Bacteria

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Bacteria

• Dr. Cserynik
• Jan. 18, 2007
• Slides by Bogdan Irimies
• PGY 4 EM Resident

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Diptheria Corynebacterium diptheriae

• Epidemiology humans are the only known
  reservoirs
• Spread is via person-person contact thru
  respiratory droplets or by direct contact w/skin
  lesion exudates
• 0-5 cases nationwide/year
• Usually seen unimmunized or under immunized
  adults in urban and poor rural areas

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Diphtheria Corynebacterium diphtheria

• Etiology/pathophysiology
• Gram bacillius koryneeclub shaped bacteria
  diphtherialeather hide looking pharyngeal
  membrane
• C. diphtheria produces exotoxin that causes
  pharyngeal membrane exudates and systemic effects
  of infection
• Causes skin, respiratory, cardiac neurological
  manifestations

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Diphtheria Corynebacterium diphtheria

• Incubation period 1-8 days
• Fever, sore throat (thick grayish-black membrane
  with sharply defined borders)
• Weakness,dysphagia, HA, change in voice, cervical
  adenopathy(bull neck appearance)
• Skin ulcer grayish membrane
• Peripheral neuropathy/muscle paralysis
• Cardiac myocarditis, CHF

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Diphtheria Membrane
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Diphtheria Bull Neck
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Diphtheria Corynebacterium diphtheria

• Complications
• Airway obstruction from edema/membrane formation
• CHF
• Cardiac conduction disturbances
• muscle paralysis

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Diphtheria Corynebacterium diphtheria

• Diagnosis throat or nasopharyngeal swabs,
  cutaneous swabs
• PCR for diphtheria gene
• Leukocytosis, mild thrombocytopenia, proteinuria
• EKG ST-T changes, AV block dysrhythmias

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Diphtheria Corynebacterium diphtheria D/Dx

• Strep/viral pharyngitis
• Tonsillitis
• Vincents angina
• Epiglottitis
• Mono

• Laryngitis
• Bronchitis
• Tracheitis
• Monilial infxn
• Rhinitis

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Diphtheria Corynebacterium diphtheria Treatment

• Place pt. in respiratory isolation
• Bronchodilators, fluids
• Equine serum antitoxin is mainstay 20,000-40,000
  units IV
• Erythromycin or procaine penicillin for 14 days
• Close contacts should be observed for 7 days,
  receive booster of diphtheria toxoid (Td) if 5
  yrs.

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Pertussis
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Pertussis Epidemiology

• Localized respiratory illness transmitted by
  respiratory droplets
• Avg incubation period 7-10 days
• Neither vaccination nor prior infection confer
  lifelong immunity

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Pertussis Etiology

• Bordetella pertussis, gram neg. coccobacilli
• Preferentially adheres to ciliated respiratory
  epithelial cells

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Pertussis Clinical

• Arises in 3 distinct clinical stages
• Catarrhal phase begins after incubation period,
  lasts 1-2 weeks, infectivity is greatest during
  this phase
• Clinically indistinguishable from an URI
  rhinorrhea, , low grade fever, malaise,
  conjunctival injection, anorexia

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Pertussis Clinical

• Paroxysmal phase fever subsides and cough
  increases(2-4 wks.)
• Staccato cough pt. coughs repeatedly in short
  exhalations followed by a short inspiratory
  whoop
• Pt. may have post-tussive emesis, syncope, brief
  apnea

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Pertussis Clinical

• Convalescent stage residual cough that lasts
  from several weeks to months
• PE low grade fever and tachypnea

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Pertussis Diagnosis

• Diagnosis should be entertained in anyone
  w/prolonged cough w/paroxysmal whoops or
  posttussive emesis
• Leukocytosis
• Lab confirmation by nasopharyngeal swab or direct
  fluorescent antibody

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Pertussis D/Dx

• Viral URI
• Pneumonia
• Bronchiolitis
• CF
• TB

• COPD Exac.
• Foreign Body Aspiration

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Pertussis Complications

• Periorbital edema
• Subconjunctival hemorrhage
• Petechiae
• Epistaxis
• Hemoptysis
• SQ Emphysema

• PTX
• Pneumomediastinum
• Diaphragmatic rupture
• Hernia exac.
• Rectal prolapse

