COVID-19: Coronavirus and hemoglobin

Hello Awesomites!

Please refer to the diagrams for better understanding.

Why do we have abnormal hemoglobin-related biochemical indices in COVID-19 patients?
Reports demonstrate that the hemoglobin and neutrophil counts decrease in most patients with SARS-CoV-2 infection, and values of serum ferritin, erythrocyte sedimentation rate, C-reactive protein, albumin, and lactate dehydrogenase increase significantly.

What makes hemoglobin an attractive molecule for the coronavirus?
Porphyrins!

Porphyrins in the human body are mostly iron porphyrins i.e heme. And a lot of heme is not free, but bound to hemoglobin. Viruses require porphyrins to survive. Therefore, the novel coronavirus targets hemoglobin, attacks heme, and hunts porphyrins.

Structure of SARS-CoV-2

Image by Upasana Yadav

The possible mechanism is that orf1ab bound to the alpha chain and attacks the beta chain, causing conformational changes in the alpha and beta chains; ORF3 attacks the beta chain and exposes heme. ORF10 then quickly attaches to the beta chain and directly impacts the iron atoms on the heme of the beta chain. The heme is dissociated into porphyrin, and orf1ab finally captures porphyrin. Orf1ab plays a vital role throughout the attack. Attack of oxidized hemoglobin by viral proteins leads to less and less hemoglobin that can carry oxygen. The invasion of viral proteins on deoxidized hemoglobin will cause less and less hemoglobin that can carry carbon dioxide.

This study found that ORF8 and surface glycoprotein had a function to combine with porphyrin to form a complex, while orf1ab, ORF10, ORF3a coordinately attack the heme on the 1-beta chain of hemoglobin to dissociate the iron to form the porphyrin. This mechanism of the virus inhibited the normal metabolic pathway of heme, and made people show symptoms of the disease.

What causes the high infectivity of the novel coronavirus?
Medical workers have detected the novel coronavirus from urine, saliva, feces, and blood. The virus can also live in body fluids. In such media, porphyrin is a prevalent substance. At the beginning of life, virus molecules with porphyrins directly move into the original membrane structure by porphyrin permeability. This study showed that the E2 glycoprotein and Envelope protein of the novel coronavirus could bind well to porphyrins. Therefore, the coronavirus may also directly penetrate the human cell membrane through porphyrin. (Means If the virus can bind with porphyrins, it can enter these secretory cells without ACE2 receptors by using the membrane permeability)

What is the importance of knowing the above information?
The drugs based on this mechanism: Chloroquine and Favipiravir.

The primary function of the Envelope protein is to help the virus enter host cells. The primary role of Favipiravir is to prevent the virus from entering host cells and catching free porphyrins. Favipiravir's ability to improve respiratory distress is lower. Favipiravir can only prevent the binding of Envelope protein and porphyrin.

Chloroquine could prevent orf1ab, ORF3a, and ORF10 from attacking the heme to form the porphyrin and inhibit the binding of ORF8 and surface glycoproteins to porphyrins to a certain extent, effectively relieve the symptoms of respiratory distress.

The infectivity of the nCoV pneumonia was not completely prevented by the drugs, because the binding of E2 glycoprotein and porphyrin was not inhibited.

Note for Diabetic patients
Diabetic patients and older people have higher glycated hemoglobin. Glycated hemoglobin was reduced by the attack, which made patients' blood sugar unstable. Since the porphyrin complexes of the virus produced in the human body inhibited the heme anabolic pathway.
Written by Upasana Yadav
(Courtesy:-Thank you Ikan for all the help) 

References:
1. Wenzhong, liu; hualan, Li (2020): COVID-19: Attacks the 1-Beta Chain of Hemoglobin and Captures the Porphyrin to Inhibit Human Heme Metabolism. ChemRxiv. Preprint. https://doi.org/10.26434/chemrxiv.11938173.v5
Link to the article: https://chemrxiv.org/articles/COVID-19_Disease_ORF8_and_Surface_Glycoprotein_Inhibit_Heme_Metabolism_by_Binding_to_Porphyrin/11938173

COVID-19: Was SARS-CoV-2 genetically engineered for biological warfare?

