Food Waterborne Diseases

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Last updated 6:12 AM on 4/4/26
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71 Terms

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What are portals of exit/how do pathogens leave the body?

same way that they entered

Respiratory Tract: droplet or airborne transmission

Gastrointestinal tract (GI): infected feces and saliva entering the mouth

  • Vehicle transmission: pathogen contaminated nonliving reservoirs (foodborne +waterborne) → transmit to mouth

Genitourinary tract: urine and secretions from the genitals

Skin: Indirect & Direct contact

Blood: contaminated needles/syringes or arthropods/animals that bite

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What is Virulence Factor

Specific tools, traits or mechanisms of the pathogen that make it harmful

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Describe a brief overview of Food and waterborne diseases

  • Infectious diseases with worldwide distribution because spread person to person

  • Involve fecal-oral route

  • Mode of Transmission: food and water that is contaminated with fecal matter and go into a person’s mouth

  • Portal of entry: Mucous membranes of the GI tract

<ul><li><p>Infectious diseases with worldwide distribution because spread person to person</p></li></ul><ul><li><p>Involve fecal-oral route</p></li></ul><ul><li><p>Mode of Transmission: food and water that is contaminated with fecal matter and go into a person’s mouth</p></li><li><p>Portal of entry: Mucous membranes of the GI tract</p></li></ul><p></p>
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What makes up the GI tract in the The Human Digestive System?

• Mouth

• Pharynx (throat)

• Esophagus

• Stomach (gastric acid is produced here to help prevent infection from contaminated food/water)

• Small and large intestine (multi-layered, semi-permeable mucosal barrier that separates the external from the internal environment, first line of defense)

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What are Primary vs Secondary reservoirs? Why do most food waterborne diseases show symptoms?

Primary reservoirs: Where the pathogen is mainly found

Secondary reservoirs: where the pathogen can also be found

Most of these food and waterborne diseases will have these typical symptoms because they are infecting and affecting the Gastrointestinal system

Signs and symptoms (S/Sx): nausea, vomiting, diarrhea, abdominal cramps

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What does Colitis, Hemorrhagic, Ulceration, and Perforation mean

Colitis: inflammation of the large intestine; colon

Hemorrhagic: a medical term referring to excessive bleeding

Ulceration: formation of an open sore/break in the skin or mucous membrane

Perforation: a hole that has developed in the organ

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What are general ways to diagnosis food and waterborne diseases?

Based on GI S/Sx (signs and symptoms) like nausea, vomiting, diarrhea, abdominal cramps

Look for pathogen in Stool sample or contaminated food/water

Serology

Polymerase Chain reaction (PCR) : Amplification of DNA

  • Create millions of DNA copies from a small sample → Cross reference the amplified DNA with genes for specific toxin production

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What are some predisposing factors of waterborne diseases? What factors increase the likelihood of getting waterborne diseases?

Inadequate cooking & Improper food handling

• Cross contamination: same cutting board + knife to cut/clean vegetables and chicken without washing in between

• Temperature Abuse: Leave food out at room temperature

• Not washing fruits and vegetables

Poor personal hygiene

• Not washing hands

Crowded & Unsanitary conditions

• Unclean environment

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What are the best preventative measures for food and waterborne diseases?

Clean: Wash your hands, fruits, vegetables and kitchen surfaces and utensils

Separate: raw meat separate from other foods

Cook: cook foods to the recommended internal temperature, Avoid raw foods if possible

Chill: refrigerate perishable foods, avoid temperature abuse

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What are the Best Treatments for food and waterborne diseases

Medication (antibacterial, antiparasitic, anthelminthic, etc.)

  • antibacterial for bacteria based diseases

  • antiparasitic for parasitic based diseases

  • anthelminthic for helminths (parasitic worm) diseases

Antitoxin

  • antibodies to the toxin

  • artificial passive immunity

Supportive therapy

  • Helps make the patient feel comfortable

  • Oral rehydration: Patient losing lots of water from symptoms

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What is the difference between Bacterial Infection vs Intoxication?

