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Excerpts have been reprinted with permission from the APHA’s Control of Communicable Diseases Manual (CCDM). Please refer to the CCDM for complete information about each disease.


BRUCELLOSIS   ICD-9 023; ICD-10 A23
(Undulant fever, Malta fever, Mediterranean fever)

1. Identification – A systemic bacterial disease of acute or insidious onset, with continued, intermittent or irregular fever of variable duration; headache; weakness; profuse sweating; chills; arthralgia; depression; weight loss and generalized aching. Localized suppurative infections of organs, including liver and spleen, as well as chronic localized infections may occur; subclinical disease has been reported. The disease may last days, months or occasionally a year or more if not adequately treated.

Osteoarticular complications occur in 20%-60% of cases; sacroiliitis is the most frequent joint manifestation. Genitourinary involvement is seen in 2%-20% of cases, with orchitis and epididymitis as common manifestations. Recovery is usual but disability is often pronounced. The case-fatality rate of untreated brucellosis is 2% or less and usually results from endocarditis caused by Brucella melitensis infections. Part or all of the original syndrome may reappear as relapses …

Laboratory diagnosis is through appropriate isolation of the infectious agent from blood, bone marrow or other tissues, or from discharges. Current serological tests allow a precise diagnosis in over 95% of cases, but it is necessary to combine a test (Rose Bengal and seroaglutination) detecting agglutinating antibodies (IgM, IgG and IgA) with others detecting non-agglutinating antibodies (Coombs-IgG or ELISA-IgG) developing in later stages. These methods do not apply for B. canis, where diagnosis requires tests detecting antibodies to rough-lipopolysaccharide antigens.

2. Infectious agents – Brucella abortus, biovars 1-6 and 9; B. melitensis, biovars 1-3; B. suis, biovars 1-5; B. canis.

3. Occurrence – Worldwide, especially in Mediterranean countries (Europe and Africa), Middle East, Africa, central Asia, central and South America, India, Mexico … Brucellosis is predominantly an occupational disease of those working with infected animals or their tissues … Sporadic cases and outbreaks occur among consumers of raw milk and milk products (especially unpasteurized soft cheese) from cows, sheep and goats. Isolated cases of infection with B. canis occur in animal handlers from contact with dogs …

4. Reservoir – Cattle, swine, goats and sheep. Infection may occur in bison, elk, caribou and some species of deer. B. canis is an occasional problem in laboratory dog colonies and kennels; a small percentage of pet dogs and a higher proportion of stray dogs have positive B. canis antibody titres. Coyotes have been found to be infected.

5. Mode of transmission – Contact through breaks in the skin with animal tissues, blood, urine, vaginal discharges, aborted fetuses and especially placentas; ingestion of raw milk and dairy products (unpasteurized cheese) from infected animals. Airborne infection occurs in pens and stables for animals, and for humans in laboratories and abattoirs …

6. Incubation period – Variable and difficult to ascertain; usually 5-60 days; 1-2 months commonplace; occasionally several months.

7. Period of communicability – No evidence of person-to-person communicability.

8. Susceptibility – Severity and duration of clinical illness vary …

9. Methods of control – The control of human brucellosis rests on the elimination of the disease among domestic animals.

A. Preventive measures:
1)   Educate the public (especially tourists) regarding the risks associated with drinking untreated milk or eating products made from unpasteurized or otherwise untreated milk.
2)   Educate farmers and workers in slaughterhouses, meat processing plants and butcher shops as to the nature of the disease and the risk in handling carcases and products from potentially infected animals, together with proper operation of abattoirs to reduce exposure (especially appropriate ventilation).
3)   Educate hunters to use protective outfits (gloves, clothing) in handling feral swine and to bury the remains.
4)   Search for infection among livestock by serological testing and by ELISA or testing of cows' milk ("ring test"); eliminate infected animals (segregation and/or slaughtering) …
5)   Rev 1 is resistant to streptomycin, and RB51 to rifampicin. This must be taken into account when treating human cases of animal vaccine infections …
6)   Pasteurize milk and dairy products from cows, sheep and goats. Boiling milk is effective when pasteurization is impossible.
7)   Exercise care in handling and disposal of placenta, discharges and fetuses …

