05-02-2014, 07:13 AM
Hey you guys,
here is my micro notes from ONLY UW... there ABC order, and at end of each question is the question ID on UW, if there is more than one number it means that was in more than one question. I also did the charts as well, but cant paste them here-- so if you want the charts please leave e-mail. If you want this in word leave e-mail since these are all jumbled up here. I did Power Points for Hem, Onc, Renal, and GU-- if anyone wants those.
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Microbiology UW (2014)
1) Actinomycosis—Gram (+) bacteria that are part of the normal flora of the mouth. These can form ‘SULFUR GRANULES” causing cervico-facial actinomycosis – abscesses in the face and neck. E.g pt with recent tooth extraction comes in complaining of a hard mass under the jaw that begins to drain yellow pus through the overlying skin. Treatment long course of parenteral penicillin and surgical debridement (Q-1678)
2) Adenovirus—(Pharyngo-conjunctival fever) these have hexon and penton capsomeres on their surface. Rodlike structures (fibers) that project from the penton base capsomeres are responsible for mediating adsorption to host cells. The cell receptor for most adenovirus fibers is a transmembrane protein of the immunoglobulin superfamily. This can cause severe upper respiratory illnesses, pneumonia, and disseminated infection in immune-suppressed patients. Common in small groups of individuals who live in crowded quarters (barraks) under conditions of fatigue or stress, military recruits, campers.
NOTE: Adenovirus is the most common viral cause of acute hemorrhagic cystitis outbreaks in children, UTI that has dysuria and hematuria is – acute hemorrhagic cystitis.
(Q-1375, 1497, 1498, 1723)
3) Arboviruses (ARthropod BOurne VIRus) are transmitted by insect bites and can cause aspectic meningitis. These include- togavirus (eastern, western, and Venezuelan equine encephalitis), flaviviridae (St. Louis encephalitis) and the bunyaviridae (California encephalitis). These viruses are most common in the summer and fall when arthropods are most active. (Q-1906)
4) Aspergillus fumigatus—is a fungal ball, comes only as a mold form, it has septate hyphae with V-shaped branching (45 degree angles).. It can colonize OLD LUNG CAVITIES e.g. those made from TB and form a “fungal ball”. Symptoms are- cough, dyspnea, and hemotysis. Pts with asthma are at high risk for developing allergic reaction to Aspergillus fumigates called allergic broncho-pulmonary aspergillosis. Signs and symptoms- cough, dyspnea, wheezing, fever, and migratory pulmonary infiltrates. Aspergillus can cause the following conditions:
a) Invasive aspergillosis- develops in immunosuppressed patients. The neutropena associated with leukemias and lymphomas is strongly associated with invasive aspergillosis. The lung is the area most commonly affected. Patients present with hemoptysis and lung granulomas. Aspergillus has a predilection for blood vessels, spreading hematogenously and potentially causing tissue infarcts in the skin, paranasal sinuses, kidneys, endocardium, and brain. Diagnosis is made by light microscopy of tissue specimens, which reveal V-shaped, branching, septate hyphae invading the tissue. Amphotericin B is used to treat invasive aspergillosis.
b) Colonizing Aspergillus- grows in old lung cavaties (produced by tuberculosis or bronchiectasis), forming aspergillomas, also called “fungus balls”. Fungus balls grow inside the cavity only, do not invade the surrounding lung tissue. Aspergillomas can be surgically removed.
c) Hypersensitivity reactions allergic bronchopulmonary aspergillosis (ABPA)- occurs in pts with asthma, Patients present with wheezing and migratory pulmonary infiltrates. Increased serum IgE and increased titers of antibodies against Aspergillus are characteristic and diagnostic. ABPA is treated with steroids.
NOTE: mucormycosis is fungal infections—commonly include: mucor, rhizopus, absidia. These differ from asperigillus b/c these have broad non-septae hyphae with right angle branching. — (Q-103,105, 107, 108, 120, 266, 267, 269)
5) Babesia divergens—is transmitted by tick bites and causes babesiosis, a malaria-like illness with a predilection for pts with spleen.
6) Bacillus anthracis—has a anti-phagocytic capsule that is unique because it has D-glutamate instead of polysaccharide. It is aerobic organism that can grow on standard culture media and make non-hemolyzing adherent colonies, on microscope it forms long chains that are described as “SERPENTINE” or “medusa head”. The anthrax exotoxin is a trimeric toxin that is made of protective antigen, edema factor, and lethal factor. The protective antigen functions to translocate both edema factor and lethal factor into the cytosol. Neither toxin can work without protective antigen. Once inside the cell- the edema factor acts as a calmodulin-dependent adenylate cyclase that increases cAMP concentration. It causes accumulation of fluid within and between cells and also cause suppression of neutrophils and macrophage function. The spores of B. anthraci are very small and once they are inhaled they go into the alveoli and get eaten by macrophages. From the lungs the organisms move fast to mediastinal lymph nodes and cause hemorrhagic mediastinitis. Once the spores germinate into vegetative cells they will begin to make 3-part anthrax toxin and pts get the clinical symptoms. It is commonly caused by exposure through contact with infected animals or animal products or through use of B. anthracis as a biological weapon. This is why occupational history of exposure to animals or animal products is important. Cutaneous anthrax in pt that no risk of occupational exposure then think bioterrorism, There is growth of vegetative organisms at the site of inoculation which causes painless, necrotic wound that is covered with black echar. B. anthracis spreads via LYMPHATICS to the bloodstream, and the organism multiplies in the blood and tissue. Cutaneous anthrax is the most common form of this disease, it occurs on exposed surfaces of the arms or hands.
NOTE:
1. Pulmonary anthrax also known as woolsorters disease, is caused by inhalation of spores most commonly while working with goat hair or hides. Hemorrhagic mediastinitis evident as widened mediastinum on chest x-ray is an important clue.
2. On microscopy it forms long chains that are described as being “serpentine” or “medusa head”
3. Bacillus anthracis produces an anti-phagocytic capsule that is required for pathogenicity. The capsule is unique in that it contains poly-y-D-glutamate instead of polysaccharide.
