WEEK 4: MicroPara Correlates Flashcards
Bacterial etiologic agents that is usual in neonates?
E coli
Listeria monocytogenes
Strep agalactiae
Bacterial etiologic agents that is usual in 6 mos to 6 years old?
H. influenza serotype B
why is Hib the most virulent among A to F?
because it has pentose and others have hexoses
Bacterial etiologic agents that is usual in >6 years old?
Streptococcus pneumoniae
Neisseria meningitidis
CSF Features of bacterial meningitis?
High WBC with neutrophilic predominance
High protein (>150 pag preterm and premature; >100 pag term)
CSF sugar is 60-75% of RBS
Low glucose concentration (<20 in preterm, <30 in term)
leading causes of
meninigitis in infants
E.coli and group B streptococci
What antigen is present in E coli in meningitis?
K1
In PCR, we are not able to detect the fragments of the virus
F. we are able.
Granulomatosis infantiseptica
• 1st 4 days of life
Causes the “’Crib Death”
• To manipulation of host cell action (actin) to propel it into
pseudopods that extend to adjacent host cells.
• Spreads from cell to cell with minimal contact with the host
immune system.
Listeria monocytogenes
• Immunocompetent and healthy children-consider if no
response to 1st line agents.
• Pregnancy- abortion, preterm birth, amniositis
• Neonates- late onset meningitis, conjunctivitis and
pneumonia.
• Immunocompromised- CNS infection, endocarditis, and
sepsis.
• Previous healthy and immunnocompetent children- rare,
associated with severe complications and high mortality rate.
Listeria monocytogenes
what drug passes through the BBB?
2nd Gen Cephalosporin
• Spore-forming toxins
• Sialic acid-rich capsular polysaccharide
• Surface proteins-interacts with human epithelial cells, binding
to extracellular matrix components, and/or evasion of host
immunity.
Streptococcus agalactiae (GBS)
Cleaves IgA present in the surface of mucosa, in moist
areas.
IgA protease
increases the virulence by participating
actively in the host invasion.
Lipooligosaccharide
Capsule • Adhesion proteins • Pili • The outer membrane proteins • igA protease
Hib
T or F? Fastidious organisms are difficult to isolate in cultures.
True
Identify if endotoxin or exotoxin?: Fever, DIC, Shock
Endotoxin
Identify if endotoxin or exotoxin: no fever, incubation period is shorter
Exotoxin
Mech of resistance of N. Meningitidis?
Penicillinase production and they cleave penicillin
Adrenal gland failure due to bleeding into the adrenal glands, commonly caused by severe bacterial infection- typically by Neisseria meningitidis.
• DIC leads to massive bleeding into one or (usually) both adrenal glands.
WATERHOUSE-FRIDERICHSEN
consumption coagulopathy, all of clotting factors are consumed.
DIC
is the most common form of CNS tuberculosis and has very high morbidity and mortality
TB meningitis
TB meningitis pathophy?
TB travels through the bloodstream to the meninges where small abscesses (called microtubercles) are formed. When these abscesses burst, TB meningitis is the result.
The typical patient will present with several weeks of headache, fever, and a subacute alteration in mental status.
TB meningitis
Stages of TB meningitis?
Stage 1 - alert
Stage 2 - lethargic
Stage 3 - coma
bacterial work up TB meningitis?
CSF GS/CS India ink AFB Cell count Differential count
If all workup for bacterial meningitis is negative but the pt has signs and symptoms, what is the dx?
Aseptic meningitis
T or F? CSF values are panic values because CSF is sterile.
T
what do we use when we culture fastidgious organism?
Chocolate agar plate
presence of encapsulated yeast cells indicate what in the India Ink?
Cryptococcus. we cannot conclude yet.
C. neoformans - for immunocompromised
C. Gatii - for immunocompetent
In CSF collection, what do we measure first?>
opening pressure in manometers
In CSF collection, what do we get in bottle 1?
CSF Proteins, sugar, LDH
In CSF collection, what do we get in bottle 2?>
Bacteriology
In CSF collection, what do we get in bottle 3?
cell diff count.
kasi need natin kunin yung least bloody to prevent alteration in hema
are DNA viruses that have properties of Latency/Dormancy
Herpes viruses
Viral meningitis agents?
Caused by o Enteroviruses o HSV o HIV o West nile virus o Varicella-Zoster virus o Mumps o Lymphocytic choriomeningitis virus
Most common causes of Viral meningitis?
