2 natural history of hiv and who clinical staging naco lac m
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Similar to 2 natural history of hiv and who clinical staging naco lac m
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2 natural history of hiv and who clinical staging naco lac m
- 1. Natural History and Clinical Staging of HIV Infection Natural History of HIV
- 2. Session Objectives By the end of the session the participant will be able • To list the modes of HIV transmission • To discuss the pathogenesis and life cycle of HIV • To describe the progression of HIV • To classify an HIV-infected patient according to the WHO clinical staging Natural History of HIV 2
- 3. Modes of HIV Transmission Semen and Vaginal Sharing Needles Needle Stick Fluids Injury & Syringes Through Infected During Pregnancy Breast Feeding Blood or Birth Images Courtesy HIV Basics Course for Nurses, I-TECH Natural History of HIV 3
- 4. HIV Transmission Risk Exposure Route HIV Transmission Blood transfusion 90-95% Perinatal 20-40% Sexual intercourse 0.1 to 1% Vaginal 0.05-0.1% Anal 0.065-0.5% Oral 0.005-0.01% Injecting drugs use 0.67% Needle stick exposure 0.3% Mucous membrane splash to eye, 0.09% oro-nasal Source: NACO PEP Guidelines Natural History of HIV 4
- 5. How HIV Infects the Body HIV makes contact with cells located within the genital mucosa Virus is carried to regional lymph nodes (1-2 Days) Exponential viral replication Widespread systemic dissemination to the brain, spleen, distant lymph nodes, etc. (5-11 Days) Natural History of HIV 5
- 6. Path of the Virus Exposure to HIV at Day 0 mucosal surface (sex) Virus collected by Day 0-2 dendritic cells, carried to lymph node Day 4-11 HIV replicates in CD4 cells, released into blood Virus spreads to Day 11 on other organs Image Courtesy Kahn JO, Walker BD. NEJ Med.1998; 339: 33-39 Natural History of HIV 6
- 7. HIV Lifecycle Image Courtesy HIV Basics Course for Nurses, I-TECH HIV Lifecycle Video Natural History of HIV 7
- 8. Stages of Untreated HIV Infection Viral transmission Acute retroviral syndrome: 2-3 weeks Seroconversion: 2-4 weeks Asymptomatic chronic HIV infection: 8 yrs (Avg.) Symptomatic HIV infection/AIDS: 1.3 yrs (Avg.) Natural History of HIV 8
- 9. Typical Course of Untreated HIV Infection 800 Acute HIV 10^6 HIV antibodies CD4 Asymptomatic count HIV cells/µl RNA Minor HIV-related Copies /ml symptoms Virologic set-point 200 Varies from patient to Opportunistic patient infections 10^2 Death 1 3 about 6mths // 5yrs 10 yrs Natural History of HIV Time 9
- 10. Progression of HIV Disease • Acute Seroconversion (Acute HIV Syndrome) • Asymptomatic HIV (Clinical latency) • Symptomatic HIV • Acquired Immune Deficiency Syndrome (AIDS) Natural History of HIV 10
- 11. Acute HIV syndrome • Transient symptomatic illness • Affects 40-90% of HIV+ individuals • Ranges from mild, non- specific illness to severe illness that can result in hospitalisation HIV Web study (www.HIV webstudy.org) Supported by HRSA Natural History of HIV 11
- 12. Acute HIV syndrome: Clinical Manifestations Small pink macules: Trunk, limbs and face Courtesy: Kahn, NEJM, 1998 Courtesy: Walker, B. 40th IDSA, Chicago 2002. Natural History of HIV 12
- 13. Patterns of HIV Progression • Typical progressors • Rapid progressors • Slow progressors • Long-term non-progressors Natural History of HIV 13
- 14. WHO Clinical Staging • WHO Clinical Staging 1 • Asymptomatic • Persistent generalised lymphadenopathy (PGL) • Painless enlarged lymph nodes >1 cm • In two or more non-contiguous sites (excluding inguinal), in absence of known cause and • Persisting for 3 months Natural History of HIV 14
- 15. WHO Clinical Staging 2 Unexplained moderate weight loss (<10% of presumed or measured body weight) Recurrent respiratory tract infections (sinusitis, tonsillitis, otitis media, pharyngitis) Herpes zoster Angular cheilitis Recurrent oral ulceration Papular pruritic eruptions (PPE) Seborrhoeic dermatitis Fungal nail infections Natural History of HIV 15
- 16. WHO Clinical Staging 3 Unexplained severe weight loss (>10% of presumed or measured body weight) Unexplained chronic diarrhoea for longer than one month Unexplained persistent fever (above 37.5oC intermittent or constant for longer than one month) Persistent oral candidiasis Oral hairy leukoplakia (OHL) Pulmonary tuberculosis Natural History of HIV 16
