Cellulitis is an acute, non-contagious inflammation of the connective tissue of the skin, resulting from Staphylococcus, Streptococcus, or other bacterial infection. It is a skin infection that also involves areas of tissue just below the skin surface. Often cellulitis begins in an area of broken skin, like a cut or scratch, but it may also start in areas of intact skin, especially in diabetics or who are taking medicines that affect the immune system.

Causes

• Streptococcus pyogenes (group A B-hemolytic streptococcus)

• Aerobic Gram-negative bacilli (eg, Escherichia coli, Pseudomonas aeruginosa)

Open wounds

• Staphylococcus aureus, aerobic Gram-negative bacilli

Animal bite

• Pasteurella multocida from dogs and cats Water injuries
• Freshwater caused by Aeromonas hydrophila
• Warm salt water- caused by Vibrio vulnificus.

Risk Factors

• Insect bites and stings
• Animal bite or human bite; injury or trauma with a skin wound
• History of peripheral vascular disease, diabetes, or ischemic ulcers
• Recent cardiovascular event
• Pulmonary, dental, or other procedures
• Immunosuppressive or corticosteroid medications.

Signs and Symptoms

• Localized skin redness or inflammation that increases in size as the infection spreads
• Tight, 9lossy, "stretched" appearance of the skin
• Pain or tenderness of the area
• Macule: sudden onset, usually with sharp borders
• Rapid growth within the first 24 hours
• Boils, blisters, pustules, or similar lesions
• The thin red line (along a vein) from the cellulitis toward the heart (lymphangitis)
• Warmth over the area of redness
• Fever
• Other signs of infection
• Chills
• Warm skin, sweating
• Fatigue
• Myalgias
• Malaise
• Nausea and vomiting
• Joint stiffness caused by swelling of the tissue over the joint
• Hair loss at the site of infection

DIAGNOSIS

Differential Diagnosis

• Perianal cellulitis
• Acute gout
• Fasciitis
• Thrombophlebitis
• Osteomyelitis
• Herpetic whitlow
• Cutaneous diphtheria
• Mycotic aneurysm
• Ruptured baker's cyst Pseudogout

Investigations

• CBC
• Blood culture

TREATMENT

Goal

Eliminate the source of infection and treat the condition appropriately

Non-Pharmacological Treatment

If pus or an open wound is present, immobilization and elevation of the affected area helps reduce edema and cool, wet dressings relieve local discomfort.

Pharmacological Treatment

Streptococcus pyogenes, Staphylococcus aureus

• Cephalosporins
• Quinolones
• Penicillins
• Macrolides
• Others- Vancomycin

Aminoglycoside-Treating concomitant tinea pedis, often eliminating the source of bacteria residing in the inflamed, macerated tissue, prevent recurrent leg cellulitis.

PATIENT EDUCATION

• Recommend hygiene

Complication

• Gangrene
• Sepsis, generalized infection, and shock
• Meningitis (if cellulitis is on the face)
• Lymphangitis

Prognosis

The cure is possible with 7 to 10 days of treatment. Cellulitis may be more severe if the chronic disease is present or if the person is susceptible to infection (immunosuppressed).

Complications

• Pneumonia
• Conjunctival scarring
• Penetration of the cornea can occur within 2 days in patients with untreated N gonorrhea
• Meningitis.

Prognosis

The prognosis is good. Conjunctivitis typically is self-limited and without long-term complications.

Endocarditis is a microbial infection of the endocardium and the heart valves, characterized by fever, heart murmurs, petechiae, anemia, embolic phenomena, and endocardial vegetations that may result in valvular incompetence or obstruction, myocardial abscesses, or mycotic aneurysm. The course may be acute or subacute and clinical findings vary greatly.

Classification

• Acute infective bacterial endocarditis (ABE)
• Subacute bacterial (SBE) endocarditis
• Prosthetic valvular endocarditis (PVE)
• Right-sided endocarditis

Causes

Native valve endocarditis: Streptococcus viridans, Enterococci, S. aureus, HACEK (Haemophilus, Actino-bacillus, Cardiobacterium, Eikenella, and Kingella).

Prosthetic valve endocarditis: Coagulase-negative staphylococci, Staphylococcus aureus, Enterococci, Gramnegative bacilli, fungi.

Endocarditis in IV drug users: S. aureus, streptococci, Gram-negative bacillus, enterococci, fungi, polymicrobial.

Culture negative (marantic endocarditis): A non-bacterial thrombotic endocarditis Acute bacterial endocarditis: S. aureus, Pneumo-coccus, group A streptococcus.

Other causes Infection may be acquired through Intravenous drug use, cardiac catheterization, and other invasive procedures, cuts, bruises and minor surgical procedures, dental procedures.

