"Tomfoolery"

The term "tomfoolery" originated from the phrase "Tom Fool," a generic name for a jester or buffoon that appeared in the Middle Ages. The word "tomfoolery" itself emerged in the early 19th century, combining "Tom Fool" with the "-ery" suffix, to describe foolish or playful behavior. Some sources suggest a potential real-life inspiration for the phrase "Tom Fool" was Thomas Skelton, a 16th-century jester at Muncaster Castle. 



• Middle Ages: "Tom Fool" was a common, generic name used to represent a foolish or jester-like person. Early written examples from the 14th century include "Thom Foole."
• By the 17th century "Tom Fool" became an established name for a buffoon or clown.
• 19th Century: The word "tomfoolery" was first recorded in the 1810s, with the Oxford English Dictionary crediting Horatio Smith in 1812. It evolved to describe the act of foolish or silly behavior, rather than a person. 

Recent Outbreak of

NDM Carbapenemase

Hardy Diagnostics was recently alerted by one of our customers in the Western United States that they are seeing an outbreak of New Delhi Metallo-beta-lactamase (NDM) Pseudomonas aeruginosa. NDM is typically a less common carbapenemase in the United States, but concerning because it can be resistant to even more antibiotics than KPC (1). Hardy Diagnostics is the exclusive distributor in the U.S. of the NG-Test® CARBA 5. CARBA 5 which offers rapid detection and differentiation of the "Big 5" Carbapenemases produced by Enterobacterales and Pseudomonas aeruginosa. CARBA 5 results are seen on the small lateral flow assay cassette in just 15 minutes, with no equipment required. CARBA 5 is more economical than PCR and, unlike molecular methods, CARBA 5 detects the bacterial gene expression, which is crucial to aiding therapeutic decisions. In addition, Hardy is now offering a complimentary product for the detection of CTX-M enzymes in ESBL producing Gram negatives. Other related chromogenic plated media products would include HardyCHROM CRE and HardyCHROM ESBL. Hardy Diagnostics is pleased to provide you with free sample kits - just let us know.

Reference: 1

300,000 infected in the U.S.

Chagas disease, also known as the “kissing bug” disease, has long been considered a rare but underreported parasitic illness in the United States. (1) However, the CDC is now proposing that it be reclassified as endemic due to growing evidence of its presence, primarily in southern states. This renewed interest will support improved surveillance, research, and public health response. (2)

Chagas disease is caused by the parasite Trypanosoma cruzi (T. cruzi), which is transmitted by the triatomine bug (top photo) that bites near the mouth or eyes when a person is asleep, hence the nickname “kissing bug.” The infection occurs when the bug’s feces enter the body though the bite site. (1, 3, 4)

Chagas disease can also be spread by:

• Consuming contaminated food.
• Being born to a person infected with the parasite.
• Receiving infected donor blood or organs.
• Exposure to the parasite while working in a lab.
• Spending time in areas where there are infected wild animals, such as raccoons and opossums.

An estimated 300,000 people in the United States live with Chagas disease. Most of these cases (~97%) have been attributed to individuals who were infected in Latin America, where the disease is considered endemic. However, T. cruzi DNA has been found in 1,000-year-old human remains from Texas, indicating that Chagas disease has existed in the United States for a very long time. Modern housing features, such as sealed windows, intact screens, and air conditioning, reduce exposure to the insect vector. (1)

A recent systematic literature review indicated that locally acquired (autochthonous) cases have been reported in southern states, particularly Texas, where insect vectors, wildlife, domestic animals, and humans have tested positive for infection. Consequently, the CDC is proposing that Chagas disease is relabeled as endemic in the United States. (2)

Chagas disease remains much more prevalent in Central and South America and Mexico. Living in these regions increases the risk of infection due to limited use of air conditioning and unsealed housing. Rural homes with mud walls and/or thatched roofs provide ideal conditions for triatome bugs to thrive. (1, 4)

Chagas disease can present as an acute infection or progress into a chronic condition. Both stages can be asymptomatic or can result in life-threatening symptoms. The trypomastigotes can be found in blood, spinal fluid, and other organ tissues. (3, 4) Acute phase symptoms can include:

• Swelling at the infection site
• Fever
• Tiredness
• Rash
• Body aches
• Eyelid swelling
• Headache
• Loss of appetite
• Nausea, diarrhea or vomiting
• Swollen glands
• A larger liver or spleen

Although acute symptoms often resolve on their own, the parasite remains in the body and may progress to chronic disease. The chronic phase may remain silent or symptoms may appear 10-20 years after the infection. (3, 4) These symptoms may include:

• Irregular heartbeat
• Heart failure
• Sudden cardiac arrest
• Trouble swallowing
• Stomach pain or constipation

Antiparasitic treatment is available during the early phase, while later treatment focuses on managing chronic complications. Most importantly, preventing contact with the “kissing bug” is the best way to reduce the risk of Chagas disease. (2)

References: 1, 2, 3, 4.

By Julie Tripp   

Technical Services Specialist II

Hardy Diagnostics

The Lyme Wars Continue

Borrelia burgdorferi, the spirochete responsible for Lyme disease (seen in the blood smear above), is typically treatable with standard antibiotics. Yet, a reported 14% of patients still experience chronic symptoms—fatigue, joint pain, cognitive fog— often lasting months or longer post-treatment. (1)

In the late 1990s, armed with limited understanding of the illness, agencies such as the Centers for Disease Control and Prevention (CDC) and Infectious Disease Society of America (IDSA) rejected persistent infection as the cause of chronic symptoms in treated patients. Instead, they described it as Post-Treatment Lyme Disease Syndrome (PTLDS), a vague label for unexplained symptoms lasting over six months post-infection. The broad definition and complexity of diagnosis led to the syndrome often being misattributed to other conditions, such as depression or fibromyalgia. This sparked a period known as the “Lyme Wars,” where patient advocates such as the International Lyme and Associated Diseases Society contested the guidelines from IDSA and CDC. (2)

In recent years, the COVID-19 pandemic has shifted the narrative and highlighted how certain infections can lead to a prolonged post-acute syndrome, such as in "Long COVID." Increased attention to long COVID renewed interest in other post-infection syndromes, including PTLDS. This similarity in symptom patterns prompted institutions like the NIH to increase funding for investigations on PTLDS. Research in this field has focused on determining possible mechanisms, determining risk factors, and symptom management. (3)

While the mechanisms behind PTLDS remains under investigation, one of the major factors appears to be pathogenic debris that remains after the infection with B. burgdorferi is treated (usually with doxycycline, amoxicillin, or cefuroxime). A unique peptidoglycan found in the cell wall of this organism can linger in host tissues for weeks or months following treatment. In some individuals, this cellular debris can trigger a chronic inflammatory response from the host’s immune system, leading to symptoms associated with PTLDS. (4) Future treatments may include targeting the host inflammatory pathways associated with this response.



The story of PTLDS highlights the importance of scientific rigor, careful interpretation of emerging evidence, and meaningful patient advocacy when navigating complex, poorly understood syndromes.

References: 1, 2, 3, 4

By Manuel Escalera

Technical Services Instrumentation Specialist I 

Hardy Diagnostics

NG Biotech CTX-M for Rapid Detection of ESBL's

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