Transcript 2014_eg ang diarrhea

Edyta Grąbczewska
Acute infectious diarrheal diseases
and bacterial food poisoning
Department of Infectious Diseases and Hepatology
Nicolaus Copernicus University
Ludwik Rydygier Collegium Medicum in Bydgoszcz
Etiological factors of infectious diarrhea
and food poisoning
Bacilli
Gram negative Bacilli
Salmonella
Campylobacter jejuni, coli
Yersinia entorocolitica,
pseudotuberculosis
Shigella
Vibrio cholerae
Escherichia coli
Gram positive Bacilli
Listeria monocytogenes
Other
Staphylococcus aureus
Aerobe
Bacillus anthracis
Bacillus cereus
Anaerobe
Clostridium perfringens A, C
Clostridium botulinum
Clostridium difficile
Virus
Rotavirus
Norwalk virus
Mechanisms causing acute diarrhea
Mechanism
Non-inflammatory
(enterotoxin)
Inflammatory
(invasion or cytotoxin)
Penetrating
Location
Proximal small bowel
Colon or distal small bowel
Distal small
bowel
Illiness
Watery diarrhea
Dysentery or inflammatory
diarrhea
Enteric fever
Stool
findings
No fecal leukocytes, mild
or no increased lactoferin
Fecal polymorphonuclear
lekocytes, substantial
increase fecal lactoferin
Fecal
mononuclear
lymphocytes
Examples
of patogens
involved
Vibrio cholerae,
enterotoxigenic E.coli,
enteroaggregative E.coli,
C. perfringens,B.cereus,
S.aureus, Rotavirus,
Norovirus, Adenovirus,
G.lamblia,
Cryptosporidium spp
Shigella spp, Salmonella
spp, Campylobacter jejuni,
enterohemorrhagic E.coli,
enteroinvasive E.coli,
Y.enterocolitica, L.
monocytogenes, C.difficile,
E.hystolitica,
S.thyphi,
Y.enterocolitica
Host defenses
The normal host can protect itself against disease
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normal flora: the large numbers of bacteria that normally inhabit
the intestine act as an important host defense by preventing
colonizaton by potential enteric pathogen
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gastric acid pH of the stomach is an important barrier to enteric
pathogen
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intestinal motility: normal peristalsis is the major mechanism for
clearence of bacteria from the proximal small intestine
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immunity: both cellular immune responses and antibody
production play importanat roles in protection from enteric
infections.
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genetic determinants
Host defense
Clinical symptoms
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stomach ache
nausea, vomiting, loose bowel movements
fever
shivery
sings of dehydration:
– mild dehydration: thirst, dry mouth, decreased axillary sweat,
decreasesd urine output, slight weight loss,
– moderate dehydration: orthostatic fall in blood pressure,
tenting of skin, sunken eyes
– severe dehydration: lethargy, obtundation, feeble pulse,
hypotension, shock
• disturbances of electrolytes and acid-base balance
• weakness
• myalgia and myasthenia
Infectious diarrhea - definition
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≥3 loose or liquid bowel movements per day
can be blood, pus or mucus in stool
Time of diarrhea
• acute diarrhea is an episode of diarrhea of <14 days in duration
• persistent diarrhea is an episode of diarrhea >14 days in duration
• chronic diarrhea is diarrhea that lasts for >28 days
Physical examination
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vital signs
- blood pressure, pulse, temperature, the number of breathes
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general assessment
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precise physical examination
- ultrasound scan of abdomen
- evaluation of peristalsis
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digital rectal examination
- blood, pus, mucus
Diagnostic approach
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many cases of noniflammatory diarrhea are selflimited or require
symptomatic treatment. There is no need to determine a specific
etiology
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routine culture should be done. All patients with fever, evidence of
inflammatory process, disease acquired outside the hospital
(Salmonella, Shigella, Campylobacter), epidemiological factors
Diagnostic approach
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evaluation of nosocomial diarrhea should initially focus on
C.difficile
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rapid enzyme immunoassys and latex agglutination test
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PCR test
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if the clinical presentation suggests the posibility of intestinal
amebiasis, stool should be examined by the rapid antigen detection
assay
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diagnose viral infection of digestive system
- enzyme immunoassays ELISA ( viral antigen) or by
techniques for detecting Viral RNA
Clinical algorithm for the approach to patients with
community-aquired infectious diarrheal diseases
and bacterial food poisoning
Diarrhea, Nausea, or Vomiting
Resolution
Yes
Symptomatic therapy
Oral rehydration therapy
No
Continued illiness
Obtain history: duration, fever appearence of stool,
frequency of bowel movement, abdominal pain,
vomiting, antibiotic use, travel, common source,
tenesmus
Obtain stool to be examined for WBC and parasites
Clinical algorithm for the approach to patients with
community-aquired infectious diarrhea and bacterial
food poisoning
Noninflammatory
No WBC
Inflammatory
WBC
Examine stool for
parasites
Continue symptomatic
therapy further evaluation
if no resolution
Culture for Shigella,
Salmonella, C.jejuni,
Consider C.difficile
Specific antiparasitic
therapy
Consider Emprical
antimicrobial therapy
Treatment - mainly symptomatic
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compensation of the water-electrolyte disorders, hydration,
analgesic medicines (Metamizolum natricum, Paracetamol)
relaxant medicines (No-Spa, Papaverine, Spasmophen)
medicines blocking diarrhea (Carbo medicinalis, Smecta,
Tanalbina)
loperamid must not be used!!!!
