# [Avian Coryza in Poultry](/knowledge/bacteria/avian-bacteria/avian-coryza-in-poultry): Clinical Management and Differential Diagnosis

## Key Takeaways

- Avian coryza is an acute upper respiratory tract disease caused by *Avibacterium paragallinarum*, a Gram-negative coccobacillus requiring NAD for growth, with three recognized serovars (A, B, C).
- Transmission occurs primarily via direct contact through respiratory droplets and contaminated fomites, with an incubation period of 1-3 days, and morbidity can reach 100% in naive flocks.
- Hallmark clinical signs include serous to mucoid nasal discharge, facial edema (periorbital swelling), conjunctivitis, and a significant drop in egg production in laying flocks.
- Definitive diagnosis relies on isolation and identification of *A. paragallinarum* via bacterial culture on enriched media (chocolate agar + NAD) and confirmation with PCR targeting the *hagA* or 16S rRNA gene.
- Treatment involves antimicrobial therapy with sulfonamides, tetracyclines, macrolides, or fluoroquinolones, guided by susceptibility testing, and control strategies include strict biosecurity and serovar-specific vaccination.
- Differential diagnoses are crucial and include other respiratory pathogens like *Mycoplasma gallisepticum*, *Pasteurella multocida*, infectious bronchitis virus, and avian influenza virus, distinguished by specific clinical signs and diagnostic tests.

---

## Etiology

[Avian coryza](/knowledge/bacteria/avian-bacteria/avian-coryza-chickens), also termed [infectious coryza](/knowledge/bacteria/avian-bacteria/avian-infectious-coryza), is an acute upper respiratory tract disease of poultry caused by the bacterium *Avibacterium paragallinarum* (formerly *Haemophilus paragallinarum*). The organism is a Gram-negative, non-motile, pleomorphic coccobacillus that requires nicotinamide adenine dinucleotide (NAD, or V factor) for in vitro growth, but does not require hemin (X factor) [<a href="#ref-1">1</a>]. This biochemical dependency distinguishes *A. paragallinarum* from other avian *Pasteurellaceae* members. The bacterium is catalase-negative, oxidase-positive, and produces acid from glucose and mannose without gas production [<a href="#ref-1">1</a>, <a href="#ref-2">2</a>]. Three serovars (A, B, and C) are recognized based on hemagglutination inhibition (HI) tests, with serovar A and C being the most prevalent in field outbreaks [<a href="#ref-2">2</a>, <a href="#ref-3">3</a>]. Serovar B is less commonly isolated but can cause significant disease [<a href="#ref-3">3</a>]. The organism is fragile and does not survive long outside the host, being susceptible to desiccation, direct sunlight, and common disinfectants [<a href="#ref-1">1</a>].

## Epidemiology

The disease is distributed worldwide and affects primarily chickens and, to a lesser extent, pheasants, quail, and guinea fowl [<a href="#ref-1">1</a>, <a href="#ref-4">4</a>]. Turkeys are generally considered resistant to natural infection with *A. paragallinarum*, although experimental infections have been reported [<a href="#ref-4">4</a>]. The primary mode of transmission is direct contact between infected and susceptible birds via respiratory droplets, aerosolized exudate, or contaminated fomites [<a href="#ref-1">1</a>, <a href="#ref-5">5</a>]. The incubation period is typically 1 to 3 days following natural exposure, but can extend to 7 days in experimental settings [<a href="#ref-1">1</a>, <a href="#ref-5">5</a>]. Morbidity can reach 100% in a naive flock, while mortality is generally low (1-5%) unless complicated by secondary pathogens such as *[Mycoplasma gallisepticum](/knowledge/bacteria/avian-bacteria/mycoplasma-gallisepticum-poultry-chronic-respiratory-disease-control)*, *Escherichia coli*, or *Pasteurella multocida* [<a href="#ref-1">1</a>, <a href="#ref-6">6</a>]. The disease is more severe in layers and breeders than in broilers, and chronic carrier states are established in recovered birds, which can shed the organism intermittently for months [<a href="#ref-1">1</a>, <a href="#ref-7">7</a>]. Stressors such as poor ventilation, high ammonia levels, overcrowding, and concurrent viral infections (e.g., [infectious bronchitis virus](/knowledge/viruses/avian-viruses/infectious-bronchitis-virus), [Newcastle disease virus](/knowledge/viruses/avian-viruses/newcastle-disease-virus)) exacerbate clinical signs [<a href="#ref-1">1</a>, <a href="#ref-6">6</a>].

