Micro 2

jdlevenson's version from 2015-06-16 22:39


Question Answer
Strongyloides larvae autoinfectionhatch from eggs laid in intestinal wall; repenetrate wall, enter blood stream.
StrongyloidesNematode; roundworm. Transmitted in soil contaminated with human feces. Larvae penetrate skin and migrate hematenously to the lungs -> aspirated -> intestine -> lay eggs, noninfectious rhabditiform larvae that migrate into the intestinal lumen to be excreted in the stool but some rhabiditiform molt directly into filariform larva and within the intestine and reinfect. AUTOINFECTION -> leading to widespread dissemination of the parasites throughout the body via HYPERINFECTION*. Can cause multiorgan dysfunction and septic shock. Occurs most in patients taking immunosuppressants or with HTLV-1 infection. Impaierd TH2 cellular immunity.
What part of immune system for helminthes/ roundwormsEos and Baso
Dx of strongyloidesLarvae in the stool as eggs and adult parasites are usually seen only in intestinal biopsies. NOT EGGS.
Cysts in stools?Intestinal protozoa like giardia and entamoeba.
Proglottids in stool?Intestinal tapeworms like taenia and diphyllobothrium.
Vibrio vs Campylobacter, how to tell differenceMedia. Vibrio –alkaline and Campylobacter not.
Since vibrio does not invade, what will you not see in stoolNo leukocytes or erythrocytes; mucus and sloughed epithelial cells instead.
Diarrhea with leukocytes with monocyte predominanceSalmonella Typhi
Diarrhea with leukocytes with neutrophil predominanceEverything else – shigella, slamonella, c. jejuni, EIEC.
Charcot-leyden crystals (eosinophil breakdown) seen in ?Intestinal parasitic infectiosn that are eosinophilic such as strong, ancylo, ascaris, toxocara, trichinella (but not giardia or entamoeba).
Intraabdominal abscess, two most likely drugs#1. Bacteriodes fragilis and # 2. E. Coli. NOT S. Aureus, which is the usual cause of abscess formation on the skin.
Argyll Robertson pupilsFail to constrict in response to light but constrict normally in response to accommodation. Probably from spirochetes damaging midbrain tectum. Pathognomonic of syphilis (I think?)
Tabes dorsalis pathogenesisDirectly damage dorsal sensory roots; secondary degeneration of dorsal columns
Tabes dorsalis clinicalSensory ataxia; lancinating pains; areflexia; neurogenic bladder with overflow incontinence*; positive Romberg
JC virus/ polyoma/ PML findingsprogressive dementia, motor deficits, visual impairment
Cryptococcus and HIV patientsSUBACUTE meningitis. Fever, malaise, headache.
Taenia solium and CNSEggs cause neurocysticercosis- multiple larval cysts develop within CNS. Headaches, seizures.
HSV encephalitis, predilection for...Temporal lobe****. Leading to aphasia, olfactory hallucinations, personality changes.
Most common cause of sporadic encephalitisHSV-1. Usually teenagers and young adults.
HSV and encephalitis, pathogenesisReactivation of latent virus living in trigem ganglion and virus’ spread along nerve into cerebral vault. Usually temporal lobe.
HSV encephalitis macroscopic brain examinationEdema and hemorrhagic necrosis of temporal lobes. Eosinophilic intranuclear inclusions in glial cells and neurons.
HSV encephalitis presentationFever, headache with viral pattern on CSF. Progresses to mental status changes, cranial nerve deficits and seizures.
Viruses that invade dorsal root sensory gangliaHSV-1, 2 and VSV.
Recurrent painful genital rash/ herpes genitaliaHSV-2 that has reactivated in sacral sensory ganglia. HSV-1 more commonly infects sensory ganglia innervating dermatomes ABOVE waist.
Shingles most common locationsThoracic or trigeminal dermatomes.
Tetanus toxin inihibitsInhibitory interneurons that regulate motor neuron, leading to unregulated action of the motor neuron and tetany.
Tetanus findingsJaw stiffness from spasmodic contraction of masseter muscle/ trismus and sustained contraction of the facial muscles producing risus sardonicus. Can extend to back and neck and even to respiratory muscles leading to resp. faiure.
Wound -> motor neuron axons vs. wound -> neuron axons -> salivary glands?Motor neuron is Tetanus vs Rabies virus travels itself from motor neuron terminal retrograde to nerves of spinal cord into cerebellum, brainstem and hippocampus and then to salivary glands.
Tetanus requires what kind of enivonrmnetAnerobic*.
Tetanus diagnosis ?History of penetrating wound and clinical features (trimus, sarconic smile, muscle spasms). Not blood cultures as disease results from toxin released from local wound.
How often is booster for Tetanus recommended?Immunization every 10 years.
Food -> systemic circulation -> peripheral nerves, what bugBotulinum toxin in adult food borne botulism.
Three types of botulinumfood-borne, wound botulism and infant botulism. All medical emergencies.
Botulinum local injections are used forFocal dystonias, achalasia and spasms (of MS and PD) and it can also be used to reduce appearance of glabellar wrinkles. Effect is only temporary since regeneration of nerve terminal occurs usually after 3 months.
Botulinum toxin, how is it released from bacteriaBacteria does not actively secrete toxin; rather, it releases toxin via autolysis.
