prof . dr. ihsan edan alsaimary department of microbiology - college of medicine - university of basrah - basrah -IRAQ ihsanalsaimary@gmail.com 00964 7801410838

1. Pathogenic Gram-Negative Bacilli
(Salmonella,Shigella and Yersinia)
Prof dr. Ihsan Edan Alsaimary
department of microbiology – college of medicine – university of basrah – mobile:
07801410838 e.mail : ihsanalsaimary@gmail.com

3. Gram-negative, motile bacilli
Important members of this group almost always
pathogenic due to numerous virulence factors
Mode of infection is through ingestion of
contaminated food or drink
Found in the intestines and feces of most birds,
reptiles, and mammals (more than 2,000 species)
Poultry and eggs are particularly common
sources of Salmonella
Salmonella :true pathogen of enterobacteriaceae

6. Classification
A. Ewing’s classification
Three species:
1) S. typhi (one serotype)
2) S. choleraesuis (one serotype)
3) S. enteritidis (> 2,400 serotypes)
Kaufman-White classification
Each serotype given a species name
(>2,400 species e.g. S.dublin, S.tamale etc)
Diseases caused by Salmonella
1. Gastroenteritis - S. typhimurium
2. Enteric fever - S. typhi (typhoid fever)
- S. paratyphi A,B,C (paratyphoid fevers)
3. Bacteremia -mostly S. choleraesuis, S. typhi

7. Salmonella
important pathogenic members
S.typhi-causes typhoid fever
S. paratyphi A, B & C –cause paratyphoid fevers
S.typhimurium, S. montevideo, S. wien -cause
salmonellosis
A complex system of classification of Salmonella based
upon antigenic structure exists (Kaufmann-White
scheme)

9. Humans are the only host
Causes typhoid fever
Infection occurs via ingestion of food or water
contaminated with sewage containing bacteria
from carriers
Bacteria can pass through the intestines into
the bloodstream and into the liver, spleen,
bone marrow, and gall bladder
Bacteria from the gall bladder can reinfect the
intestines, producing gastroenteritis and a
recurrence of bacteremia
Salmonella typhi

11. Transmission
• Animal food stuffs
• Poultry – (eggs infected trans-ovarially)
• Contaminated water and vegetables
• Ingestion of raw milk has been associated with
outbreak
• Seasonal variation – peak in summer – fall
Diseases caused by Salmonella
Gastroenteritis (Enterocolitis)
• Most common cause is S. typhimurium
• Infective dose : 10,000 bacilli or more.
Patients on antacid drugs – a smaller dose.
• Incubation period : 24-48 hours.

12. PATHOGENESIS
•After ingestion  bacilli are internalized by
induced endocytosis in the epithelial cells of ileum
& colon  penetrate to lamina propria 
inflammation and poor absorption.
•PMNL response limits infection to gut
•Bacteremia is infrequent.
CLINICAL FEATURES:
Nausea & vomiting
Abdominal cramps & diarrhea

13. Lab identification
Specimen : stool or blood
Microscopy
•Methylene blue staining to see PMNLs : if present
Culture on:
•MacConkey or Salmonella – Shigella agar (SS
Agar)
Non-lactose fermenting colonies identified by:
°Motility (motile)
°TSI – Butt – acidic, Slant – alkaline; with H2S

15. Complications of enteric fever
•Intestinal perforation in terminal ileum
•Abscess formation
•Pneumonia
•Myocarditis, damaged heart valves
•Thrombophlebitis, IVC
•Carrier state (3%)

16. In some patients the bacteria ulcerate and
perforate the intestinal wall causing
peritonitis
Treatment is through the use of
antimicrobial drugs (ampicillin,
chloramphenicol, trimethoprim-
sulfamethoxazole, )
Vaccines (TAB) are available to provide
temporary protection to individuals
traveling to areas where typhoid fever is
endemic
Salmonella typhi

17. Typhoid Carriers
Convalescent carriers &
permanent carriers
Testing of food handlers for Vi
antibodies
Treatment of carriers

19. Diagnosis of enteric fevers
During the first week of illness: blood culture
During the second week : blood culture , urine
culture
Serology: Widal test, a tube agglutination test
using antigens of S. typhi, S.paratyphi A & B to
be agglutinated by the patient serum
Stool cultures are also positive during the
second and third weeks of illness
They are indole negative and urease negative
and produce H2S in culture