B. Control of patient, contacts and the immediate environment:
1)   Report to local health authority: Case report obligatory in most countries …
2)   Isolation: Draining and secretion precautions if there are draining lesions; otherwise none.
3)   Concurrent disinfection: Of purulent discharges.
4)   Quarantine: Not applicable.
5)   Immmunization of contacts: Not applicable.
6)   Investigation of contacts and source of infection: Trace infection to the common or individual source …
7)   Specific treatment: A combination of rifampicin (600-900 mg daily) or streptomycin (1 gram daily), and doxycycline (200 mg daily) for at least 6 weeks is the treatment of choice. In severely ill toxic patients, corticosteroids may be helpful. Tetracycline should preferably be avoided in children under 7 to avoid tooth staining. Trimethoprim-sufamethoxazole is effective, but relapses are common (30%). Relapses occur in about 5% of patients treated with doxycycline and rifampicin and are due to sequestered rather than resistant organisms; patients should be treated again with the original regimen …

C. Epidemic measures: Search for common vehicle of infection, usually raw milk or milk products, especially cheese, from an infected herd. Recall incriminated products; stop production and distribution unless pasteurization is instituted.

D. Disaster implications: None.

E. International measures: Control of domestic animals and animal products in international trade and transport …

F. Measures in the case of deliberate use: Their potential to infect humans and animals through aerosol exposition is such that Brucella species may be used as potent biological weapons.

 
 
CAMPYLOBACTER ENTERITIS   ICD-9 008.4; ICD-10 A04.5
(Vibrionic enteritis)
 
1. Identification – An acute zoonotic bacterial enteric disease of variable severity characterized by diarrhea (frequently with bloody stools), abdominal pain, malaise, fever, nausea and/or vomiting. Symptoms usually occur 2-5 days after exposure and may persist for a week. Prolonged illness and/or relapses may occur in adults. Gross or occult blood with mucus and WBCs is often present in liquid stools. Less common forms include a typhoid-like syndrome, febrile convulsions, meningeal syn­drome; rarely, post-infectious complications include reactive arthritis, febrile convulsions or Guillain-Barre syndrome. Cases may mimic acute appendicitis or inflammatory bowel disease. Many infections are asymp­tomatic and occasionally self-limited.
Diagnosis is based on isolation of the organisms from stools using selective media, reduced oxygen tension and incubation at 43°C (109.4°I) …
 
2. Infectious agentsCampylobacter jejuni and, less commonly, C. coli are the usual causes of Campylobacter diarrhea in humans. At least 20 biotypes and serotypes occur; their identification may be helpful for epidemiological purposes … standard culture methods may not detect C. fetus.
 
3. Occurrence – These organisms are an important cause of diar­rheal illness in all age groups, causing 5%-14% of diarrhea worldwide … In industrialized countries; children under 5 and young adults have the highest inci­dence of illness.Persons who are immunocompromised show an increased risk for infection and recurrences, more severe symptoms and a greater likelihood of being chronic carriers. In developing countries, illness is confined largely to children under 2 … Common-source outbreaks have occurred, most often associ­ated with foods, especially undercooked poultry, unpasteurized milk and nonchlorinated water. The largest numbers of sporadic cases in temperate areas occur in the warmer months.
 
4. Reservoir – Animals, most frequently poultry and cattle. Puppies, kittens, other pets, swine, sheep, rodents and birds may also be sources of human infection. Most raw poultry meat is contaminated with C. jejuni.
 
5. Mode of transmission – Ingestion of the organisms in under­cooked meat, contaminated food and water, or raw milk; from contact with infected pets (especially puppies and kittens), farm animals or infected infants. Contamination of milk usually occurs from intestinal carrier cattle; people and food can be contaminated from poultry, especially from common cutting boards. The infective dose is often low. Person-to-person transmission with C. jejuni appears uncommon.
 
6. Incubation period – Usually 2 to 5 days, with a range of 1-10 days, depending on dose ingested.
 
7. Period of communicability – Throughout the course of infection; usually several days to several weeks. Individuals not treated with antibi­otics may excrete organisms for 2-7 weeks … Chronic infection of poultry and other animals constitutes the primary source of infection.
 
8. Susceptibility – Immune mechanisms are not well understood, but lasting immunity to serologically related strains follows infection. In developing countries, most people develop immunity in the first 2 years of life.
 
9. Methods of control­
A. Preventive measures:
1)  Control and prevention measures at all stages of the food­chain…
2)   Pasteurize all milk and chlorinate or boil water supplies. Use irradiated foods or thoroughly cook all animal foodstuffs, particularly poultry. Avoid common cutting boards...
3)   Reduce incidence of Campylobacter on farms through ... comprehensive control programs and hygienic measures … Further reduction of contamination through freez­ing poultry.
4)   Recognize, prevent and control Campylobacter infections among domestic animals and pets … Stress handwashing after animal contact.
5)   Minimize contact with poultry and their feces; wash hands when this cannot be avoided.
 
