Paragonimus

Paragonimiasis is a zoonotic infection caused by a highly evolved parasite with a complex life cycle that includes at least three hosts. Two intermediate hosts, a snail and a crustacean, and a mammalian definitive host are necessary to complete the life cycle of this parasite. Human and animal infections result from the consumption of raw or undercooked crustaceans (i.e., the second intermediate host) or through consumption of raw or undercooked meat from a paratenic host. Paragonimus is the only human parasite where the adults reside in the human lung. The genus Paragonimus is highly successful and is endemic in Asia, Africa, and the Americas. Paragonimus kellicotti is the species endemic to North America. Physicians in countries without endemic disease may encounter patients with paragonimiasis who have immigrated with the disease or who contracted the disease while traveling or through ingestion of imported contaminated food. Many infections are subclinical and cause only mild disease. Sometimes, however, severe infections occur and may be fatal. Two of the five patients with P. kellicotti infections that have been reported over the past three decades were associated with relatively severe disease. These patients required surgery, with one requiring a second course of praziquantel. The most recently reported patient had a remote P. kellicotti infection, but the residual pleural effusion caused by the Paragonimus infection became infected by bacteria and directly contributed to his demise.

The diagnosis of paragonimiasis should be considered when the appropriate clinical signs and symptoms, radiologic findings, and food history are supportive. Cough and hemoptysis are the most common presenting symptoms in patients with paragonimiasis. Diagnosis may be achieved through the demonstration of the characteristic operculate eggs in respiratory secretions, stool, or tissue biopsy specimens. Immunodiagnostics are excellent tools for assisting with the diagnosis of imported paragonimiasis, particularly for patients who do not have demonstrable eggs in clinical specimens. The utility of immunodiagnostics for detecting infections caused by P. kellicotti remains to be determined. Praziquantel is an effective treatment, but surgery may be necessary for patients with complicated pleural disease or cerebral paragonimiasis. Control of paragonimiasis in animals is impractical because of wild animal reservoirs, but in humans infections may be averted through the avoidance of certain foods and by thorough cooking. Crayfish in North America may harbor P. kellicotti and therefore should be thoroughly cooked prior to consumption.

Sleep deprivation, dopamine and addictive behaviors

For a number of years now science has born out linkages between sleep deprivation, compulsive actions and addictive behaviors.

I googled, “sleep deprived hedonic desires” and was met with many first quality links. The following are a handful from the first page of search results.

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3763921/

https://www.nature.com/articles/ncomms3259

https://www.medicalnewstoday.com/articles/307203.php#2

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4597336/

Be Easy! – mJL

why do statins work and what on?

Statins work because they are antimicrobial. Stopping the microbial process results in there not being what they call cholesterol from being used to repair the microbial damage. We also call it scar tissue.

1. Bacteria
2. Archaea
3. Fungi
4. Protazoa
5. Algae
6. Viruses

If you have use for statins in your body it is because you have one, some or all of these overgrowing in or on your person. So not really a waste of time if you have one of these living in or on you.

Just sayin…Statins might be the lesser of the evils.

Unexpected antimicrobial effect of statins

Is There Potential for Repurposing Statins as Novel Antimicrobials?

How do statin drugs affect aging?

https://www.ncbi.nlm.nih.gov/pubmed/29085751

Carpal tunnel syndrome caused by cysticercosis

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3010786/

ABSTRACT: We present a case of carpal tunnel syndrome (CTS) due to compression of the median nerve within the carpal tunnel, caused by cysticercosis. Nerve conduction studies revealed severe CTS. Magnetic resonance imaging suggested an inflammatory mass compressing the median nerve in carpal tunnel. The histological diagnosis was consistent with cysticercosis. The case resolved with conservative treatment. Such solitary presentation of entrapment median neuropathy as CTS caused by cysticercosis is extremely rare. To our knowledge, this is the only case of its kind reported in literature till date.

