This document summarizes various Gram-negative bacterial pathogens. It describes Salmonella, Escherichia, Campylobacter, and other enteric bacteria that can cause diseases like salmonellosis, E. coli infections, and campylobacteriosis. It also mentions non-enteric bacteria like Pseudomonas, Brucella, Bordetella, and Mycoplasma that can cause opportunistic infections. Key information provided includes the bacteria involved, the diseases they cause, their pathogenesis and virulence factors, how they spread, and methods for diagnosis.
CLOSTRIDIUM SEPTICUM
Pleomorphic bacillus
Oval, central/subterminal spores
Anaerobic. saccharolytic, abundant gas
Four distinct toxins
Alpha toxin is hemolytic, demonecrotic and lethal
Gas gangrene in humans
CLOSTRIDIUM NOVYI
Large, pleomorphic bacillus
Oval, subterminal spores
Strict anaerobe
Type A – causes gas gangrene
Large amounts of edema fluid, little or no observable gas, high mortality
CLOSTRIDIUM HISTOLYTICUM
Oval, subterminal, bulging spores
Proteolytic
Gas gangrene in humans
Infection – exogenous/endogenous
Exogenous – implanted foreign particles
Endogenous – clean surgical procedures
ANAEROBIC WOUND INFECTIONS
Simple wound contamination – no invasion of tissue
Anaerobic cellulitis – invasion of fascial planes, minimal toxin production, no invasion of muscle tissue
Anaerobic myositis – gas gangrene, invasion of muscle tissue, abundant formation of exotoxins
GAS GANGRENE
Rapidly spreading, edematous myonecrosis in association with severe wounds of extensive muscle mass
Etiology
C. perfringens
C. novyi
C. septicum
C. histolyticum
Incubation period – 7 hours to 6 weeks
C. perfringens – 10–48 hours
C. septicum – 2–3 days
C. novyi – 5–6 days
Increasing pain, tenderness and edema over the affected part
Accumulation of gas – crepitus
Untreated – profound toxemia and prostratio
LABORATORY DIAGNOSIS
Diagnosis on clinical grounds
Laboratory – confirmation of diagnosis and identification of infecting organism
SPECIMEN
Films – edge of affected area, tissue from necrotic area, exudate from deeper part of wound
Exudate collected from depth of wound – collected by capillary pipette or swab
Necrotic tissue/muscle fragments
C. perfringens – Gram-positive bacilli without spores
C. septicum – boat- or leaf-shaped pleomorphic bacilli
C. novyi – large bacilli with oval or subterminal spores
Naegler reaction
Reverse CAMP test
Surgery – most important therapeutic and prophylactic measure in gas gangrene
Damaged tissue removed extensively and promptly
Hyperbaric oxygen
CLOSTRIDIUM SEPTICUM
Pleomorphic bacillus
Oval, central/subterminal spores
Anaerobic. saccharolytic, abundant gas
Four distinct toxins
Alpha toxin is hemolytic, demonecrotic and lethal
Gas gangrene in humans
CLOSTRIDIUM NOVYI
Large, pleomorphic bacillus
Oval, subterminal spores
Strict anaerobe
Type A – causes gas gangrene
Large amounts of edema fluid, little or no observable gas, high mortality
CLOSTRIDIUM HISTOLYTICUM
Oval, subterminal, bulging spores
Proteolytic
Gas gangrene in humans
Infection – exogenous/endogenous
Exogenous – implanted foreign particles
Endogenous – clean surgical procedures
ANAEROBIC WOUND INFECTIONS
Simple wound contamination – no invasion of tissue
Anaerobic cellulitis – invasion of fascial planes, minimal toxin production, no invasion of muscle tissue
Anaerobic myositis – gas gangrene, invasion of muscle tissue, abundant formation of exotoxins
GAS GANGRENE
Rapidly spreading, edematous myonecrosis in association with severe wounds of extensive muscle mass
Etiology
C. perfringens
C. novyi
C. septicum
C. histolyticum
Incubation period – 7 hours to 6 weeks
C. perfringens – 10–48 hours
C. septicum – 2–3 days
C. novyi – 5–6 days
Increasing pain, tenderness and edema over the affected part
Accumulation of gas – crepitus
Untreated – profound toxemia and prostratio
LABORATORY DIAGNOSIS
Diagnosis on clinical grounds
Laboratory – confirmation of diagnosis and identification of infecting organism
SPECIMEN
Films – edge of affected area, tissue from necrotic area, exudate from deeper part of wound
Exudate collected from depth of wound – collected by capillary pipette or swab
Necrotic tissue/muscle fragments
C. perfringens – Gram-positive bacilli without spores
C. septicum – boat- or leaf-shaped pleomorphic bacilli
C. novyi – large bacilli with oval or subterminal spores
Naegler reaction
Reverse CAMP test
Surgery – most important therapeutic and prophylactic measure in gas gangrene
Damaged tissue removed extensively and promptly
Hyperbaric oxygen
This presentation describes the morphology and cultural characteristics of veterinary important Clostridia; their main virulence factors, pathogenesis and the common diseases in animals.
