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Explain the classification, characteristics,

virulence factors, pathogenesis, clinical


manifestations, laboratory diagnosis and
treatment of the microbial agents that cause
infections in the womens reproductive
system
topics discussed:
Vaginitis
Pelvic Inflammatory disease
Infections occurring during pregnancy
Common infections:
Bacterial vaginosis, Vulvovaginal Candidiasis,
Trichomonal vaginitis
Uncommon Infections:
Atropic vaginitis with secondary infection, Foreign
body with secondary infection, desquamative
inflammatory vaginitis, streptococcal vaginitis,
ulcerative vaginitis associated with S. aureus and
TSS, idiopathic vulvovaginal ulceration associated
with HIV
Non-infectious vaginitis
BV is a disorder in the vaginal ecosystem
characterized by a shift from the normal
predominant lactobacillus to a
predominant mixture of flora including
Gardnerella vaginalis, Prevotella,
Bacteroides and Mycoplasma species.
Candidiasis caused by:
Candida albicans
Candida tropicalis
Candida stellatoidea
Candida pseudotropicalis
Vaginitis caused by Trichomonas vaginalis
Includes
Pelvic Inflammatory Disease (PID)
Postpartum endometritis and Cesarean Section
Episiotomy Infection
Postabortion Sepsis
Postoperative Gynecologic Infections
Common etiologic agents of PID Other system
Aerobic bacteria Neisseria gonorrhoea Urogenital
Chlamydia trachomatis Urogenital
Gardnerella vaginalis
Eschericia coli Urogenital
Streptococcus spp. Respiratory
Haemophilus Influenzae Respiratory
Anaerobic bacteria Bacteroides spp.
Peptostreptococcus
spp.
Peptococcus spp.
Prevotella spp.
Porphyromonas spp.

Mycoplasma Mycoplasma hominis Respiratory


Mycoplasma genitalum
Potential Etiologic Agents of Post-op Other System
Pelvic Infection
Aerobic bacteria Streptococcus spp. Respiratory
Enterococcus faecalis Urogenital
Staphylococcus aureus Respiratory
Staphylococcus Urogenital
epidermidis
Eschericia coli Urogenital
Klebsiella pneumoniae Urogenital
Gardnerella vaginalis

Anaerobic Bacteroides spp.


bacteria Peptostreptococcus
spp.
Prevotella bivia
Prevotella disiens
Fusobacterium spp.

Mycoplasma Mycoplasma hominis Urogenital


Ureaplasma urealyticum Urogenital
Potential etiologic agents of Post-Abortion Other system
Infection
Aerobic Streptococcus spp. Respiratory
Enterococcus faecalis Urogenital
Staphylococcus aureus Respiratory
Staphylococcus Urogenital
epidermidis
Eschericia coli Urogenital
Klebsiella pneumoniae Urogenital
Gardnerella vaginalis
Anaerobic Clostridium perfringens
bacteria Clostridium tetani
Bacteroides spp.
Peptostreptococcus spp.
Prevotella bivia
Prevotella disiens
Fusobacterium spp.
Mycoplasma Mycoplasma hominis Urogenital
Ureaplasma urealyticum Urogenital
Implication of Specific Infection on Pregnancy
Infection Impact on Mother and Child
Malaria More frequent or severe in pregnancy
Low Birth Weight, Intrauterine Growth
Retardation, preterm birth, abortion and still
birth increased
Congenital malaria
Listeriosis Mild maternal infection, but increased
susceptibility
Serious impact on the fetus:amnionitis, preterm
birth, septic abortion, stillbirth
Varicella zoster Rare in adultrisk of varicella pneumonia
Risk of abortion, stillbirth
Congenital varicella
Measles Increased maternal mortality (pneumonia)
Risk of prematurity
Developmental abnormality (heart defect, cleft
lip)
Group B Sepsis in 1-3/1000 neonates, high mortality rates
streptococci
Implication of some STDs on Pregnancy
Infection Impact on mother and
child
Neisseria gonorrhoea Ophtalmus neonatorum,
preterm delivery, puerperal
infections
Chlamydia trachomatis Ophtalmia neonatorum,
puerperal infections, preterm
delivery
Bacterial vaginosis Risk of preterm delivery
Trichomonas vaginalis Risk of preterm delivery
Condylominata acuminatum Risk of respiratory
papillomatoses 1/80-1/1500
Herpes simpleks Neonatal herpes 50% in
mother with primary herpes at
delivery
HIV Transmission in 25-45%
Risk of abortion, preterm
delivery, puerperal infection
Agents of congenital Infection
VIRUS BACTERIA
Herpesviruses Treponema pallidum
Parvoviruses Mycobacterium
tuberculosis
Rubella viruses Listeria monocytogenes
Enteroviruses Campylobacter fetus
Measles virus Salmonella typhi
HIV-1, HIV-2 Borrelia burgdorferi
Hepatitis B virus Brucella spp.
vaccinia PROTOZOA
Small pox virus Toxoplasma gondii
Adenovirus Plasmodium spp.
Found in the urogenital tract
In a large number bacterial vaginitis
Decrease in Lactobacillus increase of
G.vaginalis, anaerobic gram neg
bacilli, peptostreptococci, mycoplasma
Taxonomy remained unsolved
Member of haemophylus or corynebacterium
based on the growth characteristics or
morphology
DNA-hybridization studies: Genus gardnerella
Gardnerella vaginalis

