NAVLE Respiratory

Bovine Contagious Pleuropneumonia Study Guide

March 28, 2026 25 min read 6 views
Contagious Bovine Pleuropneumonia (CBPP) is a severe infectious respiratory disease of cattle caused by Mycoplasma mycoides subspecies mycoides small colony type.

Overview and Clinical Importance

Contagious Bovine Pleuropneumonia (CBPP) is a severe infectious respiratory disease of cattle caused by Mycoplasma mycoides subspecies mycoides small colony type. It is classified as a World Organization for Animal Health (WOAH) notifiable disease and represents one of the most economically devastating cattle diseases in endemic regions.

CBPP is characterized by severe fibrinous pleuropneumonia, distinctive "marbled lung" appearance, and the formation of pulmonary sequestra in chronic cases. The disease continues to cause significant economic losses across sub-Saharan Africa, where it remains endemic.

Status Regions/Countries Year of Eradication/Last Case
Endemic Sub-Saharan Africa (24 countries), Parts of Asia Ongoing transmission
Eradicated USA, Canada, UK, Australia, Most of Europe USA (1892), UK (1898), Australia (1973)
Recent Control Portugal, Spain, Italy, China Portugal (1999), China (1996)

Etiology and Pathogenesis

Causative Agent

Mycoplasma mycoides subsp. mycoides small colony type (MmmSC) is the etiological agent of CBPP. This organism belongs to the class Mollicutes and is characterized by:

  • Lack of cell wall, making it resistant to beta-lactam antibiotics
  • Small genome size (500-1500 bp) requiring complex media for growth
  • Formation of characteristic small colonies on solid media
  • Environmental fragility due to absence of protective cell wall
High-YieldMmmSC was the first mycoplasma ever isolated (1898) and belongs to the Mycoplasma mycoides cluster, which includes several ruminant pathogens. European and African strains show distinct genetic lineages with varying virulence patterns.

Pathogenesis

The pathogenesis of CBPP involves multiple mechanisms that result in the characteristic lesions:

1. Initial Colonization: Following aerogenous infection, MmmSC adheres to bronchiolar and alveolar epithelial cells via specific adhesins. The organism colonizes mucosal surfaces and begins local multiplication.

2. Immune-Mediated Vasculitis: MmmSC triggers unregulated TNF-? production and immune-mediated vasculitis affecting pulmonary arteries, arterioles, veins, and lymphatic vessels. This leads to thrombosis and lobular infarction.

3. Galactan Production: The organism produces galactan polymers that modulate immune responses and promote dissemination while causing tissue damage.

Form Duration Clinical Signs Mortality Rate
Hyperacute Hours to 1 day Sudden death with fever (41.5°C), minimal respiratory signs Up to 100%
Acute 5-7 days Fever, anorexia, painful dyspnea, characteristic stance 50-70%
Subacute 3-4 weeks Intermittent fever, cough, gradual weight loss 10-25%
Chronic Months to years Asymptomatic carriers, sequestra formation Low, reservoir risk

Epidemiology and Global Distribution

Global Distribution

CBPP demonstrates a distinct global distribution pattern reflecting historical control efforts:

NAVLE TipRemember the mnemonic 'USA-UK-AUS: 1890s-1970s' for major eradication dates. The USA (1892), UK (1898), and Australia (1973) represent successful historical control programs using stamping-out policies.

Transmission and Risk Factors

Primary transmission route: Aerosol droplets from infected animals during coughing, with close and repeated contact typically required for infection.

Secondary transmission routes include:

  • Saliva, urine, and fetal membranes from infected animals
  • Transplacental transmission (vertical transmission possible)
  • Airborne transmission up to 200 meters under favorable conditions
Method Sensitivity Specificity Clinical Application
PCR High (95-100%) High (98-100%) Gold standard for acute cases, rapid results
Culture Moderate (70-85%) Very High (100%) Definitive but slow (5-21 days), requires fresh samples
CFT Moderate (75-90%) Good (85-95%) Traditional screening, OIE standard test
C-ELISA Good (80-95%) Good (90-98%) Mass screening, automation possible

Clinical Manifestations

CBPP manifests in four distinct clinical forms, each with characteristic presentations and timelines:

Pathognomonic Clinical Signs

Characteristic CBPP stance: Animals with acute CBPP adopt a distinctive posture to minimize respiratory pain:

