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Micro:Cardiovascular
| Question | Answer |
|---|---|
| Infective endocarditis Pathogenesis: | altered endothelium assists in bacterial colonization and making of biofilm |
| Infective Endocarditis Caused By: | Transient bacteremia. |
| Examples of Transient Bactremia | childbirth, bronchoscopy surgical procedures, dental procedures, toothbrushing, etc. |
| Bacteria Causing Infective Endocarditis | Most often normal flora. S. aureus = 40% S. viridans = 40% Enterococci = 20% |
| Infective endocarditis: Microbial adherence to damaged endothelial surfaces leads to: | Complement activation, inflammation--causing more damage. As a result, microorganisms are protected by a deposition of platelets and fibrin mesh. |
| Streptococcus pneumoniae is: | alpha hemolytic, and optochin sensitive (sensitive to P disc) |
| Gram negative bacteremia can lead to: | Shock and imapired O2 exchange, lung tissue damage, or Hemorrhage. |
| In Gram - bacteremia, if cytokines are released due to macrophage activation, what S&S occur? | decreased muscle tone of heart and arteries, fever, increased adhesiveness of PMNs (neutrophils), increased leakage of plasma from blood vessels--> These things all lead to shock |
| In gram - bacteremia, if complement is activated, what S&S occur? | Leukocytes are attracted to lung tissue, increased capillary leakage of plasma, and lysosomal enzymes are released from leukocytes--> These result in lung tissue damage |
| In gram - bacteremia, if clotting is activated, what S&S occur? | disseminated intravascular coagulation results in depletion of clotting proteins, and tissue damage results from clots in capillaries--> Hemorrhage |
| What is Bacterial Endocarditis? | a syndrome resulting from microbial infection f the endothelial surfaces of the heart--particularly the heart valves. |
| What is the MOA of bacterial endocarditis? | Microorganisms attach to a fibrin-platelet matrix formed on damaged cardiac valves or artificial synthetic materials |
| What infectious rmcroorganisms are usually invovled in bacterial endocarditis? | Usually bacteria, Rickettsia (scarlet fever), mycoplasma (don't have peptidoglycan walls), and chlamydia |
| What structures are normally affected by bacterial endocarditis? | mitral valve, aortic valve, tricuspid valve, mural endocardium, and myocardial abcesses can develop. |
| What are the symptoms of bacterial endocarditis? | Fever, chills, sweats, anorexia, altered or new heart murmurs, systemic emboli, splenomegaly. Usually the left side of the heart is affected. |
| What are the demographics of bacterial endocarditis? | Most commonly affects pts 45-65 yoa and males are affected 2x more often then women. |
| What increases your risk of getting bacterial endocarditis? | IVDU, and Alcoholism increases the chances of infection by Strep. pneumoniae. Immunosupression is also a risk factor. Diabetes. Chronic Renal Dz. Dental, pulmonary, GI, and GU procedures. |
| Endocarditis: | Infection of the heart valves, or infection of the inner tissue or the heart. |
| Acute Endocarditis | Sx appear abruptly, often as a result of an infection in another area of the body. |
| Acute endocarditis is caused by: | Staphylococcus aureus, and Streptococcus pneumoniae. |
| Subacute Bacterial Endocarditis (SBE) | Often caused by alpha-hemolytic streptococci when a dental procedure is done. Also occurs if bacteremia is introduced through the skin (surgery or catheterization). |
| SBE is most commonly caused by: | staphylococcus aureus or enterocicci (as a consequence of abnormalities in the GI tract or Urinary tract). |
| Sepsis | presence of pathogen in blood or tissues |
| Sepsis syndrome | evidence of altered organ perfusion |
| Septic Shock | hypotension |
| Multi-organ failure | caused by sepsis--affects kidneys, lungs, liver |