- 17. WHO Clinical Staging 3 Severe bacterial infections (e.g. pneumonia, empyema, pyomyositis, bone or joint infection, meningitis, bacteraemia) Acute necrotizing ulcerative stomatitis, gingivitis or periodontitis Unexplained Anaemia (<8 g/dl) Neutropenia (<0.5 x 109 /L) and or Chronic thrombocytopenia (<50 X 109 /L) Natural History of HIV 17
- 18. WHO Clinical Staging 4 HIV wasting syndrome Pneumocystis pneumonia (PCP) Recurrent severe bacterial pneumonia Chronic herpes simplex infection (orolabial, genital or anorectal of more than one month’s duration or visceral at any site) Oesophageal candidiasis (or candidiasis of trachea, bronchi or lungs) Extra pulmonary tuberculosis Kaposi’s sarcoma Natural History of HIV 18
- 19. WHO Clinical Staging 4 Cytomegalovirus infection (retinitis or infection of other organs) Central nervous system toxoplasmosis HIV encephalopathy Extra pulmonary cryptococcosis including meningitis Disseminated non-tuberculous mycobacteria infection Progressive multifocal leukoencephalopathy Chronic cryptosporidiosis Chronic isosporiasis Natural History of HIV 19
- 20. WHO Clinical Staging 4 Disseminated mycosis (extra pulmonary histoplasmosis, coccidiomycosis) Recurrent septicaemia (including non-typhoidal salmonella) Lymphoma (cerebral or B cell non-Hodgkin) Invasive cervical carcinoma Atypical disseminated leishmaniasis Symptomatic HIV associated nephropathy or Symptomatic HIV associated cardiomyopathy Natural History of HIV 20
- 21. WHO Clinical Staging Case Studies (17) • Each trainee has to discuss one case study • Look into the clinical photograph / X-ray • Describe the lesion, as you observe • Discuss Differential Diagnosis • Identify Clinical staging of HIV infection Natural History of HIV 21
- 22. Case Study 1 and 2 Source: GHTM, Tambaram, Chennai • Describe the lesion • Identify Clinical staging of HIV infection Natural History of HIV 22
- 23. Case Study 3 Source: GHTM, Tambaram, Chennai Natural History of HIV 23
- 24. Case Study 4 Image Courtesy: GHTM/ITECH Fellowship Programme, Tambaram, Chennai WHO Clinical Staging in CLHIV 24
- 25. Case Study 5 & 6 Image Courtesy :GHTM, Tambaram, Chennai OI Curriculum, GHTM-I-TECH, 2004 Natural History of HIV 25
- 26. Case Study 7 Images Courtesy: I-TECH-GHTM Fellowship Programme, Tambaram, Chennai Natural History of HIV 26
- 27. Case Study 8 • Describe the lesion • What are the differential diagnosis? • Clinical staging? Image Courtesy: Bowring Hospital, Bangalore Natural History of HIV 27
- 28. Case Study 9 Image Courtesy GHTM , Tambaram HIV Fellowship Programme Natural History of HIV 28
- 29. Case Study 10 Images Courtesy: GHTM/ITECH Fellowship Programme, Tambaram, Chennai WHO Clinical Staging in CLHIV 29
- 30. Case Study 11 Case Study 12 Images Courtesy: Indian Academy of Pediatrics WHO Clinical Staging in CLHIV 30
- 31. Case Study 13 Image Courtesy: Indian Academy of Pediatrics WHO Clinical Staging in CLHIV 31
- 32. Case Study 14 Image Courtesy: GHTM/ITECH Fellowship Programme, Tambaram, Chennai WHO Clinical Staging in CLHIV 32
- 33. Case Study 15 • 5 year old child • Respiratory distress • Cough+ • No sputum • Respiratory Rate: 45/mt • Lung signs: Bilateral basal inspiratory crackles Image courtesy: TRC, Chennai 33
- 34. Case Study 16 • 37 year-old HIV positive male • Lost 9 kg in last 3 months (Previously his body weight was 75 kg) • Reports having a fever for the past month • Treated for pulmonary TB 5 months ago What is his WHO clinical staging? Natural History of HIV 34
- 35. Case Study 17 • 34 year-old HIV positive male • Suffers from bacterial sinusitis and a fungal infection on his toes • Has no problem keeping up with his usual activities and weight is stable • Treated for herpes zoster 4 years ago What is his WHO clinical staging? Natural History of HIV 35
- 36. Key Points • The most common mode of HIV transmission in India is sexual • Understanding the natural history of HIV is important in predicting progress of the disease • Clinical staging allows clinicians to reliably predict in patients: – The risk of opportunistic infections and death – The need for disease prevention & pre ART Care – ART Initiation Natural History of HIV 36
Editor's Notes
