Cardiovascular Diseases

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Disease

Features

Intravascular Infections: Bacteremia

bacteria in blood; major player in dx/management of infxns (occasionally fungi or viruses)

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Intravascular Infections: Sepsis and septicemia

major clinical symptom complexes associated w/bactermia; Acute (septic shock) and Slowly progressing (most infective endocarditis)

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Intravascular Infections: Intracardiac

endocarditis

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Intravascular infections: thrombophlebitis

infections of veins

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Intravascular infections: arteries

endarteritis

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Infective Endocarditis: Pathogenesis

Altered endothelium assists colonization; deposition of platelets/fibrin; turbulence (valvular insufficiency, intracardiac shunts, direct trauma); Bacterial biofilm forms for protection

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Infective Endocarditis: Pathogenesis - Transient bacteremia

childbirth, bronchoscopy, surgical/dental procedures, toothbrushing; not usu signif d/t normal flora w/ low virulence; Staph aureus can be pathogenic; Irregardless of virulence, changes to endothelium could allow colonization in heart

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Infective Endocarditis: Pathogenesis - microbial adherence to damaged endothelial surfaces leads to:

Complement activation, Inflammation and more damage; Fibrin/platelet mesh protect microbes from immune system making it difficult to treat; deposits obstruct blood flow and embolize to brain or coronary arteries

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Etiologic agents of infective endocarditis

Viridans streptococci (30-40%), Other Strep (15-25%), Staph aureus (14-40%), Enterococci, coagulase-negative staph, Gram-neg bacilli, Fungi (candida, aspergillus)

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Gram-negative Bacteremia

Endotoxin in blood activates 1. macrophages, 2. complement cascade, 3. clotting cascade

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Gram-negative Bacteremia: Macrophage activation

cytokines: dec muscle tone of heart/arteries, fever, inc adhesiveness of PMNs, inc leakage of plasma ==> Shock, impaired O2 exchange

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Gram-negative Bacteremia: Complement cascade

Leukocytes attracted to lung tissue, inc capillary leakage of plasma, lysosomal enzymes released from leukocytes ==> Lung tissue damage

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Gram-negative Bacteremia: Clotting cascade

Disseminated intravascular coagulation, depletion of clotting proteins, tissue damage from clots in capillaries ==> Hemorrhage

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Bacterial Endocarditis

d/t microbial infxn of endothelial surfaces of heart (esp. valves); Microbes attach to fibrin-platelet matrix on damaged valves/artificial materials (mitral, aortic, tricuspid, mural endocardium, myocardial absesses)

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Bacterial endocarditis: microbes

bacteria: Rickettsia, Mycoplasma, Chlyamidia

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Bacterial endocarditis: symptoms

fever, chills, sweats, anorexia, altered/new murmurs, systemic emboli, splenomegaly, usu on L side of heart

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Bacterial endocarditis: epidemiology

10-20,000/yr; 25% nosocomial; 45-65yo M2x>F; IVDA (high risk for initial and recurring); Alcoholism (inc risk of Strep pneumoniae)

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Bacterial endocarditis: risk factors

immunosuppression (AIDS, transplant, malignancies susceptible to fungal endocarditis); IDDM; chronic renal Dx; dental/pulmonary/GI/GU procedures

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Actue Bacterial Endocarditis

abrupt presentation; often a result of pneumonia or other body infxn; Staph aureus, Strep pneumoniae (infect normal/abnormal valves; destruction of valves, abscesses in myocardium ==> heart failure)

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Subacute Bacterial Endocarditis (SBE)

d/t less virulent microbes: alpha-hemolytic strep = dentistry; Staph aureus = bacteremia via skin/surgery/catherization; Enterococci = GI/GU tract and nosocomial endocarditis

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Sepsis: 1. Sepsis syndrome, 2. Septic Shock, 3. Multiorgan failure

suspicion of infxn, 1. Evidence of altered organ perfusion (reduced urine output, systemic acidosis, hypoxemia; 2. Hypotension; 3. kindey, lungs, liver, DIC

