HIV/AIDS introductory course for nurses

1. HIV/AIDS
For BSc Nursing
Gugsa Nemera

2. Objective
• Describe pathogenesis of HIV/AIDS
• List prevention strategies to reduce the spread of HIV
infection in the country
• List mode of transmissions of HIV and body fluid that
contain HIV in higher rate
• Describe the global and national HIV/AIDS
epidemiological profile
• Describe HIV/AIDS staging and clinical manifestations
• Elaborate the initiation of PEP

3. HIV and AIDS
History
1981
AIDS was 1st
recognized in USA among homosexual
men
PCP developed with out any other reason
Kaposi’s sarcoma seen in 26 health homosexuals
1983
HIV virus was isolated from patient with
lymphadenopathy
1984
HIV virus was clearly demonstrated to be the cause of AIDS

4. Historical Overview of HIV/AIDS in Ethiopia
1984: The first evidence of HIV infection in
Ethiopia
1986: The first two AIDS cases reported to the
Ministry of Health
1989: HIV/AIDS surveillance started
2003: Fee base ART started
March, 2005: Free ART program started

5. Definitions:
AIDS
Sever disease syndrome
Final result of infection with a retrovirus, HIV
HIV infection is a progressive disease leading to
AIDS, as defined by the CDC (January 1994): “persons
with CD4 cell count of under 200 (with or without
symptoms of opportunistic infection) who are HIV-
positive

6. Etiologic agent & phathophysiology
Human Immuno deficiency virus (HIV) is a
retrovirus belonging to the family of
lentiviruses.
 Retroviruses have the ability to use their
RNA and host DNA to make viral DNA and are
known for their long incubation periods.
HIV consists of a cylindrical center
surrounded by a sphere-shaped lipid bi-layer
envelope

7. Etiologic agent & phathophysiology cont’d
 two major proteins in this lipid bi-layer,
gp120 and gp41 which helps to:
 mediate recognition of CD4+ cells, thereby
Enabling the HIV virus to attach to and invade the
CD4+ cells.

8. Etiologic agent & phathophysiology cont’d
The inner sphere contains
two single stranded copies of the genomic
material – (RNA)
multiple proteins and enzymes necessary in
the process of HIV replication and maturation:
p24
p17
reverse transcriptase
integrase
protease

9. Etiologic agent & phathophysiology cont’d
Unlike other retroviruses, HIV utilizes nine
genes to code for the necessary proteins and
enzymes.
The three principal genes are gag, pol, and
env.
The gag gene encodes core proteins.
The pol gene encodes the enzymes reverse
transcriptase, protease, and integrase.
The env gene encodes the HIV structural
components known as glycoproteins.

10. structure o f HIV

11. Continium of HIV/AIDS
Initial exposure
Primary infection (acute infection)
Flue-like syndrome, antibodies develops to HIV in 1to 6 months
Asymptomatic HIV infections (HIV sero positivity)
Infectious but no evidence of HIV infection except positive antibody test
Early HIV disease (symptomatic infections)
Persistent unexplained fever, night sweating, weight loss,
lymphadenopathy; S/S will not occur until 8-10 years after HIV exposure
Advanced disease

12. HIV life cycle
• Host cells infected with the virus have
shortened life span, b/se the virus uses them
as a “machine” to produce multiple copies of
new HIV.
• Thus the virus continuously uses host cells to
replicate it self.
• As many as 10 million to 10 billion viruses
produced each day.

13. HIV life cycle cont’d
• 24 hr after exposure, HIV captured by
dendritic cells in skin and mucus membrane.
• With in 5 days after exposure, the infected
cells make their way to Lymph node and
eventually to peripheral blood where viral
replications become very rapid.

14. HIV life cycle cont’d
• CD4
+ cells responds to viral antigen migrate to
Lymph node; generalized lymphadenopathy
which characterised by acute viral syndromes
seen in adult and adolescent.
• Monocyte act as reservoir of HIV

15. The life cycle includes the following steps.
1.Binding and entry /Attachment
Attach→ Fusion→ Uncoting

16. The life cycle includes the following steps
cont’d
2.Reverse transcription/ Conversion of RNA to
DNA)
• Enzyme RT mediates reverse transcription.
• It produce single stranded DNA from the viral RNA
• The single stranded DNA than replicated in to double
stranded viral DNA , & translation to the nucleus

17. The life cycle includes the following steps
cont’d
3. Integration
• Carried out by integrase
• Remoulding to the host chromosomes
• Enzyme integrase integrate viral DNA in to
Nucleus
• CD4+ now changed in to a “machine” used to
produce more HIV.

