R2 ??? / Vs. ?????

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• R2 ??? / Vs. ?????

2
History

• This 12-year-old boy was suffered from fever,
  cough, and abdominal pain for 3 days.
• He is a victim of acute rheumatic fever,
  including arthritis and carditis and received
  regular Penicillin-G treatment monthly for 1 year.

3
History

• He got an insert bite in his right lower leg with
  a small infected wound the wound was treated at
  home and improved.

4
History

• However, about 1 week later, the symptoms of
  low-grade fever, cough and abdominal pain with
  fullness sensation were noted.
• 3 days later, progressive dyspnea during exertion
  was noted and then he was sent to our hospital
  for help.

5
Physical examination

• The physical examination showed respiratory
  distress, bilateral coarse breathing sounds,
  grade ?-?/? systolic murmurs over LSB, distended
  abdomen, dilated jugular and superficial veins,
  hepatosplenomegaly and pitting edema of bilateral
  lower legs.
• A small healed insert bite wound over right lower
  leg.

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Image

• The CXR showed minimal right side pleural
  effusion with normal heart size.

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Laboratory data

• WBC14100
• Neutrophil67 (40-74)
• Lymphocyte20 (19-48)
• Monocyte11 (3.4-9)
• CRP8.4 mg/dl (0-0.5)
• Albumin3.0 g/dl (3.4-4.8)
• BUN8 mg/dl (7-20) Creatinine0.5 (0.5-1)
• AST126 U/L (-37) ALT107 U/L (-41)
• Total bilirubin 1.2 mg/dl
• Na135 mmol/L (136-145) K3.4 mmol/L (3.5-5.1)
  Cl98 mmol/L

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Admission course

• Echocardiography
• Tricuspid valve regurgitation
• Mitral valve regurgitation
• Pulmonary valve regurgitation

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Admission course

• Abdominal sonography
• Hepatosplenomegaly
• Patent hepatic artery and portal vein
• Mild to moderate ascites

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Subjective findings

• Fever
• Cough
• Abdominal pain with fullness
• Exertional dyspnea
• Insert bite

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Objective findings

• Coarse breathing sounds
• Systolic heart murmurs over LLSB
• Pitting edema over bilateral lower legs.
• Hepatosplenomegaly
• Wound of insert bite

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Objective findings

• Liver function impairment
• Hypoalbuminemia
• Hyponatremia
• Elevated CRP level
• Elevated WBC count
• Pleural effusion
• MR, TR, PR.

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Problems

• R/O Heart failure
• Fever
• Insert bite
• Hepatosplenomegaly
• Impaired liver functions
• Pleural effusion
• Ascites

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Question

• Patient traveling history
• EKG finding (arrhythmia, ST or T wave change)
• Echocardiography findings (compared with
  previous)
• Arterial blood gas (hypoxia, hypercapnea)
• Bacterial culture (blood,pleural effusion)
• Virus isolation and identification
• Pleural effusion study (transudate or exudate,
  AFB stain)
• Heart rate, blood pressure (arrhythmia,
  hypertension)
• Anemia or thrombocytopenia (hematologic
  abnormalities)
• Urine routine (Proteinuria ,hematuria)
• Indirect fluorescent antibody assay serology

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Causes of splenomegaly

• Infection
• Bacterial Typhoid fever, endocarditis,
  septicemia, abscess
• ViralE-B virus, CMV, and others
• Protozoal Malaria, toxoplasmosis
• Hematologic processes
• Hemolytic anemia Congenital, acquired
• Extramedullary hematopoiesis thalassemia,
  osteopetrosis, myelofibrosis
• Neoplasms
• Malignant Leukemia, lymphoma, histiocytoses,
  metastatic tumors
• Benign Hemagioma, hamartoma
• Metabolic diseases
• Lipidosis Niemann-Pick, Gaucher disease
• Mucopolysaccharidosis infiltration Histiocytosis
• Congestion
• Cirrhosis
• Cysts
• Miscellaneous

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Causes of ascites

• Hepatic (cirrhosis, fibrosis, obstruction)
• Renal (nephrotic syndrome, obstrutive, PD)
• Cardiac (heart failure, constrictive
  pericarditis)
• Infectious (abscess,TB, Chlamydia, schistosomia)
• Gastraointestinal (infarcted bowel perforation)
• Neoplastic (lymphoma, neuroblastoma)
• Pancreatic (pancreatitis, ruptured pancreatic
  duct)
• GYN (ovarian tumor, torsion, rupture)
• Miscellaneous (SLE, VP shunt, chylous,
  hypothyroidism)

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Heart failure

• Symptoms
• Fatigue, effort intolerance, anorexia, abdominal
  pain, dyspnea, cough
• Sign
• Engorged jugular vein, hepatomegaly, basilar
  rales, edema, cardiomegaly, gallop rhythm,
  holosystolic murmur of mitral or tricuspid valve
  regurgitation may be heard when ventricular
  dilatation is advanced.

