Clinical Management of the Common Opportunistic Infections Unit 13 HIV Care and ART: A Course for Physicians

Clinical Management of the Common Opportunistic Infections

Unit 13HIV Care and ART: A Course for

Physicians

2

Learning Objectives

Identify when HIV-related opportunistic infections (OIs) occur in relation to CD4 cell count

Describe the syndromic diagnosis and treatment of common OIs

Describe the primary and secondary prophylaxis for common OIs

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Syndromes Considered in This Unit

Fever Cough Headache w/ and w/o neurological findings Gastrointestinal disease Rash

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Opportunistic Infection: Definition

Infections that develop as a result of damage to the immune system are called opportunistic infections or OIs

These infections take advantage of the opportunity provided by a weakened immune system

Infections tend to appear at predictable stages of immune deterioration

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WHO Staging and Disease Correlation

WHO Stage Some Typical Diseases* CD4 Count Viral Load**

I

Asymptomatic

No symptoms or signs of any illness

Persistent Generalized Lymphadenopathy

>500103 to106***

II Minor Symptoms

Cutaneous Manifestation Folliculitis, Dermatomal Herpes (Varicella) Zoster

500 to 350 103 to 104

IIIModerate Symptoms

Oral Candidiasis, Oral Hairy Leukoplakia, Pulmonary Tuberculosis

350 to 200 104 to 105

IVAIDS-defining

Illness

Kaposi’s Sarcoma (KS), Oral KS MAC, Severe Chronic Herpes Ulcers, Toxoplasmosis, Cryptococcis

<200 105 to 106

*Staging of diseases is approximate and not the same for all individuals**HIV RNA copies per ml of plasma***Viral load spikes shortly after infection and then drops quickly when antibodies are formed

Information courtesy of WHO

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Principles of OIs with HIV

Caused by defect in cell-mediated immunity, so common viral and bacterial infections are not increasedExceptions: S. pneumoniae and Salmonella

Nearly all OIs respond to HAARTException: PML (progressive multifocal leukoencephalopathy)

Immune Reconstitution Inflammatory Syndrome (IRIS)Paradoxical illness associated with improving immunityMost common with CD4 <50, following initiation of effective

HAARTTreatment: continue ART and OI treatment +/- steroids

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Case 1

Sisay, a 42 year-old merchant, presented to the OPD complaining of two weeks high grade and intermittent fever that usually comes in the afternoon

He has no complaints except fever. Specifically, he denies:Cough or shortness of breathAbdominal pain, diarrhea or vomitingLoss of appetite or weight lossUrinary complaintsHeadache or neck painTravel to malaria endemic area

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Discussion

What would you include in your initial differential diagnosis?

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Additional Information

Sisay had been seen in the local health center where blood film (BF) was done. He was treated with antibiotics after the BF turned out to be negative but showed no improvement

He was screened for HIV five years back and was seropositive. He has never been ill and has received no treatment

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Discussion

How does this additional information affect your differential diagnosis?

What might you expect to find on physical examination?

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Physical Examination

Healthy looking adult in no distress

Vital signs PR 104/m RR 18/m T 39° C BP 120/80 Wt 80 kg

Skin: no pallor or icterus Lymph nodes: none

palpable

Chest: clear to auscultation

Cardiovascular: normal findings

Abdomen: soft, tipped spleen, no CVA tenderness

Musculoskeletal: normal findings

No meningeal signs

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Discussion


How do you investigate this patient?

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Differential Diagnosis: Infections

Protozoal: malaria, toxoplasma, leishmania, others Bacterial

Local pyogenic infection of the chest, urinary tract, the CNS, sinuses, etc

Bacteremia/septicemia due to Salmonella, Streptococcus, Staphylococcus, H. influenza, meningococcus, etc

Mycobacterial infection – M. tuberculosis, atypical mycobacteria (disseminated)

Viral infections: upper respiratory tract infections, CMV, EBV, herpes, others

Fungal infections: PCP, Cryptococcosis, nocardia, mycoplasma, disseminated candidal infection, etc

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Differential Diagnosis (2)

NeoplasmsLymphoma (NHL)Kaposi's sarcoma

OthersDrug reaction

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Approach to Fever in HIV PatientsDetailed Clinical History

SymptomsOnsetDurationPatternSeverity (degree) of

feverAccompanying

symptoms, related complaints

Past medical historyTravel historyPrior illnesses and

treatmentDrug intakeExposure to animals

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Approach to Fever in HIV PatientsMeticulous Physical Exam

HEENT, including sinuses and ears

Lymphoglandular system Chest, including inter-

costal tenderness and cardiac evaluation

Abdominal exam including PR

Genitourinary system, including gynecological evaluation

Musculoskeletal Integumentary CNS, including meningeal

signs and fundoscopy

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Discussion

How would you approach the laboratory evaluation of a patient with fever of undetermined origin?

