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Microbiology Exam #4

Terms in this set (158)

- rod-shaped obligate aerobe; G(+); id. by Robert Koch
- waxy cell capsule; called "acid fast;" require special staining techniques; waxy capsule allows microbe to survive prolonged drying and resists digestion by lysozymes inside a phagocyte; can remain viable for as long as 8 months upon entering the air when a patient coughs.
- other species also cause tuberculosis.
- Tuberculosis - leading killer among infectious diseases today; in 2005 it's estimated that 1.6 million deaths occurred;
- Doesn't just infect the lungs! can also spread to the lymphatic, genitourinary, skeletal, & nervous systems.
- transmission - respiratory droplets
- primary infection - microbes enter the lungs & are phagocytized by alveolar macrophages, but are not killed; several weeks later, T cells are activated, eliciting a cell mediated immune response & tuberculin Ag hypersensitivity (Type IV, delayed); cellular immunity helps control the infection - hypersensitivity causes most of the tissue damage associated with severe cases; the bacteria are isolated within nodules called tubercules or granulomas (dense collections of activated macrophages & lymphocytes); if host cells in the center of a tubercle die, the dead tissue looks dry & crumbly, like cheese (called caseation necrosis - "cheeselike death"); bacteria can persist in these granulomas for many years; progressive primary infection can occur - cellular immunity fails to control the microbes and they spread to other parts of the body; miliary tuberculosis is a life threatening form of the disease - infection sites are so numerous, they look like seeds of millet (grain) scattered throughout the body.
- secondary (reactivation) infection - walled-off bacilli inside old tubercles may escape; the ensuing hypersensitivity reaction can destroy the lungs; patients suffer a chronic cough (consumption); without treatment, the disease is fatal
- X-ray: consolidation in upper lobes
- prevention - BCG vaccine (Bacilllus of Calmette-Guerin) - made from attenuated M. bovis; not entirely reliable; not widely used in U.S., but is used in other parts of the world; not used because people will then test positive for tuberculin skin test. Tuberculin skin testing - tuberculin antigen is injected under skin; raised bump is positive indicating Ag-Ab binding.
- treatment - people who have a positive skin test but do not have active tuberculosis are treated with a single drug (ex. isoniazid) for 1 yr. (prevents reactivation infection); people with active infections receive multi-drug therapy (MDT) for 2 years (rifamycin,e tc.); biggest problem with control of disease is compliance with drug treatment (patients get tired of taking antibiotic)
- Important: The number of cases in the U.S. is on the rise. New drug-resistant strains have been identified in patients who did not finish their full course of medication and are lost to medical follow-up.
- Leading cause of death in AIDS patients
- Elephant-to-human transmission of tuberculosis officially confirmed in 2009
(Hansen's Disease or Leprosy)
- intracellular in macrophages; acid fast G(+) rods like M. tuberculosis
- 2 forms of disease: 1.) tuberculoid - areas of skin lose pigment (hypopigmentation) and sensation; 2.) lepromatous - nodular form where a granulomatous response causes enlarged, disfiguring skin lesions called lepromas; can involve the eyes; may cause thickening of the skin classic "leonine facies" (lion face).
- This is the only bacterium known to destroy peripheral nerve tissue; it "likes" cooler parts of body (nose, ears, fingers, etc.)
- Highest incidences in Brazil and India.
- Symptoms: Infected individuals will notice skin lesions in early stages, leading to paralysis or loss of sensation in those areas, Because of the lack of sensation in affected areas of the skin, people with leprosy often do not notice burns and injuries to their fingers and toes and fail to treat them. These injuries can then become infected with other types of bacteria that cause tissue damage. Gradually, damaged tissue and bone are resorbed by the body, causing the digits to become shorter. However, leprosy does not, as myth would have it, cause parts of the body to fall off. Blindness can occur as the disease advances.
- Incubation period can be up to 20 yrs!
- Transmission: most often spread by respiratory droplets; shared clothing, bedding, etc. may be a source - bacteria may enter a break in the skin; not as contagious as we are led to believe. Well-known case of Father Damien, a Belgian missionary who contracted the disease while caring for leprosy patients on the Hawaiian island of Molokai during the late 1800s, appears to be the exception rather than the rule. Only very rarely do health-care workers who care for patients with leprosy develop the disease themselves.
