Module 12 - Immunology & Infectious Diseases PDF

Care of Clients MODULE – IMMUNOLOGY & INFECTIOUS DISEASES IMMUNOLOGY IMMUNE RESPONSE A. INNATE IMMUNITY...

Care of Clients MODULE – IMMUNOLOGY & INFECTIOUS DISEASES IMMUNOLOGY IMMUNE RESPONSE A. INNATE IMMUNITY ― body's first line of defence against pathogens. ― general and non-specific response, which means it does not differentiate between types of pathogens ― immediate response HUMORAL ― Complement: consists of a group of proteins in the blood plasma that work together to fight infections o Complement proteins tag pathogens (like bacteria or viruses) for destruction, making them more recognizable to immune cells like macrophages. o increase the inflammatory response by attracting immune cells to the site of infection and triggering the release of histamine and other inflammatory molecules. ― Cytokines: are signaling proteins released by immune cells to regulate immune responses. o recruit and activate other immune cells, such as neutrophils and macrophages, to enhance their ability to fight infections. o promote inflammation, which helps contain infections by increasing blood flow and bringing immune cells to the affected area. o inhibiting viral replication in infected cells and signaling nearby cells to heighten their antiviral defenses. CELLULAR MONOCYTES  circulate in peripheral blood and have the ability to not only CONCEPTS / COMPONENTS OF THE IMMUNE SYSTEM migrate to the inflammatory site ANTIGEN but also exhibit the plasticity to ― any foreign substance capable of stimulating an transform themselves into tissue immune response macrophages. Once in the tissue, these cells are named ― some cells both recognize and react against macrophages. antigens.  Engulfs as long as it does not ― Include pathogens (bacteria, fungi, or viruses), recognize the foreign food proteins, and pollens. substance/body) ― Host defenses include physical protective barriers  Non-selective including the skin, mucous membranes, cilia, and MACROPHAGES  The largest type of leukocyte normal flora.  Can differentiate into ALLERGEN macrophages and myeloid lineage dendritic cells ― mediating substances are released that cause  Influence the process of adaptive tissue injury and allergic symptoms. immunity PHAGOCYTOSIS ― the destruction of the invaders. MACROPHAGES NONSPECIFIC RESPONSES  In the tissue ― include complement, phagocytes, and natural killer  Phagocytosis: will not kill the cells. microorganism, but ingests and SPECIFIC RESPONSES digests it.  After ingesting and digesting the ― include antibody production and cellular immunity. pathoges, macrophages present TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients antigens (pieces of pathogens) granules rich in histamine and on their surface to alert and heparin activate lymphocytes or adaptive  Mediate inflammatory response immunce cells (like T cells) (hypersensitivity and allergic o Antigens are usually on the reaction) surface of the microorganism  Langerhans Cells  releases and stimulates  Dendrites can be found in the cytokine secretion neurons  Modulate immune response DENDRITIC  Act as messengers between the  Participate in tissue CELLS innate and the adaptive immune reorganization / tissue repair systems  Immediate inflammatory  Antigen presenting cells response  Stimulate long lasting immune  Natural Killer Cells responses of the Antibody- NK CELLS  Are white blood cells that destroy Mediated Immunity (AMI) and infected and diseased cells Cell-Mediated Immunity (CMI) (particularly cancer cells) ― If you palpated your lymph nodes:  are effector cells that o (-) Pain: malignant predominate during the early or o (+) Pain: infectious acute phase of the innate immune response.  main function is to identify, B. ADAPTIVE IMMUNITY ingest, and destroy microbial ― a type of immunity that is built up as we are exposed pathogens through receptors, to diseases or get vaccinated. oxidative mechanisms, and enzymes including lysozyme, ― is initiated when an innate immune response fails to collagenase, and elastase, etc. eliminate a new infection  This group of cells is composed ― is much slower than an innate response, taking of neutrophils, eosinophils, days or even weeks to develop on first encounter basophils and mast cells (the primary immune response), but is specific to o Basophils = allergy the antigen(s) present and can retain a long term o Eosinophils = parasitic “memory” to enable a faster response if it is infection encountered again in the future. o Monocytes = nonselective GRANULOCYTES o Leukocytes = infection HUMORAL o Lymphocytes = B cells for producing antibodies to ― Antibodies: aka immunoglobulin neutralize pathogens and T o are proteins that protect you when an unwanted cells for killing pathogens substance enters your body.  