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

3. 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

4. Diphtheria: Corynebacterium diphtheria
Etiology/pathophysiology:
Gram + bacillius: korynee=club shaped bacteria; diphtheria=leather hide looking pharyngeal membrane
C. diphtheria produces exotoxin that causes pharyngeal membrane exudates and systemic effects of infection
Causes skin, respiratory, cardiac neurological manifestations

5. 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

6. Diphtheria Membrane:

7. Diphtheria Bull Neck:

8. Diphtheria: Corynebacterium diphtheria
Complications:
Airway obstruction from edema/membrane formation
CHF
Cardiac conduction disturbances
muscle paralysis

9. 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

10. Diphtheria: Corynebacterium diphtheria: D/Dx:
Strep/viral pharyngitis
Tonsillitis
Vincent’s angina
Epiglottitis
Mono
Laryngitis
Bronchitis
Tracheitis
Monilial infxn
Rhinitis

11. 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.

12. Pertussis:

13. Pertussis: Epidemiology
Localized respiratory illness transmitted by respiratory droplets
Avg incubation period 7-10 days
Neither vaccination nor prior infection confer lifelong immunity

14. Pertussis: Etiology Bordetella pertussis, gram neg. coccobacilli
Preferentially adheres to ciliated respiratory epithelial cells

15. 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

16. 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

17. Pertussis: Clinical
Convalescent stage: residual cough that lasts from several weeks to months
PE: low grade fever and tachypnea

18. 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

19. Pertussis: D/Dx Viral URI Pneumonia Bronchiolitis CF TB COPD Exac.
Foreign Body Aspiration

20. Pertussis: Complications
Periorbital edema
Subconjunctival hemorrhage
Petechiae
Epistaxis
Hemoptysis
SQ Emphysema
PTX
Pneumomediastinum
Diaphragmatic rupture
Hernia exac.
Rectal prolapse

21. Pertussis:Treatment O2, suctioning, hydration
Antibiotics doesn’t appear to reduce the severity of illness or duration especially if started in paroxysmal phase
Erythromycin>Azithromax> Bactrim
Postexposure prophylaxis w/erythromycin is recommended for household contacts of pts. w/pertussis regardless of previous vaccination status

22. Tetanus:

23. 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

24. 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

25. 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

26. 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

27. 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

28. Tetanus: Clinical Generalized:
Opisthotonus is a prolonged tonic contraction that resembles decorticate posturing
Autonomic dysfunction: tachy, HTN, fever, cardiac dysrythmia and diaphoresis

29. Opisthotonus:

30. Sardonic smile:

31. Tetanus: Clinical
Localized: persistent muscle spasm located near site of injury
Most cases do not progress to generalized tetanus

32. 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

33. Tetanus: Clinical Neonatal form: generalized tetanus of newborn
Symptoms begin during 1st week of life
Irritability and poor feeding seen

34. 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.”

35. 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

36. 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 & fx’s, long bone fx’s, shoulder & TMJ joint dislocations

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

38. 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

39. Tetanus: Treatment Administer Td immediately for active immunization
Prevention of further toxin production is thru wound debridement and irrigation
Metronidazole is antibiotic of choice

40. 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

41. Td Prophylaxis:

42. Botulism:

43. 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

44. 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

45. 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

46. 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

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

48. 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

49. Botulism: Clinical
Ocular signs: ptosis, extraocular palsies, dilated & fixed pupils
Muscle weakness: upper extremities more affected than lower, proximal weakness>distal muscles
Sensory exam is normal

50. 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

51. Infant Botulism:

52. Wound Botulism:

53. 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

54. Botulism: D/Dx Pharyngitis Gastroenteritis Guillain Barre Syndrome
Tick paralysis
Myasthenia Gravis
Poliomyelitis
Diphtheria
Eaton Lambert Syndrome
Anticholinergic toxicity
Organophosphate toxicity
Heavy metal poisoning
Mg+2 toxicity

55. Botulism: Complications
Complications are related to respiratory failure
Weakness of respiratory muscles

56. 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

57. 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

58. Pneumococcus:

59. 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.

60. 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 < 2 y/o
Risk Factors for pneumococcemia: chronic respiratory or CV disease, chronic ETOH abuse, cirrhosis, DM, impaired spleen(sickle cell), CRF, AIDS, cancer, organ transplant

61. 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

62. Pneumococcus:

63. 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

64. 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

65. 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

66. 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

67. 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

68. 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

69. 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

70. Meningococcemia: Epidemiology
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%!

71. 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

72. 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

73. 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

74. Purpura:

75. Petechiae:

76. 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

77. 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

78. 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

79. Meningococcemia: Complications
Most common complication is myocarditis w/CHF or conduction abnormalities
Respiratory failure
Renal failure
Cranial nerve palsies
Vasculitis
Purulent arthritis

80. 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

81. 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.

83. Kawasaki’s Disease:
KD is an acute febrile systemic vasculitis of unknown etiology
Also called Acute Febrile Mucocutaneous Lymph Node Syndrome

84. Kawasaki’s 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

85. Kawasaki’s 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

86. Kawasaki’s 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

87. Mucocutaneous involvement:

88. Edema of hands:

89. Kawasaki’s 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

90. Coronary Artery Aneurysm:

91. Kawasaki’s Disease: Diagnosis
Fever > 5 days plus 4/5 criteria
No definitive test
EKG, Echo
CBC, CRP, ESR, CMP w/LFT’s
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

92. Kawasaki’s 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

93. Kawaski’s 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

94. Kawasaki’s Treatment:
Hospitalize pt.
Includes administration of ASA and IV gamma globulin
ASA mg/kg/day for 6-8 wks
If coronary artery abnormalities exist, can use dipyridamole
Coumadin or heparin for severe coronary disease

96. 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%

97. 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

98. 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

99. 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 LFT’s, bili
Heme: plts. <100,000
CNS: Altered mental status

100. 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

101. 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

102. TSS: Clinical Fever, chills N/V/D Myalgias Pharyngitis HA
Sepsis w/organ dysfunction
Rash
Altered mental status
Conjunctival erythema
Strawberry tongue
Peripheral edema

103. Erythematous rash:

104. TSS: Diagnosis See case definitions
May see leukocytosis or leukopenia, bandemia
CXR
LP prn
EKG

105. TSS: D/Dx Kawasaki’s Disease Staph Scaled skin syndrome Scarlet fever
Drug rxns/Stevens Johnson
RMSF
Leptospirosis
Meningococcemia
Gram neg. sepsis
Measles
Viral illness

106. TSS: Complications ARDS Shock Gangrene DIC Rhabdo/Renal failure
Seizures
Pancreatitis
Pericarditis
Cardiomyopathy
Neuropsychiatric symptoms

107. 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