B. Control of patient, contacts and the immediate environment:
1)   Report to local health authority: Obligatory case report in several countries, Class 2 …
2)   Isolation: Enteric precautions for hospitalized patients. Ex­clude symptomatic individuals from food handling or care of people in hospitals, custodial institutions and day care centres … Stress proper handwashing.
3)   Concurrent disinfection: Cleaning of areas and articles soiled with stools …Terminal cleaning required.
4)   Quarantine: Not applicable.
5)   Immunization of contacts: Not applicable.
6)   Investigation of contacts and source of infection: Useful only to detect outbreaks …
7)   Specific treatment: None generally indicated except rehydra­tion and electrolyte replacement (see Cholera, 9B7) … In some areas (USA) quinolone resistance of campylobacter is increasing.
 
C. Epidemic measures:Report groups of cases … to the local health authority …
 
D. Disaster implications:A risk when mass feeding and poor sanitation coexist.
 
E. International measures:WHO Collaborating Centres; see also Joint FAO/WHO Expert Committee on Risk Assessment of (. . .) Campylobacter spp. in broiler chickens, 2001, http://whglibdoc.who.int/hq/2001/WHO_SDE_PHE_FOS_01.4.pdf
 
 
 
  
CHOLERA AND OTHER VIBRIOSES   ICD-9 001; ICD-10 A00
 
I. VIBRIO CHOLERAE SEROGROUPS O1 AND O139
 
1. Identification – An acute bacterial enteric disease characterized in its severe form by sudden onset, profuse painless watery stools (rice-water stool), nausea and profuse vomiting early in the course of illness. In untreated cases, rapid dehydration, acidosis, circulatory collapse, hypogly­caemia in children, and renal failure can rapidly lead to death. In most cases infection is asymptomatic or causes mild diarrhea, especially with organisms of the El Tor biotype; asymptomatic carriers can transmit the infection. In severe dehydrated cases (cholera gravis), death may occur within a few hours, and the case-fatality rate may exceed 50%. With proper and timely rehydration, this can be less than 1%.
Diagnosis is confirmed by isolating Vibrio cholerae of the serogroup O1 or O139 from feces. V cholerae grows well on standard culture media, the most widely used of which is TCBS agar. The strains are further charac­terized by O1 and O139 specific antisera. Strains that agglutinate in O1 antisera are further characterized for serotype … For epidemiological pur­poses, a presumptive diagnosis can be based on the demonstration of a significant rise in titre of antitoxic and vibriocidal antibodies. In nonen­demic areas, organisms isolated from initial suspected cases should be confirmed in a reference laboratory through appropriate biochemical and serological reactions and by testing the organisms for cholera toxin production or for the presence of cholera toxin genes. A one-step dipstick test for rapid detection of V cholerae Ol and O139 has been developed and should soon be available on the market to improve application of effective public health interventions. In epidemics, once laboratory con­firmation and antibiotic sensitivity have been established, it becomes unnecessary to confirm all subsequent cases. Shift should be made to using primarily the clinical case definition proposed by WHO as follows:
• Disease unknown in area: severe dehydration or death from acute watery diarrhea in a     patient aged 5 or more
• Endemic cholera: acute watery diarrhea with or without vomiting in a patient aged 5 or more
• Epidemic cholera: acute watery diarrhea with or without vomiting in any patient.
However, monitoring an epidemic should include laboratory confirma­tion and antimicrobial sensitivity testing of a small proportion of cases on a regular basis.
 
2. Infectious agent – Only Vibrio cholerae serogroups O1 and O139 are associated with the epidemiological characteristics and clinical picture of cholera. Serogroup Ol occurs as two biotypes – classical and El Tor­ – each of which occurs as 3 serotypes (Inaba, Ogawa and rarely Hikojima) … The current seventh pandemic is characterized by the Ol serogroup El Tor biotype … V. cholerae O139 remains confined to South East Asia.
 
