Vibrio cholerae Bacteremia causing severe lactic acidosis and multiorgan failure in alcoholic cirrhosis: A report of a fatal case

Abstract

Non-O1, non-O139 Vibrio cholerae (NOVC) infections can cause sepsis in patients with liver cirrhosis. NOVC bacteraemia is a rare condition, with the highest number of cases reported in Asia. Despite increasing recognition of non-O1, Non-O139 Vibrio cholerae as emerging pathogens associated with gastroenteritis, wound infections, and septicaemia, there is limited knowledge on disease patterns, complications, and survival dynamics of the disease. Here, NOVC strains were isolated from an elderly female with a known history of alcoholic cirrhosis, who presented with severe abdominal pain and altered sensorium leading to hepatic coma. The patient was admitted to the intensive care unit (ICU) with a provisional diagnosis of acute-on-chronic liver failure (ascites, jaundice, coagulopathy, and hepatic encephalopathy) complicated by septic shock and multiorgan failure. Hepatitis panel (Hepatitis A IgM, Hepatitis B surface antigen, Anti-Hepatitis C antibody) and Human Immunodeficiency Virus (HIV) screening were negative. Despite aggressive supportive measures, the patient’s condition deteriorated, and she succumbed to her illness on day 4 of ICU admission. Informed consent was obtained from the patient’s relatives.

Background

There are more than 200 serogroups of Vibrio cholerae, identifiable by the “O antigen” on the cell wall lipopolysaccharide (LPS). Only two serogroups (O1 and O139) which carry the cholera toxin (CTX) gene, are associated with all cholera outbreaks (characterised by severe acute diarrhoea with gastroenteritis) and pandemic spread. These are identified by serogrouping using O1 and O139 antisera. V. cholerae strains that do not agglutinate with either O1 or O139 antisera were previously referred to as non-agglutinating (NAG) Vibrio, and are now classified as NOVC—non-O1, non-O139 Vibrio cholerae. These strains generally lack the CTX gene and typically do not cause severe diarrhoea [1]

NOVC bacteremia is a rare condition; only 185 cases have been reported globally between 2000 and 2023, with the highest number from Asia. Cases have also been reported in Middle Eastern countries including Kuwait, Qatar, Oman, Lebanon, and Saudi Arabia [2]

Human infection with non-O1/non-O139 can occur through the consumption of raw or undercooked contaminated meat and seafood, or exposure of skin lesions to contaminated seawater, or swimming in freshwater lakes. Associated seafoods include oysters, fish, shrimps, clams, and mussels [3].

V. cholerae non-O1, non-O139 is an uncommon cause of septicaemia that can lead to fulminant illness, particularly in individuals with liver disease due to impaired immune responses [4].

Cirrhotic patients are especially vulnerable to severe infections because of compromised innate immunity, increased intestinal permeability, and the liver's reduced capacity to clear pathogens [5], [6]

In this case report, we present a known case of alcoholic liver cirrhosis who presented to the emergency department with septic shock, in whom NOVC strains were isolated, and resulting in a fatal outcome.

Case

A 35-year-old female with a known history of alcoholic cirrhosis presented with severe abdominal pain and altered sensorium for 1 day. A detailed history could not be obtained as the patient was confused and lived alone. She denied any recent alcohol binge, fever, or diarrhoea. On clinical examination she was icteric, conscious but confused (Glasgow Coma Scale: 14/15). The abdomen was mildly distended with generalised tenderness; however, rebound tenderness was absent and bowel sounds were normal. Respiratory and cardiovascular examinations were unremarkable.

Her initial vital signs in the emergency room (ER) were as follows: heart rate 109/min, blood pressure 84/62 mmHg, respiratory rate 29/min, and oxygen saturation (SpO₂): 97 % on room air. Capillary blood glucose was critically low at 37 mg/dL, indicating hypoglycaemia, and low glucose and high lactate (20 mmol/L) indicate liver failure.

Investigations

Blood gas

The first venous blood gas analysis, obtained in the ER, showed: pH: 7.15, PCO₂: 23 mmHg, PO₂: 37 mmHg, HCO₃⁻: 9 mmol/L, lactate: 20 mmol/L. Her initial laboratory investigations were severely deranged (Table 1), showing significant abnormalities in liver and kidney function, along with severe electrolyte imbalances. Her hepatitis panel (Hepatis A IgM, Hepatitis B surface antigen, Anti Hepatitis C antibody) and Human Immunodeficiency Virus (HIV) screening were negative.

