Microbiology 1.6 Dr. Januario E.

Sia-Cunco
THE GRAM POSITIVE BACILLI JULY 8, 2013

OUTLINE
I. Gram Positive Spore Forming Bacilli Cultural characteristics
a. Bacillus o Inoculate on 5% Blood Agar Plate under aerobic conditions
i. B. anthracis o Produces large, raised, opaque, grayish white plumose colonies with
ii. B. cereus irregular fringe-like edge (Medusa head) with ground glass
iii. B. subtilis appearance.
iv. B. stearothermophilus o No hemolysis
b. Clostridium (anaerobic)
i. C. botulinum
ii. C. tetani
iii. C. perfringens
iv. C. difficile Medusa Head
II. Gram Positive Non-spore Forming Bacilli
a. Corynebacterium
i. C. diphtheriae
ii. C. pseudotuberculosis
iii. C. pseudodiphtheriticum and C. xerosis
b. Listeria monocytogenes
c. Erysipelothrix rhusiopathiae
d. Actinomycetes
May also be Acid Fast Figure 2 Medusa Head with ground glass appearance
e. Nocardia
Laboratory identification
GRAM (+) SPORE FORMING BACILLI
o Virulent strains produce ROUGH colonies when grown in the absence
BACILLUS
of CO2
 Large ,aerobic, Gram (+) rods occurring in chains
o Virulent strains produce MUCOID colonies when grown under 5% CO2
 Most are prevalent on soil, water, air and/or on vegetation
with NaHCO3
 Typical organisms have square ends and are arranged in long chains with
o String of Pearls Test: B. anthracis produces colonies that resemble a
spores in the center of the bacilli
string of pearls when grown on a medium containing Penicillin (PCN).
 Some members of the genus are the source of the antibiotics Polymixin B
B. cereus would be negative because it is not sensitive to PCN
and Bacitracin (Topical Antibiotics)
o Bacteriophage (a gamma phage) added to a diffusely inoculated plate is
expected to cause lysis only of B. anthracis. (No lysis of B.cereus)
Bacillus anthracis
o Inoculation of a mouse with organisms produces death in 2-5 days and
 Causative agent of Anthrax, a disease of sheep and cattle and to a lesser organisms can be recovered in heart blood
extent horses, hogs and goats
 Humans may acquire this in an agricultural setting or in an industrial
setting (processing of hides or animal hair with inhalation of spores).
 Infection is usually initiated by the subcutaneous inoculation of spores
through incidental skin abrasions = Cutaneous Anthrax.
 Also by inhalation of spore-laden dust (Pulmonary Anthrax)
 B. anthracis spores may remain viable for many years in contaminated
pastures and in bones, wool, hair, hides, and other animal materials.
 Potential use as a bioterrorism agent can be easily grown in large
quantities and the spores are resistant to destruction and can be
formulated into an aerosol for wide dissemination.

Morphology Figure 3 String of Pearls Test

o Straight rods with square ends occurring singly, in pairs or in chains.
o With centrally located oval spores
o Spores may be formed in culture, in the soil and in the tissues and
exudates of dead animals but NOT in the blood or tissues of living
animals (living tissues have a lot of nutrients, thus there is no need for
sporulation). Spores are highly resistant. 120⁰C x 15 minutes will
inactivate spores.
o Nonmotile