3. Occurrence – Cholera is one of the oldest and best understood epidemic diseases. Epidemics and pandemics are strongly linked to the consumption of unsafe water, poor hygiene, poor sanitation and crowded living conditions … Typical settings for cholera are periurban slums where basic urban infrastructure is missing. Outbreaks of cholera can also occur on a seasonal basis in endemic areas of Asia and Africa … Man-made or natural disasters such as complex emergencies and floods resulting in population movements as well as overcrowded refugee camps are conducive to explosive outbreaks with high case fatality rates.
Cholera is one of the 3 diseases requiring notification under the International Health Regulations. In 2002, 52 countries officially re­ported 142 311 cases … The actual number of cholera cases, however, is likely to be much higher because of underreporting and poor surveillance systems …During the latter half of the 20th century, the epidemiology of cholera has been marked by: 1) the relentless global spread of the seventh pandemic of cholera caused by V. cholerae O1 El Tor; 2) recognition of environmental reservoirs of cholera such as on the shore of the Gulf of Bengal and along the Gulf of Mexico coast of the USA; 3) the appearance for the first time of large explosive epidemics of cholera caused by V. cholerae organisms of a serogroup other than Ol (V. cholerae O139) …
Cases of cholera are regularly imported into industrialized countries … However, safe water and adequate sanitation limit the potential for outbreaks.
The occurrence of laboratory and sporadic cases in the USA since 1911 over many years in the Gulf coast area, all due to a single indigenous strain, has led to the identification of an environmental reservoir of V. cholerae Ol El Tor Inaba in the Gulf of Mexico.
 
4. Reservoir – The main reservoir is humans. Observations in the Australia, Bangladesh and the USA have shown that environmental reser­voirs exist, apparently in association with copepods or other zooplankton in brackish water or estuaries.
 
5. Mode of transmission – Cholera is acquired through ingestion of an infective dose of contaminated food or water and can be transmitted through many mechanisms ... V. cholerae O1and O139 can persist in water for long periods and multiply in moist leftover food … Vegetables and fruit "freshened" with untreated sewage wastewater have also served as vehicles of transmission. Outbreaks or epidemics as well as sporadic cases are often attributed to raw or undercooked seafood. In other instances, sporadic cases of cholera follow the ingestion of raw or inadequately cooked seafood from nonpolluted waters. Cases have been traced to eating shellfish from coastal and estuarine waters where a natural reservoir of V. cholerae O1,serotype Inaba, exists in an estuarine environment not characterized by sewage contamination. Clinical cholera in endemic areas is usually confined to the lowest socioeconomic groups.
 
6. Incubation period – From a few hours to 5 days, usually 2-3 days.
 
7. Period of communicability – As long as stools are positive, usu­ally only a few days after recovery. Occasionally the carrier state may persist for several months … Rarely, chronic biliary infection lasting for years, associated with intermittent shedding of vibrios in the stool, has been observed in adults.
 
8. Susceptibility – Variable; gastric achlorhydria increases the risk of illness, and breastfed infants are protected. Cholera occurs significantly more often among persons with blood group O. Infection with either V. cholerae Ol or O139 results in a rise in agglutinating and antitoxic antibodies, and increased resistance to reinfection. Serum vibriocidal antibodies, which are readily detected following O1 infection (but for which comparably specific, sensitive and reliable assays are not available for O139 infection), are the best immunological correlate of protection against O1 cholera … In endemic areas, most people acquire antibodies by early adulthood. However, infection with Ol strains affords no protection against O139 infection and vice-versa …
 
9. Methods of control­
A. Preventive measures:
1)   See Typhoid fever …
2)   Traditional injectable cholera vaccines based on killed whole cell microorganisms provide only partial protection (50% efficacy) of short duration (3-6 months) they do not prevent asymptomatic infection ... Their use has never been recommended by WHO.
Two oral cholera vaccines (OCV) that are safe and provide significant protection for several months against cholera caused by O1 strains have become available on the international market … One is a single-dose live vaccine (strain CVD 103-HgR); the other is a killed vaccine consisting of inactivated vibrios plus B-subunit of the cholera toxin, given on a 2-dose regimen. As of 2003, these vaccines were not licensed in the USA …
 
