CDC Outbreak Investigation: Multistate Outbreak of Listeriosis Linked to Whole Cantaloupes from Jensen Farms, Colorado

Infectious Disease Epidemiology
Kristin Lake

Disease: Listeriosis

Causative Agent:Listeria monocytogenes

Scientific Classification:

  • Kingdom: Bacteria
  • Division: Firmicutes
  • Class: Bacilli
  • Order: Bacillales
  • Family: Listeriaceae
  • Genus: Listeria
  • Species: L. monocytogenes

Morphology: L. monocytogenes bacteria are Gram-positive, motile, non-sporulating, short rods that can form longer chains.


Cover photograph
 (Copyright © 2011, American Society for Microbiology. All Rights Reserved.): Listeria monocytogenes is capable of efficient growth within the porcine gallbladder. Shown is a false-colored scanning electron micrograph of L. monocytogenes in the lumen of the porcine gallbladder. (http://iai.asm.org/content/79/1/F1.medium.gif)


Outbreak Starting Location: 
Jensen Farms in Granada, Colorado U.S.
Date of Occurrence: Between July 31, 2011 through October 27, 2011

Epidemiological Data:Gender, Age, Location, Time, Dietary Determinants, etc.

  • A total of 146 persons infected with any of the four outbreak-associated strains of Listeria monocytogenes were reported to CDC from 28 states. The number of infected persons identified in each state was as follows: Alabama (1), Arkansas (1), California (4), Colorado (40), Idaho (2), Illinois (4), Indiana (3), Iowa (1), Kansas (11), Louisiana (2), Maryland (1), Missouri (7), Montana (1), Nebraska (6), Nevada (1), New Mexico (15), New York (2), North Dakota (2), Oklahoma (12), Oregon (1), Pennsylvania (1), South Dakota (1), Texas (18), Utah (1), Virginia (1), West Virginia (1), Wisconsin (2), and Wyoming (4).
  • Among persons for whom information was available, reported illness onset ranged from July 31, 2011 through October 27, 2011.
  • Ages ranged from <1 to 96 years, with a median age of 77 years. Most ill persons were over 60 years old.
  • 58% of ill persons were female. 42% of ill persons were male.
  • Among the 144 ill persons with available information on whether they were hospitalized, 142 (99%) were hospitalized.
  • Thirty deaths were reported. In addition, one woman pregnant at the time of illness had a miscarriage.
  • Thirty deaths reported by state: Colorado (8), Indiana (1), Kansas (3), Louisiana (2), Maryland (1), Missouri (3), Nebraska (1), New Mexico (5), New York (2), Oklahoma (1), Texas (2), and Wyoming (1).
  • Among persons who died, ages ranged from 48 to 96 years, with a median age of 82.5 years.
  • Seven of the illnesses were related to a pregnancy; three were diagnosed in newborns and four were diagnosed in pregnant women. One miscarriage was reported.
  • Among the 140 ill persons with available information on what they ate, 131 (94%) reported consuming cantaloupe in the month before illness onset.

Etiology and Details of Outbreak Investigation: In the Colorado cantaloupe outbreak, the bacteria were found to be in the packing center of the Colorado farm that the produce was harvested from.  The floors of the facility had standing water due to poor design which made them difficult to clean.  The production line belts, which were also difficult to sanitize, tested positive for Listeria monocytogenes rods as well.  L. monocytogenes is able to proliferate in refrigerator temperatures (39° F) as well as the temperature of the human body (98.6° F).  These bacteria can also be found in soil, animal products such as meat, unpasteurized milk and cheeses, some processed foods, vegetables and animal waste.  Alcohol and chlorine bleach are able to kill this bacteria on surfaces.

Clinical Features, Signs and Symptoms: The incubation period prior to the onset of symptoms can last from one week to several weeks.  Otherwise healthy patients infected with Listeriosis experience fever, myalgia, gastrointestinal distress, nausea, diarrhea, flu-like symptoms, and invasive infection in other parts of the body such as the bloodstream.  Some people may develop more severe symptoms such as meningitis, encephalitis, mental changes, brain abscesses, or death.  Pregnant women and patients with compromised or weakened immune systems can experience severe symptoms of fever, myalgia, gastrointestinal distress, nausea, diarrhea, headache, stiff neck, confusion, loss of balance, and convulsions in addition to a flu-like illness.  However, infection during pregnancy can lead to miscarriage, stillbirth, premature delivery, or life-threatening infection in the newborn since the illness can be transmitted from mother to child.  Diagnosis is confirmed when Listeria bacteria are isolated from the patient’s blood, cerebrospinal fluid, or other body fluid.

Treatment: Treatment of Listeriosis consists of immediate IV antibiotic therapy using Vancomycin, Azithromycin, Ciprofloxacin, Flouroquinolones, Ampicillin, Rifampicin, Trimethoprim-sulfamethoxazole, and Linezolid.

Prevention: The CDC effectively recalled all cantaloupes from Jensen Farms in Granada, Colorado via press release and believe the outbreak to be over although some consumers that are unaware of the outbreak may still have tainted cantaloupes in their possession if they’ve frozen them.  They recommended consumers to first dispose of cantaloupes in a sealed plastic bag so they cannot come into contact with humans and animals.  They then recommended consumers to sanitize their refrigerator shelves, storage bins, countertops and cutting boards with a chlorine bleach solution and reminded consumers the importance of hand washing before and after handling foods.

References

CDC - December 8, 2011 - CDC - Multistate Outbreak of Listeriosis Linked to Whole Cantaloupes from Jensen Farms, Colorado. (2011, December 8). Centers for Disease Control and Prevention. Retrieved June 13, 2012, from http://www.cdc.gov/listeria/outbreaks/cantaloupes-jensen-farms/120811/index.html#advice-consumers

Davis, C., Nettleman, M., & Stoppler, M. (n.d.). Listeriosis (Listeria monocytogenes Infection). MedicineNet. Retrieved June 13, 2012, from www.medicinenet.com/listeria/article.htm

Information on the Recalled Jensen Farms Whole Cantaloupes. (2012, January 9). U S Food and Drug Administration Home Page. Retrieved June 13, 2012, from http://www.fda.gov/Food/FoodSafety/CORENetwork/ucm272372.htm

Ohio State University. (2005, April 25). Food Microbiology-Lecture Listeria monocytogenes and Listeriosis. http://class.fst.ohio-state.edu/fst636/lecture/Listeria%20lecture.pdf. Lecture conducted from Micro 636.01/ FST 636.01, Columbus.

Crimean-Congo Hemorrhagic Fever

Infectious Disease Epidemiology
Kristin Lake

Background Information: Crimean-Congo Hemorrhagic Fever is a zoonotic, tick-borne disease caused by the arbovirus Crimean-Congo Hemorrhagic Fever Virus of the Bunyaviridae family and Nairovirus genus and has a mortality rate as high as ~30%.  It is endemic in parts of Africa, Asia and Europe due to the locale of at least 31 known species of ixodid ticks primarily of the Hyalomma plumbeumRhipicephalus sanguineus, and Boophilus calcaratusgenera.

Causative agent: Infected ixodid ticks are mechanical vectors as well as reservoirs of this disease and transmit Crimean-Congo Hemorrhagic Fever Virus to humans and animals through bite exposures which exchange fluids between the tick and its host.  CCHFV is also transmitted through contact with infected tissues and/or blood so transmission via animal product exposure and patient-caregiver nosocomial outbreaks and are a real threat.