Bacterial Infection

• Pathogen is consumed in the food or water

• Pathogens invade and multiply in the intestinal lining

• Incubation period is long (Hours to days)

• Signs/Symptoms occur slowly: Nausea, vomiting, diarrhea, usually fever

Bacterial Intoxication

• Toxin (made from pathogen) is consumed in the food or water

• Toxins can cause toxemia (spread into the blood and throughout the body)

• Incubation period is short (Minutes to hours)

• Signs/Symptoms occur quickly: Nausea, vomiting, diarrhea, usually NO fever

• Most likely gram positive

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What are endotoxins and exotoxins?

Critical bacterial virulence factors: allow pathogens to cause damage, evade immune responses, etc.

Low LD50 value; small amount of toxin needed to cause fatality (more dangerous)

<p>Critical bacterial virulence factors: allow pathogens to cause damage, evade immune responses, etc.</p><p>Low LD50 value; small amount of toxin needed to cause fatality (more dangerous)</p><p></p>
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Staphylococcal Food Intoxication: causative agent, virulence factor, and reservoirs

• Also known as “Food poisoning”

Causative agent: Staphylococcus aureus/MRSA (Gram positive cocci bacteria, cocci)

Virulence Factor: Toxin is produced when the bacteria incubates in food at temperature abuse

• Produces a heat-stable enterotoxin (Type I Exotoxin; SuperAntigen)

• Boiling may kill bacteria, but toxins will not be destroyed

Reservoir: Human skin

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Staphylococcal Food Intoxication: Mode of Transmission, Incubation Period, and S/Sx

Mode of transmission: Dirty hands with bacteria contaminate food, Temperature abuse

Incubation Period: acute/fast, within a day

S/Sx

• Acute symptoms (quick): Nausea, vomiting, diarrhea, abdominal cramps, and Fever (Type I Exotoxin: Superantigen)

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Staphylococcal Food Intoxication: diagnosis, prevention, and treatment

Diagnosis: Based on fast symptom onset of s/sx

Best preventative measures: Good hygiene, avoid temperature abuse

Treatment: Antibiotics will not work: Target the pathogen, not the toxin. Symptoms are acute, let it process

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Botulism intoxication: causative agent, virulence factor, and reservoirs

Causative Agent: Clostridium botulin (Gram positive bacteria, bacilli, endospore forming, obligate anaerobe)

Virulence factor: potent, heat-labile neurotoxin (Exotoxin) with low LD50

Reservoir: contaminated foods

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Botulism intoxication: Mode of Transmission, Incubation Period, and S/Sx

Mode of transmission: canned foods with neurotoxin (DO not buy dented canned goods because it would potentially allow bacteria to enter)

Incubation Period: 12-72 hours

S/Sx:

• intoxication comes from Exotoxin -> to toxemia and spreads to the nervous system

• Causes flaccid paralysis, Muscle paralysis, Death comes from respiratory or cardiac failure (involves Diaphragm + heart + Low LD50)

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Botulism intoxication: diagnosis, prevention, and treatment

Diagnosis: bacteria (drum stick appearance) with endospore is found at the end of the cell of the stool sample

Look for neurotoxin in serum, stool or gastric fluid

Best preventative measures:

• Proper canning methods

• Treat canned meats with nitrite (prevents spore germination). No germination = no vegetative cells = no toxin production

Treatments: respiratory assistance + antitoxins

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What is Infant Botulism

• “Floppy baby syndrome “

• infant cannot respond to stimuli because weak muscle tone (floppiness) + feeding problems

• Develops when an infant ingests C. Botulinum spores

• Associated with infants eating contaminated honey

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What is Wound Botulism

• Growth of C. botulinum in puncture wounds (Common in IV drug users)

• Obligate anaerobes with no oxygen present

• Common S/Sx: Difficulty swallowing/speaking, Facial weakness, paralysis

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Clostridium defficile Associated Diarrhea: causative agent, virulence factor, and reservoirs

• Also known as “C. diff” colitis (inflammation of the colon/the large intestine)

• A common Hospital Acquired Infection

Causative Agent: Clostridium difficile (Same genus as the Botulism pathogen)

• Gram-positive bacteria, bacilli, endospore forming, obligate anaerobe

Virulence Factors: Produces Exotoxins (No LPS layer with Lipid A because gram positive)

• caused by extended use of antibiotics because Antibiotics kill pathogens, commensal, and beneficial bacteria in your gut = Reduces competitive exclusion/microbial competition = C. defficile can multiply and produce toxins to damage the GI tract

Reservoirs:

