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Infectious Disease 2

Infectious Disease

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