Microbiology
SMALLPOX – Poxviridae, linear, DS DNA, E.C., orthopoxvirus (smallpox and cowpox);
carries some enzymes
X-T: airborne; quickly becomes blood borne; used in germ warfare
Clinical: Spots/rash (responsible for lesions
[fluid filled vesicles] all over the body) formed on the body; leaves permanent
scars, permanent disfigurement, death, loss of special senses.
Note: 1948 last case in USA;
1980 last case in world (says WHO)
One of the first viral diseases noted
about 10,000BC
Seasonal disease (late spring/early
summer)
Rx: vaccinia virus (discontinued 1974) – artificial immunization developed by Edward Jenner (late 1700,s) via observation of a milkmaid that suffered from cowpox w/lesion on finger but did not suffer from small pox. Lady Mary Wortley Montaque passed on the idea of VARIOLATION – process of making pox vaccine with a thread passed through smallpox lesions.
Note: similar to Monkey pox
Human
papillomavirus – Papovaviridae; N.P.; warts
Genital warts a.k.a. condyloma acuminata®cervical and penile
cancer.
X-T: Direct contact, sexual contact
Clinical: specifically attack skin and mucous membranes; viral infection lasts a lifetime - remains in surrounding tissue. Most are benign, a few are malignant. Warts grow larger in people with AIDS.
Rx: surgical removal cervical, women 2 PAP tests a year; cryotherapy (CO2 or N2) with excision; podophylin, salicylic acid and glutaraldehyde; surgery; antimetabolites (such as 5-fluorouracil and interferon). Still has high recurrence.
Molluscum Contagiousum - orthopoxviruses and parapoxviruses; DNA common in immunocompromised and AIDS people - severe lesions around mouth
Rubella (German) Measles virus togaviridae ( an arbovirus – meaning transmission by arthropods except that this has nothing to do with insects)
X-T: Airborne, droplet route
Clinical: not a very serious disease; produces skin
rash (exanthema); crosses the placenta and causes severe damage to fetus; 30%
of American females enter childbearing age w/o being exposed to German Measles virus
(therefore w/o developing any immunity to it) first trimester is the most risky
– produces early cataract for fetus.
Can cause “pearly cataract.”
Starts in the trunk area and then goes deep.
NOTE: most risky congenital disease.
Dx: ELISA-Rubella--enzyme linked immuno assay
Rx: immunize w/attenuated live virus (“R” in MMR); avoidance of pregnancy for 3 months following vaccination.
NOTE: Do not confuse with Morbilli Measles (1st “M” in MMR)
Measles (Morbilli) (a.k.a. Rubeola) - not a member of the same family as Rubella; paramyxoviridae; SS RNA, E.H.
X-T: airborne, droplet®mouth, nose, upper respiratory
Clinical: Koplik's spots (red spots w/central bluish specs on face); fever producing disease—childhood; leads to rash starting at face and moving distally. Complications: upper respiratory and middle ear infections; Measles Encephalitis (30% mortality rate); Subacute sclerosing panencephalitis (SSPE) resulting from measles remaining in the brain tissue 6-8 years after infection usually in children who had it before age 3. 300,000 children die every year from measles
Rx: The 1st “M” in MMR
Dengue fever (a.k.a. breakbone fever), Flaviviridae, RNA
Vector: Aedis aegypti mosquito
Clinical: self-limiting; 10 day duration
No vaccine
Yellow fever (Panama Canal)
Flaviviridae, RNA
Vector: Aedis aegypti
mosquito
Reservoir: Monkeys
Clinical: Fever, nausea, vomiting, Jaundice (hence name)
No Rx; Vaccine by Theiler
Ebola Filoviridae; E.F.,
filovirus, first appeared in Kikwit, Zaire.
Produces hemorrhagic fever
Lassa fever; arenavirus, RNA, poor
prognosis, severe liver damage
AIDS -
HIV, retroviridae (enzyme - reverse transcriptase and protease), E.S.
NOTE: may have come from some of the animal viruses like primates
(African Green Monkey)
How did it come to humans not clearly defined
- maybe a hunter working w/contaminated animals
1979 - found cure/treatment
for almost every infectious
disease then AIDS came about; Luc
Maontagniey-French and Robert Gallo-US first ID’ed the virus in the blood of
people who had the disease
1980 – Named “Acquired Immuno-Deficiency”
Since 1980, AIDS in adults
took a very heavy toll
Seen in most countries around the world -
some more affected than others
250K died since recognition of AIDS
Clinical: About 5M+ are HIV+ in U.S.; Incubation is months to years,
some w/ HIV after 16 years have no symptoms.
