Lyme Disease and the digestive tract

Topics with information and discussion about published studies related to Lyme disease and other tick-borne diseases.
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Yvonne
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Re: Lyme Disease and the digestive tract

Post by Yvonne » Sun 20 Apr 2008 11:47

Am J Med. 1995 Apr 24;98(4A):63S-68S. Links

Muscle, reticuloendothelial, and late skin manifestations of Lyme disease.
Ilowite NT.
Division of Pediatric Rheumatology, Schneider Children's Hospital, Long Island Jewish Medical Center, New Hyde Park, New York 11040, USA.

In addition to classic organ system involvement, Lyme disease may be characterized by myositis, liver and spleen involvement, and atypical cutaneous manifestations. Myositis is characteristically localized near an involved joint or localized neuropathy. Nuclear imaging with gallium-67 may be useful for detection. Myositis responds to treatment with intravenous or oral antibiotics. Patients with erythema migrans have been observed to have liver function test abnormalities in the absence of symptomatic hepatitis. Splenomegaly has been noted infrequently in patients with Lyme disease. Chronic cutaneous manifestations of Lyme disease--including erythema migrans, acrodermatitis chronica atrophicans, and lymphadenosis benigna cutis--have been observed more frequently in Europe than in the United States. It appears that they are caused primarily by the Borrelia afzelii genomic group of Borrelia burgdorferi, which has been found exclusively in Europe.

PMID: 7726194
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Yvonne
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Re: Lyme Disease and the digestive tract

Post by Yvonne » Sun 20 Apr 2008 11:48

Klin Med (Mosk). 2000;78(4):36-40. Links

Clinical characteristics and risk factors of hepatic damage in lyme borrheliosis
[Article in Russian]


Bessonova EN, Lesniak OM, Podymova SD, Bazarnyĭ VV.
The study is based on the study of data on 33 patients with Lyme Borrelia infection in the presence of typical erythema migrans in whom elevated levels of serum bilirubin or transaminases were detected simultaneously with erythema or just shortly. The obligatory criterion was no history evidence of hepatitis and abnormal hepatic functional tests. Higher levels of serum aminotransferases were a major manifestation of Lyme hepatitis in the Sverdlovsk region. In 32 patients, ALT was increased, on the average, up to 176 U/l, and AST activity was up to 113 U/l within the first 2 weeks of the disease in the absence of clinical manifestations of hepatic and biliary diseases. There were changes in the levels of serum transaminases and bilirubin following 3- and 8-month antibiotic therapy. The presence of viruses A and C in moderate chronic hepatitis induced long-term increases in the activity of transaminases in 3 cases, as evidenced by histological studies of hepatic biopsy specimens.

PMID: 10833889
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Yvonne
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Re: Lyme Disease and the digestive tract

Post by Yvonne » Tue 20 May 2008 10:16

Liver Function in Early Lyme Disease

DISCUSSION

Elevations of liver function tests occurred in 40% of
our study population of patients with early-stage Lyme
disease. These elevations were mild, were usually not
associated with anorexia, nausea, or vomiting, gener
ally resolved or improved within 3 weeks of therapy
and were not related to duration of disease, borrelial
culture result, or ELISA antibody status. Patients with
early disseminated Lyme disease, however, were sig
nificantly more likely to have one or more liver function
abnormalities than patients with localized disease
Liver function abnormalities were most consistent with
mild hepatocellular injury
This is the first prospective report of sequential liver
function studies of patients with early Lyme disease
in whom other common causes for liver disease were
excluded. In addition, a large number (49 of 99 tested)
of patients were proved to have Lyme disease by use
of culture. This is also the first study of liver function
abnormalities in Lyme disease in which a local control
group was included for comparison
Although the control group was significantly younger
than patients, the small age differences between these
two groups is unlikely to have resulted in the observed
differences in liver function tests.14 The sex differences
between controls and patients would also not explain
the differences in liver function study abnormalities
between them, because sex (among nonpregnant
adults) is not a determinant of liver function test results
among adults
Our data may, if anything, overestimate the fre
quency of Lyme-associated liver disease because of the
inclusion of seven (6%) patients who had elevations in
creatine phosphokinase. Some of the abnormalities of
AST and ALT in these patients may represent myosi
tis,15 which also occurs in Lyme disease.16 If these pa
tients are not included, then 37% of patients had liver
function abnormalities. Moreover, among controls, 19%
had abnormal liver studies

http://www3.interscience.wiley.com/cgi- ... 1&SRETRY=0
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Re: Lyme Disease and the digestive tract