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PertussisTreatment

• O2, suctioning, hydration
• Antibiotics doesnt appear to reduce the severity
  of illness or duration especially if started in
  paroxysmal phase
• ErythromycinAzithromax Bactrim
• Postexposure prophylaxis w/erythromycin is
  recommended for household contacts of pts.
  w/pertussis regardless of previous vaccination
  status

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Tetanus
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Tetanus Epidemiology

• Tetanus is a toxin mediated disease characterized
  by uncontrolled skeletal muscle spasms
• Avg. 43 cases reported to CDC/year
• Most common portals of entry are puncture
  wounds, lacerations, abrasions
• Primary risk factors are inadequate primary
  immunization and waning immunity

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Tetanus Etiology

• Clostridium tetani gram positive, spore forming,
  anaerobic bacillus
• Found in soil, dust, feces
• Development of clinical tetanus requires a portal
  of entry for infecting spores as well as tissue
  conditions that promote germination and growth in
  an immunologically susceptible host

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Tetanus Etiology

• C. tetani produces a neurotoxin that causes
  clinical illness
• C. tetani produces the neurotoxin
  tetanospasmin(TS) at the site of tissue injury
• TS binds to the motor nerve ending and then moves
  by retrograde axonal transport to the CNS
• Preferentially binds to GABA and blocks
  presynaptic release of GABA resulting in muscle
  spasm

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Tetanus Clinical

• Tetanus typically occurs as a result of a deep
  penetrating wound
• Incubation period is 1 day to several months
• There are 4 types of clinical tetanus
  Generalized, localized, cephalic, and neonatal

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Tetanus Clinical

• Generalized tetanus
• Most common form
• Trismus(lockjaw), characteristic sardonic
  smile(risus sardonicus)
• Early symptoms include irritability, weakness,
  myalgias, muscle cramps, dysphagia, hydrophobia,
  drooling

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Tetanus Clinical

• Generalized
• Opisthotonus is a prolonged tonic contraction
  that resembles decorticate posturing
• Autonomic dysfunction tachy, HTN, fever, cardiac
  dysrythmia and diaphoresis

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Opisthotonus
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Sardonic smile
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Tetanus Clinical

• Localized persistent muscle spasm located near
  site of injury
• Most cases do not progress to generalized tetanus

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Tetanus Clinical

• Cephalic form rare variant
• Results in cranial nerve palsies and muscle
  spasms
• Usually ipsilateral to site of injury
• Commonly affected nerves 3, 4,7, 9, 10, 12

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Tetanus Clinical

• Neonatal form generalized tetanus of newborn
• Symptoms begin during 1st week of life
• Irritability and poor feeding seen

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Tetanus Diagnosis

• Clinical diagnosis
• No lab test that confirm or exclude disease
• CDC clinical case definition
• Acute onset of hypertonia or painful muscular
  contractions and generalized muscle spasms
  without other apparent medical cause.

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Tetanus D/Dx

• Acute abdomen
• Black widow spider bite
• Dental abscess/peritonisillar abscess
• Dislocated mandible/TMJ
• Dystonic rxn
• meningoencephalitis

• Head trauma/SAH
• Hyperventilation
• Hypocalcemia
• Rabies
• Psychogenic
• Sepsis
• Status Epilepticus
• Strychnine poisoning

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Tetanus Complications

• Acute respiratory failure results from
  respiratory muscle spasms, laryngospasm and
  airway obstruction
• Dysrythmias, HTN, myocarditis, pulm. Edema
• Forceful contractions can cause vertebral
  subluxations fxs, long bone fxs, shoulder
  TMJ joint dislocations

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Tetanus Treatment

• 4 treatment strategies
• 1. Aggressive supportive care
• 2. elimination of unbound TS
• 3. Active immunization
• 4. Prevention of further toxin production

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Tetanus Treatment

• Benzodiazepines are DOC for supportive care
• Mechanical ventilation w/neuromuscular blockade
• Autonomic instability use labetalol
• Human tetanus immunoglobulin(TIG) neutralizes
  unbound toxin
• Administer at a site separate from toxoid

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Tetanus Treatment

• Administer Td immediately for active immunization
• Prevention of further toxin production is thru
  wound debridement and irrigation
• Metronidazole is antibiotic of choice

