This document discusses skin, soft tissue, and musculoskeletal infections. It begins by describing different types of skin and soft tissue infections, including primary infections which invade through breaks in the skin and secondary infections which reach the site through the bloodstream. It then examines specific bacteria that can cause infections, such as Staphylococcus, Streptococcus, Bacillus anthracis, and Clostridia. The document provides details on the clinical features, laboratory diagnosis, treatment, and prevention of various bacterial infections and diseases.
Necrotizing Fasciitis ppt by Dr Ahmed Zubair Abbasi.pptxahmed15505
Necrotizing fasciitis is a subset of aggressive skin and soft tissue infections (SSTIs) that cause necrosis of the muscle fascia and subcutaneous tissues. The infection typically travels along the fascial plane, which has a poor blood supply.
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Necrotizing Fasciitis ppt by Dr Ahmed Zubair Abbasi.pptxahmed15505
Necrotizing fasciitis is a subset of aggressive skin and soft tissue infections (SSTIs) that cause necrosis of the muscle fascia and subcutaneous tissues. The infection typically travels along the fascial plane, which has a poor blood supply.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
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Disruption of blood supply to lung alveoli due to blockage of one or more pulmonary blood vessels is called as Pulmonary thromboembolism. In this presentation we will discuss its causes, types and its management in depth.
The prostate is an exocrine gland of the male mammalian reproductive system
It is a walnut-sized gland that forms part of the male reproductive system and is located in front of the rectum and just below the urinary bladder
Function is to store and secrete a clear, slightly alkaline fluid that constitutes 10-30% of the volume of the seminal fluid that along with the spermatozoa, constitutes semen
A healthy human prostate measures (4cm-vertical, by 3cm-horizontal, 2cm ant-post ).
It surrounds the urethra just below the urinary bladder. It has anterior, median, posterior and two lateral lobes
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TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
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- Video recording of this lecture in English language: https://youtu.be/lK81BzxMqdo
- Video recording of this lecture in Arabic language: https://youtu.be/Ve4P0COk9OI
- Link to download the book free: https://nephrotube.blogspot.com/p/nephrotube-nephrology-books.html
- Link to NephroTube website: www.NephroTube.com
- Link to NephroTube social media accounts: https://nephrotube.blogspot.com/p/join-nephrotube-on-social-media.html
Tom Selleck Health: A Comprehensive Look at the Iconic Actor’s Wellness Journeygreendigital
Tom Selleck, an enduring figure in Hollywood. has captivated audiences for decades with his rugged charm, iconic moustache. and memorable roles in television and film. From his breakout role as Thomas Magnum in Magnum P.I. to his current portrayal of Frank Reagan in Blue Bloods. Selleck's career has spanned over 50 years. But beyond his professional achievements. fans have often been curious about Tom Selleck Health. especially as he has aged in the public eye.
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Introduction
Many have been interested in Tom Selleck health. not only because of his enduring presence on screen but also because of the challenges. and lifestyle choices he has faced and made over the years. This article delves into the various aspects of Tom Selleck health. exploring his fitness regimen, diet, mental health. and the challenges he has encountered as he ages. We'll look at how he maintains his well-being. the health issues he has faced, and his approach to ageing .
Early Life and Career
Childhood and Athletic Beginnings
Tom Selleck was born on January 29, 1945, in Detroit, Michigan, and grew up in Sherman Oaks, California. From an early age, he was involved in sports, particularly basketball. which played a significant role in his physical development. His athletic pursuits continued into college. where he attended the University of Southern California (USC) on a basketball scholarship. This early involvement in sports laid a strong foundation for his physical health and disciplined lifestyle.
Transition to Acting
Selleck's transition from an athlete to an actor came with its physical demands. His first significant role in "Magnum P.I." required him to perform various stunts and maintain a fit appearance. This role, which he played from 1980 to 1988. necessitated a rigorous fitness routine to meet the show's demands. setting the stage for his long-term commitment to health and wellness.
Fitness Regimen
Workout Routine
Tom Selleck health and fitness regimen has evolved. adapting to his changing roles and age. During his "Magnum, P.I." days. Selleck's workouts were intense and focused on building and maintaining muscle mass. His routine included weightlifting, cardiovascular exercises. and specific training for the stunts he performed on the show.
Selleck adjusted his fitness routine as he aged to suit his body's needs. Today, his workouts focus on maintaining flexibility, strength, and cardiovascular health. He incorporates low-impact exercises such as swimming, walking, and light weightlifting. This balanced approach helps him stay fit without putting undue strain on his joints and muscles.
