Gastro Micro Flashcards
Slender, curved Gram- rods
Motile with polar flagella
Microaerophilic (can only be grown under very low oxygen tension)
H pylori
virulence in H pylori
holes in cells?
Type III SS?
Re-arranges cytoskeleton?
VacA – vacuolating cytotoxin – holes in cells cell death
PAI (pathogenicity associated island – different G+C content) encoding Type III secretion system
Cag – rearranges cytoskeleton
Most common bacterial GI infection in developed countries
low infection dose
animal reservoir
spiral, G- rods, microaerophilic
Camplybacter jejuni
Can lead to Guillian-Barre syndrome
Camplybacter
Diarrhea w/ C jejuni?
watery that progresses to blood/pus and lasts about 3-7 days
Curved, Gram- rods
Motile, polar flagellum
Oxidase positive
Commonly found in saltwater, disease in warm months
Vibrio
Lives in organisms in the water
O1 and O139 outbreaks (200+ serotypes)
rice-water stools
high infectious dose to survive stomach pH
Vibrio cholera
Free-living in sea water
Seafood-associated food poisoning
Most common foodborne illness in Japan
Gulf and Pacific Coasts of US, warm months
Watery diarrhea often with abdominal cramps nausea, vomiting, low-grade fever, 24 hrs after exposure
Self-limiting, rare treatment needed
vibrio parhaemolyticus
Free-living in sea water
Consumption of raw oysters or wound infection (cellulitis)
Vomiting, diarrhea, abdominal cramps
vibrio vulnifus
Gram negative coccobacillus Antiphagocytic capsule Major component of the human GI tract Opportunistic pathogen Most common anaerobic infection
Bacteroides fragilis
Gram negative coccobacillus Antiphagocytic capsule GI tract, nasopharyngeal and vaginal flora Opportunistic pathogen, abscesses Pulmonary Periodontal
Prevotella melaninogenica
Large, “boxcar” Gram+ rods
Found in soil and intestines of humans and animals
Most human infections from spores in soil or food
Gas gangrene and cellulitis
Food poisoning
Clostridium perfringens
Spore contamination of wounds
Tetanospasmin (tetanus toxin) is an AB neurotoxin
Enters at neuromuscular junction and is transported by motor neurons to ganglia
Incubation time depends on distance of wound from CNS
Cuts a V-snare
C tetani
Consumption of contaminated food
Infants: ingesting spores from carpets
Infection of wounds with spores
AB toxins
C botulinum
Most common diarrheal disease associated with antibiotic use (creates niche)
Endogenous or hospital spores are source
Toxins A and B work synergistically to produce disease (2 separate toxins)
A: enterotoxin»_space; diarrhea
B: cytotoxin»_space; inflammation
C diff
E coli: Lactose? Glucose? Oxidase? Nitrates? Motile?
Lactose? - ferment Glucose? - ferment Oxidase? -neg Nitrates? to nitrites Motile? yep
Shiga toxin, HUS
O157:H7
cow reservoir - bad meat industry practices!!!
