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Cardiovas. Disease
Medical Microbiology
| Name | Features |
|---|---|
| Bacteremia | Presence of bacteria in the blood |
| Sepsis and septicemia | Major clinical symptoms complexes associated with bacteremia; acute = septic shock and slow progressing = infective endocarditis |
| Thrombophlebitis | Infections of veins |
| Endarteritis | Infections of arteries |
| Pathogenesis of Infective Endocarditis | Altered endothelium to assist in colonization by bacteria --> aid in deposition of platelets and fibrin = biofilm formation and protection of the microorganisms --> turbulence of blood flow + more difficult to treat |
| Transient bacteremia | from normal flora, low virulence, toothbrushing, not clinically significant |
| Etiologic agents of infective endocarditis | Viridians Streptococci (30-40%), enterococci (5-18%), Fungi (least) |
| Bacterial endocarditis | affects heart valves mostly |
| Sx of bacterial endocarditis | Anorexia, altered or new heart murmurs, systemic emboli, slenomegaly, usu affects the left side of the heart |
| Bacterial endocarditis | more males, more cases are nosocomial, IV drug users, immunosuppression, diabetes mellitus, chronic renal disease, and dental, GU, GU procedures at high risk; alcoholism increase risk of infection by strep pneumonia |
| Acute Endocarditis | Symptoms appear abruptly, often as result of infection in another area of the body, staph aureus, strep pneumonia --> valve destruction, abscesses to heart muscle, heart failure |
| Subacute Bacterial Endocarditis | caused by less virulent microorgarnisma; alpha-hemolytic strep when a dental procedure is done; If bacteremia introduced thru skin: staph aureus; enterococci are causative microorganisms as a consequence of abnormalities in GI and urinary tract |
| Sepsis syndrome | Reduction in urine output, systemic acidosis, hypoxemia |
| Septic shock | Hypotension |
| Septicemia | Gram - bacteria possess endotoxin --> macrophages respond = hypersensitivity |
| Release of endotoxin | Macrophage response --> TNF released --> raised temperature+ neutrophils adhere wall = accumulation of inflammatory cells; activated complement factors --> leukocytes --> release of tissue-damaging llysozymes --> plasma leads from capillaries |
| Exotoxins | A-B toxins, Membrane damaging toxins, superantigens |
| Endotoxins | LPS, Septic shock d/t overwhelming innate immune response, heat stable |
| AB toxins | Neurotoxins, Enterotoxins, Cyroroxins |
| Neurotoxins | Clostridium tetani (blocks inhibitory neurons), Clostridium botulinum (block nerve signals to muscle) |
| Enterotoxins | Vibrio cholerae - regulatory protein in intestinal cells is modified to induce cells to secrete electrolytes and water |
| Cytotoxins | Corynebacterium diphteriae, Shigella dysenteriae (inhibits protein synthesis --> cell death) |
| Membrane damaging Toxins | Insert into membranes forming pores and remove polar heads of phospholipid molecules by phospholipases --> damage to membrane (Streptolysin O and Clostridium perfringens) |
| Endotoxins | Activates innate immune syst, stimulates macrophages to secrete TNF & IL1 which causes fever in humans (in large amount: inflammation =hypotension, reduced PMN and platelets counts, hermorrhaging that can lead to irreversible shock); Lipid A =toxic of LPS |
| Positive blood culture | autnomatic panic value |
| Intravenous catheter bacteremia | Usu skin flora, staph epidermidis or staph aureus, candida and IV solution contaminated by enterobac and pseudomonas sp. |
| Extravascular infections | Microorganisms escape from an infected area and reach the venous circulation thru lymphatic sys; not predictable |
| Group B Strept Disease --> Strep agalactiae | most common cause of sepsis and meningitis in newborns(gram +), frequent cause of newborn pneumonia, early onset less than 7d, highrisk gps: infants born to infected women, less than 20yro, of black decent, prolonged rupture of memb,preterm delivery |
