Bacteria Flashcards
G+ coccus?
Streptococcus & Staphylococcus
G+ Spore forming rods
Bacillus and clostridium
G+ non-spore forming rods
Corynebacterium, listeria
which G- pathogen is spiral shaped?
Spirochetes, including Treponema pallidum (syphilis)
Layers of G+ cells? lipid content of G+? what can kill it?
- inner cytoplasmic membrane
- outer thick peptidoglycan layer
low lipid content
vulnerable to lysozyme and penicillin attack
Layers of G- cell?
lipid content?
endotoxin?
what can attack it?
(1) inner cytoplasmic, (2) thin peptidoglycan layer, (3) outer LPS layer
high lipid content, endotoxin is LPS - Lipid A, periplastic space, porin channel, RESISTANT to lysozyme and penicillin attack.
G+ , but seen best with Acid Fast stain?
Mycobacteria - TB and Leprosy
G- bacteria with addition phospholipid membrane to protect from immune recognition, with periplastic flagella
Spirochetes
G- Coccus?
Neisseria and Moraxella
G+ Rod (bacillus)
Corynebacterium listeria bacillus clostridium mycobacterium (acid fast)
G- Rod (bacillus)
ENTERICS = escherichia coli, shigella, salmonella, yersina, klebsiella, proteus, enterobacter, serratia, Vibro, campylobacter, helicobacter, pseudomonas, bacteroies (anaerobic) other = Haemophilus, bordetella, legionella, yersinia, francisella, brucella, pasteurella, gardnerella
G- spiral?
Spirochetes = Treponema, Borrelia, Leptospira
G- pleomorphic?
Chlamydia and Rickettsiae
G+ Obligate Aerobes?
Nocardia, bacillus cereus
G- Obligate Aerobes
Neisseria, pseudomonas, bordetella, legionella, brucella
No cell wall?
Mycoplasma
G+ Facultative Anaerobes
Staphulococcus bacillus anthracis Corynebacterium listeria actinomyces
G- Faculatative anaerobes
Most other G- Rods
G+ Microaerophilic
enterococcus
streptococcus (some are anaerobes)
G+ obligate anaerobes
clostridium
G- Obligate Anaerobes
Bacteroides
Proc vs Euk ribosomes
Proc are 70s and Euk and 80s
G+ and Catalase+
Staphlococcus
G+ and Catalase -
Steptococcus
G+, Catalase +, Coagulase +
Staphylococcus Aureus
What do you use and india ink stain for?
Fungi like cryptococcus that has a capsule.
What are the two endospore formers and what are the layers?
Bracillus and clostridium (G+) (5 layers) cell membrane thick peptidoglycan mesh another cell membrane a wall of keratin-like mesh and outer layer call the exosporium
Exotoxin vs Endotoxin
Exotoxin is released from G+ bacteria, wherase endotoxins are portions of the cell walls
bacteremia
bacteria in the blood
define sepsis
bacteremia that causes a systemic immune response to infection
define septic shock
sepsis (bacteria in blood causing immune response) that results in dangerous drops in blood pressure and organ dysfunction (endotoxic shock when with bacteria)
TNF, IL-1, NO
help cause Septic shock
TNF = cachexia, hypotension, death
IL-1 = released from MQ and endothelial cells that trigger inflammatory responses.
NO = vasodilation
exchange of genetic material allows bacteria to?
become pathogenic, resist antibiotic therapy, and survive.
example of genetic transformation
streptococcus pneumoniae can change their capsle from rough to smooth
define bacteriophages
bacteria that carry a piece of bacterial DNA from one bacterium to another
Lysogenic immunity
the term used to describe the ability of an integrated bacteriophage to block subsequent infection by a similar phage.
define conjugation
BACTERIAL SEX ;)
what is needed for conjugation to occur?
must have the F+ plasmid for the sex pilus
define transposons
the DNA does not need marker to inject itself into the cell. no DNA homology required. rapid spread and resistance.
What is the hemolytic reaction in blood agar?
killing the local RBCs
four disease associated with streptococci Group A?
streptococcal pharyngitis
streptococcal skin infections
scarlet fever
streptococcal toxic shock syndrome.
Virulence factors for Streptococci? (5)
C carb = separates groups A and C M protein = major virulence factor for group A streptococcus, inhibits complement and protects the organism from phagocytosis Streptolysin O = inactivated oxygen that is antigenic for Beta hemolytic group A strep Streptolysin S = oxygen stable, not antigenic Pyrogenic Exotoxin (erythrogenic toxin) = cause scarlet fever
two diseases caused by beta-hemolytic group A strepyococci
these are delayed antibody mediated disease
rheumatic fever
glomerulonephritis
classic strep throat with red swollen tonsils and pharynx with a purulent exudate on the tonsils, high temp, swollen lymph nodes. lasts 5 days and then recovery.
test to know the diagnosis?
streptococcal pharyngitis
rapid antigen detection test (RADT) will be pos for this bacteria
Skin infections with streptococci and Staphlococcus aureus
folliculitis (infection of the hair follicles), pyoderma, erysipelas, cellulitis (deep infection of the skin producing a red, swollen skin that is hot to the touch) and impetigo
near a cut there is swelling, heat, and redness that moves rapidly from the initial skin infection site. skin color changes from red to purple to blue and large blisters form. skin died and muscle has become infected.
caused by? follows what path?
necrotizing fasciitis (flesh eating streptococcus)
group A hemolytic streptococcal, staphylococcus, clostridium sps
caused by M proteins that block phagocytosis
necrotizing fasciitis involving the male genital area and perineum.
disease name?
caused by?
Fournier’s gangrene
Streptococcus pyrogenes
rash begins on the trunk and neck, and then spreads to the extremities, sparing the face, the skin may peel off in fine scales during healing.
scarlet fever
beta-hemolytic group A streptococci
caused by exotoxin pyrogenic toxin, erythrogenic toxin
severe skin infections, necrotizing facititis
Streptococcal toxic shock syndrome
beta-hemolytic group A streptococcal similar (strep pyrogenes) to staph aureus
mediated by the release of pyrogenic toxin
5-10 years of age, pharyngitis (without a skin infection), fever, myocarditis, arrythmia, joint swelling (arthritis), Chorea that begins 2-3 weeks pose pharyngitis, subcutaneous rubbery nodules under the skin, rash (erythema marginatum - red margin that spreads out from its center).
name the disease?
how is it caused?
fatal outcome?
Rheumatic Fever
antibody mediated
beta-hemolytic group A steptococci
heart disease develops with chronic disease
face is puffy, urine is darker than normal tea, hematuria, hypervolemia, high BP, sore throat or skin infection a week ago
Acute Post-streptococcal glomerulonephritis
post and infection of either the PHARYNX OR SKIN by nephritogenic
caused by beta-hemolytic group A streptococci
genus and species name of Group B streptococci?