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Septicemia: Gram-negative bacteria

Possess endotoxin (macrophages respond defensively as a form of Hypersensitivity); Release of endotoxin into circulation triggers macrophages; Macrophages release TNF to raise body temp; PMNs (neutrophils) adhere to capillaries and accumlate inflam cells

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Septicemia: Macrophages

release complement factors which can be activated by endotoxin to attract leukocytes w/tissue-damaging lysozymes, and cause capillaries to leak plasma

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Gram-negative Toxins: Exotoxins

A-B toxins: neurotoxins, enterotoxins, cytotoxins; Membrane Damaging; Superantigens

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Gram-negative Toxins: Endotoxin

LPS (outer membrane of G-neg); Septic shock d/t overwhelming innate immune response; Heat stable

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Gram-negative Exotoxins: A-B Neurotoxins

Clostridium tetani - blocks inhibatory neurons; Clostridium botulinum - blocks nerve signals to muscle

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Gram-negative Exotoxins: Enterotoxins

Vibrio cholerae, strains of E. coli; Regulatory protein in intestinal cells is modified to induce cells to secrete elecrolytes and water

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Gram-negative Exotoxins: Cytotoxins

Corynebacterium diptheriae, Shigella dysenteriae, strains of E. coli (O157:H7); Inhibits protein synthesis in eukaryotic cells leading to cell death

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Exotoxins: Membrane-damaging toxins - Streptolysin O

exotoxin from Streptococcus pyogenes; creates b-hemolysis on blood agar; Inserts into membrane and makes pores

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Exotoxins: Membrane-damaging toxins - a-toxin phospholipases

produced by C. perfringens (causes gas gangrene); polar heads of phospholipid molecule in membrane are removed;

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Endotoxins: LPS (the lipid A is toxic)

Gram-negative infxns; activated innate immune system; stimulates macrophage TNF/IL-1 secretion for fever in nanogram quantities; Larger secretions produce inflammation (hypotension/reduced PMN & platelet counts/hemorrhaging & DIC/irreversible shock

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Blood Cultures

aseptic venipuncture; cultured in specific media (aerobic/anaerobic); multiple sites are drawn to rule out contamination

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Blood Cultures - pts on antibiotics

presence of antibiotics can inhibit microbial growth

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Blood cultures - ARD

antimicrobial removal device; resin that removes antimicrobials from blood

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Blood cultures - FAN

fastidious antimicrobial neutralization; activated charcoal neutralizes antibiotic

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Complete Blood Count (CBC)

RBC, WBC (WBC differential); platelent count (plt); hemoglobin (hgb); hematocrit (hct); MCV; MCH; MCHC; RDW

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Red Blood Cell Count: Normals

Women: 4.3x10^6/mL; Men: 4.8x10^6/mL

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White Blood Cell Count: Normals

4500 - 10,500/mL

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White Blood Cell differential: neutrophils

40-60%; bacterial infections

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White Blood Cell differential: lymphocytes

20-40%; viral infections

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White Blood Cell differential: monocytes

2-8%; severe infections; phagocytosis

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White Blood Cell differential: eosinophils

1-4%; allergic disorders; parasitic infections

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White Blood Cell differential: basophils

0.5-1%; parasitic infections; some allergic disorders

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White Blood Cell differential: bands

0-3%

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CBC: Leukocytosis

>11,000/mL; usu involves increase in only one type of leukocyte; occurs in acute infections

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CBC: Leukopenia

<4,000/mL; viral infections, some bacterial; overwhelming bacterial infections

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CBC: MCV

mean corpuscular volume; normal = 82-98; average RBC volume; aid in classification of anemias;

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CBC: MCV - larger than normal

macrocytosis/macrocytic anemias (B12 or folate deficiency

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CBC: MCV - smaller than normal

microcytosis or mycrocytic anemias (iron deficiency)

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CBC - hemoglobin (hgb)

normal for Women: 12-16g/dL; Men: 14-17g/dL; transports O2; aids in diagnosis of anemias and in monitory therapy for anemias

