Microbial Diseases of the Skin

and Soft Tissues I

Mr. Mohamed Yusuf Abdi
M.Sc. Medical Microbiology and Immunology
 Anatomy of the Skin
• Skin is thickened keratinized epithelium made of multiple layers of
cells that is largely impervious to water, skin is part of integumentary
system (skin, hair, nails & exocrine glands).
• The skin consists of 3 layers:
I. Epidermis (external cellular layer)
II. Dermis (deep connective tissue layer)
III. Subcutaneous (hypodermis)
• Sweat gland ducts, hair follicles, and oil gland ducts are found in the
dermis and penetrate into the subcutaneous layer.
Anatomy of the Skin
 How the skin prevents microbial infections
• The continuous sloughing off of keratinocytes from the surface of the
epidermis does not allow colonizers to overgrow and cause disease.
• The sebaceous glands and the sweat glands secrete substances that
inhibit the growth of many organisms. Sebaceous glands in the dermis
secrete sebum, which contains a variety of fatty acids and lactic acid.
• Fatty acids kill bacteria, Lactic acid in the sebum reduces the pH of the
skin surface and inhibits the growth of many microorganisms.
• The high content of sodium chloride in sweat can inhibit the growth of
many bacteria.
 Normal Flora of The Skin

• The normal flora have the ability to prevent most pathogens from
colonizing by preventing their attachment to the surface of the skin or by
producing toxins that inhibit the growth of other microorganisms.
• Most microorganisms live in the superficial layers of the stratum corneum
and in the upper parts of the hair follicles.
• The normal resident skin microbiota is made up of a relatively small and
stable array of bacteria and fungi. Bacteria such as Staphylococcus
epidermidis, Corynebacterium, Lactobacillus, Bacteroides, Prevotella,
Haemophilus; yeasts such as Malassezia, Candida are part of skin normal
flora.
 Factors associated with skin infections
• A break in the barrier (skin), lacerations, bite (human, animals),
scratches, burns (most common route)
• Pre-existing skin conditions wounds (e.g., diabetes)
• Surgery and medical intervention (instrumentation eg, needles)
• When body loss the defence mechanism (e.g., lost normal flora)
• Seawater or hot tubs.
 Microbial disease of the skin
Microbial disease of the skin may result from:
Breach of intact skin, allowing infection from the outside
Skin manifestations of systemic infections, which may arise as a result
of blood-borne spread from the infected focus to the skin.
Toxin-mediated skin damage due to production of a microbial toxin at
another site in the body (e.g. toxic shock syndrome).
 Naming Skin Lesions
• Variations in these lesions are often useful in describing the symptoms of
the disease. Lesion is the clinical term for any observable abnormality of the skin.
• For example, small, fluid-filled lesions are vesicles.
• Vesicles larger than about 1 cm in diameter are termed bullae.
• Flat, distinct, discolored area of skin less than 1 cm are known as macules.
• Raised lesions are called papules or, when they contain pus, pustules.
• A skin rash that arises from disease conditions is called an exanthema.
• Pyodermas are a group of inflammatory skin disorders caused
by bacteria that produce pus.
Naming Skin
Lesions
Bacterial Diseases of the Skin
 MRSA Skin and Soft Tissue Infections
• Methicillin-resistant staphylococcus aureus (MRSA) is a common
cause of skin lesions.
• Staphylococcus aureus is a gram-positive coccus that grows in
clusters. It can be pathogenic, but it also appears as “normal”
biota on the skin.
• This species withstand high salt (7.5% to 10%), extremes in ph,
and high temperatures (up to 60°C for 60 minutes).
 Pathogenesis and Virulence Factors
• S.aureus produce different types of enzymes and toxins, to facilitate
tissue adhesion, immune evasion, and host cell injury.
• Pathogenic S.aureus strains typically produce coagulase, an
enzyme that coagulates plasma.
• Other enzymes expressed by S. aureus include hyaluronidase,
which digests the intercellular “glue” (hyaluronic acid) that binds
connective tissue in host tissues; staphylokinase, which digests
blood clots; a nuclease that digests DNA (DNase); and lipases that
help the bacteria colonize oily skin surfaces.
 Diagnosis and Culture
• Polymerase chain reaction (PCR) is routinely used to diagnose MRSA.
• Alternatively, primary isolation of S. aureus is achieved by inoculation
on blood agar or selective media such as mannitol salt agar are used.
• A catalase test can be used to differentiate the staphylococci, which is
catalase positive, from the streptococci, which is catalase negative.
• One key technique for separating S.aureus from species of
Staphylococcus is the coagulase test. By definition, any isolate that
coagulates plasma is S. aureus; all others are coagulase-negative.
 Prevention and Treatment

Prevention is only possible with good hygiene.

