Skin Biome Diagram

~Content Source – Wikipedia

Skin Biome Diagram

Actinobacteria are a group of Gram-positive bacteria with high guanine and cytosine content in their DNA, which can be terrestrial or aquatic. Though they are unicellular like bacteria, they do not have distinct cell wall, but they produce a mycelium that is nonseptate and more slender.

Proteobacteria is a major phylum of Gram-negative bacteria. They include a wide variety of pathogens, such as Escherichia, Salmonella, Vibrio, Helicobacter, Yersinia, Legionellales and many other notable genera. Others are free-living (non-parasitic) and include many of the bacteria responsible for nitrogen fixation.

Cyanobacteria also known as Cyanophyta, are a phylum of bacteria that obtain their energy through photosynthesis and are the only photosynthetic prokaryotes able to produce oxygen. The name cyanobacteria comes from the color of the bacteria.

Bacteroidetes are gram-negative bacteria that ferment polysaccharides and otherwise indigestible carbohydrates and produce short-chain fatty acids (SCFAs) that have many beneficial effects in the gut. 

Ascaris suum, an Intestinal Parasite, Produces Morphine

~Content Source-The Journal of Immunology-J Immunol July 1, 2000, 165 (1) 339-343; DOI:


The parasitic worm Ascaris suum contains the opiate alkaloid morphine as determined by HPLC coupled to electrochemical detection and by gas chromatography/mass spectrometry. The level of this material is 1168 ± 278 ng/g worm wet weight. Furthermore, Ascaris maintained for 5 days contained a significant amount of morphine, as did their medium, demonstrating their ability to synthesize the opiate alkaloid. To determine whether the morphine was active, we exposed human monocytes to the material, and they immediately released nitric oxide in a naloxone-reversible manner. The anatomic distribution of morphine immunoreactivity reveals that the material is in the subcuticle layers and in the animals’ nerve chords. Furthermore, as determined by RT-PCR, Ascaris does not express the transcript of the neuronal μ receptor. Failure to demonstrate the expression of this opioid receptor, as well as the morphine-like tissue localization in Ascaris, suggests that the endogenous morphine is intended for secretion into the microenvironment.

Successful parasitism, in which the host survives for extended periods, can be characterized as an equilibrium between the parasite and the host, more specifically between the host’s immune system and the parasite’s ability to create a permissive microenvironment in situ. One mechanism that a parasite may use to modify the host immune response is to down-regulate the host’s response (123). Capron and colleagues (4567) suggested that parasites may communicate with their hosts via common signaling molecules that diminish host immune surveillance. In this regard, morphine is generally acknowledged as an immune down-regulating agent (8). This finding is enhanced by the fact that morphine is present in several mammalian tissues, including brain and adrenal gland (91011121314151617181920), supporting its role as a neural or inflammatory mediator.

Recently, we have demonstrated that free-living and parasitic invertebrates produce several major opioid peptide precursors, i.e., prodynorphin, proopiomelanocortin, and proenkephalin (21). These mammalian-like opioid peptides exhibit high sequence identity to their mammalian counterparts. For example, Mytilus adrenocorticotropin has greater than 90% sequence identity with its mammalian counterpart (21). We have also identified a tentative morphine-like molecule in Schistosoma mansoni by way of radioimmunoassay (22).

Given this and the fact that the pig intestinal parasite Ascaris suum can live in its host for extended periods of time, we surmised that it might be using morphine to escape detection by the host’s immune system. In this study, we report for the first time that A. suum synthesizes morphine, thereby strengthening the common-signal molecule hypothesis, i.e., using either similar or identical host signaling to escape host immunosurveillance.

What if?-2019.06.24-Strange Day

Almost 2 years into this different life.

What if…It’s not us sticking our dirty fingers in our mouth that [possibility]make us sick, but our fingers become dirty, under the nails and cracks etc., from sticking them in our ears, nose and mouth?

I ask this because I have been rather shocked to see that my digital health has improved DRASTICALLY since I quit, with GREAT intentionality, sticking my fingers in my ears, nose and mouth.

The reason I started this practice was to eliminate any possibility of auto-infection of any sort happening.


Strongyloides hyper-infection causing life-threatening gastrointestinal bleeding

~Content Source

In hyper-infection syndrome, complete disruption of the GI mucosa, ulcerations, paralytic ileus with exudative enteropathy as well as massive GI bleeding may also occur due to the direct invasion of the larvae. Profound diarrhea, malabsorption with consequent hypo-albuminemia and electrolyte disturbances were all consistent with hyper-infection related enteropathy in our patient. On the other hand, effective anthelminthic treatment in hyper-infected patients can lead to mass-destruction of intraluminal and intramural larvae and to release of huge amounts of different toxic inflammatory and vaso-active compounds[7,8].

