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 April
2008: VOLUME
1, NUMBER 10
Infectious
Diarrhea in Adults
In
this Issue...
Cases of infectious diarrhea,
especially from food and water-borne sources, are common in adults,
and particularly in travelers and immunocompromised individuals. In
this issue we focus on new data in 4 areas within this broad field,
reviewing: the pros and cons of a new medication (rifaximin) for the
treatment of travelers’ diarrhea, the domestic outbreak potential of
enterotoxigenic Escherichia coli (ETEC), post-infectious complications
of infectious diarrhea, and the etiologies of bacterial diarrhea in
HIV-infected populations. |
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Course
Directors
John
G. Bartlett, MD
Professor of Medicine
Department of Medicine
The Johns Hopkins
University
School of Medicine
Baltimore, MD
Paul
G. Auwaerter, MD
Associate Professor
of Medicine
Clinical Director
Division of Infectious
Diseases
The Johns Hopkins
University
School of Medicine
Baltimore, MD
Sara
E. Cosgrove, MD, MS
Assistant Professor
of Medicine
Division of Infectious
Diseases
Director
Antibiotic Management
Program
Associate Hospital
Epidemiologist
The Johns Hopkins
University
School of Medicine
Baltimore, MD |
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GUEST
AUTHOR OF THE MONTH |
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Commentary
& Reviews: |
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Beth
D Kirkpatrick, MD
Associate
Professor of Medicine
Unit
of Infectious Diseases
The University
of Vermont College of Medicine
Burlington,
VT |
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Guest
Faculty Disclosures
Beth
D Kirkpatrick, MD has disclosed that she serves as a principal
investigator for ACE Biosciences.
Unlabeled/Unapproved Uses
The author has indicated
that there will be no reference to unlabeled or unapproved uses of
drugs or products in the presentation.
Program
Directors' Disclosures |
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At
the conclusion of this activity, participants should be able to:
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Describe
to colleagues the indications and limitations of rifaximin use for
the prevention of travelers’ diarrhea |
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Identify
for colleagues which patients are at risk for post-infectious irritable
bowel syndrome after a gastrointestinal infection |
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Describe
to colleagues the most common enteric bacterial pathogens in persons
with HIV infection |
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COMPLETE
THE
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If you have participated in a
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Complete the post-test and course
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Print out your certificate.
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Approximately
211-375 million cases of infectious diarrhea occur in the United States
each year, resulting in 900,000 hospitalizations and 6000 deaths.1 Food-borne
diseases contribute significantly to these numbers, and are estimated
to cause 6-81 million illnesses annually, with 325,000 hospitalizations
and 5000 deaths.2 Our
understanding of the etiologies of community-acquired diarrhea is limited
to those causative agents which can be detected with available diagnostic
microbiologic cultures and assays, and may under-represent both the
overall incidence of diarrhea due to infectious agents as well as the
role of specific pathogens. Using the CDC’s FoodNet database, pathogens
currently identified as causing the most diarrhea include Salmonella, Campylobacter, Shigella, E.
coli 0157:H7 and Cryptosporidium.3 Etiologic
agents of diarrhea for which adequate diagnostic tests are not readily
available include all strains of pathogenic E. coli, the noroviruses,
and toxigenic strains of both Staphylococcus aureus and Clostridium
perfringens.1
Infectious diarrhea and gastroenteritis
caused by food and water contamination are an ongoing concern, particularly
with increasing rates of antibiotic resistance and the growing importation
of fresh fruits and vegetables. Recent outbreaks have implicated tomatoes
(Shigella flexneri), spinach (E. coli 0157:H7), and
delicatessen food (enterotoxigenic E. coli [ETEC]).4,5 Nevertheless,
the incidence of Campylobacter, E. coli 0157:H7, Salmonella,
and Yersinia infections have decreased substantially between
1996-2003 according to FoodNet surveillance data.3 Fluoroquinolone
use in poultry has now also been discontinued in the US, and should
decrease the food-borne transmission of quinolone-resistant strains
of enteric bacteria.6 Concurrently,
other transmission methods of enteric agents are becoming increasingly
recognized, including zoonotic routes (pets, petting zoos, farm animals,
wildlife), recreational water sources, and sexual transmission.
