IUI and infections in pregnancy Flashcards

1
Q

Hutchinson’s triad (from congenital syphylis)

A
  • ocular interstitial keratitis
  • 8th nerve deafness
  • Hutchinson’s teeth (murberry molars and Hutchinson’s incisors)
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2
Q

The cdc and USPSTF recommend screening for HBV, HCV:

A

-All adults age 18-79
-Pregnant people, each pregnancy

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3
Q

The incidence of UTI (pyelonephritis, cystitis) asymptomatic bacteriuria in pregnancy

A

5-10 %

Untreated asymptomatic UTI has 25% risk of pyelonephritis and 2.5% with treatment
وفي رواية:
Pyelonephritis develops in 30-40% w/o treatment and in 3-4% with treatment

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4
Q

Leading bacterial killing in neonate is

A

GBS

If term 1-2% colonized develops infection, mortality 5%
If preterm, 8% of colonised develop infection, mortality rate 25 %

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5
Q

Complications of pyelonephritis in pregnancy

A

Sepsis
Cunningham’s syndrome (ARDS)

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6
Q

50% of women who are colonized with GBS will transmit the bacteria to their newborns.

A

In the absence of intrapartum antibiotic prophylaxis, 1–2% of those newborns will develop GBS EOD.

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7
Q

ACOG recommends performing universal GBS screening between

A

36 0/7 and 37 6/7 weeks of gestation.

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8
Q

Regardless of planned mode of birth, all pregnant women should undergo antepartum screening for GBS unless

A

unless intrapartum antibiotic prophylaxis for GBS is indicated because of GBS bacteriuria during the pregnancy or because of a history of a previous GBS-infected newborn.

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9
Q

If the prenatal GBS culture result is unknown when labor starts, intrapartum antibiotic prophylaxis is indicated for women who have risk factors for GBS EOD.

A

At-risk women include those who present in labor with a substantial risk of preterm birth, who have preterm prelabor rupture of membranes (PPROM) or rupture of membranes for 18 or more hours at term, or who present with intrapartum fever (temperature 100.4°F [38°C] or higher).

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10
Q

If intraamniotic infection is suspected, broad-spectrum antibiotic therapy that provides coverage for poly-microbial infections as well as GBS should replace the antibiotic that provides coverage for GBS prophylaxis specifically.

A

T

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11
Q

GBS prophylaxis in case of penicillin allergy/anaphylaxis

A

First-generation cephalosporins (i.e., cefazolin) are recommended for women whose reported penicillin allergy indicates a low risk of anaphylaxis or is of uncertain severity. For women with a high risk of anaphylaxis, clindamycin is the recommended alternative to penicillin only if the GBS isolate is known to be susceptible to clindamycin.

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12
Q

the only pharmacokinetically and microbiologically validated option for intrapartum antibiotic prophylaxis in women who report a high-risk penicillin allergy and whose GBS isolate is not susceptible to clindamycin.

A

Intravenous vancomycin, The dosage for intrapartum GBS prophylaxis should be based on weight and baseline renal function (20 mg/kg intravenously every 8 hours, with a maximum of 2 g per single dose.)

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13
Q

the most common perinatal infection in the developed world.

A

(CMV) is a ubiquitous DNA herpes virus that eventually infects most humans. The virus is secreted into all body fluids, and person-to-person contact.
Naturally acquired immunity during pregnancy results in a 70-percent risk reduction of congenital CMV infection in future pregnancies

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14
Q

Transmission rates for primary infection of CMV are – TO – percent in the 1st trimester, –to– percent in the 2nd, and – to – percent in the 3rd trimester
(ACOG, 2017; Picone, 2017).

A

Transmission rates for primary infection are 30 to 36 percent in the 1st trimester, 34 to 40 percent in the 2nd, and 40 to 72 percent in the 3rd trimester
(ACOG, 2017; Picone, 2017).

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15
Q

CMV infection. Congenital infection is a
syndrome that may include

A

growth restriction, microcephaly, intracranial calcifications”Periventricular”, chorioretinitis, mental and motor retardation, sensorineural deficits, hepatosplenomegaly, jaundice, hemolytic anemia, and thrombocytopenic purpura

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16
Q

Routine prenatal CMV serological screening is currently not recommended by the Society for Maternal–Fetal Medicine (2016).

A

Pregnant women should be tested for CMV if they present with a mononucleosis-like illness or if congenital infection is suspected based on
abnormal sonographic findings.

