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Congenital Infections: TORCH

by Dr. Jaclynn Moskow

Pregnant woman cuddling her belly
By obtaining proper prenatal and perinatal care, pregnant women can optimize their chances of preventing, detecting, and treating congenital infections.

 

Congenital infections are caused by pathogens transmitted from a mother to her offspring during pregnancy or delivery. These infections can cause significant fetal and neonatal morbidity and mortality. The mnemonic “TORCH” is often used to refer to common congenital infections:

 

T – Toxoplasma

O – Other (Syphilis, Parvovirus B19, Varicella-Zoster, etc)

R – Rubella

C – CMV

H – Herpes Simplex Virus

 

Congenital Toxoplasmosis

Congenital toxoplasmosis is caused by the parasite Toxoplasma gondii. It can be acquired when a pregnant woman consumes raw or undercooked meat, or contacts contaminated water, soil, or cat feces (generally from outdoor cats that hunt.) The classic triad of congenital toxoplasmosis is 1) chorioretinitis 2) hydrocephalus and 3) cerebral calcifications. 

Symptoms often do not occur until months after birth and may include seizures, cognitive impairment, and cerebellar dysfunction (1). The retinal disease associated with congenital toxoplasmosis is progressive. Other clinical manifestations may include fever, rash, hydrocephalus or microcephaly, sensorineural hearing loss, congenital nephro­sis, hematologic abnormalities, hepatosplenomegaly, various endocrinopathies, and myocarditis. Infection can lead to spontaneous abortion, prematurity, stillbirth, and perinatal death. 

Congenital toxoplasmosis is more severe when acquired in early pregnancy. The incidence is highest in the Eastern Mediterranean and Africa (2). Rates are estimated at 1 per 3000-10000 live births in the United States (3) and 6.7 per 10000 live births in Europe – with 81% of all confirmed cases in the EU/EEA occurring in France (4). Spiramycin can decrease the risk of vertical transmission, but will not treat the fetus if the infection has already occurred. Infants born with this disease may benefit from pyrimethamine, sulfadiazine, and leucovorin. 

To help prevent infection, pregnant women should avoid consuming raw and undercooked meat, wear gloves when gardening, and avoid changing cat litter.

 

Congenital Rubella

Rubella, also known as “German measles,” is caused by the Rubella virus (Togaviridae family). It is most severe when acquired during the first trimester of pregnancy when the maternal infection will lead to fetal demise in 40-90% of cases (5). Congenital rubella can cause cardiac abnormalities, including patent ductus arteriosus and pulmonary artery stenosis. It can also cause ophthalmic abnormalities such as cataracts, glaucoma, retinopathy, and microphthalmia. Sensorineural deafness is common, and microcephaly, cognitive impairment, and meningoencephalitis may occur. Hepatosplenomegaly, hepatitis, hemolytic anemia, and thrombocytopenic purpura may also be observed. 

The incidence of congenital rubella has plummeted in countries that employ widespread vaccination. In recent times, documented cases of rubella in the United States are virtually all imported. Cases and outbreaks continue in Europe but at a very low rate. In 2008, 48% of all cases occurred in Southeast Asia and 38% in Africa (6). There is no effective treatment for congenital rubella.

 

Regional comparison of Congenital Rubella Syndrome prevalence, 1999 – 2019

Congenital infections - Congenital Rubella Syndrome prevalence: comparison between regions worldwide, 1999 - 2019

 

Congenital CMV

Congenital cytomegalovirus (CMV) is the most common congenital viral infection in the developed world. Clinical manifestations include sensorineural hearing loss, visual impairment, cerebral palsy, and cognitive difficulty. It can also cause neonatal cholestasis, pulmonary hypertension, and epilepsy. 10-20% of all hearing impairment in children is caused by congenital CMV (7).

CMV is identified in 5 to 7 per 1000 live births in the USA, Canada, Western Europe, and Australia; and 10-30 per 1000 live births in Latin America, Africa, and most Asian countries (8). Symptomatic infants may benefit from treatment with valganciclovir. It is difficult to prevent the acquisition of CMV, but some have suggested that pregnant women can decrease risk by avoiding contact with the saliva and urine of young children.

 

Congenital HSV

Congenital herpes simplex virus (HSV) most commonly occurs when an infant is exposed to the mother’s genital tract during delivery. Both herpes simplex-1 and herpes simplex-2 can cause congenital HSV. The risk of transmission from mother to infant depends primarily on when the maternal infection was acquired. When a mother is infected close to the time of delivery, the fetal infection rate is estimated at 25-60%. This rate drops to less than 2% when a mother is infected during the first half of pregnancy or earlier (9).

Signs of congenital HSV infection may occur between birth and six weeks of age. Disseminated disease may involve the liver, lung, central nervous system, and skin. “SEM disease” is limited to the skin, eyes, and/or mouth. Congenital HSV may cause a vesicular rash, hypothermia, lethargy, seizures, respiratory distress, hepatosplenomegaly, thrombocytopenia, hepatic dysfunction, cerebrospinal fluid pleocytosis, and sepsis. Congenital HSV is fatal in 50% of cases (10). The incidence of congenital HSV is estimated to be between 1 in 3000-20000 live births. All pregnant women should be tested for HSV, and those who are positive should receive prophylactic acyclovir or a similar drug at the time of delivery. Infected infants should be treated as well.

 

Congenital Syphilis

Congenital syphilis occurs when the bacterium Treponema pallidum is transmitted transplacentally or via the birth canal. The rate of vertical transmission increases as the pregnancy advances and transmission is more likely when the mother is experiencing early disease (11). Congenital syphilis can sometimes be detected by the appearance of nonimmune hydrops fetalis on ultrasound examination.

Congenital syphilis may be divided into two clinical syndromes: early congenital syphilis and late congenital syphilis. The early disease manifests within the first two years of life and is characterized by rash, adenopathy, and hepatosplenomegaly. Mucous patches and condylomata lata may be seen.  The eyes may be affected, and cranial nerve palsy and seizures may occur. Thrombocytopenia with petechiae and purpura are often noted. Other manifestations can include anemia, myocarditis, pancreatitis, nephrotic syndrome, and malabsorption. Osteochondritis is often seen on imaging. 

Late congenital syphilis manifests after two years of age. Dental findings include “Hutchinson’s teeth” and “mulberry molars.” Interstitial keratitis and eighth cranial nerve deafness can occur. Rhagades may be seen. Bone and joint abnormalities may include frontal bossing, saddle nose deformity, protuberant mandible, short maxilla, high palatal arch, sternoclavicular joint thickening (Higouménakis sign), saber shin, and Clutton’s joints. Central nervous system involvement can include cognitive impairment, hydrocephalus, seizures, cranial nerve palsy, paralysis, and optic nerve atrophy.

 

Congenital infections, Syphilis in the United States, 1941 – 2019

 

Graph illustrating the prevalence of congenital infection - Syphilis in the United States, 1941 - 2019

 

The WHO estimates that there were approximately 661,000 total cases of congenital syphilis in 2016, resulting in over 200,000 stillbirths and neonatal deaths (12) – with most cases occurring in South America and Africa. The CDC reports that congenital syphilis is on the rise in the United States, with the number of cases in 2018 being highest since 1998 (13).

All pregnant women should be tested for syphilis at their first prenatal visit. Penicillin is the only known effective antimicrobial agent for the prevention of vertical transmission and treatment of fetal and neonatal infection.

 

Congenital Parvovirus B19

Parvovirus B19 is estimated to infect 1-5% of pregnant women. Most infections are without consequence to the fetus, but in rare cases, serious fetal disease can arise (14). In infected fetuses, ultrasound may show nonimmune hydrops fetalis. 

Congenital parvovirus B19 often causes severe anemia and may also cause thrombocytopenia. Neurological manifestations include hydrocephalus, cerebellar hemorrhage, and polymicrogyria. Cardiac complications can include Ebstein’s anomaly, ventricular septal defect, cardiomyopathy, second‐degree heart block, and myocarditis. Ocular involvement may include corneal opacification, aphakia, and microphthalmia. Gastrointestinal manifestations include meconium peritonitis, fetal liver calcifications, portal tract fibrosis, and hypoplasia of the abdominal muscles. Congenital parvovirus B19 can also cause cleft lip and palate, micrognathia, bifid scrotum, secundum atrial septal defect, and micropenis with perineoscrotal hypospadias.

Intrauterine fetal blood transfusion can be used to treat the severe fetal anemia associated with congenital parvovirus B19 infection. 

 

Congenital Varicella-Zoster

Varicella-zoster congenital infections are caused by the virus that causes chickenpox and shingles. Infection may be characterized by low birth weight, hypoplasia of the extremities, dermal scarring, focal muscular atrophy, encephalitis, cortical atrophy, chorioretinitis, and microcephaly. Neonatal varicella zoster may occur when a mother contracts varicella virus between five days before delivery – to 48 hours after delivery. Neonatal varicella has a fatality rate of up to 30% (15). Congenital Varicella-Zoster virus infection is rare since most women are immune by childbearing age – having either been infected during childhood or vaccinated. Infants born with congenital varicella zoster may improve with acyclovir. 

 

Additional Congenital Infections

Additional viral agents of fetal and neonatal morbidity and mortality include HIV, Hepatitis B and C, measles, enteroviruses, adenovirus, lymphocytic choriomeningitis virus, West Nile virus, Zika virus, and Chikungunya virus. Additional bacterial causes include Group B Streptococcus, Chlamydia trachomatis, Neisseria gonorrhoeae, , Escherichia coli, Mycobacterium tuberculosis, and Coxiella burnetii. A parasite, Plasmodium falciparum (the causative agent of malaria) is also associated with congenital infection. 

By obtaining proper prenatal and perinatal care, pregnant women can optimize their chances of preventing, detecting, and treating congenital infections. 

 

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References

(1) Hampton MM. Congenital Toxoplasmosis: A Review. Neonatal Netw. 2015;34(5):274-8. doi: 10.1891/0730-0832.34.5.274.

(2) Rostami A, Riahi SM, Contopoulos-Ioannidis DG, Gamble HR, Fakhri Y, Shiadeh MN, Foroutan M, Behniafar H, Taghipour A, Maldonado YA, Mokdad AH, Gasser RB. Acute Toxoplasma infection in pregnant women worldwide: A systematic review and meta-analysis. PLoS Negl Trop Dis. 2019 Oct 14;13(10):e0007807. doi: 10.1371/journal.pntd.0007807.

(3) McAuley JB. Congenital Toxoplasmosis. J Pediatric Infect Dis Soc. 2014 Sep;3 Suppl 1(Suppl 1):S30-5. doi: 10.1093/jpids/piu077.

