Microsoft word - ej insted 2012 jan review_of_literature_dinesh.doc
Patterns of STI in HIV affected
Dineshkumar D Registrar, Department of Pediatric Dermatology, KK Child's Trust Hospital, Chennai, Tamil Nadu, India Address for correspondence: [email protected] Introduction
Sexually Transmitted Diseases (STD), includes diseases that are transmitted by
the sexual route. Sexually Transmitted Infections (STI), differs from STD in that, STD
includes infections that result in clinical disease, whereas STI in addition includes
infections that may not cause clinical disease, but are transmitted by the sexual route.
Nonetheless, for all practical purposes both STI and STD are being used synonymously.
Sexual transmission requires the agent to be present in one partner, the other
partner to be susceptible to infection with that agent and that the sexual partners engage
in sexual practice which can transmit the pathogen. Globally the majority of Human
Immunodeficiency Virus (HIV), is through heterosexual transmission, HIV infection is
thus by definition is one of the sexually transmitted infections or diseases.
HIV /AIDS and STD
Acquired Immunodeficiency Syndrome (AIDS), represents the late clinical stage
of infection with Human Immunodeficiency Virus (HIV). A total of 39.5 million
(34.1-47.1 million estimated) people are living with HIV in 2006, about 2.6 million more
than in 2004. This figure includes the estimated 4.3 million (3.6 million-6 million) adults
and children who are newly infected with HIV in 2006,1 so that for decades to come HIV
will remain the most widespread, deadly and costly of all STI.
Epidemiologic studies have estimated the risk of HIV transmission to range from
5 in 10,000 to 26 in 10,000 penile/vaginal acts.2 The sense of rarity of transmission
conveyed by such statistics is misleading, particularly when it is considered that many
populations have very high prevalence rate of HIV infection occurring as a result of what
must certainly be much lower numbers of sexual encounters.
In fact there are a number of factors that amplify risk of transmission and that
needs to be taken into account in efforts to prevent transmission. Factors that amplify the
risk of HIV transmission include those that increase infectiousness, such as stage of HIV
disease and presence of certain co-infections (e.g.: malaria, helminthic infections,
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tuberculosis) and those that can increase both infectiousness and susceptibility, such as
other sexually transmitted diseases.3 Lethal synergy between HIV and STD
A strong association exists between the occurrence of HIV infection and the
presence of other STD. Both ulcerative and non ulcerative STD promote HIV
transmission, augmenting HIV infectiousness and HIV susceptibility via different
biological mechanisms.4 Classic STD could facilitate HIV transmission by increasing
either the infectiousness of the index case, the susceptibility of the partner or both.5, 6
The risk of HIV transmission is markedly elevated for individuals with genital
ulcer versus those without genital ulcer at every level of plasma viral load.7 HIV
seroconversion risk is 4.7 times higher among men who acquire a genital ulcer from a sex
worker.8 Studies from India have also shown increasing prevalence of HIV infection
among STD clinic attendees, prevalence was found higher among genital ulcer patients
than non-ulcerative STD patients.9, 10
In HIV infected individuals, not only may symptomatic and asymptomatic STI
enhance sexual transmission of HIV-1 by increasing virus shedding from the genital
tract11, 12,13 but also at the same time HIV infection itself increases susceptibility to STI.14
There is also considerable evidence that STI may increase HIV-1 susceptibility in
uninfected individuals15,16 although differentiating cause from effect is more difficult in
On susceptibility side, STD can reduce physical and mechanical barriers of the
virus (e.g. by causing lesions of the mucosa), increase the number of receptor cells or
density of their receptors (e.g. by causing persistent inflammation). On infectiousness
side, STDs might evoke a more infectious HIV variant18 and can increase HIV
concentrations in genital lesions, semen or both.11
Several mechanisms of cofactor effect of ulcerative and non ulcerative STD on HIV
transmission by augmenting HIV infectiousness and HIV susceptibility have been put
forth:3,6,12,19,20, 21, 22,23
Lack of mechanical skin / mucous membrane / endocervical epithelial barrier makes an easy viral exit and entry due to ulceration or micro ulceration
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Genital ulcers may increase susceptibility to HIV by not only disruption of mucosal and skin integrity but also by increase in the number and activation of the HIV susceptible cells in the genital tract.