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Heart failure

• Sign
• Pitting edema occurred usually in the legs.
• Pitting edema of the arms and face occurs rarely
  and then only in the late course of HF.
• Ascites occurred most frequently in patients with
  tricuspid valve disease or constrictive
  pericarditis

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Heart failure

• Chest X ray
• Exaggeration of the pulmonary arterial vessels to
  the periphery of the lung fields. (Patients with
  cardiomyopathy may have a relatively normal
  pulmonary vascular bed early in the course of
  disease)
• Cardiomegaly is invariable noted.
• Pleural effusion was more frequent in the right
  side than in the left side.

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Heart failure

• EKG
• Left or right ventricular ischemic changes may
  correlate well with clinical and other non
  invasive parameters of ventricular function.
• Low voltage QRS morphologic characteristic with
  ST-T wave abnormaluties may also suggest
  myocardial inflammatory disease but can be seen
  with pericarditis
• Rhythm disease is also a potential cause of heart
  failure.

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Diagnosis of congestive heart failure(Framingham
criteria)

• Major criteria (at least 1)
• Paroxysmal nocturnal dyspnea
• Neck vein distention
• Rales
• Cardiomegaly
• Acute pulmonary edema
• S3 gallop
• Increased venous pressure (gt16 cm H2O)
• Positive hepatojugular reflux
• Minor criteria (at least 2)
• Extremity edema
• Night cough
• Dyspnea on exertion
• Hepatomegaly
• Pleural effusion
• Vital capacity reduced by 1/3 from normal
• Tachycardia (gt120 bpm)

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Acute versus Chronic

• Acute Sudden development of myocardial infection
  or rupture of a cardiac valve, no cardiomegaly,
  no peripheral edema.
• Chronic Dilated cardiomyopathy, multiple
  valvular heart disease, cardiomegaly, peripheral
  edema.

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Right sided versus left sided

• Left Dyspnea or orthorpnea as the result of
  pulmonary congestion.
• Right Edema, congestive hepatomegaly, systemic
  venous distention.

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Carditis in rheumatic fever

• Rheumatic carditis is characterized by
  pancarditis, with active inflammation of
  myocardium, pericardium, and endocardium.
• Endocarditis, which is manifest by one or more
  cardiac murmurs, is a universal finding in
  rheumatic carditis.
• Most case consist of mitral valvular disease or
  combined aortic and mitral valvular disease.
• Isolated aortic or right side valvular
  involvement is uncommon.

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Rheumatic heart disease

• Mitral valve MR will result in increased atrium
  pressure and pulmoary congestion and symptoms of
  left side heart failure. Spontaneous improvement
  usually occurs with time even in sever cases. In
  chronic MR, pulmonary arterial pressure elevated
  and right ventricle and atrium become enlarged
  and right side heart failure develops.
• MS will result in increased pressure and
  enlargement and hypertrophy of the left atrium,
  pulmonary venous hypertension, increased vascular
  resistance and pulmonary hypertension.
• Aortic valve AR will lead to volume overload
  with dilatation of LV.
• Right-sided heart manifestations are rare.
• Tricuspid valve Primary tricuspid involvement is
  rare after rheumatic fever. TR is more common
  secondary to right ventricular dilatation
  resulting from unrepaired left side lesion.
• Pulmonary valve PR usually occurs on a
  functional basis secondary to pulmonary
  hypertension and is a late finding with severe
  mitral valve stenosis.

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Pulmonary regurgitation

• Isolated congenital pulmonary regurgitation is
  rare.
• Pulmoary valvular insufficiency most often
  accompanies other cardiovascular disease or may
  be secondary to severe pulmonary hypertension.

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Tricuspid regurgitation

• Tricuspid regurgitation usually functional.
• Secondary to marked RV dilatation of any cause
  and often associated with pulmonary hypertension.
• When volume overload or intrinsic myocardial
  disease -gt dilated right ventricle.
• Tricuspid regurgitation often accompanies with
  right ventricular dysfunction.