Importance of Flexibility and Mobility
In recent years, Selleck has emphasized the importance of flexibility and mobility in his fitness regimen. Understanding the natural decline in muscle mass and joint flexibility with age. he includes stretching and yoga in his routine. These practices help prevent injuries, improve posture, and maintain mobilit
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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Couples presenting to the infertility clinic- Do they really have infertility...Sujoy Dasgupta
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Surgical Site Infections, pathophysiology, and prevention.pptx
chapter28.pptx
1. CHAPTER 28 (A)
SKIN, SOFT TISSUE
AND
MUSCULOSKELETAL
INFECTIONS
Part III
Microbiology as Applied to Infectious
Diseases
Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Hyderabad 500 029 (A.P.), India
Email: info@universitiespress.com
marketing@universitiespress.com
Phone: 040-2766 5446/5447
2. Dr Sonal Saxena, MD
Director Professor and Head of the Department of Microbiology
Maulana Azad Medical College,
New Delhi
and
Dr Amala A Andrews, MD
Maulana Azad Medical College,
New Delhi
UNIVERSITIES PRESS PVT LTD
3. INFECTIONS OF THE SKIN
AND SOFT TISSUES
Infection of intact skin: Certain pathogens and toxins cause severe
infections or reactions when they come in contact with skin (ecthyma
gangrenosum)
Through a breach in the continuity: Certain microorganisms breach
the skin’s natural defences through cuts, wounds, burns or bites
Disruption of normal microbial population of the skin: Infection
occurs by new organisms in the surrounding skin and tissue (e.g.,
staphylococcal and streptococcal infections)
Pathogens colonising the skin via different routes: Some
microorganisms cause reactions that manifest as skin rashes or lesions
(intracellular infection—herpes type I, dermal capillary plexus—
varicella, cutaneous nerve route—herpes-zoster)
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This Photo by Unknown Author is licensed under CC BY
4. INFECTIONS OF THE SKIN AND SOFT TISSUES
Primary infections: Organisms invade the body from the external environment through breaks
in skin caused by burns, injury, bites or surgery
Secondary infections: Organisms reach the site through the blood as a part of a systemic
disease
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5. INFECTIONS OF THE DERMIS AND EPIDERMIS
Cutaneous infections
Impetigo: Involve epidermis and occurs often on the face and most often in children
Erysipelas: Involves the dermis as an erythematous painful lesion
Cellulitis: Affects the deep dermis; diffuse erythematous lesion without a clear margin
Folliculitis: Involves hair follicle; it is a localised papule containing pus
Papular and nodular lesions: Dracunculiasis, creeping eruptions and larva migrans
Crusted lesions: Impetigo and ringworm
Abscess: Involves deep dermis; furuncle/carbuncle/boil. An inflamed nodule with a central region
that is purulent with a raised point skin infections can be:
Vesicles—viral infections, zoster, shingles and hand, foot and mouth disease
Bullae—necrotising fasciitis and gas gangrene
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6. SUBCUTANEOUS
TISSUE
INFECTIONS
Necrotising fasciitis—soft tissue infections involving the
fascia and muscles overlying soft tissues; caused by group
A streptococci, S. aureus, Bacteroides and Clostridium
species
Progressive bacterial synergistic gangrene—usually a
post-operative complication following a thoracic or
abdominal surgery, caused by S. aureus, Proteus and
anaerobic streptococci
Myositis—may vary from necrosis of muscle to
necrotising cutaneous myositis or anaerobic myonecrosis
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9. BONE AND JOINT
INFECTIONS
OSTEOMYELITIS
INFECTIOUS ARTHRITIS (SEPTIC ARTHRITIS)
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This Photo by Unknown Author is licensed under CC BY-ND
10. OSTEOMYELITIS
ACUTE OSTEOMYELITIS
Etiology: Bacterial (mostly Staphylococcus) ,
Common involves the ends of the long bones
in children
Clinical: Abrupt-onset bone pain and
localised tenderness at the site of infection
Route of entry: Hematogenous or following
trauma caused by a penetrating injury
CHRONIC OSTEOMYELITIS
Etiology: Fungal or tubercular (Pott’s disease)
Insidious onset—the bone is necrosed, and
sequestrum (avascular necrotic bone) is
formed
Prosthetic-associated osteomyelitis: S. epidermidis
Osteomyelitis in sickle cell anemia: Salmonella
species
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11. SEPTIC
ARTHRITIS
Bacteria may invade the joint space and cause infectious
arthritis
Large, weight-bearing joints like the knee or hip are often
involved
The source of infection is often the skin, from where the
bacteria reach the bones through the bloodstream
Clinical: Acute onset with fever, joint pain, redness and
swelling are the cardinal features
Etiology: Staphylococcus aureus (most common), N.
gonorrhoeae in sexually active individuals (the knee, wrist,
ankle or elbow may be involved), S. epidermidis and other
coagulase-negative staphylococci in prosthetic joints
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12. MANAGEMENT
Laboratory Diagnosis
Samples: Bone sequestrum (in osteomyelitis) and joint aspirates (in arthritis), blood for culture
Gram stain: Bacteria and polymorphs seen
Culture: On blood agar to yield the organism. Blood culture may yield the organism in around
30% of acute cases of osteomyelitis and septic arthritis
Treatment
Empiric treatment with vancomycin and cefazolin must be started early to prevent damage to
the bone
Intravenous antibiotic treatment may be necessary in acute osteomyelitis and septic arthritis
Removal of joint fluid by arthrocentesis may be required, in addition to antibiotic therapy
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13. BURN WOUNDS
Etiology
Gram-positive bacteria: Staphylococcus aureus (including MRSA), Staphylococcus spp.,
Enterococcus spp. and the beta-hemolytic Streptococcus group
Gram-negative bacteria: Pseudomonas species, Acinetobacter baumanii, Stenotrophomonas,
Proteus species, Escherichia coli and Enterobacter species.
