Pasteurella multocida pleural effusion: A case report and review of literature.

We describe a man who developed pleural effusion with Pasteurella multocida, and review the reported literature concerning this entity. We identified 21 such cases, including our own. Most patients with P. multocida pleural effusions are immunocompromised and/or have significant co-morbidities. These effusions are typically complicated parapneumonic effusions that are grossly purulent (87%) with a low pleural fluid pH (mean 6.8), high protein (mean 4.8 g/dl) and high LDH (mean 1911 U/L) and low glucose (28.6 mg/dl). Pleural fluid drainage with tube thoracostomy was required in the majority (62%) of cases.

Introduction

Pasteurella multocida (P. multocida) empyema is a rare clinical entity. We describe a patient with P. multocida empyema, as well as analyze all the available reports previously published in the medical literature. We describe the clinical and pleural fluid characteristics of these cases.

Methods

We performed a PubMed search for P. multocida empyema using keywords ‘Pasteurella multocida’, ‘empyema’ and ‘pleural effusion’. We identified 20 case reports in addition to our own and present their pleural fluid findings in Table 1, Table 2. The mean and standard deviation (for quantitative variables) are also presented. Findings of pleural fluid analysis are reported in conventional units wherever possible.

Table 1

Clinical characteristics and outcomes.

Reference number	Age (years)	Sex	Side of pleural effusion	Significant comorbidities	Chest tube	Outcome
[1]	63	M	Left	None known	Yes	Death
[2]	8	F	Right	Noonan syndrome	Yes	Survived
[3]	57	F	Bilateral	CHF	Yes	Survived
[4]	64	F	Left	Liver cirrhosis	Yes	Survived
[5]	86	F	Left	None known	No	Survived
[6]	69	F	Right	Liver cirrhosis	Yes	Death
[7]	54	F	Left	COPD	Yes	Survived
[8]	60	M	Right	None known	No	Death
[9]	57	F	Left	Liver cirrhosis, asplenia	Yes	Death
[10]	85	F	Bilateral	None known	Yes	Survived
[11]	65	F	Right	RA on steroids and methotrexate	Yes	Survived
[12]	88	M	Right	None known	Yes	Death
[13]	90	M	Right	None known	No	Survived
[14]	76	M	Right	Prostate CA, PVD, smoking	Yes	Survived
[15]	76	F	Right	None known	No	Death
[16]	77	M	Right	None known	No	Survived
[17]	51	M	Right	Bronchiectasis and BPF	No	Survived
[18]	72	F	Right	Chronic bronchitis	No	NR
[19]	75	M	Bilateral	None known	No	Death
[20]	67	F	Right	Liver cirrhosis and CHF	Yes	Death
Present Case	75	M	Left	ESRD, valvular/coronary disease	Yes	Death
Mean	67 (±17.7)	40% M, 60% F	57% Right, 29% Left, 14% Bilateral	57% Present, 43% None known	62% Chest tube placed	45% Death

F = Female, M = Male, CHF = congestive heart failure, COPD = chronic obstructive pulmonary disease, RA = rheumatoid arthritis, CA = cancer, PVD = peripheral vascular disease, BPF = bronchopleural fistula, ESRD = end stage renal disease, NR = not reported.

Table 2

Summary of findings of pleural fluid analysis.

Reference number	Appearance	pH	Total protein G/DL	LDH (U/L)	Glucose Mg/DL	WBCacount	PMN %
1	Purulent	NR	NR	NR	NR	NR	NR
2	Chylous	NR	8.8	NR	NR	8014	89
3	Purulent	NR	12.6	1590	3	10,500	98
4	Serosanguinous	NR	3.2	NR	100	19,150	91
5	Purulent	6.53	5.6	403	4	7000	96
6	Purulent	6.69	3	NR	5.4	10,500	98
7	NR	6.9	NR	NR	12	5140	NR
8	NR	NR	NR	NR	NR	NR	NR
9	Purulent	NR	NR	NR	NR	NR	NR
10	NR	6.8	4.9	NRb	1.44	160	60
11	NR	7.23	4.3	4209	44	13,900	43
12	Purulent	NR	4.2	NR	69	74,888	84
13	Purulent	NR	0.004	1676	59	17,100	95
14	Purulent	6.6	3.4	2052	11.7	1800	88
15	Purulent	NR	NR	NR	NR	NR	NR
16	Purulent	NR	NR	NR	NR	NR	NR
17	Purulent	NR	NR	NR	NR	NR	NR
18	NR	NR	NR	NR	NR	NR	NR
19	NR	NR	NR	NR	NR	NR	NR
20	Purulent	NR	NR	NR	NR	NR	NR
Present Case	Purulent	7.04	3.3	1535	<5	45,160	99
Meanc	87% Purulent	6.8 ± 0.2	4.8 ± 3.3	1911 ± 1255	29 ± 34	17,776 ± 21,472	86 ± 18

LDH: lactate dehydrogenase; PMN = polymorphonuclear leukocytes; WBC: white blood cell; NR = not reported.