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Tetanus Vaccination

• Tetanus toxoid is an inactivated form of TS
• Immunity wanes after 5-10 years
• Those younger than 7 years should receive DPT
• No evidence that Td is teratogenic
• TIG is not contraindicated in pregnancy

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Td Prophylaxis
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Botulism
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Botulism

• Caused by neurotoxins produced by Clostridium
  botulinum
• 5 forms of the disease
• 1. Food born botulism
• 2. Infant botulism
• 3. Wound botulism
• 4. Unclassified botulism
• 5. Inadvertent botulism

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Botulism Epidemiology

• 7 types of toxins produced but only types A,B,E,F
  cause illness in humans
• 110 cases/year reported to CDC
• Food borne botulism results from the ingestion of
  preformed heat labile toxin which is found from
  exposure to home canned foods

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Botulism Epidemiology

• Infant botulism is most common form, caused by
  ingestion of spores w/in vivo production of
  toxin. Found in honey and corn syrup
• Wound botulism is rare, 1 case/year, assoc. w/IV
  drug abuse
• Inadvertent botulism is iatrogenic, occurs in
  people who have been injected w/botulism toxin
  for dystonia, movement disorders and cosmetic
  purposes

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Botulism Etiology

• C. botulinum anaerobic, gram positive rod
• Bacteria produces a potent exotoxin that is
  responsible for the disease
• Botulinum toxin targets peripheral neuromuscular
  junctions and autonomic synapses causing flaccid
  paralysis
• Blocks the release of acetylcholine resulting in
  neuromuscular blockade

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Botulism Clinical

• Botulism manifests by cranial nerve palsies,
  parasympathetic blockade, descending flaccid
  paralysis
• Food borne botulism is prototype of disease
• Symptoms begin 18-36 hrs. after ingestion of
  toxin containing food

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Botulism Clinical

• Early symptoms include weakness, malaise,
  lightheadedness, N/V, constipation
• Neurologic symptoms cranial nerves affected
• Diplopia, blurry vision, dysphonia, dysphagia,
  dysarthria
• Symmetric descending muscular weakness occurs
  involving upper and lower extremities and
  respiratory muscles

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Botulism Clinical

• Ocular signs ptosis, extraocular palsies,
  dilated fixed pupils
• Muscle weakness upper extremities more affected
  than lower, proximal weaknessdistal muscles
• Sensory exam is normal

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Botulism Clinical

• Infant botulism
• Constipation is common symptom, poor feeding,
  weak cry, loss of head control, hypotonia,
  decreased muscle tone, depressed deep tendon
  reflexes
• Wound botulism incubation period is longer 4-14
  days
• Clinical presentation is similar to food borne
  botulism

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Infant Botulism
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Wound Botulism
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Botulism Diagnosis

• Initial diagnosis is clinical suspect in someone
  who presents with constellation of GI, Autonomic,
  cranial nerve dysfunction
• Confirmed by
• 1. botulinum toxin in pts. Blood
• 2. Botulinum toxin or C. botulinum in GI
  contents, stool, or wound
• 3. Toxin in the food source
• Notify CDC

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Botulism D/Dx

• Pharyngitis
• Gastroenteritis
• Guillain Barre Syndrome
• Tick paralysis
• Myasthenia Gravis
• Poliomyelitis
• Diphtheria
• Eaton Lambert Syndrome

• Anticholinergic toxicity
• Organophosphate toxicity
• Heavy metal poisoning
• Mg2 toxicity

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Botulism Complications

• Complications are related to respiratory failure
• Weakness of respiratory muscles

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Botulism Treatment

• Treatment consists of supportive care,
  administer antitoxin
• ICU, NG tube, foley
• Antitoxin contains antibodies to toxins types
  A,B, E
• Neutralizes only circulating toxins and has no
  effect on bound toxin
• One vial is required

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Botulism Treatment

• Infant botulism antitoxin is not recommended b/c
  not efficacy, there is a risk of anaphylaxis to
  horse serum
• Use human botulism immunoglobulin(BIG)
• Wound botulism
• Debridement and antibiotics should be given only
  after antitoxin has been given

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Pneumococcus
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Pneumococcemia

• Strep. Pneumoniae clinical presentation ranges
  from mild illness to fulminant, life threatening
  systemic syndrome
• Also causes localized infections such as OM,
  pneumonia, meningitis, endocarditis, septic
  arthritis, peritonitis.