General discription about E coli.. Classification scheme of E coli. Pathogenecity of E coli. Pathological characters of E coli. slide contains animations and may not support in mobile.. Use laptop for full view
1. GRAM
–ve
Bacteria:
BACILLI
ENTEROBACTERIACEAE
‘Coliforms’
BACTERIA
Salmonella
Escherichia
Campylobacter
S.enterica
E.coli
C.jejuni
C.fetus
PATHOGENISIS
Primary
pathogen
Acute
enteritis
and
systemic
infection
(septicemia/abortion)
Phagocytosed:
Facultative
intracellular
Salmonellosis
1°/Opportunistic
UTI,
Pyometra
(dog/cat)
Acute
mastitis
Avian
colibacillosis
Colisepticemia
Thermophillic
Humans:
Enteric
disease
C.jejuni:
enteropathogen
of
man
and
animal;
food
poising
-‐>
Collitis
Non-‐thermophilic
Sheep
&
Cattle:
Infertility
and
abortion
C.coli
Pigs
TOXIN
Cytotoxicity
for
enterocytes
(diarrhea)
α-‐haemolysin
High
affinity
Fe-‐a
(Aerobactin)
K-‐antigens:
capsules
(prevent
phag/mimic
antigen)
ETEC:
Enterotoxin
(LT
&
ST)
EPEC:
effacing
lesions
EHEC:
SLT;
haemorragic
Verotoxin:
Oedema
&
haem:
pigs
Colonisation,
attachment,
invasion
and
toxin
production
Colon
damage
=
necrosis
of
absorptive
epi
cells,
erosion
of
mucosa,
crypt
abscesses
and
infiltration
of
inflame
cells
Functional
flagella:
Virulence
factors
(non-‐flagellate
do
not
colonise
in
vivo)
SPREAD
Persist
in
gut/gall
bladder:
con’t
excreted
in
faeces
after
clinical
recovery/stress
Flora
of
colon
(L.I):
abundant
in
faeces
Extraintestinal
Blood
-‐>
septicemia
Cattle,
sheep,
dog,
chickens,
wild
birds
carry
C.jejuni
in
intestines
–
Hyperendemic
on
farms
Alimentary
tract
of
reptiles
and
mammals
CHARACTERISTICS/
STERILISATION
Facultative
anaerobe
Classification:
O
(group)
and
H
(serovar)
agglutination
with
known
antiserum
Grouped:
Kauffmann-‐White
scheme*
Aerobic
O
and
H
antigens
AND
K
(fimbrial)
Classification:
Antigen
combinations
Fimbriae:
adhesion
Curved
G-‐ve
Microaerophilic
=
hard
to
grow
V.sensitive
to
drying
Active
immunity
can
develop,
but
sterile
env
means
not
exposed.