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Pulmonary regurgitation Tricuspid regurgitation

• Pulmonary hypertension
• Cardiovascular disease -gt RV dysfunction

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Causes of pulmonary hypertension

• Conditions directly affecting pulmonary
  arteriesPrimary pulmonary hypertensionToxin-indu
  ced (ie, anorexic agents)VasculitisGranulomatose
  s, collagen-vascular disorders, arteritisHepatic
  cirrhosis/portal diseaseCongenital heart disease
  (Eisenmenger syndrome ASD, VSD,
  PDA)InfectionHuman immunodeficiency virus

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Causes of pulmonary hypertension

• Conditions affecting pulmonary
  parenchymaChronic obstructive lung
  diseaseInfiltrative/granulomatous
  diseasesSarcoidosis, pneumoconiosis, radiation,
  fibrosis, neoplasm, pneumonia, collagen-vascular
  diseasesCystic fibrosisUpper airway
  obstructionHigh-altitude diseaseArteriovenous
  fistulas within the lungRestrictive lung
  diseases

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Causes of pulmonary hypertension

• Conditions affecting the thoracic cage and
  neuromuscular systemObesity-hypoventilation/sleep
  apneaPharyngeal-tracheal obstructionKyphoscolio
  sisPleural fibrosisNeuromuscular
  disordersMyasthenia gravis, poliomyelitis,
  central respiratory disorders

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Causes of pulmonary hypertension

• Conditions causing left atrial/or pulmonary
  venous hypertensionElevated left ventricular
  diastolic pressureSystolic failure, diastolic
  dysfunction, constrictive pericarditisAortic
  valve diseaseMitral valve diseaseCor
  triatriatumLeft atrial massesMyxoma or
  neoplasm, thrombusFibrosing mediastinitisCongeni
  tal pulmonary vein stenosisAnomalous pulmonary
  venous connectionPulmonary venoocclusive disease

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Causes of pulmonary hypertension

• Nonvasculitis conditions that result in pulmonary
  artery obstructionAcute and chronic
  thromboembolismHemoglobinopathies (eg, sickle
  cell disease)Primary or metastatic
  malignanciesPeripheral pulmonic stenosis
• Congenital pulmonary hypoplasia

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Vasculitis syndrome

• Goodpasture disease
• Pulmonary hemorrhage and glomerulonephritis.
• Symptoms signs
• Hemoptysis, hematuria, proteinuria and
  hypertension.

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Vasculitis syndrome

• Wegener Granulomatosis
• Fever, myalgia, cough, nasal discharge, hematuria
  proteinuria.
• Hemoptysis and dyspnea from lung lesion.
• Uveitis, conjuctivitis.
• Peripheral granuloma.
• Palpalbe purpuric nodules and ulcers

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Vasculitis syndrome

• Polyarteritis Nodosa
• Associated with infection of group A
  streptococcus, hepatitis B, CMV, parvovirus , TB,
  E-B virus.
• Symptoms signs.
• Fever
• Abdominal pain (mesenteric arterial inflammation)
• Hypertension, hematuria, proteinuria (renal
  vessels)
• Purpura, edema, painful nodule (skin involvement)
• Heart failure (myocarditis, myocardial ischemia)
• Elevated liver function (hepatitis B infection
  more common in adults)
• Elevated ESR, anemia and leukocytosis

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An algorithm for the workup of a patient with
unexplained pulmonary hypertension
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Pulmonary embolism

• Precipitating factor
• CVP insertion, immobility, heart disease, oral
  contraceptives, ventriculoatrial shunt, trauma,
  infection, dehydration, collagen vascular
  disease, shock , obesity, hematologic disorder.
• Symptoms
• Chest pain, dyspnea, cough, fever, hemoptysis.
• Signs
• Rales, heart murmurs, tachycardia, fever,
  diaphoresis, phlebitis, wheezing.

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Pulmonary embolism

• Lab
• ABG Respiratory alkalosis, arterial hypoxemia
• Elevated WBC count, D-dimer, fibrinogen, protein
  C, protein S.
• Chest Often normal in patient with PE.
• EKG Nonspecific ST segment change and signs of
  cor pulmonale
• Ventilation-perfusion image Regional blood flow
  and ventilation defects . But normal V-P scan
  cant exclude a PE and are interpreted as high
  probability, intermediate probability, low
  probability, very low probability and normal.
  Lung disease can limit the utility of this study.
  
• Pulmonary angiography is the gold standard
  diagnostic test for pulmonary embolism.

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Cause of heart failure in child

• Rheumatic fever
• Acute hypertension
• Thyrotoxicosis
• Hemochromatosis-hemosiderosis
• Cancer therapy (radiation, doxorubincin)
• Sickle cell anemia
• Endocarditis
• Cardiomyopathy (Viral myocarditis, nonviral)
• Myocarditis, hypertrophic, dilated.)
• Cor pulmoale (cystic fibrosis)

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Pulmonary regurgitation Tricuspid regurgitation

• Pulmonary hypertension
• Infection
• Pulmonary embolism
• Cardiovascular disease -gt RV dysfunction
• Rheumatic fever
• Endocarditis
• Cardiomyopathy (carditis, dilated, hypertrophic )

