Know about Impetigo in under 5 minutes

Know about Impetigo in under 5 minutes

Impetigo is a superficial skin infection that is seen most commonly in children. Most common during hot, humid weather, which facilitates microbial colonization of the skin. Minor trauma, such as scratches or insect bites, allows entry of organisms into the superficial layers of skin, and infection ensues. The infection is generally classified as bullous or non-bullous based on clinical presentation.

AETIOLOGY

Most cases of impetigo were caused by S. pyogenes, but recently S. aureus, either alone or in combination with S. pyogenes, has emerged as the principal cause of impetigo. So, the bullous form is caused by strains of S. aureus capable of producing exfoliative toxins.

PRESENTATION

Exposed skin, especially the face, is the most common site.

SIGNS & SYMPTOMS

Nonbullous impetigo indeed manifests initially as small, fluid-filled vesicles. Moreover, Purulent discharge from the lesions dries to form golden yellow crusts that are characteristic of impetigo In the bullous form of impetigo, the lesions begin as vesicles and turn into bullae containing clear yellow fluid. Bullae soon rupture, forming thin, light brown crusts. As a result, regional lymph nodes may be enlarged. Pruritus is common, and scratching of the lesions may further spread infection through excoriation of the skin. In general, Weakness, fever, and diarrhoea sometimes are seen with bullous impetigo

DIAGNOSIS

Crusted tops of lesions should be raised so that purulent material at the base of the lesion can be cultured. A complete blood count is often performed because leukocytosis is common.

TREATMENT

Although impetigo may resolve spontaneously, antimicrobial treatment is indicated to relieve symptoms, prevent the formation of new lesions, and prevent complications, such as cellulitis. Penicillinase- resistant penicillins are preferred for treatment because of the increased incidence of infections caused by S. aureus. On the whole, Penicillin, administered as a single intramuscular dose of benzathine penicillin G (300,000 to 600,000 units in children, 1.2 million units in adults) or as oral penicillin VK, is effective for infections known to be caused by S. pyogenes. So, penicillin-allergic patients can be treated with clindamycin. Additionally, the duration of therapy is 7 to 10 days. Moreover, topical therapy with mupirocin ointment (applied three times daily for 7 days) is as effective as erythromycin. Removal of crusts by soaking in soap and warm water also may be helpful in providing symptomatic relief.

Oral Agents

NAMEDOSEFREQUENCY
Amoxicillin Clavulanate875 mgBD
Cefadroxil250 – 500 mgBD
Cephalexin250 – 500 mgQID
Ciprofloxacin500 – 750 mgBD
Clindamycin300 – 600 mgTID/QID
Dicloxacillin250 – 500 mgQID
Doxycycline100 – 200 mgBD
Erythromycin250 – 500 mgQID
Levofloxacin500 – 750 mgOD
Metronidazole250 – 500 mgTID
Penicillin VK250 – 500 mgQID

Parenteral Agents

NAMEDOSEROAFREQUENCY
Ampicillin1 – 2 gmIVQID
Cefazolin1 gmIVQID
Cefepime1 – 2 gmIVBD
Cefotaxime1 – 2 gmIVTID
Ceftriaxone1 gmIVOD
Ciprofloxacin400 mgIVBD
Clindamycin300 – 600 mgIVTID

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Learn About Tuberculous Meningitis In The Next 5 Minutes

Learn About Tuberculous Meningitis In The Next 5 Minutes

Tuberculous meningitis is a Meninges infection. Meninges are the Tissues Surrounding the Brain and Spinal Cord. It is due to the presence of granulomatous inflammation that leads to the Cerebral Leptomeninges inflammation [1,2]. Mycobacterium Tuberculosis / Koch Bacilli [4] causes tuberculous meningitis. This bacterium is known to cause infectious disease Tuberculosis [1] that usually affects the lungs [3,4], and is a communicable infectious disease [4,10]. It is transmitted through the respiratory tract and primarily affects the lungs but can spread to the brain, bones, eyes and skin via the bloodstream and lymphatic system [14].

Tuberculous meningitis develops in two stages. Mycobacterium Tuberculosis enters the human body through inhalation of a droplet. Localized infection grows rapidly in the lungs and spreads to regional lymph nodes [7], reaching the bloodstream and spreading to other parts of the body. Microtubercles are formed when the bacteria travel to the Meninges (layers that protect the brain) [11] and brain tissue. These Microtubercles can burst and cause Meningitis Tuberculosa. This can be acute or chronic, resulting in increased skull pressure resulting in serious damage to the nerve and brain tissue [8]. The structural portion of Mycobacterium Tuberculosis bacilli is classified as Tuberculosteraic acid [6] (IUPAC: 10 – Methyloctadecanoic acid) [5].

PATHOPHYSIOLOGY

At the initial stage, the Mycobacterium Tuberculosis bacilli enter the human body by droplet inhalation, the initial point of infection being the alveolar macrophage. Localized infection escalates throughout the lung and spreads to primary complex producing area lymph nodes. There is a presence of brief but important bacteremia during this stage which can seed tubercle bacilli into other organs in the human body. For those persons who acquire Tuberculous Meningitis, after the original pathological studies of Rich and McCormick [14], small subpial or subependymal foci called Rich Foci are developed by the bacilli seed to meninges or brain parenchyma [6,12].

The size of the rich concentration is increased during the second stage until it splits into the subarachnoid space [6,12]. This indicates the onset of meningitis which results in serious and irreversible neurological pathology if left untreated [12]. Inflammation is caused by the development of a thick gelatinous exudate which infiltrates the vessels of the cortical or meningeal blood [7]. This exudate develops and spreads along with the growth of focal and diffuse ischemic and brain infarction due to vasculitis, with small proliferating blood vessels. Entrapment of large cerebral arteries, including large artery vasculitis, contributes to infarction.

The exudate envelops the arteries and cranial nerves, resulting in obstruction of cerebrospinal fluid flow at tentorial opening level, leading to hydrocephalus. Tuberculomas can be combined to form granulomas.
Complications of tuberculosis meningitis are hydrocephalus and tuberculoma [14]. Multiple small cerebral and spinal tuberculomas are found when tuberculous meningitis is an indication that military tuberculosis is present [15]. The bacilli may also cross the Blood-Brain Barrier and enter the Cerebro Spinal Fluid (CSF), which helps to control intracranial pressure and functions as a hydraulic shock absorber [10,11].

CLINICAL MANIFESTATIONS

  • Fever and Chills
  • Altered Sensorium
  • Photophobia (Sensitivity to Light)
  • Severe Headache
  • Stiff Neck (Meningismus)
  • Agitation
  • Unusual Posture
  • Fatigue
  • Lethargy
  • Unconsciousness
  • Loss of appetite
  • Tiredness

RISK FACTORS

  • HIV/AIDS
  • Excessive ALCOHOL Use
  • Weakened Immune System
  • Diabetes Mellitus
  • Immigrants
  • Children Less than 5 yrs of Age
  • Advancing Age

CONCLUSION

Proper details, along with medication descriptions, must be given to the patient about the current medical condition. Infection eradication with an increase in signs and symptoms. Because the patient is hypertensive, dietary sodium intake must be limited to 1.5 g / day, with the cessation of alcohol and smoking. Diabetes mellitus and chronic kidney disease are reduced in the amount of sugar and protein intake.

