Lyme Pregnancy
Citations, Abstracts, Articles
Gestational Lyme borreliosis. Implications for the fetus.
MacDonald AB
Rheum Dis Clin North Am 1989 Nov 15:657-77
Great diversity of clinical expression of signs and symptoms of gestational Lyme borreliosis parallels the diversity of prenatal syphilis. It is documented that transplacental transmission of the spirochete from mother to fetus is possible. Further research is necessary to investigate possible teratogenic effects that might occur if the spirochete reaches the fetus during the period of organogenesis.
Autopsy and clinical studies have associated gestational Lyme borreliosis with various medical problems including fetal death, hydrocephalus, cardiovascular anomalies, neonatal respiratory distress, hyperbilirubinemia, intrauterine growth retardation, cortical blindness, sudden infant death syndrome, and maternal toxemia of pregnancy.
Whether any or all of these associations are coincidentally or causally related remains to be clarified by further investigation. It is my expectation that the spectrum of gestational Lyme borreliosis will expand into many of the clinical domains of prenatal syphilis.
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Death 8-Day Old Californian Baby Boy
Culture positive seronegative transplacental Lyme borreliosis infant mortality.
Lavoie PE;Lattner BP;Duray PH; Barbour AG; Johnson HC.
Arthritis Rheum 1987; Volume 30, Number 4, 3(Suppl):S50.
"Transplacental infection by Borrelia burgdorferi (Bb), the agent of Lyme Borreliosis (LB), has recently been documented (L.E. Markowitz, et al; P.A. Schlesinger, et al). Fetal infection confirmed by culture has been reported by A.B. MacDonald (in press) from a highly endemic region (Long Island, NY).
We report a culture positive neonatal death occurring in California, a low endemic region. The boy was born by C-section because of fetal distress. He initially appeared normal. He was readmitted at age 8 days with profound lethargy leading to unresponsiveness. Marked peripheral cyanosis, systemic hypertension, metabolic acidosis, myocardial dysfunction, & abdominal aortic thrombosis were found. Death ensued. Bb was grown from a frontal cerebral cortex inoculation. The spirochete appeared similar to the original Long Island tick isolate. Silver stain of brain & heart was confirmatory of tissue infection.
The infant was the second born to a California native. The 20 m/o sibling was well. The mother had been having migratory arthralgias and malaise since experiencing horse fly & mosquito bites while camping on the Maine coast in 1971. The family was seronegative for LB by ELISA at Yale. Cardiolipin antibodies were also not found."
http://www.angelfire.com/punk/lymedisease/M8.html
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JAMA. 1986 Jun 27;255(24):3394-6. Related Articles, Links
Lyme disease during pregnancy.
Markowitz LE, Steere AC, Benach JL, Slade JD, Broome CV.
Lyme disease is an increasingly recognized tick-borne illness caused by a spirochete, Borrelia burgdorferi. Because the etiologic agent of Lyme disease is a spirochete, there has been concern about the effect of maternal Lyme disease on pregnancy outcome.
We reviewed cases of Lyme disease in pregnant women who were identified before knowledge of the pregnancy outcomes. Nineteen cases were identified with onset between 1976 and 1984. Eight of the women were affected during the first trimester, seven during the second trimester, and two during the third trimester; in two, the trimester of onset was unknown.
Thirteen received appropriate antibiotic therapy for Lyme disease.
Of the 19 pregnancies, five had adverse outcomes, including syndactyly, cortical blindness, intrauterine fetal death, prematurity, and rash in the newborn.
Adverse outcomes occurred in cases with infection during each of the trimesters. Although B burgdorferi could not be implicated directly in any of the adverse outcomes, the frequency of such outcomes warrants further surveillance and studies of pregnant women with Lyme disease.
PMID: 2423719 [PubMed - indexed for MEDLINE]
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Acta Eur Fertil 1988 Sep-Oct;19(5):279-81
Lyme Borrelia positive serology associated with spontaneous abortion in an endemic Italian area.
Carlomagno G; Luksa V; Candussi G; Rizzi GM; Trevisan G
Dept. of Obstetrics and Gynecology, University of Trieste School of Medicine.
Lyme borreliosis acquired during pregnancy may be associated with stillbirth and fetal malformations. This paper reports preliminary results of a study intended to evaluate the frequency of Borrelia burgdorferi infection associated with spontaneous abortion in an endemic Italian area.
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Lyme disease during pregnancy.
Schutzer SE; Janniger CK; Schwartz RA
Department of Allergy and Immunology, New Jersey Medical School, Newark 07103-2714.
