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Infectious Disease 2
Infectious Disease
| Question | Answer |
|---|---|
| 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:
Abarnard
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