21. Gram-negative, nonmotile bacteria,
nonlactose fermenters
Primarily a parasite of the digestive
tract of humans
Infective dose is small
Produce a diarrhea-inducing
enterotoxin
Cause a severe form of dysentery
called shigellosis
Shigella

22. Classification of Shigella
4 groups on the basis of :
•Different somatic (O) antigens &
•Fermentation of glucose & mannitol
S.dysenteriae- 10 serotypes
°(Type I – Shiga bacillus) – causes severe dysentery
S. flexneri- most commonly isolated in developing
countries
S.boydii
S.sonnei- cause a mild form of diarrhea, patients
are ambulatory
Shigellosis is treated with fluid and electrolyte replacement

23. Pathogenesis
•Very low Infective Dose (ID50)
°Ingestion of as few as 100 bacilli can cause disease as
bacteria are not easily killed by stomach acid
°Vibrio cholerae and Salmonella typhi – 105 bacilli.
•Transmission from person to person by “Four
Fs” : fingers, flies, food, faeces
•Causes Shigellosis (dysentery)
•Only a human disease
•Disease of GIT – invasion of mucosa of distal
ileum and colon.

24. Shigella are taken up by M cells in
the large intestine by endocytosis.
Bacteria are quickly released from
endosomes and leaving shigella free in
the cytoplasm. The bacteria multiply &
enter the inferior and lateral aspects of
the epithelial cells
Actin filaments quickly form a tail and
push the bacteria into next cell where
they multiply. Macrophages that take
up Shigella are killed and release organism.
Infected cells die and slough off.
Acute inflammatory response occurs
with bleeding and abscess formation.
Pathogenesis of ShigellaEpithelial cellM cell Shigella
Endosome
Macrophages

25. Shigella
Infections are mostly localized to the
intestines with formation of
microabscesses in the wall of the large
intestine and terminal ileum leading to
superficial ulceration
They are highly communicable (foods,
fingers feces, flies)
Shigella dysenteriae produces an
exotoxin (Shiga toxin) which acts as an
enterotoxin and a neurotoxin
(meninngismus and coma)

26. Lab identification
Specimen : stool
Microscopy
• Methylene blue staining to see PMNLs : if present
(Invasive organisms like Shigella, Salmonella, Camphylobacter
rather than: toxin producing organisms like V. cholerae, E. coli,
C. perfringens).
Culture on:
• MacConkey or Salmonella – Shigella agar (SS Agar)
Non-lactose fermenting colonies identified by:
° Motility (non-motile)
° TSI – Butt – acidic, Slant – alkaline; no H2S
Serological Grouping : A-D subtypes

27. Diagnosis, Treatment
Stool culture or rectal swab culture
Treatment is by chloramphenicol,
trimethoprim-sulfamethoxazole,
ampicillin
If the case is not severe it is better
not to give drugs because they do not
eradicate the organisms and permit
establishment of the carrier state.

28. Treatment
Rehydration
Antibiotics - Ciprofloxacin is drug of choice
- Ampicillin
Antispasmodics are contraindicated
Immunity:
Short lived; Preparation of oral live attenuated vaccine is on
the way to stimulate mucosal IgA.
Prevention
Sanitary precautions
Good personal hygiene (hand-washing)

29. Normal pathogens of animals
3 important species
Y.enterocolitica
• Acquired via consumption of food or
water contaminated with animal feces
• Causes inflammation of the intestinal
tract
Y.pseudotuberculosis
• Similar to Y.enterocolitica but produces
a less severe intestinal inflammation
Yersinia

30. Y.pestis
•Bubonic plague-characterized by
high fever and swollen, painful
lymph nodes called buboes
•Pneumonic plague-rapidly
developing infection of the lungs
Yersinia

31. Figure 20.16

32. Diagnosis and treatment must be rapid
due to the fast progression and deadliness
of the plague
Diagnosis
Characteristic symptoms are usually
sufficient for diagnosis
Treatment
Many antibacterial drugs are effective
against Yersinia
Diagnosis, Treatment, and Prevention

33. Figure 20.18