GI tract Pathogens Flashcards
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>
Calciviridae-Norovirus (GI)
- Star of David virus particles
- Positive ssRNA-NON enveloped icosahedral
- Found in GI tract
- High risk:
- Food & water enviromentally stable
- Outbreak in large groups (cruise ships)
- Virus alters integrity of SI brush border
- Symptoms: Incubation 1-2 days fever
- Rapid onset of Vomiting & diarrhea 2-3 days
- “winter vomiting disease”
- Diagnosis: Clinical signs 1st
- Treat: Self-limiting BUT use oral rehydration
- Prevention: Sanitation
- Resistant @ 60C, Low PH, & detergents/Chlorination
- Re-infection or infection w/other genotype
Reoviridae-Rotavirus (GI)
- Wheel-like=Rota/Segmented 11 parts
- dsDNA,<em><u> NON-enveloped</u></em> icosahedral nucleocaspid
- Stable over a WIDE range of temp/pH
- High risk: Infants/children
- Winter-spring months
- Causes shortening & blunting of villi w/Mononuclear cell infiltration
- Disease: Gastroenteritis
- Icubation 1-3 days w/symptoms 3-8 days
- Clinical triad=Fever, vomiting, diarrhea (coryza/infection of URT & cough)
- #1 cause of diarrhea in 6-24 months
- Diagnosis: ID in stool
- Treat: Children w/immunodef=Rotavirus-specific immunoglobulin prep (<u>orally)</u>
- Vaccine-
- Rotarix-HumanAttenuated-G1&P8 2 doses
- RotaTeq-Bovine strain-express human VP4-7 (3) doses
Adenovirus (GI)
- ds DNA, NON-eveloped 12 protruding fibers (penton) from corners of caspid
- Found in Late fall-winter
- High risk: Infants
- Disease: Infantile diarrhea Inoculation 7-8 days w/symptoms 8-12 days
- Watery diarrhea & fever
- Diagnosis: Serotype 40/41 in stool
- Other serotype:
- Pharyngoconjunctival fever (pools)
- Acute Rep disease (military)
- Pneumonia
Astrovirus (GI)
- Star-like shape for each virus particle
- (+) ssRNA non-eveloped
- #2 cause of infantile diarrhea (#1 rota)
- High risk: Institutionalized Elderly & immunocomprimised children
- Disease: Gastroenteritis (milder than rota)
- Icubation 3-4 days, symptoms 5+ days
- Winter Peak in temperate climates
- NO vaccine
Shigella (inflammatory)
- “Daycare Diarrhea”
- Endemic=homosexual males & children
- Dyenteriae <strong>(most severe)</strong> & Sonnei <strong>(common in USA)</strong>
- Flexneri (poor) & Boydii (rich)
- Gram (-) rods/Non-motile (salmonella is motile)
- 4 F’s <strong>(finger, food, flies, feces)</strong> Low dose <strong>(survives acidity)</strong>
- Virulence-
- Invasiveness (moving to neighbor cell w/o leaving)
- Enter through M-cells, Enter macrophages which recruit IL-1 &8, Break out of macro to infect Epi cells @ basal surface, Final POLYMERIZE actin filaments (movement)
- Enterotoxins & Shiga-toxin (verotoxin)
Shigella (inflammatory)-Virulence/Pathogenesis
- Enterotoxins-Common in all 4
- ShET1 & 2 (also found in EAEC)=Blocks absorption of electrolytes, glucose, & amino acids in GI lumen (watery diarrhea)
- Shiga Toxins (AB)-S.Dysenteriae
- <em><strong>Cytotoxin(stx)=Shiga</strong></em> kills GI epi & endo cells
- Inhibits protein synthesis inactivating 60S
- Synergy w/LPS=Inflammatory cytokines=Damage to endo of BV (<em><strong>bloody diarrhea)</strong></em>
- Bacillary Dysentery (watery-Bloody) <strong>incubation 36-72hrs</strong>
