Communicable Test 2

Foodborne Disease Outbreak
Click the card to flip 👆
1 / 158
Terms in this set (158)
Foodborne Disease Outbreak
According to CDC, when two or more people become ill from eating the same contaminated food or drink
Symptoms of Foodborne Illness
-Symptoms often affect the stomach and intestines
-Nausea, vomiting, diarrhea, abdominal pain, fever, malaise,
-Systemic disease depending on the agent
Foodborne illness
Disease caused by ingestion contaminated food
Produce are biggest cause
Host Status and Illness
-Ability to cause illness also depends on host
-Low risk, healthy individuals - more resistant to becoming ill
- High risk (immunocompromised, elderly, small children, pregnant women)
-Some infected individuals are without symptoms but are carriers EX) Hep A, Salmonella, Shigella (weeks - prolonged)
-Foodborne illness in the host is usually short-lived. Chronic sequelae are relatively rare but can occur Reactive arthritis, Guillain-Barre Syndrome (neurological), Septicemia
Impact of Foodborne Illness
Each year causes 48 million cases (1 in 6 Americans)
128,000 hospitalizations
3,000 deaths
Up to $83 billion spent annually overall - loss of productivity, healthcare, loss of business
Major threat to PH: LHD are the frontline of defense against foodborne disease outbreaks
Foodborne Illness Surveillance Systems
Notifable disease
NORS
FoodNet
PulseNet
CalciNet
NoroSTAT
Only 1-5% of cases are reported to CDC
National Outbreak Reporting System (NORS)
Originally CDC collected voluntary reports from PH agencies about foodborne disease outbreak investigations
Expanded to also include enteric diseases transmitted through water, p2p, direct contact with animals
CDC, USDA/FSIS, FDA, and other investigators analyze the data to improve the understanding of the human health impact of foodborne disease outbreaks and the pathogens, foods, and settings involved in these outbreaks
FoodNet
Active sentinel surveillance system at 10 participating sites in the US in collaboration with CDC, USDA, FDA
Population-based surveillance for lab-confirmed cases of certain disease (7 bacteria, 2 parasites)
Represents ~15% of the US population
Concentrates on foodborne disease documented by lab testing
Determines burden of foodborne illness in US; monitors trends in the burden of specific foodborne illnesses
PulseNet
National network of local, state, territorial, and fed labs coordinated by CDC that perform molecular testing on selected enteric pathogens Pulsed field gel electrophoresis Using whole-genome sequencing for certain pathogens
Allows comparisons of agents involved in an outbreak with patterns of other isolated pathogens to identify linkages
Vastly improved rapid detection of even relatively small foodborne disease outbreaks that occur in multiple sites across the county Save ~500 million in medical costs and loss productivity each year
Norovirus Reporting
Individual cases aren't required to be reported
All outbreaks of acute gastroenteritis, including suspected outbreaks of norovirus, should be reported
HD are encouraged to report suspected and confirmed norovirus outbreaks to the NORS and CalicNet
NoroSTAT combines NORS and Calcinet Data
CalciNetCollects lab specimens of norovirus (a calcivirus) associated with gastrointestinal outbreaks Compares norovirus genetic sequences to rapidly link norovirus outbreaks with common food source and ID emerging strains Started in 2009 and 15 states CDC links lab data to clinical and epidemiological data from NORSNoroSTATSentinel testing and tracking network of 12 SHD and CDC Est standard practices for norovirus outbreaks reporting to improve timeliness, completeness, and consistency of reporting Combines NORS an CalciNetMost prevalent foodborne pathogensNorovirus (5.5 million/58%) Nontyphoidal Salmonella spp. (1 million/11%) C perfringens (1 million, 10%) Staphylococcus aureus (0.2 million/3%)Leading cause of foodborne hospitalizationsNontyphoidal Salmonella spp. (35%) Norovirus (26%) Campylobacter spp (15%) Toxoplasma gondii (8%)Leading cause of foodborne deathsNontyphoidal Salmonella spp. (28%) Toxoplasma gondii (24%) Listeria monocytogenes (19%) Norovirus (11%)Associated Microorganisms with raw seafoodVibrio spp, hep A, norovirusesAssociated Microorganisms with raw eggsSalmonellaAssociated Microorganisms with undercooked meat or poultrySalmonella, Campylobacter spp, Shiga toxin-producing Escherichia coli, Clostridium perfringensAssociated Microorganisms with unpasteurized milk or juiceSalmonella, Campylobacter, Yersinia spp, STECAssociated Microorganisms with soft cheesesSalmonella, Campylobacter, Yersinia Listeria Monocytogenes, STECAssociated Microorganisms with raw hot dogs, deli meatlisteria monocytogenesAssociated Microorganisms with home canned goodsClostridium botulinumLocal, state, and federal rolesLocal: most foodborne outbreaks are local. PH officials in just on city or LHD investigate State: Investigates outbreaks that spread across cities or counties. Often works with State Dept of agriculture and federal food safety agencies Fed: Outbreaks that involve large numbers of people or severe or unusual illnesses CDC usually leads investigations that affect more than 1 state, collaborates with FDA and USDASteps in a foodborne outbreak investigation3 components: env health assessment, lab analysis, epid assessment 1) Est outbreak 2) Define cases 3) Generate hypotheses 4) Test hypothesis 5) If find associations, find point of contamination and source of food 6) Control an outbreak 7) Decide if outbreak is overRoles and Resp of Investigators in Foodborne outbreak-Env health: receives complaints from consumers, investigates establishment -Epid: analyze surv, characterize outbreak, plan studies, interview cases and control, analyze and interp -PH Nurse: interview patients, collects specimens, administer questionnaires, advises patients, provides edu -Lab: analyze specimens and interpCouncil to Improve Foodborne Outbreak ResponseMultidiscplinary working group comprised of 12 PH entities including FDA, USDA, CDC To reduce foorborne illness in the US, developed guidelines for outbreak response Emphasis on more detailed interviews of patients to build hypotheses regarding clusters, active soliciting cases, and lab analysesHypothesis Generation in Foodborne Outbreak InvestigationInterviews: interview sick people that disclose what and where they ate in the days or weeks before they got sick If no obvious place then give shotgun questionnaire. A standardized question with a list of questions about food, meals, shopping, habits, travel, restaurants, and eventsInterview Tips in Interviewing in Foodborne InvestigationConversational, empathy, explain reasoning10 Cardinal Rules for Conducting Foodborne Interviews1. Do a practice run until you are comfortable with the questionnaire 2. Find a quiet place to conduct your interviews 3. Be non-judgmental 4. Avoid leading the case 5. Accurately record what people say 6. Ensure confidentiality, beginning with conducting interviews in a private location 7. Gently re-direct as needed 8. Probe if answers are vague, particularly about time of symptom onset 9. Work with epid staff to provide lang interp 10. Thank interviewee at closing and explain how the info will be usedWhat is the timeline from first exposure to cases reported as an outbreak in a foodborne illness2-3 weeksWhat's the percentage of foodborne outbreaks that actually get solved30%What percentage of food outbreaks involve more than one state2% 98% -> one stateUSDA, FDA, CDCUSDA: ENFORCE. food and safety inspections responsible for ensuring meat, poultry, and processed egg products are safe, wholesome and labeled correcty FDA: ENFORCE. protecting consumers against impure, unsafe, and fraudulently labeled products. CDC: no authority to enforce - NONREGULATORY. Gather data on foodborne illnesses, investigates outbreaks, monitors preventionMechanism of Illness: Infection Infection with toxin production Foodborne intoxication-Infection: dis that results from eating food containing pathogenic microorgs that colonize the intestinal track and invades body causing symptoms - Infection with toxin production: dis results from eating food containing live organisms that colonize the stomach or intestinal lining, making toxin as they live and grow, the toxin produced inside the body causes the symptoms -Foodborne intoxication: dis results from eating food contaminated with preformed toxins from bacteria, molds, or chemicals. These toxins are usually odorless, tasteless, colorless, and can cause dis even after the organisms in the food have been killedCase characteristics suggest mode of transmission Foodborne Waterborne P2PF: distinctive demographic, reflecting food, similar geographic distribution W: widespread, less distinction, P2P: cases cluster in social units, cases in waves separated by one incubation period for the diseaseAgent and Mechanism: VirusInfection Hep A, Noro, Rotavirus, AdenovirusAgent and Mechanism: ParasiteInfection Cyrptospiridium, toxoplasma gondiiAgent and Mechanism Marine algae toxinsPreformed toxin Paralytic shellfish, ciguateraAgent and Mechanism Fungal toxinsPreformed toxin Alfatoxin, mushroom toxinsAgent and Mechanism Fish toxinsPreformed toxins Scombroid, tetrodotoxin from puffer fishAgent and Mechanism: ChemicalsChemical interaction Arsenic, Fluoride, Lead, Mercury, NitritesAgent and Mechanisms: Bacteria1) Preformed toxin (Bacillus cereus, Staph aureus) 2) infection and production of enterotoxins (Perfringens, Bacillus Cereus) 3) Infection (Camplybacter, bacillus anthracis)Norovirus Symptoms and incubation period-Leading cause of foodborne illness -Single-strand RNA, non-enveloped viruses -Activity all year round with peaks in winter -Symptoms in 1-2 days: nausea, vomiting, diarrhea, stomach cramping. Sometimes fever, headache, fatigue, muscle aches. -Incubation period: 24-48 hoursNorovirus Communicability-Fecal oral, p2p, contaminated food -Highly contagious -Spreads in daycare, nursing homes, schools, cruises -Chlorine bleach rec bc survives on surfacesSalmonella (non-typhoidal) Symp, transmission, incubation-2000 serotypes -Symp: diarrhea, fever, vomiting, abdominal cramps -Trans: poultry and other animals (ovarian tissue), eggs, melons, reptiles, fowl, rodents, surfaces -Incubation: 1-3 daysShigella-Symp: watery or bloody diarrhea, fever, abdominal cramps, malaise -Trans: contaminated food (poultry), p2p -Children -Incubation period: 1-7 days (usually 2-4)Escherichia Coli 6 pathotypesSTEC (shiga toxin producing) EPEC (enteropathogenic) EDEC(enteroaggregative) EIEC (enteroinvasive) DAEC (diffusely adherent)Escherichia Coli: STEC 0157:H7 Symp, trans, incub-Symp: watery or bloody diarrhea, abdominal cramps, nausea, vomiting NO fever -Complications: chemolytic uremic syndrome (children, elderly) -Trnas: contam food (lettuce, sprouts, produce, raw milk and juice), water, animal manure, ruminant reservoirListeria-Symp: febrile gastroenteritis, meningitis -Elderly, pregnant -Complications: sepsis, death, miscarriage, stillbirth -Trans: contam food/H2O, mother to baby -Incubation: days-weeksWhat was the cause of the 2 deadliest fooborne outbreaks?Listeria 1985: cali cheese 2011: US cantaloupeCampylobacter Symp, Trans, Incub-Symp: diarrhea, abdominal cramps, fever -Trans: contam food/H2O (poultry), contact with cats and puppies -Incub period: 2-10 days (2-5)Staph Aureus Symp, Incub, Trans-Foods: meat, poultry and egg, salads, cream-filled pastries, milk -Symp: nausea, vomiting, retching, diarrhea, prostration -Incub: 30 mins - 8 hours (2-4 hours)Bacillus cereus Two main types-Toxin producing gram positive bacteria found in env -Multiplies in room temp 1) Nausea and vomiting (rice) 30 mins - 6 hrs 2) Diarrheal: production of toxin when in intestine, 6-15 hoursHep A Incub, trt, description-Long incubation: 28 days (15-50) -RNA virus -Can be stable in env for months killed by temp >185F -Chlorine kills -Trt: NONE -Diagnosis: Cannot distinguish clinical presentation, made by serology (IgM: 5-10 days before onset of sympt)Hep A Serology IgM neg + IgG pos = IgM pos =past infection or vaccination acute/recentHep A Symp, complications-Virus excretion is highest before symptom development -Replicates in liver in ~10 days enters blood -Sympt: Abrupt fever, malaise, anorexia, nausea, dark urine, jaundice -Children usually asymptomatic -Last < 2 moths, doesn't become chronic -Complications: severe manifestations rare, fulminant hep is most severe mort up to 80%, 0.3%-0.6% all agesHep A Risk factors and chain of infectionRF: international travelors, contacts of recent adoptees from HAV countries, men who have sex with men, use of injection and non-infection drugs, persons with clotting factor disorders, persons working with primatesHep A chain of infectionReservoir: humans Transmission: fecal-oral (primarily p2p) - sharing syringes, eating, unwashed hands, sex with people who have Hep A Communicability: 2 weeks before illness to 1 week after jaundice Break chain with vaccination and washing hands, at hostHep A VaccineInactivate whole virus Persists 10 years 2 doses near 100%, but 1st does usually works Combo vaccine with Hep B (Twinrix) Rec 12-23 months No benefit if already have Hep APost-exposure ProphylaxisFor unvaccinated with exp Hep A in prior 2 weeks -Hep A vaccine for all people over 12 months age -Hep A virus-specific immunoglobulin to those 40 yr/older. Consider age, immune status, exp type, availability of IGHep A Trends and Outbreaks-Nationally reportable in 1966. -1996 rec Hep A vaccine. -2006 routine vaccination for all children -2013: pomegranates 2016: scallops and frozen strawberries 2017: homeless, illicit drugs (Largest P2P since vaccine)MI Hep A outbreak2017, has decreased but not over 920 cases, 30 deaths (3.3% mort rate) Most patients had USD followed by coinfection with Hep C Increase vaccinations and educationClostridium botulinum-Anaerobic gram-positive bacteria; live and grow in low ozygen conditions -Can form protective spores in poor conditions; can survive in this dormant place for years -Found naturally in soil and marine sediments, worldwide, most commonly found in spore phaseBotulism Spores-Dormant, protective phase of Clostridium botulinum -Bacteria harmless in spore form -Spores are heat resistant, survive at boiling water. Can be killed if 248F for 5 minutes -Spores can germinate into vegetative form, the active-producing form of the bacteria: restricted O2, low acidity pH>4.6, and temp 77-98FBotulinum Toxin-Most potent toxin known to man -8 toxin A-H; one strain=one toxin -A is most potent, B, F -A and B produce an enzyme that denatures (spoils) food and leaves unpleasant appearance, odor, taste, but other strains don't overly change food -Resistant to degradation by grastric acidity -Sensitive to temp; inactivated by 185F for 5 mins -No smell or tasteMechanism of BotulinumNeuromuscular junction, axon terminal Flaccid muscles, no signal to contractTypes of BotulismFoodborne Infant Wound Adult intestinal toxemia Iatrogenic InhalationalFoodborne Botulism-Caused by ingestion of food contaminated by preformed botulinum toxin -Onset of symp 12-36 hours after ingestion of the preformed toxin -Symp may vary depending on dose of exp -Canned foods!! Conducive to creating anaerobic conditions that allow spores to germinate. High acidic foods are at higher risk. Pressure canning allows water to boil at higher temp.Infant Botulism-Honey -Most common for of botulism (80-100 cases/yr) -Occurs when spores are ingested, colonize GI tract, then release toxin.Wound Botulism-Substance use -Contamination of wound with C botulinum spores from env w/ subsequent germination of spores and production of toxin in anaerobic env -Rare until 1990s -Clinical syndrome indistinguishable from foodborne -Often the skin infection/abscess is a minor lesion -IncreasingAdult Intestinal Toxemia-Rare, intestinal colonization in a few adults in US -Might occur in presence of underlying bowel abnormality that allows colonization of clostridial species -Diagnosis made after excluding other formsIatrogenic BotulismHigher doses injected for treatment of muscle disordersInhalational BotulismNot natural, deliberate dissemination of toxin by aersolClinical Syndrome-Symmetrical cranial nerve palsies with blurry vision, double vision, ptosis, expressionless faces, difficulty swallowing -Descending paralysis, resp compromise -Sensory system UNAFFECTED and intellectual function preserved -NO feverPresumptive Diagnosis BotulismCluster of 2 or more cases is essentially pathogonomic -Diagnosis of sporadic cases is frequently missed -History EVERY CASE is a ph emergency and clinicians should report immediately -Presumptive diag can be made on clinical findings alone, antitoxin should be given immediatelyConfirm Botulism Diagnosis-Foodborne: serum up to 12 days following ingestion, stool, vomit, food source -Infant: isolate and ID in stool -Wound: wound -Bioterrorism: level of toxin in serum may not be high enough to detectBotulism Toxin DetectionGold standard is mouse bioassay -Mice injected with or without antitoxin and followed for symp -Only in special labsTreatment of Botulism-Administer antitoxin as soon as possible. This only neutralizes toxin that is not bound to nerve endings. Doesn't reverse paralysis. -May req antibiotics and wound debridement -Supportive care, no isolation -Hospitalized 1-3 monthsTwo Kinds of LegionellaCaused by gram-neg bacteria legionella symp occur 2-10 days (up to 14) after exp 1) Legionnaires' -Causes pneumonia. Cough difficulty breathing, fever, muscle aches, headache, diarrhea, nausea, confusion -1/10 die, 1/4 in HC facility -1976 outbreak at American legion conference: 221 cases and 34 deaths 2) Pontiac Fever -Mild form, acute respiratory infection without pneumonia, often undiagnosed -1986, cross tracked backLegionella Risk Factors-Age GE 50 years -Smoking -Chronic lung dis (COPD) -Immune system disorders due to dis or meds -Systemic malignancy -Underlying illness such as diabetes, renal failure, or hepatic failure -Recent travel with an overnight stay outside of the home, including stay in HC facility -Exp to hot tubsDiagnosis of Legionnaires and Pontiac FeverL: urine antigen tests only tests for serogroup 1, rapid test, doesn't allow molecular comparison. Resp culture: special media, slow, detect serogroups not from urine test, allows for molecular comparison PF: no lab testTreatment for LegionellaNo treatment for PF Antibiotics for legionnaires'Environment for Legionella-Found naturally in freshwater -Grows and multiplies inside amoeba where they get nutrients and are protected -Human alveolar macrophages can provide a similar env -Not as much risk in env, but when growth is amplified and aerosolization occurs there's riskGrowth Conditions for Legionella-Warm water 68-122F (can survive in lower and higher temp) -Stagnant water (encourages biofilm and reduces temp and levels of disinfectant) -Presence of organic matter -Absence of disinfectants: Chlorine, heating/storing/filtering -Buildings with large, complex water systems can have these if not well maintained: construction, water main breaksExamples of where Legionella can Grow-Hot and cold water storage tanks -Water heaters, filters, arrestors -Expansion tanks -Faucets, aerators, restrictors, hoses, showerheads -Pipes, valves, fittings, humidifiers, misters -Ice machines -Hot tub -Fountains -Internal and external factorsCases of Legionella are Increasing-More legionella in env -Increased awareness and testing -More people susceptible -Older, complex buildings -Most likely multifactorialLegionella Endemic in NY2015 Legionnaires': 138 cases, 16 deaths Linked to single cooling tower Traced back to single strain, genetic homogeneity my complicate future investigationsLegionella Focus on Prevention-Investigations focus on finding sources of exp -Focus on env health interventions to limit growth -Water management engineering practices Est a team Describe building system Identify risk areas Decide control measures Est interventions when controls aren't met Ensure program running smoothly Document activitiesOrgs the Provide Legionella Guidance-CDC -American Society of Heating Refrigerating and Air Conditioning Engineers -American Industrial Hygiene AssociationsReproduction NumberAvg number of secondary cases resulting from an infected person in a completely susceptible population Influenced by: -Transmissability of pathogen -Probability of infection resulting from a contact -Duration of infectious period -Proportion of susceptibles -Duration of immunity -Population dynamics Pattern(s) of mixing of individualsMeasles Incub, symp, Complications, Ro-Acure viral illness: rna paramyxovirus family -Human reservoir -Symp: fever, cough, coryza, conjuctivitis, rash -Incub: 7-18 days (usually 10-14) -Highly infectious: airborn Ro=12-18 -Communicable 4-6, 4 days before and after rash -Complications diarrhea, otitis media, pneumonia, death, subacute sclerosing panencephalitis -Long term damage, immune amnesia, risk of other illnessesMeasles Diag, PEP-Diagnosis suspected based on clinical presentation and confirmed lab testing -Live measles vaccine (MMR) provides perm protection and may prevent dis if given within 72 hours after exp -Immune globulin may prevent or modify dis and provide temp protection if given within 6 days of exp: susceptible household contacts, close contacts, contacts <1 year of age, pregnant women, immunocompromisedPublic health response to measles-Assemble resp team -Determine immunity coverage -Enhance surveillance -Inform PH authorities -Educ cases about measures to minimize spread -Proper case management -Lab confirmation -Implement controls: MMR to unvaccinated, PEP to susceptible, isolation -Collected data on cases and outbreak resps -Analyze outbreakMeasles TimelineIncub: 14 days Prodome: 2-4 days Infectious: 1 day before prodome to 4day after rash onset Immunize prev dis if given <3 days after exp and IG <6 dayssubacute sclerosing panencephalitisFatal measles complication Fatal degenerative brain disease 8 years after infection 1 in 100,000 cases 1 in 1,367 < 5 y/o 1 in 600 < 12 y/oChallenges with MeaslesHighly communicable Contagious period > 1 week Ro = 12-18 Req high thresholdMeasles: In our favorLifelong immunity following dis or immunization Measles vaccine highly effective and safe Humans are sole reservoirBurden of Measles PRE-VACCINE4 million cases 400-500 deaths 1,00 cases chronic disabilityMeasles eliminated in2000 Vaccine 1963 Resurgence 1989-1991 2019: 1282 cases Vaccine hesitancy a threat to global healthMI Measles Outbreak-46 in 2019 (96 cases from 2000-2019) 61% no vaccine, 30% unknown adults 52% 20+ Due in part from increases in other areas of the world: airport = vector Mimics nationalCurrent Status of Measles-Eliminated (this does not mean eradicated): the absence of any continuous chain of measles virus transmission within a defined geographic area (i.e. the US) for more than 12 months) Interruption of year-round transmission. Doesn't imply 0 incidence. Measured by duration of outbreak, not number of cases -Elimination attempted 3 times in US: 1966-1970, 1978-1988, 1996-2000 -NOT JUST CHILDHOODEconomic Evaluation of Measles VaccinePrevents nearly 42,000 early deaths Prevents 20 million cases of disease Saves $13.5 billion in direct costs and $68.8 societal10 Threats to Global Health in 2019Air pollution and climate change Noncommunicable disease Global flu pandemic Fragile and vulnerable settings Antimicrobial resistance Ebola and other high-threat Weak primary care Vaccine hesitancy Dengue HIVAirborne vs Droplet TransmissionA: indirect, aerosolize droplet nuclei, exhaling/singing/coughing/sneezing, long distance, suspended in air Ex) varicella, measles, mumps, TB D: direct, droplets >10, coughing/sneezing, short dist(3-6ft), spread through fomites ex) Rubella, pertussis, flu, pneumoccoccus, meningococcusMumps Agent, TransParamyxovirus, enveloped RNA; human reservoir Acute viral illness associated with inflamed parotid gland Resp transmission: p2p Virus replicates in nasopharynx and regional lymph nodes, then spreads to multiple tissues including salivary glands, meninges, pancreas, testes, and ovaries