in cases of poisoning with enterotoxine do not inhibit vomiting
in cases of poisoning with Salmonella rods, antibiotics are not
administered when there are no complications (prolonging of the
period of discharge with excrements)
Treatment - antibiotic therapy
- in exeptional cases
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patients with immunity deficits,elderly patients
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in the typhoid form (symptoms of sepsis),
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administrative indications (professional contact with food,
with children)
- cephalosporin, quinolone, ampicillin, trimetoprimsulphamethoxazol
Clinical course: poisoning with Salmonella spp
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incubation period: 12 – 36 hours,
in the history: consumption of eggs (raw egg yolk with sugar…)
sudden onest
most often gets a form of acute gastroenteritis
stomachache
• intensive diarrhea - sometimes
with addition of mucus and blood
(particularly common in infections
with Salmonella enteritidis),
• nausea and vomiting seldom occur
Clinical course: Salmonella spp poisoning
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fever up to 38-40oC
chills
weakeness
headache
muscles pain
symptoms of dehydration:
feeling of dryness in the
mouth cavity, thirst, anuria
Clinical course: physical examination
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furred, dry tongue and mucosa,
live peristalsis,
decreased RR,
increased heart rate,
in cases of poisoning with S. enteritidis the symptoms suggesting
acute abdomen accompanied by peritoneal symptoms can occur
Clinical course
Dysenteric form:
• stronger stomachache, often similar to colic pain,
• visible admixture of fresh blood in the stool
Typhoid form:
• breaking the intestinal barrier
by Salmonella, high fever for
7-10 days, strong headaches,
ill-being (occasionally
enlarged spleen, slow
recovery)
Clinical course: Staphylococcal poisoning
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fever over 38ºC (occurs at the beginning of the illness and recedes
normally when vomiting stops),
diarrhea is not characteristic, occurs slightly later and lasts for a
short time,
• the symptoms of vascular
collapse may occur
(lowering of RR, paleness
of skin integument,
abnormal consciousness),
• the disease usually lasts
for several hours
Bacterial dysentery (Dysenteria bacterica)
- definition
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infectious and contagious disease,
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caused by various species of rods SHIGELLA,
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similar symptoms may be caused by:
• proteus vulgaris,
• escherichia coli
• pseudomonas aeruginosa
• some rods of Salmonella,
• in children - infections with some viruses,
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dysentery syndrome
Epidemiology
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worldwide occurrence,
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the highest level of incidence in the countries with warm climate,
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reservoir of the germ is a sick person or a carrier,
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infection through the alimentary way (fecal-oral),
it spreads directly (through the contact with the sick person) and
indirectly through food products infected with stools (vegetables,
fruit, milk), objects, rarely by contaminated by excrements water
or mechanically by flies
Differential diagnosis
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acute surgical diseases of the peritoneum („acute abdomen”)
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typhoid fever
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extrauterine pregnancy complications
abdominal form of the cardiac infarct
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mesenteric infarct
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exacerbation of chronic colitis
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diarrhea related to antibiotic use
Differential diagnosis
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bacterial enteritis (enterohaemorrhagic and enteroinvasive E.coli,
Campylobacter jejuni, Salmonella enteritidis, Clostridium difficile)
parasites – Entamoeba histolytica
ulcerative colitis , Leśniowski-Crohn’s disease
sigmoid and rectum tumour
colon diverticulitis
subacute poisoning with heavy metal salts
uraemia
haemorrhoidal nodules
appendicitis
Prevention
Avoid:
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not fresh products
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unproperly stored food
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food coming from uncertain sources
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raw eggs
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tap water, raw milk etc.
Botulism
Botulinum toxin – is the most toxic substance known
Etiology
1895 – van Ermengem – first isolation of bacterium
Clostridium botulinum – anaearobic gram-positive organisms
that form subterminal spores. The hardy spores can survive
enviromental condition and ordinary cooking procedure
Botulinum toxin – 7 types : A, B, C, D, E, F, G
C. botulinum = 1 type neurotoxin
Toxin serotypes A, B, E cause human disease
Botulinum toxin is active in the anaerobic condition and
temerature can be from 30ºC to 2ºC, but sensitive for high
temperature 100ºC about 10min
Mechanism
Inhibition of acetylocholine realease by any seven toxin serotypes
results in characteristc flaccid paralysis. Recovery follows sprouting
of new nerves terminals. Toxin binding is irreversible
Epidemiology
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Food-borne botulism is caused by consumption of food
contaminated with botulism toxin. All of the events caused by
homemade foods
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Wound botulism is caused by contamination of wounds with
C.botulinum spores. Exclusively it has occured in injection drug
useres.
