CLOSTRIDIAL DISEASES
General characters of clostridia describe in several points:
 Clostridia are large, anaerobic, Gram-positive bacteria.
 Most of which produce spores that are resistant to high temperatures and many disinfectants.
 They able to produce toxins.
 There are 8 antigenically different toxigenic groupings (A, B, C alpha, C beta, D, E, F and G).
 Human disease has been associated mainly with type A, B, E and F.
Botulism “limber neck “
western duck sickness".
Intoxication due to ingestion of Clostridium botulinum type C
(exotoxins) under anaerobic conditions at 10° - 47°C with
optimal toxin production 35-37°C"
Free ranging and confinement reared poultry and feral birds
can be affected.
• CL. botulinum is a Gram positive, spore forming
bacterium capable of elaborating potent exotoxins.
• Cases of botulism in chickens, ducks, pheasants and
turkey caused primarily by type C toxigenic group while
A, B, E have caused disease in birds.
Hosts:
Poultry: Chickens, turkeys, ducks, pheasants and ostriches.
In broiler chickens, ages ranged from 2 to 8 weeks outbreak
in older broiler chickens has been reported.
Mammals: affected by type C toxin include mink, ferrets,
cattle, horse, dog and variety of zoo animals.
Transmission:
1. External toxins: Contaminated feed / water, animal
carcasses, maggots, litter, stagnant ponds and decaying
vegetation and insects.
2. The sites of production of Internal Toxins include caecum
and crop and high intake of iron in the D.W / feed.
3. Type C organisms grow in GIT of birds as obligate
parasites.
4. Concentration of these organisms in the environment
and their opportunity to produce toxins can be
influenced by standard of management.
Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT.
Distribution:
Ulcerative Enteritis (Quail Disease, UE)
An Acute bacterial infection in young chickens’ turkeys
characterized by high onset and rapidly increasing
mortality.
The disease was first seen in quail and was, therefore,
named quail disease, it has since been established that
many avian species other quail are susceptible, and
earlier name has superseded by ulcerative enteritis.
Aetiology
• Clostridium colinum, Gram positive bacillus that
occurs singly as a straight or singly curved rod with
rounded ends.
• Sporulation is rarely seen in media but if spores are
subterminal
Epidemiology
Hosts:
1. Wide range of avian hosts, + quail all ages (young).
2. Natural infections have been found in bob white
quail.
3. Domestic chickens, turkeys are commonly affected of
(4-10 weeks).
Transmission
1. UE is transmitted through droppings, birds become
infected by ingestion contaminated feed, water, or
litter.
2. The organism produces spores, resulting in permanent
contamination of premises.
3. Influencing factors as coccidiosis, immuno-
suppressive factors such as IBD, CAV and other and
also overcrowding and inadequate hygiene.
 They are ubiquitous worldwide, being found in soil, dust, animals, insects’ larvae and they are frequently found in low
numbers in the intestinal tract of normal birds.
 Some are opportunistic pathogens and for these there are factors which predispose to outbreaks of disease in a flock or
individual birds.
Influencing factors:
 These factors include management particularly associated with feed, overcrowding and inadequate hygiene.
 In addition, perhaps genetic constitution may also be significance.
Gangrenous Dermatitis (GD)= Gangrenous cellulitis = Wing rot
Necrotic Enteritis (NE)
= Blue wing = Avian malignant edema = Necrotic Dermatitis,
Def
Disease of primarily young chickens, caused by infection & toxin It is skin disease of chickens and turkeys caused by
production by Clostridium perfringens type A and type C. Clostridium perfringens type A, CL. septicum or/+
The clinical infection is characterized by sudden onset, high Staphylococcus aureus.
mortality and necrosis of the mucous membrane of small Primary lesion is necrosis of the skin and subcutaneous tissue
intestine. usually involving the breast, abdomen, wing or thigh.
• C. perfringens type A and type C (Gram positive, spore • Caused by Clostridium perfringens type A, CL. septicum
forming, anaerobic), both of these strains are capable of or/+ Staphylococcus aureus.
producing various toxins and enzymes which are responsible • Rarely CL. novyi and other clostridial organisms.
for the associated lesions and clinical signs.
Hosts: Hosts:
1. Chickens: 2 weeks to 6 months of age. Chickens and turkeys and most commonly seen in broilers of
2. A majority of NE have been in 2- to 5-week-old broiler 4-7 weeks.
chickens. Transmission:
3. 3-6 months old commercial layers, turkey poults, 7-12 weeks 1. Clostridia are present in soil, feces, dust, contaminated
old turkey litter or feed and intestinal contents.
Mode of transmission: 2. Staph. aureus is common inhabitant of skin and mucous
Oral route Found in feces, soil, dust, contaminated feed and litter membrane.
or intestinal contents. 3. Contamination of skin wounds by toxigenic clostridia.
Flies
Economic significance:
The economic impact of GD is primarily to the degree of GD-
associated mortality that occurs within a flock.
GD usually affects mature broilers and turkeys and the
economic losses due to the disease. associated with lost in
production.
Poultry Medicine, Bacterial Diseases | 1
 Botulism “limber neck “ Gangrenous Dermatitis (GD)= Gangrenous cellulitis = Wing rot
Ulcerative Enteritis (Quail Disease, UE) Necrotic Enteritis (NE)
western duck sickness". = Blue wing = Avian malignant edema = Necrotic Dermatitis,

• Toxin C acts as neurotoxin at the peripheral chlorogenic
nerve terminus, combining with cell mm. which can result in
blocking releases of acetyl choline leading to muscle
paralysis.
NO PM due to nervous symptoms.
Empty intestine.
Maggots & feathers may present in crop.
Pathogenesis
Lesions
1- Acute:
• Haemorrhagica enteritis (duodenum).
• Small round superficial abscesses & ulcers on the
epithelium of the small intestine, cecum and upper
large intestine. Perforate →… peritonitis.
2- Subacute:
• Liver (necrotic lesions) yellow mottling to large,
irregular yellow areas along the edges.
• Spleen is enlarged and haemorrhagica.
• Cecal ulcer: central depression filled with dark
material.
MO Growth requirement:
• The best medium for isolation C. colinum is tryptase-
phosphate agar 0.2% glucose and 0.5% yeast extract
are added, liver lesions incubated anaerobically for 1-2
days at 35-42°C.
• Colonies convex, circular and have filamentous margins
growth in broth media, growing cultures produce gas.
1. Proliferation o in the L. intestine and cecum. migrate to the S. Probably associated with the nature of the skin wounds which
intestine where toxin is produced (an increase in the pH and allow the clostridia to multiply and produce lethal toxins.
reduced oxygen content in the small intestine)
2. Together with the digestive enzymes, toxins destroy epithelial
Lesions
cells of the gut.
1. Under the wings, between the thighs and over the ribs
and flanks.
Lesions:
2. Skin: dark, reddish, purple, & devoid of feathers
1. Lower small intestine (jejunum + ileum): friable, dilated, and 3. S/C: extensive blood tinged with edema with or without
distended with gas + flacks of blood (NOT heamorrhage) + gases
necrotic epithelial debris 4. There is extensive sloughing.
2. Thick wall + extensive necrotic mucosa which is lined by 5. Red and swollen areas are found on the feet, legs and
tightly adherent yellow to Green Pseudo Membrane "Turkish occasionally round feather follicles of the wings.
towel".
6. Under lying muscle is gray + edema + gas
3. The contents of the intestine may consist of ingesta and 7. Kidney, heart and liver are often congested, the lungs
necrotic epithelial debris, dark brown in colour and are congested and edematous and resemble a mass of
sometimes containing flecks of blood. dark-red jelly.
4. In cholangiohepatitis in broilers, the livers are enlarged, firm 8. Liver may also show changes of inclusion body hepatitis.
and mottled but paler than normal and gall bladders are
also enlarged and may rupture with peritonitis

