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BACTERIOLOGY SUMMARY [ SEM 5.

]
Lec 1
Joseph Lister(1860) = father of aseptic techniques
Robert Hooke(1876) = Cell theory + proved that a specific bacteria caused
disease
Kochs Postules Exceptions = Vaccination
Edward Jenner (1796)= invented vaccines (vacc. of cowpox protected from
smallpox too)
Anton van Leuwenheuk(1673) = 1st microscope
Louis Pasteur: disproved spontaneous generation, fermentation,
Pasteurization, Silkworm disease cause, Rabies vaccine, Aerobes and
Anaerobes + Pasteur Institute
Protozoa = unicellular eukaryotes
Quinine= to treat malaria
Salversan = to treat syphilis, discovered by Paul Ehlrich
Compound light microscope resolution = 0.2um
Numerical aperture= ability to gather light
Phase contrast microscopy= useful for examining live specimens
UV light = short wavelength
Pseudomonas fluoresce naturally under light
Flagellar H protein is an antigen in E.coli
Fimbriae and Pilli(proteins) = for attachment not motility
Exotoxin= LPS eg. O antigens !! Endotoxin(fatal causes septic schock)=protein
eg.Lipid A
Mycoplasma and Nocardia = Acid fast (coz they contain mycolic acid)
Mycoplasma lacks cell wall
Archeas cell wall has NO peptidoglycan
Protoplast = product of destruction of gram +ve cell wall
Spheroplast = remain of partial destruction of gram ve cell wall
Bacteria contain plasmids = extrachromosomal DNA molecules
Antibiotics work on prokaryotic ribosomes(70s)not eukaryotic ribosomes(80s)
Inclusion bodies(reserve deposits) = found in prokaryotic and eukaryotic cells
Gram +ve Endospores = resting structures formed by BACILLUS(aerobes) AND
CLOSTRIDIUM(obligate anaerobes)
Sporulation = process of endospore formation
Germination = return of endospore to vegetative state
E.coli O157:H7 causes bloody diarrhea
(E.coli also causes food poisoning)
Gram ve strictly aerobes = PSUEDOMONAS + NEISSERIA(causes gonorrhea)

Gram ve facultative anaerobes = ECHERICHIA + SALMONELLA + PROTEUS


Gram ve obligate anaerobes = FUSOBACTERIA +BACTERIODS
Gram +ve cocci = MICROCOCCUS+STAPHYLOCOCCUS + STREPTOCOCCUS
Gram +ve sporing= BACILLUS + CLOSTRIDIUM
Gram +ve non sporing = LACTOBACILLUS
Gram +ve irregular rods = CORYNEBACTERIUM DIPTHERIAE
Holoenzyme = Apoenzyme(protein pt.) and Cofactor(non protein pt.)
Competitive inhibitors for enzymes active site= Penicillin and Sulfanilamide(in
enzyme that converts PABA to folic acid
Incubation requirements:
1. Tempreature :

I.
II.
III.
IV.
V.

2. PH

I.
II.
III.
IV.

Pschrophiles (cold-loving)
Mesophiles (moderate temp loving)
Thermophiles (heat-loving)
= 60
Physchrotrophes
Hyperthermophiles (grow at 80 degrees eg. Archea)

Acidophilic
Neutrophilic
Basophilic
Halophilic (salt loving)

3. Osmotic

I. Hypertonic
(causes Plasmolysis = cell shrinkage)
II. Isotonic
III. Hypotonic
(causes cell burst)
4. Oxygen [SOD enzyme is to break down superoxide free radicals,
NOT FOUND IN Anaerobes or Microaerophiles]

I.

Obligate Aerobes(must have SOD and catalase/peroxidase)


(EG.PSEUDOMONAS
II. Facultative Anaerobes (eg. E.coli, Staphylococci and some yeasts)
(same as above)
III. Obligate Anaerobes( EG. CLOSTRIDIUM TETANI)
IV. Aerotolerant anaerobes (have SOD enzyme)(EG LACTOBACILLUS)
V. Microaerophiles (EG.CAMPYLOBACTER)
Eg. Of reducing media = Sodium thioglycolate
Candle jar = free of oxygen
Capnophiles = microbes that require high CO2 concentration
Bacteria that do not grow on artificial media:
1) Mycobacterium leprae(leprosy)--------- grows in armadillos
2) Troponema pallidum(syphilis)---------grows in rabbit testicles
3) Obligate intracellular bacteria( EG. Rickettsia and Chlamydia)--------- only grows in
host cells

Selective Media

a. Sabouraud Dextrose Agar = to isolate fungi


b. Brilliant green agar = suppresses gram +ve and isolates SALMONELLA(gram ve)

Differential media
a. Blood agar = bacteria that destroys RBCS(hemolysis) eg. S.PYOGENES

Selective and differential media


1. Mannitol Salt Agar = to distinguish S.AUREUS (has 7.5% NaCl to inhibit other organisms and phenol
red indicator for when mannitol is fermented to acid: red TO yellow)
Enrichment Culture = Used for microbes found in small amounts (eg. For soil and fecal samples)
Most common method of Isolation [to obtain a pure culture] = Streak Plate(using a sterile loop) [ use a fine needle
in obtaining a specific microbe from a culture sample bcz it wont be pure!]
Lyophilization = freeze drying

Reproduction in Prokaryotes
1.Binary fission (main method for bacteria)
2.Budding
3.Conidiospores (eg.actinomycetes)
4.Fragmentation of filaments
Generation time = time required for a cell to divide and its population to double
Bacterial growth curve:
I.
Lag phase= adjustment to new conditions
II.
Log phase= cells produced more than cells dying(affected by radiation and antibiotics)
III.
Stationary phase= cells produced = cells dying ( rate of prod decreased due to) :
Accumulation of toxic waste material
Acidic ph of media
Limited nutrients
Insufficient oxygen supply
IV.
Death or decline phase = cells dying greater than cells produced
Biosafety levels : 1 - 4 (eg. Ebola)
Commercial sterilization: killing CLOSTRIDIUM BOTULINUM endospores
Sterilization : by autoclave (121 C for 15 mins)
Pasteurization includes
63 C for 30 mins
2 C for 15 sec
140 C for <1 min
*** DESTRUCTION OF ENDOSPORES:

115 C for 70 mins

OR

125 C for 7 mins

Desiccation (absence of water) = prevents metabolism


Actions of Microbial Control Agents
1. Alteration of membrane permeability
2. Damage to proteins
3. Damage to nucleic acids
Halogens (Iodine= alters protein synthesis and membranes) OR (Chlorine= oxidizing agents)

Lec 2
ANTIBIOTICS

Mycobacteria = isonaziade and streptomycin


GRAM -VE bavteria = streptomycin + tetracycline
Gram +ve bacteria = penicillin G + tetracycline
Intracellular bacteria =tetracycline
Fungi = Ketonazole
Protozoa = Mefloquine eg. MALARIA
Viruses = Acylovir

Penicillin G = staph,strept and spirichaetes


Oxacillin =MRSA
Uses of penicillin
1.Skin infections
2.Dental infections
3.Ear infections
4.Resp. tract infections
5.UTI
6.gonnorhea
Cephalosporins
1st generation (eg Cefalexin by IV) works on gram +ve
2nd generation(eg.cefaclor) (extended spectrum)
3rd generation (eg Cefixime) more activity on gram -ve and
PSEUDOMONAS
4th generation(eg.Cefepime) most extended spectrum
Bacitricin
gram +ve bacteria(eg. Staph and Strept.), used for tropical application
Vancomycin = derived from Streptomyces,narrow spectrum, used against
MRSA
Mycobacterium TB = Izoniazide(inhibits mycolic acid SYNTHESIS)
+rifampin
Ethambutol = Mycobacterium(inhibits mycolic acid INCORPORATION)
Chloramphenicol
binds to 50s portion and blocks peptide bond formation
Tetracycline = binds to mRNA(ribosomes) and blocks binding of tRNA
Streptomycin (Aminoglycosides)= binds to 30s portion disrupts reading
of mRNA

F factor +ve = fertility factor (in males)


F factor -ve = NO fertility factors (in females)
R factor = resistance factor to antimicrobial drug

Criteria for drug classification


1. Mecahnism of action
2. Chemical structure
3. spectrum of microbes it acts on
Chloramphenicol

- binds 50s subunit


Inhibits peptide bond formation
Affects bone marrow activity
Causes aplastic anemia

Aminoglycoside
antibiotics = Streptomycin+ Gentamycin + Neomycin
Works on 30s
Against gram -ve bacteria
Cause auditory nerve damage and kidneys
Streptomycin _____ TB
Gentamycin_______ Pseudomonas
Neomycin______ tropical application
Tetracyclines

Works on 30s
Produced by Streptomyces spp.
Effective against gram + and -ve as well as intracellular bacteria
Reacts with 30s subunit interferes woth attachment of tRNA at ribosome
Used to treat UTI, syphillis and gonnorhea

Macrolides
(eg erythromycin) and (azithromycin)
Bacteriostatic acts on protein synthesis
Against gram +ve cocci
Used to treat RTI, GIT and genital

Rifampin

Inhibits bacterial transcription


Effective against intracellular bacteria eg.Mycobacteria
Used against TB and Leprosy
Causes red- orange urine

Quinolone
Inhinits DNA gyrase reponsible for DNA replication
Used for UTI
Floroquinolones
(eg Norfloxacin and Ciprofloxacin)broad spectrum , for UTI skin infections
and resp infections
Cipro = for anthrax
Polymyxin B
fungicidal, acts on cell membrane, narrow spectrum
Effective against gram -ve (Pseudomonas)

Sulfonamides
inhibit mtabollic processes(EG.septrin = bacteriostatic and broad
spectrum)
Inhibits folic acid synthesis by PABA
Inhibitory activity of sulfa drugs is by SIMILARITY in structure with PABA
NOTE: READ ALL TESTS IN LEC 3 SLIDE 41-48

LEC 5-6
Common causes of nosocomial infection:

1. Staphylococci
2. S.aureus
3. Enterococcus
4. C.difficile

Weather changes = Hantavirus


Ecological disaster (eg. War ) = Coccidiomycosis
Resp.tract = most common route of entry
ID50(Infectious dose) = no. Of microbes required to produce infection in 50% of the
population
LD50(lethal dose) = amount of toxin or pathogen necessary to kill 50% of the popn in a
particular time frame
Microbe adherence by Ligands (most common = mannose) frequently assos with fimbraie
Exotoxin (from gram +ve only, protein, has an antitoxin and is highly toxic)

3 types of exotoxin
1. AB toxin (eg.botulinum and tetanus toxin)
2. Membrane disrupting toxins(eg leukocidins) and (hemolysins like S.pyogenes)
3. Superantigens cause release of cytokines( eg. Staphylococcus)
TYPES OF EXOTOXINS:
1) Cytotoxin
i) Diptheria toxin( AB Toxin that inhibits protein synthesis)
-from Corynebacterium diptheria
ii) Erythrogenic toxin (superantigens that damage capillaries) -from S.pyogenes

2)Neurotoxin
i)Botulinum toxin (AB toxin that prevents nerve impulse transmission, results in flaccid
paralysis)
- from Corynebacterium botulinum
ii)Tetanus toxin or Tetanospasmin (AB toxin that prevents inhibitory nerve impulse
transmission, results in spasmodic muscle contractions)
-from Clostridium tetani