- Step 1: Introduction and Session Objectives, HIV Transmission Concepts (Slides 1-4) - 7 minutes Trainer Notes: This session should take approximately 60 minutes to implement. Step 1: Introduction and Session Objectives, HIV Transmission Concepts (Slides 1-4) - 7 minutes Step 2: Pathogenesis, Progression (Slides 5-13) - 15 minutes Step 3: WHO Clinical Staging of HIV infection (Slides 14-20) - 10 minutes Step 4: Case Studies on WHO Clinical Staging (Slides 21-35) - 26 minutes Step 5: Summary (Slide 36) - 2 minutes
- Trainer Notes: Present the session learning objectives Ask participants “Why it is important to understand the progression of HIV and the clinical stages of HIV infection?” Answers: Enables clinicians to identify the appropriate time to start ART Helps targeted drug development to arrest the infection at various stages Identifies time to initiate preventive therapy
- Trainer Notes & Reader Notes: The next two slides summarise the basic HIV transmission concepts. Mention more will be discussed during the PPTCT session. This information is essential to understand HIV epidemiology patterns and prevention approaches discussed in this session. Review the body fluids that transmit HIV: Semen Vaginal Fluids Blood Breast Milk Review the main modes of HIV transmission: Sexual (vaginal or anal) Injection Drug Use Mother to Child Occupational Exposure Mother to Child How HIV is transmitted: HIV is transmitted from one person to another through the exchange of blood and certain bodily fluids during sexual activity. Vaginal secretions and semen contain HIV. Sexual intercourse (vaginal and anal) is one way in which HIV is transmitted. Sharing needles, syringes and other paraphernalia receiving a blood transfusion, or getting a deep needle stick injury from a person infected by HIV during an occupational exposure, are ways through which transmission occurs when blood from an infected person is transmitted to another. Mothers can transmit the virus to their babies during pregnancy, delivery, or during breast feeding. This does not happen all the time - approximately 30-48% of the time as reported in India, but abroad it is less than 30%.
- Trainer Notes & Reader Notes: The percentage of contact infectivity of HIV from sexual transmission varies depending on sexual activity (Royce and others 1997). Anal intercourse carries a higher transmission probability than penile-vaginal intercourse and male-to-female transmission is more likely than female-to-male transmission. Discuss the following briefly: Why anal intercourse is more risky?? Why women are more vulnerable? Mention about circumcision?? Why oral transmission is so low?? Infective fluids?? Refer PEP session. Needle exchange Source: Guidelines On The Management Of Occupational And Non-occupational Exposure To HIV And Post-exposure Prophylaxis, Draft -January 2007.
- Step 2: Pathogenesis, Progression (Slides 5-13) - 15 minutes Trainer Notes: Use the image on the following slide to illustrate the steps involved in the pathogenesis of HIV infection. Ask participants to quickly name the modes of HIV transmission Reader Notes: HIV transmitted through sexual activity enters the bloodstream via mucous membranes lining the vagina, rectum and mouth. Macrophages and dendritic cells on the surface of mucous membranes bind virus and shuttle it into the lymph nodes, which contain high concentrations of Helper T cells (CD4+ T cells). Once HIV has entered the body, the immune system initiates anti-HIV antibody and cytotoxic T cell production. However, it can take one to six months for an individual exposed to HIV to produce measurable quantities of antibody. The immune response is weakened as memory T cells (CD4+ CCR5+) are destroyed. HIV enters the body and binds to dendritic cells which carry the virus to CD4+ T cells in lymphoid tissue establishing infection. Virus replication accelerates producing massive viremia and wide dissemination of virus throughout the body's lymphoid tissues. An immune response against virus causes some protection but a chronic persistent infection is established. The production of cytokines and cell divisions that regulate the immune response for protection also cause HIV replication. There is a rapid turnover of CD4+ T cells that ultimately leads to their destruction and to a change in lymphoid tissues that prevent immune responses.
