Lectures on Gynecology 
Dr Magda Helmi
Genital infections are one of the most common reasons 
for women of all age groups to present to a medical 
practitioner. 
Sexually transmitted infections form one subgroup of 
infections, however the more common infections are 
vulvovaginal candidiasis and bacterial vaginosis. 
Chlamydia and gonorrhoea affect the sexually active 
woman, with HlV. 
These infections can be asymptomatic and can have 
serious consequences to a woman’s fertility by causing 
tubal infection and damage. 
Appropriate diagnosis and treatment are fundamental 
not only to provide symptom relief, but also to prevent 
recurrences and long-term squeals
It is important to differentiate normal 
physiological 
changes from true infections. Thus, a thorough 
history and examination with the back up of 
laboratory testing is fundamental before a 
diagnosis is made. 
However, the sensitivity of clinical diagnosis 
and testing in pelvic inflammatory disease 
(PID) 
can be low, so if there is a clinical suspicion of 
PID, 
empiric treatment is recommended.
Anatomy and physiology: 
The vaginal epithelium is lined by stratified squamous epithelium during the 
reproductive age group under the influence of oestrogen. The pH is usually 
between 3.5 and 4.5 and lactobacilli (Figure 6.1a) are the most common 
organisms present in the vagina. Following the menopause, the influence of 
oestrogen is diminished making the vaginal epithelium atrophic with a more 
alkaline pH of 7.0, the lactobacillus population declines and the vagina is 
colonized by skin flora. 
Physiological discharge occurs in response to hormonal levels during the 
menstrual cycle. It is usually white and changes to a more yellowish colour due 
to oxidation on contact with air. 
There is increased mucous production from the cervix at the time of ovulation 
followed by a thicker discharge/cervical plug under the influence of 
progesterone. The discharge mainly consists of mucous, desquamated 
epithelial cells, bacteria (lactobacillius) and fluid. 
Ascending infection can occur from the vagina and cervix to the uterine cavity 
and to the Fallopian tubes through direct spread or via the lymphatics leading 
to severe pelvic inflammatory disease and pelvic peritonitis. 
Infections can be broadly divided into lower and upper genital tract depending 
on the site and affection of the infective organism.
 Vaginal and cervical 
flora (all ><1000 
magnified). Normal: 
lactobacilli - seen as 
large Gram-positive 
rods 
 - predominate. 
Squamous epithelial 
cells are Gram negative 
with a large amount of 
cytoplasm. (b) 
Cnandidiasis: (c) (d) :
Lower genital tract 
infections 
Vulvovaginal candidiasis 
Candida, a commensal organism, is found in 
small population densities in the vaginal 
ecosystems of nearly one third of healthy 
women. Symptomatic infection arises, 
however, when proliferation causes a shift 
from colonization to frank adherence and 
infection. It is caused by Candida albicans in 
around 80-92 per cent of cases. Other non 
albican species like C.tropicalis, C. glabmta, 
C. krusei and C. parupsilosis can also cause 
similar symptoms, although sometimes more 
severe and recurrent. C. albicans is a diploid 
fungus and is a common commensal in the 
gut flora. 
The patent complain of: Vulval itching and 
soreness, thick curdy vaginal discharge 
dyspareunia and dysuna. Vulval oedema, 
vulvai excoriation, redness and erythema. 
Normal vaginal pH, 
there are speckled Gram-positive 
spores and log pseudohyphae visible. 
There are numerous polymorphs 
present and the bacterial flora is 
abnormal, resembling bacterial 
vaginosis.
Microscopy of the discharge with 
10% KOH will often reveal hyphae 
or budding yeast in 50%-70% of 
cases albicans organisms are 
easiest to identify, as they have 
long hyphae with blastospores 
along their length and a terminal 
cluster of chlamydiaspores . The 
"atypical" species of yeast, 
however, may only have features 
of budding yeast (resembling 
small snowmen), which are easily 
obscured within surrounding 
cellular debris.