18. The life cycle includes the following steps
cont’d
4.Latency Proviron may remain latent
5.Replication
• The new DNA, which has been formed by the
integration of the viral DNA into the CD4+ cell,
causes the production of messenger DNA that
initiates the synthesis of HIV proteins

19. The life cycle includes the following steps
cont’d
6.Budding /Assembly
The viral proteins and RNA needed to form new
virus gathered at CD4+ cell membrane to push
through the cell wall by budding.
The new virus leave CD4+ cell.
7. Maturation
HIV protease enzyme cuts the long HIV protein
in to smaller functional unit that then reassemble
to form a mature virus which is ready to infect
other cells

20. HIV life cycle

21. Video summary of HIV life cycle
• Video summary

22. HIV Types
• Two types of HIV cause AIDS i.e.
HIV-1
HIV -2
HIV-1
• Has molecular heterogeneity that comprises
three groups.

23. HIV Types
• Group m (major) comprises sub type; I.e. A, B,
C, D. E, F, G, H, I & J
Sub type A-central & sub-Saharan Africa
Sub type B- S. America, Brazil, USA, Thailand,
Europe, India, Japan
Sub type C- South Africa
• Group O relatively rare found in Gabon,
Cameroonian women and France
• Group N Fist found Cameroonian women

24. Effects of HIV on Immune System
Introduction to Immune system
• The immune system protects the body by
recognizing antigen on invading bacteria and
virus reacting to them.
• Antigen is any substance that induces state of
sensitivity and immune responsiveness.

25. Effects of HIV on Immune System
• antigens interacts with antibodies and
immune cells initiating the immune response
which results in destruction of antigen and
allowing body free of infection.
• If weakened or destroyed by virus like HIV
causes body vulnerability to infection

26. Component of Immune system
• Lymphoid organ and tissue
• B-Lymphocyte /B-cells
• T-Lymphocyte /T-cells
• Phagocyte
• Complement system

27. Cells of the Immune System
Stem Cell
Myeloid
Precursor
Lymphoid
Precursor
Helper T-Cell
Suppressor
T-Cell
Cytotoxic
T-Cell
Plasma Cell
Platelets
Eosinophil
Basophil
Mast Cell
Macrophage
Neutrophil

28. HIV-Infected T-Cell
HIV
Virus
T-Cell
HIV Infected
T-Cell
New HIV
Virus

29. Effects of HIV on Immune system is by
• Depletion of CD4+ count & Function by single
cell killing and syncytium formation
• Also by action of Cytotoxic CD8+ T-cells

30. After HIV infection
• CD4+ decrease in 1st
month and become
normal constant until 4 year when it starts to
decline slowly (13 years)
• HIV Specific antibody rises slowly until 8
month and remains constant.
• Viral load rises rapidly in the 1st
3 month and
decline to lower level until 6month and
variable lower until 10 years when it starts to
rise rapidly.

31. Window Period
• This is the period of time after becoming
infected when an HIV test is negative
• 90 percent of cases test positive within three
months of exposure
• 10 percent of cases test positive within three
to six months of exposure

32. HIV Infection and Antibody Response
6 month ~ Years ~ Years ~ Years ~ Years
Virus
Antibody
InfectionInfection
OccursOccurs
AIDS Symptoms
---Initial Stage---- ---------------Intermediate or Latent Stage-------------- ---Illness Stage---
Flu-like Symptoms
Or
No Symptoms
Symptom-free
<
----
----

33. Epidemiology of HIV/AIDS
• AIDS did not come to public attention until
mid 1981, after a cluster of death from PCP
and Kaposi’s sarcoma was reported among
previously health young mono sexual men in
• New York City,
• Sanfrancisco
• losanangles.

34. Epidemiology of HIV/AIDS cont’d
• The disease were called “slim” diseases as it
associated with profound weight loss and
diarrhoea
• It is widely believed that HIV is the result of
animal to human (Zoonotic) transfer of simian
immuno deficiency virus (SIV-HIV) similar to
SIV that infect chimpanzees

35. Global
• Around 34.5 million people have HIV in their
blood

36. HIV/AID in Ethiopia
Prevalence
Adult prevalence of 1.5%.
Rural areas(0.6%)
Urban areas(4.2%)

37. HIV indicators in Ethiopia (2006)
• Number of PLWHA 929,699
• Estimated new annual infection 122,971
• PLWHA requiring ARVs 244,835
• Annual AIDS deaths 88,997
• Adults and Children on ART
Ever started 122,243
Current on ART 90,212
Pediatrics 4484 (January 10, 2008)

38. HIV Mode of Transmission
HIV enters the bloodstream through:
Open Cuts
Breaks in the skin
Mucous membranes
Direct injection

39. HIV Mode of Transmission
The following fluids of infected person contain
HIV;
Blood
semen,
vaginal secretion,
Breast Milk
CSF
peritoneal fluid
synovial fluid
Pericardial fluid pleural fluid.

