Ch. 11 - Food and Waterborne Bacterial Diseases Flashcards
(25 cards)
Dental carries
Tooth decay
Causative agents: streptococcus mutans, streptococcus sobrinus
Results from:
Plaque building, Dietary carbohydrates (into acid by bacteria), Acidogenic bacteria (acid-producing)
Bacterial cells on pellicle will start metabolizing carbohydrates into acids
Symptoms: toothache, sensitivity
Plaque
Biofilm
Contain salivary proteins, food debris, and bacterial cells and their products
Gingivitis
Inflammation of gums around the teeth
Bacterial cells in plaque multiply and build up between teeth and gums
Subgingival plaque - between teeth and gums
Symptoms: swollen, soft gums; bleeding gums
Periodontal disease (periodontitis)
Disease of soft tissue and bone supporting teeth
Bacteria in dental plaque - subgingival plaque
Symptoms: Ulcers and bleeding along gingival margin; Degradation of periodontal ligaments and bone - bond resorption; Loosened or lost teeth
Etiological agents: mixed infections by anaerobic gram negative bacteria – secrete toxins (hyaluronic acid) that directly injure the periodontal tissues
Streptococcus mutans
Gram pos
Major cause of dental caries (with streptococcus sobrinus)
Ferment dietary carbs (sucrose) into lactic acid
Acids in plaque cause demineralization of enamel – lead to cavity (tiny hole or lesion in enamel)
Intoxication
bacterial toxins ingested
(botulism, staph and clostridial food poisoning)
Infection
live bacteria ingested
(salmonellosis, cholera)
longer incubation period than intoxication –> bacterial cells must establish themselves in body after ingestion
Gastroenteritis
inflammation of the stomach and intestines
nausea, vomiting, stomach cramps, diarrhea
Staphylococcal food poisoning
causative agent: staphylococcus aureas (anaerobic, Gram Pos)
intoxication - enterotoxin ingested– consumed in protein-rich foods (dairy, meat, fish)
enterotoxin heat resistant (100C will not kill)
incubation period: 3-5hrs
Symptoms: cramps, pain, vomiting, nausea – gastroenteritis for several hours rapid, complete recovery
Botulism
causative agent: Clostridium botulinum (anaerobic, Gram Pos)
intoxication - exotoxin ingested
neurotoxin - inhibits release of neurotransmitter AcCH; prevents muscle contraction
Causes: flaccid paralysis - limbs lose tone, become flabby respiratory distress - failure of diaphragm and rib muscles
Treatment: antitoxin, breathing assistance (ventilators)
Prevention: heating foods before eating for at least 10 min (toxin destroyed on exposure to temp of 90C for 10 min)
Floppy Baby Syndrome
infant botulism
infants 3-24 mo. - not established normal microbiome
produce low muscle tone
no honey
Botox
Botulism toxin type A
Relieve movement disorders by involuntary sustained muscle contractions (stuttering, crossed eyes)
temporary relive of facial wrinkles and frown lines
relief of excessive sweating and migraines
Inflammatory Gastroenteritis
bacterial gastroenteritis
diarrhea, vomiting, fever, no bloody stools
Invasive Gastroenteritis
bacterial gastroenteritis
bacterial invasion beyond intestinal lumen
fever, diarrhea, vomiting, dysentery (blood and mucus in stool)
Cholera
Inflammatory gastroenteritis
causative agent: Vibrio cholerae (aerobic, Gram Neg)
V. cholerae: -often cosumed with raw oysters and water -fecal contamination of water
cells susceptible to stomach acid – need large infectious dose to colonize intestines
cells secrete exotoxin; exotoxin = choleragaen
loss of fluid and electrolytes = rice water stools (up to 1 L/hr)
untreated: fluid loss thickens blood – slow blood flow to brain – shock and coma
Treatment: oral rehydration therapy
Prevention: clean water and food
Clostridium difficile infection
Inflammatory gastroenteritis
causative agent: clostridium difficile (anaerobic, Gram Pos, spore-forming rod)
transmission: fecal-oral route toxins
enterotoxin - fluid loss and diarrhea
cytotoxin - further mucosal injury (pseudomembranous colitis)
pseudomembranous colitis - inflammation of colon; colon can rupture
drug resistance and virulence (potent toxins)
Factors: antibiotics; exposure in hospital setting (endospores transferred via healthcare workers’ hands)
Treatment: start/stop antibiotics; vancomycin, fluid replacement; fecal transplants
Listeriosis
Inflammatory Gastroenteritis
causative agent: Listeria monocytogenes
transmission: oral-fecal route, water, milk - contaminated food
psychrophilic - thrive in cold environment (4C); fridge temps do not supress
immunocompromised - form of meningitis: infected macrophages cross blood-brain barrier - inflammation of CNS
pregnant - perinatal infection - miscarriage or stillbirth
E. coli
anaerobic, Gram Neg
human colon contains (indigenous) – other E. coli serotypes can be pathogenic
transmission: fecal-oral route
E. coli diarrheas cause various forms of gastroenteritis
- Enterogenci E. coli (ETEC)
- Enteropathic E. coli (EPEC)
- Enterohemorrhagic E. coli (EHEC)
Enterogenic E. coli (ETEC)
inflammatory gastroenteritis
produce 2 toxins: heat labile - similar to cholera; heat stable - traveler’s diarrhea
low fluid loss, vomiting, cramps, nausea, diarrhea 3-7 days
Enteropathic E. coli (EPEC)
inflammatory gastroenteritis
fecal-oral transmission
watery diarrhea
diarrhea in infants (esp. when sanitation lacking)
Enterohemorrhagic E. Coli (EHEC)
Invasive Gastroenteritis
produce Shiga toxin = Shiga toxin producing E. coli (STEC)
Shiga toxin: acid tolerant; block protein synthesis
most dangerous of E. coli serotypes: E. coli 0157:H7
Hemorrhagic colitis - bloody diarrhea
Hemolytic Uremic Syndrome (HUS) - kidney failure; damaged RBC clog glomerulus
Reservoir - cattle – exists in intestine of healthy cattle -cattle feces -undercooked hamburger
Salmonellosis
Invasive Gastroenteritis
causative agent: salmonella enteritidis - found in unpasteurized milk or poultry products
transmission: fecal-oral route; live animlas; foodborne and waterborne -salmonella species infect chickens and turkeys when normal bacterial species of gut are absent
large infectious dose required to initiate illness
Campylobacteriosis
Invasive Gastroenteritis
causative agent: camplylobacter jejuni
transmission: oral-fecal route - contaminated food/water; consumption of contaminated poultry or dairy products
most common cause of bacterial gastroenteritis in the US
Recent outbreaks due to drinking raw milk
Treatment: fluid replacement; erythromycin
Gastric Ulcer Disease
Invasive Gastroenteritis
causative agent: Helicobacter pylori
Transmission: person-to-person; likely involved contaminated food/water
gastric ulcer - penetrate stomach mucasa layer; attached to stomach wall
secretes enzyme urease - digests urea, produce ammonia
ammonia neutralize acid in area of stomach (allow bacteria to survive)
urea->ammonia + CO2
ammonia + H. pylori cytotoxin—cause destruction of mucus-secreting cells – expose underlying tissue to stomach acid
