Lecture 48 to 53 GIT Infections Flashcards
Colonisation of GIT
- Immediately after birth: E. Coli & Strep
- 4 d after birth: facultative anaerobes appear and create reducing environment; Bifidobacterium, clostridium, bacteroides
- Breast fed: only Bifidobacterium levels remain high, all others decline
- Formula fed: Lactobacilli present
- Beginning of weaning: E. coli, strep, and clostridium return to high levels
- Completion of weaning: adult flora
Normal commensal flora of Mouth
- Strep, Neisseria, Actinomyces, Lactobacillus, Veillonella
- Eruption of 1st teeth: Porphyromonas, Prevetella, Fusobacterium.
- Growth of teeth: Strep. mutans, strep. salivarius, strep. sanguis
Stomach: normal commensal flora
- nl: sterile or up to 1000 bacteria (strep, staph, lactobacilli, peptostrep)
- pathological: H. pylori, 10e5 to 10e7 in achlorhydria or malabsoprtion syndrome
Duodenum: normal commensal flora
- sparse but increases w distance away from stomach (0 to 10e5)
- fluctuating: Strep, Staph, Lactobacilli, some yeasts
-
Note: complete absence of coliforms & Bacteroides
- coliform: rod-shaped Gram-negative non-spore formingbacteria which can ferment lactose Ex. E. coli
Jejunum-Ileum: nl flora
- high counts of Enterobacteriaceae
- some Strep, Staph, Lactobacillus, Bacteroides, Bifidobacterium, Clostridium
- bacteria numbers increase at ileocecal junction and highest, richest at large intestine
- bacteroides
- other anaerobes: bifidobacterium, eubacterium, peptobacterium, clostridium, enterobacteriacea
- also facultative anaerobes: E. coli
Upper GI Infections
Dental plaque=Biofilm infection
- Strep. mutans & 39 other bacterial spp
- bacteria secrete dextran for adherence
- fusobacteria & actinomyces
- Lactibacilli produce lactic acid that destroy enamel of teeth
Periodontal disease & Tartar
- Porphyromonas causing gingivitis
Oral abscess
- infection in tooth
Major causes of Gastroenteritis
50% Norovirus
50% bacterial
- Campylobacter
- Salmonella
- Shigella
- STEC O157:H7 E. coli strain
- STEC non-O157:H7
Food-poisoning: toxemia
- consumption of foods containing toxins so **short incubation period **(except C. bot -> long incubation; below)
- only Clostridium botilinum, Staph. aureus, B. cereus (1 form),
- some fungi: Amanita, Clitocybe & Psilocybes, Aflatoxin
- and marine toxin: Ciguatera, Scromboid, shellfish
- contrast w food-associated infections caused by wide variety of pathogens
- Sx: usually rapid (minutes to hours)
- C. botulinum: 6h to 8 d
- no fever, no fecal leukocytes
- toxins affect:
- C. bot -> only CNS
- S. aureus & B. cereus: -> CNS and intestines

Staph. aureus: food-poisoning
- Catalase +ve, Coagulase +ve, Beta-hemolytic
- produces 8 exotoxins (A, B, C1, C2, C3, D, E)
- water-soluble, HEAT STABLE (ST) (chromosomal)
- frequently implicated are A & D singly or combination
- Mechanisms: unknown
- neurogenic: vomitting via CN X
- diarrhea: enteric but no cAMP activation
- Contaminant: Ham, meat & poultry products, cream-filled pastries, whipped butter, cheese
- Onset: 1 to 6 h
- Duration: 6 to 24 h
Sx: self-limiting illness
- some emesis but not all vomit
- recovery in 24 to 48 h
- other common sx: headaches, nausea, ab cramps, prostration, muscle aches
- Foods: cooked meats (fish & poultry), cream-filled foods, dairy products, fuit, veggies, salads
- Highest: summer and holiday seasons
Dx & isolation: variety of media available (MSA)
- Baird Parker (selective, diagnostic, recovery)
- Confirm w coagulase test
Bacillus cereus (food poisoning)