4. The anthrax exo-toxin is a trimeric toxin made of protective antigen, edema factor, and lethal factor
5. This makes endospores that are resistant to heat, acid, and antibiotics.
6. Bacillus can survive past the boiling point of water, 100C.
(Q-971, 972, 1101, 1389, 1678, 1779)
7) Bacillus cereus—re-fried rice, survives on steamed rice where it produces a heat-stable enterotoxin. (Q-1097, 1422)
8) Bartonella Henselae—is a Gram (-) bacteria, it causes cat-scratch fever which can be caused by a cat scratch or bite. Immunocompromised pts can develop bacillary angiomatous which is characterized by the development of red or purple papules on the skin that can look like kaposi’s sarcoma lesions. (Q-1676)
9) Blastomyces- is a encapsulated fungus with single broad-based bud “owls eyes”, it is common in Great Lakes, Ohio and Mississippi river areas. It is present in soil and rotten organic matter. It is a dimorphic fungus—meaning it takes on different forms in different temperatures. The mold form (branching hyphae) is common in temperatures of 25-30C, in the yeast form (single cell) is common in humans with temperature of 37-40C. Infection occurs by inhaling the aerosolized fungus from the environment, In lungs, Blastomyces assumes yeast form, multiples and induces a granulomatous response. In majority of immune-competent pts blastomycosis stays asymptomatic. In others—they get flu-like illness such as fever, chills, myalgia, headache, non-productive cough or pneumonia. In immunocompromised pts it causes disseminated disease—pts get fever, weight loss, night sweats, lung issues- cough, dyspnea, skin lesions- ulcers, pustules, papules, and bone pain- caused by lytic lesions. Pulmonary blastomycoses is diagnosed by KOH prep of sputum. Blastomyces causes both lung disease and disseminated mycosis, Its microscopic appearance in tissue is – round yeast with broad-based budding and a thick, doubly reflective wall. (Q-103, 105, 117, 120)
10) Bordetella Pertussis—(whooping cough) pertussis toxin aka AB toxin stimulates intracellular G-proteins to increase cAMP production causing increased insulin production, lymphocyte and neutrophil dysfunction, and increased sensitivity to histamine. It makes pertussis toxin and exotoxin called adenylate cyclase toxin, like edema factor of B. anthracis – the adenylate cyclase toxin also functions as a calmodulin-dependent adenylate cyclase that causes phagocyte dysfunction and edema. The immune-suppression caused by pertussis toxin and adenylate cyclase toxin are needed so that this bacteria can colonize the respiratory tract. Bordet-Gengou medium is used to culture the very sensitive Bordetella pertussis, the causative agent in whooping cough.
(Q-1101, 1390, 1094, 1095)
11) Borrelia Burgdorferi—IXODES tick, is a spirochete that causes Lyme disease. Symptoms of Lyme disease involve skin rash (erythema chronicum migrans- occurs at site of tick bite), fever, myalgias and malaise. Systemic disease can progress to cause arthritis, facial paresis, and/or cardiac inflammation. Prolonged untreated disease causes CNS issues seen in tertiary syphilis. The rash begins as an erythematous macule that enlarges with an advancing erythematous border as the bacteria migrate slowly through the skin outward from the inoculation site. The classic lesion is erythemaytous (red) and ring-shaped (annular) due to development of a central clearing. (Q-1313, 1676, 1678)
12) Brucella melitensis—is acquired by drinking infected milk or by direct contact with infected sheep and goats. Fever, malaise, lymphadenopathy, and hepatosplenomegaly characterize the resultant “brucellosis” which is extremely rare in the United States. (Q-278)
13) Campylobacter—is an enteric pathogen, gram (-) curved rod with a filament that lets it move in a “corkscrew” fashion. It is the most common cause of acute gastroenteritis in children and adults in industrialized countries. Transmission is via fecal-oral route. Campylobacter jejuni can cause Guillain-Barre syndrome- a demyelinating syndrome of the peripheral nerves which is characterized by ascending muscle weakness and paralysis. The organisms can be acquired by:
A) Domestic animals e.g dogs, chickens, cattle
B) Contaminated food e.g. undercooked chicken and unpasteurized milk
Campylobacter species causes inflammatory diarrhea (initially watery then bloody), accompanied by abdominal cramps, tenesmus and leukocytes in stool. The abdominal pain can mimic appendicitis.
*campylobacter is the most common infectious agent associated with Guillain-Barre syndrome*
Treatment Erythromycin (b/c its becoming resistant to Fluoroquinolones)
(Q-1422, 1601)
14) Campylobacter fetus—is a Gram (-) rod that causes mild enteritis in immune-competent pts and mild systemic bacteremic illness in immunocompromised pts. (Q-1313)
15) Candida—fungus, blood cultures are used to diagnose disseminated mycoses. a) Albicans-- part of normal human flora, causes disseminated infection in immunocompromised patients. Clinical findings: oral thrush which are white plaques on the oral mucosa that can be EASILY SCARPPED OFF revealing a reddened mucosal surface underneath. It also causes vaginitis—associated with intense vaginal itching, WHITE-CURD like discharge, and labial erythema. Microscope exam of KOH-treated scrapings show candida yeast and pseudohyphae. This forms germ tubes (sprouts of hyphae from yeast cells) if incubated in 37C serum for 3 hours. This test helps to differenciate C. albicans from other candida species. * Oral thrush occurs in pts that wear dentures, DM, immunosuppressed, pts on steroids, antibiotics or chemotheraphy--- any pt that is otherwise healthy and comes in with oral thrush think HIV infection* b) Cutaneous candidiasis—causes diaper rash, occurs in areas that are exposed to heat and high humidity like groin or perianal areas of infants. c) Vulvovaginal candidiasis—associated with antibiotic and contraceptive use, pregnancy, DM, and HIV. d) Candida endophthalmitis—diagnosed using ophthalmoscopy
(Q- 103, 105, 107, 111, 1929, 266, 267, 269, 118)
16) Chlamydia trachomatis—this is a flagella protozoa that causes vaginitis, it is associated with YELLOW-GREEN FOAMY FOAL smelling discharge. On wet mount you see motile trophozoites with flagella. Chlamydia trachomatis is the pathogen that causes lymphogranuloma venereum (LGV), a disease characterized by an ulcer or vesicular lesion on the external genitalia followed by significant regional lymphadenopathy. Proctitis with tenesmus and bloody discharge can be seen in this disease. LGV is a STD.
