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Pertussis, or whooping cough, is an upper respiratory infection caused by the Bordetella pertussis or B. parapertussis bacteria. There are 30–50 million cases per year, and about 300,000 deaths per year. This is a serious disease that can cause permanent disability and/or death in infants.
Pertussis is on the increase and is viewed as a re-emerging disease. Children, especially those who are not immunized or who are not yet fully immunized against pertussis, are at the highest risk of getting severe whooping cough and suffering from the serious, potentially life-threatening, complications. Treatment of cases with certain antibiotics such as erythromycin can shorten the contagious period. People who have or may have pertussis should stay away from young children and infants until properly treated.
Pertussis begins as a mild upper respiratory infection with symptoms similar to those of a common cold, including sneezing, runny nose, low-grade fever and a mild cough. Within two weeks, the cough becomes more severe and is characterized by episodes of numerous rapid coughs followed by a crowing or high-pitched “whoop”. A thick, clear mucous may be discharged. These episodes may recur for one to two months, and are more frequent at night. Older people or partially immunized children generally have milder symptoms.
Complications of pertussis may include pneumonia, middle ear infection, anorexia, dehydration, seizures, encephalopathy, apneic episodes, and death. Pertussis is primarily spread when infected people cough or sneeze, expelling droplets that contain the bacteria. Older siblings or adults who may be harboring the bacteria in their nose and throat can infect an infant. Young children who have not been immunized have the most severe symptoms.
Infants less than six months of age, adolescents, and adults often don’t have the characteristic whoop. Therefore, a person with a cough that lasts more than a week without improvement should see a health care provider to ensure the cough is not pertussis.
Stage One: This is the most contagious stage and occurs before the actual “whoop” begins. The first stage presents as an upper respiratory disease with fever, malaise and coughing, which increases in intensity over about a 10-day period. Adult immunization may be ineffective, so adults are at risk as well as children.
The incubation period is usually five to ten days, but may be as long as 21 days. . Pertussis should always be considered when vomiting occurs with coughing. In infants, choking spells are common. The initial diagnosis is usually based on the symptoms. However, when the symptoms are not obvious, pertussis may be difficult to diagnose. During this stage the organism can be recovered in large numbers from pharyngeal cultures, and the severity and duration of the disease can be reduced by antimicrobial treatment.
Stage Two: (can last 4-6 weeks). The second or toxemic stage of pertussis follows relatively nonspecific symptoms of the colonization stage. It begins gradually with prolonged and paroxysmal coughing that often ends in a characteristic inspiratory gasp (whoop). Pertussis is most easily recognized during this stage, because this is when the classic ‘whooping’ cough is heard. The cough usually produces thick, glue-like mucus, which makes it very hard for infants and young children to eat, drink, and breathe. A child may also experience vomiting and gagging episodes after the coughing spells; this can often leave the child completely exhausted.
Stage Three: The convalescent or recovery stage can last several weeks to several months. This is the stage when the person begins to get better. The cough and other symptoms gradually get milder and eventually go away.
B. Pertussis produces a variety of substances with toxic activity in the class of exotoxins and endotoxins. It secretes its own invasive adenylate cyclas that enter the mammalian cells. This toxin acts locally to reduce phagocytic activity and probably helps the organism initiate infection. A lethal toxin is then produced which causes inflammation and local necrosis adjacent to sites where B. pertussis is located. This causes necrotic skin lesions. Finally, it produces a substance, cytotoxin, that is toxic to ciliated respiratory epithelium and which will stop the ciliated cells from beating. This toxin kills ciliated cells and causes their extrusion from the mucosa.
The pertussis toxin, (PTx), is a protein that mediates both the colonization and toxemic stages of the disease. PTx is a two component: A+B bacterial exotoxin. This has the effect of disrupting cellular function, and in the case of phagocytes, to decrease phagocytic activities such as chemotaxis, engulfment, the oxidative burst, and bactericidal killing.