Treatment of these infections often starts with incision of the lesion
and drainage of the pus.
• Antimicrobial treatment should include more than one antibiotic.
• Clindamycin + trimethoprim/sulfamethoxazole or doxycycline.
• These recommendations, of course, will change based on antibiotic-
resistance patterns.
 Acne
(the most common skin disease in humans)

• Acne, refers to clogging of the sebaceous glands by oil (sebum) and

their expansion or inflammation, affecting 80 percent of teenagers and
young adults at some point.
• Normally, skin cells that are shed inside the hair follicle are able to
leave, but acne develops when cells are shed in higher than normal
numbers, they combine with sebum, and the mixture clogs the follicle.
As sebum accumulates, whiteheads form; if the blockage protrudes
through the skin, a blackhead forms. The dark colour of black heads is
due not to dirt , but to lipid oxidation and other causes.
 Acne
• There are three main types: comedonal acne (mild), inflammatory acne
(moderate), and the most severe and scarring form nodular cystic acne.
• While mild and moderate forms of acne are common, their causes are
not uniform or fully understood. The overarching cause of acne relates
to the clogging of skin pores and hair follicles.
• A range of factors contribute to the severity of acne in different
individuals, including, but not limited to, an individual’s sebum
production, genetics, hormone levels, cosmetics, and usage of certain
drugs or medications. Despite what people might have once thought,
diet, dry skin, and hygiene have not been shown to affect acne.
 Acne
• Propionibacterium acnes bacteria, however, have been shown to play a
major role in at least some types of acne. P. acnes bacteria are Gram-
positive rods that are normal residents of the skin.
• P.acnes have enzymes that allow them to use sebum as a nutrition
source. When pores become clogged with sebum, oxygen levels in the
pores decrease, leading to an ideal environment for P. acnes. As the
bacteria proliferate in the pores they can generate an inflammatory
response, leading to the characteristic acne.
 Acne
• Some patients with acne progress to nodular cystic (severe) acne.
• Nodular cystic acne is characterized by nodules or cysts, which are
large, red, swollen and painfu linflamed lesions filled with pus deep
within the skin.
• These leave prominent scars on the face and upper body, which often
leave psychological scars as well.
• Because they are so deep, topical acne treatments aren't all that
effective. Instead, oral medications like Accutane (isotretinoin) are the
best option here.
 Different types of acne In a clogged pore, or comedo, diverse substances such as
sebum, keratin, or dead skin cells may cause the obstruction, which may either close the pore or allow it to
remain open. The type of acne lesions that develop depend on the nature of the comedo.
Comedonal acne
Acne
 Folliculitis
• Folliculitis is an inflammation and infection of hair follicles.
• S.aureus is the most common causative agent of folliculitis, although
P.aeruginosa has been implicated in cases acquired from contaminated
swimming pools or hot tubs.
• Lesions appear as small, erythematous papules and often evolve to
form pustules with a whitish or yellowish central zone.
• Sycosis barbae is a deep-seated form of folliculitis occurring in
bearded areas of the face due staphylococcus aureus infection.
Folliculitis
 Furuncles
• A furuncle results when the inflammation of a single hair follicle or
sebaceous gland progresses into a large, red, painful and extremely
tender abscess or pustule especially in warm, moist areas of the body
and areas subjected to friction.
• S.aureus is the most common causative pathogen.
• Draining pus from the abscess is frequently a preliminary step to
successful treatment
 Carbuncles
• A carbuncle involve a group of hair follicles and have similar symptoms as
furuncles but are clustered and form a lump deep in the skin
• It consists of multiple abscesses that can drain at several adjacent sites along
hair follicles.
• Carbuncles commonly occur at the nape of the neck and on the back of the
thighs and are often associated with fever and systemic symptoms
• Bacteremia can be a complicating event, and surgical drainage is
needed for most carbuncles.
• Purulent drainage should be cultured to confirm the organism, which is
typically S.aureus.
Furuncles and Carbuncles
 Paronychia

• Paronychia is an infection of the cuticle surrounding the nail bed.

