Non-respiratory bacterial diseases in poultry Flashcards

1
Q

Another term for salmonelloses in poultry.

A

Pullorum disease
Fowl typhoid
Fowl paratyphoid

These are all caused by different salmonella spp.

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2
Q

Pullorum disease is a disease of chicks caused by

A

Salmonella pullorum and characterized by septicaemia and high mortality.

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3
Q

Fowl typhoid is a chronic disease of older chicks and adult birds caused by

A

Salmonella gallinarum, characterized by diarrhea, drowsiness and emaciation.

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4
Q

Fowl paratyphoid is a zoonotic infectious disease caused by

A

a variety of Salmonella spp., characterized with latent course in birds, but causing
disease in humans who eat inadequately cooked poultry meat or eggs.

Notifiable disease!

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5
Q

Describe Salmonella spp.

A

Motile, facultatively anaerobic Gram- bacteria.

Zoonotic!

Two species, more than 2600 serotypes.

Salmonella enterica
Salmonella bongori
+ all the various subspp.

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6
Q

Salmonella enterica: six subspecies, S. enterica subsp. enterica has pathogenic serotypes.

Name 2 main subspp. to affect poultry.

A

S. Pullorum ja S. Gallinarum:
non-motile, variable in size, host-specific (chickens, turkeys, quails, pheasants, ducks, geese and pigeons).

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7
Q

Virulence factors in Salmonella spp.

A

Virulence factors: fimbriae, invasins, enterotoxins, endotoxins

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8
Q

Which salmonella spp. are more dangerous to humans?
Where do humans get them from?

A

Salmonella Typhimurium, Salmonella Infantis and Salmonella Enteritidis

Source: fresh chicken eggs and chicken meat, contaminated food, cross
contamination in the kitchen.

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9
Q

Salmonella Pullorum typically affects what age birds?
Causes what?

A

in chicks up to 3 weeks of age

Septicemia, white bacterial diarrhea

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10
Q

Salmonella Gallinarum typically affects what age birds?
Causes what?

A

in adults and young birds, but also in chicks

Septicemia, acute or chronic course.

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11
Q

Source of salmonella infection:

A

 Birds (incl. wild birds)
 Animals (incl. wild animals and rodents)
 Insects (incl. blood-sucking)

Recovered birds become asymptomatic carriers with local ovarian infection.

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12
Q

transmission of salmonella

A

Excretion: faeces

Transmission:
 Direct horizontal: eating eggs, birds, blood-sucking insects, people

 Indirect horizontal: contaminated water, feed, fomites, etc.

 Aerogenic: aerosols, dust (chicks)

 Vertical: transovarial

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13
Q

IP of salmonelloses.

A

Incubation period: 4-6 days

Recovered birds become asymptomatic carriers with local ovarian infection.

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14
Q

Where is salmonella found?

A

Salmonelloses are always a threat in poultry farms with gross and intensive production.

Prevalent everywhere. Every year people get infected. One of the four major causes of diarrhea globally.

Salmonella spp. has some resistant serotypes affecting the food chain.

Eggs and meat from infected or sick birds shall not be allowed to be resold or processed for human consumption.

Notifiable disease!

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15
Q

Clinical signs of Pullorum disease and fowl typhoid in chicks.

A

Peracute illness: sudden deaths

Acute illness: chicks seek heat,
drowsiness, not eating, white pasty
diarrhea, feathers around the cloaca are dirty, wings dropped.

Less commonly blindness, breathing
difficulties, hock joint swelling.

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16
Q

Clinical signs of Pullorum disease and fowl typhoid in older chicks and adult birds.

A
  • Not characteristic
  • depression, body temperature increase 1-3’C.
  • Loss of appetite, anorexia
  • White diarrhoea, dehydration
  • Poor plumage, comb paleness
  • Breathing difficulties
  • Decrease in egg production and fertility
  • Joint (especially hock joint) inflammation
  • Low mortality
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17
Q

Clinical signs of Fowl paratyphoid
in chicks.

