CLOSTRIDIAL DISEASES Introduction - PowerPoint Presentation

Slide1

CLOSTRIDIAL DISEASES

Slide2

Introduction

Clostridial

diseases are caused by bacteria of the genus Clostridium. (ANAEROBES)

Clostridia are widespread in the environment and are normally found in soil and

faeces

.

They are also present in the gastrointestinal tract and as spores in tissues of healthy animals.

Slide3

CLASSIFIACTION

The clostridia can be divided into four major groups according to the kind of disease they produce. 

Slide4

The

Histotoxic

clostridia causes a variety of tissue (often muscle) infections frequently following wounds or other trauma (

eg

).

Cl.

chauvoei

Cattle,

sheep

(pigs

)

Many

Spescies

Black quarter

(Black leg

)

Cl.

septicum

Cattle 

Sheep 

Chicken

Malignant

oedema in

Equne

.

 

Braxy

 

Necrotic dermatitis

Cl.

novyi

 

Type

A

Sheep 

Cattle and Sheep

Big head of rams 

Gas gangrene

Type B

Sheep (Cattle)

Black disease

(necrotic hepatitis)

Type C

Water

buffaloe

Osteomyelitis

Slide5

Hepatotoxic

clostridia produces their toxins in the liver, thus resulting in the disease Bacillary

haemoglobinuria

and Black disease (

Eg

.)

C.

haemolyticum

 

Cattle, (sheep)

Bovine Bacillary

haemoglobinuria

C.sordellii

Cattle, Sheep, Horses

Gas gangrene

C. colinum

Birds

Quail disease

, Ulcerative

enteritis

C. piliforme

foals, laboratory animals

Calves, dogs and cats

Slide6

The

Enterotoxigenic

clostridium produces mainly enterotoxaemia and food poisoning although they are occasionally

histotoxic

(

Eg).

C. 

perfringens

-

Type

A

Humans

Lambs

Broiler chickens

Gas gangrene,

Food

poisoning,

Enterotoxaemic

Jaundice

(Yellow lambs disease) Necrotic enteritis

C.

perfringens

-

Type

B

Lambs (Under 3 weeks old)

Lamb dysentery

C.

perfringens

-

Type

C

Piglets, lambs, calves and foals

Broiler chickens 

Adult sheep and goat

Struck,

Haemorrhagic Enterotoxaemia

(

Clostridial

enteritis)

Necrotic

enteritis

C.

perfringens

-

 Type D

Sheep(except neonates)

Pulpy kidney disease

C. perfringens

-

 Type E

Calves and lambs

Enterotoxaemia

Slide7

The

Neurotoxic

clostridia cause the disease by the production of the potent

exotoxins

(Neurotoxins) (

eg.)

C.

t

etani

Tetanus

C.

b

otulinum

Botulism

Slide8

Tetanus

Tetanus has been known from very early times, having been described by Hippocrates.

But the knowledge of the disease was achieved only in 1884.

Rosenbach

–1886 -

 demonstrated a slender bacillus with round terminal spores in a case of tetanus.Kitasato –1889 –

 isolated 

C.tetani

 in pure culture and reproduced the disease in animals by inoculation of pure culture.

The Greek term “tetanus” which means ‘contracture’ has been taken from the Latin medicine “rigor”.

Slide9

HABITAT

Soil, especially that contaminated by animal faeces, is the natural habitat as 

C.tetani

 is often transient in the intestines of horses and other animals.

It is ubiquitous and has been recovered from a wide variety of other sources, including street and hospital dust, cotton wool, bandages, catgut, plaster of

paris, clothing etc.

It may occur as an apparently harmless contaminant in wounds.

Slide10

tetnus

Synonym 

: Lock jaw

Definition

Acute fatal infectious disease of man and animals characterized by involuntary contraction of voluntary muscles caused by toxins of 

Clostridium tetaniHorse is more susceptible and birds

is resistant.