Potential increases in HIV infectiousness also occur as a result of bleeding of genitals during the sexual intercourse.
Plummer et al., detected HIV in the genital ulcer exudate in HIV infected individuals by means of culture and PCR.
Increased number of HIV containing white blood cells in both ulcerative and inflammatory genital secretion.
Due to inflammation in genital tract, there is increased shedding of HIV virus in the genital tract as was noted by Ghys PD et al., who detected a significant increase in HIV-1 DNA in cervicovaginal fluids of patients with gonorrhea and chlamydial infections.
STD produces a vaginal environment that is more conducive to transmission (e.g. via presence of bacterial vaginosis and increased levels of anaerobes or amines.)
Impact of HIV infection / AIDS on other STD Herpes genitalis24
Herpes genitalis is caused by a double stranded DNA virus Herpes virus hominis
also known as the Herpes Simplex Virus (HSV).
There are two types: type 1 and type 2. The predominant type isolated from the
genital area is type 2, although in one third of the cases, type 1 may be isolated.
Herpes virus infection can be classified as:
True primary: Infection occurring in a herpes seronegative individual.
Non-primary: The first episode occurring in a previously infected individual.
Recurrences generally follow the first episode of infection. Recurrent episodes are
generally milder, lasting for only 5 to 7 days. The duration of viral shedding is usually
about 3 to 4 days and healing is usually complete by 7 to 10 days. After the primary
infection, patients with HSV 2 have more frequent and earlier recurrences than those
infected with HSV 1. Patients with more severe and prolonged first episode disease (>5
weeks) have more frequent recurrences than those without.
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A synergistic relationship exists between HSV and HIV leading to enhanced
replication of viruses and potentiation of HIV transmission.25 HSV infections occur more
frequently and are of more severity in immunocompromised patients secondary to HIV
infection. HSV was isolated in 13% of HIV seropositive women as compared with only
3.6% of HIV seronegative women in a cross sectional study.26 HSV doubles the risk of
HIV acquisition in the heterosexual population.27
HSV is an important cofactor for HIV expression and transmission. In tissues
co-infected with HSV-1, HIV appears to be able to infect keratinocytes that lack CD4
receptors and are not usually vulnerable to HIV infection.28 The HSV regulatory proteins
ICPO and ICP4 (infected cell protein number 0 and 4) can up regulate the rate of HIV
replication in vitro.29 ICPO and ICP4 transactivate the long terminal repeat (LTR) of
HIV-1 and both ICPO and ICP27 can up regulate HIV expression in CD4 lymphoid cells.
There is increased expression of HIV on mucosal surfaces as a result of infiltration of
CD4+ lymphocytes in the herpetic lesions. Subclinical viral shedding is significantly
increased and common in the perianal area. HIV RNA levels in plasma significantly
increase in patients with active herpes lesions.30
Severe episodes of anogenital herpes may be the first clinical signs of
immunosuppression.31 Herpetic lesions in immunosuppressed, persist or may progress to
chronic painful ulcers with raised margin, involving large areas of perianal, scrotal or
penile skin and may bleed easily. The lesions are atypical, large often hemorrhage, deep,
painful ulcers with raised margins in advanced HIV disease.
There is an increased rate of ulcers due to HSV-2 in patients in HIV infection/
AIDS, owing to immunosuppression. Patient experiences twice the frequency of recurrent
ulcers due to HSV-2 (4 episode/yr) instead of 2 and twice the duration of ulcers
(2 wks to 1).32
The severity and frequency of recurrence increase over time as HIV induced
immunosuppression progresses. Chronicity
Non-healing perianal ulcerative herpes simplex is not an uncommon presentation in HIV
infected individuals. The CDC revised the surveillance case definition for AIDS in 1987
and included chronic ulcers caused by HSV-2 of more than 1month duration as AIDS
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Clinical picture can simulate donovanosis, syphilis, or giant chancroid. Other
atypical lesions are erythema multiforme like eruption, hyperkeratotic verrucous lesions
and vegetating plagues. Lesions of herpes simplex may acquire a zosteriform
appearance.34 Tzanck smear biopsy and viral cultures are useful for diagnosis.
