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Trypanosoma cruzi

Kaitlin Black — Mon, 18 Nov 2024 04:17:17 +0000

Pathogen Safety Data Sheets: Infectious Substances – Trypanosoma cruzi

SECTION I – INFECTIOUS AGENT

Name: Trypanosoma cruzi

Agent type: Parasite

Family: Trypanosomatidae

Genus: Trypanosoma

Species: cruzi

Synonym or cross–reference: Chagas disease, American trypanosomiasis.

Characteristics

Trypanosoma cruzi (T. cruzi) is a protozoan parasite. Cellular features include a kinetoplast comprised of 20,000 to 30,000 circular mitochondrial DNA molecules, and the presence of a flagella for 2 of the 3 morphological stages^Footnote1^Footnote2. The epimastigote form is flagellated, measures 20 to 40 μm in length, and has replicative activity^Footnote3. Trypomastigotes have a long slender shape with a shorter flagella, are non-replicating, and measure 12 to 20 μm in length^Footnote1^Footnote3. The amastigote forms are non-mobile, roughly spherical and measure 2 to 6.5 μm in diameter^Footnote3. The genome of T. cruzi is arranged in 41 chromosome pairs^Footnote4. The genome varies in size and structure for different strains, ranging from approximately 45 to 95 mega base pairs (Mbp) in length^Footnote5.

Properties

T. cruzi is the causative agent of Chagas disease. The life cycle of T. cruzi begins when an insect takes a blood meal from an infected host with T. cruzi trypomastigotes circulating in the blood. The trypomastigotes migrate to the insect midgut where they differentiate into epimastigotes and replicate^Footnote2. In the rectum of the insect, T. cruzi differentiates into the infectious metacyclic trypomastigote form that is excreted in insect feces and comes into contact with mucosal tissue or the bloodstream of a vertebrate host^Footnote2. In a newly infected host, the metacyclic trypomastigote invades a host cell and differentiates into the amastigote form^Footnote2^Footnote6; the amastigotes then multiply by binary fission in the cytoplasm. Amastigotes can persist within the host cell as a transient, dormant non-proliferating amastigote form^Footnote7^Footnote8, or differentiate into a trypomastigote, lyse the infected cell, and proceed to infect adjacent cells or migrate through the bloodstream to infect other host tissues^Footnote2. T. cruzi can infect many types of host cells, but have high affinity for cardiac and other muscle tissue (e.g., colon, esophagus)^Footnote9^Footnote10. Genetic exchange through sexual reproduction occurs, but appears to be rare^Footnote11.

Seven discrete typing units of T. cruzi have been defined: TcI-TcVI and TcBat^Footnote12^Footnote13^Footnote14. Chagas disease progression^Footnote15 and virulence varies according to strain^Footnote16.

Section II – Hazard identification

Pathogenicity and toxicity

There are two distinct phases of T. cruzi infection. During the acute phase of illness, approximately 90% of T. cruzi-infected individuals are asymptomatic or have mild symptoms^Footnote9^Footnote17. Clinical signs of illness include fever, anorexia, malaise, headache, generalized or local edema, and enlargement of the liver, spleen, and lymph nodes^Footnote9^Footnote17. Some signs will vary according to the portal of entry^Footnote9. There may be swelling (chagoma) on the skin at the site of the insect bite, or in the case of parasite entry via ocular mucous membranes, signs may include unilateral conjunctivitis and swelling of the eyelid (Romaña sign)^Footnote9. The duration of the acute phase is 1 to 2 months^Footnote17. Approximately 1-5% of symptomatic acute cases are severe with hemorrhagic, jaundice, cardiac, and meningoencephalitis manifestations^Footnote9^Footnote17. Acute illness mortality is less than 5% of symptomatic cases^Footnote9, although infections acquired via oral route have higher mortality (8 to 35%)^Footnote9^Footnote18. The majority of T. cruzi-infected individuals (70%) remain asymptomatic for life with the indeterminate chronic form of Chagas disease^Footnote17. Approximately 20-30% of individuals with the chronic form of Chagas disease will develop cardiomyopathy and/or digestive disease slowly over decades following initial T. cruzi infection^Footnote17^Footnote19.

The clinical manifestation of T. cruzi infection in dogs is similar to disease in humans^Footnote20^Footnote21^Footnote22. Cardiac changes have been observed in other T. cruzi-infected animals, including raccoons and opossums^Footnote23^Footnote24. Severe manifestations have been reported in some species (e.g., horse, red panda) but appear to be infrequent^Footnote25^Footnote26.

Epidemiology

Chagas disease is endemic in Mexico, Central America, and South America, where an estimated 5.7 million people are infected with T. cruzi in these regions^Footnote27. Estimated T. cruzi infection prevalence varies according to the country, from less than 1% of the population in many Latin American countries to 6% of the population in Bolivia^Footnote27. There was a significant decline in Chagas disease prevalence (17.4 million to 7.7 million cases)^Footnote28, deaths (45,000 to 12,000 per year)^Footnote28^Footnote29, and incidence (700,000 to less than 50,000 new cases per year)^Footnote28^Footnote29 from the 1980s to 2005, due in part to widely implemented vector control measures^Footnote27. Outbreaks in Chagas-disease endemic areas due to consumption of contaminated fruits and/or fruit juices are not uncommon^Footnote30^Footnote31^Footnote32.

Global prevalence of T. cruzi infection is 6 to 7 million cases^Footnote6^Footnote27. Chronic Chagas disease is increasingly observed in non-endemic areas including the United States, Canada, Europe, and Western Pacific countries due to migration of individuals from Chagas disease-endemic areas^Footnote33^Footnote34. Locally acquired cases of Chagas disease in the United States are rare (28 cases from 1955 to 2015)^Footnote35.

The genetic polymorphism IL17A rs2275913 has been associated with Chagas disease susceptibility^Footnote36. Immunosuppressed individuals with chronic Chagas disease have a higher risk of disease reactivation^Footnote9^Footnote17^Footnote37^Footnote38.

Host range

Natural host(s): T. cruzi can infect many mammalian species, including humans, non-human primates^Footnote39^Footnote40, armadillos^Footnote6, anteaters^Footnote40, goats^Footnote41, horses^Footnote26, swine^Footnote6, otters^Footnote40, raccoons^Footnote6, skunks^Footnote6, bats, domestic and exotic felids^Footnote40^Footnote42, cervids^Footnote43, canids (e.g., dogs, wolves, fox)^Footnote40, bears^Footnote25^Footnote40, and rodents (e.g., squirrels, wood rats)^Footnote6^Footnote44, as well as marsupials (e.g., opossum)^Footnote6.

Other host(s): None.

Infectious dose: Unknown.

Incubation period

7 to 15 days for vectorborne transmission, 8 to 120 days for transfusion transmission, 3 to 22 days for oral transmission^Footnote9^Footnote17.

Communicability

In Chagas disease-endemic areas, T. cruzi is primarily transmitted via contact with excretions and body fluids of infected triatomine insects^Footnote9. T. cruzi can gain entry through contact with mucous membranes or through broken skin when feces of an infected triatomine is inadvertently rubbed into the bite wound. Transmission can also occur via consumption of food and drink, especially fruits and fruit juices, contaminated with T. cruzi^Footnote17^Footnote45^Footnote46. Modes of T. cruzi transmission also include sexual transmission^Footnote47, congenital transmission (5%)^Footnote48, blood transfusion, and solid organ transplantation^Footnote6^Footnote17. T. cruzi transmission in breastmilk is possible but not efficient^Footnote49. In some animal species, such as dogs, transmission can occur via intentional ingestion of triatomine insects^Footnote22^Footnote50.

Section III – Dissemination

Reservoir

Reservoirs in the sylvatic transmission cycle include rodents (e.g., wood rats)^Footnote44^Footnote51, raccoons^Footnote52, and opossums^Footnote23^Footnote24^Footnote53. In some areas, dogs are a reservoir host in the domestic transmission cycle of T. cruzi^Footnote54^Footnote55.

Zoonosis

Direct transmission between animals and humans has not been documented. Transmission occurs between animals and humans via a triatomine vector.

Vectors

T. cruzi can be transmitted through the feces of triatomine insects of the Reduviidae family. There are 152 species of triatomine insects, some of which have common names, including the kissing bug^Footnote24^Footnote56^Footnote57^Footnote58. Some vector species include Triatoma infestans, Panstrongylus megistus, T. dimidiata, and Rhodnius prolixus^Footnote6. Different species have different transmission efficiencies^Footnote33. Triatomine insects can colonize nests of reservoir hosts and human dwellings. Indoor residual spraying interventions, using pyrethroids (e.g., deltamethrin), have been an effective means of vector control, although resistance has been described in some areas^Footnote59^Footnote60.

Section IV – Stability and viability

Drug susceptibility/resistance

T. cruzi is susceptible to benznidazole and nifurtimox, which are used to treat clinical Chagas disease^Footnote61. Azoles in phase I or II clinical studies include posaconazole, ravuconazole, itraconazole, voriconazole, and albaconazole. Many other compounds have shown antitrypanosomal activity in vitro and/or small animal studies, including amiodarone and fexinidazole^Footnote61^Footnote62. Drug repurposing studies have identified many candidates for the treatment of Chagas disease, such as benidipine, clofazimine, and tamoxifen^Footnote62^Footnote63. Natural compounds from plants have shown activity against T. cruzi and are a promising source for discovery of new drugs^Footnote64.

T. cruzi strains that are highly resistant (e.g., Colombian strain) and partially resistant to benznidazole have been described^Footnote10^Footnote65.

Susceptibility to disinfectants

Unknown for T. cruzi. Sodium hypochlorite (0.05%), TriGene (0.2%), liquid hand soap, and ethanol are effective against other Trypanosoma species^Footnote66.

Physical inactivation

Heat treatment at 70 °C for 10 seconds and 50 °C for 5 minutes effectively eliminated Trypanosoma species^Footnote66^Footnote67. Riboflavin/UV light treatment has been used to inactivate T. cruzi in donated blood products^Footnote68.

Survival outside host

T. cruzi can survive for up to 72 hours on sugar cane and fruits^Footnote69^Footnote70. T. cruzi can survive in juice for up to 144 h at 4 °C and in refrigerated blood for over 18 days^Footnote70^Footnote71.

Section V – First aid/medical

Surveillance

For acute phase disease, T. cruzi trypomastigotes can be observed by microscopy of a blood smear^Footnote17. PCR has been used to detect T. cruzi DNA in blood for the diagnosis of acute phase of the chagas disease^Footnote6^Footnote12^Footnote72. In the chronic phase of Chagas disease, IgG antibodies against T. cruzi can be detected in serum and saliva using ELISA and immunofluorescence assays^Footnote6^Footnote17^Footnote73. Xenodiagnosis has also been used^Footnote74.

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 (CBH).

First aid/treatment

Acute phase illness can be treated successfully with benznidazole or nifurtimox (for 2 to 3 months)^Footnote17^Footnote75^Footnote76. Indeterminate chronic phase Chagas disease treatment can decrease the risk of developing, but not the progression of pre-existing, cardiomyopathy^Footnote10. Cure rates are low when drugs are administered during the chronic phase of disease^Footnote6^Footnote61.

