clinical management of the common opportunistic infections unit 13 hiv care and art: a course for...
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Clinical Management of the Common Opportunistic Infections
Unit 13HIV Care and ART: A Course for
Physicians
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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 does this additional information affect your differential diagnosis?
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
41
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
What would you include in your initial differential diagnosis?
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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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Additional Information
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
What would you include in your initial differential diagnosis?
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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?
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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
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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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Additional Information
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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Additional Information
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
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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
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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
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Discussion
What would you include in your initial differential diagnosis?
What would you expect to find on physical examination?
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Physical Examination
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 does this additional information affect your differential diagnosis?
How do you investigate this patient?
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Differential Diagnosis
Esophageal candidiasis CMV esophagitis HSV esophagitis Kaposi's sarcoma or lymphoma Idiopathic ulcers (aphthous ulcers) Gastroesophageal reflux disease Combination of 2 or more
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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
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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
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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
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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
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Discussion
What would you include in your initial differential diagnosis?
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Additional Information
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
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Discussion
How does this additional information change your initial differential diagnosis?
What would you expect to find on physical examination?
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Physical Examination
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
How does this additional information change your initial differential diagnosis?
What laboratory tests would you perform?
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Differential Diagnosis
Enteropathogenic bacteria Shigella Salmonella E. coli
CMV Mycobacteria
M. tuberculosis M. bovis
Parasites E. histolytica G. lamblia Cryptosporidium parvum Isospora belli Strongyloides stercoralis,
others
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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)
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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
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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
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Skin Kaposi
Courtesy of the Public Health Image Library/CDC/ Dr. Steve Kraus
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Additional Information
On physical examination, you also note a lesion in the eye
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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
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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
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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
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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
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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
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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
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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
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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.
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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
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Pruritic Papular Eruption (PPE )
Photograph courtesy of Charles Steinberg MD
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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
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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
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Eosinophilic Folliculitis
© Slice of Life and Suzanne S. Stensaas
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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
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Varicella Zoster LesionsTypical Distribution
Courtesy of the Public Health Image Library/CDC
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Zoster SequenceVaricella Zoster LesionsTypical Distribution (2)
Courtesy of Tom Thacher, MD
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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
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Effect of Use of PIs on Mortality
Copyright © 1998 Massachusetts Medical Society
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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
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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