opprotustic infection among HIV patients

opportunistic infection in HIV

1. . Prevention, Screening, and Management of Opportunistic Infections

2. Enabling Objectives By the end of this chapter, participants should be able to: - Describe primary and secondary prophylaxis - Manage respiratory problems in HIV-infected individuals - Manage GI and CNS problems - Address Leishmaniasis and STIs - Screen for NCDs and advanced HIV diseases

3. , Opportunistic infections (OIs) are infections that occur more often or are more severe in people with weakened immune systems than in people with healthy immune system. Opportunistic infections are the predominant causes of morbidity and mortality.

4. The common causative agents of the OI in HIV are bacteria, fungi, viruses and protozoa. Main areas affected are the nervous, gastrointestinal, respiratory systems and the skin.

5. General Strategies to Prevent Opportunistic Infections - Reduction of exposure - Preventive therapies ( chemophrophylaxsis like CPT,TPT, FPT) - Immunization - ART treatment - Cervical Cancer screening and management

6. Co-trimoxazole Preventive Therapy (CPT) Implemented as an integral component of HIV/AIDS care Benefits: - Pneumocystis pneumonia prevention - Toxoplasmosis and bacterial infection prevention

7. CPT indication for primary prophylaxis Children ≥5 years of age, and Adults with HIV infection Any WHO stage and CD4 count ≤350 cells/mm3 Or WHO stage3 or 4, irrespective of CD4 level HIV exposed infants In all, starting at 6 weeks after birth HIV infected children < 5 year of age In all

8. COTRIMOXAZOLE TOXICITY Grade 1 Erythema, pruritus Prescribe Antihistamine and continue CPT & close Follow-up Grade 2 Diffuse maculopapular rash, dry desquamation Prescribe Antihistamine and continue CPT & close Follow-up Grade 3 Vesiculation , minor mucosal ulceration STOP CPT, manage .re-introduce after 2 weeks with observation ( desensitization)

9. Grade 4 Exfoliative dermatitis, Steven-Johnson syndrome or erythema multiform, moist desquamation STOP CPT NEVER RESTART CO- TRIMOXAZOL

10. Dapsone as an alternative dapsone can be used instead of CTX if available. It is primarily effective as prophylaxis against PCP but does not have the other prophylactic benefits of cotrimoxazole . Dapsone will contribute to anaemia in most clients, and causes haemolytic anaemia in some clients, so clients should have a baseline Hgb before starting dapsone and Hgb monitored every 1-2 weeks for the first couple of months

11. . Dapsone is not recommended during breastfeeding. When dapsone is being used as PCP prophylaxis, it is only recommended for clients in WHO Stage 4 and/or absolute CD4 count < 200 cells/mm (Or For children CD4 % < 25% for children less than 5)

12. Management of Respiratory System OIs - Bacterial Pneumonia - Pneumocystis Pneumonia (PCP) - Tuberculosis (TB)

13. Bacterial pneumonia Bacterial pneumonia occurs during the whole spectrum of HIV disease, but tends to be more severe and recurrent as the CD4 counts drops significantly; in addition pneumonia can concomitantly present with sinusitis and/or bacteremia.

14. If not treated promptly, extra pulmonary complications like empyema, meningitis, pericarditis, hepatitis and arthritis can follow. Streptococcus pneumonia and Haemophylus influenza are the most common etiologies of community acquired pneumonia.

15. Clinical Manifestations - Onset usually 3-5 days - Cough, fever, chills, rigors, - Chest pain and pleurisy - Tachypnea and decreased oxygen saturation - May consider hospitalizing clients - Egophony and pleural effusion on examination - Grunting and chest in-drawing are severity signs in children younger than 5 years

16. Diagnosis: - Predominantly clinical findings - Radiology may assist in confirmation of diagnosis - Leukocytosis may be seen in CBC

17. Pneumocystis Pneumonia Pneumocystis pneumonia is caused by Pneumocystis jiroveci formerly known as pneumocystis carini pneumonia (PCP), a ubiquitous organism that is classified as a fungus but also shares biologic characteristics with protozoa.