T. cruzi-infected dogs treated with a combination of itraconazole and amiodarone showed clinical improvement and tested negative for T. cruzi DNA in blood^Footnote20^Footnote21.

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 CBH.

Immunization

No vaccine is currently available.

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

Prophylaxis

None.

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

Section VI – Laboratory hazard

Laboratory-acquired infections

Sixty-five T. cruzi laboratory-acquired infections prior to 2001 were documented^Footnote77. The most common route of exposure was parenteral^Footnote77. In 2003, a laboratory technician was infected with T. cruzi following an accidental autoinoculation incident^Footnote78.

Note: Please consult the Canadian Biosafety Standard (CBS) and CBH for additional details on requirements for reporting exposure incidents. A Canadian biosafety guideline describing notification and reporting procedures is also available.

Sources/specimens

Blood, saliva, tissue biopsy, cerebrospinal fluid.

Primary hazards

Primary hazards include autoinoculation with infectious material and exposure of mucous membranes or abraded skin to infectious material^Footnote79. Work with triatomines infected with T. cruzi poses an additional risk to personnel^Footnote79.

Special hazards

None.

Section VII – Exposure controls/personal protection

Risk group classification

T. cruzi is a Risk Group 2 (RG2) Human Pathogen and RG2 Animal Pathogen^Footnote80^Footnote81.

Containment requirements

Containment Level 2 facilities, equipment, and operational practices outlined in the CBS are required 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 CBS to be followed. At minimum, use of a labcoat and closed-toe cleanable shoes, 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 devices 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 with work involving animals or large-scale activities.

Additional information

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

Section VIII – Handling and storage

Spills

Allow aerosols to settle. 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 (CBH).

Disposal

All materials/substances that have come in contact with the regulated materials should 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 / 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 (CBH).

Storage

The applicable Containment Level 2 requirements for storage outlined in the CBS 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 T. cruzi require a Human Pathogens and Toxins Licence, issued by the Public Health Agency of Canada^Footnote80. The following is a non-exhaustive list of applicable designations, regulations, or legislations:

Last file update

2020

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.

This Trypanosoma cruziersinia pseudotuberculosis MSDS / PSDS document, provided by Public Health Agency of Canada (PHAC), is offered here as a FREE public service to visitors of www.EHS.com. As outlined in this site’s Terms of Use, VelocityEHS is not responsible for the accuracy, content or any aspect of the information contained therein.

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Yersinia pseudotuberculosis

Kaitlin Black — Mon, 18 Nov 2024 04:08:39 +0000

Pathogen Safety Data Sheets: Infectious Substances – Yersinia pseudotuberculosis

SECTION I – INFECTIOUS AGENT

NAME: Yersinia pseudotuberculosis

SYNONYM OR CROSS REFERENCE: Yersiniosis, pseudotuberculosis (yersinia).

CHARACTERISTICS: Yersinia pseudotuberculosis is a gram negative, facultatively anaerobic, non spore-forming, coccoid bacillus of the genus Yersinia, of the family Enterobacteriaceae ^{1 2}. It is motile at room temperature but non-motile at 37 ºC ¹. Members of this species usually range from 0.5-0.8 µm by 1-3 µm in size ¹. Of 15 different of serotypes, (8 thermostable groups (I-VIII) with nine subtypes and 5 thermolabile H antigens (a-e)) the O:1 serotype is responsible for 60-70% of human pseudotuberculosis (yersinia) cases ^1–3. The serogroups are determined by the antigens present in the bacterium ².

SECTION II – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Yersinia pseudotuberculosis is a rare cause of acute enteric disease with symptoms such as acute mesenteric lymphadenitis and gastroenteritis associated with abdominal pain and fever (diarrhea is unusual). ^3–5. One to 3 weeks after the acute phase of the disease, post-infectious complications can occur, such as reactive arthritis and erythema nodosum. The arthritic phase of the disease can last up to 6 months ³. Other complications include lesions to lymph nodes, spleen and liver, as well as septicaemia in immunocompromised patients ⁴. The disease is most common in children and young adults and immunocompromised individuals are at greater risk of severe disease or death ¹⁵.

EPIDEMIOLOGY: Worldwide distribution, and most common in younger patients ²³. In an outbreak in Finland due to contaminated lettuce, the median age of patients was 19 years old ⁶. The number of infections peaks in late fall to spring and epidemics have been caused by contaminated food or water ³⁴.

HOST RANGE: The bacterium is found mostly in wild mammals, pigs, cattle, pets and wild birds ¹⁴. Humans are incidental hosts ⁴.

INFECTIOUS DOSE: The infectious dose is of 10⁸ bacteria or more orally ⁵.

MODE OF TRANSMISSION: The disease can be spread from human-to-human or animal-to-human primarily by fecal-oral transmission ⁴. Consumption of contaminated foods (infections by pasteurized milk, chocolate milk, tofu, beans and home slaughtered pork have been reported) and water, as well as contact with infectious soil, can cause an infection ¹³⁴.

INCUBATION PERIOD: The incubation period is 5-10 days although it can be as long as 21 days ³⁵.

COMMUNICABILITY: The disease can be spread from human-to-human and can still be present in stool weeks after the clinical symptoms have ceased ⁷.

SECTION III – DISSEMINATION

RESERVOIR: The reservoir hosts for this disease are rabbits, rodents, cattle, pigs, pets and wild mammals and birds ¹⁴.

ZOONOSIS: The disease can be spread from animals to humans by contact with infected animals and their feces ⁴.

VECTORS: None

SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: Susceptible to ampicillin, third generation cephalosporins, aminoglycosides, tetracyclines, and chlorampheinicol ⁴.

SUSCEPTIBILITY TO DISINFECTANTS: Susceptible to 2-5% phenol, 1% sodium hypochlorite, 70% ethanol, 4% formaldehyde, 2% glutaraldehyde, 2% peracetic acid, 3-6% hydrogen peroxide and 0.16% iodine ⁸⁹.

PHYSICAL INACTIVATION: Bacteria are sensitive to moist heat (121 ºC for at least 12 minutes) and dry heat (170 ºC for 1 hour) ¹⁰.

SURVIVAL OUTSIDE HOST: Yersinia pseudotuberculosis survives up to 15 days in river water and 3-4 days in seawater at 6-8 ºC ¹¹. It can also survive up to 9 months in soil ¹².

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Diagnosis can be confirmed by serology, culture of samples from blood, tissue or lymph nodes, ELISA, immunohistochemical staining, and PCR ¹³.

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

FIRST AID/TREATMENT: In some cases, antibiotics may be needed although infections by this bacterium are usually self limiting ¹³.

IMMUNIZATION: None

PROPHYLAXIS: None

SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: None have been reported to date.

SOURCES/SPECIMENS: The bacterium can be found in stool, blood or lymph node tissues ¹.

PRIMARY HAZARDS: Accidental parenteral inoculation is always a risk when working with pathogens and ingestion of the infectious agent (via contaminated hands) is a hazard for laboratory personnel working with enteric pathogens ⁵.

SPECIAL HAZARDS: Contact with infected animals ⁴.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk group 2 ¹⁴.

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures ¹⁵¹⁶.

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 ¹⁵.

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 ¹⁵.

SECTION VIII – HANDLING AND STORAGE

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

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

STORAGE: The infectious agent should be stored in leak-proof containers that are appropriately labelled.

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: December 2011

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.

This Yersinia pseudotuberculosis MSDS / PSDS document, provided by Public Health Agency of Canada (PHAC), is offered here as a FREE public service to visitors of www.EHS.com. As outlined in this site’s Terms of Use, VelocityEHS is not responsible for the accuracy, content or any aspect of the information contained therein.

Need an SDS? Search our entire SDS database containing millions of documents.

The post Yersinia pseudotuberculosis appeared first on VelocityEHS.

Zika virus

Kaitlin Black — Mon, 18 Nov 2024 04:05:38 +0000

Pathogen Safety Data Sheets: Infectious Substances – Zika virus

SECTION I – INFECTIOUS AGENT

Name: Zika virus

Agent type: Virus

Family: Flaviviridae

Genus: Flavivirus

Species: Zika virus

Synonym or cross-reference

Abbreviated to ZIKV¹. Zika virus is one of several arthropod-borne viruses, which are commonly referred to as “arboviruses”². Disease associated with Zika virus infection is often termed “Zika fever”³.

Characteristics

Zika virus is a positive-sense, single-stranded RNA arbovirus belonging to the genus Flavivirus and family Flaviviridae, which include other notable human pathogens such as West Nile virus, Dengue virus, Tick-borne encephalitis virus and Yellow fever virus³. Based on non-structural protein 5 gene homology, three main Zika virus lineages have been identified: Asian, East African and West African⁴⁵. The genome is approximately 11 kilobases in length and encodes one large polyprotein that is processed by viral and host proteases into three structural and seven non-structural proteins¹. Virions are spherical, enveloped, and 40-60 nm in diameter⁶.

Properties

Zika virus is maintained in transmission cycles involving humans, non-human primates, and mosquitoes⁷.

Section II – Hazard identification

Pathogenicity and toxicity

Approximately 80% of Zika virus infections are asymptomatic or subclinical, suggesting many cases likely go unreported³⁸. Symptomatic cases typically manifest as a mild, nonspecific and self-limiting febrile illness lasting up to 7 days; severe disease is uncommon³⁸. Common clinical symptoms include maculopapular rash, fever, fatigue, arthralgia, myalgia, headache and conjunctivitis³⁸. Less frequent symptoms include sore throat, dry cough, anorexia, nausea, vomiting, loose stool, dizziness, retro-orbital pain, retinal abnormalities and hypertensive iridocyclitis⁸.

Though rare, neurological complications such as Guillain–Barré syndrome, myelitis and meningoencephalitis may develop approximately 5 to 10 days after acute disease onset⁹¹⁰. Other complications that may occur include potential impacts on male fertility and cardiovascular diseases such as myocarditis, heart failure and arrhythmia¹¹¹². In adults, Zika virus infection is associated with an extremely low case fatality rate, with the majority of deaths occurring in older patients with pre-existing conditions¹³.

Vertical (i.e., mother-to-fetus) transmission of Zika virus may occur during all trimesters of pregnancy¹⁰. Zika virus infection during pregnancy is associated with an increased risk of preterm birth, fetal death, still birth, and congenital Zika syndrome¹. Congenital Zika syndrome is characterized by microcephaly, abnormal brain development, limb contractures, eye abnormalities, brain calcifications and other neurological complications. Estimates of neonatal mortality in the first week of life range from 4 to 7% among infants with congenital Zika syndrome¹⁰. Despite lacking clinical or radiological signs of congenital Zika syndrome, children born to Zika virus-infected mothers may later experience seizures, hearing loss, visual impairment, dysphagia and developmental deficits¹⁰.

