MICROBIAL AGENTS

OF OB-GYN INFECTIONS

Objective
Be able to explain:
Classification, characteristics, virulence
factors, pathogenesis & clinical
manifestations, laboratory diagnosis and
treatment
of
Microbial agents of obstetric and
gynecological infections

TOPICS
Microbial agents of:
Vaginitis
Infection of the female Pelvis
Maternal Infections in Pregnancy

VAGINITIS

CAUSES OF VAGINITIS IN ADULT

Common
Infection

Bacterial vaginosis
Vulvovaginal Candidiasis
Trichomonal vaginitis

Uncommon
Infection

Atropic vaginitis with secondary infection

Foreign body with secondary infection
Desquamative inflamatory vaginitis
Streptococcal vaginitis
Ulcerative vaginitis associated with Staph.
aureus & Toxic Shock Syndrome
Idiopathic volvovaginal ulceration
associated with HIV

Non-infectious vaginitis

Bacterial Vaginosis (BV)

Is a disorder of the vaginal ecosystem
characterized by a shif in the vaginal
flora from the normally predominant
Lacto-bacillus to one dominated by a
mix flora including Gardnerella
vaginalis and Provotella, Bacteroides,
and Mycoplasma species.

MICROBIAL AGENTS OF INFECTIOUS

VAGINITIS

VAGINITIS

AGENTS

Bacterial vaginosis Gardnerella vaginalis

Provotella spp.
Bacteroides spp.
Mycoplasma spp

Vulvovaginal
candidiasis

Trichomonal
vaginosis

Candida albicans
Candida tropicalis
Candida stellatoidea
Candida pseudotropicalis
Trichomonas vaginalis

INFECTION OF FEMALE PELVIS

Pelvic Inflamatory Disease (PID)
Postpartum Partum Endometritis and
Cesarean Section
Episiotomy Infection
Postabortion Sepsis
Postoperative Gynecologic Infections

COMMON ETHIOLOGIC AGENTS OF PID

Aerobic Bacteria

OTHER SYSTEM

Neisseria gonorrhoeae

Urogenital

Chlamydia trachomatis

Urogenital

Gardenella vaginalis
Escherechia coli
Streptococcus spp.

Urogenital
Respiratory

Haemophillus influenzae Respiratory

Anaerobic Bacteria

Bacteroides spp.
Peptostreptococcus spp.
Peptococcus spp.
Provotella spp.
Porphyromonas spp.

Mycoplasma

Mycoplasma hominis
Mycoplasma genitalium

Respiratory

POTENTIAL ETIOLOGIC AGENTS OF

POST-OP PELVIC INFECTION
Aerobic Bacteria

OTHER
SYSTEM

Streptococcus spp.
Enterococcus faecalis

Respiratory
Urogenital

Staphylococcus aureus
Staphyl. epidermidis

Respiratory
Urogenital

Escherechia coli

Urogenital

Klebsiella pneumoniae

Urogenital

Gardnerella vaginalis
Anaerobic Bacteria

Bacteroides spp.
Peptostreptococcus spp.
Prevotella bivia
Prevotella disiens
Fusobacterium spp.

Mycoplasma

Mycoplasma hominis

Urogenital

POTENTIAL ETIOLOGIC AGENTS OF

POST-ABORTION INFECTION
Aerobic Bacteria

Streptococcus spp.
Enterococcus faecalis

Respiratory
Urogenital

Staphylococcus aureus
Staphyl. epidermidis

Respiratory
Urogenital

Escherechia coli

Urogenital

Klebsiella pneumoniae

Urogenital

Gardnerella vaginalis
Anaerobic Bacteria

OTHER
SYSTEM

Clostridium perfringens
Clostridium tetani
Bacteroides spp.
Peptostreptococcus spp.
Prevotella bivia
Prevotella disiens
Fusobacterium spp.