Pleural fluid WBC count reported in several different units among these references; we therefore displayed the pleural WBC counts in units consistent with the peripheral WBC count in each reference.

LDH was elevated but could not be converted to conventional units.

±standard deviation, if applicable.

Case report

A 75-year-old man was hospitalized for 3 weeks of progressive shortness of breath. He had a history of an ischemic cardiomyopathy and valvular heart disease, and had undergone coronary artery bypass grafting, aortic and mitral valve repair. He also had hypertension, atrial fibrillation and had not been anticoagulated because of gastrointestinal bleeding. He had end stage renal disease presumed secondary to hypertension and had required renal replacement therapy for the last 3 years. He was a former smoker of 70 pack-years and had a pet dog.

Physical examination at the time of transfer to medical ICU showed that he was in mild respiratory distress with temperature 38.2 C, respiratory rate of 18/min, blood pressure 95/54 mmHg, irregularly irregular pulse 101/min and oxygen saturation 94% on 3L/min supplemental oxygen. Lung auscultation revealed decreased breath sounds with dullness to percussion at the posterior left base.

Laboratory data included: white blood cell count 16,100 cells/μl, hemoglobin 9.4 mg/dl, platelet count 152,000/μl. A chest radiograph showed a large left pleural effusion. Bedside ultrasonography revealed a homogeneously echogenic pleural effusion. A small-bore chest tube was introduced under ultrasound guidance. Purulent fluid was aspirated.

Pleural fluid analysis showed: pH 7.04, glucose <5 mg/dl, protein 3.3 gm/dl, LDH 1535 U/L, WBC 45,160/μl with 99% neutrophils, RBC 12,000/cmm. Pleural fluid Gram stain was negative. Piperacillin/tazobactam and linezolid were initiated.

P. multocida was detected on pleural fluid culture within 24 hours that was resistant to ampicillin but sensitive to amoxicillin/clavulanate. Linezolid was discontinued. Intra-pleural tPA and DNase were instilled through the chest tube that resulted in evacuation of the space (total fluid drained = 1.6L) with a residual pneumothorax suggestive of lung entrapment (trapped lung physiology). His dyspnea improved and he was transferred to the general medical ward. His fever resolved; oxygenation and leukocytosis continued to improve. However, the patient developed massive gastrointestinal bleeding resulting in cardio-respiratory arrest leading to death.

Discussion

We report the case of an elderly man with P. multocida empyema. He received timely and aggressive antibiotic therapy and complete drainage of the pleural space. Although therapy resulted in clinical improvement; he died from gastrointestinal bleeding and cardiac problems.

P. multocida is a gram negative encapsulated non-motile coccobacillus. It forms part of the normal flora in the oropharynx and nasopharynx but can also be a pathogen [21]. Animal exposure; usually from the scratch, bite or lick of a domestic cat or dog, is an important risk factor and is present in most cases of Pasteurella infection [21], [22].

Infection due to P. multocida is usually limited to the skin and soft tissue with regional complications [23]. P. multocida infection of the respiratory tract is uncommon, as is pleural infection that has been described in isolated case reports [22]. We identified 21 published reports, including our own, of P. multocida infected pleural effusions. In Table 1; we describe the clinical characteristics and outcome of these cases. Table 1 suggests that most patients with P. multocida pleural infection have underlying cardiopulmonary disease and/or are immunocompromised (12/21, 57%) and majority of patients had exposure to animals (15/21, 71%). Pleural drainage is often required (13/21, 62%) and the condition carries a high mortality (9/20, 45%).

Table 2 displays the available pleural fluid characteristics of these patients. The effusions are predominantly complicated parapneumonic effusions with 87% (13/15) described as purulent, and the following pleural fluid findings: very low pH (mean 6.8), high protein (mean 4.8 g/dl), high LDH (mean 1911 U/L) and a very low glucose concentration (mean 28.6 mg/dl). The mean pleural WBC count in the reported cases was 17,776 and there was a predominance of polymorphonuclear leukocytes in the large majority of the cases (mean 86%, 10/11 cases > 50%). Pleural fluid culture was positive in 90% of reported cases (18/20).

Our case report and literature review highlight that P. multocida may cause significant pleural disease. Pleural fluid findings typically reveal a complicated parapneumonic pleural effusion that often requires drainage. Pleural infection with P. multocida is often fatal, which may reflect the severity of infection or the moribund state of the patients who develop this infection.

Conflict of interest

SNJ, RS, AC: None.

MAJ: Consultant – Mallinckrodt, Biogen. Grant Support – Mallinckrodt, Foundation for Sarcoidosis research.