B. Control of patient; contacts and the immediate environment:
1)   Report to local health authority: Case report universally required by International Health Regulations; Class 1 (see Reporting).
2)   Isolation: Hospitalization with enteric precautions is desir­able for severely ill patients; strict isolation is not necessary.Less severe cases can be managed on an outpatient basis with oral rehydration and an appropriate antimicrobial agent to prevent spread …
3)   Concurrent disinfection: Of feces and vomit and of linens and articles used by patients, using heat, carbolic acid or other disinfectant. In communities with a modern and adequate sewage disposal system, feces can be discharged directly into the sewers without preliminary disinfection.Terminal cleaning.
4)   Quarantine: Not applicable.
5)   Management of contacts: Surveillance of persons who shared food and drink with a cholera patient for 5 days from last exposure. If there is evidence or high likelihood of secondary transmission within households, household members can be given chemoprophylaxis … Mass chemoprophylaxis ofwhole communities is never indicated, is a waste of re­sources and can lead to antibiotic resistance.
6)   Investigation of contacts and source of infection: Investi­gate possibilities of infection from polluted drinking water and contaminated food. Meal companions for the 5 days prior to onset should be interviewed. A search by stool culture for unreported cases is recommended only among household members or those exposed to a possi­ble common source in a previously uninfected area.
7)   Specific treatment: The cornerstone of cholera treatment is timely and adequate rehydration … As rehydration therapy becomes increasingly effective, patients who survive from hypovolaemic shock and severe dehydration may manifest certain complications, such as hypoglycaemia, that must be recognized and treated promptly.
Most patients with mild or moderate fluid loss can be treated entirely with oral rehydration solutions … replacing over 4-6 hours a volume matching the estimated fluid loss (approximately 5% of body weight for mild and 7% for moderate dehydration). Continuing losses are replaced by giving, over 4 hours, a volume of oral solution equal to 1.5 times the stool volume lost in the previous 4 hours.
Severely dehydrated patients or patients in shock should be given rapid IV rehydration with a balanced multielectrolyte solution … Useful solutions include Ringer lactate (4 grams NaCl, 1 gram KCl, 6.5 grams sodium acetate and 8 grams glucose/L), and "Dacca solution" (5 grams NaCl, 4 grams NaHCO3 and 1 gram KCl/L), which can be prepared locally in an emergency … In severe cases, appropriate antimicrobial agents can shorten the duration of diarrhea, reduce the volume of rehydration solutions required, and shorten the duration of vibrio excretion …
 
C. Epidemic measures:
1)   Educate the population at risk concerning the need to seek appropriate treatment …
2)   Provide effective treatment facilities.
3)   Adopt emergency measures to ensure a safe water supply …
4)   Ensure careful preparation and supervision of food and drinks …
5)   Initiate a thorough investigation designed to find the vehicle of infection and circumstances (time, place, person) of transmission, and plan control measures accordingly.
6)   Provide appropriate safe facilities for sewage disposal.
7)   Parenteral whole cell vaccine is not recommended.
8)   Use of the currently available oral cholera vaccines is under study …
 
D. Disaster implications:Outbreak risks are high in endemic areas if large groups of people are crowded together without safe water in sufficient quantity, adequate food handling or sanitary facilities.
 
E. International measures:
1)   Governments are required to report cholera cases due to V. cholerae Oland O139 to WHO. In the USA, suspected cases are reported to the State epidemiologist, State health departments then notify the CDC, which confirms the case and notifies WHO.
2)   Measures applicable to ships, aircraft and land transport arriving from cholera areas are specified in International Health Regulations
3)   International travellers: Immunization with the parenteral whole cell vaccine is not recommended by WHO. No country requires proof of cholera vaccination as a condi­tion of entry and the International Certificate of Vaccina­tion no longer provides a specific space for the recording of cholera vaccination …
4)   WHO Collaborating Centres. Further information on http://www.who.int/csr/disease/cholera or http://www.who.int/emc/diseases/cholera
 
 
CHOLERA AND OTHER VIBRIOSES ICD-9 001; ICD-10 A00
 
 
II. VIBRIO CHOLERAE SEROGROUPS OTHER THAN O1 AND O139    
ICD-9 005.8; ICD-10 A05.8
 
1. Identification – Of the more than 200 V. cholerae serogroups that exist, only O1 and O139 are associated with the clinical syndrome of cholera and can cause large epidemics. Organisms of V. cholerae sero­groups other than O1 and O139 have been associated with sporadic cases of foodborne outbreaks of gastroenteritis, but have not spread in epidemic form. They have been associated with wound infection and also, rarely, isolated from patients (usually immunocompromised hosts) with septice­mic disease.
 
2. Infectious agentV. cholerae pathogens of serogroups other than O1 and O139.
Serogroups of V. cholerae have been defined on the basis of their surface antigen (lipopolysaccharide O antigen). Vibrios that are biochem­ically indistinguishable but do not agglutinate in V. cholerae serogroup O1 or O139 antisera (non-O1 non-O139 strains, formerly known as nonagglu­tinable vibrios [NAGs] or noncholera vibrios [NCVs]) are now included in the species V. cholerae. Some strains elaborate cholera enterotoxin, but most do not … The reporting of nontoxinogenic V. cholerae O1or of non-O1/nonO139 V. cholerae infections as cholera is inaccurate and leads to confu­sion.
 
