264 terms

Infectious Diseases


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How can environmental organisms cause disease in humans?
Opportunists. They infect debilitated hosts, or the host is exposed to an unusual environment.
Molecular detection of organisms
no longer need a live organism in order to determine species. growth on culture not necessary.
How does a commensal change into a disease-causing pathogen
Motive- intrinsic virulence of the organism - does it have the right stuff to cause disease?
Opportunity - host susceptibly - genetic predispositions or disruption of normal barriers. these barriers are often disrupted in hospital settings.
staph aureus
Primary ecological niche: anterior narex
- 20% of people are persistent carriers. 30% are intermittent carriers.
can colonize the skin and GI as well.
Gram positive cocci in grape like clusters. Virulence factors: Protein A - binds Fc-IgG prevent complement fixation and phagocytosis. also, has catalase. bad strands of staph have coagulase. they can form fibrin clots around themselves, and this may form abscesses.

potential to cause inflammatory disease, toxin mediate disease - toxic shock syndrome, scaled skin synrome, rapid onset food poisoning.

TSST is a superantigens that binds to MHC II and T cell receptor --> polyclonal T cell acivation. leads to fever, vomiting, desquamation, shock, end-organ failure. TSST is an exotoxin.

when multiplying, produces different toxins than when quiescent.
community acquire methicillin resistance staph aureus. this is the predominant strain of MRSA. a lot of different virulence factors. destructive skin pathogen.
pathogenesis of staph skin infections
organisms enter through breaks in the skin - generally entering around roots of hair follicles. stimulate a vigorous host immune/inflammatory response including neutrophils and macrophages. there is an accumulation of neutrophils, but these are not effective at fighting staph. therefore, get inflammation and may form boils.
usually commensals, rarely pathogens.
distribution of bacteria in the body
depends on location. also, if have a disease, the distribution will differ. somebody with gastric ulcers has H pylori and has a completely different composition in their stomach in comparison to people without it.
relationships between bacteria and humans
Symbiosis - hanging out together.

commensalism = neutral. usually this term is used because we do not fully understand the relationship yet.

mutualism = reciprocal benefits

parasitism = benefit only to the parasite.
clostridium difficile
disruption of the microbiome and disease. causing diarrhea. can re-establish normal fecal flora by giving people a stool transplant. anti-toxin therapy is an option, but often is not a permanent solution.

C difficile is often secondary to antibiotic use, especially ampicillin. this disrupts the normal flora in the gut.
gram positive
only have one cell bilayer. thicker peptidoglycan wall - response for support. also has lipoteichoic acid.
gram negative
two bilayers and a peptidoglycan wall between them. has endotoxin lipopolysaccharide - LPS - as its major surface antigen. CV stain washes off with bilayer (when using alcohol), and cell stains with safranin red to become pink in appearance
steps in gram stain
step 1: crystal violet. both stain purple at this point.
step 2: gram iodine. remain stained
step 3: decolorizer = acetone/alcohol. gam negatives lose stain, and gram positives remain stained with CV.
step 4: safranin red - stains both gram + and gram - but pink only seen in gram - because gram + remains CV.
shape of bacteria
coccus - spherical. bacillus - rod. coccobacillus = somewhere in between. fusiform bacillus. vibrio. spirochete.
classifying bacteria by genetics
identify organisms by DNA homology. most commonly based on variations in conserved regions of DNA - 16S rDNA - comparing sequences to large databases. 16S rDNA is highly conserved in same species. identification gives family tree even if pathogen is unknown.

does not require viable organisms.
Lifestyle of bacteria
Aerobic and anaerobic. the majority our facultative - can handle oxygen, but do not need it.
true anaerobes = grow poorly in ambient oxygen concentrations.

anaerobic - 90% of normal colonic flora, important in oral flora, vaginal flora, some skin sites
intracellular pathogens
many invasive bacteria grow freely on surfaces and in the environment, but also survive in human cells.

staph aureus - can live in neutrophils
salmonella typhi - macrophages
listeria, legionella
obligate intracellular pathogens
chlamydia, chlamydophila, ehrilicha, rickettsia

must detect by non-culture methods. these are more difficult to detect because they do not grow on a dish.
classification of bacteria by habitat
outside of humans:
zoonoses - animals/fish
surfaces in the healthcare environment - nosocomial
primary habitats of bacteria in humans
may have multiple habitats - e. coli. habitat as commensal may differ from habitat as a pathogens. different strains from same species may have different genetic traits/virulence factors allowing them to thrive in different habitats.
E. coli
gram negative rods that ferment lactose. fimbriae - cystitis, pyelonephritis. k capsule - pneumonia, neonatal meningitis. lps endotoxin - septic shock.

often a urinary and intestinal pathogens. can attach to uroepithelial cells. leads to colonization of bladder, and from here these cells can move. some hosts are predisposed to these infections. these hosts may have better surfaces for adhesion or may be more accessible.
interpreting the gram stain
is the stain properly colored? there needs to be enough dye, and do not want to decolorize with alcohol too long. organisms are either positive, negative, or variable. reference: WBCs should be pink with purple nuclei. if these are seen, it is an indication of proper staining.
gram positive cocci
grape clusters = staphlococci, pairs or short chians = streptococci. pairs, but more elongated, lancid shaped, with halo around the bacteria (areas with no dye) = pneumococci.

bubble test
catalase positive = staph.
catalase negative = strep.

clumping test:
coagulase positive = staph aureus.
coagulase negative = staph epidermidis
gram positive rods
holes seen indicate spores: these have ones in the center = clostridium. filamentos forms = anaerobes and lactobacillus grow like this.
smaller = listeria.
bacillus anthracis = bacillus morphology, appearance of boxcars and are elongated
catalase negative gram positive cocci
hemolysis on blood agar plates.
viridians = streptococci. multiple species. commensals or pathogens found in mouth, GI tract. bacteria endocarditis. other.

strep pneumonia - lancet shaped, diplococci. sterile sites: CSF, blood, other. respiratory specimens: must distinguish from viridans strep. both of these are alpha hemolytics.
hemolysis on blood agar plates
alpha: incomplete hemolysis. ring of green present. beta = complete hemolysis. get cloud or clearing around it. complete clearing --> yellowish color. gamma = no hemolysis/no clearing.
beta hemolytic streptococci
complete clearance on blood agar. identification by latex agglutination tests, hemolysis patterns.

Group A (s. pyogenes) - strep throar, cellulitis, severe skin and soft tissue infections. sepsis, toxic shock

group b - s. agalactiae - neonatal sepsis. gu infections.

group c/g - skin and soft tissue infection, bacteremia

D - s. gallolyticus - bacteremia/colon cancer
non-hemolytic/gamma streptococci
Enterococcus. normal GI, skin, GU flora. lower virulence than S. aureus or beta strep. biliary and intestinal, urinary infections, bacteremia. relatively antibiotic resistant.

E. faecalis = most common species, less antibiotic resistant. 70%
E. faecium - 20% - common nosocomial pathogen.
gram positive rods
aerobes vs. anaerobes.
distringuishing potential pathogens from commensals/colonizers.
gram positive rod aerobes
cornebacterium (diptheroids), bacillus species (anthrax), listeria, lactobacilli
gram positive rod anaerobes
gram negative cocci
neisseria species. meningitidis (meningitis), gonnorhea (genital tract infections, septic arthritis, dissemination infection).
normal flora

fastidious organisms that require enriched media - e.g. chocolate agar - for growth. when collected from nonsterile specimens (genital specimens), need inhibitors to suppress other organism growth
in CSF: see as diplococci. ingenital specimen, see them intracellularly (gonorrhea)
aerobic gram negative rods
enterobacteraciae - E. coli, klebsiella, enterobacter, other. enteric pathogens: salmonella, shigella. proteus and related (can lead to UTIs), pseudomonas. fastidious organisms = haemophilus and related species (causing respiratory infections).

