INFECTIONS IN

PREGNANCY
Departemen Mikrobiologi
FK USU Medan
INFECTIONS IN PREGNANCY
Etiology :
 Bacteria

 Virus

 Fungi

Risk :
 Mother

 Neonatus
Reproductive tract infections :
A. Vaginitis & Bacterial Vaginosis (BV)
B. Discharge as major manifestation :
- Gonorrhoeae
- Chlamydia
- NGU (Non Gonococcal Urethritis)
C. Genital ulcer as major manifestation :
- Syphilis
- Chancroid
D. Group B Streptococcus “colonization”

Other infections :
 Tetanus
 Mycobacterium tuberculosis
 Erysipelas
VAGINITIS
 An inflammation of the vagina, most commonly
caused by Candida albicans

 Vulvovaginal candidiasis nearly always an

opportunistic infection

 Women with HIV infection experience frequently

recurring yeast infection
 CANDIDA SPECIES

 A yeast and the most common cause of fungal infection

 Candida albicans is responsible for 90% of infection

 Small ovoid cells that reproduce by budding

 C. albicans may be found in soil, food and hospital

environment.
 They are commensal of human (skin, sputum, GI tract,
female genital tract, etc)
CANDIDA SPECIES
Pathogenesis
 The rise of Candida sp. infection relates to the
increase in medical intervention :
- The use of antibiotics (supressing normal
bacterial flora and permitting proliferation of
Candida organism
- Intravenous catheters (providing route of entry)
CANDIDA SPECIES
Pathogenesis
 Immune supression mediated by disease
(e.g.HIV) or therapy such as steroids are also
associated with increase rates of infection
 Immune response to Candida infection is
mediated by humoral and cellular mechanism
 Candida sp. virulence factors include surface
molecules that permit organism adherence to
other structures ( human cells), acid protease
 CANDIDA SPECIES

Diagnosis
 Can be confirmed using a KOH smear or gram stain to
demonstrate hyphae and yeast form
 Culture : smooth white colony

 Presumtive identification of C. albicans is possible by

inoculating organism from a colony into a small tube of
serum, germ tube should form within 90 minutes.
BACTERIAL VAGINOSIS
 Gardnerella is associated with vaginosis that
has a discharge but no inflammation in the
vagina.
 Vaginosis could lead to complications such as
PID (Pelvic inflammatory disease)

 PMNs generally absent from exudate

 Mostly in women 20-30 years old
 Clinical manifestation:
 decreased H2O2 -producing Lactobacilli
 increase of other vaginal bacteria (esp.
anaerobes); Gram negative coccobacilli and
curved rods adhering to epithelial cells (clue
cells)
BACTERIAL VAGINOSIS
Etiology:
 Gardnerella vaginalis - small, non-motile, gram
negative/variable facultative anaerobic
coccobacilli present in most healthy women

 Mobiluncus sp. - thin, curved, gram negative

anaerobic bacilli; recently demonstrated to be the
chief cause (not normal flora)

 Trichomonas vaginalis - parasite

 Yeast/fungi - mostly Candida spp
 Mycoplasma hominis and Ureaplasma, etc.
BACTERIAL VAGINOSIS
Diagnosis criteria:
 watery, gray discharge - no PMNs

 vaginal pH 4.5+ (normal 3.8-4.2)

 positive amine (fish) odor with 10% KOH

 presence of “clue cells” - epithelial cells covered

by Gardnerella like organisms spreading past cell
boundries
NEISSSERIA GONORRHOEA
Morphology and structure :
 Gram negative cocci `kidney bean’ shape, appear in
pairs, flattened opposing sides
 Readily phagocytosed by polymorphonuclear cell
(PMN)
 Rapidly killed by drying, sun light, moist heat and
many disinfectants
 Size varies 0.6 - 1.5 µm depending on
– species, source of isolates and age of culture.

