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Microbiology > Exam 7 (CNS, Circulatory, RES, Lymphatic Infections) > Flashcards

Exam 7 (CNS, Circulatory, RES, Lymphatic Infections) Flashcards

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1
Q

Prior to immunization, what was the leading cause of pediatric meningitis?

A
  • H. influenzae type B
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2
Q

In what locations of the heart do most infective endocarditis infections occur?

A
  • Cardiac valves (natural or prosthetic) on the mitral or aortic valves
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3
Q

Leading cause of fungal meningitis

A
  • Cryptococcus neoformans
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3
Q

Define septic shock

A
  • Severe sepsis (microbial etiology + at least two of four conditions + one ore more signs of organ failure) with hypotension (systolic less 90 mmHg)
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3
Q

Pathogen of African trypanosomiasis? Vector? Location in intracellular stage?

A
  • Trypanosoma brucei (gambiense or rhodesiense) = protozoa - Vector = Tsetse fly - No intracellular stage
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4
Q

Protozoa responsible for infections of CNS

A
  • Entamoeba histolytica - Trypanosoma brucei - Plasmodium falciparum - Opportunistic = acanthamoeba, naegleria, balamuthia - Toxoplasma gondii
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4
Q

Diseases caused/associated by/with EBV?

A
  • Infectious mononucleosis - Oral hairy leukoplakia - Burkitt’s lymphoma - Hodgkin’s disease/lymphoma - Nasopharyngeal carcinoma - Post-transplantation lymphoproliferative disorder
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5
Q

What is visceral larva migrans? Diseases caused? Symptoms? Diagnosis? Treatment?

A
  • Zoonotic disease. Infection of humans by ascarid-type nematode (roundworm), which normally infect dogs (Toxocara canis) and cats (Toxocara cati) through accidental ingestion of eggs. - Eggs hatch in intestines releasing larvae that enter bloodstream and migrate to numerous body sites. Development is arrested as humans aren’t host. Lesion develop commonly in liver, spleen, lung and eye (most common). Symptoms include fever and depend on location of larval dissemination. Lesions in brain result in epilepsy or encephalopathy. - Diagnosis: eosinophilia, serology, history, clinical presentation, no eggs - Treatment: steroids
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6
Q

Categories of CNS infections

A

1.) Affecting meninges = meningitis 2.) Affecting brain parenchyma = encephalitis

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6
Q

Patterns of bacteremia

A

1.) Transient 2.) Intermittent 3.) Continuous: infective endocarditis and catheter bacteremia

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7
Q

More likely microbial agents to cause sepsis

A
  • Bacteria - Fungi and other agents can, but less frequently
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7
Q

Pts at risk for infective endocarditis

A
  • Prosthetic valve pts - IV drug users - Immunosuppressed - HIV pts esp if IV drug user
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7
Q

Genes involved in EBV carcinogenesis

A

1.) LMP1 (latent membrane protein): CD40 homologue, which is constitutively active increasing cell growth and suppressing apoptosis 2.) LMP2: increases growth in B cells 3.) EBNA1 (Epstein Barr Virus Nuclear Antigen 1): inhibits apoptosis

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8
Q

Staph aureus. Characteristics, how does it cause sepsis/toxic shock?

A
  • G pos cocci clusters, catalase pos, coagulase pos - Sepsis/toxic shock caused by TSST-1, which is a superantigen that links APCs and T-cells leading to cytokine storm
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9
Q

LaCrosse (CA) Encephalitis Virus. Characteristics, transmission, disease caused/symptoms, endemic areas/epidemiology

A
  • Characteristics: Bunyavirus - Transmission: chipmunks/tree squirrels (reservoir) with transmission = via mosquito to humans - Disease caused: initially as non-specific summer illness with symptoms = fever, HA, nausea, vomiting and lethargy. Severe disease (50% of cases) = seizures, coma, paralysis. Less than 1% are fatal. - Endemic areas/epidemiology: primary in Midwest and Mid-Atlantic states
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10
Q

Which of the following diseases are arthropod borne? West Nile, Rabies, Eastern/Western/Venezuelan Equine encephalitis, Lymphocytic Choriomeningitis, St. Louis encephalitis, LaCrosse (California) Encephalitis and Japanese Encephalitis.

A
  • Rabies and Lymphocytic Choriomeningitis are directly transmitted from mammals to humans - The rest are arthropod borne
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11
Q

Most common cause of bacterial meningitis in infants and young children

A
  • Strep pneumoniae
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12
Q

Zygomycoses. Species, characteristics, diseases caused, pathogenesis, diagnosis, treatment, source, risk factors

A
  • Species = rhizopus, absidia, mucor - Characteristics = non-septated hyphal fungi with sporangia with spores - Diseases: a.) Rhinocerebral mucormycosis: infection in sinuses via inhalation of spores, infection extens to neighbouring tissue including brain. Symptoms: nasal congestion, blood-tinged rhinorrhea, tender sinuses, HA, fever. Progresses to facial / periorbital edema, visual disturbances, AMS, coma and death - Diagnosis: a.) hyphal elements in clinical material (broad-aseptated hyphae branching at 90 degrees) b.) culture - Treatment: amphotericin B - Source: ubiquitous in environment (soil, vegetation, food) - Risks: immunosuppression, diabetes (esp rhinocerebral mucormycosis) and burn patients. Infection rare in normal healthy individuals
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13
Q

What is the most common cause of vaccine-preventable death in US?

A
  • Pneumococcal disease (strep pneumoniae)
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13
Q

What is refractory septic shock?

A
  • Septic shock lasting more than 1 hour and not responding to fluid/pharmacologic treatment
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14
Q

Pathogen of Chagas’ disease? Vector? Location in intracellular stage?

A
  • Trypanosoma cruzi = protozoa - Vector = Reduvid bugs - Skeletal, cardiac and others
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15
Q

Naegleria. Characteristics, disease caused / symptoms, pathogenesis, diagnosis, treatment, source

A
  • Characteristics: opportunistic free living amoebal protozoa - Disease caused = primary amebic meningoencephalitis (PAM). Symptoms = fever, HA, vomiting, confusion, rapidly progress to coma and death. Typically fatal in 1 week. - Pathogenesis: intranasal inoculation - Diagnosis: observation of protozoa in biopsy/CSF - Treatment: amphotericin B may be helpful, usually cases are fatal in 1 week - Source: acquired typically by swimming in warm water (hot springs, heated pools, hot tubs). Recent outbreak associated with use of Neti pot. Most outbreaks in Southern USA
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16
Q

Granulomatous amoebic encephalitis. Caused by, symptoms, pathogenesis, diagnosis, treatment, source, risk

A
  • Caused by: Acanthamoeba, Balamuthia - Symptoms: slow onset of fever, HA, vomiting, confusion, coma and death - Pathogenesis: amoeba invade brain resulting in slow developing granuloma/ulcerative lesion - Source: fresh water - Risk: infection in AIDS pts may disseminate
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16
Q

Cardinal symptom of adult T-cell lymphoma?

A
  • Hypercalcemia
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17
Q

CMV caused/associated illnesses/diseases

A
  • Infectious mononucleosis-like illness - Cytomegalic inclusion body disease - Immunosuppressed: CMV pneumonitis, GI tract illness, GVHD, CMV retinitis
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17
Q

Babesiosis. Pathogen, characteristics, pathogenesis/life cycle, symptoms, risk factors, diagnosis, treatment, epidemiology

A
  • Pathogen: Babesia spp (microti and divergens) - Characteristics: sporozoan flagella - Pathogenesis/life cycle: tick bite transmits protozoa from reservoir = rodents and cattle - Symptoms: many asymptomatic infections a.) symptomatic = fever, chills, myalgia, hemolytic anemia - Risk factors: elderly, asplenic, immunosuppressed at high risk for symptomatic infection - Diagnosis: blood smear = Maltese cross in RBC - Treatment: atovaquone and azithromycine (or qunine and clindamycin) - Epidemiology: US (upper Midwest, New England, CA)
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18
Q

Pathophysiology underlying sepsis/septic shock

A

1.) LPS/Endotoxin (lipid A) from gram negs: binds CD14 and TLR4 on phagocytes and APCs leading to inflammation via IL-1, IL-6 and TNF 2.) Peptidoglycan or exotoxins from gram pos (eg. TSST-1 from Staph) 3.) Polysaccharides (eg. C. albicans) 4.) Teichoic acid (eg. Staph) 5.) Capsules (eg. Strep pneumo)

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19
Q

Protozoal cause of brain abscess

A
  • Entamoeba histolytic
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20
Q

Hemorrhagic skin lesions in a septic person who recently ate raw oysters is suggestive of infection by what organism?

