AGE Newborns and older adults have reduced defenses against infection HEREDITY Genetic susceptibility STRESS Stressors elevate blood cortisone. epinephrine NUTRITIONAL STATUS Adequate nutritional status will increase resistance to infection MEDICAL THERAPIES Chemotherapy and Radiotherapy decrease resistance CO-MORBID CONDITIONS Diabetes, COPD, Chronic Diseases will all weaken the defense barriers
1. Viruses:- depends on host cell metabolism for their replication- obligate intracellular parasites- Some do not cause any disease, some cause acute illness (colds, influenza)- Some cause lifelong latency and long term reactivation (herpesviruses)- Some cause chronic disease ( hepatistis B)
2. Bacteriophages, Plasmids, Transposons)- Mobile genetic elements that encode bacterial virulence factors(adhesisns, toxins or enzymes that confer antibiotic resistance)- Can infect bacteria and incorporate themselves into their genome, thus converting an otherwise harmless bacteria into virulent one or an antibiotic sensitive organism into a resistant one.
3. Bacteria- Next to viruses, they are the most frequent and diverse class of human pathogens4. Fungi- Affecting the superficial layer of skin – tinea , dermatophytes- Affecting the subcutaneous tissue – causing abscesses or granulomas- Deep fungal infection – systemic infection- Oportunistic fungi - ( Candida, Mucor, Aspergillus)
- Are arthropods ( lice, ticks, bedbugs, fleas that attach to and live on the skin
1. Intact host skin and mucosal surfaces and secretory- excretory products example – lysozyme , gastric juicesRespiratory tract- Larger inhaled microbes are trapped in mucociliary blanket of the upper airway passages- Those that reached the trachea are either coughed up or pushed backward toward the throat by ciliary action, then swallowed and cleared.- -particle 5um or smaller in size reach the alveoli
Gastrointestinal tract - Pathogens are transmitted by food or drink contaminated with fecal material Normal defenses Against Ingested pathogens:1. Acid gastric juice2. The Viscous mucous layer covering the gut3. Lytic pancreatic enzymes and bile detergents4. Secreted IgA antibodies
1. They can contact or enter host cells and directly cause cell death.2. They may release endotoxins or exotoxins that kill cells at a distance , release enzymes that degrade tissue components, or damage blood vessels and cause ischemic necrosis.3. Induce host-cellular responses that may cause additional tissue damage, including suppuration, scarring, and hypersensitivity reactions.
Viral Respiratory Infections- Most frequent, least preventable- Self-limiting to life threatening pneumonias- May lead to superinfection with bacteria- Most important and most studied: rhinovirus and influenza virus
50% common colds Member of picornavirus family (small RNA viruses) which include poliovirus, hepatitis virus and coxsackie virus Single -stranded RNA unecapsulated Infect humans and higher primates Infection confined to upper respiratory tract (grow best at 33 C to 35 C) Induce serotype specific IgG and IgA antibodies
Larger and more complex than rhinoviruses Single-stranded RNA Types: A, B, and CType A- Infect humans, pigs, horses and birds and are the major cause of pandemic and epidemic flu infections.- Antigenic shift
Type B and C- Does not show antigenic shift or drift- Infect mostly children who develops antibodies against reinfection.
Haemophilus Influenzae Infection:- Pleomorphic gram-negative organism- Major cause of life-threatening acute lower respiratory tract infections and meningitis in young children.- Major cause of suppurative meningitis in children upto five years of age- Purulent conjunctivitis in children- Ubiquitous colonizer of the pharynx 5%- encapsulated 95% - unencapsulated
Six serotypes of encapsulated form:- A to F type b is the most frequent cause of severe invasive disease.- Nonencapsulated type:- Produces otitis media- Sinusitis and bronchopneumonia
Two species that cause tuberculosis:1. Mycobacterium tuberculosis – transmitted by inhalation2. Mycobacterium bovis- transmitted by milk from diseased cows and first produces intestinal or tonsilar lesions.3. *Mycobacterium leprae – causes leprosy
MYCOBACTERIA- Are aerobic, non-sporforming non-motile bacilli with waxy coat that retain the red dye when treated with an acid.- Grow very slow ( 4 to 6 wks to obtain colony)
Primary tuberculosis –- Begins with inhalation of the mycobactria and ends up with a T-cell mediated immune response that induces hypersensitivity to the organisms- Most often seen in the periphery of one lung*Ghon complex – calcified scar in the lung parenchyma and in the hilar lymphnode
Secondary and disseminated Tuberculosis- Some individuals become reinfected with mycobacteria- Reactivate dormant disease- Progress directly from primary mycobacterial lesions into disseminated disease.- * the granulomas most often occur in the apex of the lungs but may be widely disseminated in the lungs, kidneys, meninges, marrow and other organ
*Miliary tuberculosis- Refers to the hematogenous dissemination of tuberculous lesions through out the body.Frequent Cite:Lungs, cervical lymphnodes (scrofula), meningesKidneys, adrenals, bones (osteomyelitis), fallopian tubes, epididymis, vertebral TB (Pott’s dse.)Resistant Cite:Heart,Striated muscle,Thyroid gland and pancreas
Histoplasmosis and Coccidioidomycosis :- Both are granulomatous disease of the lungs- Both are caused by fungi that are thermaly dimorphic.
