Foodborne and Waterborne Infectious Diseases PDF

Foodborne and Waterborne Diseases 1 Foodborne and Waterborne Diseases: An Overview These are infectious diseases with worldwide distribution Involves fecal-oral route: Mode of transmission Contaminated food & water Portal of entry Mucous membranes of GI tract Big Picture: Pathogens (in fecal matter)...

Foodborne and Waterborne Diseases 1 Foodborne and Waterborne Diseases: An Overview These are infectious diseases with worldwide distribution Involves fecal-oral route: Mode of transmission Contaminated food & water Portal of entry Mucous membranes of GI tract Big Picture: Pathogens (in fecal matter) ðà contaminate food & water ðà pathogens ingested ðà disease in the host 2 Foodborne and Waterborne Diseases: An Overview Reservoirs - 1° (primary) reservoir vs 2° (secondary) reservoir Symptoms - typically GI symptoms Ex - nausea, vomiting, diarrhea, abdominal cramps Diagnosis Based on GI symptoms Look for pathogen in food/water or in stool sample Serology Predisposing factors Inadequate cooking, improper food handling, poor personal hygiene, unsanitary conditions 3 Foodborne and Waterborne Diseases: An Overview Best preventive measures Washing hands, well-cooked food Best treatments Medications Antitoxins Supportive therapy: Oral rehydration 4 Bacterial Infection vs Bacterial Intoxication Bacterial Infection Pathogen is consumed in food/water Pathogens invade & multiply in the intestinal lining Incubation period - long! Hours to days S/Sx - happen slowly Nausea, vomiting, diarrhea, usually fever Bacterial Intoxication Toxin is consumed in food Toxins made by pathogen ðà toxemia Incubation period - short! Minutes to hours S/Sx - happen quickly Nausea, vomiting, diarrhea, usually NO fever 5 Staphylococcal Food Intoxication AKA “Food Poisoning” Caused by Staphylococcus aureus Gram-positive bacteria, cocci, clusters; present on skin and most surfaces Reservoir - human skin Virulence factor = a heat-stable enterotoxin (Type I exotoxin) Toxins NOT destroyed by boiling Toxins produced when bacteria allowed to incubate in food (temperature abuse) 6 Staphylococcal Food Intoxication Mode of transmission - dirty hands with bacteria ðà food contaminated ðà bacteria make heat-stabile enterotoxins Acute symptoms - nausea, vomiting, diarrhea, abdominal Text cramps, fever (type I exotoxin - Super Ag!) Best preventive measures Safe food handling Good personal hygiene/washing hands Proper food temperature or refrigerate food Treatment- Why will antibiotics not work? Supportive care - oral rehydration 7 The Sequences of Events in A Typical Outbreak of Staphylococcal Food Poisoning Figure 25.6 8 Botulism Production of toxin AKA Clostridium Botulism Intoxication/Foodborne Botulism will only grow at the Caused by Clostridium botulinum bottom of test tube Gram-positive bacteria, bacilli, endospore-forming, obligate anaerobe ---- No Oxygen required. Diagnosis Culture body fluid then prep a slide Exospores Bacteria with endospore found at end of cell ðà “drumstick” appearance Spore forming bacteria: Clostridiuquim, Bacillus 9 Botulism What makes pathogen dangerous Low LD50 Value Heat sensitive, Heat will kill it Toxin targets nervous system and damage the nerves Exotoxins are mostly gram- positive Virulence factor - a potent heat-labile neurotoxin (exotoxin), No muscle stimulation endospores Forms spores in favorable conditions --> paralysis Reservoir - contaminated food Mode of transmission - canned food with neurotoxins Cans provide anaerobic condition (no O2) Spores can be found in the the canned food 10 Botulism Symptoms - intoxication comes from ingesting the botulinum exotoxin ðà toxemia Gets targeted by exotoxin Affects nervous system ðà causing flaccid paralysis Death usually comes from respiratory or cardiac failure Best preventive