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Infant botulism results from absorption of toxin produced in situ by
toxogenic Clostridia colonizing the intestine of children ≥ 1 year old
Colonization is believed to occur because the normal bowel flora is
not yet fully establish.
Clinical manifestations
The incubation period from ingestion of food containing botulinum
toxin to onset symptoms is usually 18 –36 h, can range from few
hours to several days.
Symptoms:
• Prodromal symptoms: weakness, nausea, vomiting, stomachache
 Inability to suck and swallow, dysarthria, weakend voice, ptosis,
floppy neck, flaccidity, respiratory compromised
 Constipation
 Retention of urine, anuria
Symetric cranial nerve palsies, symetric descending flaccid
paralysis that may progress to respiratory arrest and death.
 Extraocular muscle paralysis, diplopia, blurred vision, inability
to acomodate
 Facial paralysis, ptosis, strabismus
Clinical manifestations
Remember !
 No sensory disturbances
 No disorders of consciousness
 Temperature is normal except complications (infection of
urinary tract, aspiration pneumonia
Diagnosis and treatment
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Botulism in a symptomatic patient can be confirmed in the
laboratory by demonstration of toxin in clinical specimens
(serum, stool, sterile water or saline enema, gastric aspirates,
wound material
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The treatment for botulism are meticulous intensive care with
frequent monitoring of vital capacity and mechanical ventilation
if required and immidiate administration of botulinum antitoxin
(equine antitoxin).
Cholera – definition and etiology
Cholera is an acute diarrheal disease that can in a matter of hours, result in
profound rapidly progressive dehydration and death.
3mln cases of cholera occur yearly (of which only 200000 are reported to the
WHO, resulting in 100000 deaths annually (of which 5000 are reported to the
WHO
Cholera – definition and etiology
Bacteria of Vibrio kind,
Pathogenic for a human: V. cholerae, V. parahaemolyticus, V. mimicis,V.
fluvialis.
V. cholerae : serologic group 01 or 0139, there are groups with epidemic
potential To be reported to sanitary authorities Toxins: Enterotoxins,
neuraminidase, genes (ctxAB, zot, ace, cep)
Typical symptom: painless watery, intensive diarrhoea, epidemic spread
Epidemiology
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The disease takes epidemic or pandemic form, mainly in poor, developing
countries, in the tropical and subtropical climate in Asia, Africa and South
America
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The infection spreads through alimentary tract, the infectious dose must be
high – over a billion of bacterial cells . It is markedly reduced in
hypochlorhydriac person, in those using antacids, when gastric acidityis
bufffered by a meal
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Source of infection – water contaminated with human excrements (much less
frequently consumption of the infected dishes), germ reservoir – a sick person
or carrier,
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Mortality approx 1% (in extreme cases up to do 20%) when treated properly
and 50% without the treatment
Clinical course
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Incubation period 1-2 days
(in extreme cases - several hours), sudden onset of the disease, lack of fever,
vomiting,
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Intensifying rapidly diarrhoea – to a few or even over a dozen litres a day
(without rectal tenesmus and abdominal pains)
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The stool reminds of water after the rinsing of rice, “the rice-like stool” –
completely fluid, with scarce amount of mucus, colourless, grey, without
admixture of blood, with slightly sweet smell,
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Spasmodic muscle pains (electrolyte disorders – can lead to damaging or
necrosis of renal tubule)
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Thirst, dryness in the mouth cavity, hoarseness, sueaky voice (vox cholerica),
wrinkled skin, not flexible, Facies cholerica (hollowed eyes, sharpened face
features) In the more serious cases orientation disorders, coma, death,
Laboratory examinations:
Laboratory examinations:
high Ht,
RBC (normal or higher), in the smear test, shift towards the left,
higher urea and creatinine
(extrarenal uraemia)
diselectrolytemia
disorders of acid-base balance
Therapy
1. Symptomatic treatment: immediate compensation of water-electrolyte
disorders,
Administration of liquids orally ( WHOORS – recommended by WHO solution
for oral watering – NaCl, KCl, sodium citrate, glucose) and also intravenous
infusions
2. Casual treatment:
Supportive, not necessary,
Shortens diarrhea period, limits the period of liquids administration, necessity to
examine resistance of local strains against antibacterial medicines
Adults may choose: tetracycline, alternatively: doxycycline, ciprofloxacin,
erythromycin, children may choose: tetracycline, alternatively:
sulfamethoxazolum
Prevention
The most crucial – supply people with clean water, use of boiled water for
drinking purposes,
Protection against contamination of food resources,
Treating of asymptomatic carriers,
Vaccines from killed vibrio give very little protection, during epidemic they can
cause more harm than benefit (large general reaction, that may shorten the
incubation period and cause more serious course of illness if administered to an
infected person),
Certain hope for live vaccines, attenuated…
Clostridium difficile