 Cell wall
- typical of gram negative bacteria
- peptidoglycan backbone, endotoxic
LPS complex and outer membrane protein
 Capsule and pili - may be demonstrated
NEISSSERIA GONORRHOEA
Grow well on chocolate agar
- specialized medium (enriched)
- require CO2 supplement
- 48 hours incubation - well developed
- colony – smooth, non – pigmented
smaller than other spp
Produce autolytic enzyme
- swelling and lysis at 25 oC and at alkaline pH
GONORRHOEA
Symptoms :
- may be mild or absent
- 2 - 7 days after exposure
Men :
Primary site - urethra
Purulent urethral discharge and dysuria
Local extension - epididymitis
-prostatitis
Women :
Primary site - endocervix
Increase vaginal discharge
Urinary frequency, dysuria
Abdominal pain
Menstrual abnormalities
GONORRHOEA

Transmissions:
 sexual contact
 non sexual transmission - extremely rare
Difficult to control:
- changed sexual modes and practices
- lack of effective means to detect asymptomatic
case
- increase antibiotic resistance
- lack of appreciation of the importance of the
disease
- asymptomatic reservoir
-  50% infected women
- 5% infected male

Untreated symptomatic case will become

asymptomatic but infectious
GONORRHOEA
Other localized infections
Rectal gonorrhoea - rectal intercourse
- infected vaginal secretion
- generally asymptomatic
- may cause tenesmus,
discharge or rectal bleeding

Pharyngeal gonorhoea
- asymptomatic (majority)
- sore throat and cervical adenitis
- oro-genital sex
Bartholin abscess
- infection of bartholin gland in
women
Conjunctivitis - severe, acute purulent
- any age including neonates
GONORRHOEA

Risk to mothers:
Pelvic Inflamatory Disease
Infection spread to:
Fallopian tube  salpingitis
Pelvic cavity  pelvic peritonitis and
abscess
 Fever
 Lower abdominal pain and rectal tenderness
 Leukocytosis
Complication - ectopic pregnancy
- infertility.
GONORRHOEA
Specimens:
Pus and secretion from appropriate site:
urethra, cervix, rectum, conjunctiva, throat,
synovial
Gram smear
 Direct smear of specimen from genital site
 Multiple gram negative diplococci `been
shaped'
 Intra or extracellularly
 Male : > 95% sensitive and 99% specific
 Female : 50 - 70% sensitive and 95% specific
 Positive urethral smear and conjunctiva are
diagnostic
 Others – need culture confirmation
Gram Staining of gonococcus:
Bacteria from culture Direct smear -
pus
GONORRHOEA
Culture

 Fragile organism, often mixed with normal flora

 Protect specimen from adverse environmental
effect
 Culture on appropriate enriched selective media
(Modified Thayer-Martin medium)
 Direct streaking at the bed side
 Or transport to the lab (<4 hours) in suitable
transport medium
 Specify the request for culture
 Incubated at 37oC containing 5% CO2 for 24-48
hours
CHLAMYDIA

 5-7% reproductive population

 Risk to mothers: Pre-term labour, PPROM,
Chorioamnionitis, Endometritis
 Conjunctivitis (18-50%), Pneumonia (18%)

 Most are asymptomatic

 Screening needed
CHLAMYDIA LIFE CYCLE
CHLAMYDIA
 Women
 Intermenstrual or postcoital bleeding
 Lower abdominal pain
 Fever (in PID)
 No symptoms in 80%
 Men
 Unilateral pain and swelling of the scrotum
 Fever
 Asymptomatic in 50%
 Neonates
 Injected conjunctivae
 Mucopurulent discharge from eyes
 Bilateral involvement of the eyes
 CHLAMYDIA
 Physical:
 Men may have any, all, or none of the following:
 Mucopurulent urethral discharge
 Unilateral epididymal tenderness and swelling
 Mucopurulent rectal discharge (from anal intercourse)
 Women may have any, all, or none of the following:
 Mucopurulent cervical or vaginal discharge
 Cervical motion tenderness
 Adnexal tenderness
 Lower abdominal tenderness
 Upper right quadrant abdominal tenderness
(Fitz-Hugh and Curtis syndrome)
 Mucopurulent rectal discharge (from anal intercourse)
CHLAMYDIA

 Lymphogranuloma venereum
 Localized inguinal adenopathy or buboes
 Genital ulceration
 "Groove sign" - Separation of inguinal and
femoral lymph nodes by the inguinal ligament
(15-20% of patients)
CHLAMYDIA
Diagnosa Lab:

 Chlamydia membentuk sitoplasmik inklusi 

hanya dpt dilihat dgn pewarnaan khusus spt
pewarnaan Giemsa atau dengan
immunofluorescence

 Pewarnaan Gram: tidak dapat dilihat

 Jika dalam cairan exudat, bakteri dalam sel

epitel diidentifikasi dengan pewarnaan
Fluorescent Antibody atau DNA probe assay
CHLAMYDIA
Diagnosa Lab:

 Antigen Chlamydia di dalam exudat/cairan

tubuh atau urine dapat dideteksi dengan ELISA

 DNA dari Chlamydia dalam exudat/cairan tubuh

atau urine dapat dideteksi dengan PCR
(Polymerase Chain Reaction)

 Kultur Chlamydia sudah jarang dilakukan untuk

mendeteksi bakteri ini
CHLAMYDIA
Diagnosa Lab :

 Jika kultur, dilakukan kultur sel dengan

penambahan cycloheximide (inhibitor protein
sintesis pd sel host tapi tidak pada chlamydia 
replikasi)

 C. trachomatis membentuk inklusi mengandung

glikogen  dpt dilihat dgn pewarnaan Iodine.

