Lesson 5
THEMES:
1. METHODS OF EXAMINATION OF PATIENTS WITH SEXUALLY TRANSMITTED DISEASES. PRIMARY SYPHILIS. HARD CHANCRE. REGIONAL LYMPHADENOPATHY. CLINIC OF SECONDARY SYPHILIS. CLINICAL AND LABORATORY DIAGNOSIS OF PRIMARY AND SECONDARY SYPHILIS. LATE SYPHILIS.
2.CONGENITAL (HEREDITARY) SYPHILIS. SYPHILIS OF PLACENTA, UMBILICAL CORD, FETUS. HEREDITARY SYPHILIS OF SUCKLING CHILD, CHILDREN OF EARLY YEAR (1–4). DIAGNOSTIC OF LATE AND CONGENITAL SYPHILIS, MODERN PECULIARITY OF CONGENITAL SYPHILIS, PROPHYLAXIS.
3.GONOCOCCI INFECTION, TREATMENT.
COMPLICATIONS: GONOCOCCI PHARYNGITIS, GONOCOCCI INFECTION OF AN ANORECTIC ZONE.
DIAGNOSTIC, TREATMENT, CONTROL OF THE TREATMENT.
4. DERMATOLOGICAL ASPECTS OF HIV-INFECTION. CONTROL WORK.
SEXUALLY TRANSMITTED DISEASES
SEXUALLY TRANSMITTED DISEASES
Chlamydia*
Gonorrhea*
Syphilis*
Genital herpes*
Condyloma acuminatum (genital warts)* HPV
Chancroid
Infectious Mononucleosis**
HIV – AIDS
Trichomoniasis
Granuloma inquinale
Hepatitis B, C, D
Others
Three Approaches to Diagnosis of STD
1. Clinical approach
2. Etiological approach
3. Syndromic approach
1. Syndromic Approach
u In this approach, diagnosis is based on the identification of syndromes, which are combinations of the symptoms the patient reports and the signs the health care provider observes
u The recommended treatments are effective for all the diseases that could cause the identified syndrome
Components of Syndromic Approach
Classification by Syndrome:
Classifying the main causal pathogens by the syndromes they produce
Use of Algorithms:
Using flowcharts to guide the management of a given syndrome
Treatment and Counseling:
Using often more than one treatment that addresses all the pathogens with potential to cause a given syndrome
Treatment of Partners:
Promoting treatment of sex partners
STI Risk Assessment
Questions focus on
u Age
u Marital status
u Current or past STI symptoms
u Number of partners
u Nature of relationships
u The possibility of partners having other sexual partners
u Current symptoms in partners
Classification by Syndromes
u STIs are classified by syndrome
u Each syndrome is made up of a combination of symptoms and clinical signs identified upon examination
u The four main syndromes are:
Urethral discharge: men
Lower abdominal pain: women
Vaginal discharge: women
Genital ulcer: men or women
CLINICAL ASSESSMENT OF PATIENTS WITH SEXUALLY TRANSMITTED DISEASES
http://www.stdservices.on.net/management/clinical_assessment.htm
The STD consultation aims to:
Define the presenting complaint.
Assess sexual and social behaviours for risk factors and risk markers.
Screen the patient for sexually transmitted infections and associated
conditions.
Diagnose and treat infection.
Educate the patient on risk modification and offer vaccination.
Promote safe sex practices
Limit the spread of STDs in the population and conduct contact tracing.
General principles of the sexual consultation include:
Ensuring privacy and maintaining confidentiality between the doctor and patient.
It is always best never to make assumptions about the patient or their behaviour and to maintain a non judgemental attitude to patient behaviours.
If there is doctor or patient discomfort this can be acknowledged.
Maintaining a relaxed body language and using terms that the patient understands and is comfortable with helps rapport development.
I. Rationale and General Clinical Approach
A. Epidemiological and medical goals of the STD intervention:
1. Identify specific diagnosis and treatment of active disease.
2. Detect asymptomatic disease, prevent disease sequelae, transmission in the
community, and vertical disease transmission.
3. Support protective sexual health behavior. Promote behavioral change in “at
risk” individuals and groups.
4. Protect public health, current and future sex partners.
5. Promote awareness of the linkage of sexual risk-taking, substance abuse and
STD/HIV.
6. Promote reproductive and sexual health.
B. Taking a sexual history:
1. General considerations:
a) Introduce yourself and establish your role as clinician.
b) Take the history while the patient is fully clothed.
c) Interview patient alone or with an unrelated translator.
d) Focus on quality of patient-provider interaction.
e) Assure confidential nature of patient-provider information.
f) State the medical necessity of an accurate, complete, specific sexual
behavioral history (testing, counseling, therapies, etc.).
g) Make no assumptions regarding gender or gender role.
h) Make no assumptions regarding gender of partners or specific sexual
behaviors; always use gender-neutral terminology.
i) Be non-judgmental and objective to enhance patient behavioral outcomes.
j) Use active listening, open-ended questions, and clarify/verify your own
and patient understanding.
k) Actively listen for informational content, emotional content,
comprehension, omitted information, etc.
l) Begin with least sensitive questions (e.g.; general health history), then
progress to sexual behaviors, substance use, etc.
m) Discuss the specific sexual and substance use behavior; do not use labels
(“straight,” “bisexual,” “gay,” “queer,” “shooter,” etc.).
n) Clinician should be comfortable with the use of a wide range of sexual
terms, but should not assume the patient knows the meaning of sexual
terms (e.g.; fellatio, anal sex).
2. A sexual history should
a) Reinforce confidentiality.
b) Establish patient-provider rapport.
c) Ensure accurate definition of the problem.
d) Elicit accurate clinical and behavioral information.
e) Identify specific STD/HIV risk behaviors.
f) Lead to successful medical and epidemiological management.
g) Define sexual activity using a range of specific anatomic and behavioral
terms.
3. Diagnostic or epidemiologic STD risk indicators:
a) Genital symptoms, especially vaginal, urethral or anal discharge, skin
lesions, ulcers, warts
b) A sex partner with a known STD diagnosis
c) A sex partner with genital symptoms
d) Diagnosis with a concurrent STD
4. STD behavioral and partner risk indicators (varies by STD):
a) Adolescence
b) Residence in high prevalence area or sexual networks with high
prevalence of STDs
c) Residence in a high poverty area; certain racial/ethnic groups; poor
access to health care
d) A history of prior STD diagnosis and treatment (past 1-2 years)
e) New partner in the last two or three months
f) More than one sex partner (past 1-4 months, past year)
g) Sex partner with other sex partners (past 1-4 months, past year)
h) Inconsistent use of condoms with casual or multiple partners
i) Commercial sex or exchange of sex for drugs
j) A recent or past history of sexual assault, family violence, or intimate
partner abuse
k) Current use or a history of injection drug use or substance abuse by
patient or sex partners
l) Men who have sex with men (MSM) with high risk behaviors
m) HIV-infected patients with high risk behaviors
II. Chief Complaint and History of Present Illness
A. Reason for visit (elicit with an open-ended question):
1. Patient’s desire for routine STD/HIV screening (new relationship, unprotected
intercourse, sexual assault, etc.)