18. Clinical Manifestations - Sub-acute onset of progressive dyspnea, - Fever - Non-productive cough, and - Chest discomfort that worsens within days to weeks. - In children highest incidence is seen between 2-6 months of age and is characterized by abrupt onset of fever, tachypnea, dyspnea and cyanosis.

19. Diagnosis: - Mainly clinical when clients have severe and advanced immunosuppression (CD4<200/mm3) in resource limited settings - Presumptive diagnosis of PCP is based on clinical judgment and typical chest X-ray findings revealing a perihilar interstitial infiltration with tendency to spread outwards. - Physical examination of the chest may be normal in mild cases and early presentation.

20. - Note that the chest X-ray can be normal in 20% of clients. - Definitive diagnosis of PCP is based on demonstration of the organism from an induced sputum sample using special stains like Giemsa or methylamine silver stains, but these tests are not routinely done in Ethiopia

21. treatment - Trimethoprim 15-25 mg/Kg and sulphamethoxazole 75-125mg/kg, three or four times daily for 21 days. Spo2 less than 92% administer oxygen - In severely ill adults with marked respiratory distress prednisolone has to be given simultaneously; o 40mg BID for the first five days then, o 40 mg daily for the next 6 days and o 20 mg daily until completion of intensive co- trimoxazole therapy.

22. - For severe cases of PCP in children provide prednisolone 2mg/kg per day for the first 7 - 10 days followed by a tapering regimen for the next 10 - 14 days. - Secondary prophylaxis should be started immediately. Alternative regimens for mild to moderate cases of PCP include: 1. Clindamycin 600 mg qid plus primaquine 15 mg bid Or 2. Clindamycin 600 mg qid plus dapsone 100 mg daily NB: Consider spontaneous pneumothorax in clients with sudden deterioration in clinical condition.

23. Lymphoid Interstitial Pneumonitis (LIP) Epidemiology : LIP is one of the most common chronic lower respiratory conditions occurring in up to 25% of children with HIV/AIDS.

24. Clinical manifestations Range from asymptomatic disease with isolated radiographic findings to bullous lung disease with pulmonary insufficiency. insidious onset of tachypnea, cough, and mild to moderate hypoxemia with normal auscultatory findings or minimal rales or wheezing. Progressive disease is accompanied by digital clubbing and symptomatic hypoxemia. Associated physical findings include generalized lymphadenopathy, hepato -splenomegaly and parotid enlargement.

25. Diagnosis: Usually based on findings of clinical examination. . Diffuse bilateral reticulonodular infiltrate on X-ray with mediastinal lymphadenopathy. It is important to exclude tuberculosis and other infectious etiology.

26. Treatment: Provide symptomatic treatment (hydration, oxygen). Use antibiotics if there is a superimposed bacterial infection. Bronchodilators may be helpful in mild to moderate disease. Corticosteroids are usually reserved for children with significant hypoxemia and symptoms of pulmonary insufficiency. Give prednisolone 1 – 2 mg/kg/24 hrs for 6 – 8 weeks and then taper as tolerated.

27. Tuberculosis TB remains the leading cause of mortality among people living with HIV, despite substantial scale-up of ART, accounting for 30% of the AIDS-related deaths reported in 2019. TB increases HIV replication through the process of immune activation leading to increased viral load and this results in a more rapid progression of HIV disease. On the other hand, HIV increases susceptibility to be infected with M. Tuberculosis, the risk of progression to TB disease and the incidence and prevalence of TB

28. . The lifetime risk of HIV positive individuals to develop TB is 50%, the annual risk is 10%. WHO recent estimation indicates the risk of developing active TB disease is 18 times higher PLHIV. In Ethiopia, a national level data report indicated that the prevalence of TB in PLHIV is 7.3%.