 Exudat dr mata, sal.nafas atau sal.genital

kultur positif pada 50% kasus
NON GONOCOCCAL URETHRITIS (NGU)
 Mycoplasma hominis and Ureaplasma
urealyticum
 Bacteria without cell walls, fried egg colonies
slow growers on fat/cholesterol enriched
media
 Risk to mothers and neonates: Post
abortion fever, post- partum sepsis and
neonatal sepsis,pneumonia and meningitis
 Ureaplasma urealyticum
 Also associated with chorioamnionitis, low
birth weight (risk to mothers and
neoneates) and nongonococcal urethritis (in
men)
GROUP B STREPTOCOCCI
“COLONIZATION”
 25% women are carriers
 50% of babies born will be colonized

 1-2% will have Grp B Strep infection

 1:1000 babies

 Pneumonia (early), Meninigitis (Late)

FEMALE GENITAL TRACT NORMAL FLORA
 Lactobacilli
 Gram positive rod in large numbers indicate a
healthy vagina
 Produce lactic acid which helps maintain pH
needed for their survival
 May play a role in protecting women from
gonococcal infections
 Group B betahemolytic Streptococcus agalactiae
colonization
 May be transmitted to neonate
 Can cause systemic disease
GROUP B STREPTOCOCCI
Epidemiology:

 Colonizes the genital tract; risk groups include:

 Infants: Colonization during delivery may
results in invasive disease
 Pregnant and post-partum women
 Non-pregnant adults
 Elderly

 Individuals with chronic underlying disease

GROUP B STREPTOCOCCI
Clinical Presentation:
 Neonates:
 Sepsis, meningitis, pneumonia, cellulitis,
osteomyelitis, septic arthritis
 Pregnant and post-partum women:
 Mild UTI, sepsis; less commonly: osteomyelitis,
endocarditis, meningitis
 Non-pregnant adults
 Bacteremia, skin or soft tissue infections >
pneumonia > urosepsis > endocarditis >
peritonitis > meningitis > empyema
MOTHER TO INFANT GBS
TRANSMISSION
10 – 35%
GBS colonized mother

50% 50%
Non-colonized Colonized
newborn newborn

98% 2%
Early-onset sepsis,
Asymptomatic pneumonia, meningitis

5%
Neurologic Death
sequelae
 Gram Stain Colonies on sheep
blood agar plate

Group B betahemolytic Streptococcus agalactiae

SYPHILIS
 Treponema pallidum
 <1:1000 pregnant women

 Can infect trans placenta from 15th week

 Second stage by birth if not treated

 Screening – VDRL, RPR

 Diagnostic tests – TPI, FTA-Abs

 High dose Penicillins

 PRIMARY SYPHILIS
 During the 1st 10-90 days after sexual encounter
with infected person disease incubates within
body.
 Infected area will develop a sore also called a
Chancre or multiple sores
 The sore is highly infectious
 Chancre sore will resolve in 3-8 weeks if left
untreated
 Chancre sore may not be visible and may be
painless
PRIMARY SYPHILIS
SECONDARY SYPHILIS
 Symptoms occur 6-8 weeks after initial sore
disappears and may include:
 A rash on the palms of the hands and soles of
the feet lasting 2-6 weeks
 Hair loss and patchy areas
 Grayish-white sores in the mouths and throat
 Sense of not feeling good
 It can last for 3-6 months with symptoms
disappearing then reappearing
 Person infected is still capable of transmitting
the disease
 Syphilis begins to affect the entire body
 LATENT SYPHILIS
 Called the Hidden Stage
 Begins when the Secondary symptoms disappear

 The bacteria begins to infest the bone marrow,

lymph glands, vital organs, and the central nervous
system

 It may last up to a month or a lifetime

 1/3 of the cases left untreated will proceed to tertiary

stage
TERTIARY SYPHILIS

Disease is not infectious at this stage

Lesions develop on the skin, bones, and vital organs
Patient experiences: lack of coordination, paralysis,
gradual blindness, dementia, and vomiting.
Gummas or painful tumors may appear on the skin
Late syphilis can result in mental illness, blindness,
other neurological problems, heart disease, and
death.
DIAGNOSES
 Syphilis is diagnosed in 3 ways

1) First recognize the signs and symptoms of

each stage.
2) Blood samples need to be obtained to test for
syphilis antibodies that the body produces
after the infection occurs.
3) A microscopic examination may be performed
of an active lesion to confirm diagnosis.
LABORATORY TESTS
In the later stages of syphilis, blood or
cerebrospinal fluid for serological tests are
necessary for diagnosis.
 Non-specific non-Treponemal tests RPR, VDRL
May cross-react resulting in low-level
false positive tests during pregnancy,
other infections, drug abuse, connective tissue
disease and aging.
Levels usually relate to disease activity and
are used for monitoring treatment.
After effective treatment of syphilis these
tests usually become negative but in some
people, may retain positive at low levels
 LABORATORY TESTS

 Specific anti-treponemal antibody tests TPHA,

EIA
These detect antibody due to past or
present infection with Treponema
pallidum or another treponema species.
They cannot distinguish between different
types of Treponema infection ex. Yaws Syphilis
of the duration of the infection.
Most people with reactive treponemal tests
will continue to have reactive tests for the
remainder of their lives, regardless of
treatment or disease activity.
TETANUS
 Tetanus is an acute,often fatal,disease caused
by an exotoxin produced by the bacterium
Clostridium tetani.
Can be prevented by immunization with tetanus
toxoid.

Characterized by generalized rigidity and

convulsive spasms of skeletal muscles.
The muscle stiffness usually involves the jaw
(lockjaw) and neck and then becomes generalized.
TETANUS
 Clostridium tetani is a slender,gram-
positive,anaerobic rod that may develop a
terminal spore,giving it a drumstick
appearance.
 The organism is sensitive to heat and cannot
survive in the presence of oxygen.
 The spores,in contrast,are very resistant to heat
and the usual antiseptics.
 They can not survive autoclaving at 249.8 °F
(121 °C) for 15-20 minutes.
 The spores are also relatively resistant to
phenol and other chemical agents.
Courtesy : Google Image on tetanus
TETANUS
 The spores are widely distributed in soil and in
the intestines and faeces of
horses,sheep,cattle,dogs,cats,rats, guinea pigs.
 Spores may persist for months to years.
 C. tetani produces two exotoxins, tetanolysin and
tetanospasmin.
 The function of tetanolysin is not known with
certainty.
 Tetanospasmin is a neurotoxin and causes the
clinical manifestations of tetanus.
 Tetanospasmin estimated Human lethal dose 2.5
ng/kg
•Occurrence: Tetanus occurs worldwide but is most
frequently encountered in densely populated regions in
hot,damp climates with soil rich in organic matter.
•Reservoir: Organisms are found primarily in the soil and
intestinal tracts of animals and humans.
•Mode of Transmission :Transmission is primarily by
contaminated wounds,Tissue injury( surgery,burns,deep
puncture wounds,crush wounds,Otitis media ,dental
infection,animal bites, abortion,and pregnancy).
•Communicability: Tetanus is not contagious from person to
person.It is the only vaccine-preventable disease that is
infectious but not contagious.
Incubation Period: 8 DAYS ( 3-21 DAYS)
MATERNAL TETANUS
•Maternal tetanus, defined as tetanus occurring during
pregnancy or within 6 weeks after any type of
pregnancy termination, is one of the most easily
preventable causes of maternal mortality.
•It includes postpartum or puerperal tetanus
(i) postpartum or puerperal tetanus, usually resulting
from septic procedures during delivery,
(ii) postabortal tetanus, following septic maneuvers
during induced abortion
(iii) tetanus during pregnancy, generally resulting from
inoculation through a non genital portal of entry
 TETANUS TOXOID

 Tetanus toxoid was developed by Descombey in 1924,

 Tetanus toxoid immunizations were used extensively in
the armed services during World War II.
 Tetanus toxoid consists of a formaldehyde-treated toxin.
 There are two types of toxoid available —adsorbed
(aluminum salt precipitated) toxoid and fluid toxoid.
 Although the rates of seroconversion are about
equal,the adsorbed toxoid is preferred because the
antitoxin response reaches higher titers and is longer
lasting than that following the fluid toxoid.
 TUBERKULOSIS
 Tuberkulosis adalah penyakit yang disebabkan oleh
infeksi Mycobacterium tuberculosis.

