Microbiology 🦠 Flashcards

1
Q

classification of genital system infections

A
  • Venereal disease: Transmitted by sexual intercourse
  • Non-venereal disease: Not transmitted by sexual intercourse
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2
Q

what are bacteria causes of venereal diseases of genital system?

A
  • Gonorrhea ➱ Neisseria gonorrhea.
  • Syphilis ➱ T. pallidum
  • Lympho-granuloma venereum➱ Chlamydia
  • Non-gonococcal urethritis (NGU)➱ Chlamydia
  • Soft sore ➱ Hemophilus ducrii
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3
Q

what are viral causes of venereal diseases of genital system?

A
  • Herpes Simplex type 2
  • HPV (Human Papilloma virus)
  • HIV
  • HBV
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4
Q

Non-venereal diseases of male and its causes

A

Prostatitis and urethritis may be due to:
- Staphylococcus aureus
- Proteus.
- Streptococcus pyogenes
- Mycoplasma.

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5
Q

Non-venereal diseases of female and its causes

A

Salpingitis, oophoritis and endometritis are due to:
- Staphylococcus aureus
- Proteus.
- Streptococcus pyogenes
- E. coli

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6
Q

Morphology of Neisseria gonorrhea

A
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7
Q

what are the Virulence factors of Neisseria gonorrhea?

A
  • Pili (fimbriae) and outer membrane proteins: adhesion.
  • IgA proteases: inactivate human IgA.
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8
Q

what are the diseases caused by Neisseria gonorrhea?

A

Gonorrhea

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9
Q

clinical picture of Gonorrhea in males

A

Acute urethritis: characterized by profuse purulent discharge

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10
Q

clinical picture of Gonorrhea in females

A

Cervicitis: characterized by profuse vaginal mucopurulent discharge & sometimes acute urethritis & dysuria

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11
Q

clinical picture of Gonorrhea in newborns

A

Ophthalmia neonatorum:
- occur in newborns who are exposed to infected secretions in the birth canal.

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12
Q

Specimens for diagnosis of N. gonorrhea

A
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13
Q

Direct film stained by Gram stain For the diagnosis of N. gonorrhea

A

Detection of intracellular and extracellular Gram-negative diplococci is diagnostic.

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14
Q

culture of N. gonorrhea

A
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15
Q

identification of colonies of N. gonorrhea

A

a) Film stained by Gram stain to show characteristic morphology.

b) Biochemical reactions:
* Ferments Glucose with acid production only.
* Oxidase test: positive.

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16
Q

shape of Treponema pallidum

A

Slender, Spiral filaments with regular coils (coils are small and large in numbers).

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17
Q

what are special contents of Treponema pallidum?

A

The cells have a high lipid content (cardiolipin, cholesterol), which is unusual for most bacteria.

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18
Q

staining of Treponema pallidum

A
  • Stained by Giemsa and Fontana stains
  • not by Gram stain,
  • In tissues can be visualized by silver impregnation methods
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19
Q

Treponema pallidum microscopy

A
  • Cannot be seen by light microscopy
  • Can be seen unstained by dark-field microscopy (motile).
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20
Q

motility of Treponema pallidum

A
  • Have axial filaments, which are otherwise similar to bacterial flagella.
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21
Q

Diseases caused by Treponema pallidum

A

Syphilis

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22
Q

what is the mode of transmission of syphilis?

A

by sexual contact:

  • Organisms penetrate mucous membranes or enter minute breaks in the skin.
  • Less than 10 organisms are capable of producing infection.
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23
Q

clinical picture of syphilis

A

The disease passes into 3 clinical stages:

1- Primary Syphilis: chancre

2- Secondary Syphilis:
- mucous patches on mucous membranes
- Wart-like lesions called β€œcondylomata” in moist intertriginous areas.

3- Tertiary syphilis:
- gumma (granulomatous-like lesion),
- cardiovascular and neurosyphilis.

Can affect all areas of the body and be fatal.

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24
Q

specimens for diagnosis of syphilis

A

Exudate from chancre, mucous patches, blood for serology.

