Blood and Blood Products & Infections & Vaccines PDF

Blood and blood products Blood borne infections & Vaccines 1 Blood cells 2 History of Blood Transfusion 1628 British physician William Harvey discovers the circulation of blood. 1658 Microscopist Jan Swammerdam observes and describes red blood...

Blood and blood products Blood borne infections & Vaccines 1 Blood cells 2 History of Blood Transfusion 1628 British physician William Harvey discovers the circulation of blood. 1658 Microscopist Jan Swammerdam observes and describes red blood cells. 1665 The first recorded successful blood transfusion occurs in England: Physician Richard Lower keeps dog alive by transfusing blood from other dogs. 1667 Jean-Baptiste Denis in France and Richard Lower and Edmund King in England separately report successful transfusions from sheep to humans. 1818 British obstetrician James Blundell performs the first successful transfusion of human blood to a patient for the treatment of postpartum hemorrhage. 1901 Karl Landsteiner, an Austrian physician, discovers the first three human blood groups. 1907 Reuben Ottenberg performs the first blood transfusion using blood typing, cross-matching. 1914 Long-term anticoagulants, among them sodium citrate, are developed, allowing longer preservation of blood. 1939-1940 The Rh blood group system is discovered by Karl Landsteiner, Alexander Wiener, Philip Levine and R.E. Stetson. The first studies on blood transfusion in our country were initiated by Prof.Dr.Burhanettin Toker in 1921. The first transfusion was performed at Cerrahpaşa Medical Faculty in 1938. 3 Blood groups-AB0 Rh system There are more than 600 surface antigens on erythrocytes. The most important is the ABO blood group system. ABH, Lewis, P and I antigens are carbohydrate in nature and can be found in cell membranes and dissolved in body fluids. Rh, MNS, Kell, Lutheran, Kidd, Duffy antigens are in protein structure. 4 Blood groups-AB0 Rh system O A B AB Rh (+) Rh (-) 5 A BLOOD GROUP B BLOOD GROUP AB BLOOD GROUP 0 BLOOD GROUP 6 7  BLOOD AND BLOOD PRODUCTS Whole Blood Red Blood Cells Platelet-Rich Plasma Fresh Frozen Plasma Platelet Suspension Liquid Plasma Cryoprecipitate 8 BLOOD COMPONENT (PRODUCT) USE Whole blood: blood collected from a suitable donor using sterile and nonpyrogenic anticoagulants and a bag. Today, whole blood is considered source material; use blood components. The purpose of separating whole blood into its products (component); is to prepare the most useful, safe, needed and effective blood product for the patient. 9  WHOLE BLOOD — 450 (± 10%) ml of blood, which is stored in 63 ml of anticoagulant after it is taken from the blood donor, is called whole blood. ◦ ~ 450 (± 10%) ml (~ 250 ml plasma + ~ 200 ml erythrocytes) ◦ Hematocrit (Hct): 36-37% ◦ Storage at 2-6 ºC ◦ Storage time varies depending on the type of anticoagulant — When first taken, it contains erythrocytes, leukocytes, platelets, plasma and coagulation factors. — Platelets lose their function in 48 hours at +4 °C — Coagulation factors lose their function in 5-7 days — Requires cross-match — Blood that does not exceed 24 hours after collection is called fresh whole blood. 10  ERYTHROCYTE SUSPENSİON — The erythrocyte suspension is obtained as a result of the separation of the plasma of the whole blood by centrifugation method. — 200-250 ml (contains only 50 mL of plasma) — Htc % 65-75 Hb: 40-45 gr — Storage at 2-6 ºC, 42 day (SAG-M ) — Requires cross match Use the “leukocyte filter” to obtain leukocyte-poor ES. Leukocyte-poor Erythrocyte suspension is important in preventing FNHTR and transmission of CMV enf. Transfusion should be started within 30 minutes after leaving the refrigerator. No medication should be added to the bag, the transfusion should be completed within 4 hours. 11 Leukocyte-reduced erythrocyte suspension It is an erythrocyte suspension prepared by removing the buffy coat and using a leukocyte filter. < 1 x 106 leukocytes per target unit Significantly reduces CMV transmission. It does not prevent GVHD. Its use is the same as with other erythrocyte suspensions. 