CHANCROID AS COFACTOR IN HIV

TRANSMISSION

DISUSUN OLEH :
Justicia Andhika Perdana
030.07.129
Pembimbing :
dr. Suswardana, Sp.KK

KEPANITRAAN KLINIK SUB DEPARTEMEN ILMU PENYAKIT KULIT

DAN KELAMIN RUMAH SAKIT AL Dr. MINTOHARDJO
FAKULTAS KEDOKTERAN UNIVERSITAS TRISAKTI
PERIODE 24 MARET 2014 26 APRIL 2014
JAKARTA

CHANCROID AS COFACTOR IN HIV

TRANSMISSION

Justicia Andhika Perdana1, Suswardana2

1

Dokter Muda Fakultas Kedokteran Trisakti di

Sub Departemen Ilmu Kesehatan Kulit dan Kelamin RSAL dr. Mintohardjo
2

Sub Departemen Ilmu Kesehatan Kulit dan Kelamin RSAL dr. Mintohardjo

Abstract

di perkirakan 2 % dari wanita di seluruh

Genital

important

dunia beresiko terinfeksi herpes selama

cofactors of HIV transmission in the

kehamilan, dan memiliki komplikasi serius

countries

terhadap

most

ulcers

are

severely

affected

by

janin

yang

dikandungnya.

HIV/AIDS. Chancroid is a common cause

Diperkirakan apabila terdapat 9 orang

of genital ulcer in countries where adult

wanita yang terinfeksi herpes simpleks

HIV prevalence surpasses 8% and is rare

saat mendekati proses persalinan, 4 dari 9

in

anak yang dilahirkan tertular herpes saat

countries

epidemics.

with

low-level

HIV

1, 4

proses persalinan, 1 anak meninggal dunia,

Keywords : Chancroid, HIV Transmission,

dan 1 anak dapat mengalami sekuel

Soft Chancre, Ulcus Molle

neurologis.

Pemeriksaan

serologis

terhadap HSV dapat mengetahui secara

HERPES PADA KEHAMILAN
Infeksi virus herpes simpleks pada masa
kehamilan diketahui berhubungan abortus
spotan, prematuritas, dan dapat terjadi
gangguan perkembangan janin intrauterin.
Sedangkan pada saat proses persalinan
dapat menyebabkan neonatus terinfeksi
virus herpes simpleks apabila mengalami
kontak dengan lesi herpes, dan dapat
menyebabkan komplikasi serius seperti
gangguan perkembangan otak yang berat,
serta memiliki angka kematian tinggi
apabila tidak ditangani.

dini. Perlu dilakukan konseling untuk

meningkatkan kewaspadaan terhadap virus
herpes simpleks, dan tindakan abstinens
sex dan penggunaan kondom dianjurkan
terutama pada trimester ketiga kehamilan.5
Human Immunodeficiency Virus
Retroviruses

human

immunodeficiency virus type 1 and type 2

(HIV-1 and HIV-2), has reached pandemic
proportions. Therefore, it is critical to
understand how HIV causes AIDS so that
appropriate therapies can be formulated.
Primarily, HIV infects and kills CD4 + T

Infeksi herpes simpleks diketahui

lymphocytes, which function as regulators

tidak dapat menular antara ibu dan janin

and amplifiers of the immune response. In

yang dikandung selama kehamilan, namun

the absence of effective anti-retroviral

therapy, the hallmark decrease in CD4 + T

edges. The ulcer of chancroid is classically

lymphocytes during AIDS results in a

described as a nonindurated soft sore, or

weakened immune system, impairing the

ulcus molle, as distinct from the

body's ability to fight infections or certain

indurated ulcer of syphilis.1,3, 4

cancers such that death eventually ensues.

The major mechanism for CD4+ T cell
depletion

is

programmed

cell

death

(apoptosis), which can be induced by HIV

through multiple pathways. Death of HIVinfected

cells

can

result

from

the

propensity of infected lymphocytes to

form short-lived syncytia or from an
increased susceptibility of the cells to
death. There is also evidence that as AIDS
progresses cytokine dysregulation occurs,
and the overproduction of type-2 cytokines
(IL-4, IL-10) increases susceptibility to
AICD whereas type-1 cytokines (IL-12,
IFN-) may be protective. Clearly there are
multiple causes of CD4+ T lymphocyte
apoptosis in AIDS and therapies that block
or

decrease

that

death

could

have

significant clinical benefit.5

Genital

ulcer

disease

is

recognized risk factor for HIV infection.

Strong

associations

between

HIV

seropositivity and genital ulcer disease

have been reported and the odds and risk
ratios are higher than for non-ulcerative
STDs. Cross-sectional and prospective
population studies do not accurately
measure the increased risk of HIV
infection.

Chancroid

facilitates

the

transmission of HIV by increasing both the

infectiousness

of

HIV

and

the

susceptibility to infection by the virus.

Subjects

with

HIV

infection

and

concomitant chancroid ulcer demonstrate

increased

infectiousness

through

the

following: 1. There is increased HIV

shedding into the genital tract from ulcer
exudates. 2. Genital ulcers bleed during

Cofactors in HIV Transmission

intercourse, resulting in potential increases

The incubation period of H.

in viral shedding and HIV infectiousness.

ducreyi is between 4 and 7 days with no

3. In men with genital ulcer disease, there

prodromal symptoms. This may be longer

is

with pre-existing HIV infection. There

concentration, especially in those with

may be a history of recent sexual

nongonococcal urethritis. This is attributed

exposure, possibly with a commercial sex

to an increased plasma viral load from

worker. The primary lesion starts as a

advanced disease or systemic immune

tender papule with an erythematous halo

activation by H. ducreyi. Chancroid

that evolves into a pustule. Central

genital

necrosis of the pustule leads to the

susceptibility to HIV infection through the

characteristic

nonindurated,

following: 1. Disruption of mucosal

sharply defined ulcer with undermined

integrity provides a portal of entry for

painful,

increased

ulcer

seminal

disease

fluid

viral

increases

HIV. 2. Haemophilus ducreyi increases the

Chancroid can be treated with

presence and activation of HIV-susceptible

macrolides, quino- lones, and some third-

cells in the genital tract. This is part of the

generation cephalosporins. Single doses of

organisms

immune

certain antibiotics, such as ciprofloxacin

response. Specifically, CD4+ T-helper

and azithromycin, are highly effective

cells and macrophages are found in

although longer treatments may be more

significant numbers in both early lesions

effective in uncircumcised males and

of chancroid and in the advancing edge of

patients with HIV infection. Antibiotics

established ulcers. These cells are the

may also provide some protection from

primary targets of HIV. 3. Haemophilus

reinfection: one study estimated that the

ducreyi has also been found to increase

prophylactic effect of a single dose of

CCR-5

induced

receptor

macrophages,

cellular

expression

on

azithromycin against new H. ducreyi

increasing

the

infection lasted as long as two months

thus

susceptibility of these cells to HIV

invasion. 4. Specific T-cell-stimulating
antigens have been demonstrated in H.

after treatment.3
References

ducreyi, and this can result in increased

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viral replication in these cells. 5. A

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79(9).

and

HIV

seroconversion

has

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STDs (89% chancroid) from female sex

Stratov I, Spelman DW. Chronic

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reported to have seroconverted, and those

Haemophilus

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and

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immunodeficiency virus infection.

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Journal

of

Dermatology 2008, 47, 18

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