Re: Any connection between ARDS and Lyme?
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Date: 07/09/04
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Date: 9 Jul 2004 01:16:16 -0700
"Jan" <rangoons.one@verizon.net> wrote in message news:<6rmHc.14911$Xb4.5377@nwrdny02.gnilink.net>...
> Does anyone have any information regarding Acute Respiratory Distress
> Syndrome and Lyme Disease? I met someone who has ARDS and has also been
> diagnosed with CFS and fibromyalgia. I couldn't help but wonder if Lyme
> could be at the root of all her problems. I would appreciate any
> information and/or articles.
>
> Thanks,
> Jan
FYI and Good luck:
N J Med 1995 Jun;92(6):381-5 Related Articles, Books
Ehrlichiosis with pancytopenia and ARDS.
Paparone PW, Ljubich P, Rosman GA, Nazha NT.
Shore Memorial Hospital, USA.
As illustrated by the case described in this report, the possibility
of
ehrlichiosis should be considered in the differential diagnosis of
sulfasalazine toxicity/drug fever and other febrile illnesses
presenting with
pancytopenia/leukopenia and pulmonary abnormalities, when patients
have been
exposed to known tick-infested areas. Furthermore, the possibility of
delayed
serologic confirmation of Ehrlichia infection should be integrated
into the
diagnostic process as well.
PMID: 7617311 [PubMed - indexed for MEDLINE]
--------
Title ARDS (acute respiratory distress syndrome)
Near fatal acute respiratory distress syndrome in a patient with human
ehrlichiosis.
Author
Patel RG ; Byrd MA
Address
Department of Medicine, University of Mississippi Medical Center,
Jackson, USA.
Source
South Med J, 92(3):333-5 1999 Mar
Abstract
Human ehrlichiosis is not a common cause of acute respiratory distress
syndrome
(ARDS). Physicians should be aware of this life-threatening but
treatable
entity. Progression to ARDS may be related to delay in diagnosis and
treatment.
Fever, leukopenia, thrombocytopenia, and a history of tick exposure in
an
endemic area during the spring and summer months should alert the
physician to
the possibility of human ehrlichiosis, since a definitive diagnosis
requires
serologic testing that may take weeks to confirm. We describe a case
of ARDS
resulting from human ehrlichiosis. A unique feature in our case was
that
despite the early use of doxycycline, the patient had near fatal ARDS
that
responded dramatically to high doses of steroids.
Language
Eng
Unique Identifier
99192093
---------------------------------------------------------------------
Major MeSH Headings
Ehrlichiosis CO ; Respiratory Distress Syndrome, Adult MI
Minor MeSH Headings
Anti-Inflammatory Agents, Steroidal TU ANTIINFLAMMATORY AGENTS
STEROIDAL ; Case
Report ; Human ; Male ; Methylprednisolone TU ; Middle Age ;
Respiration,
Artificial ; Respiratory Distress Syndrome, Adult TH
---------------------------------------------------------------------------
Publication Type
JOURNAL ARTICLE
ISSN
0038-4348
Country of Publication
UNITED STATES
Entry Month
-----------------------------------------------------------------------------
Ehrlichiosis which we do have locally is usually treated effectively
by
Doxy if caught early.
-- >>>>>>>>
"......This case alerts physicians to the serious end of the disease
spectrum
that can occur even though patients are given prompt, appropriate drug
treatment at the onset of illness...."
South Med J 1999 Mar;92(3):336-9
Ehrlichiosis with severe pulmonary manifestations despite early
treatment.
Weaver RA, Virella G, Weaver A
Department of Microbiology and Immunology, Medical University of South
Carolina, Charleston, USA.
It is generally thought that if patients with ehrlichiosis are treated
promptly, life-threatening illness can be avoided. We report a patient
who
sought medical attention 1 day after the onset of symptoms, was
immediately
given doxycycline, and still had serious illness with generalized
edema,
pulmonary infiltrates, acute respiratory distress syndrome, and
noncardiogenic
pulmonary edema, while receiving replacement intravenous fluids. This
case
alerts physicians to the serious end of the disease spectrum that can
occur
even though patients are given prompt, appropriate drug treatment at
the onset
of illness. Further studies are needed to clearly define the
mechanisms
involved in pulmonary complications and generalized edema, including
noncardiogenic pulmonary edema, in patients with ehrlichiosis.
PMID: 10094281, UI: 99192094
"...... unique feature in our case was that despite the early use of
doxycycline, the patient had near fatal ....."
South Med J 1999 Mar;92(3):333-5
Near fatal acute respiratory distress syndrome in a patient with human
ehrlichiosis.
Patel RG, Byrd MA
Department of Medicine, University of Mississippi Medical Center,
Jackson, USA.
Human ehrlichiosis is not a common cause of acute respiratory distress
syndrome
(ARDS). Physicians should be aware of this life-threatening but
treatable
entity. Progression to ARDS may be related to delay in diagnosis and
treatment.
Fever, leukopenia, thrombocytopenia, and a history of tick exposure in
an
endemic area during the spring and summer months should alert the
physician to
the possibility of human ehrlichiosis, since a definitive diagnosis
requires
serologic testing that may take weeks to confirm. We describe a case
of ARDS
resulting from human ehrlichiosis. A unique feature in our case was
that
despite the early use of doxycycline, the patient had near fatal ARDS
that
responded dramatically to high doses of steroids.
PMID: 10094280, UI: 99192093
--------------------------------------------------------------------------
Chest 1994 Oct;106(4):1299-301 Related Articles, Books
Delayed onset adult respiratory distress syndrome in babesiosis.
Horowitz ML, Coletta F, Fein AM.
Pulmonary & Critical Care Medicine Division, Winthrop-University
Hospital,
Mineola, NY.
Reported herein is a second case of a patient who developed adult
respiratory
distress syndrome secondary to babesiosis. The features of acute lung
injury
after babesiosis will be described.
Publication Types:
Review
Review of reported cases
PMID: 7924525 [PubMed - indexed for MEDLINE]
1: Am J Respir Crit Care Med 1994 Jun;149(6):1689-91 Related Articles,
Books,
LinkOut
Acute respiratory failure in patients treated for babesiosis.
Boustani MR, Lepore TJ, Gelfand JA, Lazarus DS.
