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Personal Repro > Session 4: Infections of the Genital Tract > Flashcards

Session 4: Infections of the Genital Tract Flashcards

1
Q

What is the difference between an STI and STD? Describe other infections of the genital tract

A

[*] Sexually transmitted infection (STI):

  • Includes both symptomatic and asymptomatic cases
  • Sexual activity is the principle mode of transmission

[*] Sexually transmitted disease (STD):

  • Symptomatic cases only​

[*] There are infections when sexual activity is a possible mode of transmission (e.g. blood borne viruses – Hep B, Hep C and HIV)

[*] Sexual transmission of intestinal pathogens can also occur especially in men who engage in MSM.

  • E.g. salmonella, shigella, giardia, entamoeba, etc
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2
Q

Describe the epidemiology of sexually transmitted infections (STIs) and other infections of the genital tract.

A
  • National data is available from Genitourinary Medicine (GUM) clinics, which notify sexually transmitted diseases centrally.

[*] Open access, walk-in clinics that offer free, confidential sexual health services including diagnosis and treatment of STIs

[*] The data from the GUM services will underestimate the true incidence of STIs as patients may be seen in a variety of other settings, i.e. GP surgeries, family planning clinics etc

Epidemiology data is also available from communicable disease surveillance centres

[*] Notified of aggregate data via regular returns from GUM clinics and receive data on gonorrhoea, genital chlamydia, genital herpes and syphilis through voluntary or statutory reporting.

National data is also available from the National Chlamydia Screening Programme.

[*] The greatest impact of STIs in young heterosexuals and men who have sex with men (MSM). The latter groups has seen a significant rise in gonorrhoea diagnoses.

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3
Q

Who is at risk of STIs?

A

At risk groups

[*] Young people

[*] Minority ethnic groups

[*] Those affected by poverty and social exclusion

[*] Low socio-economic status groups

[*] Those with poor educational opportunities

[*] Unemployed people

[*] Individuals born to teenage mothers

[*] Specific aspects of sexual behaviour

  • Age at first sexual intercourse
  • Number of partners
  • Sexual orientation
  • Unsafe sexual activity

[*] Men who engage in MSM

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4
Q

What morbidities are associated with STIs?

A

[*] Pelvic Inflammatory Disease (PID)

[*] Impaired fertility

[*] Reproductive tract cancers

[*] Risk of infection with blood-borne viruses – HBV, HIV

[*] Risk of congenital or peripartum infection of neonate

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5
Q

List the most common sexually transmitted infections, identifying the infecting organism in each case.

A

*Molluscum contagiosum is an example of a disease can be transmitted by sexual activity but is more commonly seen in young children (umbilicated lesions) (not sexually transmitted).

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6
Q

Provide a differential diagnosis for Genital skin and mucous membrane lesions

A

[*] Genital ulcers – HSV (Herpes Simplex Virus), syphilis, chanchroid (Haemophilus ducreyi)

[*] Vesicles of Bullae – HSV

[*] Genital papules – transient manifestations of STIs, condylomata acuminate (anogenital warts), umbilicated lesions of Molluscum contagiosum virus

[*] Genital ulcers – number, size, tenderness, base, edge

[*] Anogenital warts

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7
Q

Provide a differential diagnosis for Urethritis

A

Urethritis – Discharge, Dysuria, Frequency

[*] Gonococcal urethritis

[*] NGU (Non-gonococcal urethritis) – Chlamydia trachomatis, ureaplasma, mycoplasma, trichomonas HSV

[*] Non-specific urethritis

[*] Post-gonococcal urethritis

[*] Non-infectious urethritis

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8
Q

Provide a differential diagnosis for Vulvo-vaginitis and Cervicitis

A

[*] Vulvovaginitis – candiasis, trichomoniasis, staphylococcal, foreign body, HSV

[*] Cervicitis – C. trachmatis, N. gonorrhoeae, HSV, HPV

[*] Bartholinitis – polymicrobial infections with endogenous flora or rarely STIs