12 Washed erythrocyte suspension It is used in uncontrollable febrile and anaphylactic reactions, in patients with IgA deficiency or anti-IgA antibodies, in patients who develop antibodies against plasma proteins. In ES washed with sterile SF, 98% of the plasma, 85% of the leukocytes, all of the platelets and cellular wastes are removed. The usage time is “24 hours” after washing. The way of use is like other erythrocyte suspensions. 13 ERYTHROCYTE SUSPENSİON INDICATIONS — Symptomatic Anemia; If Hb is below 5 g, transfusion should be done. In chronic anemia, Hb up to 7 g can be tolerated. — Patients with non-massive bleeding; 14  PLATELET SUSPENSİON Random Platelet Apheresis Platelet Susp. — Obtained from one unit of — Apheresis platelet suspension whole blood by is obtained by separating only platelets from donors, thanks centrifugation to apheresis devices in the — 50-60 ml blood bank and special sets. — For adults, 4-6 units of — 200-250ml random platelets are used — One unit of apheresis platelet by pooling. suspension is generally the effective dose for adults. 15  PLATELET SUSPENSİON — Platelet suspensions are stored at 20-24 °C and in an agitator.* — Storage time: 5 days — It is used in thrombocytopenia of various causes. — No cross-match is required for platelet tranfusion — ABO, Rh blood group compatibility is sufficient 16  FRESH FROZEN PLASMA — It is plasma that is separated from whole blood within 6 hours after the blood is bagged and stored at at least -40 ºC. — Shelf life 1 year when stored at -40 ºC — 200 ml — Contains all coagulation factors — Crossmatch is not required, ABO compliance is sufficient** — Fresh frozen plasmas should be thawed in a special device at 37 ºC for 20 minutes before use. — It is used in multiple coagulation factor deficiencies (liver disease., K vitamin deficiency, DIC etc.) 17  CRYOPRESPITATE It is the protein-rich part that precipitates in the cold during the thawing of fresh frozen plasma at 1-6 ºC. After separation, 5-20 ml of plasma is added and refrozen. 18  STORAGE CONDITIONS OF BLOOD COMPONENTS Whole blood Blood storage fridge at +4 ⁰C Erythrocyte susp. Blood storage fridge at +4 ⁰C Platelet susp. At +20-24 ⁰C in agitator Fresh frozen plasma Deep freezer (-20 ⁰C and low) Cryoprecipitate Deep Freeze minimum (-20 ⁰C and low) 19 All blood and blood components tested for ** Hepatitis B (HBsAg) Hepatitis C, (Anti-HCV or HCV Ag+Ab) Syphilis (Treponema pallidum Total Ab) HIV infections (HIV 1/2 Ag+Ab) https://www.kanver.org/Upload/Dosya/ulusal_kan_rehberi.pdf 20  Bloodborne Infectious Diseases: HIV/AIDS, Hepatitis B, Hepatitis C Exposures to blood and other body fluids occur across a wide variety of occupations. Health care workers, emergency response and public safety personnel, and other workers can be exposed to blood through needlestick and other sharps injuries, mucous membrane, and skin exposures. The pathogens of primary concern are the Human immunodeficiency virus (HIV), Hepatitis B virus (HBV), and Hepatitis C virus (HCV). https://www.cdc.gov/niosh/topics/bbp/default.html 21 Bloodborne Pathogens & Aerosols In dentistry, the diseases we are most concerned about are those caused by bloodborne pathogens (BBP): Hepatitis B and C and human immunodeficiency virus (HIV). Transmission may occur from a patient to a dental health care provider (DHCP), from a DHCP to a patient, or from one patient to another patient. The best way to prevent the transmission of BBP is adherence to Standard Precautions. 22  Standard Precautions Standard Precautions are the minimum infection prevention practices that apply to all patient care, regardless of suspected or confirmed infection status of the patient, in any setting where health care is delivered. These practices are designed to both protect DHCP and prevent DHCP from spreading infections among patients. Standard Precautions include — Hand hygiene. Use of personal protective equipment (e.g., gloves, masks, eyewear, protective clothing, face shields. Respiratory hygiene / cough etiquette. Sharps safety (engineering and work practice controls). Safe injection practices (i.e., aseptic technique for parenteral medications). Sterile instruments and devices. Clean and disinfected environmental surfaces. Also, equipment or items in the patient environment likely to have been contaminated with infectious body fluids must be handled in a manner to prevent transmission of infectious agents (e.g., wear gloves for direct contact, contain heavily soiled equipment, properly clean and disinfect or