Clinical Signs
Depending on toxin dose Incubation Period 1-3 days, course of disease in flock 3 1. Birds may be found dead without clinical signs 1. Dark reddish-purple area of skin of breast & wing
IP = 1-2 days and duration up to 5 days. weeks. 2. Depression, movements, appetite, & diarrhea 2. Depression, incoordination, & leg weakness (ataxia) and
1. Neck paralysis (limber neck) & drowning in water fowl. 3. In turkeys, the disease is more explosive, they tend to huddle, death with a few hrs and carcasses rapidly decomposed
2. Leg paralysis. Lameness. Clinical sings suffer diarrhea and develop a high-pitched voice. with a foul odour.
3. Drop wing. 1. Acute: death (NO signs). 4. Morbidity and mortality vary from 1-40% with a mean of 10%. 3. Morbidity and mortality can reach 8-9% in untreated
4. Eyelid paralysis. 2. Watery, white droppings; they are usually well flocks agnosies.
5. Gasping, ruffled feathers, & white diarrhea (urate) in muscled and fat and have feed in crop. Predisposing Factors:
broilers. 3. Depression, ruffled feathers, atrophy in breast muscle Predisposing factor:
6. In birds in captivity, the signs may be predominantly 1. Coccidiosis (Eimeria bruntii and E. necatrix) lead to damage
in affected birds seen 1 week or longer. 1. Skin wounds.
statuesque. to the intestinal wall + Provide Plasma Protein for Cl.
4. Mortality in young quail 100%,
perfringens Proliferation 2. Immune suppressive agents (IBD, CA,
7. Weakness with incoordination of legs → then wings → 5. Chicken losses typically range from 2-10%.
2. Diet-high energy: high protein particularly fish meal, cereals reticuloendotheliosis, avian adeno and reovirus and
neck → flaccid paralysis.
(Wheat / barely) Marek’s) + Mycotoxicosis
8. Mortality & Morbidity: 3. Changes in the diet composition and texture or when 3. Nutritional factors inadequate protein for feather and skin
- Low levels of intoxication produce little mortality and change from starter to grower. Associated with alternation in growth, insufficient vitamin E for immunity and as an
morbidity which can confuse diagnosis. pH. antioxidant, rancid fat in the diet will require an increase
- In severe cases up to 40% Mortality.
4. Litter-old, coarse quality (high fiber) and litter eating by in vit E.
9. Broiler chickens showing signs of botulism may have
stock. 4. Inadequate salt which exacerbates fighting and skin
diarrhea with excess urates in loose droppings.
5. Over-crowding and production of high levels of damage.
10. In many chickens, but not turkeys, the feathers of the
neck are loose and easily shed. corticosteroids.
5. Management factors (overcrowding, unhygienic
6. Inadequate cleaning and disinfection of premises, material.
conditions and inadequate provision of feed and water.)
7. Immuno suppression.
8. Genetics susceptible strains of chickens 6. Removal of contaminated litter and carcasses, and
inadequate cleaning and disinfection between flocks.

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 2
 Botulism “limber neck “ Gangrenous Dermatitis (GD)= Gangrenous cellulitis = Wing rot
Ulcerative Enteritis (Quail Disease, UE) Necrotic Enteritis (NE)
western duck sickness". = Blue wing = Avian malignant edema = Necrotic Dermatitis,

Diagnosis
Clinical signs, absence of gross and microscopic lesions. 1. On the basis of gross lesions. Isolation and identification of organism: 1. Gross lesions.
1- Detection of toxin in crop, GIT washing, & serum 2. Typical intestinal ulcerations accompanied by 1- From intestinal content, the scrapings of intestinal wall by 2. Demonstration of the presence of pathogens which may
Serum is the preferred diagnosis sample. Because C. necrosis of the liver and an enlarged haemorrhagica aerobically incubation over night at 37°C on blood agar include Staph. aureus.
botulinum is found in the gut of normal chickens, toxin spleen plates 3. Presence of immuno suppression is supportive evidence.
can be produced in decayed body tissues. Therefore, 3. Isolation and identification: - Inner zone of complete hemolysis + outer zone of
finding toxin in tissue of dead birds doesn't confirm incomplete hemolysis.
4. Confirmation by cultivation of the organism from DDX
botulism. 2- Sandwich ELIZA, PCR
intestine, liver and spleen. Can be obtained in pure
2- The mouse bioassay is a sensitive and reliable method for 1. Exudative diathesis.
culture from liver.
confirming heat-labile toxin in serum. 2. Ulcerative dermatitis.
5. Biochemical identification. DDX
Groups of mice are inoculated with suspect serum 3. Inf. Cellulitis.
6. Serology: FAT (high specific) + Agar gel Diseases that must be differentiated with NE are.
samples … death in 48hrs
immunodiffusion. 1. NE
Other mice receive samples inoculated with serum
Caused by CL. perfringens
samples + specific antiserum. protected + alive
DDX Lesions in jejunum and ileum with little or no involvement of
3- Ag- capture ELIZA. ceca.
1. Coccidiosis
Isolation of C. botulinum requires anaerobic culture, 2. Ulcerative enteritis
samples inoculated in to cooked-meat medium at 30°C 2. Necrotic enteritis
CL. colinum
after 3-5 days incubation. 3. Histomoniasis.
Multiple areas of focal necrosis and ulceration in the distal S.
4. Frequently, coccidiosis in turkey, chickens and intestine, ceca, & liver
Organism can be detected using the fluorescent
pheasants occur concurrently with UE.
antibody technique. 3. Coccidiosis.
Eimeria brunette Gross lesions similar to CL perfringens, but
microscopically of fecal smears intestinal section show
DDX presence or absence of coccidian.
1. Monensin poisoning in turkeys.
2. Aeromonas intoxication or perhaps lead poisoning of
water fowl.
3. Marek's disease of chickens.

Treatment
• Antibiotics as bacitracin (100g/ton in feed) streptomycin Treatment: Control of Necrotic enteritis Prevention:
(1g/L in water. Penicillin was ineffective
1. Streptomycin (prophylactic and therapeutic) 1. Antimicrobials and coccidiostats (effective against clostridial 1. Good management and practice high standard of
• Sodium selenite and vitamins A, D3
(1g/gallon of D.W) or 60g/ton in feed. and coccidian). hygiene.
Prevention: 2. Bacitracin: 100gm/ton. 2. Antibiotics: tylosine, Penicillin, Ampicillin, Bacitracin. 2. Avoidance of overcrowding of stock.
1. Isolation of sick bird 3. Penicillin 50-100gm/ton Amoxicillin/ Terramycin.
3. Avoidance of supply of contaminated food and water.
2. Disposal of dead carcass 4. Chlortetracycline 20-45mg/kg. 3. Competitive exclusion, probiotics such as lactobacillus
4. Protection of birds against immuno- suppressive agents
3. Fly control reduce severity of NE.
4. D.W acidification by citric acid 4. Diet-maize is less likely than other cereals to support necrotic Treatment:
Prevention:
5. Disinfect contaminated litter by formalin or iodophor enteritis (certain enzymes added to the diet probably 1. Chlortetracycline, erythromycin, oxy, Cu-sulphate
6. Inactivated bacterins and toxoids as vaccines but they 1. Removal of contaminated litter through reducing the viscosity to gut contents).
2. Avoid stresses (overcrowding, coccidiosis under 2. Water acidification by citric acid or propionic acid
are too costly 5. Clean containers with 5% soda hypochlorite or 0.4% QAC.
control, and use preventative measures against viral Vaccination:
6. Litter management by adding NaCl to dirt floor with
diseases which may act as immunosuppressive 1. Mixed clostridia bacterin at one day old
thorough cleaning + acidified litter
factors)
2. OR 5 weeks old chickens with mixed E coli and S. aureus
3. NOT mix carriers with unexposed birds Vaccination: Rare + Not Practical
and C. perfringens bacterin
4. Prebiotic + probiotics 1. Active and passive immunity through vaccination against C.
perfringens
2. Immunizations of chickens with avirulent strain of C.
perfringens followed by an antibiotic treatment
3. oral vaccination with alive alpha-toxin deficient isolate of C.
perfringens.
4. Also, vaccinations against coccidiosis indirect prevent NE
development

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 3
 SALMONELLOSIS
Pullorum Disease = Pd = Bacillary White Diarrhea & Fowl Typhoid FT Paratyphoid infections Paratyphoid Infections: Arizonosis
It is septicemic diseases affecting chicken and turkeys caused by Highly Host Specific M.O. Infection with any organism of salmonella other than S. Acute or chronic disease affecting turkey poults
gallinarum & S. Pullorum characterized by ocular & neurological signs.

