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

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Presentation on theme: "Dr. Cserynik Jan. 18, 2007 Slides by Bogdan Irimies PGY 4 EM Resident"— Presentation transcript:

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

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