• Cases generally follow minor trauma, such as removing a hangnail
• The involved part of the finger at the nail margin becomes painful, red,
warm, and swollen, and pus may be expressed from around the nail bed.
• Candida or staphylococci are usually the causative organisms.
• Paronychia usually responds to warm soaks, which often lead to
spontaneous drainage of pus and resolution.
• Systemic antimicrobial therapy is usually not required.
Paronychia
Paronychia
 Erysipelas
• Erysipelas: is a type of superficial skin infection that involves not
only the epidermis but also the underlying dermis and lymphatic
system.
• The lesions of erysipelas are characterized as painful, indurated areas
of inflammation with raised borders that are sharply demarcated from
the adjacent normal skin.
• The involved skin usually has a bright red to crimson hue, and patients
often have fever.
• Streptococcus pyogenes is the main cause of erysipelas.
 Erysipelas
• In erysipelas, the bacteria enter the
skin through a small cut or break in
the skin
• Twenty percent of erysipelas cases
are seen on the face, with 80%
affecting the legs.
 Treatment:
• Penicillin or erythromycin is
generally used for therapy.
Erysipelas
 Necrotizing Fasciitis
• Necrotizing Fasciitis also known as flesh-eating disease, is rare aggressive
life-threatening bacterial infection that cause necrosis of the skin and
surrounding muscles and organs (fascia) and fat.
• It can be caused by S.pyogenes (referred as “flesh-eating bacteria” ).
• Bacteria is introduced into the tissue through a break in the skin.
• Symptoms begin in a similar as folliculitis or erysipelas.
• Bacteria that cause this condition have great toxigenicity and invasiveness
because of special enzymes and toxins.
Streptolysins
Streptokinase Exotoxin B that
Hyaluronidase rapidly destroy
Leukocidin tissues
M-proteins Necrotizing Fasciitis
• The enzymes digest the connective tissue in skin, and the toxins
poison the epidermal and dermal tissue.
• As the flesh is killed, it separates and sloughs off, forming a pathway
for the bacteria to spread into deeper tissues such as muscle.
• More dangerous cases involve polymicrobial infections (include
anaerobic bacteria) and the systemic spread of the toxin to other
organs.
 Necrotizing Fasciitis
• Some patients have lost parts of their limbs and faces, and others have
suffered amputation, but early diagnosis and treatment can prevent
these complications.
• Risk factors are diabetes mellitus and abdominal surgery.
• Treatment is with powerful broad-spectrum antibiotics and surgery to
remove dead and damaged tissue and bone. Amputation may be
necessary in severe cases.
Flesh-eating disease
Flesh-eating disease
 Impetigo
• Impetigo is a superficial bacterial infection that causes the skin to
flake or peel off. It is not a serious disease but is highly contagious,
and children are the primary victims. Impetigo can be caused by either
Staphylococcus aureus or Streptococcus pyogenes.
Signs and Symptoms:
• The “lesion” of impetigo looks variously like peeling skin, crusty
and flaky scabs, or honey-colored crusts and it itches.
• Lesions are most often found around the mouth, face, and extremities,
though they can occur anywhere on the skin.
 Impetigo Caused by Staphylococcus
aureus
Pathogenesis and virulence factors
• The most important virulence factors relevant to S.aureus impetigo are
exotoxins called exfoliative toxins.
• The toxins cause a separation of the skin layers. This leads to the
characteristic blistering seen in the condition.
• S.aureus strains typically produce coagulase, causes fibrin to be
deposited around the bacteria, concentrating the exotoxins in an area
of local damage.
 Impetigo Caused by Streptococcus pyogenes

• S.pyogenes is a gram-positive coccus in Lancefield group A and is

beta-hemolytic on blood agar and sensitive to bacitracin.
Pathogenesis and Virulence Factors
• The M protein allows the microbe to evade phagocytosis and killing
by neutrophils. It also appears to help the bacteria adhere to and
colonize mucous membranes.
 Impetigo Caused by Streptococcus pyogenes
• The GAS produce substances that promote the rapid spread of
infection through tissue and by liquefying pus. Among these are
streptokinases (enzymes that dissolve blood clots), hyaluronidase (an
enzyme that dissolves the hyaluronic acid in the connective tissue),
and deoxyribonucleases (enzymes that degrade DNA).
• These streptococci also produce certain enzymes, called streptolysins,
that lyse red blood cells and are toxic to neutrophils.
Impetigo
 Transmission and Epidemiology of Impetigo

• Impetigo, whether it is caused by S. pyogenes, S. aureus, or both, is

highly contagious and transmitted through direct contact but also
via fomites and mechanical vectors.