Histoplasma capsulatum- Is acquired by inhaalation of dust particles from soil contaminated with bird or bat droppings that contain small spores (microconidia)n- the infectious form of the fungus.
Clinical manifestations:1. Coin lesion on the chest x-ray2. Chronic , progressive secondary lung disease which is localized to the lung apices and causes cough, fever and night sweats3. Localized lesions in extrapulmonary sites, including mediastinum, adrenals, liver or meninges4. Widely disseminated involvement (immunosuppressed)
Coccidioidomycosis- Inhalation of the spores of Coccidioides immitis- Most are assymptomatic- 10% with lung lesions, fever, cough and pleuritic pains- 1% disseminated C. Immitis involving the meninges and skin
Rotavirus-- Major cause of diarrhea in infants- Spread by fecal-oral route- Invade and destroy mature host epithelial cells in the middle and upper villus- Older children and adults are resistant- ( secretory immunity)- Antirotavirus antibodies is present in mother’s milk
Norwalk-like viruses- Cause of epidemic gastroenteritis with diarrhea, nausea, and vomiting among children.Coronaviruses- Causes diarrhea and upper respiratory tract infections and are usually endemic rather than epidemic.
Enteric adenoviruses- The second leading cause of diarrhea among infants
SHIGELLA BACILLARY DYSENTERY*dysentery – refers to diarrhea with abdominal cramping and tenesmus in which loose stools contain blood, pus and mucus.- Caused by Shigella dysenteriae. S. Flexneri, S. Boydii and S. Sonnei as well as certain O-type of enterotoxic E. coli
Transmission is fecal-oral route *S. flexneri is the major cause of bacillary dysentery in endemic locations of poor hygiene, including large regions of the developing world and institutions in the developed world. * epidemic shigellosis occurs when individuals consume uncooked foods at picnics or other events.
CAMPYLOBACTER ENTERITIS- Comma shaped, flagelatted, gram –negative organism- Important cause of chronic gastritis, enterocolitis, and septicemia- Infection occurs by ingestion of contaminated liquid or solid food such as milk, poultry, or water.
- Epidemic cases affecting both children and adults- Sporadic infections may be derived from human or zoonotic sources; domestic dogs are frequent carriers.Clinical manifestations:1. Watery diarrhea( toxin-induced)2. Bloody diarrhea ( invasion and proliferation within the intestinal epithelium)3. Enteric fever( organism penetrated the intestinal mucosa)
SALMONELLOSIS AND TYPHOID FEVER:Salmonella – are flagellated, gram negative bacteria that cause a self limited food-borne and water-borne gastroenteritis ( S. enteritidis; S. typhimurium and others) or a life threathening systemic illness marked by fever (S. typhi)
Major source of contamination (other than S. typhi)– feces contaminated meat and chicken that are insufficiently washed and cooked.S. typhi – human is the only host which is shed in the feces, urine, vomitus and oral secretions by acutely ill persons and in the feces by chronic carriers without overt disease.
Clinical manifestations:- Fever and chills during the first week- Widespread reticuloendothelial involvement with rash , abdominal pain, during the 2nd week- Ulceration of the Peyer’s patches with intestinal bleeding at the 3rd week.- * gallbladder colonization – causes a chronic carrier state.
CHOLERA- Caused by Vibrio cholerae- Are comma shaped, gram –negative bacteria- Causing severe watery diarrhea caused by an enterotoxin secreted by 01-serotype V. Cholerae and a non-01 sero-type causes diarrhea associated with eating contaminated shellfish- *never invade the enteric epithelium but instead remain within the lumen and secrete their enterotoxin
AMEBIASIS- Brought about by Entamoeba histolytica- Protozoan parasite- Major cause of dysentery and liver abscess- E. histolytica cysts – infectious form of the parasite because they are resistant to gastric acid.