  • Head lowered and extended forward
  • Back arched and elbows abducted away from chest
  • Preference for standing in shade when hot
  • Visible "heave marks" from labored breathing
Drug Class Examples Dosing Efficacy
3rd Gen Macrolides Tulathromycin, Gamithromycin 2.5 mg/kg SQ once 80-90% protection
Oxytetracycline Long-acting formulations 20 mg/kg IM, repeat PRN Effective, widely available
Fluoroquinolones Danofloxacin 2.5 mg/kg daily x 3 days Highly effective
Traditional Tylosin 10 mg/kg BID x 6 doses Variable, resistance noted

Pathological Findings

Gross Pathology

CBPP produces characteristic gross lesions that are pathognomonic for the disease:

1. Pleural Lesions:

  • Unilateral distribution (80-90% of cases affect only one lung)
  • Massive fibrinous pleuritis with up to 10 liters of straw-colored exudate
  • Pleural adhesions between visceral and parietal pleura

2. Pulmonary Lesions:

  • Marbled lung appearance due to thickened, edematous interlobular septa
  • Red and gray hepatization of lung lobules
  • Pulmonary sequestra (encapsulated necrotic tissue) in chronic cases
High-YieldThe "marbled lung" appearance is virtually pathognomonic for CBPP. It results from massive interlobular septal thickening due to fibrin and edema accumulation, creating a marble-like pattern when the lung is sectioned.

Microscopic Pathology

Histopathological examination reveals specific patterns consistent with mycoplasmal pneumonia:

  • Severe necrotizing bronchopneumonia with neutrophilic infiltration
  • Vasculitis affecting pulmonary vessels with thrombosis formation
  • Tertiary lymphoid follicle formation in chronic cases
  • MmmSC antigen detectable in bronchiolar/alveolar epithelium by immunohistochemistry
Region Type Strategy Implementation
Free Countries Stamping-out policy Quarantine, testing, culling of positive animals
Endemic Areas Mass vaccination Biannual vaccination, 80%+ coverage needed
Border Regions Combined approach Vaccination + treatment + movement control

Diagnostic Approaches

Definitive diagnosis of CBPP requires laboratory confirmation due to the potential for subclinical carriers and similar presentations with other respiratory diseases.

Laboratory Diagnostic Methods

Sample Collection Guidelines

Live Animals: Nasal swabs, broncho-alveolar lavage, transtracheal washing, and pleural fluid collected aseptically

Necropsy Samples: Lung tissue, lymph nodes, pleural exudate, and sequestra (if present)

NAVLE TipPCR positive but seronegative animals may indicate early infection (6-9 days post-infection). Complement fixation test becomes positive first (6-9 dpi), followed by immunoblotting (9-13 dpi) and competitive ELISA (13-16 dpi).
Disease Key Features Distinguishing Points Diagnosis
Pneumonic Pasteurellosis Acute pneumonia, bilateral lesions Cranioventral distribution, no marbling Culture, PCR
Haemorrhagic Septicaemia Acute septicaemia, gelatinous edema Characteristic edema, rapid course Blood smear, culture
Mycoplasma bovis Pneumonia, arthritis, mastitis Multi-systemic, no sequestra Species-specific PCR
Tuberculosis Chronic granulomatous lesions Caseous lesions, acid-fast bacilli Tuberculin test, PCR

Treatment and Management

Antimicrobial Therapy

While traditionally considered ineffective, recent research has demonstrated efficacy of specific antimicrobial protocols when used appropriately:

High-YieldThird-generation macrolides (tulathromycin, gamithromycin) show mycoplasmacidal activity and can achieve metaphylactic protection up to 80%. They represent a paradigm shift from "antibiotics don't work" to evidence-based treatment protocols.

Control and Prevention Strategies

Vaccination

Live attenuated vaccines remain the cornerstone of CBPP control in endemic areas:

  • T1/44 strain: Used in East and Central Africa
  • T1sR strain: Streptomycin-resistant variant used in West Africa
  • Protection: 40-60% after single vaccination, higher with boosters
  • Duration: 6 months to 2 years, requiring biannual revaccination

Control Strategies by Region

NAVLE TipFor effective control, herd immunity must reach 80%, achievable only through biannual vaccination as immunity wanes after 6 months. Combined vaccination-treatment programs can eliminate CBPP from defined populations within 6 months under optimal conditions.

Differential Diagnoses

Several respiratory diseases can mimic CBPP, requiring careful differentiation:

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