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anaerobic, Gram-positive, spore-forming bacillus
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opportunistic patogen
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Clostridium difficile infection is a unique colonic disease that is
aquired associated with antimicrobial use and the consequent
disruption of the normal colonic flora
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the most commonly diagnosed diarrheal
illiness aquired in the hospital
Highly virulant strain of C.difficile NAP1/027
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epidemic organism is ability to produce 18-23 times higher level
of toxin production (toxin A and B)
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new toxin - binary toxin
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produce much more spores
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3-fold mortality rate than less virulant strains
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easier transmission
in 2001 type hiperviralent represented 0,23% of all isolates but
currently this type of bacteria represents 84% in Quebec
High-level resistance to all fluoroquinolone
Clinical manifestations of infection C.difficile
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MILD: Postantibiotic diarrhea
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MODERATE: Postantibiotic colitis
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SEVERE: Pseudomembranous enterocolitis
Pseudomembranous enterocolitis
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Enterocolitis with toxin-producing C. difficile
severe clinical manifestation
there are about 20-25% infection of C. difficile
characteristic clinical syndrome
endoscopic image of pseudomembranous colitis with yellow
pseudomembrances seen of the wall of the sigmoid colon.
Nosocomial infection C.difficille
Reservoirs of toxigenic C.difficile
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asymptomatic fecal carriage:
• neonates: first 6 months of live 15-75%
• healthy adults: 1-3% - healthcare workers: ≈ 20%
• hospitalized patients: 10-20%
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sick patients (C.difficile Infection)
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indirect infection
• Envionmental surfaces (medical equipment, electronic rectal
thermometers, floor, toilet + hands of hospital personnel)
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contaminated food
Risk of factors C.difficile
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advance age > 65 y
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diseases and procedures
• antibiotic use (cephalospoins, clindamycin and fluoroquinolones)
• inflammatory bowel diseases (C.ulcerosa; Ch.L.Crohna)
• chemotherapy/transplantation
• chronic kidney disease
• HIV
• blood-borne infection (sepsis, endocarditis)
• antiacid therapy : proton pump inhibitor (PPI)
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hospitalization or residence in nursing homes or rehbilitation
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contact with children ↓ 2 y.o
Clinical manifestation
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diarrhea
> 3 do >30 loose bowel movements with a characteristic odor
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abdominal pain, fever, dehydration, lethargy
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hypoalbuminemia, oedema (enteropathy)
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complications life-threatening:
• fulminant colitis
• ileus
• megacolon toxic
• perforatio
• SIRS (Systemic Inflammatory Response Syndrome)
Hallmarks of severe Clostridium difficile colitis
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age >70
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leucocytosis > 20 000/mL
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creatinine level >2mg%
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ileus
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enterocolitis in imagining CT
Diagnostic approach CDI
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clinical manifestation
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laboratory tests
• stool culture
• enzyme immunoassay for toxin A or B in stool
• enzyme immunoassay for C.difficile common antigen in stool
• PCR for C.difficile toxin A and B gene in stool
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colonoscopy or sigmoidoscopy
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CT abdomen
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USG abdomen (megacolon toxicum!)
Treatment of infection C.Difficile
guidelines IDSA/SHEA 2010
Clinical setting
Definition
Treatment
Mild to
moderate
WBC < 15000 lub Cr
≤1.5 X baseline value
metronidazol 500 mg q8h 10-14 days
Severe
WBC >15000 lub Cr
>1.5 baseline value
vancomycin 125 mg q6h 10-14 days
Severe /
complications
Shock/
hypotonia/ileus
vancomycin 500 mg q6 po + metronidazole
500mg i.v q8h and consider rectal instillation of
vancomycin 500mg in 100ml of normal saline as
retention enema q6-8h
First recurrence
Second
recurrence
Same as an initial epizode
Vancomycin in tapered + pulsed regimen Typical taper/plused; 125mg
qid; 10-14 days, bidx1week, then dailyx1 week, then q2-3d for 2-8 weeks
IDSA – Infectious Diseases Society of America
SHEA – The Society for Healthcare Epidemiology of America
Causes of reccurance
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antibiotic continuation
low level of albumin
bad general condition
IPP use
advanced age
operation
incontinence of stool
chronic ischemic bowel disease
Stool transplantation
New strategy of treatment CDAD