Figure 4 Presence of Lysis on B. anthracis

Virulence Factors
o Poly D-Glutamic Capsule (capsule usually interferes with phagocytosis)
o Exotoxin
Figure 1 Bacillus anthracis
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 MICROBIOLOGY 1.6
 Gradually accumulates in the infected animal with a maximum
accumulation at the time of death
 The toxin acts on the CNS producing respiratory failure and anoxia.
o With 3 active proteins that act synergistically to produce the systemic
effects of anthrax. Individually, the three proteins have no known toxic
activity
 Protective Antigen (PA)
 Edema Factor (EF)
 Lethal Factor (LF)
o The PA binds to cell receptors and is proteolytically activated
o PA mediates entry of EF and LF into the cell by endocytosis
o PA with EF forms the Edema Toxin which causes inhibition of
neutrophil function and elevation of intracellular cAMP, resulting in
impaired maintenance of water homeostasis and characteristic severe
edema usually seen in B. anthracis infections.
o LF with PA forms the Lethal Toxin which is a major virulence factor of
the organism and causes apoptosis and is responsible for tissue
necrosis. It causes death in infected animals and humans.
o LF also causes rapid release of inflammatory mediators that may
contribute to the sudden death that occurs with anthrax.
Clinical infection
o Anthrax affects principally domestic herbivores (e.g. sheep, goats, and
horses) and is transmitted to humans by contact with infected animal
products or contaminated dust
o In the terminal stages of the disease in animals, bacilli are shed in large
numbers from all orifices which sporulate in the soil and remain a
source of infection
o B. anthracis spores may remain viable for many years in contaminated
pastures and in bones, wool, hair, hides, and other animal materials.
These spores are highly resistant to physical and chemical agents
(recommendation is to autoclave it).
o Human infection can occur by:
 Cutaneous Route – organisms gain access through wounds and
multiply locally producing a dramatic inflammatory response.
 Inhalation/Pulmonary – organisms are inhaled, multiply in the
lungs, spread to the draining hilar lymph nodes where
hemorrhagic necrosis may occur and goes into the blood stream.
 Ingestion – from infected meat producing gastric ulceration
o From these invasion of the bloodstream follows producing profound
toxemia. Metastatic infections like meningitis may occur.
Clinical Manifestations
o Cutaneous Anthrax
 Accounts for 95% of cases
 Begins 2-5 days after infection as a papule that develops within a
few days to a vesicle filled with black fluid. Rupture leaves a black
eschar surrounded by an inflammatory ring reaction. This is
called a Malignant Pustule.
 There is lymphadenopathy, fever & headache
 The lesion is painless and is found in the hands, forearms or
head.
 The organisms may invade regional lymph nodes and then the
general circulation, leading to fatal septicemia, meningitis and
death.
o Inhalational Anthrax or Wool-sorter’s Disease
 Due to inhalation of spores by people who handle raw wool,
hides or horsehair
 Fever, malaise and cough which progresses to a severe infection
with respiratory distress and cyanosis. Death occurs within 24
hours.
o Gastrointestinal Anthrax
 Rare form.
 Due to ingestion of meat contaminated with spores
Group 35 | J.L. Villaflor, F.A. Villamor, M.K. Villanueva, M.E. Villanueva, M.L. Villanueva
 Nausea, vomiting, diarrhea and hematemesis and/or blood in
the stool, eventual shock and death.
o Anthrax infection provides permanent immunity.
Figure 5 Black Eschar
Laboratory diagnosis of clinical manifestations
o Specimens for culture can be obtained from malignant pustule, sputum
or blood. Stained smears will show Gram positive blunt-ended bacilli
that occur singly, in pairs, or frequently in long chains
o Can be identified in dried smears by immunofluorescence techniques
o On Blood Agar Plate (BAP) – non hemolytic gray to white colonies with
a rough texture and ground glass appearance. The edge of the colonies
may have a fringed or Medusa Head appearance
o B. anthracis and B. cereus are similar in morphology. B. anthracis is non
motile, sensitive to penicillin and Gamma-phage positive.
o Antibodies to the organism can be demonstrated by serology (ELISA)
o Acute and Convalescent sera can be used to confirm infections.
Treatment
o Penicillin not recommended because of inducible β-lactamase in B.
anthracis.
o Cutaneous anthrax responds to Ciprofloxacin
o Multidrug therapy: Ciprofloxacin plus Rifampicin plus Vamcomycin is
recommended for pulmonary anthrax
o Prophylaxis for potential exposure: Ciprofloxacin or Doxycycline for 4
weeks together with 3 doses of vaccine. Give prophylaxis for 8 weeks if
no vaccine is given.
o Erythromycin is an alternative (but may cause GI irritation)
o A cell-free vaccine is available for workers in high-risk occupations
Prevention
o The soil is contaminated by spores from the carcasses of dead animals.
o Animals are infected by spores that enter injured mucous membranes
or injured skin. Humans by contact with animal carcasses.
o Dispose of animal carcasses by burning; Autoclave animal products;
Wear protective clothing when handling carcasses; Immunization of
domestic animals with live attenuated vaccine.; Immunization of farm
personnel.
Bacillus cereus
 Cause of food-borne illness
 Similar in morphology with B. anthracis
 It is usually motile, not susceptible to PCN or the Gamma phage
 Types of diseases:
o Emetic Type of Disease
 B. cereus is a soil organism that usually contaminates rice. When rice
is cooked and allowed to cool the spores germinates and starts
producing the toxin.
 Starts 1-5 hours after ingestion of reheated fried rice or pasta
dishes.
 There is nausea, vomiting, abdominal pain and occasionally diarrhea.
Recovery occurs in 24 hours.
 B. cereus may be found in the normal stool so it is not diagnostic.
Concentration of 100,000 bacteria per gram of food is diagnostic.
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 Clindamycin is the Drug Of Choice (DOC). May use Aminoglycosides,