What tests would you include in your initial evaluation?

If these were non-diagnostic, what additional tests would you consider?

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Laboratory Investigation

CBC including blood film Blood culture Mycobacterial culture Serologic studies Blood chemistry Antigen tests (CMV, cryptococcal)

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Additional Tests

Chest x-ray and other imaging studies (sonography, CT scan)

Lumbar puncture (CSF analysis) Biopsy of lymph nodes, skin lesions CD4 count, viral load (if not done already) Bone marrow, splenic aspirate examination

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Case Study Discussion

How would you manage Sisay?

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Fever Management

Definitive management of the causative agentTherapeutic trial may be considered if tests are non-diagnostic

Supportive – catabolic febrile state may require various supportive measures. Based on the patient, consider:RehydrationElectrolyte replacementCalorie replacementRespiratory supportPalliative control of fever, e.g., with antipyretic, sponging

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Examples of Fever-causing Agents

Leishmaniasis Mycobacterium avium complex

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Visceral Leishmaniasis and HIV Co-infection Caused by L. donovanii, an important OI among persons

infected with HIV-1 Reports mainly from S. Europe, E. Africa, N. and S.

America and Asia Most co-infected patients with clinically evident

leishmaniasis have CD4 cell less than 200/µl HIV and L. donovanii affect the same cell lines, causing

cumulative deficiency of the immune response Leishmania parasites suppress Th1 activity

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Visceral LeishmaniasisClinical Manifestations

Patients present with fever, organomegaly, anemia or pancytopenia

Presentation could be atypical, but VL should be suspected in those with travel history to endemic areas

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Visceral LeishmaniasisDiagnosis and Treatment

DiagnosisSerology less sensitive in immunocompromised hosts.Parasite could be detected in peripheral blood of

immunocompromised patients.Bone marrow aspirate more sensitive, and splenic aspirate most

sensitive.

TreatmentFirst line – Pentavalent antimonials (Sb)Alternatives – Pentamidine, Amphotericin B Relapse and toxicity are common in patients co-infected with

HIV.

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Mycobacterium Avium Complex (MAC)Overview

Ubiquitous in the environment: soil, water, food, house dust, domestic and wild animals

History of TB is associated with decreased risk (US, Sweden, Africa)

Low CD4 and high VL are predictors of disseminated disease

Pre-HAART, MAC was the most common OI, affecting up to 43% of AIDS patients

Dramatic treatment impact

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MAC Clinical Presentation

Symptoms and Signs Percentage Fever 93 Night sweats 87 Anorexia 74 Weight loss 60 Hepatomegaly 42 Diarrhea 40 Splenomegaly 32 Abdominal pain 28 Elevated alkaline phosphate 95

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MAC Fever with Treatment

5

Days

T

E

M

P

37.5

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1 2 3 4

Tx

BC +

BC -

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MAC Treatment

At least two medicationsClarithromycin 500mg bid po (or Azithromycin 500-

600 mg qd po) ANDEthambutol 15mg/kg qd po

Add 3rd or 4th drug if: CD4 count <50; high mycobacterial loads; or absence of effective ARTRifabutin 300 mg qd poCiprofloxacin 500-750 mg bid poLevofloxacin 500 mg qd poAmikacin IV 10-15mg/kg qd

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Case Two

Belaynesh is a 34 year-old woman presenting with two months history of non productive cough, and two weeks of fever with progressively worse shortness of breath

Also notes three months of generalized body weakness, loss of appetite and 8 kg. weight loss

Her husband died two years ago of “bird” (pulmonary disease) leaving her with two children who are now 12 and 14

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Discussion


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Differential Diagnosis

Mycobacterial or bacterial pneumonia TuberculosisStrep, staphH. influenzae LegionellaOthers

Viral pneumoniaCMVInfluenza virus

Fungal pneumoniaPneumocystisCryptococcalNocardiaHistoplasmosis etc.