Transmission of Strongyloides stercoralis Through Transplantation of Solid Organs

What is added by this report?

Donor-derived Strongyloides infection might be more common than previously believed. In these investigations, a single donor was the source of infection for three of four organ recipients. Testing of pretransplant serum contributed to the determination that infection was donor derived.

Strongyloides stercoralis is an intestinal nematode endemic in the tropics and subtropics. Immunocompetent hosts typically are asymptomatic, despite chronic Strongyloides infection. In contrast, immunocompromised patients are at risk for hyperinfection syndrome and disseminated disease, with a fatality rate >50% (1–3)The infection source for immunocompromised patients, such as solid organ transplant recipients, is not always apparent and might result from reactivation of chronic infection after initiation of immunosuppressive therapy or transmission from the donor. In October 2012, the United Network for Organ Sharing (UNOS) notified CDC of a left kidney and pancreas recipient in Pennsylvania diagnosed with strongyloidiasis. This report summarizes the results of the investigation of the source of Strongyloides infection in three of four organ recipients. Testing of pretransplant donor and recipient sera confirmed that infection in the recipients was donor derived. This investigation underscores the importance of prompt communication between organ procurement organizations, transplant centers, and public health authorities to prevent adverse events in recipients when transmission is suspected. Additionally, it emphasizes the utility of stored pretransplant samples for investigation of suspected transplant-transmitted infections and the need to consider the risk for Strongyloides infection in organ donors.

Case Investigation

On October 4, 2012, UNOS notified CDC of a left kidney and pancreas transplant recipient diagnosed with strongyloidiasis. UNOS also identified three additional organ recipients: the right kidney recipient, who received his transplant at the same institution as the index case; the liver recipient, who died within a few days after the transplantation; and the heart recipient, who was diagnosed with suspected reactivation of chronic strongyloidiasis 2 weeks earlier. CDC requested stored pretransplant serum from all organ recipients, along with stored donor serum for testing, to determine if infection with Strongyloides in the recipients was donor derived or reactivation of chronic infection. Evaluation of these specimens revealed that no recipient had detectable Strongyloidesantibody before transplantation, but the donor had evidence of chronic infection based on positive serologic results.

Organ donor. In July 2012, a Puerto Rico-born Hispanic man, aged 24 years, was admitted to a local emergency department with multiple gunshot wounds. After a 9-day hospitalization, he died, and his heart, kidneys, pancreas, and liver were transplanted into four recipients the next day. History obtained from his mother indicated that the donor was a healthy young male who often visited Puerto Rico. Strongyloides infection risk was not considered; therefore, testing was not performed before organ recovery.

Kidney and pancreas recipient. This recipient is a U.S.-born white man, aged 64 years, with end-stage renal disease secondary to long-standing diabetes mellitus who had never traveled outside the United States. Nine weeks posttransplant, he developed severe nausea, anorexia, and abdominal distention and was admitted to the hospital. Stool studies and biopsies performed during an esophagogastroduodenoscopy revealed S. stercoralis adult worms; larvae were found in urine studies. The patient was treated with ivermectin and albendazole, and after a hospitalization complicated by Enterobacter cloacae bacteremia, periduodenal abscess, and loss of pancreatic transplant function, he was discharged in stable condition on ivermectin. Repeat stool analyses were negative 3 days after starting therapy.

Kidney recipient. This recipient is a U.S.-born adolescent, aged 14 years, with end-stage renal disease as a result of a single dysplastic kidney; he had never traveled outside the United States. He was contacted for evaluation 10 weeks posttransplant, after the left kidney and pancreas recipient received a diagnosis of strongyloidiasis. He was discovered to be ill with fever, rash, malaise, anorexia, nausea, vomiting, and diarrhea. He was diagnosed with strongyloidiasis via esophagogastroduodenoscopy-obtained biopsy and stool testing. He was treated with ivermectin for 4 weeks and albendazole for 2 weeks. Repeat stool specimens were negative 3 days after starting therapy and remained negative as of November 2012.

Liver recipient. This recipient was a Hispanic man, aged 66 years, with a history of hepatic failure secondary to chronic hepatitis C infection. He tolerated surgery and was clinically stable until postoperative day 4, when his heart stopped and he was unresponsive to attempts at resuscitation. At autopsy, no evidence of Strongyloides infection was found; cause of death was undetermined.