A

Mortality is highest in the first few weeks of
life - Sudden deaths.

Huddling, Progressive depression, drowsiness, lethargy, closed eyes.

  • Droopy wings, poor feathers
  • Slow growth, weight loss, anorexia
  • Profuse watery diarrhoea, dehydration
  • Secondary infection → acute septicaemia.
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18
Q

Clinical signs of Fowl paratyphoid
in older chicks and adult birds.

A

Clinical disease is not characteristic.

  • Decreased egg production and quality
  • Infected eggs → high embryonic
    mortality.
  • Anorexia
  • Diarrhea
  • In some cases, blindness and limping.
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19
Q

Post mortem signs of Pullorum disease and fowl typhoid in chicks.

A

Peracute (sudden deaths): no findings.

Acute:
* Retained yolk sac, creamy caseous yolk sac contents.

  • Enlarged, dense liver, spleen and kidneys
  • Greyish-white spots in the liver, white nodules in the lungs, spleen, heart, intestines and gizzard.
  • Creamy caseous cecal crusts
  • Thickened pericardium, yellow serous/fibrinous exudate in pericardial cavity.
  • Swollen joints, accumulation of the yellow viscous liquid
  • Excessive exudate in the anterior chamber of the eyes
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20
Q

Post mortem signs of Pullorum disease and fowl typhoid in adult birds.

A

Damage often minimal.

  • Egg follicles of irregular shape, unnatural color, cystic or nodular follicles with oily and/or caseous content.
  • Caseous exudate in the oviduct
  • White caseous lumps may be present in the lungs and air sacs.
  • Swollen, brittle and often bile-stained liver.
  • occasionally Fibrinous peritonitis and perihepatitis, adhesions between organs.
  • Roosters: white nodules can be found in testicles
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21
Q

Post mortem signs of fowl paratyphoid in both chicks and adults.

A
  • Septicaemia, high mortality, few
    visible lesions.
  • Omphalitis, yolk sac inflammation
  • Bloody or watery yellow fluid in a
    yolk sac.

Longer course: enteritis, necrosis of
the intestinal mucosa.

  • Reddish-brown pseudomembrane
    and white to yellow caseous
    exudate in the ceca.
  • Enlarged liver, pale to hemorrhagic foci of necrosis.
  • Accumulation of fibrin or fibrinopurulent exudate on the surface of the heart, liver, lungs and other internal organs, as well
    as in the eye (hypopyon) and wing or leg joints (arthritis).
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22
Q

Material for Diagnosis of salmonelloses in poultry.

A

Material: faeces, blood, live birds and
carcasses

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23
Q

Lab analyses for Diagnosis of salmonelloses in poultry.

A

Analyses: guide to standard procedures in
EU (ISO 6579-1:2017). Strict! You must follow the standards.

Bacteriological analysis: gives a true
diagnosis.
- Faeces, organs cultured on specific media
- Diagnosis is based on isolated and confirmed Salmonella spp.
- Serotyping: White–Kauffmann–Le Minor’
system

Blood agglutination test
- Regular study of 10% of the breeding birds
(Salmonella monitoring plan).

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24
Q

Treatment of salmonella in birds.

A

Production birds are not treated.

No drug is able to completely eliminate the pathogen.

Other birds:
- Drugs With the feed or water
- Prophylactic and therapeutic treatments

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25
Q

Prevention of salmonelloses in birds.

A

biosecurity, vaccination

Strict veterinary sanitary regulations & National control programs.
Rules for the control of salmonellosis (surveillance).

Vaccination, longer downtime
Control of wild birds, rodents and other pests

New chicks from serologically tested flocks
Prevention of pullorum disease: spraying eggs with neomycin and fumigation.

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26
Q

Surveillance of salmonelloses.