29. All clients living with HIV infection should be screened for active TB with any one of the following symptoms: Adult and adolescents: • Current cough • Fever • Weight loss or poor weight gain • Night sweats

30. Children less than 10 years: • Current cough, • Fever, • Poor weight gain • Close contact with a person with TB disease Clients with any one of the above symptoms should be investigated for active TB

31. Diagnosis of TB is challenging in HIV positive individuals, especially when the stage of the disease is advanced. the sensitivity of sputum smear microscopy for the diagnosis of TB is low in PLHIV due to poor quality sputum production and low bacillary concentration. in severely immunocompromised clients, the sensitivity of sputum smear microscopy is significantly reduced. Other challenges that make TB diagnosis difficult include non-specific clinical presentation of TB that is attributable to high prevalence of extra-pulmonary and disseminated forms of TB in individuals with advanced HIV disease.

32. Urine LF LAM To minimize the challenges that are associated to sputum based diagnostic tests, urine based rapid TB diagnostic tests are recommended to detect TB in PLHIV with Advanced HIV Disease. Alere lipoarabinomannan (LAM) assay is one of the urine based rapid diagnostic tests for TB detection in PLHIV.

33. Eligible PLHIV for LF_LAM Test In patient settings With signs and symptoms of TB (pulmonary and/or extra pulmonary) With advanced HIV diseaseb or who are seriously ill a  Irrespective of signs and symptoms of TB, with a CD4 cell count of less than 200 cells/mm3 a. “ Seriously ill” is defined based on four danger signs: respiratory rate of b. “ advanced HIV disease ” . All children with HIV who are aged under 5 years should be considered as having advanced disease. For Above 5 and adult CD4 less than 200 and stage 3 &4

34. In outpatient settings • With signs and symptoms of TB • Irrespective of signs and symptoms of TB and with a CD4 cell count of less than 100 cells/mm3

35. LF-LAM should be used as an add-on to clinical judgement in combination with other tests. It should not be used as a replacement or triage test.

36. Molecular Rapid Diagnostic tests for TB include Xpert MTB/RIF Ultra assay: Line Probe Assays (LPAs): Loop-Mediated Isothermal Amplification (TB-LAMP): AFB microscopy: when access to XPERT MTB/RIF test is limited . 2 spot tests with in 1 hour. Chest radiography: Sputum culture (gold standard)

37. Histopathology: Pathology can play a complementary role in confirming the diagnosis of EPTB, such as tuberculous lymphadenitis, pleural effusion etc. FNAC of the lymph nodes Effusions of the serous membranes can be aspirated Tissue biopsy (serous membranes, skin, endometrium and bronchial, pleural, gastric or

38. New HIV positive Clients presumptive tuberculosis cases Clients with tuberculosis found to be HIV positive HIV positive clients taking ART diagnosed with TB Rapid ART initiation clinical assessment and to PLWH with signs and symptoms suggesting TB. Except for central nervous system disease (meningitis), initiate ART while rapidly investigating for TB, with close follow-up within seven days to initiate TB treatment if TB is confirmed. ART should be started in all TB clients, including those with drug-resistant TB, irrespective of the CD4 count. • ART should be started as soon as possible within two weeks of initiating TB treatment, regardless of CD4 count, , except when signs and symptoms of meningitis are present. • ART should be delayed at least four weeks (and initiated within eight weeks) after treatment for TB meningitis is initiated. Corticosteroids should be considered adjuvant treatment for TB meningitis. Start anti-TB • Modify ART regimen to avoid drug-drug interaction • Evaluate for treatment failure • DTG should be used as the preferred drug in clients starting ART while on Antituberculosis treatment but dose of DTG should be doubled (50 mg BID). • When second line is initiated LPV/r is preferable. Note that the dose of the ritonavir should be doubled to counter the effect of Rifampicin on the Protease inhibitors.

39. Tuberculosis Preventive Therapy Latent tuberculosis infection (LTBI) is the state of persistent immune response to stimulation of mycobacterium tuberculosis antigens without evidence of clinically apparent active tuberculosis (TB). Treatment of LTBI to prevent progression to active disease is one of the global key strategies to ending the TB epidemic. Increasingly, eligible targets and treatment options are expanding, with significant implications in the programmatic management of LTBI.

40. TPT is the use of Isoniazid, rifapentine or other medications to sterilize latent TB infection. Screening for exclusion of active TB in HIV infected persons is the single most important step that should precede the decision to initiate TPT. Concerns regarding the development of INH resistance should not be a barrier to providing TPT.