(4) “Congenital toxoplasmosis – Annual Epidemiological Report for 2016”, European Centre for Disease Prevention and Control, 2021. [Online]. Available: https://www.ecdc.europa.eu/en/publications-data/congenital-toxoplasmosis-annual-epidemiological-report-2016. 

(5) Best JM. Rubella. Semin Fetal Neonatal Med. 2007 Jun;12(3):182-92. doi: 10.1016/j.siny.2007.01.017. 

(6) Bouthry E, Picone O, Hamdi G, Grangeot-Keros L, Ayoubi JM, Vauloup-Fellous C. Rubella and pregnancy: diagnosis, management and outcomes. Prenat Diagn. 2014 Dec;34(13):1246-53. doi: 10.1002/pd.4467. 

(7) Goderis J, De Leenheer E, Smets K, Van Hoecke H, Keymeulen A, Dhooge I. Hearing loss and congenital CMV infection: a systematic review. Pediatrics. 2014 Nov;134(5):972-82. doi: 10.1542/peds.2014-1173. 

(8) Fowler KB, Boppana SB. Congenital cytomegalovirus infection. Semin Perinatol. 2018 Apr;42(3):149-154. doi: 10.1053/j.semperi.2018.02.002.

(9) Fernandes ND, Arya K, Ward R. Congenital Herpes Simplex. 2021 Jan 11. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2021 Jan–. PMID: 29939674.

(10) Westhoff GL, Little SE, Caughey AB. Herpes simplex virus and pregnancy: a review of the management of antenatal and peripartum herpes infections. Obstet Gynecol Surv. 2011 Oct;66(10):629-38. doi: 10.1097/OGX.0b013e31823983ec.

(11) Cooper JM, Sánchez PJ. Congenital syphilis. Semin Perinatol. 2018 Apr;42(3):176-184. doi: 10.1053/j.semperi.2018.02.005.

(12) “WHO publishes new estimates on congenital syphilis”, World Health Organization, 2021. [Online]. Available: https://www.who.int/reproductivehealth/congenital-syphilis-estimates/en/.

(13) “STD Facts – Congenital Syphilis”, Cdc.gov, 2021. [Online]. Available: https://www.cdc.gov/std/syphilis/stdfact-congenital-syphilis.htm.

(14) Ornoy A, Ergaz Z. Parvovirus B19 infection during pregnancy and risks to the fetus. Birth Defects Res. 2017 Mar 15;109(5):311-323. doi: 10.1002/bdra.23588. 

(15) “GIDEON”, App.gideononline.com, 2021. [Online]. Available: https://app.gideononline.com/explore/diseases/varicella-12550.

Dr. Oli prepares medical students for real-life situations

Multi ethnic group of medical students in uniform looking on the x-ray sitting at the desk in the modern classroom
Dr. Oli has created the “GIDEON diagnostic game” where students take on different roles to diagnose a disease

 

Due to the COVID-19 pandemic, universities all over the world had to accelerate their digital teaching programs. This has created a greater need for online tools that support the challenges of preparing students for life after graduation. This is especially true when teaching medical students – it is critically important future health professionals are taught practical and critical thinking techniques that are based on real-life situations.

Dr. Monika Oli has been speaking with Times Higher Education about the challenges of teaching microbiology online and how GIDEON can bring value to the virtual classroom. Dr. Oli explains that traditional teaching techniques may focus on identifying a few pathogens found in most laboratories, which can create “a completely artificial scenario which would never happen in the real world”.

How can a future medical doctor learn to differentiate between diseases with similar symptoms, such as Rocky Mountain Spotted Fever and Lyme disease? In a real-world scenario, you can’t “just open page 510 of the textbook and diagnose the patient…You have to think outside the box” and this is where Dr. Oli brings GIDEON in.

Dr. Oli has created the “GIDEON diagnostic game” where students take on different roles – epidemiologist, doctor, microbiologists, etc. – and use GIDEON’s Bayesian analysis-driven diagnostic tools to help create the list of likely diseases. This is followed by exploring the database to determine the best treatment plan and even speculating whether the patient would have survived or not in a given scenario!

The game proved to be very popular with students. But Dr. Oli didn’t stop there, she further encouraged future medics to analyze issues relevant today by building an exam around secondary infections of COVID-19.

“Many COVID-19 patients get secondary infections that are bacterial, so I built my whole exam around it. Students were given data and had to use GIDEON to analyze the secondary infection, how it should be treated, whether it will contribute to COVID-19 resistance, so the role play continued even during the exams.”

If you are a teacher looking for new ways to engage and challenge your students, GIDEON might be the right tool for the job. Try it free!

Read the original Times Higher Education article here

 

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Pathogen of the month: Chikungunya virus

by Dr. Jaclynn Moskow

 

Chikungunya virus, 3D illustration. Emerging mosquito-borne RNA virus from Togaviridae family that can cause outbreaks of a debilitating arthritis-like disease
3D illustration of the Chikungunya virus

 

Chikungunya refers to an infection caused by the Chikungunya virus, an alphavirus of the Togaviridae family. Like its close relative, the Semliki Forest virus, the Chikungunya virus is transmitted from human to human via mosquito bites. 

Chikungunya is characterized by fever, joint and muscle pain, and rash.  The disease was discovered in Tanzania in 1952, and since that time has been identified in over 60 countries around the world. The word “Chikungunya” means “that which bends up” in the Makonde language, spoken by a group indigenous to Tanzania and Mozambique. It is thought that this term was coined to describe the posture of patients affected with severe disease.

 

Transmission

Mosquito species that carry Chikungunya include Aedes aegypti in the tropics, Aedes albopictus in the tropics and colder areas, and approximately one dozen Aedes species in Africa, including Aedes furcifer and Aedes taylori. Transmission occurs after a mosquito bites someone infected with Chikungunya and then subsequently bites someone else. Mosquitos pick up the Chikungunya virus from human blood, the virus then replicates inside the mosquito and can be transmitted via their salvia. Once a mosquito acquires the virus, it will likely carry it for the rest of its life. There is evidence that some animals, including non-human primates, rodents, and birds, may act as reservoirs for the Chikungunya virus.

Aedes aegypti Mosquito. Close up a Mosquito Mosquito on leaf,Mosquito Vector-borne diseases,Chikungunya.Dengue fever.Rift Valley fever.Yellow fever.Zika virus.
Aedes aegypti mosquito, the vector of Chikungunya

 

Signs and Symptoms

Signs and Symptoms of Chikungunya develop after a 2-12 day incubation period. Cases vary in severity, and asymptomatic infection may occur. The rate of asymptomatic cases is estimated to be between 4% and 28%.

Cases often begin with an abrupt onset of fever. Polyarthralgia occurs in 70% of cases, usually involving small joints. Swelling of joints may also occur, typically without fluid accumulation. In greater than 50% of cases, a maculopapular rash on the palms, soles, limbs, torso, and/or face is present. This rash may progress to desquamation. Fever generally resolves within one week, but joint pain may persist for months. Sometimes, a “saddle-back fever curve” is seen, with fever resolving and then returning. Moderate to severe lymphopenia is often noted. Thrombocytopenia, leukopenia, elevated liver enzymes, anemia, and elevated creatinine may also be observed.

Facial and neck erythema and conjunctival suffusion may be noted. Headache, photophobia, retro-orbital pain, pharyngitis, nausea, and vomiting can occur. Sometimes, pneumonia and dry cough are seen. Pruritus is common. Patients may complain of exhaustion and insomnia. Symptoms of Chikungunya can persist from one week to several months. Residual chronic joint pain may continue in some cases. Chronic disease is more common in older patients and patients with prior rheumatological disease.

Chikungunya can also cause neurological and ophthalmologic complications. Eye involvement may include retinitis, retinal detachment, optic neuritis, uveitis, dendritic lesions, and Fuchs heterocyclic iridocyclitis. Neurological manifestations can include altered mental function, encephalitis, seizures, myelopathy, Guillain-Barré syndrome, bulbar palsy, acute flaccid paralysis, focal neurological deficit, and sudden sensorineural hearing loss.

Additional rare complications of Chikungunya include hemorrhagic syndrome, cardiovascular shock, arrhythmias, myopericarditis, renal failure, rhabdomyolysis, and thrombocytopenic purpura.

Children with Chikungunya are more likely to experience neurological and dermatological symptoms, and less likely to have arthralgia. Transplacental transmission of the virus can occur and may result in neonatal encephalopathy, neonatal respiratory distress, sepsis, necrotizing enterocolitis, and cardiologic complications. Infants who become infected during the perinatal period may experience fever, rash, peripheral edema, lymphopenia, and thrombocytopenia. Congenital and perinatal infections are associated with poor neurodevelopmental outcomes. Transmission of Chikungunya via breastfeeding has not been noted.

Fatalities from Chikungunya are rare, occurring in about 1 per 1,000 cases. Fatalities are more common in newborns and individuals with multiple medical comorbidities. The use of NSAIDs prior to hospitalization is associated with an increase in disease severity. Infection with Chikungunya is likely to protect against future disease. 

 

Diagnosis and Treatment

A diagnosis of Chikungunya should be considered in individuals living in – or having traveled to – areas with known outbreaks presenting with acute onset of fever and joint pain. Dengue fever and Zika virus infection should be considered in a differential diagnosis of Chikungunya, as they are also carried by Aedes species mosquitoes and may present with similar signs and symptoms.

PCR, serology, and viral culture can be used for laboratory confirmation of Chikungunya. Chikungunya is classified as a biosafety level-3 pathogen, and samples should be handled accordingly. Blood-borne transmission from patients to healthcare workers and laboratory personnel has been documented.

Patients with Chikungunya are treated with supportive care, including hydration and pain management. It is important to prevent mosquito bites during the first week of illness, in order to prevent additional transmission.

 

Chikungunya outbreaks

Between 1952 and 2013, Chikungunya virus outbreaks were identified in Africa, Asia, Europe, and the Indian and Pacific Oceans. In 2013, cases were first identified in the Americas and nations of the Caribbean, and today the majority of cases occur in these locations – where populations have no preexisting immunity.

Over the past decade, the countries that reported most cases of Chikungunya have included Haiti, Dominican Republic, Guadeloupe, Martinique, El Salvador, Honduras, Nicaragua, Columbia, Bolivia, Brazil, Ethiopia, Chad, India, Laos, and French Polynesia. If you have a GIDEON account, click to explore Chikungunya Outbreak Map.

Between 2004 and 2006, an outbreak of Chikungunya that began in Kenya resulted in 500,000 cases in countries of the Indian Ocean, including one-third of the population of La Reunion Island. This outbreak spread to India, where almost 1.5 million people were infected. Ongoing outbreaks have been occurring in Brazil since 2014, with over 300,000 cases occurring in 2016. It is thought that a mutation occurred around 2005 that enabled the virus to survive in Aedes albopictus; and that having this additional species as a vector has fueled recent outbreaks.