3)Enterotoxin
i)Vibrio enterotoxin(AB toxin stimulates secretion of fluid and electrolytes causing
diarrhea.
-from Vibrio Cholerae
ii)Staphylococcus aureus(superantigen)
-from Staphylococci
S.pyogenes = membrane disrupting exotoxin. Erythrogenic.
Endotoxins = from Lipid A component of gram ve only, LPS, has fever, no antitoxin, large
LD50 and less toxic
Endotoxins are released by= bacterial cell death, antibiotics and antibodies
Endotoxins cause macrophages to release large amounts of cytokines(symptoms fever and
shock)
Organisms that have endotoxins include:
1. Salmonella typhi
2. Proteus sp.
3. Neisseria meningitides
S.aureus (superantigen) causes eith food poisoning, or toxic shock syndrome
Clostridim sp. (membrane disrupting) (eg. C.perfringes gas gangrene and food poisoning)
(eg.C.difficileantibiotic-assosciated diarrhea)
E. coli and Shigella cause Travellers diarrhea
S.pneumonie alpha hemolytic, optochin sensitive, bile soluable and capsulated(+ve quelling test)
S.viridans (eg.mutans or sanguis), optochin resistant, not bile soluable and no capsule

S.pyogenes = Group A beta hemolytic, bacitricin sensitive


S.agalactiae = Group B beta hemolytic, bacitricin resistant
Enterococcus (eg. E.fecalis and E.fecium) = gamma hemolysis( no hemolysis)

(Lec 7)

DIGESTIVE SYSTEM
Tooth decay or DC = Endogenous infection
PORPHYROMONAS GINGIVALIS:
A. Most likely cause of periodontal disease
B. Belongs to bacteroids
C. Non motile
D. Gram ve
E. Rod-shaped
F. Pathogenic bacterium

Trench moth AKA (Vincents Disease or Acute Necrotizing Ulcerative Gingivitis


= ANUG) caused by
o Troponema and Fusobacterium species
o Sign = pyorrhea, recession of the gum
o All ages susceptible
All oral diseases can cause bacterial endocarditis
Infection = due to pathogen in GIT, incubation period is 12 hrs to 2 weeks,
symptom delayed = FEVER
Intoxication = due to ingestion of preformed bacterial toxins, incubation
period= 1-48 hrs (rapid onset), Fever is NOT A SYMPTOM
Both infection and intoxication causes diarrhea and dysentery
Staphylocoocal food poisoning( Exotoxin= heat resistant), cause of
gastroenteritis. (1 6 hrs)

Enterobacteriaceae
1. Grow in aerobic or anaerobic conditions
2. Ferment glucose
3. All motile EXCEPT: Shigella and Klebsiella
4. 2 toxins [Exotoxin = Enterotoxin and Cytotoxin called shiga] and
[Endotoxin = E.coli]
5. Other eg. Yersinia, Salmonella, Klebsiella, Enterobacter and Proteus
Antigenic structure
A. O antigen: LPS (endotoxin) is Heat stable
B. H antigen: flagellar protein is Heat labile
C. K antigen: capsular(surface)

E.coli :

Indicator organism for fecal contamination


Most frequent human bacterial infection
Have fimbriae
Infections = UTI, peritonitis, appendicitis, postoperative wound infection,
neonatal meningitis and Sepsis
Lactose fermentors, capsulated have O,K,H and fimbrial antigens
1. Enterotoxigenic E.coli
Produce enterotoxins
Cause Travelers diarrhea
Not invasive
In children = watery diarrhea
In adults = cholera like symptoms
2. Enteroaggregative E.coli
3. Enteroinvasive E.coli
Results in cell destruction bloody diarrhea
Cause Shigella-like dysentery
4. Enteropathogenic E.coli = wasting form of infantile diarrhea
5. Enterohemmorhagic E.coli: [E.coli 0157:H7]
L: intestines of animals
Produce Shiga toxin
Causes hemorrhagic colitis

Hemolytic Uremic Syndrome


Symptom = blood in urine

Shingella
Shigellosis = non motile, non lactose fermenting and causes Bacillary
Dysentry
Shigellosis or bacillary dysentery primary causes:
Shigella dysenteriae
Shigella sonnei
Shigella flexneri
Shigella boydi

SHIGELLA IS CHARACTERIZED BY INVASIVE PROPERTIES


Transmission = Orofecal route, toxin = Shiga toxin, diarrhea
containing blood+mucus+pus, commonly fatal in infants.
Salmonella-shigella agar:
- E.coli will ferment the lactose in media, No H2S produced
- Salmonella does Not ferment lactose, H2S produced
- Shigella does not ferment lactose nor produces H2S

Salmonella:

Gram ve rod
Motile pertrichious
Most produce Hydrogen Sulphide
Detected by growing on ferrous sulfate
Cause = typhoid fever, paratyphoid fever and food-borne illnesses
Sources ( Peter)= birds and turtles/ food= egg, meat and chicken
L: tract of humans and other animals
Impo. Species = S.typhi, S.paratyphi, S.enteritidis (almost all are
pathogenic)
Transmission = eating raw or undercooked food/ Orofecal route
Salmonellosis = food-borne disease
Salmonella typhi and paratyphi cause TYPHOID FEVER
S.typhi= humans are the only reservoir mafi in animals, spread through
human feces, does not produce H2S gas in lab.
Typhoid fever= usually assoc with ulceration of intestinal wall, often resides
in gallbladder of asymptomatic hosts (eg. Typhoid Mary), treatment=
antibiotic and vaccine
Coliform bacteria = E.COLI

Klebsiella
Impo species. = Klebsiella pneumonie [ Opportunistic pathogens]
Causes Chest infections, bronchopneumonia, lung abscesses, UTI,
septicemia.

