Cholera(Vibrio Cholerae O1 or O139)◊

 

Literature Recommendations

Exclusion-Case in SOS*
(Symptomatic)

Yes [1, 2, 3a, 4a, 5]
Grade III-A

Exclusion-Case in SOS*
(Asymptomatic or previously symptomatic but now recovered)

Data from literature are conflicting
See comment below c

Clearance-Case in SOS*

Yes
2 consecutive negative stools 24hr apart [3, 4, 5]
Grade III-A

Exclusion of Contact
(Symptomatic)

Yes [1, 2, 3a, 4, 5]
Grade III-A

Exclusion of Contact
(Asymptomatic)

No [1b, 2, 3b, 4]
Grade III-A
Surveillance recommended (preventive measure #3)

Exclusion-Case in Children
(Group setting with children ≤ 5 years of age)
(Symptomatic)

Yes [2, 12]
until diarrhea resolves
Grade III-A

Exclusion-Case in Children
(Group setting with children ≤ 5 years of age)
(Asymptomatic or previously symptomatic but now recovered)

No [2, 12]
Grade III-A

◊ Applicable Code

CCR 2556
* SOS (Sensitive Occupations or Situations) is not defined precisely in either the Code of Regulations or Health & Safety Code. See Attachment 2 for the definition of food workers.
◊ See California Code of Regulations, Attachment 1, for details.
+ Local health departments may elect to follow more restrictive exclusion and clearance criteria

a Recommendation to exclude until 48hrs after 1st normal stool.
b Recommends surveillance of contacts to a case for 5 days from exposure for any symptoms.
c In light of conflicting guidance from literature (see preventive measure #1, 2, 4, 5 and 7): evidence from past outbreaks and potential modes of transmission (see disease trends below) seem to point out greater risk is posed by allowing asymptomatic food handlers back into sensitive occupational setting (SOS), but possibly not by allowing others in SOS back to work.

Disease Trends in the U.S.:

According to Steinberg et al. (2001) the number of identified laboratory confirmed cases in US of V. cholerae O1 and O139 reported from 1995-2000 include Sixty-one cases all caused by O1. Thirty-seven of these cases were acquired in foreign countries, fourteen were contracted from eating undercooked seafood in the US, two were obtained as a result of consuming sliced cantaloupe that had been contaminated by an infected, asymptomatic food handler [in this case the person who had sliced the cantaloupe had sliced it for family members and was not working as a commercial food handler], and no source could be identified for eight infections (21).

Mahon et al. (1996) states that from 1992-1994 there were 160 cases of V. cholerae (154 from O1 and 6 from O139) reported. One hundred fifty-one got their infections abroad (125 in Latin America and 26 while in Asia); of the cases that were associated with travel to Latin America 75 cases were a result of an outbreak among passengers on a commercial airline flight that stopped in Lima, Peru. The implicated vehicle was a seafood salad.  Six cases were acquired in the U.S. (Two from contaminated Gulf coast seafood and four from atypical foods from outside the US) and one in Guam (unknown source of infection). In none of the outbreaks was there evidence of secondary transmission (14).

An outbreak affecting 37 construction workers occurred in Singapore in 1982. The source was traced to squid prepared by food handlers infected with V. cholerae O1 (18).

Cholera is an acute, diarrheal illness caused by infection of the intestine with the bacterium Vibrio cholerae. The infection is often mild or without symptoms, but sometimes it can be severe (1, 14, 24). Approximately one in twenty infected persons has severe disease as evidenced by profuse watery diarrhea, vomiting, and leg cramps. There can be rapid loss of body fluids, dehydration and shock. Without treatment, death can occur within hours since a cholera patient can pass up to 20 liters of stool in one day (15). The World Health Organization (WHO) has estimated that more than 120,000 people die yearly from cholera (24).