Most abundant, make up between 55%-70% of WBC CHARACTERISTICS OF ANTIBODIES / IMMUNOGLOBULINS  Presence of large granules SERUM present inside each cell. Inside CONCEN- CLASS LOCATION CHARACTERISTICS the granules are antimicrobial TRATION (%) enzymes and proteins that destroy pathogens.  Only immuno- globulin that crosses  They destroy invaders (mostly placenta bacteria and fungi) by the process of Phagocytosis and  Responsible for Enzyme Digestion secondary immune response  Highest opsonization  Least abundant (only 1% of the Plasma, tota WBC count) and neutralizstion IgG 76 interstitial activities  Have granules containing fluid chemicals that act on blood  Classified into four BASOPHILS vessels (heparin, histamine, subclasses (IgG1, serotonin, kinins and IgG2, IgG3, and leukotrienes) IgG4)  Are involved in allergic and viral  First to increase the IgM  chronic processes infection  Migrant cells of connective MAST CELLS Body  Lines mucous tissues that contains many IgA 15 secretions, membranes and TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients inc. tears, protects body ― B Cells originate in the bone marrow where they saliva, surfaces develop from plasma or memory cells. breast  Expressed in ― Their major function is to produce antibodies or milk, mucosal tissues immunoglobulins. colostrum  Forms dimers after o These immunoglobulins bind to and destroy secretion specific antigens.  Responsible for primary immune o When an antibody is formed in response to a response particular antigen, it becomes specific to that  Forms antibodies to antigen. ABO blood antigens ― Memory cells are responsible for retaining the  Produced first upon formula or ability to produce specific IgM 8 Plasma antigen invasion (first immunoglobulins. to react)  Increases transiently T LYMPHOCYTES  First to increase than ― thymus to lymph nodes and spleen IgG  acute ― TYPES: infection A. Naïve T Cells  Unknown o Has not yet encountered an antigen  Present on lymphocyte surface o Immature T cells IgD 1 Plasma o Ready to be activated by antigen-  Aids in the differentiation of B presenting cells lymphocytes o Once they recognize an antigen, they  Causes symptoms of differentiate into specific types of T cells allergic reactions (helper, killer, or regulatory) Plasma,  Fixes to mast cells B. Regulatory T Cell IgE 0.002 interstitial and basophils o Modulate the immune system to avoid fluids  Aids in defense attacking the body’s own cells against parasitic o prevent autoimmune disease infections C. Memory T Cells o Augmented immune response after TIP: reintroduction of pathogen G = Greatest plasma o Are long-lived T cells that “remember” a A = sAliva, teArs, etc. previously encountered pathogen. M = Mega; activates compleMent easily o Since they have encountered it already, they rapidly respond by producing a strong D = Di alam and quicker immune response. E = allergEE (allergy) o remembers the infection/virus (Introduction of vaccine  presence of CELLULAR antigen  production of antibodies  ― The major organs of the immune system are the production of memory cells thymus, liver, bone marrow, spleen, tonsils, lymph o will fade over time; the body will try to nodes, and blood. forget the virus thus the need for booster ― All of the cells of the immune system originate in the shots (ex: Hepa B booster) bone marrow where they develop from stem cells. D. Helper T Cells (CD4 cells) o Lymphocytes (B cell), produced in the bone o Assist other lymphocytes to mature and marrow travel to different parts of the body, activate where they function. o Activates and directs other immune cells o In the thymus, lymphocytes mature into T o In HIV, the virus attacks the T-Helper cells cells. E. Cytotoxic (Killer) ― In other organs, such as the tonsils and spleen, o Destroy virus-infected cells, and tumor lymphocytes collect and communicate with each cells other. o Bind to infected cells and release enzymes o The liver synthesizes the proteins of the that trigger cell death, effectively killing the complement system and contains large target cells. numbers of phagocytes to ingest and destroy bacteria. TYPES OF IMMUNITY A. HUMORAL IMMUNITY B LYMPHOCYTES ― immunity created by antibody production or B lymphocyte involvement. TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients ― Helper T cells recognize an antigen and activates CENTRAL DOGMA: DNA TO RNA TO PROTEIN B lymphocyte. ― Specific immunoglobulins that mark the antigen for destruction. (e.g., Escherichia coli) ― specific antigen enters the body and identified by T lymphocytes ― B-cell grows rapidly. ― Within 6 days, IgM present in the bloodstream. o peaks at 14 days and then declines ― On day 10, antigen-specific IgG production begins o remains high for several weeks ― Memory cells develop after the first exposure. 