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Spontaneous bacterial peritonitis with Pasteurella multocida in cirrhosis: case report and review of literature.

Abstract: Most Pasteurella multocida human infections involve skin and soft tissues and invariably develop after a bite or a scratch from a dog or a cat. However, other infections with this organism occur infrequently. Enteric microorganisms are the common cause of spontaneous bacterial peritonitis (SBP). We report a case of SBP in a cirrhotic patient from P multocida. English literature (Pubmed) review revealed 12 adult cases of SBP in cirrhotic patients with P multocida. Nine patients were exposed to animals, though a break in the skin or a bite was not reported in each case. The SBP was fatal in four of these patients.

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)

Case Report

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.

Discussion

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.

Conclusion

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.

References

1. Zurlo J. Pasteurella species; Levison ME, Bush LM. Peritonitis and other intra-abdominal infections, in Mandell, Douglas and Bennetts's Principle and Practice of Infectious Diseases. 5th edition, 2000, pp 2402-2405; pp 821-855.

2. Vakil N, Adiyody J, Treser G, et al. Pasteurella multocida septicemia and peritonitis in a patient with cirrhosis: case report and review of the literature. Am J Gastroenterol 1985;565:80-87.

3. Patton F, Dumas M, Cannon NJ. Pasteurella multocida septicemia and peritonitis in a cirrhotic cock trainer with a pet pig. N Engl J Med 1980;303:1126-1127.

4. Szpak CA, Woodard BH, White JO, et al. Bacterial peritonitis and bacteremia associated with Pasteurella multocida. South Med J 1980;73:801-803.

5. Gerding DN, Khan MY, Ewing JW, et al. Pasteurella multocida peritonitis in hepatic cirrhosis with ascites. Gastroenterology 1976;70:413.

6. Koch CA, Mabee CL, Robyn JA, et al. Exposure to domestic cats: risk factor for Pasteurella multocida peritonitis in liver cirrhosis? Am J Gastroenterol 1996;91:1447.

7. Beales IL. Comment. Am J Gastroenterol 1999;94:1110-1111.

8. Honberg PZ, Frederiksen W. Isolation of Pasteurella multocida in a patient with spontaneous peritonitis and liver cirrhosis. J Clin Microbiology 1986;5:340.

9. Tseng HK, Su SC, Liu CP, et al. Spontaneous bacterial peritonitis due to Pasteurella multocida without animal exposure. J Microbiol Immunol Infect 2001;34:293-296.

10. Fernandez-Esparrach G, Mascaro J, Rota R, et al. Septicemia, peritonitis and empyema due Pasteurella multocida in a cirrhotic patient. Clinical Infect Dis 1994;18:486.

11. Jacobsen JA, Miner P, Duffy O. Pasteurella multocida bacteremia associated with peritonitis and cirrhosis. Am J Gastroenterol 1977;5:489-491.

12. Runyon BA. Ascitis and spontaneous bacterial peritonitis, in Feldman M, Friedman SL, Sleisinger MH (eds): Sleisenger and Fordtran's Gastrointestinal and Liver Disease. 7th edition, 2002, pp 1517-1542.

13. Griego RD, Rosen T, Orengo IF, et al. Dog, cat, and human bites: a review. J Am Acad Dermatol 1995;33:1019.

14. Holst E, Rollof J, Larsson L et al. Characterization and distribution of Pasteurella species recovered from infected humans. J Clin Microbiol 1992;30:2984-2987.

15. Suzuki K, Takikawa Y. Marked improvement in the resolution of, and survival rates in, spontaneous bacterial peritonitis. J Gastroenterol 2002;37:149-150.

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.
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Title Annotation:Case Report
Author:Ravakhah, Keyvan
Publication:Southern Medical Journal
Date:Nov 1, 2004
Words:2039
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