Local transmission was reported for the first time in Europe in 2007, with 197 cases occurring in north-eastern Italy. The source of this outbreak was traced to a single individual who had returned from India with the infection. A second outbreak occurred in Europe in 2014, centered mainly in France and the UK and resulting in about 1500 cases.

Chikungunya cases in United States, 2006 - 2020, GIDEON graph

 

In 2014, local transmission of the Chikungunya virus was identified in the territories of the United States for the first time, with 4,659 cases occurring between American Samoa, Puerto Rico, the U.S. Virgin Islands, and Florida. Since that time, the rate of local transmission in the United States has decreased each year, with 179 cases occurring in 2016, 8 cases in 2018, and no cases in 2020.

 

Prevention

There is currently no vaccine to prevent Chikungunya. The CDC recommends the use of the Environmental Protection Agency (EPA)-registered insect repellents when traveling to areas with outbreaks. Wearing long sleeves and pants can also reduce transmission, as can sleeping in places with air conditioning and window and door screens. The CDC also recommends using 0.5% permethrin to treat clothing and gear to repel mosquitos.

During outbreaks, measures should be taken to control mosquito populations by reducing both natural and artificial water-filled habitats where they may breed. Any items that may hold water, such as pools, buckets, planters, and trash containers, should be regularly emptied and cleaned.

 

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This blog was written using data from the GIDEON database, CDC, and WHO.

Hospital-Acquired Infections

by Dr. Jaclynn Moskow

Hospital-acquired infections, also known as “healthcare-associated infections” or “nosocomial infections,” refer to infections that were not present before seeking medical care and were acquired in a healthcare setting. Hospital-acquired infections can be contracted in hospitals, ambulatory clinics, surgical centers, nursing homes, long-term care facilities, dialysis centers, and diagnostic laboratories. 

Hospital setting: male nurse pushing stretcher gurney bed in hospital corridor with doctors & senior female patient

Hospital-acquired infections are defined by symptoms presenting 48-or-more hours after hospital admission, within three days of discharge, or 30 days postoperatively (1). The vast majority of hospital-acquired infections are caused by bacteria, and the propagation of these infections is worsened by the increasing presence of multi-drug resistant bacterial strains.

 

Prevalence of hospital-acquired infections

In the United States, approximately 1 in 25 hospitalized patients will contract an infection (2). Data collected by the Centers for Disease Control and Prevention identified an estimated 1.7 million hospital-acquired infections in the United States during 2002, resulting in 99,000 associated deaths (3).

Estimates from the UK place the prevalence of hospital-acquired infections at approximately 1-in-10 patients (1). In developing nations, the prevalence is higher and may occasionally exceed 25% (4).

CDC data show that urinary tract infections make up approximately 36% of all hospital-acquired infections in the ICU, surgical site infections 20%, pneumonias 11%, bloodstream infections 11%, and other infections 22% (3).

 

Risk Factors

Immunocompromised individuals, such as those undergoing chemotherapy, are at an increased risk for hospital-acquired infection. Geriatric patients are also at increased risk, as are those with multiple medical comorbidities. The incidence of hospital-acquired infections increases as the length of hospital stay increases. Patients in the ICU, receiving mechanical ventilator support, undergoing surgery, and having indwelling devices are also at increased risk.

One large study that examined 231,459 patients across 947 hospitals in Europe found that 19.5% of patients in the ICU experienced at least one hospital-acquired infection (5).

 

Catheter-Associated Urinary Tract Infections (CAUTI)

Catheter-associated urinary tract infections are the most common forms of hospital-acquired infection. Approximately 75% of all UTIs contracted in the hospital are associated with catheter use, and the most important risk factor for developing a catheter-associated urinary tract infection is prolonged catheter use (6). Common pathogens identified in catheter-associated urinary tract infections include Escherichia coli, Enterococcus species, Staphylococcus aureus, Pseudomonas aeruginosa, Proteus mirabilis, Klebsiella pneumoniae, Morganella morganii, and Candida albicans. Some organisms, including Pseudomonas and Proteus, can form biofilms around catheters.

 

Surgical Site Infections (SSI)

Surgical site infections occur postoperatively in the skin, internal organs, or implanted materials involved in the surgery. Diabetic patients are at an increased risk of developing surgical site infections. The incidence of surgical site infections increases as procedure duration increases and the use of antimicrobial prophylaxis decreases the risk of such infections. Common causes of surgical site infections include Staphylococcus aureus (including MRSA), coagulase-negative Staphylococcus, Escherichia coli, Enterococcus faecalis, Pseudomonas aeruginosa, Klebsiella pneumoniae, and Acinetobacter baumannii. In developed nations, between 2-5% of all patients who undergo surgery develop a surgical site infection; and in developing nations, between 12%-39% do (4).

 

Hospital-Acquired Pneumonia (HAP) and Ventilator-Associated Pneumonia (VAP)

The Infectious Diseases Society of America (IDSA) defines hospital-acquired pneumonia as “pneumonia that occurs 48 hours or more after admission to the hospital and did not appear to be incubating at the time of admission”; and defines ventilator-associated pneumonia as “pneumonia that develops more than 48 to 72 hours after endotracheal intubation.” Common bacterial causes of both hospital-acquired pneumonia and ventilator-associated pneumonia include Staphylococcus aureus (including MRSA), Streptococcus pneumoniae, Haemophilus influenzae, Escherichia coli, Pseudomonas aeruginosa, and Klebsiella pneumoniae. Common viral causes include rhinovirus, parainfluenza virus, influenza virus, respiratory syncytial virus, and coronavirus. 

The incidence of ventilator-associated pneumonia in patients who require mechanical ventilation for more than 48 hours is estimated at 25-to-30% (7).

 

The male patient with intravenous catheter. Central Line-Associated Bloodstream Infection (CLABSI) is one of the types of hospital-acquired infections

Central Line-Associated Bloodstream Infection (CLABSI)

Central line-associated bloodstream infections occur at the site of central venous catheters. The mortality rate for central line-associated bloodstream infections is between 12% and 25% (8). Common causes of central line-associated bloodstream infections include coagulase-negative Staphylococci, Staphylococcus aureus (including MRSA), Enterobacte, Klebsiella pneumoniae, and Candida albicans. Central lines can be placed in the neck, chest, arm, or groin. The use of femoral-site lines is associated with an increased risk of infection and is no longer recommended (9). Antibiotic lock therapy can reduce the incidence of central line-associated bloodstream infections.

 

Clostridium Difficile Infections (CDI)

An estimated 12.1% of all hospital-acquired infections are caused by Clostridium difficile, making Clostridium difficile the most common cause of hospital-acquired infections (10). Approximately 75% of all Clostridium difficile infections are hospital-acquired (11), and an estimated 2.3% of all US hospital costs are related to these infections (12). Click to see how you can use Gideon to explore Clostridium difficile. 

 

Hospital-Acquired COVID-19

The incidence of hospital-acquired COVID-19 remains unknown. A meta-analysis of studies examining COVID-19 cases in China found that 44% of cases were likely to have originated from a healthcare setting (13). A hospital in South Africa reported that a single case led to six major outbreak clusters in several hospital wards, a nursing home, and a dialysis unit. Ultimately this episode resulted in 135 infections and 15 deaths (14). Up to 1-in-4 cases of COVID-19 in the UK are likely to have been hospital-acquired (15).

In contrast, a recent study from the United States suggests that hospital-acquired COVID-19 is actually quite uncommon when rigorous infection-control measures are followed. This study looked at all patients admitted to Brigham and Women’s Hospital in Boston, Massachusetts, between March 7 and May 30, 2020. They determined that of 697 COVID-19 diagnoses, only two were hospital-acquired, including one case that likely resulted from a visit by a pre-symptomatic spouse (16).

The World Health Organization estimates that healthcare workers may comprise as many as one-in-seven COVID-19 cases (17), reflecting a high incidence of hospital-acquired disease. The CDC is not currently collecting data on hospital-acquired COVID-19, as hospitals are required to report to the U.S. Department of Health and Human Services. 

 

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References 

(1) Inweregbu, K., Dave, J. and Pittard, A., 2005. Nosocomial infections. Continuing Education in Anaesthesia Critical Care & Pain, 5(1), pp.14-17.

(2) Magill SS, Edwards JR, Bamberg W, et al., 2014. Emerging Infections Program Healthcare-Associated Infections and Antimicrobial Use Prevalence Survey Team. Multistate point-prevalence survey of healthcare-associated infections. N Engl J Med, 27;370(13), pp. 1198-208.

(3) Klevens, R., Edwards, J., Richards, C., et al., 2007. Estimating Health Care-Associated Infections and Deaths in U.S. Hospitals, 2002. Public Health Reports, 122(2), pp.160-166.

(4) Allegranzi, B. and Pittet, D., 2007. Healthcare-Associated Infection in Developing Countries: Simple Solutions to Meet Complex Challenges. Infection Control & Hospital Epidemiology, 28(12), pp.1323-1327. 

(5) European Centre for Disease Prevention and Control, 2013. Point-prevalence survey of healthcare-associated infections and antimicrobial use in European acute care hospitals. Stockholm: EDC.

(6) Cdc.gov. 2021. Catheter-associated Urinary Tract Infections (CAUTI) | HAI | CDC. [online] Available at: https://www.cdc.gov/hai/ca_uti/uti.html.

(7) Cornejo-Juárez, P., González-Oros, I., Mota-Castañeda, P., Vilar-Compte, D. and Volkow-Fernández, P., 2020. Ventilator-associated pneumonia in patients with cancer: Impact of multidrug resistant bacteria. World Journal of Critical Care Medicine, 9(3), pp.43-53.

(8) Dumont, C. and Nesselrodt, D., 2012. Preventing central line-associated bloodstream infections CLABSI. Nursing, 42(6), pp.41-46. 

(9) Palmer, E., 2021. Avoiding the femoral vein in central venous cannulation: an outdated practice. [online] Acphospitalist.org. Available at: https://acphospitalist.org/archives/2018/08/perspectives-avoiding-the-femoral-vein-in-central-venous-cannulation-an-outdated-practice.htm.

(10) Monegro, A., Muppidi, V. and Regunath, H., 2020. Hospital Acquired Infections. StatPearls, [online] Available at: https://www.ncbi.nlm.nih.gov/books/NBK441857/.

(11) Louh, I., Greendyke, W., Hermann, E., e al., 2017. Clostridium Difficile Infection in Acute Care Hospitals: Systematic Review and Best Practices for Prevention. Infection Control & Hospital Epidemiology, 38(4), pp.476-482.