Mammals infected with Zika virus display few, if any, clinical signs¹⁴. A sentinel rhesus monkey infected with Zika virus showed only mild pyrexia but this was not conclusively attributed to the virus¹⁵. There are no reports of disease clearly associated with Zika virus in other natural animal hosts in which neutralizing antibodies against the virus have been detected. Experimentally inoculated monkeys develop viremia and show signs of lethargy, decreased motility, rash, fever, lymphadenopathy and conjunctivitis¹⁶¹⁷. Inoculation of pregnant non-human primates with Zika virus results in vertical transmission and signs of congenital Zika syndrome in the fetus¹⁸.

Epidemiology

Zika virus was first isolated in 1947 from a sentinel rhesus monkey in the Zika forest of Uganda, and was also isolated from mosquitoes collected in this region shortly thereafter¹⁵. The first well-documented report of human Zika virus infection occurred in 1964¹⁹. From 1947 to 2007, only 14 sporadic cases of human infection with Zika virus were reported⁵²⁰. The first Zika virus outbreak occurred on Yap Island, Polynesia in 2007, comprising 49 confirmed and 59 probable cases of infection²⁰. Serological testing of the general population of Yap Island estimated that 5005 of the 6892 (73%) residents aged 3 years or older were infected²⁰. A second outbreak involving 30,000-32,000 symptomatic cases (11.5% of the population) occurred in French Polynesia in 2013-2014, and seroprevalence following the outbreak was 49% in the general population²¹. Evidence of current or past Zika virus transmission has been reported in Africa, Asia, the Pacific Islands, and the Americas¹⁹. Zika virus spread to the Americas in March 2015, where it was first identified in Brazil¹⁹. It is estimated that 440,000-1,300,300 cases of Zika virus infection occurred in 2015 in Brazil²².

Zika virus viremia has been reported in non-human primates in Africa and South America¹⁴¹⁶²³, and serological studies suggest several animal species in Africa, Asia and the Americas may be susceptible to Zika virus infection¹⁴.

Factors influencing the likelihood and severity of symptoms and sequelae associated with Zika virus infection remain unclear¹. Zika virus infection during pregnancy is known to cause fetal complications, such as microcephaly, central nervous system abnormalities and fetal death¹¹⁰. A patient with immunosuppression showed prolonged persistence of Zika virus RNA in semen, which was detectable for more than 900 days following symptom onset²⁴. In adults, death associated with Zika virus infection is rare and primarily occurs in older patients with pre-existing comorbidities¹³.

Host range

Natural host(s): Humans and non-human primates are considered to be the primary vertebrate hosts of Zika virus⁷. Serological evidence of infection has been reported for sheep, goats, horses, cattle, carabao, ducks, bats, pigs, buffalo, elephants, rodents, hippos, impala, kongoni, lions, wildebeest and zebras; however, serological studies should be interpreted with caution as cross-reactivity with other flaviviruses may occur¹⁴²⁵.

Other host(s): Following experimental inoculation with Zika virus, viremia was detected in frogs, armadillos, neonatal pigs, mice, bats and non-human primates, and seroconversion was observed in goats, rabbits, ducks, frogs, and pigs¹⁴²⁶²⁷²⁸.

Infectious dose

The infectious dose for Zika virus in humans is unknown. In Aedes aegypti mosquitoes, the 50% infectious dose (ID⁵⁰) was 6.1-7.5 log₁₀ plaque-forming units (PFU)/mL, with a minimum infectious dose of 4.2 log₁₀ PFU/mL²⁹. In rhesus monkeys, intramuscular injection of 1 x 10³ PFU resulted in viremia³⁰³¹. Infection of macaques was also achieved through intravaginal or intrarectal inoculation with 7.0 log₁₀ PFU³². In guinea pigs, the median infectious subcutaneous dose was 10^3.5 PFU³³.

Incubation period

3 to 14 days post-exposure²¹¹.

Communicability

Zika virus transmission primarily occurs through the bite of an infected mosquito vector¹¹. In Africa, Zika virus is maintained in a sylvatic transmission cycle between non-human primates and Aedes mosquitoes⁷. Human-to-human transmission in urban and peri-urban settings largely occurs through Aedes mosquito vectors⁸¹¹.

Vertical transmission in utero from mother to fetus can occur during pregnancy²¹¹. Sexual transmission is suspected, as evidenced by the report of a traveller who infected his partner after returning from an endemic region²³¹¹. Transmission through blood transfusion has been documented¹¹. Transmission through breastfeeding may also occur as the virus has been detected in breast milk, but this has not been confirmed¹¹³⁴. Zika virus is detected in the saliva of infected individuals; however, the role of saliva in human-to-human transmission remains unclear²⁸¹¹. A case of Zika virus infection was reported in an individual who was bitten by a monkey, although mosquito-borne transmission was also possible³⁵. Laboratory-acquired infection was reported in a graduate student who was bitten by a Zika virus-infected mouse³⁶.

Section III – Dissemination

Reservoir

Humans and non-human primates³⁷.

Zoonosis

Zika virus is maintained in transmission cycles involving humans, non-human primates, and mosquitoes⁷³⁷. A case of Zika virus infection was reported in an individual who was bitten by a monkey, although mosquito-borne transmission was also possible³⁵, and a laboratory-acquired infection was reported in a graduate student who was bitten by a Zika virus-infected mouse³⁶.

Vectors

Aedes mosquitoes, primarily A. aegypti⁷¹¹³⁸. Other vectors include A. africanus, A. albopictus, A. hensilii, A. polynesiensis³⁸. Zika virus has also been isolated from Aedes opok, A. apicoargenteus, A. vittatus, and A. furcifer³⁸.

Section IV – Stability and viability

Drug susceptibility/resistance

Currently, there are no approved drugs to treat Zika virus infection, although antivirals such as nucleoside analogs are being evaluated for potential anti-Zika virus activity³⁹⁴⁰. Arbidol (also known as umifenovir) showed dose-dependent inhibition of Zika virus in vitro⁴¹. The antimicrobial peptides GF-17 and BMAP-18 showed strong in vitro efficacy against Zika virus⁴².

Susceptibility to disinfectants

Zika virus stocks are inactivated by 70% isopropanol, 70% ethanol, 70% incidin, 70% DMSO/E, 1% hypochlorite, 2% paraformaldehyde, or 2% gluteraldehyde following a 1-minute incubation period⁴³. Dried virus was also inactivated by 5 minutes exposure to the aforementioned disinfectants⁴³.

Physical inactivation

Complete inactivation of Zika virus in 2.5% fetal calf serum (FCS) occurred following 10 minute exposure to UV radiation; however, longer exposure is required in the presence of higher concentrations of FCS⁴³. Exposure to temperatures greater than or equal to 60°C for 5 minutes inactivated the virus⁴³. Zika virus in cell culture medium was inactivated after 5 minutes at 56°C in the absence of serum⁴⁴. Zika virus was also inactivated by 10 minute incubation at pH less than or equal to 4 or greater than 11⁴³.

Survival outside host

Zika virus remains infectious up to 84 hours after drying on a cell culture plate⁴³ but persists less than 3 days in human breast milk⁴⁵.

Section V – First aid/medical

Surveillance

Clinical diagnosis of Zika virus infection is difficult as symptoms often resemble other flavivirus infections²⁴⁶. During the symptomatic phase (i.e., within 7 days of symptom onset), molecular testing using reverse transcription polymerase chain reaction (RT-PCR) on whole blood or serum is the diagnostic method of choice²¹¹⁴⁶⁴⁷. Zika virus RNA is also detectable for more than 10 days in urine¹¹. Serological methods such as enzyme immunoassays, immunofluorescence assays, and neutralization assays are typically used at 7 or more days post-symptom onset; although these methods are limited by potential cross-reactivity with other flaviviruses²¹¹. Infection can also be diagnosed through viral culture⁴⁷.

First aid/treatment

To date, there are no specific therapeutics for the treatment of Zika virus infection³⁹⁴⁰⁴⁶. Treatment is supportive and includes antipyretics, hydration and rest³⁹⁴⁶.

Immunization

There is no approved vaccine currently available; however, dozens of candidate vaccines are currently under development, some of which have entered clinical trials³⁹.

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

Prophylaxis

None.

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

Section VI – Laboratory hazard

Laboratory-acquired infections

A case of a laboratory-acquired Zika virus infection was reported in 1973 and involved an individual working in an arboviral laboratory in Uganda; the route of exposure was unknown⁴⁸⁴⁹. Laboratory-acquired infection was reported in a graduate student in Brazil who was bitten by a Zika virus-infected mouse³⁶. Global laboratory surveys conducted in 1976 and 1978 documented three cases of laboratory-acquired Zika virus disease; the suspected sources of exposure were aerosols or unknown⁴⁹. Four cases of laboratory-associated Zika virus disease were reported in the United States between 2016-2019⁴⁹. Two of these cases were associated with needlestick injury, and the route of exposure was unknown for the other two cases. Death or serious sequelae resulting from laboratory-acquired Zika virus infection has not been reported to date³⁶⁴⁸⁴⁹.

Sources/specimens

Zika virus can be detected in amniotic fluid, brain tissue, placenta, vaginal secretions, tears, breast milk, semen, testes, blood and serum, saliva, urine¹¹.

Primary hazards

Contact with infectious material³⁶⁴⁹. Needlestick injury and aerosols pose a significant risk of infection⁴⁹.

Special hazards

Handling of Zika virus-infected animals poses a risk of infection³⁶.

Section VII – Exposure controls/personal protection

Risk group classification

Zika virus is a Risk Group 2 human pathogen and a Risk Group 2 animal pathogen, and is listed on Schedule 2 of the Human Pathogens and Toxins Act.

Containment requirements

Containment Level 2 facilities, equipment, and operational practices outlined in the CBS and in the Biosafety advisory for Zika virus for work involving infectious or potentially infectious materials, animals, or cultures.

Learn more about:

Biosafety advisory for Zika virus

Protective clothing

The applicable Containment Level 2 requirements for personal protective equipment and clothing outlined in the CBS to be followed. At minimum, it is recommended to use a labcoat and closed-toes cleanable shoes, gloves when direct skin contact with infected materials or animals is unavoidable.

Other precautions

Use of needles and syringes are 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 with work involving animals or large-scale activities.

For diagnostic laboratories handling primary specimens that may contain Zika virus, the following resources may be consulted:

Section VIII – Handling and storage

Spills

Disposal

Storage

Section IX – Regulatory and other information

Canadian regulatory information

Controlled activities with Zika virus require a Human Pathogens and Toxins licence issued by the Public Health Agency of Canada⁵⁰. Zika virus is a non-indigenous animal pathogen in Canada; therefore, importation of Zika virus requires an import permit, issued by the Canadian Food Inspection Agency. The following is a non-exhaustive list of applicable designations, regulations, or legislations:

Last file update

September, 2021

Prepared by

Centre for Biosecurity, Public Health Agency of Canada.

Disclaimer

This Zika virus MSDS / PSDS document, provided by Public Health Agency of Canada (PHAC), is offered here as a FREE public service to visitors of www.EHS.com. As outlined in this site’s Terms of Use, VelocityEHS is not responsible for the accuracy, content or any aspect of the information contained therein.

Need an SDS? Search our entire SDS database containing millions of documents.