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17
Q

fetal abnormalities associated with CMV infection may be seen antenatal with US, CT, MRI INCLUDES:

A

Findings include microcephaly, ventriculomegaly, and cerebral calcifications; ascites, hepatomegaly, splenomegaly, and hyperechoic bowel; hydrops; and
oligohydramnios (Society for MFM 2016).

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18
Q

the gold standard for the diagnosis of CMV fetal infection.

A

CMV nucleic acid amplification testing (NAAT) of amniotic fluid (Sensitivity is highest when
amniocentesis is performed at least 6 weeks after maternal infection and after 21
weeks’ gestation) A negative result from amniotic
fluid polymerase chain reaction (PCR) testing does not exclude fetal infection and
may need to be repeated if suspicion for fetal infection is high.

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19
Q

Varicella–zoster virus VZV Mortality is predominately due to

A

VZV pneumonia, which is thought to be more
severe during adulthood and particularly in pregnancy, 2 to 5 % of infected pregnant women develop
pneumonitis. Risk factors for VZV pneumonia include
smoking and having more than 100 cutaneous lesions

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20
Q

congenital varicella syndrome. Some features include

A

chorioretinitis, microphthalmia, cerebral cortical atrophy, growth restriction, hydronephrosis, limb
hypoplasia, and cicatricial skin lesions

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21
Q

If the fetus/neonate is exposed to active infection just before or during delivery, and therefore before maternal antibody has been formed, the newborn
faces a serious threat. Attack rates range from 25 to 50%, and mortality rates approach 30%.

A

neonates develop disseminated visceral
and CNS disease, which is commonly fatal. For this reason, (VZIG) should be administered to neonates born to mothers who have clinical evidence of varicella 5 days before and up to 2 days after delivery.

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22
Q

Maternal varicella Diagnosis

A

is usually diagnosed clinically. Infection may be confirmed by NAAT of vesicular fluid. The virus may also be isolated by scraping the vesicle base during primary infection and performing a Tzanck smear,
tissue culture, or direct fluorescent antibody testing.

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23
Q

Varicella Management, when to give Varicella Immunoglobulins ?

A

Although best given within 96 hours of exposure, its use is approved for up to 10 days to prevent or attenuate varicella infection. + Acyclovir to be started 24 hours after the onset of Rash.
In women with known history of varicella, VariZIG is not indicated.

VZIG to the baby&raquo_space; if the fetus was delivered within 5 days of infection.

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24
Q

management of influenza virus?/ what are the available option of antivirals?

A

Neuraminidase inhibitors are highly effective for the treatment of early influenza A and B. include ORAL oseltamivir (Tamiflu), INHALER zanamivir (Relenza); IV peramivir (Rapivab).

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25
Q

Influenza vaccine in pregnancy

A

for mothers vaccinated during pregnancy, several studies found lower rates of influenza in their infants up to 6 months of age.
A live attenuated influenza virus vaccine is available for intranasal use but is not recommended for pregnant women

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26
Q

MEASLES characteristics

A

Fever, coryza, conjunctivitis, and cough are typical symptoms. characteristic erythematous maculopapular rash develops on the face and neck and then spreads
to the back, trunk, and extremities. Koplik spots are small white lesions with surrounding erythema found within the oral cavity. Immediate or delayed
neurological sequelae of measles may manifest in several forms, making diagnosis difficult

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27
Q

Diagnosis of acute measles infection

A

most commonly performed by serological evidence of IgM antibodies, although RTPCR tests are available.

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28
Q

fetal complications of measles infection

A

The virus does not appear to be teratogenic (Siegel1973). However, rates of spontaneous abortion, preterm delivery, and low-birthweight neonates are
increased with maternal measles. If a woman develops measles shortly before birth, risk of serious infection developing in the neonate is considerable, especially in a preterm neonate.

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29
Q

fetal complications of rubella infection

A

poses significant risk for abortion and severe congenital malformations amenable in prenatal diagnosis like cardiac septal defects, pulmonary stenosis, microcephaly, cataracts, microphthalmia, and
hepatosplenomegaly, sensorineural
deafness, intellectual disability, neonatal purpura, and radiolucent bone disease.

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30
Q

rubella infection transmission

A

Transmission occurs via nasopharyngeal secretions, and the transmission rate is 80% to susceptible individuals. The peak incidence is late winter and spring in endemic areas

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31
Q

clinical presentation of Maternal rubella infection:

A

Maternal rubella is usually a mild febrile illness with a generalized maculopapular rash beginning on the face and spreading to the trunk and extremities. That said, 25 to 50 percent of infections are asymptomatic.

