Contagious caprine pleuropneumonia

GENERAL INTRODUCTION: MOLLICUTES

Introduction

Contagious caprine pleuropneumonia (CCPP) is one of the most severe diseases of goats. It presents as an acute, highly contagious disease characterized by fever, coughing, severe respiratory distress and high mortality, and is caused by Mycoplasma capricolum subsp. capripneumoniae (Mccp). It has also been described in certain wild ruminants.

The history of the disease is rather complex since there are several mycoplasmas that may produce pneumonia or pleuropneumonia in goats, and the causative agent was only isolated and characterized in 1976. Due to the fastidiousness of the agent and its antigenic relations with other mycoplasmas, it took many years before CCPP was recognized as a specific disease entity. Its history should therefore be reconsidered in the light of our present knowledge. The past literature on the disease was comprehensively reviewed by Thiaucourt in 1994.⁶⁸

In 1873, in Algeria, a French military veterinary surgeon, Philippe Thomas, described a disease called Bou Frida with the characteristic clinical signs and lesions of what is now known as CCPP. This description seems to be the first one.⁷³ A few years later in 1881 in South Africa, Duncan Hutcheon reported a disease in goats imported from Turkey that had spread to local goats and which appeared to be CCPP.²² He carried out experiments that gave valuable information on the length of the incubation period and the epidemiology of the disease.^{22, 23}

From the beginning of the twentieth century, there were many reports of outbreaks of CCPP from different parts of the world, mainly the Mediterranean area or Africa, and attempts to reproduce it and isolate the causative organism were carried out. The latter, however, led to a growing confusion since several diseases caused by various Mycoplasma spp. were involved.^{5, 31, 37, 39, 49, 50, 55}

It was only in 1976 that Macowan and Minette⁴¹ isolated a mycoplasma strain in Kenya that was called F38 and that was different in its growth inhibition test from the strains previously isolated from caprine pleuropneumonia, such as Mycoplasma mycoides subsp. capri or M. capricolum. Experimental reproduction of the disease, in which the clinical signs and lesions observed in natural cases were manifested, was obtained by inoculating pure cultures of this strain into goats, and F38-like strains were subsequently isolated from such experimentally induced cases.^{21, 42, 59} Since then CCPP has been considered a specific disease entity and this has been confirmed by the application of Koch postulates.¹⁸ In 1993 the F38 strain was given a definitive name.³³

Aetiology

It has been established that the sole agent responsible for CCPP is Mycoplasma capricolum subsp. capripneumoniae (Mccp). Like all mycoplasmas, it is a small pleomorphic micro-organism lacking a cell wall. It shares serological and genetic properties with five Mycoplasma spp. that are pathogens of ruminants. It is included in the so-called Mycoides cluster (Table 1).⁷

Table 1 Evolution of the Mycoplasma mycoides cluster taxonomy from 1987¹³ to 2009⁴⁸

*MAKEPS: Mastitis, Arthritis, Keratoconjunctivitis, Pneumonia, Septicaemia

In vitro, Mccp is a slow-growing mycoplasma compared to the other species, and it does not hydrolyse arginine, while M. capricolum does. In addition, the use of substrates by the oxydative route, such as pyruvate, is typical of Mccp. 1 Molecular studies permit the F38-type strains to be classified as a subspecies of M. capricolum. A comparison of the genomic relationships between M. capricolum strains and F38 strains resulted in intra-group DNA-DNA relatedness values of 85 to 90 per cent, while the relatedness was only 70 per cent between the two groups. The M. capricolum species, therefore, had to be divided into two new subspecies.³³

Mycoplasma capricolum subsp. capripneumoniae is a very vulnerable micro-organism and is not able to survive for long in the external environment.

Epidemiology

Mycoplasma capricolum subsp. capripneumoniae has been isolated in Kenya,⁴¹ Ethiopia,⁷⁰ Eritrea, Sudan,¹⁹ Uganda,⁹ Chad,³⁴ and Niger, but there is serological evidence of its wider presence in West Africa, for example in Mali.⁶² It has also been isolated in Turkey in the Middle-East⁷⁴ and Oman²⁴ and the United Arab Emirates⁶⁰ in the Arabian Peninsula. More recently it has been isolated in East Turkey,¹¹ Mauritius,⁶⁶ Tajikistan,² China (both from...