2. Current, recent or recurrent symptoms
3. Treatment for recurrent genital herpes or warts
4. Sexual partner with symptoms or recent STD diagnosis
5. A positive test result requiring treatment or prompting questions
6. Routine pelvic, Pap test, and/or birth control
7. Use of or need for emergency contraception
8. Immunization and/or testing for Hepatitis A or B, or immunization for HPV
9. Other
B. Characterize and document all symptoms and signs:
1. Oral/pharyngeal symptoms, including oral lesions, cold sores
2. Lymph node swelling or tenderness
3. Urethral discharge (male)
4. Vaginal discharge or odor (female)
5. Dysuria, frequency, urgency
6. Itching or irritation (vulvar, anal, penile, pubic area, perineum)
7. Abnormal vaginal bleeding (spotting between periods, abnormal menses)
8. Genital sores/ulcers/lesions, bumps/warts, masses, or rashes (painful,
Recurrent); document size and location of all lesions
9. Non-genital skin rashes
10. Pelvic pain/pain with intercourse (dyspareunia)
11. Testicular pain, swelling, masses
12. Rectal/perianal symptoms (pain, discharge, bleeding, itching, sores, masses)
13. Abdominal complaints (nausea, vomiting, constipation, diarrhea)
14. Systemic or constitutional symptoms
15. Acute arthritic symptoms
16. Neurologic symptoms
C. History of symptoms and signs:
1. Anatomic location, dimensions, distribution
2. Onset, duration, change since onset
3. Recurrence, history of similar symptoms
4. Alleviating, exacerbating factors
5. Relation of symptoms to menses, sexual intercourse
III. Past Medical and STD History
A. Past medical history:
1. General health and pre-existing medical conditions
2. Past history of underlying genitourinary pathology, urologic or gynecologic
Procedures
3. History of immunizations and testing for Hepatitis A, Hepatitis B, Hepatitis C,
HPV
B. Current medications and medications taken in the past month (including topical preparations)
C. Allergies or other side effects to medications in the past:
1. Name of medication
2. Record the type of reaction, (e.g.; rash, difficulty breathing)
3. Record side effects (e.g.; nausea)
D. Prior History of STDs and genitourinary infections (note number of episodes, when last treated):
1. Gonorrhea
2. Chlamydia
3. Nongonococcal urethritis (NGU), urethritis, epididymitis (males)
4. Cervicitis or mucopurulent cervicitis (MPC) (females)
5. Pelvic inflammatory disease (PID) (females)
6. Syphilis: note stage or symptoms, treatment, year, city or state, last VDRL
titer, if known
7. Genital herpes: note recurrence rate per year
8. Genital or anal warts
9. Trichomoniasis
10. Bacterial vaginosis (females): note frequency, last episode
11. Yeast: note frequency, treatment
12. Urinary tract infections
13. Hepatitis
14. HIV
15. Other STDs: lymphogranuloma venerium (LGV), other
16. Genital dermatoses
D. History of STD testing:
1. Frequency of chlamydia and gonorrhea testing
2. Last syphilis test; frequency of testing
3. History of HSV testing, including HSV-2 type-specific serology test
4. HIV testing history; frequency of testing.
IV. Gynecologic History
A. Last menstrual cycle (LMP):
1. First day of last menstrual period
2. LMP normal in flow and duration
3. Currently pregnant
B. Parity (pregnancy history):
1. Gravida = number of times pregnant
2. Para = deliveries
3. Ab-sp, SAB = spontaneous abortions or miscarriages
4. Ab-in, TAB = induced or therapeutic abortions or termination or pregnancy
5. Tubal (ectopic) pregnancies
6. Cesarean sections
7. Currently breast feeding (therapy ramifications, etc.)
C. Hygiene practices:
1. Douching – how often and what is used. Other genital cleansing – internally, perfumes, soaps; opportunity to educate and advise against douching.
2. Shaving/waxing practices; opportunity to educate about potential skin
damage, increased susceptibility to infection, and autoinoculation spread of
HPV infection (applies to male patients as well)
D. Current contraception:
1. Pregnancy intention and plans
2. Method used, if pregnancy not desired
3. Satisfaction with current method; side effects; adherence and appropriate use
4. Confidential access to family planning/reproductive care providers; need for
Referral
5. Need for advance prescription for emergency contraception
E. Pap smear:
1. Last Pap – date, results
2. History of abnormal Pap, year, treatment, follow-up
3. HPV test result (if done)
V. Sexual History
A. General considerations:
1. Style and content vary by patient gender, age, sexual orientation, presenting
symptoms and signs, and possibly culture.
2. Emphasize confidentiality, and provide a private setting. Clinic setting and
level of privacy may impact patient comfort, and the details elicited.
3. Specifics of the sexual history and follow-up questions generally depend on
the patient’s response to open-ended screening questions.
4. Responses to questions may warrant risk-reduction counseling.
5. The time frame for eliciting specific risk behaviors depends on presenting
symptoms and the disease of interest. Many clinics use a time frame between
1 and 4 months. A shorter time frame increases the likelihood of accuracy.
6. A focused sexual history should cover the five “Ps”: Partners, Practices,
Pregnancy Prevention, Protection from STDs, and Past STDs. See Appendix
A for examples of focused sexual history-taking tools.
7. To normalize or explain, use opening questions such as: “I ask all patients
questions about their risk for STDs and HIV,” or “In order to provide the best
care for you today, and to understand your risk for certain infections, it is
necessary for us to talk about your sexual behavior.”
8. Give assurance (and limitations) of confidentiality.
9. For adolescents, you may need to establish their level of sexual activity:
“Have you begun having any kind of sex?”
B. Sex partners:
1. Define “sex partners” as anyone the patient has had intimate sexual contact
at oral, genital and anal sites
2. Sex with men, women or both
3. Number of days since last sexual exposure
4. Number of days since last unprotected sexual exposure (without condom)
5. Was there unprotected sex with a steady sex partner or a casual/new sex
partner (may need to define)
6. Number of sex partners in the past 1-4 months
7. Number of new sex partners in the past 1-4 months
8. Total number of sex partners in the past 12 months
9. Partner with other sex partners
10. Partner who has HIV infection
11. Partners who inject drugs
12. Partner with known diagnosis of STD or current STD symptoms
13. Commercial sex, exchange of money or drugs for sex
14. Venues for meeting partners – Internet, commercial sex sites, parks
15. Anonymous partners
C. Sites of recent sexual exposure (past 1-4 months); explain why you are asking these sensitive questions:
1. Vaginal intercourse (penis to vagina)
2. Anal intercourse (penis to anus), receptive (“bottom”) and/or insertive (“top”)
3. Oral sex (mouth to penis, vagina, or anus)
4. Other sexual practices may be important in certain situations: use of sex toys
or devices, masturbation, “fisting”, exposure to blood during sex
D. Condom use for sexual practices:
1. Pattern of use (never, sometimes, and always)
2. Use with different sites of exposure (vaginal, rectal, oral)
3. Condom use with last sexual intercourse
4. Use with steady and non-steady partners, if applicable
5. Circumstances of non-use (e.g.; substance use)
6. Condom breakage and correct use
7. Opportunity to educate and discuss risk reduction
8. Opportunity to discuss contraception
E. Disclosure of STD/HIV status to partners (if positive):
1. Disclosure of HIV status
2. Disclosure of HSV-2/genital herpes status
VI. HIV Risk Assessment:
A. Date and result of most recent HIV test..
B. Patient history of injection drug use, shared needles.
C. Patient history of crack cocaine/methamphetamine (“speed”) use.
D. History of exchanging drugs/money for sex.
E. History of transfusion or hemophilia: note dates.
F. History of occupational contact to bodily fluids.
G. Sexual contact with men who have sex with other men.
H Sexual contact with known HIV-positive person.
I. Sexual contact with injection drug user.
J. Sexual contact with crack cocaine/methamphetamine (“speed”) user.
VII. Social History
A. History of or current sexual abuse, domestic violence
B. Drug use, heroin, cocaine/crack, methamphetamine (“speed”), alcohol; IV, IM, or
Subcutaneous injection, needle-sharing
C. Sex under the influence of alcohol or drugs
D. Homelessness
E. Commercial sex work, exchange of money or drugs for sex
F. Piercing and/or tattooing
G. Incarceration history; sex/substance abuse while incarcerated
H. Recent or past history of travel, sexual exposure while traveling, partner travel
history
VIII. Clinical Management
A. Screening tests as indicated by age and other risk indicators; because of the high prevalence of asymptomatic carriage and transmission of STDs/HIV/Hepatitis, the decision about screening testing should not be dependent on the presence of symptoms.
1. Sexually active young women age 25 and younger should be screened for
chlamydia (and generally gonorrhea) on an annual basis.
2. Sexually active women should receive periodic cervical cytology testing
starting at age 21, with follow-up as indicated. In certain situations, HPV
testing may be warranted in conjunction with cervical cytologic testing.