(12) Jump, R., 2013. Clostridium difficile infection in older adults. Aging health, 9(4), pp.403-414.

(13) Zhou, Q., Gao, Y., Wang, X., et al., 2020. Nosocomial infections among patients with COVID-19, SARS and MERS: a rapid review and meta-analysis. Annals of Translational Medicine, 8(10), pp.629-629.

(14) Lessells, R., Moosa, Y. and de Oliviera, T., 2020. Report into a nosocomial outbreak of coronavirus disease 2019 (COVID‐19) at Netcare St. Augustine’s Hospital. [online] Available at: https://www.krisp.org.za/manuscripts/.

(15) Discombe, M., 2021. Covid infections caught in hospital rise by a third in one week. [online] Health Service Journal. Available at: https://www.hsj.co.uk/patient-safety/covid-infections-caught-in-hospital-rise-by-a-third-in-one-week/7029211.article

(16) Rhee, C., Baker, M., Vaidya, V., et al., 2020. Incidence of Nosocomial COVID-19 in Patients Hospitalized at a Large US Academic Medical Center. JAMA Network Open, 3(9), p.e2020498.

(17) Nebehay, S., 2021. One in 7 reported COVID-19 infections is among health workers, WHO says. [online] U.S. Available at: https://www.reuters.com/article/us-health-coronavirus-who-healthworkers/one-in-7-reported-covid-19-infections-is-among-health-workers-who-says-idUSKBN2681TR?il=0

‘It’s not just COVID-19’ – Dr. Berger on Outbreak News Today podcast

HazMat team in protective suits decontaminating public transport, bus interior during virus outbreak

The global pandemic caused by COVID-19 has rightly taken center stage in media and scientific journals but overshadowed other concerning outbreaks that could do with some attention. GIDEON co-founder Dr. Stephen A. Berger has been speaking with Outbreak News Today to discuss the diseases that are flying under the radar in the media but are still being tracked and reported by GIDEON. 

Listen to the podcast or watch a video recording here.

In 2020, significant outbreaks of Cholera in Yemen, Dengue in Brazil, and neighboring South American countries have been recorded in addition to the COVID-19 pandemic. Numerous diseases such as Ebola, Lassa fever, Chikungunya, Plague, and Monkeypox have broken out in regions of Africa and Asia in recent years as well. Ebola and Monkeypox have proved a persistent threat in the Democratic Republic of Congo, with thousands of cases in the last couple of years alone. Meanwhile, Lassa fever cases in Nigeria in 2020 were the highest recorded by any country in history (nearly 7,000). The disease spreads through rodents, leaving many of its surviving victims deaf.

These and other diseases have historically been considered tropical or exotic and don’t trouble the western population too much, however, the spread of COVID-19 has proven that diseases can and will spread given the opportunity. For instance, Monkeypox, Plague, and West Nile Fever have all had outbreaks within the US in the past. 

Tune in to Outbreak News Today and hear from Dr. Berger and Robert Herriman on this timely subject.

Haven’t got a GIDEON account yet? Sign up for a free trial here.

 

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The Gut Microbiome and Its Role in Health and Disease

by Dr. Jaclynn Moskow

Intestinal bacteria, Gut microbiome helps control intestinal digestion and the immune system, Probiotics are beneficial bacteria used to help the growth of healthy gut flora
The gut microbiome helps control intestinal digestion and the immune system.

 

It is difficult to overstate the importance and complexity of the gut microbiome. Humans live in symbiosis with hundreds (and possibly thousands) of species of bacteria (1). Additionally, archaea, fungi, viruses, and protozoa are also present in our gut. In fact, only about 10% of the cells within our bodies are “ours” and contain human DNA. The remaining 90% of cells we carry with us are microbial. The exact makeup of the gut microbiome varies greatly from individual to individual and is influenced by variables that include diet, exercise, medication use, sleep, stress, hormonal changes, aging, and disease. Associations have been found between the composition of the microbiome and obesity, diabetes, hypertension, heart disease, autoimmune disorders, allergies, mood disorders, and more.

 

Why Do We Have a Gut Microbiome?

The bacteria in our gut participate in the digestion, absorption, and metabolism of proteins and carbohydrates and in the breakdown of endogenous intestinal mucus. They also synthesize vitamin K2 and various B group vitamins; and they influence the development of gut-associated lymphoid tissues and the development of cells of the immune system (2), and serve to limit the colonization of pathogenic bacteria. The majority of these bacteria are anaerobic. Common genera include Escherichia, Bifidobacterium, Lactobacillus, and Enterococcus.

 

The Gut Microbiome and COVID-19

A recent study examined the connection between the gut microbiome and COVID-19. Researchers found that patients hospitalized for COVID-19 had an increase in certain bacterial species and a decrease in others when compared to a control group, even after antibiotic use was accounted for (19). They found a negative correlation between disease severity and concentrations of Faecalibacterium prausnitzii and Eubacterium rectale. Patients were monitored for 30 days post-recovery, and the observed changes persisted. The researchers postulated that these changes may contribute to the persistence of symptoms and multi-system inflammation that is sometimes seen with patients who have recovered from COVID-19.

 

Gut flora vector illustration. Flat tiny gastrointestinal microbe person concept. Abstract digestive stomach living organisms for healthy life. Lactobacilli, coli and intestinal system environment.

 

The Gut Microbiome and Obesity

In recent years, many studies have examined associations between the gut microbiome and obesity. When germ-free mice are colonized with gut bacteria from obese mice, they gain weight; but when they are colonized with gut bacteria from lean mice, they do not gain weight (3). Mice also gain weight when they are colonized with bacteria from obese humans. In a discordant twin study, colonization from obese twins caused mice to gain weight while colonization from their lean siblings did not (4). Some believe the ratio of Bacteroidetes to Firmicutes may play a significant role in obesity. One study found that as obese individuals lose weight, the concentration of Bacteroidetes increases (5). Furthermore, genetically obese mice contain a higher proportion of Firmicutes than thin mice consuming the same diet, and thin mice contain more Bacteroidetes than obese mice consuming the same diet (6). When researchers employed machine learning to study this topic, they concluded that the association between the Bacteroidetes / Firmicutes ratio and obesity is relatively weak and that existing studies lack significant sample sizes (7). The science is far from settled.

 

The Gut Microbiome and Diabetes 

Studies have also investigated the link between the gut microbiome and diabetes. Some speculate that in individuals who are genetically susceptible to type 1 diabetes, it is ultimately a shift in the gut microbiome that triggers the onset (8).  The gut microbiome of children with type 1 diabetes has been found to be less diverse than that of children without the disease (9). A recent review of 42 studies that examined the gut microbiome and type 2 diabetes found Bifidobacterium, Bacteroides, Faecalibacterium, Akkermansia, and Roseburia to be negatively associated with type 2 diabetes; and Ruminococcus, Fusobacterium, and Blautia to be positively associated (10). Other work has shown that when individuals with metabolic syndrome were given fecal transplants from healthy donors, insulin-resistance improved (11).

 

The Gut Microbiome, Hypertension, and Cardiovascular Disease

The ratio of Bacteroidetes to Firmicutes has also been implicated in hypertension. Consuming milk fermented with Lactobacilli can lower blood pressure in some cases, and Lactobacilli produce peptides that can inhibit ACE1 (12).  The same bacterial species found within the atherosclerotic lesions of individuals with cardiovascular disease are found in their gut (13). Additionally, Akkermansia muciniphila may have a cardioprotective effect. Researchers observed that when mice were fed a Western diet, they experienced a decrease in Akkermansia muciniphila and an increase in atherosclerotic lesions. When these same mice were recolonized with Akkermansia muciniphila, a reversal in atherosclerotic lesions was observed (14). 

 

The Gut Microbiome, Autoimmune Disorders, and Allergies

Components of the gut microbiome may be involved in eliciting or quelling immune responses that lead to the development of autoimmune disorders and allergies. Antibodies directed against a yeast species, Saccharomyces cerevisiae,  have been found in patients with rheumatoid arthritis, systemic lupus erythematosus, antiphospholipid syndrome, and Crohn’s Disease (15). Individuals with these conditions show an increase in the numbers of certain bacterial species and a decrease in other species –  as do individuals with multiple sclerosis, Sjögren’s syndrome, and celiac disease. The ratio of Clostridium difficile to Bifidobacterium in infants has been associated with food and aero-allergies, and high levels of fecal Escherichia coli in infants are associated with IgE-mediated eczema (16).

 

The Gut Microbiome and Neuropsychiatric Disorders

The central nervous system and enteric nervous system (together known as the gut-brain axis) are both influenced by the gut microbiome. Bacteria in the gut can directly secrete neurotransmitters, including serotonin, dopamine, norepinephrine, GABA, and histamine. Several studies have shown that patients with bipolar and major depressive disorder have an increase in Actinobacteria and Enterobacteriaceae, and a decrease in Faecalibacterium (17). Mice treated with Lactobacillus rhamnosus have reduced anxiety/depression-like behavior and altered expression of GABA receptors (18). Differences in microbiome composition have also been noted in patients with schizophrenia, Parkinson’s disease, and an autism spectrum disorder.

 

Fecal microbiota transplant (FMT) stool transferring bacteria microbes
Fecal microbiota transplantation (FMT)

 

Fecal Microbiota Transplantation and Clostridium Difficile Colitis

Fecal microbiota transplantation (FMT) is currently being used as a treatment for Clostridium difficile colitis. In fact, FMT is more effective than vancomycin at treating recurrent Clostridium difficile colitis. Most commonly, FMT is performed via colonoscopy. Nasoduodenal tubes, nasogastric tubes, and enemas can also be used. FMT made headlines in 2019 when a transplant recipient died, and several others became seriously ill, after becoming colonized with multi-drug resistant Escherichia coli. This led the FDA to recommend new safety measures for FMTs, including screening donors for risk factors associated with carrying multi-drug-resistant organisms and testing all donor stools for such organisms.

 

Optimizing the Microbiome

In many regards, studying the gut microbiome often leads to more questions than answers. When a change in bacterial levels is observed in a disease state, it is sometimes difficult to know whether that change contributed to the disease state or merely resulted from it. Anyone who seeks to convince you that they know the perfect solution to optimizing gut health is misleading you. While a host of food products and health supplements are touted to enhance the gut microbiome, in most cases the details of this “enhancement” are not defined. As additional studies are conducted, we will gain a better understanding of this vast topic and will likely see an increase in the utilization of fecal transplants in treating various diseases.

 

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References

(1) Almeida A, Mitchell AL, Boland M, et al. A new genomic blueprint of the human gut microbiota. Nature. 2019 Apr;568(7753):499-504. Available: 10.1038/s41586-019-0965-1.