Post by Yvonne » Thu 17 Jul 2008 21:28

MMW Fortschr Med. 2008 Mar 27;150(13):38-40. Links

Mesangioproliferative IgA-nephritis in a patient with lyme borreliosis

[Article in German]


Zachäus M.
Facharzt für Innere Medizin und Gastroenterologie, Klinik für Innere Medizin II, Park-Krankenhaus Leipzig-Südost GmbH. markus.zachaeus@parkkrankenhaus-leipzig.de

PMID: 18522356
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Re: Lyme Disease and the digestive tract

Post by Yvonne » Thu 17 Jul 2008 21:30

Am J Clin Pathol. 1989 Jan;91(1):95-7. Links

Spirochetes in the spleen of a patient with chronic Lyme disease.

Cimmino MA, Azzolini A, Tobia F, Pesce CM.
Istituto Scientifico di Medicina Interna, Università di Genova, Italy.

A 54-year-old man had intermittent evening fever, arthralgia, transient erythematous macular eruption on the skin, and splenomegaly of two year's duration. Immunofluorescence tests for Borrelia burgdorferi serum antibodies had positive results, but G-penicillin treatment was ineffective. Splenectomy with lymph node biopsy was performed to rule out lymphoproliferative disorders. Borrelia-like spirochetes were identified histologically in the spleen; this finding was consistent with persistence of B. burgdorferi organisms in inner organs in chronic Lyme disease.

PMID: 2910019


Clin Infect Dis. 1992 Jul;15(1):180-1. Links

Vesicular rash, radicular pain, and splenomegaly in a patient with Lyme borreliosis.
Nelson JA, Nemcek AA Jr.
PMID: 1319756
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Yvonne
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Re: Lyme Disease and the digestive tract

Post by Yvonne » Sun 7 Dec 2008 14:56

https://secure.muhealth.org/~ed/student ... 4_1206.pdf

Gastrointestinal and Hepatic Manifestations of Tickborne Diseases in the United States

Signs and symptoms related to the gastrointestinal tract and liver may provide important clues for the diagnosis
of various tickborne diseases prevalent in different geographic areas of the United States. We review clinical
and laboratory features that may be helpful in detecting a tickborne infection. Physicians evaluating patients
who live in or travel to areas where tickborne diseases are endemic and who present with an acute febrile
illness and gastrointestinal manifestations should maintain a high index of suspicion for one of these disease
entities, particularly if the patient has received a tick bite. If detected early, many of these potentially serious
illnesses can be easily and effectively treated, thereby avoiding serious morbidity and even death.


LYME DISEASE

Gastrointestinal manifestations. Gastrointestinal
signs and symptoms are common in the early stages of
Lyme disease. In a study of 314 patients with early Lyme
disease, the predominant clinical findings included anorexia
(in 23% of patients), nausea (in 17%), vomiting
(in 10%), abdominal pain (in 8%), right upper-quadrant
tenderness (in 8%), hepatomegaly (in 5%), splenomegaly
(in 6%), and diarrhea (in 2%) [1]. Approximately
10% of the patients had symptoms that were
suggestive of hepatitis. Subclinical hepatitis occurred in
27% of patients during the early stages of disease, according
to one study [2]. Abnormal liver function test
(LFT) findings generally indicate mild hepatocellular
injury. Patients with early disseminated Lyme disease
are more likely to have abnormal LFT findings than are
patients with localized disease [3]. The results of 3 dif
ferent studies that evaluated abnormal LFT findings in patients
with Lyme disease are compared in table 2. However, elevations
in aspartate aminotransferase and alanine aminotransferase levels
may indicate Lyme disease–associated myositis in some patients
and may not be related to underlying hepatic injury.
The prognosis for patients with Lyme disease–associated hepatic
dysfunction is excellent with appropriate antimicrobial
treatment [3]. LFT elevations usually decrease or resolve within
3 weeks after starting treatment. Hepatitis has not been reported
as a late complication of the disease. In 1 case report, liver
function abnormalities occurred late in the course of Lyme
disease; however, recurrence of Lyme disease could not be distinguished
from relapse in that case [4].

