Transcript Dr Farzin Khorvash
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Dr.Farzin khorvash
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Dr Farzin Khorvash
Dr.Farzin khorvash
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Dr.Farzin khorvash
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Enteric Host Defenses
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Host species, genotype, and age
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Personal hygiene
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Gastric acidity and other physical barriers
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Intestinal motility
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Enteric microflora
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Specific immunity
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Phagocytic
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Humoral
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Cell–mediated
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Nonspecific protective factors and human milk
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Intestinal receptors
Dr.Farzin khorvash
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MICROBIAL FACTORS
• Toxins
• Attachment
• Invasiveness
Dr.Farzin khorvash
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Gastrointestinal infections
•exception of Helicobacter pylori gastritis
• noninflammatory ; syndromes of diarrhea or
vomiting that tend to involve infection in the upper
small bowel
• inflammatory infection in the colon.
• Other enteric infections and infestations cause
predominantly systemic symptoms.
Dr.Farzin khorvash
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MECANISM
• (1) a shift in the delicate balance of
bidirectional water and electrolyte
fluxes in the upper small bowel by
intraluminal toxins or minimally invasive
organisms
• (2) inflammatory destruction of the ileal
or colonic mucosa
• (3) penetration through an intact
mucosa to the reticuloendothelial
system.
Dr.Farzin khorvash
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Infectious Doses of Enteric Pathogens
Shigella
10 to 102
Campylobacter jejuni
102 to 106
Salmonella
105
Escherichia coli
108
Vibrio cholerae
108
Giardia lamblia
10 to 102 cysts
Entamoeba histolytica
10 to 102 cysts
Cryptosporidium parvum
1 to 103 oocysts
Dr.Farzin khorvash
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ACUTE NONINFLAMMATORY DIARRHEA IN
ADULTS
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Rotaviruses
Norwalk-like viruses
adenoviruses
Coxsackieviruses
toxigenic Clostridium difficile
food poisoning such as Clostridium
perfringens, Bacillus cereus, or
Staphylococcus aureus
• cholera
• undercooked shellfish
• enterotoxigenic E. coli
Dr.Farzin khorvash
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ACUTE NAUSEA AND VOMITING (WINTER
VOMITING DISEASE)
• acute nausea and vomiting
• “intestinal flu,” or “viral gastroenteritis”
• commonly occurs in winter months in
temperate climates
Dr.Farzin khorvash
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• Norwalk-like viruses (including Norwalk or
Montgomery County agent and Hawaii, Snow
Mountain, and Taunton agents)
• caliciviruses
• astroviruses
• enteroviruses (especially echovirus types 11, 14, and
18)
• enteric adenoviruses
• human coronaviruses
• Pestiviruses
• toroviruses
• Picobirnaviruse
Dr.Farzin khorvash
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DIFFERENTIAL DIAGNOSIS OF ACUTE
NONINFLAMMATORY DIARRHEA
• osmotic diuresis nonabsorbable agents such as
sorbitol , Ipecac fluid
• Heavy metal poisoning (with As, Sn, Fe, Cd, Hg, Pb)
• non–b-islet cell tumors, medullary carcinoma of the
thyroid, carcinoid tumors, vasoactive intestinal
polypeptide
• thyrotoxicosis and adrenal or parathyroid
insufficiency
• lactase deficiency and pancreatic or biliary
insufficiency
• HUS with or without enterohemorrhagic E. coli
O157:H7
• dermatitis herpetiformis
Dr.Farzin khorvash
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CHRONIC NONINFLAMMATORY DIARRHEA
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Giardiasis
tropical spruelike syndromes
syndromes of bacterial “overgrowth,”
Cryptosporidium
I. belli infection
Dr.Farzin khorvash
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ACUTE DYSENTERY
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fecal blood and pus have
frequent, small bowel movements
blood and mucus
tenesmus
pain on defecation
an inflammatory invasion of the colonic
mucosa resulting from bacterial,
cytotoxic, or parasitic destruction.
Dr.Farzin khorvash
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Bacillary dysentery (Shigella dysenteriae, Shigella flexneri, Shigella
sonnei, Shigella boydii; invasive Escherichia coli)
Campylobacteriosis (Campylobacter jejuni)
Amebic dysentery (Entamoeba histolytica)
Ciliary dysentery (Balantidium coli)
Bilharzial dysentery (Schistosoma japonicum, Schistosoma mansoni)
Other parasitic infections (Trichinella spiralis)
Vibriosis (Vibrio parahaemolyticus)
Salmonellosis (Salmonella typhimurium)
Typhoid fever (Salmonella typhi)
Enteric fever (Salmonella choleraesuis, Salmonella paratyphi)
Yersiniosis (Yersinia enterocolitica)
Spirillar dysentery (Spirillum spp.)
Proctitis
Gonococcal (Neisseria gonorrhoeae)
Herpetic (herpes simplex virus)
Chlamydial (Chlamydia trachomatis)
Syphilitic (Treponema pallidum)
Other syndromes
Necrotizing enterocolitis of the newborn
Enteritis necroticans
Pseudomembranous enterocolitis (Clostridium difficile)
Diverticulitis
Typhlitis
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Syndromes without known infectious
etiology
• Idiopathic ulcerative colitis
• Crohn's disease
• Radiation enteritis
• Ischemic colitis
• Allergic enteritis
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Antibiotic-Associated Colitis
• Nearly 15% of hospitalized patients
receiving b-lactam antibiotics develop
diarrhea
• Clostridium difficile
• Staphylococcus aureus
• Candida
• Enterotoxigenic Clostridium perfringens
Dr.Farzin khorvash
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Dr.Farzin khorvash
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CLINICAL MANIFESTATIONS
• after 5 to 10 days of antibacterial treatment or as
late as 10 weeks after cessation of therapy
• may be brief and self-limited or cholera-like,
resulting in more than 20 stools per day
• fever (30 to 50% of patients),leukocytosis (50 to
60%) and abdominal pain or cramping (20 to 33%)
• Nausea, malaise, anorexia, hypoalbuminemia, occult
colonic bleeding, dehydration
• Infrequently, C. difficile colitis presents without
diarrhea as an acute abdominal syndrome or toxic
megacolon
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Dr.Farzin khorvash
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Autopsy the cecum of a patient with
pseudomembranous colitis.
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CHRONIC INFLAMMATORY PROCESSES
• Weight loss, fever, headache, and colicky
abdominal pain ,steatorrhea , malabsorption
• Enteropathogenic and Enteroaggregative
Escherichia coli
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Syphilis
Gastrointestinal Tuberculosis
Gastrointestinal Mycosis
Parasitic Enteritis
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Slide 23
Parasitic Enteritis
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coccidiosis
Isospora belli
Cryptosporidium
Cyclospora
G. lamblia
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differential diagnosis of chronic
inflammatory diarrhea
• Idiopathic inflammatory bowel disease
including regional enteritis, granulomatous
colitis, and ulcerative colitis
• Sarcoidosis
• lymphoma
• Carcinoma
• Radiation enterocolitis
• ischemic colitis
• diverticulitis
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Abdominal Symptoms with Fever
• (1) Enteric fever : fever, headache, abdominal pain,
splenomegaly, bacteremia, and occasionally skin
rash, is by several bacteria. A number of systemic
bacterial, rickettsial, viral, fungal, and parasitic
infections, such as malaria, may mimic enteric fever
• (2) Mesenteric adenitis, a syndrome that may mimic
acute appendicitis, can be caused by several bacteria
• (3) Eosinophilia:abdominal cramps or diarrhea often
accompanied by fever, parasites, usually helminths,
several diseases of unknown cause, and neoplasms.
