congenital transmission of Lyme disease
JWissmille
heart and other cardiac anomalies. Spirochetes compatible with B. burgdorferi
were found in the spleen, kidneys, and bone marrow; however, no inflammatory
response to the organisms was seen. [i.e no further testing would have been
"needed"]."
INFECTIOUS DISEASE CLINICS OF NORTH AMERICA
VOLUME 11 NUMBER 1 MARCH 1997
INFECTIONS IN OBSTETRICS:
LYME DISEASE DURING PREGNANCY
Helayne M. Silver, MD
From the Department of Maternal-Fetal Medicine, Women & Infants Hospital of
Rhode Island, and Brown University, Providence, Rhode Island
Because of the similarities of disease caused by Borrelia burgdorferi to
Syphilis, initially there was great concern regarding possible fetal infection
and teratogenicity if Lyme disease was contracted during pregnancy. Although
the Initial retrospective case reports were alarming, more recent prospective
data have been reassuring. This article reviews the evidence that currently
supports the assurance of the benign nature of this infection with respect to
the fetus.
EARLY CASE REPORTS
The first case of perinatal transmission of presumed B. burgdorferi was
reported by Shirts et al in 1983.(8) The infant was born at 38 weeks to a
mother who had two episodes of high fever of unknown origin at 30 weeks and 32
weeks of gestation. The mother was treated initially with erythromycin and then
cefamandole. At delivery the neonate was pale, had hepatosplenomegaly,
petechiae, severe thrombocytopenia, and hyperbilirubinemia. On a peripheral
smear, spirochetes were seen, and a diagnosis of borreliosis was made.
Histologic evaluation of the placenta revealed spirochetes within the villous
capillaries. Serologic testing and specific antigen testing of the spirochete
were not performed, and results of syphilitic testing were not reported. The
patient, however, lived in an area endemic for Lyme disease and remembered
moving a woodpile 10 days before the onset of symptoms.
The first well-documented case of perinatal transmission of B. burgdorferi was
reported by Schlesinger et al in 1985. The infant was born at 35 weeks to a
mother with a clinical history consistent with erythema migrans in the first
trimester, which subsequently resolved without antibiotic therapy. The infant
had severe congenital cardiac defects resulting in neonatal death at 39 hours
of life. Postpartum, the mother developed arthritis, and serologic tests
revealed an IgG titer to B. burgdorferi of 1:128 by indirect
immunofluorescence. The neonatal autopsy revealed hypoplastic left side of
heart and other cardiac anomalies. Spirochetes compatible with B. burgdorferi
were found in the spleen, kidneys, and bone marrow; however, no inflammatory
response to the organisms was seen. [i.e no further testing would have been
"needed"]
The placenta was not examined. Although spirochetes were not originally
reported in the infant's myocardium, there was a subsequent report of
immunohistochemical techniques that did reveal the organism. (4)
The third reported case was from MacDonald et al of a full term stillbirth
delivered to a mother with a clinical history consistent with erythema migrans
in the first trimester that resolved without antibiotic therapy. (3) The infant
had a small ventricular septal defect (cardiac malformation) but no other
congenital anomalies. B. burgdorferi was found in the fetal liver, brain,
adrenal glands, heart, and placenta, again without evidence of inflammatory
response.
Maternal serology was positive for antibodies to B. burgdorferi and negative
for syphilis.
[The later two case reports involved women who were not prospectively diagnosed
with Lyme disease and therefore were not treated with antibiotics.]