Mortality 67% after clinicals
Note: M. tuberculosis, P. carinii prevalent; 10% weight loss, prolonged
fever (> 1 month), diarrhea, Kaposi’s sarcoma, repeated respiratory
infections
X-T: Homosexual 67-70% (virus present in semen, enters anal blood
vessels), I.V. drug use 20%, Heterosexuals (fastest growing) 6-7%, congenital
2%, blood transfusion <1-2%, accident <1%
Dx: clinical features and serologic:
ELISA test for antibodies: may take months – false (-) = 1/50K
Western Blot: may take a month or more - false (-) = 1/500K
PCR (polymerase Chain RXN) test for viral nucleic acid: takes 2-4 days - false
(-) = 1/2.5M
Rx: nothing is 100%; drug combination therapy will prolong a patient's
life; better nutrition and exercise increased chance of later development of
disease; some people believe 100% mortality once AIDS symptoms dovilup. Best Rx is prevention through education.
See two handouts on drugs
and progression of disease
Staphylococcus - See handout w/Table
12-1
Three Staphylococci (G+ cocci)
S.
aureus S. epidermidis S. saprophyticus
Colonies Golden
Yellow Chaulky white Muddy
Coagulase Yes
(fibrinogen®fibrin)
Mannitol ferment Yes
Hemolysis Delta None None
Salt tolerence Yes
(7%NaCl)
Heat resistant Yes(most heat resistant
non-sporing)
Pus formation Yes
Penicillinase Yes
(90%)
(b
Lactamases)
Normal flora Yes Yes
S. epidermidis – (a.k.a. S. albus) associates w/ middle ear infections, endocarditis, cardiac surgery patients.
S. aureus
Clinicals: Trivial furuncles, carbuncles, boils; osteomyelitis (in young boys); metaphysis, empyema, pericarditis, purulent arthritis, tissue abscess, endocarditis, kidney cortex disease, pneumonia (high mortality); Toxic shock syndrome (TSS); scalded skin syndrome; food poisoning; blepharitis (eye infection).
Note: TSS – prevelant in menstruating
females®shock
death. Found that “Rely” tampons
damaged vaginal wall allowing pathogenicity into blood system. TSS1 TSS2 TSS3
ID’ed.
Scalded skin syndrome – seen in 0-4
year-olds, destruction of granular layer of skin. The toxin was epidermolytic toxin (exfoliative) [a.k.a. Ritter’s
syndrome].
Food poisoning – [note that
Salmonella enteritidis is actual #1 food poison source]; results from a heat
stable exotoxin (enterotoxin), stable at 120° for 30 min. Found in improperly stored left-over foods.
Microbes – resistance – penicillin G
Methicillin
Cephalosporins I (G+), II (G+ AND G-), III (G-)
Streptococcus-largest group of organisms
that fall in this category; G(+) 50-60 cell long crooked filaments.
Lancefield grouping – A through R (some do not have a grouping) – based on presence
of carbohydrates (as polysaccharides) attached to the cocci (Thanks to Lady
Lancefield). Useful to quickly ID the
specific microbe.
S. pneumoniae - no Lancefield group
S. pyogenes - known in detail
Viridans group - has no Lancefield group (S mitis, S. mutans)
causes dental caries and endocarditis
S. pneumoniae - a.k.a. Pneumococcus [earlier known as Diplococcus pneumoniae –
typically found as pairs w/in a capsule that causes pathogenicity. Capsule
demonstrates as a smooth, wet, shiny texture in sputum. On blood agar it caused a-hemolysis (green) in a long
chain hence the change from diplo- to strepto- designation].
Transport from upper to lower respiratory tract leads to serious
pneumonia; found in upper respiratory tract of 40% of the population, though it
does not necessarily lead to infection.
Of the 100 or more serotypes, serotype 3 is most serious/deadly form
and was the #1 killer in early 1900's.
X-T: droplet
Vaccine: polyvalent type made for different kinds of serotypes expected
during yearly outbreaks (at time of typical flu season).
Clinical: today, killer of older, debilitated people
ago, killer of young adults
60K-70K U.S. people die
every year from pneumonia and influenza together (influenza and pneumonia go
hand in hand). See Handout - right
side of page.
Tx: many chemotherapies developed - penicillin G and V, and
cephalosporin
Dx: 1. autolytic colonies
on agar plate shows colonies w/central depression resulting from toxin made by
the organism that kills center of colony; also identifiable via a-hemolysis from lung
puncture (when difficult for patient to expel sputum for use as a good culture,
also note that it grows naturally in the upper respiratory tract).