Streptococcus agalactiae
Name for Group A Beta hemolytic Streptococci?
Streptococci pyogenes
Age group related to Group B strep? and clinical manifestations
most common in neonates
Three most common pathogens associated with meningitis in neonates and infants less than three months of age?
Group B strep (Strep agalactiae), Listeria, E. coli (G-)
test when you suspect meningitis in a neonate? and clinical symptoms
Lumbar puncture
two bacteria associated with meningitis later in life after maternal Abs wane and new Abs haven’t been produced?
Neissaria meningitis and Haemophilus influenzae
secondary complications that can increase the risk of Group B strep?
diabetes, malignancy, renal or liver failure, neurological disease, and elderly >65y/o.
bacteria that cause a greenish discoloration in the blood agar?
and four members of this group?
Viridans group streptococci
mitis, salivarius, Mutans, Anginosus
(alpha hemolytic)
Where do the Viridans group strep normally live?
GI tract, Nasopharynx, gingivia
Three main infections with Viridans strep?
dental, endocarditis (subacute bacterial endocarditis), and Abcess
low grade fever, fatigue, anemia, heart murmurs secondary to valve destruction.
subacute bacterial endocarditis (SBE)
viridans strep - will eat the heart slower.
also caused by group D streptococci
drug abuse, abrupt onset of shaking chills, high spiking fevers, and rapid valve destruction.
acute infective endocarditis
staphylococcal aureus will eat the heart quickly
order of bacteria causing SBE
streptococci pyrogenes causes the rheumatic fever, damaging the heart valves and then viridans and group D strep can then invade the valves causing SBE
subgroups of strep viridans that cause brain and abdominal abscesses?
where are these normally found?
clinical diagnosis?
Anginosus sp. = intermedius, constellatus, and anginosus.
normal GI flora
intermedius grows in blood culture, suspect an abscess
Six clinical G+
Streptococcus, Staphlococcus, Bacillus, Clostridium, Corynebacterium, Listeria
subgroups of Group D strep
Enterococci - enterococcus faecalis and enterococcus faecium
non-enterococci = streptococcus bovis, and streptococcus equinus
where doe group D strep normally live?
they are normal bowel flora and cause similar diseases
what are the conditions for the Group D strep?
where are they common infectious agents, and diseases?
enterococci = 40% bile and 6.5% NaCl (UTI, biliary tract, wound infections, mative and prosthetic valve, bacteremia, sub acute endocarditis and sepsis after infecting intravenous catheters. pray and weak hospitalized pts. non-enterococci = only 40% bile
bacteria with a common association with colon cancer?
Sreptococcus bovis - from polyps causing adenocarcinomas
the most common community acquired and lobar pneumonia of the middle of the right lobe and lower lobe on the left?
Streptococcus pneumoniae (group D strep)
major cause of meningitis in adults and otitis media in children?
streptococcus pneumonia (group D strep)
G+ cocci arranged in pairs (diplococci)?
streptococcus pneumonae (group D)
Major cause of meningitis in adults and children?
adults = Steptococcus pneumoniae children = group B streptococcus
three organisims that are associated with otitis media?
streptococcus pneumoniae, Haemophilius infuenzae, Moraxella catarrhalis
Quellung reaction?
pneumococci on a slide smear mixed with small amounts of antiserum (abs for the capsular antigens) and methylene blue, the capsule will appear to swell. used for rapid identification of streptococcus pneumoniae.
who gets a streptococcus pneumoniae vaccination??
given to people whom are pneumococcal pneumoniae would be exceptionally deadly like the immunocompromised or elderly, people without spleens, HIV disease.
wont work well in children
Genus and species of Staphylococci?
Staph aureus (MOST IMPORTANT)
Staph epidermis
Staph saprophyticus
testing for the three strains of staph?
aureus = G+, Cat +, Coagulase + (activates prothrombin to clot blood) epidermis = G+, Cat +, Coagulase - saprophyticus = G+, Cat+, Coagulase -
proteins that disable immune defenses for staph aureus?
Protein A (bind to Fc on IgG and protects from oponization)
Coagulase (leads to fibrin formation)
hemolysins (destroy, RBC, Neutrophils, MQ, and platlets)
leukocidins (causes CA-MRSA, Panton-Valentine Leukocidin (PVL))
Penicillinase (disrupts penicillin molecules)
Novel penicillin binding protein (transpeptidase used for inhibition of penicillin.
Staph Aureus exotoxins and diseases
Exfaliation (causes skin to slough off - scalded skin syndrome)
Enterotoxins (heat stable) - cause food poisening, resulting in vomiting and diarrhea
Toxic Shock Syndrome Toxin (TSST-1) - causes a t cell response to out pour cytokines.
three diseases caused by staph aureus exotoxin release?
Gastroenteritis (food poisoning)
Toxic shock syndrome
scalded skin syndrome
pneumonia, meningitis, osteomyelitis, quick acute bacterial endocarditis with vegetation on valves, septic arthritis, skin infections, bacteremia, UTI, necrotizing sickness. associated with IV drugs.
Staph Aureus
causes of ankylosis of a joint?
Staph aureua, hemophalis influenzae, untreated gonorrhea.
bacteria that causes indwelling catheters, prosthetic devises with biofilms leading to sepsis?
S. epidermis
a leading cause (but second to E. coli) of community-aquired UTI’s in sexually-active young women?
S. saprophyticus
name the aerobic, G+, spore forming rod bacteria with a capsule made of protein (poly-d-glutamic acid) that prevents phagocytosis. It is acquired by contact with an infected animal or soil, or infected animal products. pt has widening of the mediastinum and hemorrhagic mediastinhtis. phagocytosed and released by MQ.
Bacillus Antharacis
means of infection of Bacillus Antharacis?
skin, pulmonary, GI
skin lesion with local tissue necrosis, evidenced by a painless found black lesion with a rim of edema. called a malignant pustule. can resolve spontaneously.
Bacillus anthracis
Bacillus Antharacis exotoxins of pOX1
Edema factor (inc cAMP disrupting the homeostasis) Protective Ag (promotes EF into phagocytosed cells) Lethal factor (zinc Metalloprotease that inactivates protein kinase) stimulates release of Il-1 and TNFalpha
Bacillus Antharacis plasmids leading to virulence?
pXO1 (collection of EF, PA, and LF) and pXO2 (poly-glutamyl capsule fo synthesis of the genes.
motile, non-encapsulated, and resistant to penicillin that causes food poisoning (nausea, vomiting,diarrhea)
Bacillus cereus
Anaerobic, G+, spore-forming, rod need a rapid diagnosis or pt will die
Clostridium
rapidly fatal food poisoning, due to neurotoxin that blocks the release of Ach from presynaptic nerve terminals on the automatic nervous system and motor endplates, causing flaccid muscle paralysis.