## Clinical Signs

The hallmark clinical signs of [avian coryza](/knowledge/bacteria/avian-bacteria/avian-coryza-etiology-diagnosis-control) are confined to the upper respiratory tract. Affected birds present with serous to mucoid nasal discharge, sneezing, and facial edema (periorbital swelling) [<a href="#ref-1">1</a>, <a href="#ref-8">8</a>]. The swelling is often unilateral initially, becoming bilateral as the disease progresses [<a href="#ref-8">8</a>]. Conjunctivitis with frothy ocular exudate is common, and in severe cases, the eyelids may become adherent [<a href="#ref-1">1</a>, <a href="#ref-8">8</a>]. Submandibular edema (wattles) may also be observed [<a href="#ref-8">8</a>]. In laying flocks, a marked drop in egg production (10-40%) is typical, and egg quality may decline with increased numbers of misshapen, thin-shelled, or pale-shelled eggs [<a href="#ref-1">1</a>, <a href="#ref-9">9</a>]. Respiratory rales and dyspnea are less common but can occur if secondary bacterial infections or environmental irritants are present [<a href="#ref-1">1</a>, <a href="#ref-6">6</a>]. Anorexia, depression, and reduced water intake are frequently noted [<a href="#ref-1">1</a>]. The clinical course is usually 2 to 3 weeks in uncomplicated cases, but can persist for several weeks in the presence of secondary infections [<a href="#ref-1">1</a>].

## Pathology

Gross pathological lesions are primarily confined to the upper respiratory tract. The nasal passages, infraorbital sinuses, and trachea contain catarrhal to mucopurulent exudate [<a href="#ref-1">1</a>, <a href="#ref-10">10</a>]. The nasal mucosa is hyperemic and edematous [<a href="#ref-10">10</a>]. In chronic or complicated cases, the exudate may become caseous and inspissated, leading to sinus occlusion and facial distortion [<a href="#ref-1">1</a>, <a href="#ref-10">10</a>]. Conjunctival sacs may contain fibrinopurulent exudate [<a href="#ref-10">10</a>]. The lungs and air sacs are typically unaffected unless secondary pathogens are involved [<a href="#ref-1">1</a>, <a href="#ref-10">10</a>]. Histologically, the nasal mucosa shows acute to subacute inflammation with heterophil infiltration, epithelial hyperplasia, and goblet cell proliferation [<a href="#ref-10">10</a>]. The lamina propria is edematous with variable numbers of lymphocytes and plasma cells [<a href="#ref-10">10</a>]. In chronic cases, fibrosis and granuloma formation may be observed [<a href="#ref-10">10</a>].

## Differential Diagnosis

Differential diagnosis is critical because several other respiratory pathogens present with similar clinical signs. The table below summarizes key differentiating features.

| Disease | Etiologic Agent | Key Clinical Features | Key Diagnostic Tests |
| :--- | :--- | :--- | :--- |
| [Avian coryza](/knowledge/bacteria/avian-bacteria/avian-coryza-etiology-diagnosis-control) | *A. paragallinarum* | Nasal discharge, facial edema, conjunctivitis, egg drop | Bacterial culture, PCR, HI serotyping |
| Mycoplasmosis | *M. gallisepticum* | Chronic respiratory rales, airsacculitis, sinusitis | Serology (ELISA, HI), PCR, culture |
| [Fowl cholera](/knowledge/bacteria/avian-bacteria/avian-cholera-fowl-cholera-in-poultry) | *P. multocida* | Acute septicemia, cyanosis, diarrhea, high mortality | Bacterial culture, PCR |
| Infectious bronchitis | Coronavirus (IBV) | Tracheal rales, nephritis (some strains), egg drop | RT-PCR, virus isolation, serology |
| Newcastle disease | Paramyxovirus (NDV) | Respiratory signs, nervous signs, high mortality | Virus isolation, RT-PCR, serology |
| [Avian influenza](/knowledge/bacteria/avian-bacteria/avian-influenza-cdc-global-surveillance) | Influenza A virus | Respiratory signs, edema, cyanosis, high mortality | RT-PCR, virus isolation |
| Avian pneumovirus (TRT) | Metapneumovirus | Swollen head, nasal discharge, egg drop | RT-PCR, ELISA |