Inflammation leads to characteristic symptoms of parotitis and aseptic meningitis No treatmentMumps Clinical FeaturesIncub: 16-18 days (12-25) Prodome: myalgia, anorexia, malaise, headache, low-grade fever, parotitis -> resolve after 10 days Diagnosis suspected based on clinical presentation and confirmed with lab (serology, PCR, culture) Orchitis (testicular inflammation), nausea, vomiting, fever, ovarian inflammation, aseptic meningitis, pancreatitis, Postvaccine era these are rare <1%Mumps OutbreaksOccurring despite people receiving 2 dose MMR 2018 rec 3rd dose for those at higher risk Close contact settings because waning immunity and increase in vaccine exemption rates Unvaccinated individuals have higher mumps attack rateMumps timeline-Incub: 16-18D -Prodome: 1-2D -Dis: resolved after 10D -Infectious 7D before onset until 5D after protitisRubella Agent, Symp, TrtAcute viral illness Low-grade fever, rash, arthralgia and arthritis, conjunctivitis, testalgia, orchitis, 50% symptoms subclinical Rash 14-17 days after exposure, starts on face, lasts 3 days Associated with congenital rubella syndrome Togavirus, enveloped RNA virus No trt Rubella vaccine nor immune globulin is effective for post-exposure prophylaxis Complications not common, more in adults than children Encephalitis, arthitisRubella TransmissionResp transmission: p2p Replication in nasopharynx and regional lymph nodes then spreads Incub: 14 days (12-23 days) Prodrome: rare in children, low grade fever, lymphadenopathy occurs before rash and last weeks Moderately contagious 7 days before and after rash Confirm with lab (viral culture, detection PCR, serology IgM) cases decreasingCongenital Rubella SyndromeInfection most severe in early gestation May affect all organs and lead to death or premature Manifestations may be delayed after delivery 2-4 years Deafness, eye defects, cardiac defects, microcephaly, mental retardation, bone alterations, liver and spleen damageRubella TimelineIncub: 14D-17D Prodome: 1-5D Dis: rash last 3D Infect: 7D before to 7D after rashVaccine History1963 Live attenuated and killed measles 1967 Killed measles vaccine withdrawn. Live mumps 1969 Live rubella vaccine 1971 Licensure of combined MMR 1989 Two dose MMR 1995 Varicella vaccine 2005 Licensure of MMRVMMR VaccineLiven attenuated Rec all children get 2 doses (1st at 12-15 mo, 2nd at 4-6yr) Given later than some other vaccines because antibody transferred from mother to baby can provide some protection and make MMR vaccine less effective Safe for breastfeeding women to receive MMR vaccine; shouldn't be given to pregnant womenVaricella Zoster Virus Agent, ComplicationHerpesvirus, DNA Primary infection with virus results in chickenpox Reactivation of disease results in shingles (zoster) Associated with aging, immunosuppression, illness, stress, varicella at <18 month of age Skin lesions appear first on head, fever, itching, Varicella Complications Bacterial infections of skin lesions Pneumonia Central nervous system Hospitalization: 2-3 per 1,000 cases Death: 1 per 60,000 Increased risk for infants <1, immunocompromised, persons >15 years with initial infection, newborns with maternal rash onset within 5 days before to 48 hours after delivery Zoster Complications Prostherpetic neuralgia: pain in the area of the occurrence that persists after the lesions have resolved, may last a year or longer after the episode of zoster Ocular nerve and other organ involvement with zoster can occur, often with severe sequelaeVaricella Zoster PathogenesisEnters through resp tract (airborne) and conjunctiva (close contact) Rep at site of entry in nasopharynx and lymph nodes Primary viremia occurs 4-6 days after infection and disseminates the virus to other organs Further rep in viscera, secondary viremia, viral infection of the skin (chickenpox)Varicella Diagnosis, Trt,Diagnose with clinical specimen, serology, or rapid virus identification (PCR, direct fluorescent antibody) Treat with antiviral medications Report individual cases PEP: varicella vaccine for all susceptible person exp to varicella (70-100% effective within 72 hrs exp)Varicella EpidHuman reservoir Airborne droplet and direct contact Highly contagious, secondary AR 90%, 1-2 days before rash have crusted or no new lesions after 24 hrsVaricella VaccinesVaricella vaccine: 12 mo+ and second dose 4-6 yrs, live attenuated MMRV: 12mo-12yr, live attenuated Herpes zoster: 60yr+, live attenuated or recombinant vaccine for 50yr+, preferred shingles vaccine Persons with break through infection may transmit virus Increasing prop of cases are a result of break through infectionVaricella TimelineIncub: 14-16D Prodome: 0-2D Dis: 5D Infect: 1-2D before and 5D after rashPertussis (whooping) Agent,Highly contagious Fastidious gram neg bacteria Many antigenic and biologically active components Primarily