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 factor5. 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) B ordetella 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, cattleB) 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 tenderness2) Salpinitis and tubo-ovarian abscess3) Periotoneal inflammation including Fitz-Hugh Curtis syndrome from inflammation of hepatic capsuleTreatment 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 <100 are at increased risk for cytomegalovirus which causes retinitis in pts with AIDS. NOTE: Finding of interstitial pneumonia in a transplant patient with intranuclear and cytoplasmic inclusion bodies histologically points to opportunistic infection with CMV. CMV is an enveloped double-stranded DNA virus. (Q-278, 376, 1375, 1576, 1593, 1666, 1723)

26) Diphyllobothrim latum —is the human tapeworm, occurs after eating larvae from raw freshwater fish. Disease classically causes vitamin B12 deficiency and megaloblastic anemia. (Q-854)

27) Echinococcus granulosus —is a tapeworm from dogs, the most common cause of hydatid cysts in humans. Disease can occur after ingesting foods contaminated with dog feces. Treatment Albendazole ( Q-1574, 8541)

28) E. Coli —TRAVELERS DIARRHEA, is a Gram (-) rod that is inhibited by colistin and trimethoprim. It is the most common cause of gram (-) sepsis. E.coli have the ability to make pili by bacterial CONJUGATION. The most common source of E. coli bacteremia is the urinary tract. The common predisposing factors to urosepsis are urinaryobstruction (BPH), fecal incontinence, neurogenic bladder secondary to diabetes, and indwelling catheterization. Gram (-) sepsis or septic shock occurs b/c of the body’s systemic reaction to lipopolysaccharide endotoxin (part of the membranes of some bacteria). Signs of sepsis are- hyper or hypothermia, tachycardia, high respiratory rate, increased WBC count, hyperventilation can cause respiratory alkalosis. Severe sepsis is marked by organ dysfunction from poor blood flow. Oliguria from poor renal perfusion and altered mental status from poor cerebral perfusion are also present.

-E. coli can cause hemolytic uremic syndrome (HUS) which is characterized by micro-angiopathic hemolytic anemia, thrombocytopenia and renal insufficiency. It can occur after gastrointestinal infection caused by E.coli strain 0157:H7 (EHEC). The usually clinical picture is—hemorrhagic colitis with hemorrhagic diarrhea and severe abdominal cramping caused by E.coli’s ability to secrete a toxin just like the shiga toxin. HUS occurs more commonly in children under 10yrs of age. Most cases of HUS linked to E.coli are b/c of undercooked, contaminated ground beef. Transmitted via person to person contact. Infection can also occur after drinking contaminated raw unpasteurized milk and after swimming in or drinking sewage contaminated water. - E. coli is the most common cause of UTI in both healthy and elderly pts. E.coli is part of the normal bowel flora and special adhesive proteins let some of the strains to colonize and ascend the urinary tract. This causes pyelonephritis or bacteremia and sepsis from access to the bloodstream. The most common cause of E.coli bacteremia is a urinary tract infection. - Traveler’s diarrhea is most frequently related to ETEC that produces heat labile (LT, choleragen-like) and heat stable (ST) enterotoxins. LT activates adenylate cyclase leading to increased intracellular cAMP, and ST activates guanylate cyclase leading to increased intracellular cGMP. Both cause water and electrolyte loss and watery diarrhea. -Lactose fermentation as a source of energy is seen in E. coli using the Lac-operon. The lac-operon is an inducible and repressible genetic sequence in the E.coli genome that codes for the enzymes necessary for the fermentation of lactose in the absence of glucose. It is activated by a sensed glucose deficit and repressed when glucose is again available. NOTE: E.coli and other Gram (-) enteric rods such as.. Pseudomonas, Klebsiella, Acinetobacter are the most common causes of health care facility acquired pneumonia. From the lungs, these organisms can easily gain access to the bloodstream and cause sepsis. NOTE: “stacked brick” intestinal adhesion is seen for enteroaggregative E.coli (EAEC), these stick to human jejuna, ileal, and colon mucosa and aggregate so it looks like a stacked brick. This is seen as persistent diarrhea in infants in developing countries. NOTE: “shiga toxin” is also made by E. coli type EHEC, its similar to shiga toxin made by shiigella dysenteriae—both inactivate 60s ribosomal subunit in human cells which inhibits human cell protein production and causes cell death. (Q-963, 973, 1100, 1024, 1136, 1389, 1140, 1142, 1097, 1099)

29) Enterobius vermicularis —pinworm that infects children 5-10years of age, it migrates out of the anus at night and deposits its eggs on the surrounding perianal folds. The adult worm lives in the human intestine- specifically the cecum and appendix. The female worm migrates out through rectum and onto the skin around the anus and deposits her eggs. The larvae inside the eggs mature within 6 hours and can either get ingested by some (auto-infection) or spread to others. This pinworm causes enterobiasis. Diagnosis is via scotch tape test. It shows oval, asymmetrically flat eggs with a bean-shaped appearance. Treatment Albendazole or Mebendazole. If patient is pregenant then—Pyrantel pamoate. (Q-1142, 8538, 8873)

30) Enterococcus faecalis —causes many infections such as- endocarditis, meningitis, and urinary tract infections. It can also cause vertebral osteomyelitis after a recent urinary tract infection which has spread. (Q-646)

31) EnteroVirus— infection is the most common cause of aseptic meningitis (90%), these are single-stranded RNA viruses that includes- coxsackieviruses, echoviruses, and polioviruses. They are transmitted fecal-orally and replicate in the GI tract. (Q-1906)

32) Epstein-Barr Virus—B-cells, is part of the Herpes-viridae family and they get there envelopes by BUDDING from the nuclear membrane. There ICOSAHEDRAL core surrounded by a lipo-protein envelope and has a double-stranded linear DNA. E. barr virus induced mono-nucleosis symtoms- fever, pharyngitis, lymphadenopathy, hepato-splenomegaly, atypical lymphocytosis, and a (+) monospot test (+ hetrophil antibodies). It is transmitted from an asymptomatic virus shedder to another person via saliva. Pts that are HIV (+) usually have reactivation of latent Epstein-Barr virus, EPV replication is linked to non-Hodgkins lymphoma and oral hairy leukoplakia- which presents as single or multiple white plaques on the lateral tongue margins. Epstein-Barr virus commonly infects B-cells, stimulating them to enter the cell cycle and proliferate continuously (Transformation or Immortalization). This process is accomplished when EBV binds to the cell surface and the EBV-encoded oncogenes activate proliferative and anti-apoptotic signaling pathways within the B-cell. EBV-infected Bcells can be propagated indefinitely in vitro. In an immunocompetent host, EBV-induced B cell proliferation is held in check by a vigorous cell-mediated and humoral immune response. The ability to secrete immunoglobulins and B-cell activation products (CD23) is maintained by the immortalized B cell population, with very few cells releasing virus particles at any one time. One serologic means of diagnosing EBV infection is the monospot test- this detects a heterogeneous group of IgM antibodies that react with the hetrophil antigens present on horse red blood cells. Agglutination of these horse RBCs by human serum is a sensitive and highly specific test for EBV infection in the B-cell compartment of the human host. The means by which EBV stimulates this particular immune response remains unclear, it appears that EBV either induces a humoral response or stimulates a non-specific polyclonal activation of B-cells. EBV is a ubiquitous herpes virus that causes acute infectious mononucleosis, nasopharyngeal carcinoma, lymphoma, and Burkitt’s lymphoma. More than 90% of the normal adult population is seropositive for EBV, which is primarily transmitted through contact with oropharyngeal secretions. The EBV envelope glycoprotein gp350 binds to the cellular receptor for C3d complement (CR2 or CD21). CD21 is normally present on the surface of B-cells and nasopharyngeal epithelial cells, thus a monoclonal anti-CD21 antibody could interfere with the attachment of EBV to cells. Primary CNS lymphoma is made of B-lymphocytes and most commonly occurs in immunocpromized patients (AIDs) (Q-376, 1375, 1593, 1594, 1595, 1723, 1724, 2083)

33) Gardnerella vaginalis— VAGINOSIS, Grey vaginal discharge, this causes bacterial vaginosis, in this there is alterations in the normal vaginal flora (loss of lactobacilli and overgrowth of mixed anaerobic organisms) that make grey-discharge and a “fishy” odor that becomes more prominent with addition of potassium hydroxide (whiff test). Wet mount microscopy of the discharge shows CLUE-CELLS, which are vaginal squamous epithelial cells covered in small dark particles (G. vaginalis organism). This is treated with metronidazole. (Q-1929, 1932)

34) Giardia lamblia —transmitted from drinking contaminated water, look for history of camping, hiking in the mountains and white-water rafting. you see trophozoites and cysts in the stool of pts with intestinal protozoa infection. If examined for ova and parasites (stool smear with iodine staining) the stool will reveal ellipsoidal cysts with smooth, well defined walls and 2+ nuclei. Giardia is the most common enteric parasite in the US and Canada. When an individual drinks contaminated water from an endemic area without first boiling it, Giardia can colonize the duodenal and jejuna mucosal lining. Giardiasis causes chronic diarrhea, malabsorption and Flatulence. Treatment- Metronidazole (this drug is also used for H. pylori, amediasis, trichomoniasis). (Q-1574, 8873, 1422, 1574)

35) Group A streptococcus aka Streptococcus pyogenes-- it is a Gram (+) cocci that is coagulase (-), catalase (-), and pyrrolidonly arylamidase (PYR) (+). It forms small colonies with a wide zone of beta-

hemolysis and is sensitive to bacitracin. Strep pyogenes is transmitted via wounds and spreads fast to deep layers of the skin and fascia b/c it makes hyaluronidase and other hydrolytic enzymes. M protein is another major virulence factor that lets the bacteria avoid phagocytosis by preventing activation of the alternative complement pathway. The bacteria can also secrete many extracellular toxins such as Hemolysins O & S (cyto-toxins that cause hemolysis), and pyrogenic exotoxins (super-antigens that cause tissue injury and septic shock. - This bacteria causes Necrotizing fasciitis (flesh eating disease)—is a severe soft-tissue infection that

is characterized by tissue necrosis and high mortality. There is sudden onset of pain and swelling at the site of trauma or recent surgery, pts become hypotensive and develop septic shock. Necrotizing fasciitis is initially treated with aggressive surgical debridement of all the necrotic tissue along with empiric broad-spectrum antibiotics b/c there is so many organisms that can cause the infection.

