Transcript Syndrom of diarrhea

TASHKENT MEDICAL ACADEMY
Infectious and children infectious
diseases department
Theme: Early and Comparative
diagnosis of diseases with the
syndrome of diarrhea
Lecturer:
Definition
Bacillary dysentery is a type of dysentery caused by Shigellosis.
Bacillary dysentery is associated with species of bacteria from the
Enterobacteriaceae family. The term is usually restricted to Shigella
infections. Shigellosis is caused by one of several types of Shigella
bacteria. Three species are associated with bacillary dysentery :
Shigella sonnei, Shigella flexneri and Shigella dysenteriae. One study
in China indicated that Shigella flexneri was the most common
serotype. Salmonellosis caused by Salmonella enterica (serovar
Typhimurium) has also been described as a cause of bacillary
dysentery, though this definition is less common. It is sometimes listed
as an explicit differential diagnosis of bacillary dysentery, as opposed
to a cause. Bacillary dysentery should not be confused with diarrhea
caused by a bacterial infection. One characteristic of bacillary
dysentery is blood in stool which is the result of invasion of the
mucosa by the pathogen.
Synonyms
• Shigella
• Shigella infection
• Salmonella infection
Morphological Description of Biologic
Agent
• Shigella is a genus of gram-negative, non-spore forming rodshaped bacteria closely related to Escherichia Coli and
Salmonella. The causative agent of human shigellosis, Shigella
cause disease in primates, but not in other mammals. It is
only naturally found in humans and apes. During infection, it
typically causes dysentery.
Mode of Transmission
• Shigella infection is typically via ingestion
(fecal–oral contamination); depending on age
and condition of the host as few as ten
bacterial cells can be enough to cause an
infection.
Signs and Symptoms
• Most people who are infected with Shigella develop diarrhea,
fever, and abdominal cramps. Severity of the disease ranges
from mild to very severe diarrhea. Diarrhea is bloody 25-50
percent of the time and most often contains mucus. Rectal
spasms are common. The illness starts 12 hours to 6 days,
usually 1-2 days, after exposure. Dehydration is also a
common symptom of Shigella infection. Nausea or vomiting
may also be experienced. Muscle aches also occur. In some
cases, white blood cell count is lower than normal at the
onset.
Diagnostics/Lab Tests
• Your own observation of symptoms.
• Medical history and physical exam by
a doctor.
• Laboratory stool culture.
• Blood counts.
Period of Communicability
• Shigellosis is spread during the acute infection
and until the infectious agent is no longer
present in feces. This can last as long as four
weeks. Asymptomatic carriers have the ability
to transmit disease. The duration of carriage
may be reduced with the use of antibiotics.
Incubation Period
• The incubation period may range from 12 to
96 hours (one to three days).
Outcome of Disease
• Most shigella infections are mild and don't
require drastic treatment. However, in a
severe attack, excessive dehydration can be
fatal (especially in infants and young children)
if treatment is unsuccessful.
Treatment
• Fluids and electrolyte replacement if excessive fluid loss
through diarrhea or vomiting.
• Agents are not recommended as they may prolong the course
of disease.
• Treatment is recommended for most symptomatic patients.
Use of antibiotics will shorten the period of fecal excretion of
the infecting strain and will shorten the clinical course of
disease often to a few days.
• Antibiotics
- for adults and children, if the strain is susceptible, are
ciprofloxacin or
TMP/SMX or azithromycin.
• Antibiotic resistance frequently develops after treatment.
Control Measures
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Good personal hygiene
Toilet hygiene
Wash soiled clothing and bed linen
Handling food
While you are suffering from diarrhea you should not go
to work/school.
• Sanitation of food utensils
General Characteristics of Salmonella
 Coliform bacilli (enteric rods)
 Motile gram-negative facultative anaerobes
 Non-lactose fermenting
 Resistant to bile salts
 H2S producing
Classification and Taxonomy of
Salmonella (Confused)
Old: Serotyping
& biochemical assays used to
name individual species within genus
(e.g., Salmonella enteritidis, S. choleraesuis, S. typhi)
 Over 2400 O-serotypes (referred to as species)
(Kauffman-White antigenic schema)
 Bioserotyping (e.g., S. typhimurium)
DNA homology shows only two species
Salmonella enterica (six subspecies)
and S. bongori
New:
 Most pathogens in S. enterica ssp. enterica
Epidemiology
of Salmonella
Infection
Annual Reported Incidence
of Salmonella Infection
(excluding typhoid fever)
Clinical Syndromes of Salmonella
Salmonellosis = Generic term for disease
Clinical Syndromes
 Enteritis (acute gastroenteritis)
 Enteric fever (prototype is typhoid fever and
less severe paratyphoid fever)
 Septicemia (particularly S. choleraesuis, S. typhi,
and S. paratyphi)
 Asymptomatic carriage (gall bladder is the
reservoir for Salmonella typhi)
Epidemiology and Clinical Syndromes of
Salmonella (cont.)