Clostridium botulinum
botulism
home-canned food, smoked fish, secreting a neurotoxin that will be potent when ingested. bilateral cranial nerve palsy, double vision (diplopia) and difficulty swallowing (dysphagia). followed by general weakness, rapidly leading to sudden respiratory paralysis and death.
Adult Botulism
TREAT WITH ANTITOXIN IMMEDIATELY to neutralize the free toxins.
ingest infected honey, constipated for 2-3 days, difficulty swallowing, followed by flaccid paralysis. pos BIG-IV.
infant botulinum
give human derived antitoxin.
rusty nails, anaerobic, found in soil and animal feces, releases tetanospasmin exotoxin leading to lock jaw and skeletal ms tetany. blocks the interneurons (Renshaw cells preventing GABA and glycine)
Clostridium tetani
Tetanus
inhibition of the inhibitory neurons.
wounded in battle. necrotic skin, moist, spongy, crackling, pockets of gas (crepitus). myonecrosis, diarrheal illness due to hemorrhagic jejunum.
clostridium perfringens
Gas Gangrene
antibiotic associated pseudomembranous (on the surface of the large intestine) colitis (diarrhea), follow by the use of longterm antibiotics. Toxin A causes diarrhea and toxin B is cytotoxic to colonic cells. characterized by severe diarrhea, abdominal cramping, fever.
pseudomembranous enterocolitis
clostridium difficile
can become difficult if you give Abs.
non-spore forming G+ rods?
Corynebacterium, Listeria
These are primarily pathogens of the pediatric age groups?
Corynebacterium dipttheriae and Listeria monocytogenes
child with a sore throat and fever has a grey exudate that seems darker and thicker than strep in the back of the throat that looks necrotic. what is it made from and what bacteria is colonizing? what should you do?
Corynebacterium Diptheriae and
composed of fibrin, leukocytes, necrotic epithelial cells
do not scrap off the membrane because the exotoxin will be released into the blood stream damaging heart and neural cells by interfering with protein synthesis. get cultures on potassium tellurite agar and Loeffler’s coagulated blood serum and give antitoxin, penicillin, and DPT vaccine.
explain how corynebacterium diptheriae looks on culture.
on potassium-tellurite plates the colonies turn grey to black within 24 hrs. on Loffler’s after incubation for 12 hrs by staining with methylene blue will reveal rod-shaped pleomorphic bacteria.
How are group A hemolytic strep an corynebacterium toxins related, in terms of interactive process resulting in pathogenicity, with external agent?
for nonimmunized children, not all C. diph secrete exotoxin, just like group A strep must first be lysogenized by a temperate bacteriophage to produce erythrogenic toxin that causes scarlet fever, C. diph must be lysogenized by a temperate bacteriophage which codes for the diphtheria exotoxin.
G+ aerobic bacillary bacteria that infects animals. in HIC pts it can cause necrotizing pneumonia in the upper lobe lung nodules and cavities with air fluid levels. can stain partially acid fast, leading to diagnostic confusion with TB.
Rhodococcus equi had the air fluid levels
TB rarely has air-fluid levels.
small facultatively anerobic, non-spore forming G+, 1-5 flagella when grown at 25 degrees Celsius. can also be cultures 4-10 degrees. virulence factors is Listeriolysin O does what?
Listeria monocytogenes
listerolyn O allows them to escape phagolysosomes of MQ and avoid intracellular killing.
causes placentitis in the third trimester of pregnant women due to eating infected coleslaw, milk, soft cheeses, butter, deli meats. causes neonate meningitis. causes meningitis in elderly and immunocompromised if with lymphoma, on corticosteroids or receiving organ transplants. also meningitis in AIDS pts.
Listeria monocytogenes
Diagnosed with a LP that will have high neutrophils, high protein, low glucose, G+ rods
Listeria monocytogenes
The only G- pathogenic diplococci
Neisseria meningitidis - treat quickly with nuchal regidity.
Neisseria gonorrheae
Virulence factors with Neisseria meningitidis
capsule separates sterogroups - ABC cause meningitis
Endotoxin (LPS) - causes blood vessel destruction and sepsis tiny petechiae and possible hemorrhage of adrenal gland.
IgA1 protease - cleave IgA in half
Pili - allow attachment to the nasopharyngeal cells and undergo antigenic variation.
groups susceptible to Neisseria meningitidis?
infants 6 months to 2 years.
army recruits
college freshman
invasive petechial rash, develops into vascular necrosis, high temp, high WBC, and hemorrhage on skin. diplococci seen on gram stain as G- that is cultured from petechiae.
Neisseria Meningitidis
abrupt onset of spiking fever, chills, arthralgia, muscle pains, petechial rash, G- diplococci cultured from blood, CSF, or petechial scrapings.
meningococcemia (N. meningitidis)
septic shock, bilateral hemorrhage into adrenal glads, abrupt hypotension, tachycardia, large petechiae. leads to DIC and coma or death in 6-8 hrs.
Fulminant Meningococcemia (Waterhouse Fiderichensen syndrome)
Number one cause of meningitis in adults in the US?
Neisseria meningitidis #2 is H. Influenzae
Characteristic culture medium for Neisseria meningitidis?
Thayer-Martin VCN vancomycin kills G+ colistin kills all G- but neisseria Nystatin eliminates fungi and high CO2
Male with painful urination and thick purulent discharge? infection spreads to epididymitis, prostatitis, and urethral strictures.
N. Gonorrhoea
female with painful urination, purulent discharge, reddened cervix, lower abdominal discomfort, dyspareunia, can progress to PID causing endometritis, salpingitis, oophoritis, fever, lower abdominal pain, abnormal bleeding, cervical tenderness.
relationship with menses and IUD?
greatest complications? what is untreated?
Neisseria gonorrhoeae
with menses the bacteria are able to spread from the cervix to the upper genital tract. IUD increases the risk of progression to PID.
complications infertility! (ectopic preg, abcess, peritonitis, peri-hepatitis)
untreated lead sto septic arthritis, rarely bacteremia.
Fitz-Hugh-curtis syndrome
peri-hepatitis - neisseria gonorrhoeae infect the capsule around the liver. upper right quadrant tenderness. may also follow chlamydial pelvic inflammatory disease.
opthalmia neonatorum
eye infection in the first or second day of life that can damage the cornea and cause blindness. erythromycin given to protect children from Gonorrhoea and Chlamydia of the eyes.