• Primary: Humans

• Secondary: Contaminated medical equipment

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Clostridium defficile Associated Diarrhea: Mode of Transmission, Incubation Period, and S/Sx

Mode of transmission: fecal contaminated water & contaminated medical equipment

• 17% of all Hospital-Associated infections (HAI’s) are GI infections

• ~12% of HAI’s are caused by Clostridum difficile

Incubation Period: 1 day or up to 10 weeks or more after exposure

S/Sx:

• Mild diarrhea -> colitis

• Life threatening colitis: ulceration (form open sore on mucous membrane) and perforation (made a hole) of the intestinal wall → sometimes leads to bloody diarrhea

• Fecal mater potentially enter your body and spreading

• May lead to septic shock (Sepsis)

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Clostridium defficile Associated Diarrhea: diagnosis, prevention, and treatment

Diagnosis: PCR- looking for genes in stool sample to see if anything produce toxins

Prevention: wearing disposable PPE in a hospital setting

Treatment: Antiprotozoal drugs & Antibiotics

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What are the microorganisms/pathogens involved in HAI (hospital acquired infections)

staphylococcus aureus and clostridium difficile

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Salmonellosis: causative agent, virulence factor, and reservoirs

• AKA Salmonella Gastroenteritis (inflammation of the stomach and intestines)

Causative Agent: Salmonella enterica serovar Typhimurium

• Serovar: strain or subspecies

• Gram negative bacteria, bacillus, facultative anaerobe, motile

Virulence factor:

• Invades intestinal mucus membrane and multiplies in phagocytes leads to bacteremia (the presence of bacteria in the bloodstream which can spread the infection elsewhere on the body)

Reservoirs

• Raw eggs, Contaminated meats (specifically poultry), fruits and vegetables washed with contaminated water

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Salmonellosis: Mode of Transmission, Incubation Period, and S/Sx

Mode of Transmission: Zoonoses

• A disease that can be transmitted from animals to humans

Incubation period: 12 – 36 hours; faster than typhoid

S/Sx: Fever, nausea, abdominal cramps and diarrhea

• Chronic carriers: infected patients shed bacteria in feces for up to 6 months!

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Salmonellosis: S/Sx, diagnosis, prevention, and treatment

Diagnosis:

• Get a food sample and running a PCR analysis

Prevention:

• Avoid consumption of raw eggs

• Wash all fruits and vegetables with clean water

• Avoid petting animals, wash hands after handling

Treatment:

• Oral rehydration + antibiotics

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Typhoid Fever: causative agent, virulence factors, and reservoir

Causative Agent: Salmonella enterica serovar Typhi

• Same Genus & species, different strain/serovar as Typhimurium

Virulence Factors: Bacteria can multiply in phagocytes and can cause bacteremia

Reservoir: humans

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Typhoid Fever: Mode of Transmission, Incubation Period, and S/Sx

Mode of transmission: usually by fecal-contaminated food and water

Incubation Period: 2 – 3 week (Slow compared to Salmonellosis)

S/Sx:

• prolonged high fever (104), skin rash on trunk (rose spots), headache, muscle aches, abdominal cramps & diarrhea

• Severe cases: intestinal wall ulceration and perforation leading to bloody diarrhea

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Typhoid Fever: diagnosis, prevention, and treatment

Diagnosis:

• Pathogen in blood or stool sample

• Based on symptoms like Presence of rose spots and High fever

Prevention:

• Good personal hygiene (after going to bathroom)

• Before and after handling food

Treatment:

• Antibiotics (because bacterial infection not intoxication) and oral rehydration

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Typhoid Fever: Chronic Carriers and Typhoid Mary

• 1-3% of patients become chronic carriers (someone who is infected with the pathogen for a long time)

→ shed bacteria in feces

• Chronic carriers may require weeks of antibiotic treatment

Ex: “Typhoid Mary” , an Asymptomatic Chronic carrier

• Was a cook and caused 51-122 people infected + 3 confirmed deaths

• Forcibly quarantined twice

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Shigellosis: causative agent, virulence factor, and reservoirs

• AKA Bacillary/Bloody Dysentery (Dysentery = severe damage to intestinal mucus membranes -> ulceration -> bloody mucous diarrhea)

Causative Agent: Genus Shigella (multiple species)

• Gram-negative bacteria, bacillus, fimbriae, facultatively anaerobe

• Four species that cause Shigellosis like S. dysenteriae (most virulent; harmful)

Virulence Factor:

• Release Shiga toxin (potent exotoxin) → pathogen multiply in epithelial cells of the GI tract

Reservoir:

• Primary : fecal contaminated water

• Secondary : Humans

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Shigellosis: Mode of Transmission, Incubation Period, and S/Sx

Mode of Transmission: Fecal-oral route

Incubation period: 12 hours to 2 weeks

S/Sx: inflammation of intestines and bloody diarrhea due to Shiga toxin

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Shigellosis: diagnosis, prevention, and treatment

Diagnosis: PCR (Looking for genes in stools that produce Shiga toxins + symptoms)

Prevention: Good personal hygiene (washing hands), disinfect/sterilize, drink water

Treatment: Often treated with antibiotics and oral rehydration

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Bacterial Gastroenteritis: causative agent, virulence factor, and reservoirs

• Also known as Pathogenic E. coli Gastroenteritis (inflammation of stomach and intestines) or Travelers Diarrhea

Causative Agent: Enterotoxigenic E. coli strain (ETEC)

• Enterotoxigenic: Bacteria that produce toxins that affect the GI tract

• Gram-negative bacteria, bacillus, facultative anaerobe, motile, coliform bacteria

• Coliform bacteria: General bacterial class found in human and animal digestive tracts

• Used as an indicator of fecal contamination of water

Virulence factor: Enterotoxin (an exotoxin) that damages the GI tract

• An example of Gram-negative bacteria producing an exotoxin!

Reservoirs: infected humans, animals (poultry, cattle, pigs, pets), and contaminated environmental sources like water

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Bacterial Gastroenteritis: Mode of Transmission, Incubation Period, and S/Sx

Mode of transmission: Fecal contaminated water

Incubation Period: 1 to 3 days

S/Sx:

• GI disturbances like nausea, vomiting, diarrhea

• Less severe S/Sx than E. coli 0157:H7 strain

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Bacterial Gastroenteritis: diagnosis, prevention, and treatment

Diagnosis: stool test sample

Prevention: boil water/ chemically treat water before consumption

Treatment: oral rehydration + bismuth containing medicines/over the counter antidiarrheal medications

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Hemorrhagic Colitis: causative agent, virulence factor, and reservoirs

Also known as Shiga Toxin E. Coli

Causative Agent: Enterohemorrhagic E. Coli (EHEC) strain (E. Coli 0157:H7 strain)

• Gram negative, rod shaped, fimbriae, facultative anaerobe, motile, coliform bacteria

Virulence factor: produces shiga toxin

• From bacterial Genus Shigella

• Organisms from the Shigella and Escherichia genus can do horizontal gene transfer: Shiga toxin genes from the Shigella plasmid get transferer via conjugation pilus to Escherichia = E. coli can now make Shiga Toxin

Primary Reservoir: Cattle

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Hemorrhagic Colitis: Mode of Transmission, Incubation Period, and S/Sx

Mode of transmission: fecal contaminated food (ground beef; mainly found in cattle)

Incubation Period: 1 to 10 days

S/Sx:

• Symptoms: colitis and profuse bloody/hemorrhagic diarrhea due to ulceration of intestinal mucous membrane

• Severe cases can lead to Hemolytic Uremic Syndrome (HUS) and lead to death

  • Red Blood cell destruction

  • Low platelet count

  • Kidney failure

  • Neurological problems such as seizures or strokes

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Hemorrhagic Colitis: diagnosis, prevention, and treatment

Diagnosis: PCR- stool cultures and tests for genes that produce Shiga toxin

Prevention: routine meat inspection, proper cooking temperature for meat (specifically ground beef)

Treatment: Oral rehydration and supportive care

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Cholera: causative agent, virulence factor, and reservoirs

Causative Agent

• Vibrio cholerae serovar O1 : Primary cause of cholera pandemics

• Vibrio cholerae serovar O139; emerged in 1990s and responsible for outbreaks in Asia

• Halophiles, Slightly curved, gram-negative bacteria, bacillus with a single flagellum at one end.