Herpetic infections can be treated with oral acyclovir 400mg thrice a day till clinical
lesions have resolved (7 to 10 days). Treatment of herpes genitalis are given in table 135 . Treatment of herpes genitalis CDC 2006 guidelines35
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In severe cases or if oral absorption is unreliable then 5 to 10mg of acyclovir, 8th
hourly can be given intravenously till clinical resolution.Recommended regimen for daily
suppressive therapy (to decrease the frequency of recurrences) in persons infected with
HIV is acyclovir 400-800mg orally twice or thrice a day.36 Long-term suppressive
therapy with acyclovir may prolong survival in AIDS patients with a history of severe
HSV infections.36 Human Papilloma Virus Infection
Condylomata acuminata is a viral infection caused by Human Papilloma Virus
(HPV). In the United States, estimated prevalence of genital warts among men and
women between 15-49 years of age is 1.4 million and 19 million have subclinical
infections.37In India the prevalence of genital warts has been reported to be 5.1 % to
25.2% of STD patients.38, 39 Among the HIV infected individual, the incidence of
condylomata accuminata has increase from 7.2% to 8.8% over the last few years.40
HIV infection and immunosuppression play an important role in modulating the
natural history of HPV infection.41 HIV infection influence local immunity by altering
HPV infection and by systemic immunodeficiency.42 HIV infected patients have multiple
lesions and even diffuse involvement of anogenital area.43
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In these individuals, very large genital warts may develop and on rare occasions
these become locally invasive and destructive, however these tumours called giant
condylomas or Buschke-Lowenstein tumours are non-metastasizing,44 but carry a
significant risk of squamous cell carcinoma.
There exists a local immunodeficiency in the perineal region, which may account
for higher rate of HPV occurrence in the perianal area than on the penile shaft.45 As per
CDC 200635 guidelines treatment modalities for external genital warts should be no
different in the setting of HIV-infection.
Topical 5% imiquimod cream and podofilox 0.5% solution or gel can be used by
the patient till clinical resolution. Cryotherapy with liquid nitrogen or cryoprobe,
podophyllin resin 10%-25% in a compound tincture of benzoin, topical trichloroacetic
acid (TCA) or bichloroacetic acid (BCA) 80%-90%, surgical removal either by tangential
scissor excision, tangential shave excision, curettage, or electrosurgery, intralesional
interferon, LASER surgery are physician administered treatment modalities. Women
infected with HIV need to undergo a comprehensive gynaecological examination
including a PAP smear as a part of their initial evaluation.
Syphilis is caused by Treponema pallidum of the order spirochaetales. Syphilis
has of late received renewed attention, due to the emergence of the HIV/AIDS epidemic.
A more aggressive course and atypical presentation have been observed in HIV
seropositive individuals. The immunosuppressed state alters the serological tests used in
the diagnosis and these individuals show unreliable response to therapy.46 Syphilis
includes primary, secondary and tertiary lesions.
HIV infected persons have a greater likelihood of multiple chancre in primary
stage and an overlap of primary and secondary stages can occur. The usually painless
chancre can become painful due secondary infection and giant primary chancre can also
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Usually malignant syphilis (Lues maligna) is a feature, characterized by nodule
ulcerative (rupia) lesions with systemic symptoms. Florid cutaneous, mucocutaneous
lesions, pustular, nodular, necrotizing secondary lesions, hyperkeratotic verrucous plaque
type lesions can occur.48,49
It seems that the cellular immune functions in an immunocompetent host protect
against severe and ulcerating skin lesions. Consequently, rupia like skin lesions, which
are an almost pathognomonic sign of this type of secondary syphilis, should be
recognized by physicians taking care of HIV infected patients.