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25
Q

Direct smear for diagnosis of syphilis

A

Examined by:

  • Dark ground microscope for motile treponemes.
  • Fluorescent microscope for smears stained with fluorescein-labelled anti-treponemal antibodies
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26
Q

Sirological tests for the diagnosis of Syphilis

A

A. Non treponemal antigen tests: directed against lipid antigens, principally cardiolipin).

B. Treponemal antigen tests: detect specific antibodies directed against protein constituents of T -pallidum.

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27
Q

compare between Non-treponemal antigen tests & Treponemal antigen tests in terms of:

  • Antigen
  • Examples
  • Effect of treatment and recovery
A
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28
Q

treatment of syphilis

A

Penicillin is the drug of choice in the treatment of syphilis.

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29
Q

morphology, and the characters of Chlamydia trachomatis

A
  • Obligate intracellular bacteria
  • Elementary body/reticulate body
  • Not seen by Gram stain
  • Cannot make ATP
  • Cell wall lacks muramic acid
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30
Q

what properties of bacteria do Chlamydia trachomatis show?

A
  1. They contain both DNA and RNA.
  2. They have Gram negative cell wall.
  3. They contain prokaryotic ribosomes.
  4. They multiply by binary fission.
  5. They are susceptible to many antibiotic
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31
Q

what are the diseases caused by Chlamydia trachomatis?

A

Lymphogranuloma venereum: is a venereal disease spread sexually characterized by genital lesions and regional lymph node involvement (buboes).

Non gonococcal urethritis: in men and acute salpingitis and cervicitis in women.

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32
Q

Life cycle of Chlamydia trachomatis

A
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33
Q

specimen (Laboratory Diagnosis of Chlamydia)

A
  • Scrapping from the urogenital tract.
    • Urethral or Cervical exudates.
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34
Q

microscopic examination (Laboratory Diagnosis of Chlamydia)

A

Inclusion bodies in scraped tissue cells are detected by staining with:
βœ“ Giemsa
βœ“ iodine.
βœ“ fluorescent monoclonal antibodies staining

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35
Q

Culture (Laboratory Diagnosis of Chlamydia)

A

On McCoy cells:
- After incubation, typical cytoplasmic inclusions are seen:

Yolk sac of embryonated egg:
- Have been used to isolate Chlamydia.

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36
Q

Serological tests (Laboratory Diagnosis of Chlamydia)

A

Detection of chlamydial antigen:
- Directly in specimens by using specific immunofluorescent antibodies prepared against C- trachomatis.

Detection of anti-Chlamydia antibodies:
- in sera from infected humans by the complement fixation or micro immunofluorescence tests.

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37
Q

Molecular techniques (Laboratory Diagnosis of Chlamydia)

A

DNA probes:
- It is possible to diagnose C. trachomatis in tissue specimens by hybridization with a specific DNA probe.

  • PCR.
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38
Q

Treatment of Chlamydia

A
  • Tetracycline and Erythromycin is the drug of choice.
  • No role for penicillin
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39
Q

what are viral infections that affect the Genital system?

A
  • herpes viruses
  • Human papilloma viruses
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40
Q

what are the species of Herpes viruses?

A
  • Eight human Herpes virus species are known.
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41
Q

what can Herpes viruses enter?

A
  • All can enter a latent state following primary infection and to be reactivated later
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42
Q

Structure of Herpes viruses

A

Virion: Icosahedral

Genome: ds DNA, Linear

Envelope: with glycoprotein spikes.

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43
Q

what are types of herpes simplex virus?

A
  • There are 2 distinct herpes simplex viruses (HSV-1 and HSV-2)
  • The two viruses cross-react serologically but some unique proteins exist for each type.
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44
Q

compare between HSV-1 & HSV-2 in terms of:
- Terms of transmission
- Multiplication
- Site of lesion

A
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45
Q

what does primary infection with HSV-1 cause?

A
  • Acute gingivostomatitis.
  • Herpes libialis (cold sores)
  • Herptic whitlow: is a pustular lesion of the skin of finger or hand of medical personnel.
  • Keratoconjunctivitis, encephalitis.
  • Disseminated infections, such as pneumonia in immuno-compromised.
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46
Q

where does HSV-1 rest in its latent phase?

A
  • Trigeminal ganglia
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47
Q

what does reactivation of HSV-1 cause?

A
  • In response to stimuli as common colds, hormonal changes and sunlight.
  • They cause Cold sores, Keratitis
48
Q

what does primary infection with HSV-2 cause?

A

Genital herpes:

  • Vesiculo-ulcerative lesions on external genitalia as well as the cervix.