sterilize reusable equipment before use on another patient). https://www.cdc.gov/oralhealth/infectioncontrol/summary-infection-prevention-practices/standard- precautions.html#print 23 Potentially infectious body fluids Blood Saliva, vomit, urine Semen or vaginal discharge Skin, tissue and cell cultures Other body fluids 24  Infectious Factors Transmitted by Blood Those found in the blood at some point in their life cycle; Hepatitis D (HDV-DELTA) Syphilis CMV (Cytomegalovirus) Malaria, Leishmania Babesiosis Brucellosis Leptospirosis, Trypanasoma, Filaria Arboviral İnf. Relapsing fever (Borrelia recurrentis) Creutzfeldt-Jakob Hastalığı Human T-Lymphotropic Virus Type I (HTLV-Tip I) Crimean-congo hemorrhagic fever (CCHF) virüs, Ebola virüs, Hanta virus, Parvovirus B19 25 Infectious Factors Transmitted by Blood EBV spreads most commonly through bodily fluids, especially saliva; EBV can also spread through blood and semen during sexual contact, blood transfusions, and organ transplantations. CMV is transmitted by direct contact with infectious body fluids, such as urine, saliva, blood, tears, semen, and breast milk. CMV can be transmitted sexually and through transplanted organs and blood transfusions. Parvovirus B19 spreads through respiratory secretions, such as saliva, sputum, or nasal mucus, when an infected person coughs or sneezes. Parvovirus B19 can also spread through blood or blood products Leptospirosis: Drinking or contact with water (such as by swimming, rafting or kayaking) or soil that has been contaminated by urine or body fluids of infected 26  Hepatitis B Virus (HBV) Hepadnavirus , DNA virus, enveloped 42 nm, partially double-stranded circular DNA , icosahedral genome The virions are unusually stable for an enveloped virus; they resist treatment with ether, low pH, freezing, and moderate heating. (important for transmission and disinfection). Although it is a DNA virus, it encodes reverse transcriptase; intermediate RNA replication Hepatitis-B virion It is called Dane particle Infected cells contain mature virions (Dane particles) and spherical and tubular particles without non-infective nucleic acid (All carry HBsAg) The viral genome consists of S, C, P and X gene regions. S (surface) gene region: encodes HBs Ag (S, PreS1, PreS2 proteins) C gene region: encodes HBcAg (core antigen) and HBeAg ( precore antigen ) P gene region: longest gene; encodes viral DNA polymerase (reverse transcriptase and ribonuclease H activity) X gene region: HBxAg protein (oncogene ) codes. 27 Schematic diagram of hepatitis B virus (HBV) particles 28  Hepatitis B Virus (HBV) Pathogenesis : Replication of hepatitis B virus (HBV). 1. After entry into the hepatocyte and uncoating of the nucleocapsid core, the partially double-stranded DNA genome is delivered to the nucleus 2. and completed (by viral DNA depended DNA polymerase) in the nucleus. A double-stranded circuler DNA is formed. This DNA serves as a template for mRNA synthesis by cellular RNA polymerase. 3. Transcription of the genome produces four messenger RNAs (mRNAs), including an mRNA larger than the genome. The mRNA then moves to the cytoplasm and is translated into protein. 4. Core proteins assemble around the 3500 base mRNA, and negative-sense DNA is synthesized by a RNA depended DNA polymerase: reverse transcriptase (viral DNA depended DNA polymerase) activity in the core. 5. The ribonucleic acid (RNA) is then degraded while a positive-sense (+) DNA is synthesized. 6. The filled core associates with HBsAg-containing endoplasmic reticulum membranes, is enveloped before completion of the positive-sense DNA, and is then released by exocytosis with HBsAg- containing particles. There are 10 genotypes,serotypes of HBV ; (D most common genotype in Turkey) 29 Viral life cycle of hepatitis B virus: 30  Hepatitis B Virus (HBV) Pathogenesis : is a noncytolytic virus that causes disease by initiating inflammation of the liver can cause acute or chronic, symptomatic or asymptomatic disease (Which of these occurs is determined by the person’s immune response to the infection) The major source of virus is blood, but HBV can be found in semen, saliva, milk, vaginal and menstrual secretions, and amniotic fluid. After entering the blood, the virus infects hepatocytes, and viral antigens are displayed on the surface of the cells. Immune attack against viral antigens on infected hepatocytes is mediated by cytotoxic T cells; inflammation and necrosis occur. 