New England Medical Center, Pulmonary and Critical Care Division,
Boston, MA
02111.
Babesiosis is a tick-borne protozoal disease with infrequent clinical
complications. We report three cases of noncardiogenic pulmonary edema
in
patients from Nantucket Island, MA, with a history of Lyme disease and
review
the clinical presentation of babesiosis and its treatment. Respiratory
complications in our patients, as well as in the four previously
reported cases
in the literature, occurred a few days after initiation of medical
therapy. We
hypothesize that the pathophysiology of the pulmonary edema is
multifactorial,
due to decreased deformability of the infected erythrocytes, increased
cytoadherence of red blood cells in capillaries and venules, and a
possible
role of excessive production of certain cytokines, such as tumor
necrosis
factor and interleukin-1.
Publication Types:
Review
Review of reported cases
PMID: 8004331 [PubMed - indexed for MEDLINE]
1: Chest 1984 Oct;86(4):633-4 Related Articles, Books
Adult respiratory distress syndrome in babesiosis.
Gordon S, Cordon RA, Mazdzer EJ, Valigorsky JM, Blagg NA, Barnes SJ.
A patient is described who contracted transfusion-induced babesiosis,
and later
developed acute respiratory distress syndrome (ARDS) as a fatal
complication.
ARDS has been reported in patients with Plasmodium falciparum malaria,
but to
our knowledge has not been observed as a complication of babesiosis.
PMID: 6541117 [PubMed - indexed for MEDLINE]
-----------------------------------------------------------------------------
http://internalmedicine.medscape.com/MedscapeWire/1999/07.99/medwire.0715.improved.html
Improved Outcomes for Tick-Borne Pulmonary Disease
July 15, 1999
CHEST/MedscapeWire
Effective antibiotic therapy can lead to greatly improved
outcomes for tick-borne pulmonary disease, according to new
recommendations on diagnosis and management published in the
July issue of CHEST.
Writing in the monthly peer-reviewed journal of the American
College of Chest Physicians, Stephen J. Ruoss, MD, of the
Division of Pulmonary and Critical Care Medicine, Stanford
University Medical Center, Palo Alto, California, along with four
associates, said that effective therapy is available for most
tick-borne diseases. However, when the illnesses are left
undiagnosed and untreated, they can be crippling and fatal.
>From May through August, numerous ticks, who suck blood
while feeding, are found on rodents and small mammals that
inhabit woods, gardens, and parklands over a wide geographic
area of the United States.
"Disease prevention therefore depends on the use of tick repellent
ointments, long sleeved clothing, and the avoidance of activities in
endemic areas," said Dr. Ruoss.
According to the authors, the diagnosis of tick-borne disease is
most often based on a number of clinical signs, plus a history of
outdoor activities, skin rash, or tick bites. Also, tests of blood
serum for infection or antibodies have become widely available so
physicians can confirm infection by the more common tick-borne
pathogens.
The article reviews the clinical features, the pulmonary aspects,
and treatment options of major tick-borne diseases, including
Lyme disease, Rocky Mountain Spotted Fever, and tularemia.
Lyme Disease
As the most commonly reported vector-borne illness in the U.S.
and Europe, Lyme disease is transmitted through the bite of the
black-legged tick, the American dog tick, or the Lone Star tick.
Caused by a spiral-shaped microorganism (spirochete) found on
rodents and deer, the disease is transmitted by ticks as a result of
outdoor activities. Over 50,000 cases of Lyme disease were
reported between 1982 and 1992 in the U.S., primarily in the
northeastern coastal states, the upper Midwest, and Northern
California.
Most tick nymphs, which are very small and quite hard to detect,
remain attached to the skin for a minimum of 36 to 48 hours to
cause infection in humans. Within one week, skin rash occurs at
the bite site. This rash is accompanied by fever, headache,
fatigue, pain in the joints, and diffuse muscle pain. Stage 1 Lyme
disease symptoms usually resolve themselves in 4 weeks with no
treatment. In Stage 2 disease, various neurologic manifestations
can surface, along with shortness of breath due to cardiac
involvement or to palsy of nerves that control the diaphragm.
Cardiac complications occur in about 8 percent of U.S. patients.
According to the authors, a cortisone-like drug, prednisone, can
be helpful for these problems, rather than early antibiotic therapy,
which can assist with other features of the illness.
"Death in Lyme disease is believed to be related to cardiac
involvement and to acute respiratory distress syndrome or
ARDS," said Dr. Ruoss.
"But Lyme disease can be prevented by avoiding tick exposure
and by using antibiotic therapy early in the disease, after
diagnosis," said Dr. Ruoss. "Yet, in the absence of any clinical
disease, systemic antibiotic therapy does not seem to help treat
tick bites. "Finally, the U.S. Food and Drug Administration has
approved a vaccine against this spirochete, although no other
vaccines for tick-borne diseases are available."
Rocky Mountain Spotted Fever
This illness is caused by bacteria-like microorganisms (Rickettsia)
that live as parasites in American dog ticks in the eastern states
and in Rock Mountain wood ticks in western states. Almost
1,000 cases of the disease are reported annually. Children are at
special risk.
Within two weeks of the tick bite, victims report fever and a
general feeling of weakness and illness, headache, diffuse muscle
pain, and vomiting. Typically, a rash appears widely on the body
from 1 to 14 days after disease onset.
Pulmonary manifestations include cough, sore throat, and chest
pain. Up to 36 percent of patients show fluid in the pleural cavity
on their chest radiograph. ARDS is reported to develop in 7
percent of the patients.
Diagnosis is made by immunofluorescent examination of skin
biopsy samples. Antibodies to rickettsii are detectable 7 to 10
days after disease onset.
Chloramphenicol or tetracycline antibiotic therapy reduces the
death rate from 25 percent to 5 percent. Antibiotic therapy is
continued until patients are without fever for 1 to 2 days.
Tularemia
The causative agent for tularemia was discovered in 1912 in
Tulare County, California. It results from an oval bacterial cell
found in rabbits, hares, rodents, and ticks. Transmission may
occur by direct contact, inhalation, ingestion, or tick bite. The
primary disease areas, Arkansas, Missouri, and Oklahoma,
report 200 to 300 cases per year.