- Trainer Notes: The arrows indicate the path of the virus. The viral-envelope protein binds to the CD4 molecule on dendritic cells. Entry into the cells requires the presence of CCR5, a surface chemokine receptor. Dendritic cells, which express the viral co receptors CD4 and CCR5, are selectively infected by R5 (macrophage-tropic) strains. Within two days after mucosal exposure, virus can be detected in lymph nodes. Within another three days, it can be cultured from plasma. Cytotoxic lymphocyte production follows the rise of HIV in the blood. HIV specific CD4+ T cells may be especially susceptible to attack and destruction by HIV. HIV binds to CD-SIGN, a glycoprotein expressed on dendritic cells. Migration of HIV bearing activated dendritic cells to helper T cell areas of lymph nodes may specifically infect helper T cells specific for HIV peptides. Reductions in HIV specific helper T cell numbers may lead to decreased activation and survival of cytotoxic CD8 T cells. Reduced CD4 T cells may also result in an incomplete activation of CD8 T cells that can remove HIV infected cells, resulting in a decreased ability to destroy virally infected cells. The rapid loss of memory helper T cells and the inability to replace these cells leads to increasing immunodeficiency. High mutation rates of HIV also allow the virus to escape adaptive immune responses. Reader Notes: The arrows indicate the path of the virus. The viral-envelope protein binds to the CD4 molecule on dendritic cells. Entry into the cells requires the presence of CCR5, a surface chemokine receptor. Dendritic cells, which express the viral co receptors CD4 and CCR5, are selectively infected by R5 (macrophage-tropic) strains. Within two days after mucosal exposure, virus can be detected in lymph nodes. Within another three days, it can be cultured from plasma. Cytotoxic lymphocyte production follows the rise of HIV in the blood. HIV specific CD4+ T cells may be especially susceptible to attack and destruction by HIV. HIV binds to CD-SIGN, a glycoprotein expressed on dendritic cells. Migration of HIV bearing activated dendritic cells to helper T cell areas of lymph nodes may specifically infect helper T cells specific for HIV peptides. Reductions in HIV specific helper T cell numbers may lead to decreased activation and survival of cytotoxic CD8 T cells. Reduced CD4 T cells may also result in an incomplete activation of CD8 T cells that can remove HIV infected cells, resulting in a decreased ability to destroy virally infected cells. The rapid loss of memory helper T cells and the inability to replace these cells leads to increasing immunodeficiency. High mutation rates of HIV also allow the virus to escape adaptive immune responses.
- Trainer Notes: Carefully review this slide with participants. How to play the video? Check the functioning of the video before the session. Link to the video is given in the slide in the red colour box indicating HIV Lifecycle Video. Right Click on the box to select Open Hyperlink to open the video If the link is not functioning, right click on the red box and select Hyperlink. An INSERT HYPERLINK window will appear. Browse for the video through this window and select ‘ok’ and the hyperlink will be established. Again right click on the red box & select Open Hyperlink to play the video Play Johns Hopkins' video on viral replication: duration 2 minutes. Source: http://www.jhu.edu/Johns Hopkins' video on HIV viral replication. Stop the video at the appropriate stage and explain the different stages in the viral replication: Viral entry. Single stranded viral RNA conversion into double stranded viral DNA. Cleavage of larger proteins into smaller viral proteins by the protease enzyme. Reader Notes: The 6 stages of the HIV life cycle are essential to understand the site of action of ARVs on HIV. HIV uses the CD4 cell like one factory to reproduce itself: HIV attaches to the CD4 cell & releases RNA & enzyme on entry. The enzyme ‘Reverse Transcriptase’ makes a DNA copy of the viral RNA. New viral DNA is then integrated into the CD4 cell nucleus using ‘Integrase.’ New viral components are then produced, using the cell’s machinery. These are assembled together using the enzyme ‘Protease’ and then released as new viruses. The host CD4 cell gets destroyed during this process. Source video: http://www.jhu.edu/Johns Hopkins' video on HIV viral replication: duration 2 minutes. Stages: Attachment, Fusion and entry of the virus, RNA >> DNA, Integration into Host Genome, Production on viral proteins, Cleavage of viral proteins into functional proteins, assembly and release of virions.
