Management Factors That Affect the Development of Passive Immunity in the Newborn Calf

Total Page:16

File Type:pdf, Size:1020Kb

Management Factors That Affect the Development of Passive Immunity in the Newborn Calf Beef Cattle Handbook BCH-2240 Product of Extension Beef Cattle Resource Committee Management Factors that Affect the Development of Passive Immunity in the Newborn Calf Glenn E. Selk, Extension Animal Reproduction Specialist, Oklahoma State University Introduction the immunoglobulin was acquired, not synthesized by A successful cow/calf operation requires that a large per- the neonate’s own immune system) protection against centage of cows wean a live calf every year. A live calf at systemic disease. Part of the immunoglobulin remains weaning time requires survival of the offspring from in the gut where it can neutralize pathogenic bacteria birth to weaning. USDA beef researchers and rancher and help prevent the development of diarrhea. surveys report that diseases including scours and pneu- In addition, colostrum contains “transferrin” and monia cause significant numbers of young calf deaths. “lactoferrin”, which bind iron and also restrict bacterial Resistance to disease is greatly dependent on anti- growth. These factors, together with immunoglobulin, bodies or immunoglobulins and can be either active or help limit growth of bacteria in the gut. passive in origin. In active immunity, the body produces antibodies in response to infection or vaccination. Formulation and Composition of Colostrum Passive immunity gives temporary protection by trans- Cow colostrum contains about 22 per cent solids com- fer of certain immune substances from resistant individ- pared with the 12 per cent solids of normal whole milk. uals. An example of passive immunity is the passing of Much of this extra solid is immunoglobulin, but antibodies from dam to calf via the colostrum (or first colostrum is also a rich source of casein, fat and vita- milk after calving). This transfer only occurs during the mins—especially A and E. There is also a trypsin first 24 hours following birth. inhibitor, which helps protect immunoglobulin from digestion in the calf’s gut as well as protein fractions that Colostrum and Passive Immunity in Baby Calves facilitate absorption of immunoglobulins in calves. Lack of colostral immunity continues to be a major pre- In cows, immunoglobulin “IgG1” is the principal disposing factor to newborn calf diseases and economic colostral immunoglobulin. In cows, immunoglobulin is loss in cattle. In recent years, our knowledge of concentrated in colostrum from about five weeks colostrum feeding has advanced, but a completely reli- prepartum, probably in response to rising estrogen con- able method for preventing hypogammaglobulinemia centration in the dam. Special receptors on the mamma- (low blood concentrations of immunoglobulins) has yet ry epithelium selectively bind serum IgG1, and this is to be described. taken into the cell by transcapillary exchange and trans- Calves are born with incompletely developed host ported to the lumen of the mammary gland, where it is disease defense mechanisms, and colostral protection released into colostrum. Serum IgG1 concentrations fall plays an important role in early life. Feeding colostrum to 50 percent, as colostral concentrations rise to 3 - 12 provides the newborn with a source of pre-formed times that of serum. Other colostral immunoglobulins immunoglobulin, some of which is actively absorbed called “IgM” and “IgA” also reach higher concentrations across the small intestine and provides passive (because than are found in serum, and they are derived partly BCH-2240 1 from the serum pool and partly from local synthesis by colostrum decreases linearly from birth. (See Table 2.) lymphocytes within the mammary gland. Immunoglobulins are fairly resistant to digestion by A number of factors influence the total amount of intestinal enzymes and are further protected by the pres- immunoglobulin found in colostrum. The volume of ence of a trypsin inhibitor in bovine colostrum. colostrum produced is affected by breed, for instance, “Intestinal closure” occurs when macromolecules dairy cows produce much more colostrum than beef are no longer released into the circulation and this cows. Cows produce more than heifers. Feeding energy- occurs before the specialized absorptive cells are deficient diets markedly reduce colostral volume (Table sloughed from the gut epithelium. In calves and lambs, 1 and Table 2). Also prepartum nutrition of the cow will closure is about 24 hours after birth, although efficiency affect colostrum quality as will be discussed later in this of absorption declines from birth, particularly after 12 paper. hours and some calves fail to absorb immunoglobulin if fed after 12 hours of age. Feeding may induce earlier Table 1. Volume of Colostrum Produced by Cows as First Milking closure, but there is little colostral absorption after 24 or First Suckling by Calf. hours of age even if the calf is starved. This principle of timing of colostrum feeding holds true whether the Average colostrum is directly from the first milk of the dam, or Colostrum Yield supplied by hand feeding