Treponema pallidum: Infectious substances pathogen safety data sheet

For more information on Treponema pallidum, see the following:

• Syphilis: Symptoms and Treatment
• Syphilis: Key Information and Resources

Section I – Infectious agent

Name

Treponema pallidum

Agent type

Bacteria

Taxonomy

Family

Treponemataceae

Genus

Treponema

Species

pallidum

Synonym or cross-reference

Formerly Spirochaeta pallida, also known as venereal syphilis, pale treponema, non-venereal syphilis, endemic syphilis, bejel, yaws; commonly known as syphilis^{Footnote 1 Footnote 2}.

Characteristics

Brief description

Treponema pallidum is a spiral-shaped, microaerophilic, non-spore-forming, motile bacterium, measuring 6–20 µm in length and 0.1–0.2 µm in diameter^{Footnote 3 Footnote 4}. Due to its double-membrane structure, T. pallidum is often described as a Gram-negative bacterium, but its outer membrane lacks lipopolysaccharides and has a markedly different phospholipid composition than the outer membranes of typical Gram-negative bacteria^{Footnote 4}. As with all spirochetes, T. pallidum consists of a protoplasmic cylinder and cytoplasmic membrane bound by a thin peptidoglycan sacculus and outer membrane. T. pallidum previously comprised three subspecies, namely T. pallidum subsp. pallidum, T. pallidum subsp. endemicum, and T. pallidum subsp. pertenue, all of which were morphologically and antigenically indistinguishable but each caused a distinct disease^{Footnote 4}. However, T. pertenue (formerly T. pallidum subsp. pertenue) is currently considered a distinct species^{Footnote 1}. T. pallidum cannot be grown in pure culture^{Footnote 4}; however, successful long-term cultivation of T. pallidum subsp. pallidum in a tissue culture system was reported in 2018^{Footnote 5}. The genome is composed of a circular chromosome, approximately 1,138 kbp in size, with an overall genome identity greater than 99.7% between T. pallidum subspecies and a G+C base composition of 52.8% for T. pallidum subsp. pallidum^{Footnote 6 Footnote 7}.

Properties

Although T. pallidum expresses abundant lipoproteins, these molecules reside predominantly below the surface^{Footnote 4}. This paucity of surface-exposed pathogen-associated molecular patterns (PAMPs) enables T. pallidum to avoid triggering innate host surveillance mechanisms, facilitating local replication and early dissemination. Its limited surface antigenicity promotes the evasion of adaptive immune responses (i.e., antibody recognition), facilitating persistence. Small amounts of surface-exposed lipoproteins potentially enhance infectivity, including Tp0751, a laminin-binding lipoprotein and zinc-dependent metalloproteinase capable of degrading clots and the extracellular matrix^{Footnote 4}. T. pallidum lacks genes responsible for encoding key enzymes in oxidative phosphorylation and the tricarboxylic acid cycle, and instead uses an optimized conventional glycolytic pathway to generate ATP, resulting in limited metabolic activity and dependence on its host for many nutrients^{Footnote 4 Footnote 8}. Conversely, T. pallidum maintains a complex assortment of ABC transporters and symporters (comprising ∼5% of its genome) to transfer essential molecules from the periplasm to the cytosol^{Footnote 4}. It also expresses several antioxidant enzymes to counteract oxidative stress, as well as repeat proteins (Tpr) which undergo antigenic variation, further contributing to pathogenicity^{Footnote 4 Footnote 9}.