Slide11

Tetanus

Aetiology

Clostridium

tetani

Exotoxin

- CI. Tetani

 - Gram positive

sporulating

, anaerobic, rod shaped anaerobe, Spores – “Drum Stick”

Incidence

Tetanus occurs in all parts of the world

Slide12

Slide13

Tetnaus

Susceptibility

Hores

and mules are susceptible

Transmission

Wound infection

Slide14

Pathogenesis

The organisms enter the body through the nail prick, castration, docking, shearing, umbilical wound (tetanus

neonatorum

) or during parturition

Anaerobic condition allows germination of spores and release

exotoxin

Reaches brain ether blood circulation or through nerve

Slide15

Pathogenesis

The tetanus toxin gets fixed to a substance called

protagon

(

made of cerebroside

+ oligosaccharides

)

in the nervous tissue.

It acts on the

inhibitoty

synapses interfering with the action of the inhibitory transmitter thus producing spastic action

The toxin causes hyperirritability responsible for the

tetanic

spasms.

Slide16

Tetnaus

Three types of toxins

Haemolysin

– Tetanolysin – Not important

tetanospasmin

- Neurotoxin - responsible for the nervous symptoms

Fibrinolysin

- not very potent

Slide17

Tetnaus

The toxin causing spasmodic contraction of muscles, stiffness and immobilization.

Slide18

symptoms

Contraction of muscles

Arched back

Twisting neck

Dropping of third eyelid

ConvulsionsSensitive to loud sound.

Slide19

Tetanus

Clinical signs

Involuntary, persistent, intense painful contraction of one or more group of muscles.

Horse- Stiffness and moves like 

'wooden horse'

.Raised Tail, third eyelid Protrusion, and Stiffness of Jaw muscle -‘ 

Lock Jaw’

Ruminants – Symptoms are less severe

Slide20

Tetanus

Gross lesion

No characteristic lesion

Death due to Toxaemia

Microscopic lesions

No specific microscopic lesions. Degeneration of the neurones in the brain and spinal cord (due to

anoxaemia

)

Slide21

Tetanus

Diagnosis

Characteristic clinical signs.

Organisms are local but not

septicaemic

Demonstration of toxin in the serum

Slide22

BOTULISM

Definition

Botulism is a rapidly and fatal motor paralytic condition caused by ingestion of 

CIostridium

botulinum exotoxin.

 

Botulism is a food poisoning, the toxin being elaborated as an

exotoxin

by 

CIostridium

botulinum

 

.

Slide23

For the poisoning to occur, the toxin should be present in the food before ingestion, since the organism cannot generate the toxin in the alimentary tract

A, B, C, D, E, types

A

– Limber neck – Poultry

D

–

Lamsiekte

C

– Forage poisoning in horses

E

– Fish and fish products

Slide24

Botolisum

By

clostridum

botulinumDisease which occur by ingestion of pre-formed toxin.The toxin donot enter CNS but affect PNS.

The toxin block release of acetylcholine

The toxin through blood or nerves reach PNS and inhibit release of

inhibtory

neurotransmitters like GABA,

glycine

etc.

Due to this muscle remain in relaxed state.

Slide25

Botolisum

The disease is also known as Bulbar paralysis or loin disease.

The animal died of respiratory paralysis.

In birds disease is known

as Limber neck and in hourse also known as Shakers foal syndrome.

Slide26

Clinical signs

Cattle -Pica-Chew bones (due to deficiency of phosphorus) which may contain toxin in the decaying meat and get poisoning.

Cattle and Horse: Forage Poisoning (Ingestion of hay contaminated with dead animals or poultry litter)

Wound botulism – Horses

Salivation, paralysis with difficulty of movement and impaired vision.

Tongue paralysed leads to swallowing is impossible.

Slide27

Swine are resistant since the toxin is poorly absorbed.

