Atrophic rhinitis is a chronic bacterial disease of pigs that destroys the delicate scroll-shaped bones inside the nasal passages, called turbinates, leading to snout deformity, impaired breathing, and slower growth. Two bacteria are responsible: Bordetella bronchiseptica and toxin-producing strains of Pasteurella multocida. The disease has been a persistent headache for pig producers worldwide because it chips away at productivity in ways that are not always obvious until slaughter, and because the environmental conditions inside many commercial pig barns actively make it worse.
The Two Bacteria and Why the Combination Matters
Atrophic rhinitis comes in two forms, and the distinction matters for understanding severity. The milder form, sometimes called non-progressive atrophic rhinitis, is driven mainly by Bordetella bronchiseptica alone. This bacterium colonizes the nasal lining and causes turbinate damage, but the damage tends to be moderate and can partially reverse once the infection clears. The severe form, called progressive atrophic rhinitis, involves toxigenic strains of Pasteurella multocida, usually in combination with Bordetella. Progressive atrophic rhinitis causes irreversible destruction of the turbinate bones, visible snout distortion, and meaningful production losses.
The reason the combination is so damaging is that Bordetella acts as a pathfinder. It damages the nasal lining first, making it easier for toxigenic P. multocida to colonize and establish a foothold. Research using specific pathogen-free piglets showed that both Bordetella and toxigenic P. multocida could individually cause turbinate atrophy when given intranasally, but the combined infection produced the clinical picture recognized as progressive atrophic rhinitis.1PubMed Central. Vaccination against progressive atrophic rhinitis with a recombinant Pasteurella multocida toxin derivative Not every strain of P. multocida causes the disease. Only strains that produce a specific dermonecrotic toxin are culprits, which is why laboratory identification of toxigenic strains is central to diagnosis.
How the Toxin Destroys Bone
The damage in progressive atrophic rhinitis is not caused by inflammation in the usual sense. If you looked at affected turbinates under a microscope, you would not see the classic signs of an immune battle like swelling and masses of white blood cells. Instead, the damage is driven almost entirely by the dermonecrotic toxin produced by P. multocida, which hijacks the signaling pathways inside bone cells.2PubMed. The pathogenesis of atrophic rhinitis in pigs induced by toxigenic Pasteurella multocida
Bone is constantly being remodeled, even in healthy animals. Cells called osteoblasts build new bone, while cells called osteoclasts break old bone down. In a healthy pig’s nose, these processes balance out. The P. multocida toxin tips that balance dramatically. It activates osteoclasts, ramping up bone resorption, while simultaneously poisoning osteoblasts so they stop making new bone and eventually die. The result is that the turbinate bones thin out and disappear, sometimes almost completely.3PubMed Central. Pasteurella multocida toxin – lessons learned from a mitogenic toxin
At the molecular level, the toxin enters cells through receptor-mediated endocytosis and targets specific G proteins, permanently switching them on. This triggers a cascade of signals that stimulate osteoclast activity and suppress osteoblast function.4PubMed Central. Pasteurella multocida toxin – lessons learned from a mitogenic toxin Ultrastructural studies confirmed that osteoblasts exposed to the toxin show telltale signs of cellular distress before dying off entirely, leaving the bone without any repair capacity.5PubMed. Turbinate osteoporosis in pigs following intranasal inoculation of purified Pasteurella toxin: histomorphometric and ultrastructural studies Even purified toxin alone, applied to the nasal passages without any live bacteria, produces moderate turbinate atrophy, confirming that the toxin itself is the weapon, not the bacterial infection per se.6PubMed Central. Effects of purified Pasteurella multocida dermonecrotoxin on the nasal ventral turbinates of fattening pigs: histological observations
What You Actually See in Affected Pigs
In mild cases, the only outward sign may be sneezing, a slight nasal discharge, and occasional tear staining below the eyes. Many producers overlook these early signals because sneezing in a pig barn is practically background noise. As the disease progresses, the destruction of the turbinates leads to visible changes. The snout may twist to one side or shorten noticeably, giving the pig’s face a pushed-in appearance. In severe cases, the upper jaw can appear concave. These deformities are permanent because the turbinate bone, once destroyed, does not regenerate.
The turbinates serve an important function: they warm, humidify, and filter air before it reaches the lungs. Without intact turbinates, pigs are more vulnerable to secondary respiratory infections, including pneumonia. The cumulative effect on growth is real. Pigs with progressive atrophic rhinitis gain weight more slowly and convert feed less efficiently than unaffected herdmates, though the exact magnitude of the production hit varies widely between herds depending on severity, secondary infections, and management quality.7PubMed Central. The effect of atrophic rhinitis on growth rate
Air Quality Inside the Barn Is Part of the Problem
One of the more striking findings in atrophic rhinitis research is how much the air inside pig barns contributes to disease severity. Ammonia and organic dust, both common in intensive housing, don’t just make the environment unpleasant — they actively promote colonization by toxigenic P. multocida and worsen turbinate damage.
In controlled studies, pigs exposed to ammonia at concentrations as low as 5 parts per million showed significantly worse turbinate atrophy when also infected with P. multocida, compared with infected pigs kept in clean air. The effect peaked at around 10 ppm and, interestingly, declined somewhat at concentrations above 25 ppm, possibly because very high ammonia levels become so irritating that pigs reduce their breathing rate or because the extreme environment suppresses bacterial growth. Even in the absence of any bacterial infection, ammonia exposure at 10 ppm or higher caused mild but measurable turbinate atrophy on its own.8PubMed Central. Synergistic role of gaseous ammonia in etiology of Pasteurella multocida-induced atrophic rhinitis in swine
When researchers added organic dust to the mix alongside ammonia, the picture got worse. Pigs exposed to both pollutants and then challenged with P. multocida developed the most severe atrophy of any group tested. Clean-air control pigs had normal turbinate measurements, while pigs exposed to both pollutants and bacteria had atrophy roughly 75% more severe.9PubMed Central. Contributory and exacerbating roles of gaseous ammonia and organic dust in the etiology of atrophic rhinitis The practical implication is clear: ventilation, manure management, and reducing dust levels inside barns are not just welfare improvements — they directly influence the severity of atrophic rhinitis in herds where toxigenic P. multocida is circulating.
Diagnosing the Disease
Diagnosing atrophic rhinitis involves two separate questions: is there turbinate damage, and is toxigenic P. multocida present in the herd? The first question is usually answered at slaughter, by cross-sectioning the snout and scoring the turbinates visually. This is the gold standard for assessing lesion severity, but it obviously comes too late to help the individual pig. In live animals, veterinarians rely on clinical signs and nasal or tonsillar swabs to detect the bacteria.
Identifying whether a P. multocida isolate is toxigenic has historically been done through mouse inoculation or cell culture assays, but these methods are slow and either ethically problematic or technically demanding. An ELISA test developed for detecting the dermonecrotic toxin proved highly sensitive and more specific than both animal inoculation and tissue culture, making it a practical screening tool for herds.10PubMed. Use of ELISA to detect toxigenic Pasteurella multocida in atrophic rhinitis in swine
PCR-based testing pushed sensitivity further. In a comparison study across herds known to be infected with toxigenic P. multocida, standard bacterial culture identified the organism in 22 out of 346 swab specimens, the ELISA found it in 28, and the PCR assay picked it up in 40. Critically, when the PCR assay was tested on swabs from herds certified free of the toxigenic strain, it returned only two false positives out of 372 specimens.11PubMed. A specific and sensitive PCR assay suitable for large-scale detection of toxigenic Pasteurella multocida in nasal and tonsillar swabs specimens of pigs A later evaluation noted that all three methods gave similar results in detecting the toxin, though full agreement between them required strong PCR signals to be counted as positive.12PubMed. Evaluation of techniques for the detection of toxigenic Pasteurella multocida strains from pigs For large-scale herd surveillance, PCR has become the method of choice because it catches more carriers than either culture or ELISA.