[*] Bacterial vaginosis (BV) – common cause of vaginal symptoms such as discharge, irritation and odour. Laboratory diagnosis is based on a vaginal pH of greater than 4.5, a pungent odour with the KOH (‘whiff test’), and the presence of clue cells on a wet mount lacking many PMNs (granulocytes). BV is postulated to result from a synergistic infection involving the overgrowth of normal flora including Gardnerella vaginalis

  • Symptoms: vaginal discharge, odour, itch, dyspareunia, soreness
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9
Q

Provide a differential diagnosis for Infections of the female pelvis

A

[*] Pregnancy related – chorioamnionitis, post-partum endometriosis, episiotomy infections, puerperal ovarian vein thrombophlebitis, osteomyelitis pubis

[*] Pelvic Inflammatory Disease (PID)

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10
Q

Provide a differential diagnosis for Prostatitis, Epididymitis and Orchitis

A

[*] Prostatitis – acute bacterial prostatitis, chronic bacterial prostatitis, chronic pelvic pain syndrome

[*] Epididymitis – non-specific bacterial epididymitis, sexually transmitted epididymitis

[*] Orchitis – viral (mumps, coxsackie B) orchitis, pyogenic bacterial orchitis

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11
Q

Describe recent trends in the incidence of sexually transmitted infections

A

Data for the year 1990 to 1999 shows a gradual and sustained increase in STIs since 1995.

  • Uncomplicated Gonorrhoea- 102% increase
  • Genital Chlamydia – 107% increase
  • Infectious Syphilis – 57% increase
  • GUM clinic workload – 34% increase

[*] Prior to this there had been a decline in or at least plateauing of numbers of diagnoses of many STIs. This is thought to possibly reflect changes in sexual behaviour in response to the HIV epidemic.

[*] The reason for the increase since 1995 is thought to be due to multiple factors – increased transmission, acceptability of GUM services => increased GUM attendance, greater public, medical and national awareness (e.g. with campaigns) and development in improved diagnostic methods including screening programs (allowing us to identify pathogens in more patients).

[*] People are much more aware of the benefits of going to GUM clinics

Additionally many infections are asymptomatic, for example it is thought that in the case of chlamydia only 10% of cases may attend GUM services.

NB: Very large portion men who engage in MSM have Syphilis and/or gonorrhoea

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12
Q

Describe the burden of STIs

A

[*] Both acute and chronic/relapsing infections

[*] Stigma – impact on diagnosis and tracing contacts

[*] Consequent pathology

  • Pelvic inflammatory disease and infertility
  • Reproductive tract cancers
  • Disseminated infections
  • Transmission to foetus/neonate
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13
Q

Describe the diagnosis of STIs

A

[*] Patient presents with genital lesions/problems to GP or GUM clinic

  • Ulcers, vesicles, warts etc
  • Urethral discharge or pain
  • Vaginal discharge

[*] Clinicians note non-genital clinical features suggestive of STI

  • Disseminated disease

[*] Detection of asymptomatic cases (contact tracing /screening). In pregnant females, for certain infections there is a high risk of transmission across the placenta.

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14
Q

Describe the management of STIs

A

[*] Treatment preferably single dose/short dose (to avoid compliance/adhesion issues)

[*] Co-infections are common – screen and consider empiric treatment for other STIS.

[*] Consensus UK national guidelines: http://www.bashh.org/guidelines

[*] Contact tracing – patient and public health management

[*] Sexual health education, advice on contraception and detailed instruction on the practice and need for safer sex (recognition of risk to other individuals etc)

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15
Q

Describe Chlamydiae

A
  • Chlamydiae are obligate intracellular bacteria. As such, they do not grow on routine laboratory media, which has implications for diagnostic methods.
  • Non-specific genital chlamydial infections

[*] Serotypes D - K

  • The infective form is the elementary body, which develops within the host cell into the reticulate body. The reticulate body replicates eventually reverting back to elementary bodies, which leave the cell to infect other cells.
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16
Q

Describe Chlamydial infection in the female

A

[*] Commonly asymptomatic but can cause: urethritis, cervicitis, salpingitis, peripheaptitis

[*] The organism infects and replicates within the epithelium of the cervix and urethra.

[*] An ascending infection with the involvement of the upper genital tract occurs and can result in clinical or subclinial pelvic inflammatory disease (PID) presenting in endometritis or salpingitis.

