Spontaneous bacterial peritonitis with Pasteurella multocida in cirrhosis: case report and review of literature.
Key Words: cirrhosis, Pasteurella multocida, spontaneous bacterial peritonitis
A 48-year-old man with a history of hepatic cirrhosis, ascites, esophageal varices, hepatitis C, and anemia was admitted for lower abdominal pain, increasing abdominal girth, and diarrhea for 2 days. The patient had two healthy pet dogs but he denied any dog bites, scratching, or licking of open wounds. (1-11)
Examination revealed an afebrile, tachycardic man with blood pressure of 164/84 mm Hg. There was no evidence of bite or scratch marks. The abdomen was distended and tender with evidence of massive ascites. A paracentesis showed ascitic fluid white blood cell count of 21,300/[mm.sup.3] with 89% neutrophils and a negative Gram stain. Fluid was cultured in the following media: blood, McConckey, calcium nutrient agar plate, kanamycin-vancomycin, phenylethyl alcohol, chocolate agar, and thioglycolate. None grew any organism. The patient was empirically treated with cefotaxime. Blood cultures grew Pasteurella multocida in all of the four bottles sent simultaneously with the ascitic fluid. The antibiotic was changed to amoxicillin. The patient improved significantly and was discharged on the eighth day.
Culture-negative neutrocytic ascites (CNNA) is diagnosed when the ascitic fluid culture grows no bacteria, the ascitic fluid polymorphonuclear neutrophil (PMN) count is [greater than or equal to]250 cells/[mm.sup.3], no antibiotics have been given, and there is no other explanation for an elevated ascitic PMN. It may be difficult to recover organisms from peritoneal fluid cultures, presumably because the burden of organisms is low. Also, most episodes of CNNA are diagnosed by insensitive culture methods for which there are insufficient numbers of bacteria to reach the threshold of detectability. Inoculation into blood culture bottles can lead to detection of a single organism in the cultured aliquot of fluid. (12)
The route of infection for spontaneous bacterial peritonitis (SBP) is presumed to be hematogenous, lymphatogenous, or transmural migration. It is postulated that the hematogenous route is most likely in cirrhotic patients. The hepatic reticuloendothelial system is known to be a major site for removal of bacteria from blood, and animal studies have suggested that destruction of blood-borne bacteria by this system is impaired in experimental cirrhosis and alcoholic liver disease. The decrease in phagocytic activity seen with alcohol abuse and cirrhosis is due to inadequate intracellular killing of monocytes and neutrophils and impaired opsonisation. (1)
The most frequently recovered pathogen in SBP is Escherichia coli (37%), followed by Klebsiella pneumoniae (17%) and other streptococci including enterococci.
P multocida is an aerobic, facultatively anaerobic, Gramnegative coccobacillus that inhabits the oral cavity and the gastrointestinal tract of 70 to 90% of cats and 50 to 66% of dogs. (13)
It is most commonly a pathogen in acute skin, soft tissue, bone, and joint infections after an animal bite or a scratch or from licking of open wounds by these animals. The infections are also known to develop in patients exposed to animals but without a history of bites or scratches. (1) Respiratory tract and intra-abdominal infections have been associated with possible inhalation of the organism. (14) P multocida wound infection, septic arthritis, pneumonia, or meningitis can cause bacteremia, with or without metastatic lesions. (6) Nasopharyngeal colonization with P multocida with transient bacteremia and seeding of the peritoneum in immunocompromised cat owners could play an important role in the development of SBP. (6)
Several in vitro studies indicate that penicillin is the best treatment of virtually all forms of P multocida infections. Many cephalosporins demonstrate in vitro activity against P multocida, and activity increases with the later generation cephalosporins.
The Table summarizes the characteristics of 13 patients with P multocida SBP. Nine of these had positive blood cultures and two had a proven CNNA. Eleven patients received antibiotics. Four patients died, of which all but one received antibiotics. All of the treated patients received a cephalosporin or penicillin, except the two patients who finally died of the SBP.
Two of the four deaths occurred in the patients who were not treated with the appropriate antibiotics. It might have been secondary to a delay in diagnosis or a failure to suspect P multocida as a causative organism for the SBP in the respective patients. With early recognition of the disease and prompt and appropriate antimicrobial treatment, the in-hospital mortality rate of SBP has been reduced to approximately 20%. The lowest mortality rate, which was achieved with a combination treatment of cefotaxime and albumin, was 10%, (15) as opposed to 33.33% in our case series.
We propose that a high level of suspicion should be maintained, particularly for patients with a history of cirrhosis and animal contact. Cirrhotic patients with a risk of SBP should completely avoid animal contact. These patients may benefit from empirical antibiotic coverage for P multocida, which may reduce the high mortality rate associated with this kind of infection.