Vaccination Through the Sow
Because piglets are most vulnerable to infection in the first weeks of life, the main vaccination strategy targets the sow rather than the piglet. Pregnant sows are vaccinated during gestation so they develop high antibody levels that transfer to piglets through colostrum. This passive immunity protects piglets during the critical early window when Bordetella and P. multocida are most likely to colonize the nasal passages.
The approach works well in practice. In challenge studies where piglets from vaccinated sows were deliberately inoculated with both Bordetella and toxigenic P. multocida, the vaccinated groups showed significantly lower nasal lesion scores and better daily weight gain compared with piglets from unvaccinated sows.13PubMed. Protection of piglets against atrophic rhinitis by vaccinating the sow with a vaccine against Pasteurella multocida and Bordetella bronchiseptica The challenge organisms were also recovered less frequently from piglets in the vaccinated group, suggesting that maternal antibodies not only reduced lesion severity but also limited bacterial colonization itself. Similar results have been seen with newer vaccine formulations: piglets from vaccinated sows had significantly lower nasal lesion scores even after deliberate dual-organism challenge.14The Pig Site. Safety and Efficacy of a New Vaccine for Preventing Porcine Atrophic Rhinitis
Experimental work on recombinant toxin derivatives has shown promise too. In one trial, piglets from gilts vaccinated with a modified form of the P. multocida toxin were largely protected from clinical and pathological signs of disease after challenge, while roughly 90% of piglets from unvaccinated controls developed severe turbinate atrophy.15PubMed Central. Vaccination against progressive atrophic rhinitis with a recombinant Pasteurella multocida toxin derivative The fact that the infection rate with toxigenic P. multocida was also significantly reduced in the vaccinated groups at five and eight weeks of age suggests the colostral antibodies were interfering with bacterial establishment, not just neutralizing the toxin after it was produced.
Antibiotics and the Resistance Picture
Antibiotics play a supporting role in managing atrophic rhinitis, particularly for controlling acute outbreaks or reducing bacterial shedding, but they are not a replacement for vaccination and environmental management. The antibiotic susceptibility picture for P. multocida is mixed and regionally variable. A study of Argentine strains associated with both progressive atrophic rhinitis and porcine pneumonia found that roughly 70% of strains were sensitive to common veterinary antibiotics including enrofloxacin, ceftiofur, ampicillin, tilmicosin, florfenicol, spectinomycin, gentamicin, oxytetracycline, and trimethoprim-sulfamethoxazole. However, all strains were resistant to lincomycin, and about 70% resisted tylosin. Resistance to other antibiotics ranged from 7% for ceftiofur up to 48% for erythromycin.16PubMed Central. Characterization and comparison of strains of Pasteurella multocida associated with cases of progressive atrophic rhinitis and porcine pneumonia in Argentina
These resistance patterns underscore why culture and sensitivity testing should ideally guide antibiotic choice in affected herds. Blanket use of a macrolide like tylosin, which was once a go-to for respiratory disease in pigs, would be ineffective against the majority of strains in that study. The broader trend in swine medicine is moving away from routine antibiotic use toward prevention-first strategies: vaccination, improved ventilation, and biosecurity measures that keep toxigenic strains out of the herd in the first place.
Breed Differences in Susceptibility
Not all pig breeds respond to the bacteria equally. A follow-up study at a test station found that Yorkshire and Hampshire pigs had higher prevalences and greater severity of both pneumonia and atrophic rhinitis compared with other breeds.17Journal of the American Veterinary Medical Association. Pneumonia and atrophic rhinitis in pigs from a test station—a follow-up study This is worth knowing for producers who run multiple breed lines and see uneven disease expression within a shared environment. Breed susceptibility can interact with stocking density, ventilation quality, and vaccination coverage to create pockets of disease that seem arbitrary but actually reflect underlying genetic vulnerability.