[*] Perihepatitis is a rare complication.

[*] Cervical Infection: the majority are asymptomatic but it is an important cause of mucopurulent cervicitis

[*] Urethral infection => urethritis: the ‘acute urethral’ syndrome is now recognised as a sequel of urethral infection, and presents as dysuria and frequency, most common in young sexually active women.

[*] Ocular inoculation - conjunctivitis

[*] Complications:

  • Pelvic Inflammatory Disease: Chlamydia trachomatis is the most important cause of P.I.D. in the western world. The major complication of P.I.D. is tubal damage leading to infertility and ectopic pregnancy
  • Perihepatitis: Neisseria gonorrhoea is a well-established cause but Chlamydia trachomatis also has a role to play.
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17
Q

Describe Chlamydial infection in the male. What is Reiters syndrome?

A

[*] Usually presents as urethritis but also can be urethritis, prostatitis, proctitis and epididymitis

[*] Complications – Acute Epididymitis

  • Reiters syndrome: urethritis, conjunctivitis and arthritis are the classical triad of clinical manifestations associated with this syndrome. It predominantly occurs in male patients.
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18
Q

Describe what occurs in both female and male infections, and describe neonatal infection

A
  • Infections in men and women: ocular infections caused by Chlamydia trachomatis are common in sexually active individuals
  • Neonatal Infection: cervical infection in pregnant women in a source of Chlamydia trachomatis in the neonate. The most common infection is neonatal conjunctivitis. Untreated, this may progress to neonatal pneumonia
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19
Q

Describe the specimen collection of chlamydiae

A

Specimen Collection: with any test, quality of specimen is important. This is particularly so with Chlamydia trachomatis as it is an intra-cellular pathogen – it is essential that cells are present in the sample.

[*] Males: urethral swab (NAAT) or first catch/ first void urine (first urine voided in the morning) (NAAT)

[*] Females: endocervical swab (NAAT). It is important that any pus is first removed from the cervix and that good quality, cellular material is obtained.

  • Urine: urine may be used for molecular methods but is less sensitive than an endocervical swab. The potential value of using urine specimens is that for population screening, patients may provide their own specimens whereas an endocervical swab is time consuming, requires a trained member of staff to take the specimen and is less acceptable to the patient.

[*] Neonatal infection – conjunctival swab (NAAT)

[*] Neonates:

  • Eye swab: remove any pus. Invert eyelid and scrape conjunctiva surface to obtain cellular material.
  • Pneumonia – Serology is useful. A differential on a WCC (white cell count) may show eosinophilia.
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20
Q

How do you diagnose a Chlamydial infection?

A

[*] Obligate intracellular pathogen therefore will not grow on laboratory media.

[*] Early techniques employed tissue culture, but this is extremely expensive and could only be carried out in specialised laboratories. This has now been replaced by alternative methodologies (NAAT)

Antigen Detection: Immunofluorescence

  • Specimens may be fixed to a slide and stained with a monoclonal antibody that is tagged with fluorescein. Slides are examined under an ultraviolet microscope – drawbacks are that results are subject to observer error and the method is time consuming and therefore only suitable for small numbers of patients.
  • One advantage is that the quality of the specimen in terms of cells can be assessed using this technique.

Enzyme Immunoassays (EIA)

  • Such tests allow large numbers of specimens to be processed with relative ease.
  • Commercial kits may vary in their sensitivity and specificity but some kits have good sensitivity/specificity. The tests are relatively cheap.

Molecular Methods

  • Molecular methods (Nucleic Acid Amplification Tests – NAATs) offer high sensitivity and specificity however clinical specimens may contain inhibitors that will interfere with the assay, and commercial kits may yield significant false positives and negatives.
  • NAATs are now widely used in Chlamydia (and gonococcal) diagnosis especially in the national screening programme
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21
Q

Describe treatment for Chlamydial infections

A

Treatment: Chlamydia trachomatis contain relatively little peptidoglycan, the target for Beta-lactam antibiotics.

[*] The mainstay of treatment is the macrolides (erythromycin/clarithromycin/azithromycin) and tetracyclines (doxycycline).