Section II – Hazard identification

Pathogenicity and toxicity

T. pallidum subsp. pallidum causes venereal syphilis, which is generally divided into primary, secondary, latent, and tertiary stages^{Footnote 4}. Patients with primary syphilis present with a localized skin lesion (chancre), or multiple lesions, on the genitals or other body sites involved in sexual contact associated with mild to moderate regional lymphadenopathy approximately 3 weeks after infection^{Footnote 4}. Primary lesions are typically painless and resolve spontaneously. Within 6 to 8 weeks after resolution of primary lesions, untreated individuals develop systemic disease that represents secondary syphilis^{Footnote 10}. However, a large proportion of patients with secondary syphilis (40-85% of women, 20-65% of men) do not report a history of a primary chancre. As with primary syphilis, the acute clinical manifestations of secondary syphilis typically resolve spontaneously, even in the absence of therapy. Occasionally, untreated patients experience episodes of relapsing secondary syphilis, which can occur up to 5 years after infection. Secondary syphilis is associated with a wide variety of signs and symptoms^{Footnote 4}. Systemic symptoms include fever, headache, malaise, sore throat, anorexia, weight loss, and generalized lymphadenopathy^{Footnote 10 Footnote 11}. Rashes are the most characteristic clinical presentation of secondary syphilis, and are classically diffuse and symmetrical, although certain forms may be localized in certain anatomical sites^{Footnote 10}. Macular or papular eruptions are most common and involve the trunk and extremities, including the palms and soles. On occasion, the rash may be pruritic. Other dermatologic findings include pustular or follicular syphilide (syphilitic rash), mucous patches, whitish erosions on the oral mucosa or tongue, raised and grey-white lesions (condylomata lata), and alopecia^{Footnote 10}. Non-resolving severe ulcerative lesions called lues maligna have been reported in HIV patients. Gastrointestinal (parotitis, gastritis, gastric ulceration, hepatitis, hepatomegaly, splenomegaly), musculoskeletal (arthralgia, arthritis, periostitis, bursitis), and renal (glomerulonephritis, nephrotic syndrome) syndromes have also been reported in secondary syphilis^{Footnote 10}. Latent syphilis occurs between resolution of secondary syphilis symptoms and onset of tertiary syphilis, during which patients are asymptomatic^{Footnote 11}.

Approximately 15-40% of untreated patients develop tertiary syphilis with onset of symptoms between 3 and 30 years from primary infection^{Footnote 11}. Symptomatic manifestations include cardiovascular syphilis, which can present as aortitis, angina, aortic regurgitation, coronary artery stenosis or aneurysms, gummatous syphilis, characterized by granulomatous or ulcerative lesions occurring in a variety of organs, or late neurosyphilis^{Footnote 11}. Left untreated, tertiary syphilis is associated with a mortality rate of 8-58%, with a greater case-fatality rate in males.

Neurosyphilis can occur at any time after initial infection; T. pallidum may be frequently identified in the cerebrospinal fluid (CSF) of patients with early disease, although most patients with early syphilis and CSF abnormalities are asymptomatic^{Footnote 4}. Early symptomatic neurosyphilis can manifest as symptomatic syphilitic meningitis, characterized by severe headache, confusion, nausea, vomiting, and neck stiffness. Syphilitic meningitis usually occurs within the first 6 months of infection or at the time of secondary rash. Cranial nerve involvement may lead to sensorineural deafness in up to 20% of patients and ocular abnormalities such as optic neuritis^{Footnote 4}. Late neurosyphilis may present as meningovascular syphilis, characterized by apathy, vertigo, poor attention, seizures, and aphasia, general paresis (progressive dementia mimicking a variety of psychotic syndromes), or tabes dorsalis, which presents as intense pains, paresthesia, papillary changes, and diminished reflexes^{Footnote 4 Footnote 11}. Congenital syphilis can result in abortion, stillbirth, prematurity, or clinical signs that mimic neonatal sepsis, including poor feeding, lethargy, rash, jaundice, hepatosplenomegaly, and anemia^{Footnote 4}.

T. pallidum subsp. endemicum causes endemic syphilis, also known as bejel^{Footnote 12}. As with yaws, bejel is not known to cause congenital infection and mostly occurs in children between 2 and 15 years of age. The primary lesion appears as a small, painless mucous papule or ulcer of the mucous membranes of the oral cavity or nasopharynx but is often not clinically apparent until secondary lesions develop^{Footnote 12}. Secondary disease is characterized by mucous patches on the oral mucosa, tonsils, tongue, lips, and nasopharynx. Split papules at the labial commissures (angular stomatitis, as in yaws patients), non-pruritic skin eruptions, generalized lymphadenopathy, and laryngitis are common manifestations. Secondary skin lesions include condyloma lata in intertriginous body areas; maculopapular or papulosquamous lesions and non-pruritic generalized rash are observed in a minority of patients. As in yaws, secondary bejel may be accompanied by osteitis and periostitis resulting in nocturnal bone pain^{Footnote 12}. Secondary manifestations resolve in 6 to 9 months, and untreated bejel progresses to a latent phase. The tertiary stage may manifest earlier than for yaws (6 months to several years) but is also characterized by gummatous lesions of the skin, mucosa, and bone as well as gangosa^{Footnote 12}. In contrast to venereal syphilis, cardiovascular and neurological manifestations do not occur in tertiary bejel^{Footnote 2 Footnote 12}.