Systemic effects of the toxin include lymphocytosis and alteration of hormonal activities such as increased insulin production (resulting in hypoglycemia) and increased sensitivity to histamine (resulting in increased capillary permeability, hypotension and shock). PTx also affects the immune system in experimental animals. B cells and T cells that exit the lymphatics show an inability to return. This alters both acquired cell mediated immunity (AMI) and cell mediated immunity (CMI) responses and may explain the high frequency of secondary infections that accompany pertussis (the most frequent secondary infections during whooping cough are pneumonia and otitis media).
To be certain, a culture should be created in the lab. Although this provides an accurate diagnosis, the test takes time to analyze and treatment is usually started before the results are ready.
Pertussis is on the rise, and often misdiagnosed as bronchitis or a cold. Early treatment offers the highest probability of avoiding complications, especially in children. Cultures may be indicated for definitive diagnosis. Vaccines are the best deterrent; however, in some communities people are choosing not to vaccinate which may account for the rise in rates of occurrence in the U.S.
Erythromycin is a good choice of antibiotic if there is an early diagnosis. The toxins produced by the bacteria can create permanent B or T cell degeneration, and therefore has been shown to affect the immune system and create a secondary opportunistic infection to occur, such as pneumonia or otitis media.
C. difficile is a spore-forming, gram-positive anaerobic bacillus. In the United States alone C. difficile causes approximately three million cases of diarrhea and colitis per year. C. difficile infection represents one of the most common nosocomial infections around the world.
The emergence of a new strain of C. difficile has been reported by the CDC. Strain 630 is multi-drug resistant, and was isolated from a patient who had spread the infection to dozens of other patients on the same ward in Zurich, Switzerland. Strain 630 has the genetic attributes of a fully virulent, highly transmissible, drug resistant strain. Laboratory studies show that when C. difficile colonize the gut, they release toxin A and toxin B, two potent toxins which bind to certain receptors in the lining of the colon and ultimately cause diarrhea and inflammation of the large intestine, or colon (colitis) This strain is the epidemic type X variant that has been extensively studied in research. The new strain appears to be more virulent, with ability to produce greater quantities of toxins A and B.
The increased rates and/or severity of disease may be caused by changes in antibiotic use, changes in infection control practices, or due to increased virulence and/or antimicrobial resistance. This disease involves, initially, alterations of the beneficial bacteria that are normally found in the colon. One of the main characteristics of C. difficile-associated colitis is severe inflammation in the mucosa in the colon associated with destruction of cells of the colon (colonocytes).
While patient-to-patient spread and environmental contamination are some of the reasons for cross-infection in C. difficile-associated diarrhea and colitis, antibiotic therapy is the major risk factor for this disease. Healthy people are not usually at risk for C. difficile, however when one is on prolonged antibiotic therapy, the immune system often becomes compromised, especially when hospitalized. The risk even increases for those on cancer treatment, antibiotics, and advanced age.
C. difficile is shed in feces. Any surface, device, or material (e.g., commodes, bathing tubs, and electronic rectal thermometers) that become contaminated with feces may serve as a reservoir for the C. difficile spores. C. difficile spores are transferred to patients mainly via the hands of healthcare personnel who have touched a contaminated surface or item.
Most cases develop 4 to 9 days after the beginning of antibiotic intake. It should be noted, however, that some patients develop diarrhea after antibiotics are discontinued and this may lead to diagnostic confusion. Although nearly all antibiotics have been implicated with the disease, the most common antibiotics associated with C. difficile infection are ampicillin, amoxicillin, cephalosporins, and clindamycin.
The most common presentation is either mild colitis, or simple diarrhea that is watery and contains mucus but not blood. Examination by sigmoidoscopy usually reveals normal colonic tissue. General symptoms are commonly absent and diarrhea usually stops when antibiotics are discontinued. C. difficile can also cause non-specific colitis quite reminiscent of other intestinal bacterial infections such as Shigella or Campylobacter.
Pseudomembranous colitis represents the characteristic manifestation of full-blown C. difficile-associated colitis. Sigmoidoscopic examination reveals the presence of characteristic plaque-like pseudo membranes scattered over the colonic tissue, which is a distinctive indicator of C. difficile infection in patients with diarrhea following antibiotic treatment.
