Type of co-infection Co-pathogens Route of transmission Person to person transmission Possible Mechanism of co-infection and pathogenesis Possible Outcomes
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).