14 month old, female, Holstein-Friesian (Bos Taurus). This heifer was part of an experimental
setting and inoculated by the intranasal and intratracheal route with 109
CFU of Mycoplasma mycoides subsp. mycoides (Mmm). The animal was
humanely destroyed 4 weeks later and submitted for necropsy.
Lung: Multifocally, the pulmonary pleura
was thickened and fibrotic with multiple adhesions to the thoracic wall. Only
the right pulmonary caudal lobe was markedly enlarged and consolidated (25 cm
in diameter). On cut section, there were variably sized bulging yellowish-grey
to pale red and dry areas (necrosis) with marked interlobular fibrosis and
distension of thrombosed lymph vessels. The left cranial lobe was diffusely
Lung: There are multifocal to coalescing areas of
coagulative necrosis effacing 60% to 90% of the parenchyma (depending on
location). Multifocally, there is mineralization in the central core of
necrosis. Preexisting alveolar and bronchiolar lumina are replaced and expanded
by an exudate composed of eosinophilic beaded fibrillar material (fibrin)
admixed with large numbers of degenerate and few viable neutrophils,
karyorrhectic debris and fewer alveolar macrophages, lymphocytes, and plasma
cells. Adjacent and surrounding the necrotic foci the interlobular septa are
markedly expanded up to 20 times by fibrovascular tissue (fibrosis) with
numerous aggregated lymphocytes (lymphoid hyperplasia), scattered plasma cells
and histiocytes (sequestration). Necrotic debris and homogenous eosinophilic
material is present in various lymphatic vessels (thrombosis). Medium sized
bronchi are surrounded by thick layers of connective tissue. In less
consolidated areas alveoli coalesce and are expanded by clear space (emphysema)
or partially contain eosinophilic fluid (edema).
Lung: Pleuropneumonia, fibrinonecrotizing, chronic, multifocal to
coalescing, severe, with sequestrum formation, lymphoid hyperplasia, and interlobular
specific for Mmm in lung tissue - positive
Contagious bovine pleuropneumonia
Specific gross lesions in CBPP depend on the course of
disease. Severe congestion and hemorrhage are characteristic in the acute phase
of fibrinous pleuropneumonia leading to red discoloration of lung tissue. The
pleuropneumonia derives from early deposition of fibrinous exudate on
the pleural surface resulting in accumulation of abundant yellow material in
the pleural cavity. There is marked thickening and inflammation of the pleura
leading to fibrinous pleurisy. On cut surface, dilatation and thrombosis of
lymph vessels accompanied with interstitial edema lead to distension of
interlobular septa giving the lung a marbled appearance. In chronic cases,
areas of coagulative necrosis eventually develop into
sequestra by which
necrotic lung parenchyma is encapsulated by connective tissue.2
Due to the fact that the animal in this case was part of a challenge model targeting the immune response, necropsy was performed only in the chronic phase of disease. Thus, histological lesions of the early stages of CBPP-=like hyperemia, interstitial edema and marked lymphangiectasia with lymphatic thrombosis and obstruction as well as diffuse fibrinous exudation were not present in the slides. Later on, neutrophils invade diffusely within the parenchyma and the fibrin deposits.2,3,4 Since the branches of the bronchioles within the necrotic foci remain unchanged, the demarcation starts in an angiocentric way. From here and in broad layers with peripheral leukocyte accumulation and demarcation, a fresh granulation tissue extends towards the surrounding necrosis and yields the sequestrum.4
The pathogenicity of CBPP is not completely understood. Virulence factors of Mycoplasma species seem to be determined by intrinsic metabolic or catabolic pathway functions or by proper constituents of the mycoplasmal outer surface. It is unclear by which mechanisms Mmm can evade the killing by phagosome-lysosome fusion, which toxic molecules are produced that are responsible for cellular damage, and how vasculitis and thrombosis are induced. It is assumed that the bacterial membrane lipoprotein LppQ, is involved in the pathogenesis. The virulence of some Mmm strains seems to be related to the release of H2O2 which is cytotoxic.5 Toxic galactan production, ciliary dysfunction, TNF-alpha dysregulation and immune-mediated vasculitis are also discussed to be involved in the pathogenic process of CBPP. Vasculitis and thrombosis of arteries, small caliber blood and lymphatic vessels are known to be crucial for the development of coagulative necrosis of lung tissue.3 Little is known why CBPP is mainly restricted to the caudal pulmonary lobes and often occurs unilaterally.