• Linked to countries with poor sanitary conditions and regions that are affected by natural disasters = Leads to a limited supply of clean drinking water

Virulence Factor
• Produces an exotoxin

Reservoirs

• Primary: contaminated water sources

• Secondary: humans

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Cholera: Mode of Transmission, Incubation Period, and S/Sx

Mode of Transmission

• Contaminated water and (Raw/Undercooked) seafood

Incubation Period

• Within a day

S/Sx

• Sudden loss of water and electrolytes in ”large volumes” → causes “rice water” stools → lead to shock, circulatory collapse, organ failure, and/or death

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Cholera: diagnosis, prevention, and treatment

Diagnosis, prevention, and treatment

• Stool sample

Prevention

• Boiling water or chemical treatment

Treatments

• Oral rehydration with electrolyte replacement

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Brucellosis: causative agent, virulence factor, and reservoirs

• Undulating Fever: constant ride and fall fever pattern

Causative Agent

• Caused by Brucella abortus: Gram-negative bacteria, coccobacilli

Virulence Factors

• Multiply in phagocytes

Reservoirs

• Found in livestock and wildlife (Found in elk, bison and cows)

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Brucellosis: Mode of Transmission, Incubation Period, and S/Sx

Mode of transmission:

• Zoonotic Disease

• consumption of unpasteurized milk/dairy products from infected animals or contact with infected animals/tissues

• Pasteurization: A process that heats milks to a specific temperature for a set amount of time to kill harmful bacteria and extend shelf life; Developed by Louis Pasteur

S/Sx:

• Undulant fever, Chills, sweating, headache, fatigue and loss of appetite

• Typically NOT fatal

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Brucellosis: Diagnosis, prevention, and treatment

Diagnosis:

• Laboratory tests to find pathogen

Prevention:

• Vaccination of livestock & pasteurization of milk products

• PPE when handling infected tissues or dairy products (People who work in the dairy industry, leather makers, meat processors and hunters)

Treatment:

• Prolonged use of antibiotics (~6 weeks of antibiotics)

• Rare in the United states; typically found in the developing world

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Hepatitis A: Causative Agent, Virulence Factor, and Reservoirs

• Hepatitis: Inflammation of the Liver → severe liver damage or Jaundice

• Liver is involved in the detoxification of your blood (bilirubin, toxins, drugs and alcohol)

Causative Agent:

• Hepatitis A virus (HAV)

• Non-enveloped, single-stranded RNA virus, No multiplying/replication while on surfaces, but can survive for several days on surface; obligate intracellular parasite

Virulence Factors:

• Multiplies in the epithelial lining of intestinal tract (like Shigellosis) → lead to viremia and systemic spread →

Spreads to the liver, kidneys and spleen

• Resistant to chlorine treatment of water

Reservoirs:

• Primary: Found in contaminated food & water

• Secondary: Humans

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Hepatitis A: Mode of Transmission, Incubation Period, and S/Sx

Mode of Transmission:

• Fecal-oral Route

Incubation Period:

• 2-6 week incubation period

S/Sx:

• Asymptomatic in children; symptomatic in adults

• Nausea, diarrhea, headache, fever, chills and liver damage → cause Jaundice

• Symptoms can last 2-21 Days

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Hepatitis A: Diagnosis, Prevention, and Treatment

Diagnosis:

• Serology (indirect blood test) → look for the production of antibodies to the virus

Prevention:

• Inactivated HAV vaccine

Treatment:

• Immunoglobulins/ antibodies injection = Artificial/Natural

• Not a chronic disease

• Low mortality rate

• Recovery results in life-long immunity (Memory B & T cells = Adaptive immunity)

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Viral Gastroenteritis: causative agent, virulence factor, and reservoirs

• Also known as: Stomach Flu (Inflammation of the stomach and intestines) caused by viruses

Causative Agent:

• 2 different viruses that cause Viral Gastroenteritis: Rotavirus vs. Norovirus

Virulence Factor:

• ability to multiply in motor neuron

Reservoirs:

• Primary: Water

• Secondary: Human

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Viral Gastroenteritis with Rotavirus: Mode of Transmission, Incubation Period, S/Sx, Diagnosis, and Prevention

Rotavirus: Double stranded RNA virus

Mode of Transmission:

• Common in children

• Prevalent during the winter months; commonly occurring in day care centers

Incubation Period:

• 2–3-days

S/Sx:

• Low grade fever, diarrhea and vomiting for ~1 week

Diagnosis:

• Viral antigens in fecal/stool sample

Prevention:

