STD&HIV AIDS FOR KRCHN NORTH COAST MEDICAL TRAINING COLLEGE LECTURES

Sexually
TransmittedTransmitted
Infections&Infections&
MANAGEMENT4nursesMANAGEMENT4nursesMANAGEMENT4nursesMANAGEMENT4nurses
Common Diseases
WALTER WASWA,BSC.MLS
WALTER WASWA,BSC.MLS 1

STDs
• STDs are diseases and infections which
are capable of being spread from
person to person through:
– sexual intercourse
–oral-genital contact or in non-sexual ways.
–IV drug
–Congenitally transmitted

STD CLASSIFICATION
1. BACTERIAL
2. VIRAL2. VIRAL
3. PROTOZOAL
4. FUNGAL
5. ECTOPARASITES

BACTERIA
a) Neisseria gonorrhea
b) Chlamydia trachomatis
c) Treponema pallidumc) Treponema pallidum
d) Hemophilus ducreyi-chancroid
e) Calymmatobacterium granulomatis-
granuloma inguinae
f) Gardnerella vaginalis

VIRAL
a) HERPES SIMPLEX VIRUS (Genital
Herpes)
b) HPV Genital Warts
c) HBVc) HBV
d) HIV
e) CYTOMEGALOVIRUS
f) MOLLUSCUM CONTAGIOSUM VURUS
g) (HSV-2)

protozoan
a) TRICHOMONA
S VAGINALIS
b) ENTOMOEBA
HISTOLYTICAHISTOLYTICA
(HOMOsexual)
c) GIARDIA
LAMBLIA
(HOMOsexual)WALTER WASWA,BSC.MLS 6

fungal
Candida albican-
vulvovaginitis

ECTOPARASITE
a) Phthirius
pubis-pubic
lice
infestation
infestation
b) Sarcoptes
scabiei-
scabies

WHY SHOULD NURSES STUDY STDS
1. Major cause of infertility in men and women
2. Co factor in HIV and HBV
3. Common as malaria 333m cases every year

CHLAMYDIA
• Chlamydia trachomatis
• Small intracellular bacteria
• MOST COMMON STD
• FEMALES OUTNUMBER MALES 6:1
• Cervix is the site of infection• Cervix is the site of infection
• Most women are asymptomatic until the pain
and fever from PID occur
• Potential to transmit to newborn during
delivery
– Conjunctivitis, pneumonia

CHLAMYDIA
• If asymptomatic-discharge ,painful
urination ,lower abdominal pain,
bleeding, fever and nauseableeding, fever and nausea
• Complication include cervicitis,
infertility, salpinitis, ectopic
pregnancy, stillbirths, reactive
arthritis WALTER WASWA,BSC.MLS 11

Laboratory Tests for ChlamydiaLaboratory Tests for Chlamydia
• Tissue culture has been the standard
– Specificity approaching 100%
– Sensitivity ranges from 60% to 90%
• Non-amplified tests
– Enzyme Immunoassay (EIA), e.g. Chlamydiazyme
• sensitivity and specificity of 85% and 97% respectively
Drips
12
• sensitivity and specificity of 85% and 97% respectively
• useful for high volume screening
• false positives
– Nucleic Acid Hybridization (NA Probe), e.g. Gen-Probe Pace-
2
• sensitivities ranging from 75% to 100%; specificities greater than
95%
• detects chlamydial ribosomal RNA
• able to detect gonorrhea and chlamydia from one swab
• need for large amounts of sample DNA

Laboratory Tests for Chlamydia
(continued)
• DNA amplification assays
–polymerase chain reaction (PCR)
–ligase chain reaction (LCR)
13
• Sensitivities with PCR and LCR 95% and
85-98% respectively; specificity
approaches 100%
• LCR ability to detect chlamydia in first
void urine

Chlamydia Direct Fluorescent
Antibody (DFA)
14
Source: Centers for Disease Control and Prevention

Healthy/unhealthy cervix

Mucopurulent Cervicitis
16Source: Seattle STD/HIV Prevention Training CenterWALTER WASWA,BSC.MLS

CHLAMYDIA/COMPLICATION
• Urethratis
• Epididymitis
• Proctitis
• Cervicitis
• Endometritis
• Salpingitis
• Perihepatitis
• Otitis media in infants • Cervicitis
• Otitis media in infants
• Inclusion conjuctivitis
• sterility

LAB DIAGNOSTICS
• Direct fluorescent antibody
• Enzyme immunoassay
• DNA PROBE• DNA PROBE
• Cell culture
• DNA amplication

CHLAMYDIA/treatment
• Doxycycline
100m orally 2
times day fortimes day for
seven days
• Azithromycin 1g
orally

GONORRHEA
-females
• Gonococcal cervicitis-slightl yellow-green discharge or
vulvar irritation
-Males-Males
• Gonococcal urethritis,odorous cloudy
discharge,urianary burning ,swollen ,tender lymph
glands in groins

GONORHOEA
• Gram negative

GONORRHEA
• Mucus membranes affected
include cervix,anus,throata nd
the eyesthe eyes
• The bacteria attacks the cervix
as first site of infection

GONORRHEA
• Symptoms are thick discharge,
burning urination and severe
menstrual or abdominal crampsmenstrual or abdominal cramps
• 10-40% of women develop PID
• Untreated gonorrhea can result in
arthritis, dermatitis and tenosynivitis

GONORRHEA
COMPLICATIONS
1. Urethritis
2. Epididymitis
3. Proctitis
4. Endometritis4. Endometritis
5. Cervicitis
6. Salpingitis
7. Pharyngitis
8. Conjuctivitis
9. Amniotic infection syndrome
10. Disseminated gonococcal

GONORRHEA
Consequences
• Female:PID with sterility,ectopic
pregnancy,severe pelvic pain,infantpregnancy,severe pelvic pain,infant
conjuctivitis
• Male:
• Prostate absesses with fever,difficult
urination,epididymitis with sterility

GONORRHEA
• Transmitted to eyes,anus,throat
may enter the blood stream and
invade joints,heart,liver and CNSinvade joints,heart,liver and CNS
• Treatment:special treatment
resistant bacteria may require
special treatment

GONORRHEA/drugs
• Azithromycin igm daily/
doxycycline 100mg
twice daily
• Ceftriaxone 125mgCeftriaxone 125mg
IM/4OOmg orally
• is the best
treatment99.1%

Diagnosis not Easy
• Three levels of diagnosis are
defined on the basis of clinical
findings or the results of
laboratory diagnostic tests. A
findings or the results of
laboratory diagnostic tests. A
definitive diagnosis of
gonorrhoea must be obtained for
medico legal purposes.