measures Commercial/proper canning methods Treat meats with nitrites Inhibit spores from germination Treatmentwith respiratory assistance and antitoxins Youcan treat with antitoxin since batulism produces toxins 11 Other Types of Botulism Infant Botulism Affects infants Will germinate and produce toxins Develops when infant ingests C. botulinum spores Associated with infants eating honey Weakened muscle tone (floppiness), trouble feeding DEEP! Puncture wounds. The deeper the wound the less oxygen there Botulism is Anaerobic (No O2 required to grow Wound Botulism Growth of C. botulinum in wounds Common in IV drug users 12 Clostridium difficile-Associated Diarrhea Inflammation of colon (life-threatening) AKA “C. diff” Colitis Caused by Clostridium difficile Gram-positive bacteria, bacilli, endospore-forming, obligate anaerobe Produces exotoxins EX: Improper cleaning Reservoirs - 1° = humans; 2° = contaminated medical equipment Mode of transmission - fecal-contaminated water, contaminated medical equipment Mostly acquired in health-care settings has no competition since normal microbiota was Caused by extended use of antibiotics! C.Diff destroyed by extended use of antibiotics 13 Clostridium difficile-Associated Diarrhea Symptoms - mild diarrheaCaused ðà colitis by toxin Makes holes Life-threatening colitis: ulceration & perforation of the intestinal wall; sometime leads to bloody diarrhea Aka Dysentery Diagnosis via PCR - looking for gene in stools sample that produces toxins Prevention - wearing a gown, gloves, and using disposable equipment in hospital settingantiparasitic Best choice Treatment- antiprotozoal drug (Metronidazole) & antibiotic (Vancomycin) C. difficile caused almost 500,000 infections in U.S. in a single year (CDC study 2015) 14 Clostridium Difficile-Associated Diarrhea Long term use of antibiotic Antibiotics killed normal microbiota Was exposed to C. Diff. Has symptoms 15 Salmonellosis G.I. Type of issue AKA Salmonella Gastroenteritis Genus subspecies/strain Caused by Salmonella enterica serovar Typhimurium Can move Gram-negative bacteria, bacillus, facultative anaerobe, motile Virulence factors Prefers O2, but can grow without O2 Invades intestinal mucosa and multiplies in phagocytes ðà bacteremia Spreads through blood 16 Salmonellosis Especially Bird meat like chicken Washer with contaminated water Reservoirs - contaminated meat/fruits/vegetables, raw eggs, pet reptiles Turtles, iguanas Mode of transmission - contaminated food Very fast Incubation of 12 to 36 hours Infection to 1st sign of symptoms 17 Salmonellosis Symptoms Typical fever, not very high Fever, nausea, vomiting, abdominal cramps, diarrhea No symptoms, but infectious Chronic carriers - patients shed bacteria in feces for up to 6 months Isolate DNA Diagnosis of serovar/strain in food by PCR Best preventive measures - avoid consumption of raw eggs, wash all fruits and vegetables with clean water, avoid pet reptiles Treatment- oral rehydration and antibiotics Because bacterial disease 18 TyphoidFever VS Typhimurium(Salmonellosis) Caused by Salmonella enterica serovar Typhi Gram-negative bacteria, bacillus, facultative anaerobe, motile Virulence factors Bacteria multiply in phagocytes ðà bacteremia Reservoir - humans Mode of transmission Usually by fecal-contaminated water/food 2 - 3 weeks incubation period Take a lot longer to develop symptoms vs salmonellosis Global Distribution - TyphoidFever 19 TyphoidFever VS typical fever Symptoms - prolonged high fever (104°F), headache, muscle aches, abdominal cramps, diarrhea, skin rash on trunk (rose spots) In severe cases - intestinal wall ulceration & perforation ðà bloody diarrhea AKA Dysentery Diagnosis Pathogen in blood or stool sample Based on symptoms Ex - presence of rose spots TyphoidFever Skin Rash - Rose Spots 20 TyphoidFever