Epidemiology: Most of the people that become infected with CCHF are men that work outdoors and/or with livestock.  Due to the viruses ability as a causative agent of severe hemorrhagic fever “it is classified as a biosafety level 4 pathogen and a potential bioterrorism agent due to its aerosol infectivity and its ability to cause HF outbreaks with high case fatality.” (Y. Guo, et al., 2012)  Due to outbreaks of epidemic proportions in recent years, renewed interest has been applied to this infectious disease.  Rising numbers of cases of tick-borne diseases in the last decade have also garnered increasing attention from the scientific community who recognize the serious pathogenic potential of these arthropods.

Morphology: The Crimean-Congo Hemorrhagic Fever Virus is monomeric, segmented, circular, negative sense, single-stranded RNA.  “Its morphology is helical and the virus is enveloped.” (Standford, n.d.)
 


Transmission Electron Micrograph of the morphology
of Crimean-Congo Hemorrhagic Fever Virus 
(Stanford University http://www.stanford.edu/group/virus/pox/2000/b6.gif)

Clinical Manifestations: The incubation period varies depending upon the type of exposure to CCHFV.  If a tick-bite exposure is the cause, the incubation period lasts between 1-3 days and if tissue and/or blood exposure is the cause, the incubation period lasts between 5-6 days.  The onset of flu-like symptoms then becomes apparent to the infected individual and hemorrhage occurs 3-5 days after the initial onset of symptoms.  Fever, malaise, mood instability, agitation, mental confusion, throat petechiae, epistaxis (nosebleeds), hematuria (blood in urine), vomiting, gastrointestinal bleeding, black stools, hepatomegaly (enlarged liver), elevated transaminase levels, disseminated intravascular coagulation, leukopenia, thrombocytopenia, acute kidney failure, acute respiratory distress syndrome, and shock are soon to follow.  Most deaths occur within the second week of illness and recovery begins around the 9th or 10th day after the onset of symptoms.  Treatments include immunotherapy, antiviral drugs such as Ribavirin, surgical stemming of internal hemorrhage, blood transfusion, intensive supportive care, isolation, and increased infection control standards with body substance isolation.  Current treatments have not shown to be very effective making this disease extremely deadly.  However, there is currently a vaccine awaiting FDA approval.
 


 A patient with Crimean-Congo hemorrhagic fever with profound
ecchymosis of the left upper extremity is shown. (Medscape
http://img.medscape.com/pi/features/slideshow-slide/bioterrorism/fig13.jpg)


References

Congo-Crimean Hemorrhagic Fever Virus. (n.d.). Stanford University. Retrieved June 5, 2012, from http://www.stanford.edu/group/virus/pox/2000/Congo.html

Guo, Y., Wang, W., Lou, Z., Rao, Z., Ji, W., Deng, M., et al. (2012, March 14). Crimean–Congo hemorrhagic fever virus nucleoprotein reveals endonuclease activity in bunyaviruses . PNAS: Proceedings of the National Academy of Sciences . Retrieved June 5, 2012, from http://www.pnas.org/content/109/13/5046.abstract

Papa, A., Christova, I., Papadimitriou, E., & Antoniadis, A. (n.d.). Crimean-Congo Hemorrhagic Fever in Bulgaria - Vol. 10 No. 8 - August 2004 - Emerging Infectious Disease journal - CDC. Centers for Disease Control and Prevention. Retrieved June 5, 2012, from http://wwwnc.cdc.gov/eid/article/10/8/04-0162_article.htm

Tahmasebi, F., Ghiasi, S., Mostafavi, E., Moradi, M., Piazak, N., Mozafari, A., et al. (n.d.). Molecular epidemiology of Crimean- Congo … [J Vector Borne Dis. 2010] - PubMed - NCBI. National Center for Biotechnology Information. Retrieved June 5, 2012, from http://www.ncbi.nlm.nih.gov/pubmed/21178213

Whitehouse, C. (n.d.). Crimean-Congo hemorrhagic fever. [Antiviral Res. 2004] - PubMed - NCBI. National Center for Biotechnology Information. Retrieved June 5, 2012, from http://www.ncbi.nlm.nih.gov/pubmed/15550268

Case Study

Bacteria, Viruses and Health

Kristin Lake

A 38 year old man named Brian visited his local doctor complaining of high fever, malaise, loss of appetite and headache. Patient history revealed that Brian is a photojournalist for a travel magazine. In the past 30 days Brian has traveled on assignment to Italy, London, and France. Brian is very careful not to drink local water when traveling and he only eats well cooked foods. He did mention being bit by a ferret on the street of France, but the animal seemed fine and the owner took it away after the incident. Brian did not seek medical care because he thought it would be too complicated to deal with while overseas and the bite was very small. He does have pain and itching at the site of the animal bite. Lab tests on Brian’s blood did not show the presence of any gram-positive or gram-negative bacteria.


1. What microorganism do you believe is to blame for this illness (be specific)? Provide background information on this organism, history, morphology, virulence factors, toxins, etc.

I believe that Lyssavirus rabies is responsible for Brian’s illness.  The rabies virus is neurotropic and is part of the rhabdovidae family and small mammals are especially susceptible to this disease but it can be transmitted to any mammal including humans.  “Rabies has been noted in history since about 2000 BC when owners of rabid dogs were cautioned against getting bitten. The word rabies is derived from the Latin word rabies, which meant ‘madness or rage.’  In the 15th century, Italian physician Girolamo Fracastoro studied rabies and concluded that it was a communicable disease transmitted to people by direct contact with saliva from infected animals. He termed the disease “rabies.” In 1895, after studying the data presented by Fracastoro centuries before, Louis Pasteur was able to produce a vaccine against the disease-causing viruses without actually discovering or isolating the viruses.  The virus that causes rabies is Lyssavirus (Lyssa is the Greek goddess of madness, rage, and frenzy) rabies, a cylindrical or bullet-shaped virus that is enveloped and contains a negative-sensed RNA that makes up its genetic material.” (MedicineNet, 2012)

Lyssavirus Rabies Virus

This transmission electron micrograph reveals the bullet-shaped morphology of the rabies virus. Courtesy of:  http://www.ppdictionary.com/viruses/rabies.htm 

2. What information from the patient’s symptoms contributed to your decision? Did this information allow you to rule out any other possible culprits? What information from the patient’s history and/or lab samples that contributed to your decision? Support your answers with factual evidence and logical reasoning.

