Cardiovascular and Lymphatic Diseases PDF

Cardiovascular and Lymphatic Diseases Week 10 The Cardiovascular and Lymphatic Systems Heart and Blood Vessels Heart: Lies in the peicardium Interior: endocardium Middle: myocardium Outer: epicardium Closed system of flow to and from th...

Cardiovascular and Lymphatic Diseases Week 10 The Cardiovascular and Lymphatic Systems Heart and Blood Vessels Heart: Lies in the peicardium Interior: endocardium Middle: myocardium Outer: epicardium Closed system of flow to and from the heart Gasses, nutrients, and lymphocytes The Blood Water, proteins and cells Lymph is derived from blood Proteins and lymphocytes Travels in lymph vessels to nodes Nodes contain B-cells and T-cells and macrophages No normal microflora! modification of work by NCI and NIH Agenda Bacterial Bacteremia and Septicemia Acute and Sub-Acute Bacterial Endocarditis Plague Lyme Disease Anthrax Rocky Mountain Spotted Fever Viral Infectious Mononucleosis and Burkitt’s Lymphoma: Epstein Barr Virus Ebola Virus Hemorrhagic Fever West Nile Fever Protozoan Malaria Toxoplasmosis Bacteremia & Septicemia Bacteremia/Viremia/Toxemia: present in the blood. Septicemia: toxin-producing bacteria multiplying in the bloodstream Sepsis occurs in 2 of every 100 hospital admissions. Inflammation is out of control and becomes harmful SIRS: Systemic Inflammatory Response Syndrome Most common with pneumonia Causative agents: Streptococci, Staphylococci, nosocomial bacteria (Gram-negatives) or multiple organisms Transmission: An infection elsewhere in the body & nosocomial (intravenous lines, surgical wounds, surgical drains, ulcers, bedsores) Sepsis and Septicemia Signs/Symptoms: Lymphangitis Shock (vasodilation) Confusion Blood-clotting abnormalities petichiae Organ Shutdown Diagnosis: Blood culture Treatment: IV Antibiotics Usually penicillin or vancomycin Gram negative more difficult to treat → why? Must be caught early By James Heilman, MD [CC BY-SA 3.0 (https://creativecommons.org/licenses/by-sa/3.0) or GFDL (http://www.gnu.org/copyleft/fdl.html)], from Wikimedia Commons Acute & Subacute Bacterial Endocarditis An infection of the endocardium and/or valves leading to inflammation. May develop slowly (sub-acute) or it may occur suddenly (acute) Risk groups: People with a damaged heart valve, an artificial heart valve or other heart defects. Causative agent: Acute endocarditis: S. aureus is the usual cause Sub-acute bacterial endocarditis: Caused by alpha hemolytic Streptococci & Staphylococci (mostly part of oral microbiota) Acute & Subacute Bacterial Endocarditis Transmission: A damaged valve accumulates clots Bacteremia occurs Bacteria sticks to clots → Vegetations Can break off and block vessels What virulence factor might be involved? What benefit is it to the bacteria? modification of work by Centers for Disease Control and Prevention Acute & Subacute Bacterial Endocarditis Signs and Symptoms: Fatigue, fever, anemia, a new heart murmur, weakness, chills, aching joints & muscles, night sweats, cough, shortness of breath, swelling in the legs, ankles or feet, loss of appetite, unexplained weight loss, blood in urine, headache & spleen tenderness Endocarditis can also involve red skin rashes Can be fatal in a few days (acute) or months (sub-acute) if untreated. Acute & Subacute Bacterial Endocarditis Diagnosis: Blood cultures, heart sounds, ECG, echocardiogram, chest X-ray. Treatment: High doses of IV antibiotics for 4-6 weeks. Acute: Ampicillin, nafcillin, and gentamicin If prosthetic heart valve: vancomycin, rifampin, and gentamicin May require valve replacement surgery Prevention: Antibiotics prior to certain medical or dental procedures that may allow bacteria to enter your bloodstream Plague 3 previous pandemics Justinian: 5K deaths per day Black Death: 50 million dead Orientalis: 1890s In the U.S., 1 - 40 cases reported annually NM, AZ, CO, & CA. Risk Groups: Highest rates in Native Americans and people who have contact with animals Causative agent: Yersinia pestis (Gram-negative rod) CDC  Transmission credit “diagram”: modification of work by Stenseth NC, Atshabar BB, Begon M, Belmain SR, Bertherat E, Carniel E, Gage KL, Leirs H, and Rahalison L; credit “cat”: modification of work by “KaCey97078”/Flickr Bubonic Plague Bacteria travel through the lymphatic system to the nearest lymph node & multiply The lymph nodes become inflamed & buboes form. Hemorrhages associated with lymph node enlargement Pneumonic: Bacteria multiply in lungs usually progressing from buboes. Septicemic: Travels to tissues or enters through wound Bacterial proteins prevent phagocytosis Yop proteins are injected into macrophages. Other virulence genes disrupt inflammatory response, destroy complement & degrade fibrin clots to aid spreading of organism. American Society of Microbiology Plague Bubonic Plague Buboes: Enlarged, tender lymph nodes Fever Chills Prostration Signs/Symptoms (Pneumonic plague) Fever, chills, cough and difficulty breathing; rapid shock and death if not treated