3. All pregnant women should be screened for HIV, syphilis, hepatitis B surface
antigen, and chlamydia as early in pregnancy as possible. Pregnant women
should be screened for gonorrhea depending on age and risk factors.
Screening for hepatitis C should be based on risk factors.
4. Sexually active MSM should be screened at least annually for HIV, syphilis,
urethral gonorrhea and chlamydia, rectal gonorrhea and chlamydia (if
exposed), and pharyngeal gonorrhea (if exposed). More frequent screening
(every 3-6 months) should be based on specific risk factors.
5. HIV-infected patients should be screened for chlamydia, gonorrhea, and
syphilis at least annually or more frequently (every 3-6 months) depending on
risk factors. Women infected with HIV should be screened for trichomonas.
6. Gonorrhea, chlamydia, syphilis, and HIV screening for other risk groups (e.g.;
heterosexual males) depends on specific risk factors.
7. Screening for HSV-2 using type-specific serology tests may be considered for
certain high-risk patients (e.g.; MSM, HIV-infected, partners of those infected
with genital herpes).
8. HIV screening should be available for all sexually active patients aged 13-64,
particularly those who have never received an HIV test. Patients seeking
evaluation and treatment for STDs should be screened for HIV infection.
Persons with interim or on-going risk for HIV infection should be screened at
least annually, or as indicated by risk.
B. Diagnostic tests as indicated by symptoms and signs
C. Presumptive treatment based on known contact to disease, symptoms, signs,
and stat lab findings
D. Specific treatment based on lab findings
E. Partner management, treatment and counseling based on specific STD diagnosis
F. Referral of HIV-positive patients to Partner Counseling and Referral Services (PCRS), as indicated, for assistance iotifying sex and needle-sharing partners about possible exposure to HIV
G. Possible need for follow-up appointment.
IX. Patient Education
A. Asymptomatic nature of many STDs and the need for screening
B. Relationship of STDs to HIV transmission
C. Need for partner treatment, as indicated
D. Partner notification, disclosure, and communication issues
E. Re-testing or other follow-up as indicated
F. Specify STDs that were included in the clinical assessment and lab tests
G. Contraception, as indicated
H. Drug or alcohol counseling, as indicated
I. Advise to avoid douching, as indicated
J. Identify support, referrals for social services, domestic violence, substance
abuse, as indicated.
K. Referral for other clinical services, as indicated.
L. In addition to patient education, client-centered counseling to assess risk,
increase risk perception if appropriate and negotiate risk-reduction plan as
indicated by assessment. See curriculum module titled “Behavioral Counseling
for STD/HIV Risk Reduction”.
Reference:
1. Ramjee G, van der SA, Chipato T, et al. The diaphragm and lubricant gel for prevention of cervical sexually transmitted infections: results of a randomized controlled trial. PLoS One 2008;3:e3488.
2. Lin JS, Whitlock E, O‘Connor E, et al. Behavioral counseling to prevent sexually transmitted infections: a systematic review for the U.S. Preventive Services Task Force. Ann Intern Med 2008; 149:497–9.
3. Karim SA, Coletti A, Richardson BS. Safety and effectiveness of vaginal microbicides BufferGel and 0.5% PRO 2000/5 gel for the prevention of HIV infection in women: results of the HPTN 035 trial. In: 16th Conference on Retroviruses and Opportunistic Infections, Montreal, Canada, 2009.
4. Microbicides Development Programme. Technical fact sheet for scientists (MDP 301). London, 2009. Available at http://www.mdp.mrc.ac.uk.
5. Martin ET, Krantz E, Gottlieb SL, et al. A pooled analysis of the effect of condoms in preventing HSV-2 acquisition. Arch Intern Med 2009;169:1233–40.
6. Koss CA, Dunne EF, Warner L. A systematic review of epidemiologic studies assessing condom use and risk of syphilis. Sex Transm Dis 2009;36:401–5.
7. Auvert B, Sobngwi-Tambekou J, Cutler E, et al. Effect of male circumcision on the prevalence of high-risk human papillomavirus in young men: results of a randomized controlled trial conducted in Orange Farm, South Africa. J Infect Dis 2009;199:14–9.
8. Sobngwi-Tambekou J, Taljaard D, Lissouba P, et al. Effect of HSV-2 serostatus on acquisition of HIV by young men: results of a longitudinal study in Orange Farm, South Africa. J Infect Dis 2009;199:958–64.
9. Sobngwi-Tambekou J, Taljaard D, Nieuwoudt M, et al. Male circumcision and Neisseria gonorrhoeae, Chlamydia trachomatis and Trichomonas vaginalis: observations after a randomised controlled trial for HIV prevention. Sex Transm Infect 2009;85:116–20.
10. Tobian AA, Serwadda D, Quinn TC, et al. Male circumcision for the prevention of HSV-2 and HPV infections and syphilis. N Engl J Med 2009;360:1298–309.
11. Smith DK, Taylor A, Kilmarx PH, et al. Male circumcision in the United States for the prevention of HIV infection and other adverse health outcomes: report from a CDC consultation. Public Health Rep 2010;125(Suppl 1):72–82.
12. Public Health Agency of Canada. Canadian guidelines on sexually transmitted infections. 2006 ed. Centre for Communicable Diseases and Infection Control; 2010. Available at http://www.phac-aspc.gc.ca/std-mts/sti-its/
13. CDC. HIV/AIDS Surveillance Report, 2008. Vol. 20. Atlanta, GA: US Department of Health and Human Services, Centers for Disease Control and Prevention; 2010. Available at http://www.cdc.gov/hiv/topics/surveillance/resources/reports/.
14. DHHS. Guidelines for the use of antiretroviral agents in HIV-infected adults and adolescents. Washington, DC: US Department of Health and Human Services; 2010. Available at http://AIDSinfo.nih.gov..
15. CDC. FDA licensure of bivalent human papillomavirus vaccine (HPV2, Cervarix) for use in females and updated HPV vaccination recommendations from the Advisory Committee on Immunization Practices (ACIP). MMWR 2010;59:626–9.
16. CDC. FDA licensure of quadrivalent human papillomavirus vaccine (HPV4, Gardasil) for use in males and guidance from the Advisory Committee on Immunization Practices (ACIP). MMWR 2010;59:630–2.
17.Karim QA, Karim SS, Frohlich JA, et al. Effectiveness and safety of tenofovir gel, an antiretroviral microbicide, for the prevention of HIV infection in women. Science 2010;329:1168–74.
Syphilis – Cause
Syphilis is caused by the bacterium Treponema pallidum.
Transmission
Transmission of the bacteria usually occurs during vaginal, anal, or oral sex. The syphilis bacteria are passed from person to person through direct contact with:
- The open sore (chancre) that appears during the primary stage.
- Mucous membrane or other sores during the secondary stage and sometimes during the latent stage.
Sores mainly occur on the external genitals, vagina, anus, or rectum. Sores can also occur on the lips and in or around the mouth. The bacteria most commonly enter the body through mucous membranes, usually in the area around the genitals and urinary system.
In rare cases, syphilis enters the body through openings in the skin, such as cuts and scrapes, or even through wet kisses, if the infected person has a sore on the mouth or lips. Syphilis may also be transmitted by using a needle previously used by an infected person. Syphilis can be transmitted through a blood transfusion. But this is very rare, because all donated blood in the United States and Canada is screened for some sexually transmitted infections (STIs). And syphilis bacteria cannot survive more than 24 to 48 hours in blood stored using modern blood-banking methods.
A pregnant woman with syphilis can pass the infection through the placenta and infect her baby any time during pregnancy or delivery (congenital syphilis).
Syphilis cannot be spread through casual contact with toilet seats, door knobs, swimming pools, hot tubs, bathtubs, shared clothing, or eating utensils.
Having been infected with syphilis in the past does not protect a person from becoming infected again.