40. HIV in Body Fluids
Semen
11,000 Vaginal
Fluid
7,000
Blood
18,000
Amniotic
Fluid
4,000 Saliva
1
Average number of HIV particles in 1 ml of these body fluids

41. Ways of transmission of HIV.
1. Sexual transmission
Major route
Viral load increase with increased Monocyte
and lymphocyte in fluid as in STDs
Male to female transmission is 8 times more
efficient than female to male transmission.

42. Ways of transmission of HIV cont’d
2. Through Blood and blood products
• B/d transfusion
90-100% chance of acquiring infection, which
now a day reduced because of the availably of
p24 antigen test.
• Use of contaminated needle, blade, and other
sharp objects

43. Ways of transmission of HIV cont’d
3. Occupational risk
• Needle prick injury 0.3%
• Mucocutaneous risk/exposure = 0.1%
• Minimal risk from Health Worker to Patent

44. Ways of transmission of HIV cont’d
4. Mother to child transmission MTCT
• Exposure through pregnancy, child birth &
Breast feeding
• Rate of MTCT is varying from 20% -30% with
out ART.
– Labour and deliver→ 15-20% = 18%
– Breast feeding → 5-10% = 7.5%
– Pregnancy → 5-10% = 7.5%

45. Ways of transmission of HIV cont’d
Factor that MTCT are
High maternal load of viremia
Advanced stage of diseases (low CD4+ count)
Prolonged labour
Prolonged rupture of membrane
STD, during pregnancy
Preterm labour
Obstetric procedure like amniocenteses
C/S reduces by 50% the risk during labour.

46. Ways of transmission of HIV cont’d
5. HIV does not transmitted through the
following ways
• Respiratory route
• Causal contact in any setting ; house hold,
social, work area, school or prison
• Shared eating and drinking utensils
• Swimming together
• Second hand clothing and telephone

47. Clinical Categories of HIV Infection& Classification
system
1. Classification system
• The U.S. Centers for Disease Control and
Prevention (CDC) categorizes HIV-infected
adults and adolescents based on their CD4+
counts and clinical conditions.
• The system is Used to guide health care
professional in making Rx decisions for HIV
infected persons.

48. Clinical Categories of HIV Infection&
Classification system
The system is based on
• CD4+ count,
• T-Lymphocyte count,
• three clinical categories (A, B&C) in adult and
Clinical and immunological categories in
children.
• The classification based on Patient lowest CD4+
count at any given time, not on the most
recent count.

49. Clinical Categories of HIV Infection&
Classification system
Category 1 = > 500 cells /UL
Category 2 = 200-499 UIS/UL
Category 3 =<200 cells /UL

50. Cells susceptible to HIV infections
Hematopoietic
• T-cells (CD4+ or CD8+)
• Macrophages/monocytes
• Dendritic cells
• Fetal thymocytes and thymic epithelium
• B-cells
• NK cells

51. Cells susceptible to HIV infections cont’d
Central Nervous
• Microglia
• Capillary endothelial cells
• Astrocytes and Oligodendrocytes
Large Intestine: Columnar epithelium
Other
• Kupfer cells (liver)
• Synovial cells
• Placental trophoblast cells

52. Clinical Categories
Clinical Category A (primary infection or Acute
retroviral syndrome)
• Period of time when HIV 1st
enter the body
• Time of primary infection with HIV;A person’s
blood demonstrates very high viral load (A
number of viral copies exceeded 1,000,000
virus per ml of plasma or blood)
• Newly infected adult experience acute viral
syndromes

53. Clinical Categories cont’d
• The sign and symptom usually occurs two –
four month after infection
• CD4+ increase markedly
• Virus targets CD4+ in lymph nods and thymus
gland
• ELISA (Enzyme-linked immunosorbent assay)
or EIA (Enzyme immunoassay) yields positive
result

54. Clinical Categories cont’d
Clinical category A (clinical latency)
Patient experience “clinical latent”
HIV replication and host immune response exist
from the on set of infection
No s/s of HIV infection
The phase may last 8 to 10 years in adult
ELISA, western blot, Rapid tests or immuno
fluorescence assay (IFA) will be positive
CD4+ count is >500clls/mm3

55. Clinical Categories cont’d
Early of sign and symptoms of HIV (Clinical
category B)
• After being health for years minor s/s of HIV
infection then begin to appear.
• Pt may develop Candidiasis,
Lymphadenopathy ,cervical carcinoma, HZ and
/or peripheral neuropathy
• Viral load increases
• CD4+ count falls about to 500 clls/mm3

56. Clinical Categories cont’d
Late s/s of HIV (clinical category C)
Infected pt. develops life threatening
infection and malignancies.
Pt. may be wasted or have low body weight
Viral load continuous to increase
CD4+ count falls less than 200 clls/mm3
Pt meets definition of AIDS once in category
C
Pt. remains in category even if condition
resolves.