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Acute rheumatic fever

• Major (least 2 major or 12 minor)
• Carditis, polyarthritis, erythema marginatum,
  subcutaneous nodules
• Minor
• Fever, arthralgia, elevated ESR or CRP, prolonged
  PR interval
• Supported evidence of GAS infection
• Positive throat culture or streptococcal antigen
  test
• Elevated or increased streptococcal antibody titer

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Infectious endocarditis

• Etiology Viridans-type streptococci and
  staphylococcus aureus are the leading causative
  agents responsible for endocarditis in pediatric
  patients.
• Infective endocarditis is often a complication of
  congenital or rheumatic heart disease
• Prolonged fever without other manifestation.
• Low grade fever, fatigue, myalgia, arthralgia,
  headache, and at times, chills, nausea, and
  vomiting.
• Splenomegaly and petechiae are relative common.
• Osler nodes (tender, pea-sized intradermal
  nodules in the pads of the fingers and toes),
  Janeway lesion (painless small erythematous or
  hemorrhagic lesion on the palms and soles),
  splinter hemorrhages (linear lesions beneath the
  nails)
• Embolic strokes, cerebral abscess, mycotic
  aneurysm, and hemorrhage in staphylococcus
  disease.

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Infectious endocarditis

• History
• Congenital or rheumatic heart disease
• Preceding dental, urinary tract or intestinal
  procedure
• Intravenous drugs abuse
• Central venous catheter
• Prosthetic heart valve
• Symptoms
• Fever, chills, chest and abdominal pain,
  arthralgia, myalgia, dyspnea, malaise, night
  sweats, weight loss, CNS manifestations

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Infectious endocarditis

• Signs
• Elevated temperature, tachycardia, embolic
  phenomena (Roth spots, petechia, splinter nail
  bed hemorrahge, Osler nodes, CNS or ocular
  lesions), Janeway lesions, New or changing
  murmur, splenomegaly, arthritis, heart failure,
  arrythmias, Metastatic infection (arthritis,
  meningitis, mycotic arterial aneurysm,
  pericarditis, abscesses, septic pulmonary
  emboli), clubbing
• Labs
• Blood culture (), ESR ?, CRP?, anemia,
  leukocytosis, immune complexes,
  hypergammaglobulinemia, hypocomplementemia,
  rheumatoid factor, hematuria, renal failure
• Chest X ray bilateral infiltration, nodules,
  pleural effusions
• Echocardiography valve vegetations, prosthetic
  valve dysfunction or leak, myocardial abscess,
  new-onset valve insufficiency.

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Infectious endocarditis

• Duke criteria
• Major 1.Blood culture () 2.Evidence of
  endocarditis on echocardiography (intracardiac
  mass on a valve or other site, regurgitation flow
  near a prosthesis, abscess, partial dehiscence of
  prosthetic valves or new valve regurgitation
  flow)
• Minorfever, embolic-vascular signs, immune
  complex phenomena (GN, arthritis, rheumatoid
  factor, Osler nodes, Roth spots),
• 2 major 1 minor
• 1 major 3 minors
• 5 minors

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Infectious endocarditis

• Etiology
• Common Native valve or other cardiac lesions
• Viridans group streptococcus (dental procedure)
• Staphylococcus aureus (drugs abuse)
• Group D streptococcus (GU or GI tract procedures)
• Uncommon Native valve or other cardiac lesions
• Streptococcus pneumoniae
• Haemophilus influenzae
• Coagulase-negative staphylococci
• Coxiella burnetii (tick borne)
• Neisseria gonorrhoeae (in human, sexual ,
  intimate contact)
• Brucella (zoonotic disease, contact with infected
  animals)
• Chlamydia psittacli, Chlamydia trachomatis,
  Chlamydia pneumoniae (human, sexual,respira)
• Legionella (fresh water or aerosols containing
  bacteria)
• Bartonella (cat scratch)
• HACEK group (H respiratoryAtrauma, aspiration
  to lung, )
• Streptobacillus moniliformis
• Pasteurella multocida (chesse, milk )
• Campylobacter fetus

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Myocarditis

• Symptoms
• Fever, severe heart failure, respiratory
  distress.
• Incubation time1-7 days of the onset of
  symptoms.
• Signs
• Cyanosis, distant heart sounds, weak pulses,
  tachycardia, Gallop rhythm, acidosis, and shock.
• Evidence of hepatitis, aseptic meningitis,
  associated rash may be present.

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Myocarditis

• Lab
• Elevated CK, LDH
• EKG Sinus tachycardia, reduced QRS voltage,
  ST-segment and T-wave abnormalities, arrhythmia.
• Echo poor ventricular function, pericardial
  effusion, mitral valve regurgitation, absence of
  congenital heart lesion or coronary artery

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Etiology of myocardial disease

• Familial-Hereditary (myopathy, cardiomyopathy)
• Infection (Virus, Richettsiae, Bacteria,parasite,f
  ungus)
• Metabolic, nutritional, endocarine
• Connective tissue-Granulomatous
  disease-infiltrative (SLE, vasculitis,
  Scleroderma, sarcoidosis, dermatomyositis,
  leukemia)
• Drugs-Toxins (chemo, alcohol,irradiation.)
• Coronary arteries (Kawasaki disease, meidal
  necrosis, anomalous left coronary artery)
• Other (anemia, ischemia)

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Etiology of myocardial disease

• Infection
• Virus
• Coxsackievirus A and B
• Adenovirus
• HIV
• Echovirus
• Rubella
• Varicella
• Influenza
• Mumps
• Epstein-Barr
• Measles
• Poliomyelitis.

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Etiology of myocardial disease

• Infection
• Richettsiae
• Psittacosis
• Q fever, Coxiella burnetii(Ticks)
• Rocky Moutain spotted fever. (Tick bites)
• Bacterial
• Diphtheria (respiratory, cutaneous)
• Mycoplasma (airborne, human to human)
• Meningococcus (respiratory)
• Leptospirosis (water or soil contaminated with
  rat urine)
• Lyme disease (tick bites)
• Typhoid fever (foods or water contaminate with
  human feces)
• Tuberculosis (airborne, human to human)
• Streptococcus (respiratory, dental procedure)
• Listeriosis (food(cheese, milk) contaminate with
  feces of animals)

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Etiology of myocardial disease

• Infection
• Parasites
• Chagas disease (kissing bugs)
• Toxoplasmosis (food or water comtaminated by cat
  feces)
• Loa loa (biting flies)
• Toxocara canis (dog feces)
• Schistosomiasis (contact water contaminated with
  cercaria)
• Cysticercosis
• Echinococcus
• Trichinosis. (meat with larvae of trichinella)
• Fungi
• Histoplasmosis.
• Coccidiomyocosis.
• Actiomycosis.

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Differential problems

• R/O Pulmonary hypertension
• R/O Pulmonary embolism
• R/O Cardiomyopathy
• Hepatosplenomegaly
• Insert bite transmitted disease

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Richettsial infection

• Spotted fever group
• Typhus
• Scrub typhus
• Ehrlichioses and Anaplasmosis
• Q fever

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Richettsial infection

• Spotted fever group
• Rocky Mountain spotted feverr
• Mediterranean Spotted fever
• African tick-bite fever
• Rickettsialpox
• Murine typhus-like

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Spotted fever group

• Rocky mountain spotted fever
• Tick bite transmission disease (HostDogs,
  rodents)
• United states, southwestern, Canada, Mexico,
  Central America, South America
• The incubation period 2-14 days (median 7 days)
• Headache, fever, anorexia, myalgia, restlessness.
• GI symptoms(39-63) Nausea, vomiting, diarrhea,
  abdominal pain.
• Skin rash Maculopapules onset after the 3rd day
  of illness -gt petechia or purpura after several
  days. (4974) (1st day 14, 3rd day49)
• Hepatosplenomegaly (33)
• Clinical triad Headache, fever, rash
• Lab data Low leukocyte count with left shift
  low platelet count low serum sodium are clues
  for RMSF, impaired liver function (38)
• Severe case may present myocarditis, facial
  edema, DIC, non cardiogenic pulmonary edema,
  respiratory distress.
• Diagnosis Immunohistologic demonstration of
  specific rickettsial antigen (IFA, DFA, IH
  sensitivity 70) (single IFA tiltergt164 or 4
  fold increased between acute and convalescent
  sera (2-4 wk apart))
• Treatment Doxycycline (2.2mg/Kg/dose
  q12h-gt2.2mg/Kg/D divided q12h)
• Tetracycline (25-50mg/Kg/D q6h po)
  Chloramphenicol (50-100mg/Kg/D q6h iv) at least 5
  days until afebrile 2-4 days.

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Spotted fever group

• Mediterranean Spotted fever
• Tick bite transmission disease (Host Dogs,
  rodents)
• Pathogen R. conorii
• India, Pakistan, Russia, Ukraine, Georgia,
  Israel, Ethiopia, Kenya, South Africa, Morocco,
  and Southern Europe.
• Fever, headache, myalgias, maculopapular rash
  which appears 3-5 days after onset of symptoms.
• 70 of patient have eschar, tache noire, regional
  lymphadenopathy.
• 6 of cases Purpuric skin lesion, neurologic
  signs,myocarditis, respiratory distress, acute
  renal failure, thrombocytopenia.
• Diagnosis Immunohistologic demonstration of
  specific rickettsial antigen
• Treatment tetracycline, doxycycline,
  chloramphenichol
• Azithromycin (10mg/Kg/D once daily po) and
  clarithromycin (15mg/Kg/D bid po)

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Spotted fever group

• Rickettsialpox
• Mite bite transmission disease (Host Mouse,
  rodents)
• Pathogen R. akari
• United States, Europe, and Asia.
• 90 papular or ulcerative lesion at the initial
  site of inoculation.
• Varicelliform rash (maculopapular rash may become
  vesicular), fever, headache, chills
• The infection resolves spontaneously even without
  therapy.

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Scrub typhus

• Scrub typhus
• Chigger bite transmission disease (Host Rats, )
• Pathogen Orientia tsutsugamushi
• Southern Asia, Japan, Indonesia, Australia,
  Korea, Asiatic Russia, India, China
• Incubation period6-21 days.
• lt50 of cases necrotic eschar with an
  erythematous rim
• Fever, headache, myalgia, cough and GI symptoms.
• Regional or generalized lymphadenopathy is
  common.
• lt50 of patients presents maculopapular rash.
• Complications Meningoencephalitis, myocarditis,
  interstitial pneumonitis.
• Diagnosisindirect fluorescent antibody assay or
  immunoperoxidase serologic tests of O.
  tsutsugamushi antigen
• Treatment Doxycycline tetracycline
  chloramphenicol at least 5 days until afebrile
  2-4 days.

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Typhus Group Rickettsioses

• Murine Typhus
• Rat flea or cat flea feces transmission disease
  (Host Rats )
• Pathogen Richesttsia typhi (mouse flea) R.
  felis(cat flea)
• Distribution Worldwide.
• Incubation period 1 to 2 weeks
• Fever, rash (48-80), myalgias (29-57), vomiting
  (29-45), cough (15-40), headache (19-77), and
  diarrhea or abdominal pain(10-40)
• Usually maculopapule rashs distributed on the
  trunk and extremities.
• Neurologic involvement(photophobia, confusion,
  stupor, coma, seizures, meningismus and ataxia)
  may be a frequent finding in adults 17 of
  hospitalized and 6 of outpatients of infected
  children.
• Lab data Leukopenia with left shift(36-40)
  thrombocytopenia(43-60) Hyponatremia(20-66)
  Hypoalbuminemia (46-87) elevated AST and ALT
• DiagnosisIndirect fluorescent antibody assay
  serology
• Treatmet Doxycycline, tetracycline,
  chloramphenicol at least 5 days until afebrile
  2-4 days.

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Typhus Group Rickettsioses

• Epidemic typhus
• Louse feces (via wound or conjunctiva) disease
  (Host Human )
• Pathogen Richesttsia prowazekii
• Distribution Africa, South Amercia. Central
  America. Mexico, Asia.
• Incubation periodlt14 days.
• Fever, severe headache, abdominal pain, rash in
  most people
• Chills(82) myalgias(70) arthralgia(70)
  anorexia (48), nonproductive cough (38),
  dizziness (35), photophobia (33), nausea (32),
  abdominal pain (30), tinnitus (23) meningismus
  (17), visual disturbances (15), vomiting (10)
• Treatment Doxycycline tetracycline
  Chloraphenicol at least 5 days until afebrile 2-4
  days.

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Ehrlichioses and Anaplasmosis

• Ehrlichiosis and anaplasmosis
• Tick bite disease (Host Deer, dogs(HME) deer
  rodents, ruminants (HGE))
• Pathogen E. chaffeensis (Human monocytic
  ehrlichiosis (HME))
• Anaplasma phagocytophilum (Hauman anaplasmosis
  Human granulocytic ehrlichiosis (HGE))
• Distribution United states, Europe, Africa
• Incubation period2 days to 3 weeks.
• Fever(97), headache (81), myalgias(68),
  malaise (84) anorexia, and nausea or vomiting,
  maculopapular rash(2/3 of children with HME),
  conjunctivitis, pharyngitis and lymphadenopathy
  (minority),
• Hepatomegaly and splenomegaly (frequent),
  systolic ejection murmur (often)
• Lab data leuopenia (58-72) lymphopenia
  (75-78) thrombocytopenia(80-92) Granulomas
  and granulomatous inflammation in 75 in bone
  marrow examinations of HME Elevated transaminase
  levels Hyponatremia prolonged PT/PTT Morulae
  in peripheral blood monocyte or neutrophil.
• Diagnosis The demonstration of morulae, single
  high tilter (gt1128) of A. phargocytophilum
  antibodies or seroconversion (gt164)
• Treatment Doxycycline, Tetracycline at least 5
  days until afebrile 2-4 days.