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Strep. Pneumoniae Epidemiology

• Exact incidence is unknown. Spread from person to
  person by close contact
• The introduction of the heptavalent vaccine has
  decreased incidence of disease by 69 in children
  
• Risk Factors for pneumococcemia chronic
  respiratory or CV disease, chronic ETOH abuse,
  cirrhosis, DM, impaired spleen(sickle cell), CRF,
  AIDS, cancer, organ transplant

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Strep. Pneumoniae Etiology

• Encapsulated, gram positive anaerobic coccus that
  occurs in pairs and chains
• Over 90 serotypes
• Prevnar vaccine account for 7 serotypes which
  cause 80 of invasive disease in children

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Pneumococcus
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Strep. Pneumoniae Etiology

• Strep Pneumo enters bloodstream by one of two
  routes
• 1. Begins as pulmonary infection, thru lymphatics
  and into bloodstream
• 2. Colonizes or cause URI and spreads to
  Subarachnoid space, then to arachnoid villi to
  venous sinus to blood
• Can cause a clinical picture from a minor febrile
  illness to septic shock

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Strep. Pneumoniae Clinical

• Presents as SIRS syndrome
• Also may present as lethargy, signs of poor
  tissue perfusion, cyanosis, hypo/hyperventilation
• Findings on physical exam vary with site of
  localized infection

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Strep. Pneumoniae Diagnosis

• The only specific test is blood culture
• Check CBC w/diff, blood urine cultures,
  electrolytes, CXR, sputum, ABG prn, LP prn, coags
  prn

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Strep. Pneumoniae Complications

• CV collapse, DIC, Septic emboli, Respiratory
  failure, meningitis, hypothermia, GI Bleeding,
  hepatic coma, renal failure, MI
• Pneumococcemia can cause hematogenous seeding
  which results in peritonitis, arthritis,
  endocarditis, meningitis, cellulitis

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Strep. Pneumoniae Treatment

• Prompt initiation of antibiotics Penicillin G,
  ceftriaxone(covers also N. meningitis, H. flu)
• PCN allergic pt cefotaxime, ceftriaxone, vanco,
  chloramphenicol
• For PCN resistant Strep. Pneumo use ceftriaxone,
  cefotaxime, vancomycin or imipenem
• For suspected pneumococcal meningitis use vanco
  cefuroxime or cefotaxime

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Pneumococcal Vaccine

• Effective in preventing disease, accounts for
  85-90 of pneumococcus infections
• Recommended for children ages 2-23 months
• Recommended for adults with the following
• Chronic illness CV/Pulm, DM, ETOHics
• Immunocompromised people including asplenic
  pts.,HIV

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Meningococcemia

• Think of this in a patient who appears relatively
  well on initial presentation, then becomes
  morbiund and critically ill w/fulminant infection
  several hours later

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Meningococcemia Epidemiology

• 2400-3000 cases annually
• Crowded living conditions increase the risk
  military recruits, college freshman
• Risk Factors close contact w/an infected pt.,
  complement def., asplenia, chronic ETOH abuse,
  smoking, chronic steroid use, recent respiratory
  infection
• Overall mortality rate is 10!

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Meningococcemia Etiology

• Caused by Neisseria meningitidis a gram neg.
  diplococcus, aerobic, encapsulated organism w/13
  serotypes
• N. meningitidis attaches to nonciliated
  epithelial cells in the nasopharynx and either
  becomes an asymptomatic carrier state or produces
  a mild URI syndrome.
• If it enters the bloodstream may see localized
  infection, bacteremia, sepsis or fulminant
  infection

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Meningococcemia Clinical

• Clinical presentation ranges from mild febrile
  illness to fulminant disease and death w/in hours
• May see fever, irritability, lethargy, myalgias,
  emesis, diarrhea, cough, rhinorrhea
• Only 60 of pts. Have classic signs of
  meningococcemia fever, petechiae or purpura