Occurrence: worldwide & rarely zoonotic.
Aetiology: S. Pullorum → Pullorum Disease & S. gallinarum →
Fowl typhoid FT.
• Aerobic or facultative anaerobe, non-spore forming,
non-motile belong to serotype D
• It possesses only somatic Antigen (1,9, &12) but S.
pullorum show changes in 12 O antigen
Epidemiology
Transmission:
Source of infection: droppings of infected birds – carrier birds
– vectors (wild bird or rodents) – contaminated feed (e.g., bone
meal)
Way of entrance of Salmonella spp. in the flock: Animals,
Cages, Environment, Feed, Hatchery, Pests, Pullets, Trucks.
Liner Mode of transmission:
Distribution: Worldwide Zoonotic importance (food). Distribution: Worldwide.
Aetiology: Aetiology: Salmonella var Arizona.
• S. tyhimurium & S. entertides (the most common causes). Same as Paratyphoid salmonella but it ferments
• Motile & have flagella (Somatic O + Flagellar H antigen). lactose.
• Aerobic or facultative anaerobe, non sporogenic. Host:
Zoonotic importance: most frequent cause of food poisoning. - Turkey poults less than 5 weeks.

Host: Chicken & Turkey. - Other birds can be infected.
Age susceptibility:
Chicks & poults (few days up to 3 weeks) highly susceptible to
S. Pullorum & SG S. gallinarum.
Adults are more susceptible to SG & occasionally to SP
Routes of transmission: Inhalation and Ingestion.
1- Vertical transmission mainly transovarian
2- Horizontal/Lateral transmission
a- Direct contact: vertically infected chicks (in
hatcheries, brooder, & rearing areas)
b- Indirect contact: contaminated litter, contaminated
feed and water, equipment’s, attendants, sexers, &
hatching egg trays.
Host: - Other birds are susceptible.
Wide host range (All spp of domestic birds, Transmission:
Age Susceptibility: Source of infection: Reptiles (lizards).
Common in birds from 2 d to 2 weeks. Mode of transmission:
Rare in birds over 4 weeks. Primary infection was from reptiles to turkeys.
Transmission: same as S. pullorum. Same as other Paratyphoid salmonella.
Source of infection: Human sewage & infected workers.
Mode of transmission:
- Vertical transmission: Egg shell route.
- Lateral transmission as PD & FT.
Routes of transmission: Inhalation & Ingestion.

Pathogenesis:
M.O → Birds → Intestine → Bacteremia → Multiplication in visceral organs in mononuclear phagocytic system & produce • Adherence & invasion of intestinal mucosa.
thermostable endotoxins. →. Pathological problems in different organs.
• Toxin production (Endotoxins, Enterotoxins, Cytotoxins, &
Plasmids).
• M.O. → bird → invade intestinal epith → Series of
pathological changes in fluids & electrolytes regulation.
• It may invade blood → visceral organs.

Clinical signs
a- Chicks & Poults b- Growers & Mature birds 1. 20-100 % mortality 1. Mortality up to 90 %.
1- General signs as, depression, huddling, anorexia, & poor 1. In Pullorum Disease; No or general signs 2. In chicks & turkeys’ poults less than 2 weeks: 2. General signs.
weight gain. 2. In Fowl typhoid: a. Deaths of newly hatched chicks without clinical signs 3. Diarrhea with pasty vent.
2- Death may occur without any signs. 3. Listless, pale, & shrunken combs and drop in feed intake. b. Visual impairment (corneal opacity + caseous plug on 4. Visual impairment (Corneal opacity + Caseous
3- White viscous diarrhea that adhere to the feathers around 4. Reduced egg production, low fertility, and hatchability. eye ball). plug on eyeball/anterior chamber).
the vent. c. Diarrhea with pasty vent. 5. Nervous signs: Ataxia, Convulsions, Trembling,
5. Watery to mucoid yellow diarrhea.
4- Respiratory distress (panting + stretching of head & neck). 3. In Ducklings (keel disease): Opisthotonos, Paralysis, & Torticollis.
5- Survivors: poor growth rate, poor feathering, blindness, & Above signs + Swelling of eyelid & Edema+ Trembling + 6. Adults show NO signs & become carriers.
lameness due to swollen hock joints. Sudden death.
4. Birds above 4 W: uneven, stunted birds, & bad feathering
5. In layers: drop in egg production.
6. In Pigeon:
a. Arthritis.
b. In ability to fly; soft S/C swellings near the wing, leg
joint.
c. Nervous manifestation (Twisting of head). localization
of infection in the brain.
7. Adults: Symptoms are absent in Carrier birds.

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 4
 Pullorum Disease = Pd = Bacillary White Diarrhea & Fowl Typhoid FT Paratyphoid infections Paratyphoid Infections: Arizonosis
PM
In Young Chicks & Poults In adults 1. Acute septicemia; swelling & congestion in internal organs. 1. Septicemia: swelling & congestion in internal
• Peracute: NO specific signs. 1. In PD: small nodular regression in ovarian follicles 2. Unabsorbed inflamed yolk sac. organs.
• Acute: chick die shortly after hatching. 2. Lesions are found frequently in chronic carriers 3. Typhlitis; cecal core. 2. Liver: swollen, yellow with necrosis
1. Septicemia: congested enlarged visceral organs (liver, 3. Ovaries: irregular cystic, misshaped, discoloured, 4. Duodenitis. 3. Enteritis, Peritonitis, Pericarditis, & Air sacculitis.
spleen, kidney, & lungs) pedunculated ova with promin anent thick stalk. 4. Typhlitis + unabsorbed yolk sac.
5. Necrotic lesions on liver with haemorrhagic streaks.
2. Liver: swollen, friable, dark red or almost black with coppery 4. Salpingitis. caseous material in oviduct 5. Hard, white circular disc of inspissated caseous
6. Soft S/C swelling of leg joints.
bronze color in FT only 5. Dysfunction of ovaries and oviduct → Egg peritonitis material in eye.
7. Pericarditis + perihepatitis.
3. Liver necrosis. (yellowish cheesy material around ovary/ abdominal
cavity). 8. In adults: ovarian lesions.
4. Catarrhal enteritis. Peritonitis, Pericarditis, & Air sacculitis.
5. Typhlitis: Creamy semisolid or hard material in cecal core. 6. Arthritis, perihepatitis, and pericarditis.

