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Septicemia (Blood Poisoning): Causes, Management

Overview

What is septicemia?

Septicemia, sometimes called blood poisoning, is an infection that occurs when germs get into the bloodstream and spread. The germs are usually bacteria but also can be viruses or fungi.

Septicemia vs. sepsis: How can I tell the difference?

Some people use the words septicemia and sepsis as if they mean the same thing. But technically, septicemia is an infection that happens when bacteria or other germs enter the bloodstream and spread throughout the body. That can trigger sepsis, which is the body’s reaction to the infection.

Who might get blood poisoning?

Anyone can get septicemia, but it’s more common in people who:

  • Are in the hospital or have had recent surgery (especially those who have catheters or IVs).
  • Are very old or very young.
  • Have had septicemia before.
  • Have infections or other chronic medical conditions (for example, diabetes or cancer).
  • Have severe injuries, such as extensive burns or open wounds.
  • Have weak immune systems.

What germs can cause septicemia?

Almost any type of germ can cause septicemia. The ones most often responsible are bacteria, including:

How does septicemia affect my body?

Septicemia can lead to sepsis, which is a life-threatening medical emergency. It can cause tissue damage, organ failure and even death.

Symptoms and Causes

What causes septicemia?

Bacteria, viruses and fungi can enter the bloodstream in many ways, for example:

The body usually can remove a small number of germs naturally. But if germs continue to grow and spread, that can lead to septicemia.

What are the signs of septicemia?

Early septicemia symptoms are:

  • High fever.
  • Chills.
  • Weakness.
  • Sweating.
  • Drop in blood pressure.

Diagnosis and Tests

How is septicemia diagnosed?

Septicemia diagnosis is based on:

  • Presence of septicemia symptoms.
  • Blood tests to identify a bacterium, virus or fungus.

Depending on your symptoms, you might need other tests to check for damage to tissues and organs.

Management and Treatment

How is septicemia treated?

Septicemia requires immediate treatment to prevent the condition from worsening to sepsis. Infections caused by bacteria are treated with antibiotics. The type of antibiotic you need depends on the type of bacteria that caused the infection. If the infection is caused by a virus or fungus, treatment will include an antiviral or antifungal medication. Your healthcare provider also may recommend draining blood and fluid from the infected area.

How soon after septicemia treatment will I feel better?

If treatment is effective, you can start to feel better in weeks or months. More serious cases may take longer.

Prevention

How can I reduce my risk of septicemia?

You can lessen the chances of developing septicemia by:

  • Getting all recommended vaccines.
  • Keeping any wounds clean and covered.
  • Taking good care of any medical conditions by following your healthcare provider’s instructions.
  • Washing your hands regularly.

Outlook / Prognosis

What is the outlook for people with septicemia?

Septicemia must be treated quickly to be effective. If not, septicemia can lead to sepsis and septic shock, which is often fatal.

People who’ve had septicemia and recovered are more likely to have it again in the future.

Living With

Is septicemia contagious?

You can’t spread septicemia to other people. But you can spread germs easily, so wash your hands often.

When should I seek medical attention for septicemia?

Septicemia is a medical emergency. Be aware of the signs, and call a healthcare provider if you have any the following:

  • High fever.
  • Chills.
  • Weakness.
  • Sweating.
  • Drop in blood pressure.

A note from Cleveland Clinic

Septicemia is an infection that occurs when germs get into the bloodstream and spread. It’s a serious condition that requires immediate medical attention and antibiotic treatment. You can reduce your risk of septicemia by practicing good hand-washing, taking proper care of wounds and managing other health conditions properly.

Why five patients in the same hospital contracted a rare blood infection

As an infectious disease doctor, Nasia Safdar is a detective of sorts at the University of Wisconsin Hospital in Madison. She tracks the patterns of infections, from the type of illness to the organism at its root, and in spring 2014, she noticed something odd: A cluster of bloodstream infections caused by an uncommon, and potentially deadly, bacteria.

The microbe, Serratia marcescens, can infect the lungs, bladder, blood, and skin, and usually causes a few infections per year at Safdar’s hospital; some studies estimate that about 1 out of 100,000 people fall prey to a blood infection from the bacteria annually. So it was strange that five cases had occurred in just five weeks, and Safdar did a double take.

“There were more cases than we had been used to,” Safdar said. “I thought that needed investigation.”

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Because the bacteria were all the same strain, Safdar was confident the cluster stemmed from a single source. But what was it? To find out, Safdar scanned each patient’s chart, searching for a common thread.

Related:

This dentist broke his own opioid habit. Can the dental profession do the same?

For example, Safdar said, “Serratia is a moisture-loving organism, so we looked at all the medications and fluids the patients were getting.”

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The patients infected by the bacteria had received the same drugs as those who hadn’t gotten sick. What differed was their location: All but one of the patients had spent time in the post-surgery recovery unit. What’s more, some of these patients reported pain after the operation that was poorly controlled by opioid medicines.

“Because we try to be diligent about pain control, that set off a red flag,” Safdar said.

Syringes with missing caps

Little did Safdar know, her colleagues in the pharmacy department at the hospital were conducting their own investigation. In mid-March 2014 — less than two weeks after the first Serratia case — a nurse had discovered that the tamper-resistant caps had been removed from 10 syringes of opioids. Less than a month later, three more were discovered. Lab testing revealed the tubes held next-to-no medicine; instead, they’d been filled with saline solution.

Subsequent testing of an additional 10 random opioid syringes in the hospital’s pharmacy and medication dispensers showed one contained only a tiny fraction of its original medicine.

The findings spurred an intensive investigation, including installing surveillance cameras. Over the next two months, investigators discovered more than 40 opioid syringes hospital-wide that had been emptied and refilled with salt water. The path led to a nurse working in the post-operative area; she had entered her password to remove medications from drug dispensers just before four of the patients who contracted Serratia received their medicine. The fifth patient who came down with the bloodstream infection lived with the nurse; he was her father.

Investigators believe the saline the nurse used to re-fill the syringes was contaminated by Serratia, although the containers were destroyed before they could be tested for the bacteria. They concluded she likely brought the liquid from home.

“It was very frustrating because it took awhile to link a person to all these cases, and we felt helpless,” said Safdar, who recently published the team’s findings in the journal Infection Control & Hospital Epidemiology. “We felt very relieved to find the culprit.”

The nurse, who reported struggling with opioid addiction, was swiftly fired for stealing the drugs. That ended the string of Serratia infections. She also lost her nursing license and was convicted on four counts of narcotics possession and placed on five years of probation; at the time of the trial, the investigation into the Serratia outbreak hadn’t yet linked her to the infections.

Still, for the five patients who endured severe pain after surgery, then got sick — one of whom died — the answer came too late.

An ongoing problem

In the midst of the opioid crisis, the risk of medication diversion — when a legal controlled substance is used or distributed illegally — is greater than ever. After all, opioids are the most commonly diverted drugs. Although drug theft occurs most often in outpatient facilities, such as clinics and urgent care centers, it can happen anywhere. Health care workers struggling with addiction face their own obvious dangers, but when a substance use disorder leads to events like those in Madison, patients’ lives also are on the line.

The last decade has seen numerous outbreaks of infections caused by health care employees siphoning medications intended for patients, from technologists to nurses to respiratory therapists, according to the Centers for Disease Control and Prevention. Yet many in the health care field remain unaware that drug diversion is a major problem.

Related:

Where have all the opioids gone? Most prescribed pills go unused after surgery

“It’s become screamingly obvious that there are a lot of other people endangered” by a hospital employee’s addiction, said Dr. Keith Berge, an anesthesiologist at the Mayo Clinic in Rochester, Minn., who was not involved in the recent investigation but has written about controlled substance diversion. “It puts vulnerable patients at risk.”

Drug diversion is a complex problem that requires a multifaceted solution, starting with making it simple and acceptable for health care workers with addiction to seek help, according to Lauren Lollini, secretary of the International Health Facility Diversion Association, a nonprofit group dedicated to preventing drug diversion founded in 2015.

“Health care workers need to have a safe place to land if they are struggling,” said Lollini, who in 2009 was one of 19 patients infected with hepatitis C when a surgical technician stole opioids from a hospital in Colorado.

“It’s criminal to divert drugs, but somebody needs that drug to survive, so they are doing what they have to do,” Lollini said. “Breaking the law is separate from the addiction issue.”

Signs that an employee is struggling with addiction or is siphoning medicines can be subtle; vigilance for erratic behavior or other signs of substance use is vital, experts say, but red flags aren’t always obvious.

“They are often your best employees,” Berge said. “They may show up for work when they are supposed to be on vacation.”

When employees report suspicions that a colleague is stealing drugs, by law hospitals must relay these suspicions to the Drug Enforcement Agency within 24 hours. They may be reluctant to do so, fearing bad press and the financial and reputational losses that may follow. But Berge emphasized that it’s a crime to hide suspected diversion.

Along with health care institutions making it easy to report addiction or suspected theft, establishing a task force to investigate suspicious activity is key, said Berge, who helped create a 2012 road map to address drug diversion for the Minnesota Department of Health.

“The goal is to create a team that consistently investigates and learns from every diversion,” Berge said, adding that employees who divert drugs can be extremely clever.

That’s why tracing infections back to the theft that caused them is a team effort that requires persistence and vigilance.

“You have to follow the clues you’re confronted with,” said Safdar.

Allison Bond is a hospitalist at Massachusetts General Hospital. If you have dealt with a diagnostic puzzle that has been solved, either as a caregiver or a patient, please email Allison at [email protected]

Bloodstream Infection | Riley Children’s Health

Bloodstream Infection | Riley Children’s Health

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Bacteria, viruses or fungi that spread through the bloodstream cause bloodstream infections. Some blood infections are fairly harmless while others are life-threatening. Germs that cause these infections may come from outside the body or from inside the body where they normally live.

Bloodstream infections can be serious for any child, but the risk of worse outcomes is greater in children with:

There are many types of bloodstream infections including:

  • Catheter-related infections (from the use of tubes placed in veins)
  • HIV
  • Salmonella
  • Sepsis
  • Staph

The symptoms of bloodstream infection include:

  • Fever
  • Fatigue
  • Body aches
  • Stomach pain
  • Vomiting
  • Chills
  • High heart rate
  • Rapid breathing
  • Low blood pressure
  • Rash
  • Confusion

Diagnosis of Bloodstream Infection

Pediatric infectious disease specialists at Riley at IU Health use the following tests to diagnose bloodstream infections:

  • Blood tests. These tests are performed to see if bacteria are in the blood.
  • Urinalysis. In this test, a urine sample is looked at under a microscope and cultured to check for bacteria.
  • Imaging tests. A chest X-ray or computed tomography (CT) scan may be performed to check for infections in organs.
  • Spinal tap. In this test, a sample of spinal fluid is tested for meningitis, an infection that causes inflammation of the membranes that cover the brain and spinal cord.

Treatments

Treatments

If your child has a blood infection, intravenous (IV) antibiotics that fight against a wide range of germs are the first course of treatment. Once blood cultures identify a specific disease-causing germ, your child receives more targeted antibiotics.

The duration of treatment depends on the type of bacteria found in the blood and the overall health of the child. Your child’s pediatric infectious disease specialist will decide if your child should receive treatment in the hospital or at home. Your child should take all medicines as directed and have follow-up visits with the doctor

Key Points to Remember

Key Points to Remember

  • Bacteria, viruses or fungi can cause blood infections that spread through the bloodstream to organs and other parts of the body.
  • Bloodstream infections are serious for a child with a weak immune system or other health conditions.
  • IV antibiotics are the first line of treatment, because they work against a wide range of germs.

Locations

Locations

Locations

In addition to our primary hospital location at the Academic Health Center in Indianapolis, IN, we have convenient locations to better serve our communities throughout the state.

Departments Treating This Condition

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©2021 Riley Hospital for Children at
Indiana University Health
Find adult services at iuhealth.org


Blood in Urine (Hematuria) Causes, Treatments, and Symptoms

Blood in your urine (i.e., your pee) does not always mean that you have kidney disease, but it may mean something is wrong with your kidneys or another part of your urinary tract.

What is blood in urine?

Blood in your urine can look red, pink or brown. Sometimes, you may not know you have blood in your urine until you have a urine test. A urine test may also find white blood cells, which can be a sign of an infection in your kidneys or another part of your urinary tract.

Be sure to tell your doctor if you have blood in your urine so they can decide what to do next.

If you notice a lot of blood, or any blood clots in your urine, contact your doctor right away.

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What are the causes of blood in urine?

There are many causes of blood in your urine, including:

  • An infection, such as a UTI (urinary tract infection) or virus
  • Kidney stones
  • Having your period (menstruation)
  • Sexual activity
  • Injury, such as from sports

Other, more serious problems can also cause blood in your urine, such as:

  • Kidney or bladder cancer
  • Irritation or swelling in your kidneys, prostate (in men) or another part of your urinary tract
  • Polycystic kidney disease
  • Blood clots or diseases that cause blood clotting
  • Sickle cell disease

Anyone can have blood in their urine, but it is more likely if you:

  • Have a family history of kidney disease
  • Have an enlarged prostate (usually in middle age or older men)
  • Have a history of kidney stones
  • Are taking certain medicines, such as pain relievers, blood thinners and antibiotics
  • Have or recently had certain types of infections

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What is the treatment for blood in urine?

The treatment depends on the cause of the blood in your urine. To find out the cause, your doctor may ask about your family history and test your urine. A lab will test the urine sample for signs of an infection, kidney disease or other problems.

If an infection is causing the blood in your urine, your doctor may give you antibiotic medicine. Other causes may need different treatments.

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Contact with Blood or Body Fluids: Protecting against Infection

Blood and body fluids, such as saliva, semen and vaginal fluid, can contain viruses that can be passed on to other people. If you have contact with a person’s blood or body fluids you could be at risk of HIV, hepatitis B or hepatitis C, or other blood borne illnesses. Body fluids, such as sweat, tears, vomit or urine may contain and pass on these viruses when blood is present in the fluid, but the risk is low.

What should I do if I come into contact with blood or body fluids?

If you come into contact with blood or body fluids, always treat them as potentially infectious. If you prick yourself with a used needle, hold the affected limb down low to get it to bleed. Do not squeeze the wound or soak it in bleach. Wash the area with warm water and soap.

If you are splashed with blood or body fluids and your skin has an open wound, healing sore, or scratch, wash the area well with soap and water. If you are splashed in the eyes, nose or mouth, rinse well with water. If you have been bitten, wash the wound with soap and water.

If you are sexually assaulted, go to the hospital emergency department as soon as possible. Reporting the incident immediately after a sexual assault can help to ensure that as much evidence as possible is obtained. For more information about sexual assault and to learn what support services are available, visit JusticeBC at www2.gov.bc.ca/gov/content/justice/criminal-justice/bcs-criminal-justice-system/reporting-a-crime/what-is-a-crime/crime-examples/sexual-assault.

If you have come into contact with blood or body fluids in any of the ways described above, you may need treatment (such as a vaccine or medication) as soon as possible to protect against infection. It is important that you are assessed as soon as possible after the contact.

What will happen at the emergency department?

You will be asked to give informed consent in order for your blood to be tested for HIV, hepatitis B and C. Your treatment will be determined based on the type of exposure to blood or body fluids and your test results. The health care provider may also try to determine whether the person’s blood or body fluid with which you had contact may be infectious for HIV, hepatitis B and C.