1. Cell-mediated immunity and inflammation are responsible for causing the symptoms and effecting resolution of the HBV infection by eliminating the infected hepatocyte. 2. Necrosis (ground glass) develops in liver parenchyma cells. The pathogenesis of HBV is the result of this cellmediated immune injury, because HBV itself does not cause a cytopathic effect. 31  Hepatitis B Virus (HBV) Pathogenesis : A chronic carrier is someone who has HBsAg persisting in their blood for 6 months or longer The main determinant of whether a person clears the infection or becomes a chronic carrier is the adequacy of the cytotoxic T-cell response Infants and young children have an immature cell-mediated immune response ; 90% of infants infected perinatally become chronic carriers. (adult 5%) Viral replication persists in these people for long periods. A high rate of hepatocellular carcinoma (HCC) occurs in chronic carriers. Antigen–antibody complexes cause (type III hypersensitivity) the early symptoms (e.g., arthralgias, arthritis, and urticaria) the complications in chronic hepatitis (e.g., glomerulonephritis, cryoglobulinemia, and vasculitis. (associated with Poliarteritis nodosa) 32  Hepatitis B Virus (HBV) Pathogenesis : The e antigen is the indicator of transmissibility Lifelong immunity occurs after the natural infection and is mediated by humoral antibody against HBsAg. Antibody against HBsAg (HBsAb) is protective because it binds to surface antigen on the virion and prevents it from interacting with receptors on the hepatocyte (HBsAb neutralizes the infectivity of HBV). Antibodies to HBc and HBe are present in serum but cannot neutralize infection, nonprotective. Anti-HBc is free to be detected throughout and after the course of the infection. 33  Hepatitis B Virus (HBV) Epidemiology Transmission: Sexual, parenteral and perinatal routes*** Contaminated blood&blood components transfusion (reduced donor screening programmes),*needle sharing, acupuncture, ear piercing, or tattooing, through very close personel contact (semen, saliva, vaginal secretion exchange): e.g sexual contact, childbirth Perinatal (from mother to baby), body secretions Medical personnel (accidental): needle-sticks or sharp instruments sharing certain items that can break the skin or mucous membranes (e.g., razors, toothbrushes, and glucose monitoring equipment), resulting in exposure to blood through poor infection control practices in healthcare settings (e.g., dialysis units, diabetes clinics). 34  Hepatitis B Virus (HBV) Clinical Syndromes Acute hepatitis develops after about 30-100 days of incubation. (long incubation period and an insidious onset) It can be asymptomatic , icteric or anicteric course. 90% cases heal; 10% become chronic enfection; 1% fulminant Weakness, nausea, vomiting, yellowing of the sclera and body, tea-colored urine, diarrhea, increased transaminase levels are seen. Immune complex rxn: (urticaria, arthritis, glomerulonephrits, PAN ) Most people with chronic HBV infection are asymptomatic. Chronically infected people are the major source for spread of the virus and are at risk for fulminant disease if they become co-infected with HDV. Some people develop chronic hepatitis (elevation of AST/ALT), cirrhosis, or hepatocellular carcinoma (i.e., primary liver cancer). Primary Hepatocellular Carcinoma The World Health Organization estimates that 80% of all cases of PHC can be attributed to chronic HBV infections. 35 36  HBsAg : The surface antigen found in the envelope. The first to appear Ag. Anti HBs: stays for life ; immunity indicator HBsAg and Anti HBs are not found together in blood HBeAg : shows replication and transmissibltyinfectivity. It appears in the blood shortly after HBsAg. HBV DNA: The most reliable indicator of replication. * HBcAg (core antigen): It is not found in blood, it is found only in hepatocytes. It cannot be detected serologically in serum. Anti- HBc IgM Acute HBV inf. indicator; diagnosis during the window period** Anti- HBc IgG : is not protective, lifelog persist, it only shows that it has encountered the agent. 