- Non-specific symptoms-fever & cramping
- 48 hrs after watery diarrhea
- Dysentery (invasion & damage mucosa)
Shigella (inflammatory)-Clinical
- HUS-Assoc w/Dysenteriae (shiga toxin)
- Causes hemolysis, renal failure <u><strong>(uremia)</strong></u>, DIC
- Primary disease of infants & children
- Reiter’s syndrome (reactive arhritis)-Autoimmune
- 2-4 weeks after Flexneri (poor) infection
- Triad-“<strong>Can’t see, Can’t pee, Can’t climb a tree”</strong>
- Men 20-40 years & HLA-B27 <u><strong>(Spondyloarthropathy)</strong></u>
- Shigellosis=Self limiting w/water & electrolyte therapy
- Antidiarrheal compounds inhibit peristalsis NOT recommended
- Diagnosis-Non/lactose fermenter
- Hektoen enteric agar(shigella/salmonella) Faint green color NON-H2S producer (differs from Salmonella)
Salmonella Enterica (Non-Typhodial Inflammatory)
- Gram(-) rod, non-lactose fermenter
- DOES make H2S & Motile (unlike Shigella)
- Found in poultry, eggs, dairy products
- Need HIGH infective dose=Acid sensitive
- High risk: Children & elderly due low acid
- Local invasion-ingestion, colonization in ileum/cecum, mucosal invasion (M-cells), inflammation, ulcers=Bloody diarrhea
- Enterotoxins-Adenylate cyclase(cAMP), fluid production (large/small)=Watery diarrhea
- Systemic invasion-Multiply in endosome/phagosome
- Growth inside macrophage-Goes to lymphatics
Salmonella Enterica (Non-Typhodial Inflammatory)-Clinical
- Gastroenteritis/Salmonellosis:
- Incubation time 6-48hrs
- Inflammatory diarrhea w/orw/o blood
- Lasts 2-7 days self limiting
- Systemic infection (sicklecell pts more susceptible):
- Enter blood through lymph=Septicemia
- Brain <strong>(meningitis)</strong>, bone (osteomyelitis), lungs (pneumonia)
- Treat: neonates, elderly, sickle cell w/antibios
- Diagnose: Hektoen enteric agar (blue-green) w/Hydrogen sulfide production <strong>(black center)</strong>
Campylobacter Jejuni-Inflammatory
- Gram (-) comma or S shaped ROD
- Polar flagella motile
- Microaerophilic (O2 but lower lvls than atmosphere) & grows best @ 42C
- Zoonotic<strong>(cattle, chickens, pets)</strong>
- Transmission: Oral-fecal, water-food w/animal feces
- Poultry, beef, milk-Food
- Pets-Children
- High risk: Young children, immunocompromised, decreased/neutral stomach acids (antiacids/milk)
- Common cause of diarrhea in US & UK <u><strong>(treat w/antibiotics longer than 1 week)</strong></u>
- <u><strong>Diagnose:</strong></u> <em><strong>Campy-BAP or Skirrow</strong></em> <u>(antibiotics-Vancomycin, polymyxin B)</u> selective of other enteric microorganisms, which grows @ 42C
Campylobacter Jejuni-Inflammatory (clinical)
- Virulence & Pathogenesis:
- Toxin production-invasion of epicells & survival in monocytes (salmonella)
- Enterotoxin-Electrolyte movement (watery diarrhea)
- Followed by inflammatory diarrhea-Invasion of epi=<em><strong>ulcers in bowel mucosa</strong></em>
- Watery diarrhea <em><strong>w/foul smelling bloody feces (10+stools/day)</strong></em>
- <em><strong>Mimic acute appendicitis (self-limiting)</strong></em>
- <em><strong><u>Systemic infection:</u> </strong></em>survives in monocytes then carried to other parts of body=Septicemia