T. pertenue is the causative agent of yaws and causes primary, secondary, and tertiary lesions^{Footnote 12}. The primary lesion (mother yaw) appears at the site of initial infection and is usually a solitary erythematous papule that may develop into a papilloma of 2-5 cm in diameter. The lesion is not painful but may be pruritic, and is often found on the lower extremities but may also occur on the buttocks, arms, hands, or face. Regional lymphadenopathy and arthralgia may also occur. Secondary lesions appear a few weeks to two years after the primary lesion, resulting from dissemination of T. pertenue, and consist of a solitary papillomatous nodule or ulcer resembling the primary lesion or an eruption of multiple smaller excrescences that cover a region of the body^{Footnote 12}. Other secondary manifestations include condyloma lata in moist crevices (e.g., axilla and groin), a measles-like eruption, palmar and plantar hyperkeratotic plaques, fever, and malaise. Periostitis and osteitis may affect the bones of the upper and lower limbs (tibia, fibula, and forearm) and the proximal phalanges of the fingers and toes, resulting in bone pain and digital swelling^{Footnote 12}. If untreated, clinical manifestations spontaneously regress and a stage of latency begins, characterized by absence of physical signs but persistence of serological evidence of infection. Relapse of secondary infection can occur up to 10 years after initial infection. Tertiary yaws occurs in approximately 10% of untreated patients and consists of late lesions that develop after five or more years of infection^{Footnote 12}. This stage is characterized by subcutaneous gummatous nodules, chronic periostitis that can cause apparent bowing of the tibia (saber shin), and destructive processes leading to saddle nose and perforation/collapse of the palate and nasal septum (gangosa). Bilateral hypertrophic periostitis of the perinasal maxilla and nasal bridge causes the clinical manifestation known as goundou. Yaws is not known to cause congenital infection and occurs primarily in children less than 15 years of age (with a peak between 6 and 10 years)^{Footnote 12}.

Epidemiology

T. pallidum subsp. pallidum has a worldwide distribution, with an estimated global incidence of 7.1 million cases in 2020, as reported by the World Health Organization (WHO)^{Footnote 13}. The WHO African region had the highest prevalence rate, followed by the Americas. In 2016, the reported incidence rate of congenital syphilis was 473 cases per 100,000 live births, a 12% decrease since 2012. In Canada, syphilis is the third most reported notifiable sexually transmitted and blood borne infection (STBBI), with over 9,000 cases reported in 2020, corresponding to a rate of 24.7 cases per 100,000 population and a 536% increase in reported cases since 2011^{Footnote 14}. From 2011 to 2020, rates in males were consistently higher than rates in females; however, from 2016 to 2020, rates amongst females increased by 773%, compared to 73% among males. The highest rate in 2020 was observed in individuals aged 25-29 years. Confirmed early congenital syphilis cases increased considerably from previous years, with 50 cases reported in 2020, compared to 4 cases in 2016^{Footnote 14}. Indigenous communities are disproportionally affected by STBBI, including syphilis^{Footnote 15}. Risk factors for venereal syphilis include male sex, age between 25 and 29 years, HIV coinfection, sexually active men who have sex with men (MSM), inconsistent condom use, incarceration, prostitution, and recreational drug use during sexual activity^{Footnote 14}. Predisposing factors for congenital syphilis include poor access to prenatal care, inadequate treatment of syphilis during pregnancy, socioeconomic factors (e.g., homelessness, substance abuse, and incarceration), and children born to mothers with HIV coinfection^{Footnote 16}.

