GI tract Pathogens Flashcards
(40 cards)
Dental Plaque (Strep Viridans)
- Gram (+) cocci & catalase (-)-NO cap
- Alpha hemolytic NO Lancefield Ag
- Optochin resistant
- Found in normal flora:
- Mouth
- Upper resp tract
- Intestinal tract
- High risk:
- Poor mouth hygiene
- Tooth extraction
- Oral surgery/Trauma
-
Enter blood <u>(bacteremia)</u>
- Endocarditis=abnormal heart valve
- Virulence factors: No toxins
- Adherence & formation of biofilm
- Makes dextrans/levans (large polysacs) from sucrose-enhances attachment
- Production of acid from sugars
- Lower PH=Mineralization of enamel
Dental Plaque (Strep Viridans)-Clinical
- Disease:
- Dental cavities
- Gingivitis
- Periodontitis
- Strep is initiating organism>once plaque becomes polymicrobal
- Subacute endocarditis:
- After beacteremia
- Settles on heart valves (precondition more susceptable)
- vegetation forms
- Made of fibrin bacteria, inflamm cells
- Osler node
- Janeway lesions
- Petechiae in EYE
- Splinter hemorrhages <u>(nail bed)</u>
- Treat: Penicillin (increasing resistance)
Mumps (Paramyxoviridae)
- Enveloped (-) ssRNA
- H & N spikes
- F peplomer=Fusion
- Helical necleocapsid w/Pleomorphic envelope (RNA dep/RNA poly)
-
Affects salivary glands:
- Sublingual
- Parotid (largest)
- Submandibular
- High risk: Unvaccinated children<u> (winter/spring)</u>
- Infection starts in resp tract>enters blood…
-
1st systemic site of infection=<strong><em>Parotid gland</em></strong>
- Multiplies in ductal epi cells>Swelling w/pain
- secondary sites=Testes, ovaries, CNS, & pancreas (juvenile diabetes)
Mumps (Paramyxoviridae)-Clinical
- Contagious 7 days prior to onset of symptoms
- Transplacental infection
- Prodormal=Fever, malase, anorexia
-
Parotitis=Swelling of all or ONE of salivary glands (unilateral or bi)
- gone w/in 1 week
-
Orchitis=Inflammation of testes (post-pubertal)
- painful & can present bilateral=<u><strong>Sterility</strong></u>
- Due to fiborous <strong><u>Tunica Albuginea</u></strong>
-
Oophoritis=Inflammation of ovaries
- Mimic appendicites w/Rt ovary
- Meningitis or Ecephalitis (CNS)
- Pancreatitis (Juvenile diabetes)
- Treat: No antiviral drugs
- Vaccine=Live attenuated MMR/MMRV <u><strong>w/2 doses</strong></u>
Peptic Ulcers (H. Pylori)
- Gram (-) curved rod/spiral HIGHLY motile
- Urease (+) catalase & oxidase (+)
- Life long colonization if NOT treated
- Spread through oral-fecal route
- Virulence factors:
- Mucinase-Enzyme hydrolyzes mucopolysac substances <u>(mucins)</u>
-
Phospholipases-Hydrolyze phospholipids
- <strong>Urease</strong>-Breaks urea to Co2/NH3=<em>Neutralize gastric acid</em>
- <u>Vacuolating cytotoxin </u>A-Damage epi cells w/vacuoles
-
Cytotoxin assoc gene-Destroy epi cell cytoskelton
- <strong>Type 4 secretion-<u>"</u></strong><u>Inject" </u>CagA to epicells
- Cag+ = Gastroadenocarcinoma
- LPS-Inflammatory response <u>(PMN/Mononuclear cells)</u>
-
Further destruction done internally by digestive enzymes/acid
- Ulcer formed
H. Pylori-Clinical
- Chornic conditions:
- Lymphoproliferative disease-Malt B-cell lymphoma
- Atrophic gastritis>Gastric adenocarcinoma
- Assoc w/Cag+ strains
-
Presents:
- Upper ab pain
- Feeling full
- Nausea
- Bleeding into Gi tract
- Diagnose:
- Urease breath test-Ingest radioactive urea
- Detects radioactive CO2 in breath
- _Treat: _
- PPI <u>(omeprazole)</u>
- Macrolides (<u>clarithromycin)</u>
- Beta-lactam (<u>amoxicillin)</u>
- Metronidazole
Enteric Infections (Diarrhea)
- Proximal Small intestine (non-Inflammatory):
- Watery diarrhea &+/- vomit w/Superficial invasion
- Pathogen alter water/electrolyte movement
- Larger vol of feces w/<em><u>NO leukocytes</u></em>
- Ex. E. coli, Viral, Protozoas
- Distal SI or Colon (inflammatory):
- Dysentery (blood),diarrhea
- Cytotoxins, superficial ulceration w/gut cell destruction
- Small vol of feces w/Leukocytes