In case of possible exposure to HIV, the health care provider may start you on a course of antiviral medications without waiting for test results. These medications should be started as soon as possible, and are most effective if started within 2 hours of exposure. You will be referred to your own health care provider if you need to continue taking these medications for 1 full month.

To help protect you from hepatitis B disease, you may be given a hepatitis B vaccine and hepatitis B immune globulin. Hepatitis B immune globulin contains antibodies that provide immediate but short-term protection against hepatitis B virus. The hepatitis B vaccine provides long lasting protection by helping your body make its own antibodies against the virus.

There is no vaccine to prevent infection with hepatitis C. Blood tests will show if you were exposed to hepatitis C or have acquired the virus.

If you have a serious cut or wound you may need to get the tetanus vaccine depending upon the type of wound and your immunization history.

To find out if you have acquired an infection as a result of the incident, you will need follow-up blood tests at 3 and 6 weeks and then at 3 months after the exposure.

What is the risk of getting HIV, hepatitis B or hepatitis C?

The risk of getting HIV, hepatitis B or C depends on the amount of virus in the blood or body fluid and the type of contact. For example, a piercing through the skin poses a greater risk than a splash on the skin.

The emergency department health care provider will tell you whether your exposure puts you at risk of these infections.

How do I prevent the spread of infection to others?

Sometimes it is not possible to know for a few months if you have acquired an infection after an exposure to blood or body fluids. If you have, you can potentially transmit the infection to others. While you are waiting for your test results, follow these steps to help prevent spreading the infection to others:

  • Do not have sex (vaginal, oral or rectal). If you have sex, use a male or female condom every time. For information on preventing STIs, see HealthLinkBC File #08o Preventing Sexually Transmitted Infections (STIs).
  • Do not donate blood, plasma, organs, breast milk, tissue, or sperm.
  • Do not share toothbrushes, dental floss, razors, or other items that may have blood or body fluids on them.
  • Cover open cuts and scratches until they heal.
  • Carefully throw away anything with blood on it, such as tampons, pads, tissues, dental floss, and bandages. Put sharp items such as used razors or needles into a container and tape shut. Throw away in the garbage – do not place in a recycling box.
  • Do not share drug snorting, smoking or injection equipment such as needles and syringes, straws and pipes.

Women who are breastfeeding and have been exposed to blood or body fluids should speak with their health care provider to find out if it is recommended that they continue to breastfeed.

If you become pregnant, see your health care provider or call the Oak Tree Clinic at BC Women’s Hospital and Health Centre at 604-875-2212 or toll-free in B.C. at 1-888-711-3030.

How can I safely clean a spill or a wound?

When cleaning spills, wear clean, disposable gloves and always use absorbent material, such as paper towels, first. Then clean the area of the spill more thoroughly with soap and water, and then disinfect it with household bleach. A fresh solution of bleach should be used for disinfecting and can be prepared by mixing 1 part of bleach to 9 parts of water. The bleach solution should be left in contact with the spill area for at least 10 minutes before wiping it up.

Wear gloves when handling any body fluids or cleaning cuts, scrapes or wounds. Wash your hands carefully after disposing of your gloves in a plastic bag. Add gloves to your first aid kit so you are prepared.

How do I protect myself and others?

Teach children to never touch used needles, syringes or condoms, and to tell an adult immediately if they find one. It is important to dispose of a used condom, needle or syringe quickly and carefully. Always wear clean disposable gloves or use tongs, pliers or another object to pick up used condoms, needles and syringes. Discard condoms in a plastic bag. Needles and syringes should be placed in a metal or plastic container with a puncture-proof lid and disposed of in the regular garbage or according to local by-laws. Always discard used gloves in a plastic bag and wash your hands carefully with warm water and soap. If the item used to remove the condom, needle or syringe is not disposable it should be disinfected with bleach.

Hand washing is the best way to prevent the spread of germs. Wash your hands carefully with soap and warm water for at least 15 to 20 seconds. Waterless alcohol-based hand rinses can be used as long as hands are not heavily soiled.

Wash your hands before and/or after the following activities:

  • before preparing food and after handling uncooked foods;
  • before eating or smoking;
  • before breastfeeding;
  • before and after providing first aid;
  • before and after providing care to a person;
  • after using the toilet or changing diapers;
  • after handling blood or body fluids; and
  • after coughing or sneezing.

For more information, see the following:

Peripheral Blood Examination Findings in SARS-CoV-2 Infection | American Journal of Clinical Pathology

Abstract

Objectives

Peripheral blood abnormalities in severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) have not been fully elucidated. We report qualitative and quantitative peripheral blood findings in coronavirus disease 2019 (COVID-19) patients and compare them with a control group.

Methods

We reviewed electronic medical records, complete blood counts, peripheral blood smears, and flow cytometry data in 12 patients with SARS-CoV-2. These were compared with 10 control patients with symptoms suspicious for SARS-CoV-2 but who tested negative.

Results

No significant differences were noted in blood counts, except that absolute lymphopenia was present frequently in the control group (P < .05). Acquired Pelger-Huët anomaly (APHA) was noted in all COVID-19 cases, in most cases affecting over 5% of granulocytes. This contrasted with APHA in only 50% of control cases, affecting fewer than 5% of granulocytes in all cases (P < .05). Monolobate neutrophils were exclusive to COVID-19 cases. COVID-19 patients had greater frequency of plasmacytoid lymphocytes (P < .05). Flow cytometry data revealed absolute CD3+ T-cell count reduction in 6 of 7 patients; all of them required mechanical ventilation.

Conclusions

Lymphopenia was infrequent in our COVID-19 cohort; however, flow cytometric analysis revealed absolute T-cell count reduction in most cases. COVID-19 cases had significant APHA with monolobate neutrophils and plasmacytoid lymphocytes as compared to controls.

• This is the first study where a detailed qualitative and quantitative examination of peripheral smear findings in COVID-19 patients was performed and compared against a control group.

• Absolute lymphopenia is not specific to COVID-19. Acquired Pelger-Huët anomaly with monolobate neutrophils is significantly more common in COVID-19 patients compared to the control group.

• A spectrum of variant lymphocytes is seen in COVID-19 cases, albeit constituting less than 10% of lymphocytes in most cases. Plasmacytoid lymphocytes are more common in COVID-19 cases.

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the causative agent of the coronavirus disease 2019 (COVID-19) pandemic, is a highly contagious enveloped single-stranded RNA virus that belongs to the family of Betacoronaviruses.1 This virus shares genomic and clinical similarities with the other highly pathogenic coronaviruses, namely severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV), which caused fatal epidemics in 2002 and 2012 respectively.2 SARS-CoV-2 infections can range from asymptomatic carriers to mild respiratory symptoms and fatal acute respiratory distress syndrome. The virus is thought to cause T-cell immune dysregulation, especially in immunocompromised patients, resulting in monocyte/macrophage activation, uncontrolled cytokine release, and fatal multiorgan dysfunction.3 Laboratory findings reported in association with COVID-19 include leukopenia, lymphopenia, monocytosis, neutrophilia, eosinopenia, and thrombocytopenia.4-6 To the best of our knowledge, peripheral blood smear morphologic findings are reported in detail in less than 5 publications to date in the literature.7-10 The reported abnormalities in peripheral blood smear include a range of reactive lymphocytes, abnormal platelet morphology, leukoerythroblastosis, and one publication on acquired Pelger-Huët anomaly (APHA). In this study, we report peripheral blood abnormalities, with emphasis on peripheral blood smear morphology, in 12 cases of SARS-CoV-2 infection and compare them with a control group.

Materials and Methods

The study was approved by the institutional review board. The list of all patients tested for SARS-CoV2 infection was retrieved. Clinical criteria recommended by the Centers for Disease Control and Prevention (CDC) were adopted by our institution for COVID-19 testing. Detection of SARS-CoV-2 was carried out using a modified CDC emergency use authorization–approved polymerase chain reaction (PCR) assay that had been successfully validated in our laboratory. This method involves nucleic acid extraction from nasopharyngeal swabs using Nuclisens easyMAG (bioMérieux) or Maxwell RSC 48 (Promega). Reverse transcription and then real-time PCR reactions were performed using 2 sets of CDC primers targeting the SARS-CoV-2 nucleocapsid genes N1 and N2 on the QuantStudio-3 Real-Time PCR system (ThermoFisher). Specimens were considered positive if either N1 or N2 was detected, and they were considered negative if neither was detected in the presence of appropriately detected controls.

As of April 22, 2020, a total of 1,584 cases were tested, among which SARS-CoV-2 virus was detected by PCR in 98 patients. Electronic medical records of the positive cases were reviewed for evidence of any hematologic tests performed. Twelve patients had peripheral blood smears available for review, and 6 of them had flow cytometric studies performed. Ten patients who met symptomatic criteria for COVID-19 testing, but who tested negative, had smears available for review. These 10 were reviewed as the control group. The peripheral blood smears were reviewed by 4 board-certified pathologists, which included 2 board-certified hematopathologists. The pathologists were blinded to the COVID-19 test result of patients during smear review. Statistical analysis was performed on the Microsoft Excel platform.

Complete blood cell counts (CBCs) were performed using Sysmex XN-9000. Leukocyte differential counts were performed using Sysmex DI-60 Cellavision software, and manual differential counts were performed when flagged for abnormalities. Peripheral blood smears were stained with Wright stain.

With regard to granulocytes, the presence of APHA, monolobate neutrophils, and toxic changes were recorded as a percentage of total granulocytes. These changes were reported as present if they were noted in more than 1% of granulocytes. Left shift of granulocytes is reported as present using the following cutoffs per total granulocyte count: bands, 10%; metamyelocytes and myelocytes, 5%; promyelocytes, 1%; and blasts, greater than 0%. Toxic changes in granulocytes were defined as presence of at least 2 of the following features: prominent cytoplasmic granulation, cytoplasmic vacuolization, and Döhle bodies, present in at least 5% of granulocytes.

The presence of atypical lymphocytes was noted, and atypical lymphocytes were further classified as Downey type I, Downey type II, Downey type III, plasmacytoid lymphocytes, large granular lymphocytes (LGL above normal ranges), and other atypical lymphocytes. The individual categories of atypical lymphocytes were reported as a percentage of total lymphocytes. Flow cytometric immunophenotyping for lymphocyte subsets was performed using BD FACSCanto II (Becton Dickinson). The antibodies analyzed included CD3, CD4, CD8, CD19, and CD16/56 with percentages and absolute counts reported.

Results

The 12 COVID-19 cases included 7 men and 5 women, with an age range of 25 to 100 years (mean, 55 years). The patients presented predominantly with respiratory symptoms (11/12) and fever (6/12) Table 1. Most patients had comorbidities at presentation, which included hypertension (3/12), asthma (3/12), HIV/AIDS (2/12), bacterial infections (2/12), malignancy (1/12), chronic kidney disease (1/12), and diabetes (1/12). Both patients with HIV/AIDS had less than 20 RNA copies/mL by PCR. Seven patients (58%) were admitted directly to the intensive care unit and required mechanical ventilation, of which 2 patients (16%) died. The demographics and symptoms in the control group were similar Table 2. The 10 patients in the control group included 8 men and 2 women, with an age range of 27 to 77 years (mean, 56 years). The comorbidities in this group of patients included bacterial infections (7/10), malignancy (3/10), hypertension (2/10), diabetes (2/10), HIV/AIDS (1/10), renal disease (1/10), congestive heart failure (1/10), and chronic obstructive pulmonary disease (1/10). Two patients (20%) required mechanical ventilation and died in this group.

