Infections

Question 1

Neisseria meningitides

Answer 1

G-ve diplococci
Transmission: resp droplets
ROS: usually just mild “flu” sx’s (carrier)
Complication: invasion of blood stream causing septicemia and meningococcemia
*meningitis in some pt’s

Question 2

Meningitis Pathogenesis

Answer 2

Pathology: pyogenic inflamm of leptomeninges and SA space
Gross: meninges are dull, congested w/ purple to exudate
Microscopically: PMN cells, fibrin, vascular congestion (acute inflamm)

Question 3

Meningitis Clinical Features

Answer 3

ROS: fever, HA, cloudy consciousness, nuchal rigidity
Dx: CSF w/ PMNs and increased protein, low glucose
Other causes: TB, viral or fungal

Question 4

Meningitis Course Features

Answer 4

Complications: shock, purpura, toxemia, DIC
Epidemiology: N. meningiditis common at all stages except neonates

Question 5

Waterhouse Friderichsen Syndrome

Answer 5

Bilateral adrenal hemorrhages

Question 6

Neisseria gonorrhoeae Features (and male sx’s)

Answer 6

G-ve diplococci, sexually transmitted
Male ROS: urethritis, epididymitis, urethral d/c, dysuria
Homosexual male ROS: oropharyngitis and proctitis

Question 7

Neisseria gonorrhoeae (female sx’s)

Answer 7

ROS: cervicitis, salpingitis, peritonitis, vaginal d/c, dysuria, intermenstrual bleeding, PID,
Course: chronic can cause scarring of Fallopian tubes leading to infertility

Question 8

Gonorrhea Course

Answer 8

Rarely hematogenous - can cause tenosynovitis, arthritis, hemorrhagic skin lesion, endocarditis, rarely causes meningitis

Question 9

Ophthalmia Neonatorum (Gonorrhea)

Answer 9

Transmission: during parturition
ROS: purple to conjunctivitis
Tx: erythromycin/silver nitrate eye drops after birth for prevention

Question 10

Salmonella typhi Features

typhoid fever

Answer 10

G-ve bacilli
Transmission: ingestion of contaminated food/water
Mechanism: enters ileal wall, enters blood stream and causes bacteremia during (week 1)

Question 11

Typhoid Fever Organ Affects

Answer 11

Hepatomegaly: typhoid nodules composed of Kupffer cell hyperplasia, minute fo i of hemorrhagic necrosis, collections of macrophages during (week 2)
Splenomegaly: soft spleen w/ splenetic, typhoid nodules

Question 12

Typhoid Fever Course

Answer 12

Excretion through bile into gut, re-enter gut wall through ileum, sensitization has occurred an contact w/ the organism produces lymphoid hypertrophy and necrosis in the mucosa (week 3)

Question 13

Typhoid (enteric) Fever Lesions

Answer 13

Ileum: lymphoid hypertrophy of Peyer’s patches, necrosis, ulceration
Features: no PMNs, only macrophages, erythrophagocytosis, mesenteric LN enlarged, hemorrhagic necrosis

Question 14

Typhoid (enteric) Fever Clinical Features

Answer 14

ROS: fever, toxic appearance, leucopenia*, bradycardia, endotoxin produces depression of heart and bone marrow, ulcers heal w/o scarring
Complications: perforation peritonitis, bleed (week 3 and 4)

Question 15

Typhoid Fever Diagnosis

Answer 15

Week 1: blood culture (lysis of macrophages release large # of bacilli)
Week 2: organisms can be demonstrated in feces and sometime sin urine
Week 3: demonstrate Ab’s (Widal test)

Question 16

Typhoid Carrier State

Answer 16

Persistent/chronic infection leads to colonization of gallbladder, carrier has no sx’s but can shed the bacteria in feces/urine
Tx: need to undergo choelcystectomy

Question 17

G-ve Sepsis

Answer 17

ROS: fever, DIC, hypotension, shock
Organisms: normally commensalism but become pathogenic in situations (immunodeficiency, break in mucous membrane)
E.g. - E. coli, h influenzae, pseudomonas aergunosa, klebsiella, proteus, serratia

Question 18

Staphylococci

Answer 18

G+ve, normally colonize human skin
Infectious: most commonly S. aureus
Lesions: inflammatory or toxin mediated

Question 19

Inflammatory Staphylococci Lesions

Answer 19

Skin, postpartum mastitis, bacteremia, endocarditis (tricuspid valve, common in drug addicts), osteomyelitis, pneumonia, bacteremic abscess
*MRSA

Question 20

Toxin Mediated Staphylococci Lesions

Answer 20

Food poisoning (enterotoxin), TSS, Scalded Skin Syndrome (exfoliatintoxin)

Question 21

Streptococci

Answer 21

G+ve cocci, present in pairs or chains, hemolytic

Lancefield grouping: Group A are beta hemolytic (e.g. - S. pyogenes), Group B are hemolytic

Question 22

Streptococci Infection

Answer 22

Direct damage: suppurative - cellulitis, abscess, pneumonia
Exotoxins mediated: Scarlet Fever
Indirect damage: caused by immune response

Question 23

Strep Pneumonia (pneumococcal pneumonia)

Answer 23

Causes: lobar pneumonia in healthy young adults
ROS: cough, fever, CP, hemoptysis
Early stage: exudate rich in fibrin, RBCs, few PMNs seen in lumen of alveoli
Progression: bronchioles and alveolar walls not damaged bc pt is immunocompetent
Spread: via pores of Kohn to involve the entire lobe
Course: total resolution w/in 10 days

Question 24

Red Hepatization

Answer 24

Exudate consists of RBCs, fibrin, more PMNs

- lung loses spongy consistency and feels solid and red like liver

Question 25

Grey Hepatization

Answer 25

Congestion and fibrin disappear, PMNs replaced by macrophages Resolution: macrophages clear up the debris a few days later Tx: abx accelerate the process Complications: rare dev of abscess, fibrosis, emphysema

Question 26

Rheumatic Fever Course

Answer 26

Initial: streptococcal ST, or skin infection Lag: 2-3 wks after initial infection Mechanism: Ab's generated to M protein of the bacteria cross react w/ tissue glycoproteins in joints, heart, skin, etc.

Question 27

Rheumatic Fever Sx's

Answer 27

ROS: fever, poly arthritis, carditis, chorea, skin nodules, erythema (ACCNE) Complication: carditis showing Aschoff bodies on biopsy, can become chronic and cause mitral stenosis Tx: to prevent chronic rheumatic heart dz give pt prophylactic abx tx s/p RF

Question 28

Post-Streptococcal Glomerulonephritis Course

Answer 28

Initial: steptococcal ST or skin infection Lag: 1-4 wks after initial infection Mechanism: Ab-ag immune complexes form and get deposited in BM of glomeruli, activates complement and induce acute inflammation *type III hypersensitivity

Question 29

Post-Streptococcal Glomerulonephritis Sx's

Answer 29

ROS: acute malaise, fever, oliguria, hematuria, azotemia (👆🏽BUN, Creatinine and 👇🏽GFR) Resolution: resolves spontaneously in most pt's as immune complexes are cleared

Question 30

Diphtheria

Answer 30

Myocarditis is the complication

Question 31

Pseudomembranous Colitis (C. diff)

Answer 31

Clostridium difficult: G+ve bacillus Cause: tx w/ broad spectrum abx is assoc w/ colitis bc they eliminate the normal flora of the gut that normally afford protection

Question 32

C. difficile Mechanism

Answer 32

Exotoxin causes severe mucosal suppurative inflamation, small vascular thrombosis, necrotic mucosa forms pseudomembrane

Question 33

Rickettsia Infections

Answer 33

Small, obligate intracellular, resemble G-ve

Question 34

Epidemic Typhus

Answer 34

Organism: Rickettsia prowazeki Transmission: head/body lice ROS: hemorrhagic nodules on skin, vasculitis, thrombosis, hemorrhage Complications: pneumonia, hepatitis, CNS involvement (typhus nodule) Severe: necrosis of earlobes, scrotum, nose, finger Dx: immunofluorescence and Weil Felix test (Ab's cross react w/ Proteus ag)

Question 35

Rocky Mountain Spotted Fever

Answer 35

Organism: Rickettsia rickettsii Transmission: tick bite Geography: OK, TN, AR, GA ROS: fever, HA, myalgia followed by skin rash Complications: vascular necrosis, hemorrhage, vasculitis, thrombosis (severe lung and CNS involvement) Dx: immunofluorescence on biopsy

Question 36

Q Fever

Answer 36

Organism: Cloxiella burnetti Transmission: airborne droplets from sheep/cattle ROS: no skin rash, pneumonia (affects liver, spleen and bone marrow) Biopsy: ring granuloma in liver biopsy - central fat, fibrinoid material surrounded by epithelioid cells Dx: immunofluorescence, serology