| DIC | hemorrhagic disorder that occurs following the uncontrolled activation of clotting factors and fibrinolytic enzymes throughout small blood vessels, resulting in tissue necrosis and bleeding |
| Septicemia | gram - bacteria have endotoxin to which the MQs respond (hypersensitivity). Release of toxins triggers MQs all over and they release TNF (increasing body temp) and complement factors |
| What is the importance of complement factors released by MQs in septicemia? | Macrophages release complement factors which can be activated by endotoxin. These complement factors attract leukocytes which release tissue-damaging lysozymes and cause capillaries to leak plasma. |
| Exotoxins | Gram +/-, three kinds: A-B toxins, Membrane damaging toxins, and Superantigens. |
| Exotoxins A-B toxins | Neurotoxin, Enterotoxin, and Cytotoxin |
| A-B toxins | A portion is pathogenic, and B portion mediates attachment to host cell. |
| Neurotoxin | C. tetani--blocks inhibitory neurons. C. botulinum--blocks nerve signals to muscles |
| C. tetani | a neurotoxin that blocks inhibitory neurons |
| C. botulinum | a neurotoxin that blocks nerve cell signals to muscles. |
| Enterotoxin | E.coli and V.cholera--GI cells start secreting electrolytes and H2O. |
| Cytotoxin | C.diphtheriae, S.dysenteriae, E.coli (0157:H7)--inhibits protein synthesis in humans causing apoptosis. |
| Membrane damaging toxins | cytotoxins and hemolysins do the damage by 2 means. Streptolysin O, which makes pores, and Phospholipases which remove polar heads of phospholipids in membrane |
| Streptolysin O | a membrane damaging exotoxin that makes pores in the cell membrane (ie: S. pyogens) |
| Phospholipases | membrane damaging exotoxins that remove poalr heads of phospholipids in the membrane (ie C. perfringens) |
| Endotoxins | found in Gram - bacteria only!!! |
| LPS | Lipid A is toxic. It activates the innate immune system, telling MQs to make TNF and IL-1 causing inflammation. Septic shock occurs d/t overwhelming immune response. These bad boys are heat stable. |
| Superantigens | cause septic shock d/t overwhelming immune response (ie: toxic shock syndrome) |
| Blood Culture | two bottles (aerobic and anaerobic) collected from at least 3 sites to r/o contamination. |
| If blood cultures are being drawn on a pt on abx? | ARD--antimicrobial removal device (resin that attaches to Abx) or FAN (fastidious antimicrobial neutralization (activated charcoal) |
| ARD | antimicrobial removal device--used in blood cultures that are taken when the patient is on Abx. ARD has resin that removes antimicrobials from the blood. |
| FAN | fastidious antimicrobial neutralization--used in patients that need blood cultures but are on abx--uses activated charcoal to neutralize the abx. |
| CBC | Complete blood count--drawn in the lavender tubes. |
| What is included in the CBC? | RBC count, WBC count, Platelets, Hemoglobin, Hematocrit, MCV (mean corpuscular volume) MCH (mean corpuscular Hb) MCHC (mean corpuscular Hb concentration) and RDW (RBC distribution width) |
| RBC count | Normal is 4.8x10^6/ml for men and 4.3x10^6/ml for women. |
| WBC count | Normal is 4500-10,500/ml |
| WBC differential | (Nobody Likes Mary Ellen's Brownies) Neurtophils = 40-60% Lymphocytes = 20-40% Monocytes = 2-8% Eosinophils = 1-4% Basophils = .5-1% Bands = 0-3% |
| Neutrophils | 40-60% of WBC diff. Elevated in bacterial infections |
| Leukocytes | 20-40% of WBC diff. Elevated in viral infections |
| Monocytes | 2-8% of WBC diff. Elevated in severe infections |
| Eosinophils | 1-4% of WBC diff. Elevated in allergic reactions or parasitic infections |
| Basophils | 0.5-1% of WBC diff. Elevated in allergic reactions and parasitic infections |
| Leukocytosis | increase in WBC (more that 11,000)--usually one type d/t acute infections |
| Lerukopenia | Decreace in WBC (less than 4000) d/t viral and overwhelming bacterial infections |
| Shift to the Left | Increase in number of immature neutrophils |