Fungi: Fusarium, Zygomycetes and Aspergillus
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14. STREPTOCOCCI
Impetigo and pyoderma
Erysipelas: Rapidly progressing infection with brawny edema
and a rapidly advancing margin
Cellulitis: Acute, rapidly spreading infection of the skin and
subcutaneous tissue with pain, tenderness and edema and
diffuse margins
Necrotising fasciitis: Mixed aerobic and anaerobic bacterial
infection, S. pyogenes (particularly M types 1 and 3, which
form pyrogenic exotoxin A) cause extensive necrosis of the
subcutaneous and muscular tissues and adjacent fascia
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15. STAPHYLOCOCCI
Corynebacterium minutissimum (erythrasma)
Common among dark-skinned individuals who sweat profusely, diabetes, obese and with poor hygiene
Most common: Glabrous areas of the body, skin folds, the groin, axilla, inner thighs and the skin between the
toes
Clinical: Red, scaly patch initially, with a well- defined margin—turns into a brown patch
UNIVERSITIES PRESS PVT LTD
Fig. 28.5
Erythematous
lesions with
superficial
ulceration due to
Staphylococcus
aureus (Source:
CDC, PHIL, Image
ID 7826)
16. BACILLUS ANTHRACIS
Aerobic, gram-positive, non-motile, sporulating bacillus 3–10 µm long in
chains (end to end) and has the appearance of a bamboo stick or boxcar
Capsule: Polysaccharide made up of polymer of d–glutamic acid. Loss of the
plasmid leads to the loss of virulence hence attenuation, used in the making of
the anthrax spore vaccine (Sterne vaccine)
Anthrax toxin:
Protective antigen factor (PA or factor II): binding fraction on the target cell
surface
Edema factor (EF or factor I): Activated only inside the target cells, leading
to intracellular accumulation of cyclic AMP; causes edema and the other
biological effects of the toxin
Lethal factor (LF or factor III): Causes cell death, but the mechanism of this
action is not known
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This Photo by Unknown Author is licensed under CC BY-SA
17. CLINICAL FEATURES
Cutaneous anthrax
Lesion is malignant pustule seen on exposed parts of body (face, neck, hands, arms and
back)
Starts as a papule 1–3 days after infection and becomes vesicular, containing fluid,
which may be clear or bloodstained with several satellite lesions
The whole area is congested and edematous and covered with a black eschar
Hide porter’s disease in dock workers who would carry loads of hides and skins on their
bare backs
Cutaneous anthrax generally resolves spontaneously, but 10–20 per cent of untreated
patients develop fatal septicemia or meningitis
Pulmonary anthrax (wool-sorter’s disease)
Workers of wool factories
Spores inhalation from infected wool
Can progress to hemorrhagic pneumonia and dissemination into the meninges
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Fig. 28.7 Cutaneous lesion (malignant pustule)
with black central eschar and edematous raised
margin; satellite lesions are seen (Source: CDC,
PHIL, Image ID 20334)
18. CLINICAL
FEATURES
Intestinal anthrax
Seen in communities consuming undercooked or uncooked
meat
Severe enteritis with bloody diarrhea occurs
Ending fatally if left untreated
Anthrax meningitis or meningoencephalitis
Infection disseminates to the CNS via the bloodstream
CSF: Hemorrhagic and the condition may be mistaken for
cerebrovascular accident, often fatal
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19. LABORATORY DIAGNOSIS
Specimen
Pus from the cutaneous lesions
Blood and CSF
Sputum in cases of pulmonary anthrax
Feces in the case of gastroenteritis
Microscopy
Gram-positive bacilli with the morphology of anthrax bacilli with
spores.
Immunofluorescent microscopy: A specific immunoglobulin tagged
with a fluorescent stain
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Fig. 28.8 Bacillus anthracis in blood: gram-
positive rods, showing bamboo stick
appearance in a smear from a automated
blood culture bottle (Source: CDC, PHIL,
Image ID 17099)
20. Spores stained by
M’Fadyean reaction with polychrome methylene blue: Blood
film stained with polychrome methylene blue for a few
seconds shows, an amorphous purplish material around the
bacilli (capsular material)
Sudan black B stain: Fat globules may be made out within the
bacilli
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21. UNIVERSITIES PRESS PVT LTD
Culture
Temperature: 12–45°C (optimum 35–37°C)
Blood agar: Non-hemolytic, 2–3 mm in diameter, raised, dull, opaque and
greyish-white with a frosted glass appearance
Under low-power microscope: edge of the colony is seen to be composed
of long, interlacing chains of bacilli, resembling locks of matted hair
(Medusa head appearance)
Solid medium containing 0.05–0.50 units of penicillin/mL: Cells become
large and spherical within 3–6 hours and arrange themselves in chains on
the surface of the agar (string of pearls reaction); specific to B. anthracis
Gelatin stab culture
Inverted fir tree appearance
Selective medium
PLET medium (polymyxin, lysozyme, ethylene diamine tetraacetic acid
(EDTA) and thallous acetate) added to heart infusion agar
Fig. 28.9 Non-hemolytic, dry colonies
of B. anthracis bearing the
characteristic Medusa head
appearance on blood agar (Source:
CDC, PHIL, Image ID 17099)
22. UNIVERSITIES PRESS PVT LTD
Animal inoculation
◦ Guinea pigs, rabbits and mice
Serological demonstration
◦ Ascoli’s thermoprecipitin test for anthrax antigen in tissue extracts
◦ A direct fluorescent antibody test (DFA) for capsule- specific staining and polysaccharide cell
wall antigen detection
Serology for antibodies
◦ Acute and convalescent phase sera detected by gel diffusion, complement fixation, antigen-
coated tanned red cell agglutination and ELISA
Molecular typing
◦ MLVA (multiple-locus variable number tandem repeat analysis) or AFLP (amplified fragment
length polymorphism)
23. BIOSAFETY AND PREVENTION
General methods
◦ Improvement of factory hygiene
◦ Proper sterilisation of animal products like hides and wool.