Brian’s symptoms consisted of a high fever, malaise, loss of appetite and a headache which are consistent with a systemic infection of some etiology.  Brian’s bite wound itself had localized inflammation since itching and pain were associated with it.  Considering the patient’s history, it is unlikely that his symptoms are due to fungal, prionic, or parasitic infection(s) but are not entirely ruled out due to his recent travels and potential exposure to pathogens of this nature despite his diligence to avoid exposure.  Brian’s blood cultures showed that there was no Gram positive or Gram negative bacteria at the site of the bite wound which was indicative that bacteria was not responsible for his symptoms.  The next logical option was that his infection was viral in nature.  Given the type of animal the bite was received from, and their susceptibility as carriers of disease, the etiology of Brian’s infection can most likely be traced back to the ferret he came in contact with.  Ferret saliva can carry both bacteria and viruses making it capable of transmitting a potential pathogen if the integrity of the skin is compromised.  Furthermore, itching and pain at the wound site, fever, and headache are all classic symptoms of the early stage of rabies in humans.  “After the first exposure (in most people, an animal bite), the symptoms of itching or discomfort like pins or needles pricking the skin occur at the bite area. In addition, the person may develop fever and a headache. Investigators suggest these symptoms may last from about two days to weeks.  This is the acute phase or the acute incubation phase of the disease.” (MedicineNet, 2012)  In addition to this evidence, Brian’s infection is consistent with the known timeline of exposure to the development of symptoms in humans.  According to the history given, it is unclear whether the ferret was quarantined or experienced latent neurological stages of the illness which ultimately resulted in death.  It is unclear if public health officials in France have been made aware of the incident so it is assumed that the animal is not available for necropsy and thus cannot contribute to any diagnostic decisions.

3. What is the epidemiology of this disease? Identify risk factors for this disease and describe the disease course/outcome in humans.

Ferrets are capable of contracting the raccoon and skunk strains of the virus in the U.S. and the fox strain in Europe.  Despite their propensity to contract and transmit diseases, it is highly unusual that a ferret would infect a human with rabies through a bite exposure but it is not impossible or absolutely unheard of.  Cats, dogs and livestock represent the largest rabies risks to humans due to our close contact with them.  Also, there is a low incidence of rabies vaccinations for domestic animals in many countries making it endemic in parts of the world.  Bats, skunks, foxes and raccoons represent the largest rabies risks in the wild but again, the virus can be transmitted to any mammal.  There are two ways to contract rabies, bite and non-bite exposures with an infected mammal.  “Exposure requires that there be infective virus and penetration of the virus into wounds or mucous membranes.  Non-bite exposures include scratches, licks, inhalation of aerosols and other events that lead to contamination of an open wound or mucous membrane.” (Rabies and the Domestic Ferret, 2009)  The fact that the owner of the ferret that bit Brian took the animal away after the incident could be attributed to the owner’s knowledge that the ferret was not immunized.  Most responsible ferret owners are aware of the potential risks that ferrets can pose and that euthanasia can sometimes be the result of a bite investigation if a ferret is not vaccinated for rabies.  Most likely the owner was aware of this and to avoid any trouble he took the ferret away.  It’s also possible that the owner noticed that the ferret had been acting strangely and realized that the ferret may have contracted rabies after the bite occurred and took him away to avoid trouble.

4. What steps can be taken to treat the illness? How and why are the treatments effective (or ineffective)? Are there any concerns or other complications of this disease?

Due to Brian’s exposure, symptoms and the lack of knowledge regarding the state of the ferret, cleansing of the wound and immediate preemptive treatment with rabies immune globulin and a rabies vaccine schedule should be administered to avoid late stage neurologic involvement while laboratory RT-PCR tests confirm this diagnosis through the detection of rabies antibodies in Brian’s blood.  “As of 2010, the CDC recommends additional doses (injections) of rabies vaccine [Imrab 3] on the third, seventh, and 14th day after exposure. This schedule is for people who have had no previous treatment (vaccination) against rabies. For people previously vaccinated against rabies, only two doses of the vaccine are recommended; one as soon as possible after the exposure (no rabies immune globulin is recommended) and one more three days later.  The reason human rabies immune globulin is used (and sometimes even injected into the bite area) is that it immediately attacks the virus and slows or stops viral progression through the nerves. [The rabies] vaccine is used to stimulate the body’s immune response enough to make the body develop enough of an immune response to eventually kill all of the virus population in the body.”  (MedicineNet, 2012)  Brian should be continually monitored for anxietystress, tension, delirium, drooling, convulsions, exaggerated sensation at the bite site, excitability or combativeness, hallucinations, loss of feeling in an area of the body, loss of muscle function, muscle spasms, numbness and tingling, restlessness, insomnia, and difficulty swallowing as these are indicative of the progression of neurological involvement and thus the latent stages of illness which will require more intensive supportive care and may lead to death.  Containment and quarantine are only necessary in late stage human cases where the infected individual is a danger to themselves and/or their caregivers and require substantial supportive care and additional infection control standards.  Human-to-human transmission of rabies is rare and mostly occurs through organ transplantation.  The prognosis for patients who receive immediate treatment is extremely good.  However, death is usually imminent for patients who display the latent stages of illness.


References

Management of Bites to Humans, Animal Bites and Rabies Risk - Minnesota Dept. of Health. (n.d.). Minnesota Department of Health. Retrieved March 20, 2012, from http://www.health.state.mn.us/divs/idepc/diseases/rabies/risk/human.html

Rabies. (n.d.). MedicineNet. Retrieved March 20, 2012, from www.medicinenet.com/rabies/article.htm

Rabies and the Domestic Ferret. (n.d.). Kansas State University. Retrieved March 20, 2012, from www-personal.ksu.edu/~sprite/RABIES.HTML

Table 1: Human Rabies Risk Evaluation: Species of the Biting Animal. (n.d.). Minnesota Department of Health. Retrieved March 20, 2012, from www.health.state.mn.us/divs/idepc/diseases/rabies/risk/table1.pdf

Woerpel, R., & Rosskopf, W. (n.d.). Ferret Facts . Animal Health Center . Retrieved March 20, 2012, from http://www.caringtogether.com/exotics/ferrets.html

Emerging Infectious Disease: Lyme disease

Bacteria, Viruses and Health

Kristin Lake

Organism, Transmission and Disease

Lyme disease is caused by the bacterium Borrelia burgdorferi in the United States, as well as Borrelia afzelii and Borrelia garinii in Europe.  About 90% of the time it is transmitted through the bites of nymph ixodes ticks, more commonly known as deer ticks.  Ticks are opportunistic, parasitic, arthropods that feed on the blood of their hosts.  During a blood meal with a Lyme infected animal or human, the bacteria is transmitted from the host’s bloodstream into the tick’s stomach.  The tick then becomes a mechanical vector of disease.  During the next feeding, the B. burgdorferi spirochetes are transmitted between the tick and its host, passing on the bacteria and continuing its life cycle in a new host.  This is a very effective method of transmission.  ”The ticks’ saliva has components which disrupt the normal immune response to a bite and which afford protection to the infectious spirochaetes allowing them to establish themselves in the local area.” (Matthews, 2011)  

An image demonstrating the size of a lxodes deer tick in its nymph stage when it is most likely to transmit B. burgdorferi bacteria to its host(s). Some ticks in their nymph stage are as small as the period at the end of a sentence. Picture of a deer tick. N.d. MedicineNet. Web. 21 Mar. 2012.
An image demonstrating the size of a ixodes deer tick in its nymph stage when it is most likely to transmit B. burgdorferi bacteria to its host(s). Some ticks in their nymph stage are as small as the period at the end of a sentence.
Picture of a deer tick. N.d. MedicineNet. Web. 21 Mar. 2012.

Lyme Disease pathology  infection with Borrelia burgdorferi sensu lato Lyme disease pathology borellia bacteria infection. N.d. Lyme Disease Guide. Web. 21 Mar. 20
Lyme disease pathology – infection with Borrelia burgdorferi sensu lato
Lyme disease pathology borellia bacteria infection. N.d. Lyme disease Guide. Web. 21 Mar. 2012. 