41. For adults and adolescents living with HIV, TPT should be provided to those who are unlikely to have active TB based on appropriate clinical algorithm, irrespective of CD4 count, ART status, pregnancy status or history of treatment for prior episode of TB before three years. Children and infants less than 1 year of age should be provided preventive therapy only if they have a history of household contacts with pulmonary TB and active TB in the child has been excluded in investigation.

42. Population group Age group and ART regimen Selection of TPT regimen Preferred regimen Alternative regimen Persons living with HIV Adults, adolescents, children, and infants of all ages taking a PI- based ART regimen Daily isoniazid preventive treatment for 6 months (6H) Children and adolescents aged <15 years taking a DTG-based ART regimen Daily isoniazid preventive treatment for 6 months (6H) Children and adolescents aged <15 years taking EFV-based ART regimen Weekly isoniazid Plus rifapentine for 3 months (3HP*). Weekly isoniazid Plus rifapentine for 3 months (3HP). Adolescents and adults living with HIV (≥ 15 years of age) taking non- PI based ART regimen Weekly isoniazid Plus rifapentine for 3 months (3HP). Daily isoniazid preventive treatment for 6 months (6H) HIV-negative persons Infants and children <2 years of age) Daily rifampicin Plus isoniazid for 3 months (3RH). Daily isoniazid preventive treatment for 6 months (6H Eligible adolescents and children aged between ≥2 -14 years (refer to eligibility criteria specified above Weekly isoniazid Plus rifapentine for 3 months (3HP). - Daily isoniazid preventive treatment for 6 months (6H) - 3RH will be used as alternative to 3HP

43. Contraindications for TPT Individuals with any one or more of the following conditions should not receive TPT: • Symptoms compatible with tuberculosis even if the diagnosis is not yet confirmed; • Active hepatitis (chronic or acute); • Regular and heavy alcohol consumption; • Prior allergy or intolerance to medicine(s) in the regimen; and • Symptoms of peripheral neuropathy In addition, rifapentine is not currently indicated for children below 2 years, PLHIV receiving PI or NVP based ART regimens, and pregnant and breastfeeding women.

44. Completion of isoniazid-based TPT is defined as “completed” if a client completed the full course of therapy within nine months period (i.e. the six months of doses should be finished in nine months). If If the client discontinues isoniazid-based TPT for a period of less than three months: Resume the same course by adding for the missed doses at the end. If the client discontinues treatment for a period of more than three months, then re-initiate new course of treatment. Completion for 3HP is defined when the client took at least 11 doses of treatment in 16 weeks.

45. If a pregnant woman is found to have pulmonary TB shortly before delivery, then the baby, and if possible, the placenta, should be investigated for evidence of congenital TB infection. If the result is positive, the newborn should be treated accordingly. If asymptomatic, the newborn should receive TB preventive treatment followed by BCG immunization. Breastfeeding can be safely continued during this period.

46. Management of CNS OIs Neurological conditions in HIV clients may be due to: - HIV (HIV encephalopathy) - OIs (Toxoplasmosis, Cryptococcal meningitis) - Neurosyphilis - Malignancies (primary CNS lymphoma) and - Drugs, example EFV, the obsolete d drugs ( ddi and D4T) etc

47. Toxoplasma gondii Encephalitis (TE) is caused by the protozoan Toxoplasma gondii . Disease appears to occur almost exclusively because of reactivation of latent tissue cysts. . Sero -prevalence varies substantially in different communities; in Ethiopia, general prevalence is about 80%.

48. Clinical Manifestations Focal encephalitis with headache, confusion, or motor weakness and fever. non-specific headache and psychiatric symptoms. In the absence of treatment, disease progression results in seizures, stupor, and coma.

