Peritonitis due to brucellosis in a patient newly diagnosed with liver cirrhosis complicated by ascites: A case report and literature review

Abstract

Brucellosis is a common zoonotic disease with a wide variety of clinical manifestations. Spontaneous bacterial peritonitis (SBP) is a rare form among them. Here, we present the case of a 63-year-old woman with newly diagnosed liver cirrhosis complicated with ascites and diagnosed as spontaneous bacterial peritonitis with Brucella spp. growth in culture, and the literature is reviewed.

Clinical Pearls

• Unique Features of the Case: Brucella-related SBP revealed previously undiagnosed cirrhosis with ascites. Diagnosis was challenging because serum Brucella tests were negative, yet peritoneal fluid cultures were positive after raw-milk cheese exposure.

• Primary Lesson for Clinicians: In endemic areas, consider Brucella in cirrhotic patients with new-onset ascites or atypical/nonresponding SBP, even when serology is negative; culture-based diagnosis can enable timely targeted treatment.

Introduction

Brucellosis is a zoonotic infection transmitted from infected animals to humans by ingesting food products or contacting tissues and fluids.^[1] Its endemic regions include the Mediterranean basin countries, the Middle East, and Central Asian countries.^[2] In particular, Eastern Mediterranean countries such as Syria, Turkiye, and Iraq show the highest prevalence rates, ranging from 0.029 to 200.41 cases per 100,000 people.^[3] Brucellosis typically manifests with insidious onset of fever, fatigue, night sweats, and joint pain. Brucellosis can affect any organ system and present a wide range of symptoms. Intra-abdominal manifestations are rare, including cholecystitis, hepatic or splenic abscess, pancreatitis, ileitis, colitis, and peritonitis.^[4]

SBP related to brucellosis is particularly difficult to recognize. It can be fatal if misdiagnosed and left untreated. A review of the literature shows that most of the cases reported with Brucella peritonitis had a previous diagnosis of chronic liver or kidney disease. Detection of Brucella spp. as the causative agent of SBP in immunocompetent individuals is rare.^[5–7]

To further emphasize the importance of brucellosis in the differential diagnosis in regions where the disease is endemic, such as the Mediterranean basin, we present the case of newly diagnosed liver cirrhosis in a patient who developed SBP due to brucellosis. In addition, we provide a comprehensive review of the clinical manifestations, diagnostic methods, and therapeutic interventions of this rare condition.

Case Report

A 63-year-old woman presented with abdominal distension that started two months ago and gradually increased, weakness, and low blood pressure for the last week. She had no complaints of abdominal pain, high fever, nausea, or vomiting at presentation. She had a history of type 2 diabetes mellitus (DM) for 20 years, total colectomy for liposarcoma in the colonic mesentery five years ago, and cholecystectomy for cholelithiasis two months ago. On physical examination: fever: 36°C, pulse: 92/min, blood pressure: 82/43 mmHg, SpO₂: 92% (room air). On physical examination, the abdomen was found to be severely distended. There was diffuse tenderness on palpation. There was no defense or rebound. On percussion, a matte with an upward-pointing opening was detected. Biochemical test results are given in Table 1.

Table 1.

Biochemical test results

	Patient value	Reference range
Hemoglobin (g/dL)	12.7	13.0–17.5
Leukocyte count (per mm3)	9240	4000–11000
Platelet count (per mm3)	190,000	150,000–450,000
International normalized ratio (INR)	1.1	0.4–1.2
Creatinine (mg/dL)	0.89	0.7–1.1
Sodium (mEq/Liter)	131	135–145
Aspartate aminotransferase (U/L)	126	0–32
Alanine aminotransferase (U/L)	83	0–33
γ-glutamyl transferase (U/L)	140	0–42
Alkaline phosphatase (U/L)	166	35–104
Total bilirubin (mg/dL)	0.32	0.3–1.2
Direct bilirubin (mg/dL)	0.05	0.1–0.3
Albumin (g/dL)	2.7	3.5–5.2
Total protein (g/dL)	4.9	6.6–8.7
C-reactive protein (mg/L)	4.4	0–5

On abdominal ultrasonography, the contours of the liver were micro-lobulated, and the left lobe corner section was blunted. The spleen was normal, and 11 cm of free fluid was observed in the deepest perihepatic area in each quadrant. Esophageal varices were detected in esophagogastroduodenoscopy. Viral hepatitis serology results are given in Table 2.

Table 2.

Viral hepatitis serology

HBsAg	Negative
Anti-HBc total	Negative
Anti-HBs	Positive (98 mIU/mL)
Anti-HAV IgG	Positive
Anti-HCV	Negative
HCV-RNA	Negative

HBsAg: Hepatitis B surface antigen; HBc: Hepatitis B core; HBs: Hepatitis B surface; HAV: Hepatitis A virus; IgG: Immunoglobulin G; HCV: Hepatitis C virus; RNA: Ribonucleic acid.

Autoimmune test results are given in Table 3. Because she had type 2 DM with a BMI of 30 kg/m², metabolic dysfunction-associated fatty liver disease (MAFLD) was considered as the cause of liver cirrhosis. Diagnostic paracentesis results are given in Table 4. Ascitic fluid cultures were taken. On the second day of follow-up, abdominal pain and high fever (maximum 38°C) developed. Blood cultures were taken. Gram-negative coccobacilli were detected on direct Gram staining of peritoneal fluid. The patient was diagnosed as having spontaneous bacterial peritonitis and was put on piperacillin-tazobactam therapy. Brucella species growth was detected on the 5^th day in the peritoneal fluid culture taken from two different samples. However, the serum Brucella agglutination test (Brucella standard tube agglutination test and Brucella ELISA test) was negative. We diagnosed the patient with seronegative Brucella peritonitis due to a negative serum serology titer for Brucella. Empirical piperacillin-tazobactam treatment was stopped, and rifampicin (600 mg/dose, once daily, PO) and doxycycline (100 mg/dose, twice daily, PO) were administered. When her anamnesis was detailed, we learned that she had been consuming cheese made from raw milk until about two weeks ago. On the 7^th day of treatment, the patient's fever returned to normal, abdominal pain decreased, and in control paracentesis, neutrophils were 84 in the peritoneal fluid cell count.

