Identify Cell Morphohlogy of

 Helicobacter pylori Gastritis

• Gram -, Vibrio shaped, rod
• motile
• acid tolerant
• microaerophilic
• non-invasive

Identify Virulence Factors for

Helicobactor pylori Gastritis

• Ability to produce Cytoxin A (VacA) required for ulcer formation
• pathogenicity island produces CagA - induces IL-8->cancer
• LPS cross-reacts w/ host Ag -> Ab-> cancer
• Acid tolerent due to production of copious amts. of usease

Identify the epidemiology of

Helicobactor pylori Gastritis

• 1 of the most prevalent bacterial infections
• Humans = reservoir
• Transmission-> fecal-oral; gastric-oral; oral-oral
• Age+Gender-> carriage increases w/ age; NO gender differences
• Responsible for ALL type B gastric + duodenal ulcers (class I carcinogen, cancer can occur w/o ulcer)

Identify Clinical Manifestations of

Helicobacter pylori - Gastritis

• Abdominal pain
• Hematologic changes (idiopathic thrombocytopenic purpura, iron def., anemia

How do you diagnose

Helicobacter pylori Gastritis?

• Invasive(GOLD STANDARD) -> Endoscopy or esphagogastroduodenscopy
• Non-invasive: Breath test (¹³C) Urea; ELISA or LA; Stool Ag test detected by monoclonal Ab

What is treatment for

Helicobacter pylori Gastritis?

• Combo, sequential, or both
• Bismuth salts
• Metronidazole or Tinidazole
• Tetracycline or amoxicillin
• Anti-secretory therapy may enhance healing
• protonix, clarithromycin, amoxicillin

TREAT ALL PERSONS INFECTED!!

What are MO associatde w/ afebrile

watery diarrhea?

• Vibrio cholerae
• Enterotoxigenic E. Coli
• Aeromonas Sp.

What is cell morphology + metabolism

of Vibrio cholerae?

• Gram -, vibrio shaped, rod
• halophile
• falcultative anaerobe
• non-invasive

How do you classify

Vibrio cholerae?

• O-Antigens
• Type O-1 - classical
• Type O139 - new

What are the virulence factors

of Vibrio cholerae?

• Heat labile, ENTEROtoxin ->
• Stimulates activty of adenylatre cylase (which converts ATP to cyclic AMP -> Diarrhea)

What is epidemiology of

Vibrio cholerae?

• Humans + zooplankton = Resevoir
• Vehicle is FOOD + WATER
• Seasonality -> warmer months
• travelers to endemic or epidemic area are @ high risk!

Describe the pathogenicity of

Vibrio cholerae

• Incubation = 1-5d
• HIGH dose MO
• Diseae of small intestine - grows in lumen of small intestine + elaborates ENTEROtoxins -> fluid + electrolyte loss in feces (1L/h)
• hypovolemic shock
• metabolic acidosis
• hemoconcentration

What are the clinical manifestations of

Vibrio cholerae?

• Abrupt onset
• effortless vomiting
• profuse water diarrhea assuming rice water appearance w/ flecks of floating mucus + possess a sweet fishy odor
• little if any fever
• Fluid loss in feces maybe 1L/h (hypovolemic shock, hemoconc., + metabolic acidosis)

How does lab diagnose

Vibrio cholerae?

• micorscopic exam of stool for presence fo commma-shaped MO + absence of fecal leukocytes
• culture
• serological confirmation

What is the treatment for

Vibrio cholerae?

• Supportive -> rehydration
• Tetracycline is used to shorten the duration + carrier state

What are virulence factors

of Enterotoxigenic E. coli (ETEC)?

• Plasmid encoded ENTEROtoxins
• LT toxin
• heat labile, antigenically/strucaturally similar to + same moa as cholera enterotoxin
• ST toxin
• NON-antigenic -> stimulates guanylate cyclase -cGMP system

What is epidemiology of

Enterotoxigenic E. coli (ETEC)?

• WW incidence
• Cause of traveler's + weanling's disease
• Vehicle - FOOD + WATER
• Transmission -> Fecal-oral

What is the pathogencity of

Enterotoxigenic E. coli (ETEC)?