- Epidemiology: most cases in India; Brazil is #2; endemic in Texas & Louisiana - armadillos are reservoirs (may be spread by touching/eating armadillos)
- Culture: never grown in the lab in artificial culture (only in animal reservoirs)
- Diagnosis: lepromin skin test like tuberculin skin test
- Treatment: can be cure with antibiotics (same MDT and antibiotics as tuberculosis since bacteria are in same genus)
(Inhalation or Respiratory Anthrax)
- G(+) rod; form endospores; facultative anaerobe
- Forms: inhalation (pulmonary or respiratory), cutaneous, gastrointestinal (rare from eating endospore-contaminated meat); over 95% of cases are the cutaneous form; cutaneous form discussed under skin diseases.
- Mode of Transmission for Inhalation Anthrax: Inhalation anthrax may occur if aerosolized endospores are inhaled. Any anthrax bacteria that enter the body in their normal, vegetative state are disposed of by our nonspecific defenses and immune system. Anthrax bacteria that are infecting another person are not forming endospores so they cannot infect another person; in other words inhalation anthrax is usually not communicable by respiratory droplets - only endospores can cause an infection (ID 50 is 8,000-10,000 spores).
- Inhalation anthrax symptoms: Mild fever, malaise, nonproductive cough. Then acute dyspnea and cyanosis. Stridor may be present. A widened mediastinum is a classic hallmark sign of anthrax infection. Shock and death occur shortly. Endopores are inhaled and are engulfed by white blood cells. Inside the wbc's, the spores germinate into vegetative cells and they begin to divide. The bacteria break out of the wbc's and escape into the blood, where they release their toxin. The toxin causes white blood cells to release dangerous amounts of "inflammatory hormones." Body goes into septic shock - systemic vasodilation occurs, blood pressure drops, organs fail.
- Vaccine: The vaccine, licensed since 1970, is considered safe and effective. It is recommended only for high-risk populations, such as military personnel, people who work with the organism in the lab and those who handle potentially infected animal products. The vaccine contains no live anthrax bacteria and cannot cause anthrax infection. However, it requires many more shots than other vaccines and sometimes causes swelling and pain. Current immunization guidelines call for six shots during 18 months, followed by a booster shot every year there after. Researchers are currently working on another vaccine.
- Treatment - penicillin has been the drug of choice until resistance was found; now Cipro may be used in combo with penicillin or by itself; unfortunately, it's the toxin that does the damage, so by the time the disease is diagnosed a dangerous amount of toxin is already present.
- Orthomyxoviridae
- composed of 8 separate pieces of RNA; this and its ability to infect an already infected cell enables the virus to undergo genetic recombination (antigenic shift); this contributes to the virus's genetic variability & potential to cause epidemics.
- different strains: A (avian or bird virus that has crossed into mammals; most severe; responsible for pandemics), B (common cause in children), & C
- transmission - animal reservoirs are critical; virus can jump species; "swine flu" or "bird flu"
- H1N1 strain -Caused a flu pandemic, reportedly killing more than 18,000 people. This virus was a unique combination of influenza virus genes never previously identified in either animals or people. First described in April 2009, the virus appeared to be a new strain of H1N1 which resulted when a previous triple reassortment of bird, swine and human flu viruses further combined with a Eurasian pig flu virus, leading to the term "swine flu" to be used for this pandemic [thanks to the American media]. Initial outbreak occurred in Mexico. The virus is currently less lethal than previous pandemic strains and kills about 0.01-0.03% of those infected [fewer deaths than in an average flu season overall, but with higher risk for those under 50]. Controversy over a reported "campaign of panic" supposedly instigated to sell more vaccines.
- H3N2 strain - first seen in humans in 2011; swine origin; variant of a strain that has been circulating for more than a decade in swine; has acquired the "M" gene from H1N1 that makes the virus more transmissible; closely related to a virus that circulated in the early 1990's, so many people over the age of 20 may have some antibodies that offer some protection.
- H7N9 strain - recently circulating in China. So far is it only transmitted bird to human and is not communicable between humans. It is a deadly strain - as of July 2013 there have been 133 lab confirmed cases, including 43 deaths. In July 2013 a coinfection case was reported - a young both was infected with both H3N2 and H7N9 - this kind of case could results in mutations, giving rise to new strains that could make H7N9 communicable between people.
- clinical syndrome - fever, headache, muscle aches, cough; tracheobronchitis; person becomes prone to secondary bacterial infections because ciliated columnar epithelial cells are killed; can also cause pneumonia; usually not runny nose, which characterizes the common cold
- treatment - antibiotics only prevent secondary bacterial infections; antiviral agents like Tamiflu and Relenza can speed recovery if it is administered during the first 2 days of illness; antivirals may not work against all strains.
- prevention - immunization (Flumist is attenuated; Injected vaccine in inactivated/killed); changing Ag's require a new vaccine every year.
- G(-) bacillus; lactose & sucrose nonfermenter; glucose fermenter; produce H2S; urease negative
- A true infection, not a foodborne intoxication.
