conditions that may indicate advanced HIV disease or AIDS. Areas to focus include:
Head, eyes, ears, nose, and throat (HEENT) Funduscopic examination may suggest findings of CMV retinitis. Oral cavity lesions may suggest thrush, oral hairy leukoplakia, HSV (more commonly located on the vermilion border of the lip), or Kaposi’s sarcoma.
Dermatologic examination
Kaposi’ssarcoma lesions, cutaneous candidiasis, scabies, seborrheic dermatitis, molluscum contagiosum, and paronychia
Gastrointestinal Hepatomegaly, splenomegaly, and hepatosplenomegaly can give clues to systemic comorbid infections.
Genitourinary can help uncover other sexually transmitted diseases such as human papillomavirus (HPV) and HSV infections
Lymph node Lymphadenopathy, localized or generalized, can
help strengthen suspicions of OIs.
Neurologic Level cognitive function and peripheral neurologic status should be determined
A comprehensive physical examination should be performed on initial evaluation including a careful eye, skin, and rectal examination. This can help to diagnose conditions that may indicate advanced HIV
disease or AIDS. Areas to focus include:
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Laboratory Studies
is most commonly used and has a reported sensitivity and specificity of over 99%.
Positive or indeterminate EIA results must be confirmed with a more specific assay such as the Western blot (WB).
False-positive results can occur with recent immunization (hepatitis B virus [HBV], infl uenza), autoimmune diseases
False-negative results can occur during acute HIV infection prior to antibody development (this can range from 12 to 22 days); this period is otherwise known as the window phase.
The most recent EIA tests combine detection of antibodies with HIV p24 antigen to allow earlier diagnosis.
Point of care rapid screening tests are available to screen in appropriate clinical situations
A positive EIA test still needs confirmation with a WB
Enzyme immunoassay (EIA)
The CDC recommends a policy of performing HIV testing routinely for everyone between ages 13 and 64 in healthcare settings.
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This is essentially an EIA test to detect specific HIV proteins after they are subject to electrophoresis with separation on a membrane. The false-positive rate without EIA is estimated at 2%.
Western blot (WB)
Detects HIV-1 p24 protein in an EIA-based format. Only 30% to 90% sensitive
p24 antigen capture assay.
Three molecular techniques are available and
include: reverse transcriptase polymerase chain reaction (PCR), branched
DNA (bDNA), and nucleic acid sequence based amplification (NASBA).
Can be used in making a diagnosis of primary HIV infection especially in the window period.
These tests are more useful in monitoring the effects of therapy
Direct detection of HIV
Immunologic monitoring
CD4 T lymphocyte counts are commonly determined by flow cytometry and are useful to stage disease, assess risk for OIs, diagnose AIDS, and monitor immunologic response to therapy.
It’s commonly measured at the time of diagnosis and every 3 to 6 months thereafter.
a. Standard assays use molecular methods and can detect as few as 20 to 40
copies of HIV RNA per milliliter of plasma.
Virologic monitoring
b. Measure approximately 2 to 8 weeks after initiation of ART and then every 3 to 6 months to evaluate continued effectiveness. In most instances HIV RNA will drop to less than 50 copies per milliliter within 6 months after the initiation of antiretroviral treatment.
Resistance testing
a. Usually performed at baseline HIV evaluation (due to the frequency of
transmission of resistant viruses) and in cases of virologic failure (persistent viral detection on a seemingly adequate regimen).
b. Generally must have a viral load greater than 1,000 copies/mL to
obtain an accurate result
PREVENTION
MANAGEMENT OF HIV/AIDS
Treatment of HIV Infection. The treatment for HIV infection consists of using a combination of antiretroviral agents (usually a combination of three agents) with the goals of suppressing viral replication to undetectable levels, reducing HIV associated morbidity, and prolonging the duration and the quality of the patient’s life.
Adherence counseling is a major prerequisite of starting HIV treatment. Usually, a physician trained in HIV care is consulted when ART is being started or changed.
The treatment for HIV is called antiretroviral therapy (ART). ART involves taking a combination of HIV medicines (called an HIV treatment regimen) every day.
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INFECTION CONTROL POLICIES
When Standard Precautions alone cannot prevent transmission, they are supplemented with Transmission-Based Precautions. This second tier of infection prevention is used when patients have diseases that can spread through contact, droplet or airborne routes (e.g., skin contact, sneezing, coughing) and are always used in addition to Standard Precautions. Transmission-based precautions are based upon the mode of transmission of the infectious agent.