- This bacteria causes Scarlet fever. Scarlet fever is associated with streptococcal pharyngitis which begins after 1-5 days of infection, initial symptoms are fever, malaise, abdominal pain and sore throat. The pharynx is erythematous, swollen, and sometimes covered with grey-white exudates. The tongue can have inflamed red papillae – so it looks like strawberry tongue. After 1-2 days a rash shows on the neck, armpits, and groin then spreads to rest of body. The rash begins as scarlet spots or blotches, as it spreads it begins to look like a sunburn with goose pimples (sandpaper-like rash). The cheeks look flushed so area around the mouth looks pale (circumoral pallor). Toward end of week- desquamation begins and is seen mostly in armpits, groin, and tips of fingers and toes. Scarlet fever can pre-dispose to acute rheumatic fever and glomerulonephritis. Treatment penicillin V which can prevent rheumatic fever. NOTE: scarlet fever is characterized by fever, pharyngitis, sandpaper-like rash, circumoral pallor, and a strawberry tongue. It is caused by strains of Group A streptococcus that produce pyrogenic exotoxins. Scarlet fever can predispose to acute rheumatic fever and glomerulonephritis.

- Group A streptococcus pharyngitis can cause acute rheumatic fever which can be prevented by giving early anti-biotic treatment of group A streptococcus pharyngitis , this is still a major problem in some developing nations. Acute rheumatic fever primarily affects the joints, CNS, and heart. Inflammation of the heart involves all layers from the pericardium to the endocardium (pancarditis). Over the course of 10-20years chronic inflammation can eventually progress to rheumatic heart disease, a form of acquired valvular disease. The mitral valve is most frequently affected, but the aortic valve can also be involved. Many pts with rheumatic heart disease eventually require cardiac surgery. Rheumatic fever is caused by a form of molecular mimicry in which antigens on group A streptococcus (M. protein) activates B and T cells that are auto-reactive against homologous self-antigens in the heart and central nervous system. Recurrent, untreated streptococcal pharyngitis will lead to faster onset and increased severity of rheumatic heart disease due to increased autoimmune activity. This is of particular concern in developing countries due to poor living conditions, overcrowding, and little access to health care. Acute rheumatic fever can be prevented through prompt administration of penicillin. NOTE: Streptococcus pyogenes makes pyrogenic exotoxin and streptolysin O & S. Pyrogenic toxin is the toxin that causes scarlet fever and streptococcal toxic shock syndrome. IT is only present in strains of S. pyogenes that have been lysogenized with bacteriophage. (Q- 723, 726 1101, 8565, 8857)

36) Group B Streptococcus aka Streptococcus agalactiae – is a Gram (+), coagulase (-), catalase (-) cocci that grows in CHAINS. The colonies make a narrow zone of beta-hemolysis that enhances when plated

perpendicular to Staphylococcus aureus (+ CAMP test). This causes skin and soft-tissue infections and SEPSIS and MENINGITIS in NEWBORNS (Q-8857)

37) Haemophilus influenza —this is a Gram (-) coccobacillus. This is a BLOOD-LOVING organism and requires both X-factor (exogenous hematin) and V factor (NAD+) to grow. The 5% sheep blood agar used for growth have V-factor which inactaivates enzymes for growth. Growth of H. influenza species can be done on 5% sheep blood agar by cross streaking the medium with staphylococcus aureus. Colonies of H. influenza will grow around the hemolytic S. aureus resulting in the characteristic “satellite” phenomenon. When the enzymes of beta-hemolytic S. aureus lyse the RBCs in the medium X factor (hematin) is relased, and V factor (NAD+) is activaely secreted by staphylococcus aureus into the growth medium. S. aureus thereby provides the X and V factors needed to support growth of H. influenza species in sheep blood agar. There are 6 serotypes (a-f), the capsular type b is the most invasive strain of H. influenza and can cause sepsis, meningitis, pneumonia, and other diseases. There are unencapsulated strains called non-typable H. influenza because serotyping is based on antigens in the polysaccharide capsule. Immunity to this and other infectious diseases is accomplished during the 1st months of life by IgG antibodies acquired transplacentally from the mother, but this protection is only temporary. H. influenza type b conjugate vaccines prevent disease oropharyngeal carriage of H. influenza type b. This is becoming less common because of vaccination with the Hib capsule vaccine- a protein capsule polysaccharide conjugate vaccine. Since H. influenza species is part of the normal flora of the upper respiratory tract, it is important to differenciate it from other bacteria through biochemical means. Part of the identification criteria is to demonstrate that colonies suspected of being H. influenza species require X and V factor for growth. NOTE: Epiglottitis is mainly caused by H. influenza type b and is commonly seen in children between 2-7 years of age. H. influenza is made of a linear polymer of ribose, ribitol, and phosphate all together called- polyribose-ribitol-phosphate (PRP). Antibodies to PRP cause complement-dependent phagocytosis and killing through opsonization. Due to the Hib vaccine- which is a polysaccharide protein conjugate, this is not seen often now. (Q-1103. 735, 962, 963, 964)

38) Heliobacter pylori —is the major cause of duodenal ulcers, screening is by urease test, confirmation is by culturing the organism from gastric biopsy. In the urease breath test—a pt consumes a solution that has isotopically-labeled urea. If H. pylori is present- then the urease will degrade the urea into carbon dioxide and ammonia. The isotopically-labeled carbon dioxide is absorbed into the bloodstream and exhaled in the patients breath. The breath samples are collected 30minutes after the labeled urea is ingested. This test has excellent sensitivity and specificity for both the initial diagnosis and monitoring treatment. Treatment via- antibiotic or proton pump inhibitors. (Q-1602)

39) Hepatitis A virus -- is an RNA picornavirus, it incubates for 30 days, and is transmitted via fecal-oral route and is common in areas with over-crowding and poor sanitation. Outbreaks are b/c of contaminated water or food, with raw or steamed shellfish being the cause. Onset is acute and symptoms include- malaise, fatigue, anorexia, nausea, vomiting, mild abdominal pain, and an aversion to smoking. AST and ALT spike in early illness, then bilirubin and alkaline phosphatase. This is an infection passed from fecal-oral route, it is usually silent or subclinical (anicteric) in children but can present as an acute self-limited illness seen as jaundice, malaise, fatigue, anorexia, vomiting, right upper quadrant pain, or an aversion to smoking. Clinical disease is less common in adults but if present it is more severe. Treatment is supportive with complete recovery 3-6 weeks. Close contacts given immune globulin. NOTE: Anicteric hepatitis A virus is common in children

* anti-HAV IgM antibodies—active disease and means there is re-infection*anti-HAV IgG antibodies- means pt is immune from future infections

(Q-48, 372, 373,386, )

40) Hepatitis B virus —is a member of the Hepadna-viridae family. The mature virion called DANE PARTICLE, is made of a hexagonal protein core (capsid) that is covered with a lipid bilayer envelope which is studded with proteins and carbohydrates. The HBV- is a partially double-stranded circular DNA molecule housed within a capsid. After this virion gets inside the cell, the capsid gets released into the cytoplasm and the virus genome is transferred into the nucleus. The virus DNA is then repaired to form a fully-double stranded circular mini-chromosome that can transcribe virus mRNAs. Replication of the genes occurs inside the newly made capsid which has full length virus mRNA transcripts. Reverse transcriptase (which has both RNA and DNA-dependent DNA polymerase activity) acts on the RNA template to make a single-stranded DNA intermediate that is then converted back into circular, partially double stranded DNA. The mature capsid had partially double stranded circular DNA and reverse transcriptase. HBV is transmitted from pregnant female to the fetus via VERTICLE transmission when there is active hepatitis B infection. Usually this infection gets transmitted when the fetus passes through the birth canal, but can also occur via placenta. Transmission of Hepatitis B from mother to newborn is common in those women who get acute hepatitis B infection in the 3rd trimester. In mothers that are hepatitis B virus (+) BUT HBeAg (-) the neonates risk of getting infection is 20%. In mothers who are HBeAg (+) the neonates risk is 95%. Once the infant is infected, rapid viral replication occurs and the chance for hep B to progress to chronic hepatitis is 90%. There is only mild liver injury b/c the neonates immune system is immature but later on these newborns are at high risk for chronic disease that progresses to cirrhosis and/or hepatocellular carcinoma. a) HBeAg- marker of virus replication and infectivity b) HBcAg- is not seen in serum b/c it gets sequestered within the HBsAg coatc) HBsAg- is the 1st virus marker detected in the serum after inoculation, it comes before both symptoms

start or aminotransferase increases. It can be detected during the entire time person has symptoms of acute hepatitis B infection and suggests infectivity.

d) Anti-HBc—shows in serum shortly after HBsAg shows up, and remains detectable after pt has recovered. The IgM part tells you its acute phase of the disease, the IgG part tells you pt is recovering.

e) Anti-HBc IgM—present in the window perioid, it is important tool for diagnosis when HBsAg is cleared and Anti-HBs is cannot be seen. Anti-HBc IgM is the most specific marker for diagnosis of acute hepatitis B.

f) Anti-HBe- low infectivity and tells you viral replication has stopped.g) Anti-HBsAg IgG—shows in the serum after either hepatitis B virus vaccination or when hepatitis

BsAg is cleared and it show up for life. It is an indicator of NON-infection and immunity.

NOTE: Neonates born to HBsAg(-) and HBeAg(+) mothers are at high risk of chronic infection, experience fast HBV replication, and demonstrate mild hepatic injury histologically. NOTE: The hepatitis B virus replicates via – double-stranded DNA template+ RNA progency double-stranded DNA. (Q-46, 47, 48, 372, 374, 376, 377, 378, 386, 1374)

41) Hepatitis C virus —this is a flavivirus that gets its envelope by budding through the plasma membrane of the host cell. It has 6 or more genotypes and many subgenotypes- this is seen in the genetic differences in the encoding of its 2 envelope glycoproteins. These genetic differences is what causes the hyper-variable area of the envelope glycoprotein that is prone to mutation. There is NO-proof reading 3’5’ exonuclease activity built into the virus-encoded RNA polymerase—therefore the RNA polymerase makes a lot of errors during replication, and many many subspecies of hepatitis C are seen in the blood of an infected person at one time. Diagnosis—cryoglobulins- which are cold precipitable serum proteins that have immunoglobulins. NOTE: Hepatitis C virus is genetically unstable because it does NOT have proof-reading 3’5’ exonuclease

activity in its RNA polymerase and its envelope glycoprotein has a hypervariable area prone to frequent genetic mutations. NOTE: Because of the remarkable variety in the antigenic structure of hepatitis C virus envelope proteins, the production of host antibodies lags behind the production of new mutant strains of HCV and effective immunity against infection is not conferred. (Q- 388, 386, 44, 48, 1408, 1594)

42) Hepatitis D virus —this is usually called the delta agent or the hepatitis delta virus—this is a 35mm, double-shelled particle that looks like the DANE particle of Hepatitis B virus. The internal polypeptide assembly of HDV is designated HDAg. There is a very short circular molecule of single-stranded RNA that is associated with this antigen. HDAg is considered replication-defective because it must be coated by the external coat antigen HBAg of the hepatitis B virus. Therefore, HDV infection can start either as an acute co-infection with hepatitis B virus (but hepatitis B infection occurs first) or as an super-infection of a chronic HBV carrier. Once the hepatitis D virus is coated with HBsAg the hepatitis D virus can get into hepatocytes, survive within the cell, replicate its virus RNA, and translocate its genome into protein. Pt with anti-HDV IgG antibody means they are immune from it. NOTE: The HBsAg of hepatitis B virus must coat the HDAg of hepatitis D virus before it can infect hepatocytes and multiply. (Q-47, 373)