2. Two tests to differentiate
pneumococci from S. pyogenes
1)
Bile
solubility – pneumococci are sensitive to bile salts
2)
Optochin
test - pneumococci are sensitive to ethylhyrocupreine HCl
Special Note: first organism
to show genetic transformation (acceptance of foreign DNA by an organism)
[Griffith, 1940] leading to
biotechnological usefulness.
S. pyogenes G(+), [Billroth, 1874], found in wounds. Most often b-hemolytic, Group A (responsible for most strep infections, other than pneumoncocci-caused); has 200 serotypes. Close relative of S. pneumoniae. Very deadly.
Present in society during
winter. Known for more than 100
years. Associates with many different
diseases. See handout.
Infections due to S. pyogenes - All these require the
organism’s presence:
Strep throat, pharyngitis, scarlet fever, peritubular abscess, otitis
media, bronchopneumonia—almost always deadly, pleuritis, empyema, puerperal
fever—80%, pyoderma, erysipelas. Can lead to more serious
infections if not treated.
Auto-immune post-infections
Post-streptococcal glomerulonephritis (Bright’s Disease), Rheumatic Fever
“licks the joints but bites the heart”
Dx: DICK TEST – skin immune status test for scarlet fever
SCHULTZ-CHARLESTON REACTION – diagnostic test for scarlet fever rash; antibodies against Erythrogenic toxin injected to middle of rash – blanching is (+) result.
Tx: No vaccine available; prevent is best; Ab therapy has success - penicillin G or V; drug resistance is low; acid sensitive; penicillianase sensitive; ampicillin (for gram negative bacteria)
Mycobacterium – cause of TB and Leprosy; Mycobacteriaceae, acid fast rod with mycolic acid, lipids, and waxes on cell wall; most impervious to stains and antibiotics, though new drugs are effective; survive in macrophages and multiply.
Clinical: night sweats, weakness, cough, chest pain, spitting up blood, lethargy,
fever, discomfort, sudden weight loss.
X-ray reveals tubercles in lungs, old tubercles show ragged cavities;
confirm with Ziehl-Neelsen stain w/carbol Fuschsin®pink-red rods (acid fast). TB was more common
in the past than today.
M. tuberculosis – main cause TB.
M. bovis - milk borne; controlled by
law for pasteurization, inspection of cattle.
M. avium (MAC complex) –
intracellular - TB like disease transmitted from birds and swine; potential
AIDS link.
M. fortuitum complex – wound infections
M. kansasii – TB-like disease
M. leprae – Hansen’s disease
(Leprosy)
M. marinum – cutaneous lesions in
humans, TB in fish
M. ulcerans – ulcerative lesions
M. tuberculosis
Primary site is lungs, but almost any site of the body can come under attack (miliary TB spreads tubercles – allergic granulomas). Organism grows well on glycerol rich media – a pathogenic form in a cord-like growth (serpentine cords) b/c of cord factor, TRAHALOSE, that also associates with pathogenicity.
Closely related to poor nutrition more so than any other disease. AIDS caused a serious problem for those who are suffering from this; TB developed a drug resistance
Dx: Past - positive tuberculin test on skin used tuberculin.
Today -
purified protein derivative (PPD), used to scan population to see how many
people had exposure.
Mantoux test - quantitative test (known amount of TB injected, record
reaction).
Normal, healthy person can undergo exposure and will not suffer; some say TB can pass from parents to children (genetic disposition) - shown not true.
Tx: Past Therapy: before 1945 - rest away from
work; placement in sanitarium.
Today: chemotherapy is very successful; drug therapy that can penetrate
macrophages and kill them; several drugs are available:
Streptomycin was first [Waksman, 1945] ® loss of hearing
w/permanent damage to CNVIII - not used today;
Combination therapy:
Ethambutol + INH (iso-nicotinic hydrazid)
Rifampin + INH
Prevention of TB was major WHO concern; vaccine is
not recommended in US, in other countries it is important. BACILLE CALMETTE GUERIN (attenuated form of
vaccine developed in Paris, very effective for prevention).
U.S. has above average nutrition so no recommendation. NOTE: lack of sunlight is a predisposing
factor to TB.
Mycobacterium leprae – leprosy (Hanson); similar to TB; not subject to Koch’s postulates (unculturable – except armadillos can express the disease).