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CBC - hematocrit (hct)

normal Women: 36-48%; Men: 42-52%; ratio of the volume of packed RBCs to the total vol of whole blood; estimates number of RBC mass which aid in diagnosis anemias

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CBC - MCH

mean corpuscular hemoglobin; Normal: 26-34pg/cell; average amt of hemoglobin per RBC; useful for diagnosis pts w/severe forms of anemia

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CBC - MCHC

mean corpuscular hemoglobin concentration; normal: 32-36g/dL; useful for monitoring therapy in treating anemias

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CBC - RDW

RBC distrib. width; norm: 11.5-14.5 CV (S.D. of RBC size divided by MCV x 100); measures degree of variation of RBC sizes; larger than normal variation = Anisocytosis (typical of anemias; reticulocytes d/t stressed erythropoiesis; poikilocytosis (shapes)

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Intravascular Disease: Blood is sterile

circulating microorgaisms in blood is called bacteremia; a positive blood culture is an autonomic panic value!!

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Intravascular Disease: Bacteremia

reflection of uncontrolled infection or part of the natural course of an infectious diseases

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Intravenous Catheter Bacteremia

(or any other medical device) colonized w/bacteria; usually skin flora (Staph epidermidis, Staph aureus, or Candida); Sometimes intravenous soltions are contaminated (enterobacteriaceae; pseudomonas or other G-neg rods)

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Intravascular disease: Bacteremia from extravascular infections

microbes escape from infected area and reach venous circulation via lymphatics; most common sources are urinary tract/respiratory tract/skin&wound infxns; NOT predictable (depends on site and microbe involved)

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Bacteremias: Group B Streptococcal Disease

d/t Strep. agalactiae; most common cause of sepsis and meningitis in newborns; frequent cause of newborn pneumonia (more common than rubella/congenital syphilis/spina bifida); early onset <7days OR late onset >7days; Approx 25% occur in premies;

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Bacteremias: Group B Stretococcal Disease - epidemiology

Gram-positive cocci; Newborns - bacteremia/pneumonia/meningitis; Adults - sepsis/soft tissue infxn/pregnancy related (amnionitis/sepsis/UTIs/stillbirth); 19,000 cases/yr in US...7,500 in newborns

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Group B Streptococcal Disease - High risk groups

infants born to women colonized w/GBS (or w/anti-GBS capsular antibody); Infants born to women <20yo; Infants born to black women; prolonged rupture of membranes; preterm delivery

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Rheumatic Fever

begins w/strep throat or scarlet fever, follows a latent period after Group A strep infxn; Common manifestations - polyarthritis/carditis; Inflammatory disease - affects CT (heart/joints/brain/skin)

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Rheumatic Fever - epidemiology

Common worldwide (less in US); low socioeconomics d/t more virulent GAS; responsible for many cases of damaged heart valves; affects kids btw 6-15yo (20days after strep infxn); Rheumatic fever pts have flare-ups of repeated strep infxns

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Rheumatic Fever - symptoms

fever, joint pain/swelling (knees, ankles, elbows, wrists); abdominal pain; skin rash; muscle weakness; uncoordinated jerky movements; nosebleeds; cardiac involvment (SOB, chest pain)

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Rheumatic Fever - Role of Group A Streptococci

possible autoimmune mechanism; antigenic similarities btw strep and human tissue antigens; pts w/sterp pharyngitis have high levels of: anti-strep and autoreactive antibodies & T-cells that react w/heart tissue in addition to strep antigens!