43) Hepatitis E virus —is an UNenveloped, SINGLE-stranded RNA virus that spreads through fecal-oral route. Infection with HEV occurs in young, middle class adults living in Asia, sub-Saharan Africa and Mexico—incubation time is about 6-weeks. The virus gets shed in the stool during acute illness, the disease is self-limited and does not cause chronic liver disease. HEV Ag or HEV RNA can be found in the stool or liver in its earliest stages of infection—when pt DOES NOT have symptoms. Later the serum transaminases and IgM anti-HEV are high when there is symptoms of illness. The MOST CONCERNING FEATURE OF HEV is the high mortality rate seen in INFECTED PREGNANT WOMEN.NOTE: Hepatitis A & E transmitted via fecal-oral route (Q-48)

44) Herpes virus—which includes cytomegalovirus—get there envelope from the host nuclear membrane. They bud through the regular membrane. (Q-1408)

45) Herpes simplex virus —is associated with recurrent painful vesicular skin rash, erosions, and ulcerations of the cervix that can cause cervical discharge. Cervix cytology shows multi-nucleated giant cells with intranuclear inclusions. Diagnosed by Tzanck smear, in this material is obtained from base of vesiculoulcerative lesion- then the epithelial cells scaraped from ulcer base are prepaired with Wright-Giemsa stain and examined for multinucleated giant cells and intranuclear inclusion. (Q-1553, 1594, 1929)

46) Herpes zoster virus —arises when latent Varicella Zoster Virus (VZV) gets re-activated within a SINGLE- dorsal root sensory ganglion. Pts develop a unilateral vesicular rash localized on a single dermatome in an elderly patient. They get localized dermatomal pain that persists for more than one month after a zoster eruption is called post-herpetic neuralgia and is the most common neurological complication of VZV infection. It’s described as “stabbing”, it affects 10% of pts. Diagnosed by Tzanck smear, in this material is obtained from base of vesiculoulcerative lesion- then the epithelial cells scaraped from ulcer base are prepaired with Wright-Giemsa stain and examined for multinucleated giant cells and intranuclear inclusion. NOTE: herpes zoster virus when it infects the trigeminal ganglion of cranial nerve 5:1, it can cause visiual impairment – the condition is called herpes zoster ophthalmicus. (Q-1549, 1553, 1594)

47) Histoplasma capsulatum —is found in ohio and Mississippi, it is present in bird and bat droppings. Pts have history of cleaning bird coops or exploring caves. It causes lung disease, the yeast form is found inside the cell within macrophages. It looks like ovoid bodies within macrophages. These can survive intracellularly and cause systemic disease. In healthy pts histoplasma infections are asymptomatic or can be self-limited pulmonary disease. In immunocompromised pts they get systemic histoplasmosis that can be fatal. Disseminated histoplasmosis causes hepatosplenomegaly b/c of predilection for the mononuclear phagocyte system. Ulcerated lesions on the tongue are classic for histoplasma. CXR of pts with disseminated histoplamosis shows diffuse pulmonary infiltrates with HILAR ADENOPATHY. The radiographic changes of chronic lung disease resemble those of pulmonary tuberculosis, cavitary lesions form in the upper lung lobes, and calcified nodes and fibrotic scarring can also be seen. This is a dimorphic fungus that can cause tuberculosis like pulmonary disease and disseminated mycosis in immunocompromised patients. It is found intracellularly in tissue (within macrophages) appearing as small ovoid, budding yeast cells. (Q-105, 111, 117, 120, 266, 267, 269)

48) Human immunodeficiency virus (HIV) —is part of the lentivirus subgroup of retro-viruses. It has a BAR-shaped protein core surrounded by a glycoprotein envelope that includes the gp120 and gp41 glycoproteins. The genome is diploid, made of 2+ single stranded RNA molecules that are transcribed into double-stranded DNA by a reverse transcriptase present in the capsid. HIV is a retro-virus that is enveloped and has SS-RNA packaged with reverse transcriptase, an RNA-dependent DNA polymerase. Diagnosed via Papanicolaou (PAP) smear- you screen cervical sytology specimens for dysplasia caused by oncogenic strains of HPV. HIV attaches to their major target host cells (CD4+ T cells) primarily via the binding of viral envelope glycoprotein gp120 to the cellular CD4 transmembrane glycoprotein and the coreceptor (CCR5 or CXCR4). The HIV envelope then undergoes a conformational change that activates gp41 and initiates membrane fusion. -Radiographic findings of ring-enhancing lesions in both cerebral hemispheres is Toxoplasmosis. Treatment is Pyrimethamine & sulfadiazine - Primary CNS lymphoma is made of B-lymphocytes and most commonly occurs in immunocpromized patients (AIDs) therefore think Epsitein-Barr virus. a) Only the polyprotein protein of the env gene is glycosylated to become gp160b) The gp160 gets broken down in the endoplasmic reticulum and golgi to make—gp120 and gp41c) gp120 mediates viral absorbtion by binding to the CD4 receptor of susceptible cellsd) gp41 is a transmembrane protein- it anchors gp120 through non-covalent bonds- mediating the fusion process between virus and target cells.e) HIV polyprotein cleavage is mediated by viral proteasef) HIV DNA intergration into the host genes is by viral intergraseg) HIV synthesis from an RNA template is by reverse transcriptase (RT), once the polyprotein precursor of RT is translated from the pol gene, it is then incorporated into an immature virus and proteolytically cleaved into various viral enzymes during virus maturation. (Q-374, 376, 1373, 1375, 1594, 1672, 1723, 2082)

49) Human papilloma-virus (HPV)— this is a non-enveloped papovirus, causes anogenital squamous cell cancer and their proposed precursors – squamous intraepithelial lesions are linked to HPV. Intraepithelial neoplasias of the cervix, vulva, penis, and anus have a clear and well-developed association with HPV types 16 and 18. Immunodeficiency states e.g. AIDS increases the hosts susceptibility to HOV infection and more severe infection. HIV infection is linked to higher incidence of anogenital carcinoma. causes condyloma acuminate and cervical cancer. HIV pts with CD4 <100 are at increased risk for

cytomegalovirus, which usually causes retinitis in AIDS pts, GIT involvement can be esophageal ulcers or colitis. NOTE: HPV causes warts, cervical intraepithelial neoplasia, and carcinoma of the cervix. (Q-1408, 1498, 1929, 1723)

50) Hydrophila - is a Gram (-) rod, that is oxidase (+), and non-lactose fermenting. It causes gastro-enteritis, wound infections, and bacteremia after exposure to water that is contaminated. (Q-8857)

51) Isospora belli- causes chronic, watery, profuse diarrhea in immunocompromised patients, especially those with AIDS. (Q-278)

52) Kawasaki disease —this is a vasculitis disease of children characterized by high fever, palmoplantar erythema with periungal desquamation, oral mucosal and conjunctival inflammation and cervical lymphadenopathy. The most scariest complication of Kawasaki disease is – CORONARY ARTERY ANEURYSM, this presents with fever, strawberry tongue, rash, bilateral conjunctival injection. (Q-724, 8565)

53) Influenza A —is a orthomyxo-virus that has SS-RNA, for this virus to replicate in the host an RNA-dependent RNA polymerase within the intact virion must also get entry into the host cell. (Q-1373)

54) Klebsiella —NECROTIZING PNEUMONIA in elderly or immunocompromised pts, is a Gram (-) rod that is inhibited by colistin and trimethoprim. It causes nosocomial pneumonia, UTI, and sepsis. Since it is a normal part of the mouth flora- it causes pulmonary infections b/c of aspiration -- It is most known for causing aspiration pneumonia in hospital settings or in alcoholic pts. Pneumonia caused by Klebsiella causes hemoptysis and is classically associated with “current jelly” sputum. Klebsiella pneumonia is the most common cause of nosocomial urinary tract infections, nosocomial pneumonia, and pneumonia in alcoholics and IV drug abusers. Causes- UTI, spontaneous peritonitis and nosocomial pneumonia. (Q-973, 1137, 1024, 1146, 1666)

55) Leptospirosis— is a disease caused by the spirochete (leptospira interrogens) it occurs when exposed to infected animal urine. L. interrigans produces no characteristic cutanous manifestations. Infection is usually asymptomatic and self-limited although serious cases can progress to Weil’s syndrome (jaundice, renal dysfunction, thrombocytopenia, and bleeding). (Q-1676)

56) Leukoplakia —is caused by Tobacco use, this is a precancerous lesion that shows as white patches or plaques on the oral mucosa. This is JUST LIKE candidiasis except the plaques of leokoplakia DO NOT scrap off easily. (Q-111)

57) Listeria monocytogenes —is a facultatively intracellular, motile Gram (+) rod, it is the 3rd most common cause of meningitis in neonates after group B streptococcus and E. coli. It also causes meningitis in immunosuppressed pts and elderly. (Q-735, 1666)

58) Loa Loa African sleeping sickness, treatment diethylcarbamazine (Q-8538)59) Malassezia furfur —causes cutaneous mycosis (HYPOPIGMENTED SKIN PATCHES), KOH prep of

skin scraptings shows short hyphae and spores (Spaghetti and meatballs). (Q-103)60) Measles virus (Rubeola) and German measles (Rubella)— both these are acute viral exanthems whose

maculopapular rashes begin on the head and neck and spread downward. Generalized lymphadenopathy specifically POST-AURICULAR and occipital is because of rubella. Most adult women with rubella develop polyarthritis and polyarthralgia. Fetal infection with rubella virus during the 1st trimester can cause sensoineural deafness, cataracts, and cardiac malformations like PDA. This is associated with neurological complications such as encephalitis (acute infection), disseminated encephalomyelitis (during recovery), and subacute sclerosing panencephalitis (years later) (Q-1575, 8565)

61) Molluscum contagiosum — is more common in children, it affects skin and mucous membranes. This virus produces localized, DOME-SHAPED, flesh-colored pruritis papules with an umbilicated center that has white, curdlike material. These lesions are found in anogenital area or on the trunk. (Q-1497, 1932)

62) Moraxella catarrhalis- is part of the normal flora of the upper respiratory tract. It causes otitis media and sinusitis in healthy individuals and ususully the cause of exacerbation of chronic obstructive pulmonary disease. (Q-646)