Dr.Farzin khorvash
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Dr.Farzin khorvash
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Dr.Farzin khorvash
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MESENTERIC ADENITIS
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fever
right lower quadrant pain
vomiting
diarrhea
rebound tenderness
Rectal tenderness
Leukocytosis , polymorphonuclear leukocytes
Sonographic, radiographic contrast studies or CT
examination
• Stool cultures were positive in 56%
• Serologic confirmation
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MESENTERIC ADENITIS
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Y. enterocolitica
Y. pseudotuberculosis
nontyphoidal Salmonella spp
S. typhi infections
tuberculous mesenteric lymphadenitis
intestinal anthrax
Penicillium marneffei infection
hemolytic streptococci
Staphylococcus aureus
Bacteroides and Clostridium spp
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Differential Diagnosis
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Tuberculosis
nontyphoidal Salmonella infections
Salmonella typhi infections
Actinomycosis
Mycobacterium avium-intracellulare infection
P. marneffei infections
parvovirus B19
Epstein-Barr virus
Adenovirus infection
Angiostrongylus costaricensis
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chronic enteric inflammatory
• abdominal pain, weight loss, diarrhea,
or malabsorption
• gastrointestinal mycoses
• Mycobacterioses
• bacterial infections
• certain parasitic infections such as
coccidiosis.
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SYNDROME OF ABDOMINAL PAIN OR
DIARRHEA WITH EOSINOPHILIA
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NematodesStrongyloides stercoralis
Ascaris lumbricoides
small bowel)Visceral larva migrans (Toxocara canis, Toxocara cati
Trichinella spiralis
Anisakiasis
Capillaria philippinensis
Angiostrongylus costaricensis
TrematodesSchistosoma spp
Clonorchis sinensis
Opisthorchis spp
Metorchis conjunctus
Fasciola hepatica
Fasciolopsis buski
Heterophyes heterophes
Metagonimus yokogawi
Nanophyetus salmincola
CestodesEchinococcosis
ProtozoaIsospora belli
Dientamoeba fragilis
causeEosinophilic gastroenteritis
Polyarteritis nodosa and other forms of vasculitis
Inflammatory bowel disease
Malignancies
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Etiology of Traveler's Diarrhea
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Enterotoxigenic Escherichia coli
Shigella
Salmonella
Campylobacter jejuni
Vibrio parahaemolyticus
Rotavirus
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DIARRHEA IN PATIENTS WITH AIDS
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Cytomegalovirus
Cryptosporidium
Microsporidium
Entamoeba histolytica
Giardia lamblia
Salmonella spp.
Campylobacter spp.
Shigella spp.
Clostridium difficile toxin
Vibrio parahaemolyticus
Mycobacterium spp.
Isospora belli
Cyclospora
Blastocystis hominis
Candida albicans
Herpes simplex
Chlamydia trachomatis
Strongyloides
Intestinal spirochetes
Dr.Farzin khorvash
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simple examination
• fresh stool specimen is mixed with a drop of
methylene blue on a slide and examined for
the presence of fecal leukocytes
• In most cases, no leukocytes are noted. This
suggests a noninflammatory process in which
diarrhea usually arises from the upper small
bowel by the action of a true enterotoxin or
agents such as Giardia or viruses.
• The presence of numerous
polymorphonuclear leukocytes documents an
inflammatory or invasive process that usually
arises from the colon or distal small bowel.
Dr.Farzin khorvash
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Dr.Farzin khorvash
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• Of greatest importance in the treatment
of microbial diarrhea, regardless of the
cause or category, is fluid replacement
(ORT).
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degree of volume depletion
• examining the turgor of the skin and
mucous membranes
• by noting the amount of lacrimation
• by obtaining a history of urinary output
• changes in pulse and blood pressure
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• Electrolyte losses in severe watery
diarrhea are similar to the electrolyte
composition of serum, and fluid
replacement should contain
approximately these concentrations of
electrolytes
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standard ORT regimen
• contains 3.5 g NaCl, 2.5 g NaHCO3, 1.5 g
KCl, and 20 g glucose per liter of boiled water
• sodium 90, potassium 20, bicarbonate 30,
chloride 80, and glucose 110 mmol/liter
• A similar solution may be prepared with 3
level tablespoons of sugar, ¾ teaspoon salt,
½ teaspoon sodium bicarbonate in 1 cup of
orange juice to make up 1 liter (1.05 qt) in
water.
Dr.Farzin khorvash
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Therapy IV
Na+
Cl–
K+
HCO3–
Glucose
Intravenous solutions
Ringer's lactate
130
109
4
28*
0
Normal saline
154
154
0
0
0
90
80
20
30†
111
WHO ORS
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BRAT DIET
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Banana
Rice
Apple
Tosted bread
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ANTIMUTILITY AGENT
• Inflammatory infections: non use
• non Inflammatory infections:use
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THERAPY OF ACUTE DYSENTERY
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shigellosis : fluoroquinolones
Salmonella gastroenteritis :ciprofloxacin
C. jejuni :ciprofloxacin or azithromycin
E. histolytica :metronidazole is effective
in eradicating hepatic amebiasis and
may eradicate intestinal disease, the
iodoquinol
• Schistosomal: Praziquantel
Dr.Farzin khorvash
Slide 45
Therapy of Enteric Fever
• ampicillin, trimethoprimsulfamethoxazole, and chloramphenicol
• Fluoroquinolones, such as ciprofloxacin
or ofloxacin
• Third-generation cephalosporins, such
as ceftriaxone
• aztreonam
Dr.Farzin khorvash
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Therapy OF MESENTERIC ADENITIS
• self-limited
• Y. enterocolitica : trimethoprimsulfamethoxazole, second- and thirdgeneration cephalosporins, ciprofloxacin and
other fluoroquinolones, piperacillin,
imipenem, tetracycline, and chloramphenicol
• Yersinia pseudotuberculosis : tetracycline,
cephalosporins, aminoglycosides and
chloramphenicol
Dr.Farzin khorvash
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Treatment of Clostridium difficile–
Associated Diarrhea and Colitis
• 1. discontinue the offending antibiotic and/or
modify the regimen to include an agent less
commonly associated with C. difficile disease
• 2. Replace fluid and electrolyte losses
• 3. Avoid antiperistaltic agents
• 4. oral metronidazole, 250 mg qid for 10 days
• 5. Do treat asymptomatic patients colonized
with C. difficile
• 6. Retreat first–time recurrences with the
same regimen used to treat the initial episode
• 7. Avoid vancomycin use, if possible
Dr.Farzin khorvash
Slide 48
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Metronidazole 250 mg qid × 10 d
500 mg tid × 10 d
Vancomycina 500 mg tid × 10 d
500 mg qid × 10 d
125 mg qid × 7 d
125 mg qid × 5 d
Teicoplanin 400 mg bid × 10 d
100 mg bid × 10 d
Fusidic acid 500 mg tid × 10 d
Bacitracin 25,000 U qid × 10 d
Dr.Farzin khorvash
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SHIGELLOSIS
•acute infectious inflammatory colitis
•"bacillary dysentery,"
Dr.Farzin khorvash
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ETIOLOGIC AGENT
• small, gram-negative, nonmotile bacilli
• family Enterobacteriaceae
• (S. dysenteriae, S. flexneri, S. boydii,
and S. sonnei) on the basis of somatic
O antigens and carbohydrate
fermentation patterns.
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EPIDEMIOLOGY
• high rate of secondary household
transmission
• often symptomatic in children
• asymptomatic in adults
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PATHOGENESIS AND PATHOLOGY
• extensive ulceration of the epithelial
surface of the colonic mucosa
• exudate consisting of desquamated
colonic cells, PMNs, and erythrocytes
that may resemble a pseudomembrane
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CLINICAL MANIFESTATIONS
• is typically a pediatric ambulatory disease
• presenting as a self-limited nonbloody but
inflammatory watery diarrhea containing
many neutrophils.
• over the first 24 to 48 h, one-fourth
developed transient fever
• one-fourth had fever and self-limited watery
diarrhea
• the remaining one-fourth had fever and
watery diarrhea that progressed to bloody
diarrhea and dysentery
Dr.Farzin khorvash
Slide 54
• In young children in particular fever 40°
to 41°C
• sometimes resulting in generalized
seizures
Dr.Farzin khorvash
Slide 55
Severe dysentery
• due to S. dysenteriae type 1, occurs
less commonly with S. flexneri, and is
least likely with S. sonnei or S. boydii
• mild disease generally recover without
specific therapy in a few days to a week
• Severe shigellosis can progress to toxic
dilatation and colonic perforation
Dr.Farzin khorvash
Slide 56
Endoscopy
• shows the mucosa to be hemorrhagic,
with mucous discharge and focal
ulcerations
• sometimes an overlying exudate
resembling a pseudomembrane.