laboratory work up: growth on Maconkey agar = crystal violet plus lactose plus pH indicator. crystal violet is responsible for inhibiting growth of gram positive bacteria. the outer membrane of gram negative is protective.
pinkish/red indicate lactose fermentation

can compare lactose vs. non lactose fermenters.
placed in specific jar container (a vacuum) that prevents oxygen from getting in. also special media. grown in a CO2 rich or nitrogen rich environment.
wright-giemsa - general morphology. gram. acid fast- mycobacteria. probes - antibodies.
shape/appearance/size - bacilli/rods - beaded, filamentous, branched. cocci - single, diplo, clusters, chains. spirochetes.
localization - intra/extra cellular, infected cell type
culture features
plate medium preference. BAP, choc = fastidious (picky). Maconey stain = Gram negatives, lactose fermenters. Maconey stain has CV as well as lactose; the CV will eliminate the gram positives and prevent them form growing in the sample.
hemolysis - alpha (moderate), beta (complete), gamma (none)
liquid culture - streaming, turbidity, scummy...
carbohydrate utilization - sugar preference. fermenter/non-fermenter.
amino acid metabolism
substrate utilization
susceptibility profiles
molecular methods
based on detection/analysis of genetic material. can use PCR, RFLP, fingerprinting, microarray.

sensitivity = can ID organisms that are difficult to detect by direct observation. too small and/or rare; hard to stain/differentiate; infected tissue difficult to sample.

speed/cost - can deliver rapid diagnosis for slow-growing organisms that would take weeks to culture. can test for different organisms in same small samples.

specificity = discriminate between related/similar organisms. detect genetic features such as drug resistance. therapeutic and epidemiological purposes.
polymerase chain reaction. can detect a single gene target, a single organism in the sample being analyzed. rapid method. results can be obtained within 1-3 hours. useful in virology. can use agarose gel or rt-PCR for quantitative analysis. real time uses fluorescently labeled sequence specific probe. amount of fluorcesence accumulated during the reaction is directly proportional to initial concentration.

problems: contamination - false positives.
presence of inhibitors that inhibit the polymerases.
genetic variants = false negatives. bacteria evolve rapidly, so the primers added may not anneal to these mutants.
TB nucleic acid amplification test
NAAT. combine highly specific PCR-mediated amplification of mycoplasmic TB rRNA sequences with much higher sensitvity assays. transcription mediated amplification of targets, and fluorescence based detection of products. this is preferable to use because MTB grows very slowly in culture. also small numbers needed for infection.
transcription step is added to amplification process. the primer contains a promoter sequence, and RNA can be amplified rapidly; transcription generates multiple copies of product. increasing the number of RNA templates, and using RT to convert back to DNA.
HPA uses fluorescent oligonucleotide probes carrying a fluorochrome that is protected from hydrolysis only after hybridization to target.
tb diagnosis
culture remains gold standard for TB diagnosis
gonoccus(gonorrhea) and chlamydia trachomatis NAATs
infections are often asymptomatic. two most prevalent causes of bacterial STDs. need for high specificity, non-invasive, possibly low-cost tests for Dx/screen suitable for large scale screening. broad patient population screenings recommended, depending on risk factors and populations.

suitable samples: urethral, vaginal, cervical, rectal, and/or pharyngeal swabs, urine.

Ng/Ct NAATs can be carried out in parallel on urine or urethral/vaginal/cervical swabs
use probes immobilized on slide/chips or bead support structures. detect products labeled with different fluorescent markers. allows for BROAD scale comparisons of many target products in parallel samples. quantitative, rapid, automated, accurate profiling.
exploits genetic variation between related species/strains/isolates to ID or type microorganisms.
can use PCR, genetic material from isolates or cultured samples. hybridizations, RFLPs, microarrays, sequence analysis are used to detect variants.
can detect differences in karyotypes as well or to analyze chromosomes = pulsed field gel electrophoresis. useful for epidemiological purposes such as tracking nosocomial infections.
serological methods
diagnosis based on detection of pathogen antigens, or of the patient's own antibodie response to pathogens.
antigens and antibodies can be easier to detect than direct observation or culture.
methods are very sensitive and specific, often quantitative, technically easy. antigens and antibodies are produced in large quantities and can be found in body fluids.

antibody detection: immunodiffusion, agglutination, RAST, ELISA, western blot.

antigen detection - agglutination, RIA, ELISA, western blot
syphillis screening
T. pallidum infection elicits strong antibody response a few weeks after infection, often before primary syphilis symptoms appear. IgM is first responder, followed by IgG (by 4 weeks), IgG persists after therapy and in latent disease.

non-treponemal tests: VDRL, rapid plasma reagent. inexpensive, rapid, easy to read. false positive risk. quantitative, can be used to assess response (titers often decline). assess response to treatment in particular. tests assay for antibodies that react with organism phospholipids, but cross react with common self antigens = the issue.

treponemal test - detect organism-specific antigens by various techniques. titers persist.
HIV screening
Western blot followed by gel electrophoresis. look for various band that may indicate whether or not somebody is HIV positive, negative, or indeterminate.
Serology HBV
test to see whether or not resistance is present for hepatitis B - from having the disease previously, or from the vaccination. anti-HBs is needed for immunity. anti Hbs is found in people chronically infected, but it is not detectable in serum.
opportunistic fungal pathogens. high morbidity infections require early diagnosis. criptococcal antigen = CrAg = fungal capsule = abundantly shed in EC spaces = can be detected before initial symptoms present.
these fungal pathogens cause pulmonary and CNS infections. often associated with HIV, high morbidity and mortality.
detection of antibody responses to vaccines - MMR titers/Holly's law
NJ = first sstate to allow opt-out from mandatory 2nd MMR vaccination for schoolchildren with sufficiently higher titers after first vaccine. titer measurements: ELISA, functional. positive titer = fulfills vaccination requirements for school admission in lieu of records of a second immunization
immune deficiencies
primary/congenital: >100 types, but relatively rare. mostly genetic, not always defined.

secondary/acquired - more common than PIDs (primary immunodeficiency disorders), several mechanisms: HIV/AIDs, drug induced, cancer, diabetes, etc.

mechanisms: recurrent infections, rare opportunistic pathogens, association with autoimmune/hypersensitivity like reactions or neoplasia
time above the minimum inhibitory concentration
post-antibiotic effect
rubella virus brief
rubella. rash begins on head and moves down. fine truncal rash. postauricular lymphadenopathy.
measles virus brief
measles. a paramyxovirus, beginning at head and moving down, rash preceded by cough, coryza (cold symptoms), conjunctivitis, and blue-white (KOPLICK) spots on buccal mucosa
VZV brief
chickenpox. vesicular rash begins on trunk: spreads to face and extremities with lesions at different stages.
hhv-6 brief
roseola - a macular rash over body appears after several days of high fever. can present with febrile seizures. usually affects infants
parvovirus brief
erythema infeciousum. slapped check rash on face - can cause hydrops fetalis in pregnant woen.
streptococcus pyogenes brief
scarlet fever. erythemaotus sandpiper like rash with fever and sore throart.
coxsackie virus type a brief
hand foot and mouth disease. vesicular rash on plams and soles. ulcers in oral mucosa.
flat, circumscribed, nonpalpable lesion.

