Late Lesions of Experimental Contagious Caprine Pleuropneumonia Caused by Mycoplasma capricolum ssp. capripneumoniae

Abstract

A clinical, bacteriological, serological and patho-anatomical study was carried out on 12 goats surviving the acute stage of contagious caprine pleuropneumonia (CCPP), experimentally produced with Mycoplurma raprimlum ssp. capnpneumoniae (M. rapnipneumoniae), with the major aims of investigating the chronic stage of the disease and elucidating the possibility of a carrier state beyond the acute fulminant phase. The goats were killed 9, 16, 82 or 126 days after the onset of acute clinical sips. On day 9, clinical signs included low grade fever and persistent coughing. Thereafter, only intermittent coughing was recorded. Serum titres of complement-fixing antibodies to M. rapnpeumoniae were high at the period of fever but dropped thereafter. Post-mortem examination showed acute fibrinous pleuropneumonia on days 9 and 16, and chronic pleuropneumonia on days 82 and 126, including sequester formations in goats killed on day 126. Mymphma cap+nenmoniae was isolated on days 9 and 16 but not on later occasions. The study showed that goats recovered from acute CCPP may have lesions for a long time thereafter but provide no evidence of a carrier state among long-term survivors.

Experimental Contagious Caprine Pleuropneumonia: A Long Term Study on the Course of Infection and Pathology in a Flock of Goats Infected with Mycoplasma capricolum subsp. capripneumoniae

“…These features are collectively consistent with chronic fibrinous bronchopneumonia [8,15] and thus compatible with poor resolution of pneumonia from M. capripneumoniae infection. However, the agent was not grown from the lungs, in accordance with previous experiences from attempts to cultivate M. capripneumoniae from pulmonary or pleural lesions late in experimental infection [18,28,35]. In our study, cultivation was negative despite use of pyruvate-containing media known to markedly support growth [4,22].…”

“…Paraffin sections of the lungs of 6 goats that died with acute fibrinous pneumonia in the early phase of CCPP and with M. capripneumoniae confirmed on culture [36,35] were positive control tissues. For control of antigenic specificity of the primary antiserum, the following procedures were performed: the antiserum was (i) absorbed with M. capripneumoniae antigen (2 ml antiserum mixed with 0.2 mg antigen, kept at +4°C overnight and centrifuged) and then applied diluted 1:100 and 1:200; (ii) substituted by normal rabbit serum (Dako); (iii) applied on sections of pneumonic goat lungs with M. ovipneumoniae, M. capricolum, M. mycoides subsp.…”

“…Long term survivors of acute disease may display chronic pleuropneumonia or chronic pleuritis [13,28] but cultural recovery of the agent has not been demonstrated in such late stage pulmonary lesions [18,35]. Still, negative results of cultivation of M. capripneumoniae is not proof of freedom of infection [32] and the use of complementary techniques for microbial identification is indicated.…”

Diagnostic pathology in microbial diseases of sheep or goats

“…capripneumoniae (Caswell and Williams, 2007;Nicholas et al, 2012). Unilateral pleural and pulmonary involvement rather than bilateral is the norm and lesions can be either focal, multifocal or extensive (Wesonga et al, 2004;Nicholas and Churchward, 2012). Pleurisy (and pericarditis) can be fibrinous or fibrous and serous fluid is often present in the pleural cavity (Supplemantary material 16).…”

“…Lung lesions are those of granular consolidation and focal necrosis, sometimes evolving to sequestra, but no thickening of interlobular septa (as in the bovine homologue). Histologically, acute lesions consist of a fibrino-purulent to necrotic bronchopneumonia with vasculitis and thrombosis and peribronchiolar lymphoid cuffs; in advanced cases, pulmonary fibrosis and granulation tissue in alveoli are observed (Wesonga et al, 2004).…”