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Meningococcemia Clinical

• Meningococcal meningitis may present as fever,
  HA, photophobia, vomiting and signs of meningeal
  inflammation
• Infants and small children may present as fever,
  irritability, vomiting
• Purpura fulminans occurs in children, usually
  assoc. w/DIC.
• characterized by rapidly spreading ecchymosis
  and gangrene of the extremities

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Purpura
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Petechiae
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Meningococcemia Clinical

• Fulminant meningococcemia Waterhouse
  Friderichsen Syndrome
• Extreme severity of illness, shock like state
• Diffuse petechiae and purpuric rash
• Shock, CHF, DIC, Renal failure, coma possible
• Bilateral adrenal hemorrhage

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Meningococcemia Diagnosis

• Diagnosis of N. meningitidis is confirmed by
  isolation from blood cultures, CSF, synovial,
  pleural or pericardial fluid
• WBC count may be high, low or normal
• Bandemia is typically present

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Meningococcemia D/Dx

• Strep. Pneumo
• H. Flu
• N. Gonorrhea
• Viral exanthem
• RMSF
• Typhus
• Endocarditis
• Vasculitis(HSP)

• Toxic Shock
• Acute Rheumatic fever
• Drug rxns
• ITP
• TTP

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Meningococcemia Complications

• Most common complication is myocarditis w/CHF or
  conduction abnormalities
• Respiratory failure
• Renal failure
• Cranial nerve palsies
• Vasculitis
• Purulent arthritis

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Meningococcemia Treatment

• Immediate antibiotics lab ID use PCN G or
  ampicillin
• Alternatives are cefotaxime, ceftriaxone,
  chloramphenicol
• Airway mgmt, IVF support and vasopressor support,
  glucocorticoid therapy for refractory shock

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Meningococcemia Prophylaxis Vaccination

• Antibiotic prophylaxis for close contacts such as
  household, nursery school, daycare, intimate
  contacts, health care workers
• Use rifampin for 4 doses or Cipro
• Vaccine to children 2 years or older in high risk
  groups such as functional or anatomic asplenia or
  complement def.

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Kawasakis Disease

• KD is an acute febrile systemic vasculitis of
  unknown etiology
• Also called Acute Febrile Mucocutaneous Lymph
  Node Syndrome

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Kawasakis Disease Epidemiology

• Peak incidence is in 1-2 year olds
• Most prevalent in Asian descent
• 3000 cases annually
• Overall mortality is 2.5 and is a result of
  cardiac complications

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Kawasakis Disease Etiology

• KD is a systemic vasculitis
• There is some link between mechanism of vascular
  injury and immune system activation
• Vasculitis affects medium sized vessels
• Inflammation in the coronary arteries can cause
  myocarditis and aneurysms

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Kawasakis Disease Clinical

• Fever for at least 5 days and four of the
  following 5 signs
• 1. Bilateral conjunctival injection
• 2. Oral mucosa changes
• Erythematous dry fissured lips
• Strawberry tongue
• Erythematous oropharynx
• 3. Hand and feet changes
• Erythema of palms soles
• Edema of hand feet
• Periungal desquamation
• 4. Rash
• 5. Cervical lymphadenopathy

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Mucocutaneous involvement
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Edema of hands
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Kawasakis Disease Clinical

• Cardiac involvement is the hallmark of the
  disease
• KD is most common cause of acquired pediatric
  heart disease in U.S.
• May see myocarditis, CHF, Tachycardia
• Coronary artery aneurysms
• Mortality is from coronary artery aneurysm
  rupture or MI

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Coronary Artery Aneurysm
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Kawasakis Disease Diagnosis

• Fever 5 days plus 4/5 criteria
• No definitive test
• EKG, Echo
• CBC, CRP, ESR, CMP w/LFTs
• May see elevated WBC w/left shift, normochromic
  normocytic anemia, elevated plt ct 1,000,000
• Pts. w/KD should have UA, blood cx, CXR, ASO
  titer, GABHS throat cx to exclude other diagnosis

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Kawasakis Disease D/Dx

• Measles
• Toxic shock
• Scarlet Fever
• Leptospirosis
• Stevens Johnson Syndrome
• Staph. Scalded skin syndrome
• Influenza

• RMSF
• Juv. RA
• Drug rxn
• Viral infection
• Mercury toxicity
• Retropharyngeal abscess
• GABHS infections