3. Occurrence – Non-O1/non-O139 V. cholerae strains are associated with 2%-3% of cases (including travellers) of diarrheal illness in tropical developing countries … Most non-O1 non-O139 V. cbolerae are of little public health importance.
 
4. Reservoir – Non-O1/non-O139 V. cholerae are found in aquatic environments worldwide, particularly in mildly brackish waters where they constitute indigenous flora. Although halophilic, they can also proliferate in fresh water (e.g. lakes). Vibrio counts vary with season and peak in warm seasons. In brackish waters they are found adherent to chitinous zooplankton and shellfish. Isolates of V. cholerae other than O1 and O139 are able to survive and multiply in a variety of foodstuffs.
 
5. Mode of transmission – Cases of non-O1/non-O139 gastroenteri­tis are usually linked to consumption of raw or undercooked seafood, particularly shellfish. In tropical endemic areas, some infections may be due to ingestion of surface waters. Wound infections arise from environ­mental exposure, usually to brackish water or from occupational accidents among fishermen, shellfish harvesters, etc. In high-risk hosts septicemia may result from a wound infection or from ingestion of contaminated seafood.
 
6. Incubation period – Short, 12-24 hours in outbreaks and an average of 10 hours in experimental challenge of volunteers (range 5.5-96 hours).
 
7. Period of communicability – It is not known whether in nature these infections can be transmitted from person to person or by humans contaminating food vehicles …
 
8. Susceptibility – All humans are believed to be susceptible to gastroenteritis if they ingest a sufficient number of non-Ol/non-O139 V. cholerae in an appropriate food vehicle or to develop a wound infection if the wound is exposed to vibrio-containing water or shellfish. Septicae­mia develops only in hosts such as those who are immunocompromised, have chronic liver disease or severe malnutrition.
 
9. Methods of control­
A. Preventive measures:
1)   Educate consumers about the risks associated with eating raw seafood unless it has been irradiated or well cooked for 15 minutes at 70°C/158°F.
2)   Educate seafood handlers and processors on the following preventive measures …
 
B, C. and D. Control of patient, contacts and immediate environment; Epidemic measures and Disaster implica­tions: See Staphylococcal food intoxication (section I, 9B except for B2, 9C and 9D). Isolation: Enteric precautions.
 
Patients with liver disease or who are immunosuppressed (because of treatment or underlying disease) and alcoholics should be warned not to eat raw seafood. When disease occurs in these individuals, a history of eating seafood and especially the presence of bullous skin lesions justify early institution of antibiotherapy …
 
 
 
III. VIBRIO PARAHAEMOLYTICUS ENTERITIS ICD-9 005.4; ICD-10 A05.3
(Vibrio parahaemolyticus infection)
 
1. Identification – An intestinal disorder characterized by watery di­arrhoea and abdominal cramps in nearly all cases, usually with nausea, vomiting, fever and headache. About one quarter of patients experience a dysentery-like illness with bloody or mucoid stools, high fever and high WBC count. Typically, it is a disease of moderate severity lasting 1-7 days; systemic infection and death rarely occur.
Diagnosis is confirmed by isolating Vibrio parahaemolyticusfrom the patient's stool on appropriate media (typically TCBS media); or identifying 105 or more organisms per gram of an epidemiologically incriminated food (usually seafood).
 
2. Infectious agentVibrio parahaemolyticus, a halophilic vibrio …
 
3. Occurrence – Sporadic cases and common-source outbreaks have been reported from many parts of the world, particularly Japan, southeast­ern Asia and the USA … Cases occur primarily in warm months.
 
4. Reservoir – Marine coastal environs are the natural habitat. During the cold season, organisms are found in marine silt; during the warm season, they are found free in coastal waters and in fish and shellfish.
 
5. Mode of transmission – Ingestion of raw or inadequately cooked seafood, or any food contaminated by handling raw seafood, or by rinsing with contaminated water.
 
6. Incubation period – Usually between 12 and 24 hours, but can range from 4 to 30 hours.
 
7. Period of communicability – Not normally communicable from person to person (except fecal-oral transmission).
 
8. Susceptibility and resistance – Most people are probably suscep­tible, especially in case of liver disease, decreased gastric acidity, diabetes, peptic ulcer or immunosuppression.
 
9. Methods of control­
A. Preventive measures:See non toxigenic V. cholerae infec­tions; monitor shellfish and coastal waters for pathogenic V. parahaemolyticus.
 