Table 1.

Initial laboratory investigations performed in the emergency room (all values in SI units).

Parameters	Values	Normal value
Haemoglobin	13	12–15 gm/dL
White blood cell count (WBC)	5.48	(4.0–10) x109/L
WBC differential
Neutrophil Lymphocyte	79.6 12.9
Platelet	139	109/L (40–400)
Total bilirubin	296.6	1.7–20.5 µmol/L
AST	133.95	(0–45) U/L
ALT	70	(13–39) U/L
Serum Albumin	17	35–50 g/L
Serum creatinine	225.82	50–110 (µmol/L)
Blood Urea	4.2	2.5–7.1 mmol/L
INR	3.41	1
Prothrombin time	41.4	10–13 s
Serum sodium	121	135–145 mmol/L
Serum Potassium	2.8	3.5–5.0 mmol/L
Serum Chloride	82	98–106 mmol/L
Arterial Ammonia	126	15–45 µmol/L
C-Reactive protein (CRP)	82	< 10 mg/L

µmol/L: micromoles per litre; mmol/L: millimoles per litre; mg/dL: milligrams per decilitre.

Imaging and bedside findings

Non-contrast CT of the brain revealed no acute abnormalities. Bedside chest X-ray showed bilateral basal patchy infiltrates and blunting of the costophrenic angles, indicating pleural effusion (Fig. 1).

Fig. 1.

Chest X-ray (anteroposterior view) showing an endotracheal tube in the correct position. Bilateral basal haziness and blunting of the costophrenic angles are noted, suggestive of pleural effusion.

A contrast-enhanced CT of the abdomen (PCT Abdomen) was planned to rule out acute intra-abdominal pathology, particularly mesenteric ischemia, but could not be done due to the patient’s hemodynamic instability.

Bedside abdominal ultrasound

Ultrasound revealed a cirrhotic liver with no evidence of dilated intrahepatic biliary radicles. The portal vein diameter was normal. Moderate ascites was noted.

Microbiological laboratory investigation

On day 1, both aerobic and anaerobic blood culture bottles were incubated in the Bactec FX 40 instrument. The system flagged the culture as positive on day 2. On day 2, Gram stain from the positive blood culture bottle revealed curved gram-negative rods (Fig. 2).

Fig. 2.

Gram stain from positive blood culture bottle showing curved gram-negative rods (100x oil immersion).

Subcultures were prepared using conventional media according to standard operating procedures and incubated. On day 3, after 24 h of incubation, β-haemolytic colonies measuring 3–5 mm with greenish hue were observed on blood agar (Fig. 3).

Fig. 3.

24-h subculture from a blood culture bottle showing large β-haemolytic colonies with a greenish hue on 5 % sheep blood agar, typical of Vibrio spp.

McConkey agar showed 2–3 mm non-lactose fermenting colonies. The isolate was catalase-positive and oxidase-positive. Microscopy revealed curved gram-negative rods, typical of Vibrio spp. Motility testing demonstrated darting motility (Fig. 4).

Fig. 4.

24-h subculture from a blood culture bottle showing non-lactose fermenting colonies on MacConkey agar.

The isolate was identified as Vibrio cholerae by Microscan WalkAway plus System (Beckman Coulter) automated ID and AST(Identification and Antibiotic Specification Testing) system, using the Neg Breakpoint Combo 50 panel. The isolate was also tested using the Phoenix 100 system with the NMIC/ID-431 panel similarly identified as V. cholerae.

The biotype code from Microscan WalkAway was 60010154045, with the following significant biochemical reactions: Glucose and Sucrose fermenting, Indole + , VP+ , Citrate + , ONPG+ , Nitrate+ , and OF/G + . The isolate was susceptible to ampicillin (MIC ≤8), cephazolin (MIC ≤2), cefuroxime (MIC ≤4), cefotaxime (MIC≤1), ciprofloxacin (MIC ≤1), and cotrimoxazole (MIC ≤ 2/38) (Fig. 5).

Fig. 5.

Oxidase test performed from colonies on blood agar; the result is positive.

Agglutination testing performed at a reference laboratory showed that the isolate did not agglutinate with O1 or O139 antisera. It was sent to the National Public Health Laboratory where V. cholerae was confirmed by Matrix-Assisted Laser Desorption/Ionization Time-of-Flight (MALDI-TOF).