macular erythematous rash.
raised, circumscribedm palpable lesion. <0.5-1cm. small, solid, elevated skin lesion less than 0.5 cm in daimeter. the top of a papule can be flat, pointed, or rounded.
deep-seated, roundish lesion <1.5 cm in diamter that can involve dermis or subcutaneous tissue.
small cluster of cells arising from skin and forms a swelling.
punctate purpuric lesions <1 mm in diameter.
nonblanching - does not change color when touch glass to it.
macular or papular nonblanching lesion formed by extravasation of RBCs.
larger purpuric lesions usually several cm in diameter.
skin blisters <0.5-1cm in diameter.
small fluid-filled bubble that is usually superficial.
(pl. bullae) vesicle >0.5--1 cm in diameter that contains serous fluid.
hemorrhagic bullae.
pus-filled vesicle. a small (<1 cm in diamater), circumscribed superficial elevation of the skin that is filled with purulent material.
also described as a vesicle filled with pus.
shedding of a layer of skin
pay attention to size, color, morphology, pattern, distribution, arrangement on the body. progression of rash. presentation related to fever.
general history:
age of patient, season, travel history, geographic location, exposures, immunizations and history of childhood illnesses, immune status, sex contacts.
physical examination
vital signs and patient's overall general appearance --> toxic, lethargic, altered mental status? mucus membrane involvement? physical findings consistent with multi-organ involvement.
any eruptive disease or fever. an eruption characterizing an eruptive fever.
mucous membrane eruption, especially one occurring in connection with one of the exanthemas.
viral exanthems
most common cause of fever and rash.
mobilliform (measles-like) - most common.
generalized discrete red to pink macules, some lesions slightly raised, giving it a texture.
preceded by fever and prodromal symptoms. malaise rhinorrhea, cough or abdominal complaints. these symptoms, along with history, may help differentiate viral from other causes. some viral infections associated with fever are important to diagnose
highly contangious. single stranded RNA paramyxovirus, genus morbillivirus. hemaglutinin - important surface protein. respiratory transmission. replication in nasopharynx and regional lymph node. primary viremia (2-3 days) followed by secondary viremia (5-7 days) after exposure with spread to tissues. occurs in unimmunized/travelers. vaccine preventable.
measles symptoms
cough, coryza, conjunctivtis (three C's). fever, light sensitivity, myalgia, sore throat. APPEAR MISERABLE.

rash: usually 3-5 day after first signs of being sick. may last 4-7 days. usually starts on the head and spreads to other areas, moving down the body. rash may appear as fat, discolored areas (macules), and solid, red, raised areas (papules) that join together (become confluent).

enanthem: KOPLICK spots = tiny red or white spots with red halo on buccal mucosa.
The symptoms of such infections are generalized inflammation and sepsis. If such colonizations occur in critical body organs, such as the lungs, the urinary tract, and kidneys, the results can be fatal. Because it thrives on most surfaces, this bacterium is also found on and in medical equipment, including catheters, causing cross-infections in hospitals and clinics. FOUND ON SKIN FLORA.
gram negative aerobic.
Vaccine preventable.
Mild disease in adults.

Togavirus - genus Rubivirus. Enveloped RNA virus.
Respiratory transmission, replication occurs in the nasopharynx and regional lymph nodes. Viremia 5-7 days later. Spreads to the tissues. possibility that the placenta and fetus infected during viremia.
Normally, incubation: 14 days.
Prodrome - low-grade fever.
Rash: diffuse macules and papules, 14-17 days after exposure. Last ~3 days.
Behind the ear swollen lymph node = postauricular lymphadenopathy. also suboccupital.
polyarthralgia/polyarthritis in adult women = joint pain.
Petechia on the hard plata = FORCHHEIMERS SIGN.
Unvaccinated/travel/immigrant = most susceptible.
Koplick spots
Spots on buccal mucosa. My be white or blue with red halos. Measles
Forchheimer's sign
Petechiae on hard palate. Rubella.
Human Herpes Virus 6
Roseola. Exanthem subitum.
Mild viral illness.
Occurs in children between 6-19 months. Abrupt onset of high fever for 2-3 days. Associated with febrile seizures in about 10-15%.
Rash will develop after the fever subsides.
Appearance of rash: Rosy-pink over the entire body, but mostly on the torso, neck, and arms.
Accounts for ~20% of al ER visits for febrile infants 6-12 mos
Parvovirus B19
Fifth disease = erythema infectiosum.
common rash illness usually acquired in childhood.
transmission: contact with infected persons, fomites, large airborne droplets.
prodrome - fever, mild malaise.
rash - SLAPPED cheek, circumoral pallor, peripheral and mild macular distribution.
in adults - polyarthropathy syndrome. can cause transient aplastic crisis, hydrops fetalis.
polyarthropathy syndrome
arthritis (pain and inflammation) that affects five or more joints. often caused by autoimmune diseases, but can also be caused by infections. E.g. parvovirus in adults, and rubella in adult women may cause polyarthritis.
parvovirus b19 pathophysiology
Parvovirus B19 has a tropism for human erythroid progenitor cells. The virus requires the P blood antigen receptor (also known as globoside) to enter the cell. Rare individuals who lack the P antigen are immune to parvovirus B19 infection. Once inside the host cell, viral DNA enters the nucleus. The 3' end of the DNA strand folds back on itself, forming a hairpinlike bend that functions as a self-primer for viral DNA replication. The virus is cytotoxic to host cells.[2, 11] This, coupled with the tropism for rapidly dividing erythrocyte precursors (particularly pronormoblasts and normoblasts, wherein they replicate to high titers), leads to the suppression of erythrogenesis seen during infection. No reticulocytes (immature erythrocytes) are available to replace aging or damaged erythrocytes as they are cleared by the reticuloendothelial system.
hydrops fetalis
serious condition in which abnormal amounts of fluid build up in two or more body areas of a fetus or newborn. may occur if pregnant woman gets parvovirus b19. rarely occurs.
aplastic crisis
reticulocytopenia. reticulocytes are immature RBCs. this occurs in parvovirus b19: low count of reticulocytes contributes to severe anemia because RBCs are not able to be replaced. this is compounded in patients with sickle cell anemia - they need to make more reticulocytes because they replace RBCs more often. aplastic crisis likely would be reached more quickly.
VZV, Chickenpox. A DNA herpes virus. Persists in sensory nerve ganglia as latent infection.
virus enters through respiratory tract/conjunctiva.
replicates at site of entry/regional lymph nodes.
within 4-6 days - dissemination to other organs/sensory ganglia. this is PRIMARY viremia.
further replication occurs in the viscera, secondary viremia --> viral infection of skin. Incubation 10-21 days after exposure.

primary infection: chicken pox
Reactivation: Herpes zoster/shingles

Successive crops over several days. with lesions in several stages of development. may begin at trunk, but often on head. Vesicular rash.
After being infected with VZV, virus remains dormant in nerve cells without causing any symptoms.
later in life, virus can travel back down a sensory nerve to skin, causing the rash of zoster.
painful blisters on ONE side of the bdoy in distribution of the nerve.
rash will usually heal in a few weeks.
Some experience residual pain in the area for months or years --> postherpetic neuralgia.
sharp, shocking pain that follows the path of a nerve and is due to irritation or damage to the nerve
treatment of zoster
antiviral acyclovir/valacyclovir
nonpoliovirus enteroviruses
includes coxsackie virus. hand foot and mouth disease.
RNA viruses.
leading cause of exanthematous disease.
hand foot and mouth disease
Leading cause of exanthematous disease. Caused mostly by Coxsackievirus A16 (at leat in the US).
ubiquitous fecal-->oral transmitted viruses.
detection via PCR.
SUMMER AND FALL predominance.
HFMD clinically
Prodrome: fever, poor appetite, malaise, sore throat.
1-2 days after fever, painful sores usually develop in the mouth (herpangia). Begin as small red spots that blister and ulcerate.
rash develops over 1-2 days - flat or raised red spots, sometimes seen with blisters. USUALLY, on palms and soles. may appear on knees, elbows, butt, or genitals.
sores are often in the back of the mouth as well.
acute pharyngotonsillitis
most commonly caused by Group A Strep
Scarlet fever
Scarlatina. Bacterial infection. Usually occurs in association with pharyngitis (which is often caused by Group A strep). caused specifically by erythrogenic exotoxin produce by GAS (when GAS is infected by a certain BACTERIOPHAGE).

severe scarlet fever occurs? rarely.
usually scarlet fever will occur in children between ages 4 and 8.
scarlet fever clinical
Illness often begins with a sore throat.
patients then deveop a fever, develop a diffuse, palpable SANDPAPER like eruption.

scarlatiniform eruption starts on abdomen and disseminates from there.
frequently associated with STRAWBERRY TONGUE (often with a white membrane and prominent red papillae poking through the coating).
normal conjunctiva and lips.
circumoral sparing (surrounding the mouth no rash, but rest of face will have it).