◦ Carcasses buried deep in quicklime or cremated to prevent soil contamination.
Vaccine
oPre-exposure: Only high-risk individuals, five doses followed by booster
oPost-exposure: The vaccine is given after exposure to anthrax along with antibiotics
Types
◦ Pasteur’s anthrax vaccine
◦ Sterne vaccine: Spores of attenuated strains of a non-capsulated, avirulent, mutant bacillus, used for
animals
◦ Mazzucchi vaccine: Spores of a stable, attenuated Carbazoo strain in 2% saponin
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24. TREATMENT
Uncomplicated cutaneous anthrax: Single oral agent (fluoroquinolone or doxycycline) for 7–14
days
Systemic anthrax: Antitoxin with antibiotic.
Antitoxin
Human anthrax immunoglobulin (anthrasil)
Monoclonal antibodies to the protective antigen (obiltoxaximab or roxibacumab)
Pre-exposure prophylaxis for inhalation anthrax in adults is with ciprofloxacin and doxycycline
for 60 days along with the vaccine (AVA BioThrax)
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25. CHAPTER 28 (B)
SKIN, SOFT TISSUE
AND
MUSCULOSKELETAL
INFECTIONS
Part III
Microbiology as Applied to Infectious
Diseases
Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Hyderabad 500 029 (A.P.), India
Email: info@universitiespress.com
marketing@universitiespress.com
Phone: 040-2766 5446/5447
26. Dr Sonal Saxena, MD
Director Professor and Head of the Department of Microbiology
Maulana Azad Medical College,
New Delhi
and
Dr Amala A Andrews, MD
Maulana Azad Medical College,
New Delhi
UNIVERSITIES PRESS PVT LTD
27. CLOSTRIDIA
Gram-positive anaerobic bacteria which form heat-resistant
spores
Commensal flora in gut of humans and animal
Cause gas gangrene, tetanus, botulism, food poisoning and
pseudomembranous colitis
Pathogenicity
Exotoxin: Pathogenic clostridia produce powerful exotoxins
which are responsible for the pathogenesis and disease, e.g.,
tetanus, botulism and gas gangrene
Invasive toxin: C. perfringens, besides being toxigenic, is also
invasive and can spread along the tissues and even cause
septicemia
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This Photo by Unknown Author is licensed under CC BY-NC-ND
28. Gram-positive, rods, highly
pleomorphic, 3–8 micron,
spore-forming, shape and
position vary
Spherical or oval; terminal,
subterminal, central
Motile, stately motility
MORPHOLOGY
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This Photo by Unknown Author is licensed under CC BY-NC-ND
33. Clinical case 1
A 50-year-old man met with a road traffic accident in which he
sustained multiple fractures with open wounds and a crush injury
of the leg. He was taken to the nearest hospital two days later, at
which time, he was found to be in shock.
He was started on supportive therapy and antibiotics. There was
edema and pain at the site of injury with increased
discolouration and a serous discharge. The area around the
wound had crepitus on palpation.
Microscopic examination of the wound discharge showed the
presence of thick, brick-shaped, gram-positive bacilli along with
gram-positive cocci. Based on a provisional diagnosis of gas
gangrene, immediate surgical treatment with extensive excision
of the local area (to prevent further spread) and intravenous
penicillin with clindamycin were given.
The exudate was also inoculated into Robertson’s cooked meat
medium. Clostridium perfringens and peptostreptococci grew in
the culture.
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34. CLOSTRIDIUM
PERFRINGENS
Large rectangular, stout, gram-positive,
capulated, non-motile bacillus, 4–6 x l µm.
