STD's Flashcards

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1
Q

What is an STI?

A

More than 1 million sexually transmitted infections (STIs) are
acquired every day worldwide.
*
Each year, there are an estimated 357 million new infections with 1
of 4 STIs: chlamydia, gonorrhoea, syphilis and trichomoniasis.
*
The majority of STIs have no symptoms or only mild symptoms
that may not be recognised as an STI.

*
STIs such as HSV type 2 and syphilis can increase the risk of HIV
acquisition.
*
Over 900 000 pregnant women were infected with syphilis
resulting in approximately 350 000 adverse birth outcomes
including stillbirth in 2012.
*
In some cases, STIs can have serious reproductive health
consequences (e.g., infertility or mother to child transmission)

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2
Q

What is Syphilis?

A

Caused by the spirochete Treponema
pallidum
*
T. pallidum is a helically coiled microorganism
usually 6 15 μm long and 0.1 0.2 μm wide.
*
T. pallidum does not have a tricarboxylic acid
cycle or oxidative phosphorylation resulting in
low metabolic activity.
*
Often considered Gram but lacks LPS!
*
Extremely hard (almost impossible to culture)
due to long time culture requirements.

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3
Q

What are the characteristics of syphilis?

A

T. pallidum has a worldwide distribution, with
syphilis remaining a serious health problem.
*
Complex systemic illness.
*
Used to be known as “the great imposter”.
*
Transmitted by sexual contact.
*
Cannot be diagnosed by isolating causative
organism as T. pallidum does not normally
grow in in vitro cultures.

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4
Q

Pathogenesis of T. pallidum

A

Not all patients go through all three stages; a substantial proportion remains
permanently free of disease after suffering the primary or secondary stages of
infection.
*
Unlike most bacterial pathogens, T. pallidum can survive in the body for many
years despite a vigorous immune response.
*
The healthy treponeme evades recognition and elimination by the host by
maintaining a cell surface rich in lipid.
*
This layer is antigenically unreactive. T. pallidum membrane antigens are only
uncovered in dead and dying organisms when the host is then able to respond.
*
Tissue damage is mostly due to the host response.

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5
Q

Stages of disease

A

Initial contact
2-10 wks
primary syphilis
1-3 mnths
secondary syphilis
2-6 wks
latent syphilis
3-30yrs
tertiary syphilis

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6
Q

How does primary syphilis present?

A

Enlarged inguinal nodes

Spontaneous healing

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7
Q

How does secondary syphilis present?

A

Flu like illness
Myalgia
Fever
Headache
Mucocutaneous rash
Spontaneous resolution

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8
Q

Pathogenesis of initial contact of syphilis

A

Multiplication of treponema at site of infection.

Associate host response.

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9
Q

Pathogenesis of primary syphilis

A

Proliferation of treponema in regional lymph nodes

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10
Q

Pathogenesis of secondary syphilis

A

Multiplication and production of lesion in lymph nodes
liver
joints
skin
muscles
mucous membranes

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11
Q

Pathogenesis of latent syphilis

A

Treponemas dormant in liver or spleen

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12
Q

Pathogenesis of syphilis in 3-30yrs

A

Re-awakening and multiplication of treponema

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13
Q

Tertiary syphilis
Symptoms

A

Neurosyphilis
General paralysis of the insane
Tabes dorsalis
Cardiovascular syphilis
Aortic lesions
Heart Failure
Progressively destructive disease

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14
Q

Pathogenesis of tertiary syphilis

A

Further dissmination and invasion and host response

Cell-mediated hypersensitivity

Gummas in skin, bones, testis

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15
Q

What is congenital syphilis?

A

An infected woman can transmit T pallidum to
her baby in utero
*
Congenital syphilis is acquired after the first 3
months of pregnancy The disease may manifest as

Serious infection resulting in intrauterine death

Congenital abnormalities, which may be obvious at
birth

Silent infection, which may not be apparent until
about 2 years of age (facial and tooth deformities
“Hutchinson’s Teeth”)

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16
Q

How is syphilis diagnosed by lab>

A

T. pallidum partile agglutination assay

Rapid plasma reagin

As T. pallidum cannot be grown in vitro.
*
Exudate from the primary chancre used to be
examined by microscopy (silver stain on picture).
*
Antibody detection.