- Clinical Signs - diarrhea (can be bloody), abdominal cramps, fever, nausea, vomiting, can develop into severe dehydration or systemic bloodborne infection (bacteremia); onset of illness is usually 1-2 days.
- Transmission - poultry, eggs, unpasteurized milk are the main source; estimated that about 1 in 4 chickens are contaminated; is also transmitted through exposure to reptiles,farm animals, and pets (turtles, etc.); have been outbreaks in veterinary clinics; "egg beater" type products are ok, since they are pasteurized (so if you like raw cookie dough, use "egg beaters"!)
- Outbreaks: ice cream (1994); unpasteurized orange juice from Mexico (1999); sprouts (2000); chicken/turkey pot pies (2007); spinach (2007); salsa (2008); peanut butter (2009) - one of nation's worst know outbreaks of food-borne disease; eggs (2010); custard-filled pastry at bakery in Rhode Island (2011); Cantaloupes from Guatemala (2011); Jennie-O turkey burgers (2011); Papayas from Mexico (2011),
- Prevention - using nonporous cutting boards; disinfecting cutting boards and cooking utensils; thoroughly cooking foods; washing hands.
- Treatment - antibiotic treatment of uncomplicated salmonellosis is medically inadvisable (treatment may cause them to become chronic carriers if bacteria are develop resistance); growing drug resistance among strains due to widespread use of antibiotics in animal feed.
- curved G(-) bacillus (vibrio), microaerophilic; not recognized until the 1970's because they are so difficult to cultivate in the lab.
- A true infection, not a foodborne intoxication
- Clinical Signs - I.P. 2-5 days; frequent episodes of bloody diarrhea, abdominal pain, fever; major cause of diarrheal illness and dysentery; duration is 2-10 days; causes over 2 million illnesses in the U.S. each year. Illness can be severe in immunocompromised.
- Most common cause of bacterial foodborne illness in the U.S.
- Guillain-Barre Syndrome may develop - affects the nerves of the body beginning several weeks after the diarrheal illness. This occurs when a person's immune system is "triggered" to attack the body's own nerves resulting in paralysis that lasts several weeks and usually requires intensive care. It is estimated that approximately 1 in every 1000 reported cases of campylobacteriosis leads to Guillain-Barre syndrome. As many as 40 percent of Guillain-Barre syndrome cases in the USA may be triggered by campylobacteriosis.
- Mechanism of pathogenesis/invasiveness - destroys epithelial lining; produce a toxin and invade cells.
- Transmission - grows in intestinal tract of cattle, sheep, poultry, dogs, cats; human infection probably occurs from ingesting contaminated meat or milk (big one); direct person-to-person transmission may occur; has a low ID50. Public health authorities, including FDA and the CDC, have expressed concerns about the hazards of drinking raw milk for decades.
- Treatment - usually non-life threatening and self-limiting (lasts about a week).
- Outbreaks - unpasteurized milk in Wisconsin (2011)
- G(-) bacillus, lactose & glucose fermenter; IMViC: + + - -
- Most abundant facultative anaerobe in large intestine of humans - part of normal flora; most strains are harmless; also important pathogen of urinary tract.
- A true infection, not a foodborne intoxication
- Diseases - Clinical signs - I.P. 1-8 days; may involve nausea, vomiting, diarrhea, bloating, malaise and abdominal pain; a typical case of t.d. causes 4-5 loose stools per day for 3-4 days; the toxin causes excessive water and electrolyte secretion; can invade intestinal epithelium and cause dysentery; certain strains can cause HUS in young children (destruction of rbc's releases hemoglobin; kidneys have work harder and may fail; 4-5% die);
- Strain 0157:H7 - undercooked hamburgers at Jack in the Box (1993) changed the way fast food restaurants cook their hamburgers and changed FDA regulations; unpasteurized apple juice (1996); lettuce at Taco Bell (not scallions as originally thought) (2006); Ground beef - 2nd largest beef recall in U. S. history (2007); spinach (2006, 2007); Nestle Toll House refrigerated cookie dough (2009), U.S. Hazelnuts (2010); Alabama water park (2011)
- Strain 0104:H4 - STEC strain (Shiga toxin producing E. coli) Summer 2011 - recent epidemic in Europe (France, Germany, Denmark, Poland, Spain, Sweden, UK) linked to fenugreek seeds imported from Egypt; these seeds are used as a spice, herb, and vegetable (common ingredient in curries)
- Mechanism of pathogenesis - causes a dysentery syndrome almost identical to shigellosis; produce proteins that allow bacteria to invade human cells; its "Shiga-like toxins" inhibit protein synthesis; not as virulent as Shigella.
