BACTERIAL
INFECTIONS
OF GIT
Assistant Professor Microbiology
Syed Yousaf Kazmi
College of Medicine, Majmaah University
OBJECTIVES
1. Maj Bacteria causing GIT Infections, epidemiology,
etiology and pathogenesis
2. Mechanism of transmission, Enlist clinical conditions
3. Discuss laboratory diagnosis
INTRODUCTION
• Digestive system-maj route
of entry of pathogen
• Local defenses are strong to
keep infection away
o Mechanical & Physiological
o Immunity (MALT etc)
o Microbial Flora
• Digestive diseases are usually
associated with:
o Crowding
o Poor hygiene
o Contaminated food or water
INTRODUCTION
• GIT Infections are of two types
o Exogenous infection-where org are
introduced from outside
o Endogenous infection-where infection is
associated due to normal flora
• Endogenous infections are caused by organisms that are
part of the normal flora.
o Viridans Streptococcus, Actinomyces isreali
• In the right circumstances they can cause:
o Dental diseases.
o Infections of the bowel, appendix, and liver.
o Diverticular abscesses.
CLINICAL CONDITIONS
1. GASTROENTERITIS
a. Non inflammatory (No WBCs in
stool)
b. Inflammatory (WBCs in stool)
c. Invasive (WBCs, RBCs, Mucus in
stool)
3. FOOD POISONING
4. DYSENTERY
5. ENTEROCOLITIS,
PSEUDOMEMBRANOUS COLITIS
6.
7.
8.
9.
PEPTIC ULCER DISEASE
DIVERTICULITIS
APPENDICITIS
DENTAL CARIES, PERIODONTITIS
GASTROENTERITIS
• Most infections of GIT are Gastroenteritis
• Mainly of two types
o Intoxication (Ingestion of toxins) e.g. Staph aureus, Bacillus cereus,
Clostridium perfringens
o Infections ( Ingestion of bacteria) e.g. Vibrio cholerae, Shigellosis,
Campylobacter jejuni
• Modes of contamination of food or water
•
•
•
•
Many microbes are present in healthy animal’s intestinecontaminate during slaughter e.g. Campylobacter spp,
Salmonella spp
Washing of fruits/ veg with contaminated water
Hands of food handler
Sewage contamination of drinking water
NON INFLAMMATORY
GASTROENTERITIS
INTOXICATIONSTAPH AUREUS
• Gram positive cocci, Catalase
& coagulase +ve
• Secretes enterotoxin
• Food contaminated from boil/
abscess of food handler or
from nose during sneeze
• Type of food meat, fish, cream
filled pastries, egg salad
• Incubation Period 1-6hrs
• Nausea, vomiting, abdominal
cramps, diarrhea
• Mnemonic: (Staph starts with S,
Shank for vomiting)
INTOXICATIONCLOSTRIDIUM PERFRINGENS
 C. pergringens-Obligate
anerobe, Gram +ve spore
forming rod
 Protein rich food-beef, poultry,
fish,
 Survive cooking-germinate &
secrete enterotoxin
 Moderate to severe abdominal
cramps, diarrhea
 Recovery usually in 1-2 days
 Antimicrobials usually not req
 Mnemonic C. perf starts with C,
C for Commode
INTOXICATIONBACILLUS CEREUS
• Gram +ve spore
forming rod
• Spores germinate after
reheating of rice/
Chinese food
• Vomiting after 2-6
hours
• Recovery in 2-3 days
• Antimicrobials usually
not req
INFLAMMATORY
GASTROENTERITIS
INFECTIONVIBRIO CHOLERAE
• Gram –ve curved rod
• Contaminated water or raw
seafood
• Extremely susceptible to acid
• 105 -108 org req
• Release toxin-enterocytes ↑cAMP-loss of water &
electrolytes
• Profuse vomiting and diarrhea
(rice water stool)
• Extreme dehydration
• Renal failure, acidosis- death
INFECTION-ESCHERICHIA
COLI
• Gram –ve facultative anaerobe
• Normal fecal flora but various serotypes can be
pathogenic
• Enterotoxigenic E. coli (ETEC) T for Traveller
o
o
o
o
o
Commonest cause of Traveller’s diarrhea
Secrete enterotoxins like cholera
Eating of raw veg, fruits, drinking unhygienic water
Diarrhea, vomiting, abd cramps, fever
Diarrhea last for 3-7 days
• Enteropathogenic E. coli (EPEC) P for Pediatric
o Diarrhea in infant
o Associated with poor sanitation
INVASIVE
GASTROENTERITIS
SHIGELLOSIS
• Shigella spp are Gram –ve
facultative anaerobe, non motile
bacillus
• Shigella dysenteriae most severe,
Shigella sonnei most benign form
• Outbreaks in school, daycares, etc.
