written Presentation about HIV AND AIDS

39 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 277

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.

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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

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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)

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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)

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(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)

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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

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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)

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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)

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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)

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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)

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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)

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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.pdf. Accessed 4/21/2012.

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 :