- Prevention of t.d. - Some travelers take antibiotics prophylactically - not recommended (not effective and contributes to development of mutant strains); a better practice is to keep an antidiarrheal medicine available and use it only after symptoms appear. To be safe, drink the beer and ask for well done!
- short, curved G(-) bacillus (vibrio); flagellated
- An infection, not a foodborne intoxication
- Pandemics in the 18OO's led to the adoption of modern systems of sewage disposal and public sanitation; The current pandemic (#7) is caused by the El Tor strain (started in 1961 in Indonesia). It began in Indonesia in 1958 and is still rampant in parts of Africa (remember the thousands of Rwandan refugees that contracted it?), South America, and Asia. Rare in the United States. There was a small outbreak in Alabama (Dauphin island) in 1991 - officials had to close an oyster reef - this prevented an epidemic. Most recent outbreaks in Haiti after June 2010 earthquakes - by Sep 2012, cholera has sickened at least 600,000 and killed more than 7,400.
- Clinical Signs - dehydration from diarrhea (lose as much as a liter an hour); characteristic rice water stools (water flecked with small particles of mucous); dehydration is sudden & dramatic; a person can die in a day.
- Mechanism of pathogenesis - cholera exotoxin causes epithelial cells to secrete large quantities of sodium and chloride ions into intestine, causing water to follow and leave body as diarrhea.
- Transmission - fecal-oral (contaminated water, infected shellfish, fish); can travel around oceans in algae.
- Prevention - sanitation; 2 cholera vaccines (Dukarol & Shanchol) are licensed and available in countries where cholera is prevalent; not used in U.S.
- Treatment - #1: ORT [oral rehydration therapy]: administer water & electrolytes intravenously; tetracycline if necessary, but not administered in most cases.
- G+ bacillus, endospore-former, strict anaerobe
- toxin production depends on a viral prophage; bo-tox is the most poisonous natural substance known (as little as .000005 micrograms can kill a mouse - one oz. would kill the entire U.S. population!
- Classic botulism is food-borne intoxication; wound botulism (see skin disorders) and infant botulism (see below) can also occur
- Clinical Signs - I.P. 12-72 hours; duration days to a month; dizziness; flaccid paralysis (muscle weakness); muscle paralysis starts with the eye muscles, resulting in blurred vision; no fever; usual cause of death is respiratory paralysis; many cases are subclinical
- Mechanism of pathogenesis - produces a neurotoxin that affects the nervous system.
- Transmission - C. botulinum endospores are present in soil and so can contaminate raw produce. Endospores germinate when placed in an anaerobic environment, resulting in bacterial growth and toxin production. Disease most often from improperly home-canned low-acid foods & herb-infused oils; less prevalent in tomato based products which are acidic and fruit jams/jellies which have a lot of sugar added to them (creates a hypertonic environment). Recent outbreak in U.S. from packaged potato soup that was not kept refrigerated.
- Prevention - Add an acidifying agent such as citric or phosphoric acid to foods; use proper canning techniques (time & temp); low acid foods cannot be safely canned using boiling water bath unless acidified; pressure is required to get temp above boiling; produce should be washed well (scrub root vegetables); store foods at proper temperature.
- Treatment - antitoxin
- G(+) rod; endospore former; facultative anaerobe
- Forms: inhalation (pulmonary or respiratory), cutaneous, gastrointestinal (rare from eating endospore-contaminated meat); over 95% of cases are the cutaneous form
- Mode of transmission for G.I. Anthrax: GI anthrax usually occurs after eating undercooked or raw meat from infected animals. For this reason, GI anthrax is more common in countries where animals are not routinely vaccinated against anthrax. In the US, annual vaccination of livestock is recommended in parts of the country where animals have had anthrax in the past. Disease control programs are conducted by veterinary and public health authorities to control outbreaks in livestock and wild animals. These practices, and the inspection of food animals to ensure they are healthy at the time of slaughter, minimize the risk of contaminated meat causing anthrax in the US. This disease is not communicable between humans.
- Symptoms: Incubation period is usually 1-7 days. Symptoms include flu-like symptoms including fever and tiredness, sore throat, neck swelling, difficulty swallowing, nausea, loss of appetite, mild to severe vomiting (may be bloody), mild to severe diarrhea (may be bloody), and severe abdominal pain. When swallowed, anthrax spores may cause lesions from the oral cavity to the cecum. These ulcerative lesions may bleed; hemorrhaging in severe cases may be massive and fatal. GI anthrax can result in severe, systemic disease that is fatal in 25% to 60% of cases.