6. Inflamed unabsorbed yolk sac (in > 3-day old poults). 7. In males: caseous granules on testicles.

7. Nodules on visceral organs as lung and heart. Ascites.

8. Arthritis: swollen hock joint with excess orange exudates.

Diagnosis
I) Field diagnosis: 1- Rapid plate agglutination test (Pullorum test). I) Field diagnosis: I) Field diagnosis:
a. Flock history. 2- Tube agglutination test. a. Flock history. a. Flock history.
• PD & FT are diseases of chicks & poults / FT cause 3- ELIZA; flock screening. b. Clinical Investigation. b. Clinical Investigation.
significant disease in growers & adults 4- Micro agglutination test. c. Post-mortem investigation. c. Post-mortem investigation.
• Morbidity is higher than mortality • Rapid Plate Agglutination Test = Pullorum test == WBT II) Lab diagnosis II) Lab diagnosis
• Mortality varies from 0-100% acc. to: age, concurrent 0.04 ml coloured Pullorum antigen + 0.02 ml of whole blood on 1- Samples: 1- Samples:
disease, flock management, strain of birds, nutrition, & porcelain dish (12 wells) → agitation for 2 minutes. • Live: cloaca! swabs and droppings. • Egg shell, sell membrane, & shell
route and dose of exposure (experimentally) Results:
• Dead: liver, gall bladder and yolk sac. • Young & adults: sites of lesion
b. Clinical Investigation. Visible clumping within 2 minutes (Positive).
Absence of clumping within 2 minutes (Negative). • In adults: intestine and ceca 2- Isolation: as PF & FT
c. Post-mortem investigation.
Regulations: • Environmental samples: swabs from different parts of 3- Identification: as paratyphoid salmonella but it
II) Lab diagnosis of PD & FT
1- Age: Minimum 4 months. farm before and during population. ferments lactose if incubated for several days.
1- Samples:
2- Positive results of birds that less than 4 weeks due to 2- Isolation: 4- Serological tests:
Young: liver, gall bladder, spleen
maternal antibody. a. Pre-enrichment: Buffered peptone water with a. Pullorum test.
Adult: ovarian follicles + testicles
3- All positive and doubtful birds are culled for further environmental and feed samples b. ELISA: Flock screening.
2- Isolation
isolation of SP. b. Enrichment: Selenite F broth, Tetrathionate broth, RV c. Tube Agglutination Test.
a. Enrichment by Selenite F- broth or Tetrathionate broth with antibiotics →24 hr at 41-42C → Aerobic to inhibit
4- The negative reactors retested after 1 month.
b. Plating media: MacConkey agar, SS agar, brilliant growth of other MO.
Advantage: Fast, Easy, & no need to label birds. • Use O and H Ag specific for S. Arizona.
green agar, and blood agar c. Plating media: MacConkey agar, SS agar, brilliant
Disadvantage: Not used in turkey, Qualitative, False positive
c. Incubation for broth and media at 24 hrs at 37c under green agar and XLD → 24 hr at 37C aerobic. • The infected birds do not show detectable ab levels
due to cross agglutination
aerobic conditions & be +ve transiently.
• Tube Agglutination Test: 0.02 ml Ag + 0.02 ml serum. d. Identification:
3- Identification • The Ab titer reaches the maximum levels at the point
Quantitative & used as backup check for Pullorum test. 1) Colony morphology: non lactose fermenters.
of lay.
a. Colony morphology: both are non-lactose fermenters 2) Staining characters: G -ve rods.
(i.e., pink)
III) Differential Diagnosis: 3) Biochemical characters: produce H2S.
b. Staining: gram negative rods
a. Joint lesions: Mycoplasma synoviae, Staph aureus, & 3- Serological tests:
c. On blood agar (SP = transparent) & (SG = blue gray) Passarella multocida a. Rapid plate agglutination test (Pullorum test).
d. Biochemical characters: SP ferments dulcitol while SG b. Ovary lesions: (chronic carriers): Coliform, Staph, Strept, b. Tube agglutination test.
ferments ornithine both produce H2s & P. multocida.
c. ELISA; flock screening.
4- Serology c. White nodules on heart: Marek’s Diseases MD.
III) Differential Diagnosis:
To identify the M.O. if we use reference Ab or to detect the
antibody titer in vaccinated, infected, & carriers’ birds if we’ve a. S. pullorum and S. gallinarum.
known antigens b. Duck viral hepatitis.
Antibodies take several days to appear & maximum antibody
production may not occur until 100 days of initial infection

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 5
 Pullorum Disease = Pd = Bacillary White Diarrhea & Fowl Typhoid FT Paratyphoid infections Paratyphoid Infections: Arizonosis
Prevention & Control of Salmonella
A. Antimicrobial (control + prophylaxis): 2. Hatching egg hygiene. 5. Staff hygiene.
1. Used after sensitivity test. a. Nest boxes .... clean, dry litter and regularly changed. a. Restricted visitors to poultry units.
2. Furazolidone, Tetracycline, potentiated Sulphonamide, & Enrofloxacin. b. Disinfection of nest box every 2 W. b. Protective clothing.
3. Chicks & poults. prophylactic antibiotics following hatching in feed & c. Regular collection of eggs not less than 3 times each day. c. Staff should not attend other animals on the farm.
water for first 1-2 weeks to minimize morbidity & mortality. d. Cracked, dirty and floor eggs should not be used for hatching. 6. Feed and water hygiene.
Disadvantages: e. Lightly soiled eggs may be cleaned by gentle buffing to not damage. a. Heat treatment of poultry feed in the pelleting process
1- Number of birds may become carriers and prolong shedding.
f. All eggs used for hatching should be disinfected on the farm as soon as b. Treating feed with chemicals such as formic or propionic acid.
2- antibiotic resistant strain of salmonella may appear.
possible after collection and cleaning. c. Water tanks be wermins and wild bird proof.
B. Biosecurity:
3. Hatchery hygiene. d. Chlorination is desirable
keeping pathogens away from poultry house.
a. Prevent incubation unidentified infected eggs.
1. Continuous monitoring for farms and hatcheries.
b. One way system for the flow of eggs, chicks and trays. C. Competitive Exclusion CE: (probiotics & prebiotics) using normal gut flora from
a. Annual serological monitoring to breeding and layer stock.
c. Effective disinfectant. the cecal content in limiting intestinal colonization by several enteric
b. If infection is present retesting should be carried out every 2-4w until no pathogens including salmonella. protection develops within 32 hrs
d. Uniform air flow from clean to dirty areas.
reactors are found in two consecutive tests.
e. All waste should be enclosed in pest-proof container. Site & route of application:
c. All reactors: removed and sold for slaughter, never sold alive.
4. Poultry farm hygiene. At the hatchery or the farm before the birds are exposed to salmonella.
d. Cull the whole flock if percentage of reactors exceeds 10%.
a. After poultry building has been depopulated all manure should be Coarse sprayer or automatic spray at least 1 mm.
e. After removing of all reactors, the premises and equipment should be
removed and the buildings should be thoroughly clean. In drinking water in the farm, but it may be late for achieving maximum protection.
thoroughly clean and disinfect.
b. Buildings should be soaked with detergent/ sanitizer and then power D. Vaccination:
f. New stock, either adult, grower, one day old chicks, eggs for hatching
washed. S. tyhimurium: Live autotrophic vaccines. drinking water.
should be purchased from pullorum free flocks.
c. Surfaces should be kept dry before apply phenolic disinfectant. S. entertides: Autogenous oil adjuvant vaccine / Formalin killed vaccine.
g. Continuous sampling and culturing swabs from around different parts
of hatcheries and farms (broiler, layer and breeder) even after d. House and equipment should be of sterilized with formaldehyde solution. S. Arizona: Oil adjuvant bacterine in breeders.
disinfection. e. Control and eradication of vermin from poultry sites.
h. Examination of samples of rodents around the farm. f. Bird proof farm.
g. Control of domestic files and beetles.
h. Hygienic disposal of old litter and keep the fresh one always dry.

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 6
 INFECTIOUS CORYZA IC & FOWL CHOLERA FC (PASTEURELLOSIS)
Fowl / Infectious Coryza IC Fowl Pasteurellosis = Avian pasteurellosis, or Avian Haemorrhagic Septicemia
It is acute, rapidly spreading respiratory disease of chickens, characterized by nasal discharge, It is contagious disease affecting domestic and wild birds.
swelling of the eye lids, conjunctivitis and in many cases by swelling of the orbital sinuses. It is septicemic disease associated with high morbidity and mortality but chronic or benign conditions often occur.