B., C. and D. Control of patient, contacts and immediate environment; Epidemic measures and Disaster implica­tions:See Staphylococcal food intoxication (section 1, 9C and 9D). Isolation: Enteric precautions. Reporting of outbreaks man­datory in some areas.
1)   Specific treatment: Rehydration as appropriate. If septicemia, effective antimicrobials …
 
 
 
IV. INFECTION WITH VIBRIO VULNIFICUS  ICD-9 005.8; ICD-10 A05.8
 
1. Identification – Infection with Vibrio vulnificus produces septice­mia in persons with chronic liver disease, chronic alcoholism or hemo­chromatosis, or those who are immunosuppressed. The disease appears 12 hours to 3 days after eating raw or undercooked seafood, especially oysters. One-third of patients are in shock when they present for care or develop hypotension within 12 hours after hospital admission. Three-­quarters of patients have distinctive bullous skin lesions; thrombocytope­nia is common and there is often evidence of disseminated intravascular coagulation. Over 50% of patients with primary septicemia die; the case-fatality rate exceeds 90% among those who become hypotensive. V. vulnificus can also infect wounds sustained in coastal or estuarine waters; wounds range from mild, self-limited lesions to rapidly progressive cellu­litis and myositis that can mimic clostridial myonecrosis in the rapidity of spread and destructiveness.
 
2. Infectious agent – A halophilic, usually lactose-positive (85% of isolates) marine Vibrio that is biochemically quite similar to V. parahaemolyticus. Confirmation of species identity sometimes requires use of DNA probes or numerical taxonomy in a reference laboratory. V. vulnifi­cus expresses a polysaccharide capsule, of which there are multiple antigenic types on its surface.
 
3. OccurrenceV. vulnificus isthe most common agent of serious infections caused by the genus Vibrio in the USA. In coastal areas the annual incidence of V. vulnificus disease is about 0.5 eases per 100 000 population; approximately two-thirds of these cases are primary septicemia. V. vulnificus infection has been reported from many areas of the world (e.g. Israel, Japan, the Republic of Korea, Spain, Taiwan (China) and Turkey).
 
4. ReservoirV. vulnificus is a free-living autochthonous element of flora of estuarine environments. It is recovered from estuarine waters and from shellfish, particularly oysters. During warm summer months it can be isolated routinely from most cultured oysters.
 
5. Mode of transmission – Among persons at high risk, including those who are immunocompromised or have chronic liver disease, infection is acquired through ingestion of raw or undercooked seafood. In immunocompetent normal hosts, infections typically occur after exposure of wounds to estuarine water (e.g. boating accidents) or from occupa­tional wounds (oyster shuckers, fishermen).
 
6. Incubation period – Usually 12 to 72 hours after eating raw or undercooked seafood.
 
7. Period of communicability – This is not considered to be an infection that is transmitted from person to person, either directly or via contamination of food...
 
8. Susceptibility – Persons with cirrhosis, hemochromatosis and other chronic liver disease and immunocompromised hosts (from either underlying disease or medication) are at increased risk for the septicemic form of disease. For the period 1981-1992 the annual incidence of V. vulnificus illness among adults with liver disease in Florida (USA) who ate raw oysters was 7.2 per 100 000 versus 0.09 for adults without known liver disease.
 
9. Methods of control­
A. Preventive measures:The same as those for prevention of non-O1/non-O139 V. cholerae infections.
 
 
V. INFECTION WITH OTHER VIBRIOS   ICD-9 005.8; ICD-10 A05.8
 
Infection with certain other Vibrio species has been associated with sporadic cases of diarrheal disease and rarely with outbreaks. These include V. cholerae of serogroups other than O1 and O139, V. mimicus (some strains elaborate an enterotoxin indistinguishable from that pro­duced by V. cbolerae O1 and O139), V. fluvialis, V. furnissii and V. hollisae. Septicaemic disease in hosts with underlying liver disease, severe malnutrition or immunocompetence has, rarely, been associated with V. hollisae. V. alginolyticus and V. damsela have been associated with wound infections.
Vibrio species other than O1 and O139 have never been associated with large outbreaks. The clinical picture of infections with these strains is different from cholera and does not deserve reporting as such.
 