49. Diagnosis HIV-infected clients with TE are almost uniformly seropositive for anti-toxoplasma immunoglobulin G (IgG) antibodies. The absence of IgG antibody makes a diagnosis of toxoplasmosis unlikely but not impossible. - _ Anti-toxoplasma immunoglobulin M (IgM) antibodies usually are absent. Definitive diagnosis of CNS toxoplasmosis requires a compatible clinical syndrome; identification of one or more mass lesions by CT, MRI, or other radiographic testing

50. detection of the organism in a clinical sample. In the absence of imaging support, empirical treatment is justified when clients present with focal neurological findings and the CD4 count is < 200 cells μL .

51. Failure to respond to conventional therapy, based on presumptive clinical diagnosis within a week or two of initiation of therapy, suggests the diagnosis to be unlikely. With empirical treatment for toxoplasmosis, nearly 90% of clients will demonstrate clinical improvement within days of starting therapy. Radiological evidence of improvement is usual after 14 days of treatment.

52. Treatment First line treatment regimen for toxoplasma encephalitis in the Ethiopian context is For Adults: Trimethoprim/sulfamethoxazole 80/400 , oral, 4 tablets 12 hourly for 28 days , followed by 2 tablets 12 hourly for 3 months in adults. For children: 10mg of trimethoprim + 50mg of sulfamethoxazole/kg per dose every 12 hours for 28 days followed by maintenance therapy at 50% reduced dosage for three months. Secondary prophylaxis: use co- trimoxazole 960mg daily for adults .

53. Alternative regimen I . Sulfadiazine , PLUS Pyrimethamine , II. Pyrimethamine and Folinic Acid ( Leucovorin ): (standard dose) PLUS Clindamycin

54. Adjuvant corticosteroids should be used for clients with radiographic evidence of midline shift, signs of critically elevated intracranial pressure or clinical deterioration within the first 48 hours of therapy. Dexamethasone Anticonvulsants should be administered to clients with a history of seizures, but should not be given routinely for prophylaxis to all clients with the presumed diagnosis of TE

55. Cryptococcal infection Cryptococcal meningitis is one of the most important opportunistic infections and a major contributor to high mortality before and after ART is initiated. The main reasons for this high death rate include delayed presentation, together with poor availability of diagnostic Most HIV-associated cryptococcal infections are caused by Cryptococcus neoformans .

56. immediate ART initiation is not recommended for adults, adolescents and children living with HIV who have cryptococcal meningitis. ART initiation should be deferred 4–6 weeks from the initiation of antifungal treatment because of the risk of increased mortality.

57. Clinical manifestations - Subacute meningitis or meningoencephalitis with fever, malaise, and headache. - Neck stiffness and photophobia, occur in only one-quarter to one-third of clients. - lethargy, altered mentation, personality changes, and memory loss that are usually a result of increased intracranial pressure, thought to result from impaired cerebrospinal fluid (CSF) absorption.

58. Diagnosis prompt lumbar puncture (LP) with measurement of cerebrospinal fluid (CSF) opening pressure and rapid cryptococcal antigen assay is recommended as the preferred diagnostic approach no contraindication for lumbar puncture: A. If both access to a cryptococcal antigen assay and rapid results are available: LP with rapid CSF cryptococcal antigen assay is the preferred diagnostic approach. B. If access to a cryptococcal antigen assay is not available and/or rapid results are not available: LP with CSF India ink test examination is the preferred diagnostic approach

59. Settings without immediate access to LP or when LP is clinically contraindicated such as significant coagulopathy or suspected space-occupying lesion based on focal nervous system signs or recurrent seizures: A. I rapid serum, plasma, or whole blood cryptococcal antigen assays are the preferred diagnostic approaches. B. If a cryptococcal antigen assay is not available and/or rapid access to results is not ensured: prompt referral for further investigation and treatment as appropriate.

60. LP and CSF analysis: o The opening pressure may be markedly elevated. o CSF analysis  Protein 30-150 mg/dl  WBC 0-100 /mm3 (monocyte)  Culture positive 95-100%  Indian ink positive 60-80%  Cryptococcal Ag > 95 % sensitive and specific

61. Management A. Induction phase The following is recommended as the preferred induction regimen . A single high dose (10 mg/kg) of Liposomal Amphotericin B with 14 days of flucytosine (100 mg/kg per day divided into four doses per day) and fluconazole (1200 mg/daily for adults; 12 mg/kg per day for children and adolescents up to a maximum of 800 mg daily) should be used as the preferred induction regimen .