The genetics angle has not been extensively explored beyond these observational studies, but it aligns with what is known about breed-level variation in immune responses to respiratory pathogens more broadly. Crossbreeding programs and terminal sire selection often focus on growth traits and carcass quality; resistance to atrophic rhinitis rarely enters the conversation, though it arguably should in herds with persistent problems.
Eradication Through Depopulation and Repopulation
For herds with deeply entrenched disease, the most effective long-term solution has historically been to start over. Depopulation followed by thorough cleaning and repopulation with specific pathogen-free (SPF) pigs has a strong track record. In a series of 23 herds established using this repopulation method, 22 remained free of both atrophic rhinitis and enzootic pneumonia over the observation period.18PubMed Central. Attempts at Establishing Swine Herds Free from Atrophic Rhinitis and Virus Pneumonia: II. Repopulation with Specific Pathogen-Free Pigs
This approach is expensive and disruptive, but it highlights a key feature of the disease: toxigenic P. multocida is maintained within pig populations, not in the environment. Once the carrier animals are removed and facilities are cleaned, the buildings themselves are not a reservoir. The challenge is keeping the disease out afterward. Strict biosecurity, including closed-herd policies, quarantine of replacement animals, and testing of incoming stock for toxigenic P. multocida, is essential to protect the investment of repopulation.
Distinguishing Atrophic Rhinitis from Other Nasal Conditions
A runny-nosed, sneezing pig does not necessarily have atrophic rhinitis. Several other conditions can look similar on the surface. Porcine cytomegalovirus (PCMV), for example, can infect the nasal passages but causes a different pattern of damage. Experimental work in gnotobiotic piglets showed that PCMV lesions were confined to the lamina propria, the connective tissue layer beneath the nasal lining, and did not produce turbinate bone atrophy. In contrast, Bordetella infection caused bone atrophy and changes to the nasal epithelium itself.19PubMed. Relationship of porcine cytomegalovirus and B bronchiseptica to atrophic rhinitis in gnotobiotic piglets Histochemical analysis has further shown that nasal epithelial cells change their sugar residue profiles differently depending on whether the pig has PCMV infection or atrophic rhinitis, with certain sugar molecules tending to disappear during PCMV infection but increase during atrophic rhinitis.20Journal of Veterinary Medical Science. Histochemical and Lectinhistochemical Studies on Nasal Mucosa of Pigs with or without Respiratory Diseases
Dust irritation, poor ventilation, and other respiratory infections can also cause nasal discharge and sneezing. The definitive distinction is turbinate atrophy, which requires either snout cross-sectioning at slaughter or, in live animals, confirmation that toxigenic P. multocida is present through laboratory testing. Producers who assume every sneeze is atrophic rhinitis may vaccinate or medicate unnecessarily, while those who dismiss nasal signs as “just dusty conditions” may miss a progressive disease that is slowly degrading their herd’s performance.
Age and Timing of Infection
Young piglets are far more susceptible to severe turbinate damage than older pigs. The turbinate bones in neonates are thin, rapidly growing, and highly metabolically active, which makes them vulnerable to the osteoblast-killing effects of the P. multocida toxin. Experimental work demonstrated that clinical atrophic rhinitis could be induced in piglets as young as three weeks old using Bordetella, and that P. multocida could still cause measurable atrophy in piglets challenged at 16 weeks, though lesion development was generally less severe in older animals. This age-dependent susceptibility is why maternal vaccination is the linchpin of prevention: the goal is to protect piglets through the window when their turbinates are most vulnerable, roughly the first six to eight weeks of life. By the time colostral antibody levels wane, the turbinates have matured enough to be somewhat less susceptible, and the pig’s own immune system is better equipped to handle colonization.
Herds that rely solely on piglet vaccination rather than sow vaccination sometimes see disappointing results, partly because the piglet’s immune system at one or two weeks old does not mount as robust a response as the sow’s, and partly because the infection may already be establishing itself by the time piglet-directed immunity kicks in. The sow-focused strategy delivers ready-made antibodies on day one of life, exactly when they are needed most.