The effect of an experimental Mycoplasma (M.) hyorhinis infection (3 times intranasal instillation of 3-5 ml bouillon with 10(7) Colony forming units [CFU]/ml) in combination with a standard thermomotoric stress (swimm-test) was studied in piglets using pathomorphological, immunomorphological and microbiological methods. The 92 piglets were divided into the following 5 groups: swimmers with infection (S-I; n = 19); swimmers without infection (S; n = 19); control piglets with infection (K-I; n = 21); controls without infection, but direct (K1; n = 16) or indirect contact (K2; n = 17) with experimentally infected animals. The experimental or spontaneous infection (direct or aerogen infection) with M. hyorhinis caused in 30.4 % of the piglets an acute or subacute, catarrhal-purulent bronchopneumonia with an interstitial component. Incidence and intensity of pneumonia were significantly higher in the groups with thermomotoric stress (independent from the mode of infection) than in the non-stressed groups. The M. hyorhinis pneumonia was characterized by a limited expansion and a trend to restitution. The causal agent (M. hyorhinis) was demonstrated with immunomorphological methods (immunofluorescence and PAP) in the ciliary zone of the nasal, tracheal and especially on the bronchial mucosa, and occasionally in the bronchioles and alveoli.

Electron microscopic investigations on the respiratory tract of piglets with and without Mycoplasma hyorhinis infection (10th day of life) partly combined with swim stress (15 degrees C water temperature) (n = 20/20) yielded the following results: colonization of Mycoplasma hyorhinis in the ciliary zone of trachea and bronchi in 15 out of 40 piglets (37.5%); the evidence rate of Mycoplasma hyorhinis in pneumonic lungs (8 out of 12 = 66.7%) was significantly higher than in nonpneumonic lungs (7 out of 28 = 25.0%) and highest in experimentally infected piglets with swim stress (9 out of 16 = 56.2%). Ultrastructural lesions: loss of cilia; bleb-formation; hydropic degeneration and desquamation of ciliary cells; the occurrence of cilia-free and immature epithelial cells; alveolar collapse; microatelectasis; oedematous swelling of pneumocyte I; accumulation of surfactant in the alveoli; hyperplasia of pneumocyte II; exudation of mononuclear macrophages and neutrophils with numerous digestion vacuoles; several lymphocytes and plasma cells, only a little lymphohistiocytic interstitial and peribronchial infiltration. Phagocytized mycoplasmas were found within the resorption vacuoles of neutrophils in the tracheobronchial area, for this once in alveoli, not (more) against in alveolar macrophages. The results were discussed with regard to etiology and pathogenicity of enzootic pneumonia in pigs.

SummaryExperimental studies on effects of chronic aerogenous toxic gas stress on unweaned piglets with ammonia of varying concentrations 3. Light‐ and electronmicroscopic studies on the pathology and pathogenesis of chronic aerogenous ammonia damage to the respiratory apparatus of the pigletTistopathological and EM studies on the respiratory tract of sucking piglets after chronic aerogenous NH3‐exposure (50 and 100 ppm for 4.5–6 weeks) showed, in comparison with controls without NH3exposure, the following changes: 1. Proliferation and hypersecretion of goblet cells in the tracheobronchial mucosa, with production of an acid mucus in the upper trachea after 100 ppm compared with reduction and death of goblet cells. 2. Occurrence of necrobiotic changes in ciliary cells (vesicular widening of microvilli; cytoplasmic protruberances with and without inclusion of cilia; nodular swelling of cilia; local or extended loss of cilia etc.). 3. Destruction of pneumocyte‐1 extensions, in part with exposure of the alveolar membrane; partial or complete alveolar collapse; proliferation of pneumocytes‐II; freeing of lamellar bodies and uptake of these by alveolar macrophages. 4. Reactive inflammatory processes in the tracheobronchial mucosa (massive cellular infiltration) and in lung parenchyma (slight to medium grade interstitial pneumonia). The changes are discussed in relation to the pathogenesis of NH3effects on the respiratory tract of the sucking pig.ZusammenfassungPathohistologische und transmissionselektronenmikroskopische Untersuchungen am Atmungsapparat von Saugferkeln nach chronischer aerogener NH3‐Exposition (50 und 100ppm; Exposition 4,5–6 Wochen) ergaben im Vergleich mit Kontrolltieren ohne NH3‐Einwirkung folgende Veränderungen: 1. Vermehrung und Hypersekretion von Becherzellen in der Tracheobronchialschleimhaut mit Produktion eines sauren Schleims, in der oberen Trachea nach 100 ppm dagegen Verringerung und Untergang von Becherzellen. 2. Auftreten degenerativ‐nekrobiotischer Veränderungen an den Zilienzellen (blasige Auftreibung von Mikrovilli; zytoplasmatische Protuberanzen ohne und mit Einschluß von Zilien; kolbenartige Anschwellung von Zilien; umschriebener oder ausgedehnter Zilienverlust…). 3. Destruktion von Pneumozyten‐I‐Ausläufern z.T. mit Freilegung der alveolären Basalmembran; partieller oder vollständiger Alveolenkollaps; Vermehrung von Pneumozyten‐II; Abgabe von Lamellarkörperchen und Aufnahme derselben durch Alveolarmakrophagen. 4. Reaktiv‐entzündliche Prozesse an der Tracheobronchialschleimhaut (mäßige zellige Infiltration) und am Lungenparenchym (gering‐ bis mittelgradige interstitielle Pneumonie). Die Veränderungen werden unter dem Gesichtspunkt der Pathogenese der NH3‐Wirkung auf den Atmungsapparat des Saugferkels diskutiert.