• Live oral vaccine; thorough handwashing and sanitation practices

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Viral Gastroenteritis with Norovirus: Mode of Transmission, Incubation Period, S/Sx, Diagnosis, and Prevention

Norovirus: Single stranded RNA virus

Mode of Transmission:

• Infects both adults and children

• Low ID50 (Infectious dose 50): the number of pathogens needed to cause an infection in 50% of the population; Highly infectious

• Prevalent all year long, common on cruise ships and classrooms -> causes outbreaks

Incubation Period:

• 18-48 hours

S/Sx:

• Diarrhea and vomiting for 2-3 days

Diagnosis:

• PCR of stool sample

Prevention

• No vaccine, thorough handwashing and sanitation practices

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Poliomyelitis: Causative Agent, Virulence Factor, and Reservoirs

aka “Paralytic Polio”

Causative Agent:

• Caused by Poliovirus (Non-enveloped RNA virus, single stranded)

Virulence Factor:

• Ability to multiply in motor neuron

Reservoirs:

• Primary: Water

• Secondary: Human

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Poliomyelitis: Mode of Transmission, Incubation Period, and S/Sx

Mode of transmission:

• Fecal-oral route; contaminated water containing the Poliovirus

S/Sx:

• Commonly found in children

• Mostly asymptomatic, but less than 1% become paralytic/paralyzed

• Initial symptoms: sore throat and nausea

• Viremia may occur (virus spreads into the blood → enters the central nervous system to multiply in motor neurons (obligate intracellular parasite; causes the death/destruction of host cells)

• Lower limb paralysis

• Muscle wasting/atrophy

• Death via respiratory failure (Of the 1% of those affected with paralytic polio, 5-10% of patients will die)

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Poliomyelitis: Diagnosis, Prevention, and Treatment

Diagnosis: PCR

Prevention:

1. Salk vaccine: injected; inactivated/killed virus vaccine

2. Sabin vaccine: oral; attenuated live vaccine

Treatment: None

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Giardiasis: Causative Agent, Virulence Factor, and Reservoirs

Causative Agent:

• Caused by Giardia intestinalis (Kingdom Protista, Subkingdom Protozoa, parasite with flagella)

Virulence factor:

• Multi-stage lifecycle: ingested dormant cysts in feces and water → activates trophozoites that attach to intestinal walls

Reservoirs: contaminated water

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Giardiasis: Mode of Transmission, Incubation Period, and S/Sx

Mode of transmission:

• Giardia intestinalis cyst contaminated water

Incubation Period:

• 1-3 weeks

S/Sx:

• prolonged diarrhea, hydrogen sulfide gas (smell like rotten gas), weight loss and cramps

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Giardiasis: Diagnosis, Prevention, and Treatment

Diagnosis: microscopic examination of stool sample, looking for cyst form

• Predisposing factors: Drinking from contaminated rivers or streams

Prevention: Boiling water, chemical treatment of water

Treatment: antiparasitic/antiprotozoal drugs

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Amoebiasis: Causative Agent, Virulence Factor, and Reservoirs

Amoebic Dysentery “bloody diarrhea”

Causative Agent:

• Caused by Entamoeba histolytica (Kingdom Protista, Subkingdom Protozoan; parasite)

Virulence Factor:

• Multistage life cycle

• Ingested dormant cysts either in feces or contaminated water → Activates the trophozoites that attach to

the Intestinal walls

Reservoirs: water

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Amoebiasis: Mode of Transmission, Incubation Period, and S/Sx

Mode of Transmission:

• contaminated water → oral

Incubation Period:

• 2 to 4 week

S/Sx:

• Nausea, fever, abdominal cramps

• Ulcerations and perforations of intestinal walls by trophozoites → bloody diarrhea → Trophozoites may invade the liver and cause necrotic (cell or tissue death) liver abscess (collection of pus in the liver)

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Amoebiasis: Diagnosis, Prevention, and Treatment

Diagnosis:

• Microscopic examination of trophozoites with ingested erythrocytes via medical imaging techniques (ultrasound, CT scans & MRI) may be used to see the liver abscesses

Prevention:

• boiling water, chemical treatment of water

Treatment:

• Antiparasitic/antiprotozoal drugs

(Metronidazole)

• 10% mortality if left untreated

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What is the study of tapeworms belong to? Describe the life cycle of Tapeworms. Where are tapeworms common to? Can tapeworms be EID?