 
 
DIARRHEA, ACUTE ICD-9 001-009; ICD-10 A09
 
Diarrhea is often accompanied by other clinical signs and symptoms including vomiting, fever, dehydration and electrolyte disturbances. It is a symptom of infection by many different bacterial, viral and parasitic enteric agents. The specific diarrheal diseases—cholera, shigellosis, salmonellosis, Escherichia coli infections, yersiniosis, giardiasis, Campylobacter enteritis, cryptosporidiosis and viral gastroenteropathy—are each described in detail under individual listings elsewhere in this book. Diarrhea can also occur in association with other infectious diseases such as malaria and measles, as well as chemical agents. Change in the enteric flora induced by antibiotics may produce acute diarrhea by overgrowth and toxin production by Clostridium difficile.
Approximately 70%-80% of the vast number of sporadic diarrheal episodes in people visiting treatment facilities in less industrialized countries could be diagnosed etiologically if the complete battery of newer laboratory tests were available and utilized. In the USA, where 5 million cases per year are estimated to occur and approximately 4 million are seen by a health care provider, the comparable figure is about 45% of cases. From a practical clinical standpoint, diarrheal illnesses can be divided into 3 clinical presentations:
1) Acute watery diarrhea (including cholera), lasting several hours or days; the main danger is dehydration; weight loss occurs if feeding is not continued. For severe dehydration (one or more of the following: child lethargic or unconscious, drinking poorly or not at all, eyes very sunken and dry, mouth very dry, very slow skin pinch— corresponding to a fluid deficit > 10% of body weight), the preferred treatment is rapid intravenous therapy followed by oral rehydration; in other cases (no or some dehydration) give oral rehydration solution (ORS) by mouth;
2) Acute bloody diarrhea (dysentery), caused by organisms such as Shigella, E. coli O157:H7 and other organisms; the main dangers are intestinal damage, sepsis and malnutrition; other complications including dehydration may occur.
3) Persistent diarrhea, lasting 14 days or longer; the main danger is malnutrition and serious extraintestinal infection; dehydration may also occur.
The details pertaining to the individual diseases are presented in separate chapters.
 
 
 
DIARRHEA CAUSED BY ESCHERICHIA COLI ICD-9 008.0; ICD-10 A04.0-A04.4
 
Six major categories of Escherichia coli strains cause diarrhea: 1) enterohemorrhagic; 2) enterotoxigenic; 3) enteroinvasive; 4) enteropathogenic; 5) enteroaggregative; and 6) diffuse-adherent. Each has a different pathogenesis, possesses distinct virulence properties, and comprises a separate set of O: H serotypes. Different clinical syndromes and epidemiological patterns may also be seen. Transmission is usually through contaminated food, water or hands; an outbreak in 2003 in Ohio was attributed to respiratory transmission via contaminated sawdust.
 
I. DIARRHEA CAUSED BY ENTEROHEMORRHAGIC STRAINS      ICD-9 008.0; ICD-10 A04.3
(EHEC, Shiga toxin producing E. coli [STEC], E. coli O157:H7, Verotoxin producing E. coli) [VTEC]
 
1. Identification – This category of diarrhea-causing E. coli was recognized in 1982 when an outbreak of hemorrhagic colitis occurred in the USA and was shown to be due to an unusual serotype, E. coli O157:H7, not previously incriminated as an enteric pathogen. The diarrhea may range from mild and nonbloody to stools that are virtually all blood. Lack of fever in most patients can help to differentiate this infection from that due to other enteric pathogens. The most severe clinical manifestation of EHEC infection is the hemolytic uraemic syndrome (HUS) (sometimes diagnosed as thrombotic thrombocytopenic purpura (TTP) in adults). About 8% of persons with E. coli O157:H7 diarrhea progress to this syndrome. Rates are likely to vary for other serotypes. EHEC elaborate potent cytotoxins called Shiga toxins 1 and 2 (also called verocytotoxins and previously called Shiga-like toxins). Shiga toxin 1 is identical to the toxin elaborated by Shigella dysenteriae 1; HUS is also a complication of S. dysenteriae 1 infection. The structural genes for the toxins are found on chromosomally-encoded phages. Most EHEC strains have a chromosomal pathogenicity island containing multiple virulence genes, including those encoding proteins that cause attaching and effacing lesions.
In North America most strains of the most common EHEC serotype, O157:H7, can be identified in stool cultures on sorbitol-MacConkey media by their inability to ferment sorbitol. Because most other EHEC strains ferment sorbitol, other techniques must be used, among which are demonstrating the ability to elaborate Shiga toxins (a commercial assay is available), or the use of DNA probes that identify the toxin genes. All EHEC strains should be sent to the state health department laboratory for serotyping to monitor the frequency of various serotypes and to help detect outb