For clinical and prognostic reasons ulcerating secondary syphilis with general
symptoms and neurosyphilis are of special importance in an immunocompromised host.48
The latent period is usually shortened with premature development of neurosyphilis
within the first year of infection.46 Diagnosis
Atypical serological courses have been described in HIV infected individuals with
syphilis. Evolutions of non-treponemal test; Venereal Disease Laboratory Test (VDRL)
appears similar in HIV-seropositive and HIV seronegative patients.49 False negative
reactions are more frequent in HIV infected individuals compared to general population,
because of an excess of non-treponemal antibodies, presumably produced by HIV
induced B cell dysfunction, preventing the antigen-antibody reaction in standard test by
Among the treponemal tests, Treponema pallidum Haemagglutination Test
(TPHA) can serorevert in HIV seropositive patients; whereas seroreversion is never or
very rarely observed in HIV seronegative patients. Seroreversion of the Fluorescent
Treponemal Antigen-Antibody absorption test (FTA-Abs) was observed among both
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HIV-seropositive and seronegative patients, and was associated with a low baseline
CD4+ count in HIV seropositive patients. Falls in titer of the FTA-Abs test were more
rapid in HIV seropositive patients.49
As TPHA may serorevert in HIV seropositive patients, a non-reactive TPHA does
not exclude a past syphilis in such patient. The VDRL test remains adequate for
monitoring the efficacy of treatment in these patients. However, in cases where there is a
strong clinical suspicion and inconclusive serological results, then dark field microscopy
and histopathological examination may be required.
Parenteral penicillin is a preferred drug for the treatment of all stages of syphilis.
The preparation used, the doses and length of treatment depend on the stage and clinical
manifestations of the disease. Recommended regimens for various stages of syphilis in
HIV infected adult patient are given in table 235 Recommended regimens for various stages of syphilis in HIV infected adult patient (CDC 2006 guidelines) 35 Treatment Follow-up
2.4 million units IM in a single at 3, 6, 9, 12 and 24 months
2.4 million units IM in a single at 6, 12, 18 and 24 months
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Neurosyphilis or Aqueous crystalline penicillin G, If CSF pleocytosis was initially
administered as 3-4 million units every 6 months (for upto 2 years) or
IV every 4 hours or as a until this parameter returns to
In HIV seropositive patients sensitive to penicillin, the following regimen as used
Cap. Doxycycline, 100mg, twice a day, orally, for l4 days.
Cap. Tetracycline, 500mg, four times a day, orally, for 14 days.
Inj. Ceftriaxone, 1g, given daily, either IM or IV, for 8-10 days.
However, the uses of alternatives to penicillin have not been well studied in HIV
positive patients and thus have to be used with caution. The management of syphilis in a
HIV seropositive individual remains a area which is yet to be fully delineated.50
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Chancroid is also known as soft sore, soft chancre and ulcus molle. Chancroid is
an acute infectious disease caused by a gram-negative bacillus, Haemophilus ducreyi.
Chancroid may be both a marker for increased risk of HIV infection and co-
infection and also a cofactor for HIV transmission. HIV seropositive patients have an
increased number of ulcers, of longer duration and also the ulcer takes a significantly
longer time to heal.51 Occurrence of giant and phagedenic ulcer is frequent. Multiple,
multilocular inguinal buboes also occur.
A painful ulceration associated with tender inguinal lymphadenopathy is
suggestive of chancroid, whereas the development of associated suppurative adenopathy
is almost pathognomonic.52 HIV infection alters the disease process of H.ducreyi,
Causes for delayed healing could include:51
Autoinoculation with Haemophilus ducreyi.
Suboptimal treatment prior to presentation.
Co-existing HSV infection (the presence of HIV-induced immunosuppression
producing reactivation of genital herpes).
H. ducreyi elicits a cell mediated immune response of the delayed type
indistinguishable between HIV infected and un-infected patients and thus cannot readily
explain the clinical differences observed. Individuals with clinically latent HIV infection
have an altered response to H. ducreyi infection, which may be due to functional defects
in the lymphocytes and macrophages.51 This explains why single dose microbial therapies
for chancroid fails more often in HIV infected individuals even when microbiological
cure us obtained. Thus failure of single dose antimicrobial therapy may be due to a failure
of the healing process.51
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The CDC 2006 recommends any one of the following regimen for the treatment
of chancroid: 35
Tab. Azithromycin 1g orally in a single dose;
Inj. Ceftriaxone 250mg intramuscularly in a single dose;
Tab. Ciprofloxacin 500mg orally two times a day for 3 days;
Tab. Erythromycin 500mg orally four times a day for 7 days.