| Hemoglobin count | Normal values:In men, 14-17.4 g/dl. In women 12-16. Aids in the dx of anemias. |
| Hematocrit | Ratio of packed RBCs to total blood. Used to estimate RBC mass and dx anemia. Normal values: Women, 36-48% Men, 42-52% |
| MCV | mean corpuscular volume--aid in the classification of anemia. Normal range is 82-98 fL. Larger than normal is Macrocytosis, smaller than normal is Microcytosis. |
| Classifiacations of anemia | Macrocytic and Microcytic |
| Macrocytic anemia | B12/folate deficiency |
| Microcytic anemia | Fe deficency |
| MCH | mean corpuscular Hb--average Hb per RBC. Normal range is 26-34 pg/cell. Useful to find severe anemias. |
| MCHC | Mean corpuscular Hb concentration--average Hb per RBC volume. Normal range is 32-36g/dl. Useful to monitor therapy. |
| RDW | RBC distribution width. Normal is 11.5-14.5 cv. Measures the degree in variation of RBC sizes. |
| Anisocytosis | variation in RBC size |
| Poikilocytosis | variation in RBC shape |
| IV catheter bacteremia | Usually colonized by skin flora or the IV solution was contaminated |
| What skin flora usually colonize in IV catheter bacteremia? | S.aureus, S.epidermiditis, or Candidia |
| What bacteria usually colonize the IV fluid in IV catheter bacteremia? | Enterococci, Pseudomonas |
| Bacteremia from extravascular infection: | Microbes escape from infected area and reach veins through lymphatics. |
| Most common sources for bacteremia from extravascular infections? | UTI, respiratory, skin, wound infections. |
| Group B Streptococcal Disease (GBS) | Caused by S.agalactiae. |
| What does GBS cause in newborns? | sepsis, pneumonia and meningitis |
| What does GBS cause in adults? | sepsis, soft tissue infections, and amnionitis. |
| When are babies at high risk of getting GBS? | High risk if mom has GBS colonization, if mom is less than 20 yoa, if mom is black, if mom had ruptured membranes, or if baby is premature. |
| Rheumatic fever | begins with strep throat or scarlet fever |
| Manifestations of Rheumatic Fever | Polyarthritis, carditis, inflammatory dz affecting conecctive tissue of the heart, joints, brain and skin. |
| Epidemiology of Rheumatic Fever: | affects children between the ages of 6 and 15 yoa. There is an increased risk of repeat infections if you have it once. |
| Sx of Rheumatic Fever | fever, joint pain, skin rash, SOB, chest and abd pain, uncoordinated jerky movements (chorea). |
| Pathogenesis of Rheumatic Fever | bacterial antigen (m-protein) looks like myosin, so antibidies bind to heart sarcolemma. |
| Signs of Rheumatic Fever | Pts have increased T-cells, and antistrep and autoreactive antibodies. |
| Complications of Rheumatic Fever | Endocarditis, Arrhythmias, Pericarditis, and Heart Failure |
| Bubonic Plague | caused by bacteria Yersinia pestis |
| Yersinia Pestis | gram negative, non-motile, non spore forming rods, grow at 28C, which cause bubonic plague. |
| Vectors of Bubonic Plague today | Rock squrrels, prarie dogs, and chipmunks spread by fleas (Xenopsylla cheopis) |
| Xenopsylla cheopis | flea that carries Yersinia pestis, which causes bubonic plague. |
| Pathogenesis of Bubonic Plague | Y.pestis is carried in the lymph nodes and is taken up by MQs. They replicate w/in the MQs and destroy the MQs to release new bacteria. Inflammatory rxn leads to tender, enlarged lymph nodes called buboes. |
| Manifestation of Bubonic Plague | 2-7 days after bite. Onset is marked by painful buboes, usually in inguinal nodes. |
| If Bubonic Plague is not treated: | 75% goes to bacteremia and death occurs via gram negative septic shock within days of the first bubo. |
| Secondary Pneumonia due to Bubonic Plague (aka Pneumonic Plague) | Bacteria gets into blood and travels to lung causing secondary pneumonia which is HIGHLY contageous. |
| S&S of Pneumonic Plague | mucoid, bloody sputums, fever, malaise, tightness in the chest, terminal cyanosis (necrosis--this is why it is called the black death). Death can occur on the 2nd or 3rd day of the illness. |