A

The prevalence is continuously
monitored at farm level.
- Before slaughter, in slaughterhouses,
before the start of lay.

Only Eggs and meat from farms, where
Salmonella spp. is monitored, can be
sent to the food industry (otherwise youre unable to sell it).

For bacteriological examination;
fecal and cloacal swabs, or sock samples are collected and tested.

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27
Q

What is a sock sample/boot swab?

A

a method used to collect environmental samples from poultry houses.

Before changing/refreshing bedding.

Special socks are placed on sterile footwear.

Walking at least 100 steps to cover the entire building and all departments.

The stool should remain on socks → dirty.

Socks removed from the shoes are placed in a sterile container. Samples must be immediately and accordingly sent to the
laboratory. Samples must not be in a hot environment before testing.

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28
Q

Review this table on sample types in salmonella surveillance.

A

sock samples, fecal samples, and other samples can be taken.

from egg-layers, meat birds or other flocks.

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29
Q

Salmonella Control program in Finland

A

Vaccination of birds and treatment with antimicrobials is prohibited.

Less than 50 birds on the farm → rules are not so tight.

Active monitoring: regular sample collection and investigation –
frequency depends on bird species and production goal.

Samples represent all the birds in the farm.

The result is known before the birds are sent to the slaughterhouse.

Resampling and testing 6 weeks later (if necessary).

Where and when needed, the study of feedstuffs is done.

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30
Q

If a sample if found positive for salmonella:

A

Positive sample: slaughtering of birds, sending eggs for sale or meat for poultry production, or introduction of new birds is prohibited.

Sending birds for eradication is allowed, but the farm is quarantined, dogs must not roam the farm freely.

Decontamination program: emptying, cleaning and disinfecting buildings, followed by testing.

 Pos. result → it’s necessary to redo the
decontamination
 Neg. result → the aviary can be repopulated

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31
Q

Clinical signs of Salmonellosis in humans

A

Incubation period: 6-72h, if not treated, acute phase lasts 4-7p, carrier status for 2
months afterwards.

Stomach cramps, fever, vomiting and diarrhea, tenesmus.

Reactive arthritis, eye irritation, painful urination rare.

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32
Q

Diagnosing Salmonellosis in humans

A

Diagnosing via faecal and blood samples (antibodies), vomited masses, food residues.

 DNA fingerprint, serotyping and culture, electrophoresis

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33
Q

Treatment of Salmonellosis in humans

A

Fluid therapy + broad-spectrum AB, elongated periods.

Empirical treatment: ampicillin, biseptol, fluoroquinolones, gen. III cephalosporins,
ciprofloxacin.

Resistance plasmids: fluoroquinolones, gen. III cephalosporins.

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34
Q

Clostridiosis is an acute infectious disease of the Gallinaceae, characterized by

A

hemorrhagic-ulcerative inflammation of small intestine and parenchymal dysfunction.

35
Q

Describe Clostridial spp.

A

Gram+, facultatively anaerobic, endospores-forming rod-shaped bacteria.

Approx. 80 species, 12 are pathogenic.

Live in soil, food, litter.

Better developed in high humidity and temperature and low oxygen content.

Some are part of the normal microflora of animals (incl. humans) → morbidity due
to immunosuppression.

Produce toxins: Alpha, Beta, Epsilon, Iota

36
Q

Describe the Epidemiology of clostridium spp.

A

Widespread everywhere

Can cause major economic losses, especially after stopping the use of prophylactic antimicrobials.

Different age groups are susceptible, especially young ones.

Risk factors: intestinal wall damage, imbalanced feeding, bad housing conditions.

37
Q

Transmission of clostridiosis.

A

Excretion: feces

Transmission:
- Contaminated feed, drinking water, bedding, soil, equipment, etc.

Direct contact: latent carriers

The course is fast, mortality varies (dependent on species).

Infected birds often remain carriers.