The post Zika virus appeared first on VelocityEHS.

Alkhumra virus

Kaitlin Black — Fri, 15 Nov 2024 04:41:04 +0000

Pathogen Safety Data Sheets: Infectious Substances – Alkhumra virus

SECTION I – INFECTIOUS AGENT

Name: Alkhumra virus

Agent type: Virus

Family: Flaviviridae

Genus: Flavivirus

Species: Kyasanur Forest disease virus

Subspecies/strain/clonal isolate: Alkhumra virus

Synonym or cross–reference: Alkhumra virus (ALKV), Alkhumra hemorrhagic fever virus ¹², Alkhurma’ virus ³⁴.

Characteristics

ALKV is closely related to Kyasanur Forest disease virus ¹². ALKV is a single-stranded, positive-sense RNA virus. Its genome is approximately 10.5 kb in length ¹. ALKV has icosahedral symmetry, is surrounded by a lipid envelope, and measures approximately 40 nm in diameter ⁵.

Section II – Hazard identification

Pathogenicity and toxicity

ALKV is the causative agent of Alkhumra hemorrhagic fever⁶⁷. ALKV infections can be subclinical in some individuals⁸. Symptomatic individuals may experience influenza-like symptoms including fever (96-100%), malaise (59-86%), anorexia (62%), or nausea (60%)⁹¹⁰. Hemorrhagic manifestations have been reported in 26-55% of patients⁹. Neurological manifestations are less common and include confusion (3-25%), hallucination (4.3%), neck rigidity (1-9%), and convulsion (2-5%)⁹¹¹. Disease is biphasic in 3% of symptomatic cases⁷. In these cases, the initial fever persists for 9 to 10 days, followed by a symptom-free period for 2 to 3 days, and a second febrile period for 2 days⁷. Complications including encephalitis have been reported in 12-20% of cases⁷⁹. Overall case fatality rate is approximately 1%⁷, while one outbreak had a mortality rate of 25%⁶.

Epidemiology

ALKV is endemic in Saudi Arabia, since being discovered in 1995, with outbreaks occurring sporadically⁷¹⁰¹². Since 2009, approximately 38-93 new cases of Alkhumra hemorrhagic fever are reported in Saudi Arabia every year¹⁰¹¹. Recently travel-related cases, and cases in the surrounding geographic areas have become more prevalent¹¹³.

Predisposing factors include individuals who handle, or work closely with, raw meat or blood from infected animals. This includes abattoir workers, butchers, and shepherds¹²¹⁴.

Host range

Natural host(s): Humans, sheep¹⁵, camels¹, goats¹¹.

Other host(s): Mice have been experimentally infected with ALKV¹⁶.

Infectious dose: Unknown.

Incubation period: Approximately 3 to 8 days⁶.

Communicability

No evidence of human-to-human transmission. ALKV can be transmitted via bites from infected ticks and direct contact with blood or raw meat from infected animals⁷¹²¹⁵. Although other flaviviruses can be transmitted to humans via consumption of raw milk products¹⁷¹⁸, there is currently insufficient evidence to support this transmission pathway for ALKV⁸¹⁹.

Section III – Dissemination

Reservoir

Potential reservoirs include goats, sheep, and camels²⁰.

Zoonosis

ALKV can be transmitted to humans from infected livestock via direct contact with blood or raw meat from infected animals¹²¹⁵.

Vectors

ALKV is transmitted to mammalian hosts via tick bites. ALKV has been found in soft tick Ornithodoros savignyi²¹, and hard ticks Hyalomma dromedarii and Amblyomma lepidum¹⁹²².

Section IV – Stability and viability

Drug susceptibility/resistance

An adenosine analog (NITD008), 6-Azauridine, 2′-C-methylcytidine, and interferon alpha 2a inhibited ALKV replication in vitro²³²⁴. Perylenyltriazoles, an aglycon analogue of the antibiotic teicoplanin (LCTA-949), and Arbidol (Umifenovir), a broad-spectrum antiviral drug approved in China and Russia for influenza treatment, showed antiviral activity against other flaviviruses in vitro²⁵²⁶²⁷.

Susceptibility to disinfectants

Ethanol (70%) effectively inactivates ALKV¹. Other members of the Flavivirus genus are inactivated by iodine-based disinfectants (1%), hypochlorite (1%), paraformaldehyde, and glutaraldehyde (2%)²⁸²⁹.

Physical inactivation

ALKV is inactivated by heat treatment at 60 °C for 3 minutes and 56 °C for 30 minutes³⁰. Flaviviruses can be inactivated by UV radiation and extreme pH, (pH ≥ 9)²⁸²⁹.

Survival outside host

No literature currently provides information on survival of ALKV outside host. Other tick-borne flaviviruses are stable in milk for 72 hours at refrigeration temperature but are not detectable after 48 hours at room temperature³¹.

Section V – First aid/medical

Surveillance

Diagnosis is accomplished through the monitoring of clinical symptoms. ALKV can be detected in blood using reverse transcriptase PCR⁸³². ELISA can be used to detect ALKV antibodies in blood, but cross-reaction with other flaviviruses (e.g., dengue, yellow fever, West Nile) can be problematic⁸¹⁴.

First aid/treatment

There is no available antiviral treatment for Alkhumra hemorrhagic fever; treatment includes supportive care to manage symptoms¹⁴²⁸.

Immunization

No vaccine is currently available.

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

Prophylaxis

None.

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

Section VI – Laboratory hazard

Laboratory-acquired infections

None have been reported to date.

Sources/specimens

Blood/serum and biopsy specimens can be sources of ALKV.

Primary hazards

Exposure of mucous membranes or wounded skin to infectious material, and bites/scratches of an infected animal are the primary hazards associated with ALKV exposure.

Special hazards

None.

Section VII – Exposure controls/personal protection

Risk group classification

Alkhumra virus is a Risk Group (RG) 4 human pathogen and a RG 4 animal pathogen³³³⁴.

Containment requirements

Containment Level 4 facilities, equipment, and operational practices outlined in the CBS for work involving infectious or potentially infectious materials, animals, or cultures.

Protective clothing

The applicable Containment Level 4 requirements for personal protective equipment and clothing outlined in the CBS to be followed. The use of a positive-pressure suit or use of a Class III biological safety cabinet (BSC) line is required for all work with RG4 pathogens.

Other precautions

All activities involving open vessels of infectious material are to be performed in a certified biological safety cabinet (BSC) or other appropriate primary containment device. Centrifugation of infected materials must be carried out in closed containers placed in sealed safety cups, or in rotors that are unloaded in a biological safety cabinet. The integrity of positive pressure suits must be routinely checked for leaks. The use of needles, syringes, and other sharp objects to be strictly limited. Open wounds, cuts, scratches, and grazes are to be covered with waterproof dressings. Additional precautions must be considered with work involving animal activities.

Section VIII – Handling and storage

Spills

The spill area to be evacuated and secured. Aerosols must be allowed to settle for a minimum of 30 minutes. Spills of potentially contaminated material to be covered with absorbent paper-based material (e.g., paper towels), liberally covered with an effective disinfectant (e.g., 1% sodium hypochlorite), and left to soak for an appropriate amount of time (e.g., 10 minutes) before being wiped up. Following the removal of the initial material, the disinfection process is to be repeated. Individuals performing this task must wear PPE, including particulate respirators (e.g., N95 or higher). Disposable gloves, impermeable gowns and protective eye wear are to be removed immediately after completion of the process, placed in an autoclave bag, and decontaminated prior to disposal (CBH).

Disposal

All materials/substances that have come in contact with the infectious agent must be completely decontaminated before they are removed from the containment zone. This can be achieved by using decontamination technologies and processes that have been demonstrated to be effective against the infectious material, such as chemical disinfectants, autoclaving, irradiation, incineration, an effluent treatment system, or gaseous decontamination (CBH).

Storage

The applicable Containment Level 4 requirements for storage outlined in the CBS are to be followed. Pathogens, toxins, and other regulated materials to be stored inside the containment zone.
Inventory of Risk Group 4 (RG4) pathogens in long-term storage to be maintained and to include:

specific identification of the pathogens, toxins, and other regulated materials; and
a means to allow for the detection of a missing or stolen sample in a timely manner.

Section IX – Regulatory and other information

Canadian regulatory information

Controlled activities with ALKV require a Human Pathogens and Toxins Licence, issued by the Public Health Agency of Canada. ALKV is a non-indigenous animal pathogen in Canada; therefore, importation of ALKV requires an import permit, issued by the Canadian Food Inspection Agency.

The following is a non-exhaustive list of applicable designations, regulation, or legislation:

Last file update: October, 2019

Prepared by: Centre for Biosecurity, Public Health Agency of Canada.

Disclaimer

This Alkhumra virus MSDS / PSDS document, provided by Public Health Agency of Canada (PHAC), is offered here as a FREE public service to visitors of www.EHS.com. As outlined in this site’s Terms of Use, VelocityEHS is not responsible for the accuracy, content or any aspect of the information contained therein.

Need an SDS? Search our entire SDS database containing millions of documents.

The post Alkhumra virus appeared first on VelocityEHS.

Acanthamoeba castellanii

Kaitlin Black — Fri, 15 Nov 2024 04:34:28 +0000

Pathogen Safety Data Sheets: Infectious Substances – Acanthamoeba castellanii

SECTION I – INFECTIOUS AGENT

Name: Acanthamoeba castellanii

Agent type: Parasite

Family: Acanthamoebidae

Genus: Acanthamoeba

Species: castellanii

Synonym or cross-reference

Also known as Acanthamoeba castellani and Acanthamoeba sp. ATCC 30011¹. Acanthamoeba castellanii is a causative agent of Acanthamoeba keratitis and granulomatous amoebic encephalitis.

Characteristics

A. castellanii is a free-living amoeba². The reference genome sequence for castellanii, NEFF-v1, is based on the Neff strain and contains a linear double-stranded DNA genome of approximately 42 Mbp with a G+C content of 58%². Morphological characteristics vary depending on environmental conditions³⁴. A. castellanii can adopt an oval-shaped or elongated infective trophozoite form, measuring approximately 15 to 50 μm, or a dormant, stress-resistant, double-walled cyst form measuring 10 to 25 μm³⁴.

Properties

Acanthamoeba species are ubiquitous in the environment and have been isolated from numerous aqueous-associated sources (e.g., public water supplies, swimming pools, bottled water, surface water samples), air-conditioning units, sewage, compost, sediments, soil, vegetables, air, and contact lenses and their cases³⁵. They have also been recovered from hospitals, dialysis units, and eye wash stations⁵. Its biphasic life cycle allows for this prevalent distribution in the environment³⁵.

The vegetative trophozoite form exists when environmental conditions are favourable for growth; in this form, A. castellanii moves slowly using acanthopodia (spine-like hyaline protrusions) and feeds on other microbes, including bacteria, algae, yeasts, or small organic particles³⁵. Under adverse environmental conditions, such as extreme temperatures, pH, osmolarity, nutrient depletion, and desiccation, A. castellanii can differentiate into a metabolically inactive cyst. Its double-walled structure enables A. castellanii to survive under hostile conditions for prolonged periods³. Cysts are airborne, which may help spread the species into the environment. A. castellanii reproduces asexually by binary fission³⁵.