An article published in Nature Medicine noted that it is improbable that SARS-CoV-2 emerged through laboratory manipulation of a related SARS-CoV-like coronavirus. This article disproves most conspiracy theories about the artificial origin of the SARS-CoV-2 virus.

I am going to try to explain what the article says in simplified terms but you need to have some background in biochemistry to understand what it says. Let's begin!

COVID-19: Structure of the novel coronavirus (SARS-CoV-2)

Okay, let's start right away.

Molecular structure of SARS-CoV-2

Rickettsia mnemonic

Hi!

Do you want to learn about Rickettsia today?

Rickettsia mnemonic (Rickettsia typhi, flea vector)

COVID-19: Pathophysiology and microbiology

COVID-19: Pathophysiology and microbiology

Everything you need to know about coronavirus COVID-19

Resources: CDC, UpToDate, WHO website.
Video by Drashtant Prajapati, MBBS.

Corona virus

Corona virus:
A) Virology:
1) Coronaviruses are classified as a family within the Nidovirales order, viruses that replicate using a nested set of mRNAs. The coronavirus subfamily is further classified into four genera: alpha, beta, gamma, and delta coronaviruses. 
2) Positive mRNA strand virus. It is largest known RNA strand.

B) Routes of transmission — Respiratory coronaviruses probably spread in a fashion similar to that of rhinoviruses, via direct contact with infected secretions or large aerosol droplets. Immunity develops soon after infection but wanes gradually over time.

C) Clinical Manifestation:
Characterized by
1) Upper respiratory tract infections
2) Acute otitis media
3) Pneumonia
4) Temporarily linked to asthma attacks in both adults and children
5) The idea that coronaviruses produce diarrhea in humans is intriguing because of their clear intestinal pathogenicity in animals
6) Gastrointestinal manifestations -diarrhea, vomiting, nausea, and abdominal pain.
7) There is one reported case of encephalitis due to corona virus
8)Also seen in association with Kawasaki disease.

D) Diagnosis:
Until recently, no sensitive, rapid method existed to detect all of the known human coronavirus strains. Rapid techniques that can be used to detect coronaviruses from nasopharyngeal samples include reverse-transcriptase polymerase chain reaction (RT-PCR) and immunofluorescence antigen detection assays.

E) Treatment:
1) There is currently no treatment recommended for coronavirus infections except for supportive care as needed
2) Chloroquine has shown some activity against cultured cells.

F)Prevention:
1) Preventive measures are the same as for rhinovirus infections, which consist of handwashing and the careful disposal of materials infected with nasal secretions. Several antiseptic/disinfectant solutions used commonly in hospitals and households, including chloroxylenol, benzalkonium chloride, and cetrimide/chlorhexidine, have been shown to be ineffective against coronaviruses

That's it!

Source: Up-to-date.

Leptospirosis

Rats, rains, ricefields? Ring any bells? Sewer workers coming in with jaundice and fever? Still no?
Assam/Odisha/Kerala floods?

D-lactic acidosis in short bowel syndrome

Hello everyone!

D-lactic acidosis is an unusual form of lactic acidosis.

Which patients develop D-lactic acidosis?
1. In patients with jejunoileal bypass, small bowel resection, or other causes of the short bowel syndrome.
2. Patient who receives or ingests a large amount of propylene glycol
3. Patients with diabetic ketoacidosis

In this post, I'm going to specifically talk about D-lactic acidosis in patients with small bowel syndrome.

How do patients with D-Lactic acidosis present?

Increased anion gap metabolic acidosis.
Neurologic findings of intermittent confusion, slurred speech, and ataxia.

Why does it happen in patients with small bowel syndrome?

Glucose and other carbohydrates are normally absorbed by the small bowel. If the small bowel is bypassed, removed, or diseased, then delivery of these substances to the colon increases.