• The majority of lesions are in the distal
colon
Dr.Farzin khorvash
Slide 57
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Mild dehydration is common
severe dehydration is very rare
protein-losing enteropathy can occur
extraintestinal complications of
shigellosis arise in patients in
developing countries caused by S.
dysenteriae type 1 and S. flexneri and
to the poor nutritional state of the
hosts.
Dr.Farzin khorvash
Slide 58
HUS
• with S. dysenteriae type 1
• STEC strains (such as E. coli O157:H7)
• usually develop toward the end of the first week of
shigellosis, when dysentery is already resolving
• Oliguria and a marked drop in hematocrit (by as
much as 10% within 24 h) are the first signs
• may progress to anuria with renal failure and to
severe anemia with congestive heart failure
• Even with advanced therapy, 5 to 10% of patients
with HUS die of the acute illness.
Dr.Farzin khorvash
Slide 59
HUS
• Leukemoid reactions
• with leukocyte counts of <50,000/uL
• thrombocytopenia, with 30,000 to 100,000
platelets/uL, is common and in adults can
lead to TTP
• profound hyponatremia and severe
hypoglycemia
• may underlie central nervous system
abnormalities such as seizures and altered
consciousness.
Dr.Farzin khorvash
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Ikari syndrome
• S. flexneri is associated with a rare toxic
encephalopathy that is manifested by
bizarre posturing and lethal cerebral
edema
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Slide 61
Reactive arthritis
• with S. flexneri
• antigen HLA-B27
• the full triad of Reiter's syndrome
sometimes develops weeks to months
after diarrheal illness
• Pneumonia, meningitis, vaginitis (in
prepubertal girls), keratoconjunctivitis,
and "rose spot" rashes are rare events
Dr.Farzin khorvash
Slide 62
DIAGNOSIS AND LABORATORY
FINDINGS
• The specific :culture of Shigella from the stool
• PCR have been developed but are not yet
widely available
• enzyme immunoassay to detect Shiga-family
toxins in stool : S. dysenteriae type 1
• More than one differential selective medium
should be used for culture— i.e., MacConkey
and one other medium, such as Hektoen
enteric or xylose-lysine-deoxycholate.
Dr.Farzin khorvash
Slide 63
TREATMENT
• The mild to moderate dehydration in
shigellosis is readily corrected with oral
rehydration solutions
• Since S. sonnei infection is usually selflimited, culture results generally do not
become available until the patient is
better and there is little clinical need for
further therapy.
Dr.Farzin khorvash
Slide 64
• Trimethoprim-sulfamethoxazole 10/50
mg/kg bid × 3-5 d
• Ciprofloxacin 15 mg/kg q12h × 3-5 d;
500 mg max/dose 500 mg bid × 3 d
• Azithromycin 12 mg/kg on day 1 (max,
500 mg), 6 mg/kg on days 2-5
(max,250 mg/d) ,1 g (single dose)
• Cefiximeb 8 mg/kg (max, 400 mg) once
daily × 5 d ,400 mg/d × 5 d
Dr.Farzin khorvash
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HUS
• often requires dialysis
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Dr.Farzin khorvash
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Cholera
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VIBRIO
• 1. Aerobic, motile Gram negative rods
• 2.a profuse watery diarrhea that is
potentially fatal
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Dr.Farzin khorvash
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Vibrio cholerae
Microbiology: Gram stain
• Comma-shaped, curved Gram negative
rod
• Can’t differentiate from other
Gram negative rods
Dr.Farzin khorvash
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Dr.Farzin khorvash
Slide 72
LAB DIAGNOSIS
Organism can be seen in stool by direct microscopy
after gram stain and dark field illumination
Cholera can be cultured on special alkaline media
like triple sugar agar or TCBS agar.
Serologic tests are available to define strains, but this
is needed only during epidemics to trace the source of
infection.
Dr.Farzin khorvash
Slide 73
OTHER LAB FINDINGS
Dehydration leads to high blood urea & serum
creatinine. Hematocrit & WBC will also be high due to
hemoconcentration.
Dehydration & bicarbonate loss in stool leads to
metabolic acidosis with wide-anion gap.
Total body potassium is depleted, but serum level
may be normal due to effect of acidosis.
Dr.Farzin khorvash
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Dr.Farzin khorvash
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Dr.Farzin khorvash
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Dr.Farzin khorvash
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Dr.Farzin khorvash
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Dr.Farzin khorvash
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Dr.Farzin khorvash
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Cholera:
‘Rice water’ stool
Dr.Farzin khorvash
Slide 82
نقش مواد غذایی در انتقال ویبریوکلره:
استفاده از آب آلوده در پخت برنج
آب میوه رقیق شده با آب آلوده
شستشوی میوه و سبزی با آب آلوده
مواد غذایی دریایی (خرچنگ ،میگو و ماهی خام)
گوشت خوک پخته نشده
فرنی گندم
غذاهای خیابانی
شیر نارگیل فریز شده
Dr.Farzin khorvash
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Dr.Farzin khorvash
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Dr.Farzin khorvash
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CHOLERA
Clinical manifestation
&
Assessment of dehydration
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PATHOPHYSIOLOGY
• Non inflammatory
• Enterotoxin induced diarrhea
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Slide 87
PATHOPHYSIOLOGY
• Infective dose
Normal condition
Abnormal condition
• Enterotoxin structure
Component A
Component B
Dr.Farzin khorvash
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Dr.Farzin khorvash
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Dr.Farzin khorvash
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CLINICAL MANIFESTATION
• Depends on :
biotype
age
number of bacteria
status of immunity
blood group O ?
Dr.Farzin khorvash
Slide 91
CLINICAL MANIFESTATION
• Sub clinical
• Clinical :
profuse , watery diarrhea “rice water”
vomiting
leg cramps
convulsion,fever,hypoglycemia(children)
sometimes “cholera sica”
Dr.Farzin khorvash
Slide 92
LABORATORY FINDINGS
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Hemoconcentration
Leuckocytosis
Hyperglycemia
Hypocalemia
Increased protein , phosphate , lactate
Increased BUN , Cr
Metabolic acidosis
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Slide 93
CLINICAL MANIFESTATION
• Dehydration
some dehydration
severe dehydration
Dr.Farzin khorvash
Slide 94
CLINICAL MANIFESTATION
• Some dehydration
Restlessness and irritability
Sunken eyes
Dry mouth and tongue
Increased thirst
Skin goes back slowly when pinched
Dr.Farzin khorvash
Slide 95
CLINICAL MANIFESTATION
• Severe dehydration
Lethargy or unconsciousness
Very dry mouth and tongue
Skin goes back slowly when pinched
Weak or absent pulse
Low blood pressure
Dr.Farzin khorvash
Slide 96
ASSESSMENT OF DIARRHEA PATIENTS FOR DEHYDRATION
NO
DEHYDRATION
CONDITION
EYE
TEARS
MOUTH&TONGUE
THIRST
SKIN PINCH
SOME
DEHYDRATION
SEVER
DEHYDRATION
WELL,ALLERT
RESTLESS , IRRITABLE
LETHARGIC OR
UNCONSCIOUS,FLOPPY
NORMAL
SUNKEN
VERY SUNKEN AND
DRY
PRESENT
ABSENT
ABSENT
MOIST
DRY
VERY DRY
NOT THIRSTY
DRINK NORMALLY
THIRSTY
DRINK EAGERLY
DRINK POORLY OR
NOT ABLE TO DRINK
GOES BACK QUICKLY
GOES BACK SLOWLY
GOES BACK VERY
SLOWLY
Dr.Farzin khorvash
Slide 97
Dr.Farzin khorvash
Slide 98
Dr.Farzin khorvash
Slide 99
The goal of therapy
• to restore the fluid losses caused by diarrhea
and vomiting
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Slide 100
• treatment of patients without severe
dehydration is easy
• treatment of patients with severe
dehydration requires experience and
proper training.
Dr.Farzin khorvash
Slide 101
Basic training
• in how to recognize the degree of
dehydration
• how to select the proper intravenous
solution
• how rapidly to rehydrate the patient is
crucial
Dr.Farzin khorvash
Slide 102
• Guidelines to rehydrate cholera patients
have been written and reviewed
elsewhere
Dr.Farzin khorvash
Slide 103
intravenous route
• should be restricted to patients with
moderate dehydration who do not
tolerate the oral route
• those who purge more than 10 to 20
ml/kg/hour
• patients with severe dehydration.