Lyme disease, caused by infection with Borrelia burgdorferi, can affect those exposed to a vector tick. Pregnant women are no exception, and such infection places the fetus at risk. It is particularly important to recognize the disease early so that effective therapy may be instituted. Although the present patient had a favorable outcome, not all do. Clinical diagnosis is especially important since conventional laboratory tests may be inadequate or require lengthy periods of time before a positive result occurs. The dermatologic sign of Lyme disease, erythema migrans, although occurring in only 50 percent of cases, is likely to be the most important diagnostic sign.
NLM PUBMED CIT. ID: 2070648 NLM CIT. ID: 91300895
SOURCE: Cutis 1991 Apr;47(4):267-8
http://www.cdc.gov/epo/mmwr/preview/mmwrhtml/mm4834a3.htm
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Congenital Syphilis
Of the 801 reported cases, 651 (81.3%) occurred because the mother received no penicillin treatment or inadequate treatment before or during pregnancy; in 233 (35.8%) of these cases, the mother received no prenatal care.
Infants of mothers who had an unknown or equivocal response to therapy accounted for 91 (11.4%) of all cases; in 30 of these cases, the infant was evaluated and found to have evidence of CS radiographically or by examination of CSF.
The remaining 59 (7.4%) infants were reported to have CS because of inappropriate serologic response to therapy in the mother (4), evidence of treatment failure or reinfection, or other reasons.
Of the reported 801 infants, 748 (93.4%) were live born, 45 (5.6%) were stillborn; eight (1.0%) of those born alive were reported to have died, six within the first 2 days of life.
CS surveillance is complicated by difficulty in establishing the diagnosis. Most infants born with CS have no signs of the disease at birth. If untreated, symptoms may begin within 3 months after birth and may include anemia, skin rash, hepatosplenomegaly, and nasal discharge.
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About 1 out of every 10 newborns in the United States--375,000 per year--is exposed prenatally to one or more drugs. In major cities, many hospitals report that the percentage of newborns showing the effects of drugs is 20 percent or even higher.
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Fatal outcomes were observed in 26% of infants with congenital syphilis, including late fetal death (7%), stillbirth (16%), or neonatal death (3%). CONCLUSIONS: In the Russian Federation, the frequency of congenital syphilis is high, risk factors for congenital syphilis are modifiable, and the consequences of congenital syphilis are severe.
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Infectious diseases and pregnancy:
Infections during pregnancy can pose a threat to the fetus. Even a simple urinary tract infection, which is common during pregnancy, should be treated immediately. An infection that goes untreated can lead to premature labor and rupture of the membranes surrounding the fetus.
https://www.lpch.org/DiseaseHealthInfo/HealthLibrary/pregnant/conds.html
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Infectious syphilis in a pregnant woman usually results in miscarriage, stillbirth, or a congenitally infected baby. Risk of transmission diminishes as maternal syphilis advances, but in early latent (asymptomatic) syphilis the risk of vertical transmission remains about 30% to 60%
Seventeen children born in the United Kingdom were reported as meeting case definitions for congenital syphilis. Three children had clinical abnormalities; two had signs on x ray pictures (one osteochondritis of the skull), and the third had hepatosplenomegaly, rhinitis, oedema, and thrombocytopenia.
http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=28738
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Congenital Syphilis
When a pregnant woman has syphilis, she can transmit the infection to her unborn child, causing congenital syphilis.
By the age of 2, children born with congenital syphilis show symptoms such as problems affecting the skin, teeth, bones, liver, blood, kidneys, eyes, nerves, and brain.
* Secondary Syphilis
This stage usually begins 2 to 10 weeks after the chancre heals. Syphilis bacteria enter the blood and spread through the body causing many different symptoms, including rash (small red bumps), fever, headache, loss of appetite, weight loss, sore throat, muscle aches, joint pain, a generally ill feeling, and enlarged lymph nodes. Gray or white wart-like patches of skin called condylomata lata can appear on the moist areas around the anus and vagina. In this stage, syphilis may attack the liver, kidneys, and eyes or cause meningitis.
* Late (Tertiary) Syphilis
After the secondary stage passes, some people with syphilis progress to a latent stage where they have no more symptoms. Others go on to have symptoms of late syphilis that affect the eyes, large blood vessels, nerves (neurosyphilis), and brain. Late syphilis has many different signs and symptoms, including memory loss, psychological problems, difficulty walking, loss of balance, loss of feeling (especially in the legs), problems with bladder control, impotence, vision problems, and symptoms of heart disease.
Pregnant women with syphilis can also pass the infection to their unborn children at any time during pregnancy or even during birth.
http://kidshealth.org/parent/infections/std/syphilis.html
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Medscape Womens Health. 1998 Jan;3(1):5.