T. pallidum subsp. endemicum is mainly restricted to the arid areas of Sahelian Africa (southern border of the Sahara Desert), including Burkina Faso, Mali, Niger, Mauritania, Côte d'Ivoire, Ghana, Togo, and Benin^{Footnote 12}. In these areas, high rates of seropositivity (12-22% in children under 14 years old) have been reported. Endemic syphilis has also been described among nomadic populations in Saudi Arabia. Four cases were reported in Turkey in 1995, where the disease was considered to be eliminated^{Footnote 12}. One case was reported in Iran in 2013^{Footnote 12}. Predisposing factors for endemic syphilis include age between 2 and 15 years and hot and dry (semiarid/arid) climates^{Footnote 12}.

T. pertenue is endemic mainly in warm, humid equatorial regions of Western/Central Africa, Southeast Asia, and the Pacific Islands^{Footnote 12}. Between 2010 and 2013, 256,343 cases were reported to the WHO from 13 countries known to be endemic for yaws^{Footnote 17}. In 2020, over 87,000 suspected cases of yaws were reported to the WHO from 11 countries, with the majority from Papua New Guinea (over 81,000 reported cases in 2020)^{Footnote 18}. Other countries that reported yaws cases in West Africa and the Pacific Region include Ghana, Cameroon, Cote d'Ivoire, Togo, the Democratic Republic of the Congo, the Solomon Islands, Vanuatu, and Indonesia. Risk factors for yaws include age younger than 15 years, tropical (hot and humid) environments, and living in rural communities with scarce water supply and poor sanitation^{Footnote 12}.

Host range

Natural host(s)

Humans^{Footnote 4 Footnote 12}.

Other host(s)

Mice, rabbits, guinea pigs, rhesus macaques, and nine-banded armadillos have been experimentally infected with T. pallidum subsp. pallidum^{Footnote 19 Footnote 20 Footnote 21 Footnote 22}. T. pertenue antibodies have been detected in wild-caught olive baboons, vervet monkeys, yellow baboons, and blue monkeys^{Footnote 23}.

Infectious dose

The estimated median infectious dose (ID₅₀) for T. pallidum subsp. pallidum is 57 organisms by intradermal injection in humans^{Footnote 24 Footnote 25}.

Incubation period

Primary venereal syphilis has a median incubation period of 21 days (range 3–90 days)^{Footnote 11}. Early congenital syphilis is characterized by onset of clinical signs of disease before two years of age, usually appearing by 3 months of age, most often by 5 weeks^{Footnote 26}. Late congenital syphilis is characterized by onset of clinical manifestations after two years of age. The mean incubation period of early stage yaws is 21 days (range 9–90 days)^{Footnote 12}. The primary stage of endemic syphilis occurs approximately 2 to 4 weeks following exposure^{Footnote 27}.

Communicability

The primary mode of transmission of T. pallidum subsp. pallidum is direct contact with an infectious lesion during sexual activity, which requires exposure to open lesions with organisms present, as seen with the primary chancre and with some manifestations of secondary syphilis (mucous patches and condyloma lata)^{Footnote 11}. Sexual transmission of syphilis occurs during the first 1-2 years after infection (i.e., during primary, secondary, and early latent stages of infection), with an estimated transmission efficiency (a measure of transmission through one sexual exposure) of 30% from an individual with primary syphilis^{Footnote 4 Footnote 28}. Transplacental transmission of T. pallidum subsp. pallidum may occur at any time during gestation but occurs more frequently during later stages of pregnancy, with an overall risk of transmission of 60-80%^{Footnote 29}. The risk of congenital transmission is higher in women with untreated primary or secondary syphilis (60-80%) than in those with latent or tertiary disease (approximately 20%). Congenital syphilis is occasionally transmitted through direct contact with an infectious lesion during birth.

T. pallidum subsp. endemicum is transmitted by direct skin and mucosal contact and by indirect contact via fomites (e.g., shared use of communal eating or drinking utensils)^{Footnote 11}. T. pertenue is transmitted by direct skin contact with an infectious lesion and is facilitated by damaged skin of traumatic or other etiology (e.g., scratches, insect bites, scabies)^{Footnote 11}. Arthropod-mediated transmission (flies) has been suggested without conclusive evidence.