Associated with Rose spots A real person who was infected but didnt stay home. she went around and infected a lot of people 1 - 3% of patients become chronic carriers; shed bacteria in feces Ex - “TyphoidMary” Prevention - good personal hygiene (washing hands) Treatedwith antibiotics and oral rehydration Chronic carrier may require weeks of treatment 21 The Prevalence of Salmonellosis and TyphoidFever in U.S. Not important to know this slide Figure 25.9 22 Shigellosis Myltiply in epithelial cells of GI tract Shiga toxin Bloody Diarrhea AKA Bacillary Dysentery Dysentery - severe damage to intestinal mucosal lining ðà Due to Shiga toxin ulceration ðà bloody mucous diarrhea ðà “Bloody Dysentery” Caused by the bacterial Genus Shigella of several species Gram-negative bacteria, bacillus, fimbriae, facultatively anaerobe Four species - S. sonnei, S. boydi, S. dysenteriae, S. felxneri Shigella dysenteriae is the most virulent Virulence factor Shiga toxin Multiply in epithelial cells of GI tract Text4species - s. sonnei, S. soydi, S. dysenteriae Most Virulent 23 Shigellosis Reservoir: 1° = water; 2° = humans Mode of transmission: fecal-contaminated water From hours to weeks, typically weeks 12 hours to 2 weeks incubation period Symptoms - inflammation of intestines & bloody diarrhea due to Shiga toxin Diagnosis via PCR - looking for gene in stools that produces Shiga toxins; based on symptoms Prevention - good personal hygiene (washing hands) Often treated with antibiotics and oral rehydration Bc bacterial disease 24 Bacterial Gastroenteritis AKA Pathogenic E.coli Gastroenteritis, TravelersDiarrhea Impprtatnt to know that this is Will NOT lead to death Is not deadly,just very uncomfortable NOT a 0157:H7 strain Strain that produces toxin Caused by Enterotoxigenic E. coli (ETEC) strain ( a non-0157:H7 strain) Gram-negative bacteria, bacillus, facultative anaerobe, motile, coliform bacteria Coliform bacteria (“coliforms”) Bacteria that originates in humans or animals and this type of E.coli ends up in water supply Broad class of bacteria (E. coli) found in human & animal GI tract Coliform water pollution - indication of fecal contamination of water From humans/animals 25 Bacterial Gastroenteritis Virulence factor - enterotoxin (exotoxin) Mode of transmission - fecal-contaminated water by coliforms GI disturbances - nausea, vomiting, diarrhea E.coli from humans/animals Hemorrhagic Colitis Less severe symptoms than E. coli O157:H7 strain Causes Severe symptoms Prevention - boiling water before consumption peptobismal Treatment- oral rehydration therapy and bismuth-containing preparations/over-the-counter antidiarrheal medications 26 Hemorrhagic Colitis AKA Pathogenic E.coli Hemorrhagic Colitis, Shiga Toxin E. coli Can lead to death in severe cases Caused by Enterohemorrhagic E. coli (EHEC) strain (E. coli O157:H7 strain) G.ITract Bleeding Gram-negative bacteria, bacillus, fimbriae, facultative anaerobe, motile, coliform bacteria 27 Hemorrhagic Colitis you can DIE from this! Virulence - produces Shiga toxin Shigella and Escherichia capable of Horizontal Gene Transfer Shiga toxin genes from Shigella plasmid get transferred (via pilus) to Escherichia plasmid ðà now E. coli will make Shiga toxin! Cattle are the main reservoir 28 meansBLEEDING INFLAMMATION OF COLON Hemorrhagic Colitis GROUND BEEF Mode of transmission - fecal-contaminated food Symptoms - inflammation of colon (colitis) and profuse bloody (hemorrhagic) diarrhea due to ulceration of intestinal mucosal Severe cases can lead to Hemolytic Uremic Syndrome (HUS) ðà death Diagnosis DNA TEST DNA-->RNA--.PROTEIN BLOOD VESSELS OF KIDNEY DAMAGED!