Risk Factors

• Underlying heart disease: Rheumatic valvular damage, Congenital heart disease, mitral valve prolapse, prosthetic valves, hypertrophic cardiomyopathy, and previous bacterial endocarditis are predisposing factors for endocarditis. With more virulent organisms, such as Staphylococcus aureus, previous valvular damage is present in only about 50% of the cases. 
• Events predisposing patients to bacteremia such as intravenous drug use, intravenous catheters, dental and genitourinary procedures.
• Age greater than 50 years

Signs and symptoms

Acute bacterial endocarditis

• Acute onset of fever, chills, arthralgias
• Sepsis
• Aseptic meningitis
• Ventricular failure and heart block
• Mycotic aneurysms
• Peripheral Janeway lesions

Subacute bacterial endocarditis

• Night sweats
• Fatigue
• Heart murmurs
• Hematuria
• Fever and chills
• Tachycardia
• Arthralgias
• Flank pain
• Abdominal pain
• Roth spots
• Splenomegaly
• Petechiae over the upper trunk
• Conjunctiva
• Osler nodes
• Acute arterial insufficiency

DIAGNOSIS

Differential Diagnosis

• Brain abscess
• Cerebral hemorrhage
• with fever
• Connective tissue
• diseases
• Glomerulonephritis
• Cerebral embolus
• Fever of unknown
• origin
• Intra-abdominal
• infections
• Meningitis
• Rheumatic fever
• Tuberculosis
• Salmonellosis
• Osteomyelitis
• Myocardial infarction
• Pericarditis
• Septic pulmonary infarcts

Investigations

• Blood cultures
• IgE
• Complete blood examination
• Echocardiograph
• Rheumatoid factor

TREATMENT

Goal

• Identification of causative organisms and decide on an optimal antibiotic regimen.
• Prevention of relapse.

Pharmacological Treatment

• Native Heart Valve (Acute infective endocarditis)
• Cloxacillin/Nafcillin
• Oxacillin plus Penicillin G or Ampicillin
• Penicillin allergy Vancomycin plus Gentamicin Prosthetic Heart Valve
• Vancomycin plus gentamicin plus rifampicin Penicillin-susceptible streptococci (Pen MICmcg/mL)
• Penicillin G plus gentamicin Penicillin-resistant Streptococci (Pen MICo.5mcg/mL)
• Penicillin G/ampicillin plus gentamicin. Methicillin-susceptible (H Staphylococcus aureus)
• Cloxacillin/nafcillin/oxacillin with or without rifampicin or gentamicin Methicillin-resistant (H Staphylococcus aureus)
• Vancomycin plus gentamicin and rifampin HACEK microorganisms (Haemophilus parainfluenza, H. aphrophilus, Actinobacillus actinomyces-temcomitans, Cardiobacterium hominis, Eikenella corrodens, Kingella kingae)
• Ceftriaxone

Surgical Treatment

Cardiac valve surgery is indicated in early-onset PVE progressive CHF, multiple embolic events, fungal endocarditis, persistent bacteremia, an extension of infection into the conducting system, relapse of infection, and abscess on echo.

PATIENT EDUCATION

Emphasize patient regarding dental hygiene

Complications

• Congestive heart failure
•  Emboli
• Arrhythmias
• Stroke
• Glomerulonephritis
• Brain abscess
• Jaundice
• Severe heart valve damage
• Brain or nervous system changes

Prognosis

Untreated, infective endocarditis is always fatal. A poor prognosis is associated with heart failure, old age, aortic or multiple valve involvement, large vegetations, polymicrobial bacteremia, antimicrobial resistance, delay in initiating therapy, prosthetic valve infections, mycotic aneurysms, valve ring abscess, and major embolic events. After cardiac surgery, the mortality rate is higher in early-onset than in late-onset infective endocarditis and in fungal endocarditis.relapse after therapy usually occurs within 4 weeks.

An infection caused by herpes virus 1 or 2- which primarily affects the mouth or genital area. The virus may be transmitted even in the absence of symptoms or visible lesions. Once the virus is acquired, it spreads to nerve cells and remains dormant. It may intermittently reactivate and cause symptoms (flares). Recurrences may be precipitated by overexposure to sunlight, fever, stress, acute illness, and medications or conditions that weaken the immune system (such as cancer, HIV-AIDS, and use of corticosteroids). The herpes virus causes a wide range of diseases, including gingivostomatitis, keratoconjunctivitis, encephalitis, genital disease, and newborn infection.

Classification

• Herpes simplex virus 1 (HSV-1) is usually associated with infections of the lips, mouth, and face. It is the most common herpes simplex virus among the general population and is usually acquired in childhood.
• Herpes simplex virus 2 (HSV-2) is sexually transmitted and is usually associated with genital ulcers or sores.

• HSV-1- Transmitted through direct contact with infected saliva or direct contact with contaminated utensils
• HSV-2- usually acquired as an STD

Risk Factors

• Immune compromise
• Newborns
• Prior HSV infection
• Sexual contact with an infected person
• Occupational exposure

Signs and Symptoms

Lesions usually are vesicular or ulcerative on an erythematous base and are very painful. Many primary infections are asymptomatic. Recurrent lesions are common. Tender bilateral lymphadenopathy OCCurs with the lesions.

• Neurologic symptoms
• Headache
• Confusion
• Fever
• Tenesmus, itching with anal/perianal lesions
• Dysuria with genital lesions
• Sore throat with oral lesions
• Constitutional symptoms (usually present With the development of herpes lesions)
• Anorexia
• General malaise
• Prodromal symptoms (present in advance of herpes lesions)
• Burning
• Itching

DIAGNOSIS

Differential Diagnosis

• Chancroid
• .Pharyngitis
• .Proctitis
• Syphilis
• Male-Urethritis
• Hand-Foot-and-Mouth Disease
• Meningitis and Encephalitis

Investigations

• Tzanck smear
• Viral culture
• Serology
• CSF analysis
• CT scan
• MRI
• Lumbar puncture
• Brain biopsy
• Monoclonal antibody testin9
• Polymerase chain reaction
• Slit-lamp examination

TREATMENT

Goal

• To shorten the clinical course
• To prevent complications and the development
• of latency and/or subsequent recurrences
• To decrease transmission
• To eliminate established latency

Pharmacological Treatment

Class of drugs used is:

Antiviral agents:-

• Acyclovir
• Famciclovir

PATIENT EDUCATION

• Educate patients that Hsv-2 is an STD and advise to follow deterrence measures.
• Avoid contact with immune-compromised persons including neonates.
• Wash hands often to help prevent autoinoculation and spread to others.