- Ex. Shigella, entamoeba, C. difficle
- Distal SI or Colon:
- <em><u>Systemic penetration</u></em> (Blood>lymph) with or w/o dysentery
- Small vol of feces w/Leukocytes
- Ex. Salmonella, Yersinia
-
Diagnosis: Important to know frequency/volume of feces
- 3+ in a 24 hr period=Diarrhea
Staph Aureus (GI)
- Gram (+) cocci, Catalase/Coagulase (+)
- Growth @ 7.5 NaCl
- Found in nose, skin, LOW lvls in colon/vagina
- Consumption of contaminated foods-
- Food handler<u> <em>(picks nose)</em></u>
- Grows better on Carb & protein rich foods
- Ex. Custards, potato-egg salad, processed meat
- High risk in warmer months w/foods not refrigerated
- Diagnose: Detect on food or in vomit
- Self-limiting (24-40 hrs) w/rehydration
- Virulence factors-Non-infectious w/8 serotypes
- Heat stable @ 100c for 30 min
- Resitant to gastric acid<strong><u> (ingesting toxin)</u></strong>
- Emetic activity<strong>(<u>cereulide)</u></strong>=Stims vagus nerve in stomach lining <u>(vomit)</u>
- SuperAg activity=Stims T-cell proliferation=<em><u>Release of TNFa/IFNy into BS</u></em>
- Sudden onset less than an HOUR
Bacillus Cereus (GI)
- Gram (+) spore forming rod-Aerobic
-
Consumption of contaminated cooked food w/soil
- Rice, grains, root vegetables
- High risk: Heat resistant endospores germinate/multiply on food inadequately refrigerated
- Clinical: 2 types of food poisoning
- Emetic (strict intox)-ingestion of pre-formed heat stable toxin
- Carb rich food (<u>boiled rice/pasta</u>) held @ ambient temp too long
- Enterotoxin superAg=<u><strong>Cereulide</strong></u>-stims vagus nerve (vomit)
- <u>Rapid onset </u>1-6 hrs symptoms 24 hrs
- PROFUSE vomiting w/<u><strong>NO fever or diarrhea</strong></u>
- Diarrheal (infection/intox)-ingestion of organism & production of heat-labile toxin
- Stimulates cAMP-GI fluid secretion=Diarrhea
- Protein rich foods Or vegatable dishes, pudding, milk
- <em><u>Slower onset</u></em> 6-16 hrs
- <u><em>Watery diarrhea</em></u>, vomiting, cramps
Bacillus Cereus-Other infections
- GI-
- Diagnose: Toxin in stool or food
- Treat: self-limiting w/hydration
- Other infections:
- Eye infection:
- Severe keratitis (inflammation of cornea w/scar)
- endophthalmitis (inflammatory cond of inner eye)
- panophthalmitis (inflammation of enire eye)
- High risk: eye trauma, non-sterile contact lens sol OR IV drug users
- Rapid progression-12-48 hrs of injury
- Loss of sight in 2 days
- Treat w/multiple antibios or surgery to remove affected eye
Clostridium Botulinum (GI)-General
- Gram (+) spore formiing rods-Strict anarerobe
- Tennis racket appearance
- Strict Anaerobe (NO o2)
- Found in Colon flora or in neutral/alkaline soil
- Transmission:
- Ingestion of preformed toxin
- Trauma & wound infection
- _High risk: _
- Canned foods <em><u>(Homemade)</u></em>
- Fermented fish <em><u>(Alaska)</u></em>
- Improperly sterilized commercial canned alkaline veges <u>(green beans, peppers,mushrooms)</u>
- IV-black tar heroin
- Infants less than 1 year old w/honey <u>(inhalation common)</u>
- Prison wine outbreak
Clostridium Botulinum (GI)-Disease
- Produces invasive enzymes: Lipases, gelatinase (lead wound infection)
- Neurotoxin-8 different serotypes (A,B,E common)
- Carried by phage (Bacterial virus):
- Highly potent-letal dose 1-2ug/kg
- Type A/B associated w<u>/canned foods</u>
- Type E associated w/<u>Fish</u>
- Absorbed in gut>blood stream
-
Binds @ pre-synaptic neuron>cleaves protein involved w/release of Ach (exotoxin)
- SNARE proteins <u><em>(synaptobrevin/Syntaxin)</em></u>
- Causes bilateral flaccid paralysis
- Food borne (Intoxication)-
- Heat Libile dead after 10 min
- Incubation 18-72 hrs after ingest
- Recovery months to years
- Presents w/ab pain <em><u>(diarrhea or constipation)</u></em> untreated bilateral DESCENDING paralysis
- Wound (infection)-Incubation 1-4 days symptoms similar to food borne <strong><u>(Black-tar heroine)</u></strong>