17
Q

What is the treatment for syphilis?

A

Penicillin is the drug of choice for treating people with syphilis and
their contacts
*
Penicillin is very active against T. pallidum .
*
For patients who are allergic to penicillin, treatment with doxycycline
should be given.
*
Only penicillin therapy reliably treats the foetus when administered to a
pregnant mother.
*
Prevention of secondary and tertiary disease depends upon early
diagnosis and adequate treatment.

Contact tracing with screening and treatment is also important. Several
STIs may be present in one patient concurrently.
*
Patients with other STIs should be screened for syphilis.
*
Congenital syphilis is completely preventable if women are screened
serologically early in pregnancy (< 3 months) and those who are positive
are treated with penicillin.

18
Q

What is Gonorrhoea?

A

Is caused by the Gram negative coccus
Neisseria gonorrhoeae (the gonococcus
*
This bacterium is a human pathogen that does
not cause natural infection in other animals
*
Therefore, its reservoir is human and
transmission is direct, usually through sexual
contact, from person to person

The organism is sensitive to drying and does not
survive well outside the human host, so intimate
contact is required for transmission.
*
Asymptomatically infected individuals form the
major reservoir of infection.
*
Infection may also be transmitted vertically from
an infected mother to her baby during childbirth
*
Infection in babies usually manifests as
ophthalmia neonatorum.

19
Q

What is the clinical presentation of gonnorhea

A

Symptoms develop within 2 7 days of infection and are characterised:
*
In the male by urethral discharge and pain on passing urine (dysuria).
*
In the female by vaginal discharge.
*
At least 50% of all infected women have only mild symptoms or are completely
asymptomatic.
*
Women may not be alerted to their infection unless or until complications arise,
such as:

Pelvic inflammatory disease (PID)

Chronic pelvic pain

Infertility resulting from damage to the fallopian tubes.

20
Q

How to diagnose gonorrhea

A

Microscopy and culture of appropriate
specimens
*
Urethral and vaginal discharges.
*
Purulent discharge is characteristic.
*
Culture is essential in the investigation of
antibiotic susceptibility.
*
Commercial nucleic acid based
approaches (PCR) are now routinely
used, providing reliable results.

21
Q

Treatment of gonorrhoea

A

Antibiotics used to treat gonorrhoea are cefixime or ceftriaxone
*
Penicillinase producing N. gonorrhoeae were first observed in 1976 with
increasing resistance that has severely compromised the effective treatment of
gonorrhoea in many parts of the world.
*
Resistance to fluoroquinolones has also occurred.
*
Since patients with gonorrhoea may also be infected with chlamydia, treatment
regimens often include a combination of agents targeting both organisms (e.g.
ceftriaxone and doxycycline, respectively).
*
Infection can be prevented by the use of condoms.
*
Follow up of patients and contact tracing are vital to control the spread of
gonorrhoea.

22
Q

What is Chllamydial infection?

A

Chlamydia trachomatis cause sexually
transmitted genital infections.
*
Chlamydiae are very small Gram bacteria.
*
Considered obligate intracellular parasites.
*
They have a more complicated life cycle than
free living bacteria because they can exist in
different forms:

The elementary body (EB).

The reticulate body (RB).

Asymptomatic infection is common,
especially in women.