1. DNA → RNA (Transcription) ― The main type of immunoglobulin produced in a  is the process where DNA is copied into mRNA by secondary response is IgG RNA polymerase, which reads a gene in the DNA COMPLEMENT ACTIVATION and synthesizes a complementary RNA strand. 2. RNA → Protein (Translation) ― composed of 20 different proteins, when activated by antigen–antibody contact, these molecules  mRNA is used by ribosomes to assemble amino begin a cascade response that leads to increased acids into a protein, with tRNA bringing the vascular permeability, smooth muscle contraction, appropriate amino acids based on the mRNA chemotaxis (“calling” leukocytes into the area), codons. phagocytosis, and lysis (killing) of the foreign 3. RNA → DNA (Reverse Transcription) antigen.  RNA is converted into DNA by the enzyme reverse transcriptase, used by retroviruses like HIV to copy B. CELL-MEDIATED IMMUNITY their RNA genome into DNA, which can then integrate into the host's genome. ― is the type of immune response caused by T-  HIV has reverse transcriptase so it will insert itself lymphocyte activity. by copying their RNA genome and replicating the ― Cytotoxic T cells attack directly destroy invading normal DNA. HIV will then form its own DNA and antigens replicate o through the release of chemical compounds onto the antigen membrane LYTIC CYCLE: VIRUS REPLICATION o through the injection of a toxin directly into the STEP 1: ATTACHMENT antigen  bacteriophage (virus) attaches to the surface of a o through the secretion of lymphokines bacterial cell DELAYED HYPERSENSITIVITY ― if the T-lymphocyte activity occurs solely without an STEP 2: PENETRATION accompanying humoral response.  phage injects its DNA (or RNA) into the bacterial cell  Viral DNA is injected into the host. TYPES OF ACQUIRED SPECIFIC IMMUNITY ACTIVE STEP 3: TRANSCRIPTION ― Natural: Natural contact with antigen through actual  host's enzymes begin transcribing the viral DNA into infection (e.g., chicken pox, measles, mumps) Mrna ― Artificial: Immunization with antigen (e.g., vaccines  Viral DNA is transcribed into mRNA for chicken pox, measles, mumps) STEP 4: REPLICATION OF PHAGE DNA AND PASSIVE SYNTHESIS OF PROTEIN ― Natural: Transplacental and colostrum transfer from  The phage DNA is replicated, and viral proteins are mother to child (e.g., maternal immunoglobulins synthesized passed to baby) ― Artificial: Injection of serum with antibodies from 1 STEP 5: ASSEMBLY person (e.g., injection of hepatitis B immune  The newly synthesized viral DNA and proteins are globulin) to another person who does not have assembled into complete, functional antibodies. bacteriophages (viral particles) STEP 6: RELEASE  The host cell bursts (lysis), releasing hundreds of new phage particles into the environment, which can go on to infect other bacterial cells TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients disease, or a disease that affects your immune INFECTIOUS DISEASES system ― Do not drink unpasteurized camel milk or eat raw A. MERS COV camel meat ― Middle East Respiratory Syndrome Coronavirus ― Originated in Saudi Arabia (Arabian Peninsula) B. H1N1 OR SWINE FLU ― September 2012 ― Swine Flu ― Republic of Korea in 2015 ― Influenza virus (VARIANT) ― Severe respiratory illness with symptoms of fever, ― United States in April 2009 cough, and shortness of breath ― WHO declared a Pandemic June 11, 2009 ― 3 or 4 out of every 10 patients died ― Combined gene virus of pigs and birds (Avian) ― Infection came from bats to camels ― H1N1 virus that caused that pandemic is now a SYMPTOMS & COMPLICATIONS regular human flu virus and continues to circulate seasonally worldwide. ― Symptoms of MERS start to appear about 5 or 6 days after a person is exposed, but can range TRANSMISSION from 2 to 14 days ― Flu can spread between pigs and people ― S/sx: Fever, Cough, Vomiting, Dyspnea, Diarrhea, o Infection for people exposed to pigs, including Pneumonia, Renal Failure (similar to COVID-19) people who enter the swine barns at agricultural ― MERS-CoV can cause serious and sometimes fairs or people who raise pigs for show or deadly illness. farming ― There is no vaccine or specific treatment for o It can spread through direct contact, surface MERS-CoV, however, by adopting certain contact and air (droplet or dust) precautions you can protect yourself and others PIG TO PERSON PERSON TO PIG TRANSMISSION  A person becomes  An infected ― Through respiratory secretions infected when virus person touches ― Lived in the Arabian Peninsula or recently traveled enters through the eyes, nore, or from the Arabian Peninsula eyes, nose, or mouth and mouth after coming comes in contact ― Direct contact with camels is a risk factor in contact with an with a pig. The o Camels are often used as mode of DIRECT infected pig pig then transportation and direct contact to them CONTACT becomes increases risk of being infected with MERS infected when COV virus enters through their PREVENTION & TREATMENT eyes, nose or ― Currently no vaccine (but currently trying to develop mouth one)  The infected pig  The infeced ― Hand hygiene comes into contact person may ― Cough etiquette with a surface (e.g., leave virus ― Avoid personal contact (to the infectious animals equipment or an particles on and people) enclosure) surfaces by ― Clean & disinfect touching them  The virus is then after sneezing, ― Treatment is supportive coughing or SURFACE transferred from ― if you have fever (38C and higher), cough or that surface to a thouching their difficulty in breathing, contact your nearest health CONTACT human who face worker touches their face ― Cover your mouth with a disposable tissue when without proper  This can happen coughing or sneezing. If a tissue is not available, hand hygiene on farm cough or sneeze into your upper sleeve equipment, feeding troughs, ― Wash your hands regularly with soap and water and enclosures or maintain good personal hygiene even clothin ― Avoid close contact with people who have been Pigs/Humans can release respiratory diagnosed with MERS-CoV AIR droplets when they sneeze, cough or ― Avoid close contact with camels especially if you (DROPLETS exhale. These droplets may contain virus have a chronic disease, such as diabetes or lung OR DUST) and can be inhaled by the non-infected organism TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients  All people 6 months and older to get a flu vaccine ANTIGENIC DRIFT & SHIFT every year ― Creates a new variant of a virus  All vaccines should be given in settings where ― are two mechanisms by which influenza viruses allergic reactions can be recognized and treated evolve, leading to changes in their surface proteins quickly (antigens) that help them evade the immune  Vaccine is injected intranasally because the nose or system. the sinuses also has blood vessels ― The difficulty when creating a vaccine: virus  WOF patients with autoimmune disease or is mutates and tries to change itself making it difficult immunocompromised as they cannot be given live for the vaccines to address the virus vaccines  Small, gradual changes in the flu TREATMENT virus over time due to mutations.  Antivirals ANTIGENIC o oseltamivir phosphate (available as a generic  Leads to the need for updated DRIFT version or under the trade name Tamiflu®), seasonal flu vaccines every year.  Causes seasonal flu outbreaks. o zanamivir (trade name Relenza®)  Sudden, major changes in the o peramivir (trade name Rapivab®) virus when two different strains o baloxavir marboxil (trade name Xofluza®) ANTIGENIC combine to form a new subtype. SHIFT  Can cause pandemics because C. COVID-19 most people have little to no immunity to the new virus.  Virus associated with the outbreak originating in Wuhan, China, has been designated severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2)  The disease caused by the virus is now officially called COVID-19 SIGNS & SYMPTOMS  Most common: Fever, Cough, Tiredness, Loss of taste/smell  Less common: Sore throat, Headache, Aches and Pains, Diarrhea, Skin rash, Skin discolouration (fingers/toes), Red/Irritated eyes LONG COVID / LONG-HAUL COVID  Post-COVID Conditions (PCC)  last weeks, months, or years  wide range of ongoing health problems  more often in people who had severe COVID-19 illness  People reinfected multiple times  People who are not vaccinated SIGNS & SYMPTOMS S/SX COLD FLU SIGNS & SYMPTOMS Symptom Onset Gradual Abrupt Brain ENT Fever Rare Usual Fatigue, brain fog, trouble Ringing in ears, loss of Aches Slight Usual sleeping, mood disorders taste/smell, sore throat Heart Spleen & Kidneys Chills Uncommon Fairly common Chest pain, tachycardia Organ damage Fatigue / Sometimes Usual Lungs GI Tract Weakness Dyspnea, chest pain, cough, Diarrhea, nausea Sneezing Common Sometimes SOB Musculoskeletal Chest Discomfort Mild to Common Liver, Pancreas, Spleen & Muscle and joint pain / Cough Moderate Kidneys Stuffy Nose Common Sometimes Organ damage Sore Throat Common Sometimes Headache Rare Common VACCINES  A (H1N1) virus, an influenza A(H3N2) virus and two influenza B viruses TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients DIAGNOSIS VARIANTS RAPID RAPID  Alpha (B.1.1.7) TYPE OF RT-PCR ANTIBODY ANTIGEN  Beta (B.1.351, B.1.351.1, B.1.351.3) TESTS SWAB TEST TEST TEST  Gamma (P.1, P.1.1, P.1.2) Sample Nasal/Throat  Delta (B.1.617.2, AY.1, AY.2, AY.3) Nasal/Throat Plasma Taken Swab swab sample sample Sample TREATMENTS What It Detects anti- Detects Detects the  Antivirals Measures bodies prod- certain virus’ genetic  Dexamethasone uced against proteins in material  Convalescent Plasma the virus the virus What It Tells Diagnoses Indicates an  Monoclonal Antibodies Indicates a Us an active active past infection infection infection D. NIPAH VIRUS When Do We 24-72 hours 15 min. 15 min.  Zoonotic Virus Get Results  Fruit bats (Animal reservoir) VACCINES  Associated with Encephalitis EFFICACY &  Mild disease to Death TYPE DESCRIPTION DOSING  was first identified in 1999 during an outbreak Encapsulated mRNA 95 % effective among pig farmers in Malaysia and Singapore Vaccine (US/UK strain)  It gets its name from Sungai Nipah, a Malaysian BioNTech/ mRNA encoding for the village, where pig farmers became ill with Pfizer Spike protein is protected 0.3mL – 2 doses – encephalitis in a lipid nanoparticles 21 days apart  In subsequent outbreaks, there were no (like soap bubbles). Once 94.1% (US/UK absorbed, the cell intermediate hosts. strain) Moderna expresses the spike  In Bangladesh in 2004, humans got infected after protein resulting in an 0.5mL – 2 doses – consuming date palm sap that had been immune response. 28 days apart contaminated by infected fruit bats 82% (US/UK strain) SIGNS & SYMPTOMS Oxford / 10% (SA strain)  NiV infection in humans has a range of clinical Astrazeneca presentations, from asymptomatic infection to acute Viral Vector Vaccine 2 doses – 12 days respiratory syndrome and fatal encephalitis dsDNA encoding for the apart (inflammation of the brain) Spike protein is protected 72% (US/UK  After exposure and an incubation period of 5 to 14 in a safe virus. The strain) Johnson & days, illness presents with 3-14 days of fever and infected cell expresses 57% (SA strain) Johnson headache, followed by drowsiness, disorientation the Spike protein which leads to an immune 1 dose and mental confusion response 91% (US/UK  These signs and symptoms can progress to coma strain) within 24 to 48 hours Gamaleya (Sputnik V) 0.5mL – 2 doses – TREATMENT 28 days apart  There is no vaccine for either humans or animals Virus-like Particle 89% (US/UK  The primary treatment for human cases is intensive Vaccine strain) supportive care Nanoparticles are coated 49% (SA strain) with synthetic spike PREVENTION Novavax proteins. An additional 2 doses – 21 days  Infection can be prevented by avoiding exposure to element called adjuvant is apart sick pigs and bats and by not eating fruits bitten by added which allows to bats boost the immune reaction  Avoid contact with infected persons Inactivated Virus 79% (US/UK Vaccine strain) E. HIV / AIDS Sinopharm SARS-CoV2 is chemcally  Retrovirus inactivated (with a 2 doses – 3 wks  came from a type of chimpanzee in Central Africa chemical called beta- apart  First cases of AIDS were reported in the United propiolactone) so it --% (US/UK/SA Bharat States in 1981 cannot replicate but all the strain) Biotech  36,400 new infections occur annually proteins remain intact 2 doses – 21  MSM largest group  Chronic condition TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients  Average age group nowadays are those aged as host's DNA, becoming part of the cell's genetic pre-adolescent to adolescence (13 to 34) material (human DNA). TRANSMISSION 5. Viral Replication:  contacted with infected blood, semen, vaginal  Once integrated, the viral DNA can be transcribed secretions, or breast milk into viral RNA, which is used to produce viral  transmitted through: proteins. o use of non-sterile syringes and tools  These viral components are assembled into new o pregnancy and breastfeeding viral particles inside the host cell. o blood transfussion o organ transplant 6. Assembly and Release: o unprotected sex  Newly formed viral particles are assembled and  not spread by tears, saliva, urine, emesis, sputum, budded off from the host cell, ready to infect other feces, sweat, respiratory droplets, or enteric routes immune cells.  cannot be transmitted through hugging, dry  The enzyme protease breaks viral proteins into kissing, shaking hands, sharing eating utensils, or functional pieces, completing the assembly of the using toilet seats, sharing of clothes/towels, sharing new virus. of food RISK FACTORS  Sharing infected injection drug use equipment  Having sexual relations with infected persons (both genders like MSM or Male Sexual contact to Male)  Infants born to mothers with HIV infection or who are breast-fed by HIV-infected mothers  People who received organ transplants, HIV- infected blood, or blood products (especially between 1978 and 1985) PATHOPHYSIOLOGY (HIV Infection Cycle) 1. Viral Attachment (gp120 proteins and CD4 Receptors):  The HIV virus has gp120 proteins on its surface that bind to CD4 (Helper T-cells) receptors on the surface of a human immune cell.  Additionally, chemokine receptors (CXCR4 and TIMELINE CCR5) help stabilize the attachment.  HIV antibody test becomes positive after 3 weeks  This interaction is crucial for the virus to to 3 months successfully enter the host cell and is often targeted by HIV medications. CLINICAL MANIFESTATIONS ORAL THRUSH 2. Receptor-Mediated Endocytosis:  Candida albicans  After attachment, the virus enters the cell via a  Normal resident flora of the mouth process called endocytosis, where the host cell  If immune system is very low, oral engulfs the virus, allowing it to enter into the thrush will occur because of infection even if it’s a normal flora cytoplasm. ORAL LEUKOPLAKIA 3. Reverse Transcription:  “Leuko” = white  Once inside, the viral RNA is released into the cell.  Presence of white substance on  Reverse transcriptase, a viral enzyme, converts the tongue the single-stranded viral RNA into single-  Caused by EBV or Epstein-Barr stranded viral DNA, and then into double- Virus stranded viral DNA. KAPOSI SARCOMA 4. Integration into Host DNA:  Manifests onto the skin  The viral DNA is transported to the nucleus of the  Develops malignancy = already a host cell. sign of late stage of AIDS  Very painful  With the help of another viral enzyme called integrase, the viral DNA is incorporated into the TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients FACIAL LIPODYSTROPHY 3. One of the following opportunistic cancers: Loss of facial fats  Burkitt's lymphoma  Immunoblastic lymphoma  Invasive cervical cancer  Kaposi sarcoma  Primary lymphoma of the brain 4. Wasting syndrome. Wasting is defined as a loss of 10% or more of ideal body mass. CLINICAL STAGES OF HIV-AIDS  Asymptomatic (No symptoms of HIV OPPORTUNISTIC INFECTIONS disease)  Short, flu-like illness occurs 1-6 weeks STAGE 1 after infection  Infected person can infect other people  Mild symptoms  Average 10 years STAGE 2  HIV in blood drops to very low levels  Antibodies are detectable in the blood  Advanced symptoms  The immune system deteriorates STAGE 3  Opportunistic infections (OI) start to appear  Severe symptoms AIDS  Rapid decline in the number of CD4 T STAGE 4 cells  Opportunistic infections become severe and cancer may develop AIDS DIAGNOSTIC CRITERIA AIDS is diagnosed when a person with HIV develops at least one of the following conditions: 1. CD4+ T cell count drops below 200 cells/µl.  Normal CD4 count: 80 to 1200  500 can still be considered normal depending on the references  Less than 200 is a sign of AIDS  AIDS normally causes Pneumonia, TB (possible also for POTTS) 2. One of the following opportunistic infections (Ols):  Bacterial: TB (any site); any disseminated or extrapulmonary mycobacte- ria, including Mycobacterium avium complex (MAC) or Mycobacterium kansasii; recurrent pneumonia; recurrent Salmonella septicemia  Fungal: Candidiasis of bronchi, trachea, lungs, or esophagus; PCP; disseminated or extrapulmonary coccidioidomycosis; disseminated or extrapulmonary histoplasmosis  Protozoal: Toxoplasmosis of the brain, chronic intestinal isosporiasis, chronic intestinal cryptosporidiosis  Viral: Cytomegalovirus (CMV) disease other than liver, spleen, or nodes; CMV retinitis (with loss of vision); herpes simplex with chronic ulcer(s) or bronchitis, pneumonitis, or esophagitis; progressive multifocal leuko- encephalopathy (PML); extrapulmonary cryptococcosis TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients DIAGNOSTIC STUDIES o Needlestick injury precautions  Antibody tests, Antigen/Antibody tests, Nucleic Acid o Post-Exposure Prophylaxis (PEP) (RNA) tests  ASAP not more than 72 hours after  All test results are confidential exposure  CD4 cell count and viral load  Not given / recommended for low risks o Normal range CD4 cells: 800 - 1200 cells/Μl  HIV testing at baseline and at 6 weeks, 12 weeks, and 6 months after exposure LABORATORY  TDF + E + Raltegravir INDICATIONS  Testing every 3 weeks to 6 months since TEST HIV-1 / HIV-2  Test for both HIV-1 and HIV-2 first exposure Immunoassay antibodies HIV-1 / HIV-2  Tests for both virus (Antigen) NOTE: Antigen / Antibody and antibody for both HIV-1 and  David Kirby was the face of Time Magazine in the