Also, overgrowth of gram-positive anaerobes, such as Lactobacilli seen in small bowel syndrome contributes to lactic acidosis.

How is it metabolized?

D-lactate is not metabolized by L-lactate dehydrogenase, the enzyme that catalyzes the conversion of the physiologically occurring L-lactate into pyruvate. Thus, D-lactate is slowly metabolized in humans, accumulates in body fluids, and generates metabolic acidosis.

Diagnosis:
Laboratory studies show increased anion gap metabolic acidosis with normal plasma lactate levels, because the D-isomer is not measured by conventional laboratory assays for lactate. Diagnosis is confirmed by specifically measuring D-lactate.

Treatment:
Sodium bicarbonate if D-lactic acidosis and acidemia are severe.

Oral antimicrobial agents (such as metronidazole, neomycin, or vancomycin) can be used when D-lactic acidosis that decrease the number of D-lactate-producing organisms.
FYI: Although antimicrobials are sometimes helpful, they can occasionally precipitate D-lactic acidosis in susceptible subjects by causing an overgrowth of lactobacilli.

Low-carbohydrate diet (or the use of starch polymers rather than simple sugars) is also helpful because it diminishes carbohydrate delivery to the colon.

That's all!

-IkaN

INTERNSHIP DIARIES EPISODE 05 – Who Resides In Your Blood? (Blood Cultures)

It was a bright day. You reached the ICU ward and introduced yourself to the resident there.You got ready with cap and mask and asked to take vitals of patient.

"He developed a spiking fever, and the central venous catheter was removed on day 14 of treatment. Fever is not responding to antibiotics, Sir." said one resident to the  consultant.

"Send the blood for culture and inform me." said the consultant.

"Dr. Kesh , Can you arrange the items for sampling and fill up the laboratory forms?" the senior resident looks at you.

"Yes, Sir." Says you excited to know and expand your knowledge about blood culture.

**********************************

5.1 BLOOD CULTURES:

INDICATION FOR BLOOD CULTURE:

1.Where the possibility of septicemia or bacteremia is suggested by the presence of fever,shock or other signs and symptoms occurring in association with a known or suspected local infection such as sepsis in a surgical wound ,Osteomyelitis,peritonitis,Arthritis,Enteric fever.

2.Pyrexia of unknown origin (temperatures of >38.3°C (>101°F) on several occasions with fever of >3 weeks and failure to reach a diagnosis despite 1 week of inpatient investigation)

3.Unexplained leucocytosis or leucopenia

4.Suspected fungemia specially in Immunocompromised patients, HIV patients.

STEPS:

I)Obtain consent

II)Hand washing

III)Arranging items for sampling (MATERIALS REQUIRED)

·        70% isopropyl alcohol swabs

·         10% Povidone iodine swabs

·        dry cotton

·        Sterile gloves of suitable size

·        2 syringes (adult: 20 cc, paediatric: 5 cc)

·        2 needles (adult: 22 gauge or preferably larger butterfly or standard needle; paediatric: 25- or 23-gauge butterfly or standard needle)

·        Blood culture bottle (Aerobic and anerobic)

IV) vein selection

• Arterial vs venous blood

 • Indwelling arterial or venous lines

• Central or peripheral

V)Hand washing and Gloving

VI)Preparation of a skin

VII)Venepuncture and drawing a blood sample

VIII)Inoculating in blood culture bottle and shake the bottle

IX)Labelling, storing and documenting

• Ask the patient about allergies to iodine.

• Apply the tourniquet, select the site.

(Be careful that the ends of the tourniquet do not fall onto the puncture site, thereby contaminating it, if the tourniquet does accidentally touch the prepared puncture site, the site must be recleaned)

• Apply alcohol/acetone pad at the puncture site for 30 seconds till it dry.

• Apply the iodine swab, apply to puncture site, move the iodine in concentric circles outward. Keep it for 60 seconds (till it dry).