- Trainer Notes: Acute retroviral syndrome occurs when the virus is disseminated. It is characterised by fever, rash, lymphadenopathy and sore throat (like other viral infections). On recovery, the patient will have antibodies to HIV that can be detected by tests like ELISA. The patient remains without symptoms for many years until he or she develops symptomatic HIV or AIDS about 8 years down from the time of infection. This period, as also the time period between development of AIDS to death is highly variable. Reader Notes: Acute retroviral syndrome occurs when the virus is disseminated. It is characterised by fever, rash, lymphadenopathy and sore throat (like other viral infections). On recovery, the patient will have antibodies to HIV that can be detected by tests like ELISA. The patient remains without symptoms for many years until he or she develops symptomatic HIV or AIDS about 8 years down from the time of infection. This period, as also the time period between development of AIDS to death is highly variable.
- Trainer Notes: Explain the graphic in detail. Pink color depicts the viral load. It reaches the maximum level during acute retroviral syndrome, then it settles down to the “viral set point” and this set point is maintained over a period of years. After 5-8 years the viral load starts increasing again and the patient progresses to the stage of AIDS. Importance of viral set point may be described here. The blue line depicts the CD4 count. The CD4 count is depleted initially and then reaches a set point which is maintained over a period of 5-8 years. When the patient reaches the stage of AIDS, CD4 count starts declining very fast. Green dotted line represents the development of antibodies to HIV and their presence throughout the infection; Introduce the concept of window period here. Reader Notes: Pink color depicts the viral load. It reaches the maximum level during acute retroviral syndrome, then it settles down to the “viral set point” and this set point is maintained over a period of years. After 5-8 years the viral load starts increasing again and the patient progresses to the stage of AIDS. Importance of viral set point may be described here. The blue line depicts the CD4 count. The CD4 count is depleted initially and then reaches a set point which is maintained over a period of 5-8 years. When the patient reaches the stage of AIDS, CD4 count starts declining very fast. Green dotted line represents the development of antibodies to HIV and their presence throughout the infection; introduce the concept of window period here.
- Trainer Notes: Acute seroconversion: Fever, rash and adenopathy Usually 3-6 weeks after exposure Asymptomatic HIV (clinical latency): Patient often unaware of infection, antibodies detectable. Immune system able to control virus to limited extent and CD4 >350/cu.mm Able to transmit HIV to others Symptomatic HIV: Minor to moderately severe symptoms Recurrent symptoms AIDS: Severe immuno-suppression associated with opportunistic infections or cancers Reader Notes: Acute seroconversion: Fever, rash and adenopathy Usually 3-6 weeks after exposure Asymptomatic HIV (clinical latency): Patient often unaware of infection, antibodies detectable. Immune system able to control virus to limited extent and CD4 >350/cu.mm Able to transmit HIV to others Symptomatic HIV: Minor to moderately severe symptoms Recurrent symptoms AIDS: Severe immuno-suppression associated with opportunistic infections or cancers
- Trainer Notes: Acute HIV syndrome Usually 3-6 weeks after exposure
- Trainer Notes: Acute HIV syndrome Fever, rash and adenopathy Usually 3-6 weeks after exposure
- Trainer Notes: The progression to AIDS among individuals is variable. Following infection with HIV, some people progress rapidly (within 1-2 years) to a low CD4 count, become ill and, without treatment, dies. Other people may become infected and remain healthy with relatively normal CD4 counts for many years (>10). Typical progressors have a drop of 35-50 CD4 cells/year. Rapid progressors ("CD4 crash") have a drop of 50 CD4 cells per month after seroconversion. Slow Progressors have a CD4 decline that is very slow compared to the typical progressors. Long term non-progressors have CD4 counts that are stable at a baseline for many year Reader Notes: The progression to AIDS among individuals is variable. Following infection with HIV, some people progress rapidly (within 1-2 years) to a low CD4 count, become ill and, without treatment, dies. Other people may become infected and remain healthy with relatively normal CD4 counts for many years (>10). Typical progressors have a drop of 35-50 CD4 cells/year. Rapid progressors ("CD4 crash") have a drop of 50 CD4 cells per month after seroconversion. Slow Progressors have a CD4 decline that is very slow compared to the typical progressors. Long term non-progressors have CD4 counts that are stable at a baseline for many years.