HACEK pathagens are what? what do they cause?
endocarditis: Haemophilus sp Actinobacillus sp Cardiobacterium sp eikenella sp Kingella sp
otitis media and upper respiratory infection in pts with COPD or elderly.
Moraxella catarrhalis
bacteria that cause no cell invasion diarrhea? clinical features
enterotoxigenic E. coli, vibro Cholera
watery diarrhea without blood
bacteria that cause diarrhea with invasion of the cells. clinical features?
local immune response at Peyers patches. few WBC in stool and may have RBC with a fever. enterichia coli, shigella, and salmonella
bacteria that cause diarrhea with invasion of local lymph and blood? clinical features.
systemic features: fever, headache, WBC elevated, RBC in stool, bacteremia.
salmonella typhi, yersinia enterocolitica, and camplylobacter jejuni
The hospital acquired G- or nosocomial G- bacteria? examples?
enteric bacteria
E. Coli, Klebsillapneumoniae, Proteus mirabilis, Enterobacter, Serratia, Pseudomonas aerginosa.
Testing for coliforms?
when you find E. coli in a water source, it means there is fecal matter, but does not tell you if E. coli is causing the diarrhea to the community.
three tests: presumptive, confirmed, complete.
Presumptive test?
lactose fermenters = E. Coli, and enterobacteriae
Confirmed Test?
EMB agar plate, E. coli will grow with a metallic green sheen at 45.5 degrees.
completed test?
metallic green ecoli colonies placed in broth again. the produce acid and gas.
enterics that can hydrolyze Urea?
proteus mirabilis, sqalmonella
Antigen classifications for Enterics?
O antigen is LPS of G-, K antigen is the capsule that covers the O antigen. H antigen make up bacterial flagella.
How can E. coli cause diarrhea?
nonpathogenic E. coli (normal flora) + virulence factors = DISEASE
Diseases caused by E. coli in the presence of virulence factors? (4)
Diarrhea, UTI, neonatal meningitis, G- sepsis in hospitalized pts.
How can E. coli cause death?
diarrhea to dehydration
ETEC?
travelers diarrhea, pili colonization factor is heat labile toxin causes NaCl reabsorption and Cl and HCO3 secretion into intestinal lumen. RICE WATER STOOL
EHEC
pili colonization factor that is Shiga-toxin (verotoxin) that inhibits protein synthesis of the 60s ribosome causing epithelial cell death. (like shigella toxin). bloody diarrhea with severe abdominal cramps is called hemorrhagic colitis.
Hemolytic uremic syndrome (HUS)
anemia, thrombocytopenia, renal failure, infection of EHEC called E. coli 0157:H7. outbreaks from infected hamburger.
EIEC
virulence factor shared by shigella and E. coli. E. coli INVADE the epithelial cells. immune mediated inflammatory reaction with fever, WBC in vade intestine, diarrhea blood with WBC.
Two types of diarrhea E. Coli can be indistinguishable from?
Vibro and Shigella
E. coli UTI?
due to pili that can climb the urethra and infect and cause cystitis, pyelonephritis, dysuria, and frequency.
most commmon cause of G- sepsis?
E. coli
and hospital acquire pneumonia
capsulated, G-, without flagella, hospital acquired, cavitary pneumonia with thick, coughed up “red current jelly” sputum. high mortality rate.
Klebsiella pneumoniae
can break down urea, OX-19, OX-2, OX-K that can cross react with Rickettsia for diagnosis, UTI and nosocomial infection. alkaline urine due to NH3
Proteus mirabilis
Enterobcter and serratia (family enterobacteriaceae)
enterobacter is highly mobile G-
serratia is non-mobile, bright red pigment, caused UTI, wound infections, and pneumonia.
never part of the normal gut flora, humans are the only host, causes dysentery that strikes preschool age children and nursing homes. colon will have shallow ulcers, fever, abdominal pain, diarrhea with flecks of bright red blood and pus, colon can become inflamed and unable to absorb electrolytes.
Enterobacteriaceae family
shigella - A and B subunits are bound. A subunit inactivates Ribosome 60s protein synthesis and kills the intestinal epithelia cells.
four species of shigella?
dysenteriae, flexneri, boydii, sonnei
found in animal feces, therefore acquired from fecally-contaminated water and is zoonotic infection (exept one species?) commonly from chicken or eggs. causes 4 diseases states in humans?
salmonella
salmonella Typhi isn’t zoonotic
typhoid, carrier, sepsis, gastroenteritis/diarrhea
salmonella antigen?
Vi antigen. this is a polysaccharide capsule that surrounds the O antigen.
fever with rose colored spots on the belly. 1-3 weeks after exposure, headache, abdominal pain that is diffuse or localized to the right lower quadrant (terminal ileum), spreads to regional lymph and seeds in multiple organs. spread by not washing hands. Facultative intracellular parasite. diagnosis?
typhoid fever/enteric fever
salmonella typhi
culture from blood, urine, or stool
how can one be a carrier or salmonella typhi?
can live in the gallbladder and can constantly be excreting bacteria.
causes of salmonella sepsis?
salmonella choleraesuis
patients with sickle cell anemia are prone to what type of sepsis?
salmonella osteomyelitis. vigorous antibiotic therapy needed.
most common type of salmonella infection and clinical apperance?
gastroenteritis: nausea, abdominal pain, diarrhea that is normally watery and less commonly has traces of blood. fever is half of pts. caused by a cholera-like toxin and sometimes has ileal inflammation. only fluid replacement needed.
not truly enteric bacteria but causes acute gastroenteritis. motile, G- rod. closely related to? how is it transferred?
drank milk, fever, diarrhea, abdominal pain, right lower quadrant pain with a mucosal ulceration in the terminal ileum.
Yersinia enterocolitica, closley related to Yersinia pestis (plague).
Fecal-oral
virulence of yersinia enterocolitica?
systemic invasion into lymph and blood. heat-stable enterotoxin of E. coli to cause diarrhea.
curved, G-, single flagella, fast moving, fecal-oral contamination, NO epithelial cell invasion, attach to epithelial and secrete what toxin? cause “rice water” stool/diarrhea. shock from isotonic fluid loss. death by dehydration. NO WBC in stool or RBC.
Vibrio Cholera
choleragen toxin - associated with cAMP production increases secretion of Na and Cl.
leading cause of diarrhea in Japan due to eating sushi?
Vibro parahemolyticus
three more common causes of diarrhea?
Camplylobacter Jejuni, ETEC, and Rotavirus
G- rod, single polar flagella, lives in jejunum, fecal-oral contamination, unpasteurized milk. common diarrhea in children. prodrome of fever, headache, followed by abdominal cramps, and BLOODY, loose diarrhea, spreads systemically and secretes LT toxin similar to that of E. Coli to destroy mucosal cells.
