Shigella flexneri

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Shigella flexneri
Simon Flexner
Discoverer of Shigella dysenteriae (1899)
Compiled by Else Marais, Marlene Kassel, Naseema
Aithma, Angela Potgieter Rob Stewart, Branca
Fernandes, and Janet Loakes
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Gastro-intestinal infections

• Acute inflammatory enteritis
• Campylobacter
• Salmonella
• Shigella
• Certain parasites

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Acute dysentery

• Frequent small bowel movements
• Blood and mucous
• Tenesmus
• Pain on defecation
• Inflammatory invasion of intestinal mucosa
• Bacterial, cytotoxic or parasitic destruction

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Overview of Shigella species

• Small, Gram-negative rods
• Non-motile, non-encapsulated
• Family Enterobacteriaceae Tribe
  Escherichieae Genus Shigella
• 40 serotypes, 4 groups
• A - Shigella dysenteriae
• B - Shigella flexneri
• C - Shigella boydii
• D - Shigella sonnei

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Overview of Shigella species

• Sensitive to heat, kill in 55 c in 1 hr
• S.sonnei survive in soil room temprature for
  9-12 days
• Survive on fingers for sometime transmit
  through hand contact
• If suitable,survive in milk other food(15 days
  in sea water)

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Overview

• Shigella species
• 140-200 million people infected annually
• 650,000 deaths per year,
• worldwide(esp. developing countries)
• intracellular pathogens
• Incubation 6 hrs to 9 days(1-7 days)
• AB resistance (multiple)
• 2/3 of all cases and most of deaths in lt 10 y/o
• Developing countries 1-4 y/o but in
• epidemics of S. dysenteriae all age group equal

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Overview

• In 5-15 of diarrhea 30-50 of dysentry
• S.flexeneri the most important in endemic
  shigellosis
• Africa 15 country with outbreak (30 attack rate
  in general population 50 in lt 5 y/o
• Developed countries children, daycare centers,
  immigrant workers, travelers to developing
• 2/3 of cases in lt 10 y/o

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Iran

• Tehran 52 S.flexeneri, 37 S.sonnei
• Resistance to ampi, co-trimoxazole, tetra, amoxi,
  chloramphenicole, cephalotin(more in S.flexeneri)
• The most effective AB is ciprofloxacin then
  ceftizoxime
• Shiraz 60 S.flexeneri, 28 S.sonnei, 12
  S.boydii, 34 in preschool age
• Resistance to ampi, co-trimoxazole
• Sensitive to nalidixic acid, ceftriaxone,
  ceftazidime, ciprofloxacin(100)

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Descriptive epidemiology

• Time trend
• More common in warm seasons
• Equal in both sexes
• In temperate climate warm season
• In tropics rainy season
• Preschool early school age
• 1-4 y/o (adult get disease from children)
• Infants(1- 6 mo) are resistant due to nursing

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Predisposing factors

• HIV ( chronic relapsing and causing bateremia
  in spite of AB)
• Septicemia in Malnutrition, early infancy
  S.dysenteriae type 1
• EL-Nino phenomenon
• a dry not rainy winter rainy spring
  increase in dysentery in summer

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Sensitivity resistance

• 10-100 micro-organism ingestion in volunteers
  diarrhea in 10-40
• More virulent in children, malnutrition,
  debilitated old-mostly sub-clinical in adults
• Oral vaccine some success (short- term)
• Attenuated oral vaccine prevent clinical dx
• 2nd attack rate in household contact 40
• Epidemics in crowding, bad public health( day
  care center, long term care center)

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Transmission

• Fecal-Oral(direct or indirect) from patient or
  carrier
• No handwashing after bowel movement( direct
  contact)
• Contaminated food( not usual but can cause major
  epidemics)
• Carrierswithout treatment microorganism shedding
  for 1-4 wks( but the number is low, so
  communicability is lower than pts)
• Nosocomial infection from pts to healthworkers
  to other pts.
• Shigella can survive on lab equipments for some
  time
• Homosexual oral-anal, penile-oral

