Salmonella infections

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Salmonella infections

• (salmonelloses)

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• The Enterobacteraceae comprise Salmonella,
  Shigella, Escherichia, Klebsiella, Enterobacter,
  Serratia, Proteus, Morganella, Yersenia, and
  other less common genera. This oxidase-negative,
  Gr. (-), catalase-positive organisms are readily
  cultured on ordinary media, ferment glucose and
  reduce nitrates to nitrites.

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The 2200 known serotypes of Salmonella may be
grouped into these

• highly adapted to human hosts
• adapted to non-human hosts
• unadapted to specific host

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• The first group includes S. typhi and S.
  paratyphi A, B and C, which are pathogenic only
  in humans and commonly cause enteric fever.
• The second group causes disease almost
  exclusively in animals, although 2 strains within
  this group, S. dublin and S. choleraesuis also
  cause disease in humans.
• The third group designated S. enteritidis,
  includes gt than 2000 serotypes that cause
  gastroenteritis.

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Typhoid fever

• A systemic disease caused by S. typhi and
  characterized by fever, prostration, abdominal
  pain, and a rose-colored rash

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Pathogenesis

• S. typhi invades first the alimentary tract by
  ingestion, then via the lymphatic system, via the
  thoracic duct into the blood stream.
• This first septicemic phase leads to infection of
  the reticuloendothelial system and the gall
  bladder.
• Infection of the gall bladder causes discharge of
  organisms into the intestine, with heavy
  infection of the Peyers pathes and septicemia
  and the onset of symptoms.

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Symptoms and signs

• IP 8-14 (14-21 days)
• Onset is usually gradual, with fever, headache,
  arthralgias, pharyngitis, constipation, anorexia,
  and abdominal pain and tenderness.
• If no therapy is began the temperature raises in
  steps over 2 to 3 days, remains elevated (usually
  to 39-40?C) for another 10 to 14 days, begins to
  fall gradually at the end of the 3rd wk, and
  reaches normal levels during the fourth week.
• Prolonged fever is often accompanied by relative
  bradycardia and prostration and CNS symptoms such
  as delirium, stupor, or coma occur in severe
  cases.

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• In about 10 of the patients discreet pink,
  blanching lesions (rose spots) appear in crops on
  the chest and abdomen during the 2nd wk and
  resolve in 2 to 5 days.
• Intestinal perforation, usually involving the
  distal ileum, occurs in 1-2 of patients.
• Splenomegaly, leucopenia, anemia, liver function
  abnormalities, proteinuria, and a mild
  consumption coagulopathy are common
• Diarrhea is a late symptom, usually in the third
  week of illness and still may contain blood. In
  about 2 of patients, severe bleeding occurs
  during the third week with a mortality rate of
  about 25.

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• In addition bacteriemia, occasionally leads to
  focal infections, such as osteomyelitis,
  endocarditis, menengitis, soft tissue abscesses,
  glumerulonephritis, or GU tract involvement.

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Complications

• Relapse, intestinal perforation and hemorrhage
  are the most serious. Relapse is common, with
  recrudescence of symptoms about a week after the
  end of the primary illness
• Carriers around 2-5 of patients with typhoid
  fever become chronic carriers, owing to
  persistent infection of the gall bladder.

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Diagnosis

• Best made by isolation of the infecting organism
  from feces, blood and urine. Blood culture is
  positive in over 80 of patients in the first
  week of illness.
• Blood and urine Mac Conkey medium
• Feces use selective and enrichment media

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• Identification biochemical reactions S
  typhi, unlike other salmonellae, produces no gas
  on fermentation of sugars.
• serological preliminary identification
  with salmonella polyvalent H and O antisera
• phagotyping

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• Serology the classic test is the Widal test
  agglutination test for antibodies to flagellar H
  antigens and somatic O antigens of S. typhi and
  S. paratyphi A and B, but the results are
  difficult to interpret, especially if the
  patients has been immunized with typhoid vaccine.
  This test is no longer used in routine diagnostic
  laboratories.