Cholera:
Life threatening disease
Results in hypovolemic shock and acidosis

Cause = Vibrio cholera


Source = surface or stagnant water
V. cholerea = Non invasive, has 2 biotypes O1(more common, ya classical
or El Tor) and O139
Gram ve slightly curved rod, with a single polar flagella
Grows in ph = 7.4 9.6
Impo. Species= V.cholerae, V. parahemolyticus, V.vulnificus
Vibrio enterotoxins causes a rise in Camp
V. cholerae v. sensitive to stomach acids
V. cholera in the small intestine produces an exotoxin, that causes excretion
of K+
Incubation period = 6 48 hours
Sign = rice-water stool
Lab diagnosis= culture stool sample in thiosulfate-citrate bile-sucrose or
slide agglutination test.
V. parahemolyticus = halophilic, assoc with enteritis and acquired by raw or
improper cooked food
Antibiotic treatment = Doxycycline

Campylobacter Gastroenteritis
Cause = Campylobacter jejuni
Campylobactor species = gram ve, microaerophilic,nonferemnting,motile,oxidase-+ve, grow at 37 and 42 C, source = birds and
untreated birds, transmission = orofecal route, most common cause of
diarrhea.
Lab diagnosis = darting motility, in dark field microscopy, capnophilic,
thermophilic, oxidase and catalase +ve, sensitive to nalidixic acid,
antibiotic = Modified Skirrow medium( Erythromycin and Ciprofluxacin)
Guillian Barre Syndrome= most coomon cause of acute neuro-muscular
paralysis, due to formation of antibodies against C.jejuni

Helicobacter pylori:
Major transmission = person to person contact
Assoc with Chronic Superfiscial Gastritis
Responsible for most peptic ulcer diseases(gastric and duodenal ulcers)

Usually asyptomatic
Cariogenic bacterium and gastric cancer
Lives in mucus layer over but protected from gastric acid
Most effiecient producers of urease hence relaeases NH3 to buffer acidity
Highly motile
Survives at acidic ph (2-3)
Lab diagnosis= Urea breath test, Upper gastrointestinal endoscopy, gram
stain
.

Clostridium:
Sporing bacteria
Source = soil and GIT of humans and animals
Cause= gas gangrene,tetanus, botulism, and PMC
Clostridia= gram +ve, large, rod-shaped bacteria, anaerobe, all form
endospores, grow under aerobic conditions

Clostridium difficile-assosciated diarrhea:


1. Colitis and PMC
2. Found in stools of healthy person
3. Cause by antimicrobial chemotherapy. Elimination of
competing bacteria
4. Exotoxin production (toxins are very unstable),detected by PCR
assays
5. Nosocomial disease
6. Cell cytotoxicity test = tissue culture
Clostridium perfringes:
1. Causes gastroenteritis
2. Has endospores survive heating and germinate
3. Exotoxin causes symptom
4. Diagnosis: bacteria in stool samples
5. Lab: Nagler test
Mumps = belongs to paramyxovirus, transmitted via saliva and respiratory
secretions, entrance = respiratory tract, treatment = MMR vaccine, orchitis in
males

Read hepatitis table in lec 7 slide 59 [V.impo]


Rotavirus = the cause is Reoviridae (dsDNA), causes diarrhea in infants
Norovirus = the cause is Caliciviridae(ssRNA) enveloped
treatment=rehydration

Lec 8
RESP SYSTEM
Infections of the upper respiratory system are most common
Lower respiratory system is usually sterile because of the mucociliary
escalator action.
Normal respiratory tract flora:
i. Staphylococcus
ii. Corynebacterium
iii. Moraxella
iv. Hemophilus
v. Bacteroids
vi. Streptococcus
S.pneumonie and S.pyogenes can cause Laryngitis or Tonsilitis
Strep throat:
Cause = erthrogenic toxin( produced by S.pyogenes)
Drug of choice = penicillin

Post streptocoocal infection[Complications of S.pyogenes] eg. Acute


Rheumatic fever, Acute GN
Test for strep throat =1. Rapid Strep Test, if results is ve may be due to
viral infection/typical bacteria(eg. Hemophilus influenza)/atypical
bacterium(eg. Mycoplasma)
ASO(antistreptolysine 0 test) neutralization test. Infected individuals
produce Ab to streptolysin(Hemolysin) indicator used = Sheep RBCs
Diptheria
Gram +ve, aerobes
Pleomorphic, often club shaped rod
Genus: Corynebacterium
Have terminal volutin granules visible as metachromatic dots
Stained by = Alberts stain & Eleks test
Cause = exotoxin produced by Corynebacterium diptheriae( gram +ve
rod)
Results in necrotic injury to epithelial cells and characterized by slow
healing skin ulcerations
Froms Pseudomembrane (containing fibrin and dead cells) forms in the
throat can lead to resp. blockage
Pathogenicity = Invasion +
Exotoxin = Diptheria toxin (type is AB)--- A = toxic activity , B = binding
to receptors of target cells, fragment A irreversibly blocks protein
synthesis therefore may damage heart, kidneys and nerves
Lab diagnosis = based on isolation and identification
Treatment = antitoxin and antibiotics
Prevention = boosters every 10 years
Otitis Media:
Pus accumulation causes pressure on the eardrum
Bacterial causes:
1. S.pneumonie (35%)
2. H.influenzae (25%)
3. S.pyogenes(10%)
4. S.aureus(1%)
LRS diseases
Bronchitis
Bronchiolitis
Pneumonia
Pertussis (Bordtella pertussis)--- WHOOPING COUGH
TB
Typical pneumonie = S.pneumonie + H.influenzea

Atypical pneumonie = Mycoplasma pneumonie + Legionella pneumophilia +


Chlamydophilia psittaci

Bordetella Pertussis

Small, coccoid, non-motile, gram ve rod, nutritionally fastidious


Culturing requires 3-4 days and rich media supplemented with blood
L: cilia of the mammalian resp epithelium
Highly contagious
May cause rib fracture,pneumonia, apnea, seizures and eye bruising from
severness of cough
Transmission = highly contagious
Colonizing factors:
1. FHA = Filamentous Hemagglutinin
2. Various toxins:
A. Tracheal cytotoxin: damage ciliated cells
B. Exotoxins (Pertussis toxin) (AB toxin)
3 stages of the disease:
1) Catarrhal stage [1 -2 weeks]
2) Paraoxysmal stage [ 1 -6 weeks]
3) Convalescence stage [ weeks months]
Lab diagnosis : Nasopharyngeal specimens, Bordet-Gengou medium
Vaccination = Pertussis vaccine

Classification of pneumonia:
1. CAP (Community acquired pneumonia) caused by = S.pneumoniae &
H.influenzae
2. HAP(Hospital Nosocomial infection) caused by = Klebsiella sp., E.coli,
Pseudomonas and MRSA
3. Chronic pneumonia: caused by = M.TB, Nocardia, Actinomyces, Cryptococcus
neoformans and Aspergillus
4. Atypical pneumonia: caused by = Mycoplasma, Chalmydia and Coxiella
burnetti