Vancomycin, Tetracycline & Erythromycin
o Diarrheal Type of Disease
 Incubation of 1-24 hours. Characterized by profuse diarrhea and
abdominal pain. Vomiting is uncommon.
 Associated with meat dishes and sauces
o Other Diseases
 Keratitis, endophthalmitis, panophthalmitis (whole eye) due to
organisms introduced by foreign bodies through eye trauma.
 The presence of a medical device or in IV drug use may predispose to
endocarditis, meningitis, osteomyelitis, and pneumonia. Figure 7 Babes-Ernst granules
 Treatment is Clindamycin or Vancomycin with or without an
Aminoglycoside.
o The diseases produced are more of intoxication due to toxins produced
by the organism rather than an infection. The enterotoxin is preformed
in the food or intestine

Bacillus subtilis
 Present in air, dust, brackish water and vegetable matter
 Common Lab contaminant but can produce infections in the
immunocompromised host
 Seen in bacteremias and eye infections in heroin addicts
 Treatment: β-lactam antibiotics Figure 8 Palisade or “Fence” formation

Bacillus stearothermophilus Cultural characteristics

 The spores are used to evaluate the efficacy of autoclaving o Aerobic to facultative anaerobic
o Grows as a waxy pellicle on the surface of liquid media
GRAM (+) NON-SPORE FORMING BACILLI o Growth is scant on ordinary media. Enrichment with blood, serum or
Corynebacterium diphtheriae egg is necessary for good growth
 Small, slender, pleomorphic, gram-positive rods that are non motile, o On Loeffler’s coagulated serum medium there is minute white
unencapsulated, and do not form spores. glistening colonies after 12-24 hours.
 Causative agent of Diphtheria o Loeffler’s is useful for primary isolation because it does not support
o a disease that produces a lesion in the throat or nasopharynx the growth of streptococci and pneumococci.
characterized by the presence of a spreading grayish o Tellurite Media
pseudomembrane.  Reduces the number of contaminants only Diphtheria will grow.
o Produces an exotoxin which is transported by blood to other organs  Colonies assume a grey or black color
and causes necrotic damage.  Gravis Colonies: large, flat, gray to black with dull surface
o Only strains that produce toxin cause manifestations associated with  Mitis Colonies: medium sized colonies that are smaller,blacker,
fatal illness. glossy and more convex
 Intermedius strains are very small and either smooth or rough

Figure 9 Tellurite Media

Figure 6 Diptheria caused by Corynebacteriumdiptheria

Morphology
o Non spore-forming Gram (+) bacilli that appear in palisade or as
individual cells lying at sharp angles to each other in V or L formations
(Chinese character-like formations)
o Club shaped swellings and beaded and barred forms are common.
Babes-Ernst granules are responsible for the beaded appearance.
o Non motile

Figure 10 Loeffler’s Serum for Corynebacterium diphtheriae

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 MICROBIOLOGY 1.6

Resistance  There is enlargement of regional lymph nodes in the neck

o Resistant to drying and freezing with marked neck edema (Bull neck)
o Organisms can survive on dried pseudomembrane for 14 weeks  There is risk of suffocation and death due to mechanical
o Killed by 1 minute exposure to 100⁰C or 10 min exposure to 58⁰C obstruction of the airway
o Susceptible to most disinfectants.  Restore airway patency by tracheotomy or intubation

