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Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

BOTULISM

1- The causative organism Clostridium botulinum,
2- a spore-forming anaerobe
3- produces neurotoxins during vegetative growth
4- Spores can survive in the environment for over 30 years.
5- The organism is present in the alimentary tract of animals

that have recently ingested contaminated material

6- Bacteria can be introduced into new areas by birds and

blowflies.

7- Source of infection are associated with

a- the ingestion of preformed toxin (forage botulism)
b- growth with toxin production in wounds (wound botulism)
c- growth and toxin production in the alimentary tract

(toxicoinfectious botulism) .

d- Forage botulism occurs when pH, moisture, and anaerobic

conditions in the feedstuff allow the vegetative growth of
C. botulinum and the production of toxin

e- Poultry manure and ensiled poultry litter have caused

outbreaks of botulism when used as cattle feed, as has
poultry litter used for bedding cattle.

f- Wound botulism is rare but is recorded in horses following

castration

8- The meat and milk from cattle that have botulism should not

be used for human consumption.

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

PATHOGENESIS:

1- Botulinum toxins are absorbed from the intestinal tract or the

wound and carried

2- via the bloodstream to peripheral cholinergic nerve terminals

including neuromuscular junctions, postganglionic
parasympathetic nerve endings, and peripheral ganglia.

3- The heavy chain of the toxin is responsible for binding to the

receptors and translocation into the cell

4- the light chain of the toxin for resultant blockade of the

release of acetylcholine at the neuromuscular junction.

5- Flaccid paralysis develops and the animal dies of respiratory

paralysis.

6- The toxins of C. botulinum are neurotoxins and produce

functional paralysis without the development of histological
lesions.

CLINICAL FINDINGS:

Cattle and horses

1. Peracute cases die without prior signs of illness
2. the characteristic clinical picture is one of progressive

symmetric muscular paralysis affecting particularly the limb
muscles and the muscles of the jaw, tongue, and throat

3. obvious muscle tremor and fasciculation, often sufficient to

make the whole limb tremble

4. In most cases the disease is subacute.

Sheep

1. Sheep do not show the typical flaccid paralysis

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

2. There is stiffness while walking, and incoordination and

some excitability in the early stages

3. The head may be held on one side or bobbed up and down

while walking (limber neck)

4. In the terminal stages there is abdominal respiration, limb

paralysis, and rapid death.

NECROPSY FINDINGS

There are no specific changes detectable at necropsy.

Differential diagnosis:

Ruminants:

1.  Tick paralysis
2.  Paralytic rabies
3.  Poisoning by Phalaris aquatica
4.  Organophosphate/carbamate poisoning
5.  Louping ill in sheep

Horses:

1.  Equine protozoal myelitis
2.  Equine encephalomyelitis
3.  Hepatic encephalopathy
4.  Paralytic rabies
5.  lonophore toxicity

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

INFECTIOUS NECROTIC HEPATITIS

(BLACK DISEASE)

Epidemiology

1. The disease occurs in sheep and cattle and rarely in pigs and

in horses

2. Clostridium novyi, type B
3. it is resident in soil and may be present in the liver of normal

animals

4. Well-nourished adult sheep in the 2-4-year age group are

particularly susceptible

5.  lambs and yearlings rarely being affected
6.  liver fluke are important risk factor
7.  Fecal contamination of the pasture by carrier animals is the

most important source of infection

PATHOGENESIS

1) Spores of C. novyi are ingested and carried to the liver in the

lymphatic system

2) migrating flukes cause severe tissue destruction
3) the organisms already present in the liver proliferate
4) liberating alpha toxin, which is necrotoxic and causes local

liver necrosis and more diffuse damage to the vascular
system.

5) The nervous signs observed may be due to this general

vascular disturbance or to a specific neurotoxin.

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

CLINICAL FINDINGS

Sheep

1) Affected sheep commonly die during the night and are found

dead without having exhibited any previous signs of illness.

2) clinically affected sheep are seen to segregate from the rest of

the flock, lag behind and fall down if driven.