Epidemiology

This disease was first noted in 1975 in Lyme, Connecticut, a small, very rural town.  Resident mothers received diagnoses of rheumatoid arthritis in their children, all of whom lived in close proximity of one another.  The mothers reached out to researchers from Yale who noted the statistically improbable, unusual, grouping of cases occurring in this small, rural town.  The investigation led Dr. Allen Steer, M.D.  and his researchers to the discovery of the borrelial organism responsible for the illness officially designated as Lyme disease in 1982.  They traced the cutaneous manifestations post tick bite inoculation, and their antibiotic responsiveness to the 1950s literature written by European researchers.  The organism in the European literature was a different strain (B. afzelii) of the borrelial organism which was confirmed as the causative agent in the Connecticut epidemic.  However, this was not the first literary incidence of the bacteria B. burgdorferi.  In 1883, German physician Alfred Buchwald first described the dermatological manifestation known as acrodermatitis chronic atrophicans (ACA).  In 1912, Swedish dermatologist Arvid Afzelius first described the “bull’s-eye” rash, erythema chronicum migrans (ECM) which is now known as erythema migrans.  “In the 1920s, [Dr. Charles] Garin and [Dr. A.] Bujadoux described a patient with meningoencephalitis, painful sensory radiculitis, and erythema migrans following a tick bite, and they postulated the symptoms were due to a spirochetal infection.  The neurologic manifestations and the association with lxodes ticks (also known as deer ticks) were recognized by the mid 1930s and were known as tick-borne meningoencephalitis.  In the 1940s, [Dr. Alfred] Bannwarth described several cases of chronic lymphocytic meningitis and polyradiculoneuritis, some of which were accompanied by erythamatous skin lesions.” (Medscape, 2011)

Clinical manifestations of Lyme disease consist of:

  • Acute Erythema Migrans Rash or the “bull’s-eye” rash appears within 24-48 hours. Cutaneous inflammation surrounds the initial site of the bite, then clears, with another circular pattern of inflammation in the localized area.  However more than 1 in 4 patients never develop a rash in this stage.

Erythema Migrans
Lyme disease initially affects the skin, causing an expanding reddish rash similar to a target or a bulls-eye
Lyme disease rash N.d. MedicineNet. Web. 21 Mar. 2012.

  • Subacute flu-like syndrome with fever, general malaise, stiff neck, headache, and diffuse aches and pains in the early dissemination stage.
  • In some, bacterial dissemination will result in a multicentric erythema migrans.
  • Fewer than 5% of patients will develop cardiac conduction abnormalities.
  • Others may develop a mild hepatitis or myositis, whereas some will develop arthralgias or frank arthritis.
  • 10% to 15% of patients will develop nervous system involvement that typically consists of all or part of the triad of lymphocytic meningitis, cranial neuritis, and painful radiculitis.
  • Late stage involvement may also cause chronic Lyme arthritis in the joints (particularly the knees), neurological symptoms consisting of facial palsies, confusion, numbness, pain or weakness in the limbs (peripheral neuropathy and peripheral radiculopathy), poor motor coordination, and heart problems which manifest as arrhythmias, palpitations, lightheadedness, fainting, chest pain, shortness of breath and heart failure.

    (Halperin and Roos, 2011), (University of Maryland Medical Center, 2011)

Disease Process

“Variation in environmental and host conditions promotes different gene expression and changes in the composition of the membrane proteins of the spirochete.  This adaptation is a critical step in the pathogenesis and transmission of Lyme disease.” (Medscape, 2011) During transmission, spirochetes take advantage of the protein plasmin found in ticks’ saliva.  This protein prevents the first line of defenses, neutrophils, from congregating in the affected area.  “The plasmin confounds the immune system’s efforts which are further obstructed by the spirochaetes ability to reduce the expression of surface proteins that would be targeted by such [B. burgdorferi] antibodies.  This avoidance of detection involves alterations in the VIsE surface protein which effectively inactivates certain immune system components.”  (Matthews, 2011)  B. burgdorferi may also make it complicated for the immune system to target by positioning itself inconspicuously in the extracellular matrix.  

Early Disseminated Lyme Disease Pathology

Over the days and weeks after a bite from an infected tick, the spirochaetes slowly enter the bloodstream from where they can gain access to almost every tissue in the body through the circulation. Infection can then spread quickly through the system and cause symptoms at places far away from the initial tick bite. The erythema migrans rash may now arise in other locations on the body as well as the original location as the spirochaetes cause other localised inflammation. Once again, the body’s normal response leading to the elimination of the spirochaetes through the action of neutrophils is inhibited by the pathogen’s use of the protease plasmin from the ticks’ saliva. The Borrelia bacteria are also adept at other tactics to avoid detection by the immune system. These tactics employed by the Lyme disease bacteria have potential ramifications for the development of autoimmune complications. Exposure to the spirochaetes creates a chronic inflammatory response which may begin to damage ordinary bodily tissues due to molecular mimicry employed by the bacteria to avoid detection. In their imitation of normal body cells the bacteria can confuse the immune system into attacking ordinary body tissues which goes some way to explaining the chronic symptoms of Lyme disease experienced by some patients even after eradication of the infection by antibiotics. Where the immune system has produced antibodies against its own cells it will continue to attack these cells even in the absence of the Borrelia bacteria, leading to persistent symptoms including joint pain. Effectively, Lyme disease may induce an autoimmune condition similar to rheumatoid arthritis which persists even after the causative agent, the Borrelia bacteria, is removed.

A Multisystem Effect

Borrelia burgdorferi s.l. infection creates multiple symptoms due to it multisytem effects. In a large number of those infected, the symptoms only go as far as an acute flu-like illness which is effectively fought by the body and which leads to no other persistent effects from the tick bite. Stage II, early disseminated Lyme disease, involves the cardiovascular system and/or the central nervous system, leading to myocarditis, meningoencephalitis, and polyradiculitis. The levels of inflammation during this stage are much higher in these tissues than anywhere else in the early acute stage and can lead to significant tissue damage if the infection continues unchecked. Progression into Stage III Lyme disease involves more bodily systems, including the joints, and exerts more serious effects such as dementia and transverse myelitis.

- L. Matthews, 2011


Distribution

For the most part, rural areas provide the proper environment for deer ticks to thrive.  Lyme endemic areas are mostly concentrated in the Northeastern United States but are also predominantly found in the Midwest and Pacific Northwest of the continental U.S.  Colorado, Wyoming, Hawaii, Oklahoma, and South Dakota have the least cases reported according to the CDC in 2010, but Lyme has been reported in all 50 states.  “Epidemiologic data suggest that the actual incidence of Lyme disease could be as much as 10 times higher than the CDC data indicate.  This is probably a result of a restrictive case definition from the CDC, inevitable misdiagnosis, and the fact that physicians tend to underreport reportable diseases of all kinds.” (Medscape, 2011) 


Lyme disease found in United States. N.d. MedicineNet. Web. 21 Mar. 2012.

On a global scale, Lyme disease can be found in Canada, Scandinavia, Central Europe, Southern Europe, Western Europe, Russia, Japan, China and have even been reported in Australia.