The trichomonad parasite is a 
flagellated protozoan that 
causes up to 25% of vaginitis 
cases. While trichomonas 
infection is asymptomatic up to 
50% of the time,when clinical 
signs are present they include 
irritation and soreness of the 
vulva, perineum, and thighs, 
with dyspareunia and dysuria. 
Typically, the trichomonas 
infection is accompanied by a 
copious, greenish-yellow frothy 
discharge. Unlike bacterial 
vaginosis, it seems that 
trichomonas is primarily a 
sexually transmitted infection.
. The diagnosis is made by observation of 
the following features (Table I): 
A foul-smelling frothy discharge (present 
in 35% of cases 
Vaginal pH >4.5 (70% of cases) 
Punctate cervical microhemorrhages 
(25%) 
Motile trichomonads on wet mount (50%- 
75%) 
Papanicolaou smear is quoted to be 70% 
sensitive in identifying trichomonads. 
The current primary treatment 
recommendation is a single 2g dose of 
oral metronidazole. For those who cannot 
tolerate this single large dose, 500mg bid 
for 7 days is equally efficacious if the 
patient completes her regimen. The male 
partner(s) must also receive treatment.
 Bacterial vaginosis: there is 
an overgrowth of anaerobic 
organisms, including 
Gardnere/Ia vagina/is (small 
Gram-variable cocci), and a 
decrease in the numbers of 
lactobacilli. A 'clue cell’ is 
seen. 
 On wet preparation of 
vaginal fluid, absence of 
WBCs and stippling of 
epithelial cells support a 
diagnosis of bacterial 
vaginosis.
The diagnosis of BV requires the presence of at least 3 of the following 4 criteria. 
A homogenous noninflammatory discharge (not many WBCs). 
Vaginal pH >4.5. 
Clue cells (bacteria attached to the borders of epithelial cells, >20 % of epithelial cells; 
Whiff test positive for fishy or musty odor when alkaline KOH solution added to smear. 
For years, oral metronidazole has been the primary indicated regimen. Other systemic options 
include oral clindamycin. 
Pap smear showing clue cells consistent with bacterial 
vaginos
According to 2008 WHO estimates, 
499 million new cases of curable 
sexually transmitted infections (ie, 
syphilis, gonorrhoea, chlamydia, 
trichomoniasis) occur annually 
throughout the world in adults aged 15- 
49 years. 
Tubal scarring as a result of PID can 
cause infertility in 20%, ectopic 
pregnancy in 9%, and chronic pelvic 
pain in 18% of women[ 
Complicated PID resulting in tubo-ovarian 
or pelvic abscess may 
contribute to patient mortality.
PID is a complex polymicrobial disease that is 
due to the ascending spread of pathogens from 
the cervix or vagina, most 
commonly Chlamydia, trachomatis or Neisseria 
gonorrhoeae (60-75%) , which then spreads 
into the endometrium, fallopian tubes, ovaries, 
and adjacent structures. 
Other pathogens include Mycoplasma 
hominis, Haemophilus 
influenzae,Streptococcus 
pyogenes, Bacteroides species, 
and Peptostreptococcus species. Less 
commonly, direct spread from a nearby 
infection such 
as appendicitis ordiverticulitis may occur. 
Hematogenous infection is a rare cause of PID 
except in cases of tuberculous. 
Douching is a potential risk factor for PID as it 
can result in a change of the vaginal flora and 
introduce bacteria from the vagina into the 
upper reproductive organs. Usage of 
intrauterine contraceptive device or 
gynecologic interventions may also predispose 
a patient to PID. Direct extension of infection 
from adjacent viscera and uterine 
instrumentation are more important risk factors 
in postmenopausal PID
 Abdominal, pelvic pain and 
dyspareunla. 
 Mucopufulent vaginal 
discharge 
 Pyrexia (>38‘C). 
 Heavy/ime.rmenslrual 
bleedlng 
 Pelvic tenderness and Tender 
adnexal or palpable pelvic 
mass, 
 Generalized sepsis in severe 
and sysmmic infection 
 Tubal damage leading to tubal 
occlusion, abscess and 
hydrosalpinx.