The most serious manifestation of C. difficile infection, fulminant colitis (severe sudden inflammation of the colon), is frequently associated with very serious complications, and occurs in 3% of patients. Patients with this form of the disease experience severe lower abdominal pain, diarrhea, high fever with chills, and rapid heart beat. Timely treatment of fulminant colitis is essential; this condition can be life threatening. It is well documented that C. difficile is responsible for 4 to 12% of diarrhea in AIDS patients.
The detection of C. difficile toxins in the stool can be made by a cytotoxic assay where the toxins can be easily observed in the microscope.
Therapy of C. difficile is directed against eradication of the microorganism from the colonic microflora. Diarrhea following treatment with either vancomycin or metronidazole is expected to improve after 1 to 4 days with complete resolution within 2 weeks.
Recent reports suggest, however, that the new strain may not respond well to treatment with metronidazole even though there is no laboratory evidence of metronidazole resistance. This may be due to increased virulence in the new strain. Depending upon the severity of the C. difficile-associated disease, metronidazole is likely to be the appropriate first-line therapy for most cases.
Bubonic plague is an infectious disease that is believed to have caused several epidemics or pandemics throughout history. Bubonic plague is the most common form of plague. It is characterized by swollen, tender inflamed lymph glands (called buboes). Other forms of plague are Septicemic (which occurs when plague bacteria multiply in the blood) and Pneumonic (which occurs when the lungs are infected).
Plague is primarily a disease of rodents, particularly marmots, black rats, prairie dogs, chipmunks, squirrels and other similar large rodents. Marmots often carry the most virulent strains of plague. Human infection most often occurs through a fleabite from a flea that previously fed on an infected rodent.
In 1896 the bacteriologist Alexandre Yesin isolated the bacterium responsible for the transmission of plague. The disease is caused by the bacterium yersinia pestis, transmitted by the bite of fleas from an infected host. The bacillus multiplies in the stomach of the flea. When fleas bite a mammal, the consumed blood is regurgitated along with the bacillus into the bloodstream of the bitten animal. The disease becomes evident 2–7 days after infection. Initial symptoms are chills, fever, headaches, and the formation of buboes. If unchecked, the bacteria can infect the bloodstream (septicemic plague), progress to the lungs (pneumonic plague).
In septicemic plague there is bleeding into the skin and other organs, which creates black patches on the skin, hence the name Black Death. Septicemic plague that is left untreated is universally fatal, but early treatment with antibiotics is effective (usually streptomycin or gentamicin), reducing the mortality rate to around 15% (USA 1980s).
With pneumonic plague there is possibility of person-to-person transmission through respiratory droplets. The incubation period for pneumonic plague is usually between two to four days, but can be as little as a few hours. The initial symptoms of headache, weakness, and coughing with hemoptysis are indistinguishable from other respiratory illnesses. Without diagnosis and treatment the infection can be fatal in one to six days; mortality in untreated cases may be as high as 95%. The disease can be effectively treated with antibiotics.
In 1999 Scientists decoded the genetic make-up of the Strep A bacterium, an organism responsible for more human diseases than any other; including sore throat, scarlet fever and rheumatic fever. Through research, health experts have learned that there are more than 120 different strains of Group A streptococci, Streptococcus pyogenes each producing its own unique proteins. These infections can range from a mild skin infection or sore throat to severe, life-threatening conditions such as toxic shock syndrome and necrotizing fasciitis, commonly known as flesh eating disease. Necrotizing fasciitis occurs when the bacteria attacks soft tissue, usually in an extremity following minor trauma. There are also many cases of this occurring after surgery, usually abdominal surgery.
Today there are about 15,000 people in the U.S. who get complications from Strep A, according to the CDC, so it is worth noting here. Yes, this is the same strep that causes strep throat, although perhaps mutated. Strep is normally found in the throat or on the skin of up to 10% of children and 1% of adults. However, occasionally the bacterium is able to make it past the normal defenses of the body and enter the blood or other tissues in the body where bacteria do not normally live. This is known as invasive strep infection, and can lead to pneumonia, bone and joint infections, necrotizing fasciitis or “strep toxic shock syndrome”. Strep toxic shock syndrome occurs when the strep bacteria spread quickly inside the body and release toxins to cause shock and failure of many organs and tissues. Necrotizing fasciitis and strep toxic shock syndrome can either occur separately or together. It is only when necrotizing fasciitis is part of the picture that the disease is called flesh-eating disease.
