Transcript Microorganisms causing abortion By Dr. Sahar Zakaria

Microorganisms
causing abortion
By
Dr. Sahar Zakaria
Lecturer of Microbiology and Medical
Immunology
Abortion
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It is the expulsion of a fetus from the uterus
before it has reached the stage of viability
(usually about the 20th week of gestation).
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An abortion may occur spontaneously, in which
case it is also called a miscarriage, or it may be
brought on purposefully, in which case it is often
called an induced abortion.
Microorganisms causing abortion:
(1) Treponema pallidum (Syphilis).
(2) Listeria monocytogenes.
(3) Rubella virus.
(4) Cytomegalovirus.
(5) Varicella-Zoster virus.
(6) Parvovirus B19.
(7) Toxoplasma.
Syphilis
 Causative agent:
 It is caused by a spirochaete called Treponema
pallidum.
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It is a delicate spiral filaments with small regular
coils and a characteristic motility.
Seen by dark-ground microscopy.
Stained by silver impregnation and
immunofluorescence methods.
Cultural characters:
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Not cultivated on artificial media.
Grown anaerobically in digest broth enriched
with serum.
Nichol’s strain of T. pallidum can be
propagated in the testicles of rabbit.
 Serological characters:
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Antigenic structure is unknown.
Stimulates the formation of two types of
antibodies:
(1) A treponemal antibody → reacts with
treponema suspensions.
(2) A second antibody (reagin) → reacts with a
non-specific antigen (cardiolipin).
Virulence factors:
(1) The outer membrane → associated with
adherence to the surface of host cells.
(2) Production of hyaluronidase → facilitates
perivascular infiltration.
Transmission:
(1) Sexually.
(2) Transplacentally → from mother to fetus.
(3) By blood transfusion.
(4) As a clinical hazard → in hands of doctors and
nurses by contact with patients.
Pathogenesis:
Three stages:
(1) The primary stage:
• A hard painless ulcer called chancre at the
site of inoculation.
• Begins as a papule that ulcerates.
• Appears 2-10 weeks after exposure.
• Appears mainly on genitalia.
• Regional lymph nodes are enlarged.
• Heals spontaneously within 4-6 weeks.
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(2) The secondary stage:
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6-12 weeks after the appearance of chancre.
Generalized manifestations → skin rash, condylomata
of anus and vulva, and mucous patches in the mouth.
Systemic manifestations → fever, weight loss, joint
pains, hair loss.
T. pallidum is present in large numbers in the lesions.
Symptoms disappear spontaneously in 3-6 months.
Followed by a latent stage which is characterized by:
- Asymptomatic.
- Lasts for few months or for lifetime.
- The organism is still present in the blood.
(3) The tertiary stage:
• Occurs in 30% of untreated cases.
• Granulomas (gumma) appear in the skin and
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bones.
CNS lesions → tabes, paresis.
Cardiovascular lesions → aortitis, aneurysm of
aorta.
Treponema are rarely seen in the lesions.
Congenital syphilis:
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A syphilitic woman transmits the infection to
the fetus transplacentally.
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This leads to 1. abortion.
2. stillbirth.
3. congenital
syphilis.
Congenital syphilis → interstitial keratitis,
Hutchinson’s teeth, saddle nose, CNS anomalies,
IgM antitreponemal antibodies.
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Diagnosis:
I. Detection of spirochaetes in the lesion:
(1) Dark-ground microscopy.
(2) Direct immunofluorescence.
(3) PCR.
II. Serological diagnosis:
Two types according to the type of antigen used:
(1) Non-specific → using nontreponemal
antigens.
(2) Specific → using treponemal antigens.
(1) Non-treponemal antigen tests:
Detect the “reagin” antibody which react with a
non-specific antigen “cardiolipin”.
 1. Venereal Disease Research Laboratory
(VDRL).
2. Rapid Plasma Reagin (RPR).
3. Toluidine Red Unheated Serum Test
(TRUST).
 Used in: 1. Screening.
2. Evaluation of treatment.
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(2) Treponemal antigen tests:
Detect antitreponemal antibodies.
 1. Fluorescent treponemal antibody absorption
(FTA-ABS) tests.
2. T. pallidum haemagglutinin (TPHA) tests.
3. T. pallidum particle agglutination (TPPA) tests.
4. Enzyme-linked immunosorbent assay (ELISA).
 Used as confirmatory tests.
 Remains positive for life.
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Listeria monocytogenes
Morphology:
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Gram-positive, non-spore forming bacilli.
Motile → tumbling movement at 22-28°C but
not at 37ºC.
Produce β-hemolysis on blood agar.
Transmission:
Found in animals, soil, and plants.
 Transmitted by:
(1) Contact with domestic farm animals or their
faeces.
(2) Ingestion of contaminated unpasteurized
milk or cheese.
(3) Contaminated vegetables.
 Can grow at refrigerator temperature.
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Pathogenesis:
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Listeria is an intracellular organism.
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Listeria → phagocytosed by mononuclear
phagocytic cells → phagosome → fused with
the lysosome to form a phagolysosome → the
listeria produces listeriolysin O which lyses the
membrane of the phagolysosome → listeria
escape destruction → move from one cell to
another.
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Host defense is by cell-mediated immunity.
Listeriosis:
(1) Transplacental infection → granulomatosis
infantiseptica → skin lesions and intrauterine sepsis
→ abortion, stillbirth, or premature labour.
(2) Infection during delivery → neonatal meningitis.
(3) Infection in immunosuppressed adults →
meningoencephalitis and bacteremia.
(4) Gastroenteritis → watery diarrhea, fever,
headache, myalgia, abdominal cramps, but little
vomiting → outbreaks may occur.