Recognizing and treating syphilis in pregnancy.
Larkin JA, Lit L, Toney J, Haley JA.
Division of Infectious Disease at the University of South Florida College of Medicine in Tampa, Fla, USA.
The number of primary and secondary syphilis cases in young women rose dramatically in the late 1980s and early 1990s, due to illicit drug use and the exchange of drugs for sex. Of infants born to mothers with primary or secondary syphilis, up to 50% will be premature, stillborn, or die in the neonatal period; further, most of these children are born with congenital disease that may not be apparent for years. While appropriate treatment of the pregnant female can prevent congenital syphilis, the major deterrent has been the inability to effectively identify these women and get them to undergo treatment.
In determining a penicillin regimen, the clinician must consider the stage of maternal infection, the length of fetal exposure, and physiologic changes in pregnancy that can affect the pharmacokinetics of antibiotics. Treatment decisions may be further complicated in patients who are allergic to penicillin or infected with HIV.
The pathogenesis of congenital syphilis is not completely understood, but placental invasion is the presumed major route. All women should be screened for syphilis with a nontreponemal test (eg, rapid plasma reagin [RPR] or venereal disease research laboratory [VDRL] test) in the first trimester.
Those at high risk should be retested at 28 weeks and near delivery. Even with appropriate treatment of syphilis during pregnancy, fetal infection may still occur in up to 14% of cases. Treating syphilis during pregnancy can be difficult due to physiologic changes that can alter drug levels and the risk that drugs will induce uterine contractions or compromise the health of the fetus.
While there are added risks and potential complications, treatment regimens parallel those in nonpregnant women.
PMID: 9732090 [PubMed - indexed for MEDLINE]
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Am J Obstet Gynecol. 2002 Mar;186(3):569-73.
Congenital syphilis after maternal treatment for syphilis during pregnancy.
Sheffield JS, Sanchez PJ, Morris G, Maberry M, Zeray F, McIntire DD, Wendel GD Jr.
Department of Obstetrics and Gynecology, University of Texas Southwestern Medical Center, Dallas 75235-9032, USA.
OBJECTIVE: The purpose of this study was to characterize pregnancies that were complicated by maternal syphilis that had been treated before delivery in which the newborn infant was diagnosed with congenital syphilis.
STUDY DESIGN: Prospective surveillance from January 1, 1982, to December 31, 1998, involved women who received antenatal treatment for syphilis. Infants who were born with congenital syphilis were identified by clinical or laboratory criteria. Antepartum factors such as gestational age, time to delivery and VDRL titers were then analyzed and compared with those of women who had been treated and who were delivered of an uninfected infant. The 1:1 match was based on the stage of syphilis and the gestational age at treatment.
RESULTS: Forty-three women who received antepartum therapy for syphilis were delivered of an infant with congenital syphilis.
Most of the women had been treated for early syphilis; the mean gestational age at treatment was 30.3 weeks. Thirty-five percent of the women were treated >30 days before delivery.
Fifty-six percent of the infants were preterm. The 1:1 match revealed that treatment and delivery high VDRL titers, prematurity, and a short interval from treatment to delivery were significantly different in those infants who were diagnosed with congenital syphilis.
CONCLUSION: High VDRL titers at treatment and delivery, earlier maternal stage of syphilis, the interval from treatment to delivery, and delivery of an infant at < or =36 weeks' gestation are associated with the delivery of a congenitally infected neonate after adequate treatment for maternal syphilis.
PMID: 11904625 [PubMed - indexed for MEDLINE]
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Symptoms and Signs
The signs and symptoms of congenital syphilis are arbitrarily divided into early manifestations , which appear in the first 2 years of life, and late manifestations , which appear thereafter.
Early congenital syphilis usually starts in between birth and about 3 months of life, with most cases occurring within the first five weeks of life. Because of their frequency and early appearance the changes in the bones, especially the femur and humerus, are of diagnostic value.
Other symptoms include rhinitis , coryza , or snuffles. Snuffles usually occur in the first week of life, are very persistent and often bloody.
A syphilitic rash, typically consisting of small spots that are dark red to copper, usually appears after 1- 2 weeks of rhinitis and is most severe on the hands and feet. As the rash fades, the lesions become coppery or dusky red.
Fissures often develop about the lips and anus. They bleed readily and heal with scarring. White mucous patches may be found on any of the mucous membranes. Ectodermal changes include exfoliation of the nails, loss of hair and eyebrows, and iritis (inflammation of the iris).