A
  • Vibrio vulnificus
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21
Q

80 year old male with prosthatic heart valve goes to dentist for tooth extraction. You are concerned about what type of infection?

A
  • Concerned about SBE (subacute bacterial endocarditis) caused by Viridans strep group of bacteria that are normal flora of the oropharynx entering the blood stream
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22
Q

Malaria. Pathogen, characteristics, pathogenesis/life cycle, symptoms, complication, diagnosis, treatment, epidemiology

A
  • Pathogen: Plasmodium falciparum/vivax = most cases, others from ovale and malariae - Characteristics: sporozoan protozoa - Pathogenesis/life cycle: female mosquitos (Anopheles) transmit the protozoa during blood meal feeding, hepatocytic stage of life cycle and erythrocytic stages where they lyse respective cells, vivax and ovale can enter a hypnozoite stage in the hepatocytic cycle and lay dormant for years/decades becoming reactivated during immune status/physiological/stress event - Symptoms: characteristic feature = malarial paroxysm = synchronous lysis and release of merozoites from RBCs where pt presents with flu-like symptoms including fever, chills, HA and myalgias. Paroxysms dependent on species. Cold stage, hot stage, sweat stage. - Complications: anemia (most severe in falciparum infection), splenomegaly, hypoglycemia, lactic acidosis, cerebral malaria d/t microvascular occlusion by “sticky” RBCs - Diagnosis: clinical syndrome, history of travel a.) Blood smear: ring and banana/crescent-shape = P. falciparum - Treatment: no vaccines yet, antimalarial (chloroquine) for active infection and prophylactically, resistance to drug is an issue - Epidemiology: worldwide distribution: Central/S. America, Africa, Asia, transmission in US eradicated in 70s, outbreaks in US are from airports or via competent mosquito vectors feeding on human exposed elsewhere, cases in US mostly around travelled
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23
Q

Leishmaniasis (visceral). Pathogen, characteristics, pathogenesis/life cycle, symptoms, diagnosis, treatment, epidemiology

A
  • Pathogen: visceral by Leishmania donovani/infantum/chagasi - Characteristics: flagellated protozoa - Pathogenesis/life cycle: reservoirs = canines and rodents, bite of infected female sand flies transmit protozoa after blood meal, protozoa enter macrophages in human and disseminate throughout reticuloendothelial system and are found in liver, spleen, bone marrow, no antibody response as intracellular only - Symptoms: +/- lesion where bite occurred, presentation is irregular low grade fever, most infections asymptomatic and resolve. Full blown disease = fever, weight loss, hepatosplenomegaly, wasting/cachexia, immunosuppression and secondary infections leading to death in very old and young or malnourished. - Diagnosis: blood smear - Treatment: heavy metal compounds with high toxicity - Epidemiology: widespread (big issue in S. America), rare to have cases acquired in US possibly in Southern, opportunistic in HIV+ individuals of Mediterranean descent
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24
Q

Organisms responsible for toxic shock

A
  • Staph aureus via TSST-1 - Strep pyogenes via pyrogenic toxins (SpeA/B/C)
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24
Q

Pathogen of Leishmaniasis? Vector? Location in intracellular stage?

A
  • Leishmania spp. - Vector = sandflies - Macrophages
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25
Q

Pathogen of Babesiosis? Vector? Location in intracellular stage?

A
  • Babesia spp. - Vector = ticks - RBCs
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25
Q

Mechanisms underlying anemia in malaria

A

1.) RBCs lysed by mature intracellular protozoa 2.) Suppression of erythropoiesis by cytokines TNFalpha and IL-1 3.) Destruction of RBCs by spleen

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26
Q

CMV. Characteristics, pathogenesis, transmission, diagnosis, treatment

A
  • Characteristics: herpesviridae virus, enveloped, dsDNA - Pathogenesis: Binds and enter mucosal epithelium, viremia occurs, latency in monocytes - Transmission: saliva, breast milk, urine, fomites, sexual contact - Diagnosis: viral DNA from disease tissue, seroconversion - Treatment: a.) 1st line = gancyclovir (IV or oral: drug converted to DNA pol inhibitor by CMV enzymes), valganciclovir (oral: converted to gancyclovir in body has increased bioavailability, same action) – these have bone marrow toxicity and cause drug-related neutropenia b.) 2nd line (if virus resistant to 1st line drugs) = cidofivir (IV: converted to DNA pol inhibitor by enzymes) or foscarnet (IV: direct inhibitor of DNA pol) – both are more toxic than 1st line, foscarnet has renal toxicity
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27
Q

Common virulence factor(s) in bacterial causes of meningitis

A
  • Capsule - Fimbriae, pili, outer membrane proteins
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27
Q

In what cell types does EBV virus reside? What does this virus use to gain entry?

A
  • Epithelial and B-cells - Used 3d component of complement
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27
Q

In the year 2030, you develop an effective CMV vaccine. In 2040, you expect to see a dramatic reduction in disease d/t CMV infection in immunocompromised invidiuals and immunocompetent ___________. A. neonates B. school-aged children C. adults

A
  • Answer = A. neonates. Awaiting email from Nguyen with why only neonates and not all groups?
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27
Q

Viral myocarditis. Symptoms, most common causes, diagnosis, treatment, prognosis, risk, epidemiology

A
  • Symptoms: SOB, exercise intolerance, fatigue = typical presentation, also chest pain, abdominal pain, palpitations and syncope – could mimic infarction - Causes: adenovirus (types 2 and 5), enterovirus (esp coxsackievirus type B), B19 parvovirus and HHV-6. Less frequently = influenza, echovirus, mumps virus - Diagnosis: CXR, ECG and endomyocardial biopsy - Tx: manage symptoms and arrhythmias, rest and observation - Prognosis: 50% have full cardiac function restored, 25% will have ECG/CXR abnormalities w/o symptoms - Risk: CHF with unknown etiology - Epidemiology: more commonly in men
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28
Q

Are antivirals of use in HHV-8 (Kaposi’s sarcoma) infections?

