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MedMicro - Y2S1B2
Cardiovascular Diseases
| Disease | Features |
|---|---|
| Intravascular Infections: Bacteremia | bacteria in blood; major player in dx/management of infxns (occasionally fungi or viruses) |
| Intravascular Infections: Sepsis and septicemia | major clinical symptom complexes associated w/bactermia; Acute (septic shock) and Slowly progressing (most infective endocarditis) |
| Intravascular Infections: Intracardiac | endocarditis |
| Intravascular infections: thrombophlebitis | infections of veins |
| Intravascular infections: arteries | endarteritis |
| Infective Endocarditis: Pathogenesis | Altered endothelium assists colonization; deposition of platelets/fibrin; turbulence (valvular insufficiency, intracardiac shunts, direct trauma); Bacterial biofilm forms for protection |
| 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 |
| 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 |
| 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) |
| Gram-negative Bacteremia | Endotoxin in blood activates 1. macrophages, 2. complement cascade, 3. clotting cascade |
| 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 |
| Gram-negative Bacteremia: Complement cascade | Leukocytes attracted to lung tissue, inc capillary leakage of plasma, lysosomal enzymes released from leukocytes ==> Lung tissue damage |
| Gram-negative Bacteremia: Clotting cascade | Disseminated intravascular coagulation, depletion of clotting proteins, tissue damage from clots in capillaries ==> Hemorrhage |
| 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) |
| Bacterial endocarditis: microbes | bacteria: Rickettsia, Mycoplasma, Chlyamidia |
| Bacterial endocarditis: symptoms | fever, chills, sweats, anorexia, altered/new murmurs, systemic emboli, splenomegaly, usu on L side of heart |
| 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) |
| Bacterial endocarditis: risk factors | immunosuppression (AIDS, transplant, malignancies susceptible to fungal endocarditis); IDDM; chronic renal Dx; dental/pulmonary/GI/GU procedures |
| 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) |
| 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 |
| 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 |
| 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 |
| Septicemia: Macrophages | release complement factors which can be activated by endotoxin to attract leukocytes w/tissue-damaging lysozymes, and cause capillaries to leak plasma |
| Gram-negative Toxins: Exotoxins | A-B toxins: neurotoxins, enterotoxins, cytotoxins; Membrane Damaging; Superantigens |
| Gram-negative Toxins: Endotoxin | LPS (outer membrane of G-neg); Septic shock d/t overwhelming innate immune response; Heat stable |
| Gram-negative Exotoxins: A-B Neurotoxins | Clostridium tetani - blocks inhibatory neurons; Clostridium botulinum - blocks nerve signals to muscle |
| 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 |
| Gram-negative Exotoxins: Cytotoxins | Corynebacterium diptheriae, Shigella dysenteriae, strains of E. coli (O157:H7); Inhibits protein synthesis in eukaryotic cells leading to cell death |
| Exotoxins: Membrane-damaging toxins - Streptolysin O | exotoxin from Streptococcus pyogenes; creates b-hemolysis on blood agar; Inserts into membrane and makes pores |
| Exotoxins: Membrane-damaging toxins - a-toxin phospholipases | produced by C. perfringens (causes gas gangrene); polar heads of phospholipid molecule in membrane are removed; |
| 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 |
| Blood Cultures | aseptic venipuncture; cultured in specific media (aerobic/anaerobic); multiple sites are drawn to rule out contamination |
| Blood Cultures - pts on antibiotics | presence of antibiotics can inhibit microbial growth |
| Blood cultures - ARD | antimicrobial removal device; resin that removes antimicrobials from blood |
| Blood cultures - FAN | fastidious antimicrobial neutralization; activated charcoal neutralizes antibiotic |
| Complete Blood Count (CBC) | RBC, WBC (WBC differential); platelent count (plt); hemoglobin (hgb); hematocrit (hct); MCV; MCH; MCHC; RDW |
| Red Blood Cell Count: Normals | Women: 4.3x10^6/mL; Men: 4.8x10^6/mL |
| White Blood Cell Count: Normals | 4500 - 10,500/mL |
| White Blood Cell differential: neutrophils | 40-60%; bacterial infections |
| White Blood Cell differential: lymphocytes | 20-40%; viral infections |
| White Blood Cell differential: monocytes | 2-8%; severe infections; phagocytosis |
| White Blood Cell differential: eosinophils | 1-4%; allergic disorders; parasitic infections |
| White Blood Cell differential: basophils | 0.5-1%; parasitic infections; some allergic disorders |
| White Blood Cell differential: bands | 0-3% |
| CBC: Leukocytosis | >11,000/mL; usu involves increase in only one type of leukocyte; occurs in acute infections |
| CBC: Leukopenia | <4,000/mL; viral infections, some bacterial; overwhelming bacterial infections |
| CBC: MCV | mean corpuscular volume; normal = 82-98; average RBC volume; aid in classification of anemias; |
| CBC: MCV - larger than normal | macrocytosis/macrocytic anemias (B12 or folate deficiency |
| CBC: MCV - smaller than normal | microcytosis or mycrocytic anemias (iron deficiency) |
| 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 |
| 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 |
| CBC - MCH | mean corpuscular hemoglobin; Normal: 26-34pg/cell; average amt of hemoglobin per RBC; useful for diagnosis pts w/severe forms of anemia |
| CBC - MCHC | mean corpuscular hemoglobin concentration; normal: 32-36g/dL; useful for monitoring therapy in treating anemias |