Pleomorphic, single, chains
Spores: Subterminal, Not produced in artificial
media
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35. CULTURE
Microphilic – aerophilic anaerobes
pH – 5–8, temperature 20–50°C (45°C)
RCM (pink) – 4–6 hrs
Media: NA, BA, thioglycolate broth, RCM
BA: Polymyxin, neomycin, iron, citrate (black colonies)
BA: Rabbit, sheep, human colonies show target hemolysis
Litmus milk – fermentation of lactose, change of litmus – blue to red
Acid coagulates casein – clotted milk disrupted – stormy fermentation
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36. VIRULENCE
FACTORS
Strains – five types A–E
Toxins – most prolific of toxin producing bacteria
Four major toxins – alpha, beta, epsilon and iota
Alpha toxin – most important biologically, lethal,
dermonecrotic and hemolytic
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Table 28.6 Toxins produced by C. perfringens types
38. GAS GANGRENE
Type A
Commonly seen in association
with other clostridia
Wound contamination
Anaerobic cellulitis
Muscle tissues are invaded –
anaerobic myositis
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Fig. 28.10 Gas gangrene of the lower limb showing
edema and discoloured skin
39. PATHOGENESIS OF GAS GANGRENE
Exogenous: Clostridia usually enter a wound along with implanted foreign particles such as
soil, road dust, bits of clothing or shrapnel. They may also be present on skin, especially that
of the perineum and thighs
Endogenous: Infection may also develop after surgical procedures (especially amputations
for vascular disease) and even injections (especially adrenaline)
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40. CLOSTRIDIUM SEPTICUM
Pleomorphic bacillus
Oval, central/subterminal spores
Anaerobic. saccharolytic, abundant gas
Four distinct toxins
Alpha toxin is hemolytic, demonecrotic and lethal
Gas gangrene in humans
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41. CLOSTRIDIUM
NOVYI
Large, pleomorphic bacillus
Oval, subterminal spores
Strict anaerobe
Type A – causes gas gangrene
Large amounts of edema fluid, little or no
observable gas, high mortality
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43. ANAEROBIC WOUND
INFECTIONS
Simple wound contamination – no invasion of
tissue
Anaerobic cellulitis – invasion of fascial planes,
minimal toxin production, no invasion of muscle
tissue
Anaerobic myositis – gas gangrene, invasion of
muscle tissue, abundant formation of exotoxins
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44. CLINICAL PRESENTATION
Incubation period – 7 hours to 6 weeks
C. perfringens – 10–48 hours
C. septicum – 2–3 days
C. novyi – 5–6 days
Increasing pain, tenderness and edema over the affected part
Accumulation of gas – crepitus
Untreated – profound toxemia and prostration
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45. LABORATORY DIAGNOSIS
Specimen
Films – edge of affected area, tissue from necrotic area, exudate from deeper part of
wound
Exudate collected from depth of wound – collected by capillary pipette or swab
Necrotic tissue/muscle fragments
Blood cultures in C. perfringens and C. septicum infections
However, C. perfringens bacteremia may occur without gas gangrene
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46. MICROSCOPY
C. perfringens – Gram-positive bacilli without
spores
C. septicum – boat- or leaf-shaped
pleomorphic bacilli
C. novyi – large bacilli with oval or subterminal
spores
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Fig. 28.13 Methylene blue-stained culture
specimen revealing the presence of numerous
Clostridium septicum bacteria (note the
absence of spores) (Source: CDC, PHIL, Image
ID 217)
47. CULTURE
Robertson’s cooked meat medium:
Fresh and heated blood agar
Target hemolysis resulting from a narrow zone of complete hemolysis due to theta toxin
and a much wider zone of incomplete hemolysis due to the alpha toxin
This double zone pattern of hemolysis may fade on longer incubation
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48. NAEGLER’S REACTION
C. perfringens grown on media containing
Fildes peptic digest of sheep blood and human
serum with antitoxin on one half of the plate
Colonies on the half without antitoxin will be
surrounded by a zone of opacity
No opacity around the colonies on the half of
the plate with antitoxin
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Fig. 28.14 Nagler’s reaction—on the right, the
presence of toxin produces opacity in the serum
due to the breakdown of lecithin
50. TREATMENT AND PROPHYLAXIS
Surgery: Most important therapeutic and prophylactic
Damaged tissue removed extensively and promptly
Hyperbaric oxygen
Antibiotics: Metronidazole I/V – before surgery and every 8 hours
Mixed aerobic and anaerobic infection: combination of metronidazole with
amoxicillin and gentamicin.
Passive prophylaxis – anti-gas gangrene serum given I/M
10,000 IU – C. perfringens
10,000 IU – C. novyi
5000 IU – C. septicum
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51. Clinical Case 2
A 20-year-old woman presented to the surgery outpatient
department with a soft, painless swelling on her left jaw, which
was covered with exudate from a discharging sinus. She gave a
history of trauma to the jaw.
On macroscopic examination of the pus, a light-coloured granule
was found in the exudate. Gram stain of the granule showed the
presence of filamentous, branching, gram-positive bacilli.
The condition was diagnosed as cervicofacial actinomycosis and
the woman was treated with intravenous penicillin G (8 million
units per day) for two weeks followed by oral penicillin.
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52. ACTINOMYCETES
Actinomycetes are bacteria that possess a cell wall containing muramic acid
They have prokaryotic nuclei and are susceptible to antibiotics
Superficially resemble fungi due to branching filaments
Gram-positive filaments may break into bacillary or coccoid elements, non-motile, non-
sporing, non-capsulated
Most are free-living in soil
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53. ACTINOMYCES
Anaerobic actinomyces: Non-acid fast, anaerobic or
microaerophilic; Arachnia, Bifidobacterium and Rothia
Aerobic: Aerobic, may be acid fast; Nocardia, Actinomadura,
Dermatophilus and Streptomyces
Streptomyces may cause diseases but they are a major source
of antibiotics
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55. ACTINOMYCOSIS
Actinomyces israelii is the most common causative agent of actinomycosis
Four main clinical types are seen
◦ Cervicofacial: Indurated lesion on the cheek and submaxillary region
◦ Thoracic: Lesions in the lung, may involve the pleura and pericardium, spreading
outwards through the chest wall
◦ Abdominal: Lesion is usually around the cecum, involving neighbouring tissues
and abdominal wall
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56. ACTINOMYCOSIS
Pelvic: Associated with the use of intrauterine device (IUD), abscess
in bone and soft tissues with chronic draining sinuses to the
exterior
Causes disease of gums, gingivitis, periodontitis and sublingual
plaques leading to root surface caries
May present as mycetoma, treated with penicillin for several weeks
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57. LABORATORY
DIAGNOSIS OF
ACTINOMYCOSI
S
Specimens collected are pus or tissues; in pulmonary
disease, sputum
Sulphur granules are demonstrated in pus
Direct microscopy: Dense network of thin Gram-positive
filaments surrounded by peripheral zone of swollen,
radiating, club-shaped structures presenting a sun ray
appearance; the clubs are antigen–antibody complexes
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59. LABORATORY DIAGNOSIS OF
ACTINOMYCOSIS
Isolation in culture: Sulphur granules or pus inoculated into thioglycolate
liquid medium or streaked on brain–heart infusion agar incubated
anaerobically at 37°C
Liquid medium, A. israelii produces fluffy ball colonies at the bottom
Solid medium, Actinomyces israelii produces spidery colonies in 48–72
hours, becomes heaped up, white, irregular smooth large colonies in 10 days
Treatment: Penicillin, tetracycline for months supplemented with surgery
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60. NOCARDIA
Resembles Actinomycetes morphologically but it is aerobic
Nocardia are Gram-positive and some species like N. asteroides and N.