For a more detailed comparison, refer to the article on [Infectious Coryza in Poultry and Ducks: Etiology, Clinical Signs in Chickens, Differential Diagnosis from Avian Influenza, and Prevention Strategies](/knowledge/bacteria/avian-bacteria/infectious-coryza-poultry-ducks-etiology-clinical-signs-differential-diagnosis). Also consult [Common Viral Diseases in Poultry: Diagnosis and Differential Considerations](/knowledge/bacteria/avian-bacteria/common-viral-diseases-poultry-diagnosis-differential) for a broader overview of viral differentials.

## Diagnostics

Definitive diagnosis of [avian coryza](/knowledge/bacteria/avian-bacteria/avian-coryza-in-poultry) relies on isolation and identification of *A. paragallinarum* from clinical specimens. Nasal swabs, sinus exudate, or infraorbital sinus aspirates are the preferred samples [<a href="#ref-1">1</a>, <a href="#ref-11">11</a>]. The organism is fastidious and requires enriched media such as chocolate agar supplemented with NAD (1% yeast extract or 5% horse serum) [<a href="#ref-1">1</a>, <a href="#ref-11">11</a>]. Selective media containing antibiotics (e.g., bacitracin, clindamycin) can be used to suppress contaminating flora [<a href="#ref-11">11</a>]. Colonies appear as small, dewdrop-like, translucent colonies after 24-48 hours of incubation at 37°C in 5-10% CO2 [<a href="#ref-1">1</a>, <a href="#ref-11">11</a>]. Biochemical confirmation is performed using the catalase, oxidase, and fermentation tests [<a href="#ref-1">1</a>]. Molecular diagnostics, particularly PCR targeting the 16S rRNA gene or the *hagA* gene (encoding the hemagglutinin), are highly sensitive and specific [<a href="#ref-12">12</a>, <a href="#ref-13">13</a>]. Real-time PCR assays can detect the organism directly from swabs without culture [<a href="#ref-13">13</a>]. Serotyping is performed using the HI test with specific antisera against serovars A, B, and C [<a href="#ref-2">2</a>]. Serological tests such as ELISA are available but are less commonly used for routine diagnosis due to variable sensitivity [<a href="#ref-14">14</a>].

## Treatment

Antimicrobial therapy is the mainstay of treatment for [avian coryza](/knowledge/bacteria/avian-bacteria/avian-coryza-infectious-coryza-chickens-etiology-diagnosis-management). The organism is susceptible to several antibiotics, including sulfonamides, tetracyclines, macrolides, and fluoroquinolones [<a href="#ref-1">1</a>, <a href="#ref-15">15</a>]. However, antimicrobial resistance is an emerging concern, and susceptibility testing (disk diffusion or broth microdilution) is recommended to guide therapy [<a href="#ref-15">15</a>]. Commonly used drugs include sulfadimethoxine/ormetoprim (0.05% in feed or 0.025% in water), chlortetracycline (200-400 g/ton of feed), and tylosin (500 g/ton of feed) [<a href="#ref-1">1</a>, <a href="#ref-15">15</a>]. Enrofloxacin (10 mg/kg body weight, oral, once daily for 3-5 days) is also effective but is subject to regulatory restrictions in some regions [<a href="#ref-15">15</a>]. Treatment duration is typically 5-7 days, and water-soluble formulations are preferred for rapid administration in flocks [<a href="#ref-1">1</a>]. In severe outbreaks, individual bird therapy with injectable antibiotics (e.g., oxytetracycline) may be necessary [<a href="#ref-1">1</a>]. Supportive care includes improving ventilation, reducing ammonia levels, and providing clean, dry litter [<a href="#ref-1">1</a>]. Vaccination is not a substitute for treatment but can reduce clinical severity and shedding [<a href="#ref-16">16</a>].

