Tb, Zoonosis, Bioterrorism, Stds

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TB staining? aerobe or anaerobe?

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obligate aerobe. Acid fast when stained with ziehl-neelsen stain.

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transmission of TB

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respiratory via droplets. Droplets remain suspended for hours.

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Pathogenesis (primary infection of TB)

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small droplets reach alveoli. Ingested by alveolar macrophages and multiply intracellularly. Bacilli are released and ingested by other macrophages. Infected macs are carreid to regional lymphnodes. Ghon complex - lung inflammation with enlarged hilar lymph nodes

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Disseminated TB

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hematogenous spread --> miliary TB. Spread to vertebra --> Pott's disease

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reactivation TB (time frame for highest risk? Risk factors? Common site?)

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highest risk is within first two years after infection. HIV, corticosteriods or immunosuppressive drugs, diabetes, end-stage renal disease, malnutrition, malignancy. Commonly occurs in lung apex

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symptoms and signs TB

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productive cough for 8 months,night sweats, fevers, wieght loss for 4 months, hemoptysis, extrapulmonary sites.

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Diagnosis TB

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PPD test. Valid result after 48 - 72 hours. BCG results can result in false positive. Quantiferon (IFN gamma release assay) has no cross reactivity with BCG. PCR

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Treatment TB

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Standardized regimen: INH, rifampin, pyrazinamide, ethambutol for 6 months. Patient becomes non-infections after 2 weeks

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INH side effects

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peripheral neuropathy, rash hepatitis, lethargy

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rifampin side effects

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GI, hepatitis, cyp450 activation

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pyranzinamide (side effects)

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arthralgia, hepatitis, GI

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ethambutol (side effect)

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retrobulbar neuritis

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how does infection cause fever (4 mechanisms)

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1. upregulation of thermostatic set point in pre-optic area. 2. redirection of blood flow from cutaneous to deep vascular beds. 3. shivering, seeking warmth. 4. increased glucocorticoids and decreased secretion of vasopressin

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pyrogenic cytokines

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IL-1, TNF alpha, IL-6, IFN-gamma (induces IL-1 and TNF-alpha

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how does LPS cause fever?

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LPS binds to CD14/TLR-4 --> NF-KB mediated macrophage activation.

Front 16

What is SIRS (systemic inflammatory response syndrome)?

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temp >38 or less than 36. heart rate > 90 bpm. Resp >20/min or PaCo2 <32 mmHg. Wbc > 12000 or >10% band form

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what is sepsis?

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SIRS + evidence of infection

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what is septic shock?

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Sepsis + hypotension

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treatment of septic shock

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ABC. Identify infection and make diagnosis. Treat infection. Give CV support. Control coagulopathy.

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characteristics of spirochetes (4)

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lots of lipids. Flagella. Limiting membrane. Corkscrew

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lyme disease pathogen and life cycle

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Borrelia burgdorferi. Transmitted by the ixodes tick. Infected adult tick --> eggs in the spring --> hatch into uninfected larvae (summer time) --> larvae feed on infected deer mouse --> infected nymph --> molt to become infected adult form. Dual peak of disease: spring (nymphs) and fall (adults)

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how to break cycle (lyme disease)

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cotton balls containing insecticide. Tick checks. Antibiotic prophylaxis.

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stages of lyme disease (3)

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1. Early localized -->erythema chronic migrans. 2. Early disseminated --> multiple annular lesions, lymphadenopathy, pain on neck flexion, headache, muscle tenderness, myalgias, elevation of LFTs, hepatomegaly and splenomegaly etc. Ab to organism (igm first, then IgG), migration to nerves, bell's palsy, carditis (AV blocks). 3. late persisitent --> chronic encephalitis, arthritis, acrodermititis chronic atrophicans)

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diagnosis of lyme disease (early stage? late stage?)

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1. ECM -- clinical diagnosis. 2. Later stages --> serology (elisa)

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treatment of lyme disease

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1. ECM, Bell's palsy or midl cardiac disease --> treat with doxycycline or tetracycline (or amoxicillin for children) for 14 - 28 days. 2. for serious disease IV ceftriaxone for 14 - 28 days.