63) Mucormycosis —caused by Mucor, Rhizopus, and Absidia. Commonly seen in pts with DM. All grow in the blood vessel walls and cause necrosis of the downstream tissue, Black necrotic eschar are seen in the nasal cavity. Mucormycosis can spread fast to the CNS causing confusion, neurological deficits and death. Histologic exam of the affected tissue is needed to diagnose. These fungi appear as BROAD NON-SEPTAE hyphae with RIGHT ANGLE BRANCHING. Tissue invasion by hyphae is seen along blood vessels, vascular thrombosis and tissue necrosis. Mucormycosis can be differentiated from Aspergillus fumigates b/c Aspergillus has septate hyphae with V-shaped branching (45 degree angles). (Q-103, 105, 106, 107)

64) Mumps —enveloped virus with RNA genome, it is a para-myxovirus that gets its envelope by budding through the plasma membrane of the host cell. The most common complication is ORCHITIS, mumps presents with fever, malaise, headaches, myalgias then parotitis within 48 hours. Mumpms causes- parotitis, orchitis, and sometimes aseptic meningitis. (Q-1374, 1408, 1498, 8565)

65) Mycobacterium avium intracellulare —causes disseminated disease in AIDS. (Q-1666)66) Mycobacterium kansasii - causes tuberculosis-like symptoms (Q-1666)67) Mycobacterium leprae —causes Hansen Disease aka leprosy a deforming infection mostly of the skin

and nerves. It is known for causing cutaneous leprosy. Its transmitted via respiratory route, direct contact, or contact with armadillo’s. Leprosy has a range of clinical features which depend on the strength of the cell-mediated immune response of the person infected. The most severe form of leprosy is called “ Lepromatous leprosy” this occurs in people with a weak cell-mediated (Th1) immune response. If there is no cell-mediated response then macrophages cannot signal to kill the mycobacterium. This causes M. leprae to multiply and disseminate. M. Leprae grows best at temperature lower than the bodies core temperature that is why it is seen in skin, superficial nerves, eye, and testes. Lepromatous clinically shows as: diffuse skin thickening, cutaneous hypopigmentation in plaques (accompanied by hair loss), leonine facies, paresis and regional anesthesia of motor and sensory nerves, and testicle destruction and blindness. The least severe form called “tuberculoid leprosy” is self-limited and infection is limited—there is mild skin plaques with hypopigmentation, hair follicle loss, and decreased sensation of the area. (Q-1313, 1666)

68) Mycobacterium scrofulaceum —is commonly found in and around environmental water sources. It causes scrofula, a disease characterized by lymphadenitis (usually cervical) that occurs in children. Causes cervical lymphadenitis in children. (Q-1676)

69) Mycobacterium Tuberculosis —(Q-1666, 1767) 70) Mycoplasma pneumonia —WALKING PNEUMONIA, this is an infection that causes hemolysis b/c of

antigenic similarity between antigens in the cell membrane of M. pneumonia and in the cell membrane of erythrocytes. When the immune system mounts a response against these M. pneumonia antigens it also destroys RBCs which leads to anemia. These antibodies that cross-react between M. pneumonia and RBCs are called “cold-agglutins” because they are able to agglutinate RBCs in vitro at low temperatures. After the infection has been eliminated and the immune system is no longer activate against M.

pneumonia- the concentration of these antibodies decreases and the anemia spontaneously resolves. M. pneumonia can also cause steven-johnson syndrome and joint paint. NOTE: Mycoplasma pneumonia—is the agent that causes walking pneumonia and tracheobronchitis. It is an organism with NO peptidoglycan cell wall, it only has a phospholipid bilayer cell membrane. It shares antigens with human erythrocytes, and when the body mounts a response against these antigens it also lyses red blood cells leading to anemia. The antibodies causing this RBC destruction are referred to as cold agglutins. (Q-957, 1767)

71) Neisseria gonorrhea —has pili which are hair-like protein polymers that project from the surface of the cell and are involved in the attachment of the organism to mucosal surfaces. Those gonococci that have pili are able to adhere to susceptible cells and thereby begin the infectious process. When the host produces antibodies against gonococcal pili, adherence to the mucosa is inhibited. In a given strain at a given time, only a single pilus gene is functional, so only one pilus type is expressed, but the pilus genes are known to undergo antigenic variation at a high frequency. Antigenic variation is a process by which the structural genes for pilus proteins undergo recombination with each other to produce new antigenic types of pili, and the array of different antigenic pilus types produced by this mechanism theoretically may be quite large. This diversity of pilus protein expression is one reason why development of an effective vaccine directed against gonococcal pilus is so challenging. a) --causes pelvic inflammatory disease (PID), infection by neisseria gonorrhea 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. Pts present with fever> 38C, rebound abdominal tenderness, purulent endocervical discharge, and cervical motion and adnexal tenderness on bimanual examination. Severe PID can cause ectopic pregnancy. 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 tenderness2) Salpinitis and tubo-ovarian abscess3) Periotoneal inflammation including Fitz-Hugh Curtis syndrome from inflammation of hepatic capsuleTreatment of gonoccal PID must also always include treatment with Chlamydia trachomatis—since Chlamydia will also 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. b) causes pharyngeal exudates, but since pharyngeal exudates are made of both gram (+) and gram (-) micro-organisms—to find out which organism it is causing infection requires different medium. N. gonorrhea can be separated by using a medium that can inhibit growth of the other bacteria found normally in the mouth. The medium used to find N. gonorrhea is called the Thayer-Martin—it is a chocolate agar that has antibiotics- --Vancomycin which blocks growth of Gram (+) bacteria--Colistin e.g. polymyxin- which blocks growth of Gram (-)--Nystatin- to block growth of yeast--Trimethoprim to block growth of Proteus species. NOTE: gonococci use their pili to mediate adherence to the mucosal epithelium. An antibody against the specific pilus protein expressed by a gonococcus would prevent mucosal adherence and initiation of infection, but each gonococcus possesses the ability to modify the pilus protein that it expresses by the process of antigenic variation and thus avoid host defense to some degree as well as make vaccination directed against pilus protein difficult.

NOTE: mucopurulent cervicitis with cervical motion tenderness is a frequent indicator of pelvic inflammatory disease caused by either N. gonorrhea or Chlamydia trachomatis—PID can lead to ectopic pregnancy and infertility b/c of salpingitis leading to scarring of the fallopian tubes if not treated appropriately. (Q-1007, 1008, 1024, 1025, 1027, 1095, 1912, 1932)

72) Neisseria meningitides — is a bean-shaped Gram (-) diplococcus, this is the 2nd most common cause of meningitis in pts <60yrs of age. It occurs in outbreaks where many individuals live in close quarters e.g. dormitories, army barracks. Meningococci are usually isolated from the oripharynx and nasopharynx of asymptomatic carriers. Colonization of N. meningitis can be for several weeks to months and occurs in 5-15% of individuals. Transmission of meningococcis is usually because of respiratory droplets or direct contact with respiratory secretions. The most likely route by which meningococci enter the blood from the pharynx is via pilus-mediated adherence to and penetration of the mucosal epithelium which then leads to enterance into circulation. N. meningitides then makes an IgA protease that facilitates survival of the organism in the mucosa by destroying antibodies that could potentiallu prevent the attachment and penetration of the bacteria. N. meningitides has many virulence factors such as:a) Polysaccharide capsule - this impairs phagocytosis of the bacteriab) Lipo -polysaccharide (LPS)- this is an exotoxin, pilli which is for attachment to respiratory mucosac) IgA protease - this cleaves secretory IgA that would otherwise inactivate the pili.

Antibodies against the polysaccharide capsule causes immunity to N. meningitides, the meningococcal vaccine has many of the N. meningitides capsular polysaccharides and stimulates the production of anti-capsular antibodies. This vaccine is not complete so its only offered to high-risk patients like militart recruits and college students.

The lipo-oligosaccharide of N. meningitides is analogous to the lipopolysaccharide (LPS) of enteric-gram (-) rods. This outer membrane LOS acts as an endotoxin and is associated with many of the toxic effects of meningococcal disease. Plasma levels of LOS are linked to disease manifestations and outcomes in meningococcal infections. High levels have been associated with increased rates of severe septic shock, acute respiratory distress syndrome, and death secondary to multi-organ failure. As with other gram (-) infections, during infection the growth and lysis of meningococci causes the relase of outer membrane vesicles (OMV) with membrane attached LOS into the bloodstream. The severity of N. meningitides is b/c of high concentrations of OMV bound LOS. LOS causes sepsis by the induction of a systemic inflammatory response characterized by the production of tumor necrosis factor alpha (TNF-a), interlukin-1b (IL-1b), IL-6, IL-8, much of which are formed secondary to LOS’s interaction with Toll-like receptor-4. NOTE: Meningococcal lipo-oligosaccharide (LOS) is responsible for many of the toxic effects observed in meningitis and meningococcemia. Blood levels of LOS correlate with morbidity and mortality. (Q-735, 1005, 1006, 1853)

73) Norwalk virus - is part of calcivirus family, causes epidemic outbreaks of viral gastroenteritis. Its called Norwalk b/c it was discovered in a public elementary school that had outbreak in Norwalk, ohio. (Q-1497, 1498)

74) Paramyxovirus —is family of viruses that includes parainfluenza virus—causes croup (Laryngo-tracheo-bronchitis) in children, respiratory syncytial virus (RSV)- causes bronchiolitis in infants, measles virus, mumps virus. (Q- 1497)

75) Parovo-virum B19— P antigen is a small NON-ENVELOPED ICOSAHEDRAL virus with a linear, single-stranded DNA genome. The blood group P antigen, globoside is a parvo-virus B19 receptor that is expressed in high concentrations on mature erythrocytes and erythroid progenitors, because of this reason parvovirus B19 is highly tropic for erythrocyte precursors specifically pronormoblasts and normoblasts, and replicates mainly in the BONE MARROW. P antigen is also found on megakaryocytes, endothelial cells, placental trophoblasts, and fetal liver and heart cells. Pts with parvo-virus infection have low grade fever, headache, malaise, and upper respiratory symptoms followed by sudden appearance of erythematous malar rash with circumoral pallor 2-5 days later—erythema infectiosum aka fifth disease. When the rash on the face disappears an erythematous rash in reticular, lacelike pattern appears on the trunk and extremities. The rash of erythema infectiosum is believed to occur b/c of local immune complex deposits once serum levels of virus-specific IgM and IgG are at high levels. In pts with sickle cell anemia or those that are immunocompromised and get infected with parovo-virus they can get aplastic anemia - It is believed that parovirus B19 attaches to human erythroid cells via the blood group P antigen. The

P antigen is expressed by mature erythrocytes, erythroid progenitors, megakaryocytes, placenta, and the fetal liver and heart. Immature cells of the erythroid family are most vulnerable to parovirus B19 infection, which is why adult bone marrow and fetal liver are principal targets. Viral replication causes cell death.