3) There is fever (40-42°C)
4) which subsides to a premortal (subnormal) level
5) some hyperesthesia; respiration is rapid and shallow
6) the sheep remains in sternal recumbency
7) often dies within a few minutes

N ECROPSY FINDINGS

1.  Bloodstained froth may exude from the nostrils.
2.  The carcass undergoes rapid putrefaction.
3.  There is pronounced engorgement of the subcutaneous

vessels and a variable degree of subcutaneous edema.

4. The dark appearance of the inside of the skin, particularly

noticeable on drying, has given rise to the name black disease

5. Bloodstained serous fluid is always present in abnormally

large amounts in the pericardial, pleural, and peritoneal
cavities

6. The liver is swollen, gray-brown and exhibits characteristic

areas of necrosis.

7. These are yellow areas 1-2 cm in diameter and are

surrounded by a zone of bright red hyperemia

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

DIFFERENTIAL DIAGNOSIS

1.  Acute fascioliasis
2.  Other clostridial disease: blackleg, malignant edema
3.  Anthrax

CONTROL

1. Vaccination
2. control of the liver fluke

BACILLARY HEMOGLOBINURIA

1.  Clostridium haemolyticum (C novyi type D)
2.  is a soil-borne anaerobe
3.  organism is often found in the livers of healthy cattle
4.  Damage to the liver from telangiectasis, necrobacillosis

caused by Fusobacterium necrophorum, and fascioliasis
have been suggested as precipitating causes

5. is a disease of the summer and autumn months
6. The disease is spread from infected to noninfected areas by

flooding, natural drainage, contaminated hay from infected
areas, or carrier animals

Pathogenesis:

1. Migrating flukes are the primary factor leading to liver

necrosis and the establishment of anaerobic conditions in the
liver that will lead to the multiplication of the causative
organism.

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

2. bacteria are carried to the liver and lodge there until damage

to the parenchyma of the liver and the resulting hypoxia
create conditions suitable for their proliferation.

3. The development of an organized thrombus in a subterminal

branch of the portal vein produces the large anemic infarct
that is characteristic of the disease

4. the necrotoxic and hemolytic beta toxin is released

systemically to result in toxemia, generalized vascular
damage and intravascular hemolysis.

CLINICAL FINDINGS:

1) animal found dead
2) sudden onset, with complete cessation of rumination,

feeding, lactation, and defecation.

3) Abdominal pain is evidenced by disinclination to move and

an arched back posture

4) Grunting may be evident on walking
5) Respiration is shallow and labored
6) The pulse is weak and rapid
7) Fever (39.5-41°C)
8) Edema of the brisket is a common finding.
9) The urine is dark red.
10)

Jaundice is present but is never very obvious

CLINICAL PATHOLOGY:

1) The red color of the urine is due to the presence of

hemoglobin

2) Anemia

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

NECROPSY FINDINGS

1.  Rigor mortis develops quickly.
2.  The perineum is soiled with bloodstained urine and feces.
3.  Subcutaneous, gelatinous edema, which tends to become

crepitant in a few hours

4. extensive petechial or diffuse hemorrhages in subcutaneous

tissue are characteristic

5.  Generalized subserous hemorrhages
6.  Hemorrhagic abomasitis and enteritis
7.  The characteristic lesion of bacillary hemoglobinuria is an

ischemic infarct in the liver.

8. One or more infract may be present in any part of the liver

and vary from 5-20 cm in diameter.

9. The infarct is pale, surrounded by a zone of hyperemia, and

has the general appearance of local necrosis.

DIFFERENTIAL DIAGNOSIS

1.  Other clostridial diseases
2.  Anthrax
3.  Acute leptospirosis
4.  Postparturient hemoglobinuria
5.  Hemolytic anemia caused by cruciferous plants
6.  Babesiosis and anaplasmosis
7.  Enzootic hematuria
8.  Chronic copper poisoning (sheep)

TREATMENT

A. high doses of penicillin or tetracyclines
B. antitoxic serum

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

C. Supportive treatment including blood transfusion, parenteral

fluid, and electrolyte solutions

BRAXY (RADSOT)

Is an acute infectious disease of Weaners and yearling sheep in
winter characterized by inflammation of the Abomasal wall,
toxemia, and a high mortality rate. Caused by Clostridium
septicum predisposing factor are ingestion of frosted feedstuffs,
The sheep becomes recumbent, comatose and dies within a few
hours of first becoming ill.