In 1988, however, a disturbing case was reported by Weber et al of a poor
perinatal outcome in a woman diagnosed in the first trimester with erythema
migrans and treated with oral penicillin. (10) She delivered her infant by
vacuum extraction at term, following an uncomplicated pregnancy. The infant
developed respiratory distress at 23 hours of life and died within 30 minutes,
of respiratory failure. On autopsy there was cerebral edema and small
intracranial hemorrhages. Other than extreme congestion of the lungs, no other
abnormalities were seen. The diagnosis was respiratory failure secondary to
perinatal brain damage. Spirochetes were found in the brain and liver and were
confirmed by immunohistochemical techniques to be B. burgdorferi. The authors
concluded that oral penicillin therapy was inadequate therapy for Lyme disease
during pregnancy and recommended intravenous penicillin for 10 to 14 days. This
patient, however, received oral penicillin three times daily for 7 days, less
than the recommended oral therapy of four times daily for 3 weeks, and
therefore may not represent a failure of oral therapy.
EPIDEMIOLOGIC STUDIES
In 1986, a joint study from the Centers for Disease Control and Prevention and
Yale University was published reviewing the outcomes of pregnancies over a
10-year period that were complicated by Lyme disease. (5)
To reduce bias, only patients who were diagnosed with Lyme
disease prior to knowledge of preganancy outcome were enrolled:
Nineteen cases were identified,
eight with onset in the first trimester,
seven in the second trimester,
two in the third trimester,
and two with unknown time of onset.
Thirteen patients received antibiotic therapy and six did not.
There were five patients with abnormal pregnancy outcome as follows:
one preterm delivery at 36 weeks,
one neonate with syndactyly,
one infant with cortical blindness and developmental delay,
one intrauterine demise at 20 weeks,
and one neonate with a vesicular rash.
In no case was infection with B. burgdorferi documented in the fetus or infant,
(antibody testing?)
and there was no association of an increased risk of abnormal outcome with
disease exposure earlier in pregnancy. (same risk for all trimesters)
Two large serologic surveys of pregnant women living in endemic areas have been
published, one from Westchester County, New York and the other from Zurich,
Switzerland.
The first report from Westchester County was a cohort study of 2014 prenatal
patients. (9) Eleven women (0.7%) were seropositive at the initial prenatal
visit, and 5 of the 11 reported a past diagnosis of Lyme disease. Obstetric
outcomes were similar in comparison to seronegative patients. Born to initially
seropositive women were two infants with minor congenital anomalies (metatarsus
adductus and stomach reflux) and one with major anomalies consisting of the
VATER association. Postpartum antibody testing was performed in 1290 women.
Only one patient demonstrated seroconversion, and her infant was normal.
In 1995, a second report was published from the same authors comparing
serologic status of 2504 infants born to mothers in the endemic region to 2507
infants born to mothers living in a neighboring, nonendemic region. (11)
Twenty-eight women in the endemic region reported a history of Lyme disease,
compared to one in the nonendemic region. Six women in the endemic region
reported Lyme disease during the index pregnancy, and all were treated with
(some form of) antibiotic therapy.
Eight percent of infants from the endemic region had IgG positive cord blood
for B. burgdorferi versus 0.8% in infants from the nonendemic region. None were
IgM positive. There was a slightly increased rate of malformations in infants
from the nonendemic region, 8.9% versus 7.8%; however, there was a significant
increase in cardiac malformations in infants from the endemic region.
Among the twenty seropositive infants, one had cryptorchidism, but no other
anomolies were seen. Among the six women who reported Lyme disease during
pregnancy (treated women), one infant had hypospadias, and the rest had no
anomalies.
In Zurich, 1416 pregnant women and their infants had serologic testing
for antibodies to B. burgdorferi.(6) [Only] Twelve women and their infants
were IgG seropositive for a rate of 0.85%. Five of the women had symptoms
consistent with Lyme disease prior to pregnancy, one had undiagnosed, untreated
Lyme disease during the first trimester of the index pregnancy, and five had no
history consistent with clinical disease. The infant of the mother with
untreated Lyme disease had a ventricular septal defect (cardiac malformation),
but no other congenital anomalies were seen in the infants of the other eleven
seropositive women.