62. Consolidation phase Fluconazole (400–800 mg daily for adults or 6–12 mg/kg per day for children and adolescents up to a maximum of 800 mg daily) is recommended for the consolidation phase (for eight weeks following the induction phase).

63. Maintenance phase Fluconazole is recommended for the maintenance phase. Discontinuation of maintenance treatment (or secondary prophylaxis) will be when clients are stable and adherent to ART and anti-fungal maintenance treatment for at least one year and have a CD4 cell count of greater than or equal to 200 cells/mm3 (two measurements six months apart).

64. Management of elevated Intracranial pressure (ICP): >90 % of deaths in the first two weeks and 40% of deaths in weeks 3-10 are due to increased ICP. Failure to manage elevated ICP is the most common and most dangerous mistake in management (Since the ICP is non-communicating hydrocephalus there is no risk of CSF tapping within the recommended volume).

65. Daily serial LP should be done to control increased ICP by drawing 20-30 ml of CSF based on client’s clinical response. Signs of ICP include headache, altered mental status, meningismus and changing in hearing or vision should be closely monitored, if possible opening pressure should be measured.

66. Timing of ART initiation Immediate ART initiation is not recommended among adults, adolescents and children living with HIV who have cryptococcal meningitis because of the risk of increased mortality and should be deferred 4–6 weeks from the initiation of antifungal treatment. Depending on the cases, the scenario may differ

67. Prevention of cryptococcal disease Screening for cryptococcal antigen is the preferred approach for identifying infection when managing people aged 10 years or older When cryptococcal antigen screening is not available, fluconazole primary prophylaxis should be given to those who have a CD4 cell count of < 100 cells/mm3. All PLHIV with a positive cryptococcal antigen result should be evaluated for signs and symptoms of meningitis, and

68. if symptomatic they should undergo a LP. CSF cryptococcal antigen assay should be done to exclude active cryptococcal disease or at time there is no cryptococcal antigen assay test, India ink can be used. (India ink has lower sensitivity). The following algorithm guides how to decide whether a client needs prophylactic fluconazole treatment following screening positive for CrAg and for asymptomatic clients with CD4 count <100 cells/mm3.

69. Who is eligible for FPT? • Follow algorithm and blood- CrAg (+) ve without symptom and sign of CCM • When cryptococcal antigen screening is not available, fluconazole primary prophylaxis should be given to adults and adolescents living with HIV who have a CD4 cell count of < 100 cells/mm3.

70. Who is eligible for FPT? • Follow algorithm and blood- CrAg (+) ve without symptom and sign of CCM • When cryptococcal antigen screening is not available, fluconazole primary prophylaxis should be given to adults and adolescents living with HIV who have a CD4 cell count of < 100 cells/mm3.

71. What will be given as FPT: • Treat with Fluconazole 800 mg daily for two weeks • Initiate/re-initiate ART after 2 wks of fluconazole then • Fluconazole 400 mg daily for 8 weeks, then • Fluconazole 200 mg daily until: Client on ART for at least 6 months and CD4>200 cells/mm3 or CD4>100 cells/mm3 and Viral suppression (VL< 50)

72. Tuberculosis meningitis Tuberculosis meningitis is one of the neurological manifestations in HIV infected clients. About 10% of AIDS clients present with TB will show signs of meningial involvement. Symptoms include: fever, confusion, headache, meningismus , and focal neurological deficit (20%) especially cranial nerve palsy. Sometimes seizure and loss of consciousness is seen.