Table 1

Clinical and Laboratory Findings in Patients With COVID-19

Patient
Clinical History
CBC Abnormalities on Admission
Flow Cytometry Abnormalities
Peripheral Smear Findings on Admission
Clinical Follow-up
44 yo F with asthma presented with SOB and fever and found to have multifocal pneumonia. She was admitted to the ICU. Clinical condition deteriorated rapidly and she was pronounced dead shortly after. No OP medications were listed in the chart.  Absolute neutrophilia (12.13 × 103/μL)  CD3 abs: 4,824 H  (723-2,737/μL) CD4 abs: 3,326 H  (404-1,612/μL) CD8 abs: 1,631 H (220-1,129/μL)  APHA >10%, monolobate, PMNL, toxic changes, leukoerythroblastosis, left shift to blast, Pl-ly <5%, T2-ly <5%, Other-ly <5%  Progressed to respiratory failure, MV, deceased 
25 yo M presented with SOB. He was admitted to the ICU and went into respiratory failure requiring MV. No OP medications were listed in the chart.  Thrombocytosis (519 × 103/μL)  CD3 abs: 517 L CD4 abs: 239 L  APHA >10%, monolobate, PMNL, left shift to myelocytes, Pl-ly 5%-10%, T2-ly 5%-10%, LGL 5%-10%  Progressed to respiratory failure, MV, recovered and discharged 
52 yo M with hypertension, presented with SOB. He was admitted to the ICU and found to have hypoxic respiratory failure due to pneumonia. OP medications included oseltamivir, cetirizine, and benzonatate.  Leukocytosis (18.75 × 103/μL) Absolute neutrophilia (14.49 × 103/μL)  CD3 abs: 594 L CD8 abs: 113 L  APHA >10%, left shift to metamyelocyte, Pl-ly <5%, T2-ly 5%-10%, T3-ly 5%-10%, LGL <5%  Progressed to respiratory failure, MV, recovered and discharged 
50 yo M presented with SOB and fever. No OP medications were listed in the chart.  Absolute monocytopenia (0.16 × 103/μL)  —  APHA <5%, left shift to myelocytes, Pl-ly <5%, T2-ly 5%-10%, LGL >10%, Other-ly <5%  Stable clinical course, recovered and discharged 
32 yo F presented with cough, headache, and SOB. OP medications included acetaminophen and clindamycin.  Anemia (Hb: 10.9 g/dL) Thrombocytopenia  (112 × 103/μL)  —  APHA 5%-10%, monolobate, PMNL, left shift to myelocytes, Pl-ly <5%, T1-ly <5%, T2-ly 5%-10%, T3-ly <5%, LGL <5%, Other-ly <5%  Stable clinical course, recovered and discharged 
67 yo M with HIV/AIDS and COPD was admitted to the ICU with hypoxemic respiratory failure. HIV RNA PCR <20 copies/mL. OP medications included Isentress, Descovy, metoprolol, clonazepam, and amlodipine.  Anemia (Hb: 11.9 g/dL) Leukocytosis (10.53 × 103/μL) Absolute neutrophilia (9.23 × 103/μL)  CD3 abs: 252 L CD4 abs: 108 L CD8 abs: 172 L  APHA >10%, monolobate, PMNL, left shift to myelocyte, PL-ly 5%-10%, T2-ly 5%-10%, T3-ly <5%, LGL <5%, Other-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
100 yo F with hypertension, thyroid and ovarian cancer, and chronic kidney disease presented with fever and cough. OP medications included metoprolol, sertraline, and cetirizine.  None  —  APHA >10%, left shift to bands, Pl-ly 5%-10%, T2-ly 5%-10%, T3-ly <5%, LGL 5%-10%, Other-ly <5%  Stable clinical course, recovered and discharged 
72 yo M presented with fever, SOB, and diarrhea. He was admitted to the ICU. No OP medications were listed in the chart.  Leukocytosis (35.6 × 103/μL) Absolute neutrophilia (32.68 × 103/μL)  CD3 abs: 244 L CD4 abs: 197 L CD8 abs: 62 L CD19 abs: 21 L  (80-616/μL)  APHA <5%, monolobate, PMNL, toxic changes, left shift to bands, T2-ly <5%, T3-ly <5%, LGL <5%, Other-ly <5%  Progressed to respiratory failure, MV, recovered and discharged 
49 yo M with schizophrenia and history of polytrauma and Pseudomonas infection was admitted to the ICU for hypoxemic respiratory failure. OP medications included benztropine, escitalopram, and acetaminophen.  Anemia (Hb: 11.1 g/dL) Absolute lymphopenia (0.44 × 103/μL)  CD3 abs: 592 L CD4 abs: 353 L CD16/56 abs: 71 L  (84-724/μL)  APHA 5%-10%, monolobate, PMNL, toxic changes,T2-ly 5%-10%, LGL <5%  Progressed to respiratory failure, MV, recovered and discharged 
10  61 yo M with HIV/AIDS, hypertension, COPD, and asthma presented with fever, cough, and diarrhea and was admitted to the ICU. HIV RNA PCR <20 copies/mL. OP medications included Triumeq, aspirin, amlodipine, Nexium, and Flonase.  Anemia (Hb: 11.6 g/dL) Leukocytosis (11.02 × 103/μL) Absolute lymphopenia (0.85 × 103/μL) Absolute neutrophilia (8.92 × 103/μL)  CD3 abs: 507 L CD4 abs: 145 L  APHA >10%, Pl-ly <5%, T2-ly <5%, LGL 5%-10%  Progressed to respiratory failure, MV, recovered and discharged 
11  77 yo F with type 1 diabetes, asthma, and CAD presented with SOB and was found to have viral and bacterial pneumonia. OP medications included Advair, aspirin, enalapril, amitriptyline, albuterol, Lipitor, and Macrobid.  Anemia (Hb: 10 g/dL) Leukocytosis (12.41 × 103/μL) Absolute neutrophilia (10.11 × 103/μL)  —  APHA <5%, T1-ly <5%, T2-ly <5%, LGL <5%, Other-ly <5%  Stable clinical course, recovered and discharged 
12  33 yo F presented with cough, SOB, and fever. No OP medications were listed in the chart.  None  —  APHA 5%-10%, toxic changes, Pl-ly <5%, T2-ly <5%, LGL <5%  Stable clinical course, recovered and discharged 
Patient
Clinical History
CBC Abnormalities on Admission
Flow Cytometry Abnormalities
Peripheral Smear Findings on Admission
Clinical Follow-up
44 yo F with asthma presented with SOB and fever and found to have multifocal pneumonia. She was admitted to the ICU. Clinical condition deteriorated rapidly and she was pronounced dead shortly after. No OP medications were listed in the chart.  Absolute neutrophilia (12.13 × 103/μL)  CD3 abs: 4,824 H  (723-2,737/μL) CD4 abs: 3,326 H  (404-1,612/μL) CD8 abs: 1,631 H (220-1,129/μL)  APHA >10%, monolobate, PMNL, toxic changes, leukoerythroblastosis, left shift to blast, Pl-ly <5%, T2-ly <5%, Other-ly <5%  Progressed to respiratory failure, MV, deceased 
25 yo M presented with SOB. He was admitted to the ICU and went into respiratory failure requiring MV. No OP medications were listed in the chart.  Thrombocytosis (519 × 103/μL)  CD3 abs: 517 L CD4 abs: 239 L  APHA >10%, monolobate, PMNL, left shift to myelocytes, Pl-ly 5%-10%, T2-ly 5%-10%, LGL 5%-10%  Progressed to respiratory failure, MV, recovered and discharged 
52 yo M with hypertension, presented with SOB. He was admitted to the ICU and found to have hypoxic respiratory failure due to pneumonia. OP medications included oseltamivir, cetirizine, and benzonatate.  Leukocytosis (18.75 × 103/μL) Absolute neutrophilia (14.49 × 103/μL)  CD3 abs: 594 L CD8 abs: 113 L  APHA >10%, left shift to metamyelocyte, Pl-ly <5%, T2-ly 5%-10%, T3-ly 5%-10%, LGL <5%  Progressed to respiratory failure, MV, recovered and discharged 
50 yo M presented with SOB and fever. No OP medications were listed in the chart.  Absolute monocytopenia (0.16 × 103/μL)  —  APHA <5%, left shift to myelocytes, Pl-ly <5%, T2-ly 5%-10%, LGL >10%, Other-ly <5%  Stable clinical course, recovered and discharged 
32 yo F presented with cough, headache, and SOB. OP medications included acetaminophen and clindamycin.  Anemia (Hb: 10.9 g/dL) Thrombocytopenia  (112 × 103/μL)  —  APHA 5%-10%, monolobate, PMNL, left shift to myelocytes, Pl-ly <5%, T1-ly <5%, T2-ly 5%-10%, T3-ly <5%, LGL <5%, Other-ly <5%  Stable clinical course, recovered and discharged 
67 yo M with HIV/AIDS and COPD was admitted to the ICU with hypoxemic respiratory failure. HIV RNA PCR <20 copies/mL. OP medications included Isentress, Descovy, metoprolol, clonazepam, and amlodipine.  Anemia (Hb: 11.9 g/dL) Leukocytosis (10.53 × 103/μL) Absolute neutrophilia (9.23 × 103/μL)  CD3 abs: 252 L CD4 abs: 108 L CD8 abs: 172 L  APHA >10%, monolobate, PMNL, left shift to myelocyte, PL-ly 5%-10%, T2-ly 5%-10%, T3-ly <5%, LGL <5%, Other-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
100 yo F with hypertension, thyroid and ovarian cancer, and chronic kidney disease presented with fever and cough. OP medications included metoprolol, sertraline, and cetirizine.  None  —  APHA >10%, left shift to bands, Pl-ly 5%-10%, T2-ly 5%-10%, T3-ly <5%, LGL 5%-10%, Other-ly <5%  Stable clinical course, recovered and discharged 
72 yo M presented with fever, SOB, and diarrhea. He was admitted to the ICU. No OP medications were listed in the chart.  Leukocytosis (35.6 × 103/μL) Absolute neutrophilia (32.68 × 103/μL)  CD3 abs: 244 L CD4 abs: 197 L CD8 abs: 62 L CD19 abs: 21 L  (80-616/μL)  APHA <5%, monolobate, PMNL, toxic changes, left shift to bands, T2-ly <5%, T3-ly <5%, LGL <5%, Other-ly <5%  Progressed to respiratory failure, MV, recovered and discharged 
49 yo M with schizophrenia and history of polytrauma and Pseudomonas infection was admitted to the ICU for hypoxemic respiratory failure. OP medications included benztropine, escitalopram, and acetaminophen.  Anemia (Hb: 11.1 g/dL) Absolute lymphopenia (0.44 × 103/μL)  CD3 abs: 592 L CD4 abs: 353 L CD16/56 abs: 71 L  (84-724/μL)  APHA 5%-10%, monolobate, PMNL, toxic changes,T2-ly 5%-10%, LGL <5%  Progressed to respiratory failure, MV, recovered and discharged 
10  61 yo M with HIV/AIDS, hypertension, COPD, and asthma presented with fever, cough, and diarrhea and was admitted to the ICU. HIV RNA PCR <20 copies/mL. OP medications included Triumeq, aspirin, amlodipine, Nexium, and Flonase.  Anemia (Hb: 11.6 g/dL) Leukocytosis (11.02 × 103/μL) Absolute lymphopenia (0.85 × 103/μL) Absolute neutrophilia (8.92 × 103/μL)  CD3 abs: 507 L CD4 abs: 145 L  APHA >10%, Pl-ly <5%, T2-ly <5%, LGL 5%-10%  Progressed to respiratory failure, MV, recovered and discharged 
11  77 yo F with type 1 diabetes, asthma, and CAD presented with SOB and was found to have viral and bacterial pneumonia. OP medications included Advair, aspirin, enalapril, amitriptyline, albuterol, Lipitor, and Macrobid.  Anemia (Hb: 10 g/dL) Leukocytosis (12.41 × 103/μL) Absolute neutrophilia (10.11 × 103/μL)  —  APHA <5%, T1-ly <5%, T2-ly <5%, LGL <5%, Other-ly <5%  Stable clinical course, recovered and discharged 
12  33 yo F presented with cough, SOB, and fever. No OP medications were listed in the chart.  None  —  APHA 5%-10%, toxic changes, Pl-ly <5%, T2-ly <5%, LGL <5%  Stable clinical course, recovered and discharged 

Table 1

Clinical and Laboratory Findings in Patients With COVID-19

Patient
Clinical History
CBC Abnormalities on Admission
Flow Cytometry Abnormalities
Peripheral Smear Findings on Admission
Clinical Follow-up
44 yo F with asthma presented with SOB and fever and found to have multifocal pneumonia. She was admitted to the ICU. Clinical condition deteriorated rapidly and she was pronounced dead shortly after. No OP medications were listed in the chart.  Absolute neutrophilia (12.13 × 103/μL)  CD3 abs: 4,824 H  (723-2,737/μL) CD4 abs: 3,326 H  (404-1,612/μL) CD8 abs: 1,631 H (220-1,129/μL)  APHA >10%, monolobate, PMNL, toxic changes, leukoerythroblastosis, left shift to blast, Pl-ly <5%, T2-ly <5%, Other-ly <5%  Progressed to respiratory failure, MV, deceased 
25 yo M presented with SOB. He was admitted to the ICU and went into respiratory failure requiring MV. No OP medications were listed in the chart.  Thrombocytosis (519 × 103/μL)  CD3 abs: 517 L CD4 abs: 239 L  APHA >10%, monolobate, PMNL, left shift to myelocytes, Pl-ly 5%-10%, T2-ly 5%-10%, LGL 5%-10%  Progressed to respiratory failure, MV, recovered and discharged 
52 yo M with hypertension, presented with SOB. He was admitted to the ICU and found to have hypoxic respiratory failure due to pneumonia. OP medications included oseltamivir, cetirizine, and benzonatate.  Leukocytosis (18.75 × 103/μL) Absolute neutrophilia (14.49 × 103/μL)  CD3 abs: 594 L CD8 abs: 113 L  APHA >10%, left shift to metamyelocyte, Pl-ly <5%, T2-ly 5%-10%, T3-ly 5%-10%, LGL <5%  Progressed to respiratory failure, MV, recovered and discharged 
50 yo M presented with SOB and fever. No OP medications were listed in the chart.  Absolute monocytopenia (0.16 × 103/μL)  —  APHA <5%, left shift to myelocytes, Pl-ly <5%, T2-ly 5%-10%, LGL >10%, Other-ly <5%  Stable clinical course, recovered and discharged 
32 yo F presented with cough, headache, and SOB. OP medications included acetaminophen and clindamycin.  Anemia (Hb: 10.9 g/dL) Thrombocytopenia  (112 × 103/μL)  —  APHA 5%-10%, monolobate, PMNL, left shift to myelocytes, Pl-ly <5%, T1-ly <5%, T2-ly 5%-10%, T3-ly <5%, LGL <5%, Other-ly <5%  Stable clinical course, recovered and discharged 
67 yo M with HIV/AIDS and COPD was admitted to the ICU with hypoxemic respiratory failure. HIV RNA PCR <20 copies/mL. OP medications included Isentress, Descovy, metoprolol, clonazepam, and amlodipine.  Anemia (Hb: 11.9 g/dL) Leukocytosis (10.53 × 103/μL) Absolute neutrophilia (9.23 × 103/μL)  CD3 abs: 252 L CD4 abs: 108 L CD8 abs: 172 L  APHA >10%, monolobate, PMNL, left shift to myelocyte, PL-ly 5%-10%, T2-ly 5%-10%, T3-ly <5%, LGL <5%, Other-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
100 yo F with hypertension, thyroid and ovarian cancer, and chronic kidney disease presented with fever and cough. OP medications included metoprolol, sertraline, and cetirizine.  None  —  APHA >10%, left shift to bands, Pl-ly 5%-10%, T2-ly 5%-10%, T3-ly <5%, LGL 5%-10%, Other-ly <5%  Stable clinical course, recovered and discharged 
72 yo M presented with fever, SOB, and diarrhea. He was admitted to the ICU. No OP medications were listed in the chart.  Leukocytosis (35.6 × 103/μL) Absolute neutrophilia (32.68 × 103/μL)  CD3 abs: 244 L CD4 abs: 197 L CD8 abs: 62 L CD19 abs: 21 L  (80-616/μL)  APHA <5%, monolobate, PMNL, toxic changes, left shift to bands, T2-ly <5%, T3-ly <5%, LGL <5%, Other-ly <5%  Progressed to respiratory failure, MV, recovered and discharged 
49 yo M with schizophrenia and history of polytrauma and Pseudomonas infection was admitted to the ICU for hypoxemic respiratory failure. OP medications included benztropine, escitalopram, and acetaminophen.  Anemia (Hb: 11.1 g/dL) Absolute lymphopenia (0.44 × 103/μL)  CD3 abs: 592 L CD4 abs: 353 L CD16/56 abs: 71 L  (84-724/μL)  APHA 5%-10%, monolobate, PMNL, toxic changes,T2-ly 5%-10%, LGL <5%  Progressed to respiratory failure, MV, recovered and discharged 
10  61 yo M with HIV/AIDS, hypertension, COPD, and asthma presented with fever, cough, and diarrhea and was admitted to the ICU. HIV RNA PCR <20 copies/mL. OP medications included Triumeq, aspirin, amlodipine, Nexium, and Flonase.  Anemia (Hb: 11.6 g/dL) Leukocytosis (11.02 × 103/μL) Absolute lymphopenia (0.85 × 103/μL) Absolute neutrophilia (8.92 × 103/μL)  CD3 abs: 507 L CD4 abs: 145 L  APHA >10%, Pl-ly <5%, T2-ly <5%, LGL 5%-10%  Progressed to respiratory failure, MV, recovered and discharged 
11  77 yo F with type 1 diabetes, asthma, and CAD presented with SOB and was found to have viral and bacterial pneumonia. OP medications included Advair, aspirin, enalapril, amitriptyline, albuterol, Lipitor, and Macrobid.  Anemia (Hb: 10 g/dL) Leukocytosis (12.41 × 103/μL) Absolute neutrophilia (10.11 × 103/μL)  —  APHA <5%, T1-ly <5%, T2-ly <5%, LGL <5%, Other-ly <5%  Stable clinical course, recovered and discharged 
12  33 yo F presented with cough, SOB, and fever. No OP medications were listed in the chart.  None  —  APHA 5%-10%, toxic changes, Pl-ly <5%, T2-ly <5%, LGL <5%  Stable clinical course, recovered and discharged 
Patient
Clinical History
CBC Abnormalities on Admission
Flow Cytometry Abnormalities
Peripheral Smear Findings on Admission
Clinical Follow-up
44 yo F with asthma presented with SOB and fever and found to have multifocal pneumonia. She was admitted to the ICU. Clinical condition deteriorated rapidly and she was pronounced dead shortly after. No OP medications were listed in the chart.  Absolute neutrophilia (12.13 × 103/μL)  CD3 abs: 4,824 H  (723-2,737/μL) CD4 abs: 3,326 H  (404-1,612/μL) CD8 abs: 1,631 H (220-1,129/μL)  APHA >10%, monolobate, PMNL, toxic changes, leukoerythroblastosis, left shift to blast, Pl-ly <5%, T2-ly <5%, Other-ly <5%  Progressed to respiratory failure, MV, deceased 
25 yo M presented with SOB. He was admitted to the ICU and went into respiratory failure requiring MV. No OP medications were listed in the chart.  Thrombocytosis (519 × 103/μL)  CD3 abs: 517 L CD4 abs: 239 L  APHA >10%, monolobate, PMNL, left shift to myelocytes, Pl-ly 5%-10%, T2-ly 5%-10%, LGL 5%-10%  Progressed to respiratory failure, MV, recovered and discharged 
52 yo M with hypertension, presented with SOB. He was admitted to the ICU and found to have hypoxic respiratory failure due to pneumonia. OP medications included oseltamivir, cetirizine, and benzonatate.  Leukocytosis (18.75 × 103/μL) Absolute neutrophilia (14.49 × 103/μL)  CD3 abs: 594 L CD8 abs: 113 L  APHA >10%, left shift to metamyelocyte, Pl-ly <5%, T2-ly 5%-10%, T3-ly 5%-10%, LGL <5%  Progressed to respiratory failure, MV, recovered and discharged 
50 yo M presented with SOB and fever. No OP medications were listed in the chart.  Absolute monocytopenia (0.16 × 103/μL)  —  APHA <5%, left shift to myelocytes, Pl-ly <5%, T2-ly 5%-10%, LGL >10%, Other-ly <5%  Stable clinical course, recovered and discharged 
32 yo F presented with cough, headache, and SOB. OP medications included acetaminophen and clindamycin.  Anemia (Hb: 10.9 g/dL) Thrombocytopenia  (112 × 103/μL)  —  APHA 5%-10%, monolobate, PMNL, left shift to myelocytes, Pl-ly <5%, T1-ly <5%, T2-ly 5%-10%, T3-ly <5%, LGL <5%, Other-ly <5%  Stable clinical course, recovered and discharged 
67 yo M with HIV/AIDS and COPD was admitted to the ICU with hypoxemic respiratory failure. HIV RNA PCR <20 copies/mL. OP medications included Isentress, Descovy, metoprolol, clonazepam, and amlodipine.  Anemia (Hb: 11.9 g/dL) Leukocytosis (10.53 × 103/μL) Absolute neutrophilia (9.23 × 103/μL)  CD3 abs: 252 L CD4 abs: 108 L CD8 abs: 172 L  APHA >10%, monolobate, PMNL, left shift to myelocyte, PL-ly 5%-10%, T2-ly 5%-10%, T3-ly <5%, LGL <5%, Other-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
100 yo F with hypertension, thyroid and ovarian cancer, and chronic kidney disease presented with fever and cough. OP medications included metoprolol, sertraline, and cetirizine.  None  —  APHA >10%, left shift to bands, Pl-ly 5%-10%, T2-ly 5%-10%, T3-ly <5%, LGL 5%-10%, Other-ly <5%  Stable clinical course, recovered and discharged 
72 yo M presented with fever, SOB, and diarrhea. He was admitted to the ICU. No OP medications were listed in the chart.  Leukocytosis (35.6 × 103/μL) Absolute neutrophilia (32.68 × 103/μL)  CD3 abs: 244 L CD4 abs: 197 L CD8 abs: 62 L CD19 abs: 21 L  (80-616/μL)  APHA <5%, monolobate, PMNL, toxic changes, left shift to bands, T2-ly <5%, T3-ly <5%, LGL <5%, Other-ly <5%  Progressed to respiratory failure, MV, recovered and discharged 
49 yo M with schizophrenia and history of polytrauma and Pseudomonas infection was admitted to the ICU for hypoxemic respiratory failure. OP medications included benztropine, escitalopram, and acetaminophen.  Anemia (Hb: 11.1 g/dL) Absolute lymphopenia (0.44 × 103/μL)  CD3 abs: 592 L CD4 abs: 353 L CD16/56 abs: 71 L  (84-724/μL)  APHA 5%-10%, monolobate, PMNL, toxic changes,T2-ly 5%-10%, LGL <5%  Progressed to respiratory failure, MV, recovered and discharged 
10  61 yo M with HIV/AIDS, hypertension, COPD, and asthma presented with fever, cough, and diarrhea and was admitted to the ICU. HIV RNA PCR <20 copies/mL. OP medications included Triumeq, aspirin, amlodipine, Nexium, and Flonase.  Anemia (Hb: 11.6 g/dL) Leukocytosis (11.02 × 103/μL) Absolute lymphopenia (0.85 × 103/μL) Absolute neutrophilia (8.92 × 103/μL)  CD3 abs: 507 L CD4 abs: 145 L  APHA >10%, Pl-ly <5%, T2-ly <5%, LGL 5%-10%  Progressed to respiratory failure, MV, recovered and discharged 
11  77 yo F with type 1 diabetes, asthma, and CAD presented with SOB and was found to have viral and bacterial pneumonia. OP medications included Advair, aspirin, enalapril, amitriptyline, albuterol, Lipitor, and Macrobid.  Anemia (Hb: 10 g/dL) Leukocytosis (12.41 × 103/μL) Absolute neutrophilia (10.11 × 103/μL)  —  APHA <5%, T1-ly <5%, T2-ly <5%, LGL <5%, Other-ly <5%  Stable clinical course, recovered and discharged 
12  33 yo F presented with cough, SOB, and fever. No OP medications were listed in the chart.  None  —  APHA 5%-10%, toxic changes, Pl-ly <5%, T2-ly <5%, LGL <5%  Stable clinical course, recovered and discharged 

