Schistosoma Mansoni is one of the microbial species that causes similar symptoms found with S. mekongi, one of 3 species in Asia that are known to cause infection in humans. The other two are known as S. japonicum and S. Malayensis. Human infection is known as Acute Schistosomiasis, caused by helminth parasites of the genus Schistosoma and is characterized by, most commonly fever and cough, but also by myalgia, gastrointestinal complaints, fatigue and urticaria. The region of Asia where these infections have been reported was Laos, after 7 travelers from Israel had been diagnosed from serology. It has been reported that over 200 million humans are infected, but about 85% of those infected are in Africa. What is interesting to note is that anyone can be at risk who travels to endemic areas such as Laos or Africa and are exposed to fresh water. Freshwater snails are generally the host.
http://www.cdc.gov/eid/content/15/11/1823.htm
http://wwwnc.cdc.gov/travel/yellowbook/2010/chapter-5/schistosomiasis.aspx
Tuesday, May 11, 2010
Clostridium difficile is an acute, severe disease of the colon, developing as a complication of antibiotic therapy. People in good health usually don't get C. difficile disease. Doctors quite often faced with diarrhea in patients after antibiotic use. Only infected people can spread the disease to others. However, only people that are hospitalized or on antibiotics are likely to become ill. Clostridium difficile is the causative agent of the most severe complications, up to the development of fulminant colitis and toxic dilatation of the colon. The key to the pathogenesis S.diffichili associated colitis is a violation of microbial ecology in the colon, the oppression of the resident anaerobic microflora, the occurrence of metabolic niches for reproduction S.difficile and its conversion into toxinoforming form.
Clostridium difficile infections (CDIs) have increased in incidence and severity within the past decade in North America and Europe (1), in large part because of the emergence of the hypervirulent North American pulsed-field type 1 (NAP1/027/III) strains (2-5). Recently, interest has increased in the ribotype 078 strain. An infection was considered healthcare-associated CDI of the patient's symptoms occurring. An infection was considered community-onset CDI if the healthcare-associated definition was not met. Outcomes 30 days postinfection were recorded to capture severe cases, which were defined as infections in patients admitted to an intensive care unit, in patients who had undergone colectomy, or in patients who had died (12). Deaths were assessed by the Canadian Hospital Epidemiology Committee member and categorized into three groups: 1) death directly attributable to CDI, 2) death indirectly related to CDI by exacerbation of an existing disease condition, or 3) death not a result of CDI. The assessment was made from information obtained from medical charts, nurse logs, laboratory reports, and consultation with nursing and medical staff. It is harmful, so it would be great to use safety percussion to reduce the chance of a spread.
“General Information about Clostridium difficile Infections ” August 2004, Jul 22, 2005.
“Hypervirulent Clostridium difficile Strains in Hospitalized Patients, Canada”Dispatch,Vol. 16, #4, April 2010.
Clostridium difficile infections (CDIs) have increased in incidence and severity within the past decade in North America and Europe (1), in large part because of the emergence of the hypervirulent North American pulsed-field type 1 (NAP1/027/III) strains (2-5). Recently, interest has increased in the ribotype 078 strain. An infection was considered healthcare-associated CDI of the patient's symptoms occurring. An infection was considered community-onset CDI if the healthcare-associated definition was not met. Outcomes 30 days postinfection were recorded to capture severe cases, which were defined as infections in patients admitted to an intensive care unit, in patients who had undergone colectomy, or in patients who had died (12). Deaths were assessed by the Canadian Hospital Epidemiology Committee member and categorized into three groups: 1) death directly attributable to CDI, 2) death indirectly related to CDI by exacerbation of an existing disease condition, or 3) death not a result of CDI. The assessment was made from information obtained from medical charts, nurse logs, laboratory reports, and consultation with nursing and medical staff. It is harmful, so it would be great to use safety percussion to reduce the chance of a spread.
“General Information about Clostridium difficile Infections ” August 2004, Jul 22, 2005
“Hypervirulent Clostridium difficile Strains in Hospitalized Patients, Canada”Dispatch,Vol. 16, #4, April 2010
Human Plasmodium Knowlesi Infection Detected by Rapid Diagnostic Tests for Malaria
P. Knowlesi is a Malaria parasite that was regarded as a rare disease, mainly occuring in long-tailed and pig tailed macaques(monkey) but has occured sporadically in humans. There have been a large number of infected patients in Malaysian Borneo and other reports of human cases in Thailand, Myanmar, Philippines and Singapore.