- Treatment - penicillin has been the drug of choice until resistance was found; now Cipro may be used in combo with penicillin or by itself; unfortunately, it's the toxin that does the damage, so by the time the disease is diagnosed a dangerous amount of toxin is already present.
- Caused by 3 strains of polioviruses (Types 1, 2, 3) that have an affinity for motor neurons of the spinal cord/brain.
- Clinical signs: High fever, back pain, and muscle spasms can occur. Most infections are asymptomatic, or mild and nonparalytic. In < 1% of cases, partial or complete paralysis of muscles can occur, usually in the legs; nature and degree of paralysis depends on which neurons in the spinal cord and brain are damaged. Paralysis remaining after several months is permanent. Spinal paralysis is the most common form of paralytic poliomyelitis, affecting the lower extremities. Spinal polio is the most common form of paralytic poliomyelitis (virus invasion causes inflammation of motor neurons; death of neurons can occur, leading to weakness of respective muscles innervated those neurons; muscles atrophy, becoming weak, floppy and poorly controlled, and finally completely paralyzed).
- Transmission - fecal-oral route and from pharyngeal secretions; once a danger in fecally contaminated swimming pools; virus is shed in feces!
- Absence of animal reservoirs plus availability of effective vaccines made health authorities in 1988 choose polio as the next disease to eradicate from the planet. Polio is now endemic in only 3 countries: Pakistan, Nigeria, and Afghanistan. OPV is still used in these countries. Pakistan is the biggest contributor to the world's polio cases. Taliban campaign claims polio vaccines are a conspiracy by the West to sterilize Muslims (similar to what happened in Nigeria).
- Vaccines:
-- Salk vaccine (IPV - inactivated polio vaccine) - injectable, inactivated (killed) with formalin; requires boosters
-- Sabin vaccine (OPV - oral polio vaccine) - oral, attenuated (live); provides longer-lasting immunity, but in a small number of cases (about 6 each year in the US), viruses have mutated into virulent viruses and have caused disease; no longer administered in most countries since risk of getting disease form vaccine is now greater than getting it naturally from the environment.
G(+) acid-fast bacilli like M. tuberculosis; intracellular in macrophages
2 forms of disease: 1.) tuberculoid - areas of skin lose pigment and sensation; 2.) lepromatous - nodular form where a granulomatous response causes enlarged, disfiguring skin lesions called lepromas; can involve the eyes; may cause thickening of the skin classic "leonine facies" (lion face).
This is the only bacterium known to destroy peripheral nerve tissue; it "likes" cooler parts of body (nose, ears, fingers, etc.)
Symptoms: Infected individuals will notice skin lesions in early stages, leading to paralysis or loss of sensation in those areas, Because of the lack of sensation in affected areas of the skin, people with leprosy often do not notice burns and injuries to their fingers and toes and fail to treat them. These injuries can then become infected with other types of bacteria that cause tissue damage. Gradually, damaged tissue and bone are reabsorbed by the body, causing the digits to become shorter. However, leprosy does not, as myth would have it, cause parts of the body to fall off. Blindness can occur as the disease advances.
Incubation period can be up to 20 yrs!
Transmission: probably spread by respiratory droplets; shared clothing, bedding, etc. may be a source - bacteria may enter a break in the skin; not as contagious as we are led to believe. Well-known case of Father Damien, a Belgian missionary who contracted the disease while caring for leprosy patients on the Hawaiian island of Molokai during the late 1800s, appears to be the exception rather than the rule. Only very rarely do health-care workers who care for patients with leprosy develop the disease themselves.
Epidemiology: most cases in India; Brazil is #2; endemic in Texas & Louisiana - armadillos are reservoirs (may be spread by touching/eating armadillos)
Culture: never grown in the lab in artificial culture (only in animal reservoirs)
Diagnosis: lepromin skin test like tuberculin skin test
Treatment: can be cure with antibiotics (same as with tuberculosis)
rabies = "to rage"
Reservoirs - any mammal can be a reservoir! Most common in U.S.: raccoons (#1), skunks (#2), bats (#3), foxes (#4), cat (#5), cattle (#6), dogs (#7); there are even cases in horses and squirrels!. Globally, dogs are a major reservoir, but numbers of cases in dogs in U.S. has decreased due to vaccination program.
In 2000 there were 7,369 animal cases (domestic and wild) and 5 human cases in the U.S
Rabies does not exist in Hawaii or Australia.
Transmission - most often from bite from an animal (viruses are shed in saliva); transmission from person to person is extremely rare, though it can happen through organ transplant; exposure to infected brain/spinal cord tissue could also result in transmission.