REFERENCES

  1. Arnold Lentnek, Meningitis – tuberculous [Internet] Medlineplus Medical Encyclopedia. 2016 [updated 2016 Nov 27; cited 2018 Nov 21]. Available from: https://medlineplus.gov/ency/article/000650.htm
  2. Tuberculous Meningitis [Internet] Medical Definition.2018 [cited 2018 Nov 21]. Available from: https://www.medilexicon.com/dictionary/54120
  3. James McIntosh, All you need to know about Tuberculosis [Internet] Medical News Today. 2017 [updated 2017 Nov 27; cited 2018 Nov 22]. Available from: https://www.medicalnewstoday.com/articles/8856.php
  4. H. Mohan. Textbook of Pathology.7th ed. Delhi: Jaypee; 2014.Chapter 6, Inflammation and Healing; p.149-152
  5. Morrison R. T, Boyd R. N. Organic Chemistry. 6th ed. Delhi; Pearson; 2007. Chapter 33, Lipids, Problem – 8; p.1300
  6. G. L French, C. Y Chan, S.W Cheung, et al. Diagnosis of Tuberculous Meningitis by detection of Tuberculostearic acid in Cerebrospinal Fluid. The Lancet. 1987 Jul 18; 330(8551):117-119 doi:10.1016/S0140-6736(87)92328-2
  7. Tarakad. S. Ramachandran, Tuberculous Meningitis [Internet] Medscape. 2017 [updated 2017 Dec 02; cited 2018 Nov 22]. Available from: https://emedicine.medscape.com/article/1166190-overview#a2
  8. TB Meningitis[Internet] Meningitis Now. 2018 [updated 2018 July; cited 2018 Nov 22]. Available from: https://www.meningitisnow.org/meningitis-explained/what-is-meningitis/types-and-causes/tb-meningitis/
  9. Barbara G. Wells, Joseph T. DiPiro, Terry L. Schwinghammer, Cecily V. DiPiro. Pharmacotherapy Handbook. 9th ed. United States of America: McGraw Hill Education; 2015. Chapter 49, Tuberculosis; p.476
  10. Gerard J. Tortora, Derrickson B, Anatomy and Physiology. 2014 India ed. New Delhi: Wiley: 2014. Chapter 14, The Brain and Cranial Nerves; p.440-445
  11. Satyanarayan U, Chakrapani U. Biochemistry. 3rd ed. Delhi; Books and Allied; 2012. Chapter 22, Tissue Proteins and Body Fluids; p.497
  12. Thwaites G, Chau TT, Mai NTH, et al. Tuberculous Meningitis. Journal of Neurology, Neurosurgery & Psychiatry 2000;68:289-299. doi:10.1136/jnnp.68.3.289
  13. K. Ilango, P. Valentina. Textbook of Medicinal Chemistry. Vol 2. 2nd ed. Chennai: Keerthi Publishers; 2015. Chapter 4, AntiTubercular agents; p.69
  14. AR Rich, HA McCordick. The pathogenesis of tuberculous meningitis. Bulletin of John Hopkins Hospital 1933;52:5–37
  15. Mei Ling Sharon Tai, Tuberculous Meningitis: Diagnostic and Radiological Features, Pathogenesis and Biomarkers. Neuroscience and Medicine.2013 Jun 18; 4:101-107. doi:10.4236/nm.2013.42016
  16. Garg R. K, Malhotra H. S, Jain A. Neuroimaging in tuberculous meningitis. Neurology India. 2016; 64(2):219-227 doi:10.41030028-3886.177608
  17. Burke D, Luo E, Meningeal Tuberculosis [Internet]. 2017 [updated 2017 May 09; cited 2018 Nov 22]. Available from: https://www.healthline.com/health/meningitis-tuberculosis

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Diphtheria: Clinical Manifestations and Treatment

Diphtheria is a severe bacterial infection which typically affects nose and throat mucous membranes. This usually triggers a sore throat, cough, swollen glands, and fatigue, but the main symptom is a layer of thick, a grey substance that covers the back of the throat that blocks the airway and triggers a person to struggle for breath.

TYPES

DIPHTHERIA

Diphtheria is a severe bacterial infection which usually affects nose and throat mucous membranes.

CUTANEOUS (SKIN) DIPTHERIA

The second form of diphtheria may affect the skin, resulting in the normal pain, redness and swelling associated with other infections of the bacteria. Ulcers that are filled with a grey the membrane can also grow in cutaneous diphtheria.

PATHOPHYSIOLOGY

Diphtheria adheres to mucosal epithelial cells where the endosomal released exotoxin causes a localized inflammatory reaction that is accompanied by tissue degradation and necrosis. The toxin is composed of two joined proteins. The B fragment binds on the surface of the susceptible host cell to a receptor, which proteolytically cleaves the membrane lipid layer allowing segment A to enter.