Tularemia has about a 1 to 3 percent mortality rate. After a 3- to
5-day incubation period, patients have sudden onset of fever,
headache, weakness, and fatigue. Up to 40 percent have cough,
and up to 50 percent have an inflamed pharynx. Fluid in the
pleural cavity occurs in 20 to 30 percent of the patients at the
early disease stage and up to 55 percent in later stages.
Pneumonia occurs in 25 percent of the cases and is associated
with increased mortality.
"Either streptomycin or gentamicin therapy for 10 to 14 days
appears effective," said Dr. Ruoss. "A considerable clinical
improvement usually occurs within 48 hours of therapy."
-----------------------------------------------------------------------------
http://www.medscape.com/viewarticle/448899?mpid=10801
Endemic Babesiosis in Another Eastern State: New Jersey
Barbara L. Herwaldt, Paul C. McGovern, Michal P. Gerwel, Rachael M.
Easton,
Rob Roy MacGregor
Emerg Infect Dis 9(2), 2003. © 2003 Centers for Disease Control and
Prevention (CDC)
Posted 02/28/2003
Abstract and Introduction
Abstract
In the United States, most reported cases of babesiosis have been
caused by
Babesia microti and acquired in the northeast. Although three cases of
babesiosis acquired in New Jersey were recently described by others,
babesiosis has not been widely known to be endemic in New Jersey. We
describe a case of babesiosis acquired in New Jersey in 1999 in an
otherwise
healthy 53-year-old woman who developed life-threatening disease. We
also
provide composite data on 40 cases of babesiosis acquired from 1993
through
2001 in New Jersey. The 40 cases include the one we describe, the
three
cases previously described, and 36 other cases reported to public
health
agencies. The 40 cases were acquired in eight (38.1%) of the 21
counties in
the state. Babesiosis, a potentially serious zoonosis, is endemic in
New
Jersey and should be considered in the differential diagnosis of
patients
with fever and hemolytic anemia, particularly in the spring, summer,
and
early fall.
Introduction
In the United States, most of the hundreds of reported cases of
babesiosis
have been caused by Babesia microti, a parasite of small mammals
transmitted
by Ixodes scapularis (deer ticks); these ticks also transmit Borrelia
burgdorferi and Anaplasma (Ehrlichia) phagocytophila. Most reported
cases of
babesiosis have been acquired in the northeast, specifically in New
York,
Massachusetts, Connecticut, and Rhode Island. Another focus of B.
microti
infection is in Wisconsin and Minnesota.[1]
Although three cases of babesiosis acquired in New Jersey in 1998 were
described by Eskow et al.,[2] babesiosis has not been widely known to
be
endemic in New Jersey. Of interest, the index case-patient who
acquired B.
microti infection in the northeast (on Nantucket Island in 1969)
actually
was hospitalized in New Jersey.[3] We describe a case of babesiosis
acquired
in New Jersey in 1999 and provide composite data that include this
case, the
three cases previously reported by Eskow et al.,[2] and 36 other cases
acquired in New Jersey from 1993 through 2001. Our data strengthen the
conclusion that babesiosis is endemic in New Jersey.
Methods
Case Detection and Definition
We learned of additional babesiosis cases because they were reported
to the
New Jersey Department of Health and Senior Services or because
health-care
providers contacted the Centers for Disease Control and Prevention
(CDC)
about the diagnosis or treatment of babesiosis. Although babesiosis is
not a
nationally notifiable disease, some states have made cases of
babesiosis
reportable. Cases became reportable in New Jersey in 1985; however,
reporting was discontinued in 1990 because no cases had been reported.
Reporting was reinstated in 1995, and 1997 was the first year in which
cases
were reported to the health department.
We defined a case of babesiosis as an infection occurring in a
symptomatic
person whose illness was consistent with babesiosis, most likely was
acquired in New Jersey, and most likely resulted from a tick bite
rather
than a blood transfusion. In addition, supporting laboratory data had
to be
provided and include at least one of the following: identification by
light
microscopy of intraerythrocytic Babesiaparasites in a peripheral blood
smear, isolation of the parasite from a whole blood specimen (by
inoculating
hamsters [Mesocricetus auratus] intraperitoneally and examining smears
of
blood obtained by tail snip, weekly for up to 2 months), demonstration
of B.
microti DNA in a whole blood specimen by polymerase chain reaction
(PCR)
analysis at a reference laboratory, or demonstration of a
Babesia-specific
antibody titer of at least 1:256 with an indirect fluorescent antibody
assay
for total immunoglobulin (Ig) or IgG. If only serologic data met the
diagnostic criteria, the case was considered probable rather than
confirmed.
Case Report
A previously healthy 53-year-old woman was admitted to a community
hospital
on June 24, 1999, because she had had 1 week of fever (38.9°C-39.4°C),
rigors, a nonproductive cough, an occipital headache, and increasing
malaise. Three days before her hospitalization, she started therapy
with
cefuroxime axetil for presumed bronchitis but did not improve. She had
a >50
pack-year history of smoking and drank two to three beers per day. She
lived
in Burlington County (Figure 1) in southcentral New Jersey and had not
traveled outside the county recently. Although she did not recall
recent
exposure to deer ticks, she occasionally had seen deer in her backyard
and
she gardened frequently.
On admission to the hospital, she had a temperature of 39.2°C, a blood
pressure level in the 80/60 mm Hg range, and otherwise unremarkable
results
on physical examination. She was anemic and thrombocytopenic, with
elevated
total bilirubin and lactate dehydrogenase values (Table). On the basis
of a
blood smear from June 24, which showed intraerythrocytic ring forms in
approximately 5% of the erythrocytes on her peripheral blood smear,
treatment for babesiosis was begun on June 25. The treatment included
intravenous clindamycin, 900 mg three times a day, and oral quinine,
650 mg
three times a day; and she was transfused with two units of packed
erythrocytes. Also on June 25, hypoxic respiratory failure developed,
and
she was intubated. A chest radiograph showed diffuse alveolar
infiltrates,
which were attributed to the adult respiratory distress syndrome
(ARDS).
