Listeriosis and Colibacillosis

1. Listeriosis & Colibacillosis
Muhammad Asfar Zaman
Roll no. 106
Muhammad Asfar Zaman
Roll no. 106

3. Introduction
• Listeriosis, a serious infection
caused by eating food
contaminated with the
bacterium Listeria-
Monocytogenes.
• Listeriosis primarily causes
infections of the central
nervous system.
• Common name is “Circling
disease”.

4. Listeria Monocytogenes
• Listeria Monocytogenes is a
rod-shaped aerobic and gram
positive pathogenic bacterium
that invades the cytoplasm of
living cells. It develops a
distinctive rocket tail structure
to help push through the
cytoplasm. Eventually, these
"rockets" push bacteria into
neighboring cells, propagating
the infection

5. Listeriosis
• More common in domestic animal (domestic
mammal and poultry), especially ruminants, than
in human beings.
• It can also occur in feral animals among others, game
animals as well as in poultry and other birds.
• The causative bacterium lives in the soil and in poorly
made silage and is acquired by ingestion.
• The disease is usually sporadic, but can occur as farm
outbreaks in ruminants.

6. Cont.
Three main forms are usually recognized throughout the
affected species:
• encephalitis, the most common form in ruminants
• late abortion
• gastro-intestinal septicemia with liver damage,
in monogastric species as well as in preruminant calves
and lambs

7. Common Hosts
Common hosts includes:
• Sheep
• Horses
• Pigs
• Dogs
• Cats
• Rabbits
• Humans.

8. Zoonotic

9. Effects
• Can cause meningitis and
Meingoenphalitis
• In particularly in neonates
and elderly
• Abortions in pregnant
women, and still birth
• Asymptomatic colonization
in vagina produces
infertility

10. Who are at risk
• Pregnant women
• New-borns
• People with weakened
immune systems
• People who are taking
immuno-suppressing
medication.

11. 20 times more likely than
other healthy adults to get
New-borns rather than the pregnant
women themselves suffer the serious
effects of infection in pregnancy.

12. Signs
• Vomiting
• Nausea
• Cramps
• Diarrheal
• Severe Headache
• Constipation
• Stiff Neck
• Confusion
• Persistent fever.

13. Events

17. Etiology
Listeria monocytogenes Gram-positive,
rods.
Sheep blood agar  haemolytic
(virulence).
Soil (one year), decayed herbage, feces,
saliva, grow at 3-45 ͦ C, pH 4.5 – 9.
Susceptible to common disinfectants.

18. Epidemiology
• Case fatality high.
• Source of infection by environmental even
milk from infected dams in bacteraemia.
• Mode of infection  ingestion 
abrasions in buccal cavity  cranial
nerve.

19. Predisposing factors
• Factors decrease the animal resistance
(sudden change in weather, poor
nutrition,)
• Feeding on silage with improper
fermentation (pH > 5)

20. Pathgenesis
• Ingestion  intestine bacteremia  localized in
various organs or septicaemia.
• invasion of placenta  necrosis of placenta  abortion.
• inflammation of brainstem  unilateral.

21. Clinical Signs
• Circling
• Head deviation
• unilateral facial paralysis
• dropped jaw
• drooling saliva
• Ataxia with falling to one side,
recumbence
• May be fever 40c
• Death due to respiratory
failure.
• Course 1-2 weeks.

22. Cont.
• Sporadic abortion
• Last 3rd
of pregnancy
• Retained placenta
• Some ewes die from
septicaemia
• Start with fever
• Diarrhoea
• Die in 12 hours.

23. Postmortem Lesions
• Aborted lambs  miliary gray-white
necrotic foci on liver, placentitis.
• Microscopically; medulla oblongata,
pons unilateral microabscessation,
• Acute vasculitis and prevascular cuffing.