Aetiology:
• Haemophilus paragallinarum, Gram negative, non-motile rods or coccobacilli which may
show bipolar staining, non-spore forming and capsulated.
Colony morphology:
• H. paragallinarum typically give tiny dewdrop, non-haemolytic. On serum or dextrose-starch
agar are iridescent, circular, and smooth after 24hrs incubation 5-10% CO2, greyish-yellow
pigment is typically produced.
• Variation from high virulence to very low occurs. It is known that the presence of the capsule
and the specific HA antigens are necessary for the pathogenicity of H. paragallinarum. It is a
delicate bacterium die quickly outside the host tissues.
Susceptible Hosts:
• The chicken is the natural host for H. paragallinarum
• Turkey, pigeon, sparrow, duck, rabbit, guinea fowl. are refractory to experimental infection
Age of Host most commonly affected: -
• All ages of chickens are susceptible but older birds tend to react more severely
• Long Course in mature birds, especially hens with active egg production
Mode Of Infection:
• Infection is introduced by carrier birds and spreads by contact or airborne infected dust.
• Drinking water contaminated with infective nasal discharge serves
• Stress factors as Avitaminosis, Mycoplasmosis.
Economic significance: -
Epidemiology
Aetiology Age susceptibility:
• Pasteurella multocida is gram negative, non-motile, non-spore • All ages are highly susceptible but usually occurs in mature birds.
forming rod occurring singly, in pair and occasionally, as chain or • Turkeys are more susceptible than chicken. Under 16 weeks of
filaments. Using indirect staining methods. age are quite resistant.
• In tissues, blood and recently isolated culture the organism stains • Death losses from FC in chickens usually occur in laying flocks
bipolar. M.O is susceptible to disinfectants and drying.
• Because birds of this age are more susceptible than younger
• P. multocida grows aerobically or anaerobically. The optimal growth chick.
temperature is 37°C. the optimal pH 7.2-7.8.
Mode of Infection:
Colony Morphology
• The respiratory tract is the common portal of entry and less
- By obliquely transmitted light as iridescent rough colonies and differ in commonly via digestive tract.
shape according to virulence and iridescence related to presence of
• The organism lives in the upper respiratory tract of healthy "carrier
capsule.
birds" under unfavorable climatic conditions sudden change →
- Organisms from blue colonies also mutated and produced gray they invade tissues.
colonies, which have not been reported in primary cultures from
Spread in a Flock is Primary by
birds.
• Excretion of the organism from the mouth of infected birds which
Sub grouping of P. multocida
contaminate feed and water.
• Conventional sub grouping of P. multocida entails serological
• Mechanical spread can occur through the hands, feet and
determination of capsular and somatic antigen.
clothes of attendants and contaminated equipment’s.
• Specific capsule serogroup antigens are recognized using passive
• Chronically infected birds are considered to be a major source
hemagglutination tests. Five capsular types (A, B, D, E and F) are
of infection.
currently recognized. At least 16 serotypes have been present.
• No, egg transmission in pasteurellosis
Natural and experimental Hosts: -

Poor growth performance in growing birds. Most reported outbreaks of FC affected chickens, turkeys, ducks or
geese. However, this disease also affects other type of poultry game birds
Marked reduction (10-40%) in egg production in layers.
raised in captivity, birds in zoos and wild birds.
Increase culling rate in broilers.

Pathogenesis
1. Adherence of the organisms to the ciliated mucosa of the upper respiratory tract se. The capsule 1. The ability of P. multocida to invade and reproduce in the host is enhanced by the presence of capsule.
and the HA antigen play an important role in colonization. Toxic substances released from the 2. It enters through mucous membranes of pharynx or upper air passages, but may also enter through conjunctive or cutaneous wounds
organism during proliferation are associated with the appearance of lesions in the mucosa and
3. The Eustachian tube is the most likely route of infection, because the infection localized in air spaces of the cranial bone, middle ear, and
clinical signs.
meninges.
2. H. paragallinarum is a non-invasive bacterium with strong tropism to the ciliated cells and
4. Turkey is much more susceptible than chickens to infection with P. multocida, and mature chickens are more susceptible than young ones, heavy
migrates to lungs and air sacs after synergistic interaction with other infection agents.
losses in mature chickens, but no losses in birds under 16 weeks of age

Clinical Signs
1. IP is short develops within 24-48hrs after inoculation of chickens with either culture or exudates. Acute FC Chronic FC
2. By low mortality and high morbidity variations in age and breed may influence the clinical Signs in acute FC are often present for only a few hours before 1. Chronic FC may follow an acute stage of the disease or result from infection
picture. death. with organism of low virulence.
3. An acute inflammation of the upper respiratory tract including. 1. Fever, anorexia, ruffled feather mucous discharge from the 2. Signs generally are related to localized infections. Wattles, sinuses, leg or wing
4. Nasal discharge serous to mucoid. * Facial edema. * Swollen wattles. mouth, & increase respiratory rate, Cyanosis prior to death. joints, foot pads and sternal bursae often become swollen.
5. Rales may be heard in infection of the lower respiratory tract. 2. Diarrhea is initially watery and whitish in colour later become 3. Exudative conjunctival and pharyngeal lesions may be observed
6. Difficult breathing. greenish and mucoid. 4. Torticollis.
7. In severe cases marked conjunctivitis with closed eyes. 5. Tracheal and rales and dyspnea may be result from respiratory tract infection
8. As swollen head like syndrome associated with H. paragallinarum has been reported in broilers in
the absence of avian pneumovirus.

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 7
 Fowl / Infectious Coryza IC Fowl Pasteurellosis = Avian pasteurellosis, or Avian Haemorrhagic Septicemia
PM
1. Catarrhal inflammation of mucous membranes of the nasal passage and sinuses. Acute Form Chronic Form
2. Catarrhal conjunctivitis and subcutaneous edema of the face and wattles. 1. General hyperaemia, most evident in veins of 1. Otitis media form/Chronic localized form involved in middle ear and cranial bones.
3. Pneumonia and aracialities are rarely present. abdominal viscera. (In duodenal mucosa). Yellow caseous exudates in air spaces of the clavicular bones.
2. Petechial heamorrhage also ecchymotic are 2. Catarrhal or group form: - catarrhal or caseous exudates in the nasal passages,
frequently found. infraorbital sinuses, trachea, air sacs and conjunctival sacs.
3. Increase pericardial and peritoneal fluid 3. Wattle form: - Fluid or caseous exudates in the wattle.
frequently occur.
4. Arthritic form: - Fluid or caseous exudates in the limb joints, tendon sheaths, and foot pads.
4. Ovaries of laying hens are commonly affected
5. Ovarian or peritonitis form: - cheesy material around the ovary and in the peritoneal
mature follicles are flaccid. Yolk material from
cavity.
ruptured follicles may be found in the peritoneal
cavity.

Diagnosis
Isolation and identification of causative agent: - Isolation and identification: -
• While H. paragallinarum is considered to be a fastidious organism, it is not difficult to isolate. • In acute cases, liver, heart impression smear, or blood stained with Methylene Blue or Giemsa will reveal bipolar staining round ended rods.
• Swabbing from infraorbital sinus (nasal exudates is frequently contaminated) on agar blood plates • The isolation of the organism on blood agar and its identification by biochemical and serological tests preferred for culture: - bone narrow, liver,
and cross streaked with Staphylococcus epidermidis incubation for 24-48hrs at 37°C in 5% CO2. Tiny heart blood.
translucent colonies appear adjacent to feeder culture • In chronic cases, culture is made from localized lesion.
• PCR confirmation, other tests as Ag, HI, florescent antibody and monoclonal antibody based • Animal inoculation is frequently used to diagnose the acute form chronic Rabbits or mice inoculated subcutaneously or intraperitoneally with
blocked ELISA. 0.2ml of tissue from suspected birds will die within 24-48hrs and from them the organism can be recovered in pure culture.
DDx: DDx
1. Chronic respiratory disease 1. Chronic Respiratory Disease and Infectious Bronchitis IB.
2. Chronic fowl cholera 2. In laying: acute egg peritonitis as salmonella or E coli.
3. Fowl pox 3. Swollen head syndrome confused with chronic pasteurellosis → E. coli infection.
4. Swollen Head Syndrome SHS
5. A-hypovitaminosis.