Most common symptoms of botulinum, 3 D’sDysphagia, dysphonia and diplopia
Botulinum treatmentAntitoxin that blocks circulating toxin; it is unable to block toxin that has already gained access to nerve cells; further treated with supportive measures like intubation and mechanical ventilation
Fibrinous exudate -> systemic circulation -> cortical neuronsDiptheria toxin. From pseudomembranous exudate to blood stream and to cardiac and cerebral cortical tissues.
Neonatal meningitis causesGroup B Strep, E. Coli and Listeria. E. Coli via K1 capsule. Allows bacteria to survive in the blood stream and establish meningeal infection.
E. Coli’s K1 capsular polysacPrevents phagocytosis and complement mediated lysis. Leads to neonatal meningitis.
N. Meningitis releases LOS which is important to measure in blood beauseLOS, analgous to LPS in gram negative rods, correlates closely with morbidity and mortality. LOS causes induction of systemic inflammatory response with TNG-a and IL-6, 7
What role of capsular polysac of N MeningitidisFor group B, it is a poor immunogen and so not covered by vaccine; does not cause morbidity and mortality of disease but does assist in resisting phagocytosis.
Bugs with exotoxinsTetanus, Staph TSST and enterotoxin, Botulinum, Dipthetria and Pertussis.
Most common causes of viral meningitisEnteroviruses** as well as arboviruses and HSV2.
Rabies prodrome (hence why we do not have rabies)Fever, pharyngitis and pain around bite sites.
ALS vs PolioPolio purely LMN (anterior horn) whereas ALS UMN and LMN.
Meningoencephalitis in HIV + patientCryptococcus Neoformans
Cryptococcus neoformans is present in soil and pigeon droppings and transmitted viaRespiratory route with lungs as site of entry
CSF fluid with oligoclonal bands of virus antibodiesSubacute sclerosing panencephalitis
CSF fluid with oligoclonal IgGMS.
Efflux pumps confers resistance to which antibioticsThose that require entry into the cell to function such as tetracyclines and macrolides. (PCN functions outside of cell at peptidoglycan cell wall.
Vanco moaBinds to terminal D-alanine reisudes of cell wall glycoproteins and prevents transpeptidases from forming cross-links.
Name of penicillin binding proteins that PCN irreversibly binds toTranspeptidases, which function to cross-link peptidoglycan in bacterial cell wall. Inhibition leads to cell wall instability and bacteriolysis.
CSF viral meningitisLymphocytes (pleocytosis), normal glucose, increased protein.
White-yellow chorioretinal lesions with scattered intracranial calcifications and hydrocephalus (triad)Congenital toxoplasmosis. In-utero infection/ transmitted transplacentally. Reason pregnant women should stay away from cat litters.
Why is in-utero toxoplasmosis rare?Most healthy individuals have been already exposed to toxoplasma and are immune.
Toxoplasma leads to what complicationRing-enhancing lesion -> Seizures from brain lesions and resulting edema. Especially in HIV patients.
Toxoplasmosis treatmentPyrimethamine and Sulfadiazine
Ring engancing lesions in HIV patients, #1 is HIV but if no response to therapy after 1-3 weeks, then...Primary central nervous system Lymphoma, 2nd most common cause of ring enhancing lesions with mass effect in HIV. Diffuse large cell non-Hodgkin lymphoma of B Cell*** origin that occurs as late complication.
In CNS brain lymphoma in HIV patients, what is always foundEBV*. Recall, B-lymphocytes make up the tumor.
Aspergillus fumigatus cause sbrain abscesses in immunocompromised and especiallyNEUTROPENIC patients and transplant recepients more so than HIV patients.
Pharynx -> lymphatics -> meninges meningitisH. Flu. Infants and young children.
Pharynx -> blood -> choroid plexus -> meningesN. Meningitidis. College, etc. Remember, many are carriers in nasopharnx that are asymptomatic; only 1 in 500 develop infection.
N. Meninigitis vaccinePolysac quiadrivalent vaccine and conjugate vaccines. Made from outer polysac capsule and conjugate are made from capsular polysac antigens with diphtheria toxoid protein.
Primary lung focus -> blood -> meningesThis is the route of TB OR Strep Pneumo meningitis. Recall TB is a chronic meningitis with a lot of monocytes and infects lower meninges.
Traumatic wound -> leaking CSF -> meningesStaph aureus meningitis or CNS abscess following skull trauma or neurosurgery.
Middle ear -> contiguous tissues -> meningesStrep pneumo.
Leading cause of aseptic meningitisEnterovirus (90%)
Enterovirus confusing nameFecal oral and replicate in GI, yes, but do not cause gastroenteritis. Single stranded RNA viruses that include coxsackie, echo and polio. If accompanied by severe myalgias and asymmetric paralysis, polio.
If you are vaccinated for VZV, you are or are not protected from zoster late in lifeare not.
Children who experience chickenpox are resistant to episodes of chickenpox but not...To herpes zoster later in life.
VZV is from reactivation from whereReactivation of latent VZV from within DRG.
Botulinum toxin has what toxic effectInhibits Ach release from presynaptic neurons leading to descending skeletal muscle paralysis beginning with CNerves