Coxsackie, echovirus, other non-poliovirus enteroviruses
o Torulosis
o European Blastomycosis
what is the agent?
Cryptococcus neoformans
• Both differ from non pathogenic species by:
o Ability to grow at 37C
o Production of laccase (catalyzes melanin production)
• 22 strains: 5 serotypes (A-D & AD)
• 3 human variants
Cryptococcus
o Neoformans (AIDS &immunocompromised) o Gatii, grubri (non-immunocompromised)
MOT: cryptoccoccus species
Pathophysio
inhalation of yeast cells;
Pathogenesis: inhaled -> alveolar spaces of host’s lung, establish colonies and produce capsule-> BV-> CNS
what agent has this virulence factors?
• Capsule
o Long unbranched polymenrs consisting of alpha 1,3 linked polymannose backbone with betalinked monomeric branches of xylose and glucoronic acid
• Laccase
o Painless pustules/papules/nodules, hemorrhagic, waxy, umbilicated & ulcerated.
what type of cryptococcosis
Cutaneous Cryptococcosis
o Acute:
immunocompromised patients asymptomatic to mild flu-like s/sx
o Chronic: lobar pneumonia, cavitations due to production of granulomas with encapsulated fungi at the center.
what type of cryptococcosis?
Pulmonary Cryptococcosis
o Mainly CNS: subacute/chronic meningitis
o S/Sx: visual loss, seizures, hydrocephalus, etc
o Other organs: endopthalmitis, chorioretinitis, conjunctivitis, sinusitis, pericarditis, gastritis, bone infection
what type of cryptococcosis?
Disseminated Cryptococcosis
What are the serotypes of cryptococcus?
Serotype A- most human infections • Serotype B- US West Coast, AIDS-rare • Serotype C- Tropical areas *Philippines • Serotype D- Europe • Serotype AD • C. neoformans -A, D or AD • C. gattii- B or C
how to measure antibody titers in cryptococcus?
• Fluorescent Antibody Test
o tissue studies & serotyping cultures
• Whole Yeast Cell Tube Agglutination Test and EIA
o Cryptococcus in serum
- Dome shaped, shiny white to tan, yellow to light pink or light brown mucoid colonies (+ capsule)
- Yeast form ONLY!!!
- *Dry and dull – age
What organism has this macroscopic morph?
Cryptococcus neoformans
o Thin-walled globose or oval-shaped
o Singly or in pairs with narrow points of attachment between the mother and daughter cells
No mold form= MONOMORPHIC
o NO pseudohyphae nor true hyphae refractile mucopolysaccharide capsule
what organism has this microscopic morphology?
Cryptococcus neoformans
Treatment for cryptococcus?
Combination of Amphotericin B with or without Flucytosine
what can cause african sleeping sickness?
Trypnaosomes (hemoflagellates)
There must be a history of travel because we don’t have Kissing Bugs here
what trypanosoma is C- shaped?
T. cruzi
what trypanosoma is slender shaped?
T. gambiense; T. rhodesiense
95% of Human African Trypanosomiasis (HAT) is caused by
gambiense; 5% rhodiense
African sleeping sickness what organism?
Trpanosoma brucei complex
vector of Trypanosoma brucei complex
tsetse fly or (glossina)
subspecie of trypanosoma that is east african/ acute
T. brucei rhodesiense
subspecie of trypanosoma that is West African /chronic
T. brucei gambiense
daytime biters? night time biters?
tse tse flies - glossina species
night time - triatopic, kissing bug, cone nose bug
Identify is West African or East African? T. Brucei gambiense
west
Identify is West African or East African? Glossina morsitans group
east
Identify if west african or east african? Primary reservoirs:
humans
West african
Identify is West African or East African?
Chronic (late CNS
invasion) months to
years
west
Identify is West African or East African? High parasitemia
east
Identify is West African or East African? Rural population
west
what stage of Tryponasoma disease is this?
• Fever, headache, ms/jt pains, malaise, anemia, myocardial inflammation, DIC, renal insufficiency
winterbottom sign
hemolymphatic stage
early stage
what is winterbottom sign?
–posterior cervical lymphadenopathy – large, non-tender
- Apathy, behavioral changes, headache, sleep pattern changes, convulsion,tremors speech defects
- Kerandel’s sign
- Gambian > Rhodesian
- Frontal lobe, pons, medulla, perivascular areas
what stage of trypanosoma infection?
• Meningoencephalitic stage; late (5 to 10 months)
Kerandel’s sign?
deep, delayed hyperesthesia
CSF findings in Meningoencephaltic stage of Trypanosoma infections
Increase in : ▪ Cell count ▪ Opening pressure ▪ Protein concentration ▪ IgM levels (pathognomonic for the meningoencephalitic stage)
Treatment in the first stage of Trypanosoma infection?
IV suramin (rhodesian and Gambian)
Treatment for gambian?
IM Pentamidine
treatment for trypanosoma infection if it is in CNS stage already?
IV melarsoprol; if ineffective: nitrofurazone oreflomithine (gambian only)
transient clinical phenomenon that occurs in patients infected by spirochetes who undergo antibiotic treatment
Jarisch Herxheimer reaction
what agent? Primary amoebic meningoencephalitis
Acanthamoeba / Hartmanella culbertsoni
• Motile trophozoites o Amoeboid o Flagellate (w/ 2 flagella) – shed flagella then resume amoeboid motility and reproduction Mga freeliving • Non motile resistant cysts
Naegleria fowleri
o Findings - Like fulminant bacterial meningitis
o Amoebae in exudates
o Diagnosis : swimming in thermal/stagnant water 3 to 6 days prior; CSF; histopath
o Prognosis: fatal within a week
o Treatment: none; Amphotericin B and Sulfadiazine
what parasite?
Naegleria fowleri
Amoebic meningoencephalitis, uveitis and ulceration of cornea
• Active trophic forms
o No flagellate form
• Resistant cysts – resistant to chlorine and can withstand drying
• Slow movement of acanthopodia
Acantho= meaning thorny
what parasite?
Acanthamoeba culbertsoni
what are the species of Acanthamoeba species?
- A. culbertsoni
- A. polyphaga
- A. castellanii
- A. Astronyxis
how to diagnose Acanthamoeba
Amoebae in CSF, scrapings from lesions in cases of corneal or cutaneous infections; cultures of material from those sources; stained vaginal smears; purulent discharge from infected ear
Treatment of Acanthamoeba?
Amphotericin B and Sulfadiazine
Determine of Acanthamoeba or Naegleria? Olfactory
neuroepithelium
Naegleria
Determine of Acanthamoeba or Naegleria?
broken/ulcerated skin or eye; lungs or genitourinary tract
Acanthamoeba
Determine of Acanthamoeba or Naegleria? faster course?
Naegleria
Determine of Acanthamoeba or Naegleria? Granuloma formation?
Acanthamoeba
Determine of Acanthamoeba or Naegleria? gradual onset and prolonged chronic course
Acanthamoeba
Determine of Acanthamoeba or Naegleria? Chronically ill /
immunosuppressed
Acanthamoeba
Determine of Acanthamoeba or Naegleria? broad pseudopods
Naegleria
Determine of Acanthamoeba or Naegleria? sluggish motility
Naegleria
Determine of Acanthamoeba or Naegleria? does not form flagellate stage?
Acanthamoeba
Determine of Acanthamoeba or Naegleria? double walled cysts?
Acanthamoeba
Determine of Acanthamoeba or Naegleria? may have pores or osteioles
Acanthamoeba
Determine of Acanthamoeba or Naegleria? no encystment in tissue?
Naegleria
Criteria of Amoeba?
Chromatin dot, central karyosome, peripheral chromatin
Pathophysiology of Eosinophilic meningoencephalitis
• Eggs hatch in lung of rodent host → larvae migrate to trachea → swallowed → 1st stage larva expelled in feces → molluscan intermediate host and reach 3rd (infective) larval stage in 2 wks → ingested by rat/man → infective larvae migrate to brain → migrate to pulmonary arteries → bloodstream → gravid females lay ova
Not usually common because it is in Rats but humans can be infected as well.
called rat lung worm.
Barber’s pole appearance
Eosinophilic Meningoencephalitis
Definitive host is rat, infection is via the ingestion of 3rd stage larva
Angiostrongylus cantonensis/ Parastronglyus cantonensis
intermediate host of Angiostrongylus cantonensis/ Parastronglyus cantonensis
molluscan or freshwater
o snails / slugs
o infection via ingestion or active
o penetration of 1st stage larva
what is paratenic host Angiostrongylus cantonensis/ Parastronglyus cantonensis
may act as reservoir hosts in which different larval stages can persist but not develop further –freshwater shrimp, crabs, flatworms and frogs
humans and other mammals, birds – permit development from larval to subadult stage but are dead-ends for the parasite – these hosts are infected primarily through consumption of raw or undercooked intermediate or paratenic hosts, either intentionally or accidentally via contaminated produce.