(2) Wu HJ, Wu E. The role of gut microbiota in immune homeostasis and autoimmunity. Gut Microbes. 2012 Jan-Feb;3(1):4-14. Available: 10.4161/gmic.19320.

(3) Turnbaugh PJ, Ley RE, Mahowald MA, et al. An obesity-associated gut microbiome with increased capacity for energy harvest. Nature. 2006 Dec 21;444(7122):1027-31. Available: 10.1038/nature05414. 

(4) Ridaura VK, Faith JJ, Rey FE, et al. Gut microbiota from twins discordant for obesity modulate metabolism in mice. Science. 2013 Sep 6;341(6150):1241214. Available: 10.1126/science.1241214.

(5) Ley RE, Turnbaugh PJ, Klein S, Gordon JI. Microbial ecology: human gut microbes associated with obesity. Nature. 2006 Dec 21;444(7122):1022-3. Available: 10.1038/4441022a.

(6) Ley RE, Bäckhed F, Turnbaugh P, et al. Obesity alters gut microbial ecology. Proc Natl Acad Sci U S A. 2005 Aug 2;102(31):11070-5. Available: 10.1073/pnas.0504978102.

(7) Sze MA, Schloss PD. Looking for a Signal in the Noise: Revisiting Obesity and the Microbiome. mBio. 2016 Aug 23;7(4):e01018-16. Available: 10.1128/mBio.01018-16.

(8) Zheng P, Li Z, Zhou Z. Gut microbiome in type 1 diabetes: A comprehensive review. Diabetes Metab Res Rev. 2018 Oct;34(7):e3043. Available: 10.1002/dmrr.3043.

(9) Giongo A, Gano KA, Crabb DB, et al. Toward defining the autoimmune microbiome for type 1 diabetes. ISME J. 2011 Jan;5(1):82-91. Available: 10.1038/ismej.2010.92.

(10) Gurung M, Li Z, You H, et al. Role of gut microbiota in type 2 diabetes pathophysiology. EBioMedicine. 2020 Jan;51:102590. Available: 10.1016/j.ebiom.2019.11.051.

(11) Vrieze A, Van Nood E, Holleman F, et al. Transfer of intestinal microbiota from lean donors increases insulin sensitivity in individuals with metabolic syndrome. Gastroenterology. 2012 Oct;143(4):913-6.e7. Available: 10.1053/j.gastro.2012.06.031.

(12) Jose PA, Raj D. Gut microbiota in hypertension. Curr Opin Nephrol Hypertens. 2015 Sep;24(5):403-9. Available: 10.1097/MNH.0000000000000149.

(13) Tang WH, Kitai T, Hazen SL. Gut Microbiota in Cardiovascular Health and Disease. Circ Res. 2017 Mar 31;120(7):1183-1196. Available: 10.1161/CIRCRESAHA.117.309715.

(14) Li J, Lin S, Vanhoutte PM, et al. Akkermansia Muciniphila Protects Against Atherosclerosis by Preventing Metabolic Endotoxemia-Induced Inflammation in Apoe-/- Mice. Circulation. 2016 Jun 14;133(24):2434-46. Available: 10.1161/CIRCULATIONAHA.115.019645.

(15) De Luca F, Shoenfeld Y. The microbiome in autoimmune diseases. Clin Exp Immunol. 2019 Jan;195(1):74-85. Available: 10.1111/cei.13158.

(16) Pascal M, Perez-Gordo M, Caballero T, et al. Microbiome and Allergic Diseases. Front Immunol. 2018 Jul 17;9:1584. Available: 10.3389/fimmu.2018.01584.

(17) Huang TT, Lai JB, Du YL, et al. Current Understanding of Gut Microbiota in Mood Disorders: An Update of Human Studies. Front Genet. 2019 Feb 19;10:98. Available: 10.3389/fgene.2019.00098.

(18) Bravo JA, Forsythe P, Chew MV, et al. Ingestion of Lactobacillus strain regulates emotional behavior and central GABA receptor expression in a mouse via the vagus nerve. Proc Natl Acad Sci U S A. 2011 Sep 20;108(38):16050-5. Available: 10.1073/pnas.1102999108.

(19) Yeoh YK, Zuo T, Lui GC, et al. Gut microbiota composition reflects disease severity and dysfunctional immune responses in patients with COVID-19. Gut. 2021 Jan 11:gutjnl-2020-323020. Available: 10.1136/gutjnl-2020-323020.

Examining Salmonella Typhi and Typhoid Fever

by Dr. Jaclynn Moskow

Typhoid fever refers to the disease caused by Salmonella typhi (Salmonella enterica subsp. enterica serovar Typhi), a facultative anaerobic Gram-negative bacillus. Both typhoid fever and its close relative paratyphoid fever are sometimes referred to as “enteric fever.” As the name enteric fever implies, the illness is often characterized by gastrointestinal symptoms and fever.

Green houseflies feeding on ripe mango using their labellum to suck the meat

Transmission

Humans are the only natural reservoir for Salmonella typhi, and transmission occurs via the fecal-oral route. Transmission may occur after eating food that was prepared by someone carrying the bacterium or after using a contaminated toilet and failing to follow proper hand hygiene. Transmission can also occur by drinking water contaminated by sewage, or by eating food prepared in contaminated water. Flies can carry the bacteria from sewage to food.

The average incubation period for typhoid fever is 15 to 21 days, but symptoms may develop as soon as 5 days post transmission or as late as 34 days. Both children and adults contract typhoid fever. In some outbreaks, typhoid fever has primarily affected school-aged children, with cases in infants and toddlers being quite rare. In recent years, very young children have also proven extremely susceptible to the disease.[1]

Chronic Carriers and the Case of Typhoid Mary

Salmonella typhi may continue to shed in feces after a patient has recovered from the disease, and such individuals may become asymptomatic carriers of the bacteria. Approximately five percent of people who contract Salmonella typhi infection will become chronic carriers. 25% of carriers experienced no signs or symptoms of the disease.[2]  Females are more likely than males to become chronic carriers.  In chronic carriers, Salmonella typhi takes refuge in macrophages [3] and the gall bladder.

The most infamous carrier of typhoid fever was Mary Mallon, also known as “Typhoid Mary.” Mary was born in Ireland and immigrated to New York at the turn of the 20th century. She worked as a cook for eight affluent families, seven of which contracted Typhoid Fever.[4] These high-profile infections eventually led to an investigation and to Mary’s forced quarantine. After her release, she defied orders and continued to work as a cook, using various aliases. She stopped working for private clients and worked instead at several public restaurants as well as at Sloane Maternity Hospital.

51 cases of typhoid fever were traced to Mary, including three fatalities. [5] It is likely that Mary actually infected and killed many times this amount. In 1915, she was located and detained a second time, eventually dying after a period of 23 years in forced quarantine. Mary never believed she was the source of any infections, as she had no symptoms of the disease.

Signs and Symptoms

Typhoid fever can have a very nonspecific clinical presentation. Generally, initial enterocolitis develops, without associated fever. Patients may experience constipation or diarrhea, associated with abdominal pain and vomiting. Hematochezia may occur. Hepatosplenomegaly is present in 50% of cases and jaundice may also develop. Some patients develop cholecystitis or pancreatitis.

A short asymptomatic phase may proceed with the onset of fever.  Once fever develops, it often follows a “step-ladder” pattern, rising and subsequently falling before rising again. Additional flu-like symptoms may include chills, diaphoresis, headache, sore throat, cervical lymphadenopathy, cough, and myalgia. Pneumonia may develop and bradycardia is often noted. During the second week of illness, 30% of patients develop a rash referred to as “rose spots.” Initial leukocytosis is often seen, followed by leukopenia. Thrombocytopenia, coagulopathy, and hepatic dysfunction may also be noted.

Some patients will go on to develop an intestinal perforation, generally in the 3rd or 4th week of illness. Intestinal perforation is more common in males than in females. Typhoid fever is dangerous for pregnant women, with 70% of untreated cases ending in miscarriage. Additionally, transmission from mother to fetus and subsequent neonatal typhoid can occur.

Systemic inflammation may lead to such complications as myocarditis, endocarditis, pericarditis, and mycotic aneurysm. Some patients develop meningitis or encephalitis. Spondylitis/spondylodiscitis, rhabdomyolysis, and hemophagocytic lymphohistiocytosis have also been seen – as have endophthalmitis, cranial nerve palsy, and Guillain-Barre syndrome.

Typhoid fever can induce neuropsychiatric symptoms. Encephalopathy occurs in 21% of cases. Psychosis or confusion occurs in 5 to 10%. Seizures and coma occur less commonly. The term “typhoid state” (from the Greek word “typhos” –  meaning “clouded”) is sometimes used to refer to changes in mental status.

Without treatment, symptoms of typhoid fever will generally resolve in approximately one month. About ten percent of patients with typhoid fever will experience relapse, more common among those who received treatment than those who did not. Typhoid fever is more severe among patients with HIV infection, malaria, and sickle cell anemia. Long-term carriers have a higher incidence of cancers of the gallbladder, pancreas, colon, and lung. The case-fatality rate for untreated typhoid fever is approximately 15% – vs. 0.8% with treatment.

Illustration of typhoid fever

Diagnosis and Treatment

Diagnosis is made via culture of blood, urine, sputum, or bone marrow. Stool cultures are often negative except in very late infection. Previously, the Widal test was used to detect serum antibody titers against Salmonella typhi O and H antigens. However, this test has a high rate of both false negatives and false positives and is thus unreliable. 

Both Ceftriaxone and Azithromycin can be used to treat typhoid fever. Fluoroquinolones are no longer recommended, in view of the emergence of resistant strains. Corticosteroids may be used when there is evidence of widespread systemic involvement. Health-care personnel should follow stool precautions. Most carriers can be cured with antibiotics. Carriers with cholelithiasis usually remain positive after antibiotic treatment and will require cholecystectomy.

Prevalence 

Over the last three decades, typhoid fever has affected between 11 to 21 million people per year, worldwide.  Incidence has been declining in many countries. 

Typhoid, estimated cases worldwide 1990 - today

The countries reporting most cases include Bangladesh, China, India, Indonesia, Laos, Nepal, Pakistan, and Vietnam. High rates also occur in Africa and Central and South America. If you have a GIDEON account, click to explore the typhoid fever outbreak map. 

The CDC reports that approximately 350 people in the United States receive treatment for typhoid fever each year and that as many as 5,700 people are likely to be infected.[6]  Most cases in the United States result from travel to endemic areas. Occasionally, cases arise from other sources, such as from contaminated imported food. A review of outbreaks in the United States can be found here.