a) Is one of the main causes of pelvic inflammatory disease (2nd most common being neisseria gonorrhea). Infection by either of these causing PID can be asymptomatic but if there are symptoms they will initially cause purulent urethritis followed by ascension to the cervix where infection can further spread and cause purulent infection and inflammation in the endometrium, fallopian tubues, and peritoneal cavity. Conditions associated with this ascension of infection into the female genital tract and peritoneum include:
1) PID which shows as purulent cervical discharge and cervical motion tenderness
2) Salpinitis and tubo-ovarian abscess
3) Periotoneal inflammation including Fitz-Hugh Curtis syndrome from inflammation of hepatic capsule
Treatment of gonoccal PID must also always include treatment for both Chlamydia trachomatis and neisseria gonorrhea—since Chlamydia will co-infect with Neisseria gonorrhea. A 3rd generation cephalosporin will treat the gonococcal infection, and further treatment with azithromycin or doxycycline is required to treat the Chlamydia which is not sensitive to the beta-lactams. (Q-1027, 1929, 1723)
17) Clostridium botulinum—(CANNED foods), inhibits ACETYCHOLINE, makes botulinum toxin which works by blocking the PRE-synaptic release of acetycholine at the neuromuscular junction which causes flaccid paralysis. This makes endospores that are resistant to heat, acid, and antibiotics. In studies, more than 12% of tested honey samples have C. botulinum species. Infant botulism is due to baby consuming C. botulinum spores, which then germinate in the infant GI tract. Intracelluar toxin production, bacteriolysis resulting in toxin release and mild systemic absorption of toxin ensues. In infant botulism, constipation usually precedes the characteristic signs of neuromuscular paralysis by a few days or weeks. Other symptoms include mild weakness, lethargy, and reduced feeding. Some infants however show more severe symptoms like weakened suck, swallowing, and crying, generalized muscle weakness, and diminished gag reflex. In severe cases the generalized muscle weakness and loss of head control can cause infant to appear “floppy”. Infant botulism can be diagnosed based on the patients clinical presentation and food consumption history. Culture and isolation of the organism and bioassay of toxins are time-consuming procedures, but rapid in vitro procedures have been developed for the detection of types A, B, E, F botulinum toxin-producing organisms and their toxins. The tests are based on ELISA and polymerase chain reaction techniques. CHECK stool for bacterial toxins
(Q-966, 1101, 1390, 1396, 1399, 1097, 1400)
18) Clostridium difficile—(Pseudomembranous colitis) this is an anaerobic Gram (+) spore forming bacillus that colonizes about 3% of healthy individuals and up to 50% of hospitalized adults. Makes cyto-toxin which works by inducing actin depolymerization which leads to mucosal cell death, necrosis of colon mucosa, and pseudomembrane formation. This has endospores that are resistant to heat, acid and antibiotics. Treatment with antibiotics such as fluoroquinolones, clindamycin and broad spectrum penicillins and cephalosporins tens to kill most of the intestinal microbial flora—but C. difficle can survive them. C. difficile grows when other normal flora is dead. It spreads throughout the colon, vegetative cells begin secreting eneterotoxin A, which causes watery diarrhea, and cytotoxin B which causes colonic epithelial cell necrosis and fibrin deposits, PCR detection of toxin A and B genes in stool is the best method for diagnosing C. difficile colitis. (Q-966, 1101, 1390, 1396)
19) Clostridium Perfringens—LECITHINASE, Gram (+) rod, catalase (-), coagulase (-), large spore forming anaerobe, it causes food poisoning, clostridial myonecrosis (gas grene), and bacteremia. The main toxin is LECITHINASE its concentration is what causes the lethal and necrosis effects. Lecithinase is also known as PHOSPHOLIPASE C or ALPHA TOXIN, it is an enzyme that catalyzes the splitting of phospholipid molecules. Phopholipase C hydrolyzes lecithin-containing lipo-protein complexes in cell membranes causing cell lysis (including RBC lysis), tissue necrosis and edema. There are at least 12 toxins in C. perfringens- Alpha toxin is the most injurious one. Clostridium Perfringens uses carbohydrates for energy, its rapid metabolism of muscle tissue carbohydrates produces the gas—which can be seen on xray or ct scans. On blood agar it makes DOUBLE-zone of beta-hemolysis. ** Human phopholipase A2 is the enzyme that catalyzes arachiodonic acid release from phospholipid cell membranes in the 1st step of leukotriene, thromboxane, and prostaglandin synthesis** NOTE: Lecithinase aka alpha toxin is the main toxin made by Clostridium Perfringens. Its function is to degrade lecithin, a part of the cells phospholipid membrane, leading to membrane destruction, cell death, and widespread necrosis and hemolysis. (Q-1136, 1395, 1390, 1094, 8857)
20) Clostridium tetani—GLYCINE, have spores that only germinate and produce toxin in anaerobic environments like necrotic wounds. C. tetani produces disease by the production of a potent protein exotoxin, not by bacterial invasion of tissue. Even small amounts of tetanus toxin can be deadly. At first, the toxin binds to receptors on the presynaptic membranes of the motor neurons. From there, the toxin migrates by the retrograde axonal transport system to the cell bodies of these neurons and next to the spinal cord and brain stem. Release of the inhibitory neurotransmitter glycine and GABA from these inhibitory neurons is blocked. The suppression of inhibitory nerve function results in an increased activation of nerves innervating muscles, causing muscle spasms, spastic paralysis and hyper-reflexia. The muscle spasms involve both flexor and extensor muscles. Patients with tetanus have spastic muscle contractions, difficulty opening the jaw (lockjaw or trismus), a characteristic smile called “risus sardonicus” and contractions of back muscles resulting in backward arching known as opisthotonos. Patients are extremely irritable, and develop titanic seizures, brought about by violent, painful muscle contractions following minor stimuli such as a noise. Illness causes by C. tetani can be prevented by proper immunization with a childhood series and a booster immunization every 10 years thereafter in adulthood. An immunized mother will be able to pass IgG through the placenta to the fetus and provide passive immunity against neonatal tetanus until the child receives its first tetanus vaccination at 2 months of age. Neonatal tetanus usually occurs from C. tetani colonization of the umbilical stump.