37 DIAGNOSIS Serological tests are very important. PCR HBV-DNA. https://www.cdc.gov/hepatitis/hbv/interpretationOfHepBSerologicResults.htm 38 Hepatitis B Virus (HBV) Treatment in acute hepatitis. Supportive therapy. In chronic hepatitis, pegylated interferon (IFN) α + antiviral: lamivudine, entecavir, telbivudine, tenofovir adefovir, dipivoxil, famciclovir 39  Prevention 1. Pre-contact prevention with HBV a) non-specific protection Universal blood body fluid precaution Screening blood and blood products for HBsAg Sterilization and disinfection b) Specific Protection Active immunization : Vaccine. Recombinant vaccine is in the routine childhood immunization schedule. 3 doses (0,1,6 months) Immunity is determined by Anti HBs.** HBV immunoglobulin ( HBIG) 2. Protection after exposure to HBV a) Babies born to HBV (+) mothers à HBIG+ vaccine (first 12 hours). Vaccination protocol is completed (0-1-6. months) b) Needle injury (parenteral contact) – healthcare personnel ànotification. Anti HBs negative: HBIG + vaccine in the first 48 hours ** then vaccination protocol is completed (0-1-6 months ) In the vaccinated individual, the protective antibody titer is checked; reminder dose? 40  Hepatitis C Virus (HCV) HCV is the only member of the Hepacivirus genus of the Flaviviridae family. Enveloped, positive-sense RNA genome There are seven different genotypes (types 1-7). Most common HCV- genotype in Turkey is 1b The genome of HCV encodes 10 proteins, including two glycoproteins (E1, E2) Structural proteins are Nucleocapsid (cor, C), and envelope (E1 and E2) glycoproteins The fastest changing gene is E2 non-structural (NS) proteins The viral RNA-dependent RNA polymerase is error prone and generates mutations in the glycoprotein and other genes. This generates antigenic variability and antiviral drug resistance and vaccine development diffuculty 41  HCV Transmission: HCV is transmitted primarily and efficiently in infected blood and less efficiently sexually. In blood, semen, and vaginal secretions (HBV: saliva and mother’s milk) Risk groups: High risk: Intravenous drug abusers and tattoo recipients are at the highest risk of acquiring HCV infection. Screening procedures have led to a reduction in the levels of transmission by blood transfusion and organ donation Babies born of HCV-positive mothers are also at increased risk for infection and hemodialysis healthcare personnel (needlstick injury) Clinical Syndromes HCV causes three types of disease (1) acute hepatitis with resolution of the infection and recovery in 15% of cases, (2) chronic persistent infection with possible progression to disease much later in life for 70% of infected persons, and (3) severe rapid progression to cirrhosis in 15% of patients The most important complications of chronic hepatitis C are cirrhosis and hepatocellular carcinoma (HSK ) ** 42 43  HCV Diagnosis The diagnosis and detection of HCV infection are based on ELISA recognition of anti-HCV antibody or detection of the RNA genome. ELISA: Anti-HCV (not indicate recovery) PCR: HCV-RNA Treatment PEG IF+Ribavirin+protease inhibitors (boseprevir, telaprevir) HCV NS5A replication complex inhibitor ledipasvir+NS5B polymerase inh. nucleotide analog (sofosbuvir) Prevention Prevent transmission NO vaccine : due to genetic and antigenic variability 44  Hepatitis D Virus (HDV) HDV RNA genome is very small Single-stranded, defective RNA virus The genome is surrounded by the delta antigen core, which, in turn, is surrounded by an HBsAg-containing envelope. The delta agent can replicate and cause disease only in people with active HBV infections. Because the two agents are transmitted by the same routes, a person can be coinfected with HBV and the delta agent. A person with chronic HBV can also be superinfected with the delta agent. The delta agent exacerbates the HBV disease. 45  Hepatitis D Virus (HDV) Parenteral (in blood), sexually transmitted, and perinatally. Acute ( coinfection , superinfection , fulminant hepatitis), chronic or latent infection may develop. If infection develops at the same time (HBV+HDV) , it is called coinfection , If it is added to the existing HBV infection, it is called superinfection More rapid, severe progression occurs in HBV carriers superinfected with HDV than in people co-infected with HBV and the delta agent 46 Hepatitis D Virus (HDV) DIAGNOSIS ELISA à anti - Delta IgG and IgM , HDAg RT-PCRà Demonstration of HDV-RNA Anti-HBc IgM (if positive, coinfection) test is performed to distinguish between coinfection and superinfection. TREATMENT: Support + close monitoring PROTECTION: HDV decreases with HBV vaccination. 