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157 Cards in this Set
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manifestation of prions?
|
spongiform encephalopathies
(kuru, Creutzfeldt-Jakob dz, BSE, variant CJD) |
|
what are silver stains used to ID?
|
fungi, legionellae, pneumocystis
|
|
what is PAS used to ID?
|
fungi, amebae
|
|
what is mucicarmine used to ID?
|
cryptococci
|
|
what is the Giemsa stain used to ID?
|
campylobacteria, leishmaniae, malaria, parasites
|
|
what defenses prevent organism entry through the skin?
|
keratinized layer, low pH, presence of fatty acids
|
|
what are the normal defense mechanisms of the GI tract?
|
layer of viscous mucus, lytic pancreatic enzymes and bile detergents, mucosal antimicrobial peptides, normal flora, secreted IgA
|
|
what type of viruses are resistant to bile and digestive enzymes?
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non-enveloped viruses
|
|
what is the mechanism of gastrointestinal disease of staphylococci?
|
enterotoxins released in contaminated food
|
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what is the mechanism of gastrointestinal disease of V. cholerae and ETEC?
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multiply inside mucous layer overlying gut epithelium and release exotoxins that cause epithelium to secrete large amts of fluid
|
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what is the mechanism of gastrointestinal disease of Shigella, Salmonella, and Campylobacter?
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invade and damage intestinal mucosa and lamina propria and cause ulceration, inflammation and hemorrhage --> dysentery
|
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what is the mechanism of gastrointestinal disease of Salmonella typhi?
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passes from damaged mucosa thru Peyer patches and mesenteric LNs and into blood, resulting in systemic infection
|
|
what is the mechanism of respiratory disease of influenza virus?
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hemagglutinin proteins bind to sialic acid on epithelial cells, which leads to phagocytosis where the virus replicates, then neuraminidase cleaves sialic acid to release it from the cell
|
|
which bacteria can impair respiratory ciliary activity?
|
H. influenzae, Bordetella pertussis, M. pneumoniae
(P. aeruginosa can cause infxn in pts with CF) |
|
infections common in pts with CF?
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respiratory infxns with P. aeruginosa, S. aureus, Burkholdaria cepacia
|
|
granulomatous inflammation is usually evoked by what type of infectious agents?
|
ones that resist eradication and are ca[pable of stimulating strong T cell-mediated immunity
E.g. M. tuberculosis, Histoplasma, schistosome eggs |
|
acute diffuse mononuclear interstitial inflammation is often a response to what?
|
viruses, intracellular bacteria or intracellular parasites
|
|
what characterizes cytopathic-cytoproliferative reactions and what is the usual cause?
|
cell necrosis or cellular proliferation, usually with sparse inflammatory cells
|
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mechanisms of immune evasion?
|
1. growth in inaccessible areas
2. antigenic variation 3. resistance to innate immune defenses 4. impairment of effective T cell antimicrobial responses |
|
what characterizes necrotizing inflammation and what is the usual cause?
|
severe tissue necrosis w/o inflammation
caused by rampant viral infection (fulminant HBV), secreted bacterial toxins (C. perfringens), or direct protozoan cytolysis of host cells (E. histolytica) |
|
what viruses are specific to the respiratory tract?
|
adenovirus
rhinovirus influenza A/B RSV |
|
what viruses are specific to the GI tract?
|
mumps
rotavirus norovirus hepatitis A-E |
|
what viruses are systemic w/ skin eruptions?
|
measles
rubella VZV HSV1/2 |
|
what viruses are systemic with hematopoeitic disorders?
|
CMV
EBV HIV1/2 |
|
what are the species of arboviral and hemorrhagic fevers
|
dengue virus
yellow fever virus |
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what viruses cause skin/genital warts?
|
papillomavirus
|
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what viruses are specific to the CNS?
|
poliovirus
JC virus |
|
cell surface receptors of measles (rubeola)?