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Treatment

• Ciprofloxacin 500mg po q12h is the drug of
  choice, especially with the emergence of
  multiresistance involving other antibiotics but
  care is needed with children. Ceftriaxone is a
  useful alternative in such cases.
• Ceftriaxone 30mg/kg/day im or iv in 2 divided
  doses for 2 week (eg. 1 g iv q 12h for adults).
• Cefoperazone is given 60mg/kg/day iv in 2 divided
  doses for 2 weeks.
• Co-trimoxazole.

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Paratyphoid fever

• Causal organisms S. paratyphi A, B and C
• Clinically a milder febrile illness than typhoid
  fever, with a shorter duration and incubation
  period. Transient diarrhea and symptomless
  infection are common.
• Carriers patients become carriers less
  frequently than after typhoid fever.
• Diagnosis best made by isolation of the
  infecting organism from feces, blood and urine.
  Blood culture is positive in over 80 of patients
  in the first week of illness.
• Treatment Ciprofluxacin is the drug of choice,
  but care is needed with children. Ceftriaxone is
  a useful alternative in such cases.
  Chloramphenicol is as effective, but resistance
  is now a problem. Co-trimoxazole is less good
  than Chloramphenicol, but has less serious side
  effects.

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Non-typhoidal Salmonella infections

• Formerly the commonest cause of diarrhea in
  Europe and the USA.
• Diarrhea due to Salmonella is traditionally
  called food poisoning, although this term is
  somewhat misleading. Infected meat-producing
  animals, poultry, raw milk, eggs and egg products
  are common sources of Salmonella.
• There are more than 2000 serotypes of Salmonella,
  but only about 14 are important or common causes
  of infection.
• In recent years the commonest serotype has been
  S. enteritidis. Other common Salmonellae are S.
  typhi murium, S. heidelberg, S. Newport, S. agona

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Pathogenesis

• Sight of infection is the small or large
  intestine. Many strains produce enterotoxins
  similar to those of toxigenic strains of E.
  colli. NB! The Salmonella enterotoxins are still
  poorly defined. Other Salmonellae invade the
  mucosa of the small intestine like Shigellae.

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Symptoms and signs

• Salmonella infection may present clinically as
  gastroenterits, enteric fever (S. paratyphi A, B
  and C), a bacteremic syndrome, or focal disease.
  
• IP is short around 12-36-48 hours.
• Main symptoms are acute onset of abdominal pain
  and diarrhea, sometimes with fever and vomiting.
  Dehydratation may require correction, especially
  in babies.
• Usually the stool is watery, but made be paste
  like semisolid. Rarely, mucus or blood is
  present.

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Bacteremia

• (S. choleraesuis, S. typhimurium, S. heidelberg).
  Although blood cultures are positive, stool
  cultures are generally negative.

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Focal manifestation

• of Salmonella infections may occur with or
  without sustained bacteriemia. In patients with
  bacteriemia localized infection may occur,
  involving the GI tract (liver, gall bladder and
  appendix), endothelial surfaces.(heart valves),
  pericardium, meninges, lungs, joints, bones, GU
  tract.

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Diagnosis

• Is made by isolating the organism from stool or
  another infected site. The prognosis is usually
  good unless severe underlying disease is present.
  Asymptomatic carriage is usually self-limited and
  antibiotics treatment is rarely required.
  Eradication may be attempted with Ciprofluxacin
  500 mg po q12h for 1 month, but follow up stool
  cultures should be obtained in the weeks after
  drug administration to document elimination of
  Salmonella.

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Treatment

• Rarely necessary rehydratation may be required
  in babies oral isotonic fluid replacement can be
  life-saving in infants with diarrhea.
• Antibiotics are contraindicated except in
  septicemia cases they do not affect symptoms and
  may prolong convalescent carriage of the
  organism they also contribute to the emergence
  of antibiotic resistant strains.
• Trimethoprim-Sulphamethaxazole (TMP-SMX) 5mg/kg
  of TMP component po every 12h for children, or
  Ciprofluxacin 500mg po q12 hours for adults.
• Neledix 50mg/kg
• Gentamycin - 2-5mg/kg
• Amikacin 5-15mg/kg.

