Sexually Transmitted Infections II

Dr Sana Jamil
Assistant Professor(Microbiology)
SIUT
 Bacterial
1. Pathogenic Chlamydia:
Obligate intracellular pathogen
C. psittaci: pneumonia
C. pneumoniae acute respiratory disease
atherosclerosis?
C. trachomatis: trachoma
STD
LGV
Chlamydia trachomatis:
NGU--Non-gonococcal urethritis
Asymptomatic (particularly in women)
3 catagories of serovars associated with
disease
Bacterial: C. trachomatis

Chlamydia trachomatis: serovar catagories

*
 Bacterial: C. trachomatis

Properties of the bacterium:

Gram negative bacteria lacking a cell wall

-do not respond to b-lactam antibiotics
-many cross-linked molecules on surface
protein-protein sulphydryl groups

Two primary phases of lifecycle:

EB = elementary body (infectious)
RB = reticulate body (fragile)
Bacterial: C. trachomatis

“Developmental lifecycle”

EB = spore-like; metabolically less active

RB = bacteria-like; metabolically active
 Bacterial: C. trachomatis
Pathogenesis and clinical features (continued)
C. trachomatis disease (serovars D-K) is clinically
similar to gonococcal infection:
SYMPTOMS:
males: usually symptomatic;
in addition to urethritis can
develop an orchitis and epididymitis

females: often asymptomatic;

salpingitis (ectopic pregnancy)
PID
newborns: conjunctivitis
pneumonia
Bacterial: C. trachomatis

Purulent cervicitis
 Bacterial: C. trachomatis

Pathogenesis and clinical features

Lymphogranuloma venereum--LGV
1. Papule formation (painless)
2. Spread to inguinal lymph nodes (bubo formation)
3. Lymph nodes swell, rupture, drain through skin
4. Skin rash (like 2˚ syphilis)
5. Elephantiasis particularly in genitalia
6. Fever, malaise, loss of appetite
Bacterial: C. trachomatis

Pathogenesis and clinical features

Lymphogranuloma venereum—LGV (Rectal)

Swelling around the rectum (perirectal) bloody

rectal discharge, painful defecation (tenesmus),
diarrhea and lower abdominal pain.

Women may develop fistulas between the vagina

and rectum
LGV
Bacterial: C. trachomatis

Pathogenesis and clinical features

Lymphogranuloma venereum--LGV

Elephantiasis of the vulva

Bacterial: C. trachomatis

Diagnosis

Serology is unreliable

Cell culture
Infect McCoy cells in tissue culture
Form inclusions in 48-72 hours

Direct antigen detection

Direct fluorescent antibody (DFA) test
 Diagnosis of Chlamydia
• Tissue culture
– Difficult and not performed in few labs
– Sensitivity 60-90%

• DNA probe
Sensitivity 73-96%
Specificity 85-99%

• Enzyme Immunoassay
Sensitivity 65-95%
Specificity 95% or >
 Nucleic Acid Amplification
Techniques

PCR

• Sensitivity on endocervical specimens for

women: 82-85% for chlamydia

• Sensitivity in urine of men: 82-97%

Culture Specificity nears expensive, labor
100% intensive,
cervical
specimens,
sensitivity 80%
DNA probe more stable cervical
transport specimens,
Less expensive sensitivity 65%

EIA Less technically cervical

demanding specimens,,
Less expensive sensitivity 60%

Nucleic acid 90 % greater More expensive

amplification sensitivity and than DNA probe
specificity or EIA
Can be used
urine or cervical
specimens
Bacterial: C. trachomatis

Diagnosis

Inclusions stained with iodine

DFA stain
Bacterial: C. trachomatis

Treatment:

Treatment is with tetracycline antibiotics

-No cell wall therefore unresponsive to b-
lactam’s
-Suspect concurrent infection with GC
 Bacterial: Chancroid

Etiologic agent: Haemophilus ducreyi (gram neg. rod)

Chancroid is also referred as “soft chancre”

Worldwide in distribution
Manifests soon after genital inoculation
Painful, non-indurated genital ulcer
-contrast to syphilitic chancre
Local lymphadenopathy
Confused with genital herpes
-lesions tend to be larger
CHANCROID
 Bacterial: Chancroid

Diagnosis and Treatment:

Gram stains of aspirates from lesion or lymph node
may reveal short gram neg. chains--“school of fish”
Can be cultured on chocolate agar at 30--34˚C (2-9 d)

Treat with erythromycin

 Bacterial: Donovanosis

Etiologic agent:
Calymmatobacterium granulomatis (gram neg. rod)
Referred as “Donovanosis”
Common in tropical climates
Nodules on genitalia that erode, forming
granulomatous lesions that bleed upon contact;
purulent exudate
Secondary infections can occur
No lymphadenopathy (contrast to LGV)
Invade and multiply in mononuclear cells
 Bacterial: Donovanosis

Diagnosis:
Examination of smear from lesion stained with
Giemsa or Wright’s
“Donovan bodies”
Clustering of encapsulated bacteria seen in monocyte is
diagnostic

Prevent phagosome-lysosome fusion

Escape from phagosome
Treatment:
Tetracyclines
Bacterial: Mycoplasma

Etiologic agents:
Mycoplasma hominis
Ureaplasma urealyticum
Found in genital tracts of sexually active men and
women
Not found as often in populations who are not
sexually active
Associated with NGU, especially
U. Urealyticum -urethritis and prostatitis in men

