Sei sulla pagina 1di 94

HIV/AIDS pada kulit

Human immuno Deficiency Virus(HIV) is retrovirus


that can lead to acquired immunodeficiency syndrome
( AIDS).
AIDS is condition in human in which the immune
system begin to fail, leading to life-threating
opportunistic infections .

So AIDS is a collection of symtoms and infections


resulting from the specific damage to immune
system caused by the human immunodefienciency
virus ( HIV ).The late stage of the condition leaves
individuals prone to opportunistic infection and
tumors.
CDC ( 1993) When HIV kills CD4+ T cells so that
there are fewer than 200 CD+ T cells per microliter
(L)of blood,cellular immunity is lost,leading to the
condition known as AIDS .

Structure and genome

Tropism
The term viral tropism refers to
which cell types HIV infects.
HIV can infect a variety of
immune cells such as CD4+ T
cells, macrophage,and
microglia cells.
HIV Entry to macrophages and
CD4+ T cells is mediated
through interaction of the virion
envelope glycoprotein (gp120)
with the CD molecule on the
target cells and also with
chemokine coreceptors.
4

HIV has genes that encode the structural


protein of virus :gagprotein that form the
core of the virion ( P24 antigen);
pol the enzymes responsible for protease
processing of viral proteins, reverse
transcription , and integration.and env
the envelope glycoproteins. It also
contain at least six other genes tat, rev, nef,
vif, vpr, and vpu modification of the host
cell to enchance virus growth and the
regulation of viral genes expression.

Replication cycle

Dermatologi manifestations of HIV infection


Dermatologic problem occur in > 90% of patients with
HIV infection.
From macular, roseola-like rash seen with the acute
seroconversion syndrome to extensive end-stage KS.
Cutaneous manifestation of HIV diesases can be seen
throughout the course of HIV infection .
Among the more common nonneoplastic problem are
Seborrheic dermatitis, folliculitis ,and opportunistic
infections. Extrapulmonary pneumocystosis may cause a
necrotizing vasculitis.

Macular and papular conditions


Erythematous macular and papular exanthem in acute
HIV infection

10

Seborrheic dermatitis( Sd)


Sd occur in 3% of the general
population and in up to 50% of
patient with HIV infection.
Sd increases in prevalence and
severity as the CD 4+T cell count
decline.
More severe,persistent and
recalcitrant condition, especially
those with advanced stage of
HIV disease.
. InHIV-infected pateint,Sd may be
aggravated by concomitant
infection with pityrosporum.
11

Patients treated with with antiretroviral therapy enjoyed


regression of the condition.
Topical ketokonazole cream ,
and oral ketokonazol,200mg
perday for 4 weeks,itraconazole
200mg,fluconazole .

12

Folliculitis
The most prevalent dermatologic
disorder in patient with HIV infection
and is seen in 20 % of patient.
It is more common in patien with CD
4+ Tcell Count< 200 cell/l.
One form of folliculitis, eosinophilic
pustular folliculitis, is a rare
dermatologic condition that is seen
with increased frequency in patient
with HIV infection .
Chronic pruritic, edematous papule
distributed over the face,neck,and
upper trunk.
Respon poorly to antibacterials.
Respons to combination of
ultraviolet-B light therapy,highpotency topical steroid,and non 13
sedating antihistamines.

Staphylococcal infection
can occur as abscesse
Staphylococus aureus is the most
skin and systemic bacterial
pathogen in HIV-infected patients.
Around 50%chronic
staphylococcus nasal carriage.

14

Staphylococcal infection can occur as ulcers

15

Numerous ecthymatous lesion due to S.aureus

16

Staphyloccocal infection can occur as


folliculitis.

17

Staphylococcal infection can occur as


cellulitis.

18

Prurigo nodularis
Pruritus is common symptom in
patients with HIV infection and can
lead to prurigo nodularis.
More frequently seen in patients with
CD4+ cell counts below 50/l

numerous papule smaller than those


typically seen in prurigo nodularis.

19

Norwegian scabies with hyperkeratotic


psoriasiform lesion
Increased incidence of atypical
manifestations of scabies, including
face and scalp involvement, nodular
lesion, and hyperkeratotic ( crusted or
norwegian ,CD4<150cells/mm3)scabies.
The teatment of choice is topical
scabicide, such permethrin 5% cream.
Single-dose oral ivermectin,200g/kg.