TRANSMISSION
Faecal-‐Oral
route:
large
dose
due
to
gastric
acidity
&
gut
flora/fauna
Faeces
Respiratory
Blood
Fecal-‐oral
and
passive
(colostrum)
DIAGNOSIS
Isolate;
enrichment
(selenite
broth);
incubate
to
inc
N0;
inc
sensitivity;
strong
selective
medium
(XLD)
Urease
-‐ve
Indole
-‐ve
Non-‐lactose
fermenter
Utilise
citrate
as
sole
C
Produce
H2S
(Black
colonies)
Lactose
fermenter
(Yellow)
Vaccination
(passive;colostrum)
–
insufficient=overgrowth
in
S.I.
endotoxin
absorption
and
death
(watery
mouth
in
lambs)
Oxidase
test:
-‐ve
Reduce
NO3
-‐
to
NO2
-‐
Proteolytic
digestion
of
gelatine
Identify
with
API
20E
system
of
20
biological
tests
ETEC:
Enterotoxigenic
EPEC:
Enteropathogenic
EHEC:
Enteroheamoragic
2. GRAM
–ve
Bacteria:
BACILLI
NON-‐ENTERIC
BACTERIA
Psudomonas
Brucella
Bordatella
Pasturella
Mannheimia
Mycoplasma
P.aeruginosa
B.abortus
B.bronchispetica
B.avium
P.multocida
M.haemolytica
Spirochaetes:
swine
dysnentry,
lyme
disease,
leptospirosis
Rickettsia:
Tick
&
Louse
borne
Chlamydophilia:
live
in
cells,
look
viral;
enzootic
abortion,
feline
conjunctivitis
*No
cell
wall
peptidoglycan
PATHOGENISIS
Opportunistic
Facultative
intracellular
Brucellosis
Disease
when
infects
LOWER
RESP
tract
Brodatellosis
Kennel
Cough
Rhinotra
cheitis
in
poultry
1°:
Fowl
cholera
(septicemia)
and
epizootic
haem
sep
(cattle
–
not
in
UK)
Atrophic.r
(pigs)
Snuffles;
pasteurellosis
(rabbits)
2°:
LUNGS
following
mycoplasmal;
Pig
enzootic
pneumonia/
wound
infections
Previously
Pasteurella
haemolytica
Epizootic
pneumonia
(cattle)
and
sheep;
pasteurellosis
Severe
mastitis
(sheep/goats)
Colonise
(use
pili)
in
ciliated
tracheal
epithelium:
exudate;
nasal
discharge
TOXIN
Secretes
pyocyanin
(green/blue
puss)
Fimbria
Exotoxin
A
(inhib
host
protein
syn),
Elastase
(destroy
elastin),
proteases,
hydrolytic
enzymes
Penetrate
mucosa;
Phagocytosed;
Granulomatou
s
inflame
reactions
Adenylate
cyclase
cytolysin:
(w/RTX):
immobilises
neutrophils
LT
dermonecrotic
toxin:
turbinate
atrophy
in
pigs
Fimbriae,
filamentous
haemaglutanin
=
adhesion
5
capsular
serotypes
(A,B,D,E,F)
A&D;
normal
flora.
Some
produce
osteolytic
toxin
B&E;
haem
sept
cattle
Cytotoxin;
leukotoxin:
RTX
group
toxins:
crucial
for
pathogenicity
in
septicaemia
and
pneumonia
SPREAD
Look
like
enterobacteria
Free
living
Smell!
Multiple
antibiotic
resistance
–
plasmids
w/R-‐factors
and
chromosomally-‐
encoded
efflux
pump
genes
Grow
on
MacConkey
Spleen,
liver,
lymphatics
UPPER
RESP
tract
of
dogs,
cats,
pigs,
rabbits
(*NOT
ruminants)
UPPER
RESP
mucosa
and
GI
tracts
of
domestic
and
wild
animals
CHARACTERISTICS
Small
G-‐ve
coccobacilli
Major
O-‐
antigen
Eradicated
in
UK
Grow
on
MacConkey
Short
rods
Some
coccobaccili
Bipolar
staining
Catarrhal
odour
Large,
grey
colonies
on
blood
agar
Do
NOT
grow
on
MacConkey
Stains
β-‐haemolytic
on
blood
agar
Grows
weakly
in
MacC
DIAGNOSIS
TREAT:
Gentamicin/Tobramy
cin/
3
rd
generation
cephalosporins
(fluorinated
4-‐
quinolones)/surgery
Serological
tests
(milk
ring)
Non-‐fermenters:
Strict
aerobes
Respiratory
metabolism
Glucose
fermenters
Oxidase
+ve
(cytochrome
C)
-‐>
O2