Botulism in birds is exhibited by

torticollis

– ‘

Limber neck

’ caused by eating infected blow fly maggots and vegetable matterHead and neck droopDeath – Respiratory failure and asphyxiaNo characteristic lesions

Slide28

Entertoxaemia

There are 5 strains and there production of toxins

A

–

alpha

– Gas gangrene, food poisoning in human.

B

–

alpha, beta, epsilon & iota

-

Lamb

dysentery, Hemorrhagic enteritis in sheep & goat.

C

–

alpha, beta

- Struck in sheep & enteritis in lambs, calves & piglet. Enteritis

necroticans

( Human)

D –

alpha& iota

- Enterotoxaemia in sheep &

Pulpy

Kidney

E

–

alpha& iota

- Enterotoxaemia in Calves

and Lambs .

Slide29

Cl.

Perringens

( H, Co

2 Gas formation in tissue)

ExotoxinAlpha – ToxinPhospholipase

Phosophlipids

Phospholipid

lecithin

Which is in cell wall of RBC, WBC & Muscle cells

Produce characteristic

hemolysis

&

myconecrosis

Myconecrosis with accompanying gas formation known as Gas gangrene.

Slide30

Cl. Per produce multiple other pathogenic toxin heat- labile

entrotoxin

which causes Cl. Food poisoning manifested abdominal pain & Diarrhea

The typical

synerio

involves meat i.e kept warm for long period of time alowing

spore to germinate & produce bacteria in

vegiate

state that produce

exotoxin

.

Cl. Food poisoning

rerarly

fatal but gas gangrene can be rapidly lethal & lead to shock unless to death.

Slide31

CI.

perfringens

type ‘A’

Enterotoxaemia occurs in lamb and calves

Haemolytic anaemia,

Haemoglobinuria

and

Icterus

- acute syndrome

Slide32

Lamb dysentery

CI.

perfringens

type ‘B’

Lamb – Less than 3 weeks

Also occurs in calves and foalsHaemorrhagic enteritis with ulceration

Beta toxin

Acute – Abdominal pain, depression and reluctance to suckle

Peracute

-death without symptoms

Microscopic lesions : Haemorrhagic enteritis and ulceration.

Slide33

‘Struck’

CI.

Perfringens

type 'C' 

Adult Sheep – Haemorrhagic enteritis and ulceration of Jejunum and duodenum

Peritionitis with large volume of clear yellow fluid accumulation

Another form -

CI.

Perfringens

type 'C'

 – Haemorrhagic enterotoxaemia

Affects lambs, calves and piglets within a few days of birth and  fatal

Slide34

“

Puply Kidney disease”, 

Synonym - “Over eating disease”

Definition

Acute toxaemia of fattening lambs and sheep which receive sample milk and high concentration of diet characterized by nervous symptoms and sudden death with development of pulpy kidney

Slide35

“

Puply Kidney disease”, 

Incidence

It is occurs throughout the world including India

Susceptibility

It is an important disease of goats, sheep (fattening lambs) and less commonly in adult sheep

Enterotoxaemia has also been reported in calves

Slide36

Pathogenesis

Organism is a normal inhabitant of alimentary tract and the toxin produced are removed by normal movement of

ingesta

When excessive starch food is fed, the bacteria proliferate and liberate

toxin.Hence

the name “Over eating disease”

Atony

of intestine & Stasis of ingests also favours growth of organisms

The epsilon toxin produced will be

abosrbed

immediately by intestinal mucosa resulting in toxaemia

Slide37

Smaller quantities of alpha and

b

eta

fractions

Toxins reaches the brain causing opisthotonus, convulsion and coma.

