Airborne Infectious Diseases PDF

Airborne Diseases 1 Airborne Diseases: An Overview Transmission Contact transmission Droplettransmission, Less than 1 Meter Vehicle transmissionAirborne, More than 1 meteraway What is the major portal of entry? respiratorytract(Mucosal membrane in mouth, nose) Respiratory symptoms Coughing Sneez...

Airborne Diseases 1 Airborne Diseases: An Overview Transmission Contact transmission Droplettransmission, Less than 1 Meter Vehicle transmissionAirborne, More than 1 meteraway What is the major portal of entry? respiratorytract(Mucosal membrane in mouth, nose) Respiratory symptoms Coughing Sneezing/nasal discharge Difficulty/noisy breathing shortness ofbreath Other symptoms Droplet Airborne Skin manifestations skin rashes ex: Chickenpox, measles 2 Airborne Diseases: An Overview What are the most effective preventive measures? Good respiratoryhygiene -wearmask, sneeze in to yourelbow, nothands What is a common predisposing factor? Crowds What are the most common type of infectious diseases world-wide? Respiratorytractinfections W e don' thave a choice whatairto breathe. 3 Structures of The Respiratory System Head region Upper respiratory tract U.R.T throat Nose, oral cavity, pharynx, ear middle ear, and auditory tube below the head Lower respiratory tract L.R.T Larynx, trachea, bronchial airsacks tubes, and alveoli gas exchange Ciliary escalator Cilia on colomnarcells Respiratory mucus traps pathogens Voice Box Figure 24.1 Figure 24.2 4 Immunity Host Defenses against Airborne Pathogens Normal microbiota LRT compete againstinvading pathogens Mucus traps pathogens Lysozyme enzyme thatdestroys pathogens Ciliary escalator moves mucus up and outofthe body pathogen orantigen 5 Common Airborne Diseases Bacterial Upper Respiratory Tract Diseases Streptococcal Pharyngitis, Scarlett Fever, Diphtheria Bacterial Lower Respiratory Tract Diseases Pertussis, Pneumococcal Pneumonia, Tuberculosis Viral Diseases Influenza, COVID-19, Smallpox, Chickenpox, Shingles, Measles, Rubella 6 GENUS Streptococcus, and ithas several species Streptococcal Infections & Differential Media (EX: Blood agar) differentiating between 2 species Bacterial growth on blood agar Helps differentiate between different streptococcal species that cause airborne diseases Toxigenic Bacteria  Ex - Streptococcus pyogenes vs Streptococcus pneumoniae make a toxin Hemolysin RBCs - serve as nutrient source Gram + FEVER  RBCs lysed by toxins called hemolysins (type I exotoxin) in the process called hemolysis: 1. Complete hemolysis/RBC lysis = β hemolysis 2. Partial hemolysis/RBC lysis = α hemolysis orIncomplete hemolysis can be observed on Blood Agarplate 7 Streptococcal Infections & Differential Media β hemolysis β hemolysins completely destroy RBCs  clear zone Ex - Streptococcus pyogenes partiallylysed Green Zone α hemolysis incomplete α hemolysins partially destroy RBCs  green zone Ex - Streptococcus pneumoniae Clearzone, RBCs completely Lysed Inserttexthere 8 Streptococcal Pharyngitis AKA Strep Throat Upper respiratory tract infection Causative agent: Streptococcus pyogenes characteristics misc involves Lacefield classification system Classifies Streptococcus bycell wall differences Gram-positive bacterium, chains; group A streptococci (GAS) Produces: toxin β hemolysin - completely lyses RBCs Clearzone on blood agar Streptokinase - dissolves/prevents blood clot formation dissolves hyaluronic acid between connecting tissue cells Hyaluronidase - dissolves connective tissue Capsules and M proteins - allow for adherence Verulence factor so the bacteria can spread throughoutthe body found ofCell W all 9 Streptococcal Pharyngitis Symptoms Inflammation of throat, tonsils, otitis middle ear media in some cases; fever 1Diagnosis by serological tests (rapid antigen detection tests),looking forpathogen in blood 2β hemolysis on blood agar complete destruction, Clearzone Prevention by covering mouth & nose, wearing masks (practice good Figure 24.3 respiratory hygiene) is used forGram+ bacteria; Antibiotics (Penicillin) Penicillin Ineffective againstGram Neg. Erythema aka redness AKA Antibacterial 10 Scarlet Fever BACTERIA PHAGE INVADES BACTERIA AND PASSES ON GENE TO MAKE TOXIN (ERYTHROGENIC TOXIN) AKA Scarlatina Upper respiratory tract infection 2 differentdiseases: Strep Throatand Scarlet Causative agent: Streptococcus pyogenes Causes Fever Gram-positive bacterium, chains; group A streptococci (GAS) Produces: β hemolysin, streptokinase, hyaluronidase, capsules, M proteins Erythrogenic toxin - produced by lysogeny VIRAL INFECTION Virulance Factor  Toxin gene from bacteriophage  incorporated into chromosome of S. pyogenes (prophage)  S. pyogenes will now produce erythrogenic toxin 11 Scarlet Fever TARGETS UPPER RT (FLAT RASH) Toxemia: sore throat, high fever, bright red sandpaper-like rash mostly upper body, “strawberry tongue” (red and bumpy tongue covered with a white coating) INFLAMED TONGUE 12 Scarlet Fever Diagnosis by serological tests (rapid antigen detection tests), β hemolysis on blood agar Prevention by covering mouth & nose, wearing masks (practice good respiratory hygiene) Antibiotics (Penicillin)  very rare disease today Most common in children ages 5 - 15 1830 -1880 pandemic: most common cause of death in children 13 Diphtheria Upper respiratory tract infection Causative agent: Corynebacterium diphtheriae Gram-positive bacilli NOT ALL RODS LOOK THE SAME Pleomorphic (irregular clubbed-shaped) IRREGULAR SIZE AND SHAPES Very resistant to drying Two strains of C. diphtheriae: 1. C. diphtheriae toxigenic strain 2. C. diphtheriae non-toxigenic strain C. diphtheriae 14 Corynebacterium diphtheriae Strains C. diphtheriae toxigenic strain Diphtheria toxin = powerful Low LD50 VERULANCE Diphtheria exotoxin (produced by lysogeny) probablyGram+ symptoms Toxemia: causes heart & kidneys damage, partial paralysis of soft palate & pharynx  death Treat with antibiotics & Diphtheria antitoxin Ab againsttoxin C. diphtheriae non-toxigenic strain No toxin produced Early symptoms: sore throat & fever Later symptoms: formation of tough grayish pseudo-membrane in the throat  blocks air passage to the lungs  death Treat with antibiotics Pseudo-membrane collection ofdead cells and puss 15 NO LIFE LONG IMMUNITY Diphtheria Diagnosed usually by culturing sample from throat swab, but treatment is started immediately in suspected cases Prevented by Diphtheria vaccines: Triple combo vaccines en under6 yo 1. DTaPprChildr events 3 diseases: Less concentrated Added immunity  Diphtheria, Tetanus, acellular Pertussis 2. TDaP forTeens and young adults  Tetanus, Diphtheria, acellular Pertussis 3. Td longertoxic  Tetanus & Diphtheria toxoid no toxin 16 Tuss refers to cough Pertussis People will be coughing a lot! Smokers especially. sound AKA Whooping Cough Lower respiratory tract infection Causative agent: Bordetella pertussis Shape, Gram-negative, coccobacillus OVAL veryshortrod Produces a capsule - for attachment to ciliated cells in the trachea Tracheal cytotoxin - damages ciliated Varulance cells & shuts down the ciliary Paralyzes the Cilia, shutting down escalator Varulance Ciliaryescalator! Leads to no mucus movement, mucus stays, clogs the airways bodywants to cough. Mucus staying mightlead to infection 17 Pertussis Time between infection and symptoms showing up After 5 - 10-day incubation period: whooping sound in children Cold-like symptoms  uncontrollable violent coughing so violentchildren are known to break theirribs as a resultofcoughing  gasping for air Misc Diagnosis by culture of throat mucus sample In lab Triple prevention vaccine Vaccine is nota treatments, itis a prevention Prevented by DTaP, TDaP vaccines ectonlysmall portion ofcell, notthe acellularpertussis inj Ant ibact er ials whole pathogen Treated with antibiotics Highly contagious https://www.youtube.com/watch?v=l5SHtdczSBc 18 Pneumonias: Typical Pneumonia vs Atypical Pneumonia Broken down into 2 types.Bacterial is Typical Pneumonia, ifnon-bacterial Atypical Pneumonia Typical Pneumonia Caused by bacteria Ex - Streptococcus pneumoniae  bacterial Pneumonia (AKA Pneumococcal Pneumonia) Scarletfevercaused byspecies pyogenes Atypical Pneumonia Caused by non-bacterial microbes Ex - Influenzavirus  viral Pneumonia Ex - Pneumocystis jirovecii  fungal Pneumonia  Seen in immunocompromised hosts (Ex - HIV/AIDS) weakened immune system Untreated 19 Pneumococcal Pneumonia AKA Typical Pneumonia bc caused bybacteria Lower respiratory tract infection Causative agent: Streptococcus pneumoniae Gram-positive bacterium Encapsulated diplococci 90 serotypes/strains subspecies Produces: Based on capsule Anti-phagocytotic Too big to eat Very large capsules! α hemolysin - partially lyses RBCs Varulence factor Toxin incomplete --> green zone on blood Agar S. pneumoniae B hemolysin (complete)-S.pyogenes -->Strepthroatand Scarletfever 20 Pneumococcal Pneumonia Acute symptoms: high fever, difficulty breathing Chest pain, fluid accumulation at level of alveoli  interferes with airsacks in lung gas exchange The layerbetween alveoli and pulmonaryvein has to be verythin!Ifthere is fluid, gas exchange cantoccur Serological test Diagnosis: blood tests, α hemolysis on blood agar, presence of looking forGreen zone (incomplete) capsular antigen in urine Age is a predisposing factor Infants and the elderly(poorimmune system) Prevented with the pneumococcal conjugate vaccine (PCV13 or Prevnar 13®) - protects against 13 strains based on capsule mostcommon strains structure Treated with antibiotics (Penicillin) Used forgram positive bacteria 21 Myc means Fungus like growth Tuberculosis Mycolic acid in cell wall, and you still have peptidoglycan.BC you have mycolic acid, you cantdo a gram stain you need to do Acid-faststain Caused by Mycobacterium tuberculosis Acid-fast bacterium, bacilli, rod shape obligate aerobe require O2 Slow Fungus-like growth, mycolic acid (waxy lipid) in the cell wall V.F. Mycolic acids - make bacteria can survive on surfaces resistant to drying; allow bacteria to multiply in macrophages Lower respiratory tract infection Droplet Transmission LESS than 1 meter Mycolic acid inhibits digestive enzymes oflysosome allows pathogen to survive and multiplyinside macrophages Mycobacterium stains pink Non-Mycobacterium stains blue ACID FAST STAIN 22 Developmentofdisease The Pathogenesis of Tuberculosis Pulmonory #1 pathogen engulfed Tubercle is formed M.P have pathogens inside more macrophages #2 recruited #3A Macrophage dies and releases pathogens Figure 24.8 23 The Pathogenesis of Tuberculosis #3B-1 Tubercle did notrupture, butbacteria stopped growing, disease stops (Dormant=LATENT) #3B-2 Tubercle ruptured, spreading the pathogens to lungs or blood stream (liver, brain etc) Figure 24.8 24 Pathogenesis of Tuberculosis 1. Inhaled bacteria phagocytized by alveolar macrophages  bacteria multiply  cause inflammatory response bc mycolic acid inhibited digestive enzymes oflysosome 2. More macrophages recruited  surround & isolate bacteria inside a tubercle (aggregation of activated macrophages with bacteria inside)  tubercle lesions form bc itis too full ifTB bacteria 3. Dying macrophages release bacteria: TUBERCLE DOES NOT RUPTURE a. IF Bacteria stop growing in tubercle lesion & disease process stops for now  lesions heal & become calcified; bacteria remain dormant = Latent Tuberculosis LOCAL TB INFECTION b. IF Bacteria grow/multiply outside macrophages  tubercle ruptures  releasing bacteria into the lungs and cardiovascular SPREAD BLOOD STREAM system 25 Monocyte detects presence of pathogen & goes into Alveoli. A: The pathogen will keep multiplying buteventuallywill run outofspace and the bacterium gets released.The keyis thatthe bacterium stays, itdoesn' t spread -LATENT TB orLocal TB infection. Co-collection or aggregation of activated macrophages B A B: The pathogen multiplies, gets released BUT NOW itspreads to the blood stream orotherparts ofthe lungs! Ifin the blood stream theywill target differentparts ofthe bodylike liver, brain, bone -SYSTEMIC TB Infection The alioral cells and the blood vessel would need to be damaged forB option to happen.Also the blood can enterAlviolus and resultin Bloody Cough. 26 Symptoms of Tuberculosis Chronic symptoms Symptoms take years to develop Is this a local or systemic infection? Systemic infection bc ofspread ofpathogens like 99*formonths Persistent low-grade fever, night sweats, weight loss, weakness Bloody cough indicates alveolar damage Blood enters alveolus Bacteria can spread from the primary lesion (alveolus) to other areas of the lung, liver, nervous system and bone  called Miliary Tuberculosis you can TB in liver, lungs, NS, bone etc means spreads through blood Notj ustin yourlungs BACT CAN SPREAD ALSO TO LUNG -PUMANARY TB 27 Steps for Diagnosis of Tuberculosis 1. Tuberculin Skin Test (Mantoux Test) Subdermal injection of Tuberculin protein  check for induration 48 - 72 hours later bump orhardness underthe skin TD cells react to Tuberculin protein (delayed immune response bc ofTd Cell (Delayed Response T Cell) fNeg Testyou stop tests, Ifpositive Positive reaction means a current or previous infection Ineed more tests to run #2,#3. 2. Chest X-ray (or CT scan) FORMATION White spots on chest x-ray indicate tubercle formation Positive chest x-ray means a current or previous infection Mycobacterium Stain Pink 3. Acid-fast staining Culture sputum sample from lung Stain sample  look for pink acid-fast bacilli Mycobacterium 28 Chest X-rays BLACK MEANS AIR W HITE MEANS TUBERCLE FORMATION  Which chest x-ray is normal vs tubercle formation? TB normal 29 Treatment of Tuberculosis Minimum of 6 months of multi-drug therapy due to slow growth LatentForm and dormancy, drug-resistance ITK!!--Needs to use multidrug therapy!! IffirstLine doesntwork, Use Second-Line drugs First-line drugs Ex - Isoniazid, Rifampin, Ethambutol, Pyrazinamide dontneed to know names Second-line drugs Used for treatment of drug-resistant Tuberculosis use 2nd Multi-drug-resistant (MDR) strains: resistant to first-line drugs must line Extensively drug-resistant (XDR) strains: resistant to second-line drugs 30 Tuberculosis TB is #1 in death from infection disease #2 Malaria #3 AIDS W hywe study!A lotofpeople die from itin the world. 10 million people develop Tuberculosis annually & 2 million die annually 1/3of the world's population has Latent Tuberculosis (“dormant” bacteria) Leading cause of death from infectious diseases worldwide BCG vaccine - not used in U.S. Howeverthere is a problem with this vaccine.Itgives false positives. Ithas variable efficacy(Itis inconsistent). BCG vaccine scar Figure 24.10 31 Influenza VIRAL DISEASE AKA Flu name forindividual viruses Causative agent: Influenza Virus Enveloped, contains eight RNA ITK segments, spikes ITK ication based Influenza Types A, B, C, D - Classif on type ofcapsomere based on capsid protein surrounds the genetic material DNA/RNA Figure 24.14 32 Influenza Protein spikes: Verulance HA (H) spikes NA (N) spikes Spikes can change the structure/shape Antigenic variation of the spikes - involves genetic recombination & formation of hybrid viruses Hybrid is a mix ofhuman spike and non-human spike Mix & match different types of spikes; Ex - H1N1 (Swine Flu), H5N1 mixing and matching differentcombinations ofH and N spikes (Avian Flu), H3N1, etc.  “genetic recombination” Can mix human virus spikes with non-human virus spikes this is hybrid  Ex - HSWNHK  “hybrid” Hsw=pig Hhk= human HK= Hong Kong Why does antigenic variation make it difficult for the immune antigenic determinants change system to destroy virus? because the spikes change (antigenic variation).Since the spikes change the immune system needs time to respond 33 Influenza 3 types oftransmission Droplet and airborne transmission Zoonoses jumping from animals to humans Reservoirs: 1° = human 2° = birds, farm animals Quick Acute symptoms - chills, fever, headache & muscle aches No intestinal symptoms Some viral strain Viral Pneumonia pneumonia caused bybacterium is called TYPICAL pneumonia caused byVirus is called ATYPICAL Atypical bc notcaused bybacterium 34 Influenza symptoms are ACUTE, bythe time you getto Difficult to diagnose from clinical symptoms BC doctor, yoursymptoms are gone < 1% mortality lybc theyhave weak immune systems Which age groups are most at high risk? infants and elder (immuno-compromised) immunized formultiple strains Prevention Multivalent vaccine (contains killed, multi-strains of the virus) INJECTED Composition of the vaccine determined annuallyyou dontgetsame vaccine everyyear Does not provide long-term immunity - Why not? bc ofantigenic variation."Spikes change" Prevention Nasal spray flu vaccine - live, weakened virus SPRAY 35 Influenza anti-viral drugs end in VIR (usually) bc caused byviruses Treated with antivirals: Zanamivir (Relenza) - inhaled NITK  Oseltamivir (Tamiflu) - oral; effective against Influenza Type A if taken within 30 hours of symptom onset NITK Misc Supportive treatment make person comfy Type A - potential cause of most Flu pandemics 3,000 to 50,000 deaths in the United States annually 1918 Spanish Flu pandemic killed more than 20 million people 36 Coronavirus Disease 2019 (COVID19) Coronavirus Disease 2019 AKA 2019 Novel Coronavirus  COVID-19 (on 02/11/2020) Caused by virus: SARS-CoV-2; Coronaviridae Family ITK Single-stranded RNA, enveloped, spikes Several human variants (serotypes): Strains/Subspecies  Alpha variant (B.1.1.7)  Beta variant (B.1.351)  Gamma variant (P.1)  Delta variant (B.1.617.2)  Epsilon variant (B.1.427 & B.1.429)  Omicron variant (B.1.1.529)  Why are these SARS-CoV-2 variants of great concern? BC HIGH MUTATION RATE (ANTIGENIC VARIATION)OF SPIKES 37 VF VF Coronavirus Disease 2019 (COVID19) High mutation rates of the protein spikes! Ability to multiply in ciliated epithelial cells of respiratory tract Coronaviridae Family responsible for several diseases: SARS (Severe Acute Respiratory Syndrome)  Caused by SARS-CoV 1 DONT NEED TO KNOW YEARS FOR ANY  Identified in 2003  Epidemic MERS (Middle Eastern Respiratory Syndrome)  Caused by MERS-CoV  Identified in 2012 EPIDEMIC COVID-19 SARS-COV-2  Pandemic First detected in open food markets in Wuhan, China (12/2019) 38 Coronavirus Disease 2019 (COVID19) Reservoir:  1° = animals (bats, intermediate animal hosts)  2° = humans Transmission: zoonotic, non-living droplet transmission, fomites, object airborne Pangolin 39 Coronavirus Disease 2019 (COVID19) How do you prevent COVID-19?  Wash hands frequently, maintain social distancing, practice respiratory hygiene  Vaccines - Emergency Use Authorization by U.S. FDA 40 Coronavirus Disease 2019 (COVID19) - Vaccines (USA) Pfizer-BioNTech mRNA vaccine, 2 shots (21 days apart) FDA approved 12/11/2020 High efficacy rate (>92%) Moderna mRNA vaccine, 2 shots (28 days apart) FDA approved 12/18/2020 High efficacy rate (>94.1%) Johnson & Johnson/Janssen Viral vector vaccine, 1 shot FDA approved 02/27/2021 Efficacy rate (66.3%) 41 Coronavirus Disease 2019 (COVID19) Incubation period: up to 14 days (average time 4 - 5 days) Symptoms: mild  severe Fever, headache, fatigue, dry cough, loss of taste/smell Shortness of breath  respiratory failure Drop in BP  Septic shock  multiple organ failure Predisposing Factors? Crowds, poorhealth (obesity, high BP, Diabetes), immuno compromised Diagnosis: PCR & antigen test (from saliva, nasal/throat swab); antibody test (serology) High IgM low IgG Treatment? About 80% of people recover without treatment Severe cases - Remdesivir, steroids, antibodies Mild-to-moderate cases - Paxlovid (Nirmatrelvir & Ritonavir tablets - available since 12/2021) and Lagevrio; started within 5 days of first feeling symptoms 42 Differential Diagnosis: COVID-19 vs. Influenza vs. Cold NOT TESTED ON THIS SLIDE 43 Differential Diagnosis: COVID-19 vs. Influenza NOT ON THE EXAM more infectious quick longer 44 World Health Organization and COVID-19 NOT ON THE TEST 45 COVID-19 in the U.S. Inserttexthere 46 Smallpox AKA Variola Causative agent: Variola Virus; enveloped, ds DNA virus Two strains: Variola major - 20 - 60% mortality Variola minor - < 1% mortality Virulance Produces protein called SPICE (Smallpox Inhibitor of Complement Enzymes) How does SPICE act as a virulence factor? Transmitted via the respiratory route inactivates complementproteins AIRBORNE TRANSMISSION 47 Smallpox virus enters blood stream, virus will targetskin, will call skin rush filled with pus = RAISED RASH. prevention Viremia: skin infections/pus-filled lesions dead cells & W BCs Serological tests for diagnosis look forpathogen orantibody Vaca (cow)Cowpox virus Vaccine = live Vaccinia Virus Mild to severe side effects Smallpox Completely eradicated from the human population by vaccination lastcase 1978 Highly contagious Potential for bioterrorism Leaves "pock marks"= pitted scars (indentations) Figure 21.10 48 HHV Chickenpox human herpes virus HHV-1 Cold sores HHV-2 Genital herpes HHV-3 Chickenpox AKA Varicella Causative agent: Varicella-Zoster Virus, Herpesviridae family, HHV-3; enveloped, ds DNA virus Who is the primary reservoir? Human What is the major mode of transmission? Droplettransmission Virulence Fact Multiplies in epithelial cells of upper respiratory tract  viremia will targetthe skin;Skin rash Virus becomes latent in CNS can reemerge years lateras shingles Hidden in CNS (protected from host' s immune system) Abilityto hide in CNS is Unique to Herpesviridae 49 Testquestion mightsaythatthe rash started on chest/face Chickenpox affects children mostly 3 weeks Incubation period of 10 - 21 days RAISED Fever, headache, itchy rash, fluid-filled vesicles on face, chest & back NOT pus Diagnosis based on type of rash & Flatvs Raised location Predisposing factors? schools, daycare weakened Varicella vaccine - live, attenuated virus treatment Calamine lotion to relieve itching, notmuch non-aspirin medication in children you can do Raised, fluid filled forms scab, scab falls, you leftwith a pit(pitted scar)aka "pock" bc aspirin mightlead to brain disfunction in children crustforms 50 Shingles reactivation ofchickenpox AKA Herpes Zoster Causative agent: reactivation of the latent Varicella-Zoster Virus B & T cells How effective is adaptive immunity against latent infections? Noteffective because Virus is in CNS Reactivation - virus travels along sensory nerves of the skin chickenpox virus is goin from skin to rash CNS Virus goes from CNS to Skin.Its called Reactivation CNS to Skin shingles  Limited to one side of the Virus does notcross midline body unique to Shingles Reactivation can usuallyhappens when immune system