Late manifestations of congenital syphilis are the result of scarring from the early systemic disease and include involvement of the teeth, bones, eyes, and gummas in the viscera, skin, or mucous membranes.
Characteristic changes of the teeth include a notched appearance on the biting edges of the upper central incisors, these are called Hutchinson's teeth. Interstitial keratitis is the most common late lesion. Bony changes include sclerosing lesions, saber shin, frontal bossing and gummatous or destructive lesions within long bones.
http://www.hon.ch/Dossier/MotherChild/neonatal_problems/congenital_syphilis.html
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If a woman with syphilis gets pregnant, her child may be born with congenital syphilis. 40% of infected fetuses die before birth; newborns suffer from secondary-stage syphilis and enter the latent stage if they survive their first year.
http://www.everything2.com/index.pl?node=syphilis
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* IN A PREGNANT WOMAN:
* If untreated, all children born with syphilis develop secondary and tertiary syphilis. The infected children do not live long enough.
* Treatment for tertiary Stage
* At this point, many of the effects of this disease can not be treated. It is too late!!
http://www.skinchoice.com/Syphilis.htm
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Clin Infect Dis. 2002 Oct 15;35(Suppl 2):S200-9.
Treatment of syphilis in pregnancy and prevention of congenital syphilis.
Wendel GD Jr, Sheffield JS, Hollier LM, Hill JB, Ramsey PS, Sanchez PJ.
Department of Obstetrics and Gynecology, The University of Texas Southwestern Medical Center at Dallas, Dallas, TX 75390-9032, USA. george.wendel@utsouthwestern.edu
Studies about the management of syphilis during pregnancy were reviewed. They lacked uniformity in diagnostic criteria and study design. Currently recommended doses of benzathine penicillin G are effective in preventing congenital syphilis in most settings, although studies are needed regarding increased dosing regimens.
Azithromycin and ceftriaxone offer potential alternatives for penicillin-allergic women, but insufficient data on efficacy limit their use in pregnancy. Ultrasonography provides a noninvasive means to examine pregnant women for signs of fetal syphilis, and abnormal findings indicate a risk for obstetric complications and fetal treatment failure. Ultrasonography should precede antepartum treatment during the latter half of pregnancy to gauge severity of fetal infection.
However, optimal management of the affected fetus has not been established; collaborative management with a specialist is recommended. Antepartum screening remains a critical component of congenital syphilis prevention, even in the era of syphilis elimination.
PMID: 12353207 [PubMed - indexed for MEDLINE]
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Lyme borreliosis as a cause of facial palsy during pregnancy.
Grandsaerd MG; Meulenbroeks AA
Department of Otorhinolaryngology, Rijnstate hospital Wagnerlaan 55 6815 AD, Arnhem, The Netherlands
The medical history of a pregnant woman in whom the initial pattern of complaints suggested hyperemesis gravidarum is described. After about 18 days the patient developed left facial palsy. Repeated tests eventually confirmed the diagnosis of neuroborreliosis. The problems concerning diagnostics, therapy and the possible complications of Lyme borreliosis during gestation are described.
Eur J Obstet Gynecol Reprod Biol 2000 Jul 1;91(1):99-101
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Maternal Lyme disease and congenital malformations: a cord blood serosurvey in endemic and control areas.
Williams CL; Strobino B; Weinstein A; Spierling P; Medici F
Child Health Center, American Health Foundation, Valhalla, New York 10595, USA.
This report describes a cohort study of over 5000 infants and their mothers who participated in a cord blood serosurvey designed to examine the relationship between maternal exposure to Lyme disease and adverse pregnancy outcome. Based on serology and reported clinical history, mothers of infants in an endemic hospital cohort are 5 to 20 times more likely to have been exposed to B. burgdorferi as compared with mothers of infants in a control hospital cohort.
The incidence of total congenital malformations was not significantly different in the endemic cohort compared with the control cohort, but the rate of cardiac malformations was significantly higher in the endemic cohort [odds ratio (OR) 2.40; 95% confidence interval (CI) 1.25, 4.59] and the frequencies of certain minor malformations (haemangiomas, polydactyly, and hydrocele), were significantly increased in the control group. Demographic variations could only account for differences in the frequency of polydactyly.
Within the endemic cohort, there were no differences in the rate of major or minor malformations or mean birthweight by category of possible maternal exposure to Lyme disease or cord blood serology. The disparity between observations at the population and individual levels requires further investigation. The absence of association at the individual level in the endemic area could be because of the small number of women who were actually exposed either in terms of serology or clinical history. The reason for the findings at the population level is not known but could be because of artifact or population differences.