Combination of sulphonamide-trimethoprim, tetracyclines and enrofloxacin, norfloxacin for 5-7 days.
After that, relapse may occur due to the presence of agent in some birds and environment. So,
vaccination is a must.
Treatment
• Peracute cholera is so rapid that treatment is rarely of value.
• In acute: Trimethoprim/ Sulphadiazine preparation in the food or water + tetracycline injection
• In Ducks, Streptomycin and Dihydrostreptomycin
• In some outbreaks therapeutic treatment for 7-10days may be followed by a longer period during which drugs are administered at a lower dosage.

Prevention & control

Management: - Good management
Depopulation, good sanitation, traffic control and avoiding birds of multiple ages may break the 1. New birds introduced on a premise should be
cycle. To eliminate agent the infected birds … reservoir. After cleaning, disinfection and resting the as chicks and reared in isolation from adult
building for at least 1-week, new birds (one day or older) known to be free from the infection. flock.
Vaccination 2. Different species of poultry should be reared
• Inactivated whole culture of organisms containing adjuvant, two doses given S/C, 3-6 weeks apart and housed separately
at 16 weeks of age. 3. Utensils and equipment’s should be thoroughly
• Protect against fall in egg production and induce maternal antibodies to progeny. disinfected before being used.
• If a commercial bacterin is unable to induce protective immunity an autogenous bacterin should 4. Prevention of wild birds from getting access to
be used. poultry yards and combating rodents.
Vaccination
Commercially produced bacterins and live vaccine are available.
– Bacterin (killed vaccines): - are used effectively in endemic areas in some countries
including Egypt. Two or more injections S/C or I/M at month interval are usually given.
– Live vaccines: - produced from virulent strains and administered via drinking water have
been reported.
• Three live vaccines available for use in the United States are (Cu) (Clemson university), a
strain of low virulence; M-9 a mutant of Cu with very low virulence and PM-1, a mutant of
Cu intermediate in virulence between Cu and M-9.
• Vaccination of chickens and turkeys with this live vaccine induced protection against
heterologous serotype challenge.
• Disadvantage, resulting in mortality in the vaccinated birds. Its mortality post-vaccination
become excessive; it can be reduced by administration of an antibiotic.
• Some of the more commonly used vaccination programs consist of administration of live
vaccine in the wing web at 10-12 weeks of age followed by either another live vaccine or
bacterin at 18-20 weeks.

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 8
 COLIBACILLOSIS
Definition
Localized or systemic infection caused by Avian Pathogenic Escherichia coli (APEO).

Epidemiology
1- Aetiology: E. coli, gram –ve flagellated motile rods with peritrichous flagella 2- Transmission: Routes of transmissions are inhalation & ingestion
It had somatic (O), Flagellar (H), capsular (K), & pilus antigens a- Vertical Transmission: Egg shell
The most pathogenic serovars are O1:K1, O2:K1, & O78:K80 b- Lateral Transmission: Direct & indirect contact
Predisposing Factors: Direct contact: vertically infected chicks in hatcheries brooders & rearing
areas.
a. Temperature. e. Unhealed navel & wounds.
Indirect contact: contaminated litter, contaminated feed water,
b. Stocking density. f. Contamination.
equipment & hatching egg trays.
c. Poor ventilation. g. Mycoplasmosis, Coccidia.
3- Economic Loss:
d. Concurrent infection. h. IB, NDV, AI, & IBD
High mortality in young birds
4- Host & Age: Increase downgrade carcasses
Broiler, turkeys, & waterfowl Slow growth & poor food conversion rate
Age susceptibility differ according to form Reduce hatchability

Pathogenesis
• E. coli strains presents in large intestine & cecum (Non-pathogenic presents in lower small intestine).
• Pathogenic strains commonly present in the environment → Ingestion & Inhalation → Established in region of nasopharynx → Stress factors → Systemic disease.

Clinical Signs
A. Systemic Forms
Colisepticemia Coli Granuloma (Hjarre’s Disease)
It is an acute septicemic infection causing Polyserositis in chicken, turkeys, & • Chronic granulomatous condition of the domestic fowl & Turkey.
pheasants • Sporadic mainly in hens in the end of laying period.
1. In young chicken (2-12 weeks)
2. Serious Disease in intensive system, high density, & poor ventilation.
3. The origin of E. coli in blood is either enteric or respiratory.
4. It needs predisposing factors.

Clinical Signs
1. Mortality 5%. Emaciation.
2. Morbidity 50%. Unthriftiness.
3. General signs of Colisepticemia.
4. Respiratory signs cough, laboured breathing, gasping, & sniking
5. Severe diarrhea.
6. Recovered birds: uneven unsatisfactory, & high condemnation

Lesions
1. Septicemic carcass → Congested liver, spleen, & kidney. 1. Intestine: Hard, yellow, nodular granuloma (TB Like) in mesentery wall of intestine
2. Peritonitis + Air sacculitis → Thick opaque with white deposits. (cecum).

3. Greenish discoloration of tissues following exposure to air “Indole production” 2. Liver: Hard, Blotchy, Discoloured, & Swollen.
and characteristic odour. 3. Spleen is NOT AFFECTED.
4. Fibrinous pericarditis → Thick white pericardial sac adhered to the surface of
heart.
5. Fibrinous perihepatitis → Fibrin layer on liver.

Sequel of Colisepticemia
1. Joints: osteoarthritis & synovitis
2. Hock joint → lameness.
3. Thoracolumbar vertebrae: Spondylitis, paresis, & paralysis.
4. Eyes: Panophthalmitis (uncommon): unilateral, swollen eye, cloudy, opaque,
& hyperaemic.
5. Immature oviduct: Juvenile Salpingitis.
6. Brain: meningitis.

DDx
1. Synovial Lesions: Reo Virus + Mycoplasma. 1. TB: (Acid fast bacilli)
2. Septicaemia: Pasteurella, Salmonella, & Streptococcus. a. Nodules are encapsulated
b. Easily removed from tissues
c. Crepitate sound on cutting
2. Leucosis: NOT easily removed + Lardaceous
3. Tape worm: adult in intestine +NO bacterial growth on EMB Eosin Methylene Blue
Agar
4. Coligranuloma: grow on EMB media

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 9
 Clinical Signs
B. Localized Forms
1. Yolk Sac Infection (Omphalitis) = Mushy Chick Disease
• It is inflammation of navel in newly hatched chicks. Clinical signs:
• It is the most common cause of chick mortalities in first week. 1. General weakness and huddling under heaters.
• Dry hatching conditions increases the incidence. 2. Fluffy body, Swollen abdomen, Wet and dirty skin (Mushy chicks).
Route of infection 3. The navel (which normally heals within 72 hrs post hatching) is inflamed, red,
Omphalitis swollen, moist, & oedematous.

Through faecal contamination of egg shells 4. Sudden death with high mortality rate.

- Embryo death in late incubation Lesions

- Infected unhealed navel after hatching from contaminated incubators 1. Septicemic carcass.

Yolk sac infection 2. Yolk sac

E. coli translocate from navel, intestine, or blood stream (hence navel may not be a. Blood vessels engorged and dilated.
affected). b. The yolk becomes yellow inspissated or brownish green with fetid odour.
Experimentally reproduced in ducks by dipping eggs at 18 days of incubation. 3. Peritonitis with haemorrhage on serosal surface of intestine.