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Tick borne disease

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rickettsia, ehrlicia, coxiella burneti, bartonella

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Ehrilichiosis (2 types)

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Human granulocytic ehrlichiosis (erhlichia phagocytophila. tick is ixodes scapularis--> same one that causes lyme disease and babesiosis). Human Monocytic ehrlichiosis (ehrilichia chaffeensis. Tick is amblyomma americanum)

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symptoms ehrilichiosis

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febrile flu-like illness with low white count (usually do not expect influenza during the spring). Mild hepatitis, non-descript rash)

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diagnosis ehrilichiosis

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leukopenia, thrombocytopenia, elevated LFTs, serology (four fold rise in ab titer)

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treatment ehrilichiosis

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tetracyline, chloramphenicol (risk of aplastic anemia)

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Diagnosis of Babesiosis

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RBC with Babesia forming a maltese cross

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Treatment for Babesiosis

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Clindamycin plus quinine or atoviquone and azithromycin

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ricketsial diseases (pathogenesis)

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tick bite --> replication in skin --> invades endothelial cells of capillaries --> vasculitic rash --> eschar at site of bite (for all other ricketsial diseases, not rmsf though)

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symptoms of ricketstisal diseases

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eschar, vasculitic rash (on palms and soles), gangrene, fever, edema, hepatosplenomegaly, meningeal signs, conjunctivitis

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diagnosis of RMSF (3)

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fluorescent antibody staining of biopsy tissue, direct culture from blood, serology (complement fixation and wiel-felix test --> sera would agglutinate certain strains of proteus)

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treatment of RMSF (3)

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tetracyline, chloramphenicol (children under 7), quinolones

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etiological agent for typhus

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R. prowazekii. Reservious of thyus in fly-squirrels. Transmission via the body louse.

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signs and symptoms (thyphus)

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macular erythematous rash

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Brill-Zinsser disease

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Reactivation of latent thyphus in an individual as they get older or become immunesuppressed. Typhus is latent in adipocytes

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Q fever pathogen

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Coxiella brunetti

Front 41

where is coxiella found?

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plancenta of infected animals. Lives in the phagosome because it needs low pH to survive)

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Diagnosis of coxiella

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phase 1 antigen serology (complement fixation titer). Used to diagnose active infection.

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symptoms of coxiella

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acute --> flu-like pneumonia with hepatitis. Chronic --> endocarditis, ostemyelitis, neurological disease. Fever.

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treatment of coxiella

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tetracycline, TMP-SMX, Rifampin, quinolones.

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Three toxins of Anthrax

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Lethal factor, Edema factor, Protective antigen

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clinical presentation of anthrax(cutaneous)

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blistering and swelling at site of innoculation. Development of black eschar with edema (in excess of what you would expect). Also, fatigue, sore throat, headaches, nausea, myalgias, sweats)

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clinical presentation of anthrax (pulmonary)

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via inhalation. No runny nose, widened mediastinum (due to hemorrhagic lymph nodes, bilateral pleural effusions, pneumonia

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clinical presentation of anthrax (GI)

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via ingestion. Upper and lower GI bleed, severe nausea and vomiting. Black eschar and edema in GI tract

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Clinical presentation of small pox

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sick first, then infectious later (until scabs separate) (unlike VZV), synchronous pox, scars (because occurs in the dermis-- deeper than VZV), affects the periphery > trunk

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transmission of small pox

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respiratory aerosols, direct contact, fomites

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complications of small pox vaccine

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erythema multiforme, accidental auto-inoculation (commonly mouth and nose), generalized vaccina, exzema vaccinatum, progressive vaccinia, encephalitis, myocarditis, death

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General characteristics of F. tularensis

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Gram-negative coccobacillus, grows best with special media containing cysteine

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transmission of tularemia

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direct innoculaton (skinning rabbits), inhalation, ingestion, ticks and other insect bites

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clinical manifestation of tularemia

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high fever, chills, head and muscle ache. Depending on the site of infection: cutaneous ulcers, conjunctivitis, exudative pharyngitis, ulcerating lymphadenitis, bronchopneumonia,

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treatment of tularemia

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Doxycycline, quinolone or steptomycin

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Microbiology of Yersinia pestis

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gram- negative coccobacillus. Safety pin apperaance. Grows in routine media

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transmission of the plague

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infected flea, intentional release

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clinical presentation of the plaque

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Bubo - swelling of lymph node upstream from the flea bite, DIC -- rotting of fingertips and nose, Pneumonia with hemoptysis

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prophylaxis and treatment of plaque

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Doxycycline, quinolone or steptomycin

Front 60

Microbiology of C. botulinum

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Anaerobic, spore forming, gram-postive rod. Exotoxin prodced. Stable spores

Front 61

transmission of botulinism (adult vs infant)

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ingestion (adults eat preformed toxin), infants eat the spore (in honey) and the toxin is made in vivo resulting in floppy babies.