| 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) |
| Intravascular Disease: Blood is sterile | circulating microorgaisms in blood is called bacteremia; a positive blood culture is an autonomic panic value!! |
| Intravascular Disease: Bacteremia | reflection of uncontrolled infection or part of the natural course of an infectious diseases |
| 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) |
| 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) |
| 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; |
| 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 |
| 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 |
| 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) |
| 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 |
| 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) |
| 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! |
| 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 |
| Rheumatic Fever - Complications | Endocarditis (friable/inflamed heart valves; w/time valves thicken/scar/shorten/stenotic); Arrhythmias; Pericarditis; Heart Failure |
| 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 |
| 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) |
| Bubonic Plague "Black Death" - Disease of Rodents | zoonotic disease; humans accidental hosts; rodents (particularly rats) are primary reservoir; spread by fleas (Xenopyslla cheopis) |
| 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 |
| 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 |
| 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 |
| 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") |
| 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! |
| 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 |
| 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 |
| 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 |
| Viremias - Mumps - Tx, At risk groups, Prevention | bed rest, fluids, medication for fever; unvaccinated school-aged kids; vaccine is available: MMR |
| 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 |
| 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) |
| 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 |
| 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 |
| Mononucleosis: Antibodies -3 types | Heterophile, EBV, autoantibodies |
| 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) |
| Mononucleosis: Antibodies - EBV | EBV-VCA (IgM), EBV-VCA (IgG), EBNA, EBV-EA; most commonly measured when Monospot is negative is: VCA (viral capsid antigens) |
| Mononucleosis: Antibodies - Autoantibodies | RBCs, WBCs, platelets, cold agglutinins |
| Mononucleosis: EBV-VCA | IgM antibody to viral capsid antigen; present in 1st week of infxn; BEST indicator of current infxn |
| 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 |
| Mononucleosis: EBNA | antibody to EBV nuclear antigen; appears in 1st MONTH and persists indefinately; indicates past infxn |
| Mononucleosis: EBV-EA | antibody to EBV early antigen complex; seen in <5% of normal healthy subjects; indicates EBV-carrier state |
| 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 |
| Mononucleosis: Infectious Mononucleosis | + Heterophile Antibody and + Repeat Heterophile Antibody |
| Heterophile-negative Infectious Mononucleosis | + EBV-IgM Antibody |
| CMV Mononucleosis | + CMV-IgM and Negative Hepatitis/toxoplasma titer/viral culture |
| 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 |
| 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 |
| Fungemia | can be dt complications from venous or arterial catheterization (AIDS, antimicrobial therapy, radiation, antineoplastic drugs); represents failure of host immune system |
| Fungemia: Etiology | mc: Candida albicans (causes candida endocarditis in IVDA); Others include: Histoplasma capsulatum, Coccidioides immitus, Cryptococcus neoformans |
| 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!! |
| 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) |
| Fungemia: Candidemia - Clinical Manifestations | 4 overlapping invasive forms: 1. Catheter related candidemia; 2. Acute disseminated candidiasis; 3. Chronic disseminated candidiasis; 4. Deep organ candidiasis |
| 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 |
| 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 |
| 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 |
| 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 |
| Fungemia: Disseminated Forms - Coccidiodes immitus | pericardium |
| Fungemia: Cryptococcus neoformans | myocarditis, pericarditis, endocarditis |
| Fungemia: Histoplasma capsulatum | lymphadenitis, endocarditis |
| 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 |
| Malaria: Plasmodium falciparum | most severe form; parasites infect all stages of erythrocytes; rigid RBCs stick to capillary walls; up to 2.7million deaths/yr |
| 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 |
| Malaria: Plasmodium malariae | produce long-lasting infxns; most often asymptomatic |
| Malaria: incubation period | btw 7-30 days after bite (P. falciparum - shorter; P. malariae - longer) |
| Malaria: clinical manifestations | delayed (wks to months) dt prophylaxis Tx; P. vivax and P. ovale; can lead to misdiagnosis |
| 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" |
| Malaria: uncomplicated malaria | fever, chills, sweating, headaches, nausea, vomiting ,body aches, malaise, enlarged spleen; P. falciparum (mild jaundice, enlarged liver, inc respiratory rate) |