the newborn calf previously Breed Management (Liters) obtained colostrum. Beef-Hereford-Cross* Out wintered: poor 0.6 nutrition 1.7 Table 2. Effect of Time of Colostrum Feeding (hours after birth) In wintered: silage ad lib on Total Immunoglobulin Absorption in Calves. Dairy-Ayrshire Plasma Jersey Time of Feeding Concentration (mg/ml) Absorption Holstein-Friesian 2.2 (hours after birth) 24 hours after feeding (%) 2.2 2.4 6 52.7 66 12 37.5 47 There are marked breed differences in colostral 24 9.2 12 immunoglobulin concentration. Low colostral IgM and 36 5.4 7 IgA concentrations in Guernsey’s have led to the specu- 48 4.8 6 lation that this may result in high calf mortality in this breed. Cows also affect the colostral immunoglobulin If parturition is induced in cows using very slow-act- concentrations and serum immunoglobulin concentra- ing corticosteroids (9 - 19 days), the efficiency of absorp- tions of their one-day-old calves. An important factor tion of colostral immunoglobulin is reduced in the calf. that influences colostrum quality (immunoglobulin con- However, there is no evidence that more rapid-acting centration) is the age of the cow. Heifers have poor corticosteroid preparations (two days) induce closure or quality colostrum while older cows have the best quality that treating calves with ACTH or cortisone at birth colostrum. Another very important factor is milking affects immunoglobulin absorption. stage. In general, colostral immunoglobulin content is halved with each successive milking; therefore, the first Behavioral Factors milking colostrum has twice the immunoglobulin con- Behavioral factors are very important in determining the tent of the second milking colostrum. Colostrum leakage final immunoglobulin concentration attained by calves. and premilking will both adversely influence colostrum Following birth the cow licks the calf dry and may eat the quality. Administration of long-acting corticosteroids, placenta. The calf nuzzles upwards, along the dark under- which takes 9 - 19 days to induce parturition, will side of the cow, and in this way ends up in the region of depress colostral immunoglobulin concentration. the udder. In cows with good conformation, the teats are Limited evidence suggests that the commonly used set at a high point between the thighs and are in the North American corticosteroid preparations, which take calf’s path. Cows with poor udder conformation have about two days to induce calving, do not adversely dropped teats, and the calf has trouble finding them as it affect the immunoglobulin concentrations attained by nuzzles up into the darker region of the thighs. The initial calves if the cow was over 260 days into gestation at licking dry of the calf appears to be very important to the induction. However, in one study, both induced and con- cow-calf bond, and the dam will not allow the calf to trol calves had a very high incidence of poor colostral suck if this phase of behavior has not been successfully immunity. completed. Calves born in stalls can mistake walls for the dam and orient to the dark corners. This is particularly Timing of Colostrum Feeding and the Principle of likely to happen if the cow remains lying down. In gener- “Intestinal Closure” al, beef cows mother their calves better than dairy cows, Timing of colostrum feeding is important because the and cows have better maternal instincts than heifers. If efficacy of absorption of immunoglobulin from the calf does not suck its dam in the first eight hours of 2 Beef Cattle Handbook life, it will be hypoimmunoglobulinemic. Despite behav- Table 3. Effect of Calving Difficulty on Serum Immunoglobulin ioral differences, calves born to dairy heifers attain Concentration 24 hours after Birth, Interval from Calving to serum immunoglobulin concentrations similar to calves Standing, and Mothering Score born to cows—better mothering behavior in cows is Calving Difficulty Score* compensated by better udder conformation in heifers. 12 3 Calves born to beef and dairy animals also attain similar Interval from immunoglobulin concentrations, possibly because, while Calving to Stand beef cows are better mothers, they do not produce as (minutes) 39.8 50.9 84.3 much colostrum. Mothering has a tremendous beneficial effect on the Mothering Score 1.2 1.5 1.5 efficiency of absorption of immunoglobulin. Mothered calves absorb 70 per cent more immunoglobulin from a IgG1 (mg/dl) 2401 2191 1918.5 standard feed than non-mothered calves. This benefit is still seen if the calf obtains the colostrum by sucking its IgM (mg/dl) 194.8 173.0 135.6 dam, but is separated from its dam between feedings. Field surveys implicate separating the calf from its dam *1=unassisted; 2=assisted after at least one hour of labor, easy pull; as one cause of hypoimmunoglobulinemia. Dairy calves 3=assisted after at least one hour of labor, difficult pull kept with their dams attained higher serum immunoglobulin concentrations then hand-fed calves, even though the mothered calves may suckle less colostrum than hand-fed calves. Table 4. Effect of Time of Suckling and Calf Vigor on Immuno- Temperature stress adversely affects colostral globulin Absorption immunoglobulin absorption.
