Did you know that hepatitis C and malaria can coexist

Hey, everyone..

I will now share a topic that often does not occur as often as other clinical entities, and that its medical diagnosis and management is a challenge.

As we know, malaria is the parasitic disease that needs a vector in this case the bite of the mosquito of the genus Anopheles carrying Plasmodium with its infectious form to be able to replicate in man and cause disease.

Currently, more than 150 thousand species of Plasmodium have been described, but only 4 are capable of generating disease in man, and these are: Plasmodium falciparum, Plasmodium vivax, Plasmodium malariae and Plasmodium ovale.

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In this last decade, cases of malaria caused by Plasmodium knowlesi have been reported, being a species previously exclusive to the macaque monkey, but in areas that are the habitat of this animal and that have been populated by man, this parasite has taken on the capacity to take man as a host and generate the disease.

Although, this pathological entity by itself, has generated a high rate of incidence and mortality is the result of a failure in the treatment, by mixed infections, the immunological state of the host in this case the man, and by failures in the epidemiological system in the prevention of this disease.

Now, associated to the Hepatitis "C" Virus (HCV), which is originated by a totally different etiological agent, being this an RNA virus of the Hepacivirus genus from the Flaviviridae family. Its mechanism of transmission is more complex in relation to other hepatitis viruses such as HAV and HBV, it reaches the hepatocyte where it replicates through blood transfusions, intravenous drugs, reuse of non-sterile syringes, sexual relations, among others.

The present clinical case, was brought with the purpose of making known that it is possible and viable the coexistence of these pathological entities, despite being totally different etiological agents has in common its reproduction cycle for life as it is the hepatocyte.

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Clinical case

A 30-year-old male patient, with no significant pathological history, is admitted to the emergency unit. He started the current disease approximately 2 months ago, characterized by unquantified heat waves without a predominant time schedule, preceded by chills, which partially subsided with common antipyretics, accompanied by frontal headache of strong intensity, of oppressive character, retro ocular pain and photophobia, likewise it is associated finally with liquid evacuations in number of 4 per day, without mucus, without blood, in view of symptomatology it is taken to the emergency where it is admitted, for 18 days during its intrahospital evolution multiple paraclinical studies are requested. He was treated for 3 days with metronidazole and ceftriaxone for 8 days, plus an animal-based scheme for 3 days. He is then discharged with clinical improvement. After one week, the feverish picture reappears with 39º C without prevalence of time, preceded by shivers, which partially disappears with common antipyretics, concomitant asthenia, hyporexia, and he is admitted again.

Some important patient history:

Denies MD, ATH, previous blood transfusions and surgery.

Asthma since childhood.

Helicobacter pylori at age 21, receives tto for more than 6 months unspecified.

Tattoo on right arm in 2016.

Chikungunya in 2015 without complications.

Habits:

Non-smoker, occasional wineballs, caffeine 1 cup a day. I consume a sweet called "chmio" which has a high alcohol content 1 pack every 3 days from the age of 12.

Occupation: Mechanical Engineer.

heterosexual: 10 couples during his life.

Functional test:

Loss of 12 kg in 2 months.

Fever with current illness, night sweats, denies tremors.

Frontal headache, denies photophobia.

Left nasal polyp diagnosed in childhood, not documented.

Denies manifestations of bleeding.

Denies dyspnea, coughing, palpitations.

Daily Bristol 5 evacuation pattern, no mucus, no blood, number one.

Refers to nocturia, spurt and retained voiding volume.

Generalized arthralgia to predominance of lower limbs.

Denies convulsions.

Physical Entrance Examination:

SV: TA: 100/40mmHg.

Heart rate: 79 bpm.

Breathing rate: 18rpm.

Patient Stable Clinical Conditions, afebrile to touch, hydrated, eupneic, skin and mucous membrane colored, tolerating oral, and ambient oxygen. Normocephalic skull, isocoric pupils reactive to light. Mobile neck without adenopathies.

Symmetrical thorax, normo-expanding, RsCsRs without presence of murmur, audible breathing sounds in both hemi thorax, no added auscultation.

Painful depressible soft abdomen on superficial and deep palpation in right hypochondrium, RsHsAS present with mild hepatosplenomegaly.

Symmetrical extremities without edema. Neurological: conscious oriented in time, space and person.

^{Public domain Wikipedia}

Relevant paraclinic of the 1st hospitalization:

White beads 5000.

Segmented 65%.

Lymphocytes 38%.

Hemoglobin 8.

Platelets 91,000.

Urea 21.

creatinine 0.8.

Glutamic oxalacetic transaminase 202.

Transaminase of enzyme group present 180.

Serologies

Elisa's HIV IV generation negative.

VDRL negative.

Febrile antigens negative.

Dengue IgM and IgG negative.

Thick drop on three occasions, one positive for P. falciparum. He is treated with Artemether + Lumefantrine at a rate of 4 tablets (dose corresponding to his weight) every 12 hours for 3 days together with Primaquine at a dose of 0.50mg /kg/ single dose. The patient's clinical and laboratory condition improves and he is discharged.

However, he presents again 8 days after his discharge, fever, headache, myalgia and arthralgia, so he is reevaluated and admitted.

Paraclinic of 2nd hospitalization.

White beads 4700.

Segmented 66%.

Lymphocytes 23%.

Hemoglobin 7.3.

Platelets 94,000.

Urea 30.

Creatinine 0.9.

Glutamic oxalacetic transaminase 129.

Transaminase of enzyme group present 98.

Alkaline phosphatase 43.

Lactate dehydrogenase 577.