Diagnosis

Diagnosis begins with the observation of the skin for the erythema migrans rash that is typical in 70% to 80% of patients.  However, many patients cannot recall being bitten by a tick due to their size and the location of the bite.  For instance, a bite on the scalp can easily allow the tick to feed on its host without the host being aware of its presence.  After considering the history of present illness, and ruling out other conditions during physical examination, the differential diagnosis can include other tick-borne illnesses such a babesiosis, Rocky Mountain Spotted Fever, “Spotless” Rocky Mountain Spotted Fever, bartonellosis, anaplasmosis, mycoplasmosis and ehrlichiosis which may be present as secondary and tertiary coinfections from the same bite.  The differential diagnosis also can include autoimmune, rheumatoid, neurologic, and cardiac conditions, viral infections, and even clinical depression due to the array of nonspecific symptoms.  To confirm or rule out a Lyme diagnosis, there are several diagnostic tests that can be done.  Blood samples are subjected to ELISA or enzyme-linked immunosorbent assay and the Western Blot tests to detect B. burgdorferi antibodies but both tests can also provide false positive or false negative results so an ELISA is first performed and then confirmed with the Western blot test.  Cerebrospinal fluid, urine, and fluid drawn from an infected joint can also be evaluated for IgG antibodies.  Synovial fluid, which is drawn from the knee arthroscopically, can be subjected to a PCR or polymerase chain reaction test which detects bacterial DNA in the fluid.  Positive serology is confirmed by a 2-tiered testing approach.  “In patients with positive serologies and atypical disorders, or with negative serologies and typical syndromes, the diagnosis is possible but must be entertained with caution.” (Halperin and Roos, 2011)

Treatment and Prognosis

Oral antibiotics such as Doxycycline (Vibramycin) are the usual treatment for Lyme disease.  For more involved infections, intravenous antibiotics consisting of Cefuroxime (Ceftin), Penicillin, Amoxicillin, Ceftriaxone (Rocephin) and Amoxicillin/Clavulanate (Augmentin) are administered.  Chronic Lyme Arthritis is not well understood but is accepted by most of the medical community.  However, long-term administration of antibiotics is discouraged if symptoms persist due to the negative side effects outweighing the benefits of prolonged treatment.  Generally speaking people who contract Lyme disease have a very good prognosis with proper treatment during the early stages.  When Lyme goes undetected for long periods of time and is allowed to enter late stages of the disease it has more permanent effects on the body.  The neurologic, cardiac, and musculoskeletal effects of the disease can have serious complications in patients especially if multisystem involvement is present.  Memory, cognition, and concentration can also become particularly difficult for Lyme sufferers.  Despite the wealth of knowledge regarding tick-borne illnesses in humans and animals, many doctors are not aware of how to help Lyme patients beyond the usual battery of diagnostics and prescribed antibiotic therapy.  There is still much to be learned about this illness and its long-term consequences for patients.  Prevention is always the best method of treatment and you can protect yourself and your family from ticks, Lyme disease and other tick-borne illnesses by wearing long pants and sleeves when walking through heavily wooded or grassy areas,  using insect repellents with DEET, pyrethroids or Permethrin on yourself and children above 3 years of age, tick-proofing your yard by clearing woodpiles, brush and leaves where ticks live, and by thoroughly checking yourself and your family for ticks each time you spend a day outdoors.

Human Vaccines

Unfortunately there is no longer a vaccine to combat Lyme disease in humans, but there are Lyme vaccines for your family pets.  In 1998 GlaxoSmithKline developed and released the human Lyme vaccine which was then pulled from the market in 2002 due to poor sales from lack of understanding of vaccination guidelines and side effects.  However, the number of cases reported have been skyrocketing ever since and pharmaceutical manufacturers have yet to re-release it.  This is a serious public health dilemma.  “The vaccine was made from a single protein found on the surface of Borrelia burgdorferi, the bacterium that causes Lyme. When given to people, the vaccine prompted the production of antibodies that then entered ticks as they sucked vaccinated blood.  Instead of killing pathogenic bacteria in the human body, like other vaccines do, these Lyme antibodies actually immunized the insects by killing bacteria in their bodies. The vaccine was shown to prevent Lyme in about 80 percent of exposed adults.” (Sohn, 2011)  Due to the public outcry, “early clinical trials are underway for at least one new candidate vaccine. A combined phase 1/2 study is estimated to be completed in October 2013.” (The History of Lyme disease Vaccine, 2012)

Veterinary Testing, Vaccines and Prevention

A wide array of mammals are at risk of developing Lyme disease due to tick bite exposures.  There have been many more advances in Lyme disease detection in the veterinary field and there are several diagnostic options available at this time.  Depending upon the hypothetical or proposed timeline of tick bite inoculation, antibody titers which measure B. burgdorferi antibody levels, and multiplex testing which detect B. burgdorferi antigens in serum can be used.  However, the most common testing for Lyme disease in companion animals such as canines consists of an in-house 4Dx Snap Test which can test serum, plasma or anticoagulated whole blood combined with conjugate for heartworm disease, ehrlichiosis, anaplasmosis and Lyme disease.  ELISA, Western blot and PCR testing can be performed to rule out false positives and false negatives in the 4Dx tests.  There is also an extremely effective vaccine for dogs which consists of a series of two killed, adjuvanted vaccine inoculations, given subcutaneously two weeks in succession of one another, and then it is continually boostered on an annual basis.  There are also topical flea and tick repellent treatments for dogs and cats with varying mechanisms of action.  Medicated shampoos and oral medications are more effective against fleas than ticks.  In addition to topical treatments and vaccinations, physically checking your pets’ coat, underside and ears can help to reduce the incidence of Lyme disease and ensure that ticks are not being brought into your home.  

Bibliography

CDC - Cases by State - Lyme disease. (n.d.). Centers for Disease Control and Prevention. Retrieved March 21, 2012, from http://www.cdc.gov/lyme/stats/chartstables/reportedcases_statelocality.html
CDC - Lyme disease Home Page. (n.d.). Centers for Disease Control and Prevention. Retrieved March 21, 2012, from http://www.cdc.gov/Lyme/
Halperin, J., & Roos, R. (2011, May 18). Lyme disease. Medlink. Retrieved March 21, 2012, from www.medlink.com/medlinkcontent.asp
Littman, M., Goldstein, R., Labato, M., Lappin, M., & Moore, G. (n.d.). ACVIM  Small Animal Consensus Statement on Lyme disease in Dogs: Diagnosis, Treatment, and Prevention. NC State College of Veterinary Medicine. Retrieved March 21, 2012, from www.cvm.ncsu.edu/vhc/documents/LymeconsstmtACVIM.pdf
Lyme disease. (2011, September 16). MedicineNet. Retrieved March 21, 2012, from www.medicinenet.com/script/main/art.asp?articlekey=407&pf=3&page=1
Lyme disease. (2010, June 14). University of Maryland Medical Center |  Home. Retrieved March 21, 2012, from http://www.umm.edu/altmed/articles/lyme-disease-000102.htm
Lyme disease - MayoClinic.com. (n.d.). Mayo Clinic. Retrieved March 21, 2012, from http://www.mayoclinic.com/health/lyme-disease/DS00116/METHOD=print
Matthews, L. (n.d.). Lyme disease Pathology. Lyme disease. Retrieved March 21, 2012, from http://lymediseaseguide.org/lyme-disease-pathology 
Sohn, E. (2011, June 17). Lyme disease: Where’s the Vaccine? : Discovery News. Discovery News: Earth, Space, Tech, Animals, History, Adventure, Human, Autos. Retrieved March 21, 2012, from http://news.discovery.com/human/lyme-disease-ticks-vaccine-110617.html
The American Animal Hospital Association. (n.d.). 2011 AAHA Canine Vaccination Guidelines. Retrieved March 21, 2012, from https://www.aahanet.org/PublicDocuments/CanineVaccineGuidelines.pdf
The History of the Lyme disease Vaccine - History of Vaccines. (n.d.). History of Vaccines - A Vaccine History Project of The College of Physicians of Philadelphia. Retrieved March 21, 2012, from http://www.historyofvaccines.org/content/articles/history-lyme-disease-vaccine