A
  • No. Virus is in latent phase
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30
Q

Children (2-18 years) bacterial meningitis causes

A
  • N. meningitidis - S. pneumoniae
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31
Q

Japanese Encephalitis Virus. Characteristics, transmission, disease caused, epidemiology

A
  • Characteristics: flavivirus - Transmission: birds/livestock = reservoir and transmitted to humans via mosquito - Disease caused: encephalitis similar to WNV and St. Louis Encephalitis - Epidemiology: leading cause of viral encephalitis in Asia
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32
Q

Symptomatology associated with bacterial CNS infections

A
  • Fever, headache, stiff neck (nuchal rigidity), altered mental status - 50% of pts present with first three - Nearly 100% present with combination of two of 4
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32
Q

African Trypanosomiasis (Sleeping Sickness). Pathogen, characteristics, pathogenesis/life cycle, symptoms, diagnosis, treatment, epidemiology

A
  • Pathogen: Trypanosoma brucei (gambiense in W. Africa and rhodesiense in E. Africa) - Characteristics: flagellated protozoa - Pathogenesis/life cycle: Tsetse fly ingests them during blood meal, part life cycle within salivary gland of fly, enters human through bite site when fly refeeds, maturation in blood / lymph of human, later invasion into CNS. Protozoa expresses variable surface glycoproteins and undergoes antigenic variation, which is rapid switching of the glycoproteins to avoid absolute clearance of all organism by hosts immune system - Symptoms: more acute with E. African form a.) Early (when organism in blood and peripheral LNs): painless chancre at site of entry, fever, myalgia, chills, lymphadenopathy b.) Late (when organism in CNS): HA, seizures, tremors, encephalitis, sleeplessness, lethargy, coma and death - Diagnosis: parasite in blood smear, lymph node aspirates or CSF - Treatment: melarsoprol (highly toxic), difluoromethylornithine (DFMO) - Epidemiology: W. and E. Africa
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33
Q

A patient’s sepsis was initiated by a gram-neg bacterium. If abx were not given to the patient and three blood cultures were taken over an 8 hour period, there is a 99% chance that the gram-neg bacterium will be detected in the blood. True/False.

A
  • False. Only about 50% of pts with sepsis will have bacteremia to begin with. Idea about taking multiple cultures over time is that if the pt is bacteremic, first culture will only be about 80-90% positive, second culture 90-95% positive and third culture 99% positive.
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34
Q

An unexplained encephalitis or meningitis in summer/early fall in adults over 50 years of age should lead to suspicious of what disease(s)?

A
  • West Nile and other arboviral diseases
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34
Q

Multiorgan failure definition

A
  • Dysfunction of >1 organ AND - DIC
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35
Q

Treatment of sepsis/septic shock

A

1.) If shock, ie. With hypotension: IV fluids 2.) Hypoxia: ventilator 3.) DIC: transfuse with FFP and platelets OR heparin to stop bleeding 4.) Antibiotics: broad spectrum such as vancomycin and gentamicin to cover G+ and G-

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36
Q

What is cytomegalic inclusion body disease? Cause? Symptoms? Population affected? Risk factors? Epidemiology? Prevention? Treatment?

A
  • Congenital infection of newborn by CM - Symptoms: commonly = hepatosplenomegaly, jaundice, petechial rash. Less commonly = microcephaly, growth retardation, inguinal hernias, chorioretinitis - Population affected: commonly newborn to seronegative mother (infected with CMV for first time) - Risk factors: seronegative pregnant women infected with CMV during pregnancy – risk of transmission = 33% - Epidemiology: most common congenital viral infection - Prevention: interrupt CMV transmission - Tx: none – CMV immunoglobulin under investigation
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36
Q

Filariasis (aka elephantiasis). Pathogen, characteristics, pathogenesis/life cycle, symptoms, diagnosis, treatment, epidemiology

A
  • Pathogen: Wuchereria bancrofti an Brugia malayi - Characteristics: nematodes (roundworms) - Pathogenesis/life cycle: mosquito (including Anopheles) take up microfilariae, development in mosquito, bite human, larvae migrate into lymphatics where they develop into adults and mate releasing microfilariae, these enter bloodstream at night in hopes of mosquito feeding - Symptoms: a.) Acute = fevers, chills and lymphadenitis lasting for weeks and recur frequently b.) Elphantiasis = chronic debiliting swelling/clogging of lymphatics of upper/lower extremities and male genitalia c.) Tropical pulmonary eosinophilia = asthma attacks during to high IgE/eosinophilia - Diagnosis: eosinophilia with pulmonary involvement, clinical, microfilariae in blood (collected at night) - Treatment: DEC, steroids to counteract allergic response to dying worms, surgery if disease severe - Epidemiology: Bancrofti in Africa, Mediterranean coast, Asia, Caribbean and S/Central America. Malayi in Asia
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37
Q

True / False. Bacteremia is typically present with infective endocarditis.

A
  • True, more than 95% of cases of infective endocarditis yield positive blood cultures
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38
Q

Rabies virus (aka Lyssavirus). Characteristics, transmission, disease caused/symptoms/pathogenesis, diagnosis, treatment, endemic areas/epidemiology

A
  • Characteristics: rhabdoviridae - Transmission: reservoirs = humans and other mammals (dogs, cats, raccoons, bats) with transmission via infected saliva (bites, mucous membrane, aerosolized), most infections via infected dogs, bats, skunks and foxes; rare cases via corneal transplant - Disease/pathogenesis: virus proliferates locally, enters peripheral nerves and transported to CNS, non-specific flu-like signs (few days to more than month after incubation) = fever, malaise or headache, virus disseminates within CNS and spreads to peripheral nerves, behavioral changes (anxiety, confusion, agitation, delirium, abnormal behavior, hallucinations, insomnia) including hydrophobia (fear of water) in 50% of cases, end result is coma and death. Once clinical signs appear, disease is nearly always fatal in ~ 2 weeks. - Diagnosis: serology, confirmation of Negri bodies in animals thought to have infected human - Treatment: pooled immune globulin and 5 doses of vaccine (over 28 day period) - Endemic areas: Worldwide (except Australia, Gr. Britain and Hawaii)
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38
Q

Post-transplantation lymphoproliferative disorder (PTLD). What is it? Symptoms? Risk factors? Diagnosis? Treatment?

A
  • Abnormal proliferation of lymphoid cells in a transplant patient, benign or malignant - Symptoms = fever, fatigue, weight loss, progressive encephalopathy - Risk factors = EBV infection at time of transplant - Diagnosis: detect of EBV genome in specimen via in situ hybridization - Tx: reduce immunosuppression, rituximab anti-CD20, conventional chemo
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39
Q

Streptococcus. Characteristics, how does it cause toxic shock?

A
  • G pos cocci in pairs or chains, catalase neg - Strep pyogenes produces pyrogenic exotoxins (SpeA and SpeC), which are superantigens that bind APCs and T-cells lead to cytokine storm
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40
Q

EBV. Characteristics of virus, general pathogenesis/virology

A

1.) Characteristics: herpesviridae, enveloped, dsDNA 2.) Pathogenesis/virology - Uses 3d component of complement to gain entry into epithelial and B-cells where replication occurs - Induces proliferation of B cells, induces production of heterophile antibodies (to non-specific antigens) - Becomes latent - In carcinogenesis

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41
Q

50% of N. meningitidis invasive disease in children less than 2 years of age are due to which serotype? Why?

A
  • B. No effective vaccine
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43
Q

Fungi that cause CNS infections

A
  • Histoplasma capsulatum* - Blastomyces dermatitidis* - Paracoccidioides brasiliensis* - Coccidioides immitis* - Cryptococcus neoformans = encapsulated yeast * dimorphic: molds in environment, yeast in tissue other less commonly: Candida albicans and zygomycetes
44
Q

Pathogen of Malaria? Vector? Location in intracellular stage?

A
  • Plasmodium spp. (falciparum, vivax, ovale and malariae) - Vector = Mosquitoes (Anopheles) - RBCs and hepatocytes
45
Q

Differentiate between staph and strep toxic shock

A
  • Most pts with streptococcal toxic shock are bacteremic and many have necrotizing fasciitis.
45
Q

How to diagnose sepsis/septic shock?

A
  • Symptoms - Blood cultures (~50% are not bacteremic) – not a requisite
45
Q

Pathophysiology of bacterial endocarditis

A
  • Cardiac abnormality creates attachment site on heart - Blood contacts subendothelial factors = promotion of coagulation - Pathogens bind and activate factors creating vegetations and damage on heart valves - Vegetations can break off from heart leading to septic emboli commonly to brain, spleen or kidney
47
Q

Vector for West Nile Virus, Dengue, Yellow Fever Virus and St. Louis Encephalitis Virus?

A
  • Mosquito
48
Q

Pathogen of filariasis? Vector?

A
  • Wuchereria bancrofti and Brugia malayi = roundworms (nematodes) - Vector = mosquito (including Anopheles)
50
Q

Non-common causes of meningitis

A
  • Mycobacterium tuberculosis - Staph aureus
51
Q

Distinguish between acute bacterial endocarditis and subacute bacterial endocarditis, include most common causes of each

A
  • ABE (acute bacterial endocarditis): high fever, acutely ill, rapid damage to heart, death in weeks – most common cause = Staph aureus (more virulent) - SBE (subacute bacterial endocarditis): low grade fever, night sweats, weight loss, vague constitutional problems, slower damage to heart, death over weeks to months – most common cause = Viridans strep (less virulent)
52
Q

Streptococcus agalactiae (GBS). Characteristics, diseases (including CNS) caused, pathogenesis, diagnosis, treatment, vaccines, epidemiology/risk

A
  • Characteristics: gram pos cocci - Diseases caused: a.) Newborns: i.) early onset: during first week of life = bacteremia, pneumonia and meningitis with symptomatology: resp distress, labored breather, fever, lethargy, irritability. Permanent neurological sequela post infection ii.) late onset: one to three weeks after birth = meningitis more common, but others in early onset are possible, survival rate is higher, neuro complications more common b.) Adults: sepsis, UTIs, soft tissue infections - Pathogenesis: a.) Polysaccharide capsule: impedes phagocytosis, disrupts complement lysis - Diagnosis: a.) Culture: gram pos cocci that grow in chains, catalase neg, beta-hemolytic, bacitracin resistant, positive CAMP test b.) Serology: group B strep - Treatment: a.) Penicillin b.) Provide intrapartum antibiotics (penicillin) greater >= 4 hours before delivery to those at risk (fever, ROM greater than 18 hours, preterm, bacteuria, previous infant with GBS) - Vaccines: no vaccines, universal screening during perinatal period between 35-36 weeks gestation. - Epidemiology: higher incidence during first 90 days of newborn life, infections rates increase in elderly population, high incidence in African American population - Risk: African American, mother who is GBS carrier (in LGI/GU tract), absence of maternal antibodies, obstetric issues such as PROM/preterm delivery/intrapartum fever - mothers are GBS carriers in LGI/GU tracts which is risk factor for early onset in infants (25% more likely to deliver infants with invasive GBS), another risk factor = absence of maternal antibodies
53
Q

Haemophilus influenzae. Characteristics, diseases (including CNS) caused, pathogenesis, diagnosis, treatment, vaccines, epidemiology

A
  • Characteristics: gram neg rod - Diseases caused a.) Non-encapsulated cause (non-typeable): pinkeye, otitis media, sinusitis b.) Encapsulated cause (typeable): meningitis, epiglottitis i.) Meningitis: fever, nuchal rigidity, headache. Neurological sequelae = hearing loss - Pathogenesis a.) Encapsulated strains have polysaccharide coat. Type b has PRP (polyribitol phosphate capsule = most pathogenic. - Diagnosis a.) Culture of CSF: gram neg rod, requires chocolate agar with factors X (hemin) and V (NAD) for growth b.) Latex agglutination - Treatment: similar to other forms of bacterial meningitis, which is empiric treatment first = Vancomycin and cephalosporin. Treat appropriately after culture and sensitivity testing - Vaccines: a.) PRP conjugated, previous non-conjugated vaccine, which was poorly immunogenic
54
Q

How to differentiate strep pneumoniae from Viridans strep species?

A
  • Optochin test - S. pneumo are optochin sensitive - Viridans are optochin resistant
55
Q

Neisseria meningitidis. Characteristics, meningitis symptoms, other diseases caused, pathogenesis, diagnosis, treatment, vaccines, epidemiology

A
  • Characteristics: gram neg diplococci - Meningitis: abrupt onset of fever, nuchal rigidity, headache and AMS with accompanying septicemia symptoms: hypotension, petechial/purpuric rash, organ failure – DIC - Other diseases: bacteremia/septicemia with/wo meningitis, pneumonia, arthritis, otitis media, epiglottitis - Pathogenesis: a.) Pili: attach to epithelial cells in nasopharynx, transcytose to submucosa b.) Polysaccharide capsule: protective against phagocytosis, resist complement lysis c.) LOS (endotoxin): inflammatory response, likely facilitates entry into CNS by weakening BBB, crosses BBB in neutrophils (hematogenous spread) - Diagnosis: a.) Culture of CSF/blood: gram neg diplococci coffee or kidney-bean appearance, oxidase pos, catalase pos, glucose and maltose fermenter, requires chocolate agar with CO2 supplementation for growth b.) Anitgen detection in CSF, other serological methods - Treatment: a.) Empiric tx = vancomycin +/- cephalosporin b.) Most are susceptible to penicillin c.) Prophylactic treatment of exposed individuals - Vaccines: a.) MPV/4: tetravalent (A, C, Y, W135) polysaccharide vaccine – not effective in children less than 2 years, not part of routine vaccination, recommended for high risk groups: immune deficiency, asplenics, travelers, lab workers b.) MCV/4: tetravalent (A, C, Y, W135) polysaccharide conjugated to non-toxic diphtheria toxin, used in 11-55 year olds, currently being evaluated to younger groups - Epidemiology: epidemic in sub-Saharan Africa, outbreaks common in close quarter dwellings, invasive diseases in US caused by 5 serotypes (C, B, Y, W125, A) most commonly C, B and Y. B doesn’t have effective vaccine, there are 12 serotypes
56
Q

CSF differences between bacterial and viral meningitis

A
  • Bacterial: PMNs high, decreased glucose, increased protein, increased pressure - Viral: Monocytes/lymphocytes high, rare PMNs, normal glucose, normal or slightly increased protein and pressure
57
Q

Pathogenesis of EBV in B cells?

A
  • DNA circularizes after entry. Induces proliferation of B cells and induces production of heterophile antibodies (antibodies to non-specific antigens). Becomes latent and can reactivate and become lytic.
58
Q

Distinguish between clinical diagnosis of opportunistic protozoal CNS infection

A
  • Primary amoebic meningoencephalitis (PAM) caused by Naegleria onset is acute - Granulomatous amoebic encephalitis (GAE) caused by Acanthamoeba and Balamuthia has slower course and onset
59
Q

Leading infectious cause of neonatal morbidity and mortality

A
  • Group B strep, Strep agalactiae
60
Q

Sepsis accompanying petechial rash is suggestive of infection by what organism?

A
  • Neisseria meningitidis
61
Q

What is acanthamoeba keratitis? Treatment?

A
  • Chronic infection of cornea associated with corneal ulceration and ocular pain. It can lead to requisition of corneal transplantation or eye enucleation. It is caused by Acanthamoeba protozoa. Associated with contact lens use and homemade cleaning solutions. - Tx = topical ointment
63
Q

Differentiate between West Nile, St. Louis Encephalitis and Japanese Encephalitis Virus clinically?

A
  • Cannot
65
Q

True / False. Sepsis can occur with and without a bacteremia

A
  • True. Not a requisite to have bacteremia
66
Q

What is the most common congenital viral infection?

A
  • CMV causing cytomegalic inclusion body disease
68
Q

What are zoonoses?

A
  • Diseases of vertebrate animals transmitted to man either directly or via insect vector (arboviral = arthropod borne)
69
Q

Clinical features of bacterial endocarditis

A
  • Mnemonic: FROM JANE (Fever, Roth spots, Osler’s nodes, Murmur, Janeway lesions, Anemia, Nail hemorrhages (Splinter), Emboli) - Heart murmur (new/unchanging) - Splenomegaly - Skin lesions (petechiae, splinter hemorrhages, Osler’s nodes, Janeway lesions) - Retinal lesions (Roth spots)
71
Q

St. Louis Encephalitis Virus. Characteristics, transmission, disease caused, diagnosis, treatment, epidemiology, risks

A
  • Characteristics: flavivirus - Transmission: birds/horses = reservoir, transmitted to humans (incidental dead-end hosts) via mosquitos - Disease caused: a.) Mild disease: sudden fever with headache b.) Severe disease: sudden high fever, headache, nuchal rigidity, stupor, disorientation, coma, tremors, occasional convulsions, spastic paralysis – requires hospitalization - Diagnosis: serology - Treatment: supportive, no vaccine - Epidemiology: temperate areas of US with summer/early fall illness, in Southern US with cases all year round - Risks: high mortality in aged
73
Q

Cause of sleeping sickness

A
  • Protozoa = trypanosoma brucei
74
Q

Categories of meningitis

A

1.) Acute pyogenic (bacterial) 2.) Aseptic (viral) 3.) Chronic (any class of microbe)

75
Q

What is Infectious mononucleosis-like illness? What causes it? Symptoms? Who is affected? Diagnosis?

A
  • Caused by primary CMV infection, not reactivation - Symptoms = fever, fatigue, pharyngitis (non-exudative) - Affected = immunocompetent adults and adolescents - Diagnosis = no heterophile ab production (like EBV mono), Downey (atypical T cells) are seen
76
Q

Names of opportunistic amoeboid protozoa infections of CNS. Source of these infections?

A
  • Acanthamoeba - Naegleria - Balamuthia - Source = fresh water
77
Q

Prion diseases. Types, nature of prions, transmission, clinical presentation, diagnosis, treatment

A
  • Types: a.) Human spongiform encephalopathies: Kuru, CJD, Gestermann-Straussler-Scheinker Dz, Fatal Familial Insomnia b.) Animal spongiform encephalopathies: scrapie, transmissible mink encephalopathy, BSE (mad cow), chronic wasting dz - Nature of prions: aggregates of chemically resistant hydrophobic glycoprotein known as PrP (prion protein), with normal form superscript C (unknown functions), infectious subscript Sc. Abnormal binds to normal, induces release and conversion to abnormal. Aggregates form and are internalized by neurons. Neurons become vacuolated and amyloid plaques are deposited. - Transmission: infectious prion proteins or inherited/spontaneous mutation of PrP. Thought to be species specific, but unknown with mad cow. - Clinical presentation: slow progressive neurological degeneration, incubation is years to decades, death ensues months once symptoms appear such as loss of muscle control, shivering, jerks, tremors, behavioral changes, dementia - Diagnosis: postmortem - Treatment: no current treatment
78
Q

Transmission of EBV

A
  • Saliva
80
Q

Methods of pathogenic entry into CNS

A

1.) Hematogenous spread (bacteremia) 2.) Spread from site adjacent/contiguous with CNS 3.) Direct inoculation (surgery, trauma) 4.) Neuronal spread (typically viral)

81
Q

Lymphocytic Choriomeningitis Virus (LCMV). Characteristics, transmission, disease/symptoms caused, treatment, risk

A
  • Characteristics: arenavirus - Transmission: reservoir = rodent (incl. common house mouse), transmission to humans via inhaled aerosolized particles of rodent urine, feces or saliva or my ingesting food contaminated with virus, vertical transmission between mother and fetus - Disease: meningitis, encephalitis or meningoencephalitis a.) Biphasic illness: Febrile illness (fever, malaise, anorexia, myalgias, HA, nausea and vomiting), remission, followed by meningitis or encephalitis. Most pts recovery fully. - Treatment: supportive - Risk: vertical transmission between mother and fetus, associated with abortion and neurological deficits in newborn
82
Q

Chagas’ Disease. Pathogen, characteristics, pathogenesis/life cycle, symptoms, diagnosis, treatment, epidemiology

A
  • Pathogen: Trypanosoma cruzi - Characteristics: flagellated protozoa - Pathogenesis/life cycle: Reduvid bug ingests protozoa during blood meal and as it is filling up shed protozoa in feces, which enters the bite site or mucosa/conjunctiva, enters cells and spreads systemicatically to cardiac muscle, smooth muscle, ganglia etc. - Symptoms: a.) First sign = chagoma (local swelling) at entry site or Romaña’s sign (painless periorbital edema) if entry into eye b.) Acute phase = fever, malaise, myalgia, hepatosplenomegaly c.) Indeterminate phase = asymptomatic. Majority of individuals go into this phase. Few parasites remain in blood d/t high levels of Ab. d.) Chronic phase = infection of cardiac and myenteric plexus decades after infection = CHF, myocarditis, megacolon and megaesophagus - Diagnosis: acute = parasites in blood, chronic = serology - Treatment: ? - Epidemiology: common in S. and Central America, rare to acquire infection in US, however many living immigrants in US with parasite, concern for US blood supply
84
Q

Infant (less than 2 years) bacterial meningitis causes

A
  • S. pneumoniae - N. meningitidis
85
Q

25 yo male present to office feeling tired and feverish. No significant history other than IV drug user, using heroin regularly in last 2 months. PE revealed that pt was febrile and had a heart murmur. Splinter hemorrhages seen and fundoscopic exam revealed Roth spots. Echo demonstrated vegetation the tricuspid valve. Blood cultures were positive. What is the likely diagnosis? What bacteria are you suspicious of?

A
  • Bacterial endocarditis - Staph aureus or viridans strep are two common causes
86
Q

Most common cause of bacterial meningitis in newborn

A
  • Group B strep: S. agalactiae
88
Q

15 yo female presents with severe HA, fever, nausea, vomiting, myalgias, athralgias, disorientation and petechial rash for 6 hours. PE reveals BP 90/55, pulse 125, temp 39.4 C, lethargy alternating with restlessness, generalized purpuric rash and nuchal rigidity. LP reveals CSF that is clear with 22 WBCs, of which 75% are PMNs, increased protein, decreased glucose. Gram stain shows few gram neg cocci. a.) What is the likely pathogen? b.) What is likely pathogen if gram stain indicates gram pos cocci? c.) What might you expect if this were a neonate? d.) What might you expect if an India Ink stain were positive?

A
  • A.) N. meningitidis - B.) Strep pneumoniae - C.) Strep agalactiae - D.) Cryptococcus neoformans
89
Q

Human T-cell Leukemia/Lymphotropic Virus.(HTLV-1). Characteristics, transmission, pathogenesis, diseases/symptoms, diagnosis, treatment, epidemiology

A
  • Characteristics: retrovirus, enveloped, +ssRNA genome, cell-associated virus (CD4/8 T cells) - Pathogenesis: infects CD4/CD8 T cells, life cycle like HIV virus except they use glut-1 receptor. HAM = demyelination of neurons in spinal cord, possibly autoimmune. - Transmission: nursing, blood transfusion, sexual transmission (more efficient = male to female) - Diseases: a.) Adult T-cell lymphoma (ATL): lymphadenopathy, hepatosplenomegaly, hypercalcemia, skin infiltration (papules, plaques, ulcers) of tumor cells b.) HTLV-1 associated myelopathy (HAM) aka tropic spastic parapesis: stiff gait, lower extremity weakness, back pain, incontinence, 1/3rd patients are bedridden 10 yrs post diagnosis - Diagnosis: a.) ATL: flower cell in peripheral blood, anti-HTLV-1 antibodies - Treatment: combined chemo - Epidemiology: ATL common in Southern Japan, Caribbean, Central Africa, age of onset = 55 years of age, survival = 7 months. Childhood transmission has greatest risk for ATL. HAM has highest incidence in women.
91
Q

Slow occurring/chronic bacterial meningitis cause

A
  • Mycobacterium TB. Most history includes pulmonary disease
92
Q

Following resolution of infectious mononucleosis, latent EBV is found in what cells? A. T cells B. Memory B cells C. Sensory neurons

A
  • Answer = B. Memory B Cells
93
Q

Risk factors for sepsis

A
  • Indwelling catheters, mechanical devices, immunosuppression
94
Q

Petechial skin lesions in person bitten by tick is suggestive of what organism?

A
  • Rickettsia rickettsii, causative agent of Rocky Mountain Spotted Fever
95
Q

Hodgkin’s disease. Pathogenesis/viral involvement/cell type, symptoms, diagnosis, population affected, treatment

A
  • Pathogenesis: B-cell origin CA, 20-40% contain proliferation of EBV-infected cells (latent) - Symptoms: fever, night sweats, weight loss, neck/supraclavicular/axilla lymphadenopathy and commonly enlargement of mediastinal lymph nodes - Diagnosis: a.) Biopsy: Reed-Sternberg cell, which are large cells with two or more nuclei or lobes each containing large eosinophilic nucleolus - Population: many populations - Tx: radiation, chemo
96
Q

What is the body’s barrier to protect against CNS infections? How?

A
  • BBB: blood brain barrier - Tight junctions bw endothelial cells, epithelial cells - Cells rarely demonstrate pinocytosis, lack fenestrations or channels
97
Q

Oral hairy leukoplakia. Caused by, symptoms, population affected, pathogenesis, treatment

A
  • Caused by: EBV - Symptoms: white patches on side of tongue - Population affected: immune suppressed (eg. HIV pts) with CD4 T cell count ~ 300 - Pathogenesis: lytic EBV replication in epithelial cells - Treatment: antiherpetic drugs, podophyllin resin
98
Q

Burkitt’s lymphoma. Pathogenesis/viral involvement/cell type, symptoms, population affected, risk factors, treatment

A
  • Pathogenesis/viral involvement: endemic form highly associated with latent EBV infection, B cells: translocation of myc gene that gets placed under Ig promoter leading to cell being pushed into S phase. - Symptoms: presents often in jaw of children (in endemic form), most rapidly progressing tumor of B-cell origin - Population affected: high incidence in equatorial Africa, 20% of US cases associated with EBV - Risk factors: chronic malaria, immune suppression - Treatment: chemotherapy
100
Q

Causes of helminth infections of the CNS

A
  • Cestode (aka tapeworm): Taenia solium - Nematode (aka roundworm): Ascarid-type worms that normally infect dogs (Toxocara canis) and cats (Toxocara cati), which cause visceral larva migrans
101
Q

What diseases/viruses are associated with the following findings under microscope? A. Spindle cells B. Downey cells C. Reed-Sternberg cells D. Flower cells

A
  • A. HHV-8, Kaposi’s Sarcoma - B. EBV in infectious mononucleosis and CMV in infection mononucleosis-like illness - C. EBV in Hodgkin’s disease/lymphoma - D. HTLV-1 in Adult T-cell lymphoma (ATL)
102
Q

Typical pathophysiology of bacterial CNS infections

A
  • Inflammation d/t toxins leads to edema, increased ICP, seizures, coma and death
103
Q

Predisposing factors to meningitis

A
  • Pneumonia - Chronic otitis media - Viral URTI (breaks down respiratory barriers) - Immune system deficiency, including complement deficiencies - School/military barrack dwelling
104
Q

Streptococcus pneumoniae. Characteristics, meningitis symptoms, other diseases caused, pathogenesis, diagnosis, treatment, vaccines, epidemiology

A
  • Characteristics: gram pos cocci - Meningitis symptoms: Abrupt onset of fever, headache, nuchal rigidity and AMS. It may or may not follow clinically recognized syndrome (from other diseases it causes). - Other diseases: pneumonia, bacteremia, otitis media - Pathogenesis a.) Colonization of oropharynx with choline binding proteins b.) Pneumolysin and IgA protease prevent clearance from resp tract by destroying ciliated epithelial cells and degrading IgA. Pneumolysin may also interfere with macrophage clearance c.) Polysaccharide capsule: prevents phagocytotic destruction, protects against complement – aids dissemination - Diagnosis: a.) Culture of CSF/blood: gram pos cocci (oval/lancet, diplo in specimens, chains in liquid culture), catalase neg, alpha-hemolytic (green) on blood agar, susceptible to optochin, susceptible to bile (last tests differentiate it from other alpha-hemolytic strep) b.) Latex agglutination: detect presence of capsular antigens - Treatment: must treat empirically as meningitis is a medical emergency a.) Vancomycin + cephalosporin b.) Penicillin: 1/3rd of strains are resistant - Vaccines: a.) 23-valent: not effective in children less than 2 years of age, less effective in pneumococcal pneumonia, given to aged and greater than 2 years of age with other predisposing factors b.) 7-valent and 13-valent conjugated to diphtheria toxin - Epidemiology: higher incidence of dz in very old and very young, 90+ serotypes
105
Q

Adult (greater than 18 years) bacterial meningitis causes

A
  • S. pneumoniae - N. meningitidis - L. monocytogenes
106
Q

CMV diseases typically seen in transplant recipients, symptoms? Treatment?

A
  • CMV pneumonitis: fever, hypoxia, interstitial lung infiltrates - GI illness: diarrhea, abdominal pain, nausea, vomiting – complication = perforation and hemorrhage of GI epithelium - GVHD • these are from the transplanted organ or from latent CMV infection • Treatment = prophylaxis / preemptive
107
Q

17 yo female presents to the clinic with onset of fever, sore throat and lymphadenopathy for the past 4 days. Physical exam reveals moderately sized anterior cervical lymphadenopathy with a severely erythematous posterior oropharynx with exudate. Pt is suspected to have strep throat given here clinical presentation and is sent home with a rx for ampicillin. Pt returns to the clinic with worsening symptoms. Examination reveals the same findings as on previous visit, but also mild splenomegaly with a diffuse rash. What is the mostly like diagnosis given her return visit? Is she allergic to the antibiotic?

A
  • Pt likely has EBV. This is common occurrence when infectious mononucleosis pts are treated with abx for suspected strep pharyngitis. She likely isn’t allergic.
109
Q

Compare and contrast paralysis seen in tetanus and botulism

A
  • Tetanus = spastic paralysis - Botulims = flaccid paralysis
111
Q

Define bacteremia

A
  • Bacteria in the blood due commonly to: UTIs, respiratory infections, skin/soft tissue infections. Can occur from manipulation/trauma to body site that has normal flora (such as during brushing of teeth)
113
Q

What cancers are EBV associated with?

A
  • Burkitt’s lymphoma - Hodgkin’s disease/lymphoma - Nasopharyngeal carcinomas - Post-transplantation Lymphoproliferative Disorder (PTLD)
114
Q

Listeria monocytogenes. Characteristics, CNS diseases caused, source

A
  • Characteristics: gram pos motile coccobacillus, rod - Diseases: meningitis (neonates, older adults, immunosuppressed and pregnant women). In utero infection results in stillbirth, premature delivery with neuro sequelae in infant - Source: water, soil, feces of many animals, infection from contaminated food (milk, soft cheeses, poultry)
115
Q

Define severe sepsis

A
  • Sepsis (microbial etiology + at least two of four conditions) with one or more signs of organ failure
116
Q

Nasopharyngeal carcinoma. Which virus can be involved in this cancer? Cell origin? Symptoms? Population affected? Treatment? Risk factors?