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Kawaskis Disease Complications

• Coronary artery aneurysm is most serious
  complication
• Occurs in 20-25 of untreated pts., occurs in
  3-4 of those treated w/IV immunoglobulin and ASA
• Other complications MI, CHF, myocarditis

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Kawasakis Treatment

• Hospitalize pt.
• Includes administration of ASA and IV gamma
  globulin
• ASA 80-100mg/kg/day for 6-8 wks
• If coronary artery abnormalities exist, can use
  dipyridamole
• Coumadin or heparin for severe coronary disease

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Toxic Shock Syndrome Epidemiology

• Toxic Shock Syndrome is a toxin mediated systemic
  inflammatory response syndrome
• Menstruation remains most common setting
• 200 cases a year
• Nonmenstrual TSS is assoc. w/superinfection of
  various skin lesions/soft tissue infections
  strep TSS
• Mortality rate of staph TSS is 3, strep TSS is
  30-70

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Toxic Shock Syndrome Etiology

• Staphylococcal TSS is caused by colonization or
  infection w/toxigenic strains of S. aureus
• Streptococcal TSS is caused by infection
  w/toxigenic strains of group A strep(GAS).
• Staph. Aureus produces toxic shock syndrome
  toxin(TSST-1)
• GAS produces streptococcal pyrogenic exotoxin

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Toxic Shock Syndrome Risk Factors

• Use of super absorbent tampon
• Post-op wound infection
• Post-partum period
• Nasal packing
• Bacterial infections

• Varicella or Influenza A infection
• DM
• HIV
• Chronic cardiac pulmonary disease

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Toxic Shock Syndrome Case Definition for Staph.
Aureus TSS

• Fever 38.9C
• Diffuse erythroderma rash
• Palm and sole desquamation rash 1-2 wks later
• Hypotension
• Multisystem involvement 3 or more of following
• GI N/V/D
• Muscular myalgias or incr. CPK
• Mucus Membrane hyperemia
• Renal elevated BUN/Cr.
• Hepatic elevated LFTs, bili
• Heme plts.
• CNS Altered mental status

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Toxic Shock Syndrome Case Definition for Strep
TSS

• Isolation of group A strep from body site
• Clinical signs 2 or more
• Hypotension and
• Renal impairment
• Coagulopathy
• Liver abnormalities
• ARDS
• Necrotizing fasciitis
• Erythematous rash

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TSS Clinical

• The clinical presentations of strep TSS and staph
  TSS are similar
• The primary difference is an identifiable
  infectious source is always present w/strep TSS
  and colonization alone may be the only source in
  staph TSS

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TSS Clinical

• Fever, chills
• N/V/D
• Myalgias
• Pharyngitis
• HA
• Sepsis w/organ dysfunction
• Rash
• Altered mental status

• Conjunctival erythema
• Strawberry tongue
• Peripheral edema

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Erythematous rash
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TSS Diagnosis

• See case definitions
• May see leukocytosis or leukopenia, bandemia
• CXR
• LP prn
• EKG

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TSS D/Dx

• Kawasakis Disease
• Staph Scaled skin syndrome
• Scarlet fever
• Drug rxns/Stevens Johnson
• RMSF

• Leptospirosis
• Meningococcemia
• Gram neg. sepsis
• Measles
• Viral illness

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TSS Complications

• ARDS
• Shock
• Gangrene
• DIC
• Rhabdo/Renal failure
• Seizures
• Pancreatitis
• Pericarditis
• Cardiomyopathy
• Neuropsychiatric symptoms

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TSS Management

• Aggressive fluids
• O2, monitor
• Source of bacteria removed(tampons, nasal
  packing, wound debridement)
• Antibiotics clinda, nafcillin or oxacillin
• Refractory case use IV immunoglobulin

108
Summary

• All pts. Appearing septic should be treated
  w/broad spectrum antibiotics ASAP
• Immunity to Diphtheria, pertussis, tetanus wanes
  in adults. Think of pertusssis as a cause of
  persistent cough in adults. Update Td in trauma
  or infection
• Botulism should be in differential for infant who
  presents w/failure to thrive, constipation or
  decreased muscle tone. Also in IV drug abuser
  w/neurologic symptoms
• IV GG should be given as soon as KD is diagnosed