Morphology: pleomorphic bacilli-


coccobacilli
Gram stain: varies
Microsc: club form, metachromatic granules
Non-motile; non-capsulated
Facultatively anaerob
Fastidious in nutritional requirements
Do not require hemin nor nicotinamide
adenine nucleotide
Blood agar B-hemolysis
Pale yellow pigment
Clue Cells : Squamous epithelial cells covered with tiny
esp on the periphery
Gardnerella vaginalis

Laboratory Identification:
Swab from cervix, urethra and vagina
Blood as a sign of sepsis
Gram staining
Culture: not recommended
Amsels Criteria for Presumptive Diagnosis
of BV
3 out of 4
Homogenous vaginal discharge
Clue cells upon direct wet mount of vaginal
discharge
Fishy odor
pH higher than 4.5
Features Candida vaginitis Bacterial vaginosis Trichomonas
vaginitis

amount Scant to moderate moderate Profuse


colour white White/gray Yellow
consistency Clumped; variable Homogenous, uniformly Homogenous
coating walls

bubbles absent present Present


pH <4.5 >4.7 5-6
Amine test (KOH neg pos Occasionally present
10%)
Saline Normal flora, Clue cells, PMN +++, mitile
microscopy blastospore, 40-50% coccobacillary flora trichomonas 80-90%,
pseudohypha predominant, absence of no clue cells,
leucocytes abnormal flora
Gram Blastospore, Clue cells, Gram -, PMN +++.
pseudohyphae, Gram + coccobacilli, no PMN Trichomonad, no clue
rods cells
Vulvovaginal Candidiasis superficial
fungal infection
Normal flora of the skin and mucosal tissue
Colonization occurs under predisposing
factor:
Impaired cellular immunity (neutropenia)
Prolonged antibiotic use
Invasive procedure
Candidiasis

Order Cryptococcales
Genera: Candida
Spesies:
C. albicans, C.tropicalis, C.parapsilosis, C.
guilliemondi, C.kefyr, C.krusei, C.lusitaniae,
C.glabrata
Morphology:
Dimorphic fungi(yeast-like)
Yeast cells budding or fission
Pseudohyphae (C. albicans)
True hyphae = mycelium
Chlamydospores (big, round)
blastospores
Candida

On Saborauds agar, 24 hr, 37oC : soft, cream


coloured, yeasty odour, pseudohyphae (only
for Candida albicans) below the agar surface
Candida in serum at 37OC for 90 minutes
produces germ tubes and mycelium/true hyphae
On corn meal agar Candida produces
blastospores, pseudohyphae, chlamydospores
Chemical test for identification: sugar
fermentation and assimilation tests
Candida

Pathogenesis of superficial Candidiasis


Increased local census of candida cause
damage to the skin and epithelium
Damage on the skin/epithelial surface
permits local invasion of yeast/
pseudohyphae Inflammatory reaction
Pathogenesis of systemic Candidiasis
enters the blood stream
phagocytic host defense unable to stop
growth/dissemination of the yeast
Candida