Diagnosis of GonorrhoeaDiagnosis of Gonorrhoea
• Suggestive diagnosis is defined by
the presence of:
1. A mucopurulent endocervical or1. A mucopurulent endocervical or
urethral exudate on physical
examination and sexual exposure to
a person infected with N.
gonorrhoea.

2.Presumptive diagnosis of gonorrhoea is made
on the basis of one of the following three
criteria:
• Typical gram-negative intracellular diplococci on
microscopic examination of a smear of urethral
exudate from men or endocervical secretions
from women*;
• Growth of a gram-negative, oxidase-positive• Growth of a gram-negative, oxidase-positive
diplococcus, from the urethra (men) or
endocervix (women), on a selective culture
medium, and demonstration of typical colonial
morphology, positive oxidase reaction, and
typical gram- negative morphology;

3. Definitive diagnosis of gonorrhoea
requires:
• Confirmation of isolates by biochemical,
enzymatic, serologic, or nucleic acid testing
e.g., carbohydrate utilization, rapid enzyme
substrate tests, serologic methods such as cosubstrate tests, serologic methods such as co
agglutination or fluorescent antibody tests
supplemented with additional tests that will
ensure accurate identification of isolates, or a
DNA probe culture confirmation technique.

Newer Methods in Diagnosis of
Gonorrhoea
• Detection of N. gonorrhoea by a
nonculture laboratory test (Antigen
detection test (e.g., Gonozymedetection test (e.g., Gonozyme
[Abbott]), direct specimen nucleic
acid probe test (e.g., Pace II
[GenProbe]), nucleic acid
amplification test (e.g., LCR
[Abbott]). WALTER WASWA,BSC.MLS 32

NONGONOCOCAL URETHRITIS
• Female-few or no
symptoms,may itch,urinary
burning,mild vaginal
discharge of pus
• Male-penile discharge,urinary
burning
• Etiology:
– 20-40% C. trachomatis
– 20-30% genital mycoplasmas
(Ureaplasma urealyticum,
Mycoplasma genitalium)
– Occasional Trichomonas
vaginalis, HSV
– Unknown in ~50% cases
burning
– Unknown in ~50% cases
• Sx: Mild dysuria, mucoid
discharge
• Dx: Urethral smear ≥ 5
PMNs (usually ≥15)/OI field
Urine microscopic ≥ 10
PMNs/HPF
Leukocyte esterase (+)

SYPHILISSYPHILIS –– THETHE ““““““““GREAT IMITATORGREAT IMITATOR””””””””
• Infectious Dose: ~57 organisms1
• Incubation Period – 21 days (median)
• 3 clinical stages of syphilis
– Primary:
• Painless sore (chancre) at inoculation
sitesite
– Secondary:
• Rash, Fever, Lymphadenopathy, Malaise
– Tertiary/Latent:
• CNS invasion, organ damage
• “The physician that knows syphilis knows
medicine.”
– Sir William Osler
6

Primary SyphilisPrimary Syphilis

Primary Syphilis - Chancre

Primary Syphilis Chancre
38
Source: Florida STD/HIV Prevention Training Center

Secondary Syphilis Rash
Sores
39

40

41
Source: Cincinnati STD/HIV Prevention Training Center

Secondary Syphilis
42
Source: Diepgen TL, Yihune G et al. Dermatology Online Atlas

Congenital Syphilis
• Congenital syphilis
usually occurs following
vertical transmission of
T. pallidum from the
infected mother to theinfected mother to the
fetus in utero, but
neonates may also be
infected during passage
through the infected
birth canal at delivery.

First /(primary)Stage Syphilis
Chancres (shangker) (painless open
sore) appear on the body.
They disappear in about 14They disappear in about 14
days.
Signs
Appearance of red painless sore on
mouth,fingers,reproductive organs in priamry syphilis-
chancers

If gone untreated…
Third/tertiary Stage Syphilis
• Transmission to sex
partners and newborns
• Nerve and brain damage
• Blindness
• Physical damage• Physical damage
• Death
• Tertiary syphilis linked to HIV
• Destructive lesion,organ
destruction,meningitis
Degenerative lesions called
gummas appear as a result of
hypersensitivity

SYPHILIS
Symptoms
• Inflamed
cervix/PID;spread to
prostate/epididymis,rar
CondylomataCondylomata
LataLata
prostate/epididymis,rar
e cases of arthritis
Treatment
• Doxycline or
erthromycin

Diagnosis of Syphilis
• History and clinical examination.
• Evaluation based on three factors:
–Clinical findings.
– Demonstration of spirochetes in clinical specimen.
– Present of antibodies in blood or cerebrospinal
fluid.
• More than one test should be performed.
• No serological test can distinguish between
other Treponemal infections.

Laboratory Diagnosis of Syphilis
The Uncommon Methods
1.Rabbit Infectivity Test (RIT)
– High Sensitivity and Specificity
– Long turn-around-time
– Limited to research settings
2.Dark Field Microscopy
http://www.els.net
– Useful only during primary infection
– Technician expertise required
3.Immunostaining
– Direct fluorescent antibody or silver stain
4.Polymerase Chain Reaction (PCR)
– Not commercial available
textbookofbacteriology.net
7WALTER WASWA,BSC.MLS 48

• RPR and VDRL are agglutination assays
Reagin
Serologic Tests for Syphilis:
Non-Treponemal Assays
Cardiolipin
Charcoal
Serum
or
CSF

6.VDRL
• VDRL (venereal disease research laboratories)
- It is useful for the screening, diagnosis and follow up.
- The results can be qualitative or qualitative
• Each preparation of antigen suspension should first be examined by testing with known
positive or negative serum controls.
• The antigen particles appear as short rod forms at magnification of about 100x. Aggregation
of these particles into large or small clumps is interpreted as degrees of positivity
• Reactive on left, non-reactive on right

7.RPR
• Test Procedure:
– Serum or plasma added to circle on card and spread.
– One drop of antigen from a needle capable of delivering 60 drops/mL
is added.
– Rotate at 100 rpms/minute for 8 minutes.
– Results are read macroscopically.– Results are read macroscopically.
• Daily quality control:
– 20 gauge needle checked for delivery of 60 drops/mL
– Rotator checked for 100 rpms/minute
– Room temperature must be 23-29 C.
– Three levels of control must be run and give appropriate results.
• RPR appears to be more sensitive than the VDRL.

