Cholera, non-O1 - Netherlands ex Spain (02): (CN)
Date: Thu 13 Aug 2009
Source: Eurosurveillance [edited]
<http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19298>
In July 2009, a Dutch man in his 50s presented to an emergency
department in Amsterdam with profuse diarrhea. He had recently been
diagnosed with systemic sclerosis complicated by a renal crisis,
myositis and reduced motility of the stomach and small bowel
(especially the duodenum). His medication included prednisone and esomeprazole.
The patient became ill the day before presentation with severe
diarrhea (more than 30 times per day), vomiting and abdominal cramps.
A day before onset of symptoms he had returned from [Fuerteventura,
one of the Canary Islands], Spain. He had not swum in natural water
nor eaten seafood during his stay. None of his family members who had
accompanied him on his holiday had symptoms of gastroenteritis. On
examination he was afebrile with normal pulse and blood pressure. He
was severely dehydrated having lost more than 10 percent of his body
weight. Laboratory tests showed an acidosis, hypokalemia and elevated
creatinine and C-reactive protein. He was hospitalised and treated
with intravenous fluids and potassium.
A fecal culture was sent to the microbiology department. Its rice
water appearance guided the technician to include testing for _Vibrio
cholerae_. A lactase-negative, oxidase-positive, Gram-negative rod
was identified by the Vitek system (Biomerieux, France) as _V.
cholerae_. Serotyping classified it as non-O1, non-O139 serotype.
Disk diffusion results showed susceptibility to cefotaxime,
ciprofloxacin, trimethoprim-sulfamethoxazole and tetracycline.
When culture results became available 6 days later, the patient was
still having diarrhea (diminished to 10 times a day) and was feeling
unwell. Antibiotic treatment was started with oral doxycycline 100 mg
for 3 days and this led to quick recovery from his gastroenteritis.
Further worsening of the systemic sclerosis prevented the patient
from being discharged in the following days.
In contrast to _V. cholerae_ serotype O1 and O139, the non-O1,
non-O139 _V. cholerae_ (NCV) are not associated with cholera
epidemics but with sporadic cases or small outbreaks of
gastrointestinal disease (1,2). Occasionally these can cause
extraintestinal disease including wound infections and septicemia
(1,2). Few NCV strains produce cholera enterotoxin, the toxin
responsible for massive dehydrating diarrhea. Some strains can have
other virulence genes leading to less severe intestinal symptoms
(1,2). The presence of typical choleric rice water stools and the
extent of dehydration in our patient are uncommon in NCV infection
and suggest cholera enterotoxin production (3). The predisposition of
this patient may have contributed to the severity of disease. He was
on immunosuppressive medication, his gastric acid production was
blocked by esomeprazole and the intestinal mobility was impaired (4,5).
NCVs are part of the normal bacterial ecosystem of estuaries and
coastal areas and these strains seem to persist in the environment,
similar to _V. cholerae_ O1 and O139 strains (5). NCVs are found in
salt and fresh water in both the Mediterranean and temperate parts of
Europe. Warm summer months favor _Vibrio_ growth and it is in late
summer and early fall that most cases occur, either through eating
contaminated seafood or by direct contact with contaminated water
(6-8). A recent study in Italy, in a population with high dietary
seafood intake, showed that 3.4 percent of the acute diarrhea cases
admitted to hospital were caused by NCV infection (7). Most European
countries do not routinely check for the presence of NCV in clinical
samples, foodstuff or the environment. Our case underlines the
importance of testing for _V. cholerae_ in potentially exposed
patients with acute diarrhoea, especially when predisposing factors
like immunosuppression and acid-blocking medication are present.
References
----------
1. Kaper JB, Morris JG, Levine MM: Cholera. Clin Microbiol Rev. 1995;8: 48-86.
2. Sack DA, Sack RB, Nair GB, Siddique AK: Cholera. Lancet. 2004;363: 223-233.
3. Spira WM, Daniel RR, Ahmed QS, et al: Clinical features and
pathogenicity of O group 1 non-agglutinating Vibrio cholerae and
other vibrios isolated from cases of diarrhea in Dacca, Bangladesh.
In: Takeya J, Zinnaka Y, editors. Proceedings of the 14th Joint
Conference US-Japan Cooperative Medical Science Program Cholera
Panel; 1978. Toho University: Tokyo; 1978. p. 137-153.
4. Nalin DR, Levine RJ, Levine MM, et al: Cholera, non-vibrio
cholera, and stomach acid. Lancet. 1978;2: 856-859.
5. Tobin-D'Angelo M, Smith AR, Bulens SN, et al: Severe diarrhea
caused by cholera toxin-producing Vibrio cholerae serogroup O75
infections acquired in the southeastern United States. Clin Infect
Dis. 2008;47: 1035-1040.
6. Lukinmaa S, Mattila K, Lehtinen V: Territorial waters of the
Baltic Sea as a source of infections caused by Vibrio cholerae
non-O1, non-O139: report of 3 hospitalized cases. Diagn Microbiol
Infect Dis. 2006;54: 1-6.
7. Ottaviani D, Leoni F, Rocchegiani E; Prevalence and virulence
properties of non-O1 non-O139 Vibrio cholerae strains from seafood
and clinical samples collected in Italy. Int J Food Microbiol. 2009;132: 47-53.
8. Stypulkowska-Misiurewicz H, Pancer K, Roszkowiak A: Two unrelated
cases of septicaemia due to Vibrio cholerae non-O1, non-O139 in
Poland, July and August 2006. Euro Surveill. 2006;11(48):pii=3088.
Available from:
<http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=3088>.