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32
Q

dx of rubella infection:

A

Specific IgM antibody can be detected using enzyme-linked immunoassay for 4 to 5 days after onset of clinical disease, but antibody can persist for up to 6 weeks after appearance of the rash.

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33
Q

rubella infection fetal transmission

A

Pregnant women with rubella and a rash during the first 12 wks GA have an affected fetus with congenital infection in up to 90% of cases, At 13 to 14 wks’ GA, this incidence is 50%, and by the end of the second trimester, it is 25% . Defects are rare after 20 WKS’ GA.

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34
Q

Management and Prevention of rubella infection:

A

There is no specific treatment for rubella. Droplet precautions for 7 days after the onset of the rash are recommended. Postexposure passive immunization with polyclonal immunoglobulin may be of benefit if given within 5 days of exposure.

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35
Q

causes erythema infectiosum, or fifth disease.

A

PARVO B19 virus

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36
Q

Fetal infection has been associated
with

A

anemia, which is its primary fetal effect. (In women with severe hemolytic anemia‒for example, sickle-cell disease‒parvovirus infection may cause an aplastic crisis), abortion, nonimmune hydrops, and stillbirth. Comorbid fetal myocarditis may induce hydrops with
lesser degrees of anemia.

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37
Q

clinical presentation of Maternal Infection of parvo B19 virus

A

20 to 30% is asymptomatic. Fever, headache, and
flulike symptoms may begin in the last few days of the viremic phase. Several days later, a bright red rash with erythroderma affects the face and gives a slappedcheek appearance. The rash becomes lacelike and spreads to the trunk and extremities. symmetrical
polyarthralgia

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38
Q

vertical transmission rate to the fetus in parvo virus infection

A

in up to a third of maternal parvovirus
infections

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39
Q

the rate of fetal loss with serologically proven parvovirus infection is

A

8 to 17 percent before 20 weeks’ gestation, and 2 to 6 percent after midpregnancy.
Hydrops develops in only approximately 1 percent of fetuses of women infected with parvovirus. Still, it is the most frequent infectious agent of nonimmune hydrops in autopsied fetuses

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40
Q

parvo virus Fetal infection is diagnosed by

A

detection of B19 viral DNA in amniotic fluid or IgM antibodies in fetal serum obtained by cordocentesis

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41
Q

important points to be counseled with a mother with parvo virus induced non-immune hydrops

A

Mortality rates as high as 30% have been reported in hydropic fetuses without transfusions. With transfusion, 94% of hydrops cases resolve within 6 to 12 wks, and the overall mortality rate is <10%. Most fetuses require only one transfusion because hemopoiesis resumes as infection resolves. Concurrent fetal thrombocytopenia worsens the prognosis.

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42
Q

important points to be counseled with pregnant woman regarding parvo virus infection

A

Pregnant women should be counseled that risks for infection approximate 5 percent for casual, infrequent contact; 20 percent for intense, prolonged work exposure such as for teachers; and 50 percent for close, frequent interaction such as in the home.
Workers at day-care centers and schools need not avoid infected children because infectivity is greatest before clinical illness. Finally, infected children do not
require isolation.

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43
Q

In the most severely affected fetuses, a congenital Zika
syndrome has been described that includes

A

microcephaly, lissencephaly, ventriculomegaly, intracranial calcifications, ocular abnormalities, and congenital contractures.

44
Q

Diagnosis of zica virus infection in pregnant women is made with

A

detection of Zika virus RNA in blood or urine or by serological testing. Detection of Zika virus RNA by
PCR confirms infection. Serological assays for Zika IgM antibodies may cross react with other flaviviruses. Thus, a positive assay result is followed by another assay containing virus-specific neutralizing antibodies

45
Q

the most common cause of severe maternal postpartum infection and death worldwide

A

Group A Streptococcus Infections caused by Streptococcus pyogenes
Can cause also streptococcal pharyngitis, scarlet
fever, and erysipelas are not life threatening. Treatment, usually with penicillin, is similar in pregnant and nonpregnant women.

46
Q

streptococcal toxic shock syndrome, manifested by

A

hypotension, fever, and evidence of multiorgan failure
with associated bacteremia.

47
Q

streptococcal toxic shock syndrome treatment

A

Treatment includes clindamycin plus penicillin therapy and often surgical debridement

48
Q

S agalactiae (GBS) has been implicated in adverse pregnancy outcomes that include

A

preterm labor, prematurely ruptured membranes, clinical and subclinical chorioamnionitis, and fetal infections. Can also cause maternal bacteriuria, pyelonephritis, osteomyelitis, postpartum mastitis, and
puerperal infections.