Flu’s Evolutionary Strategy

Bacteria, Viruses and Health

Kristin Lake 

Some surprising discoveries made while performing a study on the evolutionary strategy of Influenza were first published in 2010.  The study was lead by Professor Baek Kim Ph.D. of the University of Rochester Medical Center Department of Microbiology and Immunology.  Dr. Kim believes he has disproven a widely believed theory regarding how Influenza replicates its genome and is able to produce the mutations necessary to cross the host species barrier.  Increased research to close the gaps of our knowledge is necessary to understand the evolutionary strategy of Influenza due to its highly pathogenic abilities in both veterinary and human public health.  In April 2009, the Influenza strain H1N1 reached pandemic proportions across the globe in a matter of months.  This highly contagious respiratory pathogen is estimated to have resulted in one million infections in the United States alone, with an acute respiratory illness and Influenza-like illness generation time between 2-3.1 days according to the Center for Disease Control (CDC).  Epidemiologic and virologic data collected from the 2009 H1N1 pandemic allows us to better understand how Influenza subtypes emerge and establish themselves within human populations.  Dr. Kim’s research contributes to the continual improvement of our understanding of the Influenza genome as well as the molecular determinants for increased pathogenicity which are necessary for virulent evolution.

Influenza belongs to the Orthomyxoviridae family and is a negative sense, single-stranded RNA virus.  Influenzaviruses A, B and C all have the ability to infect humans, but Influenza A has spawned many serotypes which infect vertebrates of avian, equine and swine varieties and are the culprit of all flu pandemics.  Current immunotherapies include live-attenuated and agricultural Influenza vaccinations, and antiviral drugs such as Amantadine (Symmetrel), Rimantidine (Flumadine), Oseltamivir (Tamiflu), and Zanimivir (Relenza).  Influenzavirus A has not yet shown any resistance to these treatments.  Despite having these prophylactic measures in our arsenal, we need to continue our surveillance of avian, equine, swine and human Influenza viruses due to their continued abilities to effectively mutate and produce new virulent strains which are capable of bridging the gap between species.  Genetic novelty and mutations are becoming more exotic as the tropics are a perpetual source of variance.

Dr. Kim’s study set out to discover why the flu is able to spawn so many mutations, so quickly.  He compared and contrasted the replication processes of HIV and Influenza and documented new evidence regarding the flu’s genetic evolution which was once thought to be incredibly error-prone.  In Kim’s experiment, he studied a virus that is well known as a control against the flu virus, whose genome we are still working to fully ascertain.  While studying the biochemical analyses of each virus, Kim and his team noted that HIV only has a limited number of opportunities per infection to replicate its genome and spur adequate mutations.  This means of replication differs significantly from Influenza’s replication process.   Kim discovered that the flu has an abundance of chances to accrue genomic mutations in each of its infection cycles in addition to producing highly sufficient mutations.   Prior to his findings, it was widely believed that the flu’s enzymes, or polymerases, which are liable for viral replication, were extremely prone to error and this resulted in highly varied mutations allowing the flu to evolve its virulence and adapt to its host.  The highly sufficient mutations that Kim witnessed disproved this error-prone polymerase theory.  Kim concluded that the flu’s multiple replication strategy, independent of the numerous amounts of changes in its genome, was the crux which allows the flu to produce genetic mutations of sufficient quality.  However, the AIDS virus polymerases were indeed error-prone in addition to the virus having decreased chances to produce sufficient mutations per cycle.  Essentially, Influenzavirus’ replication process strikes an ideal balance in natural selection that allows it to generate adequate mutations for the virus to multiply and adapt to its host. But, the virus does not produce so many mutations as to lead to catastrophic mutagenesis which would ultimately result in its demise.

I believe that Kim’s experiment will prove to be highly beneficial to the general public.  Now, that we have a base of knowledge and understanding of how the flu is able to evolve so rapidly and efficiently, we can begin to use this information to our advantage and eventually save lives.  I believe that our best use of this information in the near future will be against the almost inevitable H5N1 outbreak when this subtype transmits across the host species barrier to infect populations of pandemic proportions.  I believe that his use of the AIDS virus was a wise choice considering so much research has been done in the past 20 years to further our knowledge and ultimately assist HIV patients and prevent new infections.  The HIV virus proved to be a good control against the flu since there are such stark contrasts in their replication processes.  However, I also believe that further study is necessary to provide additional support to the conclusions extrapolated from this study.

This research gives us deeper insight into the functions of the Influenza polymerases which could potentially lead to the improvement of research methodology in addition to the advent of new Influenza antiviral drugs and control measures as this virus continues to evolve.  With further examination, we will be able to steadily close our gap of knowledge in regard to Influenza.  We still have much to learn about its transmissibility, pandemic potential, host susceptibility, antigenic variability and the roles of reservoirs.  We still do not know the full usage potential of Influenza vaccines, the long-term effects and potential consequences of vaccinations, or the possible ramifications of anti-Influenza drug resistance.  Some of the stated research goals for Influenza in the future include complete genomic and proteomic analysis, the development of genetically resistant hosts, the attempt to explain why H5N1 doesn’t spread as efficiently in humans as H1N1 of swine origin, and continued investigations to discover how we can eradicate H5N1 on a global scale.  Experts have projected that the “next decade will bring much knowledge thanks to a multidisciplinary approach between virology, evolutionary biology, immunology and clinical outcomes.” (4) It is my personal belief that our attempts to stay one step ahead of nature will ultimately be futile because nature is adapting more quickly to us than we are to it.  Despite this harsh reality, it is worth every step of our journey in exploring our world to attempt to improve the quality of life for all of those in it. 