38
Q

3 main spp. of clostridium to cause clostridiosis:

A

Cl. perfringens
Cl. colinum
Cl. botulinum

39
Q

Clostridium perfringens: necrotic enteritis
Susceptible species
Reservoir hosts

A

Susceptible species: birds, cattle, sheep, pigs, dogs, people
- Especially broilers and turkeys

Reservoirs: rodents

40
Q

Clostridium colinum: ulcerative enteritis, quail disease
Susceptible species
Reservoir hosts

A

Susceptible species: birds (quails, turkey and chicken chicks)

Reservoirs: flies, frogs, rodents

41
Q

Clostridium botulinum: paralysis, rare in birds
Susceptible species
Reservoir hosts

A

Susceptible species: birds, cattle, horses, people, mink
Reservoirs: fish

42
Q

Course of disease in Cl.perfringens.
Clinical signs?
Post mortem findings?

A

Acute or subclinical.

Signs: bloody diarrhea, salivation, depression, death in 3 days when acute.

Post mort.: SI mucosa thick, hemorr., necrotized. Hepatomegaly with hemorr.
Spleenic atrophy.

43
Q

Course of disease in Cl.colinum.
Clinical signs?
Post mortem findings?

A

Acute or chronic.

Clin.signs:
sudden death
hemorrhagic enteritis
kyphosis (hunchback)

Post mort.:
SI hemorrhagic enteritis
GI tract ulcers
peritonitis
liver/spleenic necrosis

44
Q

Cl.botulinum.
Clinical signs?
Post mortem findings?

A

Clin.signs:
diarrhea
visual, auditory, resp. impairment
paralysis

Post mort.:
gaseous gangrene
enterotoxemia
parenchymal organ necrotic inflammation

45
Q

Diagnosis of clostridiosis in birds.

A

Can be tricky due to being part of the normal microflora.

 Cl. perfringens – jejunum, PCR
 Cl. colinum – intestines, liver, blood, spleen, PCR, IFA.
 Cl. botulinum – bird food or tissue, PCR,
inoculation (mouse).

Microbiological isolation of the bacterium.

Preparation, staining and microscopy of the smear preparation of intestinal contents, intestines, intestinal lymph nodes or liver.

Serological examination for effective treatment.

46
Q

treatment of clostridiosis in birds.

A

Antibiogram!

First choice: penicillins, tetracyclines, bacitracin, furazolidone, streptomycin.

Resistance: clindamycin, metronidazole

47
Q

Prevention of clostridiosis in birds.

A

Good keeping and feeding conditions, avoiding stress and new birds, quick removal of sick and dead birds.

Keeping the diet in balance, pro- and prebiotics. Control of contamination of feed
and drinking water, clean environment.

Vaccine is available (Cl.perfringens)

Control of parasites and rodents.

48
Q

clostridiosis in humans

A

Cl. perfringens – food poisoning and gaseous gangrene.

Cl. botulinum – nausea, vomiting, diarrhea

Mostly followed by neurological symptoms (e.g. swallowing difficulties).

In more severe cases, cessation of breathing causes death.

Death as a result of cardiac arrest is less frequent.

49
Q

Colibacteriosis is an infectious disease in many animals that is characterized by

A

fatal septicemia or subacute pericarditis, airsacculitis, salpingitis and/or peritonitis in birds.

50
Q

APEC stands for?

A

avian pathogenic Escherichia coli

51
Q

Causative agent of colibacteriosis in birds?

A

APEC (avian pathogenic Escherichia coli)
- Gram–, rod-shaped, facultatively aerobic bacterium.

Part of the intestinal normal microflora.
Healthy, adult animals and birds rarely get sick.

Occurrence in water or feed → fecal contamination.

Destroyed by temp. over 80’C and disinfectants.

By lysis of the bacterium, the endotoxin of the cell wall is released → triggers septic shock.

52
Q

Epidemiology of colibacteriosis in birds.