Because of concern about the similarities between syphilis and Lyme disease, a
survey was performed by Gerber and Zalneraitis to evaluate whether congenital
neuroborreliosis existed as a diagnosable entity.(2) In a survey of 162
neurologists practicing in endemic areas for Lyme disease, only one reported
caring for patients with congenital Lyme disease. In all three patient cases,
none of the three mothers had histories meeting the Centers for Disease Control
and Prevention criteria for the diagnosis of Lyme disease
.
This survey raises doubt about the existence of prenatally acquired
neuroborreliosis.
Recent serologic survey studies suggest that antepartum Lyme disease is
uncommon, even in endemic regions, and that although there have been case
reports of transplacental transmission of the spirochete, fetal immologic
response is lacking, and association with congenital [cardiac] anomalies is
strong.
As the disease is uncommon, and anomalies less common, ............
larger epidemiologic studies are required for a definitive resolution to the
question of fetal risks with perinatal infection.
TREATMENT OF LYME DISEASE DURING PREGNANCY
The American College of Obstetrics and Gynecology recommends treatment of deer
tick bites or suspected early disease with oral amoxicillin or penicillin for 3
weeks.(1) There is no evidence that more aggressive, intravenous therapy is
warranted, except for the usual indications of severe acute disease, neurologic
complications, or chronic disease.
References
1., American College of Obstetrics and Gynecology Committee Opinion: Lyme
disease during pregnancy. Int J Gynaecol Obstet 39:59, 1992
2. Gerber M, Zalneraitis E: Childhood neurologic disorders and Lyme
disease during pregnancy. Pediatr Neurol 11:41, 1994
3.MacDonald A, Benach J, Burgdorfer W: Stillbirth following maternal Lyme
disease. N Y State J Med 87: 615, 1987
4. MacDonald A: Gestational Lyme borreliosis. Rheum Dis Clin North Am
15:657, 1989
5. Markowitz L, Steere A, Benach J, et al: Lyme disease during pregnancy.
JAMA
255:3394, 1986
6. Nadal D, Hunziker U, Bucher H, et al: Infants born to mothers with
antibodies against Borrelia burgdorferi at delivery. Eur J Pediatr 148:426,
1989
7. Schlesinger P, Duray P, Burke B, et al: Maternal-Fetal transmission of
the Lyme disease spirochete, Borrelia burgdorferi. Ann Intern Med 103:67, 1985
8. Shirts S, Brown M, Bobitt J: Listeriosis and Borreliosis as causes of
ante-partum fever. Obstet Gynecol 62:256, 1983
9. Strobino B, Williams C, Abid S, et al: Lyme disease and pregnancy
outcome: A prospective study of two thousand prenatal patients. Am J Obstet
Gynecol 169:367, 1993
10. Weber K, Bratzke H, Neubert U, et al: Borrelia burgdorferi in a newborn
despite penicillin for Lyme borreliosis during pregnancy. Pediatr Infect Dis J,
7:286 1988
11. Williams C, Strobino B, Weinstein A, et al: Maternal Lyme disease and
congenital malformations: A cord blood serosurvey in endemic and control areas.
Pediatr Perinatal Epid 9:320, 1995.
Address reprint requests to:
Helayne M. Silver, MD
Women & Infants Hospital of Rhode Island
101 Dudley Street
Providence, RI 02905
______________
REPOST: This information was compiled by Bella...@aol.com - a registered
nurse very knowledgeable on the subject of Lyme and pregnancy.
PEDIATRIC RN, BSN IN CT
GINNY (BELLA...@AOL.COM)
georgia
______________________
80 pages on Lyme with a focus on CLD...by Tessa Gardner- She is a pediatric
infectious disease specialist in the midwest....she lists 400+ references...