ETEC is a common cause of travelers’ diarrhea, but is not part of the
standard diagnostic workup for infectious diarrhea. As described in
the article by Beatty et al (reviewed herein), ETEC may also be an under-recognized
cause of large domestic outbreaks in the United States. This pathogen
is responsible for up to 30-40% of travelers’ diarrhea (TD) cases, although
rates vary by geographic region.7 A
new non-absorbable antibiotic (rifaximin) for the treatment of traveler’s
diarrhea is additionally reviewed below (Taylor et al).
Whether acquired domestically
or while traveling, post-infectious sequelae of food-borne diseases
and infectious diarrhea are an increasing area of interest. Reactive
arthritis, Guillain-Barre syndrome, and post-infectious irritable bowel
syndrome have occurred following infection with Salmonella, Shigella and Campylobacter.
Post-infectious irritable bowel disease (PI-IBS) has been described
since 1962, and it appears that this patient population differs from
the larger group of individuals who suffer IBS from other causes.8,9 The
risk of PI-IBS appears to have re-invigorated the debate over use of
prophylactic agents against traveler’s diarrhea, although PI-IBS has
less association with ETEC than with the "invasive" enteric bacteria,
and prompt treatment of infection remains a reasonable approach. The
meta-analysis of post-infectious bowel syndrome by Halvorson et al further
provides further insight.
Infectious diarrhea in immunocompromised
patients is associated with increased morbidity, and exhibits a more
diverse range of pathogens than in immunocompetent individuals. Recent
articles describe infectious causes of diarrhea in solid organ and stem
cell transplant patients.10,11 Bacterial
causes of infectious diarrhea in persons with HIV infection have been
evaluated by Sanchez and colleagues, reviewed herein.
Finally, exciting data on our
understanding of infectious diarrhea will likely emerge from a new
NIH-initiative to understand normal human flora "the microbiome," and
its effect on human immunity, metabolism and nutrition.12
References
| 1. |
Thielman
NM, Guerrant RL. Clinical practice. Acute
infectious diarrhea. N Engl J Med. 2004;350(1):38-47. |
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| 2. |
Mead
PS, Slutsker L, Dietz V, et al. Food-related
illness and death in the United States. Emerg Infect Dis. 1999;5(5):607-625. |
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| 3. |
CDC:
Preliminary FoodNet Data on the Incidence of Infection with Pathogens
Transmitted Commonly Through Food. MMWR Morb Mortal Wkly
Rep. 2006;(14):392-395. |
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| 4. |
Reller
ME, Nelson JM, Molbak K, et al. A
large, multiple-restaurant outbreak of infection with Shigella flexneri
serotype 2a traced to tomatoes. Clin Infect Dis. 2006;42(2):163-169. |
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| 5. |
Ongoing
multistate outbreak of Escherichia coli serotype O157:H7 infections
associated with consumption of fresh spinach—United States,
September 2006. MMWR Morb Mortal Wkly Rep. 2006;55(38):1045-1046. |
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| 6. |
Nelson
JM, Chiller TM, Powers JH, Angulo FJ. Fluoroquinolone-resistant
Campylobacter species and the withdrawal of fluoroquinolones from
use in poultry: a public health success story. Clin Infect
Dis. 2007;44(7):977-980. |
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| 7. |
Steffen
R. Epidemiology
of traveler's diarrhea. Clin Infect Dis. 2005;41 Suppl
8:S536-540. |
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| 8. |
Chaudhary
NA, Truelove SC. The
irritable colon syndrome. A study of the clinical features, predisposing
causes, and prognosis in 130 cases. Q J Med. 1962;31:307-322. |
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| 9. |
DuPont
AW. Postinfectious
irritable bowel syndrome. Clin Infect Dis. 2008;46(4):594-599. |
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| 10. |
Kamboj
M, Mihu CN, Sepkowitz K, Kernan NA, Papanicolaou GA. Work-up
for infectious diarrhea after allogeneic hematopoietic stem cell
transplantation: single specimen testing results in cost savings
without compromising diagnostic yield. Transpl Infect Dis. 2007;9(4):265-269 |
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| 11. |
Arslan
H, Inci EK, Azap OK, Karakayali H, Torgay A, Haberal M. Etiologic
agents of diarrhea in solid organ recipients. Transpl Infect
Dis. 2007;9(4):270-275. |
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| 12. |
Li
M, Wang B, Zhang M, et al. Symbiotic
gut microbes modulate human metabolic phenotypes. Proc Natl
Acad Sci U S A. 2008;105(6):2117-2122. |
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RIFAXIMIN
FOR THE TREATMENT OF TRAVELERS' DIARRHEA |
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Taylor
DN, Bourgeois AL, Ericsson CD, et al. A randomized, double-blind,
multicenter study of rifaximin compared with placebo and with
ciprofloxacin in the treatment of travelers' diarrhea. Am
J Trop Med Hyg. 2006;74(6):1060-6.