ENTEROTOXEMIA ASSOCIATED WITH CLOSTRIDIUM
PERFRINGENS TYPES B, C, AND E

ETIOLOGY:

The diseases that are produced by these organisms in the different
animal species, and the organisms' names, are as follows:

1. Lamb dysentery associated with C. perfringens type B.
2. An enterotoxemia of young lambs is also associated with C.

perfringens type C

3. Goat enterotoxemia associated with C. pelfringens type C

and rarely by type B

4. Foal enterotoxemia associated with C. perfringens types C

and B

5. Calf enterotoxemia associated with C. perfringcns types B

and C

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

6. Struck, associated with C. perfringens type C, affects adult

sheep, particularly when feed is abundant.

7. Their predominance in very young animals may be due to the

immaturity of their alimentary tracts, the beta toxin being
readily inactivated by trypsin, and because of the ready
colonization of the gut by C. perfringens in the absence of a
mature intestinal flora

PATHOGENESIS

1. The organism is ingested from soil and fecal contamination

on the surface of the dam's udder.

2. It proliferates and attaches to the surface of the epithelial

cells of the intestinal villus

3. Toxigenic strains of C. perfringens types B and C both

produce both alpha and beta toxin.

4. The alpha toxin is a lethal toxin It is a phospholipase, cause

hydrolysis of membrane phospholipids in erythrocytes,
platelets, leukocytes, and endothelial cells results in cell lysis
or other forms of cytotoxicity.

5. The beta toxin causes increased capillary permeability and

may facilitate its uptake from the intestine.

6. Beta toxin is a necrotizing toxin and initially produces

damage to the microvilli with eventual destruction and
desquamation of the intestinal epithelial cells and the
production of a hemorrhagic enteritis and ulceration of the
intestinal mucosa.

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

CLINICAL FINDINGS

Lamb dysentery

1. can be manifest by sudden death without premonitory signs

in peracute cases.

2. In the more common acute form, there is loss of sucking

drive and severe abdominal pain manifest by bleating,
stretching, and looking at the abdomen.

3.  Lambs pass brown, fluid feces sometimes containing blood,
4.  defecation is often accompanied by painful straining.
5.  Death usually occurs after a period of recumbency and coma

and within 24 hours of the onset of illness

6. A chronic form of the disease in older lambs called 'pine',

and manifest with chronic abdominal pain and reluctance to
suck but no diarrhea, is recognized and responds to treatment
with specific antiserum.

Foals

1. severe depression, pronounced toxemia, and marked

abdominal pain

2.  acute attack of collapse with bloody feces
3.  subnormal temperature, fast pulse and respiratory rate
4.  death within a few hours

In calves

1. signs include diarrhea, dysentery, and acute abdominal pain

accompanied by violent bellowing and aimless running

2. In very acute cases, death occurs in a few hours
3. In less severe cases, the illness lasts for about 4 days and

recovery is slow, usually requiring 10-14 days.

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

adult sheep

1. Struck in is manifested only by sudden death

NECROPSY FINDINGS

With type B infections:

1.  the lesions occur as localized areas of necrosis,
2.  usually most evident in the ileum.
3.  The intestinal mucosa is dark red and the ulcers are large (up

to 2.5 cm in diameter) and almost transmural.

4. Intestinal contents are bloodstained and may contain fibrin

clots.

With type C infection:

1. the areas of necrosis are more extensive, involving entire

segments of small intestine and often inducing a peritonitis.

