By Author
  By Title
  By Keywords

April 2018, Volume 68, Issue 4

Case Reports

Non O1, non O139 Vibrio cholerae bacteraemia in an infant; case report and literature review

Mirza Zain Baig  ( Medical College )
Umme Hani Abdullah  ( Medical College )
Yusra Shafquat  ( Section of Microbiology, Department of Pathology and Laboratory Medicine, Aga Khan University, Karachi )
Khadija Nuzhat Humayun  ( Department of Paediatrics and Child Health, Aga Khan University, Karachi. )
Afia Zafar  ( Section of Microbiology, Department of Pathology and Laboratory Medicine, Aga Khan University, Karachi )


Non 01, Non O139 Vibrio cholerae bacteraemia is a rare but potentially fatal occurrence. There have been very few incidents of this infection from around the world. The treatment regimen of antibiotics also varies in literature. We present a case of bacteraemia caused by Non O1, Non O139 Vibrio cholerae along with associated risk factors, disease manifestations, laboratory diagnosis and treatment regimen. This serves to add additional information regarding symptoms and signs of this infection along with management of patient. Knowledge regarding this topic shall be highly useful to professionals if further cases are detected. In the discussion section, a review of literature of previous cases is also presented.
Keywords: Vibrio cholera, Bacteraemia, Non O1, Non O139, Pakistan.


Vibrio cholerae is a gram negative oxidase positive bacterium. Its O1 and O139 serotypes are notorious for causing epidemics and pandemics of severe watery diarrhoea known as cholera. Strains that do not agglutinate with O1 and O139 antisera are known as non O1, non O139 Vibrio cholerae species. These strains — although can also cause diarrhoeal illness, are reputable more due to their extra intestinal manifestations — most prominent of which is bacteraemia. Non O1, non O139 bacteraemia is rare and very few cases of it in infants has been presented in the previous literature.

Case Report

A two-month old baby boy presented with a 10-day history of fever and abdominal distension. He had abdominal pain for the past 3 days and was taken to a local doctor who administered a single dose of metronidazole. However, the condition of the baby worsened and the infant became lethargic. After which he was subsequently brought to a tertiary care hospital. Within a span of one month he was admitted thrice. He had an uneventful antenatal history with an emergency caesarian section. He was born with bilateral lamellar cataract. His birth weight was 3.5 kg and he had neonatal jaundice on the third day of birth. On 19th day his weight increased by 200grams. On his third visit, on examination he was found to be drowsy with a temperature of 38°C, a heart rate of 160 beats per minute and a respiratory rate of 35 breaths per minute. His oxygen saturation was 98 percent. He also appeared anaemic and had jaundice along with pitting oedema. On Cardiovascular system examination S1 and S2 were audible while pulses and perfusion were poor. Glasgow coma scale revealed a 14/15 score. Abdomen was tense, distended with a positive fluid thrill. He also had hepatomegaly, splenomegaly, oedematous skin with an everted umbilicus and sluggish bowel sounds. Chest X ray was clear. The patient was started on cefotaxime, amikacin and vitamin K and a nasogastric tube was inserted. Ultrasound showed dilated bowel loops. Blood cultures were sent. Gram stain revealed curved gram negative rods. After 24 hours of incubation, growth of beta haemolytic colonies were noted on sheep blood agar. On MacConkey agar there was growth of non-lactose fermenters that were oxidase positive. Hanging drop showed darting movements. On Thiosulfate- citrate- bile salts- sucrose (TCBS) agar there was growth of yellow colonies that were opaque in center and pale at periphery. API-20E (bioMérieux) confirmed identification of Vibrio cholera while slide agglutination tests were negative for O1 and O139 antigens. On third day of admission the patient started to have symptoms of respiratory distress. Abdominal swelling increased and patient became drowsy with laboured breathing. Oxygen saturation reduced to 84% from 95%. Parents were advised for intubation. However, they refused and due to poor prognosis, withdrew support.
Consent from parents was taken prior to the writing of the manuscript. Ethical review committee granted us permission to publish this research.


Non O1 and non O139 Vibrio cholerae have been known to cause extra intestinal disease in adults with underlying malignancies, chronic syndromes, renal dialysis, liver pathologies, post-transplants and immunosuppressive disorders.1 Previously it is well established that chronic liver disease is one of the most prominent predisposing factor for systemic bacterial infections. It has been postulated that increased infection in cirrhotic patients may be attributable to a defective reticuloendothelial system leading to increased survival of bacteria in the bloodstream.2 This patient was admitted with hepatosplenomegaly, jaundice and ascites which suggests that maybe he was syndromic or suffering from primary immunodeficiency. Unfortunately, during his hospital stay he was not investigated in that direction. Infantile Non O1 and non O139 Vibrio cholera infections are a rare entity. There have only been a few such cases reported in literature. Previous case reports (Table-1)