NeoplasticKaposi sarcoma

(pulmonary Kaposi)Lymphoma

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On examination . . .

She was in respiratory distress Mild cyanosis of the finger tips Bilateral fine diffuse rales Vital signs

BP 110/70 mm HgTemp 38 oCPulse 112/mResp 36/mWT 48 Kgs

What tests would you like to order?

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Potential Diagnostic Tests

CBC Sputum culture & stain for AFB, bacteria, fungal CXR HIV serology LFT, RFT, etc Bronchoalveolar lavage (BAL)

Methenamine silver stain for Pneumocystis CD4 Viral load

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Belaynesh’s Laboratory Results

WBC 2500/mm3 TLC 750/mm3 Hgb 12g/dl Gram stain no gram positive diplococcus AFB negative 3x HIV serology positive (done after counseling) CD4 72 cells/µl CXR as follows

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PCP Chest X-Ray

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Discussion

How do these results change your differential diagnosis?

How would you manage this patient?

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Focused Differential Diagnosis

PCP Pulmonary tuberculosis (atypical appearance) in

late stage HIV disease Viral interstitial pneumonia, e.g., CMV PCP superimposed with tuberculosis

(or some other combination of pathogens)

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Pneumocystis Jiroveci Pneumonia

Most humans infected early in life Diagnosis via induced sputum or

bronchoalveolar lavage (bronchoscopy)Stains with Wright-Giemsa, methenamine silver, and

direct immunofluorescence

Typical presentationNon-productive coughExertional dyspneaGradual fever

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Pneumocystis Treatment

Standard regimen:Cotrimoxazole (15-20 mg TMP + 75-100 mg

SMX)/kg/day in 3 doses IV or PO for 3 weeks

Alternative treatments:Dapsone 100 mg qd + Trimethoprim 15 mg/kg/day

PO divided tid x 3 wksPentamidine 4 mg/kg IV qd x 3 weeksPrimaquine 15-30 mg qd + Clindamycin 450 mg po

q8h x 3 wksAtovaquone 750 mg bid with food x 3 wks

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Adjunctive Corticosteroids in Pneumocystis Therapy

Adjunctive corticosteroids are indicated for severe hypoxemia (pO2<70, AaDO2>35)

Reduces mortality by 50% Start within 72 hours of presentation Regimen

Prednisone 40 mg po bid x 5 days, followed by40 mg qd x 5 days, followed by20 mg qd x 11 days

No benefit for salvage therapy or mild episodes Use cautiously if diagnosis is not confirmed, and watch

for other OIs

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Benefit of Corticosteroids in Pneumocystis Therapy

Survival in PCP depends on patient’s level of oxygenation

Adjunctive corticosteroids can have a significant effect on clinical outcome, including survivalBegin within 72 hours of specific antipneumocystis therapy

Caution should be taken in treating patients with tuberculosis, fungal pneumonia, or pulmonary Kaposi's sarcomaSteroids can have detrimental effectVigorous attempts to confirm a diagnosis of PCP should be

made rather than initiating adjunctive corticosteroids empirically

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Pneumocystis ProphylaxisIndications

Primary prophylaxis (to prevent disease)CD4 < 200/mm3

HIV-associated oral candidiasisUnexplained fever

Secondary prophylaxis (after pneumonia, to prevent recurrence)Prior episode of PCP

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Pneumocystis Prophylaxis Agents

Standard regimenCotrimoxazole (TMP/SMX) 1 tab daily

Alternate regimensDapsone 100mg dailyAtovaquone 1.5 gm PO qd Inhaled pentamidine 300 mg monthly

Duration of treatment: lifelong, but May safely discontinue if immune system restored from

ARTMust have CD4 > 200 for 3 months

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Resolution

Belaynesh was started with Bactrim and steroids After seven days of treatment she started to

show marked clinical improvement She was discharged with: 1) oral Bactrim, 2) an

appointment to be seen at the OPD, and 3) instructions to return before her appointment if she worsened

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Case Three

Amare, a 38 year-old English teacher from Bahir Dar, presents to the general OPD with 10 days history of fever and headache

For the past two days he has vomited any ingested matter

Today he had one seizure with inability to communicate

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Amare’s sister also reports:Amare has had slight right-side body weakness and 2

days difficulty with speechHe had pulmonary tuberculosis 2 years agoHe received an HIV positive test result 6 months ago,

after he lost considerable weight for no apparent reason. He shared this information with her, but was afraid to seek medical care

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Discussion


49

Additional Findings

Chronically ill appearing Vital signs

Temp. 38.8° C Wt 52 Kg

Facial seborrhoeic dermatitis Fundoscopy – bilateral papilledema Right extremity power 3/5, brisk DTR

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Discussion

How does this additional information change your initial differential diagnosis?

