V311 Bacterial Pneumonia and Lung Abscesses of Adult Horses M. Keith Chaffin, DVM, MS, DACVIM Professor, Equine Internal Medicine, Large Animal Medicine and Surgery, College of Veterinary Medicine, Texas A&M University 1. Definition: colonization of pulmonary parenchyma by pathogenic bacteria. 2. Pathogenesis: bacterial pneumonia occurs when normal host defense mechanisms are compromised or overwhelmed. a. Pulmonary defense mechanisms include: i. Mucociliary clearance. ii. Phagocytic cells (alveolar macrophages, neutrophils): a) Alveolar macrophage is primary line of defense of the alveolar space. b) Alveolar macrophages phagocytize and process bacteria that gain access to the alveoli. c) Neutrophils are attracted to alveoli when bacterial infection occurs. Neutrophils important in engulfing and killing bacteria. iii. Cellular immunity: a) T-lymphocytes important against intracellular bacteria. iv. Humoral immunity: a) Upper airways protected by IgA. b) Lower airways protected by IgG. b. Bacteria gain access to lungs via inhalation, aspiration or hematogenous spread. Infection occurs when defense mechanisms are compromised or are overwhelmed by sheer numbers of bacteria. i. Mucociliary clearance may be compromised by: a) Viral infection b) Toxic gases (ammonia in poorly ventilated barns) c) Stressors ii. Phagocytic cell function may be compromised by: a) Viral infections b) Endotoxemia c) Neutropenia d) Stressors iii. Immune defenses can be compromised by: a) Poor nutrition b) Immunosuppressive drugs (corticosteroids) c) Immunologic disease d) Stressors iv. Pulmonary defense mechanisms may be overwhelmed by: a) Aspiration of oropharyngeal contents: (1) Laryngeal or pharyngeal dysfunction (2) Esophageal reflux (3) Esophageal obstruction (choke) b) Aspiration of foreign objects. c. Stressors that may compromise pulmonary defense mechanisms and increase susceptibility to bacterial pneumonia: i. Long-distance transport ii. Overcrowding iii. Poor nutrition iv. Inclement weather v. Smog, ammonia vi. Poor ventilation vii. Exercise (racing, training) viii. Viral infections d. Once bacteria colonize the lung, mixed infections facilitate microbial growth: i. Microbial synergy: a) Polymicrobic infections b) Mixed aerobic/anaerobic infections e. Bacterial growth results in tissue destruction and further recruitment of neutrophils and inflammatory mediators: i. There is accumulation of cellular debris, exudation of serum, and deposition of fibrin in alveolar spaces. ii. Gas exchange is thus compromised and ventilation/perfusion mismatches occur, resulting in hypoxemia. 3. Epidemiology a. Associated with antecedent viral infection, stress or aspiration: i. Performance horses are at higher risk of developing bacterial pneumonia because of their association with long distance transport, competitive performance, exposure to large numbers of horses and lack of rest between stressful events. Aspiration of dirt during racing may be a prominent factor as well. b. Management factors and vaccination status are important factors in the pathogenesis of bacterial pneumonia. 4. Etiologic Agents a. Streptococcus zooepidemicus—most common cause of bacterial pneumonia in adult horses and foals: i. Is a B-hemolytic Streptococcus. ii. Is a normal inhabitant of the pharynx and tonsillary tissue of normal horses. iii. Is an opportunistic organism: a) It cannot invade normal intact mucous membranes. b) Secondary invader after stress or viral infection. iv. Can also cause upper respiratory infection: a) Sinusitis b) Guttural pouch empyema c) Retropharyngeal lymphadenopathy b. Streptococcus equi: i. Causes lymphadenopathy “strangles” much more commonly than pneumonia. c. Gram negative organisms commonly isolated from horses with bacterial pneumonia include: i. Pasteurella spp ii. Klebsiella spp iii. E. coli iv. Bordetella bronchiseptica d. Anaerobes: i. Bacteroides fragilis, Bacteroides melaninogenicus, Clostridia spp. ii. Gain access often by aspiration of oropharyngeal contents. iii. Require anaerobic environment. iv. Complicate aerobic pneumonia. e. Polymicrobic isolates are common as are mixed aerobic/anaerobic isolates. 5. Clinical Signs: Horses with bacterial pneumonia usually present with all, some of or any combination of the following: a. Fever: may be intermittent—necessitates multiple daily monitoring to detect a fever spike. b. Cough: may or may not be spontaneous or may be inducible by tracheal palpation and/or rebreathing bag. c. Elevated respiratory rate (tachypnea). d. Nasal discharge: serous to mucopurulent. e. Anorexia (partial to complete). f. Exercise intolerance. g. Weight loss: associated with chronic pneumonia. h. Putrid odor to the affected horse’s breath is associated with anaerobic infection. i. Absence of putrid odor does not rule out anaerobic infection. 