Vibrio Cholerae, Serovar 01

Vibrio Cholerae

PATHOGEN SAFETY DATA SHEET – INFECTIOUS SUBSTANCES

SECTION I – INFECTIOUS AGENT

NAME: Vibrio cholerae, serogroup O1, serogroup O139 (Bengal)

SYNONYM OR CROSS REFERENCE: Cholera

CHARACTERISTICS: Vibrio cholerae is a gram negative, non-spore forming, curved rod that is oxidase positive(1,2,3). It is very motile and has a single polar flagellum(1). The bacterium is 1- 3 µm by 0.5-0.8 µm, is a facultative anaerobe and is part of the Vibronaceae family(1,3). Serogroups O1 (classical and El Tor biotypes) and O139 are primarily responsible for cholera outbreaks(1,3). Pathogenic serogroups produce cholera toxin (CT) while non pathogenic strains may or may not produce this toxin(2). Recently, V. cholerae serougroup O75 strains possessing the cholera toxin gene were isolated from patients with severe diarrhoea, and serogroup O141 has been associated with sporadic cholera-like diarrhoea and bloodstream infections in the United States(4,5). Some serotypes may serve as a reservoir for the cholera toxin phage genome(6,7). Serotypes that do not produce cholera toxin can still cause illness in humans (i.e. enteritis)(8).

SECTION II – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Vibrio cholerae can cause syndromes ranging from asymptomatic to cholera gravis(3). In endemic areas, 75% of cases are asymptomatic, 20% are mild to moderate, and 2-5% are severe forms like cholera gravis(3). Symptoms include abrupt onset of watery diarrhoea (a grey and cloudy liquid), occasional vomiting and abdominal cramps(1,3). Dehydration ensues with symptoms and signs such as thirst, dry mucous membranes, decreased skin turgor, sunken eyes, hypotension, weak or absent radial pulse, tachycardia, tachypnea, hoarse voice, oliguria, cramps, renal failure, seizures, somnolence, coma and death(1). Death due to dehydration can occur in a hours to days in untreated children and the disease is dangerous for pregnant women and their foetuses during late pregnancy as abortion, premature labor and fetal death may occur(3,9,10). In cases of cholera gravis involving severe dehydration, up to 60% of patients can die; however, less than 1% of cases treated with rehydration therapy are fatal. The disease typically lasts from 4-6 days(3,11). Worldwide, diarrhoeal disease, caused by cholera and many other pathogens, is the second leading cause of death for children under the age of 5 and at least 120,000 deaths are estimated to be caused by cholera each year(12,13). In 2002, the WHO deemed that the case fatality ratio for cholera was about 3.95%(3).

EPIDEMIOLOGY: In the past 200 years, there have been 8 main cholera pandemics, with the disease being most common in tropical and subtropical areas(2,14). Most of the cases are in the Indian subcontinent and Africa (in 2002 the WHO estimated that 97% of the cholera cases were in Africa)(2,3). There are several million cases of cholera each year and in endemic areas, these tend to be most common in children aged 2-9 and in women who are of child-bearing age(3,12). Epidemics in endemic areas tend to occur during the hot season(1).

HOST RANGE: Humans, water birds, shellfish, fish, and herbivores have been found to contain the infectious agent(1).

INFECTIOUS DOSE: The infectious dose ranges between 106 and 1011 ingested vibrios(1). The infectious dose depends on gastric acidity (lower acidity levels reduces the number of vibrios required for infection)(1).

MODE OF TRANSMISSION: Cholera is typically spread by consumption of water that is contaminated with infectious feces(1,2). Epidemics caused by infectious raw fish and seafood have been reported(1).

INCUBATION PERIOD: The incubation period can range from a few hours to 5 days after infection(1).

COMMUNICABILITY: Symptomatic patients may shed vibrios before clinical signs of illness and up to 2 weeks after, whereas asymptomatic patients typically only shed vibrios for 1 day(12). A carrier state (where the patient has the infectious agent without any clinical manifestations) can exist for several weeks where vibrios are shed in small and intermittent quantities (15), (16).