57. Clinical Categories cont’d
Advanced HIV disease (clinical category C)
Pt continue to develop new OI such as
cytomegalovirus virus infection,
mycobacterium Avium complex, streptococcal
meningitis, progressive multifocal
leukoencephalopathy and other infection that
commonly occur secondary to depressed
immunity.
 Viral load is high, CD4+ count is less than 50
cells/mm3,
and Death is imminent

58. OI and cutaneous manifestation of HIV
1. Kaposi’s Sarcoma
• A vascular malignancy that can occur any
place in the body, including the internal
organs.
• First lesions often appear subtly on the face or
in the oral cavity.
• 1st
described by Moritz Kaposi in 1982

59. KS cont’d
• Involves endothelial layer of blood and
lymphatic system thus it is;
– vascular neoplasm
– Associated with infection with human herpes virus
8 (HHV8)
– Characterised by red or brown macular, popular
or nodular lesion seen on skin and mm
– Commonly appear age b/n 20 and 40

60. 2.Cutaneous infection with Herpes simplex virus
CXRS
Skin lesion Characterised by micro vesicles soon
ruptured to form Yellow crust (Small and blister
like lesion)
More common in children and found at adjacent
areas of mm and skin
Diagnosed by viral culture if available
Rx
 Acyclovir 10-20mg/kg dose 4x4-7 days for children
 Acyclovir 400mg po/dose 5x5 -7days.

61. 3. Herpes Zoster (Shingles)
Definitions :
An inflammatory viral condition in which the
virus produce pain full vesicular eruption
along the area of sensory nerve distribution.
Cause: Varicella virus

62. HZ cont’d
C/M
Linear vesicular unilateral eruption along the side
of sensory nerve distribution that may be
accompanied by radiating pain.
Clinical course varies from 1 to 3 weeks
Rx
Analgesics
Systemic corticosteroid
Acyclovir
Broad spectrum antibiotics
Wound care and Psychological support

63. 4. Mulluscum Cantageosum
Mainly involve the face
Hyper follicular warts
Umblicated
Treated by puncture of individual
lesion

64. 5. Bacterial skin infection (pyoderma
• Two types of bacterial skin infection
Primary bacterial skin infection
secondary bacterial skin infections
• Causes
– Staphylococcus aurous
– Group A Streptococcus
– And others

65. Primary bacterial skin infection
includes;
Folliculitis: inflammation and infection of hair
follicle which caused by staphylococcus aurous
Cellulites: Inflammation of skin and
subcutaneous tissue characterized by oedema,
erythema and pain which Caused by
staphylococcus, streptococcus and Haemophilus
influezae
Skin abscess/carbuncles: Localized accumulation
of pus; multiple boils. May be complication of
untreated cellulites

66. Primary bacterial skin infection cont’d
Furuncle /Boils
Acute tender, perifollicular inflammatory
nodules resulting from infection by
staphylococci.
It may result from, Folliculitis and may involve
one or more hair follicles.
Appear as small red, raised pain full pimple
(small hard inflammatory spot)
The lesion has central necrosis with yellowish
appearance

67. Primary bacterial skin infection cont’d
Impetigo: Superficial skin infection caused by
staphylococcus, Streptococcus and other
multiple bacteria characterised by vesicle or
bulla that become pustule, rupture and form
yellow crust

68. Treatment of bacterial skin infection
• Antibiotics e.g. Cloxacillin
• Topical therapy
• Surgical for boils
• Antipain
• Incision and drainage for abscess

69. 6. Fungal skin infection (Mycosis)
• Fungal skin infection in HIV/AIDS includes
Candidiasis and dermatophytosis
• Candidiasis: Mycosis caused by Candida
albicans and affects oral cavity, genitalia
commonly and oesophagus, trachea, and skin
folds some times. Appear as whitish coat of
tongue and vaginal discharge

70. Rx
Oropharyngeal Candidiasis
Nystatin suspension or miconazol oral gel
 In Sever and persistent cases; Fluconazol 3-
6mg/kg/d (100-200mg) once po/d for 7-14 days
or Ketoconazol 200mg po daily for 7-14 days
Oesophageal Candidiasis
Flucanazol 200-400mg po for 14-21 days
Ketoconazol 200mg po BID for 14-21 days

71. Rx cont’d
Cutaneous Candidiasis
• G.V (1%) aqua’s solution 3 time a day for 3
days
• Nystatin ointment applied 3 times a day

72. Dermatophytosis
• usually occur as tinea (ring worms)
• Common forms are
• Tinea pedis (ring worm of feet
• Tinea corporis (ring worm of body) common in
HIV/AIDS
• Tinea capites ( “ “ “) common in HIV/AIDS
• Tinea cruis ( “ “ “ )
• Tinea unguim (onychomycosis /nail

73. C/M
• Itching and scaly skin lesion
• Hard and fragile nail
• Cellulites
• Hair loss
• Discoloration of the skin
• Lyphangitis

74. Rx
Broad spectrum antifungal
Topical Clitromatol 1% applied BID
until rash resolves
Systemic antifungal

75. 7. Drug eruption
• As for example SJS

76. 8.Seborrhoeic dermatitis
Occur up to 85 % of cases; May be early sign
of HIV characterized by thick, yellow scales
occurring on scalp but may be seen deeper
areas
Rx
• Ketoconazol shampoo or salicylic acid
• 1% Hydrocortisone cream for inflammation.