• Again, clean the site with alcohol/acetone and allow it to dry.

• Perform the venepuncture, following routine venepuncture procedures. Do not repalpate the site.

• If the blood culture is one of a series of samples to be drawn from a patient, the blood culture must be collected first.

• Withdraw needle from vein and insert into the top of the blood culture container.

(Other than syringe and needle, by closed system, consisting of vacuum bottle and double needle collection tube can be done.)

• Do not change the needle.

• Do not hold the container in your hand, this may result in a needle exposure.

• Do not push the blood. Mix the content. (An adequate space above broth ensures that blood is not injected under undue pressure and some air is still available for strict aerobes)

• Keep at room temperature.

• Label the blood specimen collected, following standard labelling procedures. Be sure to include the site used and the number of the specimen in the series ordered.

Blood Cultures should NOT be taken from the following sites

•       Veins which are immediately proximal to an existing peripheral IV cannula.

•       A femoral vein due to difficulty in skin disinfection of the site. This area poses a high risk of contamination.

•       Catheter drawn blood cultures are equally likely to be truly positive (associated with sepsis), but more likely to be colonized.

(One drawn through catheter and other drawn through vein PPV of 96%)

VOLUME OF BLOOD drawn is the single most important factor influencing sensitivity

• For adult: minimum 10 ml

 • For infant and children: 1-5 ml

1-2 ml= neonate

 2-3ml= 1 month - 2year age

 3-5ml= Older children

 • 20 ml of blood obtain in sequence is more effective and sensitive (98%) specially in intermittent bacteremia.

 • Patients who have received antibiotics should give 3 separate collections of blood. Also, one or two of which on 2nd day also.

TIMING OF BLOOD CULTURE

• Before starting antimicrobial therapy

• At the time of fever peak

 • Minimum 30-60 minute interval between 2 samples except in critically ill septic patient.

 • In continous bacteremia-timing of blood culture is not important, but in intermittent bacteremia 2 or 3 culture should be spaced an hour apart.

TEST PERFORMED AFTER SAMPLE REACH TO LABORATORY

Blood to broth ratio: 1:5 only, should not be <1:5 or > 1:10

• Agitation during incubation

-  Length of incubation: • Not more than 7 days • 5 days is sufficient • >5 day-contaminants • 7 days is useful for: • Fungemia • Bacteremia due to fastidious organisms like HACEK group, brucella, legionella • For patients suspected of endocarditis who has been treated with antimicrobial before obtaining blood culture • Mycobacterial culture > 4 weeks

• Atmosphere of incubation: aerobic and anaerobic

ASK YOUR MICROBIOLOGICAL DEPARTMENT TO HELP YOU IN SELECTION OF BROTH :

• Glucose broth: useful in endocarditis

• Bile broth: In enteric fever

• Trypticase soy broth (inhibits Neisseria and S.pneumoniae)

• Brain heart infusion broth: multipurpose broth

• Thioglycolate broth: for anaerobes

• Columbia or brucella broth

• Mycobacteria: Middlebrook 7H9 with 0.05% SPS, BHI with 0.5 % polysorbate 80

• Fungus broth

Additives in broth: • Anticoagulant- bacteria are trapped in blood clot • Antimicrobial- if patient is already in antibiotics • Anticomplementry agents- to inactivates complement action • Antiphagocytic

 Type of blood culture bottle (AEROBIC AND ANAEROBIC CULTURE BOTTLE)

• Standard aerobic bottles- most common bacterial pathogens, including aerobes, facultative anaerobes and for candidemia

• Smaller bottles are used for neonates and young children

• After inoculation, bottles are incubated aerobically.

SIGNS OF BACTERIAL GROWTH:

• Macroscopically:

-Generalized turbidity

-Hemolysis

- Gas production

- Discreate colonies on the surface of the sedimented red cells

-recoverable bacterial growth may occur before turbidity is evident.

Subculture from bottles as a routine

  • For subculture:

- Subcuture should be done at least once during the first day after 5-6 hours and at interval thereafter which should be at least twice during first 2-3 days.