Complications

• Encephalitis
• Neonatal infections
• Compromised host progressive and disseminated disease
• Genital infection acute urinary retention

Prognosis

• The high recurrence rate for genital HSV-2 infection.
• More than 85% of patients with one symptomatic episode will experience another.
• Recurrences may be frequent; 38% of the population with genital herpes have more than 6 recurrences per year; 20% have more than 10 recurrences per year.

Meningitis is an inflammation of the leptomeninges and underlying subarachnoid cerebrospinal fluid (CSF). approximately 75% being subacute. Bacterial seeding usually occurs by hematogenous spread, once in the CSF, the bacteria flourishes. Bacterial cell wall components initiate a cascade of complement- and cytokine-mediated events that result in at least 3 critical events: increased permeability of the blood-brain barrier, cerebral edema, and presence of toxic mediators in the CSF. Bacterial exudates extend throughout the CSF, particularly to the basal cisterns, damaging cranial nerves, obliterating CSF pathways, and inducing vasculitis and thrombophlebitis.

Causes

• Neonates Group B or D streptococci, nongroup B streptococci, E. coli, and L monocytogenes
• Infants and children H. influenza, S. pneumonia, and N  meningitidis
• Adults-S. pneumonia, H. influenza, N. meningitides, Gram-negative bacilli, staphylococci, streptococci, and Listeria species.

• Aged >60 years or <5 years or younger
• Sex: In neonates, the male-to-female ratio is 3:1.
• Race blacks
• Crowding
• Immunosuppressed patients
• Splenectomy and sickle cell disease
• Alcoholism, diabetes, and cirrhosis
• Contagious infection, bacterial endocarditis
• Dural defect
• Intravenous drug abuse Ventriculoperitoneal shunt
• Malignancy
• Thalassemia major
• Some cranial congenital deformities

signs and Symptoms

Classic symptoms

• Headache
• Nuchal rigidity (Signs of meningeal irritation)
• Fever and chills
• Prodromal upper respiratory tract infection (URTI) symptoms (viral and bacterial)
• Altered sensorium
• Photophobia
• Seizures
• Vomiting
• Focal neurologic symptoms

Symptoms in infants

• Fever
• Lethargy and/or change in the level of alertness
• Poor feeding and/or vomiting
• Respiratory distress, apnea, cyanosis

Symptoms of partially treated meningitis

• Seizures
• Fever
• Changes in the level of alertness or mental status

• Headache
• Low-grade fever
• Lethargy

Symptoms of tuberculous meningitis

• Fever
• Night sweats
• Malaise, with or without the headache
• Weight loss
• Meningismus

DIAGNOSIS

Differential diagnosis

• Brain abscess
• Tremens encephalitis Herpes simplex
• Delirium
• Herpes simplex.
• Febrile seizures (Pediatrics)
• Neoplasms
• Herpes simplex encephalitis
• Meningitis and encephalitis subarachnoid hemorrhage

Investigations

• Complete blood count Serum electrolytes(CBC)
• Serum glucose
• Urinary electrolytes
• BUN and/or creatinine and liver profile
• Serum cryptococcal antigen
• Chest X-ray
• Serum test
• Cultures blood, nasopharynx, respiratory secretions, urine, and skin lesions.
• Latex agglutination or counter immunoelectrophoresis (CIE) of blood, urine, and CSF.
• Head CT scan with contrast or MRI

TREATMENT

Goal

identify the causative organism, treat patients with acute bacterial meningitis, assess whether a central nervous system (CNS) infection is present in those with suspected subacute or chronic meningitis.

Pharmacological Treatment

Antibiotics

• Infants <3 months: Ampcilline plus Cefotaxim, Gentamicin
• Children -3 months-12 yr: Cefotaxime, ceftriaxone,meropenem
• Adults-19-50yr: Cefotaxime, Ceftriaxone, ampicillin
• Adults> 50yr: Ampicillin plus cefotaxime or Ceftriaxone

S. pneumonia Pen MIC mcg/mL

• Penicillins
• Vancomycin
• Cephalosporins

Neisseria meningitidis

• Penicillins
• Chloramphenicol or cefoperazone/sulbactam
• Cephalosporins

Haemophilus influenza

• Cephalosporin8
• Chloramphenicol or cefoperazone/sulbactam
• Meropenem

Aseptic meningitis

Antivirals: Acyclovir

mycobacterium tuberculosis

• Isoniazid, rifampicin, pyrazinamide, ethambutol, streptomycin

PATIENT EDUCATION

• Regular follow-up
• Advise patients to report any sign of fever, sore throat, rash, or symptoms of meningitis.
• Complications
• Immediate: Septic shock, coma with loss of protective airway reflexes, seizures, cerebral edema, septic arthritis, pericardial effusion, and hemolytic anemia.
• Subdural effusions
• Delayed: Decreased hearing or deafness, other cranial nerve dysfunction, multiple seizures, focal paralysis, subdural effusions, hydrocephalus, intellectual deficits, ataxia, blindness, Waterhouse-Friderichsen syndrome, and peripheral gangrene

Prognosis

Pneumococcal meningitis has the highest rates of mortality and morbidity.