Keywords: Carpal tunnel syndrome, cysticercosis, entrapment neuropathy, median nerve

INTRODUCTION: Carpal tunnel syndrome (CTS) is a constellation of signs and symptoms resulting from compression of the median nerve in the carpal tunnel.[1] CTS is the most commonly encountered entrapment neuropathy with an incidence of 139 per 100,000 person-years for men and 506 per 100,000 person-years for women.[2] The classic symptoms of CTS are numbness and paraesthesia in the first three fingers of the hand, which is commonly exacerbated at night.[3] The diagnostic signs include sensory loss along the lateral aspect of the hand, motor weakness and wasting of abductor pollicis brevis (APB) muscle and eliciting Tinel’s and Phalen’s sign at the wrist.

The nerve conduction study (NCS) study is a definite diagnostic test for CTS, with a high degree of sensitivity and specificity(4). Taenia solium, the pork tapeworm is endemic in Mexico, Central and South America, Africa, India, Pakistan and China. Human cysticercosis is caused by dissemination of embryos of T. solium from the intestine via the hepatoportal system to the tissues and organs of the body.[5] Apart from the involvement of the central nervous system, subcutaneous tissue and muscle by cysticercosis, less frequently, cysticerci may localise in other organs like eyes, tongue, oral cavity, breast, heart and lungs.[68]

We present a case of CTS due to compression of the median nerve within the carpal tunnel, caused by cysticercosis.

CASE REPORT: A 38-year-old man presented with progressively worsening tingling, pins and needles in the radial four digits, loss of strength and awakening nocturnal pain in the right hand of 2 years duration. Physical examination showed swelling measuring 3–4 cm over volar aspect of the wrist. A mild thenar atrophy was observed and phalen’s test and tinel’s sign were positive. NCS of the median nerve revealed an absence of digit to wrist sensory Nerve Action Potential (NAP) on the right side and distal motor latency was 6.2 ms. Needle Electro Myo-graphy findings included fibrillation activity, decreased recruitment and abnormalities (large and long duration polyphasic Motor Unit Potentials (MUPs) in configuration of MUPs. The left hand was neurophysiologically intact. Both clinical symptoms and signs and neurophysiological tests [according to American Association of the Electro diagnostic Medicine (AAEM) criteria] showed severe CTS in right hand, while the left hand was completely healthy, implying a secondary disease. Magnetic resonance imaging (MRI) [Figure 1] with contrast revealed a sharply defined elliptical mass enhancing with contrast, in the deep palmar space extending into the carpal tunnel and compressing the median nerve. Fine needle aspiration cytology revealed a chronic inflammatory mass infiltrated with predominantly macrophages and lymphocytes and parasitic fragments, consistent with cysticerosis. Cysticercus serology was positive. He was started on a short course of steroids for 2 weeks, along with nonsteroidal anti-inflammatory drugs. The hand was put on a splint and physiotherapy was started. There was remarkable improvement in symptoms with reduction of swelling size. Although surgical excision was initially planned, since he improved by conservative management alone, it was abandoned. He became asymptomatic and his deformity completely corrected in 2.5 months of follow-up.

It is widely known that idiopathic CTS usually presents with bilateral symptoms.[911] In patients who present with unilateral symptoms, 38–50% were reported to have positive electro diagnostic test results in the asymptomatic, contralateral hand.[12] CTS is the most common entrapment neuropathy, with a prevalence of 10–20% for symptoms in the population-based studies.[13] Space-occupying lesions are known to cause CTS and the incidence of space-occupying lesions in unilateral CTS is higher than that in bilateral CTS.[14] Cysticercosis is a systematic illness caused by dissemination of the larval forms of the pork tapeworm, T. solium. Man is the definitive host for T. solium, and humans acquire this disease by ingesting the eggs of T. solium from food or water contaminated by human faeces or autoinfection. The larvae enter the bloodstream, migrate, and encyst in tissue, usually striated muscle or brain. Less frequently, cysticerci may localise in other organs. The encysted larvae may remain asymptomatic or may provoke granulomatous inflammatory response depending on the anatomical site.[5]

The presenting muscle symptoms of cysticercosis vary greatly. Unlike ceberal disease, muscle cysticercosis is not grave but can cause morbidity of varying severity.[15,16] Most of the patients are asymptomatic, and characteristic elliptical, calcified lesions are detected incidentally on plain X-Ray films of the extremities. It can also present as acute myositis as a result of a host inflammatory response to dying larvae, as mass lesions, myopathy, or rarely as muscular pseudo hypertrophy, depending on the parasite burden.[15]