Every Pregnant women Needs
Screening

VIRAL STDS
1.HSV
2.HPV2.HPV
3.HBV
4.HIV

HPV
• Recurrent,incurable
viral disease
• HSV-2=genital herpes
• 80%asymptomatic• 80%asymptomatic

HSV
• HSV-1 cold sores,blisters,primarily
around the mouth and affects 80%
of all adults
• HSV-2 genital herpes infects 1:6• HSV-2 genital herpes infects 1:6
adult
• Contagious through direct skin
contact particularly oral and genital
areas

HSV 2
• Active phase may include itching ,burning , swelling
and flu like symptoms
• Appearance of small painful blisters of genitals
rupture, crust over and healrupture, crust over and heal
• The virus travels down nerve to ganglia near spine
and reamins dormant until another outbreak and
virus travels up nerve to skin
• Control difficult because 75% are unaware they are
infected

HSV 2
• No cure
• Acyclovir is prescribed form minimizing the
discomfort
• Sexual activity should be avoided when sores are
activeactive
• Antiviral drugs neither eradicate latent virus nor
affect the risk, frequency or severity of recurrences
• Treatment
• On first clinical episode
• Acyclovir 400mg orally 5 times a day for 7-10 days

HPV
• Ref to 70 different viruses a third of which causes
genital problems
• Common in 40% of sexually active women in their
20’s
• A small percentage develop genital warts which can• A small percentage develop genital warts which can
lead to a precancerous condition
• Spread through direct contact on vaginal/and are
anal area
• Warts remain undetected when located inside the
vagina/cervix/anus

HPV
• HPV
16,18,31,45=CERVICAL
CANCER
• Genital warts affect 1 %Genital warts affect 1 %
of sexually active adult
• 75% of adult have been
infected with greater
than one type 0f HPV

HPV
• No cure for HPV although lessions can be removed
• Methods include cyrotherapy, chemicals and laser
therapy
• HPV is associated with cervical cancer or cervical• HPV is associated with cervical cancer or cervical
dysplasia
• Early detection reduces mortality
• Also linked to cancers of the cavity

HPV
• TREATMENT
• Patient apply podofilox 0.5% solution or gel
• Cryotherapy
• Podophyllin resin 10-25%• Podophyllin resin 10-25%
• Sugery, intralesional interferon, laser

HBV
• Transmission as HIV
• Bloodborne, sex, tattoo, eearpiercings, injection and ocupuncture
• Easily transmitted than HIV
• Almost 95% of person with HBV recover
• Vaccination of health personnels
• RISK GRP• RISK GRP
• Hemodialysis pts
• Injectable drug users
• Health workers
• Infants born of mothers infected
• Gay men
• Sexually active heterosexuals

HBV
• Present in body fluids
• Severe HBV include jaundice and may result in
prolonged illness or death

HIV
• Retrovirus that targets and destroys helper T-4
cells that assist the immune response to disease

Beginning of HIV/AIDS
• The first published article related to AIDS
was in 1981. The principal author’s name
was Michael Gottlieb and it appeared in
the Morbidity and Mortality Weeklythe Morbidity and Mortality Weekly
Report for June 5th. This article reported
that there was a random increase in
pneumocystis carinii pneumonia (PCP), a
rare lung infection.

Discovery of HIV infection.
• In 1982, the term Acquired Immune Deficiency
Syndrome is used for the first time. The name was
designated by the CDC.
• In 1983, French scientists at the Institute Pasteur
found a new virus that they called lymphadenopathy-found a new virus that they called lymphadenopathy-
associated virus or LAV. About a year later, Dr. Robert
Gallo, of the National Cancer institute discovered
HLTV-III. The first discovery was made in France at
the Institute Pasteur, but shared credit is given to Dr.
Robert Gallo, the discoverer of AIDS and his French
counterparts for discovering HIV on April 23, 1984.

History of HIV
•• The HIV virus first came to light during theThe HIV virus first came to light during the
early 1980’s.early 1980’s.
•• A number of healthy gay men in New YorkA number of healthy gay men in New York
began to develop rare opportunistic infectionsbegan to develop rare opportunistic infectionsbegan to develop rare opportunistic infectionsbegan to develop rare opportunistic infections
& cancers, that were resistant to treatment.& cancers, that were resistant to treatment.
•• One such viral opportunistic infection isOne such viral opportunistic infection is
cytomegalovirus that causes blindness &cytomegalovirus that causes blindness &
inflammation of the coloninflammation of the colon

What is Human Immune DeficiencyWhat is Human Immune Deficiency
VirusVirus
•• Genus RetroviridaeGenus Retroviridae
•• Lentivirus, which literally means slow virusLentivirus, which literally means slow virus -- it takesit takes
such a long time to develop adverse effects in thesuch a long time to develop adverse effects in the
body.body.body.body.
•• This virus attacks the immune systemThis virus attacks the immune system
•• There are two strainsThere are two strains –– HIV 1 & HIV 2HIV 1 & HIV 2

What is Human ImmuneWhat is Human Immune
Deficiency VirusDeficiency Virus
•• These contain RNA, the genetic material ofThese contain RNA, the genetic material of
HIVHIV
•• The outer layer of the HIV virus cell is coveredThe outer layer of the HIV virus cell is covered
in coat proteins, which can bind to certainin coat proteins, which can bind to certainin coat proteins, which can bind to certainin coat proteins, which can bind to certain
WBCs. This allows the virus to enter the cell,WBCs. This allows the virus to enter the cell,
where it alters the DNA.where it alters the DNA.
•• The virus infects and destroys the CD4 lymphocytesThe virus infects and destroys the CD4 lymphocytes
which are critical to the body’s immune response.which are critical to the body’s immune response.

Origin of AIDS; controversial, similar
to SIV
71WALTER WASWA,BSC.MLS

Family : Retroviridae
Subfamily : Lentivirus
• RNA virus, 120nm in
diameter
• Envelope gp160; gp120 &
gp41
• Icosahedral symmetryIcosahedral symmetry
• Nucelocapsid
– Outer matrix protein (p17)
– Major capsid protein (p24)
– Nuclear protein (p7)
• Diploid RNA with several
copies of reverse
transcriptase

Types of HIVTypes of HIV

Subtype C is Major type in India
• Subtype C is
predominant in
Southern and East
Africa, India and Nepal.
It has caused theIt has caused the
world's worst HIV
epidemics and is
responsible for around
half of all infections.