The data is limited concerning the therapeutic efficacy of the recommended single
dose regimens in HIV infected patients; hence these regimens should be used for such
patients only if follow up can be ensured, some specialists suggest using 7 day
erythromycin regimen for HIV infected person.35 Granuloma inguinale (Donovanosis)
Donovanosis is a chronic destructive and slowly progressive, mildly contagious
disease caused by Calymmatobacterium granulomatis and is characterized by
granulomatous ulceration affecting primarily the genitalia. Also known as Granuloma
venereum, Granuloma inguinale tropicum. As it is a genital ulcer disease it facilitates
transmission of HIV. Genital ulcers due to Donovanosis take a longer time to heal and
tend to produce more tissue destruction.53 There also appears to be a increased incidence
of squamous cell carcinoma in HIV seropositive young patients with donovanosis.54
Crush tissue smear or histopathological examination of the ulcer is useful for diagnosis.
CDC 2006 guidelines for treatment of Granuloma inguinale are as follows:35 Recommended Regimen
Tab. Doxycycline 100 mg orally twice a day.
Alternative Regimens include
Tab. Azithromycin 1 g orally once per week. or
Tab. Ciprofloxacin 750 mg orally twice a day or
Tab. Erythromycin base 500 mg orally four times a day or
Trimethoprim-sulfamethoxazole one double-strength (160 mg/800 mg) tablet
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Therapy should be continued at least 3 weeks and until all lesions have
completely healed. Some specialists recommend the addition of an aminoglycoside (e.g.,
Gentamycin 1 mg/kg IV every 8 hours) to these regimens if improvement is not evident
within the first few days of therapy. Response to treatment should be noticed in a week;
otherwise alternate regimen may have to be considered. WHO (2001) recommends that
treatment should be continued until all lesions have completely epithelialized. HIV
seropositive patients with Donovanosis can have a failure rate to first line antibiotic
therapy. CDC 2006 recommends injection Gentamycin 1mg/kg every 8hours for such
patients.35 Lymphogranuloma venereum (LGV)
LGV is a sexually transmitted infection affecting primarily the lymphatic system,
caused by Chlamydia trachomatis serovars L1, L2, and L3. It is characterized by regional
suppurative lymphadenopathy, which is preceded by a small transient, inconspicuous
lesion at the site of inoculation, usually the genitalia. HIV appears to have no adverse
effect on clinical features of LGV.55 CDC recommends the same line of treatment for
LGV in HIV seropositive individuals as with HIV seronegative individuals, with a
CDC 2006 recommendations for treatment of LGV are as follows:35
Tab. Doxycycline 100mg orally twice a day, for 3 weeks or
Tab. Erythromycin 500mg orally four times a day, for 3 weeks.
It is also recommended to either aspirate with a wide bore needle through normal
skin or incise and drain the buboes as and when required.
Urethritis and HIV
Urethritis is defined as inflammation of urethra. It is mostly a sexually transmitted
disease. Urethritis manifested by urethral discharge, dysuria or itching at the tip of
urethra is the response of the urethra to inflammation of any etiology. The urethral
inflammation and discharge help in the transmission of HIV and thus increases the
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chances of individuals acquiring HIV infection. Urethritis, of any etiology increases the
chances of acquiring HIV infection by the way of inflammatory cells, which phagocytose
the virus and then take the virus to systemic circulation. Also, breach in the mucosa of
urethra facilitates easy entry of the virus into the body.
Classification of Urethritis
Gonococcal Urethritis - Caused Neisseria gonorrhea.
Non-Gonococcal Urethritis (NGU) - Caused Chlamydia trachomatis, Ureaplasma urealyticum, Mycoplasma genitalium, Trichomonas vaginalis, Yeasts, Herpes
simplex virus, Adenovirus, Hemophilus species.