Tuberuculosis
Leading killer of HIV positive people
Cause: M. tuberculosis, M.bovis and M.avium
M.TB = transmitted via aerosol, non motile rod-shaped bacterium,
obligate aerobe has Mycolic acids, incubation period = 1 -3 weeks
Test +ve reaction to tuberculin test

TB infection(culture ve) is not infectious but TB disease(culture


+ve) is !
Normal chest X-ray
Symptoms of TB disease = cough, fever and weight loss
MTB is attacked by activated macrophages--- tuberculin +ve
Tubercle formation begins characterized by Caseous necrosis and
cheesy appearance
Hematogenous spread of MTB may cause extrapulmonary TB (AKA
MILITARY TB)
Characterized by = Ghon focus= hilar lymphadenopathy and
primary focus lesion[ seen on X-ray]
Diagnosis of TB = Sputum sample, decontaminated by N.acetyl L
cysteine + NaOH / Radiometric method/ PCR/ Serology (ELISA Latex
agglutination/ Skin testing = Tuberculin or MANTOUX test
Detection = acid fast stain (eg. Ziehl Nelson stain = hot method)
(eg.Kinyoun = cold method) or by Florescent stain (eg. Auramine/
Fluorochrome stain) or by culture [Lowenstein Jenson medium = egg
based medium called Conventional method/ Middlebrooks medium=
agar based medium]
Vaccine = BCG vaccine (containing M.bovis)
Treatment = Rifampin and INH and Ethambutol or Streptomycin
MDR-TB (multi drug resistant MTB)
Tb lesion of Mantoux test when PPD(Purified protein derivative) is
given is characterized by : erythema, swelling and induration

Pneumococcal pneumonia [typical pneumonia]


Cause : Encapsulated S.pneumoniae
Production of alpha-hemolysins, inhibition of Optochin, bile solubility
and serological test
Illness due to immune suppression, smoking and viral infection
Symptoms = fever, chest-pain, breathing difficulties and rust
coloured sputum
Treatment : penicillin

( Lec 9)
NERVOUS SYSTEM
Encephalitis = inflammation of brain (eg. Mami)
Meningioencephalitis = inflammation of both brain and meninges
Myelitis = inflammation of SC
Bacterial
meningitis(most
dangerous)

Viral meningitis(called
aseptic meningitis)
Usually mild. Clears up

Fungal meningitis

NEISSERIA
MENINGITIDUS
HEMOPHILUS
INFLUENZAE
S.PNEUMONIAE

within a week or two


without specific
treatment.
CRYTOCOCCUS
NON POLIO
NEOFORMANS
ENTEROVIRUS
MEASLES
C. ALBICANS

MUMPS
INFLUENZA
ARBOVIRUS
HERPES

Opportunistic pathogens that may causes meningitis = L.monocytogenes +


S.pyogenes + S. aureus
First thing give cephalosporins before pathogen identification

Hemophilus Influenzae type b =


encapsulated (to protect cell from phagocytosis),
gram ve rods,
only occurs in humans,
causes URT and LRT infections in immunocomprimized patient
MOST COMMON CAUSE OF MENINGITIS IN CHILDREN LESS THAN 4!
Also causes Pneumonia, Otitis media and Epiglottises
its fastidious (needs factor in blood)
Cultured on chocolate blood agar
Required preformed growth factors( factor X and V)
Identification of pathogen is = CSF, blood,pus or purulent sputum
Direct detection by latex agglutination test
Detection by microscopy and culture(inability to grow in absence of facto X
and V)
Treatment = polysaccharide conjugated vaccine

NEISSERIA MENINGITIDIS:

Coffee-bean-shaped cocci
Normally found in :oro-and naso-pharynx, and vagina
concentration of 510%CO2 encourages proliferation
cultures requires medium containing blood.
Highly contagious
Has polysaccharide capsule
frequently pleomorphic

Gram-negative
Humans are the only pathogen reservoir
Probable mode of spread to the meninges is through the blood.
13 meningococcal serogroups have been identified
Group A meningococcus accounts for an estimated 8085% of all cases
in the meningitis belt.
N.meningitidis is a major cause of epidemic
Meningococci are parasites of the nasopharynx
Transmission : through droplets of respiratory or throat secretions from
carriers
live in leukocytes in CSF
The symptoms are due to endotoxin
headache, fever, neck stiffness, and severe malaise, rash
disease occurs most often in young children < 2 y of age.
Sporadic outbreaks among young adults.
Diagnosis based on isolation and identification of the organisms from
either the blood or the CSF.
CSF sample :turbid due to large no. of pus ells
Serology (detection of antigen by Latex agglutination test
Meningococci are capsulate
Culture: N. meningitidis :Cultivation requires (blood) chocolate agar and
incubation in 5% to 10% carbon dioxide atmosphere
Selective media Modified Thayer-Marten (MTM) media containing
antibiotics
Biochemical tests : Oxidase +, sugar fermentation test.
Serology : Detection polysaccharide capsular antigen
Treatment : Penicillin G.
Prevention : immunization can be achieved with a vaccine made from
the purified capsule polysaccharides A, C, Y, and W-135
(tetravalent).MCV4
NB. There is no serogroup B. Conjugate vaccine

S. PNEUMONIE

Human pathogen spread by droplet.