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Rheumatic Fever - Autoimmune mechanism

most likely antigen to stimulate antibody production is "M-protein" (adhesion molecule for strep), Group A CHO is also a possibility; M-protein is similar to myosin in heart sarcolemma membranes

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Rheumatic Fever - Complications

Endocarditis (friable/inflamed heart valves; w/time valves thicken/scar/shorten/stenotic); Arrhythmias; Pericarditis; Heart Failure

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Bubonic Plague "Black Death"

d/t Yersinia pestis; non-motile/non-spore forming/ G-neg rod/grows at 28*C; original source may be rats and flea carriers in Egypt Nile Valley - sent to India and spread via trade routes westward during war/famine/typhoid epidemic/pestilence

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Bubonic Plague "Black Death" - Stats

3000 cases worldwide/yr; In the US, rock squirrels (and their fleas) cause infxn in southwest (also pairie dogs and chipmunks; domesticated animals may bring fleas home)

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Bubonic Plague "Black Death" - Disease of Rodents

zoonotic disease; humans accidental hosts; rodents (particularly rats) are primary reservoir; spread by fleas (Xenopyslla cheopis)

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Bubonic Plague "Black Death" - pathology

Y. pestis obstructs flea GI tract; repeatedly bite victim and infect wounds; Y.pestis carried to lymph nodes & taken up by macrophages; replication kills macrophages and acute inflam rxn enlarges tender nodes = Bubo

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Bubonic Plague "Black Death" - Disease manifestations

incubation is 2-7days after bite; onset fever/painful bubo (usu in groin); w/o Tx, 50-75% progress to bacteremia and die of G-neg septic shock w/in hrs to days of bubo appearance; also progresses to lung infxn

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Bubonic Plague "Black Death" - Secondary pneumonia

d/t bacteremic spread to lungs; aka: Pneumonic Plague; highly contagious person-person coughing; clearly shows how plague speas so quickly thru crowded European cities in 14th century

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Bubonic Plague "Black Death" - Secondary infxn Pneumonic Plague pathology

2-3day incubation; pts develop mucoid, bloody sputums; begins w/fever malaise, tightness in ches; cough/sputum production/dyspnea/cyanosis; Death occurs on 2nd or 3rd day of illness; Terminal cyanosis seen in pneumonic plague (hence "black death")

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Bubonic Plague "Black Death" - Primary pneumonic plague d/t biologic attack

inhaled aerosozlized Y. pestis would cause primary plague; incubation 1-6days (typ 2-4); blood, watery, purulent sputum; nausea, vomiting, abdominal pain, diarrhea; MAIN DIFFERENCE btw 1* and 2* pneumonic plague = No buboes w/primary!

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Bubonic Plague "Black Death" - First indication of clandestine biological attack...

sudden outbreak of severe pneumonia/sepsis; overlooked b/c similar to bacterial/viral pneumonias; few western Drs seen plague, but healthy individuals w/cough, SOB, chest pain & death should suggest bubonic plague or inhalation anthrax

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Viremias - Mumps

paramyxovirus: ssRNA virus, lipid-envelope, parainfluenzae fam; detect in saliva/CSF/blood/urine; d/t respir drops; replic in nasopharynx/regional nodes; after 12-25days viremia occurs; spread to meninges/salivary glands, pancreas, testes, ovaries

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Viremias - Mumps - Symptoms

myalgia/anorexia/malaise/HA/low fever; 1+ salivary glands involved (first notes as earache or jaw tenderness); usu resolves 7-10days; Complications - aseptic meningitis/ovarian or testicular inflam/pancreatitis/deafness

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Viremias - Mumps - Tx, At risk groups, Prevention

bed rest, fluids, medication for fever; unvaccinated school-aged kids; vaccine is available: MMR

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Intravascular Disease; Infectious Mononucleosis

aka: Kissing disease; Inc in mononuclear leukocytes; transitory/nonmalignant/self-limiting infxn; dt Epstein-Barr Virus (EBV; dsDNA herpes family) w/affinity for B-lymphocytes; oral spread/contagious

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Mononucleosis: Symptoms

fatigue, fever, sore throat, lymphadenopathy; leukocytosis by 2nd week (leukopenia possible in 1st week); inc in LYMPHOcytes on differential (not monocytes); resolved 3-4wks; (<5% complications: b-hemolytic strep or ruptured spleen)

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Mononucleosis: lymphocytes...

minimum of 10-20% reactive/atypical (xtra cytoplasm) lymphocytes on diff (activated Tcells responding to viral infxn); invasion and killing of Bcells by EBV seen as degenerated lymphocytes on peripheral blood smear