NOTE: A febril upper respiratory illness in a child followed by the sudden appearance of red, flushed cheeks approximately 2-5 days later is characteristic of erythema infectiosum (parvovirus B19 infection). This virus is highly tropic for erythroid precursor cells and replicates mainly in the bone marrow. NOTE: Parvo-virus replicates via One-stranded DNAtemplate double-stranded DNAprogeny one-stranded DNANOTE: Parvovirus B19- is responsible for aplastic crisus in pts with chronic hemolytic disorders e.g sickle cell anemia, the childhood viral exanthema of childhood termed erythema infectiosum (5th disease) and hydrops fetalis. (Q-8565, 376, 374, 1374, 1375, 1495, 1497, 1498)

76) Pasteurella multocida —is a Gram (-) rod that is part of normal flora of the mouth of cats and dogs. It can causes fast growing soft tissue infection if an animal (usually cat) bites. You can have draining cutaneous singus tracts, lympadenopathy, osteomylitis, and septic joints. It is an acute infection. (Q- 1678)

77) Plasmodium vivax & Plasmodium ovale —both cause malaria. Pts get fever, chills, sweats that occur every 48hrs after traveling to tropical areas such as South America, Africa, India, Southeast Asia. Giemsa smear shows—red blood cells with inclusions. All species of malaria have similar life cycle. A person gets bitten by Anopheles mosquito, the mosquito releases merozoites into the blood stream. Merozoites then go and infect erythrocytes which start to lyse and this causes the relapsing fevers and sweats. The unique quality to Plasmodium Vivax and Plasmodium Ovale- is that they cause a latent hepatitis infection (exo-erythrocytic cycle) in the form of hypnozoites. Treatment chloroquine for Plasmodium in the bloodstream. Primaquine is for the latent hepatic infection. There both these Chloroquine and Primaquine should be used together to get rid of infection. Side effect of Chloroquine is retinopathy(Q-1965)

78) Picronavirus family —Coxsackie, Echovirus, Poliovirus, Rhinovirus, Hepatitis A virus. Only one that can die in acid is Rhinovirus, once ph drops to below 5 (like in stomach) the rhinovirus gets inactivated. (Q-1410)

79) Poxvirus —family which includes smallpox, vaccine, cowpox, monkeypox, and the molluscum contagiosum virus. Small pox (variola) has been eradicated b/c of vaccine. Molluscum contagiosum virus is more common in children, it affects skin and mucous membranes. This virus produces flesh-colored pruritis papules with an umbilicated center that has white, curdlike material. These lesions are found in anogenital area or on the trunk. (Q-1497)

80) Proteus mirabilis —has peritrichous flagella which is found all over there surface making them motile. (Q-972)

81) Pseudomonas aeruginosa —NEUTROPENIC-immunosuppressed pt, ECTHYMA GANGRENOSUM, this is a gram (-) rod, that is non-lactose fermenting, is ubiquitous in nature and is commonly isolated from water sources. Its oxidase (+), and produces pigment during culture with pyocyanin, pyoverdin. -makes a lot of extra-cellular products such as EXOTOXIN A, COLLAGENASE, ELASTASE, FIBRINOLYSIN, PHOSPHOLIPASE C, and DNAse. These substances help it to invade and disseminate in human tissues. The exotoxin A ribosylates and inactivates elongation factor-2 (EF-2), stopping human cell protein synthesis and causing cell death. Exotoxin A is a major virulence factor and is the cause of high mortality with pseudomonas aeruginosa infections. Cornybacterium Diptheria has diphtheria toxin which works the same way, it also ribosylates and inactivates EF-2 which stops protein synthesis. - causes “hot tube folliculitis”, this is a superficial pseudomonal infection of the hair follicle. The presentation is commonly seen as outbreaks from public or hotel swimming pools or hot tubes where the chemicals in the pool water have not been maintained at the appropriate concentrations therefore P. aeruginosa grows in the pool water. Many infections begin with exposure to a water source or creation of a moist environment e.g. swimmers ear, hot tub folliculitis, burn wound. - Pseudomonas aeruginosa is a NON-lactose fermenting, oxidase (+) motile Gram (-) rod. It is the most common cause of malignant otitis externa (MOE), a serious infection of the ear seen in elderly diabetic patients. MOE presents with exquisite ear pain and drainage, and granulation tissue is usually seen within the ear canal.

(Q-973, 974, 1146, 1390, 8342)

82) Rabies —caused by bats, clinical symptoms is—restlessness, agitation, dysphagia that progresses to coma in 30-50days. (Q-1465, 8541, ) Treatment Killed vaccine

83) Respiratory syncytial virus (RSV)—is a paramyxovirus that has enveloped, SS-RNA. In order for this virus to replicate in a host cell, an RNA-dependent RNA polymerase within the intact virion must also gain entry into the host cell. (Q-1373, 1374)

84) Rhinovirus- is a naked, non-enveloped RNA molecule in the picornavirus. For any naked RNA molecule to induce virus protein synthesis in the host cell—then it must act like an mRNA capable of using the hosts intracellular machinery for translation. The RNA molecule must be single-stranded and positive sense (SS+). (Q-1373, 1408)

85) Rhizopus —is a mucormycosis, it has a high affinity for ketones and high blood glucose because of its enzyme, ketone reductase. These fungi of mucormycosis e.g. mucor, absidia and rhizopus—all grow in the blood vessel walls and cause necrosis of the downstream tissue, Black necrotic eschar are seen in the nasal cavity. Mucormycosis can spread fast to the CNS causing confusion, neurological deficits and death. Histologic exam of the affected tissue is needed to diagnose. These fungi appear as BROAD NON-SEPTAE hyphae with RIGHT ANGLE BRANCHING. Tissue invasion by hyphae is seen along blood

vessels, vascular thrombosis and tissue necrosis. Mucormycosis can be differentiated from Aspergillus fumigates b/c Aspergillus has septate hyphae with V-shaped branching (45 degree angles). (Q-103, 105, 106, 107)

86) Rickettsia rickettsiae —causes rocky mountain spotted fever. This is a tick born illness caused by contact with dogs exposed to wooded areas or grassy fields. It is characterized by cutaneous lesions are palmo-plantaer erythematous macules that migrate centri-petally toward the trunk. Treatment doxycycline (Q-1678, 1676, )

87) Rotavirus —is a reovirus that has double-stranded RNA. This virus replicates if a specific viral RNA polymerase has to be present in the intact virion for it to get into host cell. (Q-1373)

88) Rubella (German measles) & Rubeola (regular measles )— togavirus, enveloped RNA virus, both these are acute viral exanthems whose maculopapular rashes begin on the head and neck and spread downward. Generalized lymphadenopathy specifically POST-AURICULAR and occipital is because of rubella. Most adult women with rubella develop polyarthritis and polyarthralgia. Fetal infection with rubella virus during the 1st trimester can cause sensoineural deafness, cataracts, and cardiac malformations like PDA. This is associated with neurological complications such as encephalitis (acute infection), disseminated encephalomyelitis (during recovery), and subacute sclerosing panencephalitis (years later). Congenital rubella syndrome is characterized by neonatal defects of the head (microcephaly, mental retardation) eyes (cataracts), ears (deafness), and heart/cardiovascular system (PDA, peripheral pulmonic stenosis). The most classic triad of congenital rubella is—cataracts (white pupils), sensory-neural deafness, and PDA. Current recommendation is—live attenuated virus vaccine for children 12-15 months and again at 4-6 years of age, but also in NON-pregnant woman of childbearing age who do not have serum antibodies against rubella. At the time of vaccination woman are advised to avoid pregnancy for next 4 weeks. (Q-1374, 1464, 1575, 1669, 8565)

89) Salmonella —raw EGGS, chicken, improper food handling, this is the most common cause of osteomyelitis in pts with sickle cell anemia. The 2nd most common cause is E.coli. Pts with sickle cell disease have functional asplenia 2nd to multiple infarctions of the spleen which makes them more prone to infection by ENCAPSULATED organisms. Salmonella has a special capsule called “ Vi ANTIGEN” (Vi stands for virulence) which protects the bacteria from opsonization and phagocytosis. (Q-1137, 1097)

90) Salmonella typhi or Salmonella paratyphi —causes the life-threatening illness typhoid fever aka enteric fever, it is transmitted via fecal-oral route that begins after ingestion of S. typhi or paratyphi. These organisms penetrate the gut mucosa both via transporters or enterocytes and via phagocytosis by M cells in Peyer’s patches. The organisms are then phagocytosed bymacrophages, within which Salmonella (para) typhi are adapted to survive. Macrophages carry the infective organisms to the liver, spleen, and bone marrow. Hepato-spleno-megaly from organism growth ensues. From here, these species are able to cause bacteremia and sepsis. Salmonella typhi and paratyphi also colonize the gallbladder, which lets access to the gut lumen. In the gut lumen, S. typhi and paratyphi disseminate, cause inflammation within peyer’s patches, causing intestinal hemorrhage and gut perforation which can cause polymicrobial peritonitis and sepsis, the mechanisms by which typoid fever can cause death. Pts who do not get fulminant disease are at risk for becoming chronic carriers of the bacterium and can affect many people. S. typhi and paratyphi are shed from the bile into the stool. Contaminated water and the handling of food with unwashed hands then allows the bacteria to be ingested. The clinical features of the disease are- mild abdominal cramping with a low fever and diarrhea or constipation initially, then pts get salmon –colored “rose spots” on the abdomen, develop hepatosplenomegaly and recolonization of the gut, leading to hemorrhagic diarrhea and sepsis. (Q-1136, 1138)

91) Scarlet fever —is caused by Group A streptococcus which makes pyrogenic exotoxins. Scarlet fever is associated with streptococcal pharyngitis which begins after 1-5 days of infection, initial symptoms are fever, malaise, abdominal pain and sore throat. The pharynx is erythematous, swollen, and sometimes covered with grey-white exudates. The tongue can have inflamed red papillae – so it looks like strawberry tongue. After 1-2 days a rash shows on the neck, armpits, and groin then spreads to rest of body. The rash begins as scarlet spots or blotches, as it spreads it begins to look like a sunburn with goose pimples (sandpaper-like rash). The cheeks look flushed so area around the mouth looks pale (circumoral pallor). Toward end of week- desquamation begins and is seen mostly in armpits, groin, and tips of fingers and toes. Scarlet fever can pre-dispose to acute rheumatic fever and glomerulonephritis. Treatment penicillin V which can prevent rheumatic fever. NOTE: scarlet fever is characterized by fever, pharyngitis, sandpaper-like rash, circumoral pallor, and a strawberry tongue. It is caused by strains of Group A streptococcus that produce pyrogenic exotoxins. Scarlet fever can predispose to acute rheumatic fever and glomerulonephritis. (Q- 8565)