• HIGH dose MO
• Incubation period -> 1-2d
• similar mechanism as V. cholerae

What are the clincal manifestations

of Enterotoxigenic E. coli (ETEC)?

• Spectrum of clincal mani. is like cholera -NOT as severe
• aburpt onset of diarrhea which last 1-3d

What are some prevention and treatment measures

for Enterotoxigenic E. coli (ETEC)?

• Prevention: pepto-bismol OR Rifaximin
• Treatment: TMZ + Rifaximin

• Staphlococcus aureus
• Bacillus cereus
• Clostridium perfringens, type A

• Characteristics: Coagulase +, Gram + cocci in clusters
• ENTEROtoxin: water-soluble, heat stable, colorless, odorless, + tasteless

What are epidemiology factors of

Staphylococcal aureus?

• Humans = Reservoir + Source
• Mode of intoxication:
• toxin is produced by S. aureus growing in improperly prepared food
• Persons ingests the pre-formed toxin in: custard filled baked goods, potato salad, canned foods, processed meats, meat pies

What is pathogenicity of

Staphlococcal aureus?

• Incubation period = 1-6h post-ingestion
• Enterotoxin is absorbed in gut
• disseminates to the CNS
• acts on vomiting center

What are clincal manifestations of

Staphlococcal aureus?

• symptoms last <12h
• nausea, acute salivation, pronounced vomiting, less pronounced diarrhea may occur, abdominal cramps, illness is SELF-LIMITING -> recovery 1-4d

How do I diagnose

Staphlococcal aureus?

• Short incubation period- NO neurological signs, NO fever
• Epidemiological investigations
• Test entertoxin
• Phage typing of MO

What is morphology + metabolism

of bacillus cereus?

• Gram +, spore forming rod
• produces 2 ENTEROtoxins

What is the epidemiology of

bacillus cereus?

• WW distribution, in soil
• spors are found on
• grains - rice
• potatoes
• vegis

What is pathogenicity and clinical

manifestations of bacillus cereus?

• Emetic form: food poisining caused by heat-stable ENTEROtoxin produced in food
• Diarrheal form:food poisining caused by heat-labile ENTEROtoxin -> production of adenylate cyclase in small intestine
• symptoms 10-12h post ingestion + last <24h
• SELF- LIMITING
• profuse watery diarrhea, abdominal cramps, pain, less pronounced N/V may occur

• Suspect B. cereus food poisoning whenever upper GI illness develops 1-5 hours after eating, or lower-intestinal-tract illness develops 6-24h after eating
• Diagnosis is confirmed by detecting, quatitating, and identifying large #s of this aerobe in the incriminated food + pt's feces

What is cell morphology + metabolism

Clostridium perfringens, type A?

• Gram +, spore forming rod
• anarobic
• produces ENTEROtoxin
• heat labile, acid labile, protein
• toxin produced in gut
• toxin inhibit glucose + Cl^- absorption

What is epidemiology of

Clostridium perfringens, type A?

• WW - common in: soil + the gut of humans + other animals
• Food-borne disease is associated w/ ingestion of: meat, poultry, meat or poultry gravy

What is pathogenicity of

Clostridium perfringens, type A?

• Heat labile ENTEROtoxin produced in gut agter ingestion of food containing large # of MO

What are the clincal manifestations

of Clostridium perfringens, type A?

• Lower GI symptoms appear 10-12h after ingestion of contaminated food
• SELF-LIMITING
• symptoms last <24h
• Symptoms -> profuse water diarrhea, abdominal cramps/pain, less pronounced N/V may occur

How to diagnose

Clostridium perfringens, type A?

• confirmed by detecting, quantitating, and identifying larger #s in the incriminated food + pt's feces

• Giardia lamblia
• Cryptosporidium parvum
• Cyclospora spp. Isospora
• Microsporidia

what is pathogenicity of

Giardia lamblia?

• Trophozoites adhere to mucose of upper small intestine but do NOT invade - they interfere w/ absorption of fat + protein

What are clincal manifestations

of Giardia lamblia?