Apart from peripheral neuropathy, cranial nerve neuropathies caused by cysticerosis, involving the second, third, fourth and fifth cranial nerves, have been described in the literature.[1718]

Investigations in entrapment neuropathy cases are directed to confirm the area of entrapment and to document the extent of the pathology. Cysticerci are rarely seen in plain radiographs as multiple fusiform, cigar shaped calcifications within the muscles or as multiple punctuate soft tissue calcifications. MRI is far superior to computed tomography in detecting and evaluating the stage of cysticercosis.[19] The radiographic appearance of cysticercosis correlates with its pathological features and reflects the stage of maturation of the disease. Initially, when the parasite is viable, a fluid-filled cyst without peripheral enhancement is observed. Later, as in our case, peripherally enhancing cystic lesions after gadolinium injection are observed and correlate with the inflammatory host-tissue response that occurs during leakage of fluid or during death of the parasites associated with varying amounts of oedema. The final radiographic appearance is that of an elliptical, non–fluid-filled, calcified lesion. The role of MRI is increasing in diagnosing entrapment neuropathies and other pathological conditions of the wrist. Definitive diagnosis requires histopathological demonstration of the cysticercus. A needle or an open biopsy is used in determining the aetiology of cutaneous and muscular nodules.[18] It should be emphasised, however, that the appearance of the parasite varies with the degree of cyst degeneration or the plane of sectioning. In our case, we found a dense accumulation of mononuclear cells probably representing vigorous granulomatous inflammatory response to dying larvae. Serological diagnosis of cysticercosis gives additional clues to the diagnosis as in our case.

In cases of entrapment neuropathy, conservative approach in the form of limb positioning using splints, physiotherapy and anti-inflammatory drugs is tried initially. Surgical intervention is indicated if increasing paraesthesia occurs despite adequate conservative treatment and at the first sign of motor changes. For symptomatic cysticercus cysts outside the central nervous system, the most favourable approach is surgical resection. Hence, in our case, although initially surgical approach was planned, surgical intervention was withheld as the case showed dramatic improvement with conservative management.

CONCLUSION: In endemic countries, cysticercosis can have an extremely varied presentation and should be a part of differential diagnosis while evaluating CTS. Imaging studies, especially MRI, which are usually not used in idiopathic CTS should be remembered in patients with unilateral symptoms, especially with a long history and when the symptomatic hand shows severe neurophysiological impairment. Early identification of the cause of CTS is essential as early appropriate intervention helps to avoid surgery and promotes complete recovery.

A Topical Gel From Flax Seed Oil Compared With Hand Splint in Carpal Tunnel Syndrome: A Randomized Clinical Trial

https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5871162/

ABSTRACT: This study compared the therapeutic effect of flax seed oil topical gel and hand splint in the treatment of carpal tunnel syndrome. This study was a randomized clinical trial. Forty-nine patients, 96 hands, with mild to moderate idiopathic carpal tunnel syndrome were divided into 2 groups randomly. One group was treated by topical gel and the other group by hand splint. Intensity of symptoms and function before and after intervention was measured via Boston Carpal Tunnel Questionnaire. After intervention, the ANCOVA showed a significant difference between the symptom and function scores of the 2 groups. In both cases, recovery was higher in the gel group (P < .001). The topical use of flax seed oil gel is more effective in the improvement of symptoms and function of patients with mild to moderate carpal tunnel syndrome as compared with hand splint, and it can be introduced as an effective treatment.

Keywords: Persian medicine, carpal tunnel syndrome, flax seed oil

CONCLUSION: The results showed that for patients with the clinical and electro-diagnostic diagnosis of mild to moderate idiopathic carpal tunnel syndrome, topical application of flax seed oil gel, twice a day for 3 weeks, was more effective than a hand splint for short-term reduction of symptoms and functional improvement. This method can be introduced as an effective and supportive alternative treatment for patients who are unwilling to use a hand splint. It should be mentioned that further studies are needed for determining the long-term effects of the proposed method.