2. Coliform Cellulites
(Necrotic Dermatitis)
• On the lower abdomen
below the vent and thigh of
broilers.
• Down grading of carcass
causing economic loss.
Aetiology
E. coli: O1, O2, & O78 group.
3. Swollen Head
Syndrome
• In broilers, broilers breeders,
and commercial layers.
• Usually following upper
respiratory viral infection as
IB, Avian Influenza, or
Ammonia.
Lesions:
1. Oedematous swelling over
the eyes.
2. Caseous exudates in the
conjunctiva, facial S/C, and
lachrymal glands.
3. Gelatinous edema in the
facial skin & periorbital
tissues.
4. Coliform Salpingitis 5. Diarrheal Disease 6. Venereal Colibacillosis
(Egg Peritonitis) (Acute Vaginitis)
Infection of oviduct with variety • Considered rare. • Acute and fatal vaginitis that
of E. coli serotypes. • Enterotoxigenic E. coli (ETEC) affect turkey breeder hens
Route of infection: Elaborate Toxins + Diarrhea. shortly after they are first
inseminated due to
• Air sac infection. • Lesions are most common in
puncturing of hymen & severe
• Ascending from the cloacae. the Cecum.
localized E. coli infection.
It occurs at onset of laying due • It is characterized by
to hormonal changes at sexual
1. Vaginitis.
maturity.
2. Peritonitis.
Lesions:
3. Egg binding and internal
1. Abdominal Cavity: filled with
laying.
yolk debris, inspissated yolk,
caseous material or milky 4. Cloacal and intestinal
fluid. prolapse.
2. Ovaries & Oviduct are
inflamed, distorted, and
distended with offensive
caseous material.

Lab Diagnosis
Sampling Culturing Identification

Septicemia: Liver, heart, lung, & air sacs EMP MacConkey Tregitol -7 agar Blood agar • Colony morphology
Omphalitis: Yolk sac & abdominal viscera • Staining characters: Gram –ve, motile rods
Egg peritonitis: Oviduct & inspissated yolk Aerobic / 24 hrs / 37oc with peritrichous flagella
• Biochemically: Eijkman test
Green black Bright pink colony Yellow colony Smooth, convex,
Samples must be taken immediately • Serology:
colonies with with precipitate & gray
after death to avoid swarming of E. coli metallic sheen around them a. K Antigen: Plate agglutination test
Confluent growth from fresh carcass is b. O Antigen: Tube agglutination test
indicative for +ve sample

Prevention & Control

Antimicrobials Competitive Exclusion (CE)
Used after sensitivity test. Def: using normal gut flora from the cecal contents in limiting intestinal colonization by several enteric pathogens
Types: Protection develops with 32 hrs
1. Ampicillin. Site & route of application
2. Apramycin. - At the hatchery or the farm
3. Chloramphenicol. - Coarse spray or automatic spray cabinet at least 1mm
4. Chlortetracycline. - In the drinking water in the farm, it may be too late to achieve max. protection
5. Gentamycin.
6. Neomycin. Probiotics & prebiotics
7. Nitrofurans. Vaccination
8. Oxytetracycline. A. Live vaccine: from a naturally occurring non-pathogenic piliated strain (BT-7)
Reducing the numbers of organisms in the 1. In chicken older than 14 days
digestive tract and prevent bacteremic in
2. Protection against both homologous & heterologous stains
chickens.
B. Killed vaccine: against certain strains of E. coli involved in colisepticemia
Biosecurity
1. S/C at 2-3 weeks
1. Hatching egg hygiene
2. The efficacy not yet sufficiently tested under field conditions
2. Hatchery hygiene
C. Vaccination against the primary respiratory infections (ND/ IBD)
3. Poultry farm hygiene
4. Staff hygiene
5. Feed & water hygiene

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 10
 AVIAN MYCOPLASMOSIS
General Criteria Mycoplasma Of Concern to Poultry:
1. Prokaryotes, very small size, small genome. 1. M. gallisepticum.
2. No cell walls and bounded by a plasma membrane only, consequently: 2. M. synoviae.
a. Resistant to antibiotics that affect cell wall. 3. M. meleagridis.
b. Complex nutritional requirements. 4. M. iowae.
c. Fragile in environment.
3. Mycoplasmas are non-invasive, except for: M. gallisepticum and M. synoviae.

Mycoplasma gallisepticum M. synoviae (Infectious Synovitis) M. meleagridis in turkey

Chronic Respiratory Disease (CRD) → in Chickens. Infections Sinusitis → in Turkey.

Aetiology
• Same as general criteria. M. synoviae M. meleagridis

• Flask shape with lipoprotein tip attaches to the epithelial cells. Criteria same as MG except Criteria same as MG except: Less HA characters &
1. NO attachment organelle. not included in virulence.
• By EM, it has filaments involved in motility, adherence, and pathogenicity.
• By Giemsa, it’s coccid (no gram stain). 2. Less sensitive to antimicrobials.

• There are variable virulence strains (i.e., high virulent & low virulent). However, there is no markers for virulence through molecular identification. 3. Inconsistent HA properties.

Epidemiology
1- Occurrence: worldwide 1- Occurrence: worldwide. 1- Occurrence: Sporadic cases (outbreaks).
2- Host: 2- Host: 2- Host: Turkey only especially young ages.
a. Chicken and turkey more often in young ages (0-14 days). Chicken & turkeys (all ages). 3- Transmission: Same as MG except for:
b. Turkeys are more susceptible. Other birds. 1- Vertical Route: oviduct infected from
c. Other birds can be infected. 3- Transmission & predisposing factors: a. Contact with infected air sacs.
d. There are carriers (as salmonella and E. coli) (i.e., shedding the mo. throughout its life). Same as MG but NO venereal transmission. b. Ascending from cloaca or bursa of
3- Economic importance: fabricius infected during embryonic
stage.
1. Increased condemnations or down grading of carcasses.
2- Horizontal Route: AI & Sexing.
2. Layers: ↓ egg production.
3- Venereal route: male. phallus. semen.
3. Breeders: Slaughter and restriction of exportation to eggs and progeny.
female.
4. Coasts of diagnosis, medication, vaccination and biosecurity.
4- Transmission:
a- Source of infection: Respiratory excretions of infected birds, carrier birds, and its infected eggs.
b- Route of transmission is inhalation & conjunctiva.
c- Mode of transmission
1- Vertical transmission → infected eggs
i- Death before hatch (virulent strain).
ii- Hatching → infected progeny.
2- Venereal transmission by semen of infected cock (low importance).
3- Lateral transmission:
a- Direct contact
i- Vertically infected chicks (hatcheries, Brooders, Rearing area, during spiking) (introduction of new young cockles to the herd to
increase fertility rate).
ii- Contaminated vaccines from infected eggs (i.e., the egg is not SPF and free from mycoplasma).
b- Indirect contact
i- Egg debris in hatchery.
ii- Contaminated litter, equipment, and personals.
5- Seasonal Incidence: Winter.

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 11
 Mycoplasma gallisepticum M. synoviae (Infectious Synovitis) M. meleagridis in turkey

Pathogenesis
Source of M.O. → Inhalation& conjunctive → Motility and attach to upper resp. epithelium by lipoprotein tip → Ciliostasis & colonization. Source of mo. → Inhalation → R. tract → Source of MO → Routes of transmission → Immune
If there is concurrent infection as E. coli ↑ severity of the disease. ciliostasis → colonization → blood → joints suppression and dystrophy due to lake of nutrition to
→ Immune response by T- cell induce → bone
Pathogenic factors of M. gallisepticum: arthritis. • Exact mechanism is unknown
1. Hydrogen peroxide secretion causing → Oxidative stress on host cell membrane→ Irritation to respiratory cells.
• Same predisposing factors.
2. Invade the cells → Escape the immune response and medication. Pathogenic factor:
3. Phenotyping switching (i.e., change its surface antigens) → Skip immune response and stay for long time in host. Phenotyping switching → skip immune
4. One type of Mg S6 → Neurotoxin in turkeys → Arteritis in brain. response & stay for long time in the host
5. Immune Modulatory Effect → Increase cytotoxicity of immune cells and activate complement cascade.
NB: The clinical signs & lesions occur due to host immune and inflammatory response to the M.O. rather than the direct effects of Mycoplasma's
toxicity.
6. Exit of M. gallisepticum
o Excretions of respiratory tract.
o Genital tract → egg or semen.
Factors affecting disease severity (These stress factors initiates ciliostasis & MG colonization)
1- Concurrent respiratory infections as bacterial E. coli (CCRD) or viral infection.
2- Environmental stress as ammonia, dust, poor nutrition, immune suppressive factors, and stocking density.
3- Sex: more in males.
4- Season: winter.