• The peak incidence is in the summer and fall.

• S.pyogenes is more often the cause of impetigo in newborns, and S.aureus is

more often the cause of impetigo in older children, but both microbes can cause
infection in either age group.
 Culture and/or Diagnosis
• Doctors usually diagnose impetigo by visual inspection.
• However, when an infection requires identification (for instance, if
initial treatment fails), sample can be cultured on blood agar.
• A catalase test can be used to differentiate the staphylococci, which is
positive, from the streptococci, which is negative.
 Prevention and Treatment
Prevention: The only current prevention for impetigo is good hygiene
Treatment
• Impetigo is sometimes treated with a drug that will target either
bacterium, S.pyogenes or S.aureus, eliminating the need to determine
the exact etiologic agent.
• The drug of choice is topical mupirocin or Retapamulin.
• Trimethoprim-sulfamethoxazole is the first alternative for methicillin-
resistant S. aureus (MRSA).
 Cellulitis
• Cellulitis is an acute spreading infection of the dermis and
subcutaneous tissues and results in pain, erythema, edema, and warmth.
• Cellulitis generally follows the introduction of bacteria or fungi into the
dermis, either through trauma or by subtle means (with no obvious
break in the skin). Cellulitis is very common on the lower leg.
• The most common causes of the condition in healthy people are
Staphylococcus aureus and Streptococcus pyogenes, although almost
any bacterium and some fungi can cause this condition in an
immunocompromised patient
 Cellulitis
Pathogenesis:
• A diffuse infection occurs in patients with cellulitis due to S.pyogenes
because streptokinase, DNase, and hyaluronidase break down cellular
components that otherwise would contain and localize the
inflammation.
• Spreading factors such as hyaluronidase, protease, and DNase are
present in other bacteria and appear to be important in the
pathogenesis of this disease.
 Cellulitis
• The signs of cellulitis
include the indistinct
border, spreading erythema.
• In infants, group B
streptococci are a frequent
cause of this infection.
 Cellulitis

• Treatment:

• Mild cellulitis responds well to oral antibiotics chosen to be effective

against both S. aureus (if it is S. aureus, it is nearly always MRSA)
and S. pyogenes. More involved infections and infections in the
immunocompromised require intravenous antibiotics.
Staphylococcal Scalded Skin Syndrome (SSSS)

• This syndrome is another dermolytic condition caused by

Staphylococcus aureus. Although children and adults can be affected,
SSSS develops predominantly in new-borns and babies.

• Exfoliative toxins are responsible for the damage. Unlike impetigo,

the toxins enter the bloodstream from the site of initial infection (the
throat or vagina) and then travel throughout the body, interacting with
the skin at many different sites.
 Staphylococcal Scalded Skin Syndrome