Dr.Farzin khorvash
Slide 104
Rehydration
• should be accomplished in two phases
• rehydration phase
• maintenance phase
Dr.Farzin khorvash
Slide 105
The purpose of the rehydration phase
• is to restore normal hydration status
• it should last no more than 4 hours
Dr.Farzin khorvash
Slide 106
Intravenous fluids
• should be infused at a rate of 50 to 100
ml/kg/hour in severely dehydrated
patients.
• Ringer's lactate solution is the most
frequently recommended solution
Dr.Farzin khorvash
Slide 107
Electrolyte Concentration of Cholera Stools and Common Solutions Used for Treatment
Electrolyte and Glucose Concentration (mmol/L)
Cl–
Na+
HCO3–
K+
Glucose
Cholera stool
Adults
130
100
20
44
Children
100
90
33
30
Ringer's lactate
130
109
4
28*
0
Normal saline
154
154
0
0
0
WHO ORS
90
80
20
30†
111
Intravenous
solutions
*Ringer's lactate does not contain HCO –; it has lactate instead.
†Bicarbonate is replaced by trisodium citrate, which persists longer than bicarbonate in
sachets.
Abbreviation: WHO ORS, World Health Organization oral rehydration solution.
3
Dr.Farzin khorvash
Slide 108
• Normal saline solution is not
recommended because it does not
correct the metabolic acidosis.
Dr.Farzin khorvash
Slide 109
• When intravenous access proves
difficult
• nasogastric tubes
• or intraosseous catheters can be used
Dr.Farzin khorvash
Slide 110
finishing the rehydration
• all signs of dehydration should have
abated
• the patient should pass urine at a rate
of 0.5 ml/kg/hour or greater
• Then starts the maintenance phase.
Dr.Farzin khorvash
Slide 111
maintenance phase
• During this phase the objective is to
maintain normal hydration status by
replacing ongoing losses
• The oral route is preferred during this
phase
• use of oral rehydration solutions at a
rate of 500 to 1000 ml/hour is highly
recommended
Dr.Farzin khorvash
Slide 112
Oral rehydration therapy
• uses the principle of common
transportation of solutes, electrolytes,
and water by the intestine not affected
by the cholera toxin
• People with diarrhea can undergo
successful rehydration with simple
solutions containing glucose and
electrolytes that may be prepared at
home.
Dr.Farzin khorvash
Slide 113
Evaluation of rehydration status
• accurate recording of intake and output
volumes are essential
• Patients without severe dehydration
who tolerate the oral route can be
rehydrated with oral rehydration
solutions exclusively and discharged
promptly from the health center
Dr.Farzin khorvash
Slide 114
Discharge patients
• urine volume higher than 40
ml/hour
• diarrhea output below 400
ml/hour
• oral ingestion of rehydration
solutions between 600 and 800
ml/hour
Dr.Farzin khorvash
Slide 115
Case-fatality rate
• during epidemics may be reduced to
values below 1% even in disaster
situations, provided that adequate
access to health care centers and
proper management of patients can be
ensured
• Figures as high as 10% have been
reported in epidemic settings when
patients had no access to health care or
received improper treatment
Dr.Farzin khorvash
Slide 116
Antimicrobial agents
• play a secondary role in the treatment of
cholera
• patients with severe dehydration are given
antibiotics
• duration of diarrhea is decreased
• volume of stool is reduced by nearly half
• Early discharge and lessened hydration
decrease hospital expense
• These benefits are critical in epidemic
conditions.
Dr.Farzin khorvash
Slide 117
• Oral tetracycline and doxycycline are the
agents of choice in areas of the globe where
sensitive strains predominate
• A single dose of doxycycline (300 mg) is the
preferred regimen
• Tetracyclines are not safe in children younger
than 7 years
• alternatives such as trimethoprimsulfamethoxazole, erythromycin, and
furazolidone are preferred over tetracyclines
• Pregnant women can be treated with
erythromycin or furazolidone
Dr.Farzin khorvash
Slide 118
• In the last 2 decades the appearance of
strains resistant to tetracyclines and
other antimicrobial agents
• New agents :with quinolones being the
most effective
• Ciprofloxacin has been more
extensively studied than other
quinolones.
Dr.Farzin khorvash
Slide 119
• Two regimens of ciprofloxacin
• a single dose of 1 g
• once-daily regimens of 250 mg for 3
days.
Dr.Farzin khorvash
Slide 120
Therapy of Cholera
1.Evaluate the degree of dehydration on arrival
2.Rehydrate the patients in two phases:
Rehydration phase: lasts 2–4 h
Maintenance phase: lasts until diarrhea abates
3.Register output and intake volumes in predesigned charts and
periodically review the data
4.Use the intravenous route only for
Severely dehydrated patients during the rehydration phase, in whom an
infusion rate of 50–100 ml/kg/h is advised
Moderately dehydrated patients who do not tolerate the oral route High
stool purgers (>10 ml/kg/h) during the maintenance phase
5.Use ORS for patients during the maintenance phase at a rate of 800–
1000 ml/h, matching ongoing losses with ORS
6.Discharge patients to the treatment center if the following conditions
are fulfilled:
Oral tolerance, 1000 ml/h
Urine volume, 40 ml/h
Stool volume, 400 ml/h
Dr.Farzin khorvash
Slide 121
Dr.Farzin khorvash
Slide 122
Prevention
• V. Cholerae is spread through contaminated
food and water, therefore, prevention depends
upon the interruption of fecal-oral transmission
• Anti-biotic prophylaxis, vaccines and
surveillance of new cases are the answer to
preventing the spread of disease.
Dr.Farzin khorvash
Slide 123
Cholera is not transmissible personto-person, but can easily be spread
Dr.Farzin khorvash
through contaminated
food and water
Slide 124
Sari Cloth Filtration:
Preventative Measure
Using Sari cloth to filter
Water
Dr.Farzin khorvash
Slide 125
Vaccines
• Two types of cholera vaccines are
currently approved for use in humans.
– Killed-whole-cell formulation: killed
bacterial cells from both biovars of serovar 01
and purified B subunit of the cholera toxin.
Provides immunity to only 50% of adult victims
and to less than 25% of child victims.
– Live-attenuated vaccine, genetically
engineered
Provides >90% protection against classical biovar
and 65-80% agaisnt E1Tor biovar.
Dr.Farzin khorvash
Slide 126
Vaccines: Problems
• The live vaccine is associated with certain
problems:
• Side Effects:
• Cause mild diarrhea, abdominal cramping
and slight fever
• Possible virulence of live strain
• Upon infection of the vaccine strain by
cholera toxin
Dr.Farzin khorvash
Slide 127
Chemoprophylaxis of household
contacts
• published data do not support this concept
• More recently it has been shown that when
transmission of the disease is low, as occurs
in endemic areas, the utility of
chemoprophylaxis is not significant
• Prophylaxis with antibiotics might be
considered in situations in which the rate of
transmission of the disease is high, along
with other measures to curtail transmission
Dr.Farzin khorvash
Slide 128
Dr.Farzin khorvash
Dr.Farzin khorvash
Slide 2
Dr Farzin Khorvash
Dr.Farzin khorvash
Slide 3
Dr.Farzin khorvash
Slide 4
Enteric Host Defenses
•
Host species, genotype, and age
•
Personal hygiene
•
Gastric acidity and other physical barriers
•
Intestinal motility
•
Enteric microflora
•
Specific immunity
•
Phagocytic
•
Humoral
•
Cell–mediated
•
Nonspecific protective factors and human milk
•
Intestinal receptors
Dr.Farzin khorvash
Slide 5
MICROBIAL FACTORS
• Toxins
• Attachment
• Invasiveness
Dr.Farzin khorvash
Slide 6
Gastrointestinal infections
•exception of Helicobacter pylori gastritis
• noninflammatory ; syndromes of diarrhea or
vomiting that tend to involve infection in the upper
small bowel
• inflammatory infection in the colon.
• Other enteric infections and infestations cause
predominantly systemic symptoms.