Diagnosis - IFAT (immunofluorescent antibody test) developed in 1958; animal is killed and its brain is examined for rabies antigens; prior to 1958, brain was examined for Negri bodies (inclusion bodies-clusters of viruses in neurons).
The Disease - virus replicates in injured tissues and then slowly migrates to nerves where it eventually reaches the central nervous system (brain/spinal cord); the length of time required for symptoms to appear is proportional to the distance between the wound and the brain and is affected by the accessibility of nerve fibers (think about a face bite vs. a foot bite).
Clinical Signs - 2 forms of disease:
o Furious - "mad dog form"; animal highly irritable/excitable, animals lose caution/fear of other animals/humans; death results from progressive paralysis
o Paralytic - "dumb form"; paralysis of the throat and masseter muscles, often with profuse salivation and inability to swallow; dropping of the lower jaw is common in dogs; animals may not be vicious and rarely attempt to bite; animals develop hydrophobia because it is so painful to swallow; paralysis progresses rapidly to all parts of the body, and coma and death follow in a few hours.
Treatment - Ordinarily there is sufficient time for the bitten individual to be vaccinated and to respond by making enough protective antibodies to prevent onset of the disease - this is due to very slow replication of virus! Once symptoms have occurred it is often too late to vaccinate and death usually follows quickly. No longer administer 20 abdominal injections/day to treat rabies! The current inactivated vaccine is given intramuscularly on days 0, 3, 7, 14, and 28. Passive antibody is also placed deep in the wound and infiltrated around the wound. Pasteur discovered vaccine. Milwaukee Protocol: In the past several years doctors have had some success with recovery from inducing coma in infected individuals exhibiting symptoms
Prevention -
Rabavert, etc - inactivated vaccine given to dogs and cats; once given every year, now every 3 years is sufficient; however, new schedule is more difficult for pet owners to keep track of.
Rabies Bait Drop (ORVP - oral rabies vaccination program): 12 year old program; For several weeks in January, about 3.3 million baits filled with rabies vaccine are dropped from five specially-equipped airplanes flying across 44 South and West-Central Texas counties. The specialized bait of fish meal was designed for coyotes, and a dog-food bait containing molasses and vanilla flavoring was designed for gray foxes.
- G(-) coccobacilli
- zoonosis; spread from infected rodents (rats, squirrels, prairie dogs) to humans by fleas; in West Texas, prairie dogs are reservoirs; recent report in a dog in New Mexico and a cat in Colorado (June 2011) - pets could acquire bacteria by eating an infected rodent or by being bitten by an infected flea; pneumonic plague is communicable between humans via respiratory droplets
- Bacteria clump together in the flea, blocking the digestive tract and driving the flea into a feeding frenzy.
- Two distinct forms of plague occur in human populations:
1. Bubonic plague occurs within a week of being bitten by an infected flea. Symptoms include sudden onset of fever, headache, weakness. Multiplication of the bacteria produces the characteristic "bubo" (swollen, painful lymph node especially in axillary region, groin, or neck). The bacteria escapes from the infected bubo into the bloodstream, causing septicemia (bacteremia). Disseminated intravascular coagulation (DIC) with subsequent cutaneous hemorrhage may well have been what was called the 'Black Death' in the Middle Ages. Death occurs in about 50-75% of those infected if not treated. Bubonic plague can turn into Pneumonic plague (see below).
2. Pneumonic plague Bubonic plague can turn into pneumonic plague if bacteremia occurs and bacteria travel to lungs, so then becomes communicable as it can be transmitted via respiratory droplets. This form is characterized by a shorter incubation period and greater mortality (90%); extremely communicable! Sudden onset of flu-like symptoms includingfever, chills, headache, generalized body pains, weakness and chest discomfort. A cough develops with sputum production, which may be bloody, and increasing chest pain and difficulty in breathing. As thedisease progresses, hypoxia (low oxygen concentration in the blood) and hemoptysis (coughing up blood) are prominent. Fatality rate is high.

- History: During the 6th century AD, the plague ravaged the known world over a 50 year period causing 100 million deaths. The "black death" again devastated Europe during the 14th century over a 5 year period causing 25 million deaths (25% of the European population). In Germany and Switzerland especially, Jews were falsely accused of and persecuted for having deliberately poisoned the waters with the disease. They were, after all, the only ones who drank well water, not stream water, and were not affected by the plague.
- Bioterrorism - in WWII the Japanese dropped infected fleas on China
- G(+) rod; form endospores; facultative anaerobe
- Forms: inhalation (pulmonary or respiratory), cutaneous, gastrointestinal; over 95% of cases are the cutaneous form. See other descriptions of inhalation anthrax respiratory system notes.