Bronchitis is an inflammation of the tracheobronchial tree. It is generally self-limiting and with eventual complete healing and return of normal function. Commonly, it is mild but may become serious in debilitated patients and in those with chronic lung, or heart disease. The cause is usually infectious, but allergens and irritants can produce a similar clinical picture. Bronchitis typically occurs in the setting of an upper respiratory illness and therefore is seen more frequently In the winter.

Causes

• Virus:-Adenovirus, coronavirus, influenza A and B viruses, parainfluenza virus, respiratory syncytial virus, coxsackievirus A21, rhinovirus, and the viruses that cause rubella and measles.
• Bacteria:-Mycoplasma pneumoniae, Bordetella pertussis, and Chlamydia pneumoniae, Moraxella catarrhalis, Mycoplasma, Streptococcus pneumoniae.

Risk Factors

• Chronic pulmonary diseases
• Chronic sinusitis Bronchopulmonary allergy
• Hypertrophied tonsils and adenoids in children
• Immunocompetent
• Air pollutants
• Elderly
• Infants
• Smoking, passive smoking
• Alcoholism
• Reflux esophagitis
• Tracheostomy
• IgA deficiency
• Environmental changes

Signs and Symptoms

• Preceding respiratory tract infection, such as a common cold with coryza, malaise, chills, fever,sore throat, back and muscle pain.
• Cough, dry and productive initially later productive.
• Dyspnea.
• Rales Ronchi, wheezing.
• Infected pharynx.

DIAGNOSIS

Differential Diagnosis

• Influenza
• Bronchopneumonia
• Bronchiectasis
• Acute sinusitis
• Aspiration
• Cystic fibrosis
• Reactive airways disease
• Bacterial tracheitis

Investigations

• Chest X-ray
• Arterial blood gases should be monitored when the serious underlying chronic respiratory disease is present.
• Gram stain and sputum culture should be performed to determine the causative organism.
• Pulmonary function tests.

TREATMENT

Goal

Provide symptomatic relief and treat according to the predominant organism.

Non-Pharmacological Treatment

• Stop smoking
• Steam inhalations
• Rest

Pharmacological Treatment

Antipyretic analgesic

Antibiotics:-Antibiotics are indicated when there is pertussis infection or when purulent sputum is present, or when high fever persists

• Oral tetracycline
• Trimethoprim-sulfamethoxazole
• Amoxicillin--If M. pneumoniae or C. pneumoniae is the causative agent
• Macrolides

PATIENT EDUCATION

• Stop smoking
• Rest until the fever subsides
• Recommend oral fluids up to 3-4 L/day during the febrile course

Complications

• Bronchopneumonia
• Acute respiratory failure

Prognosis

Usually, complete healing, can be serious with elderly or debilitated patients, cough may persist for several weeks after initial improvement.

It is a bacterial or viral infection in the middle ear, usually secondary to an upper respiratory tract infection (URTI). Although acute otitis media can occur at any age, it is most common in young children, particularly from age 3 mo to 3 yr. Microorganisms may migrate from the nasopharynx to the middle ear by moving over the surface of the Eustachian tube's mucous membrane or by propagating in the lamina propria of the mucous membrane as spreading cellulitis or thrombophlebitis.

Causes

In newborns

• Gram-negative enteric bacilli, Escherichia coli, Staphylococcus aureus

After the neonatal period

• E. coli rarely cause acute otitis media. In older infants and children< 14 yr: Streptococcus pneumoniae, Haemophilus influenzae, group A B-hemolytic streptococci, Moraxella (Branhamella) catarrhalis, and S. aureus
• Viral otitis media is usually complicated by secondary invasion by one of these bacteria. In those > 14 yr, S. pneumoniae, group A
• B-hemolytic streptococci, S. aureus, H.influenzae.

Risk Factors

• Daycare
• Formula feeding
• Passive smoking
• Male
• Family history of middle ear disease
• Acute otitis media in the first year of life is a risk factor for recurrent acute otitis media

• Severe earache
• Hearing loss
• Fever (up to 40.50°C [105.0°FI)
• Nausea and vomiting
• Diarrhea
• Bulged erythematous tympanic membrane
• Serosanguineous
• Purulent otorrhea

DIAGNOSIS

Differential Diagnosis

• Referred pain from the jaw or teeth

Investigations

• Tympanometry
• Acoustic reflectometry
• Hearing testing
• Tympanocentesis
• Nasopharyngeal cultures

TREATMENT

Goal

• To relieve symptoms
• Hasten resolution of the infection
• Reduce the chance of labyrinthine and intracranial infectious
• Reduce the complications and residual damage to the hearing mechanism in the middle ear.

Pharmacological Treatment

Antibiotic therapy

• 1st line agents: Amoxicillin, co-trimoxazole, erythromycin
• 2nd line agents: Amoxicillin/clavulanate, cefdinir, cefpodoxime, cefuroxime axetil, clarithromycin
• 3rd line agents: Ceftriaxone, clindamycin, levofloxacin

Surgical Treatment

Myringotomy should be considered if the tympDanie the membrane has bulged or it pain, fever, vomiting, and diarrhea are severe or persistent.