23
Q

What is the cycle of life for chlamydia>

A
  1. Attachment and entry of elementary body to target cell
  2. Formation of reticulate body
  3. binary fusion of reticulate bodies
  4. Reorganisation of reticulate bodies into elementary bodies
  5. Multiplication ceases
  6. Release of elementary bodies
24
Q

What is the clinical manifestation of Chlamydia

A

Can be asymptomatic.
*
Common symptoms include unusual discharge from vagina or penis
and pain when peeing.
*
Most people with chlamydia do not notice any symptoms and do not
know they have it.
If symptoms are developed, patients may experience:

Pain when peeing

Unusual discharge from the vagina, penis or bottom

In women, pain in the tummy, bleeding after sex and bleeding between
periods

In men, pain and swelling in the testicles

25
Q

Pathogenesis and diagnosis of chlamydiae

A

Chlamydiae enter the host through abrasions in the mucosal surface.
*
The clinical effects of C. trachomatis infection appear to result from cell
destruction and the host’s inflammatory response.
*
Laboratory tests are essential to diagnose chlamydial urethritis and
cervicitis.

Chlamydial urethritis and cervicitis cannot be reliably distinguished from
other causes of these conditions on clinical grounds alone.
*
Detection used to be performed by cell culture.
*
Antigen detection (i.e. ELISA).
*
Detection of antibodies anti chlamydia.
*
Modern laboratories use PCR based assays to detect genetic markers.
These will detect both C. trachomatis and N. gonorrhoeae (co infection
occurs frequently).

26
Q

What is genital herpes?

A

Herpes simplex virus (HSV) 2 is the most common cause of genital
herpes, but HSV 1 is being detected more frequently
*
Herpes simplex virus (HSV) infection is a ubiquitous infection of humans
worldwide.
*
HSV 1 is generally transmitted via saliva, causing primary oropharyngeal
infection in children.
*
Cold sores occur after virus reactivation.
*
HSV 2 emerged as a result of independent transmission by sexual route
*
Both HSV 1 and HSV 2 are double stranded DNA viruses.

HSV 2 shows biologic and antigenic differences from HSV 1 and can be
distinguished by molecular typing methods.
*
HSV 2 is one of the most common STIs. O ver 500 million individuals with
HSV 2 globally.
*
Patients may be asymptomatic.
*
HSV 2 infection = increased risk of developing HIV infection (due to
breaches in the mucosal barrier as a result of the HSV ulcers).

27
Q

Clinical presentation of herpes

A

Genital herpes is characterised by ulcerating vesicles that can take up to 2
weeks to heal.
*
The primary genital lesion on the penis or vulva is seen 3 7 days after infection.
*
It consists of vesicles that soon break down to form painful shallow ulcers.
*
Symptoms include: fever, headache and malaise.
*
Occasionally the lesions are on the urethra, causing dysuria or pain on micturition.
*
Healing takes up to 2 weeks, but the virus in the lesion travels up sensory nerve
endings to establish latent infection in dorsal root ganglion neurones.
*
From this site it can reactivate, travel down nerves to the same area, and cause
recurrent lesions (‘genital cold sores’).
*
Meningitis or encephalitis occurs in adults as a rare complication.Genital herpes is characterised by ulcerating vesicles that can take up to 2
weeks to heal.
*
The primary genital lesion on the penis or vulva is seen 3 7 days after infection.
*
It consists of vesicles that soon break down to form painful shallow ulcers.
*
Symptoms include: fever, headache and malaise.
*
Occasionally the lesions are on the urethra, causing dysuria or pain on micturition.
*
Healing takes up to 2 weeks, but the virus in the lesion travels up sensory nerve
endings to establish latent infection in dorsal root ganglion neurones.
*
From this site it can reactivate, travel down nerves to the same area, and cause
recurrent lesions (‘genital cold sores’).
*
Meningitis or encephalitis occurs in adults as a rare complication.