49
Q

the leading infectious cause of morbidity and
mortality among infants in US

A

GBS infection

50
Q

neonates Complications of GBS Infection

A

septicemia involves signs of serious illness that usually develop within 6 to 12 hours of birth. These include respiratory distress, apnea, and hypotension.

51
Q

GBS early-onset disease Vs. Late-onset disease

A

GBS Infection <7 days after birth is defined as early-onset disease while Late-onset disease caused by GBS is noted in 0.32 per 1000 live births and usually manifests as meningitis 1 week to 3 months after birth

52
Q

GBS +VE Women with a penicillin allergy and no history of anaphylaxis are given —— (Briody, 2016). Those at high risk for anaphylaxis should have antimicrobial susceptibility testing performed to exclude —— resistance.

A

CEFAZOLIN, If +ve h/o anaphylaxis clindamycin, if resistant vancomycin should be administered. Erythromycin is no longer used for penicillin-allergic patients.

53
Q

MRSA risk factors include

A

prior MRSA infection, hospitalization, dialysis or surgery within the past year, and indwelling catheters or
devices

54
Q

treatment of MRSA infections Uncomplicated superficial infections/ Severe superficial infections

A

antibiotic therapy in addition to incision and drainage of smaller abscesses.
Severe superficial infections, especially those that fail to respond to local care or those in patients with medical comorbidities, are treated with Vancomycin remains the first-line therapy for inpatient serious MRSA infections. Purulent cellulitis should be treated empirically for CA-MRSA (trimethoprim-sulfamethoxazole and clindamycin) until culture results are available.

55
Q

+VE CULTURE MRSA PROPHYLAXIS

A

For women with culture-proven CA-MRSA infection during pregnancy, we add single dose vancomycin to routine beta-lactam perioperative prophylaxis for cesarean deliveries and higher-order perineal lacerations. Breastfeeding in these women is not prohibited, but optimal hygiene and attention to minor skin breaks is encouraged.

56
Q

Treatment of listeriosis

A

ampicillin plus gentamicin is usually recommended because of synergism against Listeria species
Trimethoprim-sulfamethoxazole can be given to penicillin-allergic women.

57
Q

listeriosis fetal presentation

A

Occult or clinical infection also may stimulate
labor. Discolored, brownish, or meconium-stained amnionic fluid is common with fetal infection, even in preterm gestations. fetal infection that characteristically produces disseminated granulomatous lesions with
microabscesses. Chorioamnionitis is common, and placental lesions include multiple, well-demarcated macroabscesses. Early- and late-onset neonatal
infections are similar to group B streptococcal sepsis.

58
Q

enteric (typhoid) fever caused by salmonella treatment

A

Fluoroquinolones and third-generation cephalosporins are the preferred treatment.

59
Q

Shigellosis Clinical manifestations range from

A

mild diarrhea to severe dysentery, bloody stools, abdominal cramping, tenesmus, fever, and systemic toxicity.

60
Q

Shigellosis treatment

A

Antimicrobial therapy is imperative, and effective
treatment during pregnancy includes fluoroquinolones, ceftriaxone, or azithromycin.

61
Q

toxoplasmosis Maternal infection is associated with a —fold increased preterm delivery rate
before 37 weeks

A

toxoplasmosis Maternal infection is associated with a fourfold increased preterm delivery rate
before 37 weeks

62
Q

The incidence and severity of fetal toxoplasmosis depend on gestational age at the time of maternal infection.

A

Risks for fetal infection rise with gestational age. A
metaanalysis estimated the risk to be 15 percent at 13 weeks, 44 percent at 26 weeks, and 71 percent at 36 weeks. Conversely, the severity of fetal infection is much greater in early pregnancy, and these fetuses
are much more likely to have clinical findings of infection

63
Q

fetal complications of toxoplasmosis

A

Clinically affected neonates usually have low birthweight, hepatosplenomegaly, jaundice, and anemia, microcephaly. learning disabilities. This classic triad—chorioretinitis, intracranial calcifications, and hydrocephalus—is often accompanied by convulsions.