Paediatr Perinat Epidemiol 1995 Jul;9(3):320-30
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[Manifestation of Lyme arthritis in the puerperal period]
Bussen S; Steck T
Universitatsfrauenklinik Wurzburg.
Lyme disease, a tick-transmitted spirochetal illness caused by Borrelia burgdorferi, usually begins with a characteristic erythema chronicum migrans accompanied by flu-like symptoms. This phase may later be followed by meningitis, neuritis, carditis or arthritis. Congenital abnormalities due to maternal infection during pregnancy have been described. We report on a case of a 36-year old V gravida III para. After a normal pregnancy and a Cesarean section the patient developed postpartal an acute Lyme arthritis.
Z Geburtshilfe Perinatol 1994 Aug;198(4):150-2
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Congenital infections and the nervous system.
Bale JF Jr; Murph JR
Department of Pediatrics, University of Iowa College of Medicine, Iowa City.
Despite vaccines, new antimicrobials, and improved hygienic practices, congenital infections remain an important cause of death and long-term neurologic morbidity among infants world-wide. Important agents include Toxoplasma gondii, cytomegalovirus, Treponema pallidum, herpes simplex virus types 1 and 2, and rubella virus.
In addition, several other agents, such as the varicella zoster virus, human parvovirus B19, and Borrelia burgdorferi, can potentially infect the fetus and cause adverse fetal outcomes. This article provides an overview of these infectious disorders and outlines current strategies for acute treatment and long-term management.
Pediatr Clin North Am 1992 Aug;39(4):669-90
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[Borrelia infections from a dermatological viewpoint]
Vocks E; Engst R; Borelli S
Dermatologische Klinik und Poliklinik Technischen Universitat Munchen. ABSTRACT:
Erythema migrans (EM), Borrelia lymphocytoma (BL) and acrodermatitis chronica atrophicans (ACA) are the established dermatological manifestations of borrelia infection, a complex multiorganic disease. Analogous to syphilis Borrelia infection can be classified by three stages, at which stage I (localized infection) and II (disseminated infection) are manifestations of early infection and stage III (persistent infection) a symptom of late infection.
At all stages skin manifestations can be present, the above mentioned as stage-marker as well as other non-specific polymorphous skin lesions which sometimes appear at stage II. Because of its frequent (60-80%) occurrence in all borrelia infections EM has a pathognomonic importance for borrelia infection. In diagnosis serology is currently the only practical laboratory aid. False negative and false positive results must be considered. Treatment of choice is ceftriaxone, penicillin G (or amoxycillin) or tetracycline. Prophylactic antibiotic therapy for tick bites is not recommended. Congenital borrelia infections seem to be unusual, but it is likely that they can occur and cause different adverse fetal outcome or abortion.
Monatsschr Kinderheilkd 1991 Jul;139(7):425-8
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Lyme disease during pregnancy.
Schutzer SE; Janniger CK; Schwartz RA
Department of Allergy and Immunology, New Jersey Medical School, Newark 07103-2714.
Lyme disease, caused by infection with Borrelia burgdorferi, can affect those exposed to a vector tick. Pregnant women are no exception, and such infection places the fetus at risk. It is particularly important to recognize the disease early so that effective therapy may be instituted.
Although the present patient had a favorable outcome, not all do. Clinical diagnosis is especially important since conventional laboratory tests may be inadequate or require lengthy periods of time before a positive result occurs. The dermatologic sign of Lyme disease, erythema migrans, although occurring in only 50 percent of cases, is likely to be the most important diagnostic sign.
Cutis 1991 Apr;47(4):267-8
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Infants born to mothers with antibodies against Borrelia burgdorferi at delivery.
Nadal D; Hunziker UA; Bucher HU; Hitzig WH; Duc G
Abteilungen fur Infektionskrankheiten und Immunologie der Universitat, Zurich, Switzerland.
A serological survey over a 1-year period of 1416 mothers at delivery and their 1434 offspring for the presence of anti-Borrelia burgdorferi antibodies revealed a prevalence of 0.85%. Clinically active Lyme disease during pregnancy was found in 1 of these 12 women with elevated titres and the child was born with a ventricular septal defect.
Of six affected children, two had hyperbilirubinaemia, one muscular hypotonia, one was underweight for gestational age, one was macrocephalic, and one had supraventricular extrasystoles. Anomalous findings could not be attributed to B. burgdorferi due to a lack of serological evidence of intrauterine infection. Our data do not imply the need for serological screening in pregnancy, however, the importance of recognition and treatment of Lyme disease in pregnancy is emphasized.