On June 28, she was transferred to the Hospital of the University of
Pennsylvania. When admitted, her blood pressure was 84/52 mm Hg,
despite
therapy with dopamine. She continued therapy for babesiosis for a
total of
15 days (the dose of clindamycin was decreased to 600 mg three times a
day
on June 28). Although the level of parasitemia had decreased to 0.3%
by June
29, she had ongoing hemolysis and received six more units of packed
erythrocytes during her hospital stay (Table). No parasites were noted
on a
blood smear on July 9, the last day of antibabesial therapy. She had
been
successfully weaned from inotropic blood-pressure support on July 2
and
underwent extubation on July 4.
Additional laboratory testing at CDC provided further evidence that
she was
infected with B. microti. Serum specimens assayed in parallel, in
serial
fourfold dilutions, by indirect fluorescent antibody testing for
antibody to
B. microti,[4] had titers of 1:1,024 (June 30, 1999) and 1:16 (July
16,
2000). In addition, PCR analysis of whole blood from June 30, 1999, by
using
B. microti-specific primers,[5] confirmed she was infected with B.
microti.
Serologic testing performed at the Hospital of the University of
Pennsylvania by enzyme immunoassay for antibody to Borr. burgdorferi
was
negative.
Complications during her hospitalization unrelated to babesiosis
included
nosocomial pneumonia, acute tubular necrosis from hypoperfusion,
bilateral
deep venous thromboses, pulmonary embolism, and thrombocytopenia
temporally
associated with the initiation of heparin therapy (Table). On July 23,
after
30 days in the hospital, she was sent home. She was continuing to do
well as
of October 2002.
Composite Data
The 40 cases in our analyses include the case described above, the
three
cases previously described by Eskow et al.,[2] and 36 other cases. We
did
not include six other reported tick-borne cases that occurred in New
Jersey
residents, because the laboratory data did not meet our criteria or
information about the probable state in which infection was acquired
was not
known or provided.
The number of reported cases of babesiosis increased over time (Figure
2);
28 (70.0%) of the 40 cases occurred in 2000 or 2001. The 40 cases were
acquired in eight (38.1%) of the state's 21 counties (Figure 1).
Burlington
County, on the inner coastal plain, and Ocean County, on the outer
coastal
plain, which are neighboring counties in southcentral New Jersey,
accounted
for 25 (62.5%) of the 40 cases; these two counties are the 7th (Ocean)
and
10th (Burlington) most populous counties in the state. None of the
cases
were acquired in the northernmost or southernmost counties of New
Jersey.
Most of the cases were in elderly persons (median age, 67 years;
range,
11-87 years). Over half of the cases (22 [55.0%]) were in male
patients. The
median date of diagnosis was July 20 (range, June 10-September 9;
n=36). Two
patients (5.0%) died: an 86-year-old man with multisystem organ
failure and
an 80-year-old man with ARDS. The patient whose case we described here
also
developed ARDS.
The following information about the patients was not collected
systematically. However, three patients were reported to be asplenic,
18 to
have recalled tick bites, 34 to have been hospitalized, and three to
have
had Lyme disease (no details available). Underlying conditions
included HIV
infection in one patient, who had a CD4 count of 50; diabetes in five
patients; a history of breast or prostate cancer in three patients (no
details available); and a condition that led to chemotherapy in one
person
(no details available).
Various types of laboratory tests were used to diagnose the 40
babesiosis
cases. Not all patients were tested with the same methods. However, 34
patients had positive blood smears; for 27 of these patients, the
positive
smear was the only laboratory result that met our diagnostic criteria.
All
three cases reported by Eskow et al. were in patients who had negative
blood
smears.[2] One of the two patients who had whole blood inoculated into
hamsters had positive results (i.e., the hamsters became parasitemic).
Four
patients had positive PCR results from a reference laboratory; for one
of
these patients, these results were the only ones that met our
diagnostic
criteria. Twelve patients had serologic data that met our criteria;
for four
patients, the serologic results were the only data that met our
diagnostic
criteria. These cases were considered probable rather than confirmed.
CDC
confirmed the diagnosis of Babesia infection in 11 (27.5%) of the 40
cases;
specimens from the other 29 case-patients were not sent to CDC.
Discussion
Our report strengthens the evidence that New Jersey is one of the
eastern
states in which babesiosis is endemic. In addition, the risk for
acquisition
of infection is widely distributed in the state. Whether the fact that
most
of the reported cases occurred in southcentral and northcentral
counties
reflects the degree of endemicity of babesiosis in various areas of
New
Jersey is unknown.
The fact that babesiosis is endemic in New Jersey is not surprising,
given
that Lyme disease, the etiologic agent of which also is transmitted by
I.
scapularis, is highly endemic in New Jersey[6, 7] and given the
geographic
proximity of New Jersey to areas in the northeast where babesiosis is
highly
endemic. In a 1996 study, of 100 I. scapularisticks collected in
Hunterdon
County, New Jersey, 43 were infected with Borr. burgdorferi, 5 were
infected
with B. microti, and 2 were infected with both organisms.[8]
The increase in reported cases of babesiosis, which began in 1998
(Figure 2)
and was even more notable in 2000 and 2001, could indicate an
increased risk
for B. microtiinfection and illness. If true, possible reasons for the
increased risk could include a growing abundance of local I.
scapularis
populations or the introduction of a more virulent strain of B.
microti.[9]
However, the increased numbers of reported cases could simply
represent an
increased awareness of the disease and increased reporting. Even so,
the 40
cases of babesiosis that we tallied probably represent only a fraction
of
the clinical cases of B. microti infection acquired in New Jersey from
1993
through 2001. Presumably, other symptomatic cases (as well as many
more
subclinical cases) occurred but were not diagnosed or reported. In
fact,
several other possible symptomatic cases were reported that we did not
count
because we received insufficient information about them. Also, as is
commonly true for surveillance data, the amount and quality of the
information provided to the health department and CDC about the cases
varied
widely; some of the information might have been inaccurate, and not
all of
the cases were confirmed by reference laboratories (e.g., not all of
the
blood smears that were reported as positive were reexamined by a
reference
laboratory).
The laboratory tests CDC offers for babesiosis, when indicated,
include
examination of blood smears, hamster inoculation, and PCR[5] for
parasitologic diagnosis and an indirect fluorescent antibody assay for
total
immunoglobulin for serologic diagnosis.[4] Using PCR for detection of
DNA
from Babesia spp. has not yet become a routine diagnostic method, and
the
analysis should be conducted by experienced reference laboratories.