"Human Plasmodium Knowlesi infection detected by rapid diagnostic tests for malaria". Dispatch, volume 15 number 9 September 2009 http://www.cdc.gov/eid/content/15/9/478.htm
P. Knowlesi is transmitted from monkeys to humans by mosquitos. Sx's of malaria include fever and flu like sx's, headach, muscle aches and tiredness, nausea, vomitting and diarrhea. May also cause juandice(yellow coloring of the skin and eyes). If not treated the infection can cause kidney failure, seizures, mental confusion, coma and death.
http://www.cdc.gov/malaria/about/faqs.htm
"Human Plasmodium Knowlesi infection detected by rapid diagnostic tests for malaria". Dispatch, volume 15 number 9 September 2009 http://www.cdc.gov/eid/content/15/9/478.htm
P. Knowlesi is transmitted from monkeys to humans by mosquitos. Sx's of malaria include fever and flu like sx's, headach, muscle aches and tiredness, nausea, vomitting and diarrhea. May also cause juandice(yellow coloring of the skin and eyes). If not treated the infection can cause kidney failure, seizures, mental confusion, coma and death.
http://www.cdc.gov/malaria/about/faqs.htm
Lymphocytic Choriomeningitis Virus Meningitis, New York, NY, USA, 2009
Lymphocytic choriomeningitis virus (LCMV)belongs to the family of the arenaviruses, which are associated with rodent-transmitted disease in humans and are zootonic. Humans can come into contact with arenaviruses by ingesting contaminated food and having direct contact with rodent excrement. Such arenavirus infections can cause severe illnesses and are more common in humans.The rodent hosts of arenaviruses have been known to be chronically infected with viruses, which do not show obvious symptoms inside the hosts. Some arenaviruses are also associated with nosocomial transmission and secondary person to person. Nosocomial transmission occurs when a person is exposed and then infected with the arenavirus from the rodent host. Once the person is infected the virus, he or she can spread it to other humans. However, person to person transmission is associated with having direct contact with one another's blood and other excretions that contain virus particles of infected individuals.
Since LCMV belongs to the family of the arenavirus, it has been discovered in the common house mouse (MUS musculus and M. domesticus), pets, and research rodents, such as hamsters and guinea pigs. LCMV is transmitted through inhalation, fomites, and direct contact with blood from infected rodents. Such a virus has also been transmitted by infected mothers during pregnancy to the fetus and through solid organ transplantation. The incubation period for LCMV is from one to two weeks and infected individual usually experience symptoms, such as fever chills, myalgia, pharyngitis, testicular pain, and photophobia.
In the article, "Lymphorcytic Choriomeningitis Virus Meningitis, New York, NY, USA, 2009," it mentioned about how a forty-nine year old man (taxi driver) received treatment for LCMV. The patient also had all the symptoms for the virus, such as chills, headache, vomiting, generalized weakness, nausea, and a seven day history of fever. The article also stated that he received a corneal transplant the previous year that may have caused LCMV. After the patient received supportive care, he fully recovered and was discharged on day twelve.
Although the patient received a corneal transplant the previous year, it was not actually the source of infection. The Centers for Disease Control and Prevention concluded that the patient experienced meningitis during the fall-winter season. Then,a febrile illness followed by brief remission before an onset of neurological illness, and CSF with a hypoglycorrachia and lymphocytosis. After the case, the Center for Disease Control and Prevention implemented new rules and regulations for diagnosing LCMV. Within the preceding three months, patients with a history of organ transplantation should be evaluated to determine whether infected organs were the primary souce of LCMV. Patients with LCMV should also be questioned about potential rodent exposure. By having a better understanding of the true incidence of LCMV, authorities will be able to prevent and control the virus.
Asnis, Deborah, "Lymphorcytic Choriomeningitis Virus Meningitis" Center for Disease Control and Prevention, February 2010, http://www.cdc.gov/eid/content/16/2/328.htm.
"Arenaviruses," Special Pathogens Branch, August 2005, http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/arena.htm.
Since LCMV belongs to the family of the arenavirus, it has been discovered in the common house mouse (MUS musculus and M. domesticus), pets, and research rodents, such as hamsters and guinea pigs. LCMV is transmitted through inhalation, fomites, and direct contact with blood from infected rodents. Such a virus has also been transmitted by infected mothers during pregnancy to the fetus and through solid organ transplantation. The incubation period for LCMV is from one to two weeks and infected individual usually experience symptoms, such as fever chills, myalgia, pharyngitis, testicular pain, and photophobia.
In the article, "Lymphorcytic Choriomeningitis Virus Meningitis, New York, NY, USA, 2009," it mentioned about how a forty-nine year old man (taxi driver) received treatment for LCMV. The patient also had all the symptoms for the virus, such as chills, headache, vomiting, generalized weakness, nausea, and a seven day history of fever. The article also stated that he received a corneal transplant the previous year that may have caused LCMV. After the patient received supportive care, he fully recovered and was discharged on day twelve.
Although the patient received a corneal transplant the previous year, it was not actually the source of infection. The Centers for Disease Control and Prevention concluded that the patient experienced meningitis during the fall-winter season. Then,a febrile illness followed by brief remission before an onset of neurological illness, and CSF with a hypoglycorrachia and lymphocytosis. After the case, the Center for Disease Control and Prevention implemented new rules and regulations for diagnosing LCMV. Within the preceding three months, patients with a history of organ transplantation should be evaluated to determine whether infected organs were the primary souce of LCMV. Patients with LCMV should also be questioned about potential rodent exposure. By having a better understanding of the true incidence of LCMV, authorities will be able to prevent and control the virus.
Asnis, Deborah, "Lymphorcytic Choriomeningitis Virus Meningitis" Center for Disease Control and Prevention, February 2010, http://www.cdc.gov/eid/content/16/2/328.htm.