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Shigellosis(Dysenteriae)

• Shigellosis is an acute infectious inflammatory
  colitis due to one of the members of the genus
  Shigella. The less severe illness predominates in
  industrialized countries, whereas more severe,
  often fatal dysenteria occurs in patients in
  developing countries.

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The four species of Shigella are

• ? S. dysenteriae
• ? S. flexneri
• ? S. boydii
• ? S. sonnei
• All the species except S. sonnei contain several
  distinguishable serotypes.
•  

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Pathogenesis and pathology

• Shigella are orally ingested and because they
  survive low pH better than other enteric
  pathogens, they seem to have little difficulty in
  passing the gastric acid barrier
• An essential step in pathogenesis is invasion of
  colonic epithelial cells and cell-to-cell spread
  of infection.
• Invasion and cell-to-cell spread involve the
  initial attachment of the organism to colonic
  cells, entry by and an endocytic mechanism, in
  which organisms are initially incased in and then
  escape from plasma membrane-enclosed vesicles,
  and a jet propulsion-like movement to the
  epithelial cell surface that is powered by
  bacteria-induced actin polymerization at the
  trailing end of the bacterium

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• A second property of apparent importance in
  virulence, at least for S. dysenteriae type I is
  the ability to produce cytotoxic proteins. Shiga
  toxin composed of two distinct peptide subunits,
  each with highly conserved active regions.

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• Shigella organisms penetrate the mucosa of the
  lower intestini, causing mucous secretion,
  hyperemia, leucocytic infiltration, edema and
  often superficial mucosal ulceration. The watery
  diarrhea associated with shigella infection may
  be mediated by an enterotoxin that causes
  increased intestinal secration.

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• S. dysenteriae has invasive properties and
  produces a powerful neurological exotoxin, but
  this probably does not play a role in shiga
  dysenteriae. An enterotoxin and cytotoxin are
  also produced their role is uncertain, but they
  may be partly responsible for invasiveness. Shiga
  toxin, is very closely related to E. colli
  verocytotoxin 1(VT1). Cytotoxins, which cause
  destruction of mucosal cell and associated
  inflammatory diarrhea and neurotoxins, which act
  directly on the central or peripheral nervous
  system.

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Symptoms and signs

• IP 1-9 days.
• Diarrhea with blood, mucus and often pus in the
  stools, which varies from a severe life
  threatening to a mild and symptomless infection.
• In young children onset is sudden, with fever,
  irritability or drowsiness, anorexia, nausea or
  vomiting, diarrhea, abdominal pain and distention
  and tenesms. The number of stools may increase to
  more than 20/day, and weight loss and
  dehydratation may become severe.
• In adults first symptoms may be episodes of
  abdominal pain, urgency to defecate and little or
  no tenesms.

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Complications

• severe mucosal ulcerations may cause significant
  acute blood loss.
• Intestinal perforation
• Hemolytic-uremic syndrome in children
• Arthritis, myocarditis, toxic neuritis

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Laboratory findings and diagnosis

• ? Diagnosis isolation culture feces and rectal
  swabs on MacConckey medium and selective media.
  Identify by biochemical tests, then serology.
• ? WBC count is often reduced at onset
  hemoconcentration is common, as is
  diarrhea-induced metabolic acidosis.
• ? The mucosal surface, as seen through a
  prostoscope, is diffusely erithematous with
  numerous small ulcers.

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DD

• Should include invasive E. colli, Salmonella,
  Yersenia, Campylobacter, Amebiasis, and viral
  diarrheas.