Neonatal infection:

  • Originates chiefly from contact with vesicular lesions within the birth canal.
  • Neonatal herpes varies from a severe generalized disease often involving the CNS, through milder local lesion (keratitis) to asymptomatic infection.
  • Aseptic meningitis
49
Q

Where does HSV-2 rest during its latent period?

A

Sacral ganglia.

50
Q

what does reactivation of HSV-2 cause?

A
  • In response to stimuli as common colds, hormonal changes and sunlight.
  • It Occurs more frequently.
  • Often asymptomatic but still results in viral
    Reactivation shedding.
51
Q

diagnosis of herpes simplex virus

A
52
Q

treatment of herpes simplex virus

A
  • Acyclovir, Famciclovir, and Valacyclovir are the treatment of choices.
  • It shortens the duration of the lesion and decreases shedding of the viru
  • No drug treatment prevents recurrences.
  • No effect on the latent state.
53
Q

what is the structure of human papilloma virus (HPV)?

A
54
Q

what are the types of human papilloma virus (HPV)?

A

There are more than 100 different types of HPV

55
Q

what are the most common sexually transmitted virus?

A

HPV

56
Q

what is the mode of transmission of human papilloma virus (HPV)?

A
  • It requires direct contact with infected individuals
    e.g. sexual contact or contaminated surfaces and common bathroom floors.
57
Q

Hpv type, Clinical lesion and either they are begnin or malignant

  • HPV 1
  • HPV 2,4
  • HPV 16,18
  • HPV 6,11
A
58
Q

what are Condylomata (genital wart)?

A

Condylomata (genital wart) are irregular, soft, pink growths that are found on external genitalia or the anus.

59
Q

what is the virulence factor of HPV?

A
  • HPV virulence factors include proteins (E6 and E7)
  • That are capable of inactivating tumor suppressor proteins (P53),
  • Lleading to uncontrolled cell division and the development of cancer.
60
Q

Laboratory diagnosis of HPV

A
  1. Virus has not been isolated in cell line
  2. Serologic tests rarely done (large number of serotypes)
  3. PCR to detect virus DNA is available.
  4. Screening by Pap smear for all women above 30 in USA. (koilocytes)

In this image, the cervical cells on the left are normal and those on the right show enlarged nuclei and hyperchromasia (darkly stained nuclei) typical of HPV-infected koilocytes.”

61
Q

vaccine for HPV

A
  • Virus-like particle (VLP) vaccine. (L1 and/ Or L2 protein)
  • There are 3 versions of the L1 only HPV vaccine:
    1. Gardasil: HPV16, 18, 6 and 11.
    2. Cervarix: HPV 16, 18.
    3. Gardasil 9: HPV 6, 11, 16, 18, 31, 33, 45, 52, and 58
  • The vaccine is given to females through 10 – 25 years of age.
62
Q

Treatment of HPV

A
63
Q

what do viral infections cause in pregnancy?

A
  • Viral infections in pregnancy are major causes of maternal and fetal morbidity & mortality.
  • Some causative agents resulting in congenital malformation.
64
Q

what are the factors affecting clinical manifestations of viral infections during pregnancy?

A
  • Viral agent and gestational age at exposure
  • The risk of infection is usually inversely related to gestational age at acquisition.
65
Q

Transmission of Viral infections in pregnancy

A

Infections that develop in the neonate can be transmitted through:

  • Transplacental (through placenta),
  • Perinatal (from vaginal secretions or blood),
  • Postnatal (from breast milk or other sources).
66
Q

what are the causative organisms of congenital defects?

A

Infections causing congenital defects described with the acronym TORCH:

T ➱Toxoplasma, Treponema
O ➱ Others,
R ➱ Rubella,
C ➱ Cytomegalovirus
H ➱ Herpes, HIV

67
Q

what are viruses that cause congenital infections?

A
  • Parvovirus B19 (B19V),
  • Varicella-zoster virus (VZV)
  • Zika virus
  • Measles virus
  • Enteroviruses, Adenovirus, West Nile virus, HIV
  • Hepatitis E virus
  • Lymphocytic choriomeningitis virus.
68
Q

what could TORCH infections cause?