A

Prevalent all over the world.

Causes great economical losses –
mortality increases, low productivity
of surviving birds.

Acute infectious disease In birds of all ages.
- Hatchlings are more susceptible

Causes a variety of manifestations of illness.
- Airsacculitis, cellulitis, coligranuloma, omphalitis, septicemia etc.

53
Q

Clinical signs of colibacteriosis.

A

Review this table.

54
Q

Post mortem signs of colibacteriosis.

A

Review this table.

55
Q

Diagnosis of colibacteriosis.

A

Microbiological study of organs with pathological changes.

Samples: heart, liver, spleen, bone marrow

 McConkey agar, Drigalski agar

Blood and excretions

Isolation & clarification of the
pathogenicity of the E. coli strain.

 PCR, ELISA

56
Q

Treatment and prevention of colibacteriosis.

A

 Resistance to many antimicrobials
 “Use as often as needed and as
rarely as possible”

Fluoroquinolones have proved to be
the most effective antimicrobials.
 Enrofloxacin and marbofloxacin.

 Live vaccines exist for extraintestinal
coliforms, but not for much use.
 Vaccinate also against disease-causing diseases.

57
Q

Campylobacteriosis is an infectious disease occurring in many animal species,
characterized mostly by

A

subclinical course or transient diarrhea in birds, but causing acute gastrointestinal disease in humans.

58
Q

Describe the causative agent of campylobacteriosis.

A

Campylobacter spp.
 Gram– microaerophilic spiral bacterium

 Optimum growth at 37-42 °C
 Mammalian, reptilian, and avian bacterium

Most common in birds:
C. jejuni (most pathogenic), C. coli and C. lari

 C. jejuni survives less than 1 week in the environment

 Neutral pH and at least 10% moisture are needed for survival

 C. jejuni is one of the most common food poisoning agents

 C. hepaticus, C. bilis – laying hens, „spotty liver disease“

59
Q

one of the most common food poisoning agents

A

C. jejuni

60
Q

Epidemiology of Campylobacteriosis

A

Zoonosis!
Widespread in the world

Susceptible species: chicken, turkey, goose, dove, duck, etc.
Mostly in chicks

Usually asymptomatic carriers, pathogen is found in the intestines.

Spontaneous recovery and recurrence are characteristic.

61
Q

Transmission of Campylobacteriosis

A

Spreads through the herd within a couple of weeks. Spreads with faeces, respiratory droplets.

62
Q

Mortality of Campylobacteriosis

A

Particularly high mortality is observed among fledglings.

In adults, the mortality is low, in laying chickens up to 15%.

63
Q

Campylobacteriosis Clinical disease usually occurs in birds with

A

coccidiosis and/or roundworms

64
Q

Clinical signs of Campylobacteriosis in chicks.

A

Incubation period 1-4 days

  • Lethargy, anorexia
  • Diarrhoea (usually yellowish in colour, small amount of blood may occur)
65
Q

Clinical signs of Campylobacteriosis in adults.

A

In the peak period of egg laying, in
free range systems.

  • Decrease in egg production up to 25%

Sudden deaths: septicaemia and
toxaemia.

  • Dull, ruffled, discoloured feathers
  • Beak/nail overgrowth
  • Lethargy, weakness
  • Shrunken comb
  • Signs do not occur in all birds
66
Q

Post mortem signs of Campylobacteriosis in chicks.

A
  • Enlarged, pale or greenish liver
  • Catarrhal/haemorrhagic enteritis, mostly in the end of small intestine and caeca
  • Mucus and blood in the intestinal content
67
Q

Post mortem signs of Campylobacteriosis in adults.

A
  • Focal hepatic necrosis of various
    degrees of severity (spotted liver)
  • The liver may be slightly enlarged with moderately rounded edges
  • Foci of necrosis may coalesce
68
Q

Diagnosis of Campylobacteriosis

A

 Isolation of bacteria from damaged tissues.