- Dry-Furrowed tongue
Clostridium Botulinum (GI)-Clinical
- Infant botulism: “floppy baby”
- Most common in US
- Incubation=3-30 days
- Ingestion of spore and germinates in GI due to low flora<u><em>(multiply in gut-make toxin)</em></u> absorbed in blood
- Associated w/Honey & dust inhalation
- <u><strong>Symptoms:</strong></u> Lethargy, constipation, poor feeding <u><em>(sucking reflex)</em></u>, Facial paralysis
- Diagnosis: Toxin in pt’s blood/Infant’s stool
-
Treat: Antiobios=Wound (not infants could worsen)
- Passive immunization <strong>ANTI-toxin</strong> (A,B,E)
- Anti-bios NOT used in Infants due to worsening the condition <u>(killing flora)</u>
- Prevention: Heating canned foods
Clostridium Perfringens (GI)-General
- Enterotoxin NOT Gangrene
- Gram (+) spore forming rod-Type A (anaerobic)
- Found in normal GI (large intestine)
- Transmission: Ingestion of large # of bacteria grown on pre-cooked meats (not refrigerated)
- Gravy, Meats, poultry
- Food poisoning (toxin/infection):
- HIGH dose 108 to 109 of bacteria needed=small intestine
- <strong><em>Enterotoxin-</em></strong>Heat liable <em><u>(B.cereus) </u></em>Increase cAMP=<u><em><strong>Watery diarrhea</strong></em></u>
- <em>Increases intracellular Ca+2 </em>alters membrane perm=Loss of fluids/macomols
- Incubation: 8-16 hours will last 24 hours in immunocomprimised 1-2 weeks
Enterobacteriaceae (GI)-Non/inflammatory
- All Gram (-) non-spore bacilli
- Faculative anaerobes=Ferment glucose
- Oxidase (-) Reduce Nitrates>Nitrites (UTI)
- Class based on tests (carb fermentation & AA decarboxylase) & antigenic prop of <em><strong>O-Ag</strong><u> (LPS)</u></em>
- MacConkey & Eosin methylene blue agar for Lactose fermentation:
- Low pH = Pink in MAC
- Gram (-) ONLY
-
TSI: Contains 3 sugars (glucose, sucrose, lactose)
- Lactose & Sucrose=<u>Large amount of acid</u>
- Glucose=<u>Less amount of acid</u>
- Contains Ferrous sulfate (black)
- OKH Ag serotypping:
-
O terminal sugar used to ID different strains
- A core endotoxin common in all
- K (capsular) virulence Ag
- H flagellar found on motile strains
E. Coli (GI)-General
- 5 groups classified by virulence factor
- Non-inflammatory <strong>(Small intestine-lumen)</strong>
- <u>Enterotoxigenic (ETEC)</u>: travelers & infants in developing countries=<em><u>Watery diarrhea & nausea</u></em>
- <u>Enteropathogenic (EPEC)</u> & <u>Enteroaggregative (EAEC)</u>: Childhood diarrhea
- Gram (-) Rod=Lactose fermenter
- Most common bacilli in GI tract
- _Virulence factor: _
- Exotoxins-
- <u>Heat stable toxin </u><em><u><u>(ST</u>)-</u></em><strong>Excess cGMP</strong>=Blocks ion transport INTO cells>water moves into LUMEN
- <u>Heat liable toxin </u><em><u>(LT)-s</u>imilar to cholera toxin</em>
- <em>binds to GM1 ganglioside receptors on Gut>I<strong>ncrease cAMP </strong>outflow of Cl-<strong>=Inihibition of Na+ absorption</strong></em>
- Ion imbalance=Water loss=<strong>Diarrhea</strong>
- Shiga like toxin <em><u>(STx)</u></em>
- Adhesion-
- <u>Colonizing factor adhesions </u><em><u><u>(CFA)</u>-</u></em>Fimbriae recognize host glycoprotein receptor
- bundle forming pili <em><u>(Bfp)</u></em>
- adherance fimbriae <em><u>(AAF)</u></em>
EAEC-Enteroaggregative (GI)
- Aggregative adherence fimbriae (AAF):
- Bacterial clumping into small aggregates
- Stacked bricks-Bacteria parallel rows<u> (autoagglutination)</u>
- <u>Stimulates mucus production-</u>Mucus + Bacterial aggregates =<em><strong> Biofilm</strong></em>
- Biofilm>ST toxin <u>(heat stable</u><em>)=Excess cGMP </em>interferes w/ ion absorption
- <strong><em>Cytotoxin/hemolysin</em></strong>=Shortening of microvilli><strong><em>Decreased</em></strong> fluid absorption
- Disease: Presistant watery diarrhea w/vomiting & dehydration NO fever
- Lasts 14 + days
