Infectious Coryza

Infectious coryza is an acute to subacute respiratory disease of chickens primarily caused by the Gram-negative, non-motile, pleomorphic bacterium Avibacterium paragallinarum (formerly Haemophilus paragallinarum). The disease is characterized by catarrhal inflammation of the upper respiratory tract, including the nasal passages, sinuses, and conjunctiva, with pronounced facial edema and mucoid to purulent nasal discharge. It predominantly affects commercial layers and broiler breeders, causing significant economic losses due to decreased egg production (10-40%), increased culling, and elevated mortality (up to 20% in complicated cases). In broilers, the disease is less common but can occur, leading to respiratory distress and increased condemnations at processing. The disease is distributed worldwide, with higher prevalence in multi-age layer flocks and in regions with poor biosecurity. Infectious coryza is often complicated by secondary infections such as Mycoplasma gallisepticum, Escherichia coli, and infectious bronchitis virus, exacerbating clinical signs and lesions. The disease is not zoonotic and is reportable in some countries due to its impact on poultry health and trade.

The primary causative agent is Avibacterium paragallinarum, a member of the family Pasteurellaceae. It is a Gram-negative, encapsulated, non-spore-forming, non-motile rod that exhibits pleomorphism, appearing as coccobacilli or filaments. The bacterium requires nicotinamide adenine dinucleotide (NAD, V-factor) for growth, hence its historical classification as Haemophilus. Three serovars (A, B, C) are recognized based on agglutination tests, with serovar A being most common in many regions, followed by C and B. The bacterium possesses various virulence factors, including a polysaccharide capsule that resists phagocytosis, fimbriae for adhesion to respiratory epithelium, and a cytotoxin that damages ciliated epithelial cells. The capsule is a key immunogen, and vaccines typically contain inactivated whole-cell bacterins of multiple serovars. The organism is fragile in the environment, surviving only a few days in droppings or water, but can persist longer in nasal exudates. It is susceptible to common disinfectants, heat (56°C for 30 minutes), and drying.

Infectious coryza primarily affects chickens, with commercial layers and broiler breeders being most susceptible, especially during the laying period. Broilers can be affected but often show milder signs. The disease is more prevalent in multi-age layer complexes, where continuous introduction of susceptible pullets into infected flocks perpetuates the cycle. Age susceptibility: all ages are susceptible, but clinical disease is more severe in adults, particularly during peak production. Housing systems: birds in high-density, poorly ventilated houses with high ammonia levels are at increased risk. Free-range and deep-litter systems may also facilitate transmission via contaminated water and feed. Seasonality: higher incidence in cooler months due to reduced ventilation and increased bird confinement. Morbidity can reach 100% in susceptible flocks, while mortality is typically low (1-10%) unless secondary infections occur, then it may rise to 20%. Egg production drops of 10-40% are common, with a delay in peak production. Feed conversion ratio (FCR) may worsen by 5-10% due to reduced feed intake. Transmission occurs via direct contact, aerosol, and contaminated fomites (feed, water, equipment). Wild birds and rodents can act as mechanical vectors. The bacterium can persist in carrier birds for months, serving as a reservoir.

Avibacterium paragallinarum colonizes the nasal mucosa and upper respiratory tract, adhering to ciliated epithelial cells via fimbriae. The cytotoxin causes ciliostasis and destruction of the epithelium, leading to loss of mucociliary clearance. The bacteria multiply in the submucosa, inducing an intense inflammatory response with infiltration of heterophils and macrophages. The release of endotoxin (lipopolysaccharide) triggers vasodilation and increased vascular permeability, resulting in edema of the facial tissues, particularly the infraorbital sinuses and wattles. The inflammatory exudate accumulates in the nasal passages and sinuses, causing the characteristic nasal discharge and swelling. In severe cases, the infection can spread to the lower respiratory tract (trachea, lungs, air sacs) and to the conjunctiva, causing conjunctivitis. Secondary bacterial infections (e.g., E. coli, M. gallisepticum) can exacerbate the lesions, leading to airsacculitis, pericarditis, and perihepatitis. The systemic effects are mediated by endotoxemia, causing fever, depression, and reduced feed intake. In laying hens, the stress of respiratory disease can cause a temporary cessation of ovulation, leading to egg production drops. The immune response involves both humoral (IgG, IgA) and cell-mediated immunity, but protection is serovar-specific.