Resistance
• The virus are inactivated in 10 minutes at 600c and in seconds
at 1000c
• At room temperature survive for seven days
• HIV are inactivated in 10 minutes by treatment with 50%
ethanolethanol
• 35% Isopropanol.
• 0.5% Lysol and paraformaldehyde
• 0.3% hydrogen
• 10% house hold bleach
• Hypochlorite solution at 0.5%
• 2% Glutaraldehyde

HIV Replication
– Attachment
– Penetration
– Uncoating
– Reverse Transcription– Reverse Transcription
– Integration
– Replication
– Assembly
– Release

Life Cycle of HIV
1. Attachment: Virus binds to surface molecule
(CD4) of T helper cells and macrophages.
• Coreceptors: Required for HIV infection.
• CXCR4 and CCR5 mutants are resistant to infection.
2. Fusion: Viral envelope fuses with cell2. Fusion: Viral envelope fuses with cell
membrane, releasing contents into the cell.

HIV Life Cycle: Attachment Requires CD4 ReceptorHIV Life Cycle: Attachment Requires CD4 Receptor
plus a Coreceptorplus a Coreceptor

• The HIV receptor
•• Gp160Gp160 is composed ofis composed of gp41gp41 andand gp120gp120 and forms theand forms the
receptor for binding to the host cell (CD4 positive cells).receptor for binding to the host cell (CD4 positive cells).
•• The gp41 portion is half embedded in the membraneThe gp41 portion is half embedded in the membrane
envelope and interacts with gp120 portion on theenvelope and interacts with gp120 portion on the
The gp41 portion is half embedded in the membraneThe gp41 portion is half embedded in the membrane
envelope and interacts with gp120 portion on theenvelope and interacts with gp120 portion on the
exterior side of the membrane.exterior side of the membrane.
•• Each receptor is composed of 3 subunits of gp41 and 3Each receptor is composed of 3 subunits of gp41 and 3
subunits of gp120.subunits of gp120.

The HIV ReceptorThe HIV Receptor

Lifecycle of HIV
HIV particles enter the body in a fluid as it can notHIV particles enter the body in a fluid as it can not
survive without a support medium.survive without a support medium.
The virus targets any cell expressing CD4, including TThe virus targets any cell expressing CD4, including T
helper cells, macrophages, dendritic cells andhelper cells, macrophages, dendritic cells and
monocytes.monocytes. WALTER WASWA,BSC.MLS 83

Life Cycle of HIV
3. Reverse Transcription: Viral RNA is
converted into DNA by unique enzyme
reverse transcriptase.
Reverse transcriptase
RNA ---------------------> DNARNA ---------------------> DNA
Reverse transcriptase is the target of
several HIV drugs: AZT, ddI, and ddC.

Infection spread throughout the BodyInfection spread throughout the Body
• Within the inflammatory cells of the infection (T
cells)
• Site of replication shifts to lymphoid tissues:
• Lymph nodes
• Spleen• Spleen
• Liver
• Bone marrow
• Macrophages and Langerhans cells become
reservoirs and sites of
• replication but do not die themselves.

Effects of HIV on the immune systemEffects of HIV on the immune system
3 areas:3 areas:
1. Destruction of CD4+ T cells population1. Destruction of CD4+ T cells population
2. Immune effects due to HIV infection2. Immune effects due to HIV infection
3. Progression of HIV infection to AIDS3. Progression of HIV infection to AIDS

2.Host’s immune responses2.Host’s immune responses
•• Both humoral and cellBoth humoral and cell--mediated immune responsesmediated immune responses
partially control the viral production but in thispartially control the viral production but in this
process they destroy the infected CD4+T cells,process they destroy the infected CD4+T cells,
leading to a gradual decline of CD4+ T cellsleading to a gradual decline of CD4+ T cells
HIVHIV--specific CTLs kill infected CD4+ T cellsspecific CTLs kill infected CD4+ T cells•• HIVHIV--specific CTLs kill infected CD4+ T cellsspecific CTLs kill infected CD4+ T cells
•• Antibodies that recognize a variety of HIV antigensAntibodies that recognize a variety of HIV antigens
are producedare produced -- Antibody dependent cellAntibody dependent cell--mediatedmediated
cytotoxicitycytotoxicity
•• Apoptosis of infected cellsApoptosis of infected cells

Blood and Body fluids contain HighBlood and Body fluids contain High
concentration of Viral particlesconcentration of Viral particles
• Blood
• Semen/Vaginal
fluids (as high asfluids (as high as
blood)
• Breast milk
• Pus from sores

Low concentrations of HIVLow concentrations of HIV
It is highly unlikely you will be infected
if you come into contact with:
• Sweat
• Tears• Tears
• Urine
• Saliva (-highly possible if blood from
mouth sores is present)

High Risk Populations:
1. Males, homosexuals & bisexuals
2. IV drug users
3. Improperly screened transfusion recipients
4. Sexual partners of persons infected with HIV
5. Infants of HIV –infected mothers

How is HIV Spread?
• ANY type of sexual activity (highest risk)
• Sharing used drug needles
• Pregnancy-from mother to child
• Sharing razors- if blood is present• Sharing razors- if blood is present
• Kissing- if even the smallest amount of blood
is present. (-membranes of mouth are thin
enough for HIV to enter straight into the
body.)
• Tattoos/body piercing if equipment is not
clean.

HIV in Body FluidsHIV in Body Fluids
Semen
11,000 Vaginal
Fluid
7,000
Blood
18,000
Amniotic
Fluid
4,000 Saliva
1
Average number of HIV particles in 1 ml of these body fluidsWALTER WASWA,BSC.MLS 93

Transmission
• Vaginal Intercourse
• Anal Intercourse (10x higher infection rate than
vaginal intercourse because of tissue tear is higher
• Oral Intercourse
• Blood Transfusion (risk greater than 90% if sample is• Blood Transfusion (risk greater than 90% if sample is
already infected)
• Needles (tattoos, injections)
• Infected mother to the infant through:
• Pregnancy (placenta), Birth, and breastfeeding

Window Period
• This is the period of time after becoming
infected when an HIV test is negative
• 90 percent of cases test positive within three• 90 percent of cases test positive within three
months of exposure
• 10 percent of cases test positive within three
to six months of exposure

Pathogenesis of HIV / AIDSPathogenesis of HIV / AIDS
Infected TInfected T--CellCell
HIV
Virus
T-Cell
HIV Infected
T-Cell
New HIV
Virus

• Immune responses fail to eradicate all viruses.
• Viral load is maintained at low level
• Continuous decline of CD4+ T cells