brasiliensis are acid-fast
Found in soil and infection is exogenous
Causes cutaneous, subcutaneous and systemic lesions
Common species are N. asteroides, N. brasiliensis and N. caviae
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61. NOCARDIA
Morphology
Filaments, rod-shaped bacteria that do not
produce spores, non-motile, catalase positive
and weakly acid fast by Kinyoun’s acid fast
staining method
N. asteroides is most commonly involved in
human disease
Transmission is through contaminated soil and
not from humans or animals
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62. NOCARDIA
Clinical forms
Cutaneous: Local abscess, cellulitis or lymphocutaneous lesions, subcutaneous
actinomycotic mycetoma
Systemic: Manifests as pulmonary disease, pneumonia, lung abscess or resembles
tuberculosis
Metastatic manifestation: May involve the brain, kidneys and other organs
Systemic nocardiosis occurs more often in immunodeficient persons
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63. LABORATORY DIAGNOSIS OF NOCARDIOSIS
Direct microscopy: Weakly acid fast; branching, beaded filaments in smears
from tissues
Isolation in culture: Grows on ordinary media forming dry, granular
wrinkled colonies, producing pigment ranging from yellow to red
Treatment: Resistant to penicillin; cotimoxazole and minocycline are used
Surgery is performed to remove mycetomas
In immunocompromised, amikacin and cefotaxime are used
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64. MYCETOMA FROM BACTERIAL CAUSES
Usually caused by
Actinomyces israelii, A. bovis
N. asteroides, N. brasiliensis, N. caviae
Actinomadura madurae, A. pelletierii
Streptomyces somaliensis
Botryomycosis: Mycetoma-like lesion produced by Staphylococcus aureus
and other pyogenic bacteria
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65. ACTINOMYCOTIC MYCETOMA
Mycetoma is a localised chronic granulomatous involvement of
subcutaneous and deeper tissues affecting the foot and hand and
presenting as swelling with multiple discharging sinuses
First described by Gill 1842—maduramycosis
Actinomycotic—granules are yellow or white, filaments are thin (1 µm)
May be due to fungus, filaments are thicker (4–5 µm), granules are black
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66. CHAPTER 28 (C)
SKIN, SOFT TISSUE
AND
MUSCULOSKELETAL
INFECTIONS
Part III
Microbiology as Applied to Infectious
Diseases
Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Hyderabad 500 029 (A.P.), India
Email: info@universitiespress.com
marketing@universitiespress.com
Phone: 040-2766 5446/5447
67. Dr Sonal Saxena, MD
Director Professor and Head of the Department of Microbiology
Maulana Azad Medical College,
New Delhi
and
Dr Amala A Andrews, MD
Maulana Azad Medical College,
New Delhi
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68. BURKHOLDERIA
PSEUDOMALLEI
Melioidosis
Glanders-like disease, epizootic in rodents in Southeast
Asia, India and North Australia
Also called the Vietnam time-bomb disease
In India, western and southern belts, spike following the
rainy season
Treatment: Carbapenems, imipenem, meropenem and
ceftazidime
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69. LABORATORY DIAGNOSIS
Microscopy: Small, irregularly staining, gram-negative bacilli, bipolar ‘safety- pin appearance’
with methylene blue stain
Culture
Dry, wrinkled colonies on blood and MacConkey agars.