Toxaemia (Few hours - chronic convulsions)Hyperglycaemia and glycos

uria

are also observed

Slide38

Gross lesions

Petechial

or

ecchymotic

haemorrhages of

epicardium, endocardium, serous surface of intestine, abdominal muscles, diaphragm and

hydropericardium

Catarrhal or haemorrhagic gastroenteritis

Kidneys – swollen and pulpy – “

Puply

Kidney disease”

Reaching the brain causing symmetrical

encephalomalacia

Slide39

Microscopic lesions

Kidney:

Cloudy swelling and necrosis of epithelium of proximal

convuluted

tubules

Liver and spleen- Congested

Brain:

Lysis

and liquefaction of the white matter, while the grey matter is oedematous.

Hyperglycaemia due to increased

glycogenolysis

of liver glycogen

Slide40

BLACK QUARTER

Synonym

: 

Black leg, quarter ill, Symptomatic anthrax

Definition

Acute febrile disease of cattle (6 month to 2 years), less often of  sheep, goat and swine characterized by emphysematous,

sero

haemorrhagic swelling in the heavy muscles, especially of the hind limbs.

Slide41

BQ

Etiology

Clostridium chauvoei

- 

Gram + (positive), spore forming, rod shaped bacterium

Slide42

B Q

This disease is spread generally in Rainey Season.

Slide43

BQ

Incubation period: 1- 5 days

Slide44

Pathogenesis

Infection is by ingestion of spore of Cl.

Chauvoi

The organisms multiply in the intestinal mucosa.

Goes into the intestinal

macrophase

Inters the lymph & blood

Precipitates'

in the heavy muscle of thigh& limb & shoulder.

Slide45

B Q

During devitilization , when some injury to the muscles anaerobic condition sets up. ( due to wound or heave exercise anaerobic condition developed)

The bacteria vegetates in bacilli form.

start causing necrosis by release of toxins.

Causing emphysematous necrotizing myositis of the muscles.

Black gas gangrenous muscles with crepitating sound.

Slide46

B Q

Filled with

serosaguinous

fluid ( foul smelling)

FeS

deposition

Toxemia

Death within 24 hrs to 60 hrs. Death may be due to toxaemia

Slide47

Different types of toxins are releases by Cl.

Chauvoea

α

– toxin is most imp toxin.

β

γ

δ

These toxins causes necrosis of muscles (

Gluteal

)

Here breakdown of RBC

RBC

lysis

---- Iron is release & due to necrosis of muscle

H

2

S

is release.

Slide48

B Q

H

2

S

+ Fe = Fe2S - which is black in colour of affected muscles.Release of gas is due to fermentation of sugar in anaerobic medium.

Slide49

B Q

Clinical signs

Fever

lameness,

visible swelling of muscles- Tongue, diaphragm, myocardium and

gluteal muscles

In early stages, the swelling is hot and painful to the touch but soon cold and painless and oedema and emphysema can be felt

Slide50

Gross lesions

Crepitating swelling of the muscle(extremities)

Rubber sponge and dark brown or black

sero

sanguineous fluid exudes with gas bubbles -Gas gangrene

Affected muscles appears blackMuscle – Centre area is dry and have odour of rancid butter

Regional lymph nodes – Swollen and oedematous

Large muscles – Diaphragm and tongue

Internal organs – Heart, lung, kidneys, liver, spleen and intestine showed acute congestion

Slide51

Microscopic lesions

Muscle fibres separated and showed waxy degeneration and coagulation necrosis

Streaks of haemorrhages - Collection of

neutrophils

, lymphocytes and Gram positive organisms demonstrated in tissue sections

Slide52

Diseased muscle from a heifer that died suddenly from blackleg. The muscle tissue is dark red and has a dry appearance due to gas formation.

Slide53

Blackleg -

generalised

discoloration/gaseous

degeneration of carcass in Blackleg case.

Slide54

Blackleg – accurately located typically ‘dry’ lesion (area to right of label) from PM.

Slide55

Diagnosis

May be confirmed by gross lesions

Demonstration of organism – from the fluid incised swelling

Biological tests using guinea pigs

Fluorescent Antibody Technique (FAT)

Fatal course and found dead before signs of illness are seen