Exaggerated in creases (PASTIA's lines)
Desquamation during RECOVERY.

treatment: PENICILLIN
pastia's lines
exaggerated in creases.
pink or red lines formed of confluent petechiae are found in skin creases, particularly the crease in the antecubital fossa, the soft inside depression on the inside of the arm; the folding crease divides this fossa where the forearm meets the (upper) arm (the biceps, triceps, humerus section of the upper extremity); the inside of the elbow (the inside flexor depression (fossa) of the elbow.
indication of SCARLET FEVER.
toxic shock syndrome (TSS)
diffuse inflammatory response syndrome.
characterized by fever, rash, constitutional symptoms, hypotension, and multi-organ involvement.
caused by toxin producing GAS or STAPH AUREUS.
toxins act as superantigens: production of large amount of inflammatory mediators.

more often in younger individuals wo have no neurtalizing antibody to toxin produced by SA or GAS
toxic shock syndrome toxin 1: major toxin produced by Staph Aureus.
Exotoxin A, B
SPEA and SPEB: Major toxins produced by GAS (group a step)
toxic shock clinically
acute serious illness: sudden onset of high fever, chills, ehadache, muscle ache, vomiting, diarrhea.
next 24-48 hrs: patient's develop erythroderma (sunburn like diffuse reddening of skin).
hypotension, conjunctival hyperemia (red eyes - more blood flow to the eyes), STRAWBERRY TONGUE, and multiorgan disfunction - including rapidly progressive renal failure.
other manifestations: peripheral cyanosis and edema, pulmonary edema, myocarditis, mental status changes.
CONSIDER IN PATIENTS WITH FEVER AND ERYTHRODERMA. or in patients with fever and hypotension.

during recovery: full thickness desquamation of the skin.
sunburn like diffuse reddening of the skin. may be a sign of TSS if patient presents with fever.
strawberry tongue
Kawasaki disease - may see a strawberry tongue (red in this case).
In scarlet fever - this one with a white membrane and prominent red papillae.
toxic shock - may see it.
staph and strep tss
staph: moreso in women btwn 15-35. severe pain is rare. hypotension. ERYTHRODERMA. low chance of bacteremia. tissue necrosis is rare. tampons -- predisposition. mortality rate 3%.

strep: 20-50 yo. women=men. severe pain is common. not often with erytheroderma. common renal failure. 60% bacteremia. common tissue necrosis.
predisposition: cuts, burns, bruises, varicella.
mortality rate = 30-70%
staph scalded skin syndrome (SSSS)
toxin mediated disease caused by circulation of exfoliative toxins A and B.
low grade fever followed by top layer of skin peeling off in sheets, leaving exposed moist, red/tender areas.
hallmark: toxin mediated cleavage of stratum granulosum layer of the epidermis (NIKOLSKY sign). clinical picture dominated by RAPIDLY evolving exanthem, with loss of skin in sheets as well as PURULENCE around eyelids and nose.
rash will spread to other parts of body: includes arms, legs, trunk.
children have variable degrees of illness. manifestations are age related (Ritters).

Desquamation occurs during the crescendo phase as maximal disease manifestations evolve.
nikolsky sign
cleavage of stratum granulosum layer of the epidermis.
ritter disease
staph scolded skin syndrome- age related illness. generalized exfoliation in the newborn. localized lesions are often found in the diaper area or found around the umbilical cord
petechiae-purpuric rashes
rocky mountain spotted fever

meningococcemia and purpura fulminans.
rocky mountain spotted fever
tick-borne (American dog tick) illness caused by gram negative INTRACELLULAR bacterium Rickettsia ricketsii (cannot see on gram stain).
prevalent in south central US.

majority of cases between april and october. suspect it in males <15 yo.

prodrome: fever, nausea, vomiting, ab pain, HA, malaise, photophobia.

following exposure, bacteria multiply iwthin endothelial cells of small vessels and disseminate in bloodstream --> leads to endothelial cell inury, thrombosis and capillary leak --> edema and petechiae.

classic rash: begins 2-5 day as blanching macules and papules 2-3 mm on wrists and ankles (petechiael).
rash then spreads centripetally (INWARD) to arms, thighs, trunk.
eventual involvement of PALMS AND SOLES.

classic rash only seen in 35-60%. 10-15% never have rash.
rocky mountain spotted fever progression and treatment
can result in widespread necrosis, purpura, gangrene, death. requires high index of suspicion - early empiric treatment with antibiotics: DOXYCYCLINE!!!!!!!!!
do not wait for definitive diagnosis or classic rash.
Neisseria meningitidis
meningococcus. oxidase + aerobic gram negative diplococcus. divided into serogroups based on polysaccharide capsule.
MeninGococci ferment Maltose and Glucose.
Serogroups: A, B, C, Y, and W-135: major pathogens causing human disease.

Colonizes the nasopharynx - transmitted by the exchange of respiratory and throat secretions. epidemic bacterial meningitis.
onset of infection often abrupt with fever, chills, malaise, myalgia, limb pain, prostration and rash.
neisseria meningitidis rash and treatment
initially can be macular, mauclar and papular, then petechiael followed by purpura. can result in purpura fulminans.
risk factors: late complement deficiency, close contact with case!

treatment: third generation cephalosporin like ceftriaxone. (prophylax contacts).
purpura fulminans
cutaneous hemorrhage and tissue necrosis, low blood pressure and disseminated intravascular coagulation.
Kawasaki disease
Febrile exanthematous multisystem medium vessel vasculitis. cause unknown. 80% in children. highest rates in children of azn ancestry.
sequences of events and duration of fever = clues to the diagnosis.

can resemble measles, scarlet fever, and even toxic shock syndrome! -- due to rash!
inflammation of the blood vessels
kawasaki disease sequence
start with fever and irritability (not much different than viral illness). concerns heighten as the symptoms progress.
diagnosis is made with 5 days of fever and 4 out of 5 clinical features:
1. bilateral bulbar conjunctival injection without exudate.
2. erythematous mouth and pharynx, strawberry tongue, red/cracked lips.
3. polymorphous, generalized, ertyhematous rash - can be mobilliform, maculopapuler, or scarlinitform. typically fiery red with an exaggeration at the groin.
4. changes in peripheral extremeties: induration (hardening) of hands/feet with ertyehmmatous palms and sole - later desquamation. - painful edema/erythema of the hands and feed. may have demarcated stocking/glove distribution of ertyehma and induration === digital cyanosis and gangrene.
5. acute unilateral cervical lymphadenitis - at least one node >1.5 cm)
kawasaki consequences and treatment
if untreated ~ ~20% of children may develop coronary artery abnormalities - including aneurysm.

treatment: IV administration of high-dose of pooled human Igs and oral aspirin therapy.
infects 300-500 million persons worldwide annually. causes 1-3 million deaths annually. plasmodium ____. symptoms: headache, fever, fatgiue, pain, back pain, chills, sweating, dry cough, spleen enlargement, nausea, vomiting.
complicated malaria
hyperparasitemia (>5-10% parasitized RBCs). altered mental status with seizures. hepatic failure. disseminated intravascular coagulation. hemolysis. metabolic acidosis. renal failure. hypoglycemia.
malaria diagnosis
thick and thin peripheral blood smears.
molecular diagnostics - rapid tests, PCR.
malaria treatment options
*CHLOROQUINE. malarone, coartem, mefloquine (Lariam), quinine, quinidine, doxycycline with quinine, clindamycin with quinine.

quinine is a heme polymerase inhibitor.
west nile virus infection
vector: culex mosquito. peak incidence in late summer and early fall. asymptomatic in 80% of cases. neuroinvasive disease in <1%.
west nile virus symptoms
self-limited febrile illness, fatigue, rash, myalgia, headache, anorexia, backache.
meningitis, encephalitis, myelitis.
focal weakness.
acute flaccid paralysis.
respiratory failure
extrapyramidal signs (various movement disorders).
west nile lab/imaging diagnosis
lymphocyte predominant CSF pleocytosis (increase in WBCs, specifically in bodily fluid, indicating inflammation or an infectious condition).
MRI: normal, or nonspecific.
IgM antibody in CSF.
Cross reactivity with other flaviviruses
lyme disease
borrelia burgdorferi. most common arthropod borne infection in the US. spread by the deer tick - ixodes scapularis.
stages of lyme
early localized - 1-2 weeks following infection. erythema migrans.