What tests would you like to order?

51

Test Results

WBC 3500/mm3 TLC 800/mm3 Hgb 10 g/dl Blood Film negative VDRL non-reactive ESR 85 mm/hr CXR normal Node FNA pending Serology for toxoplasma and CT of the brain could not

be done as these investigations are not available.

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Discussion

How does this additional information change your thinking?

How would your thinking change if you knew the brain CT showed 2 ring-enhancing lesions?

How would your thinking change if the toxoplasma serology were negative?

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(Partial) Differential Diagnosis

Cerebral toxoplasmosis Tuberculoma CNS lymphoma Cryptococcosis

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Toxoplasmosis Facts

Is caused by Toxoplasma gondii Cats are definitive host; excrete organism in

feces Cysts also found in inadequately cooked meat Seropositivity in Ethiopia reaches 80% For an immunosuppressed patient with focal

neurologic signs, cerebral toxoplasmosis is the most likely diagnosis

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Treatment Considerations

The presentation is so characteristic that many guidelines suggest routine treatment for toxoplasmosis

A lack of response to such therapy indicates other possible conditions:Central nervous system lymphomaTuberculomaCryptococcoma

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Treatment Response

With empiric treatment for Toxoplasmosis, what should we expect?Nearly 90% of patients will respond clinically within

days of starting therapyRadiologic evidence of improvement should appear

by 14 days following treatment initiation

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Cerebral Toxoplasmosis

When no imaging is available, it is appropriate to initiate treatment for two weeks to assess for clinical improvement

If improvement occurs, continue treatment until the CD4 count responds to ART and increases to more than 200

Use the maintenance therapy after initiating acute therapy for 6 weeks

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Toxoplasmosis Brain CT Scan

Courtesy of HIV Web Study, www.hivwebstudy.org

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Toxoplasmosis Treatment

Loading dose of Pyrimethamine 200 mg once, followed by:Pyrimethamine 50-75 mg/day, plus Sulfadiazine 1.0-1.5 gm q 6 hrs, plus Folinic acid 10-20 mg/d

Corticosteroids (dexamethasone 4mg PO or IV q6hrs) used if cerebral edema present, and discontinued as soon as clinically feasible

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Additional Treatment Questions

How long will you continue the primary treatment for toxoplasmosis?

Could alternatives to the standard regimens be used?

Which drugs do we commonly use to treat toxoplasmosis in the Ethiopian context?

What about suppressive therapy in this patient?

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Primary Treatment Duration

Duration of Rx is 6 weeks, or 3 weeks after complete resolution of lesions on CT (if repeat CT is available)

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Alternative Regimens

Pyrimethamine and Leucovorin (standard dose) PLUS Clindamycin 600 mg q 6 hrs, or

Cotrimoxazole (TMP 5 mg + SMX 25 mg)/kg IV or PO bid, or

Atovaquone 1.5 gm PO bid, or Pyrimethamine and Leucovorin (standard dose)

PLUS Azithromycin 900-1200 mg PO qd

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Ethiopian Toxoplasmosis Treatment

In Ethiopian context, Fansidar (Pyrimethamine plus Sulfadoxine) is usedA loading dose of two tabs of Fansidar bid for 2 days,

followed byFansidar one tab daily for life

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Suppressive Therapy

Pyrimethamine 25 mg + sulfadiazine 500 mg + folinic acid 10-25 mg PO qd

Cotrimoxazole DS tablet daily Can be stopped when the CD4 count remains ≥

200 for 6 months

Are Therapies Potentially Toxic?

YES

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Common Toxicities

Bone marrow suppression, including:ThrombocytopeniaLeucopenia Anemia

If signs of folate deficiency develop, reduce the dosage or discontinue the drug

Folinic acid (Leucovorin) 5 to 15 mg daily should be administered with pyrimethamine

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Primary Prophylaxis for Toxoplasmosis

When is it indicated? What is used?