Intrinsic factors: Genetic susceptibility varies among chicken lines; high-producing layers are more prone due to metabolic stress. Age: adults are more susceptible than young birds. Immune status: flocks with waning maternal antibodies or incomplete vaccination are at higher risk. Concurrent immunosuppressive diseases (e.g., infectious bursal disease, Marek's disease) increase susceptibility. Extrinsic factors: Poor biosecurity allowing introduction of the bacterium from infected flocks or contaminated equipment. High stocking density and poor ventilation leading to high ammonia levels (>25 ppm) damage respiratory epithelium, facilitating infection. Wet litter and poor sanitation increase environmental contamination. Stressors such as moving, vaccination, or extreme temperatures can precipitate outbreaks. Inadequate nutrition, particularly vitamin A deficiency, compromises mucosal integrity. Vaccination failures due to improper storage, administration, or serovar mismatch. Presence of other respiratory pathogens (e.g., Mycoplasma gallisepticum, infectious bronchitis virus) that cause immunosuppression or epithelial damage.

The incubation period is 1-3 days, and clinical signs develop rapidly. Early signs include serous nasal discharge, sneezing, and mild conjunctivitis. Within 24-48 hours, the discharge becomes mucoid to purulent, and facial edema becomes pronounced, especially around the infraorbital sinuses and wattles. Birds may shake their heads to expel exudate, and the feathers around the face become soiled. Swelling of the wattles is common in males. Affected birds are depressed, huddle together, and have reduced feed and water intake. Respiratory rales and coughing may be heard, especially when secondary infections are present. In layers, egg production drops sharply, often within a few days, and may take 2-3 weeks to recover. Egg quality may be affected, with thin-shelled or misshapen eggs. Mortality is usually low but can increase if the disease is complicated by colibacillosis or chronic respiratory disease. In severe cases, birds may develop sinusitis with caseous exudate, leading to swelling and distortion of the face. Neurological signs are rare but can occur if the infection spreads to the central nervous system. In broilers, signs are similar but less severe, with increased respiratory distress and reduced weight gain.

1. Avian influenza (AI): High mortality, severe systemic signs, cyanosis of comb and wattles, edema, and hemorrhages. PCR and virus isolation differentiate. 2. Newcastle disease (ND): Respiratory and neurological signs, with gastrointestinal lesions. HI test and PCR. 3. Mycoplasmosis (M. gallisepticum): Chronic respiratory disease, airsacculitis, and sinusitis. Serology (ELISA, HI) and PCR. 4. Infectious bronchitis (IB): Respiratory signs, tracheal rales, and nephritis in some strains. PCR and serology. 5. Fowl cholera (Pasteurella multocida): Acute septicemia with high mortality, cyanosis, and petechial hemorrhages. Bacterial culture. 6. Ornithobacterium rhinotracheale (ORT): Respiratory disease with airsacculitis and pneumonia. Culture on blood agar. 7. Avibacterium paragallinarum infection (coryza) is confirmed by isolation and PCR. 8. Vitamin A deficiency: Causes nasal discharge and conjunctivitis, but no facial edema. Histopathology shows squamous metaplasia. 9. Aspergillosis: Respiratory distress with gasping, but typically affects lower respiratory tract. Fungal culture. 10. Infectious laryngotracheitis (ILT): Severe respiratory distress with bloody expectoration. PCR and histopathology.

Step 1: Flock history and clinical signs – acute onset of facial edema, nasal discharge, and drop in egg production in layers. Step 2: Physical examination of affected birds – observe characteristic swelling of infraorbital sinuses and wattles. Step 3: Gross necropsy – examine nasal passages, sinuses, and trachea for catarrhal exudate; note any caseous plugs in sinuses. Step 4: Sample collection – collect nasal swabs, sinus exudate, and tracheal swabs from acutely affected birds (3-5 birds) for bacterial isolation and PCR. Also collect blood samples for serology. Step 5: Bacterial isolation – culture on chocolate agar or blood agar with a nurse colony (Staphylococcus) to provide V-factor; incubate at 37°C with 5-10% CO2 for 24-48 hours. Identify colonies as small, dewdrop-like, and Gram-negative. Perform biochemical tests (catalase, oxidase, urease) and serotyping with specific antisera. Step 6: Molecular confirmation – PCR targeting the HPG2 gene or 16S rRNA gene. Step 7: Serology – serum plate agglutination (SPA) or hemagglutination inhibition (HI) test to detect antibodies; a four-fold rise in titer between acute and convalescent sera is confirmatory. Step 8: Histopathology – if needed, examine nasal turbinates for epithelial necrosis and heterophilic infiltration. Step 9: Differential diagnosis – rule out other respiratory pathogens via PCR and culture. Step 10: Final diagnosis based on isolation and identification of A. paragallinarum.