INFECTIOUS DISEASES OF THE FETUS AND NEWBORN INFANT--CHAPTER 11
______________________________________________
Source # 1:
Text: Lyme Disease (tiny green hardcover book @ local hospital
library)
by Patricia Coyle of State University of NY @ Stonybrook
Chapter 23 Lyme Disease in Pregnancy
Genevieve Sicuranza and David Allen Baker
Lyme borreliosis became a reportable disease in the United States in 1982, and
in 1991 a national surveillance case definition was established. The Centers
for Disease Control in its June 1991 report indicated an eighteenfold increase
in the number of cases from 1982 through 1989(13,500). Lyme disease was first
described in 1977 in Old Lyme, Connecticut, as a juvenile-arthritis type
syndrome associated with tick bites.'(ref 12) Although cases are concentrated
in the northeastern, midwestern, and Pacific United States, Lyme disease has
now been reported from most states. It is clearly an international problem,
with a marked increase in infected and symptomatic people in Europe and Asia as
well. Due to the rising numbers of cases each year, there has been increasing
concern about the potential impact of Lyme disease on the pregnant woman and
her fetus.
Lyme disease is caused by a spirochete, Borrelia burgdorferi, classically
carried by the deer tick, hodes dammini.(ref10) Other vectors have been
identified in New Jersey and Texas (Amblyomma americanum). (ref 11) Although
the deer is the preferred host of the adult tick, almost any bird or domestic
animal can act as an intermediate host. It is known that the fetus is quite
vulnerable to the transplacental passage of the syphilis spirochete, Treponema
pallidum. Because the causative agent of Lyme disease is also a spirochete,
there is concern that B. burgdorferi might also affect the fetus. This chapter
reviews the available information pertaining to Lyme disease in pregnancy and
discusses the diagnosis and management in this selected population. (See Color
Plate 8.)
PREGNANCY
Maternal infection may involve transmission of the invading microorganism to
the fetus. This may have no adverse consequences or may produce a range of
sequela from minor transient problems to fetal death and abortion. Among the
spirochetal bacterial infections, syphilis is known to cause abortion,
stillbirth, and congenital abnormalities. Maternal relapsing fever and
leptospirosis have also been associated with an increased risk of fetal loss.
Among animals, borreliae have been associated with bovine abortion. Whether
Lyme disease affects the pregnancy or the fetus has been a subject of several
studies. In 1985, Schlessinger (ref 8) documented transplacental transmission
of B. burgdorferi for the first time. The infant involved showed congenital
heart anomalies. An autopsy revealed numerous spirochetes in the spleen, kidney
and bone marrow. The chorionic villi had histologic evidence of involvement
with increased numbers of Hofbauer cells. The mother in question had been
infected during the first trimester and had not received treatment. The Centers
for Disease Control conducted a retrospective study on 19 women with Lyme
disease. (ref 5) There were five poor outcomes:
prematurity. cortical blindness, fetal demise, syndactyly, and rash. No
association was noted between a poor outcome and the trimester in which
infection occurred, or whether treatment was given. A second study conducted by
the Centers for Disease Control (ref 5) involved a prospective analysis of 17
females infected during the first trimester. In this small prospective study,
one infant was born with syndactyly and there was one spontaneous loss at 13
weeks. All the other pregnancies resulted in normal infants.
From 1986 through 1987, Nadal et a (ref 17) surveyed over 1000 mothers at
deliveries where anti-B burgdorferi antibody titers were obtained. ** see
note below
Of these 1000 mothers, 12 had elevated titers, but only one mother was
symptomatic with Lyme disease during her first trimester. Her child was born
with a ventricular-septal cardiac defect (VSD). None of the children born to
mothers with a positive titer had detectable antibodies. Of the 12 mothers with
positive titers, 8 delivered at term, 2 were preterm and 2 were postterm. Seven
infants had problems in the newborn period: there were two cases of
hyperbilirubinemia and one case each of hypotonia; (attributed to medication),
microcephaly, supra-ventricular extrasystoles, VSD, and small for gestational
age when examined between 9 and I7 months of age; however, only the child with
the VSD remained abnormal.
MacDonald published two papers regarding
Lyme disease in pregnancy. He described four cases of fetal borreliosis found
while prospectively studying abortuses.(ref 4) His findings included one term
stillbirth and three second-trimester losses. One of the second-trimester
losses was complicated by toxemia and another by systemic lupus erythematous.