SECTION III – DISSEMINATION

RESERVOIR: Humans are a reservoir for the disease as are animals around aquatic environments(1). The bacterium has been found in birds and herbivores surrounding freshwater lakes and rivers as well as in algae, copepods (zooplankton), crustaceans and insects(1,3).

ZOONOSIS: None.

VECTORS: None.

SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Susceptible to antibiotics. Tetracycline has been the drug of choice, although resistance to this antibiotic is becoming more common(17,18). Ciproflaxin, doxycycline and co-trimoxazole can also be used(1). An outbreak in 1979 in Bangladesh was caused by multi-drug resistant strains of El Tor biotype(18). 36% of strains in this outbreak were resistant to tetracycline, ampicillin, kanamycine, streptomycin, and trimethoprim sulfamethoxazole(18).

DRUG RESISTANCE: Resistance has been shown to nalidixic acid, furazolidone, and co- trimoxazole, V. cholerae O1 lnaba isolates have been found to be muli-antibiotic resistant, when increasing resistance to ciprofloxacin(19).

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 2-5% phenol, 1% sodium hypochlorite, 4% formaldehyde, 2% glutaraldehyde, 70% ethanol, 70% propanol, 2% peracetic acid, 3-6% hydrogen peroxide, and 0.16% iodine(14).

PHYSICAL INACTIVATION: Vibrio cholerae is sensitive to cold (loss of viability after a cold shock at 0ºC)(20).

SURVIVAL OUTSIDE HOST: Cholera can survive in well water for 7.5 ± 1.9 days and the El Tor biotype can survive 19.3 ± 5.1 days(21). The bacterium can survive in a wide variety of foods and drinks for 1-14 days at room temperature and 1-35 days in an ice box(21). It has also been found on fomites at room temperature for 1-7 days(21).

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Confirm diagnosis by dark field microscopy of a wet mount of fresh stool, PCR or ELISA(1,3,11).

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Fluid replacement, electrolyte replacement and base i.v. fluid replacement followed by the WHO’s oral rehydration solution (Na+ 90 mmol/L, K+ 20 mmol/L, Cl- 80 mmol/L, citrate (10 mmol/L and glucose 110 mmol/L) is the recommended treatment for dehydration(1). Administering an antibiotic like ciproflaxin, doxycycline or co-trimoxazole reduces the duration of the illness(1).

IMMUNIZATION: Routine vaccination for laboratory workers and travellers is not recommended(22,23). Traditional parenteral inactivated vaccine strains are available though not recommended for widespread use as they only provide protection for 3-6 months(3,14). Oral vaccines that provide protection for several years (up to 3) are available but their efficacy in endemic areas has not been confirmed(3,13).

PROPHYLAXIS: Chemoprophylaxis with antibiotics has not been shown to be effective(1). Proper hygiene, sanitary measures, water treatment and careful food preparation are the best prophylactic measures in endemic areas(1).

SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: 12 cases of infection with 4 deaths were reported up to 1979(24). The deaths were associated with mouth pipetting, contact with infectious feces and contaminated laboratory laundry(24).

SOURCES/SPECIMENS: Feces and naturally or experimentally infected animals are the main specimens which contain the infectious agent(22).

PRIMARY HAZARDS: The primary hazards when working with this agent are ingestion and accidental parenteral inoculation(9,14,22). The risk of aerosol exposure is not known(22).

SPECIAL HAZARDS: The risk of infection is higher in people who don’t have gastric acid (i.e. due to gastrectomy or achlorhydria)(2).

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk group 2(25).

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk to splashes(26).

OTHER PRECAUTIONS: All procedures that may produce aerosols, or involve high concentrations or large volumes should be conducted in a biological safety cabinet (BSC). The use of needles, syringes, and other sharp objects should be strictly limited. Additional precautions should be considered with work involving animals or large scale activities(26).