Globular sedimentation rate 45.

C-reactive protein test: Positive.

Serologies

HIV negative.

HBV anti-core negative.

HBV Surface Antigen: Negative.

HCV positive.

Thick drop in 7 occasions, evidencing in the 2 positive thick drop control for P. falciparum. It was decided to start treatment again in animals.

Uroanalysis, within normal parameters.

Coproanalysis, no parasitic elements are observed.

Ultrasounds in 2 opportunities

1st Report mild hepato-plenomegaly.

2nd elaborated by the Gastroenterology service: Hepatic Steatosis grade I Splenomegaly.

Intrahospital evolution

Patient who during his intrahospital evolution, remains feverish, quantified in 38.The first two weeks, at the time of admission, third generation cephalosporin was indicated, but without criteria it was omitted on the fourth day. A paraclinic was performed in search of an infectious focus or the cause of the feverish picture, among which a blood biometry was requested, which was evaluated by the hematology service where red blood cells were found to be parasitized.

Physical examination showed hepato-plenomegaly, and with a negative first large drop, a GRL evaluation was requested for ultrasound, where grade I hepatic steatosis and splenomegaly were reported.

The patient, after completing the animalarium scheme, showed a feverish peak, with evident focus of skin and soft tissues (phlebitis at the site of venipuncture), which resolved with topicals. The patient is discharged from the hospital with satisfactory outpatient gastroenterology and internal medicine controls.

Clinical case discussion

It is interesting to note that this patient was initially diagnosed with Dengue Fever on his first hospitalization, with signs of alarm due to both symptoms and paraclinical admission, with a torpid intrahospital evolution associated with enteral disease due to liquid evacuation for more than 10 days, as well as nosocomial respiratory infection, multiple pathological entities, which were treated together with a thick drop positive for P. falciparum.

It is very probable that in this first opportunity that the patient receives animal treatment, he attended with enteral picture given by liquid evacuations of more than 5 per day accompanied by nausea and vomits, therefore, the absorption and excretion of drug was not the correct one being evidenced only a partial improvement with a minimum load of parasites nondetectable in the control drop.

Physiopathology

As mentioned above, both the malaria parasite and the hepatitis C virus require the hepatocyte to fulfill part of their life cycle.

^{Life Cycle of the Malaria Parasite. Public domain wikipedia}

In relation to Malaria, this etiological agent needs two hosts to complete its complete cycle, in this case Anopheles (mosquito) and Man who is the accidental host.

Once the Plasmodium completes its cycle in the host, its infectious form lodges in the salivary glands of the mosquito which is inoculated during the bite, this enters the bloodstream in the form of sporozoites and goes to the hepatocyte, and according to the infectious species, it can continue its replication and transform into merozoites or remain in latent form as hypnozoites, only in the case of P. Vivax and Ovale. Once it leaves the hepatocyte it goes to the erythrocyte and becomes a trophozoite.

In relation to HCV it also cycles in the hepatocyte, and that both Plasmodium and this virus bind to the hepatocyte through membrane receptors sharing one in common as is CD-81, generating greater competition and severity of the disease by excessive increase with the need to replicate and take more easily the union to the hepatocyte, causing competition and severity of the disease.

Diagnosis and treatment

The diagnosis is simple for both diseases, in the case of malaria it is done by means of a direct smear examination under the microscope or also called coarse drop, it is the standard gold.

The hepatitis C virus is serological (antigens of HCV) simple and rapid and if positive we must request the viral load (RNA) of the same to determine whether to initiate treatment or not. It is advisable to complement the paraclinic with ultrasound, tomography if necessary and even liver biopsy, where the diagnosis is uncertain.

Regarding treatment, for malaria it will depend on the species observed in the thick drop and its presentation if it is uncomplicated or complicated malaria.

Finally, HCV can remain asymptomatic for years and even decades to generate disease, with more than 80% of cases originating from liver cirrhosis and hepatocarcinoma. Those cases of acute presentations or with high viral load should begin treatment.

Conclusion

Both malaria and HCV are diseases that represent a global health problem, and their coexistence generates atypical and cumbersome presentations of these medical entities.

We must bear in mind that the liver is the target organ, both for the plasmodium parasite and for the hepatitis C virus, which is why its function must be constantly monitored, by means of laboratory tests, (TGO, TGP, Bilirubins, GGT, coagulation times, glycaemia, proteins, among others) and the patient's clinic that make us think of liver failure.

In view of all the above, the need arises to diagnose on time, treat correctly, avoid complications that may be generated and preserve the life of the patient.

Sources:

^_link

^{Human Infections and Detection of Plasmodium knowlesi Balbir Singhcorresponding authora and Cyrus Daneshvarb._link}

^{Why do we need to know more about mixed Plasmodium species infections in humans?. Peter A. Zimmerman, Rajeev K. Mehlotra, Laurin J. Kasehagen, and James W. Kazura_link}

^{Malaria Parasite Liver Infection and Exoerythrocytic Biology Ashley M. Vaughan and Stefan H.I. Kappe_link}

^{Biology of Human Malaria Plasmodia Including Plasmodium Knowlesi Spinello Antinori, Laura Galimberti, Laura Milazzo, and Mario Corbellino_link}

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^{The Origin of Hepatitis C Virus. in Current topics in microbiology and immunology 369:1-15 · March 2013_link}

^{The history of hepatitis C virus (HCV): Basic research reveals unique features in phylogeny, evolution and the viral life cycle with new perspectives for epidemic control_link}

^{Hepacivirus C_link}

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Dr. Ana Estrada

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