Based on clinical findings: 
Raised white cell count (neutrophilia 
suggestive of acute inflammatory 
process) 
Reduced white cell count 
(neutropenia in severe infections) 
Raised C reactive protein and ESR 
(erythrocyte sedimentation rate) 
Adnexal masses on ultrasound 
Laparoscopy is the gold standard to 
give a definitive diagnosis, however, 
in mild cases it may 
not be very obvious.
 Depending on the severity of the infection, patients with mild/moderate 
disease can be managed on an outpatient basis with easy access to hospital 
admission if the infection becomes more severe. An intrauterine 
contraceptive device, if present, should be removed and alternative 
emergency contraception or other modes of contraception (combined pill, 
oral/parenteral progesterone) should be offered. A 
 pregnancy test should be done in all cases to rule out ectopic pregnancy. 
 There are several differing antibiotic regimes that are used; however, the 
following is recommended by the RCOG Green Top Guideline (2008) which 
is evidence based. 
Mild/moderate infection (outpatient treatment) 
 Oral ofloxacin 400 mg twice a day + oral 
 metronidazole 400 mg twice a day x 14 days 
 Ceftriaxone 250 mg single intramuscular injection + oral doxycycline 100 mg 
twice a day 
 oral metronidazole 400 mg twice a day x 14 days 
 Single intramuscular dose of ceftriaxone 250 mg azithrornycin 1 g/week x 2 
weeks. 
The data supporting the use of azithromycin are limited and should not be used 
in isolation.
Causative organism 
Herpes simplex virus type I (usually oral) or 
type II (usually genital). 
Clinical features 
Painful vesicles and multiple ulcerations on 
vulva, Retention of urine. 
Diagnosis 
Swab from ulcer, Serum from vesicle, Virus 
seen on electron microscopy, Culture. 
Treatment 
Acyclovir 200 ml five times/ day 
Famciclovir, Valaciclovir, 
Analgesics and local unaesthetic gels
Causative organism: 
Human papillomavirus, HPV6and11, HPV 16 and 18, 
linked to cervical caner. 
Clinical features: 
Warty lesions on the vulva, vagina, cervix and perianal 
area. 
Also seen around mouth, lips and larynx if orogenital 
contact. 
Diagnosis: 
Clinical examination: 
Histology of removed wart Seen on cervical smear and 
colposcopy 
Treatment: 
Podophyllin; local application twice a week, Surgical 
excision, Laser, Cryotherapy.
Causative organism: 
Treponema pallidum 
Clinical features: 
Primary syphilis: Painless ulcer/ulcers on vulva, vagina or cervix, Enlarged 
groin/inguinal lymph nodes 
Secondary syphilis: maculopapular, rash on palms and soles. Mucous 
membrane ulcers, Generalized lymphadenopath, arthritis 
Neurosyphilis: meningitis, strok, tabes dorsalis 
Cardiovascular: aortic aneurysm 
Congenital syphilis: intrauterine death, interstitial keratitis, VIII nerve 
deafness, abnormal teeth 
Diagnosis: 
TPPA: Treponema pallidum particle agglutination. 
TPHA: Treponema pallidum haemagglutinatio assay. 
FTA: Fluorescent treponemal antibody. 
Dark Held illumination: serum from base of ulcer + saline taken and seen 
under the microscope. Spiral organisms with characteristic movements 
are diagnostic 
Treatment: 
Penicillin mainstay of treatment Procaine, penicillin, 1.2 MU daily, i.m. x 
12 days, Benzathine penicillin, 2.4 MU i.m. repeated after 7 days. 
Doxycycline 100 mg bd x 14 days. 
Erythromycin 500 mg qds x 14 days mm.
Causative organism: 
Mycobacterium tuberculosis. 
Clinical features: 
Usually following pulmonary tuberculosis through blood and lymphatics, 
Amenorrhoea (affects endometrium) Infertility (affects tube), Acute/ chronic pelvic 
pain, Frozen pelvis due to severe multiple adhesions. 