MY CONCLUSION: Carpal Tunnel: It’s Dermal Origins

Psoriasiform Dermatoses: Microscopic Approach

~Content Source

Psoriasiform dermatoses often pose challenges to both dermatologists and pathologists alike. With proper clinicopathologic correlation and a systematic approach, it is possible to arrive at a specific diagnosis in most cases. This article attempts to outline a practical, step-wise method of looking at these cases and highlights some important clues in individual conditions.

Keywords: Histopathologypsoriasiform dermatosespsoriasis


What was known?

1. Psoriasiform dermatoses comprise of a wide variety of diseases that resemble each other both at clinical and histologic levels.

2. Correct diagnosis is reached with good clinico-pathologic correlation.


Psoriasiform dermatoses (PD) encompass a wide array of diseases, some of which show both clinical and histologic overlap. It is an intimidating task even to experienced microscopists to give a precise diagnosis every time and one relies heavily on clinical correlation. However, it is possible to assign specific diagnoses in most cases with a logical, systematic approach. Many textbooks give detailed descriptions about individual diseases and this review does not attempt to replicate them.[1,2] This article outlines the microscopic approach and emphasizes certain important principles and clues that should always be at the back of one’s mind when evaluating these cases.

Psoriasis literally mean “itchy condition,” derived from Greek.[3] Psoriasiform pattern is defined histologically by the finding of elongated rete ridges of roughly equal length, which alternate with long dermal papillae. According to Ackerman et al., psoriasiform pattern forms a major subset of perivascular dermatitis, the largest group of inflammatory skin diseases.[3] Perivascular dermatitis can be associated with epidermal changes such as psoriasiform, interface/lichenoid, ballooning or spongiotic patterns. Often, these changes are found in combination and the components of this mixture give important clues to the correct diagnosis. PD can be broadly classified as:

  1. Psoriasiform only: Even or uneven psoriasiform
  2. Combinations: Psoriasiform lichenoid, Spongiotic psoriasiform, Spongiotic psoriasiform lichenoid

These can be further deciphered based on the dominant inflammatory cell infiltrate i.e., lymphocytes only or admixture with other cells such as eosinophils, histiocytes or plasma cells. These, coupled with a detailed, stepwise analysis of findings beginning right from the top of the stratum corneum, help one arrive at the right diagnosis.

Stratum corneum often holds the most important but often subtle features that aid diagnosis. It mirrors the temporal evolution of a disease. The normal basket-weave pattern is lost in most PD and it is common to find parakeratosis. Parakeratosis refers to the presence of nuclei within the cornified layer and is the consequence of a rapid turnover of the epidermal keratinocytes, instead of the usual 4 weeks.[3] The presence of a normal basket-weave pattern above this indicates a recent onset.

Parakeratosis can be present in small mounds or may be broad and confluent.[3] Often, it is associated with collections of neutrophils and/or plasma, called “scale crust.” Mounds of parakeratosis can be present throughout the epidermis in conditions like psoriasis and dermatophytosis, confined to the infundibular ostia (Seborrheic dermatitis) or seen in both locations, like in pityriasis rubra pilaris (PRP).[1,2,3] The classic “checkerboard” pattern of PRP i.e., parakeratosis staggered in both vertical and horizontal fronts is often difficult to find, even on multiple sections [Figure 1a].[1] Confluent parakeratosis is seen in dermatophytosis, syphilis, pityriasis lichenoides chronica and most importantly, in mycosis fungoides (MF). Sharply defined, thick zones of parakeratosis alternating with orthokeratosis and mild papillomatosis is a feature of inflammatory linear epidermal nevus (ILVEN).[3] Crowding and atypia of parakeratotic nuclei is seen in Bowen’s disease.[4]

