Microbiology UW (2014)

1) ActinomycosisGram (+) 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 fumigatusis 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 infectionscommonly 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 divergensis transmitted by tick bites and causes babesiosis, a malaria-like illness with a

predilection for pts with spleen.

6) Bacillus anthracishas a anti-phagocytic capsule that is unique because it has D-glutamate instead of

polysaccharide. It is aerobic organism that can grow on standard culture media and make non-

hemolyzing adherent colonies, on microscope it forms long chains that are described as SERPENTINE

or medusa head. The anthrax exotoxin is a trimeric toxin that is made of protective antigen, edema

factor, and lethal factor. The protective antigen functions to translocate both edema factor and lethal

factor into the cytosol. Neither toxin can work without protective antigen. Once inside the cell- the edema

factor acts as a calmodulin-dependent adenylate cyclase that increases cAMP concentration. It causes

accumulation of fluid within and between cells and also cause suppression of neutrophils and

macrophage function. The spores of B. anthraci are very small and once they are inhaled they go into the

alveoli and get eaten by macrophages. From the lungs the organisms move fast to mediastinal lymph

nodes and cause hemorrhagic mediastinitis. Once the spores germinate into vegetative cells they will

begin to make 3-part anthrax toxin and pts get the clinical symptoms. It is commonly caused by exposure

through contact with infected animals or animal products or through use of B. anthracis as a biological

weapon. This is why occupational history of exposure to animals or animal products is important.

Cutaneous anthrax in pt that no risk of occupational exposure then think bioterrorism, There is growth of

vegetative organisms at the site of inoculation which causes painless, necrotic wound that is covered with

black echar. B. anthracis spreads via LYMPHATICS to the bloodstream, and the organism multiplies in

the blood and tissue. Cutaneous anthrax is the most common form of this disease, it occurs on exposed

surfaces of the arms or hands.

NOTE:

1. Pulmonary anthrax also known as woolsorters disease, is caused by inhalation of spores most

commonly while working with goat hair or hides. Hemorrhagic mediastinitis evident as widened

mediastinum on chest x-ray is an important clue.

2. On microscopy it forms long chains that are described as being serpentine or medusa head

3. Bacillus anthracis produces an anti-phagocytic capsule that is required for pathogenicity. The capsule

is unique in that it contains poly-y-D-glutamate instead of polysaccharide.

4. The anthrax exo-toxin is a trimeric toxin made of protective antigen, edema factor, and lethal factor

5. This makes endospores that are resistant to heat, acid, and antibiotics.

6. Bacillus can survive past the boiling point of water, 100C.

(Q-971, 972, 1101, 1389, 1678, 1779)

7) Bacillus cereusre-fried rice, survives on steamed rice where it produces a heat-stable enterotoxin.

(Q-1097, 1422)

8) Bartonella Henselaeis 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 kaposis 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

fungusmeaning 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 othersthey get flu-like illness such as

fever, chills, myalgia, headache, non-productive cough or pneumonia. In immunocompromised pts it

causes disseminated diseasepts get fever, weight loss, night sweats, lung issues- cough, dyspnea, skin

lesions- ulcers, pustules, papules, and bone pain- caused by lytic lesions. Pulmonary blastomycoses is

diagnosed by KOH prep of sputum. Blastomyces causes both lung disease and disseminated mycosis, Its

microscopic appearance in tissue is round yeast with broad-based budding and a thick, doubly

reflective wall. (Q-103, 105, 117, 120)

10) Bordetella Pertussis(whooping cough) pertussis toxin aka AB toxin stimulates intracellular G-

proteins to increase cAMP production causing increased insulin production, lymphocyte and neutrophil

dysfunction, and increased sensitivity to histamine. It makes pertussis toxin and exotoxin called adenylate

cyclase toxin, like edema factor of B. anthracis the adenylate cyclase toxin also functions as a

calmodulin-dependent adenylate cyclase that causes phagocyte dysfunction and edema. The immune-

suppression caused by pertussis toxin and adenylate cyclase toxin are needed so that this bacteria can

colonize the respiratory tract. Bordet-Gengou medium is used to culture the very sensitive Bordetella

pertussis, the causative agent in whooping cough.

(Q-1101, 1390, 1094, 1095)

11) Borrelia BurgdorferiIXODES 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 melitensisis 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) Campylobacteris an enteric pathogen, gram (-) curved rod with a filament that lets it move in a

corkscrew fashion. It is the most common cause of acute gastroenteritis in children and adults in

industrialized countries. Transmission is via fecal-oral route. Campylobacter jejuni can cause Guillain-

Barre syndrome- a demyelinating syndrome of the peripheral nerves which is characterized by ascending

muscle weakness and paralysis. The organisms can be acquired by:

A) Domestic animals e.g dogs, chickens, cattle

B) Contaminated food e.g. undercooked chicken and unpasteurized milk

Campylobacter species causes inflammatory diarrhea (initially watery then bloody), accompanied by

abdominal cramps, tenesmus and leukocytes in stool. The abdominal pain can mimic appendicitis.

