Download Infectious Diseases in Obstetrics and Gynecology, fifth Edition (Infectious Diseases in Obstetrics & Gynecology) PDF

TitleInfectious Diseases in Obstetrics and Gynecology, fifth Edition (Infectious Diseases in Obstetrics & Gynecology)
TagsInfectious Disease Infectious Diseases Obstetrics
File Size11.8 MB
Total Pages1044
Table of Contents
Part I General Considerations
1 Understanding the bacteriology of the female genital tract
2 Immunological defense mechanisms in the female genital tract
3 Anaerobic infections
4 Antibiotic selection in Obstetrics and Gynecology
5 Antibiotics and pregnancy
6 Timing of antibiotic therapy
7 Antibiotic induced diarrhea
8 Prophylactic antibiotics
Part II Organisms
9 Congenital viral infections
10 Cytomegaloviruses
11 Enteroviruses
12 The hepatitis viruses
13 Herpes simplex viruses, types 1 and 2 (HSV-1, HSV-2)
14 Human immunodeficiency viruses
15 Human papilloma viruses
16 Human B-19 parvovirus
17 Influenza viruses
18 Measles
19 Mumps
20 Rubella
21 Varicella-zoster virus (chickenpox)
22 Calymmatobacterium granulomatis
23 Haemophilus ducreyi
24 Haemophilus influenzae
25 Listeria monocytogenes
26 Neisseria gonorrhoeae
27 Salmonella typhi
28 Streptococcus pneumoniae
29 Group A β-hemolytic streptococci
30 Actinomyces israelii
31 Bacteroidaceae
32 Clostridium perfringens
33 Clostridium sordellii
34 Escherichia coli
35 Gardnerella vaginalis (Haemophilus vaginalis)
36 Klebsiella/Enterobacter
37 Mobiluncus species
38 Peptostreptococci
39 The Proteus group
40 Staphylococci
41 Group B streptococci
42 Group C beta-hemolytic streptococci
43 Enterococci and group D streptococci
44 Group F streptococci
45 Group G beta-hemolytic streptococci
46 Chlamydia trachomatis
47 Chlamydia trachomatis lymphogranuloma venereum (L) strains
48 Mycoplasma
49 Borrelia recurrentis
50 Borrelia burgdorferi
51 Leptospira
52 Treponema pallidum
53 Entamoeba histolytica
54 Plasmodial infections
55 Toxoplasma gondii
56 Trichomonas vaginalis
57 Candida albicans
58 Coccidioides immitis
59 Mycobacterium tuberculosis and M. bovis
Part III Problem Areas: Obstetrics
60 Chorioamnionitis
61 Infectious morbidity associated with intrauterine monitoring
62 Postpartum endometritis/ endomyometritis
63 Septic pelvic thrombophlebitis
64 Infectious complications associated with legal termination of pregnancy
65 Septic shock
66a Appendicitis in pregnancy
66b Puerperal mastitis
66c Breast abscess
67 Vaccination of women in pregnancy
68 Urinary tract infections in pregnancy
69 Bacterial endocarditis in pregnancy
Part IV Problem Areas: Gynecology
70 Infectious vulvovaginitis
71 Infectious complications associated with the intrauterine contraceptive device
72 Toxic shock syndrome
73 Nosocomial infections
74 Postoperative infections
75 Acute salpingitis
76 Ruptured tubo-ovarian abscess
77 Pelvic abscess
78 Wound infections
Appendix I
Appendix II
Appendix III
Appendix IV
Document Text Contents
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Page 522