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Treatment

• Fluid therapy. Diarrhea usually causes isotonic
  dehydratation (equal salt and water loss), with
  metabolic acidosis and significant potassium
  loss. Thirst from dehydratation can lead to a
  proportionately excessive water intake, causing
  hypotonicity.
• Antibiotics. The decision to use antibiotics
  requires consideration of disease severity, age
  of the patient and other factors. In children,
  TMP-SMX at 4mg/kg/po of the TMP component q12h is
  the treatment of choice.
• In adults the dose is one double strand tablet
  q12h (320 mg TMP). An alternative for adults is
  norfluxacin or ciprofluxacin 500mg po bid (two
  times a day). Many shigella isolates are likely
  to be resistant to Ampicillin and Tetracyclin

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Cholera

• An acute infection by Vibrio cholerae involving
  the entire small bowel characterized by profuse
  watery diarrhea, vomiting muscular cramps,
  dehydratation, oliguria, and collapse.

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Etiology

• ? The causative organism, V. cholerae, serogroups
  01 and 1039. Epidemic cholera is caused by V.
  cholerae serogroup 01. which is divided into
  three serotypes, Ogava, Inaba, Hikojima. However,
  antigenic structure may change within the human
  gut.
• ? Biotypes two biotypes of V. cholerae 01,
  classic and El Tor. Any serotype can be of either
  classic or El Tor biotype.
• ? Non-01 vibrios, deficient in the 01 antigen,
  were classified as non-cholera vibrios but a
  cholera epidemic in Bangladesh in 1992 was due to
  serogroup 0139.

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Pathogenesis

• V. cholerae produces a potent exotoxin cholera
  toxin (CT), vary similar to the LT enterotoxin of
  ETEC, which is plasmid coded. The toxin
  stimulates the activity of the enzyme
  adenylcyclase, which raises the concentration of
  cyclic AMP is cell this causes an increase in
  the flow of water and electrolytes into the bowel
  lumen. The fluid lost has relatively high
  concentration of bicarbonate and potassium.
• V. cholerae is not invasive and does not
  penetrate the gut mucose membrane, although
  adhesion to gut epithelium plays a part in its
  pathogenesity.

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Clinical feature

• ? IP 6h to 5 days.
• ? Acute onset of abdominal pain and diarrhea
  the diarrhea being typically of exceptional
  severity, progressing to the continuous passage
  of rice-water stools.
• ? Vomiting, dehydratation, acidosis and collapse
  may follow.
• Some cases are much les severe with only mild
  diarrhea. Two forms of disease are recognized
• severe classic cholera
• milder cholera associated with the 01 El Tor
  biotype.

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CHOLERA
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Diagnosis

• Culture feces on alkaline selective medium.
  Observe for typical colonies, which can be
  identified by slight agglutination, with
  polyvalent antiserum.

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Treatment

• ? Correction of dehydratation by intravenous
  administration of fluid and electrolytes to
  restore the acid-base balance. Mortality can be
  reduced from more the 50 to 0 with fluid
  replacement treatment.
• ? Tetracycline, given orally or intravenously,
  may help to limit the duration of diarrhea and
  reduce fluid loss.

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• ? Composition of World Health Organization oral
  rehydratation solution (WHO ORS).
• In 1000ml pre-boiled water
• 20g glucose
• 3.5g NaCl
• 2.5g NaHCO3
• 1.5g KCl
• Concentration (mmol/l) Na 90, K 20, HCO3 30
• ex tempore
• Rehydrin
• - Phillips solution

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Esherichioses intestinales

• (Colibacilloses)

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• Enteric infections are common cause of diarrhea
• infantile gastroenteritis
• travelers diarrhea
• hemorrhagic diarrhea
• hemorrhagic colitis
• hemolytic-uremic syndrome

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• ETEC enterotoxigenic E. coli travelers
  diarrhea (Delhi belly, Tokyo two step etc)
• EPEC enteropathogenic (eneteroadherent) E. coli
  childhood diahhrea.
• EIEC enteroinvasive E. coli a dysentery-like
  disease
• EHEC enterohemorrhagic E. coli hemorrhagic
  colitis and HUS in children.