Diagnosis: 
Histological confirmation from endometrium and Fallopian tube, Mantoux test, Heaf 
test, Chest x-ray. 
Treatment: 
Rifampicin, Isoniazid, Pyrazinamide. Treatments can, last from six to 12 months.
Causative organism: 
Haemophilus ducreyi. 
Clinical features: 
Painful shallow multiple ulcers, Regional 
lymphadenopathy with suppuration. 
Diagnosis: 
Isolation of Ducrey’s bacillus on biopsy on 
biopsy. 
Treatment: 
Single oral dose of azethromycin, Ceftriaxone, 
Erythrofpycin.
Causative organism: 
Klebsiella grarnulomatoses. 
Clinical features: 
Painless nodule. 
Diagnosis: 
Donovan bodies:intracellular inclusions seen in 
phagocytes or histiocytes. 
Treatment: 
Erythromycin.
Painful ulcers, Local tissue, destruction, treated with Streptomycn, 
tetracyclin
ONE IS TERMED LACTOBACILLOSIS OR 
DÖDERLEIN CYTOLYSIS. THIS ENTITY IS 
CHARACTERIZED BY AN OVERGROWTH OF 
THE COMMENSAL LACTOBACILLI HENCE, 
ON SALINE WET MOUNT, ONE FINDS AN 
EXCESSIVE NUMBER OF BACILLI AMONG 
THE BACKGROUND FLORA. THE PH IS 
TYPICALLY LOW-NORMAL. TREATMENT, 
THEREFORE, IS DIRECTED AT 
CORRECTING THE DISRUPTION OF THE 
VAGINAL ECOSYSTEM IN ORDER TO LIMIT 
THE EXCESSIVE PROLIFERATION OF 
THESE PROTECTIVE ORGANISMS. 
INFLAMMATORY VAGINITIS, FEATURES A 
VAGINAL PH ABOVE 4.2, LARGE NUMBERS 
OF LEUKOCYTES, AND SOME PARABASAL 
AND BASAL VAGINAL CELLS, WITH A 
PAUCITY OF SUPERFICIAL SQUAMOUS 
CELLS. CLINICIANS OFTEN FIND THAT 
PATIENTS ARE INFECTED WITH GROUP A 
OR GROUP B STREPTOCOCCUS 
THEREFORE, BECAUSE INFECTION IS 
SUSPECTED TO UNDERLIE THE 
INFLAMMATION AND DESQUAMATION, 
TREATMENTS DIRECTED AGAINST 
BACTERIAL VAGINOSIS ARE 
RECOMMENDED.

Genital infections in gynecology

  • 1.
    Lectures on Gynecology Dr Magda Helmi
  • 2.
    Genital infections areone of the most common reasons for women of all age groups to present to a medical practitioner. Sexually transmitted infections form one subgroup of infections, however the more common infections are vulvovaginal candidiasis and bacterial vaginosis. Chlamydia and gonorrhoea affect the sexually active woman, with HlV. These infections can be asymptomatic and can have serious consequences to a woman’s fertility by causing tubal infection and damage. Appropriate diagnosis and treatment are fundamental not only to provide symptom relief, but also to prevent recurrences and long-term squeals
  • 3.
    It is importantto differentiate normal physiological changes from true infections. Thus, a thorough history and examination with the back up of laboratory testing is fundamental before a diagnosis is made. However, the sensitivity of clinical diagnosis and testing in pelvic inflammatory disease (PID) can be low, so if there is a clinical suspicion of PID, empiric treatment is recommended.
  • 4.