| Malaria: Lab results (esp P. falciparum) | mild anemia, thrombocytopenia, elevated bilirubin, aminotransferases, albuminuria, urinary casts |
| 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 |
| Malaria: Malarial relapses | usu a/w P. vivax dt dormant liver stage of life cycle; can occur after months or yrs w/o symptoms |
| Malaria: microscopic diagnosis | prepare blood smear w/Giemsa or Wright's stain |
| Malaria: antigen detection diagnosis - Malarial RDTs | rapid diagnostic test; dipstick or cassette (solid phase immunoassay); controversial; not approved for use in US |
| Malaria: molecular diagnosis | PCR |
| Malaria: Serology | detect antibodies to antigens; IFA (indirect fluorescent assay); ELISA (ezyme-linked immunosorbent assay) |
| 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 |
| Schistosomiasis: Penetration of skin | via cercarine; causes "swimmer's itch"; physical damage to skin caused by proteases secreted by cercariae |
| Schistosomiais: Bladder | granulomatous lesions; hematuria; urethral occlusions |
| Schistosomiais: Intestines | polyp formation can lead to life-threatening dysentery |
| Schistosomiasis: Liver | eggs cause hepatomegaly dt periportal fibrosis and protal hypertension |
| Schistosomiasis: Nervous system | headaches, disorientation, amnesia, coma |
| Schistosomiasis: Heart | arteriolitis and fibrosis leading to enlargement and failure of right ventricle |
| 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 |
| Schistosomiasis: Host immune responses | IgE; eosinophil-mediated cytotoxicity |
| 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) |
| Trypanosomiasis: T. cruzi | Chagas' disease |
| Trypanosomiasis: T. brucei gambiense | Chronic form of African sleeping sickness |
| Trypanosomiasis: T. brucei rhodesiense | Acute African sleeping sickness |
| Chagas disease | primarily affects nervous system and heart; chronic infxn (dementia, damaged myocardium, death if untreated); vectors (Triatoma infestans, Rhodnius proxilis, Panstrongylus megistus) |
| 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 |
| 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 |
| 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 |
| Chagas Disease: Indeterminate Stage | asymptomatic 8-10wks after infxn; can last years |
| 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 |
| Human African Trypanosomiasis (HAT): T. brucei gambiense | slow-progressing; can be self-limiting or develops into chronic disease involving CNS and lymphatics |
| Human African Trypanosomiasis (HAT): T. brucei rhodesiense | rapidly progressing disease |
| Human African Trypanosomiasis: Kinetoplastids | mitochondrial DNA |
| African Sleeping Sickness: Lifecycle (MT, LS, SS, PT, E) | metacyclic trypomastigotes ==> long slender ==> short stumpy ==> procyclic trypomastigotes ==> epimastigotes |
| African Sleeping Sickness: Metacyclic trypomastigotes | reside in salivary gland of tsetse fly; transferred to bloodstream of host |
| African Sleeping Sickness: Long slender, short stumpy | trypomastigotes display different morphologies in bloodstream; their antigenic variance eludes the immune system |
| African Sleeping Sickness: Procyclic trypomastigotes | when tsetse fly ingests trypomastigotes from blood meal, these develop in the gut and travel to salivary gland |
| African Sleeping Sickness: epimastigotes | in salivary gland of tsetse fly, these attach to epithelial cells by their flagella and develop into metacyclic trypomastigotes |
| 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 |
| 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 |
| Leishmaniasis | obligate-intracellular protozoan transmitted by sandflies; amastigote found in reticuloendothelial cells of viscera (spleen/nodes/liver/intestines) |
| 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 |
| 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 |
| Leishmaniasis: LD Bodies | amastigote intracellular parasites on microscope smear |
| 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 |
| Babesiosis: emerging zoonosis | caused by animal specific protozoan parasites in ticks; parasites invade RBCs and induce febrile disease; hemolytic anemia, hemoglobinuria, shock, death |
| 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 |
| 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 |
| Babesiosis: Demographics | Northeastern US coastal reagions (offshore islands of MA, NY); scattered cases elsewhere |
| 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 |
| 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 |
| 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 |
| 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) |
| Filariasis: Wuchereria bancrofti | tropical areas worldwide; migrates to lymphatics in host to develop into microfilaria-producing adults |
| Filariasis: Brugia malayi | Asia; migrates to lymphatics in host to develop into microfilaria-producing adults |
| Filariasis: Brugia timoria | certain Indonesian islands |
| 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 |
| Filariasis: Loa loa, Mansonella streptocerca | Africa; Loa Loa migrates to subcutaneous tissue in host to develop into microfilaria-producing adults |
| Filariasis: Mansonella perstans | Africa, South America |
| 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 |
| Lymphatic filariasis: Clinical manifestations | asymptomatic microfilaremia; some pts develop lymphatic dysfxn (lymphedema, elephantiasis in lower extremities); Febrile lymphangitis and lymphadenitus; Eosinophilia |
| 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) |
| 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 |
Created by:
bscaryp