early disseminated - several weeks following infection. fever, myalgia, headache, fatigue, multiple EM lesions, lymphadenopathy. localized infection - cardiac (myocarditis) and CNS (cranial nerve palsy, aseptic meningitis, radiculopathy)

late: arthritis. encephalopathy.
cranial nerve palsy
a type of palsy that involves one or more of the cranial nerves. palsy occurs when a muscle becomes paralyzed, or someone loses control of it, experiencing erratic movements or jerks or other problems. cranial nerve palsies involve facial muscles and people's face's change in response to this. patient may find it difficult to smile, control eye movements, or engage in other facial movements.
a set of conditions in which one or more nerves are affected and do not work properly (a neuropathy). emphasis is on the nerve root. can result in pain, weakness, numbness, or difficulty controlling specific muscles. the pain or other symptoms often radiate to the part of the body served by the nerve, even though the problem occurs at or near the root of the nerve along the spine.
bell's palsy
form of facial paralysis resulting from a dysfunction of the cranial nerve VII - the facial nerve - that results in the inability to control facial muscles on the affected side. lyme disease can cause bell's.
most common acute mononeuropathy.
unilateral. usually self-limiting.
diagnosis of lyme
early clinical diagnosis. later stages - serologic testing for antibodies.
two stage approach.
confirmatory western blot.
neuro - CSF pleocytosis and positive CSF serum antibody. CSF PCR.
treatment of lyme
oral: doxycycline, amoxicillin, cefuroxime.

IV: ceftriaxone.
southern tick-associated rash illness - STARI
indistinguishable from early Lyme.
geographically distinct distribution in the south-east, mid-atlantic, and south central US.
vector: lone STAR tick - amblyomma americanum.

EM skin lesion, fever, headache, myalgia.

DX: clinical
RX: doxycycline
babesia microti. same vector tick species as lyme (ixodes scapularis). same geographic distribution. coinfection. person to person transmission after transfusion from asymptomatic donor.
clinical manifestation babesiosis
mild infection - fever hemolysis (jaundice, splenomegaly, hepatomegaly).
severe - hemolytic anemia, acute renal failure, heart failure, shock, DIC.

risk factor: asplenia, older age, HIV infection, other immunocomprses.
babesiosis lab and diagnosis
macrocytic anemia. elevated bilirubin and LDH, decreased haptoglobin, thrombocytopenia, elevated liver enzymes.
diagnosis: PCR using whole blood.
examination of thin blood smear
babesiosis treatment
mild disease. atovaquone and azithromycin.
or quinine and clindamycin.

severe: quinine and clindamycin.
>10% parasitemia = exchange transfusion.
rickettsial infection
obligate intracellular gram negative bacteria.
transmitted by fleas, lice, mites, ticks.
outbreaks during war and natural disasters.
symptoms: fever, headache, malaise, rash (maculopapular, petechiael, vesciular)
DX: PCR, immunohistochemical analysis of tissue, culture.

rocky mountain spotted fever
found throughout continental US.
rickettsia rickettsii.
reservoir: dogs, rabbits, wild rodents.
vector: wood-tick (dermacentor andersoni in western us)
dog tick (dermacentor variabilis in eastern us)

incubation: 2-14 days.
fever + headache, myalgia, confusion, GI symptoms. Rash in 90% and progression of rash.

LAB: normal WBC count, thrombocytopenia, elevated liver enzymes.

diagnosis: immunohisto studies of skin biopsy.
serology: 4 fold rise in antibody titer. seroconversion on a convalescent serum sample obtained 2-4 weeks after acute illness.
human monocytic ehrlichiosis *HME.
erlichia chaffeenis.
lone star tick.
southeast, south central, mid atlantic US.
human granulocytic anaplasmosis. due to anaplasma phagocytophilum. deer tick. northeast and north central us.
clinical manifestation of ehrlichiosis and anaplasmosis
incubation 1-2 weeks.
symptoms: fever, myalgia, fatigue.

rash in <30% with HME (maculopapular or petechial) and very few with HGA.
meningoencephalitis in 20% with HME.

leukopenia, thrombocytopenia, elevated liver enzymes.

diagnosis and treatment:
intraleukocytic clusters of bacteria (morulae) on a buffy coat stain (20%). antibodies appear 2-4 weeks after clinical illness.

treat with doxycycline.
yersinia pestis. gram negative rod. with a capsule.
reservoirs: rats, gerbils, squirrels, field mice.
transmission: via flea from one of these animals. human to human if serious bronchopneumonia from yersinia.

clinical ilness:
fever, hypotension (septicemic)
fever, very swollen lymph nodes in axilla or groin. may be followed by generalized spread and multisystem illness (bubonic). severe bronchopneumonia. high mortality without treatment.

diagnosis: use gram, giemsa or fluorescent stain from lymph node aspirates. can be cultured as well.
treat with: streptomycin, DOXYCYCLINE, quinolones.
prevention - quarantine, vaccines, rodent control, chem-prophylaxis, isolation.
anthrax quick facts
bacillus anthracis. large gram positive rod. aerobic, non-motile; spore forming (can survive years in soil). grows in chains(?). disease of herbivores. humans infected through contact with infected animals, or contact with spores in animal products. infections in developed countries rare.
anthrax exotoxins
Protective antigen (PA), lethal factor (LF), edema factor (EF)
PA will bind cell receptor ATR. PA is cleaved. Heptamer forms. Allows translocation of EF and LF (from anthrax) to endosomes (because comes in via vesicle from heptamer endocytosis)
Low pH? EF and LF are free. EF = binds calmodulin. EF is a calmodulin activated adenylyl cyclase edema.
LF cleaves MAPKK = death.
anthrax clinical
skin is usual site of entry; mucous membrane is possible, respiratory tract is less common.

bacteria replicates once inside host, produces anthrax toxins --> leads to edema and other toxic products. painless papule develops --> turns into eschar (piece of dead tissue that falls off from healthy skin). can spread into lymphatics leading to severe illness and death.

ingestion - major intestinal lesions and high mortality.

airborne exposure to spores --> pneumonia, mediastinal hemorrhage, bloodstream infection, and death.
anthrax diagnosis and treatment
culture of skin or blood, PCR test available.

treatment: ciprofloxacin. PCN, doxycycline has also been used.
cutaneous anthrax should be treated (20% of dissemination).
francisella tularensis.
very small, gram negative coccobacillus. fastidious. strictly aerobic. subspecies infect different mammalian species.
route of infection via contact with SKIN of infected animal. also possible via inhalation.
tularemia clinical presentation
several forms based on presentation

ulceroglandular: skin lesion and lymph nodes.
oculoglandular: eye and cervical lymph nodes.
glandular: lymph nodes.
typhoidal: fever, systemic signs of sepsis.
pneumonic - can be severe, with sepsis.
oropharyngeal and GI disease (after ingestion)
tularemia diagnosis
usually via serology. culture on CHOCOLATE agar or BCYE can be done, but lab should be warned. BC takes more than 1 week to turn positive.
tularemia treatment
streptomycin, gentamicin. doxycycline and cipro for milder infections.
prevention: avoid ticks, use gloves.
q fever
coxiella burnetti: rickettsia, resistant to desiccation, heat and sunlight - can infect environmental materials "endospore like form"
infects many species of animals. largest numbers of bacteria in placenta, but also in urine. can be present in farmland or anywhere an infected animal gives birth.
route of infection usually inhalation, but also can be ingestion.
q fever clinical
usually pneumonia (atypical), with fever and headache.
hepatitis is common (granulomatous is common).
acute: may resolve spontaneously, some cases become chronic. culture negative endocarditis, osteomyelitis possible.
q fever diagnosis and treatment
PCR in early illness. serology later (>1 wk). increase in Ab titers measured by indirect immunofluorescence assay.

treatment: ACUTE - tetracyclines
CHRONIC: combo therapy - rifampin + doxycycline or TMP/sulfa
small gram negative coccobaccili.
4 species.
primarily animal pathogens, humans are infected by CONTACT with infected animals or products.
B abortus - cows, mid.
b melintensis - goats, sheep in mexico, mediterranean, more sever disease.
b suis - pigs - US, SA, SE asia - SEVERE
b. canis - dogs, mild disease in humans
brucellosis transmission
cause abortion in animal. can be shed in milk for prolonged time, also shed in urine and feces.