Section III – Dissemination

Reservoir

Humans are the only known natural reservoir of T. pallidum, although African non-human primates (olive baboons, vervet monkeys, yellow baboons, and blue monkeys) may be a potential reservoir^{Footnote 23 Footnote 30}.

Zoonosis

The high prevalence of non-human primate infection in areas of tropical Africa where yaws is common in humans suggests that cross-species infection may occur^{Footnote 30}. However, zoonotic transmission between humans and non-human primates has not been conclusively established.

Vectors

Mechanical transmission of T. pertenue by sucking flies (Hippelates pallipes), suspected to inoculate the pathogen through wounds, has been suggested but has not been definitely demonstrated^{Footnote 12}.

Section IV – Stability and viability

Drug susceptibility/resistance

Susceptible to penicillin, tetracycline, doxycycline, minocycline, ceftriaxone, cefixime, amoxicillin with probenecid, and azithromycin^{Footnote 16}. Azithromycin resistance has been described in T. pallidum subsp. pallidum and T. pertenue^{Footnote 16}. There are a few reports of possible penicillin failure for treatment of T. pertenue infection in Papua New Guinea^{Footnote 31} and Ecuador^{Footnote 32}, although these findings could not be proven microbiologically.

Susceptibility to disinfectants

T. pallidum cells are highly susceptible to disinfection with common alcohols, such as 70% isopropanol^{Footnote 24}. Treatment with 70% ethanol, 10% sodium hypochlorite, or other disinfectants is typically adequate for routine disinfection^{Footnote 33}.

Physical inactivation

T. pallidum cells die readily upon desiccation or exposure to atmospheric levels of oxygen^{Footnote 24}. They are also inactivated by heat treatment at 56°C in 10% rabbit serum for 30 minutes^{Footnote 34} and by dissolution in 65% InterSol platelet additive solution^{Footnote 35}. Laboratory experiments have demonstrated that T. pallidum can be inactivated by photochemical treatment in single-donor platelet concentrates containing 3.0 x 10¹¹ to 6.0 x 10¹¹ platelets suspended in 300 mL of 35% plasma and 65% normal saline, with addition of 150 µmol/L amotosalen HCl and treatment with 3 J/cm² UVA light (320-400 nm) for 3-4 minutes^{Footnote 35}. T. pallidum is also susceptible to UV radiation at 120 J^{Footnote 36}.

Survival outside host

T. pallidum can survive in banked donor blood for 72 to 120 hours^{Footnote 37}. However, treponemes only survive for a few hours in plasma, whole blood, or serum at body or room temperatures^{Footnote 38}. Motile organisms were observed for 8 to 14 days in sealed slides kept at room temperature.

Section V – First aid/medical

Surveillance

Darkfield examinations and molecular tests for detecting T. pallidum infection directly from lesion exudate or tissue are the definitive methods for diagnosis of early syphilis and congenital syphilis^{Footnote 16}. Although no T. pallidum direct-detection molecular nucleic acid amplification tests (NAATs) are commercially available, certain laboratories provide locally developed and validated PCR tests for detecting T. pallidum DNA. A presumptive diagnosis of syphilis requires use of two laboratory serologic tests: a C (i.e., Venereal Disease Research Laboratory (VDRL) or rapid plasma reagin (RPR) test) and a treponemal test (i.e., the T. pallidum passive particle agglutination (TP-PA) assay, various enzyme immunoassays, chemiluminescence immunoassays and immunoblots, or rapid treponemal assays). Use of only one type of serologic test (nontreponemal or treponemal) is insufficient for diagnosis and can result in false-negative results among persons tested during primary syphilis and false-positive results among persons without syphilis or previously treated syphilis. Further testing with CSF evaluation is recommended for individuals with clinical signs of neurosyphilis (e.g., cranial nerve dysfunction, meningitis, stroke, acute or chronic altered mental status, or loss of vibration sense), and can include CSF cell count, protein, or reactive CSF-VDRL^{Footnote 16}.