- Gram +ve rods, chains, aerobic or facultative
- spore former
- Encapsulated w protein (Poly-D-Glutamic Acid)
- emetic toxin or enterotoxin
- easily spread to food: cross-contamination
- 2 types of gastro
- Emetic resembles Staph. aureus
- Incubation: short 2 to 3 h
- Duration: 6 to 24 h
- Toxins: ST neurotoxin (peptide), EF (Edema Factor), LF (Lethal Factor)
- Foods:
- boiled rice, ex. Chinese restaurant syndrome
- pulses=lentils, split peas
Sx:
- Nausea, vomiting; sometimes diarrhoea & cramps
- Most common effect of Bacillus infections are cutaneous black eschar
Dx & isolate: implicated foods contains > 10e5
- non-selective medium: blood agar
- EF causes incr cAMP
Rx:
- Fluoroquinolones
- Cyclosporin
C. bot (food poisoning)

C. bot
- variable size Gram +ve
- Obligate anaerobic
- ferment range of carbs -> gas
- spore former, produce exotoxins, susceptible to penicillin
- habitat: lower GI of human & animals
2 types of botulism:
- food poisoning: rare
- Sausages & fermented foods
- canned foods
- infant bot: most common bot in US
Neurotoxin: Cleves SNARE protein and decr ACh
- 8 types: A, B, C1, C2, D, E, F, G
- Humans: A, B, E, rarely F
- US frequent isolate type A, then B & E
- Europe frequent isolate type B (A rare)
Food poisoning botulism:
- Foods:
Type A&B: vegetables, fruits, meat, fish & poultry
Type E: fish
- Onset: 12 to 36 h
- Duration: months
Etiopath: INGESTION OF PRE-FORMED TOXINS
- almost all GI disturbances from toxin E; 1/3 Pt (toxin A or B)
Sx: mild illness or serioues disease (fatal within 24 h)
- nausea, vomting, and ab pain, diarrhea often present
- constipation
- diplopia
- dysphagia
- no fever in absence of complicating infections
- Descending flaccid paralysis
- Ptosis
Dx:
- presumptive dx: presence of rapidly descending paralysis
- confirmative dx: demonstrate botox in serum/faeces or food (mouse toxin-neutralization test)
Infant Botulism

Infant botulism: NOT FOOD POISONING (2wk to 6 mo)
- Toxins: Types A & B implicated
Etiopath:
- INGESTION OF SPORE
- From environment -> entry into baby -> spore germination (GI tract) -> vegetative cells -> replicate & release toxin
- Spores commonly found in honey
Sx:
- illness & constipation (overlooked)
- Floppy baby syndrome
- lethargy, sleep more than normal
- suck & gag reflex diminished
- dysphagia becomes evident as drooling
- later: head control lost -> infant becomes flaccid -> resp. arrest
Dx: botox in feces
Rx:
- botulism antitoxin heptavalent (A, B, C, D, E, F, G) (Equine)
- baby botulism Ig (BIG-IV) for A & B toxins
Types of diarrhea
non-inflammatory= watery; from non-invasive diarrhea or viruses inflammatory = blood or pus -\> from invasive bacteria or those producing cytotoxins
- Invasive diarrhea: do not give anti-diarrheal; cause inflammatory diarrhea; salmonella; break mucosal walls
chronic>4 wk due to:
- medication
- parasites
- malabsorption
Mushroom toxin
Short acting: wild mushrooms
- toxins: psilocybine, muscarine, museino, coprius artermetaris, ibotenic acid
- incubation < 2h: vomitting, diarrhea
Long acting: amantia mushroom
- toxin: amantia
- incubation 4 to 8 h: cramps, diarrhea
Mycotoxigenic fungi
- Mycotoxins: aspergillus, fusarium, penicillium
- Aflatoxins: Aspergillus flavus & A. parasiticus
- peanuts, corn & cotton (oil seeds) contamination
- SOA: liver cirrhosis & carcinoma, acute necrosis
Marine toxins
- Ciguetera poisoning; heat stable toxin so cooking does not destroy
- dinoflagellates produce ciguetera toxin; big fish eat dinoflagellates (Barracuda, Amberjacks, Grouper)
- Sx: acute GI sx 3 to 6 h
- watery diarrhea
- nausea
- abdominal cramp (12 h)
- Complication: neuro sx (extremity paresthesia, severe itching, hot/cold temp reversal)
Scromboid poisoning: non-allergic histamine
- Bacteria: Stentorophomonas maltophilia, M. morganii
- Toxin: Histamine (scrombotoxin); heat & cold stable toxin so cooking and freezing does not destroy
- Scrombridae fish: tuna, mahi mahi, marlin & bluefin
- Sx: acute GI sx -> minutes to 3 h afger ingestion
- Burning sensation in mouth, a metallic taste
- Watery diarrhea, nausea, lasting 3 to 6h
- dizziness, rash, facial flushing, generalised itching, paresthesias
Neurologic shellfish poisoning
- dinoflagellate algae: Karenia brevis
- Toxins: brevetoxins
- Incubation: < 1 to 3 h
- Duration: 2 to 3 d
- Paresthesia, mouth numbness, tingling sensation of mouth & extremities, GI upset
Paralytic shellfish poisoning
- dinoflagellate algae: Alexandrium spp., Gymnodinium catenatum, Pyrodinium bahamense, Gonyaulax spp.
- Toxin: Saxitoxin
- Incubation: < 2 h; duration: 3 days
- Sx: GI sx less common
- tingling & numbness of mouth spread to extremities
- ataxia (muscular in-coordination)
- severe cases: muscular paralysis, respiratory paralysis
Non-Inflammatory diarrhea
Bacterial
- E. coli (ETEC, EHEC)
- V. cholera
- C. perfringens
- B. cereus
Viral
- Rotavirus
- Norovirus
- Adenovirus
- other
EnteroToxigenic E. coli (ETEC)