References

  1. CDC Novel H1N1 Flu | 2009 H1N1 Early Outbreak and Disease Characteristics. (2009, October 27). Centers for Disease Control and Prevention. Retrieved March 5, 2012, from http://www.cdc.gov/h1n1flu/surveillanceqa.htm
  2. Flu’s evolution strategy strikes perfect balance. (2010, June 10). Science Daily: News & Articles in Science, Health, Environment & Technology. Retrieved March 5, 2012, from http://www.sciencedaily.com/releases/2010/06/100610104621.htm
  3. Forest, H., & Webster, R. (n.d.). Animal Health Research Reviews. Perspectives on Influenza Evolution and the Role of Research. Retrieved March 5, 2012, from http://apps.webofknowledge.com.ezproxy.umuc.edu/full_record.do?product=BIOSIS&search_mode=GeneralSearch&qid=2&SID=1Cl4PGoleN3DOa4gaFN&page=2&doc=19&cacheurlFromRightClick=no
  4. Simonsen, L., Viboud, C., Taylor, R., & Miller, M. (n.d.). Birkhauser Advances in Infectious Diseases. The Epidemiology of Influenza and Its Control. Retrieved March 5, 2012, from http://apps.webofknowledge.com.ezproxy.umuc.edu/full_record.do?product=BIOSIS&search_mode=GeneralSearch&qid=2&SID=1Cl4PGoleN3DOa4gaFN&page=2&doc=13

West Nile Virus: Background, Pathogenesis, Dissemination, and Prognosis

Bacteria, Viruses and Health

Kristin Lake

West Nile virus (WNV) is endemic to the Middle East, Europe and Africa.  A member of the Flaviviridae family, it is a neurotropic flavivirus which is related to dengue, yellow fever and Japanese encephalitis viruses.  In 1999 an outbreak of West Nile affected New York and has since disseminated across the Americas and Caribbean.  Usually an enzootic affliction, WNV has breached the cycle in vertebrate animals due to the mosquito bug.  West Nile is transferred from infected avian hosts when a mosquito feeds on their blood.  The virus then is transmitted to vertebrate animals and humans alike once the infected mosquito feeds again and transfers fluids between itself and its newest host.  Once WNV enters the human body, replication is then believed to occur in Langerhans dendritic cells of the skin.  WNV is an enveloped virus with a single-stranded, positive sense, ~11-kb RNA genome. (1)  Since Langerhans dendritic cells are thought to be the targets, reservoirs and vectors of dissemination of the virus, it is understandable why WNV affects young, elderly, pregnant, and the immunocompromised more severely than the immunocompetent. 

Once the mechanism of action has begun in vivo, clinical manifestations of the central nervous system (CNS) develop in about 1:150 patients.  The mechanisms which allow West Nile and other neurotropic flaviviruses to cross the blood-brain-barrier (BBB) are not well understood.  However it is believed that hematogenous spread is the likely cause of viral entry into the CNS.  Additional mechanisms may contribute to WNV CNS infection including (i) infection or passive transport through the endothelium or choroid plexus epithelial cells, (ii) infection of olfactory neurons and spread to the olfactory bulb, (iii) a “Trojan horse” mechanism in which the virus is transported by infected immune cells that traffic to the CNS and (iv) direct axonal retrograde transport from infected peripheral neurons.  Although the precise mechanisms of WNV CNS entry in humans require additional study, changes in cytokine levels that may modulate BBB permeability and infection of blood monocytes and choroid plexus cells have been documented in animal models. (1)

Once WNV has taken hold in an immunocompromised patient, West Nile Fever which consists of dangerous inflammation begins and lasts anywhere between 3 and 8 days.  West Nile Encephalitis and West Nile Meningitis (WNEM) are common complications which may lead to brain damage, permanent muscle weakness reminiscent of poliomyelitis, and death.  Goals of hospitalization include proper diagnosis through histology and/or serology tests of cerebrospinal fluid (CSF) and blood to screen for antibodies, RT-PCR (reverse-transcription polymerase chain reaction) testing if a more rapid diagnosis is necessary, supportive care to decrease the risk of complications of neuroinvasive damage, administration of corticosteroids, intravenous immunoglobulin (IVIG), and continued management of febrile symptoms.  Antibiotics are ineffective against primary infection but may be supportive in preventing secondary infection.  At this time there have been no effective antiviral therapies or vaccines developed for human protection against West Nile Virus.  About 10% of people diagnosed with WNEM die from overwhelming inflammation of the brain or meninges.  Despite the grim statistics for immunocompromised patients, immunocompetent patients fare much better against WNV.  Very few people exposed to West Nile by being bitten by an infected mosquito actually develop symptoms or the disease of West Nile Fever.  Most people that develop WNF display typical flu-like symptoms and are usually misdiagnosed but are able to fight off the virus on their own without medical intervention.

References

  1. Diamond, M., & Samuel, M. (n.d.). Pathogenesis of West Nile Virus Infection: a Balance between Virulence, Innate and Adaptive Immunity, and Viral Evasion. National Center for Biotechnology Information: Journal of Virology. Retrieved March 4, 2012, from www.ncbi.nlm.nih.gov/pmc/articles/PMC1617273/pdf/1122-06.pdf
  2. Epidemic/Epizootic West Nile Virus in the United States: Guidelines for Surveillance, Prevention, and Control. (n.d.). Center for Disease Control. Retrieved March 4, 2012, from www.cdc.gov/ncidod/dvbid/westnile/resources/wnv-guidelines-aug-2003.pdf
  3. Medscape: Medscape Access. (n.d.). Medscape: Medscape Access. Retrieved March 4, 2012, from http://emedicine.medscape.com/article/210367-overview
  4. West Nile virus - PubMed Health. (n.d.). National Center for Biotechnology Information. Retrieved March 4, 2012, from http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0004457/

If a patient is vomiting, hydrochloric acid (HCl) from the stomach is removed from the body in the act of vomiting. How will prolonged vomiting affect the pH of the patient’s blood?

Human Health and Disease

Kristin Lake

If a patient is vomiting and hydrochloric acid is being continually removed from the body, the blood pH will raise and become more alkaline or basic, due to the loss of hydrogen ions (H+) and increase in bicarbonate (HCO3-), a condition called metabolic alkalosis. Depletion of chloride increases bicarbonate reabsorption rendering the buffer system out of balance. With loss of fluid, blood volume is diminished and bicarbonate is concentrated within smaller volumes and increases blood pH. H+ is needed to restore the balance in pH so intravenous replacement fluids are given to bypass the gastrointestinal system as a whole until vomiting ceases so that blood volume is increased, more hydrogen ions are able to be replenished and blood pH is restored to normal ranges.

Shiga Toxin (Verotoxin) of Enterohemorrhagic Escherichia coli (EHEC)

Bacteria, Viruses and Health

Kristin Lake

Shiga toxin is a protein comprised of A-moiety and B-moiety subunits which are responsible for the toxic actions of the protein as well as for binding to specific types of cells.  The B-moiety binds to cells with glycosphingolipid, Gb3, receptors in the cellular membrane.  Once adhered, endocytosis occurs and the A subunit which consists of an N-glycosidase transports intracelluarly via the Golgi complex to the endoplasmic reticulum and then to the cytosol where intoxication begins.  The N-glycosidase acts upon the RNA by removing the adenine from a specific adenosine of a ribosome subunit.  The Shiga toxin mechanism of action ultimately terminates protein synthesis in the cell.  In addition, Shiga toxin is capable of inducing apoptosis as well as generating expression and secretion of cytokines which cause an inflammatory response in some cell types.

The highly pathogenic Shiga toxin genes exist on bacteriophages in the chromosomes of enterohemorrhagic E. coli bacteria (EHEC).  This toxin isneurotoxic, cytotoxic and enterotoxic and is very effective against the vascular endothelium found in the digestive tract, glomerulus of the kidneys, lungs and heart.  Several sites of the central nervous system are affected as well.  Vascular endothelium locations which are plentiful in Gb3 receptors become damaged by the toxin which results in impaired function.  Human infection with EHEC is generally attributed to consumption of contaminated undercooked bovine products, direct contact with cattle, birds, other animal species, and infected humans, unpasteurized apple cider and juice, lettuce, cantaloupes, alfalfa sprouts, radish sprouts, as well as contaminated sources of drinking water and water for bathing. 