20

Psoriasis
Although they are not reported to be
increased in frequency,may be particularly severe when they occur in
patient with HIV infection.
Individual infected with HIV do have
increased prevalence of arthritis
associated with psoriasis.
can have unusual presentation
((inverse psoriasi )

21

Inverse psoriasis of the feet. Inverse psoriasis of the under


arm

22

Varicella-zoster
Scattered facial verrucous lesion
of ACV-resistant VZV.
In HIV, Vzv can be the cause of
varicella, even in adults,and can
cause manifestation more severe.
Chronic verrucous or vegetative
nodules can develop.
Herpes zoster in young, sexually
active adults is one of the common
presenting feature of HIV .
Multi-dermatomal herpes zoster is
often seen ( widespread
dissemination).
Post-herpetic neuralgia is more
common.
Dermatomal vesiculo-pustular lesion,
preceded by localized itching,
tenderness,or burning painthe
23
hallmark.

Chronic vegetative nodules of varicella


lesions.

24

Reactivation herpes zooster


(shingles)
10-20 % of patients with HIV infection.
This reactivation syndrome of varicellazoster virus indicates a modes decline in
immune function and may be the first
indication of clinical immunodeficiency .
AIDS was more likely to develop if the
outbreak of zoster was associated with
severe pain, e xtensive skin involvement
,or involvement of cranial or cervical
dermatomes.

25

Herpes simplex virus


With advanced HIV diseases, HSV can
manifest itself as very painful, persistent,
progresive,clean-based ulcers.
Sometimes HSV can also present with
atypical deep ulcers, verrucous or
vegetative erosion, or folliculitis.
Extensive lesions are usually seen when
the CD4<50 cells/mm3
Disseminated HSV from hematognous
spread of the virus rarely occurs.
Widespread HSV ,knows as eczema
herpeticum.

26

Chronic, progressive, clean based ulcer of HSV


infection.

27

Molluscum
contangiosum(MC)
Diffuse skin eruption due to MC may be
seen in patient with advanced HIV
infection.
Lesions tend to be more numerous and
may be nodular ( so-called giant
molluscum if 1 cm or more ) and
disfiguring .
Treatment option :cryoterapy, electro
dessicasi, gentle curettage,topical
trtinoin,and superficial chemical peeling.
Respon well to effective antiretroviral
therapy .

28

CD4+ cell count < 100/l

29

Giant Molluscum contangiosum.


CD4 cell < 50 cells/mm3

30

Human Papilloma virus (HPV)


To be infected with more HPV types.
HPV infection has also been shown to
facilitate HIV gene expression.
Frequently manifestations of HPV
infection :multiple common warts on
hands, facial warts, intra-oral warts, and
anogenital warts (conyloma acumoinata
)
IEN can develop more frequently in HIV.
Extensive diseases can often be seen
when the CD4 cell count< 500
cells/mm3.
Treatment:cryoterapy,CO2,laser
surgery, ED,podophylin,and 5%
imiquimod Cr .
HPV infection refractory to conventional
31
Topical treatment and recurrence can
usually be anticipated.

32

Mosaic warts

33

Mycobacterial infections
Skin mycobacterial infection in
HIV patient are caused primarily
by Mycobacterium tuberculosis.
Skin manifestation : papulonecrotic lesion, papulo pustular
lesion, nodules, plaque,
abscesses, ecthyma and ulcer.
Scrofuloderma is also not
uncommon.
papulo-pustular lesions of
disseminated tuberculosis.

34

Drug eruption
Drug reaction producing full-body
erythema.CD 4+ cell counts< 50l.
Skin of patient with HIV infection is
often a target organ for drug
reaction.
Patient may have particularly
severe cutaneous reaction,
including erythoderma and stevensjohnson syndrome.

35

Toxic epidermal necrolysis due to trimethoprim


sulfamethoxazole.

36

Photosensitive
Photodermatitis of the face andvee
Patient with HIV infection are often
of the neck
quite photosensitive and burn easily
following exposure to sunlight or as a
side effect of radiation therapy .
HIV infection itself is photosensitizing,
and patient with low CD4 +cell count
may receiving photo sensitizing drugs
Such as trimethoprim/sulfamethoxa
zole.

37

Photodermatitis of the arm and hand.