When parakeratosis with neutrophils is seen beneath a basket-weave cornified layer, one has to look carefully for the presence of fungal hyphae. One must remember that large amounts of plasma and a rapidly proliferating epidermis are hostile to fungi, which prefer the comfort of the niche just below the orthokeratotic zone, constituting the “sandwich” sign.[5] It is useful to lower the condenser of the microscope when attempting this, as the hyphae are better seen. Parakeratosis with neutrophils is seen alternating with zones of orthokeratosis vertically, reflecting the periodicity of eruptive/guttate psoriasis [Figure 1b]. Significant amounts of plasma in the scale crust go against a diagnosis of psoriasis, except on volar skin. Debris and fragments of mites are frequently seen in Norwegian scabies.[1]

Stratum corneum is completely absent in diseases with a markedly accelerated epidermal turnover, clinically presenting as erythroderma. This is commonly seen in psoriasis, MF, and sometimes, in PRP.[1,3]

Diminished or absent granular layer is seen in classic psoriasis. But, classic psoriasis is rarely biopsied. What one sees under the microscope are clinically atypical or treated, unresponsive lesions. In such instances, the granular layer may be normal or thickened, as in other diseases like pityriasis rosea (PR), lichen simplex chronicus or allergic contact/nummular dermatitis.[1,6] Too much stress should not be placed on this feature.

Pallor of keratinocytes in the upper epidermal layers is seen in psoriasis, PR and most importantly, in certain nutritional deficiency diseases [Figure 1c].[1,3,7] In psoriasis, pallor is mediated by neutrophils that migrate through the epidermis into the stratum corneum.[3] Presence of neutrophils in between keratinocytes with early spongiosis indicates either psoriasis or dermatophytosis. In diseases like pellagra, acrodermatitis enteropathica and glucagonoma syndrome, the keratinocytes appear extremely pale due to accumulation of glycogen.

Although psoriasis is primarily spongiotic, it never eventuates in the formation of spongiotic vesicles. The finding of spongiotic vesicles in a PD are seen in allergic contact/nummular dermatitis and seborrheic dermatitis. These begin as purely spongiotic diseases in the early phase and psoriasiform hyperplasia develops in the subacute and chronic phases. In seborrheic dermatitis, the finding of scale crusts at the dilated infundibular openings accompanied by spongiosis points to the diagnosis.[1,3] Spongiotic psoriasiform pattern is also encountered in patch-stage MF.[3Table 1 summarizes some of the important differentiating microscopic features in common PD.

Psoriasis is characterized by thinning of supra-papillary plates and elongated dermal papillae that contain dilated, tortuous capillaries. This is in keeping with the “squirting papilla” concept that explains its pathogenesis.[8] The presence of extravasated erythrocytes is a sign of acuteness and is seen in eruptive psoriasis and PR.[3]

Vertical streaks of collagen with uneven psoriasiform acanthosis and compact orthokeratosis is diagnostic of lichen simplex chronicus (LSC).[1,3] In fact, the biopsy resembles volar skin on scanning magnification, except for the presence of pilosebaceous structures, giving rise to the “hairy palm” sign [Figure 1d].[9] Changes of LSC can be superimposed on any chronic, itchy dermatitis including psoriasis. In contrast, thin haphazard, wiry bundles of collagen are seen in the papillary dermis in PLC and MF. This finding reflects the chronicity of the infiltrate and one should look carefully for other features of early MF.

Most PD are dominated by lymphocytes in the dermis. When one meets eosinophils among them, it indicates allergic/contact dermatitis or a drug eruption. However, eosinophils are not a pre-requisite for diagnosis of either of these conditions.[1,3] Histiocytes and plasma cells in a PD with scale crusts should ring a bell for secondary syphilis.[1,3] It is also common to find some ill-formed granulomas in such instances and special stains for spirochaetes must be employed. However, plasma cells are absent in early lesions.[3]

Superficial and deep infiltrates are seen in syphilis and lichen striatus (LS).[3] In LS, there is a psoriasiform lichenoid pattern with deep infiltrates of lymphocytes along the adnexae, specially so around the eccrine glands.