[Byline: Rozemeijer W, Korswagen LA, Voskuyl AE, Budding AE]
Source: Eurosurveillance [edited]
<http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=19298>
In July 2009, a Dutch man in his 50s presented to an emergency
department in Amsterdam with profuse diarrhea. He had recently been
diagnosed with systemic sclerosis complicated by a renal crisis,
myositis and reduced motility of the stomach and small bowel
(especially the duodenum). His medication included prednisone and esomeprazole.
The patient became ill the day before presentation with severe
diarrhea (more than 30 times per day), vomiting and abdominal cramps.
A day before onset of symptoms he had returned from [Fuerteventura,
one of the Canary Islands], Spain. He had not swum in natural water
nor eaten seafood during his stay. None of his family members who had
accompanied him on his holiday had symptoms of gastroenteritis. On
examination he was afebrile with normal pulse and blood pressure. He
was severely dehydrated having lost more than 10 percent of his body
weight. Laboratory tests showed an acidosis, hypokalemia and elevated
creatinine and C-reactive protein. He was hospitalised and treated
with intravenous fluids and potassium.
A fecal culture was sent to the microbiology department. Its rice
water appearance guided the technician to include testing for _Vibrio
cholerae_. A lactase-negative, oxidase-positive, Gram-negative rod
was identified by the Vitek system (Biomerieux, France) as _V.
cholerae_. Serotyping classified it as non-O1, non-O139 serotype.
Disk diffusion results showed susceptibility to cefotaxime,
ciprofloxacin, trimethoprim-sulfamethoxazole and tetracycline.
When culture results became available 6 days later, the patient was
still having diarrhea (diminished to 10 times a day) and was feeling
unwell. Antibiotic treatment was started with oral doxycycline 100 mg
for 3 days and this led to quick recovery from his gastroenteritis.
Further worsening of the systemic sclerosis prevented the patient
from being discharged in the following days.
In contrast to _V. cholerae_ serotype O1 and O139, the non-O1,
non-O139 _V. cholerae_ (NCV) are not associated with cholera
epidemics but with sporadic cases or small outbreaks of
gastrointestinal disease (1,2). Occasionally these can cause
extraintestinal disease including wound infections and septicemia
(1,2). Few NCV strains produce cholera enterotoxin, the toxin
responsible for massive dehydrating diarrhea. Some strains can have
other virulence genes leading to less severe intestinal symptoms
(1,2). The presence of typical choleric rice water stools and the
extent of dehydration in our patient are uncommon in NCV infection
and suggest cholera enterotoxin production (3). The predisposition of
this patient may have contributed to the severity of disease. He was
on immunosuppressive medication, his gastric acid production was
blocked by esomeprazole and the intestinal mobility was impaired (4,5).
NCVs are part of the normal bacterial ecosystem of estuaries and
coastal areas and these strains seem to persist in the environment,
similar to _V. cholerae_ O1 and O139 strains (5). NCVs are found in
salt and fresh water in both the Mediterranean and temperate parts of
Europe. Warm summer months favor _Vibrio_ growth and it is in late
summer and early fall that most cases occur, either through eating
contaminated seafood or by direct contact with contaminated water
(6-8). A recent study in Italy, in a population with high dietary
seafood intake, showed that 3.4 percent of the acute diarrhea cases
admitted to hospital were caused by NCV infection (7). Most European
countries do not routinely check for the presence of NCV in clinical
samples, foodstuff or the environment. Our case underlines the
importance of testing for _V. cholerae_ in potentially exposed
patients with acute diarrhoea, especially when predisposing factors
like immunosuppression and acid-blocking medication are present.
References
----------
1. Kaper JB, Morris JG, Levine MM: Cholera. Clin Microbiol Rev. 1995;8: 48-86.
2. Sack DA, Sack RB, Nair GB, Siddique AK: Cholera. Lancet. 2004;363: 223-233.
3. Spira WM, Daniel RR, Ahmed QS, et al: Clinical features and
pathogenicity of O group 1 non-agglutinating Vibrio cholerae and
other vibrios isolated from cases of diarrhea in Dacca, Bangladesh.
In: Takeya J, Zinnaka Y, editors. Proceedings of the 14th Joint
Conference US-Japan Cooperative Medical Science Program Cholera
Panel; 1978. Toho University: Tokyo; 1978. p. 137-153.
4. Nalin DR, Levine RJ, Levine MM, et al: Cholera, non-vibrio
cholera, and stomach acid. Lancet. 1978;2: 856-859.
5. Tobin-D'Angelo M, Smith AR, Bulens SN, et al: Severe diarrhea
caused by cholera toxin-producing Vibrio cholerae serogroup O75
infections acquired in the southeastern United States. Clin Infect
Dis. 2008;47: 1035-1040.
6. Lukinmaa S, Mattila K, Lehtinen V: Territorial waters of the
Baltic Sea as a source of infections caused by Vibrio cholerae
non-O1, non-O139: report of 3 hospitalized cases. Diagn Microbiol
Infect Dis. 2006;54: 1-6.
7. Ottaviani D, Leoni F, Rocchegiani E; Prevalence and virulence
properties of non-O1 non-O139 Vibrio cholerae strains from seafood
and clinical samples collected in Italy. Int J Food Microbiol. 2009;132: 47-53.
8. Stypulkowska-Misiurewicz H, Pancer K, Roszkowiak A: Two unrelated
cases of septicaemia due to Vibrio cholerae non-O1, non-O139 in
Poland, July and August 2006. Euro Surveill. 2006;11(48):pii=3088.
Available from:
<http://www.eurosurveillance.org/ViewArticle.aspx?ArticleId=3088>.
[Byline: Rozemeijer W, Korswagen LA, Voskuyl AE, Budding AE]
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