• Asympotomatic cyst passers
• Acute infection-> 3-4d w/ little or no fever, watery, greasy, foul smelling stools, nausea, abdominal distension, flatulence
• Chronic infection-> ≤2yrs ->abdominal pain + distension, greasy foul-smelling stools (malabsorption), wt. loss

How is

Giardia lamblia, Cryptosporidium parvum, Cyclospora spp. Isospora, + Microsporidia transmitted?

• Fecal-Oral route via FOOD or WATER

• Giardia lamblia + Cryptosporidium -> DIRECT contact OR sexually (oral-anal sex)

What is etiology of

Cryptosporidium parvum + cyclospora spp.?

• Acid-fast
• broad host range
• Obligate intracellular parasite
• undergo sexual reproduction-> producing oocysts

who do the clinical manifestations affect

for Cryptosporidium parvum + cyclospora spp.?

• immunocompetent hosts
• explosive, profuse watery diarrhea w/ vomiting + flatulence + self-limiting
• duration ~2wks
• immunocompromised hosts
• prolonged, severe, watery diarrhea w/ wt. loss >2mo w/ dissemination to all of GI tract, liver, pancreas
• symptomatic resp. infections can occur

What are etiologic agents of Cyclospora spp?

(LIKE crytosproidium)

• Mildly acid-fast
• have intracellular as well as extracellular existance 

What is the epidemiology of

Cyclospora spp.?

(i.e. incidence + prevalance)

• Highest incidence in natives + travelers to Asia + S. America 

• Microscopic examinations (LARGE oocytes)
• U.V floresence
•  Acid Fast +

What is MOST common cause of chronic

diarrhea in HIV/AIDS pt?

Microsprodidians - Enterocytozoan bieneusi, Encephalitzoon spp. are causes of chronic diarrhea in the immnocompromised

They ARE the MOST COMMON cause of chronic diarrhea in HIV/AIDS pts.

How to diagnose

Microsporidians (Enterocytozoan bieneusi, Enchpalitozoon spp.)?

• STEC - Shinga-producing E. Coli
• EHEC 0157:H7 - Enterohemorrhagic E. coli 

What is epidemiology of STEC - Shinga-producing E. Coli + EHEC 0157:H7 - Enterohemorrhagic E. coli ?

• Zoonosis
• Food-borne outbreaks + sporadic cases occur
• Childern + eldery more commonly affected
• peaks in warmer months
• RISK FACTORS: undercooked beef, raw milk, _ unpasteurized A.J., + poor personal hygiene 

T/F

STEC + EHEC are non-invasive

What are the clinical manifestations

of EHEC + STEC?

• Afebrile bloody diarrhea
• Become bloody after 1-3d
• may have cramps, N/V, w/ fever in 1/2 pts.
• 1/3 of pts HAVE fecal leukocytes 

• HUS
• Microangiopathis hemolytic anemia
• thrombocytopenia
• acute renal failure
• CNS involvement
• Mortatlity is HIGH
• Toxemia
• Toxinn is potentiated by TMX-SMX in vitro + in vivo!!!

• invasive
• anarobic
• eucaryotic protzoan
• FORMS CYSTS -- infectious form - LOW dose MO
• consumes human RBC
• Virulence Factors-> produce soluble cytotoxins -lyse PMNs

• Humans are the difinitve host and ONLY reservior
• LOW dose MO
• Transmitted -> fecal/oral(food/water), direct contact, sexually (oral/anal sex)
• RISK GROUPS: travelers to endemic coutnries SE Asia, persons who practice oral/anal sex 

What are clincal manifestations of

Entamoeba histolytica?

• Acte amebic colitis (varies): bloody,loose watery diarrhea, abdominal pain, urgency to defecate, fever + constituational symptoms seen in many
• Extrainsetinal amoebiasis: Mostly necrotic amebic liver abscess (symptoms: upper right quadrent pain, fever, pleuritic pain, liver involvement-liver faulure s/s of hepatitis) 
• NOT self-limiting

Detection of trophozoites in diarrhea or cysts in formed stools

Few fecal RBC + WBC

What is cell morphology of

Bacillus anthracis?