Table 52.4 Alternative therapy advocated for a gravida with secondary syphilis* Medication and
route Rationale
I. 10 million units of
penicillin G (intravenous) Forty or sixty percent of pregnant patients with secondary syphilis will
exhibit a Jarisch-Herxheimer reaction. A comparable phenomenon may
occur Involving the placenta, causing acute placental insufficiency and
possible abortion. If the reaction occurs, diminish but do not discontinue infusion, administer oxygen and antipyretic drugs; intravenous route of
administration is chosen to give better drug control. If no reaction occurs, discontinue intravenous therapy.
II. 2.4 million units of
slowly released
benzathine penicillin Standard treatment of the non-pregnant female as advocated by the CDC.
III. Ampicillin 2 grams
q 12 hours ×10 days (oral)
Penicillin traverses the placental barrier poorly. Despite
in utero treatment with standard therapy,
T. pallidum may not be eradicated. To
treat fetus, as opposed to mother,
the placental drug gradient must be
stacked. Ampicillin traverses the placental barrier more effectively than
penicillin. Replication time for
T.pallidum is 33Œ36 hours. Because of non-synchronous replication, the fetu
s should be treated for a minimum of 7 days.
*The above therapy differs significantly from that
advocated by the Center for Disease Control and
is not FDA-approved advocated a policy of initiating penicillin th
erapy through a controllable vehicle (Table
52.4). Five million units of penicillin G in a liter of five percent dextrose are administered
by a slow intravenous drip. If a Jarisch-He
rxheimer reaction occurs, the infusion is
temporarily discontinued. Oxygen is given by a Venture mask with the patient lying on
her left side. Antipyretics are given to maintain the temperature below 38.5ºC. The fetal
heart rate is monitored. If non-stress test
s remain positive and good fetal heart rate
variability persists, the infusion is cautiously reinstated. If evidence of fetal distress is
identified, the situation is discussed with the mother and an individualized program of
therapy is instituted.
The conversion from intravenous penicillin to
oral ampicillin is predicated upon fetal
considerations. The difference in lipid solubility and ionic binding between benzathine
penicillin and ampicillin is such that ampi
cillin more readily tr
averses the placental barrier. The level of penicillin in cord
and amniotic fluid is governed by the
maternal/fetal gradient. The maternal levels attainable with benzathine penicillin are low
and vary from individual to individual.
The use of benzathine penicillin assures compliance and effective maternal therapy
which is a cornerstone of public health policy.
Without a collaborative multiple institu
tional double-blinded comparative study
spanning at least a five to ten year period, documentation of the superiority or otherwise
of this regimen will be wanting.
Treponema pallidum (syphilis) 507

Page 523

CONGENITAL SYPHILIS Congenital syphilis is primarily a reflection of
inadequate prenatal care. In a review of 54
cases of congenital syphilis in the state
of Massachusetts, 18 mothers had received no
prenatal care, 23 had received inadequate pr
enatal care, 10 cases resulted from maternal
infection or reinfection following initial prenatal examination, and 3 were due to the
failure of the physician to obtain the appropriate tests. Now, a significant number of
congenital syphilis cases have been identified
in which the mother had received adequate
maternal therapy during gestation.
Analysis of infant therapeutic failures after maternal treatment for syphilis in
pregnancy has documented the significance of proximity to maternal spirochetemia and

probably the magnitude of its occurrence. Sheffield
et al.
identified 43 gravidas who had
received antepartum therapy for syphilis acco
rding to the CDC guidelines and who were
delivered of a newborn with congenital syph
ilis. The majority of these women had been
treated for secondary or early latent syphilis
. Thirty-five percent of these women were
treated within 30 days of delivery. Fifty-six percent of the infants were delivered before

36 weeks and 26% of them were stillborn infants. Similarly, Alexander
et al.
that 73% of their treatment failure occurred in women with either secondary or early
latent syphilis.
Why did these therapeutic fa
ilures occur and is there a relationship of therapy to
preterm delivery?
The incidence of occult neonatal infection or disease does not parallel the incidence of
syphilis in pregnancy. Maternal therapy given
early in the infection is often adequate to
eradicate spirochetal replication prior to spirochetemia. If the occurrence of
spirochetemia antedates the establishment of pregnancy, the probability of subsequent