a toxin-mediated disPertussiss PathogenesisDroplets with bacteria are inhaled, attach to ciliated epithelial cells in resp tract, release toxin that paralyze cilia and kill cillia, local tissue damangePertussis Communicable PeriodIncub: 5-10 days, up to 21 Communicable period Catarrhal stage: 1-2 weeks Insidious onset, similar to upper resp infect Paroxysmal stage: 1-6 weeks Severe burst of coughing, long inspiratory effort, cyanosis, vomiting, exhaustion, paroxysmal attacks Convalescent stage: weeks to months Mild to moderate cough, fever minimalPertussis Trt, DiagnosisSerious for infants: half req hospitalization, 1/4 get pneumonia, 3/5 have apnea, 1/100 die Diagnosed by clinical history, culture, PCR (rapid, high sensitivity) Treat with antibiotics Human reservoir Milder in adults AntibioticsPertussis TrendsIncreasing Peaks every 3-5 years Cases have gotten higher (awareness, diagnostic tests, better reporting, more circulation of bacteria, waning immunity, genetic shifts) Cannot rely on herd immunity because it spreads so easily, vaccine protection decreases with time, acellular vaccines doesn't prevent colonizationWhole Cell Pertussis Vaccine (wP)Mid 1930s and combined with DTwP in mid 1940s 70-90% efficacy after 3 doses Protection for 5-10 years Fever common, local adverse rxns, No longer available in USCellular pertussis vaccine (aP)Purified subunit vaccines Several made for dif groups (DTaP, Tdap) DTaP (pediatric) 6wk-6yr Tdap 10-64 yrs (boostrix) and 11-64 (Adacel) Contains lesser amount of diphtheria toxoid and acellular pertussis antigen than DTaP Licensed for full series 1996Pertussis Timeline:Incub: 9-10D Catarrhal: 7-14D Paroxysmal: 1-6w Convalescent: 1-6wTB-5th LCOD worldwide -TB has been responsible for the death of more people than any other infectious disease in history - over 1 billion deaths in the past 200 years -Airborne dis caused by Mycobacterium tuberculosis Tuberculosis complex (M. tb, bovis, africanum, microti, canetti, caprae, pinnipedii, orygis, suricattae, mungi) -Acid fast bacilli (Stain AFB+ = TB)Transmission of TBAirborne particlesPathogenesis of TB-2-8 weeks, special immune cells called macrophages ingest and surround the tubercle bacilli. The cells form a barrier shell, call a granuloma, that keeps the bacilli contained and under control (latent TB, LTBI) -IF the immune system cannot keep the tubercle bacilli under control, the bacilli begin to multiple rapidly (TB disease). This process can occur in different areas in the body, such as the lungs, kidneys, brain, or bone.Active TB-Pulmonary (lungs): most common site; usually infectious Symp: chronic cough, coughing up blood (hemoptysis), weight loss, night sweats -Extrapulmonary: any site outside of lungs; usually not infectious unless concomitant pulmonary dis or in oral cavity -Miliary: occurs when bacilli spread to all parts of the body; rare, but fatal if untreated -CNS: usually occurs as meningitis, but can occur in brain or spineHigh Risk for TB Infection-Have HIV/AIDs -Use IV drugs -Are in contact with infected individuals -Are from a country where TB is common, such as several countries in Latin America, Africa, and Asia -Live or work in areas where TB is common, such as prison or nursing homes -Work in HC and treat people with a high risk of TB -Are children and are exp to adults at risk of TBHigh Risk for Progression for Dis-Persons infected with HIV -Children younger than 5 y/o -Persons who were recently infected with M. tuberculosis (within the past 2 years) -Persons with a history of untreated or inadequately treated TB disease -Persons who are receiving immunosuppressive therapy -Persons with silicosis, diabetes mellitus, chronic renal failure, leukemia, or cancer of the head, neck, or lung -Persons who have had a gastrectomy or jejunoileal bypass -Persons who weigh less than 90% of their ideal body weight -Cigarette smokers and persons who abuse drugs and/or alcohol -Populations defined locally as having an increased incidence of disease due to M. tuberculosis, including medically underserved, low-income populationsPercentage Risk of TB10% over life time with TB infection and no risk factors 30% over lifetime with TB infection and diabetes 7-10% PER YEAR for TB infection and HIVPrevalence of TB-1/3 of world's population is infected with TB -Each year there's 9 million cases (6 million know) -An undiagnosed, untreated person with active pulmonary TB dis can infect an est 10-14 people in a year -Resurgence in US in 1980s but has been decreasing -2017 National avg is 2.8 cases per 100,000TB Control StrategiesDiagnose and treat all persons with TB Detect and treat LTBI Contact investigation and case management Prevent transmission through infection controlHow to Diagnose TBSymp: cough, weight loss, night sweats RF TB test Chest radiograph MicrobiologyChest Radiograph(abnormalities may suggest TB but cannot be used to definitely diagnose; negative x-ray can help rule out active dis) Consolidation in upper lungs, cavitation in upper lungs, enlargement at hilum due to lymphadenopathyDirect Identification with nucleic acid amplification or DNA probe. Proper specimen collection for TBDirect: Newer tests can also test for rifampin resistance, Amplified mycobacterium TB direct, Molecular beacon assay (genotyping helps match cases) Proper specimen: at least 3 sputum at 8- 24- hour intervals, at least 1 morningTB SpecimenGOLD standard: more sensitive than a smear, mycobacteria can take weeks, allows for susceptibility testingTreatment for TB (what's the 4 main drugs?)Combo of drugs to start (usually 4) then based on response to treatment, usually 2 drugs Isoniazid, Rifampin, Pyrazinamide, Ethambutol -> RIPE Takes 2 weeks then likely not contagious Directly observed therapy: healthcare worker watches patient swallow each dose Can reduce drug resistance, treatment failure, and relapseDetecting LTBIHigh risk then screen. If identified TB then clinical eval for active vs latentLTBI11 million people in US Not everyone with LTBI will develop disease, about 5-10% will if not treated Treatment substantially reduces the risk that persons infected with M tuberculosis will progress to TB dis Targeted testing programs should be designed to ID persons who are at a high risk for disease who would benefit from treatmentTest for LTBITB skin test (TST, PPD) TB blood test (IGRA)TB Skin Test-Purified protein derivative extract from M tuberculosis -Intradermal injection on inner surface of forearm -Immune cells respond causing wheal to rise -Must be read within 48-72 hours after placement -After exp and infection it takes 2-8 weeks for immune system to reactTB Skin Test Reaction False-positive False-negativeA) FP: Nontuberculous mycobacteria, BCG vaccination, problems with admin, recent initial skin test B) Anergy (lack immune resp), coinfection, recent infection, very young or old, live-virus vaccination, renal failure, lymphoid dis, low protein states, immunosuppressive drugs, problems with adminAdv and Dis of TB Skin TestA) Cost effective, minimally invasive, simplistic test, widely available, can be used in children as young as 6 month, well est definitions of TST conversion - useful for serial testing D) Req trained personnel, req 2 visits, may need to be boosted (2 step), can be affected by BCG vaccine, results more susceptible to errors, doesn't distinguish latent vs active diseaseTB Blood TestIn vitro T cell-based assays that measure interferon-gamma release by sensitized T cells in response to highly specialized M tb antigensTB Blood Test Adv and DisadvA) 1 visit, not affected by vaccine, more objective, no booster D) More invasive, costly, finicky, limited data on use in children <5, doesn't distinguish between latent and active, inconsistent reproducibility, complicated interpGeneral Recommendations with TB Blood Test-Preferred when testing person who might not return for TST reading or have received BCG vaccine -Not for children <5 -Preferred over TST for all older than 5Patient Monitoring for TB (Before starting treatment for LTBI)-Exclude possibility of dis -Determine if patient has history of prior treatment for LTBI or dis -Determine if any contraindications to treatment -Obtain info about current and previous drug therapy, including adverse reactions -Recommend HIV testing, unless patient declinesLBTI Treatment RegimensRifampin (daily for 4 months), or Isonizaid (daily for 9 months), or Isonizaid and rifapentine once a week for 12 weeks Latent TB doesn't req LHDTB Laws-LHD responsible for TB prevention and control and early case management -Private providers must report suspected and confirmed casesTo be considered noninfectious (TB) must have1) 3 consecutive negative AFB sputum smears collected in 8- to 24- hour intervals 2) Their symptoms have improved clinically (cough, no fever) 3) Compliant with an adequate trt regimen for 2 weeks or longersFactors associated with infectiousness and noninfectious of TBNON: No cough, no cavity in lung, no acid-fast bacilli, extrapulmonary TB dis, not undergoing cough-inducing procedures, negative cultures INF: cough, cavity, acid-fast bacilli, TB dis of the lungs, not receiving adequate trt, undergoing cough-inducing procedures, positive sputum culturesBacillus Calmette-Guerin Vaccination-Live, attenuated strain of Mycobacterium bovis -Can't give to immunocompromised or pregnant -Used in countries with high prevalence -Not for US because low risk infectionHow to Tell a Person Has TB-Large amount of active TB bacteria -May spread TB bacteria to others -May have cough, fever, and weight loss -TB skin test or blood test positive -Radiograph abnormal -Sputum smears and cultures positive -Needs trt -May req isolation