    Anatomy and physiology: The vaginal epithelium is lined by stratified squamous epithelium during the reproductive age group under the influence of oestrogen. The pH is usually between 3.5 and 4.5 and lactobacilli (Figure 6.1a) are the most common organisms present in the vagina. Following the menopause, the influence of oestrogen is diminished making the vaginal epithelium atrophic with a more alkaline pH of 7.0, the lactobacillus population declines and the vagina is colonized by skin flora. Physiological discharge occurs in response to hormonal levels during the menstrual cycle. It is usually white and changes to a more yellowish colour due to oxidation on contact with air. There is increased mucous production from the cervix at the time of ovulation followed by a thicker discharge/cervical plug under the influence of progesterone. The discharge mainly consists of mucous, desquamated epithelial cells, bacteria (lactobacillius) and fluid. Ascending infection can occur from the vagina and cervix to the uterine cavity and to the Fallopian tubes through direct spread or via the lymphatics leading to severe pelvic inflammatory disease and pelvic peritonitis. Infections can be broadly divided into lower and upper genital tract depending on the site and affection of the infective organism.
  • 5.
     Vaginal andcervical flora (all ><1000 magnified). Normal: lactobacilli - seen as large Gram-positive rods  - predominate. Squamous epithelial cells are Gram negative with a large amount of cytoplasm. (b) Cnandidiasis: (c) (d) :
  • 6.
    Lower genital tract infections Vulvovaginal candidiasis Candida, a commensal organism, is found in small population densities in the vaginal ecosystems of nearly one third of healthy women. Symptomatic infection arises, however, when proliferation causes a shift from colonization to frank adherence and infection. It is caused by Candida albicans in around 80-92 per cent of cases. Other non albican species like C.tropicalis, C. glabmta, C. krusei and C. parupsilosis can also cause similar symptoms, although sometimes more severe and recurrent. C. albicans is a diploid fungus and is a common commensal in the gut flora. The patent complain of: Vulval itching and soreness, thick curdy vaginal discharge dyspareunia and dysuna. Vulval oedema, vulvai excoriation, redness and erythema. Normal vaginal pH, there are speckled Gram-positive spores and log pseudohyphae visible. There are numerous polymorphs present and the bacterial flora is abnormal, resembling bacterial vaginosis.
  • 7.
    Microscopy of thedischarge with 10% KOH will often reveal hyphae or budding yeast in 50%-70% of cases albicans organisms are easiest to identify, as they have long hyphae with blastospores along their length and a terminal cluster of chlamydiaspores . The "atypical" species of yeast, however, may only have features of budding yeast (resembling small snowmen), which are easily obscured within surrounding cellular debris.
  • 8.
    The trichomonad parasiteis a flagellated protozoan that causes up to 25% of vaginitis cases. While trichomonas infection is asymptomatic up to 50% of the time,when clinical signs are present they include irritation and soreness of the vulva, perineum, and thighs, with dyspareunia and dysuria. Typically, the trichomonas infection is accompanied by a copious, greenish-yellow frothy discharge. Unlike bacterial vaginosis, it seems that trichomonas is primarily a sexually transmitted infection.
  • 9.
    . The diagnosisis made by observation of the following features (Table I): A foul-smelling frothy discharge (present in 35% of cases Vaginal pH >4.5 (70% of cases) Punctate cervical microhemorrhages (25%) Motile trichomonads on wet mount (50%- 75%) Papanicolaou smear is quoted to be 70% sensitive in identifying trichomonads. The current primary treatment recommendation is a single 2g dose of oral metronidazole. For those who cannot tolerate this single large dose, 500mg bid for 7 days is equally efficacious if the patient completes her regimen. The male partner(s) must also receive treatment.
  • 10.
     Bacterial vaginosis:there is an overgrowth of anaerobic organisms, including Gardnere/Ia vagina/is (small Gram-variable cocci), and a decrease in the numbers of lactobacilli. A 'clue cell’ is seen.  On wet preparation of vaginal fluid, absence of WBCs and stippling of epithelial cells support a diagnosis of bacterial vaginosis.
  • 11.
    The diagnosis ofBV requires the presence of at least 3 of the following 4 criteria. A homogenous noninflammatory discharge (not many WBCs). Vaginal pH >4.5. Clue cells (bacteria attached to the borders of epithelial cells, >20 % of epithelial cells; Whiff test positive for fishy or musty odor when alkaline KOH solution added to smear. For years, oral metronidazole has been the primary indicated regimen. Other systemic options include oral clindamycin. Pap smear showing clue cells consistent with bacterial vaginos
  • 12.
