salmonella - pathogenesis

Salmonella - pathogenesis

Ingested orally (acid-labile)

1,000,000-100,000,000 live bacteria for

infection

(only 1,000 to 10,000 for S. typhi)

Must survive in gastric acid

• Lower pH increases number for infection

• People on antacids show increased risk

Salmonella - clinical syndromes

Gastroenteritis (diarrhea)

• Most common infection seen with Salmonella spp. = salmonellosis

• Invade cells of GI tract

• Loss of water from cells gives rise towatery diarrhea, fever, cramps

• Spontaneous resolution in days to a week

Salmonella - clinical syndromes

Typhoid Fever (S. Typhi)

• Pass through cells into bloodstream

• Picked up by macrophages to liver, spleen,

bone marrow (ulceration, perforation,

endotoxin shock)

• High fever, diarrhea, cramps

ShigellaMedically important species

–S. dysenteriae (most serious)

–S. sonnei (most common in developed)

–S. flexneri (most common in underdeveloped)

Epidemiology

–Human reservoir (fecal-oral through hands)

– Hardy in nature - survives long time on surfaces

– >50% of cases are in children

Shigella - pathogenesis

● Ingested orally - only 200 live bacteria for infection

Acid stable (unlike Salmonella)

Attach to & invade cells & replicate

Spread cell to cell (protected from immunity)

DO NOT spread through bloodstream

Endotoxin causes inflammation

Produces original shiga toxin (Sh. dysenteriae type 1)

Enterotoxins (Sh. flexneri)

Shigella – clinical syndromes

Shigellosis

• Starts with watery diarrhea

• Turns grossly bloody with pus

• Severe cramps

• Self-limiting

• Complication: HUS

Miscellaneous Enterobacteriaceae

• Klebsiella pneumoniae– community-acquired pneumonia

– diarrhea

• Enterobacter, Serratia, Citrobacter

– opportunistic pathogens = they cause infections

in patients that are very sick and have weakened

defences

– hospital-acquired infection are primary source

Proteus (UTI), Enterobacter, Citrobacter etc.

Yersinia pestis, enterocolitica,

pseudotuberculosis

• Gram-negative rod

• Intracellular pathogen

• Zoonotic infection

Epidemiology

– World-wide problem

– Usually associated with contact with squirrels &

other urban animals

Yersinia pestis - clinical syndromes

Bubonic Plague

–Flea bite

–Bacilli travel to lymph nodes (multiply in

lymph nodes – can survive within

macrophages)

– Infection results in swelling and pain

–High fever, chills, headache, nausea

Yersinia pestis - clinical syndromes

Septicemic Plague

Can penetrate & invade bloodstream

• All organs infected

• Lungs (secondary pneumonic plague)

50-75% mortality when it goes to

bloodstream• Endotoxin shock primary problem

Yersinia pestis - clinical syndromes

Primary Pneumonic Plague– spread via respiratory droplets

– 1 bacilli can cause disease in patient

– severe hemorrhages

– death in hours

– 100% mortality if untreated or late treatment

Diagnosis and Treatment

– symptoms & patient history key

– must act fast with treatment

Clinically important nonfermentative

GN bacilli

General characteristics of nonfermenters

Oxidative GN bacilli, facultative anaerobes &

microaerophiles

Produce acid from glucose or other carbohydrates only

in the presence of oxygen (nonfermenters)

NOTE: Enterobacteriaceae, Aeromonas and Vibrio are

fermentative & can utilize carbohydrates in the absence

of oxygen

Pseudomonas aeruginosa oxidizes but does not

ferment glucose

Pseudomonas

aeruginosa

(Family Pseudomonadaceae)

Pseudomonas aeruginosa

• GN long & thin rods

• Pigmented growth on agar & distinct odor– usually green or red & smells like grapes or juicy fruit gum

• Ubiquitous in environment, especially in

water– Hospital environment loaded with this pathogen

• Hardy, survive extreme conditions

• Rarely part of normal flora

• Primarily opportunistic pathogen

Pseudomonas aeruginosa

Virulence Factors

– Attachment by fimbriae

– Capsule - anti-phagocytic

– Endotoxin – inflammation

– Exotoxin A

•blocks protein synthesis

•kills cells

•skin or lung damage depends on infection

– Many other toxins & enzymes

Virulence factors associated with

Pseudomonas aeruginosa

Pseudomonas aeruginosa

Epidemiology

– Opportunistic infections

– Require weak defense systems

– Colonize hospitalized patients

• respirators

• solutions

• cut flowers

• instruments

Diverse sites of infection by P. aeruginosa

Pseudomonas aeruginosa

Pulmonary Infections

– Colonization

– Benign bronchitis to necrotic fatal pneumonia

– Cystic Fibrosis

• mucoid encapsulated strains

• exacerbations of disease happen frequently

• invasive pneumonia

– Neutropenic patients

• respiratory equipment is a primary source

• serious pneumonia

Pseudomonas aeruginosa

Skin Infections

– Most common in burn victims

• moist environment

• lack of WBC reaching damaged tissue

• vascular damage

• tissue necrosis

• blood stream invasion

– Folliculitis (hot tubs, whirlpools, pools)

Pseudomonas aeruginosa

Other infections associated with contaminated

water or liquid solutions

– outer ear infections (swimmers ear)

– eye infections (contact lens wearers especially)

– endocarditis (drug abusers)

Treatment challenges

– multiple antibiotic resistance problems

– develops resistance overnight

Diseases Associated with Burkholderia spp.