(Q-966, 968, 1389)
21) Coccidioides immitis—thick walled spherules- that contains endospores, a dimorphic fungus that has a mold form (hyphae) at 25C- 30C and an endospore form (spherules with endospores- a unique feature of coccidioides) at body temperature of 37C-40C. C. immitis is endemic to the southwest USA e.g. southern and central California, Arizona, New mexico, and western texas, northern mexico and some areas of central and south America. Patients with coccidioidomycosis are likely to live in or have recently traveled to these areas. It is transmitted by breathing in spores, the spores are made by fragmentation of hyphae. Once inside the lungs, the spores turn into spherules that have endospores. The spherules subsequently rupture and release endospores that disseminate to other organs and tissues. Each endospore is capable of forming a new spherule. In healthy pts C. immitis causes lung disease which is asymptomatic or flu-like e.g. cough, fever, myalgia and erythema nodosum. In general C. immitis can present in 5 ways- acute pneumonia (most common), chronic progressive pneumonia, pulmonary nodules and cavities, exrapulmonary nodules and cavities, extrapulmonary non-meningeal disease, and meningitis. The more severe is seen in immunocompromised pts. NOTE: Coccidioides immitis is a dimorphic fungus endemic to the southwest USA. It exists in the environment as a mold (with hyphae) that forms spores. These spores are inhaled and turn into spherules in the lungs. C. immitis causes lung disease in immunocompetent people and disseminated mycosis in immunocpmpromised individuals. In tissue samples it appears as large, irregularly sized, thick walled spherules that have small round endospores. (Q-105, 117, 118, 120, 267, 269)
22) Corynebacterium diphtheria—AB-EXOTOXIN, is a Gram (+) rod, catalase (+), aerobic or facultatively anaerobic, club-shaped rods. that causes diphtheria. One of the characteristics of this organism is the intracellular polyphosphate granules—these can be seen on microscopy after growth on Loeffler medium and staining with methylene blue. The diphtheria exotoxin an AB exotoxin is specific for neural and cardiac tissues it works by ribosylating and inactivates elongation factor-2 (EF-2) which stops protein synthesis and causes cell death in humans. This is same way exotoxin A made by pseudomonas aeruginosa works. C. diphtheria is an acute toxin-caused disease but not all strains of c. diphtheria express the disease causing exotoxin. C. diphtheria gets its virulence via bacterio-phage mediated “infection” with the TOX gene, this codes for the diphtheria AB exotoxin. The bacteriophage responsible is called Corynephage beta. The phage TOX gene incorporates into the bacterial chromosome as a prophage and codes for toxin production by C. diphtheria. This process whereby a bacteriophage infects a host bacterium and integrates its genome into the host bacterium’s genome is called lysogenization. Acute infection of the naso- and oropharynx causes pseudomembranous pharyngitis with exudates and cervical lymphadenopathy in a group where vaccination status is unknown. Diptheria can cause MYOCARDITIS and HEART FAILURE. Clinical symtoms: sore throat, fever, lymphadenopathy, upper airway dyspnea, and odynophagia. Corynebacteria diphtheria will grow on cystein-tellurite agar as dark black slightly iridescent colonies. It can also grown on Loffler’s medium where it will develop cytoplasmic metachromatic granules (visualizable after staining with an aniline dye such methylene blue). Because culturing the organism may take days, and because diphtheria has high mortality that warrants immediate treatment, more rapid diagnostic mechanisms such as the immune-chromagraphic strip assay are being developed. Treatment Diphtheria anti-toxin (1st) , Penicillin or Erythromycin (2nd) , DPT vaccine (passive immunization) Active immunization with the diphtheria toxoid (given as part of childhood DTaP vaccine) prevents diphtheria. It is also given as tetanus boosters in adults.
NOTE: Corynebacterium diphtheria causes diphtheria, an acute bacterial disease that initially affects the oropharynx. The organism is spread by respiratory droplet transmission and causes disease via it’s A/B exotoxin. The B (think: binding) subunit allows penetration of the A (think: active) subunit into the cell to inhibit ribosome function. Neural and cardiac toxicity are serious potential sequelae. Immunization with diphtheria toxoid induces production of circulating IgG against the exotoxin B subunit, effectively preventing disease.
(Q-1313, 1388, 1389, 1390, 1024, 1092, 1094, 1095, 972)
23) Coxsackie virus—is part of the picorna-viridae family and is made of an ICOSAHEDRAL nucleocapsid and a (+) single-stranded RNA genome. The RNA has a protein on the 5’ end that acts as a primer for transcription by RNA-dependent RNA polymerase. (Q-376)
24) Cryptocossus neoformans—the yeast form is found in pigeon droppings. This is a fungal infection seen in AIDS pts causing Cryptococcus meningitis, to diagnose it you need to do a lumbar puncture then CSF is stained with India ink which shows encapsulated yeast. It causes lung disease and meningitis in immunocompromised pts. It forms NARROW BASED BUDS, with a thick polysaccharide capsule that appears clear with india ink staining and stains red with mucicarmine. A pt with history of viral esophagitis and pneumocystis pneumonia think HIV, then they present with headache, confusion, and inflammatory CSF think meningitis which is probably caused by Cryptococcus neoformans. Mucicarmine stain is used to find the polysaccharide capsule of Cryptoccus neoformans. The polysaccharide capsule is the major virulence factor—it stains red, and seen in tissues as round yeast cells with narrow-based buds. C. neoformins affects immunocompromised patients (e.g. kidney transplant). It is transmitted via respiratory route and can cause pulmonary disease. Usually its aymptomatic but lung disease can cause pneumonia like symptoms. Pts complain of cough with little sputum production and pleuritic chest pain, with dyspnes and hemoptysis. The diagnosis is made by seeing C. neoformins in sputum, bronchoalveolar washings, or tissue samples. Methenamine silver (GMS) and mucicarmine stains are used. NOTE: C. neoformins is a neurotropic fungus—most common presentation is subacute or chronic meningo-encephalitis.
NOTE: causes meningitis in AIDS pts, India ink stain of CSF shows—encapsulated yeast. (Q-103, 105, 107, 120, 266, 267, 269, 118, 117)
25) Cytomegalovirus—ICOSAHEDRAL core that is surrounded by a lipo-protein envelope and has double-stranded, linear DNA. In order for this virus to get into host cell it requires initial contact with glycosaminoglycan chains on host cell surface proteoglycans for entry. This family of viruses are in the Herpes-viridae family and they get there envelopes by BUDDING from the nuclear membrane. Pts with CD4
here is my micro notes from ONLY UW... there ABC order, and at end of each question is the question ID on UW, if there is more than one number it means that was in more than one question. I also did the charts as well, but cant paste them here-- so if you want the charts please leave e-mail. If you want this in word leave e-mail since these are all jumbled up here. I did Power Points for Hem, Onc, Renal, and GU-- if anyone wants those.