Recommended publications
  • IFM Innate Immunity Infographic
    UNDERSTANDING INNATE IMMUNITY INTRODUCTION The immune system is comprised of two arms that work together to protect the body – the innate and adaptive immune systems. INNATE ADAPTIVE γδ T Cell Dendritic B Cell Cell Macrophage Antibodies Natural Killer Lymphocites Neutrophil T Cell CD4+ CD8+ T Cell T Cell TIME 6 hours 12 hours 1 week INNATE IMMUNITY ADAPTIVE IMMUNITY Innate immunity is the body’s first The adaptive, or acquired, immune line of immunological response system is activated when the innate and reacts quickly to anything that immune system is not able to fully should not be present. address a threat, but responses are slow, taking up to a week to fully respond. Pathogen evades the innate Dendritic immune system T Cell Cell Through antigen Pathogen presentation, the dendritic cell informs T cells of the pathogen, which informs Macrophage B cells B Cell B cells create antibodies against the pathogen Macrophages engulf and destroy Antibodies label invading pathogens pathogens for destruction Scientists estimate innate immunity comprises approximately: The adaptive immune system develops of the immune memory of pathogen exposures, so that 80% system B and T cells can respond quickly to eliminate repeat invaders. IMMUNE SYSTEM AND DISEASE If the immune system consistently under-responds or over-responds, serious diseases can result. CANCER INFLAMMATION Innate system is TOO ACTIVE Innate system NOT ACTIVE ENOUGH Cancers grow and spread when tumor Certain diseases trigger the innate cells evade detection by the immune immune system to unnecessarily system. The innate immune system is respond and cause excessive inflammation. responsible for detecting cancer cells and This type of chronic inflammation is signaling to the adaptive immune system associated with autoimmune and for the destruction of the cancer cells.
    [Show full text]
  • Discussion of Natural Killer Cells and Innate Immunity
    Discussion of natural killer cells and innate immunity Theresa L. Whiteside, Ph.D. University of Pittsburgh Cancer Institute Pittsburgh, PA 15213 Myths in tumor immunology • Cancer cells are ignored by the immune system • Immune responses are directed only against “unique” antigens expressed on tumor cells • Tumor-specific T cells alone are sufficient for tumor regression • Tumor are passive targets for anti-tumor responses Tumor/Immune Cells Interactions Tumor cell death C G DC M TUMOR NK Th B Tc Ab Ag Ag/Ab complex NK cells as anti-tumor effectors • LGL, no TCR, express FcγRIII, other activating receptors and KIRs • Spare normal cells but kill a broad range of tumor cells ex vivo by at least two different mechanisms • Produce a number of cytokines (IFN-γ, TNF-α) • Constitutively express IL-2Rβγ and rapidly respond to IL-2 and also to IL-15 and IFNα/β • Regulated by a balance of inhibitory receptors specific for MHC class I antigens and activating signals • NK-DC interactions at sites of inflammation Heterogeneity of human NK cells • Every NK cell expresses at least one KIR that recognizes a self MHC class I molecule • Two functionally distinct subsets: 1) 90% CD56dimCD16bright , highly cytotoxic, abundant KIR expression, few cytokines 2) 10% CD56brightCD16dim/neg, produce cytokines, poorly cytotoxic, low KIR expression Expression of activating and inhibitory receptors on NK cells Interaction with CD56 Interaction with MHC ligands non-MHC ligands KIR CD16 CD2 CD94/NKG2A/B β2 NKp46, 44, 30 CD94/NKG2C/E NK Cell 2B4 NKG2D Lair1 LIR/ILT A
    [Show full text]
  • COVID-19 Natural Immunity