Some bacteria and viruses ingested by trophozoites are able to evade digestion. For example, Mollivirus⁶, adenovirus⁷, Lausannevirus⁸, murine norovirus⁹, and Medusavirus¹⁰ can replicate within trophozoites. Bacteria including Legionella pneumophila¹¹¹², Protochlamydia amoebophila¹³, Porphromonas gingivalis, Prevotella intermedia¹⁴, Bacillus anthracis¹⁵, Vibrio cholerae¹⁶, and Mycobacterium spp.¹⁷¹⁸ are able to survive and grow within A. castellanii trophozoites. Depending on conditions and pathogenicity of the microorganisms and the amoebae, the interactions vary leading to lysis of the microorganisms or amoebae, intake of microorganisms without any changes, incubation and growth of the microorganisms within the amoebae, or increase in virulence of the microorganisms¹⁹. Thus, both trophozoites and cysts may serve as reservoirs for a number of pathogenic microorganisms, leading to co-infection¹⁹.

Section II – Hazard identification

Pathogenicity and toxicity

Several Acanthamoeba species, including A. castellanii, have been reported to cause Acanthamoeba keratitis (AK)⁵²⁰. Onset of symptoms may range from a few days to several weeks, depending on the inoculum size and/or the extent of corneal trauma, and clinical signs include foreign body sensation in the eye, redness, itching, pain, photophobia, epiphora, edema, and blurred vision or loss of vision⁵²¹²². A ring-like stromal infiltrate appears in approximately 50% of patients in the advanced stage of Acanthamoeba keratitis³. Usually only one eye is affected²³²⁴. Acanthamoeba sclerokeratitis (ASK) is an uncommon complication of AK and presumably has an immune-mediated origin³. ASK is estimated to occur in 14–16% of AK cases and is characterized by severely reduced vision and severe pain, which may lead to necrotizing scleritis and corneal perforation²⁵. The prognosis of ASK is generally poor and occasionally requires enucleation to alleviate severe ocular pain²⁵. A. castellanii cysts may resist drug treatment and persist within the host for prolonged periods. Recurrent infection occurs in approximately 10% of cases²⁶, and has been reported up to 5 years after initial infection²⁷. Early diagnosis and treatment are necessary to prevent permanent ocular damage and vision loss⁵²⁸.

A. castellanii can also cause granulomatous amoebic encephalitis (GAE), particularly in immunocompromised or otherwise debilitated individuals⁴⁵. Onset of GAE is slow and follows a chronic course characterized by several weeks to months of headache, low-grade fever, stiff neck, mental state abnormalities, nausea, vomiting, lethargy, visual disturbances, and focal neurologic deficits, depending on the topographic site of lesions, followed by loss of consciousness, hemiparesis, seizures, and coma in later stages⁵²⁹. Although rare, GAE has been reported in otherwise healthy individuals. For example, an otherwise healthy Taiwanese farmer presented with general weakness and difficulty of defecation and urination two weeks after aspiration of muddy water, and subsequently developed nausea, vomiting, severe headache, and gradual altered consciousness and emotional agitation during hospitalization³⁰. Despite antibiotic treatment, he developed hypotension, bradycardia, and myoclonus. The patient recovered following antimicrobial, corticosteroid, and diuretic therapy, although slow response to time, place, and person orientation was noted. The mortality rate of Acanthamoeba central nervous system (CNS) infection may exceed 90%³¹.

Cutaneous manifestations of A. castellanii are characterized by hard erythematous nodules and/or skin ulcerations, including the presence of firm papulonodules with purulent drainage which develop into non-healing indurated ulcerations, and demonstrate Acanthamoeba trophozoites and cysts⁵²⁰. In otherwise healthy individuals, these infections are very rare and are typically self-limiting. However, in immunocompromised individuals, disseminated infection may follow, leading to fatal outcomes⁵. The reported mortality rate for Acanthamoeba cutaneous infection without CNS involvement is approximately 73% in AIDS patients, while that for cutaneous infection with concomitant CNS infection is 100%²⁰.

A rare cause of osteomyelitis of a bone graft of the mandible associated with A. castellanii infection was reported in a 32-year-old prediabetic woman³². A. castellanii sinusitis was reported in an HIV-infected patient and was characterized by sinus congestion, epistaxis, nasal crusting, and frontal headache³³. Acanthamoeba spp. also appear to be a vector in transmission of bacterial pathogens to susceptible hosts; approximately 24% of Acanthamoeba spp. isolates from clinical and environmental sources appear to carry intracellular bacteria³⁴.

A case of acute, hemorrhagic, necrotizing meningoencephalitis was reported in a dog; A. castellanii was isolated from the canine’s lung and kidneys, which were presumed to be the primary sites of lesions³⁵. A. castellanii has also been isolated from cornea swab samples from cats with keratitis³⁶. Disseminated disease associated with Acanthamoeba spp. infection has been reported in dogs³⁷³⁸³⁹ and horses⁴⁰.

Epidemiology

Acanthamoeba spp. occur worldwide and are ubiquitous in the environment³⁵. A. castellanii has been isolated from the nasal mucosa of approximately 4% of healthy individuals⁴¹, whereas A. castellanii genotype T4 antibody prevalence rates of over 85% were detected in 114 healthy individuals from 37 countries⁴².

A. castellanii genotype T4 has been implicated in AK and GAE worldwide⁵. The estimated annual incidence of AK is 0.1 to 14.9 cases per 100,000 contact lens wearers³. An outbreak in the United States linked to use of a particular contact lens solution affected approximately 158 people in 2007⁴³. GAE incidence is rare. Less than 200 cases have been reported worldwide, making accurate diagnosis and treatment difficult³¹⁴⁴.

Use of contact lenses and ocular trauma are risk factors for AK ²³; over 93% of reported AK cases were associated with use of contact lenses²²²³⁴⁵. Improper usage, such as extended wear and poor hygiene during lens storage and handling, is usually a contributing factor²³.

Immunocompromised individuals are predisposed to GAE⁴⁵⁴⁶. GAE is generally associated with individuals with comorbidities, including malignancies, Hodgkin’s disease, systemic lupus erythematosus, diabetes, renal failure, cirrhosis, tuberculosis, skin ulcers, and HIV infection²⁰. Predisposing factors include alcoholism, drug abuse, steroid treatment, cancer chemotherapy, radiotherapy, organ transplantation, and excessive use of antibiotics²⁰⁴⁷.

Host range

Natural host(s): Humans³⁵, dogs³⁵⁴⁸, and cats³⁶⁵³.

Other host(s): Pigs⁴⁶, hamsters⁴⁹, mice, and rats⁵⁰ are notable experimentally infected hosts.

Infectious dose

Unknown. However, infectious doses (ID₅₀) were experimentally determined in mice infected with A. castellanii strain HN-3 by intranasal exposure; an ID₅₀ of 811 organisms was determined with brain invasion as an endpoint response, whereas the ID₅₀ in an acute meningoencephalitis model was 2,483 organisms⁵¹. A median lethal dose (LD₅₀) of 5,276 amebae was also determined⁵⁶.

Incubation period

Varies from days in cases of Acanthamoeba keratitis to several weeks to months in cases of GAE, cutaneous lesions, and sinusitis²⁰.

Communicability

The preferred mode of transmission is contact of A. castellanii with mucous membranes or damaged skin²³⁵²⁵³⁵⁴. In immunocompromised individuals, A. castellanii can enter via skin lesions or inhalation of cysts and cause cutaneous or lower respiratory tract infections, respectively²³. Transmission by ingestion of contaminated water has been reported in otherwise healthy individuals³⁰, while transmission by direct contact with intact skin has resulted in cutaneous infection⁵⁵. Transmission by injection was reported in a peripheral stem cell transplant recipient⁵⁶.

Section III – Dissemination

Reservoir: None.

Zoonosis: None.

Vectors: None.

Section IV – Stability and viability

Drug susceptibility/Drug resistance

Diamidines (e.g., hexamidine⁵⁷, pentamidine⁵⁷⁵⁸, propamidine); biguanides (e.g., chlorhexidine⁵⁷, polyhexamethylene biguanide); azoles (e.g., clotrimazole⁵⁷, voriconazole⁵⁷, itraconazole⁵⁹); amphotericin B⁵⁷; neomycin⁶⁰; flucytosine and miltefosine⁵⁷⁶¹ have been used in the treatment of Acanthamoeba infections and were effective against A. castellanii in vitro.

High resistance to polyhexamethylene biguanide was described in clinical isolates in Taiwan⁶², whereas strains resistant to erythromycin, chloramphenicol, and oligomycin were reported in the United States⁶³. Treatment failure with rifampin and ketoconazole was reported in an HIV-infected patient with A. castellanii infection³³. Generally, Acanthamoeba cysts are more resistant to drugs than trophozoites²⁰.

Susceptibility to disinfectants

Treatment with povidone-iodine resulted in a reduction of viable trophozoites and, to a lesser degree, cysts⁶⁴⁶⁵. Formalin (10%)⁶⁶ treatment and sodium hypochlorite (2.5%) treatment for 15 minutes showed cysticidal effects⁶⁷. Ethanol (60-70%)⁶⁷⁶⁸ and isopropanol (20%)⁶⁶⁶⁸ are effective against trophozoites and moderately effective against cysts. Treatment with peracetic acid (0.2%) at 55°C for 10 minutes, ortho-phthalaldehyde (0.55%) for 10 minutes, and hydrogen peroxide (7.5%) for 20 minutes were effective against Acanthamoeba cysts⁶⁷.

Physical inactivation

Acanthamoeba cysts can be inactivated by moist heat treatment at 65°C for 15 minutes⁶⁷⁶⁹. A. castellanii ATCC 50370 trophozoites may be completely inactivated by cold atmospheric gas plasma (CAP) for 2 minutes, whereas complete inactivation of A. castellanii cysts was reported after 4 minutes of exposure to CAP⁷⁰.

Survival outside host

A. castellanii is ubiquitous in the environment and has been isolated from soil, fresh and marine water, and air samples⁴⁵⁷¹. A. castellanii cysts, and the viable microbes they may contain, can survive for prolonged periods¹⁷⁷²⁷³. Acanthamoeba cysts can survive for several years⁷⁴⁷⁵.

Section V – First aid/medical

Surveillance

A. castellanii can be detected in patient samples using culture-based methods and PCR³⁵². Patient samples can be examined microscopically to detect trophozoites and/or cysts. Experimental diagnostic techniques including autofluorescence signatures of pathogens are under investigation⁷⁶.

First aid/treatment

Treatment for AK usually involves topical application of a biguanide (e.g., polyhexamethylene biguanide, chlorhexidine gluconate) in combination with a diamidine (e.g., hexamidine)²⁶⁷⁷. Duration of treatment is usually about 6 weeks²⁶, but may last up to 26 months⁷⁸. Surgical intervention may be required. GAE has been treated successfully using various combinations of drugs including antibiotics such as pentamidine, cotrimoxazole, propamidine isethionate, azoles, amphotericin B, flucytosine, rifampin, azithromycin, amikacin, and anticancer drugs such as miltefosine, phenothiazines and thioridazine²⁶⁴⁶⁷⁹.