- Complications-Autoimmune
- Guillain-Barre: Acute neuromuscular paralysis
- Cross reactivity w/O Ag & glycosphigolipids <u><strong>(peripheral NS)</strong></u>
- Reactive arthritis: inflammation of joints
Yersinia Spp-Inflammatory
- Gram(-) rod NON-lactose fermenters
- Grows @ 25C (cold enrichment) & motile BUT not @ 37C
- Found in GI of animals
- Contaminated food, Pet feces, High dose needed
- High Risk: Any one in cold climate (North)
- Virulence/Pathogenesis: Enterotoxin & invasion of mucosa-Inflammation=Ulceration
- Systemic to mesenteric lymph=Mesenteric adentitis
- SEVERE ab pain in LRQ pseudo-appendicits
- Complication=Reiter’s syndrome (HLA-B27-Same as shigella)
- Diagnose: Stool culture “cold enrichment” 2-4 weeks Yersinia INCREASE and other microbes DIE
Clostridium Difficile-Inflammatory/General
- Gram + rod & anaerobic spore former
- Found in GI tract-High % colonies in Hospital pts
- Transmission:
- Endogenous or via spores
- Fecal-oral <u>(clothing, surfaces)</u>
- High Risk: Hospital
- Long term Antibiotic use (ampicillin, cephalosporins, clindamycin)
- Hospital pts-Long term stay (4weeks)
- Anibiotic Assoc Diarrhea-Mild diarrhea to pseudomembranous colitis (4-10 days after antibio & 2weeks after termination)
- Most common nosocomial diarrhea <u>(hospital)</u>
Clostridium Difficile-Inflammatory/Clinical
- Adhesion (surface layer proteins)
- Toxin A (enterotoxin)=Hypersecretion of fluid, induce inflammation (cytokine production & Hemorrhagic necrosis)
- Toxin B (cytotoxin)=Depolymerization of actin, loss of cytoskeleton & cell death
- Toxin C (Super BUG)=Deletion of A/B reg gene tcdC-Makes 20x more <u>(resistant to antibios)</u>
- Pseudomembranous colitis- Severe ab pain, watery diarrhea w/high # of neutrophils in stool
- Irreg yellow plaques nectotic debris (fibrin&mucus)
- Diagnose: Toxin detection in stool or ELISA for A/B
- Treat: Stop current antibio & use Metronidazole/Vancomycin
- Restore normal GI flora=Saccharomyces boulardii or fecal transplant
Typhoidal Salmonella spp (Gen)
- Typhi & Parathyi
- Gram(-) rod/motile, non-lactose, produces H2S
- Found in gallbladder up to 1 year
- High risk: Poor hygiene & traverlers to endemic areas under 30 yrs old
- Virulence: Multiplies in macrophages w/LPS
- 1st week=Fever w/bradycardia (no GI)
- 2nd week=GI w/rash on trunk/ab <strong>(Rose spots)</strong>
- 3rd week=hepatosplenomegaly w/GI bleeding <strong>(erosion to peyer’s patches)</strong>
- <u><strong>Complications=</strong></u>shock, stupor, seizures, psychosis, myelitis, and pneumonia.
Typhoidal Salmonella spp (clinical)
- W/GI perforation=Fatty degeneration
- Accum of fat in cells w/enlarged spleen, liver, mesenteric glands, kidney, & heart
- DIC-Thrombophlebitis (vein inflammation=Blood clot)
- _Diagnose: _
- Specimen-Blood, bone, urine, stool w/chornic pt
- Culture=Hektoen (non-lactose fermenter)
- Serology=Widal test (test tube agglutination)-Detect Ab against O/H Ag
- Treat: Borad spec fluroquinolones, cipro, ceftriaxone
- Prevention: ID & treat carriers (removal of gallbaldder)
- Vaccine: Capsular=VI & live attenuated=Ty21a
- Both taken <u><strong>oral for traverler's</strong></u> in endemic areas