EHEC
Leading bacterial cause of diarrhea worldwide
Non-inflammatory, high volume ~ cholera
LT~ binds to GM1 gangliosides on cell surface; cholera toxin (activates adenylyl cyclase chloride efflux)
ST ~cGMP, activates PKA which regulates CFTR, may also decrease sodium reabsorption
Adhesins – fimbriae, species specific
ETEC
very similar to Shigella Lac- Non-motile Dysentery similar to shigellosis Infectious dose much higher Low incidence in US Children under 5 yo in developing countries
EIEC
Infantile diarrhea in developing countries
No toxins
Apical adhesion, moderate invasion, flattens villi
EPEC adherence factor – EAF
EPEC – attached by pili, injects a receptor for other bacteria to produce a pedestal for other colonization (change the locks to fit your own keys) - attachment & effacement
Profuse, watery infant diarrhea in developing countries
Clustered microcolonies in small intestine that degenerate with loss of brush border and microvilli
Pedestal formation via LEE, but no Stx, ST or LT
Attachment and effacing (A/E) lesion
EPEC
Gram-, Lac-, Glu+, produce H2S
Symptoms begin 20-72 hrs post consumption of improperly cooked food
Nausea, vomiting, followed by or concomitant with abdominal cramps and diarrhea lasting 3-4 days
Fever in half of patients
Diarrhea ranges from loose stools to dysentery
Antibiotics usually not necessary
Salmonella
Gram-, Lac-, Glu+
Invade M cells, survive in macrophages
Vi capsule antigen inhibits neutrophil uptake
Spread to mesenteric lymph nodes and RES in macrophages
Subsequent spread to blood
Sepsis can occur
Perforations of GI tract at necrotic Peyer’s patches can lead to severe hemorrhage
Insidious, rising fever with headache, abdominal pain
Slow pulse, mental confusion
Diarrhea late if at all
Death possible by ruptured spleen or intestine
Chronic infection of gall bladder possible
Culture from blood (or feces)
DOC: ceftriaxone
Oral vaccine for travelers to endemic areas (70%)
S typhi
Epidemics in Central and South America 1000X Stx compared to other species HUS High fatality rate (20%) Gram-, non-motile rod Lac-, Glu+, no gas, no H S Leukocytes prominent in stool samples Acute inflammatory colitis and bloody diarrhea– dysentery like EIEC S. sonnei often less bloody, more watery Very low infectious dose: 10-100 cfu Entry into M cells in gut Escape from phagocytic vesicle Extension to neighboring enterocytes Rarely leaves GI tract
Shigella
Gram- coccobacilli with bipolar staining
Primarily animal pathogens
Human outbreaks linked to consumption of milk, pork in US
Gastroenteritis
Relatively rare
Abdominal pains can mimic appendicitis – “pseudoappendicitis”
Usually self-limiting
Siderophilic (more common in people w/ hemochromatosis) repliacates in terminal ilieum, can cuase reactive arthritis
Yersinia enterocolitica
Single most important cause of diarrheal disease of infants & children world-wide
Non-enveloped, dsRNA 2-3 concentric icosahedral particles: double shelled virion – very stable (fomites)
Potential for antigenic shift: segmented genome, dsRNA
mRNAs are capped, but not polyadenylated
lytic
1-4 day incubation
Rotavirus
Non-enveloped, (+) strand RNA viruses
– Total estimated cases of food-borne illness in U.S: ~38,600,000/yr
– Noroviruses responsible for ~23 million of total (~60%)
• Symptoms include:
– Nausea, vomiting, fever, followed by “watery diarrhea”
– No blood or leukocytes in stool
– Vomiting more prominent with norovirus infections
1 day incubation
Norovirus
Agent for Hand Foot Mouth Disease
Coxsackivirus A16
HAV Family
Picornaviridae
ET
ssRNA+
HBV Family
Hepadnaviridae
PT
dsDNA (cannot be cured)
*transferred to infant during birth not in utero
*Dane particles - 20nm particles that can titrate antibody response
HBV markers
a vaccinee?
a resolved acute infection?
a low risk carrier?
a high risk carrier?
Will see high levels of HBe antigen w/o much antibody response
HBV markers
a vaccinee? –antiHBs (only component in vaccine)
a resolved acute infection? (anti-surface antigen antiHBs, anti-HBc – if antibody to core is present, they had a natural infection) IgM anti-HBc (acute/ recent infection)
a low risk carrier? Will be able to see surface antigen but not surface antibody, will see HBe in low risk and antiHBe
a high risk carrier? Will see high levels of HBe antigen w/o much antibody response
HCV family
Flaviridae, ssRNA
85% chronic
genotype determines prognosis
HDV
Delta Virus
ssDNA
co-infection w/ HBV required
HEV family
Calciviridae
ssRNA+ nonenveloped
1/5 fatal in pregnant women