Complications

• Acute mastoiditis
• Petrositis
• Hearing loss
• Labyrinthitis
• Cholesteatoma
• Facial paralysis
• Conductive and sensorineural hearing loss
• Epidural abscess
• Atrophy and scarring of eardrum, chronic perforation, and otorrhea
• Meningitis, brain abscess, lateral sinus thrombosis, subdural empyema, and otitic hydrocephalus.

Prognosis

Symptoms of otitis media usually improve in 48-72hrs; otitis media with effusion following acute otitis media resolved in 90% by 3 months. Otitis media with effusion have a lesser percentage of complications.

Pharyngitis is an inflammation of the pharynx. which frequently results in a sore throat and

may be caused by a variety of microorganisms. Chronic pharyngitis is a chronic inflammation of

the pharyngeal mucous membrane and submucous Lymphoid tissues. In infectious pharyngitis, bacteria

or viruses may directly invade the pharyngeal mucosa, causing a local inflammatory response.

Causes

• Virus
• Adenovirus
• Arcanobacterium (Corynebacterium) haemolyticus
• Coxsackieviruses A and B
• Herpes Simplex virus
• HIV
• Influenza virus
• Mononucleosis
• Respiratory Syncytial virus
• Rhinovirus
• Bacteria
• Arcanobacteriumn
• Chlamydia pneumoniae
• Corynebacterium
• Group Ab Streptococcus
• Group C, G, and F Streptococci
• Mycoplasma pneumonia
• Neisseria gonorrhoeae
• Other causes of pharyngitis
• Oral thrush is due to candidal species (immunocompromised patients).
• Dry air, allergy/postnasal drip, chemical injury, gastroesophageal reflux disease (GERD), smoking, neoplasia, and endotracheal intubation.

Riak Factors

• Colder months-during respiratory disease season.
• Infected family member

Signs and Symptoms

• Sore throat
• Strep throat may be accompanied by fever, headache, swollen lymph nodes in the neck
• Viral pharyngitis may be associated with rhinorrhea and postnasal discharge
• Difficulty in swallowing and breathing

DIAGNOSIS

Differential Diagnosis

• Candidiasis
• Diphtheria
• Epiglottitis (adult)
• Gonorrhea
• Herpes Simplex
• Mononucleosis
• Pediatrics
• Croup or Laryngotracheobronchitis (pediatrics)
• Epiglottitis Pediatrics
• Hand-Foot-and-Mouth Disease (pediatrics)
• Pharyngitis (pediatrics)
• Scarlet Fever
• Peritonsillar abscess
• Pharyngitis Pneumonia
• Mycoplasma Retropharyngeal Abscess
• Rheumatic Fever

Investigation

• GABHS rapid antigen detection test
• Throat culture
• Antistreptolysin-O (ASO)
• Mono spot
• Peripheral smear
• Fluorescent monoclonal antibody test
• .Lateral neck film
• Chest X-ray

TREATMENT

Goal

• Decrease the duration of the illness and infective period
• Provide symptomatic relief
• Decrease the incidence of relapses and complications.

Non-Pharmacological Treatment

Viral infections are managed with supportive measures Such as warm saline gargles, analgesics, and fluids.

Pharmacological Treatment

Antibiotic therapy

• 1st line treatment: Penicillins, erythromycin
• 2nd line treatment: Penicillins, cephalosporins, macrolides
• Gonococcal pharyngitis: Ceftriaxone plus doxycycline or azithromycin, or ciprofloxacin plus doxycycline or azithromycin

PATIENT EDUCATION

• A complete full course of antibiotic therapy
• The risk of recurrence
• Regular follow-up

Complications

• Otitis media
• Mastoiditis
• Sinusitis
• Epiglottitis
• Pneumonia

Prognosis

• Most cases of pharyngitis resolve spontaneously within 10 days.
• Treatment failures are frequent (poor compliance, antibiotic resistance, untreated close contacts, carrier states, and antibiotic-related or co-pathogenic suppression of host immunity and necessary flora).

Osteomyelitis is an infection of the medullary bone that results in progressive inflammatory destruction of the bone and the apposition of new bone, caused by aerobic and anaerobic bacteria, mycobacteria, and fungi. Osteomyelitis occurs in vertebrae and bones of the feet in patients with diabetes or at sites of bone trauma or surgery. In children, osteomyelitis usually affects the metaphysis of the tibia or femur as well as growing bones with a rich blood supply.

Classification

• Hematogenous osteomyelitis is an infection caused by bacterial seeding from the blood.
• Direct or contiguous inoculation osteomyelitis-is caused by direct contact of the tissue and bacteria during trauma or surgery.
• Chronic osteomyelitis
• Osteomyelitis secondary to peripheral vascular

Causes

Bacterial causes of acute and direct osteomyelitis include

the following:

• Acute hematogenous osteomyelitis
• Newborns (younger than 4 months): S. aureus, Enterobacter species, and group A and B Streptococcus species
• Children (aged 4 months to 4 yr): S. aureus, group A Streptococcus species, Haemophilus influenzae, and Enterobacter species
• Children, adolescents (aged 4 yr to adult): S. aureus (80%), group A Streptococcus species, H influenzae, and Enterobacter species
• Adult: S. aureus and occasionally Enterobacter or Streptococcus species
• Direct osteomyelitis
• Generally: S. aureus, Enterobacter species, and Pseudomonas species
• Puncture wound through an athletic shoe: S aureus and Pseudomonas species
• Sickle cell disease - S. aureus and Salmonellae species