Gram-positive diplococci that usually occur in pairs or short chains
thick capsule that prevents phagocytosis
when cultured : a-hemolytic colonies
Typically associated with pneumonia, but may cause pneumococcal meningitis
and pneumococcal septicemia

70% of people are healthy nasopharyngeal carriers


Diagnosis : Solubility in bile + Sensitivity to Optochin + Quelling test
(capsular test)

LISTERIOSIS

Listeria monocytogenes:
Gram-positive rods
Peritrichous flagellation
Motile at 20 C
Can be cultured aerobically on blood agar.
Reproduce in phagocytes
Acquired by ingestion of contaminated food
May be asymptomatic in healthy adults
On isolated culture confused with diptheroids
Cultures will take 1-2 days for growth
Causes meningitis in newborns, immunosuppressed, pregnant women, and
cancer patients.
Can cross placenta and cause spontaneous abortion and stillbirth
Diagnosis: blood or spinal fluid test

TETANUS
Appearance under microscope :drum-stick
Clostridium tetani : Gram-positive bacilli, endospore-forming,
obligate anaerobe
Motile, clear zone of hemolysis, Robertson cooked media
Puncture wounds (such as those caused by rusty nails, splinters,
or insect bites.)
clinical manifestations do not result directly from the invasive
infection, but are rather caused by a strong neurotoxin =
TETANOSPASMIN (blocks inhibition pathway)
characteristic motor spasm of tetanus
Germinates under anaerobic conditions

Clinical features

1.Sardonic grin: Contraction of the muscles at the angle of mouth


and frontalis.
2. Trismus (Lock Jaw): Spasm of Masseter muscles.
3. Opis-thotonus: Spasm of extensor of the neck, back and legs to form a
backward curvature.
4. Muscle spasticity
5. Neonatal tetanus: contamination of umbilical cord, circumcision
6. can cause fractures and muscle tears.
7. If respiratory muscle is involved apnoea
Diagnosis. :The preferred method is toxin detection
Robertsons cooked meat broth is useful medium.
Treatment :Tetanus toxoid (DTaP): tetanus immune globulin. Principle of
Treatment
Prevention of further toxin production by Human tetanus
immunoglobulin 2. Neutralization of unbound toxin with Antibiotics
(Metronidazole)

BOTULISM
Clostridium botulinum :Gram-positive, Endospore-forming, Obligate
anaerobe, ubiquitous in soil and H2O
Intoxication (ingestion of botulinum toxin): Botulinum Toxin: Most Potent
Toxin on Earth
7 different Neurotoxins
Mechanism of action: Irreversible inhibition of ACh acetylcholine release
from motor neuron .
Resulting in flaccid paralysis of the musculature
3- Forms of Botulism
1. Food-borne botulism: Intoxication not infection, Due to improper
canning procedures
2. Wound botulism symptoms start ~ 4 days after wound infection
3. Infant botulism: Due to ingestion of endospores C. botulinum in
food (e.g., honey).
Diagnosis: Based on toxin detection by means of the mouse
neutralization test.
Therapy : Urgent administration of a polyvalent antitoxin.(A, B &E)
Prevention: Proper canning

LEPROSY OR HANSENS DISEASE


Mycobacterium leprae (acid-fast rod)
Grows best at 30C cooler body regions (peripheral nerves and
skin cells

Transmission requires prolonged contact with an infected person.


Mostly via nasal secretions of lepromatous leprosy patients
Incubation time: Months to 10 years
Two forms depending on immune response
Tuberculoid (neural) form: Loss of sensation in skin areas;
Lepromatous (progressive) form: Disfiguring nodules over body;.
Treatment can reverse ALL nodules
VIRAL DISEASES OF THE NERVOUS SYSTEM
1.
2.
3.
4.

Poliomyelitis
Rabies
Viral meningitis
Viral encephalitis

ARBOVIRAL ENCEPHALITIS

Arboviruses are arthropod-borne viruses


Prevention by mosquito control.
Affects horses and humans
Sentinel animals, e.g.: caged chickens
Caused by = Western equine virus, Eastern equine virus, California virus,
St.Louis and West Nile

CRYPTOCOCCUS NEOFORMANS MENINGITIS

(Also called cryptococcosis)


Soil fungus associated with pigeon and chicken
Transmitted by the respiratory route
spreads through blood to the CNS
Primarily affects AIDS patients
Diagnosis: Serology to detect cryptococcal antigens in serum or CSF
Treatment: Amphotericin B and flucytosine
Super thick Capsule
Urinary bladder and upper urinary tract are sterile
Lactobacilli are predominant in the vagina and Produce H 2O2

RENAL DISEASES OF THE NERVOUS SYSTEM


CYSTITIS
Usual causative agents: E. coli + S. saprophyticus

Symptoms:Dysuria (difficult or painful urination) + Pyuria (pus in


urine)
Diagnosis: >100 CFU/ml potential pathogens
Treatment: Trimethoprim-sulfamethexazole

PYELONEPHRITIS

Causative agent: Usually E. coli


Symptoms: Fever; back or flank pain
Diagnosis: 104 CFUs/ml and
Treatment: Cephalosporin

LEPTOSPIROSIS
Causative agent: Leptospira interrogans
Is a Gram negative, obligate aerobe spirochete, flagella
Reservoir: Dogs and rats
Transmission: Skin/mucosal contact from urine-contaminated water
Symptoms: Headaches, muscular aches, fever, kidney failure a possible
complication
Diagnosis: Serological test
Treatment: Doxycycline

BACTERIAL DISEASES OF REPRODUCTIVE SYSTEM


(STIS)
GONNORHEA
Sexually transmitted disease
Affect both male & female
Caused by Neisseria gonorrhoeae
Gram-negative, coffee-bean-shaped cocci that are frequently pleomorphic,
they are non motile and feature a polysaccharide capsule.
Can occur intra or extra cellular
If left untreated, may result in
o Endocarditis
o Meningitis

o Arthritis
o Ophthalmia neonatorum
NB. N.meningitidus and N.gonnorhea are BOTH coffee- bean shaped !!!