Prevention

Cases of typhoid fever and other waterborne diseases will decline as access to clean water increases and as sanitary conditions improve.  The CDC recommends receiving a typhoid fever vaccine prior to travel to countries with high incidence. Both oral and injectable vaccines are available – both with approximately 50 to 80% efficacy in preventing disease. When traveling, precautions should include adherence to proper hand hygiene, drinking only bottled water, and avoiding uncooked food.

Paratyphoid Fever and Typhus

Typhoid fever is clinically similar to Paratyphoid fever and some forms of Typhus. Paratyphoid fever is a form of enteric fever caused by a Salmonella paratyphi (Salmonella enterica serotypes Paratyphi A, Paratyphi B, or Paratyphi C). Clinically, it may be indistinguishable from typhoid fever and it is transmitted via the same routes. Salmonella paratyphi causes fewer cases of enteric fever than Salmonella typhi

Typhus refers to diseases caused by Rickettsia typhi, Rickettsia prowazekii, and Orientia tsutsugamushi.  Typhus is transmitted by fleas, mites, or lice. During the 19th century, typhoid and typhus were believed to be two forms of a single disease. Like typhoid fever, typhus usually causes flu-like symptoms and a rash, and often with gastrointestinal symptoms. The various forms of typhus are less common than typhoid – and are each reported in specific geographical regions. 

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References

[1] A Sinha, S Sazawal, R Kumar, et al., “Typhoid fever in children aged less than 5 years”, Lancet, vol. 28, num. 354, pp. 734-7, 1999. Available: 10.1016/S0140-6736(98)09001-1

[2] C Parry, T Hien, G Dougan, et al., “Typhoid fever”, N Engl J Med, vol. 347, num. 22, pp. 1770-82, 2002. Available: 10.1056/NEJMra020201

[3] N Eisele, T Ruby, A Jacobson et al., “Salmonella require the fatty acid regulator PPARδ for the establishment of a metabolic environment essential for long-term persistence”, Cell Host Microbe, vol. 14, num. 2, pp. 171-182, 2013. Available: 10.1016/j.chom.2013.07.010

[4] Marineli F, Tsoucalas G, Karamanou M, Androutsos G. Mary Mallon (1869-1938) and the history of typhoid fever. Ann Gastroenterol. 2013;26(2):132-134. [Online]. Available: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3959940/

[5] “’Typhoid Mary’ Dies Of A Stroke At 68. Carrier of Disease, Blamed for 51 Cases and 3 Deaths, but Immune”, The New York Times, November 12, 1938. [Online]. Available: https://www.nytimes.com/1938/11/12/archives/typhoid-mary-dies-of-a-stroke-at-68-carrier-of-disease-blamed-for.html

[6] Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Foodborne, Waterborne, and Environmental Diseases (DFWED), “Typhoid Fever and Paratyphoid Fever: Questions and Answers”. [Online]. Available: https://www.cdc.gov/typhoid-fever/sources.html 

Pathogen of the Month: Yersinia Pestis

by Dr. Jaclynn Moskow

The most researched pathogen on GIDEON in January was Yersinia pestis, a facultative anaerobic, Gram-negative, coccobacillus. It is the causative agent of the Plague and responsible for some of the most deadly pandemics in history.  While Yersinia pestis is no longer a cause of mass mortality, outbreaks do still occur. Over the last decade, there have been up to 2,000 cases per year reported to the World Health Organization, and likely thousands more unreported.[1]

Yersinia pestis illustration
Yersinia pestis – the agent of Plague

Transmission

Rodents are the natural reservoirs for Yersinia pestis, including rats, mice, squirrels, chipmunks, voles, prairie dogs, and marmots. The bacteria can also be transmitted to a wide variety of other mammals, including rabbits, coyotes, sheep, and cats. There are currently animals carrying Yersinia pestis on all continents except for Oceania.[2]

Fleas transmit Yersinia pestis from animals to humans, and flea bites are the most common route of infection for humans. Humans can also become infected by coming into contact with fluid or tissue. For example, this could happen when a hunter skins a diseased animal. When respiratory infection occurs, Yersinia pestis can become airborne and spread between humans. In rare cases, Yersinia pestis has been contracted via ingestion of infected meat. Dr. Berger discusses transmission here

Both children and adults are at risk of becoming sick with Plague, and there does not appear to be a significant difference in infection rates between men and women.

Yersinia pestis in history

Yersinia pestis likely emerged around 6,000 years ago, evolving from a close relative – Yersinia pseudotuberculosis. [3] The first major Plague pandemic occurred in the 6th century and is known as The Justinian Plague. The disease spread throughout Europe, Asia, and North Africa by way of ship. Its death toll is disputed, with some researchers estimating it claimed half the world’s population and others believing it was less severe.[4]

The second major Plague pandemic occurred between 1346 and 1353, once again striking Europe, Asia, and North Africa. This outbreak, known as The Black Death, took the lives of 75 to 200 million people. It decimated cities quickly upon arrival, sometimes killing over half the population in just a few weeks. In Ragusa, a Venetian port city, incoming sailors were isolated for 40 days, a practice which was known as a “quarantino” …the origin of the word “quarantine”.[5]

Images of physicians wearing bird-like beak masks are often associated with The Black Death. Microbes had yet to be discovered, and many doctors believed Plague was transmitted through smell. To combat this smell, the beak mask had a space for flowers, herbs, and spices. This mask, however, was actually not invented during The Black Death, but rather during a different Plague outbreak in 1619. After the Black Death subsided, Plague outbreaks continued in Europe every few years for the next 300 years, culminating with “The Great Plague” of London in 1665.

 

 

The next significant Plague pandemic occurred in 1894, originating in China, spreading through Asia and Europe, and eventually arriving in the United States in 1900. In 1894 Swiss physician Alexandre Yersin and Japanese physician Kitasato Shibasaburō simultaneously discovered the bacterial origin of Plague. Yersin named the bacterium Pasteurella pestisSoon after, fleas were identified as a vector of transmission. Pasteurella pestis was renamed Yersinia pestis in 1944. Notable 20th-century plague outbreaks occurred in Los Angeles between 1924 to 1925 and in Vietnam from 1965 to 1975.

Bubonic Plague

There are 3 main types of Plague, with Bubonic Plague being the most common type. Bubonic Plague is transmitted via flea bites or via the handling of tissue or fluids. It has an incubation period of 2-to-6 days. Bacteria multiply in lymph nodes close to the site of infection. A maculopapular lesion may appear at the infection site. The lymph nodes become painful and swollen and are known as “Buboes.” Buboes are usually inguinal (60% to 90%), axillary (30%), cervical (10%), or epitrochlear (10%). Other symptoms of Bubonic Plague are flu-like, including fever, headache, chills, pharyngitis, muscle aches, extreme weakness, and tachycardia. Without treatment, Bubonic Plague has a mortality rate of around 50-60%. With treatment, this drops to about 10%. Human to human transmission of Bubonic Plague is extremely rare.

 

Bubonic plague transmission - illustration

 

Pneumonic Plague

Pneumonic Plague occurs when Yersinia pestis enters the lungs. This can happen from inhaling respiratory droplets, or from the bloodstream during untreated Bubonic Plague. The incubation period when the bacteria is inhaled is 1-to-3 days. Pneumonic Plague presents with fever, headache, weakness, tachycardia, coughing, chest pain, and shortness of breath. Hemoptysis is common. With treatment, it has a fatality rate of around 15%. Untreated Pneumonic Plague is almost always fatal.

Septicemic Plague

When Yersinia pestis enters the bloodstream, Septicemic Plague can occur. This may happen directly from a flea bite, or as a complication of untreated Bubonic or Pneumonic Plague. Septicemic Plague may begin with flu-like symptoms. Additionally, it may cause nausea, vomiting, diarrhea, abdominal pain, and sometimes hematemesis and/or hematochezia. Acrocyanosis, ecchymosis, petechiae, and digital gangrene may be noted. Septicemic Plague may progress to cause meningitis, osteomyelitis, kidney failure, DIC, and septic shock. The fatality rate is around 28% with treatment and around 100% if untreated.

Rare forms of Plague include cutaneous, pharyngeal, meningeal, and gastrointestinal.

Diagnosis and treatment

A presumptive diagnosis of Plague may be made through isolation of Yersinia pestis from pus, blood, sputum, or other infected material. 

When Plague is suspected, treatment should be initiated prior to laboratory confirmation. Gentamicin, Streptomycin, Doxycycline, and Chloramphenicol are all effective. Patients with Plague should be isolated. When Pneumonic Plague is suspected, standard respiratory droplet precautions should be followed. Individuals exposed to Plague patients should begin prophylaxis. 

Prevalence

Today, there are approximately 1,000 to 2,000 reported cases of Plague globally each year – and 100 to 200 deaths.

Plague deaths worldwide, GIDEON graph

 

About 95% of current Plague cases occur in Madagascar and the Democratic Republic of Congo.  Brazil, Myanmar, Peru, Vietnam, and The United States also report cases almost every year. If you have a GIDEON account, click to explore Plague outbreak map

According to the CDC, about 7 people in the United States contract Plague each year, with the areas reporting cases usually being Northern New Mexico, Northern Arizona, Southern Colorado, Southern Oregon, Western Nevada, and various rural and semi-rural parts of California.

In 2009, University of Chicago scientist Malcolm Casadaban contracted Plague while conducting vaccine research and unfortunately died. Between 2019 and 2020 there were at least 5 cases of Plague in China linked to eating marmot meat and a few others of unknown origin.

 

Prevention

People who live in areas with Plague outbreaks can take precautions to minimize the risk of infection. The CDC recommends the following:

  • Reduce rodent habitat around your home, workplace, and recreational areas. Remove brush, rock piles, junk, cluttered firewood, and possible rodent food supplies, such as pet-  and wild anima- food. Make your home and outbuildings rodent-proof.
  • Wear gloves if you are handling or skinning potentially infected animals to prevent contact between your skin and the plague bacteria. Contact your local health department if you have questions about disposal of dead animals.
  • Use repellent if you think you could be exposed to rodent fleas during activities such as camping, hiking, or working outdoors. Products containing DEET can be applied to the skin as well as clothing and products containing permethrin can be applied to clothing (always follow instructions on the label).
  • Keep fleas off of your pets by applying flea control products. Animals that roam freely are more likely to come in contact with plague infected animals or fleas and could bring them into homes. If your pet becomes sick, seek care from a veterinarian as soon as possible
  • Do not allow dogs or cats that roam free in endemic areas to sleep on your bed.