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Microbiology UW (2014)
1) Actinomycosis—Gram (+) bacteria that are part of the normal flora of the mouth. These can form ‘SULFUR GRANULES” causing cervico-facial actinomycosis – abscesses in the face and neck. E.g pt with recent tooth extraction comes in complaining of a hard mass under the jaw that begins to drain yellow pus through the overlying skin. Treatment long course of parenteral penicillin and surgical debridement (Q-1678)
2) Adenovirus—(Pharyngo-conjunctival fever) these have hexon and penton capsomeres on their surface. Rodlike structures (fibers) that project from the penton base capsomeres are responsible for mediating adsorption to host cells. The cell receptor for most adenovirus fibers is a transmembrane protein of the immunoglobulin superfamily. This can cause severe upper respiratory illnesses, pneumonia, and disseminated infection in immune-suppressed patients. Common in small groups of individuals who live in crowded quarters (barraks) under conditions of fatigue or stress, military recruits, campers.
NOTE: Adenovirus is the most common viral cause of acute hemorrhagic cystitis outbreaks in children, UTI that has dysuria and hematuria is – acute hemorrhagic cystitis.
(Q-1375, 1497, 1498, 1723)
3) Arboviruses (ARthropod BOurne VIRus) are transmitted by insect bites and can cause aspectic meningitis. These include- togavirus (eastern, western, and Venezuelan equine encephalitis), flaviviridae (St. Louis encephalitis) and the bunyaviridae (California encephalitis). These viruses are most common in the summer and fall when arthropods are most active. (Q-1906)
4) Aspergillus fumigatus—is a fungal ball, comes only as a mold form, it has septate hyphae with V-shaped branching (45 degree angles).. It can colonize OLD LUNG CAVITIES e.g. those made from TB and form a “fungal ball”. Symptoms are- cough, dyspnea, and hemotysis. Pts with asthma are at high risk for developing allergic reaction to Aspergillus fumigates called allergic broncho-pulmonary aspergillosis. Signs and symptoms- cough, dyspnea, wheezing, fever, and migratory pulmonary infiltrates. Aspergillus can cause the following conditions:
a) Invasive aspergillosis- develops in immunosuppressed patients. The neutropena associated with leukemias and lymphomas is strongly associated with invasive aspergillosis. The lung is the area most commonly affected. Patients present with hemoptysis and lung granulomas. Aspergillus has a predilection for blood vessels, spreading hematogenously and potentially causing tissue infarcts in the skin, paranasal sinuses, kidneys, endocardium, and brain. Diagnosis is made by light microscopy of tissue specimens, which reveal V-shaped, branching, septate hyphae invading the tissue. Amphotericin B is used to treat invasive aspergillosis.
b) Colonizing Aspergillus- grows in old lung cavaties (produced by tuberculosis or bronchiectasis), forming aspergillomas, also called “fungus balls”. Fungus balls grow inside the cavity only, do not invade the surrounding lung tissue. Aspergillomas can be surgically removed.
c) Hypersensitivity reactions allergic bronchopulmonary aspergillosis (ABPA)- occurs in pts with asthma, Patients present with wheezing and migratory pulmonary infiltrates. Increased serum IgE and increased titers of antibodies against Aspergillus are characteristic and diagnostic. ABPA is treated with steroids.
NOTE: mucormycosis is fungal infections—commonly include: mucor, rhizopus, absidia. These differ from asperigillus b/c these have broad non-septae hyphae with right angle branching. — (Q-103,105, 107, 108, 120, 266, 267, 269)
5) Babesia divergens—is transmitted by tick bites and causes babesiosis, a malaria-like illness with a predilection for pts with spleen.
6) Bacillus anthracis—has a anti-phagocytic capsule that is unique because it has D-glutamate instead of polysaccharide. It is aerobic organism that can grow on standard culture media and make non-hemolyzing adherent colonies, on microscope it forms long chains that are described as “SERPENTINE” or “medusa head”. The anthrax exotoxin is a trimeric toxin that is made of protective antigen, edema factor, and lethal factor. The protective antigen functions to translocate both edema factor and lethal factor into the cytosol. Neither toxin can work without protective antigen. Once inside the cell- the edema factor acts as a calmodulin-dependent adenylate cyclase that increases cAMP concentration. It causes accumulation of fluid within and between cells and also cause suppression of neutrophils and macrophage function. The spores of B. anthraci are very small and once they are inhaled they go into the alveoli and get eaten by macrophages. From the lungs the organisms move fast to mediastinal lymph nodes and cause hemorrhagic mediastinitis. Once the spores germinate into vegetative cells they will begin to make 3-part anthrax toxin and pts get the clinical symptoms. It is commonly caused by exposure through contact with infected animals or animal products or through use of B. anthracis as a biological weapon. This is why occupational history of exposure to animals or animal products is important. Cutaneous anthrax in pt that no risk of occupational exposure then think bioterrorism, There is growth of vegetative organisms at the site of inoculation which causes painless, necrotic wound that is covered with black echar. B. anthracis spreads via LYMPHATICS to the bloodstream, and the organism multiplies in the blood and tissue. Cutaneous anthrax is the most common form of this disease, it occurs on exposed surfaces of the arms or hands.
NOTE:
1. Pulmonary anthrax also known as woolsorters disease, is caused by inhalation of spores most commonly while working with goat hair or hides. Hemorrhagic mediastinitis evident as widened mediastinum on chest x-ray is an important clue.
2. On microscopy it forms long chains that are described as being “serpentine” or “medusa head”
3. Bacillus anthracis produces an anti-phagocytic capsule that is required for pathogenicity. The capsule is unique in that it contains poly-y-D-glutamate instead of polysaccharide.