B. burgdorferi was cultured from the fetal liver in each case. From the term
stillbirth, spirochetes were found in the liver, heart, adrenal, brain, kidney,
meninges, and subarachnoid. Three of the cases had identifiable cardiac
malformations:
atrial-septal defect, VSD, and coarctation of the aorta. He questioned whether
or not B. burgdorferi could be a cause of fetal demise, congenital heart
defect, or fetal loss after toxemia. In l989, MacDonald described several other
cases. One was a 25-year-old black woman at term in labor who delivered a male
fetus who was small for gestational age with multiple anomalies including VSD
in addition to central nervous system (CNS) anomalies. B. burgdorferi was
identified in the fetal autopsy. Another was a term intrauterine
growth-retarded infant who succumbed to a large VSD and absence of the left
hemidiaphragm. This autopsy also found spirochetes in tissue. MacDonald also
reports several second-trimester losses, with and without anomalies, that at
autopsy revealed B. burgdorfen. In the same article, MacDonald refers to a
retrospective study of 10 sudden infant deaths; he reported that 2 had
spirochetes consistent with B. burgdorferi in the brain. No other laboratory,
however, has confirmed this high report of spirochetal invasion of the fetal
and placental tissue.
In contrast to these reports of MacDonald, (ref 3,4) the Fourth International
Conference on Lyme Borreliosis held in Stockholm in June of 1990 concluded that
there is little risk to the fetus.(ref 9) The symposium examined a large
retrospective study in which there was no increased rate of congenital
malformations in infants with seropositive mothers. The symposium referred to a
study in which there were six pregnant women with Lyme disease, all of whom had
healthy infants. Another study, which surveyed pediatric neurologists in areas
highly endemic for Lyme disease, failed to discover any (??!!) records of
neurologic cases that could be attributed to Lyme disease.
In a series of 143 pregnant women from Wisconsin, titers for B. burgdorferi
exposure were examined and correlated with pregnancy outcome. In the group, the
incidence of first-trimester spontaneous abortions was no greater for
seropositive women than for seronegative women.
DIAGNOSIS
According to the Centers for Disease Control (ref 5) a diagnosis of Lyme
disease in pregnancy can be made with certainty if erythema migrans (EM) is
present or if there is the new onset of typical neurologic, cardiac, or joint
involvement in a pregnant woman accompanied by laboratory confirmation of
infection (typically diagnostic antibody levels or a significant rise in acute
versus convalescent antibody levels; isolation of spirochetes from a clinical
sample is also acceptable). In reality, however, patients in whom there is a
reasonable clinical suspicion for Lyme disease warrant treatment.
TREATMENT
According to the Centers for Disease Control, any pregnant woman with the
diagnosis of Lyme disease, or the suspicion of it, should be treated.(ref 5)
The diagnosis should be a clinical one and not based on serology because
serologic conversion may occur too late in the disease process. The problems
with current antibody assays, and the problem of seronegativity, are addressed
in Chapters 14 and 25. In the Centers for Disease Control study, 3 of
13 patients treated had abnormal fetal outcomes (23%), as did 2 of the 6
patients who were not treated (33%). According to their study, the time of the
disease in relation to poor outcome and whether the patient was treated were
not significant. The Centers for Disease Control admitted that none of these
adverse outcomes was documented to be a direct sequela of Lyme disease. These
adverse outcomes are only possible associations of Borrelia burgdorferi
maternal infection (Table 23-1).
Table 23-1 Adverse pregnancy outcomes with possible association to Lyme disease
Congenital anomlies (especially heart, great vessels)
Congenital cortical blindness
Miscarriage
Small for gestational age
Stillbirth
Toxemia
According to Mikkelsen and Palle, (ref 6) to avoid a potential adverse effect
on the fetus, the mother should be treated aggressively. Treatment is guided by
the clinical manifestations of the disease (Table 23-2).