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Mononucleosis: EBV pathophysiology

viral pharyngitis; virions enter lymph nodes and blood stream; virions infect Bcells (either latent or productive); Bcells replicate w/"heterophile Ab" and Tcells destroy the Bcells; Latent bcells are immortal and can be activated later

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Mononucleosis: Antibodies -3 types

Heterophile, EBV, autoantibodies

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Mononucleosis: Antibodies - Heterophile

react w/unrelated antigens on cells from diff species; can be absorbed by bovine RBCs but not guinea pig kidney cells (Rapid slide differential "Monospot" test); Test can be negative in kids <10 (use sensitive EBV antibody test)

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Mononucleosis: Antibodies - EBV

EBV-VCA (IgM), EBV-VCA (IgG), EBNA, EBV-EA; most commonly measured when Monospot is negative is: VCA (viral capsid antigens)

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Mononucleosis: Antibodies - Autoantibodies

RBCs, WBCs, platelets, cold agglutinins

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Mononucleosis: EBV-VCA

IgM antibody to viral capsid antigen; present in 1st week of infxn; BEST indicator of current infxn

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Mononucleosis: EBV-VCA

IgG antibody to viral capsid antigen; present 7days after exposure; indicates current or past infxn; a rise in titer MUST be demonstrated on acute and convalescent sera

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Mononucleosis: EBNA

antibody to EBV nuclear antigen; appears in 1st MONTH and persists indefinately; indicates past infxn

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Mononucleosis: EBV-EA

antibody to EBV early antigen complex; seen in <5% of normal healthy subjects; indicates EBV-carrier state

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Mononucleosis: Series of Tests

1. Heterophile Antibody Test; 2. Repeat Heterophile (1 wk later); EBV-IgM Ab test; CMV-IgM test; Hepatitis tests/Toxoplasma titer/viral culture

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Mononucleosis: Infectious Mononucleosis

+ Heterophile Antibody and + Repeat Heterophile Antibody

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Heterophile-negative Infectious Mononucleosis

+ EBV-IgM Antibody

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CMV Mononucleosis

+ CMV-IgM and Negative Hepatitis/toxoplasma titer/viral culture

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Other clinical symptoms: Epstein Barr Virus - Bcell Latency

infected Bcells can have a latent infxn; EBV incorporates into host genome; EBNA (EBV genes) transform Bcells into immortal/constantly dividing cells; *a healthy immune system can keep these immortalized Bcells in check

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Epstein Barr Virus: Burkitt's Lymphoma

Bcell lymphoma; High levels of antibodies to EBV antigens; EBV detected in tumor cells; viral particles in blood cell culture

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Fungemia

can be dt complications from venous or arterial catheterization (AIDS, antimicrobial therapy, radiation, antineoplastic drugs); represents failure of host immune system

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Fungemia: Etiology

mc: Candida albicans (causes candida endocarditis in IVDA); Others include: Histoplasma capsulatum, Coccidioides immitus, Cryptococcus neoformans

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Fungemia: Candidemia

defined by Candida sp in blood; 25-75% mortality (all pts get therapy); 4th most common cause of nosocomial bloodstream infxns in the 1990s!!

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Fungemia: Candidemia - epidemiology

C. albicans (~50% of cases); C. tropicalis/glabrata (inc freq in adults); C. parapsilosis (pediatric pts); C. krusei (bone marrow transplant pts)

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Fungemia: Candidemia - Clinical Manifestations

4 overlapping invasive forms: 1. Catheter related candidemia; 2. Acute disseminated candidiasis; 3. Chronic disseminated candidiasis; 4. Deep organ candidiasis

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Candidemia: Catheter-related

primary infxn from catheter or the fibrin clot on catheter; high density w/seeding; catheter removal helps; antifungal therapy required to remove local infx and prevent hematogenous spread

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Candidemia: Acute Disseminated Candidiasis

may originate from contaminated catheter; infxn spread to 1+ organs; Tx - remove primary focus/control Sx of sepsis; Drug therapy to remove all sites of infxn