77. 9.Scabies
• An infestation of skin with itch mite
commonly appear in finger webs, hand, arm
pit, buttock, groin
C/M
• itchy scratch syndrome ,Vesicle, pustule,
excoriation, crust

78. Rx
1. Benzyl benzoate lotion – applied daily for 3-5
days and body both before and after
application
2. Sulphur ointment apply daily for 3days 4
body both p 24 hr
3. Personal hygiene
4. Wash cloth
5. Treat the whole family
6. Treat 2o
bacterial infection

79. 10. Other systemic opportunistic infection
CNS toxoplasmosis:
• occur as a reactivation of latent infection when CD4<100
C/F fever, head ache, vomiting, Hemi paresis (with out body
weakness) and Change in mental status
• Rx –
– Fansider 2 tabs po BID for 2 days loading dose then 1 tab
daily for 3-6 wks followed by co-trimoxazol 2 tabs po daily
as secondary prophylaxis
– Prophylaxis – Co-trimoxazol 960 po daily.

80. Other cont’d
Cryptococcus meningitis: Fungal infection caused by
Cryptococcus neoformans occur at CD4 <100
C/F-fever, sever head ache, change in mental status
and rare hemi paresis
• Diagnosed by Indian Ink staining of CSF
RX
• Amphotericin B. not routinely available
• Fluconazol 400 mg po BID x 2 wks and then 400 mg po daily
for 8 wks
• Secondary prophylaxis Fluconazol 200mg po daily until
CD4>200 for 3month with ART

81. Other cont’d
Respiratory manifestation of HIV
• Common causes of respiratory symptoms
include:
• Bacterial pneumonia
• Pneumocystis jirovecii pneumonia (PCP)
• TBC
• Fungal infections

82. PCP
Respiratory fungal infection caused by
Pneumocystis jirovecii which usually occur at
CD4 <200
C/F:
 Scanty cough or no sputum
 Progressive respiratory distress
 Minimal chest findings, may have crackle
 Chest X-ray bilateral interstitial infiltrates

83. Rx of PCP
Co-trimoxazol 100-120mg/kg/d in 3-4 divided
dose for 21 days
Steroid added for sever cases
Prophylaxis
 Cotrimoxazole 2 tabs per day until CD4+
increases greater than 200 for greater than three
consecutive months.
Indication prophylaxis
◦ Symptomatic HIV oral Candidiasis
◦ CD4 count <200
◦ history of PCP

84. HIV/TB co- infection
• About a third of the global population living
with HIV is also infected with tuberculosis
(TB).
• Worldwide, particularly within developing
countries, TB is the leading cause of death
amongst people living with HIV.
• HIV and TB co-infection is a term to describe
infection with both HIV and TB.

85. HIV/TB co- infection cont’d
• Greater chance of progression to TB disease if
HIV-infected (10%/year).
• More rapid progression– from 2 years to
weeks/months
• Higher mortality (15%-50%)
• Higher with MDR TB (75%-100%)
• TB is most common OI and most common
cause of death among HIV-infected persons

86. HIV/TB co- infection cont’d
In Ethiopia 50% or TB/HIV co infection varies by
region and ranges 11% to 40% (average 25%)
from routine data
Symptomatic TB increase in 5-10 folds which
implies the Needs for HCT for person with TB and
Needs for TB screening in HIV +ve cases
TB Accelerates the HIV progression
In late stage of HIV Extra pulmonary is more
common and Atypical PTBC (involves lower lung)

87. HIV/TB co- infection cont’d
• The diagnosis is difficult because SSE is usually –ve
for AFB and Difficult to differentiate from other
condition by Chest X-Ray
• Problem Encountered when treating TB and HIV
• High pill burden which leads to poor adherence
• Over lapping of slide effect
• Hepatotoxicity and rash from INH, prazinamide,
Rifampin and NVP (EFV)
• Drug interaction Rifampin level of NVP, EFV & PIS

88. ART and TB
Pt develops TB while on ART
• Start anti TB while on ART
• Continue ART with appropriate change in
regimen I.e. NVP by EFV
• Increase dose of EFV in Rifampin if EFV not
possible continue NVP with close follow up