SECTION VIII – HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply appropriate disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up (30 min)(26).

DISPOSAL: All wastes should be decontaminated before disposal either by steam sterilization, incineration or chemical disinfection(26).

STORAGE: The infectious agent should be stored in a sealed and identified container(26).

SECTION IX – REGULATORY AND OTHER INFORMATION

REGULATORY INFORMATION: The import, transport, and use of pathogens in Canada is regulated under many regulatory bodies, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment Canada, and Transport Canada. Users are responsible for ensuring they are compliant with all relevant acts, regulations, guidelines, and standards.

UPDATED: September 2010

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada.

Although the information, opinions and recommendations contained in this Pathogen Safety Data Sheet are compiled from sources believed to be reliable, we accept no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information. Newly discovered hazards are frequent and this information may not be completely up to date.

Vesicular Stomatitis Virus

PATHOGEN SAFETY DATA SHEET – INFECTIOUS SUBSTANCES

SECTION I – INFECTIOUS AGENT

NAME: Vesicular stomatitis virus (VSV)

SYNONYM OR CROSS REFERENCE: Vesiculovirus(1,2), vesicular stomatitis(1,2,3,4,5), VS(1,2,3,4,5,6), vesicular stomatitis virus disease(3,7), vesicular stomatitis fever, and Indiana fever(3).

CHARACTERISTICS: A member of the Vesiculovirus genus, in the family Rhabdoviridae(3,6). VSV is a bullet-shaped, enveloped virus, approximately 70 nm in diameter and 170 nm in length(3), and has a single-stranded, negative-sense RNA genome(5,8). VSV has two main serotypes: VSV serotype Indiana (with its subtypes Cocal virus and Alagoas virus), and VSV serotype New Jersey(1,2,3,5,6,8).

SECTION II – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Most human infections with VSV appear to be subclinical(1,6,8). In patients that show clinical manifestations, the initial symptom is high fever that is often biphasic. Subsequent symptoms are “flu-like” including severe malaise, headaches, myalgia, arthralgia, retrosternal pain, eye aches, and nausea(1,3,6,7). Occasionally a disease course with haemorrhages similar to dengue fever has been seen(6). Vesicle formation on the oral mucosa, lips, and nose is possible, but these are rare symptom of vesicular stomatitis (VS)(3,6,7). Most human cases of VS have been diagnosed in laboratory workers(3). In the laboratory, VSV has been engineered to target cancer cells or to stimulate immunity against diseases such as AIDS or influenza(8).

EPIDEMIOLOGY: VS exists in North and South America, Africa and Asia but not in central Europe(6). Serological surveys indicate that the prevalence of infection may be high among some populations in enzootic areas. For example, in a rural locality in Panama, more than 90% of the adult population is affected(3); however, the precise frequency of VS is not well established, as the disease often goes unnoticed due to its benign course.

HOST RANGE: Humans(1,2,4,5,6,8), horses(2,4,6,8), cattle, pigs, mules(2,6), sand flies(5,6), grasshoppers(4), and rodents(2).

INFECTIOUS DOSE: Unknown.

MODE OF TRANSMISSION: Bite of an infected sand fly(1,5,7,8); by direct contact with abrasions on the skin; by contact with infected domestic animals; or by inhaling aerosols via the nasopharyngeal route(1,3). The virus has also been transmitted via accidental autoinoculation or inhalation of aerosols in a laboratory setting(3,8).

INCUBATION PERIOD: A wide range of incubation periods have been reported from 30 hours(1,6) to 6 days(7).

COMMUNICABILITY: There is no documented evidence of person-to-person transmission of VSV.

SECTION III – DISSEMINATION

RESERVOIR: The main reservoir is the sand fly, although arboreal rodents and non-human primates may also harbour VSV(7). Grasshoppers have also been implicated as a potential reservoir for VSV(4).