| Primary Pneumonic Plague | If inhalation of the aerosolized microbe from another individual, but no buboes. |
| S&S of Primary Pneumonic Plague | bloody waters purulent sputum, nausea, vomiting, abd pain and diarrhea. |
| Mumps | Viremia--caused by the Paramyxovirus |
| Paramyxovirus | ssRNA, lipid containing envelope--causes Mumps |
| Mumps is acquired... | ...when person is exposed to infective respiratory droplets. |
| Mumps replicates | in nasopharynx and lymph nodes. |
| How soon does mumps viremia occur? | Within 25 days. |
| Sx of Mumps | myalgia, anorexia, HA, fever, salivary gland involvement. |
| Complications of Mumps | Aseptic meningitis, ovarian/testicular inflammation, pancreatitis |
| Prevention of Mumps | MMR vaccine |
| Infectious Mononucleosis | Characterized by an increase in monomuclear LEUKOCYTES |
| Etiologic agent in Mono | Epstein-barr virus (EBV) which has an affinity for b-lymphocytes |
| EBV | dsDNA virus in the herpes virus family--spread by oral contact |
| Sx of Mono | Fatigue, fever, sore throat, lymphadenopathy. Leukocytosis by 2nd week of infection, leukopenia possible during 1st week of infection. |
| Reactive (atypical) lymphocytes | Often present in viral infections--in Mono, 10-20% of lymphocytes are atypical on a differential. These lymphocytes are said to have a "blue skirt' |
| In Mono there are three types of antibodies | Heterophile, EBV, and autoantibodies |
| Heterophile Antibodies | react with unrelated antigens on cells from different species. |
| What is the basis for the Monospot test? | Heterophile antibodies belonging to IM can be absorbed by bovine erythrocytes, but not by guinea pig kidney cells. |
| When is the Monospot test falsely negative? | In IM occuring in children under the age of 10. |
| EBV antibodies | EBV-VCA (IgM), EBV-VCA (IgG), EBNA, EBV-EA |
| Most commonly measured EBV antibodies | EBV-VCA (IgM) and EBV-VCA (IgG) |
| When is the EBC antibody test done? | When IM is suspected, but the heterphile antibody test is negative. |
| Mono Autoantibodies: | RBCs, WBCs, platelets, cold agglutinins |
| EBV-VCA (IgM) | IgM antibody to capsid antigen. Present at detectable levels in 1st week of infection; the best indicator of current infection. |
| EBV-VCA (IgG) | IgG antibody to capsid antigen. Present at detectable levels about 7 days after exposure; indicates either current or past infection; a rise in titer must be demonstrated on acute and convalescent sera. |
| What is the order of operations for testing for Mono? | 1) Heterophile antibody test. If +, tx for IM. If -, 2)repeat heterophile test in 1 week. If +, IM. If -, 3)EBV-IgM antibody test. If +, IM. If -, CMV-IgM test. If +, CMV mono. If -, run hepatitis tests, toxoplasma titer, or viral cultures. |
| Other Clinical Syndromes of EBV: | B-cell latency, EBNA,Burkitt's Lymphoma |
| B-cell latency | EBV infects B-cells and establishes a latent infection. EBV incorporates its genome into host cell DNA. |
| EBNA | (EBV genes) transforms B-cells into immortal, constantly dividing cells. A healthy host immune system keeps these bad boys in check. |
| Burkitt's Lymphoma | B-cell lymphoma. There are high levels of antibodies to EBV antigens. EBV genome is detected in tumor cells. Viral particles detected in BL cell culture. |
| Fungemia | can be caused by complications due to venous or arterial catheterization |
| Fungemia occurs in: | Host with compromised immune system ie: AIDS, Antimicrobial therapy, Radiation, and antineoplastic drugs |
| Which fungemia is mc in IVDUs? | Candida albicans--causing candida endocarditis. |
| Etiologic agents of fungemia include | Candida albicans, other Candida sp, Histoplasma capsulatum, Coccidioides immitus, Cryptococcus neoformans |
| Candidemia | the isolation of candida sp from blood specimens. Associated with significant M&M. This is the 4th most common cause of blood stream infections in the 1990s. |