(For non-journal subscribers, an additional fee may apply
for full text articles.) |
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Taylor
et al. evaluated adult travelers to compare the efficacy of the non-absorbable
antibiotic rifaximin to ciprofloxacin for treating travelers’ diarrhea.
Subjects were enrolled from travel health clinics in Peru, Guatemala,
India, and Mexico. All subjects had acute diarrhea of less than 72
hours of duration, and were randomized in a 2:1:1 fashion to receive
rifaximin (200 mg orally, three times daily), ciprofloxacin (500
mg orally, twice daily with a placebo once daily), or placebo (three
times daily). All regimens were received for three days, and subjects
documented all symptoms, including fever, in a daily diary for five
days after dosing. Stool specimens for microbiologic analysis were
collected pre- and post-dosing. The primary study endpoint was time
to last unformed stool (TLUS), measured from the start of study medication.
Secondary endpoints included "clinical wellness," treatment failures,
and microbiologic eradication. Data was evaluated for all subjects,
as well as two subgroups. The first compared subjects with microbiologically
confirmed “non-invasive” pathogens (diarrheagenic E. coli,
ETEC, and enteroaggregative E. coli [EAEC]) to groups with
invasive pathogens (Salmonella, Shigella, Campylobacter)
or no defined pathogen. The second subgroup evaluated subjects with
no evidence of clinically invasive disease, defined as subjects without
fever or blood in the stool. Rifaximin minimal inhibitory concentrations
(MIC) were performed on microbiologic isolates obtained pre-and post-treatment
with rifaximin.
Three hundred ninety-nine
adult subjects were enrolled in the trial with similar baseline characteristics
in each group. The isolation rate of enteric pathogens was also similar
between centers (with the exception of Goa, India which had significantly
more Campylobacter infections). No pathogen could be isolated
in 36% of subjects. Overall, the primary endpoint of TLUS was significantly
shorter in the ciprofloxacin (28.8 hours) and rifaximin (32 hours)
groups (P values of 0.0003 and 0.0014, respectively) when compared
to the placebo group (TLUS, 65.5 hours). There was no significant
TLUS difference between the rifaximin and ciprofloxacin groups (P
=0.35); however, more subjects in the rifaximin group had treatment
failure (14.7%) than with ciprofloxacin (6.9%). Not surprisingly,
in subjects with microbiologically confirmed non-invasive E.
coli infections, the rifaximin and ciprofloxacin groups had
comparable TLUS and percentages reaching clinical wellness. Data
were similar for the subset of patients without fever or blood in
the stool. In contrast, ciprofloxacin was superior for subjects with
microbiologically-confirmed invasive pathogens. In this sub-analysis,
68% subjects receiving rifaximin reached "clinical wellness" with
a TLUS of 43.7 hours, compared to the ciprofloxacin group, where
85.7% achieved wellness, with a 24.4 hour TLUS. Overall microbiologic
eradication rates were 61.6% in the rifaximin group and 80.7% in
the ciprofloxacin group. MIC data demonstrated that for subjects
receiving rifaximin, 10 of 19 ETEC isolates recovered post-treatment
had a ≥4-fold increase in the MIC to rifaximin, particularly in
isolates with a relatively high baseline MIC of ≥4 µg/ml.
Clinical response rates in subjects with these isolates did not differ,
and adverse event rates between groups were similar.