Classic psoriasis is rarely biopsied, as stated earlier. Problems arise in interpretation of treated lesions. In a study of treated psoriasis by Boer, et al., dilated, tortuous capillaries emerged as the most reliable sign of psoriasis in all its stages and forms.[6] This is retained even when the granular layer and supra-papillary plates have returned to normal. On the scalp, psoriasis is accompanied by papillomatosis, atrophy of sebaceous glands and necrotic keratinocytes in the epidermis, features helpful in distinction from seborrheic dermatitis.[10]

Psoriasis on volar skin shows large amounts of plasma in the scale crust and is difficult to tell apart from allergic contact/dyshidrotic dermatitis. In such an instance, one should look for the tortuous dermal capillaries and presence of neutrophils in the epidermis. Neutrophils are not seen in allergic contact dermatitis, unless the lesions are secondarily infected due to excoriation.[3] But, in practice, it is not very easy to render a specific diagnosis every time. One must recall that finding significant numbers of eosinophils is not a feature of psoriasis and is absent, even when it is triggered by a drug.[11] Pustular psoriasis is also a teaser, especially when occurring de novoand classic changes may not be found. Finding neutrophils amidst the keratinocytes at the periphery of the pustule is helpful, together with tortuous dermal vessels.[12]

In patients with a predisposition to psoriasis, its histologic changes are seen even with other dermatologic conditions, the most important being with MF. It is important to recognize both the conditions. This process is a result of Koebnerization.[3]

There are some diseases that appear identical under the microscope, but can be told apart clinically. The most important group includes allergic contact dermatitis, nummular dermatitis, id reaction, dyshidrotic dermatitis (pompholyx) and photoallergic dermatitis.[3] Allergic contact dermatitis corresponds to the site of its trigger. Nummular dermatitis appears as discoid/coin-shaped lesions. Pompholyx occurs on acral skin, at the side of the digits while photoallergy is seen in sun-exposed sites like the V of the neck. “Actinic reticuloid” histologically is photoallergic dermatitis with superimposed LSC-like changes.

PR and erythema annulare centrifugum are histologic twins and one has to go back to the clinical presentation.[3]

The most important condition in this category is MF. Virtually every combination of patterns, i.e., psoriasiform, spongiotic psoriasiform, psoriasiform lichenoid and spongiotic psoriasiform lichenoid is seen in MF.[3] Mild to moderate amounts of spongiosis is seen, but never to the extent ending in vesiculation. The most important feature is the presence of lymphocytes in the epidermis disproportionate to the amount of spongiosis. These are disposed in a linear fashion along the basal layer and may also be present in a pagetoid fashion, reaching almost up to the granular layer.[13] Other signs like dermal papillae stuffed with lymphocytes, wiry collagen, absence of dermal edema also help.[12] It cannot be overemphasized that this diagnosis should be made in the right clinical context and never on a single biopsy specimen. If there are features suspicious for MF, it is prudent to request repeat biopsies from multiple, preferably non-sun exposed sites for a specific diagnosis. Ancillary tests like immunostains and T-cell gene rearrangements are often futile in early lesions.

Psoriasiform hyperplasia can occur over a dermatofibroma [Figure 2a].[3] Bowen’s disease also shows psoriasiform acanthosis and is generally not difficult to pick up as the keratinocyte atypia is striking. Clear cell acanthoma is a rare tumor with a psoriasiform appearance [Figure 2b]. There are broad, uneven rete ridges with marked pallor of the keratinocytes throughout the epidermal thickness.[14]

One may also find some neutrophils and nuclear debris in the spinous layer.

  1. Use a step-wise, logical approach.
  2. Start with scanning magnification: Uneven vs. even psoriasiform, purely psoriasiform or combination of epidermal patterns.
  3. Spend time in examining the stratum corneum, especially to elicit subtle changes.
  4. Observe changes in the rest of the epidermis, particularly the follicular infundibula.
  5. Determine the nature of the inflammatory cell infiltrate and its depth.
  6. Pay attention to the changes in dermal vasculature.
  7. Don’t forget that MF and drugs can mimic any of these patterns.
  8. Be aware of the temporal evolution of lesions, their pitfalls and simulators.
  9. Never sign out a PD without employing fungal stains.
  10. Look at the clinical findings AFTER you have made a preliminary impression and note the site of the biopsy, this is the simplest tool for clinico-pathologic correlation.
  11. If one is unable to arrive at a specific diagnosis despite all this, give descriptive reports using language understood by the dermatologist. This should include the epidermal pattern and nature of the infiltrate, at least.
  12. Remember that the terms acute, subacute and chronic are clinical and their use in histopathology reports do not reflect specificity. For example, psoriasiform spongiotic pattern with lymphocytes is far better than saying “chronic dermatitis.” To the clinician, who has access to the complete history and clinical findings, this implies allergic/contact dermatitis and he will proceed accordingly.
  13. When in doubt, ask. Incomplete requisition forms are a major problem faced by pathologists world over and it is important to pick up the phone and obtain that missing piece of information that will solve the puzzle.