64
Q

diagnosis of toxoplasmosis

A

With IgG antibody confirmed before pregnancy, there is no risk for a congenitally infected fetus. Although IgM antibodies appear by 10 days after infection and usually become negative within 3 to 4 months, they may remain detectable for years. Thus, IgM antibodies are not used alone to diagnose acute toxoplasmosis. , if a high-avidity IgG result is found, infection in the preceding 3 to 5 months is excluded. Multiple tests are available that allow high avidity results to confirm
latent infection with a 100-percent positive-predictive value. Prenatal diagnosis of congenital
toxoplasmosis is performed using PCR amplification of toxoplasma DNA in amnionic fluid. The sensitivity of PCR varies with gestational age and is lowest before 18 weeks.

65
Q

Congenital toxoplasmosis is suspected when sonography reveals findings such as

A

hydrocephaly, intracranial or hepatic calcifications, ascites, placental thickening, hyperechoic bowel, and growth restriction.

66
Q

Prenatal treatment is based on two regimens

A

spiramycin alone or a pyrimethamine–sulfonamide combination given with folinic acid.
most experts will use spiramycin in women with acute infection early in pregnancy to reduce vertical
transmission. Because it does not cross the placenta, spiramycin may not be used to treat fetal infection. Pyrimethamine–sulfadiazine with folinic acid is selected for maternal infection after 18 weeks’ gestation or if fetal infection is suspected.

67
Q

TOXOPLASMOSIS management

A

Maternal&raquo_space; Spiramycin 1G Q8h till delivery.
Fetal infection&raquo_space; Pyrimethamine , sulfadiazine and folinic acid for 1 year

68
Q

most serious congenital infection.

A

Rubella

69
Q

most common congenital infection occurring in 0.2-2.2%

A

CMV

70
Q

classification of neonatal HSV infection:

A

1) localized disease of the skin , eye and mouth &raquo_space; the most common 45% , not associated with mortality.
2) CNS disease with to without skin , eye and mouth disease&raquo_space; 30%
3) Disseminated disease&raquo_space; 25 % , 30% mortality rate.

71
Q

what situations should cesarean delivery be considered for prevention of neonatal HSV?

A

If there is active genital lesions or symptoms such as vulvar pain or burning at delivery .

72
Q

When does hydrops develop due to parvovirus B19 virus ?

A

Within 10 weeks of maternal infection.

73
Q

During what weeks of pregnancy is the risk of congenital varicella syndrome is the highest?

A

Between 13-20 weeks.

74
Q

How should HIV RNA levels be monitored in pregnancy?

A

4 weeks after initiation of treatment , then monthly until undetectable , then every 3 months including a value near term.

75
Q

What is the regimen of zidovudine antepartum ?

A

100 mg orally five times a day , 200 mg three times daily or 300 mg twice daily.

75
Q

What is the regimen of zidovudine antepartum ?

A

100 mg orally five times a day , 200 mg three times daily or 300 mg twice daily.

76
Q

When should IV zidovudine be started prior to elective cesarean section ?

A

3 hours prior to surgery

77
Q

what is the maternal treatment if the HIV RNA level is >1000 copies/mL?

A

Combination antiretroviral therapy ( CART )

78
Q

What is the recommended mode of delivery ?

A

Scheduled cesarean section at 38 weeks is recommended for women with a viral load >1000 copies/mL.

79
Q

Whats the detection rate of quad test for trisomy 21?

A

75% for women younger than 35 yo. 90% for women whose older than 35 yo.

80
Q

Without intervention, the risk of HIV transmission Intrapartum is

A

50%

81
Q

most genital infections with HSV are caused by

A

HSV-2.
However, HSV-1 infections are becoming increasingly common as a cause of oral and genital infections, particularly among adolescent women and young women!

82
Q

the incidence of new HSV-1 or HSV-2 infection during pregnancy is approximately

A

2%

83
Q

diagnosis of herpes simplex virus

A

The tests used to confirm the presence of HSV infection can be divided into two basic groups: 1) viral detection techniques and 2) antibody detection techniques.
Virologic tests are preferred for patients who present with genital vesicles, ulcers, or other mucocutaneous lesions and include viral culture and HSV antigen detection by polymerase chain reaction (PCR).

84
Q

If both IgG and IgM are positive what test can be done to know whether there is an acute infection or chronic persistent

A

Avidity test
If high means chronic
If low means acute

85
Q

What happens During the S phase ?

A

new DNA is synthesized.

86
Q

The G2 (premitotic) phase is characterized by

A

cells having twice the DNA content as they prepare for division.

86
Q

The G2 (premitotic) phase is characterized by

A

cells having twice the DNA content as they prepare for division.

87
Q

،actual mitosis and chromosomal division take place during the — phase.