A
  • Spontaneous abortion
  • premature birth.
  • Intrauterine growth restriction (IUGR).
  • Abnormalities in the CNS, the skeletal and endocrine systems, and the internal organs (e.g., cardiac defects, vision and hearing los
69
Q

Prevention of Infections that cause congenital defects

A
  1. Primary prevention includes vaccination for varicella and rubella (prior to pregnancy),
  2. Hygiene measures (washing hands)
  3. Affected infants require regular follow-ups to monitor for hearing loss, ophthalmological abnormalities, and developmental delays.
  4. Prophylaxis is of great importance during pregnancy
70
Q

what special ability do herpesviridae have?

A
  • have the ability to enter a latent state following primary infection and to be reactivated at a later time.
71
Q

Structure of herpes viruses

A
72
Q

Classification of herpes viruses

A

Alpha herpes-virinae:
- HSV-1
- HSV-2
- VZV or (HHV-3).

Beta herpes-virnae:
- CMV (HHV-5),
- Human herpes viruses types 6 and 7.

Gamma herpes-virinae:
- EBV (HHV-4)
- Human herpes virus 8.

73
Q

Transmission & Pathogenecity of Cytomegalovirus

A
74
Q

Clinical picture of Cytomegalovirus in primary infection in healthy individuals

A
  • Asymptomatic infection may be associated with intermittent shedding in saliva and urine.
  • Infectious mononucleosis-like syndrome:
    clinically similar to EBV infection. However, they are heterophil antibodies negative.
75
Q

Clinical picture of Cytomegalovirus in primary infection in Immunodeficient individuals

A
  • Hepatitis and pneumonia are common.
  • In AIDS patients, diarrhea and retinitis may also occur.
76
Q

Clinical picture of Cytomegalovirus in primary infection in Congenital infections

A
  • CMV is the most common intrauterine viral infection.
77
Q

Clinical picture of Clinical picture of Cytomegalovirus in latency period

A

Latency is established in monocytes, macrophages and kidney.

78
Q

Clinical picture of Cytomegalovirus after reactivation

A

Repeated episodes of asymptomatic virus shedding over prolonged periods of times.

79
Q

Laboratory diagnosis of Cytomegalovirus

A
  • Virus isolation in cell culture
  • Direct diagnosis
  • Indirect diagnosis
  • Diagnosis during pregnancy
80
Q

Virus isolation in cell culture (Cytomegalovirus)

A
  • CPE in the form of typical swollen and translucent cells with intra nuclear inclusion bodies.
  • The inclusion bodies have an oval (Owl’s eye) shape.
81
Q

Direct diagnosis of Cytomegalovirus

A
  • Fluorescent antibody and histological staining of inclusion bodies in urine and in tissue (viral Ags).
  • PCR for detection of CMV (nucleic acid) in tissues or body fluids e.g. CSF.
82
Q

Indirect diagnosis of Cytomegalovirus

A
  • Serological diagnosis to detect (viral Abs).
83
Q

Diagnosis of Cytomegalovirus infection during pregnancy

A
84
Q

Treatment of Cytomegalovirus

A

Ganciclovir is effective for treatment of retinitis and pneumonia in AIDS patients.

85
Q

Prevention of Cytomegalovirus

A
  • For pregnant women: the saliva and urine of infected children are the main sources of CMV infection.
  • Secondary source is sexual contact.
  • Pregnant women can become infected from their children and no actions can eliminate all risks of catching CMV for them.
86
Q

Prevention behaviors of CMV

A

However, there are some hygiene and behavioral measures that may be taken in order to reduce the viral spread:

  • Hand washing whenever there is contact with a child saliva or urine,
  • Do not sharing drinking glasses or eating utensils with young children, and
  • Do not kissing young children on the mouth or cheek
87
Q
A

..

88
Q

structure of Parvoviruses

A
89
Q

Types of Parvoviruses

A

Dependo-viruses: they require helper virus for their replication which usually an adenovirus
(e.g. Adeno-associated virus).

Autonomous parvoviruses: they are capable of independent replication (e.g. human parvovirus B19).

90
Q

What does Parvovirus B19 target?

A

immature cells of the erythroid lineage (RBCs).

91
Q

Diseases caused by Parvovirus B19

A
  • Transient aplastic crisis in patients with sickle cell disease.
  • Erythema infectiosum (fifth disease or slapped cheek disease).
  • Hydrops fetalis and fetal death due to severe anemia if infection occurs during pregnancy.
92
Q

Why is Fifth Disease or Erythema infectiosum called β€œslapped cheek syndrome”?