enters human via skin or alimentary tract, or via inhalation (farmers, vets, abattoir workers). unpasteurized milk is a possible source.

no human to human spread
brucellosis patho
go from portal of entry to lymph nodes, and bloodstream. can survive for prolonged periods in the liver, spleen, bone marrow, lymph nodes. chronic granulomatous infection occurs.

infection may be subclinical, or gradual development of fever, malaise, sweats. undulant fever described (intermittent). enlarged lymph nodes, hepatitis may occur, osteomyelitis and endocarditis rare.

infection USUALLY resolves, but some may develop chronic infections with fatigue, intermittent fever, waxing and waning symptoms.
brucellosis diagnosis and treatment
blood culture, or bone marrow or lymph node culture. serology: IgM is present in acute brucellosis. IgG and IgA in chronic. Cultures are negative in chronic.

treatment: DOXYCYCLINE, streptomycin, TMP/SULFA.
leptospirosis transmission
leptospira interrogans - spirochete. infects many domestic and wild animals worldwide. dogs and rats are important in human transmission. infected animals secrete large numbers of bacteria in URINE. bacteria can live in wet environments. humans infected through exposure to or ingestion of contaminated water or food. farmers, water sport participants at risk.

RARE person to person transmission.
leptospirosis clinical
bacteria enter through break in skin or mucous membrane or via ingestion.
reach blood 1-2 weeks. cause febrile illness (flu like). most cases resolve, but some SOME patients then develop hepatitis, jaundice, renal failure, aspetic meningitis, conjunctival or scleral hemorrhage (biphasic illness).

weil's disease - severe form with hemorrhage, kidney, and liver failure. 5-10% of patients.
leptospirosis diagnosis
can be isolated from blood, csf, urine (depending on time since infection)
serology can be used in diagnosis: rise in agglutinating Ab is seen.
treatment: penicillin or doxycycline are effective if started early enough
psittacosis transmission
chlamydophila psittaci: chlamydiae. Obligate intracellular aerobes. Coccoid.
infects parrots and most other bird species.
organisms will be present in blood, tissues, feces, and feathers of an infected bird.
infection in humans occurs through handling birds, or aerosolization of bacteria from infected bird.

person-> person = rare.
psittacosis clinical
bacteria enter resp tract then spread to RETICULOENDOTHELIAL cells of liver, spleen, and can lead to hematogenous spread. pneumonia (atypical, interstitial, usually can be severe) usually occurs. can also have ASEPTIC meningitis and sepsis presentations.
psittacosis diagnosis and treatment
rarely diagnosed. need suspicion regarding exposure.

based on serology. 4fold increase in titer by CF testing of acute and convalescent sera.

treatment: doxycycline or macrolides
bartonella transmission
3 species associated with human illness.
gram negative, coccobacilli, fastidious.
many animal reservoirs, human infection can occur with DIRECT contact or via VECTOR.
bartonella quintana
B quintana - transmitted by lice, no animal reservoir. causes TRENCH FEVER - WWI - as well as infection in HIV and immunocompromised patients -- angiomatosis, bacteremia, endocarditis.
bartonella bacilliformis
restricted to andres area of s. america (peru, ecuador, columbia). sandfly transmission.
causes illness with fever, hemolytic anemia (OROYA FEVER), followed by formation of cutaneous nodules that are angiproliferative, may persist for years (verruga peruana).
bartonella henselae
cats, flea reservoir.
cat scratch disease - regional lymphadenopathy that may drain. dissemination may occur to liver spleen, CNS.
bacillary angiomatosis in immunocompromised patients; vascular proliferative nodules in the skin - can also occur in liver (peliosis hepatitis) or spleen.
bacteremia or endocarditis
bartonella diagnosis
blood culture for endocarditis. may be positive in blood agar. can also culture skin and lymph node specimens in blood agar.

cat scratch: serology.

treatment: doxycycline or macrolide.
treponemal test
measures antibodies against t. pallidum antigens. principal use is to verify positive nontreponemal tests
treatment for syphillis
failure of nontreponemal tests to decline fourhold within 6 months after therapy
may indicate treatment failure. repeat HIV testing. retreat three weeks unless neurosyphilis
pregnancy and syphilis
screening at first prenatal visit.
any woman who delivers a stillborn after 20 week gestation should be tested.
penicllin regimen appropriate at this stage.
gram negative, fastidious, facultative anaerobe.
ulcerative disease.
special culture media for haemophilus ducreyi. sensitivity <80%.
PCR - not FDA approved. silver stain to identify.
painful genital ulcer and tender suppurative inguinal adenopathy suggestive of diagnosis.
probably diagnosis if all met:
one or more painful ulcers
darkfield and serology negative for syphilis
ulcer exudate negative for syphilis
ulcer exudate negative hsv
genital ulcer and adenopathy
chancroid treatment
azithromycin. ceftriaxone. ciprofloxacin. erythromycin. clinical imporvement in 3-7 days. large ulcers may need more than 2 weeks.
if no chancroid improvement
diagnosis correct? coinfection? HIV positive? compliance? resistance?
granuloam inguinael (donovanosis)
intracellular gram negative bacteria = klebsiella granulomatis.
endemic in some tropical and developing areas.
painless, slowly progressive ulcers on genitals or perineum WITHOUT regional adenopathy.
subcutaneous granulomas = pseudobuboes may occur. lesions highly vascular and bleed easily. can present as hypertrophic, necrotic, or sclerotic variants. can extend to pelvis, organs in abdomen, bones, mouth
granuloma inguinale diagnosis
visualized of DONOVAN bodies on tissue culture. use a giemsa stain. rod shaped organisms in cytoplasm of monocyte.
lymphgranuloma venereum
caused by chlamydia trachomatis serovars - L1, L2, L3.
inguinal and/or femoral adenopathy that is typically unilateral. rectal exposure can result in proctocolitis (mucoid adn/or hemorrhagic rectal discharge, anal pain, constipation, fever, and or tenesmus.
if not treated can lead to chronic colorectal fistulas and structures.
can develop secondary bacterial infections.
suspicious and serology to determine if have it.
LGV treatment
doxycycline for 3 weeks. erythromycin or azithromycin.
herpes simplex virus
hsv1 and 2 can cause genital herpes. most infected with hsv-2 have not been diagnosed with genital herpes but shed virus intermitently in the genital tract.
hsv1 increasing in first episodes of anogenital herpe (anus).
diagnosis: cell culture or PCR. PCR more sensitive.
treatment of HSV
acyclovir. famciclovir. valacyclovir.
recurrent: same but more days.

suppressive therapy: reduces frequency of recurrence by 70%. over time outbreaks will diminish. reassess yearly. likely to reduce transmission in those with multiple partners.
inflammation of the urethra. discharge, dysuria, pruritis (itchy). asymptomatic.
- gonorrhea, non-gonococcal = chlamydia, trichomonas, mycoplasm, ureaplasma.