    COVID-19 natural immunity Scientific brief 10 May 2021 Key Messages: • Within 4 weeks following infection, 90-99% of individuals infected with the SARS-CoV-2 virus develop detectable neutralizing antibodies. • The strength and duration of the immune responses to SARS-CoV-2 are not completely understood and currently available data suggests that it varies by age and the severity of symptoms. Available scientific data suggests that in most people immune responses remain robust and protective against reinfection for at least 6-8 months after infection (the longest follow up with strong scientific evidence is currently approximately 8 months). • Some variant SARS-CoV-2 viruses with key changes in the spike protein have a reduced susceptibility to neutralization by antibodies in the blood. While neutralizing antibodies mainly target the spike protein, cellular immunity elicited by natural infection also target other viral proteins, which tend to be more conserved across variants than the spike protein. The ability of emerging virus variants (variants of interest and variants of concern) to evade immune responses is under investigation by researchers around the world. • There are many available serologic assays that measure the antibody response to SARS-CoV-2 infection, but at the present time, the correlates of protection are not well understood. Objective of the scientific brief This scientific brief replaces the WHO Scientific Brief entitled “’Immunity passports’ in the context of COVID-19”, published 24 April 2020.1 This update is focused on what is currently understood about SARS-CoV-2 immunity from natural infection. More information about considerations on vaccine certificates or “passports”will be covered in an update of WHO interim guidance, as requested by the COVID-19 emergency committee.2 Methods A rapid review on the subject was undertaken and scientific journals were regularly screened for articles on COVID-19 immunity to ensure to include all large and robust studies available in the literature at the time of writing.
    [Show full text]
  • THE IMMUNE SYSTEM Blood Cells Cells of the Immune System
    THE IMMUNE SYSTEM Blood Cells Cells of the Immune System White Blood Cells • Phagocytes - Neutrophils - Macrophages • Lymphocytes Phagocytes • Produced throughout life by the bone marrow. • Scavengers – remove dead cells and microorganisms. Neutrophils • 60% of WBCs • ‘Patrol tissues’ as they squeeze out of the capillaries. • Large numbers are released during infections • Short lived – die after digesting bacteria • Dead neutrophils make up a large proportion of puss. Macrophages • Larger than neutrophils. • Found in the organs, not the blood. • Made in bone marrow as monocytes, called macrophages once they reach organs. • Long lived • Initiate immune responses as they display antigens from the pathogens to the lymphocytes. Macrophages Phagocytosis Phagocytosis • If cells are under attack they release histamine. • Histamine plus chemicals from pathogens mean neutrophils are attracted to the site of attack. • Pathogens are attached to antibodies and neutrophils have antibody receptors. • Enodcytosis of neutrophil membrane phagocytic vacuole. • Lysosomes attach to phagocytic vacuole pathogen digested by proteases Lymphocytes • Produce antibodies • B-cells mature in bone marrow then concentrate in lymph nodes and spleen • T-cells mature in thymus • B and T cells mature then circulate in the blood and lymph • Circulation ensures they come into contact with pathogens and each other B -Lymphocytes • There are c.10 million different B- lymphocytes, each of which make a different antibody. • The huge variety is caused by genes coding for abs changing slightly during development. • There are a small group of clones of each type of B-lymphocyte B -Lymphocytes • At the clone stage antibodies do not leave the B- cells. • The abs are embedded in the plasma membrane of the cell and are called antibody receptors.