73. Diagnosis LP- it is mostly safe and CSF analysis characteristically reveals - Lymphocytosis (<500 cells/mm3) - Low glucose - High protein(100-500mg/dl) - CSF geneXpert AFB - seldom positive (10-40%) - Examine the deposit after centrifugation of 10cc - Examine at least for 30 minutes - Repeat several CSF samples over several days

74. Treatment - TB treatment according to the national protocol - Delay ART for at least 4 weeks and initiate within 8weeks after treatment of TB meningitis is initiated - Start prednisolone 1mg/kg for 2-4 wks then taper off over 4-8wks with Anti-TB for all clients

75. Prevention and Management of STIs - Screening and treatment strategies for STIs - Safe sexual practices education

76. Visceral Leishmaniasis and HIV Co-infection Screening, diagnosis, and treatment considerations

77. Visceral leishmaniasis (VL) is a systemic parasitic illness, transmitted primarily by the phlebotomine sand fly from animal or human reservoirs. Visceral Leishmaniasis is endemic in Ethiopia, with patchy distribution in the southern and north-western lowlands ..

78. The causative parasite is L. donovani . VL has emerged as a major OI associated with HIV. In HIV clients, VL represents reactivation of latent infection with Leishmania parasite

79. Clinical features: The cardinal signs of VL in clients with HIV infection are unexplained fever, splenomegaly and pancytopenia. Presentation may not be typical. The bone marrow is packed with parasites but two-thirds of cases have no detectable anti Leishmania antibodies. CD4+ cell count in co-infected clients is usually <200cells/ml.

80. Diagnosis: • Parasitological diagnosis: Isolation of the organism from samples taken from reticuloendothelial tissue and examined with Giemsa, Wright’s or Leishmanial stain. • Immunological diagnosis: - Antibody detection- rapid test rk39 tests , - Antigenic test-DAT freeze dried Antigen test- Confirmatory - negative or positive results,

81. Treatment The first line regimen - AmBisome ® at a total dose of 30 mg/kg (5 mg/kg on day 1, 3, 5, 7, 9, 11) and miltefosine 2.5 mg/kg/day for 28 days, starting from day 1 (100 mg/day for clients weighing more than 30 kg, 150 mg/day for clients weighing more than 45 kg).

82. Second-Line regimen - AmBisome ® monotherapy - A total dose of 40 mg/kg given on days 1, 2, 3, 4, 5, 10, 17 and 24 has shown to have an efficacy of 50%. - Drug combinations - Paromomycin in combination with AmBisome ® or - miltefosine ). Another option could be the combination of sodium stibogluconate (SSG) 20 mg/kg/d for 30 days with paromomycin 15 mg/kg/day for 17 days. - Pentavalent antimonials - Due to the high toxicity of antimonials and risk of mortality in HIV/VL co-infected clients, this should be the last option. They are administered intravenously or

83. Cutaneous Manifestations in HIV-positive Individuals

84. early manifestations of HIV infections frequently occur in the skin. Different kinds of OIs, such as herpes zoster, and other viral, fungal and bacterial infections occur in the skin. Manifestations of adverse drug reactions and noninfectious conditions also occur in the skin.

85. Agent CD4 Symptom Diagnosis Treatment E. Hystolitica Any bloody stool, colitis Stool microscopy Metronidazole Giardia Any Watery diarrhea Stool microscopy Metronidazole Strongloides stercoralis Any Watery diarrhea Stool microscopy Ivermectin or Albendazole Cryptosporidium <150 Watery diarrhea Modified AFB ART Isospora belli <100 Watery diarrhea Modified AFB TMP-SMX Microsporidium <50 Watery diarrhea Giemsa stain Albendazole CMV <50 Watery/bloody diarrhea, colitis Tissue biopsy Ganciclovir

86. a . Pruritic Papular Eruption Pruritic Papular Eruption is common among HIV infected clients causing substantial morbidity in sub-Saharan Africa. Its prevalence ranges from12-46% and it is uncommon in HIV negative clients.The pathogenesis is unknown but it may be related to hypersensitivity to arthropod bites. In extreme form, eosinophilia and eosinophilic infiltrates of the skin are present. Severity of rash often correlates with CD4 count.

87. Clinical manifestations • Intensely pruritic discrete, firm papules with variable stages of development and predilection for extremities, though they can involve trunk and face. • Pigmentation, scarring and nodules due to excoriation.

88. Treatment: Treat with topical steroid and oral antihistamines; however it is often refractory to treatment and hence short course prednisolone may be used. HAART is often effective.