89. ART and TB cont’d
Pt. presents with TB before initiating of ART
• Start anti TB immediately
• Decision to start ART depends on CD4 count If:
CD4 <200 initiate anti TB then ART with in 2 wks
to 2 months
CD4 200-250 immediate anti TB then ART after
intensive phase
CD4 350 deter ART

90. INH prophylaxis therapy( IPT)
• Administration of INH to prevent symptomatic infection and
to reduce life time risk
• Life time risk in a symptomatic TB infection is
5-10% in non HIV person
over 50% with HIV
decrease to 4% with IPT
• Indication of IPT
– HIV positive
– Person with out active TB
• Dose of INH 5 mg/kg/d (max 300mg) for 6 month

91. Co-trimoxazol prophylaxis
Bactrim has broad spectrum activity that can
prevent different infection such as
PCP
toxoplasmosis,
 bacterial pneumonia,
diarrhoea by Isospora and bacteria

92. Co-trimoxazol prophylaxis cont’d
• Indication
• CD4 < 200
• WHO stage 3
• Symptomatic HIV infection
• It should be stated before ART
• Dose 2 tabs po daily for until CD4 count
persistently increase above 200/mm3
for at
least 3 months

93. The effect of HIV infection on symptoms and signs of TB
Symptom/sign HIV
positive
(%)
HIV negative
(%)
Dyspnea 97 81
Fever 79 62
Sweats 83 64
Weight loss 89 83
Diarrhea 23 4
Hepatomegaly 41 21
Splenomegaly 40 15
Lymphadenopathy 35 13

94. The Three I’s for HIV/TB; WHO Department of HIV/AIDS
Intensified TB case finding
• Assessing TB status of people living with HIV
at every contact with the health service with
full TB investigation for those who are
symptomatic and those who are
asymptomatic should be considered for IPT

95. Three I’s cont’d
Isoniazid preventive therapy (IPT)
• Six month treatment with Isoniazid is
recommended for all people living with HIV
who do not have evidence of active TB disease
in order to reduce the risk of TB.

96. Three I’s cont’d
Infection Control
• Every effort must be made to reduce the risk
of TB transmission in all settings where HIV
care is provided; this includes rapid triage of
TB suspects and adequate sunlight and
ventilation in waiting

97. WHO staging system for HIV infection and Diseases
Clinical Stage I
• Asymptomatic
• Persistent Generalized L/Adenopathy (PGA)
• Performance scale 1 Asymptomatic normal
activity

98. WHO staging cont’d
Clinical stage 2
Wt. loss <10% of body weight
Minor mucocutaneous manifestation
(seborrhoeic dermatitis, fungal nail infection,
recurrent oral ulceration, angular chilitis)
HZ with in last 5 years
Recurrent URTI i.e. bacterial sinusitis
Performance scale 2 –Asymptomatic, normal
activity

99. WHO staging cont’d
Clinical stage 3
Wt. Loss, <10% body wt
Un explained chronic diarrhoea > 1 month
Oral Candidiasis (thrush)
Oral hairy leukoplakia
Pulmonary TBC with in the past year
Sever bacterial infection (i.e. pneumonia,
pyomyosite)
And/Or performance scale 3: bed ridden <50%
of the day during last month

100. WHO staging cont’d
Clinical stage 4
HIV wasting syndrome (wt loss >10%, Plus either
unexplained Chronic diarrhoea >1month, or
chronic weakness and unexplained fever
>1month.
PCP
Toxoplasmosis of the brain
Cryptosporidiosis with diarrhoea > 1 month
Cryptococcosis,
EPTB

101. Clinical stage 4 cont’d
Cytomegalovirus (CMV) diseases of an organ
other than spleen liver and lymph nods
HSV infection, CMV >1month or visceral
Progressive multifocal leukoencephalopathy
(PML)
Any disseminated endemic mycosis
histoplasmoxis coccid mycosis
Candidiasis of oesophagus, trachea, bronchi
or lungs

102. Clinical stage 4 cont’d
• Atypical micobacteriosis, disseminated
• Non typhoid salmonella septicaemia
• EP
• Lymphoma
• KS

103. Clinical stage 4 cont’d
• HIV encephalopathy (Clinical findings of
disabling cognitive and/or motor dysfunction
interfering activity of daily living, progression
over weeks or absence of a concurrent illness
or condition other than HIV infection that
could explain findings and/or performance
scale 4, bed ridden >50% of the day during the
last month (ADC)

104. HIV diagnostic methods
• HIV testing technologies

105. WHO clinical criteria for HIV Diagnosis
Major sign/disease
• Wt loss of 10% or more
• Chronic diarrhoea
• Prolonged fever for more than one month