- Mode of Transmission for Cutaneous Anthrax: Humans usually acquire a cutaneous infection from contact with infected animals (cattle, sheep, etc.) or contaminated animal products (wool, hides) - once called "wool sorter's disease". Recently (2010) there has been an outbreak in Scotland & England associated with heroine use (contaminated heroine is injected). Can also be transmitted through bite of a fly (ex. stable fly) & mosquitoes.
- Cutaneous Anthrax symptoms: The endospore is introduced a the site of a cut or abrasion. The primary lesion appear 1-7 days after the introduction of the endospore (painless papule). Within 1-2 days small vesicles develop around the papule. One vesicle will enlarge, filling with clear fluid. The vesicle ruptures, undergoes necrosis, and enlarges, forming an ulcer covered by a characteristic black eschar. The lesion looks similar to a brown recluse spider bite. The eschar dries and falls off in 1-2 weeks with little scarring.
- Vaccine: The vaccine, licensed since 1970, is considered safe and effective. It is recommended only for high-risk populations, such as military personnel, people who work with the organism in the lab and those who handle potentially infected animal products. The vaccine contains no live anthrax bacteria and cannot cause anthrax infection. However, it requires many more shots than other vaccines and sometimes causes swelling and pain. Current immunization guidelines call for six shots during 18 months, followed by a booster shot every year there after. Researchers are currently working on another vaccine.
- Treatment - penicillin has been the drug of choice until resistance was found; now Cipro may be used in combo with penicillin or by itself; unfortunately, it's the toxin that does the damage, so by the time the disease is diagnosed a dangerous amount of toxin is already present.
- A skin disease caused by the molluscum contagiosum virus (MCV) usually causing one or more small lesions/bumps.
- MCV is generally a benign infection and symptoms may self-resolve. MCV was once a disease primarily of children, but it has evolved to become a sexually transmitted disease in adults.
- It is believed to be a member of the pox virus family.
- Transmission: may be sexually transmitted by skin-to-skin contact (does not have to be mucous membranes); transmission through sexual contact is the most common form of transmission for adults; MCV may be transmitted from fomites such as towels and clothing; transmission has been associated with swimming pools and sharing baths with an infected person; MCV also may be transmitted by autoinoculation (touching a lesion and touching another part of the body).
- Symptoms: lesions are usually present on the thighs, buttocks, groin, lower abdomen, external genital and anal region; children typically develop lesions on the face, trunk, legs and arms; lesions may begin as small hard bumps which can develop over a period of several weeks into larger sores/bumps; they can cause itching or tenderness in the area, but in most cases the lesions cause few problems; lesions can last from 2 weeks to 4 years -- the average is 2 years.
- Complications: People with AIDS or others with compromised immune systems may develop extensive outbreaks.
- Treatment: most symptoms are self-resolving, but generally lesions are removed; lesions can be removed surgically and/or treated with a chemical agent; cryotherapy is an alternative method of removal.
- spirochete bacterium; difficult to isolate in patient
- std; can also be transmitted in saliva
- 3 disease stages: primary (genital chancres), secondary (rash can look like chicken pox or heat rash), tertiary (damage to all organs, death) - latent stages occur between these disease stages
- has periodic latent stages (no symptoms) that make patients sometimes think that they do not have an STD
- called the "great imitator" because its symptoms mimic those of so many other diseases; heart valves, blood vessels, and meninges can be affected
- mental illness accompanies neural damage
- congenital syphilis occurs when bacteria cross the placenta from mother to baby - infant may show signs such as notched incisors ("Hutchinson's teeth"), a perforated palate, a "saber tibia" (deformed shin bone), an aged face with a saddle-shaped nose
- less common than gonorrhea
- can be cured with antibiotics (penicillin & tetracycline)
- Pyrotherapy - There was no cure for the STD until the early 1900s, when Viennese neurologist Wagner von Jauregg got the idea to treat syphilis sufferers with malaria-infected blood. Predictably, these patients would develop the disease, which would cause an extremely high fever that would kill the syphilis bacteria. Once that happened, they were given the malaria drug quinine, cured and sent home happy and healthy. Von Jauregg won the Nobel Prize for malaria therapy, and the treatment remained in use until the development of penicillin came along and gave doctors a better, safer way to sure the STD.
- About the virus: This virus is called a retrovirus (retro means backward). This virus uses the enzyme reverse transcriptase to make DNA from its RNA. This DNA can be integrated into the host cell's chromosome (now called a provirus). The provirus can stay in a latent stage in which it is replicated along with host cell DNA, causing the host cell no damage. AZT (azidothymidine), which is used against HIV, helps stop reverse transcription by targeting the enzyme reverse transcriptase. There are 3 major groups of HIV and 10 subtypes; most cases in U.S. caused by type I.