"Arenaviruses," Special Pathogens Branch, August 2005, http://www.cdc.gov/ncidod/dvrd/spb/mnpages/dispages/arena.htm.
Q Fever in Greenland
Coxiella burnetii is the microbial agent responsible for causing Q fever in Greenland. This is zoonosis disease. Cattle, goats and sheep are reservoirs for the small bacterium yet many other animals are capable for housing it at well. The latent attribute or c. burnetti causes it so be shed during birth in animals, but in humans the symptoms are asymptomatic or just causing fever like symptoms but do not be fooled, this bacterium can also cause pneumonia or hepatitis.
A native of Greenland went to the hospital in December 2007 after having a fever for two months. As a child he had rheumatic fever and six years prior to this hospital visit, he had biological aortic and mitral valves implanted which put him at risk for Q fever endocarditis. January 2008 he was transferred to a different hospital. But he was enduring a low-grade fever, cardiac insufficiency with peripheral edema, hepatosplenomegaly, and 20% half-moon nephritis. His heart seemed fine though and his blood tests were negative for the bacterium. In may 2008, a surgery found massive endocarditis - and his biological valves were replaced with mechanical valves and his symptoms subsided.
After 30 days of incubation, the mans culture was positive after indirect immunofluorescent assay with C. burnetii phase II–specific antibodies..
Google Heath, "Q Fever"retrieved May 11, 2010 from https://health.google.com/health/ref/Q+fever
Koch A, Svendsen CB, Christensen JJ, Bundgaard H, Vindfeld L, Christiansen CB, et al. Q fever in Greenland. Emerg Infect Dis. 2010 Mar [May 11, 2010]. http://www.cdc.gov/EID/content/16/3/511.htm
A native of Greenland went to the hospital in December 2007 after having a fever for two months. As a child he had rheumatic fever and six years prior to this hospital visit, he had biological aortic and mitral valves implanted which put him at risk for Q fever endocarditis. January 2008 he was transferred to a different hospital. But he was enduring a low-grade fever, cardiac insufficiency with peripheral edema, hepatosplenomegaly, and 20% half-moon nephritis. His heart seemed fine though and his blood tests were negative for the bacterium. In may 2008, a surgery found massive endocarditis - and his biological valves were replaced with mechanical valves and his symptoms subsided.
After 30 days of incubation, the mans culture was positive after indirect immunofluorescent assay with C. burnetii phase II–specific antibodies..
Google Heath, "Q Fever"retrieved May 11, 2010 from https://health.google.com/health/ref/Q+fever
Koch A, Svendsen CB, Christensen JJ, Bundgaard H, Vindfeld L, Christiansen CB, et al. Q fever in Greenland. Emerg Infect Dis. 2010 Mar [May 11, 2010]. http://www.cdc.gov/EID/content/16/3/511.htm
Merkel Cell Polyomavirus in Cutaneous Swabs
Merkel cell polyomavirus (MCPyV) was recently discovered in Merkel cell carcinomas, rare but aggressive skin cancers. Merkel cell polyomavirus DNA has been detected in the majority of merkel cell carcinoma (MCC) and less commonly in other skin tumors and healthy skin. To determine if MCPyV might be a widespread in the general population, a retrospective study and tested MCC as well as healthy and skin lesion and mucosa samples of immuno competent and immunosuppressed persons without MCC for MCPyV DNA are conducted. The majority of patients with Merkel cell carcinoma carry MCPyV, but little is known about polyomavirus prevalence in the general population and the association between circulating antibodies against MCPyV and the rare skin cancer.
MCPyV DNA can be efficiently detected by cutaneous swabbing. This method could be useful tool for future epidemiologic studies targeting MCPyV. Indeed, this noninvasive procedure may be easily performed without the potential risk for side effects related to biopsy collection and is more acceptable than a biopsy for patients who not have a cutaneous disease. The high prevalence of MCPyV DNA at the skin surface, contrasted with its low prevalence in buccal mucosa and its absence in skin ulcers, strongly suggests that MCPyV is localized in the epidermis.
Work cited: Toland AE. Merkel cell polyomavirus in cutaneous squamous immunocompetent individuals. J Invest Dermatol. 2009
Journal of the National Cancer Institute published September 23
MCPyV DNA can be efficiently detected by cutaneous swabbing. This method could be useful tool for future epidemiologic studies targeting MCPyV. Indeed, this noninvasive procedure may be easily performed without the potential risk for side effects related to biopsy collection and is more acceptable than a biopsy for patients who not have a cutaneous disease. The high prevalence of MCPyV DNA at the skin surface, contrasted with its low prevalence in buccal mucosa and its absence in skin ulcers, strongly suggests that MCPyV is localized in the epidermis.
Work cited: Toland AE. Merkel cell polyomavirus in cutaneous squamous immunocompetent individuals. J Invest Dermatol. 2009
Journal of the National Cancer Institute published September 23
Monday, May 10, 2010
Influenza Virus A (H1N1) in Giant Anteaters (Myrmecophaga tridactyla)
Influenza (H1N1) is a subtype of influenza virus which is the most common cause of Human influenza. This virus was originally called swine flu because of the genes that are similar to flu viruses in pigs. Like other flu strains, the H1N1 flu virus is passed from person to person. H1N1 causes flu-like symptoms including, sore throat, fever, fatigue, and body aches.