Immunoblot testing for IgG and IgM is investigational. However, an
immunoblot test for IgG performed well in a recent evaluation, with a
sensitivity of 96% and a specificity of 99%.[10] A positive serologic
result
for IgM[11] is insufficient for diagnosis without a positive result
for IgG.
If the IgM result is positive but the IgG result is negative, a
follow-up
specimen should be tested. If IgG seroconversion is not noted, the IgM
result likely was a false positive. Future serologic testing might
involve
recombinant and synthetic antigens[12] rather than whole parasites or
soluble antigens.
The case we described in detail demonstrates that babesiosis can be
life
threatening.[1,13,14] In fact, two (5.0%) of the 40 case-patients
died. In
the patient we described, the following conditions developed: severe
anemia,
for which she was transfused with eight units of packed erythrocytes;
hypotension that required inotropic support; ARDS, which has
previously been
reported;[13-17] and various nosocomial complications. The fact that
she was
ill for approximately 1 week before therapy for babesiosis was
initiated
might have contributed to the severity of her illness. Fortunately,
treatment for babesiosis was begun soon after she was hospitalized.
Although
she was treated successfully with clindamycin and quinine, a recent
clinical
trial indicated that the combination of azithromycin and atovaquone is
also
effective.[18] However, patients with life-threatening babesiosis were
excluded from the study. Severely ill patients, particularly those
with high
levels of parasitemia (e.g., >/= 10%), may benefit from exchange
transfusion.[1, 19]
In summary, babesiosis, a potentially serious zoonosis, is endemic in
New
Jersey and should be considered in the differential diagnosis of
patients
with fever and hemolytic anemia, particularly in the spring, summer,
and
early fall.
References
Boustani MR, Gelfand JA. Babesiosis. Clin Infect Dis 1996;22:611-5.
Herwaldt BL, Kjemtrup AM, Conrad PA, Barnes RC, Wilson M, McCarthy MG,
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Herwaldt BL, Persing DH, Precigout EA, Goff WL, Mathiesen DA, Taylor
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al. A fatal case of babesiosis in Missouri: identification of another
piroplasm that infects humans. Ann Intern Med 1996;124:643-50.
Quick RE, Herwaldt BL, Thomford JW, Garnett ME, Eberhard ML, Wilson M,
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1993;119:284-90.
Persing DH, Herwaldt BL, Glaser C, Lane RS, Thomford JW, Mathiesen D,
et al.
Infection with a babesia-like organism in northern California. N Engl
J Med
1995;332:298-303.
McQuiston JH, Childs JE, Chamberland ME, Tabor E. Transmission of
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United States. Transfusion 2000;40:274-84.
Cable RG, Trouern-Trend J. Tickborne infections. In: Linden JV, Bianco
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Filstein MR, Benach JL, White DJ, Brody BA, Goldman WD, Bakal CW, et
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Serosurvey for human babesiosis in New York. J Infect Dis
1980;141:518-21.
Hatcher JC, Greenberg PD, Antique J, Jimenez-Lucho VE. Severe
babesiosis in
Long Island: review of 34 cases and their complications. Clin Infect
Dis
2001;32:1117-25.
White DJ, Talarico J, Chang H, Birkhead GS, Heimberger T, Morse DL.
Human
babesiosis in New York State: review of 139 hospitalized cases and
analysis
of prognostic factors. Arch Intern Med 1998;158:2149-54.
Meldrum SC, Birkhead GS, White DJ, Benach JL, Morse DL. Human
babesiosis in
New York State: an epidemiological description of 136 cases. Clin
Infect Dis
1992;15:1019-23.
Chisholm ES, Ruebush TK II, Sulzer AJ, Healy GR. Babesia microti
infection
in man: evaluation of an indirect immunofluorescent antibody test. Am
J Trop
Med Hyg 1978;27:14-9.
Persing DH, Mathiesen D, Marshall WF, Telford SR, Spielman A, Thomford
JW.
Detection of Babesia microti by polymerase chain reaction. J Clin
Microbiol
1992;30:2097-103.
Wong SJ, Brady GS, Dumler JS. Serological responses to Ehrlichia equi,
Ehrlichia chaffeensis, and Borrelia burgdorferi in patients from New
York
State. J Clin Microbiol 1997;35:2198-205.
Linden JV, Wong SJ, Chu FK, Schmidt GB, Bianco C.
Transfusion-associated
transmission of babesiosis in New York State. Transfusion
2000;40:285-9.
Grabowski EF, Giardina PJV, Goldberg D, Masur H, Read SE, Hirsch RL,
et al.
Babesiosis transmitted by a transfusion of frozen-thawed blood. Ann
Intern
Med 1982;96:466-7.
Slovut DP, Benedetti E, Matas AJ. Babesiosis and hemophagocytic
syndrome in
an asplenic renal transplant recipient. Transplantation 1996;62:537-9.
Perdrizet GA, Olson NH, Krause PJ, Banever GT, Spielman A, Cable RG.
Babesiosis in a renal transplant recipient acquired through blood
transfusion. Transplantation 2000;70:205-8.
Krause PJ, Lepore T, Sikand VK, Gadbaw J Jr, Burke G, Telford SR III,
et al.
Atovaquone and azithromycin for the treatment of babesiosis. N Engl J
Med
2000;343:1454-8.
Acknowledgements
We thank the laboratory staff of the Division of Parasitic Diseases,
Centers
for Disease Control and Prevention; Adeleh Ebrahimzadeh from the New
York
City Public Health Laboratory; and Rich Gallo and staff from the New
York
State (Westchester County) Department of Health.
Joseph Z. Lux, Don Weiss, Jeanne V. Linden, Debra Kessler, Barbara L.
Herwaldt, Susan J. Wong, Jan Keithly, Phyllis Della-Latta, Brian E.
Scully;
Columbia University College of Physicians and Surgeons, New York; New
York
City Department of Health, New York; Wadsworth Center, New York State
Department of Health, Albany; New York Blood Center, New York; Centers
for
Disease Control and Prevention, Atlanta, Georgia; Columbia
Presbyterian
Medical Center, New York, New York
Dr. Lux is an infectious diseases fellow at Columbia University
College of
Physicians and Surgeons.