Organism: Gram-negative curved rods with singular polar flagella which are divided into several serogroups (r). Two specific serogroups (O1 and O139) have been associated with the clinical picture of cholera and are known to cause epidemics (1, 6, 18). Serogroup O1 has 2 biotypes (classical and El Tor each of which has 3 serotypes) (1, 18). These 2 serogroups coexist and have caused substantial outbreaks in India and Bangladesh (1, 6, 20). Both serogroups create a toxin (enterotoxin), which is responsible for the clinical disease (1, 13).

Reservoir of infection: Often described as a water-borne disease, it is found in brackish waters and thrives and proliferates in the sheaths of blue-green algae, the shells of crustaceans, zooplankton and phytoplankton independent of humans. Humans also serve as a reservoir of infection (1, 3, 6, 7, 8, 9, 13, 14, 15). Feces from acutely infected persons are the primary source of infection in epidemic settings (15, 18).

Modes of transmission: Predominately via consumption of polluted and untreated water, but also through consumption of contaminated food (raw or undercooked shellfish, food washed with contaminated water) (1, 3, 4, 6, 10, 11, 13, 18).  Symptomatic or asymptomatic food handlers can serve as a source of an outbreak (3, 4, 13, 18, 21, 22). Secondary transmission is rare in areas with adequate sanitation and safe drinking water (14).

Attack rates: Highest attack rates are in children two to four years old (6) and highest incidence in children two to nine in endemic areas (13, 20). High attack rates of cholera were found in homes where food handlers had recently been ill (15).
           
Infectious dose: Infectious dose of 100000000 bacteria is needed to cause severe cholera in healthy volunteers, but a much lower dose (1000000) is sufficient if given in persons who are taking antacids to neutralize stomach acid (6, 16, 24)

Incubation Period: Average of two to three days (range eight hours to five days) (1, 6, 20)

Infectious Period: As long as stools are positive (usually only for a few days after recovery) (1). Persons with V. cholerae O1 infection may emit vibrios in their stool for two weeks (22).

Asymptomatic carrier state: Long term carriers of V. cholerae are rare and aren’t important in disease transmission (6), but there is documentation of an asymptomatic carrier who excreted V. cholerae O1 El Tor for ten years in his feces (23).

Diagnosis: Culture on thiosulfate citrate bile salts sucrose (TCBS) medium remains the gold standard for cholera diagnosis and conformation (19). Culture seeks to isolate serogroups O1 or O139 from feces. V. cholerae survives in fecal samples if kept moist but if a delay of hours is possible then Cary-Blair transport medium should be used to transport specimen to the lab (6, 18). Rectal swabs or stool swabs should be plated (for culture) onto thiosulfate citrate bile salts sucrose (TCBS) agar, and presumptive identification of V. cholerae O1 or O139 is made on basis of oxidase-positive colonies that have positive agglutination reactions with O1 or O139 antiserum (6, 14, 18). Dark field microscopy can be used for rapid testing. Wet Mounted liquid stool is examined for “darting” organisms that are stopped by the addition of O1 or O139 antiserum (6). PCR and DNA probes are also available and are particularly valuable when there are low concentrations of V. cholerae in the samples (19). Vibriocidal antibody titers can be done on serum samples at Center for Disease Control and Prevention (CDC) lab and titers of 1280 or higher suggest recently acquired infection (22).

Preventive Measures
Exclusions:

  1. According to Heymann (2004) in his section on V. cholerae epidemic measures, “Persons with active diarrhea should not prepare food or haul water for others (1- Guidelines and Consensus document).” According to the Public Health Laboratory Service (PHLS) (2004), “Persons with active diarrhea should be excluded from work until 48 hours after 1st normal stool. Where indicated, microbiological clearance with two consecutive negative stools 24 hours apart (3, 4- Guidelines and Consensus documents).” {Grade III-A}
  2. According to a joint collaborative project of The American Academy of Pediatrics, American Public Health Association & National Resource Center for Health and Safety (2002), “in child care settings, caregivers with “diarrhea (defined as 3 or more stools in 24 hr or blood in stool) shall be excluded from childcare. Exclusion for acute diarrhea shall continue until diarrhea stops or stools are deemed non-infectious by appropriate public health professional. Children who develop diarrhea should be isolated from other children pending arrival of parent who should remove them from the facility. Children and caregivers who excrete intestinal pathogens but no longer have diarrhea generally may be allowed to return once diarrhea stops (2- Guidelines and Consensus document).” {Grade III-A}
  3. Heymann (2004) and PHLS (2004) agree that, “surveillance of contacts should occur for those that shared food or drink with a case for 5 days from shared exposure (1, 3- Guidelines and Consensus documents).” {Grade III-A}
  4. According to Guerrant et al (2001), “because food handlers and health care workers can transmit bacterial and parasitic diseases even if they are asymptomatic, it is recommended that the have 2 consecutive negative stool samples 24 hours apart and at least 48 hours after symptom resolution before returning to work. If the patient had taken antibiotic therapy, then stool specimen should be retrieved at least 48 hours after the last dose (5- Evidence based reviews with guidelines formed out of reviewed literary sources).” {Grade III-A}
  5. According to Cruickshank (1990) referencing a 1988 working party of the WHO states that “In line with other expert bodies it concluded that asymptomatic carriers of non-typhoid salmonella, shigella, Vibrio Cholerae, and enteric viruses don’t pose a significant risk if they practice good hygiene (17- Evidence Based Literature).” {Grade III-A}
  6. According to the American Academy of Pediatrics (2005), “Temporary exclusion is recommended when a child has diarrhea: defined as more watery stools, decreased form of stool that is not associated with dietary changes and increased frequency of passing stools that is not contained by the child’s ability to use the toilet. Exclusion until diarrhea resolves, except in the case of Toxin producing E. coli or Shigella which require 2 negative stool cultures after resolution and S. Typhi requiring 3 negative stool cultures and clearance from health professional or health department(12- Guidelines and Consensus document).” {Grade III-A}
  7. According to Estrada-Garcia & Mintz (1996), “in cases where the source of Vibrio contamination was established, 2 main sources are water and food handlers. Food handlers play an important role in cholera transmission. Persons infected with V. cholerae and those in close contact with them may harbor organisms on their hands. High attack rates of cholera were found in homes where food handlers had recently been ill (15- Review of Outbreaks and Epidemiology.).” {Grade II-A}

References:

    1. Heymann, D.L. ed. Control of Communicable Disease Manual, 18th edition.2004. American Public Health Association, Washington, DC. Pgs 103-114. Guidelines and Consensus document
    2. APHA, AAP, & NRCHS. Exclusion and Inclusion of Ill Children in Child Care Facilities and Care of Ill Children in Child Care. National Health and Safety Performance Standards: Guidelines for Out-of-Home Child Care. Second Edition. 2002. A Joint Collaborative Project of The American Academy of Pediatrics Elk Grove Village, IL., The American Public Health Association Washington, D.C. & The National Resource Center for Health and Safety in Child Care, University of Colorado Health Sciences Center at Fitzsimons Campus Aurora, CO. Guidelines and Consensus document
    3. Public Health Laboratory Service, Advisory Committee on Gastrointestinal infections. Preventing Person to Person Spread Following Gastrointestinal Infections: Guidelines for Public Health Physicians and Environmental Health officers. Communicable Disease and Public Health 2004; 7(4):362-384. Guidelines and Consensus document
    4. Communicable Disease Report Review. The Prevention of Human Transmission of Gastrointestinal infection, infestations, and bacterial infestations. A Guide for Public Health Physicians and Environmental Health officers in England and Wales 1995; Volume 5 Number 11: R158-172. Guidelines and Consensus document
    5. Guerrant RL, Van Gilder T, Steiner TS, et al. Practice Guidelines for the Management of Infectious Diarrhea. Clinical Infectious Disease 2001; 32:331-350. Evidence based reviews with guidelines formed out of reviewed literary sources.
    6. Sack DA, Sack RB, Nadir GB, and Siddique AK. Cholera. Lancet 2004; 363:223-233. Evidence Based Literature.
    7. Nair GB, Oku Y, Takeda Y, et al. Toxin profiles of Vibrio cholerae non-O1 from environmental sources in Calcutta, India. Applied Environmental Microbiology 1988; 54: 3180–82. Evidence Based Literature.
    8. Huq A, Small EB, West PA, Huq MI, Rahman R, Colwell RR. Ecological relationships between Vibrio cholerae and planktonic crustacean copepods. Applied Environmental  Microbiology 1983; 45: 275–83. Evidence Based Literature
    9. Islam MS, Drasar BS, Bradley DJ. Long-term persistence of toxigenic Vibrio cholerae 01 in the mucilaginous sheath of a blue-green alga, Anabaena variabilis. JTrop Med Hyg1990; 93: 133–39. Evidence Based Literature
    10. CDC. Cholera Associated with Food Transported from El Salvador-Indiana, 1994. MMWR 1995 44(20):385-386. Review of Outbreaks and Epidemiology
    11. CDC. Epidemiology notes and Reports Toxogenic Vibrio Cholerae O1 Infection acquired in Colorado. MMWR 1989; 38(2):19-20. Review of Outbreaks and Epidemiology
    12. American Academy of Pediatrics. Managing Infectious Diseases in Child Care and Schools: A Quick Reference Guide 2005 Aronson SS and Shope TR eds. Chapter 5. Accessed on 7/30/07 at www.aap.org. Guidelines and Consensus document
    13. Rabbani G, and Grennough WB. Food as a Vehicle of Transmission of Cholera. Journal of Diarrhoel Disease Research 1999; 17(1): 1-9. Review of Outbreaks and Epidemiology.
    14. Mahon BE, Mintz ED, and Greene KD et al. Reported Cholera in the United States 1992-1994: A Reflection of Global Changes in Cholera Epidemiology. JAMA 1996; 276(4):307-312. Review of Outbreaks and Epidemiology
    15. Estrada-Garcia T and Mintz ED. Cholera: Foodborne Transmission and its Prevention. Euorpean Journal of Epidemiology 1996; 12:461-469. Review of Outbreaks and Epidemiology.
    16. Katz U, Zilberman N, Inbar R and Schwartz E. Caring for the Caregivers. Journal of Travel Medicine 2006;13(2):63-66. Editorial
    17. Cruickshank JG. Food Handlers and Food Poisoning. BMJ 1990; 300(6917):207-208. Evidence Based Literature.
    18. Alpert JM, Neira M, and Motarjemi Y. The role of Food in the Epidemiology of Cholera. World Health Organization Stat Q. 1997; 50(1-2): 111-118. Review of Outbreaks and Epidemiology.
    19. Shears P. Recent Developments in Cholera. Current Opinions in Infectious Disease 2001; 14:553-558. Evidence Based Literature.
    20. Das P, Mukherjee D, & Sarkar AK. Study of a Carrier Dependent Infectious Disease-Cholera. Journal of Biological Systems 2005; 13(3):233-244. Review of Outbreaks and Epidemiology.
    21. Steinberg EB, Greene KD, Bopp CA et al. Cholera in The United States, 1995-2000: Trends at the End of the Twentieth Century. Journal of Infectious Disease 2001; 184:799-802. Review of Outbreaks and Epidemiology.
    22. Ackers M, Pagaduan R, Hart G et al. Cholera and Sliced Fruit: Probable Secondary Transmission from an Asymptomatic Carrier in the U.S. International Journal of Infectious Disease 1997; 1:212-214. Review of Outbreaks and Epidemiology.
    23. Didion JJ. Cholera carriers. In: Barua D Burrows W, eds. Cholera. Philidelphia: WB Saunders, 1974:359-366. Guidelines and Consensus document
    24. Zuckerman JN, Rambo L and Fisch A. The True Burden and Risk of Cholera: Implications for Prevention and Control. Lancet Infectious Disease 2007; 7:521-530. Review of Outbreaks and Epidemiology