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

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Title: R2 ??? / Vs. ?????


1
?????????
  • ?????
  • 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.

6
Image
  • The CXR showed minimal right side pleural
    effusion with normal heart size.

7
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

8
Admission course
  • Echocardiography
  • Tricuspid valve regurgitation
  • Mitral valve regurgitation
  • Pulmonary valve regurgitation

9
Admission course
  • Abdominal sonography
  • Hepatosplenomegaly
  • Patent hepatic artery and portal vein
  • Mild to moderate ascites

10
Subjective findings
  • Fever
  • Cough
  • Abdominal pain with fullness
  • Exertional dyspnea
  • Insert bite

11
Objective findings
  • Coarse breathing sounds
  • Systolic heart murmurs over LLSB
  • Pitting edema over bilateral lower legs.
  • Hepatosplenomegaly
  • Wound of insert bite

12
Objective findings
  • Liver function impairment
  • Hypoalbuminemia
  • Hyponatremia
  • Elevated CRP level
  • Elevated WBC count
  • Pleural effusion
  • MR, TR, PR.

13
Problems
  • R/O Heart failure
  • Fever
  • Insert bite
  • Hepatosplenomegaly
  • Impaired liver functions
  • Pleural effusion
  • Ascites

14
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

15
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

16
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)

17
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.

18
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

19
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.

20
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.

21
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)

22
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.

23
Right sided versus left sided
  • Left Dyspnea or orthorpnea as the result of
    pulmonary congestion.
  • Right Edema, congestive hepatomegaly, systemic
    venous distention.

24
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.

25
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.

26
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.

27
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.

28
Pulmonary regurgitation Tricuspid regurgitation
  • Pulmonary hypertension
  • Cardiovascular disease -gt RV dysfunction

29
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

30
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

31
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

32
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

33
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

34
Vasculitis syndrome
  • Goodpasture disease
  • Pulmonary hemorrhage and glomerulonephritis.
  • Symptoms signs
  • Hemoptysis, hematuria, proteinuria and
    hypertension.

35
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

36
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

37
An algorithm for the workup of a patient with
unexplained pulmonary hypertension
38
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.

39
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.

40
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)

41
Pulmonary regurgitation Tricuspid regurgitation
  • Pulmonary hypertension
  • Infection
  • Pulmonary embolism
  • Cardiovascular disease -gt RV dysfunction
  • Rheumatic fever
  • Endocarditis
  • Cardiomyopathy (carditis, dilated, hypertrophic )

42
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

43
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.

44
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

45
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.

46
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

47
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

48
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.

49
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

50
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)

51
Etiology of myocardial disease
  • Infection
  • Virus
  • Coxsackievirus A and B
  • Adenovirus
  • HIV
  • Echovirus
  • Rubella
  • Varicella
  • Influenza
  • Mumps
  • Epstein-Barr
  • Measles
  • Poliomyelitis.

52
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)

53
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.

54
Differential problems
  • R/O Pulmonary hypertension
  • R/O Pulmonary embolism
  • R/O Cardiomyopathy
  • Hepatosplenomegaly
  • Insert bite transmitted disease

55
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56
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58
Richettsial infection
  • Spotted fever group
  • Typhus
  • Scrub typhus
  • Ehrlichioses and Anaplasmosis
  • Q fever

59
Richettsial infection
  • Spotted fever group
  • Rocky Mountain spotted feverr
  • Mediterranean Spotted fever
  • African tick-bite fever
  • Rickettsialpox
  • Murine typhus-like

60
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.

61
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)

62
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.

63
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.

64
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.

65
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.
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