- Symptoms: infection typically causes flu-like symptoms, followed by an asymptomatic period of months or years during with the patient can transmit the disease; HIV specifically targets and destroys T helper cells and macrophage, thus affecting both the B cell and cytotoxic T cell responses, so person can die of a secondary infection; see page 520 for symptoms; most patients develop Kaposi's sarcoma (caused by a herpes virus; tumors of blood vessels are seen as purplish spots on skin, but occur throughout the body)
- ARC (AIDS Related Complex) is a condition in which antibody tests are positive for HIV. Patients with ARC show the mild symptoms of HIV infection, which include enlarged lymph nodes, fatigue, night sweats, weight loss, and diarrhea.
- Transmission: sexual contact (all forms), sharing of needles, blood transfusions, mother to infant; development of a vaccine is difficult due to high mutation rate of virus
- First reported in 1980; thought that the virus could have jumped species (from primates to humans)
- AIDS has become the 5th leading cause of death among 25 to 44 yr. olds!
- At of the end of 2000, an estimated 36.1 million people are HIV positive.
- An estimated 5.3 million new infections occurred worldwide during 2000 (15,000 new infections a day)
- In 2000, AIDS associated illness caused the death of 3 million people worldwide; common infections include herpes, CMV, Toxoplasma (protistan), Crytptococcus (fungus), Cryptosporidium (protistan), Candida (fungus).
- Worldwide, more than 80% of all adult HIV infections have resulted from heterosexual intercourse.
- Estimated 800,000 to 900,000 U.S. residents are living with HIV, 1/3 of whom are unaware of their infection.
- RNA virus
- not identified until 1989; blood, blood products (plasma, platelets, antibody), & organs not screened until 1992, so were a source of infection prior to this time!
- the most common blood-borne infection in the United States, affecting at least 4 million people
- The Centers for Disease Control and Prevention urges people born between 1945 and 1965 to be tested, noting that roughly 75 percent of people with the disease are baby boomers. The number of baby boomers
dying from a "silent epidemic" of hepatitis C infections is increasing so rapidly that federal officials are planning a new nationwide push for widespread testing.

Transmission:
- HCV usually spreads through contact with blood, most commonly by sharing needles and other equipment used to inject illegal drugs, but also through blood/organ donations, body piercing and tattoos; health care workers face a risk (although low, less than 2%) of infection from accidental needle sticks and other occupational exposures; can also be spread from using same tooth brush, razor, etc.
- Sexual transmission of HCV is considered to be an inefficient and rare mode of transmission. However, concurrent HIV infection results in increased HCV RNA levels (viral load), which are thought to increase infectiousness of HCV acquired through sexual contact. Of further concern among persons who are coinfected is that HIV accelerates HCV disease progression, even in its early stages. A recent report suggests high-risk sexual behavior as a cause of HCV transmission among HIV-infected MSM in New York City. Unprotected receptive anal intercourse with ejaculation and sex while high on methamphetamine were the most important predictors of HCV infection. Any sexual practices that involve higher levels of trauma to anogenital mucosa ("rough sex") can increase risk
- Vertical transmission to the fetus is possible
- Blood, blood products (plasma, platelets, antibody), & organs not screened until 1992, so were a source of infection prior to this time
- Not transmitted through food/water like Hep A & E.

Acute Infection: occurs 2 weeks to 6 months after infection, usually is so mild that most people don't know they are sick. Older children and adults may develop some mild symptoms, such as fatigue, sore muscles, headache, widespread abdominal pain or pain that is concentrated in the upper right quadrant of the abdomen, nausea, dark urine, light (clay-colored) stools, loss of appetite or weight loss, aversion to some foods, particularly those that are fatty or fried or high in protein, jaundice.
Chronic Infection: About 80% of people who become infected with HCV develop a chronic infection, which they often have for the rest of their lives. However, the majority of people with chronic HCV infection will not develop severe liver damage. Although it may take many years, up to 20% of people who have chronic HCV infection develop liver scarring (cirrhosis). Of these people, 1% to 4% also develop liver cancer. HCV infection is the most common reason for liver transplantation in the United States. In 2007, deaths from the disease
surpassed those linked to HIV, and the numbers of fatalities are expected to continue increasing, researchers reported. Disease is severe in immunocompromised patients. Most people, especially young children, have no symptoms. If symptoms do develop, they may include:
• Constant tiredness (fatigue)
• A general sense of not feeling well (malaise)
• Mild abdominal pain