• Gram stain:  Should be made and examined at the subculture stage. Any positive finding should be reported at once to clinician as the morphological type of organism may guide the physician to start antibiotic.

• Quantitative counts of bacteria in blood: Inoculate 1 ml amounts of blood into several tubes of melted agar and make pore plates either directly from patients. Another method is treat the patient sample with lytic agent. Then lysed sample is centrifuged and harvested organism cultured directly on a suitable solid medium to allow identification and to give a semi-quantitative indication of its presence in blood. (When monitoring colonization associated with a prosthesis or catheter) 

INTERPRETATION OF POSITIVE BLOOD CULTURE REPORT:

1. Whether true or contaminant (ASEPSIS, ASSES RISK FACTOR PRESENT IN PATIENT)

2.FIND THE SOURCE

3.DETERMINE THE NEED FOR TREATMENT (whether patient is toxic and in shock)

4.ADDRESS UNDERLYING INFECTIOUS FOCUS

5.LOOK FOR PATHOGEN SPECIFIC FACTORS DURING ANTIBIOTIC TREATMENT (Toxins that are produced)
6.HELPS IN IDENTIFYING OTHER RISK FACTOR WITH INFECTION (The identification of S.bovis organism also prompted the ultimate identification of colonic carcinoma, which is an underlying risk factor for S. bovis bacteremia)
7.LOOK FOR REASON OF IMMUNOCOMPROMISED STATE (Rule out malignancy or HIV as bactremia may be a result of oppurtunistic infection)

Therefore,clinical examination is of utmost important. As positive blood culture is not a disease in itself. It may be a result of underlying disease or part of complication.

After starting treatment, document the blood culture clearance duration.

SOME DEFINITIONS:

Bacteremia – presence of bacteria in blood stream.Some conditions have a period of bacteremia as part of the disease process (ex. Meningitis, endocarditis)

Septicemia – bacteremia plus clinical signs and symptoms of bacterial invasion and toxin production

Transient bacteremia lasts for minutes or a few hours and most frequently occurs after manipulation of nonsterile body sites—for example, during dental procedures; after gastrointestinal biopsy; after percutaneous catheterization of the vascular system, bladder, or common bile duct; and after surgical debridement or drainage—that is, after procedures involving contaminated or colonized skin and/or mucosal surfaces are performed and also at the onset of acute bacterial infections.

Intermittent bacteremia is defined as bacteremia due to the same microorganism that is detected intermittently in the same patient because of a cycle of clearance and recurrence. Intermittent bacteremia is often associated with undrained closed-space infections, such as intra-abdominal or soft-tissue abscesses, and may also occur in patients with liver abscesses, cholangitis, and focal infections, including pneumonia, osteomyelitis, and spondylodiscitis. 

Persistent bacteremia is a characteristic of infective endocarditis (IE) and other intravascular infections, such as vascular-graft infection, a mycotic aneurysm, or an infected thrombus. Persistent bacteremia also occurs during the early stages of systemic bacterial infections, such as brucellosis and typhoid fever.

********************************
After labelling the sample, storing and documentation, you went to ICU again. Taking vitals and documenting it in files. Feeling happy to learn about blood culture. 

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HAPPY STUDYING !

UPASANA Y. AND JAY

Catheter Removal Timing

Removal — Following diagnosis of catheter-related infection, catheter removal is warranted in the following circumstances :

●Severe sepsis

●Hemodynamic instability

●Endocarditis or evidence of metastatic infection

●Erythema or exudate due to suppurative thrombophlebitis

●Persistent bacteremia after 72 hours of antimicrobial therapy to which the organism is susceptible

Source :Uptodate

Bhopalwala. H

Lung Biopsy in VAP

Lung biopsy in Ventilator-associated Pneumonia may be reserved for patients in whom infiltrates are progressive despite antibiotic therapy or patients in whom a non-infectious etiology is suspected.