Incubation period
An incubation period is the time between exposure to a disease and the first symptom. A skin sore called a chancre is usually the first symptom of sexually transmitted syphilis. A chancre appears between 3 weeks to 3 months after a person has been infected with syphilis.
Contagious period
A person with syphilis can easily pass the infection (is contagious) to physically intimate partners when primary- or secondary-stage sores are present. But the person may be contagious for years, off and on, and is always contagious whenever an open sore or skin rash from syphilis is present.
Syphilis – What Happens?
About 3 weeks-although the range is from 10 to 90 days-after being infected with syphilis, a sore (chancre) that is usually painless often appears on the genitals. This first stage in the course of syphilis is referred to as the primary stage. The chancre usually heals without treatment in 3 to 6 weeks.1
If syphilis is not treated during the primary stage, it often progresses to later stages.
In the secondary stage of syphilis, a skin rash will usually develop about 2 to 8 weeks after the chancre appears. The symptoms usually disappear without treatment within two months.1
After the rash clears, a person may have a period with no symptoms. This symptom-free period is called the latent (hidden) stage. Even though symptoms disappear, the bacteria that cause syphilis remain in the body and begin to damage the internal organs. The latent period may be as brief as 1 year or range from 5 to 20 years.
A person is contagious during the primary and secondary stages and may still be contagious during the early part of the latent stage. During this time, symptoms of the second stage of syphilis may reappear. This is called a relapse and can occur several times.
If not detected and treated, syphilis may then progress to the tertiary (late) stage, the most destructive stage of syphilis. During this stage, syphilis may cause serious blood vessel and heart problems, mental disorders, blindness, nerve system problems, and even death. It may begin as early as 1 year after infection or at any time during the infected person’s life. About one-third of untreated people who are infected with syphilis will have the complications of tertiary (late) syphilis. Any organ system (such as the central nervous system) may become involved.
Syphilitic Chancres
n Genital (95%) and extragenital (5%).
n Highly infectious.
n Usually single.
n Indurated.
n Painless.
n Edge regular.
n Floor clean.
n Heal in 3-6 weeks.
Primary Syphilis Chancre, Tongue
Oral chancres in primary syphilis
Chancre of Hard Palate
Chancre of the Lip
Regional lymphadenopathy
n Firm, discrete, mobile, nonsuppurative and painless without overlying skin changes
n It may persist for months, despite healing of the chancre.
Secondary Syphilis
Ddx “Great Imitator”
Pityriasis rosea
Drug eruptions (pruitic)
Lichen planus; Wickham’s striae, Koebner’s, pruitic
Psoriasis; no adenopathy
Sarcoidosis; need serology and silver staining of biopsy
Infectious mononucleosis, false pos RPR
Geographic tongue
Aphthous stomatitis
Distribution of skin lesions of secondary syphilis
• Macular lesions most often found in pink colored areas
• Papular lesions in light blue areas
• Pustular lesions in the purple areas
Mouth
Bacterial-Syphilis
Condylomata lata:
n Wart-like lesions in moist intertriginous areas.
n Sessile
n don’t bleed easily.
n D.D.: Condyloma accuminata:
n Pedunculated
n Bleed easily.
n All of these lesions teem with treponemes and are highly contagious
Naso-Labila fold
CONGENITAL SYPHILIS
1. Mucous patches and skin lesions in an infant
2. Hutchinson’s teeth
n Characteristic notched edges
n “screwdriver” shaped central incisors
3. Moon’s molar of congenital syphilis
4. Saddle nose
5. Perforation of the hard palate (resulting from gummatous destruction)
TERTIARY SYPHILIS
Latent stage: After the rash clears, a person may have a period with no symptoms. This is often called the “hidden stage.” Even though symptoms go away, the bacteria that cause syphilis are still in the body and begin to damage the internal organs. This stage may be as short as 1 year or last from 5 to 20 years. Often, a woman with latent-stage syphilis doesn’t find out that she has the infection until she gives birth to a child with syphilis.
Late (tertiary) stage: If syphilis is not found and treated in the early stages, it can cause other serious health problems. These can include blindness, problems with the nervous system and the heart, and mental disorders. It can also cause death.
Palatal gumma
Complications of tertiary (late) syphilis include:
Gummata, which are large sores inside the body or on the skin.
Cardiovascular syphilis, which affects the heart and blood vessels.
Neurosyphilis, which affects the nervous system.
Congenital syphilis refers to syphilis passed from the mother to the baby during pregnancy or during labor and delivery. Congenital syphilis can cause complications iewborns and children.
Laboratory Testing
Direct examination of clinical specimen by dark-field microscopy or fluorescent antibody testing of sample.
Non-specific or non-treponemal serological test to detect reagin, utilized as screening test only.
Specific Treponemal antibody tests are used as a confirmatory test for a positive reagin test.
1. Non-treponemal Reagin Tests
Non-specific or non-treponemal serological test to detect reagin, utilized as screening test only.
o Reagin is an antibody formed against cardiolipin.
o Found in sera of patients with syphilis as well as other diseases.
o This type of reagiot to be confused with same word originally used to describe IgE.
o Non treponemal tests become positive 1 to 4 weeks after appearance of primary chancre.
o in secondary stage may have false negative due to Prozone, in tertiary 25% are negative, after successful treatment will become nonreactive after 1 to 2 years.
VDRL
RPR
USR-unheated serum reagin test
RST-reagin screen test
ELISA.
Laboratory – VDRL
Flocculation test, antigen consists of very fine particles that precipitate out in the presence of reagin.
Utilizes an antigen which consists of cardiolipin, cholesterol and lecithin.
o Antigen very technique dependent.
o Must be made up fresh daily.
Serum must be heated to 56 C for 30 minutes to remove anti-complementary activity which may cause false positive, if serum is not tested within 4 hours must be reheated for 10 minutes.
Calibrated syringe utilized to dispense antigen must deliver 60 drops/mL +/- 2drops.
Performing the test:
o 0.05 mL of serum added to circle on ceramic slide and spread.
o Add one calibrated drop of antigen to each circle.
o Rotate at 180 rpms for 4 minutes.
o Read microscopically at 100x and grade reaction if positive.
o Perform titer on positive samples, report out titer.
Quality control:
o Run three levels of control: Non-reactive, weakly reactive and reactive.
o Glass syringe with 18g delivery needle must be checked daily to ensure delivery of 60 drops/mL.
o Rotator rpms must be checked to ensure 180 rpms.
o Room temperature must be 23-29 C.
VDRL used primarily to screen cerebral spinal fluid.
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.
Rapid Plasma Reagin Test – RPR
General screening test, can be adapted to automation.
CANNOT be performed on CSF.
Antigen
o VDRL cardiolipin antigen is modified with choline chloride to make it more stable
o attached to charcoal particles to allow macroscopic reading
o antigen comes prepared and is very stable.
Serum or plasma may be used for testing, serum is not heated.
Test Procedure:
o Serum or plasma added to circle on card and spread.
o One drop of antigen from a needle capable of delivering 60 drops/mL is added.
o Rotate at 100 rpms/minute for 8 minutes.
o Results are read macroscopically.
Daily quality control:
o 20 gauge needle checked for delivery of 60 drops/mL
o Rotator checked for 100 rpms/minute
o Room temperature must be 23-29 C.
o Three levels of control must be run and give appropriate results.
RPR appears to be more sensitive than the VDRL.
Clumping of the carbon particles indicates the person’s serum contains nonspecific antilipid (reagin) antibodies.
RPR
In the first test, the patient’s serum has caused flocculation of the carbon particles; indicative of active syphilis.
After six months, however, the test is negative.
0This indicates that the antimicrobial therapy given at the time of the first test has been successful.
Although the RPR test is a non-specific test, it is an excellent indicator of the success of therapy.
Neg/Pos controls at top of slide, patient bottom right.
Specific Treponemal Tests
Performed to confirm a positive non-specific reagin test.
Treponema Pallidum Immobilization
Treponema pallidum hemagglutination
Fluorescent treponemal antibody absorption test
ELISA
1. Treponema Pallidum Immobilization – TPI
An antibody present in the serum of a syphilitic patient, in the presence of complement, causes the immobilization of actively motile Treponema pallidum obtained from testes of a rabbit infected with syphilis.