47  Human Immunodeficiency Virus The genome of the retroviruses consists of three major genes: Gag (group-specific antigen, capsid, matrix, and nucleic acid–binding proteins), Pol (polymerase:RT, protease, and integrase), Env (envelope: glycoproteins) Tat, nef, rev, vif, vpu, vpr the other genes. gp 120** glycosylated viral protein the most antigenic determinant of the virus, Binding to the CD4 receptor can be protected from antibodies, gp 41** fusion of the virus envelope and the cell membrane, the entry of the virus into the host cell. 48 Human Immunodeficiency Virus Replication and pathogenesis The virus binds with gp120 to CD4 molecule on the surface of CD4+ T lymphocytes, monocytes, macrophages, dendritic cells, CNS glia cells with the help of CCR5 chemokine receptor; It enters the cell by fusion with the help of gp 41. Primary receptors: CD4 T cell receptors Co-receptors : CCR5 chemokine receptor, CxCR4 chemokine receptor 49  HIV receptors HIV binds to 2 surface proteins in cells: CD4 ( Th , monocytes , neurons) and CXCR4 or CCR-5. M tropic viruses (Macrophage type viruses-R5 Virus): The virus can bind to CD4 and CCR5. M-tropic viruses are transmitted by sexual contact. They do not induce syncytium formation ; infect macrophages and T cells. T tropic viruses (T lymphocyte type viruses- X4 virus): The virus can bind to CD4 and CXCR4 (naive CD4+T cells). These induce syncytium formation and infect T cells. 50 51 Clinical Syndromes HIV disease progresses from an asymptomatic nonspecific or mononucleosis-like disease to profound immunosuppression, referred to as AIDS. Acute phase, 2 to 4 weeks after infection: The initial symptoms may resemble influenza or heterophile antibody negative mononucleosis; these symptoms subside after 2 to 3 weeks followed by a period of asymptomatic infection or a persistent generalized lymphadenopathy that may last for several years. During this period, the virus is replicating in the lymph nodes. Deterioration of the immune response is indicated by increased susceptibility to opportunistic pathogens. AIDS (CD4 T-cell counts less than 200/μL) may be manifested in several different ways, including lymphadenopathy and fever, opportunistic infections, malignancies, and AIDS-related dementia 52 Are there symptoms? For many, yes. Most people have flu-like symptoms within 2 to 4 weeks after infection. Symptoms may last for a few days or several weeks. Having these symptoms alone doesn’t mean you have HIV. Other illnesses can cause similar symptoms. Some people have no symptoms at all. The only way to know if you have HIV is to get tested. Transmission of HIV Routes Specific Transmission KNOWN ROUTES OF TRANSMISSION Inoculation in blood Needle sharing among intravenous drug abusers Needlestick, open wound, and mucous membrane exposure in health care workers Tattoo needles Sexual transmission* Anal and vaginal intercourse Perinatal transmission Intrauterine transmission Peripartum transmission Breast milk ROUTES NOT INVOLVED IN TRANSMISSION Close personal contact Household members Health care workers not exposed to blood *Sexual transmission (most common transmission route) 54  Laboratory Diagnosis Specific HIV Antigen/Antibody detection ELISA:HIV Ag+Ab Screening test p24 Antigen: early indicator of infection Western blot: Ab detected; Confirmatory test Viral genetic material (PCR) HIV RNA: The diagnosis is confirmed by viral genome determination. Quantification of virus in blood (viral load) CD4 T cell counts, CD4:CD8 T cell ratio HIV disease indicator Treatment follow-up: CD4 count and viral load tracking 55 Antiretroviral Therapy&Antiretroviral Drugs The management of HIV/AIDS includes the use of multiple antiretroviral drugs as a strategy to control HIV infection. There are several classes of antiretroviral agents that act on different stages of the HIV life- cycle. The use of these is known as: Highly Active Antiretroviral Therapy (HAART) decreases the patient's total burden of HIV, maintains function of the immune system, prevents opportunistic infections that often lead to death. prevents the transmission  Prevention and