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七院聯合病例討論會 三軍總醫院 R2 李宗翰 / Vs. 喩永生主任 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. History • He got an insert bite in his right lower leg with a small infected wound; the wound was treated at home and improved. 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. Physical examination • The physical examination showed • respiratory distress, bilateral coarse breathing sounds, grade Ⅰ-Ⅱ/Ⅳ 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. Image • The CXR showed minimal right side pleural effusion with normal heart size. Laboratory data • • • • • • • • • • WBC:14100 Neutrophil:67% (40-74) Lymphocyte:20% (19-48) Monocyte:11% (3.4-9) CRP:8.4 mg/dl (0-0.5) Albumin:3.0 g/dl (3.4-4.8) BUN:8 mg/dl (7-20) Creatinine:0.5 (0.5-1) AST:126 U/L (-37) ALT:107 U/L (-41) Total bilirubin: 1.2 mg/dl Na:135 mmol/L (136-145) K:3.4 mmol/L (3.5-5.1) Cl:98 mmol/L Admission course • Echocardiography: • Tricuspid valve regurgitation • Mitral valve regurgitation • Pulmonary valve regurgitation Admission course • Abdominal sonography • Hepatosplenomegaly • Patent hepatic artery and portal vein • Mild to moderate ascites Subjective findings • Fever • Cough • Abdominal pain with fullness • Exertional dyspnea • Insert bite Objective findings • Coarse breathing sounds • Systolic heart murmurs over LLSB • Pitting edema over bilateral lower legs. • Hepatosplenomegaly • Wound of insert bite Objective findings • Liver function impairment • Hypoalbuminemia • Hyponatremia • Elevated CRP level • Elevated WBC count • Pleural effusion • MR, TR, PR. Problems • R/O Heart failure • Fever • Insert bite • Hepatosplenomegaly • Impaired liver functions • Pleural effusion • Ascites 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 Causes of splenomegaly • Infection – – – Bacterial: Typhoid fever, endocarditis, septicemia, abscess Viral:E-B virus, CMV, and others Protozoal: Malaria, toxoplasmosis – – Hemolytic anemia: Congenital, acquired Extramedullary hematopoiesis: thalassemia, osteopetrosis, myelofibrosis – – Malignant: Leukemia, lymphoma, histiocytoses, metastatic tumors Benign: Hemagioma, hamartoma – – Lipidosis: Niemann-Pick, Gaucher disease Mucopolysaccharidosis infiltration: Histiocytosis • Hematologic processes • Neoplasms • Metabolic diseases • • • • Congestion Cirrhosis Cysts Miscellaneous 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) 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. 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 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. 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. 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 (>16 cm H2O) Positive hepatojugular reflux – – – – – – – Extremity edema Night cough Dyspnea on exertion Hepatomegaly Pleural effusion Vital capacity reduced by 1/3 from normal Tachycardia (>120 bpm) • Minor criteria (at least 2) 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. Right sided versus left sided • Left: Dyspnea or orthorpnea as the result of pulmonary congestion. • Right: Edema, congestive hepatomegaly, systemic venous distention. 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. 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. 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. 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 -> dilated right ventricle. Tricuspid regurgitation often accompanies with right ventricular dysfunction. Pulmonary regurgitation & Tricuspid regurgitation • Pulmonary hypertension • Cardiovascular disease -> RV dysfunction Causes of pulmonary hypertension Conditions directly affecting pulmonary arteries Primary pulmonary hypertension Toxin-induced (ie, anorexic agents) Vasculitis Granulomatoses, collagen-vascular disorders, arteritis Hepatic cirrhosis/portal disease Congenital heart disease (Eisenmenger syndrome [ASD, VSD, PDA]) Infection Human immunodeficiency virus Causes of pulmonary hypertension Conditions affecting pulmonary parenchyma Chronic obstructive lung disease Infiltrative/granulomatous diseases Sarcoidosis, pneumoconiosis, radiation, fibrosis, neoplasm, pneumonia, collagen-vascular diseases Cystic fibrosis Upper airway obstruction High-altitude disease Arteriovenous fistulas within the lung Restrictive lung diseases Causes of pulmonary hypertension Conditions affecting the thoracic cage and neuromuscular system Obesity-hypoventilation/sleep apnea Pharyngeal-tracheal obstruction Kyphoscoliosis Pleural fibrosis Neuromuscular disorders Myasthenia gravis, poliomyelitis, central respiratory disorders Causes of pulmonary hypertension • Conditions causing left atrial/or pulmonary venous hypertension Elevated left ventricular diastolic pressure Systolic failure, diastolic dysfunction, constrictive pericarditis Aortic valve disease Mitral valve disease Cor triatriatum Left atrial masses Myxoma or neoplasm, thrombus Fibrosing mediastinitis Congenital pulmonary vein stenosis Anomalous pulmonary venous connection Pulmonary venoocclusive disease Causes of pulmonary hypertension • Nonvasculitis conditions that result in pulmonary artery obstruction Acute and chronic thromboembolism Hemoglobinopathies (eg, sickle cell disease) Primary or metastatic malignancies Peripheral pulmonic stenosis • Congenital pulmonary hypoplasia Vasculitis syndrome • Goodpasture disease • Pulmonary hemorrhage and glomerulonephritis. • Symptoms & signs • Hemoptysis, hematuria, proteinuria and hypertension. 