Enterobacteriaceae/Salmonella Flashcards
Enterobacteriaceae- where do they live?
Important pathogens of mammals, birds and humans
a number are zoonotic: foodborne, water borne, vector borne
typical habitat: intestinal tract of vertebrates
Enterobacteriaceae- general characteristics
gram negative rods or coccobacilli usually MOTILE and flagellated facultative anaerobes Fermentative organisms: produce acid and gas Oxidase negative- distinguished from non-fermenters Grow well on MAC agar Lactose fermenters: E. coli, Klebsiella NLF: Salmonella, Proteus, Yersinia
ID of enterobacteriaciae
E. coli resists action of bile salts. Produce acidic reaction which lowers pH and a color change results (pink). If NLF, colonies are colorless or yellow (increased pH)
E. coli is hemolytic on sheep blood agar
Subdivision/serotyping of enterobacteriaceae
All species subdivided using a scheme based on O (somatic) and H (flagellar) antigens
Different pathoypes cause different types of disease.
Enterobacterial surface antigens
Flagella: H antigen
Fimbriae/pili: F (K) antigen
LPS: O antigen- on outside of LPS, chain of sugars which is variable–> antigenically variable–> use serotypes to recognize antigen with generation of antibodies.
Capsule: K antigen (kelbsiella and E. coli have capsules)
Salmonella-general characteristics
Non-lactose ferementers, pathogens of warm blooded-animals, commensals of cold blood animals. Reptiles and amphibs. carry organisms but may cause disease also.
Generally infection via fecal-oral route.
Salmonella are invasive (get inside epithelial, endothelial cells and macrophages)
Facultative intracellular pathogens.
Important salmonella syndromes
- enteritis resulting in diarrhea- reistricted to gut tissue- organisms generally don’t invade beyond mesenteric LN- acute diarrheal disease with inflammation of ileum or colon— enteritis is often zoonotic
- septicemia-organisms spread through body may lead to abortion or joint infections or pneumonia- may or may not be accompanied by diarrhea–septicemia is generally NOT zoonotic
After recovery, chronic infection and carrier state may follow- organism persists in body, transmits infection to other animals, humans and/or environment.
Salmonella “species”
S. enterica; 1. subspecies >1300 serotypes isolated- infects warm blooded animals
S. enterica II, IIIa,IIIb, IV, VI and S. bongori all infect cold blood animals and account for less than 1% of clinical isolates.
NB: s. tymphimurium=S. enterica subspecies I serotype typhimurium
Distinct antigen differences for over 2500 serotypes of salmonella.
Salmonella species
Only 2- s. enterica and S. bongori
S. enterica subdivided by O and H antigens into serotypes
Serotypes of Salmonella enterica
O antigens identified using sera against LPS denoted as 1,2,3 etc (1-13)
Similar O types are grouped into serogroups A, B, C and D
Can produce one of two types of antigenically distinct flagella
Phase I H antigen
Phase II H antigen
Capsules present on only a few salmonella serovars
Non-host specific (non-host adapted serovars)
broad host range e.g. S. typhimurium, S. enteritidis
cause enteritis, mainly of young animals
v. important cause of food poisoning in humans
Host-specific (host-adapted) serotypes
often cause systemic infection, young or adult animals
i.e. s. gallinarum, s. abortusovis and S. typhi
Host-restricted serovars
preferentially infect one host but can infect others
S. dublin: cattle- septicemia, enteritis, abortion, meningitis, joint ill, terminal dry gangrene- also found in pigs
S. cholerasuis: pigs- septicemia, simialr to swin fever- can also be found in cattle.
Both CAN, but rarely infect humans; infectiosn are serious. systemic–> causes focal infections in organs.
Chronic salmonellosis
S. dublin, calf post-septicimia–> necrotic ear tips
peripheral vascular shutdown. tissue went gangrenous, surgically removed, dry gangrene at periphery.
Septicemic salmonellosis
S. cholerasuis: acute speticemia, periphery becomes cyanotic in favor of blood supply to critical organs- get disseminated vascular coagulation
Pig with megacolon resulting from rectal stricture, S. typhimurium- eventual peritonitis–> die of overwhelming infection.
Pathogenesis of Salmonella infection- enteritis
Organism ingested–> reaches gut–> invades cell through epithelium/enterocytes into submucosa or via M cell. If non-host adapted, neutrophils into lamina propria–> massive inflammatory response. Acute neutrophil infiltration results in diarrhea and enteritis.
Pathogenesis of Salmonella infection- septicemia
preferentially attracts macrophages to lamina propria. infection doesn’t stop at gut. Macrophages go to mediastinal LNs. Bacteria grow in macrophages–> go around body–> liver and spleen (reticulo-endothelial system) –> septicemia.
Salmonella attachment: fimbriae
each serotype can produce many different types of fimbriae/pilli. S. tymphimurium has genes for 13 different types of pili, except fimbriae aren’t well expressed in the lab so we don’t know which of the 13 is responsible for adhesion in the gut.
Salmonella membrane ruffling
Adhesion via fimbriae to cell–> contacts host cell–> molecular syringe is produce–> engulfment by host. Bacteria mediates its own engulfment via membrane ruffling.
Type III secretion systems (TTSS)
molecular syringes produced by TTSS. Molecular syringe injects host cell. Effector proteins bring out ruffling.
Pathogenicity islands
Large chromosomal regions (30-200 kb) that encode virulence genes (toxins, adhesins, invasins, secretion systems)
Have a different G+C component in comparison to the rest of the chromosomal DNA- come from another organism through evolution
Acquired horizontally: from another organism–> have phage remnants
Patho. islands for salmonella
All genes required for membrane rufflin on SPI 1
SPI 1: TTSS, invasion of epithelial cells, enteritis
SPI 2: important for survival in macs should organism go systemic- TTSS, survival in macs
17 PIs identified in salmonella, strain may not have all PIs
Expressed in different environments
SPI I expressed in gut
SPI2 expressed in tissue of reticuloendothelial system
SPI 1: invasion of epithelial cells
Salmonella contacts surface via fimbriae–> SPI 1 TTSS produces molecular syringe and injects effector proteins–> membrane ruffling–> bacteria goes into phagosome–> delivered to basal lateral surface of enterocyte–> within lamina propria, attracts n’phils –> inflammation
Salmonella enteritis- what causes destruction of epithelium?
Destruction of epithelium is largely d/t inflammatory response marked by massive n’phil influx elicited by salmonella. Leads to diarrhea (nb: diarrhea is very efficient for transmission and dissemination of salmonella). H2O absorption is prevented–> tissue damage may result in diarrhea with blood
Is gut inflammation beneficial to salmonella?
Inflammation induced is important for clearing out normal flora. if you get rid of normal flora by ABX, animal is susceptible to salmonella. antimicrobial peptides and n’phils flush out normal flora in diarrhea, but not necessarily salmonella
Survival strategies of salmonella species in macrophages
normally, fusion of phagolysosome kills organisms, however, bacteria prevents the fusion of the phagolysosome. salmonella can then survive and grow in macrophages. it remodels the vacuole (mediated by SPI 2) and allows replication within the vacuole.
SPI 2 is essential for replication in the macrophage, but there are also many other genes important for survival in the macs.
Salmonella Zoonosis
CDC estimates ~70k americans have contracted salmonella from a reptile
Veggies (due to manuring with infected feces)/meat can also carry salmonella infection