Immune defects due to HIV infectionImmune defects due to HIV infection
B cellsB cells –– impaired humoral responseimpaired humoral response
•• BB--cell hyper reactivitycell hyper reactivity
•• Polyclonal hypergammaglobulinemia due to enhanced nonspecificPolyclonal hypergammaglobulinemia due to enhanced nonspecific
IgG and IgA production.IgG and IgA production.
•• Impaired AbImpaired Ab--isotype switching and inability to respond toisotype switching and inability to respond to
specific antigen.specific antigen.
•• High incidence of BHigh incidence of B--cell lymphomascell lymphomas•• High incidence of BHigh incidence of B--cell lymphomascell lymphomas
Lymph nodesLymph nodes
•• HIV kills cells in the lymph nodesHIV kills cells in the lymph nodes
•• Early HIV infection: destruction of dendritic cellsEarly HIV infection: destruction of dendritic cells
•• Late stage: extensive damage, tissue necrosis, a loss of follicularLate stage: extensive damage, tissue necrosis, a loss of follicular
dendritic cells and germinal centres.dendritic cells and germinal centres.
•• An inability to trap Ag or support activation of T+B cellsAn inability to trap Ag or support activation of T+B cells

CDC Classification of HIV
• Category 1: > 500 cells/mm3 (or CD4% > 28%)
• Category 2: 200-499 cells/mm3 (or CD4% 14% -
• 28%)• 28%)
• Category 3: < 200 cells/mm3 (or CD4% <
14%)(CD4+ T-lymphocyte counts per
microliter of blood)

normal
Slightly
Acute HIV disease
Exposure to
HIV
Clinical latency period
competence
Progression of HIV infection
Progression of HIV infection
•• After initial infection withAfter initial infection with
HIV, there is usually anHIV, there is usually an
acute fluacute flu--like illness.like illness.
•• This illness may includeThis illness may include
•• FeverFever
•• HeadacheHeadache
•• TirednessTiredness
Severely
impaired
Abnormal
Slightly
reduced
Time
Clinical latency period
-declining CD4+ T cell amount
AIDS
Immunecompetence
Opportunistic
infections
•• TirednessTiredness
•• Enlarged lymph nodesEnlarged lymph nodes
•• But after this mostBut after this most
individuals are clinicallyindividuals are clinically
asymptomatic for years.asymptomatic for years.
This is called the clinicalThis is called the clinical
latency period.latency period.

WHO clinical case definition for AIDS in
South-East Asia
• WHO clinical case definition for AIDS in South-East Asia
Clinical AIDS in an adult is defined as an individual who has
been identified as meeting the two criteria A and B below:
A. Positive test for HIV infection by two tests based on
preferably two different antigens.
B. Any one of the following criteria:
• - Weight loss of 10% body weight or cachexia, not known to
be due to a condition unrelated to HIV infection
- Chronic diarrhoea of one month's duration, intermittent or
constant

WHO clinical case definition for AIDS in SouthWHO clinical case definition for AIDS in South--
East AsiaEast Asia
• Disseminated, miliary or extra pulmonary
tuberculosis
• Candidiasis of the oesophagus; diagnosable as
dysphasia, odynophagia and oral Candidiasisdysphasia, odynophagia and oral Candidiasis
• Neurological impairment restricting daily
activities, not known to be due to a condition
unrelated to HIV (e.g. trauma)
• Kaposi's sarcoma.

Stage 1Stage 1 -- PrimaryPrimary
• Short, flu-like illness - occurs one to six weeks
after infection
• no symptoms at all
• Infected person can infect other people• Infected person can infect other people

Stage 2Stage 2Stage 2 ---- AsymptomaticAsymptomaticAsymptomaticAsymptomatic
• Lasts for an average of ten years
• This stage is free from symptoms
• There may be swollen glands• There may be swollen glands
• The level of HIV in the blood drops to very low
levels
• HIV antibodies are detectable in the blood

- Symptomatic
• The symptoms are mild
• The immune system deteriorates• The immune system deteriorates
• Emergence of opportunistic infections and
cancers

- HIV AIDS
• The immune
system weakens
• The illnesses• The illnesses
become more
severe leading to
an AIDS diagnosis

Progression to AIDSProgression to AIDS
•• During the latency period, lymph nodes and the spleen areDuring the latency period, lymph nodes and the spleen are
sites of continuous HIV replication and cell destruction.sites of continuous HIV replication and cell destruction.
•• The immune system remains competent at handling mostThe immune system remains competent at handling most
infections with opportunistic microbes but the number ofinfections with opportunistic microbes but the number of
CD4+ T cells steadily declines.CD4+ T cells steadily declines.
Symptoms often experienced months to years before the onsetSymptoms often experienced months to years before the onset
of AIDS.of AIDS.
•• Lack of energyLack of energy
•• Weight lossWeight loss
•• Frequent fevers and sweatsFrequent fevers and sweats
•• Persistent or frequent yeast infectionsPersistent or frequent yeast infections
•• Persistent skin rashesPersistent skin rashes
•• Dysfunction of CNSDysfunction of CNS

•• FinalFinal stage of HIV infectionstage of HIV infection -- AIDSAIDS
•• Occurs when the destruction of peripheral lymphoid tissue isOccurs when the destruction of peripheral lymphoid tissue is
complete and the blood CD4+ T cell count drops belowcomplete and the blood CD4+ T cell count drops below 200200
cells/mmcells/mm33. (Healthy adults usually have CD4+ T. (Healthy adults usually have CD4+ T--cell counts ofcell counts of
1,000 or more).1,000 or more).
•• AIDSAIDS –– acquired immunodeficiency syndromeacquired immunodeficiency syndrome –– is marked byis marked by
Progression to AIDSProgression to AIDS
•• AIDSAIDS –– acquired immunodeficiency syndromeacquired immunodeficiency syndrome –– is marked byis marked by
development of various opportunistic infections and malignancies.development of various opportunistic infections and malignancies.
•• The level of virus in the blood and CD4+ T cell count can predictThe level of virus in the blood and CD4+ T cell count can predict
the risk of developing AIDS. Vthe risk of developing AIDS. Voral titers often accelerate asoral titers often accelerate as
the patient progresses towards AIDS.the patient progresses towards AIDS.
•• Without treatment, at least 50% of people infected with HIVWithout treatment, at least 50% of people infected with HIV
will develop AIDS within ten years.will develop AIDS within ten years.