Heart recipient. This recipient was a U.S.-born Hispanic man, aged 59 years, with ischemic cardiomyopathy; he lived in Puerto Rico for 6 months as a teenager. He remained clinically stable posttransplant and was discharged 11 days after surgery. He experienced multiple episodes of organ rejection and was treated with high doses of steroids. Seven weeks posttransplant, he was readmitted to the hospital with fever and a respiratory illness and required intubation in response to rapid decompensation. He was diagnosed with a viral respiratory illness and given oseltamivir and antibiotic and antifungal medications. A bronchoscopy performed on hospital day 3 showed S. stercoralis larvaeHe was started on ivermectin and albendazole for treatment of suspected reactivated chronic strongyloidiasis. He developed gram-negative and enterococcal bacteremia and vancomycin-resistant enterococcal meningitis and became neurologically compromised. Life support was withdrawn, and he died 11 weeks posttransplant.

Reported by

Anjum Hasan, MD, Marie Le, MD, Jessica Pasko, MD, Karen A. Ravin, MD, Geisinger Medical Center; Heather Clauss, MD, Temple Univ Hospital; Richard Hasz, MFS, Gift of Life Donor Program; Elizabeth A. Hunt, MPH, Pennsylvania Dept of Health. Elizabeth Bosserman, MPH, Isabel McAuliffe, MS, Susan P. Montgomery, DVM, Div of Parasitic Diseases and Malaria, Center for Global Health; Matthew J. Kuehnert, MD, Susan N. Hocevar, MD, Div of Healthcare Quality Promotion, National Center for Emerging and Zoonotic Infectious Diseases; Francisca Abanyie, MD, EIS Officer, CDC. Corresponding contributor: Francisca Abanyie,, 404-718-4775.

Editorial Note

Most Strongyloides infections in organ transplant recipients are thought to be caused by reactivation of chronic infection after initiation of immunosuppressive therapy. Donor-derived infection has been reported, but the incidence of transmission is unknown (4,5). During 2009–2012, CDC assisted in seven investigations of organ donors and associated recipients with strongyloidiasis determined to be donor derived. Donor-derived infection is difficult to prove, especially if the infected recipient is from a region in which Strongyloides is endemic. Archived pretransplant serum samples were available for recipient testing in this investigation. Results of that testing contributed to the determination that infection was donor derived and not reactivated chronic infection in the recipients.

This investigation revealed several gaps in current understanding and assessment of the risk for transplant-transmitted strongyloidiasis. Specific recommendations are lacking for Strongyloides testing of organ donors from areas in which it is endemic. The parasitic infections sections of the American Society for Transplantation’s guidelines for screening prior to solid organ transplantation recommend testing donors and recipients for Toxoplasma and Trypanosoma cruzi (the cause of Chagas disease), but only recommend screening for Strongyloides in recipients from areas in which the nematodes are endemic, with no mention of donor screening (6,7). These guidelines are not policy, thus screening of donors and recipients for parasitic infections is voluntary, resulting in varied practices among organ procurement organizations and transplant centers based on the perceived risk in their respective patient populations. The growing evidence of transplant transmission of Strongyloides, reported here and in the recent literature, might support development of recommendations for specific testing of donors and recipients from endemic regions to prevent severe strongyloidiasis in recipients (1,4,5). A minimum of three serial stool examinations for larvae, using specialized concentration techniques, is the gold standard for diagnosis of Strongyloides infection, but this might not be feasible in patients who have poor gastrointestinal function or are brain dead. Tests to detect parasite-specific antibody, such as an enzyme-linked immunoassay, also are available and are valuable in identifying Strongyloides infection (8). If infection is confirmed in the donor, prophylaxis could be given to recipients to avert adverse outcomes.

Rapid communication among transplant centers with patients who received organs from a single donor also is essential. The Organ Procurement and Transplant Network encourages organ procurement organizations and transplant programs to communicate promptly through its Patient Safety System, especially when there is concern for potential transmission of disease or medical conditions to the organ recipient from the donor. Such communication ideally should occur within 24 hours after knowledge of or concern for transmission, because multiple recipients might be adversely affected (9).

This investigation illuminates two gaps that need to be filled to improve transplant safety in solid organ recipients at risk for Strongyloides infection: 1) developing recommendations for screening of donors from Strongyloides-endemic areas, and 2) improving communication among transplant centers and organ procurement organizations. Advances in these areas might be life-saving for immunocompromised hosts.