4. The anthrax exo-toxin is a trimeric toxin made of protective antigen, edema factor, and lethal factor
5. This makes endospores that are resistant to heat, acid, and antibiotics.
6. Bacillus can survive past the boiling point of water, 100C.
(Q-971, 972, 1101, 1389, 1678, 1779)
7) Bacillus cereus—re-fried rice, survives on steamed rice where it produces a heat-stable enterotoxin. (Q-1097, 1422)
8) Bartonella Henselae—is a Gram (-) bacteria, it causes cat-scratch fever which can be caused by a cat scratch or bite. Immunocompromised pts can develop bacillary angiomatous which is characterized by the development of red or purple papules on the skin that can look like kaposi’s sarcoma lesions. (Q-1676)
9) Blastomyces- is a encapsulated fungus with single broad-based bud “owls eyes”, it is common in Great Lakes, Ohio and Mississippi river areas. It is present in soil and rotten organic matter. It is a dimorphic fungus—meaning it takes on different forms in different temperatures. The mold form (branching hyphae) is common in temperatures of 25-30C, in the yeast form (single cell) is common in humans with temperature of 37-40C. Infection occurs by inhaling the aerosolized fungus from the environment, In lungs, Blastomyces assumes yeast form, multiples and induces a granulomatous response. In majority of immune-competent pts blastomycosis stays asymptomatic. In others—they get flu-like illness such as fever, chills, myalgia, headache, non-productive cough or pneumonia. In immunocompromised pts it causes disseminated disease—pts get fever, weight loss, night sweats, lung issues- cough, dyspnea, skin lesions- ulcers, pustules, papules, and bone pain- caused by lytic lesions. Pulmonary blastomycoses is diagnosed by KOH prep of sputum. Blastomyces causes both lung disease and disseminated mycosis, Its microscopic appearance in tissue is – round yeast with broad-based budding and a thick, doubly reflective wall. (Q-103, 105, 117, 120)
10) Bordetella Pertussis—(whooping cough) pertussis toxin aka AB toxin stimulates intracellular G-proteins to increase cAMP production causing increased insulin production, lymphocyte and neutrophil dysfunction, and increased sensitivity to histamine. It makes pertussis toxin and exotoxin called adenylate cyclase toxin, like edema factor of B. anthracis – the adenylate cyclase toxin also functions as a calmodulin-dependent adenylate cyclase that causes phagocyte dysfunction and edema. The immune-suppression caused by pertussis toxin and adenylate cyclase toxin are needed so that this bacteria can colonize the respiratory tract. Bordet-Gengou medium is used to culture the very sensitive Bordetella pertussis, the causative agent in whooping cough.
(Q-1101, 1390, 1094, 1095)
11) Borrelia Burgdorferi—IXODES tick, is a spirochete that causes Lyme disease. Symptoms of Lyme disease involve skin rash (erythema chronicum migrans- occurs at site of tick bite), fever, myalgias and malaise. Systemic disease can progress to cause arthritis, facial paresis, and/or cardiac inflammation. Prolonged untreated disease causes CNS issues seen in tertiary syphilis. The rash begins as an erythematous macule that enlarges with an advancing erythematous border as the bacteria migrate slowly through the skin outward from the inoculation site. The classic lesion is erythemaytous (red) and ring-shaped (annular) due to development of a central clearing. (Q-1313, 1676, 1678)
12) Brucella melitensis—is acquired by drinking infected milk or by direct contact with infected sheep and goats. Fever, malaise, lymphadenopathy, and hepatosplenomegaly characterize the resultant “brucellosis” which is extremely rare in the United States. (Q-278)
13) Campylobacter—is an enteric pathogen, gram (-) curved rod with a filament that lets it move in a “corkscrew” fashion. It is the most common cause of acute gastroenteritis in children and adults in industrialized countries. Transmission is via fecal-oral route. Campylobacter jejuni can cause Guillain-Barre syndrome- a demyelinating syndrome of the peripheral nerves which is characterized by ascending muscle weakness and paralysis. The organisms can be acquired by:
A) Domestic animals e.g dogs, chickens, cattle
B) Contaminated food e.g. undercooked chicken and unpasteurized milk
Campylobacter species causes inflammatory diarrhea (initially watery then bloody), accompanied by abdominal cramps, tenesmus and leukocytes in stool. The abdominal pain can mimic appendicitis.
*campylobacter is the most common infectious agent associated with Guillain-Barre syndrome*
Treatment Erythromycin (b/c its becoming resistant to Fluoroquinolones)
(Q-1422, 1601)
14) Campylobacter fetus—is a Gram (-) rod that causes mild enteritis in immune-competent pts and mild systemic bacteremic illness in immunocompromised pts. (Q-1313)
15) Candida—fungus, blood cultures are used to diagnose disseminated mycoses. a) Albicans-- part of normal human flora, causes disseminated infection in immunocompromised patients. Clinical findings: oral thrush which are white plaques on the oral mucosa that can be EASILY SCARPPED OFF revealing a reddened mucosal surface underneath. It also causes vaginitis—associated with intense vaginal itching, WHITE-CURD like discharge, and labial erythema. Microscope exam of KOH-treated scrapings show candida yeast and pseudohyphae. This forms germ tubes (sprouts of hyphae from yeast cells) if incubated in 37C serum for 3 hours. This test helps to differenciate C. albicans from other candida species. * Oral thrush occurs in pts that wear dentures, DM, immunosuppressed, pts on steroids, antibiotics or chemotheraphy--- any pt that is otherwise healthy and comes in with oral thrush think HIV infection* b) Cutaneous candidiasis—causes diaper rash, occurs in areas that are exposed to heat and high humidity like groin or perianal areas of infants. c) Vulvovaginal candidiasis—associated with antibiotic and contraceptive use, pregnancy, DM, and HIV. d) Candida endophthalmitis—diagnosed using ophthalmoscopy
(Q- 103, 105, 107, 111, 1929, 266, 267, 269, 118)
16) Chlamydia trachomatis—this is a flagella protozoa that causes vaginitis, it is associated with YELLOW-GREEN FOAMY FOAL smelling discharge. On wet mount you see motile trophozoites with flagella. Chlamydia trachomatis is the pathogen that causes lymphogranuloma venereum (LGV), a disease characterized by an ulcer or vesicular lesion on the external genitalia followed by significant regional lymphadenopathy. Proctitis with tenesmus and bloody discharge can be seen in this disease. LGV is a STD.