[*] Erythromycin in children

[*] As conjunctivitis (both neonatal and adult) is part of a more widespread infection, this should always be treated with systemic antibiotics

Many cases asymptomatic especially in women

[*] >200,000 cases diagnosed each year

[*] Nearly half of all STIs

[*] 50% cases diagnosed in GUM

[*] 50% cases from chlamydia screening programme (national programme particularly targeted at sexually active people <25)

  • Urine (M&F) or swab (F)
  • Nucleic acid amplification test (NAAT) – dual testing (with N. gonorrhoeae) available
22
Q

Describe the organism that causes gonorrhoea infections

A

Member of the Neisseriaceae family.

They are gram-negative diplococci that will only grow on enriched media e.g. chocolate agar

23
Q

Describe gonorrhoea in females

A

Infection in female patients: the gonococcus primarily infects the cervix and urethra. This may lead to acute cervicitis with vaginal discharge and “urethral syndrome” where the urethra is infected.

[*] Clinical presentation in females: asymptomatic, endocervicitis, urethritis, PID

[*] Complications

  • Pelvic Inflammatory Disease: occasionally with tubo-ovarian abscess
  • Bartholins abscess
  • Disseminated gonococcal infection: a rare complication that affects women more than men, particularly young females - the common symptoms are pain on the joints, tenosynovitis and rash.
  • Bacteraemia, skin and joint lesions
24
Q

Describe gonorrhoea in males

A

Infection in male patients: clinical presentation - gonococcal urethritis, epididymitis, prostatitis, proctitis, pharyngitis

[*] Complications:

  • Epididymitis
  • Disseminated gonococcal infection
  • Bacteriaemia, skin and joint lesions
25
Q

Describe diagnosis of gonorrhoea including specimen collection

A

Diagnosis: fragile organism and does not survive transportation well. Ideally, specimens should be taken and plated directly onto media at the bedside (as occurs in GUM clinics)

Specimen collection: smear and culture

[*] Females: endocervical swab (throat, rectum), urethral swab, rectal and pharyngeal swab

[*] Males: urethral, rectal and pharyngeal swabs

Laboratory Diagnosis: the characteristic appearance of gram-negative diplococcic allows a presumptive diagnosis to be made on the basis of gram stain in some patients

Culture/Sensitivities

[*] Culture is far more sensitive that microscopy.

[*] Organisms that resemble Neisseria on culture must be confirmed as Neisseria gonorrhoeae on the basis of biochemical tests in order to distinguish them from other species.

[*] Sensitivity testing is important, as antibiotic resistance patterns are valuable in guiding future management guidelines.

[*] NAATs (nucleic acid amplification test) for Chlamydia and gonococci is now available and may be utilised in both screening and clinical diagnosis.

26
Q

Describe the treatment for gonorrhoea

A
  • Neisseria gonorrhoeae may vary in its sensitivity.
  • Initial therapy is usually guided by severity of symptoms and local knowledge of sensitivity patterns. Penicillin resistance is common. Ceftriaxone (intramuscular injection) is usually initial therapy and there is increasing resistance to many other agents. Single dosage is usually curative.
  • All patients are treated (and tested) for chlamydia with azithromycin, which also may prevent emergence of resistance to cephalosporins.
27
Q

What kind of virus is the Herpes Simplex Virus? And describe the clinical presentation of genital herpes

A

Herpes Simplex Virus is an encapsulated, double stranded DNA virus

Clinical presentation of Primary Genital Herpes

[*] Extensive, painful genital ulceration, dysuria, inguinal lymphadenopathy (enlarged lymph nodes), fever

Clinical presentation of Recurrent Genital Herpes

[*] Asymptomatic -> moderate (latent infection in dorsal root ganglia)

28
Q

Describe the diagnosis and treatment for genital herpes

A

Diagnosis of Genital Herpes

[*] Smear and swab of vesicle fluid and/or ulcer base

[*] PCR of vesicle fluid and/or ulcer base

Treatment: Aciclovir (primary and severe disease)

[*] Aciclovir prophylaxis for frequent recurrences

Barrier contraception – reduce risk of transmission

There are 2 distinct serological types of HSV: HSV-1 and HSV-2. HSV-1 infection is typically asymptomatic and nearly ubiquitous. It is transmitted by primary infection of the respiratory tract. HSV-2 has a predilection for genital disease and much more likely to become a latent infection of the sacral ganglion and to cause neonatal disease.