24. Diagnosis
• Signs.
• History of silage feeding.
• Histopathology of brain.
• Demonstrate the Listeria and
culturing it.
• From CSF, Blood, and other
fluids

25. Treatment
• Penicillin 44,000 iu/kg especially after abortion and in
early septicemia.
• Ampicillin – amoxicillin+ sulphonamide.
• Gentamycin and Ampicillin on clinical basis.
• Intravenous Trimethoprim – Sulphmethoxazole
• Cephalosporins and Fluroquinoles are not active against
l.monocytogens

26. Control
• Provide good silage; no mould, good fermented, no
grazing in silage fields.
• Rodent control will prevent spread of bacteria.
• Avoid spoiled or moldy silage and silage from the top
layer (few inches) which has been exposed to air. Any
leftover silage should be removed from the feedbunk
after feeding.
• Vaccines are available in some countries, however
results are questionable, which leads to questions about
the cost-benefit of vaccination.

28. Introduction
• Colibacillosis is a broad term that refers to any infection
or disease caused by the bacteria Escherichia coli.
• These infections include colisepticemia, coligranuloma,
veneral colibacillosis, coliform cellulitis, peritonitis,
salpingitis, orchitis and enteritis.
• In mammals, colibacillosis is usually a primary intestinal
or urinary tract infection.
• Colibacillosis in poultry is usually a secondary disease
that occurs when the host’s immune system has become
overwhelmed with virulent E. coli strains.

29. Cont.
• Diarrhea associated with Escherichia coli can occur in
young within a few days of birth through well after
weaning. Occasional cases of septicemia are attributable
to E. coli.
• It is associated with many different kinds of diseases
ranging from respiratory tract infection to swollen head
syndrome in poultry to urinary tract infections.
• Colibacillosis is a common disease that is seen
worldwide and is of significant economic importance
concerning the loss of livestock.

30. Cont.
• There are many different types
of E. coli, each of which may
possess several of many
virulence factors.
• Many outbreaks occur within the
first week after birth.
• 1-2 weeks after weaning or
following abrupt changes in
environment or nutrition.
• E. coli can infect hosts as either
a primary or secondary
pathogen.

31. Common Hosts
It is the most common infectious bacterial disease
in:
• Cattle.
• Goats.
• Poultry.
• Pigs.
• Most of avian species.
• Some other mammals.

32. Etiology
• Pathogenic strains of E. coli are easily isolated, Gram-
negative, flagellated bacilli. Most pathogenic strains form
smooth to mucoid colonies; some are beta-hemolytic.
• Virulence factors include fimbria (pili), enterotoxins
(exotoxins), endotoxins, and capsules. Fimbria are the
small hair-like processes on the bacterial surface that
allow attachment to specific receptors on the surface of
mucosal enterocytes of the small intestine.

33. Epidemiology
• Potentially pathogenic E. coli are present in the intestinal
tract and feces of many normal animals. Dams often act
as immune carriers. Poor sanitation and chilling, can
increase the risk of colibacillosis.
• Pathogenic coliforms are magnified by fecal shedding to
further increase exposure of littermates. Disease
occurrence and severity is related to dose ingested and
the level of immunity derived from colostral immunity.

34. Cont.
• Pathogenic coliforms survive in
contaminated buildings and can infect
successive litters of other.
• Once present, E. coli tend to persist
unless vigorous efforts are given to
maintaining sanitation, husbandry, and
environment.

35. Pathogenesis
• Ingested pathogenic E. coli adhere to receptors on microvilli of
enterocytes via pili. There they colonize, proliferate, and elaborate
enterotoxins that cause excessive secretion of fluid and electrolytes
by crypt epithelial cells which markedly exceeds absorptive capacity
resulting in a net flow of tissue fluids into the lumen. This reduces
the absorption of electrolytes, water and endogenous secretions
from the lumen.
• The large intestine, sometimes also affected, is unable to absorb the
excess fluid and diarrhea results. Damage to epithelial cells
sometimes leads to septicemia. Diarrhea usually continues until
death results from dehydration and metabolic acidosis or from
terminal septicemia.
• Environmental factors (temperature, humidity, sanitation, etc.) are
critical.

38. Clinical signs
• Colibacillosis usually is signaled by the appearance of
diarrhea. The severity of the diarrhea varies. The
hypersecretory diarrhea usually has an alkaline pH but
varies in color. It may be clear and watery, especially in
neonates, but may be white or yellow, influenced by type
of ingesta and duration of the disease.
• As diarrhea continues, there is progressive dehydration
and the hair coat becomes roughened. Body
temperature often is subnormal. Shivering often is noted
unless an adequate supplementary heat source, such as
heat lamps, is available

39. Signs
• Severe diarrhea
• lack of appetite and water consumption
• Unresponsiveness
• lameness
• Stunted growth

40. Severity
• Morbidity and mortality are very variable
depending on which infection/infections the E.
coli strain causes in a particular flock of animals.
However, almost all flocks exhibit some degree
of mortality due to an outbreak of colibacillosis.
• Highly virulent strains of E. coli cause the hosts
to become sick and die within a few hours,
• Mildly affected flocks can take days to show
morbidity.