Cumbersome and expensive, no longer used in US.
2. Treponema pallidum hemagglutination (TPHA)
Adapted to microtechniques (MHA-TP)
Tanned sheep RBCs are coated with T. pallidum antigen from Nichol’s strain.
Agglutination of the RBCs is a positive result.
Based on the agglutination of colored gelatin particle carriers sensitized with T. pallidum antigen.
Patient sera incubated with sensitized particles in microtiter wells and unsensitized gelatin particles in control wells.
Patient sera containing specific antibodies will react only with the antigen to form a smooth mat of agglutinated particles.
A compact button formed by the settling of the non-agglutinated particles in the microtiter wells containing sensitized particles indicates lack of specific antibody in patient sera (-).
If agglutination is seen with both sensitized and unsensitized particles, nonspecific agglutination is indicated.
3. Positive FTA Test for Syphilis Viewed with a Flourescent Microscope
4. Fluorescent Treponemal Antibody Absorption Test (FTA-ABS)
Diluted, heat inactivated serum added to Reiter’s strain of T. pallidum to remove cross reactivity due to other Treponemes.
Slides are coated with Nichol’s strain of T. pallidum and add absorbed patient serum.
Slides are washed, and incubated with antibody bound to a fluorescent tag.
After washing the slides are examined for fluorescence.
Requires experienced personnel to read.
Highly sensitive and specific, but time consuming to perform.
In the diagnosis of the primary and secondary stages of syphilis, lumbar puncture (spinal tap) is needed in some cases. A lumbar puncture may be done in adults:
If there is evidence of tertiary syphilis (such as aortic aneurysm, gumma, or iritis) or if neurosyphilis is suspected.
If penicillin or another recommended antibiotic cannot be used for treatment in latent syphilis. If the appropriate antibiotic cannot be used, it is important to find out whether fluid from the spinal column and brain (cerebrospinal fluid) is infected, because specific treatment methods are needed to effectively treat infected cerebrospinal fluid.
Infected with HIV. Some experts recommend lumbar puncture in all HIV-infected people who have syphilis.
To check whether a person is cured of neurosyphilis.
Iewborns and children, a lumbar puncture may be done if:
There are signs of congenital syphilis.
The child’s mother had syphilis and she was not treated, was not treated adequately, or was treated after the 20th week of pregnancy.
The child’s mother was treated with an antibiotic other than penicillin.
Additional testing should be done to find out if other sexually transmitted infections are present, especially:
Human immunodeficiency virus (HIV). People who have syphilis have a greater chance of being exposed to HIV.
The diagnosis of syphilis can be delayed or complicated because its symptoms are very similar to those of many other diseases and are sometimes not recognized. Syphilis has historically been called “the great imitator.”
GONORRHEA
1. http://emedicine.medscape.com/article/218059-overview
2. http://www.youtube.com/watch?v=Eww8tGkqGRw
Gonorrhea, an important public health problem and the second most commootifiable disease in the United States, is a purulent infection of mucous membrane surfaces caused by the gram-negative diplococcus Neisseria gonorrhoeae.
Neisseria gonorrhoeae
n Gram-negative diplococcus
n Infects non-cornified epithelium
n Second most common bacterial STD
n Estimated >1 million US cases per year
n Incidence highest among adolescents and young adults
n Causes a range of clinical syndromes
Many infections are asymptomatic.
In women, the cervix is the most common site of gonorrhea, resulting in endocervicitis and urethritis, which can be complicated by pelvic inflammatory disease (PID). In men, gonorrhea causes anterior urethritis. Gonorrhea can also spread throughout the body to cause localized and disseminated disease. Complications also include ectopic pregnancy and increased susceptibility to human immunodeficiency virus (HIV) infection. Most commonly, the term gonorrhea refers to urethritis and/or cervicitis in a sexually active person.
Gonococcal infections following sexual and perinatal transmission are a major source of morbidity worldwide. In the developed world, where prophylaxis for neonatal eye infection is standard, the vast majority of infections follow genitourinary mucosal exposure.
Gonococcemia is defined as the presence of N gonorrhoeae in the bloodstream, which can lead to the development of disseminated gonococcal infection (DGI). Gonococcemia occurs in about 0.5-3% of patients with gonorrhea (see the image below).
TRANSMISSION OF GONORRHEA
• Transmission is almost exclusively by sexual contact
• Disseminated gonococcal infection (DGI) may occur
• Transmission by inanimate objects is very rare
• Vertical transmission during parturition
Pathophysiology
The pathophysiology of N gonorrhoeae and the relative virulence of different subtypes depend on the antigenic characteristics of the respective surface proteins. Certain subtypes are able to evade serum immune responses and are more likely to lead to disseminated (systemic) infection.
Well-characterized plasmids commonly carry antibiotic-resistance genes, most notably penicillinase. Plasmid and nonplasmid genes are transmitted freely between different subtypes. The ensuing exchange of surface protein genes results in high host susceptibility to reinfection. The exchange of antibiotic resistance genes has led to extremely high levels of resistance to beta-lactam antibiotics. Fluoroquinolone resistance has also been documented on multiple continents and in widespread populations within the United States.
Infection of the lower genital tract, the most common clinical presentation, primarily manifests as male urethritis and female endocervicitis. Infection of the pharynx, rectum, and female urethra occur frequently but are more likely to be asymptomatic or minimally symptomatic. Retrograde spread of the organisms occurs in as many as 20% of women with cervicitis, often resulting in pelvic inflammatory disease (PID), with salpingitis, endometritis, and/or tubo-ovarian abscess. Retrograde spread can lead to frank abdominal peritonitis and to a perihepatitis known as Fitz-Hugh-Curtis syndrome.
Long-term sequelae of PID, such as tubal factor infertility, ectopic pregnancy, and chronic pain, may occur in up to 25% of affected patients. Epididymitis or epididymo-orchitis may occur in men after gonococcal urethritis. Lower genital infection is a risk factor for the presence of other sexually transmitted diseases (STDs), including human immunodeficiency virus (HIV).
Conjunctivitis can occur in adults, as well as children, following direct inoculation of organisms (usually as a result of hand-eye inoculation in adults) and can lead to blindness.
Disseminated gonococcal infection
Disseminated gonococcal infection (DGI) occurs following approximately 1% of genital infections. Patients with DGI may present with symptoms of rash, fever, arthralgias, migratory polyarthritis, septic arthritis, tendonitis, tenosynovitis, endocarditis, or meningitis.
N gonorrhoeae organisms spread from a primary site, such as the endocervix, the urethra, the pharynx, or the rectum, and disseminate to the blood to infect other end organs. Usually, multiple sites, such as the skin and the joints, are infected. Neisserial organisms disseminate to the blood due to a variety of predisposing factors, such as host physiologic changes, virulence factors of the organism itself, and failures of the host’s immune defenses.
For example, changes in the vaginal pH that occur during menses and pregnancy and the puerperium period make the vaginal environment more suitable for the growth of the organism and provide increased access to the bloodstream. (Three fourths of the cases of DGI occur in women; susceptibility is increased if the primary mucosal infection occurs during menstruation or pregnancy.)
Defects in the host’s immune defenses are also involved in the pathophysiology, with certain patients more likely to develop bacteremia. Specifically, patients with deficiency in terminal complement components are less able to combat infection, as complement plays an important role in the killing of neisserial organisms. As many as 13% of patients with DGI have a complement deficiency.
A study of 22 patients with DGI revealed that total serum complement activity was greater than 25% below the normal mean. Other causes of immunocompromise (eg, HIV, SLE) also predispose to dissemination of infection.
Etiology
N gonorrhoeae is a gram-negative, intracellular, aerobic diplococcus; more specifically, it is a form of diplococcus known as the gonococcus. N gonorrhoeae is spread by sexual contact or through vertical transmission during childbirth. It mainly affects the host’s columnar or cuboidal epithelium. Virtually any mucous membrane can be infected by this microorganism. The physiologic ectopy of the squamocolumnar junction onto the ectocervix in the adolescent female is one factor that causes particular susceptibility to this infection.