Immunization

No vaccine currently available.

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

Prophylaxis

No known post-exposure prophylaxis.

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

Section VI – Laboratory hazard

Laboratory-acquired infections

None reported to date.

Sources/specimens

Corneal scrapings³, corneal biopsy specimens³, cerebrospinal fluid⁵, brain tissue⁵, saliva⁴², nasal and skin biopsy specimens³³.

Primary hazards

Exposure of mucous membranes/skin to infectious material²³⁵², inhalation of airborne or aerosolized infectious material²³, and autoinoculation with infectious material⁵⁶ are the primary exposure hazards associated with A. castellanii.

Special hazards

A. castellanii is capable of harbouring a variety of microbes, including some that are pathogenic to humans and animals⁶⁷⁸⁹¹⁰¹¹¹²¹³¹⁴¹⁵¹⁶¹⁷¹⁸.

Section VII – Exposure controls/personal protection

Risk group classification

A. castellanii is a Risk Group 2 Human Pathogen and Risk Group 2 Animal Pathogen⁸⁰⁸¹.

Containment requirements

Containment Level 2 facilities, equipment, and operational practices outlined in the CBS 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 CBS are to be followed. The personal protective equipment could include the use of a labcoat 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, PM 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.

Other precautions

A biological safety cabinet (BSC) or other primary containment devices 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, the handling of high concentrations of regulated materials, or the handling of large volumes of regulated materials.

Additional information: For diagnostic laboratories handling primary specimens that may contain Acanthamoeba castellanii, the following resources may be consulted:

Section VIII – Handling and storage

Spills

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 / 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 (CBH).

Storage

Section IX – Regulatory and other information

Canadian regulatory context

Controlled activities with A. castellanii require a Human Pathogens and Toxins licence issued by the Public Health Agency of Canada.

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

Last file update: May 2023

Prepared by: Centre for Biosecurity, Public Health Agency of Canada.

Disclaimer

This Acanthamoeba castellanii MSDS / PSDS document, provided by Public Health Agency of Canada (PHAC), is offered here as a FREE public service to visitors of www.EHS.com. As outlined in this site’s Terms of Use, VelocityEHS is not responsible for the accuracy, content or any aspect of the information contained therein.

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The post Acanthamoeba castellanii appeared first on VelocityEHS.

Bovine Spongiform Encephalopathy Agent

Kaitlin Black — Mon, 10 Apr 2017 04:00:00 +0000

Bovine Spongiform Encephalopathy Agent

Bovine Spongiform Encephalopathy Agent (BSE) is a progressive, fatal disease of the nervous system of cattle.

Please visit this link to view more information on Bovine Spongiform Encephalopathy Agent:

http://www.inspection.gc.ca/english/anima/disemala/bseesb/bseesbe.shtml

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The post Bovine Spongiform Encephalopathy Agent appeared first on VelocityEHS.

Actinobacillus spp.

Kaitlin Black — Fri, 07 Apr 2017 04:00:00 +0000

Pathogen Safety Data Sheets: Infectious Substances – Actinobacillus spp. and Aggregatibacter spp.

SECTION I – INFECTIOUS AGENT

NAME: Actinobacillus spp. and Aggregatibacter spp.

SYNONYM OR CROSS REFERENCE: Actinobacillus spp: Actinobacillus lignieresii, Actinobacillus ureae (formerly Pasteurella ureae), Actinobacillus hominis, Actinobacillus suis actinobacillosis (1-4); Aggregatibacter spp. (formerly Actinobacillus and Haemophilus species), Aggregatibacter actinomycetemcomitans (formerly Actinobacillus actinomycetcomitans), Aggregatibacter aphrophilus (formerly Haemophilus aphophilus) and Aggregatibacter segnis (formerly Haemophilus segnis) (4, 5)

CHARACTERISTICS: Actinobacillus and Aggregatibacter spp. both belong to the family Pasteurellaceae ⁽¹⁾. They are facultative anaerobic, non-motile, non-spore-forming, coccoid to small gram negative rods (mean size 0.1 – 1.0 um) ^(1, 3). They have what is described as a Morse-code appearance and irregular staining ⁽³⁾. The colonies are translucent and 1-2 mm in diameter on blood agar ⁽³⁾. Growth requires enriched media and is improved by a 5 % – 10 % CO2 atmosphere ⁽¹⁾. Aggregatibacter spp. are as for Actinobacillus, except that some strains may require V factor (that is, NAD or NADP) for growth but no strain in either genus requires X factor (heme).

SECTION II- HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Aggregatibacter actinomycetemcomitans, Actinobacillus. ureae, and A. hominis exclusively colonize humans ⁽¹⁾. The other Actinobacillus species colonize animals, which can act as a reservoir for opportunistic human infections. A. actinomycetemcomitans is part of the normal flora of the human oral cavity and is one of the major causes of endocarditis, soft tissue infections, abscess formation, and adult and juvenile periodontis ^(1, 3). A. ureae and A. hominis have primarily been found in the sputum and tracheal secretions in patients with chronic respiratory tract diseases or pneumonia, although systemic infections have been reported ⁽¹⁾. It is assumed that they also colonize the respiratory tract of healthy individuals. A. lignieresii causes actinobacillosis, a granulomatous disease in cattle and sheep. A few human soft tissue infections, originating from contact with, or bites from, cattle or sheep have been reported. A. equuli and A. suis cause a variety of diseases in horses and pigs and human infection are mostly due to horse or pig bites. Both species have also been isolated from the human upper respiratory tract. A. pleuropneumoniae causes porcine pleuropneumonia, a highly contagious and often fatal respiratory disease of major economic importance to the pig industry ⁽²⁾. The disease, which occurs in pigs of all ages, is characterized by necrotizing, haemorrhagic bronchopneumonia and serofibrinous pleuritis.

EPIDEMIOLOGY: Worldwide distribution. Aggregatibacter actinomycetemcomitans is commonly found in Asian populations and several studies showed a clear predominance of serotype c in Japanese, Chinese, Vietnamese, and Korean individuals ⁽⁶⁾. Conversely, the JP2 clone of A. actinomycetemcomitans has enhanced virulence and causes significantly higher prevalence of aggressive periodontitis in adolescents whose descent can be traced back to the Mediterranean and Western parts of Africa⁽⁶⁾.

HOST RANGE: Actinobacillus and Aggregatibacter spp. infect humans and animals, including sheep, pigs, horses, cattle, hares and swans ⁽⁷⁾^{(1, 2, 6, 8)}

INFECTIOUS DOSE: Unknown.

MODE OF TRANSMISSION: Aggregatibacter actinomycetecmcomitans can be transmitted to humans from animal bites (sheep, pigs, horses, cattle) ^(1, 2, 6) or between humans via direct contact with human saliva ^(9, 10).

INCUBATION PERIOD: Unknown.

COMMUNICABILITY: Capable of transmission from person-to-person. Studies demonstrate that family members commonly harbour the same strain of A. actinomycetemcomitans ⁽¹⁰⁾.

SECTION III – DISSEMINATION

RESERVOIR: Humans, animals ^(1, 2, 6).

ZOONOSIS: Capable of zoonosis. Actinobacillus or Aggregatibacter spp. can be transferred to humans by animal bites ⁽¹⁾.

VECTOR: None.

SECTION IV- STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY/RESISTANCE: Actinobacillus or Aggregatibacter strains are generally susceptible to a range of antibiotics, including cephalosporins, cefotaxime, cefazolin, doxycycline and aminoglycosides ^(1, 3).

DRUG RESISTANCE: Aggregatibacte. actinomycetemcomitans is resistant to penicillin and macrolides ^(1, 3). A. lignieresii is sensitive to chloramphenicol, chlortetracycline, oxytetracycline and streptomycin, and resistant to neomycin, novobiocin and oleandomycin ⁽³⁾.

SUSCEPTIBILITY TO DISINFECTANTS: Generally susceptible to glutaraldehyde, sodium hypochlorite, hydrogen peroxide and sulfathiazole ^(11, 12). A. pleuropneumoniae has been shown to also be susceptible to mercurochrome, high concentrations of iodine, and a quaternary ammonium compound formulation containing combinations of benzalkonium chloride, glutaraldehyde, glyoxal and formaldehyde ⁽¹²⁾.

PHYSICAL INACTIVATION: Heat at 121 °C for 15 minutes under pressure. Specific species may be heat inactivated at lower temperatures ⁽³⁾.

SURVIVAL OUTSIDE HOST: Survives less than 24 hours when dried on paper ⁽³⁾.

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Infection can be confirmed by bacterial isolation on enriched growth media such as blood agar with appropriate supplements followed by morphological assessment and biochemical testing (i.e. PCR for surface polysaccharides, immunofluorescence) ^(1, 3).

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

FIRST AID TREATMENT: Administer appropriate antibiotic therapy ^(1, 3).

IMMUNIZATION: None.

PROPHYLAXIS: None.

SECTION VI – LABORATORY HAZARD

LABORATORY ACQUIRED INFECTIONS: None reported to date.

SOURCES/SPECIMENS: Human and animal samples: tracheal secretions, bronchial washings and lavages, oral cavity samples (subgingival plaque samples, dental plaque samples), pus and exudates from lesions, blood, cerebrospinal fluid, respiratory tract samples ^(1, 3).

PRIMARY HAZARD: Accidental parenteral inoculation or mucous membrane exposure.

SPECIAL HAZARD: None.

SECTION VII- EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk group 2 ⁽¹³⁾. This risk group applies to the genus as a whole, and may not apply to every species within the genus.

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials, animals, or cultures. These containment requirements apply to the Actinobacillus spp. as a whole, and may not apply to each species within the genus.

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 ⁽¹⁴⁾. Additional precautions should be considered with work involving animals or large scale activities.

SECTION VIII- HANDLING AND STORAGE

SPILLS: Allow aerosols to settle; wearing protective clothing, 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 (14, 15).

DISPOSAL: Decontaminate all wastes before disposal; steam sterilization, chemical disinfection, incineration (14).

STORAGE: In sealed containers that are appropriately labelled ⁽¹⁴⁾.

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: August 2010

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

Public Health Agency of Canada, 2010

Canada

This Actinobacillus spp. MSDS / PSDS document, provided by Public Health Agency of Canada (PHAC), is offered here as a FREE public service to visitors of www.EHS.com. As outlined in this site’s Terms of Use, VelocityEHS is not responsible for the accuracy, content or any aspect of the information contained therein.

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Actinomyces spp.

Kaitlin Black — Fri, 07 Apr 2017 04:00:00 +0000

Pathogen Safety Data Sheets: Infectious Substances – Actinomyces spp.

SECTION I – INFECTIOUS AGENT

NAME: Actinomyces spp.