Riek Factors

• sickle cell disease
• Local trauma
• Neuropathy
• Vascular insufficiency IV drug use
• Presence of orthopedic implant
• Other conditions that predispose to bone infarcts
• Hemodialysis
• Open fractures
• Diabetes mellitus

Signs and Symptoms

• Fatigue
• Malaise
• Tenderness
• Febrile
• Afebrile
• Nonhealing ulcer
• Restriction of movement
• Hematogenous long-bone osteomyelitis
• Abrupt onset of high fever
• Local edema, erythema, and tenderness
• .Hematogenous vertebral osteomyelitis
• History of an acute bacteremic episode
• .May be associated with contiguous vascular insufficiency
• Local edema, erythema, and tenderness
• Localized back pain with a paravertebral muscle spasm that is unresponsive to conservative treatment.
• Acute osteomyelitis of peripheral bones
• Localized warmth, swelling, erythema, and tenderness.
• Irritability
• Insidious onset
• Sinus drainage.
• Weight loss and fatigue
• Chronic osteomyelitis
• Sinus tract drainage
• Low-grade chronic osteomyelitis
• Intermittent (months to many years) bone pain
• Chronic fatigue
• Malaise

DIAGNOSIS

Differential Diagnosis

• Cellulitis
• Hand Infections
• Gout and Pseudogout Sickle Cell Disease
• Spinal Cord Infections
• Gas Gangrene
• Neoplasma
• sickle cell disease

• WBC count
• ESR
• CBC
• C-reactive protein
• CT
• X-rays
• Bone biopsy
• Radiograph
• Radioisotope bone scans
• Blood culture results
• MRI

TREATMENT

Goal

• To eliminate the infection and prevent the development of chronic infection

Pharmacological Treatment

Hematogenous

• Nafcillin, oxacillin, cefazolin, vancomycin.Sickle cell
• Ciprofloxacin, levofloxacin, ofloxacin, cefotaxime,Ceftriaxone.

Contiguous without vascular insufficiency

• Nafcillin or cloxacillin and ciprofloxacin or vancomycin and ceftazidime

Contiguous with vascular insufficiency

• Imipenem, meropenem

Surgical Treatment

• In chronic infection, surgical removal of the dead bone tissue is indicated. The open space left by the removed bone tissue may be filled with bone graft, or by packing material to promote the growth of new bone tissue. Antibiotic therapy is continued for at least 3 weeks after surgery.
• The infection of an orthopedic prosthesis may require surgical removal with debridement of the infected tissue surrounding the area. A new prosthesis may be implanted in the same operation, or delayed until the infection has resolved, depending on its severity.

PATIENT EDUCATION

• Avoid further stress and weight-bearing until healing.

Complications

• Bone abscess
• Loosening of the prosthetic implant
• Overlying soft-tissue cellulitis
• Draining soft-tissue sinus tracts
• Local spread of infection
• Reduced limb or joint function
• Bacteremia
• Fracture

Prognosis

The prognosis is variable but markedly improved with timely diagnosis and aggressive therapeutic intervention. The outcome is usually good with adequate treatment of acute osteomyelitis, and worse for chronic osteomyelitis, even with surgery. Resistant or complicated chronic osteomyelitis may result in amputation.

Malaria is an acute and chronic protozoan infection transmitted by Anopheles mosquitoes to humans. Four parasitic protozoa of the genus Plasmodium (Plasmodium ovale, Plasmodium vivax, Plasmodium malaria, Plasmodium falciparum) cause malaria. Of the 4 species, P falciparum causes the most severe morbidity and mortality. Malaria can also be transmitted via a blood transfusion or congenitally between mother and fetus, although these forms of infection are rare. According to the World Health Organization estimate, there are around 300-500 million cases of malaria and more than one million people die due to malaria.

Causes

• Bites from infected Anopheles mosquitoes
• Transfusion of infected blood

Risk Factors

• Traveling and/or living in endemic area

Signs and Symptoms

• Fever
• Flu-like illness
• Chills
• Headache
• Muscle ache
• Tiredness
• Nausea
• Hemolysis
• Diarrhea
• Anemia

DIAGNOSIS

Dirferential dlagnosis

• Babesiosis
• Q Fever
• Viral Hemorhagic Fevers
• Dengue Fever
• Encephalitis
• Endocarditis
• Gastroenteritis
• Giardiasis
• Hepatitis
• Hypothemia
• Leishmaniasis
• Meningitis
• Mononucleosiss
• Pneumonia
• Tropical splenomegaly
• Blood dyscrasias

Investigations

• Malarial smear
• Indirect fluorescent antibody (IFA)
• ELISA
• DNA probe
• Renal function tests
• Urine and blood cultures
• .Chest X-ray
• CT scan of the head
• Microhematocrit centrifugation
• Giemsa-stained thick and thin peripheral blood smears
• Polymerase chain reaction
• parasite F (dipstick test)

TREATMENT

Goal

• identity the type of parasite and treat accordingly

• Antipyretics
• Antiprotozoal
• Antimalarials

PATIENT EDUCATION

• Take prophylactic drugs at proper intervals if traveling to endemic regions... Use topical insect repellent (30-35% diethyltoluamide [DEET]),especially from dusk to dawn.
• Wear long-sleeved permethrin-coated clothing if not allergic to permethrin; spray under beds,chairs, tables, and along walls.
• Sleep under fine-nylon netting impregnated with permethrin.
• Seek medical attention immediately upon contracting any tropical fever or flu-like illness.