Determinants of Pathogenecity
o Capable of colonizing mucous membranes
o K Antigen
 Heat – labile protein located at the surface of the cell wall.
 Antiphagocytic property of K antigen allows the organism to colonize
cells
o Cord Factor: produces disruption of the mitochondria.
o Neuraminidase & N-Acetylneuraminate lyase: degrades N-
Acetylneuraminic acid residues from mucinous environments,
providing bacteria a ready source of energy.
o Exotoxin
 Accounts for all the pathologic systemic effects
 Produced by organisms infected with a bacteriophage carrying the
gene for toxin production Figure 11 Enlargement of regional lymph nodes in
 Low iron conditions induce toxin expression, whereas high iron the neck with marked edema (BULLNECK)
conditions repress toxin production.
o Extrarespiratory Disease
 Diphtheria is caused by the local and systemic effects of a single
 The most common is Cutaneous diphtheria, due to secondary
exotoxin
infection of septic skin lesions
 The toxin molecules are composed of fragments, A and B.
 Appears as a chronic, spreading, non healing ulcer covered with a
 Fragment B binds to susceptible cell membranes and mediates the
grayish membrane
delivery of fragment A to its target.
 Strep. pyogenes and Staph. aureus are usually also present in the
 Inside the cell, fragment A separates from fragment B and catalyzes
lesion. Lesions fail to heal until appropriate therapy is given for
a reaction between nicotine adenine dinucleotide (NAD+) and the
these organisms.
eukaryotic polypeptide chain elongation factor.
 The toxin causes fatty myocardial degeneration resulting in
 Inhibits eukaryotic protein synthesis, produces DNA cleavage and
circulatory collapse and accounts for more than half of case
cell lysis.
fatalities.
 Cranial nerve paralysis may lead to paralysis of the soft palate with
Clinical infection
resultant difficulty of swallowing and nasal regurgitation of fluids.
o The primary habitat is the respiratory tract, and is transmitted by
 The most common manifestation of peripheral nerve involvement
symptom-free carriers, by persons in the incubation stage and by
is Polyneuritis of the lower extremities producing a mild
convalescents.
weakness to paralysis.
o Transmission is via droplet inhalation or from discharges in
cutaneous infections.
o Less frequently spread by direct contact with an infected individual
or a contaminated fomite.
o There is NO lifelong immunity to diphtheria
o Presence in the blood of antitoxin due to infection or immunization
with toxoid confers immunity. Determined by:
Schick Test:
 Injection of the volar forearm skin with 0.1ml of highly purified
toxin. Toxin treated with heat is injected in the other arm as
control.
 Absence of immunity to diphtheria is characterized by an
inflammatory reaction that becomes maximal in 4-7 days Figure 12 Cutaneous Diphtheria due to secondary infection of septic skin lesion
o Respiratory Disease Diagnosis
 Initial lesion on the tonsils and oropharynx and may spread to o Specific treatment must be started if the clinical picture is suggestive
the nasopharynx, larynx and trachea. of diphtheria.
 There is exotoxin production that is absorbed in the mucous o Dacron swabs collected from beneath the membrane is taken from
membranes and causes necrosis of cells in the area. suspected lesions BEFORE antibiotics are started. Place swabs in semi
 When the necrotic epithelium is embedded in fibrin, RBC & solid transport media such as Amies.
WBC, a grayish pseudomembrane is formed over the tonsils, o Inoculate specimens on a
pharynx or larynx.  Blood Agar Plate to rule out hemolytic strep
 Removing the pseudomembrane would tear capillaries and  Loeffler’s Slant, in 12-18 hours organisms with diphtheria-like forms
result in bleeding. can be identified by Gm stain
 Clinical Findings:  Tellurite Plate and incubate, in 36-48 hours the colonies can be
 Sorethroat and fever followed by prostration and dyspnea identified
because of obstruction caused by the membrane o Gram stain