*campylobacter is the most common infectious agent associated with Guillain-Barre syndrome*

Treatment Erythromycin (b/c its becoming resistant to Fluoroquinolones) (Q-1422, 1601)

14) Campylobacter fetusis a Gram (-) rod that causes mild enteritis in immune-competent pts and mild

systemic bacteremic illness in immunocompromised pts. (Q-1313)

15) Candidafungus, 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 vaginitisassociated

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 candidiasiscauses diaper rash, occurs in areas that are exposed to heat and high humidity

like groin or perianal areas of infants.

c) Vulvovaginal candidiasisassociated with antibiotic and contraceptive use, pregnancy, DM, and HIV.

d) Candida endophthalmitisdiagnosed using ophthalmoscopy

(Q- 103, 105, 107, 111, 1929, 266, 267, 269, 118)

16) Chlamydia trachomatisthis is a flagella protozoa that causes vaginitis, it is associated with

YELLOW-GREEN FOAMY FOAL smelling discharge. On wet mount you see motile trophozoites with

flagella. Chlamydia trachomatis is the pathogen that causes lymphogranuloma venereum (LGV), a

disease characterized by an ulcer or vesicular lesion on the external genitalia followed by significant

regional lymphadenopathy. Proctitis with tenesmus and bloody discharge can be seen in this disease.

LGV is a STD.

a) Is one of the main causes of pelvic inflammatory disease (2nd most common being neisseria

gonorrhea). Infection by either of these causing PID can be asymptomatic but if there are symptoms

they will initially cause purulent urethritis followed by ascension to the cervix where infection can

further spread and cause purulent infection and inflammation in the endometrium, fallopian tubues,

and peritoneal cavity. Conditions associated with this ascension of infection into the female genital

tract and peritoneum include:

1) PID which shows as purulent cervical discharge and cervical motion tenderness

2) Salpinitis and tubo-ovarian abscess

3) Periotoneal inflammation including Fitz-Hugh Curtis syndrome from inflammation of hepatic capsule

Treatment of gonoccal PID must also always include treatment for both Chlamydia trachomatis and

neisseria gonorrheasince 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 florabut 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 PerfringensLECITHINASE, 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 gaswhich

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 tetaniGLYCINE, 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 immitisthick 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 diphtheriaAB-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 granulesthese 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 bacteriums 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 Lofflers 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 its 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 virusis 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 neoformansthe 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 factorit 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 fungusmost common presentation is subacute or

chronic meningo-encephalitis.

NOTE: causes meningitis in AIDS pts, India ink stain of CSF showsencapsulated yeast. (Q-103, 105,

107, 120, 266, 267, 269, 118, 117)

25) CytomegalovirusICOSAHEDRAL 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

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 ishemorrhagic colitis with

hemorrhagic diarrhea and severe abdominal cramping caused by E.colis 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.

- Travelers 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

dysenteriaeboth 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 vermicularispinworm 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 thenPyrantel pamoate. (Q-1142, 8538, 8873)

30) Enterococcus faecaliscauses 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) EnteroVirusinfection 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 VirusB-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

Burkitts 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 vaginalisVAGINOSIS, 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 lambliatransmitted 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 pyloriis the major cause of duodenal ulcers, screening is by urease test, confirmation is

by culturing the organism from gastric biopsy. In the urease breath testa 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 antibodiesactive 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 virusis 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 coat

c) 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-HBcshows 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 IgMpresent 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 IgGshows 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 virusthis 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 35 exonuclease activity built into the virus-encoded RNA polymerasetherefore 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. Diagnosiscryoglobulins- which are cold precipitable serum proteins

that have immunoglobulins. NOTE:

Hepatitis C virus is genetically unstable because it does NOT have proof-reading 35 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 virusthis is usually called the delta agent or the hepatitis delta virusthis 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 virusis 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

Mexicoincubation 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 infectionwhen 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 viruswhich includes cytomegalovirusget there envelope from the host nuclear membrane.

They bud through the regular membrane. (Q-1408)

45) Herpes simplex virusis 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 virusarises 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. Its 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 capsulatumis 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 gp160

b) The gp160 gets broken down in the endoplasmic reticulum and golgi to makegp120 and gp41

c) gp120 mediates viral absorbtion by binding to the CD4 receptor of susceptible cells

d) 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 protease

f) HIV DNA intergration into the host genes is by viral intergrase

g) 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

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 diseasethis 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 Ais 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) KlebsiellaNECROTIZING 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) Leptospirosisis 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 Weils syndrome (jaundice,

renal dysfunction, thrombocytopenia, and bleeding). (Q-1676)

56) Leukoplakiais 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 monocytogenesis 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 furfurcauses 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) Mucormycosiscaused 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) Mumpsenveloped 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 intracellularecauses disseminated disease in AIDS. (Q-1666)

66) Mycobacterium kansasii- causes tuberculosis-like symptoms (Q-1666)

67) Mycobacterium lepraecauses 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 armadillos. 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 scrofulaceumis 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 pneumoniaWALKING 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 pneumoniais 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 gonorrheahas 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 tenderness

2) Salpinitis and tubo-ovarian abscess

3) Periotoneal inflammation including Fitz-Hugh Curtis syndrome from inflammation of hepatic capsule

Treatment of gonoccal PID must also always include treatment with Chlamydia trachomatissince

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-organismsto 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-Martinit 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 trachomatisPID 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

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 latererythema 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 DNA

NOTE: 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 multocidais 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 ovaleboth 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 showsred 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 familyCoxsackie, 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) Poxvirusfamily 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 mirabilishas peritrichous flagella which is found all over there surface making them motile.

(Q-972)

81) Pseudomonas aeruginosaNEUTROPENIC-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) Rabiescaused by bats, clinical symptoms isrestlessness, 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 cellthen 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) Rhizopusis 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 rhizopusall 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 rickettsiaecauses 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) Rotavirusis 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 iscataracts (white pupils), sensory-

neural deafness, and PDA. Current recommendation islive 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) Salmonellaraw 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 paratyphicauses 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 Peyers 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

peyers 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 feveris 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 haematobiumcauses 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 destinationsthe 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 flowportal hypertension. (Q-8541)

93) Shigellacauses 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) Sporotrichosisbegins 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 c