| Rheumatic Fever | Begins with strep throat or scarlet fever (follows a latent period after a group A strep infection, common manifest.: polyarthritis, carditis), inflammatory disease (connective tissue), damaged heart valves, pts have flare-ups of repeated of strep infect |
| Rheumatic Fever | Possible autoimmune mechanism (pts with strep pharyngitis have high levels of antistrep and autoreactive antibodies and T cells; M protein (binds to human heart sarcolemma memb), adhesin molec |
| Bubonic Plague "Black Death" | Caused by Yersinia pestis: nonmotile, nonspore forming, gram - rods, grows at 28degC; in US, carriers: rock squirrels and their fleas(Xenopsylla cheopis); disease of rodents (zoonotic, human accidental host) |
| Black plague MOA | Yersinia obstructs GI tract of infected fleas, fleas bite and regurgitate infected material into the wounds, bacteria carried to lymph nodes and taken up by macroph, yersinia kills leuko, acute inflammat=enlargement and tenderness of lymph nodes (BUBO) |
| Black Plague: Disease manifestation | incubation=2-7dy, onset: fever and painful bubo (usu in groin area), w/out tx: 50-75% of pts progress to bacteremia and die of gram - septic shock w/in hrs, progression to disease leads to blood infection then to lung (plague septicemia) |
| Pneumonic Plague | Some pts can develop a 2ndary pneumonia by bacteremic spread to the lungs, highly contagious person-to-person by respiratory droplets (coughing), pts dvp mucoid, bloody sputums, dyspnea, cyanosis, death after 2-3 days |
| Primary pneumonic plague | following a biological attack, bloody, watery purulent sputum, N&V, abdo pain --> NO BUBOES present in primary pneum |
| Mumps | Paramyxvirus(ss-RNA, lipid-containing envelope) acquired by exposure to infective respiratory droplets, virus replicates in nasopharynx and regional lymph node |
| Mumps: Symptoms | Myalgia, anorexia, malaise, low-grade involved, single or mutliple salivary glands can be involved (can be 1st noted as earache or tenderness to jaw), usu resolves wi/in 1 week-10d; complications: aseptic meningitis, pancreatis,deafness, ovarian/test infl |
| Mumps: Tx and prevention | Bed rest, fluids, meds for fever, MMR vaccine, At risk gps: Unvaccinated, school-age children |
| Kissing disease --> Epsein-Barr Virus (EBV) | Increase in mononuclear leukocytes, transitory nonmalignant, self-limiting, infectious disease, EBV has affinity for B-lymph (ds-DNA), contagious by oral contact |
| Kissing disease | Symptoms: fatigue, fever, sore throat, lymphadenopathy; leukocytosis by 2nd week of infection, leukopenia possible during 1st week, increase in lymphocytes on differential |
| Infectious Mononucleosis | Heterophile, EBV, Autoantibodies |
| Heterophile antibodies | react with unrelated antigens on cells from different species, can be absorbed by bovine erythrocytes but not by guinea pig kidney cells (for differential: monospot), test can be negative in IM occuring in child under 10 yr, ab agglutinate horse/sheep RBC |
| EBV antibodies | EBV-VCA (IgM to viral capsid--> best indicator), EBV-VCA (IgG), EBNA (nuclear antigen), EBV-EA (early antigen complex) |
| B cell latency | EBV infects B cells and establishes a latent infection, EBNA transforms B cells into immortal, constantly dividing cells |
| Burkitt's Lymphoma | B cell lymphoma, high levels of antibodies to EBV antigens, EBV genome detected in tumor cells, viral particiles detected in BL cell culture |
| Fungemia | can be caused by complications d/t venous or arterial catheterization, represents failure of host immune system, most common CANDIDA, significant morbidity and mortality rates, one of the most importt nosocomial infections |
| Candida albicans | 1/2 of all cases of candidemia |
| C. tropicalis and C. glabrata | increased frequency in adults |