    According to 2008WHO estimates, 499 million new cases of curable sexually transmitted infections (ie, syphilis, gonorrhoea, chlamydia, trichomoniasis) occur annually throughout the world in adults aged 15- 49 years. Tubal scarring as a result of PID can cause infertility in 20%, ectopic pregnancy in 9%, and chronic pelvic pain in 18% of women[ Complicated PID resulting in tubo-ovarian or pelvic abscess may contribute to patient mortality.
  • 13.
    PID is acomplex polymicrobial disease that is due to the ascending spread of pathogens from the cervix or vagina, most commonly Chlamydia, trachomatis or Neisseria gonorrhoeae (60-75%) , which then spreads into the endometrium, fallopian tubes, ovaries, and adjacent structures. Other pathogens include Mycoplasma hominis, Haemophilus influenzae,Streptococcus pyogenes, Bacteroides species, and Peptostreptococcus species. Less commonly, direct spread from a nearby infection such as appendicitis ordiverticulitis may occur. Hematogenous infection is a rare cause of PID except in cases of tuberculous. Douching is a potential risk factor for PID as it can result in a change of the vaginal flora and introduce bacteria from the vagina into the upper reproductive organs. Usage of intrauterine contraceptive device or gynecologic interventions may also predispose a patient to PID. Direct extension of infection from adjacent viscera and uterine instrumentation are more important risk factors in postmenopausal PID
  • 14.
     Abdominal, pelvicpain and dyspareunla.  Mucopufulent vaginal discharge  Pyrexia (>38‘C).  Heavy/ime.rmenslrual bleedlng  Pelvic tenderness and Tender adnexal or palpable pelvic mass,  Generalized sepsis in severe and sysmmic infection  Tubal damage leading to tubal occlusion, abscess and hydrosalpinx.
  • 15.
    Based on clinicalfindings: Raised white cell count (neutrophilia suggestive of acute inflammatory process) Reduced white cell count (neutropenia in severe infections) Raised C reactive protein and ESR (erythrocyte sedimentation rate) Adnexal masses on ultrasound Laparoscopy is the gold standard to give a definitive diagnosis, however, in mild cases it may not be very obvious.
  • 16.
     Depending onthe severity of the infection, patients with mild/moderate disease can be managed on an outpatient basis with easy access to hospital admission if the infection becomes more severe. An intrauterine contraceptive device, if present, should be removed and alternative emergency contraception or other modes of contraception (combined pill, oral/parenteral progesterone) should be offered. A  pregnancy test should be done in all cases to rule out ectopic pregnancy.  There are several differing antibiotic regimes that are used; however, the following is recommended by the RCOG Green Top Guideline (2008) which is evidence based. Mild/moderate infection (outpatient treatment)  Oral ofloxacin 400 mg twice a day + oral  metronidazole 400 mg twice a day x 14 days  Ceftriaxone 250 mg single intramuscular injection + oral doxycycline 100 mg twice a day  oral metronidazole 400 mg twice a day x 14 days  Single intramuscular dose of ceftriaxone 250 mg azithrornycin 1 g/week x 2 weeks. The data supporting the use of azithromycin are limited and should not be used in isolation.
  • 17.
    Causative organism Herpessimplex virus type I (usually oral) or type II (usually genital). Clinical features Painful vesicles and multiple ulcerations on vulva, Retention of urine. Diagnosis Swab from ulcer, Serum from vesicle, Virus seen on electron microscopy, Culture. Treatment Acyclovir 200 ml five times/ day Famciclovir, Valaciclovir, Analgesics and local unaesthetic gels
  • 18.
    Causative organism: Humanpapillomavirus, HPV6and11, HPV 16 and 18, linked to cervical caner. Clinical features: Warty lesions on the vulva, vagina, cervix and perianal area. Also seen around mouth, lips and larynx if orogenital contact. Diagnosis: Clinical examination: Histology of removed wart Seen on cervical smear and colposcopy Treatment: Podophyllin; local application twice a week, Surgical excision, Laser, Cryotherapy.
