Viral |
Influenza |
Respiratory |
Yes |
IFN induced overexpression of
ACE2 triggered by influenza virus aids SARS-CoV-2 infection
(Suwanwongse & Shabarek, 2020). |
Influenza co-infection can provoke COVID-19 hyper-inflammatory states.
Higher incidence of acute cardiac injury was reported
(Ma, Lai, Chen, Tu, & Qin,
2020) |
|
HBV |
Body fluid |
Yes |
Increased liver tissue damage and
inflammatory responses due to COVID-19 may aid HBV co-infection by
overexpressing host cell receptors (Wu,
Song, Cao, & Li, 2020). It may also fuel the reactivation of
pre-existing chronic HBV
(Lozano-Sepulveda, Galan-Huerta,
Martínez-Acuña, Arellanos-Soto, & Rivas-Estilla, 2020). |
Elevation of
ALT, AST, TBIL, ALP, and γ-GT. (Zou et
al., 2020) Higher risk of liver injury.
(Y. Lin et al., 2020) |
|
Dengue |
Mosquito bite |
No |
NR |
Increase the severity of symptoms
(Verduyn et al., 2020). Decrease in
white blood cell, neutrophils, lymphocytes and platelets count and
eventual higher mortality rate (Saddique
et al., 2020) |
|
HIV |
Body fluid |
Yes |
Suppression of T lymphocyte mediated immunity
(as observed in HIV patients) leads to the prognosis of increased
disease severity and higher mortality rate during COVID-19 co-infection
(Xu et al., 2020). |
HIV Patients under
ART exhibits mild COVID-19 symptoms. But ART-naïve patients show acute
COVID-19 clinical representation (Hu, Ma,
Huang, & Vermund, 2020). Higher maximum body temperatures, longer
duration of fever and longer improvement time of chest CT image was
reported due to co-infection (R. Yang et
al., 2020) |
|
HCV |
Body fluid |
Yes |
Both SARS-CoV-2 E and HCV p7 proteins can
form similar ion channels which ensure their success in attacking their
host and effective replication during co-infection
(Alothaid, Aldughaim, El Bakkouri,
AlMashhadi, & Al-Qahtani, 2020). |
The actual outcome is not reported
till date. It has been speculated that some investigational COVID‐19
drugs may adversely affect the HCV‐related decompensated cirrhosis
patients (Reddy, 2020). |
|
Rhinovirus |
Respiratory |
Yes |
Major disease-causing rhinovirus
serotype HRV-A16 infection upregulates ACE2 and TMPRSS2 expression in
epithelial cells by inducing by IFNb1. This event facilitates SARS-CoV-2
transmission and further disease severity
(Murphy et al., 2020) |
One case has been
reported in a young patient expressing critical illness as the outcome
of co-infection (Orozco-Hernández,
Montoya-Martínez, Pacheco-Gallego, Céspedes-Roncancio, &
Porras-Hurtado, 2020) |
|
Adenovirus |
Respiratory |
Yes |
Similar ion channel forming
capability of SARS-CovV-2 E and Adenovirus 6K proteins facilitates
co-infection (Alothaid et al., 2020) |
Unfavorable prognostic outcome including ARDS
(Motta & Gómez, 2020) |
Bacterial |
Streptococcus pneumoniae |
Respiratory |
Yes |
Opportunistic normal flora of human upper respiratory track |
Severe
respiratory distress followed by pleural effusion and necrotizing
pneumonia (Nieto‐Moro et al., 2020),
higher mortality rate (Rodriguez-Nava et
al., 2020) |
|
Staphylococcus aureus
|
Respiratory/
Digestive/ Contact
|
Yes
|
Opportunistic normal flora of human upper respiratory track, gut mucosa
and skin
|
Necrotizing pneumonia (Duployez et al.,
2020).
Bacteremia and higher mortality (Cusumano
et al., 2020)
|
|
Pseudomonas aeruginosa |
Contact |
Yes |
Opportunistic pathogen
causing HAI mostly related with poor hygiene, mechanical ventilation and
urinary catheterization. |
NR |
|
Acinetobacter baumannii |
Contact |
Yes |
Mechanical
ventilation |
NR |
|
Klebsiella pneumoniae |
Respiratory/ Contact |
Yes |
Opportunistic normal flora of human mouth, skin, and intestines |
Fatal
sepsis (Hosoda et al.,
2020) |
|
Mycoplasma pneumoniae |
Respiratory/ contact |
Yes |
NR |
Severe pneumonia (Oliva et al., 2020).
Increased morbidity, mortality and disease severity
(Amin, McKitish, & Shah,
2020) |
|
Clamydia pneumoniae |
Respiratory/ contact |
Yes |
NR |
Severe
pneumonia (Oliva et al.,
2020). |
|
Legionella pneumophila |
Digestive/ Respiratory |
Yes |
NR |
Elevated aspartate aminotransferase, blood urea nitrogen, creatinine,
lactate dehydrogenase and C-reactive protein
(Arashiro et al., 2020) |
|
Haemophilus influenzae |
Respiratory/ contact |
Yes |
Opportunistic normal flora of human upper respiratory track |
NR |
|
Neisseria meningitides |
Respiratory/ contact |
Yes |
NR |
Convulsion (Moriguchi et al., 2020),
elevated C-reactive protein, headache, neck stiffness, rigors,
confusion, and a new purpuric rash over hands and feet
(Gallacher & Seaton,
2020) |
|
Mycobacterium tuberculosis |
Respiratory |
Yes |
Cytokine storm
produced by COVID-19 may reactivate latent TB or boost the development
of active TB. Lung damages caused by TB may also escalate the disease
severity caused by SARS-CoV-2
(Crisan-Dabija et al., 2020). |
Co-infection is associated with disease severity and disease progression
rate (Liu et al., 2020). 2.17 times
higher risk-of-death and 25% lower risk-of-recovery was reported. Also
shorter time-to-death and longer time-to-recovery was found
(Sy, Haw, & Uy, 2020). |
Fungal |
Aspergillus spp.
|
Respiratory |
No |
Pro-inflammatory cytokines (especially IL-6 and IL-10 released during
COVID-19 results in tissue necrosis and ARDS, which eventually makes
patient more vulnerable to Aspergillosis
(Lai & Yu, 2020). |
Invasive pulmonary
aspergillosis, higher case fatality rate (64.7% reported)
(Lai & Yu, 2020) |
|
Candida spp.
|
Perinatal/ Contact |
No |
Opportunistic
pathogen found in human skin. |
Candidemia and increased mortality rate
(Al-Hatmi, Mohsin, Al-Huraizi, & Khamis,
2020). |