Dr.Farzin khorvash
Slide 7
MECANISM
• (1) a shift in the delicate balance of
bidirectional water and electrolyte
fluxes in the upper small bowel by
intraluminal toxins or minimally invasive
organisms
• (2) inflammatory destruction of the ileal
or colonic mucosa
• (3) penetration through an intact
mucosa to the reticuloendothelial
system.
Dr.Farzin khorvash
Slide 8
Infectious Doses of Enteric Pathogens
Shigella
10 to 102
Campylobacter jejuni
102 to 106
Salmonella
105
Escherichia coli
108
Vibrio cholerae
108
Giardia lamblia
10 to 102 cysts
Entamoeba histolytica
10 to 102 cysts
Cryptosporidium parvum
1 to 103 oocysts
Dr.Farzin khorvash
Slide 9
ACUTE NONINFLAMMATORY DIARRHEA IN
ADULTS
•
•
•
•
•
•
Rotaviruses
Norwalk-like viruses
adenoviruses
Coxsackieviruses
toxigenic Clostridium difficile
food poisoning such as Clostridium
perfringens, Bacillus cereus, or
Staphylococcus aureus
• cholera
• undercooked shellfish
• enterotoxigenic E. coli
Dr.Farzin khorvash
Slide 10
ACUTE NAUSEA AND VOMITING (WINTER
VOMITING DISEASE)
• acute nausea and vomiting
• “intestinal flu,” or “viral gastroenteritis”
• commonly occurs in winter months in
temperate climates
Dr.Farzin khorvash
Slide 11
• Norwalk-like viruses (including Norwalk or
Montgomery County agent and Hawaii, Snow
Mountain, and Taunton agents)
• caliciviruses
• astroviruses
• enteroviruses (especially echovirus types 11, 14, and
18)
• enteric adenoviruses
• human coronaviruses
• Pestiviruses
• toroviruses
• Picobirnaviruse
Dr.Farzin khorvash
Slide 12
DIFFERENTIAL DIAGNOSIS OF ACUTE
NONINFLAMMATORY DIARRHEA
• osmotic diuresis nonabsorbable agents such as
sorbitol , Ipecac fluid
• Heavy metal poisoning (with As, Sn, Fe, Cd, Hg, Pb)
• non–b-islet cell tumors, medullary carcinoma of the
thyroid, carcinoid tumors, vasoactive intestinal
polypeptide
• thyrotoxicosis and adrenal or parathyroid
insufficiency
• lactase deficiency and pancreatic or biliary
insufficiency
• HUS with or without enterohemorrhagic E. coli
O157:H7
• dermatitis herpetiformis
Dr.Farzin khorvash
Slide 13
CHRONIC NONINFLAMMATORY DIARRHEA
•
•
•
•
•
Giardiasis
tropical spruelike syndromes
syndromes of bacterial “overgrowth,”
Cryptosporidium
I. belli infection
Dr.Farzin khorvash
Slide 14
ACUTE DYSENTERY
•
•
•
•
•
•
fecal blood and pus have
frequent, small bowel movements
blood and mucus
tenesmus
pain on defecation
an inflammatory invasion of the colonic
mucosa resulting from bacterial,
cytotoxic, or parasitic destruction.
Dr.Farzin khorvash
Slide 15
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Bacillary dysentery (Shigella dysenteriae, Shigella flexneri, Shigella
sonnei, Shigella boydii; invasive Escherichia coli)
Campylobacteriosis (Campylobacter jejuni)
Amebic dysentery (Entamoeba histolytica)
Ciliary dysentery (Balantidium coli)
Bilharzial dysentery (Schistosoma japonicum, Schistosoma mansoni)
Other parasitic infections (Trichinella spiralis)
Vibriosis (Vibrio parahaemolyticus)
Salmonellosis (Salmonella typhimurium)
Typhoid fever (Salmonella typhi)
Enteric fever (Salmonella choleraesuis, Salmonella paratyphi)
Yersiniosis (Yersinia enterocolitica)
Spirillar dysentery (Spirillum spp.)
Proctitis
Gonococcal (Neisseria gonorrhoeae)
Herpetic (herpes simplex virus)
Chlamydial (Chlamydia trachomatis)
Syphilitic (Treponema pallidum)
Other syndromes
Necrotizing enterocolitis of the newborn
Enteritis necroticans
Pseudomembranous enterocolitis (Clostridium difficile)
Diverticulitis
Typhlitis
Dr.Farzin khorvash
Slide 16
Syndromes without known infectious
etiology
• Idiopathic ulcerative colitis
• Crohn's disease
• Radiation enteritis
• Ischemic colitis
• Allergic enteritis
Dr.Farzin khorvash
Slide 17
Antibiotic-Associated Colitis
• Nearly 15% of hospitalized patients
receiving b-lactam antibiotics develop
diarrhea
• Clostridium difficile
• Staphylococcus aureus
• Candida
• Enterotoxigenic Clostridium perfringens
Dr.Farzin khorvash
Slide 18
Dr.Farzin khorvash
Slide 19
CLINICAL MANIFESTATIONS
• after 5 to 10 days of antibacterial treatment or as
late as 10 weeks after cessation of therapy
• may be brief and self-limited or cholera-like,
resulting in more than 20 stools per day
• fever (30 to 50% of patients),leukocytosis (50 to
60%) and abdominal pain or cramping (20 to 33%)
• Nausea, malaise, anorexia, hypoalbuminemia, occult
colonic bleeding, dehydration
• Infrequently, C. difficile colitis presents without
diarrhea as an acute abdominal syndrome or toxic
megacolon
Dr.Farzin khorvash
Slide 20
Dr.Farzin khorvash
Slide 21
Autopsy the cecum of a patient with
pseudomembranous colitis.
Dr.Farzin khorvash
Slide 22
CHRONIC INFLAMMATORY PROCESSES
• Weight loss, fever, headache, and colicky
abdominal pain ,steatorrhea , malabsorption
• Enteropathogenic and Enteroaggregative
Escherichia coli
•
•
•
•
•
Syphilis
Gastrointestinal Tuberculosis
Gastrointestinal Mycosis
Parasitic Enteritis
Dr.Farzin khorvash
Slide 23
Parasitic Enteritis
•
•
•
•
•
coccidiosis
Isospora belli
Cryptosporidium
Cyclospora
G. lamblia
Dr.Farzin khorvash
Slide 24
differential diagnosis of chronic
inflammatory diarrhea
• Idiopathic inflammatory bowel disease
including regional enteritis, granulomatous
colitis, and ulcerative colitis
• Sarcoidosis
• lymphoma
• Carcinoma
• Radiation enterocolitis
• ischemic colitis
• diverticulitis
Dr.Farzin khorvash
Slide 25
Abdominal Symptoms with Fever
• (1) Enteric fever : fever, headache, abdominal pain,
splenomegaly, bacteremia, and occasionally skin
rash, is by several bacteria. A number of systemic
bacterial, rickettsial, viral, fungal, and parasitic
infections, such as malaria, may mimic enteric fever
• (2) Mesenteric adenitis, a syndrome that may mimic
acute appendicitis, can be caused by several bacteria
• (3) Eosinophilia:abdominal cramps or diarrhea often
accompanied by fever, parasites, usually helminths,
several diseases of unknown cause, and neoplasms.
Dr.Farzin khorvash
Slide 26
Dr.Farzin khorvash
Slide 27
Dr.Farzin khorvash
Slide 28
MESENTERIC ADENITIS
•
•
•
•
•
•
•
•
fever
right lower quadrant pain
vomiting
diarrhea
rebound tenderness
Rectal tenderness
Leukocytosis , polymorphonuclear leukocytes
Sonographic, radiographic contrast studies or CT
examination
• Stool cultures were positive in 56%
• Serologic confirmation
Dr.Farzin khorvash
Slide 29
MESENTERIC ADENITIS
•
•
•
•
•
•
•
•
•
•
Y. enterocolitica
Y. pseudotuberculosis
nontyphoidal Salmonella spp
S. typhi infections
tuberculous mesenteric lymphadenitis
intestinal anthrax
Penicillium marneffei infection
hemolytic streptococci
Staphylococcus aureus
Bacteroides and Clostridium spp
Dr.Farzin khorvash
Slide 30
Differential Diagnosis
•
•
•
•
•
•
•
•
•
•
Tuberculosis
nontyphoidal Salmonella infections
Salmonella typhi infections
Actinomycosis
Mycobacterium avium-intracellulare infection
P. marneffei infections
parvovirus B19
Epstein-Barr virus
Adenovirus infection
Angiostrongylus costaricensis
Dr.Farzin khorvash
Slide 31
chronic enteric inflammatory
• abdominal pain, weight loss, diarrhea,
or malabsorption
• gastrointestinal mycoses
• Mycobacterioses
• bacterial infections
• certain parasitic infections such as
coccidiosis.