a) Is one of the main causes of pelvic inflammatory disease (2nd most common being neisseria gonorrhea). Infection by either of these causing PID can be asymptomatic but if there are symptoms they will initially cause purulent urethritis followed by ascension to the cervix where infection can further spread and cause purulent infection and inflammation in the endometrium, fallopian tubues, and peritoneal cavity. Conditions associated with this ascension of infection into the female genital tract and peritoneum include:
1) PID which shows as purulent cervical discharge and cervical motion tenderness
2) Salpinitis and tubo-ovarian abscess
3) Periotoneal inflammation including Fitz-Hugh Curtis syndrome from inflammation of hepatic capsule
Treatment of gonoccal PID must also always include treatment for both Chlamydia trachomatis and neisseria gonorrhea—since Chlamydia will co-infect with Neisseria gonorrhea. A 3rd generation cephalosporin will treat the gonococcal infection, and further treatment with azithromycin or doxycycline is required to treat the Chlamydia which is not sensitive to the beta-lactams. (Q-1027, 1929, 1723)
17) Clostridium botulinum—(CANNED foods), inhibits ACETYCHOLINE, makes botulinum toxin which works by blocking the PRE-synaptic release of acetycholine at the neuromuscular junction which causes flaccid paralysis. This makes endospores that are resistant to heat, acid, and antibiotics. In studies, more than 12% of tested honey samples have C. botulinum species. Infant botulism is due to baby consuming C. botulinum spores, which then germinate in the infant GI tract. Intracelluar toxin production, bacteriolysis resulting in toxin release and mild systemic absorption of toxin ensues. In infant botulism, constipation usually precedes the characteristic signs of neuromuscular paralysis by a few days or weeks. Other symptoms include mild weakness, lethargy, and reduced feeding. Some infants however show more severe symptoms like weakened suck, swallowing, and crying, generalized muscle weakness, and diminished gag reflex. In severe cases the generalized muscle weakness and loss of head control can cause infant to appear “floppy”. Infant botulism can be diagnosed based on the patients clinical presentation and food consumption history. Culture and isolation of the organism and bioassay of toxins are time-consuming procedures, but rapid in vitro procedures have been developed for the detection of types A, B, E, F botulinum toxin-producing organisms and their toxins. The tests are based on ELISA and polymerase chain reaction techniques. CHECK stool for bacterial toxins
(Q-966, 1101, 1390, 1396, 1399, 1097, 1400)
18) Clostridium difficile—(Pseudomembranous colitis) this is an anaerobic Gram (+) spore forming bacillus that colonizes about 3% of healthy individuals and up to 50% of hospitalized adults. Makes cyto-toxin which works by inducing actin depolymerization which leads to mucosal cell death, necrosis of colon mucosa, and pseudomembrane formation. This has endospores that are resistant to heat, acid and antibiotics. Treatment with antibiotics such as fluoroquinolones, clindamycin and broad spectrum penicillins and cephalosporins tens to kill most of the intestinal microbial flora—but C. difficle can survive them. C. difficile grows when other normal flora is dead. It spreads throughout the colon, vegetative cells begin secreting eneterotoxin A, which causes watery diarrhea, and cytotoxin B which causes colonic epithelial cell necrosis and fibrin deposits, PCR detection of toxin A and B genes in stool is the best method for diagnosing C. difficile colitis. (Q-966, 1101, 1390, 1396)
19) Clostridium Perfringens—LECITHINASE, Gram (+) rod, catalase (-), coagulase (-), large spore forming anaerobe, it causes food poisoning, clostridial myonecrosis (gas grene), and bacteremia. The main toxin is LECITHINASE its concentration is what causes the lethal and necrosis effects. Lecithinase is also known as PHOSPHOLIPASE C or ALPHA TOXIN, it is an enzyme that catalyzes the splitting of phospholipid molecules. Phopholipase C hydrolyzes lecithin-containing lipo-protein complexes in cell membranes causing cell lysis (including RBC lysis), tissue necrosis and edema. There are at least 12 toxins in C. perfringens- Alpha toxin is the most injurious one. Clostridium Perfringens uses carbohydrates for energy, its rapid metabolism of muscle tissue carbohydrates produces the gas—which can be seen on xray or ct scans. On blood agar it makes DOUBLE-zone of beta-hemolysis. ** Human phopholipase A2 is the enzyme that catalyzes arachiodonic acid release from phospholipid cell membranes in the 1st step of leukotriene, thromboxane, and prostaglandin synthesis** NOTE: Lecithinase aka alpha toxin is the main toxin made by Clostridium Perfringens. Its function is to degrade lecithin, a part of the cells phospholipid membrane, leading to membrane destruction, cell death, and widespread necrosis and hemolysis. (Q-1136, 1395, 1390, 1094, 8857)
20) Clostridium tetani—GLYCINE, have spores that only germinate and produce toxin in anaerobic environments like necrotic wounds. C. tetani produces disease by the production of a potent protein exotoxin, not by bacterial invasion of tissue. Even small amounts of tetanus toxin can be deadly. At first, the toxin binds to receptors on the presynaptic membranes of the motor neurons. From there, the toxin migrates by the retrograde axonal transport system to the cell bodies of these neurons and next to the spinal cord and brain stem. Release of the inhibitory neurotransmitter glycine and GABA from these inhibitory neurons is blocked. The suppression of inhibitory nerve function results in an increased activation of nerves innervating muscles, causing muscle spasms, spastic paralysis and hyper-reflexia. The muscle spasms involve both flexor and extensor muscles. Patients with tetanus have spastic muscle contractions, difficulty opening the jaw (lockjaw or trismus), a characteristic smile called “risus sardonicus” and contractions of back muscles resulting in backward arching known as opisthotonos. Patients are extremely irritable, and develop titanic seizures, brought about by violent, painful muscle contractions following minor stimuli such as a noise. Illness causes by C. tetani can be prevented by proper immunization with a childhood series and a booster immunization every 10 years thereafter in adulthood. An immunized mother will be able to pass IgG through the placenta to the fetus and provide passive immunity against neonatal tetanus until the child receives its first tetanus vaccination at 2 months of age. Neonatal tetanus usually occurs from C. tetani colonization of the umbilical stump.