MATERNAL INFECTIONS
IN PREGNANCY

IMPLICATION OF SPECIFIC INFECT ON PREGNANCY

INFECTION

IMPACT ON MOTHER & CHILD

Malaria

More frequent, ore severe in pregnancy

LBW, IUGR, pre-term birth, abortion and
stillbirth 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 adult riks of varicella pneumonia

Risk of abortion, stillbirth
Congenital varicella
Measles

Increased maternal mortality (pneumonia)

Risk of prematury
Developmental abnormality (heart d, cleft lip)

Group B
Streptococci

Sepsis in 1-3/1000 beonates, high mortality rates

IMPLICATION OF SOME STDs ON PREGNANCY

INFECTION OF

IMPACT ON MOTHER & CHILD

Neisseria gonorrhoeae

Ophthalmia neonatorum, pre-term

delivery, puerpural infections

Chlamydia trachomatis

Ophthalmia neonatorum, puerpural

infections, pre-term delivery

Bacterial vaginosis

Risk of pre-term delivery

Trichomonas vaginalis

Risk of pre-term delivery

Condylomata acuminatum

Risk of respiratory papillomatoses 1/80

1/1500

Herpes simplex

Neonatal herpes 50% in mother with

primary herpes at delivery

HIV

Transmission in 25-45%
Risk of abortion, pre-term delivery,
puerpural infection

AGENTS OF CONGENITAL INFECTIONS

VIRUS
BACTERIA
Herpes viruses
Triponema pallidum
Parvoviruses
Mycobacterium tuberculosis
Rubella virus
Listeria monocytogenes
Enteroviruses
Campylobacter fetus
Measles virus
Salmonella typhi
HIV-1 & HIV-2
Borellia burgdorferi
Hepatitis B virus
Brucella spp.
Vaccinia
PROTOZOA
Small pox virus
Toxoplasma gondii
Adenovirus
Plasmodium spp.

MICROBES WILL BE DISCUSSED

FACULTATIVE ANAEROBES

Gardnerella vaginalis

ANAEROBE BACTERIA
Basil negative-gram Bacteroides fragilis group .
Provotella spp.
Porphyromonas spp.
Fusobacterium spp.
Basil positive-gram Clostridium perfringens
Coccus positive-gram Peptostreptococcus spp.
Peptococcus spp.
PARASITE
Flagellate Trichomonas vaginalis
Sporozoan Toxoplasma gondii

Gardnerella vaginalis

Gardnerella vaginalis:
Found in the human urogenital tract
In BV large number Serves as one
indicator organism of the syndrome
In BV hydrogen peroxide producing
Lactobacillus increase of:
- G. vaginalis,
- anaerobic negative-gram bacilli
- Peptostreptococci
- Mycoplasma

CLASSIFICATION-TAXONOMY
Taxonomy position of Gardnerella vaginalis
remained unsolved
On the basic of superficial growth
characteristic or morfology classified as
a member of genus:
- Haemophilus, or
- Corynebacterium
But by DNA-hybridization studies: new
genus Gardnerella

GENERAL CHARACTERISTICS
Pleomorfic tiny bacilli, coccobacil
Gram-negative to gram variable
Club form & metachromatic granules: often
present
Non-motile & non-capsulated
Most strain: facultatively anaerobic
Fastidious in nutritional requirements
Not required neither hemin nor nicotinamide
adenine nucleotide
-hemolysis on human blood agar
Pigment: pale yellow

Gardnerella vaginalis Gram stain

LABORATORY IDENTIFICATION
Specimens:
- Cervical, urethral & vaginal swabs
- Sign of sepsis : blood
Can be detected best by Gram stain
Culture not recommended result not
specific enough to predict reliability the
presence of the syndrome.

PRESUMPTIVE DIAGNOSIS OF BV
Amsels criteria 3 of the following 4:
Homogenous vaginal discharge
Direct wet mount of vaginal discharge
shows clue cells
Characteristic fishy odor of material,
particularly after addition of 10% KOH
(potassium hydroxide)
pH >4.5

CLUE CELL
squamous epithelia
cells covered with
tiny bacilli,
especially around
the periphery,
giving the cell a
stippled
appearance.