NONGONOCOCCAL URETHRITIS (NGU)


Chlamydia are obligate intracellular parasites, and are among the smallest
living organisms and they form
Chlamydia trachomatis
Gram-negative bacteria
Chlamydia Trachomatis is the organism responsible for diseases such as
trachoma and the STD Chlamydia.
Chlamydia is the most common STD
They divide by binary fission.
It prevents the fusion of the phagosome and lysosome
Symptoms: Painful urination and watery discharge; in women, possible
complications, such as PID
Diagnosis: Culturing, PCR
Treatment: Doxycycline, azithromycin

SPIROCHAETES:
1. Treponema,
2. Borrelia,

Syphilis
Lyme disease

3. Leptospira,

Weils
N. MENGITIDUS

Fermentatio
Ferments glucose and
n test
maltose
Microscopic
Encapsulated
features
Transmission
Respiratory or oral
secretions

N. GONNORHEA
Ferments glucose but
NOT maltose
Un encapsulated
Sexually or vertical
Usually found

intracellularly in
LEUKOCYTES

Syphilis
Contagious, sexually transmitted disease
Spirochete Treponema pallidum = Microaerophilic.
Not been cultivated on artificial media in the lab.
Identification: darkfield microscopy or fluorescent antibody techniques
Congenitally transmitted syphilis ( Vertical: Mother to child), pass
through the placenta.
Invades mucosa or through skin breaks

Types:
Primary Syphilis
Forms at site of inoculation

Forms a chancre on the tongue( painless)


Mainly the genitalia

Secondary Syphilis
Spread to local lymph nodes & then to the blood stream
Signs and Symptoms:
Usually occurs 4-8 weeks after primary chancre
Skin manifestations, Rash (75-90%),
Early on face, shoulders, flanks, palms and soles, anal or genital areas
Patchy alopecia or hair loss
The rash and ulcer will disappear in (3-6) months
Early Latent
Can involve of many body organs (2o and latent)
Late latent = Late Syphilis (tertiary)
Late disease (tertiary) infection/inflammation of the blood vessels in the central nervous
system and cardiovascular systems
involuted, a latent period occurs
few months or a lifetime
No clinical manifestations
Is positive serologic tests.

60-85% remain asymptomatic for years without treatment.


Divided into two stages for treatment purposes:
Early latent syphilis: <1yr duration
Late latent syphilis: >1yr duration
The presence of signs or symptoms usually point to primary or secondary syphilis
that late syphilis can manifest neurologic symptoms.
Patients with positive syphilis serologies who have no signs or symptoms of disease have
latent syphilis
Tertiary Syphillis
Congenital:
Pregnant syphilitic women can transmit T.P. to fetus
Central nervous system involvement:
General paresis, tabes dorsalis, optic atrophy
Cardiovascular involvement
Gummas: (Granulomas)destructive lesions of soft tissue, cartilage,
internal organs and bone
70% of untreated patients remain asymptomatic
30% of untreated patients progress to tertiary stage in 5-20 years
Diagnosis of Syphilis
1- Non-treponemal antigen test = Detect reagin antibody with react with
non-specific antigen {cardiolipin
2- Treponemal antigen tests = FTA-ABS tests for anti-treponemal
antibodies
Treatment = Penicillin is the drug of choice

VIRAL DISEASES OF THE REPRODUCTIVE SYSTEMS


GENITAL HERPES
Caused by herpes simplex virus 2 , thats characterized by painful
vesicles on genitals
Recurrences from viruses latent in nerves
Suppression: Acyclovir

GENITAL WARTS
Human papillomaviruses= characterized by warts in genital area
Cause : HPV 16 causes cervical cancer and cancer of the penis
Prevention: Vaccination against HPV strains

CANDIDIASIS:
Causative agent: Candida albicans Grows on mucosa of mouth, intestinal
tract, and genitourinary tract that grows on pH: <4
Vulvovaginal candidiasis, yeasty discharge
Diagnosis: microscopic and culture
Treatment: Clotrimazole; fluconazole

LEC 10

MEDICALLY IMPORTANT GRAM +VE BACILLI


Sepsis may be called systemic inflammatory response syndrome (SIRS).
reactions including widespread inflammation, swelling and blood clotting
can lead to a significant decrease in blood pressure, eventually lead to
multiple organ failure and death.
Fever, rapid heart or respiration
High WBC count
Often leads to lymphangitis, inflammation of the lymph vessels
Two major forms of sepsis
1. Gram sepsis
2. Gram + sepsis
Gram Negative Sepsis:
Outer LPS layer of Gram bacteria
Gram positive sepsis :
Gram positive bacteria are the leading cause of sepsis.
Often nosocomial in origin

Various species of Staphylococcus and Enterococcus are the cause

BACILLUS ANTHRACIS
Gram-positive, endospore-forming, rods, nonmotile, nonhemolytic
Bamboo stick appearance
Referred to as medusa head appearance (culture
Aerobic and catalase positive
Primary habitat is soil.
Spike-like projections at the colony edge, ground glass texture exhibited
by the colonies
The disease strike primarily grazing animals, such as cattle and sheep.
Zoonotic disease of grazing animals
Not generally considered to be contagious
2 SPECIES OF MEDICAL IMPORTANCE:
1. Bacillus anthracis
2. Bacillus cereus
Occupational hazard
depends on the death of its host for formation of spores, which are the main
transmissible source of the disease.
It enters through: Cuts in the skin, Respiratory tract, Mouth.
Infection by B. anthracis are initiated by endospore
In the body taken by macrophages
Virulence factors are:
Two exotoxins
third toxic component, a cell receptor-binding protein called the protective
antigen, that binds the toxins to target cells and permit their entry.
1. The edema toxin
o Cause local edema, interfere with phagocytosis.
2. The lethal toxin
Specifically targets and kill microphages
capsule of B. anthracis is very unusual it has (amino acids instead of
polysaccharide) thats one of the major virulence factors
When enter the blood, proliferate without inhibition,until it kills the
macrophages

3 types of anthrax:
1- CUTANEOUS ANTHRAX
Over 90%
Entry through minor skin lesion
incubation period of 1-7 days
Symptoms: papule ---- vesicular ---- pustule (malignant) ---- depressed black
eschar + Edema
In most cases the pathogen does not enter the bloodstream

2- GASTROINTESTINAL ANTHRAX

Gastrointestinal anthrax is caused by ingestion of undercooked food


containing the spores
Causes severe nausea ,abdominal pain and bloody diarrhea.
Symptoms: Ulcerative lesions

3- INHALATIONAL (PULMONARY) ANTHRAX


Inhalation anthrax (woolsorters' disease), results most commonly from
inhalation of spore-containing dust where animal hair or hides are being
handled
The most dangerous form
Spores germinate in the mediastinal L. nodes
Initial symptoms following inhalation of spores are non-specific and flu-like
Diagnosis is based on isolation and identification of the bacteria from clinical
specimen (slow), Gram stain, capsular staining, and direct fluorescent
antibody (DFA) testing on capsule antigen and cell wall polysaccharide.
malachite green staining for spores.
Confirmatory identification of B. anthracis tests for motility, capsule
production and visualization, hemolysis.
Treatment : Ciprofloxacin is the drug of choice. Doxycycline is used.
Vaccines : Anthrax Vaccine for human (AVA, BIOTHRAX ), killed vaccine.