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EPEC (055 0111) strains

• cause childhood diarrhea, especially in
  underdeveloped countries and in nursery
  outbreaks. These bacteria bind to the membranous
  cells of Peyers patches and disrupt the
  overlying mucous gel of the host cell.
• EPEC do not produce toxins and are non-invasive,
  but produce an attaching end effacing lesion in
  the small intestine

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• ETEC there are more than 100 0 serogroups.
  Important examples are 06, 078.
• ETEC produce heat-labile toxin (LT) or
  heat-stabile toxin (ST) or both. They also posses
  colonization factors, which facilitate the
  attachment of the organism to the epithelium of
  the small intestine.
• EIEC (0124, 0164) invade the host cell and
  provoke significant inflammatory response.
  Manifestations are those of bacterial dysentery
  with fever and bloody diarrheal stool, containing
  polymorphonuclear leukocytes.

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EHEC strains

• all belong to the serotype 0157H7, cause
  hemorrhagic colitis.
• These strains produce shiga-like toxins that kill
  certain cells in tissue culture.
• Although the typical patient is afebrile the
  sequel can be severe. In the elderly the disease
  is often confused with ischemic colitis. It can
  lead to death. Children (1-4 years) and
  occasionally adults with EHEC infection can
  develop HUS, which also can lead to death. HUS is
  seen occasionally with bacteria other than
  0157H7, including other E.coli serotypes and
  Shigella.

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• ? HUS in children diarrheal prodrome, followed
  by uremia, throbocytopenia and hemolytic anemia.
• ? Shiga-like toxins have a cytopathic effect on
  Vero (monkey kidney) cells. There are two Vero
  cytotoxins, VT1 and VT2, which are antigenically
  distinct from each other. Vero cytotoxin
  producing E.coli strains are known as VTEC. Over
  80 phagotypes of serogroup 0157 can be
  distinguished.

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Diagnosis

• ? Culture feces on MacConckey medium.
• ? Identify by serology and biochemical tests.

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Treatment

• Rehydratation with correction of fluid loss and
  electrolyte and acid base balance
• Antibiotics therapy is of doubtful value,
  although it may be useful in severe cases
• Treatment may be started empirically, than
  modified on the basis of antibiotic sensitivity
  studies. Although many strains are still
  sensitive to Ampicillin (Piperacillin,
  cephalosporins, amynoglucosides, TMP-SMX, and
  quinolons in adults).

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Dehydration syndrome

• Rehydration
• ? oral rehydratation WHO ORS
• In 1000ml pre-boiled water
• 20g glucose
• 3.5g NaCl
• 2.5g NaHCO3
• 1.5g KCl
• Concentration (mmol/l) Na 90, K 20, HCO3 30,
  Cl 80
• ex tempore
• Rehydrin a commercial solution

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i.v. fluids

• Classification of dehydratation in infants
• Ist grade up to 5 loss of body weight (infuse
  with 80-100ml/kg/24h)
• IInd grade between 5-10 loss of body weight
  (120-150ml/kg/24h)
• IIIrd grade more than 15 loss of body weight
  (150-170ml/kg/24h)

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• At the end of the rehydratation period (about 4
  hours), the patient should be reassessed. If
  signs of dehydratation persist, rehydratation
  therapy should be repeated until dehydratation is
  corrected

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Metabolic acidosis phlt7.37

• The amount of NaHCO3 can be approximated by the
  formula
• NaHCO3 required (mEq) BE(base excess) x 0.4 x
  body wt(kg)
• First 1/3rd of the received quantity is applied
  and if fails to correct the acidosis, the rest is
  added.

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Hypokaliemia

• a decrease in the serum potassium concentration,
  below 3.5 mEq/l. It is a result of excessive
  losses of K from GI tract. It is characterized my
  muscle weakness and can lead to paralysis and
  respiratory failure. ECG ST depression.
• Treatment i.v. KCl amp.15 10ml 2mEq/kg
  slowly!

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• The use a antibiotics therapy in bacterial
  diarrheas is controversial and generally not
  necessary in patients with mild or resolving
  disease, but should be considered in patients
  with Shigellosis, travelers diarrhea, cholera.

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• Reference
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