Discharge Features of Infectious Vaginosis

FIATURES CANDIDA
VAGINITIS

BACTERIAL
VAGINOSIS

TRICHOMONAS
VAGINITIS

Amount

Scant to
moderate

Moderate

Profuse

Color

White

White/gray

Yellow

Consistency

Clumped but
variable

Homogenous,
Homogenous
uniformly coating
walls

Bubbles

Absent

Present

Present

pH

<4.5

>4.7

5.0 6.0

Amine test
10% KOH

Negative

Positive

Occasionally present

Saline
microscopy

Normal flora,
Blastospore, 4045% pseu
dohype

Clue cells,
coccobacillary
flora predominant, absent of
leukocytes

PMNs +++, motile

trichomonands (8090%), no clue cell,
abnormal flora.

Gram

Blastospore
Pseudohyphe

Clue cells, Gr-neg

coccobacil, no

PMNs +++,
Trichomonad, no clue

CANDIDA

VULVOVAGINAL CANDIDIASIS
Superficial Candidiasis:
The most common candidiasis skin &
mucosa
By NF of skin & mucosa colonization
Predispose factors :
- Impaired cellular immunity or
neutropenia
- Prolonged antibiotic therapy
- Invasive procedure

CLASSIFICATION
Order: Cryptococcales
Genera: Candida
Species:
.

C. albicans : paling patogen.

C. tropicalis,
C. parapsilosis,
C. guilliemondi,
C. kefyr,
C. krusei,
C. lusitaniae,
C. glabrata

MORPHOLOGY
C. albicans : dimorphic
fungi
budding yeast cells,
reproduce by budding or
fission
pesudohyphae,
true hyphae = mycelium
chlamydospores : big and
round
blastospores

A. Blastospores & Pseudohyphae

B. Clamydospores, pseudohypha & blastospora
C. Yeast cells form germ tubes

COLONIES
On agar Sabouraud (24 hr at 37oC):
- soft, cream-colored
- yeasty odor
- pesudohyphae grow below the agar surface

Only C. albicans produce pseudohyphae

In serum for 90 at 37oC:
germtubes & true hyphae

On corn-meal agar :
- blastospores,
- pseudohyphae
- chlamydospores

Identification confirmation:
Sugar fermentation & assimilation tests

PATHOGENESIS
Superficial Candidiasis
(mucocutaneus): increased local census of
candida damage the skin or epithelium
permit local invasion of the yeast &
pseudohyphae imflamatory reaction:
pyogenic abscesses to chronic granulomas.

Systemic Candidiasis
candida enter the blood stream &
phagocytic host defences are inadequate to
contain the growth and dissemination of the
yeasts.

CLINICAL FINDING
Cutaneus and Mucosal Candidiasis
- Vulvovaginitis
- Oral trush
- Cutaneus Candidiasis
- Oncomycosis

Systemic Candidiacis: everywhere, eg:

- arthritis
- meningitis
- endphthalmitis

Chronic Mucocutaneus Candidiasis:

onset in early childhood, associated with cellular
immunodeficiency & endocrinopathies chronic
superficial disfiguring infections of skin or mucous.

DIAGNOSTIC LABORATORY TESTS

Specimen
scraping from superficial lesion, exudates, blood, spinal fluid, tissue
biopsies, urine, material from removal intravenous catheter

Microscopic examination
- Gram stain of tissue, centrifuged spinal fluid, & other:
pseudohyphae & budding cells (strongly Gram-positive)
- Skin & nail scraping 10% KOH

Culture
- Yeast colonies: wet mount or Gram: pseudohyphae,
chlamydospore, germ tubes

- Biochemical reaction

Serology (limited used: sensitivity & specificity )

Ab titers & cell mediated immunity

Microscopic Figure
in lactophenol cotton blue

TREATMENT
Mucocutaneus candidiasis
- nystatin, ketokonazole, or fluconazole
(topical)
- eliminating contributing factors

Systemic candidiasis:
- systemic amphotericin, sometimes +
- flucytonsine, fluconazole, or caspofungin orally

Chronic mucocutaneus candidiasis

- ketoconazole or other azones
- lifelong treatment

EPIDEMIOLOGY & CONTROL

Avoid disturbing:
- the normal balance of microbial flora and
- intact host defenses
Candidiasis not communicable, since all
person normally harbor the organism.