suggests a strong association with meningitis in infants and a high mortality and morbidity rate. It is therefore imperative that early diagnosis be made and early intervention in the form of intravenous antibiotics should be started.  Unlike their O1 and O139 counterparts, non O1 and non O139 Vibrio cholera do not produce the cholera toxin. They are hence termed as non-toxigenic. The virulence factors for non-toxigenic Vibrio cholera have not yet been well established. Haemolysin, which would explain the invasive nature of these bacterium appears to be the most likely candidate in these serotypes.3 Cytotoxic and haemolytic activity has been previously demonstrated in a Non-O1 strain causing bacteraemia in a patient.4 It has also been postulated that the invasive nature of the bacteria can be attributed to a toxin named the zot toxin which functions by disabling the tight junctions between the epithelial cells of the intestine.5 Infections in humans arise most commonly due to ingestion of contaminated water and raw or undercooked seafood. Foreign travel to endemic regions and contact of contaminated water with broken skin are also known risk factors. In infants, sterility of artificial feeds and cleanliness of bottles are highly recommended and reinforced by Kerketta et al.6 In neonates, we may also consider perinatal infections from maternal faecal flora as well as low birth weight5 and prematurity.7 The source of infection in this case could not be ascertained though it is possible the child may have ingested polluted water. As reported previously the disease may present as fever, chills, lethargy, irritability and refusal to feed.5-10 Generalized convulsions have also been reported.6-10 It is important to note the absence of diarrhoeal disease in both, previous literature as well as this case report. This patient presented with abdominal distension that was probably associated with coexisting pathology. The patient reported by Kerketta6 also developed metastatic endopthalmitis. Antibiotic susceptibilities vary in different reports. However, the organism is most commonly found sensitive to ampicillin and cefotaxime.7 Antibiotic sensitivity is also observed in aminoglycosides, fluoroquinolones and chloramphenicol.6,9,10
Table lists down salient features of published case reports in recent years.


Through this communication, we are reporting a life-threatening condition due to a non O1, non O139 Vibrio cholera. Therefore,we suggest that clinicians should
always be vary of such infections in extremes of ages and immunocompromised states.

Disclaimer: This article has not been presented or published in a conference.
Conflict of Interest: None to declare.
Funding Disclosure: None to declare.


1.  Lan N, Nga T, Yen N, Dung L, Tuyen H, Campbell J et al. Two Cases of Bacteriemia Caused by Nontoxigenic, Non-O1, Non-O139 Vibrio cholerae Isolates in Ho Chi Minh City, Vietnam. J Clin Microbiol. 2014; 52: 3819-21.
2.  Yang C, Wang C, Lu P, Chen T, Chen Y, Huang M et al. Bullous cellulitis in cirrhotic patients — a rare but life-threatening infection caused by non-O1, non-O139 Vibrio cholera bacteraemia. J Med Microbiol. 2011; 60: 861-2.
3.  Albuquerque A, Cardoso H, Pinheiro D, Macedo G. Vibrio cholerae non-O1 and non-O139 bacteremia in a non-traveler Portuguese cirrhotic patient: First case report. Gastroenterol Hepatol. 2013; 36: 309-10.
4.  Namdari H, Klaips C, Hughes J. A Cytotoxin-Producing Strain of Vibrio cholera Non-O1, Non-O139 as a Cause of Cholera and Bacteraemia after Consumption of Raw Clams. J Clin Microbiol. 2000; 38: 3518-9.
5.  Sarwar S, Hannan A, Sultana Q, Saleem S, Sohail M, Arshad M et al. Non-O1Vibrio choleraebacteraemia in an infant, first case report from Pakistan. J Infect Dev Ctries. 2016; 10: 188-9.
6.  Kerketta J, Paul A, Kirubakaran C, Jesudason M, Moses P. Non-01 Vibrio cholerae septicemia and meningitis in a neonate. Indian J Pediatr. 2002; 69: 909-10.
7.  Ismail E, Shafik M, Al-Mutairi G. A Case of Non-O:1 Vibrio cholerae Septicemia with Meningitis, Cerebral Abscess and Unilateral Hydrocephalus in a Preterm Baby. Euro J ClinMicrobiol Infect Dis. 2001; 20: 598-600.
8.  Naidu L, Bakerman P, Saubolle M, Lewis K. VIBRIO CHOLERAE non-O: 1 meningitis in an infant. Pediatr Infect Dis J. 1993; 12: 879-81.
9.  Rubin L, Altman J, Epple L, Yolken R. Vibrio cholerae meningitis in a neonate. J Pediatr.1981; 98: 940-2.
10.  Hao Y, Wang Y, Bi Z, Sun B, Jin Y, Bai Y et al. A case of non-O1/non-O139 Vibrio cholerae septicemia and meningitis in a neonate. Int J Infect Dis. 2015; 35: 117-9.

Journal of the Pakistan Medical Association has agreed to receive and publish manuscripts in accordance with the principles of the following committees: