Infectious Disease
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| TB arthritis: clinical presentation | pain & swelling dev in affected joint over mos / yrs; knee & hip > ankle, shoulder, elbow
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| TB arthritis: occurs as: | part of disseminated primary disease or through reactivation; usu a chronic monoarticular process
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| tetanus pathology | Spores in wound => bacteria produce tetanospasmin: interferes w/neurotransmission at spinal synapses of inhibitory neurons
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| tetanus incubation period is: | 5 days - 15 weeks (average 8-12 days)
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| Tetanus clinical features | Uncontrolled spasm & hyperreflexia. Minor stimuli precipitate painful tonic convulsions. Spasms of glottis & resp muscles may lead to death.
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| diphtheria complications | myocarditis; CN neuropathy 2/2 exotoxin
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| pertussis stages | catarrhal; paroxysmal; convalescent
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| Reye syndrome | fatty liver w/encephalopathy; may dev 2-3 wks post flu A onset, usu kids; jaundice, sz, hypoglycemia, inc LFTs; supportive tx
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| Acute joint pain; swollen, warm, erythema = | Septic arthritis (synovial fluid = leukocytosis, low glucose)
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| Bacterial meningitis organisms in Neonates: | Group B Strep (S agalactiae); Enterococci; Enterobacteriaceae/ Listeria
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| Bacterial meningitis organisms: <2 mo: | Group B Strep (S agalactiae); E. coli (tx < 1yo = Vanco + Rocephin)
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| Bacterial meningitis organisms: 3 mos - 6 yrs | Strep pneumo (DRSP); N. meningitidis; H flu
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| Bacterial meningitis organisms: 7-50 yrs | Strep pneumo (DRSP) (No. 1 cause); N. meningitidis; L. monocytogenes
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| Bacterial meningitis organisms: Adults >50 yrs | usually Strep pneumo (DRSP)
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| Pertussis: catarrhal stage sx/sx | sneezing, coryza, hacking cough
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| Pertussis: paroxysmal stage s/s | whooping cough fits
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| Pertussis: convalescent stage sx/sx duration | until 4 weeks post onset
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| botulinum toxin MOA | Spore-forming anaerobe found in soil. Inhibits acetylcholinesterase release at NM junction
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| botulism S/S | 12-36 hours post-ingestion: diplopia, loss of accommodation/EOMs; ptosis, CN palsy; UE weakness; respiratory paralysis; normal mental status
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| GPR, vesicular papule w/blue-black center 2 weeks post-exposure => painless necrotic eschar => sepsis/ meningitis = | anthrax
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| Gangrene = | Clostridium infection: anaerobic bacteria; tx w/ hyperbaric oxygen, PCNs, surgical excision
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| Inhalation anthrax clinical features | Biphasic pattern: first 1-3 days (flulike) fever, LAD, malaise, cough, substernal pressure (hemorrhagic mediastinitis) 10 days post-exposure. Then sudden fulminant phase -> sepsis to death in 1-2 days
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| Infectious disease that may cause Addison disease | TB
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| Brucellosis pathology | Aerobic, slow growing, non-motile facultative intracellular GNCB. In cattle, hogs, goats. Endemic in Mexico, S America, Spain. Eating dairy.
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| Brucellosis clinical features | Insidious: fever, weakness, arthralgia, HA, wt loss. Undulant fevers in chronic. HSM, LAD.
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| Cat scratch clinical features | Papule / ulcer in days. Fever, HA, malaise in 1-3 weeks. Tender LAD in 1-7 weeks, regress in 2-4 months.
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| Bacillary angiomatosis & peliosis hepatis are disseminated forms of: | Bartonella (cat scratch dz) in HIV-positive patients
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| Brucellosis tx in immunosuppressed patients | Macrolides or doxy
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| MAC organism | Mycobacterium avium: acid-fast, rod-shaped nonmotile organism: not communicable from person to person
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| MAC clinical features | Disseminated dz occurs in late HIV in patients with low CD4. Fever & wt loss
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| Erysipeloid etiology | Erysipelothrix rhusiopathiae: seen in many animals worldwide, esp hogs. Infection follows skin abrasion or puncture from contact with shellfish, meat, poultry
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| Erysipeloid clinical features | 2-7 days incubation. Skin burning, severe pain, itching. Nonpitting edema.