The purpose of acquiring tissue under these circumstances is to identify a pathogen that may have been missed with previous sampling or a pathogen that is difficult to culture (eg, fungus, herpes viruses) or to identify a noninfectious process masquerading as infection (eg, cancer, cryptogenic organizing pneumonitis, lymphangitis, interstitial pneumonitis, vasculitis).

Source: Uptodate

Bhopalwala. H

Catheter Related Candidemia Treatment Indications

Empiric therapy for suspected catheter-related candidemia should be administered for septic patients with the following risk factors:

●Total parenteral nutrition

●Prolonged use of broad-spectrum antibiotics

●Hematologic malignancy

●Hematopoietic cell or solid organ transplant

●Femoral catheterization

●Colonization due to Candida species at multiple sites

Source: Uptodate

Bhopalwala. H

Antibiotic Lock Therapy

Antibiotic lock therapy —

The premise of ALT is to achieve sufficient therapeutic concentrations to kill microbes growing in a biofilm . ALT may be a useful adjunctive therapy together with systemic antibiotic therapy for intraluminal infections due to coagulase-negative staphylococci or gram-negative organisms in the setting of CRBSI (Catheter Related Blood Stream Infection) when the catheter cannot be removed .

ALT should not be used for extraluminal infections nor for management of infections due to S. aureus, P. aeruginosa, drug-resistant gram-negative bacilli, or Candida.

Source: Uptodate

Bhopalwala. H

Timing of Catheter Replacement in CRBSI

In general, the patient should receive antibiotic therapy for at least two to three days following device removal prior to device replacement. At the time of device replacement, the patient should be hemodynamically stable with negative blood cultures and no sequelae of bloodstream infection .In addition, for patients with CRBSI ( Catheter Related Blood Stream Infection) due to S. aureus, a new catheter may be placed if additional blood cultures demonstrate no growth at 72 hours

Source: Uptodate

Bhopalwala. H

HAP and VAP

Pneumonia types — The 2016 Infectious Diseases Society of America (IDSA)/American Thoracic Society (ATS) guidelines distinguish the following types of pneumonia :

●Hospital-acquired (or nosocomial) pneumonia (HAP) is pneumonia that occurs 48 hours or more after admission and did not appear to be incubating at the time of admission.

●Ventilator-associated pneumonia (VAP) is a type of HAP that develops more than 48 hours after endotracheal intubation.

Bhopalwala. H

qSOFA Score for Sepsis

The qSOFA (quick Sequential Organ Failure Assessment) score is easy to calculate since it only has three components, each of which are readily identifiable at the bedside and are allocated one point:

●Respiratory rate ≥22/minute

●Altered mentation

●Systolic blood pressure ≤100 mmHg

Bhopalwala. H

True or False #2

1. Herpangina involves the anterior oropharynx with grey vesicles and ulcers. T or F

2. Pleurodynia is also known as Bornholm disease. T or F

ANSWERS

1. False

Herpangina is caused by Coxsackievirus and involves the posterior oropharynx

Herpetic gingivostomatitis caused by HSV involves the anterior oropharynx and grey vesicles and ulcers

2. True

Pleurodynia — Pleurodynia is an acute enteroviral illness characterized by fever and paroxysmal spasms of the chest and abdominal muscles . Most cases occur during localized summer outbreaks among adolescents and adults. Regional and nationwide outbreaks involving a large number of older children and young adults have been reported at infrequent intervals, often separated by decades. The role of the group B coxsackieviruses, the most important cause of epidemic pleurodynia, was established in 1949 . Other agents rarely implicated in pleurodynia include echovirus serotypes 1, 6, 9, 16, and 19 and group A coxsackievirus serotypes 4, 6, 9, and 10 .

Pleurodynia can mimic more serious diseases, including bacterial pneumonia, pulmonary embolus, myocardial infarction, acute surgical abdomen, and herpes zoster infection. Most patients are ill for four to six days. Children have milder disease than adults, who are often confined to bed.