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Q fever

• Acute Q fever
• Inhalation of infectious aerosols, ingestion of
  contaminated dairy products, ticks disease (Host
  Cattle, sheep, goats, cats, rabbits )
• Pathogen Coxiella burnetii
• Distribution Worldwide
• Incubation day 3-30 days.
• Fever, sever headache, arthralgia, myalgia,
  cough, fatigue, vomiting, abdominal pain.
• Hepatomegaly and splenomegaly may be detected in
  some patients.
• Fever (91), respiratory involvement (34) rash
  (11), neurologic findings (4)
• Lab data Leukopenia with left shift (50),
  thrombocytopenia (9-48), reative thrombocytosis
  in recovery state results in DVT, Elevated
  transaminase levels (62), elevated ESR (50)
• Hepatitis (40), Myocarditis, pericarditis.
• Right side endocarditis results in pulmonary
  embolism is reported.
• Self-limited illness that last for 2-36 weeks.

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Q fever

• Chronic Q fever
• Chronic Q fever occurred months to years after
  acute Q fever or even in the absence of any
  history of acute Q fever.
• Presents with endocarditis, hepatitis,
  myocarditis, FUO, pneumonia, osteomyelitis.
• Q fever endocarditis Fever may be absent in up
  to 15 of cases. More than 75 of all identified
  have congestive heart failure.
• Data ESR gt 20 mm/hr (80), hypergammaglobulinemia
  (54), hyperfibrinogenemia (67). Rheumatoid
  factor (gt50) , antiplatelet antibodies,
  anti-smooth muscle antibodies, antimitochondrial
  antibodies, positive direct Coombs test.
• Diagnosis (children with fever of unknown
  origin, atypical pneumonia, culture negative
  endocarditis) 4-fold increase in indirect
  fluorescent antibody tilters to phase 1 and phase
  2 antigens in acute and convalescent (2-4 weeks)
  sera
• Treatment AcuteTreated within 3 days of onset
  of symptoms with tetracycline or doxycycline.
• ChronicTetracycline or doxycycline rifampin,
  ofloxacin or pefloxacin. (18months until phase 1
  tilters of lt1200 for IgG and negative IgA
  tilters)

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Relapsing fever (Borrelia)

• Human louse, tick disease (Host Human )
• Pathogen Borrelia. Recurrentis
• Distribution Worldwide
• Incubation time 5-15 days(median 8 days)
• Fever lasting 2-9 days then a febrile periods of
  2-7 days.
• Symptoms High fever, delirium, lethaygy,
  headache, myalgia, arthralgia, photophobis,nausea,
  vomiting, abdominal pain, productive cough, mild
  respiratory distress, bleeding tendency(epistaxis,
  hemoptysis, hematuria, hematemesis), skin rash
• Sings lymphadenopathy, splenomegaly, hepatic
  tenderness with hepatomegaly is a common sign,
  jaundice (50)
• Severe complication CNS, mycocarditis, hepatic
  failure, DIC.
• Diagnosis spirochete in Giemsa or Wrights stain
• Treatment Doxycycline (500mg po q6h),
  erythromycin (50mg/Kg/D) for lt12 years old
  children.

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Lyme disease

• Lyme disease
• Tick bite disease (Host Deer, Rodent)
• Pathogen Borrelia burdorferi
• DistributionWorldwide
• Early localized disease typical annular rash,
  erythema migrans(90) occurs in 7-14 days after
  the bite, it appear as a target lesion with
  central clearing and may be associated with
  systemic features including fever, myalgia,
  headache, malaise. Without treatment, the rash
  will expands to an average diameter of 15cm and
  remains present at least 1-2 wks.
• Early disseminated disease Multiple skin lesion,
  accompanied by fever, myalgia, headache, malaise
  conjunctivitis and lymphadenopathy may develop.
  Aseptic meningitis, uveitis, focal neurologic
  findings, especially cranioneuropathies, carditis
  with varying degrees of heart block, palalysis of
  the facial nerve is relatively common in
  children.
• Late disease Arthritis, especially the large
  joints (gt 90 in knees) with swollen and tender
  joints, chronic demyelinating encephalitis,
  polyneuritis, impairment of memories

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Lyme disease

• Diagnosis The presence of EM rashes gt 5cm in
  diameter or serologic confirmation of infection
  with evidence of at least one manifestation of
  musculo skeletal, neurological or cardiovascular
  disease .
• The culture of B. burgdorferi in
  Barbour-Stoenner-Kelly medium from the specimen
  of plasma, biopsy samples of erythema migrans
  lesions, occasionally from cerebrospinal fluid
  samples in patients with meningitis can permit a
  definitive diagnosis.
• Serologic tests was used as diagnostic method in
  public health surveillance and in clinical
  diagnosis. This Western Blot detects the presence
  or absence of antibodies and is not quantitative.
  Antibody can still be detected with Western blot
  even after a successful. It was used to confirm
  equivocal and positive serology results obtained
  by ELISA or IFA.
• Treatmentdoxycycline (100mg bid for 14-21 days)
  in children older than 8 yr of age Amoxicillin
  (50 mg /Kg/D tid po 14-21 days) cefuroxime
  (30mg/kg/D bid po for 14-21 days ) erythromycin
  (30-50mg/Kg/D qid for 14-21 days.)
• Meningitis Ceftriaxone 50-80 mg/Kg/D iv qd for
  14-28 days.
• Carditis Mild to moderate as EM Severe as
  meningitis
• Late disease the same as for EM except for 28
  days-gtrecurrence choose second dose or
  meningitis.