  • 90% of women with primary genital HSV-2 infection shed virus from their cervix during the acute infection. 50% of pregnant women with primary genital HSV, will transmit infection to the neonate. Neonatal herpetic infections are life-threatening. They may be prevented by appropriate use of caesarean delivery.
29
Q

What causes anogenital warts? Describe the clinical presentation

A

Anogenital warts caused by Human Papilloma Virus (HPV) are the commonest viral STI diagnosed in GUM clinics throughout the UK. (~4% young adults in their life)

[*] ~73,000 cases per year in UK (M=F)

HPV is a small double-stranded DNA virus.

Clinical presentation:

[*] Cutaneous, mucosal and anogenital (anus and genital) warts

  • Mainly HPV 6 and II
  • Benign, painless, verrucous epithelial or mucosal outgrowths, penis, vulva, vagina, urethra, cervix, perianal skin
30
Q

Describe the diagnosis and treatment for anogenital warts

A

Diagnosis:

[*] Clinical, biopsy and genome analysis, hybrid capture

Treatment

[*] None – frequent spontaneous resolution (70% 1 year, 90% 2 years)

[*] Topical podophyllin, cryotherapy, intralesional interferon, imiquimod, surgery

31
Q

Describe screening for HPV and the HPV vaccine

A

Screening

[*] Cervical pap smear cytology

[*] Colposcopy (close examination of the lining of the cervix) + acetowhite test (patches of white are seen after acetic acid washes away mucus – allows abnormal areas to be seen more clearly by staining them white)

[*] Cervical scab – HPV hybrid capture (40% of 20-24 year olds positive)

First episode, recurrent and re-registered cases accounted for 22% (131 140 out of 590 909) of all diagnoses in GUM clinics in 1999

More than 100 HPV types have been described, however the vast majority of infected individuals fail to develop warts. Apart from being unsightly and difficult to treat, the main concern is the strong association of certain high risk types with cervical carcinoma. Highest risk is attributed to HPV 16 and 18.

[*] Associated with cervical (>70%) and anogenital cancer

[*] 2500 cases cervical cancer in 2012 – most common cancer in women 15-34

HPV vaccine

[*] Two types

Cervarix (HPV 16 & 18) initially used in UK
Gardasil (HPV 6, 11, 16, & 18) from 2011

[*] Vaccine offered to girls 12-13 (2 doses)

[*] 99% effective in preventing HPV 16 & 18 – related cervical abnormalities in those not already affected

32
Q

Apart from gonorrhoea, chlamydia, herpes and HPV, what are other aetiological agents of STIs?

A

[*] HIV

[*] Trichomonas vaginalis

[*] Herpes simplex virus

[*] Hepatitis B virus

[*] Treponema pallidum (Syphilis)

[*] NB: Trichomonas vaginalis, Herpes simplex virus and Syphilis are common STIs. You should be able to describe the clinical presentation, diagnosis and management of these STIs.

33
Q

Describe treatment of STIs generally

A

[*] Multiple infections are common, so patients presenting with one infection should be screened for a number of other infections. This is especially the case as many infections as asymptomatic or only become symptomatic later in the course of the disease.

[*] Antibiotic therapy is usually initiated on the initial visit and regimes that ensure compliance are utilised.

[*] An important part of management is contract tracing of sexual partners for which GUM clinics are resourced.

Patients should also receive health education, advice on contraception and instruction in safe sex.