| Most common cause of Candidemia | Candida albicans (1/2 of all cases) |
| Most common cause of Candidemia in bone marrow patients | C.krusei |
| 4 overlapping forms of invasive candidiasis | catheter related candidemia, acute disseminated candidiasis, chronic disseminated candidiasis, deep organ candidiasis. |
| Catheter related candidemia | Primary infection is on the catheter or related to the fibrin clot which forms on the catheter. Anitfungal therapy is required to remove local infection. |
| Acute disseminated candidiasis | May have originated from contaminated catheter. Infection has spread to one or more organs. |
| Chronic disseminated candidiasis | also called hepatosplenic candidiasis--occurs almost exclusively following prolonged episodes of bone marrow dysfunction and neutropenia. Liver, spleen and kidneys are involved. Positive blood cultures at this stage are rare. |
| Deep Organ Candidiasis | Any organ can be affected. |
| Fungemia also includes disseminated forms of | Coccidioidomycosis, Cryptococcosis, and Histoplasmosis. |
| Fungemia forms of Coccidioidomycosis | Coccidioides immitus, Pericardium |
| Fungemia forms of Cryptococcosis | Cryptococcus neoformans, Myocarditis, pericarditis, and endocarditis. |
| Fungemia forms of Histoplasmosis | Histoplasma capsulatum, Lymphadenitis, endocarditis |
| Maliaria | Mosquito (named ANOPHELES) ingests blood infected with malarial gametocytes and then spreads it to another host. |
| When a mosquito infected with malaria bites a human | the sporozoites are transferred from the saliva to the human. |
| Once in the human blood, malarial sporozoites | travel to the liver where they invade the liver cells and replicate into merozoites. |
| From the liver, malarial merozoites | leave the liver through the circulatory system and invade RBCs. They continue to replicate, lyse RBCs, and invade other RBCs. Some develop into male and female gametocytes. |
| The male and female gametes of the malaria do what? | They get transferred to a mosquito when it bites the infected host. |
| In the mosquito, the malarial gametes | mature and fuse to become zygotes. |
| malarial zygotes | in the mosquito develop into oocytes. The oocytes multiply into many sporozoites. |
| Malarial sporozoites in the mosquito | migrate from the gut to the salivary glands and then get transferred to a new host when the mosquito bites. |
| Species of Malarial carrying mosquito | Anopheles |
| Plasmodium falciparum | is the most sever form of malaria. These paracytes infect all erythrocytes. RBCs become rigid and stick to eachother and to capillary walls. |
| Plasmodium vivax and P.ovale cause | relapsing malaria. Recurring infections can cause severe anemia. |
| Plasmodium malariae | produce long-lasting infections which are most often asymptomatic. |
| Malaria incubation period | 7-30 days after bite. P.falciparum is shorter, Pmalariae is longer. |
| Clinical manifestations of malaria | are delayed due to prophylaxis tx. Antimalarial medications can delay onset of sx by weeks or months, often leading to misdiagnosis--especially in vivax or ovale. |
| S&S of Uncomplicated malaria | fever, chills, sweating, HA, N/V, body aches, general malaise, enlarged spleen, mild jaundice |
| Physical findings of malaria | elevated temp, perspiration, weakness, enlarged spleen |
| Additional physical findings with P.falciparum | mild jaundice, enlarged liver, increased RR. |
| Malarial Lab Results (Particularly with P.falciparum infections): | mild anemia, thrombocytopenia, elebated bilirubin, animotransferases, Albuminuria, urinary casts. |
| S&S of Severe Malaria | cerebral malaria, hemoglobinuria, pulmonary edema, abnormal blood coags, thrombocytopenia, cardiovascular collapse, kidney failure, metabolic acidosis associated with hypoglycemia, acute kidney failure, hyperparasitemia, metabolic acidosis |