Table 2

Clinical and Laboratory Findings in Control Group of Patients

Patient
Clinical History
CBC Abnormalities on Admission
Flow Cytometry Abnormalities
Peripheral Smear Findings on Admission
Clinical Follow-up
77 yo F with hypertension, type 2 diabetes, and breast cancer presented with SOB, fever, and hypotension. She was found to have metapneumovirus infection and Clostridium difficile colitis. OP medications included metformin, metoprolol, and levothyroxine.  Anemia (Hb: 10.2 g/dL) Absolute lymphopenia (0.67 × 103/μL)Absolute monocytopenia (0.19 × 103/μL)  —  APHA 5%-10%, toxic changes, left shift to myelocytes, T2-ly 5%-10%, LGL 5%-10%  Recovered and discharged 
39 yo M presented with SOB and new onset heart failure. He was found to have metapneumovirus and Rhinovirus by PCR. OP medications included acetaminophen, guaifenesin, albuterol, dicyclomine, and ondansetron.  None  —  Pl-ly <5%, T2-ly <5%, T3-ly <5%, Other-ly <5%  Recovered and discharged 
39 yo M presented with SOB and pneumonia. His tracheal swab was positive for Escherichia coli. OP medications included metoprolol, sertraline, buspirone, and trazodone.  Anemia (Hb: 7.3 g/dL)Leukocytosis (18.38 × 103/μL)Absolute lymphopenia (0.74 × 103/μL)Absolute neutrophilia (16.54 × 103/μL)  —  APHA <5%, toxic changes, left shift to bands, PL-ly <5%, T2-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
67 yo M with history of oral cancer presented with fever and cough. He was found to have Streptococcus agalactiae bacteremia. OP medications included prednisone, metoprolol, atorvastatin, levothyroxine, guaifenesin, and furosemide.  Anemia (Hb: 7.4 g/dL)Leukocytosis (12.04 × 103/μL)Absolute lymphopenia (0.24 × 103/μL)Absolute neutrophilia (8.67 × 103/μL)  CD3 abs: 118 L (723-2,737/μL)CD4 abs: <40 L (404-1,612/μL)CD8 abs: 87 L (220-1,129/μL)  APHA <5%, left shift to myelocytes, T2-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
63 yo M with hypertension, congestive heart failure, and COPD presented with fever and SOB. He was found to have metapneumovirus infection and secondary bacterial pneumonia. OP medications included metoprolol, lisinopril, aspirin, atorvastatin, cetirizine, and prednisone.   Anemia (Hb: 11.4 g/dL)Leukocytosis (23.97 × 103/μL)Absolute lymphopenia (0.46 × 103/μL)Absolute neutrophilia (21.89 × 103/μL)  —  Toxic changes, T2-ly <5%, LGL <5%  Recovered and discharged 
61 yo M with end-stage renal disease and type 2 diabetes presented with fever and SOB. He was found to have Staphylococcus aureus bacteremia. OP medications included amlodipine, atorvastatin, furosemide, and Keppra.  Anemia (Hb: 11.3 g/dL)  —  APHA <5%, toxic changes, left shift to metamyelocytes, Pl-ly <5%  Recovered and discharged 
27 yo M presented with fever and sore throat. Monospot test was positive. No OP medications were listed in the chart.  Leukocytosis (13.15 × 103/μL)Absolute lymphocytosis (5.65 × 103/μL)Absolute monocytosis (1.58 × 103/μL)  —  PL-ly <5%, T1-ly >10%, T2-ly >10%, T3-ly <5%, LGL >10%  Recovered and discharged 
62 yo M with chronic neutropenia and history of Kaposi sarcoma presented with fever and pneumonia. He was positive for rhinovirus/enterovirus on PCR. OP medications included metoprolol, amlodipine, and Zoloft.  Anemia (Hb: 9.9 g/dL)Leukopenia (1.85 × 103/μL)Absolute lymphopenia (0.39 × 103/μL)Absolute neutropenia (1.28 × 103/μL)  —  PL-ly 5%-10%, T1-ly <5%, T2-ly <5%, LGL <5%  Recovered and discharged 
59 yo M with HIV and autoimmune hemolytic anemia presented with fever. He was found to have rhinovirus/enterovirus on PCR and Pseudomonas in urine sample. HIV RNA PCR <20 copies/mL. OP medications included BIKTARVY.  Anemia (Hb: 11.6 g/dL)Absolute lymphopenia (0.24 × 103/μL)Thrombocytopenia (95 × 103/μL)  —  Toxic changes, left shift to bands, T1-ly 5%-10%, T2-ly <5%, LGL 5%-10%  Recovered and discharged 
10  64 yo F presented with cough and fever. She was found to have bacterial pneumonia. No OP medications were listed in the chart.  Leukocytosis (16.91 × 103/μL)Absolute neutrophilia (12.83 × 103/μL)  —  APHA <5%, toxic changes, left shift to metamyelocytes, PL-ly: <5%, T2-ly 5%-10%, T3-ly <5%, LGL <5%  Recovered and discharged 
Patient
Clinical History
CBC Abnormalities on Admission
Flow Cytometry Abnormalities
Peripheral Smear Findings on Admission
Clinical Follow-up
77 yo F with hypertension, type 2 diabetes, and breast cancer presented with SOB, fever, and hypotension. She was found to have metapneumovirus infection and Clostridium difficile colitis. OP medications included metformin, metoprolol, and levothyroxine.  Anemia (Hb: 10.2 g/dL) Absolute lymphopenia (0.67 × 103/μL)Absolute monocytopenia (0.19 × 103/μL)  —  APHA 5%-10%, toxic changes, left shift to myelocytes, T2-ly 5%-10%, LGL 5%-10%  Recovered and discharged 
39 yo M presented with SOB and new onset heart failure. He was found to have metapneumovirus and Rhinovirus by PCR. OP medications included acetaminophen, guaifenesin, albuterol, dicyclomine, and ondansetron.  None  —  Pl-ly <5%, T2-ly <5%, T3-ly <5%, Other-ly <5%  Recovered and discharged 
39 yo M presented with SOB and pneumonia. His tracheal swab was positive for Escherichia coli. OP medications included metoprolol, sertraline, buspirone, and trazodone.  Anemia (Hb: 7.3 g/dL)Leukocytosis (18.38 × 103/μL)Absolute lymphopenia (0.74 × 103/μL)Absolute neutrophilia (16.54 × 103/μL)  —  APHA <5%, toxic changes, left shift to bands, PL-ly <5%, T2-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
67 yo M with history of oral cancer presented with fever and cough. He was found to have Streptococcus agalactiae bacteremia. OP medications included prednisone, metoprolol, atorvastatin, levothyroxine, guaifenesin, and furosemide.  Anemia (Hb: 7.4 g/dL)Leukocytosis (12.04 × 103/μL)Absolute lymphopenia (0.24 × 103/μL)Absolute neutrophilia (8.67 × 103/μL)  CD3 abs: 118 L (723-2,737/μL)CD4 abs: <40 L (404-1,612/μL)CD8 abs: 87 L (220-1,129/μL)  APHA <5%, left shift to myelocytes, T2-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
63 yo M with hypertension, congestive heart failure, and COPD presented with fever and SOB. He was found to have metapneumovirus infection and secondary bacterial pneumonia. OP medications included metoprolol, lisinopril, aspirin, atorvastatin, cetirizine, and prednisone.   Anemia (Hb: 11.4 g/dL)Leukocytosis (23.97 × 103/μL)Absolute lymphopenia (0.46 × 103/μL)Absolute neutrophilia (21.89 × 103/μL)  —  Toxic changes, T2-ly <5%, LGL <5%  Recovered and discharged 
61 yo M with end-stage renal disease and type 2 diabetes presented with fever and SOB. He was found to have Staphylococcus aureus bacteremia. OP medications included amlodipine, atorvastatin, furosemide, and Keppra.  Anemia (Hb: 11.3 g/dL)  —  APHA <5%, toxic changes, left shift to metamyelocytes, Pl-ly <5%  Recovered and discharged 
27 yo M presented with fever and sore throat. Monospot test was positive. No OP medications were listed in the chart.  Leukocytosis (13.15 × 103/μL)Absolute lymphocytosis (5.65 × 103/μL)Absolute monocytosis (1.58 × 103/μL)  —  PL-ly <5%, T1-ly >10%, T2-ly >10%, T3-ly <5%, LGL >10%  Recovered and discharged 
62 yo M with chronic neutropenia and history of Kaposi sarcoma presented with fever and pneumonia. He was positive for rhinovirus/enterovirus on PCR. OP medications included metoprolol, amlodipine, and Zoloft.  Anemia (Hb: 9.9 g/dL)Leukopenia (1.85 × 103/μL)Absolute lymphopenia (0.39 × 103/μL)Absolute neutropenia (1.28 × 103/μL)  —  PL-ly 5%-10%, T1-ly <5%, T2-ly <5%, LGL <5%  Recovered and discharged 
59 yo M with HIV and autoimmune hemolytic anemia presented with fever. He was found to have rhinovirus/enterovirus on PCR and Pseudomonas in urine sample. HIV RNA PCR <20 copies/mL. OP medications included BIKTARVY.  Anemia (Hb: 11.6 g/dL)Absolute lymphopenia (0.24 × 103/μL)Thrombocytopenia (95 × 103/μL)  —  Toxic changes, left shift to bands, T1-ly 5%-10%, T2-ly <5%, LGL 5%-10%  Recovered and discharged 
10  64 yo F presented with cough and fever. She was found to have bacterial pneumonia. No OP medications were listed in the chart.  Leukocytosis (16.91 × 103/μL)Absolute neutrophilia (12.83 × 103/μL)  —  APHA <5%, toxic changes, left shift to metamyelocytes, PL-ly: <5%, T2-ly 5%-10%, T3-ly <5%, LGL <5%  Recovered and discharged 

Table 2

Clinical and Laboratory Findings in Control Group of Patients

Patient
Clinical History
CBC Abnormalities on Admission
Flow Cytometry Abnormalities
Peripheral Smear Findings on Admission
Clinical Follow-up
77 yo F with hypertension, type 2 diabetes, and breast cancer presented with SOB, fever, and hypotension. She was found to have metapneumovirus infection and Clostridium difficile colitis. OP medications included metformin, metoprolol, and levothyroxine.  Anemia (Hb: 10.2 g/dL) Absolute lymphopenia (0.67 × 103/μL)Absolute monocytopenia (0.19 × 103/μL)  —  APHA 5%-10%, toxic changes, left shift to myelocytes, T2-ly 5%-10%, LGL 5%-10%  Recovered and discharged 
39 yo M presented with SOB and new onset heart failure. He was found to have metapneumovirus and Rhinovirus by PCR. OP medications included acetaminophen, guaifenesin, albuterol, dicyclomine, and ondansetron.  None  —  Pl-ly <5%, T2-ly <5%, T3-ly <5%, Other-ly <5%  Recovered and discharged 
39 yo M presented with SOB and pneumonia. His tracheal swab was positive for Escherichia coli. OP medications included metoprolol, sertraline, buspirone, and trazodone.  Anemia (Hb: 7.3 g/dL)Leukocytosis (18.38 × 103/μL)Absolute lymphopenia (0.74 × 103/μL)Absolute neutrophilia (16.54 × 103/μL)  —  APHA <5%, toxic changes, left shift to bands, PL-ly <5%, T2-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
67 yo M with history of oral cancer presented with fever and cough. He was found to have Streptococcus agalactiae bacteremia. OP medications included prednisone, metoprolol, atorvastatin, levothyroxine, guaifenesin, and furosemide.  Anemia (Hb: 7.4 g/dL)Leukocytosis (12.04 × 103/μL)Absolute lymphopenia (0.24 × 103/μL)Absolute neutrophilia (8.67 × 103/μL)  CD3 abs: 118 L (723-2,737/μL)CD4 abs: <40 L (404-1,612/μL)CD8 abs: 87 L (220-1,129/μL)  APHA <5%, left shift to myelocytes, T2-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
63 yo M with hypertension, congestive heart failure, and COPD presented with fever and SOB. He was found to have metapneumovirus infection and secondary bacterial pneumonia. OP medications included metoprolol, lisinopril, aspirin, atorvastatin, cetirizine, and prednisone.   Anemia (Hb: 11.4 g/dL)Leukocytosis (23.97 × 103/μL)Absolute lymphopenia (0.46 × 103/μL)Absolute neutrophilia (21.89 × 103/μL)  —  Toxic changes, T2-ly <5%, LGL <5%  Recovered and discharged 
61 yo M with end-stage renal disease and type 2 diabetes presented with fever and SOB. He was found to have Staphylococcus aureus bacteremia. OP medications included amlodipine, atorvastatin, furosemide, and Keppra.  Anemia (Hb: 11.3 g/dL)  —  APHA <5%, toxic changes, left shift to metamyelocytes, Pl-ly <5%  Recovered and discharged 
27 yo M presented with fever and sore throat. Monospot test was positive. No OP medications were listed in the chart.  Leukocytosis (13.15 × 103/μL)Absolute lymphocytosis (5.65 × 103/μL)Absolute monocytosis (1.58 × 103/μL)  —  PL-ly <5%, T1-ly >10%, T2-ly >10%, T3-ly <5%, LGL >10%  Recovered and discharged 
62 yo M with chronic neutropenia and history of Kaposi sarcoma presented with fever and pneumonia. He was positive for rhinovirus/enterovirus on PCR. OP medications included metoprolol, amlodipine, and Zoloft.  Anemia (Hb: 9.9 g/dL)Leukopenia (1.85 × 103/μL)Absolute lymphopenia (0.39 × 103/μL)Absolute neutropenia (1.28 × 103/μL)  —  PL-ly 5%-10%, T1-ly <5%, T2-ly <5%, LGL <5%  Recovered and discharged 
59 yo M with HIV and autoimmune hemolytic anemia presented with fever. He was found to have rhinovirus/enterovirus on PCR and Pseudomonas in urine sample. HIV RNA PCR <20 copies/mL. OP medications included BIKTARVY.  Anemia (Hb: 11.6 g/dL)Absolute lymphopenia (0.24 × 103/μL)Thrombocytopenia (95 × 103/μL)  —  Toxic changes, left shift to bands, T1-ly 5%-10%, T2-ly <5%, LGL 5%-10%  Recovered and discharged 
10  64 yo F presented with cough and fever. She was found to have bacterial pneumonia. No OP medications were listed in the chart.  Leukocytosis (16.91 × 103/μL)Absolute neutrophilia (12.83 × 103/μL)  —  APHA <5%, toxic changes, left shift to metamyelocytes, PL-ly: <5%, T2-ly 5%-10%, T3-ly <5%, LGL <5%  Recovered and discharged 
Patient
Clinical History
CBC Abnormalities on Admission
Flow Cytometry Abnormalities
Peripheral Smear Findings on Admission
Clinical Follow-up
77 yo F with hypertension, type 2 diabetes, and breast cancer presented with SOB, fever, and hypotension. She was found to have metapneumovirus infection and Clostridium difficile colitis. OP medications included metformin, metoprolol, and levothyroxine.  Anemia (Hb: 10.2 g/dL) Absolute lymphopenia (0.67 × 103/μL)Absolute monocytopenia (0.19 × 103/μL)  —  APHA 5%-10%, toxic changes, left shift to myelocytes, T2-ly 5%-10%, LGL 5%-10%  Recovered and discharged 
39 yo M presented with SOB and new onset heart failure. He was found to have metapneumovirus and Rhinovirus by PCR. OP medications included acetaminophen, guaifenesin, albuterol, dicyclomine, and ondansetron.  None  —  Pl-ly <5%, T2-ly <5%, T3-ly <5%, Other-ly <5%  Recovered and discharged 
39 yo M presented with SOB and pneumonia. His tracheal swab was positive for Escherichia coli. OP medications included metoprolol, sertraline, buspirone, and trazodone.  Anemia (Hb: 7.3 g/dL)Leukocytosis (18.38 × 103/μL)Absolute lymphopenia (0.74 × 103/μL)Absolute neutrophilia (16.54 × 103/μL)  —  APHA <5%, toxic changes, left shift to bands, PL-ly <5%, T2-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
67 yo M with history of oral cancer presented with fever and cough. He was found to have Streptococcus agalactiae bacteremia. OP medications included prednisone, metoprolol, atorvastatin, levothyroxine, guaifenesin, and furosemide.  Anemia (Hb: 7.4 g/dL)Leukocytosis (12.04 × 103/μL)Absolute lymphopenia (0.24 × 103/μL)Absolute neutrophilia (8.67 × 103/μL)  CD3 abs: 118 L (723-2,737/μL)CD4 abs: <40 L (404-1,612/μL)CD8 abs: 87 L (220-1,129/μL)  APHA <5%, left shift to myelocytes, T2-ly <5%  Progressed to respiratory and multiorgan failure, MV, deceased 
63 yo M with hypertension, congestive heart failure, and COPD presented with fever and SOB. He was found to have metapneumovirus infection and secondary bacterial pneumonia. OP medications included metoprolol, lisinopril, aspirin, atorvastatin, cetirizine, and prednisone.   Anemia (Hb: 11.4 g/dL)Leukocytosis (23.97 × 103/μL)Absolute lymphopenia (0.46 × 103/μL)Absolute neutrophilia (21.89 × 103/μL)  —  Toxic changes, T2-ly <5%, LGL <5%  Recovered and discharged 
61 yo M with end-stage renal disease and type 2 diabetes presented with fever and SOB. He was found to have Staphylococcus aureus bacteremia. OP medications included amlodipine, atorvastatin, furosemide, and Keppra.  Anemia (Hb: 11.3 g/dL)  —  APHA <5%, toxic changes, left shift to metamyelocytes, Pl-ly <5%  Recovered and discharged 
27 yo M presented with fever and sore throat. Monospot test was positive. No OP medications were listed in the chart.  Leukocytosis (13.15 × 103/μL)Absolute lymphocytosis (5.65 × 103/μL)Absolute monocytosis (1.58 × 103/μL)  —  PL-ly <5%, T1-ly >10%, T2-ly >10%, T3-ly <5%, LGL >10%  Recovered and discharged 
62 yo M with chronic neutropenia and history of Kaposi sarcoma presented with fever and pneumonia. He was positive for rhinovirus/enterovirus on PCR. OP medications included metoprolol, amlodipine, and Zoloft.  Anemia (Hb: 9.9 g/dL)Leukopenia (1.85 × 103/μL)Absolute lymphopenia (0.39 × 103/μL)Absolute neutropenia (1.28 × 103/μL)  —  PL-ly 5%-10%, T1-ly <5%, T2-ly <5%, LGL <5%  Recovered and discharged 
59 yo M with HIV and autoimmune hemolytic anemia presented with fever. He was found to have rhinovirus/enterovirus on PCR and Pseudomonas in urine sample. HIV RNA PCR <20 copies/mL. OP medications included BIKTARVY.  Anemia (Hb: 11.6 g/dL)Absolute lymphopenia (0.24 × 103/μL)Thrombocytopenia (95 × 103/μL)  —  Toxic changes, left shift to bands, T1-ly 5%-10%, T2-ly <5%, LGL 5%-10%  Recovered and discharged 
10  64 yo F presented with cough and fever. She was found to have bacterial pneumonia. No OP medications were listed in the chart.  Leukocytosis (16.91 × 103/μL)Absolute neutrophilia (12.83 × 103/μL)  —  APHA <5%, toxic changes, left shift to metamyelocytes, PL-ly: <5%, T2-ly 5%-10%, T3-ly <5%, LGL <5%  Recovered and discharged 

Among the COVID-19 patients, CBCs revealed anemia in 5 cases (mean hemoglobin, 12.5 g/dL; range, 10-16.1 g/dL), leukocytosis in 4 cases (mean, 7.3 × 103/μL; range, 3.9-35.6 × 103/μL), thrombocytosis in 1 case, and thrombocytopenia in 1 case. Absolute lymphopenia was present in 2 cases; one of them had HIV/AIDS. Absolute neutrophilia was seen in 6 cases (mean, 9.24 × 103/μL; range, 2.3-32.6 × 103/μL). Absolute monocyte count was low in 1 patient and within reference ranges in others. Absolute eosinophil count was within reference ranges in all patients. The control group showed CBC findings similar to the COVID-19 group; however, absolute lymphopenia was present in 6 control group patients as compared to only 2 COVID-19 patients (P < .05).

Peripheral blood smear review showed presence of APHA in all COVID-19 cases, with 50% of cases (6/12) having over 10% pelgeroid neutrophils, 25% cases (3/12) having 5% to 10%, and the remaining 25% cases (3/12) having less than 5%. Monolobate neutrophils were noted in 50% of COVID-19 cases (6/12). Rare neutrophils showed prominent apoptotic changes. In contrast, the control group showed APHA in 50% of cases (P < .05), and in 4 of 5 of these cases, pelgeroid cells comprised less than 5% of neutrophils. Notably, monolobate neutrophils were not present in any of the control cases. Morphologic findings in granulocytes are illustrated in Image 1A, Image 1B, Image 1C, and Image 1D. Two patients with HIV/AIDS had APHA greater than 10%; however, both patients had less than 20 HIV RNA copies/mL detected by PCR. None of these patients had a history of myeloid neoplasms. Review of outpatient medications revealed no definite evidence of medications reported to be associated with APHA. Inpatient medications were not pertinent, as the peripheral blood studied were drawn during hospital admission.

Image 1

Morphologic findings in peripheral smears in coronavirus disease 2019 patients (Wright stain, ×100). A, Acquired Pelger-Huët anomaly. B, Monolobate neutrophil. C, Apoptotic neutrophil. D, Left shift to blast stage. E, Atypical lymphocyte with irregular nuclear contours. F, Plasmacytoid lymphocyte. G, Downey type I lymphocyte. H, Downey type II lymphocyte. I, Downey type III lymphocyte. J, Large granular lymphocyte.

Image 1

Morphologic findings in peripheral smears in coronavirus disease 2019 patients (Wright stain, ×100). A, Acquired Pelger-Huët anomaly. B, Monolobate neutrophil. C, Apoptotic neutrophil. D, Left shift to blast stage. E, Atypical lymphocyte with irregular nuclear contours. F, Plasmacytoid lymphocyte. G, Downey type I lymphocyte. H, Downey type II lymphocyte. I, Downey type III lymphocyte. J, Large granular lymphocyte.

In only a minority of COVID-19 cases did granulocytes show prominent toxic changes. In 1 severely ill patient with multifocal pneumonia and respiratory failure, the peripheral smear showed leukoerythroblastosis and toxic changes in greater than 10% neutrophils. The patient died soon after. In the remaining 11 cases, toxic changes were present in less than 10% of granulocytes. However, granulocytic left shift was a prominent feature in a majority of cases (8/12). Among the cases with left shift, 62% of cases (5/8) showed left shift to metamyelocyte/myelocyte stage, 25% of cases (2/8) showed presence of circulating bands, and the 1 case described above with leukoerythroblastosis showed rare circulating blasts (<1% blasts). In the control group, 6 of 10 cases showed extensive toxic changes and granulocytic left shift; however, most of those cases also had concurrent bacterial infections.

All COVID-19 cases showed varying types of atypical lymphocytes, albeit constituting less than 10% of lymphocytes in the majority of cases Image 1E, Image 1F, Image 1G, Image 1H, Image 1I, and Image 1J. The most common and least specific type of reactive lymphocyte, the Downey type II lymphocyte, was noted in all cases; however, it constituted less than 10% of lymphocytes in all cases. Large granular lymphocytes were noted in 11 of 12 cases, but only 1 case showed mildly increased numbers of LGLs comprising greater than 10% of lymphocytes. Plasmacytoid lymphocytes were noted in 9 of 12 cases, Downey type III lymphocytes in 5 of 12 cases, and Downey type I lymphocytes in 2 of 12 cases, with each individually comprising less than 10% of total lymphocytes. Rare atypical lymphocytes with markedly irregular nuclear contours and scant to moderate basophilic cytoplasm were noted in 7 of 12 cases but comprised less than 5% of total lymphocytes in each case. Plasmacytoid lymphocytes were seen in greater frequency in COVID-19 patients, compared to controls (P < .05), although they constituted less than 10% of lymphocytes in all cases. Otherwise, the control group had a comparable qualitative and quantitative spectrum of atypical lymphocytes, except 1 case of infectious mononucleosis.

Of the 12 cases, flow cytometric studies for lymphocyte subsets were performed in 7 cases. This included 2 patients with HIV/AIDS; however, both patients had less than 20 HIV RNA copies/mL detected by PCR. Decreases in absolute numbers of CD3+ T-cells, CD4+ T-cells, and CD8+ T-cells were identified in 6, 5, and 3 cases respectively. B cells and NK cells were enumerated only in 4 cases, of which the majority showed absolute counts in normal ranges. One case had a low B-cell count and another case had a low NK-cell count. Although the numbers are too few to draw meaningful comparisons, cytopenia of CD3+ T cells appears to be a common finding. All patients with decreased T cells required mechanical ventilation. The control group only had flow cytometry performed in 1 case.