Eur J Pediatr 1989 Feb;148(5):426-7
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Fetal outcome in murine Lyme disease.
Silver RM; Yang L; Daynes RA; Branch DW; Salafia CM; Weis JJ
Department of Obstetrics and Gynecology, University of Utah School of Medicine, Salt Lake City 84132.
Lyme disease is an inflammatory syndrome caused by infection with Borrelia burgdorferi. Although this syndrome has important implications for human pregnancy, little is known about gestational infection with B. burgdorferi. Fetal death occurred in 33 of 280 gestational sacs (12%) in 39 C3H/HeN female mice infected by intradermal injection of B. burgdorferi 4 days after mating (acute infection), compared with 0 of 191 sacs in 25 control mice (P = 0.0001).
Forty-six percent of acutely infected mice suffered at least one fetal death, compared with none of the control animals (P = 0.0002). There were no fetal deaths in 18 C3H/HeN mice infected 3 weeks prior to mating (chronic infection). A sensitive PCR technique detected B. burgdorferi DNA in the uteri of acutely infected mice but did not detect DNA in the uteri of controls or chronically infected mice.
Spirochete DNA was only rarely detected in fetal tissues, and its presence was not required for fetal death. The inclusion of an internal competitive PCR target indicated that the lack of B. burgdorferi sequences in fetal DNA was not due to the presence of a PCR inhibitor. Histologic analysis of gestational tissues from infected animals demonstrated nonspecific pathology consistent with fetal death.
These findings indicate an association between murine fetal death and acute infection with B. burgdorferi early in gestation but not with chronic infection. Our data suggest that fetal death is due to a maternal response to infection rather than fetal infection. These findings could provide an explanation for observations in humans in which sporadic cases of fetal death in women infected with B. burgdorferi during pregnancy have been reported, while previous infection has not been associated with fetal death.
Infect Immun 1995 Jan;63(1):66-72
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Intrauterine transmission of Borrelia burgdorferi in dogs.
Gustafson JM; Burgess EC; Wachal MD; Steinberg H
Department of Medical Sciences, University of Wisconsin-Madison, School of Veterinary Medicine 53706.
To determine whether intrauterine transmission of Borrelia burgdorferi could exist in dogs, 10 female Beagles were inoculated intradermally with approximately 1,000 B burgdorferi on day 1 of proestrus; inoculation was repeated every 2 weeks during the gestation period. Ten female control Beagles were similarly inoculated with phosphate-buffered saline solution.
Prior to the start of the study, all females and 3 males used for breeding were seronegative for B burgdorferi on the basis of results of the indirect fluorescent antibody test and immunoblot (western analysis. Similarly, results of culture of blood for B burgdorferi were negative. All 20 of the females were bred naturally. Blood samples were collected weekly for serologic testing and culture.
Blood samples were obtained from live pups on day 1 of life, then weekly until pups were 6 weeks old when they were euthanatized. Tissues were obtained for culture and testing by use of polymerase chain reaction (PCR). Of 10 spirochete-inoculated (SI) females, 8 became infected with B burgdorferi as evidenced by spirochete culture results and/or PCR-detected B burgdorferi DNA in the tissues of females or their pups.
Of the 10 SI females, 8 delivered litters (3 to 7 pups) that had at least 1 neonatal or 6-week-old pup with B burgdorferi DNA-positive tissues (by PCR), and spirochetes were cultured from tissues from pups of 2 litters. (ABSTRACT TRUNCATED AT 250 WORDS)
Am J Vet Res 1993 Jun;54(6):882-90
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Borrelia burgdorferi infection in dairy cows, rodents, and birds from four Wisconsin dairy farms.
Burgess EC; Wachal MD; Cleven TD
Department of Medical Science, University of Wisconsin, School of Veterinary Medicine, Madison 53706.
A combination of culture and subsequent spirochete identification with the polymerase chain reaction technique was used to identify cows, rodents, and birds infected with Borrelia burgdorferi. Animals were trapped on four Wisconsin dairy farms during the summer of 1990. Farms 1 and 2 were located in counties nonendemic for Lyme disease and Farms 3 and 4 were located in counties endemic for Lyme disease.
The results of the rodent and bird samples were as follows given as the number yielding organisms number tested: Farm 1, 1/17 Mus musculus and 2/52 Peromyscus domesticus; Farm 2, 4/49 M. musculus, 1/2 P. maniculatus, 1/1 P. leucopus, and 1/35 P. domesticus; Farm 3, 0/27 M. musculus, 0/5 P. leucopus, 0/12 P. maniculatus and, 3/58 P. domesticus; and Farm 4, 1/24 M. musculus, 2/19 P. leucopus, 1/12 Microtus pennsylvanicus, and 0/17 P. domesticus.