38

Perioral dermatitis

39

Pomholyx Eczema as manifestation


of HIV infection

40

Bacillary angiomatosis(BA)
Characteristic exophytic angiomatous
nodules of BA with and without surrounding cellulitic.
Bartonella henselae and B.quintana
As solitary or multiple vascular lesion
that clinically resemble Kaposis
sarcoma.
Involvement of the liver, spleen, lymph
nodes, bone, lung and central nervous
system.
BA HIV-infected patients withCD4 >
100 cells/l.
Typical :dermal vascular proliferastion,
with plump endothelial cell lining the
vessels.
Erythromycin,500po qid 8 weeks.
41

Kaposis sarcoma( KS)


KS on the face of a homosexually
active man with AIDS
The lesion typically violaceous
papule and nodule that can be single,
few, or multiple and widely scattered.
No symtom, the lesions progressively
extend into the subcutaneous and
lympahatic tissue, chronic lymphedema
may form .

42

43

Sifilis
Generalized rashed can develop in
patiens with secondary syphilis,
including the macular and papular
variants.
Papular > maccular form.
Incidence of the Jarisch Herxheimer
reaction is 95 % in patient with
seropositive primary syphilis or
secondary .
Papular lesions are typically on
the face, flexural fold ,and trunk.
Annular lesion > seen on the faces
of black ,can resembles sarcoidosis
or tinea.
44

45

Fungal infection
Manifestation can be very extensive
and have unusual morphologies.
In advanced HIVCentral clearing
may be absent and patients can
have widespread dermatophytosis.
Fungal nail infection most
commonly presents as distal
subungual onychomycosis.
Trichophyton rubrum is the most
frequently encountered fungal
pathogen.
Systemic antifungal : itraconazole,
terbinafine,use of antifungal shampoo.

46

Generalized dermatophytosis with


onychomycosis.

47

Deep or systemic fungal infections


Penicilliosis, histoplasmosis, and
Crytococcosis are common systemic fungal
Infection in HIV infected patient .
70% of patient with penicillinosisskin
lesion.
10-20 % of histoplasmosis and
crytococcosisskin lesion.
The most common skin lesion is the
molluscum-like lesion .
Treatment : Systemic antifungal agent
( amphotericin,itraconazole,fluconazole).
Crytococcus neoformans

48

49

Nodular lesion with overlying serosanguinous


crusting caused by H.capsulatum.

50

51

52

53

54

Erythema nodosum

55

Infection due to helicobacter cinaedi can


mimic erythema nodosum in appearance.

56

Infection due to Campylobacter species can


mimic erythema nodosum in appearance.

57

HIV and hepatitis C virus coinfection


associated vasculitis.

58

Epidemiology
38.6 million people now
living with the diseases
world wide.
As of january 2006,the
joint United Nations
Programme On
HIV/AIDS(NAIDS) and
WHOAIDS has killed
more than 25 million
people.
In 2005AIDS claimed
an estimated 2,4-3,3
million lives,of which more
than 570.000 were
59
children.

60

Transmission
Three main transmission routes for HIV :
Sexual route : genito-genital
genito-anal
genito-oral
Blood or blood product route.
Mother-to child transmission ( MTCT). without
treatment transmission rate is 25 %.Where drug
treatment and cesarian section are available, can be
reduced to 1 % .Breast feeding also a risk of infection for
the baby .

61

Estimated per act for acquisition of HIV by exposure


route .
Exposure route

Blood Transfusion
Childbirth
Needle-sharing injection
drug use
Receptive anal intercourse
Percutanous needle stick
Receptive penile-vaginal
intercourse
Insertive anal intercourse
Insertive penile-vaginal
intercourse
Receptive oral intercourse
Insertive oral intercourse

Estimated infectious per


10,000 exposure to an infected
source.
9,000
2,500
67
50
30
10
6,5
5
1
0,5

62

Perjalanan infeksi HIV


gejala klinis melalui 3 fase:
Fase infeksi Akut.
3 sampai 6 minggu setelah terinfeksi virus dengan
gejala umum Flu like sindrom :
Kelainan sistem saraf (meningitis ,ensefalitis, neuropati
perifer &mielopati).
Gejala dermatologi yaitu ruam makropapuler eritematosa
dan ulkus mukokutan.

63

Fase infeksi laten.