combination HIV-2 90s for HIV. He is an HIV positive patient who took immunoassay a picture hugging an his father. The picture, along HIV-1 differentia-  Differentiates HIV-1 from HIV-2 with the scientific studies, debunked the belief of tion assay how HIV is transmitted – which is not via direct HIV-1 nucleic acid  Test directly for virus amplification test contact like hugging or talking HIV-1 p24 antigen  Tests directly for virus  Window Period for HIV: there will be no viral load during this period (from day o to 2nd wk so you WINDOW PERIOD FOR HIV TESTS cannot test for the viral load within this time frame because viral load will be low/very low Nucleic Acid Test (NAT) 10 – 33 days  After 3 wks to 3 months: usual testing for HIV since the possible transmission. If tested earlier, Antigen/Antibody Lab 18 – 45 days there might be a false result. Test Rapid Antigen/Antibody 18 – 90 days Test Antibody Test 23 – 90 days PREVENTION  Health Education  Behavioral interventions o Condoms o PrEP o Abstinence o Monogamy o Dental dams o Safe Sex Practices  HIV testing  Pre-exposure prophylaxis (PrEP) o Tenofovir disoproxil fumarate 300 mg + Emtricitabine 200 mg o HIV status checked every 3 months o does not prevent other sexually transmitted infections o Usual dosing schedule for PrEP:  2-1-1 ( 2 tabs 2-24 hrs before coitus, 1 tab 24 hrs and 1 tab after 48 hrs of loading dose  Downside is it only prevents HIV not STIs  Avoid having unprotected sex with another HIV- seropositive person. Cross-infection with that person’s HIV can increase the severity of infection  U=U (Undetectable = Untransmittable)  Healthcare providers and Healthcare team o Hand hygiene o PPEs TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients DRUG THERAPY F. MPOX  previously known as monkeypox  In Africa, most cases are among children under 15  is a viral illness caused by the monkeypox virus, a years old. species of the genus Orthopoxvirus.  Outside of Africa, the disease appears to be more  It’s found mostly in areas of Africa, but has been common in men who have sex with men (MSM) seen in other regions of the world. SIGNS & SYMPTOMS  causes flu-like symptoms such as fever and chills, The rash starts as flat, red spots and a rash that can take weeks to clear. STAGE 1 - MACULE (lasts for 1-2 days)  There’s no proven treatment for mpox, but it usually The spots become hard, raised goes away on its own. STAGE 2 - PAPULE bumps (lasts for 1-2 days)  There are two known types (clades) of mpox virus The bumps get larger. They o Clade I: originated in Central Africa STAGE 3 - VESICLE look like blisters filled clear fluid o Clade II: One that originated in West Africa. (lasts for 1-2 days)  Is what caused the current world outbreak The blisters fill with pus (lasts for STAGE 4 - PUSTULE (2022 to 2023) 5-7 days)  a subtype of the less severe West African The spots crust over and clade STAGE 5 - SCABS become scabs that eventually fall off (lasts for 7-14 days) TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients OTHER SIGNS & SYMPTOMS  Orthoebolaviruses were discovered in 1976 in the  Fever, Rash, Swollen lymph nodes, Chills, Democratic Republic of the Congo and are found Headache, Muscle aches, Fatigue primarily in sub-Saharan Africa.  Flu-like symptoms, then a rash. Some people don’t  is a rare but severe illness in humans. It is often get a rash at all. fatal. People get infected with Ebola by touching:  A rash can be widespread, but some people only a o infected animals when preparing, cooking or have few bumps or blisters. eating them  swollen lymph nodes usually distinguish mpox from o body fluids of an infected person such as saliva, other poxes. urine, feces or semen o things that have the body fluids of an infected TRANSMISSION person like clothes or sheets.  Person-to-person spread  It is thought that fruit bats of the Pteropodidae o occurs when you come in contact with the family are natural Ebola virus hosts. sores, scabs, respiratory droplets or oral fluids  is introduced into the human population through of a person who’s infected, usually through close contact with the blood, secretions, organs or close, intimate situations like cuddling, kissing other bodily fluids of infected animals such as fruit or sex. bats, chimpanzees, gorillas, monkeys, forest  Animal-to-person antelope or porcupines found ill or dead or in the o occurs through broken skin, like from bites or rainforest. scratches, or through direct contact with an infected animal’s blood, bodily fluids or pox TRANSMISSION lesions (sores).  