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Toxoplasmosis Primary Prophylaxis

Indications: Positive toxoplasma serology, andCD4 count <100 cells/mm3

RegimensTMP/SMX DS tab daily (preferred)TMP/SMX 3 times weeklyTMP/SMX SS tab daily

TMP/SMX prophylaxis serves dual purpose: for PCP and to prevent toxoplasmosis of the brain

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Toxoplasmosis Primary Prophylaxis (2)

Alternative regimenDapsone 50 mg/day, plus

pyrimethamine 50mg weekly, plusfolinic acid 25 mg weekly (if available)

Primary prophylaxis can be stopped if CD4 count >200 cells/mm3 for more than three months following HAART

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Retinal Toxoplasmosis

Courtesy of: C. Stephen Foster M.D., Copyright © 1996-2005,

All Rights Reserved

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Variation on Headache

What if the patient did not have a seizure or focal neurological findings, but still had persistent fever and severe headache?

How would this change your thinking and/or your management?

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No neck stiffness LP was done:

Opening pressure = 300 mm H2O30 WBC/mm3Protein 35 gm%Glucose: normalIndia ink stain: pending

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Discussion

How do you interpret these findings? What is normal OP? What additional tests will you do?

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Results from additional tests:India ink was positive for CryptococcusCSF Cryptococcal culture: PositiveOther tests in the CSF: Negative

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Cryptococcal Meningitis

Caused by a yeast-like fungus, C. neoformans Infection acquired through inhalation Occurs in advanced disease (CD4<100) Rarely, presents as pneumonitis, or as

disseminated disease that includes skin (umbilicated vesicles, like molluscum)

Clinical manifestations may be subtle

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Clinical Signs of Cryptococcal Meningitis

Clinical Manifestations % of Cases

Headache 70-90

Fever 60-80

Meningeal signs 20-30

Photophobia 6-18

Seizures 5-10

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Cryptococcal Meningitis Treatment

Amphotericin 0.7 mg/kg/day IV plus flucytosine 25 mg PO qid for 2 weeks followed by Fluconazole to 8 weeks If potassium drops dangerously, switch amphotericin to

fluconazole PO

If Amphotericin not available, use Fluconazole 400-800 mg/day

Treatment continued for 8-10 weeks, or until CSF is sterile

After treating acute illness, continue preventive therapy (Fluconazole 200 mg PO qd) until asymptomatic and CD4 > 200 x 6 months

78

Additional PatientManagement Issues

HAARTAdherence issuesSide effectsDrug interactions, etc

Prophylaxis for PCP Support and follow up Nutrition and healthy lifestyles, including

disclosure and risk reduction issues

79

Case Four

Sara, a 32 year-old accountant, presented with retrosternal pain associated with swallowing of both solid and liquid foods of two weeks duration

She also reports generalized body weakness and weight loss

One month back she developed whitish oral lesions, treated with topical antifungals

80

Discussion


What would you expect to find on physical examination?

81


She was chronically sick looking Vital signs were all in normal range Small, unremarkable posterior cervical lymph

nodes Extensive oral candidiasis Chest clear No other pertinent findings

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Discussion


How do you investigate this patient?

83


Esophageal candidiasis CMV esophagitis HSV esophagitis Kaposi's sarcoma or lymphoma Idiopathic ulcers (aphthous ulcers) Gastroesophageal reflux disease Combination of 2 or more

84

Diagnostic Interventions

KOH from oral lesion Barium swallow Endoscopy and tissue biopsy

Tissue staining for CMVFluorescent antibody testsAntigen detection tests (CMV & HSV)Polymerase chain reaction (PCR) Viral culture

Therapeutic trials with systemic antifungals

85

Therapy

Esophageal candidiasis would be the most likely diagnosis in this patientFluconazole 200mg/day PO (up to 400mg/day) for

14-21 daysAlternative treatments

• Ketoconazole 200-400 mg PO qd for 14-21 days

• Itraconazole 200 mg PO qd for 14-21 days

86

Therapy (2)

CMV esophagitis requires systemic ganciclovirOral ganciclovir has poor oral absorption so IV

treatment is preferred

HSV esophagitis may be treated with acyclovir, valacyclovir, or famciclovir

Kaposi sarcoma should be treated with HAART and/or other therapies as described previously

Idiopathic ulcers may respond to oral steroids Reflux is treated as for non-HIV patients