Note: The specific recommendations for surveillance in the laboratory should come from the medical surveillance program, which is based on a local risk assessment of the pathogens and activities being undertaken, as well as an overarching risk assessment of the biosafety program as a whole. More information on medical surveillance is available in the Canadian Biosafety Handbook.

First aid/treatment

Parenterally delivered penicillin G is the treatment of choice for all stages of syphilis caused by T. pallidum subsp. Pallidum^{Footnote 16}. In patients without neurosyphilis, the appropriate formulation is penicillin G benzathine. In the case of penicillin allergy, alternative antimicrobial agents include tetracyclines (e.g., doxycycline, tetracycline, minocycline) and cephalosporins (e.g., ceftriaxone, cefixime)^{Footnote 16}. In non-pregnant individuals with yaws (T. pertenue infection), treatment with either azithromycin or injectable penicillin G benzathine is favoured^{Footnote 12}.

When serologic tests do not correspond with clinical findings indicative of primary, secondary, or latent syphilis, presumptive treatment is recommended for persons with risk factors for syphilis, and use of other tests (e.g., biopsy for histology and immunostaining and PCR of lesion) should be considered^{Footnote 16}.

Note: The specific recommendations for first aid/treatment in the laboratory should come from the post-exposure response plan, which is developed as part of the medical surveillance program. More information on the post-exposure response plan can be found in the Canadian Biosafety Handbook.

Immunization

No vaccine currently available. Possible vaccine candidates include selected subsets of the Tpr protein family (targeting susceptibility and persistence) and the treponemal adhesin protein Tp0751 (targeting dissemination). Immunization of rabbits with Tp0751 resulted in attenuated lesion development, inhibition of T. pallidum dissemination, and increased cellular infiltration at lesion sites^{Footnote 39}. Experimental induction of immunization using a TprC/TprK/Tp0751 tri-antigen vaccine attenuates chancre development, bacterial load, and inhibits dissemination of T. pallidum in rabbits^{Footnote 40}. However, complete protection against infection was not achieved.

Note: More information on the medical surveillance program can be found in the Canadian Biosafety Handbook, and by consulting the Canadian Immunization Guide.

Prophylaxis

Parenteral penicillin G benzathine is the preferred treatment for post-exposure prophylaxis, including in pregnant women^{Footnote 16}. Although further studies are required to determine the effectiveness of antimicrobial STBBI pre- or post-prophylaxis, small studies on doxycycline pre- and post-prophylaxis in MSM have been associated with a 73% reduction of incident syphilis^{Footnote 16}.

Note: More information on prophylaxis as part of the medical surveillance program can be found in the Canadian Biosafety Handbook.

Section VI – Laboratory hazard

Laboratory-acquired infections

As of 1964, at least 15 cases of laboratory-acquired infection with T. pallidum have been reported^{Footnote 41}. One case occurred in 1964 and involved a finger prick while inoculating a rabbit with a concentrated suspension of T. pallidum obtained from an experimental rabbit orchitis^{Footnote 42}, while another case occurred in 1975 and resulted from splashing of treponemes by a laboratory technician who did not use a self-lock needle and syringe^{Footnote 43 Footnote 44}. Information was not available for other cases.

Note: Please consult the Canadian Biosafety Standard and Canadian Biosafety Handbook for additional details on requirements for reporting exposure incidents.

Sources/specimens

Cutaneous and mucosal lesions and exudates, nasal cavity/nasopharyngeal aspirates, semen, vaginal secretions, blood, lymph node aspirates, amniotic fluid, umbilical cord, cerebrospinal fluid, biopsy tissues, urine, and saliva^{Footnote 16 Footnote 25 Footnote 45 Footnote 46 Footnote 47 Footnote 48}.

Primary hazards

Parenteral inoculation and contact of mucous membranes or broken skin with infectious clinical materials are the primary hazards associated with exposure to T. pallidum^{Footnote 24}.

Special hazards

Work with experimentally infected animals can present a special hazard^{Footnote 24}. Rabbit-adapted T. pallidum, including the Nichols strain and possibly others, retains virulence for humans^{Footnote 24}.