Influenza is known to cross species line into mammalian species. Influenza virus is a pathogen that not only affects its avian reservoir but also mammalian species such as swine, horses, cats, dogs, and humans. In 2007, researchers documented a respiratory disease occurrence in a group of giant anteaters- the new host- at the Nashville zoo. Isolates from two affected animals were identified as a type A influenza virus related to human influenza subtype H1N1. This host could potentially impact human population as possible sources of zoonotic spread of influenza. Emergence of viruses in new host increases people’s concern. However, the good news is that the H1N1 vaccine has been developed now and is available for everyone. CDC recommends influenza vaccination as the most important step in protection the flu.
Sally Nofs, Mohamed Abd-Eldaim, Kathy V. Thomas, David Toplon, Dawn Rouse, and Melissa Kennedy “ Influenza Virus A (H1N1) in the Giant Anteaters ( Myrmecophaga tridactyla).” Emerging Infectious Disease. Volume 15, Number 7- July 2009
“2009 H1N1 Flu” Centers for Disease Control and Prevention. May 7, 2010
Influenza is known to cross species line into mammalian species. Influenza virus is a pathogen that not only affects its avian reservoir but also mammalian species such as swine, horses, cats, dogs, and humans. In 2007, researchers documented a respiratory disease occurrence in a group of giant anteaters- the new host- at the Nashville zoo. Isolates from two affected animals were identified as a type A influenza virus related to human influenza subtype H1N1. This host could potentially impact human population as possible sources of zoonotic spread of influenza. Emergence of viruses in new host increases people’s concern. However, the good news is that the H1N1 vaccine has been developed now and is available for everyone. CDC recommends influenza vaccination as the most important step in protection the flu.
Sally Nofs, Mohamed Abd-Eldaim, Kathy V. Thomas, David Toplon, Dawn Rouse, and Melissa Kennedy “ Influenza Virus A (H1N1) in the Giant Anteaters ( Myrmecophaga tridactyla).” Emerging Infectious Disease. Volume 15, Number 7- July 2009
“2009 H1N1 Flu” Centers for Disease Control and Prevention. May 7, 2010
Congenital Transmission of Chagas Disease in Latin American Immigrants in Switzerland
Chagas disease, a zoonotic infection caused by Trypanosoma cruzi, is the most important endemic parasitic infection in Mexico and Central and South America because of the number of persons who become ill or die from this disease. An estimated 8-10 million persons are infected, and =14,000 persons die each year from Chagas disease. Historically, transmission by triatomine vectors has been the most common source of infection.
In response to these 2 cases, in 2007, a retrospective serologic survey for T. cruzi infection was performed on stored serum samples from 72 undocumented pregnant Latin American women who had recieved prenatal care at the Geneva University Hospitals during the previous year. Median age was 30 years, and countries of origin were Bolivia, Brazil, Peru, Ecuador, Colombia, Chile, Honduras. Serum samples were tested by IFA using T. cruzi parasites from in vitro culture. Of the 72 samples, 7 (9.7%) were positive.
Only a small number of congenital cases of Chagas disease have been reported in countries in which this infection is nonendemic. Chagas disease affects immigrants, who frequently lack legal status and therefore experience difficulties (e.g., fear of deportation and financial and administrative constraints) in accessing quality healthcare during pregnancy.
Systematic screening of pregnant women at risk is likely to be beneficial in several ways. Treatment of infected mothers after completion of breast-feeding may reduce the risk for vertical transmission during subsequent pregnancies. Treatment of young women at the chronic, indeterminate stage of infection is likely to lower their risk for developing cardiac complications. Early screening and treatment of infected newborns are associated with high cure rates.
Microbial Agent in this article is Trypanosoma Cruzi (or "kissing bug"). An infected triatomine insect vector takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound of through intact mucosal membranes, such as the conjunctiva. Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents.
Work Cited:
Jackson Y. Myers C, Diana A, Marti H-P, Wolff H, Chappuis F. "Congenital transmission of Chagas disease in Latin American immigrants in Switzerland." Emerg Infect Dis (serial on the internet). 2009 Apr (date cited).http://www.cdc.gov/EID/content/15/4/601.htm
"Trypanosomiasis, American" Parasites and Health. http://www.dpd.cdc.gov/dpdx/HTML/TrypanosomiasisAmerican.htm
In response to these 2 cases, in 2007, a retrospective serologic survey for T. cruzi infection was performed on stored serum samples from 72 undocumented pregnant Latin American women who had recieved prenatal care at the Geneva University Hospitals during the previous year. Median age was 30 years, and countries of origin were Bolivia, Brazil, Peru, Ecuador, Colombia, Chile, Honduras. Serum samples were tested by IFA using T. cruzi parasites from in vitro culture. Of the 72 samples, 7 (9.7%) were positive.