| C parapsilosis | affinity for pediatric patients |
| C. krusei | increased frequency of occurence with bone marrow transplant patients |
| 4 overlapping forms of invasice candidemia | catheter related candidemia, acute disseminated candiasis, chronic disseminated cadidiasis, deeo organ candidiasis |
| Catheter-related candidemia | primary infection is on catheter or related to the fibrin clot which forms on the catheter, tend to be of high density, removal of catheter betterm antifungal therapy still needed to remove local infection and foci from hematogenous spread |
| Acute disseminated candidiasis | from contaminated catheter?, infection has spread to 1 or more organs, tx focuses on elimination of primary focus, controlling symptoms of sepsis, drug therapy to remove all sites of infections |
| Chronic disseminated candidiasis | also hepatosplenic candidiasis, occurs mostly after prolonged episodes of bone marrow dysfxn and neutropenia (tx for leukemia), liver, speen and sometimes kidney involved, positive blood culture rare |
| Deep organ candidiasis | any organ can be affected, an episode of candidemia must precede the organ infection, only manifestation: focal infection of a specific organ |
| Coccidioides immitus | pericardium |
| Cryptococcus neoformans | myocarditis, pericarditis, endocarditis |
| Histoplasma capsulatum | lymphadenitis, endocarditis |
| Malaria | Mosquito ingest blood infected with malarial gametocytes (which mature in mosquitoe's gut=zygotes --> oocytes --> sporozoites in salivary glands); sporozoites travel to host liver --> merozoites then invade RBC |
| Plasmodium falciparum | most severe form of malaria, infect all erythrocytes, RBC membrane = rigid and stick to each other |
| Plasmodium vivax and P. ovale | cause a relapsing malaria, after tx, tx-resistant parasites reside dormant in the liver, later multiply in an exoerythrocytic cucle, eventually invade RBCs and begin typical erythrocyte cycle, recurrent infections --> anemia |
| Plasmodium malariae | produce long-lasting infections; most often asymptomatic |
| Incubation period | 7-30 days, P falciparum: shorter, P. malariae: longer |
| Clinical manifestations | delayed because of prophylaxis tx, antimalarial medications can delay onset of symptoms by weeks or months |
| Schuffner's dots | RBCs paratized by Plasmodium vivax display small purplish red granules with Wright's stain; common "ring stage" found intracellularly |
| Uncomplicated malaria | enlarged spleen, mild jaundice, body aches, general malaise, sweating, fever, chills, increased respiratory rate in P. falciparum |
| Lab results of Malaria | Mild anemia, thrombocytopenia, elevated bilrubin, aminotransferases, albuminuria, urinary casts |
| Cerebral malaria | abnormal behavior, impaired consciousness, coma, seizures |
| Severe malaria | cerebral, severe anemia, hemoglobinuria, pulmonary edema, abnormal blood coags, metabolic acidosis a/w hypoglycemia, cadivascular collapse, kidney failure |
| Malarial relapse | usu with P. vivax (has dormant liver stage) |
| Antigen detection of Malaria | Malarial RDT, not approved yet |
| Molecular diagnosis | PCR |
| Serology | Indirect fluorescent assay (IFA), ELISA, detection of antibodies |
| Schistosomiasis "blood flukes" | Individuals infected through contaminated water --> cercaria penetrate the skin and enter the venous system |
| Blood flukes | polyp formation in intestines, hepatomegaly, hematuria, urethral occlusions, headache, disorientation, amnesia, coma, arteriolitis and fibrosis leading the enlarg, of R ventricle, Swimmer sitch |
| Blood flukes - clinical manifestations | Katayama's fever, bloody diarrhea, hepatoslenomegaly, eosinophilia, S. japonicum eggs in brain and S. mansoni in spinal cord, pulm hypertension, cystitis, ureteritis with hematuria --> bladder cancer |
| Diagnosis | stool or urine (S. haematobium) dx, antibody detection using purified adult worm antigen, ELISA |