Non-chlamydial non-gonococcal urethritis (NCNGU)- When C. trachomatis and
N. gonorrhoeae is not isolated form urethral specimen by various methods, in
urethritis patients, then the terminology NCNGU is used. The most likely causes
are Ureaplasma urealyticum and Mycoplasma genitalium.
It is shown that semen and cervical secretions may also harbor infectious
virus.12,56Neisseria gonorrhea and Chlamydia trachomatis infections of urethra or
cervix, increases infectiousness of HIV by increasing the viral load in genital
secretions.57,58 The risk for female to male HIV transmission was doubled in gonorrhea
patients.59 Ghys and co-workers found that the detection of HIV-1 in cervicovaginal
lavage samples from patients with gonorrhea, chlamydial infection, cervicovaginal ulcer
or cervical mucopus, a week after STD treatment HIV-1 decreased from 42% to 21% in
this group, however changes in detection rate were not observed in women whose STD
were not cured.12
Treatment for gonococci infections of the cervix, urethra, and rectum as per CDC
2006 guidelines is:35
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Recommended regimens include any one of the following
Inj. Ceftriaxone 125 mg IM in a single dose:
Tab. Cefixime 400 mg orally in a single dose.
Tab. Ciprofloxacin 500 mg orally in a single dose.
Tab. Ofloxacin 400 mg orally in a single dose.
Tab. Levofloxacin 250 mg orally in a single dose.
Inj. Spectinomycin 2 g in a single IM dose.
Treatment for non-gonococcal urethritis as per CDC 2006 guidelines is:35 Recommended regimens
Tab. Azithromycin 1 g orally in a single dose. or
Tab. Doxycycline 100 mg orally twice a day for 7 days.
Alternative Regimens can be one of the following
Tab. Erythromycin base 500 mg orally four times a day for 7 days.
Tab. Ofloxacin 300 mg orally twice a day for 7 days.
Tab. Levofloxacin 500 mg orally once daily for 7 days.
In case of recurrent or persistent urethritis; metronidazole 2 g orally in a single
dose or tinidazole 2 g orally in a single dose plus azithromycin 1 g orally in a single dose
Trichomoniasis is caused by Trichomonas vaginalis. T. vaginalis is almost
exclusively transmitted by sexual intercourse. T.vaginalis is a flagellated parasitic
protozoan that elicits a broad range of clinical symptoms. It is estimated that up to 30%
of infected women are asymptomatic (with normal vaginal pH and flora) with about one
third of these women developing symptoms within 6 months.60 In acute symptomatic
infections, clinical manifestations can include punctate hemorrhagic spots on the vaginal
and cervical mucosa and yellow green discharge.61 In chronic infections, symptoms are
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milder and may include and pain during sexual intercourse.60 Men generally remain
asymptomatic and are classified as carriers, although, some develop urethritis62 and
Contact with T.vaginalis damages the epithelium, the primary line of defense
against infection, causing cytotoxicity and epithelial cell disruption and allowing HIV-1
access to underlying immune cells. Trichomonads also induce HIV-1 replication through
cytokine pathways such as TNFα.64 One or both of mechanisms may lead to T.vaginalis
patients being more susceptible to HIV-1 infection. Augmented viral replication in co-
infected patients would make them more likely to infect their sexual partners, thereby
increasing HIV-1 transmission.64Patients who have trichomoniasis and also are infected
with HIV should receive the same treatment regimen as those who are HIV negative.
CDC 2006 guidelines for treatment of trichomoniasis are as follows: 35 Recommended Regimens
Tab. Metronidazole 2 g orally in a single dose or
Tab. Tinidazole 2 g orally in a single dose
Metronidazole 500 mg orally twice a day for 7 days.