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Transmission

• Contaminated water milk
• 4-6 wks survive in water( shorter in sun-exposed
  water)
• Pasteurization eliminate the mo.
• Insects
• Fly mechanical, biological
• Communicable for 4 wks

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• Humans and primates only reservoirs
• Crowded living conditions
• Poor quality water supplies
• Inadequate sewage disposal
• Increase risk of infection

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Clinical features

• From asymptomatic to severe (Mortality rates
  vary from 5-10 )
• Bacilli ingested by epithelial cells of the
  intestinal villi
• Organisms multiply and spread laterally into
  lamina propria
• Inflammatory reaction develops with capillary
  thrombosis
• Necrotic epithelium sloughed leading to
  ulceration
• Severe cases may become life threatening

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Clinical features natural history

• 7-12 bowel movement/day
• Watery, green or yellow, containing mucous blood
  or undigested food
• Convulsion, Acute bloody dysentery
• Fever, malaise, headache, abdominal pain
• Usually self limited and recovery after 4-7 days,
  sometimes persistent diarrhea
• HUS
• Mortality in hospital 20

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Virulence

• S.dysenteriae forms potent exotoxin
• Fluid transuding action as well as
• Lipo-polysaccharide endotoxin
• Described as a neurotoxin
• Toxin levels of S.dysenteriae, highest
• S.sonnei causes mild illness(short symptomatic
  period and very low mortality)
• S. flexneri and S.boydii range in severity
• S.flexneri bacteremia, predisposed by ulcers

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Virulence

• Commonly a self-limited disease(mild or mod)
• 4-7 days(several days to weeks)
• S.dysenteriae cause more severe disease(20
  mortality in admitted patients)
• If untreated stool culture for 30 days or more

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Molecular methods of detection

• Isolation difficult
• Genetic probe to the virulence-plasmid developed
  and being tested
• PCR not routinely done for detection

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Outbreaks

• From contaminated water or food
• contaminated potato salad
• inadequate toilet facilities
• Origin of infection- food handler
• Secondary transmission may occur
• Flies aid transmission
• Infants resistant to shigellosis
• More in formula fed)

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Patterns of outbreaks

• Cyclic patterns of 20-30 years
• From 1900-1925 S.dysenteriae predominated while
  from 1926-1938, S.flexneri was common
• Currently S.sonnei predominates in Europe and
  USA
• S.flexneri is predominant in developing
  countries( with boydii dysenteriae)

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Controlprimary prevention

• Chlorinated water, waterborne sewage
• Rigorous hand washing
• Institutional outbreaks Isolation of the
  infected
• Infected food handlers - 2 negative cultures
• Insecticides
• After P/E of the patient hand washing,
  disinfection of exam. Equipments
• Vaccination under trial

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primary prevention

• Enteric precaution, disinfection of contaminated
  equipment stool( if there is not modern sewage)
  
• Infected person withhold from children, other pts
  and food handling 2 consecutive stool culture in
  24 hr interval 48 hr after D/C of AB
• AB treatment of carriers( without any sign or
  symptoms) not recommended
• Common writing equipment(pen,)
• nursing

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Secondary Prevention

• Early treatment shorten acute phase of disease
  mo. shedding

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Treatment

• Fluid replacement
• Antimicrobial therapy- reduces duration of
  symptoms
• Reduces secretion of organisms
• Adults- oral ciprofloxacin or ofloxacin
• Children- cotrimoxazole, ampicillin,nalidixic
  acid, ceftriaxone, azithromycin
• Agents decreasing intestinal motility should not
  be used
• Untreated lasts 1 day - 1 month (average 7days)
• Complications - dehydration, seizures,
  septicaemia, pneumonia, keratoconjunctivitis and
  arthritis

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• Travellers
• Eat well cooked food
• Bottled water
• Peel all fruit and vegetables
• Perhaps use prophylactic flouroquinolones