The features described above are neither complete nor exhaustive. The approach outlined here is simple, practical and repeatable. It cannot be emphasized too much that the bottom-line of a good histopathology report is clinico-pathologic correlation and the pathologist should take the onus of signing out meaningful reports.

What is new?

1. A stepwise, systematic histopathologic approach enables one to arrive at a specific diagnosis in most cases of PD.

2. Stratum corneum holds a lot of subtle, but important clues, which should be elicited carefully.

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Spongiosis

Spongiotic reaction pattern is characterised by inter and intracellular oedema of the epidermis and elongation of the intercellular bridges.

Progressive psoriasiform hyperplasia occurs with chronicity.

In the past this reaction pattern was known as ‘eczematous tissue reaction’.

The spongiosis may vary from microscopic foci to grossly visible vesicles.

Inflammatory cells are present in the dermis and their distribution and type may aid in making a specific diagnosis.

Five patterns of spongiosis :

1. Neutrophilic spongiosis (where there are neutrophils within foci of spongiosis)

Example- Pustular Psoriasis

2. Eosinophilic spongiosis (where there are numerous eosinophils within foci of spongiosis).

Example- Bullous Pemphigoid

3. Miliarial (acrosyringial) spongiosis (where edema is related to the acrosyringium).

Example – Miliaria Rubra.

4. Follicular spongiosis (where the spongiosis centered on the follicular infundibulum.

Example – Infundibulofolliculitis

5. Haphazard spongiosis (other spongiotic disorders in which there is no particular pattern).

Example- Spongiotic Drug Reaction


1. Neutrophilic spongiosis (where there are neutrophils within foci of spongiosis)

Examples of Neutrophilic Spongiosis:

Pustular psoriasis;

IgA pemphigus;

Palmoplantar pustulosis;

Dermatophytosis/candidosis;

Acute generalized exanthematous pustulosis.

2. Eosinophilic spongiosis (where there are numerous eosinophils within foci of spongiosis)

Examples of Eosinophilic Spongiosis:

Pemphigus (precursor lesions)

Pemphigus vegetans

Bullous Pemphigoid

Arthropod bites

Allergic contact dermatitis

Eosinophilic folliculitis

Incontinentia pigmenti (first stage)


3. Miliarial (acrosyringial) spongiosis (where edema is related to the acrosyringium).

Example: Miliaria

4. Follicular spongiosis (where the spongiosis centered on the follicular infundibulum

Example: Infundibulofolliculitis, atopic dermatitis

5. Haphazard spongiosis (other spongiotic disorders in which there is no particular pattern).

Other Spongiotic Disorders:  

Irritant contact dermatitis

Allergic contact dermatitis Image

Nummular dermatitis ; Dermatopathology Case 122

Seborrheic dermatitis ;

Atopic dermatitis ;

Pityriasis rosea;

Stasis dermatitis ;

Chronic superficial dermatitis ;

Spongiotic drug reaction.

Histopathological features of some spongiotic diseases:  

Irritant contact dermatitis:  

Superficial ballooning, necrosis and neutrophils; mild irritants produce spongiotic dermatitis mimicking allergic contact dermatitis.

Allergic contact dermatitis:

Variable spongiosis and vesiculation at different horizontal and vertical levels, mild exocytosis, progressive psoriasiform hyperplasia with chronicity.

Superficial dermal oedema and eosinophils in superficial dermal infiltrate.

Seborrheic dermatitis:

Variable spongiosis and psoriasiform hyperplasia depending on activity and chronicity.

Scale crust and spongiosis may localize to follicular ostia.