|
CD46 (complement regulatory protein that inactivates C3 convertases)
SLAM (involved in T-cell activation) |
|
blotchy, red-brown rash on face, trunk, limbs; ulcerated mucosal lesions in mouth near Stensens duct; follicular hyperplasia and germinal centers in lymph organs; multinucleated cells w/ eosinophilic nuclear and cytoplasmic inclusion bodies?
|
Measles (rubeola)
(paramyxovirus) |
|
B/L enlarged parotid glands; possible involvement of testes, pancreas, CNS; lesions show interstitial edema, diffuse macrophage, lymphocyte, and plasma cell infiltrates?
|
Mumps
(paramyxovirus) |
|
usually asxs, but can invade CNS, replicate in motor neurons of spinal cord or brain stem, causing muscular paralysis or respiratory paralysis?
|
Poliovirus
(unencapsulated RNA enterovirus) |
|
What is an arbovirus?
|
arthropod-borne virus
|
|
birds are major reservoir; usually asxs, but 20% mild fever, HA, myalgia, 50% maculopapular rash; carries risk of CNS complications w/ acute flaccid paralysis; CCR5 is essential for host immune defense
|
West Nile virus
|
|
infxns w/ fever and hemorrhage; wide range of presentations from fever, HA, myalgia, rash, neutropenia, thrombocytopenia to severe hemodynamic deterioration; usually infect endothelial cells
|
Viral hemorrhagic fevers
(enveloped RNA viruses: arenavirus, filovirus, bunyavirus, flavivirus) |
|
replication in skin and mucous membranes at site of entry causes vesicular lesions; lesions show multinucleated cells with pink-purple intranuclear inclusions visible on Tzanck smear?
|
Herpes simplex virus
|
|
which viruses are the α-group chronic latent infections?
what cells infected? |
HSV 1/2, VZV
infect epithelial cells and latent infxn in neurons |
|
what are the lymphotropic β-group viruses?
|
CMV, Human herpes virus 6 (causes exanthem subitum), Human herpes virus 7
|
|
what are the γ-group viruses?
|
EBV, KSHV (HHV-8; cause of Kaposi sarcoma)
Latent virus is in lymphoid cells |
|
infxn with rash starting on trunk, spreading to head and limbs, progresses rapidly from macule to vesicle?
|
VZV
latent virus in sensory ganglia |
|
latently infect monocytes, reactivated when immunity is depressed; asxs or mononucleosis-like infxn in normal pts, severe systemic infxn in neonates and immunocompromised; cells are large w/ large purple inclusions surrounded by clear halo
|
CMV
|
|
most common opportunistic pathogen in AIDS pts?
how does it manifest in these pts? |
CMV
mononucleosis-like illness: fever, atypical lymphocytosis, lymphadenopathy, hepatomegaly, mild hepatitis |
|
how does CMV avoid host defenses?
|
downmodulating MHC I and II moelcules and producing homologues of TNF receptor, IL-10 and MHC I molecules
|
|
what determines whether a person will resolve or be a carrier after HBV infection?
|
the effectiveness of the CTL response
|
|
benign lymphoproliferative dz w/ fever, sore throat, lymphadenopathy, splenomegaly, increased WBC (especially large, atypical lymphocytes); B-cells are reservoir of latent infxn; may be associated with B-cell lymphoma in immunocompromised
|
EBV
|
|
EBV-associated Burkitt lymphoma is associated with what mutation?
|
translocation of the c-myc oncogene into the immunoglobulin heavy chain region
|
|
pyogenic, G+ cocci; grow in clusters
|
staphylococci
|
|
what are the virulence factors of S. aureus?
|
surface proteins that allow binding to host endothelial cells
polysaccharide capsule resist phagocytosis enzymes that degrade host proteins (lipase - skin abscesses, protein A binds Fc on Ig's to avoid Ab-mediated killing) Hemolysins (damage membranes) Exfoliative toxins (induce skin sloughing by degrading desmoglein 1 which holds epidermal cells together) Enterotoxins (vomiting) Superantigens (shock) |
|
what kind of pts do less virulent staphylococci infect?