Pathogenesis and histopathologic findings. The pathogenesis
of liver injury in patients with Lyme disease includes
an interplay of direct hepatic invasion by the spirochete and
immunologic responses. B. burgdorferi has been shown to penetrate
through vascular endothelial cells in vitro [5], and it is
this invasive capacity of the organism that is responsible for its
tissue colonization in vivo [6]. Cellular and humoral immunologic
mechanisms also contribute to the abnormal LFT findings
commonly observed in the early stages of Lyme disease.
Lyme disease can result in a variety of histologic abnormalities
in the liver—in particular, sinusoidal infiltration by a mixed
inflammatory infiltrate [4]. Kupffer cell hyperplasia, microvesicular
fat, and hepatocyte ballooning are less commonly observed
[7]. Spirochetes have been identified within hepatic sinusoids
and parenchyma [4, 7]. This is most common in early,
disseminated infection. Rarely, B. burgdorferi infection can result
in a granulomatous hepatitis, which suggests that Lyme
disease should be included in the differential diagnosis of febrile
granulomatous hepatitis



EHRLICHIOSIS

Gastrointestinal manifestations. Gastrointestinal manifestations
of ehrlichiosis are frequently nonspecific and include
nausea, vomiting, diarrhea, abdominal pain, and, occasionally,
jaundice; these manifestations usually occur early in the course
of illness, sometimes at the time of presentation. Although
gastrointestinal hemorrhage is uncommon, Wallace et al. [10]
have described 3 patients with gastrointestinal hemorrhage.
Death following gastrointestinal and pulmonary hemorrhage,
partly in relation to thrombocytopenia, has been reported
among elderly patients. In contrast, younger patients may have
mild or subclinical illness [11], although severe abdominal pain
was the presenting symptom of a 5-year-old girl with human
granulocytic ehrlichiosis [12]. Diarrhea occurs in up to 10%
of patients and may be the primary manifestation [13]. Therefore,
ehrlichiosis should be included in the differential diagnosis
of febrile diarrhea in patients in areas of endemicity, especially
in the presence of leukopenia, thrombocytopenia, or elevated
aminotransferase levels. Hepatic involvement occurs in 180%
of patients, usually resulting in mild, transient elevations of
aminotransferase levels [14]. Occasionally, elevations in transaminase
levels may be more marked and cholestasis and liver
failure may occur. However, these conditions generally resolve
with appropriate therapy [11]. Progressive hepatosplenomegaly
has been described in association with ehrlichiosis, with resolution
preceding and paralleling recovery with antibiotic therapy

Pathogenesis and histopathologic findings. Liver injury
occurs by proliferation of organisms within hepatocytes and by
stimulation of immunologic and nonspecific inflammatory
mechanisms. The types of histologic lesions in the liver vary from
focal hepatic necrosis to ring granulomas and cholestatic hepatitis
[14]. Usually, there is evidence of a mixed portal infiltrate and
sinusoidal lymphoid cellular infiltrate; foamy Kupffer cells and
apoptotic hepatocytes are less frequently seen [14, 16].
Conclusions. Ehrlichiosis should be considered in the differential
diagnosis of an acute febrile illness with gastrointestinal
symptoms, especially in the presence of cytopenia, hepatosplenomegaly,
elevated transaminase levels, and appropriate
history of travel or exposure. PCR may be a useful tool for
early diagnosis of Ehrlichia species. Progression to multiorgan
failure and death can be avoided with early clinical suspicion
and timely treatment with doxycycline.