28
Q

Diagnosis of herpes

A

Spread of infection from mother to infant at the time of delivery can give
rise to neonatal disseminated herpes or encephalitis.
*
Herpes simplex virus DNA can be detected in vesicle fluid or ulcer swabs.
*
A number of antivirals, including oral acyclovir, valaciclovir and famciclovir
can be used for treatment of severe or early lesions, and acyclovir may
need to be given intravenously if there are systemic complications.
29

29
Q

What is Human papillomavirus infection

A

There are over 200 distinct types of human papillomaviruses, all infecting skin
or mucosal surfaces.
*
Many papillomavirus types are transmitted sexually and cause genital warts.
*
Warts appear on the penis, vulva and perianal regions after an incubation
period of 1 6 months.
*
The lesion on the cervix is a flat area of dysplasia visible by colposcopy as a
white plaque after the local application of 5% acetic acid.
*
Because of their association with cervical cancer, especially types 16 and 18,
cervical lesions are best removed by laser or loop excision.

30
Q

What is HIV?

A

Human immunodeficiency virus (HIV) is a retrovirus, so called because this
single stranded RNA virus contains a gene that codes for a reverse transcriptase
(Latin: retro ,
*
Acquired immune deficiency syndrome (AIDS) was first recognised in 1981 in the
USA.
*
Patients had evidence of impaired immune function, and depletion of CD4
positive T helper ( Th ) lymphocytes.
*
This immunodeficiency syndrome appearing in an individual without a known
cause such as treatment with immunosuppressive drugs was referred to as
‘acquired immune deficiency syndrome’ (AIDS).
*
Human immunodeficiency virus, the causative virus of AIDS, was isolated from
blood lymphocytes in 1983.

31
Q

what is the pathogenesis for HIV?

A

The HIV transmission route for more than 80% of adults involves mucosal
surfaces, in particular cervicovaginal , penile and rectal.
*
The remainder may be infected by intravenous or percutaneous routes.
*
The immune system begins to suffer gradual damage, and the number of
circulating CD4 positive T cells steadily falls and the HIV load rises.
*
As AIDS develops, responses to HIV and unrelated antigens are further
depressed. The immune system has lost control.

32
Q

Progression to AIDS from HIV

A

Viral invasion of the CNS, with self limiting aseptic meningoencephalitis
as the most common neurological picture, occurs in early infection.
*
Infections by HSV, varicella zoster virus (VZV), Toxoplasma gondii , JC
virus and Cryptococcus neoformans , Cryptosporium spp , and many
*
AIDS, symptomatic disease, consists of a large spectrum of microbial
diseases acquired or reactivated as a result of the underlying
immunosuppression due to HIV.
*
The disease picture of AIDS is therefore an indirect result of infection with
HIV.

33
Q

Treatment of HIV/AIDs

A

Antiretroviral therapy results in a dramatic
improvement in disease prognosis.
*
In the 1990s, a range of antiretroviral therapies was
introduced.
*
These were developed further over the next two
decades in terms of new drugs in all classes and
combinations.
*
This had a dramatic effect on progression to AIDS
and led to the term highly active antiretroviral
therapy (HAART).
*
Drawback side effects altered fat distribution:
lipodystrophy.

34
Q

Measures to control spread of HIV/AIDS

A

Many resource rich countries have taken measures to reduce the spread of
HIV.
*
Up to 2010, the number of new HIV infections fell by nearly 20%.
*
The risk of transmitting HIV via blood and blood products is reduced considerably
by donor screening programmes.
*
HIV has a delicate outer envelope and is highly susceptible to heat and chemical
agents.
*
The main effort in the prevention of HIV infection concerns mass public education
programmes.
*
These involve advice to change sexual behaviour and the use of barrier
contraceptives such as condoms.

35
Q

Key facts

A

*
STIs have a profound impact on sexual and reproductive health worldwide.
*
More than 1 million STIs are acquired every day.
*
STIs can have serious consequences beyond the immediate impact of the
infection itself.
*
STIs like herpes and syphilis can increase the risk of HIV acquisition three fold
or more.
*
Mother to child transmission of STIs can result in stillbirth, neonatal death, low
birth weight and prematurity, sepsis, pneumonia, neonatal conjunctivitis, and
congenital deformities.
*
HPV infection causes 528 000 cases of cervical cancer and 266 000 cervical
cancer deaths each year.
*
Prevention by barrier protection is key as vaccines are unavailable for the
majority of STIs.