ANAEROBIC BACTERIA

FISIOLOGY & GROWTH

CONDITION FOR ANAEROBES
Anaerobic bacteria:
not grow in a presence of O2 and are killed
by O2 or toxic O2 radical.
pH oxidation-reduction potential (E h) also
important in establishing condition that
favor growth of anaerobes
Anaerobes grow at a low or negative Eh

 Aerobic bacteria:
require O2 as a terminal electron acceptor and will
not grow under anaerobic condition.

Facultative anaerobic bacteria:

Do not use O2 for growth and metabolism but
obtain their energy from fermentation condition.
So they require reduced O2 tension for growth and
fail to grow on the surface of solid medium in 10%
CO2 in ambient air.

Aerobes and facultative anaerobes often have

the metabolic system listed below, whereas
anaerobic bacteria frequently not.

Cytochrome systems for the metabolism of O 2

Supeoxide dismutase, which catalyzes the following reaction:

O2- + O2- + 2H+ H2O2 + O2

Catalase, which catalyzes the following reaction:

2H2O2 2H2O + O2

Anaerobic bacteria do not have cytochrome

system.

ANAEROBIC BACTERIA FOUND IN

HUMAN INFECTIONS
BACTERIA

NORMAL SITE

Cocci (Spheres)
Gram positive Peptostreptococcus Colon
Peptococcus

Gram negative Veillonella

Bacilli (Rods)

Mouth, colon

BACTERIA

NORMAL SITE

Bacilli (Rods)
Gram negative Bacteriodes fragilis
group

Colon

Provotella spp

Mouth

Fusobacterium

Mouth, colon

Gram Positive Actinomyces

Mouth

Lactobacillus

Vagina

Propionibacterium

Skin

Mobiluncus

Vagina

Eubacterium, bifido- Mouth, colon

bacterium & arachnia
Clostridium
Also found in soil

Colon1

BACTEROIDES
Very important anaerobes that cause
human infections.
Large group of gram-negative bacilli:
slender rods or coccobacilli.
Normal flora of the bowel & other site
Most common isolated:
B. fragilis group :
- B. fragilis
- B. avatus
- B. distasonis,
- B. vulgatus
- B. thetaiotaomicron

Bacteroides fragilis

GENERAL CHARACTERISTICS
Slim, pale staining, gram-negative rods
Has surface pili & capsule composed of polymer
of two polysaccharides
The LPS endotoxin in the outer membrane is less
toxic than that of most other negative-gram
bacteria
One of the most hardier & more easy grown
anaerobes ( misleading name)
Most strain produce superoxide dismutase and are
relatively tolerance to atmospheric O2
Produce enterotoxin enteric disease in animal

Bacteroides fragilis

ANTIGENIC STRUCTURE
Thermo labile protein & thermos table
lipopolysaccharides antigen: a basis for
serologic classification of B. fragilis
B. fragilis can be divided into serotypes on
the basis of agglutination, gel diffusion, and
fluorescent-antibody assays.
A species-specific capsular polysaccharide
antigen has been demonstrated (capsule
only in clinical isolate)

PATHOGENESIS
Endogenous infection, opportunistic
The relative tolerance of B. fragilis
survive in oxygenated tissue in the period
between its displacement from intestinal
flora.
Pili has adhesive properties
Polysaccharide capsule anti-phagocytosis
& inhibit macrophage migration.
Capsule may stimulates abscess formation
Produce extra cellular enzymes:
collagenase, fibrinolysin, heparinase,
hyaluronidase abscess formation

CLINICAL MANIFESTATION
Onset : Deep pain & tenderness anywhere
below the diaphragm
The bacteria not invasive, mucosal break
maybe the result of trauma or other
diseases, such as diverticulitis.
Fever & acute abdomen may occur depend
on extent of intra-abdominal abscess.