• Coma (cerebral malaria)
• Seizures
• Renal failure
• Hemoglobinuria (blackwater fever)
• Noncardiogenic pulmonary edema
• .Profound hypoglycemia
• Lactic acidosis
• Hemolysis resulting in severe anemia and
• jaundice
• Bleeding (coagulopathy).

Prognosis

• Most patients with uncomplicated malaria exhibit marked improvement within 48 hours after the initiation of treatment and are fever-free after 96 hours.
• Only P falciparum infection carries a poor prognosis with a high mortality rate if untreated. However, if diagnosed early and treated appropriately, the prognosis Is excellent.

Gingivitis is an inflammatory process limited to the mucosal epithelial tissue surrounding the cervical a portion of the teeth and the alveolar processes. Gingivitis proceeds through an initial stage to produce early lesions, which then progress to advanced disease. The initial stage of an acute exudative inflammatory response begins within 4 or 5 days of plaque accumulation. Both gingival fluid and transmigration of neutrophils increase. At approximately 1 week, the transition to early lesions is marked by the change to predominately lymphocytic infiltrates. With time, lesions become chronic and are characterized by the presence of plasma cells and B lymphocytes. As chronic local inflammation progresses, pockets develop where the gingiva separates from the tooth. These pockets deepen and may bleed during tooth brushing, flossing, and even normal chewing. As this persistent inflammation continues, periodontal ligaments break down and destruction of the local alveolar bone occurs. Teeth loosen and eventually fall out.

Classification

Gingivitis has been classified on the basis of:

Clinical appearance:-

• Ulcerative
• Hemorrhagic
• Necrotizing
• Purulent

Etiology:-

• Drug-induced
• Hormonal
• Nutritional
• Infectious
• Plaque-induced

Duration:-

• Acute
• Chronic
• Causes
• Bacteria
• Inadequate oral hygiene
• Inadequate plaque removal
• Blood dyscrasias
• Allergic reactions
• Chronic debilitating disease

• .Gingival bleeding -Anticoagulants and fibrinolytic agents.
• Gingival hyperplasia Phenytoin, oral contraceptive agents, calcium channel blockers
• Gingivitis - Protease inhibitors (eg, saquinavir, ritonavir), vitamin A and analogues, danazol, pentamidine, misoprostol, methotrexate, and gold compounds
• Gingivostomatitis- Exposure to arsenic, gold, bismuth, mercury, nickel, sulfur dioxide, lead, thallium, zinc, methyl violet, and topical chlorhexidine.

Risk Factors

• Use of tobacco or ethanol
• Immune incompetence
• Diabetes mellitus
• Malocclusion
• Poor dental hygiene
• Faulty dental restoration

Signs and Symptoms

.Chronic gingivitis:-

• Bleeding gums while toothbrushing, flossing, and eating

Acute necrotizing ulcerative gingivitis:-

• Apparently spontaneous bleeding or bleeding in response to very minimal local trauma
• Local pain, malaise, and alterations in taste, such as a metallic flavobr.
• .Foul breath
• Erythema, edema, tenderness, and induration of affected areas

DIAGNOSIS

Differential Diagnosis:-

• Adrenal insufficiency and Adrenal crisis
• HIV
• Pericoronitis

• Smear to identify causative agents

Pharmacological treatment

Classes of drugs used are:-

Antibiotics:-

• Amoxicillin/Clavulanate
• Erythromycin
• Penicillin V
• Metronidazole
• Tinidazole

Antiseptic

Analgesics

Topical anesthetics

PATIENT EDUCATION

• Good oral hygiene
• Regular dental check-ups

Complications

• Local and systemic complications
• Noma
• Periodontal disease and tooth loss
• Osteomyelitis of alveolar bone.

Prognosis

• Untreated chronic gingivitis eventually results in tooth loss. After initial cleaning and scaling in its early stages, gingivitis usually is reversible with good dental hygiene.

• Gingivitis generally responds well to appropriate treatment.

Conjunctivitis describes the inflammatory process that involves the conjunctiva; most causes of conjunctivitis are benign. Cellular infiltration and exudation characterize conjunctivitis on a cellular level. Classification is based on the underlying cause, as visual conjunctivitis, bacterial, fungal.

CAUSES

Bacterial

• Staphylococcus aureus
• Streptococcus pneumonia
• Haemophilus influenzae
• N. gonorrhoeae
• Neisseria meningitidis
• .Rarely Streptococcus sp., Pseudomonas, Branhamella catarrhalis, Coliforms, Klebsiella, Proteus, Corynebacterium diphtheriae, Mycobacterium tuberculosis, Treponema pallidum.

Viral

• Adenoviruses types 3, 4, 7, 8, 11 and 19
• Herpes simplex, Herpes zoster
• Enterovirus type 70
• Coxsackievirus type A24 and A28
• Molluscum contagiosum
• Varicella
• Measles virus

Chlamydial

• Chlamydia trachomatis (trachoma)
• Chlamydia oculogenitalis (inclusion conjunctivitis)
• Chlamydia lymphogranulomatis (lymphogranu-loma venereum)

Allergic

• Rhinoconjunetivitie (hay fever) humoral
• Vemal conjunctivitis
• Giant papillary conjunctivitis
• Autoimmune

Chemicals or irritants

• Topical medication
• Home/industrial chemicals
• Wind, smoke, ultraviolet light

Other

• Rickettsial, fungal, parasitic, tuberculosis, syphilis, Kawasaki disease
• Thyroid disease, gout, carcinoid, sarcoidosis, psoriasis, Stevens-Johnsons syndrome, Ligneous conjunctivitis, Reiter's syndrome.