Clinical finding in cutaneus and mucosal


candidiasis:
Vulvovaginitis
Oral thrush
Cutaneus candidiasis
onycomycosis
Clinical finding in systemic candidiasis:
Arthritis
Meningitis
endophtalmitis
Chronic mucocutaneous candidiasis:
Early childhood, assoc. with immunodeficiency and
endocrinopathies chronic superficial disfiguring
infections of skin or mucous
Candidosis

Laboratory diagnosis:
Specimen: scrapings from lesions, exudates,
blood, spinal fluid, tissue biopsy, materials from
removed I.V. cathether
Gram staining of tissue, spinal fluid, skin
scrapings Gram positive
Culture: yeast colonies, wet mount or Gram:
pseudohyphae, chlamydospores, germ tubes
Biochemical reactions
Serology (limited use) lack sensitivity or
specificity
Candida

Treatment:
Mucocutaneous candidiasis: Nystatin,
ketokonazole, fluconazole (topical)
And eliminate contributing factors
Systemic candidiasis:
Amphotericin (systemic)
Flucytosine, fluconazole, caspofungin
Chronic mucocutaneous candidiasis
ketoconazole
Candida
Epidemiology and Control
Avoid disturbing the normal flora and
the intact host defenses
Candidiasis is not communicable
disease, candida is a normal flora
Anaerobic pathogens:
Gram positive cocci Peptostreptococcus and peptococcus
Gram negative cocci Veillonella
Gram negative bacilli Bacteroides fragilis, prevotella spp,
fusobacterium
Gram positive bacilli Actinomyces, Lactobacillus,
Propionibacterium, Mobiluncus, Eubacterium,
Bifidobacterium, Arachnia, Clostridium
Gram negative bacilli normal flora of the gut
become pathogenic under
circumstances involving disruption of
the normal intestinal mucosa such as
trauma, or surgery.
surface pili and capsule
The LPS endotoxin in the outer membrane is less
toxic than that of most other gram negative bacteria
Superoxide dismutase relatively tolerance to O2
Enterotoxin producing bacteria enteric disease in
animal
Bacteroides fragilis

Serologic classification is based on


thermolabile and thermostable LPS antigen
Serotyping is based on agglutination, gel
diffusion and fluorescent-antibody assays
A species-specific capsular polysacharide
has been demonstrated (capsule only in
clinical isolate)
Bacteroides fragilis

it constitutes 1-2% normal flora, causing


abscesses, soft tissue infect., diarrhea
Causes endogenous infection, opportunistic
Pili adhesion
Polysacharide capsule anti-phagocytosis
and inhibition of macrophage migration
Capsule may stimulate formation of abscess
B.fragilis produce enzymes such as
collagenase, fibrinolysin, heparinase and
hyaluronidase abscess formation
B.fragilis

Upon onset of disease, deep pain and


tenderness below the diaphragm
Abscess formation is due to mucosal
break caused by a trauma or other
diseases such as diverculitis.
Fever and acute abdomen may occur
depending on the extent of intra
abdominal abscess.
B. fragilis