    [Show full text]
  • Innate Immunity and Inflammation
    ISBTc ‐ Primer on Tumor Immunology and Biological Therapy of Cancer InnateInnate ImmunityImmunity andand InflammationInflammation WillemWillem Overwijk,Overwijk, Ph.D.Ph.D. MDMD AndersonAnderson CancerCancer CenterCenter CenterCenter forfor CancerCancer ImmunologyImmunology ResearchResearch Houston,Houston, TXTX www.allthingsbeautiful.com InnateInnate ImmunityImmunity andand InflammationInflammation • Definitions • Cells and Molecules • Innate Immunity and Inflammation in Cancer • Bad Inflammation • Good Inflammation • Therapeutic Implications InnateInnate ImmunityImmunity andand InflammationInflammation • Definitions • Cells and Molecules • Innate Immunity and Inflammation in Cancer • Bad Inflammation • Good Inflammation • Therapeutic Implications • Innate Immunity: Immunity that is naturally present and is not due to prior sensitization to an antigen; generally nonspecific. It is in contrast to acquired/adaptive immunity. Adapted from Merriam‐Webster Medical Dictionary • Innate Immunity: Immunity that is naturally present and is not due to prior sensitization to an antigen; generally nonspecific. It is in contrast to acquired/adaptive immunity. • Inflammation: a local response to tissue injury – Rubor (redness) – Calor (heat) – Dolor (pain) – Tumor (swelling) Adapted from Merriam‐Webster Medical Dictionary ““InnateInnate ImmunityImmunity”” andand ““InflammationInflammation”” areare vaguevague termsterms •• SpecificSpecific cellcell typestypes andand moleculesmolecules orchestrateorchestrate specificspecific typestypes ofof inflammationinflammation
    [Show full text]
  • The Relationship Between Maternal Postpartum Psychological State and Breast Milk Secretory Immunoglobulin a Level
    View metadata, citation and similar papers at core.ac.uk brought to you by CORE provided by Tsukuba Repository The Relationship Between Maternal Postpartum Psychological State and Breast Milk Secretory Immunoglobulin A Level 著者 Kawano Atsuko, Emori Yoko journal or Journal of the American Psychiatric Nurses publication title Association volume 21 number 1 page range 23-30 year 2015-01 権利 Authors URL http://hdl.handle.net/2241/00124572 doi: 10.1177/1078390314566882 The relationship between maternal postpartum psychological state and breast milk secretory immunoglobulin A level. Kawano A, Emori Y. J Am Psychiatr Nurses Assoc. 2015 Jan-Feb;21(1):23-30. doi: 10.1177/1078390314566882. Epub 2015 Jan 14. PMID:25589451 Abstract BACKGROUND: Maternal psychological state may influence the passive transfer of immune factors (e.g., immunoglobulin) via the mother’s breast milk. OBJECTIVE: The aim of this study was to determine whether a correlation exists between mothers’ postpartum psychological state and their breast milk secretory immunoglobulin A (SIgA) levels. STUDY DESIGN: Eighty-one mothers who delivered at an urban general hospital were included in our analysis. Two weeks after delivery, we measured their breast milk SIgA levels and simultaneously documented their psychological state using the Profile of Mood States (POMS), General Health Questionnaire (GHQ), and State-Trait Anxiety Inventory (STAI) scales. RESULTS: Breast milk SIgA levels were negatively correlated with negative POMS states (tension-anxiety, depression-dejection, anger-hostility, fatigue, and confusion). A negative correlation was also observed between SIgA levels and GHQ mental health (r = −.625, P = .000), and a similar negative correlation was observed with STAI trait and state anxieties.
    [Show full text]
  • Understanding the Immune System: How It Works
    Understanding the Immune System How It Works U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES NATIONAL INSTITUTES OF HEALTH National Institute of Allergy and Infectious Diseases National Cancer Institute Understanding the Immune System How It Works U.S. DEPARTMENT OF HEALTH AND HUMAN SERVICES NATIONAL INSTITUTES OF HEALTH National Institute of Allergy and Infectious Diseases National Cancer Institute NIH Publication No. 03-5423 September 2003 www.niaid.nih.gov www.nci.nih.gov Contents 1 Introduction 2 Self and Nonself 3 The Structure of the Immune System 7 Immune Cells and Their Products 19 Mounting an Immune Response 24 Immunity: Natural and Acquired 28 Disorders of the Immune System 34 Immunology and Transplants 36 Immunity and Cancer 39 The Immune System and the Nervous System 40 Frontiers in Immunology 45 Summary 47 Glossary Introduction he immune system is a network of Tcells, tissues*, and organs that work together to defend the body against attacks by “foreign” invaders. These are primarily microbes (germs)—tiny, infection-causing Bacteria: organisms such as bacteria, viruses, streptococci parasites, and fungi. Because the human body provides an ideal environment for many microbes, they try to break in. It is the immune system’s job to keep them out or, failing that, to seek out and destroy them. Virus: When the immune system hits the wrong herpes virus target or is crippled, however, it can unleash a torrent of diseases, including allergy, arthritis, or AIDS. The immune system is amazingly complex. It can recognize and remember millions of Parasite: different enemies, and it can produce schistosome secretions and cells to match up with and wipe out each one of them.