Gonococci attach to the host mucosal cell (pili and Opa proteins play major roles) and, within 24-48 hours, penetrate through and between cells into the subepithelial space. A typical host response is characterized by invasion with neutrophils, followed by epithelial sloughing, formation of submucosal microabscesses, and purulent discharge. If left untreated, macrophage and lymphocyte infiltration replaces the neutrophils. Some gonococcal strains cause an asymptomatic infection, leading to an asymptomatic carrier state in persons of either sex.
The ability to grow anaerobically allows gonococci, when mixed with refluxed menstrual blood or attached to sperm, to secondarily invade lower genital structures (vagina and cervix) and progress to upper genital organs (endometrium, salpinx, ovaries).
Gonococcal infection usually follows mucosal inoculation during vaginal, anal, or oral sexual contact or perinatally.
Sexually transmitted infection
Gonococcal infection usually follows mucosal inoculation during vaginal, anal, or oral sexual contact. It also may be caused by inoculation of mucosa by contaminated fingers or other objects. Transmission through penile-rectal contact is fairly efficient.
The risk of transmission of N gonorrhoeae from an infected woman to the urethra of her male partner is approximately 20% per episode of vaginal intercourse and rises to 60-80% after 4 or more exposures. In contrast, the risk of male-to-female transmission approximates 50-70% per contact, with little evidence of increased risk with more sexual exposures.
Persons who have unprotected intercourse with new partners frequently enough to sustain the infection in a community are defined as core transmitters.
Neonatal and pediatric gonococcal infection
Neonatal gonococcal infection may follow conjunctival infection, which is obtained during passage through the birth canal. In addition, direct infection may occur through the scalp at the sites of fetal monitoring electrodes.
In children, infection may occur from sexual abuse by an infected individual or possibly nonsexual contact in the child’s household or in institutional settings.
Autoinoculation
Autoinoculation can occur when a person touches an infected site (genital organ) and contacts skin or mucosa.
Risk factors
Risk factors for gonorrhea include the following:
Sexual exposure to an infected partner without barrier protection (eg, failure to use a condom or condom failure)[12]
Multiple sex partners
Male homosexuality
Low socioeconomic status
Minority status – Blacks, Hispanics, and Native Americans have the highest rates in the United States
History of concurrent or past STDs
Exchange of sex for drugs or money
Use of crack cocaine
Early age of onset of sexual activity
Pelvic inflammatory disease (PID) – Use of an intrauterine device (IUD)
Prognosis
With adequate early therapy, complete cure and return to normal function are the rule. Most gonococcal infections respond quickly to cephalosporin therapy. Late, delayed, or inappropriate therapy may lead to significant morbidity or, on rare occasions, death.
Complications in males
Urethral strictures secondary to gonococcal infection in men are less common than previously thought. Some strictures in the preantibiotic era likely resulted from treatment by urethral irrigation using caustic compounds rather than from the gonorrhea itself.
Other complications, such as penile lymphangitis, periurethral abscess, acute prostatitis, seminal vesiculitis, and infection of the Tyson and Cowper glands, are now rare.
Gonococcal Urethritis
n Incubation 2-7 days
n Abrupt onset of severe dysuria
n Purulent urethral discharge
n Most urethral infections symptomatic
Complications in females
Tubal scarring and infertility are the major complications of gonococcal infection in females. The incidence of involuntary infertility is estimated at 15% after one attack of pelvic inflammatory disease (PID) and approximately 50%-80% after 3 attacks. (However, infertility may be more common after chlamydial PID than after gonococcal PID, presumably because the more acute inflammatory signs associated with gonorrhea prompt women to seek diagnosis and treatment sooner.)
Failure to diagnose PID can result in acute morbidity, including tuboovarian abscess, endometritis, Fitz-Hugh-Curtis syndrome (perihepatitis), and other chronic sequelae. Perihepatitis secondary to gonorrhea presents as right upper quadrant pain and nausea.
The incidence of ectopic pregnancy is increased from 7-fold to 10-fold in women with previous salpingitis, with resultant increased fetal and maternal mortality rates.
Gonococcal infections in women may also manifest as gonococcal urethritis or infection of periurethral (Skene) or Bartholin glands.
Gonococcal Cervicitis
Gonococcal Bartholinitis
Bartholin’s Abscess
Pelvic inflammatory disease
PID is generally the most feared complication of gonococcal infection, because it is one of the leading causes of female infertility and often leads to hospitalization. This can be devastating to any woman, especially an adolescent who potentially has many years of childbearing ahead of her. In a 2011 study, female adolescents with PID were more likely than older women to have a rapid recurrence of PID or to become pregnant despite reporting more consistent condom use.[26]
Tubo-ovarian abscess and, rarely, tubal perforation with peritonitis and death, can occur, especially if the tubo-ovarian abscess was recurrent. Females with recurrent PID have high rates of ectopic pregnancy and infertility.
Epididymitis and orchitis
Epididymitis and orchitis occur infrequently in males who go untreated. These conditions usually respond well to the same antibiotics used for uncomplicated urethritis, but the drugs are administered for a longer course.
Arthritis
Gonorrhea is the most common cause of arthritis in the adolescent. However, arthritis (septic or reactive) is a rare complication of this disease.
Because it mimics septic arthritis, excluding the possibility of gonococcal infection in any adolescent with acute onset of pyogenic arthritis is important. Adequate diagnosis may require culturing extraarticular sites for N gonorrhoeae.
Additional complications
Corneal scarring after ocular gonococcal infections
Destruction of cardiac valves in gonococcal endocarditis
Death from congestive heart failure related to endocarditis
Central nervous system (CNS) complications of gonococcal meningitis
It has been suggested that a person with a gonococcal infection may be at a 3- to 5-fold increased risk of acquiring HIV infection, if exposed to the virus.
DGI is an acute illness that causes fever, asymmetrical polyarthralgias, and skin pustules overlying small joints in patients with gonorrhea. Disseminated infection may also lead to meningitis or endocarditis.
Iewborns, vertical transmission can cause conjunctivitis, known as ophthalmia neonatorum, and permanent damage and blindness, if untreated.
Oral sex with an infected partner can result in pharyngitis, and, similarly, anal infection can arise from anal sex or local spread from a vaginal source.
Clinical Presentation
History
The incubation period for gonorrhea is usually 2-7 days after exposure to an infected partner. In all patients who present with a possible STD, the history should include the following:
· Past history of STDs (including HIV infection and viral hepatitis)
· Treatment history for known STDs
· Known symptoms of STDs in current or past sexual partners
· Type of contraception used
· Any history of sexual assault
In women, the history should also include the date of the last menstrual period and the details of parity, including any history of ectopic pregnancies.
Female genitourinary tract
The most common site of gonococcal infection in women is the endocervix (80%-90%), followed by the urethra (80%), rectum (40%), and pharynx (10%-20%). If symptoms develop, they often manifest within 10 days of infection.
Major symptoms include vaginal discharge, dysuria, intermenstrual bleeding, dyspareunia (painful intercourse), and mild lower abdominal pain.
When gonococcal cervicitis is either asymptomatic or unrecognized, the patient may progress to PID, often in proximity to a menstrual period. PID may also be asymptomatic or silent and occurs in 10-20% of infected women.
Symptoms of PID include the following:
· Lower abdominal pain (most consistent symptom of PID)
· Increased vaginal discharge or mucopurulent urethral discharge
· Dysuria (usually without urgency or frequency)
· Cervical motion tenderness
· Adnexal tenderness (usually bilateral) or adnexal mass
· Intermenstrual bleeding
· Fever, chills, nausea, and vomiting (less common)
Acute perihepatitis (Fitz-Hugh-Curtis syndrome) occurs primarily through direct extension of N gonorrhoeae or Chlamydia trachomatis from the fallopian tube to the liver capsule and overlying peritoneum.