Treatment of abscess is by drainage of


abscess and debridement of necrotic tissue
Antibiotic:
Penicillins are of no use due to -lactamase
Use Cephalosporin which is resistant to -
lactamase
Sensitive to Chloramphenicol, Clindamycin,
metronidazole
Still effective: Cefotaxim, imipenem (-lactams)
Combination of clavulanate and Sulbactam (-
lactamase inhibitor) or Ampicillin and Ticarcillin
(-lactams)
Classification:
Pigmented Prevotella and Porphyromonas
Non pigmented Prevotella spp
Found along with other anaerobs in brain
and lung abscess, in PID and tubo-ovarian
abscess
Prevotella bivia
Gram negative rods, anaerob
Small coccobacillus, in pair or short chain
Requires hemin
Many strains produces -lactamase
Resistant to penicillin and old cephalosporins
Vaginal flora
Common isolated from GT infection
Porphyromonas spp
Gram negative bacilli
Normal flora of the mouth culture obtained
from gingival and periapical tooth infection
More commonly found in breast, axillary and
male genital infections
Fusobacterium spp. is frequently isolated
from mixed bacterial infections caused by
normal mucosal flora (NF of GIT & upper
resp), occasionally it is the only bacteria in
an infection (eg. Osteomyelitis)
Most common strain: F.nucleatum
Microscopically:
thin, pleomorphic gram negative bacilli,
pointed ends resembling scattered paddy
straw
Generally isolated from oral infection, lung
abscess, pleuropulmonary infections, and
amniotic fluid infections.
A cause of BV
Newly designed genus
Curved anaerobic bacilli
Cell wall is gram positive freq stained
negative or positive
M. mulieris and M. curtisii assoc.
with BV
Slow growing bacteria
Normal flora of the mouth and GI tract
Predominant flora in the vagina
Most species have minimal pathogenic
potential
L. catenaforme is assoc. with
pleuropulmonary infection
Spore forming bacilli, distributed in nature;
soil and intestinal tract of human and
animals
Usually gram positive (gram negative in
older culture)
Mostly obligate anaerob, a few
aerotolerant
Pathogenic species produce high potential
soluble toxin
Clostridium

Spore forming, Gram positive rods


Anaerob
Motile pertrichous flagella
Spore:
Wider than the diameter of the rod
Located centrally, sub terminally or terminally
Commonly implicated in gas gangrene and
certain types of food poisoning
Isolated from 60-90% of clostridial
myonecrosis
5 types of C.perfringens (Type A-E) according
to their production of 4 major lethal toxins
type A strains causing diseases in human;
clostridial myonecrosis, less severe wound
infection and food poisoning
Type B-E: in animals intestinal tract, only
occasionally in human
General Characteristics of C.perfringens
Short, plump, gram positive rods, uniform
Capsulated and Non-motile
Aerotolerant anaerobic
Does not produce spore in ordinary media;
spore formed in special media
Capsule may be demonstrated by direct
examination of wounds, but not uniformly
demonstrable in culture
Clostridium perfringens Antigenic structure
C. perfringens produce 12 soluble substances or toxins
a1 protein in nature and is antigenic
TOXINS of C.perfringens are exotoxins (-, -, -, -). The
most important is -toxin, produced by all 5 types of
C.perfringens
Other soluble subtances are enzymes, non lethal, minor
antigenic. These are collagenase (-Ag) destroys
tissue/liquefy muscles, deoxyribonuclease (-Ag),
hyaluronidase (-Ag) destroys intercellular cement
substance
Clostridium perfringens