-------------------------------------------------------------------------------
Respiratory Manifestations of Tick-Borne Diseases in the Southeastern
United
States
RYLAND P. BYRD, JR., MD, JOSE VASQUEZ, MD, and THOMAS M. ROY, MD,
Johnson City,
Tenn
ABSTRACT: Pulmonary signs and symptoms may provide important
differential clues
to the diagnosis of tick-borne illness incurred in the southern United
States.
IN THE UNITED STATES, most vector-borne diseases are transmitted by
ticks. With
migration of our population into rural areas and increased outdoor
recreational
activity, tick-borne viral, rickettsial, bacterial, and protozoal
infections
have become more prevalent (Table 1). Each of these diseases typically
occurs
with the constellation of symptoms of fever, chills, headache, and
myalgia.
Pulmonary involvement, however, is not uniform. In this article we
review the
respiratory manifestations of tick-borne diseases (Table 2).
COLORADO TICK FEVER
Colorado tick fever is an acute viral illness transmitted by the tick
Dermacentor andersoni. The pathogen is a double-stranded RNA virus of
the
Orbivirus genus. Between 200 and 300 cases are reported each year in
the
mountain regions of Colorado, Wyoming, Montana, Idaho, Washington,
Oregon,
California, New Mexico, Nevada, Utah, and South Dakota. Since the
disease is
relatively benign, the annual incidence is probably much higher.1
The illness begins 3 to 6 days after inoculation, with an abrupt onset
of
constitutional complaints. Although 34% of patients will have a sore
throat,
more extensive involvement of the respiratory system is rarely
seen.2-4 A
single patient with an atypical pneumonitis has been described in the
medical
literature.2
RELAPSING FEVER
Relapsing fever can be caused by one of several spirochete organisms
within the
genus Borrelia. The waxing and waning nature of this disease is
thought to be
due to the spontaneous appearance of antigenic variants under pressure
from the
hostís immune system.5 Several ticks are important in the transmission
of this
disease to human beings. In the western forested mountains above 300
meters,
Ornithodoros hermsii serves as the vector for Borrelia hermsii. In the
semiarid
plains, Ornithodoros turicata serves as the reservoir for Borrelia
turicatae,
and Ornithodoros parkeri harbors Borrelia parkeri.6
The incubation period for relapsing fever is generally 7 days but
ranges from 4
to 18 days. Illness usually begins with an abrupt onset of systemic
malaise.
Nonproductive cough is present in only 9% of patients.7 Pharyngitis,
pleuritic
chest pain, pneumonia, and pleural effusions have not been reported.
There has
been one case of adult respiratory distress syndrome (ARDS) associated
with
relapsing fever.8
LYME DISEASE
Lyme disease has been well publicized in recent years. Borrelia
burgdorferi is
the spirochete that causes this illness. Ixodes scapularis in eastern
and upper
midwestern states and Ixodes pacificus in western states serve as the
vectors
for human inoculation.
Lyme disease may cause both an acute and chronic multisystem illness.
Lyme
disease is typically divided into three stages.9 Stage 1 is the early
localized
stage occurring 7 to 10 days after infection. This is the point at
which the
typical dermatitis, erythema migrans, develops at the site of the tick
bite.
The patient may have a low-grade fever, headache, fatigue, arthralgia,
myalgia,
and regional lymphadenopathy. Respiratory symptoms are unusual, but
cough may
be present.
In stage 2, dissemination from the primary site commonly occurs a few
weeks
after the initial infection. Patients may have multiple secondary
cutaneous
annular lesions. Fever, adenopathy, and cranial neuritis are common.9
Respiratory symptoms are again unusual, but cough may be present.
Pharyngitis
has been reported in 17% of patients in stage 2 of Lyme disease.10 One
case of
adult respiratory distress syndrome during stage 2 has been
reported.11
The late manifestations of Lyme disease (stage 3) include chronic
arthritis,
chronic central nervous system impairment, chronic dermatitis, and
keratitis.
There are no reports of respiratory symptoms during stage 3 of Lyme
disease.
BABESIOSIS
Babesiosis is the only known tick-borne protozoal infection in the
United
States. Babesia microti is the causative agent in the northeastern
United
States, Babesia equi in California. Other organisms within the genus
Babesia
may also cause disease. Transmission is by the tick Ixodes scapularis
in the
Northeast. Other ticks, such as Ixodes pacificus in California, may
serve as
the vector when disease is contracted outside the normal range of
Ixodes
scapularis. Most cases occur in the northeastern United States, but
cases are
reported as far south as Virginia and Georgia. There are sporadic
reports of
babesiosis in California, Washington, Wisconsin, and Minnesota. Since
Lyme
disease is transmitted through the same tick vector, babesiosis occurs
concurrently with Lyme disease in 23% of the patients.12
Symptoms of malaise, fatigue, and anorexia begin 1 week after
inoculation.
Several days later, patients typically have fever, sweats, myalgia,
and
headache. Respiratory symptoms include cough in 14% and pharyngitis in
7% of
patients.13-16 Pleuritic chest pain, pleural effusion, and pneumonia
have not
been reported. Six patients have had adult respiratory distress
syndrome
associated with babesiosis. Each of these patients had been receiving
therapy
for babesiosis for several days. This leaky capillary syndrome is
unique in
that it occurs after the institution of therapy with a variety of
antimicrobials.13-16
EHRLICHIOSIS
Ehrlichiosis is one of the two rickettsial diseases transmitted by
ticks.
Ehrlichia chaffeensis is the sole causative agent in the United
States. The
tick vector may include both Dermacentor variabilis and Amblyomma
americanum.
Most cases of ehrlichiosis have occurred in the south central and
southeastern
United States.
Infection with E chaffeensis usually causes a nonspecific illness 7
days after
exposure. The most common clinical features are high fever with
headache, but
the patient may complain of malaise, myalgia, nausea, vomiting, and
anorexia.
Cough is present in 39% of patients.17 Sore throat and pharyngitis
occur in 22%
to 33% of patients.17,18 The risk of pneumonia in ehrlichiosis varies
with the
age of the patient. Pulmonary infiltrates develop in 75% of the
children with
this rickettsial infection but in only 39% of the adults.17 Adult
respiratory
distress syndrome occurred in 11% to 18% of the cases reported in the
literature.17
ROCKY MOUNTAIN SPOTTED FEVER
Rickettsia rickettsii is the organism responsible for Rocky Mountain
spotted
fever, the most common rickettsial disease in the United States.