ZOONOSIS: Yes, humans can contract VSV through direct contact with infected animals, or indirectly through the bite of an infected fly(1,5,7,8).

VECTORS: Sand fly ( Phlebotomus spp.) appears to be the most important vector for VSV(2,6,8). Black flies ( Simuliidae )(2,5,6), midges ( Culicoides spp.), mosquitoes ( Aedes spp.)(2,5,8) and other diptera(2,5,6) have also been implicated.

SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Unknown.

SUSCEPTIBILITY TO DISINFECTANTS: VSV is inactivated by 1% cresylic acid, phenolics, chlorinated phenol, 2.5% phenol, 0.4% HCl, 2% sodium orthophenylphenate(9), and sodium hypochlorite(1,9).

PHYSICAL INACTIVATION: Inactivated at low pH (1.5)(9), and immediately upon heating to 60 °C(10,11). VSV in stroma-free haemoglobin can also be inactivated by phototreatment (for example, with red light-emitting diode (655 nm), 1,9-dimethylmethylen blue (DMMB), or methylen blue (MB))(11).

SURVIVAL OUTSIDE HOST: VSV can survive for 3 to 4 days in infected saliva on milking pails, mangers and hay(1).

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Human VSV infections are confirmed by virus isolation from throat swabs or blood(1,2,6). Other methods of detection include PCR(1,2,6), ELISA(1,2), neutralisation(2), compliment fixation, immunofluorescence, and electron microscopy(1).

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: No specific therapy is currently available. Symptomatic treatment and prevention of secondary infections is important(6).

IMMUNIZATION: None currently available for use in humans.

PROPHYLAXIS: None.

SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: 46 recorded cases (with no deaths) until 1980(12).

SOURCES/SPECIMENS: Blood(3,4,6), throat secretions(1,3,6), saliva(1,3,4), exudates, or epithelium from open vesicles(1,3,4).

PRIMARY HAZARDS: Exposure of skin and mucous membranes to VSV via infectious aerosols and/or droplets(3).

SPECIAL HAZARDS: Handling infected livestock is a well documented hazard(1,2,3,6,7).

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 3.

CONTAINMENT REQUIREMENTS: Containment Level 3 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures.

PROTECTIVE CLOTHING: Personnel entering the laboratory should remove street clothing and jewellery, and change into dedicated laboratory clothing and shoes, or don full coverage protective clothing (i.e., completely covering all street clothing). Additional protection may be worn over laboratory clothing when infectious materials are directly handled, such as solid-front gowns with tight fitting wrists, gloves, and respiratory protection. Eye protection must be used where there is a known or potential risk of exposure to splashes(13).

OTHER PRECAUTIONS: All activities with infectious material should be conducted in a biological safety cabinet (BSC) or other appropriate primary containment device in combination with personal protective equipment. Centrifugation of infected materials must be carried out in closed containers placed in sealed safety cups, or in rotors that are loaded or unloaded in a biological safety cabinet. The use of needles, syringes, and other sharp objects should be strictly limited. Open wounds, cuts, scratches, and grazes should be covered with waterproof dressings. Additional precautions should be considered with work involving animals or large scale activities(13).

SECTION VIII – HANDLING AND STORAGE

DISPOSAL: Decontaminate all materials for disposal by steam sterilisation, chemical disinfection, and/or incineration(13).

STORAGE: In sealed, leak-proof containers that are appropriately labelled and locked in a Containment Level 3 laboratory(13).

SECTION IX – REGULATORY AND OTHER INFORMATION

UPDATED: September 2010.

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada.

Trichomonas Vaginalis

PATHOGEN SAFETY DATA SHEET – INFECTIOUS SUBSTANCES

SECTION I – INFECTIOUS AGENT

NAME: Trichomonas vaginalis

SYNONYM OR CROSS REFERENCE: Trichomoniasis, vaginitis.