 Kuman penyebab tuberkulosis ditemukan pertama kali

oleh Robert Koch pada tahun 1882.

 Mycobacterium tuberculosis berbentuk batang ramping

lurus, berukuran kira-kira 0,4x3 µm, kuman ini tahan
terhadap asam.

 Kuman biasanya masuk ke dalam tubuh manusia

melalui udara pernafasan ke dalam paru dan dapat
menyebar dari paru ke bagian tubuh lainnya melalui
sistem peredaran darah, saluran lymphe.
 TUBERKULOSIS

 Tuberkulosis paru merupakan penyakit yang prevalensi

tinggi dibanding dengan tuberkulosis lainnya seperti
TB-Miliar,TB-Tulang, TB Meningitis dan TB ekstra
paru lainnya.

 Gejala umum dari TB adalah batuk terus menerus,

berdahak, dahak pernah bercampur darah, dan nyeri
dada yang berlangsung selama 3 minggu atau lebih,
berat badan menurun, berkeringat malam padahal
tidak melakukan kegiatan, demam dan sesak nafas.
TUBERCULOSIS IN PREGNANCY
 Maternal mortality a sensitive indicator of
women’s health
 TB increasing cause of maternal mortality

 Risk of vertical transmission of TB to infant

 Risk of mothers: Maternal TB associated with

higher rates of prematurity,low birth weight,and
intra uterine growth retardation
TUBERCULOSIS IN PREGNANCY
 Diperkirakan bahwa diantara semua wanita hamil
kira-kira 1% menderita tuberculosis paru. Di negara-
negara berkembang dan kurang makmur frekuensi itu
dapat lebih tinggi lagi.

 Di Indonesia berkisar lebih kurang 1,6% (menurut

Sarwono P dan Soemarto).

 Mengenai apakah kehamilan mempunyai pengaruh

buruk atau tidak terhadap penyakit tuberculosis paru
tidak ada persesuaian paham, ada yang berpendapat
bahwa kehamilan dapat menyebabkan progresifitas
dari penyakit tuberculosis paru (dikaitkan dengan
adanya malnutrisi pada ibu hamil).
TUBERCULOSIS IN PREGNANCY
 Penularan tuberkulosis dari ibu ke bayinya dapat
terjadi karena :
1. Hematogen,yakni dari plasenta yang
terinfeksi tuberkulosis.
2. Tertelan cairan amnion yang terinfeksi
tuberkulosis.
3. Aspirasi cairan amnion yang terinfeksi
tuberkulosis.
Ketiga cara tersebut dapat menyebabkan
tuberkulosis kongenital (jarang terjadi)
4. Tertular dari droplet infection dari ibunya
setelah lahir.
 Gejala Klinis
Wanita hamil yang menderita tuberkulosis paru
gejalanya sama dengan yang tidak hamil, masalahnya
tidak mudah untuk mengenal ibu hamil yang
menderita tuberkulosis paru terutama pada stadium
dini dimana si ibu tampak sehat dan tidak
menunjukkan gejala yang khas.

Kemungkinan ibu hamil menderita tuberkulosis paru

apabila :
1. Ibu hamil dengan batuk darah.
2. Ibu hamil dengan keluhan nyeri dada, demam dan
efusi pleura dengan respon terhadap antibiotik tidak
ada.
3. Ibu hamil dengan keadaan sakit kronis yang disertai
berat badan menurun, demam, rasa capek yang
berlebihan, disertai dengan keringat malam.
 4. Ibu hamil dengan gambaran foto thoraks TB paru,
sedangkan gejala klinis yang lainnya tidak
menyokong.
5. Ibu hamil yang pada pemeriksaan tes tuberkulin
berulang terdapat konversi dari negatif menjadi
positif .

Pemeriksaan pendukung untuk menegakkan diagnosa

tuberkulosis paru pada ibu hamil :
1. Foto thoraks
2. Pemeriksaan sputum BTA.
3. Tes tuberkulin
 PENANGGULANGAN :
- Pemberian OAT seperti kombinasi Rifampisin,
Isoniazid dan Pirazinamid aman untuk ibu dan
janin.

- Penderita dengan TB paru aktif dirawat di RS

- Pencegahan kehamilan sementara atau permanen

bagi ibu yang telah mempunyai beberapa anak

- Setelah bayi lahir segera dipisahkan dari si ibu,

lakukan tes tuberkulin, foto thoraks, periksa urin
dan
kumbah lambung.