- Step 3: WHO Clinical Staging of HIV infection (Slides 14-20) - 10 minutes Trainer Notes: Refer to Handout on WHO Clinical Staging in the Participant Manual Discuss WHO Clinical staging 1
- Trainer Notes: Refer to Handout on WHO Clinical Staging in the Participant Manual Discuss WHO Clinical staging 2
- Trainer Notes: Refer to Handout on WHO Clinical Staging in the Participant Manual Discuss WHO Clinical staging 3
- Trainer Notes: Refer to Handout on WHO Clinical Staging in the Participant Manual Discuss WHO Clinical staging 3 (continued)
- Trainer Notes: Refer to Handout on WHO Clinical Staging in the Participant Manual Discuss WHO Clinical staging 4
- Trainer Notes: Refer to Handout on WHO Clinical Staging in the Participant Manual Discuss WHO Clinical staging 4 (continued)
- Trainer Notes: Refer to Handout on WHO Clinical Staging in the Participant Manual Discuss WHO Clinical staging 4 (continued)
- Step 4: Case Studies on WHO Clinical Staging (Slides 21-35) – 26 minutes Trainer Notes: Explain to participants that the next several slides will present a case including an accompanying clinical image and a few “clues” to assist them in making a clinical diagnosis and categorise the patient according to WHO Clinical Staging Guidelines Handout 1: WHO Clinical Staging will assist them with questions regarding WHO clinical staging. For each slide: Project the image and review the clinical history for participants. Ask for volunteers to answer the questions below. Give the correct answers to participants
- Trainer Notes: Project the image and review the clinical history for participants. Ask for volunteers to answer the questions below. Give the correct answers to participants. Reader Notes: Clinical History: Case Study 1: A 30 year-old HIV-positive male patient presented with these types of lesions over the gums and inner aspect of the upper and lower lips. Question 1: What is the diagnosis? Answer: Oral candidiasis. Question 2: What clinical stage does this patient belong to? Answer: WHO Clinical Stage III. Case Study: Ask them to watch the involvement of palate and pharynx with candida. Ask the trainees, if the patient is presenting with odynophagia, then what will be the Clinical Staging in this patient? Answer: Stage IV (Oro-Oesophageal Candidiasis)
- Trainer Notes: Project the image and review the clinical history for participants. Ask for volunteers to answer the questions below. Give the correct answers to participants. Reader Notes: Clinical History: An adult HIV-positive male patient presented with white linear, vertical, raised, lesions over the side of the tongue and they are not easily removable. Question 1: What is the diagnosis? Answer: Oral Hairy Leukoplakia (Caused by Ebstein Barr Virus). Question 2: What clinical stage does this patient belong to? Answer: WHO Clinical Stage III.
- Trainer Notes: Ask participants the questions below and show the lesions on the trunk which appears healed using the laser pointer. Review the answers Question 1: “Name the clinical finding in the child Answer: There is extensive Herpes Zoster lesions which are healing. Question 2: “Name the clinical staging?” Answer: Stage II
- Trainer Notes: Project the image and review the clinical history for participants. Ask for volunteers to answer the questions below. Give the correct answers to participants. Reader Notes: Case Study 5: A 29 year old HIV positive woman came with fever and painful vesicular lesions over the lips and at the angle of the mouth of 3 days duration. Question 1: What is the diagnosis? Answer: Herpes simplex labialis Question 2: What clinical stage does this patient belong to? Answer: WHO Clinical Stage II. Case Study 6: Chronic ulcerative lesions present for more than one month in adult male with HIV seropositivity Question 1: What is the diagnosis? Answer: Herpes simplex Question 2: What clinical stage does this patient belong to? Answer: WHO Clinical Stage IV.
- Trainer Notes: Project the image and review the clinical history for participants. Ask for volunteers to answer the questions below. Give the correct answers to participants. Reader Notes: Clinical History: Two middle aged HIV-positive male patients presented with extensive scaly hypo-pigmented lesions over his face and body. Question 1: What is the diagnosis? Answer: Seborrheic dermatitis, Patient is showing the signs of moderate wasting (you can observe the prominent clavicles and the ribs, supra clavicular and infra clavicular hollowing, Prominent intercostals spaces, the malar prominence is very much present and the cheeks are hallowed out.) Question 2: What clinical stage does this patient belong to? Answer: . If the diagnosis is only Seborrheic dermatitis, then he fits into WHO Clinical Stage II. If you consider the wasting also and if it is more than 10% of his presumed body weight, then he fits in to WHO Clinical Stage III. If it is less than 10% of his presumed body weight, then he fits in to WHO Clinical Stage II only. So the final answer depends upon his presumed body weight and present body weight.