early. Treatment Tetracycline, streptomycin Vaccine Available worldwide Not recommended for immediate protection Only recommended for high-risk groups. CDC Lyme Disease Named in 1977 when arthritis was observed in a cluster of children in & around Lyme, Connecticut. Over 25,000 infections in the US in 2014 Causative agent: Borrelia burgdorferi Gram negative, spirochete Lyme Disease Risk Groups: Human encroachment on wooded areas White tailed deer Most common tick-borne illness in the US Tick must feed for at least 36 hours to transmit Tick Life Cycle credit “mouse”: modification of work by George Shuklin Lyme Transmission a: modification of work by Jerry Kirkhart; credit c: modification of work by Centers for Disease Control and Prevention) Lyme Disease Signs/Symptoms: A red bull’s eye rash (erythema migrans) & flu-like symptoms Rash in 70-80% of cases 1 week- 4 months later: Large joints become stiff, swollen Pain (due to myelin loss) Cardiac symptoms (myocarditis) Neurological symptoms Paralysis: Bell’s Palsy CDC Lyme Disease Diagnosis, Treatment, and Prevention Anthrax A zoonosis that affects mostly herbivorous animals (sheep, goats and cows) Causative agent: Bacillus anthracis Gram-positive, endospore former 3 Forms of Anthrax Cutaneous, Respiratory, and Gastrointestinal Transmission: Not spread from one person to another. Anthrax from animals Handling products from infected animals Inhalation of anthrax spores from infected animal products (wool) Anthrax from food: Eating undercooked meat from infected animals. Anthrax Bacteria produces virulence factors Protective antigen: binds the toxins to target cells, permitting their entry Edema toxin: causes local swelling and interferes with phagocytosis Lethal toxin: targets and kills macrophages Amino acid capsule that avoids an immune response Cutaneous Anthrax: Signs and Symptoms Small sore→ Blister → Distinctive Ulceration Most common form (90%) 2 to 5 days incubation 10-20% fatal without treatment 1% with treatment CDC GI and Pulmonary Anthrax: Symptoms and Treatment Gastrointestinal: Less common (5%) Contaminated food products → Made from infected animal Nausea, loss of appetite, bloody diarrhea, and fever → bad stomach pain 25-50% fatal Inhalation: 5% of all cases Flu-like symptoms → cough, chest discomfort, shortness of breath, fatigue & muscle aches Almost always fatal, even with treatment In 2001, 50% fatality rate Treatment: Ciprofloxacin (Cipro), penicillin, doxycycline, erythromycin, chloramphenicol Anthrax- Prevention Prevention: Prophylactic antibiotics combined with the anthrax vaccine Livestock Hygiene Risk Bioterrorism potential Category A agent Has been used recently (2001) FBI Rocky Mountain Spotted Fever Rickettsia rickettsii Despite name, most cases in Appalachia and Southeastern US Transmission: Dog Tick CDC RMSF: Signs and Symptoms Signs and Symptoms One week after bite Headache, fever, nausea & a rash usually on the arms or ankles/wrists Joint & stomach pain, & diarrhea Pathogenesis Invasion of blood vessel endothelia Petichiae: local hemorrhages 5-80% mortality depending on strain Treatment: Doxycycline Prevention: Tick bite prevention CDC Viral Cardiovascular and Lymphatic Disease Epstein Barr Virus Ebola Virus Hemorrhagic Fever West Nile Fever Infectious Mononucleosis Causative agent: Epstein-Barr Virus (EBV) Human Herpesvirus 4 EBV is found worldwide In developing world most are infected soon after birth → asymptomatic In the US: 95% of adults between 35 - 40 years have been infected When infected with EBV during adolescence or young adulthood, infectious mononucleosis results 35-50% of the time Infects and replicates within mature memory B cells B cells produce antigens that T cells recognize causing them to proliferate leading to excess lymphocytes Proliferation is limited by cytotoxic T cells Failure of this suppression can lead to Hodgkin’s Lymphoma or Burkitt’s Lymphoma Infectious Mononucleosis Transmission Person-to-person usually via contact with saliva EBV enters body through the oropharynx, infects epithelial cells & eventually B cells Incubation period 4 - 6 weeks Signs/ Symptoms: Fever, sore throat, & swollen lymph glands. Sometimes, a swollen spleen or liver involvement may develop. Diagnosis: Elevated white blood cell count, a positive antibody test. Treatment: None Protection of the spleen and symptomatic Burkitt’s Lymphoma Occurs about 6 years after primary EBV infection A tumor of the jaw & viscera (liver or spleen) Seen mainly in malaria endemic areas Co- or past infection with malaria may interfere with suppression or enhance viral replication modification of work by Bi CF, Tang Y, Zhang WY, Zhao S, Wang XQ, Yang QP, Li GD, and Liu WP Ebola Virus Hemorrhagic Fever A severe syndrome affecting multiple organ systems often accompanied by hemorrhaging. Causative agent: Ebola virus (highly virulent) Ebola is fatal in 50-90% of cases Transmission: Person-to-person contact (blood, body fluids or organs), fomites (contaminated needles and syringes), & sexual