| Host immune responsed to blood flukes | IgE, eosinophil-mediated cytotoxicity |
| Chagas' Disease --> Trypanosoma cruzi | affects nervous sys and heart, chronic infections can lead to dementia, damage to heart muscle and death if untreated, spread by triatoma infestans, rhodnius prolixis, panstrongylus megistus |
| Chagas's disease | triatomine (reduviid) bug "kissing bug", infection by triatomine fecal material (uncooked meat or bite), high risk gp: in central and south america |
| Acute Stage of Chagas | Romana's sign (eye on 1 side swells), enlarged spleen or liver, swollen lymphn glands |
| Indeterminate Stage | asymptomatic, 8-10 weeks after infection, could last for years |
| Chronic Stage | 10-40 yrs after infections, can develop cardiac pbs (enlarged heart, arrhythmia, heart failure, enlarged esophagus --> severe constipation and pb in swallowing) |
| Human African Trypanosomiasis (HAT) "African Sleeping Sickness" | Trypanosoma brucei gambiense, slow-progressing that can be self-limiting or develop into a chronic disease involving the CNS and lymphatic system; T. brucein rhodesiense: rapidly profess, Kinetoplastids: mito DNA |
| Life Cycle | Metacyclic trypomastigotes resided in salivary glands of tsetse fly, different morphology in blood stream (long slender, short stumpy), develop into procyclic trypomas in gut, epimastigotes attach to epithelial cells in salivary glands by flagella |
| Disease progression of HAT | 1-2 week incubation, acute blood stage (fever, headaches), invasion of lymphatics (febrile attack, weight loss, weakness), relapse occur d/t antigenic variation of trypanosomal surface |
| Hallmark of this disease | Invasion of CNS: 6-12 months after infections with gamibiense, cross BBB results in meningoencephalitis, apathy, fatigue, confusion, tics, changes in sleep patterns (extreme fatigue during day and agitation at night) |
| Leishmaniasis | transmitted by sandflies, caused by obligate-intracellular protozoa, amastigote forms found in reticulo-endothelial cells of visceral (asmatigotes =LD bodies) |
| Symptoms of Leishmaniasis | Low-grade fever, general malaise, anemia, progressive wasting, protusion of abdomen (d/t enlargement liver and spleen) |
| Acute Leishmaniasis | Edema (in face), bleeding mucus membrane, breathing difficulties, diarrhea; pb: patients can recover with post Kala-azar dermal leishmanoid; face is badly disfigured |
| Babesiosis --> Babesia microti, Babesia divergens | emerging zoonosis; caused by animal-specific protozoan parasites which invade RBCs and induce a febrile disease |
| Hosts in Babesiosis | White-footed mouse (peromyscus leucopus), Deer tick (Ixodes dammini); human: accidental hosts (no human to human transfer) |
| DX of Babesiosis | Tetrad formation in blood smears, IFA, antibody titers more than 1:1024 in 1st weeks then 1:16 after 6 months, drenching sweats, loss of appetite, Low BP, pt with removed spleen more likely for complications |
| Filariasis | caused by infections with nematodes |
| Filariasis - Life Cycle | Infective larvae transmitted by arthropods,depending on species, larvae migrate to a particular area of host's body --> dvp into microfilaria-producing adult (fem); subcut tissues (onchocerca volvulus, loa loa; lymph: brugia malayi, whuchereria bancrofti) |
| Filariasis- Clinical Manifestations | Asymptomatic microfilaremia, some pts dvp lymphatic dysfxn --> Lymphedema, elephantiasis (usu in lower extremities), febrile lymphangitis and lymphadenitus, eosinophilia prominant |
| Filariasis- DX | identify microfilariae in blood and skin (sometimes need to concentrate blood specomens), antigen detection, Ab detection (not useful b/c of cross-activity btw filarial antigens and antigens from other helminths), serology cant distinguish past fr present |
Created by:
gladho
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