Ch. 11 - Food and Waterborne Bacterial Diseases Flashcards Preview

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Flashcards in Ch. 11 - Food and Waterborne Bacterial Diseases Deck (25):

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




Contain salivary proteins, food debris, and bacterial cells and their products



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)



bacterial toxins ingested

(botulism, staph and clostridial food poisoning)



live bacteria ingested

(salmonellosis, cholera)

longer incubation period than intoxication --> bacterial cells must establish themselves in body after ingestion



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



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



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)



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



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

1. Enterogenci E. coli (ETEC) 

2. Enteropathic E. coli (EPEC) 

3. 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



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



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