Dermacentor
variabilis in the eastern United States and D andersoni in the western
United
States are responsible for the transmission of this infection to
humans. Most
infections occur in the southeastern and coastal Atlantic states.
Rocky Mountain spotted fever is classically manifested by the triad of
fever,
rash, and history of tick exposure. However, as with all tick-borne
illnesses,
the tick bite is recalled by only 50% of the patients. A rash is
present in 80%
of the patients. The usual onset of illness is 5 to 7 days after
inoculation.
Fever, malaise, frontal headache, myalgia, and vomiting are common.
Cough is
present in 14% to 33% of patients, with sore throat and/or pharyngitis
in 6% to
9% of the patients.19,20 About 17% of patients will complain of
pleuritic chest
pain,19 and between 10% to 36% will have a pleural effusion on chest
radiograph.19,21
Vasculitis is responsible for the rash found in the typical patient
with Rocky
Mountain spotted fever. This vasculitis also affects the pulmonary
vasculature.
Approximately 12% to 42% of patients will have a pulmonary infiltrate
on chest
radiograph.19,21-24 Since the vasculitis is thought to be responsible
for the
radiographic finding, it is not surprising that an interstitial
pattern
predominates (85%). The remaining 15% of patients with Rocky Mountain
spotted
fever and pulmonary infiltrates have a pattern of consolidation on
chest
films.19
Rocky Mountain spotted fever leads to adult respiratory distress
syndrome in 6%
to 9% of patients19,20,22 in whom catheterization of the right side of
the
heart has shown noncardiac pulmonary edema. Hemodynamic monitoring is
essential
in critically ill patients with Rocky Mountain spotted fever and
pulmonary
edema because the vasculitis associated with this illness can also
affect the
blood vessels of the myocardium, resulting in poor pump function.
About 30% of
patients with Rocky Mountain spotted fever have cardiogenic pulmonary
edema.
This is the only tick-borne disease to directly cause congestive heart
failure.21,25,26
TULAREMIA
Tularemia is caused by the bacterium Francisella tularensis. The tick
vector
includes Amblyomma americanum in the southeastern and south central
United
States and Dermacentor andersoni and D variabilis in the West. The
severity of
illness is variable. Classically, the illness begins 3 to 5 days after
inoculation with a sudden onset of fever, chills, headache, malaise,
fatigue,
and myalgia. Tularemia that is acquired by a tick bite occurs as
either the
ulceroglandular or typhoidal form. Respiratory symptoms are not
significantly
different with either of these forms. Cough is present in 23% to 40%
of
patients27-30 and pharyngitis in 15%-50%.28,29 Effusions due to
pleural
inflammation occur in 21% to 31% of patients early in the course of
the
disease,27,29,31,32 but this may exceed 50% in later stages.33 The
tendency
toward involvement of serosal surfaces also causes exudative
pericarditis.32
Pneumonia is encountered in 15% to 25% of tularemic patients,27,31,32
74% of
whom have a patchy air-space opacity.31,32 More unusual chest
radiographic
findings (Table 3) have not been reported with other tick-borne
diseases.31,32
The classically described radiographic triad of oval opacities, hilar
adenopathy, and pleural effusion is encountered in a minority of
patients.31,32
Tularemia progresses to adult respiratory distress syndrome in 12% of
patients.27 As with Rocky Mountain spotted fever, right heart
catheterization
is often helpful in the treatment of critically ill patients with
tularemia.
CONCLUSIONS
Pulmonary signs and symptoms may aid in the clinical diagnosis of
tick-borne
disease. Cough, sore throat, and pharyngitis are nonspecific findings
in
tick-borne infections. Pneumonia should point away from a diagnosis of
Colorado
tick fever, relapsing fever, Lyme disease, or babesiosis. However,
pneumonia
does occur in tularemia,31,32 Rocky Mountain spotted fever,19 and
ehrlichiosis.17 Since these three illnesses have an overlapping
geographic
distribution in the southeastern United States, recognition of the
disease
pattern on chest radiograph can be helpful in the differential
diagnosis.
Although the radiographic pattern of pulmonary disease due to
ehrlichiosis has
not been well classified because cases are infrequent, the great
majority of
patients with Rocky Mountain spotted fever and pulmonary infiltrates
have an
interstitial radiographic pattern.19 Tularemia, on the other hand,
produces
primarily a patchy alveolar process on chest roentgenogram.31,32
Pleural
effusion with any type of infiltrate is evidence against ehrlichiosis
and
narrows the differential to tularemia27,29,31,32 and Rocky Mountain
spotted
fever.19,21 If the infiltrate is interstitial or if the effusion is a
transudate consistent with increased hydrostatic pressures, then Rocky
Mountain
spotted fever is most likely.
Adult respiratory distress syndrome can occur with tick-borne
illnesses and
should be anticipated in Rocky Mountain spotted fever,19,20,22
tularemia,27 and
ehrlichiosis.17 Adult respiratory distress syndrome has not been
reported in
patients with Colorado tick fever, and there has been only one
reported case of
ARDS associated with relapsing fever8 and one with Lyme disease.11
Importantly,
adult respiratory distress syndrome in babesiosis occurs only after
starting
effective treatment.13-16
References
1. Emmons RW: An overview of Colorado tick fever. Prog Clin Biol Res
1985;
178:47-52
2. Goodpasture HC, Poland JD, Francy B, et al: Colorado tick fever:
clinical,
epidemiologic, and laboratory aspects of 228 cases in Colorado in
1973-74. Ann
Intern Med 1978; 88:303-310
3. Spruance SL, Bailey A: Colorado tick fever: a review of 115
laboratory
confirmed cases. Arch Intern Med 1973; 131:288-293
4. Earnest MP, Breckinridge JC, Barr RJ, et al: Colorado tick fever:
clinical
and epidemiologic features and evaluation of diagnostic methods. Rocky
Mountain
Med J 1971; 68:60-62
5. Barbour AG: Antigenic variation of a relapsing fever Borrelia
species. Annu
Rev Microbiol 1990; 44:155-171
6. Felsenfeld O: Borrelia: Strains, Vectors, Human and Animal
Borreliosis. St.