Management and outcomes

Upon arrival at the ER, resuscitation was initiated with intravenous fluid boluses, empirical ceftriaxone, sodium bicarbonate, and 50 % dextrose.

During initial resuscitation, the patient developed bradycardia followed by three episodes of cardiac arrest, requiring 15 min of cardiopulmonary resuscitation (CPR). She was subsequently intubated. High-dose norepinephrine and vasopressin were initiated for hemodynamic support.

The patient was admitted to the intensive care unit (ICU) with a provisional diagnosis of acute-on-chronic liver failure (ascites, jaundice, coagulopathy, and hepatic encephalopathy) complicated by septic shock and multiorgan failure. A septic screen (blood, urine, tracheal aspirate cultures) was sent, and antibiotics were upgraded to meropenem and vancomycin. Ultrasound guided diagnostic paracentesis revealed a serum-ascites albumin gradient (SAAG) of 1.4 gm/L with no evidence of spontaneous bacterial peritonitis (''ascitic''fluid WBC: 325 cells/mm³; polymorphs: 33 %).

The patient’s condition continued to deteriorate in the ICU. She developed worsening metabolic acidosis and anuria. Continuous renal replacement therapy was initiated for refractory metabolic acidosis, hyperkalaemia, and volume overload.

Despite all the supportive measures, her condition continued to decline, and she succumbed to her illness on day 4 of ICU admission.

Discussion

This 35-year-old female with alcoholic cirrhosis presents with several concerning features: 1) abdominal pain, altered mental status (confusion, Glasgow Coma Scale 14/15), and hypoglycaemia; and 2) laboratory findings indicating severe metabolic acidosis with elevated lactate, severe electrolyte disturbances, and markedly deranged liver and kidney function. These findings are highly suggestive of acute decompensated cirrhosis with complications such as hepatic encephalopathy, sepsis, and hepatorenal syndrome. Cirrhotic patients face an increased risk of severe infections due to impaired innate immune responses, heightened intestinal permeability, and reduced hepatic clearance of pathogens. These vulnerabilities render them particularly susceptible to invasive infections [7].

The isolation of V. cholerae NOVC strains from the patient’s bloodstream adds a significant and rare complication. While V. cholerae is typically associated with gastrointestinal infections and cholera caused by O1 or O139 serogroups, non-O1/non-O139 strains can cause extraintestinal infections, including sepsis and bacteraemia. Prior studies, including those conducted in Australia, have identified chronic liver disease and malignancy as key predisposing factors for NOVC bacteraemia.

Rodríguez-Negrete (2024) highlighted the concept of cirrhosis-associated immune dysfunction (CAID), which involves a combination of systemic inflammation and immune suppression. This dysfunction increased the risk of infections, particularly those originating from the gastrointestinal tract. The study also discusses emerging therapies aimed at modulating immune pathways to reduce infection risk in patients with cirrhosis [8].

Host risk factors for NOVC infection include immunocompromised status and chronic illnesses, particularly liver disease. In cirrhosis, intestinal mucosal inflammation, oedema and increased intestinal permeability facilitate bacterial translocation and bloodstream invasion. Additional risk factors include alcoholism, diabetes, haematological malignancies, cancers and long-term corticosteroid therapy [9].

Although NOVC infections are rare, they are associated with a high mortality rate, especially in immunosuppressed individuals [10]. These strains can cause extraintestinal complications such as wound infections or septicaemia, with manifestations resembling Vibrio vulnificus. A reported case involved a 52-year-old man with no known pre-existing conditions who succumbed to a. NOVC infection within 72 h of admission to the ICU [11]

The primary challenge in this case was the persistently elevated serum lactate levels, observed from the outset. Severe lactic acidosis contributed to multiple episodes of cardiac arrest and the development of post-cardiac arrest syndrome, further worsening the patient’s critical condition and ultimately leading to irreversible multiorgan dysfunction syndrome (MODS). The extremely high lactate levels were likely due to both overproduction—secondary to tissue hypoxia and aerobic glycolysis—and impaired hepatic clearance. As the liver is responsible for clearing approximately two-thirds of the body’s lactate, liver dysfunction can significantly impair lactate clearance [12]

The antibiotic was upgraded to meropenem as a carbapenem is known for its strong effectiveness against a variety of Gram-negative bacilli, including numerous multidrug-resistant (MDR) strains. Although NOVC strains are typically sensitive to multiple antibiotics, the presence of invasive infections (such as bacteremia, deep wound infections, and sepsis) warrants the administration of a broad-spectrum antibiotic like meropenem, particularly when the initial resistance pattern is unclear. Research conducted by Deshayes et al. (2015) supports the administration of carbapenems for severe Gram-negative infections when there is a suspicion of resistance or virulence [13].

