Lecture 11: Enterobacteriaceae

enterobacteriaceae

enterobacteriaceae are ubiquitous and can be found in the soil, water, vegetation and intestinal flora.

• causes 30-35% of all bacteremia
• causes more than 70% of all UTI infections

• bacteremia
• UTIs
• intestinal infections

• Animal reservoirs (mostly salmonella species & Yersenia species)
• Human Carriers ( shigella species and some salmonella

Enterobacteriaceae are Gm^- rods and can either be motile or non-motile. They do not form spores and are facultative anaerobes. They are not fastidious. Test results show that enterobacteriaceae are catalase positive and oxidase negative. LPS is a major cell wall antigen in enterobacteriaceae. Peritrichous flagella & fimbriae are also present.

• O polysaccharides: present in each genus. detected by agglutination with specific antibodies
• Capsular K antigens: heat-labile. can interfere with O polysaccharide typing
• Flagellar H proteins: heat-labile flagellin proteins. not always present. can undergo antigenic variation

• fermenation of lactose
• resistance to bile salts

• the release of its endotoxin causes many symptoms of disease
• the capsule protects the sell from phagocytosis
• the antigenic phase variation expresses the capsular K and flagellar H antigens and protects the cell from antibody-mediated death
• the type III secretion systems deliver virulence factors into the host cell. Without TTSS, bacteria loses virulence
• the sequestration of iron produces siderophones or iron-chelating compounds. Releases iron from host cells using hemolysins

• Entertoxigenic E. coli (ETEC)
• Enteropathogenic E. Coli (EPEC)
• Enteroaggregative E. Coli (EAEC)
• Enteroinvasive E. Coli (EIEC)
• Enterohemorrhagic E. Coli (EHEC)

Entertoxigenic E. coli (ETEC) is most common in developping countries and among children because it is spread through the fecal-oral route

Entertoxigenic E. coli (ETEC) is spread through he fecal-oral route but requires high inoculum, thus there is no person to person spread. The bacteria then adhere to the intestinal mucosa, but arouses no inflamation or intestinal changes

• Heat-labile
• Heat-stable
• Result in secretion of fluids and electrolytes into bowel

• Enteropathogenic E. Coli (EPEC) typically causes diarrhea in infants in impoverished nations
• Symptoms include watery diarrhea (severe and extended), fever and vomiting

Enteropathogenic E. Coli (EPEC) is spread through person to person contact since only a low infectious dose is needed.

the bacteria attach to the epithelial cells of the small intestine and destroy microvilli due to the formation of pedestals of actin under the site of attachement. This results in the aggregation of bacteria on the epithelial surface mediated by plasmid-encoded pili.

TTSS initiates the secretion of proteins into the host cell. Tir inserts into the epithelial cell and functions as receptor for the outer membrane adhesin, intimin. The intimin-Tir binding results in the polymerization of actin and the accumulation of cytoskeletal elements beneath the attached bacteria. The cell then loses surface integrity and dies

• EAEC binds small intestinal cells into small aggregates. The bacteria is non invasive and causes no intestinal changes.
• The bacteria causes watery diarrhea with dehydration, and usually occurs in infants.

Aggregative adherence fimbriae (adhesins) adheres to the intestinal surface, stimulates mucus secretion and leads to the formation of thick biofilm

• Enteroaggregative heat stable toxin
• Plasmid encoded toxin

• the consumption of contaminated foods such as: undercooked meat, water, unpasteurized milk or fruit juice and uncooked vegetables and fruits
• EHEC usually infects the large intestine
• *usually requires very low inoculum and so can be spread person to person

• Watery diarrhea followed by grossly bloody diarrhea with adominal cramps.
• little to no fever usually occurs
• can sometimes progress to hemolytic uremic syndrome

• acute renal failure
• thrombocytopenia
• can be fatal

• infection is mediated by cytotoxi Shiga toxins which disrupt protein synthesis.
• causes attaching/effacing lesions with destruction of intestinal microvilli that results in decreased absorption

Shigella. symptoms from EIEC are often indistinguishable from from shigellosis, which is usually less severe.

• Invasion & destruction of epithelial cells lining the colon is plasmid mediated.
• After invasion of the colonic epithelium, the bacteria lyse the vacuoule, replicate in the cytoplasm and spread to adjacent cells.
• can cause colonic ulceration

• develops mainly in the large intestine and causes fever, cramping & watery diarrhea.
• may progress to dysentry (inflammation of intestine) with scant, bloody stools

• caused by : salmonella
• symptoms: nausea, vomiting, non-bloody diarrhea, fever, abdominal cramps, myalgias (muscle pain) & headache

Salmonella enterica serovar. Typhi

• The patient is suffereing from typhoid/enteric fever that is caused by Salmonella Typhi.
• Infection is treated with an effective antibiotic such as fluoroquinolones, chloramphenicol, trimethoprimsulfamethoxazole or a broad-specturm cephalosporing

It is not recommended because it may prolong the duration of the disease

• shigella dysenteriae
• shigella flexneri
• shigella boydii
• shigella sonnei
• Technically, all shigella species are sub-groups of E. Coli

Shigellosis

antibiotic therapy, although not necessary to recovery, is recommended in order to shorten the course of symptomatic disease and fecal shedding.

Yersinia

• Bubonic (urban) plague: spread by fleas and rats
• Pneumatic (sylvatic) plague: spread by squirrels, rabbits, rats and cats

Yersinia enterocolitica