Only a small number of congenital cases of Chagas disease have been reported in countries in which this infection is nonendemic. Chagas disease affects immigrants, who frequently lack legal status and therefore experience difficulties (e.g., fear of deportation and financial and administrative constraints) in accessing quality healthcare during pregnancy.
Systematic screening of pregnant women at risk is likely to be beneficial in several ways. Treatment of infected mothers after completion of breast-feeding may reduce the risk for vertical transmission during subsequent pregnancies. Treatment of young women at the chronic, indeterminate stage of infection is likely to lower their risk for developing cardiac complications. Early screening and treatment of infected newborns are associated with high cure rates.
Microbial Agent in this article is Trypanosoma Cruzi (or "kissing bug"). An infected triatomine insect vector takes a blood meal and releases trypomastigotes in its feces near the site of the bite wound. Trypomastigotes enter the host through the wound of through intact mucosal membranes, such as the conjunctiva. Trypanosoma cruzi can also be transmitted through blood transfusions, organ transplantation, transplacentally, and in laboratory accidents.
Work Cited:
Jackson Y. Myers C, Diana A, Marti H-P, Wolff H, Chappuis F. "Congenital transmission of Chagas disease in Latin American immigrants in Switzerland." Emerg Infect Dis (serial on the internet). 2009 Apr (date cited).http://www.cdc.gov/EID/content/15/4/601.htm
"Trypanosomiasis, American" Parasites and Health. http://www.dpd.cdc.gov/dpdx/HTML/TrypanosomiasisAmerican.htm
Botulism from Drinking Pruno
According to the article, “Botulism from Drinking Pruno” by Dub Vugia, four inmates from a prison in Riverside California, came down with food borne botulism. After a massive investigation, it was found that the prisoners created a home-made alcoholic beverage called “Pruno.” The prisoners used ingredients such as: unpeeled potatoes, apples, old peach jelly, and ketchup. The combination of these ingredients were mixed in a plastic bag and fermented with different heating stages over several days. The investigation led them to the conclusion that the potatoes used in making pruno were the main contributor to botulism toxin. Clostridium botulism is found in soil and the spores have been found on raw potatoes. From further research, it was found that the spores on the surface of raw potatoes can survive baking and lead to production of C. botulinum toxin. Additionally, the warm fermentation process of making pruno can enhance the production of C. botulinum toxin.
When a person ingests food borne botulism toxin signs will appear within approximately 12-36 hours. The main symptoms of food borne botulism are: double vision, drooping eyelids, difficulty swallowing, dry mouth, distorted voice which causes difficulty in speaking, muscle weakness which may move down the body, typically shoulders first, upper arms, lower arms, thighs, and calves. Additionally, the paralysis can cause breathing problems which can ultimately cause the person to die.
"CDC Botulism | Clinical Description." CDC Emergency Preparedness & Response Site. 14 June 2006. Web. 10 May 2010..
"CDC | Facts About Botulism." CDC Emergency Preparedness & Response Site. 14 Oct. 2001. Web. 10 May 2010..
Vugia, Duc J. "Botulism from Drinking Pruno|CDC EID." Centers for Disease Control and Prevention. 1 Jan. 2009. Web. 10 May 2010..
Dictionary.com|Find the Meanings and Definitions of Words at Dictionary.com. Web. 10 May 2010..
When a person ingests food borne botulism toxin signs will appear within approximately 12-36 hours. The main symptoms of food borne botulism are: double vision, drooping eyelids, difficulty swallowing, dry mouth, distorted voice which causes difficulty in speaking, muscle weakness which may move down the body, typically shoulders first, upper arms, lower arms, thighs, and calves. Additionally, the paralysis can cause breathing problems which can ultimately cause the person to die.
"CDC Botulism | Clinical Description." CDC Emergency Preparedness & Response Site. 14 June 2006. Web. 10 May 2010.
"CDC | Facts About Botulism." CDC Emergency Preparedness & Response Site. 14 Oct. 2001. Web. 10 May 2010.
Vugia, Duc J. "Botulism from Drinking Pruno|CDC EID." Centers for Disease Control and Prevention. 1 Jan. 2009. Web. 10 May 2010.
Dictionary.com|Find the Meanings and Definitions of Words at Dictionary.com. Web. 10 May 2010.
Yersinia pestis in bobcats and pumas
Yersinia pestis is a causative agent of plague in mammals. Y. pestis is a group A bioterroism agent causes zoonotic disease transmitted to humans through flea bites, usually appear swollen and tender. Domestic cats are a high source of human plaque infections in North America, which puts pet owners and veterinarians at risk for Y. pestis infections. Twelve cases of transmission of plaque from nondomestic animals have been reported, including direct contact with puma which eventually resulted in death.
Pumas and bobcats are the most widepsread felids in U.S. because the distance they travel. They both may reintroduce Y. pestis positive fleas into distant regions which can greatly contribute to the spread of the plague. The study collected samples from both bobcats and pumas in western United States to analyze for Y.pestis antibody using hemagglutination assay. 17.7% had Y.pestis.Geographic location, capture season, and age were significant factors to the percentage. Colorado had 38% positive animals, whereas California had limited plague seroreactivity of 2.2% of animals tested positive for plague exposure. Death caused by plagues have been documented in wild felids and still remains a concern for vets and hunters.