TREATMENT
Drainage of abscess & debridement of necrotic
tissue
Most strain B. fragilis produce -lactamase:
- No penicillins
- Cephalosporin R to -lactamase needed.
R to tetracyclin common
Most strain S to chloramphenicol, clindamycin, &
metronindazole
Still effective among -lactams: cefotaxime &
imipenem
Effective: combination of Calvulanate &
Sulbactam (has -lactamase inhibitors) and
Ampicillin & Ticarcillin (-lactams)

PREVOTELLA
Be classified as:
Pigmented Prevotella & Pophyromonas
Non-pigmented Prevotella spp
Prevotella spp found + other anaerobes in :
brain & lung abscess
PID
Tubo-ovarian abscesses

Prevotella or Pophyromonas

CLASSIFICATION
Prevotella & Pophyromonas
PIGMENTED

NON-PIGMENTED

Pophyromonas asaccharosa

Prevotella buccae

Pophyromonas ginggivalis

Prevotella bivia

Prevotella intermedia

Prevotella oralis

Prevotella melanogenica

Prevotella oris
Prevotella disiens
Prevotella buccalis
Prevotella veroralis

Prevotella bivia

GENERAL CHARACTERISTICS
Anaerobic gram-negative rods
Small coccobacillus, often occuring in pair
or short chain
For growth need hemin
Many strains produce -lactamase
R to penicillin & old cephalosporin
Vaginal flora
Mostly common isolated from GT infection
Can be pathogenic in other body sites

Porphyromonas spp

 Gram-negative bacilli
Part of normal oral flora and occur other
anatomic site
Newly name species previously included
in genus Bacteroides.
Can be cultured from gingival & periapical
tooth infection
More commonly: breast, axillary, and male
genital infections.

FUSOBACTERIUM
Pleomorphic gram-negative rods
Most species produce butyric acid and
convert threonine to proprionic acid
Fusobacterium spp. frequently isolated
from mix bacterial infections caused by
normal mucosal flora.
Occasionally a Fusobacterium spp. Will be
the only bacteria in an infection. (eg.
osteomyelitis)

Fusobacterium nucleatum
The most common Fusobacterium isolated
from infection
Normal flora mouth and occasionally UGT
F. nucleatum characteristically is thin with
pointed ends and may resembles scattered
paddy straw, or a very long, thin filament.
Important agents of oral infections, lung
abscesses, other pleuropulmonary infections
and amniotic fluid infections.

Fusobacterium

Mobiluncus spp
New designed genus
Curved anaerobic bacilly
Has gram-positive type of cell wall, but
strain frequently stain gram-negative or
gram-positive
Mobiluncus mulieris & Mobiluncus curtisii
are highly associated with bacterial
vaginosis what role ??? Still unclear
Slow growth bacteria small colony
together with other bacteria.

Lactobacillus
Normal flora in the mouth and GI Tract
Predominant flora in the vagina
Most species apparently have minimal
pathogenic potential
But Lactobacillus catenaforme is
occasionally associated with
pleuropulmonary infection.

Predominant lactobacilli in Gram stain from

healthy vagina

Clostridium

Spore-forming bacilli
Usually Gram-positive
Most species obligate anaerobe
A few species aero tolerant & will grow
minimally in air at atmosphere pressure
Pathogenic species produce high
potential soluble toxin
Clostridia are widely distributed in nature
Present in soil and in the intestinal tract of
humans and animals.

PROPERTIES
Large Spore-forming gram-positive rods
Spore:
- wider than diameter of rod
- centrally, sub terminally, or terminally
Anaerobe
Motile: pertrichous flagella

Clostridium perfringens
Isolated from 60-90% of clostridial
myonecrosis
There are 5 types of C. perfringens: A E,
according to their production of 4 major
lethal toxins.
Type A: primary responsible for human
diseases: clostridial myonecrosis, less severe
wound infection, and food poisoning.
Type A found in intestinal almost every
animal, but less common cause disease in
animal than in human.

 C. perfringens types B, C, D, and E, occur in

intestinal tract of animal, only occasionally
in human, produce a variety of naturally
occurring diseases of domestic animal.
This types do not permanently inhabit the
soil, as the type A does.

GENERAL CHARACTERISTICS

Short, plump, strongly gram-positive rods

Uniform
Non-motile
Aero tolerant anaerobic
Does not produce spore in ordinary media
To demonstrate spore : special media
Capsule may be seen by direct examination
of smear of wounds, but not uniformly
demonstrable in culture.

Clostridium perfringens

ANTIGENIC STRUCTURE
Strains of C. perfringens produce 12 soluble
substances or toxins al protein in nature
and antigenic.