- Disease: Traveler’s diarrhea
- Contaminant: contaminated food & water
- Onset: 10 h to 3 d
- Duration: 3 to 5 d
Common E. coli features
- encapsulated
- Catalase +
- Green colonies on EMB agar
- Lactose fermenter -> pink colonies on Mac agar
- K antigen can lead to neonatal meningitis
- Fimbri allow bacteria to cause UTI infection (#1 cause; see UGI FC)
- Can lead to sepsis
Etiopath:
- bacterial must colonize small intestine:
- CFA pii (colonizing factor)
- heat LABILE LT toxin: binds GM1 at brush border of epithelial cells -> facilitate entry of subunit A -> cAMP -> Cl transporter -> watery diarrhea
- heat STABLE ST toxin: activates cGMP -> watery diarrhea
Sx: rapid onset of watery diarrhea w/o fever, sometimes cramps, nausea & vomiting
Rx: E. coli resistant to trimethroprim
Enteropathogenic (EPEC) strain of E. coli
- Disease: childhood diarrhea
- developing countries (50% mortality)
- Etiopath: not fully understood
- Plasmid-borne (EAF) Bundle-forming Pilus (BFP) used to adhere to microvilli -> cell necrosis
- So, mechanism similary to Shigella
- Rx: ORT and trimethoprim/fluoroquinolones
Vibrio cholerae

Toxin: Vibrio toxin Vibrio cholerae
- single curved Gram -ve rods
- S-shaped when joined together
- “Shooting-star” motililty
- spore forming
- Oxidase +
- Acid-labile
- Antigens: O & S
- O1: El Tor strain
- O139: more recent
Epi: Asia, Africa, Americas
- Contaminant: Fecal-oral -> Food or water contaminated by faeces of infected individuals
- Onset: 2 to 3 d
- Duration: 1 wk
Etiopath: similar to ETEC in:
- Toxin: Vibrio toxin
- fimbriae attaching to GM1
- activates Gs -> AC -> cAMP -> watery diarrhea
- hypokalemia & metabolic acidosis (loss of bicarb)
Sx: rice watery diarrhea (20 to 30 L/d), vomiting, dehydration; fatal if untreated
Dx:
- clinical presentation
- screening of stool sample
- Grows on alkaline media
- Thiosulphate Citrate Bile Salts (TCBS) agar
- Sucrose differentiation media: only Vibrio cholerae sp can ferment sucrose (other Vibro spp cannot)
Rx: ORT & tetracycline
Prevention: sanitation and hygiene
C. perfringens

- Obligate anaerobe
- Diseases: 2 different disease
- necrotizing enteritis (rare, Papua New Guinea)
- type A food-borne infection; major cause of food-borne infection in US
Contaminant:
- Cooked meat & meat gravy
- Spores in soil; common in military, motorcycle accidents, and trauma
- Onset: 8 to 24 h
- Duration: < 24 h, slow
Etiopath:
- Clostridium Perfringens Enterotoxin (CPE) in the intestinal villi cause cramps and diarrhea
- alpha-toxin affects cell membrane (lecintinase) and hemolysis
Sx:
- slow onset watery diarrhea, severe ab pain, no fever, nausea & vomitting rare
- gas gangrene aka clostridial myonecrosis/osteomyelitis
- gas in tissue on CT scan
- crepitance
Dx:
- Double zone of hemolysis when plated
- case hx & sx
Rx: penicillin












