Module 5-Path Continued: Men, Salmonella Flashcards
What are the 4 different etiologies of Meningitis?
Bacterial
Viral
Fungal
Tuberculous
What is meningitis ?
Inflammation of leptomeninges (pia and arachnoid)
How is meningitis spread?
Via inhalation of respiratory droplets == colonizes in nasopharynx —- spreads directly to brain via sinuses to meninges but can also spread via blood (via thoracic duct into lymphatics to bloodstream to CSF)
What are the symptoms of meningitis?
Headache, fever, stiff neck and photophobia
What is the best investigation for meningitis?
Spinal Tap
What examination should you do on a patient before spinal tapping the patient?
Fundoscopy to check for papilledema
if a patient has papilledema and you as the physician do a lumbar puncture the patient will get an uncal herniation (or transtentorial herniation)
CNIII is damage so patient pupil is dilated (mydriasis)
What would you find in the CSF of a patient with bacterial meningitis?
Increased Protein
Decreased Glucose (Bacteria eats it)
Increased PMNs
CSF will also be cloudy due to pus – exudate
What would you find in the CSF of a patient with viral meningitis?
Slightly Increased Protein
Slightly low/normal glucose
Increased lymphocytes (CD8 T cells –remember its viral thats why)
What would you find in the CSF of a patient with fungal meningitis?
Increased protein
Slightly decreased glucose
Mix of PMNs and lymphocytes (remember acute and chronic cells for fungal)
What would you find in the CSF of a patient with TB meningitis?
Increased Protein
Decreased Glucose
Increased CD4 T lymphocytes
A neonate up to 2 months, what bacterial meningitis would you find?
Strep. Agalactiae (group B) (gram positive bacteria)
group B colonizes the vagina of a pregnant women so baby can get meningitis during birth in the birth canal.
Infancy through childhood, what bacterial meningitis would you find?
Strep. Pneumoniae (gram positive bacteria, diplocci)
In adolescences what bacterial meningitis would you find?
Neisseria meningitides (gram negative bacteria)
During adulthood what bacterial meningitis would you find?
Strep Pneumoniae (gram positive bacteria, diplocci)
on gross image of the brain of a patient with bacterial meningitis what do you find?
Hyperemic (increased active blood volume) blood vessels
purulent exudate in subarachnoid space
What is one of the best investigations for TB?
Acid fast stain for CSF
What is the first investigation for TB?
xray
What is one complication to bacterial meningitis?
Gram negative septic shock (aka neisseria meningitides )
N. meningitides leads to gram negative septic shock from meningococcal septicemia
Meningococcal Septicemia can lead to DIC how?
LPS binds to LBP and this complex is now taken up by macrophages , secrete —- TNFalpha, recruits —– neutrophils, secrete —- IL-1 and procoagulant which causes endothelial damage —– systemic microthrombi —- DIC
How does a gram positive bacteria cause DIC?
Via superantigens
What are the internal and external bleeding spots in DIC?
Internal: adrenal glands hemorrhage
External: purpura and petechiae and ecchymosis
this leads to Waterhouse-Friderichsen Syndrome which can lead to Addison’s disease.
What investigations would you do for Meningococcal Septicemia?
Increased D-dimer
Increased bleeding time
Increased PT and PTT
So the first complication of Bacterial meningitis was meningococcal septicemia due to N. meningitides, what are the other 3 complications of bacterial meningitis?
- Deafness
- Communicating Hydrocephalus
- Spread of infection can cause encephalitis (these patients are usually immunocompromised)
Clostridium Perfringens is a gram positive bacilli, anaerobic bacteria that produces spores and is found in the soil and invades traumatic and surgical wounds. what type of infection does this bacterial cause?
Myonecrosis aka gas gangrene
gas forming organisms: degradative enzymes produce gas in tissues
Deadly form of gangrene –> medical emergency
Perfringens perforates a gangrenous leg
Clostridium Perfringens secretes 12 exotoxins= necrosis
most important is alpha toxin (lecithinase) what exactly do these exotoxins do?
Degrade lecithin – a major component cell membrane
Destroys RBCs, platelets, muscle fibers (myonecrosis)
Enzymes released from necrotic tissue
Schistosoma is a parasite that has what significant effects on the body if contracted?
Bladder carcinoma
hepatomegaly, fibrosis and portal HTN
Eggs induce granulomas –> fibrosis and this leads to liver failure and hence ascites
Staphylococci lesions can either be inflammatory mediate or toxin mediated. Name some inflammatory mediated examples:
- Skin- folliculitis, furuncle, carbuncle, cellulitis, impetigo, paronychia, surgical wound infection
- Post Partum-mastitis
- Bacteremia
- Endocarditis: tricupsid valve
- Osteomyelitis
- Pneumonia: bronchopneumonia, abscess wit hwatery pus
- Bacteremic abscess- lung, kidney, brain
- MRSA
What are examples of toxin mediated staphylococci lesions?
- Food poisoning: enterotxoin
- Toxic Shock Syndrome (TSS)- intravaginal tampon if left in longer leads to growth of staph – release of exotoxin into circulation —rash, conjunctivitis and vomiting
- Scaled skin Syndrome
Neisseria gonorrhoeae is a gram negative, diplococci, sexually transmitted disease. What are the signs and symptoms in males, homosexual males and females?
Males:
1. Urethritis and Epididymitis
–urethral discharge and dysuria
Homosexual Males:
1. oropharyngitis and proctitis (inflammation of rectum)
Females:
1. Cervicitis, salpingitis (infection/inflammation of fallopian tubes) and peritonitis, PID (pelvic inflammatory disease)
–vaginal discharge, inter menstrual bleeding
–if untreated can lead to scaring of the fallopian tubes
Neisseria gonorrhoeae disseminated via what methods?
- Rare via hematogenous (carried in blood)
- Tenosynovitis (inflammation of the lining of sheath that surrounds tendon), arthritis
- Hemorrhagic skin lesions
- Endocarditis
- Rarely meningitis
Neisseria gonorrhoeae can occur in a newborn, explain the mechanism for this
infections acquired during passage of the fetus through cervix during labor purulent conjunctivitis (opthalmia neonatorum) use of erythomycin/silver nitrate eye drops after birth can prevent this
How does one diagnosis Neisseria gonorrhoeae in males and females
Males: microscopy of exudate: PMNs and gram - diplococci
Females: culture of exudate - essential b/c gram - diplococci are normal part of vaginal flora
could yield false negative result if there are fewer organism
What other STI can produce similar signs and symptoms as Neisseria gonorrhoeae?
Chlamydial infection
Typhoid fever = Enteric Fever and it is caused by Salmonella Typhi: gram negative bacilli. how is this bacteria acquired?
Through ingestion of contaminated food, water (transferred in feces)
Typhoid fever (Enteric fever) affects the body differently with each week, explain the effects of the bacteria during week one
Enter ileal wall (no lesions at this time) – enter bloodstream — bacteremia
What is the effect of the salmonella typhi in week two?
Liver enlarged = typhoid nodules: composed of Kupffer cell hyperplasia
–minute foci of hemorrhagic necrosis, collections of macrophages
–Typhoid nodules: macrophages that contain bacteria, RBCs, degenerated lymphocytes
Spleen: enlarged soft spleen with splenitis, typhoid nodules
What is the effect of salmonella typhi in week three?
Bacteria excreted through gall bladder in bile – lumen of gut — re-enter gut wall through ileum
–sensitization has occurred during this period — contact with organisms produces lymphoid hypertrophy (increase lymph tissue) and necrosis in the mucosa
What are the clinical features of Enteric/Typhoid fever?
- –Fever, toxic appearance, leukopenia (decreased WBCs) and bradycardia
- –Endotoxin = depression of heart and bone marrow
- –Ulcers heal without scarring
- -Complications: perforation peritonitis bleed (3rd and 4th week)
What are the lesions of enteric/typhoid fever?
ileum — lymphoid hypertrophy (Peyer’s patches), necrosis, ulceration
- –no PMNs (Excrete a protein called invasion, that allows non phagocytic cells to take up the bacteria, where it is able to live intracelluarly; also inhibit oxidative burst of leukocytes = innate (Acute) immune response infected)
- -only macrophages, erythrophagocytosis (phagocytosis of RBCs)
- -mesenteric LN enlarged, hemorrhagic necrosis
How would you diagnosis Enteric/Typhoid fever with each week?
End of week 1: blood culture – lysis of macrophages release large number of bacilli into circulation
Week 2: organisms in feces/ urine
Week 3: Widal test (demonstrate antibodies ) — bacteria are mixed with serum containing specific antibodies from an infected individual
In some patients with Enteric/Typhoid fever, they develop chronic colonization of gallbladder, in what kind of patients does this develop?
Asymptomatic carries
Gram negative bacteria septicemia leads to septic shock, what are some features of septic shock?
Common Clinical Situation
Fever, septicemia, DIC, Shock
Normally commensual organsims — become pathogenic
immune deficiency, break in mucous membranes