A. Toxins
Four major lethal Antigens: -, -. -, and toxins, all are exotoxins.
The most important is -toxin : produce by
all 5 types of C. perfringens

B. Other soluble are Enzymes :

Minor antigenic
Non-lethal
Examples:
- collagenase (-Ag),
- deoxyribonuclease (-Ag), and
- hyaluronidase (-Ag)

VIRULENCE FACTORS
Toxin primary important is -toxin : has
lethal, dermonecroti, and hemolytic activity.
The toxin is lecithinase C which split lecithin
to phosphorylcholine and a diglycerise.
The toxin is activated by Ca2+ and Mg2- ions.
In vivo action of -toxin:
on lecithin-containing lipoprotein complexes
in the cell membrane disruption or
leakage of cell membrane lyses of
erythrocytes, destruction of tissue &edema.

PATHOGENESIS
When C. perfringens is introduced into tissue
primary requirement for initiation of infection is a
lowered oxidation-reduction potential.
In the area of reduced O2 tension, the pyruvate of
muscle is incompletely oxidized and lactic acid
accumulates, causing a drop in pH.
Combination of lowered oxidation-reduction
potential & a drop in pH activate endogenous
proteolytic enzymes tissue autolysis.
This release of nutrient and the lowered oxidationreduction potential combine to produce condition
suitable for growth of anaerobic organisms,

 Proliferation of organisms production of

soluble toxins.
In clostridial myonecrosis: toxins diffuse from the
initial site of growth and attack healthy muscle
and surrounding tissue destroy by the toxins
spread of infection into a new necrotic areas.
The edema fluid produced by action of the
clostridial toxins and enzymes on tissue and gas
accumulated from the metabolism of the
organism,
Increase the pressure within muscle bundle so
the circulation is impaired decreasing
oxidation-reduction potential & pH providing
new areas in muscle suitable for clostridial growth.

CLINICAL MANIFESTATION
1. Simple Wound Contamination: may be present
without an obvious pathologic process.
2. Anaerobic Cellulites: more serious than wound
infection
3. Clostridial Myonecrosis: the organism are
invasive with profound toxemia, extensive local
edema, variable amount of gas, massive tissue
damage & death in untreated case.
4. Uterine Infection: special type of clostridial
myonecrosis after illegal abortion,
occasionally occur as puerperal infection
5. Clostridial Septicemia: Invasion to bloodstream
may happen in malignancy with myonecrosis.

DIAGNOSIS
A. Clinically early diagnosis
B. Bacteriological confirmation
Direct smear with Gram stain
Specimen: deep within the wound
Cultures and smear
Specimens: tissue, aspirates, or deep swabs
of affected muscle.

Trichomonas vaginalis

CLASSIFICATION

1.

Kingdom: Protozoa
Phylum: Sarcomastigophora
Subphylum: Mastigophora (flagellate)
Intestinal & Genitourinary flagellates
Giardia, Trichomonas, Dientamoeba,
Chilomastrix
2. Blood & Tissue flagellates
trypanosoma, Leismania
Species:
1. Trichomonas tenax
2. Trichomonas hominis
3. Trichomonas vaginalis

MORFOLOGY
Pear shape
Axostyle
Short undulating membrane lined
with a flagellum
4 anterior flagella
Chromatin basal body
Chromatin granules
Nucleolus
Para basal fiber
Posterior flagellum
Move with wobbling & rotating
motion

LIFE CYCLE

PATHOGENESIS
Normal habitats: human vagina & prostate
gland
T. hominis & T. tenax: harmless commensals
T. vaginalis: low-grade inflammation
In : infection normally limited to vulva,
vagina and cervix
In : Prostate, seminal vesicles, and urethra
may be infected.

