Salmonella
Infections
Presented By:
Sreevarshini N
Introduction
• Enterobacteriaceae family
• Gram-negative bacilli
• Divided into
o Salmonella enterica and
o Salmonella bongori
• Infection: Most common in young children and older adults
• Transmission:
o Via contaminated food – undercooked meat, poultry and
egg
• Vaccination:
o Available for both humans and farm animals ( egg laying hens)
• Pathogenesis:
o Salmonella necessary to cause infection
absense of gastric acid
Atrophic gastritis
Acid-suppressive therapy
Salmonella possess
Bacterial growth
6
within endosomes
Actin rearrangement
5
& bacterial
Activate host Rho guanosine
endocytosis
triphosphates (GT Pases) 4
3 Into M cells and
Capable of enterocyctes
transferring
bacterial protein 2
1 Virulence encode type III
secretion system
Induces
1
Epithelial cells
Release Eicosanoid 2
hepoxillin A3 (potent
chemoattractant)
Neutrophil chemotaxis
3
into intestinal lumen
Mucosal damage 4
Activate TLR5
Flagellin and TLR4
Core protein of bacterial Inflammation
flagella and and tissue
lipopolysaccharide damage
disseminated Pathogen
salmonellosis clearance
Genetic defects in Th1 and Th17
Th17 immunity cells
Salmonella enteritis
• Non-specific
• Similar to the acute self-limited colitis of
campylobacter and shigella
• Stool culture are essential for diagnosis
Clinical Features
• Salmonella infections indistinguishable from enteric pathogen
• Symptoms:
o Loose stool to cholera – like profuse diarrhea to dysentery
o Fever : 2 days
o Organisms can be shed in the stool for several
weeks
• Therapy:
o Antibiotic therapy not recommended
Because it prolong carrier state or relapse
Not shorten the duration of diarrhea
• Complication
o Typically self-limited salmonella
o Reactive arthritis and meningitis
o Death may occur for patients with malignancies, immunosuppression,
alcoholism, cardiovascular dysfunction, sickle cell disease ( hermolytic anemia)
Morphology of S a l m o n e l l a
• Peyer patches in the terminal ileum enlarge into sharply delineated, plateau like
elevation
• Neutrophils accumulates within the superficial lamina propria along the macrophages
(bacteria, red cell, nuclear debris, lymphocytes and plasma cells).
• Mucosal damage creates oval ulcers
• Liver – presence of parenchymal necrosis
(hepatocytes replaced by macrophage
aggregates called typhoid nodules)
TYPHOID FEVER
• Enteric fever S. typhi
Salmonella
enterica
• Caused by: S. paratyphi
o S.typhi – due to major cases in endemic countries
o Infection by S.paratyphi common on traveller
o since vaccinated against S.typhi
o Transmission:
Via contaminated food or water
o Both S.paratyphi or S. typhi colonize in the Gallbladder with gallstone and
make chronic carrier state
Pa t h o g e n e s i s
Systemic
S.typhi
reactive Invade via
disseminate
hyperplasia of Resistant to small
via lymphatic
phagocyctes gastric acid intestinal M
and blood
and lymphoid cells
vessel
tissues
Clinical Features
• Acute infection
• Symptoms:
o Anorexia
o Abdominal pain
o Bloating
o Nausea
o Vomiting
o Bloody diarrhea
• Follows asymptomatic phase to bacteremia and fever with flu-like symptoms
• Abdominal tenderness – mimic appendicitis
• Rose spots, small erythematous maculopapular lesions in chest and abdomen
Clinical Features
• Systemic dissemination cause extraintestinal complications include:
o Encephalopathy
o Meningitis
o Seizures
o Endocarditis
o Myocarditis
o Pneumonia
o Cholecystitis
• Sickle cell disease patients are susceptible to Salmonella osteomyelitis
• Blood cultures are positive for 90% of affected individuals in febrile phase
• Antibotics only prevent disease progression
Non-Typhoidal Salmonellae –
S.enteritidis
• It mainly causes gastrointestinal manifestations 8% of patient with NTS
gastroenteritis
• Risk factors for bacteremia:
o NTS serotype – cattle & pig
Develops
o Age: Infant & Elderly people bacteremia
o Immunity: HIV with other low immunity
o People with pre-existing valvular heart Leads to endovascular infection / Seedling
to various organs
disease
Metastatic
infections
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