Lung:Â Bronchopneumonia, fibrinosuppurative and
necrotizing, chronic-active, diffuse, severe, with marked interlobular edema and fibrosis
and fibrosis and lymphoid hyperplasia.Â Â
The contributor has done an outstanding job in reviewing
this pathogen, which, with the eradication of rinderpest, is considered to be
the most important pathogen in affected countries.7 It is the only
bacterial disease currently on the OIEâs
A list of severe infectious animal
disease. Eradicated from much of the world, it has never been
reported in South America and several Saharan and Middle Easter countries. It
is considered eradicated in North America, much of Asia, Australia, and
countries comprising the southern part of Africa. In the remaining part of
sub-Saharan Africa, the disease is present and yet causes marked livestock
losses. Current information on outbreaks of this disease may be found at the
World Animal Health Information Service.
In the United States, the federal veterinary service, the US Bureau of Animal Industry, was founded in 1884, largely to eradicate the disease of contagious bovine pleuropneumonia. Its first director, Dr. Daniel Salmon had begun his years-long crusade to stamp out the disease in 1879, and was given the task of organizing the BAI in 1884, and established the Pathological Division in 1891. In addition to work on contagious bovine pleuropneumonia (which was eradicated from the United States in 1892, the BAI Pathological division did yeoman work in eradicating and developing vaccines for many other diseases, including foot-and âmouth disease, blackleg, tuberculosis, glanders, dourine, and Texas cattle fever (bovine babesiosis). Their groundbreaking research as a division of the USDA came to a halt in 1953 when their duties were transferred to the Agricultural Research Service, a newly created organization under the Eisenhower administration.6
MMM belongs to the so-called
mycoides cluster, containing MMM, M. mycoides susbsp capri (MMc),
M. capricolum subsp capricolum (Mcc), M. capricolum
susbsp. capripneumoniae (Mccp) and M. leachii, containing a
number of closely related previous unclassified mycoplasmas. MMMâs most
closely related member of this cluster is Mycoplasma mycoides susbsp. capri,
a bacterium which causes a syndrome called
MAKePS in small ruminants,
primarily goats, composed of mastitis, arthritis, keratitis, pneumonia, and
septicemia. It can also be identified in the ears of normal goats.7
The moderator reviewed several other severe fibrinosuppurative pleuropneumonias in cattle, and the subtle gross and histologic lesions that might help differentiate them, to include Mannhemia hemolytica, Histophilus somni, Pasturella multocida, and Mycoplasma bovis, in addition to MMM.
1. Caswell JL, Williams KJ. Respiratory system. In: Maxie MG ed. Jubb, Kennedy and Palmer's Pathology of Domestic Animals. Vol 2. 6th ed. Philadelphia, PA: Elsevier; 2016:551-554.
2. LÃ³pez A, Martinson SA. Respiratory System, Mediastinum, and Pleurae. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Mosby; 2017:519-520.
3. LÃ³pez A, Martinson SA. Respiratory System, Mediastinum, and Pleurae. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Mosby; 2017:532-533.
4. Nieberle K, Cohrs P, Lehrbuch der speziellen pathologischen Anatomie der Haustiere, Teil I, 5th ed. Jena: VEB Gustav Fischer Verlag; 1970: 270-274.
5. Pilo P, Frey J, Vilei EM. Molecular mechanisms of pathogenicity of Mycoplasma mycoides subsp. mycoides SC. Vet J. 2007;174(3):513-21.
6. Saunders, LZ. A history of the Pathological Division of the Bureau of Animal Industry, United States Departmen of Agriculture between 1891-1921. Vet Pathol 1989; 26:531-550.
7. Thiacourt F, Manso-Silvan L, Salah W, Barbe V, Vacherie B, Jacob D, Breton M, Dupuy V, Lomenech AM, Blanchard A, Sirand-Pugnet P. Mycoplasma mycoides, from
mycoides Small Colonyto
capri. A microevolutionary perspective. BMC Genomics 2011, 12:114-133.
8. Zachary JF. Mechanisms of microbial infections. In: Zachary JF, ed. Pathologic Basis of Veterinary Disease. 6th ed. St. Louis, MO: Mosby; 2017:170-171.
9. World Organization for Animal Health (2009). Contagious Bovine Pleuropneumonia. OIE, Paris. http://www.oie.int/fileadmin/Home/eng/Animal_Health_in_the_World/docs/pdf/Disease_cards/CONTAGIOUS_BOVINE_PLEUROPNEUMONIA.pdf