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Chagas disease

• Acute Chagas disease
• Kissing bugs bite transmission disease
• Pathogen Trypanosoma cruzi
• Distribution Western hemisphere (Mixeco, south
  America, Brazil, Argentina)
• Acute chagas disease mild fever, malaise, facial
  edema, lymphadenopathy, local sign of
  inflammation at the site entry(chagomas) .
• 50 with Romana sign (Unilateral, painless eye
  swelling), conjunctivitis, preauricular
  lymphadenitis
• Lymphadenopathy, hepatosplenomegaly,
  meningoencephalitis can occur in children
  younger than 2 years old.
• The heart is the primarily target organ, 4
  chamber dilatation, diffuse myocarditis and
  inflammation of the conduction system lead to the
  development of fibrosis.

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Chagas disease

• Chronic Chagas disease
• Chronic Chagas disease Cardiomyopathy included
  congestive heart failure, arrhythmia and
  thrombocytopenia events. EKG will showed complete
  A-V block, RBBB, LBBB, left ventricular apical
  aneurysm.
• Diagnosis Giemsa-stain smear will demonstrate
  motile trypanosomes.
• These are only seen in the peripheral blood in
  the first 6-12 week of the illness.
• Specific IgM antibodies in ELISA or IFA in acute
  Chagas disease.
• Complement fixation is considered the most
  reliable immunodiagnostic method for chronic
  Chagas disease.
• Treatment Nifurtimox (15-20mg/kg/D qid po(1-10
  y/o) 12.5-15mg/KG/D (11-16 y/o), 8-10mg/Kg/D(gt16
  y/o)) for 90 days and benznidazole (10mg/Kg/D bid
  po(lt12y/o) 5-7 mg/kg/D(gt12y/o)) for 60 days

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Impression

• Q fever
• Rocky mountain spotted fever

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Diagnosis of Q fever

• Q fever results from infection with C. burnetii.
• This small gram-negative microorganism (0.2 um by
  0.7 um) exists in two antigenic forms phase I
  and phase II.
• The phase I form is extremely infectious and
  exists in humans and other animals. Passage in
  cell culture or embryonated eggs results in a
  shift to the phase II form, which is avirulent.

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Diagnosis of Q fever

• C. burnetii can be isolated from buffy-coat blood
  samples or tissue specimens by a shell-vial
  technique C. burnetii since it is considered
  highly infectious.
• PCR can be used to amplify C. burnetii DNA from
  tissue or biopsy specimens. This technique can
  also be used on paraffin-embedded tissues.
• Serology is the most commonly used diagnostic
  tool. Three techniques are available complement
  fixation, indirect immunofluorescence, and
  enzyme-linked immunosorbent assay.
• Indirect immunofluorescence is sensitive and
  specific and is the method of choice.
• Rheumatoid factor should be adsorbed from the
  specimen before testing.

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Diagnosis of Q fever

• 4-fold increased in IFA titers to phase I and
  phase II antigens between acute and convalescent
  sera(2-4wks)
• An IgG titer of 1800 to phase I antigen is
  suggestive of chronic Q fever.
• In almost all instances of chronic Q fever, the
  antibody titer to phase I antigen is much higher
  than that to phase II antigen.
• The reverse is true in acute Q fever. In
  addition, in acute Q fever, it is usually
  possible to demonstrate a fourfold rise in titer
  between acute- and convalescent-phase serum
  samples.
• Elevated phase I IgA antibody are diagnostic for
  Q fever endocariditis.

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Diagnosis of RMSF

• The most common serologic test for confirmation
  of the diagnosis is the indirect
  immunofluorescence assay.
• Between 7 and 10 days after onset, a diagnostic
  titer of 164 is usually detectable.
• The sensitivity and specificity of the indirect
  immunofluorescence assay are 94 to 100 and 100
• The only diagnostic test that is useful during
  the acute illness is immunohistologic examination
  (immunofluorescence or immunoenzyme staining) of
  a cutaneous biopsy of a rash lesion for R.
  rickettsii.
• Examination of a 3-mm punch biopsy of such a
  lesion is 70 sensitive and 100 specific.