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References

[1] Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of Vector-Borne Diseases (DVBD), “Plague: Frequently Asked Questions”. [Online]. Available: https://www.cdc.gov/plague/faq/index.html#cases

[2] World Health Organization, “Plague”. [Online]. Available: https://www.who.int/health-topics/plague#tab=tab_1

[3] C Demeure, O Dussurget, G Mas Fiol, et al., “Yersinia pestis and plague: an updated view on evolution, virulence determinants, immune subversion, vaccination, and diagnostics”, Genes Immun, vol. 20, num. 5, pp. 357-370, 2019. Available: 10.1038/s41435-019-0065-0

[4] L Mordechai, M Eisenberg, T Newfield, et al., “The Justinianic Plague: An inconsequential pandemic?”, Proc Natl Acad Sci, vol. 116, num. 51, pp. 25546-25554, 2019. Available: 10.1073/pnas.1903797116

[5] P Mackowiak, P Sehdev, “The Origin of Quarantine”, Clinical Infectious Diseases, vol. 35, num. 9, pp. 1071–1072, 2002. Available: 10.1086/344062

Understanding Leprosy on World Leprosy Day

by Dr. Jaclynn Moskow
World Leprosy Day in January

Leprosy is a chronic and progressive disease that primarily affects the skin and peripheral nervous system. The disease has been with us for thousands of years. There is evidence of the disease as far back as 4000 BC, in ancient Egypt. [1] In 1873, Norwegian physician Dr. Gerhard Armauer Hansen discovered that leprosy was caused by a bacterium. [2] Today, we call this bacterium Mycobacterium leprae, and we often refer to leprosy as Hansen’s Disease, in honor of Dr. Hansen. While leprosy caused significant morbidity and mortality in the past, cases today are rare and are curable with proper treatment.

How Is Leprosy Transmitted?

Leprosy does not spread very easily. Transmission is poorly understood, but it is thought to occur via respiratory droplets. Leprosy cannot be contracted from a single exposure to someone with the disease, but only from prolonged exposure over many months.[3] Leprosy cannot be transmitted sexually, and it cannot be passed from a pregnant woman to her fetus. Once an individual has begun treatment for leprosy, they are no longer contagious.

Not everyone who experiences prolonged exposure to leprosy will go on to develop the disease. There are both genetic and environmental factors that determine susceptibility. It is estimated that only 5-20% of people are susceptible to developing leprosy.[4] Surprisingly, individuals with HIV infection do not appear to be at an increased risk of contracting leprosy nor at an increased risk for severe outcomes.[5] The reasons for this remain unclear.

In addition to human reservoirs, leprosy has been found in armadillos, wild chimpanzees, mangabey monkeys, and British red squirrels. There are well documented instances of humans contracting leprosy through contact with armadillos.  

How Does Leprosy Present Clinically?

Symptoms of leprosy typically develop from 1 to 20 years after exposure, with an average incubation period of 5 years. [6] Leprosy often causes changes in skin color, with areas becoming hypopigmented or erythematous. Painless ulcers may be seen on the soles of the feet, and loss of eyebrows and eyelashes are sometimes noted. Subcutaneous nodules are also common.

In addition to the skin, leprosy affects the mucous membranes of the nose, throat, and eyes. Leprosy may cause congestion, nose bleeds, and sometimes collapse of the nasal septum, resulting in a characteristic “saddle nose deformity.”  Other findings include difficulty in blinking, photophobia, corneal ulcers, staphylomas, and glaucoma. Untreated leprosy may result in blindness.

Leprosy can produce significant peripheral neuropathy. The skin may become numb to touch, pain, and temperature. Muscle weakness can occur, and paralysis of the hands and feet may be noted. Sometimes the disease causes nerves to become enlarged. Observation of enlargement of the great auricular nerve may lead to diagnosis. 

As the disease progresses, burning, tingling, and pain occur. The hands and feet may become crippled.  Erosion of finger bones is sometimes seen, and toes and fingers may appear to be shorter as a result of reabsorption. Advanced disease may also cause erectile dysfunction, infertility, osteoporosis, and chronic kidney disease. 

Leprosy medical bacterial infection disease.

There are also psychiatric comorbidities associated with leprosy. One study found that 44% of patients with the disease suffer from depression, anxiety, or psychosis.[7]

How Is Leprosy Classified?

Two main systems have been used to classify leprosy. 

Traditionally, the disease was categorized as “tuberculoid,” “lepromatous,” or “borderline.” Tuberculoid leprosy is usually limited to a few skin lesions. It is milder than lepromatous or borderline leprosy, and is less contagious than the latter. Patients with tuberculoid leprosy mount immune responses that prevent the disease from progressing. In lepromatous and borderline leprosy, systemic infection is present. The skin, peripheral nervous system, and other organs may become involved.

A more modern classification of leprosy divides the disease into two types: “paucibacillary” (PB) or “multibacillary” (MB).  PB is defined as ≤ 5 skin lesions with no bacteria detected via biopsy.  MB is defined by the detection of bacteria on biopsy or by the presence of ≥ 6 skin lesions.

Who Is Impacted By Leprosy?

The incidence of leprosy is declining, with approximately 200,000 new cases expected this year – worldwide.

The countries reporting most leprosy cases are India, Indonesia, Papua New Guinea, The Central African Republic, Mozambique, Brazil, and French Guiana. More than half of all new cases occur in India. 

It is estimated that currently, approximately 2 to 3 million people are living with disabilities secondary to leprosy. [8]  It is commonly stated that leprosy is twice as common in men as women. The true discrepancy between the sexes remains unknown as sociocultural factors may have led to female cases being underreported. [9]  Leprosy is more common in adults than children, and more common in older children than younger children. 

Leprosy is extremely rare in the United States, with only 77 cases reported in 2019. The vast majority of these cases were imported, occurring in immigrants and refugees. Many countries in Europe reported zero cases in 2019. 

If you have a GIDEON account, click to explore Leprosy Outbreak Map

How Is Leprosy Diagnosed And Treated?

The diagnosis of leprosy generally begins with a clinical suspicion related to characteristic signs and symptoms. The gold standard for diagnosis is a biopsy of a suspicious area of skin or peripheral nerve. PCR has also proven to be a valuable tool.

In 2008, a second species, Mycobacterium lepromatosis, was also found to cause leprosy. Neither Mycobacterium lepromatosis nor Mycobacterium leprae have ever been successfully cultured under laboratory conditions. Both are obligate intracellular organisms, biologically related to the bacterium that causes tuberculosis.

In the 1940s, Promin was developed as the first effective treatment for leprosy. Promin  is broken down by the body into Dapsone. In the 1950s, clinicians began using Dapsone itself as a treatment.  Currently, Dapsone is rarely administered alone; and multi-drug regimens are more effective and may prevent the development of drug resistance. 

Multibacillary disease is typically treated with daily Dapsone and Clofazimine – in addition to  monthly Rifampin – administered for one year. Paucibacillary disease is typically treated with daily Dapsone plus monthly Rifampin for six months. Treatment may trigger severe inflammatory reactions. Anti-inflammatory drugs such as aspirin, prednisone, and thalidomide are sometimes used to combat such episodes.

Historical stigma

Throughout history, individuals affected with leprosy were discriminated against. In part, this was a reaction to the overt disfigurement seen in advanced cases. To this day,  the expression “treated like a leper” refers to feeling ostracized.

The disease was referenced as a curse in the Bible and by the Ancient Greeks.  In fact, the precise nature of the Biblical “leprosy” is not known.  During the Middle Ages, “Leper Colonies” were built to isolate these patients, with as many as 19,000 such institutions existing across Europe.[10]  During the 19th century, hospitals known as “Leprosaria” emerged for patients with leprosy.

Despite the fact that leprosy is now curable, significant stigma regarding the disease remains. There are still 750 Leper Colonies in India, housing more than 200,000 people.[11]  In some cases, Indian law discriminates against people with leprosy, including a statute that permits the detention of leprosy patients. Hopefully, the stigma associated with leprosy will disappear from all countries.  As long as discrimination remains, leprosy patients may avoid seeking treatment, and the disease will remain uneradicated. 

 

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References

[1] J. Gilbody, “Aspects of rehabilitation in leprosy”, Int. J. Lepr, vol. 60, num. 4, pp. 608-40, 1992. Available: http://ijl.ilsl.br/detalhe_artigo.php?id=NzM0&secao=EDITORIAL#

[2] R. Bhat and C Prakash, “Leprosy: an overview of pathophysiology”, Interdiscip Perspect Infect Dis, vol. 2012, num. 181089, 2012.  Available: 10.1155/2012/181089

[3] Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of High-Consequence Pathogens and Pathology DHCPP, “Hansen’s Disease (Leprosy): Transmission”. [Online]. Available: https://www.cdc.gov/leprosy/transmission/

[4] D Blok, S de Vlas, E Fischer, and J Richardus, “Mathematical modeling of leprosy and its control”, Adv Parasitol, vol. 87, pp. 33-51, 2015. Available: 10.1016/bs.apar.2014.12.002

[5] K Ukwaja, “Interactions between leprosy and human immunodeficiency virus: More questions than answers”, J Neurosci Rural Pract, vol. 6, num. 2, pp. 135-6, 2015. Available: 10.4103/0976-3147.150291

[6] World Health Organization, “Leprosy”. [Online]. Available: https://www.who.int/news-room/fact-sheets/detail/leprosy

[7] N Mahendra, R Yaduvanshi, C Sharma, R Ali, P Rathore, and A Kuchhal, “Psychiatric Co-morbidity in Patients of Hansen’s Disease”, International Journal of Contemporary Medical Research, vol. 5, num. 1, 2018. Available: https://www.ijcmr.com/uploads/7/7/4/6/77464738/ijcmr_1822_v1.pdf

[8] Centers for Disease Control and Prevention, National Center for Emerging and Zoonotic Infectious Diseases (NCEZID), Division of High-Consequence Pathogens and Pathology DHCPP, “World Leprosy Day: Bust the Myths, Learn the Facts”. [Online]. Available: https://www.cdc.gov/features/world-leprosy-day/

[9] R Sarkar, and S Pradhan, “Leprosy and women”, Int J Women’s Dermatol, vol. 2, num. 4, pp. 117-121, 2016. Available: 10.1016/j.ijwd.2016.09.001

[10] T Tulchinsky, and E Varavikova, “Communicable Diseases”, The New Public Health (Third Edition), 2014. [Online]. Available: https://www.sciencedirect.com/topics/nursing-and-health-professions/leprosarium

[11] The Leprosy Mission Trust India, “Leprosy.” [Online]. Available: https://www.leprosymission.in/leprosy-modern-challenges-of-an-ancient-disease/

All you need to know about waterborne diseases

by Dr. Jaclynn Moskow

Woman scientist takes a water sample from polluted pond.

 

Waterborne diseases are contracted through exposure to contaminated water including drinking water, water used in food preparation, and swimming water. 