SYNONYM OR CROSS REFERENCE:, A. bovis, A. bowdenii, A. canis, A. israelii, A. denticolens, A. funkei, A. georgiae, A. gerencseriae, A. hominis, A. hongkongensis, A. hordeovulneris, A. howellii, A. hyovaginalis, A. johnsonii, A. massiliensis, A. meyeri, A. naeslundii, A. neuii, A. odontolyticus, A. oris, A, radicidentis, A. radingae, A. slackii, A. suis, A. turicensis, A. viscosus, other Actinomyces species sensu stricto ⁽¹⁾ .

CHARACTERISTICS: Actinomyces spp. belongs to the family Actinomycetaceae. They are gram positive rods, 0.4–1.0 µm in size that are straight, curved, or pleomorphic, and occur singly, in pairs, in clusters, or in short chains. Filaments (up to 50 µm in length) that are non-acid-fast and non-motile, do not form endospores or conidia, and grow well with media containing sodium carbonate ⁽²⁾. The majority of Actinomyces spp. are facultative anaerobes but some are anaerobic (A. suis).

SECTION II- HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Actinomyces spp. are part of the normal flora of the oral cavity and respiratory tract, but infection of organs and bloodstream may occur upon disruption of tissue barriers ⁽³⁾. Actinomyces spp. are common in mixed infections, and infection with Actinomyces spp. alone is often associated with lower pathogenicity than when it is part of a mixed infection ⁽⁴⁾. Mixed infections predominantly involve A. israelii and A. gerencseriae, and based on the oral habitat of the genus, manifestations mostly occur in the cervicofacial region (but may occur at any area of the body) ⁽⁵⁾. A. israelii is known to cause actinomycosis, which is characterized by abscesses of the cervicofacial, thoracic, abdominopelvic regions, and central nervous system ⁽⁶⁾. A. naeslundii, A. meyeri, A. odontolyticus and A. viscosus are more rarely associated with actinomycosis ⁽⁷⁾. Infection is caused by invasion through a break in the mucous membrane, and the presence of devitalized tissue allows for deeper penetration into body tissues. Gastrointestinal infections often occur after surgery, intra-abdominal inflammation, trauma, or presence of foreign bodies, when the integrity of mucosal membranes is fragile. The spread of the bacterial infection after the initial invasion leads to chronic infection accompanied by draining sinuses and fibrosis. Secondary hepatic actinomycosis commonly occurs with abdominal or thoracic infections, and infections that dominantly affect the liver are rare but often serious ⁽³⁾. A. israelii has been discovered in the genital tract of healthy females, suggesting that it may be the cause of such infections, which are often related to the use of an intrauterine device. Actinomyces spp. has been linked to root surface caries and periodontal disease, both are widespread human illnesses. In root surface caries, species of Actinomyces can dominate the flora of lesions in root tissue of mainly elderly people, and it also aids in plaque development in periodontal diseases, which can lead to gingivitis.

EPIDEMIOLOGY: Actinomyces spp. are found worldwide with reported cases in Canada, USA, and India ^{(8, 9)}, although it is most commonly found in regions of low socioeconomic status and poor hygiene ⁽⁶⁾. Infection is rare in infants and children ⁽⁸⁾. Many cases are found in women using intra-uterine contraceptive device (IUCD) ⁽⁹⁾. Actinomycosis is three times more common in men than women ⁽¹⁰⁾. Alcoholism, intravenous drug abuse, peptic ulcer, and biliary tract disease are risk factors for hepatic actinomycosis ⁽³⁾.

HOST RANGE: Humans and animals, including pigs, dogs, cats,horses ⁽⁷⁾,cattle and marine mammals ^(1, ^2, ^7, ¹¹⁾.

INFECTIOUS DOSE: Unknown.

MODE OF TRANSMISSION: The Actinomyces spp. commonly inhabits the oral cavity, the gastrointestinal tract, and the female genital tract, where they exist as commensals. Infection occurs when mechanical insult disrupts the mucosal barrier or organisms gain access to privileged sites. For example, actinomycosis commonly occurs after dental procedures, trauma, surgery, or aspiration ⁽¹⁰⁾. Actinomyces spp. is also presumed to be transmitted via direct contact between individuals as part of the normal oral flora ⁽⁷⁾.

INCUBATION PERIOD: The incubation period varies from several days to several years after colonization ^{(7, 8)}. The incubation period could be days to months after insult to a mucous membrane ⁽⁷⁾.

COMMUNICABILITY: The majority of infections result from Actinomyces spp. colonizing the hosts own oral or respiratory cavities ^(7, ¹¹⁾. It is presumed that Actinomyces can be transmitted from person-to-person via direct contact as part of the normal oral flora⁽⁷⁾.

SECTION III – DISSEMINATION

RESERVOIR: Humans are the natural reservoir for Actinomyces spp., especially A. israelii ^(2, ⁷⁾. They are part of the normal oral flora and form a significant component of dental plaque on tooth surfaces ⁽²⁾. Actinomyces spp. are mostly found in intestinal surfaces and mucosal surfaces of humans and animals, blood, female and male genital and urinary tracts, actinomycotic lesions, and infectious hip prosthesis ^(2, ¹²⁾.

ZOONOSIS: None known.

VECTOR: None known.

SECTION IV – STABIILTY AND VIABILITY

DRUG SUSCEPTIBILITY/RESISTANCE: Highly sensitive to β-lactam antibiotics, high to moderate sensitivity to tetracyclines, chloramphenicol, macrolides, lincomycins, fusidic acid and vancomycin. Actinomyces spp. do not generally develop antibiotic resistance, but some strains are resistant to aminoglycosides, peptide antibiotics, metronidazole, rifampicin (A. naeslundii).

SUSCEPTIBILITY TO DISINFECTANTS: Bacteria have been shown to be susceptible to low concentrations of chlorine, 70 % ethanol, phenolics, 2% aqueous glutaraldehyde, and peracetic acid (0.001% to 0.2%) ^(13, ⁽¹⁴⁾.

PHYSICAL INACTIVATION: Inactivation is obtained by exposure to UV rays or by heating to 55-65 oC ⁽¹⁵⁾. Most bacteria can be inactivated by moist heat (121°C for 15 min – 30 min) and dry heat (160-170°C for 1-2 hours) ⁽¹⁶⁾.

SURVIVAL OUTSIDE HOST: Unknown.

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. The detection of ‘sulfur’ granules, Gram staining, and histological staining remain the principal methods of direct detection of Actinomyces spp. in clinical material ⁽¹⁾. Immunofluorescent stains for Actinomyces spp. are available. Actinomyces spp. can be identified in tissue specimens using the 16s rRNA sequencing and PCR assay.
Note: All diagnostic methods are not necessarily available in all countries.

FIRST AID TREATMENT: Administer appropriate antibiotic therapy ^(7, ⁸⁾. Prolonged therapy is necessary to achieve a cure and minimize relapse ⁽¹⁰⁾. Penicillin is usually effecting, but amoxicillin, erythromycin, clindamycin, doxycycline, and tetracycline are alternative antimicrobial choices ⁽⁷⁾. Tetracyclines are not recommended for pregnant women or children younger than 8 years of age. Surgical drainage often is a necessary adjunct to medical management and may allow for a shorter duration of antimicrobial treatment ⁽⁸⁾.

IMMUNIZATION: None.

PROPHYLAXIS: None.

SECTION VI: LABORATORY HAZARDS

LABORATORY ACQUIRED INFECTIONS: One laboratory-acquired infection reported in 1976 ⁽¹⁷⁾.

SOURCES/SPECIMENS: Samples from oral cavity (dental plaque, saliva, mucosal surfaces), blood, tissue biopsy specimens, aspirates ^(2, ¹²⁾.

PRIMARY HAZARD: Actinomyces spp. adapts to mucosal surfaces and has to penetrate through epithelial barrier to produce infection ⁽¹⁸⁾.

SPECIAL HAZARD: None.

SECTION VII- EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk group 2 ⁽¹⁹⁾. This risk group applies to the genus as a whole, and may not apply to every species within the genus.

CONTAINMENT REQUIREMENT: Containment Level 2 facilities, equipment, and operational practices for all work involving infectious or potentially infectious material ⁽²⁰⁾. This containment level applies to the genus as a whole, and may not apply to every species within the genus.

SECTION VIII- HANDLING AND STORAGE

SPILLS: Allow aerosols to settle and, wearing protective clothing, gently cover spill with paper towels and apply an appropriate disinfectant, starting at the perimeter and working towards the centre. Allow sufficient contact time before clean up⁽²⁰⁾.

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⁽²⁰⁾.

STORAGE: The infectious agent should be stored in leak-proof containers that are appropriately labelled⁽²⁰⁾.

SECTION IX – REGULATORY AND OTHER INFORMATION

UPDATED: November 2011

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

This Actinomyces spp. MSDS / PSDS document, provided by Public Health Agency of Canada (PHAC), is offered here as a FREE public service to visitors of www.EHS.com. As outlined in this site’s Terms of Use, VelocityEHS is not responsible for the accuracy, content or any aspect of the information contained therein.

Need an SDS? Search our entire SDS database containing millions of documents.

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Adenovirus (Types 1, 2, 3, 4, 5 and 7)

Kaitlin Black — Fri, 07 Apr 2017 04:00:00 +0000

Pathogen Safety Data Sheets: Infectious Substances – Adenovirus types 1, 2, 3, 4, 5 and 7

SECTION I – INFECTIOUS AGENT

NAME: Adenovirus (excluding serotypes 40 and 41)

SYNONYM OR CROSS REFERENCE: Acute respiratory disease (ARD), childhood febrile illness, adenovirus species A, B, C, D, E, F, G, pharyngoconjunctival fever.

CHARACTERISTICS: Human adenoviruses are members of the family Adenoviridae and genus Mastadenovirus. Within the almost 100 different serotypes of human adenovirus, 51 are known to be pathogenic in humans ^{1 2}. The virus is nonenveloped with an icosahedral capsid at 70-90 nm in diameter and each contains a single linear, double-stranded DNA genome of approximately 36 kb ².

SECTION II – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Adenovirus cause generally mild respiratory tract infections which are self-limiting and generally asymptomatic despite virologic and serologic proof of infection ³, and only around 45% of infections are manifested by disease ¹. It is a major agent of acute respiratory disease, mainly caused by serotypes 4 and 7, and is characterized by fever, rhinitis, pharyngitis, cough, and conjunctivitis ¹. Other common illnesses can be observed in the respiratory tract, gastrointestinal tract, and eyes (acute follicular conjunctivitis) ². Common diseases caused by various adenovirus serotypes are:

Childhood febrile illness and pharyngoconjunctival fever – 1, 2, 3, 5, 7 ¹
Pneumonia and other acute respiratory illnesses – 1, 2, 3, 5, 7, 14 ¹⁴
Pertussis-like illness – 1, 2, 3, 5, 19, 21 ¹
Conjunctivitis – 1-4, 5, 7, 8, 19, 21 ¹²
Keratoconjunctivitis – 3, 8, 9, 19, 37 ¹
Acute hemorrhagic cystitis – 11 ¹
Upper respiratory illness and hepatitis – 1-3, 5, 7 ²
Lower respiratory illness – 3, 4, 7, 21 ²

General infections are commonly observed in young children, particularly by serotypes 1, 2, and 5 ¹. Symptoms of infection may include fever, nasal congestion, coryza, and pharyngitis. Other more serious illnesses such as nephritis, neutropenia, myocarditis, hepatitis, disseminated intravascular coagulation and meningoencephalitis can occur ^{2 5}. Eye infections such as acute follicular conjunctivitis, often accompanied by significant periauricular lymphadenopathy, are often mild and complete recovery is common ⁶. Neonatal disease, meningoencephalitis, myocarditis, and venereal diseases are uncommon ².