Opportunistic Infections
109WALTER WASWA,BSC.MLS

-to-Baby
• Before Birth
• During Birth• During Birth
• Postpartum
–After the birth

How is HIV not spread?How is HIV not spread?
• Shaking hands
• Hugging
• Swimming pools• Swimming pools
• Toilet seats
• Insect bites
• Donating blood

THE NATIONAL HIV TESTING POLICYTHE NATIONAL HIV TESTING POLICY
• No individual should be made to undergo a
mandatory testing for HIV
• No mandatory HIV testing should be imposed as
a precondition for
- Employment
- Providing health care services and facilities- Providing health care services and facilities
• Any HIV testing must be accompanied by a
pretest and posttest counseling services
(through VCTC)
• Testing without consent – hindrance to the
control of the epidemic

Pre--test Counseling explain to individualstest Counseling explain to individuals
• Transmission
• Prevention
• Risk Factors
• Voluntary &• Voluntary &
Confidential
• Report ability of
Positive Test
Results

Post--test Counselingtest Counseling
• Clarifies test
results
• Need for
additional testingadditional testing
• Promotion of safe
behavior
• Release of results

Three types of tests
(i) Screening tests - ELISA and simple/rapid
tests.
(ii) Confirmatory or supplemental tests-
Western Blot assay.Western Blot assay.
(iii) Nucleic acid and antigen screening tests.
Polymerase chain reaction (PCR), Ligase chain
reaction (LCR), Nucleic acid based Sequence
assays (NASBA) and some ELISA tests.

Diagnosis of HIV
•• Initial test for HIV is an indirect ELISA testInitial test for HIV is an indirect ELISA test
•• Economic, rapid, performed easily, high sensitivityEconomic, rapid, performed easily, high sensitivity
and specificityand specificity
•• Detects antiDetects anti--HIV antibodies in patient serumHIV antibodies in patient serum•• Detects antiDetects anti--HIV antibodies in patient serumHIV antibodies in patient serum
•• Antibodies are generally detectable within 3Antibodies are generally detectable within 3
months of infectionmonths of infection
•• Antibodies are typically directed at the envelopeAntibodies are typically directed at the envelope
glycoproteins (gp120 and gp41)glycoproteins (gp120 and gp41)

Absence of Antibodies to do not confirm
absence of HIV infection
•• Absence of antibody, as in ‘window period’ does notAbsence of antibody, as in ‘window period’ does not
exclude the presence of the virus which can beexclude the presence of the virus which can be
detected by PCR amplification approx. ten days afterdetected by PCR amplification approx. ten days after
infectioninfection
•• ‘Window period’‘Window period’ –– time between infection andtime between infection and
detection of serological viral markerdetection of serological viral marker
•• Direct ELISA for p24 antigen canDirect ELISA for p24 antigen can also be usedalso be used
although the false negative rate is higheralthough the false negative rate is higher

EIA/ELISA
Test
PositiveNegative
Repeat
Positive
HIV Testing
No HIV Exposure
Low Risk
HIV Exposure
High Risk
Run IFA
Confirmation
Positive
Positive
End Testing
Repeat ELISA
Every 3 months
for 1 year
Negative
PositiveNegativeIndeterminate
Repeat at
2-4 months
Repeat at
3 weeks
Low Risk High Risk
Negative
HIV
+
Repeat every
6 months for continued
High risk behavior

Diagnosis of HIV
•• Positive or indeterminate ELISA tests for antiPositive or indeterminate ELISA tests for anti--HIV antibodiesHIV antibodies
are confirmed by immunoblotting (Western Blotting) whichare confirmed by immunoblotting (Western Blotting) which
identifies specific HIV virus proteinsidentifies specific HIV virus proteins
•• PCR can also be usedPCR can also be used•• PCR can also be usedPCR can also be used
•• Detects proDetects pro--viral DNA or viral RNAviral DNA or viral RNA
•• It is highly sensitive and specific but is more costly thanIt is highly sensitive and specific but is more costly than
ELISAELISA
•• Can be used to test infants born to HIVCan be used to test infants born to HIV--infected mothersinfected mothers

Indirect ELISA test

Western blot Test
•• Confirms HIV infectionConfirms HIV infection
•• Proteins are separated by electrophoresisProteins are separated by electrophoresis
and transferred to a nitrocelluloseand transferred to a nitrocellulose
membrane by the passage of an electricmembrane by the passage of an electric
currentcurrentcurrentcurrent
•• The proteins are treated with antibodiesThe proteins are treated with antibodies
•• Similar to ELISA technique, addition ofSimilar to ELISA technique, addition of
secondary antibodies with an enzymesecondary antibodies with an enzyme
attached allows the use of colour to detectattached allows the use of colour to detect
a particular proteina particular protein

Western BlottingWestern Blotting
•• A discrete protein band represents theA discrete protein band represents the
specific antigen that the antibody recognizesspecific antigen that the antibody recognizes
•• The bands from a positive Western blot areThe bands from a positive Western blot are
from antibodies binding to specific proteinsfrom antibodies binding to specific proteins
and glycoprotein's from the HIV virusand glycoprotein's from the HIV virus
from antibodies binding to specific proteinsfrom antibodies binding to specific proteins
and glycoprotein's from the HIV virusand glycoprotein's from the HIV virus
•• The CDC recommends that the blot should beThe CDC recommends that the blot should be
positive for two of the p24, gp41 andpositive for two of the p24, gp41 and
gp120/160 markers (gp160 is the precursorgp120/160 markers (gp160 is the precursor
form of gp41 and gp120, the envelope protein)form of gp41 and gp120, the envelope protein)

HIV Western blot

Rapid Tests
•• ADVANTAGESADVANTAGES::
• quicker to perform
– do not require batching
– do not require specialised equipment or– do not require specialised equipment or
trained personnel
– results delivered on the same day
• Only ‘WHO recommended’ Rapid HIV antibody tests
should be used to ensure quality.

The ‘Window period’ Aware of
it
Follows acute infection with HIV, before HIV
antibodies can be detected in the patient’s
blood stream.
• Patient is highly infectious, despite testing HIVPatient is highly infectious, despite testing HIV
antibody negative, HIV is replicating rapidly in
all body compartments.
• Typically up to 12 weeks duration but may be
shorter in more sensitive HIV antibody assays.

Paediatric HIV Testing
Infants born to HIV infected mothers will have
antibodies to HIV in their serum as a result of:
– maternal-fetal transfer during pregnancy
– delivery– delivery
– breast-feeding
they may not necessarily be infected !