Amoeba dysentery- Bloody diarrhea, intestinal pain, fever- Frequently involves the cecum, and ascending colon followed in order by the sigmoid, rectum and the appendix.- Fullblown cases – entire colon is involved.- * flask-shaped ulcer – narrow neck and broad base- *Ameboma – napkin- like constrictive lesions
Amebic liver abscess:- Chocolate –colored odorless, pasty materials likened to be anchovy-paste- May produce pain by pressing the liver capsule as it enlarged.- Treated with drainage and drugs or drugs alone
GIARDIASIS- Caused by Giardia lamblia – most prevalent pathogenic intestinal protozoan worldwide.- May be subclinical or may cause acute or chronic diarrhea, steatorrhea, or constipation.- Endemic in public water supply
Infections Exists in Two forms:1. A dormant by infectious cysts spread by fecal-oral routefrom person to person (as well as from cats, bears and beavers to person)2. Tropozoites that multiplyin instinal lumen and cause disease.
Giardia resides in the duodenum rather than the colon Adhere to but do not invade intestinal epithelial cells Cause diarrhea rather than dysentery.
- Staphylococcus aureus – are pyogenic non- motile, gram-positive cocci- Skin lesions – boils, carbuncle, impetigo and scalded skin- Also cause pharyngitis, pneumonia, endocarditis, food poisoning and toxic shock syndrome
S. aureus is the major cause of infection of patients with burns and surgical wounds and is second only to E. coli. *S. epidermidis - causes opportunistic infections in catheterized patients, patient with prosthetic cardiac valves, and drug addicts.
Enzymes and toxins Secreted by S. aureus:1. Staphylococci infecting prosthetic valves and cathethers have an exopolysaccharide capsule that allows them to attach to the artificial matrials and to resists host cell phagocytosis2. The lipase of S. aureus degrades lipids on the skin surface, and its expression is correlated with the ability of the bacteria to produce skin abscess.
3. S. aureus enterotoxins are associated with food poisoning and appear to act by stimulating emetic receptors in the abdominal viscera and so cause vomiting and diarrhea4. Exfoliative toxins of S. aureus are associated with staphylococcal scalded-skin syndrome – forming skin blisters.5. Toxic shock syndrome toxin (TSST-1) is secreted by S.aureus colonizing the vagina of women using tampons causing shock by mechanisms similar to those of S. Aureus enterotoxins.
- Are facultative anaerobic gram-positive cocci- Cause suppurative infections of the skin, oropharynx, lungs, and heart valve and also cause poststreptococcal syndromes including rheumatic fever, immune complex glomerulonephritis, and erythema nodosum
-Most streptococci are beta-hemolytic- S. pyogenes (Group A)- which causes pharyngitis, scarlet fever, erysipelas, impetigo, rheumatic fever and glomerulonephritis- S. agalactiae (group B) – causes neonatal sepsis and urinary tract infections.- S. faecalis – (group D) – causes endocarditis and urinary tract infections- S. viridans – which is alpha-hemolytic and thus green in blood agar plates – can cause endocarditis
Streptococcus pneumoniae (pneumococcus) – major cause of community –acquired pneumonia and major cause of bacterial meningitis in adults.*Streptococcus mutans – is the major cause of dental caries.
Virulence factor of Streptococci:• M-protein – a rod like surface protein that prevents bacteria from being phagocytosed.• Pyrogenic exotoxin – causes fever and rash in scarlet fever• S. mutans produces caries by metabolizing sucrose to lactic acid• Poststreptococcal autoimmune diseases of the heart (rheumatic fever) may result from antistreptococcal M-protein antibodies that cross react with cardiac myosin.
- Gram-positive bacilli that grow under anaerobic conditions and produces spores which are frequently present in the soil.
Four Types of Clostridium:1. C. perfringens (welchii), C. septicum and other species invade traumatic and surgical wounds and cause an anaerobic cellulitis or myonecrosis (gas gangrene)- Contaminate illegal abortions and cause uterine myonecrosis, cause mild food poisoning2. C. tetani – proliferates in puncture wounds and in umbilical stump of the new born- release a potent neurotoxin tetanospasmin that causes convulsive contractions of skeletal muscles.