Table 23-2
Treatment of Lyme disease during pregnancy
Disease stage Antibiotic regimen
Uncomplicated erythema migrans after first trimester:
Amoxicillin 500 mg P0 tid-qid x 21-30 days
Erythromycin 250 mg P0 qid x 21-30 days
[Newer macrolides such as Azithromycin may prove to he superior to
erythromycin]
Avoid tetracyclines, probenecid
Disseminated or late disease; first trimester infection
Intravenous antibiotics for 2-4 weeks
Ceftriaxone 2g
Penicillin G 20 million U qd
Lyme disease limited to the skin can probably be treated with amoxicillin or
erythromycin (see Chapter 18 for a different approach). Probenecid should not
be used, and the tetracyclines should be avoided. Disseminated disease, and
infections in the first trimester, should be treated with parenteral
antibiotics (ceftriaxone or penicillin - ref 6).
In 1987, Mikkelsen and Palle (ref 6) reported the case of a 29-year-old woman
who during her 24th week was bitten by a tick. She developed EM without any
systemic manifestations, with a positive antibody titer. She was treated with
penicillin for 10
days and subsequntly delivered a term baby. Histologic study of the placenta
was negative, and the antibody titer in cord and maternal blood was not
elevated.
SUMMARY
A body of evidence (ref 3 and 4) suggests that the causative agent of Lyme
disease, B. burgdorfen, can cross the placenta and infect the fetus. There are
also several reports that suggest that this may be associated with a poor fetal
outcome. However, the majority of studies have not been able to identify B.
burgdorferi as a direct cause of spontaneous abortions, congenital anomalies,
or neurologic sequelae in infants.
It is essential to realize that in the pregnant woman Lyme disease is a
clinical diagnosis regardless of her serologic status. Because the precise risk
to the fetus from an infected pregnant female is not yet clear, it is important
to be aggressive in the diagnosis and management of Lyme disease. This is
important not only for the fetus, but also for the mother. The mother is
certainly at risk for serious and potentially debilitating manifestations of
Lyme disease including arthritis, carditis, and neurologic problems.
In conclusion, Lyme disease in pregnancy is a clinical diagnosis irrespective
of serologic status.
The diagnosis must be made promptly, and treatment must be instituted in the
interest of maternal, in addition to fetal, welfare.
REFERENCES
1. Centers for Disease Control, MMWR 40(25):417, 1991.
2. Dlesk A et al: Lyme seropositivity and pregnancy outcome in the absence
of symptoms of Lyme disease, Arthritis Rheum 32(suppl):S46, 1989.
3. MacDonald AB: Human fetal borreliosis, toxemia of pregnancy, and fetal
death, Zentralbi Bakieriol Mikrobiol Hyg
[A] 263:189, 1986.
4. MacDonald AB: Gestational Lyme borreliosis, Rheum Dis Clin North Am
15(4):657, 1989.
5. Markowitt LE et al: Lyme disease during pregnancy. JAMA
255(24):3394, 1986.
6. Mikketsen AL, Palle C: Lyme disease during pregnancy. Acta Obstet
Gynecol Scand 66:477, 1987.
7. Nadal D et al: Infants born to mothers with antibodies against Borellia
burgdorferi at delivery, Eur J Pedjair
148:426, 1989.
8. Schlessinger PA et al: Maternal-fetal transmission of Lyme disease
spirochete Borrelia burgdoDferi, Ann Intern Med
103:67, 1985.
9. Sigal LH: Summary of the Fourth International Symposium on Lyme
Borreliosis, Arthritis Rheum 34(3):367, 1991.
10. Steere AG: Lyme disease, N Engi J Med 321:586, 1989.
11. Steere AC, Malawista SE: Cases of Lyme disease in the United States:
locations correlated with distribution of Ixodes dammini, Ann Intern Med
91:730, 1979.
12. Steere AC et al: The clinical spectrum and treatment of Lyme disease,
Yale J Biol Med 57:453, 1984.