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 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 An algorithm for the workup of a patient with unexplained pulmonary hypertension 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. 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. 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) Pulmonary regurgitation & Tricuspid regurgitation • Pulmonary hypertension • Infection • Pulmonary embolism • Cardiovascular disease -> RV dysfunction • Rheumatic fever • Endocarditis • Cardiomyopathy (carditis, dilated, hypertrophic ) Acute rheumatic fever • Major: (least 2 major or 1+2 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 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. 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 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. 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) Minor:fever, embolic-vascular signs, immune complex phenomena (GN, arthritis, rheumatoid factor, Osler nodes, Roth spots), 2 major + 1 minor 1 major + 3 minors 5 minors 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: respiratory;A:trauma, aspiration to lung, ) Streptobacillus moniliformis Pasteurella multocida (chesse, milk ) Campylobacter fetus Culture negative (6% of cases) Myocarditis • Symptoms: • Fever, severe heart failure, respiratory distress. • Incubation time:1-7 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. 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 Etiology of myocardial disease • Familial-Hereditary (myopathy, cardiomyopathy) • Infection (Virus, Richettsiae, Bacteria,parasite,fungus) • Metabolic, nutritional, endocarine • Connective tissue-Granulomatous diseaseinfiltrative (SLE, vasculitis, Scleroderma, sarcoidosis, dermatomyositis, leukemia) • Drugs-Toxins (chemo, alcohol,irradiation.) • Coronary arteries (Kawasaki disease, meidal necrosis, anomalous left coronary artery) • Other (anemia, ischemia) Etiology of myocardial disease • • • • • • • • • • • • • Infection: Virus: Coxsackievirus A and B Adenovirus HIV Echovirus Rubella Varicella Influenza Mumps Epstein-Barr Measles Poliomyelitis. Etiology of myocardial disease • Richettsiae: • Infection: • 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 Etiology of myocardial disease • Parasites: • • • • • • • • • Infection: 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. Differential problems • R/O Pulmonary hypertension • R/O Pulmonary embolism • R/O Cardiomyopathy • Hepatosplenomegaly • Insert bite transmitted disease Transmission Heart Pul. hypertentsion Pul. embolism Hepatomegal y Splenomegaly Malaria Mosquitoes Yellow Fever Mosquitoes Dengue Fever Mosquitoes J. encephaliti s Mosquitoes (-) (-) (-) (-) (-) (-) (-) (-) (+) (-) (-) (-) Filariasis Mosquitoes (-) (-) (-) Colorado tick fever Tick Tick born Encephaliti s Tick (-) (-) (-) (-) (-) (-) Disease Transmission Heart Pul. hypertentsion Pul. embolism Hepatomegal y Splenomegaly Leishmanias is Sandflies Chagas Disease Tick Sleeping sickness Tsetse fly Loa loa biting flies (-) (+) (-) (+) (-) (-) (-) (-) (+) (+) (-) (-) Disease Disease Transmission Heart Relapsing fever Tick,louse Myocarditis Lyme disease Tick bite Myocarditis RMSF Tick bite Myocarditis MSF Tick bite (-) Scrub typhus Chigger bite Myocarditis Murine typhus Flea feces (-) Epidemic typhus Louse feces (-) HME, HE Tick bite (-) Q fever Tick borne Myocarditis Endocariditis Chagas disease Kissing bug Myocarditis Loa Loa Biting flies Cardiomyopathy Hepatomegaly Pul. E. Splenomegaly Pul. H. (+) (-) (+) 33% (-) (-) (-) (-) (-) (-) (+) P.E. (-) (-) (-) (-) (+) (+) (-) (+)P.E. (+) (-) (-) (-) Richettsial infection • Spotted fever group • Typhus • Scrub typhus • Ehrlichioses and Anaplasmosis • Q fever Richettsial infection • Spotted fever group • Rocky Mountain spotted feverr • Mediterranean Spotted fever • African tick-bite fever • Rickettsialpox • Murine typhus-like Spotted fever group • • • • • • • • • • • • • • Rocky mountain spotted fever Tick bite transmission disease (Host:Dogs, 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 -> petechia or purpura after several days. (49~74%) (1st day: 14%, 3rd day:49%) 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 tilter>1:64 or 4 fold increased between acute and convalescent sera (2-4 wk apart)) Treatment: Doxycycline (2.2mg/Kg/dose q12h->2.2mg/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. 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) 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. Scrub typhus • Scrub typhus • Chigger bite transmission disease (Host: Rats, ) • Pathogen: Orientia tsutsugamushi • Southern Asia, Japan, Indonesia, Australia, Korea, Asiatic Russia, India, • • • • • • • • China Incubation period:6-21 days. <50% of cases necrotic eschar with an erythematous rim Fever, headache, myalgia, cough and GI symptoms. Regional or generalized lymphadenopathy is common. <50% of patients presents maculopapular rash. Complications: Meningoencephalitis, myocarditis, interstitial pneumonitis. Diagnosis:indirect fluorescent antibody assay or immunoperoxidase serologic tests of O. tsutsugamushi antigen Treatment: Doxycycline ; tetracycline; chloramphenicol at least 5 days until afebrile 2-4 days. 