Accidental host
How does transmission to man in angiostrongylus cantonensis happen?
Ingestion of raw mollusk IH infected with the 3rd stage larva
o Ingestion of leafy vegetables of mollusk with 3rd stage larva
o Ingestion of a paratenic host, such as freshwater prawn or crab
o Drinking contaminated water
ALL STAGES ARE INFECTIVE TO MAN • INVADES ALL NUCLEATED CELLS • TRANSMISSION o INGESTION OF OOCYSTS (infective stage) o INGESTION OF INFECTED MEAT o TRANSPLACENTAL o BONE MARROW TRANSPLANTATION o WHITE CELL TRANSFUSION o ACCIDENTAL (LABORATORY)
Toxoplasma gondii
Symptoms of acquired toxoplasmosis
o RETINOCHOROIDITIS o FEVER/LYMPHADENOPATHY o HEADACHE o MYALGIA o RASHES
Symptoms of transplacental (congenital) toxoplasmosis?
o ABORTION/STILLBIRTHS ▪ PHYSICAL/ MENTAL DEFECTS • INTRACRANIAL CALCIFICATION • HYDROCEPHALY • MICROCEPHALY o DEATH CONVULSIVE/EPILEPTIC SEIZURES
manifestation of immunodeficient patients with toxoplasmosis?
Encephalitis (Sabin Syndrome)
A syndrome of toxoplasmosis like symptoms and extensive destruction of brain tissue, hydrocephalus, diffuse cerebral calcification, chorioretinopathy, microcephaly, mental
retardation, and degenerative changes of small retinal vessels.
Sabin Syndrome
how to diagnose toxoplasmosis?
• IDENTIFICATION
o TISSUE IMPRINTS
o GIEMSA STAINING
• PARASITE ISOLATION o PLACENTA o VENTRICULAR FLUID o PERITONEAL FLUID o BUFFY COAT
• SEROLOGY
o IFA/ IHA
o EIA
o DOUBLE SANDWICH ELISA
o LAT
o SABIN FELDMAN DYE TEST based on the presence of certain
antibodies that prevent methylene blue dye from entering thecytoplasm of Toxoplasma
• PCR
Normal CSF: Appearance - Opening Pressure - WBC - Protein - Glucose -
Appearance - Clear Opening Pressure - 90-180 mmHg WBC - <8 Protein - 15-45 Glucose - 50-80
Bacterial Meningitis Appearance - Opening Pressure - WBC - Protein - Glucose -
Appearance - turbid Opening Pressure - Elevated WBC - >1000 -2000, neutrophilic predominance Protein - >200 Glucose - <40
Viral Meningitis Appearance - Opening Pressure - WBC - Protein - Glucose -
Appearance - Clear Opening Pressure - Normal WBC - <300 lymphocytic predominance Protein - <200 (slightly elevated) Glucose - Normal
Fungal Meningitis Appearance - Opening Pressure - WBC - Protein - Glucose
Appearance - clear Opening Pressure - Normal -elevated WBC - <500 Protein - >200 Glucose - Normal to low
TB Meningitis Appearance - Opening Pressure - WBC - Protein - Glucose
Appearance - clear Opening Pressure - Inc, Dec, Spinal Block WBC - 100 - 600, mixed or lymphocytic Protein - 500 - 300 Glucose - decreased
Acute syphilis Appearance - Opening Pressure - WBC - Protein - Glucose
Appearance - Clear Opening Pressure - Increased WBC - About 500 lymphocytic Protein - Inc but less than 100 Glucose - normal
Spreading of viral meningitis? bacterial?
viral - Saliva/ stool
bacterial - contact with fluids from the mouth or nose of a sick person
Identify if meningococcal or meningitis? illness caused by neisseria meningitidis?
meningococcal
Identify if meningococcal or meningitis? symptoms include headcahe, stiff neck, vomiting, nausea, rash, organ problems, sensitivity to light and DIC
meningococcal
Identify if meningococcal or meningitis? death rate is variable, low with viral meningitis to as high as 73% to 95 %
meningitis
Identify if meningococcal or meningitis? caused by virus, fungi, parasites, bacteria, cancer and lupus
Meningitis
Identify if meningococcal or meningitis?
risk factors include young children of 6 months to 3 years and young people living in college dorm, military recruits etc
meningococcal