Bevins SN, Tracey JA, Franklin SP, Schmit VL, MacMillan ML, Gage KL, et al, "Wild felids as hosts for human plague, western United States"Emerging Infectious Diseases,December,2009,
Drancourt M, Roux V, Dang LV, Tran-Hung L, Castex D, Chenal-Francisque V, et al,"Genotyping, Orientalis-like Yersinia pestis, and plague pandemics" Emerging Infectious Disease,September 2004,
Pumas and bobcats are the most widepsread felids in U.S. because the distance they travel. They both may reintroduce Y. pestis positive fleas into distant regions which can greatly contribute to the spread of the plague. The study collected samples from both bobcats and pumas in western United States to analyze for Y.pestis antibody using hemagglutination assay. 17.7% had Y.pestis.Geographic location, capture season, and age were significant factors to the percentage. Colorado had 38% positive animals, whereas California had limited plague seroreactivity of 2.2% of animals tested positive for plague exposure. Death caused by plagues have been documented in wild felids and still remains a concern for vets and hunters.
Bevins SN, Tracey JA, Franklin SP, Schmit VL, MacMillan ML, Gage KL, et al, "Wild felids as hosts for human plague, western United States"Emerging Infectious Diseases,December,2009,
Drancourt M, Roux V, Dang LV, Tran-Hung L, Castex D, Chenal-Francisque V, et al,"Genotyping, Orientalis-like Yersinia pestis, and plague pandemics" Emerging Infectious Disease,September 2004,
Saturday, May 8, 2010
Methicillin- Resistant staphylococcus aureus in pultury
Methicillin resistant stapyloccocus aureus (MRSA) is a staph bacteria that does not react to certain antibiotics usually causes skin infection but can also cause other infections.MRSA can be fatal.MRSA is resistant to antibiotics including methicillin, oxacillin, penicillin, and amoxicillin. These skin infections can be spread by kin to skin contact , sharing or touching a person personal item with someone infected, or touching a surface that has been in contact with someone with MRSA.
This study was done to determine if MRSA was present in pultury. There was a random selection of farms in Belgium and at each farm there was 5 laying hens sampled and 5 broiler chickens sampled. 10 farms for laying hens and 14 farms for the broiler chickens. The samples were taken from cloaca and nasal cavity. There were many tests ran on these samples. Of all the samples MRSA was not isolated from any of the laying hens. which can either mean that is just isnt present of the laying hen or that it is but in very low numbers. MRSA was isolated from 8 broiler chicken from only 2 of the 14 farms, a relativly low number. Between the nasal and cloaca amples a total of 15 MRSA isolations were found. Of all the 15 isolated they all showed resistant to 7 drugs and suseptible to 7 drugs.Molecular typing showed that all the samples were found to be spa type t1456.
Persoons D, Van Hoorebeke S, Hermans K, Butaye P, de Kruif A, Haesebrouck F, et al. Methicillin-resistant Staphylococcus aureus in poultry. Emerg Infect Dis [serial on the Internet]. 2009 Mar [date cited]. Available from http://www.cdc.gov/EID/content/15/3/452.htm
Healthcare associated methicillin restistant staphylococcus aureus (HA- MRSA) March 3, 2010 http://www,cdc.gov/ncidod/dhqplar_mrsa.html
This study was done to determine if MRSA was present in pultury. There was a random selection of farms in Belgium and at each farm there was 5 laying hens sampled and 5 broiler chickens sampled. 10 farms for laying hens and 14 farms for the broiler chickens. The samples were taken from cloaca and nasal cavity. There were many tests ran on these samples. Of all the samples MRSA was not isolated from any of the laying hens. which can either mean that is just isnt present of the laying hen or that it is but in very low numbers. MRSA was isolated from 8 broiler chicken from only 2 of the 14 farms, a relativly low number. Between the nasal and cloaca amples a total of 15 MRSA isolations were found. Of all the 15 isolated they all showed resistant to 7 drugs and suseptible to 7 drugs.Molecular typing showed that all the samples were found to be spa type t1456.
Persoons D, Van Hoorebeke S, Hermans K, Butaye P, de Kruif A, Haesebrouck F, et al. Methicillin-resistant Staphylococcus aureus in poultry. Emerg Infect Dis [serial on the Internet]. 2009 Mar [date cited]. Available from http://www.cdc.gov/EID/content/15/3/452.htm
Healthcare associated methicillin restistant staphylococcus aureus (HA- MRSA) March 3, 2010 http://www,cdc.gov/ncidod/dhqplar_mrsa.html
Immunological response of unvaccinated wool factory workers to Anthrax
Recently there was a study performed to determine immunological reactivity to Baccillus anthrax antigens. To accomplish this task scientists conducted serological testing of workers in a factory that performed scouring of wool and goal hair. During 19th and early 20th centuries industrial anthrax was a serious threat when the wool industry was flourishing. Anthrax is a zoonotic desease caused by the spore-forming bacterium Bacillus anthracis. Its spores remain viable in the environment for years, therefore it represents a potential source of infection. The spores of B. anthracis were brought into wool factories with the organic matter that was contaminating the animal fibers. A skin contact with contaminated products from infected animals leads to cutaneous anthrax, the most common type of naturally acquired anthrax infection. In addition, it could also cause a respiratory disease through inhalation of sporulated anthrax.