Asimtomatis, Jarang ditemukan virion di plasma
sehingga jumlah virion diplasma menurun karena
sebagian besar virus terakumulasi di kelenjar limfe dan
terjadi replikasi di kelenjar limfe .
Pada fase ini jumlah limfosit T-CD4 menurun hingga
sekitar 500 sampai 200 sel/mm3.
Fase ini bisa berlangsung 3-13 tahun

64

Fase infeksi kronis.


Di dalam kelenjar limfe terus terjadi replikasi virus yang diikuti
kerusakan dan kematian sel dendritik folikuler karena banyak nya virus,penurunan limfositTlimfositT-CD4hingga dibawah200sel/mm3,
mengakibatkan sistem imun menurun dan pasien semakin
rentan terhadap berbagai macam penyakit infeksi sekunder
,mis Pneumocytis carinii, tuberkulosis, sepsis, infeksi virus
sitomegalo, dan ,juga dijumpai beberapa jenis kanker yaitu
kanker kelenjar getah bening dan kanker sarkoma Kaposis

65

66

67

Manifestasi klinis
Tahap pertama : Infeksi akut.
akut.
6 minggu pertama setelah paparan HIV dapat berupa
demam, rasa letih,nyeri otot dan sendi, nyeri telan, dan
pembesaran kelenjar getah bening .
Tahap kedua

: Asimtomatis.

Tahap ketiga : Simtomatis:


Berat badan menurun tetapi tidak sampai 10%, pada selaput
mulut terjadi sariawan berulang, infeksi bakteri pada saluran
napas bagian atas namun penderita dapat melakukan
aktivitas meskipun terganggu.

68

Tahap keempat : AIDS :


Penurunan berat badan lebih 10%.
Diare yang lebih dari 1 bulan.
Panas yang tidak diketahui sebabnya lebih dari satu
bulan
kandidiasis oral, oral hairy leukoplakia, tuberkulosis
paru, dan pneumonia bakteri.
Penderita diserbu berbagai macam infeksi
sekunder seperti pneumonia pneumokiskarinii,
toksoplasmosis otak, diare akibat kriptosporidiosis,
Infeksi virus herpes , Kandidiasis pada esofagus ,
trakea, bronkus atau paru serta Infeksi jamur lain.

69

DERAJAT BERAT INFEKSI HIV dan AIDS.


Sesuai dengan ketentuan WHO melalui stadium klinis pada
orang dewasa serta klasifikasi klinis dan CD 4 dari CDC.
Stadium Klinis I:
1. Asimtomatis
2. Limadenopati persistent generalisata.
Penampilan / aktivitas fisik skala I : Asimtomatis, aktivitas
Normal.

70

Stadium klinis II
1.Penurunan berat badan,tetapi < 10 % dari berat badan
sebelumnya.
2.Manifestasi mukokutaneus minor (dermatitis seborrohoic
prurigo,infeksi jamur pada kuku,ulserasi mukosa oral
berulang,cheilitis angularis.
3.Herpes zoster,dlam 5 tahun terakhir
4.Infeksi berulang pada saluran pernapasan atas ( mis:
sinusitis bakterial ).
Dengan atau penampilan /aktivitas fisik skala II:simtomatis,
aktivitas normal.

Stadium klinis III.


1.Penurunan berat badan ,> 10%
2.Diare kronis dengan penyebab tidak jelas ,> 1 bulan
71

3.Demam dengan sebab yang tidak jelas ( intermittent


atau tetap),> 1 bulan
4.Kandidiasis oris
5.Oral hairy leukoplakia
6.TB Pulmoner, dalam satu tahun terakhir
7.Infeksi bakterial berat ( misal :pneumonia,piomiositis)
Dengan atau penampilan /aktivitas fisik skala 3 : lemah,
berada di tempat tidur,<50% per hari dalam bulan terakhir.

Stadium klinis IV
1.
2.
3.
4.
5.

HIV wasting syndrome ,sesuai yang ditetapkan CDC.