Vaginal discharge from endocervicitis is the most common presenting symptom of gonorrhea and is usually described as thin, purulent, and mildly odorous. Many patients have minimal or no symptoms from gonococcal cervicitis. Dysuria or a scant urethral discharge may be due to urethritis accompanying cervicitis.
Pelvic or lower abdominal pain suggests ascending infection of the endometrium, fallopian tubes, ovaries, and peritoneum. Pain may be midline, unilateral, or bilateral. Fever, nausea, and vomiting may be present. The possibility of ectopic pregnancy should always be considered in patients with pelvic or lower abdominal pain.
Right upper quadrant pain from perihepatitis (Fitz-Hugh-Curtis syndrome) may occur following the spread of organisms upward along peritoneal planes.
Rectal infection is often asymptomatic, but rectal pain, pruritus, tenesmus, and rectal discharge may be present if the rectal mucosa is infected. Bloody diarrhea may also occur. Rectal infection may occur from anal intercourse or, in women, by local spread of the organism.
Male genitourinary tract
In men, urethritis is the major manifestation of gonococcal infection. Initial characteristics include burning upon urination and a serous discharge. A few days later, the discharge usually becomes more profuse, purulent, and, at times, blood-tinged.
Acute epididymitis may also be caused by N gonorrhoeae or C trachomatis, especially in men younger than 35 years. This is usually unilateral and often occurs in conjunction with a urethral exudate. The classic presentation of epididymitis is of unilateral pain and swelling localized posteriorly within the scrotum.
Urethral strictures due to gonococcal infection are now uncommon in the antibiotic era, but they can present with a decreased and abnormal urine stream, as well as with the secondary complications of prostatitis and cystitis.
Another manifestation of gonorrhea, rectal infection, may present with pain, pruritus, discharge, or tenesmus.
Sex-independent manifestations
Men and women may exhibit gonococcal infection of the pharynx, rectum, and eye. Gonococcal pharyngitis is most commonly acquired during orogenital contact, with fellatio predisposing to infection more so than cunnilingus. Pharyngitis is often asymptomatic; however, it may present as exudative pharyngitis with cervical lymphadenopathy.
Although rectal cultures are positive for gonorrhea in up to 40% of women with cervical gonorrhea (a similar percentage noted in infected homosexual men), symptoms of proctitis are unusual.
Eye involvement in adults occurs by autoinoculation of gonococci into the conjunctival sac from a primary site of infection, such as the genitals, and is usually unilateral. The most common form of presentation is a purulent conjunctivitis, which may rapidly progress to panophthalmitis and loss of the eye unless promptly treated.
Neonates
Ieonates, bilateral conjunctivitis (ophthalmia neonatorum) often follows vaginal delivery from an untreated, infected mother. However, transmission to the newborn can also occur in utero or in the postpartum period.
Symptoms of gonococcal conjunctivitis include eye pain, redness, and a purulent discharge. Neonates may also acquire pharyngeal, respiratory, or rectal infection or disseminated gonococcal infection (DGI).
The organism can cause permanent injury to the eye very quickly. Prompt recognition and treatment are essential to avoid blindness. Blindness due to neonatal gonococcal infection is a serious problem in developing countries but is now uncommon in the United States and in other countries where neonatal conjunctival prophylaxis with antimicrobial therapy is routine. Nevertheless, infants of mothers with untreated infections, poor prenatal care, and unmonitored births continue to be at risk.
Direct infection with N gonorrhoeae ieonates may also occur through the scalp at the sites of fetal monitoring electrodes.
Disseminated gonococcal infection
The symptoms of DGI vary greatly from patient to patient. By the time the symptoms of DGI appear, many patients no longer have any localized symptoms of mucosal infection.
The classic presentation of DGI is an arthritis dermatitis syndrome. Joint or tendon pain is the most common presenting complaint in the early stage of infection. About 25% of patients with DGI complain of pain in a single joint, but many other patients describe migratory polyarthralgia, especially of the knees, elbows, and more distal joints. Patients may also have tenosynovitis; the early tenosynovitis most commonly affects the flexor tendon sheaths of the wrist or the Achilles tendon (“lovers’ heels”).
Skin rash is a presenting complaint in approximately 25% of patients, but a careful examination will reveal a rash in most patients with DGI. The rash is usually found below the neck and may also involve the palms and soles.
The dermatitis consists of lesions varying from maculopapular to pustular, often with a hemorrhagic component. Lesions usually number 5-40, are peripherally located, and may be painful before they are visible. Fever is common but rarely exceeds 39°C.
Gonococcal pharyngitis
• Is seen in both men and women who have had oral sexual exposure
• Impossible clinically to differentiate from pharyngitis caused by other bacteria – must culture
• Left untreated it will resolve within 6 weeks
Ocular and periocular symptoms
Ocular and periocular manifestations of gonorrhea include the following:
- Anterior chamber – Cellular reaction, hypopyon, endophthalmitis
- Conjunctiva – Chemosis, acute purulent exudate, hemorrhages
- This patient presented with gonococcal urethritis, which became systemically disseminated, leading to gonococcal conjunctivitis of the right eye. Courtesy of the CDC/Joe Miller, VD.
- Cornea – Punctate epithelial keratitis; marginal, sterile stromal infiltrates; epithelial defects; infectious stromal infiltrates; stromal ulcerations; descemetocele; perforation; opacification
- Lids – Erythema, edema
Diagnostic Considerations
When evaluating a female patient with suspected gonococcal infection, also consider bacterial vaginosis, vaginitis, ectopic pregnancy, pregnancy, tubo-ovarian abscess, endometriosis, and mucopurulent cervicitis. In men, consider epididymitis, orchitis, and testicular torsion.
Other conditions that should be considered include the following:
- Urinary tract infections
- Pharyngitis; hepatitis
- Herpes simplex urethritis
- Rat-bite fever
- Inflammatory and septic arthritis
- Nongonococcal conjunctivitis, endocarditis, meningitis, and urethritis
References
1. Holder NA. Gonococcal infections. Pediatr Rev. Jul 2008; 29(7):228-34. [Medline].
2. Ilina EN, Vereshchagin VA, Borovskaya AD, Malakhova MV, Sidorenko SV, Al-Khafaji NC, et al. Relation between genetic markers of drug resistance and susceptibility profile of clinical Neisseria gonorrhoeae strains. Antimicrob Agents Chemother. Jun 2008;52(6):2175-82. [Medline].
3. Centers for Disease Control and Prevention. 2009 Sexually Transmitted Diseases Surveillance: Gonorrhea. Available at http://www.cdc.gov/STD/stats09/gonorrhea.htm. Accessed 5/27/11.
4. CDC, Workowski KA, Berman SM. Sexually transmitted diseases treatment guidelines, 2010. MMWR Recomm Rep. 2010, Dec 17;59(RR-12):1-110. [Full Text].
6. Centers for Disease Control and Prevention (CDC). Gonococcal Infections. Available at http://www.cdc.gov/std/treatment/2010/gonococcal-infections.htm. Accessed May 21 2012.
7. Unemo M, Shipitsyna E, Domeika M. Recommended antimicrobial treatment of uncomplicated gonorrhoea in 2009 in 11 East European countries: implementation of a Neisseria gonorrhoeae antimicrobial susceptibility programme in this region is crucial. Sex Transm Infect. Nov 2010;86(6):442-4. [Medline].
8. National Institute of Allergy and Infectious Diseases. Gonorrhea. Available at http://www.niaid.nih.gov/topics/gonorrhea/Pages/default.aspx. Accessed August 16, 2011.
9.World Health Organization. Initiative for Vaccine Research (IVR). Available at http://www.who.int/vaccine_research/diseases/soa_std/en/index2.html. Accessed August 16, 2011.
10.Trent M, Haggerty CL, Jennings JM, Lee S, Bass DC, Ness R. Adverse adolescent reproductive health outcomes after pelvic inflammatory disease. Arch Pediatr Adolesc Med. Jan 2011;165(1):49-54. [Medline].