BACILLUS CEREUS

Common airborne and dustborne


Grows in foods, spores survive cooking and reheating
No treatment
Ingestion of toxin-containing food causes nausea, vomiting, abdominal cramps
and diarrhea; 24 hour duration

INFECTIVE ENDOCARDITIS:

Deposition of platelets and fibrin nonbacterial thrombotic vegetation


(NBTE)
Classification: ACUTE OR SUBACUTE
Febrile illness + Persistent bacteremia
The hallmark of IE is he presence of valvular vegetation composed of
Amorphous mass of fibrin & platelets
Aortic valve more common than mitral
Causes of bacteremia:
1. Dental extraction
2. Periodontal surgery
3. Tooth brushing
4. Tonsillectomy

5.
6.
7.
8.

Oesophageal dilatation
Biliary tract surgery
Cardiac surgery
Injection drug use

Valve type
Nature

SUBACUTE IE

Normal valve

Previously abnormal
valves
Indolent nature,
local
Months - years

Develops to
metastatic infection
Days - weeks

Duration
Toxicity

Highly toxic

Causative agent
Fatality
untreatment

ACUTE IE

S.aureus
of

Quick

Mild toxicity
S. viridans or
enterococcus
Slow

Aetiological Agents
1. Streptococci
a. Native valves (not prosthetic)
b. Previously damaged
2. Enterococci
i. E. faecalis, E. faecium
ii. Associated with GU/GI tract
3. Staphylococci
viridans streptococci as the most common cause of
infective endocarditis
S. aureus
Acute endocarditis
S. epidermidis (Coagulase-negative staphylococci)
Prosthetic valve endocarditis
4. Gram negative organisms
P. aeruginosa most common
HACEK - slow growing, fastidious organisms
Haemophilus sp.
Actinobacillus
Cardiobacterium
Eikenella

5. Fungi
Candida species, Aspergillus species
Clinical features:

Laboratory features:

1. Fever

1. Anemia

2. Murmurs

2. Most commonly elevated WBC

3. Petechiae and cutaneous


manifestations.

3. ESR elevated,

4. Conjunctival and mucosal petechiae,


splinter hemorrhages, Osler nodes,
Janeway Lesions.

4. Microscopic hematuria

5. Splenomegaly

6. Blood cultures.

6. Embolism. Septic or sterile. CNS,


spleen, lung, retinal vessels, coronary
artery, large vessels.

7. Aerobic and anaerobic.

5. Bacteremia.

8.

Echocardiography

7. Renal disease, infarction. Multiple


abscesses. Glomerulonephritis and
uremia
8. CHF
9. General. Weight loss, anorexia,
debilitation.

65 75% of i.v. drug abusers with tricuspid IE


Prevention: treat underlying cause
o Strep. viridans oral, respiratory, eosphogeal
o Enterococcus genitourinary, gastrointestinal
o S. aureus infected skin, mucosal surfaces
Dental procedures NOT to be done on pt. suspected to have cardiac
complications:
A. Routine anesthetic injections
B. Dental radiographs
C. Adjustment of orthodontic appliances
D. Shedding deciduous teeth
E. Bleeding from lips or oral cavity due to trauma

MICROBIAL DISEASES OF THE EYE


Haemophilus influenzae, Gram-negative, coccobacilli is the most common
bacterial cause.
Viral conjunctivitis is usually caused by adenovirus.
Bacterial Diseases of the Eye =
originate from the skin and upper respiratory tract.
Caused by:
1. Staphylococcus aureus
2. Haemophilus species
3. Streptococcus pneumoniae
4. Pseudomonas aeruginosa grows in contact lens solution

OPHTHALMIA NEONATORUM

(Neonatal gonorrheal ophthalmia)


caused by the transmission of Neisseria gonorrhoeae from an infected mother to an infant
Large amount of pus are formed
If untreated ulceration of the cornea results
high risk of blindness.
treated with 1% silver nitrate, tetracycline, or erythromycin to prevent the growth of
Neisseria and Chlamydia infection.

INCLUSION CONJUNCTIVITIS OR CHLAMYDIA


CONJUNCTIVITIS
cause by Chlamydia trachomatis, a bacterium which can only live within a
host cell called an obligate intracellular parasite
transmitted to infants during birth
transmitted in unchlorinated swimming water (swimming pool conjunctivitis
effective treatment : Tetracycline applied

Trachoma: cause of blindness


caused by C. trachomatis
The disease is conjunctivitis where trachoma is transmitted by hands, fomites
(towels), and perhaps flies.
Repeated infection repeated infection with C. trachoma cause chronic
inflammation which damages the cornea
In later stages cause trichiasis (in- turning of the eye lash) that can be
corrected surgically
Scar tissue forms on the cornea (corneal abrasion).
Treatment: oral azithromycin, are useful in treatment.

Inflammation of the cornea is called keratitis.


Herpetic keratitis causes corneal ulcers.

The etiology is herpes simplex type 1 (HSV-1) that invades the central nervous
system
Trifluridine is an effective treatment for herpes keratitis.

Acanthamoeba
Protozoa (amoeba), transmitted via water, can cause a serious form of keratitis.
Damage is often severe (corneal transplant), or even removal of the eye.