EPIDEMIOLOGY: Adenovirus is of worldwide prevalence, and is ubiquitous throughout the year, especially during later winter and early spring ⁵. Serotype 5 is the most common, with serotypes 1 and 2 being highly endemic ¹. Children are especially susceptible to infection ^{2 5 7}. Adenovirus serotypes 3, 4, 7, and 21 have been associated with outbreaks of acute respiratory disease among military recruits ^{3 8}. These outbreaks have resulted in hospitalization and some mortality ⁸. Smaller outbreaks of serotypes 3, 4, and 7 occur in the summertime due to contaminated swimming pool water, which commonly resulted in conjunctivitis ^{1 2}. Serious adenovirus infections occur more frequently in immunocompromised individuals ^{2 7}.

HOST RANGE: Humans.

INFECTIOUS DOSE: Inhalation of as few as 5 adenovirus particles can cause disease in susceptible individuals ³. The National Institutes of Health lists the infectious dose for adenovirus serotype 7 as >150 viral units, administered as nasal drops ⁹.

MODE OF TRANSMISSION: Respiratory and fecal-oral routes. Infection can also spread through contaminated fomites, fingers, ophthalmic solutions, and airborne particulates^{2 5 1}

INCUBATION PERIOD: Approximately 2 to 14 days ².

COMMUNICABILITY: Children shed non enteric adenovirus in throat and stool samples for 3 to 6 weeks following lower respiratory infection or generalized illness. Chance of transmission is high in crowded and closed settings such as day cares, boarding schools and long-term care facilities. Transmission between family members is common. In rare cases, virus shedding may last for 18 months or longer ².

SECTION III – DISSEMINATION

RESERVOIR: Humans ^{3 6}. Experimentally, human adenovirus can infect virtually all mammalian species, including monkeys, cotton rats, rabbits, and rodents ⁶.

ZOONOSIS: None.

VECTORS: None.

SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: None. Many reports indicate cidofovir to be effective against adenoviruses; however, no controlled trials have been performed so far, and the drug is not currently licensed for use Footnote 5.

SUSCEPTIBILITY TO DISINFECTANTS: Adenoviruses are resistant to lipid disinfectants, but are inactivated by formaldehyde and chlorine ⁵. They can be inactivated by contact with 1:5 dilution of bleach for 1 minute or 2 minutes contact with alcohol-based hand gels ².

PHYSICAL INACTIVATION: Adenovirus can be inactivated by heat ⁵: heating to 56 °C for 30 min, 60 °C for 2 min, and autoclaving will destroy infectivity ².

SURVIVAL OUTSIDE HOST: Most serotypes are stable at 36 °C for a week, for several weeks at room temperature, and for several months at 4 °C ^{2 10}. Adenoviruses are very stable in the environment and persist for 7 days to 3 months on dry inanimate surfaces ¹⁰. They can also survive for weeks in tap water, sewage effluent and sea water ¹¹. Adenovirus type 2 can survive on common environmental surfaces for up to 8 weeks at room temperature ¹².

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms. Infected cells can be observed by microscopy, and adenoviruses can be detected using immunofluorescence, enzyme-linked immunoassay, or PCR for antigen detection ².

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

FIRST AID/TREATMENT: No formally approved effective antiviral agents exist for treatment of adenoviral infections ⁷. Illness is generally self-limiting and treatment is supportive ⁵. It has been suggested that immunocompromised patients may require drug treatment with cidofovir or other antiviral drugs ⁷.

IMMUNIZATION: A vaccine for adenovirus strains 4 and 7 was developed but is no longer in production (economic reasons) ^{2 8}.

PROPHYLAXIS: None.

SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: At least 10 cases of laboratory-acquired adenovirus infections have occurred up to 2006; however, the serotypes involved were not reported Footnote 13.

SOURCES/SPECIMENS: Generally, fecal samples, and respiratory secretions from an infected individual contain infectious virus. Other tissues may contain virus depending on symptoms ².

PRIMARY HAZARDS: Contact of mucous membranes (mouth or eyes) with virus, ingestion, or inhalation of viral particles ^{2 13 14}.

SPECIAL HAZARDS: None.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2 ¹⁵. This risk group applies to the species as a whole, and may not apply to every serotype within the species.

CONTAINMENT REQUIREMENTS: Containment Level 2 facilities, equipment, and operational practices for work involving infectious or potentially infectious materials. These containment requirements apply to the species as a whole, and may not apply to each serotype within the species.

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 ¹⁶.

STORAGE: The infectious agent should be stored in leak-proof containers that are appropriately labelled ¹⁶.

SECTION IX – REGULATORY AND OTHER INFORMATION

UPDATED: November 2011

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

This Adenovirus (Types 1, 2, 3, 4, 5 and 7) MSDS / PSDS document, provided by Public Health Agency of Canada (PHAC), is offered here as a FREE public service to visitors of www.EHS.com. As outlined in this site’s Terms of Use, VelocityEHS is not responsible for the accuracy, content or any aspect of the information contained therein.

Need an SDS? Search our entire SDS database containing millions of documents.

The post Adenovirus (Types 1, 2, 3, 4, 5 and 7) appeared first on VelocityEHS.

Adenovirus (types 40 and 41)

Kaitlin Black — Fri, 07 Apr 2017 04:00:00 +0000

Pathogen Safety Data Sheets: Infectious Substances – Adenovirus (types 40 and 41)

SECTION I – INFECTIOUS AGENT

NAME: Adenovirus (Serotypes 40 & 41)

SYNONYM OR CROSS REFERENCE: Adenovirus Species F, enteric adenovirus^(1,2), fastidious adenovirus⁽²⁾, ADV 40, and ADV 41.

CHARACTERISTICS: Human adenoviruses are members of the family Adenoviridae and genus Mastadenovirus. They are nonenveloped viruses with an icosahedral capsid, 70-90 nm in diameter and a double-stranded, linear DNA genome⁽¹⁾.

SECTION II – HAZARD IDENTIFICATION

PATHOGENICITY/TOXICITY: Adenovirus serotypes 40 and 41 cause acute gastroenteritis primarily in children. Symptoms may include fever, diarrhea, vomiting, and abdominal pain, and last for approximately 10 days. Respiratory symptoms can occur in some individuals. The disease is usually self-limiting in immunocompetent individuals; however rare fatalities can occur in immunocompromised individuals(1).
Asymptomatic infections are common, particularly in children(3).

EPIDEMIOLOGY: Enteric adenovirus is a common cause of acute gastroenteritis in children worldwide⁽¹⁾. Enteric adenoviruses have been identified in 9% of children with diarrhea. They are the third most common cause of infantile gastroenteritis after rotavirus and norovirus⁽²⁾. Sporadic and endemic infections may occur year-round⁽¹⁾.

HOST RANGE: Humans.

INFECTIOUS DOSE: Unknown.

MODE OF TRANSMISSION: The virus is transmitted via the fecal-oral route⁽¹⁾.

INCUBATION PERIOD: 3 to 10 days⁽¹⁾.

COMMUNICABILITY: Low communicability between close contacts in the same household⁽⁴⁾. Virus shedding takes place during the acute stage of the disease, since enteric adenoviruses are rarely recovered from stool samples more than a few weeks after recovery from gastroenteritis⁽¹⁾. Asymptomatic individuals (mainly children) shed adenoviruses in their stool⁽³⁾.

SECTION III – DISSEMINATION

RESERVOIR: Humans⁽⁵⁾.

ZOONOSIS: None.

VECTORS: None.

SECTION IV – STABILITY AND VIABILITY

DRUG SUSCEPTIBILITY: None. Reports indicate that cidofovir may be effective against adenoviruses; however, no controlled trials have been performed so far, and the drug is not currently licensed for use(6).

SUSCEPTIBILITY TO DISINFECTANTS: Adenoviruses are resistant to lipid disinfectants, but are inactivated by formaldehyde and chlorine⁽⁶⁾. Adenoviruses can be inactivated by contact with 1:5 dilution of bleach for 1-2 minutes, and by contact with alcohol-based hand gels⁽¹⁾.

PHYSICAL INACTIVATION: Adenoviruses are highly resistant to inactivation⁽¹⁾. Adenovirus can be inactivated by heat⁽⁶⁾: heating to 56 °C for 30 min, 60 °C for 2 min, and autoclaving will destroy infectivity⁽¹⁾. Adenovirus serotype 40 is also sensitive to UV radiation⁽⁷⁾.

SURVIVAL OUTSIDE HOST: Most serotypes are stable at 36 °C for a week, for several weeks at room temperature, and for several months at 4 °C^(1,8). Adenoviruses are very stable in the environment and persist for 7 days to 3 months on dry inanimate surfaces⁽⁸⁾. They can also survive for many days in tap water, sewage effluent, and sea water⁽⁹⁾.

SECTION V – FIRST AID / MEDICAL

SURVEILLANCE: Monitor for symptoms of gastrointestinal and/or respiratory illness. Enteric adenovirus infection can be detected by electron microscopy, agglutination tests, enzyme-linked immunosorbent assay, or by PCR⁽¹⁰⁾.

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

FIRST AID/TREATMENT: Illness is generally self-limiting. Treatment is primarily oral rehydration or, in serious cases, intravenous rehydration⁽¹⁰⁾.

IMMUNISATION: None.

PROPHYLAXIS: None.

SECTION VI – LABORATORY HAZARDS

LABORATORY-ACQUIRED INFECTIONS: At least 10 cases of laboratory-acquired adenovirus infections have occurred up to 2006; however, the serotypes involved were not reported(11).

SOURCES/SPECIMENS: Fecal samples^(1,4).

PRIMARY HAZARDS: Ingestion of virus⁽¹⁾, accidental parenteral inoculation, and droplet exposure of the mucous membranes of the eye, nose, or mouth.

SPECIAL HAZARDS: None.

SECTION VII – EXPOSURE CONTROLS / PERSONAL PROTECTION

RISK GROUP CLASSIFICATION: Risk Group 2⁽¹²⁾.

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

SECTION VIII – HANDLING AND STORAGE

SPILLS: Allow aerosols to settle, and while wearing protective clothing, gently cover the spill with paper towels and apply appropriate disinfectant, starting at the perimeter, working inwards towards the centre. Allow sufficient contact time before clean up⁽¹³⁾.

DISPOSAL: Decontaminate before disposal by steam sterilization, incineration, or chemical disinfection⁽¹³⁾.

STORAGE: In locked, leak-proof containers that are appropriately labelled and secured⁽¹³⁾.

SECTION IX – REGULATORY AND OTHER INFORMATION

UPDATED: November 2010

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

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