Question: Chicken pox

#Medicowesome
#Microbiology
#PSM

Q) True about chicken pox are all except:

1) Caused by HSV-3
2) SAR is 90%
3) Superficial rash
4) Single stage of rash

Answer in 12 hours 

 Answer is 4) Single stage of rash

So, this post will help you remember manifestation of Chickenpox rash. You can also differentiate between Chickenpox and Smallpox rash using same

So for Chicken pox remember this mnemonic:-

DCP SPAReS Iron man ( Always Marvel fan!)

D= Dew drops appearance

CP= Centripetal appearance

S= Superficial and Uniocular 

P=Pleomorphic

A= Axilla and flexor surface affected

R=Rapid evolution

S=Spares palms and soles 

I=Inflammation around vesicles present

Since we have rapid evolution in chicken pox, scabs are formed after 4-7 days itself.

Smallpox rash appears exactly in an opposite manner of chickenpox rash.

Smallpox rash manifests as follow:-

Centrifugal appearence

Deep and Multilocular appearence

Non-pleomorphic

Axilla is spared and extensor compartment affected 

Slow evolution

Palms and soles are affected

No inflammation around vesicles

Since we have slow evolution in chicken pox, scabs are formed after 10-14 days itself.

-Demotional bloke

Facebook: Microbiology Candida.

So, this post is the answer to our previous question asked on medicowesome facebook page. Question was

#Medicowesome #Microbiology

A vitreous aspirate from a case of metastatic endopthalmitis on culture yields Gram-positive round to oval cells, 12-14 mm in size. The aspirate on Gram staining show the presence of pseudohyphae. Which of the following is the most likely aetiological agent?

1)  Aspergillus.
2)  Rhizopus.
3)  Candida.
4)  Fusarium.

Answer: Option 3) Candida.

Let's analyse the question and extract the information one by one.
So, we get two things from the question.
a) The causative organism has pseudohyphae and
b) It is stained by gram stains.

Among the given options, only Candida can form pseudohyphae. All other options are filamentous fungi forming true mycelia and Candia is the only fungi that are usually gram positive on smears.

Some awesome points that must be known on Candida infections.

1) Candida is unicellular organism belonging to yeast like fungus categories. All Candida species are commensals of humans. So, their mode of transmission is endogenous while most of the fungus have mode of transmission as inhalation.
2) They form pseudohyphae.
3) Candida albicans is different from other candida because :-
   a) It forms true hyphae or germ tubes when grown in serum.
   b) It forms thick walled large spores called chlamydospores.
   c) It is dimorphic. It means it grows as yeast at 37°C and as molds at 25°C.

4) Test to differentiate between C. Albicans and other Candida is called germ tube test or Reynolds Braude phenomenon.
-C. Albicans when placed at 37°C in human serum forms germ cell tubes within 2 hours.
5)Candida albicans is the most common cause of mucosal candidiasis.
6) Candidiasis is the most common systemic mycosis. It is also the most common fungal infection in neutropenic and immunocompetent patients.
7) It causes oral thrush, oesophageal candidasis, cerebral candidasis and pulmonary candidiasis.

Extra information:

Their is one test which I learned online and some people consider it as diagnosis of candida infections.

The Spittle Test:
When you get up in the morning, and before you brush your teeth, eat or drink anything, fill a glass with bottled water at room temperature.
Spit some saliva gently into the glass.
Come back every 20 minutes for the next hour and check for some of these signs.

1) Strings coming down through the water from the saliva at the top.
2) Cloudy saliva sitting at the bottom of the glass.
3) Opaque specks of saliva.

Also, in above question we deducted that the given pathogenic organism is gram stain so we get to learn about stains as well.
Normally, fungi are stained by PAS and methenamine silver but some fungi are stained by special stains like :-

Candida is stained by gram stain.
Cryptococcus is stained by mucicarmine, India ink.
Histoplasma is stained by Giemsa stain.

Thanks for reading!
Ojas Gite.

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