PCP
Ensefalitis Toksoplasmosis
Diare karena Cryptosporidiosis,> 1 bulan.
Cryptococosis ekstrapulmoner
72

6.Infeksi virus sitomegalo


7.Infeksi Herpes simpleks > 1 bulan
8.Berbagai infeksi jamur berat ( histoplasma,coccidioido
mycosis )
9.Kandidiasis esofagus, trachea atau bronkus.
10.Mikobakteriosis atypical
11.Salmonelosis non tifoid desertai setikemia
12.TB,ekstrapulmoner
13.Limfoma maligna
14.Sarkoma Kaposis
15.Ensefalopati HIV
Dengan atau penampilan /aktivitas fisik skala 4 : sangat
lemah ,selalu berada di tempat tidur . 50% per hari dalam
bulan terakhir .
73

Klasifikasi dengan memakai hitungan sel CD4


1.Infeksi Akut : 1000>CD>750
Gejala infeksi akut biasanya timbul sesudah masa
inkubasi selama 1-3 bulan Flu like syndrome.
berlangsung 1-2 minggu.
Serokonversi terjadi pada fase ini dan antibodi
virus mulai dapat dideteksi kira-kira 3-6 bulan.
2.Infeksi kronis asimtomatik : CD4 > 500/ml.
Keadaan penderita kelihatan baik saja, meskipun
sebenarnya terjadi replikasi virus secara lambat di
dalam tubuh.
Limfadenopati generalisata persisten ( LGP)
74

Muncul penyakit penyakit autoimun,mis :ITP,Guillain


Barre akut ,poliomielitis idiopatik.
3.Infeksi kronis simtomatik
Rata-rata sesudah 5 tahun terkena infeksi HIV.
A. Penurunan imunitas sedang : CD4 200-500
Timbul penyakit yang lebih ringan ,mis :reaktivitasi
dari herpes zoster atau herpes simpleks,namun dapat
sembuh spontan atau hanya dengan pengobatan biasa.
Penyakit kulit Seperti dermatitis seboroik, veruka vulkaris
,moluskum kontangiosum atau kandidiasis oral sering
timbul.
AIDS Related complex ( ARC ) : Demam> 3 bln,diare
BB >10%, kelelahan dan keringat malam,Limfadenopati
berlangsung > 3 bulan.
75

B. Penurunan imunitas berat : CD4 < 200

Infeksi oportunistik berat, seperti Pneumocystis


carinii (PCP )toksoplasma, Cryptococcosis, tuberkulosa,
Cytomegalo virus (CMV) dan lainnya. Keganasan
juga timbul pada subfase inui meskipun sering pada fase
yang lebih awal .

Viremia terjadi untuk kedua kalinya dan boleh dikatakan


tubuh sudah dalam keadaan kehilangan kekebalannya .

76

Diagnosis
WHO disease staging system for HIV infection and
disease :
Stage I : HIV disease is asymtomatic and no categorized
as AIDS.
Stage II : Includes minor mucocutaneous manifestation and
recurrent upper respiratory tract infections.
StageIII : Includes unexplained chronic diarrhea for longer
than a month ,severe bacterial infections and
pulmonary tuberculosis.
StageIV:Includes toxoplasmosis of the brain,candidiasis of
the esophagus, trachea,bronchi or lung and
Kaposis sarcoma;these disease are indicators 77
of
AIDS .

Serologi : ELISA ( Enzyme link immunoassay ) 3

metode : Indirect ELISA ,Competitive ELISA


and sandwich ELISA ( agglutination )
Westernt Blot :
Tes virologi:
Imun compleks p24
HIV RNA with PCR
HIV RNA with bDNA

78

Management
Strategi penatalaksanaan dan pengendalian progresivitas
HIV ke AIDS dilakukan melalui :
1.Terapi antiretroviral
2.Terapi infeksi oportunistik serta malignansi
3.Dukungan nutrisi berbasis makronutrient dan
mikronutrien.
4.Konseling terhadap penderita maupun keluarga ,dan
5.Membudayakan pola hidup sehat

79

Pemeriksaan penderita suspect HIV


Pemeriksaan awal
1.Riwayat Faktor resiko
Riwayat infeksi menular seksual
Riwayat infeksi oportnistik dan penyakit yang
berhubungan dengan HIV ,termasuk TBC.
Riwayat penyakit lain
Riwayat pengobatan antiretroviral
Riwayat alergi
Tanda dan keluhan penyakit saat ini
2.Pemeriksaan klinis.
Pemeriksaan fisik
Nilai stadium klinis infeksi HIV
80

Cari infeksi oportunistik dan penyakit yang terkait


dengan HIV.
Saring kemungkinan TBC
Nilai kemungkinan adanya kehamilan.
3. Pemeriksaan Laboratorium
Pemeriksaan darah lengkap
Jumlah sel T CD 4
X-Ray dada
BTA sputum
Cari kemungkinan hepatitis dengan tes faal hati.
Tes laboratorium lain yang berhubungan dengan infeksi
HIV.
81

B.Konseling dan dukungan.