2. Subendocardial and subepicardial hemorrhages

Differential diagnosis:

All species

1.  Enteritis associated with C. perfringens type A
2.  Salmonellosis
3.  Enteric colibacillosis
4.  C ryptosporidiosis

Foals

1. Enteritis associated with:

a) Strongyloides westeri
b) Clostridium difficile
c) Actinobacillus equuli

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

TREATMENT

a) Hyperimmune serum
b) Oral and parenteral administration of penicillin may prevent

further proliferation of organisms and production of toxins.

ENTEROTOXEMIA ASSOCIATED WITH CLOSTRIDIUM
PERFRINGENS TYPE D (PULPY KIDNEY, OVEREATING
DISEASE)

ETIOLOGY

a) Enterotoxemia results from the proliferation of C.

perfringens type D in the small intestine

b) This organism produces a number of toxins, of which the

epsilon toxin

c) The affected animals are on highly nutritious diets and are in

very good condition

d) The highest incidence of the disease is in suckling lambs

between 3 and 10 weeks of age from profuse lactation ewes

e) Calves Enterotoxemia is most common between 1 and 4

months of age

f) high incidence has been observed in association with heavy

tapeworm infestation

PATHOGENESIS:

1) Ingested C. perfringens type D are destroyed in large

numbers in the rumen and abomasum

2) although some survive to reach the duodenum, where

multiplication occurs and toxin is produced

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

3) passage of large quantities of starch granules into the

duodenum when sheep overeat on grain diets

4) changed suddenly from a ration consisting largely of

roughage to one consisting mainly of grain

5) slowing of alimentary tract movement or any factor that

causes intestinal stasis

6) The epsilon toxin increases the permeability of the intestinal

mucosa to this and other toxins, thereby facilitating its own
absorption

7) Degeneration of vascular endothelium, perivascular and

intercellular edema, and microscopic foci of necrosis in the
brain

8) accumulation of protein-rich fluid effusions observable in

heart, brain, and lung

9) The postmortem autolysis of kidney tissue that occurs so

rapidly and is the characteristic of 'pulpy kidney' has the
same basis.

10)

There is a pronounced hyperglycemia due to the

mobilization of hepatic glycogen

CLINICAL FINDINGS

Lambs

1) The course of the illness is very short, often less than 2 hours
2) Acute cases may show little more than severe clonic

convulsions with frothing at the mouth and rapid death

3) Cases that survive for a few hours show a green, pasty

diarrhea, staggering, recumbency, opisthotonos, and severe
clonic convulsions.

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

Adult sheep

1) These usually survive for longer periods, up to 24 hours.
2) They lag behind the flock
3) show staggering and knuckling, champing of the jaws,
4) salivation, and rapid, shallow, irregular respiration.
5) There may be bloat in the terminal stages
6) Irritation signs, may occur but are less common than in

lambs.

Calves

1) The syndrome is similar to that seen in adult sheep, with

nervous signs predominating

2) The more common, acute cases show a sudden onset of

bellowing

3) mania, and convulsions
4) the convulsions persisting until death occurs 1-2 hours later

Goats

1) Diarrhea is a prominent sign in affected goats
2) In the peracute form, which occurs most frequently in young

kids, there are convulsions after an initial attack of fever
(40.5 C)

CLINICAL PATHO LOGY

1) A high blood sugar level of 150-200 Immo/L and marked

glycosuria are characteristic of the terminal stages of
enterotoxemia in sheep

Infectious Lecture 4th Year 7-11-2016 Dr.Osamah Muwafk

NECROPSY FINDINGS:

1. straw-colored pericardial and thoracic fluid that clots on

exposure to air

2. Many petechiae are present in the epicardium and

endocardium

3. Pulmonary edema
4. Patchy congestion of the Abomasal and intestinal mucosae is

usual

5. The small intestine often contains a moderate amount of thin,

creamy ingesta.

6. The content of the large intestine may be watery and dark

green.

7. The characteristic finding of soft, pulpy kidneys

TREATMENT

1. Hyperimmune serum
2. antitoxin in combination with orally administered

sulfadimidine may be effective in treatment in goat

CONTROL

1) Reduction in food intake while waiting for immunity to

develop after vaccination

2) Antitoxin
3) Vaccination