- NAAT test. (also approved for chlamydia).
gram stain

azithromycin - long half life, great tissue penetration (macrolide)
Doxycycline (tetracycline)
if due to trichomonas use metronidazole.
inflammation of endocervical mucosa.
two major diagnostic signs
= purulent or mucopurulent endocervical exudate. sustained endocervical bleeding easily induced by gentle passage of cotton swab.

often asymptomatic. may have weird discharge and intermenstrual bleeding.

gonorrhea, chlamydia, trichomonas, herpes
nonmotile obligate INTRACELLULAR bacteria.
prevalence highest in people younger than 25.
sequelae: PID, ectopic pregnancy, infertility.

all sexually active female should be screened!!!!
chlamydia treatment
neisseria gonorrhea. nonmotile, nonspore forming, gram negative diplococci. pili attach to epithelium. up to 50% women with mild or no symptoms - not the case for men. can lead to PID, infertility, ectopic pregnancy.
purulent discharge in men seen.

disease in gay men - throat and rectum.
need annual screening.

can become disseminated. papules can develop on hands and become necrotic.
tetracycline and pregnant women
cannot be administered!
gonorrhea treatment
ceftriaxone. pencillin allergy? azithromycin.

not cefixime.
bacterial vaginosis
polymicrobial clinical syndrome. replacement of normal hydrogen peroxide producing lactobacillus with anaerobic organisms.

diagnosis - use a gram stain.
clinical critera (at least 3 of the following)
homogenous, thin, white discharge that coats vaginal walls.
clue cells (on wet mount. rattiness border. gram stains help to identify. intracellular clearing?)
fishy odor (whiff test)
bacterial vaginosis treatment
metronidazole (orally or gel). clindamycin cream.
protozoa, worry about motile trophozoites - see a tail. t. vaginalis.
asymptomatic to copious foul smelling discharge (strawberry cervix with punctate hemorrhages)
in men asymptomatic to urethritis.
treatment: metronidazole
vulvovaginal candidiasis
candida species - usuall albicans. pruritus, thick white discharge, edema, exorations, diagnosis via wet mount.
treat with fluconazole. intravaginal antifungals.

pelvic inflammatory disease
spectrum of inflammatory disorders of the upper female genital tract.
etiology - stds, vaginal flora.

diagnosis challenging - may have abnormal bleeding, vaginal discharge, tenderness...
PID treatment
ceftriaxone and doxycycline. may give metronidazole as well.
two kinds. acute and chronic. pain, swelling, inflammation of epidiymis. most cases involve testis.

treatment: levofloxacin, ceftriaxone with doxycycline.
human papilloma virus
more than 40 types can infect genital area. most infections are asymptomatic, unrecognized, or subclincal. more than 50% sexually active infected at least once in their lifetime.

oncogenic = 16 and 18.
treatment for genital warts - cryotherapy, imiquimod....

prevention - vaccines - 6, 11, 16, and 18 covered.
treponema pallidum characteristics
few-surface exposed proteins = stealth organism.
undulating movement about its center which distinguishes it from other treponems on darkfield microscopy.
cannot be cultured on artifical media, but can be propagated in organ culture.
slow growth rate.
syphillis pathogenesis
enters through intact mucous membranes or abraded skin.
hours --> days later, enters the lymphatics with eventual dissemination throughout the body. incubation period is inverseley related to the size of inoculum.
mdan incubation period before clinical manifestations is 3 weeks
primary syphilis
button-like papule appears at site of inoculation which develops into a painless erosion, then ulcerates with RAISED boarder and scant serous exudate. can range in size up to 1 cm.
although unusual, genital lesion can be painful if secondarily infected with staph. extragenital lesions may be painful especially if on the fingers.
GENERALLY, a single lesion appears. less commonly, multiple or kissing lesion.
atypical lesions can occur in up to 60% and the absence of a primary lesionc an occur.
regional lymphadenopathy appears within 7 days. nodes are nontender, rubbery, firm, and usually unilateral. they may persist for months.
the chancre heals on its own within 3-6 weeks (range 1-12)
secondary syphilis
the disseminated or most clinically florid stage. appears 2-6 months after primary infection. 2-10 weeks after the appearance of the primary chancre. 6-8 weeks after the healing of the chancre.
IN ~15% the chancre may be present at the time the secondary lesions appear.
may experience fever, sore throat, weight loss, malaise, anorexia, HA, meningismus, mucocutaneous lesions are asymptomatic and can last for weeks.
Neisseria meningitidis
one of the most rapidly fatal of all infectious diseases. usually occurs in previously healthy individuals. typically develops after an upper respiratory tract infection, with a prodrome of headache, nausea, vomiting, myalgias, and anthralgias and subsequent development of a rash. no one feature of rash can readily distinguish meningococcemia from other processes, but petechiae are the most common initial skin lesions. typically distributed sparsely over the extremeties and trunk.
RMSF - another description
tick-borne disease caused by rickettsia rickettsii. has been referred to as the great imitator. patients may initially report fevers, chills, headache, cough, myalgias, and malaise. petechial rash typically develops 3-5 days into the illness and is the major diagnostic sign. rash initially pink to bright red, with discrete macules that blacnh. lesions start on wrist and ankles and spread to hands and soles, then centripetally to the trunk. within days, the macules progress to papules and petechiae that may coalesce to ecchymoses.
kawasaki - what does it effect?
lymph nodes, mouth, mucous membranes. AKA mucocutaneous lymph node syndrome.
kawasaki sequealae
acute stage begins with onset of fever and lasts 1-2 weeks. followed by the subacute stage, which includes desquamation of the extremities and the development of coronary aneurysms. third stage is convalescence during which findings resolve. patient may first exhibit erythema of the palms, soles, and perineal regins that gradually spreads to the trunk and extremities. more than 90% of patients present with a polymorphic rasah following the onset of fever.
in 94% of cases, patient experiences changes in the extremities. after the apperance of erythema, the palms of the hands and soles of the feet become abnormally indurated and swolen (hardened).
in subacute phase of the illness, approximately 2 weeks after onset of initial fever, 75% of patients have acral desquamatin and erythema of the fingertips that involves the nail region. later, desquamation of toes occur.
patients exhibit other change sin oral cavitiy besides strawberry tongue. often red and swollen lips that crack and bleed, as well as pharyngeal edema.
what disease has the largest amount of bacteria in the placenta or in the urine?
coxiella burnetti - Q fever. infects many species of animals. can be present in farms and/or anywhere infected animal gives birth
What is pneumocystis pneumonia?
PCP. Caused by pneumocystis jiroveci (fungus). Ubiquitous in nature. most common OI in HIV/AIDs patients.
Mode of entry of PCP
inhalation. can colonize airways without causing infections in normal host.
PCP infection
usually lungs, and is often bilaterally. organism causes an intense inflammatory reaction in the alveoli leading to interstitial pneumonitis. alveolar space appearance: filled with frothy honeycombed material.

clinical syndrome is often subacute. gradual worsening of symptoms over weeks. notice a fever, nonproductive cough, accelerated dyspnea upon exertion.
PCP Physical Exam
Decreased oxygenation on room air = HYPOXIA = hallmark sign of PCP.

precipitous drop in oxygenation with exertion.

+/- fever

lung exam usually normal.

chest x-ray: diffuse bilateral usually reticular, interstitial infiltrate.
impairment of o2 exchange due to this inflammation.
PCP diagnosis
Preferred: bronchoalveolar lavage. Use GMS stain - selectively stains for the walls of the cysts (one of the forms of PCP possible in the body). Giemsa and wright stains will identify cysts and trophozoites.

induced sputum: less invasive, lower sensitivity.
LDH: usually elevated, but not specific.
PCP therapy
Preferred: high doses of TMP-SMX.
significant oxygen impairment/inflammation? use prednisone (a steroid).
cryptococcal infection
causative agent: most often cryptococcus neoformans. oval encapsulated, yeast-like fungus. found in soil and bird droppings.

patients at risk when CD4<100. Clinically, usually presents when CD4<50.
cryptococcal mode of entry
inhalation. just like blastomycoses and histoplasmosis.
cryptococcal tropism
CNS tropism. May also see skin infections, pneumonia, skeletal system implications.
cryptococcal clinical presentation
subacute meningoencephalitis. gradually worsening headache. fever, malaise. may not have classic signs for meningitis - neck stiffness, photophobia. encephalitic type symptoms = altered mental status, lethargy, memory loss.
cryptococcal diagnosis
lumbar puncture. Hallmark of disease: elevated intracranial pressure *measured using a manometer. checking for the antigen is a highly specific and highly sensitive.
cell counts may not be elevated due to lack of inflam response to infection (=poor prognosis).

may have elevated protein. often glucose is not low.

stain using an INDIA INK stain to identify the THICK capsule surrounding the yeast.
HIV patients and LPs
CT scans prior to any LPs! Delicate balance of ICP - otherwise may lead to herniation or serious complications.
Cryptococcal treatment
amphotericin B plus flucytosine.
maintenance: fluconazole.
management of ICP (LPs can reduce the ICP).
cryptococcal skin infection
commonly appears as papule with umbilicated center. usually due to disseminated infection. diagnosis: serum cryptococcal antigen, skin biopsy--> culture.
causative agent: toxoplasma gondii. increased risk of acquisition from cats, undercooked or raw meets. presents as reactivation of prior infection in HIV patients.
toxoplasmosis presentation
predilection for CNS. presentation depends on location of the lesion. headache, altered mental status, seizures, personality changes, focal neurological.
toxoplasmosis diagnosis
imaging: CT scan of brain with contrast or MRI. usually see multiple ring enhancing lesions. similar presentation can be seen with other disease.

brain biopsy
toxoplasmosis treatment
preferred: pyrimethamine plus sulfadiazine plus leucovorin.

alternative: TMP-SMX.
double stranded DNA virus. Most persons are seropositive for CMV. disease reflects reactivation of prior infection.