CHARACTERISTICS: Trichomonas vaginalis is a parasitic protozoan flagellate, and organisms vary in size but are usually around 10 μm in length and 7 μm in width(1,2). It usually has an oval or pear-like shape, but can assume an amoeboid form when attached to vaginal epithelial cells. T. vaginalis has a total of 5 flagella, four of which are located at its anterior portion. The fifth flagellum is incorporated within the undulating membrane(1,3). The anaerobic parasite can only exist as a trophozoite and lacks a cystic stage, reproducing by longitudinal binary fission. Growth is optimized at 37°C at pH 6.0 – 6.3, but can survive at up to pH 7(4).

SECTION II – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: T. vaginalis is generally restricted to the genitourinary tract by the host’s immune system, and is the etiological agent of human trichomoniasis(2). Infection has been associated with an increased risk of human immunodeficiency syndrome in both sexes(4).

In women: Symptoms of infection include vaginal secretion that is scanty and mixed with mucus; malodorous discharge that is frothy, yellow or green, mycopurulent, and copious(4). The protozoan can be found in the vagina, cervix, bladder, Bartholin’s, Skene’s, and periurethral glands. Complications may result in cervical erosion, cervical cancer, infertility, adnexitis, pyosalpinx, and endometritis. Premature rupture of the placental membranes can occur in pregnant women, resulting in premature birth and low-birth weight(5). Acute infections are characterised by severe pruritus, vaginitis, vulvitis with dysuria and dyspareunia, and hemorrhagic spots on the mucosa (in 2% of patients) which results in colpitis macularis or petechiae (strawberry cervix). In females, 50% of cases are asymptomatic. Infection can persist for long periods of time in the urogenital tract of women. 25 – 50% are asymptomatic for the first 6 months of infection, and organisms can survive indefinitely in the lower urogenital tract if left untreated(1,6).

In men: Prevalence is lower in men, and infection is often asymptomatic(7). Infection in men can be present in the prostate, seminal vesicles, and epididymis. Complications are rare, but can potentially lead to genitourinary inflammation disease, sterility, scanty, clear to mucopurulent discharge, dysuria, non-gonococcal urethritis, prostatitis, balanoposthitis, epididymitis, and urethral disease(4). Infection is usually mild with no symptoms, thus making men potential carriers. Spontaneous resolution of infection is common as the oxidative nature of the male genital tract is speculated to be inhibitory to pathogenic factors of infection, which usually remains for 10 days or less(1).

EPIDEMIOLOGY: Worldwide – trichomoniasis caused by T. vaginalis is one of the most common non-viral sexually transmitted diseases with an estimated 170 million cases occurring annually (no seasonal variability)(1), and incidence has been found to be high in non-hispanic black women(5). Infection usually occurs in women during reproductive years, and occurrence before menarche or after menopause is rare(4). Fourteen to 60% of male infections are associated with known infected female partners(1).

HOST RANGE: Humans(1).

INFECTIOUS DOSE: Experimental studies have shown that urogenital inoculation with 10,000 to 120,000 organisms has resulted in transmission, although epidemiological examinations have shown that the infective dose in women is low and the infection rate is high(8-10).

MODE OF TRANSMISSION: Commonly spread through sexual contact with vaginal or urethral discharges of infected persons(1), and transmission of organisms via artificial insemination of infected cryobanked semen is also possible(11). Non-sexual transmission is rare but has been observed in cases involving contaminated douche nozzles, moist wash-clothes, specula, or toilet seats(1,12,13). Transmission to newborn infants from infected mothers is possible and is observed in 2 – 17% of cases, and can result in urinary tract or vaginal infections(1).

INCUBATION PERIOD: Ranges from 3 – 28 days with an average of 7 days(4,14).

COMMUNICABILITY: Infection can persist for a significant period of time in asymptomatic cases(14), from months to years. SECTION III – DISSEMINATION

RESERVOIR: Humans, typically females, while men may act as a reservoir for infection(4).