87

CMV

Typically does not cause disease until CD4 <50 Manifestations in HIV patients:

Retinitis• Unilateral or bilateral visual disturbance

• Confirmed by retina exam showing “scrambled eggs & ketchup” (exudates & hemorrhages)

GI disease• Esophagitis

• Colitis with watery diarrhea, abdominal pain

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CMV Retinitis

© Slice of Life, Suzanne S. Stensaas

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Case Five

Solomon, a 42 year-old farmer, presents to the OPD with a one month history of watery diarrhea

He reports minimal abdominal pain and bloating, with no tenesmus

He also reports generalized body weakness and significant weight loss

90

Discussion


91


He was recently admitted for this problem and treated with IV fluids and oral antibiotics

Treatment helped a little but the problem recurred

He was screened for HIV and was found positive but he was not started with ARV

Other diagnostic tests were negative He was treated for tuberculosis five years back

92

Discussion


What would you expect to find on physical examination?

93


He is chronically ill appearing and emaciated

Vital signs PB 90/60mm Hg PR 110/m RR 18/m T 36oC Wt 46 kg

Oral candidiasis No lymphadenopathy Normal chest,

cardiovascular Soft abdomen, no masses

or organomegaly Old herpes zoster scar on

the trunk No other abnormal

findings in the other systems

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Discussion


What laboratory tests would you perform?

95


Enteropathogenic bacteria Shigella Salmonella E. coli

CMV Mycobacteria

M. tuberculosis M. bovis

Parasites E. histolytica G. lamblia Cryptosporidium parvum Isospora belli Strongyloides stercoralis,

others

96

Laboratory Diagnosis

Direct microscopy of stool, including leukocyte stain

Stool culture AFB stain Modified AFB stain Endoscopy and colon biopsy Assessment of related effects (CBC, LFT, RFT,

electrolytes, blood sugar, U/A, VDRL, CD4, viral load)

97

Diagnosis and Treatment of Common Causes of Diarrhea in AIDS Patients

Agent CD4 Symptom Diagnosis Rx

E. histolytica any bloody stool, colitisStool microscopy

Metronidazole

Giardia any Watery diarrhea “ “

Cryptosporidium <150 Watery diarrhea Modified AFB ?paromomycin

Isospora belli <100 Watery diarrhea Modified AFB TMP-SMX

Microsporidium <50 Watery diarrhea Giemsa stain Albendazole

CMV <50Watery to Bloody stool, colitis

Biopsy, barium study

Ganciclovir

98

Case Six

Your colleague working in a nearby health center calls you to ask for advice in managing an HIV patient

The patient has been well, without illness, but now presents concerned about a new skin lesion

99

Skin Kaposi

Courtesy of the Public Health Image Library/CDC/ Dr. Steve Kraus

100


On physical examination, you also note a lesion in the eye

101

Conjunctival Kaposi

Courtesy of Paul T. Finger, MD, FACS. www.eyecancer.com

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Kaposi Sarcoma Epidemiology

Was most common cancer at beginning of AIDS epidemic

With use of HAART, KS incidence has declined by 66% between 1989 and 1997, and has likely declined further

Decline in KS may be due to:HAART-induced HIV down-regulation with immune recoveryChange in sexual practice may have decreased transmission

103

KS Etiology and Pathogenesis

Presumed due to Human Herpes Virus 8 (HHV8) Studies of MSM have shown that HHV-8 may be

sexually transmitted Multiple heterosexual contacts is a risk factor for

HHV-8 in Africa Other transmission via saliva; parenteral; from

mother to child

104

KS Clinical Manifestations

Can affect almost any organ system Most common sites include:

Skin: flat to nodular lesions; can progress to significant infiltration of skin with necrosis

Oral cavity: flat to invasive lesionsGI tract: can have KS anywhere in GI tract, which can

cause intestinal blockage and bleedingPulmonary: can spread along bronchi and vessels

105

Genital and Oral Lesions

Courtesy of the Public Health Image Library/CDC/ Sol Silverman, Jr., D.D.S., University of California, San Francisco

Courtesy of HIV Web Study, www.hivwebstudy.org

http://depts.washington.edu/hivaids/derm/case3/fig6d.html

106

Kaposi Sarcoma Diagnosis

Skin and oral lesions are typically diagnosed by visual exam; skin biopsy is most accurate (although invasive) way to make diagnosis