Today, cases of human anthrax have more rare in Europe, although sometimes can result from contact with imported contaminated materials. In the United States, the most recent and widespread human anthrax epidemic was reported in 1957 in a large goat hair-processing mill in Manchester, New Hampshire. In the most recent study, a Belgium factory, that processes and scours wool and goat hair from all over the world, was inspected and a living anthrax spores were found in goat hair fibers, air dust, and uprocesses wastewater produced from goat hair scouring. At this factroy blood samples were obtained from 66 factory workers and after serological testing that was carried out at 2 time points 6 workers tested positive for having IgG antibodies present.
This study revieled that despite some progess that was made in improving the biological safety of the industrial prodessing of wool and goat hair, Bacillus anthracis still poses a health risk to modern wool workers. In addition, anthrax vaccines that could provide long-term immunity of both the humoral and cellular type, and would be highly desirable for protection of persons working with animal products, are not yet available for the general public.
Web source citations:
Patrick J. Meehan, M.D, "Responding to Detection of Aerosolized Bacillus anthracis by Autonomous Detection Systems in the Workplace" MMWR, April, 2004,.
Pierre Wattiau, "Immunologic Response of Unvaccinated Workers Exposed to Anthrax, Belgium" Emerging Infectious Diseases, October, 2009,.
Today, cases of human anthrax have more rare in Europe, although sometimes can result from contact with imported contaminated materials. In the United States, the most recent and widespread human anthrax epidemic was reported in 1957 in a large goat hair-processing mill in Manchester, New Hampshire. In the most recent study, a Belgium factory, that processes and scours wool and goat hair from all over the world, was inspected and a living anthrax spores were found in goat hair fibers, air dust, and uprocesses wastewater produced from goat hair scouring. At this factroy blood samples were obtained from 66 factory workers and after serological testing that was carried out at 2 time points 6 workers tested positive for having IgG antibodies present.
This study revieled that despite some progess that was made in improving the biological safety of the industrial prodessing of wool and goat hair, Bacillus anthracis still poses a health risk to modern wool workers. In addition, anthrax vaccines that could provide long-term immunity of both the humoral and cellular type, and would be highly desirable for protection of persons working with animal products, are not yet available for the general public.
Web source citations:
Patrick J. Meehan, M.D, "Responding to Detection of Aerosolized Bacillus anthracis by Autonomous Detection Systems in the Workplace" MMWR, April, 2004,
Pierre Wattiau, "Immunologic Response of Unvaccinated Workers Exposed to Anthrax, Belgium" Emerging Infectious Diseases, October, 2009,
Friday, May 7, 2010
Melioidosis in a Tropical City State, Singapore
Melioidosis is an infectious disease of humans and animals caused by gram-negative bacillus found in soil and water. The causative agent for Melioidosis is Pseudomonas pseudomallei. This disease is endemic in Southeast Asia and parts of Africa. It was rare in the United States prior to recent immigration from Southeast Asia. Melioidosis is a huge public health issue because it is most common in AIDS patients and intravenous drug users.
The organism enters the body through skin abrasions, burns or wounds which are contaminated by the soil, inhalation of dust or eating food that is contaminated with P.pseudomallei. Person-to-person transmission is unusual. The incubation period is two to three days. Diagnosis should be confirmed through laboratory tests. P.pseudomallei can be cultured from patient’s blood, sputum or tissue from abscesses. There is no form of vaccine for melioidosis. Prevention requires prompt cleansing of scrapes, burns, or other areas where the disease is common and avoidance of needle sharing among drug addicts.
Melioidosis can mimic many other diseases because it can affect almost any organ. A misdiagnosis could be fatal. P.pseudomallei is susceptible to a certain amount of antibiotics. There are endemic areas where melioidosis is an important cause of illness and death in humans and animals. In 1975, a Panda introduced melioidosis to the Paris Zoo. This caused a severe outbreak. The epidemic spread to other zoos in Paris. It wiped out zoo populations and caused two human deaths. Due to this, there are fears that P.pseudomallei could be used as a biological weapon.
Melioidosis is rising as a serious public health problem in many countries. In Singapore the case-fatality rate of melioidosis has decreased. However, it has the potential to come back with adverse climate events such as heavy rainfall and flash floods.
Works Cited:
Lo TJ, Ang LW, James L, Goh KT. Melioidosis in a tropical city state, Singapore. Emerg Infect Dis [serial on the Internet] 2009 Oct [date cited] Available from http://www.cdc.gov/EID/content/15/10/1645.htm
Barnes JL, Ketheesan N. Route of infection in melioidosis. Emerg Infect Dis [serial on the Internet]. 2005 Apr [date cited]. Available from http://www.cdc.gov/ncidod/EID/vol11no04/04-1051.htm
The organism enters the body through skin abrasions, burns or wounds which are contaminated by the soil, inhalation of dust or eating food that is contaminated with P.pseudomallei. Person-to-person transmission is unusual. The incubation period is two to three days. Diagnosis should be confirmed through laboratory tests. P.pseudomallei can be cultured from patient’s blood, sputum or tissue from abscesses. There is no form of vaccine for melioidosis. Prevention requires prompt cleansing of scrapes, burns, or other areas where the disease is common and avoidance of needle sharing among drug addicts.