For STDs patients we mainly observe contact precaution.
Contact Precautions are intended to prevent transmission of infectious agents, including epidemiologically important microorganisms, which are spread by direct or indirect contact with the patient or the patient’s environment. Contact Precautions are indicated to reduce the risk of transmission of epidemiologically important microorganisms thru direct and indirect contact with the patient or the patient’s environment..
INFECTION CONTROL POLICIES
Following the infection control guidelines in your workplace.
Treating all blood and body fluids as though they are infectious.
Handling and disposing of needles and sharp instruments correctly.
Getting immunized for necessary vaccines
Using protective gear, such as gloves, goggles, and/or masks.
For known STD patient, wearing PPE, double gloves when doing procedures that expose you to blood.
No recapping of needles and following the proper disposal.
In Accidental needle prick, report immediately and follow protocol.
NURSING DIAGNOSIS AND INTERVENTION
The list of potential nursing diagnoses is extensive because of the complex nature of the disease.
Impaired skin integrity related to cutaneous manifestations of HIV infection, excoriation, and diarrhea.
Diarrhea related to enteric pathogens of HIV infection.
Risk for infection related to immunodeficiency.
Activity intolerance related weakness, fatigue, malnutrition, impaired F&E balance, and hypoxia associated with pulmonary infections.
Disturbed thought processes related to shortened attention span, impaired memory, confusion, and disorientation associated with HIV encephalopathy.
Ineffective airway clearance related to PCP, increased bronchial secretions, and decreased ability to cough related to weakness and fatigue.
Pain related to impaired perianal skin integrity secondary to diarrhea, KS, and peripheral neuropathy.
Imbalanced nutrition, less than body requirements related to decreased oral intake.
NURSING DIAGNOSIS AND INTERVENTION
The plan of care for a patient with AIDS is individualized to meet the needs of the patient.
Promote skin integrity. Patients are encouraged to avoid scratching; to use nonabrasive, nondrying soaps and apply nonperfumed moisturizers; to perform regular oral care; and to clean the perianal area after each bowel movement with nonabrasive soap and water.
Promote usual bowel patterns. The nurse should monitor for frequency and consistency of stools and the patient’s reports of abdominal pain or cramping.
Prevent infection. The patient and the caregivers should monitor for signs of infection and laboratory test results that indicate infection.
Improve activity intolerance. Assist the patient in planning daily routines that maintain a balance between activity and rest.
Maintain thought processes. Family and support network members are instructed to speak to the patient in simple, clear language and give the patient sufficient time to respond to questions.
Improve airway clearance. Coughing, deep breathing, postural drainage, percussion and vibration is provided for as often as every 2 hours to prevent stasis of secretions and to promote airway clearance.
Relieve pain and discomfort. Use of soft cushions and foam pads may increase comfort as well as administration of NSAIDS and opioids.
Improve nutritional status. The patient is encouraged to eat foods that are easy to swallow and to avoid rough, spicy, and sticky food items.
SUMMARY
When HIV is introduced into the body, this virus is too strong for the helper T cells and killer T cells. The virus then invades these cells and starts to reproduce itself, thereby not only killing the CD4 T cells, but also spreading to infect otherwise healthy cells.
Some people apparently remain well after infection of the AIDS virus. They may have no physically apparent symptoms of illness. However, if proper precautions are not used with sexual contacts and/or intravenous drug use, these infected individuals can spread the virus to others.
Until an effective vaccine is developed, nurses need to prevent HIV infection by teaching patients how to eliminate or reduce risky behaviors.
Confirming Diagnosis: Signs and symptoms may occur at any time after infection, but AIDS isn’t officially diagnosed until the patient’s CD4+ T-cell count falls below 200 cells/mcl or associated clinical conditions or disease.
Medical management focuses on the elimination of opportunistic infections.Treatment of opportunistic infections. For Pneumocystis pneumonia, TMP-SMZ is the treatment of choice; for mycobacterium avian complex, azithromycin or clarithromycin are preferred prophylactic agents; for cryptococcal meningitis, the current primary treatment is IV amphotericin B.
THANK YOU……!!!!
REFERENCES:
Essentials of Clinical Infectious Diseases Second Edition William F. Wright.
https://www.who.int/news-room/fact-sheets/detail/hiv-aids
https://www.healthcentral.com/condition/aids-and-hiv-infection