***Infants infected in the first trimester, do not make antibodies (soldiers to
the bacterial antigen) because their young immune system does not recognize the
infection as foreign......See Altaie, Sousan...
** NOTICE: In accordance with Title 17 U.S.C. Section 107, this material
is distributed without profit to those who have expressed a prior interest
in receiving the included information for research and educational
purposes. **
FROM ANGILOGY: THE JOURNAL OF VASCULAR DISEASES...
JANUARY 1994
R GASSER, MD,PhD GRAZ, AUSTRIA AND EIGHT OTHER DOCTORS...
LETTER TO THE EDITOR
"A MOST UNUSUAL CASE OF A WHOLE FAMILY SUFFERING FROM LATE LYME BORRELIOSIS
FOR OVER 20 YEARS"
".............HUSBAND HAD NO MEMORY OF A PRIMARY INFECTION WITH CLASSICAL
STAGE ONE SYMPTOMS BUT REMEMBERS RECURRENT EPISODES OF FLU LIKE SYMPTOMS A
YEAR AFTER THE INFECTION OF HIS WIFE. THESE EPISODES WERE SOON FOLLOWED BY
STAGE TWO AND THREE SYMPTOMS. .......
A SON WAS BORN IN 1969 WITH SEVERAL MINOR ABNORMALITIES....HUGE SACRAL
HEMANGIOMA, GLUTEAL ATROPHY, AND OTHERS......GENERALLY WEAK, RECURRENT
EPISODES OF FEVER THROUGHOUT HIS LIFE....MINOR MENTAL ABNORMALITIES LIKE
IRRITABILITY AND DEPRESSION.....
DIAGNOSIS WAS CONFIRMED IN ALL THREE BY IMMUNOBLOTTING IN OUR SPECIFIC
CLINIC FOR Bb ASSOCIATED DISORDERS.......
FROM THESE CASES TWO IMPORTANT QUESTIONS ARISE:
1. IS THERE A SEXUAL TRANSMISSION...OR OF MERE COINCIDENCE IN AN ENDEMIC
AREA?
2. IS THERE A CONGENITAL LYME DISEASE COMPARIBLE TO CONGENITAL SYPHILIS?
.THE LATTER QUESTION CERTAINLY MERITS FURTHER INVESTIGATION...
.MUCH LARGER CONTROLLED STUDIES ARE NEEDED....
ALTERNATIVELY THERE IS GROWING EXPERIMENTAL EVIDENCE FOR TRANSMISSION OF Bb
THROUGH INFECTED BODY FLUIDS. THUS IT HAS BEEN SHOWN THAT Bb CAN BE
TRANSMITTED BW CLOSELY HOUSED RESEARCH ANIMALS WITHOUT THE PRESENCE OF
INSECTS... (#11 BURGESS EC. EXPERIMENTAL INNOCULATION OF PEROMYSCUSS SPP.
WITH Bb . AMER JOUR TROP HYG 35; 355-359, 1986.)
THIS LAB EVIDENCE STRONGLY ARGUES IN FAVOR OF TRANSMISSION THROUGH INFECTED
BODY FLUIDS. FURTHERMORE MORE THAN 30% OF THE PATIENTS DO NOT REMEMBER A TICK
BITE STILL TICK BITES CAN OCCUR WITHOUT THE PT'S BEING AWARE OF THE TICK
BITE. A STRONG CORRELATION BETWEEN ANTITICK SALIVA ANTIBODY WAS RECENTLY
REPORTED...THUS THERE IS NO DOUBT THAT TICKS ARE THE MOST COMMON TRANSMITTERS
OF THE MICROORGANSIM......."
PEDIATRIC RN, BSN IN CT
GINNY (BELLA...@AOL.COM)
** NOTICE: In accordance with Title 17 U.S.C. Section 107, this material
is distributed without profit to those who have expressed a prior interest
in receiving the included information for research and educational
purposes. **