Atopic dermatitis:  

Mimics other spongiotic diseases. 

There is variable spongiosis, focal parakeratosis, prominence of vessels in the papillary dermis, psoriasiform hyperplasia, exocytosis and perivascular infiltrate of lymphocytes.

Stasis dermatitis:

Mild spongiosis only ; proliferation of superficial dermal vessels, extravasation of erythrocytes, abundant hemosiderin.

Spongiotic drug reaction:  

Spongiosis, conspicuous exocytosis of lymphocytes, rare  apoptotic keratinocytes, eosinophils, plasma cells, lymphocytes in superficial dermis and sometimes in mid dermis.

Sometimes superficial dermal oedema.

Chronic superficial dermatitis:

Mild spongiosis, focal parakeratosis, variable psoriasiform hyperplasia, superficial perivascular infiltrate with upward extension and mild exocytosis.

 

Dermatophytoses

Neutrophils in stratum corneum or compact orthokeratosis should alert observer to perform PAS stain.

Spongiotic vesicles may form on palms and soles.

Ginger and Cinnamon: Can This Household Remedy Treat Giardiasis? Parasitological and Histopathological Studies

~Content Source

Background

Giardia lamblia is one of the most common protozoal infections in human especially children. Metronidazol (MTZ) is the drug of choice for treatment of giardiasis; its chemical composition possesses major threats and is becoming less sensitive. This study aimed to search for natural extracts alternative to MTZ.

Methods

In-vivo effects of dichloromethane extracts of ginger and cinnamon in doses of 10 and 20 mg/kg/day separately were studied on 30 experimentally infected albino rats divided into 6 groups (5 rats each). Plant extracts were started on the 6th day post infection for 7 successive days. The study was evaluated by fecal cyst and intestinal trophozoite counts, histopathology, scanning and transmission electron microscopic examinations of the small intestinal mucosa.

Results

Ginger and cinnamon caused reduction of fecal cyst and trophozoites counts. Histopathology, scanning electron microscopy (SEM) and transmission electron microscopy (TEM) after exposure to each extract revealed evident improvement of intestinal mucosal damage produced by G. lamblia infection and direct structural injury to the trophozoites. However, these results were more obvious after exposure to cinnamon extracts.

Conclusion

We confirmed the potential therapeutic effects of ginger and cinnamon extracts on G. lambliainfection in albino rats as a promising alternative therapy to the commonly used antigiardial drugs.

Keywords: Giardia, Ginger, Cinnamon, Intestinal-histopathology, Electron microscopy

linkDonut-2019.07.10

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A Gnotobiotic Mouse Model Demonstrates that Dietary Fiber Protects Against Colorectal Tumorigenesis in a Microbiota- and Butyrate–Dependent Manner

Butyrate elicits a metabolic switch in human colon cancer cells by targeting the pyruvate dehydrogenase complex.

Mechanisms of primary cancer prevention by butyrate and other products formed during gut flora-mediated fermentation of dietary fibre.

G-protein-coupled receptor for short-chain fatty acids suppresses colon cancer.

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Tauroursodeoxycholic Acid May Improve Liver and Muscle but Not Adipose Tissue Insulin Sensitivity in Obese Men and Women

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https://en.wikipedia.org/wiki/Prostaglandin – PROSTAGLANDIN

Inulin-Type Fructans: Functional Food Ingredients

GUAR GUM BABY

Guar gum as a promising starting material for diverse applications: A review.

Microbiota benefits after inulin and partially hydrolized guar gum supplementation: a randomized clinical trial in constipated women.

Partially Hydrolyzed Guar Gum in the Treatment of Irritable Bowel Syndrome with Constipation: Effects of Gender, Age, and Body Mass Index

Prebiotic stimulation of human colonic butyrate-producing bacteria and bifidobacteria, in vitro

Butyrate: A Double-Edged Sword for Health?

Maternal butyrate supplementation induces insulin resistance associated with enhanced intramuscular fat deposition in the offspring.

Butyrate alleviates high fat diet-induced obesity through activation of adiponectin-mediated pathway and stimulation of mitochondrial function in the skeletal muscle of mice.