Researchers at the University of California, San Diego (UCSD) School of Medicine reported in the February 21, 2006 issue of the journal Current Biology Researchers (Flesh-Eating Bacteria Escape Body’s Safety Net) that so-called flesh-eating strep bacteria use a specific enzyme to break free of the body’s immune system. The UCSD investigators examined the interaction of Strep bacteria with neutrophils, specialized white blood cells that play a front line role in human immune defense against pathogenic microbes. Recent research by European investigators (2006, Biology/Biochemistry News, 22, 2006. Flesh-eating “Strep” bacteria use an enzyme to break free of the body’s immune system) had shown that neutrophils are particularly effective defenders because they release “nets” composed of DNA and toxic compounds to entrap and kill invading bacteria. In the current study, the UCSD scientists proved that disease-causing strep release an enzyme that degrades these DNA nets, thereby allowing the organism to escape the neutrophil net and spread in body tissues.
“Deprived of this single enzyme, the mutant Strep strain was easily killed by human neutrophils,” said John Buchanan, PhD, research scientist in the UCSD department of pediatrics. “In addition, the mutant strep bacteria no longer produced a spreading infection when injected into the skin of experimental mice. The experiments explain how this DNA-degrading enzyme contributes to the severe infections produced by certain strains of Strep bacteria, while simultaneously confirming just how important neutrophil DNA nets are to our normal immune defense,” said Buchanan.
Proper care of minor wounds and cuts immediately reduce infection opportunities. Seeking immediate medical attention if suspicious of flesh eating bacteria is critical. There is no preventative vaccine. The flesh-eating disease progresses rapidly, thus treatment usually involves surgery to remove the infected tissue and antibiotics to fight the infection.
Glanders is a highly contagious disease in horses, mules, and donkeys. It is caused by the bacterium Actinobacillus mallei. Despite the rarity of contagion from infected horses and donkeys to man, the attack rates caused by laboratory aerosols have been as high as 46% and cases have been severe. It can be transmitted to humans, but is limited almost exclusively to handlers of equine animals.
Aerosols from cultures have been observed to be highly infectious to laboratory workers. Since aerosol spread is efficient, and there is no available vaccine or a dependable therapy, B. mallei has been viewed as a potential BW agent. Work with this organism in the laboratory requires biosafety level 3 containment practices.
There are three primary sites of infection:
The bacteria can create lumps or nodules that form in the affected area. The nodules enlarge, form ulcers, and release pus that spreads the germs to other parts of the body. In the cutaneous form of the disease, craterlike ulcers form on the skin along the course of the lymph vessels of the extremities; this form of glanders is commonly called farcy. There is no effective treatment for glanders and the infected animal must be destroyed to prevent the spread of the disease. Glanders has been virtually eradicated in the United States, Canada, and Great Britain, but still occurs in Asia and South America.
Leptospirosis is an infectious disease caused by the spirochete type of bacteria. It is a reportable disease in the United States and local and state health officials must be notified of newly diagnosed cases. Leptospirosis can be transmitted by rats as well as by skunks, opossums, raccoons, foxes, and dogs. It can be transmitted to humans and it is present worldwide. However, it is most commonly acquired in the tropics. According to the Center for Disease Control and Prevention, approximately 100 cases of leptosporiasis are reported each year in the United States.
Oddly however, there has been an outbreak on an island close to Seattle as reported by the news media in April of 2006. As of this writing, there have been 32 confirmed cases (since December of 2005) of the illness where dogs contracted the disease. It is not known why there are so many cases. However, it is suspected that due to the rural nature of the locality (no sidewalks, no drainage systems), water accumulates into puddles where animals drink.