Clinical Signs
Morbidity & Mortality % increases with concurrent infections. 1. IP is relatively short in birds infected by Young:
egg transmission 1. Poor growth with 10% mortality.
A. In Chicken (CRD) B. In Turkey (Infectious Sinusitis) C. In Breeding and Layer Flocks:
2. Most Frequently: subclinical infection 2. Air sacculitis.
1. Uncomplicated infection, NO or low clinical 1. More severe disease than chicken. 1. Drop of egg production by 10-20%. with concurrent infection will be more
signs or mortality. 3. Increase condemnation rate.
2. Sinusitis with swelling of one or both 2. Keratoconjunctivitis. severe.
2. Respiratory signs: (concurrent infections) infraorbital sinuses. Adult:
3. General signs
a. Sneezing. 3. Soiled/ dirty wing feather. 1. Reduced egg hatchability.
4. Respiratory signs as MG.
b. Coryza. 4. Encephalitic for (12-16 w) due to MG S6 → 2. Osteodystrophy: expressed in the following
Arthritic Form:
c. Frothy ocular exudates & conjunctivitis. Nervous signs (As Torticollis & Opisthotonos). 3. Bowing, twisting, and shortening of the
Acute: swollen joints (hock j), Lameness, & tarsometatarsal bone.
d. Swollen facial skin and eyelids. Sterna bursitis (breast blister).
4. Deformed cervical vertebrae.
e. Moist rales, dyspnea, breathing though Chronic: persistent synovitis for life.
partly open beak. 5. Hock joint swelling.

3. Swollen hock joints → Lameness (rare). 6. Feathers of wing become protruded (aeroplane
appearance( .

PM Lesions
1. Excess mucous or catarrhal exudates in the 1. Enlarged infraorbital sinuses (excess mucoid Salpingitis (caseous exudates in the oviduct) 1. Respiratory Lesions: Same as MG but
mares, trachea, lungs. or caseous exudates) due to contact with infected air sacs. milder.
2. Edema of air sacs with caseous exudates 2. Excess mucous or catarrhal exudates in the 2. Arthritic Lesion:
(air sacculitis). mares, trachea, lungs. a. Excessive amount of viscous
3. Edema of air sacs with caseous exudates exudate (creamy to brown) in joints.
(air sacculitis). b. Thickening to synovial membrane of
4. If the disease was complicated with E. coli tendon sheath.
septicaemia (CCRD). c. Caseous exudate in sternal bursa.

a. Air Sacculitis. 3. Kidney: swollen, mottled, & pale.

b. Pericarditis. 4. Hepato & Splenomegaly.

c. Perihepatitis.
d. Peritonitis.

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 12
 Mycoplasma gallisepticum M. synoviae (Infectious Synovitis) M. meleagridis in turkey

Diagnosis
I) Field Diagnosis 2- Isolation of Mycoplasma NB: Mycoplasma and Chlamydia psittaci only Same as MG except for: Diagnosis of M. meleagridis
1. Flock History. a. Mycoplasma broth with Phenol Red Indicator at mo. can be cultured on embryonated egg. Samples from trachea NOT joints. Samples:
2. Clinical Signs 37oC for 3-5 d → Change color to orange/ yellow. 3- Identification Culture media need NAD (Nicotinamide • Young: Resp. system, cloaca and BF.
3. PM lesion b. PPLO (Pleuropneumonia Like Organism) or Chicken a. Direct: PCR. adenine dinucleotide) & Alkaline media. • Adult: phallus, oviduct (female), semen, and
Serum Agar → at 37oc, 3-5 d (in closed container) b. Colony morphology and staining cloaca
II) Lab Diagnosis
→ Dissecting microscope → Circular translucent characters.
1- Samples: Culture: good growth on agar and poor on broth
colonies with dense center (fried egg
c. IF, IP (Immunoperoxidase), and growth
a- Live: Swap from trachea, appearance).
inhibition tests.
cloaca, and phallus. NB: The media must be enriched with horse, sine, and
d. Serological tests (Ag or Ab): RSA (Rapid
b- Dead: Sinus exudates, chicken serum (for M. gallisepticum) e.g.; Penicillin (no
Serum Agglutination), ELIZA, & HI tests.
Trachea, lungs, and air sacs. effect due to lack of Cell wall).
NB: Mycoplasma has haemagglutinin
c- Dead in Shell Embryo: shell c. ECE at 7 days → Yolk sac → Incubation at 5-8 days
ag as viruses).
membrane & air sacs. → Death of embryo → CPE → Dwarfing, edema,
necrosis on liver, and enlarged spleen

Prevention and Control:

A. Anti-Microbials C. Vaccination (NO vaccination for turkey) Same as MG except for: Same as MG except for:

1. To control clinical signs NOT prevent egg transmission. Resistant to antibiotics except for NO egg heating.
Chlortetracycline. No vaccination.
2. MG susceptible to Macrolides, Tetracycline, and Fluroquinolones, etc. Killed Oil Adjuvant Vaccine (Bacterin)
Live temp. sensitive mutant vaccine Ms-H in Phallus & oviduct swaps are always monitored.
3. Resistant to Penicillin or other Antibiotics which Inhibit Cell Wall Synthesis. • S/C or I/M.
breeders. Hygienic measure should be conducted during
B. Bio Security • Given in two doses (1 month interval).
sexing & AI.
• Given to breeder pullets.
Aim: maintain breeding stocks of chicken & turkey free From MG infection then
rearing the progeny with adequate biosecurity to avoid introduction of Advantage:
organism. • Layers protect against egg production losses
1. Hatching egg hygiene + Hatching Egg Treatment. • Broilers protect from air sacculitis
• Breeders: ↓ egg transmission of MG.
2. Hatchery hygiene.
3. Farm & personal hygiene.
Live Vaccine (Mild Strain)
4. Feed & water hygiene.
1. F strain
5. Continuous serological monitoring with elimination of reactors. a. Protect against drop in egg production & reduce egg
6. Slaughter policy for infected breeder. transmission.
b. Pullets at 12-16 weeks or at 2 wk. in chicken at risk.
Hatching Egg Treatment:
c. By aerosols (may cause infection), DW (may not reach to all
I. Antimicrobial Treatment.
birds), nasal or eye drops (the safest method).
1. Egg dipping → worming eggs to 37oC. → Emersion in cold Ab solution (2-
2. Ts-11
10oC) for 20 min under vacuum pressure.
a. Temp. sensitive.
2. AB injection in air sac (chicken) or Albumin pointed end (turkeys).
b. Aerosols.
II. Heating: _Not -preferable)
c. Safer than F- strain but less protective.
Gradual warming until internal temp. 46oc for 12 hrs. return to room temp.
3. 6/85
Advantages: killing MG. a. Eye drops.
Disadvantages: low hatchability (10%) & ↑ mortality in turkey embryos. b. Safer than F- strain but less protective.

M. Iowae
It is enteric Form Host: mainly turkey and occasionally in chicken. Diagnosis: Same as MM but NO serology (NO reliable Abs).
Aetiology: Transmission As M. meleagridis. Prevention & control of M. iowae: Same as MM except that Quinolone and Tiamulin are
1. 6 serovars (I-R) with Variable virulence. Pathogenesis: Transient Immunosuppression. more effective in treatment.

2. Tropism to GIT (resist bile). Clinical sings:

3. Resist environment and antibiotics. 1. Adults (reduce hatchability 2-5) %.
4. No attachment organelle. 2. Young Poor growth and feathering, Experimentally: skeletal Deformity.

Ce: Mustafa Ahmed Abo ElEnein, BVSc., CPT. Poultry Medicine, Bacterial Diseases | 13