Transmission is through oral contact and ingestion.  EHEC easily travels through the beginning of the gastrointestinal tract due to its resistance to acid and the low pH of the stomach. When EHEC reaches the small intestine, the virulence genes of Shiga toxin receive signals from the colon to activate and EHEC binds to enterocytes in the lower gastrointestinal tract.  Within a few hours localized damage to microvilli and vascular sites directly results in the rapid onset of symptoms of severe, watery or bloody diarrhea, severe abdominal pain and cramping and sometimes is accompanied by vomiting and a low-grade fever.  Mild cases usually last between 1-3 days.  Serious complications may occur in up to 10% of cases which result in hemorrhagic colitis, dysentery, typical and atypical Hemolytic Uremic Syndrome (HUS), Thrombotic Microangiopathic Anemia (TMA), and Thrombotic Thrombocytopenia Purpura (TTP). Diagnostics include immunoassays, history of present illness, complete blood counts (CBCs), chemistry screens for electrolyte values, assessment of kidney function and urinalysis.  Supportive care consists of intravenous fluid therapy, maintenance of electrolyte levels and continued monitoring of kidney function.

 

Works Cited

The Central Role of Cattle in Transmission of Shiga Toxin-producing Escherichia Coli (STEC) to Humans. Digital image. Journal of Animal Science. Mar. 2007. Web. 18 Feb. 2012. <http://jas.fass.org/content/85/13_suppl/E45.full.pdf+html>.
Gyles, C.L. “Shiga Toxin-producing Escherichia Coli: An Overview.” Journal of Animal Science. 3 Nov. 2006. Web. 18 Feb. 2012. <Shiga toxin-producing Escherichia coli: An overview>.
Obrig, Tom G. “Escherichia Coli Shiga Toxin Mechanisms of Action in Renal Disease.” National Center for Biotechnology Information, U.S. National Library of Medicine. 24 Nov. 2010. Web. 18 Feb. 2012. <http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3032420/>.
Overview of Disease in Humans Due to Enterohemorrhagic Escherichia Coli (EHEC). Digital image. Journal of Animal Science. Mar. 2007. Web. 18 Feb. 2012. <http://jas.fass.org/content/85/13_suppl/E45.full.pdf+html>.
Sandvig, K. “Shiga Toxins.” National Center for Biotechnology Information, U.S. National Library of Medicine. Web. 18 Feb. 2012. <http://www.ncbi.nlm.nih.gov/pubmed/11595626>.
Sears, C.L., and J.B. Kaper. “Enteric Bacterial Toxins: Mechanisms of Action and Linkage to Intestinal Secretion.” Microbiology and Molecular Biology Reviews. 1996. Web. 18 Feb. 2012. <http://mmbr.asm.org/content/60/1/167.full.pdf>.
"Shiga Toxin or Verotoxin: Essential Data." CBWInfo. 1999. Web. 18 Feb. 2012. <http://www.cbwinfo.com/Biological/Toxins/Verotox.html>.
"Shiga Toxin-producing Escherichia Coli Fact Sheet." Colorado Department of Public Health and Environment. Mar. 2001. Web. 18 Feb. 2012. <http://www.cdphe.state.co.us/dc/epidemiology/stec_fs.html>.
The Structure of Stx. Digital image. The Open Toxinology Journal. 2010. Web. 18 Feb. 2012. <http://www.benthamscience.com/open/totnj/articles/V003/SI0001TOTNJ/3TOTNJ.pdf>.
Torgersen, Maria L., Nikolai Engedal, Jonas Bergan, and Kirsten Sandvig. Overview of Components Involved in the Retrograde Trafficking of Stx. Digital image. The Open Toxinology Journal. 2010. Web. 18 Feb. 2012. <http://www.benthamscience.com/open/totnj/articles/V003/SI0001TOTNJ/3TOTNJ.pdf>.
Torgersen, Maria L., Nikolai Engedal, Jonas Bergan, and Kirsten Sandvig. “The Intracellular Journey of Shiga Toxins.” The Open Toxinology Journal. 2010. Web. 18 Feb. 2012. <http://www.benthamscience.com/open/totnj/articles/V003/SI0001TOTNJ/3TOTNJ.pdf>.

Helpful Bacteria: Staphylococcus Aureus and Staphylococcus Epidermidis

Bacteria, Viruses and Health

Kristin Lake
 

Kingdom: Bacteria

Phylum: Firmicutes

Class: Bacilli

Order: Bacillales

Family: Staphylococcaceae

Genus: Staphylococcus

Species: Aureus and Epidermidis

Staphylococcus is a Gram-positive bacteria that has over 40 known species.  It is part of the normal human flora and is found on the skin, ocular conjunctiva, mucous membranes of the upper respiratory tract, the lower gastrointestinal tract and the urogenital tract in the anterior urethra and vagina.  S. aureus and S. epidermidis flourishes on the uppermost layers of the epidermis and the associated hair follicles as well as the nasal membranes.  S. aureus and S. epidermidis pose as potential pathogens and can cause overwhelming infection in many systems of the body but they are also mutually beneficial to humans.  The oral cavity contains many microbial entities and S. aureus and S. epidermidis are part of the normal flora. This normal flora provides many benefits to its human host by inhibiting and killing non-indigenous species of microbes, colonizing throughout to prevent the establishment of non-indigenous species of microbes which may be pathogenic in nature, synthesizing and excreting vitamins and nutrient byproducts, and stimulating antibody production as well as tissue development.  There is little contrast between the benefits of S. aureus and S. epidermidis, however most strains of S. epidermidis usually are not harmful to the host or pathogenic in nature unless a strain with inherent or acquired resistance is present.

S. epidermidis and S. aureus have the potential to be the culprit of nosocomial infections (hospital-borne illnesses) in patients post-surgically at wound sites.  Purulent discharge and necrosis of tissues can occur in susceptible individuals with openings on the skin to allow S. epidermidis and S. aureus an entry to deeper layers of the tissue.  Despite their pathogenic qualities, S. aureus helps to prevent pseudomembranous colitis which is another common nosocomial infection caused by the bacteria Clostridium difficile or more commonly known in the medical field as “C. diff.”  Prolonged antibiotic usage in ill patients can cause an imbalance in the gut flora which allows C. difficile to flourish.  S. aureus is found in the lower gastrointestinal tract in much smaller numbers than other enteric microbes, but remains a part of the normal flora which is responsible for keeping the numbers of C. difficile bacteria under control by acting as a microbial antagonist.

Citation:

Todar PhD., Kenneth. “Staphylococcus Aureus.” Online Textbook of Bacteriology. Web. 07 Feb. 2012. <http://textbookofbacteriology.net/staph.html>.

Todar PhD., Kenneth. “Staphylococcus and Staphylococcal Disease.” Online Textbook of Bacteriology. Web. 07 Feb. 2012. <http://textbookofbacteriology.net/themicrobialworld/staph.html>.

Todar PhD., Kenneth. “The Normal Bacterial Flora of Humans.” Online Textbook of Bacteriology. Web. 07 Feb. 2012. <http://textbookofbacteriology.net/normalflora_2.html>.

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