Leptospirosis symptoms begin from 2 to 25 days after initial direct exposure to the urine or tissue of an infected animal. This can occur via contaminated soil or water. Veterinarians and farm workers are at particularly high risk. The illness typically progresses through three phases. The first phase of symptoms includes headaches, muscle aches, eye pain with bright lights, followed by chills and fever. Watering and redness of the eyes occurs and symptoms seem to improve between five to nine days.
The second phase, called the immune phase, progresses to fever, aching, and stiffness of the neck after a one to three day symptom-free period. Some patients develop serious inflammation of the nerve to the eye, brain, spinal column (meningitis), or other nerves.
During the final phase, from 2 to 4 weeks after the initial infection, recurrent fever and muscle aching is noted. It does not fully resolve unless treated by antibiotics such as doxycycline and penicillin in the second stage; in such cases the majority experience complete recovery. A small percentage of people can have uveitis up to a year after exposure. If left untreated until the third stage the benefit of antibiotic treatment is controversial. About one per 100 die yearly in the USA (Farr, 1995)
The diagnosis of leptospirosis is made by culture of the bacterial organism, Leptospira, from infected blood, spinal fluid, or urine. However, the difficulty of the testing techniques means that many doctors rely upon rising antibody levels in the blood in order to make the diagnosis.
Leptospirosis is a zoonotic disease (transmitted from animals to humans). People can catch the disease from water that is contaminated by infected wild or domestic animals, as well as by direct contact with animals, such as rodents, raccoons, skunks and cattle.
The treatment of leptospirosis involves high doses of antibiotics.
Lyme disease is an illness caused by the spirochete bacteria, Borrelia burgdorferi, transmitted to animals and man through the bite of infected ticks. The disease was first identified in Lyme, Conn., in 1975 after an abnormally large number of children developed signs of rheumatoid arthritis, a symptom of the disease. It has now been reported in most parts of the United States affecting more than 20,000 people annually (CDC, 2004). It is currently found in about 25 states.
Lyme disease is under-reported because of differences in opinion on how the disease is diagnosed, but it is of growing concern worldwide. Most cases occur in the Northeast, upper Midwest, and along the Pacific coast. Michael Carroll’s book, “Lab 257, The Disturbing Story of the Government’s Secret Plum Island Germ Laboratory” (William Morrow, 2004), suggests that the 1970’s outbreak in Lyme, Connecticut was the result of an escaped “experiment” from the nearby Plum Island lab, just across the Long Island Sound, where they grew infected tick colonies for years in biowar research.
Although some deaths have been attributed to Lyme disease, it is not generally considered to be fatal. Once an animal or person has recovered from the disease it appears to be possible to be re-infected. Blood testing is available for animals and man. Mice and deer are the most commonly infected animals that serve as host to the tick. Most infections occur between the late spring and early fall.
The vector is a hard tick, (Ixodes dammini), and commonly attacks white-tailed deer. This is the tick responsible for most of the cases of Lyme disease in the northeastern United States because it carries the bacteria, Borrelia burgdorferi. These ticks are found in grassy areas (including lawns), and in brushy, shrubby and woodland sites, even on warm winter days. They prefer areas where some moisture is present.
The tick has three life stages in a complex two-year cycle: larva, nymph and adult. Each stage takes a single blood meal. They feed on a variety of warm-blooded animals including man, dogs, cats, horses and cows. The bite is painless so most victims do not know they have been bitten.
The nymphal stage appears to be responsible for most of the Lyme disease cases. Both the larval stage (about the size of a grain of sand) and nymphal stage (about the size of a poppy seed) attach to a variety of small mammals. The larval and nymphal deer ticks also attach to birds.
In about 50% of the cases a characteristic erythema migrans (rash or lesion) is seen. It begins a few days to a few weeks after the bite of an infected tick. The rash generally looks like an expanding red ring, a bull’s eye. It can be confused with poison ivy, spider or insect bite, or ringworm. At about the same time that the rash develops, flu-like symptoms may appear with headache, sore throat, stiff neck, fever, muscle aches, and fatigue or general malaise. Some people develop the flu-like illness without getting a rash.