| Cerebral malaria | abnormal behavior, impaired consciousness, coma, and seizures. |
| Malarial Relapses | often occurs with P.vivax which has a dormant liver stage in its life cycle. Relapses can occur after months or years w/out sx. |
| Dx of Malaria | Microscopic: preparation of blood smear stained standard blood cell stains such as Giemsa, Wrights--this is the gold standard of laboratory confirmation. Also, antigen detection (not currently approved in the US), Molecular dx by PCR, and serology. |
| Schistosomiasis "blood flukes" | Schistosoma hematobium, S.mansoni, and S.japonicum |
| How do people get infected with Schistosomiasis | through contaminated water. Cercaria penetrate the skin and enter the venous system to travel to the heart, lungs, and portal circulation. |
| S&S of blood fluke infection on skin | penetration of skin by cercariae causes swimmers itch. Physical damage to the skin caused by proteases secreted by the cercariae |
| S&S of infection with blood flukes in the bladder | granulomatous lesions, hematuria, and urethral occlusions |
| S&S of infection with blood flukes in the Intestines | Polyp formation (sometimes leading to life-threatening dysentery). |
| S&S of infection with blood flukes in the Liver | Eggs cause hepatomegaly due to periportal fibrosis and portal hypertension |
| S&S of infection with blood flukes in the Nervous system | HA, disorientation, amnesia, coma |
| S&S of infection with blood flukes in the Heart | arteriolitis and fibrosis leading to enlargement and failure of the right ventricle. |
| Clinical features of acute schistosomiasis with S.mansoni and S.japonicum | Katayama's Fever |
| Clinical features of blood fluke infection | fever, cough, abdominal pain, diarrhea (bloody) hepatosplenomegaly, eosinophilia, cystitis, ureteritis with hematuria (can lead to bladder cancer) and pulmonary hypertension. |
| Occasional clinical features of blood fluke infection | CNS lesions--Cjaponicum leaves eggs in the brain. S.mansoni and S.haematobium leave eggs in the spinal cord |
| Host immune responses to blood flukes | IgE and Eosinophil-mediated sytotoxicity |
| Dx of Schistosomiasis | Microscopy of stool (all species) or urine (s.haematobium). Also antibody detection. |
| Trypanosomiasis | T.cruzi, T.brucei gambiense, T.brucei rhodesiense |
| Trypanosoma cruzi | Chagas' dz |
| Trypanosoma brucei gambiense | Chronic form of African sleeping sickness |
| Trypanosoma brucei rhodesiense | Acute form of African sleeping sickness |
| Chagas' Dz | caused by T.cruzi--affects primarily nervous system and heart. Chronic infections can result in dementia, damage to heart muscle, and can lead to death if left untreated. |
| Chagas' Dz is spread by vectors such as: | "Kissing Bugs"--Triatoma infestans, Rhondnius prolizis, and Panstrongylus megustys |
| Chagas' Dz in the Americas | American trypanosiomiasis--primarily found in central and south america--occasionally transmitted in the US. |
| Chagas' Dz acute stage: | Romana's Sign--eye on one side swells, fever, fatigue, enlarged liver or spleen, swollen lymph glands. Brain damage and death could occur in infants and young children. |
| Chagas' Dz indeterminate stage | asymptomatic--occurs 8-10 weeks after incection and could last for years |
| Chagas' Dz chronic stage | 10-40 years after infection 20-30% of these individuals develop serious sx including cardiac problems (including enlarged heart, arrhythmia, and heart failure), enlargement of esophagus or large bowel (causing problems swallowing or severe constipation). |
| Human African Trypanosomiasis (HAT) aka African Sleeping Sickness | Trypanosoma brucei ganbiense, Trypanosoma brucei rhodesiense, Kinetoplastids |
| Trypanosoma brucei gambiense | Slow-progressing illness that can be self-limiting or develop into a chronic disease involving the CNS and lymphatic system |
| Trypanosoma brucei rhodesiense | Rapidly progressing disease |