106. WHO clinical criteria for HIV Diagnosis
Minor signs/disease
• Oropharyngeal Candidiasis
• Persistent cough for more than 1 month
• Body weakness ,Night sweating
• Loss of appetites ,KS, Pneumonia
• Generalized skin infection
• Generalized lymph adenopathy
• HZ, Chronic Herpes simplex infection

107. Illustrative summary of c/m

108. Cryptococcosis

109. Seborrhioc dermatitis

110. SJS
Reaction due to theazetazone , neverapine and others

111. Hyperemia- Erythematic
Hyperemia

112. Pressure ulcers
Ischemia
Ulceration
Necrosis- Dead
skin

113. Macule
Macule

114. Vesicle

115. bulla

116. Pustule

117. Papule

118. Plaque

119. Scale

120. Herpes zosters

121. Impetigo

122. Staphylococcal scalded skin syndrome

123. Carbuncles

124. Scabies rash

125. DERMATOPHYTES

126. Tinea Capitis

127. Tinea Unguium

128. Tinea Cruris

129. Tinea corporis

130. Tinea Pedis

131. Eczema Herpeticum

132. Molluscum Contagiosum

133. Facial eczema in a baby:

134. Per orbital
cellulitis

135. Juvenile Plantar Dermatosis

136. Management of Pt with HIV/AIDS
• While many medicines are used to treat HIV
infection none can cure HIV/AIDS

137. 1. Anti Retroviral therapy
Important terms
• ART :-Antiretroviral RX /Therapy
• ARVs:- Anti retroviral
• HAART: – Highly active antiretroviral /Rx/
therapy

138. Goals of ART
• To improve Health and prolong life of HIV
infected individuals.
• To inhibit replication or fusion of virus
• To increase Immuno response
• To reverse the progression of the infection
• To decrease viral load

139. Function ART
• Restore immunity
• Increase survival
• Improve quality life
• Restore hope
• Reduce HIV transmission

140. Factors to be considered when starting
therapy
• National Guide line
• Potential S/E
• Concurrent infection & abnormal laboratory
value
• Drug interaction
• Potential for pregnancy
• Ability to adhere is primary indicator for ART
success

141. When to start ART
• Starting anti retroviral therapy is not an
emergency
• Consider components of criteria ;
– Symptoms of HIV infection (Candidiasis or weight
loss )
– viral load (HIV RNA) >55000 copies /ml of plasma
– CD4+ count.

142. When to start ART cont’d
If CD4+ testing is available
• WHO stage IV (clinical AIDS) irrespective of
CD4 cell count
• WHO stage III, if CD4 count is <350 cell /mm3
or less
• WHO stage II,I, if CD4 count is <200 cell/mm3

143. When to start ART cont’d
If CD4 count is not available
– WHO stage IV irrespective of total lymphocyte
count
– WHO stage III “ “ “ “
– WHO stage II Plus total lymphocyte count is
<1200/mm3

144. When to start ART cont’d
• Anaemia may be an indicator to start ART
though it is out of WHO stage
• Viral Load > 55,000 copies /Ml of plasma;
Specifically not used in the absence of
symptom or CD4 count

145. When to start ART cont’d
• All pregnant women and lactating mother
with HIV irrespective of CD4 level
• CD4 count <500 cell/mm3

146. Recommended HAART Regimens in infected Adult &
Adolescent
D4T/3TC/EFZ
Or Replace NVP for EFZ in pregnancy
 D4T/3TC/NVP
ZD4/3Tc /NFZ
Or Replace NVP for EFZ in pregnancy
ZDV/3Tc/NVP
ABC or TDF or ZD4 if not taken plus dd1plus
LPV/ or SQV or NFV

147. Classes of antiretroviral therapy
1. Nucleoside reverse transcriptase inhibitor
(NRTIS)
2. NNRTIS
3. PIs (protease inhibitors)
4. Fusion Inhibitors (not available in Ethiopia
and not widely used in westerns

148. NRTIS
Blocks HIV protein RT thus preventing HIV RNA
from changing to DNA
• Stavudine (d4T)
• Zidovudine (ZDV, AZT)
• Lamovudine (3Tc)
• Didanosine (dd1)
• Tenofovir ( TDF)
• Abnacavir (ABC)

149. NNRTIs
• Also works by blocking RT Enzyme indifferent
ways than NRTI.
• Nevirapine (NVP)
• Efavirenz (EFZ)
• Delavirdine

150. Protease inhibitors /PI
Prevents protease enzyme from cleaving large
HIV precursor proteins in to smaller functional
unit
• Lipinavir /ritonavir/ LPV/R
• Nelfinavir (NFV)
• Saguinavir (SQV/ritonavir