Discussion

After its identification in December 2019 in Wuhan, China, COVID-19 has rapidly spread and evolved into a pandemic over a few months.11 The pathophysiology of this infection is not completely understood; however, the causative agent SARS-CoV-2 shares 79% genomic similarity with SARS-CoV.2 SARS-CoV infects host cells expressing the angiotensin-converting enzyme 2 (ACE-2) receptor, including airway epithelium, alveolar lining, endothelial cells, and alveolar macrophages. SARS-CoV-2 is postulated to infect cells via the ACE-2 and transmembrane protease serine 2 (TMPRSS2) receptors, leading to host cell death while triggering monocyte/macrophage activation, T-cell activation, cytokine release, and B-cell mediated antibody production.3 Furthermore, studies have demonstrated that SARS-CoV is able to infect and replicate in peripheral blood mononuclear cells.12,13 Transcriptomic analysis of peripheral blood in COVID-19 patients, however, has not demonstrated presence of SARS-CoV-2 RNA in hematopoietic cells.14 Activation of genes in the proapoptotic and p53 signaling pathway was identified in the peripheral blood mononuclear cells of patients with SARS-CoV-2.14

Laboratory abnormalities reported in COVID-19 patients include lymphopenia (>40% patients), leukocytosis, leukopenia, neutrophilia, monocytosis, and eosinopenia.4-6 These laboratory abnormalities were also reported in SARS-CoV patients.15 Lymphopenia is the predominant hematologic finding associated with SARS-CoV-2 in the literature and is reported to predict disease severity.16 Several hypotheses exist regarding mechanism of lymphopenia in COVID-19 patients, including direct viral toxicity due to ACE-2 receptor expression on lymphocytes, cytokine-induced lymphocyte apoptosis, and metabolic products causing lymphocyte inhibition.17 In our cohort of cases, absolute lymphopenia by CBC was only seen in 2 cases, but flow cytometric analysis revealed absolute T-cell count reduction in 6 of 7 cases. All patients with decreased T cells were admitted to the intensive care unit and required mechanical ventilation. Lymphocyte subset alterations are reported to be associated with disease activity in COVID-19 patients,18 and flow cytometry is a sensitive modality to detect that. No specific CBC abnormalities were identified in COVID-19 cases compared to the control group in this study.

There is limited literature on peripheral smear findings in COVID-19 patients. Zini et al8 reported presence of APHA, prominent abnormal neutrophilic granulation, monolobate neutrophils, granulocytic left shift, large abnormal platelet morphology, apoptotic cells, and few reactive lymphocytes. These abnormalities were not quantified in their study. Interestingly, the neutrophilic morphologic abnormalities almost entirely disappeared after 1 week of antiviral/anti-inflammatory treatment in a subset of cases. Our study is in concordance with that of Zini et al in that there is conspicuous presence of APHA including monolobate neutrophils in the peripheral blood of COVID-19 cases compared to control cases. Pelger-Huët anomaly is a benign hereditary condition where mutations in the lamin B receptor (LBR) result in hyposegmented neutrophils with dense chromatin.19 LBR plays an important role in maintaining the structure of nuclear membranes.20 Acquired causes of this anomaly include myelodysplastic syndrome, infections like tuberculosis, HIV/AIDS, influenza A, mononucleosis, parvovirus, and drugs such as immunosuppressive agents and some antibiotics.19 There was no evidence of medications associated with APHA identified in our patient cohort. In the 2 cases with HIV/AIDS, the viral loads were undetectable. The mechanism behind APHA is unclear. Some hypotheses include acquired mutations in LBR gene and accelerated apoptosis.21 In light of evidence regarding enriched apoptotic activity by SARS-CoV-2,14 that hypothesis is a possibility. APHA is not reported in association with SARS-CoV.

Barring myeloid neoplasms, left shift of granulocytes is conventionally interpreted as a sign of bacterial infection.22 Neutrophil kinetics in bacterial infections is thought to trigger mobilization of marrow reserves, resulting in left shift of granulocytes.22 Of the 8 patients with left shift in our study, only 2 patients had concurrent bacterial infections. SARS-CoV-2 induced cytokine release causing neutrophil migration akin to bacterial infections is a possibility. Direct myelotoxicity caused by the virus or marrow overproduction in a background of increased peripheral cell turnover are other hypotheses. Leukoerythroblastosis, defined as circulating immature granulocytes and nucleated RBCs with or without anemia, is typically associated with marrow infiltrative processes but may also represent marrow response to stressors like hypoxia, peripheral destruction/sequestration, or sepsis.23 Peripheral blood leukoerythroblastosis in a COVID-19 patient was reported by Mitra et al9 This was noted in 1 case in our cohort as well. Given the lack of any other evidence suggestive of an underlying myeloid neoplasm or malignancy causing a myelophthisic process, this may represent marrow stress and response to the viral infection.

Atypical/ reactive lymphocytes in the peripheral smear is the hallmark of some infections, such as infectious mononucleosis, Bordetella pertussis, and hantavirus.24-26 Infectious mononucleosis shows a spectrum of reactive/pleomorphic lymphocytes, while hantavirus shows predominantly Downey type III cells or immunoblasts. These are not specific findings and may be seen in varying numbers in other infections, autoimmune diseases, and malignancies. Peripheral smear review of 32 COVID-19 cases from Singapore reported presence of circulating reactive lymphocytes with predominantly lymphoplasmacytoid morphology in 72% of cases.7 Our study also shows a spectrum of atypical lymphocytes in almost all COVID-19 cases, with plasmacytoid lymphocytes present in greater frequency in COVID-19 cases compared to the control group. However, variant lymphocytes comprise a minority of lymphocytes (<10%) in most patients. This finding may be similar to SARS-CoV, where reactive lymphocytes were not identified in significant numbers by Chng et al27 and seen in only about 15% cases by Lee et al.28 Quantitation of reactive lymphocytes was not performed in other SARS-CoV or COVID-19 studies.

In summary, we report CBC and peripheral smear findings on admission in 12 symptomatic patients who tested positive for COVID-19 and compared them to a control group. To the best of our knowledge, this is the first study to quantify individual morphological findings on peripheral smear in COVID-19 cases. We acknowledge the limitations of our study, especially the number of peripheral smears available for review. Larger series of cases with peripheral smear review during and after treatment will be of interest, to study their potentially transient nature and correlation with disease activity.

Conclusion

Peripheral blood abnormalities are common in viral infections and can occasionally provide insight into underlying pathophysiologic processes. An increase in variant lymphocytes was observed in most COVID-19 patients, with plasmacytoid lymphocytes seen more often in COVID-19 patients than in controls. Morphologic abnormalities in the granulocytic series, namely APHA and left shift, were significantly more common in COVID-19 cases. The implications of these findings with respect to our understanding of SARS-CoV-2 infection are yet to be uncovered.

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Infections | Leukemia and Lymphoma Society

Cancer patients, especially those undergoing chemotherapy, are more likely to get infections because of their weakened immune systems. Cancer and certain cancer therapies can damage the immune system by reducing the number of infection-fighting white blood cells. Patients with a low white blood cell count are at a higher risk of developing infections, and these infections can be more serious and harder to treat. In severe cases, infections can lead to death.

Cancer treatment can destroy cancer cells as well as healthy, infection-fighting white cells. If your white cell counts decreases moderately, you won’t need special precautions, especially if the cells return toward normal within a short period. However, if you have a severe or prolonged low white cell count, especially after intensive drug therapy, you may be at greater risk for infection.

To prevent or manage infection, your healthcare team may 

  • Prescibe antibiotics to prevent or treat infection.
  • Prescibe growth factors to improve white cell counts 
    • Growth factors used to help your body produce more white blood cells include filgrastim (Neupogen®), pegfilgrastim (Neulasta®) and sargramostim (Leukine®). These can cuase serious side effects in some patients. Discuss the risk and benefits with your doctor. 
  • Stop or delay treatment to allow blood cell counts to rise  

Signs and Symptoms to Watch For

If you exerience any signs of infection, don’t delay in seeking medical attention. If you have even one of the following symptoms, contact your doctor immediately:

  • A temperature of 100.4° F or higher
  • Chills
  • Persistent coughing
  • Redness, swelling or tenderness, especially around a wound or IV site
  • A sore throat
  • Pain when urinating
  • Frequent diarrhea or loose bowel movements
  • Bleeding gums or white patches in the mouth 

12 Ways to Reduce Infection Risk

  1. Make sure your healthcare team takes steps to avoid exposing you to bacteria, viruses and other infection-causing agents: They should practice frequent and vigorous hand washing or, in some cases, wearing masks, gowns and/or gloves.
  2. Discuss how to avoid infection with members of your healthcare team if you’re receiving outpatient treatment. Caregivers need to be meticulous in cleaning catheters to reduce the risk of bacteria entering the body.
  3. Wash your hands thoroughly, especially before eating and before and after using the bathroom. This applies to everyone — people in treatment and those around them.
  4. Avoid crowds and individuals with contagious diseases such as colds, flu, measles or chicken pox.
  5. Check with your doctor about getting vaccinations. Find out whether you should avoid people who’ve recently been immunized with live, weakened forms of organisms or viruses that cause the disease, such as measles, and how long you should stay away.
  6. Clean your rectal area gently but thoroughly after each bowel movement. Ask your doctor for advice if irritation or hemorrhoids are a problem. Check with your healthcare team before using enemas or suppositories.
  7. Don’t cut or tear your fingernails’ or toenails’ cuticles.
  8. Avoid cuts or nicks when using scissors, needles or knives.
  9. Use an electric shaver instead of a razor to prevent cuts
  10. Uuse an extra soft toothbrush that won’t hurt the gums.
  11. Don’t squeeze, pick, or scratch at wounds or blimishes.
  12. Clean cuts and scrapes immediately. Rinse the wound under running water. Wash the skin around the wound with soap. To avoid irritation, don’t use soap on the wound.
  13. Take a warm (not hot) bath, shower or sponge bath every day. Don’t rub skin to dry it; use a light touch to pat skin dry. Use lotion or oil to soften and heal skin if it becomes dry and cracked.
  14. Wear protective gloves when gardening or cleaning up after animals, young children or others.
  15. Follow food safety guidelines. 

For Kids: The Hand-Washing Experiment

If your child has cancer, he or she should be taught how to prevent infections, especially by keeping the hands clean.

Let your child know that washing his or her hands the right way can prevent infections from spreading. Visit The Centers for Disease Control and Prevention website, where your child can read about how to wash their hands the right way.

Teach your child to wash his or her hands:

  • Before and after making or eating meals or snacks
  • Before and after changing diapers
  • After coughing, sneezing or blowing your nose
  • Before and after using the bathroom

Related Links
  • Download or order The Leukemia & Lymphoma Society’s free factsheets:

90,000 Viral Diseases – Blood Center

Viral Disease Research

There are many diseases, pathogens of which are transmitted through the blood. In Estonia, the most common are HIV (Human Immunodeficiency Virus), hepatitis B and C viruses, and the causative agent of syphilis.

The Blood Center analyzes all donated blood doses. 25 ml from each blood supply is used for testing for the presence of viruses; The blood center cannot provide hospitals with unexamined blood.

It is important for the donor to know that when the pathogen enters the body, the symptoms of the disease do not develop immediately. At this time, the causative agents of the disease are already in the body, but there are still too few of them for laboratory determination. Blood is already dangerous for transfusion to another person.

The period of time during which it is impossible to detect pathogens in donated blood by laboratory means is called the “window period”. Even the best and most modern analysis methods do not provide the ability to detect the presence of viruses immediately after infection.That is why the donor’s awareness of his health condition, a sincere desire to help those in need and constant honesty during medical examinations are so important.

If the test results require additional verification, the donor is called for repeated tests. The dose of blood in which the causative agent of the infection is found is destroyed.

In the control laboratory, donated blood is tested for HIV, hepatitis B and C and syphilis

How can get infected virus infection ?

Viruses live in the body fluids of an infected person (blood, vaginal fluid, pre-seminal fluid, semen, breast milk).Infection occurs by the ingestion of the physiological fluid of an infected person into the blood of a healthy person. This can happen in four ways:

  1. During skin piercing procedures
    A person can become infected with the virus if they use needles that were previously used by a virus carrier. Piercing and tattooing procedures can also be dangerous if they are performed with agents previously used on carriers of the virus (for example, inserting rings, tattooing, acupuncture).
  2. During sexual intercourse
    You can get the virus by coming into contact with a partner who is a carrier without using protective equipment.
    More often than other virus carriers are:
    – homo- and bisexuals
    – prostitutes
    – drug addicts
  3. From mother to child. Infection with the virus can occur during pregnancy, childbirth, and breastfeeding.
  4. For blood transfusion, if the blood transfused contains blood-borne pathogens.

love or hate – Science – Kommersant

The reaction of our body to a bacterial infection that has appeared in the bloodstream is a complex response, in which the cells and components of the immune system, the blood coagulation system participate, endothelial cells lining the blood vessels are necessarily connected, and all this is complemented by the responses of the liver and the endocrine system.

Even the reaction of one of the listed systems – the blood coagulation system – is multifaceted.The blood coagulation system is traditionally divided into two interconnected links – platelet and plasma. Platelet coagulation is the activation, adhesion (adhesion) to the surface and aggregation (sticking to each other) of cells – platelets. Plasma clotting is the sequential activation of protease proteins (enzymes that break down other proteins), leading to the polymerization of the blood plasma protein fibrinogen into long branched fibrin strands and the formation of a clot (this process resembles the formation of jelly).

Both links of blood coagulation react to a bacterial infection. Platelets form aggregates around bacteria and can absorb them (phagocytosis). Platelets also “recognize” bacterial patterns and release platelet antimicrobial agents. In all of these cases, platelets trigger the activation of the body’s immune system. In turn, bacteria form colonies on platelets and blood clots, thus becoming entrenched in the bloodstream. Plasma clotting is no less difficult to interact with a bacterial infection: in addition to starting from a foreign surface – a bacterial wall, the formation of a fibrin clot is triggered by specific bacterial proteases that also suppress fibrinolysis – the physiological process of blood clot degradation.Moreover, all the listed answers at the molecular level are specific for the genus, or even the species of pathogenic bacteria.

Our team based at the National Medical Research Center for Pediatric Hematology, Oncology and Immunology named after Dmitry Rogachev, explores all aspects of the activation of the blood coagulation system both in physiological processes and in pathology. One of the projects that we have been conducting for several years was devoted to the questions of the blood coagulation system’s response to lipopolysaccharides (LPS) – components of the cell wall of gram-negative bacteria (for example, E. coli).The level of this response turns out to be vital in acute bacterial infections that cause spontaneous blood coagulation – disseminated intravascular coagulation (DIC), when a too violent reaction of the system leads to a sharp decrease in the concentration of proteins and platelets and, as a consequence, hemorrhages in combination with impaired microcirculation in organs. Currently, in clinical practice, the treatment of DIC, depending on the phase, is carried out with antiplatelet agents (such as aspirin), anticoagulants (heparin derivatives), plasma components and platelet concentrates, that is, treatment does not normalize coagulation, but shifts the balance towards weakening or strengthening (more details – “Practical coagulology”, ed.A.I. Vorobiev, Moscow, 2012). Understanding the molecular mechanisms of the reaction of the blood coagulation system to bacteria will significantly improve modern approaches to the therapy of DIC.

In this project, we started with the interaction of the plasma link of blood coagulation with LPS. After several series of experiments, we came to the conclusion that the effect of LPS is rather weak and strongly dependent on the donor. When analyzing the data using computer modeling, it was concluded that blood coagulation can “start” from the formed (as a result of the immune system) LPS aggregates, but single LPS molecules, binding to protease proteins, rather suppress blood coagulation.