Christine McGarry, Gift of Life Donor Program; Justine Gaspari, Milton S. Hershey Medical Center, Pennsylvania. Patricia Wilkins, PhD, Div of Parasitic Diseases and Malaria, Center for Global Health, CDC.


  1. Roxby AC, Gottlieb GS, Limaye AP. Strongyloidiasis in transplant patients. Clin Infect Dis 2009;49:1411–23.
  2. Cappello M, Hotez PJ. Intestinal nemaodes: Strongyloides stercoralis and Strongyloides fuelleborni. In: Long S, Pickering LK, Prober CG, eds. Principles and practice of pediatric infectious diseases. 3rd ed. Philadelphia, PA: Churchill Livingstone-Elsevier; 2008.
  3. CDC. Parasites—Strongyloides: resources for health professionals. Atlanta, GA: US Department of Health and Human Resources, CDC; 2012. Available at
  4. Hamilton KW, Abt PL, Rosenbach MA, et al. Donor-derived Strongyloides stercoralis infections in renal transplant recipients. Transplantation 2011;91:1019–24.
  5. Weiser JA, Scully BE, Bulman WA, Husain S, Grossman ME. Periumbilical parasitic thumbprint purpura: Strongyloides hyperinfection syndrome acquired from a cadaveric renal transplant. Transpl Infect Dis 2011;13:58–62.
  6. Fischer SA, Avery RK; AST Infectious Disease Community of Practice. Screening of donor and recipient prior to solid organ transplantation. Am J Transplant 2009;9(Suppl 4):S7–18.
  7. Anonymous. Screening of donor and recipient prior to solid organ transplantation. Am J Transplantation 2004;4(Suppl 10):10–20.
  8. Genta RM. Predictive value of an enzyme-linked immunosorbent assay (ELISA) for the serodiagnosis of strongyloidiasis. Am J Clin Path 1988;89:391–4.
  9. Organ Procurement and Transplantation Network. Identification of transmissible diseases in organ recipients. Rockville, MD: US Department of Health and Human Services, Health Resources and Services Administration, Organ Procurement and Transplantation Network; 2010. Available at .

Morbidity Associated with Chronic Strongyloides stercoralis Infection

~ Content Source

Strongyloides stercoralis, a worldwide-distributed soil-transmitted helminth, causes chronic infection which may be life threatening.

Limitations of diagnostic tests and nonspecificity of symptoms have hampered the estimation of the global morbidity due to strongyloidiasis. This work aimed at assessing S. stercoralis-associated morbidity through a systematic review and meta-analysis of the available literature. MEDLINE, Embase, CENTRAL, LILACS, and trial registries (WHO portal) were searched. The study quality was assessed using the Newcastle-Ottawa scale. Odds ratios (ORs) of the association between symptoms and infection status and frequency of infection-associated symptoms were calculated. Six articles from five countries, including 6,014 individuals, were included in the meta-analysis-three were of low quality, one of high quality, and two of very high quality. Abdominal pain (OR 1.74 [CI 1.07-2.94]), diarrhea (OR 1.66 [CI 1.09-2.55]), and urticaria (OR 1.73 [CI 1.22-2.44]) were associated with infection. In 17 eligible studies, these symptoms were reported by a large proportion of the individuals with strongyloidiasis-abdominal pain by 53.1% individuals, diarrhea by 41.6%, and urticaria by 27.8%. After removing the low-quality studies, urticaria remained the only symptom significantly associated with S. stercoralis infection (OR 1.42 [CI 1.24-1.61]). Limitations of evidence included the low number and quality of studies. Our findings especially highlight the appalling knowledge gap about clinical manifestations of this common yet neglected soil-transmitted helminthiasis. Further studies focusing on morbidity and risk factors for dissemination and mortality due to strongyloidiasis are absolutely needed to quantify the burden of S. stercoralis infection and inform public health policies.


~Because…Too many tabs…8-)

WORMBOOK <—Awesome Sause

Wormbook-History Page

A Collection of Conditions Transmitted by Insects or Ticks

The biology of Strongyloides spp. from WormBook: The Online Review of C. elegans Biology [Internet].

Strongyloides stercoralis: a model for translational research on parasitic nematode biology

Host-finding behavior of Strongy

Copper – Cu Toxicity

Strongyloidiasis Hyperinfection in a Patient with a History of Systemic Lupus Erythematosus

Circulating Non-Human Microfilaria in a Patient with Systemic Lupus ErythematosusSee Below

A 12-yr-old girl with systemic lupus erythematosus requiring steroid therapy was found to have a circulating microfilaria during an exacerbation of her illness. Morphologically, the microfilaria does not correspond precisely with any previously described species, though similarities exist between the patient’s microfilaria and those of Dipetalonema reconditum of the dog and D. interstitium of the grey squirrel. The organism reported here is probably an undescribed species from a wild mammal. Although the association may be merely coincidental, this case suggests that compromised immunity might have led to this unusual infection with a non-human filaria.