Section VII – Exposure controls/personal protection

Risk group classification

Treponema pallidum is a Risk Group 2 Human Pathogen and Risk Group 1 Animal Pathogen^{Footnote 49}.

Containment requirements

Containment Level 2 facilities, equipment, and operational practices outlined in the Canadian Biosafety Standard for work involving infectious or potentially infectious materials, animals, or cultures.

Protective clothing

The applicable Containment Level 2 requirements for personal protective equipment and clothing outlined in the Canadian Biosafety Standard are to be followed. The personal protective equipment could include the use of a lab coat and dedicated footwear (e.g., boots, shoes) or additional protective footwear (e.g., boot or shoe covers) where floors may be contaminated (e.g., animal cubicles, post mortem rooms), gloves when direct skin contact with infected materials or animals is unavoidable, and eye protection where there is a known or potential risk of exposure to splashes.

Note: A local risk assessment will identify the appropriate hand, foot, head, body, eye/face, and respiratory protection, and the personal protective equipment requirements for the containment zone and work activities must be documented.

Other precautions

A biological safety cabinet (BSC) or other primary containment device to be used for activities with open vessels, based on the risks associated with the inherent characteristics of the regulated material, the potential to produce infectious aerosols or aerosolized toxins, the handling of high concentrations of regulated materials, or the handling of large volumes of regulated materials.

Use of needles and syringes to be strictly limited. Bending, shearing, re-capping, or removing needles from syringes to be avoided, and if necessary, performed only as specified in standard operating procedures (SOPs). Additional precautions are required for work involving animals or large-scale activities.

For diagnostic laboratories handling primary specimens that may contain T. pallidum, the following resources may be consulted:

• Human Diagnostic Activities Biosafety Guideline
• Local Risk Assessment Biosafety Guideline

Section VIII – Handling and storage

Spills

Allow aerosols to settle. While wearing personal protective equipment, gently cover the spill with absorbent paper towel and apply suitable disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up (Canadian Biosafety Handbook).

Disposal

All materials/substances that have come in contact with the regulated materials to be completely decontaminated before they are removed from the containment zone or standard operating procedures (SOPs) to be in place to safely and securely move or transport waste out of the containment zone to a designated decontamination area or third party. This can be achieved by using decontamination technologies and processes that have been demonstrated to be effective against the regulated material, such as chemical disinfectants, autoclaving, irradiation, incineration, an effluent treatment system, or gaseous decontamination (Canadian Biosafety Handbook).

Storage

The applicable Containment Level 2 requirements for storage outlined in the Canadian Biosafety Standard are to be followed. Primary containers of regulated materials removed from the containment zone to be labelled, leakproof, impact resistant, and kept either in locked storage equipment or within an area with limited access.

Section IX – Regulatory and other information

Canadian regulatory information

Controlled activities with Treponema pallidum require a Pathogen and Toxin licence issued by the Public Health Agency of Canada.

The following is a non-exhaustive list of applicable designations, regulations, or legislations:

• Human Pathogens and Toxins Act and Human Pathogens and Toxins Regulations
• Transportation of Dangerous Goods Act and Transportation of Dangerous Goods Regulations
• National notifiable disease (human)

Last file update

March 2023

Prepared by

Centre for Biosecurity, Public Health Agency of Canada.

Disclaimer

The scientific information, opinions, and recommendations contained in this Pathogen Safety Data Sheet have been developed based on or compiled from trusted sources available at the time of publication. Newly discovered hazards are frequent and this information may not be completely up to date. The Government of Canada accepts no responsibility for the accuracy, sufficiency, or reliability or for any loss or injury resulting from the use of the information.

Persons in Canada are responsible for complying with the relevant laws, including regulations, guidelines and standards applicable to the import, transport, and use of pathogens in Canada set by relevant regulatory authorities, including the Public Health Agency of Canada, Health Canada, Canadian Food Inspection Agency, Environment and Climate Change Canada, and Transport Canada. The risk classification and related regulatory requirements referenced in this Pathogen Safety Data Sheet, such as those found in the Canadian Biosafety Standard, may be incomplete and are specific to the Canadian context. Other jurisdictions will have their own requirements.

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