RMSF

Gastrointestinal manifestations. Gastrointestinal manifestations,
as reported from 4 different case series, are listed in
table 3. These manifestations, which include nausea, vomiting,
diarrhea, and abdominal pain, are present more frequently than
rash during the first 2–3 days of illness. The classically described
tetrad of fever, headache, rash, and a history of tick bite is
rarely encountered at this stage of the illness. Thus, to reduce
the mortality rate associated with RMSF, these clinical manifestations
must achieve wider recognition [19]. The gastrointestinal
abnormalities associated with RMSF may lead to an
erroneous diagnosis of an acute abdomen, and they have resulted
in surgical intervention in cases in which appendicitis
and acute cholangitis were clinically suspected [21–23]. Diarrhea
occurs in up to one-third of patients and may be the
primary presenting symptom. Guaiac-positive stool samples
and vomitus suggest severe underlying intestinal vasculitis [18].
Massive hemorrhage of the upper gastrointestinal tract has occurred
in some patients [18]. Hepatic involvement usually results
in mild to moderate elevation of aminotransferase levels
and occasional jaundice. The latter is a predictor of mortality
and is likely the result of a combination of inflammatory bile
ductular obstruction and hemolysis [24]. Pancreatic rickettsial
infection and vasculitis occur frequently, although the parenchymal
injury may not be severe enough to qualify as pancreatitis

Pathogenesis and histopathologic findings.

Although vasculitis
with ischemic necrosis is a possible mechanism for gastrointestinal
injury, this does not occur frequently in other
organs. The most likely mechanism appears to be an effect on
the gastrointestinal tract nerves of humoral inflammatory reaction,
edema, and ischemia without infarction [25]. The main
pathologic lesion of RMSF is vasculitis in the stomach, small
and large intestines, and pancreas [19, 26]. Rickettsiae may
infect the endothelial lining, the liver sinusoids, and the portal
vasculature, but not hepatocytes, leading to a mild focal hepatitis
and periportal inflammation. In cases of fulminant RMSF,
actively growing rickettsiae can result in vast destruction of
hepatic vasculature, with or without significant vasculitis [27].
Conclusions. The diagnosis of RMSF is often delayed, usually
because of failure to consider diagnosis at the initial presentation. Mortality rates may be decreased by the administration
of empiric treatment within the first 5 days of the illness [28].
RMSF must be included in the differential diagnosis for febrile
patients who live in or have traveled to an area of endemicity
and who present with headache, nausea, vomiting, diarrhea, or
abdominal pain, particularly in spring or summer. Receipt of
a tick bite may not be recalled by the patient, and a rash may
not yet have appeared. Awareness of the possibility of hepatic
involvement in RMSF is essential. In febrile patients for whom
an exploratory laparotomy does not demonstrate the cause of
an acute abdomen, it may be worthwhile to search for a rickettsial
vasculitis. The finding of mononuclear-predominant vasculitis,
with or without thrombosis, should lead to consideration
of a diagnosis of RMSF


BABESIOSIS

Gastrointestinal manifestations. The initial gastrointestinal
manifestations are nonspecific complaints of nausea, vomiting,
anorexia, and abdominal pain. Hepatosplenomegaly may
be present, although it is less commonly seen in patients with
babesiosis than it is in patients with ehrlichiosis. Mild LFT
elevations are usually observed, although they may be normal
in subclinical infection [50]. The degree of indirect hyperbilirubinemia
is dependent on the extent of hemolysis. Initiation
of appropriate antimicrobial therapy, along with exchange
transfusion for patients with severe hemolysis, usually results
in resolution of the abnormal LFT findings. Bovine babesiosis,
caused by Babesia divergens and Babesia bovis, has been frequently
reported in Europe and occurs in asplenic patients. It
is a fulminant infection associated with multiorgan and hepatic
failure.



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Yvonne
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Re: Lyme Disease and the digestive tract

Post by Yvonne » Sat 7 Feb 2009 10:49

http://www.wjgnet.com/1007-9327/E-Journal/WJGv14i26.pdf
Hepatic involvement is common in Lyme disease caused

by Borrelia burgdorferi, and mild elevations of GGT and

aminotransferase are commonly observed especially in

patients with early stage disease[62,63].
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Yvonne
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Re: Lyme Disease and the digestive tract

Post by Yvonne » Sun 25 Oct 2009 12:45

Am J Gastroenterol. 1998 Jul;93(7):1179-80. Links

Intestinal pseudoobstruction in acute Lyme disease: a case report.

Chatila R, Kapadia CR.
Department of Medicine, Yale University School of Medicine, New Haven, Connecticut 06520-8019, USA.