• The toxins cause bullous lesions, often appear first around the
umbilical cord (in neonates) or in the diaper or axilla area.
• The lesions begin as red areas, take on the appearance of wrinkled
tissue paper, and then form very large blisters. Eventually, the top
layers of epidermis peel off completely.
• Widespread desquamation of the skin follows, leading to the burned
appearance referred to in the name of this condition.
• Fever may precede the skin manifestations.
 Staphylococcal Scalded Skin Syndrome
• At this point, the protective keratinized layer of the skin is gone,
and the patient is vulnerable to secondary infections, cellulitis, and
bacteremia.
• Once a diagnosis of SSSS is made, immediate antibiotic therapy
should be instituted.
• Culture should be attempted so that antibiotic sensitivities can be
established.
Staphylococcal
Scalded Skin
Syndrome
 Gas Gangrene
Necrotizing fasciitis & “flesh-eating” disease
• Gas gangrene (also called clostridial myonecrosis) is a highly lethal
infection of skin and soft tissue, characterized by the presence of gas
under the skin and caused by a bacteria called Clostridium perfringens.
• Clostridium perfringens, a an anaerobic gram-positive, spore-forming
bacilli.
• The endospores of this species can be found in soil, on human skin,
intestine and vagina.
• In an anaerobic conditions, this bacterial spore germinate to bacillus
form and release the exotoxins that cause the damage in this disease.
 Gas Gangrene
Transmission and Epidemiology:
• The conditions that may predispose a person to gangrene are surgical
incisions, compound fractures, diabetic ulcers, septic abortions,
puncture and gunshot wounds and accidents injuries contaminated by
endospores from the environment.
Pathogenesis and Virulence Factors:
• Bacterial spores gather in an injury or surgical wound that has no or
poor blood supply (low-oxygen environment).
 Pathogenesis and Virulence Factors
• Low-oxygen environment stimulate endospore germination, rapid
vegetative growth in the dead tissue, and release of exotoxins.
• C. perfringens produces several active exotoxins; the most potent one,
alpha toxin (lecithinase), which damages cell membranes, including
those of erythrocytes, resulting in hemolysis, edema, and tissue
destruction.
• Virulence factors that add to the tissue destruction are collagenase,
hyaluronidase, and DNase.
• The gas formed in tissues, resulting from fermentation of muscle
carbohydrates, can also destroy muscle structure.
 Signs and Symptoms
• Two forms of gas gangrene have been identified.
• In anaerobic cellulitis, the bacteria spread within damaged necrotic
muscle tissue, producing toxins and gas as the infection proceeds.
However, the infection remains localized and does not spread into
healthy tissue.
• The pathology of true myonecrosis is more destructive. Toxins
produced in large muscles, diffuse into nearby healthy tissue and cause
local necrosis at these sites.
 Signs and Symptoms

• Initial symptoms of pain, edema, and a foul smelling bloody exudate

in the lesion are followed by fever, tachycardia, and blackened
necrotic tissue filled with bubbles of gas. Shock and death can ensue.

• If treatment is not begun early, the disease is invariably fatal.

Gas Gangrene
 Gas gangrene
Note large area of necrosis on
lateral aspect of foot. Necrosis
is mainly caused by lecithinase
produced by Clostridium
perfringens. Gas in tissue is a
feature of gangrene produced
by these anaerobic bacteria. A
large gas- and fluid-filled bulla
is seen near the ankle.
 Gas Gangrene
Prevention and Treatment:
• One of the most effective ways to prevent clostridial wound infections
is immediate and rigorous cleansing and surgical repair of deep
wounds, compound fractures, and infected incisions.
• Debridement (the removal) of diseased tissue eliminates the conditions
that promote the spread of gangrenous infection.
• Surgery is supplemented by large doses of antibiotics (clindamycin +
penicillin) to control infection.
• Extensive myonecrosis of a limb may call for amputation.
 Prevention and Treatment

• Hyperbaric oxygen therapy, in

which the affected part is
exposed to an increased oxygen
mix in a pressurized chamber,
can also lessen the severity of
infection by inhibiting the
growth of anaerobic bacteria.
 Cutaneous Anthrax
• Bacillus anthracis, the agent of anthrax, is a gram-positive rod that can
cause ulcerative skin lesions.
• B. anthracis spores enter the skin through small cuts or abrasions.
• The skin lesions most often occur in wool handlers or persons working
with other animal products that are contaminated with B. anthracis
spores.
• Germination and growth of the pathogen in the skin are marked by the
production of a papule that becomes increasingly necrotic and later
ruptures to form a painless, black eschar.
 Cutaneous Anthrax

• The diagnosis is often suspected clinically given the characteristic

skin lesions, but biopsy and culture should be performed for
confirmation.

• Penicillin has long been the drug of choice for the treatment of anthrax

• A vaccine exists but is recommended only for high-risk persons and

the military.
Cutaneous Anthrax
 Leprosy (Hansen disease)
• Leprosy, is a rare highly contagious, found in South Asia, Africa, and
South America.
• The classic skin manifestation of Mycobacterium leprae, the causative
agent of Hansen disease, is a circumscribed, hypopigmented, or less
commonly, hyperpigmented macule.
• Acid-fast bacilli and granulomas can be seen in tissue biopsy specimens,
but M. leprae cannot be cultured in vitro because it is an obligate
intracellular bacteria.
• Effective treatment usually involves combination chemotherapy with
agents such as rifampin, dapsone, and clofazimine
Leprosy
 Other Soft Tissue Infections
Bite infections:
• Bites from humans or animals are often complicated by infection
that can be quite severe and is generally caused by a mixture of
aerobic and anaerobic organisms.
• Common pathogens implicated in human bite infections include
streptococcus anginosus group, S. Aureus, eikenella, fusobacterium,
and prevotella
 Bite Infections

• Wound care, including debridement, culture of deep tissue or purulent

drainage, and prompt antimicrobial administration are important.

• Antimicrobial regimens with aerobic and anaerobic activity are

indicated; amoxicillin-clavulanic acid, ampicillin-sulbactam, or a
combination of a fluoroquinolone and clindamycin is suitable
treatment.
 Diabetic Foot Infections
• Foot infections are a very common occurrence in persons with diabetes
mellitus.
• Risk factors for foot infection include the presence of peripheral
neuropathy (damage or dysfunction of one or more nerves), trauma to the
feet, inadequate blood glucose control, impairment of kidney function, and
improper foot care, including walking barefoot.
• Ulcerative lesions and gangrene may, like cellulitis, be the result of
staphylococcal and streptococcal infection but often are mixed infections
and include Enterobacteriaceae, Pseudomonas (blue-green pus and a
grapelike odor), gram-positive bacteria, and anaerobic bacteria.
 Diabetic Foot Infections

• Cultures of open wounds are most helpful when they are

obtained from deep tissues or from collections of pus beneath the
skin surface.

• Definitive antimicrobial therapy should be based on culture results

from a deep specimen.

• Most diabetic foot wounds require debridement

 Actinomycosis
• Actinomycosis is a chronic disease characterized by the formation of
abscesses, tissue fibrosis, and draining sinuses that discharge
sulfur granules (masses of organisms).
• It is caused by gram-positive non–sporeforming anaerobic flamentous
bacterial species, especially Actinomyces israelii, although a variety of
Actinomyces species have been identifed as causing human infection.
• They are part of the normal biota of the mouth and GI and genital
tracts.
• Penicillin is the preferred treatment
Actinomycosis
 Erythema gangrenosum
• Erthyma gangrenosum is a characteristic skin lesion associated with
Pseudomonas bacteremia.
• The lesions begin as painless, flat, erythematous areas that progress
rapidly to nodules and then bullae, which subsequently ulcerate and
form a black eschar on the surface, with surrounding erythema.
• Biopsy and Gram stain of the lesions will reveal bacteria in the tissue,
and inflammation of blood vessels will also be present.
 Erythema
gangrenosum
• Lesions of ecthyma
gangrenosum begin as
red macules that enlarge
and become slightly
elevated papules, which
become hemorrhagic and
centrally necrotic with
purple-to-black
coloration
Ecthyma gangrenosum due to a Pseudomonas aeruginosa
infection of the bloodstream.
 Vibrio and Aeromonas Infections
• Vibrio vulnifcus is a gram-negative organism that is part of the
ocean microbiota
• Infection occurs through exposure of an existing wound to seawater
containing the organisms.
• Aeromonas spp. are found in fresh water and brackish water
and can cause skin lesions similar to those caused by V. vulnifcus.
However, skin infection due to Aeromonas is often the result of
contamination of a preexisting wound with water containing the
organisms.
 Lyme disease
• The tick borne spirochete of Lyme disease Borrelia burgdorferi,
characteristically produces a distinctive “bull’s eye” or target skin
lesion called erythema migrans at the inoculation site 1 to 2 weeks
after infection.
• The diagnosis of Lyme disease can be made by serologic testing
to identify antibodies against B. burgdorferi.
• A number of antimicrobials, including ceftriaxone, penicillin G,
amoxicillin, erythromycin, and tetracycline, are useful in the treatment
of Lyme disease.
 Lyme disease
• Within 3–32 days after a
patient experiences a tick bite,
a red macule will appear at the
site.
• The macule expands radially
with central clearing and
swelling (bull’s eye)
• A macule is a flat, distinct,
discolored area of skin less
than 1 centimeter (cm) wide.
 Rickettsiosis
• Dermatologically, rickettsial infections are characterized by the type and
distribution of the associated rash and the presence or absence of a black
eschar at the vector bite inoculation site.
• Clinical symptoms common to rickettsial infections include high-grade
fever, chills, malaise, headache, myalgias, rash, and conjunctival
injection.
• Rickettsiae are gram-negative intracellular pathogens that reside
within endothelial cells and macrophages. Rickettsiae have various
animal reservoirs and are transmitted to humans through several
species-specifc insect vectors (e.g., ticks, mites, lice, fleas).
Rickettsiosis
Thank You