| Kinetoplastids | Mitochondrial DNA |
| The important thing about the life cycle of african sleeping sickness | is that because it keeps changing forms, it evades the immune system. |
| Vector for African sleeping system | Tsetse fly |
| Progression of african sleeping sickness | 1-2 week incubation period (sometimes the appearance of a chancre), followed by an acute blood stage (fever, HA), and invasion of lymphatics (enlarged nodes, weight loss, weakness, rash itching, continued fever). Relapses occur. |
| The Hallmark of African sleeping sickness | is the invasion of the CNS. Nervous system impairment is 6-12 months after initial infection (T.gambiense) but can occur w/in weeks (T.rhodesiense). Trypanosomes cross the BBB resulting in meningoencephalitis. |
| Sx of CNS involvement by African Sleeping Sickness include | apathy, fatigue, confusion, motor changes (tics, slurred speech), extreme fatigue during day, extreme agitation during night. Untxd, can progress to coma or death. |
| Leishmaniasis | Vector-borne dz transmitted by sandflies and caused by obligate-intracellular protozoa. |
| Incubation of Leishmaniasis | as short as 10 days or as long as a year. Average time is 2-4 months. |
| Sx of Leishmaniasis | fever, malaise, anemia, wastihg, protrusion of abdomen due to enlarged spleen and liver. Death in 2-3 years if left untxd. |
| Acute Leishmaniasis (6-12 months) sx | edema (particularly of face), bleeding mucus membranes, breathing difficulties, diarrhea |
| Complications of Post Kala-azar dermal Leishmaniasis | Perminant disfigurement of face and/or limbs |
| Dx of Leishmaniasis | Spleen sm,ear showing amastigotes (also called LD bodies). |
| Babesiosis | caused by deer tick (which can also cause Lyme dz). |
| Babesiosis is caused by | animal-specific protozoan parasites that invade RBCs and induce a febrile dz (hemolytic anemia, hemoglobinuria, shock, and death). |
| 2 Species of Babesia responsible for the majority of human infections | B.microti, B.divergens |
| 2 hosts that carry Babesia to humans | White-footed mouse, and Deer tick. |
| How do we know that humans are accidental hosts of Babesia? | Babesia sp. so not transfer from human to human--we are 'dead end' hosts. |
| Babesiosis sx | Similar to malaria b/c RBCs are infected w/parasite. Sx include fatigue, loss of appetite, fever, sweat, muscle aches, HA--lasting from days to months. |
| Dx of Babesiosis | Babesia sp parasites found in RBCs in a thin blood smear. They take a tetrad formation. Also dx by IFA |
| Complications of Babesiosis | Low BP, liver dz, sever hemolytic anemia, kidney failure--people who have had their spleens removed are the most susceptible. |
| Filariasis | Caused by infection with nematodes (roundworms). |
| 8 species of filariasis are known to affect humans | 3 of these are responsible for most of the morbidity due to filariasis, and the other 5 are there. |
| 3 species of filariasis that most commonly affect humans | Wuchereria bancrofti, Brugia malayi, and Onchocerca volvulus |
| Lymphatic filariasis | caused by Wuchereria bancrofti and Brugia malayi |
| River blindness (Onchocerciasis | caused by Onchocerca volvulus |
| Filariasis vectors | larvae are transmitted by arthropods. |
| Lymphatic filariasis clinical manifestations | lymphedema, elephantiasis often occuring in the lower extremities. Febrile lymphangitis and lymphadenitus, and eosinophilia are also common. |
| Dx of Filariasis | Microscopic examination to identify presence of microfilariae in the blood or in the skin. Also antigen or antibody detection can be used. |
| Blood collection for filariasis | must be timed with periodicity of organism |
| Presence of microfilariae in the skin is most indicative of | Onchocerca volvulus and Mansonella streptocerca. |
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ahanna2008
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