Dr.Farzin khorvash
Slide 32
SYNDROME OF ABDOMINAL PAIN OR
DIARRHEA WITH EOSINOPHILIA
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
NematodesStrongyloides stercoralis
Ascaris lumbricoides
small bowel)Visceral larva migrans (Toxocara canis, Toxocara cati
Trichinella spiralis
Anisakiasis
Capillaria philippinensis
Angiostrongylus costaricensis
TrematodesSchistosoma spp
Clonorchis sinensis
Opisthorchis spp
Metorchis conjunctus
Fasciola hepatica
Fasciolopsis buski
Heterophyes heterophes
Metagonimus yokogawi
Nanophyetus salmincola
CestodesEchinococcosis
ProtozoaIsospora belli
Dientamoeba fragilis
causeEosinophilic gastroenteritis
Polyarteritis nodosa and other forms of vasculitis
Inflammatory bowel disease
Malignancies
Dr.Farzin khorvash
Slide 33
Etiology of Traveler's Diarrhea
•
•
•
•
•
•
Enterotoxigenic Escherichia coli
Shigella
Salmonella
Campylobacter jejuni
Vibrio parahaemolyticus
Rotavirus
Dr.Farzin khorvash
Slide 34
DIARRHEA IN PATIENTS WITH AIDS
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
•
Cytomegalovirus
Cryptosporidium
Microsporidium
Entamoeba histolytica
Giardia lamblia
Salmonella spp.
Campylobacter spp.
Shigella spp.
Clostridium difficile toxin
Vibrio parahaemolyticus
Mycobacterium spp.
Isospora belli
Cyclospora
Blastocystis hominis
Candida albicans
Herpes simplex
Chlamydia trachomatis
Strongyloides
Intestinal spirochetes
Dr.Farzin khorvash
Slide 35
simple examination
• fresh stool specimen is mixed with a drop of
methylene blue on a slide and examined for
the presence of fecal leukocytes
• In most cases, no leukocytes are noted. This
suggests a noninflammatory process in which
diarrhea usually arises from the upper small
bowel by the action of a true enterotoxin or
agents such as Giardia or viruses.
• The presence of numerous
polymorphonuclear leukocytes documents an
inflammatory or invasive process that usually
arises from the colon or distal small bowel.
Dr.Farzin khorvash
Slide 36
Dr.Farzin khorvash
Slide 37
• Of greatest importance in the treatment
of microbial diarrhea, regardless of the
cause or category, is fluid replacement
(ORT).
Dr.Farzin khorvash
Slide 38
degree of volume depletion
• examining the turgor of the skin and
mucous membranes
• by noting the amount of lacrimation
• by obtaining a history of urinary output
• changes in pulse and blood pressure
Dr.Farzin khorvash
Slide 39
• Electrolyte losses in severe watery
diarrhea are similar to the electrolyte
composition of serum, and fluid
replacement should contain
approximately these concentrations of
electrolytes
Dr.Farzin khorvash
Slide 40
standard ORT regimen
• contains 3.5 g NaCl, 2.5 g NaHCO3, 1.5 g
KCl, and 20 g glucose per liter of boiled water
• sodium 90, potassium 20, bicarbonate 30,
chloride 80, and glucose 110 mmol/liter
• A similar solution may be prepared with 3
level tablespoons of sugar, ¾ teaspoon salt,
½ teaspoon sodium bicarbonate in 1 cup of
orange juice to make up 1 liter (1.05 qt) in
water.
Dr.Farzin khorvash
Slide 41
Therapy IV
Na+
Cl–
K+
HCO3–
Glucose
Intravenous solutions
Ringer's lactate
130
109
4
28*
0
Normal saline
154
154
0
0
0
90
80
20
30†
111
WHO ORS
Dr.Farzin khorvash
Slide 42
BRAT DIET
•
•
•
•
Banana
Rice
Apple
Tosted bread
Dr.Farzin khorvash
Slide 43
ANTIMUTILITY AGENT
• Inflammatory infections: non use
• non Inflammatory infections:use
Dr.Farzin khorvash
Slide 44
THERAPY OF ACUTE DYSENTERY
•
•
•
•
shigellosis : fluoroquinolones
Salmonella gastroenteritis :ciprofloxacin
C. jejuni :ciprofloxacin or azithromycin
E. histolytica :metronidazole is effective
in eradicating hepatic amebiasis and
may eradicate intestinal disease, the
iodoquinol
• Schistosomal: Praziquantel
Dr.Farzin khorvash
Slide 45
Therapy of Enteric Fever
• ampicillin, trimethoprimsulfamethoxazole, and chloramphenicol
• Fluoroquinolones, such as ciprofloxacin
or ofloxacin
• Third-generation cephalosporins, such
as ceftriaxone
• aztreonam
Dr.Farzin khorvash
Slide 46
Therapy OF MESENTERIC ADENITIS
• self-limited
• Y. enterocolitica : trimethoprimsulfamethoxazole, second- and thirdgeneration cephalosporins, ciprofloxacin and
other fluoroquinolones, piperacillin,
imipenem, tetracycline, and chloramphenicol
• Yersinia pseudotuberculosis : tetracycline,
cephalosporins, aminoglycosides and
chloramphenicol
Dr.Farzin khorvash
Slide 47
Treatment of Clostridium difficile–
Associated Diarrhea and Colitis
• 1. discontinue the offending antibiotic and/or
modify the regimen to include an agent less
commonly associated with C. difficile disease
• 2. Replace fluid and electrolyte losses
• 3. Avoid antiperistaltic agents
• 4. oral metronidazole, 250 mg qid for 10 days
• 5. Do treat asymptomatic patients colonized
with C. difficile
• 6. Retreat first–time recurrences with the
same regimen used to treat the initial episode
• 7. Avoid vancomycin use, if possible
Dr.Farzin khorvash
Slide 48
•
•
•
•
•
•
•
•
•
•
Metronidazole 250 mg qid × 10 d
500 mg tid × 10 d
Vancomycina 500 mg tid × 10 d
500 mg qid × 10 d
125 mg qid × 7 d
125 mg qid × 5 d
Teicoplanin 400 mg bid × 10 d
100 mg bid × 10 d
Fusidic acid 500 mg tid × 10 d
Bacitracin 25,000 U qid × 10 d
Dr.Farzin khorvash
Slide 49
SHIGELLOSIS
•acute infectious inflammatory colitis
•"bacillary dysentery,"
Dr.Farzin khorvash
Slide 50
ETIOLOGIC AGENT
• small, gram-negative, nonmotile bacilli
• family Enterobacteriaceae
• (S. dysenteriae, S. flexneri, S. boydii,
and S. sonnei) on the basis of somatic
O antigens and carbohydrate
fermentation patterns.
Dr.Farzin khorvash
Slide 51
EPIDEMIOLOGY
• high rate of secondary household
transmission
• often symptomatic in children
• asymptomatic in adults
Dr.Farzin khorvash
Slide 52
PATHOGENESIS AND PATHOLOGY
• extensive ulceration of the epithelial
surface of the colonic mucosa
• exudate consisting of desquamated
colonic cells, PMNs, and erythrocytes
that may resemble a pseudomembrane
Dr.Farzin khorvash
Slide 53
CLINICAL MANIFESTATIONS
• is typically a pediatric ambulatory disease
• presenting as a self-limited nonbloody but
inflammatory watery diarrhea containing
many neutrophils.
• over the first 24 to 48 h, one-fourth
developed transient fever
• one-fourth had fever and self-limited watery
diarrhea
• the remaining one-fourth had fever and
watery diarrhea that progressed to bloody
diarrhea and dysentery
Dr.Farzin khorvash
Slide 54
• In young children in particular fever 40°
to 41°C
• sometimes resulting in generalized
seizures
Dr.Farzin khorvash
Slide 55
Severe dysentery
• due to S. dysenteriae type 1, occurs
less commonly with S. flexneri, and is
least likely with S. sonnei or S. boydii
• mild disease generally recover without
specific therapy in a few days to a week
• Severe shigellosis can progress to toxic
dilatation and colonic perforation
Dr.Farzin khorvash
Slide 56
Endoscopy
• shows the mucosa to be hemorrhagic,
with mucous discharge and focal
ulcerations
• sometimes an overlying exudate
resembling a pseudomembrane.