ZOONOSIS: None.

VECTORS: None.

SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: The only drugs that have been approved by the FDA for use in the United States are metronidazole (although the use of this drug can increase the incidence of preterm birth)(15), and Tinidazole (trade name known as Tindamax)(16). Ornidazole, secnidazole, and nimorazole can be used in countries outside of the US. In vitro testing has shown that nitroimidazole EU11100 also has similar efficacy as metronidazole(15).

DRUG RESISTANCE: Studies have shown that at least 5% of clinical cases of trichomoniasis are caused by metronidazole-resistant T. vaginalis, and cross-resistance to tinidazole is a concern as the two drugs are similar in modes of action (4).

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 1% sodium hypochlorite, and 70% ethanol(17).

PHYSICAL INACTIVATION: Inactivated below pH 5(4). Organisms cannot survive long (several hours) in dry conditions(1).

SURVIVAL OUTSIDE HOST: The organism grows best at 37°C, and specimens in urine should be considered viable for only 30 minutes to avoid false negatives (2 hours if PCR is used)(18). Live T. vaginalis have been found in swimming pool water, in urine, and semen after up to 6 – 24 hours, and up to 30 – 45 minutes when exposed to air(1,19,20). Studies have also shown that T. vaginalis organisms are able to survive through the cryopreservation process of human semen, making infection via artificial insemination possible(11).

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Current laboratory diagnoses include direct microscopic observation, cell culture, immunological techniques, PCR assay, nucleic acid probe test, immunochromatographic capillary-flow dipstick technology, DNA probing and gene amplification, and in situ hybridization(2,9,16).

Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID/TREATMENT: Topical vaginal medications and pessaries (such as clotrimazole, povidone-iodine, nonoxynol-9, and arsenical pessaries) may be prescribed for treatment in women to lessen the effects of symptoms; however, these do not consistently cure disease(4). Topical paromycin has been found to be effective, but side effects can be mild to severe(21). There are no topical medications available for men. Metronidazole can be administered orally or intravenously, with cure rates of 85-95%(1); Metronidazole should not be used by pregnant women in their first trimester as it has been linked to higher prevalence of preterm birth(22).

IMMUNISATION: No vaccinations are currently available. Two vaccines have progressed to the human clinical trials stage in the past 50 years (a heat-killed T. vaginalis vaccine, and SolcoTriovac), although they have not been proven to be effective against T. vaginalis(4).

PROPHYLAXIS: Since many males are asymptomatic and may be carriers, it is important to concurrently treat male partners of infected women to prevent re-infection(4).

SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: None reported to date.

SOURCES/SPECIMENS: Vaginal and urethral secretions, urine, human semen(4,11,18).

PRIMARY HAZARDS: Droplet exposure to mucous membrane, accidental parenteral inoculation and sexual transmission(1,23).

SPECIAL HAZARDS: None.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2(24).

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infected or potentially infected materials, animals, or cultures.

PROTECTIVE CLOTHING: Lab coat. Gloves when direct skin contact with infected materials or animals is unavoidable. Eye protection must be used where there is a known or potential risk of exposure to splashes(25).

SECTION VIII – HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, while wearing protective clothing, cover spill with absorbent paper towel. Apply appropriate disinfectant, and starting from perimeter and wipe towards the center. Allow sufficient contact time with the disinfectant before cleaning up.

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism before disposing by autoclave, chemical disinfection, gamma irradiation, or incineration(25).

STORAGE: Properly labelled and sealed containers.

SECTION IX – REGULATORY AND OTHER INFORMATION

UPDATED: November 2010

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada

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Trichomonas Vaginalis

PATHOGEN SAFETY DATA SHEET – INFECTIOUS SUBSTANCES

SECTION I – INFECTIOUS AGENT

NAME: Trichomonas vaginalis

SYNONYM OR CROSS REFERENCE: Trichomoniasis, vaginitis.