---> MOST LIKELY W ILL LEAD TO DEATH PROTEIN TOXIN PCR - stool cultures and tests for Shiga toxin Prevention - routine meat inspection, proper cooking temperatures for meat (ground beef) Treatment- oral rehydration and supportive care 50 - 500 deaths annually NOT MUCH YOU CAN DO TO TREAT 29 Shigella donatesitsgene to neighboring cell,byPILUS SHIGA TOXIN CAUSING BLEEDING 30 Cholera Caused by Vibrio cholerae O1 or 0139 strains Slightly curved, gram-negative bacteria, bacillus, with single polar flagellum Commonly found in salty waters (halophiles) OR FRESH Virulence factor -produces a powerful cholera exotoxin THIS ONE IS GRAM NEGATIVE....USUALLY EXOTOXINS ARE GRAM POSITIVE LOW ID50 PROTEIN 31 Cholera Reservoirs: 1° = water; 2° = humans Transmission- contaminated water and seafood Symptoms - toxin causes sudden loss of water and electrolytes in large volumes ðà “rice water” stools CHUCKS OF MUCOSA LINING BLOOD IS MOSTLY W ATER,NO BP... PREVENTION Can lose 12 to 20 liters of fluid per day!!! ðà causes shock, circulatory collapse, organ failure ðà death Boiling water as prevention Treatmentincludes oral rehydration and electrolyte replacement Endemic to parts of Asia Associated with natural disasters Rice Water Stool IONS IN FLUIDS K,Na etc NO ACCESS TO CLEAN W ATER OR DURING NATURAL DISASTERS 32 Brucellosis TEMP GOES UP AND DOW N AKA Undulant Fever Caused by Brucella abortus ABORTUS BC CAUSES SPONTENIOUS ABORTION IN BISON,ELK ETC Gram-negative bacteria, coccobacilli Found in elk, bison, cows Virulence factors - ability to multiply in phagocytes Reservoirs - livestock and wild animals (elk, bison) 33 Brucellosis Mode of Transmission- via unpasteurized milk from infected animals or contact with infected animals Zoonotic disease CAN JUMP FROM ANIMALS TO HUMANS --->> DRINKING UNPASTEURIZED MILK OR CONTACT W ITH INFECTED ANIMAL Symptoms Undulant fever = recurring daily high fever (104°F), chills, and night sweats Not usually fatal W AVE LIKE HIGH FEVER 34 Brucellosis VACCINES IS NOT A TREATMENT,IT IS PREVENTION Predisposing factors Dairy workers, handlers of animal hides (leather makers), hunters Prevention Vaccination of livestock and wild animal populations Pasteurization of milk products Protective clothing Prolonged treatment with antibiotics Brucellosis rare in USA 35 VIRAL DISEASES LIVER INFLAMMATION Hepatitis A ANIMAL VIRUS Caused by Hepatitis A virus (HAV), non-enveloped, single-stranded RNA ITK BUT CANT MULTIPLY CUZ VIRUS NEEDS HOST Shed in acute phase, survives for several days on surfaces Resistant to chlorine treatment of water SHED= FOUND IN FECES MUCOSA OF GI Virulence factor - multiplies in the epithelial lining of intestinal tract ðà viremia (spreads to the liver, kidneys and spleen) Reservoirs: 1° = food & water; 2° = humans Mode of Transmission- contaminated food & water (fecal-oral route) 2 - 6 weeks incubation period DNTK 36 Hepatitis A Symptoms - mostly asymptomatic in children; symptomatic in adults LOSS OF APITTIE Anorexia, nausea, diarrhea, headache, fever, chills Jaundice in later stages of disease Symptoms last 2 to 21 days YELLOW ING OF SKIN AND EYES BLOOD W ORK Diagnosis - serology: detection of antiviral Abs (IgM) Prevention - inactivated HAV vaccine Treatedwith immunoglobulins Not a chronic disease Low mortality rate Recovery results in life-long immunity NEW INFECTION ANTIBODIES ARTIFICIAL PASSIVE 37 Viral Gastroenteritis CAUSED BY 2 CAUSATIVE AGENTS AKA Stomach Flu Caused by Rotavirus, double-stranded RNA virus Common in children 2 - 3 days incubation Low-grade fever, diarrhea and vomiting for 1 week Prevalent during winter months; common in daycare centers Diagnosis - viral antigens in feces Prevention - live oral vaccine Caused by Norovirus, single-stranded RNA virus Adults and children HIGHLY INFECTIOUS Low ID50 ðà highly contagious! 