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Candidemia: Chronic Disseminated Candidiasis

aka: hepatosplenic; usu after prolonged bone marrow dysfxn and neutropenia (dt tx for leukemia); liver, spleen and sometimes kindeys; blood cultures usu negative

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Candidemia: Deep organ candidiasis

any organ can be infected; an episode of candidemia must preceed organ infxn to seed area; only manifestation is focal infxn of a specific organ

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Fungemia: Disseminated Forms - Coccidiodes immitus

pericardium

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Fungemia: Cryptococcus neoformans

myocarditis, pericarditis, endocarditis

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Fungemia: Histoplasma capsulatum

lymphadenitis, endocarditis

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Malaria: pathophysiology

Mosquito (anopheles) ingests malarial gametocytes, zygotes mature into oocytes in gut; sporozoites migrate to salivary glands at 10-14days; transfer sporozoites into next human bite; travel to liver (merozoites) and infect/lyse RBCs

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Malaria: Plasmodium falciparum

most severe form; parasites infect all stages of erythrocytes; rigid RBCs stick to capillary walls; up to 2.7million deaths/yr

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Malaria: Plasmodium vivax, Plasmodium ovale

causes relapsing Dx; after treatment, treatment resistant parasites reside dormant in liver; later multiply into exoerythrocyte cycle and eventually invade RBCs; can cause severe anemia

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Malaria: Plasmodium malariae

produce long-lasting infxns; most often asymptomatic

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Malaria: incubation period

btw 7-30 days after bite (P. falciparum - shorter; P. malariae - longer)

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Malaria: clinical manifestations

delayed (wks to months) dt prophylaxis Tx; P. vivax and P. ovale; can lead to misdiagnosis

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Malaria: Schuffner's dots

various stages of parasites may be found intracellularly; RBCs parasitized by P. vivax have sm. purple-red granules (Wright's stain); also an intracellular "ring stage"

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Malaria: uncomplicated malaria

fever, chills, sweating, headaches, nausea, vomiting ,body aches, malaise, enlarged spleen; P. falciparum (mild jaundice, enlarged liver, inc respiratory rate)

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Malaria: Lab results (esp P. falciparum)

mild anemia, thrombocytopenia, elevated bilirubin, aminotransferases, albuminuria, urinary casts

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Malaria: Severe malaria

cerebral infxn (abnml behavior/impaired consciousness/coma/seizures); severe anemia; hemoglobinuria; abnml coag/thrombocytopenia; pulmonary edema; CV collapse; kidney fail; met acidosis a/w hypoglycemia; hyperparasitemia >5% RBC infected

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Malaria: Malarial relapses

usu a/w P. vivax dt dormant liver stage of life cycle; can occur after months or yrs w/o symptoms

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Malaria: microscopic diagnosis

prepare blood smear w/Giemsa or Wright's stain

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Malaria: antigen detection diagnosis - Malarial RDTs

rapid diagnostic test; dipstick or cassette (solid phase immunoassay); controversial; not approved for use in US

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Malaria: molecular diagnosis

PCR

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Malaria: Serology

detect antibodies to antigens; IFA (indirect fluorescent assay); ELISA (ezyme-linked immunosorbent assay)

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Schistosomiasis: "Blood Flukes"

S. hematobium, S. mansoni, S. japonicum; infected via contaminated water; cercaria penetrate skin and enter venous circulation; travel to heart, lungs, and portal circulation

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Schistosomiasis: Penetration of skin

via cercarine; causes "swimmer's itch"; physical damage to skin caused by proteases secreted by cercariae

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Schistosomiais: Bladder

granulomatous lesions; hematuria; urethral occlusions

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Schistosomiais: Intestines

polyp formation can lead to life-threatening dysentery

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Schistosomiasis: Liver

eggs cause hepatomegaly dt periportal fibrosis and protal hypertension

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Schistosomiasis: Nervous system

headaches, disorientation, amnesia, coma

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Schistosomiasis: Heart

arteriolitis and fibrosis leading to enlargement and failure of right ventricle

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Schistosomiasis: Clinical features

acute: Katamaya's fever (S. mansoni, S. japonicum); fever/cough/abdominal pain/bloody diarrhea; hepatosplenomegaly; eosinophilia; CNS lesions (S. japonium eggs in brain; S. mansoni/haematobium in spinal cord); cystitis/ureteritis bladder cancer; pulm-HT