A
  • Associated with bright red rash of the cheeks gives it the nickname
93
Q

Incidence of Fifth Disease or Erythema infectiosum

A
  • Any age may be affected
  • although it is most common in children aged six to ten years
94
Q

Incubation period of Fifth Disease or Erythema infectiosum

A

4 -14 days

95
Q

Clinical picture of Fifth Disease or Erythema infectiosum

A
  • Viral prodrome with fever, headache, nausea, diarrhea
  • High fever and malaise, when the virus is most abundant in the bloodstream
  • Patients are usually no longer infectious once the characteristic rash of this disease has appeared.
  • As the fever breaks, a red rash forms on the cheeks, with relative pallor around the mouth β€œslapped cheek rash”, sparing the nasolabial folds, forehead, and mouth.
  • (Lace-like /reticular) red rash on trunk or extremities then follows the facial rash
  • Infection in adults only involves the reticular rash, with multiple joint pain predominating.
96
Q

what causes exacerbation of rash in cases of Fifth Disease or Erythema infectiosum?

A

by sunlight, heat, stress

97
Q

what causes Hydrops fetalis?

A
  • Parvovirus infection in pregnancy is associated with hydrops fetalis due to severe fetal anemia.
  • This is due to a combination of hemolysis of the red blood cells, as well as the virus directly negatively affecting the red blood cell precursors in the bone marrow
98
Q

Effect of Hydrops fetalis

A

May leading to miscarriage or stillbirth

99
Q

Risk factors of Hydrops fetalis

A
  • The risk of fetal loss is about 10% if infection occurs before week 20 of gestation (especially between weeks 14 and 20), but minimal after that.
100
Q

Prevention of Hydrops fetalis

A
  • The best approach is to recommend all pregnant women to avoid contact with children with current symptoms of infection.
101
Q

How to decrease fetal risk of Hydrops fetalis?

A
  1. Correct diagnosis of the anemia (by ultrasound scans)
  2. Correct treatment (blood transfusions).
102
Q

Morphology of Rubella virus

A
103
Q

Family of Rubella virus

A

Togavireadea family

104
Q

what is Rubella?

A

Rubella is a contagious viral infection caused by rubella virus.

105
Q

what is another name for Rubella?

A
  • It’s also called German measles (because it was first described by German physicians in mid-18th century) or three-day measles.
  • The name Rubella is derived from a Latin word that mean little red.
106
Q

Mode of transmission of Rubella virus

A

transmitted via respiratory droplets.

107
Q

Pathogenesis of rubella virus

A
  • Initial replication occurs in the oropharynx and local lymph nodes. Spreads via the blood to the internal organs (including placenta) and skin.
  • The virus is found in the blood 5 to 7 days after infection and spreads throughout the body.
108
Q

Incubation period of Rubella virus

A

14-25 days after infection

109
Q

Infectivity period of Rubella virus

A

During IP, the patient is contagious typically for about one week before development of the rash and for about one week thereafter.

110
Q

What is the clinical picture of Rubella infection in general?

A

Pink, maculopapular rash and posterior auricular lymphadenopathy.

111
Q

What is the clinical picture of Rubella infection in adult infection?

A

Other than pregnant women, symptoms in adults are rare.

112
Q

What is the clinical picture of Rubella infection in children infection?

A

In children, it is a mild febrile illness - less severe than that of measles.

113
Q

What is the clinical picture of Rubella infection in congenital infection?

A

Congenital rubella syndrome (CRS):

  • Low birth weight, deafness, CNS involvement and abortion.
  • The fetus is persistently infected (immature immune response) and continues to excrete virus after birth (a risk to doctors, nurses and other patients).
114
Q

classical triad of rubella

A
  • cataract
  • cardiac abnormality
  • deafness
115
Q

Prevention & control of rubella

A

MMR vaccine

116
Q

MMR vaccine

  • Nature
  • Mode of use
  • Doses
  • Efficacy
  • Side effects
A
117
Q

What is the clinical picture of Rubella infection during pregnancy?

A
  • Virus crosses placenta and multiplies in the fetus (infecting the placenta and the fetus).
  • Up to 85% of infants infected in the first trimester of pregnancy get congenital rubella syndrome (CRS)
  • The earlier the infection occurs in pregnancy, the more worse is the prognosis.