 Culture from the fecal sample in live birds.

69
Q

Treatment of Campylobacteriosis

A

 Can’t completely eradicate from the flock.

 Erythromycin, tetracycline or streptomycin.

 Pet birds: treating is questionable

70
Q

Prevention of Campylobacteriosis

A

All-in/all-out, decontamination, hygiene, biosecurity, proper keeping, parasite control.

71
Q

Campylobacteriosis in humans

A

Source: uncooked or insufficiently cooked
poultry products, raw milk, contaminated
water.

Most common source: poultry meat (> 50%).

Poultry carcass gets contaminated when
intestines are broken, milk contamination occurs with bad milking hygiene.

Prevention: good personal hygiene

Food warming over +70 °C, poultry meat over +75 °C.
Storing food over +60 °C or below +6 °C.
Care when preparing raw meat.

72
Q

Poultry erysipelas is an infectious disease of turkeys and birds kept close to water
bodies, characterized by

A

acute course, septicemia and sudden
deaths.

 Acute and chronic illness

73
Q

Describe the causative agent of Poultry erysipelas.

A

Gram+ Erysipelothrix rhusiopathiae
- short, nonmotile, rod-shaped bacterium

Better known as the causative agent of swine erysipelas.

Highly resistant to the environment (survives 4-8 months in urine/faeces).

74
Q

Erysipelothrix rhusiopathiae serotypes:

A

22 serotypes
- Most of the isolated strains are serotype 1 and 2.

  • Serotype 1 is considered to be the cause of acute disease.
75
Q

Epidemiology, host range, age of poultry erysipelas.

A

NB! Zoonotic pathogen! Mammals, birds, and fish can get sick (including humans).

Widespread in nature
More often in summer and autumn.

In turkeys and free-range chickens commonly.

In geese, pheasants and ducks rarely.

In all age groups, more in males and older birds.

76
Q

Transmission of poultry erysipelas.

A

Sources: sick or asymptomatically ill/carrier birds.

Excretion: urine, faeces, saliva and nasal secretions

Transmission: peroral, wound infections

Eating fish, traumas, cannibalism, blood-sucking insects, rodents, contaminated feed.

77
Q

Morbidity & mortality of poultry erysipelas

A

Morbidity 40-50%,
mortality usually <15%

 40% to 50% in naive/unvaccinated flocks

78
Q

Clinical signs of poultry erysipelas.

A
79
Q

Post mortem signs of poultry erysipelas.

A
80
Q

Diagnosis of poultry erysipelas.

A

Material: damaged tissues, blood,
dead bird

Analyses:
 Isolation and identification
(Isolation of the pathogen on blood
agar; Colonies on medium are very
small)

 PCR, ELISA and IFA

81
Q

Treatment of poultry erysipelas.

A

Treatment: antibiotics (broad-spectrum are the best), at early stage.
 Penicillin, cephalosporins, clindamycin, fluoroquinolones
 Antibiogram (drug resistance)
 given SC or with drinking water

In the event of an acute outbreak give to healthy birds also.

82
Q

Prevention of poultry erysipelas.

A

vaccination, hygiene, biosecurity

 Inactivated and live vaccines
 2 times within 2-3 weeks IM or with drinking water

 Proper handling of dead birds
 Stress reduction, health monitoring

83
Q

Define Erysipeloid.

A

The disease in ppl, that is caused by Gram+ Erysipelothrix rhusiopathiae.

alt. term ‘Fish poisoning’ because can be transmitted via raw fish too.

 Usually when handling raw meat or in direct contact with the sick animal.

 NB! Occupational risk!

Inflammation of skin and subcutaneous tissue (cellulitis). Characterized by reddening skin rash and systemic symptoms.

May also cause inflammation of the heart or kidneys, or pneumonia.

Prevention: treatment of scratches, use of
gloves.