Jelaskan tentang perjalanan penyakit dan rencana
pengobatan dan perlu kunjungan selanjutnya ( kontrol)
Berikan bimbingan cara hidup yang positif, gizi dan
hidup sehat.
Berikan bimbingan cara pencegahan penularan HIV:
Hindari kintak seksual dengan penderita HIV dan yang
sering menggunakan obat bius secara intravena .
Mitra seksual multiple memberikan kemungkinan lebih
besar mendapat AIDS .
Cara hubungan seksual yang dapat merusak selaput
lendir rektal dapat memperbesar kemungkinan
mendapatkan AIDS.
Pada orang yang bersesiko tinggi AIDS agar tidak
menjadi donor darah.
82

Berikan bimbingan tentang metode keluarga berencana,


pencegahan penularan HIV dari ibu ke anak jika
seseorang berencana, untuk memilki anak.
Bimbing untuk taat pada profilaksis infeksi oportunistik.
Siapkan terapi antiretroviral bila ada indikasi.
C.Pengamatan klinis.
Penderita HIV harus dikontrol teratur setiap 3-6 bulan
sekali jika asimtomatik dan setiap waktu jika ada keluhan
.Laboratorium : darah lengkap, sel T CD4 setiap 6
bulan, X-ray dad jika ada indikasi .
Beri profilaksis infeksi oportunistik bila ada indikasi .

83

The goal of therapy are to :


Reduce morbidity ( the occurrence of opportunistic
infections or number of hospitalizations) and mortality
( death )
Improve quality of life.
Restore or preserve immune function (CD4+ >500.)
Suppress viral load ( or the amount of HIV in a sample of
blood ) < 50 copi /ml .

84

Recommended Treatment Option :


Treatment is typically not started in individuals who have a
CD4+T cell count of greater than 350 cells/mm 3 and plasma
HIV RNA levels of less than 100.000 copies/ml .
Clinicians may consider starting therapy for individuals who
have a CD4+ count of more than 350 cells/mm 3 and plasma
HIV RNA levels of more than 100.000 copies/ml and are not
showing signs or symtoms of HIV.
Individual who have a CD 4+ count of 200 to 350 cells/mm3
and any level of plasma HIV RNA are offered the option to
start treatment, but it is up to the individual.
Treatment is recommended in those individuals who have a
CD4+ count of less than 200 cells/mm3 are not showing
signs or symtoms of HIV / AIDS .
85

Treatment is recommended in those individuals that have


severe symtoms of HIV infection or have a history of AIDS
defining illnesss ( such as multiple/recurrent bacterial
infections, fungal infection in esophagus, kaposis
sarcoma, burkitts lymphoma, herpes simplex virus, recent
pneumonia, as well as any other opportunistic infections)
no matter what their CD 4+count is.

86

ANTIRETROVIRAL THERAPY
Combination antirertoviral therapy ( ART), or higly
active antiretroviral therapy ( HAART), is the
cornerstone of management of patient with HIV
infection .
HAART consists of three or more drugs.The most
common combination given to those beginning treatment
consists of two NRTIs combined with either an NNRTI or
a boosted protease inhibitor.
Exp :Zidovudin (AZT) : 1x 500-600 mg
Lamivudin (3TC ) : 2x 150 mg
Nevirapin 1x 200mg for 14 days,then 2x 200mg.

87

The groups of antiretroviral drugs


There are four groups of anti-HIV drugs. :
Nucleoside / Nucleotide Reverse Transcriptase Inhibitors.
Non-Nucleoside Reverse Transcriptase Inhibitors.
Protease Inhibitors
Fusion or Entry Inhibitors
New class of antiretroviral drugs called Integrase Inhibitors

88

89

90

91

92

Factors affects the rate of progression from


HIV to AIDS

1.general immune function.


2.Poor acces to health care.
3.The existence of coexisting infections
such as tuberculosis.
4.Genetic inheritance ( CCR5 -32
mutation)

93

Prevention
Promoting condom use
Promotion of marriage
Promotion of monogamy
Promotion of morality
Abstinence outside marriage
Screening of blood transfusion
Needles, use clean ones( not to share needles)

94

Potrebbero piacerti anche