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 MICROBIOLOGY 1.6
 Use specimens from growth on cultures NOT from clinical specimens
obtained from patients (Chinese character-like formation)
o Presumptive diphtheria isolate should be subjected to testing for
toxigenicity
 Modified Elek Method: An antitoxin disc is placed on an agar plate
and the culture to be tested is inoculated 9mm away from the disc.
After 48 hrs the toxin will be precipitated by the antitoxin from the
disc as a whitish material between the disc and the growth
 Polymerase Chain Reaction detects toxin on patient specimens
 ELISA can detect toxin in clinical specimens
 Immunochromatographic strip assay can also detect toxin on clinical
specimens
 Animal Inoculation Test:
a)Guinea pig or rabbit is injected intracutaneously with the
organism.
b) 5 hours later, Antitoxin is injected intraperitoneally.
c) 30 minutes later, the animal is injected with the organism in a
control area. After 48 hours, if a toxigenic strain is present, the initial
injection site will have a necrotic area.
Treatment
o Treatment of choice is antitoxin, which should be given immediately on
the basis of clinical impression.
o The function of antitoxin is to neutralize the unbound toxin in the blood
o The patient must be tested for hypersensitivity before starting
treatment.
o Treatment with penicillin G or erythromycin is recommended but
neither is a substitute for antitoxin.
o Antibiotics slow the spread of infection and, by killing the organism,
prevent further toxin production.
o Supportive care directed especially at respiratory and cardiac
complications is an essential part of the management of patients with
diphtheria.
Prevention
o Vaccination with diphtheria toxoid is highly effective & it is first
administered early in infancy with (DPT) at 2,4,6 months and booster at
18 months of age.
Corynebacterium pseudotuberculosis
 Produces an exotoxin and causes ulcerative lymphangitis in warm
blooded animals
 Causes chronic lymphadenitis in humans due to contact with infected
animals.
Corynebacterium pseudodiphtheriticum and Corynebacterium xerosis
 Diphtheriticum is normal in the nasopharynx. Xerosis in the skin, mucous
membranes and conjunctica.
 Infections occur in immunocompromised patients and those with
mucocutaneous defects
 Causes prosthetic valve endocarditis
Listeria monocytogenes
 Facultative intracellular Gram (+) coccobacilli that occur in short chains of
3-5 organisms. Causes Listeriosis
 Can assume a palisade formation in stained preparations.
 Actively motile. “Tumbling-end-over-end motility” which distinguishes it
from the non motile C. diphtheriae
 The disease affects primarily pregnant women, newborns, and adults with
weakened immune systems.
Cultural Characteristics
o Aerobic to microaerophilic (can survive with little oxygen)
Group 35 | J.L. Villaflor, F.A. Villamor, M.K. Villanueva, M.E. Villanueva, M.L. Villanueva
o Can grow at Refrigerator temperature, low pH and high salt conditions,
so, it can survive food preservation methods making it an important
food borne pathogen.
o Grows well on Sheep blood agar & Tryptose Agar
 Produces Beta hemolysis on Sheep blood agar
 On Tryptose Agar colonies are blue green in color
o Catalase (+), ferments Glucose with the formation of acid, does not
ferment Mannitol
Figure 13 Tryptose Agar
 Serologic classification based on the O (somatic) antigen and H (flagellar)
antigen yielded several serotypes.
o 1/2a, 1/2b, 4b : 95% of human isolates
o 4b causes most of the food-borne outbreaks
Determinants of Pathogenicity
o Facultative intracellular organism that invades and grows in
mammalian cells including macrophages, epithelial cells and fibroblasts.
o The organism enters the cytoplasm, grows and spreads to other cells.
o Normally, the immune system eliminates the infection before it
spreads (Cytotoxic T cells). If the immune system is compromised,
systemic disease may develop.
o The organism binds to the host cell facilitated by adhesin proteins (Ami,
Fbp A & Flagellin Pr-)
o Internalin A on the cell wall of the organism interacts with E-cadherin
on the epithelial cells promoting Phagocytosis.
o The organism produces Listeriolysin O which lyses the phagolysosome
membrane allowing the organism to escape into the cytoplasm and
undergo rapid division.
o The organism becomes encapsulated by actin filaments. The filaments
reorganize into a long tail extending from one end of the organism due
to the action of Act A.
o The tail propels the organism to the surface of the host cell, protrusions
(filopods) are formed that can penetrate adjacent cells allowing the
bacterium to enter.
o Since the bacterium is intracellular, antibodies are ineffective.
o Its presence intracellularly in phagocytic cells also permits access to
the brain and probably transplacental migration to the fetus in
pregnant women.
Clinical Infection
o Found in plant-soil environment and animal feces
o Food is the most common vehicle for transmission
 Raw vegetables, dairy products, raw hotdogs, undercooked chicken
o Human to human transmission
 Transplacentally through the umbilical vein
 During delivery through contact with infective secretions
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 MICROBIOLOGY 1.6