Lung and GI-tract lesions need endoscopy and biopsy for definite diagnosis

Resolution of skin lesions with HAART supports a presumptive diagnosis

Testing for HHV-8 is not indicated for clinical management, and treating HHV-8 is ineffective

107

Kaposi Sarcoma Treatment

Local therapy for skin lesionsAlitretinoin gel (35-50% response)Local radiation (20-70% response)Intralesional vinblastine/vincristine (70-90% response)Cryotherapy (85% response)Photodynamic therapySurgical excision

Systemic therapy failure of local therapy or extensive disease

108

Molluscum Contagiosum

Small, firm, umbilicatedpapules

Typically, resolve completely with HAART

Persist for months in patients with significant immunosuppression

Implicated papules of Molluscum contagiosum and Cryptococcus have the same appearance

Diagnosis is proven through tissue biopsy

109

Molluscum Contagiosum Treatment

The goal of treatment is to remove the soft center from each lesion.

Various methods are available, including:CurettageChemical destruction with concentrated phenolCryotherapyElectrocautery

Generally lesions disappear with HAART.

110

Pruritic Papular Eruption (PPE )

Multiple, chronic, pruritic, hyperpigmented papules distributed symmetrically on the trunk and extremities

May be one of the earliest clinical manifestations of HIV, despite being a marker of advanced disease

Etiology unclear Primarily a clinical diagnosis Eosinophilia and elevated IgE are usual findings Success has been reported with UVB light, with or

without oral antipruritics, as well as pentoxifylline

111

Pruritic Papular Eruption (PPE )

Photograph courtesy of Charles Steinberg MD

112

Seborrheic Dermatitis

Characterized by reddish scaling eruption that favors the scalp, ears, sternum, face, axillae and crural folds

Occasionally the scales can be yellowish or greasy appearing

Topical treatment with corticosteroid creams are helpful

Systemic steroids are seldom needed Medicated shampoos can help the dandruff

associated with scalp involvement

113

Seborrheic Dermatitis

Courtesy of Dr. R. Ojoh, www.thachers.org

http://www.thachers.org/

114

Eosinophilic folliculitis

Characterized by multiple sterile follicular pustules and urticarial papules on the face, trunk, and extremities

Often confused with bacterial folliculitis Involved follicles show spongiotic changes with

eosinophilic and lymphocyte infiltration of the epidermis

Eosinophilia, leukocytosis, and elevated IgE levels are often present

Topical steroids are the mainstay of treatment

115

Eosinophilic Folliculitis

© Slice of Life and Suzanne S. Stensaas

116

Herpes (Varicella) Zoster

Occurs due to reactivation of varicella zoster In HIV:

Often multi-dermatomalMay be recurrentOccurs early in disease; first episode usually in

patients with CD4 count>350 cells /mm3

If treated within 72 hrs of the first appearance of symptoms (pain, redness, papular rash) the progress/appearance of vesicular lesions may be arrested

117

Varicella Zoster LesionsTypical Distribution

Courtesy of the Public Health Image Library/CDC

118

Zoster SequenceVaricella Zoster LesionsTypical Distribution (2)

Courtesy of Tom Thacher, MD

119

Varicella Zoster Treatment

Famciclovir 500 mg po tid for 7-10 days Valacyclovir 1 gm po tid for 7-10 days Acyclovir 800mg po 5x/day for 7-10 days

Superimposed bacterial infection should be treated with antibiotics.

Zoster Ophthalmicus can cause blindnessTreatment - Acyclovir 800mg po 5x daily, plusTopical acyclovir ointment applied 5x daily with topical midriatics

to prevent synechae formation and corneal opacity

120

Effect of Use of PIs on Mortality

Copyright © 1998 Massachusetts Medical Society

121

Key Points

Infections that develop as a result of damage to the immune system are called opportunistic infections or OIs

Most OIs and complications of HIV develop when the CD4 count drops below 200/mm3

OIs are leading causes of morbidity and mortality in HIV-infected persons

122

Key Points

Common OIs in Ethiopia include TB, PCP, Toxoplasmosis, and Cryptococcus

Many OIs are both preventable and treatable Standards exist for diagnosing and treating

common HIV-related OIs After appropriate OI treatment, assessment for

ART therapy is needed

Documents

Clinical Management of the Common Opportunistic Infections Unit 13 HIV Care and ART: A Course for Physicians