3. C. botulinum – grows in inadequately sterialized canned foods and releases a potent neurotoxin that block synaptic released of acetylcholine and causes a severe paralysis of respiratory and skeletal muscles.4. C. difficile – overgrows other intestinal flora in antibiotic-treated patients, release multiple toxins, and cause pseudomembranous colitis
Folliculitis is an infection of the hair follicles and produces a number of small erythematous or pustular lesions . It is usually caused by Staphylococcus aureus. Local warm compresses and topical antibiotics are all that is needed as therapy.
A particular form of folliculitis occurs in persons who have bathed in swimming pools or whirlpool baths contaminated by Pseudomonas aeruginosa A pruritic papulopustular rash, those covered by a bathing suit (the buttocks, hips, axillae and the lateral side of the trunk), develops within a day or two of exposure. no therapy is required and topical steroids should be avoided.
Small red lesion, each associated with a hair follicle and caused by Staphylococcus aureus.
Pseudomonas folliculitis. Papulopustular rash over the buttocks and thighs following use of a spa pool.
A furuncle (boil) is a S. aureus infection of an obstructed hair follicle. It begins as a red, tender, inflammatory nodule on the face, neck, axilla or other area of hairy skin. Constitutional symptoms and fever are not common. Antibiotic therapy is not usually necessary; surgical drainage or the application of warm soaks is all that is normally required.
Patients with diabetes, poor hygiene and excessive sweating may suffer from recurrent furuncles. Antibiotic ointment to the nares and/or the use of systemic rifampicin may eradicate carriage.
Small cutaneous abscess associated with hair follicle on back of neck.
A carbuncle is a larger abscess (almost always staphylococcal) extending from an infected follicle into the subcutaneous fat. It is often seen at the nape of the neck , or on the back. Carbuncles require surgical drainage and treatment with an anti-staphylococcal antibiotic.
A huge area of induration of the neck with multiple discharging follicular abscesses.
chronic, suppurative infection of apocrine sweat glands is fortunately rare. It is often due to S. aureus, and occurs principally in adults. It results in recurrent crops of abscesses, leading to sinus formation. Oral anti-staphylococcal therapy combined with moist compresses and drainage of fluctuant lesions.
Extensive scarring with multiple sinuses in and around the axilla.
Impetigo is a superficial streptococcal or staphylococcal infection of the skin. It is highly communicable; transmission is enhanced by low socioeconomic status with its associated poor living conditions and hygiene. The organisms probably cannot invade intact skin - infection occurs through minor abrasions, insect bites, etc. The infection often spreads rapidly presumably by scratching and autoinoculation. It may also complicate eczema or varicella.
Impetigenized eczema. Young Asian child with severe atopic eczema secondarily infected with impetigo.
All impetigo is initially vesicular, later becoming crusted; depend on whether the aetiological agent is Streptococcus pyogenes or S. aureus . After rupture, the discharge dries to form characteristic thick, adherent, golden-yellow crusts. Staphylococcal impetigo, on the other hand, typically produces more long-lived bullae and thin, light brown crusts (described as `varnish- like).
Streptococcal impetigo. The cluster of superficial vesicles has broken to form a row weeping surface, soon to be covered by a yellow crust.
These characteristic yellowcrusts are often the mainfeature on presentation.
Severe streptococcal impetigocrusts over the face of a young girl.
Adherent dark yellow/browncrust of impetigo in fingers.
The cause of impetigo can be determined by Gram stain or by culture of the exudate beneath the crust. Anti-DNAase B and anti-hyaluronidase titres usually rise after streptococcal skin infection, but the anti-streptolysin O (ASO) titre often does not.
Certain strains of B-hemolytic streptococci - the so-called nephritogenic strains - may give rise to immunologically-mediated acute post-streptococcal nephritis after skin infection
There are two approaches to the antibiotic treatment of impetigo. One is to use penicillin alone (or erythromycin in the penicillin-allergic individual The other approach is to use an anti- staphylococcal antibiotic
Systemic antibiotics are more effective than topical therapy Injudicious treatment with steroid skin creams removes the crusts but promotes spread of the infection, with numerous red raw lesions.
Cellulitis is a spreading superficial infection of the skin. due to streptococci or S. aureus.
Infection can occur at any age often develops at a site of previous trauma or skin lesion, the entry site may be unapparent. Patients frequently have an abrupt onset of malaise, fever, chills and headache and the involved skin becomes tender, red, warm and swollen.
Erythematous area with ill – defined margin over lower limb.
The inflammation spreads with poorly defined margins and may be accompanied by lymphangitis and lymphadenopathy. Streptococcal cellulitis occasionally becomes bullous.