contact. Signs/symptoms: Within 2 days- 3 weeks, fever, weakness, muscle pain, vomiting & diarrhea. Then, some people develop hemorrhagic rash, delirium, bleeding from the nose, mouth, eyes, ears & rectum, seizures & coma Treatment: Effective Treatments Available Vaccine in development http://apps.who.int/ebola/ Long-Term Presence of Ebola? Emory Eye Center West Nile Fever NYC 1999 → First cases surrounding LGA A potentially serious illness causing seasonal epidemics in North America (summer into the fall). Causative agent: West Nile virus (WNV) Risk Groups People over 50 Transmission Mosquitos & dead birds Incubation 2-15 days Centers for Disease Control West Nile Fever Signs/Symptoms: Vary 80% → asymptomatic 20% → fever, headache, body aches, nausea, vomiting, & swollen lymph nodes or a skin rash on the chest, stomach & back. 1 in 150 people develop severe illness with a high fever, headache, neck stiffness, stupor, disorientation, coma, tremors, convulsions, muscle weakness, vision loss, numbness & paralysis. Symptoms may last several weeks, but neurological effects may be permanent. Treatment: None; supportive Prevention: Avoid mosquitoes NYC and WNV  Cardiovascular and Lymphatic Systemic Diseases Toxoplasmosis Malaria Toxoplasmosis Causative agent: Toxoplasma gondii More than 60 million people in the US may be infected with CDC Toxoplasma. Most asymptomatic → normal immune system can suppress Risk groups Pregnant women and immunocompromised USDA  Toxoplasmosis The infectious cycle of Toxoplasma gondii. (credit: “diagram”: modification of work by Centers for Disease Control and Prevention; credit “cat”: modification of work by “KaCey97078”/Flickr) Toxoplasmosis Signs/Symptoms Variable Flulike symptoms with swollen lymph glands, muscle aches and pains that last a month or more. Severe cases can cause damage to the brain, eyes, or other sense organs Diagnosis Blood tests specific for toxoplasmosis Treatment Pyrimethamin, trisulfapyridine Prevention Avoid cat feces, especially pregnant women Wear gloves when changing litter box Hand washing & washing materials used in food preparation Cook all meat thoroughly (internal temp. = 168° F) Malaria One of the most severe of all parasitic diseases Endemic is most tropical areas Causative agent: Protozoan Plasmodium species Plasmodium are amoeboid, intracellular protozoa that infect erythrocytes and other tissues Affects 300 to 500 million globally; 2 to 4 million deaths annually Four major forms: Plasmodium vivax: mildest and most prevalent form; dormant in the liver Plasmodium ovale and Plasmodium malariae: benign; restricted geographically Plasmodium falciparum: most deadly; severe anemia; blocks capillaries; affects the kidneys, liver, and brain Malaria Mosquito bite transmits sporozoite into the bloodstream Enters the liver cells (which undergo schizogony), resulting in the release of merozoites into the bloodstream Merozoites infect RBCs and again undergo schizogony Ruptures the infected RBCs, releasing toxic compounds Causes paroxysms of chills and fever Some merozoites develop into gametocytes and are taken up by a mosquito, repeating the cycle CDC A blood smear (human blood stage) shows an early trophozoite in a delicate ring form (upper left) and an early stage schizont form (center) of Plasmodium falciparum from a patient with malaria. (credit: modification of work by Centers for Disease Control and Prevention) Malaria Prophylaxis Chloroquine; Malarone for chloroquine-resistant areas Treatment Artemisinin: reacts with iron to create free radicals Quinine: Blood stage, prevents hemoglobin digestion Chloroquine: same as quinine Primaquine: Kills hepatic form, interferes with mitochondria, prevents sexual reproduction. Prevention: Parasite develops resistance and changes antigens during life cycle Netting & spraying with insecticide Malaria Diagnosis: blood smear Complications : severe anemia, breathing problems, dehydration, liver failure, kidney failure, & rupture of the spleen Parasite-filled RBCs cells block small blood vessels to the brain leading to swelling of the brain or brain damage. This is known as cerebral malaria Malaria Descriptions of the disease date back to 1600 B.C. Malaria was common in the United States during the 19th century and early part of the 20th century Malaria remains one of the globe's leading infectious killers Estimates of annual deaths range between 700,000 and 2.7 million More than 75% of these deaths occur in children in sub-Saharan Africa Risk Groups: Virtually eradicated in temperate climates Africa, Asia, South America and Central America. Malaria Treatment: Quinine: Blood stage, prevents hemoglobin digestion Chloroquine: same as quinine Primaquine: Kills hepatic form, interferes with mitochondria, prevents sexual reproduction. Prevention: Parasite develops resistance and changes antigens during life cycle Vaccine needs to be immunogenic at the proper stage Prophylactic antibiotic therapy for endemic areas Netting & spraying with insecticide