They can be caused by bacteria, viruses, and parasites. Below is a partial list of waterborne disease pathogens, their microbial classification, and their resulting illnesses.

Bacteria, virus, and a parasite icon

Classification Microorganism Disease
Bacterium Campylobacter spp. Campylobacteriosis
Bacterium Escherichia coli E. Coli Diarrhea
Bacterium Legionella pneumophila Legionnaires’ Disease
Bacterium Salmonella enterica Salmonellosis
Bacterium Salmonella typhi Typhoid fever
Bacterium Shigella spp. Shigellosis
Bacterium Vibrio cholerae Cholera
Parasite Cryptosporidium spp. Cryptosporidiosis
Parasite Cyclospora cayetanensis Cyclosporiasis
Parasite Entamoeba histolytica Amoebiasis
Parasite Giardia lamblia Giardiasis
Parasite Naegleria fowleri Primary Amoebic Meningoencephalitis (PAM)
Parasite Schistosoma spp. Schistosomiasis
Virus Adenovirus Adenovirus
Virus Hepatovirus A Hepatitis A
Virus Norovirus Norovirus
Virus Rotavirus Rotavirus

 

WHO IS MOST AFFECTED BY WATERBORNE DISEASES?

The vast majority of waterborne diseases are contracted by individuals who lack access to safe and sanitized water for drinking and personal hygiene. This problem is pervasive around the globe. 

According to the World Health Organization (WHO), 2.2 billion people do not have access to safe drinking water, which equates to 1 in 3 people on the planet. Additionally, 4.2 billion people lack access to adequate sanitation facilities such as hygienic toilets.[1] This lack of access to safe water and sanitation results in 4  billion cases of waterborne diseases annually and 3.4  million deaths.[2] 

Increasing access to clean water worldwide is the single most critical step we can take to prevent morbidity and mortality from these devastating diseases.

Delivery of humanitarian aid and water by military helicopter

 

Symptoms of waterborne diseases are primarily gastrointestinal and include fever, nausea, vomiting, and diarrhea. 88% of all deaths that occur as a result of diarrhea can be attributed to these infections.[3]  90% of diarrhea deaths involve children under the age of five years.[4] Children are particularly susceptible to waterborne diseases, in part because their naive immune systems have not yet encountered most pathogens. 

Another group who are at increased risk for contracting waterborne diseases is people that are immunocompromised, including individuals living with HIV/AIDS. Unfortunately, the HIV epidemic has hit hardest in areas where access to clean water is lacking. 

Countries that have reported recent outbreaks of Cholera include Bangladesh, Haiti, The Democratic Republic of the Congo, Ethiopia, Somalia, and Yemen.[5]  The Democratic Republic of the Congo and Haiti have also reported recent outbreaks of Typhoid fever, as have Uganda and Pakistan.[6]

 

HOW CAN TRAVELERS AVOID WATERBORNE DISEASES?

Tourists are at increased risk for contracting waterborne diseases, in part because they lack prior exposure and immunity. To avoid waterborne illnesses when traveling to an area of concern, the Centers for Disease Control and Prevention (CDC) recommends the following[7]:

  •     Eat only foods that are cooked and served hot
  •     Avoid food that has been sitting on a buffet
  •     Eat raw fruits and vegetables only if you have washed them in clean water or peeled them
  •     Only drink beverages from factory-sealed containers
  •     Avoid ice – which may have been prepared from unclean water
  •     Only drink pasteurized milk
  •     Wash hands often with soap and water for 20 seconds, especially after using the bathroom and before eating
  •     If soap and water are not available, use a hand sanitizer that contains at least 60% alcohol
  •     Keep your hands away from your face and mouth

Travelers can also receive vaccines for some waterborne diseases, namely, Typhoid Fever, Hepatitis A, and Cholera.  Since the efficacy of these vaccines varies, general precautions including avoidance of tap water should still be taken.

Glass of contaminated water on grey background

 

WHAT WATERBORNE DISEASES ARE SEEN IN THE DEVELOPED WORLD?

Sporadic outbreaks of several waterborne diseases are also reported in industrialized countries. A well-known example occurred in 1993 in Milwaukee, Wisconsin when over a two-week period approximately 403,000 individuals experienced a diarrheal illness. The cause was determined to be Cryptosporidium that had contaminated one of the city’s water-treatment plants.[8]  A more recent example occurred in 2019 when over 2000 residents of a small island in Norway became ill as a result of Campylobacter contaminating the local water supply.[9] 

In 2015, 31% of students at a school camp in South Korea became ill as a result of water contaminated with E. coli.[10] There have also been outbreaks of typhoid fever in the United States. Outbreaks of waterborne disease increase after extreme weather events such as flooding caused by heavy rains and snowfall. After Hurricane Katrina, Salmonella enterica, Vibrio cholerae, and Norovirus were detected in individuals in evacuee camps.[11]

 

CONTRACTING WATERBORNE DISEASES WHILE SWIMMING

Waterborne diseases can also be contracted by swimming in pools, lakes, rivers, and oceans. This includes Giardia lamblia, which is one of the most common intestinal parasites worldwide, including in the United States. Giardia lamblia can enter the body in a number of ways, including ingestion of water while swimming. 

Another parasite that can be contracted while swimming is Naegleria fowleri, which is found in freshwater and often referred to in headlines as “the brain-eating amoeba.” Naegleria fowleri invades the body via the nose and travels to the brain by way of the olfactory nerve. Unlike Giardiasis, Primary Amebic Meningoencephalitis caused by Naegleria fowleri is almost always fatal. Fortunately, the condition is exceedingly rare.

Over 250 million persons suffer from Schistosomiasis – in Africa, Asia, and the Americas.  Parasites enter through the skin, usually while swimming, working, or simply walking through freshwater. The parasites travel through the bloodstream, eventually lodging in the liver, urinary system, and other organs with resultant damage to tissues, or even cancer which can develop over many years.

Recreational water areas such as pools, hot tubs, and spas are also at risk of contamination by a variety of pathogens. Between 2000 and 2014, 212 reported outbreaks of Cryptosporidium were associated with recreational water facilities.[12] Adenovirus is also known to cause outbreaks from recreational water, as is Legionella pneumophila. Legionella pneumophila is a unique waterborne pathogen in that it often must be aerosolized to cause infection. The organism is transmitted via hot tubs, showers, humidifiers, and air conditioning systems. Aerosolization allows Legionella pneumophila to enter the lungs and thus, unlike other waterborne pathogens, it can cause respiratory illness. A milder form of the disease caused by Legionella species is known as Pontiac fever, and the more severe form is known as Legionnaires’ Disease.

 

CAN SARS-COV-2 BE TRANSMITTED THROUGH THE WATER SUPPLY?

Fortunately, you cannot contract COVID-19 through contaminated water. Viruses may be classified as either enveloped or non-enveloped. Viruses with envelopes have an outer layer of proteins and lipids that surround their viral capsids. Non-enveloped viruses can survive for relatively long periods outside the body – and in much harsher conditions – than can enveloped viruses. 

Viruses that cause waterborne diseases, such as Hepatovirus A, Norovirus, Rotavirus, and Adenovirus, are all non-enveloped. In contrast, members of the Coronaviridae (such as SARS-CoV-2) are enveloped and thus cannot be spread through the water supply.

 

SARS-CoV-2 structure. Anatomy of the coronavirus

 

Although we cannot contract SARS-CoV-2 from the water supply, inactive SARS-CoV-2 viral material can still be detected in the wastewater from areas with COVID-19 outbreaks. This can be useful in tracking outbreaks. In Switzerland, for example, laboratories were able to determine that a new “British variant” of SARS-CoV-2 had arrived by simply monitoring wastewater.[13]  In fact, monitoring wastewater is an emerging epidemiological tool for tracking many pathogens, including many of the waterborne diseases discussed above.

 

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References:

[1] World Health Organization. 1 in 3 people globally do not have access to safe drinking water – UNICEF, WHO. New York, Geneva: World Health Organization; 18 June 2019. [cited 2021 Jan 10]. Available from: https://www.who.int/news/item/18-06-2019-1-in-3-people-globally-do-not-have-access-to-safe-drinking-water-unicef-who

[2] World Bank. World Development Indicators 2015. Washington, DC: World Bank Publications; 2015. [cited 2021 Jan 10]. Available from: https://openknowledge.worldbank.org/handle/10986/21634

[3] Prüss-Üstün A, et al. Safer water, better health: costs, benefits and sustainability of interventions to protect and promote health. World Health Organization. 2008.

[4] Jong-wook, L. Water, sanitation and hygiene links to health. Geneva: World Health Organization; Nov 2004. [cited 2021 Jan 10.] Available from: https://www.who.int/water_sanitation_health/publications/facts2004/en/

[5] European Centre for Disease Prevention and Control. Cholera worldwide overview. Solna: ECDC; 2021. [cited 2021 Jan 11.] Available from: https://www.ecdc.europa.eu/en/all-topics-z/cholera/surveillance-and-disease-data/cholera-monthly

[6] World Health Organization. Emergencies preparedness, response – Typhoid fever. New York, Geneva: World Health Organization; 2021. [cited 2021 Jan 11]. Available from: https://www.who.int/csr/don/archive/disease/typhoid_fever/en/

[7] Center for Disease Control and Prevention. Travels Health – Disease Directory – Typhoid Fever. Atlanta: CDC; 01 Dec 2020. [cited 2021 Jan 10.] Available from: https://wwwnc.cdc.gov/travel/diseases/typhoid

[8] Mac Kenzie WR, et al. A massive outbreak of Cryptosporidium infection transmitted through the public water supply. N Engl J Med. 1994;331:161-167.

[9] Paruch L, et al. DNA-based faecal source tracking of contaminated drinking water causing a large Campylobacter outbreak in Norway 2019. Int J Hyg Environ Health. 2020 Mar;224:113420.

[10] Park J, et al. A waterborne outbreak of multiple diarrhoeagenic Escherichia coli infections associated with drinking water at a school camp. Int J Infect Dis. 2018

[11] Center for Disease Control and Prevention. Infectious Disease and Dermatologic Conditions in Evacuees and Rescue Workers After Hurricane Katrina – Multiple States, August – September, 2005. Morbidity and Mortality Weekly Report. 30 September, 2005;54(38):961-964.

[12] Hlavsa MC, et al. Outbreaks Associated with Treated Recreational Water – United States, 2000-2014. MMWR Morb Mortal Wkly Rep 2018;67:547–551

[13] Jahn, K. Detection of SARS-CoV-2 variants in Switzerland by genomic analysis of wastewater samples. medRxiv 2021.01.08.21249379; doi: https://doi.org/10.1101/2021.01.08.21249379

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