-toxin : lethal, dermonecrotic and hemolytic


activity.
Toxin is lecithinase C which splits lecithin to
phosphorylcholine and a diglyceride
Toxin is activated by Ca2+ and Mg2- ions
In-vivo action of -toxin:
On lecithin-containing lipoprotein
complexes in the cell membrane,
disrupting the cell membrane, causing
lyses of erythrocytes, destruction of tissue
and edema.
In lowered oxidation-reduction
potential, the pyruvate of muscle is
incompletely oxidized and lactic acid
accumulates (pH decrease) both
conditions activate endogenous
proteolytic enzymes tissue autolysis
the release of nutrient and the
lowered oxidation-reduction potential
a suitable condition for the growth of
anaerobic organisms
In clostridial myonecrosis: toxins diffuse from
initial site of growth, attacking surrounding
healthy muscle and tissue
The edema fluid produced by action of the
clostridial toxins and enzymes on tissue, and
gas accumulated from the metabolism of the
organism
Increased pressure within muscle bundle
impaired circulation decreases oxidation
reduction potential and pH provides new
areas in muscle suitable for clostridial growth
1. Simple wound contamination
2. Anaerobic Cellulites: more serious condition
3. Clostridial myonecrosis; invasive clostridial infection with
profound toxemia, extensive local edema, variable amount
of gas, massive tissue damage and may cause death if
untreated
4. Uterine infection (after illegal abortion) occasionally occur
as puerperal infection
5. Clostridial septicemia: invasion to bloodstream may
happen in malignancy with myonecrosis
Clinically early diagnosis
Bacteriologically confirmation
Gram stain of a direct smear
Collect specimen deep in the wound
Culture and smear
Tissue, aspirates, deep swabs of affected
muscle
Classification: Protozoa
Phylum: Sarcomastigophora
Subphylum: Mastigophora (flagellate)
1. Intestinal and genitourinary flagellates
Giardia, Trichomonas, Dientamoeba, chilomastrix
2. Blood and tissue flagellate
Trypanosoma, Leismania
Species of Trichomonas: T. tenax, T. hominis, T.vaginalis
Trichomonas morphology
Pear shape
Axostyle
Short undulating membrane lined with a lateral
flagellum and 4 anterior flagella
Chromatin basal body
Chromatin granules
Nucleolus
Parabasal fiber
Posterior flagellum
Move with wobbling and rotating motion
Normal habitats: human vagina and prostate
gland
T. hominis and T.tenax are harmless comensals
T. vaginalis causes low grade inflammation
In women: limited to the vulva, vagina, cervix
In men, infection may occur in prostate, seminal
vesicles and urethra
Factors affecting pathogenicity:
Intensity of infection
pH and physiological status of the vagina
and other genitourinary tract surfaces
The organism do not not survive at
normal vaginal acidity (pH 3.8-4.4)
Accompanying bacterial flora
Specimen: vaginal and urethral discharge
Microscopic examination: wet preparation in
a drop physiological saline motile
trichomonas
Dried smears stained with HE, gram or giemsa
Prep culture from vaginal or urethral discharge,
prostatic secret and semen specimen if
microscopic examination is negative
Topical and systemic metronidazole (Flagyl)
Tinidazole (Fasigyn) and ornidazole (Tiberal)
are equally effective with fewer side effect
Sex partner should be examined and treated
simultaneously
Postmenopausal: may need estrogen
Definitive host: cat
Tropozoite
Boat shape
Thin wall, 4-7 x 2-4 m within tissue cells,
larger outside
Stain slightly with Giemsa
T. gondii

Oocyst
Within a sporocyst, 2 sporocysts form
4 sporozoites in each sporocyst
Life cycle of Toxoplasma gondii
Coccidian protozoan world wide, infect wide
range of animals and birds not causing disease
Normal final host: Cats in which oocyst develop
the sexual stage of toxoplasma
Sporozoites or bradyzoites (from tissue cysts)
invade mucosal cells of cats intestine and form
schizonts or gametocytes
After sexual fusion of gametes, oocyst develop
and exit from the host cell, excreted via feces.
How human become infected:
Ingestion of undercooked infected meat
containing T.gondii cysts
Ingestion of oocysts from fecal
contaminated hands or food
Tranplacental transmission
Accidental inoculation of tachyzoites
The parasite then form tissue cysts,
commonly in skeletal muscle, myocardium
and brain. Cyst may remain throughout the
life of the host
Ingested oocyst repeat the cycle in a cat
If ingested by birds, rodents or other
mammals can establish an infection. In this
case, the oocysts opens in the host cells
duodenum releasing sporozoites enter
the circulation, enters various cells
especially macrophage.
In macrophage tropozoits are formed
multiplybreak outspread to lymphnodes
and other organs
T.gondii

These rapidly multiplying crescentric cells


(tachyzoites) initiates the acute stage of disease
Can penetrate nerve cells, brain, eyes where
they multiply slowly (as bradyzoites) and
forming quiescent tissue cysts, initiating the
chronic stage of disease
The tissue cysts are infective when ingested by
cat, or by other animals, more tissue cysts are
produced
In human, T.gondii produce either congenital or
postnatal toxoplasmosis
T.gondii

Laboratory diagnosis
Microscopic examination: smears and sections
stained with giemsa or Periodic acid schiff
Cysts visible densely packed
Animal inoculation for definitive diagnosis
Serology ; IFA and ELISA tests

Specimens are blood, sputum, bone marrow, CSF


and exudates
lymphnode, tonsillar, striated muscle biopsy
T.gondii

Treatment with pyrimethamine and


sulfadiazine/trisulfapyrimidines
Alternative drugs:
Spiromycin, clindamycin, trietoprim-
sulfametoxazole

In pregnancy: spiramycin (Rovamycin), given


until delivery
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