Control Preexposure prophylaxis, or PrEP, for people who have a high risk of HIV infection (e.g., partners of HIV infected individuals and IV drug users). Currently, the suggested therapy is a single pill of a HAART that combines tenofovir and emtricitabine. This therapy is also appropriate for postexposure prophylaxis (e.g., needlestick). Education The principal way HIV infection can be prevented İts spread controlled is by educating the population about the methods of transmission and the measures monogamous relationships, safe sex, use of condoms. IV drug abusers must be taught that needles must not be shared. Blood, Blood Product, and Organ Screening Infection control procedures: wearing protective cloth, dysenfection Contaminated surfaceshould be disinfected with: 10% household bleach 70% ethanol 2% glutaraldehyde 4% formaldehyde 6% hydrogen peroxide  Vaccine Types I. Live Attenuated Vaccines Live vaccines are obtained by attenuating the disease-causing virus or bacteria in the laboratory. The microorganism in this vaccine type has the ability to multiply inside the body and induce an immune response. The antigen enables recognition of a substance by the immune system. Live vaccines should not be administered to pregnant women or people with a weakened or suppressed immune system. Examples of live vaccines are yellow fever vaccine, rotavirus vaccine, BCG vaccine, oral polio vaccine (OPV), Measles, Mumps and Rubella (MMR) (MMR) vaccine, and chickenpox vaccine. https://covid19asi.saglik.gov.tr/EN-80252/vaccine-types.html 58  Vaccine Types II. Inactivated Vaccines 1. Toksoid Vaccines Toxoid vaccines contain a form of toxin produced by toxin producing microorganisms. However, the disease-causing properties of the toxin are eliminated by changing the toxin structure, while the immunity-inducing properties are preserved. Diphtheria and tetanus vaccines are toxoid vaccines. 2. Whole-Cell Vaccines Whole-cell vaccines contain a whole microorganism in an inactivated state. They are obtained by killing the microorganism produced in the culture medium by applying heat or chemicals. Examples are hepatitis A vaccine and inactivated polio vaccine (IPV). https://covid19asi.saglik.gov.tr/EN-80252/vaccine-types.html 59  Vaccine Types II. Inactivated Vaccines 3. Fractional Vaccines Fractional vaccines contain only certain parts of an inactivated microorganism. 3.1. Protein-Based Vaccines Protein-based vaccines incorporate purified microbial protein structures or microbial protein structures obtained by recombinant technology. 3.1.1. Split Vaccines Split vaccines contain a part of microorganism after it is disrupted or split. Inactivated flu vaccine is a split vaccine. 3.1.2. Subunit Vaccines Subunit vaccines contain certain antigenic parts of the microorganism. Hepatitis B vaccine and acellular pertussis vaccine are subunit vaccines. 60 https://covid19asi.saglik.gov.tr/EN-80252/vaccine-types.html  Vaccine Types II. Inactivated Vaccines 3. Fractional Vaccines 3.2. Structural Vaccines Without Genetic İnformation This type of vaccine contains the entire capsid of the virus, but does not contain any of its enzymes or nucleic acids. E.g. the HPV vaccine. 3.3. Polysaccharide-Based Vaccines This type of vaccine is composed of long chains of polysaccharides forming the bacterial capsule. 3.3.1. Pure Polysaccharide Vaccines Examples are pneumococcal vaccine and meningococcal vaccine. 3.3.2. Conjugate Polysaccharide Vaccines Examples are pneumococcal conjugate vaccine, meningococcal conjugate vaccine and Hib vaccine. 61 https://covid19asi.saglik.gov.tr/EN-80252/vaccine-types.html  Vaccine Types III. Vaccines Containing mRNA and DNA mRNA Vaccines are vaccines that contain mRNA of the antibody- producing antigenic structure of the target microorganism.(Examples: COMIRNATY- Pfizer Biontech mRNA vaccine, Moderna mRNA vaccine) DNA Vaccines are vaccines that contain DNA of the antibody- producing antigenic structure of the target microorganism. IV. Vector Vaccines Vector vaccines are developed by adding the genetic information of the antibody-producing antigenic structure of the target microorganism to modified viruses. (Sputnik-V, ZEBOV, AZD1222) https://covid19asi.saglik.gov.tr/EN-80252/vaccine-types.html 62 Republic of Turkey Ministry of Health childhood vaccination calendar 63