This study demonstrates
that rifaximin is a well-tolerated and effective oral antibiotic
for the treatment of travelers’ diarrhea in subjects infected with
non-invasive pathogens (predominantly ETEC, EAEC) and for those in
which a pathogen cannot be identified but is assumed to be the cause
of diarrhea. The use of rifaximin in the prevention of travelers’ diarrhea
has also been recently published.1 The
benefits of this agent include its non-absorbable nature and the
potential ability to avoid fluoroquinolones for the treatment of
non-invasive pathogens (notably, 42% of the Campylobacter isolates
in this trial were shown to have MIC ≥0.25 µg/ml to ciprofloxacin,
reiterating that in some cases neither of these agents would be useful).
In anticipation of concerns about rifaximin-induced resistance, the
authors carefully point out that the clinical response rates of persons
with non-invasive travelers’ diarrhea taking rifaximin were similar
regardless of MIC increases; however ETEC isolates with higher pre-treatment
MICs were also more likely to persist post-therapy. The long term
effect of rifaximin use on antimicrobial resistance remains to be
seen, and the acceptance of this agent by travelers’ health clinics
will be interesting to follow.
References
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POST-INFECTIOUS
IRRITABLE BOWEL SYNDROME |
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Halvorson
HA, Schlett CD, Riddle MS. Postinfectious irritable bowel
syndrome—a meta-analysis. Am J Gastroenterol. 2006;101(8):1894-1899.
(For non-journal subscribers, an additional fee may apply for
full text articles.) |
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This
meta-analysis by Halverson and colleagues was performed to better estimate
the risk for post-infectious irritable bowel syndrome (PI-IBS) following
episodes of acute gastroenteritis/diarrhea. Published studies evaluating
persons with IBS after an acute intestinal illness were included in
the meta-analysis if they met predetermined inclusion and exclusion
criteria using standardized grading criteria and data abstraction. Subgroup
analysis evaluated self-reported vs laboratory-confirmed infectious
diarrhea.
One hundred-eighty-eight articles
were evaluated and 8 studies involving adults, all published from 1999
through 2005, were chosen for the meta-analysis. Individual study sizes
ranged from 97 to 584,626 subjects, and 6 of the 8 trials were cohort
studies. In these studies, 42% of the overall population was male. Two
studies were outbreak investigations (one Shigella, one Salmonella)
and 2 others involved travelers. All studies demonstrated an increased
risk (odds ratio greater than one), and 6 of the 8 studies had a significant
positive association of IBS following gastrointestinal infection. The
median prevalence of IBS in these patients was 9.8%, compared to 1.2%
in the control group (p=0.01). The summary odds ratio by the Mantel-Haenszel
model was 7.3 without significant heterogeneity. Laboratory-confirmed
gastrointestinal infection had twice the odds of PI-IBS with a pooled
odds ratio (OR) estimate of 10.9 (95% CI 6.7-17.1) vs 5.3 (95% CI 3.0-9.3)
in those without microbiologically confirmed infection. Interestingly,
male subjects were more likely to develop PI-IBS.
The link between infectious diarrhea/gastroenteritis
and PI-IBS has received significant attention, and the association is
slowly coming into better focus. This study reiterates the presence
of PI-IBS as a distinct entity, rather than a subset of IBS. As shown
in this work and that of others, subjects with PI-IBS differ from the
general population of IBS patients. Specifically, PI-IBS appears to
affect both genders equally, and is less likely to involve pre-existing
psychiatric issues.1 The
association between antecedent GI infection and PI-IBS appears to exist
in mixed populations, as well as travelers and those diagnosed as part
of an enteric disease outbreak. The increased odds ratio found in subjects
with laboratory-confirmed infections lends credence to the importance
of invasive bacterial pathogens in PI-IBS. Additionally, other studies
have suggested that protracted duration (>14 days) of initial illness
(as a measure of severity) is a critical element in the development
of PI-IBS.2 Further
work is needed to better understand the pathophysiology of PI-IBS as
well as the role of specific pathogens. Until then, Halverson’s report
refocuses our attention on providing rapid and effective treatment of
infectious diarrhea due to invasive enteric bacteria.
References
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ENTEROTOXIGENIC E.
COLI AS A CAUSE OF LARGE FOOD-BORNE OUTBREAKS IN THE UNITED STATES |
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Beatty
ME, Adcock PM, Smith SW, et al. Epidemic diarrhea due to
enterotoxigenic Escherichia coli. Clin Infect Dis. 2006;
42(3):329-34.