34
Q

Describe Syphilis including different types and consequences

A

Syphilis (great mimicker, can produce a number of different systems, affect multiple organ systems)

[*] Treponema Pallidum – spirochaete

  • Most cases are MSM

[*] May be contracted congenitally

[*] Multistage disease

  • Indurated, painless ulcer (chancre)
  • 6-8 weeks later – fever, rash, lymphadenopathy, mucosal lesions

Latent – Symptom free years

Chronic granulomatous lesions

Neurosyphilis (GPI tabes dorsalis – paralytic dementia) [CNS pathology], cardiovascular syphilis [cardiovascular pathology], gummas (local destruction – form of granuloma and can be found on liver, brain, heart, bone, testis, skin and other tissues)

[*] Congenital syphilis (the placenta is diffusely fibrotic with inflammation and necrosis of the fetal blood vessels in the placental villi. The resulting vascular insufficiency leads to poor fetal growth (intrauterine growth restriction) and stillbirth. Fibrosis of the liver and spleen cause fetal anaemia.

  • Compensatory extramedullary haematopoiesis promotes hepatosplenomegaly and the development of pleural effusions and ascites (fetal hydrops)). Congenital syphilis neonatal mortality rate is 50%.

[*] **Complications of syphilis in pregnancy include miscarriage, stillbirth, premature delivery and congenital syphilis. **

35
Q

Describe the Diagnosis and Treatment for Syphilis

A

Diagnosis: dark field microscopy (traditional), serology

  • Cannot be grown
  • Serology: Initial screening with EIA antibody test then positives

Rapid Plasma Reagin RPR titre (cross-reacting antigen) (organism reacts to normal tissues)
TP particle agglutination TPPA
Serologic pattern interpreted (false positives, response to treatment, etc)

Treatment – penicillin and test of culture follow-up.

[*] Treatment: penicillin and ‘test of cure’ follow up

36
Q

Describe Trichomonas Vaginitis

A
  • Trichomonas vaginalis – flagellated, motile protozoan
  • Thin, frothy, offensive discharge
  • Irritation, dysuria, vaginal inflammation
  • Diagnosis – vaginal wet preparation +/- culture enhancement
  • Treatment – metronidazole
37
Q

Describe Arthropods and other less common STIs (mainly tropical)

A

Arthropods

[*] Scabies mite

[*] Pubic louse

[*] Scabies can affect the genitalia and spread sexually

[*] Pubic lice (pediculosis pubis)

  • Distinct from the other human (body) lice
  • The ‘crab louse’ (Phthirus pubis)

Less common STIs (mainly tropical)

[*] Inguinal lymphadenopathy may be caused by

  • LGV (lymphogranuloma venereum)

C. trachoma serotypes L1, L2 and L3

  • Rapidly healing papule then inguinal bubo (large, red swollen lymph nodes)
  • Recent clusters of cases in Europe in MSM

Chancroid (Haemophilus ducreyi)

  • Painful genital ulcers

Granuloma inguinale / Donovanosis (Klebsiella granulomatis)

  • Genital nodules => ulcers => lymphadenopathy
38
Q

What are 3 common causes for vaginal discharge?

A

Vulvovaginal candidiasis, Bacterial Vaginosis (BV) and Trichomonas vaginalis

39
Q

Describe Vulvovaginal Candidiasis

A

Vulvovaginal Candidiasis

[*] Candida Albicans and other candida species

May be part of normal GI and genital tract flora

[*] Risk factors:

  • Antibiotics
  • Oral contraceptives
  • Pregnancy
  • Obesity
  • Steroids
  • Diabetes

[*] Profuse, itch (distinctive from other causes of vaginal discharge), white, curd-like discharge

[*] Vaginal itch, discomfort and erythema

[*] Diagnosis

  • High vaginal smear and culture (gram-positive yeast)
  • NB: most GPs make diagnosis based on symptoms

[*] Treatment

Topic azoles or nystatin, or oral fluconazole

40
Q

Describe Bacterial Vaginosis

A

Bacterial Vaginosis

[*] Not vaginitis (no inflammation of vaginal wall)

Unsettled normal flora (anaerobes, enteric gram –‘ve bacteroides, Gardnerella, mycoplasmas)

[*] Scanty, but offensive, fishy discharge

[*] Diagnosis

  • pH > 5, KOH whiff test => strong amine smell
  • NB: GPs normally make diagnosis based on symptoms
  • High vaginal smear – gram variable coccobacilli, reduced numbers of lactobacilli, absence of pus cells, ‘clue’ cells – epithelial cells studded with gram variable coccobacilli

[*] Treatment: Metronidazole

41
Q

What is PID? (Pelvic Inflammatory Disease)

A

[*] It is an ascending infection from the endocervix causing inflammation of the structures within the pelvis:

  • Endometritis: inflammation and infection of the endometrium (lining of the uterus)
  • Salpingitis: inflammation and infection of the fallopian tube
  • Tubo-ovarian abscess: late complication – a pocket of pus that forms during an infection of a fallopian tube and ovary.