Vulvovaginal candidiasis (VVC) is a common problem in women with HIV. The
number of VVC in HIV seropositive women is increasing as is the number of HIV
seropositive women. VVC is recurrent in HIV infected women and improves only
temporarily with therapeutic intervention. In women there would be complaints of
pruritus, vaginal discharge, vaginal soreness, vulvar burning, dyspareunia and external
dysuria. Examination reveals typical dusky red erythema of vaginal mucosa with curdy
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In men it commonly can present as longitudinal fissures on the under surface of
the prepuce, as transient papulopustules on the glans giving rise to superficial
erythematous erosion having a thrush like membrane.
Long term prophylactic therapy with tab. Fluconazole 200mg per orally weekly
has shown to be of benefit in controlling genital candidiasis. Therapy (CDC 2006) for
VVC in HIV-infected women should not differ from that for seronegative women.
Although long-term prophylactic therapy with tab. Fluconazole at a dose of 200 mg
weekly has been effective in reducing C. albicans colonization and symptomatic VVC
this regimen is not recommended for routine primary prophylaxis in HIV-infected
Recommended Regimens (CDC 2006) Intravaginal Agents
Clotrimazole 1% cream 5 g intravaginally for 7-14 days
Clotrimazole 100 mg vaginal tablet for 7 days.
Clotrimazole 100 mg vaginal tablet, two tablets for 3 days.
Fluconazole 150 mg oral tablet, one tablet in single dose.
Men are to be given topical clotrimazole 1% cream along with a single
Molluscum contagiosum is a common cutaneous disease caused by a pox virus.
Molluscum contagiosum virus (MCV). There are two types of viruses MCV-1 and MCV-
2. MCV-2 is common in adult men and patients with HIV infection.66 Between 10-30%
of patients with symptomatic HIV disease or AIDS have molluscum contagiosum.67
Molluscum in AIDS patients reflects the reactivation of latent MCV. The individual
lesion of molluscum contagiosum may be quite large with a diameter of 10mm or more
(giant MC). The lesions are usually in clusters, pearly with an umbilicated centre.
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Hundreds of lesions may be found between the umbilicus and the genitals in
sexually active young adults.68 Despite being recalcitrant, all MC lesions in HIV patients
are not sexually transmitted. Viral structures, consistent with MCV are present in the
clinically uninvolved epidermis adjacent to the lesions of MC in some HIV infected
patients. This may explain the large number of lesions seen in these patients and the
difficulty in controlling the spread and recurrences of MC lesions.69
No therapy is very effective in HIV seropositive patients as new lesions can erupt
frequently.68 Intralesional Interferon α, imquimod and cidofovir (topical or intravenous Ectoparasite infections70
Scabies and pediculosis pubis are the two important ectoparastic infections to be
considered in HIV seropositive patients.
Scabies is caused by itch mite Sarcoptes scabiei var-hominis and its clinical
manifestation in HIV seropositive individuals depends on the degree of
immunosuppression. HIV seropositive patients can have two unusual overlapping forms
Papular variety: Characterized by severely pruritic, generalized papules,
topped by scabietic burrows, which may be scaly.
Crusted (Norwegian) Scabies: Characterized by thick, friable, white-grey
plaques, which become crusted. Crusted scabies is associated with greater
Patients with uncomplicated scabies with HIV infection should receive the same
treatment regimens as those who are HIV negative. CDC 200635 recommends permethrin
cream (5%) applied to all areas of the body from the neck down and washed off after
8-14 hours or oral ivermectin 200 µg/kg/dose repeated in 2 weeks. Alternatively,
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Lindane (1%) applied in a thin layer to all areas of the body from the neck down and
thoroughly washed off after 8 hours. Lindane is not recommended as first-line therapy
because of toxicity. It should only be used as an alternative if the patient cannot tolerate
other therapies or if other therapies have failed. Topical scabicide application should
started form behind the ears and should involve the entire body up to the fingernail and
toenail tips. Fingernails need to trimmed.
It is an infestation of hair bearing area, most commonly pubic region and is
sexually transmitted. The causative parasite is Phthirus pubis also known as ‘pubic or
crab louse’. Infestation may be severe with extensive colonization in HIV seropositive
individuals. The treatment regimen for HIV seropositive individuals with pediculosis
pubis is same as that of HIV seronegative (Permethrin 1% cream/ lotion).