Usually occurs when CD4<50.

can cause a WIDE spectrum of disease in AIDs patients.
CMV retinitis
sight threatening infection. full thickness necrotizing retinitis. can involve one or both eyes.

dx: dilated funduscopic exam. fluffy yellow white retinal lesions with intraretinal hemorrhages.
looks like a tomato and cheese pizza!
CMV esophagitis and colitis
symptoms - pain with swallowing (odynophagia) in esophagitis.

colitis - bloody diarrhea, abdominal pain, fever with colitis.

diagnosis: endoscopy (upper or lower). also, biopsy.

pathology: will show large cells with intranuclear and intracytoplasmic inclusions.
CMV - other symptoms
CNS infection: dementia, ventriculoencephalitis, radiculopathy.

treatment: gangcyclovir (IV), oral valgancyclovir.
Mycobacterium avium complex *MAC
ubiqutious in nature. route of infection: inhalation, ingestion, inoculation. usually presents as disseminated infection. primary infection is more common then reactivation. risk of infection: CD4<50.
MAC clinical presentation
Insidious onset of fever, weight loss, night sweats, diarrhea. several weeks of symptoms.

predominantly affects bone marrow and lymph nodes - however, any organs can be involved in active infection.
clinical findings: may have enlarged lymph nodes (lymphadenopathy), enlarged spleen or liver.
may have marked anemia, neutropenia, and/or elevated alkaline phosphatase.
MAC diagnosis
mycobacterial blood culture. can take up to 8 weeks after growth. biopsy of affected organ --> usual sites include lymph node, bone marrow - culture, pathology.
MAC treatment
2-3 drug combination. most active agent: macrolides = clarithromycin.

other agents: rifabutin, aminglycosides
mucocutaneous candidiasis
causative agent: candida species. usually C. albicans. Normal flora of oropharynx. patients with immunosuppression - can have overgrowth of Candida.
HIV patients: tend to cause oropharyngeal and/or esophageal infection.
mucocutaneous candidiasis presentation
Presentation: OP-->painless, creamy white plaques/patches on mucosa (buccal, tongue, palate). can be easily removed with a tongue depressor.
Esophageal --> odynophagia, retrosternal pain. may not see evidence on exam.
mucocutaneous candidiasis diagnosis
OP: mostly based on direct visualization. can scrape patches and identify yeast on KOH prep.

esophagitis: endoscopy. visualization of plaques. biopsy.
mucocutaneous candidiasis treatment
preferred: fluconazole

resistant: echniocandins, amphotericin
diarrheal IO
cryptosporidiosis, microsporidiosis, cystoisosporiasis = protozoan infections.

At risk CD4<100.
all can cause prolonged non bloody diarrheal illness, abdominal symptoms, poor oral intake, fever. malabsorption can lead to wasting. route of infection: fecal-oral. ingest oocysts/spores.
diarrheal IOs diagnosis
stool studies: ova and parasite. modified acid fast stain will stain oocysts red.

cryptosporidium = 5-7µm, cystoisospora: 25µm.

detection of spores for microsporidia species: 1-2µm.

biopsy of small intestine.
diarrheal IOs treatment
all three will resolve with antiretrovirla therapy --> immune reconstitution.

cystoisospora - TMP-SMX. crypto - inconsistent results.
mostly in tropical and subtropical regions
risk associated with contaminated water/food (recreational, potable sources); infected animals, and raw oysters.
comprised of several species.
can cause a variety of infections in HIV patients. ESP disseminated disease.

associated with travel to/living in endemic areas (US Midwest, Puerto Rico, central/south America). Usually seen when CD4<150.
histoplasmosis symptoms
fever, weight loss, fatigue, night sweats, pulmonary infection, enlarged lymph nodes, liver, spleen.
histoplasmosis diagnosis
histoplasma antigen. usually done on urine--> highly sensitive and specific for disseminated disease.
Culture of biopsy or bronchoalveolar lavage.
histoplasmosis treatment
ampho B then oral itraconzaole.
risk associated with living in southwest desert, central/south america.

increased risk if CD4<250.
clinical presentation: focal or diffuse pneumonia, skin lesions, meningitis, liver and lymph node involvement.
diagnosis: culture, serology.
treatment: ampho B followed by azole
mycobacterium tuberculosis TB
in developing countries, most commonly seen OI. due to large number of latently infected persons with MTB. can disseminate and infect any organ, but predominantly lungs (initial portal of entry).
MTB can occur at any CD4 count, but increased risk with declining CD4 counts.
Especially when patients NOT treated for latent TB.
mycobacterium TB
presentations: pulmonary disease-->cavitary. military tb - hematogenous seeding of lung tissue.
bone marrow and lymph nodes --> can see pancytopenia. brain, bone, peritoneum, pericardium.
Epstein barr virus
DNA virus -- herpes virus. infects B cells. in hiv infected patients, has increased oncogenic potential --> primary central nervous system (CNS) lymphoma.
presents with CNS symptoms:
lethargy, confusion, seizures, constitutional symptoms.
imaging, PCR of CSF.
kaposi sarcoma associated herpes virus
HHV-8. associated with Kaposis sarcoma --> vascular malignancy. skin lesions - violaceous iregular plaques. visceral involvement can occur.
treatment: ART (antiretroviral therapy), chemo.
human papilloma virus
DNA virus. certain types associated with cervical cancer = 16, 18. hiv infected women have several fold higher risk of cervical cancer than non infected women. yearly paps recommended. hpv vaccine is not yet officially recommended in infected women.
CD4<200, >100
Cover for PCP.

treat with TMP-SMX daily or three times weekly.
cover for toxoplasmosis AND PCP

TMP-SMX daily or thrice weekly
cover for MAC, toxo, PCP

azithromycin 1200 mg once weekly.
consider primary proplhylarix for at risk patients for histo and coccidioido.
what are nosocomial infections most often caused by?
what is a hospital acquired infection
nosocomial infection. infection that first appears between 48 hours and four days after a patient is admitted to a hospital or other health-care facility.
what are the most common hospital acquired infections
utis, ventilator associated pneumonia, surgical wound infections, line related blood stream infection, c diff colitis
most common type of hospital acquired infection. shown to occur after urinary catheterization.
catherization is placement of a catheter through the urethra into urinary bladder.

bacteria usually are in or around the urethra and cannot get into the bladder. a catheter can pick up bacteria from the urethra and give them an easy route into the bladder, causing infection
ca-uti pathogens
enteric bacteria. skin flora like staph epi/staph aureus. patients with poorly functioning immune systems who are taking antibiotics are also at increased risk of UTI caused by candida.
second most common type of hospital acquired infection. bacteria/other microorganisms are easily introduced into the throat by treatment procedures performed to treat respiratory illnesses.
pneumonia pathogenesis
primary route of infection of lungs is through microaspiration of organisms that have colonized the oropharyngeal tract. (or to lesser extent GI tract). high proportion of severely ill patients aspirate routinely. although frequently regarded as partially protective, the presence of an endotracheal tube permits the aspiration of oropharyngeal material or bacteria of gi origin
c diff
gram positive anaerobe spore forming toxin producing bacillus. 20% of patients admitted with negative stools will become infected. easily transmissible. asymptomatic carrier stated exist. can be cultured from any surface. can lead to death.