Parasitology: the study of parasites; traditionally limited to protozoans, helminths (worms), and arthropods

Life cycle

1. sexual production: Occurs in definitive host

2. Asexual reproduction: occurs in intermediate host

Common to areas of Asia, Latina America and Eastern Europe

Can become an Emerging Infectious Disease (EID)

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What is taeniasis? What is cysticercosis, Ophthalmic cysticercosis, and Neurocysticercosis?

AKA taeniasis: All types of tapeworm infections, Adult tapeworm that is currently infecting the host’s intestine

• Sometimes called cysticercosis: infection with the larval stage via ingesting of tapeworm eggs

• Ophthalmic cysticercosis: larvae lodged in the eye

• Neurocysticercosis: Larvae developed in the central nervous system

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Beef tapeworm Infection: Causative Agent, Virulence Factor, and Reservoirs

Causative agent:

• Taenia saginata (Kingdom Animalia, Phylum Platyhelminthes)

• A mature worm can be 4-8 meters in length with 1000-2000 segments

Virulence factor:

• Multistage life cycle (Eggs → oncosphere → cysticeri larva → adult tapeworm)

Reservoirs:

• Primary: Human (definitive host, where tapeworm sexual reproduction will occur)

• Secondary: Cattle (intermediate host, where asexual reproduction will occur)

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Beef tapeworm infection: Mode of Transmission, Incubation Period, and S/Sx

Mode of Transmission:

• Humans eat raw or undercooked contaminated beef that contains cysticerci larvae/tapeworm oncosphere

Symptoms

• Abdominal pain, lack of appetite, weight loss and fatigue

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Beef tapeworm infection: Diagnosis, Prevention, and Treatment

Diagnosis:

• Stool sample: the presence of eggs or proglottids (reproductive body segments)

Treatment:

• Antiparasitic and anthelminthic drugs for a prolonged period

• Can take weeks to kill the parasitic worms and their eggs

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Describe Beef Tapeworm Feeding and Reproductive Structures

Feeding

• Scolex: Head that has Hooks & suckers for to physically attach to the Host’s intestinal wall

• Cuticle (the outer covering of the worm): protect and nutrient absorption

• Proglottids (body segments): Part of their reproductive system

Reproduction

• Proglottids (body segments) → Mature proglottids has male and female reproductive organs

• Capable of sexual reproduction with other tapeworms to infect the host or can do self fertilization

• Once fertilized and filled with eggs → the proglottids will be released from the tapeworm, spreading via the host’s feces

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Describe the beef tapeworm lifecycle steps

  1. Human eat raw or undercooked beef that has cysticerci larvae → gets infected

  2. A tapeworm will develop from the cysticeri larvae → The scolex (head) develops first to let the tapeworm to attach to the small intestine via hooks and suckers → produce proglottids

  3. Mature proglottids produce fertilized eggs via sexual or self fertilization → Fertilized eggs will be released into the environment with host feces

  4. Cattle (intermediate host) is infected via eating tapeworm contaminated foods

  5. Asexual Reproduction occurs inside cattle: eggs develop into oncospheres → penetrate the intestinal wall and migrate to muscles

  6. Oncospheres → Cysticeri larvae in the cattle muscle → Cattle is slaughtered so their infected meat is sold

  7. The cycle continues as humans eat infected and improperly cooked beef.

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Prion Diseases: Causative Agent, Virulence Factor, and Reservoirs

Causative agent:

• Prions = Protein Infection (Abnormally folded infectious protein particles) = Diseases of the nervous system

Virulence factor:

• Highly resilient; extremely difficult to kill

Reservoirs:

• Sheep, cattle and humans

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Prion Diseases: Mode of Transmission, Incubation Period, and S/Sx

Mode of transmission:

• Consumption of contaminated animal tissues/meats

Incubation period:

• Long, yypically years before symptoms occur

S/Sx:

• Spongiform encephalopathy = Progressive degeneration of the brain tissue

3 Types of transmissible spongiform encephalopathy

1. Mad cow disease (Bovine Spongiform Encephalopathy)

2. Creutzfeldt-Jakob Disease (CJD) – in humans

3. Sheep scrapie

71
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Prion Diseases: Diagnosis, Prevention, and Treatment

Prevention: Incineration of contaminated meats/tissue

No treatment: Chronic and fatal

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