151. 2.Prevention and Mx of OI
• Leading cause of mm
• Initiate OI Rx before ART

152. 3. Changing ART
Not done unless absolutely necessary
Reason to change
 Occurrence of TB or development of active TB
 Drug toxicity
 Intolerance leading to poor adherence
 Pregnancy
 Rx Failure
 In effective regimen
 Resistance
 Missed dose
 Mutating virus

153. Chang from 1st
to second line regimen
1st
line 2nd
line
• d4T or ZDV ABC or TDF or ZDV (if
not taken)
• And and
• 3Tc ddI
• And and
• NVP or EFV LPV/r or SQV/r or NFV

154. 4. Discontinuing therapy
• Therapy must be discontinued temporary or
permanently depending on
–Drug toxicity
–Adherence
–Potential benefit

155. 5.ART Adherence
• Ability of the pt to take drug exactly as
prescribed
• Adherence should be 100%

156. Adherence
• A shared decision making process b/n the pt
and health care provider
• The pt understands and agrees to make
behaviour change to improve their health

157. Component
Right drugs – right drug and right dose (No
of
tables)
Right time
Right ways
Take nelfinavir (NLV) Ritonavir (RTV) and
Efavirenze (EFV) with food but avoid fatty food
 Take didanosine (ddI ) and Indinavir with out
food or light meal
 Adherence is the most important part of
successful Rx

158. 6. Symptoms Management
Use principle of nursing process
NURSING PRIORITIES
1. Prevent/minimize development of new
infections.
2. Maintain homeostasis.
3. Promote comfort.
4. Support psychosocial adjustment.
5. Provide information about disease
process/prognosis and treatment needs.

159. Symptomatic management cont’d
DISCHARGE GOALS
1. Infection prevented/resolved.
2. Complications prevented/minimized.
3. Pain/discomfort alleviated or controlled.
4. Patient dealing with current situation
realistically.
5. Diagnosis, prognosis, and therapeutic
regimen understood.
6. Plan in place to meet needs after
discharge.

160. 7. Nutritional support
Important food to include
• Protein -body building
• Carbohydrate- energy giving
• Fruits /vegetable -source of many vit & mineral
• Fats /oils -source of fat
Food to avoid
• Raw eggs
• Under cooked meats
• Not boiled water
• Alcohol and Coffee

161. 8. Palliative care
Palliative means treatment relieves but does
not cure disease
Palliative care are intervention that improve
of life for pt and their families
It includes :- Prevention and relief of
suffering i.e. - pain and other physical
problems and Psychological and spiritual
issue
It starts from on set of non curable disease
to end of life

162. Component of palliative care
• Pain & symptom control – use of opoids
• Hospice care (home and hospice centre)
• Financial support
• Emotional spiritual support
• Food and shelter
• Legal help and school fee

163. Hospice
• Caring community of professional and non
professional people together with the family.
Emphasis on spiritual, emotional and medical
problems for terminally ill pt. & support
through period of bereavement for family
after the pt dies

164. Palliative care mode in Ethiopia
•Home based care.

165. Prevention& Control of HIV/AIDS
1.Safer Sex education (practice = ABC)
A. Abstinence
B. Be faith full
C. Condom
• Postponement
• Microbicides

166. Prevention& Control of HIV/AIDS cont’d
2. Free sexual discussion in the family members and
public
3. HCT
VCT
PIHCT HIV prevention intervention in which routine
confidential testing of HIV offered to pt visiting
health institution by their provider.
PIHTC

167. Prevention& Control of HIV/AIDS
4. Increase the awareness of community on
the impact of stigma and discrimination
Stigma – Social labels that undermine the
way people are viewed by other of or view
them selves. Attitude of toward HIV patients
Discrimination – Distinction, exclusion or
restriction due to personal characteristics.
More of action or behaviour

168. Prevention& Control of HIV/AIDS
• Forms of stigma & discrimination
– Self stigma – Blaming PLWHA or self Isolation
– Enacted stigma – Actual experience of
discrimination from other
– Stigma by association e.g. Effects people
associated with PLWHA

169. Prevention& Control of HIV/AIDS
6. Standard precaution for body fluid potentially infectious
Body fluids considered infectious are:
1. All body fluid containing visible blood
2. Body fluid with out visible blood but may be infectious are
Vaginal discharge
Semen
Peritoneal fluid
Amniotic fluid
CSF
Breast milk
Pericardial fluid
Synovial fluid

170. Prevention& Control of HIV/AIDS
• Body fluid considered non infectious for HIV
are
Tears
Faeces
Urine
Saliva
Nasal secretion
Sputum
Vomit
Sweat

171. Prevention& Control of HIV/AIDS
6. Post Exposure prophylaxis
• Definition: Use of therapeutic agents to
prevent establishment of infection following
exposure to pathogen.
7. Prevention of mother to child transmission

172. Thank you

173. Work toward health of
• Your self
• Individuals
• Family and
• Community