    [Show full text]
  • A Role of Inflammation and Immunity in Essential Hypertension—Modeled and Analyzed Using Petri Nets
    International Journal of Molecular Sciences Article A Role of Inflammation and Immunity in Essential Hypertension—Modeled and Analyzed Using Petri Nets Dorota Formanowicz 1 , Agnieszka Rybarczyk 2,3 , Marcin Radom 2,3 and Piotr Formanowicz 2,3,* 1 Department of Clinical Biochemistry and Laboratory Medicine, Poznan University of Medical Sciences, 60-806 Poznan, Poland; [email protected] 2 Institute of Computing Science, Poznan University of Technology, 60-965 Poznan, Poland; [email protected] (A.R.); [email protected] (M.R.) 3 Institute of Bioorganic Chemistry, Polish Academy of Sciences, 61-704 Poznan, Poland * Correspondence: [email protected] Received: 15 April 2020; Accepted: 5 May 2020; Published: 9 May 2020 Abstract: Recent studies have shown that the innate and adaptive immune system, together with low-grade inflammation, may play an important role in essential hypertension. In this work, to verify the importance of selected factors for the development of essential hypertension, we created a Petri net-based model and analyzed it. The analysis was based mainly on t-invariants, knockouts of selected fragments of the net and its simulations. The blockade of the renin-angiotensin (RAA) system revealed that the most significant effect on the emergence of essential hypertension has RAA activation. This blockade affects: (1) the formation of angiotensin II, (2) inflammatory process (by influencing C-reactive protein (CRP)), (3) the initiation of blood coagulation, (4) bradykinin generation via the kallikrein-kinin system, (5) activation of lymphocytes in hypertension, (6) the participation of TNF alpha in the activation of the acute phase response, and (7) activation of NADPH oxidase—a key enzyme of oxidative stress.
    [Show full text]
  • Vaccine Immunology Claire-Anne Siegrist
    2 Vaccine Immunology Claire-Anne Siegrist To generate vaccine-mediated protection is a complex chal- non–antigen-specifc responses possibly leading to allergy, lenge. Currently available vaccines have largely been devel- autoimmunity, or even premature death—are being raised. oped empirically, with little or no understanding of how they Certain “off-targets effects” of vaccines have also been recog- activate the immune system. Their early protective effcacy is nized and call for studies to quantify their impact and identify primarily conferred by the induction of antigen-specifc anti- the mechanisms at play. The objective of this chapter is to bodies (Box 2.1). However, there is more to antibody- extract from the complex and rapidly evolving feld of immu- mediated protection than the peak of vaccine-induced nology the main concepts that are useful to better address antibody titers. The quality of such antibodies (e.g., their these important questions. avidity, specifcity, or neutralizing capacity) has been identi- fed as a determining factor in effcacy. Long-term protection HOW DO VACCINES MEDIATE PROTECTION? requires the persistence of vaccine antibodies above protective thresholds and/or the maintenance of immune memory cells Vaccines protect by inducing effector mechanisms (cells or capable of rapid and effective reactivation with subsequent molecules) capable of rapidly controlling replicating patho- microbial exposure. The determinants of immune memory gens or inactivating their toxic components. Vaccine-induced induction, as well as the relative contribution of persisting immune effectors (Table 2.1) are essentially antibodies— antibodies and of immune memory to protection against spe- produced by B lymphocytes—capable of binding specifcally cifc diseases, are essential parameters of long-term vaccine to a toxin or a pathogen.2 Other potential effectors are cyto- effcacy.