Molecularly, it is suggested that the cellular susceptibility is also due to modification of diphthamide, dependent on types of human leukocyte antigen (HLA) predisposing to more severe infection. The diphthamide molecule is present in all eukaryotic species and is located on a translation elongation factor 2 (eEF2) histidine residue. EEF2 is responsible for altering this residue of histidine and is the basis for diphtheria toxin (DT).

Fragment A inhibits the transfer of amino acid from RNA translocase to the ribosomal amino acid chain, thus inhibiting protein synthesis is required for normal functioning of the host cell. DT triggers the catalytic transfer of NAD to diphthamide, which inactivates the elongation factor, resulting in the inactivation of eEF2, resulting in blockage of protein synthesis and subsequent cell death. Regional tissue damage enables the lymphatic and haematological transfer of the poison to other areas of the body. Diphtheria toxin development can affect distant organs like the myocardium, kidneys, and nervous system.

CAUSES

  • Airborne droplets
  • Contaminated personal items
  • Contaminated household items

CLINICAL MANIFESTATIONS

  • A thick, grey membrane covering your throat and tonsils
  • A sore throat and hoarseness
  • Swollen glands (enlarged lymph nodes) in your neck
  • Difficulty breathing or rapid breathing
  • Nasal discharge
  • Fever and chills
  • Malaise

RISK FACTORS

  • Children and adults who don’t have up-to-date immunizations
  • People living in crowded or unsanitary conditions
  • Anyone who travels to an area where diphtheria is endemic

COMPLICATIONS

  • Breathing problems: The bacteria that cause diphtheria can produce a toxin. In the immediate region of infection, this toxin destroys the tissue — typically the nose and throat. The infection at this site creates a thick, grey-coloured membrane made up of dead cells, bacteria, and other substances. This membrane can inhibit respiration.
  • Heart damage: The diphtheria toxin can spread through the bloodstream and affect other tissues in the body, including heart muscle, causing complications such as heart muscle inflammation (myocarditis). Heart damage from myocarditis can be mild, showing up on an electrocardiogram as minor anomalies, or severe, leading to congestive heart failure and sudden death.
  • Nerve damage: The toxin can also cause damage to the nerves. Typical targets are the throat’s nerves, where poor nerve conduction can cause swallowing difficulty. Nerves to the arms and legs can also get inflamed, leading to muscle weakness. When Cutaneous diphtheria toxin affects the nerves that help regulate the muscles used in breathing, it can paralyze these muscles. For a respirator or other tool, respiration can then become difficult to help with breathing.

TREATMENT

ANTITOXIN

An antitoxin is given to the infected infant or adult. The antitoxin, which is injected into a vein or muscle neutralizes the already circulating diphtheria toxin within the body.

ANTIBIOTICS

Diphtheria is also treated with antibiotics, such as penicillin or erythromycin. Antibiotics help destroy bacteria in the body, clearing up infections.

MANAGEMENT

  • Eating a healthier diet
  • Maintaining a healthy weight
  • Quitting smoking
  • Exercising regularly
  • Managing stress

PREVENTION

Usually, the diphtheria vaccine is paired with tetanus vaccinations and whooping cough (pertussis). Diphtheria, tetanus, and pertussis vaccine is known as the three-in-one vaccine. The latest version of this vaccine is named the children’s DTaP vaccine, and the teenage and adult Tdap vaccine.

BOOSTER SHOTS

After the initial series of childhood immunizations, diphtheria vaccine booster shots are required to help keep you safe. This is because, over time, the immunity to diphtheria disappears. Children who received all the necessary vaccines before age 7 would receive their first booster shot at around age 11 or 12. 10 years later, the next booster shot is prescribed, and then repeated at intervals of 10 years. Booster shots are particularly useful when you’re travelling to an area where diphtheria is common.

Tetanus booster — the tetanus-diphtheria (Td) vaccine — is paired with the diphtheria booster.
This combination vaccine is delivered by injection, normally into the arm or leg. Tdap is a combination vaccine against tetanus, diphtheria and acellular pertussis (whooping cough). It’s a one-time substitute vaccine for teenagers aged 11 to 18 and adults who haven’t had a Tdap booster before. This is also recommended for someone who is pregnant, regardless of previous vaccination status.

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