metastatic spread to the products of concep
tion in the face of an established maternal
immune response is non-existent.
Penicillin concentrations as low as 0.018 µg
/ml, sustained for seven days, results in
nearly 100% treponemacidal activity. Idsoe
et al.
demonstrated that this drug
concentration can be achieved with a single dose of 2.4 mU of benzathine penicillin in
non-pregnant adults. The physi
ology of pregnancy alters
penicillin pharmacokinetics
such that the majority of pregnant women administered a single dose of 2.4 mU of
benzathine penicillin do not attain a leve
l of 0.018 µg/ml in fetal blood for the time
required to eradicate the organism.
The risk of an adverse fetal/neonatal outcome is theoretically a function of the
magnitude of the maternal spirochetemia, the effectiveness and safety of antimicrobial

therapy and the magnitude of fetal involvement.
The placenta, like the conceptus, is involved
in the disease process. As with organ
pathology, the mass of treponema organisms determines the extent of fetal pathology. In

its most overt form, syphilitic placentitis is ma
nifested by a marked increase in placental
weight such that the placental-fetal weight ratio
is in the range of 1:3 or even 1:2. The
increase in weight reflects the presence of a
dense stroma beneath the chorionic layer of
the villus, in which a compensatory increase in the number of vascular channels may be
identified. The overall effect
is an increase in connective tissue and cellular mass between
the maternal and fetal circulation analogous to
an alveolar capillary block in the lungs.
With advanced disease, placental
erythroblastosis may be present.
Infectious diseases in obstetrics and gynecology 508

Page 1043

therapy 194
prophylaxis 199
therapy 199
VDRL test 360 Veillonella sp.,
Gram staining of 16 in vaginal flora 5 vesiculopustules, skin cultures 674 Vibrio mulieris, see under Mobiluncus mulieris viral infections, congenital 55 laboratory detection of viruses 677
see also
specific viruses by name
vulva, clinical manifestations of human papillomavirus infection 147
donovanosis of 204 fused condyloma of 155
vulvar carcinoma, lymphogra
nuloma venereum and 335 vulvar ulcers, diagnosis and therapy 680
vulvovaginal candidiasis, see under candidiasis vulvovaginitis, amebic 371 Candida glabrata 418, 547 causal organisms 531 cultures from 537 diabetic 546 discharge in 534 frequent causes 533 Gardnerella vaginalis 271, 538 monoetiological disease type, I 272
polymicrobial disease type, II 272
Haemophilus influenzae infection and 212 herpes simplex viruses, management during pregnancy 111
herpetic 101 diagnosis 688 management 689 primary 687

recurrent 687 infectious 531Œ52 laboratory procedures,
physiological saline wet mount 532
potassium hydroxide wet mount 532
normal secretions 535 prepubescent gonococcal 227 prevalence 531 primary cf recurrent 102
primary herpetic and neonatal outcome 113
pruritus in 534 signs and symptoms 532
stained smears 536 Streptococcus pyogenes 248 Trichomonas vaginalis in 538 vulvar sign 539 Index 1028

Page 1044

warts, genital, morphological types 142
virology of 142
Weil™s syndrome 351
Wendell Homes, Oliver 581 WHO, recommendations for toxoplasmosis therapy 388
wound infection, Proteus group 286 wound infections 654Œ70 classification of 655 contributory factors 658
course 659 definition of 655 diagnosis 659 epidemiology 655
Escherichia coli
270 general considerations 665 group F streptococcus 315 historical development 654 incidence 656 incision technique 667, 668 microbiology of 656
monomicrobial 657 necrotizing 661 necrotizing fasciitis 662, 664 operative field preparation 667 pathogenesis 656 polymicrobial 657
postirradiation necrosis 665 prevention 665 progressive synergistic bacterial gangrene 657, 663
prophylactic antibiotics 666
local 666 systemic 666
prophylactic measures for 669

prophylactic vaccination 670
Staphylococcus aureus in 288 Staphylococcus epidermidis 293 toxic shock syndrome 575
toxin-related 657 treatment 660 zanamivir and influenza virus infection 169
zidovudine, use in health workers exposed to HIV 595 useinHIV 129 zovir for herpetic vulvovaginitis 690 Index 1029

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