    [Show full text]
  • Recently Enacted Medical Liability Immunity Statutes Related To
    Recently enacted medical liability immunity statutes related to COVID-19 Note: State bills are hyperlinked to their respective state legislative websites Updated 11-20-2020 Disclaimer: The information and guidance provided in this document is believed to be current and accurate at the time of posting but it is not intended as, and should not be construed to be, legal, financial, medical, or consulting advice. This chart may not contain the entire text of referenced bills. In many cases, headings in bold have been added for convenience and are not part of the referenced bill’s text. Physicians and other qualified health care practitioners should exercise their professional judgement in connection with the provision of services and should seek legal advice regarding any legal questions. References and links to third parties do not constitute an endorsement or warranty by the AMA and AMA herby disclaims any express and implied warranties of any kind. State Key Provisions Alaska SB 241. Immunity for following a state standard order. A health care provider (HCP) who takes action based on a standing order issued by the chief medical officer in the Department Signed into law on of Health and Social Services is not liable for civil damages resulting from an act or omission in implementing the standing order except in cases of gross negligence, May 18, 2020. recklessness, or intentional misconduct. Duration. Standing orders shall be effective until retracted or for the duration of the COVID-19 public health disaster emergency declaration issued by the governor on March 11, 2020, and any extensions. Immunity relating to Personal Protective Equipment (PPE).
    [Show full text]
  • Humoral Immunity and Complement Humoral Immunity B Cell Antigens
    Humoral Immunity Humoral Immunity and Complement Transfer of non-cell components of blood-- Robert Beatty antibodies, complement MCB150 Humoral immunity = antibody mediated B Cell Activation of T-dependent antigens B cell Antigens T cell dependent B cell antigens T cell independent Majority of antigens. Do not require thymus. Most protein antigens. No memory. T cell help required for B cell activation and antibody production. T-cell dependent antigens T-cell independent antigens 1 B Cell Activation T-dependent antigens Location of B Cell Activation Antigen activated B cells remain in T cell zones of LN. Linked Recognition Maximize contact of Need T cell epitope along with B cell epitope to B cells with T cells. get antibody response. B cells get help from T cells, help = CD40Ligand and IL-4. Clonal proliferation In Follicles Isotype Switching Affinity maturation Somatic hypermutation 2 T cell Independent Antigens B cell mitogens (e.g. LPS) B-1 cells At low levels normal immune response to LPS Activated by repeating CHO epitopes that provide crosslinking At high levels LPS can cause non-antigen specific to induce antigen uptake and activation. activation of B cells. Mitogen effect Antigen specific immune response Lower affinity, lower numbers, no memory. Primarily IgM. Antibody Effector Functions Opsonization Neutralization Antibody Effector Functions Enhancement of phagocytosis Neutralizing abs block active site for adherence, entry into host cell, or active site of toxin Neutralizing antibodies are usually high affinity and primarily IgG. 3 Antibody-dependent cell-mediated Complement Activation cytotoxicity (ADCC) Antibody Effector Functions Antibody Effector Functions Antibody binds to pathogen or infected target cell.
    [Show full text]
  • Three Things Every Nurse Needs to Know About Antibody Testing for Covid-19
    THREE THINGS EVERY NURSE NEEDS TO KNOW ABOUT ANTIBODY TESTING FOR COVID-19 1. A POSITIVE ANTIBODY TEST DOES NOT Different immune ESTABLISH IMMUNITY responses to viruses: The human body develops and produces antibodies in response MEASLES Usually lifelong to viral infections. However, these antibodies do not always immunity is achieved provide full immunity against future infections. The World Health after one infection. Organization (WHO) published an issue brief on COVID-19 However, measles antibody testing and “immunity certificates” where they said: antibody titers have been shown to decrease over WHO continues to review the evidence on antibody responses time and there are reports to SARS-CoV-2 infection (the virus that causes COVID-19). Most that health care workers of these studies show that people who have recovered from with positive titers have infection have antibodies to the virus. However, some of these been infected. people have very low levels of neutralizing antibodies in their blood, suggesting that cellular immunity may also be critical for DENGUE Antibodies from recovery. As of 24 April 2020, no study has evaluated whether infection with one strain the presence of antibodies to SARS-CoV-2 confers immunity to may cause increased subsequent infection by this virus in humans severity of infection with a second strain. It may be years before we understand the immune response to SARS-CoV-2 and what level of protection—if any—is provided. SEASONAL CORONAVIRUSES 2. ANTIBODY TESTS CAN BE UNRELIABLE Immunity can last from AND INCONCLUSIVE a few months up to one Many antibody tests currently available have high rates of false year.
    [Show full text]