Saudi Ministry of Health (2023) reported [14] that cholera is not endemic in the Kingdom. Nevertheless, the country faces the possibility of imported cases, particularly due to travel and pilgrimages from nations experiencing ongoing cholera outbreaks. The Ministry upholds proactive epidemiological surveillance systems and consistently releases alerts and readiness plans during periods of heightened risk. However, although NOVC cases are rare, Alomar et al. in 2024 identified the first instance of wound infection caused by toxigenic NOVC in a hospitalized patient with COVID-19, confirmed through whole genome sequencing, highlighting the potential for serious infection in at-risk individuals. Alotaibi et al. in 2017 [15] reported a case of NOVC septicemia in a previously healthy adult male, demonstrating that even those with intact immune systems can be susceptible to invasive disease. • Al-Otaibi and Almuhanna in 2020 [16] recorded blood culture-positive NOVC cases in the Eastern Province and pointed out environmental and behavioral risk elements such as climate, seafood consumption, and existing health conditions. They also highlighted the under-recognition of NOVC within clinical settings. These findings indicate that although NOVC remains uncommon, there is an increasing trend in its identification in Saudi Arabia, emphasizing the need for better diagnostic awareness, microbiological monitoring, and public health preparedness.

Although this study presented practical example at real-world settings that support critical thinking, decision-making, and application of knowledge, the rarity of this disease, and unavailability of multiple cases limited generalizability, as the findings obtained from one case.

Conclusion

This case highlights the fatal interaction between advanced cirrhosis and rare infections such as NOVC. Early recognition, aggressive treatment, and preventive strategies are essential in the care of such high-risk patients, although outcomes remain poor in the setting of advanced liver disease.

Improved surveillance and infection preventive protocols are vital for managing infections in cirrhotic individuals. Additionally, earlier evaluation for liver transplantation in patients with decompensated cirrhosis may improve long-term outcomes and survival.

Future studies are needed to explore other forms of the disease, causality, and management.

Author's agreement

The content of this case discussion reflects my independent professional judgment and experience in the clinical management of a patient with alcoholic cirrhosis complicated by non-O1/non-O139 Vibrio cholerae bacteremia. We have drawn upon our knowledge of medical literature, clinical practice, and relevant diagnostic and therapeutic guidelines to present a comprehensive analysis of the case.

We confirm that this case discussion has been based on available clinical data and research, and it has been written without any influence from external commercial entities.

We have made every effort to ensure the accuracy of the information presented, and the discussion is intended to contribute to the understanding and management of similar clinical situations.

This work represents our own analysis and perspective, and any conclusions or recommendations are solely those of the authors.

The views expressed herein are not intended to represent the official stance of any affiliated institution or organization.

Ethical Approval

Due to the critical and rapidly deteriorating condition of the patient described in this case report, it was not feasible to obtain ethical approval prior to her death. The patient passed away shortly after admission, and no institutional review board (IRB) review could be conducted in advance. However, written informed consent for the publication of the case details and any accompanying images was obtained from the patient’s next of kin following her passing. This process was conducted in accordance with the ethical principles outlined in the Declaration of Helsinki. The authors affirm that all identifying details have been anonymized to protect the privacy of the patient and her family.

Funding sources

This research did not receive any specific grant from funding agencies in the public, commercial, or not-for-profit sectors.

Declaration of Competing Interest

The authors declare that there are no conflicts of interest regarding the publication of this manuscript. No financial or non-financial relationships exist that could influence the content or interpretation of the research presented in this study.

The study was self-funded by the authors. All authors confirm that they have no competing interests that would influence the findings or conclusions drawn.

Glossary

Matrix-Assisted Laser Desorption/Ionization Time-of-Flight MALDI‐TOF(MALDI-TOF)

is a rapid, accurate, and cost-effective technique used in microbiology and clinical diagnostics to identify microorganisms (bacteria, fungi, and some parasites) based on proteinprofile.

Identification and Antibiotic Susceptibility Testing (ID& AST)

Traditional methods of microbial identification that include culture, staining, and biochemical tests.