6. Clinical & Laboratory Findings/Diagnosis a. Auscultation of thorax: i. Early in disease process, increased intensity of expiratory sounds are heard. ii. In more advanced cases, may auscultate end-inspiratory crackles due to transient atelectasis and/or increased secretions. iii. Expiratory wheezes are auscultable when airways or inflamed or narrowed by thick secretions. iv. Decreased or absent ventral lung sounds suggest pleural effusion or ventral consolidation/abscessation. v. Referred large airway sounds may be ausculted over areas of consolidated or abscessed lung. vi. Horse may rapidly become tachypneic after applying a rebreathing bag. b. Thoracic percussion: i. May hear dull sounds over areas of pleural effusion, pulmonary consolidation or abscessation (does not differentiate between these). c. CBC: the following are often found but are not specific to bacterial pneumonia and their absence does not rule out bacterial pneumonia: i. Elevated WBC count ii. Neutrophilia iii. +/- bands iv. Hyperfibrinogenemia v. Hyperproteinemia (in chronic cases) a) Caused by hypergammaglobulinemia b) Decreased A:G ratio d. Thoracic radiographs: i. Allow characterization of severity and location of pulmonary parenchymal disease. ii. Allows detection of deep lung abscesses or cavitary lesions. iii. Radiographs and ultrasonography complement each other in providing characterization of pulmonary disease. e. Thoracic ultrasonography: i. Will detect and allow characterization of pleural effusion and abscessation, consolidation, necrosis and atelectasis of the peripheral lung. ii. Will not detect deep parenchymal pathology (deep to aerated lung). f. Transtracheal aspirate (TTA): i. Should be performed to obtain a sample for bacterial culture, Gram’s- stain and cytologic examination. ii. Antimicrobial agents should be discontinued 24 hours prior to performing TTA. iii. Cytologic Examination: a) Degenerative neutrophils often containing intracellular bacteria. b) Extracellular bacteria may also be visible. c) May see precipitated protein and necrotic material. iv. Gram’s-stain: a) Should be performed to guide antimicrobial therapy until culture and sensitivity results are obtained (48–72 hours). v. Bacterial Culture: a) Aerobic and anaerobic cultures should always be submitted. 7. Therapy: Ideally, antimicrobial therapy should be based on culture and sensitivity results obtained from TTA. Prior to obtaining microbiology results, S. zooepidemicus should be suspected. A mixed infection, including gram negative organisms, should be considered when initial therapy fails or when Gram-stains detect gram-negative organisms. a. S. zooepidemicus: i. Usually sensitive to potassium penicillin or sodium penicillin (22,000 IU/kg IV q 4 hrs) or procaine penicillin G (22,000 IU/kg IM q 12 hrs), ceftiofur (2.2 mg/kg IV, IM q 12 hrs). ii. Ampicillin (11 mg/kg IM or IV q 6 hrs) offers a broader spectrum against mixed infection. iii. Trimethoprim sulfadiazine (or sulfamethoxazole) is a broad spectrum alternative that can be administered orally (15–30 mg/kg PO BID). Not all S. zooepidemicus isolates are sensitive to TMS. iv. Doxycycline 10 mg/kg PO q 12 hrs. b. Mixed infections: i. In mixed infections with multiple or resistant organisms, use antimicrobial agents directed against the pathogens isolated: a) Gentamicin (6.6 mg/kg IV or IM SID) or amikacin (7 mg/kg IV BID– TID) are effective against many gram-negative organisms. (1) Combination therapy with an aminoglycoside and a penicillin or cephalosporin is often used. b) Cephalosporins c) Chloramphenicol (50 mg/kg PO QID) d) Trimethoprim—sulfas (15–30 mg/kg PO BID) e) Enrofloxacin (5 mg/kg IV q 24 hrs OR 7.5 mg/kg PO q 24 hrs) c. Anaerobic infections: i. Aggressive and early therapy is necessary for the resolution of anaerobic pulmonary infections. ii. Most anaerobes are sensitive to penicillins. a) However, Bacteroides fragilis produces a B-lactamase that renders penicillins and cephalosporins inactive. iii. Chloramphenicol is effective, but beware of human health concerns. iv. Metronidazole: a) 10–15 mg/kg BID to QID b) Effective against most anaerobes. c) Should be used in conjunction with antimicrobials against aerobic infection. d) Anorexia has been seen in some horses as a side-effect. d. Duration of therapy: i. Inadequate duration of therapy is probably the most common cause of treatment failure and relapse. ii. Should monitor clinical response (rectal temp., auscultation, clinical signs, rads, ultrasound). iii. Duration varies with severity of the individual case, but ranges from 7 days to 3–4 months. e. Rest: i. Stall rest should be enforced during treatment. Return to exercise after resolution of pneumonia should be gradual, and permitted only after complete resolution. 8. Complications a. Pulmonary parenchymal abscesses. b. Extension into pleural space (pleuropneumonia). 9. Prevention a. Depends upon management factors that impact on the normal defense mechanisms of the respiratory tract: i. Adequate ventilation. ii. Minimize stress factors discussed above. a) Especially in athletic horses that are gathered for competitive events. iii. Immunization at 3–4 month intervals against viral diseases (EHV-1 and influenza) may help reduce predisposition to bacterial pneumonia.
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