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Schistosomiasis: Host immune responses

IgE; eosinophil-mediated cytotoxicity

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Schistosomiasis: Microscopy and Antibody Detection

stool (all sp); urine (S. haematobolium); useful for confirming in travelers (use purified adult worm antigens on ELISA for 99% specificity)

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Trypanosomiasis: T. cruzi

Chagas' disease

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Trypanosomiasis: T. brucei gambiense

Chronic form of African sleeping sickness

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Trypanosomiasis: T. brucei rhodesiense

Acute African sleeping sickness

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Chagas disease

primarily affects nervous system and heart; chronic infxn (dementia, damaged myocardium, death if untreated); vectors (Triatoma infestans, Rhodnius proxilis, Panstrongylus megistus)

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Chagas Disease: American trypanosomiasis

16-18 million infxns (50,000 die/yr); latin america; rare in US; Triatomine (reduvid) bug feces in eyes, cuts, uncooked food; risk in poor dirt houses

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Lifecycle of T. cruzi

parasite leaves revudid rectum and feces enters bite on human skin; trypomastigotes reproduce as amastigotes and transform into trypomastigotes in bloodstream; vector infected when it bites infected host

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Chagas Disease: Acute Stage

1% of cases; Romana's sign (one swollen eye where feces gets rubbed in); fever, fatigue, enlarged liver/spleen; swollen lymph glands; brain damage in infants/young kids can lead to death

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Chagas Disease: Indeterminate Stage

asymptomatic 8-10wks after infxn; can last years

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Chagas Disease: Chronic stage

10-40yrs after infxn; 20-30% develop serious symptoms incl: Cardiac (enlarged heart/arrhythmias/heart failure); Enlarged esophagus or bowl (probs swallowing, severe constipation); Chronic stage symptoms don't always occur

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Human African Trypanosomiasis (HAT): T. brucei gambiense

slow-progressing; can be self-limiting or develops into chronic disease involving CNS and lymphatics

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Human African Trypanosomiasis (HAT): T. brucei rhodesiense

rapidly progressing disease

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Human African Trypanosomiasis: Kinetoplastids

mitochondrial DNA

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African Sleeping Sickness: Lifecycle (MT, LS, SS, PT, E)

metacyclic trypomastigotes ==> long slender ==> short stumpy ==> procyclic trypomastigotes ==> epimastigotes

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African Sleeping Sickness: Metacyclic trypomastigotes

reside in salivary gland of tsetse fly; transferred to bloodstream of host

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African Sleeping Sickness: Long slender, short stumpy

trypomastigotes display different morphologies in bloodstream; their antigenic variance eludes the immune system

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African Sleeping Sickness: Procyclic trypomastigotes

when tsetse fly ingests trypomastigotes from blood meal, these develop in the gut and travel to salivary gland

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African Sleeping Sickness: epimastigotes

in salivary gland of tsetse fly, these attach to epithelial cells by their flagella and develop into metacyclic trypomastigotes

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African Sleeping Sickness: Disease Progression

1-2wk incubation (trypanosomal chancre?); Acute blood stage (fever, HA); Invasion of lymphatics (large nodes; wt loss; weak; rash; itch; febrile attacks); ***Relapse occurs dt antigenic variation on trypanosomal surface from different morphologies

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African Sleeping Sickness: Hallmark of Disease

invasion of CNS 6-12 months after infxn w/T. gambiense or Within Weeks of T. rhodesiense; Trypanosomes cross BBB causing meningoencephalitis (apathy, fatigue, confusion, motor changes in speech/ticks; sleep disruption; coma; death

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Leishmaniasis

obligate-intracellular protozoan transmitted by sandflies; amastigote found in reticuloendothelial cells of viscera (spleen/nodes/liver/intestines)