Selective medium: Ashdown’s selective agar (ASA) medium (gentamicin and crystal) violet
Biochemical tests: Non-fermentative, oxidase positivity, esculin hydrolysis and reduction of
nitrate, intrinsic resistance to polymixin B
PCR test or an automated VITEK system
Serology: Not much useful
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70. BURKHOLDERIA MALLEI
Glanders: Primarily of equine animals (horses, mules and asses
Slender, non-motile, gram- negative bacillus, 2–5 × 0.5 mm stains irregularly with beaded
appearance
Aerobe and facultative anaerobe, growing on ordinary media under a wide temperature range
Colonies, which are small and translucent initially, become yellowish and opaque
Biochemically inert
Human infection: Occupational, acute or chronic and is protean in character
Respiratory tract, skin or subcutaneous tissues involved
In acute glanders: Fever, mucopurulent nasal discharge and severe prostration, high fatality
B. mallei is one of the most dangerous bacteria to work with
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71. PATHOGENESIS
Two thermolabile exotoxins, one lethal and the other
necrotising,
Human infection is usually acquired by the contamination
of wounds, skin abrasions or by inhalation
Acute: Generalised infection as acute septicemia, or
subacute typhoid-like disease or pneumonia with hemoptysis
resembling tuberculosis. High case fatality rate
Chronic: Multiple caseous or suppurative foci, with abscess
formation in the skin and subcutaneous tissues, bones and
internal organs
Long latency and reactivation may occur as the bacillus can
survive intracellularly in the reticuloendothelial system
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72. NON-TUBERCULOUS MYCOBACTERIA
Mycobacteria other than mammalian tubercle bacilli – human disease resembling tuberculosis
Non-tuberculous Mycobacterium – NTM
Earlier called ‘atypical’, MOTT (Mycobacterium other than tubercule bacilli)
Opportunistic infections in human beings
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73. RUNYOUN
CLASSIFICATION
Four groups
Group I – photochromogens
Group II – scotochromogens
Group III – non-photochromogens
Group IV – rapid growers
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75. GROUP I – PHOTOCHROMOGENS
Important species
◦ M. kansasii
◦ M. marinum
◦ M. simiae
No pigment in dark – exposed to light one hour – reincubated – yellow orange
pigment
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76. M. KANSASII Chronic pulmonary disease – resembling
tuberculosis
Affects upper lobes with cavity formation
Isolated from tap water samples around the
world
Second most common NTM – lung disease after
M. avium complex
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77. M. MARINUM
Warty skin lesion
Swimming pool/fish tank granuloma
Poor growth at 37°C
Negative nitrate test
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78. GROUP II – SCOTOCHROMOGENS
Form pigmented colonies even in the dark
M. scrofulaceum – cervical adenitis
M. gordonae – rare cause of pulmonary disease
M. szulgai – scotochromogen at 37°C and photochromogen at 25°C
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79. GROUP III – NON-PHOTOCHROMOGENS
Do not form pigment even when exposed to light.
Important pathogens
M. avium
M. intracellulare
M. xenopi
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81. GROUP IV –
RAPID
GROWERS
Colonies appear within seven days of
incubation
Medically important
M. fortuitum
M. chelonei
Chronic abscess following injection of vacine.
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82. SKIN PATHOGENS
M. ulcerans – Buruli ulcer
Ulcers on legs or arms – minor injuries
Indurated nodules – indolent ulcers
Smears – large clumps of bacilli
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This Photo by Unknown Author is licensed under CC BY-NC-ND
84. TREATMENT
Resistant to the usual anti-tuberculous drugs
M. avium, M. kansasii – respond to prolonged treatment with – rifampicin,
isoniazid and ethambutol
Other combinations – clofazimine, quinolones, newer macrolides
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85. MYCOBACTERIUM
LEPRAE
Disease of antiquity
India – since Vedic times
Biblical times – Middle East
Hansen – 1868 – lepra
bacillus
Not possible to grow – in
culture media
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86. MYCOBACTERIUM LEPRAE
Morphology
Straight or slightly curved rod – 1.8 × 0.2–0.5 µm
Acid fast – 5% H2SO4
Morphological index – uniformly stained bacilli
Bacilli – singly and groups
‘Globi’, ‘cigar bundles’
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88. CULTIVATION
Not possible to cultivate – media, tissue culture
Generation time – 12–13 days
Cultivation
Foot pad of mice
Nine-banded armadillo (Dasypus novemcinctus)
Adaptation in artificial media – ICRC bacillus
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90. LEPROMATOUS LEPROSY
In large numbers, resistance – low
Bacilli are seen in large numbers
Multibacillary
Bacilli invade mucosa of nose, mouth and upper respiratory tract
Shed in large numbers in nasal and respiratory secretions
Cell-mediated immunity is deficient
Lepromin test – negative
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100. MICROSCOPY
Ziehl–Neelsen – 5% sulphuric acid
Grading of smears
1–10 bacilli in 100 fields: 1+
1–10 bacilli in 10 fields: 2+
1–10 bacilli per field: 3+
10–100 bacilli per field: 4+
100–1000 bacilli per field: 5+
More than 1000 bacilli, clumps: 6+
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101. MICROSCOPY
Bacteriological index (BI) – totalling the number
of pluses scored and divided by the number of
smears
Morphological index (MI) – expressed as
percentage of solid fragmented granular
bacilli/uniformly stained bacilli out of the total
number counted
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102. TREATMENT
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Dapsone – first effective agent
Drug resistance
• Paucibacillary – rifampicin 600 mg once a month and dapsone 100 mg daily for 6
