Environmental ammonia and mycoplasma: a summary of Broderson et al. 1976

Mycoplasma is a respiratory disease caused by Mycoplasma pulmonis, an organism carried by all pet rats and found in wild rats too. All rats carry M. pulmonis, but not all show symptoms. These symptoms can be treated, but M. pulmonis can never be completely eradicated from a rat's respiratory system by medical treatment. Mycoplasma is therefore of enormous concern to rat enthusiasts.

Many factors are involved in triggering or worsening an outbreak of mycoplasma symptoms, and one of these factors is urine odors in the cage. Why should this be the case? What is going on in the rat's respiratory system?

Broderson et al. (1976) conducted an experiment to examine what is going on in the rat's respiratory system when rats are exposed to mycoplasma and urine odors. The authors took young adult pathogen-free rats (pathogen free means they don't carry bacteria or fungi), and divided them into several groups. The experiments lasted about 6 weeks.

Natural ammonia and mycoplasma (Experiment 1)

All rats, whether they were exposed to ammonia or not, showed mycoplasma symptoms starting at 10 days after inoculation (snuffling, head shaking). A few rats in the dirty cage groups had labored breathing and panting after 14 days.

All rats had damaged lungs, but the dirty-cage rats' lungs were more damaged than the clean-cage rats' lungs. Specifically, rats in both groups had partial or complete collapse of the lungs (atelectasis), and fluid in the lungs (consolidation). However, lung lesions were observed in more of the dirty-cage rats than the clean-cage rats, and some of the the dirty-cage rats' lungs were dilated and distorted (bronchiectasis), while the clean-cage rats' lungs were not.

Pure ammonia and mycoplasma (Experiment 2)

Rats in the ammonia groups snuffled more than the rats in the no-ammonia groups.

The pathological results were similar to Experiment 1: mamy more in the ammonia groups had dilated and distorted lungs or lung abscesses. Lung collapse and fluid in the lungs was always more common in the ammonia groups than in the no-ammonia groups. Lastly, the lesions in the nose, ears, throats and lungs of the ammonia groups were more severe than those of the no-ammonia groups.

Increasing levels of ammonia were positively associated with prevalence of lung lesions: the higher the ammonia concentration, the more rats had lung lesions.

Ammonia without mycoplasma (Experment 3)

All the rats exposed to ammonia (from the natural or pure sources) had lesions in their noses. The control rats had no nasal lesions at all. Most of the ammonia-rats' lesions were at the front of their nasal passages, and the skin of their nasal and respiratory passages (olfactory and respiratory epithelium) was three or four times thicker than normal. This damaged area had dilated vessels and swelling (edema), and some of the submucosal glands were replaced by collagen.


Effects of M. pulmonis: All rats infected with M. pulmonis (ammonia and no-ammonia groups) had inflammed nasal mucus membranes (rhinitis), inflammation of the middle ear (otitis media), and inflammation of the trachea. Lung lesions occur irregularly, but are always associated with upper respiratory disease. Therefore, under normal circumstances, M. pulmonis prefers to inhabit the upper respiratory tract and produces lung diseases as a secondary effect.

Effect of ammonia: Chronic exposure to ammonia produces nasal lesions. Rats with M. pulmonis that were exposed to ammonia were more likely to have lung lesions, and those lesions were more severe, than M. pulmonis-infected rats who were not exposed to ammonia. Therefore, chronic exposure to ammonia, perhaps through injury to the nasal mucosa, enhances the growth of M. pulmonis in the upper respiratory tract, producing more bacteria which subsequently invade the lung.

Ammonia -- produced by soiled bedding or from other sources -- drastically enhances mycoplasma in rats.

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