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Leishmaniasis: pathophysiology and symptoms

incubation 10days to 1yr (avg: 2-4mo); low fever; malaise; anemia; progressive wasting; protrusion of abdomen (large spleen/liver); death w/in 2-3 days if untreated

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Leishmaniasis: Acute form

runs course for 6-12 months; edema (face); bleeding mucous membranes; breathing difficulty; diarrhea; pts can recover w/ post Kala-azar dermal Leishmanoid; Face can be badly disfigured

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Leishmaniasis: LD Bodies

amastigote intracellular parasites on microscope smear

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Leishmaniasis: life cycle

sand fly --> promastigotes ingested by macrophages ==> form amastigotes inside MQ and other tissues; sandfly ingests amastigotes ==> they transform in midgut and divide into proboscis which infect host when bitten

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Babesiosis: emerging zoonosis

caused by animal specific protozoan parasites in ticks; parasites invade RBCs and induce febrile disease; hemolytic anemia, hemoglobinuria, shock, death

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Babesiosis: Human infections

B. microti and B. divergens carried by 2 hosts: white-footed mouse (Peromyscus leucopus) and Deer tick (Ixodes dammini); humans are accidental hosts; infxn does not transfer btw human "dead end" hosts

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Babesiosis: course

spreads thru bite from infected deer tick (they also spread lyme disease); individuals bitten can be infected by both; infxn can also occur via blood transfusions

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Babesiosis: Demographics

Northeastern US coastal reagions (offshore islands of MA, NY); scattered cases elsewhere

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Babesiosis: symptoms

similar to malaria (RBCs infected w/parasite); fatigue, loss of appetite; w/infxn progression: fever, drenching sweat, muscle aches, HA; lasts from days to months

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Babesiosis: lab and complications

Tetrad formation of parasite in RBCs; low BP, liver disorders, severe hemolytic anemia; kidney failure; pts w/o spleens are most susceptible

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Babesiosis: Diagnosis

direct blood smears; IFA - antigens to B. microti used to detect Ab in pts; titers >1:1024 in first wks can drop to 1:16 or 1:256 in 6months; although titer is low, it can be detected for one year

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Filariasis

caused by infxns w/nematodes (roundworms); 8 known species to affect humans: 3 are most responsible for morbidity (W. bancrofti, B. malavi, O. volvulvus)

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Filariasis: Wuchereria bancrofti

tropical areas worldwide; migrates to lymphatics in host to develop into microfilaria-producing adults

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Filariasis: Brugia malayi

Asia; migrates to lymphatics in host to develop into microfilaria-producing adults

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Filariasis: Brugia timoria

certain Indonesian islands

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Filariasis: Onchocerca volvulus

Africa; some foci in Latin America and the Middle East; migrates to subcutaneous tissue in host to develop into microfilaria-producing adults

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Filariasis: Loa loa, Mansonella streptocerca

Africa; Loa Loa migrates to subcutaneous tissue in host to develop into microfilaria-producing adults

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Filariasis: Mansonella perstans

Africa, South America

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Filariasis: Life Cycles

larvae transmitted via arthropods; can migrate to specific area in host body (18months; develop into microfilaria-producing adults); Female worms produce microfilariae (enter bloodstream); When arthopod bites it takes up microfilariae and grows filariform

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Lymphatic filariasis: Clinical manifestations

asymptomatic microfilaremia; some pts develop lymphatic dysfxn (lymphedema, elephantiasis in lower extremities); Febrile lymphangitis and lymphadenitus; Eosinophilia

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Filariasis: Diagnostics - microscope

ID microfilariae in blood (must collect w/periodicity of organism or concentrate blood sample); ID microfilariae in skin (snips incubated in saline for O. volvulus and M. streptocerca to migrate out of tissue)

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Filariasis: Antigen and Antibody Detection

Immunoassay for W. bancrofti (when low #s of microfilariae in bloodstream); Ab detection not useful dt cross-reactivity of filarial antigens w/those of other helminths; cannot distinguish btw past and current infxns

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