Campylobacter jejuni
most common cause of Duodenal ulcers and chronic gastritis. association with GALT lymphomas and gastric carcinomas.
Helicobacter pylori
evidence for why Helicobacter Pylori can cause stomach ulcers (4)
- cultured from ulcer craters
- feed to human volunteers and causes ulcer formation
- pepto-bismol has muth salts that inhibit growth
- antibiotics help treat duodenal and gastric ulcer disease.
comprise 99% of the GI flora by this obligate anaerobic, G- rod ?
Bacteroidaceae
one of the few G- bacteria WITHOUT lipid A in the outer membrane?
Bacteroides fragilis
normal gut flora, that during surgery, car accident, bowel perforation, or intestine ruptures leading to bacteria in the peritoneal cavity forming abscesses with a collection of WBC, fever, and dead tissue.
Bacteroides fragilis
abscesses may arise in a pt with a septic abortion, pelvic inflammatory disease, or IUD
Bacteroides fragilis
necrotizing anaerobic pneumonia, following GI aspiration. cultured from mouth and will turn black. pneumonic and peritoneal infections.
Bacteroides melaninogenicus
necrotizing anaerobic pneumonia, peritoneal infections, black pigment with cultures. WITH otitis media, and abdominal/pelvic diseases
Fusobacterium
strip or chain of cocci that are part of the normal flora of the mouth, vagina, and GI. microaeophillic, isolated from abscesses. in abscesses they’re mixed with viridans group strep.
Peptostreptococcus (anaerobic G+ cocci)
a serious complication in a very ill, debilitated, usually hospitalized. green pigment which is observable in infected wounds and at autopsy (pyroveridin and blue pigment = pyocyanin), sour/sweet smell like fermented grapes, will infect any system leading to bacteremia and septic shock
Pseuomonas aerginosa
clinical manifestations of pseudomonas aeruginosa infection?
(1) chronic pneumonia that can destroy the lungs of Cf and immunocompromised,
(2) Osteomyelitis in diabetes pts and inc risk of foot ulcer leading to osteomyelitis.
(3) burn wound infections can lead to fatal sepsis,
(4) UTI, pyelonephritis is common in nursing homes and hospitals,
(5) endocarditis on right heart valve due to IV drugs,
(6) malignant external otitis that can burrow to the mastoid bones in diabetes pts, corneal infections.
(7) sepsis due to IV or catheter infection
(8) corneal infections leading to cataracts.
G- bacillus, water and environment sources, infections on burns and ventilator pts. bronchielecasis or rapid progress from pneumonia to bacteremia. highly drug resistant. who has greatest risk?
Burkholderia (pseudomonas) cepacia
CF pts have greatest risk
G- anerobe, can cause pneumonia, line related bacteremia, burn infections, foley catheter associated UTI, may appear G+ but aren’t, coccillary or coccal appearance and in solid media form diplococci.
most common sp?
Acinectobacter
Acinectobacter baunannii is most common
G- rods that are grouped together because of they are acquired through the respiratory tract.
Haemophilis Influenzae
Bordetella pertussis
Legionella pneumophila
define hemophilus
“blood loving”, hemophilus influenzae needs hematin for cytochrome an NAD+ for metabolic activity.
how are the subtypes of Hemophilus influenzae separated? child diseases?
due to the polyribitol ribose phosphate capsule. A-F and B is the most common with invasive hemophilus influenzae in children causing meningitis, epiglottitis, and septic arthritis.
difference between type and non-type hemophilus influenzae? clinical manifestations?
non type is not and invasive causing only local infections of the upper respiratory tract in children and adults.
children = otitis media
both = respiratory disease, chronic bronchitis with smoking or recent viral infection.
age related factors in hemophilus influenzae?
pts with COPD get frequent nontypable infections worsening the wheezing, shortness or breath and cough
Abs are lacking in children 6 months - 3 years. takes 3-5 years for make own abs and only other way to get them were breast milk or transplacentally.
vaccination for hemophilus influenzae?
protective to the B capsule for children older then 18 months. within the DPT vaccine. also give vaccine at 8 months pregnant to inc antibody secretion in breast milk.
want to stimulate abs as early as possible.
obligate human parasite usually transmitted via the respiratory tract?
Hemophilus influenzae
diseases with Hemophilus influenzae, type b
(1) meningitis - 6months - 3 years
(2) acute epiglottitis - rapid sealing causing wheezing (stridor), cherry red spot on tongue, manipulation of larynx can cause obstruction.
(3) septic arthritis - most common cause in children, single joint, fluid has G- pleomorphic rods
(4) sepsis - more common is spleen is compromised or sickle cell
what causes a painful genital ulcer, unilateral painful and swollen inguinal lymph nodes that rapidly develop and can rupture releasing the pus. what else should you consider? G stain?
Hemophilus duceryi
consider syphillis (painless), Herpes 1/2 (blisters, fever, myaliga), lymphogranuloma from chlamydia (painless, matted, purulent lymph nodes, and then a slow chancoid).
G- coccobacilli
bacteria causing vaginittis with vaginal discharge with “clue cells” (tiny pleomorphic bacilli within cytoplasm)
Gardnerella vaginalis
define whooping cough and the three stages.
Whooping Cough: with adolecents and adults whent eh vaccination is waning. booster recommeneded 19-64 years. tranmission is respiratory secreations on the hands or in the aerosolized form. a week long incumation followed by three stanges.
- cararrhal stage: lasts 1-2 weeks with URI, low-grade fever, runny nose, sneezing, and mild cough. this is whent he disease is most contagious.
- Paroxysmal stage: fever sunsides and the are burts of nonproductive cough spells. followed by vomitting and gasps due to the narrowed glottis. can cause chronic cough in adolecents for about a week.
- convalescent stage: attacks stop and the pt is no longer contagious.
can cause chronic cough without these stages, will have ince lymphocyte but not neeutrophil counts.
will not grow on cotton, calcium alginate swab used to culture post a cough. made of Bordet-Gengou medium made of potato, blood, and glycerol agar.
G- that causes whooping cough with 4 major virulence factors.
Bordetella pertussis
Virulance factors:
1. pertussis toxin - A and B subunits. activate G reulatory proteins, turing on adenylate cyclase, increasing cAMP that activates the protein kinase. causing histamine sensitation, increase in insulin synthesis, and promotion of lymphocyte production and inhibition of phagocytosis.
2. extra cytoplastic adenylate cyclase. impairs chemotaxis and generation of H2O2
3. Filamentous hemagglutinin (FHA): they done invade the body. the pilli allow the bacteria to attach and release exotoxins. antibodies are protective.
4. tracheal cytotoxin that destroys ciliated epithelial cells resulting in impaired clearance of bacteria, mucus, and inflammatory exudate. this causes the violent cough.
Water loving/air conditioner loving, G- rod, that is very small and hard to gram stain, will live in amoebas and will survive within a low metabolic stage on a biofilm that can be disturbed and spread into the water.
Legionella pneumophila
Pontiac fever?
caused by Legionella pneumophila - headaches, muscle aches, fatigue, and fever with chills that are localized.
Legionnaires disease?
caused by legionella pneumophila - classic with a very high fever and pneumonia.
G-, zoonotic, agressive virulent diseases that can penetrate following a insect bits or direct contact with an animal, site of contact is usually skin and they are generally Facultative intracellular organisims who tend to spread to regional lymph nodes and then vital organs like the spleen, liver, and lungs. delayed cell mediated immunity: skin swelling and hardening 1-2 days post infection (4 bacteria)
Yersinia, Frencisella, Brucella, and Pasteurella.
bubonic plague, still in rats in Arizona and New Mexico, reservoir is rats, vectors are fleas. G- bipolar staining pattern, primarily within rodents and humans. SW US is an area of interest.
Yersinia pestis
invade the skin and will be eaten by MQ (faculative intracelluar organisim). moving to the nearest lymph noeds (buobon = groin) and will swell uop and become hot, red, and painful. fever and headache. invades lood. hemorrages under skin cause blackig discoloration to call bubonic plague the “black plague”. pneumonis plagus, and with poneuminia and human to human tranmission by aerosolized bacteria.
Yersini pestis
Virulence of Yersinia pestis
virulance =
Fraction 1 (F1) this capsular antigen has antiphagocytic properties.
V and W antigens are proteins and lipoproteins respectivly.
considered in differential with Yersini pestis and why?
Francissella tularensis but often has a characteristic skin ulcer.
can get it by touching infected rabbits and from tick/deerfly bites. hard to culture, only need ten organisms to cause disease. two major clinical manifestations. diseases caused eye and GI invasion
Francisella tularensis
(1) Ulceroglandular tularemia: skin ulcer
(2) pneumonia tularemia
oculoglandular tularemia (eyes), typhoidal tularemia (GI)
named after cows, not very common in the US, undulant fever (slowly rises during the day and declines at night), chills, sweats, loss of appetite, backache, headache, and sometimes lymphadenopathy, can culture from bone marrow, blood, or lymph. serology? what will skin look like?
Brucella - assay for anti-burcella abs
will enter skin, conjunctiva, lungs, or GI. no ulcers or buboes.
NOT a facultative intracellular organism, G-, zoonotic, colonizes in mouth of cats. will grow under a closed wound and invade local joints and bones.
Pasteurella multocida
G- , very small, obligate intracellular parasites, that need animals for ATP, energy parasites that use a ATP/ADP transporter to steal ATP.
Chlamydia and Rickettsia
tiny, G- because it stains red but does not have a peptidoglycan layer, and has no muramic acid. fond of columnar epithelial cells that line mucus membranes causing conjunctivitis, cervicitis, and pneumonia.
Chlamydia
cell cycle and cellular localization of bodies
Chlamydia Life Cycle:
- elementary body (EB - 300nm) is the infectious particle and attaches to the cell and enters with endocytosis. it likes columnar spithelial cells with the conjunctiva, cervix, and lungs.
- one in the endosome, the EB inhibits the phagolysosome fusion and it not destroyed. it grows into the initial/reticulate body (IB - 100nm).
- once enough IBs are formed, some transform back into EB.
- the life cycle is completed when the host cell liberates the EB that can now infect other cells.
primarily infects the eyes, lungs, and genitals. leading cause of preventable blindness. transmission is hand to hand transfer of infected eye secretions and by sharing contaminated clothing or towels. blindness develops slowly over 10-15 years. Leading cause of preventable blindness and most common STD in the US
Chlamydia trachomatis
inclusion conjunctivitis is caused by a baby passing through an infected birth canal. inflammation is purulent, yellow discharge, and swelling of eye lids usually 5-14 days post birth. erythromycin eye drops are given prophylactically. then 4-11 weeks of life upper respiratory symptoms followed by rapid breathing, cough, and respiratory distress. what bacteria causes this and how is it diagnosed?
Chlamydia trachomatis
inclusion conjunctivitis = intracytoplasmic inclusion bodies in cells taken from scraping of the palpebral conjunctival surface.
pneumonia = diagnosed by anti-chlamydial IgM abs and/or chamydia trachomatis.
two Chlamydial diseases that are normally associated with respiratory disease?
Chlamydia psittaci and pnumoniae (spreads person to person with a respiratory route and has a single species (TWAR - taiwan and acute respiratory).
facts to now about chlamydia and rickettsiae
size = 350, obligatory intracellular parasites, RNA and DNA, reproduction through complex fission, antibiotic sensitivity, ribosomes, metabolic enzymes, NO energy production
species and sterotpyes of chlamydia that causes disease.
chlamydia trachomatis strotypes ABC = Trachoma (leading cause of blindness)
Serotypes D-K = inclusion conjuntivitis (neonates), infant pneumonia, cervictis, nongonococcal urethritiis in men.
serotypes L1-L3 = lymphogranuloma venereum (LGV)
chlamydophila psittaci = atypical pneumonia
chlamydophila pneumoniae serogroup TWAR = atypical pneuminia
women unknown of having a UTI that leads to infertility due to inflammation and fibrosis of the fallopian tubes.
Chlamydial diseases - chlamydia trachomatis
can also have asymptomatic urethritis
epididymitis in males - unilateral scrotal swelling, tenderness, and pain associated with fever
bacteria?
chlamydia trachomatis
Reiters syndrome?
inflammatory arthritis of large joints along with inflammation of the eyes and the urethritis
Fitz-Hugh-Curtis syndrome?
infection of the liver capsule with symptoms of right upper quadrant pain that can occur in men and women. associated with chlamydia and gnonococcal infection.
painless papule or ulceration on the genitals that heals spontaneously. bacteria migrate to regional lymph nodes becoming increasingly tender and may break open and drain pus.
Lymphogranuloma vereum with chlamydia trachomatis
bacteria causing atypical pneumonia that occurs 1-3 weeks post exposure to it dried out on feathers or dried feces.
Chlamydiophila psittaci - psittacosis
atypical vs typical pneumonia
atypical have less well defined infiltrates, dry cough, fever, and are less sick appearing that typical pneumonia.
small, G-, non-motile, coccobacillary bacterium, Arthropod vector (except one?), obligate intracellular parasites that grow in cytoplasm, not motile, no exotoxins, damages endothelial cells, culture is chick yolk sac, look for abs or Weil-Felix reaction.
Rickettsia
Except Q fever
difference between rickettsia and Chlamydia
Requires an arthropod vector
– Replicates freely in the cytoplasm
– Has tropism for endothelial cells (Chlamydia prefers
columnar epithelium)
– Cause different disease manifestations; most Rickettsiae
exhibit rashes, high fevers and severe headaches
– Some Rickettsiae share antigenic characteristics with
Proteus vulgaris; which lends itself to diagnostic utility – *theWeil-Felix reaction (OX-2, OX-19, OX-k)
fever, conjunctival injection (redness), severe headache, rash on wrists, ankles, and soles/palms initially, becomes more generalized later.
Disease? bacteria? reservoir? vector? serology?
Rocky Mountain Spotted Fever rickettsia rickettsii reservoir = dogs, rabbits, and wild rodents vector = wood tick, dog tick serology = OX-19 and OX-2 POSITIVE
vesicular rash similar to chicken pox, it resolves after 2 weeks. Weil-Felix negative.
disease? bacteria? reservoir? vector?
disease = Rickettsial Pox bacteria = Rickettsia akari reservoir = house mice vector = Mites that live on house mice
abrupt onset of fever and headache, rash that spares the palms, soles, and face, delirium/stupor, gangrene of hands or feet.
disease? bacteria? reservoir? vector? Weil-Felix?
disease = Epidemic Louse-borne Typhus bacteria = Rickettsia prowazekii reservoir = humans and flying squirrels vector = human body louse Weil-Felix = OX-19
Brill-Zinsser Disease?
due to Rickettsia prowazekii, mild symptoms, no rash
Fever, headache, rash, Weil-Fleix OX-19+
disease? bacteria? reservoir? vector?
disease = endemic or murine typus bacteria = Rickettsia typhi reservoir = Rats and small rodents vector = rat flea
fever, headache, scab at the bit site followed by rash, OX-K+
disease? bacteria? reservoir? vector?
disease = scrub typus bacteria = Rickettsia tsutsugamushi reservoir = rats, shrew, mongooses, bird vector = mite larvae (chiggers)
fever, headache and back pain that last 5 days and recurs at 5 day intervals, bacteremia, endocarditis, and bacillary angiomatosis.
disease? bacteria? reservoir? vector?
Trench fever
Bartonella quintana
humans, body louse
(low yield)
cat scratch with regionally enlarged lymph nodes, low grade fever that resolves with few complications. but can cause bacillary angiomatosis, bacteremia, endocarditis “cultures negative”
disease? bacteria? reservoir? vector? Weil-Felix?
Bartonella henselae
spread through cats?
PCR no Weil-Fleix
fever, headache, viral-like pneumonia, no rash. possible complications: hepatitis and endocarditis
disease? bacteria? reservoir? vector? Weil-Felix?
Q fever Coxiella burnetii cattle, sheep, goats no arthropod vector, direct airborne transmission or consumption negative Weil-Felix (ab and PCR)
fever, conjunctival redness, severe headaches, no rash
ehrlichia chaffeensis (HME)
Tiny G- organisms with corkscrew configurations of various types, difficult to culture, use dark feild microscopy, silver stains, and serologic tests. three genra?
Sprochetes:
Treponema sp.
borrelia sp.
Leptospira sp.
Two reasons Spirochetes are unique?
two reasons they are unique:
1. they have an additional phospholidid-rish outer membrane with a few exposed proteins. making them immunoresistant.
- axial flagella come out of the ends of the spirichete cell wall, but rather than protude out of the oter membrane. this is called a periplastic flagella. this causes it to spin.
how do treponema cause disease?
they do not have any known toxins or tissue destructive enzymes. disease is caused by the host’s own immune responses such as inflammatory cell infiltrates, proliferative vascular changes, and granuloma formation.
clinical presentations of the stages of syphillis?
Primary = painless chancre (ulcer) (3-6 weeks without scar) Secondary = rash on palms and soles, condyloma latum in vulva or scrotum, CNS, eyes, bones, kidneys, and joints involved (6 weeks) Latent = 25% may relapse and develop secondary stage symptoms again Tertiary = Gummas of skin and bone (deep gnawing pain), cardiovascular (aortic aneurysm), neurosyphilis. (6-40 years)
presentation of neurosyphilis?
- Asymptomatic but CSF is pos
- subacute meningitis (fever, stiff neck, headache, high lymph, high protein, low glucose, pos for syphillis)
- meningovascular syphilis (circle of willis occlusion)
- Tabes dorsalis (affects posterior spinal cord posterior column and dorsal roots)
rule of 6 with syphillis
six looks like sex? (sexual transmission)
6 axial filaments
6 weeks incubation
6 weeks for the ulcer to heal
6 weeks after the ulcer heals secondary develops
6 weeks of secondary syphilis to resolve
6 years to develop tertiary syphilis.
66% laten stage pts resolve without tertiary
bacteria that causes syphilis?
Treponema pallidum
clinical presentation of congenital syphilis? early vs late?
can cross placenta causing a high mortality rate, still birth, abortion, neonatal death.
early = within 2 years of adult, child had rash and condymloma, snuffles, and osteities seen on X ray
late = similar to adult with cardiovascular involvement, saddle nose, saber shins, upper central notch in each tooth (hutchinson’s teeth and molars have too make cusps (mulberry molars)
diagnostic tests for syphilis
non-specific treponemal tests (anti-lipoidal abs)
specific treponemal tests ( for the spirochete)
All treponemal subspecies (often called non-venereal) tend to
cause skin ulcers and gummas of the skin, except for ? whose primary manifestation is usually skin discoloration
carateum
Jarish-Herxheimer Phenomenon
acute worsening of their symptoms when abs are started (mild fever, chills, malaise, headache, and muscle aches) becuase the killed organism is a pyrogen.
spread by sharing drinking and eating utensils, primary and secondary have oral chancres. name the subspecies
Treponema pallidum:
Endemicum (Endemic syphilis, bejel)
Pertenue (yaws)
Carateum (pinta)
Large spirichetes that can be seen under a light microscope with giema or wright stains
Borrelia
bacteria that causes lyme disease. reservoir? vector?
Borrelia burgdorferi
reservoir = white-footed mouse and white tailed deer
vector = Ixodes (ticks)
stages of lyme disease?
1: early localization - erythema chronicum migrans
2: early dissemination stage - smaller ECM, neurologic (aseptic meningitis, peripheral neuropathy, bells palsy, peripheral neuropathy), cardiac (transient heart block or myocarditis), brief attacks of arthritis of large joints (Knees).
3: late stage - chronic arthritis, encephalopathy
recurring fever about every 8 days, fever breaks with drenching sweats, rash, splenomegaly, occasional meningeal involvement. disease? bacteria? reservoir? vector?