Serology: ELISA can detect antibodies to A. paragallinarum, but sensitivity and specificity vary. HI test is more specific; titers ≥1:80 are considered positive. A four-fold increase in HI titer between paired sera is diagnostic. Molecular: PCR (conventional or real-time) targeting the HPG2 gene is highly sensitive and specific. Microbiology: Isolation on chocolate agar with V-factor (NAD) supplementation; colonies are small, smooth, and grayish. Biochemical profile: catalase positive, oxidase positive, urease negative, and nitrate reduction positive. Blood chemistry: In severe cases, heterophilia and lymphopenia may be observed. No specific blood chemistry changes are pathognomonic. Coccidiosis lesion scoring is not applicable. Mycotoxin feed assays may be performed to rule out immunosuppressive factors.

Radiography: Not typically used for diagnosis of infectious coryza, but may show soft tissue swelling of the facial region. Ultrasonography: Not applicable. Gross necropsy photography: Key findings include subcutaneous edema of the face and wattles, catarrhal exudate in nasal passages and infraorbital sinuses, and occasionally caseous plugs. The trachea may show mild congestion. In complicated cases, airsacculitis and peritonitis may be present.

Gross necropsy: The most consistent lesion is inflammation of the nasal passages and sinuses with mucoid to purulent exudate. The infraorbital sinuses may be distended with caseous material. The trachea may contain excess mucus. In layers, the ovary may show regressed follicles due to decreased feed intake. Histopathology: Microscopic examination of the nasal mucosa reveals loss of cilia, epithelial necrosis, and infiltration of heterophils and macrophages in the submucosa. There is edema and congestion of the underlying connective tissue. In chronic cases, fibrosis and glandular hyperplasia may be seen. The conjunctiva may show similar inflammatory changes. No inclusion bodies are present. Special stains (Gram) can demonstrate Gram-negative pleomorphic bacteria in the exudate.

Treatment aims to reduce clinical signs and secondary infections. Antibiotics are effective if administered early. Water-soluble antibiotics: Amoxicillin (10-20 mg/kg body weight per day, or 100-200 mg/L drinking water for 3-5 days), Oxytetracycline (10-20 mg/kg, or 200-400 mg/L for 3-5 days), Tylosin (20-40 mg/kg, or 500 mg/L for 3-5 days), Tilmicosin (10-20 mg/kg, or 75 mg/L for 3 days), Enrofloxacin (10 mg/kg, or 50-100 mg/L for 3-5 days, where legal), Florfenicol (20-30 mg/kg, or 400 mg/L for 3-5 days). In-feed antibiotics: Oxytetracycline (200-400 g/ton feed for 5-7 days), Chlortetracycline (200-400 g/ton for 5-7 days). Supportive therapy: Multivitamins (especially vitamin A and C) in water to enhance mucosal integrity. Electrolytes and glucose to maintain hydration and energy. Anti-inflammatory drugs (e.g., aspirin) may reduce fever and edema. Biosecurity: Isolate affected flocks, disinfect waterers and feeders, and improve ventilation. Vaccination: Inactivated bacterins are available and can be used in pullets before onset of lay (16-18 weeks) to prevent outbreaks. Two doses are often recommended. Treatment of secondary infections: If E. coli or Mycoplasma is involved, adjust antibiotic therapy accordingly. Withdrawal times must be observed for eggs and meat.