Ebola then spreads through human-to-human  Contact with recently contaminated materials transmission via direct contact (through broken skin or mucous membranes) with: DIAGNOSIS & TESTS o blood or body fluids of a person who is sick with  tissue sample from an open sore (lesion) for or has died from Ebola; and polymerase chain reaction (PCR) testing (genetic o objects that have been contaminated with body fingerprinting) fluids (like blood, feces, vomit) from a person  blood sample to check for the mpox virus or sick with Ebola or the body of a person who died antibodies your immune system makes. from Ebola.  Pregnant women who get acute Ebola and recover MANAGEMENT & TREATMENT from the disease may still carry the virus in  Mpox is usually a self-limited disease (gets better breastmilk, or in pregnancy related fluids and without treatment) with symptoms lasting from two tissues. to four weeks  A person with Ebola can only spread the disease  prevent dehydration once they have symptoms.  give you antibiotics to treat secondary bacterial  People can spread Ebola for as long as their body infections if they develop. contains the virus, even after they have died.  There aren’t any currently approved antiviral treatments for mpox. SYMPTOMS  If you’re very sick, your provider might prescribe  Symptoms can be sudden and include fever, antiviral drugs like cidofovir or tecovirimat. These fatigue, muscle pain, headache and sore throat. drugs are approved to treat other viral infections These are followed by vomiting, diarrhea, rash, and (like smallpox) internal and external bleeding.  The time from when someone gets infected to PREVENTION having symptoms is usually from 2 to 21 days.  getting vaccinated helps stop the spread  After recovering from Ebola, some people may  decreasing human contact with infected animals have symptoms for two years or longer. These and limiting person-to-person spread. symptoms can include:  Avoiding contact with infected animals o feeling tired  Avoiding contact with bedding and other materials o headache contaminated with the virus. o muscle and joint pain  Practicing safe sex o eye pain and vision problems o weight gain G. EBOLA o belly pain and loss of appetite  is caused by a group of viruses, known as o hair loss and skin problems orthoebolaviruses (formally ebolavirus) o trouble sleeping  These viruses can cause serious illness that, o memory loss without treatment, can cause death. o hearing loss o depression and anxiety. TRANSES BY: JONAH CASSANDRA C. LIM  Care of Clients  People should speak to a health-care professional  The Ervebo vaccine has been shown to be if they have: effective in protecting people from the species Zaire o symptoms and have been in an area known to ebolavirus and is recommended by the Strategic have Ebola, or Advisory Group of Experts on Immunization as part o been in contact with someone who may have of a broader set of Ebola outbreak response tools. had Ebola. DIAGNOSIS  It can be difficult to clinically distinguish Ebola virus disease from other infectious diseases such as malaria, typhoid fever and meningitis.  Many symptoms of pregnancy and Ebola disease are also quite similar. Hence why, pregnant women should be tested rapidly if Ebola is suspected.  Confirmation that symptoms are caused by Ebola virus infection are made using the following diagnostic methods: o antibody-capture enzyme-linked immunosorbent assay (ELISA) o antigen-capture detection tests o serum neutralization test o reverse transcriptase polymerase chain reaction (RT-PCR) assay o electron microscopy o virus isolation by cell culture. TREATMENT  Early care improves a person's chances of surviving Ebola.  Treatment includes oral or intravenous fluids and medicines provided in the hospital.  It is not safe to care for people with Ebola at home, because the person may make other people sick.  There is an effective vaccine for the Zaire type of Ebola, which is mostly found in Guinea and the Democratic Republic of the Congo. o It is treated with antibodies. These antibody medicines are given intravenously and increase the chances of survival.  Research is ongoing to find vaccines and treatments for other types of Ebola.  or all types of Ebola, supportive treatments save lives and include the following: o oral or intravenous fluids o blood transfusions o medicines for other infections the person may have, such as malaria o medicines for pain, nausea, vomiting and diarrhoea. PREVENTION & CONTROL  People can protect themselves from getting Ebola by: o washing hands o avoiding touching the body fluids of people who have, or may have, Ebola o not touching the bodies of people who have died from Ebola  getting the Ebola vaccine if they are at risk for the Zaire type of Ebola. TRANSES BY: JONAH CASSANDRA C. LIM