The mechanisms of activation of blood coagulation as a result of bacteria-induced inflammation, when either the endothelial cells themselves or the cells of the immune system on their surface exhibit a protein, a tissue factor that triggers the entire blood coagulation system, were separately considered. With the help of computer modeling, we have shown that with the death of such cells, when many membrane vesicles – “bubbles” of 10–100 nm in size, are formed, blood plasma coagulation is triggered most intensively due to the increased affinity (“love”) of coagulation proteases to the curved surface.

Blood cells, platelets, can interact with LPS through special receptor proteins on their surface, the so-called Toll-like receptors. By the way, the same receptors are responsible for the activation of the LPS cells of the immune system and lead to the development of inflammation. However, to our surprise, we could not identify direct activation of LPS for platelets, despite the presence of functional Toll-like receptors. After many experiments in collaboration with the group of Professor S.P. Gambaryan from the Institute of Evolutionary Physiology and Biochemistry named after IM Sechenov (St. Petersburg), we showed that LPS even cause a slight suppression of platelet activation.

Thus, we have obtained that the components of the bacterial cell wall, lipopolysaccharides, by themselves either do not affect the blood coagulation system, or cause suppression of coagulation activation. This behavior – suppression of blood clotting – is typical for many bacteria, because the formation of a blood clot around the bacteria can prevent its spread in the body.The acute reaction to bacterial infection described above in the case of E. coli is most likely associated with the activation of the clotting system as a result of a general process of inflammation triggered by bacteria in the body. Currently, we continue to study the activation of the blood coagulation system during inflammation and other interactions with the immune system, according to projects supported by the Russian Foundation for Basic Research and the Russian Science Foundation, as well as the Doctors, Innovations, Science for Children Foundation.

The results were obtained in the framework of the project “Identification of targets for pharmacological effects on blood coagulation in bacterial infection”, supported jointly by the RFBR and the Moscow government.

Anastasia Sveshnikova, Project Manager, Doctor of Physical and Mathematical Sciences, Leading Researcher laboratory of cellular hemostasis and thrombosis NMITs DGOI

“Intravascular blood coagulation in COVID-19 determines the entire course of the disease”

Conversation with academician A.D. Makatsaria, the largest specialist in the field of clinical hemostasiology

Today it is known that with COVID-19, first of all, the blood coagulation system suffers. That is why all those who die from the complications of the new coronavirus infection have a large number of blood clots.How can this be explained? Why was it not noticed right away? How and why does this happen? Is it possible to prevent the development of such a complication? This is what our conversation with A.D. Makatsaria, Academician of the Russian Academy of Sciences, one of the world’s largest specialists in the study of blood clotting disorders, founder of the School of Clinical Hemostasiology, Head of the Department of Sechenov University. Alexander Davidovich and his students actively collaborate with the Sorbonne University, Vienna, Rome, Milan and Tel Aviv universities, Technion in Haifa.150 candidate and doctoral dissertations have been defended under his supervision. Author of over 1200 scientific papers, including 40 monographs.

– Alexander Davidovich, recently all over the world there are more and more reports that at COVID -19, the blood coagulation system suffers. Is this so, and if so, how do you explain this phenomenon?

Of course it is. Moreover, I want to say that there is practically no such infection (viral or, moreover, bacterial) that would not affect blood coagulation.Proof of this is the doctrine of sepsis and septic shock as a universal model of disseminated intravascular coagulation syndrome. The severity of thrombotic disorders depends on the characteristics of the pathogen and the host organism (immune system, hemostasis system, the presence of concomitant diseases, etc.).

– But do not all patients develop sepsis and septic shock?

– Of course, not all of them.Therefore, the mechanism of the pathogenesis of complications caused by coronavirus infection is currently very relevant and far from being studied. This is largely due to the characteristics of the virus, as well as the characteristics of the human body, starting from the number and quality of receptors present in humans and their ability to bind to this virus. Of course, the outcomes of the disease are greatly influenced by comorbidity, that is, the presence of concomitant chronic diseases in the patient.

Why, in your opinion, this feature of the course of the disease did not manifest itself immediately?

I believe that all this manifested itself immediately, but was not adequately assessed by doctors initially: there has not yet been such a number of autopsies and widespread testing for hemostasiological markers.I must say that we have been studying this problem for a long time, almost from the very beginning of the epidemic. At the very beginning of April, we published a paper based on the first observations of our Chinese colleagues. The work was titled “COVID-19 and disseminated intravascular coagulation syndrome.” It had an extremely wide resonance, since even then doctors began to understand the role of the blood coagulation system in the infectious process.

What is the mechanism of thrombus formation in covid-19 and is it different from this process in other pathologies?

– This is a very difficult question.Today, it can be unambiguously stated that with this virus, from the very beginning, there is an activation of hemostasis, intravascular blood coagulation and thrombus formation in small-caliber vessels of vital organs. In this case, not only the lungs are damaged, but the blockade of microcirculation and its irreversible nature determine the outcome of the disease. Late initiation of anticoagulant therapy is an unfavorable factor. Moreover, this process of intravascular coagulation in the capillaries of the lung plays an important role in the development of acute respiratory distress syndrome (ARDS), which everyone is talking about.But not everyone grasped the connection between intravascular coagulation and ARDS from the very beginning.

In the Western literature, the term “pulmonary intravascular coagulation” even appeared. In almost all cases, there is an activation of the systemic inflammatory response. This is a general biological reaction, which is especially manifested in response to infection, viral pathogens. International organizations have recognized that coronavirus infection is sepsis.

On the other hand, the International Organization for Thrombosis and Hemostasis in the absolute number of cases recognized the presence of DIC in severe patients with COVID-19.The combination of sepsis and coagulopathy is septic shock. Even Chinese colleagues indicated that in 92% of cases, patients die from septic shock. Of course, it cannot be denied that, along with the virus, the addition of a secondary bacterial infection can be the cause of septic shock. In patients with COVID-19 and disorders in the hemostatic system, as a rule, hyperferritinemia occurs, which occurs in critical conditions as a reactant of the acute phase of inflammation and is characterized by a cytokine storm due to hyperactivation of macrophages and monocytes.As a result, a large amount of ferritin is produced – a complex protein complex that plays the role of the main intracellular iron depot in humans and animals. In this case, it is always an acute phase protein, a marker of severe inflammation, and not at all an indicator of iron overload, as one might think at first glance.

Thus, cytokine and thrombotic storms aggravate the patient’s condition and determine the severity. But there are also some peculiarities. Perhaps, with COVID-19, fibrinolysis is primarily damaged – part of the hemostasis system, which ensures the destruction of already formed blood clots, thereby performing a protective function of preventing clogging of blood vessels by fibrin clots.Hence the fibrinating syndrome with a lower incidence of hemorrhagic complications. And from here the prospect of using thrombolytics opens up, which is now being talked and written about so much. And for the first time such a scheme was proposed by our American colleagues.

– But there are many people with bleeding disorders. Now, during the epidemic, difficult times have come for them .

– This is true. In our population there are people not only with obvious, but also with latent disorders of hemostasis, predisposing to thrombosis – genetic thrombophilia, antiphospholipid syndrome and a number of other diseases, accompanied by excessive activation of the hemostasis system; as well as people with a high readiness for a super-inflammatory response (congenital factors and a number of rheumatological and immune diseases).Now it is important for them to control their condition, and doctors do not forget about it.

And finally, COVID-19 is blood clotting. This is, in fact, a virus-mediated NET-os model, which characterizes the close relationship of such biological processes as inflammation and thrombus formation. Neutrophils and the extracellular traps of neutrophils (NET) secreted by them play a huge role in the development of the so-called immunothrombosis. This is one of the priority research areas today, which we are now developing together with our students, including our foreign colleagues.

In general, it must be said that the discovery of NET expanded the horizons in understanding the biology of neutrophils and the role of these cells in the body. The use of chromatin by the host organism in combination with intracellular proteins as a natural antimicrobial agent has an ancient history and changes our understanding of chromatin as a carrier of genetic information. Due to the excessive and uncontrolled formation of NET, neutrophils can contribute to the development of pathological venous and arterial thrombosis, or “immunothrombosis”, and also play an important role in the processes of atherothrombosis and atherosclerosis.The release of NET has been shown to be one of the causes of thrombus formation in conditions such as sepsis and cancer. The presence of NETs in these diseases and conditions makes it possible to use them or individual components as potential biomarkers. NET and their components can be attractive as therapeutic targets. Further studies of neutrophils and NET are needed to develop new approaches to the diagnosis and treatment of inflammatory and thrombotic conditions.

Thinking about the high mortality in patients who had to use mechanical ventilation, you state that we may have gone the wrong way.Which way could be more correct?

Yes, I meant that when assessing ventilation and perfusion disorders in COVID-19, perfusion disorders and microcirculation disorders prevail, which means that the main therapeutic target is the restoration of normal tissue perfusion, that is, anti-thrombotic therapy, and possibly even fibrinolytic. Mechanical ventilation cannot resolve the issue of perfusion disturbances.

– Do you see that due to the epidemic, thrombosis problems have become more frequent in obstetric and gynecological practice?

It so happened that, largely and thanks to our efforts (lectures and publications), most obstetricians today are aware that pregnancy is a state of so-called physiological hypercoagulation, and these patients are often prescribed anticoagulants during pregnancy.However, further research is required to judge the incidence of thrombosis in pregnant women with COVID-19.

In general, it must be said that most of the complications of pregnancy are either caused or combined with a high thrombogenic potential. Genetic factors of blood clotting, especially antiphospholipid syndrome, are risk factors for a huge number of pregnancy complications – intrauterine fetal death, IVF failures, intrauterine fetal growth retardation, and premature placental abruption, which leads to severe thrombohemorrhagic complications, finally, thrombosis and thromboembolism.Therefore, of course, one can expect that in the context of COVID-19, these complications could pose an even greater danger. After all, a virus can be a factor that activates blood clotting factors. Of course, generalizing studies are needed here, but even now our individual observations indicate that the risk of such complications is increasing.

– In your opinion, are cases of severe covid-19 in pediatrics (conditions similar to Kawasaki syndrome) one of the manifestations of this problem?


WHO head Tedros Adanom Ghebreyesus urged doctors from all countries to pay special attention to reports that some children infected with coronavirus show symptoms similar to another disease – Kawasaki syndrome (multisystem inflammatory syndrome).Indeed, reports from Europe and North America indicated that a number of children were admitted to intensive care units with a multisystem inflammatory condition, with some symptoms similar to Kawasaki syndrome and toxic shock syndrome.

Kawasaki syndrome was first described in 1967 by a Japanese pediatrician named Tomisaku Kawasaki. It usually affects children under the age of five. In this syndrome, the patient develops inflammation of the blood vessels (vasculitis) and fever.Kawasaki disease has a distinct set of symptoms, including persistent high fever, redness of the eyes and around the mouth, rashes on the body, and redness and swelling of the legs and arms.

On May 13 this year, the authoritative medical publication The Lancet published a study of Italian doctors who reported that an outbreak of Kawasaki syndrome or a syndrome similar to it had been recorded in the province of Bergamo, one of the most affected by the coronavirus epidemic.

Importantly, in most cases, the children also tested positive for COVID-19 antibodies, suggesting that the syndrome followed a viral infection.

Kawasaki disease tends to show up in groups of genetically similar children and may look slightly different depending on the genetics underlying the group. This suggests that various triggers can induce an inflammatory response in children with a specific genetic predisposition.

It is possible that SARS-COV-2, caused by the COVID-19 virus, is one such trigger. This is an important issue that requires careful study.

– Alexander Davidovich, why do you think COVID -19 manifests itself differently in all ?

The problem of risk factors is very important here. The fact is that, in addition to visible diseases such as diabetes mellitus or hypertension, there are invisible diseases that we often do not even suspect about.In recent years, the doctrine of genetic thrombophilia has become widespread. Globally, it is about 20 percent of people who carry some form of genetic thrombophilia. You can live with this for a hundred years, but if an infection occurs, an injury occurs, an operation is performed, the patient may die from thromboembolism, even if the operation is performed at the highest technical level. The reason for this is latent genetic thrombophilia, a mutation that makes the carrier at high risk for blood clots.

One of the forms of thrombophilia – the so-called hyperhomocysteinemia, which can be either acquired or genetically determined, can also be an important factor in thrombosis, heart attacks, and strokes. And now there is evidence that hyperhomocysteinemia is aggravated by SARS-CoV2 infection. Accordingly, the risk group includes all those who have an increased level of homocysteine ​​in the blood, but the person may not know about it. Therefore, we have now begun a large-scale study to identify these risk groups, to isolate various forms of thrombophilia in patients with COVID-19.Our goal is to find out if these people are at risk of developing severe complications of the new coronavirus infection.

The high contagiousness of the virus and a large number of sick people involuntarily “allows” the virus to identify people with an initial clear or latent predisposition to thrombosis. These are patients not only with genetic thrombophilia or antiphospholipid syndrome, but also with diabetes mellitus, obesity, rheumatic diseases and other pathological conditions associated with increased coagulation and / or inflammation.

– What methods of prevention and treatment of covid-19 do you consider promising?

– In addition to those already mentioned, these are antiviral therapy, therapy with specific immunoglobulins, anti-thrombotic therapy and treatment aimed at reducing inflammation (the so-called anti-cytokine drugs). We still have a lot to understand about this new disease for us, but gradually we are moving towards a better explanation of many of its mechanisms.You know, I have always worked hard, but, perhaps, never before have I been so busy with research and practical work as I am now. I am sure that it will yield important results.

Interview was moderated by Natalia Leskova.


RECOMMENDATIONS
ON STRENGTHENING ANTI-EPIDEMIC REGIME IN INSTITUTIONS
BLOOD SERVICES IN THE CONDITIONS OF DISTRIBUTION OF NEW
CORONAVIRUS INFECTION COVID-19

Appendix

to the letter of Rospotrebnadzor

from 18.04.2020 N 02 / 7312-2020-23

In connection with the deterioration of the epidemiological situation on the new coronavirus infection COVID-19 in the world and the Russian Federation, it is necessary to strengthen anti-epidemic and preventive measures in the institutions of the Blood Service. Although there is currently no reliable data on the possible transmission of SARS-CoV-2 through blood and blood components, it is necessary to strengthen measures to ensure the safety of donated blood and its components for recipients, procedures for donating blood for donors and the performance of professional duties for employees of the Blood Service.Taking into account the decline in donor activity in the conditions of self-isolation, a balance must be observed between the safety measures taken and the sufficiency of the volume of blood and its components.

In order to prevent the transmission of coronavirus infection COVID-19 during the procurement of donated blood and its components and transfusion to recipients of blood and its components, in addition to the previously established requirements, it is recommended to ensure:

1. Cancellation of mass and mobile donor actions, incl.h. in medical organizations, educational institutions and enterprises.

2. Treatment of hands with alcohol-containing skin antiseptics at the entrance to the institutions of the Blood Service for all employees and visitors.

3. Conducting a thorough selection of donors, including:

3.1. Organization of a medical post at the entrance to the territory of the Blood Service institution. At the entrance to the territory of the institution, carrying out thermometry for donors, examination and questioning for the presence of symptoms of respiratory infections in order to prevent the presence of donors with fever and signs of SARS and their withdrawal from donation.