41. Lesions
• Dehydration is the most obvious clinical sign.
• The small intestine and colon may contain excess watery
fluid or may be distended and gas-filled.
• There may be mild reddening and congestion of the
stomach.
• Microscopy of the mucosa of the small intestine reveals
many coliforms adhered to microvilli of intestinal
epithelial cells. Villi usually are intact. With some strains
of E. coli, there may be necrosis of some villi and
microvascular thrombosis in the lamina propria.
• E. coli is a common cause of septicemia in neonates. In
those cases, there is fibrinous polyserositis and arthritis.

42. Diagnosis
• Typical signs and lesions are useful but not
definitive.
• The isolation of a uniform and high population of
smooth, mucoid, or hemolytic E. coli from the
small intestine is suggestive of colibacillosis.
• Isolation, sero-typing, pathology. Aerobic culture
yields colonies of 2-5mm on both blood and
McConkey agar after 18 hours - most strains are
rapidly lactose-fermenting producing brick-red
colonies on McConkey agar.

43. Dx
Diagnostic labs often use one of the following methods to
more specifically identify the pathogenic E. coli:
• A slide agglutination test can identify the serogroup but
does not confirm pathogenicity.
• Adhesin(s) can be identified using monoclonal
antibodies.
• A polymerase chain reaction (PCR) can identify the
pathogen genetically.

44. Cont.
• Diagnostic methods do not identify important contributing
factors such as chilling, poor sanitation or starvation.
These often must be corrected if prevention or treatment
is to be successful.
• Colibacillosis has to be differentiated from other diarrheal
diseases of young. These include transmissible
gastroenteritis (TGE), rotaviral infection, coccidiosis and
Strongyloides parasitism. Starvation is also a major
differential diagnosis.

45. Treatment and Prophylaxis in Travelers
diarrhea
• Doxycycline,
• Trimethoprim,
• Norfloxacillin
• Fluroquinolones
• Avoid contaminated food,
• Safe protected water ,prefer bottled water,
• Hot foods, Hot Drinks,
• Boiled milk

46. Treatment
• Amoxycillin
• Tetracyclines
• Neomycin (intestinal activity only)
• Gentamycin
• Ceftiofur (where hatchery borne)
• Potentiated sulphonamide
• Flouroquinolones.

47. Control & Prevention
• Colibacillosis is related largely to problems in housing
and management which cause the disease secondarily.
• Breeding stock should be obtained from a single source
with no problems of colibacillosis. Dams should be
acclimatized together for 3-6 weeks prior to breeding and
during gestation so they can develop immunity to
endemically occurring pathogens. This allows for the
production of an adequate amount of specific antibodies
in colostrum and milk.

48. Cont.
• To enhance the immunity by using vaccines made from
bacterial pili or toxins or both.
• Pregnant dams often are vaccinated twice at 2-3 week
intervals prior to birth.
• Increasing colostral antibodies is feeding some farrowing
house waste to sows during late gestation.
• Use of the all in/all out system of raising is suggested.
• Giving birth to young should occur in a facility thoroughly
cleaned, disinfected, and dried.
• Clean, Dry and hygienic conditions in order to reduce
stress.

49. Cont.
• When precautionary efforts fail, a system should be
available to treat young immediately if signs of
colibacillosis appear. Antimicrobials can be administered
to neonates orally or by injection.
• Antibiotics can be given in water.
• Oral electrolyte replacement solutions sometimes are
used to help control dehydration.
• Various products may aid in prevention of postweaning
colibacillosis. Plasma proteins, zinc oxide, organic acids,
and probiotics are commonly used.

50. Cont.
• Some are genetically resistant to certain
fimbriae of pathogenic E. coli. Breeding for
genetically related resistance eventually may
help control some forms of colibacillosis.