A
  • Cancer of nasopharynx of epithelial cell origin associated with HBV latent infections. Symptoms include facial pain, fullness in sinuses/throat and hearing loss. - High incidence in SE Asian population. Treatment with chemo and radiation. Risk factors include genetics and diet.
117
Q

Infectious mononucleosis. Caused by, symptoms, diagnosis, pathogenesis, population affected, complications, treatment/prevention

A
  • Caused by: EBV - Symptoms: fever, malaise, exudative pharyngitis, splenomegaly, tender lymphadenitis - Diagnosis: a.) Monospot test: for Heterophile antibodies, which agglutinate RBCs b.) Other serology: anti-EA (early antigen) and anti-VCA IgM (viral capsid antigen) can indicate lytic infection in early part of infection. Anti-EBNA (Epstein Barr Nuclear antigen) is measure in latent infections. c.) Downey cells under microscope: atypical T cells with altered nucleus and indented cell margin - Pathogenesis: immune targeting of the lytic infected B cells - Population affected: young adults in industrialized countries - Complications: splenic rupture - Treatment/prevention: no vaccine, acyclovir inhibit viral polymerase, but no impact on outcome, rest/hydrate, avoid strenuous activity to avoid splenic rupture
118
Q

West Nile Virus. Characteristics, transmission, disease caused, treatment, epidemiology, risks

A
  • Characteristics: flavivirus - Transmission: bird = reservoir, to humans/other mammals = incidental dead-end hosts via mosquito - Disease caused: 50% of cases are neuro-invasive a.) Most infections are mild b.) West Nile Fever = sudden febrile illness with malaise, anorexia, nausea, vomiting, headache, myalgias, rash, lymphadenopathy c.) Neurological (1/150) = encephalitis and meningitis w/ fever, headache, weakness, GI disturbance, ataxia, seizures, disorientation, visual disturbances, coma and paralysis - Treatment: supportive, no vaccine - Epidemiology: to US in 1999, summer months illness - Risks: transfusions/organ transplants and breastfeeding, high risk in elderly population
119
Q

Common causative agents of bacterial/infective endocarditis (include characteristics)

A

1.) Staph aureus: Gram pos cocci cluster, catalase pos, coagulase pos 2.) Viridans strep group (S. mitis and S. salivarius): Gram pos cocci in chains or pairs, catalase neg., resistant to optochin, alpha or gamma hemolytic, typically part of normal oral flora

120
Q

Coccidiodes immitis. Characteristics, diseases caused/symptoms, pathogenesis, diagnosis, treatment, endemic areas.

A
  • Characteristics: dimorphic fungi, arthroconidia easily airborne - Diseases: 60% of individuals are asymptomatic a.) Pulmonary disease: fever, cough, night sweats, malaise, chest pain – resolves in 2 to 3 weeks b.) Meningitis: slow developing with HA, fever, nuchal rigidity and other neurological signs – occurs in 1% of infected individuals - Pathogenesis: inhalation of arthroconidia, converts into spherule (multinucleated structure with hundreds of spores) - Diagnosis: a.) antigen detection in CSF b.) serology c.) cultivation rare successful - Treatment: amphotericin B - Endemic areas: Western Hemisphere: San Joaquin Valley of CA and S. Arizona follows drought-rain-drought pattern
121
Q

Criteria for bacterial/infective endocarditis diagnosis

A
  • Mnemonic: BE FIVE PM - Major = BE (also stands for bacterial endocarditis) a.) Blood culture positive (two drawn 12 hours apart) b.) Endocardial involvement (from echo or new valvular regurg) - Minor = FIVE PM a.) Fever b.) Immunologic phenomena (Osler nodes, Roth spots) c.) Vascular findings/phenomena (eg. Emboli, Janeway lesions) d.) Echo findings (suggestive, but not definitive for major criteria) e.) Predisposition (eg. Heart condition or IV drug user) f.) Microbiologic evidence (Positive blood culture not meeting major criteria) - for diagnosis: 2 major OR 1 major+3 minor OR 5 minor
122
Q

Two major predisposing risk factors for infective endocarditis

A

1.) Susceptible cardiovascular substrate (prosthatic valve or rheumatic fever) 2.) Source of bacteremia

123
Q

Togavirus (alphavirus) encephalopathies. Types of viruses, transmission, diseases/symptoms caused, endemic areas/epidemiology

A
  • Types: a.) EEE: Eastern equine encephalitis virus b.) WEE: Western equine c.) VEE: Venezuelan - Transmission: rodents/birds and horses = reservoirs and transmitted to humans/other mammals via mosquitoes - Diseases/symptoms: a.) EEE: sudden onset fever, myalgias and headache. Many individuals progress to seizures and coma. 1/3rd with encephalitis will die, many suffer permanent brain damage. b.) WEE: most infections are asymptomatic/mild. Severe = sudden onset fever, headache, nausea, vomiting, anorexia and malaise, followed by AMS, weakness, signs of meningeal irritation. Children are worse affected than adults. Low mortality rate. c.) VEE: acute viral disease with symptoms = fever, chills, HA, nausea, vomiting, lumbosacral pain and myalgia. Severity can progress to disorientation, nuchal rigidity, convulsions, paralysis, coma and death Most infections are symptomatic. Fatality rate low. - Endemic areas/epidemiology a.) EEE: Eastern/Gulf Coast/Midwest US – outbreaks primarily in summer/fall. Equine epidemics precede human infections usually b.) WEE: Western US and Canada – cases in summer c.) VEE: South and Central American
124
Q

Cause of tetanus? Characteristics, clinical symptoms, pathogenesis, diagnosis, treatment, prevention/vaccination, source

A
  • Cause = Clostridium botulinum - Characteristics: gram pos rod spore-forming - Clinical symptoms: early signs = trismus (lock jaw), neck stiffness, difficulty swallowing, abdominal muscle rigidity. Following = spastic paralysis = generalized muscle spasms, which grow more frequent and last several minutes, death results from respiratory failure - Pathogenesis: a.) Tetanospasmis neurotoxin from vegetative cells, not spores. This is AB toxin. B binds to motor neurons and inactivates release of inhibitory NTs - Diagnosis: mostly clinical a.) Culture: gram pos anaerobe - terminal drumstick shape w/spore formation, difficult to grow b.) Toxin is bound to neurons and difficult to detect - Treatment: immunoglobulin and vaccination (with inactive tetanus toxin) with goal to remove unbound toxin. Clean and administer abx to kill vegetative cells at wounds. Supportive therapy. Binding of toxin to neurons is irreversible, so symptoms can resolve on when new axonal termini are generated. - Vaccine: TDaP, DTaP with boosters - Source: soil, feces of domestic animals, entry via wound contamination or traumatic inoculation or via umbilical stumbs in neonates
126
Q

Staph are the only bacteria that lead to toxic shock syndrome. True/False.

A
  • False. Strep organisms can cause streptococcal toxic shock syndrome
127
Q

Which of the following is the target for gancylovir? A. DNA polymerase B. RNA dependent RNA polymerase C. Protease

A
  • CMV is a herpes virus, which is DNA virus. Answer = A
128
Q

Define and provide criteria for sepsis/SIRS

A
  • Sepsis = SIRS (systemic inflammatory response syndrome) that has a proven or suspected microbiological etiology with two or more of the following conditions: a.) Fever (temp greater 38 C) or hypothermia (temp less 36 C) b.) Tachypnea (RR greater 20) c.) Tachycardia (HR greater 90) d.) Abnormal WBC count (leukocytosis or leukopenia or greater 10% immature neutrophils aka bands)
129
Q

Common bacterial causes of bacterial meningitis across all age groups

A

1.) Strep pneumoniae: Gram pos cocci – ~ 50% 2.) N. meningitidis: Gram neg cocci 3.) Group B strep (S. agalactiae): Gram pos cocci 4.) Listeria monocytogenes: Gram pos rod 5.) H. influenzae: Gram neg rod

130
Q

Consequences of bacteremia

A
  • Transient/benign - Sepsis, septic shock - Endocarditis
132
Q

Cause of botulism? Characteristics, clinical symptoms, pathogenesis, diagnosis, source

A
  • Clostridium botulinum - Characteristics: gram pos rod - Symptoms: a.) Botulism: nausea, dry mouth, blurred vision, involuntary eye movement, muscle paralysis (descends from ocular, laryngeal, respiratory, trunk, extremities). Death from respiratory paralysis. b.) Infant botulism (floppy baby): tends to be milder than botulism - Pathogenesis: a.) Not typically infection, rather an intoxication of preformed botulism toxin. Toxin = AB toxin. B blocks release of ACh from neuron terminals - Diagnosis: a.) Culture: gram pos anaerobe – terminal drumstick shape w/spore formation - Source: soil, contaminated foods (meat, fish, veggies, honey), improperly canned foods (anaerobic environment)
133
Q