18 - 48-hours incubation Diarrhea and vomiting for 2 - 3 days Prevalent all year-long; common in cruise ships & classrooms ðà “outbreaks” Diagnosis - via PCR FECES ----LOOKING FOR DNA Prevention - no vaccine; thorough handwashing 38 Poliomyelitis AKA Paralytic Polio Caused by Poliovirus, non-enveloped, RNA virus Virulence factor CAUSES PARALYSIS ITK Ability to multiply in motor neurons Reservoirs: 1° = water; 2° = human Mode of Transmission Fecal-oral route; contaminated water containing the virus Common in children 39 Poliomyelitis VERY RARE!!! Mostly asymptomatic, but less than 1% become paralytic Initial symptoms: sore throat and nausea ðà viremia may occur ðà virus enters the CNS Multiply in motor neurons ðà destruction of motor neurons ðà muscle wasting ðà lower limb paralysis Death from respiratory failure Prevention Salk vaccine: injected; inactivated/killed vaccine Sabin vaccine: oral; attenuated live vaccine; lifelong immunity VERY W EAK No treatment Polio cases fell 99% from 1988 to 2000 IF YOU GET IT,NO TREATMENT!...HAVE TO BE VACCINATED TO PREVENT IT. EXTREMELY RARE 40 PARASITIC DISEASES Giardiasis G.I.TRACT Caused by Giardia intestinalis SUB KINGDOM PROTOZOA Kingdom Protista, flagellated protozoan parasite Virulence factor: multi-stage lifecycle STAGE/STATE MULTIPLE DEVEPMENTAL STAGES STAGE/STATE Ingested dormant cysts in feces and water ðà active trophozoites that attach to intestinal wall DIFFICULT TO DESTROY BC IT CAN REPRODUCE FROM ANOTHER STAGE Reservoirs: 1° = water; 2° = humans Mode of Transmission- water contaminated with cysts Symptoms - prolonged diarrhea, hydrogen sulfide gas, weight loss, cramps 41 Giardiasis ACTIVE Diagnosis - microscopic examination of stool samples Predisposing factors LOOK FOR CYST IN HUMAN Trophozoites DORMANT IN W ATER Cyst Drinking from contaminated river streams Prevention - boiling water Treatment- antiparasitic/ antiprotozoal drugs (Metronidazole) SINCE IT IS A PARASITE Figure 25.16 Giardia intestinalis 42 Amoebiasis BLOODY DIARRHEA AKA Amoebic Dysentery Caused by Entamoeba histolytica Kingdom Protista, protozoan parasite Virulence factor: multi-stage lifecycle Ingested dormant cysts in feces and water ðà active trophozoites that attach to intestinal wall Reservoirs: 1° = water; 2° = humans Mode of Transmission- water contaminated with cysts AND FECES 43 Amoebiasis Symptoms Nausea, fever, abdominal cramps Ulceration & perforation of intestinal walls by trophozoites ðà bloody mucous diarrhea (bloody dysentery) Trophozoitesmay invade liver ðà necrotic liver abscess FOUND IN RBC,THATS HOW YOU DIAGNOSE 44 Amoebiasis Diagnosis Microscopic examination of trophozoites with ingested RBCs present inside Prevention - boiling water Treatment- antiparasitic/antiprotozoal drugs (Metronidazole) 10% mortality if left untreated 45 TapewormInfections Parasitology - the study of parasites; traditionally limited to parasitic protozoa, helminths (worms), and arthropods Life Cycle - continuous sequence of morphological changes undergone by an organism, as part of its reproduction KINGDOM ANIMALIA KINGDOM PROTISTA MANY DEVELOPMENTAL STAGES OF PATHOGEN Sexual Reproduction - occurs in definitive/primary host Asexual Reproduction - occurs in intermediate/secondary host Sexual Reproduction Asexual Reproduction TapewormInfections UNSANITARY CONDITIONS....DIRTY W ATER,POOR HIGEANE Has a world-wide prevalence Endemic to areas of Asia, Latin America, and Eastern Europe Can become an Emerging Infectious Disease (EID) 47 Worldwide Prevalence of Human Infections with The Most Common Helminths, 2015 W ORMS DNTK ITK Figure 25.20 TapewormInfections AKA Taeniasis= adult tapeworm infects the intestine Sometimes called Cysticercosis: infection with the larval stage (by ingesting eggs) Ophthalmic cysticercosis: larvae lodge in the eye Neurocysticercosis: larvae develop in the CNS If caused by Taeniasaginata = beeftapeworm infection Kingdom Animalia, Phylum Platyhelminthes Mature worm 4 - 8 meters in length, with 