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XVIII.

HIV and Other


Sexually Transmitted
Infections
JUNELLE DUMANGON, MD, OHS
College of Medical Technology
Sexually Transmitted Infections
• Illnesses that have significant probability of transmission between
humans by means of human sexual behavior, including oral sex, vaginal
intercourse and anal sex
• Can also be transmitted via the use of IV drugs or by infected person
(childbirth and breastfeeding)
Global Impact of STIs
• A growing public health importance because of the increasing morbidity
and mortality they cause
• Facilitate the transmission of infection with the Human
Immunodeficiency Virus (HIV)
• Cause complications with sequelae such as infertility, ectopic pregnancy,
low birth weight, and prematurity
Failure to Control STIs
1. Low priority has been afforded by policy makers and planners in
allocating resources
2. Control efforts have been concentrated on symptomatic patients
(usually men) and have failed to identify asymptomatic individuals
(usually women) until complications develop
3. Service delivery has often been through specialized STD treatment
facilities which provide inadequate coverage and are stigmatizing
4. Ineffective low-cost antibiotics continue to be used for reasons of
economy
5. Little emphasis on education and other efforts to prevent infection
HIV/AIDS
History of HIV
• AIDS first described in 1981 and was called Gay Cancer
or GRID (Gay-Related Immune Disease)
– Started when cluster cases of pneumonia due to Pneumocystis
(carinii) jirovecii in previously healthy young homosexual men
in Los Angeles were found
– Further raised suspicion when large cluster cases of Kaposi’s
sarcoma were found in young homosexual men
• HIV-1 isolated in 1983 and HIV-2 in 1986
– Scientists later found evidence that the disease existed in the
world for some years prior after subsequent analysis of a
blood sample of a Bantu man, who died of an unidentified
illness in the Belgian Congo in 1959, made him the first
confirmed case of an HIV infection
History of HIV
• HIV-1 and HIV-2 originated in Africa
• As is often the case with microbes, a jump from one species to another is
probably to blame - chimpanzees (for HIV-1) and sooty mangabeys (for
HIV-2)
• How do you think did it jump to humans?
History of HIV
• AIDS awareness was soon brought to the public's
consciousness, when popular film star, Rock Hudson,
died of AIDS on October 2, 1985, shortly after making
public his AIDS on July 25, 1985, thus becoming the first
major public figure to announce that he had AIDS.
Human Immunodeficiency Virus
• Members of the Lentivirus subfamily of the Retroviridae family
• Called Retrovirus because they can insert their RNA genome to the host cell
via Reverse Transcription
• There are 2 types:
– HIV 1 – pandemic and aggressive
– HIV 2 – confined mainly to West Africa and less pathogenic
Human Immunodeficiency Virus
HIV Structure
• Enveloped RNA virus
• gp120 (glycoprotein 120)
– Outer membrane subunit
– Binds to CD4 receptor
• gp41 (glycoprotein41)
– Transmembrane protein
– Mediates virus membrane fusion
with host cell
HIV Life Cycle
1. Binding
2. Fusion
3. Reverse Transcription
4. Integration
5. Replication
6. Assembly
7. Budding
HIV Life Cycle
• 1. Binding
– Also called attachment
– HIV binds to receptors (gp120) on the surface of a
CD4 cell
• 2. Fusion
– HIV and CD4 cell membrane fuse together
– Transfer of viral RNA genome to the host cell
HIV Life Cycle
• 3. Reverse transcription
– HIV releases reverse transcriptase
– Converting HIV RNA to HIV DNA
• Reverse because usually RNA is created from
DNA but in this case, DNA is created out of
RNA
– This allows HIV to enter the CD4
cell nucleus and combine with cells’
genetic material
HIV Life Cycle
• 4. Integration
– HIV releases integrase in the nucleus of
CD4 cell
– Integration of the viral DNA to the cell’s
DNA