Enteritis
 Most common form of salmonellosis with major
foodborne outbreaks and sporadic disease
 High infectious dose (108 CFU)
 Poultry, eggs, etc. are sources of infection
 6-48h incubation period
 Nausea, vomiting, nonbloody diarrhea, fever,
cramps, myalgia and headache common
 S. enteritidis bioserotypes (e.g., S. typhimurium)
Pathogenesis of Salmonella
Enteritis (cont.)
Virulence attributable to:
 Invasiveness
 Intracellular survival & multiplication
 Endotoxin
 Exotoxins: Effects in host have not been identified
 Several Salmonella serotypes produce enterotoxins
similar to both the heat-labile (LT) and heat-stable
enterotoxins (ST), but their effect has not been identified
 A distinct cytotoxin is also produced and may be involved
in invasion and cell destruction
Pathogenesis of Salmonella (cont.)
Invasiveness in Enteritis
(cont.)
 Penetrate mucus, adhere to and invade into
epithelial layer (enterocytes) of terminal small
intestine and further into subepithelial tissue
 Bacterial cells are internalized in endocytic vacuoles
(intracellular) and the organisms multiply
 PMN’s confine infection to gastrointestinal (GI) tract,
but organisms may spread hematogenously (through
blood, i.e., septicemia) to other body sites
 Inflammatory response mediates release of
prostaglandins, stimulating cAMP and active fluid
secretion with loose diarrheal stools; epithelial
destruction occurs during late stage of disease
Clinical
Progression of
Salmonella
Enteritis
Lamina propria = thin
membrane between
epithelium & basement layer
Hyperplasia = abnormal
increase in # of normal cells
Hypertrophy = abnormal
increase in normal
tissue/organ size
Prostaglandins = potent
mediators of diverse set of
physiologic processes
Epidemiology & Clinical Syndromes (cont.)
Enteric Fevers
 S. typhi causes typhoid fever
S. paratyphi A, B (S. schottmuelleri) and C
(S. hirschfeldii) cause milder form of enteric fever
 Infectious dose = 106 CFU
 Fecal-oral route of transmission
 Person-to-person spread by chronic carrier
 Fecally-contaminated food or water
 10-14 day incubation period
 Initially signs of sepsis/bacteremia with sustained
fever (delirium) for > one week before abdominal
pain and gastrointestinal symptoms
Pathogenesis of Salmonella (cont.) Enteric Fevers
(cont.)
Virulence attributable to:
 Invasiveness
 Pass through intestinal epithelial cells in ileocecal region, infect
the regional lymphatic system, invade the bloodstream, and infect
other parts of the reticuloendothelial system
 Organisms are phagocytosed by macrophages and monocytes,
but survive, multiply and are transported to the liver, spleen, and
bone marrow where they continue to replicate
 Second week: organisms reenter bloodstream and cause
prolonged bacteremia; biliary tree and other organs are infected;
gradually increasing sustained fever likely from endotoxemia
 Second to third week: bacteria colonize gallbladder, reinfect
intestinal tract with diarrheal symptoms and possible necrosis of
the Peyer’s patches
Clinical
Progression of
Enteric Fever
(Typhoid fever)
Lumen (intraluminal);
ileocecal area = see
above - Anatomy of
Digestive Tract
(RES)
Liver, spleen, bone marrow
(10-14 days)
RES = sum total of
strongly phagocytic
Gastrointestinal cells; primarily found in
lymph nodes, blood,
Symptoms
liver, spleen and bone
marrow
Hyperplastic changes =
see hyperplasia above
- Clinical Progression of
Enteritis
Microbial Defenses Against Host
Immunological Clearance
ENCAPSULATION and
ANTIGENIC MIMICRY, MASKING or SHIFT
CAPSULE, GLYCOCALYX or SLIME LAYER
Polysachharide capsules Streptococcus pneumoniae,
Neisseria meningitidis, Haemophilus influenzae, etc.
Polypeptide capsule of Bacillus anthracis
EVASION or INCAPACITATION of PHAGOCYTOSIS
and/or IMMUNE CLEARANCE
PHAGOCYTOSIS INHIBITORS: mechanisms enabling an
invading microorganism to resist being engulfed, ingested,
and or lysed by phagocytes/ phagolysosomes
RESISTANCE to HUMORAL FACTORS
RESISTANCE to CELLULAR FACTORS
See Chpt. 19
Methods That Circumvent
Phagocytic Killing
, Salmonella typhi
See Chpt. 19
Epidemiology & Clinical Syndromes (cont.)