11. Centers for Disease Control and Prevention (CDC). 2010 Sexually Transmitted Diseases Surveillance: Gonorrhea. Available at http://www.cdc.gov/std/stats10/gonorrhea.htm. Accessed May 21 2012.
12. Bleich AT, Sheffield JS, Wendel GD Jr, Sigman A, Cunningham FG. Disseminated gonococcal infection in women. Obstet Gynecol. Mar 2012;119(3):597-602. [Medline].
13. García PJ, Holmes KK, Cárcamo CP, et al. Prevention of sexually transmitted infections in urban communities (Peru PREVEN): a multicomponent community-randomised controlled trial. Lancet. Mar 24 2012;379(9821):1120-8. [Medline]. [Full Text].
14. Wada K, Uehara S, Mitsuhata R, et al. Prevalence of pharyngeal Chlamydia trachomatis and Neisseria gonorrhoeae among heterosexual men in Japan. J Infect Chemother. Apr 11 2012;[Medline].
15. Update to CDC’s Sexually Transmitted Diseases Treatment Guidelines, 2010: Oral Cephalosporins No Longer a Recommended Treatment for Gonococcal Infections. MMWR Morb Mortal Wkly Rep. Aug 10 2012;61:590-4. [Medline]. [Full Text].
Human Immunodeficiency Virus (HIV) Infection
1.http://emedicine.medscape.com/article/211316-overview
2.http://www.youtube.com/watch?v=hdgNnXLY8LU
http://www.emedicinehealth.com/slideshow_pictures_hiv_aids_myths_and_facts/article_em.htm
is a progressive process that mostly leads to the development of Acquired Immune Deficiency Syndrome(AIDS).
Ú The first cases of AIDS occurred in the USA in 1981.
Ú AIDS is caused by the virus HIV.
Ú HIV is part of a family or group of viruses called lentiviruses.
Where do viruses come from?
Three major mechanisms have been proposed for the evolution of viruses:
1. ‘Escaped gene’ theory:
Viruses derive from normal cellular nucleic acids and ‘gain independence’ from the cell. DNA viruses could come from plasmids or transposable elements, while RNA viruses could derive from mRNA.
2. Regressive theory:
Gradual degeneration of procaryotes living parasitically in eucaryotic cells. Enveloped forms such as poxviruses are most likely to have been formed in this way.
3. Coevolution theory:
Independent evolution alongside cellular forms from primordial soup. Some scientists consider it unlikely that the same mechanism could account for the diversity of viruses we see today, and therefore propose that viruses must have evolved many times over. A study published in 2004 conversely proposes that all viruses share a common ancestor and may even have developed before cellular life forms.
HIV Disease Clinical Presentation
History
The history should be carefully taken to elicit possible exposures to human immunodeficiency virus (HIV).
Risk factors include the following:
Unprotected sexual intercourse, especially receptive anal intercourse (8-fold higher risk of transmission)
A large number of sexual partners
Prior or current sexually transmitted diseases (STDs): Gonorrhea and chlamydia infections increase the HIV transmission risk 3-fold, syphilis raises the transmission risk 7-fold, and herpes genitals raises the transmission risk up to 25-fold during an outbreak
Sharing of intravenous drug paraphernalia
Receipt of blood products (before 1985 in the United States)
Mucosal contact with infected blood or needle-stick injuries
Maternal HIV infection (for newborns, infants, and children): Steps taken to reduce the risk of transmission at birth include cesarean delivery and prenatal antiretroviral therapy in the mother and antiretroviral therapy in the newborn immediately after birth.
VIRAL INFECTIONS
http://www.hivguidelines.org/clinical-guidelines/infants-children/dermatologic-manifestations/
A. Herpes Simplex
Severe, chronic, or recurrent infection with herpes simplex virus (HSV) can be a complication of HIV infection.
This series demonstrates a severe primary herpes stomatitis in an 18 year old male. Note the crusting at the vermillion border on both upper and lower lips, as well as the crusting herpes blister on the upper right lip. Also note the extremely red and swollen gingiva in all three images.
B. Herpes Zoster (Varicella-Zoster Virus)
Severe hemorrhagic and necrotic lesions may extend over several dermatomes, or disseminated allover the body.
C. Molluscum Contagiosum
Widespread molluscum contagiosum can occur in HIV-infected children but has been rarely noted since the introduction of HAART.
D. Human Papillomavirus Infection
Unusual location lip wart in HIV. Used with permission from Dr M Whitfeld of St Vincent’s Hospital, Sydney.
FUNGAL INFECTIONS
http://www.hivguidelines.org/clinical-guidelines/infants-children/dermatologic-manifestations/
A. Candidiasis
Candidiasis may be an initial presentation of HIV disease. Oral thrush and recalcitrant monilial diaper dermatitis are the most common mucocutaneous manifestations of HIV infection in children.
Candidiasis (Moniliasis, Thrush) This HIV/AIDS patient presented with a secondary oral pseudomembranous candidiasis infection. Courtesy of Centers for Disease Control and Prevention/Sol Silverman, Jr., DDS
Angular Cheilitis
Kaposi Sarcoma
Ú Red, purplish or brown colored maculas, nodules or plaque.
Ú Common sites are trunk, legs, face and oral cavity.
Viral associated signs of HIV
Hairy Leukoplakia
Primary Care of the HIV-Infected Adult
I. Initial evaluation
The initial evaluation of the HIV-infected adult should include an:
Assessment of the patient’s past medical history.
Current symptoms and treatments.
A complete physical examination.
Laboratory testing.
1. Previous conditions
1. Prior medical conditions related to HIV infection should be assessed:
Mucocutaneous candidiasis.
Oral hairy leukoplakia.
Hepatitis.
Pneumonia.
Sexually transmitted diseases.
Tuberculosis.
Varicella-zoster.
Herpes simplex virus lesions.
Opportunistic infections.
2. Dates and results of earlier tuberculin skin tests should be obtained. Women should be are asked about dates and results of Pap smears. Previous immunizations and antiretroviral therapy should be documented.
2. Current conditions and symptoms
Fever.
Night sweats.
Unexplained weight loss.
Lymphadenopathy.
Oral discomfort.
Visual changes.
Unusual headaches.
Swallowing difficulties.
Diarrhea.
Dermatologic conditions.
Respiratory and neurologic symptoms are suggestive of opportunistic infections or a malignant process.
3. Social history includes
Information on past and present drug use.
Sexual behavior.
Dietary habits.
Household pets.
Employment.
And current living situation.
4. Physical examination
Weight.
Temperature.
Skin.
Oropharynx.
Fundi.
Lymph nodes.
Lungs.
Abdominal organs.
Genitalia.
Rectum.
Nervous system should be assessed.
4. Laboratory tests
A. Complete blood count, chemistry profile, and serologic studies for
Syphilis (rapid plasma reagin or VDRL).
Toxoplasma gondii (IgG antibody).
Hepatitis B (surface antigen, core antibody) should be obtained.
B. Patients should have a tuberculin skin test unless they have been reactive in the past or have been treated for the disease. In HIV-infected persons, a positive test is 5 mm or more of indurations.
C. A baseline chest film is useful because many opportunistic pulmonary infections present with very subtle radiographic findings. A chest radiograph may suggest unrecognized tuberculosis.
D. CD4+ counts assist in determination of the degree of immunologic damage, assess risk of opportunistic complications, and guide the use of prophylaxis against infections.
E. HIV RNA levels
1. Quantitation of plasma HIV RNA (viral load), a marker of the rate of viral replication, is useful in determining prognosis. It is used to estimate the risk of disease progression and to aid in making antiretroviral therapy decisions.
F. Viral markers
• The virus can be cultured (but the technique is dangerous, labor intensive and not sensitive).
• Detection of p24 antigen (30% of patients in ARS are positive).
• Polymerase chain reaction (PCR) to detect the virus is a highly sensitive method.
G.Acute Retroviral Syndrome (ARS)
Response, which is detected by ELISA or Western Blot technique, occurs much later.
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