Copyright © 1978 by The American Society of Tropical Medicine and Hygiene

Antimicrobial Effects of Antipyretics


ABSTRACT: Antipyretics are some of the most commonly used drugs. Since they are often co-administered with antimicrobial therapy, it is important to understand the interactions between these two classes of drugs. Our review is the first to summarize the antimicrobial effects of antipyretic drugs and the underlying mechanisms involved. Antipyretics can inhibit virus replication, inhibit or promote bacterial or fungal growth, alter the expression of virulence factors, change the surface hydrophobicity of microbes, influence biofilm production, affect the motility, adherence, and metabolism of pathogens, interact with the transport and release of antibiotics by leukocytes, modify the susceptibility of bacteria to antibiotics, and induce or reduce the frequency of mutations leading to antimicrobial resistance. While antipyretics may compromise the efficacy of antimicrobial therapy, they can also be beneficial, for example, in the management of biofilm-associated infections, in reducing virulence factors, in therapy of resistant pathogens, and in inducing synergistic effects. In an era where it is becoming increasingly difficult to find new antimicrobial drugs, targeting virulence factors, enhancing the efficacy of antimicrobial therapy, and reducing resistance may be important strategies.

KEYWORDS: NSAIDs, ibuprofen, acetaminophen, paracetamol, antibacterial, antimicrobial, efflux pumps

Copper in the Textile Industry

~Content Source

Copper is an essential trace element that is vital to life. The human body normally contains copper at a level of about 1.4 to 2.1 mg for each kg of body weight; and since the body can’t synthesize copper, the human diet must supply regular amounts for absorption. The World Health Organization (WHO) suggests that 10-12 mg/day may be the upper safe limit consumption.

The fact that copper is essential to life is well known, but it’s also a toxic metal, and that toxicity, except for the genetic overload diseases, Wilson’s disease and hemochromatosis, is not so well known. Humans can become copper-toxic or copper-deficient, often because of “copper imbalance” (which can include arthritis, fatigue, insomnia, migraine headaches. depression, panic attacks, and attention deficit disorder).

Copper has been used for centuries for disinfection, and has been important around the world in technology, medicine and culture.

Is copper in the environment a health risk?

The answer to this question is complex. Copper is a necessary nutrient and is naturally occurring in the environment in rocks, soil, air, and water. We come into contact with copper from these sources every day but the quantity is usually tiny. Some of that copper, particularly in water, may be absorbed and used by the body. But much of the copper we come into contact with is tightly bound to other compounds rendering it neither useful nor toxic. It is important to remember that the toxicity of a substance is based on how much an organism is exposed to and the duration and route of exposure. Copper is bioaccumulative – there are many studies of copper biosorption by soils, plants and animals. But copper in the environment, (such as that in agricultural runoff, in air and soil near copper processing facilities such as smelters and at hazardous waste sites) binds easily to compounds in soil and water, reducing its bioavailability to humans. On the other hand, many children are born with excessive tissue copper (reason unknown), and one of the ways we are told to balance a copper imbalance is to reduce your exposure to sources of copper!

There are no studies on what this increased copper is doing to the environment. Copper is listed as an EPA Priority pollutant, a CA Air Toxic contaminant, and an EPA Hazardous air pollutant; it is also a Type II Moderate Hazard by the WHO Acute Hazard Ranking. There is NO DATA on its carcinogenity, whether it is a developmental or reproductive toxin or endocrine disruptor or whether it contaminates groundwater.

Today, because of its long use as a disinfectant and because it’s required for good health, many claims are being made about using copper in various products – including fabric. Copper-impregnated fibers have been introduced, which enables the production of anti-bacterial and self-sterilizing fabrics. These copper infused fabrics are marketed to be used in hospital settings to reduce infections, as an aid to help those suffering from asthma and allergies provoked by dust mites, and in socks to prevent athlete’s foot.

These copper impregnated fabrics are said to be safe, pointing to the low sensitivity of human tissue to copper, and because the copper is in a non-soluble form. Yet, that copper is safe because it is in a non soluble form was disproven by at least one study which tried to determine whether total copper or soluble copper was associated with gastrointestinal symptoms. It was found that both copper sulfate (a soluble compound) and copper oxide (insoluble) had comparable effects on these symptoms.