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clinical presentation of botulinism

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24 - 72 hrs after ingestion. Diplopia and dry mouth. Cranial nerve palsies, descending symmetrical weakness (contrast with Guillian barre which is symmetrically ascending).

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prevention and treatment of botulinism

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Anti-toxin, respiratory support

Front 64

Causative organismof syphilis

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treponema pallidum

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clinical stages of syphillis (4)

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Primary syphillis, secondary syphilis, latent stage, tertiary stage

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characteristics of primary syphilis

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single painless ulcer with indurated edges. Treponemes can be seen on dark field microscopy

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xteristics of secondary syphilis

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Fever, malaise, lymphadenopahty, alopecia, hepatosplenomegaly, rash involving palms and soles. Wet mucosal lesions (condyloma lata - infectious)

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xteristics fo latent syphilis

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only way to detect is by blood test.

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xteristics of tertiary syphilis

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Gummas, endarteritis of aortic arch (aneurysm, aortic valve insufficiency)

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Neuromanifestation of syphilis (3)

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syphilitic meningitis (cranial nerve palsies, sensory-neural deafness), meingovascular syphilis (end-arteritis leading to infarction), parenchymatous neurosyphilis (meningoencephalitis, psychiatricl issues, argyll-robertson pupil, tabes dorsalis

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congenital syphillis (transmission)

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in utero and at time of birth

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prevention of congenital syphilis

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treatment of mother with penicillin

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clinical manifestation of congenital syphilllis

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leaky rhinits, deformities, anemia, jaundice, thrombocytopenia

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diagnosis of syphilis

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darkfield, serology (most sensitive and specific for secondary syphilis) VRDL serology for neurosyphilis

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serology for syphilis (2)

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non-treponemal (anti-cardiolipin ab detection with vdrl or RPR. Assay can cross-react with lupus, HIV, pregnancy), treponemal ( specific. FTA-ABS, MHA-TP. Detects anti-treponemal AB. Remain positive for life

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treatment of syphilis

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single injection of penicillin, or doxycycline (except in pregnancy)

Front 77

jarisch-Herxheimer reaction

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massive lysis of spriochetes with six hours of first dose of treatment (fever, chils, headache, arthralgias)

Front 78

Pathogenesis of Gonorrhea

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iron scavenging. Incorporation fo host sialic acide residues thereby blocking C3b depostition like encapsulated bacteria. Catalase, antigenic variation of OMPII (outer membrane protein for cluster formation) and pili (attachment and sex)

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manifestation of gonorrhea in males

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incubation for 3 days. Urethritis. Spontaneuous resolution after weeks. Secondary infection of prostate and epididymis)

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manifestation of gonorrhea in females

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discharge and metromenorrhagia. Secondary infection of bartholin glands. PID

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Other sites of gonorrhea infection (4)

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rectial infection, pharyngeal infection, conjunctivitis, disseminated infection (DGI)

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Diagnosis of gonorrhea (4)

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Gram stain, thayer0-martin media culture, Antigen assays, amplification assays

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tratment of gonorrhea

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3rd generation cephalosporin, or spectinomycin for penicillin allergic patients. Always treat for co-existing chalmydia infection

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Non-ulcerative STDs

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Scabies, HPV, Crabs, molluscum cntagiosum, candida, condyloma lata, pubic lice

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ulceratiive STDs

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chancroid, lymphogranuloma venerum, granuloma inguinale

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chancroid (etiology and treatment)

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hemophilus ducreyi. Papules, Pustules, Ulcer, Bubo. Treat with ceftriaxone or Cipro

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lymphogranuloma veneruem (etiology and treatment)

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chlamydia trachoatis serovars 1-3. small ulcer, inguinal nodes (groove sign). Treat with doxycycline

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Chlamydia trachomatis growth phases

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elemetary body (infective agent), reticulate body (growth and replication)

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clinical manifestations of chlamydia

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rieters syndrome (urethritis, conjunctivitis, arthritis, mucocutaneous lesions. Not as exuberant PMN respone as in GU.), Trachoma (scarring disease of eyes), Interstitial Pneumonitis (in new borns)

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treatment of chlamydia

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Azithromycin

Front 91

Causes of Vaginitis (and diagnosis)

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Candida (postive KOH stain), Trichomonas vaginalis (wet mount to see motile organism), Bacteral vaginosis (clue cells on wed mount --> epithelial cells with adherent bacteria. Fishy odor with KOH)