Factors affecting pathogenicity:

Intensity of infection
pH & physiological status of the vagina and
other genitourinary tract surfaces
The organism do not survive at normal
vaginal acidity of pH 3.8-4.4
Accompanying bacterial flora

LABORATORY DIAGNOSIS
Specimen:
Vaginal or urethral discharge
Microscopic examination:
Wet preparation in a drop physiological
saline motile trichomonas
Dried smears can be stain with hematoxylin,
Gram or Giemsa
Culture if microscopic negative
- Vaginal or urethral discharge,
- Prostatic secret
- Semen specimen

TREATMENT
Successful treatment destruction of the
trichomonands
Best: topical and systemic metronidazole
(flagyl)
Tinidazole (Fasigyn) and ornidazole
(tiberal) equally effective with fewer side
effects.
Patient sex-partner examined & treated
simultaneously.
Postmenopausal: may be need estrogen

Toxoplasma gondii

MORFOLOGY
Tropozoite:
Boat shape
Thin wall : 4-7 x 2-4m
within tissue cells larger
outside them
Stain lightly with Giemsa

MORFOLOGY
Oocyst
Within oocyst 2
sporocysts form
4 sporozoites in each
sporocyst

LIFE CYCLE
Coccidian protozoan world wide
Infect wide range animals and birds not cause
disease
Normal final host: cats in which oocystsproducing sexual stage of toxoplasma can develop.
Organisms (sporozoites from oocyts or bradyzoites
from tissue cysts) invade mucosal cells of cats
intestine form schizonts or gametocytes.
After sexual fusion of the gametes, oocysts
develop, exit from the host cell into the gut lumen
of the cat and pass out via the feces.

Human infection may acquired in several ways:

Ingestion of undercooked infected meat containing
Toxoplasma cysts
Ingestion of oocysts from fecally contaminated
hands or food
Organ transplantation or blood transfusion
Transplacental transmission
Accidental inoculation of tachyzoites
The parasites form tissue cysts, most commonly in
skeletal muscle, myocardium, and brain; these
cysts may remain throughout the life of the host

PATHOGENESIS
When oocyst is ingested, can either repeat it cycle
in a cat, or if ingested by certain birds, rodents or
other mammals, including human, can establish
an infection.
In the latter case, the oocyst opens in the humans
or other animals duodenum release the 8
sporozoites.
The sporozoites pass through the gut wall
circulate in the body & invade various cells,
especially macrophage, where they form
trophozoits multiply break out spread the
infection to the lymph nodes & other organs.

 These rapidly multiplying crescentric cells

(tachyzoites) initiate the acute stage of
disease.
Subsequently, they penetrate nerve cells,
brain & eye, where they multiply slowly (as
bradyzoites) to form 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.
Infection in human produce either congenital
or postnatal toxoplasmosis,

LABORATORY DIAGNOSTIS
Specimens:
Blood, sputum, bone marrow, cerebrospinal fluid, &
exudates.
Lymph node, tonsillar, striated muscle biopsy.

Microscopic examinations
Smears & sections stained with Giemsas, or other special
stain such as periodic acid-Schiff technique densely
packed cysts.

Animal inoculation
Commonly used for definitive diagnosis.

Serology
IFA and ELISA tests

Toxoplasma gondii
A. Tachyzoites: stained with Giemsa
B. Cysts in brain tissue

TREATMENT
Combination:
pyrimethmine & sulfadiazine/trisulfapyrimidines
Alternative drugs:
spiramycin, clindamycin, trimethoprimsulfamethoxazole
For use in pregnancy:
spiramycin (Rovamycin) until delivery.

FURTHER READING
Baron, JD; Peterson, LR; Finegold, SM: Bailey & Scotts
Diagnostic Microbioloy, 9th edition, Mosby, Sydney, 1994.
Brooks, GF; Butel, JS; Morse, SA: Jawezt, Melnick, &
Adelbergs Medical Microbiology, 23rd Edition,
International Edition, McGraw-Hill, Kuala Lumpur, 2004.
Cohen, J., et all: Infectious Diseases, Volume 1, 2nd Edition,
Mosby, Sydney, 2004.
Ryan, KJ; Ray CG: Sherris Medical Microbiology, an
Introduction to Infectious Diseases, 4th Edition, McGrawHill, Singapore, 2004.
Joklik, WK; Willett, HP; Amos, DB; Wilfret, CM: Zinsser
Microbiology, 20th Edition, Appleton & Lange,
Connecticut, 1992.
Virella, G.: Microbiology and Infectious Diseases, 3rd
Edition, Wlliams & Wilkins, Tokyo, 1997.