Table. Patient characteristics Animal, type Reference Yr/sex Clinical data of exposure Tseng HK et al 43 male Hepatitis B Sick-appearing (February 2001) Liver cirrhosis stray dogs, no Esophageal varices bite or scratch 54 male Hepatitis C-related cirrhosis Diabetes mellitus Beales et al 43 male Inactive alcoholic None, no bite or (April 1999) cirrhosis scratch Encephalopathy grade 2 Koch CA et al 66 female Biopsy-proven Cat, no bite or (March 96) alcoholic scratch cirrhosis mentioned Squamous cell carcinoma of the neck Fernandez-Esparrach 69 female Liver cirrhosis, Cat, no bite or et al (March 1994) pleural effusion scratch Honberg PZ et al 12 male Cirrhosis None, scratch- (June 1986) Acute active scar hepatitis of found unknown cause Vakil N et al 43 male Alcoholic liver Pet dog, licking (July 1985) disease and scratching Portal hypertension Patton F et al 48 male Alcoholic liver Game cocks and (November 1980) disease pet pig, no Portal hypertension bite or scratch Esophageal varices Szpak CA et al (June 55 male Micronodular None, no bite or 1980) cirrhosis scratch Acute hemorrhagic gastritis Jacobson JA et al 61 male Biopsy-proven Dog, no bite or (November 1977) cirrhosis scratch Esophageal varices Gastric ulcer Gerding DN et al 51 male 50% gastric Cat, scratch (March 1976) resection Billroth 2 anastomosis for peptic ulcer disease Chronic subhepatic abscess with a sinus tract suprahepatic abscess 62 male Bleeding None, no bite or hemorrhoids scratch Asterexis Our case (occurred in 48 male Hepatic cirrhosis 2 dogs, no bite July 2002) with ascites or scratch Esophageal varices Hepatitis C infection Ascitic fluid Blood Ascitic fluid Reference cultures cultures WBCs Tseng HK et al Not mentioned Positive Not mentioned (February 2001) Not mentioned Positive Not mentioned Beales et al Positive Negative 5,300 with (April 1999) 95% PMNs Koch CA et al Positive Not done 9,650 with (March 96) 82% PMNs Fernandez-Esparrach Positive (pleural Positive 105,000 et al (March 1994) fluid was also (pleural positive for fluid with Pasteurella 98% PMNs) multocida) Honberg PZ et al Positive Negative Not mentioned (June 1986) Vakil N et al Positive Positive 4,040 with (July 1985) 90% PMNs Patton F et al Positive Positive Not mentioned (November 1980) Szpak CA et al (June Positive Positive 760 with 76% 1980) PMNs Jacobson JA et al Negative Positive 1st set: 19,700 (November 1977) with 100% PMNs 2nd set: 2,800 with 90% PMNs Gerding DN et al Positive Negative 2,900 with (March 1976) 100% PMNs Positive Positive 2,200 with 85% PMNs Our case (occurred in Negative Positive 21,300 with July 2002) 89% PMNs Reference Antibiotics Outcome Tseng HK et al Cephalothin and No death (February 2001) gentamicin followed by ceftriaxone and amikacin then cefoxitin and gentamicin Cephalothin and gentamicin followed by oral cephalexin Beales et al 2 g cefotaxime IV BID No death (April 1999) Koch CA et al Ceftriaxone Continued abdominal (March 96) pain but no death; follow-up of abdominal pain revealed hepatic cancer with portal, celiac, and paracaval adenopathy Fernandez-Esparrach Ceftriaxone Progressive hepatic et al (March 1994) failure and death in the 3rd week Honberg PZ et al Netilmicin, No death (June 1986) metronidazole followed by penicillin Vakil N et al 12 g ampicillin QD Oliguria, drowsiness, (July 1985) development of asterixis and death on the 14th day Patton F et al 1 g ampicillin IV q 6 h Patient remained (November 1980) and 100 mg afebrile gentamicin IV q 8 h Szpak CA et al (June 2 million penicillin Recovery 1980) units IV q 4 h for 14 d Jacobson JA et al 100 mg gentamicin IV Recovery (November 1977) q 8 h and 2 g ampicillin IV q 6 h Gerding DN et al Clindamycin and Increased hepatic (March 1976) gentamicin failure and death on the 20th day Oxygen, albumin, Death 7 h after plasma, no admission antibiotics Our case (occurred in 2 g cefotaxime IV BID Recovery July 2002) followed by amoxicillin WBCs, white blood cells: PMNs, polymorphonuclear neutrophils. References 2 through 11.
Accepted July 16, 2004.
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RELATED ARTICLE: Key Points
* Spontaneous bacterial peritonitis (SBP) caused by Pasteurella multocida is rare.
* P multocida SBP has a very high mortality rate when it occurs.
* Avoidance of animal contact and empiric antibiotic coverage for P multocida is advocated.
Ila Tamaskar, MD, and Keyvan Ravakhah, MD, MBA, FACP
From the Department of Medicine, Huron Hospital, Cleveland Clinic Health System, Cleveland, OH.
Financial support of the study was provided by Huron Hospital, Department of Medicine, Cleveland, OH.
Reprint requests to Dr. Ila Tamaskar, Huron Hospital, 13951 Terrace Road, Cleveland, OH 44112.