92) Schistosoma haematobium —causes schistosomiasis, humans get this when they are in contact with freshwater habitat of SNAILS, which is the intermediate host that incubates the infected larvae. When the infection is released from the snails, larvae penetrates the intact skin of humans and enters the vascular and lymphatic vessels. They travel to the liver and mature into adults in several weeks. After maturation, the adult worms migrate to specific destinations—the mesenteric venules of the intestine (S. japonicum and S. mansoni) or the vesical venous plexus (S. haematobium). The adult worms remain in these blood vessels for life (5-30years), sticking to the vessel walls with suckers and releasing eggs into circulation. The eggs released by S. japonicum and S. mansoni have a tendency to penetrate the bowel wall and be excreted in the feces. They also frequently go into portal venous system and lodge in the liver. S. haematobium eggs can pierce the vesicle and urethral walls and get out via urine. When exposed to freshwater, these eggs release larvae that infects snails and the cycle starts over again. The clinical symptoms are caused by Th2 mediated immune response directed against the eggs. This causes granulomatous inflammation and fibrosis, which causes ulcers and scarring of the bowel or bladder/urethers, depending on infectious species. Eggs that settle in the pre-sinusoidal radicals of the portal vein cause peri-portal “pipestern” fibrosis (hepatic schistosomoasis) which causes restriction of portal vein flow—portal hypertension. (Q-8541)

93) Shigella —causes diseases via direct invasion of colon mucosa cells. It is transmitted via fecal-oral route by dirty hands, fomites in daycare centers, and food contaminated by unhygienic handlers. It is highly adapted to survive in the acidity of the stomach and the bacteriostatic action of bile. Depending on age and health of host as few as 10 shigella can cause disease. Its infectivity can be b/c of its unique way to bind to intestinal mucosal M cells. These sites are usually unoccupied by the normal flora of the gut, which lets shigella easily bind and invade. The incubation time for shigellosis is 24-72 hours. Disease begins with watery diarrhea which progresses to abdominal pain, cramps, blood diarrhea, mucous, pus, fever, vomiting, and tenesmus. Tenemus is a painful spasm of the rectum that is associated with an urge to defecate but little stool comes out. There are 4 pathogenic species which can all cause a form of bacterial dysentery called shigellosis via shiga-toxin, which is associated with severe abdominal cramping and tenesmus. The shiga-toxin causes inactivation of the 60s ribosomal subunit. (Q-1101, 1136, 1137, 1422, 1094, 1099, 1842)

94) Sporotrichosis— begins as a ulcerating papule at the site of inoculation and spreads proximally along the LYMPHATICS causing more lesions as it spreads. (Q-1678)

95) Staphylococcus aureus —(IV-drug users), Gram (+) coccus that grows in clusters, it is catalase (+), coagulase (+), and PYR(-). Staphy aureus makes the virulence factor Protein A- this can bind the Fc part

of IgG and prevent opsonization and complement mediated killing of bacteria. Staph aureus makes large colonies that show beta-hemolysis. It produces 2 toxins- Entero-toxin, and TSS toxin both these are super-antigens which acts in different areas to cause different effects. Teichoic acid and lipoteichoic acid are substances that are integrated into the peptidoglycan cell wall of some gram (+) bacteria such as staphy aureus. Staphylococcus aureus is the number one cause of osteomylitis in healthy children and adults. Staphylococcus aureus is the most common pathogen to infect central venous catheters. Staphylococcus aureus causes gastroenteritis because of action of a preformed exotoxin and is associated with consumption of certain precooked foods, dairy products, custard, and mayonnaise. This disease is more commonly causes vomiting and abdominal cramps—not diarrhea. Staphylococcus aureus can cause meningitis in neuro-surgical pts because bacteria get access to the meninges by direct inoculation during the procedure or post-op through the wound. -Gram stain and culture of a skin wound that shows gram (+) cocci in clusters that DO NOT respond to nafcillin but show sensitivity to vacomycin is classic case of methicillin-resistant staphylococcus aureus (MRSA). Staphylococcus aureus is one of the most common causes of skin infections in the USA. Most of these skin infections are minor, but S. aures can also cause serious infections like in surgical wounds, bloodstreams such as centra intravenous catheters and pneumonia. -About 95% of S. aureus isolates in the USA produce Beta-Lactamase (penicillinase) which causes resistance to penicillin, however many strains although resistant to penicillin are susceptible to penicillinase-stable penicillins such as oxacillin, nafcillin, and methicillin. Strains that are oxacillin, nafcillin, and methicillin resistant are called methicillin-resistant S. aureus. These are all resistant to B-lactam agents such as- cephalosporins, and carbepenems. Naficillin (methicillin) resistance is because of alterations in the penicillin-binding protein (PBP) structure. PBPs are the enzymes involved in cell wall synthesis. Alterations in PBPs have less affinity for all beta-lactam anti-biotics. - Protein A is a cell wall component of staphylococcus aureus, it consists of a single polypeptide chain. This polypeptide chain binds to the Fc portion of IgG causing the epitope binding sites of the IgG to face away from the bacterial cell, shielding the cell from complement fixation and phagocytosis. -Toxic shock syndrome caused by staphylococcus aureus is b/c of exotoxin-induced T-cell receptor activation called super-antigens.

NOTE: Diseases caused by “exotoxin” release by S. aureus are:a) Toxic shock syndromeb) Staphyloccal scalded syndromec) GastroenteritisNOTE: S. aureus produces an extracellular enzyme B-lactamase, which inactivates the B-lactam antibiotics (penicillins) by breaking the B-lactam ring, rendering them ineffective. NOTE: Hematogenous osteomyelitis is a disease mostly of children that usually affects the long bones. Staphylococcus aureus is most common cause. (2nd most common cause- streptococcis pyogenes- group A strep). NOTE: Staphyloccus aureus is the most common cause of TRICUSPID ENDOCARDITIS in IV DRUG USERS. These pts can develop multiple septic emboli in lungs. Pulmonary infarcts are almost always hemorrhagic b/c of the dual blood supply to the lungs—these look like wedge shaped infarcts.

NOTE: Enterotoxins, Exfoliative Toxins, and Toxix Shock Syndrome (TSST-1) are the toxins with superantigen activity. Superantigens interact with major histocompatibility complex molecules on antigen presenting cells and the variable region of the T-lymphocyte receptor to cause non-specific “widespread” activation of T-cells resulting in the release of inter-leukin-2 (IL-2) from the T-cells and IL-1 and TNF from macrophages. The immune cascade, in turn, is responsible for the effects of TSS.(Girl wearing tampo too long gets toxic shock- its caused by Staphylococcus aureus b/c of Macrophaes and T-lymphocytes). NOTE: Staphylococcus aures causes food poisoning occurs after a food handler inoculates food (usually a mayonnaise containing product on Step 1 tests) with S. aureus that is allowed to incubate at room temperature, producing heat-stable EXOTOXIN that causes rapid-onset nausea, vomiting, and abdominal cramping. (Q-642, 644, 646, 676, 677, 723, 724, 725, 735, 8282, 1137, 1390, 1666, 8857, 972, 975, 1422, 1097)

96) Staphylococcus epidermis —is a coagulase (-) bacteria that is part of the normal flora of the skin, it is the major cause of infections in pts with pre-disposing factors such as indwelling catheters or implanted foreign bodies. These bacteria have the ability to colonize intravenous catheters and prosthetic devices (heart valves, vascular grafts, peritoneal dialysis catheters) because of their ability to produce a polysaccharide slime, which allows adherence to the prosthetic devices. This is resistant to most antibiotics so initial strong treatment with vacomycin is important. S. epidermis is susceptible in vitro to vancomycin and rifampin and resistant to methicillin. (Q-645, 646)

97) Staphylococcus saprophyticus—is a gram (+) coccus that causes UTI in sexually active women. It is related to seasons, usually worse in summer. (Q-1146)

98) Streptococcus agalactiae (group B Streptococcus) – is a Gram (+), coagulase (-), catalase (-) cocci that grows in CHAINS. The colonies make a narrow zone of beta-hemolysis that enhances when plated perpendicular to Staphylococcus aureus (+ CAMP test). It usually colonizes the gastrointestinal and urogenital tracts. Infants born vaginally to mothers who have this bacteria colonizing there vagina can get infected and develop serious neonatal infections, including sepsis, pneumonia, and meningitis. This is why pregnant women that test positive for group B strep are treated with antibiotics prophylactically during labor and delivery. This causes skin and soft-tissue infections and SEPSIS and MENINGITIS in NEWBORNS. (Q-646, 8857)

99) Streptococcu bovis —think colon cancer, this is part of the normal flora of the colon. Bacteremia or endocarditis caused by S. bovis is linked to colon cancer. It causes a subacute bacterial endocarditis with symptoms like those of S. viridians subacute bacterial endocarditis. (Q-1001)

100) Streptococcus pneumonia —is a Gram (+) coccus, it is the most common cause of bacterial meningitis in adults of ALL ages, and community acquired pneumonia in adults. Certain strains express capsular polysaccharides that inhibit phagocytosis, making it a successful pathogen. Strains that do not have a capsule do not cause infection. Streptococcus pneumonia can get new genetic material from the environment that is released after the death and lysis of neighboring bacterial cells. This process is called—transformation, it allows the bacteria to take-up exogenous DNA fragments, integrate the DNA into its genome, and express the encoded proteins. Bacteria that have the innate capacity to undergo transformation are said to be naturally competent. Through this method, non-virulent, non-capsule-forming strains of S. pneumonia can acquire the genes that code for the capsule and thus gain virulence. It is inhibited by vancomycin. --streptococcus is the most common cause of bacterial meningitis in adults of ALL ages. On CSF—gram stain, lacet shaped Gram (+) cocci in pairs. It follows a pulmonary infection or mild upper respiratory infection. Alcoholics, sickle cell anemia pts, asplenic pts, and those in poor health are most at risk.

NOTE: Streptococcus pneumonia is able to undergo transformation, which allows the bacterium to take up exogenous DNA fragments and express the encoded proteins. Through this method, non-capsule-forming strains of S. pneumonia can acquire the genes that code for the capsule and thus gain virulence. Conjugation and transduction are 2 additional mechanisms by which bacteria can obtain new genetic material. Streptococcus pneumonia bacteria get there ability to make capsules by the process of transformation. The capsule is the major virulence factor for S. pneumonia; strains that do not have the capsule are not pathogenic. NOTE: The pneumococcal polysaccharide vaccine is recommended for all adults over 65 years of age and for patients with COPD, asplenia, or immunosuppression. Vaccination does not completely prevent pneumonia, as this vaccine only contains antigen from 23 of the more than 80 different CAPSULAR serotypes known. The adult pneumococcal vaccine is an unconjugated polysaccharide vaccine that, unlinke the infant vaccine does not stimulate a T-helper response. (Q-646, 734, 735, 736, 973, 1024, 1389, 1767)

101) Streptococcus pyogenes (group A streptococcus)-- it is a Gram (+) cocci that is coagulase (-), catalase (-), and pyrrolidonly arylamidase (PYR) (+). It forms small colonies with a wide zone of beta-hemolysis and is sensitive to bacitracin. Streptococcus pyogens cleaves IgA by IgA protease that is a virulence factor. Strep pyogenes is transmitted via wounds and spreads fast to deep layers of the skin and fascia b/c it makes hyaluronidase and other hydrolytic enzymes. M protein is another major virulence factor that lets the bacteria avoid phagocytosis by preventing activation of the alternative complement pathway. The bacteria can also secrete many extracellular toxins such as Hemolysins O & S (cyto-toxins that cause hemolysis), and pyrogenic exotoxins (super-antigens that cause tissue injury and septic shock. S. pyogenes is inhibited by vancomycin. - Causes rheumatic fever b/c of antigenic mimicry - causes pharyngitis that if not treated causes rheumatic fever- This bacteria causes Necrotizing fasciitis (flesh eating disease)—is a severe soft-tissue infection that

is characterized by tissue necrosis and high mortality. There is sudden onset of pain and swelling at the site of trauma or recent surgery, pts become hypotensive and develop septic shock. Necrotizing fasciitis is initially treated with aggressive surgical debridement of all the necrotic tissue along with empiric broad-spectrum antibiotics b/c there is so many organisms that can cause the infection.