(For non-journal subscribers, an additional fee may apply for
full text articles.) |
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Beatty
et al., investigating a large outbreak of acute diarrhea in Wisconsin,
performed an embedded cohort study to determine the epidemiologic risk
factors for gastrointestinal illness. The epidemic occurred in 1998
after complaints of acute gastroenteritis following events catered by
a single delicatessen. A case was defined as an individual with diarrhea
or abdominal pain after consumption of food provided by the delicatessen.
Information on patients presenting with gastroenteritis was obtained
from health departments and emergency rooms. A convenience sample of
ill persons was interviewed, which included a food questionnaire. The
cohort study evaluated persons who attended the largest events during
the suspected time of transmission. Laboratory assessment of stool specimens
were performed and included expanded bacterial cultures as well as polymerase
chain reaction (PCR) to identify the heat-labile (LT) and heat-stabile
(ST) toxins of ETEC, and serotyping for the O and H antigens. Food specimens
and environmental cultures were also performed. Serologic responses
to the E. coli O6 LPS (IgM, IgG) were measured and compared
to controls. Univariate and multivariate analyses were performed, as
well as manual stepwise logistical regression for exposure identification.
ETEC infection was linked to
a single delicatessen which catered 539 events to 16,691 people over
a 3-day time period. 405 events had guests that become ill. The cohort
study determined that the median prevalence of illness among guests
was 20%, with 3338 persons estimated to have met the case definition.
Illness was characterized by a median incubation period of 50 hours
and a median duration of diarrhea of 5 days. Foods common to all cohorts
included prepared mayonnaise-based salads and hand-cut fruit. The delicatessen
was found to have inadequate hand washing facilities as well as presumptively
inadequate plumbing and refrigeration. Stool specimens from ill persons
revealed LT and ST-producing ETEC, which was confirmed as an identical
strain by pulsed-field gel electrophoresis. Elevated anti-O6 titers
(>1:160) were found in 19 of 27 collected serum samples, but no elevated
titers were found in control serum. The source of contamination was
not determined.
This study represents one of
the largest food-borne disease outbreaks reported to date in the United
States. Based on an internal cohort study, the authors estimate that
over 3300 subjects became ill due to food-borne ETEC. Because the infective
dose of ETEC is large (>10^8 CFU),
food must be heavily contaminated to cause disease, and the epidemiologic
findings clearly linked this outbreak to a single delicatessen. The
outbreak occurred with the most common circulating strain of ETEC (serotype
0169), but a precise food source was not identified. The authors developed
an anti-06 ELISA to guide diagnostics for this outbreak; however ETEC-specific
diagnostics are not often part of the initial workup for food-borne
outbreaks.
Although ETEC is generally considered
the primary agent of travelers’ diarrhea, food-borne outbreaks of ETEC
in the United States have been reported. (The next largest outbreak
of ETEC caused 452 cases and was described in 1980.1)
This study reiterates that food-borne infectious diarrhea due to enterotoxigenic E.coli occurs
domestically as well as abroad, and that ETEC infection should be considered
if routine cultures are negative.
References
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CAUSES
OF BACTERIAL DIARRHEA IN INDIVIDUALS WITH HIV INFECTION |
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Sanchez
TH, Brooks JT, Sullivan PS, et al. Bacterial diarrhea in
persons with HIV infection, United States, 1992-2002. Clin
Infect Dis. 2005;41(11):1621-1627.
(For non-journal subscribers, an additional fee may apply for
full text articles.) |
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Sanchez
et al., analyzed the incidence and etiologies of diarrheal illnesses
caused by bacteria in a large cohort of HIV-infected individuals during
1992-2002. Data was extracted from the Adult/Adolescent Spectrum of
HIV Disease Project, a collaboration between the Centers for Disease
Control (CDC) and 11 state and local health departments. Clinical diagnosis,
microbiology, and CD4+ counts were abstracted. Diarrhea was only included
in the case definition if a bacterial etiology was microbiologically
confirmed. Specific methods of culture or diagnosis were not recorded,
and pathogenic E. coli were not captured. HIV-infected persons
were classified as "clinical AIDS" (previous diagnosis of any opportunistic
infection, regardless of CD4+ count), "immunologic AIDS" (no clinical
AIDS, but CD4+ count <200 cells/mL or CD4+ <14%) or "HIV infection
without AIDS" (all others). Changes in rates were examined using logistic
regression analysis.