CDC 200635 recommends regimens are:
Permethrin 1% cream rinse applied to affected areas and washed off after 10 minutes.
or Pyrethrins with piperonyl butoxide applied to the affected area and washed off after
Malathion 0.5% lotion applied for 8-12 hours and washed off.
Ivermectin 250 µg / kg / dose orally, repeated in 2 weeks.
Effect of STD management on HIV transmission
Prevention, early diagnosis and treatment of STD can be important for HIV
prevention strategy especially when treatment of symptomatic STD is addressed.
In a study conducted in a STD clinic, a single injection of ceftriaxone for
presumptive gonorrhea in 86 men with urethritis produced a reduction in median seminal
HIV RNA concentration from approximately 1,20,000 copies/ml to 40,000 copies/ml
over 3 weeks with no change occurring in plasma viral load.11 These findings indicate
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that the amplified transmission risk associated with high seminal HIV level can indeed be
markedly reduced on treatment of the underlying STD. Similarly treatment for
trichomoniasis in the STD clinic produced a reduction in genital tract.71 An association
does exist between HSV-2 infection and HIV-1 acquisition and provide a strong rationale
for current trials of HSV-2 suppression as an HIV-1 prevention strategy in Africa.72 Syndromic Approach
As prompt and efficient therapeutic interventions of STD have a positive impact
on the course of HIV infection, the treatment of symptomatic STD gains importance. It
was in this background, that the syndromic approach to the management of STDs was
brought out and it is endorsed by World Health Organization (WHO), National AIDS
Control Organization (NACO) and Government of India, Ministry of Health and Family
Welfare as an effective means to treat symptomatic STD, promptly when rapid and
sensitive laboratory tests are not available.
A 42% reduction in new sexually transmitted HIV infection was detected in a
randomized control trial done to evaluate the impact of improved STD case management
as per the WHO recommended syndromic STD management guidelines at primary case
level in rural Tanzania over a 2 year period.73
Syndromic treatment has a greater impact on HIV infection, as it covers
proportionately more symptomatic STI, which are stronger co-factors for HIV infection
than are asymptomatic STI.32 Effect of Highly Active Antiretroviral Therapy (HAART) on STI in people with HIV infection
Patients with partially restored immunity due to HAART show less frequency,
milder form and reduced recurrence of molluscum contagiosum and condyloma
accuminata.55 There is evidence that HAART directed at HIV may cause the regression
of HPV disease.74 Effective ART limits the effect of urethritis on increase in seminal
plasma HIV-1 RNA loads.75
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However, HAART may give a false sense of security to ill counseled patients and
they are more likely to indulge unsafe sexual practices.
Screening and Diagnostic Testing
As majority of STI are asymptomatic, deciding when to screen the patients is
critical. People often underestimate their risk of exposure to STI and HIV and don’t
understand safe sexual practices. Because self-reported sexual history is often an
unreliable indicator of the actual risk of infection, broader screening of populations in
which prevalence of STI is high should be considered.76 Conclusion
HIV infection is a major global cause of illness, long term disability and death,
with severe medical and psychological consequences for millions of men and women,
especially so when it co-exists with other STD. HIV and other STD synergize to
aggravate the associated morbidity of each other in the human body. The effective
management of one condition produces a better outcome of not only the treated
condition, but also of the existing comorbid condition.
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Aviso Importante: Laboratorios Suiphar interpreta que internet es un medio de comunicación global, sin embargo es importante considerar que la Industria Farmaceútica está regida por un marco regulatorio especíﬁco de cada país. La sección de productos está exclusivamente dedicada a satisfaccer necesidades de información de los profesionales de la salud, para uso adecuado de lo
Excerpts from Shimara’s Newsletter, THE COMPLETE SYSTEM OF HEALING WITH DIVINE ENERGIES Beloved friends,I think it is so incredibly amazing how well orchestrated the movement of Mother Earth and all of nature is, and how totally in alignment she is with the wisdom of the ancient ones. Both the Hathors and the Mayan calendar gave the time of the 9th March as the beginning of the final wave