Melioidosis can mimic many other diseases because it can affect almost any organ. A misdiagnosis could be fatal. P.pseudomallei is susceptible to a certain amount of antibiotics. There are endemic areas where melioidosis is an important cause of illness and death in humans and animals. In 1975, a Panda introduced melioidosis to the Paris Zoo. This caused a severe outbreak. The epidemic spread to other zoos in Paris. It wiped out zoo populations and caused two human deaths. Due to this, there are fears that P.pseudomallei could be used as a biological weapon.
Melioidosis is rising as a serious public health problem in many countries. In Singapore the case-fatality rate of melioidosis has decreased. However, it has the potential to come back with adverse climate events such as heavy rainfall and flash floods.
Works Cited:
Lo TJ, Ang LW, James L, Goh KT. Melioidosis in a tropical city state, Singapore. Emerg Infect Dis [serial on the Internet] 2009 Oct [date cited] Available from http://www.cdc.gov/EID/content/15/10/1645.htm
Barnes JL, Ketheesan N. Route of infection in melioidosis. Emerg Infect Dis [serial on the Internet]. 2005 Apr [date cited]. Available from http://www.cdc.gov/ncidod/EID/vol11no04/04-1051.htm
Saturday, May 1, 2010
Avian Influenza Virus A (H7N3) in Domestic Poultry, Saskatchewan, Canada, 2007
A highly pathogenic strain of Virus A was isolated from domestic poultry after an outbreak of infection and death among the hen and rooster population at a local farm barns in Regina Beach, Saskatchewan. At one barn, over two-thirds of the rooster population was dead within a couple days of noticed outbreak.
The birds were sampled and the samples sequenced and compared to known strains of the pathogen. After a successful test using RT-PCR assays revealed the identity of the agent as the H7N3 avian flu virus. Subsequently, epidemiological testing suggested of transmission of the virus through wild water birds from nearby natural body of water. Serological testing pointed out antibodies against the avian virus. In addition, phylogenetic analysis seemed to prove the hypothesis that the strain was transmitted from a wild bird of Anseriformes or Charadriiformes.
Influenza virus A belongs to the family Orthomyxoviridae with 16 HA and 9 NA subtypes currently identified. The H7N3 strain specifically targets avian creatures, but human subjects infected with the virus also occur, but are much less common.
One of the possible modes for human infections with the H7N3 results from handling of infected poutry.
Citations
Berhane Y, Hisangaga T, Kehler H, Neufeld J, Manning L, Argue C, et al. Highly pathogenic avian influenza virus A (H7N3) in domestic poultry, Saskatchewan, Canada, 2007. Emerging Infection Diseases. http://www.cdc.gov/EID/content/15/9/1492.htm
Belser J, Bridges C, Katz J, and Tumpey T, "Past, Present, and Possible Future Human Infection with Influenza Virus A Subtype H7." Emerging Infectious Diseases. June 2009. http://www.cdc.gov/EID/content/15/6/pdfs/859.pdf
Morgan O, Kuhne M, Nair P. "Personal Protection Equipment and Risk for Avian Influenza (H7N3)." Emerging Infectious Diseases. January 2009. http://www.cdc.gov/eid/content/151/1/59.htm
The birds were sampled and the samples sequenced and compared to known strains of the pathogen. After a successful test using RT-PCR assays revealed the identity of the agent as the H7N3 avian flu virus. Subsequently, epidemiological testing suggested of transmission of the virus through wild water birds from nearby natural body of water. Serological testing pointed out antibodies against the avian virus. In addition, phylogenetic analysis seemed to prove the hypothesis that the strain was transmitted from a wild bird of Anseriformes or Charadriiformes.
Influenza virus A belongs to the family Orthomyxoviridae with 16 HA and 9 NA subtypes currently identified. The H7N3 strain specifically targets avian creatures, but human subjects infected with the virus also occur, but are much less common.
One of the possible modes for human infections with the H7N3 results from handling of infected poutry.
Citations
Berhane Y, Hisangaga T, Kehler H, Neufeld J, Manning L, Argue C, et al. Highly pathogenic avian influenza virus A (H7N3) in domestic poultry, Saskatchewan, Canada, 2007. Emerging Infection Diseases. http://www.cdc.gov/EID/content/15/9/1492.htm
Belser J, Bridges C, Katz J, and Tumpey T, "Past, Present, and Possible Future Human Infection with Influenza Virus A Subtype H7." Emerging Infectious Diseases. June 2009. http://www.cdc.gov/EID/content/15/6/pdfs/859.pdf
Morgan O, Kuhne M, Nair P. "Personal Protection Equipment and Risk for Avian Influenza (H7N3)." Emerging Infectious Diseases. January 2009. http://www.cdc.gov/eid/content/151/1/59.htm
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