Parmetritis (inflammation of the ligaments around the uterus)
Oophoritis: inflammation of the ovaries
And/or pelvic peritonitis

42
Q

Describe the pathogenesis of PID

A
  • Infection of the cervix (endocervicitis) and vagina ascends, either directly or via lymphatics to the endometrium, uterine tubes and the pelvic peritoneum.
  • Inflammation causes damage to tubal epithelium (scarring) and thus adhesions to form (leading to inflammation of the parametrium (connective tissue of the pelvic floor), contributing to chronic pelvic pain)

Factors associated with the ascent of bacteria include

  • Instrumentation: cervical dilation, coil insertion
  • Hormonal changes associated with menstruation – lowers bacteriostatic effect of cervical secretion
  • Retrograde menstruation – infection more common after a period
  • Virulence of the organisms in acute chlamydial and gonococcal PID
43
Q

Describe the immediate and long term sequelae of PID. What is Fitz-Hugh-Curtis Syndrome?

A
  • *Immediate**: tubo-ovarian abscess, pyo-salpinx (fallopian tube filled and often distended, with pus)
  • *Long term**:
  • Ectopic pregnancy (1 episode of PID => 7x increased risk)
  • Infertility (1 episode of PID => 12% increased risk, 2 episodes => 25% increased risk, 3+ episodes => 50-75%)
  • Dyspareunia (painful sexual intercourse)
  • Chronic PID / Chronic pelvic pain
  • Pelvic adhesions

[*] Fitz Hugh Curtis Syndrome

RUQ pain + perihepatitis

Following Chlamydial PID (10-15% of cases)

44
Q

Describe the groups PID is more common in, and risk factors

A

[*] Disease of sexually active women

  • Incidence higher in urban areas
  • Peak incidence 20 per 1000
  • Highest incidence 20-24 year olds
  • Underestimated
  • Incidence rate in primary care approximately 280 per 100,000 person-years

[*] PID Risk Factors

  • Young age at first intercourse
  • Multiple sexual partners (polygyny)
  • High frequency of sexual intercourse
  • Lack of use of barrier contraception
  • Type of contraception used
An IUCD (intrauterine contraceptive device – coil) increases the risk of PID in the 1st few weeks of insertion.
The COCP (combined oral contraceptive pill) is considered to be protective against symptomatic PID.
  • High rate of acquiring new partners within 30 days.
  • Alcohol/drug use
  • Cigarette smoking (2x increased risk)
  • Low socioeconomic class
45
Q

What are the causative organisms of PID?

A
  • Often polymicrobial
  • Neisseria gonorrhoea (intracellular, gram negative diplococcic) (14% of cases) (STI)
  • Chlamydia trachomatis (gram negative extracellular organism) (STI)
  • 40% risk of concurrent infection
  • Bacterial vaginosis (anaerobes, enteric gram negative bacteroides)
  • Group A Streptococci
  • Haemophillis influenzae
  • Cytomegalovirus
  • Mycobacterium tuberculosis
  • Garderella, Mycoplasma and anaerobes have also been implicated
46
Q

Describe the clinical features of PID

A

Pyrexia
Pain

  • Bilateral lower abdominal tenderness
  • Adnexal (uterine appendages) tenderness
  • Cervical excitation
  • Deep dyspareunia (pain during or after sexual intercourse – pain is perceived deeply inside the vulva)

Abnormal vaginal/cervical discharge
Abnormal vaginal bleeding

[*] History

  • Lower abdominal pain
  • Abnormal vaginal bleeding/discharge
  • Deep dyspareunia
  • History of STIs in the past

[*] Examination

  • Pyrexia > 38oC
  • Lower abdominal tenderness (bilateral)
  • Do a bimanual examination to look for Adnexal tenderness and Cervical excitation (cervical motion tenderness) [one hand palpates the fundus of the uterus anteriorly, the other hand has 2 fingers in the vagina, palpating the cervix)
  • Discharge (vaginal or cervical) (can be examined using a speculum, good opportunity to do swabs)
47
Q

What are the laboratory investigations for PID?