|
catheterized pts, pts w/ prosthetic heart valves, or IV drug abusers (S. epidermidis)
Urinary tract infections (S. saprophyticus) |
|
facultative or obligate anaerobic G+ cocci growing in pairs or chains; cause suppurative infxns of skin, oropharynx, lungs, and heart valves
|
Streptococci
|
|
how are β-streptococci classified?
|
according to their CHO (Lancefield) antigens
|
|
what are the β-streptococci?
|
S. pyogenes (Group A)
S. agalactiae (Group B) |
|
pathogen that causes pharyngitis, scarlet fever, erysipelas, impetigo, RF, TSS, glmerulonephritis
|
S. pyogenes
|
|
pathogen that colonizes female GU tract, causes sepsis and meningitis in neonates and chorioamnionitis in pregnancy
|
S. agalactiae
|
|
what are the α-streptococci?
|
S. pneumoniae
S. viridans group |
|
pathogen that is common cause of adult community-acquired pneumonia and meningitis
|
S. pneumoniae
|
|
pathogen that is normal oral flora, causes dental caries and endocarditis
|
S. viridans (S. mutans = caries)
|
|
Pathogens that are often abx resistant and cause endocarditis and UTIs
|
Enterococci
|
|
Special virulence factors of S. pyogenes?
|
M protein (prevents bacteria from phagocytosis)
C5a peptidase (degrades chemotactic complement) Pyrogenic exotoxin (causes fever and rash in scarlet fever) |
|
Virulence factor of S. pneumoniae?
|
Pneumolysin (cyosolic bacterial protein released on cell disruption which lyses host cell membranes and activates classical pathway of complement activation)
|
|
How does S. mutans cause caries?
|
metabolizes sucrose to lactic acid and secretes HMW glucans that promote bacterial aggregation
|
|
what differentiates infxns by Staph and Strep?
|
diffuse interstitial neutrophilic infiltrates w/ MINIMAL host tissue destruction
|
|
G+ rod w/ clubbed ends that causes disease characterized by durable membrane at the site of growth in oropharynx, exotoxin-mediated damage to heart, nerves, and other organs
|
C. diptheriae
|
|
necrosis of epithelium by this pathogen causes production of a dense fibrinosuppurative exudate resulting in a tough, dirty gray to black, superficial membrane in airway
|
C. diptheriae
|
|
virulence factor of C. diphtheriae?
|
phage-encoded A-B toxin
B binds cell and allows entry of A A inactivates EF-2 via ADP-ribosylation, blocking protein synthesis release of toxin in pharynx causes epithelial necrosis w/ fibrinosuppurative exudate |
|
Is there immunization against C. diphtheriae?
|
Yes, but does not protect against infxn, only against lethal effects
|
|
G+ facultative intracellular rod; food-borne sepsis and meningitis in elderly and immunosuppressed, placental infections, granulomatosis infantiseptica; identified by finding bacteria in CSF, exudative inflammation w/ neutrophils.
|
Listeria monocytogenes
|
|
virulence factors of L. monocytogenes?
|
bind to E-cadherin on epithelial cells and are internalized; use listeriolysin O and two phospholipases to escape phagolysosome; ACTA induces actin polymerization to propel bacteria into adjacent cells
|
|
what can happen with Listeriosis in pregnant women?
|
amnionitis which can cause abortion, stillbirth or neonatal sepsis (granulomatosis infantiseptica)
|
|
what macrophage activator is crucial to killing of L. monocytogenes?
|
IFN-γ
(IFN-γ-activated macrophages kill phagocytosed listeria, C3-activated macrophages do not) |
|
Spore-forming G+ rod common in animals that have had contact with contaminated soil; lesions exhibit necrosis w/ neutrophils and macrophages and large, boxcar-shaped extracellular bacteria in chains
|
B. anthracis
|
|
Syndromes produced by anthrax?
|
Cutaneous: painless, pruritic papules --> edematous vesicles --> black eschar
Inhalational: release of toxins causes hemorrhagic mediastinitis; prodromal fever, cough, and chest/abd pain rapidly leads to sepsis, shock, death GI: n/v, abd pain --> severe, bloody diarrhea, death |
|
Virulence factors of anthrax?
|
A-B toxin: B = protective factor (binds host cell)
A = edema factor (converts ATP to cAMP --> water efflux) or lethal factor (protease that kills cells by destroying mitogen-activated protein kinase kinases) |
|
aerobic, G+, grows in branched chains; cause opportunistic indolent respiratory infxn w/ CNS dissemination mostly in pts T-cell immune deficiency
|
Nocardia asteriodes
|
|
pathogen that causes indolent illness with fever, weight loss, and cough; arrange in branching filaments, stain with modified acid-fast stains; sites of infection have suppurative response with central liquefaction and surrounding granulation and fibrosis (w/o granulomas)
|
Nocardia asteroides
|
|
Major aerobic G- bacterial infections
|
Neisseria
Whooping cough (B. pertussis) Pseudomonas aeruginosa Plague (Yersinia pestis) Chancroid (Hemophilus ducreyi) Granuloma inguinale (Klebsiella granulomatis) |
|
small, G- aerobic diplococci; cause suppurative, bacterial meningitis esp in <2 y.o., invasive dz occurs in crowded conditions
|
Neisseria meningitidis
|
|
What confers increased risk of Neisseria meningitis?
|
C5-C9 complement deficiencies
|
|
In males, causes symptomatic urethritis; in females, often asxs, can lead to PID; in neonates, can cause blindness; usually manifests in genital or cervical mucosa, pharynx or anorectum
|
N. gonnorhoeae
|
|
Prevention of gonorrheal blindness in neonates?
|
otic drops of silver nitrate or antibiotics
|
|
Neisseria: mechanism of immune evasion?
|
antigenic variation of surface attachment proteins (pili proteins and OPA proteins)
|
|
disseminated infection of this pathogen causes septic arthritis accompanied by a rash of hemorrhagic papules and pustules
|
N. gonorrhoeae
|
|
G- coccobacillus that causes a laryngotracheobronchitis that causes bronchial mucosal erosion, hyperemia and copious mucopurulent exudate w/ peripheral lymphocytosis resulting in violent paroxysms of coughing
|
Bordetella pertussis
|
|
Virulence factors of B. pertussis?
|
virulence factors coordinated by BVGS transmembrane protein; pertussis toxin ADP-ribosylates and inactivates guanine nucleotide-binding proteins, resulting in failure in transmitting signals from host plasma membrane receptors thus paralyzing cilia.
|
|
Opportunistic, aerobic G- bacillus; frequently seen in CF, burns, or neutropenia; in neutropenic pts, can cause extensive necrosis by vascular invasion w/ subsequent thrombosis
|
P. aeruginosa
|
|
virulence factors of P. aeruginosa?
|
Pili and adherence proteins (bind to epithelial cells and lung mucin)
Endotoxin Exotoxin A (inhibits protein sythesis by ADP-ribosylating EF-2) Exoenzyme S (ADP-ribosylates RAS and G proteins that regulate cell growth and metabolism) Alginate (forms slimy biofilm to protect it from Ab, complement, phagocytes, and abx) |
|
Which bacteria use exotoxin A?
|
Corynebacterium diphtheriae and Pseudomonas aeruginosa
|
|
Necrotizing pneumonia in terminal airways in a fleur-de-lis pattern with pale centers and red, hemorrhagic peripheral areas along with G- vasculitis w/ thrombosis and hemorrhage suggests what pathogen?
|
P. aeruginosa
|
|
G- facultative intracellular bacteria that proliferate in lymphoid tissue; cause ileitis, mesenteric lymphadenitis, pneumonia, sepsis w/ neutrophilia
|
Yersinia (pestis, enterocolitica, pseudotuberculosis)
|
|
Acute, ulcerative genital infxn, most common in Africa and SE Asia
|
Chancroid (Hemophilus ducreyi)
|
|
histological appearance of ulcer formed by chancroid?
|
contains neutrophils and fibrin w/ underlying zone of granulation tissue, necrosis, and thrombosis and lymphoplasmacytic infiltrate
|
|
sexually transmitted minute, encapsulated coccobacillus; endemic in tropical and subtropical regions; untreated leads to scarring, associated with lymphatic obstruction and elephantiasis of external genitalia
|
Klebsiella granulomatis (Granuloma Inguinale)
|
|
slender, aerobic, acid-fast rods growing in straight or branching chains
|
Mycobacterium
|
|
what increases the risk of Tb?
|
poverty, overcrowding, chronic debilitating illness, diabetes, Hodgkin lymphoma, chronic lung dz (particularly silicosis), chronic renal flr, malnutrition, alcoholism, immunosuppression
|
|
When will PPD detect active Tb infection?
|
2-4 wks after initial infection
|
|
what does a positive PPD indicate?
|
pt has T cell-mediated immunity to mycobacterial antigens; does not differentiate between infection and disease
|
|
causes of false negatives in PPD?
causes of false positives in PPD? |
False Neg: some viral infxns, sarcoidosis, malnutrition, Hodgkin lymphoma, immunosuppression, overwhelming active Tb disease
False Pos: infxn by atypical mycobacteria, prior vaccination with BCG |
|
What are the primary cells infected by M. tuberculosis?
|
Macrophages
|
|
Progression of normal M. tuberculosis infxn?
|
1. bacteria enter macrophages because macrophages bind bacterial lipoarabinomannan
2. bacteria block phagosome-lysosome fusion and proliferate 3. 2-4 wks after infxn, T cells specific to M. tuberculosis proliferate and make IFN-γ 4. IFN-γ activates macrophages to kill bacteria via N2O synthase |
|
what are the characteristic pathologic manifestations of Tb?
|
caseating granulomas and cavitation
|
|
Fosamax
|
Alendronate
a-LEN-droe-nate |
|
what is "secondary" Tb?
how is it characterized? |
pattern of dz arising in a previously sensitized host;
insidious onset of wt loss, low grade fever, and night sweats; increasing amts of mucoid to purulent sputum, 50% have hemoptysis |
|
What is the Ghon complex? With what is it associated?
|
lung and draining lymph node granulomas
associated with primary Tb |
|
what manifestation of Tb is more common in advanced HIV?
|
extrapulmonary involvement
|
|
Common environmental bacteria causing widely disseminated infxn characterized by abundant acid-fast organisms in macrophages of immunocompromised hosts?
|
M. avium-intracellulare Complex
|
|
What is the result of systemic arterial dissemination of M. tuberculosis to peripheral organs, meninges, and bone marrow?
|
Systemic miliary tuberculosis
|
|
slowly progressive infxn that affects skin and peripheral nerves (due to bacteria growing only in cooler tissues of the periphery); results in disabling deformities?
|
Leprosy (M. leprae)
|
|
Insidious infxn leading to dry, scaly skin lesions lacking sensation, w/ asymmetric peripheral nerve involvement; on microscopy, few bacteria are found?
|
Tuberculoid leprosy
|
|
Systemic infxn with disfiguring cutaneous thickening and nodules, w/ nervous system damage d/t bacterial invasion into perineural macrophages and Schwann cells; on microscopy, aggregates of lipid-laden macrophages and abundant bacteria?
|
Lepromatous (anergic) leprosy
|
|
What determines which kind of leprosy an infected individual will have?
|
T-helper lymphocyte response
(tuberculoid = Th1 cells make IL-2 and IFN-γ; lepromatous = weak Th1 response followed by ineffective Th2 response) |
|
neuronal involvement dominates which type of leprosy?
|
Tuberculoid
|
|
G-, slender corkscrew-shaped bacteria with axial periplasmic flagella?
|
Spirochetes
|
|
Infxn characterized by development of firm, nontender, raised red lesion on site of infxn 3 wks after inoculation; bacteria are present in the lesion and exudate has infiltrate of plasma cells, macrophages, lymphocytes and proliferative endarteritis
|
Primary syphilis
|
|
5-13 wks after inoculation, cutaneous spread of this pathogen causes maculopapular, scaly or pustular lesions on the palms or soles of feet, condylomata lata, and silvery-gray erosions of mucous membranes, all of which are painless; also lymphadenopathy, mild fever, malaise, wt loss
|
Secondary syphilis
|
|
chronic infection that can cause aortic valve insufficiency and aortic aneurysms, chronic meningovascular dz, tabes dorsalis, general paresis; increased inflammatory cells, protein, or decreased glucose in CSF
|
Tertiary syphilis
|
|
Disease associated with necrotic, rubbery masses which form in bone, skin and oral mucosa
|
Benign tertiary syphilis
|
|
Risks associated with congenital syphilis?
|
intrauterine death, perinatal death, nasal discharge and congestion, sloughing of the skin, hepatomegaly, skeletal abnormalities
|
|
When can VDRL and RPR detect syphilis infection?
When do they become negative? |
4 to 6 wks after infection
Tertiary syphilis |
|
What is the best test for detection of early syphilis infection?
|
immunofluorescence of chancre exudate
|
|
what sx is seen in all stages of syphilis?
|
endarteritis (inflammation of arterial inner lining; endothelial cell activation and proliferation --> intimal fibrosis)
|
|
the triad of interstitial keratitis, Hutchinson teeth, and 8th nerve deafness are the late manifestations of what disease?
|
congenital syphilis
|
|
What pathogen is transmitted by body lice or ticks and is clinically manifested by shaking chills, fever, HA, and fatigue, followed by DIC and multi-organ failure?
|
Borrelia recurrentis (relapsing fever)
|
|
what pathogen causes an erythematous papule with a pale center with fever and lymphadenopathy during the acute phase; skin lesions, migratory arthralgias and myalgias, arrhythmias and meningitis during the second stage; and chronic, destructive arthritis and encephalitis in the late chronic stage?
|
Lyme disease (Borrelia burgdorferi)
|
|
what is the usual cause of abscesses?
|
commensal bacteria from adjacent sites, usually anaerobic>aerobic
|
|
G+, anaerobic bacilli that cause cellulitis and myonecrosis of wounds, food poisoning and small bowel infection?
|
Clostridium perfringens, C. septicum
|
|
this pathogen proliferates in wounds and causes spastic paralysis
|
Clostridium tetani
|
|
MOA of tetanospasmin?
|
blocks release of GABA
|
|
pathogen that grows in canned foods and releases a toxin that blocks release of ACh leading to repiratory and skeletal paralysis
|
Clostridium botulinum
|
|
important toxin of C. perfringens and MOA?
|
α-toxin
degrades lecithin (component of cell membranes), thus destroying RBCs, PLTs, muscle cells, can also cause nerve sheath damage |
|
MOA of botulinum toxin?
|
blocks synaptobrevin which mediates fusion of NT-vesicles with neuron membrane, thus preventing ACh release at the neuromuscular junction
|
|
small, G- obligate intracellular bacteria that may be asxs or may cause urethritis, epididymitis, prostatitis, PID, pharyngitis, conjunctivitis, perihepatic inflammation and proctitis
|
Chlamydia trachomatis
|
|
which serotypes of chlamydia cause urogenital infections and inclusion conjunctivitis?
|
D through K
|
|
which serotypes of chlamydia cause lymphogranuloma venereum (chronic, ulcerative disease in Asia, Africa, Caribbean and S. America)?
|
L1, L2, and L3
|
|
which serotypes of chlamydia cause trachoma (ocular infection of children)?
|
A, B, and C
|
|
G-, intracellular bacilli that cause epidemic typhus, scrub typhus erlichiosis and spotted fever?
|
Rickettsiae
|
|
Type of Rickettsial infxn with lesions that range from a rash w/ small hemorrhages, to skin necrosis and gangrene w/ internal organ hemorrhages
|
Epidemic typhus (R. prowazekii)
|
|
Pathogens that predominantly infect vascular endothelial cells causing vascular leakage from endothelial damage, resulting in hypovolemic shock w/ peripheral edema, pulmonary edema, renal failure and CNS manifestations
|
Rickettsiae
|
|
which organisms proliferate in endothelaila cells, causing endothelial swelling, thrombosis and vessel wall necrosis (manifesting as gangrene of tips of fingers, nose, earlobes, scrotum, penis and vulva), w/ a perivascular cuff of mononuclear inflammatory cells?
|
Typhus and spotted fever (Rickettsiae)
|
|
What disease is caused by infection of neutrophils or macrophages and manifests as fever, HA, malaise, progressing to respiratory insuff., renal failure, and shock?
|
Erlichiosis (Rickettsiae transmitted by ticks)
|
|
this infxn causes a hemorrhagic rash over the entire body, including palms and soles, and is common in SE and south-central US?
|
Rocky Mountain Spotted Fever (Rickettsia rickettsii)
|
|
candida produces what diseases in healthy ppl?
|
vaginitis and diaper rash
|
|
who is susceptible to superficial candidiasis?
|
burn victims, diabetics
|
|
fungus that is spore at 20degC, forms germ tubes at 37degC; pseudohyphae
|
candida
|
|
heavily encapsulated monomorphic yeast that causes meningitis that appear as soap-bubble lesions in the brain; found in soil, pigeon droppings
|
cryptococcus
|
|
mold that causes pulmonary allergy in healthy ppl, serious sinusitis, pneumonia and invasive dz in IC; septate hyphae branching at acute angles
|
aspergillus
|
|
Mold with irregular nonseptate hyphae branching at wide (90+ deg) angles; cause dz in ketoacidotic diabetics and leukemic pts
|
mucor
|
|
intracellular protozoa that causes cyclic fever, anemia, cerebral sxs, renal flr, pulmonary edema, splenomegaly; first invades hepatocytes, then ruptures and infects RBCs
|
Plasmodium
|
|
protozoa that parasitizes RBCs and causes fever and hemolytic anemia; transmitted by ixodes tick; in RBC, has ring stages, Maltese cross
|
Babesia
|
|
intracellular protozoa transmitted by sandfly; causes chronic inflammatory dz of skin, mucous membranes; visceral dz has spiking fevers, hepatosplenomegaly, pancytopenia; macrophages contain amastigotes
|
leishmania
|
|
extracellular protozoa that cause recurring fever, enlarged LNs, splenomegaly and progressive brain dysfxn --> death; red-rubbery chancre at site of insect bite
|
Trypanosoma
|
|
intracellular protozoa that uses cell lysosome to activate; causes dCM, megacolon, megaesophagus, predominantly in S. America
|
Chagas dz (Trypanosoma cruzi)
|
|
Nematode whose larvae in soil penetrate skin --> lungs --> trachea --> mucosa of intestines cause vomiting, diarrhea, anemia, can autoinfect
|
Strongyloides
|
|
Ingestion of this helminth larvae in pork --> cysticercosis, neurocysticercosis, mass lesions in brain, also found in muscles, skin, heart
|
Taenia solium
|
|
eggs in dog feces; hatch in duodenum; can cause cysts in liver, lungs, or bones
|
Echinococcus granulosus (hydatid disease)
|
|
nematode from undercooked meat, usually pork; causes inflammation of muscle (coiled larvae encyst in striated muscle), periorbital edema
|
trichinella spiralis
|
|
snails are host of this parasite, cercariae penetrate skin, cause granulomas, fibrosis, inflammation of spleen and liver
|
Schistosoma
|
|
nematode transmitted by mosquito, causes blockage of lymphatic vessels --> fibrosis, hyperkeratosis (elephantiasis)
|
Wuchereria bancrofti (lymphatic filariasis)
|
|
nematode transmitted by black flies; causes hyperpigmented, chronically itchy skin and "river blindness"
|
Onchocerca volvulus
|