X-T: personal contact (?); germ plasma (?). Tends to run in families b/c they live
together and transmit.
NOTE: incubation period ~20 years.
Clinical: Syphilis has overlapping symptoms
w/leprosy. Severe debilitation,
disfigurement, 2°
infection to anesthetized wound area, deformities, pneumonias, can survive in macrophages,
transmits in plasma.
No other organism grows as abundantly in humans.
Disease has 2 phases:
Lepromatous
phase — special macrophages w/bacteria
Tuberculoid — areas w/lack of sensation
Both are responsible for debilitations. Can lead a normal life w/chemotherapy and if they do not to injure themselves. Health care providers acquired leprosy — very few cases.
Some
African and Asian countries - health care facilities are not available b/c of
the stigma.
Western world has Lazar Houses — specially equipped to handle lepers.
Hawaiian islands have some leper colonies.
Only 3000-5000 cases in the U.S. - most imported.
Impermeable cell wall—structure is of significant importance.
Dx: clinical symptoms along w/Lepromin test
Found more anti-leprosy drugs b/c of Armadillos
Sulfa drug and sulfones
DDS
(Diamino diphenyl sulfone) give the best results, in use for some time; only
suppresses the growth of the organism, doesn’t get rid of the organism.
Rifampin — shows progress in suppressing the progression of leprosy.
Chemotherapy; some people dovilup hypersensitivity to ENL (erythema nodosum
leprosum), a breakdown product of leprosy; may cause wounds and bleeding.
Klebsiella: G(-); Highly capsulated rod; Enterobacteriaceae; part of normal flora of GI tract – movement to respiratory tract causes problems.
Several species:
K. pneumoniae — major disease causing agent
K. azaenae — atrophy of nasal mucous membranes
K. rhinoscleromatis — scleroma in nasal passages
K. oxytoca — non pathogenic
Nosocomal transmission—acquired by using hospital equipment and facilities (catheters, trach. tubes, UT equipment)
Clinical: Can cause pneumonia in respiratory tract or cause UTI’s - depending upon transmission:
[Deadly] Pneumonia
One of the most serious pneumonia; necrotizing; more deadly b/c not Dx’ed or Rx’ed promptly; insensitive to penicillin; has multiple drug resistance. Often mistaken for S. pneumoniae (Rx: penicillin).
Most effective drugs: Tobramycin and Amikatin — members of Aminoglycosides (streptomycin).
Most of the other gram negative drugs are ineffective; predisposing factors — age, debilitation, infections, congestive heart failure, diabetes.
Yersinia pestis — (past a.k.a. Pasteurella pestis); Enterobacteriaceae; G(-) rod; capsulated (not as prominent as Klebsiella). Responsible for the Black Plague.
X-T: Past: rat [reservoir] had flea (cheopis)
[vector], upon death of rat, flea moved to humans as alternate host leading to:
1. Bubonic Plague - affected lymphatics (tumor-like growth called a bubo). Rupture of bubo allowed movement into the
vasculature;
2. Septicemic Plague - affected blood (leading to shock + death). Then movement to the lungs, if person
survived;
3. Pneumonic Plague – a.k.a. 2° pneumonic plague, that became airborne via droplets;
4. 1°
pneumonic plague – leading to 100% mortality.
Killed over 200M people
1896 – during an outbreak in India, Yersin recognized mode of transmission
1925 - last outbreak in U.S. – 150K died in San Francisco.
Pathogenicity of organism not clearly understood; PESTICIN (produced by bacterium) is contributor.
Tx: Past: none
Today: tetracycline and 3rd generation Cephalosporins;
Prophylaxis = prevention
Currently, prairie dogs in Plain States are
reservoir for fleas.
If suspected contracture of plague, person undergoes quarantine. Bubo’s are locatable in arm pit or groin
area.
Get-a-long little doggie, get-a-long.
During the days of the plaque, a vaccine became available —Haffkine vaccine, successful only for Bubonic Plaque and Septicemic Plaque - not Pneumonic Plaque.
Diphtheria - Corynebacterium diphtheriae; G(+) rod with pallisading arrangement of cells (Chinese letters); forms shiny dark, black colonies on Tellurite Media.
X-T: Airborne, droplet route
Clinical: Causes throat inflammation ® suffocation ® total airway blockage ® death by strangulation.
Dx: SCHICK TEST – verify allergic status and
immunity status
Not used today.
Rx: The “D” in DPT vaccine (Passive immunization);
Antibiotics are not effective: it is not the organism, but the toxin that makes
you ill.