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 (2
nd
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 3
rd
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 1
st
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 (1
st
) , Penicillin or Erythromycin (2
nd
)
, 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 <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 latumis the human tapeworm, occurs after eating larvae from raw freshwater fish.
Disease classically causes vitamin B12 deficiency and megaloblastic anemia. (Q-854)
27) Echinococcus granulosusis 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. ColiTRAVELERS 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
bodys 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 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 1
st
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 3
rd
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 1
st
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 <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 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 3
rd
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 1
st
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 3
rd
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 2
nd
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 bacteria
b) Lipo-polysaccharide (LPS)- this is an exotoxin, pilli which is for attachment to respiratory mucosa
c) 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 LOSs 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) Paramyxovirusis family of viruses that includes parainfluenza viruscauses 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 antigenis 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 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 (5
th
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 1
st
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 2
nd
most common cause is E.coli. Pts with sickle cell
disease have functional asplenia 2
nd
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 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 crampsnot 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 syndrome
b) Staphyloccal scalded syndrome
c) Gastroenteritis
NOTE: 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. (2
nd
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 lungsthese 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 epidermisis 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 saprophyticusis 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 bovisthink 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 pneumoniais 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
calledtransformation, 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 CSFgram
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 viridiansthis 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 stercoralisis 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 soliumtapeworm, 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) Toxplasmosiscongenital form is a transplacental infection (acquired in utero). Its classic finding
ishydrocephalus, intracranial calcifications and chorioretinitis. Expecting mothers should avoid cat
feces to help prevent exposure to toxoplasma. (Q- 1038)
107) Treponema Pallidumis 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 Hutchinsons 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 areRPR and VDRL. The confirmation tests are
FTA-ABS. (Q-1575, 1313, 1315, 1316, 1676)
108) Trypanosoma cruzicauses 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 CholeraGram (-), 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 inhibitorsthese 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 diarrheathe only thing visualized on stool exam ismucus and some epithelial cells. (Q-
976, 977,1396, 1842)
111) Vibrio parahemolyticustransmitted 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 patientsare 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 reasonsthese 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
organismsthis 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 showshigh 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 virusesbut
NO spores. B) hydrogen peroxideworks 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 glutaraldehydework 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 1
st
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