Prompt medical attention is important if any of these symptoms appear, especially after being bitten by a tick or visiting an area where Lyme disease is common. If possible, document the presence of the rash by taking a picture because it may disappear before a physician can see it.
If ignored, the early symptoms may disappear, but the later symptoms of Lyme disease can be quite severe and chronic. Muscle pain and arthritis, usually of the large joints is common. Neurological symptoms include meningitis, numbness, tingling, and burning sensations in the extremities, Bell’s palsy (loss of control of one or both sides of the face), severe pain and fatigue (often extreme and incapacitating), and depression. Heart, eye, respiratory and gastrointestinal problems can develop. Symptoms are often intermittent lasting from a few days to several months and sometimes years. Chronic Lyme disease, because of its diverse symptoms, mimics many other diseases and can be difficult to diagnose.
Isolation and culture is the best way to determine the cause of most disease. However, ELISA and Western Blot, the common serological tests, are not yet sophisticated enough to quantitatively determine the severity of infection, and reproducibility of results are not consistent. Thus many false positives and/or false negatives occur.
Typically the characteristic “bulls eye” lesion, flu-like symptoms and history of being in an area where deer ticks are present (such as being in the woods in sandals and shorts), is still considered to be the reliable diagnostic indicator.
Lyme disease is treated with a 3-to-4 week course of antibiotics administered orally (e.g., amoxicillin, doxycycline, ceftriaxone.) Advanced disease may require intravenous ceftriaxone or penicillin for 4 weeks or longer.
Timely treatment increases chances of recovery and may lessen the severity of any later symptoms in both animals and man. Treatment for later stages is more difficult, often requiring extended and repeated courses of antibiotic therapy. In animals and man treatment failures and relapses are reported.
Lyme disease is seen in dogs, cats, horses, cows, and goats. Symptoms can include fever, lameness and soreness, listlessness, loss of appetite, swollen glands and joints. Heart, kidney, liver, eye and nervous system problems are also described in animals. Laminitis (inflammation of a hoof) is reported in horses and cows, as are poor fertility, spontaneous abortions and chronic weight loss. Temperament changes have been reported in dogs and horses. Untreated animals can develop chronic progressive arthritis.
Ticks are most commonly found around the heads and necks of animals. They can also be found between the toes, on or in the ears, and in the armpit and groin areas. Because the ticks are so small, careful inspection is required.
Keep animals out of tick habitats. Check animals daily for ticks and promptly remove any that are found. Dogs and cats should be brushed as soon as they come in the house. Brush them over a light colored surface so any ticks removed can be seen and discarded.
Permethrin, sold under many brand names, is very effective for tick control. Veterinary assistance is important in selecting safe and effective tick control products and in designing a control program.
The proper and easiest method of tick removal is to grasp the tick with fine tweezers, as near the skin as possible, and gently pull it straight out. Be careful not to squeeze the tick when removing it; this could result in more bacteria being injected. Do not try to remove the tick with fingers or attempt to remove with lighted cigarettes, matches, nail polish, or Vaseline. The use of lavender oil has been said to help in tick removal, as ticks may be repelled by the smell and come out. Put the tick in a tightly closed container with a small amount of alcohol for identification.
As in most cases prevention is better than treatment. Suggestions for avoiding tick bites include:
Pertussis, or whooping cough, infects 30–50 million people per year, causing about 300,000 to die. This serious disease can cause permanent disability and/or death in infants, and it is on the rise, and often misdiagnosed. C. difficile, a spore-forming, gram-positive anaerobic bacillus causes approximately three million cases of diarrhea and colitis per year in the United States and represents one of the most common nosocomial infections around the world.
Leptospirosis is an infectious disease caused by the spirochete type of bacteria and can infects humans as secondary hosts. Although it has been a tropical disease, new reports indicate leptospirosis to be of growing concern throughout the United States. It is a reportable disease. Lyme disease is an illness caused by the spirochete bacteria, Borrelia burgdorferi, transmitted to animals and man through the bite of infected deer ticks.
As research continues to find new bacteria responsible for disease, this fascinating subject is ever changing.