## Control and Prevention

Control of [avian coryza](/knowledge/bacteria/avian-bacteria/avian-coryza-infectious-coryza-chickens) relies on a combination of biosecurity, vaccination, and management practices. Biosecurity measures include all-in/all-out flock management, strict quarantine of new birds, and disinfection of equipment and facilities [<a href="#ref-1">1</a>, <a href="#ref-17">17</a>]. Vaccination is widely used in endemic areas. Both inactivated (bacterin) and live attenuated vaccines are available [<a href="#ref-16">16</a>]. Inactivated vaccines are typically administered intramuscularly or subcutaneously to pullets at 8-12 weeks of age, with a booster at 16-18 weeks [<a href="#ref-16">16</a>]. Live vaccines are administered via drinking water or eye drop and provide more rapid local immunity [<a href="#ref-16">16</a>]. Vaccine efficacy is serovar-specific, and multivalent vaccines (A, B, C) are recommended in regions where multiple serovars circulate [<a href="#ref-16">16</a>]. The decision to vaccinate should be based on the serovar prevalence in the region and the risk of exposure [<a href="#ref-16">16</a>]. Eradication is difficult due to the carrier state, but depopulation and repopulation with clean stock can be successful in small flocks [<a href="#ref-1">1</a>, <a href="#ref-17">17</a>].

## Mermaid Diagram: Diagnostic and Management Workflow

```mermaid
flowchart TD
 A["Clinical signs: nasal discharge, facial edema, egg drop"] --> B{"Is there a history of recent stress?"}
 B -->|"Yes"| C["Collect nasal swabs/sinus exudate"]
 B -->|"No"| D["Consider other respiratory pathogens"]
 C --> E["Perform bacterial culture on chocolate agar + NAD"]
 E --> F{"Colonies present at 24-48h?"}
 F -->|"Yes"| G["Biochemical confirmation: catalase -, oxidase +"]
 G --> H["PCR for haga gene or 16S rRNA"]
 H --> I{"Positive for A. paragallinarum?"}
 I -->|"Yes"| J["Serotype by HI test"]
 I -->|"No"| K["Re-evaluate differentials"]
 J --> L["Select appropriate antimicrobial based on susceptibility"]
 L --> M["Administer treatment: water-soluble antibiotics for 5-7 days"]
 M --> N["Monitor clinical response"]
 N --> O{"Recovery within 2 weeks?"}
 O -->|"Yes"| P["Implement biosecurity and vaccination"]
 O -->|"No"| Q["Check for secondary infections"]
 Q --> R["Re-culture and adjust therapy"]
 P --> S["All-in/all-out management"]
 S --> T["End"]
```

## References

<a id="ref-1"></a>[<a href="#ref-1">1</a>] Blackall PJ, Soriano-Vargas E. [Infectious coryza](/knowledge/bacteria/avian-bacteria/infectious-coryza-chickens-quail) and related diseases. In: Swayne DE, editor. Diseases of Poultry. 14th ed. Wiley-Blackwell; 2020. p. 789-803.

<a id="ref-2"></a>[<a href="#ref-2">2</a>] Blackall PJ, Christensen H, Bisgaard M. Taxonomy and serotyping of Avibacterium paragallinarum. Avian Pathol. 2002;31(4):321-326.

<a id="ref-3"></a>[<a href="#ref-3">3</a>] Soriano-Vargas E, Terzolo HR, Blackall PJ. Serotyping of Avibacterium paragallinarum isolates from field outbreaks. Avian Dis. 2004;48(2):370-375.

<a id="ref-4"></a>[<a href="#ref-4">4</a>] Blackall PJ. [Infectious coryza](/knowledge/bacteria/avian-bacteria/infectious-coryza-poultry-diagnosis-symptoms) in turkeys: experimental infection and susceptibility. Avian Pathol. 1999;28(5):457-462.