• Consumption of water or food e.g.
eggs, veg, dairy products
contaminated by food handler, flies,
hands
• Even 101 to 102 org can initiate
infection
• Acid resistant- reach colon- secrete
toxin and invade epithelium
• Blood, mucus, WBCs passed in stool
• Severe diarrhea, tenesmus,
vomiting, dehydration
Stool exam shows WBCs, RBCs, non motile bacilli
ENTERO-HEMORRHAGIC
E. COLI
• EHEC-H for Hemolytic Uremic Syndrome
• Dangerous
• Undercooked beef, unpasteurized milk, juices,
lettuce,
• 103 org can initiate infection
• Release toxin in high conc in large intestine
• Serotype O157:H7 secretes toxin- inhibits protein
synthesis-cytolysis
• Hemorrhagic colitis
• Older, young children, weak immunity- HUS
• Hemolysis, renal failure, seizure, coma, etc
SALMONELLOSIS
• Salmonella typhi causative agent of
typhoid fever
• Salmonella enterica serotype
Enteritidis and serotype Typhimurium
• Salmonella typhi source is humans,
Salmonella enterica spp source is
poultry chicken & turkeys
• Transmitted through food handlers
• IP 6-48 hours, nausea, diarrhea,
abdominal pain, fever
• Colonic ulceration
• Infection lasts 3-7 days
• Septicemia rare
CAMPYLOBACTER
JEJUNI
• Gram negative motile curved
bacillus
• Normal gut flora of chicken, turkey,
dairy cattle
• Contaminated raw food, water,
eggs, poultry
• Fecal-oral route
• IP 2-7 days – small /large intestine
invasion
• Ulceration of mucosa
• Symptoms variable- mild to severe
dysentery
• Association with GB Syndrome
weeks later (Markus Babbel
liverpool)
LAB DIAGNOSIS OF INFECTIVE
GASTROENTERITIS
• Clinical history
• Appropriate Samples
• Vomitus
• Stool
• Left over food
• Blood
• Microbiological Testing
• Microscopy (Direct and after
Gram staining)
• Culture & Sensitivity of Stool,
vomitus, left over food or blood
• Blood complete picture
• Toxin detection in stool or
vomitus, food
Cl. Perfringens in stool
LAB DIAGNOSIS
Campylobacter jejuni in stool
Vibrio cholerae colonies on TCBS
Toxin detection kit C. difficile
PEPTIC ULCERHELICOBACTER PYLORI
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•
•
•
•
•
•
•
•
Peptic ulcer –smoking, alcohol, diet, stress
etc.
Association of peptic ulcer with infectious
etiology in 1982
Australians Dr. Barry J Marshall & J Robbin
Warren believed that infection is
responsible
Microaerophilic Gram –ve curved rod,
urease producer
Person to person via food or water
In stomach, attaches to stomach surfacesecrete urease- produces ammonia
Locally pH ↑, neutralize acid, mucus cells
destroyed
Ulcer develop
2% of ulcer patients develop cancer
Gastric ulcer
HELICOBACTER PYLORI
LAB DIAGNOSIS
• Urea breath Test
o Urea breath test- use radioactive C
labeled urea
o Patient drinks the sol- urea broken
down by urease of H. pylori- CO2
released radiolabeled detected by
special equipment
• Serological tests like ELISA
• Culture of gastric biopsy
• Rapid urease test of gastric
biopsy