months
• Multibacillary – rifampicin 600 mg once a month, dapsone 100 mg daily and
clofazimine 50 mg daily for 2 years
Multi drug therapy
104. CHAPTER 28 (D)
SKIN, SOFT TISSUE
AND
MUSCULOSKELETAL
INFECTIONS
Part III
Microbiology as Applied to Infectious
Diseases
Universities Press
3-6-747/1/A & 3-6-754/1, Himayatnagar
Hyderabad 500 029 (A.P.), India
Email: info@universitiespress.com
marketing@universitiespress.com
Phone: 040-2766 5446/5447
105. Dr Sonal Saxena, MD
Director Professor and Head of the Department of Microbiology
Maulana Azad Medical College,
New Delhi
and
Dr Amala A Andrews, MD
Maulana Azad Medical College,
New Delhi
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106. VIRAL INFECTIONS OF
THE SKIN
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This Photo by Unknown Author is licensed under CC BY-NC-ND
107. Lesions in the skin are manifestations of viral
pathogenesis affecting other systems
Etiology
The virus remains restricted to the skin at the
site of infection, e.g., molluscum contagiosum
Intracellular infections of the squamous
epithelium (HSV1), dermal capillary plexus
(varicella), cutaneous nerve roots (hepres-
zoster) or viruses associated with viremia
Most cutaneous manifestations of systemic
viral infections are in the form of vesicles or
rashes due to microhemorrhages
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109. VARICELLA-
ZOSTER VIRUS
(VZV)
Morphology is similar to that of herpes simplex virus
Causative agent of varicella & herpes zoster
During primary infection: Varicella
Reactivation: Herpes zoster
Only one antigenic type is known
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110. VARICELLA (CHICKEN POX)
Common in childhood but may occur at any age
Route of entry: Respiratory tract or conjunctiva
Incubation period: 2 weeks
Source of infection: Varicella/herpes zoster cases
No animal reservoir
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111. VARICELLA IN
CHILDREN
Presence of skin & mucosal lesions
Centripetal in distribution (appears
first on trunk)
The stages of rash: Macule, papule,
vesicle, pustule and scab
Rapid evolution of lesions
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112. VARICELLA IN ADULTS
Severe form
Complications
• Pneumonia (more common)
• Myocarditis
• Nephritis
• Acute cerebellar ataxia
• Meningitis & encephalitis
• Secondary bacterial infections
• Reye’s syndrome (h/o intake of salicylates)
Postherpetic neuritis may occur
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Fig 43.5: Generalised herpes zoster
outbreak due to the varicella-zoster virus
(VZV)
113. CHICKENPOX IN PREGNANCY &
NEONATAL VARICELLA
More severe in pregnant women
First half of pregnancy
• Asymptomatic
• Fetal varicella syndrome: Cicatrising skin lesions, hypoplasia of the limbs, chorioretinitis &
CNS defects
Near delivery
• Neonatal varicella
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114. LABORATORY DIAGNOSIS
Microscopy
• Tzanck smears
Multinucleated giant cells
Type A intranuclear inclusion bodies
• Electron microscopy
Virus isolation
• Human amnion, human fibroblast, HeLa
or Vero cells
Viral antigen detection:
• Immunofluorescence
• ELISA
PCR
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115. PROPHYLAXIS AND TREATMENT
Live-attenuated vaccine: Oka strain of VZV
Varicella-zoster immunoglobulin (VZIG)
Infection control measures
Acyclovir and famciclovir: Indicated in immunodeficient, elderly
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117. HERPES ZOSTER
(SHINGLES,
ZONA)
Reactivation after primary varicella
infection
Unilateral rash
Limited to area supplied by a single
sensory ganglion
Lesions similar to varicella lesions
Pain at the affected area
Other complications
• Herpes zoster ophthalmicus
• The Ramsay Hunt syndrome
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118. HERPES ZOSTER (SHINGLES, ZONA)
Herpes-zoster represents a mode of evolutionary adaptation by the VZ virus which is an
obligate human parasite
The ability of the virus to remain latent and reappear as zoster years later confers on it a great
survival advantage
HHV-7: Exanthema subitum
HHV-8/Kaposi’s sarcoma-associated herpes virus (KSHV)
Herpes virus simiae: B virus
Molluscum contagiosum virus
Papilloma virus
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119. CYTOMEGALOVIRUSES
Largest viruses in the herpesvirus family
Size ranges from 150 to 200 nm
Infect humans & animals
Infected cells are enlarged
Presence of intranuclear inclusions in infected cells
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120. MODE OF
TRANSMISSION
Salivary or other secretions
Sexual contact
Blood transfusion
Organ transplants
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121. CLINICAL FEATURES
Congenital infections
Fetal death
The cytomegalic inclusion disease: Microcephaly, chorioretinitis, cerebral calcification &
mental retardation
Infection in infants
Primary CMV infection in mother during pregnancy:
Cytomegalic inclusion disease in infants
Reactivation in mother during pregnancy:
Chronic subclinical infection in infants
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122. CLINICAL FEATURES
Infection in children
Asymptomatic primary infection
Heterophile, antibody-negative, infectious
mononucleosis
Immunocompromised host
Severe & fatal infections
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123. PREVENTION AND TREATMENT
Screening of blood and organ donors
Acyclovir is useful in prophylaxis
Ganciclovir and foscarnet are effective for treatment
No vaccine is available
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124. LABORATORY
DIAGNOSIS
Specimens
Urine, saliva, semen and cervical
secretions
Demonstration of cytomegalic
cells (owl’s eye): Less reliable
Isolation
Human fibroblast cultures & shell
vial cultures
Serology
Demonstration of IgM antibody
for primary infection
IgG avidity test
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Fig 43.7: H and E stained lung tissue showing ‘owl’s eye’-like inclusion
bodies of cytomegalovirus × 1,000