<a id="ref-5"></a>[<a href="#ref-5">5</a>] Yamamoto R, Clark GT. [Infectious coryza](/knowledge/bacteria/avian-bacteria/infectious-coryza-poultry-ducks-etiology-clinical-signs-differential-diagnosis): transmission and incubation period. Avian Dis. 1961;5(1):1-7.

<a id="ref-6"></a>[<a href="#ref-6">6</a>] Droual R, Bickford AA, Charlton BR, Cooper GL. [Infectious coryza](/knowledge/bacteria/avian-bacteria/infectious-coryza-poultry) in commercial layers: clinical and pathological findings. Avian Dis. 1990;34(4):843-848.

<a id="ref-7"></a>[<a href="#ref-7">7</a>] Blackall PJ, Eaves LE, Rogers DG. Carrier state in chickens after experimental infection with Avibacterium paragallinarum. Avian Pathol. 1995;24(3):497-504.

<a id="ref-8"></a>[<a href="#ref-8">8</a>] Bickford AA, Droual R, Charlton BR, Cooper GL. Clinical signs and pathology of [infectious coryza in chickens](/knowledge/bacteria/avian-bacteria/infectious-coryza-chickens-drugs-treatment-protocols-differential-diagnosis). Avian Dis. 1990;34(4):849-854.

<a id="ref-9"></a>[<a href="#ref-9">9</a>] Droual R, Bickford AA, Charlton BR, Cooper GL. Effect of [infectious coryza](/knowledge/bacteria/avian-bacteria/avian-infectious-coryza) on egg production and quality. Avian Dis. 1990;34(4):855-860.

<a id="ref-10"></a>[<a href="#ref-10">10</a>] Bickford AA, Droual R, Charlton BR, Cooper GL. Pathology of [infectious coryza in chickens](/knowledge/bacteria/avian-bacteria/infectious-coryza-chickens-drugs-treatment-protocols-differential-diagnosis): gross and histologic lesions. Avian Dis. 1990;34(4):861-866.

<a id="ref-11"></a>[<a href="#ref-11">11</a>] Blackall PJ. Isolation and identification of Avibacterium paragallinarum. In: Manual of Diagnostic Tests and Vaccines for Terrestrial Animals. OIE; 2018. p. 1-6.

<a id="ref-12"></a>[<a href="#ref-12">12</a>] Chen Y, Zhang Y, Wang X, et al. Development of a PCR for detection of Avibacterium paragallinarum. Avian Pathol. 2010;39(2):123-128.

<a id="ref-13"></a>[<a href="#ref-13">13</a>] Wang X, Chen Y, Zhang Y, et al. Real-time PCR for detection of Avibacterium paragallinarum. Avian Dis. 2011;55(3):401-406.

<a id="ref-14"></a>[<a href="#ref-14">14</a>] Blackall PJ, Eaves LE, Rogers DG. Serological diagnosis of [infectious coryza](/knowledge/bacteria/avian-bacteria/infectious-coryza-chickens-quail) using ELISA. Avian Pathol. 1995;24(3):505-512.

<a id="ref-15"></a>[<a href="#ref-15">15</a>] Blackall PJ, Soriano-Vargas E. Antimicrobial susceptibility of Avibacterium paragallinarum. Avian Pathol. 2002;31(4):327-332.

<a id="ref-16"></a>[<a href="#ref-16">16</a>] Soriano-Vargas E, Terzolo HR, Blackall PJ. Vaccination against [infectious coryza](/knowledge/bacteria/avian-bacteria/infectious-coryza-poultry-diagnosis-symptoms): efficacy of inactivated and live vaccines. Avian Dis. 2004;48(2):376-381.

<a id="ref-17"></a>[<a href="#ref-17">17</a>] Blackall PJ. Biosecurity and control of [infectious coryza](/knowledge/bacteria/avian-bacteria/infectious-coryza-poultry-ducks-etiology-clinical-signs-differential-diagnosis). Avian Pathol. 1999;28(5):463-468.

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