- Infantile chronic diarrhea=<strong><em>Growth retardation</em></strong>
- Travelers’ diarrhea in HIV pts
EPEC-Enteropathogenic (GI)
- Virulence factors:
- Bundle forming pili (Bfp)-patchy adherence>Tir insertion & intimin binding
- Attaching>effacing=<em><strong>Destruction of microvilli</strong></em>
- Forms cup-like pedestal structure in cytoplasm made of <u><em>Cytokeretin 18 =</em></u><em><strong>dense mat of actin fiber under EPEC (attaches to apical membrane)</strong></em>
- TYpe 3 injection system (Tir) allows for attachment and eventual Destruction of microvilli=<strong><em>Malabsorption=Diarrhea</em></strong>
- Disease: “Infantile diarrhea”
- Epidemics in newborn nurseries
- watery diarrhea, fever, nausea, vomitting
E.Coli-Clinical
- _Diagnosis (lactose fermenter): _
- Culture different media-
- MacConkey (pink)
- EMB (green)
- Classifying strains=API biotests
- 4 characteristics of E.coli-
- Produces indole from tryptophan
- Uses citrate as sole source of carbon
- Decarboxylate lysine
- Motile
- Treat: Rehydration, self limiting
Enteroinvasive E.Coli (EIEC)-Inflammatory
- Large Intestine
- Virulence: Plasmid mediated invasion (plnv)
- Invade colonic epi cells-Escape phagosome to multiply in cytoplasm & move to adj cells <strong>(shigella)</strong>
- NO enterotoxin
- Disease: IP 12-72 hrs
- Infective does=10
- Fever, cramping, watery diarrhea may progress to dysentery
- Primary in under-developed countries <strong>(rare in US)</strong>
Enterohemorrhagic-E.coli (EHEC)-Inflammatory
- “Child w/HUS ate @ hamburger joint”
- No human carrier ONLY cattle
- High risk: Children under 5
- Undercooked beef <strong>(hamburger)</strong>
- Veges contaminated by animal feces (O104:H4)
- Virulence factors:
- Budle forming pili (Bfp-EPEC)-Attaching-effacing-Destruction of microvilli
- Shiga-like toxin <u><strong>(verotoxin)</strong></u>-Inhibit protein synthesis kills epi/endo cells Large intestine (STEC)
- Small infective dose=100
(EHEC)-Inflammatory/Clinical
- Mild diarrhea->Hemorrhagic colitis
- Little or no fever w/severe ab cramps
- Watery diarrhea->Bloody diarrhea
- HUS: toxin can reach blood=Kidney failure w/hemolytic anemia, thrombocytopenia w/minor Neuro symptoms
- Treat: Use of antibiotics could contribute to HUS-Due to dying/dead bacteria shiga toxin & LPS released
- Diagnose: Sorbitol MacConkey agar (pink)
- O157:H7 non-sorbitol fermenter=Grey colonies
- Detection of Shiga Toxin=Destruction of cells
Vibrio Cholera (GI)-General
- “Comma shaped” bacilli
- Gram (-)/Oxidase (+)
- Motile w/single polar flagella
- Need HIGH dose for infection <strong><u>(acid sensitive)</u></strong>
- High risk:
- Contaminated Water
- Undercooked crabs, shrimps, oysters <strong><u>(V. para & vulnificus)</u></strong>
- Flooded areas
- _Disease: “cholera” _
- HUGE amount of water loss w/Rice water diarrhea <u>(contains mucus)</u>
- Hypokalemia due to massive dehydration
- Loss of skin tugor w/weak pulse
- Virulence factors: O1 & O139 make-
- Cholera toxin- Similar to ETEC (LT)>binds to GM1 gangloside
- Increase in cAMP=hyersecretion Cl-out NO Na+ in
- Toxin-co-reg pilus (TCP)-Adhesion
Vibro Cholera (GI)-Clinical
- Additional virulence factors: Absence of CT
- Zonula Occludens toxin (zot)-protease degrades tight junctions=Mild diarrhea
- Accessory cholera enterotoxin (ace)-Activates Ca+2 dependent Cl- channel
- Symptoms:
- Incubation 2-3 days
- Abrupt onset<u> (profuse watery diarrhea)</u>
- Colorless feces=”Rice water stools”
- Dark field testing of Stool
- Culture-Selective media-TCBS
- Thiosulfate citrate bile salts sucrose Agar
- Cholera turns YELLOW due acidity in <strong><em>Strong alkaline sol</em></strong>.
- Serotyping-agglutination test using polyvalent sera Anti-O1 & O139
- Treat-IV infusion <u>(NaCl, KCl, NaHCO3)</u> & Oral rehydration glcose + salt
- Prevention-Chlorination of H2O & <em>O1 oral Vaccination w/boosters</em>