is weak like infants and old people 51 Shingles Travels along sensorynerves Band-like rash after chikpox pain nerves Very painful (post-herpetic neuralgia) Blisters scab in 7 -10 days *Sensorynerves *Raised rash (fluid filled)path oftravel *Onlyone side sensorynerves One Side 52 Shingles hide in CNS elderlywho had chickenpox weak immune system (immuno-compromised) stress based on type ofrash (raise, thick, fluid filled)and location Predisposing factors? Diagnosis? prevention Prevention via the Shingles/Zoster vaccine called Shingrix® 50 years orolder treatment Antiviral drugs may relieve/suppress symptoms  Ex - Acyclovir Treatmentinvolves 2 things: EitherCURE orMANAGMENT (no Cure)ofdisease. W hen you MANAGE the disease you suppress the disease, notcuring it(suppressing symptoms) W hen you CURE the disease is gone 53 Chickenpox vs Shingles What is the final diagnosis? SHINGLES Band-like rash, only1 side Chickenpox Discreate rash (individual rashes) raised, fluid filled 54 Measles studythis hard will be on testforsure.Know the difference between Measelse and Rubella! AKA Rubeola Causative agent: Rubeola Virus Enveloped, spikes, ss RNA virus Antigenically stable Virulence igenicallyStable!No antigenic vireations ofspikes, H & F protein spikes allow for attachment Ant therefore you can use the same vaccine yearafteryear. Who is the primary reservoir? HUMAN Transmission --> inhale virus, virus enters What is the major mode of transmission? DROPLET blood stream (viremia), virus is going to targetskin --> RASH. 55 Vs.Rubella no orlow fever-thats how you tell the difference between Measles and Rubella Measles M formerging, M formeasles about2 weeks Incubation period 10 - 12 days High fever, runny nose, dry cough, conjunctivitis redness of"white"partofthe eyes Koplik spots - clustered, white lesions on the oral mucosa clumped together FLAT Merging macular rash (flat red spots) goes to Koplik Spots goes to Starts on face  neck  trunk goes to  extremities Figure 21.14 56 Measles Koplik stops mergin rash blood test Diagnosis - based on symptoms, serological tests No specific treatment available; supportive care only Prevention: Single strain ofa pathogen there is no antigenic variations, so you can use single strain Monovalent measles vaccine MMR vaccine - prevents Measles, Mumps, Rubella (Tripple combo vaccine) Complications: Encephalitis in 1 out of 1000 cases Viral Pneumonia ATYPICAL, bc notcaused bybacteria 57 Measles vs Chickenpox What is the final diagnosis? measles -merging, macular(flat)rash Chickenpox ---discreetrashes, elevated, fluid filled 58 Rubella AKA German Measles or 3-Day Measles Causative agent: Rubella Virus NOT RubeOlla virus Non-enveloped, ss RNA virus Who is the primary reservoir? Human What is the major mode of transmission? Droplet Incubation period: 2 to 3-weeks vs 2 weeks forMeasles Mild/no fever, runny nose, cough, conjunctivitis Discrete macular/flat rash lasting 3 - 5 days: Starts on face  neck  trunk  extremities vs HIGH feverforMeasles 59 Rubella studythis hard, will be on the testforsure, know the difference between Rubella and Measles Type oflocation ofrash looking pathogen orAntibody Diagnosis - based on symptoms, serological tests No specific treatment available; supportive care only Prevented by the MMR vaccine Infection confers life-long immunity bc no antigenic variation means ' born with' Complications: Congenital Rubella Syndrome Maternal infection during 1st trimester Fetal damage Cataracts, cardiac abnormalities, deafness, intellectual disabilities 15% mortality within first year of life 60 German Measles Rubeola Rubella vs Measles What is the final diagnosis? Rubella -discreet, flatrash Measles -mergin, flatrash --Rubeola 61 raised scarletfever chickenpox smallpox shingles 62