We report here a case of acute Lyme disease in a 61-yr-old man who developed a facial nerve paralysis and a relentless intestinal pseudoobstruction 2 wk after the initial prodrome. Both the facial nerve paralysis and pseudoobstruction persisted for a month until the patient sought medical attention. Both lesions resolved only after treatment for Lyme disease was initiated. The temporal association of the pseudoobstruction with the somatic cranial neuropathy and the response of both to specific therapy for Lyme disease suggest that the former was likely the result of a reversible autonomic neuropathy or dysfunction.

PMID: 9672362

Intestinal pseudoobstruction = http://en.wikipedia.org/wiki/Intestinal ... bstruction
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Dr Googlittle
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Re: Lyme Disease and the digestive tract

Post by Dr Googlittle » Fri 9 Apr 2010 13:48

Practical Enterology, 2006 April Volume: XXX Issue: 4
“Bell’s Palsy of the Gut” and Other GI Manifestations of Lyme and Associated Diseases
V.T. Sherr

Bell’s palsy signifies paralysis of facial muscles related to inflammation of the associated seventh Cranial Nerve. Physicians may not realize that this syndrome is caused by the spirochetal agent of Lyme disease until proven otherwise. Whether it is a full or hemifacial paralysis, Bell’s palsy is cosmetically disfiguring when fully expressed. Sudden loss of normal facial expression terrifies patients who naturally fear they are having a stroke. When a smile is asked for, normal countenances warp into bizarre grimaces. The amount of tooth area exposed in this attempt to smile helps doctors evaluate the degree of paralysis and its change over time (Figure 1). In every case of Bell’s, doctors need to carefully investigate by history, physical, and laboratory work every shred of evidence that might suggest the presence of cryptic tertiary Lyme, a serious multisystem, gut and neuro-brain infection even though about half of fully diagnosed patients have no evidence whatsoever of having had a tick-bite. Gastrointestinal Lyme disease may cause gut paralysis and a wide range of diverse GI symptoms with the underlying etiology likewise missed by physicians. Borrelia burgdorferi, the microbial agent often behind unexplained GI symptoms—along with numerous other pathogens also contained in tick saliva—influences health and vitality of the gastrointestinal tract from oral cavity to anus. Disruptions caused by GI borreliosis (Lyme) may include, amongst many others, distortions of taste, failure of other neural functions that supply the entire GI tract—paralysis or partial paralysis of the tongue, gag reflex, esophagus, stomach and nearby organs, small and/or large intestines.

http://www.practicalgastro.com/pdf/Apri ... rticle.pdf
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Dr Googlittle
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Re: Lyme Disease and the digestive tract

Post by Dr Googlittle » Fri 9 Apr 2010 14:05

J. Spiro and Tick-borne Diseases, Vol. 9, Spring/Summer 2002
Borrelia burgdorferi persists in the gastrointestinal tract of children and adolecents with Lyme disease
M.D. Fried, D Pietrucha, G. Madigan and A. Bal.

This study documents the persistence of B burgdorferi DNA in the gastronintestinal tract of pediatric patients who have already been treated with antibiotics for Lyme disease. Ten consecutive patients between ages of 9 and 13 years presented with an erythema migrans (EM) rash, a positive western blot for Lyme disease, chronic abdominal pain, heartburn, or bright red blood in the stool. Endoscopy assessed the gastrointestinal (GI) mucosa for inflammation and biopsies were examined for B burgdorferi using a Dieterle stain and with polymerase chain reaction (PCR) to the outer surface protein A (Osp A) of B burgdorferi. As controls 10 consecutive patients with chronic abdominal pain were also tested by GI biopsies and PCR. B burgdorferi persisted in the GI tract in all 10 patients with Lyme disease as shown by Dieterle stain of biopsies and with PCR. None of the control subjects' biopsies were PCR positive for B bugdorferi. Chronic gastritis, chronic duodenitis, and chronic colitis were found in Lyme disease patients and associated with the detection of B burgdorferi DNA in the GI tract despite prior antibiotic treatments. We have concluded that the DNA of B burgdorferi persisted in patients with Lyme disease even after antibiotic treatments.

http://www.lymepa.org/03%20Persistence% ... 0tract.pdf
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DrG
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