  • 19.
    Causative organism: Treponemapallidum Clinical features: Primary syphilis: Painless ulcer/ulcers on vulva, vagina or cervix, Enlarged groin/inguinal lymph nodes Secondary syphilis: maculopapular, rash on palms and soles. Mucous membrane ulcers, Generalized lymphadenopath, arthritis Neurosyphilis: meningitis, strok, tabes dorsalis Cardiovascular: aortic aneurysm Congenital syphilis: intrauterine death, interstitial keratitis, VIII nerve deafness, abnormal teeth Diagnosis: TPPA: Treponema pallidum particle agglutination. TPHA: Treponema pallidum haemagglutinatio assay. FTA: Fluorescent treponemal antibody. Dark Held illumination: serum from base of ulcer + saline taken and seen under the microscope. Spiral organisms with characteristic movements are diagnostic Treatment: Penicillin mainstay of treatment Procaine, penicillin, 1.2 MU daily, i.m. x 12 days, Benzathine penicillin, 2.4 MU i.m. repeated after 7 days. Doxycycline 100 mg bd x 14 days. Erythromycin 500 mg qds x 14 days mm.
  • 20.
    Causative organism: Mycobacteriumtuberculosis. Clinical features: Usually following pulmonary tuberculosis through blood and lymphatics, Amenorrhoea (affects endometrium) Infertility (affects tube), Acute/ chronic pelvic pain, Frozen pelvis due to severe multiple adhesions. Diagnosis: Histological confirmation from endometrium and Fallopian tube, Mantoux test, Heaf test, Chest x-ray. Treatment: Rifampicin, Isoniazid, Pyrazinamide. Treatments can, last from six to 12 months.
  • 21.
    Causative organism: Haemophilusducreyi. Clinical features: Painful shallow multiple ulcers, Regional lymphadenopathy with suppuration. Diagnosis: Isolation of Ducrey’s bacillus on biopsy on biopsy. Treatment: Single oral dose of azethromycin, Ceftriaxone, Erythrofpycin.
  • 22.
    Causative organism: Klebsiellagrarnulomatoses. Clinical features: Painless nodule. Diagnosis: Donovan bodies:intracellular inclusions seen in phagocytes or histiocytes. Treatment: Erythromycin.
  • 23.
    Painful ulcers, Localtissue, destruction, treated with Streptomycn, tetracyclin
  • 24.
    ONE IS TERMEDLACTOBACILLOSIS OR DÖDERLEIN CYTOLYSIS. THIS ENTITY IS CHARACTERIZED BY AN OVERGROWTH OF THE COMMENSAL LACTOBACILLI HENCE, ON SALINE WET MOUNT, ONE FINDS AN EXCESSIVE NUMBER OF BACILLI AMONG THE BACKGROUND FLORA. THE PH IS TYPICALLY LOW-NORMAL. TREATMENT, THEREFORE, IS DIRECTED AT CORRECTING THE DISRUPTION OF THE VAGINAL ECOSYSTEM IN ORDER TO LIMIT THE EXCESSIVE PROLIFERATION OF THESE PROTECTIVE ORGANISMS. INFLAMMATORY VAGINITIS, FEATURES A VAGINAL PH ABOVE 4.2, LARGE NUMBERS OF LEUKOCYTES, AND SOME PARABASAL AND BASAL VAGINAL CELLS, WITH A PAUCITY OF SUPERFICIAL SQUAMOUS CELLS. CLINICIANS OFTEN FIND THAT PATIENTS ARE INFECTED WITH GROUP A OR GROUP B STREPTOCOCCUS THEREFORE, BECAUSE INFECTION IS SUSPECTED TO UNDERLIE THE INFLAMMATION AND DESQUAMATION, TREATMENTS DIRECTED AGAINST BACTERIAL VAGINOSIS ARE RECOMMENDED.