- Trainer Notes: Project the image and review the clinical history for participants. Ask for volunteers to answer the questions below. Give the correct answers to participants. Reader Notes: Clinical History: A 39 year-old HIV-positive male patient presented with history of fever, loss of appetite and multiple matted glands in the neck. Question 1: What is the diagnosis? Answer: TB Cervical Lymphadenitis; AFB was identified in FNAC. Discuss other differential diagnoses, including Non Hodgkin Lymphoma Question 2: What clinical stage does this patient belong to? Answer: WHO Clinical Stage IV.
- Trainer Notes: Project the image and give the diagnosis to the patients. Ask for volunteers to answer the question below. Give the correct answer to participants. Reader Notes: Diagnosis: This patient has Cerebral Toxoplasmosis. Question 1: What clinical stage does this patient belong to? Answer: WHO Clinical Stage IV.
- Trainer Notes: After projecting the pictures, the trainer may request one of the participant to answer the following question; 10 yrs old, male child presented with this (using the laser pointer, point the skin lesions) the clinical problem for the past few months. Question 1: “Describe the clinical finding in this child? Name the lesion?” Answer: There are multiple, pearl like, flesh/skin coloured, dome-shaped, smooth papular lesions with central umbilication, varying in size, are present over the face. Most probably the lesions are Molluscum Contagiosum. Question 2: “ Stage the disease as per WHO clinical staging?” Answer: Stage-II.
- Trainer Notes: Conduct a discussion and brainstorming activity using the following three questions. Question 1: Name the clinical finding in the child (number-1, left side)? Answer: The child is emaciated and there is hepatomegaly. Question 2: “Name the clinical finding in the child (number-2, right side)?” Answer: There is hepatosplenomegaly. Question 3: “In both the children, the etiology was not known. All the routine tests were normal, Name the clinical staging?” Answer: Stage II.
- Trainer Notes: Ask participants the questions below and show the lesions (Parotid Swelling) using the laser pointer. Review the answers Question 1: “Name the clinical finding in the child? (the trainer may give a clue to the participants; having a swelling in left parotid region, for the past few weeks)” Answer: The child is having parotid swelling. Question 2: “ The aetiology for the parotid swelling is not known in spite of the routine tests, Name the clinical staging?” Answer: Stage II.
- Trainer Notes: The following clinical points may be provided: 8 Yrs old HIV positive female child admitted for severe breathlessness of acute onset, cough and mild fever. The x-ray is projected and one of the participants may be requested to read the x-ray chest PA view. Answer: There are infiltrations in the mid and lower zones of both the lung fields. The cardiac shadow is within normal limits. Probably PCP. Question : What is the WHO clinical stage? Answer: Stage IV.
- Trainer Notes: Project the image and give the diagnosis of the patient. Ask for volunteers to answer the question below. Give the correct answer to participants. Point out that this radiological picture is from a patient with Lymphoid Interstitial Pneumonitis (LIP), which is more commonly seen in children.
- Trainer Notes: Explain to participants that the last two case studies will be conducted in small groups. Divide participants into small groups (about 4 members). Explain to participants that they should first read over the slide and discuss the answer to the question. Allow two minutes for small group discussion. When each group has completed the activity, ask a volunteer to answer the question: “What is his WHO clinical stage?” Answer: WHO clinical stage 4 because the patient has lost more than 10% of his body weight (9 Kg out of 75 Kg); had unexplained prolonged fever (for >one month) and been treated for pulmonary TB. Loss of weight >10% with fever of more than one month duration, indicates HIV Wasting, which indicate stage 4 disease. Encourage discussion of the answer by asking if all group members were in agreement with the answer and if any other points of discussion came up within the small groups. Repeat the same for Case Study 14
- Trainer Notes: Answer: WHO Clinical Stage 2 because the patient is suffering from bacterial sinusitis and fungal infection of his toes. He also had herpes zoster in the past. His weight is stable and he is able to keep up with his regular activities.
- Step 5: Summary (Slide 36) - 2 minutes Trainer Notes: Review Key Points with participants and answer any final questions.