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Cardiovas. Disease

Medical Microbiology

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