A severe rapidly developing infection of the subcutaneous tissue of the leg with large bullae and scabs.
Large bullae in an area of cellulitis of the neck caused by Streptococcus pyogenes.
The diagnosis of cellulitis is usually a clinical one Gram stain or culture of material aspirated from the leading edge of the cellulitis.
Chains among streptococci among cellular debris in pus. Gram’s stain.
if there are no initial clues to the aetiology then a penicillinase-resistant penicillin should be given (e.g. flucloxacillin 0.5-1.0g orally every 6 hours). For the more severely ill patient parenteral therapy may be needed and for the penicillin-allergic individual, erythromycin or clindamycin would be suitable.
In children an unusual form of cellulitis may be caused by Haemophilus influenzae type b. It is commonly seen on the cheek and produces a purple-red, bruised appearance .
Cellulitis due to haemophilusinfluenzae of the cheek andpreorbit.
Following laceration or trauma during swimming in fresh water and seawater A severe form of cellulitis, often complicated by necrosis and bacteraemia
Severe infection with bullouslesions due to Vibrio vulnificansinfection following immersion of leg in brackish water.
Vibrio Cellulitis. Haemorrhagic bullous lesions of Vibrio vulnificans sepsis.
Comma-shaped cells of Vibrio vulnificans. Gram’s stain.
Erysipelas is a characteristic variant of cellulitis, almost always caused exclusively by S. pyogenes. It is a painful, bright red, shiny lesion with a raised, sharply demarcated, advancing edge . It is most common on the legs or face and often spreads across the nose to involve both cheeks (the `butterfly-wing rash ).
Well demarcated area of erythema and induration on the forehead.
A typical butterfly-wing rash on the cheeks. Both eyes are closed by oedema of the lids.
With high fever and rigors and a leucocytosi. Erysipelas is treated with penicillin, given parenterally in the more severe cases.
Scarlet fever Some group A haemolytic streptococci produce an erythrogenic toxin causing the characteristic rash of scarlet fever. Infection is usually of the pharynx or tonsils although streptococcal skin or wound infection can also be associated with scarlet fever. The rash of scarlet fever begins on the face , neck and upper chest, spreading to the abdomen and extremities: it consists of a diffuse scarlet erythema with almost confluent punctate papules. This is called punctate erythema.
Scarlatina. The face appears flushed with circumolar pallor.
There is often also slight prominence of the hair follicles, giving a sandpaper-like texture to the skin. The rash blanches upon pressure . The erythema often spares the area around the mouth but is accentuated in the creases of the elbows, groin and axillary folds (Pastias lines). The tongue is at first furred with prominent papillae (the `white strawberry tongue). After about 4 days there is extensive desquamation of the skin which may continue for 2 weeks or more.
Diffuse erythematous rashshowing blanching where fingerpressure has been applied to theabdomen.
Extensive desquamation of the skin of the trunk. This may last for several weeks.
Desquamation of the tongue also occurs leaving a raw, red tongue with prominent papillae (`red-strawberry tongue). Culture of a swab from the throat or from the infected wound will demonstrate group A b- haemolytic streptococci. The condition is treated with penicillin.
Toxic shock syndrome (TSS) is mediated by one or more of the exotoxins produced by S. aureus. It occurs predominantly in menstruating females using tampons but can occur with staphylococcal infection at other sites and in males or children.
The rash is a diffuse, blanching, macular erythema, particularly affecting the hands and feet, which desquamates 1-2 weeks after it appears.
Typical sunburn-like rash over the face and trunk. Note the dryness and hyperaemia of the lips.
Desquamation of the skin, particularly of the palms and soles, occur with recovery.
The diagnosis of TSS is clinical and the isolation of S. aureus is not necessary.
The initial treatment should be with aggressive supportive care. Intravenous anti-staphylococcal antibiotics are also given but Antibiotic therapy is usually given for 10-14 days Women who have had TSS should not use tampons again.
Certain strains of S. aureus produce an exfoliative exotoxin, release of which may cause a syndrome termed staphylococcal scalded skin syndrome (SSSS), or Ritters disease.In neonates it is also termed pemphigus neonatorum. It usually occurs in children and starts with fever and a tender scarlatiniform rash.
Within a day or two, large flaccid, clear bullae develop and exfoliation of sheets of skin (resembling cigarette paper) occurs, leaving a red, denuded base . Lateral traction of the skin causes it to wrinkle and be displaced (a positive Nikolskys sign).