(Q-966, 968, 1389)
21) Coccidioides immitis—thick walled spherules- that contains endospores, a dimorphic fungus that has a mold form (hyphae) at 25C- 30C and an endospore form (spherules with endospores- a unique feature of coccidioides) at body temperature of 37C-40C. C. immitis is endemic to the southwest USA e.g. southern and central California, Arizona, New mexico, and western texas, northern mexico and some areas of central and south America. Patients with coccidioidomycosis are likely to live in or have recently traveled to these areas. It is transmitted by breathing in spores, the spores are made by fragmentation of hyphae. Once inside the lungs, the spores turn into spherules that have endospores. The spherules subsequently rupture and release endospores that disseminate to other organs and tissues. Each endospore is capable of forming a new spherule. In healthy pts C. immitis causes lung disease which is asymptomatic or flu-like e.g. cough, fever, myalgia and erythema nodosum. In general C. immitis can present in 5 ways- acute pneumonia (most common), chronic progressive pneumonia, pulmonary nodules and cavities, exrapulmonary nodules and cavities, extrapulmonary non-meningeal disease, and meningitis. The more severe is seen in immunocompromised pts. NOTE: Coccidioides immitis is a dimorphic fungus endemic to the southwest USA. It exists in the environment as a mold (with hyphae) that forms spores. These spores are inhaled and turn into spherules in the lungs. C. immitis causes lung disease in immunocompetent people and disseminated mycosis in immunocpmpromised individuals. In tissue samples it appears as large, irregularly sized, thick walled spherules that have small round endospores. (Q-105, 117, 118, 120, 267, 269)
22) Corynebacterium diphtheria—AB-EXOTOXIN, is a Gram (+) rod, catalase (+), aerobic or facultatively anaerobic, club-shaped rods. that causes diphtheria. One of the characteristics of this organism is the intracellular polyphosphate granules—these can be seen on microscopy after growth on Loeffler medium and staining with methylene blue. The diphtheria exotoxin an AB exotoxin is specific for neural and cardiac tissues it works by ribosylating and inactivates elongation factor-2 (EF-2) which stops protein synthesis and causes cell death in humans. This is same way exotoxin A made by pseudomonas aeruginosa works. C. diphtheria is an acute toxin-caused disease but not all strains of c. diphtheria express the disease causing exotoxin. C. diphtheria gets its virulence via bacterio-phage mediated “infection” with the TOX gene, this codes for the diphtheria AB exotoxin. The bacteriophage responsible is called Corynephage beta. The phage TOX gene incorporates into the bacterial chromosome as a prophage and codes for toxin production by C. diphtheria. This process whereby a bacteriophage infects a host bacterium and integrates its genome into the host bacterium’s genome is called lysogenization. Acute infection of the naso- and oropharynx causes pseudomembranous pharyngitis with exudates and cervical lymphadenopathy in a group where vaccination status is unknown. Diptheria can cause MYOCARDITIS and HEART FAILURE. Clinical symtoms: sore throat, fever, lymphadenopathy, upper airway dyspnea, and odynophagia. Corynebacteria diphtheria will grow on cystein-tellurite agar as dark black slightly iridescent colonies. It can also grown on Loffler’s medium where it will develop cytoplasmic metachromatic granules (visualizable after staining with an aniline dye such methylene blue). Because culturing the organism may take days, and because diphtheria has high mortality that warrants immediate treatment, more rapid diagnostic mechanisms such as the immune-chromagraphic strip assay are being developed. Treatment Diphtheria anti-toxin (1st) , Penicillin or Erythromycin (2nd) , DPT vaccine (passive immunization) Active immunization with the diphtheria toxoid (given as part of childhood DTaP vaccine) prevents diphtheria. It is also given as tetanus boosters in adults.
NOTE: Corynebacterium diphtheria causes diphtheria, an acute bacterial disease that initially affects the oropharynx. The organism is spread by respiratory droplet transmission and causes disease via it’s A/B exotoxin. The B (think: binding) subunit allows penetration of the A (think: active) subunit into the cell to inhibit ribosome function. Neural and cardiac toxicity are serious potential sequelae. Immunization with diphtheria toxoid induces production of circulating IgG against the exotoxin B subunit, effectively preventing disease.
(Q-1313, 1388, 1389, 1390, 1024, 1092, 1094, 1095, 972)
23) Coxsackie virus—is part of the picorna-viridae family and is made of an ICOSAHEDRAL nucleocapsid and a (+) single-stranded RNA genome. The RNA has a protein on the 5’ end that acts as a primer for transcription by RNA-dependent RNA polymerase. (Q-376)
24) Cryptocossus neoformans—the yeast form is found in pigeon droppings. This is a fungal infection seen in AIDS pts causing Cryptococcus meningitis, to diagnose it you need to do a lumbar puncture then CSF is stained with India ink which shows encapsulated yeast. It causes lung disease and meningitis in immunocompromised pts. It forms NARROW BASED BUDS, with a thick polysaccharide capsule that appears clear with india ink staining and stains red with mucicarmine. A pt with history of viral esophagitis and pneumocystis pneumonia think HIV, then they present with headache, confusion, and inflammatory CSF think meningitis which is probably caused by Cryptococcus neoformans. Mucicarmine stain is used to find the polysaccharide capsule of Cryptoccus neoformans. The polysaccharide capsule is the major virulence factor—it stains red, and seen in tissues as round yeast cells with narrow-based buds. C. neoformins affects immunocompromised patients (e.g. kidney transplant). It is transmitted via respiratory route and can cause pulmonary disease. Usually its aymptomatic but lung disease can cause pneumonia like symptoms. Pts complain of cough with little sputum production and pleuritic chest pain, with dyspnes and hemoptysis. The diagnosis is made by seeing C. neoformins in sputum, bronchoalveolar washings, or tissue samples. Methenamine silver (GMS) and mucicarmine stains are used. NOTE: C. neoformins is a neurotropic fungus—most common presentation is subacute or chronic meningo-encephalitis.
NOTE: causes meningitis in AIDS pts, India ink stain of CSF shows—encapsulated yeast. (Q-103, 105, 107, 120, 266, 267, 269, 118, 117)
25) Cytomegalovirus—ICOSAHEDRAL core that is surrounded by a lipo-protein envelope and has double-stranded, linear DNA. In order for this virus to get into host cell it requires initial contact with glycosaminoglycan chains on host cell surface proteoglycans for entry. This family of viruses are in the Herpes-viridae family and they get there envelopes by BUDDING from the nuclear membrane. Pts with CD4