Diagnosis:
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Isolation of listeria from:
- Blood → by blood culture.
- CSF → on blood agar.
- Stool → on listeria selective media.
Cold enrichment for few days.
Identified by: 1. gram stain.
2. charateristic tumbling movement.
3. β-hemolysis on blood agar.
4. positive catalase test.
Rubella
Causative agent:
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Rubella virus
Belongs to togavirus family.
Enveloped with surface spikes.
Icosahedral nucleocapsid.
Single-stranded RNA genome.
One antigenic type.
Man is the only host.
Transmission:
(1) Respiratory route → adults.
(2) Transplacental route → from mother to fetus.
 According to the route of transmission, two
clinical forms exist:
(1) Postnatal Rubella.
(2) Congenital rubella syndrome.
Pathogenesis:
(1) Postnatal Rubella:
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Incubation period is 2-3 weeks.
Enter through the respiratory route → replicate
in the nasopharynx and regional lymph nodes →
spread via blood → reach the internal organs
and skin → fever, skin rash, and enlargement of
posterior occipital lymph nodes.
(2) Congenital Rubella Syndrome:
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Early intrauterine infection in the first trimester
may lead to
(1) Abortion / intrauterine fetal death.
(2) Congenital rubella syndrome →
congenital heart defects, deafness, blindness,
cataract, meningoencephalitis, mental
retardation, and hepatosplenomegaly. The virus
is shed in pharyngeal secretions and other body
fluids for up to 18 months after birth.
Diagnosis:
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Pregnant woman → detection of rubella
antibodies:
. IgM in a single serum sample.
. Rising IgG titre in paired sera.
Fetus → isolation of the virus from the
amniotic fluid.
Newborn → 1. detection of rubella IgM.
2. Isolation of the virus from the
newborn secretions.
Cytomegalovirus
Morphology & pathogenesis:
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Belongs to Herpesviruses family.
Enveloped.
Double-stranded DNA genome.
Causes massive enlargement of infected cells.
Causes indefinite latent infection that can be
reactivated occasionally.
Transmission:
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Fetus → transplacentally.
Newborn → 1. during passage in the birth canal.
2. in the breast milk.
Adult → 1. saliva.
2. sexually.
3. blood transfusion.
4. organ transplantation.
Clinical forms
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Normal host → may cause:
1. latent infection.
2. infectious mononuleosis-like syndrome.
3. coronary heart disease.
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Immunocompromised host → pneumonia,
retinitis, graft rejection or disseminated disease.
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Congenital infection → may lead to:
- abortion.
- stillbirth.
- cytomegalic inclusion disease →
blindness, deafness, mental retardation,
microencephaly, hepatosplenomegaly, jaundice,
and purpura.
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Newborn → subclinical infection.
Diagnosis:
(1) Detection of intranuclear cytomegalic
inclusions in tissues and desquamated cells in
the urine.
(2) PCR for detection of CMV-DNA.
(3) Isolation of the virus from urine and throat
washings.
(4) Detection of IgM or rising titre of IgG in
congenital infections.
Varicella
Causative agent:
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Varicella-Zoster virus (VZV).
Causes two distinct diseases:
(1) Varicella → the primary disease.
(2) Zoster → the recurrent form.
Belongs to the Herpesviruses family.
Enveloped, double-stranded DNA virus.
Transmission:
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In children and adults:
(1) The respiratory route.
(2) Contact with the lesions.
In neonates:
(1) Transplacentally during pregnancy.
(2) Through the birth canal during labor.
(3) The respiratory route or contact with the
lesions from the mother.
Pathogenesis:
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Incubation period is 14-21 days.
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VZV multiplies in the mucosa of the respiratory
tract → spreads via the blood to the skin causing
the typical rash → evolves from papules to vesicles,
pustules, and finally crusts → Rash starts on the
trunk and spreads to he limbs and face →
Recovery occurs without scar formation.
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The virus becomes latent in the dorsal root
ganglia.
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It is a highly contagious disease in children and
can occur in epidemics.
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The disease is mild in children but severe in
adults
Congenital varicella syndrome:
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Maternal infection with VZV can lead to
abortion, stillbirth, or congenital varicella
syndrome.
Neonates may acquire the infection from the
mother before or just after birth.
It is highly fatal. The main cause of death is
pneumonia.
Diagnosis:
(1) Stained smears of scrapings or swabs of the
base of vesicles shows multinucleated giant cells.
(2) Detection of viral antigens or DNA in
vesicular fluid, skin scrapings, or biopsy.
(3) Detection of viral particles in the vesicular
fluid by electron microscopy.
(4) Isolation of the virus by cell culture.
(5) Detection of virus-specific antibodies.
Parvovirus B19
The causative agent:
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Parvovirus B19 is a small, nonenveloped virus.
The genome is single-stranded DNA.
Transmission:
(1) The respiratory route.
(2) Blood transfusion.
(3) Transplacentally.
Pathogenesis:
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B19 virus attacks immature cells of the
erythroid lineage causing their death.
The virus replicates in the bone marrow and
fetal liver.
Red cell production is interrupted leading to
chronic anemia.
B19 is found in the blood and respiratory
secretions.
Clinical forms:
(1) Erythema infectiosum in children.
(2) Aplastic crisis in patients with sickle cell
anemia.
(3) Severe anemia and persistent infection in
immuncompromised patients.
(4) Abortion, hydrops fetalis, and fetal death in the
fetus.
Diagnosis:
(1) Detection of viral DNA by PCR.
(2) Detection of virus-specific antibodies.
(3) Detection of viral antigens in clinical samples.
(4) Immunohistochemistry to detect viral antigens
in the fetal tissues and bone marrow.