A

Urinary and/or Serum Pregnancy test

Triple swabs

  • High vaginal swab – Bacteria vaginosis organisms, Trichomonas vaginalis, Candida
  • Endocervical swab – Neisseria gonorrhoea
  • Endocervical swab – Chlamydia trachomatis
  • Urethral swabs – Chlamydia trachomatis (males only)

Positive swabs support the diagnosis, negative swabs do not exclude it

Midstream Urine

    • Leucocytes and nitrates

Screening for other STIs including HIV
Blood tests for WBC and C-Reactive Protein

    • Marker for acute infection/inflammation
48
Q

What are the differential diagnoses for PID?

A

Gynaecological

  • Ectopic pregnancy (presents almost identically to PID, need to do a blood or serum pregnancy test)
  • Endometriosis (endometrium at sites outside of uterus – causes cyclical pain)
  • Complications of an ovarian cyst (torsion, rupture, haemorrhage) (can present more suddenly than PID)

Gastrointestinal

  • Acute appendicitis
  • Irritable bowel syndrome (IBS)

Renal

    • Urinary Tract Infection (UTI)

Other:

    • Functional pelvic pain of unknown origin (difficult to exclude, need a laparotomy to show no adhesions are causing the pain)
49
Q

Describe the management for PID

A

Low threshold for empirical treatment (delayed treatment increases long term sequelae)
Severe disease requires IV antibiotics and admission for observation, and possible surgical intervention. Increased risk of long-term sequelae.

[*] Management – Medical

  • Analgesia
  • Antibiotics
Mild =\> Moderate disease (oral antibiotics)
Severe disease (IV antibiotics)

When to admit to hospital?

  • Surgical emergency cannot be excluded
  • Clinically severe disease
  • Signs of pelvic peritonitis
  • Tubo-ovarian abscess
  • PID in pregnancy (very rare)
  • Lack of response/intolerance to oral therapy
  • Other complications e.g. H.I.V

Antibiotics - Outpatient treatment:

  • IM Ceftriaxone 500mg stat and PO Doxycycline 100mg BD and PO Metronidazole 400mg BD.

Antibiotics – Inpatient treatment:

IV Ceftriaxone 500mg stat and IV/PO Doxycycline 100mg BD and IV Metronidazole (covers anaerobes) 500mg BD => PO Doxycycline 100mg BD + PO Metronidazole 400mg BD

Continue antibiotics for 14 days

Management – Surgical:

  • Laparoscopy/laparotomy may be considered if no response to therapy, clinically severe disease, presence of a tubo-ovarian abscess (walled-off area of inflammation so penetration of antibiotics can be poor)
  • Ultrasound-guided aspiration of pelvic fluid collections is less invasive
50
Q

What do you tell the patient regarding PID?

A
  • What the diagnosis is
  • What treatment is being given – possible side effects, importance of completing antibiotics
  • Future risk of
    • Ectopic pregnancy
    • Infertility (risk increases exponentially with repeat episodes of PID)
    • Chronic pelvic pain
    • Fitz Hugh Curtis syndrome

Risks increase with repeat episodes

  • Future use of barrier contraception will reduce the risk of PID
  • Contact screening
    • Empirical treatment of partners
    • Abstinence until antibiotic course complete so she doesn’t infect someone else who re-infects her

Severe disease = greater risk of complications, early treatment = lower risk of complications

51
Q

Describe Chronic Pelvic Inflammatory Disease

A

[*] Symptoms > 6 months duration

  • Pelvic pain
  • Secondary dysmenorrhoea
  • Deep dyspareunia
  • Menstrual disturbance
  • Recurrent acute painful exacerbations

[*] Sequelae

  • Infertility
  • Ectopic pregnancy
  • Chronic pelvic pain
  • Pelvic adhesions/tubo-ovarian complex
  • Abnormal/painful periods

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