Diagnosis by culture on Mycoplasma/PPLO agar

Both organisms are susceptible to tetracyclines
 Mycotic: Candida

C. albicans: normal vaginal flora

For unknown reasons, growth increases dramatically

commensurate with increase in vaginal pH

Range of disease is mild (normal) to severe

(immunocom-promised)

Presents as irritating vaginitis with cheesy/thick

discharge

Can be accompanied by urethritis and dysuria (UTI)

Balanitis--infection of male is rare and usually

asymptomatic
 Mycotic: Candida

Diagnosis:
Microscopic examination of vaginal discharge
or culture can confirm diagnosis

Treatment:
Oral: Fluconazole or Topical: Nystatin
Protozoal: Trichomonas

Etiologic agent: Trichomonas vaginalis

Found in vaginal tract in women and urethra (and

sometimes the prostate) of men

In women, infection results in vaginitis with a

copious, foul-smelling discharge
-intense vaginal itch
-foamy white/ green

In men, mild urethritis; rarely pathogenic

Protozoal: Trichomonas

Diagnosis:
Must be distinguished from BV; can be done by
examining discharge microscopically
-actively motile trophozoites present

Treatment:
Metronidazole
 Viral: Herpes simplex types I&II
HSV1: spread via saliva; oropharyngeal infection
-cold sores
HSV2: venereal route; recovered from oral and genital sites
1 week incubation--start to see vesicles
Vesicles form painful shallow ulcers
-can be found in vagina, on penis, in anus
Result in painful urination, malaise, fever
Spontaneous healing occurs
Therapy is highly supportive
Reactivation of latent virus can occur
-virus infects neurons, goes latent
 Diagnosis of Herpes Genitalis

 History and physical examination

 Confirmed by tissue culture of
lesions
 Type and stage of infection can effect
recovery of virus
 Pap and Tzanck test (60% to 70%
sensitivity)
 Polymerase chain reaction and
hybridization assays available
 Viral: Herpes simplex types I&II

Treatment:
Acyclovir helps suppress the frequency of recurrences
 Viral: Papilloma

Over 70 different types of human papilloma

viruses

All infect skin or mucosal surfaces

Types 6, 11, and 16 are associated with

cervical cancer
 Viral: Papilloma
Wart formation appears 1-6 months after inoculation
-warts can be found on penis, vulva, in
vagina, in perianal regions

Red to pink, often with a cauliflower-type of

appearance; can also be rounded

Subject to trauma during sex

Treated by electrosurgery or cryosurgery; no other

therapy

Cervical lesions best removed by laser, particularly

if type is one associated with cervical cancer
 Screening and Diagnosis of Condyloma
Accuminata

 History and physical Examination

 Confirmed by tissue biopsy (not routinely
performed)
 No data supports use of type-specific HPV
nucleic acid test for routine diagnosis
• Quadrivalent HPV vaccine is a non-infectious
recombinant vaccine prepared from the purified
virus-like particles (VLPs) of the major capsid
(L1) protein of HPV types 6, 11, 16, and 18.
• 9-valent HPV vaccine is a non-infectious
recombinant vaccine prepared from the purified
VLPs of the major capsid (L1) protein of HPV
types 6, 11, 16, 18, 31, 33, 45, 52, and 58.
 Ectoparasites: Louse

Louse borne disease spread by Phthirus pubis or

Pediculus humanus

-May or may not be sexually transmitted

-Cause severe itching
-Diagnosed by identifying eggs attached to
hair
-Associated with other STI’s
-Thrive on toilet seats, fomites
 Ectoparasites: Mites
Sarcoptes scabei: scabies
-Can be spread non-venereally also
-Pregnant female burrows into skin, lays eggs
-Eggs hatch and reside in hair folicles
-Severe itching can ensue

-Can also burrow between fingers, armpits, under

breasts, between buttocks, thighs, penis, scrotum

-Those who do not respond well to this challenge,

experience severe inflammation and to an exudate
that gives rise to an encrusted skin condition
Scabies
 What is Norwegian Scabies?
 Crusted scabies is a severe form of scabies that can occur in
some persons who are immunocompromised elderly, disabled, or
debilitated.
 Persons with crusted scabies have thick crusts of skin that
contain large numbers of scabies mites and eggs.
 Persons with crusted scabies are very contagious
 Persons with crusted scabies may not show the usual signs and
symptoms of scabies such as the characteristic rash or itching
(pruritus).
 Persons with crusted scabies should receive quick and aggressive
medical treatment for their infestation to prevent outbreaks of
scabies.
 DIAGNOSIS
 Skin Scrapings (With mineral oil)
 It is important to remember that a person can
still be infested even if mites, eggs, or fecal
matter cannot be found; typically fewer than 10-
15 mites can be present on the entire body of an
infested person who is otherwise healthy.
 Biopsy
 videodermatoscopy, dermatoscopy, reflectance confocal
microscopy, and optical coherence tomography
 PCR
 TREATMENT
 Anti allergy
 Apply a mite-killer like permethrin .
 These creams are applied from the neck down, left on
overnight, then washed off.
 This application is usually repeated in seven days.
 Permethrin is approved for use in people 2 months of
age and older and is considered to be the safest and
most effective treatment for scabies.
 Ivermectin(Norwegian Scabies)
General Conclusions

1. Persons who are sexually active will

experience STIs in their lifetime.

2. Virtually all STIs begin with an acute phase

that can become a chronic disease if
untreated.

3. STI agents have an increased capacity to

evade innate host immune responses.

4. Co-transmission, co-infections are common.

5. Few vaccines available to combat these

diseases.