Cause of cerebral malaria

A
  • Protozoa = Plasmodium falciparum
134
Q

Mumps virus. Characteristics, pathogenesis, transmission, disease/symptoms, complications, treatment, vaccine, epidemiology

A
  • Characteristics: paramyxoviridae –ssRNA, one serotype - Pathogenesis: entry into resp tract, spread to local lymph nodes, primary viremia results, spread to salivary glands/testes/ovaries/pancreas/CNS - Transmission: respiratory droplets, saliva, contaminated fomites - Symptoms: swollen tender parotid glands, sometimes submandibular swelling, prodrome = malaise / anorexia for 1-2 days. 1/5th infections are asymptomatic - Complications: meningitis, orchitis, deafness, myocarditis - Treatment: typically resolve in 10 days - Vaccine: live attenuated part of MMR(V) given IM in two dose form – after 2nd dose = 88% effective - Epidemiology: onset in adolescent groups usually, can happen in adulthood
135
Q

Describe the skin lesions commonly seen in bacterial endocarditis patients

A

1.) Petechiae 2.) Splinter lesions: red linear streaks in nail bed 3.) Osler’s nodes: painful subcutaneous nodules in pads of digits (fingers or toes) 4.) Janeway lesions: painless lesions on palms or soles of feet

137
Q

Brain abscess post trauma or surgery is likely from what pathogen?

A
  • Staph aureus
138
Q

Is CMV reactivation symptomatic in immunocompetent individuals?

A
  • Rarely
139
Q

Generalized erythroderma (sunburn-like rash) in a septic patient is suggestive of infection by what organism?

A
  • TSS with infection by Staph aureus or Strep pyogenes
140
Q

Neonatal (less than 1 month) bacterial meningitis causes

A
  • Group B strep - E. coli - Other gram neg enterics - L. monocytogenes
141
Q

Schistosomiasis. Pathogen, characteristics, pathogenesis/life cycle, symptoms, diagnosis, treatment, epidemiology

A
  • Pathogen: Schistosoma spp (mansoni, japonicum, haemotobium) - Characteristics: trematode (flatworm) - Pathogenesis/life cycle: larvae penetrate snails and undergo development, forked tail form lives in water, penetrates skin of humans, migrates to liver becoming adult, mating adults (mates for life) migrate to various locations where chronic infection results from lodging of eggs in tissue: a.) Haemotobium: to venous plexus of liver b.) Mansoni: to venous plexus of large intestine c.) Japonicum: to venous plexus of small intestine - Symptoms: a.) Japonicum/mansoni = chronic intestinal and hepatic dysfunction = portal fibrosis, portal hypertension b.) Haemotobium = hematuria, dysuria, urinary frequency, loss of bladder function, squamous cell carcinoma of bladder - Diagnosis: eggs in feces or urine - Treatment: ? - Epidemiology: S. America, Middle East, Asia, Phillipines
142
Q

CMV diseases typically seen in AIDS patients, symptoms? What is the CD4 count typically? Treatment?

A
  • CMV retinitis: blurred vision, floaters – exam indicates: white lesion with irregular necrotic border - GI illness: diarrhea, abdominal pain, nausea, vomiting - CMV pneumonitis: fever, hypoxia, interstitial lung infiltrates • CD4 counts between 50-100 • Treatment = antivirals (typically IV: cidofivir, foscarnet)
143
Q

Pathogen of schistosomiasis? Vector?

A
  • Schistosoma spp. (mansoni, japonicum, haematobium) = flatworm (trematode) - No vector. Developmental period in snails
144
Q

Toxoplasma gondii. Characteristics, diseases caused, pathogenesis, diagnosis, source, epidemiology, risk factors

A
  • Characteristics: protozoa. Oocysts found in contaminated grass and soil. Consumed by cats (definitive hosts) and livestock. Cats also consume rats/birds, which have cysts in tissue. Reproduction in cats leads to oocysts in cat feces. Livestock contain cysts in tissues. - Disease caused: a.) Toxoplasmosis: majority are asymptomatic. Symptomatic dz = flu-like = fever, HA, chills, lymphadenopathy, myalgias b.) Ocular infection (asymptomatic typically) c.) Congenital toxoplasmosis: miscarriage, stillbirth, blindness, mental retardation, neuro disorders d.) Encephalitis: in HIV/AIDS population - Pathogenesis: post ingestion, parasite differentiates and disseminates into muscle and brain, immune system walls off cyst - Diagnosis: serological, maternal and newborn testing for IgM / IgG - Source: a.) consumption of undercooked meat containing cysts b.) ingesting oocysts shed in cat feces - Epidemiology: 30-50% of world population is seropositive - Risk factors: pregnant women in contact with cats or cat litter, maternal infection in 1st trimester = up to 25% chance of fetal infection with severe disease, infection in 3rd trimester = 65% chance of fetal infection with less severe or asymptomatic dz. Immune compromised can cause reactivation, breaking open of cysts leading to encephalitis, seizures and death
145
Q

Human Herpes Virus 8 (HHV-8). Characteristics, pathogenesis, transmission, diseases/symptoms, diagnosis, treatment, epidemiology, risk

A
  • Characteristics: aka KSHV (Kaposi’s sarcoma-associated herpesvirus), herpesviridae, dsDNA, enveloped - Pathogenesis: Lesions are result of endothelial cell proliferation, virus is in latent state a.) vGPCR: IL-8 homologue b.) vIL-6: IL-6 homologue c.) K4, 4.1 and 6: chemokine homologue d.) vFLIP: apoptosis protection e.) LANA: maintenance of viral latency and binds p53 - Transmission: sexual contact, needle sharing - Disease/symptoms: a.) Kaposi’s sarcoma lesions: i.) Cutaneous lesions: pink/purple/brown, non-painful, +/- confluence. ii.) visceral lesions b.) Classic KS: rare, few lesions, rarely life-threatening c.) Endemic KS: 1.) classic like KS symptoms or 2.) aggressive form in pre-pubescent children (fatal in 3 years) d.) Transplant-related KS: immunosuppression e.) AIDS-related KS: cutaneous and visceral lesions, fatal with lung involvement. Other symptoms = fever, lymph node swelling, weight loss f.) Castleman’s disease/primary effusion lymphomas - Diagnosis: spindle cell morphology of Kaposi’s sarcoma lesion - Treatment: control immune deficiency, cannot treat with anti-herpes antivirals as virus is in latent phase, chemo/radiation/surgery - Epidemiology: spike during HIV/AIDS epidemic, classic KS associated with those of Middle Eastern / Mediterranean descent, endemic KS in equatorial Africa - Risk: immune deficiency
146
Q

Cryptococcus neoformans. Characteristics, disease caused/symptoms, pathogenesis, diagnosis, treatment, endemic areas, risk factors

A
  • Characteristics: encapsulated yeast fungus - Disease caused/symptoms: a.) Pulmonary disease: asymptomatic or mild influenza-like illness with minimal sputum production b.) Meningitis: develops slowly, intermittent bouts of HA, irritability, dizziness and other neurological symptoms present over weeks or months, acute onset in AIDS pts - Diagnosis: India Ink stain of CSF, other aspirations, skin lesions. Also cultivation and serology - Treatment: long term tx with combination amphotericin B and 5-fluorocytosine (or fluconazole), prophylactic tx = azole - Endemic areas: worldwide distribution, abundant in soil contaminated with bird droppings - Risks: 10-20% of all AIDs pts will likely become infected with C. neoformans

Microbiology (16 decks)

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