One P. leucopus and one M. musculus from Farm 2 were pregnant and fetal tissues from both were positive. Cow blood sample results were as follows: Farm 1, 7/47 in July, and 2/45 in August; Farm 2, 0/28 in August and 0/23 in October; Farm 3, 0/13 in July and 1/18 in August 29; and Farm 4, 3/45 in August.
Ticks were found on rodents on Farm 4 and on one bird on Farm 3. Spirochetemic cows, rodents, and birds were found in non-Lyme endemic counties suggesting that alternate modes of transmission other than by ticks may be important. Transplacental transmission was shown in M. musculus and P. leucopus.
Vet Microbiol 1993 May;35(1-2):61-77
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Borrelia sp. infection in coyotes, black-tailed jack rabbits and desert cottontails in southern Texas.
Burgess EC; Windberg LA
Department of Medical Sciences, School of Veterinary Medicine, University of Wisconsin, Madison 53706.
Coyotes (Canis latrans) from southern Texas were sampled for antibodies to Borrelia burgdorferi from 1980 to 1986; black-tailed jack rabbits (Lepus californicus) and desert cottontails (Sylvilagus audubonii) were sampled in 1986. Coyote fetuses, adult coyote kidneys, and black-tailed jack rabbit and desert cottontail kidneys were cultured for B. burgdorferi in 1986.
Results of indirect immunofluorescent antibody (IFA) tests for B. burgdorferi in coyotes were as follows (number positive at a dilution of greater than or equal to 1:128/number tested): 1980 (0 of 30), 1981 (0 of 21), 1982 (0 of 53), 1983 (0 of 78), 1984 (47 of 97), 1985 (20 of 88), and 1986 (42 of 80). Eight of 26 black-tailed jack rabbits and two of seven desert cottontails tested in 1986 had IFA titers to B. burgdorferi of greater than or equal to 1:128.
Borrelia burgdorferi was isolated from one of five coyote fetuses, three of 31 adult coyote kidneys, and two of 10 black-tailed jack rabbit kidneys in 1986. These results indicate that B. burgdorferi infection has been present in coyotes in Texas, at least since 1984 and that transplacental transmission occurs.
J Wildl Dis 1989 Jan;25(1):47-51
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Borrelia burgdorferi infection in Wisconsin horses and cows.
Burgess EC
School of Veterinary Medicine, University of Wisconsin, Madison 53706.
Blood samples from Wisconsin horses and cows suspected of having clinical disease due to Borrelia burgdorferi infection were submitted by veterinary practitioners. All serum, milk, colostrum, and synovial samples were tested for B. burgdorferi antibodies by immunofluorescence. Whole blood, milk, colostrum, and synovial fluid samples were cultured for B. burgdorferi.
Records were kept on the clinical signs of antibody-positive animals, date of sample, and location of the animal by county. Of the samples tested for antibodies 282/430 cow sera, 118/190 horse sera, 5/10 cow synovial fluids, 3/6 horse synovial fluids, 2/3 cow colostrums, 0/44 cow milk samples and 1 aborted fetus serum were antibody positive at a titer of 1:128 or greater.
Of samples cultured 7/156 cow bloods, 2/35 horse bloods, 1/14 cow synovial fluids, 0/4 synovial fluids, 1/3 cow colostrums, 0/44 cow milk, and 2/10 cow urine samples were B. burgdorferi culture positive. For both cows and horses October and May were the two peak months for the number of antibody-positive samples. The most frequent clinical signs in antibody-positive horses and cows were lameness and swollen joints, but many also had stiffness, laminitis, abortions, and fevers.
Not all antibody-positive animals showed clinical signs. These findings show that B. burgdorferi infection occurs in horses and cows and can cause clinical illness in some but not all animals. Infection in cows and horses occurs most frequently 1 month after the emergence of adult I. dammini. Because spirochetes could be isolated from blood, synovial fluid, colostrum, and urine, these animals could be important in providing an infected blood meal for ticks and bringing B. burgdorferi in direct contact with humans.
Ann N Y Acad Sci 1988;539:235-43
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Seasonal prevalence of Borrelia burgdorferi in natural populations of white-footed mice, Peromyscus leucopus.
Anderson JF; Johnson RC; Magnarelli LA
Borrelia burgdorferi, the etiologic agent of Lyme disease, was isolated from 111 of 237 Peromyscus leucopus captured during all seasons of the year. Borreliae were cultured from tissues of the spleen (101 mice), left kidney (76 mice), and right kidney (73 mice), from blood (12 mice), and from one fetus. Mice were infected during the winter, when immature Ixodes dammini were inactive.