Short-term: With prompt antibiotic treatment, clinical signs usually resolve within 1-2 weeks, but recovery may be slower in severe cases. Medium-term: Egg production typically returns to normal within 2-3 weeks, but may not reach pre-outbreak levels if the drop was severe. Long-term: Flocks may have reduced overall performance, and carrier birds can remain, leading to recurrent outbreaks. Mortality is usually low (<5%) unless secondary infections occur. The prognosis is guarded in flocks with poor management or concurrent diseases. Depopulation is rarely necessary but may be considered in severe outbreaks with high mortality and poor recovery.

After an outbreak, monitor the flock for 2-4 weeks for recurrence of clinical signs. Serological monitoring: Collect serum samples from sentinel birds or a random sample of the flock every 2-4 weeks to assess antibody titers. A rise in titers may indicate active infection. Cleaning and disinfection: Thoroughly clean and disinfect the house, equipment, and water lines with a disinfectant effective against Gram-negative bacteria (e.g., quaternary ammonium compounds, phenolics). Allow the house to remain empty for at least 2 weeks. Litter management: Remove and dispose of contaminated litter properly. Pullet rearing audits: Ensure that replacement pullets are vaccinated and raised in a biosecure environment to prevent introduction of the disease. Review biosecurity protocols and correct any deficiencies.

Pearls: 1. Facial edema and nasal discharge in layers are highly suggestive of infectious coryza. 2. The infraorbital sinus is a key site for lesion detection. 3. A. paragallinarum requires V-factor for growth; use a nurse colony for isolation. 4. Vaccination with a serovar-matched bacterin is effective in preventing disease. 5. Antibiotic treatment is most effective when initiated early. Pitfalls: 1. Confusing infectious coryza with other respiratory diseases such as avian influenza or Newcastle disease; always confirm with laboratory tests. 2. Failure to collect samples from acutely affected birds before antibiotic treatment, as this may prevent isolation. 3. Using antibiotics without proper diagnosis can lead to antibiotic resistance and mask clinical signs. 4. Neglecting secondary infections, which can worsen the outcome. 5. Assuming that vaccination provides complete protection; it may not cover all serovars. 6. Overlooking biosecurity lapses that allow re-infection.

Antibiotics: Amoxicillin: 10-20 mg/kg body weight orally once daily, or 100-200 mg/L drinking water for 3-5 days. Oxytetracycline: 10-20 mg/kg, or 200-400 mg/L for 3-5 days. Tylosin: 20-40 mg/kg, or 500 mg/L for 3-5 days. Tilmicosin: 10-20 mg/kg, or 75 mg/L for 3 days (not for use in layers producing eggs for human consumption in some countries). Enrofloxacin: 10 mg/kg, or 50-100 mg/L for 3-5 days (banned in poultry in some regions). Florfenicol: 20-30 mg/kg, or 400 mg/L for 3-5 days. In-feed: Oxytetracycline 200-400 g/ton for 5-7 days. Withdrawal times: Eggs: 0-7 days depending on drug; Meat: 3-7 days. Supportive: Vitamin A (10,000-20,000 IU/L water), Vitamin C (100-200 mg/L), Electrolytes (e.g., 0.5% sodium chloride, 0.5% sodium bicarbonate in water). Vaccines: Inactivated bacterins containing serovars A, B, and C are available. Administer subcutaneously or intramuscularly at 16-18 weeks of age, with a booster 4-6 weeks later. Some vaccines are oil-emulsion adjuvanted. Do not vaccinate during an outbreak.

Infectious coryza has been extensively studied. Key studies include: 1. Blackall et al. (1990) demonstrated the efficacy of a trivalent bacterin in protecting against challenge with all three serovars. 2. Bragg et al. (1996) showed that vaccination reduced egg production losses by 50% compared to unvaccinated controls. 3. A field trial by Sandoval et al. (1994) reported that antibiotic treatment with oxytetracycline reduced clinical signs and improved egg production recovery. 4. A meta-analysis by Zhang et al. (2018) found that PCR was more sensitive than culture for diagnosis. 5. The World Organisation for Animal Health (WOAH) provides guidelines for diagnosis and control. 6. The American Association of Avian Pathologists (AAAP) recommends a comprehensive approach including biosecurity, vaccination, and antimicrobial therapy. 7. Recent studies have focused on molecular epidemiology and antimicrobial resistance patterns, highlighting the emergence of multidrug-resistant strains. 8. Expert consensus emphasizes the importance of early diagnosis and treatment to minimize economic impact.