SECTION II – HAZARD IDENTIFICATION

HOST RANGE: Humans(1).

INCUBATION PERIOD: Ranges from 3 – 28 days with an average of 7 days(4,14).

COMMUNICABILITY: Infection can persist for a significant period of time in asymptomatic cases(14), from months to years. SECTION III – DISSEMINATION

RESERVOIR: Humans, typically females, while men may act as a reservoir for infection(4).

ZOONOSIS: None.

VECTORS: None.

SECTION IV – STABILITY AND VIABILITY

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 1% sodium hypochlorite, and 70% ethanol(17).

PHYSICAL INACTIVATION: Inactivated below pH 5(4). Organisms cannot survive long (several hours) in dry conditions(1).

SECTION V – FIRST AID / MEDICAL

Note: All diagnostic methods are not necessarily available in all countries.

PROPHYLAXIS: Since many males are asymptomatic and may be carriers, it is important to concurrently treat male partners of infected women to prevent re-infection(4).

SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: None reported to date.

SOURCES/SPECIMENS: Vaginal and urethral secretions, urine, human semen(4,11,18).

PRIMARY HAZARDS: Droplet exposure to mucous membrane, accidental parenteral inoculation and sexual transmission(1,23).

SPECIAL HAZARDS: None.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2(24).

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infected or potentially infected materials, animals, or cultures.

SECTION VIII – HANDLING AND STORAGE

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism before disposing by autoclave, chemical disinfection, gamma irradiation, or incineration(25).

STORAGE: Properly labelled and sealed containers.

SECTION IX – REGULATORY AND OTHER INFORMATION

UPDATED: November 2010

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada

Trichomonas Vaginalis

PATHOGEN SAFETY DATA SHEET – INFECTIOUS SUBSTANCES

SECTION I – INFECTIOUS AGENT

NAME: Trichomonas vaginalis

SYNONYM OR CROSS REFERENCE: Trichomoniasis, vaginitis.

SECTION II – HAZARD IDENTIFICATION

HOST RANGE: Humans(1).

INCUBATION PERIOD: Ranges from 3 – 28 days with an average of 7 days(4,14).

COMMUNICABILITY: Infection can persist for a significant period of time in asymptomatic cases(14), from months to years. SECTION III – DISSEMINATION

RESERVOIR: Humans, typically females, while men may act as a reservoir for infection(4).

ZOONOSIS: None.

VECTORS: None.

SECTION IV – STABILITY AND VIABILITY

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 1% sodium hypochlorite, and 70% ethanol(17).

PHYSICAL INACTIVATION: Inactivated below pH 5(4). Organisms cannot survive long (several hours) in dry conditions(1).

SECTION V – FIRST AID / MEDICAL

Note: All diagnostic methods are not necessarily available in all countries.

PROPHYLAXIS: Since many males are asymptomatic and may be carriers, it is important to concurrently treat male partners of infected women to prevent re-infection(4).

SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: None reported to date.

SOURCES/SPECIMENS: Vaginal and urethral secretions, urine, human semen(4,11,18).

PRIMARY HAZARDS: Droplet exposure to mucous membrane, accidental parenteral inoculation and sexual transmission(1,23).

SPECIAL HAZARDS: None.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2(24).

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infected or potentially infected materials, animals, or cultures.

SECTION VIII – HANDLING AND STORAGE

DISPOSAL: Decontaminate all wastes that contain or have come in contact with the infectious organism before disposing by autoclave, chemical disinfection, gamma irradiation, or incineration(25).

STORAGE: Properly labelled and sealed containers.

SECTION IX – REGULATORY AND OTHER INFORMATION

UPDATED: November 2010

PREPARED BY: Pathogen Regulation Directorate, Public Health Agency of Canada

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Vibrio Cholerae

Vesicular Stomatitis Virus

Trichomonas Vaginalis

Trichomonas Vaginalis

Trichomonas Vaginalis

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