The prevalence of infection during the winter (less than or equal to 33%) was more than twofold lower than that during the summer (ca. 75%), a time when nymphal ticks are abundant. Overwintering, infected mice are reservoir hosts for subadult ticks that begin feeding in early spring. Twenty white-footed mice from which B. burgdorferi was isolated from tissues of spleen or kidney but not from blood were parasitized by larval I. dammini or Dermacentor variabilis which harbored borreliae. We conclude that these mice were infectious to feeding ticks, even though borreliae were not isolated from blood.
J Clin Microbiol 1987 Aug;25(8):1564-6
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Lyme disease and cases occurring during pregnancy--United States.
See full-text article at:
CDC MMWR: Lyme Disease and Cases Occurring during Pregnancy -- US, June 28, 1985
NLM PUBMED CIT. ID: 3925314 NLM CIT. ID: 85240257
MMWR Morb Mortal Wkly Rep 1985 Jun 28;34(25):376-8, 383-4
[No abstract available.]
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References, citations only (i.e., no abstract available.)
Neonatal skin lesions due to a spirochetal infection: a case of congenital Lyme borreliosis?
Trevisan G; Stinco G; Cinco M:
Institute of Dermatology, University of Trieste, Italy.
Int J Dermatol 1997 Sep;36(9):677-80
[No abstract available.]
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[Pathology of pregnancy and the fetus in Lyme disease]
Elsukova LV; Korenberg EI; Kozin GA
Med Parazitol (Mosk) 1994 Oct-Dec;(4):59-62
[No abstract available.]
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Lyme disease during pregnancy. ACOG Committee Opinion: Committee on Obstetrics: Maternal and Fetal Medicine. Number 99--November 1991.
Int J Gynaecol Obstet 1992 Sep;39(1):59-60
[No abstract available.]
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Lyme disease: a review with emphasis on the pregnant woman.
Smith LG Jr; Pearlman M; Smith LG; Faro S
Department of Obstetrics and Gynecology, Baylor College of Medicine, Houston, Texas 77030.
Obstet Gynecol Surv 1991 Mar;46(3):125-30
[No abstract available.]
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Lyme disease during pregnancy.
Edly SJ
Department of Obstetrics and Gynecology, UMDNJ-Robert Wood Johnson Medical School, New Brunswick 08903.
N J Med 1990 Jul;87(7):557-60
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Lyme borreliosis during pregnancy.:
Stiernstedt G
Department of Infectious Diseases, Danderyd Hospital, Sweden.
Scand J Infect Dis Suppl 1990;71:99-100
[No abstract available.]
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Lyme disease and pregnancy.
Cartter ML; Hadler JL; Gerber MA; Mofenson L
Conn Med 1989 Jun;53(6):341-2
[No abstract available.]
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Borrelia burgdorferi in a newborn despite oral penicillin for Lyme borreliosis during pregnancy.
Weber K; Bratzke HJ; Neubert U; Wilske B; Duray PH
Department of Medicolegal Medicine, Dermatology and Microbiology, University of Munich, Federal Republic of Germany.
Pediatr Infect Dis J 1988 Apr;7(4):286-9
[No abstract available.]
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[Lyme disease in pregnancy]
Andrasova V; Svarovsky J; Matousek B
Cesk Gynekol 1988 Feb;53(1):39-41
[No abstract available.]
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Stillbirth following maternal Lyme disease.
MacDonald AB; Benach JL; Burgdorfer W
N Y State J Med 1987 Nov;87(11):615-6
[No abstract available.]
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Lyme disease during pregnancy.
Mikkelsen AL; Palle C
Department of Gynecology and Obstetrics, Hvidovre Hospital, University of Copenhagen, Denmark.
Acta Obstet Gynecol Scand 1987;66(5):477-8
[No abstract available.]
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Human fetal borreliosis, toxemia of pregnancy, and fetal death.
MacDonald AB
Zentralbl Bakteriol Mikrobiol Hyg [A] 1986 Dec;263(1-2):189-200
[No abstract available.]
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Maternal-fetal transmission of the Lyme disease spirochete, Borrelia burgdorferi.
Schlesinger PA; Duray PH; Burke BA; Steere AC; Stillman MT
Ann Intern Med 1985 Jul;103(1):67-8
[No abstract available.]
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Thanks to Art Doherty for providing some of the citations and abstracts. - Lots Of Links On Lyme Disease http://www.geocities.com/HotSprings/Oasis/6455/lyme-links.html