Septicemia
 Can be caused by all species, but more
commonly associated with S. choleraesuis, S.
paratyphi, S. typhi, and S. dublin
 Old, young and immunocompromised (e.g.,
AIDS patients) at increased risk
Epidemiology & Clinical Syndromes (cont.)
Asymptomatic Carriage
 Chronic carriage in 1-5% of cases following S.
typhi or S. paratyphi infection
 Gall bladder usually the reservoir
 Chronic carriage with other Salmonella spp.
occurs in <<1% of cases and does not play a
role in human disease transmission
Treatment, Prevention and Control of
Salmonella Infections
Enteritis:
 Antibiotics not recommended for enteritis because
prolong duration
 Control by proper preparation of poultry & eggs
Enteric fever:
 Antibiotics to avoid carrier state
 Identify & treat carriers of S. typhi & S. paratyphi
 Vaccination can reduce risk of disease for
travellers in endemic areas
Botulism
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Organism
History
Epidemiology
Transmission
Disease in Humans
Disease in Animals
Prevention and Control
Organism
• Clostridium botulinum
– Gram positive
– Obligate anaerobic bacillus
– Spores
• Ubiquitous
• Resistant to heat, light, drying and radiation
• Specific conditions for germination
– Anaerobic conditions
– Warmth (10-50oC)
– Mild alkalinity
Neurotoxins
• Seven different types: A through G
– Different types affect different species
– All cause flaccid paralysis
– Only a few nanograms can cause illness
– Binds neuromuscular junctions
• Toxin: Destroyed by boiling
• Spores: Higher temperatures to be inactivated
Neurotoxins
Neurotoxin
A
B
Human
X
X
Horses
Cattle
Sheep
D
E
F
X
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Dogs
X
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Avian
X
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X
Mink & Ferret
X
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C
X
G
History
• 1793, Justinius Kerner
– “Wurstgift”
• “Botulus” = Latin for sausage
• 1895, Emile von Ermengem
– Isolated organism during Belgium outbreak
• U.S. outbreaks led to improved industry
processing
Transmission
• Ingestion
– Organism
– Spores
– Neurotoxin
• Wound contamination
• Inhalation
• Person-to-person not documented
Epidemiology
• In U.S., average 110 cases each year
– Approximately 25% food-borne
– Approximately 72% infant form
– Remainder wound form
• Case-fatality rate
– 5-10%
• Infective dose- few nanograms
Epidemiology
• 1977, Largest botulism outbreak
– Michigan - 59 people
– Poorly preserved jalapeno peppers
• Alaska
– 27% of U.S. foodborne botulism cases
– 1950-2000
• 226 cases from 114 outbreaks
Human Disease
• Three forms
– Foodborne
– Wound
– Infant
• All forms fatal and a medical emergency
• Incubation period: 12-36 hours
Foodborne Botulism
• Preformed toxin ingested from contaminated
food
• Most common from home-canned foods
– Asparagus, green beans, beets, corn, baked
potatoes, garlic, chile peppers, tomatoes; type A
– Improperly fermented fish (Alaska); type E
Infant Botulism
• Most common form in U.S.
• Spore ingestion
– Germinate then toxin released and
colonize large intestine
• Infants < 1 year old
– 94% < 6 months old
• Spores from varied sources
– Honey, food, dust, corn syrup
Wound Botulism
• Organism enters wound
– Develops under anaerobic conditions
– From ground-in dirt or gravel
– It does not penetrate intact skin
– Associated with addicts of black-tar heroin
Adult Clinical Signs
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Nausea, vomiting, diarrhea
Double vision
Difficulty speaking or swallowing
Descending weakness or paralysis
– Shoulders to arms to thighs to calves
• Symmetrical flaccid paralysis
• Respiratory muscle paralysis
Infant Clinical Signs
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Constipation
Lethargy
Poor feeding
Weak cry
Bulbar palsies
Failure to thrive
Diagnosis
• Clinical signs
• Toxin in serum, stool, gastric aspirate,
suspected food
• Culture of stool or gastric aspirate
– Takes 5-7 days
• Electromyography also diagnostic
• Mouse neutralization test
– Results in 48 hours
Treatment
• Intensive care immediately
– Ventilator for respiratory failure
• Botulinum antitoxin
– Derived from equine source
– CDC distributes
– Used on a case-by-case basis
• Botulism immune globulin
– Infant cases of types A and G