3.2. Conducting a survey / questioning of donors before donating about the presence of contacts with a patient with COVID-19 (about cases of the disease in the family, with relatives, at the workplace, at the place of residence), visiting countries / regions unfavorable for infection caused by the coronavirus COVID-19, in within four weeks preceding the day of contacting the blood Service institutions. Conducting a telephone survey of donors about deteriorating health 14 days after donation (fever, signs of SARS, diagnosis of coronavirus infection).

3.3. Providing a temporary withdrawal from donation of citizens who have returned from foreign countries and regions of the Russian Federation with coronavirus problems who are in contact with COVID-19 patients for 4 weeks, in addition to the current list of contraindications for donating blood and its components.

The withdrawal from donation for citizens who have recovered from COVID-19 is 6 months after recovery.

4. To refrain from transfusion of blood and its components to recipients not for health reasons.

5. Quarantine of blood plasma for a period of at least 120 days in accordance with the current regulatory documents.

6. To increase viral safety, it is recommended to ensure the widespread use of methods of inactivation of pathogenic biological agents for the production of platelet concentrate. It is recommended to ensure the issuance of pathogen-reduced and leukofiltered platelet concentrates for patients with oncological and hematological diseases.

7. Clarification in the territorial bodies of Rospotrebnadzor of information on cases of coronavirus infection COVID-19 in a specific donor to resolve the issue of temporary withdrawal from donation and disposal of donor materials received from patients with COVID-19 within 4 weeks before the disease.

At present, it is not currently foreseen to carry out testing of donors for SARS-CoV-2 RNA before each donation; this recommendation may be revised when new evidence-based medicine data becomes available.

One of the key priorities of the Blood Service institutions is to ensure the safety of the donation procedure for the donor. In particular, in order to increase the safety of the blood donation procedure, in addition to the current requirements of regulatory documents, it is advisable to provide:

1.Introduction of records of donor visits to blood service institutions at a fixed time to prevent a mass gathering of citizens.

2. Observance of social distance (1.5 m) when entering and staying in the institutions of the Blood Service.

3. Provision of medical masks, shoe covers and information materials about coronavirus infection to donors at the entrance to the Blood Service institutions.

4. Separation of the flows of donors and patients (organization of a separate entrance for donors) in the institutions of the Blood Service, which are structural units of outpatient / inpatient medical organizations or functioning on the territory of other medical organizations.If it is impossible to separate the flows of donors and patients, the collection of blood and its components on the basis of these structural units is recommended to be stopped until further notice.

5. Strengthening the anti-epidemic regime in the institutions of the Blood Service.

To ensure the uninterrupted operation of the subjects of the Blood Service for the collection of blood, its components and to prevent the spread of the new coronavirus infection COVID-2019 in all institutions of the Blood Service, the requirements established by Rospotrebnadzor must be met, including:

1.Availability of a stock of disinfectants, personal protective equipment (medical masks, respirators, medical clothing, etc.).

2. Strict adherence to the temperature regime, ventilation regime, proper disinfection and disposal regime, staff compliance with the rules for the use of personal protective equipment, mask regime.

3. Conducting daily thermometry for employees, preventing the presence of employees with fever and signs of SARS; contacts for coronavirus and visited countries / regions affected by the infection caused by the coronavirus COVID-19 within 14 days.

4. Strengthening the current disinfection mode: increasing the frequency of disinfection treatment of corridors, offices, equipment, instruments, donor chairs and harnesses after each donation, common areas, disinfection of air and surfaces in rooms using ultraviolet irradiators of a recirculating (closed) type.

5. Training of medical workers in the prevention, clinic, diagnosis and treatment of coronavirus infection COVID-19.

6. Carrying out a set of anti-epidemic measures in identifying persons with respiratory symptoms that do not exclude a new coronavirus infection, detecting cases of coronavirus infection COVID-19, in accordance with the approved procedure.


FGBU RosNIIGT FMBA of Russia – Infections and infectious safety in hematology and blood service

March 22-23, 2012 All-Russian Scientific and Practical Conference “Infections and Infectious Safety in Hematology and Blood Service , dedicated to the 70th anniversary bacteriology laboratory of the Russian Research Institute of Hematology and Transfusiology.The conference was organized by the Ministry of Health and Social Development of the Russian Federation, the Federal Medical and Biological Agency of Russia, the North-West Branch of the Russian Academy of Medical Sciences, the Federal State Budgetary Institution “Russian Research Institute of Hematology and Transfusiology” of the FMBA of Russia, the All-Russian Scientific and Practical Society of Epidemiologists, Microbiologists and Parasitologists in St. Petersburg and the Leningrad Region , the city scientific society of hematologists and transfusiologists of St. Petersburg.

Conference channel on YouTube – Infection Safety 2012

Conference Organizing Committee:

Chairman of the organizing committee: memberscorr. RAMS, Doctor of Medical Sciences, Professor E.A. Selivanov
Deputy Chairmen: D.M. Sci., Professor S.S. Bessmeltsev, Doctor of Medical Sciences, Professor V.N. Chebotkevich.
Members of the organizing committee: E. I. Kaitanjan, Ph.D., T.V. Glazanova, Ph.D. E.R. Shilova, N.P. Stizhak, V.V. Burylev, N.Yu. Tsybakova, M.Sh. Grigorian.

More than 200 delegates from various cities of Russia, near and far abroad took part in the conference. More than 40 reports were presented at the plenary session and 8 sessions, reflecting a wide range of scientific research in the field of infectious safety in hematology and blood services.

At the plenary session prof. V.N. Chebotkevich dwelled on questions of the history of the formation of the laboratory of bacteriology. The laboratory was founded as a separate subdivision in 1942. The speaker noted the heroic work of the laboratory and the entire institute during the Great Patriotic War and the siege of Leningrad. In the post-war years, the main direction of the laboratory was the study of the problems of infectious safety of blood transfusions. A number of blood preservation drugs have been developed, as well as medicinal preparations from donor plasma.In recent years, the laboratory has been studying infectious complications in hematological cancer patients. The laboratory is well equipped with high-tech equipment, which allows conducting research at the most modern level.

In the report of V.N. Vavilov, associate professor of St. Petersburg State Medical University named after Pavlov, new data on the resistance of gram-negative bacteria detected in patients with neutropenia and in bone marrow recipients were presented. The report of prof. A.P. Kozlova, concerning the problems of the prevalence of HIV infection in Russia.He highlighted the widespread prevalence of infection in recent years and talked about his experience in developing an HIV vaccine. Ph.D. IV Volchek reported on the method he developed for personalized therapy of infectious and oncological diseases in humans.

Three sessions were devoted to the study of infectious complications in immunosuppression. At the session “Purulent-septic infections in immunosuppression”, the issues of the etiological structure of bacterial complications in hematological cancer patients were considered (report by M.Averyanova), reports of employees of the Department of Clinical Epidemiology of St. Petersburg State Medical Academy named after N.I. I.I. Mechnikova (Yu.S. Svetlichnaya, M.G. Dar’ina), as well as D.Sc. T.N.Suborova (VMedA). A.V. Schmidt (RosNIIGT) shared his experience in studying infectious complications when using central venous catheters in oncohematological patients. Kornienko M.N. (NIIEM named after Gamaleya, Moscow) spoke about the methods of diagnosing pneumocystis infection in hematological patients.

As usual, the session “Diagnostics, prevention and treatment of invasive mycoses” aroused great interest among the audience. Prof. N.N. Klimko and other employees of the N.N. Kashkin discussed various issues of studying invasive mycoses. N.P. Stizhak shared her experience in laboratory diagnostics of fungal infections at RosNIIGT. The issues of etiopathogenesis of viral infections in patients with immunosuppression were also considered. V.E. Karev (Research Institute of Children’s Infections, St. Petersburg) shared his experience of using pathomorphological research methods in the diagnosis of CMV infections.

The second day of the conference was devoted to the infectious safety of blood transfusions and various aspects of the study of herpesvirus infections. The session “Ensuring the infectious safety of blood transfusions” was opened by the report of prof. A.V. Chechetkina on the organizational aspects of fresh frozen plasma quarantine. V.E. Soldatenkov spoke about the need to improve the regulatory framework of the Blood Service. The rest of the reports were devoted to new technologies for ensuring viral and bacteriological safety of blood transfusions (employees of the GSPK SPb A.V. Volkov, D. S. Malysheva; RosNIIGT V. N. Chebotkevich, Yugorsk Research Institute of Cell Technologies, Khanty-Mansiysk, E.V. Korotaev; LLC “Pharmstandard”, Moscow, VB Yakimenko). The issues of blood transfusion transmission of hepatitis and HIV were also considered.

A special session was devoted to the use of molecular biological methods for the indication of pathogens. D.Sc. A.A. Yelov spoke about new trends in the technology of detection and identification of bacteria by PCR. N.S. Egorov (Moscow) reported on the prospects for the use of new generation sequencers in hematology and the Blood Service.

The conference also paid attention to the development of new technologies for inactivation of pathogens in hemocomponents. 3 reports were devoted to this problem. N.P. Sivakova pointed to the prospects of studying the antiviral and antibacterial activity of fullerenes. Marcia da Silva Cardoso (Belgium) shared her experience of using the Mirasol system to improve the safety of blood transfusions. AI Kostin touched upon the economic and legal aspects of inactivation of pathogens in hemocomponents.

Traditionally, great interest was aroused by the session “Herpesvirus infections in immunosuppression”, which was conducted by prof. V.A. Isakov. At the session, 7 reports were presented concerning the treatment of herpesvirus infections, diagnosis (E.V. Sharipova, St. Petersburg; D.S.Tikhomirov, T.A.Garanzha, State Scientific Center, Moscow) and the organization of medical care for these patients (M.V. , Samara).

In conclusion, a general discussion was held, in which, along with other issues, the need to develop regulatory documents governing the work of the Russian Blood Service was especially emphasized.

A report on the materials of the conference was prepared by
Deputy Director for Research and Development of the Russian Research Institute of Hematology and Transfusiology
Professor S.S. Bessmeltsev

90,000 Testing for coronavirus – get tested at an affordable price in Surgut

Blood for antibodies to COVID-19 can be donated in three departments of “Naj” on a first come, first served basis:

  • st. S. Bezverkhova, 3/7, Laboratory
    Monday-Friday 8: 00-15: 00
    Saturday 8: 00-12: 00
  • st.Melik-Karamova, 76V, Consultative and diagnostic department
    Monday-Friday 8: 00-12: 00
    Saturday 8: 00-12: 00
  • Tyumensky tract, 6, Center of plastic surgery
    Monday-Saturday 8: 00-12: 00

Validity of analysis results:

  • for antibodies to COVID-19 – set by the requested party
  • PCR test for COVID-19 – 72 hours.

For reliable and complete diagnosis, the study is carried out according to three methods:

Rapid ICA test (immunochemical analysis)

Detects IgG / M antibodies in the blood. Detection of IgM antibodies indicates recent infection. The presence of IgG antibodies in the blood indicates that you have already had this infection. They are produced about two weeks after the onset of the disease.

Biomaterial for analysis: capillary blood (finger sampling).

Preparation for analysis: taking a biomaterial on an empty stomach or not earlier than 4 hours after eating and drinking.

Results readiness time: 15 minutes.

ELISA diagnostics (enzyme-linked immunosorbent assay)

Determines IgG / M antibodies in the blood to the infectious agent.The presence of IgM antibodies indicates that a person is sick at the moment. IgG antibodies will clarify whether you have had a coronavirus infection in the past.

Biomaterial for analysis: venous blood (collection from a vein).

Preparation for analysis: taking a biomaterial on an empty stomach or not earlier than 4 hours after eating and drinking.

Results readiness period: up to two working days, excluding the day of taking the biomaterial.There is a possibility of urgent testing with the result in one working day.

PCR Testing

This “gold standard” of diagnostics is aimed at detecting the RNA of the virus and is guaranteed to confirm the presence or absence of coronavirus infection here and now in a particular person. The analysis is necessary to obtain a laboratory test result according to the form approved by Rospotrebnadzor.

Biomaterial for analysis: swab from the nasopharynx and oropharynx.

Preparation for analysis: taking a biomaterial on an empty stomach or not earlier than 2 hours after eating and drinking; before rinsing and irrigation with medicines. It is not recommended to use all types of local forms of drugs 24 hours before taking the material. The material is taken before hygiene procedures (brushing teeth, rinsing the mouth, instilling any substances into the nasal passages. It is necessary to exclude the intake of alcohol.

Results readiness period: up to two working days, excluding the day of taking the biomaterial. There is a possibility of urgent testing with the result in one working day.

PCR testing for a new coronavirus infection is carried out by appointment by phone (3462) 771-003.

Please note that the sampling of tests is not carried out with antiviral treatment or signs of SARS.You must have a protective mask and passport with you.

Blood composition – Regional blood transfusion station

Blood composition

Blood consists of 4 main components:

  • red blood cells – erythrocytes that transport oxygen from the lungs to human organs;
  • white blood cells – leukocytes responsible for fighting off infections that attack the body;
  • platelets – platelets that ensure blood clotting, thereby protecting the body from fatal blood loss from injuries and cuts.

All these cells are suspended in blood plasma, which is not only a transport medium for blood cells, moving them through the human body, but also contains proteins and salts necessary for the body.

Red blood cells – erythrocytes

Red blood cells perform one of the important functions of blood. A drop of blood contains millions of red blood cells, which constantly circulate through the blood vessels, delivering oxygen to the organs and removing carbon dioxide formed during cellular respiration.

Red blood cells are called red blood cells because they contain the protein hemoglobin, which is a bright red color. It is hemoglobin that carries oxygen and carbon dioxide. When blood passes through the lungs, oxygen molecules attach to hemoglobin, which carries it to every cell in our body. Having freed from oxygen, hemoglobin attaches to itself carbon dioxide molecules. In the lungs, carbon dioxide is released and excreted through respiration from the body.

The average life of an erythrocyte is 120 days.The bone marrow constantly produces blood cells, replacing their natural loss.

White blood cells – leukocytes

Leukocytes perform protective functions, as soon as an infection enters the body, white blood cells – leukocytes – enter the case. Leukocytes are constantly on guard. Some white blood cells (lymphocytes) produce protective antibodies – proteins that neutralize or destroy viruses and disease-causing bacteria.

The life cycle of leukocytes is relatively short – from several days to several weeks.One cube of blood of a healthy person contains from 4 to 8 thousand leukocytes. If the body is fighting an infection, this number may increase. A constant too large or too small number of leukocytes in the blood may indicate the presence of serious diseases.

Platelets

A person is very difficult to endure massive blood loss. However, our body has a mechanism that protects it from blood loss, and platelets play a major role in this mechanism.

Platelets are irregularly shaped, colorless little bodies circulating in the blood. They have the ability to form clots (blood clots) that stop bleeding.

If bleeding begins, platelets collect at the wound and try to block the bleeding. Calcium, vitamin K, and the protein fibrinogen help platelets to form a clot that closes a bleeding vessel. As it dries, the clot hardens, forming the well-known “crust”.

Plasma

Plasma is a transparent, straw-colored liquid, composed of 90% water, and is an extremely important component of blood.

In addition to water, plasma contains (approximately 1% by volume) dissolved salts of calcium, potassium, phosphoric acid, sodium. Proteins make up about 7% of the plasma volume. Among them is fibrinogen, which is involved in blood clotting. Plasma contains glucose as well as other nutrients and breakdown products.

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