• 5. Replication
– HIV uses the machinery of CD4 cell to
make long chains of HIV proteins
HIV Life Cycle
• 6. Assembly
– New HIV protein and HIV RNA move to the
surface of the cell and assemble into
immature HIV
• 7. Budding
– The immature HIV pushes itself outside CD4
cells
– Protease breaks the long protein chain that
form the immature virus
– Smaller protein will combine to form mature
HIV
Importance of CD4 Lymphocytes
• Central regulatory effector cells of immune
system
• Essential for preparing foreign antigen to be
phagocytized by killer T cells
• Without CD4 cells, immune system will be
dysfunctional
– Body won’t be able to kill foreign
substances
– Opportunistic infections will ensue
– Can be fatal
Transmission
1. Sexual contact
– Contact between sexual secretion of the rectal, genital or oral mucous
membranes through unprotected sex
2. Perinatal transmission
– Mother to child in utero during the last weeks of pregnancy
– 25% transmission rate with the absence of treatment
3. Blood and Blood products
– Sharing of used needles contaminated with HIV-infection for extraction, pricking,
tattoo, piercing etc
– Transfusions with infected blood/organs
Stages of HIV Infection
1. Acute HIV infection
• Within 2 –4 weeks after infection, people may experience a flu-like illness that may
last for weeks
2. Clinical latency
• Also known as asymptomatic HIV or Chronic infection
• HIV is still active but reproduces at a very low level - UNDETECTABLE
• At the end of this stage, viral load goes up and CD4 count goes down
3. AIDS – Acute Immunodeficiency Syndrome
• Most severe stage of HIV infection because of badly damaged immune system
• INCREASING NUMBER OF OPPORTUNISTIC ILLNESSES
Stages of HIV Infection
Laboratory Diagnosis
• HIV 1/2 antigen/antibody immunoassay
• Western Blot-Protein – gold standard
• Nucleic Acid Test (NAT)
– No need to wait after WINDOW phase
Antigen/Antibody test via ELISA
Western Blot
Management
1. Anti-retroviral Agents
• -Just prolongs the latency period
• Has several types
Syphilis
Syphilis
• A sexually transmitted disease cause by a bacteria,
Treponema pallidum
• This bacteria is a Spirochete - a group of spiral,
motile bacteria
• Transmitted via:
– Direct contact with a syphilis sore during sexual
intercourse (vaginal, oral and anal)
– Mother-to-baby
Stages of Syphilis
Primary Syphilis
• Local multiplication of bacteria at the site of entry
• Can spread to lymph nodes and blood stream
• Appearance of hard chancre
– Painless, solitary lesion characterized by raised and well-
defined borders.
– Appear in 10 – 90 days after infection
– Heals spontaneously
• Duration: 1-6 weeks
Stages of Syphilis
Secondary Syphilis
• Consist of a red maculopapular rash anywhere in the body including the
hands and feet.
• Appearance of moist, pale papules in the anogenital region, axilla and
mouth
Stages of Syphilis
Secondary Syphilis
– Systemic dissemination of organism
– Occurs 1 to 2 months after the primary chancre disappears
– Symptoms include:
• Enlargement of lymph nodes
• Malaise
• Fever
• Pharyngitis
• Rash on skin and mucous membranes
• Neurological signs
• Spontaneous healing
Stages of Syphilis
Latent Syphilis
• No visible signs or symptoms
• Patient is noninfectious except for maternal transmission
• Early latent stage: less than 1 year after primary stage
• Late latent stage: more than 1 year after primary stage
Stages of Syphilis
Tertiary Syphilis
• Occurs months to years after secondary infection.
• 3 major manifestations:
1. Gummatous syphilis – bones, skins, and subcutaneous tissue
2. Cardiovascular disease – destruction of tissue in aorta
3. Neurosyphilis – meningitis, spinal cord degeneration, general
paresis
Congenital Syphilis
• Transmission of T. pallidum from mother to
fetus during early or early latent syphilis
• Most affected: 2nd and 3rd trimester
• Necrotizing funisitis – inflammation of
umbilical cord
• If born alive, can develop signs of congenital
syphilis in childhood:
– Interstitial keratitis
– Hutchinson’s teeth
– Eight nerve deafness
– Periostitis
Laboratory Diagnosis
• Specimen of choice
– Tissue fluid
– Serum
• Dark-field Microcopy
• Immunofluorescence
• Serological Testing
Laboratory Diagnosis
• Serological testing
➢ Non-Treponemal – Screening test
➢ Detects antibody named Reagin which is an Ab against Cardiolipin
➢ VDRL - Venereal Disease Research Laboratory
➢ RPR – Rapid Plasma Reagin
➢ Treponemal – Confirmatory test
➢ Detects antibody against T. pallidum
➢ TP-PA – T pallidum-particle agglutination
➢ TPHA – T pallidum hemagglutination
➢ MHA – TP – Microhemagglutination T pallidum
➢ FTA-ABS – Fluorescent treponemal antibody absorption
➢ Specimen - Blood
Management
• Control Measures will depend on…
1. Prompt and adequate treatment of all discovered cases
2. Follow-up on source of infection
3. Protected sexual intercourse
• Drug of Choice
– Penicillin
Gonorrhea
Gonorrhea
• Caused by a bacteria called Neisseria gonorrhea
– A gram-negative cocci that usually occurs in pairs
– Occur intracellularly
• Causes infection in the genitals, rectum and
throat
• Common among teens and young adults (15-24
years old
• Transmitted via:
– Direct contact with a syphilis sore during sexual
intercourse (vaginal, oral and anal)
– Mother-to-baby
Pathogenesis
• Gonococci attacks mucous membrane of the
genitourinary tract, eye, rectum and throat
– Results to acute suppuration
• For infected males:
– Urethritis, with yellow, creamy pus and painful urination
– Urethral infection can be asymptomatic
• For infected females:
– Primary infection is in the endocervix and extends to the
urethra and vagina
– May progress to the uterine tubes, causing salpingitis
Symptoms
• Sore throat
• If in the rectum:
– Itching
– Soreness
– Bleeding
– Painful bowel movements
• For Females
– Vaginal bleeding
– Pain or burning urination
– Increased vaginal Discharge
• For Males
– Swollen testicles
– Pain or burning urination
– Discharge from penis

Laboratory Diagnosis
• Specimen
– Pus and secretions from urethra, cervix, rectum,
conjunctiva, throat and synovial fluid
• Stained Smear – Gram Stain
• Blood culture
– Culture medium – Modified Thayer-Martin
• Serological Testing
• Immunoblotting
• Radioimmunoassay
• ELISA
Management
• Antibiotics:
– Penicillin
– Tetracycline
– Spectinomycin
– Quinolone
– Cephalosporine
– Ceftriaxone and Azithromycin – Last recommended DUAL treatment as of today
End

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