- This bacteria causes Scarlet fever. Scarlet fever is associated with streptococcal pharyngitis which begins after 1-5 days of infection, initial symptoms are fever, malaise, abdominal pain and sore throat. The pharynx is erythematous, swollen, and sometimes covered with grey-white exudates. The tongue can have inflamed red papillae – so it looks like strawberry tongue. After 1-2 days a rash shows on the neck, armpits, and groin then spreads to rest of body. The rash begins as scarlet spots or blotches, as it spreads it begins to look like a sunburn with goose pimples (sandpaper-like rash). The cheeks look flushed so area around the mouth looks pale (circumoral pallor). Toward end of week- desquamation begins and is seen mostly in armpits, groin, and tips of fingers and toes. Scarlet fever can pre-dispose to acute rheumatic fever and glomerulonephritis. Treatment penicillin V which can prevent rheumatic fever. NOTE: scarlet fever is characterized by fever, pharyngitis, sandpaper-like rash, circumoral pallor, and a strawberry tongue. It is caused by strains of Group A streptococcus that produce pyrogenic exotoxins. Scarlet fever can predispose to acute rheumatic fever and glomerulonephritis.

- If Group A streptococcus (GAS) pharyngitis is left untreated it causes rheumatoid fever b/c of structural homology between antigenic determinants (epitopes) on Group A streptococcus and on human heart, CNS, and cutaneous tissue. Rheumatic fever is a syndrome of fever, arthritis,

subcutaneous nodules, rash (erythema marginatum), involuntary rhythmic movements of the extremities (Sydenham chorea) and myocarditis leading to valvular insufficiency of the mitral or aortic valve. NOTE: -Streptococcus pyogenes makes pyrogenic exotoxin and streptolysin O & S. Pyrogenic toxin is the toxin that causes scarlet fever and streptococcal toxic shock syndrome. IT is only present in strains of S. pyogenes that have been lysogenized with bacteriophage. -Rheumatic fever is an autoimmune reaction that occurs following untreated streptococcus pyogenes (GAS) pharyngitis. Antigenic similarity between bacterial antigens and normal “self” antigens in the heart and CNS are believes to cause formation of anti-self antibodies causes rheumatic fever. Bacterial and human epitope homology.

- Group A streptococcus pharyngitis can cause acute rheumatic fever which can be prevented by giving early anti-biotic treatment of group A streptococcus pharyngitis , this is still a major problem in some developing nations. Acute rheumatic fever primarily affects the joints, CNS, and heart. Inflammation of the heart involves all layers from the pericardium to the endocardium (pancarditis). Over the course of 10-20years chronic inflammation can eventually progress to rheumatic heart disease, a form of acquired valvular disease. The mitral valve is most frequently affected, but the aortic valve can also be involved. Many pts with rheumatic heart disease eventually require cardiac surgery. Rheumatic fever is caused by a form of molecular mimicry in which antigens on group A streptococcus (M. protein) activates B and T cells that are auto-reactive against homologous self-antigens in the heart and central nervous system. Recurrent, untreated streptococcal pharyngitis will lead to faster onset and increased severity of rheumatic heart disease due to increased autoimmune activity. This is of particular concern in developing countries due to poor living conditions, overcrowding, and little access to health care. Acute rheumatic fever can be prevented through prompt administration of penicillin. (Q- 677, 724, 726, 973, 999, 1101, 8565, 8857, 1024, 1094)

102) Streptococcus viridians —this is the most common cause of subacute bacterial endocarditis after DENTAL WORK. (Q-1001)

103) Streptokinase is an exotoxin made by Streptococcus pyogenes (Group A Strep) ( Q-1395)104) Strongyloides stercoralis —is a roundworm that causes strongyloidiasis, the infection is transmitted

by filriform larvae found in soil contaminated with human feces. On contact, the larvae penetrate the skin and migrate hematogenously to the lungs. There they enter the alveoli and travel up the bronchial tree to the pharynx, where they are swallowed. When the larvae reach the intestine, they develop into adults that lay eggs within the intestinal mucosa. These hatch into rhabditoform (non-infectious) larvae that migrate into the intestinal lumen to be excreted in the stool. Some rhabditiform larvae can mold directly into filariform larva within the intestine and re-infect the host by penetrating the intestinal wall or perianal skin. This cycle of auto-infection can cause a massive increase in worm burden, leading to widespread dissemination of the parasites throughout the body (hyper-infection). The ensuing inflammation can be severe enough to cause multi-organ dysfunction and septic shock. Hyperinfection occurs most often in patients taking immunosuppressants or those with HTVL-1 infection. These pts have impaired Th2 directed cellular immunity. Strongyloidiasis occurs in tropical and warm temperate areas like southeast asia. Most pts are asymptomatic but present with chronic, intermittent gastrointestinal or pulmonary symptoms. Pruritic, erythematous, linear streaks (called larva currens) can occur on thighs and buttocks as larvae moves away from the perianal area. Treatment is via ivermectin. (Q-8538, 8873)

105) Taenia solium —tapeworm, larvae passed in undercooked pork. Cysticercosis is a disease caused by the larval stage of the organism following ingestion of eggs found in the excrement of T. solium tapeworm carriers. (Q-8541)

106) Toxplasmosis— congenital form is a transplacental infection (acquired in utero). Its classic finding is—hydrocephalus, intracranial calcifications and chorioretinitis. Expecting mothers should avoid cat feces to help prevent exposure to toxoplasma. (Q- 1038)

107) Treponema Pallidum —is a spirochete that causes syphilis. It is a spiral shaped, gram (-) bacteria. It is very thin and cannot be seen using standard gram stain and microscopy. Darkfield microscopy of the material scrapted from the surface of the cutaneous syphilitic lesion is used. Syphilis is a STD that has 3 phases. Initially it causes a painless ulcer (Chancre) at site of infection which is usually genitalia. Systemic illness seen in secondary syphilis causes diffuse eruption of erythematous macules over the entire body including palms and soles (Condylomata lata), tertiary syphilis causes gummas of the skin and bone, ascending aortitis, and neurosyphilis. Malformed teeth such as Hutchinson’s incisors and mulberry molars are late manifestations of congenital syphilis. Most commonly, syphilis is diagnosed and confirmed using serologic testing. The serologic tests can be divided into two groups: nontreponemal tests (VDRL, RPR) which look for presence of cardiolipin – a byproduct of treponemal infection. These are best used for screening – with sensitivity of 70-99%. The treponemal tests (FTA-ABS, MHA-TP) detect specific treponemal antigens and are used for confirmation of a positive non-treponemal test or when clinical suspicion remains high- even though non-treponemal test is negative. NOTE: the more common ways to diagnose infection with Treponema pallidum is by both screening and confirmatory serolohgic tests. The screening tests are—RPR and VDRL. The confirmation tests are—FTA-ABS. (Q-1575, 1313, 1315, 1316, 1676)

108) Trypanosoma cruzi—causes Chagas disease, is a parasite transmitted by an insect called reduviid bug- which lives in the walls of the rural huts. T. cruzi produces a neurotoxin that destroys the myenteric plexus and causes intramural. Parasympathetic denervation of smooth muscle. In the esophagus, this neurotoxin incapacitates the lower esophageal sphincter, so that food gets “stuck” in the esophagus. Proximal to this obstruction, the esophagus is markedly dilated. T. cruzi infection can cause similar changes in the sigmoid colon and ureter- which causes megacolon and megaureter. (Dysphagia- for liquids and difficulty belching in association with a dilated esophagus and absent peristalsis in the smooth muscle portion of the esophagus is diagnostic of achalasia. Achalasia is usually a primary disorder (congenital). It is always caused by dysfunction of ganglion cells of the myenteric plexus. When a patient from Central or South America presents with achalasia, however suspect infection by T. cruzi. Treatment Nifurtimox(Q-278, 8538)

109) Varicella Zoster Virus (VZV) —is a herpes virus that is enveloped and has double-stranded DNA genome, it gets re-activated within a SINGLE- dorsal root sensory ganglion. Pts develop a unilateral vesicular rash localized on a single dermatome in an elderly patient. They get localized dermatomal pain that persists for more than one month after a zoster eruption is called post-herpetic neuralgia and is the most common neurological complication of VZV infection. Its described as “stabbing”, it affects 10% of pts. (Q-1374, 1553)

110) Vibrio Cholera —Gram (-), oxidase (+), comma shaped rod that can grow in alkaline medium, it can only infect humans, this organism must be swallowed in either food or water and survive passage through the acidic pH of the stomach to colonize the small intestine in order to cause disease. V. cholera is extremely sensitive to acid so under normal gastric acid conditions an individual must ingest millions or more V. cholera to become infected from ingesting water. If V. cholera causes disease b/c of food then

you need to ingest much more colonies b/c food buffers the bacteria. Achlorhydria is a condition in which there is inadequate gastric acid production to maintain the normal gastric pH of less than 4. It can be induced by many drugs such as proton pump inhibitors—these pts are more susceptible to V. cholera infection. V. cholera causes diarrhea by cholera toxin which increases cAMP by increasing the activity of adenylate cyclase in intestinal mucosal cells by a mechanism indentical to that of the heat labile toxin produced by E. coli. Increased intracellular cAMP causes increased efflux of sodium and chloride from the intestinal epithelial cells and decreased reabsorption of these ions. This leads to massive water loss and watery diarrhea—the only thing visualized on stool exam is—mucus and some epithelial cells. (Q-976, 977,1396, 1842)

111) Vibrio parahemolyticus —transmitted by eating contaminated shellfish, OYSTERS. (Q-1097, 1422,1136, )

Q-269 Neutropenic patients are at high risk for developing opportunistic mycoses, Candida albicans, Aspergillious fumigates, Mucor, and Rhizopus species can cause severe disease in this population.