Signs and Symptoms

• Bacterial conjunctivitis-acute onset, minimal pain, occasional pruritus, and sometimes, exposure history
• Ocular surface diseases predispose the patient to bacterial conjunctivitis.
• Viral conjunctivitis- acute or subacute onset, minimal pain level, and often, exposure history
• Severe photophobia and foreign-body sensation
• Chlamydial conjunctivitis chronic onset, minimal pain level, occasional pruritus, and STD history
• Allergic conjunctivitis -acute or subacute onset, no pain, and no exposure history
• Pruritus
• Shield corneal ulcers.
• Giant papillary conjunctivitis resembles vernal disease; excessive pruritus, mucous production, and increasing intolerance to contact

General

• Increased tearing
• Pain, redness and itching of the eyes
• Gritty feeling in the eyes, blurred vision
• Sensitivity to light
• Crusts that form on the eyelid overnight

Risk Factors

• Trauma
• Chemicals and foreign body

DIAGNOSIS

Differential Diagnosis

• Glaucoma, Acute Angle-Closure
• Herpes Zoster, Herpes Zoster Ophthalmicus
• Iritis and Uveitis
• Scleritis

Investigations

• Gram stain
• Giemsa staining
• Immunofluorescent antibody test

TREATMENT

Pharmacological Treatment

Classes of drugs used are:

• Antibiotics:-Tetracyclines,Cephalosporins,Macrolides
• Mast cell stabilizers
• Decongestants
• Nonsteroidal anti-inflammatory agents (NSAIDs)

PATIENT EDUCATION

Good hygiene can help prevent the spread of conjunctivitis:

• Keep your hands away from the eye.
• Wash hands frequently.
• Change pillowcases frequently.
• Replace eye cosmetics regularly.
• Do not share eye cosmetics, towels or handkerchiefs.
• Proper use and care of contact lenses.

Complications

• Pneumonia
• Conjunctival scarring
• Penetration of the cornea can occur within 2 days in
• patients with untreated N gonorrhea
• Meningitis.

Prognosis

• The prognosis is good. Conjunctivitis typically is self-
• I limited and without long-term complications.

Bursitis is defined as an inflammation of bursae. Bursae are closed, round, flattened sacs that are lined by synovium, and separate the bare areas of hone from overlapping muscles (deep bursae), or skin and tendons (Superficial bursae). They occur in areas of friction or possible impingement. When inflammed, the synovial cells increase in thickness and may show villous hyperplasia. Bursal lining eventually may be replaced by granulation tissue prior to fibrous tissue formation. The bursa becomes filled with fluid, which is often rich in fibrin.

Classification

• Subacromial (subdeltoid) bursitis
• Olecranon bursitis
• Iliopsoas bursitis
• Trochanteric bursitis
• Ischial bursitis
• Prepatellar bursitis
• Infrapatellar bursitis
• Anserine bursitis
• Calcaneal bursitis

General bursitis

• Acute trauma
• Chronic friction
• Crystal deposition (gout, pseudogout)
• Systemic diseases such as rheumatoid arthritis,ankylosing spondylitis, psoriatic arthritis,Scleroderma, systemic lupus erythematosus,pancreatitis, Whipple disease, oxalosis, uremia,hypertrophic pulmonary osteoarthropathy, and idiopathic hypereosinophilic syndrome

Infective and septic bursitis

• Bacteria
• Staphylococcus aureus most common
• Mycobacterium (both tuberculous and non tuberculous strains)
• Fungi-Candida species

Risk Factors

• .History of inflammatory disease (s)
• History of repetitive motion
• Diabetes
• Steroid therapy
• Uremia
• Alcoholism
• .Traumatic injury
• Cellulitis in the overlying skin

Signs and Symptoms

• Pain upon motion
• Decreased range of motion
• Edema
• Localized tenderness
• Warmth
• Erythema of the skin (if superficial)
• Loss of function

DIAGNOSIS

• Differential Diagnosis
• Abdominal Trauma
• Rheumatoid Arthritis
• Cellulitis
• Costochondritis
• Tendonitis strain and sprain

Investigations

• X-ray
• Bursograpny
• .Ultrasound
• CT scan
• MRI
• Bursal fluid white blood cell count

TREATMENT

Goal

• To reduce morbidity
• .To prevent complications

Pharmacological Treatment

Classes of drugs used are:

• Nonsteroidal anti-inflammatory agents (NSAIDS)
• Antibiotics
• Penicillins
• Cephalosporin
• Others - Vancomycin
• Corticosteroids

For details, refer chart on bone and joint infections

PATIENT EDUCATION

• Advice pertaining to prevention via appropriate warm-up, stretching, and avoidance of repetitive injury
• Lifestyle changes to prevent recurrent joint irritation

Complications

• Acute bursitis may progress to chronic bursitis
• Severe long-range limitation of motion

Prognosis

• Generally good as most bouts of bursitis heal without sequelae
• Repetitive acute bouts may lead to chronic bursitis necessitating repeated joint/bursal aspirations or eventually surgical excision of involved bursa.