HIV INFECTION AND OTHER SEXUALLY TRANSMITTED INFECTIONS

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HIV INFECTION AND OTHER SEXUALLY TRANSMITTED
INFECTIONS

• HIV FACILITATE HIV TRANSMISSION BY
• 1 INCREASE INFECTIOUSNESS OF THE INDEX CASE
• 2 INCRESE THE SUSCEPTIBILITY OF THE PARTNER OR
  BOTH
• 3 ALTER THE NATURAL HISTORY OF STIs AND MGT.

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RELATIONSHIP BETWEEN STIs HIV INFECTION

• PREDOMINANT MODE OF TRANSMISSION OFBOTH HIV STIs
  SEXUAL ROUTE
• STDs STIs are biological cofactors for
  acquisition, transmission course of HIV
• CONCURRENT HIV INF. alters the natural history of
  classic STDs/STIs.
• STDs/STIs are a marker for high risk behaviour
  for HIV infection.
• TARGET interventions for both the diseases are
  same.

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HOW THE COFACTOR EFFECT MECHANISMS POSTULATED.

• Lack of mechanical skin/mucous membrane/
  endocervical epithelium makes an easy viral exit
  and entry.
• By increasing the presence and activation of HIV
  susceptible cells in the genitourinary tract
  .e.g. H.ducreyi evokes a CMI response which
  attracts HIV susceptible cells to the ulcer
  surface. A susceptible cofactor effect.
• G.Ulcers bleed profusely during a sexual act
  resulting in potential increase in HIV
  infectiousness. the infectivity cofactor effect.
• Presence of HIV in g.ulcer exudate in HIV
  infected individuals has been confirmed by
  culture PCR.

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• Increased number of HIV containing white blood
  cells in both ulcerative and inflammatory genital
  secretions
• Increased shedding of HIV virus in genital tract
  particularly in non ulcerative STDs probably by
  recruiting HIV infected inflammatory cells as
  part of the normal host response. Investigators
  have noted a significant increase in detection of
  HIV-1 DNA in cervicovaginal secretions of pts.
  With gonorrhoea, Chlamydia, TV infections.

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COFACTOR MECHANISMS contd.

• Increased HIV replication by certain ulcerative
  STD pathogens e.g. Treponema pallidum
  lipoproteins and/or increased number of receptors
  expressed per cell receptive to HIV-1 e.g.
  H.ducreyi

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CERVICITIS HIV- three mechanisms

• Increased conc. Of HIV infected CD4 lymphocytes
  infected monocytes-macrophages
• HIV replication is increased in the presence of
  an inflammatory milieu
• Cervicitis is associated with micro ulceration
  and friable mucosal tissue that can provide a
  portal of exit or entry for the virus or infected
  cells.

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BACTERIAL VAGINOSIS HIV

• When lactobacilli are deficient as is seen in BV,
  pH increases, HIV multiplies.
• A high vaginal pH in BV, make the vagina more
  conducive to HIV survival and adherence
• BV increases intravaginal levels of interleukin
  10, which increases the susceptibility of
  macrophages to HIV
• A heat stable protein elaborated by G.vaginalis
  increases the multiplication of HIV in HIV
  infected cells. M.hominis is the most potent
  inducer of HIV1 expression

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EFFECT OF STD/STI Mgt. on HIV TRANSMISSION

• In a community where STDs/ STIs are prevalent and
  when there is a strong STDs/ STIs cofactor STDs/
  STIs control can very well be achieved through
  IMPROVEMENTS in there Mgt. This is done by
  PREVENTION,EARLY DIAGNOSIS and TREATMENT of
  STDs/STIs.

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SYPHILIS IN HIV co infection

• CLINICAL
• SEROLOGICAL
• DIAGNOSIS
• TREATMENT

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CLINICAL SEROLOGICAL

• Primary-painful, multiple, Giant primary
  chancres.
• Malignant syphilis, florid secondary,
  hypertrophic verrucous lesion, rapid progression
  to secondary, persistent primary, early
  neurosyphilis, precocious tertiary.

• Limited or absent antibody response due to a
  defect in TB cell function. serodiagnosis
  unreliable .

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DIAGNOSIS TREATMENT

• Rely on DF microscopy, histology , clinical
  acumen. Both HIV syphilis produce mononuclear
  pleocytosis and elevated proteins in CSF and a
  negative CSF VDRL

• Lack of response to penicillin/relapse despite
  adequate treatment. All patients whose titres
  increase/fail to decrease four folds within 6
  months should undergo csf study or retreatment.

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CHANCRIOD HIV

• There is increased risk for HIV transmission
• Genital ulcers tend to be larger persistent
• Multilocular buboes
• Frequent occurrence of giant and phagedenic ulcer
  
• Less response to standard antibiotic.
• Higher doses and prolonged treatment

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HERPES GENITALIS HIV

• Disseminated infection
• Frequency of recurrences are more
• Bleeding ulcers
• Necrotic ulcers
• Prolonged course of acyclovir
• Parenteral dosing of the drugs
• Other antiviral agents

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DONOVANOSIS L G V

• Donovanosis
• Larger lesions
• Extensive lesions
• Ulceration of pseudo bubo

• INFLAMMATORY BUBOES
• Persistence of primary

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HPV M C

• FLORID LESIONS of HPV
• INCIDENCE OF CARCINOMA
• RECALCITRANT LESIONS
• SEEN IN CLUSTERS

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VULVOVAGINAL CANDIDIASIS

• Severe and relapsing
• Prolonged treatment is necessary
• Chronic treatment is necessary

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PROBLEMS OF STD MANAGEMENT

• 500 STD Clinics all over INDIA
• 5 REGIONAL STD REFERENCE CENTRES DELHI, CHENNAI,
  NAGPUR, HYDERABAD, and KOLKOTTA
• It is estimated that 5-10 of people with STD
  attend public STD facilities. Rest of the
  patients will go to quacks, chemists, private
  practitioners, or resort to self medication
• The mgt. of STDs become inadequate.
• These patients get complications like PID,
  INFERTILITY,ECTOPIC PREGNANCY, URETHRAL
  STRCTURES,STILL BIRTH,NEONATAL DEATH and above
  all UNCONTROLLED SPREAD OF HIV.

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Thank You