• The majority of lesions are in the distal
colon
Dr.Farzin khorvash
Slide 57
•
•
•
•
Mild dehydration is common
severe dehydration is very rare
protein-losing enteropathy can occur
extraintestinal complications of
shigellosis arise in patients in
developing countries caused by S.
dysenteriae type 1 and S. flexneri and
to the poor nutritional state of the
hosts.
Dr.Farzin khorvash
Slide 58
HUS
• with S. dysenteriae type 1
• STEC strains (such as E. coli O157:H7)
• usually develop toward the end of the first week of
shigellosis, when dysentery is already resolving
• Oliguria and a marked drop in hematocrit (by as
much as 10% within 24 h) are the first signs
• may progress to anuria with renal failure and to
severe anemia with congestive heart failure
• Even with advanced therapy, 5 to 10% of patients
with HUS die of the acute illness.
Dr.Farzin khorvash
Slide 59
HUS
• Leukemoid reactions
• with leukocyte counts of <50,000/uL
• thrombocytopenia, with 30,000 to 100,000
platelets/uL, is common and in adults can
lead to TTP
• profound hyponatremia and severe
hypoglycemia
• may underlie central nervous system
abnormalities such as seizures and altered
consciousness.
Dr.Farzin khorvash
Slide 60
Ikari syndrome
• S. flexneri is associated with a rare toxic
encephalopathy that is manifested by
bizarre posturing and lethal cerebral
edema
Dr.Farzin khorvash
Slide 61
Reactive arthritis
• with S. flexneri
• antigen HLA-B27
• the full triad of Reiter's syndrome
sometimes develops weeks to months
after diarrheal illness
• Pneumonia, meningitis, vaginitis (in
prepubertal girls), keratoconjunctivitis,
and "rose spot" rashes are rare events
Dr.Farzin khorvash
Slide 62
DIAGNOSIS AND LABORATORY
FINDINGS
• The specific :culture of Shigella from the stool
• PCR have been developed but are not yet
widely available
• enzyme immunoassay to detect Shiga-family
toxins in stool : S. dysenteriae type 1
• More than one differential selective medium
should be used for culture— i.e., MacConkey
and one other medium, such as Hektoen
enteric or xylose-lysine-deoxycholate.
Dr.Farzin khorvash
Slide 63
TREATMENT
• The mild to moderate dehydration in
shigellosis is readily corrected with oral
rehydration solutions
• Since S. sonnei infection is usually selflimited, culture results generally do not
become available until the patient is
better and there is little clinical need for
further therapy.
Dr.Farzin khorvash
Slide 64
• Trimethoprim-sulfamethoxazole 10/50
mg/kg bid × 3-5 d
• Ciprofloxacin 15 mg/kg q12h × 3-5 d;
500 mg max/dose 500 mg bid × 3 d
• Azithromycin 12 mg/kg on day 1 (max,
500 mg), 6 mg/kg on days 2-5
(max,250 mg/d) ,1 g (single dose)
• Cefiximeb 8 mg/kg (max, 400 mg) once
daily × 5 d ,400 mg/d × 5 d
Dr.Farzin khorvash
Slide 65
HUS
• often requires dialysis
Dr.Farzin khorvash
Slide 66
Dr.Farzin khorvash
Slide 67
Cholera
Dr.Farzin khorvash
Slide 68
VIBRIO
• 1. Aerobic, motile Gram negative rods
• 2.a profuse watery diarrhea that is
potentially fatal
Dr.Farzin khorvash
Slide 69
Dr.Farzin khorvash
Slide 70
Vibrio cholerae
Microbiology: Gram stain
• Comma-shaped, curved Gram negative
rod
• Can’t differentiate from other
Gram negative rods
Dr.Farzin khorvash
Slide 71
Dr.Farzin khorvash
Slide 72
LAB DIAGNOSIS
Organism can be seen in stool by direct microscopy
after gram stain and dark field illumination
Cholera can be cultured on special alkaline media
like triple sugar agar or TCBS agar.
Serologic tests are available to define strains, but this
is needed only during epidemics to trace the source of
infection.
Dr.Farzin khorvash
Slide 73
OTHER LAB FINDINGS
Dehydration leads to high blood urea & serum
creatinine. Hematocrit & WBC will also be high due to
hemoconcentration.
Dehydration & bicarbonate loss in stool leads to
metabolic acidosis with wide-anion gap.
Total body potassium is depleted, but serum level
may be normal due to effect of acidosis.
Dr.Farzin khorvash
Slide 74
Dr.Farzin khorvash
Slide 75
Dr.Farzin khorvash
Slide 76
Dr.Farzin khorvash
Slide 77
Dr.Farzin khorvash
Slide 78
Dr.Farzin khorvash
Slide 79
Dr.Farzin khorvash
Slide 80
Dr.Farzin khorvash
Slide 81
Cholera:
‘Rice water’ stool
Dr.Farzin khorvash
Slide 82
نقش مواد غذایی در انتقال ویبریوکلره:
استفاده از آب آلوده در پخت برنج
آب میوه رقیق شده با آب آلوده
شستشوی میوه و سبزی با آب آلوده
مواد غذایی دریایی (خرچنگ ،میگو و ماهی خام)
گوشت خوک پخته نشده
فرنی گندم
غذاهای خیابانی
شیر نارگیل فریز شده
Dr.Farzin khorvash
Slide 83
Dr.Farzin khorvash
Slide 84
Dr.Farzin khorvash
Slide 85
CHOLERA
Clinical manifestation
&
Assessment of dehydration
Dr.Farzin khorvash
Slide 86
PATHOPHYSIOLOGY
• Non inflammatory
• Enterotoxin induced diarrhea
Dr.Farzin khorvash
Slide 87
PATHOPHYSIOLOGY
• Infective dose
Normal condition
Abnormal condition
• Enterotoxin structure
Component A
Component B
Dr.Farzin khorvash
Slide 88
Dr.Farzin khorvash
Slide 89
Dr.Farzin khorvash
Slide 90
CLINICAL MANIFESTATION
• Depends on :
biotype
age
number of bacteria
status of immunity
blood group O ?
Dr.Farzin khorvash
Slide 91
CLINICAL MANIFESTATION
• Sub clinical
• Clinical :
profuse , watery diarrhea “rice water”
vomiting
leg cramps
convulsion,fever,hypoglycemia(children)
sometimes “cholera sica”
Dr.Farzin khorvash
Slide 92
LABORATORY FINDINGS
•
•
•
•
•
•
•
Hemoconcentration
Leuckocytosis
Hyperglycemia
Hypocalemia
Increased protein , phosphate , lactate
Increased BUN , Cr
Metabolic acidosis
Dr.Farzin khorvash
Slide 93
CLINICAL MANIFESTATION
• Dehydration
some dehydration
severe dehydration
Dr.Farzin khorvash
Slide 94
CLINICAL MANIFESTATION
• Some dehydration
Restlessness and irritability
Sunken eyes
Dry mouth and tongue
Increased thirst
Skin goes back slowly when pinched
Dr.Farzin khorvash
Slide 95
CLINICAL MANIFESTATION
• Severe dehydration
Lethargy or unconsciousness
Very dry mouth and tongue
Skin goes back slowly when pinched
Weak or absent pulse
Low blood pressure
Dr.Farzin khorvash
Slide 96
ASSESSMENT OF DIARRHEA PATIENTS FOR DEHYDRATION
NO
DEHYDRATION
CONDITION
EYE
TEARS
MOUTH&TONGUE
THIRST
SKIN PINCH
SOME
DEHYDRATION
SEVER
DEHYDRATION
WELL,ALLERT
RESTLESS , IRRITABLE
LETHARGIC OR
UNCONSCIOUS,FLOPPY
NORMAL
SUNKEN
VERY SUNKEN AND
DRY
PRESENT
ABSENT
ABSENT
MOIST
DRY
VERY DRY
NOT THIRSTY
DRINK NORMALLY
THIRSTY
DRINK EAGERLY
DRINK POORLY OR
NOT ABLE TO DRINK
GOES BACK QUICKLY
GOES BACK SLOWLY
GOES BACK VERY
SLOWLY
Dr.Farzin khorvash
Slide 97
Dr.Farzin khorvash
Slide 98
Dr.Farzin khorvash
Slide 99
The goal of therapy
• to restore the fluid losses caused by diarrhea
and vomiting
Dr.Farzin khorvash
Slide 100
• treatment of patients without severe
dehydration is easy
• treatment of patients with severe
dehydration requires experience and
proper training.