Pathogenesis
o The major portal of entry is the GIT. The disease may not occur in
immunocompetent individuals after ingestion of contaminated food or
may develop gastroenteritis with fever and diarrhea.
o Intraluminal bacteria gain access to the circulation when the host
defense is altered, followed by seeding of various sites.
Clinical Manifestations
o More than half of patients have underlying disorders like malignancy,
alcoholism, diabetes, etc.
o In the healthy adult, infections are usually asymptomatic, or at most
produce a mild influenza-like disease.
o Adult Infection
 Meningitis is the most common form of listeriosis in the adult
especially in cancer patients and renal transplant recipients
 Primary Listeria bacteremia usually affects patients under 50
years of age. May produce endocarditis and pneumonia.
 In pregnant women, even though the most usual symptom is a
mild influenza-like illness without meningitis, infection of the fetus
is common and can lead to abortion, stillbirth, or delivery of an
acutely ill infant.
o Neonatal Infections
 Genital tract infections in the pregnant with infection of the
offspring. History of mild influenza-like illness.
 Granulomatosis infantiseptica
 Early form
 Results from infection in utero and appears within 2 days of
birth
 May cause abortion, premature birth, stillbirth or death within a
short period after birth.
 If the infant is born alive, septicemia develop within a few hours
followed by fetal distress, pneumonia, diarrhea, seizures, and
maculopapular lesions on the legs and trunk
 Late Form of Neonatal Listeriosis.
th
 Occurs on the 5 day of life
 Infection is acquired during or after birth rather than in utero
 Meningitis is the usual presentation.
Prevention
o Should center on the elimination of animal reservoirs (sheep, cattle,
goats and pigs)
o Listeriosis can be prevented in infants by prompt recognition and
treatment of the mother.
Erysipelothrix rhusiopathiae
 Non motile, nonencapsulated, Gram(+) bacilli
Cultural Characteristics
o Microaerophilic
o Heart Infusion Agar with rabbit’s blood is suitable for isolation
o On BAP, colonies are small, round, grayish white in color and shows
alpha hemolysis
o Catalase(-), oxidase (-), indole (-)
o On TSI agar, hydrogen Sulfide is produced turning the TSI butt black
 Produces Hyaluronidase (Spreading Factor) and Neuraminidase (increases
ability of the organism to attach to host receptors)
Clinical Infection
 Widely distributed in land and sea animals worldwide including birds.
 It occurs on the surface slime of fresh and seawater fishes, in the sewage
of abattoirs, and in the feces of infected animals
 The disease is prevalent in abattoir employees, butchers, fish handlers and
those who have contact with animal products
 Infection is via direct inoculation of a wound with animal products
 Most common E. rhysiopathiae infection in humans is Erysipeloid.
o Occurs on the fingers by direct inoculation on the site of a cut (“seal
finger” or “whale finger”)
o Severe pain and swelling occur. The lesion is raised and violaceous in
color. Pus is usually not present as differentiated from Staph infection.
Resolves in 3-4 weeks
o May also cause a diffuse cutaneous disease and bacteremia with
endocarditis.
o Dx: Culture of aspirated material from border of lesion.
o DOC is PCN. Erythromycin is an alternative

Immunity
o No second clinical infection with Listeria has been observed in patients
cured of Listeriosis

Laboratory Diagnosis
o Gram Stain of infected material and look for typical pleomorphic Gm (+)
bacilli
 Blood, CSF, Amniotic fluid and Genital tract secretions
o Tryptose Agar medium is excellent for cultivation and propagation
o Accurate identification is based on combination of Beta hemolysis,
catalase production, and tumbling motility.
o Serology is unreliable because the organism cross-reacts with other
Gm(+) organisms

Treatment
o Penicillin G or Ampicillin
o Trimethoprim-Sulfamethoxazole or Erythromycin for patients allergic to
PCN.

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