Treatment of HIVTreatment of HIV
•• Eradication of HIV infection not possible with currently availableEradication of HIV infection not possible with currently available
drugsdrugs
•• Viral replication can not be completely suppressedViral replication can not be completely suppressed
•• Latently infected CD4+ T cells established at early stageLatently infected CD4+ T cells established at early stage
•• Goals of antiretroviral therapy are to:Goals of antiretroviral therapy are to:
-- Suppress viral replicationSuppress viral replication-- Suppress viral replicationSuppress viral replication
-- Restore and/or preserve immune functionRestore and/or preserve immune function
-- Improve quality of lifeImprove quality of life
-- Reduce HIVReduce HIV--associated morbidity and mortalityassociated morbidity and mortality
•• Combinations of antiretroviral drugs are usedCombinations of antiretroviral drugs are used
•• Referred to as HAART (highly active antiretroviral therapy)Referred to as HAART (highly active antiretroviral therapy)
•• Suppress levels of plasma viraemia for long periodsSuppress levels of plasma viraemia for long periods
•• Plasma viraemia is a strong prognostic factor in HIV infectionPlasma viraemia is a strong prognostic factor in HIV infection

Antiretroviral DrugsAntiretroviral Drugs
•• Significant declines in AIDS related morbidity and mortality are seenSignificant declines in AIDS related morbidity and mortality are seen
as a result of HAARTas a result of HAART
•• Several strategies for development of effective antiviral drugsSeveral strategies for development of effective antiviral drugs
•• Potential therapies based on knowledge of the way in which HIVPotential therapies based on knowledge of the way in which HIV
gains access into the cells and its method of replicationgains access into the cells and its method of replicationgains access into the cells and its method of replicationgains access into the cells and its method of replication
•• Targets for therapeutic antiTargets for therapeutic anti--retroviral drugs:retroviral drugs:
-- Inhibiting reverse transcriptionInhibiting reverse transcription
-- Inhibiting proteasesInhibiting proteases
-- Inhibiting integrateInhibiting integrate –– interferes with integration of viralinterferes with integration of viral
DNA into host genomeDNA into host genome
-- Inhibiting fusionInhibiting fusion –– prevents virus from fusing with host cellprevents virus from fusing with host cell

Therapeutic OptionsTherapeutic Options
•• Combination of RT inhibitors protease inhibitorsCombination of RT inhibitors protease inhibitors
results in potent antiresults in potent anti--viral activityviral activity
•• In most cases, two nucleoside analogues and oneIn most cases, two nucleoside analogues and one
protease inhibitor are taken togetherprotease inhibitor are taken togetherprotease inhibitor are taken togetherprotease inhibitor are taken together
•• HAART lowers plasma viral loads in many cases toHAART lowers plasma viral loads in many cases to
levels not detectable by current methodslevels not detectable by current methods
•• Has improved the health of AIDS patients to theHas improved the health of AIDS patients to the
point that they can function at a normal levelpoint that they can function at a normal level

AIDS (Pregnancy & AIDS)
• Zidovudine(AZT) – recommended for px of maternal
fetal HIV transmission & administered after 14
months AOG (PO meds); IVIT during labor;/ neonate
post birth for 6 wks.
Restrict breastfeeding –infant/neonate is seen byRestrict breastfeeding –infant/neonate is seen by
physician at birth, 1 wk. or 2 wks., a mos., 2 mos., &
4 mos. of life
* Neonate- asymptomatic for 1st several yrs. Of life &
monitored for early sign of immunodeficiency

Antiretroviral DrugsAntiretroviral DrugsAntiretroviral DrugsAntiretroviral Drugs
• Nucleoside Reverse Transcriptase inhibitors
– AZT (Zidovudine)
• Non-Nucleoside Transcriptase inhibitors
– Viramune (Nevirapine)– Viramune (Nevirapine)
• Protease inhibitors
– Norvir (Ritonavir)

Prevention and control of HIVPrevention and control of HIV
• Education
• Prevention of blood born HIV transmission
• Anti Retro Viral treatment
• Combination therapy• Combination therapy
• Post exposure prophylaxis
• Specific prophylaxis
• Primary health care

HIV Occupational ExposureHIV Occupational Exposure
• Review facility policy and report the incident
• Medical follow-up is necessary to determine
the exposure risk and course of treatment
• Baseline and follow-up HIV testingBaseline and follow-up HIV testing
• Four week course of medication initiated one to
two hours after exposure
• AZT (200mg)-TID +lamivudine(3TC)(150mg)BID
x 4days
• Nelfinavir (750 mg) TID ,AZT/3TC
• Exposure precautions practiced

HIV NonHIV Non--Occupational ExposureOccupational Exposure
• No data exists on the efficacy of antiretroviral
medication after non-occupational exposures
PREVENTIONPREVENTION ------ FIRSTFIRST
• The health care provider and patient may decide
to use antiretroviral therapy after weighing the
risks and benefits
• Antiretroviral should not be used for those with
low-risk transmissions or exposures occurring
more than 72 hours after exposure

Play safePlay safe
• Use the common
sense
Be faithful to one
partner,partner,
Use Condom.
• Antiretroviral
drugs
• Caesarean delivery

AbstinenceAbstinenceAbstinence
• It is the only 100 %
effective method of
not acquiring
HIV/AIDS.
• Refraining from
sexual contact: oral,
anal, or vaginal.
• Refraining from
intravenous drug use

Monogamous relationshipMonogamous relationshipMonogamous relationship
• A mutually monogamous (only one sex partner)
relationship with a person who is not infected with
HIV
• HIV testing before intercourse is necessary to proveHIV testing before intercourse is necessary to prove
your partner is not infected

Sex EducationSex Education –– Best option to PreventBest option to Prevent AIDSAIDS
Move from Past to FutureMove from Past to Future

World AIDS DayWorld AIDS Day,,
• World AIDS Day, observed December 1 each
year, is dedicated to raising awareness of the
AIDS pandemic caused by the spread of HIV
infection. It is common to hold memorials toinfection. It is common to hold memorials to
honour persons who have died from HIV/AIDS
on this day. Government and health officials
also observe the event, often with speeches or
forums on the AIDS topics.

TRICHOMONIASIS
• Single celled protozoa
• Men and women can be infected
• Remains dormant in asymptomatic women
• Causes vaginal irritation,itching, and difuse• Causes vaginal irritation,itching, and difuse
malodorous dischare in symptomatic women
• Women may see red spots on the vaginal walls
• Most men are asymptomatic
• Both partner must be treated

CANDIDIASIS
• NOT sexually transmitted
Symptoms
a) Itching
b) Dischargeb) Discharge
c) Burning/irritation
• Pregnant women, diebetes, obesity, suppressed
immunity, antibiotics, corticosteroids or birth control
pills commonly experience yeast infection

Bacteria vaginosis
• Discharge is white and ordorous
Symptoms
• Cervicitis
• PID
• Pospartum endometritis• Pospartum endometritis
• Proamture labour
• Recurring UTI
TREATMENT
• Oral,cream,or gel application of flagyl
• Male partner also treated if infection recurs