Dr.Farzin khorvash
Slide 101
Basic training
• in how to recognize the degree of
dehydration
• how to select the proper intravenous
solution
• how rapidly to rehydrate the patient is
crucial
Dr.Farzin khorvash
Slide 102
• Guidelines to rehydrate cholera patients
have been written and reviewed
elsewhere
Dr.Farzin khorvash
Slide 103
intravenous route
• should be restricted to patients with
moderate dehydration who do not
tolerate the oral route
• those who purge more than 10 to 20
ml/kg/hour
• patients with severe dehydration.
Dr.Farzin khorvash
Slide 104
Rehydration
• should be accomplished in two phases
• rehydration phase
• maintenance phase
Dr.Farzin khorvash
Slide 105
The purpose of the rehydration phase
• is to restore normal hydration status
• it should last no more than 4 hours
Dr.Farzin khorvash
Slide 106
Intravenous fluids
• should be infused at a rate of 50 to 100
ml/kg/hour in severely dehydrated
patients.
• Ringer's lactate solution is the most
frequently recommended solution
Dr.Farzin khorvash
Slide 107
Electrolyte Concentration of Cholera Stools and Common Solutions Used for Treatment
Electrolyte and Glucose Concentration (mmol/L)
Cl–
Na+
HCO3–
K+
Glucose
Cholera stool
Adults
130
100
20
44
Children
100
90
33
30
Ringer's lactate
130
109
4
28*
0
Normal saline
154
154
0
0
0
WHO ORS
90
80
20
30†
111
Intravenous
solutions
*Ringer's lactate does not contain HCO –; it has lactate instead.
†Bicarbonate is replaced by trisodium citrate, which persists longer than bicarbonate in
sachets.
Abbreviation: WHO ORS, World Health Organization oral rehydration solution.
3
Dr.Farzin khorvash
Slide 108
• Normal saline solution is not
recommended because it does not
correct the metabolic acidosis.
Dr.Farzin khorvash
Slide 109
• When intravenous access proves
difficult
• nasogastric tubes
• or intraosseous catheters can be used
Dr.Farzin khorvash
Slide 110
finishing the rehydration
• all signs of dehydration should have
abated
• the patient should pass urine at a rate
of 0.5 ml/kg/hour or greater
• Then starts the maintenance phase.
Dr.Farzin khorvash
Slide 111
maintenance phase
• During this phase the objective is to
maintain normal hydration status by
replacing ongoing losses
• The oral route is preferred during this
phase
• use of oral rehydration solutions at a
rate of 500 to 1000 ml/hour is highly
recommended
Dr.Farzin khorvash
Slide 112
Oral rehydration therapy
• uses the principle of common
transportation of solutes, electrolytes,
and water by the intestine not affected
by the cholera toxin
• People with diarrhea can undergo
successful rehydration with simple
solutions containing glucose and
electrolytes that may be prepared at
home.
Dr.Farzin khorvash
Slide 113
Evaluation of rehydration status
• accurate recording of intake and output
volumes are essential
• Patients without severe dehydration
who tolerate the oral route can be
rehydrated with oral rehydration
solutions exclusively and discharged
promptly from the health center
Dr.Farzin khorvash
Slide 114
Discharge patients
• urine volume higher than 40
ml/hour
• diarrhea output below 400
ml/hour
• oral ingestion of rehydration
solutions between 600 and 800
ml/hour
Dr.Farzin khorvash
Slide 115
Case-fatality rate
• during epidemics may be reduced to
values below 1% even in disaster
situations, provided that adequate
access to health care centers and
proper management of patients can be
ensured
• Figures as high as 10% have been
reported in epidemic settings when
patients had no access to health care or
received improper treatment
Dr.Farzin khorvash
Slide 116
Antimicrobial agents
• play a secondary role in the treatment of
cholera
• patients with severe dehydration are given
antibiotics
• duration of diarrhea is decreased
• volume of stool is reduced by nearly half
• Early discharge and lessened hydration
decrease hospital expense
• These benefits are critical in epidemic
conditions.
Dr.Farzin khorvash
Slide 117
• Oral tetracycline and doxycycline are the
agents of choice in areas of the globe where
sensitive strains predominate
• A single dose of doxycycline (300 mg) is the
preferred regimen
• Tetracyclines are not safe in children younger
than 7 years
• alternatives such as trimethoprimsulfamethoxazole, erythromycin, and
furazolidone are preferred over tetracyclines
• Pregnant women can be treated with
erythromycin or furazolidone
Dr.Farzin khorvash
Slide 118
• In the last 2 decades the appearance of
strains resistant to tetracyclines and
other antimicrobial agents
• New agents :with quinolones being the
most effective
• Ciprofloxacin has been more
extensively studied than other
quinolones.
Dr.Farzin khorvash
Slide 119
• Two regimens of ciprofloxacin
• a single dose of 1 g
• once-daily regimens of 250 mg for 3
days.
Dr.Farzin khorvash
Slide 120
Therapy of Cholera
1.Evaluate the degree of dehydration on arrival
2.Rehydrate the patients in two phases:
Rehydration phase: lasts 2–4 h
Maintenance phase: lasts until diarrhea abates
3.Register output and intake volumes in predesigned charts and
periodically review the data
4.Use the intravenous route only for
Severely dehydrated patients during the rehydration phase, in whom an
infusion rate of 50–100 ml/kg/h is advised
Moderately dehydrated patients who do not tolerate the oral route High
stool purgers (>10 ml/kg/h) during the maintenance phase
5.Use ORS for patients during the maintenance phase at a rate of 800–
1000 ml/h, matching ongoing losses with ORS
6.Discharge patients to the treatment center if the following conditions
are fulfilled:
Oral tolerance, 1000 ml/h
Urine volume, 40 ml/h
Stool volume, 400 ml/h
Dr.Farzin khorvash
Slide 121
Dr.Farzin khorvash
Slide 122
Prevention
• V. Cholerae is spread through contaminated
food and water, therefore, prevention depends
upon the interruption of fecal-oral transmission
• Anti-biotic prophylaxis, vaccines and
surveillance of new cases are the answer to
preventing the spread of disease.
Dr.Farzin khorvash
Slide 123
Cholera is not transmissible personto-person, but can easily be spread
Dr.Farzin khorvash
through contaminated
food and water
Slide 124
Sari Cloth Filtration:
Preventative Measure
Using Sari cloth to filter
Water
Dr.Farzin khorvash
Slide 125
Vaccines
• Two types of cholera vaccines are
currently approved for use in humans.
– Killed-whole-cell formulation: killed
bacterial cells from both biovars of serovar 01
and purified B subunit of the cholera toxin.
Provides immunity to only 50% of adult victims
and to less than 25% of child victims.
– Live-attenuated vaccine, genetically
engineered
Provides >90% protection against classical biovar
and 65-80% agaisnt E1Tor biovar.
Dr.Farzin khorvash
Slide 126
Vaccines: Problems
• The live vaccine is associated with certain
problems:
• Side Effects:
• Cause mild diarrhea, abdominal cramping
and slight fever
• Possible virulence of live strain
• Upon infection of the vaccine strain by
cholera toxin
Dr.Farzin khorvash
Slide 127
Chemoprophylaxis of household
contacts
• published data do not support this concept
• More recently it has been shown that when
transmission of the disease is low, as occurs
in endemic areas, the utility of
chemoprophylaxis is not significant
• Prophylaxis with antibiotics might be
considered in situations in which the rate of
transmission of the disease is high, along
with other measures to curtail transmission
Dr.Farzin khorvash
Slide 128
Dr.Farzin khorvash