Relapsing fever
borrelia recurrentis
wild rodents in western US
louse (lice)
long, thin, aerobic spirochetes that are wound up in a tight coil, that hook on the ends. usually found in contaminated urine.
Leptospira
phases of Leptospria interrogans?
Phase one: bacteria invade the blood and the CSF. high spike in fever, headaches, malaise, and severe ms aches in the thighs and lower back. conjuntiva may have photophobia. lasts 1 week.
Phase two: correlates with the appearance of IgM abs. and elevated WBC in CSF.
Weil’s disease?
Weil’s disease involved renal failure, hepatitis with jaundice, mental staus changes, hemorrhage in many organs.
associated with subgroup icterohemorrhagiae
acid fact bacteria?
Mycobacteria
thin rods, liid laden cell walls, only infect humans, 10 million new cases and 3 million deaths worldwide. acid fast organism, takes two weeks to culture and will not gram stain. will stain red and acid-fast stain. Obligate aerobe. will first colonize in the lungs (intracellular facultative in early infection) and can take up to 6 weeks for visible growth. will form globs due to hydrophobic lipid nature, resulting as globs on agar and floating blobs on liquid media.
Myobacteria
virulence of myobacteria?
Mycosides involved in organism virulence, this is a large fatty acid (mycloic acid) bound to a carb.
pathogenesis of TB? necrosis?
First have faculative intracellular growth and that is recognized early with Abs with spread throughout the body. second is cell mediated MQ recognize the bacteria and make granulomas with caseous necrosis. these can calcify and scar. the bacteria are kept at bay, but are still viable.
cell mediated immunity with caseous necrosis (duh)
PPD skin test?
PPD = Purified protein derivative, will cause type 4 hypersensitivity. reveals if the person has every been infected with Tb and has Abs to the bacteria. Pos PPD is considered to have laten TB. Pos test is >5mm for a person that is immunosuppresed, >10mm for a person with common exposure to the factors (live in high incidence, medical feild, incarceration, high risk medical condition, >15 mm for normal people. Does not mean the person has active TB, means they have been exposed before. FALSE pos with a person that has recieved the BVG (bacillus Calmette-Guerin) vaccine against TB. Fasle neg means they are anergic due to lacking normal immune responce.
Clinical manifestations of TB
primary vs secondary?
Primary: is after the first exposure to mycobacterium tuberculosis and can cause an asymptomatic lung exposure. this is due to cell mediate immunity.
Secondary or reactivation is when they rise up after being dormant and create granulomas
Pathogenesis of primary TB
Primary: infected due to aerosalized TB that can be spread through a cough, singing, laughing, or talking. they will land in the middle and lower lobes due to the highest air flow. neutrophils will collect and there will be a little edema.
- Asymptomatic: cell mediate defences kick in and there is little scaring on a chest X-ray. ttiny tubercles are often too small to notice on a chest X-ray but will show up on a PPD. Ghon focus = calcified tubercles in the middle and lower lobes. normally accompanied by peripheral calcifications called Ghon (Ranke) Complex
- Symptomatic: more common in children and elderly and immunocompromised. Chest X ray will show enlargment of the mediastinum or hialar lymph nodes and possibly lower and middle lobe infiltrates. can become ill with pulmonary disease. granulomas can leak the pus and become cavitary lesions
Secondary TB
Seconday: is an infection that can occur within any other organ. Pulmonary will be in atypical areas around the lungs. pleural and pericardial infections, lymph nodes (Scrofula), Kidney (from urine it takes weeks to grow and called sterile pyuria, Skeletal (pott’s disease), Joints, central nervous system, miliary are tinny granulomas all over the body.
always suspect Tb when?
there is weight loss and an infection within a organ
how to diagnose TB?
PPD - 1/3 will be a false neg
Cest X-Ray - isolated granulomas
sputun acid fast stain culture - active pulmonary infection.
Rapid Molecular detection of MTB - with a sputum sample you can recognize MDR and XDR TB
Rules of 5 with TB
a droplet of nuclei are 5 micrometers and contain 5 mycobacterium tuberculosis bacilli.
pts infected with TB have 5% risk of reactivation in the first 2 years and the 5% in their lifetime.
pts with HIGH FIVE HIV will have a 5+5% risk of reactivation per year.
Acid fast rod that is IMPOSSIBLE to grow on artificial media. infected persions normally have a unknown reason for being susceptable. infection can occur if exposed to respiratory secreations, or less likely, skin lesions of infected individuals. it damages the SKIN sparing the warm parts of the body (arm pit, groim, perineum).
Myobacterium Leprae
disease = leprosy
Pts with this CANNOT mount a cell mediate immune responce. maybe a defective t-8 cell. facial skin will thicken causing the face to look lion like (leonine facies, nasal cartilage can be destroyed creating a saddlenose defermity, and testicular damage. along with peripheral nerve involvment leading to loss of sensation in the extremities.
Lepromatous Leprosy
pts CAN mount a immune responce leading to a milder and self limiting disease. there can be a localized superfical, unilateral skin and nerve involvment. well defined, hypopigmented, elevated, hairless, and absent sensation by nerves, moat frequwntly involes nerves closet to the skin. pts are non-infections and will spontaneously recover.
Tuberculoid leprosy
normally seen in AIDs pts. CD4 T cell count is
Mycooobacterium avium-intracellulare - MAC
bacteria without cell walls?
Mycoplasma
tiniest free living organisisms capable of self-replication. that are smaller than some virus.
mycoplasma
mild self-limiting bronchitis or pneumonia. common in teanagers and young adults. attaches to epitheliaum due to protein P1 and has a 2-3 wekk incubation period causing fever, sore throat, malaise, a persistant dry hacking. also reffered to as walking pneumonia becuase they dont feel that sick. chest X-ray will show streaky infiltrates. and will last in lungs up to two weeks post stopping of clinical symptoms.
some pts will get erythemia multiforme or stevens johnson syrdrome of a skin reaction causing vesicles and bllae over the mucocutaneous junctions of the eyes, mouth and skin.
Mycoplasma pneumoniae
diagnosis for mycoplasma pneumoniae
cold aggulations - cause the blood to clot when cold in a none clotting vial. will unclump when warm.
complement fixing
sputum culture - willlook like a fried egg and have a round bumpy appearance likened to mulbery.
mycoplasma DNA probe
PCR
named this way becuase it likes to swim in urine and break down urea. reffered to as the T-strain, makes tiny collonies in the shape of a T. normal flora of sexually active women in the lower urinary tract causing urethritis and yellow mucoid discharge. releases ammonia and carbon.
ureaplasma urealyticum