Data for 44,778 persons was evaluated
and the subject characteristics (ethnicity, age, gender) reflected the
US HIV-infected population. Eleven thousand three hundred twenty episodes
of diarrhea were reported, with a mean annual incidence of bacterial
diarrhea of 7.2 cases per 1000 person-years. Of these, 1091 (9.6%) had
a confirmed bacterial origin. The most commonly identified pathogen
was Clostridium difficile, accounting for 54% of all cases,
followed by Shigella (14%), Campylobacter (13.8%),
and Salmonella (7.4%). In subjects with "clinical AIDS", rates
of infection with all bacterial pathogens were highest. For this group, C.
difficile had an incidence of 9.6 per 1000 person-years, and infections
from other bacteria 5.1 per 1000 person-years. Nevertheless, during
the study period (1992-2002) rates from bacterial causes of diarrhea
(not including C. difficile) fell significantly in all HIV-infected
persons, from a rate of 5.6 cases per 1000 person-years to 1.9 (OR 0.3).
Similarly, the overall rate of C. difficile-associated disease
(CDAD) fell, but the decline was only significant in the "clinical AIDS" population.
This report identifies trends
in the bacterial causes of diarrhea in HIV-infected persons and spans
the time period pre-and post- use of highly active antiretroviral therapy
(HAART). Reflective of the general success of HAART therapy, the overall
rate of these infections has fallen in the post-HAART era. Notably, C.
difficile constituted the largest percentage of the identified
cases of bacterial diarrhea throughout the entire period of study. Interestingly,
despite an overall increase in United States, rates of CDAD decreased
in persons with the most advanced disease ("clinical AIDS").1 Presumably
this group of patients had both less exposure to C. difficile due
to decreasing hospitalizations as well as reconstitutions due to HAART
that permitted a better immunologic defense against clinical disease. Shigella species
were the second most common pathogen. This contrasts with infections
in the non-HIV general population, in which Shigella are less
common than Salmonella and Campylobacter. Although
48% of the current study population were men who have sex with men (MSM),
75% of the Shigella cases occurred in MSM. These data reconfirm
that Shigella species are a sexually-transmitted pathogen in
HIV-infected MSM, as shown in recent outbreaks and case-control studies.2,3
References
| 1. |
Archibald
LK, Banerjee SN, Jarvis WR. Secular
trends in hospital-acquired Clostridium difficile disease in the
United States, 1987-2001. J Infect Dis. 2004;189(9):1585-1589. |
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| 2. |
Morgan
O, Crook P, Cheasty T, et al. Shigella
sonnei outbreak among homosexual men, London. Emerg Infect
Dis. 2006;12(9):1458-1460. |
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| 3. |
Aragon
TJ, Vugia DJ, Shallow S, et al. Case-control
study of shigellosis in San Francisco: the role of sexual transmission
and HIV infection. Clin Infect Dis. 2007;44(3):327-34. |
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At
the conclusion of this activity, participants should be able to:
|
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Describe
to colleagues the indications and limitations of rifaximin use
for the prevention of travelers’ diarrhea |
|
|
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Identify
for colleagues which patients are at risk for post-infectious
irritable bowel syndrome after a gastrointestinal infection |
|
|
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Describe
to colleagues the most common enteric bacterial pathogens in
persons with HIV infection |
|
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Office of Continuing Medical Education (CME) at The Johns Hopkins
University School of Medicine is committed to protect the privacy
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As
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The Program Directors reported the following:
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John
G. Bartlett, MD has disclosed that he has served on
the HIV Advisory Board for GlaxoSmithKline, Abbott, Bristol-Myers
Squibb, Pfizer and Tibotec. He is also on the Policy Board for
Johnson & Johnson. |
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Paul
G. Auwaerter, MD has disclosed that he has served as
a consultant for Novartis, Pfizer, Ortho-McNeil, Schering-Plough,
and Genzyme. He is on the Speakers' Bureau for Schering-Plough
and has also disclosed that he is a Stock Shareholder for Johnson &
Johnson. |
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Sara
E. Cosgrove, MD, MS has disclosed that she has received
grants or research support from Merck and served on the Advisory
Boards for Ortho-McNeil, Cadence Pharmaceuticals, and Theravance/Astellas. |
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