1000 - 2000 segments REFERS TO FLAT FLAT OR ROUND Virulence factor: multi-stage lifecycle Ex - eggs, oncospheres, cysticerci larvae, adult tapeworm 49 Beef TapewormInfection Reservoirs Human = 1° Cattle = 2° Mode of Transmission Contaminated/undercooked beef 50 Beef Tapeworm:Structural Adaptations SUCKERS TAENEA SAGENATA HOOKS HEAD Anatomy of The Beef Tapeworm Scolex (Head): Hooks Suckers Cuticle ATTACHMENT TO INTESINAL W ALL ABSORTION OF NUTRIENTS OUTER COVERING Protection & nutrient absorption LIKE SUCKERS Proglottids (Body Segments) Reproductive System CONTAIN REPRODUCTIVE PARTS (BOOTH MALE AND FEMALE)LIKE EGGS ETC REPRODUCE W ITH THEMSELVES 52 Beef TapewormLifecycle Long & complex life cycle Many developmental stages Eggs ðà oncospheres ðà cysticerci larvae ðà adult tapeworm Two hosts: PRIMARY HOST SECONDARY HOST Human = definitive host (sexual reproduction) Cattle = intermediate host (asexual reproduction) Highly-developed reproductive system 53 Beef TapewormLife Cycle THIS PICTURE ON THE EXAM!!!!!! Human (definitive host) eats raw beef 1. PRIMARY HOST SEXUAL REPRODUCTION 5. Oncosphere 2. Cysticerci larvae in muscles 6. Scolex of developing adult worm attaches Adult Worms SECONDARY HOST ASEXUAL REPRODUCTION 4. eggs Cattle (Intermediate host) eats contaminated food with eggs 3. Mature proglottid with eggs * {All of these 3 developmental stages occur in humans (definitive host) as part of sexual reproduction} Summary of Beef TapewormLifecycle Human (definitive host) is infected by eating raw/undercooked beef containing Cysticerci Larvae. The definitive host is where the sexual reproduction part of tapeworm lifecycle occurs. Adult tapeworms develop from Cysticerci Larvae. The scolex develops first so adult worm can attach to small intestine of human (definitive host) using the hooks in the scolex of the developing tapeworm. MALE AND FEMALE BODY PARTS Mature proglottids (body segments of adult tapeworm) containing eggs are passed in feces & will disintegrate, releasing eggs into environment/soil. ON EXAM!! * {All of these 3 developmental stages occur in cattle (intermediate host) as part of asexual reproduction} Summary of Beef TapewormLifecycle ON EXAM!!! Cattle (intermediate host) is infected by eating contaminated food/grass containing the eggs. Asexual reproduction part of tapeworm’s lifecycle occurs here. Eggs in the cattle develop into oncospheres (infectious stage of tapeworm lifecycle). Oncospheres hatch, and the head (containing the scolex with hooks) develops first for attachment purposes. Cysticerci larvae develop & are found in striated muscle of cattle. Cattle is slaughtered and infected meat is sold. Beef TapewormInfection Symptoms - large numbers of adult worms may cause: Abdominal pain, lack of appetite, weight loss, fatigue Diagnosis Stool sample - presence of eggs or proglottids (body segments) Treatment- antiparasitic/antihelminthic drugs for a prolonged period of time Will kill parasitic worms and their eggs Can take a few weeks to fully clear an infection Tapewormwill be excreted as waste 57 Prion Diseases Caused by Prion = abnormally folded, infectious protein particles Diseases of the nervous system Virulence factor - highly resistant! Reservoirs: sheep, cattle, humans Mode of Transmission- consumption of contaminated animal tissue Incubation period - usually years 58 Prion Diseases Symptoms Progressive degeneration of brain tissue ðà spongiform encephalopathy Types of transmissible spongiform encephalopathy: Mad Cow Disease (Bovine Spongiform Encephalopathy) Creutzfeldt-Jakob Disease (CJD) - in humans Sheep Scrapie Prevention - incineration NO treatment - chronic and fatal! 59 Genus Clostidium HORISONTAL GENE TRANSFER MASIVE LOSS OF W ATER BY DIARRHEA 60 104*DEGREESE 61 FLAPPY BABY 62 IN BOTH IN HUMANS ONLY IN COW S ONLY IN BOTH 63