• Gram + box car shaped rod
• spore former
• aerobic
• encapsulated
• facultative intracellular pathogen
• produced exotoxins 

T/F

Bacillus anthracis is a disease of herbivores

TRUE

Enzootic disease:

• Sheep
• Goats
• Cattle
• Horses 

How is Bacillus anthracis

transmitted?

• Bacillus anthracis is excreted from infected animals in: feces, urine, + saliva
• Spores can surive for YEARS in the soil
• Disease requires DIRECT contact w/            -> contaminated soil, infected animals, or animal products bearing spores 

What are clinical manifestations of

Gastrointestinal Bacillus anthracis?

• fever
• N/V
• diarrhea
• GI pain
• bleeding 

What is morphlogy and characteristics of

Clostridium difficle?

Gram +, anaerobic, spore forming rod

Most produce cytotoxin (toxin A or Toxin B or BOTH)

How is Clostridium difficle

transmitted?

person-to-person

Via fomites

What are pre-disposing factors of

Clostridium difficle?

• hospitalization (malnutrition, debilitation, bedridden)
•  Antibiotic therapy for ID
• antacids, PPI
• Elderly + females disproportionately affeted (more)

What are the 4 clincal forms of

Clostridium difficle?

• short-term colonization
• acute diarrhea
• fulminant diarrhea
• recurrent C. difficle infection

Symptoms of AAD Clostridium difficle?

(AAD- Antibiotic associated diarrhea)

Diarrhea

• Sometimes accompanied by lower abdominal cramping w/ NO systemic signs!

What are symptoms of AAC Clostridium difficle?

(AAC - Antibiotic associated colitis)

• Profuse, debilitating diarrhea (foul-smelling, greenish colored) w/ abdominal pain + cramping
• Systemic signs (fever, anorexia, malaise, dehydration)
• NO pseudomembrane 

Symptoms of AAPMC Clostridium difficle?

(AAPMC - Antibiotic associated pseudomembrane colitis)

• symptoms of AAC - MORE severe
• presence of classical pseudomemraneous colitis -> elevated yellowish plaques scattered over the inflamed areas of the muscose when viewed in sigmoid or coloic endoscopic exam 

• CDI should be suspected in any person w/ diarrhea who has recieved antibiotics <2mo +/or whom diarrhea began >72h after hosp.
• gram stain stool
• EIA + latex aggulation
• Cytotoxin assay - most specific
• stool culture - most sensitive
• endoscopy
• differential 

What is treatment for

Clostridium difficle?

Supportive!

• STOP antibiotic treatment is possible
• vanco, metronidazole, or tinidaxole can be used
• probiotics 

What are some preventative measures for

Clostridium difficle?

• Barrier precautions
• isolation of pt
• careful cleaning - sporicidal agents (bleach)
• Hand hygiene (sanitizers do NOT eradicate Clostridium difficle) 

What is seasonality of:

Rotovirus

Norwalk

Norovirus

• Rotovirus -> winter
• Norwalk -> summer
• Norovirus -> summer (but ALL year round)

How are Rotovirus, Norwalk,Norovirus

tranmitted?

• fecal/oral route
• food + water can be vehicles 

What are manifestations of Rotovirus,

Norwalk, + Norovirus?

• diarrhea
• acute vomiting
• fever
• abdominal pain
• Durations:
• Rotovirus 5-7d
• Norwalk 1-2d
• Norovirus 1-2d

What is treatment for

Rotovirus, Norwalk,+ Norovirus?

Supportive!

** NOTE ** child can NOT digest disaccharides --            NO MILK!! 

What are virulence factors of

Shigella spp.?

(Bacillary Dysentery)

• Surface 0 antigens (allows MO to INVADE)
• shiga toxins (irreversable inactivation of EF-1 + Y-interferon

What is etiology of

Shigella spp.?

(Bacillary Dysentery)

• Gram -, NON-lactose fementing, non-motile, enteric bacilli
• facutlative intracellular pathogen
• 4 species based on serology
• S. dysenteriae, group a
• S. flexneri, group b **
• s. boydii, group c
• s. sonnei, group d **

**more common in US