Q-644 a) Food poisoning caused by EXOTOXIN- after eating the contaminated food is caused by Enterotoxigenic E. coli (ETEC) and Vibrio cholera which causes watery diarrhea, and EHEC, and shigella- which causes inflammatory diarrhea. B) All the enterobacteriaceae have the endotoxin Lipid A- a part of their lipo-polysaccharide outer membrane. It is released in small amounts by normally dividing Gram (-) bacteria, but can be released in large amounts during widespread bacteriolysis as with the initiation of antibiotic theraphy in a patient with gram (-) sepsis. C) Bacteria that invade the gut mucosa are Salmonella species, Shigella, Yersinia enterocolitica, Entero-invasive E.coli (EIEC), and Campylobacter jejuni. These organisms cause blood and/or inflammatory diarrhea and systemic illness.

Q-1103: The most common bacterial causes of acute otitis media, sinusitis, AND bacterial conjunctivitis in childhood: 1. Streptococcus pneumonia

2. Nontypable Haemophilus influenza 3. Moraxella Catarrhalis

Q- 1137: Sickle cell patients—are at an increased risk of infection by ENCAPSULATED organisms such as Neisseria, Haemophilus, Streptococcus pneumonia, and Salmonella species b/c they have functional asplenia. Certain vaccinations are given to patients with sickle cell disease who are asplenic for other reasons—these include pneumovax for S. pneumonia, Hib for H. influenza tybe b, and Meningitis polysaccharide capsular vaccine for N. meningitides.

Q-1595 1. Vaginal secretions harbor pathogens: HIV, Neisseria gonorrhoeae, Chlamydiae trachomatis, Trichomonas vaginalis. 2. Blood harbors pathogens: hepatitis B, hepatitis C, HIV

3. Urine harbors pathogens: cytomegalovirus, adenovirus, E. coli, Staphylococcus saprophyticus, Klebsiella pneumonia 4. Arthropods (ticks) harbor pathogens: Rickettsia rickettsii, and Borrelia burgdorferi 5. Saliva harbors pathogens: Epstein Barr virus induced mono-nucleosis

Q-1408 A virus with a phospholipid-containing particle surface is a enveloped virus. Most enveloped nucleocapsid viruses get there lipid bilayer envelopes by budding through the plasma membrane of the host cell. The herpes-viruses which includes cytomegalovirus bud through and get the lipid bilayer envelope from the host cell nuclear membrane.

Q-642 1) A mutation in RNA polymerase causes resistance to rifampin (red secretions)

2) Resistance to tetracycline and sulfonamides is b/c of decrease in the levels of drug accumulation b/c of decreased uptake and/or increased efflux

3) mutations in DNA gyrase causes resistance to quinolone antibiotics

Q-1095 1. MacConkey agar is used grow many of the enteric bacteria. MacConkey is a bile salt-containing agar that restricts the growth of most Gram (+) organisms. 2. Thayer-Martin VCN medium will encourage growth of Neisseria species while prohibiting growth of other organisms. This heated blood agar, or chocolate agar, is supplemented with the anti-microbial agents Vancomycin, Colistin (polymyxin), and Nystatin (VCN), which restrict the growth of Gram (+) organisms, Gram (-) organism other than Neisseria and yeast. 3. Blood agar has bile and hypertonic saline that can be used to culture enterococci and to differentiate enterococci from the non-enterococcal Group D Streptococci. The enterococci include E. faecalis and E. faecium and are able to grow in the presence of both bile salts and 6.5% hypertonic saline. The non-enterococci include Streptococcus bovis and Streptococcus equines. Non-enterococcal Group D streptococci grow in the presence of bile but NOT in the presence of hypertonic saline. 4. Cysteine-tellurite agar used to culture Corynebacteria diphtheria, colonies are black in color. The bacterium makes intracellular polyphosphate granules, called metachromatic granules that can be detected on microscopy after methylene blue staining.

Q-1441 Chronic granumatous disease (CGD) results from a genetic defect in NADPH oxidase. Normally, NADPH oxidase participates in the killing of microbes within neutrophil phagolysosomes. Patients with CGD develop recurrent pulmonary, cutanous, lymphatic, and hepatic infections, with a tendency toward granuloma formation, usually beginning in childhood. These infections are predominantly caused by:

1) Staphyloccus aureus 2) Pseudomonas cepacia (Burkholderia cepacia)

3) Serratia marcescens 4) Nocardia species

5) Aspergillus species

Q-1912 a) Selective medium- is used for Neisseria Gonorrhoeae which separates the normal bacterial flora, the Thayer-Martin VCN medium inhibits growth of Gram (+) organisms & Gram (-) organisms besides Neisseria G.

b) Enrichment medium- has growth factors needed for certain bacteria to grow. An example is- X & V factors needed for Haemophilus or Clostridium to grow.

c) Differential media- helps to differenciate cultured organisms based on what they need metabolically and biochemically. MacConkey agar and EMB agar are used to culture some organisms—this that ferment lactose will look purple on MacConkey agar and black on EMB agar.

d) Reducing medium- is used to culture organisms that can reduce iron or sulfur as part of their metabolic pathways.

Q- 735 Any pt that presents with confusion, headache, fever, and nuchal rigidity think meningitis. In bacterial meningitis the CSF shows—high opening pressure, neutrophils, proteins and low glucose.

Q-1215 a) N-acetylmuramic acid and N-acetylglusamine are the saccharides that combine with an amino acid chain to form the peptidoglycan layer in both Gram (+) and Gram (-) cell walls

B) Teichoic acid is a molecule linked to the peptidoglycan cell wall of Gram (+) bacteria. It serves an an antigenic determinant for organism identification in the laboratory and an antigenic target for the human immune system. C) Lipo-polysaccharide (LPS) is a component of the outer cell envelope of Gram (-) bacteria.

D) Unique to fungi ergosterol is the sterol component of fungal cell membranes. This molecule is not found in human cells membranes b/c humans have cholesterol in their membranes.

E) Acid-fast stain identifies organisms that have mycolic acid present in their cell walls, including mycobacterium and some norcardia species. Acid-fast staining is carried out by applying an aniline dye (e.g. carbolfuchsin) to a smear and then decolorizing with acid alcohol to reveal whether the organisms present are “acid-fast”

Q-8593 a) Alcohols such as ethanol and isopropanol are used as disinfectants, mostly to clean the skin before

immunization or venipuncture and to disinfect external surfaces of equipment. They work by- disorganizing the lipid structure in membrances which causes them to be leaky, and by denaturing cellular proteins. Alcohols need water for max activity and are best at 60-90% concentration. They can kill bacteria, tuberculocidal, fungus, and viruses—but NO spores. B) hydrogen peroxide—works by making hydroxyl free radicals that attack cellular components. It is great for skin cleaning and wound debridement.

C) Iodine causes halogenations of proteins and DNA, its used for antisepsis in surgical and percutaneous procedures. D) Formaldehyde and glutaraldehyde—work by alkylating and cross-linking DNA and proteins. They are used for sterilizing hospiral instructments.

Q-1099 Endotoxin release is a mechanism of toxicity for all gram (-) bacteria. Once they get inside and multiply in the bloodstream they elaborate LPS which induces inflammatory response mediated by TNF-alpha and IL-1 secreted from activated macrophages.

Q-1411 A major determinant of virus tropism for the specific tissues of specific hosts is the extent to which

the viral surface proteins can bind to complementary host cell plasmalemma receptors. In the case of an enveloped virus, whether or not the virus can attach to a specific host cell generally depends on if a viral envelope glycoprotein with a high binding affinity for a host cell surface glycoprotein is present. A mutation in a viral-encoded envelope glycoprotein can therefore dramatically affect the range of host cells that the virus can attach to or infect. One example of this mutation is hemagglutinin of an influenza A strain that was previously confined to domestic livestock. If the mutation conferred a new binding affinity for a neuraminic acid-contaning glycoprotein on the surface of human nasopharyngeal epithelial cells, then the virus would no longer be a threat only to domestic livestock and humans would be vulnerable to infection.

Q- 8282: Central venous catheters (CVCs) are commonly used in critically ill patients for hemodynamic monitoring and administration of fluids and medications that cannot be given peripherally (e.g. vasopressors, TPN, chemotheraphy). Infection, phlebitis, and bacteremia are the major complications of intravascular catheters, especially CVCs. Infection involving CVCs often originates from the patients skin flora or bacteria on the hands of health care workers. Gram (+) cocci account for the overwhelming majority of these infections, with the most common pathogens being coagulase (-) staphylococcus and Staphylococcus aureus. The most important steps for the prevention of CVCs infections are: 1. Proper hand washing

2. Full barrier precautions during insertion of a central line 3. Chlorhexidine for skin disinfection

4. Avoidance of the femoral insertion site 5. Removal of catheter (s) when no longer needed

Q-8857: Necrotizing fasciitis (flesh eating disease)—is a severe soft-tissue infection that is characterized by tissue necrosis and high mortality. There are 5 bacteria types that can cause this, the 1st 3 being most common Streptococcus pyogenes, Staphylococcus aureus, Clostridium perfringens, Streptococcus agalactiae, and Aeromonas hydrophila. There is sudden onset of pain and swelling at the site of trauma or recent surgery, pts become hypotensive and develop septic shock. Necrotizing fasciitis is initially treated with aggressive surgical debridement of all the necrotic tissue along with empiric broad-spectrum antibiotics b/c there is so many organisms that can cause the infection.

Q- 736

1) Transduction- a bacteriophage (virus) transfers DNA from one bacterial cell to another. While replicating within a host bacterium, a bacteriophage may accidentally incorporate host bacterial DNA into the phage particle. Once released, it can then transfer DNA from the previous host into a newly infected bacterium. By this mechanism, bacteria can acquire genes for virulence and anti-biotic resistance.

2) Conjugation- is a form of one-way DNA transfer performed by many species of bacteria. Only bacteria with genetic material coding for conjugative ability (e.g the F plasmid) can initiate conjugation. The process

begins with donating bacterium producing a sex pilus, which then forms a direct connection with the receiving bacterium. Next, the donating bacterium synthesizes a new DNA strand, which is passed into the recipient organism where a complementary DNA strand is synthesized.

3) Transposons are mobile genetic elements that can mediate DNA transfer from plasmids or phages to a bacterial chromosome, move genetic material from one position to another along a bacterial chromosome, or transfer genes from a bacterial chromosome to a plasmid. The location of a gene in the genome is important as it determines its proximity to promoter or suppressor regions.

4) Spontaneous or induced mutations change the nucleotide sequence of a gene, potentially altering the amino acid sequence of the protein product. Through this mechanism, bacteria from novel proteins with potentially useful functions to aid in survival.

Q-8541

Q-1374

Q-1374

Q-1092

Q-726

Q-1390:

Q-646

Q-1101

Q-8593

Q-103