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 Diagnosis:Indirect fluorescent antibody assay serology Treatmet: Doxycycline, tetracycline, chloramphenicol at least 5 days until afebrile 2-4 days. 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 period:<14 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. 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 period:2 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 (>=1:128) of A. phargocytophilum antibodies or seroconversion (>=1:64) Treatment: Doxycycline, Tetracycline at least 5 days until afebrile 2-4 days. 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. 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 > 20 mm/hr (80%), hypergammaglobulinemia (54%), hyperfibrinogenemia (67%). Rheumatoid factor (>50%) , 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: Acute:Treated within 3 days of onset of symptoms with tetracycline or doxycycline. Chronic:Tetracycline or doxycycline + rifampin, ofloxacin or pefloxacin. (18months until phase 1 tilters of <1:200 for IgG and negative IgA tilters) 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 Wright’s stain Treatment: Doxycycline (500mg po q6h), erythromycin (50mg/Kg/D) for <12 years old children. Lyme disease • • • • • • • Lyme disease Tick bite disease (Host: Deer, Rodent) Pathogen: Borrelia burdorferi Distribution:Worldwide 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 (> 90% in knees) with swollen and tender joints, chronic demyelinating encephalitis, polyneuritis, impairment of memories Lyme disease • Diagnosis: The presence of EM rashes > 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. Treatment:doxycycline (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->recurrence choose second dose or meningitis. 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. 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); 12.515mg/KG/D (11-16 y/o), 8-10mg/Kg/D(>16 y/o)) for 90 days and benznidazole (10mg/Kg/D bid po(<12y/o); 5-7 mg/kg/D(>12y/o)) for 60 days Disease Transmission Heart Relapsing fever Tick,louse Myocarditis Lyme disease Tick bite Myocarditis RMSF Tick bite Myocarditis MSF Tick bite (-) Scrub typhus Chigger bite Myocarditis Murine typhus Flea feces (-) Epidemic typhus Louse feces (-) HME, HE Tick bite (-) Q fever Tick borne Myocarditis Endocariditis Chagas disease Kissing bug Myocarditis Loa Loa Biting flies Cardiomyopathy Hepatomegaly Pul. E. Splenomegaly Pul. H. (+) (-) (+) 33% (-) (-) (-) (-) (-) (-) (+) P.E. (-) (-) (-) (-) (+) (+) (-) (+)P.E. (+) (-) (-) (-) Impression • Q fever • Rocky mountain spotted fever Laboratory Diagnosis and Treatment of Selected Rickettsial Diseases Disease Laboratory Diagnosis Treatment Mediterranean spotted fever, Japanese spotted fever, Queensland tick typhus, Flinders Island spotted fever, African tick-bite fever Isolation of rickettsiae by shell-vial culture; serology, IFA (IgM, ≥1:64; or IgG, ≥1:128); skin biopsy immunohistochemical detection of rickettsiae; PCR amplification of DNA from tissue specimens Doxycycline (100 mg bid PO for 1-5 days) or Ciprofloxacin (750 mg bid PO for 5 days) or Chloramphenicol (500 mg qid PO for 7-10 days) or (in pregnancy) Josamycina (3 g/d PO for 5 days) Rickettsialpox IFA: seroconversion to a titer of ≥1:64 or a single titer of ≥1:128; crossadsorption to eliminate antibodies to shared antigens necessary for a specific diagnosis of the spotted fever rickettsial species; skin biopsy immunohistochemistry Doxycycline (100 mg bid PO for 1-5 days) or Ciprofloxacin (750 mg bid PO for 5 days) or Chloramphenicol (500 mg qid PO for 7-10 days) or (in pregnancy) Josamycina (3 g/d PO for 5 days) Endemic (murine) typhus IFA: fourfold rise to a titer of ≥1:64 or a single titer of ≥1:128; immunohistology: skin biopsy; PCR amplification of R. typhi or R. felis DNA from blood; dot ELISA and immunoperoxidase methods also available Doxycycline (100 mg bid PO for 7-15 days) or Chloramphenicol (500 mg qid PO for 7-15 days) Epidemic typhus IFA: titer of ≥1:128; necessary to use clinical and epidemiologic data to distinguish among louseborne epidemic typhus, flying-squirrel typhus, and Brill-Zinsser disease Doxycycline (200 mg PO as a single dose or until patient is afebrile for 24 h) Scrub typhus IFA: titer of ≥1:200; PCR amplification of O. tsutsugamushi DNA from blood of febrile patients Doxycyclineb (100 mg bid PO for 7-15 days) or Chloramphenicol (500 mg qid PO for 7-15 days or (for children) Chloramphenicol (150 mg/kg per day for 5 days) 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. 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 paraffinembedded 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. 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 ≥1:800 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. 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 ≥1:64 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.