A

actual mitosis and chromosomal division take place during the M phase.

88
Q

Prophylaxis of malaria during pregnancy :

A

Mefloquin in 2nd and 3rd trimester

89
Q

Listeria monocytogenes, listeriosis microbiology description

A

food-borne infection, small, facultatively anaerobic, Gram-positive, flagellated, linear motile rod, which is non-spore forming, grows well in broth, blood agar and most routine culture media

90
Q

CDC Recommendations for the Prevention of Listeriosis

A

Thoroughly cook raw food from animal sources and Wash raw vegetables before eating
Keep uncooked meats separate from vegetables and from cooked foods and ready-to-eat foods
Avoid unpasteurized (raw) milk/ foods made from it
Wash hands, knives, and cutting boards after the handling of uncooked foods
Consume perishable and ready-to-eat foods ASAP

Do not eat hot dogs, luncheon meats, or deli meats, unless they are reheated until steaming hot
Avoid getting fluid from hot dog packages on other foods, utensils, and food preparation surfaces, and wash hands after handling hot dogs, luncheon meats, and deli meats
Do not eat soft cheeses, such as feta, brie, and camembert; blue-veined cheeses; or Mexican-style cheeses, such as queso blanco, queso fresco, and Panela, unless they have labels that clearly state they are made from pasteurized milk
Do not eat refrigerated pâtés or meat spreads. Canned or shelf-stable pâtés and meat spreads may be eaten.
Do not eat refrigerated smoked seafood, unless it is contained in a cooked dish, such as a casserole. Refrigerated smoked seafood, such as salmon, trout, whitefish, cod, tuna or mackerel, is most often labeled as “nova-style,” “lox,” “kippered,” “smoked,” or “jerky.” The fish is found in the refrigerator section or sold at deli counters of grocery stores and delicatessens. Canned or shelf-stable smoked seafood may be eaten.

91
Q

pregnant women is diagnosed with toxoplasmosis .what is the drug of choice for reducing the risk of fetal infection?

A

spiramycin

92
Q

Toxoplasmosis caused by which organism and mode of transmission?

A
93
Q

Syphilis diagnostic tests

A
94
Q

Management options of syphilis:

A
95
Q

Management (dx and prevention and treatment ) of malaria in pregnancy

A
96
Q

Toxoplasmosis management

A
97
Q

warm phase of septic shock

A

capillary leakage initially causes hypovolemia, if intravenous crystalloid is given at this point, sepsis hemodynamically can be described as a high-cardiac-output, low-systemic-vascular-resistance condition . pulmonary hypertension develops, and despite the high cardiac output, severe sepsis also causes myocardial depression

98
Q

cold phase of septic shock

A

severe and unresponsive extracellular fluid extravasation with vascular insufficiency, overwhelming myocardial depression, or both. Oliguria and continued peripheral vasoconstriction characterize a secondary, cold phase of septic shock

99
Q

Tdap vaccine offered to pregnant woman btw

A

27-36 wks GA

100
Q

Risk of intrauterine infection in case of HSV infection

A

5%

101
Q

Women chronically infected with HBV and high viral load (>106 log copies/ml (200,000 IU/ml) and higher) should be offered

A

antiviral medication with teno- fovir or telbivudine in the third trimester to reduce perinatal transmission of HBV (strong recommendation, low level of evidence). ACG Guidelines*

102
Q

Fetal infection develops in >– percent of untreated early maternal syphilis cases and in up to – percent of late latent disease.

A

Fetal infection develops in >50 percent of untreated early maternal syphilis cases and in up to 10 percent of late latent disease

103
Q

Early-stage syphilis includes primary, secondary, and early latent syphilis. These are associated with high spirochete loads, and partner transmission rates range from – to – percent (Garnett, 1997; Singh, 1999). Late-stage syphilis includes latent syphilis, unknown duration or late and tertiary syphilis. In these, transmission rates decline because of smaller inoculum sizes.

A

Early-stage syphilis includes primary, secondary, and early latent syphilis. These are associated with high spirochete loads, and partner transmission rates range from 30 to 60 percent (Garnett, 1997; Singh, 1999). Late-stage syphilis includes latent syphilis, unknown duration or late and tertiary syphilis. In these, transmission rates decline because of smaller inoculum sizes.

104
Q

15% to 45% the absence of intervention, the rate of transmission of HIV from a mother living with HIV to her child during pregnancy, labour, delivery or breastfeeding ranges from –% - –%

A

15% to 45%