Herpes Simplex Pada Kehamilan 4d2r

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 sures 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.

5

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

1

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-γ) 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

a

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

2

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

organism’s

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

1. Steen R. Eradicating Chancroid.

viral replication in these cells. 5. A

World Health Organization. 2001.

temporal sequence of chancroid infection

79(9).

and

HIV

seroconversion

has

been

documented in 39 men who acquired

2. Peel TN, Bhatti D, Boer JCD,

STDs (89% chancroid) from female sex

Stratov I, Spelman DW. Chronic

workers in Nairobi. Twenty-four were

cutaneous ulcers secondary to

reported to have seroconverted, and those

Haemophilus

with genital ulcer disease were sometimes

Med J Aust 2010; 192 (6): 348-

more likely to acquire HIV than those

350.

without

genital

ulcer

disease

after

adjustment for sexual behavior. 6. Invasive diagnostic/therapeutic

procedures

for

chancroid may also spread HIV infection. These include bubo aspiration if not properly handled and herbalist’s methods of bubo drainage, especially with the use

ducreyi infection.

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and

human

immunodeficiency virus infection. International

Journal

of

Dermatology 2008, 47, 1–8 4. Ravikanti,

Sunitha Murugesh

BR,

of unsterilized blades for other subjects,

Vishwanath,

B.

e.g. in scarification and circumcision.1,3

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Treatment

3

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immunodeficiency virus infection

Sci. 2013 Nov;1(4):590-591 5. Alimonti JB, Ball TB, Fowke KR.

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