ECTOPARASITE
• Pubic lice
• Thru sexual contact/infected clothing
• Symptoms: little to severe itchiness• Symptoms: little to severe itchiness
• Treatment:pyrinate
• Clean clothing/no sharing inner
pants

ECTOPARASITES
• Scabies:close physical /sexual
contact/infected clothing
• Symptoms
• small.,red rash arround primary
lesion,intense itching esp.night
• Treatment:topical scabicide,clean
clothing

Treponema pallidum – The Agent of Syphilis
• Spirochete
• Obligate human parasite
• Transmission
– Sexual
– Trans-placental– Trans-placental
– Percutaneous following contact with
infectious lesions
– Blood Transfusion
• No reported cases of transmission
since 1964

Pelvic Inflammatory Disease (PID)
• l0%-20% women with GC develop PID
• In Europe and North America, higher proportion of C.
trachomatis than N. gonorrhoeae in women with
symptoms of PID
• CDC minimal criteria
Drips
146
• CDC minimal criteria
– uterine adnexal tenderness, cervical motion tenderness
• Other symptoms include
– endocervical discharge, fever, lower abd. pain
• Complications:
– Infertility: 15%-24% with 1 episode PID secondary to GC or
chlamydia
– 7X risk of ectopic pregnancy with 1 episode PID
– chronic pelvic pain in 18%

Chancroid
• The combination of a painful genital ulcer and
tender Suppurative inguinal adenopathy suggests
the diagnosis of Chancroid A probable diagnosis
of Chancroid, for both clinical and surveillance
purposes, can be made if all of the following
criteria are met:
purposes, can be made if all of the following
criteria are met:
1) the patient has one or more painful genital
ulcers;
2) the patient has no evidence of T. pallidum
infection by dark field examination of ulcer
exudate or by a serologic test for syphilis
performed at least 7 days after onset of ulcers;

Chancroid
• 3) the clinical presentation,
appearance of genital ulcers and,
if present, regional
lymphadenopathy are typical for
if present, regional
lymphadenopathy are typical for
Chancroid; and
4) a test for HSV performed on
the ulcer exudate is negative.

Chancroid
• A definitive diagnosis of Chancroid
requires the identification of H.
ducreyi on special culture media thatducreyi on special culture media that
is not widely available from
commercial sources; even when
these media are used, sensitivity is
<80% (145).

Granuloma Inguinale (Donovanosis)Granuloma Inguinale (Donovanosis)
• Granuloma inguinale is a genital ulcerative
disease caused by the intracellular gram-
negative bacterium Klebsiella granulomatis
(formerly known as Calymmatobacterium(formerly known as Calymmatobacterium
granulomatis). The disease occurs rarely in the
United States, although it is endemic in some
tropical and developing areas, including India;
Papua, New Guinea; the Caribbean; central
Australia; and southern Africa (192,193).

Granuloma Inguinale
(Donovanosis)
• Clinically, the disease is commonly
characterized as painless, slowly progressive
ulcerative lesions on the genitals or perineum
without regional lymphadenopathy;without regional lymphadenopathy;
subcutaneous granulomas (pseudoboboes)
might also occur. The lesions are highly
vascular (i.e., beefy red appearance) and
bleed easily on contact.

Granuloma Inguinale
(Donovanosis)
• The causative organism is difficult to culture,
and diagnosis requires visualization of dark-
staining Donovan bodies on tissue crush
preparation or biopsy. No FDA-clearedpreparation or biopsy. No FDA-cleared
molecular tests for the detection of K.
granulomatis DNA exist, but such an assay
might be useful when undertaken by
laboratories that have conducted a CLIA
verification study.

Lymph granulomaLymph granuloma VenereumVenereum
• Lymph granuloma venereum (LGV) is
caused by C. trachomatis serovars L1, L2,
or L3 . The most common clinical
manifestation of LGV amongmanifestation of LGV among
heterosexuals is tender inguinal and/or
femoral lymphadenopathy that is
typically unilateral.

Lymph granuloma Venereum
• Diagnosis is based on clinical suspicion,
epidemiologic information, and the
exclusion of other Aetiologies for
proctocolitis, inguinal lymphadenopathy,proctocolitis, inguinal lymphadenopathy,
or genital or rectal ulcers. C. trachomatis
testing also should be conducted, if
available.

• Genital and lymph node specimens (i.e., lesion
swab or bubo aspirate) can be tested for C.
trachomatis by culture, direct
immunofluorescence, or nucleic acid detection.
NAATs for C. trachomatis are not FDA-cleared for
testing rectal specimens, although some
NAATs for C. trachomatis are not FDA-cleared for
testing rectal specimens, although some
laboratories have performed the CLIA validation
studies that are needed to provide results for
clinical management. Additional molecular
procedures (e.g., PCR-based genotyping) can be
used to differentiate LGV from non-LGV C.
trachomatis, but these are not widely available.

• chlamydia serology (complement fixation
titers >1:64) can support the diagnosis of LGV
in the appropriate clinical context.
Comparative data between types of serologicComparative data between types of serologic
tests are lacking, and the diagnostic utility of
serologic methods other than complement
fixation and some micro immunofluorescence
procedures has not been established.

Trichomoniasis• An estimated 5 million new cases occur each year in women and men.
• Occurs in vagina of women so may be sexually transmitted to men using infected
washcloths and towels.
• It is transmitted to the baby during delivery.
• It also can occur in the urethra (carries urine to penis) in men, doesn’t have
symptoms usually.
SYMPTOMS:
Appear within 5 to 28 days of exposureAppear within 5 to 28 days of exposure
Women usually have a vaginal discharge that
FEMALE SYMPTOMS:
Itching and burning at the outside of the opening of the
vagina and vulva.
Painful and frequent urination
Heavy, unpleasant smelling greenish, yellow discharge
MALE SYMPTOMS:
Usually nothing, or discomfort in urethra, inflamed head of
the penis.

Consequences of untreated STD
• Ectopic pregnancy
• Increased risk of cervical cancer
• Chronic abdominal pain
• Children can be infected at birth causing• Children can be infected at birth causing
blindness ns damage/death

PREVENTION of STIs
• Abstinence give 100% effective method to
prevention
• Avoid multiple partners
• Condoms/spermicides• Condoms/spermicides
• Most STI can be treated
• All STI can be prevented
• Early diagnosis and treatment can decrease the
possibility of serious complications such as infertility
in both men and women

WHY IS STI CONTROL DIFFICULT
• Many people carry the infections
without knowing it

Life at Risk with Sexually Transmitted Infections
Best Choice Play safe

STD&HIV AIDS FOR KRCHN NORTH COAST MEDICAL TRAINING COLLEGE LECTURES

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