Louis, WH Green, 1971, pp 37-41
7. Thompson RS, Burgdorfer W, Russell R, et al: Outbreak of tick-borne
relapsing fever in Spokane County, Washington. JAMA 1969;
210:1045-1050
8. Davis RD, Burke JP, Wright LJ: Relapsing fever associated with ARDS
in a
parturient woman. Chest 1991; 102:630-632
9. Steere AC: Lyme disease. N Engl J Med 1989; 321:586-596
10. Steere AC, Bartenhagen NH, Craft JE, et al: The early clinical
manifestations of Lyme disease. Ann Intern Med 1983; 99:76-82
11. Kirsch M, Ruben FL, Steere AC, et al: Fatal adult respiratory
distress
syndrome in a patient with Lyme disease. JAMA 1988; 259:2737-2739
12. Meldrum SC, Birkhead GC, White DJ, et al: Human babesiosis in New
York
State: an epidemiological description of 136 cases. Clin Infect Dis
1992;
15:1019-1023
13. Horowitz ML, Coletta F, Fein AM: Delayed onset adult respiratory
distress
syndrome in babesiosis. Chest 1994; 106:1299-1301
14. Gordon S, Gordon RA, Mazdzer EJ, et al: Adult respiratory distress
syndrome
in babesiosis. Chest 1984; 86:633-634
15. Boustani MR, Lepore TJ, Gelfand JA, et al: Acute respiratory
failure in
patients treated for babesiosis. Am J Respir Crit Care Med 1994;
149:1689-1691
16. Iacopino V, Earnhart T: Life-threatening babesiosis in a woman
from
Wisconsin. Arch Intern Med 1990; 150:1527-1528
17. Eng TR, Harkess JR, Fishbein DB, et al: Epidemiologic, clinical,
and
laboratory findings of human ehrlichiosis in the United States, 1988.
JAMA
1990; 264:2251-2258
18. Mathisen GE, Weiss PJ, Kennedy CA: Pneumonia, aseptic meningitis,
and
leukopenia in a 28-year-old man. Clin Infect Dis 1993; 16:809-815
19. Donohue JF: Lower respiratory tract involvement in Rocky Mountain
spotted
fever. Arch Intern Med 1980; 140:223-227
20. Kirk JL, Fine DP, Sexton DJ, et al: Rocky Mountain spotted fever:
a
clinical review based on 48 confirmed cases, 1943-86. Medicine 1990;
669:35-45
21. Lees RF, Harrison RB, Williamson BRJ, et al: Radiographic findings
in Rocky
Mountain spotted fever. Radiology 1978; 129:17-20
22. Sacks HS, Lyons RW, Lahiri B: Adult respiratory distress syndrome
in Rocky
Mountain spotted fever. Am Rev Respir Dis 1981; 123:547-549
23. Garg P, Blass DA: Rocky Mountain spotted fever manifested by
cerebritis and
pneumonitis. Md Med J 1987; 36:343-344
24. Helmick CG, Bernard KW, DíAngelo LJ: Rocky Mountain spotted fever:
clinical, laboratory, and epidemiological features of 262 cases. J
Infect Dis
1984; 150:480-488
25. McCook TA, Briley C, Ravin CE: Roentgenographic abnormalities in
Rocky
Mountain spotted fever. South Med J 1982; 75:156-157
26. Lankford HV, Glauser FL: Cardiopulmonary dynamics in a severe case
of Rocky
Mountain spotted fever. Arch Intern Med 1980; 140:1357-1359
27. Scofield RH, Lopez EJ, McNabb SJN: Tularemia pneumonia in
Oklahomaó1987. J
Okla State Med Assoc 1992; 85:165-170
28. Halstead CC, Kulasinghe HP: Tularemia pneumonia in urban children.
Pediatrics 1978; 61:660-662
29. Evans ME, Gregory DW, Schaffner W, et al: Tularemia: a 30-year
experience
with 88 cases. Medicine 1985; 64:251-269
30. Schmid GP, Kornblatt AN, Connors CA, et al: Clinically mild
tularemia
associated with tick-borne Francisella tularensis. J Infect Dis 1983;
148:63-67
31. Miller RP, Bates JH: Pleuropulmonary tularemia: a review of 29
patients. Am
Rev Respir Dis 1969; 99:31-41
32. Rubin SA: Radiographic spectrum of pleuropulmonary tularemia. AJR
1978;
131:277-281
33. Dennis JM, Boudreau RP: Pleuropulmonary tularemia: its roentgen
manifestations. Radiology 1957; 68:25-30
Back to January INDEX
---------------------------------------------------------------------------
Title ARDS (acute respiratory distress syndrome)
Fatal adult respiratory distress syndrome in a patient with Lyme
disease.
Author
Kirsch M ; Ruben FL ; Steere AC ; Duray PH ; Norden CW ; Winkelstein A
Address
Department of Medicine, Montefiore Hospital, University of Pittsburgh
School of
Medicine, PA 15213.
Source
JAMA, 259(18):2737-9 1988 May 13
Abstract
A dry cough, fever, generalized maculopapular rash, and myositis
developed in a
67-year-old woman; she also had markedly abnormal liver function test
results.
Serologic tests proved that she had an infection of recent onset with
Borrelia
burgdorferi, the agent that causes Lyme disease. During a two-month
course of
illness, her condition remained refractory to treatment with
antibiotics,
salicylates, and steroids. Ultimately, fatal adult respiratory
distress
syndrome developed; this was believed to be secondary to Lyme disease.
Language
Eng
Unique Identifier
88188323
------------------------------------------------------------------------
Major MeSH Headings
Lyme Disease DI ; Respiratory Distress Syndrome, Adult ET
Minor MeSH Headings
Aged ; Antibodies, Bacterial AN ; Borrelia IM ; Case Report ; Female ;
Human ;
IgG AN ; IgM AN ; Lyme Disease CO ; Lyme Disease DT ; Penicillin G TU
;
Respiratory Distress Syndrome, Adult DT ; Respiratory Distress
Syndrome, Adult
PA ; Support, U.S. Gov't, P.H.S. ; Tetracycline TU
------------------------------------------------------------------------
Publication Type
JOURNAL ARTICLE
ISSN
0098-7484
Country of Publication
UNITED STATES
Entry Month
8807
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