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| Purple erythema with sharp irregular margins extending peripherally but clearing centrally = | Erysipeloid
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| Hansen disease organism | Mycobacterium leprae: acid-fast gram-variable rod-shaped obligate intracellular bacterium. Respiratory transmission. Disease requires prolonged childhood exposure
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| 2 types of disease in Hansen | Lepromatous (more malignant & progressive; in pts without immune cellular resistance) and tuberculoid
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| Neurologic changes in lepromatous Hansen disease | Nodular skin lesions & slowly evolving symmetric nerve involvement.
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| Organs usually spared in Hansen disease | Kidneys (unless immune complex nephritis or amyloidosis occurs)
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| Bioterrorism agents in Category A | Highest priority: anthrax, botulism, plague, smallpox, tularemia, viral hemorrhagic fevers
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| Bioterrorism agents in Category B | Brucellosis, epsilon toxin of C perfringens, Salmonella, glanders, melioidosis, psittacosis, Q fever, ricin, staph enterotoxin B, typhus, viral encephalitis, water safety threats
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| Bioterrorism agents in Category C | Emerging threats: Nipah and hantavirus
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| The most poisonous substance known is: | Botulinum toxin (good thing people inject it into their faces, amirite?)
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| Glanders causative organism | Burkholderia mallei (small bipolar GN nonmotile aerobic bacillus)
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| Glanders geography | Eradicated in N Am in 1938; found in S Am, Asia, Africa
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| Glanders pathology | Infects horses, mules, donkeys (pigs & cattle are resistant), rarely humans. Mucosal / resp / skin contact w/animal
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| Glanders clinical features | 10-14 day incubation. Fever, rigors, night sweats, HA, pleuritic pain, LAD, diarrhea. Nodules into ulcers.
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| Glanders: crater-like ulcers along course of lymph vessels are called: | Farcy
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| Plague organism | Yersinia pestis: nonmotile GNR. Highly contagious by airborne transmission, rapidly fatal if untreated
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| 3 forms of plague | Bubonic (95% of cases), septicemic, pneumonic
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| Bubonic plague clinical features | Acutely swollen painful lymph node (bubo) in groin, axilla, cervical
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| Septicemic plague clinical features | DIC & gangrene in advanced disease (without bubo). Toxic, coma, extremities purpura (black death)
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| Pneumonic plague clinical features | Tachypnea, productive cough, frothy sputum, cyanosis. Fatal in hours if not treated
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| Q fever causative organism | Coxsiella burnettii (proteobacterium)
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| Q fever pathology | Inhalation of aerosols from livestock, dogs, or pigeons; or ingestion of raw milk / cheese.
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| Q fever clinical features | 7-21 day incubation. Fever, wt loss, severe HA, cough. May develop PNA, hepatitis, meningoencephalitis, IE, osteo, miscarriage
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| Most common finding in chronic Q fever | Culture-negative endocarditis
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| Smallpox pathology | Infectious dose is a few virions. Virus migrates & multiplies in lymph nodes, spleen, and bone marrow. ~12 days incubation
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| Smallpox clinical features | Prodrome: abrupt high fever, severe HA / backache. Exanthem: in 1-2 days, skin eruptions, esp palmar & plantar. Lesions develop all at once (not in crops like VZV)
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| Tularemia organism | Francisella tularensis: small nonmotile aerobic GN coccobacillus. Hardy non-spore-forming organism with thin lipopolysaccharide-containing envelope
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| Tularemia clinical features | 2-3 day incubation. Asx or sudden HA, fever, N/V. Papules -> ulcers. PNA if inhaled. Tender splenomegaly, rashes.
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| Tularemia pathology | Infection due to tick or insect bite or handling animal tissues
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| 4 families of viral hemorrhagic fevers | Filoviridae, Arenaviridae, Bunyaviridae, Flaviviridae
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| Filoviridae viruses | Ebola and Marburg
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| Arenaviridae viruses | Lassa fever and New World arenaviruses
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| Bunyaviridae viruses | Rift Valley fever, Crimean-Congo hemorrhagic fever virus
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| Flaviviridae viruses | Dengue, yellow fever, Omsk hemorrhagic fever, Kyasanur Forest disease viruses
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| These hemorrhagic fever viruses are not transmissible from person to person | Rift Valley fever and Flaviviridae
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| Neurologic changes in tuberculoid Hansen disease | Macular lesions & sudden severe asymmetric nerve involvement. 4th-5th fingers, posterior tibialis, peroneal; fine touch, temp, and pain. Proprioception & vibratory sensation are intact.
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