Table 3.

Autoimmune hepatitis tests

Smooth muscle antigen (SMA)	Negative
Liver-kidney microsomal antigen (LKM)	Negative
Antimitochondrial antigen (AMA)	Negative

Table 4.

Diagnostic paracentesis

Albumin concentration	0.71 g/dL
Total protein	1.28 g/dL
Total leukocyte count	1867/mm3
Neutrophils	443/mm3
Serum-ascitic albumin gradient	1.99

Discussion

Brucellosis is a multisystemic disease with diverse clinical manifestations, often characterized by non-specific symptoms or multisystemic involvement.^[8] Peritonitis, although a rare complication of brucellosis, is more commonly observed in peritoneal dialysis patients and those with liver cirrhosis due to an increased risk of bacterial translocation.^[7,9] Spontaneous bacterial peritonitis (SBP) is a frequent decompensation event in patients with cirrhosis, with an incidence of 15–20% and short-term mortality ranging from 10–33%. While Gram-negative enteric bacteria are the predominant causative agents of SBP (90%), Brucella spp. are an extremely rare etiological agent.

In our patient, Brucella spp. were isolated from the peritoneal fluid, confirming brucella-associated SBP. This diagnosis is rare and typically reported in patients with cirrhosis, chronic liver disease, or peritoneal dialysis. Although our patient lacked a prior diagnosis of cirrhosis or chronic liver disease, imaging findings (microlobulated liver contours, blunting of the left lobe corner, and hepatomegaly), endoscopic findings (grade-2 esophageal varices and portal hypertensive gastropathy), and elevated liver function tests strongly suggested underlying cirrhosis. The potential role of intestinal bacterial translocation in the decompensation process and its association with SBP has been highlighted in this case. Additionally, the patient’s two-month clinical history aligns with the typical incubation period of brucellosis, further supporting the suspicion of Brucella-related SBP.

The negative Brucella serology in our patient presents a diagnostic challenge. Seronegative brucellosis has been described in immunocompromised individuals or those with localized infections, emphasizing the importance of microbiological culture results for definitive diagnosis in such scenarios. This highlights the need for heightened clinical suspicion, particularly in endemic regions.

The decision to initiate piperacillin-tazobactam as the first-line treatment was guided by local antibiotic resistance patterns, empirical treatment guidelines, and the patient’s clinical presentation. Although this therapy initially led to clinical improvement, the absence of a follow-up diagnostic paracentesis at 48 hours is a limitation in this case. Standard SBP management protocols recommend repeat paracentesis to assess treatment response, mainly by monitoring changes in ascitic fluid white blood cell counts. The lack of such data limits our ability to confirm the efficacy of the empirical treatment and to delineate the contribution of subsequent specific brucellosis therapy to the patient’s overall recovery.

Differentiating brucella-related SBP from cirrhosis-associated SBP is crucial yet challenging. Features such as the rarity of Brucella as an SBP agent, the absence of a known source of infection in most cases, and the patient’s consumption of unpasteurized dairy products in endemic areas provide valuable diagnostic clues. Literature supports considering brucellosis in the differential diagnosis of new-onset ascites in patients with cirrhosis or those presenting with atypical features of SBP.

Brucella peritonitis lacks a standardized treatment protocol. Current guidelines for brucellosis recommend a six-week course of doxycycline combined with rifampicin or streptomycin.^[10,11] Of the 13 reported cases of brucella-associated SBP unrelated to peritoneal catheterization, most patients presented with abdominal pain, and fever was reported in a minority (Appendix 1). In our case, the patient exhibited both fever and abdominal pain, typical symptoms in brucellosis-related SBP. Notably, systemic brucellosis was absent in most reported cases (10/13), including ours.

Conclusion

In conclusion, brucella-associated SBP is a rare yet crucial diagnostic consideration, particularly in endemic regions. Patients with cirrhosis and new-onset ascites who fail to respond to standard SBP treatment should be evaluated for Brucella infection, especially if there is a history of exposure to unpasteurized dairy products or contact with infected animals. Enhanced awareness and early identification can facilitate timely and appropriate therapy, potentially improving outcomes in atypical cases.

Informed Consent

Written informed consent was obtained to publish potentially identifiable images or data in this article.

Conflict of Interest

The author(s) declared no potential conflicts of interest with respect to the research, authorship, and/or publication of this article.

Financial Disclosure

The author(s) received no financial support for the research, authorship, and/or publication of this article.

Use of AI for Writing Assistance

The study did not use AI-enabled technology.

Author Contributions

Concept: RE, TB, GB; Design: RE, MF, SO, AGA; Supervision: RE, MA, CNE; Materials – RE, EGA, ME; Data Collection and/or Processing: RE, ME, MA; Analysis and/or Interpretation: RE, TB, ME; Literature Search: RE, MF, SO, AGA, TB; Writing: RE, TB, EGA; Critical Reviews: ME, MA, CNE.

Peer-review

Externally peer-reviewed.